Textbook of Obstetrics

Textbook of
Obstetrics
Textbook of
Obstetrics
Second Edition
Edited by
Sudha Salhan
MBBS (Hons), MD (Obstetrics and Gynecology)
PGDMCH (NIHFW), CIC (IGNOU)
Professor
NDMC Medical College and Hindu Rao Hospital, Delhi
Former Professor and Head
Department of Obstetrics and Gynecology
Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi
E-mail: [email protected]
Foreword
Dr Anusuya Dass
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Textbook of Obstetrics
First Edition: 2007
Second Edition: 2016
ISBN: 978-93-85891-79-3
Printed at
Dedicated to
My patients
List of Contributors
Achla Batra Harish Chellani
Professor and Consultant Professor and Consultant
Department of Obstetrics and Gynecology Department of Pediatrics
Vardhman Mahavir Medical College and Safdarjung Hospital Vardhman Mahavir Medical College and Safdarjung Hospital
New Delhi New Delhi
Anil Kumar Jain Harsha Gaikwad
Consultant Professor
Department of Obstetrics and Gynecology Department of Obstetrics and Gynecology
New Delhi New Delhi
Anshula Gupta HP Anand
Former Senior Resident Associate Professor and Consultant
Vardhman Mahavir Medical College and Safdarjung Hospital Department of Obstetrics and Gynecology
New Delhi Vardhman Mahavir Medical College and Safdarjung Hospital
Anukriti Verma New Delhi
Senior Resident Indira Ganeshan
Department of Psychiatry
Director
Vardhman Mahavir Medical College and Safdarjung Hospital
IRENE IVF Centre
New Delhi
Safdarjung Enclave, New Delhi
Ashok Khurana
Director
Ipsita Ray
The Ultrasound Laboratory Lecturer
Defence Colony, New Delhi Department of Pharmacology
MGM Medical College, Mumbai
Banashree Das
Professor and Consultant JB Sharma
Department of Obstetrics and Gynecology Professor
Vardhman Mahavir Medical College and Safdarjung Hospital Department of Obstetrics and Gynecology
New Delhi All India Institute of Medical Sciences, New Delhi
BD Hasija Jyotsna Suri

Former Consultant Senior Specialist and Associate Professor
New Delhi New Delhi
Deepali Garg Kavita N Singh

Assistant Professor Associate Professor
NDMC Medical College and Hindu Rao Hospital, New Delhi NSCB Government Medical College, Jabalpur, Madhya Pradesh
Dheeraj Deo Bhatt Mahua Maiti

Assistant Professor Former Senior Resident
Department of Pediatric Cardiology Vardhman Mahavir Medical College and Safdarjung Hospital
Ram Manohar Lohia PGIMER, New Delhi New Delhi
Divya Pandey Manjula Sharma

Assistant Professor Consultant and Professor
New Delhi New Delhi
viii Textbook of Obstetrics
Matthews Mathai PK Shah

Former Professor Professor
Christian Medical College and Hospital, Vellore Lokmanya Tilak Municipal General Hospital
Mumbai
Meenakshi B Chauhan
Professor PK Verma
Department of Obstetrics and Gynecology Professor and Consultant
PG Institute of Medical Sciences Department of Anesthesia
Rohtak, Haryana Vardhman Mahavir Medical College and Safdarjung Hospital
New Delhi
Meenakshi Bhatt
Assistant Professor and Specialist Poonam Goel
Department of Pediatrics
Professor
New Delhi
Government Medical College
Meetu Salhan Chandigarh
Medical Officer Pratima Mittal
Professor and Consultant
New Delhi
Navneet New Delhi
Former Senior resident
Puja Jain
Government Medical College
Former Senior Resident
Chandigarh
Niharika Dhiman New Delhi
Assistant Professor
Rahul Manchanda
Maulana Azad Medical College, New Delhi Consultant Gynecologist
Former Senior Resident
Nivedita Sarda Vardhman Mahavir Medical College and Safdarjung Hospital
Professor New Delhi
Dr Baba Saheb Ambedkar Medical College, New Delhi
Rajesh Kumari
Specialist
NS Sardeshpande Department of Obstetrics and Gynecology
Consultant CGHS Hospital RK Puram, New Delhi
Lokmanya Tilak Municipal General Hospital, Mumbai Rajesh Rastogi
Consultant
Padmabati Rath Department of Obstetrics and Gynecology
Documentation Officer Vardhman Mahavir Medical College and Safdarjung Hospital
National Institute of Social Defence, New Delhi New Delhi
Pikee Saxena Rajesh Uppal

Professor Radiologist
Department of Obstetrics and Gynecology Uppal Diagnostics
Lady Hardinge Medical College and Suchitra Kripalani Hospital South Extension, New Delhi
New Delhi
Rekha Bharti
Pinkee Saxena Assistant Professor
Pool Officer Department of Obstetrics and Gynecology
Department of Obstetrics and Gynecology Vardhman Mahavir Medical College and Safdarjung Hospital
Vardhman Medical College and Safdarjung Hospital, New Delhi New Delhi
List of Contributors ix
Renuka Sinha Smiti Nanda

Professor and Head of the Department Senior Professor and Head of the Department
Rama Medical College, Ghaziabad (UP) PG Institute of Medical Sciences
Rohtak, Haryana
Reva Tripathy
Sonia Ghumman
Director–Professor
Senior Medical Officer
CGHS
MAM College and LNJP Hospital Chandigarh
New Delhi
Sonia Malik
Ritu Sharma Director
Assistant Professor Southend Infertility and IVF Centres, New Delhi
NDMC Medical College and Hindu Rao Hospital Sudha Salhan
New Delhi Former Professor and Head
Ruchi Arora Sachdeva Vardhman Mahavir Medical College and Safdarjung Hospital
Assistant Professor New Delhi
Department of Respiratory Medicine
ESI, Faridabad Medical College Sugandha Arya
Faridabad, Haryana Assistant Professor and Specialist
Ruchi Kapoor Vardhman Mahavir Medical College and Safdarjung Hospital
Assistant Professor New Delhi
Department of Anesthesia
Ram Manohar Lohia PGIMER
Sunita Malik
New Delhi Professor and Consultant
Sangeeta Tripathi Vardhman Mahavir Medical College and Safdarjung Hospital
New Delhi
Professor
Department of Radiology
Sunita Seth
Superspeciality Pediatrics Hospital and Postgraduate Institute
Specialist
Noida
Deen Dayal Upadhyay Hospital, New Delhi
Sanjay Gupte
Director Sunita Singal
Gupte Hospital NFSG
Pune Vardhman Mahavir Medical College and Safdarjung Hospital
New Delhi
Simmi Chopra
Senior Consultant Usha Gupta
Department of Obstetrics and Gynecology Professor
Mata Chanan Devi Hospital Department of Obstetrics and Gynecology
New Delhi ESI, Faridabad Medical College
Faridabad Haryana
SK Sen
Former Senior Specialist Vasantha Muthuswamy
Vardhman Mahavir Medical College and Safdarjung Hospital Former Senior Deputy Director General
New Delhi Indian Council of Medical Research, New Delhi
Foreword
I have the pleasure of going through the book Textbook of Obstetrics by Dr Sudha Salhan. During the last two decades,
there have been tremendous advances in the field of Medical Sciences. This comprehensive book is fully updated for
undergraduates, postgraduates and practitioners. This textbook is truly the work of many obstetricians under the expert
guidance of Dr Sudha Salhan. While preparing the text, the contributors and the editor have utilized their experience and
information received from a large number of students and teachers.
This book has additional new features such as counseling, ethics, medicolegal problems related to obstetrical issues.
Therefore, the book is very informative and useful for the doctors dealing with obstetric cases. I earnestly hope all these
will enhance the utility of this book for the students as well as for the practitioners. All procedures have been explained in
simple manner.
I am confident that after reading this book, students will develop special interest in Obstetrics and would like to take up
postgraduation in the subject.
I wish Dr Sudha Salhan and this book all success.
Dr Anusuya Dass
Former Principal
Lady Hardinge Medical College
New Delhi
Preface to the Second Edition
Since, the first edition many new techniques have been developed and outmoded procedures are dropped from clinical
practices. Therefore, an updated edition was required. This new edition is fully updated as well as new chapters have been
introduced for the first time (contraception) with new illustrations and images. New horizons are giving us the insights into
the abnormalities of reproductive functions in females by ongoing relentless research.
I hope this new edition will be of great help to our obstetricians, especially the students.
I am grateful to the experienced contributors for devoting their precious time for updating their chapters. I am also
thankful to Mr Jitendar P Vij (Group Chairman), Mr Ankit Vij (Group President), Ms Chetna Malhotra Vohra (Associate Director
Content Strategy), Dr Madhu Choudhary (Senior Content Strategist), Ms Nitasha Arora (Project Manager) for all their help
and support.
Sudha Salhan
Preface to the First Edition
This is a Textbook of Obstetrics with emphasis on recent advances counseling, medicolegal aspects and ethics. In this fast
mechanised world, the art of talking to the patient is fast disappearing. Therefore, a chapter on counseling is included
in the book. We must also be aware of the legislations pertaining to our subject. With this end in mind, a chapter on the
‘Medicolegal Aspects of Obstetrics’ has been written. Other often neglected but important topics which are discussed in
detail are Ethics and the Disposal of Biomedical Waste. Much of the Obstetric morbidity and mortality can be averted in
women embark on pregnancy after controlling medical ailments; hence, a separate chapter on ‘Preconceptional Check-
up’ is incorporated in this book. Finally, it is important to know about the importance given to pregnant women by the
Government of India. This book will update students on the recent endeavours of the Government to alleviate the suffering
of women by various schemes. Overall, this book will provide a comprehensive and up-to-date picture of the interesting
subject of Obstetrics.
The contributors are seasoned obstetricians dealing with obstetrical cases day in and day out. I thank them all for sparing
time from their busy schedule. I offer special thanks to Mrs Jayshree for the tying and related work. I also thank Dr Harsh
Gaikwad for actively helping me in all aspects of this book. I also thank my family for their unstinted support.
Sudha Salhan
Contents
Section 1 Basics of Obstetrics
1. Evolution of Obstetrics..............................................................................................................................................................................................................3
Sudha Salhan
2. Anatomy of Female Genital Tract...........................................................................................................................................................................................7
Sudha Salhan
3. The Bony Pelvis.......................................................................................................................................................................................................................... 24
Anil Kumar Jain, Sudha Salhan
4. Fetus and Fetopelvic Relations............................................................................................................................................................................................ 31
5. Patient-Doctor Communication.......................................................................................................................................................................................... 37
Sudha Salhan, Jyotsna Suri
6. History-taking and Examination of the Pregnant Patient.......................................................................................................................................... 42
Sunita Malik, Sudha Salhan
Section 2 Normal Pregnancy

7. Physiology of Reproduction................................................................................................................................................................................................. 53
SK Sen, Meenakshi Bhatt, Harsha Gaikwad
8. Placenta, Umbilical Cord and Fetal Membranes............................................................................................................................................................ 60
Harsha Gaikwad, Sudha Salhan, Indira Ganeshan
9. Maternal Anatomical and Physiological Changes in Pregnancy............................................................................................................................. 73
Sudha Salhan
10. Immunology of Normal Pregnancy................................................................................................................................................................................... 85
Sonia Malik, Ritu Sharma, Sudha Salhan
11. Diagnosis of Pregnancy.......................................................................................................................................................................................................... 90
Sudha Salhan, Anshula Gupta, Indira Ganeshan
12. Antenatal Care (Antenatal Exercises and Nutrition During Pregnancy)............................................................................................................... 94
Sudha Salhan, Harsha Gaikwad, Padmabati Rath, Simmi Chopra
Section 3 Abnormal Pregnancy

13. Hyperemesis Gravidarum....................................................................................................................................................................................................117
Sudha Salhan
14. Spontaneous Miscarriage or Abortion including Habitual or Recurrent Miscarriage...................................................................................120
Sudha Salhan, Indira Ganeshan, Harsha Gaikwad
15. Ectopic Pregnancy..................................................................................................................................................................................................................133
Sudha Salhan
16. Gestational Trophoblastic Disease (GTD).......................................................................................................................................................................145
Sudha Salhan, Jyotsna Suri, Divya Pandey
17. Antepartum Hemorrhage....................................................................................................................................................................................................158
Harsha Gaikwad, Kavita N Singh, Sudha Salhan
18. Multifetal Gestation...............................................................................................................................................................................................................168
Sunita Singal, Sudha Salhan, Harsha Gaikwad
19. Preterm Labor and Premature Rupture of Membranes............................................................................................................................................181
Sudha Salhan, Sunita Singal
xviii Textbook of Obstetrics
20. Disproportional Fetal Growth............................................................................................................................................................................................191

Sudha Salhan, Meenakshi Bhatt
21. Intrauterine Fetal Death.......................................................................................................................................................................................................199
Poonam Goel, Sudha Salhan, Navneet
22. Prolonged Pregnancy............................................................................................................................................................................................................205
23. Abnormalities of Placenta, Cord and Amniotic Fluid Volume................................................................................................................................209
Section 4 Normal Labor

24. Mechanism of Parturition and Labor...............................................................................................................................................................................221
Sudha Salhan, Pratima Mittal, Niharika Dhiman, Divya Pandey
25. Onset and Stages of Parturition and Labor...................................................................................................................................................................229
Pratima Mittal, Sudha Salhan, Divya Pandey
26. Initial Assessment at Onset of Normal Labor...............................................................................................................................................................236
Pratima Mittal, Ritu Sharma, Sudha Salhan, Renuka Sinha
27. Conduct of Normal Labor....................................................................................................................................................................................................246
Pratima Mittal, Ritu Sharma, Sudha Salhan
28. Induction of Labor..................................................................................................................................................................................................................252
Usha Gupta, Sudha Salhan, Deepali Garg
29. Obstetric Analgesia and Anesthesia................................................................................................................................................................................259
PK Verma
Section 5 Abnormal Labor

30. Abnormalities of the Passage.............................................................................................................................................................................................269
31. Malpositions and Malpresentations................................................................................................................................................................................274
Rekha Bharti, Sudha Salhan, Harsha Gaikwad, Sunita Malik, Mahua Maiti, PK Shah, NS Sardeshpande
32. Labor Dystocia: Dysfunctional Labor..............................................................................................................................................................................306
33. Complications of Third Stage of Labor...........................................................................................................................................................................318
Reva Tripathy, Sudha Salhan
Section 6 Puerperium
34. Normal Puerperium...............................................................................................................................................................................................................331
Sudha Salhan, Meetu Salhan, Sugandha Arya, Padmabati Rath
35. Abnormal Puerperium..........................................................................................................................................................................................................349
Sudha Salhan, Nivedita Sarda, Divya Pandey
Section 7 Medical Disorders in Pregnancy

36. Preconceptional Counseling..............................................................................................................................................................................................357
Sudha Salhan, Meetu Salhan, Meenakshi Bhatt
37. Anemia in Obstetrics.............................................................................................................................................................................................................360
Sudha Salhan, JB Sharma, Divya Pandey, HP Anand
38. Pregnancy and Heart Disease............................................................................................................................................................................................378
Dheeraj Deo Bhatt, Sudha Salhan, Manjula Sharma
Contents xix
39. Diabetes and other Endocrine Disorders in Pregnancy............................................................................................................................................386

Smiti Nanda, Meenakshi Bhatt, Ritu Sharma, Meenakshi B Chauhan
40. Hypertension in Pregnancy................................................................................................................................................................................................398
Banashree Das, HP Anand, Sudha Salhan
41. Renal Disorders Complicating Pregnancy.....................................................................................................................................................................417
Sudha Salhan
42. Liver and Pancreatic Diseases in Pregnancy.................................................................................................................................................................420
Sudha Salhan, Divya Pandey
43. Respiratory Disorders in Pregnancy.................................................................................................................................................................................427
Ruchi Arora Sachdeva, Sudha Salhan
44. Rh-Isoimmunization in Pregnancy...................................................................................................................................................................................435
Sudha Salhan, Meenakshi Bhatt, Banashree Das
45. Alteration of Hemostatic System and Coagulation Disorders in Pregnancy.....................................................................................................444
Achla Batra, Sudha Salhan, Harsha Gaikwad
46. Thyroid Disease in Pregnancy............................................................................................................................................................................................450
Sudha Salhan, Divya Pandey, Sunita Seth, Meenakshi Bhatt
47. Neurological Disorders in Pregnancy..............................................................................................................................................................................458
Section 8 Infections in Pregnancy

48. HIV in Pregnancy.....................................................................................................................................................................................................................467
Sudha Salhan
49. Malaria in Pregnancy.............................................................................................................................................................................................................479
Sudha Salhan
50. Other Infections in Pregnancy...........................................................................................................................................................................................483
Sudha Salhan
Section 9 Special Conditions

51. Dermatological Problems in Pregnancy.........................................................................................................................................................................493
Sudha Salhan
52. Care of Pregnant Patient with Previous Cesarean Section......................................................................................................................................497
Sudha Salhan
53. Psychiatric Disorders in Pregnancy and Puerperium.................................................................................................................................................500
Rajesh Rastogi, Anukriti Verma
54. Gynecological and Surgical Disorders Associated with Pregnancy.....................................................................................................................503
Sudha Salhan
55. High-risk Pregnancies...........................................................................................................................................................................................................507
Sudha Salhan, Rajesh Kumari, Sonia Ghumman
56. Obstetrical Collapse...............................................................................................................................................................................................................511
Sudha Salhan, Divya Pandey, Pinkee Saxena
57. Asepsis and Antisepsis in Operation Theater...............................................................................................................................................................515
HP Anand, Sudha Salhan
Section 10 Operative Obstetrics

58. Minor Obstetric Procedures................................................................................................................................................................................................525
Sudha Salhan, Anshula Gupta, Harsha Gaikwad, Indira Ganeshan
59. Female Sterilization, Cesarean Delivery and other Emergency Obstetric Operations..................................................................................538
Sudha Salhan, Harsha Gaikwad, PK Verma, Puja Jain, Indira Ganeshan
xx Textbook of Obstetrics
60. Destructive Operations........................................................................................................................................................................................................559

Rahul Manchanda, SK Sen, Sudha Salhan
61. Interpreting Arterial Blood Gas Sample.........................................................................................................................................................................564
PK Verma, Ruchi Kapoor
Section 11 Routine and Special Investigations

62. Ultrasound, Doppler, MRI, CT-scan and X-ray in Obstetrics.....................................................................................................................................571
Rajesh Uppal, Ashok Khurana, Sudha Salhan, Sangeeta Tripathi
63. Prenatal Diagnosis and Fetal Therapy.............................................................................................................................................................................592
Sudha Salhan, Sunita Seth, Indira Ganeshan
64. Antepartum Fetal Surveillance..........................................................................................................................................................................................603
Nivedita Sarda, Jyotsna Suri, Sudha Salhan
65. Intrapartum Fetal Monitoring............................................................................................................................................................................................611
Sudha Salhan, Divya Pandey, Indira Ganeshan
Section 12 Neonatology
66. Neonatal Resuscitation.........................................................................................................................................................................................................623
Harish Chellani, Sugandha Arya
67. Newborn Examination and Common Early Neonatal Problems...........................................................................................................................630
Sugandha Arya, Harish Chellani
68. Care of Premature Newborn...............................................................................................................................................................................................637
Meenakshi Bhatt
Section 13 Contemporary Issues in Obstetrics

69. Medicolegal, PCPNDT and Bioethics...............................................................................................................................................................................641
Sudha Salhan, Sanjay Gupte, Vasantha Muthuswamy
70. Reproductive Morbidity and Maternal Mortality........................................................................................................................................................649
Sudha Salhan, Matthews Mathai, BD Hasija
71. Government Programs for Reproductive and Child Health....................................................................................................................................660
72. Biomedical Waste Management.......................................................................................................................................................................................665
Sudha Salhan
Section 14 Pharmacotherapeutics in Obstetrics

73. Clinical Pharmacology in Obstetrics................................................................................................................................................................................675
Pikee Saxena, Sudha Salhan, Meenakshi Bhatt, Ipsita Ray, Ritu Sharma
Section 15 Practical in Obstetrics

74. Obstetrics Instruments.........................................................................................................................................................................................................689
Sudha Salhan, Renuka Sinha
75. Obstetrics Forceps and Ventouse.....................................................................................................................................................................................698
76. Specimens in Obstetrics.......................................................................................................................................................................................................706
77. Contraception..........................................................................................................................................................................................................................711
Sudha Salhan
Index.................................................................................................................................................................................................................................................737
Section 1
Basics of Obstetrics
Section Outline
1. Evolution of Obstetrics
2. Anatomy of Female Genital Tract
3. The Bony Pelvis
4. Fetus and Fetopelvic Relations
5. Patient-Doctor Communication
6. History-taking and Examination of the Pregnant Patient
Sudha Sa/hon
1 Evolution of Obstetrics
various illustrated positions of the fetus in Temkin's edition

DEFINITION
of Soranus' Gynecology. Soranus knew that the fetus can
Obstetrics is the branch of medicine that concerns man- take up various positions in the uterus and he described
agement of women during pregnancy, childbirth and the them all. He prescri ed the qualities needed for a good
puerperium. midwife, like she had to have a good memory, love for her
work, be r ~ ectab e to her patients, be sound of limbs,
HISTORICAL EVOLUTION robust and enaowed with long slim fingers and short nails.
She should be free from superstitions.
History gives an account of the changes that have taken There are records of birthing stools, made of wood, in
place in obstetrics in many centuries. Hence, obstetrics is the old testament. The front of the seat was hollowed out
as old as mankind. into a semicircle and two upright wooden rods were affixed
The development of obstetrics possibly started in the on each corner of the front so that the woman could grasp
Indus valley about 5 million years ago. Figures of women them when pushing, in the second stage of labor while the
giving birth in sitting and kneeling positions are seen witH midwife stood in front.
a figure of the goddess of fertility. The husband as aalled Oribasius (325-403 AD) of Pergamum had a high
to cut the cord (husbands still do this in Brazil) l::l t no other reputation as an Obstetrician in Byzantium.
male is allowed in, especially in Egypt and the Mil:idle East. In Baghdad, the book Liber Helchavywritten by Rhazes
Drawings of 6000-1200 BC show women squatted on (850-923 AD) was devoted mainly to midwifery. Over
the ground or on bricks to deliver. Cabor stimulants like the next few centuries, European medicine gradually
salt, onions, oil, mint, incense, wine and even ground up re-emerged until 1316 AD.
scarabs and tortoise shells were used. The first cry of the
The knowledge of anatomy was based on that of the pig.
neonate had a great significance and the cord was cut only
Mundinus at Bologna wrote a book on human dissection.
after the midwife had washed the baby. Breastfeeding
He wrote that the uterus contains several cells but rejected
was universal. Pregnancy was diagnosed by the woman
the old Greek concept of wandering uterus.
urinating on a mixture of wheat and barley seeds with
Dissection was performed, particularly by Gabrielis
dates and sand. It was believed that if the grains sprouted,
she was pregnant. If only barley grows, a girl would be born Fallopio (1523-1562) and published as the anatomical
but if only wheat sprouted, a boy was in the womb. work. He described the fallopian tubes, connecting the
A variety of Goddesses were thought to protect and ovaries to the uterus. In the eleventh century, Trotula
help the woman in labor. In India, during 1000 BC to 500 wrote a book which was translated into English in the
AD, women had a high position. Their physical health fifteenth century. This book showed abnormal fetal
was treated as being as important as that of the men (500 positions. Richard of Salerno, in thirteenth century, wrote
BC-500 AD). It is possible that obstetrics started in India a book showing some pictures of female anatomy. Albert
and gradually moved to the West reaching Greece, Italy Magnus, a Dominican monk (1193-1280 AD) produced
and then Rome. Soranus wrote his Gynecology in Greek. the first printed work in Gynecology, giving comments on
This book was quoted by Muscio (or Mustio) around the secrets of women). De Graaf (1641-1673) was able to
300-500 AD and had a portion for midwives. There are describe ovaries with follicles. In 1513, Eucharius Ri:isslin
4 Textbook of Obstetrics
produced a book the ‘Rose Garden’ which was translated Charles White (1728–1813) of Manchester empha-
to English by Richard Jonas as, ‘The Byrth of Mankynde’ in sized the need for cleanliness to prevent puerperal sepsis.
1540. It remained the most popular textbook of midwifery Soranus of Ephesus (at the coat of Turkey) provided the
till late seventeenth century. Ambroise Pare (1510–1590) first anatomical description of the ovaries (98–138 AD).
of Paris was a greatly acknowledged Obstetrician. He Leonardo da Vinci (1452–1519) drew the anatomy of the
revitalized the idea of podalic version (internal). Hotel uterus and ovaries (Andre Levret).
Dieu in Paris started by Ambroise Pare, in fifteenth century Fielding Ould (1710–1789) was considered the first
became the most famous maternity unit in Europe and in important teacher in Obstetrics in Ireland. He introduced
the World. It is still functional. the left lateral position for delivery. Lying-in wards were
In England, Henry VIII in 1512, formed an Act to added in the hospital building in 1773. The hospital was
regularise midwifery practice. Obstetric forceps were later rechristened as the Queen Charlotte’s hospital.
developed but kept as a secret for 150 years by the Thomas Bull wrote the first book on antenatal care in the
Chamberlain family in 1598. Many other varieties of forceps nineteenth century. It sold 25 editions between 1837 and
were developed by Jacob Rediff Paltine, Douglas and others. 1877. Dr A Pinard of France was one of the first to advocate
During this period, the understanding of embryology the antenatal examination of the abdomen (1895). He
and reproductive anatomy was enhanced because of the favored induction of labor. He also designed the fetal
advent of the microscope. Other instruments to deliver stethoscope. The first antenatal patient hospital, was made
the dead fetus also developed, e.g. various forms of hooks, by Madame Bequet of Vienne (France) in 1892 in Hotel
vectis and different bandages of soft leather, linen, muslin, Dieu. It had less space hence two patients used to share
a bed (as seen in government hospitals in resource poor
etc. for application of traction on breech. Eighteenth
countries, like in our hospital, i.e. Safdarjung Hospital).
century saw the beginning of scientific obstetrics. William
The term puerperal fever was given by Edward Strother
Smellie (1697–1763) introduced varieties of the obstetrics
in 1716. Oliver Wendell Holmes (1809–1894) in 1843
forceps besides studying the effect of rickets on the pelvis.
pointed out that the disease was carried to the patient by
He also studied pelvic soft tissues.
her physician or nurse. Development of antiseptics and
William Harvey, of blood circulation fame, wrote on
discovery of antibiotics, besides the all important ‘hand
labor in De Partu (De Generatione Animalium). This is
washing’ helped reduce the maternal morbidity and
the first original English book on Obstetrics in which he
mortality. Florence Nightingale (1820–1910) emphasized
advised against unnecessary interference.
the importance of a good ventilation system. Gustav
Francois Mauriceau (1637–1709), a renowed obstet-
A Michealis (1798–1848) discovered true conjugate
rician of Paris, investigated the mechanism of labor and measurement.
devised a method for delivery the after coming head in Friedrich Trendelenburg (1899–1925) introduced the
breech. He also described brow presentation. He was, position of the patient which is now named after him.
perhaps the first, to advocate delivery in bed rather than on James Mathews Duncan (1826–1886) helped formulate
a birth stool. He emphasized greatly on hygiene in his book. management of antepartum hemorrhage. Crede (1819–
Hendrik van Deventer (1651–1727) of Hague wrote 1892) of Leipzig introduced a method of separation of
about obstructed labor and deformed pelvis. Dutchmen, placenta. John Braxton Hicks (1825–1893) noted rhythmic
Hendrik Van Roenhuyze (1625–1672) advocated cesarean uterine contractions of pregnancy. Aschheim and Zondek
section in obstructed labor to prevent vesicovaginal fistula. described pregnancy test in 1927. Voge introduced
In nineteenth century, James Young Simpson (1811– detection of pregnancy by the flocculation pregnancy test
1870) of Edinburg started obstetrical anesthesia. Parro’s in 1926.
Cesarean hysterectomy (subtotal) saved many lives Nearly all breeches were delivered from below. Rhesus
(1876). In 1882, Adolph Kechrer, closed the uterine wound factor was discovered in 1940 by Landsteiner and Wiener.
and laid the foundation of modern cesarean operation. Though Hofbauer advocated pituitary extract in 1918, it
Symphysectomy (division of symphysis pubis) was known was introduced very late in practice.
to be practiced in Ireland. In Paris, Sigault (1777) is said Antenatal care is attributed to JW Ballantyne. In 1901
to have performed the first symphysectomy on a living Royal Maternity and Simpson Memorial Hospital endowed
woman. William Hunter (1718–1783) studied anatomy of one bed for the purpose. In USA, it was started in 1911 and
the pregnant and non-pregnant uterus and the embryo. in 1912 in Sydney.
Evolution of Obstetrics 5
Fig. 1.1: Dr Krishna Menon with the Department of Obstetrics and Fig. 1.2: Dr Shirodkar
Gynecology, Banaras Hindu University (BHU), India, February 1976
Though John Charles in 1811, discovered the relation Tremendous changes occurred in the understanding
of proteinuria with eclampsia, it did not receive much and management of labor, its induction and active
attention at that time. The invention of the stethoscope management of the third stage of labor in the twentieth
was done in 1819 by Rene Laennec (1781–1826) and his century. There is a gradual trend of increasing hospital
student Kergaradec. Hearing the fetal heart by applying his deliveries. Artificial rupture of membranes became
instrument to the abdomen was a great step forward. In popular at the end of the nineteenth century. Quinine
1896, the sphygmomanometer was perfected by Scipione for the induction of labor (Porak in 1878) was popular
Riva-Rocci and the relation of high blood pressure and till 1930. Oxytocin induction was started by Theobald
eclampsia was established. However, blood pressure was in 1952. Pelvic scoring system was devised by Bishop in
not often taken in antenatal check-ups. Stronganuff in 1909 1964. The use of prostaglandins, as a cervical ripening
introduced anticonvulsants and their combination with agent, was introduced by Karim and his associates in 1968.
Titration of oxytocin infusion by Turnbull and Anderson
antihypertensive started in 1960. Krishna Menon’s regime
was started around the same time. Incompetence of cervix
(Fig. 1.1) was in vogue for a long time to treat eclampsia thus
was investigated by Lash and Lash in 1950, Palmer and
lowering the maternal mortality drastically. During 1932–
Shirodkar (Fig. 1.2) in 1953 and McDonald in 1957.
1944, Mcafee’s regime helped many patients suffering
O’Driscoll and Meagher of the National Maternity
from antepartum hemorrhage and their neonates.
Hospital Dublin, revolutionized the active management
Cesarean section by 1931 was not considered a dangerous
of labor with the use of the partogram, introduced by
operation and it saved many patients with placenta previa. Philpott of Rhodesia, which helped them to intervene
The technique of ultrasound introduced by Ian Donald in before the mother and fetus were exhausted. Analgesia
1958 replaced all other invasive methods of diagnosis of and regional anesthesia is becoming popular. Caudal
placenta previa. anesthesia was replaced by epidural analgesia by mid
The abandoning of high forceps and difficult vaginal 1970. Cesarean delivery was performed in less than 2% of
deliveries, reduced the incidence of birth trauma and the labor in the beginning of twentieth century. But by 1990, it
morbidity significantly. The uterus and its contractions was about 12%. The practice of episiotomy with or without
were investigated for long by Alvarez and Caldeyro-Barcia instruments became common in 1950. Introduction of
in 1950. vacuum was a great achievement.
In 1970, parasympathomimetic agents were introduced, The crude fetal kick counting was introduced by
thus preventing neonatal deaths. The categorization of Sadovsky and his associates in 1976. Biophysical assessment
antenatal mothers into low-risk and high-risk helped the of the fetus introduced by Frank Manning and Larry Platt in
mothers and neonates immensely. Fetoplacental function the early 1980, still continues to be life saving for the fetus.
tests developed in 1961, greatly improved our insight into Electronic fetal monitoring of high-risk cases combined
the fetal condition. with Saling’s technique of fetal scalp pH monitoring,
is still of considerable value. Genetic counseling and In this chapter, we have had a brief glimpse of the
determination of genetic defects has helped a lot. journey of the primitive art of obstetrics conducted by
Maternal mortality review and audit of maternal care natives to the midwives and now by qualified obstetricians.
during antenatal, natal and postnatal period, according to It has gradually become a scientific venture from ovulation
evidence-based protocol and practices is now improving to conception, from the development of the fetus to
the maternal care to a great extent. delivery.
Self-assessment Exercise
1. What do you understand by the term obstetrics?
2. Fill in the blanks:
i. The ____________ of the neonate had a great significance and the cord was cut only after the midwife had washed the baby.
ii. ____________ was performed in less than 2% of labor in the beginning of twentieth century.
Anatomy of
2
Sudha Sa/hon
Female Genital Tract
■ Associated structures
INTRODUCTION
• Urethra and
It is important to know any deviation from normal in - Urinary b adder
anatomy or histology, as it forms the basis of most of the - Sphimsteric structures
obstetrical and gynecological diseases. Since the urethra, • Ureter
urinary bladder, ureter, pelvic colon, rectum and anus • Pelvic-colon
are closely associated with female genital organs, any • Rectum and anus.
alteration in their function or structure during childbirth ~ Blood supply of female pelvic organs
or disease will influence the gynecological procedures, ■- ~ erve supply of pelvis
and vice-versa when gynecological conditions encroach ■ L mphatic drainage of female pelvis associated struc-
them and pose difficulties in treatment and surgeries. tures.
No two women are alike in respect of anatomy. Variation
is the rule. For convenience, we can divide the female
FEMALE EXTERNAL GENITAL
genital organs into external and internal.
ORGANS (FIG. 2.1)
■ Female external genital organs (pudenda
• Vulva It includes the following exterior genital organs. Vulva or
- Mons pubis/veneris pudenda include whatever is visible on external examination.
- Labia majora It comprises mons veneris, labia majora, labia minora,
- Labia minora (nymphae) Bartholin's glands, clitoris, vestibule and bulb of vestibule,
- Bartholin's glands (greater vestibular glands) vaginal entrance, hymen, external urethral opening, the
- Clitoris openings of various glandular and vascular structures and
- Vestibule the perineum.
- Vestibule bulb
- Hymen Mons Pubis (Mons Veneris)
- Vaginal entrance It is the area over the symphysis pubis. It contains fatty
- External urethral opening and connective tissue. At puberty, it bears hair-forming
- Opening of various glandular and vascular escutcheon. The shape of escutcheon is triangular with
structures base at mons pubis and apex below on the outer surfaces
- Perineum of both labia majora.
• Vagina.
■ Internal genital organs Labia Majora
• Uterus They are skin folds filled with fats extending from the mons
• Supports pubis backwards on either side of vaginal opening (7-8 cm,
• Fallopian tubes and 1-1.5 cm). They taper posteriorly and unite to form the
• Ovaries posterior commissure and m erge into the perineal body.
Fig. 2.1: Female external genital organs Fig. 2.2: Vulval boil
The lateral sides are hairy after the puberty. They are the The round ligament can give rise to leiomyomas in
counterparts of the male scrotum. this region and the obliterated processes vaginalis can
Each labium majus is covered by stratified squamous become a dilated embryonic remnant in the adult.
epithelium.
In its substance, there are many sebaceous glands, sweat Labia Minora (Nymphae)
glands, elastic fibers, adipose tissues and plexuses of veins They are thin folds of soft skin and are on either side of
but no muscle cells. It is subcutaneous tissue like abdominal vaginal opening on the inner side of the labia majora. It
wall. The superficial tissue of this region (Camper’s fascia) is covered by non-keratinized stratified epithelium with
is fat laden, as it is on the abdomen. Deeper layer is called
no hair follicles or fat. Stroma is very vascular and has
Colles’ fascia and is similar to Scarpa’s fascia of the
sebaceous follicles and a few smooth muscles. Skin is
abdomen.
loosely attached to the underlying tissues.
Some of the sebaceous glands are large and are called
These labia minora correspond to the floor of the penile
apocrine glands; their secretions when modified by local
urethra in males. They split towards the mons side into two
bacteria give a characteristic odor. The connective tissue is
folds, the anterior folds joining to form the prepuce and
very loose and hence becomes edematous easily.
the posterior folds forming the frenulum of the clitoris.
The last part of round ligament and processes vaginalis
Posteriorly, towards the perineum, both the labia majora
(obliterated)—(canal of Nuck) are present in labia majora.
join to form the fourchette. Fossa navicularis is a small
Before puberty, there are no hair on the outer surface of
hollow between the fourchette and the hymen.
labia majora and mons. At and after the puberty, hair growth
Labia minora are hardly visible before the puberty. But
starts and fat appears. At this time of life the labia majora
in multiparous women they may project prominently.
cover the vaginal orifice. In children and postmenopausal
women the amount of fat is very less hence the vaginal
Applied Anatomy
orifice remains uncovered.
The fourchette is a sharp fold of skin that is injured
Applied Anatomy during delivery and occasionally during the first inter
Since stratified squamous epithelium covers the region, course.
the mons pubis and the labia majora are vulnerable Smooth muscle fibers enable the labia minora to become
to ordinary skin diseases like boils (Fig. 2.2) sebaceous turgid during the sexual excitement.
cysts and new growths like hidradenoma (of apocrine Since the skin is loosely attached to the underlying tissues
glands), etc. it allows easy dissection in the vulvectomy operation.
Anatomy of Female Genital Tract 9
Fig. 2.3: Bartholin’s glands and vestibular bulb Fig. 2.4: Bartholin’s cyst—40x
Courtesy: Dr Chandok, Department of Pathology, ESI Hospital
Basaidarapur, Delhi
Bartholin’s Glands (Greater Vestibular Glands) side of ischiopubic rami are narrow and are firmly attached
These lie one on either side of vaginal orifice posterolaterally to the pubic bone, continuing dorsally to lie on the inferior
(at the junction of middle and post third) (Fig. 2.3). They aspect of the pubic rami. Ischial tuberosity and free surface
correspond to the Cowper’s glands or bulbourethral glands of crura has the origin of ischiocavernosus muscle and is
in males. They are oval (pea shaped) and about 0.5–1 cm in attached to the upper crura and clitoral body and fuse just
diameter and when normal, cannot be palpated. Outside below pubic arch to form the corpus or body. The body can
the lateral margin of vagina, its ducts open (1.5–2 cm size). be palpated against the symphysis pubis.
Each Bartholin gland is a compound racemose gland and
Applied Anatomy
its acini are lined by low columnar epithelium. Multilayered
columnar cells line the duct. Its function is to secrete a The blood vessels of the clitoris have connections
colorless mucoid secretion with a characteristic odor, with the vestibular bulb and may suffer injury during
mainly in response to sexual excitation. parturition causing perfuse bleeding.
It is an erectile organ.
Applied Anatomy
Bartholin’s glands may be infected with gonorrhea or oth-
Vestibule
er bacterial infections when they may form a Bartholin’s Vestibule is a Latin term meaning a ‘hall next to the
gland abscess. It is the duct which gets distended in Bar- entrance’. On separating the labia, this area is seen in front
tholin’s cyst (Fig. 2.4). of the vaginal opening. Its boundaries are anterior clitoris
and posterior fourchette. It has the opening of urethra,
Clitoris vagina Bartholin and paraurethral glands (Skene’s) ducts.
Though separate from urethra it represents male penis. It
lies below the mons pubis hidden by the two folds of labia External Urethral Meatus
minora and is located above the external urethral opening. It is above the vaginal orifice and clitoris is anterior. Skene’s
It is attached to the under surface of the symphysis pubis (paraurethral gland) ducts open into the sides of the
by the subcutaneous suspensory ligament. It is divided urethral openings. The fossa navicularis is in the posterior
into a glans (only the glands and prepuce are visible), body part of the vestibule in nulliparous women. On either side
(corpus) and two crura. The glans has spindle shaped cells, of the urethral opening, there are small depressions called
covered by squamous epithelium. The two crura (corpora paraurethral pouches with adjacent, barely perceptible,
cavernosa with smooth muscle fibers) originate from inner urethral labia.
Vestibule Bulb
Two vestibular bulbs are counterparts of corpora spon-
giosa of males. They lie under the lining of the vestibule
on either side. They are an elongated aggregation of veins
close to the ischiopubic rami.
Applied Anatomy
During parturition, the vestibular bulbs are usually pushed
up beneath the pubic arch. They are liable to injury and
rupture causing hemorrhage or hematoma.
Hymen
The hymen is a thin incomplete membrane covered on
both the surfaces by squamous epithelium. It lies at the
entrance of the vaginal opening. It has a few openings for Fig. 2.5: Imperforate hymen
the drainage of menstrual blood. It varies in shape and can
be annular, crescentic, septate or cribriform.
Vagina
Applied Anatomy The vagina is a tubular structure containing both fibrous
The hymen is mostly torn during the first act of coitus. and muscular tissue. It lets the uterus communicate exter-
In imperforate hymen it remains intact and prevents nally to the vulva. It is directed upwards and posteriorly
flow of menstrual blood (Fig. 2.5). from the vulva forming an angle of 60–70° to the horizontal
Injury may also be caused by operations, digital inter- (Figs 2.6A and B).
ference or insertion of menstrual tampons. Vesicovaginal fascia or septum is the condensation
The type of tear will give more information about its
of connective tissue separating vagina anteriorly from
cause, e.g. during parturition the injury is greater and
the remains of the hymen are a few tags around the bladder and urethra, and posteriorly vagina is separated
vaginal opening called carunculae myrtiformes. from lower portion of rectum by the connective tissue
condensation called the rectovaginal septum or fascia.
Vaginal Entrance Cul-de-sac or rectouterine pouch of Douglas separates
The vaginal entrance lies at the posterior end of the upper fourth of vagina from rectum. Vagina pierces
vestibule and is of different shapes. the triangular ligament and the pelvic diaphragm by
A B
Figs 2.6A and B: A. Normal vagina—10x; B. Histopathology of vagina

Courtesy: A. Dr Rath, Department of Anatomy, Vardhman Mahavir Medical College, Delhi; B. Dr A Gupta, Department of Anatomy, Sikkim
Manipal Institute of Medical Sciences, Sikkim
1 cm and 2.5 cm respectively, from its lower end. The

upper end of the vagina (vault) is blind except where
it is perforated by the cervix and has the external os
projecting through its upper anterior wall. The vault of
the vagina is divided into four fornices by the cervix.
The posterior fornix is the deepest (7–10 cm) and is
called the pouch of Douglas (POD). The anterior fornix
is shallow (6–8 cm). There are two lateral fornices on
both the sides of cervix. Vaginal opening (introitus) is
functionally closed by the labia, which are in contact
with each other.
Both vaginal walls (anterior and posterior) are normally
lying close together obliterate the cavity of the vagina.
Diameter of vagina is 4–5 cm at its lower end and 8–10 cm
at its upper end. The vagina is covered by non-cornified Fig. 2.8: Normal rugae of vagina
stratified squamous epithelium. But it can become cornified
(Fig. 2.7) once it is exposed to air, as in procidentia. Prominent Superficial cells of the vaginal mucosa are rich in
longitudinal ridges project into the vaginal lumen. There are glycogen hence the vagina stains deep brown with iodine.
also many transverse ridges called rugae (Fig. 2.8) making This property is seen in mucosa of infants due to estrogen of
a corrugated surface. Below the vaginal covering, there is a the mother. This is also seen even after menopause (though
thin fibromuscular coat of smooth muscles (inner circular much less in amount). Muscles are mostly involuntary but
and outer longitudinal). It is believed by some that they are there may be a few voluntary fibers contributed by the
arranged in a criss-cross manner. There is also rich vascular levator ani at the sites of their insertion. The fascial sheets
connective tissue with a few small lymphoid nodules. This fuse with the fascia covering the levator ani muscles, the
connective tissue is the perivaginal endopelvic fascia. No triangular ligament and perineal body.
glands are present in the vagina. It is kept moist by small At birth, because of maternal estrogen, Doderlein’s
amount of uterine secretions. bacilli are present in the vagina of the female newborn and
Embryonic remnant (Gartner’s cysts) lined by columnar the pH is acidic. After a few weeks of birth, the pH rises to 7
or cuboidal epithelium can be seen in the vagina. They lie and the epithelium atrophies. At puberty, due to formation
on the side wall of vagina. Mülllerian ducts form upper part of estrogen, the pH is acidic again and Doderlein’s bacilli
and the urogenital sinus forms the lower part of vagina. increase markedly. With repeated childbirth and distension
of the vagina the rugae disappear. At menopause, the
vagina shrinks and the epithelium atrophies.
Functions
Acts as excretory channel of the uterus (secretions and
menstrual blood).
It is the organ of copulation.
It is part of the birth canal.
Applied Anatomy
Through the thin walls of the fornices, the internal
pelvic organs can be felt (by per vaginal examination).
Via the POD, after holding the posterior lip of the cervix
by the vulsellum, one can gain access to the peritoneal
cavity by culdocentesis (Fig. 2.9). If culdocentesis yields
altered blood, an ectopic pregnancy is suspected. In the
case of pelvic abscesses pus is aspirated via the same
Fig. 2.7: Cornified vaginal wall route and then colpotomy (Fig. 2.10) (opening of vagina)
Fig. 2.9: Culdocentesis Fig. 2.10: Colpotomy
is done to drain the pus. Colpotomy is also done for point into which many muscles get inserted. It supports
vaginal tubal ligation. the lower part of the vagina. Through the perineal
The length and width of the vagina varies considerably membrane and superficial transverse perineal muscles,
in different women. But anatomical shortness or the perineal body is attached to inferior pubic rami and
narrowness does not cause any difficulty in normal ischial tuberosities. Bulbocavernosus muscle and of some
functions, as the vagina is distensible due to the tone levator ani fibers are also attached to the perineal body.
and contractions of the surrounding muscles. There is indirect attachment to coccyx by the insertion of
After childbirth, small tags can get buried during healing the external anal sphincter posteriorly.
or repair of vaginal lacerations and form vaginal inclu
sion cysts.
Applied Anatomy
During pregnancy, the vaginal discharge, which is The perineal body may be torn during parturition.
acidic, is more profuse and also contains exfoliated External anal opening may also be injured. Hence, after
epithelial cells and bacteria. delivery, examine carefully to see and repair, if any injury
Doderlein’s bacilli or lactobacillus are more numerous are there and then. This prevents further damage.
in the pregnant vagina than otherwise; they act on the
glycogen within the exfoliated vaginal cells and form FEMALE INTERNAL GENITAL
lactic acid. This acidity is very important, as it is a natural ORGANS (FIG. 2.11)
resistance to infection during the reproductive age.
The vagina absorbs water, electrolyte and substances of Uterus
low molecular weight. This is important in clinical prac- The uterus is an inverted pear-shaped hollow muscular
tice as it enables administration of drugs like estrogen, organ. It is positioned in the pelvis with urinary bladder in
progesterone, prostaglandin and antibiotics, etc. per- front and rectum behind. It is divided into fundus (above
vaginally. cornua and fallopian tube) body and cervix. Isthmus is
The vaginal inlet and the tissue around it are richly the part between the body of the uterus and the cervix. The
supplied by blood vessels and so it bleeds profusely if uterus is flattened from before backwards, more so on the
injured by an accident or at operation. anterior wall. The measurements vary but the nulliparous
organ is approximately 8–9 cm in length, 6 cm across and
Perineal Body 4 cm from before backward. The walls are 1–2 cm thick.
It is situated between the vagina and anus. It is also called The normal length of the cavity is 7 cm (7–8 cm). It can be
the central tendon of the perineum, as it is the central measured during operations by uterine sound.
Fig. 2.11: Sagittal section of genitourinary system (Internal pelvic organs) Fig. 2.12: Criss-cross spiral fashion of uterine muscle
The cavity is shaped like an inverted triangle. It

communicates with the vagina through the cervix and
with the peritoneal cavity via the fallopian tubes. It is lined
by endometrium.
The uterus is covered partially by peritoneum. The
whole of the fundus, the anterior wall as low as the isthmus
and the posterior wall as low as the attachment of vagina
to the cervix are intimately covered with peritoneum
(Fig. 2.11). The sides of the uterus, between the attachment
of the two leaves of the broad ligament, the whole of the
cervix except the posterior aspect of its supravaginal part
are not covered with peritoneum. The main walls have thick
Fig. 2.13: Muscles of the myometrium
involuntary muscles (myometrium) running obliquely in
a criss-cross spiral fashion (Fig. 2.12). The more superficial
muscle fibers however, are arranged longitudinally and are Cervix
continuous with muscle fibers of the fallopian tubes and the Two parts of cervix are portio supravaginalis (which is
vagina (Fig. 2.13). Fibrous and elastic tissues are mixed with above vagina) and portio vaginalis (which projects into the
the muscles. There is no submucosa, thus the glands of the vagina). Cervix has dense fibrous connective tissue with
lining endothelium sometimes dip into the fibromuscular some smooth muscles connecting the myometrium with
tissue. the muscles of the vagina. They are circularly arranged
The lining of the uterus (the endometrium) has glands into these tissues which are attached to the cardinal, the
and a specialized stroma. uterosacral ligaments and pubocervical fascia.
Applied Anatomy Histopathology

Thick involuntary muscles (myometrium) running The portio vaginalis is covered by non-keratinizing stratified
obliquely in a criss-cross spiral fashion helps in squamous epithelium (Fig. 2.14). The cervical canal (2.5 cm)
preventing postpartum hemorrhage (PPH) (Fig. 2.12). is lined by a columnar epithelium, which secretes mucus
Endomerial in its superficial portion undergoes cyclic and is thrown into V-shaped folds giving it a characteristic
changes during the menstrual cycle under the influence appearance—plicae palmatae or arbor vitae. Endocervix
of hormones. has cylindrical columnar epithelium (Fig. 2.15).
Fig. 2.14: Histology of ectocervix Fig. 2.15: Histology of endocervix

Courtesy: Dr Yadav, Department of Pathology, RML Hospital, Delhi
A B
Figs 2.16A to C: A. Transitional zone (T-zone) junction; B. Histo-

pathology of cervix T-zone; C. Squamocolumnar junction
Courtesy: Dr A Gupta, Department of Anatomy, Sikkim Manipal Insti-
C tute of Medical Sciences, Sikkim
The internal os marks the upper border of the cervix and of transitional zone in relation to the external os varies
at the lower border is the external os. Near the external os is depending on the age and hormone levels. It may be up to
the transitional zone (T-zone) (Figs 2.16A to C) where the 1 cm in width.
change from cylindrical columnar epithelium to squamous The longitudinal axis of the uterus is approximately at
epithelium occurs (squamocolumnar junction). The level right angle to the vagina and normally lies tilted forward;
this is termed as anteversion. The uterus is also flexed

forwards on itself at the isthmus; this is termed as
anteflexion. In around one fifth of women this tilt is
backwards causing retroversion and retroflexion.
Anteriorly: The uterus is related to the bladder and is
separated by the uterovesical pouch of peritoneum.

Posteriorly: It is the POD with coils of intestines, sigmoid
colon and upper rectum. Laterally, the broad ligaments

with its contents of special importance are uterine arteries
and ureters as they are very close at the supravaginal
portion of the cervix. Cervix is double the body of uterus
in length at birth, and at puberty it is half of uterine size.
Uterus atrophies after menopause, its mucosa is thinned,
glands disappear and muscles are reduced, cervical lips
disappear and the external os becomes flush with the Fig. 2.17: Histopathology of fallopian tube
Courtesy: Dr A Gupta, Department of Anatomy, Sikkim Manipal
vaginal vault obliterating the fornices. Institute of Medical Sciences, Sikkim
Applied Anatomy
The T-zone is an active area of cellular transition; it is
here that the cervix is most susceptible to malignant
transformation when acted on by carcinogens.
Usually, retroversion of the uterus does not cause any
significant pathology.
Fallopian Tubes
They are paired tubular structures about 7–12 cm in
length. Each fallopian tube is divided into 4 distinct parts.
At the cornua, the interstitial portion starts and then is the
narrow isthmus. Next is the ampulla, the most spacious
with convoluted mucosa. Laterally is the fimbrial end
with petal-like projections providing big surface area for
the pick up of the ovum. One fimbria is long and reaches Fig. 2.18: Graafian follicle (ovary)
up to the ovary—the fimbria ovarica. Courtesy: Dr Yadav, Department of Pathology, RML Hospital, Delhi
The serosal layer consists of the peritoneum with
underlying areolar tissue. The muscle layers are the outer hilum of broad ligament. The latter transmit the vessels and
longitudinal and the inner circular muscle fibers. They nerves. Laterally, it is attached to the suspensory ligament
are fairly thick at the isthmus and thin at the ampulla. The of the ovary with folds of peritoneum, which become
mucous membrane is thrown into folds or plicae especially continuous with that over the psoas major.
at the infundibular area. It consists of columnar epithelium, Ovary has a medulla and cortex. The central vascular part
most of the cells bearing cilia, which together with the containing loose connective tissue is medulla, having many
peristaltic action which help in sperm and ovum transport. elastic fibers and non-striated muscle cells. The outer thicker
The epithelium also contains secretory cells as well as a third cortex contains a network of reticular fibers and fusiform
group of intercalary cells of uncertain function (Fig. 2.17). cells. The outer surface is covered by a single layer of cuboidal
cells called germinal epithelium. Below it is the tunica
Ovaries albuginea, an ill-defined layer of condensed connective
They are two in number. They are solid, grayish pink almond- tissue. Primordial follicles are present in the cortex but some
shaped in young adults and approximately 3 cm×1.5 cm × are seen in the medulla. They in turn develop into graafian
1 cm in volume. Before childbirth, each ovary is longitudinal follicles (Fig. 2.18), corpus luteum (Figs 2.19A and B) and
in disposition; after childbirth there are many variations. It finally atretic follicles (corpus albicans) (Fig. 2.20).
is not covered by peritoneum. Ovarian ligament attaches The ovary anteriorly is in touch with the fallopian tube,
ovaries to uterine cornua and mesovarium connects it to superiorly to the urinary bladder and uterovesical pouch
A B
Figs 2.19A and B: A. Histopathology of corpus luteum; B. Corpus luteal cyst—40x
Courtesy: Dr Chandok, Department of Pathology, ESI Hospital, Basaidarapur, Delhi
Fig. 2.20: Corpus albican and stroma (ovary) Fig. 2.21: Female internal genital organs
Courtesy: Dr Yadav, Department of Pathology, RML Hospital, Delhi
and posteriorly to POD. Superiorly are the bowels and parallel blind tubes in the mesosalpinx. Sometimes
omentum and inferiorly are the broad ligaments with between the epoophoron and the uterus are a few
their contents. Laterally, the ovary is related to the parietal rudimentary tubes—the paroophoron (Fig. 2.21). They
peritoneum and the pelvic sidewalls. may get filled with fluid forming paraovarian cysts. The
In fetal life, the ovaries are situated in the lumbar region caudal part of the mesonephric duct is well developed
near the kidney. They gradually descend into the pelvis. in some and running along side with the uterus to the
Each ovary is packed with primordial follicles. The ovaries internal cervical os as Gartner’s duct.
grow in size till puberty by increasing the stroma. With Blood supply of the ovary is from the ovarian vessels
puberty some primordial follicles develop each month into and anastomosis with uterine vessels.
graafian follicles. After menopause, the ovary atrophies is
small and shriveled. The fully involuted ovary of old age ASSOCIATED STRUCTURES
contains practically no germinal elements.
Ureter
Applied Anatomy There are two ureters connecting the kidney with the
The mesonephric ducts and tubules are always present urinary bladder. The approximate length is 25–30 cm, with
as vestigial structures. The epoophoron are a series of a diameter of about 4–6 mm. They are equally divided into
abdominal and pelvic parts. There are slight constrictions

at three points at the renal pelvis (upper isthmus) as they
cross the brim of the lesser pelvis (lower isthmus) and
also when they enter into the bladder (intramural). Each
ureter is about 3 mm thick and has 3 layers—the outer
fibrous coat becoming continuous with the bladder wall,
a second non-striated muscular layer with outer circular
and inner longitudinal layer and near bladder a third layer
of muscles—outer longitudinal layer (as in the urinary
bladder). It is lined by transitional epithelium (Fig. 2.22).
The ureter can be recognized by its peristalsis. In its
abdominal part, it is retroperitoneal traveling along the
anteromedial aspect of psoas major and is crossed by
ovarian vessels. The ureter enters the pelvis at the sacroiliac
joint and cross common iliac bifurcation (pelvic position).
On further descent, it passes posterolaterally in the pelvis
and travels in front of internal iliac artery and its anterior
division, medial to the obturator vessels and nerves. In the
true pelvis, it reaches medially and forwards on the lateral
side of the uterosacral ligament (ischial spine). From Fig. 2.23: Route of ureter
here the ureter passes through the broad ligament base
2 cm lateral to the cervix into the ureteric canal of cardinal •• Ligation
ligament and at this point the uterine vessels cross it •• Kinking and resultant obstruction
superiorly from lateral to the medial side. At this site, it •• Ischemia because of devascularization due to exten-
is anterolateral to the upper part of the vagina. Slightly sive dissection (e.g. in Wertheim’s hysterectomy)
medially it enters obliquely into the urinary bladder at the •• Segmental resection
trigone (Fig. 2.23). •• Injury by a laparoscope.
The ureter can be injured at the following points during
Applied Anatomy
operations
Operative trauma to the ureter can be of the following •• Adjacent to the cervix in the ureteric canal, where it
types: is crossed over by the uterine vessels, the ureter may
•• Crush injury due to a wrongly applied clamp. be injured or accidentally ligated while ligating these
•• Transection vessels.
•• Beyond the uterine vessels as it enters into the
cardinal ligament on its way to enter the bladder.
•• In the part of the ureter which enters in the bladder
wall (intramural).
•• Near the pelvic brim, where it is near the ovarian
vessels during broad ligament fibroid operation.
•• At or below the infundibulopelvic ligament.
•• Along the course of the ureter on the lateral pelvic
wall just above the uterosacral ligament.
•• During dissection of lymph nodes in Wertheim’s
operation as it is just lateral to inferior vena cava.
•• A high suture near the cervix in the pelvic floor repair
(PFR) occasionally injures the ureter.
•• Blind hemostatic suturing in vault bleeding is dangerous.
Fig. 2.22: Histology of ureter Most such ureteral injuries occur in the lower third of
Courtesy: Dr Yadav, Department of Pathology, RML Hospital, Delhi the ureter. The chances of damage are greater when any
tumor, like a fibroid or an ovarian cyst, distorts the pelvic pubocervical fascia below the supravaginal portion of
anatomy or the course of the ureter deviates due to a the cervix. Here, uterovesical pouch containing coils of
malignant tumor or broad ligament pathology. intestines.
The mucous membrane is transitional epithelium.
Urinary Bladder There are no glands in the bladder. The mucous membrane
It is a muscular organ capable of altering its size and shape is loosely attached to the underlying muscular wall
depending upon the amount of urine. This reservoir of and hence forms rugae, when empty. The trigone is an
urine is a retroperitoneal viscus lying behind the pubis inverted triangular area bounded above by two ureteral
symphysis. It is a tetrahedron when empty with a fundus, openings and below by urethral opening, here the mucous
a triangular base and a superior and two inferior lateral membrane is firmly attached to the underlying muscles,
surfaces. The latter meets to form the rounded border hence it appears smooth.
joining the superior surface at the apex. Meeting of the The interureteric ridge is slightly curved. The ureteric
base inferolateral surfaces at the urethral orifice and the openings are about 2.5 cm apart.
inferior forms bladder neck. This is the urethral orifice.
Normal bladder capacity is 300–600 mL, but in patients Applied Anatomy
with retention of urine several liters can be accumulated. The mucous membrane’s transitional epithelium
The bladder becomes more rounded as it fills and in responds to ovarian hormones. Therefore, menopausal
extreme cases can reach upto umbilicus. women are more prone to cystitis.
There are 3 layers of the bladder wall. Outermost is the Ureters open at an oblique angle through slit-like
peritoneum, covering only the fundus. The second layer is openings, this prevents reflex of urine when the bladder
the detrusor muscle, it is non striated and has three layers— contracts for voiding.
the middle circular, the outer and inner longitudinal. During abdominal hysterectomy, the bladder may be
Innermost lies the mucous membrane (Fig. 2.24). injured 3–4 cm above the trigone and it can be easily
The peritoneal covering in the abdomen goes from repaired.
anterior abdominal wall to fundus of the bladder. This While performing anterior colporrhaphy or vaginal
peritoneum is displaced anteriorly upwards on filling of hysterectomy the bladder can be damaged, more so if
the bladder making it bereft of peritoneum anteriorly. This previous repair was done. If this damage goes unnoticed,
is utilized in suprapubic catheterization of full bladder vesicovaginal fistula (VVF) forms.
without entering the peritoneal cavity (Fig. 2.11). Below
the reflection of the peritoneum, anteriorly is the cave Urethra
of Retzius filled with loose cellular tissue. Posteriorly the It runs anteroinferiorly from the internal meatus of the
base of bladder is separated from the upper vagina by urinary bladder. It lies behind the symphysis pubis in
close relation to the anterior vaginal wall. Its length is
approximately 1 cm and it is 6 mm in diameter. After
crossing the perineal membrane it ends at the vestibule.
The external urinary meatus is below the clitoris. Skene’s
tubules draining the paraurethral glands (homologous to
the male prostrate) open into the lower urethra.
Near the bladder, the urethra is lined by transitional
epithelium, which later converts into non-keratinizing
stratified squamous epithelium by the time it reaches the
external urethral meatus. The muscle layers are the inner
longitudinal and the outer circular, which are continuous
with those of the urinary bladder.
The urethra is anteriorly related to the symphysis pubis
with some loose cellular tissue in between. Posteriorly,
it is near the anterior vaginal wall and Skene’s tubules.
Fig. 2.24: Urinary bladder Laterally, it is in relation to the urogenital diaphragm,
Courtesy: Dr Yadav, Department of Pathology, RML Hospital, Delhi bulbospongiosus muscle and the vestibular bulb.
Near its lower end, before crossing the perineal mem- fossa, which support (otherwise slit like empty cavity)
brane it is encircled by voluntary muscles fibers—arising when distended. Anteriorly is perineal body and lower
from the inferior pubic ramus to form the so called external vagina and posterior relation is anococcygeal body.
sphincter; this allows the voluntary arrest of urine flow. The sphincteric muscles are voluntary. External sphinc-
ter is of 3 layers of striated muscles, levator ani muscles
Applied Anatomy
also surrounding the anal canal and are important in the
The urethra is kept closed by the tone and elasticity of control of defecation. The internal sphincter is involun-
its muscles, except during micturition. tary and is the thickened circular muscles of the gut wall
The decussating arrangement of vesical muscle fibers at around the anal canal just above the anorectal junction.
the urethrovesical junction acts as an internal sphincter Posterolaterally are piriformis, coccygeus and levator ani
and helps maintain continence. muscles, along with sacral (3rd, 4th and 5th) and coc-
Pelvic Colon cygeal nerves. Anteriorly can feel uterus, adnexa, upper
vagina and pouch of Douglas. Laterally is ischiorectal fossa
Descending colon continues as sigmoid colon (pelvic
(on per rectal examination).
colon) at the pelvic brim on left side. Its loop is about
40 cm in length and it lies behind the broad ligament in the Applied Anatomy
lesser pelvis. It is totally covered with peritoneum and has
While doing per rectal examination, we can feel lower
a sigmoid mesocolon. It continues as rectum at the level of
3 sacral vertebrae, the coccyx, medical sacral and
3rd sacral vertebra.
superior rectal vessels.
Its mucous membrane consists of non-ciliated
Laterally, we also feel for the cardinal ligaments for
columnar epithelium and is thrown into irregular folds.
involvement in the staging of carcinoma of the cervix.
The muscle layers are the inner circular and the outer
longitudinal with three taenia coli bands. As the taenia, Tissue layer form anterior border of rectovaginal space
are shorter they give the sacculated appearance to the by fusing to the under surface of the muscularis of the pos-
pelvic colon. There are also appendices epiploicae. terior vaginal wall. It varies in size, strength and consis-
Inferiorly, the sigmoid colon is in relation with the uterus tency in different individuals. It is a fixation point for the
and urinary bladder and on the left side is the rectum. On upper border of the perineal body and is very important
the right side above are coils of ileum. Posteriorly there clinically.
are the left ureter, the left internal iliac vessels, piriformis
muscle and the sacral plexus. Laterally are the left ovary, ANATOMICAL PELVIC SUPPORT
left external iliac vessels and the obturator nerve.
Varying degree of support to the birth canal is given by at
Rectum least nine different anatomical systems:
1. The bony pelvis.
It is 10–12 cm in length and lies on the concavity of the
sacrum and coccyx forming an anterior-posterior curve 2. Pelvic peritoneum-broad ligaments.
called the concavity of the sacral flexure. The lower end 3. Subperitoneal connective tissue reticulum including
is the ampulla bulging into the posterior vaginal wall, then •• Round ligament
continue as the anal canal. The peritoneum covers it on •• Ovarian ligament.
the front of upper and middle third and the sides of the 4. Fascia ligaments: Transverse cervical (cardinal) or
upper third only. Mackenrodt ligament
The lining is of mucous secreting columnar epithelium. •• Uterosacral ligament
When empty, the lining is thrown into transverse folds. •• Pubocervical fascia.
Horizontal folds are always present and are more 5. The paravaginal attachments of the vaginal sulci to the
pronounced during distension. There is absence of saccula arcus tendineus.
tions, appendices epiploicae and mesentry that helps to 6. The urogenital diaphragm including pubourethro-
differentiate it from the sigmoid colon. Taenia coli fuse vaginal ligament.
5 cm above the rectum and form one anterior and one 7. Pelvic diaphragm particularly the pubococcygeus
posterior band, which descend in the rectal wall. component of levator plate.
The anal canal passes downwards and backwards and 8. The fascia of Denonvilliers (rectovaginal septum).
is about 3 cm long. Laterally, there is fat in the ischiorectal 9. The perineum including the perineal body.
All of them in combination provide the support. and posterior ligaments while intermediate liga-
Bony pelvis is the ultimate fixed attachment of the pelvis ments is formed by fusion of the same facial layers.
soft tissues. It is inflexible, firm and strong and thus These ligaments contain dense collagen, smooth
resists sudden strain and stress. This response is both and striated muscles and elastic fibers. The striated
age and hormone related. Hence, any deviation from muscles may be a pubourethrovaginal continuation
normal due to trauma or any congenital abnormality of some fibers of pubococcygeus. Smooth muscles
may fail to provide adequate support to the soft tissue. have numerous nerve fibers. Hence, most of the pel-
Broad ligaments are the peritoneal covering the vic supporting ligaments have contractile elements
fallopian tubes, mesosalpinx and blood vessels and under neural control. The urogenital diaphragm is
lymphyatics. almost horizontal when the woman is standing. The
Round ligament gives some support for anteversion urogenital diaphragm support urethra by its fixation
and anteflexion positions of the uterus. to perineal body. Vesicourethral junction decreasing
Ovarian ligament a fibromuscular cord, together with
the tendency of these structures to rotate around the
the round ligament, is the homologue of the gubernac- attachment of the pubourethrovaginal ligament to
ulum of the testis of the male. the pubis.
Fascia ligaments consist principally of blood vessels
Arcus tendinei are two in number one on each side of
(largely veins), nerves, lymphatic channel and areolar the pelvis. Levator ani, arcus tendineus runs between
connective tissue. It is denser lateral to the cervix back of pubic bone and ischial spine. Medially is the
and the vagina and contains many smooth muscles.
arcus tendineus of the endopelvic connective tissue.
It lies above the levator ani muscles and has two
The former provides a soft tissue attachment for the
parts. Mackenrodt (cardinal, or transverse cervical)
connective tissue bundle of fibers attached to the
ligament attaches medially to the uterus at the internal
anterior vaginal sulcus.
os level being extensive and strong has an important
Pelvic diaphragm: It is formed by the levator ani
supportive function. It passes lateral to the pelvic wall. Its
muscle along with its superior and inferior fascial
posterior reflection—the uterosacral ligament—passes
coverings. It is derived from the fourth sacral myotome.
posteriorly around the lateral margin of the rectum and is
It was used to wag the tail in animals. In the upright
attached to the periosteum of the fourth sacral vertebrae.
It also assists in anterversion. These two ligments provide human being, it mostly supports the pelvic organs and
the major support to the uterus. helps in bladder and rectal continence. The muscle
Pubocervical fascia is inserted in the body of the pubis.
arise from pubic bones pelvic surface, ischial spines and
The anterior reflexion is weak and support bladder base the arcus tendinae. Converging in the midline, it can be
and anterior vaginal wall. It is called pubocervical divided into the puborectalis (most medial, encircling
ligament. and supporting and forming additional sphincters to
Urogenital diaphragm: It is divided into two layers—
the rectum and the vagina), the pubococcygeus (the
the superficial and the deep. most important and strongest part stretching from
1. The superficial layer contains three muscles: pubis to the coccyx) and iliococcygeus (the posterior-
i. Bulbospongiosus muscle (called sphincter vagi- most, getting attached to the coccyx).
nae as it surrounds the vaginal opening) is attached Posterior part of pelvic floor is formd by coccygeus
anteriorly to corpora cavernosa of the clitoris). muscle which arise from ischial spine and gets inserted
ii. Ischiocavernosus (covering clitoral crura). into lower sacrum and the upper coccyx. It lies in the
iii. Superficial transverse perineal muscles. same plane as iliococcygeus. Sacrospinous ligament is
2. Deep layer contains only the deep transverse perinei the tendon or aponeurosis of the coccygeus muscles.
muscle originating from inner side of ischial ramus Pelvic peritoneum also provides some supporting.
and attaching at the perineal body and urethra. Rectovaginal septum: The fascia of Denonvilliers is a
These two layers of muscles and their fascial covering distinct fibromuscular elastic.
constitute the urogenital diaphragm.
Bilateral Pubourethrovaginal ligaments (anterior, Applied Anatomy
posterior and intermediate) suspend the urethra to If a tear at this attachment occurs it may result in consti
the pubic bones. Reflection of inferior and superior pation. The laceration in the midline and occurs in exces
facial layers of urogenital diaphgram form anterior sive stretching during labor.
crosses the left ureter and the left common iliac artery
BLOOD SUPPLY TO THE FEMALE bifurcation before entering infundibulopelvic ligament.
PELVIC ORGANS (TABLE 2.1) Each artery then sends branches to the ovary through
Abdominal aorta lies to the left of midline in front of the mesovarium; branches also supply the ureter and
the vertebral column from the T12 downwards with the fallopian tube. One tributary reaches the cornua of
inferior vena cava on its right side. From its lower part the uterus and freely anastomoses with the uterine
arises the ovarian, the inferior mesenteric and superior branches to produce a continuous arterial arch.
rectal arteries anteriorly and the middle sacral and the Ovarian vein: Drain into the pampiniform plexus of
lumbar artery posteriorly. It divides into right and left veins in the broad ligament and may become varicose.
commom iliac arteries at the level of L4 which in turn The left vein drains into the left renal vein and right vein
divide into internal and external iliac arteries. discharges into inferior vena cava like respective arteries.
Ovarian branch (2-right and left): It arise below the Inferior mesenteric branch: Originated from the
renal arteries from the abdominal aorta. Right branch abdominal aorta. It descends in front of the aorta and
enters infundibulopelvic ligament after crossing then deviates to the left. En route, it crosses the left
inferior vena cava and right ureters abdominal part. common iliac artery median to the left ureter and then
While the left branch may arise from left renal artery. It into the mesentry of the sigmoid colon. It can be injured
during paraaortic lymph node dissection. Along the
way it gives a left colic branch supplying the left half
TABLE 2.1: Arterial supply of pelvic organs
of the transverse colon and the descending colon and
Organ Artery Origin then continues as the superior rectal artery nourishing
Ovary Ovarian Aorta the upper rectum and anastomosing with the middle
Vein L-Renal Uterine Internal iliac and the inferior rectal branches.
R-IVC Middle sacral artery is a branch of abdominal aorta.
Fallopian tube Ovarian Aorta
Common iliac arteries (2) have length of about 4–5 cm
divide into the internal and external iliac branches in
Uterine Internal iliac
front of the corresponding sacroiliac joint behind the
Ovarian Aorta
ureter. The artery on the right is slightly longer, running
Vagina Vaginal Internal iliac in front, the left artery passes partly lateral and partly in
Uterine front of the corresponding vein. It has no branch.
Internal pudendal •• Two external iliac arteries run on the psoas major
Middle rectal muscle (medial boarder) to the inguinal ligament
Vulva Internal pudendal Internal iliac
midpoint from where it continue as femoral artery
where femoral vein is lateral and femoral nerve is
External pudendal Femoral
medial (VAN). Round ligament and ovarian vessels
Ureter Renal Aorta
cross in front of the artery on both sides. The branches
Ovarian Aorta of external iliac artery are superficial epigastric
Uterine Internal iliac artery, superficial circumflex iliac artery, inguinal
Superior vesicle Internal iliac artery and external pudandal artery which ansto
Inferior vesicle Internal iliac moses with internal pudendal artery after supplying
the skin of vulva.
Urinary Superior vesicle Internal iliac
bladder –– Femoral artery has two main branches. The
inferior epigastric artery runs obliquely along
Inferior vesicle Internal iliac
the deep inguinal ring; after going through the
Urethra Inferior vesicle Internal iliac transverse fascia it runs up and supply nearby
Internal pudendal Internal iliac muscle (rectus abdominis) and the skin above.
Sigmoid colon Left colic Inferior mesenteric It finally anastomoses with the superior epigastic
Rectum Superior rectal Inferior mesenteric artery above the level of the umbilicus. The sec-
ond branch is the deep circumflexartery, which
Middle rectal Internal iliac
supplies the transverse abdominal and internal
Inferior rectal Internal pudendal
oblique muscles.
•• Each internal iliac (hypogastric) artery divides at TABLE 2.2: Nerve supply of pelvis
greater sciatic foramen into anterior and posterior Nerve Spinal segment Innervation
branches. Its total length is around 4 cm. Its length Ilioinguinal L1 Sensory—mons, labia majora
is 8 cm in the fetus but after delivery the abdominal Genitofemoral L1, L2 Sensory—anterior vulva
4 cm forms the lateral umbilical ligament. The ureter (genital branch)
is anterior and the internal iliac vein is behind Posterior S2, S3 Sensory—vulva, perineum
the artery. The posterior division has 3 branches femoral
cutaneous
iliolumbar, lateral sacral and superior gluteal.
Pudendal S2, S3, S4 Sensory—perianal skin
They all supply muscles of the buttocks. vulva and perineum, clitoris,
The anterior division has seven branches in urethra, vaginal vestibule
addition to parietal branches. The superior vesical Motor—external. anal
supplies the upper part of bladder. The obturator sphincter, perineal muscles,
urogenital diaphragm
branch gives the iliac, vesical and pelvic branches.
Upper vagina, the base of the bladder and the rectum
are supplied by vaginal artery (equivalent to inferior anterior columnar (innervating of bladder and ure-
vesical artery of male). After anastomosing with thra) and posterior column (innervating uterus, cervix,
branches of the uterine artery it forms two median vagina, sigmoid colon and rectum).
longitudinal azygos arteries of the vagina one in front Parasympathetic nerves originates from sacral nerves
and one behind. The middle rectal artery gives blood (second, third, and fourth). These preganglionic fibers go
supply to the lower rectal muscles and anastomoses to the pelvic plexus and parasympathetic ganglion which
with inferior rectal (branch of internal iliac) and are located close to the wall of the viscera to be supplied.
superior rectal (branch of inferior mesentric) arteries.
The uterine artery is 2 cm from cervix and it crosses Somatic Nerves Supply
the ureter and runs tortuously, to accommo date It comes from anterior primary rami of first, second and
increased uterine size in pregnancy between the third lumbar and part of fourth lumbar nerve with some
broad ligament layers and give branches. These supply fibers of 12th thoracic (subcostal) nerve form the lumbar
the cervix, and the body of uterus, part of urinary plexus (placed on psoas major) and its major branches
bladder and one branch goes to the vaginal artery. At supply the pelvic organs.
the end it anastomoses with the ovarian artery. The The iliohypogastric nerve supplies the buttocks.
uterine branches goes circum ferentially around the The ilioinguinal nerve innervates the skin of the mons
myometrium providing coiled radial branches ending and surrounding vulva (both from first lumbar nerve).
as basal arteries to supply the endometrium. Genitofemoral nerve (first and second lumbar nerve); its
genital branch supplies the skin of the labia majus. From
NERVE SUPPLY OF PELVIS (TABLE 2.2) second and third lumbar nerves arise lateral cutaneous
nerve, it supplies the thigh. The femoral nerve (second,
It is both autonomic and somatic. third and fourth lumbar nerves) is the largest branch of
Autonomic nerve supply: Pelvic plexuses supply all inter- lumbar plexus. Same is the origin of obturator nerve. They
nal pelvic organs except ovaries and fallopian tubes which both supply muscles of the hip. The lumbosacral trunks
are directly supplied by nerves from preaortic plexus arise from fourth and fifth lumbar nerves. Anterior rami
placed along ovarian vessels. of first, second and third sacral nerves join this trunk and
form the sacral plexus in front of pyriformis muscles. The
Autonomous Nerve Supply major branch is the sciatic nerve. The second branch is
Both sympathetic and parasympathetic innervations are the pudendal nerve. It re-enter the pelvis with the internal
seen. pudendal artery (on lateral side) at ischial spine via lesser
Sympathetic branches from the lower part of lumbar sciatic foramen. In the pudendal canal, it is on the lateral
sympathetic trunk join the aortic plexus and ganglia, wall of ischiorectal fossa. A pudendal block is given using a
over the bifurcation of aotra to form superior hypogas- local anesthetic at the point where the nerve curls around
tric plexus. Near rectum it bifurcates into right and left the ischial spine. The nerve gives three terminal branches.
inferior hypogastric plexus which further divides into Motor and sensory supply to anal canal, external anal
spincter and skin around the anus is by inferior rectal TABLE 2.3: Lymphatic drainage of the female pelvis
branch. Perineal branch nerve divides into the medial and Nodes Primary afferent connections
lateral posterior labial and supplies the skin of the labia
Aortic/paraaortic Ovary, fallopian tube, uterine corpus (upper)
majora and anal sphincter, levator ani, bulbospongiosus, drainage from common iliac nodes
corpus spongiosum and the urethra. The third is dorsal
Common iliac Drainage from external and internal iliac nodes
branch of clitoris after passing through pudendal canal
External iliac Upper vagina cervix, uterine corpus (upper)
supply the crura of the clitoris and the surrounding tissue. drainage from inguinal nodes.
Internal iliac
LYMPHATIC DRAINAGE OF THE
}
Lateral sacral
FEMALE PELVIS (TABLE 2.3) Superior gluteal
Inferior gluteal
The main lymph nodes are placed along the blood vessels. Obturator Vulva, lower vagina (rare: deep uterus, tube
They are important in radical surgeries of the female Vesical ovary)
reproductive malignancies. Rectal
The superficial femoral (inguinal) nodes form a chain Parauterine
just below the inguinal ligament. Lymphatics from Inguinal
Superficial
gluteal and anterior abdominal wall are received by
lateral nodes. Lymphatics from perineum, vulva, lower
vagina, the lower anal canal and from the uterus as flex iliac nodes are also members of this group. Similarly,
the lymph vessels traveling with the round ligament to internal iliac vessels have corresponding.
anterior abdominal wall are drained to medial nodes. Internal iliac nodes placed side by side to drain all the
The lymphatics both sides of the vulva anastomose pelvic viscera. The obturator lymph node in the obturator
freely hence, the importance of removing the whole of fossa and the sacral lymph nodes (on median and lateral
the vulva in cases of malignant disease. sacral vessels) are members of internal iliac group.
On the median side of femoral vein lie deep (inguinal) The common iliac lymph nodes are situated on either
lymph nodes. Lymphatics from nodes of cloquet drain side of the aorta. They receive afferents from the exter-
the clitoris and some the superficial femoral nodes. nal iliac and the internal iliac lymph nodes.
Superficial and deep inguinal lymph nodes efferents Besides those organs which receive blood supply
reach external iliac group of lymph nodes in pelvis. directly from aorta drain their lymph directly to the para-
On the corresponding vessels lie the external iliac lymph aortic lymph nodes, viz. ovary, fallopian tubes, upper
nodes and form the lateral median and anterior groups. ureter and in view of arterial anastomoses, uterine fundus.
Lymphatics from cervix, upper vagina, urinary bladder, Their efferents together form the lumbar trunk on both
lower abdominal wall and from the inguinal lymph node sides; the lumbar trunks terminate at the cisterna chyli at
drain into this group. The inferior epigastric and circum- the base of the neck.
1. Write short notes on:
i. Female external genital organ
ii. Functions of vagina
iii. Pouch of Douglas
2. True/False:
i. Urinary bladder is a non-muscular organ.
ii. Clitoris represents the male penis in female.
iii. In fetal life, the ovaries are situated in the lumbar region.
iv. More than 10 different anatomical systems give support to birth canal.
3
Anil Kumar Jain, Sudha Sa/hon
The Bony Pelvis
INTRODUCTION
The process of normal labor depends on a safe journey of
the fetus through the maternal pelvis. No two pelvis are
exactly the same and slight variation of pelvic structure
does not hamper normal delivery. At the most, the
variation may delay process oflabor, but marked deformity
may render vaginal delivery impossible.
The maternal pelvis is made up

innominate bones one on each side and sacrum witH
coccyx posteriorly. Each innominate bone is compesed of
the ilium, ischium and pubis. These bones are articulated Fig. 3.1: Pelvic inlet with its bony landmarks
together by four joints-the symphysis pubis joint Keys: 1-Center of upper border of symphysis pubis; 2-Pubic crest;
anteriorly, two sacroiliac joints posterolaterally and one 3-Pubic tubercle; 4-Pectineal line; 5-lliopectineal eminence;
sacrococcygeal joint posteriorly. The sygipijysis pubis is a 6-llial portion of lliopectineal line; 7-Sacroiliac joint; 8-Anterior
secondary fibrocartilaginous joint witho t a capsule or a border of ala of sacrum; 9-Center of sacral promontory
synovial cavity. The articular surfaces of the two pubic bones
are covered with a hyaline cartilage On the other hand, landmarks on the brim anteroposteriorly on either side
the sacroiliac joint between ilium and sacrum is a synovial are the center of the upper border of the symphysis pubis,
joint with a capsule and synovial cavity. Due to softening of
pubic crest, pubic tubercle, pectineal line, iliopectineal
ligaments during pregnancy, probably under the effect of
eminence, ilial portion of the iliopectineal line, sacroiliac
the hormone relaxin, some gliding movements are possible
joint, anterior border of the ala of sacrum and center of
at the symphysis pubis and the sacroiliac joints. These joints
sacral promontory. It is heart shaped with the promontory
may become hypermobile, thus causing enlargement of the
of the sacrum forming a slight projection into it posteriorly.
pelvic cavity during labor. Even the coccyx is pushed back
at the sacrococcygeal joint by the descending fetal head False Pelvis (Figs 3.2 and 3.3)
during labor. The pelvis is divided into two parts-upper
false pelvis and lower true pelvis: The junction of these two It mainly consists of two iliac bones with two iliac crests (one
is called the pelvic or inlet brim. on each side) forming the superior limit. The false pelvis does
not have any bony boundary anteriorly, being bounded by
Pelvic Inlet (or Brim) (Fig. 3.1) the anterior abdominal wall. Posteriorly, it is bounded by the
Pelvic inlet continuous from sacral promontory and lumbar vertebrae and laterally by iliac fossae. The false pelvis
extending along the ilium on each side in a circular has no obstetrical importance except to support the gravid
fashion, is a ridge called the brim. This is the entry way of uterus. In the past, it was thought to indicate the shape and
the fetus from the false pelvis to the true pelvis. The bony size of the true pelvis, which is not true.
The Bony Pelvis 25
Fig. 3.2: Normal female pelvis with false and true pelvis
Fig. 3.3: Innominate bone showing important landmarks Fig. 3.4: Angle of inclination
True Pelvis Plane

This part of the pelvis forms a bony canal through which It is an imaginary flat surface bounded by the bony land-
the fetus must pass during labor, hence it is of great marks of the inlet or brim and is often called the superior
significance. The true pelvis is shallow anteriorly, formed strait. This plane is not horizontal but tilted forward when
by the symphysis pubis (4–5 cm) and deep posteriorly, a woman is standing and forms an angle of around 55°
formed by the sacrum and coccyx (10 cm). It is divided with the horizontal. This is called the angle of inclination.
into three parts—inlet, cavity and outlet. Radiologically, this angle can be measured by measuring
the angle between the front of L5 and the plane of inlet and
Inlet subtracting this angle from 180° (Fig. 3.4).
The inlet is narrowest anteroposteriorly and widest from
side to side, i.e. in the transverse diameter. Therefore, the Obstetrical Significance
fetal head enters the pelvic inlet with its longest diameter When the angle of inclination is increased as in sacralization
(anteroposterior) in the widest part of the pelvis (transverse of L5, is called high inclination. Due to change of uterine
diameter). axis, as compared with the axis of inlet, engagement of
fetal head is delayed and occipitoposterior positions are

more common. Labor is prolonged as altered structure
of pelvis delays the descent of the head and a flat sacrum
hinders internal rotation of the fetal head. On the other
hand, lumbarization of S1 (first sacral piece) decreases
angle of inclination and this is called low inclination. This
favors early engagement and easy delivery.
Axis of Inlet
It is a line drawn from center of the inlet, perpendicular
to the plane of the inlet. Its direction is downwards and
backwards (Fig. 3.5). The axis passes through the umbilicus
to the coccyx. The uterine axis generally coincides with the
axis of the inlet and the fetus is easily pushed into the brim
with uterine contractions.
Fig. 3.5: The planes and axes of pelvis
Diameters of Pelvic Inlet (Figs 3.5 and 3.6) Keys: AB—Horizontal line; GB—Plane of inlet; FE—Plane of obstetrical
outlet; DC—Axis of inlet; GH—Axis of obstetrical outlet
From front to back, there are three diameters worth men-
tioning:
•• Obstetrical conjugate (10 cm): It is the distance
1. Anteroposterior diameter (Figs 3.6A and B) also
between the midpoint of the sacral promontory to
known as the true conjugate, anatomical conjugate
or conjugate vera) (11 cm): It is the distance between the prominent bony projection in the midline on the
the inner margin of the middle of upper border of the inner surface of symphysis pubis. It is the shortest
symphysis pubis to the midpoint of the sacral promon- anteroposterior diameter of the brim and cannot
tory. Its direct measurement can only be made by X-ray be measured clinically but can be estimated by
pelvimetry. By subtracting around 1.25 cm from this we deducting 1.5–2.0 cm from the diagonal conjugate
can obtain the obstetric conjugate. depending on the height, thickness and inclination
A B
Figs 3.6A and B: A. Diameters of pelvic inlet; B. Anteroposterior (AP) diameters of pelvis
Keys: OC—Obstetric conjugate; TC—True conjugate
The Bony Pelvis 27
Fig. 3.7: Vaginal examination to determine diagonal conjugate Fig. 3.8: Metal scale mounted on the wall for measuring diagonal
Keys: S—Symphysis pubis; P—Sacral promontory conjugate after vaginal examination
of the symphysis pubis. Obstetric conjugate can be The diameter usually lies slightly closer to the sacral
measured by ultrasound examination. promontory and divides the brim into an anterior and
•• Diagonal conjugate: It is the distance between the a posterior segment. The head negotiates the brim
lower borders of the symphysis pubis to the midpoint through a diameter, called available or obstetrical
on the sacral promontory. It measures 12 cm. It is the transverse. This is described as a diameter which
diameter, which can be measured clinically during bisects the anteroposterior diameter in the midpoint.
pelvic assessment in late pregnancy or in labor. Thus, the obstetrical transverse is either equal or less
How should the diagonal conjugate be measured? than the anatomical transverse.
The patient is placed in the dorsal position. Two 3. Oblique diameter (12 cm): It extends from one sacroiliac
fingers are introduced into the vagina taking aseptic joint to the opposite iliopubic eminence. There are two
precautions. The fingers are to follow the anterior oblique diameters, right and left named according to
sacral curvature. In a normal pelvis, it is not easy the sacroiliac joint from which they start, e.g. the right
to feel the sacral promontory or at best it can be oblique diameter extends from the right sacroiliac joint
felt with difficulty. However, in order to reach the to the left iliopectineal eminence. This is the diameter in
promontory, the elbow and the wrist are to be which the presenting part engages (Fig. 3.6).
depressed sufficiently while the fingers are mobilized Cavity
in the upward direction. The point at which the bone Definition: It is a space (not a plane like the brim) bounded
recedes from the fingers is the sacral promontory. above by the brim and below by the plane of least pelvic
The fingers are then mobilized under the symphysis dimensions.
pubis and a marking is placed over the gloved index Plane of least pelvic dimensions (or narrow pelvic
finger by the index finger of the left hand (Fig. 3.7). plane): It is like the plane of the inlet and this flat
The internal fingers are removed and the distance surface also has bony landmarks. It extends from the
between the marking and the tip of the middle finger lower border of the symphysis pubis to tip of ischial
gives the measurement of the diagonal conjugate spines laterally and the tip of the fifth sacral vertebra
(Fig. 3.8). Practically, if the middle finger fails to reach posteriorly. As the name indicates, it is the narrowest
the promontory, generally termed as promontory plane of the pelvis, roughly corresponding to the origin
not tipped, it is likely that the conjugate is adequate of the levator ani muscles.
for an average-sized head to pass through. Plane of cavity: Since the cavity is not a flat surface
2. Transverse diameter (Fig. 3.5): It is the distance but a space extending from S1 to S5 sacral vertebrae
between the two farthest points on the pelvic brim over posteriorly and symphysis pubis anteriorly, its plane
the iliopectineal lines. It measures 13 cm. is considered somewhere in the middle of this space.
pelvic dimensions; otherwise it forms a wedge posteriorly

(Fig. 3.9).
Diameter of mid pelvis: Anteroposterior diameter (11.5
cm). It is measured from the lower border of the symphysis
pubis to the junction of S4 and S5 or the tip of S5 (11 cm),
whichever is applicable.
Bispinous or transverse diameter (10.5 cm): It is the
distance between two ischial spines.
Obstetrical Significance of Cavity

The upper part of the pelvic cavity is cylindrical while the
lower portion is curved. If the axis of cavity is viewed from
the side, it will be clear that the fetal head descends directly
downwards till it reaches the ischial spines and then curves
forward. It is at this level where internal rotation occurs.
Fig. 3.9: Pelvic cavity and mid pelvis at the junction of S4 and S5
or tip of sacrum Importance of Ischial Spines
(Plane of Least Pelvic Dimension)
The plane of the cavity extends from the midpoint of the Ischial spines on each side are important bony landmarks
posterior surface of the symphysis pubis to the junction on the ischium at the mid pelvis.
of the second and third sacral vertebra (Fig. 3.9). As it is Ischial spines form the origin of the levator ani muscles.
the roomiest plane of the pelvis, it is also called plane of It is at this level that the internal rotation occurs (and
greatest pelvic dimensions. the level of arrest when it does not, since it is the plane
Shape of cavity: It is almost round in shape. of least pelvic dimension).
Axis of cavity: It is a mid perpendicular line drawn to the It marks the beginning of the forward curve of the pelvic
plane of the cavity. Its direction is almost downwards. axis.
Diameters The ischial spines are easily felt on vaginal examination
•• Anteroposterior diameter (12 cm): It is the distance and the degree of descent of fetal head into the pelvis
between the midpoint on the posterior surface of the (usually termed station of head) can be clinically judged
symphyis pubis to the junction of the second and third in relation to them. The level of the ischial spine termed as
sacral vertebrae. ‘0’ station, above this level, stations are –1, –2, etc. While
•• Transverse diameter (12 cm): It is the distance below this level, stations are +1, +2, etc. If the head has
between two farthest points laterally. As there are reached the level of the ischial spines, it is certain that it has
no bony landmarks and points lie on the soft tissues engaged in the pelvic brim except when there is excessive
covering the sacrosciatic notches and obturator molding and caput formation (sometimes mistaken as the
foramina, this diameter cannot be exactly measured lower limit of the head) or when face presents.
and is roughly 12 cm. They are important landmark for pudendal nerve block
for analgesia.
Mid Pelvis
It is a space bounded above by the plane of the greatest Outlet
pelvic dimensions and below by a plane called the mid From an obstetric point of view, it is better to regard the
pelvic plane. It roughly corresponds to the lower half pelvic outlet as a constricted lower portion and not merely
space of the cavity of pelvis. its lower bony limits. Therefore, the pelvic outlet is described
Mid pelvic plane: Bounded anteriorly by the lower margin as an obstetrical outlet and an anatomical outlet.
of symphysis pubis, this plane extends through the ischial
spine to the junction of S4 and S5 sacral pieces or the tip of Obstetrical Outlet
fifth sacral piece according to the structure of the sacrum. It is a shallow bony segment (and not bony landmark)
Therefore, if it meets at the tip of the S5 sacral piece, the bounded above by the plane of least pelvic dimensions
plane becomes the same as that of the plane of least and below by the anatomical outlet (Fig. 3.10).
The Bony Pelvis 29
Plane: It is represented by a line joining the lower

border of the symphysis pubis to the tip of the coccyx.
Axis: It is a line drawn at right angles to the plane of the
outlet and its direction is downwards and forwards.
Diameters
•• Anteroposterior: It extends from the center of the
lower border of symphysis pubis to the tip of the coc-
cyx. It is obvious that the length of the anteroposte-
rior diameter is reduced by forward projection of the
coccyx. During labor, however, the movement of the
Fig. 3.10: Diagrammatic representation of pelvic segments (cavity coccyx at the sacrococcygeal joint carries it back-
mid pelvis and obstetrical outlet) and bony landmarks (inlet, plane wards so that length of this diameter is increased.
of greatest and least pelvic dimensions, and anatomical outlet) But when the sacrococcygeal joint is ankylosed, this
movement cannot occur and hence, the available
This space has lateral and posterior walls. Its anterior diameter is either reduced or fracture of coccyx
wall is deficient at the pubic arch, the lateral wall includes occurs. The anteroposterior diameter with coccyx
the greater part of ischial bones and the posterior wall pushed back is 13 cm and with coccyx at normal
includes the whole of the coccyx. position is about 11 cm (2–2.5 cm less).
Shape: It is oval anteroposteriorly.
•• Transverse diameter (11 cm): It is also called the
Plane: It is the same as the plane of least pelvic

bi-ischial or intertuberous diameter or transverse
dimensions. diameter of the outlet. It is the distance between the
Axis: It is represented by a line-joining the center of
inner borders of ischial tuberosities.
•• Subpubic angle (85° ± 5°): It is formed by the joining
the plane of least pelvic dimensions with the sacral
promontory. Its direction is almost vertical. of the two descending pubic rami.
•• Waste space of Morris: Normally the pubic arch
Diameters
•• Transverse or bispinous diameter (10.5 cm): It is

is wide and a round disc of 9.4 cm (diameter of a
measured between the two ischial spines. well-flexed fetal head) can pass through the pubic
arch at a distance of 1 cm from the midpoint of the
•• Anteroposterior diameter (11 cm): It extends from
inferior border of symphysis pubic (Fig. 3.11). This
the lower border of the symphysis pubis to the tip of
is called the waste space of Morris. If the pubic
the sacrum.
arch is narrow, the fetal head is pushed backwards
Anatomical Outlet and less space is available for the fetal head to pass
through. Therefore, if the waste space of Morris is
It is a bony boundary as mentioned earlier. Viewed from
increased from normal, the fetal head has to pass
below, one can easily make out its boundaries. It is bounded
through a smaller diameter, termed as the available
in front by the inferior border of the symphysis pubis, and
anteroposterior diameter, injuring the perineum or
laterally by the ischiopubic rami, ischial tuberosities
sometimes causing arrest of the head.
and sacrotuberous ligaments. Posteriorly the tip of the
coccyx bounds it.
Thus, it consists of two triangular planes with a common
base formed by a line joining the ischial tuberosities. The
pubic arches present the sides of the anterior triangle with
the apex at the inferior border of symphysis pubis. From an
obstetric point of view this triangle is of great importance
because the fetal head must use this space to exit from the
pelvis. Women have a wide pubic arch whereas men have
a narrow pubic arch. The apex of the posterior triangle is at
the tip of coccyx.
Shape: It is diamond or rhomboid shaped. Fig. 3.11 Waste space of Morris at subpubic angle
Pelvic Axis the canal of the bony pelvis with its convexity snugly fitting
the concavity of sacrum. This is also called the curve of
Anatomical Carus and is directed at first downwards and backwards
If the axes of inlet, cavity and outlet are joined together, (axis of inlet), then gradually more and more forwards
they form a uniform curve, which traverses the center of until it reaches the axis of the oultet.
i. Diameter of pelvic
ii. Angle of inclination
iii. Mid pelvis
2. True/False
i. Axis of inlet is a line drawn between center of inlet and perpendicular plane of inlet.
ii. Bispinous diameter is about 10 cm.
iii. Obstetric outlet is a shallow bony segment.
iv. Pelvic inlet is also known as brim.
4
Fetus and Fetopelvic Relations
THE PASSENGER (THE FETUS)

As discussed earlier, maternal pelvis must be of an adequate
size and a proper configuration to allow the passage of
the fetus. However, even in such a pelvis, the birth may
be difficult if the fetus is too large or is in an abnormal
position. For a successful outcome, the fetal skull (head),
shoulders, trunk and buttocks have to pass through the
maternal pelvis. From an obstetric viewpoint, the fetal
head is the most important part of the fetus. If it can pass
through the pelvis safely, there is usually no difficulty in
delivering the rest of the body, although occasionally the
shoulders may cause some trouble (shoulder dystocia).
FETAL HEAD (SKULL CRANIUM)

(FIGS 4.1 AND 4.2)
Fetal skull can be divided into two parts—the base Fig. 4.1: Fetal skull showing landmarks and regions of obstetric
and the vault. Four bones—the sphenoid, the ethmoid importance
and the two temporal bones lie at the base of the skull.
These bones are closely knit; hence, the base is rigid and
incompressible. On the other hand, the vault is made up
of thin, pliable, flat bones, which are compressible to some
extent. These bones are the two frontal bones in front, the
occipital bone at the back and the two parietal bones
in between. These bones at birth are not closely knit but
separated by membranous interspaces called sutures and
the intersection of these sutures are known as fontanels.
There are four main sutures (Fig. 4.3):
1. The sagittal or longitudinal suture: Lies across the
vault of the skull in the midline between two parietal
bones and separates the skull into the left and the right
halves.
2. The coronal suture: It runs between the parietal and
frontal bones, extending transversally on either side Fig. 4.2: Regions of the skull showing the large, compressible
from the anterior fontanel. vault and the non-compressible face and base
–– Position of occiput in relation to the pelvis

–– Degree of flexion (or attitude of fetus)
•• It facilitates molding of the head
•• As this fontanel ossifies by one and half year, it helps
to accommodate the marked brain growth, which is
the maximum in the first year of life (brain almost
doubles its size in first year).
•• Intracranial status of fetal head is reflected—
tense and elevated in raised intracranial tension;
big fontanel with wide apart sutures may suggest
hydrocephalus and a dimpled or depressed floor
seen in dehydration.
•• Rarely—lateral angle of the fontanel is used to draw
cerebrospinal fluid (CSF) from the lateral ventricle.
Similarly blood can be withdrawn from the superior
longitudinal sinus for fetal blood sampling for pH in
Fig. 4.3: Bones, sutures and fontanel on fetal skull as viewed from
fetal distress.
above with head partially deflexed
Posterior fontanel or lambda: This triangular fontanel
is formed by the junction of three suture lines—sagittal
3. The frontal suture: It lies between the two frontal suture anteriorly and lambdoid sutures on either side.
bones, extending anteriorly from the anterior fontanel. It measures around 1.2 × 1.2 cm. It ossifies by term but
4. The lambdoid suture: It separates the occipital bone may be membranous in preterm babies. This fontanel
and the two parietal bones, extending transvesely on also helps to denote the position of the head in relation
the left and right from the posterior fontanel. to the maternal pelvis.
These sutures are of a great obstetric importance as
they allow gliding movements of one bone over the other Presenting Parts of Fetal Skull
(molding), causing a small variation in the shape of the The skull is arbitrarily divided into several regions of
fetal head necessary to negotiate the maternal pelvis. In obstetric importance. These are as follows:
addition, the digital palpation of the sagittal suture during Vertex: This is a quadrangular area bounded anteriorly
labor while performing an internal examination gives by bregma and coronal sutures, posteriorly by lambda
important information regarding the internal rotation and lambdoid sutures and laterally by arbitrary lines
of the head and the manner of engagement of the head passing through the parietal eminences. Fetal head lies
in flexion during this presentation.
(synclitism or asynclitism).
Face: This is an area bounded by the root of the nose
along with supraorbital ridges and the junction of the

Fontanels
chin or floor of mouth with the neck. The fetal head is
A wide gap at the intersection of the sutures is called a fully extended during this presentation.
fontanel. Six fontanels exist in the skull at term but only Brow: This is an area of forehead from the root of nose
two of these are of obstetrical significance. These are: and supraorbital ridges to the bregma and coronal
Anterior fontanel or bregma: Felt as a “soft spot” just sutures. The fetal head lies midway between full flexion
above the forehead of a newborn; is large and diamond and a full extension in this presentation.
shaped. It is formed by the frontal suture anteriorly, the Other areas on the fetal skull generally described are:
Sinciput: Area in front of anterior fontanel corres
sagittal suture posteriorly and the two coronal sutures
ponding to forehead.
on either side. Its average measurement is around 3 cm
Occiput: Area limited to occipital bone.
anteroposteriorly and 2 cm transversely. It ossifies by 18
Mentum: Refers to the chin of the fetus.
months and failure to do so by 24 months is pathological. Parietal eminences: As the name indicates, these are
Obstetrical and clinical significance: eminences of parietal bones on either side.
•• During internal examination: Palpation of fontanel Sub-occiput: It is the junction of the fetal neck and
along with sutures occiput, also called the nape of the neck.
–– Confirm vertex presentation (whenever in doubt) Sub-mentum: It is the junction between neck and chin.
Fetus and Fetopelvic Relations 33
Fig. 4.4: Anteroposterior diameters of fetal skull

Keys: SOB—Suboccipito-bregmatic: 9.4 cm; SOF—Suboccipito-frontal: 10 cm; OF—Occipito-frontal: 11.3 cm; MV— Mento-vertical: 13.8 cm;
SMV—Submentovertical: 11.3 cm; SMB—Submento-bregmatic: 9.4 cm
Diameters/Circumferences of Skull (Fig. 4.4) said to be engaged. In a fully flexed, vertex presentation,
the transverse biparietal diameter and the anteroposterior
The shape and diameter of the circumference of the fetal
suboccipito-bregmatic diameter measure the same and
skull varies with the degree of flexion and hence the
remain on the same plane.
presentation. A normal true pelvis permits the fetal skull,
in various vertex and face presentations, to pass through
but not a fetal head in brow presentation (diameter 13 cm). CHANGES IN FETAL SKULL DURING LABOR
The various anteroposterior diameters of fetal head
are given in Tables 4.1 and 4.2 and transverse diameter in
Molding
Figure 4.5 respectively. It is an alteration in the shape of the fetal head while
As the vault is compressible, these diameters can be passing through a resistant maternal pelvis during labor.
reduced in length to some extent if the need arises, to allow As the contents of the fetal skull are not compressible, the
the passage of the fetal head through the maternal pelvis. reduction in size is minimal, made possible by the presence
of fontanel and sutures (the unossified areas in the fetal
skull), as well as by squeezing out of some blood and CSF
ENGAGEMENT OF FETAL HEAD
from the skull (Figs 4.6A and B and 4.7A to E).
When the maximum transverse diameter of the fetal head Due to compression, the two parietal bones generally
(biparietal) passes through the pelvic brim, the head is overlap the adjacent bones as well as over each other.
TABLE 4.1: Anteroposterior diameters of fetal skull

Attitude
S. No. Name Description of fetal skull Presentation Length Circumference Shape
1. Suboccipito- From the nape of the neck to the Complete flexion Vertex 9.4 cm 27.5 Round
bregmatic center of bregma
2. Suboccipito- From the nape of the neck to Incomplete Vertex 10 cm 30 cm Oval
frontal the anterior end of bregma flexion or slight
or midpoint of frontal suture/ deflexion
sinciput
3. Occipito- From the occipital protuberance Marked Vertex 11.3 cm 34 cm Oval
frontal to the root of the nose (Glabella) deflexion
4. Mento-vertical From the mid point of the chin to Partial extension Brow 13.8 cm 37.5 cm Oval (bigger)
the highest point (generally the
center) on the sagittal suture.
5. Submento- From the angle between neck Incomplete Face 11.3 cm 34 Oval
vertical and chin to the center of sagittal extension
suture
6. Submento- From the angle between neck Complete Face 9.4 cm 27.5 cm Round
bregmatic and chin to the center of bregma extension
TABLE 4.2: Transverse diameters of fetal skull

Name Description Length Remarks
Biparietal diameter Distance between the two parietal eminences 9.4 cm This is engaging diameter of fetal skull
irrespective of position of the head.
Super-subparietal diameter Distance between a point placed below one parietal 8.5 cm
eminence to a point placed above other parietal
eminence of the opposite site.
Bi-temporal diameter Distance between the lower ends of the coronal 8 cm
sutures at the temples.
Bi-mastoid diameter Distance between the tips of the mastoid processes 7.5 cm Being at the base of the skull, it is
incompressible. Therefore, it can only
be reduced by obstetrical operations
(destructive procedures)
Thus, the edges of frontal bones anteriorly, occipital bones

posteriorly and temporal bones at sides dip under the
parietal bones. The anterior parietal bone can overlap the
posterior parietal bone. In the first vertex position (LOA),
the right parietal bone tends to overlap the left one while
in the second vertex position (ROA), the left overlaps the
right parietal bone. Compression of the girdle of contact
(engaging diameter) leads to bulging of the fetal head, in
a diameter lying at right angles to that of compression,
causing alteration in shape of the fetal head, although
the change in size is minimal. For example, compression
of suboccipito-bregmatic diameter in a fully flexed vertex
presentation will lead to compensatory elongation at the
mento-vertical diameter.
Grading
According to the severity of compression and thereby extent
Fig. 4.5: Transverse diameters of fetal skull of overlapping, Molding is divided into:
Fetus and Fetopelvic Relations 35
Figs 4.6A and B: Demonstration of principle of molding. The diameter compressed is diminished while the diameter at right angles to
it is enlarged
A B C
D E
Figs 4.7A to E: Molding when head presents (shown in dotted line) A, B, C—vertex presentation. A. Head well flexed; B. Head partially
flexed; C. Head deflexed; D. Face presentation; E. Brow presentation
Grade-1 the bones touch each other but do not overlap scalp beneath the girdle of contact, leading to effusion
Grade-2 the bones overlap but are easily separable of serous fluid into subcutaneous cellular tissue. Thus a
(reducible overlapping) diffuse, boggy swelling, not limited by sutures, appears
Grade-3 fixed, irreducible overlapping. on the fetal skull disappearing within 24 hours after birth.
In normal labor, slight molding is physiological and harm Apart from vertex presentations; caput can also form in
less and usually disappears within a few hours of delivery. the face and other presentations. The site of caput in vertex
However, extreme molding as seen in cephalopelvic dis presentations is:
proportions, may produce severe intracranial compression, LOA—posterior end of right parietal bone
resulting in tears in the tentorium cerebelli or subdural hem ROA—posterior end of left parietal bone
orrhage. ROP—middle of left parietal bone
LOP—middle of right parietal bone.

Caput Succedaneum (Fig. 4.8)
It is a localized swelling on the fetal skull due to edema of Obstetrical Significance
tissue beneath the girdle of contact. This girdle of contact may Caput signifies a static position of fetal head for a
be bony (maternal pelvic bones) or soft tissue like the dilating
long period. Therefore, this is an important sign of a
cervix or the vulval ring. Caput usually forms after rupture of
prolonged first stage of labor. The size of the caput is
membranes and always during the first stage of labor.
proportional to the degree of compression and the
As the fetal head is driven down, the tissues in contact
length of time which elapses between the rupture of
with the cervix are compressed thus hampering the venous
membranes and a full dilation of the cervix.
and lymphatic drainage from the unsupported area of
Location of caput gives an idea about the position of
the fetal head in the pelvis and the degree of its flexion.
As mentioned above, in left positions, the caput forms
on the right parietal bone and in right positions, on the
left. When the head is fully flexed, caput is placed far
back, close to or overlapping the posterior fontanel,
while when the head is incompletely flexed, it is found
to be more anterior and may even be present near the
anterior fontanel.
Secondary caput succedaneum after internal rotation—
if the head is delayed on the pelvic floor for long, a caput
will form upon the part of the scalp which presents at the
vulva, i.e. the region of occipital bone near the posterior
fontanella. Location of secondary caput succedaneum
in all positions of vertex is the same, when forward
rotation of occiput has occurred. But in cases with face
Fig. 4.8: Caput succedaneum to pubes, it is found on the sinciput.
1. Explain fetal skull with its landmarks and regions.
2. Write short note on anteroposterior diameters of skull.
3. Explain transverse diameters of fetal skull.
4. Explain changes in fetal skull during labor.
5. What is molding? Explain head representation during molding.
5
Patient-Doctor Communication
INTRODUCTION LISTENING AND LEARNING SKILLS

Besides thorough therapeutic know-how method of talking The place must be clean and orderly. A comfortable envi-
(communication) is the fundamental instrument by which ronment makes the patient feel at home. Greet her with a
physicians and patients relate to each other and attempt pleasant gesture. Accept her with dignity. Respect her as
to achieve therapeutic goals. The obstetrician ignore this an individual.
role sometimes. In that situation, the obstetrician give Managing a woman’s illness requires information
greater importance to blood tests, X-rays, ultrasound, etc. of sensitive and intimate activities. Maintenance of
But if we proceed to manage the illness without proper privacy should be ensured before probing into those
talking with the patient about the detail information or facts. Privacy in place, e.g. a separate room or at least
without understanding and respect for the autonomy of the use of curtains to make the patient or the couple feel
the patients, the treatment is mostly not proper. Effective free to bring up personal matters. Personal privacy or
communication in the medical world has been shown to
confidentiality is ensured by not sharing her/their facts
be essential to the patient’s satisfaction with the care they
with anyone. The records are kept secret (as in MTP/
receive. The development of trust, giving of full accurate
HIV) talking in a low tone so that noone else listens. She
information and for compliance, depend on the health
reassured that confidentiality will be maintained unless
care provider’s communication skills. It may be inborn in
she desires to reveal the facts to someone.
a few but the majority must acquire this by active learning.
Asking questions: Questions are asked to know the
Counseling is a way of working with people in which
purpose of the visit and to know the patient’s personal
we try to understand their feelings and help them to make
decisions. health. Both closed ended and open question are required.
Counseling skills are useful when we talk to our patients Closed ended questions are those whose answers end
as well as in our daily interactions with our colleagues, our with yes or no. They do not give us any extra information
family members and friends. besides what has been asked, e.g. Do you drink milk in
We, as doctors should make a sincere effort to be good your breakfast?
counselors, besides being astute clinicians. Open questions are those which encourage a person
The counseling skills will be discussed under two major to talk and give more information. This saves us from
headings: asking too many questions and helps us to learn more
1. Listening and learning skills in a shorter time, e.g. “What do you eat for breakfast?”
2. Building confidence and giving support. Closed questions are needed only for knowing informa
A patient often can provide the necessary piece to the tions as name, age, etc. They should be as few as
diagnosis puzzle if she listened to them effectively. As Sir possible. Open questions gives us the patient’s feelings,
William Osler once noted that the physician should listen, thoughts and explanation and thus give us to learn
for the patient will tell the diagnosis. Poor communication more about her. Do not ask leading questions as far as
is actually one of the main reasons for medico-legal cases, possible, e.g. ‘Now you won’t produce further children,
poor adherence to treatment, adverse advertisement and will you?’ These can guide the patient to give answers
termination of the physician’s care. we desire. These questions may even be judgmental.
Ask one question at a time. Be brief and clear. Only ask Remove barriers while talking with the patient or her
questions with a sense or purpose. Too many questions family. Sitting behind a table, writing notes simultane-
are not desirable. Be silent in between and give her ously, reading case papers or talking on the phone or
time to recollect. Do not interrupt unnecessarily. Ask mumbling to indicate involvement is some thinking pro-
question only, if you do not understand. cess can all act as barriers and discourage the patient.
Using supportive non-verbal communication—let patient Take time—do not show any signs of impatience, e.g.
speak more. Most of our communication should be non- looking at the watch or yawning or shifting positions
verbal. frequently while the patient is speaking. Make her feel
This means that we show our positive or helpful that you have time for her. She may not tell details of
attitude through our posture, expression, body language her illness and personal life to a provider who does not
or other means, but without speaking. Rapport and the take time to show interest in her complaints. By this,
communication of emotional support through non-verbal valuable clues for diagnosis are missed.
communication skills can help to cement the physician- Use a smooth and gentle tone of voice while talking. Do
patient relationship and their non use, interfere with not express judgment, disapproval or negative thoughts
effective care. by your tone of voice.
Touch appropriately according to the situation and the
Helpful Non-verbal Communications local customs, e.g. patting a newborn baby with the
To maintain the head level if we are sitting, the patient woman is appropriate. However, for a male doctor to pat
we are talking to should also be seated and not standing. a young female patient is not correct in a conservative
Lean forward while listening (Fig. 5.1). society like ours.
Maintain an eye-to-eye contact with the patient. Show
interest in what is being said, by nodding, smiling, Reflection and Paraphrasing
etc. Do not wrinkle your brow or raise an eyebrow in a Reflection means repeating back or reflecting what the
judgmental way. Listen with attention. Do not do any patient is saying. This helps the patient to realize that we have
other work when listening to her like playing with pen heard and understood her and she will further impart more
or paper weight, etc. information to us. It is desirable to say it in slightly different
way, so that is does not sound as if we are copying her, e.g.
if the patient says, “Doctor, I was awake the whole night due
to headache”. We can reflect on this information by saying
“You could not sleep last night because of headache?”
VALIDATION
The patient thinks that her situation is unique and is
uncomfortable. Thus, when we tell her that these feeling
are common to a particular situation, she feels reassured
that her feelings are not exceptional.
EMPATHIZE
This means to show the patient that we understand how
she feels. Empathy is different from sympathy.
Sympathy shows we are sorry for a person but from our
point of view whereas empathy is from the patient’s point
of view, e.g. if a patient says “Doctor I feel very tired since
the time I have become pregnant”. If the doctor says “Yes,
I understand how you feel; I too felt very tired when I was
pregnant.” This shows sympathy and it brings the attention
Fig. 5.1: Non-verbal communication towards the doctor. If the doctor says “You are feeling
Patient-Doctor Communication 39
very tired now-a-days. It must be very distressing to you”. mistaken idea is corrected. This has to be done in a tactful
This shows empathy to the patient. Empathy is more than way which does not sound too critical.
reflecting back what the patient says to us.
Excessive use of judging words such as good, bad, well, Recognize and Praise What a
right, normal, proper, wrong, etc. should be avoided as Patient is doing Right
they suggest a preconceived idea to the patient. Further As doctors, we are trained to look for problems and correct
the patient’s notion of what is correct or wrong may be very them. However, as counselors we must look for good
different from what is actually the fact, e.g. if the doctor practices followed by the patient and praise her. Praising
asks, ‘Are you taking your contraceptive pills or other good practices builds the patients confidence, besides
medications properly?’ The patients idea of what is ‘proper’ encouraging her to continue those good practices.
is not known to the doctor. Alternatively, the doctor can
asks, ‘How are you taking your contraceptive pills or other Give Practical Help Wherever Possible
drugs?’ This question will make the patient tell exactly how For example, helping a pregnant patient climb the examina
she takes her pills and hence gives complete information. tion table or get down, helps the patient to trust the doctor
Note, that judging questions are often closed questions. and build a rapport between them.
Using open questions helps to avoid using judging words.
Give a Little, Relevant Information
BUILDING CONFIDENCE AND Patients do not want technical details. But, want to
GIVING SUPPORT know what their problem is, how it happened and what
is to be done to treat it, chances of their cure and any
Accept what the patient thinks or feels—sometimes a
alternative method of treatment. Physicians must provide
patient may have a mistaken idea about something.
this information for all patients in simple clear and non-
It is important not to disagree with her in a blunt manner.
technical language. It is important not to overburden the
This will makes her feel wrong and reduce her confidence.
patient with too much information which may not be
She may not wish to reveal anything more after that. It is
relevant for her right now. Information should be given in
equally important not to agree with her mistaken idea.
a positive way and not in a critical manner. But it has been
So what can we do in a situation like this? We should
observed that patients usually want far more information
just accept what she feels or says. This means to respond in and detailed disclosures then their physicians assume that
a neutral way; neither agreeing nor disagreeing. they do.
Examples Use Simple Language
Patient—“Doctor, my husband will become weak if he Try to speak in the patient’s language. We should try to use
undergoes vasectomy operation?” simple, familiar terms to explain things to a patient and
Response 1. not use too much of scientific terminology. This improves
Doctor—“Oh no! There is no weakness whatsoever after our communication with the patient. She can understand
vasectomy”. better and can ask questions for clarification.
This is an inappropriate response, because it is disagreeing.
Response 2. Make One or Two Suggestions, not Commands
Doctor—“Yes, weakness after vasectomy operation can be When we counsel the patient, we suggest what she
a problem”. ‘could’ do not, what they ‘should’ do. Herein, lies the
This is also an inappropriate response because it agrees, entire basis of counseling that we leave all options open
with the patient’s mistaken idea. for the patient and let her decide what she wants to do
Response 3. in a particular situation after she has been given all the
Doctor—“I see, you are worried that your husband will relevant information. This leaves her feeling in control of
become weak after vasectomy.” the situation and helps her to feel confident.
This is an appropriate response because it shows a
neutral attitute and accepting the statement. Summarizing
After we have accepted and understood what the This skill is used to help the patient summarize what is
patient feels, we have to give her information so that her so far discussed in this session or meeting or interaction.
This help her classify the topics including medical or Intrauterine death or still birth: Parents and grand
personal information. What decision she has made and if parents are attached to the unborn children and their loss
not another session or appointment is given. She is also around the time of birth is a great trauma to them.
asked to return for follow-up. Our aim is to satisfy the The parents should see the efforts of the doctor in
patient as much as possible. reviving their baby. The dead baby should be handed
All this can be summarized in the GATHER approach over to the couple and their grief should be respected.
G—Greet the patient The use of sedatives to the mother should be avoided
A—Ask about herself and family as it delays the process of acceptance. There is a slight
T—Tell the patient about all the available options with increase in postpartum psychosis after perinatal loss.
their respective merits and demerits A discussion with the couple should be arranged to
H—Help her to choose the treatment discuss the events and possible preventive measures to
E—Explain be taken so as to avoid such incident in the future.
R—Return visit after treatment. Birth of a baby with an anomaly: Sometimes abnor
To check whether any improvement is seen or any malities are known to the patient before the child’s
problems or doubts have arisen and for check-up. Some birth, as detected by ultrasound. They should then be
times, a return visit is needed for the patient to take a told about probable cause (if known) and prognosis of
decision. these abnormalities.
Disbelief and sadness are reactions from parents of
these babies. The baby should be handed over to the
SUPPORT DURING EMERGENCY parents. In case of severe deformity, the deformed
SITUATIONS IN OBSTETRICS portion should be wrapped-up and normal portion of
baby should be exposed before the mother.
Emergency situations are very distressing for all concerned
The problem of the baby should be discussed with the
and evoke a range of emotions. Communication and
woman and her family. Correct treatment should be
genuine empathy are the most important aspects to be advised to them and for further management of the
stressed upon such situations. Each emergency situation child should be referred to a pediatrician.
is unique and has to be dealt with great sensitivity. Some of Postpartum depression: This condition requires
the common emergency situations faced by obstetricians psychological counseling and practical assistance (with
are: baby care). The doctor should listen to the woman and
Maternal mortality: This is a devastating situation for
give encouragement and assurance to the patient by
the family. At the time, the patient is in a critical position informing her that this is a fairly common condition. The
the doctor should listen to the distressed relatives and couple should be helped to come to terms to their role as
show empathy towards them along with providing parents. They are counseled to adjust to their old routine
emotional support to the family members. Speaking in activities, keeping their new responsibilities in mind.
simple local language and being honest is important. If the depression is severe then antidepressant drugs
Tell the family the exact condition of the patient and all may have to be prescribed.
the effort being made to save her. The paternalistic type of physician-patient relationship
After a patient’s death, the formalities of providing is not effective and detrimental to optimum patient
the necessary documents should be facilitated. Any care. Although the necessity of speaking with patients
questions from the family should be answered to their and fostering her assessment and self-determination
satisfaction. is an essential part of medicine in the view of ethics
Severe maternal morbidity: The condition and treatment and law, such actions does not occur naturally in
of the patient should be clearly explained to her and her clinical practice. If we want to improve our therapeutic
relatives and the treatment or referral arranged when skill, reduce medico-legal cases and adverse publicity
indicated. Show dignity and respect to the patient even if learning and improving communication skill is
she is unconscious. essential. Discuss her illness, procedures needed, her
A staff member should care for the emotional needs expectations, risks and the chance of improvement, any
of the woman and her family, if possible. Arrange for alternative method and in private practice, expenses.
follow-up visits to assess progress and discuss the During examination: If a male doctor is a examining
options of care available. a female patient, a lady doctor, nurse, female worker or
Patient-Doctor Communication 41
female relative of the patient must be standing near the We respect your right to ethical and fair treatment.
patient vice-versa, if a female doctor is examining the We respect your right to information as regards your
male patient. Help her get to the table and alight. Do health diagnosis and treatment.
not uncover suddenly and completely. Allow her to do We respect your right to know about the treatment off
so herself expose only the part to be examined. ered, medication used and treatment options available.
We respect your right to choose your treatment and
PATIENT’S RIGHTS CHARTER hence the right to a second opinion.
We respect your right of confidentiality regarding your
Healthcare is a partnership in which doctors and patients health issues.
have reciprocal obligations. Trust between them is an We respect your right to competent treatment and
essential element of the healing relationships. We recognize hence, promise to keep ourselves updated.
this sacred relationship and hence would like to pronounce We respect your social rights and hence, promise to help
that: you in case of gender violence and we promise to act
We respect you, our patient, as a person and your moral to prevent gender discrimination of any kind including
right to bodily integrity and self-determination. prenatal sex-determination.
1. How patient-doctor communication is important for a pregnant woman?
2. Explain emergency situations in obstetrics.
3. Write short note on—patient’s rights charter.
History-taking
6
and Examination
of the Pregnant Patient
INTRODUCTION Identification and Demographic Data

Name Date of first examination
Antenatal care is the care given during pregnancy in the Age Religion
interest of both the mother and the fetus and is very much Address Occupation
an exercise in preventive medicine. The great majority of Contact phone number Education
women are healthy at the outset of pregnancy and one Registration number Husband’s education
aim of antenatal care is to assess, maintain and if possible Husband’s name Husband’s occupation
improve the general condition of the patient. Of the From the above data one can have an idea of the woman’s
remainder, some will have a known preexisting disease and socioeconomic status. The woman’s age is important, for
their management may need to be altered to allow for the the risks of pregnancy is increased at the extremes of ages.
changes due to pregnancy; others may have no history or The address is required for communication if the need
symptoms suggesting disease, but by clinical examination arises.
and special tests, hitherto undetected conditions could be
diagnosed, investigated and treated. Complications may Menstrual History
arise in any pregnancy and although good management The following points should be noted:
avoids some, others will inevitably occur; and their early Age of menarche, duration of bleeding/the frequency
detection and treatment is of prime importance. in days, e.g. 3–4/28–30 days. Passage of clots, amount
of flow and dysmenorrhea should also be enquired. The
HISTORY-TAKING first day of the last menstrual period (LMP) is recorded.
It is important to establish that the last period is normal
The best way to diagnose these conditions in time, is to in amount and duration, because sometimes the woman
start with a good history. It involves asking the woman a may have conceived and experienced slight spotting when
great many personal and intimate details, which she would the period is due, known as decidual/placental bleeding.
not normally be prepared to talk about to a stranger. The LMP is reliable if the woman is having regular periods and
student should aim to achieve an air of slight informality by not taking any hormonal contraception in the preceding
showing interest in the patient as a person and by avoiding 3 months. In latter cases, estimation of gestational
the use of medical terms so that the patient can understand age should be done by other methods as described in
what is being asked and can answer in the same terms subsequent chapters.
without feeling embarrassed. With experience, everyone
develops one’s own technique for taking a history, but Calculation of Estimated Date of Delivery
until that has been gained it is essential to have some sort The average duration of pregnancy is 266 days from
of a plan. The following basic information is always needed conception and 280 day from LMP in a woman with a
although the style of notes may vary from one hospital to cycle of 28 days. This is calculated by Naegele’s rule, i.e.
another. add 7 days and 9 months (Table 6.1) to the LMP or subtract
History-taking and Examination of the Pregnant Patient 43
TABLE 6.1: Hindi and english months Nulligravida: Woman who has never been pregnant.
Hindi English
Primigravida: Woman who has conceived for the first
time.
Paush January
Multigravida: Woman who has been pregnant more
Magh February than once.
Phalgun March Multipara: A woman who has borne more than one
Chaitra April viable fetus, whether or not the offsprings were alive at
Baishakh May birth.
Grand multipara: Woman who has delivered at least
Jyestha June
four viable children.
Asharh July
Nullipara: Woman who has never delivered a child
Savan August
beyond the period of viability.
Bhadrapad September Parturient: Woman in labor.
Ashwin October Puerpera: Woman who has just given birth or aborted
Kartik November (during puerperium).

Marghshirsha December Obstetric history is taken under two headings—(1)
present obstetric history, (2) past obstetric history, (if
she has/had miscarriage, ectopic pregnancies or viable
3 months from LMP and add 7 days, e.g. if LMP is 22nd pregnancies before this one).
March then estimated date of delivery (EDD) will be 29th
December. If a leap year intervenes, add 6 days only. Present Obstetric History
Apart from specific ailments enquiries should be made
Obstetric History regarding the following points in all the three trimesters:
Before starting with the obstetric history one should be
familiar with the following terms. First Trimester (Till 12 weeks of Gestation)
Spontaneous conception or after treatment of infertility
Terms Used
Amenorrhea
Gravida: Denotes the number of pregnancies including Confirmation of pregnancy
the present one (also include number of miscarriages). Booked/unbooked
Para: Denotes the number of previous pregnancies
Number of visits for antenatal care (ANC)
(not just the number of children) beyond the period of Nausea, vomiting
viability, i.e., 20 weeks. Fever and rashes
Miscarriage: Termination of pregnancy before 20 weeks Heartburn
of gestation. Whether it was spontaneous or induced and Itching, jaundice
even an ectopic pregnancy. Drug intake including tetanus toxoid (TT) immunization
This may be expressed by one of two following methods. Radiation exposure
1. G P A L where G is Gravida, P is Para, A is Abortion and L Any episode of leaking of fluid per vaginum (LPV) or
represents number of live children at present. bleeding per vaginum (BPV)
2. G PA – B –C–D where A denotes number of term deliveries, Breast tenderness
B is number of preterm deliveries, C is number of Fatigue
miscarriage and D is number of children alive at present. Frequency of micturition, burning micturition.
For example, if a woman bears twins in the first pregnancy
and is now pregnant for the second time, she still gravida Second Trimester (12 week–28 week of Gestation)
two and para one because these terms refer to pregnancies, Continuing amenorrhea
not the number of babies. It is written as G2P1A0L2. Quickening
As far as the obstetric history is concerned it is the Second dose of TT immunization
information of previous pregnancies including the Iron folic acid (IFA) and calcium supplementation
abortions for much valuable information may be gained LPV/BPV
from knowing the manner and timing of their occurrence. Vaginal discharge or irritation
Reduced fetal movements 4. Product

History suggestive of hypertension (weight gain, head- •• The weight and sex of baby.
ache, oliguria, pedal edema, epigastric pain, giddiness •• Condition of baby at birth (any congenital anomaly/
or blurring of vision). whether cried immediately or not).
•• Whether breastfed or not, period of exclusive breast-
Third Trimester (>28 weeks) feeding.
Second dose of TT immunization •• Subsequent progress of the baby.
Frequency of micturition •• Present health status of child.
Increase/decrease fetal movements •• Immunization status of the child.
LPV/BPV •• In case of previous miscarriage, at what period of
History suggestive of hypertension (weight gain, head- gestation (POG) did it occur, whether spontaneous/
ache, oliguria, pedal edema, epigastric pain, giddiness induced or missed.
or blurring of vision) •• Any cause, whether followed by D&E (dilatation and
IFA and calcium intake evacuation) or not.
History of blood transfusion •• Specify preterm birth/still birth if applicable and
Abdominal pain or back pain possible intrauterine growth restriction (IUGR) or
Bowel habits large sized baby.
Any dai (traditional birth attendent) interference.
Past History
Past Obstetric History
Any history of medical or surgical illness is to be taken into
The record must include the following four P’s of all account as these may effect the present pregnancy and
previous pregnancies in chronological order: produce adverse effects on the mother or the fetus, e.g.:
1. Pregnancy
Heart disease, tuberculosis, diabetes, hypertension,
•• Duration of marriage, whether conceived after
thyroid disorders, epilepsy, etc.
treatment of infertility.
Sexually transmitted diseases (STDs).
•• The duration of pregnancy.
Human immunodeficiency virus (HIV) status, if known
•• Any complication during pregnancy (abortion,
Other specific conditions depending on the regional
BPV, multiple pregnancy, gestational diabetes, pre-
prevalence (e.g. hepatitis, malaria, sickle cell trait,
eclampsia/eclampsia, obstructed labor or vaginal or
thalassemia, etc).
rectal injuries).
Other diseases
2. Parturition
History of allergy.
•• Date and place of delivery and conducted by whom
Any operations—
(doctor/nurse/qualified/unqualified dai).
Blood transfusion
•• Whether labor was spontaneous or induced.
Current use of medicines—specify.
•• The duration and course of labor.
Period(s) of infertility: Timing, duration, cause(s),
•• The mode of delivery [normal/vacuum/forceps/
treatment.
lower segment cesarean section (LSCS)] indication.
•• Any complications during the third stage retained
One should be careful of any previous uterine surgery,
placenta or postpartum hemorrhage (PPH). e.g. myomectomy, uteroplasty, hysterotomy, dilatation and
•• Whether a blood transfusion was given.
curettage. Past history of surgery on the bowel or appendix
3. Puerperium may cause adhesions. Every patient should be asked
•• The course of the puerperium. whether she is taking any drugs as some of them may be
•• Any history of fever/discharge/calf tenderness/ teratogenic, and some others might be drugs of addiction.
pain in suture line (if episiotomy, stitching of tear or
cesarean is done). Genetic History
•• Any costly injection given (Rh-negative woman). A very important role of obstetrician is to identify high
•• Any visit within 6 weeks of delivery for some previous risk factor that might contribute to high risk genetic
complaint. diseases. Also, age of patients is enquired whether she is
•• Type of contraception used, if any, for spacing 35 year or above. Other enquired questions, does you or
between pregnancies. anyone in family or anyone in your baby’s father family
have disorders like Down syndrome, neural tube defects,

hemophilia, muscular dystrophy, cystic fibrosis or other
chromosomal abnormalities.
Does you or your baby’s father have any birth defects or
any one of you two have been previously married and had
a child born dead or alive with birth defects? Do any one
of you two have any close relative with mental retardation?
This is also called genetics counseling.
Family History
There are some conditions which tend to be familial and it
is well worth enquiring whether any close relative suffers
from diabetes, hypertension, mental deficiency, epilepsy, Fig. 6.1: Breast showing secondary areola and Montgomery’s
blood dyscrasias, multiple births, carcinoma or allergies. tubercles
Personal History woman often experiences tenderness and tingling

Enquire About sensation in breasts. After the 2nd month, the breasts
Dietary habits: Vegetarian/non vegetarian. increase in size and become nodular due to hypertrophy
Total daily calorie intake at home calculated from one
of mammary glands. Delicate veins become visible just
24 hour dietary recall beneath the skin. The nipples become considerably
Protein intake larger, more deeply pigmented and more erectile. The
Other nutrients areolae become broader and more deeply pigmented.
Smoking or alcohol habits Small elevations formed by hypertrophic sebaceous
Addiction of any drugs glands appear scattered through the areolae known as
History of vaccination Montgomery tubercles. After the first few months, a
Contraception history—type and duration. thick yellowish fluid, colostrum can be expressed from
the nipples (Fig. 6.1).
EXAMINATION Examination of the respiratory and cardiovascular
system includes observing for pedal edema, clubbing of
General Examination nails, varicosities, any cardiac murmur and abnormality
Look at the general appearance of patient, build and in breath sounds.
nutritional status. The vulva should be inspected for any signs of infections
Look at her gait and stance while she is enters the room. especially STDs, congenital abnormalities, scar, varico
Check for signs of severe anemia: Pale complexion, sities and edema.
fingernails, conjunctiva, oral mucosa, tip of tongue and Hernial sites are inspected.
shortness of breath. Palpation of abdomen should be done for hepatosple-
Record weight (kilograms) and height (meters). nomegaly or any other swelling apart from the gravid
Measure pulse, blood pressure, respiratory rate and uterus.
temperature.
Examine the oral cavity for dental hygiene. Obstetrical Examination
Look for skin infections such as scabies and for allergy, Uterus can be palpated abdominally after the 12th week,
pigmentation and operation scars. fetal parts are palpable after 16 weeks, fetal movements
Inspect patient neck veins (jugular venous pressure), may be felt a week or 2 weeks later and the fetal heart can
lymphadenopathy and thyroid gland. be heard after 24 weeks of gestation. Lie and presentation
A careful inspection and palpation of breasts should be can be determined from 28 weeks of pregnancy onwards.
done for any lump and nipple deformity like retracted- The abdomen should be examined systematically in the
inverted nipples, it may impair breastfeeding later. following manner:
Changes in breasts are quite characteristic in primiparas Inspection
as compared to multiparas. In the early weeks the Palpation

Auscultation
Vaginal or bimanual examination (pelvic examination).
Before starting the examination, the following precau-
tions should be taken:
The woman should be comfortable on her back with
one pillow under her head. The abdomen is exposed

from the xiphisternum to a little below the symphysis
pubis.
The bladder should be empty.
The patient should be examined from the right side.
The hands should be warm especially in cold weather
as it may stimulate uterine contractions.
Inspection
It will reveal whether the uterine ovoid is longitudinal,
oblique or transverse, whether there is overdistension due
to multiple pregnancy or hydramnios. Observe for fullness
of the flanks especially after 36 weeks of pregnancy. Look
for the status of the umbilicus, any abnormal pigmentation, Fig. 6.2: Height of uterus in relation to weeks of pregnancy
striae gravidarum, linea nigra and hernial sites for
any cough impulse. Any distension other than uterine
abnormal peristalsis and pulsation should be mentioned.
Any incisional mark (of previous operations) or any
other scar should also be observed as this may influence
the future management of the patient.
Palpation
Check the patient’s temperature whether its normal
or has fever. Is the uterus relaxed or becoming hard?
After correcting (if any) dextrorotation of the uterus and
outlining the contour of the uterus, note the height of
fundus with the ulnar border of the left hand, which should
correspond with the period of amenorrhea. Symphysis-
fundal height (in cms) and the girth of uterus (in inches)
Fig. 6.3: Measurement of the girth of the uterus
at the level of umbilicus should be measured (Fig. 6.2)
(generally corresponds with the period of gestation in
weeks) in a normal pregnancy.
By the 12th week of gestation, usually the uterus can be
felt through the abdominal wall just above the symphysis
pubis. It reaches the umbilicus by 24 weeks and near the
xiphisternum by 36 weeks. Thereafter it falls by 40 weeks
as the head starts engaging and the girth of the uterus
increases (Fig. 6.3).
The fetal parts can be felt distinctly by the 20th week.
Around 20 weeks, external ballottement may be done, i.e.
one hand taps the uterus from one side and the other hand
kept on the opposite side perceives the impulse (Fig. 6.4).
Around 16–20 weeks, the volume of fetus is small compared
to that of amniotic fluid, so a sudden pressure exerted on
the uterus may cause the fetus to sink in the amniotic fluid, Fig. 6.4: External ballottement
Fig. 6.5: Internal ballottement Fig. 6.6: Fundal grip
then rebound to its original position and the tap is felt by

the examining finger known as internal ballottement
(Fig. 6.5). This may be present with leiomyoma, ovarian
cyst and ascites and absent with scanty amniotic fluid.
Obstetric Grips
After 20 weeks of gestation, the examiner’s hand can
appreciate active fetal movements as well. In order to
determine the presentation, it is a sound practice to locate
the head, as this is by far the most easily recognized part
of the fetus. It is hard, round, smooth and ballotable. Since
in the majority of cases the head is the presenting part it is
reasonable to first palpate the lower pole of uterus. There
are two ways of doing this:
1. Fundal grip: If the head is not recognized in the lower Fig. 6.7: Umbilical or lateral grip
part of the uterus, it must be sought in the fundus as
in breech (podalic) presentation and if the head is examiner faces the patient’s head and his right hand
not found in either of these situations, the lie is not grasps the lower portion of the abdomen just above
longitudinal or the fetus is anencephalic or head is fully the symphysis pubis, between the thumb and fingers
engaged (Fig. 6.6). and gently presses into the lower pole of the uterus
2. Umbilical or lateral grip: The next procedure is to find and a hard mass with a distinctive round, smooth
out on which side the back of the fetus lies. The examiner surface will be felt. If the head presents, it should
places the palmar aspects of the hands on either side of fit into the hand of the examiner and can be moved
the uterus sliding from the fundus down the borders of from side to side. If no part of the fetal head has
uterus pressing alternatively left and right. The back is entered the pelvis and a certain amount of mobility
felt as a smooth curved solid structure on one side and is possible, it is free head. The breech will be felt to
limbs as irregular, knobby nodular structures on the be much larger in size, softer in feel and moving with
other side. The back may be anterior, lateral or posterior the rest of the body (Fig. 6.8).
on one or other side of the uterus. If the back is anterior, •• The two handed method: Here the examiner faces
it is easily felt while the limbs are difficult to palpate and the feet of woman. The hands are placed upon the
vice versa if back is posterior (Fig. 6.7). lower pole of uterus with the finger tips just above the
•• Pawlik’s grip: After asking the patient to bend her symphysis pubic and the thumbs meeting near the
knees slightly (to relax the abdominal muscles) the umbilicus. The thighs should be semiflexed to relax
Fig. 6.8: Pawlik’s grip or first pelvic grip Fig. 6.9: Two handed method for second pelvic grip
the abdominal muscles. On careful palpation, if the Auscultation

head is presenting, the fingers of one hand will feel the The fetal heart sounds give information about the viability
occiput and those of other the sinciput. If the sinciput of the fetus and the point of maximum intensity of fetal heart
is at a higher level than the occiput, then the vertex is sounds will help in the confirmation of lie, presentation
presenting; if on the other hand it is on a lower level and position. As a rule this point is below the umbilicus in
than the occiput, the face is presenting. If the fingers all cephalic presentations, above the umbilicus in podalic
of both hands converge below the presenting part, it (breech) presentation and at or just above the umbilicus
is free; if the fingers cannot meet the head is fixed or in transverse or oblique lie. This point also varies with
engaged depending on how much of the head has reference to the position of the back of the fetus. In cases
entered the pelvis (Fig. 6.9). According to Leopold where the back is on left or right the fetal heart sounds are
heard on the same side, nearest the midline in anterior
maneuvers, the fundal grip is done first followed by
position and further away in posterior position.
lateral grips and the two pelvic grips.
Fetal heart sounds are audible with a stethoscope or
One can judge the amount of amniotic fluid
a Pinard fetoscope or a doppler (Figs 6.10A and B) from
(olighydramnios/polyhydramnios). the 18th week onwards and definitely after 24 weeks. The
Approximate weight of the fetus can be judged by Doppler machine (Figs 6.11A and B) can detect the fetal
johnsons formula. heart tones as early as 12 weeks of gestation but more
Uterine contractions can be felt (Braxton Hick’s). If regularly after the 14th week. The Doppler ultrasound can
these are painful their duration and intensity are noted. detect the uterine souffle and funic souffle as well.
A B
Figs 6.10A and B: A. Fetoscope; B. Hearing fetal heart sound with fetoscope
A B
Figs 6.11A and B: A. Doppler machine; B. Hearing fetal heart sound with Doppler machine
Souffle is a soft blowing sound heard on auscultation

even with a stethoscope. Uterine souffle is heard
because of blood passing through dilated uterine
arteries especially in the last months of pregnancy—
along the side of the uterus. It is synchronous with the
maternal pulse. Funic souffle is the sound produced
by the flow of blood in the umbilical vessels. It is
synchronous with the fetal heart beat.
Lie is the relationship of axis of fetus to the long axis of A B
uterus and it may be longitudinal, transverse or oblique
Figs 6.12A and B: A. Longitudinal lie; B. Transverse lie
(Figs 6.12A and B).
Presentation is the part of the fetus, which is lowermost
in the uterus. It may be cephalic, breech or shoulder

(Fig. 6.13).
This part can be felt by vaginal examination when
the patient is in labor. In cephalic presentation also it
may be vertex, brow, deflexed or face depending on
the degree of flexion of head (Fig. 6.14). Compound
presentation is the presentation when more than one
part of fetus is presenting, e.g. head with hand.
Denominator is the lowermost point on the presenta
tion, which can be used as a reference point to

describe the degree of rotation of fetus, e.g. in a vertex
presentation it is occiput, in a face presentation it is
mentum, in a breech presentation it is sacrum and in a
shoulder presentation it is the acromion.
Position is the relation of denominator to a fixed point
in the pelvis. Fig. 6.13: Breech presentation

In the vertex presentation it may be written as follows:
If the occiput is facing the anterior aspect of pelvis it Station
is occipitoanterior (OA) and if facing the posterior half The relationship of the presenting part to the pelvis is
of pelvis it is occipitoposterior (OP). It can also be left or known as the station. The landmark used is the level of the
right depending on the position on the side of the pelvis ischial spines which is considered as the zero station (For
as shown in (Fig. 6.15). detail see Chapter 26) 0–5 station.
Engaged: The largest transverse diameter of the head,

i.e. biparietal has passed through the ischial spines,
only the sinciput may be felt per abdomen.
Attitude is the relation of fetal parts to one another.
Normal attitude is of complete flexion with the legs
drawn up and bent at the knees, arms folded across the
chest, chin pressed against the chest. In this attitude the
fetus occupies minimum of uterine space called fetal
A B C D
ovoid.
Figs 6.14A to D: Cephalic presentation. A. Vertex; B. Deflexed
head; C. Brow; D. Face Pelvic Examination
Inspection with a speculum reveals the cervix and vaginal
mucosa to appear congested and bluish, and the vaginal
discharge is mucoid and creamy white.
A pelvic examination should be done for the following
reasons:
To confirm the pregnancy and to relate the size of uterus
with the period of amenorrhea and to exclude ectopic

pregnancy in the first trimester.
To detect the presence of any other pelvic mass like a
fibroid, ovarian tumor or uterine anomaly.

To take a pap smear with a vaginal speculum in any
trimester of pregnancy (if the facility is available).

To estimate the pelvic size and to rule out cephalopelvic
disproportion at 36 weeks or later especially in a

primigravida or a multigravida with a previous cesarean
section who has never delivered normally.
The points to be noted are:
Fig. 6.15: Position of vertex in relation to pelvis
Condition of the cervix: Sacrum—is promontory
Keys: OA—Occipitoanterior; ROA—Right occipitoanterior; ROT—
Right occipitotransverse; ROP—Right occipitoposterior; OP—Occip- reachable, its curvature
itoposterior; LOP—Left occipitoposterior; LOT—Left occipitotrans- The projection of ischial spines into the pelvic cavity,
verse; LOA—Left occipitoanterior
interischial measurement
The inter tuberous diameter
Per abdomen, the landmark used is the pelvic inlet and
the relation of head to the pelvis may be described as follows: The diagonal conjugate
Free/mobile: The head is completely above the pelvic The angle of the subpubic arch
brim. Adequacy of pelvis.
Fixed: Some part of the head has passed through the The pelvic examination is generally avoided in cases
pelvic brim so very little movement of head is possible of previous history of miscarriage or vaginal bleeding in
like an egg is fixed in egg cup. present pregnancy (to prevent placenta previa bleeding).
1. Give in detail about menstrual, obstetric and genetic history of the patient.
2. Discuss different types of obstetric grips.
3. What is uterine and funic souffle?
Section 2
Normal Pregnancy
Section Outline
7. Physiology of Reproduction
8. Placenta, Umbilical Cord and Fetal Membranes
9. Maternal Anatomical and Physiological Changes in Pregnancy
10. Immunology of Normal Pregnancy
11. Diagnosis of Pregnancy
12. Antenatal Care (Antenatal Exercises and Nutrition During Pregnancy)
7
SK Sen, Meenakshi Bhatt, Harsha Gaikwad
Physiology of Reproduction
The sperm can feritilize the ovum in the fallopian tube

FERTILIZATION
within 24–48 hours after reaching the vagina.
Motherhood is the greatest joy in a woman’s life. Fertiliza- Fertilization is a union of ovum with spermatozoa
tion of the ovum by a spermatozoon is a very important following the stages as described below:
event for the continuation of mankind (Fig. 7.1). Capacitation is a physiological change in the sperma-
After intercourse, the semen liquefies within 20 minutes tozoa enabling them to bind and fertilize the oocyte. It
and thousands of motile sperms swim up through the involves cyclic adenosine monophosphate (cAMP)
cervix within a few minutes into the uterus. After ovulation, dependent phosphorylation. Capacitated sperm can
the ovum is picked up by the fimbria of the fallopian tube locate the ovum in the ampulla.
and is carried by the cilia and peristaltic movement of the This causes release of enzymes—hyaluronidase and
fallopian tube towards the uterine end. acrosin at the acrosomal cap in the sperm head. These
enzymes cause lysis of the intercellular mucopolysac-
charide of corona radiata cells of the ovum.
Zona-pellucida has sperm receptors (ZP1, ZP2, ZP3).
Only a single sperm (out of the hundreds, presents near

the zona-pellucida), can enter the ovum by a process
of physically drilling a hole, proteolytic digestion of the
pathway and secondary binding to the ZP2 molecule of
the zona by lyconidase and proacrosin/acrosin. Once a
sperm enters an ovum, further entry of any other sperm
is sealed. This sperm oocyte binding is species-specific.
Sperm penetration into the ovum triggers the comple-
tion of meiosis II (from its arrest in the metaphase stage

at ovulation) in the ovum. Arrest of meiosis I (1° oocyte
= 46 chromosome) at prophase completed just before
ovulation (1st polar body—23 chromosomes) to half
again during meiosis II (2° oocyte = 23 chromosomes)
in the metaphase stage till fertilizations when its com-
pleted. There is a rapid depolarization of the ovum sur-
face membrane thus blocking entry of any other sperm.
Tail of the sperm dissolves when it enters in the ovum
and the remaining part forms the male pronucleus which

fuses with the female pronucleus to form a zygote.
The presence of both the male and female pronucleus
Fig. 7.1: Structure of spermatozoon in the ovum is a certain proof of fertilization.

Fig. 7.2: Human blastocyst Fig. 7.3: Stages of development of the embryo
In case of non-fertilization, the ovum degenerates in

the tubal lumen after 24 hours of ovulation.
Sex asignment of fertilized ovum (zygote) is due to the
sex chromosome of the sperm which caused fertilization
(father) as a sperm can either contain 22X or 22Y chromo-
somes. The ovum always has 22X chromosomes.
The resulting zygote can have 44XX or 44XY.
The zygote with 46 chromosomes (44+2 sex chromos-
omes), with a zona-pellucida sheath around it undergoes
the first mitotic cell division to a 2 cell stage by cleavage
within 24 to 30 hours after fertilization. It moves towards
the uterine cavity through the tubal lumen with the help of
tubal peristalsis and mucosal ciliary current.
The second cell division (cleavage) occurs within the
next 12 hours to 4 cell and further cell-division occurs in
rapid succession to 8 and then 16 cells. Uneven numbers
of cells are produced since cell division does not happen
synchronously.
The morula stage (a ball of cells) with 16 or more cells
with a covering, zona-pellucida, reaches the uterine cavity
by 4 days after the fertilization.
The blastocyst and the morula on 4th and 5th day freely
floats on the endometrial surface, imbibes uterine fluid
through canaliculi in the zona-pellucida and the zona-
pellucida degenerates and forms the blastocyst (Fig. 7.2).
The blastocyst grows rapidly and forms the embryonic
disc, which has three layers, the outermost is the ectoderm,
the middle layer is the mesoderm and inner layer forms the
endoderm. The developing embryo is shown in Figure 7.3.
Fig. 7.4: Embedding of the blastocyst
IMPLANTATION (NIDATION)
The developing embryo after passing through the isthmus it goes in the compact layer of secretory endometrium
enters the uterine cavity by 68–80 hours after ovulation and [after 6–7 days of fertilization (on 20–21 day of regular
remains free floating. For 3–4 days, the blastocyst (20 cells) menstrual cycle)] (Fig. 7.4).
Physiology of Reproduction 55
The entering pole of the late stage blastocyst is at the site

of the inner cell mass. Carbohydrate selection interactions
are involved in the attachment of human embryo to the
endometrial cells. Selectin is found on human embryos
and the luminal epithelial cells of the uterus. Heparan
sulphate proteoglycan (HSPG) has been considered
a likely molecule involved in blastocyst adhesions.
The implantation involves a regulated balancing of
adhesion and invasion-inducing mechanisms of the
cytotrophoblast. The uterine receptivity is essential
for implantation. Progesterone and possibly estrogen
help in this uterine receptivity. Increasing the correct
COX-2 (cyclooxygenase–2) expression at the implanta
tion site is important. Prostaglandins are also needed as
they activate peroxisome proliferator-activated receptors
(PPARS) necessary for vascular changes in the maternal
endometrium. Fig. 7.5: Embryonal development (day 15–21)
The blastocyst burrows in the compact layer of secretory
endometrium, entry point is sealed by epithelium, is
called interstitial implantation which is completed by
Embryonic Development (Fig. 7.5)
the end of 10–11th day of fertilization. Day 15–21th (5th week of menstrual age), intra-
By this time beta human chorionic gonadotropin (b- embryonic mesoderm develops from embryonal
hCG) hormone is secreted by the trophoblast and takes ectoderm. The embryonic plate becomes trilaminar,
over the corpus luteal function of production of proges- later forming the head and tail segments. The embryo
terone. is separated from the trophoblast by extraembryonic
coelom leaving a stalk of mesoderm. This body becomes
the umbilical cord.
DEVELOPMENT OF EMBRYO AND FETUS Primitive blood vessels appear in the chorionic villi
The human embryo develops from the 15th day of and the yolk sac. The gestation sac partly occupies
fertilization to the 10th week of menstrual age. the uterine cavity and is first identified by ultrasound
From 11th to 40th week of pregnancy, a growing baby at 6–10th weeks of menstrual age. By 8th week, the
amniotic cavity becomes filled with liquor amnii,
inside the uterus is called the fetus.
enlarges rapidly to fill up blastocyst and an amniotic
Pre-embryo development at embryonic disc—on day
membrane consequently forms the inner lining of
7th of fertilization, the inner layer of cuboidal cells facing
chorion. The embryo freely floats in the amniotic fluid.
the blastocyst cavity forms one layer—the endoderm
By 10th week, the gestational sac almost fills up the
(primary embryonal ectoderm). The remaining part of
cavity of the expanded and enlarged uterus except at
the conceptus forms the placenta and outer polyhedral the isthmus.
layer forms the ectoderm. By 12th week, the fetal head is seen in the enlarged
Day 8–9th, amniotic cavity appears in the ectoderm cell uterus simultaneously, the decidua capsularis fuses
layers between inner cell mass and trophoblast. Blastocyst with decidua parietalis obliterating the uterine cavity.
(gestation sac) slightly bulges on endometrial surface. The yolk sac is partly enclosed by the growing body of
Day 10–11th, extraembryonic mesoderm develops embryo to form foregut, midgut and hindgut. The midgut
on the inner surface of trophoblast, loosely fills up remains connected with yolk sac by a vitelline duct.
blastocyst and covers the embryonic endoderm. Vitelline duct and remnant of yolk sac (umbilical
Day 12–14th, yolk sac forms adjacent to endoderm vesicle) lie in the body stalk. In the latter, a diverticulum
being lined by it. The inner cell mass lying between grows from hindgut called allantois.
the amniotic cavity and the yolk sac develops into the Principal visceral veins of the embryo are two vitelline
embryo and is called the embryonic plate. veins bringing blood from the yolk sac.
Umbilical Cord Development 11th day – Implantation completed

Details are described in Chapter 8. 12th day – Primary villi
16th day – Secondary villi
Embryonal Plate Evolution 21st day – Tertiary villi
From the embryonic plate, develops the following parts 21st–22nd day – Fetal heart, fetoplacental
of the embryo (Figs 7.6A to D). circulation
•• Ectoderm: Skin, hair, the nervous system, lens of 21st–40th day – Chorion frondosum
eye, enamel of teeth, epithelium of mouth (except 40th–50th day – Formation of cotyledons
tongue), salivary glands, tongue nasal cavity and 80th–267th day – Formation of 60 fetal primary stem
lower portion of anal canal. cotyledon anchoring and nutritive
•• Endoderm: Epithelial lining of gut, pancreas, liver,
villi where from peripheral terminal
lungs, thyroid glands, major part of urinary bladder,
villi grow.
urethra.
•• Mesoderm: The entire skeletal system, heart, blood
vessels, lymphatics, kidneys, ureters, gonads and FETAL DEVELOPMENT (FIG. 7.7)
internal genital organs, muscular system, endothelial
The end of the embryonic period is arbitrarily taken as
linings of peritoneum, pleura and pericardium.
10 weeks after fertilization. The embryo is about 3–4 cm
The ectoderm forms the brain, the spinal cord and the
skin which covers the embryo. The mesoderm forms sides long. The major part of lungs and other new organs is
and front of the embryo followed by the development of developed by this time. After this period starts the period of
limb buds to form arms and legs. fetal development which consists of growth and maturation
Organogenesis is the stage of fetal organ development of structures that were formed during the embryonic period.
also known as the embryonic stage. The length (in cm) is roughly the square of the age in
Milestones of post-fertilization events are as follows: months till the 5th month (at 1 month = 1 cm, 2 month =
1st week – Implantation 4 cm, 3 month = 9 cm, 4 month = 16 cm and 5 month =
A B
C D
Figs 7.6A to D: Development of embryo

Fig. 7.7: Fetal development in weeks of gestation
25 cm) and after that roughly five times the age in months 24 Weeks
(at 6 month = 30–35 cm, till the 10 month = 50 cm). Weighs 600–900 g
Skin is wrinkled
12 Weeks Deposition of fat begins
Comparatively large head
Crown rump length (CRL)—7 to 9 cm Recognizable eyebrows and eye darker
Ossification centers appear Lung development is almost complete (terminal sacs
Toe and finger differentiation takes place are still not formed).
Skin and nails develop 28 Weeks
Gender differentiation occurs CRL: 25–35 cm
Movements start. Weight: 1000–1500 g
Skin: Thin and red, covered with vernix caseosa
16 Weeks Pupillary membrane from eyes disappeared.
Weighs 200–300 gm 32 Weeks
Skin covered by downy hair called lanugo CRL: 28–40 cm
Few scalp hair. Weight: 1800 g–2 kg.
36 Weeks blood and helps bypass for the hepatic microcirculation.

CRL: 32–45 cm This relatively well-oxygenated blood reaching the IVC
Weight: 2000–2500 g and does not mix with the blood from the hepatic veins due
More deposition of subcutaneous fat to streaming (vide infra). This blood then preferentially
More round body, no wrinkles on face. enters into the left atrium as soon as it reaches the right
atrium via the foramen ovale as explained below. This
40 Weeks blood subsequently supplies in the brain and heart.
CRL: 35–50 cm Next, the blood from the upper part of the body
Weight: More than 2500–3500 g. draining through superior vena cava (SVC), which reaches
the right atrium, mixes with the remaining small amount
FETAL CIRCULATION (FIG. 7.8) of oxygenated blood (from hepatic vein and lower limbs)
carried by the IVC. It then proceeds to the right ventricle
In Utero and to the pulmonary artery. Since, the resistance in the
The right and the left halves of heart in the fetus run in a pulmonary vascular bed is high, this blood is diverted into
parallel circulations; they are not in series (as in adults). the descending aorta through the ductus arteriosus to
Oxygenated blood is carried to the fetus from the supply the lower part of the body.
placenta by one umbilical vein. The umbilical vein provides The separation of blood according to its oxygen content
portal branches to the left lobe of the liver; next, it gives is facilitated first by streams of blood in IVC (streaming),
rises to the ductus venosus that diverts the remaining well-oxygenated blood travels along the medial side of
blood in the vein into the inferior vena cava (IVC). This IVC and less oxygenated along the lateral wall. Secondly,
constitutes approximately half of the umbilical vein’s after entering the right atrium, the crista dividens (upper
interatrial septum) preferentially shunts well-oxygenated
blood from medial side of IVC through foramen ovale to
the left atrium and to left ventricle heart and brain. The
less oxygenated blood (lateral stream) is sent to the right
ventricle. Thus, it is ensured that most oxygen carrying
blood from placenta goes to the heart and brain. The blood
with least oxygen from upper and lower limbs is drained
into the right atrium via the SVC and IVC respectively.
The blood from the lower part of the body and limbs is
returned to placenta via the hypogastric arteries leading
to two umbilical arteries draining into the placenta for
oxygenation. Flowchart 7.1 shows fetal circulation.
After Birth
Two major changes takes place:
1. Decreased pulmonary vascular resistance following
lung expansion.
2. Increased systemic vascular resistance due to abrupt
disconnection from the low resistance placental circula
tion, heart starts working as follows:
•• The foramen ovale, which acts as a flap valve, closes
due to increase in left atrial and decrease in right
atrial pressure.
•• The ductus arteriosus constricts due to exposure
to increased PO2. Functional closure occurs within
24–48 hours. Permanent (anatomic) closure takes
about 2–3 weeks for completion and results in the
Fig. 7.8: Fetal circulation formation of the ligamentum arteriosum.
Flowchart 7.1: Fetal circulation
TABLE 7.1: Remnants of extrauterine life

HUMAN SEX RATIO
Intrauterine structure Remnants in extrauterine life
Hypogastric arteries Umbilical ligaments
At fertilization (primary sex ratio), 160 male zygotes
Umbilical vein Ligamentum teres
are produced against 100 female zygotes. This is due
to the higher mobility of the Y spermatozoa although
Ductus venosus Ligamentum venosum
equal number of X and Y spermatozoa are produced.
Ductus arteriosus Ligamentum arteriosus
At birth (secondary sex ratio), 106 males are born
against 100 females.
Remnants: The hypogastric arteries on atrophy become •• Sex ratio equals at the age of puberty.
umbilical ligaments and the umbilical vein forms the •• First borns are more likely to be males.
ligamentum teres, the closure of ductus venosus and •• Advancing age of mother favors female births.
ductus arteriosus forms the ligamentum venosum and •• Higher coital rates produce more males.
ligamentum arteriosus, respectively (Table 7.1). •• Blacks have lower male/female ratio than Caucasians.
1. Define the terms:
i. Implantation
ii. Morula stage
2. Explain fetal development in 24th week.
i. Sex ratio equals at age of _____________.
ii. The _____________ forms the brain, the spinal cord and the skin which covers the embryo.
8
Placenta, Umbilical Cord
and Fetal Membranes
The trophoblast directly comes in contact with the

PLACENTA endometrial stroma. Implantation of the blastocyst is
The word placenta comes from the Latin word flat cake. It completed on 6–7 days after fertilization.
is also called afterbirth. The decidual cells lose boundary and are called syn-
The placenta is a very important lifeline organ for the cytium or syncytiotrophoblast. Deeper to this layer, cells
fetus. It carries out the functions that the fetus is not able which retain their cell walls are called cytotrophoblast or
to perform during the intrauterine period of life (functions Langhan’s layer. The trophoblast grows in two pathways—
of the lungs, liver, kidney and endocrine organs), the core
villous and extravillous trophoblast (Flowchart 8.1).
function being transport of nutrition. The survival of fetus
depends on the integrity and efficiency of the placenta. Villous trophoblast: The syncytiotrophoblast grows and
Placental pathology is associated with growth restriction, becomes thick. Small cavities appear in this layer which
pre-eclampsia, fetal death, etc. are initially arranged irregularly and then radially around
the blastocyst. These spaces are called lacunae and are
DEVELOPMENT OF PLACENTA formed as a result of engulfing endometrial substances.
The placenta has two parts (Fig. 8.1): These lacunae are separated from each other by partitions
1. Fetal part which is expelled after birth of syncytium called trabeculae (10th and 13th day of
2. Maternal part conception).
The zygote enters the uterine cavity at the morula or the This syncytium burrows the endometrium which is
blastocyst stage with an outer layer of trophoblast and a eroded and blood fills the lacunar space. The columns of
cluster of cells called inner cell mass. cytotrophoblast extend between the blood filled lacunae
Fig. 8.1: Outline of placental structure

Placenta, Umbilical Cord and Fetal Membranes 61
Flowchart 8.1: Differentiation of trophoblast
A A
B B
Figs 8.2A and B: Primary villi Figs 8.3A and B: Secondary villi
are called and as primary villi (Figs 8.2A and B). To start and ramuli chorii. Cytotrophoblastic cells spread laterally
with they are on the entire aspect of blastocyst. Later, and meet some of the other villi forming a complete
when the fetus enlarges, the placenta remains near the cytotrophoblastic shell of tissue which multiplies and
basal plate. Extra embryonic mesoderm layer enters the increase the size of the placenta.
primary villi and forms a central core—now this structure In between the villi by branching and rebranching the
with outermost syncytial layer, middle cytotrophoblast surface area for exchange is increased.
and inner mesoderm core is the secondary villus One main stem villus and its branches constitute a
(Figs 8.3A and B). All these villi are branching further. placental lobule or cotyledon. Each has its arterial and
Blood vessels form in the core of the each villus and venous supply. It is the functional unit of the placenta.
become tertiary villi. Tertiary villi (Figs 8.4A and B) float Growing cytotrophoblastic cells divide the syncytiotro-
in the maternal blood sinuses. Some of these tertiary phoblast into two layers. The definitive syncytium on the
villi extend across to the maternal decidual cells and are fetal aspect and other peripheral syncytium on the mater-
known as anchoring villi. Each anchoring villus has a nal side. The latter degenerates and is replaced by fibrinoid
stem (truncus chorii) which is divided into rami chorii material (Nitabuch’s layer).
Figs 8.4A and B: Tertiary villi Fig. 8.5: Decidua of pregnancy
The ramuli are attached to the cytotrophoblastic Placental barrier is the area separating the maternal
shell. This branching and rebranching takes place in the and fetal streams by syncytiotrophoblast, two basal laminae
intervillus spaces; almost the whole of the intervillus and endothelium of fetal capillary. At places this placental
space becomes filled. So, the surface area for exchanges, membrane is very thin, i.e. 0.602 mm. These zones are
becomes enormous. From 21st day to end of 4 months called alpha zones for maternofetal exchange. The beta
of gestation there is both growth and remodeling of the zone is for hormone synthesis. Examples of cells passing
placenta. Chorionic villi are all around the blastocyst. The between the mother and fetus and vice versa are seen in
villus in contact with decidua basalis proliferates most and Rhesus isoimmunization and detection of Y chromosomes
is called the chorionic frondosum or leafy chorion; this is in mothers blood many years after delivering a son
the portion which will form the fetal part of the placenta. (microchimerism). It may cause autoimmune diseases in
The villi other than near the decidua basalis gradually the mother (thyroiditis, skin hyperimmune reactions, etc).
get lesser blood supply and stop growing; this part is
chorion laevae or smooth chorion. By the late 3rd month DEVELOPMENT OF MATERNAL PART
of pregnancy the latter comes in contact with amnion OF PLACENTA (FIG. 8.5)
forming an avascular amniochorion. The area merger
of decidua capsularis and decidua parietalis is called After the implantation of the embryo, the uterine endo-
decidua vera (Fig. 8.5). After the end of 4 months, the metrium is called the decidua. The features of the endo-
placenta has achieved its definitive form and there is no metrium which are seen during the secretory phase are
further modification in the anatomy. But branching of the intensified. The stromal cells enlarge, become vacuolated,
villous tree and formation of fresh villi continues till term. and store glycogen and lipids. This change is called the
The placenta now subdivides into lobes by septa that decidual reaction.
grow into the intervillous space from the maternal side The position of the decidua where placenta is to be
(during the 3rd month of gestation). formed is called decidua basalis.

The part of the decidua that separates the embryo from
PLACENTAL MEMBRANE/PLACENTAL the uterine lumen is called the decidua capsularis.

The part lining the rest of the uterine cavity is called the
BARRIER decidua parietalis.
Fetal and maternal blood are in close proximity but are The spiral arteries course through the myometrium
separated from each other by the placental membrane into the decidua. This part of placentas is called interstitial
preventing blood exchange. extravillous cytotrophoblast. Other trophoblastic cells
endothelial cell division along the entire length of the

capillary development from the extraembryonic mesoderm
resulting in the final coiling and bulging of the capillary
loop through the trophoblastic surface. These specialized
structures are the main site of diffusion of gases between the
fetus and the maternal circulation. With increase in gestation
these terminal capillaries enlarge to form large sinusoids.
Maternal glucocorticoids are also essential in early pregnancy
for the placental development and growth because they
provide stimulation for the vascular endothelial growth and
for decidual remodeling. However, in late pregnancy, these
drugs inhibit fetal metabolism. The fetus has one-fourth the
concentration of maternal corticoids due to the presence of
11-b-hydroxysteroid dehydrogenase 2 (11 β-HSD2) enzyme
(secreted by the placenta and which inactive cortisol) in late
pregnancy.
Fig. 8.6: Changes in uteroplacental vessels in the placental bed
(spiral arteries)
Important Points
Interstitial implantation is completed on 6–7 days of pregnancy.
penetrate the intradecidual portion of the spiral arteries The circulation between the chorion and the embryo is established.
and are called intravascular extravillous cytotrophoblast Placental growth begins at 6th week and is completed by
which destroy the endothelium of maternal vessels. This 12th weeks.
The placenta grows both in thickness and circumference. Sub
results in destruction of the medial elastic and muscular sequently, there is little increase in thickness but it continues to
tissue and is replaced by fibrin of maternal blood and increases circumferentially till term.
protein secreted by invading trophoblastic cells. This
process is complete by the end of the first trimester
Anatomy of Placenta
(Fig. 8.6). After that, the same changes occur in the
inner spiral arteries and they become flaccid, sac-like, The human placenta may have multiple shapes and
uteroplacental vessels passively dilating to accommodate forms, but usually it is discoidal in shape, has a diameter
of 15–20 cm and thickness of 2.5–3 cm at its center, thining
the increased blood flow through the vessels. These
off towards the periphery. The weight is approximately
changes are impaired in pre-eclampsia and gestational
500–600 g. The proportion of size of placenta to fetus is
hypertension. This is the work of intravascular extravillous
approximately 1:6 at term. It occupies 30% of the uterine wall.
trophoblastic cells. The interstitial extravascular tropho
It is hemochorial, as it is in contact with the maternal blood.
blastic cells are a major component of the placental bed and
Hemo is maternal blood bathing the syncytiotrophoblast
facilitate vascular invasion by the intravascular trophoblast.
and chorio represent chorioplacenta. It is deciduate as it
Vascular endothelial growth factor-a (VEGF-a) is shown to
sheds off after parturition. The placenta is a specialized part
initiate vasculogenesis and angiogenesis, and angiopoietin of chorion and four-fifth of the placenta is fetal in origin.
(Ang1 and Ang2) act with it in later stages of angiogenesis. Only decidua basalis is of maternal origin.
Mesenchymal derived macrophages (Hofbauer cells) The placenta has two surfaces:
expressing angiogenic growth factors, appear in the Maternal surface (Fig. 8.7)
mesenchymal secondary villi suggesting a paracrine role in Fetal surface (Fig. 8.8).
initiation of vasculogenesis and trophoblastic invasion of The maternal surface is rough and spongy; it appears
the maternal circulation. shaggy. It is dull red in color, when viewed from the
Only arteries in the maternal side of placenta are invaded maternal surface (Fig. 8.7).
by the trophoblasts. Veins are not invaded. In third trimester There are a number of slightly elevated convex areas
till term, the existing vessels increase in size due to formation called lobes or cotyledons (Fig. 8.7). The smaller ones are
of mature intermediate and terminal villi. The terminal villi called lobules. Lobules are the functional subunits of the
show decreased trophoblastic proliferation and increased placenta. The number of lobes in each placenta varies,
Fig. 8.7: Maternal surface of placenta showing lobes and cotyle Fig. 8.8: Mature placenta with umbilical cord and membranes
dons (fetal surface)
from 10 to 38. Each lobule has a tertiary villus. Relation

PLACENTAL ATTACHMENT
of lobules to cotyledon is not fixed. Centrally placed
cotyledons may have five lobules and lateral cotyledons The placenta usually attaches at the upper segment of the
may have one or two lobules. The lobes are separated, uterus, but could be low lying in location. The attachment
albeit incompletely, by grooves of variable depth, these of the uterine wall is effective due to anchoring villi
connecting the chorionic plate with the basal plate and
are called placental septa. They correspond to the major
also by fusion of decidua capsularis with decidua parietalis
part of distribution of umbilical vessels and are supplied
(vera) with the chorion laeve at the margin. The line of
with a branch (truncal) of the chorionic artery. For each
separation of placenta after the birth of baby is through
cotyledon there is a vein, and a primary stem villus.
the decidua spongiosum. The placenta does maintain an
Constituting 1:1:1 ratio of artery, vein and cotyledon
absolute integrity of the fetal and maternal circulations.
(Fig. 8.9). Very rarely, there are breaks in the placental barrier.
The fetal surface is covered by the amnion with the
umbilical cord attached at or near its center. The branches PLACENTAL PERFUSION
of umbilical vessels could be visualized radiating from the
insertion of the cord (Fig. 8.8). The uterine blood flow is about 700–750 mL/min at term,
of which about three quarters goes to the placenta and the
other one-fourth supply the myometrium. The placenta
has a low resistance and high flow rates of blood during
maternal diastoles. Maternal blood enters the intervillous
spaces via 80–100 spiral arteries as they pass the
trophoblastic shell. These arteries are eroded by the non-
villous trophoblasts, later on these arteries are partially
blocked by these trophoblast cells. Thus the terminal parts
of spiral arteries are narrow. This helps to regulate the
blood flow into the intervillous spaces. At any time about
150 mL blood is present in the placenta and it is replaced
three-four times per minute. The maternal blood from the
placenta is drained away by the uterine veins.
Fig. 8.9: Histology of normal placenta

PLACENTAL CIRCULATION (FIG. 8.10)
Courtesy: Dr Hari Om Gupta and Dr Rashmi Arora, VMMC and The fetal deoxygenated blood from the fetal heart goes
Safdarjung Hospital towards the placenta along two umbilical arteries. This is
Respiratory function
Excretory function
Nutritive function
Endocrine function
Barrier function
Placental transfer of heat
Immunological function.
Placental Transfer
Fig. 8.10: Relationship of maternal blood flow and the fetal lobule
Factors affecting placental transfer are:
Lipid solubility (facilitates transfer)
then transported through the branches to the capillaries Molecular weight of substance
of chorionic villi. The gas exchange takes place at the Ionization of substances.
capillary level after which the blood returns to the fetus by
an umbilical vein. The maternal blood flows through the Respiratory Function
placental bed in the decidua via spiral arteries and flows Oxygen and carbon dioxide: These gases diffuse freely
into the intervillous spaces surrounding the villi. Maternal across the placenta by a pressure gradient.
blood flows through the placenta due to a series of pressure The oxygen supply to the fetus is at the rate of 5 mL/
differentials. The placenta is a low resistance and a high kg/minute. Carbon dioxide crosses the placenta by the
conductance organ. There are two schools of opinion about process of simple diffusion. The placental membrane is
the direction of the maternal blood stream. One school highly permeable to carbon dioxide.
think the central space of fetal lobule is the inlet. from here
the maternal blood flows laterally and is drained by a basal Excretory Function
venous outlet. Others think that maternal vessels open Urea and uric acid are excreted in the maternal blood by
into the inter lobular spaces and then encircles the lobules simple diffusion.
in streams to form a shell around them, before draining
into the basal outlet. A functional intervillous space is only Nutritive Functions of Placenta (Table 8.1)
of a capillary caliber and here the maternofetal exchange Immunological Function
takes place.
Maternal immunoglobins protect the fetus against infec-
tive diseases like diphtheria, measles, etc.
AGEING OF PLACENTA
As the placenta ages there is decrease in thickness of the ENDOCRINE FUNCTION OF PLACENTA
syncytium, partial reduction of cytotrophoblastic cells and
decrease in stroma. These changes increase the efficiency Placental Products
of transport and exchange to meet the increasing fetal Proteins
metabolic needs. There are more terminal villi in the •• Pregnancy-specific beta-1-glycoprotein (Schwanger-
placenta and are called third trimester villi. But sometimes, schafts protein, SPI)
there is a thickening of the basement membrane, and Pregnancy-specific β-glycoprotein (SP4)
of the trophoblast capillaries, with obliteration of small •• PAPP C
fetal vessels and fibrin deposition on the surface of villi •• Relaxin
in basal and chorionic plates and the intervillous spaces. •• Leptin
This decreases the placental exchange. The placenta has a •• Placental protein 5 (PP5).
considerable functional reserve. Protein hormones
•• Human placental lactogen (hPL)
•• Human chorionic gonadotrophin (hCG)
FUNCTIONS OF THE PLACENTA
•• Hypothalamic like hormones [β-endorphin, Adreno
The most vital function of the placenta is the transfer of corticotropic hormone (ACTH), etc.]
oxygen and nutrients. It also produces hormones. The •• Human chorionic somatomammotropin (hCS or
main functions of the placenta are listed below: PAPP-D).
TABLE 8.1: Nutritive functions of placenta

Water Crosses the placenta freely. At term it reaches 3.5 L/h.
Glucose It is transported by facilitated diffusion. Fetal glucose levels are lower than the mother because of increased consumption
by the fetus
Amino acids Acidic, non-essential amino acids are transferred by concentration gradient as a result of the higher concentration in the
maternal blood
Lipids Cross the placenta freely (simple diffusion). Triglycerides, fatty acids and cholesterols are directly transported to the fetus.
Arachidonic acid levels are higher as they are synthesized from cholesterol in the placenta
Steroids They also cross the placenta readily
Water-soluble These are absorbed active mechanisms; fetal concentration is higher than that in the mother. Neither parathormone nor
Vitamin calcitonin cross the placenta
Electrolytes Sodium and potassium cross the placenta readily by simple diffusion and solvent drag. The fetus requires more water and
transfer is dependent upon the osmotic and hydrostatic pressures. The control of water exchange is also thought to be
influenced by hormones such as vasopressin, oxytocin and prolactin
Drugs Determined by their molecular weight, affinity for lipids and ionization
•• Human chorionic adenocorticotropic (hCACTH)

•• Human chorionic thyrotropin (HCT)
•• Pregnancy-associated b1-macroglobulin (b1-PAM)
•• Pregnancy-associated a2-macroglobulin (a2-PAM)
•• Pregnancy-associated major basic protein (PMBP)
•• Parathyroid hormone related protein (PTHrP).
Steroids
•• Progesterone
•• Estrogens (estrone estradiol, estriol). Fig. 8.11: Immunoassay card test (showing a positive test—2
A few hormones of the above list are given in detail below: lines, one a control line and the second the test line)
Human Chorionic Gonadotrophin (hCG)

after 48–72 hours should be performed from the same
It is also known as the pregnancy hormone. It is 38,400 daltons
laboratory to give guidance for management. Hydatidiform
molecular weight, glycoprotein with highest carbohydrate
mole (H. Mole) and choriocarcinoma secrete free alpha and
residue. hCG has alpha and beta subunits (non-covalently
beta subunits as well as intact hCG. But there is an excess
linked). hCG is mainly synthesized by placenta (by the
of alpha subunit while the level of plasma beta subunits are
syncytiotrophoblast) after synthesis from corpus luteum
very low. Biological activity is similar to LH. Plasma half-life
ceases. Fetal kidney and malignant trophoblast also produce
of its slow component is 24 hours as compared to the fast
hCG. A small amount is secreted in men and non-pregnant
women. hCG is a glycoprotein hormone like luteinizing component (5 hours) and half-life of LH, which is 2 hours.
hormone (LH), follicle-stimulating hormone (FSH) and Thirty percent of hCG is cleared by the kidney and rest is
thyroid stimulating hormone (TSH). The alpha subunit of metabolized by the liver and kidneys.
all these are identical, but the beta subunits are different. The hCG can be detected as early as 7–9 days after the
Beta subunit gives a hormone its biological activity. The rate LH surge in plasma. Maximum levels in the serum are
of synthesis of beta subunit of hCG is a very good indicator between 8 to 10 weeks. Its urine concentration parallels
of health of the pregnant woman. In a normal pregnancy, that in the plasma.
shortly after implantation, hCG can be detected in the
urine and plasma of the pregnant woman. The level falls Higher Levels of hCG
to lower levels in second and third trimesters. Laboratory Multiple pregnancy
and ‘do it yourself’ pregnancy tests using monoclonal Single pregnancy with erythroblastotic fetus, resulting
antibodies—specific to hCG, become positive as early as from maternal D antigen isoimmunization
the 1st day of the first missed period (Fig. 8.11). Different Hydatidiform mole and choriocarcinoma
laboratories have different standards hence a repeat test Mid-trimester Down syndrome pregnancy.
Low Levels of hCG are Found in Anti-insulin action.

Missed abortion Angiogenesis (formation of fetal vasculature).
Blighted ovum
Impending abortion
Other Placental Hormones
Ectopic pregnancy. Chorionic adenocorticotrophins: A protein similar
to ACTH has been isolated from placental tissue. The
Functions physiological role is unclear. The concentration of ACTH
Rescue of corpus luteum. hCG rescues and maintains in pregnancy is lower than that in the non-pregnant
the function of the corpus luteum in continuation with woman, but it increases as the pregnancy advances. The
production of progesterone. placenta might produce ACTH which is then secreted
hCG stimulates fetal testis. The peak of fetal testicular into the mother and the fetus.
secretion of testosterone corresponds to the same time Chorionic thyrotropin: The placenta produces chori-
when the serum has the maximum levels of hCG, i.e. onic thyrotropin, but its role in pregnancy is, as of now,
110 days of pregnancy, thus promoting the male sexual not clearly established.
differentiation. Relaxin: It is a peptide hormone made up of a single 105
hCG stimulation of maternal thyroid. The exact mech amino acid as prorelaxin molecule. This cleaves into A
anism is not known. and B chains. Relaxin has two genes H1 and H2, which
hCG promote relaxin secretion by corpus luteum. are transcribed in the corpus luteum of the ovary. H1
genes are expressed on the decidua, placenta and fetal
Human Placental Lactogen
membrane.
First described by Ehrhardt in 1936, hPL has a prolactin Functions: Acts on myometrial smooth muscles promo
like activity and is found to be concentrated in the ting uterine relaxation.
syncytiotrophoblast and cytotrophoblasts as early as the Parathyroid hormone related protein (PTHrP) may
2nd and 3rd week after fertilization. hPL is a single non- serve as the parathyroid of the fetus.
glycosylated polypeptide chain of molecular weight 22, Human growth hormone variant (hGHV): This hor
279 d. There are 191 amino acid residue. It is proportional mone is expressed in the placenta, producing a 191
to the placental mass. It is excreted in the urine in a small amino acid protein. It is present in the maternal plasma
amount. Its half-life is 10 to 15 minutes (Fig. 8.12). by 21 to 26 weeks increasing in concentration to a
Functions maximum by about 36 weeks.
Hypothalamic-like releasing hormones. There are
Lipolysis and increase in the levels of circulating free
analogous hormones, produced in human placenta.
fatty acids—thus helps in production of energy for both
Estrogen: The placenta produces a large amount of
maternal and fetal metabolism.
estrogen. The production and synthesis of the hormone
is dependent on the steroidal precursors in the blood.
Estriol is synthesized in the placental syncytiotrophoblast
from its fetal precursor, dehydroepiandrosterone
(DHEA) which is a product of the adrenal glands of the
fetus, and is hydroxylated (16-OH-DHA) in the fetal liver.
Deficiency of fetal adrenal activity is associated with a
low estriol levels. The bilary part of excretion undergoes
entrohepatic circulation. The hormone estrone and
estradiol are also secreted by the placenta.
•• Levels: In pregnancy, the estrogen levels are very
high than those in the non-pregnant state.
•• Fetal conditions that affect estrogen production:
–– Fetal death
–– Fetal anencephaly
Fig. 8.12: Concentrations of hCG and hPL in maternal serum in –– In the absence of the fetal adrenal cortex, the rate of
relation to weeks of gestation formation of placental estrogen is severely limited.
–– Fetal adrenal hypoplasia: Rare It is again to be emphasized that the placenta, cord
–– Placental sulfatase deficiency: Estrogen forma and membranes (with the vessels) should be examined
tion in placenta is generally regulated by the meticulously after delivery and mentioned in the case
availability of C19 steroid prohormones in the report. It may be examined by pathologist in cases of
fetal and maternal plasma. stillbirths, fetal growth abnormalities, etc.
–– Placental aromatase deficiency
–– Down syndrome UMBILICAL CORD
–– Deficiency in the fetal low-density lipoprotein
(LDL) cholesterol biosynthesis
–– Fetal erythroblastosis DEVELOPMENT (FIG. 8.13)
–– Decreased fetal adrenal use of LDL.
The yolk sac and the umbilical vesicle into which it
•• Maternal conditions that affect placental estrogen
develops are quite prominent early in pregnancy. Initially
synthesis
the embryo is a flattened disc between the amnion and
–– Glucocorticosteroid treatment: The admini
yolk sac. The dorsal surface grows faster than the ventral
stration of moderate to high dose of glucocortico-
surface. In association with elongation of the neural tube,
steroid to pregnant women causes a reduction in the embryo bulges into the amniotic sac and the dorsal
placental estrogen formation as it inhibits ACTH part of the yolk sac is incorporated into the body of the
secretion. This results in a reduction of the mater- embryo to form the gut. The allantois projects into the
nal and fetal adrenal secretion of the precursor base of the body stalk from the caudal wall of hindgut. As
dehydroepiandrosterone sulfate. pregnancy advances, the yolk sac becomes smaller and its
–– In maternal adrenal dysfunction like Addison’s pedicle relatively longer. By about the middle of the 3rd
disease, the urinary estrogen levels are reduced month, the expanding amnion obliterates the exocoelom,
specially 17b-estrone. fuses with the chorion laeve, covers the bulging placental
–– Maternal ovarian androgen producing tumors. disc and the lateral surface of the body stalk, which is
–– Maternal renal disease: Low levels of estriol then called the umbilical cord or the funis. Initially four
are seen in the urine of pregnant women with vessels are present in the umbilical cord (2 arteries and 2
pyelonephritis. The levels are normal in these veins) (Fig. 8.14). Later, by the 4th month of intrauterine
patients but it is probably because of low renal life, the right vein disappear. The cord at term normally
clearance that the levels are low in urine. has two arteries and one vein. Sections of any portions
–– Maternal hypertensive disorders and diabetes. of the cord frequently reveal near the center, a small duct
The fetal adrenal synthesis of DHEA is impaired of the umbilical vesicle, lined by a single layer cuboidal
because of a decrease in the uteroplacental blood epithelial cells. The intra-abdominal portion of the duct,
flow and not because of a reduction of placental
functions.
–– Gestational trophoblastic disease: There is no
fetal adrenal source of C19 steroid precursor.
Leptin: It regulates bone growth and immune function.
It is synthesized in both cytotrophoblast and syncytio-

trophoblast.
Progesterone: It is secreted by the corpus luteum upto
6–7 weeks of gestation. Thereafter, it is synthesized

by the placenta. Maternal cholesterol is converted to
pregnenolone in the mitochondria. It is converted to
progesterone in the endoplasmic reticulum. Unlike
estrogen, progesterone is not an indicator of fetal
well-being, fetal death, intrauterine growth restriction
(IUGR), etc.
The concentration gradually rises and it is about 250
mg/day at term. It may act as a mild immunosuppressor. Fig. 8.13: Fetal development (umbilical cord)
2 cm, the length varies between 30 and 100 cm and on

an average it is approximately 50 to 55 cm (same length
as the newborn) and any cord length less than 30 cm is
considered abnormally short. Very rarely there might
be no cord which is called achordia and there might be
unusually long cord to an extent of 300 cm.
Length of cord depends on the intrauterine movement of
the fetus. The cord might have false knots or true knots. The
false knots are because of vessels tortuosity; vessels are being
longer than the cord itself frequently creates nodulations
on its surface. The cord is covered by amniotic epithelium.
The extracellular matrix, which is a specialized connective
tissue, is rich in mucopolysaccharides with embedded
collagen fibers, mast cells and sparse flat stellate cells
around the vessels—Wharton jelly. This is metabolically
very active and has a protective effect on the cord. Further
functions may be elucidated by further research.
Fig. 8.14: Blood vessels in umbilical cord The two arteries are smaller in diameter than the vein.
One part of the blood flowing from the umbilical vein
goes via the ductus venosus into the inferior vena cava
which extends from the umbilicus to the intestine usually
(IVC) directly, and other part drain through multiple small
atrophies and disappears. Occasionally, it remains patent
openings into the fetal hepatic circulation and then into the
to form the Meckel’s diverticulum. The umbilical cord is
IVC by the hepatic vein. The blood takes the path of least
the connection between the fetus and mother (Fig. 8.14).
resistances through these alternative routes. Resistances in
the ductus venosus is controlled by a sphincter situated at
CONTENTS its origin the ductus at the umbilical recess and innervated
The umbilical cord contains two umbilical arteries, one by a branch of the vagus nerve. Nerves are not found in the
umbilical vein, Wharton’s jelly and amniotic cells. The umbilical cord.
arteries are two in number and are derived from the
ventral division of the internal iliac arteries. They transport INSERTION
deoxygenated blood from the fetus to the chorionic villi of
The attachment to the fetal end is at the caudal extremity in
the placenta. The umbilical arteries are spirally arranged
early stages of pregnancy, but by the end of the 4th month,
with a thick muscular valve. In the early part of pregnancy the
the point of attachment shifts to the center of abdomen.
umbilical veins are two in number. Later the right umbilical
Placental insertion—normal variations are:
vein, disappears and the left persists to carry oxygenated
Central insertion—usual (Fig. 8.8)
blood, from the placenta to the fetus where it joins the left
Marginal—cord is inserted at placental margin
branch of the portal vein at the porta hepatis. Blood vessels
Eccentric insertion.
going toward the heart are called veins. Thus, the umbilical
vessel carrying oxygenated blood going towards the fetal
heart is called a vein. (Other examples being pulmonary
FUNCTIONS
veins in adults). Arteries go away from heart. Umbilical Besides serving as a mechanical conduit between the fetus
arteries, though containing deoxygenated blood, go away and the placenta, it also plays a part in the movement of
from the fetal heart and are thus called arteries (adult water and other substances between the fetal circulation
pulmonary arteries also carry deoxygenated blood). and the amniotic fluid.
CHARACTERISTICS FETAL MEMBRANES (FIG. 8.15)

The umbilical cord is dull white in color, moist and covered Membranes are two in number:
by amnion. The umbilical vessels may be seen through 1. Amnion—inner
the amnion. The diameter of cord varies between 0.8 and 2. Chorion—outer
Fig. 8.15: Fetal membranes Fig. 8.16: Development of chorion
Amnion: The amnion has following layers:

•• Cuboidal epithelium
•• Basement membrane
•• Compact layer
•• Fibroblast layer
•• Spongy layer
There are no blood vessels, lymphatics or nerves in it. The
thickness of the amnion is 0.02 to 0.5 mm.
Chorion: It represents the remnant of chorion laeve
and is thicker than amnion (Fig. 8.16).

The chorion has following layers:
•• Cellular layer (fibroblast)
•• Reticular layer
•• Basement membrane
Fig. 8.17: Development of amnion
•• Trophoblast (main layer of chorion).
The chorion contains no vessels or nerve supply.
Development of Amnion
Amnion A space forms between trophoblast and embryonal
The inner layer of fetal membranes has small cells that line cell mass, this will form amniotic cavity. (Fig. 8.17).
the inner surface of trophoblasts called the amniogenic
cells, which are the precursors of the amniotic epithelium. Histogenesis of Amniotic Cells
The human amnion is first identifiable around the 7th Amnion epithelial cells: These are derived from fetal
or 8th day of embryonic development. Initially a small ectoderm of the embryonic disc. These cells line the
vesicle, the primitive amnion develops into a small sac entire inner portion of the amniotic membrane and are
that covers the dorsal surface of the embryo. As this sac responsible for most of the amniotic functions.
enlarges, it engulfs the growing embryo, which prolapses Amnion mesenchymal cells: These cells are derived
into its cavity. This sac enlargement brings it into contact from embryonic mesoderm. They belong to the
with the inner surface of the chorion laeve. The mesoblast fibroblast layer of the amnion. These are sparsely
of the chorion laeve and amnion come closer to obliterate distributed as compared to the epithelial cells. The
the space of the extra-embryonic coelom. This change tensile strength of the amniotic membrane, in terms of
takes place at the end of the first trimester. interstitial collagen, is made up solely by these cells.
These cells are responsible for synthesizing cytokines, relatively decreases and is about one liter. Recent studies
interleukins (IL-6 and IL-8). These substances are shows that the observed reduction in the amniotic fluid
responsible for the study of amniotic fluid for evidence index in the final weeks before the onset of labor, is
of labor associated accumulation of inflammatory related to the process of labor. Less amount of amniotic
mediators. fluid volume occurs with a circulatory redistribution and
The amniotic membrane has three parts: reduced production of fetal urine; this is followed by a
1. Reflected amnion: It is fused to the chorion laeve. spontaneous onset of labor (Stiger and associates 2002).
2. Placental amnion: It covers the fetal surface of the Fetal lungs secrete about 300–400 mL fluids per day. More
placenta and thereby is in contact with adventitial than 1500 mL liquor amnii at term is called polyhydramnios
surface of the chorionic vessels which traverse the and less than 300 mL is called oligohydramnios.
chorionic plate and branch into the cotyledons.
3. Umbilical amnion: It covers the umbilical cord. Composition of Amniotic Fluid
Immediately above the internal os the reflected chorion It is isotonic in early pregnancy but hypotonic by the end of
laeve is not contiguous with the decidua. the term because fetal urine (main contributor at the time)
Human amniotic epithelial cells proliferation was seen has a low electrolyte content, though the levels of urea and
to increase significantly in a dose related fashion when creatinine are high. It also contains protein, glucose, lipids,
insulin like growth factor-II (IGF-II) and relaxin were hormones and suspended particles like lanugo, exfoliated
given. Relaxin appears to affect IGF-II transcription. It fetal squamous cells, vernix caseosa, cells from respiratory
causes proliferation of human amniotic epithelium by system and, genitourinary system of fetus.
stimulating IGF-II.
Functions and Clinical Importance of
Amniotic Fluid Amniotic Fluid
Amniotic fluid is derived from the maternal plasma in very
Mainly protective in nature. Protect the growing fetus
early pregnancy. The amniotic fluid is also called liquor
from the outside world. Also protect the placenta and
amnii. It is pale straw colored, has a low specific gravity
umbilical cord from the pressure of the uterine contents.
(1080) and is alkaline in nature (pH 7.2). From the second
Helps in maintaining an even temperature.
trimester, it also receives contributions from fetal urine
Prevents any external injuries by equalizing pressure.
and lung fluid. A small amount of amniotic fluid is secreted
Allow free fetal movements and fetal activity. This also
by the amnion, specially the part covering the placenta
and the umbilical cord. Amniotic fluid has 98% water and prevents adhesion between the fetal parts.
contains around 2% of solids like inorganic salts, urea, Aspiration of amniotic fluid in the gastrointestinal tract
protein and a small amount of sugar, food substances, (GIT) and lungs of the fetus helps in their development
waste products, shed, fetal skin cells, vernix caseosa and because of PTHrP and endothelin 1, which helps in
lanugo. The amniotic cells are cuboidal over the placenta surfactant synthesis.
and flattened over the rest of the amniotic cavity. The Bacteriostatic—some protection from infection is given
amniotic cells have microvilli on their surface. They are: by the amniotic fluid.
Golgi type or During labor amniotic fluid with membranes help in
Fibrillar type. dilation of cervix.
Nutritive value of amniotic fluid is small as protein
Amount of Amniotic Fluid content is less, however, it is a good source of fluid
There is a wide variation in the volume of amniotic fluid. supply to the fetus.
12 weeks 50 mL It helps in ultrasound examination as the sound is freely
16 weeks 100 mL transmitted through it.
22 weeks 400 mL Amniocentesis helps in diagnosis of neural tube defects,
34–36 weeks 1000 mL (α-fetoprotein, cholinesterase and rapidly adherent
40 weeks 950–980 mL cells), chromosomal abnormalities, (culture of cells
41–42 weeks 500–550 mL and fibroblast in amniotic fluid), Rh-isoimmunization,
The fluid gradually increases in amount upto the 6th lung maturity (lecithin/sphingomyelin ratio) and
month of pregnancy. Towards end term, the amount chorioamnionitis (presence of WBC and bacteria).
The volume of amniotic fluid present is an important Isoimmunization: The level of bilirubin in amniotic
indicator of fetal condition. If there is oligohydramnios fluid at an optical density of 450 nm, a golden color of
fetal growth is in jeopardy (renal agenesis). The same liqor denotes hemolysis due to rhesus incompatibility
is true with polyhydramnios (diabetes mellitus in the and severity of fetal hemolysis.
mother). Lung maturity: The lecithin/sphingomyelin (L/S) ratio
It makes a good medium in the intra and extra-amniotic is a good indicator of lung maturity and, should be more
instillation of drugs for second trimester medical than two. Sometimes a lecithin phosphatidyl glycerol
termination of pregnancy (MTP). ratio may be required (especially in diabetic patients).
Color of amniotic fluid changes to green by meconium Infections: Amniocentesis is done to determine the
(fetal compromise). Dark brown color can be seen in presence of white cells and bacteria, which is diagnostic
IUD (Intrauterine death) and macerated still birth. of chorioamnionitis.
Artificial rupture of membranes (ARM) is done for It is again to be emphasized that placenta, cord and
induction of labor. membranes (with the vessels) should be examined
Villus sampling can be done to examine genetic and meticulously after delivery and mentioned in the case
metabolic disorders. Fetal blood cells in the cord (after report. It may be examined by a pathologist in cases of
birth) is useful as stem cells. They are tolerated better than stillbirths, fetal growth abnormalities, etc.
adult cells. Hence, recently they are stored for treatment of
certain cancers on other disorders of bone marrow. FUNCTIONS OF FETAL MEMBRANES
Prevention of ascending infection from vagina
COMPLICATIONS OF MEMBRANES Contributes in formation of liquor amnii
Facilitates dilatation of cervix.
These topics are covered in individual chapters.
The amnion contains arachidonic acid, the precursor of
prostaglandins and phospholipase. The release of ara-

AMNIOCENTESIS chidonic acid by phospholipase A2 provides the mech-
Access to amniotic fluid is made by performing amniocen- anism for prostaglandin E2 (PGE2) and prostaglandin
tesis, which is indicated in the following conditions. F2 (PGF2) formation which are important in normal
Neural tube defects (NTD): Concentration of labor. It also has some enzymatic action.
α-fetoprotein, acetylcholinesterase and the presence of The tensile strength of chorioamnion increases upto
rapidly adhering cells can be diagnostic of NTD. 20 weeks of gestation. It does not change till 39 weeks
Chromosomal abnormality: Fetal cells (fibroblasts) of pregnancy, after which it drops suddenly. Clinical
from amniotic fluid are cultured and arrested in the chorioamniotis alone cannot influence tensile strength. But
metaphase stage. These can provide accurate chromo- gross inflammation of the membranes does cause reduction
somal diagnosis. in the tensile strength.
1. Name two pathways of trophoblest growth.
2. Define primary villi.
3. Name two fetal membranes.
i. Placenta has two part _____________ and _____________.
ii. Zygole inter the uterine cavity at the morula stage with outer layer of _____________ and duster of cells called _____________.
Maternal Anatomical and
9
Sudha Salhan
Physiological Changes
in Pregnancy
progressively by 12 weeks. After 12 weeks, the uterus

INTRODUCTION
increases in length rapidly and becomes sac like as it grows
The anatomical, physiological, and endocrinological changes into abdominal cavity.
are a positive adaptation of the mother to accommodate
and support the fetus throughout gestation, for delivery and Position
lactation. Hormones and genetic factors are responsible for The position of uterus which was anteverted and antiflexed
most of these changes. becomes more axial and vertical, it displaces the intestines
Aims of anatomical, physiological and endocrinological to the sides of abdomen, and directly comes in contact
changes are: with anterior abdominal wall. The position of the uterus in
To fulfill the needs of the fetus the second half of pregnancy depends on the laxity of the
To provide conditions favorable for development and abdominal wall. In nulliparous patient, whose abdominal
growth of fetus wall is tense, the uterus is more vertical. In multiparous
Prepare the body for labor and lactation. women, abdomen is pendulous due to laxity of anterior
abdominal wall and its rectus abdominis muscle. As the
ANATOMICAL CHANGES OF CONCEPTION uterus grows and becomes an abdominal organ, it also
rotates on its long axis, usually to the right (dextrorotation).
Uterus
The uterus shows maximum changes because it provides Thickness
a nutritive and protective environment in which the fetus The wall of the uterus increase in thickness from 0.8 to
will develop and grow. 1 cm in non-pregnant state to 25 mm by the 12th weeks. Then
The uterus has two parts—the corpus and the cervix. the thickness of uterine wall decreases as the pregnancy
The corpus is composed of muscle and undergoes marked advances (as size of uterus is increasing) because of this
growth and hypertrophy. thinning the fetal parts becomes palpable after 24 weeks.
The pregnancy causes a progressive softening of the uterus
Size which starts with the isthmus. This is the basis of Hegar’s
The size of uterus which is approximately 7.5 × 5 × 2.5 cm sign (10 weeks).
with capacity of 4 mL increases to 28 × 24 × 21 cm and
capacity about 4 liters. The mass of the uterus varies from Uterine Musculature
30 to 60 g in non-pregnant state, increases to 750–1000 g at In the first trimester, there is a marked hyperplasia of
term. the muscle cells and mitotic figures are common. In the
second trimester, the increase in size is due to hypertrophy
Shape of the muscle, the muscle cells increases in length and
Uterine muscles mostly hypertrophy to increase the volume. They increase from 50 mm to 200–600 mm. The
mass. The increase in size also leads to change in its initial hyperplasia is because of estrogen, but hyperplasia
shape. Originally, it is pear-shaped but become spheroid is later inhibited and hypertrophy begins under the effect
of progesterone hormone. There is also simple stretching

of the uterine muscles to accommodate the enlarging
fetus, placenta and amniotic fluid. This is due to the direct
stretching effect of uterine contents. The muscle fibers
in the uterus have a bilateral symmetrical arrangement
resulting from the fusion of the two Müllerian ducts in
embryologic period. The fibers run spirally and form an
interlacing complex. In non-pregnant patient, the fibers
tend to cross each other at right angle in the fundus, but
in the lower segment it is obtuse. The uterine muscles are
arranged in three layers during pregnancy (Fig. 9.1). The
outer most layer passes over the fundus longitudinally
and merge into ligaments. The inner layers are around
the opening of the fallopian tubes and internal os act like
sphincters. The main part is the middle layer of muscles.
They have interlocking network of muscle fibers, they are
shaped in a manner that each cell has double curve and
when two muscle interlace, they get a shape of figure of eight
Fig. 9.2: Living ligatures (figure of eight) arrangement of blood
(Fig. 9.2). This is a very vital arrangement, after delivery when vessels and muscle fibers in myometrium
this muscles fibers contract, they constrict the blood vessels
between them and thus act as living ligatures preventing
postpartum hemorrhage (PPH). In pregnancy, the fibers of Decidua
the upper segment preserve their original arrangement but There is increased thickness and vascularity of the lining
the fibers of lower segment are drawn up so that these fibers of uterus; it is called decidua. These changes are brought
of lower segment become more vertical, favoring dilatation about by progesterone and estrogen. It is most developed
in labor. The pregnant lady is advised not to lie supine as at the fundus and the upper part of the body of the
the uterus falls backwards upon the vertebral column, uterus—the sites of implantation of the embryo. Decidua
compressing the inferior vena cava (IVC) and aorta. This produce relaxin which causes myometrial relaxation. It
causes the reduction in blood supply to uterus and thus may also play a role in cervical ripening and the rupture of
fetus.
membranes. The decidua also release prostaglandins for
Dextrorotation starting the process of labor.
The presence of the rectosigmoid on the left physically
Contractility
pushes the uterus slightly to the right. Hydroureter is also
more on the right side. The uterine muscles are both contractile (to push the fetus)
and elastic (to stretch and accommodate the growing
fetus).
The uterus starts contracting from as early as the 14th
weeks of pregnancy. These contractions are character-
istically infrequent, weak and arrhythmic till later in the
gestation (30–34 weeks), when it is increases in strength
and frequency—Braxton Hicks contractions. The uterine
contractions in early pregnancy are due to the uncoordi-
nated myogenic activity of individual uterine muscle fiber.
Braxton Hicks contractions are usually painless. But some
discomfort is usually felt if their pressure increases to 15
mmHg or more. These contractions facilitate blood flow
through the placental site and play a part in the develop-
Fig. 9.1: Muscle layers of uterus in pregnancy ment of the lower uterine segment.
Maternal Anatomical and Physiological Changes in Pregnancy 75
Nerve Supply
The uterus is profusely supplied by the autonomic
and central nervous system (CNS). It undergoes marked
hypertrophy in pregnancy. There is an increase in the
size of Frankenhauser’s ganglion. The fibers to the uterus
arises from the spinal cord through sacral nerves and
distributed via Frankenhauser’s ganglion to the cervix.
The Pacinian types structures have been found which may
be responsible for pain on stretching the cervix. This pain
from body of the uterus is conducted by the sympathetic
nervous system and is ischemic in origin. There is a relative
denervation of the isthmus and the stimulating effect of
neural noradrenaline is reduced, unlike the non-pregnant
uterus where noradrenergic nerves are distributed mainly
to the cervix and lower part of the uterine body. The
Fig. 9.3: Tortuous blood supply
relative denervation of the uterus may favor relaxation and
formation of the lower uterine segment.
Ferguson’s reflex: In labor, the nerve supply to the cervix with Braxton Hicks contractions. Columnar epithelium is
causes stimulation of uterine contractions on applying stimulated to grow (under the effect of estrogen) and may
pressure on the cervix by the fetal head. be seen as an erosion or ectropion which bleeds on touch.
Mucous glands are distended and increase in complexity
Isthmus (under the effect of progesterone) and form a thick viscous
During the first trimester the isthmus of the uterus mucus plug (operculum) which provides protection against
hypertrophies and elongates to three times its original ascending infections. The length of the cervix remains
length. It is soft and compressible between 10 and 12 2.5 cm throughout pregnancy. It remains firmly closed and
weeks (Hegar’s sign). The isthmus progressively opens holds the uterine contents in place. The cervix gradually
out after the 12th week as the gestational sac expand. The softens or ripens. The cervical canal dilates. In a multipara
isthmic canal is incorporated into the uterine cavity and some dilatation of the external os is seen by 24 weeks. In a
forms a part of the lower segment of the uterus. primigravida also the internal os starts opening by the 32nd
week. The ripening is caused by the enzyme collagenase
Blood Supply and by prostaglandins from local tissue or amniotic fluid.
The tortuous uterine vessels get straightened as the uterus Effacement produces a more circular orifice with paper thin
enlarges in size (Fig. 9.3). Besides, the spiral arteries lose edges (see Chapter 26). The ripening and dilatation of the
their endothelium and musculature, (see development cervix are important for normal delivery. Both before and
of placenta). At 10th weeks of gestation, the uterus has during labor the connective tissue of the cervix undergoes
a blood supply of 50 mL/minute. It reaches its maximum marked changes with loosening and dispersion of the
supply of 450–700 mL/minute at term; of this 80% goes microfibrils. The patient who has an incompetent cervix
to the placenta and 20% to the myometrium. It is important causing recurrent miscarriage, needs the placement of
to know this because prompt control of PPH prevents cervical cerclage (like McDonald’s and Shirodhar’s) to carry
active loss (450–700 mL in a minute). the pregnancy to term.
Cervix Epithelium and Glands of Cervix and Cervical Canal

The cervix is vital in pregnancy and for normal delivery. The squamous and columnar epithelium is hyperactive in
There is an increase in vascularity and softening of the pregnancy. There is abundant growth of the endocervical
cervix, it appears blue in color. These are diagnostic signs mucosa. There is also a marked increase in thickness
of pregnancy. The cervix has 10% muscular tissues, the (from 2.3 mm to 4.6 mm). This mucosa protrude from the
rest being collagenous. Muscular activity of the cervix is endocervical canal producing apparent ectropion of the
sufficient to cause constriction during early pregnancy cervix. The transition zone (squamocolumnar junction)
and early labor. Therefore, no dilatation of cervix occurs also moves peripherally producing an erythroplasia which
appears red and velvety around the external os. This might the papillae enlarge. The highly acidic vaginal discharge
even extend as far as the upper vagina. The squamous (pH 3.5–5) is caused by more desquamation of superficial
epithelium of the cervical canal is hyperactive in pregnancy vaginal cells. Thus more glycogen is released (in these
so much, so that it resembles carcinoma in situ. desquamated cells) which is converted by Döderlein
bacilli to lactic acid. Hence, the patient complains of
Cervical Mucus an increased amount of white vaginal discharge during
Ferning is absent in pregnancy. The mucus become opaque pregnancy. If there is no other symptom (itching), it is a
and viscous and fills the endocervix forming a mucus normal occurrence. The high acidic pH plays a role in
plug. It has antibacterial action as it contains abundant keeping the upper vagina free from bacteria. However, it
leukocytes. It also mechanically blocks the passage and favors the growth of yeasts and Candida albicans. As the
thus further prevents ascending infection. pregnancy advances the basophilic boat shaped navicular
cells predominate over the superficial squamous and
Ovaries basal cells.
Ovulation leads to the formation of a corpus luteum. If
fertilization occurs, the corpus luteum enlarges rapidly Ligaments, Parametrium and Peritoneum
and is called the corpus luteum of pregnancy. It occupies The round ligaments and uterosacral ligments hypertro-
one-third of the ovary. It is initially composed of granulosa phy, stretch in pregnancy. Due to the disproportionate
lutein cells (containing lipid vacuoles). By 24th weeks of growth of the uterus, the round ligament may become
gestation secretory granules are present in about one-third tender and painful. It is believe that the round ligament
of the cells, by term they disappear. The corpus luteum is and uterosacral ligaments contract during labor with
functional till 12–14 weeks of pregnancy. After that, the the uterus and thus helps in bringing the long axis of the
placenta takes over its function and the corpus luteum uterus into the long axis of the inlet of pelvis. The perito-
begins to regress. neum grows with the uterus and becomes loose; it is easily
Many follicles become temporarily active but the ova separable in the lower uterine segments (identified during
undergo cytolysis. Hence, there is no ovulation during cesarean section). The decidual reaction may be observed
pregnancy. However, in the follicles in which the ova on the ovary, posterior surface of pelvic peritoneum,
disintegrate, the theca lutein cells proliferate and form round ligament, uterosacral ligaments and the pouch of
interstitial glands of pregnancy in the first half. These Douglas (POD). The broad ligament opens out (anterior
later undergo fatty and hyaline degeneration, which are and posterior folds) to accommodate the greatly enlarged
indistinguishable from corpora albuginea. The ovarian uterine and ovarian vessels. Pelvic ligaments show marked
capsule undergoes a decidua-like reaction. changes. The same is true with the symphysis pubis, su-
perior and inferior pubic ligament, sacroiliac joints and
Fallopian Tubes sacrococcygeal joint. These fibrocartilages become soft
Its main functions are accommodation, transport and and loose. There is an increase in synovial fluid. All these
sustenance of the ovum and embryo during the first 7 days changes greatly increased the mobility of these joints.
of life. As there is disproportionate growth of the fundus, Symphysis pubis separates thus increasing the pelvic di-
at term the fallopian tube insertion is seen at half way up mensions during labor. They may become excessively re-
the uterus. The endosalpinx epithelium is flattened and laxed causing difficulty in walking (pelvic arthropathy of
irregular and cytoplasmic processes bulge. pregnancy).
Vagina, Vulva and Pelvic Floor Gastrointestinal System

There is increased vascularity in pregnancy. The veins There is delayed gastric emptying time, gallstone formation
become engorged. The vagina acquires a violet color may occure due to stasis. Constipation is usually seen.
due to hyperemia (Chadwick’s sign by 8–10th weeks of Esophageal reflux may be there.
pregnancy). The capacity, length and distensibility of the
vaginal as well as vulval connective tissue starts loosening, Skeletal System
which makes vagina more distensible during delivery. The Because of uterine growth there is protrusion of the
epithelium of vagina, like the cervical epithelium, starts abdomen and shift of the center of gravity. To counteract
undergoing hyperplasia. The vaginal rugae deepen and this, the pregnant woman keeps the shoulders back,
her spine is straightened and a slight lordosis is seen.

Gradually lumbar lordosis increases and by term there is
rotation of the pelvis and femur. With all these changes,
the waddling gait of late pregnancy is seen. There may be
pain in ligaments and muscles and hence backache.
Skin
Neurological Changes
Sometimes median nerve entrapment due to fluid retention
(carpal tunnel syndrome) causes pain, diminished
sensation and weakness of the first three fingers. Sciatica
is also sometimes seen due to fluid retention. There is an
increased blood flow to maintain the body temperature.
Sweat and sebaceous glandular activity also increases. Fig. 9.5: Breast showing secondary areola and Montgomery’s
In a few, hair growth is stimulated. Mild hirsutism may tubercles
develop on the face and extremities (Fig. 9.4). It is due to
placental androgen and elevated cortisol. Pigmentation
of the skin occurs especially on the nipples (development
of secondary areola in primigravida and Montgomery’s
tubercles) (Fig. 9.5), face, umbilicus, vulva and midline
(Fig. 9.6) due to melanocyte stimulating effect of estrogen
and progesterone. The placenta also produces melanocyte
stimulating hormone. Vascular spider nevi and palmar
erythema may be seen. Varicose veins may be seen at
the vulva (Fig. 9.7) perineum and legs. Hemorrhoids are
also seen in some pregnant women. The face is more full
due to fat deposition. A butterfly like hyperpigmented
area is seen (chloasma or mask of pregnancy) on the face
(Fig. 9.8). Fat is laid down, especially in the second and
Fig. 9.6: Abdominal changes in pregnancy
Fig. 9.4: Hirsutism Fig. 9.7: Vulval varicosities in pregnancy

development throughout gestation and after delivery till

lactation. These changes start very early in pregnancy
preceeding the needs of the fetus, e.g. 50% increase in
renal flow starts at 9 weeks of pregnancy. They are also
in excess of the requirement of the fetus, e.g. the cardiac
output increases by 25–65% during pregnancy, which is
much more than necessary. In anticipation of the needs of
the growing fetus, the mother accumulates essential stores
like deposition of fat. This provides a reserve of energy at
the time of nutritional deprivation which may occur in
late pregnancy and during lactation. Thus, the internal
environment of the mother is geared to provide favorable
conditions for the unhindered development and growth
of the fetus and later the neonate. But, all these changes
are temporary and no permanent ill effect occurs in the
Fig. 9.8: Chloasma or mask of pregnancy mother. All these changes revert to almost pre-pregnancy
levels, in due course of time, after delivery.
The knowledge of physiological changes in pregnancy
third trimesters on the thighs abdomen and buttocks. It
is very important because any deviation from normal must
helps in the puerperium for lactation.
be detected and treated promptly.
Abdominal Wall Fluid Changes
It is stretched and thinned out. The umbilicus becomes flush
Fluid retention occurs in pregnancy in the range of 6.5–8.5
with the skin. Any hernias, if present before pregnancy, are
liters, the average gain of weight being 11 kilogram. Blood
more manifested now. Because of the breaking of underlying
volume of the mother expands 1500–1800 mL (plasma
connective tissues there are irregular, wavy pink or purple
1200–1300 mL and RBC 300–400 mL) (Table 9.1). The rest of
markings called striae gravidarum. These are seen on the
the retention of fluid is in the extravascular space.
lower abdomen, buttocks and thighs (Fig. 9.6).
Intracellular fluid accumulates in the uterus, adipose
Breasts tissue and breasts. All these lead to an increase in maternal
Breasts develop in preparation of lactation in puerperium. cardiac output. This retention is by active sodium and
Unusual tenderness and tingling is experienced as water conservation, due to alteration of osmoregulation
early as 2–4 weeks of conception. Estrogen helps in the and renin-angiotensin system.
development of the duct system and progesterone is Antidiuretic hormone (ADH) secretion is controlled
responsible for alveolar growth. The growth continues by the posterior pituitary. Between 5 and 8 weeks of
throughout pregnancy with increased blood supply. The gestation, there is more water intake and, hence, increased
weight of each breast is 400–800 g. Breasts progressively body fluid. The osmoregulation threshold is reset after
increase in size due to proliferation of glands and deposition
of fat. Veins below the skin become prominent. Nipples are
larger, with more pigmentation. Montgomery tubercles TABLE 9.1: Distribution of weight gain during pregnancy
(mouths of hypertrophied sebaceous glands) are seen Tissue/fluid Gain (g)
around the areola. Secondary areola develops especially Fetus 3400
in primigravidae. This is less pigmented. Secretion of Placenta 650
colostrum starts from mid-pregnancy onwards.
Amniotic fluid 800
Uterus 970
PHYSIOLOGICAL CHANGES OF
Mammary gland 400
CONCEPTION
Blood 1250
There are profound physiological adaptations of most
Extracellular extravascular fluid 1700
organs and systems in the mother which are a positive
Fat 3500
adaptation to accommodate and support the fetus in its
8 weeks of pregnancy. ADH production is increased TABLE 9.2: Blood cell composition changes during pregnancy
but it is rapidly metabolized. There is a total of 900 mEq Component Change
increases in sodium in the body. The placenta, the fetus
Total white cell count Increase
and the amniotic fluid has 60% of this sodium, which is lost
Neutrophils Increase
after delivery. This increase in body sodium is mainly due
to enhanced tubular sodium reabsorption. Glomerular Lymphocytes No change
filtration rate (GFR) is increased during pregnancy. This Eosinophils No change
increases filtered sodium from 20,000 to 30,000 mMol/ Platelets Decrease
day and 2–6 mEq of sodium reabsorption. This may be Red cell count Decrease
due to hormonal control by modified renin-angiotensin- Hematocrit (packed cell volume) Decrease
aldosterone and atrial natriuretic peptide (ANP), besides
Hemoglobin concentration Decrease
there is also preferential increase in salt intake.
Mean cell hemoglobin No change
Renin-angiotensin-aldosterone system activity is concentration
markedly increased in pregnancy. The levels of plasma
Mean cell volume Small increase
renin are increased 5–10 times than in non-pregnant
Red cell fragility Increase
state. Angiotensinogen (renin substrate) and angiotensin
are also 4–5 fold, increased, besides these two hormones, Erythrocyte sedimentation rate Increase
(ESR)
deoxycorticosterone and estrogen levels also influence
sodium metabolism. Note that changes in cell factors are dependent on iron supplemen
ANP is an antagonist to renin-angiotensin system. It tation.
is produced by atrial myocytes (of the heart) in response
to atrial dilatation. It is a diuretic, natriuretic and a vaso Helps fill the expanded vascular system (due to vasodi-
dilator. Its level fluctuates with posture. latation in the body and placenta). This prevents sud-
Plasma osmolality decreases in pregnancy (by den hypotension after delivery. Normal vaginal delivery
10 mMol/kg), so pregnant women easily feel thirsty. The has a blood loss of about 500 mL and uncomplicated
colloid osmotic pressure (oncotic pressure) also decreases cesarean section has about 1000 mL of blood loss.
in pregnancy because plasma albumin is decreased Response to blood loss: In the non-pregnant state,
(diluted) by 20%. This is responsible for increase in GFR any blood loss causes a fall in blood volume and fluid
and peripheral edema. redistribution occurs within 24 hours and there is a
proportionate drop in hematocrit. In pregnancy, the
Changes in Blood due to Pregnancy (Table 9.2) mechanism of adaptation is different. There is no
As seen from above, there is more increase in plasma re-expansion to the prelabor level and there is less
than RBC and other circulatory factors. Plasma volume change in hematocrit after bleeding (post delivery).
starts increasing at 6 weeks of pregnancy and increases In multiple pregnancy the blood volume increase is
steadily till 30 weeks (50% higher than non- pregnant more. It correlates with the weight of the fetuses.
state). After 30 weeks it is stationary (plateau). RBC mass Iron: Its absorption occurs in the duodenum in its ferrous
start increasing slowly from 10 weeks onwards to a level form in the enterocytes in the presence of enzyme ferric
18% more than the non-pregnant state. It increases on reductase. The absorption depends on the requirement
iron supplementation (30% more than non-gravid). of the body. If the body iron stores are normal, there is a
Because plasma expands more than the RBC mass there is 10% absorption of iron in the gut. If the patient is anemic
physiological anemia in pregnancy occurring maximum with limited iron stores in her body, the iron absorption
at 30–34 weeks. RBC mass continues to increase. There increases. After absorption in the enterocytes in the small
is bone marrow hyperplasia and the reticulocyte count gut, iron is released into the circulation. It is bound to
is slightly more than in non-pregnant women, due to transferrin and carried to the liver, spleen, muscles and
increased erythropoietin synthesis. bone marrow. Here it is freed from transferrin and utilized
in the formation of hemoglobin, myoglobulin or stored as
Advantages of Increased Blood Volume ferritin and hemosiderin.
Protects the woman from the possibility of hemorrhage The total iron requirement in pregnancy is around
during pregnancy or at delivery. 1000 g (500 mg in RBC mass, 300 mg to the fetus, 200 mg to
compensate for daily iron loss of 1 mg/day). Iron supplements in vascular endothelium. This may cause vasodilatation.
are needed to replenish the iron reserves of the patient. The Calcitonin gene-related peptide (CGRP) is a vasoactive
fetus being a complete parasite, there is an adequate iron peptide produced by neural tissue and may affect the
transfer, mainly in the last trimester. Hence, even if the patient vasculature of the pregnant woman.
is anemic the fetus will absorb maternal iron, precipitating Peripheral resistance is reduced to about 20%. It is
maternal anemia in a pregnant women with low or no stores. reduced more in the uterus and the placenta. Hence, there
This can be prevented by supplementing iron. is increased blood flow. The increase depends on the stage
More recent studies show that: of pregnancy. The average is 500–800 mL/minute. Renal
Platelet count decreases in pregnancy, this may be due blood flow increases by 400 mL/min and that to the breast
to increased destruction. 200 mL/minute over and above non-pregnant levels.
Increase in leukocyte count due to elevated estrogen Blood circulation to skin (especially of hands and feet) also
and cortisol levels. increases. This helps in dissipation of heat produced by
Erythrocyte sedimentation rate (ESR) also increases increased maternal metabolism and heat produced by the
and so does the fibrinogen concentration. fetus. Vigorous exercises in uninitiated pregnant women is
discouraged as it may reduce blood flow to the uterus (as
The Heart and Blood Vessel Changes more blood is diverted to exercising muscles) hence to fetus.
There is peripheral vasodilatation. It may be due to nitric There is a 40% increase in plasma volume. The cardiac
oxide (from endothelium). The heart rate increases output also increases by 70–80 mL due to increased blood
progressively till the third trimester when it is 10–15 beats volume and hypertrophy of heart muscles. This increased
per minute more than the non-gravid state. The stroke cardiac output reaches its maximum at 24–30 weeks and
volume also increases gradually due to increased plasma remains at this level till term. Changes in body position
volume (around 10%). Cardiac output increases from less influence the cardiac output and this sensitivity increases
than 5 L/min before pregnancy to around 7 L/min at 20 with gestation. As the weight of uterus increases, on lying
weeks of gestation (30–50%). supine position it produce pressure on IVC, decreasing
There is a reduction in arterial blood pressure (BP) venous return to the heart and hence cardiac output is
due to decrease in peripheral vascular resistance and decreased. In the beginning of pregnancy, only increased
vasodilation (about 10%). If the patient was hypertensive stroke volume causes an increase in cardiac output
before pregnancy, there may be a decrease upto 15–20 (25–30%, maximum at 12–24 weeks of pregnancy).
mmHg in BP during pregnancy. This is seen in the first Gradually the heart rate also increases and it can be 15
trimester and reaches a plateau in the second trimesters. beats/minute more than the non-pregnant rate. Stroke
It usually reaches the normal pre-pregnancy level at volume and increase in heart rate can be influenced by
term but sometimes in puerperium, there may be a slight exercise, heat, emotional stress, etc.
increase of BP. Effects on cardiovascular system in labor: The patient is
The decrease in diastolic pressure is more marked advised to lie on her side at the beginning of labor. Otherwise
than systolic. Pulse pressure is increased in early there can be hypotension in the supine position due to pressure
pregnancy. Thus measurement at the fifth Korotkoff sound of the gravid uterus on the IVC causing reduced return of
(disappearance of sounds) is more accurate. blood to the heart. The pulse pressure is higher by 26%. This
There may be a systolic murmur of grade I or II. An may be harmful to a patient with heart disease. In the lateral
increased intensity and widening split of first sound and position, the cardiac output increases by 7.6%, heart rate
a third heart sound are normal in pregnancy. Increase decreases by 0.7%, stroke volume increases by 7.7% and pulse
in blood flow through the mammary vessels (supplying pressure decreases by 6% during each uterine contraction.
breasts) in late pregnancy may be heard as a continuous Uterine contractions increase blood volume by about
murmur over the chest. The apex beat moves laterally. On 300–500 mL.
X-ray of the chest the cardiac outline appears larger (12%).
There is no significant change in the electrocardiogram Metabolic Changes
(ECG) except sometimes a sinus tachycardia and left axis Plasma protein: Total plasma protein decreases from
deviation. 7 to 6 g/dL. The albumin level decrease from 3.5–2.5 g/
There is a link between the marked increase in placental dL. The globulin increases marginally from 2.75 to
hormones (estrogen and progesterone) and alterations 3 g/dL. This is because there is an increase in carrier
globulins (sex hormone-binding, thyroid binding Urinary System

globulin, transcortin and transferrin). The non-gravid Renal blood flow increases from the beginning of
albumin/globulin ratio of 1.3 is changed in pregnancy
pregnancy. By 16 weeks, it is 75% more than in the non-
to 0.8.
gravid state. This is maintained till 34 weeks of pregnancy.
The plasma oncotic pressure falls (due to fall in total
GFR increases from early pregnancy. It is 50% more than
plasma protein concentration) from 38 to 31cm of water
the non-pregnant level at the end of 12 weeks and this is
causing edema of pregnancy.
maintained till labor. It returns to normal within 3 months
Plasma lipids: Plasma lipids increase from 600 to
after delivery. This reduces creatinine (from 0.8 mg/dL to
1000 mg/dL. Triglycerides are doubled from 80 to
0.5 mg/dL) and blood urea nitrogen (BUN) 2.0–3.0 mg/dL.
160 mg/dL. Lipoprotein [mainly low-density lipoprotein
Uric acid levels rise after 24 weeks and levels of more than
(LDL)] increases from 250 to 350 mg/mL and there is
5.9 mg/dL predict a poor prognosis in cases of gestational
a fall of free fatty acids. Total plasma cholesterol falls
hypertension and reach prepregnancy levels (due to renal
in the first trimester, then rises in second and third
tubular reabsorption of urate) by term. Nocturia is caused
trimesters. This is because there is deposition of fat in
by more blood flow to kidney in lateral position.
the first half of pregnancy and increased production of
Potassium levels in maternal blood in pregnancy are
cholesterol and LDL by the liver (for steroid hormone
slightly less than non-gravid levels (due to hemodilution).
synthesis) in late gestation.
Kidneys conserve potassium because of progesterone.
Blood gases and acid base balance: Plasma bicar
Glucose excretion is increased. In non-pregnant women,
bonate falls from 24 to 20 mEq/L. PCO2 falls from 38 to
less than 100 mg/day of glucose is excreted. In pregnancy,
32 mmHg (due to hyperventilation normally occurring
it is 1 to 10 g/day, probably due to an increase in GFR
in pregnancy). Thus, there is a partially compensated
causing a greater load of glucose to reach the proximal
respiratory alkalosis with a rise in blood pH from 7.4 to
tubule. The exact mechanism by which glucose absorption
7.44. Arterial PO2 increases from 95 to 105 mmHg due to
is increased is not known.
hyperventilation. This is helpful in transfer of CO2 from
The amount of protein excreted in the urine does not
the fetus to the mother and O2 from mother to the fetus.
increase in pregnancy. However, there is increased excretion
Due to hemodilution, total plasma electrolytes fall by
of amino acid and calcium in the urine. In respiratory
10 mEq/L.
alkalosis there is increase excretion of bicarbonates. Acid
excretion is not affected by pregnancy.
Coagulation Changes
Pregnancy is a hypercoagulable state. There is venous Gastrointestinal System
stasis. Many procoagulant factors are increased (factor Nutritional needs, including vitamins and minerals, increase
I, VII, VIII, IX, X). The levels of factor II, V and XII are
during pregnancy.
unchanged and those XI and XIII decrease.
There may be a sensation of nausea or ‘morning
Plasma fibrinogen (factor I) starts increasing in first
sickness’ in early pregnancy; otherwise there is an increase
trimester and by the third trimester it is 50% higher than in
in appetite throughout pregnancy, hence intake is more.
the non-gravid state.
In rare cases, pregnant women develop some craving for
Prothrombin time (PT), activated partial thrombo-
plastin time (APTT), and thrombin time, all fall slightly. bizarre substances (pica), e.g. clay, soap, coal, etc. There
Bleeding time and clotting times are unchanged. may be heartburn due to esophageal dysmotility and
All these return to normal within 2 weeks of delivery. slower emptying of the stomach due to progesterone.
The advantage of a hypercoagulable state is at the time
There is also relaxation of the cardiac sphincter, so gastric
of placental separation in delivery. If coagulation does reflux is more frequent during late pregnancy because of
not occur, the woman can die of hemorrhage because elevation of the stomach by the enlarged uterus. Therefore,
500 mL blood flows through placental bed per minute. before giving anesthesia, it is important to assure that the
After immediate constriction of blood vessels by uterine stomach is empty to prevent regurgitation and aspiration
contractions, fibrin begin to deposit over the placental (Mendelson’s syndrome). Stomach motility and tone
site. is decreased in pregnancy due to relaxing effects of
Disadvantage: There is a potential risk of thromboem- progesterone. Motilin—a gut hormone is decreased in
bolic accident which may be life-threatening. pregnancy. Thus, there is longer gastric emptying time.
There is less incidence of peptic ulcer disease during are less active during respiration, respiration is mostly
pregnancy. This may be due to decreased maternal diaphragmatic in late pregnancy. Increasing progesterone
histamine level, increased mucin production, reduced levels in pregnancy, from 25 ng/mL at 6 weeks to 150
acid secretion and increased immunological tolerance to ng/mL at term, stimulate the respiratory center directly
Helicobacter pylori. increasing ventilation. Estrogen is suggested to increase
Intestinal motility and tone are also decreased, due to the irritability of the respiratory center thus adding to
progesterone, leading to constipation. More water can the effect of progesterone. Dead space volume is greater
be absorbed due to decrease colonic motility. The gravid due to relaxation of the conductive airway muscles. Tidal
uterus displaces the intestine and change the position of volume gradually increases (35–50%) with the duration of
appendix (see Fig. 54.1). There are more hemorrhoidal pregnancy. Lung volume is unchanged till the later half of
veins visible. pregnancy when there is decrease in expiratory reserve
Gallbladder: Because of progesterone, gallbladder muscles volume (ERV) and residual volume (RV) and 18% mean
tone is reduced and hence emptying is much slower and decrease in functional residual capacity (FRC). The vital
incomplete. Cholesterol saturation in bile is increased and capacity (VC) is unchanged (4–5%). By elevation of the
chenodeoxycholic acid level is decreased causing cholesterol diaphragm (Tables 9.3 and 9.4), increased tidal volume
calculi formation. Liver, plasma cholinesterase activity is and small residual volume, leads to increased alveolar
decreased during normal pregnancy. High levels of estrogen ventilation (65%). Inspiratory capacity is increased by
may cause spider angiomas and palmar erythema. 5–10% and it is maximum at 22 to 24 weeks of pregnancy.
The level of serum alkaline phosphatase rises 2–4 folds During rest, CO2 ventilation and oxygen consumption
in the third trimester due to the placental heat stable and carbon dioxide production are increased in pregnancy
isoenzyme. Other liver enzymes are not altered. compared to the non-pregnant state. Progesterone has a
role in the disproportionate increase in minute ventilation
Bone Changes over oxygen consumption in pregnancy. Due to the
Throughout pregnancy, maternal total calcium falls due effect of progesterone on the respiratory centre there is
to a decrease in the albumin bound calcium. However, hyperventilation which is compatible with the increased
ionized calcium levels are unchanged (which is 50% of metabolic needs of the mother causing decrease in
the total calcium). Increased calcium absorption through maternal and fetal alveolar CO2. There is a slight increase
the intestine is the main source of calcium to the fetus. in respiratory rate (15–20% more). This leads to a fall in
Maternal serum phosphate levels are almost doubled in the PCO2. This respiratory alkalosis and hyperventilation
late pregnancy causing calcium absorption. Maternal increases renal bicarbonate excretion keeping the pH in
kidney produces increased levels of 1,25-dihydroxy the normal range. Mean PO2 increases to 106–108 mmHg
vitamin D which helps calcium absorption and there in the first trimester and 101–104 mmHg in the third
is 20% increase in calcitonin causing protection of the trimester. The gradient between alveolar and arterial PO2 is
maternal skeleton from reaborption. elevated mainly near term and, hence, partially offset the
increase in arterial PO2 by hyperventilation. In the supine
Changes in Respiratory System in Pregnancy position also there is decrease in arterial PO2 compared
Capillary dilatation in the respiratory tract takes place in with sitting position in late pregnancy. However, if there
early pregnancy. This causes engorgement of the naso- is no pulmonary disease these changes have no clinical
pharynx, larynx, trachea and bronchi, causing difficulty in importance. At a high attitude, maternal PO2 is 70–75
breathing. mmHg. This decreases the umbilical venous PO2 and
The increasing size of the uterus also changes the reduce fetal growth. Maternal PCO2 increase reduces
resting position of the diaphragm and the configuration uterine vascular resistance and increases uterine blood
of the thorax. The diaphragm at rest is 4 cm above flow and elevation of PO2 in the fetal umbilical cord.
non-pregnant resting level, the transverse diameter of During labor: The patient may become dyspneic and
chest increases by 2 cm and thoracic circumference by hence, may hyperventilate and respiratory alkalosis
6 cm. Subcostal angle increases gradually from 68.5° in may develop, leading to carpopedal spasm and acid
early pregnancy to 103.5° during late pregnancy. The base imbalance. With each uterine contractions there is
movements of the elevated diaphragm are not decreased. redistribution of blood from uterus and central venous
As the tone of abdominal muscles is decreased and they pool. This helps in more efficient gas exchange. These
TABLE 9.3: Changes in lung parameters during pregnancy changes during labor has its effect on the anesthesia, if
Tidal volume (TV) Volume of air inspired Increase (200 mL)
administered. The induction of anesthesia is delayed.
or expired in each res
piration (500 mL) Changes in Endocrine Glands
Inspiratory reserve Maximum Thyroid: There is a small increase in size of the thyroid
volume amount of volume gland during pregnancy. The gland remains euthyroid.
air, which can be
There is an increase in total thyroxin (T4), from
inspired beyond
increase (300 mL) 5–12 mg/dL to 9–16 mg/dL and also triiodothyronine
Normal tidal (T3). Thyroid-stimulating hormone (TSH) slightly
volume (3000 mL) decreases in the first trimester and rises to normal
Expiratory reserve Maximum amount Decrease (200 mL) after that. Iodine in pharmacologic doses given to the
volume of volume air which mother crosses the placenta and may induce goiter
can be expired from
in the fetus. Similarly, radioactive iodine crosses the
the resting end-
expiratory position
placenta and if given may have severe adverse effect on
(1100 mL) the fetal thyroid.
Residual volume Volume of air Decrease (200 mL) Pituitary gland: The pituitary gland enlarges due to
in lungs after proliferation of prolactin-producing cells in the anterior
maximal expiration pituitary. By term serum prolactin is 10 times the non-
(excluding bronchi pregnant levels. It is instrumental in preparing the breasts
and trachea)
(1200 mL) for lactation. Maternal follicle-stimulating hormone
(FSH) and luteinizing hormone (LH) are decreased.
Alveolar Tidal volume minus
ventilation dead space Placental growth hormone variant suppresses maternal
Total lung capacity Amount of air in
growth hormone level.
lung after maximal Adrenal gland: Expansion of zona fasciculata (gluco
inspiration corticoid producing area) occurs during preg nancy.
Vital capacity Inspiratory reserve Increase in some but Corticosteroid-binding globulin (CBG) doubles by the
volume + tidal not all end of 6th month. Aldosterone, deoxycorticosterone
volume + expiratory (DOC) cortisol and free cortisol increase during
reserve volume
(4600 mL) pregnancy. Corticotropin-releasing hormone (CRH) is
greatly increased during the third trimester of pregnancy.
Functional residual Amount of air Decrease (500 mL)
capacity remaining in the The maternal level of CRH also increases due to placental
resting end- and fetal membrane production of the hormone.
expiratory position Testosterone and androstenedione levels in maternal
(2300 mL)
plasma are slightly higher. The former due to an increase
Minute volume Amount of air Increase in sex hormone-binding protein and the latter due to
inspired in a minute (3 liters/minute)
increase in its synthesis, but dehydroepiandrostenedione
(7.5 liters/minute)
levels are decreased in pregnancy.
Pancreas: In early pregnancy there is increased insulin
release due to estrogen stimulation of the β-cells of
TABLE 9.4: Lung function tests pancreas. These facilitate storage of fats needed as
Test Description energy in later gestation and puerperium. Fasting blood
Maximum breathing Maximum amount of air which can be
sugar is less in pregnancy because of constant drain of
capacity inspired or expired by forced voluntary maternal glucose by the fetus. By the third trimester
breathing over 15% the fetus take 6.0 mg/kg/minute glucose from the
Forced expiratory volume Amount of air which can be forcibly mother. In later pregnancy maternal hypoglycemia and
expired in one second hypoinsulinemia, hyperlipidemia and hyperketonemia
Peak expiratory flow rate Maximum rate air-flow during forced is the maternal response to starvation. In a normal
expiration (measured with Wright peak pregnancy glucose homeostasis is maintained by the
flow meter)
exaggerated response. If her pancreas is unable to
increase insulin production, gestational diabetes is cause insulin resistant. This diabetogenic effect is
revealed during pregnancy. Pregnancy is diabetogenic. helpful to the growing fetus after a meal by the mother.
This effect is because of a variety of hormones secreted The concentration of glucose in the fetus is roughly 20
by the placenta. Human placental lactogen (HPL) has mg/dL less than the mother. The glucose transport from
strong lipolytic and anti-insulin action and, hence, is placenta is facilitated and is energy independent. Hence
responsible for insulin resistance during pregnancy. an adequate maternal level of glucose is very important
Cortisol, prolactin, estrogen and progesterone also for an adequate supply of glucose to the fetus.
1. What are the changes in blood during pregnancy?
2. Uterus has two parts _____________ and _____________.
3. Secondary areola develops especially in _____________.
4. ESR stands for _____________.
5. Uterine contractions increase blood volume by about _____________.
10
Sonia Malik, Ritu Sharma, Sudha Salhan
Immunology of
Normal Pregnancy
BASICS OF REPRODUCTIVE TABLE 10.1: Types of immune responses
IMMUNOLOGY Component Innate Adaptive immunity

Cellular Monocytes/macrophages, T lymphocytes and
The process of eliminating the foreign substances by the natural killer cells, mast cells B lymphocytes
body is called the immune response and the substance Humoral Complement, acute phase Antibodies
is called as an antigen. The antigen can be anything plasma proteins, mannose
varying from microorganisms and their metabolites to binding lactin, clotting cascade
proteins and carbohydrates. There can be antigen specific
and antigen non-specific immune reactions. The three
components of antigen specific immunity or adaptive by cells like lymphocytes, natural killer (NK) cells and
immunity include memory, specificity and recognition. phagocytes. It is stimulated by T helper type 1 lymphocytes
The initial response to an antigen that occurs in 1–2 weeks and cytotoxic T lymphocytes and is cytokine mediated.
is called primary response. The subsequent exposure to It is effective against viral infections and intracellular
the same antigen leads to the secondary immune response pathogens. Humoral immunity is antibody mediated
aided by memory. Specificity is the immunity response immunity stimulated by T helper type 2 lymphocytes and
towards a specific antigen. The immune system is capable effective against bacterial infections.
of differentiating between self and non-self and failure of Pregnancy is a unique physiological process of immune
this leads to autoimmunity. Different antibodies develop tolerance of a fetal allograft in the mother. Paternal
in response to various antigens. On electrophoresis, five antigens contribute to 50% of fetal antigens, yet mother
major types of immunoglobulins are found—IgG, IgM, IgA, does not reject fetus. In order to understand this mystery
IgD and IgE antibodies are involved in primary immune of pregnancy immune tolerance let us first study the
response. They act as cytolytic agents by activating the preparation of the endometrium for pregnancy.
complement system. IgG, IgA and IgM are involved in The menstrual cycle is divided into two phases. First
infertility. IgD action is dependent on IgM antibodies phase is known as proliferative phase that is under the
and they affect the lymphocyte activity. IgG anibodies effect of estrogens which prepares the endometrium
are involved in secondary immune response and can for progesterone action and also increase the number
cross placental barrier. IgE antibodies are involved in of progesterone receptors. Second phase is known as
immediate hypersensitivity reactions or allergic response. secretory phase that is under the effect of progesterone.
IgA antibodies are present in seromucous secretions. As If estrogen levels are deficient, as in disordered ovulation,
a result of interaction with the surface antigens, these the endometrium will not be receptive for a pregnancy.
antibodies prevent microbial adherence to cells and Progesterone is produced by the corpus luteal cells after
subsequently their entry into the tissues. ovulation. Thus, in cases with a defect of the corpus luteum
Immune responses are of two types—cell mediated (luteal phase defect), there is poor decidualization of
immunity and humoral immunity (Table 10.1). The the endometrium and failure of the pregnancy to thrive,
foreign antigens in cell mediated immunity are removed thereby leading to either sterility or an early abortion.
THEORIES FOR IMMUNE TOLERANCE IN Modification of Immune System at

PREGNANCY (FIG. 10.1) Peripheral Level
Many theories have been put forward to explain the Pregnancy has been regarded as an immunosuppressed
phenomenon of immune tolerance. We shall now discuss state with progesterone acting as an immunosuppressant.
them in detail. But it has been found that there is no generalized immune
suppression; infact there is modification in immune
Pregnant Uterus is an Immune Privileged Site response in pregnancy to adapt the foreign fetal allograft.
It was earlier believed that all organs induce immune Modifications at various levels include the following:
response except certain organs like brain and eye. In 1948, T lymphocytes are of two types—helper T lymphocytes/
it was proposed that the presence of a mechanical barrier Th cells and cytotoxic T lymphocytes/ Tc cells. Cytotoxic
in the fetomaternal circulation just like blood-brain (BBB) T lymphocytes directly attack the foreign bodies or
barrier which prevented the movement of immune cells. infected cells and destroy them. Helper T lymphocytes
This theory has been challenged as we have evidence of produce cytokines and are further divided into type 1
fetal cells in maternal circulation. and type 2 cells. Type 1 cells produce interferon–gamma
Fig. 10.1: Theories for immune tolerance in pregnancy

Abbreviations: VEGF—Vascular endothelial growth factor; MMP—Matrix metalloproteinases; XOX—Hydroperoxinase; COX—Cyclooxygendase
LIF—Leukemia-inhibitory factor; HLA—Human leukocyte antigen; IL—Interleukin; TGF—Transforming growth factor; MHC—Major
histocompatibility complex
Immunology of Normal Pregnancy 87
(IFN-γ), interleukin-2 (IL-2) and tumor necrosis factor- TABLE 10.2: Types of cytokines
alpha (TNF-α) which are responsible for cell mediated Pro-inflammatory cytokines Anti-inflammatory cytokines
immunity while type 2 cells stimulate B lymphocytes Interleukin (IL) 1 and 2 Interleukin–4, 6,10
and produce IL-4, IL-5, IL-9, IL-10, IL-13 which are Interferon gamma (IFN-γ) Transforming growth factor
responsible for promoting systemic humoral immunity Tumor necrosis factor alpha beta (TGF-b)
and suppressing local cell mediated immunity. (TNF-a) Leukemia inhibitory factor (LIF)
In pregnancy there is a shift from type 1 to type 2
cells that is from cell mediated immunity to humoral
immunity which is essential for sustaining pregnancy. selective survival advantage over those sharing similar
So, rheumatoid arthritis which is a cell mediated antigens. It was assumed that the mother produced a
autoimmune disorder undergoes into remission while blocking antibody to fetal foreign antigens in pregnancy.
systemic lupus erythematosus (SLE) which is an antibody The failure to develop these blocking antibodies in cases
mediated autoimmune disease worsens. Th 2 shift is of similar maternal and paternal antigens would result
influenced by hormonal factors (progesterone) and in reproductive failure. This concept has, however, been
release of Th 2 stimulating cytokines by macrophages. challenged. Till date, there has been no standardized assay
Peripheral NK cells have deleterious effect on preg for determining the presence of these blocking antibodies.
nancy and their number and function is suppressed
in pregnancy. They are capable of killing target cells Cytokine Shift
that are coated with antibodies. Excessive presence of Cytokines form the link between the immune system
peripheral NK cells is associated with a miscarriage. and the other systems. They act through specific cytokine
Monocytes and granulocytes phagocytos is fetal cells receptors. These cytokines may be pro-inflammatory or
in maternal circulation. Innate immunity gets activated anti-inflammatory in nature (Table 10.2).
by hormones and placenta. In pregnancy, it has been shown that the cellular
immunity is decreased while the humoral immunity is
Role of Trophoblasts in Avoiding Maternal enhanced; hence there is a shift from the pro-inflammatory
Immune Rejection cytokines to the anti-inflammatory type, thus facilitating
There are three classes of major histocompatibility implantation. Low levels of IL-4 and IL-10 were observed
complex (MHC) antigens—class Ia, class Ib, class II. in decidual T cells of women undergoing repeated
MHC class Ia antigens are expressed on all nucleated pregnancy losses. High levels of IL-10 were observed in
cells except trophoblasts. Exact function of MHC Class Ib normal pregnancy. Leukemia inhibitory factor (LIF) is
antigens is not known but thought to have inhibitory effect another anti-inflammatory cytokine, the absence of which
on NK cells preventing lysis of trophoblasts, proliferation has been shown to result in reproductive failure. Both
of T lymphocytes and production of cytokines. MHC estrogens and progesterones affect the cytokine levels. A
class II antigens are present on B lymphocytes and some host of subclinical endometrial infections may also shift
epithelial cells. MHC class I antigens are also called the balance towards higher levels of pro-inflammatory
human leucocyte antigen (HLA) and include four types, cytokines, thereby resulting in miscarriages.
i.e. HLA-A, B, C and G.
During the early embryonal period, the fetus separates Changes in Decidua
into two groups of cells. The outer trophoblastic group and During pregnancy, there is increase in leukocyte population
the inner cell mass. Expression of MHC class Ia antigen to about 40% in decidua; among them 60–70% are uterine
on cells is responsible for rejection of allografts. But in NK cells and 20–25% are macrophages. The uterine NK
fetus the outer group of trophoblasts do not express MHC cells are different from their peripheral counterpart. Their
antigens, while the inner cell mass that forms the fetus number is increased due to either migration of peripheral
expresses all MHC antigens and hence, would be rejected NK cells or their proliferation in the uterus itself. Their
as an allograft if removed from its protective cocoon of the increased presence during early pregnancy coincides
trophoblasts. with the first invasion of the trophoblasts in the maternal
vasculature. They express inhibitory receptors which
Blocking Antibodies and HLA Sharing bind to MHC class I antigens on trophoblasts and thereby
During the 1960’s it was suggested that the fetuses that inhibiting the lysis of trophoblasts. With the help of various
shared different maternal and paternal antigens have cytokines they influence the growth differentiation,
breakdown and regeneration of the trophoblasts invading concurrent hyperprolactinemia or polycystic ovaries.
the uterine decidua and maternal vasculature. Proliferation However, in a small subset of patients the endometrium
of trophoblasts is helped by granulocyte colony stimulatory may remain poorly decidualized even in the presence
factor (GCSF), granulocyte macrophage colony stimulating of normal or high circulating levels of progesterone. In
factor (GMCSF), macrophage colony stimulating factor these patients it is believed that there is a deficiency of
(MCSF) and LIF. Implantation is helped by LIF. Their presence progesterone receptors in the endometrium which may
ensures that the trophoblast invasion of the mother does not be genetic in origin, due to a defect in the progesterone
overshoot the mark. In other words the uterine NK cells will receptor gene.
kill stray trophoblastic cells that have invaded into maternal In the background of these preparatory changes in the
sites but are not required for implantation. luteal phase endometrium, and the immunoprivilege that
is selectively conferred upon the blastocyst, its entry into
Fas-Fas Ligand System and Immune Tolerance the endometrial cavity is with a lot of fanfare. The blasto-
Induction of apoptosis (programed cell death) of cyst arrives in the endometrial cavity from the cornual end
activated immune cells is helped by certain ligands— of the tube, 5–7 days postfertilization. It has so far been
FAS Ligand (FasL) and tumor necrosis factor-related nourished by the corona radiata cells and the human fal-
apoptosis-inducing ligand (TRAIL). Fas is described lopian tubal fluid. However, with rapid cell division its nu-
as a death factor and FasL is its receptor. During the tritional requirements increase and it has, therefore, got
proliferation of trophoblast in pregnancy the surrounding to expediate implantation. For this it has to undergo three
endometrial cells undergo apoptosis. FasL is expressed in vital processes:
the trophoblast throughout pregnancy and can induce fas 1. Attachment to a preferred site on the endometrium
mediated cell death of T cell clones that recognize fetal 2. Gaining vascular foothold
antigens as thus, protecting the fetus from maternal T cell 3. Burrowing deep within the endometrium.
immune rejection.
Attachment to Endometrium—Endometrial
Genome Alteration Sulfhydral Groups and Pinopodes
During the normal menstrual cycle and during decidual- The decidualized endometrium shoots up pinopodes
ization and implantation certain genes are expressed in or cytoplasmic offshoots that are visible by electron
the endometrium that will facilitate implantation. Some of microscopy. These help in the anchorage of the blastocyst
the genes that have been studied are: to the endometrium. It is also believed that the embryo
Hydroperoxidase (HOX) A-10 gene: This gene is binds to the sulfhydryl groups and masking of these
expressed in the endometrium only in the luteal phase. It groups, in experimental swiss albino mice, results in failed
is regulated by estrogen and progesterone receptors and implantation.
is necessary for mammalian implantation. HOX A-10
deficient endometrium shows a normal histopathology Gaining Vascular Foothold—Vascular Endothelial
but lacks beta 3 integrins and will not support Growth Factor (VEGF)
implantation. In the knock out mice model as well, It has been observed that the VEGF levels rise in the
deficiency of expression of HOX A-10 results in infertility. secretory phase of menstrual cycle. The blastocyst expresses
Cyclooxygenase (COX) 2 gene: This gene regulates the messenger (m) RNA that encodes for VEGF protein. VEGF
enzyme 2 which is the rate limiting step in prostaglan- induces angiogenesis at the site of implantation to bring
din biosynthesis. COX 2 derived prostacyclin is essen- nutrition to the implanting blastocyst. It is also expressed
tial for decidualization and implantation. in the corpus luteum to help the luteal cells to multiply and
LIF gene: Helps in implantation. LIF deficient women produce progesterone that is necessary for implantation. If
are either infertile or have recurrent abortions. This the blastocyst is unable to express VEGF and mRNA, it will
cytokine has now been synthesized in the laboratory lead to failed implantation.
and is undergoing phase 2 clinical trials.
Progesterone receptor gene: It has been shown that
Burrowing within the Endometrium Matrix
implantation may be deficient in patients who have a Metalloproteinases
poorly decidualized endometrium in the luteal phase. The proteolysis of the endometrium is brought about
Often this condition may result from a luteal phase defect by protein digesting enzymes called matrix metallo-
or low levels of circulating progesterone in patients with proteinases (MMP). These are:
Immunology of Normal Pregnancy 89
Interstitial collagenase In conclusion, it must be appreciated that implantation

Gelatinase is the result of a two way dialogue between the embryo
Stromeolysins and the mother which is mediated by various chemicals,
Urokinase type plasminogen activator cytokines and enzymes (Fig. 10.1). These are in turn
Plasminogen activator inhibitors. under the control of hormones and genetic factors. It is
These are produced actively by the cells of the cytotro imperative that the right amount of endometrial digestion
phoblast and even by the cumulus oophorus of a seven- is accompanied by the right amount of cytotrophoblastic
cell embryo. However, the syncytiotrophoblast is not burrowing and vascularization. All this requires a host
invasive and does not secrete these enzymes. of physiological changes in the mother which need to be
The endometrium also secretes proteinases, which fine tuned. These changes, if not cleverly regulated could
are capable of digesting the trophoblast cells. There is a be a source of potential harm to either the mother or
temporal and topographical regulation of these enzymes the fetus. Yet in the majority of the cases these changes
from both the maternal and fetal cells to produce just the proceed under perfect balance without even being noticed
required amount of matrix degradation. The endometrial clinically.
enzymes control the trophoblast, and the trophoblastic The right balance of the hormonal mileu as well as the
enzymes control the digestion of the endometrium. right balance of cytokines, NK cells, sulfhydryl groups
Hence, we can appreciate that the implantation process and MMP in the endometrium is required for successful
is very finely tuned so as to facilitate the burrowing of implantation to occur. Fetal antigens, trophoblasts and
the embryo and yet cause no harm to the mother by over maternal immune system—all work in harmony with each
degradation of her tissues or vasculature. other for the successful outcome of the pregnancy.
1. Explain COX2 gene.
2. What is the full form of TRAIL?
3. True/False:
i. LIF gene is expressed in the endometrium only in the luteal phase.
ii. The menstrual cycle is divided into two phases.
iii. The subsequent exposure to the same antigen leads to the primary response aided by memory.
11
Sudha Salhan, Anshula Gupta, Indira Ganeshan
Diagnosis of Pregnancy
INTRODUCTION •• This symptom is present in first 3 months of pregnancy.

•• The severity of this symptom varies from mild to very
Pregnancy is the condition of carrying a developing fetus severe vomiting (hyperemesis).
in the uterus. It is a physiological state, but the diagnosis •• It is due to high levels of beta-human chorionic
of pregnancy is very important. Ordinarily, the woman gonadotropin (b-hCG) in serum.
is aware of the likelihood, or at least the possibility of Frequency of micturition: This is disturbing in the first
pregnancy when she consults an obstetrician. Mistakes in 8–12 weeks of conception.
the confirmation of conception occur more frequently in •• The big antevetred uterus cause pressure on urinary
first few weeks when the uterus is still in pelvis. bladder
Anatomical and physiological changes occurring during •• Congestion of the lining of urinary bladder
pregnancy are responsible for those symptoms and signs •• The cervix may get backwardly displaced causing
points towards pregnancy. These symptoms and signs are stretching of bladder base. When uterus straightens
classified into three groups: up after 12 weeks and becomes an abdominal organ
1. Subjective evidence this symptom no longer troubles. However, they may
2. Probable signs reappear in last 2 weeks when the presenting part
3. Positive signs of pregnancy. descent into the pelvis pressing urinary bladder.
Feeling tired: This is a common symptom in early
pregnancy.
SUBJECTIVE EVIDENCE OF PREGNANCY Breast discomfort: During first 6–8 weeks of pregnancy
It is based largely on some symptoms and a few objective (especially in primigravida) there is a sensation of full-
signs which include: ness or pinpricks due to breast development for starting
lactation after birth. Soreness of breasts is also seen.
Symptoms Perception of fetal movement (quickening): It is the
feeling of intrauterine fetal movement by the mother.
Amenorrhea: The abrupt cessation of menstruation
These are slight fluttering movements in the abdomen
in a healthy reproductive age woman, who previously
which gradually increase in intensity, becoming more
has experienced spontaneous, cyclical and predictable
pronounced in the third trimester. It is felt at 18–20 weeks
menses, is highly suggestive of conception unless
by primigravida and 2 weeks earlier in multigravida. Time
disproved. But sometimes scanty monthly staining
of quickening is useful in calculating period of gestation.
can be seen till decidual space is obliterated (upto 12 Abnormal appetite: Some pregnant women develop
weeks). It is called Hartman’s or placental sign, this strange carvings to unusual articles like chalk, wall
should not be confused with miscarriage. Sometimes plaster, etc. called pica.
pregnancy occurs during lactational amenorrhea or Constipation is a common symptom.
during infrequent periods in pubertal girls. Some complain of nasal stiffness and even nasal bleed.
Morning sickness: A feeling of nausea and vomiting Some are troubled by burping and gas formation.
affect some pregnant women during the first few Insomnia and changes in libido are also complained by
months of pregnancy, particularly in the morning. a few.
Diagnosis of Pregnancy 91
Fig. 11.1: Breast changes in pregnancy Fig. 11.2: Ferning
Signs
Breast changes (Fig. 11.1): They are of significance
only in primigravida. These changes are seen after 6–8
weeks of pregnancy. The changes being—increase in
size of the breast (stria) with vascular engorgement,
pigmentation (primary and secondary areola—at 20th
week), development of Montgomery tubercles around
the nipple, and some discharge can be expressed from
the nipple (witch’s milk).
Skin changes (see Fig. 9.8): Chloasma in the form of
hyperpigmentation on cheeks and forehead is visible by
20th weeks of pregnancy. Besides there is a linear hyper
pigmentatin from symphysis pubis to ensiform cartilage
(linea nigra Fig. 9.6 20th week). In second trimester Fig. 11.3: Non-ferning
onwards striae gravidarum (due to stretching of skin, due
to over distention of uterus) are visible on lower abdomen.
Changes in vaginal mucosa are: PROBABLE SIGNS OF PREGNANCY
•• Jacquemier‘s or Chadwick’s sign: Due to local They include are as follows:
vascular congestion the vestibule and anterior
vaginal wall acquire a pink dusky color. It is visible Uterine Changes in Shape, Size and Softness
as early as 8th week of pregnancy and becomes more Uterus is about the size of an egg of hen at 6 weeks of preg-
pronounced as the pregnancy advances. nancy, about a full term fetal head at 12 weeks. The shape
•• The walls of vagina soften. is pyriform to start with, then it changes to globular form
•• A non-irritant, mucoid discharge which is copious at 12 weeks. The uterus may increase asymmetrically if the
appear from 6th weeks of pregnancy. placenta is laterally implanted (Piskacek’s sign) when half
•• Osiander’s sign: Increased pulsations are felt through of the uterus is firmer than other half. Symmetry is restored
the lateral fornices at the 8th week. Similar pulsations, as pregnancy advances. In pregnancy the uterus becomes
however, are also felt in acute pelvic inflammation. soft and elastic. Hegar sign can be elicited at 6–10 weeks of
•• Changes in the cervical mucus. Make a smear of gestation.
the aspirated cervical mucus and examine under a
microscope. The ferning of early menstrual cycle Hegar’s Sign
disappears and gives a beaded appearance due to This sign is based on the fact that different parts of uterus
the effect of progesterone (reduce sodium chloride has different consistencies, viz. fundus is occupied by
concentration) in pregnancy (Figs 11.2 and 11.3). the ovum, isthmic part is empty and very soft and cervix
These are not, however, positive signs of pregnancy,

because similar contractions are sometimes observed in
uterine of women with hematometra and occasionally in the
uterus in which there are pedunclated submucous fibroids.
Ballottement
Near mid-pregnancy, amniotic fluid is more then the volume
of the fetus. When we give a sudden flick by the vaginal fingers
the fetus drops in the amniotic fluid and comes back. The tap
produced (ballottement) is felt by the examining finger. It is
difficult to elicit in cases with scanty liquor amnii.
External ballottement: It is elicited by around 20th
weeks of gestation.
Internal ballottement: It can be elicited between
16–28th week.
Outlining the Fetus

Fig. 11.4: Hegar’s sign
In the second half of pregnancy, the outlines of the fetal body
is relatively firmer. Because of this variable consistency of may be palpated through the maternal abdominal wall. How-
different regions of the uterus during bimanual examination ever, a positive diagnosis of pregnancy cannot be made from
the fingers on abdomen and vagina seems to meet below the this sign alone because occasionally, a subserous myoma
uterine body compressible soft isthmic region (Fig. 11.4). may be of such a size and shape as to simulate the fetal head.
Palmer’s Sign Detection of Chorionic Gonadotropins in

Urine or Serum
At the time of bimanual examination one feels regular
rthymic contraction at 4–8 weeks of pregnancy. Contrac- Pregnancy tests depends on detection of the maternal
tion phase lasts for about 30 seconds, increasing as dura serum or urine levels of hCG (produced by trophoblastic
tion of pregnancy increases and the relaxation phase cells) antigen done by monoclonal or polyclonal antibodies
increases. After 10th week, the relaxation phase is so much available as kits commercially. The immunological tests
increased that this test is difficult to perform. used are as follows:
Immunoassay without radioisotopes (Fig. 11.5)
Abdominal Enlargement Agglutination inhibition tests: This 2 line test measures
Till 12 weeks of gestation, uterus is a pelvic organ. By the upto 50 micro units of hCG. Newer do it yourself imm
12th week of pregnancy, the uterus is just palpable above unoassay are coming up, e.g. clear blue advanced digital
symphysis on abdominal examination. After 12 weeks pregnancy test weeks of gestation estimated.
of gestation, fundal height increases with progressive Direct agglutination tests (sensitivity—0.2 IU/mL;
enlargement of the uterus, and can be used to ascertain positive on 28th day of cycle).
approximate duration of pregnancy. ELISA (enzyme-linked immunosorbent assay) (sensitivi-
ty—0.05 IU/mL; positive on the first day of missed period).

Changes in the Cervix Immunofluorometric assay and first response early
The cervix becomes soft by the 6th week (Goodell’s sign). result pregnancy tests give positive results 2 days before
The consistency of a pregnant cervix at the external os the due date.
is softer (the feeling of lips) than non-pregnant cervix
(feeling of tip of nose). As vascularity is increased during
pregnancy, there is bluish coloration of cervix.
Braxton Hicks Contractions

These are irregular, infrequent, spasmodic and painless
uterine contractions without any effect on dilatation of the
cervix. Intrauterine pressure remains below 8 mmHg. The Fig. 11.5: Immunoassay card test (showing a positive test—2
patient is not conscious of the contractions. lines, one a control line and the second the test line)
Diagnosis of Pregnancy 93
Immunoassay with radioisotopes CHRONOLOGICAL APPEARANCE OF

Radioimmunoassay (β-subunit) (sensitivity—0.002 IU/
mL; positive on 25th day of the cycle)

SPECIFIC SIGNS AND SYMPTOMS OF
Immunoradiometric assay PREGNANCY
Radioreceptor assay (sensitivity—0.001 IU/mL; +ve on
First Trimester
22nd day of cycle).
Symptoms: Amenorrhea, morning sickness, loss of
When the diagnosis of pregnancy is not so urgent,
appetite, tiredness, increased frequency of micturition,
using agglutination inhibition principle, the pregnancy
test should be performed preferably 14 days following the fatigue, breast discomfort.
missed period. The test is not reliable after 12 weeks. Test Signs: Breast enlargement, engorged, blood vessels
accuracy ranges from 98.6–99%. are visible under the skin, and in primigravida there is
Radioimmunoassay: It is a more sensitive method and increased pigmentation of areola and nipple (secondary
can be employed to detect the presence of hCG in the areola). Positive Jacquemier’s sign, cervical softening,
serum as early as 8–9 days after ovulation, probably on bluish discoloration of cervix, Osiander‘s sign, positive
the day of blastocyst implantation. The assay can prove Hegar‘s and Palmer’s sign. Uterine enlargement varies
a sensitivity of even an insignificant amount of 0.002 IU/ from hen’s egg to medium-sized orange. Immunological
mL of β-subunit hCG in the serum. It is specific to hCG tests will be positive. Sonographic appearance of
and does not cross react with luteinizing hormone (LH). gestational ring helps in early diagnosis.
Radioreceptor assay gives the highest sensitivity of 0.001
IU/mL hCG in the serum, but is not usually available. Early Second Trimester
Symptoms: Around 16 weeks, all these symptoms except
POSITIVE SIGNS OF PREGNANCY amenorrhea, and fatigue and breast discomfort disappear.
Palpation of the fetal parts and perception of active fetal Signs: Increased pigmentation of primary areola and
movements by the obstetrician by 20 weeks of gestation. appearance of Montgomery tubercles and colostrum.
These findings are of value not only to diagnose pregnancy Uterus midway between pubic symphysis and umbili-
and its duration but also to identify the presentation and cus, Braxton Hicks contractions, uterine souffle, inter-
position of the fetus in later weeks of gestations. It not only nal ballottement. Appearance of sonographic evidence.
gives a positive evidence of pregnancy but that of a live
fetus as well. The intensity varies from a faint flutter in the Late Second Trimester
early months to stronger movements in later pregnancy.
Symptoms: Amenorrhea, quickening.
The auscultation of fetal heart sound (FHS) is a definite
Signs: Appearance of secondary areola (20th week), linea
clinical sign of live pregnancy (18–20 weeks). Its rates
nigra (20th week), Braxton Hicks contractions, external
varies from 120–160 bpm and is heard as a sound
resembling the tick of a watch from under a pillow. ballottement (20th week), feeling of fetal parts (20th
Fetal cardiac action can be detected almost always by week), fetal movements (20th week), FHS (20 weeks),
10 weeks by an appropriate Doppler equipment. internal ballottement (16–28 weeks), uterus at the level
Ultrasonic recognition of pregnancy: The earliest sign of of umbilicus (24th week), sonographic evidence.
conception is a characteristic small white gestational ring
seen as early as the 5th week of gestation. Subsequently, Third Trimester
the fetal pole and yolk sac are seen at the 6th week; cardiac Symptoms: Amenorrhea, perception of fetal movement and
pulsations are visible at the seventh week; embryonic reappearance of increased frequency of micturition, palpita-
movements at the eighth week. With the use of vaginal tion and breathlessness (due to the enlarged uterus).
probe, the above events can be visualized one week earlier. The fetus descend into the well-developed lower
Estimation of gestational age by crown rump length (CRL) segment of the uterus. The mother feels the baby has gone
is most precise (variation ± 5 days) in the first trimester. down. This sensation is called lightening.
1. How to diagnose pregnancy?
2. What are the signs and symptoms of early second trimester?
3. What do you understand the term abnormal appetite?
Antenatal Care
12 (Antenatal Exercises and

Nutrition during Pregnancy)
Sudha Salhan, Harsha Gaikwad, Padmabati Rath, Simmi Chopra
INTRODUCTION Instructions for child rearing.

Contraceptive counseling.
All cultures and countries promote care of the pregnant Screening for cancer of the genital tract and breast.
women. But it was first emphasized scientifically by
Some pregnancies, because of certain factors in the
Ballantyne in UK in 1901. It is preventive obstetrics. By
pregnant woman’s medical history or previous pregnancy,
antenatal care (ANC), maternal morbidity and mortality,
some demographic issues or developments during the
and fetal and neonatal dangers can be greatly reduced,
pregnancy lead to a poor outcome. Such patients are
thus ensuring healthy mother with healthy child. In
called high-risk patients. They must be detected early and
India, ANC is utilized by less than 50% of pregnant
women. The countries which have substantially reduced given special care.
maternal mortality have 100% ANC coverage. The main Women receiving inadequate or no ANC have many
reason for non-utilization of ANC services are absence complications and have a poorer outcome in pregnancy,
of felt need. Other causes include distance from medical e.g. severe anemia, preterm and intrauterine growth
facility, absence of transport, responsibilities at home restriction (IUGR) babies with perinatal deaths, pre-
and monetary factors, etc. Our country also lacks trained eclampsia and eclampsia, etc. The cost of treating them
doctors and auxilliary nurse midwife (ANM) for ANC. is much higher than ANC which is beneficial and cost-
The purpose of antenatal care is to ensure, as much as effective.
possible, an uncomplicated maternal and fetal outcome.
The obstetrician’s role in providing routine ANC is to INVESTIGATIONS DONE
reduce maternal and perinatal mortality while preserving
maternal satisfaction with pregnancy. About 8 million
DURING PREGNANCY
neonates are born with serious birth defects all over the
world per year. Congenital anomalies can contribute to
Routine Investigations on First Visit
upto 15% of perinatal deaths. Hemoglobin (Hb) estimation including thalassemia
screening
OBJECTIVES OF ANTENATAL CARE Urine examination for albumin and sugar and routine
� The diagnosis of pregnancy is confirmed and expected microscopy. If required culture sensitivity
date of delivery is calculated. Blood group ABO and Rhesus (Rh)
Health of the pregnant woman is cared for. Blood sugar estimation
Monitor fetal wellbeing including screening for con- Veneral disease research laboratory (VDRL) testing of
genital abnormalities and genetic diseases. both partners
If possible prevent and also detect high-risk pregnancies. Test for Australia antigen [hepatitis B surface antigen
Screen for infections. (HBsAg)] and hepatitis C virus (HCV)
Immunization against tetanus and other diseases. Testing for human immunodeficiency virus (HIV)
Giving advice about nutrition, drugs, investigation, exer Papanicolaou smear
cises, resolve any doubt and explain danger symptoms. Thyroid-stimulating hormone (TSH).
Antenatal Care (Antenatal Exercises and Nutrition during Pregnancy) 95
Screening for Rh-Antibodies TABLE 12.1: Recommended treatment for pregnant women with
The patient’s blood group with ABO and Rh-factor is done syphilis
for all patients. If the patient is found to be Rh-negative Category Treatment
then her husband’s blood group is ascertained. Indirect Early syphilis Benzathine penicillin G is given 2.4 million
Coomb’s test (to detect antibody) is done at the 12th week units intramuscularly (1.2 million units in
each buttocks) after testing sensitivity. Some
in Rh-negative patient with Rh-positive husband. If the recommend a second dose one week later
test is negative, it is repeated at 28th and 36th week in
Syphilis of more than Benzathine penicillin is given G 2.4 millions
primigravidae. In multigravidae, it is repeated at monthly 1 year duration intramuscularly weekly for 3 doses
intervals from the 24th week onwards.
Follow-up of treatment is done according to titers the antibody on
If the antibody screen remains negative the mother VDRL test.
should receive Rh (D) immune globulin 300 µg at 28 weeks
to prevent isoimmunization in the third trimester.
prevent the progress of syphilis and fetal or neonatal
Screening for Gestational Diabetes infection (Table 12.1).
Many screening tests are used. The 1-hour 50 gm oral
glucose test [glucose challenge test—(GCT)] screen is
Hepatitis B Surface Antigen (HBsAg) Testing
done generally between 26 and 28 weeks. In patients with Mothers with HBsAg are very likely to transmit the disease
known risk factors this test can be done earlier. Recently to their infants. Only half the mothers infected are icteric
it has shown that fasting glucose level to be better than and symptomatic. Hence, there is the need to screen all
GCT. At a cut-off level of 86.0 mg/dL or 4.8 milimol/L has mothers. If positive, do hepatitis B ‘e’ antigen (HBeAg) and
a sensitivity of 81% and specificity of 76% compared with if this is positive there is a greater chances of mother TO
69% and 91% respectively in GCT with cut-off 140.0 mg/ child transmission (MTCT).
mL or 7.8 milimol/L. It is easier cheaper and better to take Transplacental viral transfer from the mother to the
fasting sample because in first trimester nausea prevent fetus is associated with acute hepatitis but not chronic
ingestion of 50/70 gm glucose. It is repeated if the patient seropositivity. Infection rate in the fetus increases with
is booked earlier in pregnancy. Risk factors for early the period of gestation. Perinatal transmission is by
screening include: ingestion of infected material during delivery or exposure
Diabetes mellitus in parents, sibling or the patient
subsequent to birth, e.g. breastfeeding. Infection of the
Previous macrosomic, malformed or stillborn infant
newborn is prevented by giving hepatitis B vaccination
Gestational diabetes in previous pregnancy
and hepatitis B immune globulin to the newborn as soon
Maternal obesity
as possible after delivery.
Maternal age greater than 30 years
Testing for hepatitis C is also needed.
Persistent glycosuria
Chronic use of certain drugs like β-sympathomimetics

Testing for HIV
or corticosteroids
A patient with a GCT value greater than 140 mg/dL of Pre-test counseling for HIV testing is done. The test is
serum or fasting blood sugar greater than 86 mg/dL should offered to every antenatal woman, but it is optional. If
undergo a glucose tolerance test (100 gm glucose, 3 hour tested, the results are given with post-test counseling.
specimens) for confirmation of gestational diabetes.
The significance of gestational diabetes mellitus (GDM) Screening in First Trimester for Structural and
lies in the risk of excessive fetal growth with its attendant Chromosomal Abnormality (Flowchart 12.1)
birth related and neonatal morbidities. Some obstetricians
advise repeat screening at 32 weeks in high-risk patient Ultrasound Examination in First Trimester
when the initial screening is negative. It is advised around 11–13 weeks of gestation.
Screening for Syphilis Anatomical Abnormalities

It is done in all patients and their partners by VDRL test at Normal anatomical structures to be recognized in first
the initial visit. If positive, then treatment with benzathine trimester ultrasound. Anencephaly fetus has no cranium
penicillin 2.4 mega units to both the partners is given to (‘Mickey mouse’ appearance). Bowels are present in the
Flowchart 12.1: Screening in first trimester NT is measured in the midline sagittal plane, as maximum
thickness of subcutaneous translucency between the skin
and soft tissues overlapping the spine. It is seen as a black
(sonolucent) area between the fetal spine and skin at 33–83
mm CRL. The image size of the fetus should be 75% of the size
of the screen and keep the fetal neck in neutral position. NT
measurement increases till 13 weeks two days of gestation
(maximum) declining after that hence optimum gestation
umbilical cord upto crown rump length (CRL) of 46 cm. Can
period to look for this sign is approximately 11–13 weeks with a
see 4 chamber view of heart but septa are small. Kidneys
1.3% false-positive rate.
can be seen by 12 weeks in 80% and by 13 weeks in 100%
In a three dimentional ultrasound, the length of
of the cases. However, major renal tract abnormalities can
be seen in second trimester. As hands are open, we can see fetal nasal bone in first trimester is very informative in
the fingers and exclude polydactyly. detection of trisomy 21. Other soft markers for Down
syndrome are ductus venosus blood flow impediment and
Utrasound Markers of Chromosomal tricuspid regurgitation.
Abnormalities (see Figs 62.15 to 62.18) To conclude, first trimester sonography at 10–14 weeks
can detect major fetal structural defects (68%) and chro-
In most fetuses, some internal and external defects on
mosomal defects (79%).
ultrasound appear in cases of chromosomal abnormalities.
Nearly all fetuses with trisomy 13 (100%), 77 to 100% in
trisomy 18 and 33–50% in Down syndrome (trisomy 21)
Biochemical Markers
have significant sonographic signs. In first trimester, maternal pregnancy-associated plasma
There are two categories of ultrasound markers in protein A (PAPP-A) and free human chorionic gonadotropin
trisomy 21. The first category comprises major fetal (hCG) are measured. PAPP-A gives 42% and free hCG 25%
structural abnormalities like congenital heart defects, accuracy in diagnosis fetal aneuploidy.
ventriculomegaly and duodenal atresia. Using both beta-hCG and PAPP-A, the screening per-
The other category is that of soft markers which may formance is 63% accuracy with a 5.5% false-positive rate in
be present in a normal fetus but have been found in first trimester.
association with abnormal karyotype, e.g. nuchal fold
thickness, nasal bone pylectasis, hyperechogenic bowel, Combination Screening in First Trimester
choroid plexus cyst, short femur or humerus and cardiac It has been seen that Down Syndrome is suspected in
echogenic foci (golf balls). The presence of two or more 73% with ultrasound and 61% cases by biomarkers test
markers makes the possibility of an abnormal karyotype screening. If we do the combined testing, the accuracy
more likely. rises to 87–90% with a 5% false-positive rate. Detection of
one or more ultrasound markers in a pregnant mother who
Nuchal Translucency (NT)
is serum screen-positive could increase the risk of trisomy
Nuchal membranes is seen in some normal fetuses 21 by 5 to 8 folds.
representing normal development of lymphytic system.
But persistance be indicative of aneuploidy (21 trisomy Invasive Techniques in First Trimester
Down syndrome). The fluid collection at posterior neck
visualization is called nuchal fold or membrane. Its If the screening is positive, parents are counceled and the
thickness is more than 3 mm. Before 15 weeks of gestation diagnosis is confirmed by invasive tests.
Chorionic villous sampling (CVS) is a procedure
and more than 5 mm after 16 weeks is a sign of aneuploidy.
NT is quite distinct from nuchal thickness, a term applied for prenatal diagnosis performed between 9 and 12
in second trimester fetus. NT is measured as maximum weeks. CVS avoids problems associated with tradition-
thickness of subcutaneous transparency between the skin al amniocentesis such as advanced gestational age at
and soft tissue overlapping the spine. NT can be measured 16 weeks when results are communicated to the patient
in 90% and 92% of fetuses using transvaginal scan (TVS) and medical and emotional problems associated with
and transabdominal scan (TAS) respectively and in 100% termination. It can be done per vaginally or through the
with combination of both techniques. abdomen.
Amniocentesis: Obstetricians have statrted using Biochemical Markers (see Figs 63.4A and B)
early amniocentesis nowadays.
Quad screening: In this test concentrations of maternal
Fetal cells in the mother: Blood samples of pregnant
serum alpha-fetoprotein (MSAFP), total β-hCG and uncon
women contain fetal cells from 4 weeks of gestation
jugated estriol are measured (triple marker). Nowadays
upto the delivery. An increased concentration of fetal
inhibin A is added to qualify as Quad test.
DNA (fDNA) is reported in pre-eclampsia and fetal
Measurement of MSAFP is performed to detect fetal
aneuploidy especially Down syndrome (7-fold higher
neural tube defects and fetal ventral wall defects. During
than control). This can be a possible non-invasive test.
pregnancy, alfa-fetoprotein (AFP) is produced in sequence
by the fetal yolk sac, the fetal gastrointestinal tract (GIT)
Screening in Second Trimester for
and finally the fetal liver.
Structural and Chromosomal Abnormality Excretion of AFP in the fetal urine results in high
Ultrasound Examination in Second Trimester levels of AFP in the amniotic fluid. Transfer of AFP to
the maternal serum occurs via the placenta and trans-
Though the major or severe anomalies can be diagnosed in
the first trimester but spina bifida, major cardiac and limb amniotically. The interpretation of the MSAFP screening
defects are difficult to detect in first trimester. Around 17% test is gestational age dependant and should be performed
anomalies are not diagnosed in the first trimester and can at the 15th to 20th week of pregnancy. Elevated maternal
be picked up by the second trimester (Table 12.2). This is serum (> 2.5 multiples of median) and amniotic fluid AFP
because all organs are not fully formed in first trimester. (by amniocentesis) can lead to the suspicion of 85% of
Hence, a second trimester screening is essential to exclude anomalies like spina bifida, omphalocele, gastroschisis,
maximum fetal anomalies. It is done around 20 weeks of multiple gestation, incorrect dates, etc. Serial tests are
pregnancy. If there are anomalies incompatible with life required.
we can abort them within permissible medical termination According to the concentrations of these biomarkers,
of pregnancy (MTP) law period and early diagnosis makes the risk for fetal trisomies is assessed for each individual
us prepared for interventions. patient.
The ultrasound findings of hypoplasia of nasal bone,
increased nuchal fold thickness, echogenic bowel, Invasive Techniques in Second Trimester
echogenic focus in the heart, atresia of duodenum, hydro Chorionic villus sampling (CVS) or amniocentesis is
nephrosis, shortening of femur or humerus, mid-phalanx offered in the first and second trimester respectively is
hypoplasia of fifth finger of clinodactyly and sandal gap can cases who need confirmation.
be seen.
Hands are usually closed in second trimester hence Screening for Pre-eclampsia
details of fingers may not be possible. Shortening of long Hypertensive disease of pregnancy is a leading cause
bones is obvious in second trimester. of maternal death. It cause severe obstetric morbidity,
stillbirth, IUGR, preterm delivery and neonatal morbidity
TABLE 12.2: Timing of detection of fetal abnormalities by ultrasound and mortality. Risk factors at booking before 20 weeks of
First trimester Second trimester pregnancy is elicited in cases of pre-eclampsia in previous
CNS 88% 12% pregnancy, multiple pregnancy, pre-existing diabetes
Face 0% 50%
mellitus, diastolic pressure of 80 mmHg or greater, raised
basal metabolic index (BMI) before pregnancy or at the
Neck 100% 0%
time of booking, long interpregnancy intervals (10 years
CVS 37% 13%
or more), maternal age 40 years or above for multipara,
Lung 33% 33%
antiphospholipid antibodies, autoimmune disease, renal
GIT 100% 0% disease or proteinurea, chronic hypertension. Color
Renal 75% 25% Doppler (blood flow) study during early second trimester
Skeletal 0% 75% may indicate high-risk patients of this category.
Abbreviations: CNS—Central nervous system; CVS—Cardiovascular Some obstetricians advise repeat screening at 32 weeks
system; GIT—Gastrointestinal tract in high-risk patients when initial screening is negative.
Testing for Group B Streptococci TABLE 12.3: Timing and frequency of visits (classic)
Group B streptococci have been implicated in preterm labor First prenatal visit 6–8 weeks after missed period
as well as in amnionitis, endometritis and wound infections Monthly visit Upto 28 weeks
in the mother. Vertical transmission during labor or delivery Bimonthly visit Upto 36 weeks
may result in generalized sepsis in the newborn and
Weekly Until delivery
related long-term morbidity or neonatal death. The ACOG
and Centers for Disease Control and Prevention (CDC)
recommend either of two strategies. examination is done if needed. An ultrasound after
1. To treat pregnant women with chemoprophylaxis based 32 weeks of gestation is done for fetal wellbeing, placental
solely on risk factors without screening cultures. Risk position and maturity and liquer amount (two ultrasounds
factors include preterm labor, rupture of the membranes already done at 11–13 and 18–20 weeks as detailed above).
(ROM) of more than 18 hours prior to delivery, previous Examine the patient at each visit. Calculate the period
neonatal infection or maternal fever during labor of gestation in weeks and on examination confirm the
(>38°C). same. Listen to fetal heart sound (FHS). Any abnormality
2. To perform screening cultures at 35–37 weeks of all is noted down and managed.
pregnant women, obtained from lower third of vagina
and perianal area. Culture positive women are treated Maternal Weight Gain during Pregnancy
during labor with antibiotic prophylaxis to prevent Total weight gain throughout pregnancy is 9–11 kg. More
fetal-neonatal group B streptococcus infection. gain may indicate fluid retention leading to pre-eclampsia.
Hence, it is essential to watch weight gain. The weight
Papanicolaou Smear gain should be 0.3–0.5 kg/week during second and third
This should be performed on every pregnant woman, if not trimester.
done in the previous 6–12 months, preferably at the first The ideal weight gain for an individual pregnant patient
visit or subsequently when indicated. depends on several factors. The most important of these
Also look for: are the pre-pregnancy BMI and the type of gestation
Neisseria gonorrhoeae (single/multiple) (Table 12.4).
Chlamydia trachomatis in vaginal discharge
Cytological abnormality: Colposcopy may be done, if

Blood Pressure
needed, but endocervical biopsy is postponed to some At each antenatal visit, blood pressure is recorded with
time after delivery the patient in sitting or recumbent position (not supine
Follow-up visit: Usual routine investigations. as gravid uterus presses on pelvic vessels causing supine
In India, the Ministry of Health and Family Welfare hypotensive syndrome) when arm is at the level of the
has recommended minimal ANC of 3 visits (in low risk heart. Blood pressure of 90 mmHg systolic or an increase
pregnancies) of which 2 should be in the last trimester. of 15 mmHg above basal diastolic or more or a rise of
Otherwise the scheme of visits is once a month till 30 mmHg above basal systolic are accepted criteria for
28 weeks of gestation, fortnightly (after 15 days bimonthly) the diagnosis of gestational hypertention. The fifth sound
from 28–36 weeks of pregnancy and weekly after 36 weeks (Korotkoff-5) disappearance should be taken, rather
till she delivers (Table 12.3). than muffling (Korotkoff-4), to mark the diastolic blood
At each antenatal follow up visit, ask for any new pressure.
problem. Ask for pain, cramps or contraction, bleeding
or discharge, fever, pain during micturition, any diarrhea
TABLE 12.4: Weight gain in singleton pregnancy
or vomiting and movements of the fetus, etc. Give advice
Weight gain in normal
regarding diet, the importance of lactation and spacing BMI (before conception) pregnancy (kg)
at each visit. Hb estimation is repeated at 28–36 weeks <19.8 (low) 12.5–18
of pregnancy because maximum demand of iron, by
19.8–26 (normal) 11.5–16
the fetus, is in the last trimester and if not supervised
>26–29 (high) 11.5
may lead to dangerous low level of Hb in the mother.
Blood pressure and weight is measured at each visit. >29 (obese) <7
Urine is tested for proteins and sugar and microscopic Abbreviation: BMI—Body mass index
Second Visit Close to 26 Weeks need to started by the mother as early as possible in first
Weight is measured trimester even before the diagnosis CAH made.
In case of treatment as late as third trimester, one may
Blood pressure is measured
Urine analysis be just prolonging the pregnancy and the baby may
Iron, folic acid and calcium to continue have a very poor prognosis and very poor quality of life
later on as, e.g. shunting in pelvi-ureteric junction (PUJ)
Hb estimation is repeated
even if done early has a very high incidence of renal
An obstetric examination is done.
failure and a very poor outcome.
Most corrective procedures are in research stages only
Necessity of Third Trimester Screening
and not universly available.
Whenever the patient reports, she should be provided
In case of percutaneous umbilical blood sampling
comprehensive care.
(PUBS) in the third trimester, all its complications are
Certain anomalies can only be detected in the third
more likely and one may lose a viable fetus or may have
trimester as only then is the degree of anatomic distor
to surgical intervene at a premature stage to save a baby.
tion sufficient to be sonographically detectable.
If there is a history of previous malformed neonate,
In case a lethal anomaly is detected, one can avoid an
the parents are advised to come for investigation and
operative delivery, lower segment cesarean section
counseling before the next conception (pre-conception).
(LSCS) and morbidity can be reduced.
Even early detection upto 20 weeks of pregnancy by
Counseling of the patient can be done before delivery, in
ultrasound gives the obstetrician the choice of termination
order to save the sudden trauma of an abnormal birth.
of pregnancy if the malformations are incompatible with
The pediatrician can be informed well in advance for
life. Here the doctor must discuss the risk of recurrence
certain special care that the baby may need and certain
with the couple and inform them about the technology
corrective surgeries done at birth in specialized centers available for the diagnosis.
can save the baby to prevent further problems, e.g. Certain malformations which can be detected in third
hiatus hernia. trimester by ultrasound are:
The patient can be referred for delivery to a highly spe- Hydrocephalus
cialized neonatal care center. Neural tube defects (anencephaly, spina bifida, ence
Fetal therapies by means of endoscopic, pharmacologic, phalocele)
stem cell and gene therapy pre-delivery can prevent Diaphragmatic hernia
irreversible and progressive damage to the baby. Most Cardiac anomalies (echocardiography may be neces-
of these are at an experimental stage. Among these sary)
intrauterine transfusion is possible if Rh-immunization Omphalocele
is diagnosed in utero. Cleft lip with or without cleft palate
Certain metabolic disorders can be dealt with at birth Pyloric stenosis
by providing a special diet if one already knows about Renal agenesis (unilateral or bilateral)
their presence. Urethral abnormalities
In case of a known lethal anomaly in the fetus, one need Posterior urethral valves
not prolong pregnancy by tocolytics in case of preterm Limb reduction defects
labor. Osteogenesis imperfecta.
If any defect is visualized, then one should hunt for any

Disadvantages of Screening in Third Trimester associated chromosomal and genetic syndrome by other
Termination in third trimester is ethically and legally invasive techniques, if required, may be combined with
not allowed until the malformation is lethal or if only routine investigations for evaluation of the fetus.
short term viability is possible but with a certainity of Ultrasound is very useful in detecting anatomical errors.
the absence of cognitive developmental capacity. It should be performed only by experienced doctor.
Most anomalies should be treated as early as possible
either surgically or pharmacologically or by gene therapy Third Visit at Around 30 Weeks
to achieve optimal result. The third trimester is often too The patient is weighed and weight gain is confirmed.
late for such therapy, e.g. in case of congenital adrenal Blood pressure is measured.
hyperplasia (CAH) in order to prevent virilization steroids Urine is tested for protein and sugar.
Hemoglobin: Not required if previous Hb is done within

three months.
MINOR AILMENTS OF PREGNANCY
Obstetric examination is done.

Nausea and Vomiting
Breast examination: The pregnant lady is advised
regarding breastfeeding and diet. Recurrent nausea and vomiting during the first trimester
Iron, folic acid and calcium to continue. occurs in about 80% of pregnancies. The etiology is not clear.
Abnormal symptoms are watched for. Symptoms may be mild or may be so severe that the patient
Advise about spacing. needs hospital admission as she becomes dehydrated
and risks electrolyte imbalance and caloric malnutrition.
Fourth Visit at 36–38 Weeks Normally non-pharmacological measures are sufficient
She is examined with routine check-up, i.e. weight, blood to alleviate if not completely relieve the symptoms. These
pressure hemoglobin and urine examination. include avoidance of fatty or spicy foods, eating small
Obstetrical and pelvic examination is performed.
and more frequent meals, drinking ginger tea, increasing
One should look for: rest periods each day, etc. Pyridoxine, promethazine,
•• Period of gestation
metoclopramide and trimethobenzamide can be given.
•• Presentation of the fetus
Hyperemesis gravidarum (severe and persistent vomit-
•• Position of the fetus
ing) may need hospitalization.
•• FHS
•• Cephalopelvic disproportion (CPD)
Constipation
Advice about breastfeeding and spacing methods
Abnormal symptoms are explained Progesterone induced relaxation of the intestinal smooth
•• Any complaint by the mother that may indicate muscle slows peristalsis and increases bowel transit time.
hospitalization, e.g. reduced fetal movements, blee Dietary management of this common condition include
ding or leaking per vaginum, headache, etc. increased fluids and liberal intake of a high-fiber diet.
She should be advised to report to the hospital in Iron salts may exacerbate the problem. Over the counter
case there is/are any one of the following: products containing psyllium draw fluid into the intestine
•• Pain in the abdomen, pelvic pain or cramping and promote a more rapid transit time. Enemas, laxatives
•• Leaking per vaginum and strong cathartics should be avoided.
•• Bleeding per vaginum
•• Severe headache with blurring of vision Varicosities
•• High-grade fever or chills
Varicosities are seen mainly in the lower limbs and vulva
•• Epigastric pain
and are due to increased femoral venous back flow
•• Vomiting
pressure as pregnancy advances (Fig. 12.1) Treatment
•• Loose motions
consists of periodic rest with elevation of the legs and
•• High blood pressure
elastic stockings.
•• Breathlessness
•• Palpitations
•• Reduced fetal movement
•• Excessive fetal movements
•• No fetal movements
•• Swelling of face and body or any other complaint.
She is told that she should not stay at home after com-
pletion of 41 weeks, i.e. report to hospital.

She is informed that she must report to the hospital if
symptoms of commencement of labor or any other

abnormality are detected.
This is for the management of pregnant women who
do not have evidence of pregnancy related complications,
medical conditions or major health related risk factors.
The details of obstetrical examination are given in the
previous Chapter 6. Fig. 12.1: Varicosities of vulva
Hemorrhoids Travel: Most issues concerning travel involve the

Hemorrhoids of the rectal veins are due to mechanical comfort of the mother. When prolonged sitting is
compression by the enlarging uterus, as well as from con- involved the patient should try to stretch her legs and
stipation and straining at stool. Treatment includes cool walk for 10 minutes every 2 hours to decrease the
sitz baths, stool softeners, etc. If bleeding from hemor- risk of thrombosis that can occur secondary to the
rhoids occurs, hemorrhoidectomy may be required. hypercoagulable pregnancy state and mechanical
compression of venous blood flow from the extremities.
Leg Cramps She should avoid traveling on an uneven road, which
may be jerky. She should always take a copy of her
They are commonly seen at night and usually occur during
medical records with her. Long journeys during the first
the third trimester. Massage and placing the affected
and third trimesters should be avoided. However, travel
muscle on stretch relieves cramps when they occur.
in a pressurized aircraft is safe. Precautions are to be
Urinary Frequency taken regarding ingestion of unpurified drinking water
and uncooked eatables, etc.
This is seen mainly during the first 3 months of pregnancy
Footwear: Wearing of high heels sandals to be avoided
as the enlarging uterus compresses the bladder and again
as also the lifting of heavy weights.
during the last week as the fetal head descends into the
Clothes: Loose fitting cotton clothes are advised.
pelvis. If frequency occurs in conjunction with dysuria,
Teeth: She must maintain good general as well as dental
hematuria or urgency the patient should be evaluated
hygiene. If she has any dental problems, she should
for a urinary tract infection (UTI) by urine routine and
consult a dentist so that tooth extraction if required can be
microscopic examination and culture sensitivity test.
done safely in the second trimester. Pregnancy induced
Immunization gingivitis should be taken care of. Advise her to brush teeth
twice to prevent infection and chances of preterm labor.
To prevent tetanus, two dosage of 0.5 mL tetanus toxoid Sexual activity: A patient with bad obstetrical history
(TT) is given intramuscularly (IM) 4–6 weeks apart are or bleeding episodes in early pregnancy should avoid
given during 16–20 weeks of pregnancy. If the preceeding sexual activity during the first trimester of pregnancy.
pregnancy was less than 3 years ago and the patient was Patients with history of preterm labor should avoid
immunized for tetanus in that pregnancy then only one these during the last 6–8 weeks of pregnancy, for the
dose is required. Live viral vaccines are contraindicated fear of introducing infection and inducing preterm
during pregnancy (measles, mumps, rubella). Inactivated labor. Patients with placenta previa should also avoid.
or subunit as rabies, hepatis B, cholera, plague, etc. are Otherwise sexual relations are allowed to continue
allowed if there is risk of exposure. Once exposed, post- normally.
exposure prophylaxis can be given by hyperimmune Care of the breasts: If the nipples are anatomically
globulins, e.g. hepatitis B, rabies, tetanus and vericella etc.
normal, nothing needs to be done beyond ordinary
cleanliness. If they are retracted then correction can be
ADVICE TO THE PREGNANT WOMEN done by gentle manipulation with fingertips by pulling
Exercise: She should exercise sufficiently but avoid these out or by the use of nipple shields.
getting fatigued and any risk of injury to herself or her
fetus. Do not start new exercise program to which the ANTENATAL EXERCISES
women is not accustomed to as it may lead to low birth
weight (LBW) of the neonate. Many women have an exercise regimen in their non-
pregnant time. Once they become pregnant, it is better
Occupation: Any occupation that subjects the pregnant
to examine them and prescribe appropriate exercises.
women to severe physical strain should be avoided, as
Pregnancy is a healthy state and not an illness and a well-
there is an increased risk of preterm delivery, IUGR conditioned body will perform better. The obstetrician
or gestational hypertension. Women with previous should be aware of the different guidelines and
pregnancy complications that are likely to be repetitive, recommendations regarding exercises in pregnancy.
e.g. preterm labor, should minimize physical work. There are certain physiological changes in pregnancy,
Women with uncomplicated pregnancies can usually which are to be understood before advising exercises
continue to work until onset of labor. during pregnancy.
Musculoskeletal changes: These are growing breasts, Influence of Pregnancy on Exercise

uterus and fetus and lumbar lordosis. With these changes, The women who were doing weight-bearing exercises
the center of gravity of the pregnant woman is disturbed before pregnancy noted a progressive decline in perfor-
causing problems in balancing. Sudden movement may mance during pregnancy. Non-weight bearing exercises,
increase these mechanical difficulties and heighten the e.g. cycling or swimming are not affected. Exercise in the
potential for injury. Weight bearing exercises may cause first and second trimester was correlated with feeling
abdominal and pelvic discomfort due to increased uterine better in the third trimester.
mobility, pelvic instability and tension on round ligaments.
As we know hormones, lead to laxity of joints, leading to Effect of Exercise in Labor Outcome
an increased risk of strains and sprains. There is no evidence of preterm labor, premature rupture
of membranes and fetal distress due to exercise. Exercise
Temperature of the Mother and the Fetus may relieve stress, reduce anxiety and increase self-esteem.
Fetal temperature is 0.5–1°C more than mother’s It may help glucose control in gestational diabetic patients.
temperature due to heat production by fetoplacental It is found that well conditioned subjects (who exercised
metabolism. Basal metabolic rate (BMR) is increased during pregnancy) had shorter labor, lesser need for obstet-
during exercise. This generates additional heat and causes ric intervention and fewer signs of fetal compromise. So,
a rise of temperature. There is some suggestion that this there are additional benefits to the pregnant woman who
rise in temperature decreases heat dissipation to the exercise, but no advantage to the fetus is seen.
mothers and may be potentially teratogenic especially in The goal is to maintain a good fitness level throughout
the first trimester. pregnancy, but no trial to reach peak fitness or training for
competition is allowed. However, it should be emphasized
Hemodynamic Effects of Exercise
that in pregnancy, exercise is not a means to control weight.
There is an increase in heart rate, stroke volume and A physically fit pregnant woman can exercise during
cardiac output. During exercise, blood supply is diverted pregnancy, provided there are no contraindications.
to exercising muscles. This may decrease the splanchnic Similarly, a previously inactive woman can start exercise,
blood flow. However, studies of flow velocity profile in the after the advice of the doctor. Exercise with least risk
fetal aorta and the umbilical circulation have not supported should be chosen. An uninitiated pregnant woman can
these concerns. There may be ST segment depression but begin exercise with as little as 5 minutes a day and add
it may be secondary to altered sympathetic regulation. 5 minutes a week until she can stay active for continuously
30 minutes. She should exercise regularly at least three
Demand of Oxygen times per week. There are certain contraindications to
In the mother, there may be a mild increase in tidal volume exercise during pregnancy.
and oxygen consumption as an adaptation to the increased
oxygen demands of the fetus. During mild exercises the Absolute Contraindications
pregnant woman has a greater increase in respiratory Gestational hypertension and pre-eclampsia
frequency thus meeting her greater oxygen demand during Preterm rupture of membranes (PROM)
exercise. If vigorous exercises are done in pregnancy these History of preterm labor in previous pregnancy
adaptive changes cannot cope. This is partially due to the Signs and symptoms of preterm labor in this pregnancy
obstructive effect of the enlarged uterus on diaphragmatic Incompetent cervix or circlage operation
movements. Placenta previa
IUGR
Demand of Energy Multiple pregnancy.
In normal pregnancy, more energy (first two trimesters 150
calories per day and third trimester 300 calories per day) Relative Contraindications
is needed than in normal day-to-day life. This demand of Chronic hypertension
energy is even higher with exercise. There are concerns Abnormal thyroid functions
that excessive exercise may hamper fetal development Cardiac disease, valvular disease and congestive cardiac
however, overall weight gain was seen to be unchanged by failure
exercise. Diseases of the lungs
Vascular diseases Pain in abdomen or back

Severe anemia Dyspnea
Diabetes mellitus. Dizziness, faintness
Nausea and vomiting
Instructions to Pregnant Woman Headache and elevated blood pressure
Exercises are to be advised on individual health merits Chest pain
by a doctor. There should be no detrimental effect. The Cramping.
duration and intensity must not cause strain on joints
causing pain, fatigue or dyspnea. Thirst lags behind the Exercises not Allowed
body’s need for fluids. Water loss during exercise is not Contact sports (as they have an increased risk of abdominal
generally noticed. Therefore, start exercise after drinking trauma)
about half a liter of fluid and take one cup of liquid after Hockey (both field and ice hockey)
every 20 minutes of exercise. Do not exercise lying down Boxing
after the first trimester, as the gravid uterus will press on Football
the great vessels. Do not stand motionless for long. In Soccer
late pregnancy avoid exercises requiring balancing and Wrestling
sudden changes in position. Do not exercise during illness High-risk sports (as they have an increased risk of falls/
and fever. trauma)
If exercising in early morning and late evening the Gymnastics
temperature rise will be minimum. Use a fan while doing Horseback riding
stationary cycling. Avoid exercise in hot and humid Skiing (both snow and water)
weather. Hence, hot tubbaths are also to be avoided Skating
in early pregnancy. Walking is the only exercise that Gliding
can be started safely. She can be advised that if you can Vigorous racquet sports
comfortably walk and talk, that is the best pace of walking. Scuba diving
Cool down following exercise till the heart rate is less Weight lifting
than 100 per minutes. Wear comfortable cotton clothes Squash
allowing adequate ventilation and prevent hyperthermia. Sit ups and double leg lifts
Supporting brassiere and supporting footwear are a great Downhill run
help. A carbohydrate rich diet restores muscle glycogen. Mountaineering
An exercising frequency of three or four times a week is Rock climbing
adequate. Avoid jumping and bouncing exercises. Jumping.
Permitted Exercises in Pregnancy Benefits of Exercise

Walking Evaluation of possible benefits of exercise to the mother
Stationary cycling are difficult but the ones documented are:
Swimming and water exercise Increases energy
Yoga–women who show interest should be directed to a Good breathing
properly trained teacher Correct posture
Low impact aerobics Encourages flexibility and suppleness
Pilates: It is a scheme of exercises that gives mental and Reduces leg cramps
physical training. The concentration is on abdominal Better coping with labor
and pelvic floor muscle strengthening by appropriate Enhances circulation
instructors. Strengthens muscles stressed by pregnancy (abdomen,
low back and pelvic floor)

When to Stop Exercise Immediately Shorter labor
Feeling fatigue Less need for intervention
Leaking of liquor Less backache
Bleeding Less constipation.

Risk of Severe Exercises on the Mother helpful. While working on a table sitting tall is correct,
Trauma to ligaments and muscles sagging is not good (Figs 12.3 to 12.5).
More stress on the heart Standing and walking: She is advised to stand and
Hypoglycemia
walk tall. Prolonged standing is discouraged. She is
Dehydration.
instructed to not stand with front foot on a raised
Fetal risks: Strenuous and prolonged exercise may lead to: support and to not rock from foot to foot. Frequent
Fetal distress
vigorous ankle dorsiflexion and plantar flexion for
IUGR
30 seconds at a time is to be done by forward and
During severe exercise the temperature of the mother
backward movements (Fig. 12.6).
rises. This high temperature may be teratogenic during Bending and lifting: Bend the hip and knee and not the
the first trimester back. Avoid lifting or pushing heavy weights (Fig. 12.7A
Preterm labor may be precipitated.
and B). Equal weights on both sides is advised (e.g. two
Hence, vigorous exercises are avoided during pregnancy. shopping bags on each side).
Atheletes must not practice their sports during pregnancy. •• Pregnant women are more prone to backache
The following instructions are to be issued to the pregnant because of distended abdomen, increased lumbar
women during antenatal visits to relieve common ailments. curve and weight gain. A poor posture due to weight
Back care: The patient is shown in postures during lying, gain causes fatigue of interventricular joints,
sitting, standing to prevent back pain (Figs 12.2A to C). overriding and traumatizing the joint capsule
A supporting mattress, a small pillow or a rolled towel also causes pain in the back. Softness of ligaments
at the waist helps. A pillow under the thigh and knee is and increased torsional strains and sometimes
comforting. spondylolisthesis is also seen.
•• This is an era where road traffic accidents are often
Posture for Relief of Pain seen and a pregnant woman may be a victim. How to
Getting up from the bed is done by crooking the knees, tie car seat belt is to be told (Fig. 12.8A to C).
rolling on the side and sitting up sideways by pushing Pelvic floor and pelvic tilting exercises: This can be
with the arms. The process is reversed when she is to lie shown with patients sitting on the edge of the chair. This
down. Putting on elastic support stockings before getting can be practiced standing, crook lying, side lying and
out of bed helps to prevent varicose veins. Adequate rest prone kneeling (Figs 12.9A to C).
is essential. Relaxation exercises for coping with stress, fatigue and
Sitting: While sitting on a chair, the buttocks should be relaxing in between contractions (Fig. 12.10). Keeping
placed right back on the chair seat, keep a firm support the foot end of the bed raised helps in better venous
in the lumbar region. Sitting tall is advised. Prolonged return.
sitting is discouraged. Standing and some walking Leg exercises and foot exercises: This helps in proper
is advised in between. Putting feet on a low stool is circulation of blood in legs and foot. Dorsiflexion and
A B C
Figs 12.2A to C: Photos for postures for relief of backache

Fig. 12.3: Sitting postures Fig. 12.4: Sitting postures on study table
Fig. 12.5: Sitting postures on computer table Fig. 12.6: Standing positions
A B
Figs 12.7A and B: A. Lifting; B. Bending postures
A B C
Figs 12.8A to C: Car belt position. A and B. Incorrect; C. Correct
B C
Figs 12.9A to C: A. Pelvic position in crook lying; B. Sitting on a edge of the chair; C. Standing position
Fig. 12.10: Relaxing in first stage of labor Fig. 12.11: Yoga
A B C
Figs 12.12A to C: Positions to ease sacrosciatic pain
plantar flexion and circles at ankle for 30 seconds help. early labor relaxing unwind and listening to music will
While sitting she is advised not to cross the knee. If she help her (Figs 12.13 and 12.14).
is lying down in bed, feet are to be dorsiflexed and not
plantarflexed. Long sitting time must be avoided. A During Contractions
workout before bedtime and warm bath helps. Also do feet Lying in comfortable position, relaxing, breathing exercises
exercises in bed. These will prevent cramps. Lifting of legs and back massage, kneading or stroking will help.
one at a time is to be done (never lift both legs together).
Working women are given instructions: In the last During Delivery
trimester of pregnancy taking one day off in the middle Breathing exercises, back massage, assuming a comfortable
of the week will help. Alteration of lifestyle is discussed. position and keeping the legs relaxed will ease discomfort.
•• Massage with soothing stroke may help in relaxing. Braxton Hicks contractions of late pregnancy are used
•• Breathing slowly and easily is relaxing. to practice relaxation during labor. During labor, hard
•• Yoga, music, putting feet in warm water are all physical work in the form of pushing down is done by
relaxing (Fig. 12.11). Different postures may relieve the patient. Therefore, controled relaxation in between
sacrosciatic pain (Figs 12.12A to C). contractions is very useful. Deep slow breathing is one of
Visits to the labor room may help her know the process them. The face can be sponged and she can take sips of
of labor. water. Change of position helps. Keep her covered espe-
cially in cold weather, and an extra pillow for support may
Exercises to be Practiced during Labor help her to rest. Encouragement and praise are helpful.
Preparing for labor is essential. Relaxation prevents the The woman is trained to hold her breath and to push for
patient’s tiredness and she can control them herself. In longer and longer periods. She is taught to breath in and
Figs 12.13A and B: A. During the first stage of labor many women feel more comfortable leaning forwards; B. The supine position
reduces anteversion of uterus
A B
Figs 12.14A to C: Different postures in early labor
out. Then, lungful of air is taken in and she is made to push pushes are needed. After the contraction is over, one or
down while holding her breath. two deep breaths are taken.
After a contraction is over she is taught to relax and Massaging during labor in the form of stroking and
recharge her strength by changing her position, breathing kneading on the back makes the experience of labor
and sometimes massage. Drawing up of a contraction better (Figs 12.15A to D). It could be due to release of
makes the women in labor aware and less frightened. endogenous opiates relieving pain. This also gives non-
Do not force down her head on the chest while pushing, verbal psychological support to the laboring women.
it may lead to pain and inconvenience postnatally. Each Similarly light finger (Fig. 12.16) stroking of the
push lasts about 5–10 seconds and in each contraction 3–4 abdomen from one anterior superior iliac spine to other
A B C D
Figs 12.15A to D: Kneading and stroking
Fig. 12.16: Finger stroking of the abdomen Fig. 12.17: Transcutaneous electrical nerve stimulation (TENS)
passing under the bulge, stroking ascending on either side massage or abdominal electrodes this technique gives
of the midline and across the iliac crest is also soothing. sufficient relief during labor.
This can be done by the patient herself. Kneading of the Use of acupuncture may be beneficial. It has been shown
thighs relieve pain in legs. Massage of perineum is also acupuncture to be a good alternative to analgesia in labor.
taught. A birth companion, an elderly lady or the husband Hypnosis has proven to be a good method by some.
is being allowed in some labor rooms. A fully trained aromatherapist can help ease labor
Transcutaneous electrical nerve stimulation (TENS) pains. Pains in a birthing pool take advantage of the
(Fig. 12.17) is an additional non-invasive technique to ease positive mechanical and physiological effects of water but
the process of labor. Two types of TENS are there: burst or should be used in expert hands only.
train TENS and brief intense TENS. The first is self initiated
at the start of a contraction by pressing a button and NUTRITION DURING PREGNANCY AND
stopping after the end of contraction by the same button. LACTATION
The brief intense TENS is the continuous mode. TENS is In all mammals the handling of nutrients by the mother and
also helpful in post-delivery, suturing and for after pains in transfer to the fetus is done by a complex series of endocrine
the early puerperium. Electrodes are placed on the back of and metabolic changes. All parts of the fetus-organ viz.
the mother paravertebrally on T12-L1 (uterine and cervical muscles, bones, blood, skin, etc. are made from nutrients in
innervation) during the first stage of labor. Additional the food that the mother eats. Nutrient needs of a woman
electrodes on S2–S4 (birth canal and pelvic innervation) during pregnancy and lactation are higher than at any other
are placed in the second stage of labor. No adverse effect times. The better a woman takes care of herself nutritionally,
is seen on neonates by TENS. Together with abdominal the more successful her pregnancies are likely to be.
A woman needs extra calories during pregnancy to

build up her own tissues (hypertrophied uterus, breast,
etc.), to build fat stores, to make breast milk and for
the growth of the fetus and placenta. Her gut absorbs
nutrients better and her body uses them more efficiently
than when she is not pregnant. During the first six
months, tissues and fat stores are used up. Only a small
amount is needed for the growing fetus during these six
months. During the last three months of pregnancy extra
food is needed for the growing fetus and to build up the
fetus’s stores of fat, iron and vitamin A. According to the
National Nutrition Monitoring Bureau (NNMB) 2002,
the recommended dietary allowances are 2175 Kcal and
65 gm protein per day (approximately 1gm/kg weight).
Mothers pre-pregnancy nutritional status and proper
intake has profound effect on the growth of the fetus.
Stillborn, LBW, premature infants are more frequently Fig. 12.18: Vegetables rich in folic acid
born to mothers who have a poor diet prior to pregnancy. of nutritional status is vital. Health care in her childhood
An adequate supply of nutrients during pregnancy also also has influenge on the fetus. Mothers diet during
helps to assure an adequate supply of good quality of pregnancy also bear a very useful role.
breast milk during lactation. The major change of weight The recommended dietary allowances (RDA) for women
occur between 25th to 40th weeks of pregnancy. during pregnancy have been categorized according to
their work status namely sedentary, moderate and heavy
PLACENTA AND FETAL NUTRITION work and the height of the pregnant woman. The rest of
the nutrients remain the same in all three categories of
Placenta has a very important role in fetal nutrition. It
activity. She has not to eat double the pre-pregnancy
transfuses, selectively transports, processes or resynthesizes
amount (eating for two). For a pregnant woman the calorie
nutrient before they reach the fetus. Hence, amount of
requirement increases by +300 Kcal and protein by +15
maternal blood flow through the placenta, and nutrients
gm/day per fetus over and above normal requirements.
supply determine fetal health.
The fat intake is recommended to be a total of 30 gm/day,
calcium intake to be 1000 mg/day and iron to be 38 gm/
MECHANISM OF PLACENTAL TRANSFER day. Vitamin A, pyridoxine, ascorbic acid at Vitamin B12
Various factors affecting transport is depicted in Flowchart quantities remain the same as in non-pregnant state.
12.2. Thiamine, riboflavin and nicotinic acid quantities are also
increased, respectively. Folic acid (Fig. 12.18) requirement
is increased to 400 µg/day.
NUTRITION OF THE MOTHER
Pre-pregnancy nutrition status of the mother is very ENERGY AND ENERGY NUTRIENTS
important in fetal growth. Her pre-conceptional building DURING PREGNANCY
A woman can easily obtain 300 Kcal from just one extra
Flowchart 12.2: Factors affecting transplacental supply of nutrients
serving from each of the five food groups—a slice of bread,
a serving of vegetable, an ounce of lean meat, a piece of
fruit, and a cup of non fat milk. Pregnant teenagers, under-
weight women or physically active women may require
more than a sedentary woman.
For a 2000 Kcal daily intake, 300 K calories represents
about 15% more food energy than before pregnancy. The
increase in nutrient needs is greater than this, so nutrient-
dense foods should supply the 300 Kcal.
Protein Folate: It is fairly easy to obtain sufficient folate, without

The expansion of maternal blood volume and the growth of supplements, from a diet that includes fruits, juices, green
the fetus, placenta, and maternal tissue-require additional vegetables and whole-grain or fortified cereals. In addition
protein. The RDA for pregnancy is 10–15 grams per day to being good sources of folate, these foods are low in calo-
higher than for non-pregnant women (1 gm per kilogram ries, rich in other vitamins and minerals, and high in fiber.
body weight). When dietary intake is inadequate, daily supplementation
Protein needs during pregnancy can easily be met from with 300 micrograms folate is recommended.
dietary sources such as whole grains, meats, milk, eggs Iron: Pregnant women need iron to support their enlarged
and legumes. Obtaining enough protein does not pose a blood volume and to provide for placental and fetal needs.
problem, even if the diet excludes all foods of animal origin. The developing fetus draws on maternal iron stores to
Above of 20% of the diet. create stores of its own to last through the first four to six
months after birth when milk, which is poor in iron, will
Carbohydrate be its sole food. Also, the blood loss that is inevitable at
Ample carbohydrate is necessary to spare the protein delivery, especially at a cesarean delivery, can further drain
needed for growth. At least 50% of the total daily energy the mother’s supply. When these special needs are added
intake should derive from carbohydrate. For example, to the body’s usual requirements, the iron requirement of
for a daily intake of 2000 Kcal, this represents at least pregnancy totals about 1000 milligrams. Iron in diet comes
1000 Kcal or 250 grams of carbohydrate. Foods that provide from meat, eggs, green leafy vegetables etc. Only 10–15%
carbohydrate include milk, legumes, fruits, grains (breads, iron in diet is absorbed.
cereals and rice) and vegetables. Fortunately, vitamin C in fruits and vegetables can
enhance the absorption of iron. In India, very few women
Fat enter pregnancy with adequate iron stores, so a daily iron
The diet should contain about 30% of fats. In multiple supplement of 100 milligrams is recommended during the
pregnancy the exact amount is not worked out but it is second and third trimesters for all pregnant women.
recommended to add 300 Kcal and 10–15 gm of protein Zinc: It is required for DNA and RNA synthesis and thus for
per fetus over and above the standard for a singleton protein synthesis and cell development. Low blood zinc is
pregnancy. a significant predictor of LBW. The recommendation for
zinc for pregnant women is slightly higher than for non-
Vitamin B Associated with Energy and pregnant women.
Protein Intake In an average diet, zinc comes from meat, fish, and
The need for vitamin B increases in proportion to the poultry. Zinc from plant sources such as cereals and legumes
increase in energy requirements. The RDA during is not well absorbed. In vegetarian diets, the abundant fibers
pregnancy is set slightly above the non-pregnant woman’s and binders in foods of plant origin limit its absorption. Soy
RDA for thiamine, riboflavin and niacin. products, which are commonly used as meat alternates, also
Vitamin B6 recommendations increase in parallel with interfere with zinc quantity, bioavailability or both. Oysters,
protein recommendations. Fortunately, most protein-rich crabmeat and shrimp are rich sources of zinc.
foods provide ample vitamin B6. Pregnant adolescents,
and women carrying more than one fetus need to pay Nutrients for Bone Development
attention to their vitamin B6 intakes. For these women, a The nutrients involved in building the skeleton are in great
daily multivitamin supplement containing 2 milligrams demand during pregnancy. Insufficient intakes of calcium,
vitamin B6 is recommended. phosphorus, vitamin D, magnesium or fluoride during
pregnancy may result in abnormal fetal bone and teeth
Nutrients for Blood Production and Cell Growth development.
New cells are laid down at a tremendous pace as the fetus Calcium and phosphorus: Adequate calcium intake
grows and develops. The needs for folate (Fig. 12.18), is especially important for young women. Sources of
vitamin B12, iron and zinc are especially great, due to dietary calcium being milk, cheese, yogurt and other
their main role in DNA synthesis and cell manufacture, calcium rich foods. Alternatively and less preferably, they
including red blood cells (RBCs). The requirement is more may need a daily supplement of 600 milligrams calcium.
in epileptic pregnant women on therapy. Calcium intake is shown to reduce hypertension.
Diets rich in cereals and vegetables (typical of Vitamin A: Its deficiency during pregnancy has been
vegetarian diets) contain abundant fibers, phytates and associated with fetal growth restriction (FGR), preterm
oxalates-compounds that impair calcium absorption even birth, and LBW, therefore, the recommended allowances
when calcium intakes meet recommendations. Together, of either retinol 600 µg/per day or beta-carotene 24 µg/per
the strict vegetarians with low calcium in diet and more day should be strictly met. Good sources are yellow and
fiber binding calcium in meals prevent absorption along orange colored vegetables and fruits.
with the high calcium needs of pregnancy jeopardise Vitamin E: Pregnant women typically have vitamin E
the calcium status of these women. They need a reliable intakes below the RDA, which is slightly higher than for
calcium source in their diets—either a calcium fortified non-pregnant women food rich in vitamin E are vegetable
food or a calcium supplement (within physiological limits, oil, wheat germ, whole grains and nuts.
the body partially compensates for low calcium intakes by Vitamin C: It is useful to give structure to bone, cartilage,
increasing absorption). muscles and blood vessels by facilitating formation of
Phosphorus: It is closely linked with calcium metabolism. fibrin protein collagen, it also help in the absorption of iron.
Since phosphorus intakes usually exceed recommenda- Plasma vitamin C normally falls during pregnancy, largely
tions, getting enough does not present a problem for preg- because of hormonal changes, blood volume expansion,
nant women. and increased needs. The placenta transfers vitamin C into
Vitamin D: It has a vital role in the absorption of calcium the fetal blood against a concentration gradient. At term,
from GIT and utilization of calcium. It stimulates calcium the fetal vitamin C plasma concentration is 50% greater
retention by the kidneys. In these ways, vitamin D raises than maternal concentration. The RDA for non-pregnant
blood calcium. Consequently, severe maternal vitamin D women increases by 10 milligrams during pregnancy.
deficiency interferes with normal calcium metabolism, Women need to include vitamin C rich fruits like citrus
resulting in rickets in the fetus and osteomalacia in the variety and vegetables in their diets. Otherwise, they may
mother. need a daily supplement of 50 milligrams of vitamin C.
The body can synthesize vitamin D from cholesterol in Iodine: It is an integral part of two hormones released
the body in sunlight. Foods rich in vitamin D are eggs, liver, by the thyroid gland which are vital for temperature
fatty fish, butter and milk fortified with vitamin D. regulation of body, metabolism, reproduction, growth,
Magnesium: The recommendation for magnesium during blood cell formation, nerve and muscle fuctions, etc.
pregnancy is slightly higher than for non-pregnant women Deficiency of iodine in pregnant woman impairs fetal
because of its integral role in bone formation. Magnesium development, causing the extreme and irreversible mental
participates in the activation of vitamin D and in the release and physical retardation known as cretinism. To prevent
of the parathyroid hormone that acts on the kidneys and fetal damage, iodine deficiencies need to be corrected
bones to raise blood calcium. before conception.
Magnesium is commonly found in foods such as grains, Iodine needs are fulfilled by using iodised salt in cook-
seafood and green vegetables. ing, eating seafood and vegetables grown in iodine rich
Fluoride: Mineralization of the fetal teeth begins in the fifth soil.
month. Some studies report reduced tooth decay in children Foods are basically divided into five groups namely—(1)
born to women taking fluoride in diet. Supplementation in cereals, grains and their products (2) pulses and legumes
discouraged as it crosses placenta and the placenta may (3) milk and milk products (4) fruits and vegetables (5) fats
not defend well against excess fluoride. Instead, women are and sugars. Table 12.5 describes the sources of various food
encouraged to drink fluoridated water or physicians may groups and the main nutrients provided by each group.
prescribe supplements, not to exceed 1 milligram fluoride
per day. Fluid Requirements
Maternal fluid intake is required to be increased. About
Other Nutrients 30 mL/day is needed over and above the non-pregnant
The nutrients mentioned so far are the most intensely state. It can be calculated according to body weight to give
involved in cell production and bone mineralization. Of a baseline assessment 100 mL/kg for first 10 kg, 50 mL/
course, other nutrients are also needed during pregnancy kg each for the next 10 kg but more than required is not
to support the growth and health of both fetus and mother. harmful.
TABLE 12.5: Five food group system TABLE 12.6: Nutrient recommendations for multivitamin-mineral
supplements in pregnancy
Food group Main nutrients
Nutrient Amount Nutrient Amount
Cereals grains and products Energy, protein
Rice, wheat, ragi Invisible fat, vitamin B1 vitamin Vitamin B6 2 mg Iron 30 mg
Bajra, maize, jowar B2, folic acid iron, fiber Folate 300 mg Zinc 15 mg
Barley, riceflakes, wheat flour Vitamin C 50 mg Copper 2 mg
Pulses and legumes Energy, protein Vitamin D 5 mg Calcium 250 mg
Bengalgram, blackgram Invisible fat,
Greengram, redgram Vitamin B1, vitamin B2
Lentil (whole as well Folic acid, calcium, iron, Iron supplements: Iron is the only nutrient for which
as dhals) Fiber supplements are routinely recommended during preg
Cowpea, peas, rajmah, soyabeans nancy. A balanced diet alone cannot supply the iron a
Beans, etc.
pregnant woman and fetus needs. Iron supplementation
Milk and meat Products is needed to accommodate the expansion in red blood cell
Milk, curd, skimmed milk, cheese Protein, fat, vitamin B2, calcium mass that begins at the end of the first trimester. During
Meat the second and third trimesters, all pregnant women are
Chicken, liver, fish, egg, meat Protein, fat, vitamin B2 advised to take 30 milligrams of ferrous iron daily. They are
Fruits and vegetables Carotenoids (vitamin A), vitamin also advised to eat an iron-rich diet that contains meat, fish,
Fruits: C, fiber poultry and vitamin C-rich fruits and vegetables to enhance
Mango, guava, tomato (ripe), Invisible fats, carotenoids iron absorption by converting insoluble ferric iron in the
papaya, orange, sweet lime, (vitamin A), vitamin B2, folic acid,
food into more soluble ferrous form. Women who have iron
water melon calcium, iron, fiber
Carotenoids (vitamin A) folic deficiency anemia may need to take iron supplements that
Vegetables (green leafy):
Amarnath, spinach, gogu acid, calcium, fiber provide 60 to 120 milligrams a day until iron status returns
Drumstick leaves, coriander to normal.
leaves, mustard leaves and Iron supplements can cause such side effects as heart-
fenugreek leaves burn, nausea, upper abdominal discomfort, constipation,
Other vegetables: and diarrhea. These problems may be alleviated by taking
Carrots, brinjal, ladies fingers,
the iron supplements at bedtime.
capsicum, beans, onion,
Only recommended doses should be given to pregnant
drumstick, cauliflower
women because mega dose vitamin and minerals may be
Fats and sugars
harmful to the growing fetus and it should be seen that the
Fats: Energy, fat, essential fatty acids.
Butter, ghee, hydrogenated oils,
supplementation starts only, from the second trimester
cooking oils like ground nut, only. High doses of vitamin A and D (fat soluble) and
mustard, coconut, sugars selenium can cause birth defects. Larger doses of fluoride
Sugar: Jaggery Energy may cause mottled teeth of the fetus. Excess vitamin C may
interfere with copper metabolism. Similarly zinc competes
with iron for absorption. Some herbal additives like
chamomile, mint and raspberry leaves in tea are harmless
Nutrient Supplements for Pregnant Women but details about other herbal preparation are not known
Women who make wise food choices during their preg- and hence they should be avoided.
nancies can meet most of their nutrient needs. For women Figure 12.19 shows the average intake and the recom-
who do not eat adequately, daily multivitamin-mineral mended dietary intake for a pregnant and lactating mother.
supplements are recommended. Table 12.6 lists nutrient Childhood malnutrition, early and short interval
recommendations for multivitamin-mineral supplements. frequent pregnancies, reproductive tract infection along
In general, supplements should be taken between with malnutrition result in high maternal mortality. One
meals or at bedtime to enhance absorption. Calcium out of three women aged 15–29 years is undernourished.
supplements are an exception; they should be taken with Therefore, the battle for safe motherhood should start
meals to enhance absorption and limit interactions with while girls are still in their early adolescence or better from
iron and zinc supplements. cradle.
Fig. 12.19: Comparisons of energy and nutrient recommendations for non-pregnant, pregnant and lactating women
Although there are no special diets for pregnancy, most locally available. With a little guidance, they can make
pregnant women require some general dietary advice informed food choices so as to include foods from all the
as to how best to modify their usual diet so as to supply groups and thus fulfilling their nutritional needs. This will
the extra needs for nutrients. This also depends on the help the woman in giving birth to a healthy baby and also
economic status of the family and the foods which are in maintaining her own health.
1. What are the routine investigations on first visit on pregnancy?
2. What are the advices given to pregnant women?
3. What are the effect of exercise in labor outcome?
4. Does iron play an important role in pregnancy. Explain.
Section 3
Abnormal Pregnancy
Section Outline
13. Hyperemesis Gravidarum
14. Spontaneous Miscarriage or Abortion including Habitual or Recurrent Miscarriage
15. Ectopic Pregnancy
16. Gestational Trophoblastic Disease (GTD)
17. Antepartum Hemorrhage
18. Multifetal Gestation
19. Preterm Labor and Premature Rupture of Membranes
20. Disproportional Fetal Growth
21. Intrauterine Fetal Death
22. Prolonged Pregnancy
23. Abnormalities of Placenta, Cord and Amniotic Fluid Volume
13
Sudha Salhan
Hyperemesis Gravidarum
Gynecological causes
NAUSEA AND VOMITING IN PREGNANCY
•• Twisted ovarian tumor

Nausea and vomiting, as such, are usually harmless and •• Red degeneration of fibroid.
self-limiting, in early pregnancy. About 60–70% of pregnant
women, do experience them between 4 and 7 week of Vomiting in Late Pregnancy
pregnancy but in approximately 30%, they disappear by Related to pregnancy:
the 10 weeks of gestation and are no longer seen in 60% by Impending eclampsia
12 weeks of pregnancy and in 99% by around 20 weeks Continuation or reappearance of simple vomiting of
of gestation. Rarely, they can be a manifestation of some pregnancy.
underlying pathology or become severe enough to require
Associated (but not related) with pregnancy:
hospitalization to treat the complications and to know the
All medical, surgical and gynecological causes mentioned
cause.
previously.
Causes of Nausea and Vomiting in Pregnancy Hiatus hernia.
Vomiting in Early Pregnancy Nausea and vomiting are more common in the first
trimester of pregnancy in 75% of pregnant women, i.e.
Related to pregnancy:
between first and second missed period and may last till
Vomiting due to pregnancy: A simple nausea and
14 weeks. Some experience them even before the first
vomiting (morning sickness or emesis gravidarum).
missed period, being worse in the morning though in
Hyperemesis gravidarum (pernicious vomiting).
some it may persist throughout the day. This extreme form
Associated (but unrelated) with pregnancy:
is called hyperemesis gravidarum. It is diagnosed when
Medical causes
there is a compromised fluid, electrolyte and nutritional
•• Urinary tract infection (UTI)
status. It is rare (found in 0.5% of pregnancies). In this,
•• Hepatitis
•• Gastroenteritis
there is a history of persistent vomiting, loss of more than
•• Ketoacidosis of diabetes mellitus
5% of pre-pregnancy weight and ketonuria.
•• Hyperthyroidism
It is more common in multiple gestation, hydatidiform
•• Intestinal worm infestation
mole (and other trophoblastic disease), impending
•• Addison disease eclampsia and a few fetal anomalies like Down syndrome
•• Uremia (trisomy 21), partial mole and hydrops fetalis.
•• Pancreatitis
•• Migraine
Effects on the Fetus
Surgical causes It depends on the severity of the vomiting. Mild to
•• Peptic ulcer moderate vomiting does not have any effect on the fetus.
•• Appendicitis But hyperemesis, leading to weight loss of the mother, can
•• Intestinal obstruction cause intrauterine growth restriction (IUGR) in one-third
•• Cholecystitis of the infants.
Effects on the Mother TABLE 13.1: Laboratory finding in hyperemesis gravidarum

Mild to moderate nausea and vomiting have little influence Laboratory index Compared to normal value
on the health of the mother. Thyroid-stimulating hormone Suppressed <0.4 mIu/L
However, in hyperemesis gravidarum, there may Free T4 index Elevated 13–40
occur some serious complications, like Wernicke’s Free T3 index Elevated 225–350
encephalopathy (if dextrose solution is infused without
Sodium Low 125–134
replacing thiamine). In this case, there is an associated
Potassium Low 2.3–3.1
ophthalmoplegia, ataxic gait and confusion (only one
of these three complications may be seen). Hence, in Chloride Low 80–98
hyperemesis gravidarum, especially if prolonged, 100 mg Alanine aminotransferase (ALT) or High 41–324
aspartate aminotransferase (AST)
of thiamine intravenously (IV) should be started before
establishing a dextrose IV drip. Other rare complication of Amylase High 151–391
hyperemesis gravidarum are splenic avulsion, pneumo Lipase High 70–200
thorax, peripheral neuropathy (B6 and B12 deficiency), Serum creatinine High Upto 5 mg
esophageal rupture and Mallory-Weiss tear of the Abbreviations: T4—Thyroxine; T3—Triiodothyronine
esophagus, etc.
be responsible for the temporary hyperthyroidism in
Mechanism of Vomiting (Flowchart 13.1) hyperemesis gravidarum, which corresponds to the
Vomiting is caused by a complex reflex pathway, controlled degree of vomiting. These women also have a history of
through the brainstem. The trigger can be emotional, experiencing vomiting while using oral contraception,
hormonal or physical. motion sickness (during traveling) and migraine. There
Olfactory receptors, with dopamine receptor D2 (DRD2) may also be a family history. Helicobacter pylori is seen as
gene may be involved (it has been seen that women with causative agent in some.
congenital anosmia have very low incidence of nausea and
vomiting during pregnancy). Laboratory Investigations (Table 13.1)
Psychological factors also have an important role in its Many serum indices change during hyperemesis as
causation though the relation with vomiting is not well shown in Table 13.1. In moderately severe cases, there is
understood. hypochloremic metabolic alkalosis, but if the vomiting
In pregnancy the cause is not clear. It may be due to high is so prolonged as to caused dehydration, acidosis may
or rapidly rising serum levels of chorionic gonadotropin or occur. Fortunately, all these changes reverse to normal,
estrogen. once treated. Repeating these tests help analyze the
The probable relationship between human chorionic response of the patient to treatment and also allows to
gonadotropin (hCG) or a structural variant of hCG may exclude various differential diagnosis. The most sensitive
single test is thyroid-stimulating hormone (TSH) which is
Flowchart 13.1: Mechanism of vomiting always low in hyperemesis gravidarum. If it is normal, one
should look for other causes of vomiting.
Management (Flowchart 13.2)

General management:
Preconceptional multivitamin intake reduces the
incidence of nausea and vomiting in pregnancy

(prevention).
In mild cases, counseling and support from the doctor
and a strong family backing is essential. The patient and

the family must be told that it is a transient phenomena.
Frequent small feeds are advised. Foods causing
Abbreviations: hCG—Human chorionic gonadotropin; TSH—Thyroid- vomiting are to be avoided; use of ginger is advocated.
stimulating hormone; T4—Thyroxine; T3—Triiodothyronine Dietary changes may help. The patient should be given
Hyperemesis Gravidarum 119
Flowchart 13.2: Management of nausea and vomiting in pregnancy If there is no response, doxylamine 25 mg twice a
day is added. If there is still no control of vomiting
conventional antiemetics are offered (though concern
about fetus may hinder their use). Promethazine 25 mg
orally or rectally, trimethobenzamide 200 mg 6 hourly,
via rectum or prochlorperazine 25 mg every 12 hourly
rectally can be given.
If vomiting still persists
Admit the patient in the hospital.
Investigations: Ketones are measured in urine. Blood is
sent for estimation of serum electrolytes, liver enzymes,

amylase, TSH. Ultrasonography of the uterus (to rule out
multiple pregnancy or hydatidiform mole) is carried out.
The patient is kept nil per orally.
Intravenous (IV) hydration with isotonic fluid is
preferred.
IV dextrose solution is to be given only after IV thiamine
100 mg in 100 mL normal saline (slowly over 30 minutes)

to prevent Wernicke’s encephalopathy. IV fluids are
used to correct dehydration, electrolyte and acid base
imbalance and nutrition, till vomiting is controlled.
Antiemetics are continued.
Frequent, small, semisolid meals are given when the
patient is able to retain the feed.

Acupressure (by wrist bands) is an alternative treatment
to help early recovery.

Supportive psychotherapy is always needed. Psycho-
the food of her liking. Caloric intake or ratio of proteins,
fats and carbohydrates intake need not be controlled logical and social factors are important in counseling.
if the above measures are followed. A change of The perception of being trusted by the doctor is impor-
environment may help. tant.
If no relief is seen drugs may also be started. Pyridoxine If the vomiting persists, other causes of vomiting should
(vitamin B6) 10–25 mg every 8 hourly is administered. be ruled out.
1. What are the causes of nausea and vomiting in early pregnancy.
2. True/False:
i. If the vomiting is so prolonged as to caused dehydration, acidosis may not occur.
ii. In mechanism of vomiting DRD2 gene may be involved.
Spontaneous Miscarriage or
14 Abortion including Habitual or
Sudha Salhan, Indira Ganeshan, Harsha Gaikwad

Recurrent Miscarriage
colposcopy. It can produce irregular spotting or bleeding

VAGINAL BLEEDING
per vaginum during intercourse, if the erosion is
Vaginal bleeding in the first trimester is a common extensive, infected or traumatized, e.g. by examining the
complication of pregnancy and accounts for a significant cervix by speculum, performing a pap smear, etc. However,
percentage of maternal morbidity and mortality. The etiology it can also be associated with pregnancy in which case, the
is complicated and the causes can be classified as follows: presence of other signs or USG are helpful to confirm the
diagnosis.
Obstetric Causes of Bleeding in First Trimester
Implantation bleeding Cervical Polyp
Miscarriage (threatened, missed, inevitable, etc.) It is a benign mucoid or polypoidal growth from the
Ectopic pregnancy (see Chapter 15) uterine body or the cervix. It can give rise to metrorrhagia
Hydatidiform mole (see Chapter 16)
(irregular bleeding) and can present as a picture very
Implantation Bleeding similar to that of miscarriage.
This bleeding takes place about 6–8 days post-ovulation
Carcinoma Cervix
or fertilization caused by invasion of the decidua basalis
by the chorion. It is characterized usually by spotting or It is a malignancy of the cervix. It presents with irregular
slight bleeding for a day or two and can be confused with bleeding, postcoital bleeding or blood stained discharge
intermenstrual bleeding. Immunoassays, urine pregnancy per vaginum. Cervical biopsy is confirmatory. At times it
test or ultrasonography (USG) can rule out miscarriage. can be found concurrent with pregnancy.
Miscarriage
SPONTANEOUS MISCARRIAGE
The pre-embryonal period is defined upto first 5 weeks of
pregnancy from the first day of the last menstrual period. The Spontaneous miscarriage is defined as any recognized
embryonic period lies between 6 and 9 weeks of conception involuntary pregnancy loss occurring before the period
while the fetal period is from 10 weeks till delivery. of viability (without the use of any medical or mechanical
Miscarriage (previously called abortion) is defined as means to empty the pregnant uterus).
termination of pregnancy, by any means (spontaneous or
artificial) before 20 weeks (before the viability of fetus) or Incidence
when the fetus is less than 500 g in weight. Miscarriage is the most common complication of preg-
nancy because human reproduction is not an efficient
Non-obstetric Causes of Bleeding in mechanism.
First Trimester The actual incidence is difficult to assess. Approximately
Bleeding from Cervical Erosion 15% of documented pregnancies go waste. More than
It is a lesion over the cervix and can be diagnosed on 80% miscarriages occur before 12 weeks of gestation. A
visual inspection either by naked eye examination or by large number of embryos fail to implant, and pass off as a
Spontaneous Miscarriage or Abortion including Habitual or Recurrent Miscarriage 121
normal menstrual bleeding and thus the pregnancy goes Medical disorders: Relative risk of miscarriage is
unnoticed. The causes of early miscarriage are usually an increased in:
embryonic pregnancy or blighted ova. •• Cardiovascular disorders
•• Hypertensive disorders
Etiology •• Renal diseases
The exact cause is not known, but there are some factors •• Connective tissue disorders like systemic lupus
seen to be associated with miscarriage. erythematosus (SLE)
Chromosomal anomalies are responsible for at •• Chronic disease like celiac sprue
least half of all early pregnancy loss, e.g. autosomal •• Inherited thrombophilias.
trisomy, monosomy, triploidy, tetraploidy, structural Drugs and chemicals: Many drugs at higher doses and
abnormalities, dysfunction, etc. exposure early in the conception cause missed abortion
Maternal and paternal factors or have a teratogenic potential, e.g. ergot preparations.
•• Age: Extremes of maternal ages are very detrimen- Immunological causes: Antiphospholipid antibody
tal in human reproduction. Miscarriages are more syndrome and other immunological conditions cause
common after 40 years of age or in teenage pregnan- miscarriage (see Chapter 10).
cies. The incidence of miscarriage due to aneuploidy Previous history of miscarriage (especially less than 6
increases dramatically after the maternal age of 35 months before).
years. Reasons for this are not known but a genetic Anatomic abnormalities of the uterus
abnormality like isolated mutation or polygenic •• Congenital, e.g. Müllerian duct anomalies. Intra
factor may be present. As age advances, various uterine exposure to diethylstilbestrol (DES) may be
maternal factors also come into play contributing to the cause of congenital anatomical defects.
the pregnancy loss. Increased paternal age also lead •• Acquired Asherman’s syndrome, incompetent
to miscarriage due to paternal factors (ageing gam- os, embryo implanted on leiomyoma, may end in
etes and physiological systems). miscarriage.
•• Infections: Toxoplasmosis, other (syphilis, varicella- Personal habits
zoster, parvovirus B19), rubella, cytomegalovirus and •• Cigarette smoking does increase miscarriage rate
herpes (TORCHs) group of infections including syphilis especially aneuploidic ones (risk increases linearly by
may be a contributory factor in early pregnancy loss. a factor of 1.2 for each 10 cigarettes smoked per day).
•• Vaginal infection with group B streptococci, •• Alcohol consumption is also implicated by some
Mycoplasma hominis and Ureaplasma urealyticum. as causes of miscarriage during first 8 weeks of
•• Chlamydia trachomatis, Toxoplasma gondii, Neisseria pregnancy (it is computed that abortion risk increases
gonorrhoeae, Streptococcus agalactiae and Listeria by an average of 1.3 for each drink per day).
monocytogenes have been implicated in spontaneous •• Coffee consumption can also predispose to
miscarriage but their role is not yet established. miscarriage. More than 4 cups per day increases
•• Spontaneous miscarriage is independently associa the incidence in early pregnancy loss. High levels
ted with human immunodeficiency virus (HIV) of paraxanthine (a caffeine metabolite) in maternal
antibodies in the mother. blood are associated with miscarriages.
Endocrinological causes •• Radiation does cause missed abortion, but the exact
•• Thyroid autoantibodies and hyperthyroidism. dose is not clearly known.
•• Uncontrolled insulin dependent diabetes mellitus •• Contraception—intrauterine contraceptive device
especially in the first trimester leads to a marked (IUCD) failure may cause septic miscarriage in some
increase in the miscarriage rate. cases.
•• Progesterone deficiency: Manifest as luteal phase Trauma: Surgical trauma, like laparotomy during early
defect (LPD). pregnancy, may cause miscarriage. Peritonitis also
•• Androgen excess: Elevated serum levels of testos increases its incidence. Physical traumas like a direct
terone and dehydroepiandrosterone sulphate blow over the abdomen or gunshot wounds are stated
(DHEAS). as causes of miscarriage.
•• Polycystic ovary syndrome (PCOS): Elevated serum Paternal factors: Chromosomal translocation in
luteinizing hormone (LH) levels. the sperm may cause miscarriage. Besides aging and
immunological factors, some infections like adenovirus

or herpes simplex in the father may lead to miscarriage.
Environmental toxins: There is an increased risk
of spontaneous miscarriage in women anesthetists.

In addition arsenic, lead, formaldehyde, ethylene
oxide and benzene are also found to play a role in the
causation of early pregnancy loss. Increased exposure
to environmental pollutions as a cause of miscarriages
is under study. However, exposure to electromagnetic
fields (video display), shortwaves and ultrasound do
not cause miscarriage.
Spontaneous miscarriage could be categorized into:
Isolated incident
Recurrent abortions.
Pathology of Spontaneous Miscarriage

Hemorrhage into the decidua basalis is seen. Necrosis
Fig. 14.1: Threatened miscarriage
with inflammation is witnessed at the implantation site.
The products of conception are partially detached and lie
in the uterine cavity. This stimulates uterine contractions Period of amenorrhea (POA)
and dilatation of the cervix, thus expelling the conceptus. Time of onset of bleed and duration
But if the dead embryo/fetus is retained it may undergo Amount of bleeding (number of pads soaked)
maceration. Fetal skull bones collapse as there is no Any passage of product of conception (POC) or vesicles
muscle tone and its abdomen gets filled up with blood Any associated pain
stained discharge. Fetal internal organs degenerate and Was the pregnancy previously documented [by urine
get necrosed. Amniotc fluid gets absorbed, the fetus is pregnancy test (UPT) or ultrasound]
compressed upon itself. It may get dry and compressed by History of trauma
the uterine wall thus forming fetus papyraceous (mostly History of drug intake
seen in twins). Any history of interference (by dai or any other person)
Any febrile illness
Types of Spontaneous Miscarriage History of fainting attacks
Threatened miscarriage History of bleeding tendency.
Inevitable miscarriage
Incomplete miscarriage Clinical Examination
Complete miscarriage General condition of patient, her nutritional status
Missed miscarriage Pallor, temperature, pulse, blood pressure (BP)
Blighted ovum. Systemic examination
Per abdominal examination: Look for distension,
Threatened Miscarriage mass, free fluid or tenderness, size of the uterus, whether
This is a condition where the onset of the process of corresponding to the POA.
miscarriage is started but further progression can be Per speculum examination
averted (Fig. 14.1). The bleeding usually starts first, the •• Inspect the vulva, vagina and cervix for amount and
amount of bleed could be variable between mild to source of bleed.
moderate and rarely excessive. The bleeding is usually •• Any local lesion of cervix or vagina?
fresh red in color with or without mucus discharge in it. •• Is the cervix open?
The bleeding could be accompanied with pain; sometimes •• Any POC coming out through the external os?
the pain may start after a few hours of bleeding. •• Type (fresh or altered) and amount of bleeding.
History-taking should be complete. Points to be noted Pelvic examination (per vaginal examination): Do a
while taking history are: gentle digital examination to see the state of the cervix
(external os closed). See the size of uterus. It threatened To continue the medicines prescribed earlier.
abortion it corresponds to the period of gestation. Any Follow-up by β-hCG levels (if possible).
tenderness in the fornix or any mass are also noted.
Prognosis
Investigations In the majority of cases, the progress of threatened
miscarriage to inevitable or incomplete miscarriage can be
Lab investigations
averted, if immediate measures are taken. However, some
Urine pregnancy test (UPT)
percentage of patients will abort in the course of time.
Hemoglobin estimation
This possibility is increased if the bleeding starts early in
Blood group-ABO and Rh-typing
gestation. The long-term prognosis in these patients is good.
Serum progesterone level (optional)
Patients who have repeated bouts of bleeding have more
Serum beta-human chorionic gonadotropin (β-hCG)
chances of intrauterine growth restriction (IUGR), preterm
(only special cases).
labor and low birth weight (LBW) babies. However, the risk
Ultrasonography (USG): In early pregnancy transvaginal of fetal malformation is not increased in these patients.
ultrasonography is better than transabdominal scanning.
Points to be noted in ultrasound. Inevitable Miscarriage
Is it an intrauterine pregnancy, ectopic or molar preg This is a condition where the process of miscarriage has
nancy? progressed to a stage from where it cannot be averted
Look for fetal heart rate (viability). (Fig. 14.2). The patient gives a history of a POA followed
Is the gestational sac well formed and what is its position? by bleeding per vaginal. The amount of bleeding is again
Is it a singleton or multiple pregnancy? variable, but usually is more than that seen in threatened
Look for the position of the placenta whether it is at the miscarriage. The patient might give a history of leaking
upper segmentin or low lying. per vaginum due to rupture of membranes. This is usually
Is there any evidence of intrauterine collection of blood accompanied with severe abdominal pain.
or subchorionic hemorrhage?
Management
Treatment History (the points to be elicited remain the same as in
Assure the patient, as the patient may be anxious. threatened miscarriage).
Admit the patient and advise bed rest until the bleeding General physical examination: The patient is usually
stops. bleeding profusely so her general condition might not
Advise the patient to save her pads, to observe any POC be good. The patient may even be in shock.
or clot that is expelled out and to document the amount
of bleeding.
Pain relief and sedation with tablet phenobarbitone or
diazepam is to be given.
Intravenous (IV) fluid/oral fluid should be given to
correct any dehydration or hypotension (in case of
severe bleeding). This may need blood replacement too.
Hematinics, folic acid and calcium to be continued if
the gestational age is more than 12 weeks.
Anti-D prophylaxis to be given, if the patient is Rh-
negative with Rh-positive husband (100 µg IM).
Follow-up
The patient is advised to rest till the bleeding stops and
not to exert herself.
The patient should abstain from sexual intercourse.
A repeat USG after 3–4 weeks to note for the viability
and growth of the fetus. Fig. 14.2: Inevitable miscarriage
Pulse rate may be increased (tachycardia) and BP might for gastrointestinal tract (GIT) side effects of the drug.
be maintained or low. The patient may be pale, but this Parenteral prostaglandin is relatively contraindicated in
also depends on her previous hemoglobin level. patients with a history of previous uterine scar or with
Per speculum examination: Internal and external compromised lung pathologies (like asthma). These
os are open, clots and POC could be seen protruding days oral prostaglandin like misoprostol are also used
through the external os along with bleeding or POC in place of injectables.
could be seen in the vagina. After the fetus and placenta are expelled, an USG can
Pelvic examination: Clots and POC may be felt in the be performed and if the uterine cavity is empty the
vagina. Internal and external os are open, the size of the patient can be given methergine orally IM/IV to control
uterus is smaller than the POA or may correspond to it. excessive bleeding.
Sometimes POC can be felt lying in the cervical canal. In cases where fetus is expelled and the placenta is
retained, the placenta can be removed with ovum forceps
Investigations or by digital evacuation under general anesthesia or
Hemoglobulin estimation, blood grouping and cross- give 600–800 µg mesoprostol and wait for spontaneous
matching, urine routine examination, other investigations expulsion.
for pre-anesthetic checkup. In rare cases, the patient might have to be taken up for
Ultrasonography (not always needed). Usual findings are: hysterotomy.
Cardiac activity is usually absent.
The products of conception should always be sent for
POC are separated from the decidual attachment.
histopathological examination (Fig 14.3) to confirm
Products are usually seen lying in the lower part of the
conception and to rule out hydatidiform mole and
uterine cavity or cervical canal. choriocarcinoma.
Treatment Follow-up
Antibiotics, oral methylergometrine and hematinics are
Admit the patient. Treatment will start with correction
prescribed.
of the patient’s general condition and hypovolemia with
Anti-inflammatory agents and pain killers are advised.
the use of crystalloids and colloids. If required, blood is
Anti-D prophylaxis is given in Rh-negative patient
arranged and transfused. The patient should preferably
whose husband is Rh-positive (100 µg IM).
have two patent IV accesses by number 16 or 18 cannulas.
The patient is started on oral contraceptive pills for 3
The patient should be immediately prepared and taken
months, to help her endometrium to heal better and for
up for evacuation in the operation theater (OT) after
regulation of the hypothalamopituitary ovarian axis.
taking a consent. Injection tetanus toxoid (TT) 0.5 mL The patient is asked to report immediately if the
intramuscular (IM) should be given. bleeding increases, if there is fever or pain in the lower
In first trimester miscarriages: In patients whose preg abdomen. Otherwise she can report after 6 weeks for
nancy is less than 12 weeks of gestation, the procedure investigation of the cause of miscarriage.
performed is usually dilatation and evacuation (D&E) or
suction evacuation or manual vaccum aspiration (MVA)
under local anesthesia.
In second trimester miscarriages
Oxytocin IV drip with 10 units oxytocin in 500 mL
ringer lactate is started. The dose is then gradually

escalated till good uterine contractions are established
or the patient aborts the fetus (maximum 40 units in one
bottle). Special precautions should be taken to avoid
fluid over load and electrolyte imbalance, because of
antidiuretic hormone (ADH)-like action of oxytocin.
If the patient is hypotensive, oxytocin drip is a relative
contraindication.
Injection prostaglandin F2a (PGF2α) 250 mg IM
Fig. 14.3: Histopathology of products of conception
3 hourly can also be given till the patient aborts the Courtesy: Dr Hari Om Gupta and Dr Rashmi Arora, VMMC and
fetus. Special precautions in this case should be taken Safdarjung hospital
Tetanus and anti-D prophylaxis are given to the patients

who require it
Pain relief is provided.
Surgical procedure: D&E, suction evacuation or MVA.

In some cases, where the patient is stable and there is no
active bleeding use of misoprostol may suffice (medical
management) instead of surgery because both the
immediate and late complications are less with medical
management.
Follow-up: Same as in the previous case.
Complete Miscarriage
In this condition the patient had been pregnant, which
is followed by bleeding per vaginum and expulsion of all
the products of conception from the uterus. The cavity is
completely empty at the time when patient presents in
Fig. 14.4: Incomplete miscarriage
hospital. She may bring the expelled products with her.
Examination: The general condition of the patient is
usually stable. Pulse and BP are normal.

Investigations like blood sugar, venereal disease research
Per speculum examination: Bleeding may or may not
laboratory (VDRL), TORCH and if required, immuno
be observed at the vulva and vagina.
logical profile may be advised (to prevent recurrence, if
The external os is closed with no or minimum bleeding.
possible).
Pelvic examination: The size of the uterus is normal
She is advised against conception for 6 months. or slightly bulky but never corresponds to the POA. The
consistency of the uterus is firm.
Incomplete Miscarriage
USG finding: The uterus is usually normal in size or
In this condition, the patient has already aborted a major bulky and the cavity is found to be empty.
part of her conceptus and only some amount is left in � Management
the uterine cavity (Fig. 14.4). The patient gives a history •• If the patient is bleeding, methylergonovine is advised.
of amenorrhea followed by bleeding per vaginum with •• Antibiotics may be prescribed, if infection is
history of passage of clots and POC. The patient might not suspected.
be bleeding actively when she attends the hospital. •• Hematinics and calcium are to be prescribed.
On examination: The general condition depends on •• Oral contraceptives are given for 3–6 months.
the amount of bleeding and her hemodynamic status. Follow-up and investigations are the same as described
Per speculum examination: Bleeding may or may not in the previous case.
be seen in vulva and vagina. The os may be closed.
Pelvic examination: Os may be closed and may feel Missed Miscarriage (see Fig. 62.7)
firm. In some cases the os is open. The size of the uterus It is the death of the fetus before 20 weeks of gestation with
will not correspond the POA (smaller than period of retention of all POC. In this condition, the fetus dies in utero
gestation). but instead of getting expelled is retained for a variable
Investigations: Same as in inevitable miscarriage. period of time. The cause responsible for this retention is
USG findings not exactly known but there is a hypothesis that the estrogen
Uterine cavity will show POC falls reducing the contractility. The fetus which dies after 12
Cardiac activity will not be localized weeks may undergo maceration (aseptic autolysis) or may
The fetus is usually not seen. mummify as the liquor is absorbed. The fetus dies without
any symptoms of spontaneous miscarriage. The patient
Management gives a history of regression of all symptoms of pregnancy
Admit the patient and correct hypovolemia and the diagnosis is made only after clinical examination
Antibiotics are started by a doctor and confirmed by ultrasound.
Carneous Mole Coagulation profile

The bleeding and clot from a missed miscarriage can Investigations for preanesthetic checkup (PAC).
become organized and laminated; termed as carneous Surgical Procedures
mole. Histologically, there is an ovum or macerated fetus Category I
surrounded by clotted blood with a disorderly capsule of
Pregnancy less than 12 weeks.
varying thickness and evidence of degenerated chorionic
Suction evacuation, D&E or MVA under antibiotic cover.
villi scattered through it. If the pregnancy has been of a
Special precautions to be taken during evacuation to
relatively longer duration, a collapsed skull may also be
keep a watch on the amount of bleeding as coagulation
seen in the center.
disorder may be precipitated because of consumption
coagulopathy.
Clinical Features
Medical management with misoprostol may be tried
The patient gives a history of amenorrhea and typical signs under strict supervision.
and symptoms of pregnancy. These signs usually regress
after sometime but amenorrhea continues. Some patient Category II
may give a history of a brownish or dark-colored vaginal Pregnancy more than 12 weeks.
discharge. Clinical examination and ultrasound scan may Mesoprostol or dinoprostone gel instillation to soften
be the only methods for establishing the diagnosis. the cervix is followed by oxytocin drip. A close watch
is kept for expulsion of the products of conception.
On Examination Surgical evacuation may be needed.
The general condition is stable unless the patient is
bleeding. Vitals are usually maintained. Follow-up
Per abdominal examination: Fetal heart sound (FHS) Antibiotics are prescribed.
will not be localized with USG or Doppler. Tablet methergine 3 times a day for three days is advised.
Per speculum examination: Brownish discharge may Anti D prophylaxis is given to an Rh-negative patient
be observed though the os which is usually closed. whose husband is Rh-positive (100 µg).
Pelvic examination: The external os is closed and feels Investigation of miscarriage are advised.
firm. The size of the uterus is less than the POA. Oral contraceptives are given for 3–6 months.
Investigations Blighted Ovum

Urine pregnancy test (UPT): May be negative. It is diagnosed ultrasonologically. In this, the patient had
Serum b-hCG levels can be either very low or not amenorrhea which may be followed by bleeding. There is an
correspond to the POA. absent or a degenerated embryo. USG reveals a gestational
Ultrasound findings sac but no fetal pole is visualized. Fetal tissue is absent on
Cardiac activity is absent. histological examination of the products of conception.
Evidence of collapse of fetal skeletal system or a Management: Evacuation of the uterus or medical
collapsed fetal skull is seen if the pregnancy had been management with misoprostol if the patient is stable.
of more than 16 weeks duration.
Septic Miscarriage
Management of Missed Miscarriage and When an outside interference is done or the patient’s
Carneous Mole general immunity is low, the miscarriage might turn into
a septic one. This is treated vigorously with antibiotics,
Admit the patient and investigate.
evacuation and blood transfusion.
Lab Investigations
Hemoglobin, platelet count
RECURRENT OR HABITUAL MISCARRIAGE
Blood group and Rh-typing Recurrent or habitual miscarriage is defined as three or
Bleeding time (BT), clotting time (CT) and clot retrac more consecutive spontaneous miscarriages, without an
tion time (CRT) intervening live birth. This is a very distressing condition,
Blood fibrogen level hence need elaboration.
ovum or some fault in the pregnancy rather than it being

ETIOLOGY
a cause of early pregnancy loss. 17-hydroxyprogesterone
The exact etiology is not completely understood, but the is a better marker than serum progesterone.
following factors are contributory: Thyroid function abnormalities: Hypothyroidism is not
Genetic abnormalities a usual cause of abortions, but thyroid autoantibodies
Endocrine factors are associated with an increased incidence of pregnancy
Infections and chronic diseases loss despite no overt hypothyroidism.
Anatomic abnormalities of the uterus Diabetes mellitus: Patients with elevated glycosylated
Immunological causes hemoglobin levels (uncontrolled state) and elevated
Defective placentation. blood glucose levels in the periconceptional and early
conceptional period have a higher incidence of sponta-
Genetic Abnormalities neous abortion. Impaired glucose tolerance test (GTT),
Eighty percent of miscarriages in this category occur at hypertension, hypertriglyceridemia and a procoagulant
less than 8 weeks and are often associated with a blighted state (syndrome X) may also cause recurrent miscar-
ovum. Chromosomal abnormalities most commonly riage.
found in miscarriages are: Maternal hyperandrogenicity: Elevated levels of
Autosomal trisomy: Like chromosome 16, 21 and 22. serum testosterones and dehydroepiandrosterone
The most common is trisomy of chromosome 16, which sulfate (DHEAS) (either from ovarian or adrenal glands
is due to non-dysfunctional defects. or both) cause dysfunction of corpus luteum. The
Monosomy X: The karyotype usually seen in this mechanism is not well understood but androgens may
category is 45X. Many of these are not aborted and be an extra glandular source of estrogen.
present at birth as Turner’s syndrome. This occurs as a Polycystic ovarian disease (PCOD): The chances of
result of loss of X chromosome at the time of fertilization spontaneous abortion are more in these patients as
or because of non-dysfunction. compared to the rest of the population. The elevated
Triploidy: The sac might be empty or may have a malformed serum LH levels seen in this condition may cause
fetus. The cause is double fertilization of a single ovum. corpus luteal dysfunction. This high level may also
Tetraploidy directly influence the oocyte and the endometrium or
Isolated mutation or polygenic factors. indirectly the ovarian hormone production. Increased
Inherited thrombophilia in the mother. levels of LH concentration throughout the cycle (a
single high level is not predictive) increases the chance
Reasons of miscarriage.
Error in maternal or paternal meiosis. Premature ovarian failure: In this condition the oocytes
Fertilization of one ovum by more than one sperm. are defective and may cause repeated miscarriage.
A chromosomal division takes place but no cytoplasmic
division occurs. Infections and Chronic Diseases
Ascending infection: This is not a common cause of
Endocrine Factors abortion, as fetal membranes are protective. The patient
Progesterone deficiency: Progesterone is important to complains of uterine cramps and fever, and may have
maintain the quiescence of the uterus. It is beneficial leaking or bleeding per vaginum. The placenta shows signs
only in patients with luteal phase defects (LPD) and in of chorioamnionitis. The organisms which are implicated
cases of insufficient progesterone production by the are as follows:
corpus luteum or placenta. Patients with recurrent Group B streptococci
miscarriages have a greater incidence of LPD than the Escherichia coli
general population. However, the level of the serum Mycoplasma hominis
progesterone concentration during pregnancy as a Ureaplasma urealyticum
diagnostic measure, is not a very reliable method, Chlamydia
as its production is pulsatile and there is a marked Genital herpes simplex
fluctuation in the serum levels. Secondly, the low serum HIV
progesterone level may be consequence of a blighted Maternal syphilis.

A B
Figs 14.5A and B: A. Bicornuate uterus at laparotomy; B. Uterine horns on hysterosalpingography
Chronic illness like celiac sprue has been seen to cause due to surgical trauma to a large area of the endometrium
habitual miscarriage. by curettage or intrauterine infections leading to varying
degrees of obliteration of the uterine cavity depending
Anatomic Abnormalities of the Uterus on the degree of adhesions. Cervical incompetence is
These are responsible for 15% of all abortions with normal associated with recurrent second trimester pregnancy
fetal development. The anatomic abnormalities of the loss. The fetus is normal in such cases but is not retained.
uterus can be categorized into—congenital defects of The most common cause is acquired, following surgical
uterus, acquired defects of uterus. procedures like D&E, dilatation and curettage (D&C) and
Congenital defects of the uterus can be Müllerian duct
medical termination of pregnancy (MTP) or following
abnormalities, defects due to DES exposure in utero, cone biopsy of the cervix, cauterization or amputation.
or cervical incompetence. The Müllerian anomalies Rarely, cervical incompetence can be congenital.
can involve formation or fusion like septate uterus,
The size of a fibroid is not important but is the location
bicornuate uterus or unicornuate uterus. These are
of placenta in relation to the fibromyoma plays a significant
associated with early pregnancy losses because of
role in causing abortions.
deficient blood supply or because of implantation in
the relatively avascular endometrium or septum (Figs Immunological Causes
14.5A and B).
DES exposed uterus is usually a small T-shaped There is an increasing incidence in more than 30 years
uterus and can also have incompetent cervix; this [delayed child bearing in both natural and in vitro fertiliza
usually causes late or second trimester abortions. DES tion (IVF)]. The immunological causes include:
Autoimmune factors
exposure may also result in cervical hoods on Cocks
Positive antinuclear antibody (ANA) titers
Coombe cervix (transverse septa between the cervix
and vagina), hypoplastic uterus and cervix, constriction Alloimmune factors.
bands, widening of the lower two-third of the uterus.

The chances of occurrence of vaginal adenosis are more Autoimmune Factors (Immunity against Self)
than that vagina of clear cell carcinoma. Approximately 15% of recurrent pregnancy loss have
Acquired defects of uterus include an incompetent a recognized autoimmune factor. High levels of antipho
cervix, Asherman’s syndrome and fibroid uterus. spholipid (APL) antibodies [immunoglobulin G (IgG),
Asherman’s syndrome or uterine synechiae can occur IgA or IgM isotopes] lead to repeated miscarriages.
The frequency of miscarriage in the untreated group in Defective Placentation

this condition is almost 85–90%. There are several anti- During normal placentation the spiral arteries undergoes
phospholipid antibodies of which the most relevant are adaptive changes; the lack of these changes has been
lupus anticoagulant, anticardiolipin antibodies and the
named as abnormal placentation. This type of abnormal
antibodies that cause false positive syphilis test. The
placentation is seen in pre-eclampsia, severe IUGR,
majority of pregnancy loss is in the second trimester. Fetal
preterm labor and also in some cases with early fetal deaths.
death is caused by extensive thrombosis and infarction of
The frequency of abnormal placentation is the same for
placental vessels. Inhibition of endothelial cell product—
both chromosomally defective or normal fetuses. The
prostacyclin release, causes vasoconstriction and platelet
patients who have recurrent early pregnancy loss because of
aggregation hence facilitating thromboxane A2 action and
abnormal placentation are at a high-risk of developing pre-
thus resulting in thrombosis. There is also inhibition of
eclampsia and IUGR beyond the second trimester.
protein C activation. APL antibodies also directly produce
cellular injury to trophoblasts and inhibits syncytium
formation. The fetus is morphologically normal and there MANAGEMENT
are no other maternal factors detected. Despite these extensive tests, there are certain cases of
repeated miscarriage, where a cause cannot be found. The
Antinuclear Antibody (ANA) first and the most important point in evaluation of a patient
Patients with recurrent miscarriage who have positive with recurrent miscarriage is eliciting a detailed history
ANA titers should be investigated for other autoimmune and thus categorizing patients into early first trimester, late
factors and anti-DNA antibodies as well. first trimester and second trimester abortions. Further the
patient needs to be asked or records to be obtained to see
Alloimmune (Immunity against Another whether the baby was normal or abnormal, structurally
Person-Fetus and Father) Factors and genetically. Communication skills are very important
This factor is under further investigation. It is diagnosed in these high-strung women with previous pregnancy
by maternal and paternal human leukocyte antigen (HLA) losses.
comparison, detection of cytotoxic antibodies to paternal
leucocytes and testing for blocking factors for maternal- HISTORY
paternal mixed lymphocytic reactions. Immunological
abnormalities also include antithyroid antibodies, History should include the following points:
antiovarian antibodies, an increase in natural killer (NK) Was the pregnancy confirmed by laboratory test or
cells, decreased suppressor T-cells, IgA deficiency and USG?

endometriosis. What was the duration of amenorrhea before miscarri
ages took place?

Therapy Was it a genetically normal fetus or congenitally mal
Many IVF techniques have been advocated for women formed?

with recurrent pregnancy loss which, though useful in Did any cardiac activity appear before bleeding or not?
women with anatomic or genetic abnormalities, may be (any previous ultrasound report).
successful in only 12–24% and as low as 1–2% (in older Was the patient on any kind of prolonged treatment?
women). Corticosteroid therapy has been shown to be Any personal or family history of autoimmune disorder?
ineffective for immunologic miscarriage and can even Any history of endocrine disorder?
cause many complications during pregnancy (especially Any history suggestive of a sexually transmitted disease
preterm delivery). Several studies have shown significant like syphilis?

benefits of intravenous immunoglobulin (IVIg) treatment Any history of gynecological procedure undergone,
(either standard dose 400–500 mg/kg or low dose 200–250 e.g. D&E/D&C cone biopsy (to rule out cervical
mg/kg) in women with recurrent miscarriages. A study incompetence and Asherman’s syndrome)?
showed overall pregnancy success rate in the IVIG treated Any live issues (children) before?
group to be 80–88% and it appeared to be safe and effective Any history of genetic abnormality in the partner or family?
in older women. The results of larger controlled clinical Menstrual history, amount and regularity of the
trials are still awaited. menstrual cycle (to rule out PCOD).
Per speculum examination

INVESTIGATIONS
Exclude any vaginal infection. Take a swab for culture
Baseline investigations include and sensitivity and smear.
•• Hemoglobin (Hb), total leukocyte count (TLC), dif- Examine the external os.
ferential leukocyte count (DLC) and erythrocyte sed- See whether it is patulous, i.e. easy passage of number
imentation rate (ESR). 6 to 8 Hegar dilator, absence of internal os snap on
•• Blood sugar—fasting and postprandial its withdrawal, supracervical Foley’s balloon test and
•• VDRL of both partners Bragman’s traction test to be performed if indicated
•• Blood group and Rh-typing to rule out cervical incompetence in a non pregnant
•• Urine routine examination for any proteinuria and patient. Transvaginal ultrasound is preferred in a
reducing substances and microscopy. pregnant patient-measure cervical length and diagnose
� Special tests funneling (ballooning and passage of the membranes
•• Semen analysis into a dilated internal os while the external os is closed).
•• Thyroid profile Rule out Müllerian duct anomaly, e.g. double cervices,
•• Glycosylated hemoglobin level vaginal septum, etc.
•• Serum insulin (fasting) Per vaginal examination: To assess the size of the uterus,
•• TORCH consistency of the cervix and to look for any other mass
•• Anticardiolipin antibodies which could be palpated, like rudimentary horn.
•• Antiphospholipid antibodies
Pre-conceptional treatment: Checkup is done by all the
•• Lupus anticoagulant antibody
above parameters. If a cause is detected it is managed
•• Anti-DNA antibody
accordingly. Use of heparin and aspirin before pregnancy
•• Hormone profile [follicle-stimulating hormone (FSH),
may help. If there are congenital causes, karyotyping of
LH, prolactin]
both the partners and their affected child is carried out.
•• If a hyperandrogenic state is suspected:
In hyperandrogenism, suppression of ovarian androgen
–– Serum total and free testosterone
by gonadotropin-releasing hormone (GnRH) agonists
–– 17-α hydroxyprogesterone level
and adrenal androgen by dexamethasone may be
–– DHEAS levels
fruitful.
•• Karyotype
In preconceptional diagnosis of incompetent cervix,
•• USG pelvis
some surgeons perform preconceptional cerclage.
•• Hysterosalpingography (HSG) (before pregnancy)
However, if diagnosis is known, cerclage can be done
•• Hysteroscopy (before conception)
early in pregnancy. Control of diabetes before pregnan-
•• Laparoscopic evaluation of the pelvis and abdomen
cy with insulin is very rewarding.
(optional)
•• Magnetic resonance imaging (MRI) for anatomical
defects of the uterus (optional) or cervix (before TREATMENT OF SPECIFIC
pregancy). ETIOLOGY (TABLE 14.1)
Luteal Phase Defect
EXAMINATION Estimation of blood or urinary LH daily will reveal hypo
General observation of patient for health and nutriti secretion of LH, if present.
onal status Assessment of luteal phase is done by:
Height, weight and body mass index (BMI) of the patient Progesterone level at day 21 (in a 28 day cycle): Less
Pulse rate, BP and respiratory rate than 10 ng/mL

Look for anemia, galactorrhea, thyroid or a lymph node Endometrial histology and dating
swelling, hirsutism Serial ultrasound evaluating the endometrium (thick
Position of breasts, distribution of hair (rule out any ness, echogenicity)

hirsutism) Color Doppler—detection of vascularity
Systemic examination: Per abdomen examination—look Daily salivary progesterone
for any mass, scar of surgery, free fluid and inspect the Progesterone associated endometrial protein (PAP) level
hernial orifices. Progesterone receptor assay.

TABLE 14.1: Management of recurrent pregnancy loss

First trimester abortions Find genetic or non-genetic origin
Luteal phase defects Progesterone supplement
PCOD Pituitary suppression with GnRH analogs followed by ovulation induction
Hyperandrogenism Treatment with prednisone
Abnormal placentation Low dose aspirin and dipyridamole
Uterine anomalies Surgery, IVF
Immunological causes Low dose aspirin and prednisone or aspirin, heparin and IVIG
Cervical incompetence Cervical cerclage operation
Abbreviations: PCOD—Polycystic ovarian disease; GnRH—Gonadotropin-releasing hormone; IVF—In vitro fertilization; IVIG—Intravenous
immunoglobulin
In these patients progesterone supplements in the form dose heparin. The dose of heparin is 5000 units 12 hourly.
of vaginal pessary, vaginal gels or injectable progesterone It has been seen to be successful in 80% patients.
are recommended. Treatment with heparin also helps in inherited throm-
bophilia. For alloimmune causes different therapies are
Polycystic Ovarian Disease Tests under trial, viz. injection of paternal leukocytes or pooled
Patients are advised pituitary suppression with GnRH human immunoglobulin and low dose IVIG.
analogs and induction of ovulation followed by hCG The overall response rate to allogenic lymphocyte
injection. These patients after conception, are further immunization (ALI) has not been encouraging.
supported with progesterone preparations. LH levels
can be reduced by diathermy of the ovary. Laparoscopic
Cervical Incompetence
electrocautery of the ovarian surface (LEOS) helps in This group suffers second trimester pregnancy loss. The
spontaneous ovulation and achievement of conception in patient complains of leaking per vaginum followed by
some patients. painless dilatation of the cervix. The fetus is later expelled.
On per speculum examination the cervix will be seen to
Hyperandrogenism be open, and membranes can be seen bulging through the
Patients who have androgenism of adrenal origin will external os. On ultrasound the cervical length is less than
benefit from treatment with dexamethasone. 3 cm and the internal os is open. In non pregnant patients
cervical incompetence can be diagnosed by passage of 6
Abnormal Placentation and 8 Hegar dilator beyond the internal os. Funneling of
These patients are recommended low dose aspirin and the cervix is seen on USG and HSG (before pregnancy).
dipyridamole. The treatment is cervical cerclage. Contraindications of
cervical encirclage include any bleeding during pregnancy,
Uterine Anomalies uterine contraction or ruptured membranes.
Patients with uterine anomalies may benefit from surgery In an incompetent cervix, the width of the internal os is
more than 1.5 cm in the first trimester, more than 2.0 cm in
for resection of uterine septum or adhesiolysis of synechiae
the second trimester and the lower uterine segment is V or
with an operative hysteroscope. Patients having a bicornuate
U shaped not the normal Y.
uterus may sometimes be recommended metroplasty.
Funnel length + 1
Cervical index =
Immunological Causes Endocervical length
It is normally 0.32. A cervical index 0.52 is indicative of
Patients suffering from the antiphospholipid antibody an incompetent cervix.
syndrome have been seen to benefit from low dose aspirin
and prednisone. These drugs are started as soon as the Indications of USG in Recurrent Pregnancy
patient is tested positive for pregnancy or just before To know the gestational age of pregnancy and viability
conception. The dose of aspirin is usually 80 mg per To rule out blighted ovum
day and prednisone is 40–60 mg per day. This treatment To rule out morphological and structural abnormalities
culminates in live births but had greater maternal and fetal of the fetus
morbidity. In another protocol aspirin is given with low To rule out cervical incompetence
To evaluate the placenta for abnormal placentations To rule out uterine septum, especially with three
and to grade the placenta dimensional (3D) and 4D scans
To study the Doppler parameters To rule out LPD, by measuring endometrial thickness
In patients of Müllerian duct anomaly, to see the size, To rule out Asherman‘s syndrome or uterine synechiae,
shape and number of uteri with 3D or 4D scans.
1. Briefly explain vaginal bleeding and its classification during early pregnancy.
2. Why genetic abnormalities occurs? Give reasons and justify.
3. Name the types of spontaneous miscarriage.
4. True/False:
i. Anti-D prophylaxis to be given, if the patient is Rh -ve with Rh +ve husband.
ii. PCOS stands for polycystic oral syndrome.
iii. Is diabetes a genetic abnormality.
15
Sudha Salhan
Ectopic Pregnancy
infection. Many ectopic pregnancies have history

INTRODUCTION
of salpingitis. Salpingitis causes damage to the
Ectopic pregnancy (EP) occurs when a fertilized ovum fallopian tubes, especially to the lining of the
(embryo) implants outside the uterine cavity. If not tubes. It damages cilia and hence hinders the
diagnosed promptly, it is a life-threatening condition propulsion of fertilized ovum towards the uterus.
leading to maternal morbidity and mortality. In the past, Other anatomical changes caused by infection are
it was diagnosed only on postmortem examination. We adhesions in the tubal cavity, e.g. in tubercular
still get patients in critical stages in our hospital. salpingitis. This causes entrapment of the fertilized
Incidence: The exact incidence is not well-known, but ovum in the fallopian tubes. Fallopian tubes
it has increased after 1970 partly because of higher are also affected secondary to pelvic peritonitis
prevalence of risk factors and partly because of the caused by appendicitis or other causes. As a result,
development of more sensitive diagnostic techniques. tubal pregnancy is more common on the right
Higher incidence of salpingitis, increase in ovulation side. Since tubal disease is always bilateral, there
induction, assisted reproductive technology and more is a strong tendency for EP to occur first on one
tubal sterilization has in creased the incidence. The side and then recur on the other side in another
incidence of second ectopic pregnancy is 10–15%. pregnancy.
•• Distortion of the tube externally by a large tumor
EPIDEMIOLOGY or endometriosis, etc. may also cause ectopic
pregnancy.
The exact etiology of ectopic pregnancy is not well- •• Tubal sterilization and tuboplasty (post ectopic
known. But there are many risk factors, which lead to pregnancy, post salpingitis) and recanalization
ectopic pregnancy. The major ones are given below: and other tubal surgeries make the fallopian tubes
Factors of the fallopian tubes structurally vulnerable to EP.
•• Development errors: Hyperplasia, hypoplasia, undue Surgical obstruction: After tubal sterilization,
tortuosity of a segment of fallopian tube, congenital the fertilized ovum sometimes implants on the
absence of a segment of fallopian tube, fistula, stump of the tube or sometimes spontaneous
congenital diverticula and intramural polyp. Rarely, recanalization occurs with narrowing of the lumen
congenital abnormalities of the tubes are seen due to results in ectopic pregnancy. The author has seen
diethylstilbestrol (DES) exposure in the fetal life. cases who undergo MTP before 6 weeks pregnancy
•• History of previous inflammation of the tubes (where the fertilized ovum has not reached the
(Salpingitis) is present in 50–60% patients due to uterine cavity) leading to EP. The surgical procedure
septic miscarriage, medical termination of pregnancy of MTP causes removal of decidua from the uterus;
(MTP) by surgical means, pelvic inflammatory and there is blockage of uterine ostia (opening
disease, tubercular salpingitis, etc. of fallopian tubes in the uterus) due to reactive
At present, the Chlamydia trachomatis infection edema. Hence, the fertilized ovum is trapped in the
is most common. It is a very slowly damaging fallopian tube and iatrogenic EP happen.
Fertility regulatory methods: Intrauterine contra

PATHOLOGICAL ANATOMY
ceptive devices (IUCD) per se do not increase EP. But
they may be more effective in preventing intrauterine (FLOWCHART 15.1)
pregnancy and pregnancy in the medial half of the As seen in the flowchart, changes in fallopian tubes,
tube, than lateral part of the tube. The incidence of uterus and general reaction occur.
tubal pregnancy is slightly higher with progesterone- The common sites are as follows (Fig. 15.1):
containing IUCD. If IUCD inserted with all aseptic Fallopian tube: Most of them occur in the lateral half
techniques, there is no increase in salpingitis. In
of the fallopian tubes—95%
99.5% of cases, the EP is in the lateral half of the
Infundibulum and fimbrial end—17%
fallopian tubes. Similarly, users of progesterone only
Ampula—55% (most common)
oral contraceptive have a higher incidence of EP.
Isthmus—20–25% (more dangerous)
This is probably because these contraceptives are
Interstitial—2–4% (in the intramural portion of the
supposed to limit propelling effect of fallopian tube at
the ampullary-isthmic junction resulting in trapping tube, where it traverses the wall of the uterus).
Rudimentary horn of bicornuate uterus
of fertilized ovum and hence EP.
Cervix
Assisted reproductive technologies are shown to
Abdominal cavity
increase the incidence of EP due to an increased
number of ova in seminated. Broad ligament
Over development of the ovum due to delay in Cesarean section scar
transport may cause EP. Heterotropic pregnancy (combined pregnancy) is
Endometriosis pregnancy occurring simultaneously in the fallopian

Smoking tube and uterine cavity. The previous incidence was
Causes in the embryo: The embryo may have severe around one in 30,000 pregnancy. The incidence has
growth anomalies. increased with in vitro fertilization (IVF) techniques
Flowchart 15.1: Pathological anatomy of ectopic pregnancy

Ectopic Pregnancy 135
Fig. 15.1: Sites of ectopic pregnancy Fig. 15.2: Culdocentesis

Abbreviation: POD—Pouch of Douglas
to more than 1.2%. A viable intrauterine pregnancy is due to an increased level of progesterone. Cervical
seen on ultrasound which is exactly what was wanted. motion tenderness (due to stretching of fallopian tubes
The radiologist may miss the heterotopic pregnancy if in EP) may or may not be present. It is also called pain
he/she does not keep it in mind to look at the fallopian of cervical excision. On moving the cervix, the uterus
tubes as well. moves in the opposite direction. There is increased
Chronic EP. tension on the side of the EP and it causes pain. After
rupture, there is tachycardia, hypotension and signs
of shock, depending on the amount of hemorrhage.
DIAGNOSIS OF ECTOPIC PREGNANCY
Abdominal tenderness with or without distension and
Not very long back, EP was diagnosed only on post- cervical motion tenderness is present.
mortem examination. However, now, advances in Pregnancy test: Urine pregnancy test is positive in
diagnostic techniques have made it possible to diagnose 50–60% of EP cases. A negative pregnancy test is of no
it even before rupture. Meticulous history, examination value. Culdocentesis will yield blood which does not
and diagnostic tests are required for the diagnosis of EP. clot.
History: The presentation is variable. A higher index Culdocentesis is a simple technique to identify hemo-
of suspicion is a must. The three common symptoms peritoneum (Fig. 15.2).
amenorrhea, pain and bleeding may not be always A 20 gauge spinal needle is introduced through the
present (in 50% cases). posterior vaginal fornix into the cul-de-sac.
A history of amenorrhea of a few days or none with If the patient is stable, further diagnostic tests are
severe pain abdomen and fainting attack or the patient required to confirm EP.
is in a state of shock may be all that the doctor has to Ultrasonography: It is useful in the diagnosis and
look upon. There may be no need and no time for any management of EP. A positive pregnancy test with
investigation in cases of a ruptured ectopic except empty uterus is suggestive of EP. Transvaginal
hemoglobin (Hb) and blood group examination. ultrasound (TVS) gives a clear image of pelvic organs
Physical examination is performed to confirm the and intrauterine pregnancy at 5 weeks. If the uterine
diagnosis. Additional tests are often needed to establish cavity is empty, the fallopian tubes may show the
the diagnosis and to assess the risk factors. It includes fetus. Color Doppler may show a ball of fire around
eliciting vital signs and examination of the abdomen the EP. Fluid in pouch of douglas (POD) signifies
and pelvis. Before rupture, vital signs may be normal. rupture of the EP.
Abdomen may have mild tenderness with or without An adnexal mass with fetal heart is EP in unruptured
rebound tenderness. The cervix and uterus feel softer EP (Fig. 15.3).
Fig. 15.3: Ultrasonography of ectopic pregnancy Fig. 15.4: Right cornual ectopic pregnancy (laparoscopic photo)
Courtesy: Dr Rajesh Uppal, Uppal Diagnostics, Delhi
Other tests corroborating the diagnosis of EP are: Raised interleukin (IL) and tumor necrosis factor-2
•• Low Hb% alpha (TNF-2a) levels in the serum are higher in EP
•• Increased leukocyte count than in normal pregnancy and miscarriage.
•• The erythrocyte sedimentation rate (ESR) might be Glycodelin serum levels are significantly lower in
increased EP compared with intact pregnancy and abortion

•• Raised serum bilirubin is chronic EP. (glycodelin is a glycoprotein of the lipocalin super
•• Presence of porphyria in urine—suggestive of family which has a major role in the reproductive axis).
hematoma formation. Serum placental protein 14 (PP14) is a secretory endo-
Serum human chorionic gonadotropin (hCG) level less metrial protein. Low concentration is suggestive of EP.
than 6,500 IU/L is suspicious of EP or missed abortion; Serum relaxin, produced by corpus luteum of pregnancy.
but if there is no intrauterine pregnancy, a diagnosis of Its potential as marker for EP is under further evaluation.
EP is made. Human placental lactogen (HPL) assay.
•• Serum hCG levels double every 2 days in a normal Pregnancy-associated plasma protein-A assay (PAPP-A)
pregnancy. Schwangerschaft protein 1 (SP1) assay.
•• If the patient is hemodynamically stable, we can Differential diagnosis (Flowchart 15.2) from other
repeat hCG. conditions causing acute lower abdomen pain is important.
•• If the rise is less than 66% from the previous reading, Acute abdomen: Conditions like splenic rupture,
EP should be suspected. perforated appendix, acute pancreatitis, perforated

•• If the rise is double or the level is more than 6,500 gastric and duodenal ulcer, etc. In these conditions,
IU/L, USG invariably reveals a uterine pregnancy in the abdomen has board-like rigidity that is absent
95% of cases. in EP. There will be no amenorrhea and no vaginal
Serum progesterone level: A single level cannot predict bleeding in these conditions.
EP. Serum progesterone indicates the viability of the Rupture of corpus luteal hematoma: Simulates EP,
corpus luteum. Values more than 25 ng/mL, exclude EP. both in history and clinical findings and may be the
•• Serum progesterone level less than 15 ng/mL = 83% EP. cause of a few negative laparotomies.
•• Serum progesterone level more than 25 ng/mL Miscarriage of early pregnancy: Bleeding is large in
indicates normal intrauterine (IU) pregnancy. volume and pain occurs in lower midline abdominal area.
Uterine curettage: Only decidual tissues and no villi— Salpingitis: Most commonly mistaken for EP. Negative
such a picture is diagnostic of EP. pregnancy test with leukocytosis and fever confirm the
If placental tissue is seen, it is threatened or incomplete diagnosis.
abortion. Ovarian torsion or torsion of pedunculated fibroid:
Laparoscopic diagnosis may be used, if available Pain usually waxes and wanes and later becomes
(Fig. 15.4). constant as the vascular supply is compromized.
Flowchart 15.2: Differential diagnosis of ectopic pregnancy
Abbreviations: EP—Ectopic pregnancy; PID—Pelvic inflammatory disease; IU—Intrauterine
Intrauterine device—associated with severe dysmen- prospects. Treatment options are surgery, medical and
orrhea. expectant management depending on whether the
Red degeneration in fibroid with pregnancy. patient is in shock (ruptured ectopic) or is stable.
Intraperitoneal hemorrhage from any other source If in shock, the patient must be treated and simultane-
(e.g. liver). ously preparation for laparotomy should be made.
Retroverted gravid uterus with retention of urine. Acute stage: A rupture of EP can occur in very low hCG
Pyosalpinx (acute stage), usually bilateral. concentration. In ruptured ectopic surgical treatment is
Rupture of chocolate cyst. the only option.
Urinary tract infection (UTI). As soon as the diagnosis of EP is made, management
Risks of ectopic pregnancy: The blood lost may be should start.
massive endangering the woman’s life. Implications for Blood transfusion is required before, during and after
future pregnancy is not well-known. operation.
Resuscitation and operation is performed simultane
FATE OF ECTOPIC PREGNANCY ously. Depending on the availability, laparoscopic or
Fate of EP depends on many factors. Important among laparotomy surgery is performed.
them being site and duration of EP. The main serious Identifying the affected tube, clamping of the bleeding
outcome is rupture. Timing of rupture depends on the vessel may be the only means of saving the patient’s life
site of EP. Isthmic pregnancy ruptures at 6–8 weeks of as her shock is because of this bleeding of the ruptured
gestation as the isthmic region has the smallest diameter. fallopian tube.
The ampullary region rupture is late at 8 weeks. The Before deciding for the surgical treatment of the affected
rudimentary horn takes still longer to rupture. The tube, opposite tube and ovary must be examined and
greater the duration of pregnancy at the time of rupture, patient’s desire for future pregnancy is to be considered.
the more massive and life-threatening the bleeding will Indications of laparotomy: Laparotomy is done when the
be shown in Table 15.1. patient is in a hemodynamically unstable condition and
Sometimes, the EP is expelled through the fibrial end the surgeon is not an expert in laparoscopic surgery. Other
(tubal abortion) (Flowchart 15.3). If it remains attached indications are:
Most ovarian and abdominal pregnancies
to the tube after rupture, then it may continue to grow as
Chronic EP
a secondary abdominal pregnancy.
Non-availability of laparoscopic equipment
Spontaneous resolution of the EP is also seen.
Adhesions preventing laparoscopic approach
Cornual or interstitial pregnancies

TREATMENT (FLOWCHART 15.4) Started as laparoscopic approach but converted to
Whenever tubal pregnancy is diagnosed, immediate laparatomy due to complications

hospitalization is required. Treatment depends on If large blood clots, prevent estimation of intraabdo
the clinical condition of the patient and future fertility minal lesion.
TABLE 15.1: Clinical manifestation of tubal abortion and tubal rupture

Symptoms Tubal abortion Tubal rupture
Amenorrhea May or may be present May or may not be present
Pain 95% Aching in one or other iliac fossa due to distension Severe lancinating pain in one iliac fossa due to
of tube rupture and escape of large quantity of blood
Sharp stabbing pain due to choriodecidual hem- into the peritoneal cavity
orrhage and escape of blood into the peritoneal Blood trickles up to the undersurface of the
cavity (severity depends upon the intraperitoneal diaphragm; causes shoulder trip pain and
hemorrhage) epigastric pain
Abnormal vaginal bleeding Small amount; dark altered Vaginal spotting or bleeding
60–80% Due to withdrawal of hormones
Discharge of decidual cast 5–10% of case
Syncope Always associated with syncope Profound collapse
Momentary feeling of faintness to collapse Marked pallor, sweating
Retention of urine Blood collects in the pouch of Douglas—pelvic
hematocele
Forms irregular mass—displaces the cervix against
bladder neck
Fever <10% When pelvic hematocele gets secondarily infected
Sign of shock and anemia Pallor Weak rapid pulse
Subnormal temperature
Low blood pressure with marked pallor
Generalized tenderness and Over lower abdomen especially on the affected side Lower abdomen is acutely tender
muscle guarding in 45% of cases with muscle guarding
Distension of abdomen Intestinal distension Extreme tenderness can be elicited in the
Hemoperitoneum of 2–3 weeks causes bruising lower abdomen
around the umbilicus called Cullen’s sign (15% of Cervical movement causes severe pain
cases) Abdominal tenderness present on bimanual
examination
Difficult to feel the uterus and pelvic mass
Flowchart 15.3: Outcome of ectopic pregnancy

Flowchart 15.4: Treatment of ectopic pregnancy (EP) adnexal mass). Advantage of salpingectomy is that the
ovarian function will continue and during IVF ova can
be collected from this ovary also. The disadvantage of
preservation of the ovary is the theoretical danger of
transperitoneal migration of the ovum from this intact
ovary going to intact fallopian tube on the other side and
causing EP. Hemostasis is achieved by catching hold of
the bleeders and securing them. Clean the abdominal
cavity of blood and products of conception by doing a
saline lavage.
Salpingo-oophorectomy: When the ovary is completely
involved with the adnexal mass (including fallopian
tube).
Segmental resection and end-to-end anastomosis can also
be done in ruptured EP when hemostasis has been secured
by catching the bleeding vessel in the mesosalpinx.
Linear salpingostomy with scissors or diathermy or
laser is done in an unruptured ectopic and the products
Abbreviation: hCG—Human chorionic gonadotropin
of conception are sucked out, followed by suturing (Figs
15.6A to D) or not suturing (Figs 15.7A to C). The tissues
The following operations can be/done either by laparo obtained are to be sent for histopathology (Fig. 15.8)
tomy or laparoscopically. Milking (milking of the tube): If the EP is at fimbrial
Radical salpingectomy (Fig 15.5): It was first performed end or just at the outer end of the ampullary portion
by Robert Laws on Tait in 1884. Removal of entire of the tube, milking of the tube done with a grasper
fallopian tube is done when the condition of ruptured forceps through a laparoscope and products can
fallopian tube is unsalvageable or the fallopian tube is be aspirated with a suction irrigation cannula. In
diseased, e.g. tuberculosis (ovary is separated from the fimbrial EP, expulsion of embryo is achieved. But this
A B
C D
Fig. 15.5: Salpingectomy for tubal pregnancy—the tube has Figs 15.6A to D: Removal of a midampullary pregnancy. A. Mid
been delivered and the mesosalpinx is being clamped and cut ampullary ectopic; B. Antimesenteric incision with diathermy
with a succession of Kelly clamps needle; C. The pregnancy removed by grasping tissue while blunt
teasing the tissue away from the endosalpinx; D. Serosa and mus-
cularis are closed with 5.0 non-reactive suture material
Conservative surgery is not done in uncontrolled

hemorrhage when hemostasis cannot be achieved by
using conservative techniques. It is also not done in
cases of unrepairable tubal damage and in cases with no
desire for further fertility. Conservative surgery does not
give good results in isthmic and large corneal ectopic
pregnancies. Thermal needle and direction of a powerful
ultrasound beam accurately at the ectopic sac alongside
an imaging transducer, can eliminate the need for any
infection (under research).
A Treatment of unruptured EP: Options are surgical
treatment–salpingectomy, salpingostomy (both by laparo
tomy and laparoscopy), salpingotomy, evacuation and
B end-to-end anastomosis.
Surgically administered medical treatment: Around
the EP—laparoscopically by falloposcope or TVS guided
transcervical injection is given. First aspirate the contents
of the sac and then inject 50 mg of methotrexate into the
gesational sac.
Medical treatment: It can be given systemically by the
C intravenous (IV) or intramuscularly (IM) route or orally.
Surgically administered medical treatment is carried
Figs 15.7A to C: Laparoscopic salpingostomy for EP. An incision out in stable patients with unruptured EP.
is made with the monopolar diathermy needle along the It involves local administration of the following
antimesenteric border of the oviduct. The trophoblastic tissue
trophotoxic drugs in the EP sac.
is removed with forceps. The lumen is left to heal by secondary
intention A total of 5 mg of methotrexate is injected into the
gestational sac. Other drugs under research are:
Anti-hCG antibodies
Etoposide, danazol
Hyperosmolar glucose
Prostaglandins’ mifepristone
Potassium chloride.
CRITERIA FOR MEDICAL TREATMENT

Medical treatment: All the above trophotoxic drugs can
be given IV, IM and by the oral route. But methotrexate,
generally as a single dose, is most commonly used.
Whom to give methotrexate? The following selection
criteria are needed:
The patient is stable hemodynamically with no sign
or symptoms of active bleeding or hemoperitoneum.

Fig. 15.8: Ectopic pregnancy in fallopian tube
The fallopian tube is unruptured.
Courtesy: Dr A Gupta, Sikkim Manipal Institute of Medical Sciences
Mean duration of pregnancy is 54 days.
Absent fetal heart and less than 4 cm ectopic mass.
procedure is associated with a two-fold increase in the Serum progesterone less than 10 ng/mL.
rate of recurrent EP. Always send the tissue obtained Serum hCG level below 6,000 IU/mL.
for his histopathological examination to confirm the No contraindication to methotrexate therapy.
diagnosis. Persistent EP after conservative surgery.

Cervical and intestinal pregnancy where surgical The patient is instructed not to have sexual intercourse
intervention is not easy. till hCG levels are negative. She is also asked not to take
Desiring future fertility. multivitamin tablets containing folic acid and alcohol
Methotrexate is an antifolic acid drug. It interferes with consumption is prohibited. Measure the hCG level on
the synthesis of DNA in rapidly dividing trophoblast cells. days 4–7 and then repeat weekly till undetectable. TLC,
If hCG fails to fall below 15% in 4–5 days or increases a DLC and platelets are also measured repeatedly. After
dose of methotrexate is repeated. the hCG level is negative for two months, contraception
Post-treatment tubal patency is demonstrated in is advised. Failure of medical treatment is when the hCG
82% cases. Side effects of methotrexate—stomatitis is level increases or plateaus or the decrease is less than
most common. Methotrexate may also cause nausea, 15% from day 4–7 post injection. A repeat single dose of
vomiting, diarrhea, gastric upset, rarely neutropenia. methotrexate can be given.
But these side effects are rare in a single dose regimen Careful monitoring is done by:
and folinic acid is not needed. Side effects are to be told Careful clinical assessment
to the patient before starting the treatment. Follow-up Complete blood count
is essential. LFT
Serum hCG level closely monitored at least once a week
Contraindications of Medical Treatment until negative

Ultrasound scanning.
Patients with prior surgeries on fallopian tubes (tubal
ligation) and tubercular salpingitis. As chances of Advantage of medical treatment:
Minimal hospitalization
development of an EP again are more
Shorter time interval to normal activity
Breastfeeding
Outpatient treatment
Immunodeficiency
More than 90% success in selected cases.
In patients who cannot remain under follow-up
Expectant treatment, i.e. observation and monitoring
Blood dyscrasias and thrombocytopenia
until EP resolves. Ectopic pregnancy is a life-threatening
Alcoholism
condition. So expectant treatment is not frequently used
Active pulmonary diseases
and should rigidly follow the set criteria. This mode of
Sensitivity to methotrexate
treatment should be started only if the hCG is less than
Patients who have elevated liver enzymes
1000 IU/L.
Renal dysfunction
Falling level of serum hCG at 2-day intervals.
Fetal sac more than 4 cm
No sign of intrauterine pregnancy.
Fetal heart present (some authors give ultrasound-
Diameter of EP sac less than 4 cm and rapidly decreasing
guided potassium chloride injection in the fetal heart.
within 7 days (USG after 1 week).
Look for arrest of cardiac activity and then inject
No sign of rupture or acute bleeding by TVS and no fetal
methotrexate).
heart activity.
Counseling before medical treatment it is an essential
Progesterone level less than 10 ng/mL.
step. The patient should be told about the seriousness of
Constant supervision is essential.
the disease, importance of follow-up and that in case of
The selected patients are counseled about the follow-
failure of medical treatment, surgery may be needed. up and other treatment protocols and consent is taken.
For medical treatment, the following investigations In case of any danger signs, the patient is instructed to
are required: contact the emergency. Till the patient is symptoms free,
Hb level, total leukocyte count (TLC), differential leu-
she is followed with weekly hCG and USG until hCG levels
kocyte count (DLC) and platelet count are less than 20 IU/L.
Liver function tests (LFT) especially serum glutamic
Spontaneous resolution occurred in 72% of cases;
oxaloacetic transaminase (SGOT), serum glutamic py- resolution time is 20 ± 13 days.
ruvic transaminase (SGPT)
Serum hCG level
Blood group and Rh typing

HETEROTOPIC ECTOPIC PREGNANCY
Blood urea nitrogen, creatinine When one pregnancy is in the uterus and other is in
Informed consent is taken. the fallopian tube. The incidence used to be 1:30,000
pregnancies. But, now in cases of IVF, it is 12%. It may

occur due to IVF diagnosed TVS. To avoid missing it,
these cases in patients of IVF, after seeing an intrauterine
pregnancy, do not stop the ultrasound procedure; exclude
concomitant EP. On laparoscopy, two corpora lutea are
seen.
Treatment: Potassium chloride or hyperosmolar glucose
is injected into the ectopic sac either under ultrasound
guidance or laparoscopically.
Surgical removal of EP can be carried out by laparoscope
or one can give drugs in sac by laparoscopy:
Methotrexate
Ru-486.
Expectant management, i.e. observation and monito

ring until EP resolves.
PERSISTENT ECTOPIC PREGNANCY (PEP)

Fig. 15.9: Cervical ectopic pregnancy
Denotes continued growth and enlargement of residual
trophoblastic tissue. This is the complication of salpingos- 3. Products of conception entirely confined within and
tomy and evacuation of EP. Here, the removal of pregnancy firmly attached to the endocervix.
is incomplete. PEP may also occur after medical treatment 4. Internal cervical os is closed.
if residual trophoblast continues to survive. Close follow- 5. External cervical os is partially open.
up is essential. Untreated PEP can cause tubal rupture and The diagnosis is often delayed until second trimester
severe hemorrhage. Treatment consists of: when severe hemorrahge occurs leading to high
Reoperation and further evacuation morbidity and mortality. An index of suspicion is very
Salpingectomy important. TVS and hCG levels help in the diagnosis.
Segmental resection color Doppler may be useful. Classically, the treatment
Methotrexate single dose IM 50 mg/m body surface
2
is surgery with hysterectomy as the mainstay leading to
area. loss of reproductive capability. Recently, treatment by
injection of potassium chloride into the gravid sac under
CERVICAL ECTOPIC PREGNANCY (FIG. 15.9) TVS guidance is used. Methotrexate along with uterine
artery embolization helps to preserve future fertility.
It is rare occurring (0.1–0.2% of ectopic pregnancies). It is Some gynecologists give a combination of methotrexate
more common in Japan which is attributed to high rate of and mesoproston. If the fetal cardiac activity was seen
MTPs. High incidence is seen in cases of curettage. they injected KCL 2 mL (2 mg/mL) (intracardiac) under
Rubin gave three criteria for the diagnosis of cervical EP: ultrasound guidance. Medical management of cervical EP
1. Cervical glands must be opposite the placental attach is a safe and viable option in most patients with cervical
ment. EP. Early diagnosis of cervical pregnancy is crucial for
2. The placental attachment is below the uterine vessels effective conservative management with low morbidity.
or below the peritoneal reflection of the anterior and Hystrectomy may be required in massive hemorrhage.
posterior surface of the uterus. Differential diagnosis of cervical EP is from carcinoma
3. Fetal elements must be absent from the corpus uteri. of the cervix and incomplete abortion. It is important to
These criteria are difficult to evaluate unless we study differentiate from inevitable abortion because if we start
the whole of the uterus. Hence, Paalman and McElin gave evacuating (confusing it with inevitatble abortion) severe
five more criteria: hemorrhage ensures.
1. Uterine bleeding without cramping pain following a
period of amenorrhea. OVARIAN ECTOPIC PREGNANCY
2. Hour glass uterus showing soft enlarged cervix equal to Ovarian EP is also a rare condition. The exact etiology is
or larger than the fundus (Fig. 15.9). difficult to find. However, it is more often seen with IUCD
users. The ovum is fertilized within the follicle itself before pregnancy or pregnancy in the rudimentary horn ruptures
ovulation (extrusion). and attaches itself to other viscera. The placenta in the
Spiegelberg criteria for ovarian pregnancy: Besides a fallopian tube spreads to gain blood supply from perito-
preserved corpus luteum in the wall of the gestational sac, neal site also, besides the original site in the tubes. Rarely
there must be: spontaneous separation of an old cesarean section scar,
Tubes including the fimbria ovarica are intact and after perforation of the uterus in MTP or after subtotal
clearly separate from the ovary. and total hysterectomy. Fetal hemorrhage can occur after
Gestational sac definitely occupies the normal position separation of the placenta.
in the ovary. Diagnosis of abdominal pregnancy is very important.
Gestational sac is connected to the uterus by the utero- Hence, one must keep it in mind in cases who have
ovarian ligament. amenorrhea, and present with a history of sudden pain
The ovarian tissue is demonstrated in the sac. in the abdomen in the first trimester. The patient often
Differential diagnosis is a leaking corpus luteum complains of pain in the abdomen and visible fetal
hematoma. Though there is more bleeding in ovarian EP. movements in the upper abdomen. Hyperemesis late in
Treatment is surgical in both cases (to be on the safer pregnancy is also a complaint.
side). Conservative resection of the bleeding portion of the On examination, the fetus is felt superficially with
ovary is carried out. Rarely, oophorectomy is required for malpresentation and malposition. The cervix is long and
hemostasis. unaffected and the uterus can be felt separately and is
Abdominal EP (Fig. 15.10): It is very rarely seen. The small in size.
incidence varies. It is as rare as 1 in 10,000–25,000 live births. X-ray abdomen (lateral view) shows fetal parts overlying
It can be primary or secondary abdominal pregnancy. the maternal spine along with transverse or lateral position.
Studdiford (1992) criteria for primary abdominal Ultrasound: Confirms the diagnosis by an empty uterus
ectopic include the following: and the fetus lying in the abdomen. There may be
Both tubes and ovaries must be in normal condition oligohydramnios.
with no evidence of recent or remote injury. Magnetic resonance imaging (MRI) may be used, if
No evidence of uteroperitoneal fistula should be found. available.
The pregnancy must be related exclusively to the Management includes keeping blood ready and close
peritoneal surface and be early enough in the gestation fetal monitoring. Intact fetal membranes are crucial; if
to eliminate the possibility that it is a secondary they rupture, the fetus dies quickly of respiratory distress.
implantation following primary implantation in the Due to lying in restricted space, there are anomalies in the
tube. fetus like joint deformities, torticollis, etc.
Secondary abdominal pregnancy is more common of The fetus is extracted by laparotomy. Try not to remove
the two abdominal pregnancies. It occurs when a tubal the placenta if it is morbidly adherent to surrounding
viscera. Fiddling with placenta usually leads to fatal
hemorrhage. Its removal is only attempted when after
examining it, the surgeon is sure that it can be removed
completely without any damage to the surrounding
organs. Otherwise, the cord is cut as close to the placenta as
possible and the placenta is left in the abdomen. It will get
absorbed in due course of time. We can give methotrexate
orally and can follow hCG levels.
Chronic EP: The EP ruptures, patient survives this
catastrophe. The ectopic mass gets organized and present

as chronic pain. There is a pelvic mass. Treatment is
surgical removal of the mass (which is difficult because
of inflammation and subsequent adhesions).
Anti-D prophylaxis should be given in all Rh-negative
mothers with EP.

Influence on fertility: The subsequent fertility depends
Fig. 15.10: Abdominal ectopic pregnancy on the condition of the fallopian tube (damage by EP),
previous disease (tuberculosis, chlamydial infection). subsequent results may be good. It is seen that most of
With the availability of antibiotics, if there is minimum the patients with previous EP are not able to have a live
damage, the prospects are good for a subsequent child.
pregnancy. However, to tubal damage with Chlamydia Follow-up is especially important in medical treatment,
or tuberculosis is usually bilateral and irreversible and expectant treatment and conservative surgery to
hence leads to repeated EP. Definitive future outcome prevent persistent EP. Weekly hCG should be measured;
cannot be predicted. required till it becomes negative. It clears within 2–3
When the contralateral fallopian tube is normal, the weeks but may take up to 6 weeks.
1. Explain briefly sites of EP.
2. What is the difference between tubal abortion and tubal rupture?
3. True/False:
i. Rupture of EP can occur in very low hCG concentration.
ii. Tubal function with chlamydia or tuberculosis is usually bilateral.
iii. Levels of IL and TNF-2 in the serum are higher in EP than in normal pregnancy.
iv. Radical salpingectomy was first performed in year 1886.
16
Sudha Salhan, Jyotsna Suri, Divya Pandey
Gestational
Trophoblastic Disease (GTD)
Trophoblastic disease arises from trophoblastic tissue. It having hydropic swelling and hyperplasia of trophoblasts.
can be divided into: The incidence varies with geographic location and is
Gestational trophoblastic disease (GTD) greatest in South-East Asia.
Non-gestational trophoblastic disease (NGTD). Pathology: It is the most common gestational tropho-
blastic tumor. It can be complete or partial depending on
GESTATIONAL TROPHOBLASTIC DISEASE the presence or absence of an embryo or fetus.
Gestational trophoblastic disease is a term that encom Complete Hydatidiform Mole

passes a spectrum of tumors associated with the result Complete H mole occur with abnormal conception which
of an abnormal pregnancy, which arises from human do not have recognizable embryonic and fetal tissue on
placental trophoblastic tissue. They are diagnosed by microscopic examination. Gross examination shows grape
the serum marker beta-human chorionic gonadotropin like vesicles of 1–3 cm in diameter (hydropic villi) (Figs
(β-hCG) and are the first solid disseminated tumor highly 16.1A and B).
curable by chemotherapy. After treatment of chorio On microscopic examination (Figs 16.2A and 2B),
carcinoma, the patient can conceive again. Hence, any there is hydropic swelling of chorionic villi and diffuse
woman coming with a history of bleeding or tumor with hyperplasia with interstitial edema of cytotrophoblastic
a recent history of hydatidiform mole, abortion or term and syncytiotrophoblast. There is absence of fetal
pregnancy should have at least one β-hCG examination to vessels in villous stroma and lack of trophoblastic
rule out GTD. All evacuated tissues in a miscarriage should stromal invasion. A complete mole produces hCG.
be seen with naked eyes and sent for histopathology (the Karyotype: These are diploid (90% are 46XX and
author detected choriocarcinoma in one case diagnosed 10% have 46XY). Mitochondria comes from mother
as incomplete abortion). but chromosomes are totally from father. It appears
Gestational trophoblastic diseases are histologically that a complete mole arises when an empty-ovum is
divided into: fertilized by self-duplicated haploid sperm (homo
Hydatidiform mole: zygous monospermic androgenic fertilization) or
•• Complete by two haploid sperms with fusion and replication
•• Partial (heterozygotic, dispermic diandrogenetic fertilization).
Chorioadenoma destruens—invasive mole There is transformation of the embryonic cell mass just
Choriocarcinoma before lying down of endoderm. Hence, there is no
Placental site trophoblastic tumor (PSTT). differentiation into ectoderm and endoderm. This gives
rise to vesicles with loose primitive mesoderm in their
villous core.
HYDATIDIFORM MOLE (H MOLE)
The name comes from hydatis (Greek) water drop and Clinical Features
mole (Latin) mass. It is defined as an abnormal pregnancy Vaginal bleeding: History of amenorrhea is important
or conception which has no embryo, the chorionic villi are as most of them give history of first trimester bleeding.
A B
Figs 16.1A and B: A. Hydatidiform mole (gross view); B. Molar pregnancy
A B
Figs 16.2A and B: A. Hydatidiform mole (4X); B. Hydatidiform mole (microscopic view)
Molar tissue may separate from the decidua and can complete H mole causing pain. These are due to high serum
be expelled as grape like vesicles. The blood may be hCG level causing hyperstimulation of ovaries. In most of
retained inside the endometrial cavity. This gives the the cases, they regress spontaneously in 8–12 weeks after
typical ‘prune juice’ like appearance to the discharge in the evacuation of H mole. Rarely, surgical intervention
these cases. may be required, as in rupture or hemorrhage or infection
Fetal heart: No fetal heart is heard.
in these cysts. Patients with these cysts are more likely to
Uterine size larger than the gestational age: Excessive
develop choriocarcinoma.
uterine size relative to the gestational age is seen in
Pre-eclampsia: It develops in about one-fourth of the
about half the patients of complete H mole. The size of
cases of complete H mole in the first and second trimesters
the uterus often correlates with the serum hCG level
fells. before 20 weeks of pregnancy. The reason for this may be
Differential diagnosis needs consideration of the following: the release of vasoactive substances from the trophoblastic
Multifetal gestation
tissue.
Polyhydramnios Hyperemesis: Respiratory disress.
Uterine fibroid (especially with pregnancy when it Hyperthyroidism: High levels of serum hCG are sometimes
enlarges rapidly) associated with elevated free thyroxine (T4) and triiodothy-
Ovarian tumor in early pregnancy. ronine (T3). This is possibly due to the thyrotropic effect of
Theca lutein ovarian cysts: Large theca lutein cysts (6 hCG. Sometimes a limited course of antithyroid drugs may
cm or more) are seen in about half of the women with be needed.
Gestational Trophoblastic Disease (GTD) 147
Fig. 16.3: Ultrasonogram hydatiform mole Fig. 16.4: Ultrasound showing partial mole
Complete H mole is rarely seen is overnice ectopic

pregnancy.
Clinically, it is usually detected between 8 and 24
weeks of conception. Respiratory distress is seen as
trophoblasts travel to the lungs. H mole is rarely seen in
ectopic pregnancies, fallopian tubes (5%) and ovaries.
About 10% of complete H mole progress to persistent
trophoblastic disease and 3–5% go on to developing
choriocarcinoma. Microscopic examination helps because
cistern formation is not present; villi are less edematous
and are without blood vessels. Atypia of trophoblasts is not
seen. Flow cytometry also helps in differentiating the two.
Ultrasound shows snowstorm appearance (Fig. 16.3).
Partial Hydatidiform Mole (see Fig. 62.8)

The partial mole, in contrast to the complete mole, has the
presence of identifiable embryonic or fetal tissues (Figs Fig. 16.5: Partial mole (fetus with molar tissue)
16.4 and 16.5). Gross examination of the placenta shows
both normal and hydropic villi. There is variation in the size The clinical features may be different in cases of
of the chorionic villi and the microscopic examination partial mole. Less than 10% of the patients have uterine
shows focal swelling, cavitations and trophoblastic enlargement greater than the period of amenorrhea. The
hyperplasia along with normal villi. A normal amniotic incidence of theca lutein cysts, hyperthyroidism, toxemia
membrane is seen. Trophoblastic stromal invasion is and respiratory insufficiency is also very low. The ultrasound
present. Scalloping of the hydropic villi may be seen. and histopathological examination are diagnostic, hCG
Fetal vessels are often seen. There may be nucleated fetal levels are also to be tested.
red blood cells (RBC) in these vessels. The fetus in partial
mole has growth restriction and show multiple congenital INVASIVE MOLE (CHORIOADENOMA
abnormalities hCG is produced more. DETRUENS)
Karyotype: Ninety percent of the partial moles are triploid
with an extra haploid set of chromosomes of paternal Within 6 months 10–16% of complete moles progress
origin (69XXX or 69XXY with two-third of DNA of paternal to invasive moles. It mostly invades locally, distent
origin (one haploid maternal and two haploid paternal metastasis are rarely seen. Histopathology myometrium is
chromosomal sets). This occurs when a haploid ovum is invaded by trophoblasts and its blood vessels are without
fertilized by two sperms or a diploid sperm (Table 16.1). intervening endometrial stroma. Villi are not seen. There
TABLE 16.1: Comparison of complete and partial hydatidiform is made at hysterectomy only. Nowadays, the morbidity
mole and mortality is less because follow-up can diagnose the
Complete H mole Partial H mole disease in the persistent gestational trophoblastic stage
(when the b-hCG level plateaus or stops falling) and
Embryonic tissue of Not identified Identified
fetus
prompt chemotherapy cures the disease.
Complications of H mole and invasive mole:
Hydropic swelling of Generalized Localized
Bleeding which may be life-threatening
chorionic villi
Systemic disease
Proliferation of Generalized Localized
Development of malignancy—choriocarcinoma
trophoblasts
Acute pulmonary insufficiency—seen in some cases
Chorionic villi scalping Not seen Seen
of H mole with sudden dyspnea and cyanosis 4–6
Trophoblastic stromal Not seen Seen
hours after evacuation. This may be due to pulmonary
invasion
embolism. Hence, oxytocin is not used now before
Clinical diagnosis by Possible Not possible
history
evacuation is complete.
Size of uterus Mostly larger than Mostly
period of amenorrhea appropriate CHORIOCARCINOMA
for period of (FIGS 16.6, 16.7A AND B)
amenorrhea
Theca lutein cyst Present Not seen It is a highly aggressive malignancy of trophoblastic
Pre-eclampsia Seen Not seen
tissue. Gross appearance, nowadays, chemotherapy is
the mainstay of therapy and surgery is rarely required.
Hyperemesis Seen Not seen
Therefore, gross appearance of the tumor is not usually seen
Thyrotoxicosis Seen Not seen
if available gross examination shows hemorrhagic tumor
Karyotype Paternal only Both maternal with extensive necrosis with granular red appearance.
and paternal
Under the microscope we see dimorphic population of
DNA concentration— Diploid 50%, 43% Triploid cytotrophoblast and syncytiotrophoblast with numerous
flow cytometry tetraploid
mitotic figures and giant cells, without formed chorionic
Conversion to Seen (10% persistent Rare villi. There are hemorrhagic nodules and extensive necrosis.
malignancy and 3–5% develop
choriocarinoma)
Choriocarcinoma cells are positive for hCG and keratin on
immunohistochemistry. Reactivity can be seen to pregnancy
Immunochemistry Localization of hCG Localization of
epidermal growth and hPL hCG and hPL
factor detected
In situ hybridization P53 staging more P53 staging less
intense MVC intense different
MVF-ras and sis than complete
oncogenes not mole
seen
Abbreviations: hcG—Human chorionic gonadotropin; hPL—Human
placental lactogen
is cytoplasmic and syncytitial hyperplasia as well as the

persistence of villous structures. Hence, it is diagnosed only
if there is persistence of hCG in blood for a long time after
the complete mole is evacuated. Women aged more than
40 years are more prone. Due to invasion by tropho
blasts, the symptoms of bleeding, amenorrhea, pain in
the abdomen (which may be acute in case of uterine
perforation) and hemoperitoneum are seen. Molar villi are
seen in the blood vessels (deportation lesion). Diagnosis Fig. 16.6: Choriocarcinoma
A B
Figs 16.7A and B: Microscopic appearance of choriocarcinoma
specific b-1-glycoprotein and carcinoembryonic antigen

(CEA). Massive amounts of hCG is produced.
The patient is of a younger age. Previous history of
complete H mole, miscarriage or ectopic pregnancy and
normal delivery can be elicited in 25%. There is a higher
proportion of women with blood group A with the partner
also having the same blood group. The most common
complaint is continuous or intermittent bleeding which
may be quite massive. It is a very rapidly growing tumor.
Many organs show hyperplasia due to high levels of hCG
in the blood. This is seen as hyperplasia of endocervical
glands, decidual reaction of the endometrial glands,
ovarian theca lutein cysts, breast lobule hyperplasia and
Arias-Stella phenomenon.
PLACENTAL SITE TROPHOBLASTIC Fig. 16.8: Pulmonary metastasis
TUMOR (PSTT) Metastasis in the majority of cases has the histology of

It is rarely seen. There is a history of H mole or normal choriocarcinoma. Here its hematogenous spread. There is
term pregnancy before. It is limited to the uterus and local bleeding from metastatic GTD because of extensive
mostly spreads through lymphatics and rarely via vascular network of blood vessels.
channels. Metastases are very late as there is very little or no Lungs (80%), vagina (30%), pelvis (20%), liver (10%),
syncytiotrophoblast. β-hCG is not secreted, but hPL levels brain (10%), bowel, kidney and spleen (5% each) and
give the diagnosis and are useful for follow up. Recently, bones are the sites of GTD metastasis.
it has been seen that very high levels of free b-fragments Pulmonary metastasis (Fig. 16.8) is the most common
of hCG have been produced in PSTT and it is very specific and may present as hemoptysis and cough. The
test to differentiate PSTT from choriocarcinoma. radiological features can be alveolar, nodular or
miliary patterns. There may be discrete round densities.
METASTATIC GESTATIONAL Pleural effusions may also be seen. Some patients
present primarily with respiratory symptoms and their
TROPHOBLASTIC DISEASE reproductive organs may be free of the disease. In such
Complete H mole does spread locally and disseminates. cases, establishing a diagnosis is possible only after
After evacuation 15% have local uterine invasion and 4% histopathological examination of the lung or pleural
show metastasis. tissues.
•• The ratio of β-hCG in serum and cerebrospinal fluid

(CSF) is measured in cases of metastatic disease to
exclude cerebral involvement. A ratio of less than 60
is diagnostic of brain metastasis.
•• Elevated hyperglycosylated hCG (H-hCG) level is
specific in cases of H mole which later on require
chemotherapy. It is a helpful tool in identifying
molar cases in which apparent neoplasm (e.g.
choriocarcinoma) develops because this marker
rises earlier than conventional hCG thereby allowing
earlier initiation of chemotherapy.
Complete blood counts (CBC)
Hepatic, thyroid and kidney function tests.
Fig. 16.9: Vaginal metastatic lesion Radiological Studies

Always do chest X-ray to rule out metastatic lung disease.
Vaginal metastatic spots are blue in color as are very Chest computed tomography (CT) scan is very useful to
vascular and may bleed torrentially when biopsied. The evaluate any non-specific lesion. It may also demonstrate
patient presents with irregular bleeding and purulent micrometastases in the presence of normal X-ray.
discharge (Fig. 16.9). Ultrasonogram or CT scan of the abdomen and
Hepatic metastasis usually present with right upper
pelvis: Ultrasonography is the preferred diagnostic
quadrant pain due to stretching of the Glisson’s capsule. method to confirm diagnosis of GTD. It is a non-
Rarely, the hepatic lesions may cause liver rupture and invasive, cost-effective and reliable method. There is no
exsanguinating intraperitoneal hemorrhage (acute fetus in complete H mole and snowstorm appearance
abdomen). filling the uterus, confirm the diagnosis (Fig. 16.3).
When brain is metastasized it suggests widespread
Partial mole may show a fetus too (Fig. 16.4). Transverse
involvement and poor prognosis. These patients
diameter and anteroposterior diameter ratio of the
may present with headache, hemiparesis, vomiting,
gestational sac more than 1.5 is seen in partial molar
giddiness, coma, convulsions, visual disturbances,
pregnancy. There are multiple echoes.
aphasia and slurred speech. All patients have concurrent
These days, Doppler ultrasonography has been found to
pulmonary metastases.
be very useful in the diagnostic assessment of GTD.
Secondaries in gastrointestinal area cause severe
CT scan head: CT scan of the head is not routinely
hemorrhage or perforation requiring emergency inter
advocated as normally brain metastases are very rare in
vention.
the absence of lung involvement. Only if the X-ray shows
Work up before treatment:
lung secondaries should a CT scan of the head be done.
History of abortion, H mole or normal delivery
In equivocal cases use of magnetic resonance imaging
Examination of the patient including general and pelvic
(MRI) especially for cerebellum and brainstem evaluation
examination.
is useful, which are sites of occult metastasis. It can be
used for the evaluation of the abdomen and the pelvis.
INVESTIGATIONS
Abdominal and pelvic organ angiography may be
Laboratory Studies indicated in some selected cases.
Serum β-hCG: This glycoprotein hormone is secreted
by the syncytiotrophoblast. Hence is a very good marker STAGING OF GESTATIONAL
of tumor activity in non pregnant women. In normal
TROPHOBLASTIC DISEASE
pregnancy, the values are below 60,000 MIU/mL.
Values above 100,000 MIU/mL is diagnostic. It is The Federation of International Gynecologists and Obstetrics
always increased in GTD and hence must be measure (FIGO) staging system (Table 16.2) is based on the anatomic
serially for monitoring the effect of treatment. The level criteria. In GTD stage I, the disease is confined to the uterus;
corresponds to the tumor size. stage II includes disease limited to the genital structures;
TABLE 16.2: FIGO staging gestational trophoblastic tumors Metastatic GTD: The disease is spread outside the
(anatomical) uterus. In these cases, the following factors should be
Stage I Disease confined to uterus considered and noted while reporting:
Stage I A Disease confined to uterus with no risk factor •• Duration of disease: Shorter (duration less than 4
months) has better prognosis.
Stage I B Disease confined to uterus with one risk factor
•• Serum hCG level less than 40,000 mIU/mL has better
Stage I C Disease confined to uterus with two risk factor
outcome.
Stage II Gestational trophoblastic tumor extending •• Metastatic sites: Lung and pelvic metastasis has
outside uterus but limited to genital
structures (adnexa, vagina, broad ligament) better prognosis than metastasis to the brain or liver.
•• Prior chemotherapy: If no chemotherapy is given
Stage II A Gestational trophoblastic tumor (GTT) involving
genital structures without risk factor before, it has a better response.
•• GTD following abortion gives better results with
Stage II B GTT extending outside uterus but limited to genital
structures with one risk factor treatment than one following full term pregnancy.
Stage II C GTT extending outside uterus but limited to genital •• Placental site tumors should be reported separately;
structures with two risk factors histologic verification of disease is not needed.
Stage III Disease extending to lungs with or without Metastatic tumors seen are usually choriocarcinoma. It
known genital tract involvement can mimic many diseases and may present with the sign
Stage IIIA Gestational trophoblastic tumor extending to lungs and symptoms of stroke, intracranial bleeding, cerebral
with or without genital tract involvement and with or spinal cord tumors, liver infections, blood in urine or
no risk factor stools and pulmonary disease. Acute abdomen may be due
Stage IIIB Gestational trophoblastic tumor extending to lungs to rupture of liver or ovarian cyst. The hCG titer clinches
with or without genital tract involvement and with
the diagnosis. Tissue diagnosis of choriocarcinoma is
one risk factor
unnecessary; it can be misleading and may be dangerous
Stage IIIC Gestational trophoblastic tumor extending to lungs
(patient may start bleeding profusely at D and C).
with or without genital tract involvement and with
two risk factors
Stage IV All other metastatic sites
FIGO Staging and Scoring System
Stage IVA All other metastatic sites without risk factor
The FIGO 2000 staging and risk factor scoring system for
gestational trophoblastic neoplasia (GTN).
Stage IVB All other metastatic sites with one risk factor
In September 2000, a combined FIGO anatomic
Stage IVC All other metastatic sites with two risk factors
staging with a revised WHO risk factor scoring system was
Placental site tumors should be reported separately promulgated, which was accepted by the FIGO oncology
committee in 2002.
stage III involves metastasis to the lungs and stage IV is Before staging a disease, its inclusion criteria needs to
metastasis to any other site. be defined. The criteria for diagnosis of post-hydatidiform
The anatomic staging system remains basically the mole trophoblastic neoplasia are given in Table 16.3.
same (Table 16.2). The only difference in the revised 2002 Certain changes from the 1983, WHO classification have
classification is that the actual numerical risk factor is been made in this new FIGO 2002 classification for risk
mentioned in Arabic numeral after the stage in Roman scoring (Table 16.4). The risk score for ABO blood group
numeral, separated by a colon. For example, a patient who has been eliminated and risk factor for liver metastases
has been classified as stage II and has the risk scoring of 5 is upgraded from 2–4. Another major change is that the
will be expressed as FIGO stage II: 5. middle risk category of the WHO classification has been
Risk factors which affect the staging are as follows: abolished. A score of 6 or less is considered low risk while
hCG level more than 100,000 mIU/mL 7 or more is high risk.
Duration of disease longer than 6 months from the Table 16.5 shows the criteria recommended by FIGO to
termination of antecedent pregnancy. diagnose metastases in GTN.
Gestational trophoblastic disease can be non-metastatic Placental site trophoblastic tumor will be categorized
and metastatic: separately from other GTN.
Non-metastatic GTD: There is no disease outside the The actual level of hCG or the amount of rise will be
uterus. determined by the individual investigator.
TABLE 16.3: Criteria for the diagnosis of post-hydatidiform mole gestational trophoblastic neoplasia (GTN)
GTN may be diagnosed when the plateau of human chorionic gonadotropin (hCG) lasts for 4 measurements over a period of 3 weeks or
longer, that is days 1, 7, 14, 21.
GTN may be diagnosed when there is a rise of hCG on three consecutive weekly measurements over a period of two weeks or longer days
1, 7, 14.
GTN is diagnosed if there is histologic diagnosis of choriocarcinoma.
GTN is diagnosed when the hCG level remains elevated for 6 months or more.
TABLE 16.4: FIGO risk factor scoring values (modified WHO scoring) of H mole
FIGO Scoring 0 1 2 4
Age <40 >40 – –
Antecedent pregnancy Mole Abortion Term –
Interval in months from index pregnancy <4 4–<7 7–<13 ≥13
Pre-treatment serum hCG (IU/L) <103 103–<104 104-<105 ≥105
Largest tumor size (including uterus) cm <3 3–<5 ≥5 –
Site of metastases Lung Spleen, kidney Gastrointestinal tract Liver brain
Number of metastases – 1–4 5–8 >8
Previous failed chemotherapy – – Single drug 2 or more drugs
TABLE 16.5: Criteria for methods used to diagnose metastases in trophoblastic neoplasia
Chest X-ray is appropriate to diagnose lung metastases and also used for counting the number of lung metastases to evaluate the risk factor
score.
Liver metastases may be diagnosed by CT scanning or by ultrasound.
Brain metastases may be diagnosed by MRI or CT scanning.
To diagnose intra-abdominal metastases, CT scanning is preferable.
Abbreviations: CT—Computed tomography; MRI—Magnetic resonance imaging
This may not apply for patients with unexplained low metastases. The distinction between low risk and high
level hCG without clinical or imaging evidence of GTN. risk, therefore, applies to patients with stage II disease
The identification of an individual patient’s stage and (vaginal metastases) or stage III disease (lung metastases).
risk score will be expressed by allotting a Roman numeral A high-risk score is generally associated with a large
to the stage and an Arabic numeral to the risk score tumor burden (multiple metastases, large metastases), a
separated by a colon. delay in diagnosis, a non-molar antecedent pregnancy or
the failure of prior chemotherapy. Combination therapy
Anatomical Staging and Prognostic Scoring Systems treatment is needed for the patients with high-risk scores,
FIGO anatomical staging is commonly followed. A number to avoid the risk of resistance.
of adverse prognostic factors have been identified. These
include—(i) nature of antecedent pregnancy, (ii) the
duration of time from the antecendent pregnancy, (iii)
TREATMENT OF GESTATIONAL
the serum β-hCG concentration, (iv) number and size TROPHOBLASTIC DISEASE
of metastases, and (v) the site of specific metastases and
failure of prior chemotherapy with two or more drugs.
Hydatiform Mole
Based on the above factors, a prognostic scoring system Suction evacuation: It is the method of choice for
has been proposed by WHO, that reliably predicts the evacuation of complete molar pregnancies. The proce
potential for resistance to chemotherapy (Table 16.6). If dure can be carried out under intravenous (IV) sedation
the prognostic score is higher than 7, patient is considered but should always be performed in the presence of
as high risk for chemotherapy-resistant disease. A higher an anesthetist. Adequate blood should be arranged
score is generally seen in patients with liver or CNS before starting the procedure. The cervix should be
TABLE 16.6: WHO scoring system based on prognostic factors of H mole

Prognostic factor Score
0 1 2 4
Age (years) ≤39 >39
Antecedent pregnancy H mole Abortion Term
Interval (months) between antecedent pregnancy <4 4–6 7–12 >12
and start of chemotherapy
β-hCG (mIU/mL) <1000 1000–10,000 10,000–1 lac >1 lac
Largest tumor including uterine (cm) <3 3–5 >5
Site of metastases Lungs Spleen, kidney GIT, liver Brain
No. of metastases identified 1–3 4–8 >8
Prior chemotherapy One drug Two or more drugs
The total score for a patient is obtained by adding the individual score for each prognostic factor. Total score <6 = low risk, 7 or more high risk.
dilated up to 12 mm. The routine use of oxytocic agents of single drug (methotraxate/dactinomycin) but giving
should be avoided before or during the procedure prophylactic chemotherapy has the risk of developing
as the contractions of the myometrium may lead to resistance to the drugs and also over treatment of a large
embolization and dissemination of trophoblastic tissue percentage of patients with such toxic drug who in the
through the venous system from the site of placenta. normal course will not develop persistent gestational
Hence, it is recommended that where possible, trophoblastic disease. Thus, the role of prophylactic
the oxytocic infusion should commence only once chemotherapy is limited to high-risk patients and those
evacuation has been completed (RCOG Guideline No patients (in Safdarjung hospital) who are unlikely to
38, Feb 2004). However, if the patient is experiencing come for close follow-up (as most of our patients are
significant hemorrhage prior to evacuation, then from different states). It can also be given in patients in
oxytocin infusion should be started earlier. Sharp whom follow-up hCG titer is high.
Follow-up: Strict follow-up in cases of H mole is of
curettage should be done at the end of the procedure.
All the products of conception along with the curetted utmost importance. Normally, after evacuation, serum
material should undergo histological examination. β-hCG progressively declines and comes to normal
There is no role of repeat curettage after one week within 14 days. The patient is examined one week after
or later. Rhesus (Rh)-prophylaxis is to be given in Rh- evacuation and the first blood sample for β-hCG is
taken. The uterine size is examined and ovarian cysts
negative patients according to gestation period. If on
are looked for. Vulva, vagina, urethra and cervix are
ultrasound, one viable fetus is seen along with molar
inspected to rule out secondaries. She is again examined
changes, the mother is to be counseled. If she desires,
after one month. If pre-evacuation chest X-ray showed
the pregnancy can be continued till term. If she wants
pulmonary metastasis, then another X-ray is done after
termination, a medical method can be used.
4 weeks. If remission is seen, a repeat X-ray is done
Hysterectomy as the mode of treatment in H mole can
every 3 months till 1 year.
be considered if the patient does not desire further
A weekly serum β-hCG level is done. If there is a steady
pregnancy and is more than 40 years old. Ovaries need decline, the follow-up is continued in this manner till
not be removed. But post-operative follow-up monitoring three consecutive values are normal. After this, monthly
is a must for these patients also. titers are done for 1 year (i.e. a total of one year after three
Role of prophylactic chemotherapy in H mole: The consecutive negative reports). Women should avoid
role of prophylactic chemotherapy in cases of H mole pregnancy during this period, hCG monitoring at 6 and 10
after suction and evacuation is controversial. High-risk weeks post delivery in subsequent pregnancies.
patients such as those with (i) pre-evacuation β-hCG
levels more than 100,000 mIU/mL, (ii) uterine size more Persistent Gestational Trophoblastic Tumor
than the period of amenorrhea and (iii) theca lutein cysts In case the hCG titer plateaus for 3 weeks or the titer
more than 6 cm have been seen to benefit after one course rises, the diagnosis of persistent gestational trophoblastic
tumor is made after excluding pregnancy by ultrasound Adequate response to treatment is defined as fall in
examination. Such patients often present with irregular β-hCG by 1 log after a chemotherapy course. Therapy is
vaginal bleeding, they are more likely to develop dyspnea continued for three cycles after 3 consequent negative
or abnormal neurological complaint from metastasis. normal serum b-hCG levels is achieved.
A complete metastatic work up is warranted in such Single agent chemotherapy is less toxic and this toxicity
cases, which includes a chest X-ray, complete hemogram, gets reversed easily and hence is well-tolerated. In a study it
liver function test (LFT), ultrasound and CT of the whole was found that, only 14% patients developed hepatotoxicty,
abdomen and brain. The tumor should be FIGO staged. 6% granulocytopenia and 1.6% thrombocytopenia follow
WHO prognostic scoring (Table 16.6) is done and treatment ing methotrexate folinic acid therapy. The chief side effects
advocated according to the risk. of dactinomycin are nausea and vomiting. If single agent
Follow-up is the same as in H mole. therapy fails, then multidrug chemotherapy is started.
Chemotherapy Multiagent Chemotherapy
Chemotherapy has radically changed the prognosis of Multidrug chemotherapy is the first line treatment for the
GTD without surgery and hence has helped in preserving high-risk group as per the WHO prognostic scoring. It is
reproductive function. Chemotherapy is instituted for both also given for low-risk cases, which shows resistance to
non-metastatic as well as metastatic GTD as is risk scoring. single drug treatment (less than 1 log fall of β-hCG).
Some of the multiagent regimens are MAC (methotrexate,
Single Agent Chemotherapy
dactinomycin and cyclophosphamide or chlorambucil);
For low-risk patients (mostly corresponding to clinical EMA-CO (etoposide, methotrexate, dactinomycin,
stages I and II) with no metastasis, single agent cyclophosphamide and vincristine [oncovin]); EHMMAC
chemotherapy is given. The most commonly used drug for (etoposide, hydroxyurea, methotrexate, dactinomycin,
single agent chemotherapy is methotrexate. Methotrexate vincristine and cyclophosphamide) and CHAMOCA (cyclo
is an antimetabolite. It binds to dihydrofolate reductase. phosphamide, hydroxyurea, methotrexate, vincristine and
This prevents purine production, side effects are seen in dactinomycin). Pre-treatment work up is done.
Safdarjung hospital are nausea, vomiting, anorexia and EMA-CO at present provides the best results with lowest
stomatitis. Folinic acid is used as rescue in all our cases. side effects and this drug regimen is used in the department
Pretherapy hemoglobin level, total leukocyte count (TLC), of Obstetrics and Gynecology at Safdarjung hospital (Table
differential leukocyte count (DLC) platelet count, blood
16.7).
urea nitrogen, creatinine, LFT and chest radiographs are
The drugs are given on every other week schedule.
done.
β-hCG level is monitored every week. Drugs are continued
The most preferred regime is injection methotrexate
1 mg/kg/day on days 1, 3, 5 and 7 along with injection
folinic acid 0.1 mg/kg/day on 2, 4, 6 and 8. After completion TABLE 16.7: Showing EMA-CO—regimen
of each cycle, blood is sent for serum β-hCG, CBC, hepatic Course 1 (EMA) Drug Dosage
function test and renal function test. The cycle can be Day-1 Etoposide 100 mg/m2 IV over 30 min
repeated after a week depending on the marrow recovery. Methotrexate 100 mg/m2 IV bolus
The cycle is stopped if white blood cells (WBC) count less Methotrexate 200 mg/m2 IV as 12h
than 3,000, neutrophils less than 1,500 platelets less than continuous infusion
100,000 or there are alterations in blood urea nitrogen, Dactinomycin 0.5 mg IV bolus
creatinine, alanine transaminase (ALT), aspartate Day-2 Etoposide 100 mg/m2 IV over 30 min
aminotransferase (AST) and bilirubin or side effects Leucovorin 15 mg IV/IM/PO every 12 h for
(stomatitis, gastrointestinal ulceration or fever) are severe. 4 doses, beginning 24 h after
start of methotrexate
The other regime for low-risk GTD uses methotrexate
Dactinomycin 0.5 mg IV bolus
alone as 0.4 mg/kg intramuscularly (IM) or IV daily for
5 days and repeated every 7–10 days. Course 2 (CO)
Dactinomycin (actinomycin-D) as a 5-day course Day-8 Cyclopho- 600 mg/m2 IV over
sphamide 30 min
(10 mg/kg IV) every alternate week or as pulse dose of 1.25
Vincristine 1 mg/m2 (up to 2 mg) IV bolus
mg/m2 IV every two weeks are alternate regimens.
till three consecutive β-hCG values in the serum are less the tumor. There is a 50% cure. For liver metastasis
than 1 mIU/mL. Atleast three courses are given once a (difficult to control), irradiation is also used. There are
normal titer has been reached. chances of massive hemorrhage leading to death. Some
If the courses are not given according to schedule, the authorities recommend whole liver irradiation of 2,000
tumor recovers and it cannot be treated because of so- cGY in case of extensive or subcapsular metastasis.
called development of resistance. There is about 25% cure.
Arterial embolization: It is considered in cases of acute
EMA-CO Regime for High-risk GTD bleeding in brain and hepatic metastasis.
The most preferred regime for high-risk GTD is the EMA-CO
regime. This is also used for single drug-resistant low-risk ROLE OF SURGERY IN
group. The therapy is quite well-tolerated without any serious
METASTATIC DISEASE
side effects. Mild bone marrow depression, stomatitis and
alopecia are the common side effects seen in our cases in It is considered in resistant cases and cases where no
Safdarjung hospital, which are entirely reversible. reproductive function is desired.
An important point to be kept in mind while giving
chemotherapy to high-risk patients with a heavy tumor Hysterectomy
load is the possibility of hemorrhage into the tumor and Hysterectomy has a definite role in patients with bulky
surrounding tissue after initiation of chemotherapy. uterine disease to reduce the tumor load. This decreases
Any unusual symptom reported by the patient after the number of chemotherapy cycles required for complete
starting chemotherapy should be viewed with a high index cure. It is also useful in high-risk group, atypical histologic
of suspicion. findings, frequent need for salvage chemotherapy.
Treatment for refractory cases: For women who are Hysterectomy is also required in patients who have
refractory to EMA-CO and fail to achieve complete repeated and uncontrolled hemorrhage.
remission, alternative regimens are to be considered. But it should be emphasized that even after surgery,
Almost all these regimens use cisplatin as one of the drugs. chemotherapy is a must with proper follow-up. This takes
Owing to renal toxicity, cisplatin containing regimens are care of the secondaries and recurrence.
not given as primary therapy in GTD. They are, however,
an effective salvage therapy.
Craniotomy
The various regimens which have been clinically tried Craniotomy may be required in some cases of cerebral
with favorable results are: metastasis for decompression and control of bleeding.
EMA-EP: This regime uses cisplatin (100 mg/m )
2 Local resection of cerebral tumor resistant to chemotherapy
and etoposide (200 mg/m ) along with etoposide,
2 has also been tried in a few patients.
methotrexate and dactinomycin as in EMA-CO.
EMA-POMB: It combines EMA along with cisplatin,
Thoracotomy
vincristine, methotrexate and bleomycin. Thoracotomy has a role in cases of localized pulmonary
PEBA: In this regime, cisplatin, etoposide, bleomycin metastases which are not sensitive to chemotherapy. The
and doxorubcin are given. resistant focus is excised.
ICE: This consists of ifosfamide, carboplatin and etopo-
side. This regime has been used along with autologous Laparotomy
bone marrow transplantation with some success. Lung Laparotomy for perforation peritonitis in cases of gastroin-
metastases have a very good prognosis in 90% of cases. testinal metastasis is needed as an emergency procedure
Treatment failure is mostly due to bone marrow and (very rarely).
gastrointestinal toxicity.
Irradiation: It is helpful especially in brain and liver Hepatic Resection
metastasis concomitantly with multidrug chemo Hepatic resection may be required as an emergency life-
therapy. On diagnosing brain metastases on history, saving measure to control hemorrhage from the tumor in
clinical examination and CT, immediate treatment an occasional case of hepatic metastasis.
is 2,000–3,000 cGY whole brain irradiations (in 10 Hepatic resection may also be needed for focal-resistant
fractions). This prevents hemorrhage at once and treats tumor.
Follow-up in choriocarcinoma involves measuring of the same histological type. The chances of developing
weekly hCG levels till three consequent normal studies persistent disease increase by three times in case of a
are obtained. Give two more courses of drug. The repeat mole. Hence, when pregnancy occurs after proper
overall relapse rate is 3% and the incidence is maximum follow-up, β-hCG and ultrasound are essential.
in the first year. As per current guidelines, life long Recovery of fertility after chemotherapy normally takes
surveillance is recommended. Pregnancy is avoided in place within one year. The rate of premature deliveries and
first year post chemotherapy as relapse can be masked congenital malformations is the same as in the general
and teratogenic risk may be there. population. But early monitoring with ultrasound and
Placental site trophoblastic tumor (PSTT): This is a rare β-hCG is necessary for recurrent GTD. After delivery, send
variant arising at the site of placental implantation. It is a the placenta for histopathological examination and call
slow growing tumor. The presenting complaint is irregular the patient after 6 weeks and measure serum β-hCG.
vaginal bleeding. In contrast to choriocarcinoma hCG Secondary tumors: Tumors like myeloid leukemia colon
levels are low relative to tumor burden. This is because cancer and breast cancer as seen after multiple drug
of lack of syncytiotrophoblasts (which produces hCG) regimens (especially ones with etoposide) but not with
in PSTT. The treatment is surgical, i.e. hysterectomy as it single drug therapy.
is usually chemo-resistant tumor. If it has metastasized,
then EP-EMA regimen gives better results. Paclitaxel and Phenomenon of Phantom hCG
topotecan may be used in resistant cases. Phantom hCG or false positive hCG is an entity of which
physician should be aware of, as these false positive results
Epithelioid Trophoblastic Tumor may lead to unwarranted investigations and interventions
Epithelioid trophoblastic tumor is yet another recently on suspicion of diagnosis of abnormal pregnancy or
described rare tumor arising from intermediate trophob gestational trophoblastic disease. Its incidence is 1/1000
lasts. Management is similar to PSTT. to 1/10,000 tests. The false positive phantom hCG
can give a positive pregnancy test in a non pregnant
Prognosis patient and is suspected in a patient with negative urine
H mole: After evacuation, it has a very good prognosis. sample test but positive serum hCG. It is discovered with
The patient is kept under surveillance. incidental positive serum pregnancy test, done as a part of
Choriocarcinoma: Non-metastatic, survival is 90% with investigating before a surgery or a diagnostic procedure. It
chemotherapy. In metastatic tumor, EMA-CO regimen is due to interfering of the tests by presence of heterophile
has the best prognosis. Lung metastases have the best antibodies with ability to cross react with other species
prognosis. Brain and liver give 50–80% prognosis. immunoglobulins. American College of Obstetricians and
If prior chemotherapy is given and has failed, the Gynecologists (ACOG) recommends three tests to rule out
prognosis is not good. presence of heterophile antibodies—(1) The interference
Recurrence occur mostly in the first 6 months but can with hetrophile antibodies can be confirmed if urine is
be seen after 3 years. negative for hCG (as they cannot undergo glomerular
filtration due to large molecular weight) and serum level
CONTRACEPTION IN PATIENTS OF GTD is atleast 50 IU/L, (2) Non-linearity pattern not matching
with standards on serial serum dilutions goes in favor of
The patients of gestational trophoblastic disease require
interference, (3) Pre-treatment of the serum removes the
a very potent contraceptive during follow-up, as a fresh
heterophile antibodies.
pregnancy will raise the hCG levels and cause confusion
in the follow-up.
Variants of β-hCG
Combined oral contraceptives are a safe and effective
means of contraception once the hCG levels have come b-hCG is a glycoprotein produced by trophoblasts and the
back to normal. Patients with H mole should not conceive pituitary. It has a and b-subunits, of which b-subunit is
for 6 months after normal hCG levels. After completed specific to trophoblast produced hCG. The b-hCG is found
course of chemotherapy she must avoid pregnancy for one to exist in two intact forms; a regular b-hCG secreted
year (some say 2 years after choriocarcinoma). in normal pregnancy and H-hCG variant produced by
invasive trophoblasts seen in implantation phases of
Future Pregnancy Experience normal pregnancy and GTN. Besides H-hCG in GTN,
After one H mole repeat incidence is 1%. But after two fragmented b-hCG, e.g. free b-subunit, b-core, nicked
molar pregnancies it is 15–28%. The recurrence is mostly free-b and C-terminal fragments are also produced.
1. Define:
i. Gestational trophoblastic disease
ii. Phantom hCG.
2. Explain the term epithelioid trophoblastic tumor.
3. True/False:
i. H mole has an abnormal pregnancy which has no embryo.
ii. FIGO stands for International Federation of Games Obstetrics.
iii. Craniotomy may be required in some cases of cerebral metastasis for decompression and control of bleeding.
17
Harsha Gaikwad, Kavita N Singh, Sudha Salhan
Antepartum Hemorrhage
placental attachment in the lower uterine segment, or

DEFINITION
when performing vaginal examination.
Bleeding from the genital tract after 28 weeks of gestation It contributes to about one-third of all cases of APH.
but before birth of the baby is defined as antepartum The incidence ranges from 0.5–1% amongst deliveries in
hemorrhage (APH). hospitals. Incidence in the Safdarjung hospital is 2%.
The incidence is about 1–3.5%. APH is one of the major
causes of maternal mortality and morbidity in the devel- Grades
oping countries. There are four grades or types of placenta previa.
1. Grade/type I (lateral/low lying): Placental edge just
CAUSES encroaches on LUS but does not reach upto the internal
The causes (i.e. differential diagnosis of bleeding in the os (Fig. 17.1).
third trimester of pregnancy) are given in Flowchart 17.1. 2. Grade/type II (marginal): The placenta edge reaches
the internal os but does not cover it. It can be (a) anterior
or (b) posterior (Fig. 17.2).
PLACENTA PREVIA 3. Grade/type III (partial/incomplete central): The
Placenta previa is a condition in which placenta is implanted placental edge covers the internal os partly, but does
completely or partially over the lower uterine segment not cover it fully when the internal os is completely
(LUS). It may lead to painless and causeless bleeding per dilated (Fig. 17.3). It can be anterior or posterior.
vaginum. 4. Grade/type IV (total/complete/central): The placental
Bleeding may occur when uterine contractions take edge covers the internal os completely even when the
place dilating the cervix, applying shearing forces to the os is fully dilated (Fig. 17.4).
Flowchart 17.1: Causes of vaginal bleeding in third trimester of pregnancy

Antepartum Hemorrhage 159
Fig. 17.1: Type I (low lying) placenta previa Fig. 17.2: Type II (marginal) placenta previa
Fig. 17.3: Type III (partial central) placenta previa Fig. 17.4: Type IV (complete/central) placenta previa
In the last two grades the placenta can be visualized the increased incidence of placenta previa following a
through a per speculum examination. cesarean section in a previous pregnancy.
A low lying placenta seen in early pregnancy may
migrate upwards as the pregnancy advances when the Causes
lower segment forms and upper segment expands. This Theories
may also be due to differential development of placenta Dropping down theory, where implantation of the
and is influenced by previous scarring or changes in zygote in the LUS which normally implants in the upper
vascularization. Adherence to the lower segment explain segment.
Defective decidualization Diagnosis

Hyperplacentosis (bigger placenta) as seen in multiple
Clinical
pregnancy, anemia, Rh-isoimmunization
Persistence of chorion laeve. A gentle per speculum examination differentiate the condi
tion from other local causes in the vagina and the cervix, e.g.
Predisposing Factors polyp, etc. The blood in the vagina can be collected by the
Grand multiparity speculum and tested (if possible) for fetal hemoglobin (vasa
Increasing maternal age previa).
Multiple pregnancy
Rh-negative blood group of the pregnant women and
Investigations
Rh-positive husband Ultrasonography (USG)
Previous cesarean section (may have placenta accreta). Route
The incidence of placenta previa increases with each •• Transabdominal

cesarean section. The normal incidence is around 1–2%. •• Transvaginal
Once cesarean section number increases the risk to 10– •• Transperineal/translabial
35% while multiple cesarean sections increase it to 65% Three-dimensional scan and color Doppler flow study
History of previous spontaneous or induced miscar- is used.

riages and instrumentation Sonography being simple, precise and safe, is the
Previous history of placenta previa method of choice in diagnosis.

Ethnicity, e.g. more in women of Asian origin Diagnostic criteria: Placenta within 2 cm of internal os
Congenital uterine malformations. at term is labeled placenta previa.

It can be used to localize and grade the placenta and
Cause of Hemorrhage obtain other information like, amniotic fluid index
The inelastic placenta gets detached from the progressively (AFI), fetal age, maturity, etc.
thinning and dilating LUS during the last trimester of Differential diagnosis on USG (pitfalls)
pregnancy and in labor and thereby bleeding occurs •• Blood clots
from the opened maternal sinuses. Hence, it is mostly •• Thick decidual reaction
unprovoked, but sometimes there is history of recent •• Succenturiate lobe
coitus. Over distended bladder reveals placenta away from
The blood lost is almost always maternal in origin, but internal os.
in traumatic separation of the placenta, fetal blood may Before 26 weeks of gestation, LUS of the uterus is not
escape from torn villi. well formed, hence upto 45% of placentae may appear low
lying. Routine ultrasound done at 16–20 weeks raises false
Clinical Features fears. Hence, placenta previa should not be diagnozed on
Symptoms a single ultrasound observation in the second trimester.
Sudden onset of painless and apparently causeless (no The follow-up USG in late third trimester, mostly shows
history of trauma, coitus, etc.) and recurrent bleeding placenta in the upper segment (King’s phenomenon of
without onset of labor. placental migration). Transvaginal ultrasound (done by
The first bleeding is often minor and is called warning an expert cautiously) is superior to a transabdominal one
bleed. Subsequent bleeding may be life-threatening in diagnosis, because placental edge and cervical canal are
because of poor contractility of the lower segment. readily identified. It is helpful in early diagnosis of a few
complications of placenta previa.
Signs Magnetic resonance imaging (MRI): It is non-invasive,
General examination safe and excellent but expensive method of diagnosis.
Pallor is proportionate to the visible blood loss. Gadolinium enhanced MRI is helpful to diagnose placenta
Stalworthy’s sign may be seen in type IIb placenta accreta and percreta.
previa [suprapubic pressure on the fetal head elicits a Other investigations (not used nowadays)
deceleration in the fetal heart rate (FHR)]. Radiography
Fetal heart sound (FHS) and placental souffle are well Radioactive isotopes study I132 or I131 or technetium99
auscultated. Arteriography.
TABLE 17.1: Complications of placenta previa report immediately at the slightest blood staining. Active
involvement of the whole family is essential. Otherwise,
Perinatal mortality ranges from 7 to 25%
keep the patient in the hospital till she delivers.
Problems specific to placenta previa are:
Route of delivery is decided based on type of placenta
zz Placenta accreta
zz Uterine atony and postpartum hemorrhage (PPH)

previa: Type I, II anterior—induction of labor with
zz Bleeding from placental site.
artificial rupture of membrane (ARM) and oxytocin
Abruptio associated in some cases. infusion. Cesarean section done only if there is severe
Maternal mortality 0.5%: Adult respiratory failure (ARF), preterm bleeding or fetal distress or any other obstetric indication.
rupture of membranes (PROM), preterm labor (PTL), cesarean Rest of the patients deliver vaginally.
section (CS), disseminated intravascular coagulation (DIC), PPH. In type II posterior, III and IV—cesarean section is
performed.
Difficulties encountered during cesarean section in
Investigation for management: Hemoglobin (Hb), packed placenta previa
cell volume (PCV), blood group, venereal disease research Before term the lower segment is not well formed.
laboratory (VDRL), urine, if Rh-negative Coombs test, May require lower segment vertical incision.
Kleihauer-Betke test. If the placenta lies anteriorly, there can be large dilated
vessels. In such a case ligate them with catgut and then

Complications (Table 17.1) give a nick in the uterus or separate the placenta and
Mostly, it is not possible to predict which patient of approach the baby laterally or cut through the placenta.
placenta previa will bleed but it has been seen that if If there is placenta accreta hysterectomy or internal
the maternal a-fetoprotein is more than 2.0 multiples of iliac vessel ligation may be required.
medium (MOM) there is a more chance of bleeding. If the placental bed bleeds excessively, apply hotpacks,
mattress sutures or gel foam.

Management Cesarean section for placenta previa, must be done
preferrably during the day time so that there are senior
Prevention of maternal morbidity and mortality by early
doctors of the obstetrics, pediatrics and anesthesia
detection is very important.
departments either directly supervising or performing
the procedures, e.g. cesarean section, resuscitation of
Plan of Management
the neonate or administering anesthesia. This will help
Mcafee Johnson regimen: Expectant management—the prevent maternal morbidity, mortality and fetal mortality
patient and the family members are informed about the line and morbidity through prematurity (very common).
of action. If the condition of the mother is stable and the Congenital defects are also more common but development
fetus is premature. The basis of expectant management is to of intrauterine growth restriction (IUGR) is not proven
give time for fetal maturation to reduce perinatal mortality. yet. In an emergency situation keeping adequate blood
The patient is admitted in the hospital. Cross matched in hand is life saving especially in complicated cases like
blood is kept ready. Strict bed rest is advised till bleeding placenta accreta, percreta, etc. or cases with previous
stops. Betamethasone is given to improve lung maturity of history of cesarean section.
the fetus. If the membranes are intact and active uterine Placenta previa without hemorrhage: It is diagnosed in
contractions are perceived then selection of tocolytic is to the second trimester by ultrasound. Explain to the patient
be judicious. b-mimetics are not given because they cause and the family members the position of the placenta at
maternal tachycardia, hence, they are used only if there is diagnosis and reassure them that it will most probably
minimum bleeding. Calcium channel blockers (nifedipine, migrate upwards in most of the cases. The patient is
etc.) cause hypotension, indomethacin is also harmful advised to avoid strenuous work and coital activities and
(premature closure of fetal ductus arteriosus). Therefore, to report at the slightest bleeding. Active participation of
magnesium sulphate is most commonly used. If bleeding family members is essential. The ultrasound is repeated
is completely stopped and there is no other complication at 28–30 weeks. If placenta previa persists the patient
(after days of observation), if the gestation is early and in is warned against rigorous activities and intercourse
carefully selected cases who have access to telephone, who and advised to report immediately even if slight
live nearby and have transport ready, can be discharged. The bleeding occurs. Persistence of placenta previa beyond
patients are advised strict bed rest, to avoid intercourse and 32–34 weeks of gestation implies that it will remain as such
and will usually not migrate. Delivery depends on the type

of placenta previa (vide supra).
Placenta previa with hemorrhage: Management
depends on the amount of bleeding. Initial small warning
hemorrhage must alert the obstetrician. The patient is
admitted to the hospital. The maturity of fetus is assessed. If
the fetus is mature delivery can be allowed. In all active cases
of hemorrhage stabilize the maternal hemodynamic status.
An intravenous (IV) access is established (18 or 16 number
cannula) and blood is arranged. Arterial embolisation may
be life saving in some cases (if available). If the fetus is not
mature one can administer tocolytics and betamethasone
for achieving lung maturity of the fetus (when bleeding is
slight).
Immediate delivery is indicated if:
Maternal condition deteriorates despite appropriate
treatment
Persistent hemorrhage
Gestational age 36 weeks or more
Fetal distress in a viable fetus Fig. 17.5: Revealed accidental hemorrhage

Estimated fetal weight 2500 g or more
Patient in labor (28 weeks), but before delivery of the fetus. It is also known
Fetus is very small or has lethal major congenital as placental abruption. It causes perinatal mortality and
abnormalities may cause maternal mortality as well.
IUD (intrauterine devices).
Recurrence rate of placenta previa is 6–8 times greater Incidence

than in the normal population.
It occurs in one in 100 to 250 deliveries and is more
common in the developing world like India.
Indeterminate Bleeding
It has three types—(i) revealed hemorrhage, (ii)
It includes cases of APH, where a confident diagnosis of concealed hemorrhage, (iii) mixed hemorrhage.
placenta previa or abruptio placentae cannot be made, are
1. Revealed hemorrhage: The bleeding of placental
there any local lesions causing bleeding viz. (1) marginal
abruption passes into the decidua basalis. It usually
sinus hemorrhage, circumvallate placenta, (2) excessive
insinuates between the membranes and the uterus
show, (3) ruptured vasa previa and (4) marked decidual
reaction on the endocervix. These patients are managed and escapes through the cervix. The blood loss is
conservatively, and usually deliver spontaneously or after proportionate to the amount of bleeding (Fig. 17.5).
induction of labor. Close fetal monitoring is necessary. 2. Concealed hemorrhage: In this, the blood does not
escape externally but is retained between the detached
Vasa Previa placenta and the uterus. The hemodynamic instability
It can be diagnosed by looking at the insertion of the cord of the patient is out of proportion to visible blood loss
on USG. If there is bleeding, test for fetal blood (alkaline (Fig. 17.6).
pH, Ogita and Loendersloot test). Color Doppler helps 3. Mixed hemorrhage: It is a combination of revealed and
in clinching the diagnosis. Early recognition and elective concealed hemorrhages.
cesarean section reduce fetal and perinatal mortality.
Etiology/Risk Factors
ABRUPTIO PLACENTAE The primary cause of placental abruption is unknown, but
there are several associated conditions and risk factors like:
(ACCIDENTAL HEMORRHAGE) Hypertensive disorders of pregnancy (HPD): In 20–
Incidence at Safdarjung hospital is 1.5%. It is the premature 50% cases HPD is associated with concealed type of
separation of a normally situated placenta, after viability abruptio placentae
Pathology
Abruption is a Latin word meaning breaking away.
Pathology depends on the etiology. The end result is
common. Placental abruption is initiated by hemorrhage
into the decidua basalis. To start with there is vasospasm
of the uterine vessels, then they relax causing venous
engorgement and arteriolar rupture into the decidua.
The decidua then splits leaving a thin layer adherent
to the myometrium. Consequently, the process in its
earliest stages consists of the development of a decidual
hematoma that leads to further separation, compression,
and the ultimate destruction of the placenta adjacent to it.
The escaping blood may dissect the membranes from
the uterine wall and eventually appear externally, into the
amniotic sac (revealed) or may be completely retained
within the uterus concealed behind the membranes and
even between the muscles (Couvelaire uterus Figs 17.7A
and B). There is increased intrauterine pressure, which
Fig. 17.6: Concealed accidental hemorrhage further embarrasses the placental circulation. This adds to
the hypoxia of the fetus already present due to separation
of the placenta. Routine examination of the placenta after
High levels of maternal serum a-fetoprotein and human
delivery reveals retroplacental clot.
chorionic gonadotropin (hCG). Decreased inhibin A,
In severe types of abruptio placentae, a fibrin knot or
pregestational diabetes and antiphospholipid syndrome
a thrombotic lesion in the hepatic sinusoids, has been
and hyperchromocysteinemia
described as specific of abruptio placentae. In renal
Blunt external trauma, motor vehicle accident (when
changes, oliguria and anuria may develop, due to acute
seat belt is not correctly applied)
tubular necrosis in mild forms of abruptio. Renal cortical
External cephalic version
necrosis occurs in severe form.
Short cord. Rapid decompression of the uterus as seen
Chorioamnionitis is implicated in its pathophysiology.
in cases of twins and hydramnios. It causes reduction
in surface area of the uterus and hence, shearing of the
Coagulation Failure (Coagulopathy)
placenta
Preterm premature rupture of membranes (PROM),
Defibrination and Excess Fibrinolysis
prolonged rupture of membrane—three-fold increase About 5% of patients with abruptio placentae develop
in risk compared with normal pregnancy coagulation failure, excess fibrinolysis and a hemorrhagic
Uterine anomaly (septate uterus) state. Coagulation failure is detected by prolonged
Abnormal placentation (circumvallate placenta) coagulation time, lowered platelet count, low fibrinogen
Past history of abruption (recurrence ten times higher level and excess fibrinolysis is detected by elevated fibrin
than normal cases) degradation products (FDP) in maternal serum (more than
Maternal anemia, malnutrition, folate deficiency and 100 mcg/mL). The patient presents with hemorrhages from
smoking, lower socioeconomic class, young age, low needle puncture site, hematuria, cutaneous ecchymoses,
education postpartum hemorrhage, etc. In 30% of cases placental
High parity, elderly or with fibroids abruption is severe enough to kill the fetus.
Vascular accidents, supine hypotension syndrome

Clinical Features of Accidental Hemorrhage
Severe fetal growth restriction
Cigarette smoking Symptoms
Malformed fetus There may be a history of previous small vaginal bleeds.
After snake bite Pain: Severe abdominal pain occurs with concealed
Cocaine abuse. hemorrhage. If the placenta is posterior, the patient
may complain of backache. Painful uterine contractions TABLE 17.2: Clinical grading (sher’s clinical grades) of accidental
may be present which are unresponsive to tocolysis. hemorrhage
External vaginal bleeding may not be very significant Grade Retroplacental clots FHS (fetal heart sound)
but blood may accumulate retroplacentally. I 150 mL or less Present diagnosed after delivery
Shock may not be proportionate to visible blood loss II 150–500 mL 92% abnormal
(more shock than acounted for by visible blood loss). III As above Absent fetal heart
Onset of premature labor. IIIa Without coagulapathy
IIIb With coagulopathy
Signs
Tender enlarged uterus with the uterine size being
TABLE 17.3: Page’s classification (1951) of accidental hemorrhage
larger than the period of gestation. The uterus feels
Grade 0 Clinically unrecognized before delivery but diagnosed on
woody hard in consistency and has tonic contractions, examination of placenta after delivery
which give the uterine body a hard feeling. This feeling Grade I Cases with external bleeding only or mild uterine tetany
is aggravated by rare accumulation of blood between but no maternal shock, good fetal heart sound. Cases
the uterine muscle fibers (Couvelaire uterus). When with external bleeding only or mild uterine tetany but no
bleeding reaches the uterine muscle it is mostly the maternal shock, good fetal heart sound
concealed variety. Grade II Cases with uterine tetany usually with uterine tenderness
Abdominal rigidity is seen in severe cases. fetal distress or death but no maternal shock
Vaginal bleeding may be serosanguinous and non-clotting. Grade III Cases with uterine tetany, intrauterine fetal death, materal
shock or coagulation defect
Fetal distress is seen in milder cases. Absent fetal heart is
present in severe cases. Cardiotocography show regular
(one/min) small contractions superimposed on raised Ultrasonography
uterine tone. The effect on the fetus is seen in the form
To rule out placenta previa.
of tachycardia, loss of variability, late deceleration. If
Reveal the state of the fetus.
these changes are present, urgent cesarean is indicated.
Retroplacental clots at previous placental site (as seen
Blood pressure is a poor guide to the extent of bleeding.
in earlier ultrasound) is helpful.
Clinical presentation of abruptio placentae may be
divided into 3 grades as a guide to management and Differential diagnosis to rule out: Chorioamnionitis,
comparison between centers (Table 17.2 and 17.3): pyelonephritis, appendicitis, rupture uterus, placenta pre-
1. Grade I: It can not recognized clinically before deli via in labor. Concealed type is to be differentiated from
very. Diagnosed only be retroplacental clot (mild retroperitoneal hemorrhage, rupture of an appendicular
form) after examination of the placenta after delivery. abscess, acute degeneration of the uterine fibroid and its
2. Grade II: Intermediate—classical signs of abruption torsion.
but the fetus is alive. Abruption occurring in posteriorly situated placenta
3. Grade III: Severe—the fetus is dead. Grade IIIa is is very dangerous because backache is the only symptom
without coagulopathy IIIb is with coagulopathy. and the site of tenderness is not reachable.
Features of shock.
Management
Investigations Prevention is done based on the risk factors. High-risk
General pregnant women must recognize early symptoms and
Blood examination including Hb estimation and white report immediately.
blood cell (WBC) counts. Bed side bleeding time (BT)
and clotting time (CT) Principle of Management
Serum fibrinogen level, prothrombin time (PT), partial The importance of swift action after diagnosis is crucial to
thromboplastin (PTT), FDP levels, platelet count, bleed- prevent maternal mortality and fetal demise because the
ing and clotting time, D-dimer (fibrinolytic activity) level prognosis of the mother and the fetus worsen by delay.
Serum electrolytes Admit the patient, draw blood for cross matching and tests
Arterial blood gas analysis and set up an IV line (with 18 or 16 gauze cannula).
Blood group and cross-matching The principles of management are:
The Kleihauer-Betke test. Early delivery
Adequate blood transfusion Oxytocin Drip

Adequate analgesia Improves uterine activity.
Detailed monitoring of maternal condition
Hastens delivery.
Assessment of fetal condition.
General Measures COUVELAIRE UTERUS

Evaluate and replace blood loss—atleast 2 units fresh (FIGS 17.7A AND B)
whole blood or packed cell with ringer lactate. Fetal There is widespread extravasation of blood into the uterine
death usually occurs with blood loss of upto 2500 mL and muscles below the peritoneum.
indicates severe losses. Draw blood for cross matching It is a complication of severe form of placental abruption.
and screening for clotting factors and platelets count. The patient looks unwell. The abdomen is tender and the
One or two wide bore IV lines are started, Foley’s catheter uterus is woody hard. Depending on the bleeding, fetal
is introduced in urinary bladder and central venous parts may not be palpable.
pressure (CVP) line is established. This is required to know On laparotomy the uterus is of dark portwine (bluish)
about fluid requirements and to measure urine output. color. The bleed is patchy or diffuse looking like a huge bruise.
Maintain PCV 30%, pulse less than 120/min, urine Subperitoneal petechial hemorrhages are found under the
output at least 30 cc/hour, CVP 4–8 cm of water. This is uterine peritoneum and may extend into the broad ligament.
vital as it help prevent under transfusion before delivery There can be free blood in the peritoneal cavity or broad
and over hydration after delivery. ligament hematoma. Microscopically, uterine muscle over
Mark the outline of the uterus with a pen. the affected area gets necrosed and there is infiltration of
Keep on measuring abdominal girth at the level of the blood and fluid in between the muscle bundles. The blood
umbilicus every hour. vessels show acute degenerative changes or thrombosis.
Couvelaire uterus is not an indication per se for
Specific Measures hysterectomy.
Assess fetus (clinical + USG): Presentation, gestational Uterus usually contracts well once emptied and sutured.
age, size, viability, FHS. Occasionally it causes severe atonic PPH in which
Watch for disseminated intravascular coagulopathy
case internal iliac ligation uterine artery embolization
(DIC): Due to placental thromboplastin release. if possible or obstetric hysterectomy may be required.
Correlate clinical evidence of excess bleeding with
laboratory parameters.
Complications
Decision for delivery: Expectant treatment only has a Maternal
place when the diagnosis is in doubt or abruption is minor Hemorrhagic shock: The amount of blood loss in
or there are no previous episodes. Monitoring the status accidental hemorrhage is usually underestimated. This
of the fetus and the extent of the placenta separation is because part of the blood loss is behind the placenta
is important, especially if the fetus is premature. and hence, not measured before delivery. Also, since the
However small the separation, the fetus is to be closely patient may be hypertensive before the onset of bleeding
monitored, as there is always damage to the placenta. low blood pressure is not noticed to be obvious sign.
Induction of labor as early as possible is to be practised. Postpartum hemorrhage: There may be some blood
In the meantime serial Doppler studies are needed to round the uterine muscles and the high level of fibrin
decide whether to continue the pregnancy under strict degradation products can inhibit myometrial contrac-
surveillance or deliver the baby immediately. tions. It can worsen the situation if associated with
An IV oxytocin infusion is started first, then an artificial coagulopathy.
ruptures of membranes (ARM) is done (Flowchart 17.2) Disseminated intravascular coagulopathy: Once
Advantage of amniotomy artificial rupture of membrane: a coagulation disorder develops the dangers to the
Augments contraction and hastens the onset of labor. mother are increased. Here the fibrinogen level is less
Uterine contractions reduce uterine bleeding (however, if than 300 mg/mL. Besides fibrogen loss there may be
the uterus has intramyometrial bleeding it will not help). consumptive thrombocytopenia because of the clot
Decompresses the intrauterine pressure and reduces using platelets. Immediate delivery will prevent further
intravasation of blood into the myometrium. damage. Adequate blood transfusion or packed red
Reduces absorption of thromboplastin. cells to maintain circulation and platelets transfusion
Flowchart 17.2: Showing management of delivery in abruptio placenta and placenta previa
Abbreviations: APH—Antepartum hemorrhage; FHS—Fetal heart sound; ARM—Artificial rupture of membrane; USG—Ultrasonogram;
DIC—Disseminated intravascular coagulation; FFP—Fresh frozen plasma; LSCC—Lower segment cesarean section
A B
Figs 17.7A and B: Couvelaire uterus. A. Schematic; B. Photograph
if platelet counts fall below 50,000/µL. Avoid dextran Hypoxia.

as it may inhibit blood clotting and interfere with Recurrence is seen in subsequent pregnancies in 20–25%
cross matching. However, one can use cryoprecipitate. of cases.
Fibrinolytic inhibitors (aminocaproic acid or aprotinin) Difference between placenta previa and abruptio
have a controversial place and the same is true about placentae is given in the Table 17.4.
the use of heparin.
Urinary output monitoring is essential. Due to hypovo-
TABLE 17.4: Differences between placenta previa and abruptio
lemia there can be: placentae
•• Acute tubular necrosis
Placenta previa Abruptio placentae
•• Renal cortical necrosis.
Ischemic necrosis of the kidney is a serious complication. Vaginal bleeding is bright red, Vaginal bleeding is either
This is due to hypovolemia, and hence, hypoperfusion revealed, painless and recurrent concealed or revealed but dark
red, painful and continuous
during acute blood loss. Fibrin deposits from DIC also
play a part. Oliguria during the first 12 hours postpartum Abdominal pain is absent Pain in abdomen is present
may not be due to permanent damage. Diuretics are not Shock, if present correlates to Shock may be out of
indicated here. If oliguria persists after 12 hours and amount of blood loss proportion to visible blood
CVP is normal measure serum electrolytes, urea and loss (e.g. concealed accidental
creatinine. Continue conservative treatment till serum hemorrhage)
potassium, blood urea and creatinine levels start to rise Very few patients may have Upto 50% may be associated
then consult a nephrologist. hypertension with hypertension
Other complication can be: Per abdomen, uterus is relaxed Uterus is tender and tonically
•• Sheehan’s syndrome (pituitary ischemia) contracted
•• Death.
Fetal heart sound (FHS) are FHS often absent or not heard
usually normal, unless patient is because of tonically contracted
Fetal in shock uterus
High perinatal mortality is seen in abruptio placentae.
alpresentations are common Presenting part (usually vertex)
M
Perinatal death occurs in 22–40% due to: and presenting part is easily felt is felt with difficulty
Prematurity and is floating
Small for gestational age
Sonography is 98% diagnostic Is suggestive if clots seen
Congenital anomalies (2–5 times greater incidence
especially those of the central nervous system) Usually cesarean is done Usually vaginal delivery
Intrauterine fetal death (IUFD) if severe placental
[artificial rupture of membrane
(ARM)+ oxytocin]
detachment (due to anoxia and prematurity)
1. Explain all the types of placenta previa.
i. Indeterminate bleeding
ii. Abruptio placentae
3. True/False:
i. Abruptio placenta is also known as accidental hemorrhage.
ii. Excess fibrinolysis is not detected by elevated FDP.
18
Sunita Singal, Sudha Salhan, Harsha Gaikwad
Multifetal Gestation
INTRODUCTION INCIDENCE
Twin pregnancy has been a fascinating subject and has According to Hellen’s rule, the frequency in naturally
generated a lot of interest in obstetricians, many religions, occuring twins is 1 in 80, triplets is 1 in 802, quadruplets
communities and cultures. Many myths are linked to the is 1 in 803 and so on. But there are geographic variations
birth of twins. in the frequency of multiple pregnancies. The incidence is
highest in African countries and lowest in Japan. In Nigeria,
DEFINITION it is 4.5 per 100 births, as compared to 0.5 per 100 births
in far Eastern countries. The incidence is intermediate in
The development of two or more than two fetuses
Caucasians, about 1 or 1.2 per 100 births.
simultaneously in a pregnant uterus is called multifetal
pregnancy. Simultaneous development of two fetuses is ETIOLOGY
called twin pregnancy and is the most common variety of
multifetal pregnancy. The other types are the development The cause of twinning is not known. The frequency of
of three fetuses (triplets), four fetuses (quadruplets) (Fig. uniovular (monozygotic) twinning is fairly constant
18.1), five fetuses (quintuplets), six fetuses (sextuplets). worldwide, approximately 4 per 1000 births though certain
Although rare, these are more often encountered in factors like assisted reproductive technique (ART) method,
women on ovulation inducing drugs. Multiple gestations play a mojor role. There are variations in the frequency of
are high-risk pregnancies [due to an increased risk of dizygotic twinning (varying with maternal characteristics).
Certain races show an increased prevalence whereas
perinatal morbidity and mortality and maternal morbidity
postpartum hemorrhage (PPH), etc.] and thus require others show a low incidence.
Hereditary predispositions appears to play a role,
special attention (high-risk pregnancy).
specially from the maternal side.
High parity (specially para 5 and above) is associated
with a higher incidence.

Maternal age: Dizygotic twinning occurs more freque
ntly with rising maternal age, showing a peak between

35 and 39 years (due to maximum hormonal levels
leading to double ovulation).
Nutrition: Studies have shown that the twinning rate
was higher (25–30%) in taller, heavier women and

with increased nutritional level than in shorter and
nutritionally deprived women.
Iatrogenic
•• Use of ARTs: The treatment of infertility using

Fig. 18.1: Quadruplets with mother ovulation inducing drugs, or in vitro fertilization or
Multifetal Gestation 169
embryo transfer probably due to a minor trauma

to the blastocyst, make an important contribution.
Ovulation induction by clomiphene (6–8% risk of
multifetal pregnancy) or gonadotropins (20–30%
risk) increase the chances of both monozygotic and
dizygotic twins. Though Governments are passing
legislations to limit the number of embryos transfer to
a maximum of two, people are not abiding by these
laws.
•• Contraception: Progestational agents and combined
oral contraceptives (COCs) delay the transport of the
fertilized ovum through the tube and implantation.
They thus increase the risk of twinning in conceptions
occurring immediately after stopping them. Studies
of conceptions occurring soon after cessation of Fig. 18.2: Diamniotic-dichorionic fused dividing membrane has
use (>6 months) of oral contraception (OC) have four layers—two chorions separating two amnions
shown that the risk of twin pregnancy is two times
increased if the conception occurs within 1 month
after discontinuation of OC due to a sudden release of
gonadotropins.
TYPES OF TWINS
Dizygotic or Binovular Twins
They are also known as fraternal twins, result from fertiliza-
tion of two ova, either from same or both the ovaries during
a single ovarian cycle, each by a separate sperm. The babies
are not identical and may not be of same sex and show only
sibling resemblance. It is the most common variety and
nearly two-thirds (67%) of all twins are dizygotic. All dizy-
gotic twin have two placentae which are dichorionic and
diamniotic (Fig. 18.2) (see Figs 62.3 and 62.4).
Fig. 18.3: Diamniotic-monochorionic dividing membrane has
three layers—two amnions separated by one chorion
Monozygotic or Uniovular Twins or
Identical Twins
Such twinning results from fertilization of a single ovum by enclosed by a single chorion, have a single placenta but
a single sperm and is seen to occur in one-third of all twin two separate amniotic sacs (diamniotic-monochorionic).
pregnancies. There are several varieties of monozygotic Nearly, two-thirds of monozygotic twins are of this variety
twins which are determined by the time, when splitting (Figs 18.3 and 18.4).
occurs in the embryo as described below: If the cleavage occurs between 8 and 12 days after fer-
If division takes place at about the 8 cells stage, i.e. within tilization, i.e. after differentiation of amnion, there is a
3 days (72 hours) after fertilization, the resulting embryo single amniotic cavity, single chorion and a single pla-
will have two separate or a single fused placenta, two centa (monoamniotic-monochorionic). These acco
chorions and two amnions (diamniotic-dichorionic). unts for only 1–5% of monozygotic twins (Fig. 18.5).
This accounts for nearly one-third of monozygotic twins On a very rare occasions, when splitting occurs after the
(Fig. 18.2). appearance of the primitive steak, i.e. after the 13th day
If the cleavage is delayed until the inner cell mass is of fertilization, it results in the formation of conjoined
forming (4–7 days), the two embryos will develop twins within a single amnion and chorion, also called
Fig. 18.4: Diamniotic-monochorionic placenta with two cords Fig. 18.5: Monoamniotic-monochorionic twins
siamese twins. The following varieties of conjoined Molecular genetic fingerprinting of samples taken from
twins have been described according to the site of fusion: amniotic fluid from both the sacs (where the sex of the
•• Thoracopagus: Joined at the chest twin is the same).
•• Omphalopagus: Joined at the anterior abdominal Fetal growth and congenital malformations—
wall monozygotic twins have a higher risk of congenital
•• Pygopagus: Joined at the buttocks malformations and discordant growth than in dizygotic
•• Craniopagus: Joined at the head twins owing to the fact that the action of twinning may
•• Ischiopagus: Joined at the ischium. not be an equal division and is a teratogenic event.
Sonographic evaluation: Evaluate the number of
DETERMINATION OF ZYGOSITY chorions (possible event in the first trimester).
Fetal sex: In approximately 35% of cases, twins are of Presence of a single placental mass (single fused) or
the opposite sex, thus implying dizygosity. 2 separate placental sites with a thick (>2 mm) intervening
Observation of the placenta: Monochorionic pla membrane of 3 or 4 layers (in dichorionic-diamniotic
centae (irrespective of di/monoamniotic) only occur placenta).
in monozygotic twins. An examination to see if the Determination of zygosity is important because of the
two placentae are fused/separated should also be done. serious implications of monozygotic twinning such as:
Microscopic examination of the septum (T-section as Spontaneous abortion/vanishing twin
membranes join the placenta) which divides two fetal Twin-to-twin transfusion syndrome (TTTS)
cavities (in dichorionic-diamniotic–chorionic tissue Intrauterine fetal growth restriction (IFGR)/discordant
which is present between amnions while chorion is growth
absent in monochorionic-diamniotic septum). Vascular More severe, multiple and lethal congenital malformations
anastomosis in the placenta may be seen. Preterm delivery
Blood group markers (ABO, MNS, Rh, Kell, Duffy, Kidd, Conjoined twins
etc.) Acardia with twin reversed arterial perfusion (TRAP)
RBC (red blood cell) enzymes Abnormal umbilical cord conditions such as cord
Placental alkaline phosphatase (ALP). entanglement.
Analysis of DNA (deoxyribonucleic acid) polymorphism
(most accurate method)—genetic fingerprinting by PROGNOSIS
studying the similarities and differences in restriction
frequent length polymorphism (RFLP) also helps in Maternal mortality is 3–7 times higher in twin pregnancy
differentiations. than that of singleton pregnancy. The most common cause
of maternal death is PPH, which may be due to the larger Apart from increased pressure effects caused by increased
size of the uterus in twin pregnancy. The other important uterine size, there may be exacerbation of varicose veins,
causes of death are anemia and pre-eclampsia. hemorrhoids and dependent edema.
There is even an increase in maternal morbidity, which There is an increased frequency of antepartum
is due to the complications and increased incidence of hemorrhage (APH), as there is increased incidence of both
operative interference in twin pregnancy. placenta previa (due to larger size of the placenta) and
abruption in the third trimester and following the delivery
Perinatal Mortality of first baby due to shrinkage of uterine size as compared
It is markedly increased (3–11 times that of singleton to the placenta (shearing off ). Malpresentations also are
pregnancy). The causes are prematurity, growth-restricted more common. Prematurity is often seen.
fetuses and infection. The second twin is more at risk than Sepsis due to ascending infection after premature rup-
the first twin. The monozygotic twins have two and a half ture of membranes (PROM) (three times increased risk),
times higher mortality than dizygotic twins. There are hypertension and PPH (due to uterine atony, retained pla-
higher chances of congenital abnormalities, discordant centa and traumatic causes) significantly contribute to the
growth, TTTS and malpresentation. high maternal morbidity. Other complications seen more
Since, there is an increased risk to both the mother frequently are cholestatic jaundice, hyperemesis, shortness
and the fetus, twin pregnancy is considered as high-risk of breath, loss of balance, varicose veins, dependent edema
pregnancy. Twins develop lung maturity 3–4 weeks earlier and hemorrhoids.
Due to all the above reasons the mother is hospitalized
than singletons.
during pregnancy and sometimes even in the intensive
care unit (ICU).
EFFECTS OF TWIN PREGNANCY
ON MOTHER EFFECTS OF MULTIPLE PREGNANCY ON
There is an exaggerated adaptation of all body systems of FETUS
the mother specially of the cardiovascular system (CVS).
The cardiac output is higher, the normal increase in plasma Vanishing Twin
volume during pregnancy is also much greater than In one-third of the twins, one of fetuses aborts or get
singleton pregnancy. The hematocrit and hemoglobin reabsorbed within 10 weeks of pregnancy. There may
is even lower than in singleton pregnancy. The plasma be little accompanying bleeding. The fact that a viable
protein levels are lower. Other differences include a slower pregnancy is accompanied by a non-viable one, is obvious
rate of glucose disposal after a glucose load. on ultrasonography (USG). When fetal death occurs
The frequency and severity of nausea and vomiting are during the second trimester, the remains of the baby
increased in multiple pregnancy and may persist beyond get compressed and become paperlike and flattened
the first trimester. by pressure from the survivor (fetus papyraceous). The
Anemia is the most common complication of twin vanishing twin can cause complications in screening for
pregnancy. Both iron and folic acid may show a two-fold neural tube defects (elevated levels of α-fetoprotein in
decline in twin pregnancy. The iron stores in the body also maternal serum and amniotic fluid) and a discrepancy
decrease. Urinary infection is more common in multiple in the karyotyping. Thus, amniocentesis is chosen over
pregnancy. karyotyping. Monochorionic twins have a higher chance of
The incidence of polyhydramnios is higher in twin abortion. In the dichorionic twins, spontaneous abortion/
pregnancy, more so in monozygotic twins. It is common loss of one or both twins should be kept in mind when
with TTTS. diagnosing twins in very early pregnancy by transvaginal
The incidence of gestational hypertension or pre- USG. Abortion rate is increased in twin gestations.
eclampsia is higher than (nearly three times) that of
singleton pregnancy. Gestational diabetes is two to three Prematurity
fold more common than in singleton pregnancy. Preterm labor frequently occurs. It is the most important
Other differences in maternal physiological changes in complication of multiple pregnancies and the predominant
multiple gestation include a greater increase in respiratory reason for the increased perinatal loss. It is generally
tidal volume and a higher glomerular filtration rate (GFR). attributed to uterine overdistension, hydramnios and
intrauterine infections with/without PROM. Patients with Intrauterine Fetal Demise of One Twin
twin-to-twin transfusion and those showing a discordant (Acute Intertwin Transfusion)
fetal growth may require a preterm delivery as soon as
Intrauterine fetal demise of one twin can affect the surviving
lung maturity is achieved. Cerebral palsy, microcephaly,
twin, depending upon the cause of death, the gestational
porencephaly and multicystic encephalomalacia have
age at death, the chorionicity, length of death and delivery
been seen to occur more frequently in preterm twins than
of the second twin.
in preterm singletons.
The surviving twin can suffer from thromboembolism
Growth Restriction and central nervous system (CNS) dysfunction due to
embolization of toxic products via the vascular anastomoses
Diminished growth occurs at and after 30 weeks of
(more in patients with monochorionic placentations). There
pregnancy. It is more marked in monozygotic twins.
may also be renal cortical necrosis and aplasia cutis. It is due
Nearly, 90% twins are low birth weight (LBW) the cause of
to hypotension due to loss of blood to dead twin.
which is growth restriction in 25% and the rest are preterm.
Discordant Twins (Fig. 18.6) Twin-to-Twin Transfusion Syndrome

(Chronic Intertwin Transfusion)
They are due to unequal division of the zygote, unequal
placental mass, umbilical cord abnormalities, genetic In monochorionic twins, arteriovenous anastomoses on
diseases, twin-to-twin transfusion or placental insufficiency. the fetal surface of the placenta may develop leading to
The difference of birth weight of 25% or more may occur one twin (donor twin) being undertransfused and hence
amongst the twins (expressed as a percentage of the larger developing intrauterine growth restriction (IUGR), anemia
twin’s weight). The smaller twin has a higher risk of perinatal and oligohydramnios. The other fetus, the recipient,
complications and long-term physical and intellectual becomes hyperfused, large, plethoric and develops
growth restriction and most may die. hypervolemia, polyhydramnios and polycythemia
The criteria for diagnosis are—on ultrasound examina- with subsequent development of severe neonatal
tion: hyperbilirubinemia and kernicterus. It presents before 28
A difference in the head circumference of ≥5% weeks of pregnancy. The syndrome is associated with very
A difference in abdominal circumference of 20 mm high perinatal mortality. At birth, letting of blood from
A difference of 15–25% in the estimated fetal weight the umbilical vein of the hyperfused twin at 5 mL/min for
Abnormal umbilical artery Doppler waveforms 30 minutes can prevent heart failure. Serial amniocentesis
Increased head to abdomen and femur to abdomen ratios. (removing excessive amniotic fluid slowly) have reduced
the perinatal mortality. It is done when amniotic fluid
is increased with 40 cm or the deepest single pocket
is greater than 12 cm. Each 100 mL of amniotic fluid
removed decreases the amniotic fluid index (AFI) by 1 cm.
Operations like fetoscopic anastomotic vessel ablation by
laser between 16 and 25 weeks or umbilical cord ligation
in utero are still only experimental. Septostomy puncturing
the amniotic membrane may lead to restoration of the
amniotic fluid in the donor sac, allowing liquor draining
and its readjustment. Cord coagulation or ligation (by
polar diathermy, alcohol injection or endoscopic laser
under ultrasound guidance) can be used for treatment.
But it may cause severe brain injury in the surviving twin.
Selective feticide of small infant (before 14 weeks) can be
done. Sonographic picture of abnormal difference in fetal
size, amniotic volume, unchanging position of a twin in
uterus (stuck twin, smaller with lesser/no amniotic fluid
Fig. 18.6: Discordant growth surrounding it) should alert the obstetrician of a possibility
Courtesy: Dr Rajesh Uppal, Uppal Diagnostics, Delhi of twin-to-twin transfusion.
Superfetation and Superfecundation Intrauterine death (IUD)

IUGR
Superfetation involves fertilization of 2 ova occurring
Congenital abnormalities
at long intervals (time ≥1 ovulation cycle), the second
Discordant growth
ovulation occurring during the course of an established
Twin-to-twin transfusion
pregnancy (before the fusion of the decidua capsularis and
Malpresentation.
decidua vera). This entity is still to be proven in humans.
Superfecundation involves fertilization of 2 ova in the same
Cerebral Pathology
menstrual cycle within a short period of time but not with a
single act of coitus and may not be from the same partner. It is five times more common in twins than in singleton
pregnancies especially after the death of one twin due to
Cord Entanglement thromboemboli originating from the dead fetus leading
to ischemic necrosis in the brain or hypotensive cerebral
It can occur in monozygotic twins. Other factors which can
ischemia. Ninety percent of the patients with vein to vein
adversely affect the fetal and neonatal outcome are PROM
with chorioamniotis, abruptio placentae, IUGR and other anastomosis develop cerebral damage and cerebral palsy.
intrapartum complications. Other cord problems which are more common in twins
are a single umbilical artery, velamentous insertion of
Malpresentation the cord, cord prolapse, vasa previa and tension of the
It is common in twin pregnancies as compared to singleton umbilical cord.
pregnancies. The presentations in order of incidence are
shown in Figures 18.7A to G.
Congenital Anomalies
The incidence is 2–3 times higher than in a singleton
MATERNAL COMPLICATIONS pregnancy. Most common are cleft lip and palate, CNS
anomalies are also seen.
During Antenatal Period
Anemia MANAGEMENT DURING ANTENATAL
Hyperemesis

Hypertension
PERIOD
APH Many patients have sonographic diagnosis early in preg
Hydramnios nancy. However, on clinical suspicion, as in cases of
Malpresentation large for date fundal height, twin pregnancy should be
Preterm labor considered or ruled out. All cases of twin pregnancy
Mechanical distress (varicose veins, dependent edema) should be booked early in pregnancy because they require
Obstructive uropathy. additional care for better fetal and maternal outcome.
Early diagnosis is important to improve the maternal and
During Labor neonatal outcome.
History
Early rupture of membranes
Cord prolapse •• Conception after prolonged infertility by ARTs tech-
Increased operative interference niques

•• High maternal age
Abruption
•• High parity
PPH.
•• Previous history of twin delivery
Puerperium •• Family history of twins.
Ultrasound (Figs 18.8A and B) screening for spontaneous
Subinvolution
abortion/loss of one/both the twins should be kept in
Infection
mind when diagnosing twins in very early pregnancy by
Failing lactation.
transvaginal.
•• Neural tube defects or other fetal anomalies
FETAL COMPLICATIONS •• Conjoined twins, twin-to-twin transfusion syndrome
Abortion •• Fetal size and sex and IUGR/discordant growth, lie,
Prematurity presentation
A B C
D E F
Figs 18.7A to G: Presentations in order of incidence. A. Both vertex—40%; B. First vertex, second breech—25%; C. First Breech,
second vertex— 7%; D. First and second breech—9%; E. First vertex, second transverse—7%; F. First breech, second transverse—3%;
G. Others—3%
•• Placenta—localization, number, intervening, mem- insertion using the maximum magnification. Assess-
brane, its thickness, and the number of layers seen [the ment of the triangular junction of the membranes with
division in dichorionic-diamniotic placenta is thick the placental site (twin peak or lambda sign) is neces-
(more than 2 mm and with 3 or 4 layers)] better seen sary, as this is absent in monochorionic placenta (Table
in very early pregnancy and near the site of placental 18.1). A repeat ultrasound between 20 and 26 weeks
A B
Figs 18.8A and B: Sonographic appearance. A. Twin gestational sacs in 8 weeks pregnancy; B. Triplet gestation
TABLE 18.1: Ultrasound differentiation On examination

•• Unexplained maternal anemia
Character Monochorion twin Dichorion twin
•• Fundal height disproportionately larger than
Placenta Single Separate
dates (more than 5 cm in symphysiofundal height)
Number of 2 4 detected before 24th week (after ruling out other
membranes
causes of this disproportion such as—hydramnios,
Thickness <2 mm >2 mm distended bladder, wrong dates, hydatidiform mole,
Twin peak sign Absent Present uterine fibroid, obesity, ovarian tumor or a big baby)
Sex Concordant Discordant •• Abdominal palpation more than three fetal poles,
fetal lie. Abdominal girth, more than 100 cm
•• Auscultation more than one fetal heart sounds—by 2
may be required to visualize a thin membrane in case observers 10 cm apart, a difference of more than 10
of monoamniotic pregnancies beats/minute
•• Amniotic fluid volume (AFV) •• β-hCG (human chorionic gonadotropin) in plasma
•• Umbilical cord abnormalities, IUGR (abnormal

and urine elevated more than found in a singleton
umbilical artery waveforms or vascular lesions in the pregnancy.
Invasive monitoring is rarely required to diagnose
placenta using color Doppler USG)
monoamniotic twins. It includes:
•• Transvaginal sonographic assessment of cervical
•• X-ray one day after intramniotic injection of 30 mL
length and fetal fibronectin at 24–28 week gestation
iothalamate meglumine dye—presence of contrast
(for prediction of preterm labor). Repeating ultrasound
in the gastrointestinal tract (GIT) of both the twins
every 4 weeks may help in close monitoring of fetal
clinches the diagnosis of monoamniotic pregnancy
growth and umbilical cord Doppler velocimetry helps (not done now).
in evaluation of IUGR. •• After amniocentesis 0.1 mL oil mixed with 5 mL of
Maternal serum α-fetoprotein is higher, thus a higher amniotic fluid is injected into amniotic cavity under
cut off limit is used when screening for neural tube ultrasound guidance after taking a sample for genetic
defects in multiple gestational pregnancy. studies (no more performed).
If there are more than three fetuses, X-ray abdomen •• Ultrasonographic picture demonstrating microbub-
should be done to be sure of the number of fetuses. bles around both the twins can diagnose monoam-
X-ray abdomen is also needed if there is a suspicion of niotic placentation.
conjoint twins. Determination of zygosity.
Antenatal Follow-up Smoking and alcohol are completely forbidden.

Elective hospitalization at about 30 weeks, specially for
Multifetal Reduction patients from poor socioeconomic status, is advisable.
In pregnancies, especially with more than 2 fetuses Earlier admission is also needed in patients with 3 or more
or twin gestation associated with a major congenital fetuses. This will help prevent preterm delivery, toxemia
malformation, fetal reduction can be considered after and improve fetal weight besides preventing anemia.
taking an informed written consent. Selective fetocide More frequent examination of hemoglobin should be
(intracardiac or intrathoracic injection of potassium done in all twin or higher pregnancies. The patient should
chloride in the selected fetus) is performed with close be referred to a hospital equipped with neonatal care unit.
monitoring. The course of the pregnancy has been found Maternal weight gain of 15–16 kg in twin pregnancies
to reduce some complications of multifetal gestations. But is within normal limits. Constant monitoring of the fetal
complications due to the procedure, like development of wellbeing is an important component of the antenatal
premature uterine contractions, infection, hemorrhage care. NST with ultrasonographic evaluation, serial evalu-
and risk of losing all the fetuses should also be considered ation of fetal growth, biophysical profile (BPP) and Dop-
and the risk-benefit ratio evaluated before resorting to it. pler velocimetry help in deciding about the best mode and
time of delivery.
Early Detection and Possible
Prevention of Preterm Labor Cervical Score
Using transvaginal sonographic assessment of cervical Antepartum examination of the cervix gives an ongoing
length and fetal fibronectin (if possible) at 24–28 weeks risk assessment. Between 24 and 36 weeks of pregnancy
of gestation as a screening test for all multifetal gestation cervical scoring is done every 1–2 weeks. Cervical score =
helps identify high-risk for preterm delivery before 32 cervical length (cm) minus cervical dilatation of internal
weeks and their further management. Bed rest and os (cm). For example, if the cervical length is 2 cm with a
prophylactic tocolytics in selective cases for a short period closed internal os, the cervical score is +2. A cervical score
only and betamethasone administration (there are some of < zero on or before 34 weeks of pregnancy has a positive
trials of giving 3 doses 18 hours apart instead of 2 doses predictive value of 75% and a four-fold increase in relative
24 hours apart as there are more than one fetuses) are risk of delivery at <37 week. Those with a score more than
documented to prevent preterm labor. Continuous fetal 0 are less likely to go into preterm labor.
wellbeing surveillance [by nonstress test (NST)] and uterine The prospective risk of fetal death is greater for triplet
contraction monitoring can be helpful though their role is and twins than for singletons and greater for triplets than
controversial. Prophylactic elective cervical cerclage has for twins during the third trimester (Fig. 18.9). In cases with
been shown to have no role in preventing preterm labor. uteroplacental insufficiency and when the prospect of fetal
Tocolysis by magnesium sulfate can be done, if needed, death exceeds the risk of neonatal mortality, induction of
under strict supervision only for 24 hours to gain time for labor is done. It is reasonable to consider delivery of twins
in utero transfer to tertiary center and to allow time for the at 38 weeks and triplets at 36 weeks to improve perinatal
effect of cortisone for lung maturity. It can be used after outcome. Beyond this gestation, fetal morbidity and
delivery of the first twin for podalic versions. mortality increases.
Once diagnosed, frequent antenatal visits fort-nightly
till 28 weeks are recommended (more frequent in
Stillbirth
hypertensive patients). Adequate attention should be paid Its incidence is high with monochorionicity, ART, preterm
to nutrition of the patient—increase in calories (300 calories labor and consanguinity.
and 60 g protein per fetus), increase in supplements of iron, Predictors for stillbirth before 32 weeks are:
vitamin, calcium and folic acid is required. The patient is Fibronectin level (if possible)
also advised for an additional afternoon rest of 2 hours a-fetoprotein
and avoidance of physical and mental stress. Increased ALP
periods of bed rest may decrease the risk of PROM and Granulocyte-colony stimulating factor (G-CSF)
mild pregnancy induced hypertension. After 28 weeks, do At 35 weeks these predictors are less useful.
a per speculum examination to detect and treat infection Uterine and umbilical artery Doppler velocimetry and
and to assess cervical length. uterine artery scores (UAS), presence or absence of notching,
to the number of fetuses present. Keep PPH in mind,

have blood ready. The pediatrician must be present. An
anesthesiologist must be available, if need arises.
During first stage of labor: An attitude of watchful
expectancy with some additional precautions is followed.
Bed rest (to prevent PROM), careful monitoring of labor
by using partogram, with a close monitoring of both the
fetuses. Per vaginal examination (PV) should be done at
rupture of membrane to exclude prolapse of cord or limb.
An IV (intravenous) line should be established and IV fluid
started and blood should be arranged. For prevention of
neonatal group B streptococcal (GBS) infection, antibiotics
should be started in case of documented preterm labor.
The pediatrician should be informed. Careful fetal heart
Fig. 18.9: Placenta in triplet pregnancy sound (FHS) monitoring is required. Cardiotocography
(CTG) monitoring can be done by putting a scalp clip in the
and increase in pulsatility index (PI) are ultrasonologic first twin and abdominal monitoring in the second twin.
predictors of impending stillbirth. Plasma leptin level in an Augmentation with oxytocin could be done, if indicated.
IUGR twin is two-fold lower than normal twin. Usually, the first twin delivers spontaneously and timely
episiotomy should be given. After the delivery of the first
Elective Cesarean in Twin Pregnancy twin, the cord is clamped at two places to prevent bleeding
which could be deleterious in cases of monozygotic twins.
Indications for elective cesarean include all obstetric
Ergometrine is not to be given at the birth of the first baby.
conditions as in a singleton pregnancy. However, nowadays,
An active approach after this is very important. Follow-
liberal use of cesarean section for multifetal pregnancy is
ing the delivery of the first twin abdominal palpation is
practiced.
performed to ascertain the lie and FHS of the second twin
Accepted indications for cesarean section in twin
to rule out fetal distress. Per-vaginal examination is done
pregnancy are:
to confirm presentation, station and to rule out cord pro-
Non-cephalic 1st twin (23%) monoamniotic placen-
lapse and disproportion and the status of membranes—
tation (due to high-risk of cord complication and thus
ruptured or not.
fetal demise)
Undue delay in the delivery of the second twin
IUGR in dichorionic twins (<5%)
(>30 minutes) should be avoided. Look for premature
Twin 2 significantly larger (>500 gm) than twin 1
separation of placenta and cord prolapse. Continuous
Antepartum death of 1st twin (1–2%)
electronic fetal maintaining is required. Oxytocin can be
Placenta previa (1–2%)
started. If the lie of the second twin is cephalic, rupture of the
Fetal abnormality precluding safe vaginal delivery (1%)
membranes should be performed only when the presenting
Chronic TTTS in monochorionic twins (<1%)
part of the second twin is well descended and engaged, to
Monoamniotic twins (<1%).
prevent the otherwise high-risk of cord prolapse. If uterine
Contentious Indications for Cesarean in Twins contractions are inadequate oxytocin should be started and
Maternal request (5–10%) labor monitored.
Unfavorable cervix at 39 weeks in nulliparous If the second twin is breech, wait and conduct a
Death of second twin complete assisted breech delivery. If the lie is transverse
Uncomplicated monochorionic twins it may be corrected by external cephalic version (ECV)
Previous cesarean section. or external podalic version (EPV) per abdomen. If this
fails, patient is transferred to the operation theater
Management of Twins During Labor and an internal podalic version (IPV) is performed. All
(Intrapartum Management Flowchart 18.1) procedure should be done with continuous electronic
Most of the patients go into spontaneous labor by 38 weeks. monitoring of the fetal heart rate (FHR) (if available) to
The time of onset of labor is inversely proportional detect any sign of fetal distress which, if present, is an
Flowchart 18.1: Intrapartum management
Abbreviations: ECV—External cephalic version; EPV—External podalic version; IPV—Internal podalic version
indication for hastening the delivery process by forceps,

cesarean section or breech extraction, as the case may be.
Cesarean section for the second twin may be required for
the following indications:
Transverse lie where version fails
For a large second twin weighing more than 3 kg.
Thus, all facilities for emergency cesarean section

should be available.
The management of third stage requires great attention. A B
Prophylactic IV injection of ergometrine at the birth of
Figs 18.10A and B: A. Dichorionic-diamniotic placentae (fused);
anterior shoulder of second twin should be routinely B. Monochorionic-monozygotic
followed as this helps minimize the risk of PPH. It is a safe
practice to add oxytocin in the IV drip, just after the delivery of Infrequent Complications of Twin Pregnancy
the second twin or prostaglandin administration along with Apart from complications that may be encountered in a
bimanual uterine massage to prevent PPH. The placenta singleton pregnancy, the obstetrician may come across some
is delivered by controlled cord traction and examined in other conditions in twin pregnancies, leading to difficulty
detail, noting any anomalies, if present. Documentation during labor. However, these conditions are very rare.
of placenta (Figs 18.10A and B) and membrane, sex of
the babies their blood group and DNA fingerprinting Interlocking (Fig. 18.11)
(if possible). The patient is to be kept under observation for One twin may obstruct the passage of the other twin in
12 hours after delivery. the birth canal. There are several varieties of interlocking,
the most common being the after coming head of the first
baby obstructed by the forecoming head of the second
baby. An attempt should be made to dislodge the head
of the second child and push it up. If this fails, the only
option left is decapitation of the first child, as it is already
partially delivered and cord pulsation would have ceased.
The decapitated head is pushed up and the second twin is
delivered followed by delivery of the decapitated head of
the first twin. IV administration of a β-mimetic agent can
also be tried.
Sometime in case of both cephalic presentations, the head
of the second twin tries to descend into the pelvic cavity along
with the first, resulting in collision, thus impeding progress.
In such cases, the patient is put in the trendelenburg
position under general anesthesia and disengagement of Fig. 18.12: Conjoined twins
the higher head is attempted by pushing it out of the pelvis.
If both fetuses are alive cesarean should be done to save both facing each other or on repeated examination heads are
twins. Occasionally, interlocking may occur if one fetus is at same level and plane. The thoracic cages are in unusual
longitudinal and the second fetus is an oblique or transverse proximity. There is no change in relative fetus positions
presentation. It is diagnosed when difficulty is encountered with time or manipulation. An X-ray may be performed
in delivery of the first child. By careful internal examination with radiopaque dye in amniotic fluid to confirm diagnosis.
under anesthesia, the second child is pushed out of the pelvis Spontaneous delivery may occur in extreme premature
and if possible the first child is extracted; otherwise cesarean cases. Cesarean section offers a safe method of delivery for
section should be performed. the mother and should be done where the diagnosis has
Conjoined twins (Fig. 18.12) are extremely rare, and been made. Usually, obstructed labor is encountered.
may be mistaken for interlocking of twins. In all cases of Triplet and higher multifetal delivery: Cesarean section
monoamniotic twins, the possibility of conjoined twins, is recommended in all these. These fetuses are more
should be considered. Antenatal USG shows, both twins premature, growth restricited and have malpresentations.
They also need complex manipulations. If vaginal delivery
is contemplated (e.g. if at least the first two fetuses are
vertex and baby sizes are more than 1500 g each) an
experienced obstetrician with a team of pediatricians and
anesthetist are required in an operation theater so that
cesarean section can be done immediately, if required.
Postpartum: Special attention is needed in puerperium
because there can be subinvolution, and there are greater
chances of infection and failure of lactation. Cooperation
of all family members is essential to rear multiple births.
Stimulation of Lactation
Suckling is the true stimulus for lactation and no drugs
are required. Proper counseling for adequate and exclu-
sive breastfeeding is essential, especially in primiparas. If
breastfeeding is not done or babies are not sucking, effec-
tively milk production decreases. Giving sufficient, time,
encouragement and proper diet in the first few days will
establish lactation.
Hence, repeated patient education about nutrition,
Fig. 18.11: Interlocking of after coming head of first twin weight gain, signs of preterm labor and pre-eclampsia,
extra rest, proper drugs and more frequent antenatal Care of the Newborn
checkups go a long way in reducing perinatal and It is according to the weight. They are mostly treated as
maternal mortality in multiple gestations. preterm neonate.
1. Differentiate between monzygotic twins and dizygotic twins.
2. Elaborate TTTS in brief.
3. True/False:
i. Development of three fetuses is called quintuplets.
ii. Zygosity can also be determined by RBC enzymes.
iii. ECV stands for external cephalic version.
Preterm Labor and
19
Sudha Salhan, Sunita Singal
Premature Rupture
of Membranes
Nutritional status (obesity/under nutrition)

PRETERM LABOR Chronic ill health
Preterm labor is defined by the American College of Low socioeconomic status
Obstetricians and Gynecologists (ACOG) as the onset Previous spontaneous or induced miscarriage.
of labor prior to the completion of 37 weeks, after the
gestational viability (24–28 weeks) or 259 days from the Medical and Obstetrical Conditions
last menstrual period. These babies are mostly less than Anemia
2,500 g in weight at birth. If the gestational age is not Bacterial vaginosis before conception (see Flowchart
known (as in most of our patients) then a weight less than 50.1 in Chapter 50)
2,500 g is taken as the indicator of prematurity, but this has Diabetes mellitus
its limitations. Infants with birth rate less than 2,500 g are Asthma
termed as low birth weight (LBW). LBW neonates can be Pre-eclampsia/eclampsia
premature or small for gestational age. Chronic hypertension
Infant mortality has become a benchmark for interna- Bleeding in current pregnancy [antepartum hemorrhage
tional comparisons of healthcare systems. Countries with (APH)]
higher preterm delivery rates have a higher infant mortality Infection plays a role: Pneumonia, urinary tract infec-
rate, signifying the importance of prematurity. Upto 70% of tion (UTI) or asymptomatic bacteriuria, pyelonephritis,
fetal and neonatal deaths may be due to prematurity. The reproductive tract infections (RTIs) (Chlamydia,
incidence of prematurity varies from 5–15% from various Neisseria gonorrhoea), appendicitis and dental infec-
centers. tions
Short interval between pregnancies (less than 3 years).
ETIOLOGY Premature rupture of membranes (PROM) associated
The causes are mostly unknown in the majority of cases. with chorioamnionitis
Previous history of preterm labor.
Nevertheless, there are certain factors, which increase its
incidence. Congenital abnormalities of the uterus—septate,
unicornuate or bicornuate uterus.
Maternal Factors causing Preterm Labor Incompetence of cervix (cervical weakness) following
General Conditions cervical conization or previous second trimester sponta
Racial differences are important—the incidence is 9.9% neous or induced miscarriage.
for white and 11.2% for black women Substance abuse—smoking (tobacco contains nicotine
Maternal age less than 18 years or over 40 years which can lead to vasoconstriction thus, causing uteropla-
Short stature cental insufficiency). Alcohol intake (increases the risk of
Maternal weight less than 45 kg preterm birth and brain injuries in premature infants).
Strenuous work (during pregnancy) Trauma may cause premature labor
High personal stress Genetic: Many preterm deliveries are familial.
Fetal factors causing preterm labor: nancy, but not in between. Alkaline phosphatase (ALP)
•• Congenital malformation (especially those associ- greater than 90th percentile is also considered a predictor.
ated with fetal hydrops or polyhydramnios) Amniotic fluid cytokine (IL-1, IL-6 and TNF) levels are in-
•• Multiple pregnancies creased.
•• Intrauterine death (IUD). Salivary estriol—there is a potential value of salivary
Iatrogenic/elective preterm labor: Due to advance in maternal estriol in preterm labor.
neonatal care, there is a greater incidence of iatrogenic Hence, analysis of cervicovaginal fibronectin, cervical
or elective preterm labor, e.g. for bad obstetric history length, obstetric history of previous preterm birth and pres-
(e.g. previous term stillbirth), pre-eclampsia, placenta ence of bacterial vaginosis may help predict preterm labor.
previa, intrauterine growth restriction (IUGR), etc.
Miscalculation of gestational age also leads to premature PREVENTION OF PRETERM BIRTH
induction of labor.
All factors which could lead to prematurity are not clear,
but an attempt at prevention can be helpful.
PATHOGENESIS
Exact mechanism of premature labor is not known. Primary Prevention
In most cases of premature labor, there is fetal stress. This
Elimination or reduction of risk in all women. It includes:
fetal stress produce corticotropin-releasing hormone
Preventing pregnancy in teenagers
(CRH). CRH is a peptide produced by the placenta,
Management of anemia
amniochorion and decidua. This enhances prostaglandin
Prevent smoking
production by these cells. Hence, abnormalities of the
Prevent RTIs/sexually transmitted infections (STIs)
placenta and uteroplacental blood flow may lead to
Access to family planning methods to prevent unwanted
preterm birth either directly through decidua and/or
and frequent pregnancies
indirectly by inducing fetal stress.
Preconceptional counseling
Infection/inflammation → activation of prostaglandins
Improve the nutrition and general health of women
→ uterine irritability and contractions + premature
Decrease factors causing stress and give adequate rest.
cervical ripening → premature labor.
Bacterial products acts on → decidua, release → monocytes in Secondary Prevention

amniotic fluid → platelet-activating factors (PAF). Identification of pregnant women who are at risk of
↓ preterm delivery and their close surveillance. It includes:
Cytokines [IL-1, IL-6, TNF (interleukin) (tumor necrosis factor)] →
Prophylactic patient education to enable them to
arachidonic acid → prostaglandins (E2 and F2a)
↓
detect early symptoms of premature labor (rhythmic
Uterine contractions backache, sense of pelvic pressure, heavier vaginal
discharge, vaginal spotting and abdominal cramps)
Identifying mothers at risk for preterm birth is and also instruct them to reduce physical and sexual
important. History at the antenatal visit includes history activity.
of previous preterm birth, bleeding in second trimester, Medical therapy includes tocolytic drugs, progesterone
genitourinary infections, age below 18 years or above 40 therapy, antibiotics, cortisone and metronidazole
years, low weight of the mother, history of smoking and (given between 14 and 20 weeks of gestation, if bacterial
any other medical conditions which complicating the vaginosis occurs).
pregnancy, etc. Encirclage operation (if cervical incompetence is present).
Cervical length is a useful indicator. Transvaginal
ultrasound detection of cervical length (in women with pre
vious history of preterm birth) of less than 2.5 cm is a marker
DIAGNOSIS
of cervical competence. Vaginal infection in pregnancy is Cervical changes (progressive dilatation ≥ 2–3 cm and
also significant. Recently, fibronectin has emerged as a effacement of the cervix ≥ 80%) with regular uterine
useful indicator. It acts as a ‘glue’ attaching the fetal mem- contractions (at the rate of 4 in 20 minutes or 8 in 60
branes to the decidua. It is normally present before minutes at intervals of every 5–8 minutes), with or without
20–22 weeks of pregnancy and again at the end of preg- pain (low backache occurring in every 10 minutes),
Preterm Labor and Premature Rupture of Membranes 183
vaginal bleeding or rupture of membrane occurring before •• Examination of urethral discharge for gonorrhea
37 weeks of gestation is essential for the diagnosis. •• Cervical swab examination for Chlamydia.
Uterine contraction alone should not be the basis of the Per vaginal examination
diagnosis (60% false positives). If the cervical dilatation is •• Cervix ≥ 3 cm dilated and ≥ 80% effaced
≥ 3 cm, the diagnosis becomes straight-forward. •• Presence or absence of membranes
•• Presentation.
MANAGEMENT OF PRETERM LABOR Per abdominal ultrasound
•• Placental localization and maturity

It includes prompt and accurate diagnosis, proper refer- •• Amniotic fluid volume (AFV)
ral or appropriate treatment. Confirmation of the period •• Fetal wellbeing
of gestation is important. The goal is to diagnose the condi- •• Fetal presentation
tion in the reversible state and eliminate the risk factor, if •• Estimated fetal maturity and weight.
possible. Transvaginal ultrasound: Vaginal sonographic mea-
Once the diagnosis of preterm labor is established surements of the cervix are more reproducible. A
the patient is admitted to the hospital, advised bed rest, stenographic cervical length of 18 mm as optimal posi-
activities are curtailed, adequate hydration is maintain tive predictive value and 30 mm as optimum negative
and following investigations are done to try and find the predictive value and if done by transvaginal probe, it is
cause of the preterm labor and to monitor maternal and more accurate. If the cervical length is less than 3 cm,
fetal wellbeing.
tocolytic therapy can be considered.
Amniocentesis
Physical Examination
•• To assess fetal lung maturity where the estimated
Pulse
Blood pressure (BP) age is uncertain/size of fetus is in conflict with the
Temperature estimated date of conceptions or if the fetus is ≥ 34
Hydration weeks gestation (by lecithin/sphingomyelin (L/S)
Abdominal: Fundal height (to see the correlation with ratio, phosphatidylglycerol (PG) levels.
•• If suspicion of intrauterine infection (chorioamnion-
period of gestation), monitoring of contractions and
fetal heart rate (FHR) auscultation. itis) exists, amniotic fluid examination is done.
Amniotic fluid examination
Investigations •• WBCs (white blood cells) count (superior to CRP)
Hemoglobin •• Glucose (low in cases of infection)
Total leukocyte count (TLC) and differential leukocyte •• IL-6 concentration (high in case of infection).
count (DLC) •• Gram stain and culture (to diagnose the pathological
C-reactive protein (CRP), if possible organisms)
Urine examination: •• L/S ratio for maturity
•• Glucose Salivary estradiol—used to predict preterm delivery
•• Ketones (under research).
•• Protein If the patient is admitted in a primary or secondary
•• Pus cells healthcare center, then an effort should be made to delay
•• Culture and sensitivity the delivery by tocolytic drugs till the following interven-
High vaginal swab and culture [especially for Group B tions are carried out:
streptococcus (GBS)], pH and fern test Transfer the fetus in utero (before delivery) to a tertiary
Per speculum examination to look for any infection hospital equipped to be able to care of the premature
and leaking of liquor infant (i.e. the uterus is the best incubator)
Special investigations Administer glucocorticoids to decrease the fetal mor-
•• Enzyme immunoassay for fetal fibronectin: A swab bidity and mortality
is taken from the posterior fornix/external cervical Administer antibiotics to prevent neonatal CBS infec
os (if possible). The presence of fibronectin in the tions, especially in cases of PROM.
cervix and vagina after 22 weeks and before 37 weeks In the tertiary healthcare center, glucocorticoid
of gestation is diagnostic of preterm labor and antibiotics are given. In bacterial vaginosis, oral
metronidazole 250 mg TDS + ampicillin 500 mg 6 hourly Tocolytic agents are:

intramuscular (IM) + gentamicin 3–5 mg/kg body weight •• β-mimetic tocolytics, e.g. isoxsuprine, ritodrine,
8 hourly IM × 7 days. If the pregnant women is terbutaline, salbutamol
allergic or intolerant to ampicillin, then clindamycin •• Magnesium sulfate
300 mg BD or erythromycin × 7 days can be given. •• Indomethacin
Corticosteroid administration reduces the incidence •• Calcium channel blockers—nifedipine and nicardipine
and severity of respiratory distress syndrome (RDS), •• Oxytocin antagonist—atosiban
intraventricular hemorrhage (IVH), necrotizing entero •• Nitric oxide donor, e.g. glyceryl trinitrate.
colitis (NEC) and patent ductus arteriosus (PDA) and β-mimetic agents successfully prolong pregnancy
thus decreases the perinatal mortality. It is also repor for at least 48 hours. They are useful for the acute
ted to reduce circulatory instability and improve Apgar suppression of contractions by the parenteral route.
scores. Betamethasone 12 mg IM 2 doses, second Oral administration is ineffective. They cause smooth
dose after 24 hours, is better than dexamethasone muscle relaxation. Side effects include maternal
6 mg every 12 hours for 4 doses. Three doses of beta apprehension, headache, nausea and vomiting,
methasone or six doses of dexamethasone are advised by fever, tachycardia, hypotension, pulmonary edema
some, in case of multiple pregnancies. Neonatal benefit is and even heart failure. Fetal tachycardia, myocardial
maximum when the interval between the first dose and ischemia, heart failure and death can occur. These
delivery exceeds 48 hours, but some benefit always occurs drugs are contraindicated in diabetic patients (as
even after a partial or incomplete course. The benefit they can alter the glucose control), in pregnant
lasts upto 18 days. Second or subsequent courses are not patient with heart disease and multiple pregnancy
advised because of deleterious effect on both the mother use with precaution (may cause pulmonary edema).
and the fetus (smaller neonatal head circumference, They are not used often now because of side effects
increased risk of growth delay, increased risk of neonatal and other safer drugs.
sepsis and neonatal mortality). Cortisone is given to Ritodrine: 50 µg/minute in intravenous (IV) drip
mothers who are likely to deliver upto 34 weeks with intact increase every 20 minutes, if contractions occur at
membranes. With PROM upto 34 weeks the beneficial more than 10 minutes interval, to a maximum of 350
effect of cortisone on RDS is lost but the effect on IVH is µg till the labor stops. Then, reduce the dosage every
retained. 20 minutes to a lowest dose at which the contractions
Other chemotherapeutic agents, which can be given, are adequately inhibited. This rate is then maintained
if available, are surfactants (synthetic surfactant and for 12 hours, maximum dose 350 µg/minute IV, monitor
modified bovine surfactant extract) which add to and pregnant woman by pulse and blood pressure in every
synergize with the useful effect of corticosteroids to reduce 15 minutes, auscultate her lung bases, do blood sugar,
RDS. The effect of phenobarbital and thyrotropin-releasing blood urea and electrolytes.
hormone (TRH) given to the mother before delivery are Terbutaline: It has replaced ritodrine because of its
under research. Injection vitamin K to the newborn is ease of administration. Bolus, IV 250 µg followed by 10–
being tried in reducing IVH. 50 µg/minute until the labor stops. 250 µg SC every 20
A decreased incidence of IVH and cerebral palsy in minutes for 4–6 doses. A maintenance dose of 250–500
premature infants exposed to maternal magnesium sulfate mg orally may be given 4–6 times a day. Then, administer
treatment is seen retrospectively. subcutaneously (SC) 0.25–0.5 mg every 2–4 hours for 12
hours. A maintenance dose of 2.5–5 mg orally may be
Tocolytic Therapy given 4–6 times a day.
This is indicated when the patient is in labor and a delay Isoxsuprine: 100 mg in 5% Dextrose at 0.2 mg/minute
in the delivery will benefit the fetus (i.e. prevent RDS, NEC gradually increased to 0.8 mg/minute and continued at
and IVH, etc.) by giving cortisone and transferring the least 2 hours after the contractions cease. Oral adminis
fetus in utero to a better facility. tration is of no use.
Tocolytic drugs can delay the delivery for at least Magnesium sulfate: It is a safe drug with limited
48 hours (with gestational age between 24 and 34 weeks), tocolytic efficacy. It can be used in diabetic mothers. A
when effective measures can be taken to reduce the loading dose of 4–6 g IV over 20–30 minutes is followed
neonatal morbidity and mortality, e.g. giving antibiotics by infusion of 2–4 g/hour. It competes for calcium entry
and cortisone. into the muscles cells.
Combined therapy: IV terbutaline with magnesium Advanced cervical dilatation (>4 cm)
sulfate. It increases the mean duration of pregnancy Active labor.
with intact membranes.
Indomethacin: Ibuprofen (prostaglandin synthetase Fetal
inhibitors) are effective and well-tolerated tocolytics Maturity beyond 37 weeks or more (or estimated fetal
especially at less than 32 weeks gestation. However, fetal weight ≥ 2500 g)
abnormalities like constriction of ductus arteriosus, Advanced stage of labor
oligohydramnios and neonatal pulmonary hypertension IUD or congenital abnormalities incompatible with life
can occur. If used for a period of 2–4 days, it is useful in Chorioamnionitis
polyhydramnios and degenerating uterine fibroids in Acute fetal distress
association with preterm labor. 50 mg loading dose orally IUGR
or per rectal (P/R) followed by 25–50 mg 6 hourly. Erythroblastosis fetalis.
Calcium channel blockers: Nifedipine is a good Prognosis: The more immature the fetus the greater is the
tocolytic agent but should not be given sublingually risk of complications during delivery.
because it gets rapidly absorbed and can cause a
sudden fall of BP and myocardial ischemia which can be
dangerous to both the mother and the fetus. Otherwise, PREMATURE RUPTURE OF MEMBRANES
maternal side effects are low. Rupture of membranes normally occurs at the onset of
It should not be combined with magnesium or labor. Premature rupture of membranes (PROM) is defined
β-mimetics. Further studies are needed for its use. A as spontaneous rupture of chorioamniotic membrane at
common regimen is 20 mg orally followed by 10–20 mg any time prior to the onset of labor regardless of the age
every 6 hourly till the contractions cease. of gestation.
Atosiban: It is an oxytocin antagonist. Cardiovascular
side effects are much less as compared to ritodrine. There PRETERM

is some injection site inflammation. Initial, IV bolus
of 6.75 mg over 1 min, then infusion of 18 mg/hour for PROM, is when the rupture of membranes occurs beyond
3 hours, followed by 6 mg/hour upto 45 hours (maximum 37 weeks of gestation but prior to the onset of labor while
300 µg). preterm premature rupture of membranes (PPROM)
The nitric oxide donor glyceryl trinitrate is also
is when the gestational age is less than 37 weeks and
under the research to prevent preterm labor. It causes membranes rupture before onset of labor.
headache, can be given IV, intradermally or sublingually Prolonged rupture of membrane is when 24 hours have
or 10 mg patch. It does not need intensive monitoring. elapsed between the rupture of membranes and the onset
Maintenance of tocolytic treatment for a period of labor.
over 48 hours is not useful. The treatment is continued
6–12 hours after cessation or reduction in intensity and ETIOLOGY
frequency of uterine contractions. If contractions persist The exact cause is not known but some associations are
despite tocolytic treatment the usefulness of treatment is seen with:
to be reconsidered. Incompetent cervix
Overdistended uterus (polyhydramnios, multiple preg-

Contraindications for Tocolysis
nancies)
Maternal Inherent membrane defects (genetic conditions, low
Pre-eclampsia/eclampsia maternal serum copper, vitamin C deficiency)

APH—specially in accidental hemorrhage or excessive Infections like asymptomatic bacteriuria, UTIs and lower
bleeding in placenta previa genital tract infections (GTIs), bacterial vaginosis, intra-
Pulmonary hypertension uterine infections, chorioamnionitis (by organisms such
Hypersensitivity to tocolytic agent as mycoplasma, Escherichia coli, N. gonorrhoea, Chla-
Any surgical and medical conditions in which prolonga mydia trachomatis, Trichomonas vaginalis, Bacteroides
tion of pregnancy is not advised Fragilis, GBS organisms producing proteolytic enzyme).
Any bleeding more than light spotting Seminal fluid releasing collagenase like enzyme
Maternal connective tissue disorders (e.g. Ehlers- •• Look for uterine tenderness to see if chorioamnionitis
Danlos syndrome) has set in
Second and third trimester bleeding •• Determine fetal lie
External cephalic version •• Auscultate fetal heart sounds (FHR).
Amniocentesis Local examination: Per-speculum examination is
Trauma carried out to see:
Maternal smoking •• Extent of cervical dilation and effacement
Low socioeconomic status •• Cord prolapse
Family history. •• Fetal presenting part
•• Liquor may be seen draining through the cervical
DIAGNOSIS os and pooling of the amniotic fluid in the posterior

fornix. If no discharge is seen by per-speculum
Clinical Features examination, the patient is asked to cough, apply
slight fundal pressure or perform Valsalva maneuver
Symptoms
and the leak is observed. This fluid is collected. A
A sudden gush of fluid from the vagina/continued leakage clean sterile pad is given to the patient and the pad is
requires detailed history of: then observed after one hour.
Duration of the leakage
No per-vaginal digital examination should be
Quantity of the discharge
done unless the patient is in labor/POG more than
Types of discharge (clear/blood stained/ cream-
36 week because of a substantial increase in the risk
colored/green-colored) of introduction of infection even after a single per-
Consistency of the fluid
vaginal examination.
Presence of vernix.
Examination of the collected amniotic fluid:
•• Gross examination
History •• Clear, blood stained or cream/green color
Presence and duration of pain •• Foul/sweet smelling
Last menstrual period (LMP) for period of gestation •• Amniotic fluid pH
(POG) –– By litmus paper: Amniotic fluid is more alkaline
Assessment of fetal movements than vaginal pH (normal vaginal pH = 4.5 and pH
It would be very informative to obtain any history of liquor = 7.8), thus vaginal secretions containing
suggestive of infections like: the amniotic fluid result in pH changes between
•• Per-vaginal examinations 4.5 and 7.5 turning the red litmus paper blue.
•• Untrained attendant interference –– Nitrazine paper test: It turns blue in the presence
•• Fever/symptoms of lower GTI/UTI. of amniotic fluid indicating an alkaline pH
A detailed present and past obstetric, medical and surgical (sensitivity of the test is high 90–98%). False
history may help to find the pathological cause. positive values may result due to infection that
raise the vaginal pH (e.g. T. vaginalis), presence of
Differential Diagnosis blood and rarely cervical mucus or semen.
Vaginitis: Vaginal secretions are acidic •• Ferning: A drop of amniotic fluid when placed
Urinary incontinence: The urinary pH is acidic and no on a clean slide and allowed to dry demonstrates
ferning can be seen. ferning (microscopic crystallization) on microscopic
examination due to the interaction of the amniotic
Examination fluid proteins and salts.
General physical examination, hydration of the patient It is diagnostic in 85–95% cases and is unaffected by
and monitoring of vitals (temperature, pulse, BP and the presence of meconium or vaginal pH changes.
respiratory rate). False positive tests can occur if the cervical mucus
Abdominal examination has been accidentally taken but the cervical mucus
•• Confirm the period of gestation by measuring fundal shows a more floral pattern of ferning (Fig. 19.1)
height which may be small for dates (due to drainage •• 0.1% nile blue sulfate test: The collected fluid can be
of the amniotic fluid) centrifuged and examined for fetal cells staining with
Investigations on Admission
Complete blood count
Urine: Routine/microscopy examination
Urine: Culture/sensitivity test
2 swabs—a high vaginal swab and a cervical for culture/
sensitivity.
Determine the gestational age for deciding further
management.
The principle of management is to prolong the preg-
nancy till fetal lung maturity is attained by cortisone the
rapy or chorioamnionitis is suspected or diagnosed. The
prolongation of pregnancy by tocolytic agent is recom-
mended only when chorioamnionitis is absent. Surveys
of the literature still indicate that neonatal morbidity and
mortality due to prematurity exceed the complications
due to infection. The patient should be given the first
Fig. 19.1: Ferning
dose of betamethasone if less than 34 weeks of gestation
and antibiotics (ampicillin 2 g IV) and transferred to a
0.1% nile blue sulfate dye. The cells appear orange tertiary care unit (where facilities for maternal and fetal
due to the presence of exfoliated fat cells from the monitoring and care of premature infants are available)
sebaceous glands of the fetus before delivery because the uterus is the best incubator.
•• Culture and sensitivity of the amniotic fluid (for Sealing of membranes by intra-amniotic injection (IAI)
infection). of platelets and cryoprecipitates without localizing the site
Special investigations of leak amniopatch is under preliminary research.
•• Amniocentesis: If the diagnosis still remains doubt-
ful, a dilute solution of 1 ampoule of indigo carmine Indications for Immediate Delivery
dye is injected into the amniotic fluid and a pad is Irrespective of gestational age if any of the following are
kept at the vulva. A leak of blue fluid into the vagina present, immediate delivery is indicated:
confirms the diagnosis of PROM. Patient in labor
•• High vaginal swab for culture and sensitivity (for Clinical chorioamnionitis (Table 19.1)
diagnosis of infection) and fetal fibronectin (if pos- Fetal distress
sible, to diagnose prematurity). Features suggestive of cord compression or cord pro-
•• Abdomen ultrasonographic examination: lapse
–– Estimated gestational age Gross fetal congenital abnormalities
–– Amount of liquor—reduced/absent (confirms the Immunocompromized host
diagnosis) Pregnancy complications indicating delivery (heart
–– Fetal number and presentation disease, diabetes mellitus).
–– Estimated fetal weight In the absence of indications for immediate delivery, the
–– Placental localization and maturity. clinical management depends on the period of gestation.
•• Complete blood count including hemoglobin, TLC,
DLC and if possible CRP (to predict the development
DETERMINE THE GESTATIONAL AGE
of chorioamnionitis where the levels are significantly
elevated—normal levels 0.3–0.8 mg%). USING FOLLOWING PARAMETERS
•• Urine examination—routine, microscopy and culture.
Clinical
Management History
All patients suspected of PROM should be admitted in the Previous antenatal care records/first trimester PV
labor room of the hospital. They can be transferred to a examination
ward after 24 hours of observation and investigation. Clinical examination
TABLE 19.1: Signs of chorioamnionitis Placental localization/retroplacental clots

Fever ≥ 100°F/37.8°C NST (nonstress test)/BPP (biophysical profile).
Maternal tachycardia (P-R > 100 bpm or >20 bpm above the base line) During this time, the patient is monitored to evaluate
Fetal tachycardia uterine contraction and fetal wellbeing (by an electronic
Uterine tenderness cardiotocograph, if available).
Foul odor of amniotic fluid The presence of variable decleration suggests the possi-
Maternal leukocytosis (≥ 12000–15000/cc and shift to left) bility of umbilical cord compression due to oligohydram-
CRP (if possible)
nios.
Gram stain of amniotic fluid (if possible)
Amniotic fluid: Culture/sensitivity (if possible)
Biophysical profile (BPP) (if possible) MANAGEMENT PLAN ACCORDING TO
Decreased fetal breathing movements

Decreased gross fetal body movement

GESTATIONAL AGE (FLOWCHART 19.1)
Non-reactive NST POG more than 36 weeks

Abbreviations: bpm—Beats per minute; NST—Nonstress test; •• Consider delivery, if the following parameters are
CRP—C-reactive protein present:
–– Cervix dilation more than 3 cm
–– Bishop score more than 6
Ultrasound –– Documented or suspected chorioamnionitis
POG –– Immunocompromised host [e.g. on steroids or has
Estimated fetal weight acquired immune deficiency syndrome (AIDS)].
Amount of liquor Fetal
Fetal congenital abnormality –– Non-reactive NST or BPP less than 7 (for gesta-
Fetal presentation tional age more than 32 weeks)
Flowchart 19.1: Plan of management according to fetal maturity
Abbreviation: PROM—Premature rupture of membrane

–– Oligohydramnios, [amniotic fluid index (AFI) <6 •• Fetal lungs immature/non-availability of test look for
cm; are at increased risk of chorioamnionitis] signs and symptoms of infection
–– Meconium stained amniotic fluid (MSAF) Between 26 and 32 weeks POG
–– Small for gestational age fetus POG less than 26 weeks
•• No interference for 12 hour if the above conditions Patient is admitted in the hospital. Counsel the patient
are not present about the likelihood of outcome and obtain an informed
–– Repeat Bishop’s scoring after 12 hour of PROM written consent.
–– If unfavorable → Oxytocin drip after 12 hours If the patient wants expectant management:
↓ ↑ •• Ampicillin is administered first and then changed
–– If favorable Cervigel (prostaglandin gel to specific antibiotic based on sensitivity testing of
instillations) vaginal swab fluid is culture and sensitivity report.
–– Oxytocin drip: Prophylactic antibiotics •• USG is performed every 2 weeks for fetal weight and
–– Between 32 and 36 weeks POG (Flowchart 19.2) vertical pocket of amniotic fluid more than 2 cm and
Tests for fetal lung maturity (if available) as pregnancy reaches 36 weeks then do as in above
•• Test for fetal lung maturity (if the amount of pooling group.
is large) by evaluating:
–– L/S ratio EXPECTANT MANAGEMENT OF
–– PG level PATIENTS IN THE WARD
–– Shake test: This is a semiquantitative measure
of the surfactant present in a sample of amniotic Monitoring
fluid. In this test, the fluid is mixed with ethanol in
Maternal Parameters
the necessary amounts to achieve concentrations
Temperature charting 6 hourly
of 44–50%. The risk of RDS is 73% when the test
Pulse charting 6 hourly
is negative and no bubbles are formed at 44%
Abdominal examination for uterine tenderness daily
of alcohol. The chances of developing RDS is
TLC, DLC on alternate days
0.35% if bubbles are produced when the ethanol
Cervical and vaginal culture biweekly
concentration is 47%.
CRP (if possible biweekly)
•• Fetal lungs mature same as term management
Antenatal care charting biweekly (weight, BP, urine
ex-abdominal examination for size of uterus).
Flowchart 19.2: Management of PROM
Fetal Parameters
FHR monitoring 12 hourly
DFMR daily (daily fetal movement record)
NST daily (for patients with POG > 32 weeks)
AFI at least biweekly
BPP if possible biweekly
USG, 2 weekly for fetal growth.
Treatment
Steroids if POG less than 34 weeks: Give one course only
Tocolysis is not employed, except as a ‘short protocol’ in
cases of preterm labor, during the early phase in order
to gain time for the action of steroids (but not in cases of
heart disease or diabetes mellitus)
Antibiotics: Parenteral (Table 19.2)
•• Ampicillin 1 gm IV 6 hourly
Abbreviations: NR—Non-reactive; NST—Nonstress test; CA—Cho
rioamnionitis, BPP—Biophysical profile; POG—Period of gestation; •• Gentamicin 80 mg BD
EFW—Estimated fetal weight •• Metrogyl 5 doses only.
TABLE 19.2: Antibiotics Flowchart 19.3: Management of chorioamnionitis
Ampicillin 1 g IV 6 hourly + gentamicin 5 mg/kg IV 12 hourly

If patient delivers vaginally: Discontinue antibiotics postpartum
If patient undergoes CS continue the above + 500 mg
metronidazole IV 8 hourly-till afebrile for 48 hours
If fever persists 72 hours after starting antibiotics, re-evaluate and
revise diagnosis
Oral antibiotics are not necessary after stopping IV antibiotics
Abbreviations: IV—Intravenous; CS—Cesarean section
Indication for Termination of Persistent variable deceleration

↓
Expectant Management Operative delivery
POG: 34 completed weeks Prophylactic antibiotics
Signs and symptoms of chorioamnionitis (Flowchart Active management of third stage of labor
19.3) Placental tissue is sent for culture/sensitivity and
Non-reactive NST membranes for histopathology examination (in case of
BPP 6/10 liquor + fetal activity. fever/chorioamnionitis)—if possible.
Management During Labor SPECIAL CASES

CTG (cardiotocographic) monitoring If cerclage is present, it should be removed during early
Minimal per-vaginal examinations labor on after 37 weeks of gestation
If there is no vertical pocket of amniotic fluid more than If leakage stops or amniotic fluid reaccumulates as seen
2 cm and the FHS is showing variable deceleration on repeat USG examination, the patient can be dis-
An amnioinfusion is done charged. However, before discharge, confirm resealing
↓ of membranes (depending on POG).
1. Write short note on:
i. Preterm labor
ii. Premature rupture of membranes (PROM)
2. Explain management of chorioammionitis.
3. True/False:
i. DFMR stands for daily fetal movement record.
ii. Magnesium sulfate and indomethacin are not tocolytic agents.
20
Disproportional Fetal Growth
INTRODUCTION Asymmetric Intrauterine Growth Restriction

Later in intrauterine life, fetal hypertrophy is affected (fat
Neonates who are appropriate for gestation are supposed and hepatic glycogen) but head is spared (brain sparing
to be normal and have fewer complications. Both small for effect). Asymmetric IUGR is more common. It is usually
gestation and large for gestation babies are high-risk cases. caused by placental insufficiency due to maternal causes
viz. hypertension, anemia, heart disease and also due to
Fetal Growth Restriction (FGR)—Small for placental causes like premature separation [antepartum
Gestation Age (SGA) hemorrhage (APH)]. It occurs later in intrauterine life and
Fetal growth restriction (FGR) is a very important cause of these neonates catch up growth after birth. It is also called
perinatal morbidity and mortality, being 6–10 times greater type I (late flattering).
than a normally growing fetus. It causes 40% of all term still There is a mixed variety also called the intermediate type.
births. Part of these complications can be prevented, if these
intrauterine growth restriction (IUGR) fetuses are identified Etiology
early and managed properly. Way back in 1946, under The exact etiology is not known in all cases. Birth weight is
nourished full term infant was identified by McBurney as a function of both the fetus’s inherent genes (determined
failure to achieve the growth potential. FGR is a pathological growth potential) and a host of maternal environment and
decrease in the fetal growth. It is defined as fetal weight pregnancy-related variables together with their pathologic
below the 10th percentile or less than 2 SD (standard variants. Thus, IUGR has a heterogenous etiology.
deviation) below or below the 3rd centile the mean weight Etiology is arbitrarily divided into fetal, maternal or
for that gestational period. However, the exact threshold is placental causes.
still debatable. Other terms used are dysmaturity restriction
IUGR. It can be seen upon 10% of pregnancies. Fetal Causes
Chromosomal abnormalities: Trisomies (21, 13, 18,
Symmetrical IUGR 16), etc—this leads to abnormal cell replication and
The term, small for gestation fetus depicts the size reduced cell number. It upto 20% of cases
and weight. The term IUGR in addition shows the poor Genetic causes
wellbeing of the fetus. It does not include fetuses of Cretinism (hypothyroidism)
multiple gestation and fetuses with congenital anomalies. Congenital heart disease (CHD), renal agenesis and
It is called symmetrical IUGR when the growth is affected other congenital malformations like osteogenesis
before 16 weeks of pregnancy. At this time hyperplasia imperfecta
is prevented and results in an all round small fetus. It Infections: Rubella, cytomegalovirus (CMV), vericella
is mostly caused by intrauterine infections, maternal herpes, etc.
malnutrition, chromosomal aberrations or congenital Protozoa: Toxoplasmosis, malaria
abnormalities. These neonates are small in all parameters. Bacteria: Listeria monocytogenes, tuberculosis, syphilis,
They usually catch up growth poorly, after birth. It is also etc.
labelled as type II (low profile). Multiple pregnancy.
Maternal Causes etc. can lead to the diagnosis. The risk of IUGR in current
If the mother or father had FGR at the time of her/his birth: pregnancy is one in four, if there is a past history of one
Hypertension (gestational or chronic) or diabetes mellitus
IUGR baby. The risk increases four-fold, if there were
Aged elderly women or teenage pregnancy
previous two IUGR pregnancies.
Crohn’s disease or ulcerative colitis
Low maternal weight gain during the antenatal period
Severe anemia, malnutrition (low maternal weight and
should alert the obstetrician. Any sign of maternal pathology
poor maternal weight gain during pregnancy) will help the management further. In fundal height
Heavy bleeding in pregnancy
measurement if there is a lag of 4 cm (symphysiofundal
Substance abuse (tobacco, alcohol, cocaine and other
height in cm) or more than 4 weeks lag there is a suggestion
drugs) of growth restriction. Estimation of fetal size and weight by
Chronic renal disease or any other chronic illness—
abdominal examination, may alert the obstetrician. Low
malaria, tuberculosis pregnancy associated plasma protein A (PAPP-A) in the first
Periodontal disease is possibly an independent risk
trimester (<0.4 MoM) points that IUGR may happen.
for low birth weight (LBW) as treatment prevents this In severe cases screen for CMV, toxoplasmosis infec-
complication tion, thrombophilia antiphospholipid syndrome.
Bacterial vaginosis also significantly increases the Presence of risk factors should prompt ultrasound
incidence of preterm and LBW babies examination. An early pregnancy ultrasound is invaluable.
Drugs: Hydantoin, coumarin Look for any congenital abnormalities if present. In
Maternal hemoglobinopathies, e.g. sickle cell diseases estimation of fetal development different parameters are
Maternal hypoxia: Pulmonary illness, cyanotic cardiac used to determine IUGR. There are a few ratios in which
diseases, high altitude Head circumference/abdominal circumference (HC/AC)
Cardiac diseases NYHA (New York Heart Association) is one. HC/AC ratio is more than one till 32 weeks, it is one
class III and IV between 32 and 36 weeks and less than one after 36 weeks.
Connective tissue and autoimmune disorders. Proximal tibial epiphysis is present around 38 weeks of
Previous IUGR child (antiphospholipid syndrome) low gestation. Serial measurement of AC and growth velocity
interpregnancy interval is more accurate. Less than 5 mm AC increase in 14 day
Previous miscarrage SB thrombophilia. diagnosis FGR.
Femoral length/abdominal circumference (FL/AC)
Placental Causes ratio is not useful in symmetrical IUGR. The normal value
It is suggested that decidualization is impaired in IUGR is 22 ± 2 irrespective of the POG. If this ratio is more than
placentae, as a result of a complex interaction of many 24, suspect IUGR. Estimated fetal weight is determined.
endocrine placental and paracrine factors determined by The amount of liquor amnii is also important because
the placenta and ovarian steroids, corticotropin-releasing oligohydramnios is often associated with IUGR [amniotic
factors and prostaglandin-E2. Among paracrine factors, are fluid index (AFI) below 5]. Placental maturity of grade
natural killer cells (NKC) of native immunity—lymphocyte, III may alert the obstetrician. Also look for congenital
macrophages, monocytes and neutrophils. abnormalities. Biological markers like erythropoietin,
Small placenta, single umbilical artery amino acid concentration, increased glycerol in cord blood
Placenta previa and abruption (APH) can be risk factors in the child for long-term morbidity, e.g.
Abnormal cord insertion, e.g. circumvallate cerebral palsy and death.
Infection like villitis Fetal echogenic bowel in ultrasound points to IUGR.
Placental hemangiomas and other abnormalities
Infarctions in placenta Doppler Study

Placental mosaicism. Bilateral uterine artery Doppler recording is done at
11–14 weeks. The longitudinal variation in uterine artery
Diagnosis flow pattern (no notches, unilateral notches or bilateral
An accurate history of last menstrual period (LMP) notches) has a significant correlation with the birth weight,
is very important. A history of maternal malnutrition, likely reflecting the timing and degree of trophoblastic
chronic illness, drug abuse, bleeding in current pregnancy, invasion of the maternal vessels.
Disproportional Fetal Growth 193
A second ultrasound after 3 weeks will show whether diameter (BPD), HC/AC ratio, fetal weight and amniotic
growth is satisfactory or restricted. If available, Doppler fluid volume (AFV). Also exclude major congenital mal
ultrasound is advised to find the resistance to blood flow formations. For detection of chromosomal abnormali
in fetal umbilical and maternal uterine vessels. Changes in ties, amniocentesis; placental biopsy or cordocentesis
uterine artery flow preceed those in umbilical artery flow. is performed. If any lethal abnormality is detected do not
Lack of diastolic component or reversed end diastolic do a cesarean section for this indication alone. Twice a
flow are serious signs and need very close monitoring. week, nonstress test is done as long as it is reactive and
Recently, ductus venosus blood flow measurement oligohydramnios is not severe (AFI less than 5). AFV denotes
are shown to provide more accurate information. Fetal urine output, which in turn reflects renal blood flow of the
echocardiography may detect CHD. fetus. Less amniotic fluid means less renal blood supply and
A flat response to glucose tolerance test also points to hence severe degree of IUGR. Both these tests, nonstress
IUGR. The amount of subcutaneous fat store of the fetus is test and AFV together are called the modified biophysical
an important parameter (Ponderal index). profile (MBPP). If there is any doubt, perform a contraction
IUGR fetus shows umbilical blood leptin concentration stress test (CST). If that is negative, it is reassurance of fetal
significantly, lower than the normal fetus (leptin is stored
wellbeing. Daily maternal assessment of fetal kick count
in fetal adipose tissue). IUGR babies with placental
and biweekly-modified biophysical profile is performed;
insufficiency have high level of tumor necrosis factor
ultrasound examination is carried out after 3–4 weeks.
(TNF), but not in those with normal placental blood flow.
As long as fetal head growth continues and is reassuring,
Management pregnancy is continued till 37 weeks of pregnancy. Then
deliver her. Route of delivery is according to individual
One must be sure that the neonate is IUGR and not a
obstetric data.
constitutionally small fetus. The mother is advised to stop
Positive CST, fetal biophysical score 6 with oligohy
smoking or drinking alcohol. Any maternal bowel disease
dramnios and a maturity of 37 weeks, delivery should be
contributing to poor nutrition of the mother is to be treated
considered. A balance should be maintained between the
by specific therapy. Anemia and heart disease should be
consequences of prematurity and intrauterine death (IUD).
controlled as far as possible. Start nonspecific therapy like
bed rest in the left lateral position to increase placental Continuous fetal heart monitoring is carried out during labor.
blood flow. Dietary supplementation is also advised. Any late deceleration warrants immediate delivery. Prost
Adequate protein intake is ensured. Intermittent oxygen aglandin for cervical ripening is a relative contraindication in
therapy (55% oxygen by face mask) may be useful. Time IUGR.
is needed for cortisone therapy to act, [these fetuses need Doppler study is very significant in IUGR fetal surveil
cortisone to avoid intraventricular hemorrhage (IVH) and lance and reducing perinatal mortality. If normal, repeat
necrotizing enterocolitis] betamethasone 12 mg, 24 hours it every 14 days. But as soon as it shows end diastolic flow
apart (2 doses) is given to mothers with period of gestation (abnormal-showing more resistance), repeat color Doppler
(POG) less than 35 + 6 weeks. Antioxidants, low dose of twice a week. When the end diastolic flow is absent.
aspirin and dipyridamole are also practised. Amino acid Reversed end diastolic flow in the maternal umbilical artery
infusion and 10% glucose intravenous (IV) on alternate reflects severe fetal compromise (the phrase fetal distress in
days is practised. Glutamine 40 mg sachet orally twice a not used nowadays) and hence, immediate delivery is called
day for 21 days or in hypertensive patients is given by a few. for. Put the patient in the lateral position, and increase fluid
Atrial natriuretic peptide (ANP) infusion is tried by intake IV. It can also do ductus venosus blood flow which
some obstetricians to increase placental blood flow. gives better guidance or color Doppler of middle cerebral
Similarly, maternal insulin like growth factor-1 (IGF-1) artery (MCA) showing increased blood flow indicate brain
administration is in the experimental stage. sparing effect. A ratio of cerebroplacental flow (MCA P1/
Recent research shows that progestins (allylestrenol) umbilical artery P1) denotes early sign of hypogis in SGA
has good effect for the birth weight of these neonates. fetuses. It helps in deciding timming of delivery.
Fetal Surveillance Care during Delivery

Maternal monitoring of fetal movement is important. A pediatrician is to be present in the labor room. Meco-
Ultrasound is done every 3–4 weeks. Note biparietal nium aspiration can occur after 34 weeks of gestation.
Intrapartum nasopharyngeal suction, in babies born is called the barker hypothesis. The proposed mechanism
through meconium stained liquor is no longer recom- is congenital pancreatic deficiency, manifesting in later
mended. After delivery, aspiration through a direct laryn- life as insulin resistance, and alteration in sympathetic
goscope is indicated. nervous activity or adrenocortical function.
Early neonatal manifestations are: Other long-term sequences of IUGR include:
Meconium aspiration Growth lag
Birth hypoxia Poor school performance
Hypoglycemia Cerebral dysfunction ranging from minimal to cerebral
Hypocalcemia palsy
Hypothermia Stroke and hypertension in adult life
Hyperphosphatemia Adult type 2 diabetes mellitus.
Polycythemia
Hyperviscosity LARGE FOR GESTATIONAL AGE

Hyponatremia
OR MACROSOMIA
Hyperbilirubinemia
Sepsis Large for gestational age (LGA) neonate is defined as,

Necrotizing enterocolitis one who has weight at the 90th percentile or above or
Pulmonary hemorrhage. greater than 2 SD above the normal weight at any particular
Hypothermia is due to low body fat stores. The baby must gestational age. They are also called macrosomic fetuses.
be properly covered otherwise metabolic deterioration of The term is used to refer to fetuses with an estimated fetal
an already unstable IUGR infant can lead to death. weight greater than or equal to 4500 g, independent of
Hypoglycemia due to inadequate glycogen reserve gestational age and demographic variable. However, in
and gluconeogenic pathway is commonly seen. Hypo one north Indian study in Safdarjung hospital, a weight
calcemia may be due to, relative hypoparathyroidism more than 3800 g is considered LGA.
or hyperphosphatemia secondary to tissue breakdown.
Polycythemia is more common in IUGR neonates than in Mechanism
normal babies, it is due to hypoxia leading to more red cell The precise mechanism of macrosomia is not defined.
production. These red cells are broken down and cause To ensure adequate fetal supply of glucose in the second
high incidence of hyperbilirubinemia. Polycythemia can half of pregnancy, there is an increased concentration
sometimes lead to hyperviscosity, causing capillary bed of human placental lactogen, free and total cortisol
sledging and thrombosis. This may involve multiple organs, and prolactin. These together produce maternal insulin
causing pulmonary hypertension, cerebral infection and resistance, which cause postprandial hyperinsulinemia. In
necrotizing enterocolitis. patients, where this hyperinsulinemia response is absent,
Hyponatremia can be caused, centrally as a result of gestational diabetes (relative hyperglycemia) develops.
impaired renal function. Renal complications are attributed This excess glucose, crosses the placenta by facilitated
to asphyxia and nervous system insult, which in turn leads diffusion and produces fetal hyperglycemia. This leads
to inappropriate antidiuretic hormone (ADH) secretion. to fetal hyperinsulinemia with intracellular transfer of
glucose causing macrosomia. Fetal hyperinsulinemia,
Long-term Sequences IGF-I, fibroblast growth factor (FGF-2) with an increased
Neurologic outcome depends on the degree of growth expression of glucose transport (GLUT) protein promotes
restriction (especially impact on head growth), time of excessive fetal growth—excess central body obesity due to
onset, gestational age of the infant at birth and postnatal abnormal deposition and distribution of adipose tissue,
hypertrophy and hyperplasia of organs, especially liver
environment. The long-term consequences are cerebral
and pancreas.
palsy, low intelligence quotient (IQ), poor concentration
and clumsiness especially in very low birth children.
There is growing evidence to support a relation between
Causes
LBW IUGR and adult diseases. Barker proposed that LBW Maternal
infants might be at greater risk for coronary artery disease. Diabetes mellitus (gestational or insulin-dependent)
The risk of stroke and hypertension were also greater. This Maternal obesity (3–4 fold increased risk)
Postdatism Hypothermia
Multiparity Polycythemia
Advance maternal age Hyperbilirubinemia
Previous macrosomia Feeding difficulties
Tall stature of mother Greater risk of Erb’s palsy, cerebral palsy, mental retar-
Race and ethnicity. dation and seizures
Higher absolute nucleated RBC count, lymphocyte
Fetal count and packed cell volume (PCV), reflecting a
Genetic and congenital: compensatory increase in erythropoiesis, in response
•• Beckwith: Wiedemann syndrome (due to pancreatic to chronic intrauterine hypoxia (increased placental
islet cell hyperplasia) oxygen consumption and decreased fetal oxygen supply)
•• Fragile: X-syndrome Greater incidence of asymmetrical cardiac septal
•• Carpenter’s syndrome hypertrophy and cardiomyopathy.
Constitutionally large fetus
Male fetus (150 g heavier than female fetuses at each Long-term Complications
gestational age) Difficulties in feeding the child
Fetal plasma leptin levels (direct link between leptin
Obesity
level and quantity of body fat has been found). Type II diabetes mellitus
If a mother, weighs more than 300 pounds (120 kg) if she Neurological and behavioral problems
is also diabetic the risk of macrosomia is increased to 30%, Childhood onset of cancer (due to the presence of
if his/her mother is simultaneously diabetic. In post-term rapidly dividing cells in macrosomia):
babies, the risk ranges from 5–15%. A good glycemic •• Childhood leukemia
control decreases the risk of macrosomia. •• Wilm’s tumor
•• Osteosarcoma
Complications •• Nephroblastoma
Maternal Complications •• Adrenal cortical carcinoma
No progress in labor •• Hepatoblastoma.
Prolonged labor
Shoulder dystocia Prevention
Operative vaginal deliveries Primary prevention: Includes preconceptional decrease
Emergency cesarean section in weight. Counseling about diet and exercise and control
Fetal compromize of diabetes (by insulin 2–3 months before conception).
Increase reproductive tract injuries Secondary prevention: Early detection of risk factors, e.g.
Increased incidence of postpartum hemorrhage (PPH). advanced maternal age, previous history of LGA neonate,
multiparity is required. A history of previous large
Fetal Complications babies and difficulty in delivery is important however,
Birth trauma (due to vaginal delivery with shoulder in half of the shoulder dystocia cases, have no high-risk
dystocia) factor. Careful antenatal history may help. Examination
• Brachial plexus injuries revealing a big fetus may alert the obstetrician. Fetal
•• Facial nerve trauma weight estimation by ultrasound is carried out. If the
•• Fracture of humerus and clavicle baby’s weight by these methods appears more, an
Stillbirth (lethal congenital malformations or excessive elective cesarean section will be less traumatic.
prepregnancy weight of the mother). Look for factors contributing to increased birth weight
(due to obesity or diabetes).
Newborn Complications At risk patients should be assessed for fetal macrosomia.
Low Apgar score In ultrasound examination, measurement of AC at regular
Hypoglycemia intervals is an important parameter; an initial AC above
Hypocalcemia the 70th percentile is significant.
Adequate control of maternal blood glucose level is •• HC/AC ratio—less than 0.80, suggestive of dispro-
required as 1 hour postprandial, glucose levels are directly portionate central body growth (high-risk of shoulder
related to fetal AC values. dystocia and birth trauma)
•• Cheek to cheek diameter and humoral soft tissue
History thickness—can be added to the AC to improve the
Suggestive of diabetes in previous or present pregnancy. diagnosis
Previous history of macrosomia or difficult or operative •• Biparietal diameter
delivery. •• Femur length
Abnormal weight gain during pregnancy (20 kg or more •• Estimated fetal weight
during pregnancy). •• Central body skin folds thickness
•• Estimated fetal weight/femur length [normal
Examination value = 8.325 ±2.5 (2 SD)]
General examination—abnormal weight gains during •• Congenital malformations
pregnancy or obesity. •• AFV
Abdominal examination •• Placental localization and maturation.
•• Fundal height ≥4 cm, more than expected for Clinical pelvimetry—to assess fetopelvic disproportion
gestational age or contracted pelvis
•• Abdominal girth in inches more than the expected Turtle’s sign (seen in cases of shoulder dystocia)—after
for gestational age (due to disproportionate increase the head delivers, it retracts back into the maternal
in fetal size) pelvis.
•• Fetal lie
•• Fetal heart sound. Management
Because of maternal, fetal and neonatal risks, these patients
Investigations
should deliver in a tertiary care health center where proper
Hemoglobin obstetric, pediatrics and anesthetic facilities are available.
Urine examination Large bore IV line (number 16/18) is introduced and blood
Routine examination is arranged. Elective cesarean is preferred. The patient
•• Albumin
should be fully informed about the risks of vaginal delivery
•• Glucose
to her and to her baby (e.g. shoulder dystocia). However,
•• Ketones
if she still wants a vaginal delivery, an informed consent
Microscopic examination
must be taken and facilities for immediate cesarean
•• Pus cells and bacteria
section should be available, if the need arises.
•• Culture
If glucose challenge test is more than 130 mg/dL then a
glucose tolerance test (GTT) is performed
Fetal Complication
Glycosylated hemoglobin (HbA1C) levels—monitor the The fetus is at risk of asphyxia as it cannot breath by
glucose control expanding the chest. Umbilical circulation is obstructed.
Renal function tests—especially baseline serum creati- An inexperienced birth attendant may cause damage
nine to rule out nephropathy (if diabetic) to the brachial plexus (Erb’s palsy). Besides there may
Ophthalmological examination (fundoscopy) rule out be long-term complications like central nervous system
retinopathy (in diabetic patients) (CNS) damage, mental retardation, seizures and speech
Ultrasound examination: It is helpful only in conjunc disorders.
tion with clinical examination, estimated weight, past
history and assessment of risk factors. SHOULDER DYSTOCIA
Various parameters and their combination are essential
for diagnosis: Shoulder dystocia is defined as the inability of the
•• HC is usually normal in insulin dependent diabetes shoulders to deliver, after the delivery of the head. This
mellitus (IDDM) but may be increased is an acute obstetric emergency and prompt and skilled
•• HC is increased—probably being the most reliable management is warranted to prevent injury or death of the
sonographic parameter for detection of LGA fetus.
Shoulder dystocia sometimes can be anticipated by

looking at the size of the fetus. However, it can only be
diagnosed during labor, after delivery of the head, when
gentle downward pressure on the head fails to deliver the
anterior shoulder from behind the pubic symphysis.
When the maternal pelvis is of a sufficient size to allow
the delivery of the fetal head but is not large enough for
the passage of the fetal shoulder, shoulder dystocia can
occur. This is also seen in women with short stature (4 feet
10 inches) or platypelloid pelvis.
Patient is advised to stop bearing down and a senior
obstetrician, a pediatrician and an anesthestist should be
called immediately to conduct this delivery.
Methods for Conduction of Delivery in

Cases of Shoulder Dystocia
An adequate generous episiotomy is performed after
anesthetizing the patient and assessing the posterior space Fig. 20.2: Suprapubic pressure
of the pelvis after delivery of the head. The application of
downward pressure on the head is stopped (Fig. 20.1).
Suprapubic pressure: The maternal legs are hyperflexed
on her abdomen (McRoberts maneuver). This results

in flattening of her lumbar spine and increase in the
size of the posterior space of the outlet. Suprapubic
pressure may be applied by an assistant to dislodge the
anterior shoulder. Now the obstetrician applies gentle
downward pressure on the head. The shoulders are thus
delivered (Figs 20.2 and 20.3).
McRoberts maneuver: The maternal legs are hyperflexed
onto her abdomen and suprapubic pressure is applied

to dislodge the anterior shoulder along with a gentle Fig. 20.3: Maternal legs hyperflexed on her abdomen
downward pressure on the head. This will ease the

delivery of the shoulder.
Rubin maneuver: If the above procedure fails, an
attempt is made to rotate the shoulders into an oblique
position by using two fingers against the posterior
shoulder and pushing it around towards the fetal chest.
Woods maneuver (corkscrew maneuver) (Clockwise
180°) if the McRoberts maneuver is unsuccessful try to
rotate the fetal shoulder into the oblique position. Put
2 fingers against the posterior shoulder and attempt to
push it towards the fetal chest (Rubin maneuver). One
can also push the posterior shoulder towards the fetal
back (Fig. 20.4).
Reversed woods: Pressure is applied to the posterior
surface of the anterior shoulder in order to produce a
Fig. 20.1: Fundal pressure should never be used counterclockwise rotation of the posterior shoulder.
Fig. 20.4: Wood’s maneuver Fig. 20.5: Posterior arm extraction
Delivery of posterior arm: Posterior arm extraction Subcutaneous symphysiotomy: Symphysiotomy by

is usually attempted when the above mentioned subcutaneous incision at the central cartilage of the
maneuvers have failed. The operator flexes the arm symphysis pubis can be carried out by an experienced
then gently brings down and delivers the shoulders. obstetrician.
A hand is inserted into the hollow of the sacrum, Cleidotomy can be practised in experienced hands. The
gentle pressure is applied on the antecubital fossa, clavicles are divided.

causing flexion of the arm. As the arm flexes across If all the above techniques fail the fetal head is replaced
the chest the forearm is caught and the hand and the in the vagina and a cesarean section is performed (Zavanelli
maneuver).
forearm are gently delivered. The posterior shoulder is
In a dead fetus, destructive operations under anesthesia
brought anterior by rotating the trunk and the free arm
are required.
is delivered anteriorly. The assistant gives suprapubic
Prolonged second stage of labor or arrest of descent of
pressure and posterior shoulder is delivered. Otherwise fetus is further indications for cesarean section.
rotate the trunk to bring the free arm anteriorly and Weight loss is strongly recommended in obese women
effect delivery (Fig. 20.5). before embarking on next pregnancy. Counseling should
Zavanelli maneuver: It can be performed when all be done, if there is a previous history of LGA fetus as the
the above procedures fail. The head is rotated back risk of LGA babies is greater.
to direct occipitoposterior position and is flexed and Further efforts are done to diagnose these pregnancies
pushed into the vagina subsequently cesarean section early so that they can be managed early and electively,
is carried out. rather than as an emergency.
1. Define IUGR.
2. Explain LGA/macrosomia and shoulder dystocia.
3. True/False:
i. Doppler study is useful in IUGA fetal surveillance.
ii. Shoulder dystocia is the ability of the shoulders to deliver after delivery of the head.
21
Poonam Goel, Sudha Salhan, Navneet
Intrauterine Fetal Death
indices). Roughly, 3 million IUFD occurs throughout the

INTRODUCTION
world every year.
Intrauterine fetal death (IUFD) or intrauterine death (IUD) is
one of the greatest tragedies in obstetrics. IUFD embraces all ETIOLOGY
fetal deaths occurring after the 24th week of gestation, both
during pregnancy (antepartum death) and during labor (in- Finding of the cause helps the parent in coping with their
trapartum death) . It is early fetal death if its weight is atleast loss and in counseling for future pregnancy.
500 g or period of gestation (POG) after 22 weeks with a The fetal deaths during pregnancy and labor are due to
crown rump length (CRL) of 25 cms or more. Late fetal a number of fetal, maternal and placental factors and in
death is labeled when weight is 1000 gm or more, POG more about 25–35% cases, the cause remains unknown.
than 28 weeks or CRL is 35 cms or more. When the fetus dies
in utero in the antenatal period, it is usually retained in the Fetal Causes (25–40%)
uterus for some days before it is expelled and usually results Congenital malformations: As a result of chromosomal
in the delivery of a macerated stillbirth (Fig. 21.1). Death and non-chromosomal disorders of which neural tube
during labor ends in delivery of a fresh stillborn and does defects, isolated hydrocephalus and complex congenital
not pose a problem for management. The fetal death rate is heart diseases (CHD) (rubella) are the most common.
the number of fetal deaths per 1000 infants born. Hemoglobinopathies in fetus are also a cause. Glycogen
Incidence varies between 115 and 125 per 1000 births.
storage disease, X-linked congenital disorders or
Incidence in Safdarjung hospital is 3.6%. It contributes
autosomal dominant (skeletal dysplasias) are also causes
significantly to perinatal mortality (an important health
etiology.
Rh-incompatibility: In an Rh-negative mother with an
Rh-positive fetus, maternal red cell antibodies against
Rh-antigen of IgG (immunoglobulin G) type cross the
placenta and cause fetal hemolytic anemia and hydrops
fetalis. Fetuses with hydrops may die in utero from
profound anemia and circulatory failure. Now, with
administration of anti-D immunoglobulin during and
after pregnancy, antenatal intrauterine transfusions
and screening for Rh-sensitization in pregnancy there
has been a decrease in Rh-incompatibility as a cause of
fetal death.
Infections: Congenital syphilis, cytomegalovirus, toxo-
plasmosis, parvovirus B19, rubella, varicella infections
and listeriosis.
Fig. 21.1: A macerated stillborn Male fetus.
Placental (25–35%) Abnormal labor, mismanaged labor, obstructed labor

Placental abruption and placenta previa are the leading and uterine rupture can also cause fetal death
causes of obstetrical hemorrhage and can cause fetal Post-term pregnancy: While unexpected death may
death by producing acute placental insufficiency. occur during pregnancy due to placental insufficiency,
the risk is likely to be more in labor
Placenta with two types of cell lines in a euploid
Systemic lupus erythematosus (SLE)
conception (placental mosaicism).
•• Antiphospholipid antibodies: The presence of lupus
Placental and cord abnormalities: Pregnancies with
anticoagulant (LA) and anticardiolipin antibodies
circumvallate placenta, velamentous (vasa previa),
(ACA) is associated with decidual vasculopathy,
membranous or marginal insertion of cord to placenta,
placental infarction, fetal growth restriction and fetal
true knots in the cord, tight cord round the neck,
death.
torsion, stricture and hematoma in the cord are rare
•• Other coagulation disorders: Prothrombin, gene
causes of fetal death. Prolapse of the umbilical cord is
mutation, factor V Leiden mutation, lll deficiency, etc.
an important cause.
Hyperpyrexia due to any cause
Intrapartum asphyxia: Usually manifests itself by
Adolescent or elderly gravidas
(a) signs of fetal distress or (b) fetal death, according to
The mother’s educational level less than the 10th stan-
its severity.
dard
Twin-to-twin transfusion syndrome: It is a common
Male fetus, low socioeconomic status, multiple gestation,
cause of fetal death in monochorionic multifetal preg-
drug abuse are other associated causes
nancy.
Third trimester IUFD correlates significantly with
Chorioamnionitis frequently associated with pro-
thrombophilia
longed membrane rupture and long labors and if fetal
Smoking
infection ensues, fetal death can occur.
Coffee: Drinking coffee during pregnancy increase
Maternal (5–10%) stillbirth rate.
Surprisingly, maternal disorders make only a small
Unexplained (25–35%)
contribution to fetal death. Common maternal causes for
Usually one-fourth of fetal deaths are unexplained, but
IUD are:
with careful assessment of the clinical course, meticulous
Hypertensive disorders: The combination of prote
examination of fresh stillborn and appropriate laboratory
inuria and hypertension markedly increases the risk of
investigations including autopsy only about 10% of fetal
fetal death in utero. Fetal death in these women is due
deaths remain unclassified.
to large placental infarcts, abruption placentae and
markedly small placental size
Diabetes mellitus: Stillbirths without identifiable cause
PATHOLOGY
unexplained fetal demise are a phenomenon unique When the fetus dies in the antenatal period, it is usually
to pregnancies complicated by overt and uncontrolled retained in the uterus for some days before it is expelled,
diabetes and it undergoes a process of maceration. The epidermis
Thyroid disorders becomes soft and sodden, bullae appear containing turbid
Obesity fluid beneath them and it peels off in patches exposing
Cholestatic disease of pregnancy areas of dark red cutis. The entire fetus becomes swollen
Multiple pregnancy and of a dusky red color. The articular ligaments are
No or inadequate antenatal care softened, allowing free separation of bones to occur. The
Severe anemia in mother skull bones overlap, become loose and the skull collapses.
Infections: Toxoplasmosis, other—rubella, cytomega- The solid viscera becomes soft and diffluent. The umbilical
lovirus and herpes (TORCH) and other infections of the cord is swollen and stained. The liquefaction of the tissues is
mother due to a process of aseptic autolysis as there is no bacterial
Trauma, sepsis, acidosis, shock and other medical decomposition. These changes vary in degree with the
disorders like heart disease and renal disease can affect length of retention in utero of the dead fetus. Peeling off of
the general maternal condition adversely enough to skin becomes evident after 24 hours (Fig. 21.2); the more
cause fetal death and sometimes, even cause maternal advanced changes in solid viscera and other parts require
mortality several days.
Intrauterine Fetal Death 201
To confirm the diagnosis real time ultrasonography

(USG) is used. In the past, radiograph of the abdomen was
used to establish fetal death.
Ultrasonography (Fig. 21.3)

Failure to detect heart motion by real time ultrasound
is reliable evidence of fetal death. Other findings on
sonography include scalp edema and collapsed cranial
bones which are overlapping (Spalding’s sign). USG can
also provide some clue to the cause of death in a few cases
(congenital abnormalities, retroplacental clot, etc).
Straight X-ray Abdomen (Fig. 21.4)

Fig. 21.2: Macerated stillbirth with peeling of skin Signs on the X-ray are seen, if fetal demise has occurred
several days previously. These following are the principal
CLINICAL FEATURES radiological signs of fetal death:
Significant overlap of skull bones (Spalding’s sign) caused
Patient may present with abdominal pain and cessation by liquefaction of the brain, a process that requires several
of fetal movements, which were previously experienced days to develop. There is also abnormal increase of the
by the patient. This loss of fetal movements must not be cranial soft tissue as a result of maceration (the Halo sign).
accepted as conclusive evidence of fetal demise unless Exaggerated curvature of the fetal spine. Because this
confirmed by other signs. There may be regression of sign depends on maceration of the spinous ligaments,
symptoms of pregnancy like breast tenderness, nausea, its development requires several days. Moreover, mild
etc. Note her age and POG. Ask for history of bleeding, degree of curvature of spine in the living fetus may be
trauma, any recent severe illness or fever, etc. Elicit any misleading (Ball’s sign).
drug abuse history or any medical disease. Try to find Demonstration of gas [carbon dioxide (CO ) due to
2
miscarriage, intrauterine growth restriction (IUGR), IUFD anerobic metabolism] in the fetus is an uncommon but
or neonatal demise in previous pregnancy. reliable sign of fetal death. Appearance of gas shadow
On examination, gradual retrogression of height of (Robert’s sign) in the chambers of the heart and great
uterus occurs and it becomes smaller than the period of vessels (e.g. aorta) may appear as early as 12 hours but
amenorrhea. Dead fetus in utero feels quite different from is difficult to interpret.
Crowding of ribs (concertina effect).
the living; because of loss of muscle tone, the limbs do not
stand out distinctly and the fetus feels like a homogenous Routine and Special Investigations
mass. Fetal movements are not felt during palpation. Egg-
They are done to find the cause of death. Hemoglobin level,
shell crackling feel of the fetal head, if elicited is almost
ABO-Rh typing, platlet count, venereal disease research
pathognomonic. Abnormal fetal posture and decreased
laboratory (VDRL) of both partners, fasting and postprandial
liquor may be associated findings. On auscultation, the
blood sugar, thyroid function, renal function tests (RFTs),
fetal heart sound (FHS) is absent. Further confirmation of
liver function tests (LFTs) and bile salts, coagulation profile,
the fetal heart on ultrasound examination is mandatory
TORCH screening, urine complete examination and culture
before disclosing the diagnosis of fetal death.
and vaginal swab and in selected cases LA and ACA and
thrombophilia screening is done. Coagulation profile inclu
MANAGEMENT (FLOWCHART 21.1) ding bedside bleeding time (BT) and clotting time (CT) is
needed. Work-up for thrombophilia includes prothrombin
Investigations maturation, factor V Leiden mutation, antithrombin II level.
The investigation protocol is directed at confirming the If available perform maternal anti-Ro, anti-La antibodies,
diagnosis, followed by investigations to identify the cause and antiplatelet antibodies. Do parental karyotyping.
of death and lastly, the coagulation profile to follow-up Examine the baby: Do a comprehensive assessment of
these patients. all stillbirths. See color of the liquor (meconium smeared
Flowchart 21.1: Schematic management of intrauterine fetal death
Abbreviations: VDRL—Venereal disease Research Laboratory; GTT— Glucose tolerance test; IUFD—Intrauterine fetal death; PGE2 PGE1—
Prostaglandin E2 and E1; TORCH—Toxoplasmosis, other rubella, cytomegalovirus and herpes
Fig. 21.3: Ultrasound showing fetal stillbirth (Spalding’s sign) Fig. 21.4: X-ray showing intrauterine fetal death
Intrauterine Fetal Death 203
or blood staining). Look for time of death (fresh or Induction of Labor

macerated), any congenital abnormality. Note, weight Weekly assessment of fibrogen level is helpful. Until
of the baby and color of its skin. A photograph of the fibrogen levels fall below 100 mg/mL clinically relevant
stillborn baby or an ultrasound should be preserved (if coagulopathy does not occur.
possible). Take consent and perform an autopsy to know
Active intervention is required if the patient does not
the cause. A negative consent is to be documented. If
go into spontaneous labor within 2 weeks of fetal death,
consent is not given, perform limited autopsy [consists of
signs of coagulopathy are imminent or the patient is much
physical examination, biopsy from skin, heal and liver,
depressed emotionally because of carrying a dead fetus.
a photograph, ultrasound and if possible magnetic
Cervical assessment and Bishop scoring is done and
resonance imaging (MRI)] of the newborn. Cytogenetic
if the Bishop score is poor, the treatment is begun with
studies by karyotyping of the baby are helpful in the
cervical priming, which is done by using prostaglandins.
presence of congenital malformation or IUGR. Try to
find the maturity (palmar or sole creases). Examination Prostaglandins used for cervical ripening are prostaglandin
of umbilical cord for any knots, its length, attachment E2,, i.e. cerviprime gel containing 0.5 mg of PGE2 which
and any abnormality is noted. Cord blood may be taken is instilled intracervically and prostaglandin E1 (PGE1),
for cytogenetic studies in fresh stillbirth. i.e. misoprostol which can be used orally and vaginally.
Examination of the placenta: Gross examination for Prostaglandins are also used for induction of labor,
any anatomical abnormality is done. Note the weight, along with cervical ripening, and they are more effective,
size, thickness any staining, calcification, attachment of especially when the patient is remote from term.
the cord, any retroplacental clot, etc. Do macroscopic In near term, oxytocin administered intravenously (IV)
examination of the membranes. Microscopic examina- is usually effective in stimulating uterine activity. When the
tion may be sent for bacteriological studies which are POG is remote from term, oxytocin is less likely to prove
done if infection is suspected. Send swab or part of pla- effective unless given in higher concentration.
centa for microbiological tests. Surgical induction by artificial rupture of membranes
is contraindicated, as a dead fetus offers a greater
TREATMENT opportunity for sepsis to be established than a living one
and also because of a chance of failure of induction.
Pshycological Support
It is of paramount importance. The diagnosis is gently Complications
revealed to the patient and relatives and consent for treatment Blood coagulation disorders: If the fetus is retained in
taken. There are symptoms like loss of sleep, anger, hostility, utero for sometime before being expelled consumptive
etc. but they often regresses soon. The adaptation is easy, if coagulopathy, presumably mediated by thromboplastin
the attending obstetrician is considerate and substantial from the dead products of conception, becomes opera
information is imparted (suggesting probable cause, human tional. Prospective studies indicate that gross disruption
behavior and counselor consultation). of maternal coagulation mechanism rarely developed
The medical team and nursing staff should provide all earlier than one month after fetal death. If the dead
support and sympathy to the bereaved couple and their fetus is retained longer, however, about 25% of women
relatives. Long-term anxiety-related symptoms in the develop coagulopathy. Typically, the fibrinogen
mother are reduced if she sees her stillborn baby and if she concentration falls (hypofibrinogenemia) and in some
has an ultrasound or picture of the child or she has gone cases, the decrease may reach potentially dangerous
through the ritual of burial of the child because in this way concentrations of less than 100 mg/dL. Simultaneously,
easing her stress is helped. fibrin degradation products are elevated and platelet
counts tends to decrease, but severe thrombocytopenia
Expectant Management is uncommon. Rarely disseminated intravascular
The majority of women enter spontaneous labor within coagulation (DIC) and hemorrhage can be seen.
2 weeks of fetal death. In the absence of other complica- Psychological upset: The psychological stress experi-
tions, attempts to evacuate the uterus may be delayed for enced by carrying a dead fetus, needs special attention.
this interval. The patient and her relatives are likely to be Infection: Until the membranes are intact, infection
upset psychologically but they should be assured of the is unlikely but once the membranes rupture, infection
safety of non-interference. especially by gas forming organisms like Clostridium
welchii may occur. The dead tissue favors microbial Prediction of fetal compromise in present pregnancy
growth with disastrous consequences causing chorio- may be done by the following tests which may bring out
amnionitis and septicemia. high-risk patients.
During labor: Uterine inertia, retained placenta and In first trimester, pregnancy associated plasma protein-A
postpartum hemorrhage (PPH) may occur. (PAPP-A) is less than 5th percentile it require special vigil.
High doses of IV oxytocin may lead to hyponatremia Similarly, in second trimester screening, if a-fetoprotein
and rupture uterus. and b-human chorionic gonadotropin (b-hCG), levels are
more than 95th percentile there are more chances of fetal
Prevention compromise.
If she comes in preconceptional period after a previous During each visit emphasise the importance of
IUFD investigate on the line to find the etiology. reporting immediately if the fetal movements increase
or decrease. In cases of postmaturity, delivery should be
Early start of a good antenatal care and institutional delivery
monitored under cardiotocography (CTG).
help. But prevention of stillbirth is not always possible however
While IUFD cannot be totally prevented, regular ante-
in the following circumstances a vigil can be kept.
natal care and screening of at risk mothers and intensive
Previous history of IUFD or growth restriction or
fetal and maternal monitoring may help in achieving a
neonatal death (upto 10% chances of recurrence)
good outcome in pregnancy.
History of vaginal bleeding during this pregnancy
especially placental abruption Inhibition or Suppression of Lactation

Hypertensive disorders of pregnancy
In stillbirth, we advise the patient to avoid nipple stimulation,
Pregnancy with diabetes mellitus
and not to express milk by hand or pump. The patient should
Other placental and fetal abnormalities seen be instructed not to massage or apply heat to the breast.
Postmaturity.
The patient should wear a supporting brassiere. Analge-
Preconceptional period: Detail history of previous IUFD sics are sometimes needed. Apply cold compresses to the
(of mother’s antenatal course and dead child examination breast to reduce swelling and pain.
report). Try to eliminate and correct as many causes as Milk production by the breast depends upon the suck-
possible (illicit drugs, smoking, obesity). Genetic disorders ling. As there is no suckling in the case of stillbirth, no milk
in parents are to be probed. is produced. In about 2–3 days engorgement will start
When she comes in antenatal period with above high receding. There is no indication of medical suppression of
risk history do tests to find the cause (if any). lactation in this case.
1. Explain the causes of intrauterine fetal death.
2. Explain briefly the management of intrauterine fetal death.
3. True/False:
i. High doses of intravenous oxytocin leads to rupture of uterus.
ii. For cytogenetic studies, cord blood is taken.
22
Prolonged Pregnancy
INTRODUCTION ETIOLOGY
Prolonged pregnancy can also be called postmaturity, The most frequent cause of post-dated pregnancy is
postdates and post-term pregnancy. incorrect dates. Fetal and placental anomalies are more
Ballantyne (1902) was the first to draw attention to often seen in post-term pregnancies. Fetal anomalies
postmaturity. The American College of Obstetrician and include hypothalamic-pituitary-adrenal axis abnormalities,
Gynecologist (ACOG), the World Health Organization e.g. anencephaly where a marked adrenal hypoplasia is
(WHO) and the International Federation of Gynecology seen in the fetus because of pituitary insufficiency causing
and Obstetrics (FIGO) have defined prolonged pregnancy low estrogen levels leading to a decreased synthesis and
as pregnancy at 42 completed weeks of gestation [i.e. secretion of precursor hormone dehydroisoandrosterone
294 days after last menstrual period (LMP) or more]. sulfate, and therefore, insufficient conversion to estradiol
However, recently a significant increase in fetal mortality and estriol in the placenta.
from 41 weeks gestation onwards. Since, there is a gradual It has been seen that low levels of placental corticotropin
decline in placental vascularity and therefore, its function, releasing hormone (CRH) can also cause post-term
a post-dated pregnancy may culminate in fetal distress
pregnancy.
and occasionally fetal death. Hence, we must closely
Deficiency of placental sulfatase (an X-linked recessive
observe fetal wellbeing and induce labor, if need be, after
disease in male fetuses) is seen to produce less estrogen
41 completed weeks. It is estimated that 4–19% of preg
and hence post-term pregnancy.
nancies reach or exceed 42 weeks of gestation and 2–7%
In others, primiparity is sometimes associated with
complete 43 weeks. Incidence in Safdarjung hospital is 4%.
post-term pregnancy. In multigravida, if there is a history
of previous post-term pregnancy, approximately half will
POSTMATURITY SYNDROME deliver a post-dated fetus in the current pregnancy too.
It is characterized by prolonged gestation, sometimes There may be a family history of prolonged pregnancies.
a large-sized fetus and diminished placental capacity The father’s genes may play some role in determining
for exchange associated with cutaneous and nutritional how long a pregnancy lasts. Previous prolonged pregnancy,
changes in the newborn infant. specially with the same partner is an important risk factor
Pregnancy should not be permitted to go beyond term for new post-term delivery.
in conditions like:
Gestational hypertension
CAUSES OF POST-TERM PREGNANCY
Pre-eclampsia
Eclampsia Incorrect dates (most frequent cause)

Renal diseases associated with pregnancy Fetal congenital abnormalities:
Chronic hypertension associated with pregnancy •• Anencephaly (without hydramnios)
Rhesus (Rh) isoimmunization in pregnancy •• Adrenal hypoplasia
Diabetes mellitus Maternal factors:
Antepartum hemorrhage. •• Primipara
•• Previous post-term pregnancy cord compression and fetal hypoxia. The latter in turn
•• Family history causes relaxation of the rectal sphincters and meco-
Placental factors: nium discharge. If placental blood flow is decreased
•• Deficiency of placental sulfatase significantly, restriction of fetal growth and loss of sub-
•• Deficiency of placental CRH cutaneous fat is seen. Oligohydramnios is more often
Past history seen in growth-restricted fetus. It causes variable
Family history. deceleration due to cord compression in cardiography
tracings.
Cord compression
DIAGNOSIS
Macrosomia
Diagnosis is often difficult because of inaccuracy of the date Placenta insufficiency (fetal hypoxia)
of the LMP (as most of the women do not remember their Fetal distress.
LMP). It is also not possible in cases of irregular periods,
lactational amenorrhea preceding pregnancy and post-
During Labor
pill amenorrhea. In these cases, the earliest examination Maternal
of the size of the uterus are helpful. The time of diagnosis Labor dysfunction (e.g. incoordinate uterine action)
of pregnancy by urine test is also important. The date of Obstetric trauma
quickening is useful. Most accurate is the earliest ultrasound Increase operative/instrumental delivery
examination. Hemorrhage.
On Examination Fetal
General examination: Weight-falling/stationary Macrosomia
on serial examinations Shoulder dystocia—greater risk of operative delivery
Abdominal examination Decreased molding capacity (because the skull bones
•• Uterine size—to assess the period of gestation are no longer pliable and soft)
•• Girth of the abdomen—steady decline due to reduced Cord compression
amniotic fluid volume Fetal asphyxia.
•• Increased prominence of the fetal parts to palpation
Ultrasound abdomen
Following Delivery
•• Assessment of gestational age Appearance of the neonate at birth—the post-term
•• Fetal weight newborn has a wrinkled and yellow—greenish colored
•• Fetal maturity [by biparietal diameter (BPD), head skin, which is peeling at places. This may be due to loss
circumference (HC), abdominal circumference (AC) of protective effect of vernix caseosa. The body is long
and femur length (FL)] and thin suggestive of wasting. The newborn is usually
•• Restriction of fetal growth alert, has wide open eyes and has a wisened look. Skin
•• A loss of fetal subcutaneous fat wrinkles are accentuated (especially in palms and
•• Amount of liquor (oligohydramnios, amniotic fluid soles). Finger and toe nails are long with an appearance
index ≤ 5 cm) of advanced maturity.
•• Placental localization and maturity (Grade 3) Increased incidence of neonatal convulsions
Rule out cephalopelvic disproportion Severe meconium aspiration syndrome (due to oligo-
Doppler ultrasound has no proven value, till date, in the hydramnios if the liquor is meconium stained, thick
surveillance of post-term fetuses. and viscous).
Atelectasis of lungs
Hypoglycemia
COMPLICATION Polycythemia
Hyperbilirubinemia
During Pregnancy Low Apgar score (<4 at 5 minutes)
Oligohydramnios: Reduced amniotic fluid volume in Abnormal neurological signs
the absence of ruptured membranes or fetal urinary Sleep disorders
abnormalities is due to poor placental function leading Inadequate social competence during the first year of
to less renal blood flow and less urine output. It causes life.
Prolonged Pregnancy 207
The last three complications are still under investiga- on post-contraction fetal heart auscultation, an immediate
tions. delivery is indicated (vaginal or abdominal), depending on
Post-term delivery is associated with a significant cervical dilation, to prevent fetal morbidity and mortality.
increase in the incidence of shoulder dystocia, labor dys- It is necessary to initiate fetal surveillance at 41st weeks of
function, obstetric trauma and maternal bleeding. Due pregnancy. A biophysical profile biweekly is advised. More
to the complications mentioned above neonatal inten- important are nonstress test and an assessment of amniotic
sive care unit (NICU) admissions are needed more often fluid volume. Induction of labor is carried out if the nonstress
in these neonates. There is greater morbidity as well. For test is non-assuring and amniotic fluid volume is 5 cm or less.
long-term outcome, large scale follow-up is needed. Estimating fetal weight by ultrasound is important in man-
agement. Oxytocin stress test is performed. If abnormal, it is
an indication for delivery. Induction of labor should also be
MANAGEMENT (FLOWCHART 22.1)
done in women complaining of decreased fetal movements.
A pregnant woman, who has completed 41 weeks of preg- However, induction of labor should be carried out at
nancy, should be admitted in the hospital and put on fetal 42 completed weeks in all pregnancies. Sweeping and
surveillance. Expected fetal weight is assessed, and any stripping of the membranes can be performed along with
cephalopelvic disproportion is meticulously ruled out. The prostaglandin gel (PGE2 dinoprostone gel) 3 mg instillation
level of fetal fibronectin in cervical secretion (if possible), in the non-dilated cervix. With a favorable cervix, oxytocin
is measured (level of 50 mg/mL is observed to correlate drip is started combined with amniotomy. Early artificial
with spontaneous labor within 3 days). rupture of membranes (ARM) helps in detection of thick
A small amount of amnioinfusion in cases of oligohy- meconium, which is important. To prevent its aspiration
dramnios can help. (may lead to severe respiratory distress and death)
The patient should be instructed to keep a daily fetal immediately delivery is a must. After rupture of membranes,
movement record. scalp electrode can be applied and an intrauterine
Fetal circulation is compromized and the fetus can not pressure catheter can be passed to give a more accurate
tolerate hypoxia (during uterine contractions) and dies faster impression of fetal heart rate and contraction of the uterus
than a term fetus. If fetal growth restriction is superimposed, if available. If the baby is big, try to avoid vaginal operative
morbidity and mortality is greatly increased. Therefore, in deliveries and prevent traction on the impacted shoulders.
case of any abnormalities on cardiotocographic tracings or It is best for this baby to be delivered by cesarean section.
Flowchart 22.1: Management of post-term pregnancy
Abbreviations: U/S—Ultrasound; BPP—Biophysical profile; NST—Nonstress test; CTG—Cardiotocography; LSCS—Lower segment cerarean section
1. Explain prolonged pregnancy.
2. Write note on etiology and management of prolonged pregnancy.
3. True/False:
i. It is necessary to initiate fetal surveillance at 41 weeks of pregnancy.
ii. Incorrect dates is a cause of most frequent post-dated pregnancy.
Abnormalities of
23
Placenta, Cord and
Amniotic Fluid Volume
Amniotic fluid abnormalities

INTRODUCTION
Hydramnios
Anatomy of placenta: There is a wide variation in the Oligohydramnios.
normal anatomy of placenta. No two placentae are the
same. There are some distinct anatomical variations.
ABNORMALITIES OF PLACENTA
Certain placental abnormalities are documented and are
of clinical significance. Their knowledge is very important Placenta Bipartite or Bilobate (Fig. 23.1)
in managing during the antenatal period and the third It is not a very common condition but occasionally, the
stage of labor. placenta is separated in two lobes. The separation may be
Abnormalities of placenta
incomplete or complete. The incomplete ones are known
Placenta bipartite or bilobate
as placenta bipartite or bilobate. Here the vessels of
Succenturiate placenta
fetal origin extend between the two lobes before joining
Ring-shaped placenta
to form the umbilical cord. While in the placenta duplex
Membranous placenta or placenta diffusa
the lobes are completely separated and so are the vessels.
Fenestrated placenta
Occasionally, three distinct lobes may be seen which is then
Extrachorial placenta
Large placenta
known as placenta triplex or tripartite placenta.
Placenta accreta, placenta increta and placenta percreta
Clinical significance: Evidence of missing lobe on exami-
Placental infarcts and calcification
nation of placenta after delivery must lead to exploration
Placenta previa.
of the uterus without any loss of time.
Abnormalities of cord
Succenturiate Placenta (Incidence 5%)
Cord prolapse
False knots
In this type, one or more small accessory lobes or cotyle-
True knots don are developed in the membrane away from the main
Long cord and short cord placenta; the lobe has vascular connections (of fetal ori-
Torsion gin), (Fig. 23.2) to the main part of the placenta.
Stricture Clinical significance: The smaller accessory lobe might be
Hematoma retained in the uterus after the placenta is expelled causing
Cyst severe postpartum hemorrhage (PPH).
Edema. Retention of succenturiate lobe is suspected if the
Cord insertion abnormalities placenta expelled is not complete and shows a defect in
Vellamentous the membrane towards the periphery and also if vessels
Battledore. extend from the placenta to the margin of the tear.
Complications of membranes
Premature rupture of membranes (PROM)/early rup-
Ring-shaped Placenta
ture of membrane This abnormality is not usually seen. The placenta may be
Chorioamnionitis annular in shape, sometimes a complete ring or horseshoe
Fig. 23.1: Placenta bipartite or bilobate Fig. 23.2: Succenturiate placenta
shaped. This anomaly may be a variant of membranous

placenta.
Clinical significance: This abnormality is associated with
an increased incidence of antepartum hemorrhage (APH)
and PPH and intrauterine growth restriction (IUGR).
Membranous Placenta or Placenta Diffusa

This too is a very uncommon abnormality. In this, the
whole of the chorion is covered by a functioning villi and
thus the placenta appears as a thin membranous structure
on ultrasonography.
Clinical significance: Chances of retention of the placenta
leading to a severe PPH is very high as membranous placenta
may not separate easily. More chances of occurrence of a
severe PPH due to placenta accreta/placenta previa associ
ated with it.
Fig. 23.3: Fenestrated placenta—note the absence of placental
tissue in the center
Fenestrated Placenta
A rare condition, here the chorionic plate is intact, but
smaller, than the basal plate on the maternal side. In these
there may be a defect in the villous structure, there might
kinds of placentas there might be a central depression in
be a hole in the placenta (Fig. 23.3).
the fetal surface, which is surrounded by a thickened ring.
Clinical significance: When the placenta is examined This is called circumvallate placenta. It is composed of
after delivery, the hole might be mistaken for retained bits a double fold of amnion and chorion, with degenerated
of placenta in the uterus. But there are no vessels leading decidua and fibrin, in between presenting as a cup-shaped
to this hole. placenta with raised edges. When the ring coincides with
the placental margin, without any central depression then
Extrachorial Placenta it is called circummarginat placenta (Fig. 23.4).
As opposed to the previously described conditions, this Circumvallate placenta is more often associated with
is not an uncommon abnormality. This condition is seen adverse fetal and maternal outcomes. Elderly gravida are
when the chorionic plate, on the fetal side of the placenta is more prone to this placental abnormality.
Abnormalities of Placenta, Cord and Amniotic Fluid Volume 211
Uterine peforation
Infection.
Attempts to remove manually may cause severe and
uncontrolled PPH leading to hysterectomy to save the
patient.
Placental Infarcts
It is a common finding occurring even in some normal
uncomplicated pregnancies, but its incidence is increased
in patients who have gestational hypertension, pre-
eclampsia or eclampsia. It may be associated with aging
of placenta (see Grannum’s grading of the placenta in
Chapter 62) or due to impairment of the uteroplacental
Fig. 23.4: Circumvallate placenta—note that the membranes of circulation causing infarction.
the chorion laeve are not inserted at the edge of the placenta but
at some distance from the margin. At the margin there is varying Placenta Previa
amount of fibrin and blood
It is given in detail in APH Chapter 17.
Clinical significance
Antepartum hemorrhage (APH) (from both maternal
and fetal blood vessels)

Preterm delivery
Perinatal death
Intrauterine growth restriction
Fetal congenital malformations may occur.
Large placenta: It may be seen in multiple pregnancy, and

in case where the mother is anemic or has syphilis. An Rh-
negative pregnancy may also present with a large placenta.
A B
Placenta Accreta, Placenta Increta and
Placenta Percreta (Figs 23.5A to D)
Placenta accreta: It is a type of placental implantation
where the placental villi are abnormally attached to the
myometrium due to partial or total absence of decidua
basalis (Figs 23.5B) and fibrinoid layer (nitabuch layer).
Where the invading trophoblasts meet the decidua,
there is absence of this layer.
Placenta increta: The placental villi invade the myome
trium (Fig. 23.5C).

Placenta percreta: The placental villi penetrate through
the myometrium and the serosa as well (Fig. 23.5D).

Their incidence is increased probably due to increased
cesarean sections now. Most common sites are lower C D
uterine cesarean section scar or previous curettage. Figs 23.5A to D: A. Cross-section at site of implantation of a
In suspected cases ultrasound and Doppler color flow normal placenta. The decidua basalis intervenes between the
placenta and uterine wall; B. Placenta accreta—the decidua basalis
helps. D-dimer increase may be a markerdly.
is absent and the villi directly implant on the uterine muscle;
Clinical significance C. Placenta increta—the villi partially penetrate into the uterine
Postpartum hemorrhage musculature; D. Placenta percreta—the villi completely invade
Retained placenta into the myometrium extending upto the serosal surface percreta
A B
Figs 23.6A and B: A. True and false knots (schematic representation); B. True and false knots (photographs)
ABNORMALITIES OF CORD
True knots: In a fetus with a long cord, fetal movements
causes entanglement in its own cord and sometimes
knotting of the cord occurs (Figs 23.6A and B).
False knots: These are due to accumulation of Wharton’s
jelly or due to varices (Figs 23.6A and B).
Short cord: It is a cord with a length less than 30 cm.
It may predispose to accidental hemorrhage, IUGR or
congenital abnormalities.
Long cord: It is a cord with a length more than 60 cm.
Maternal systemic diseases and delivery complications
like cord prolapse are seen.
Torsion (cord coiling): It occurs sometime because
of excessive fetal movements. The cord get twisted
and at times it is so severe that it compromises the Fig. 23.7: Marginal attachment of placenta
fetal circulation. It may be a cause of intrauterine fetal
demise. Higher rate of preterm delivery and cocaine Cord insertion abnormalities
abuse is detected in these cases. •• Marginal insertion of cord (Fig. 23.7)
Stricture: The actual reason is not known but it is •• Battledore insertion of the cord: The cord is
associated with focal deficiency of Wharton’s jelly. attached to the very edge of the placenta. It is also
Strictures may be associated with torsion and stillbirth. called Racket Handle attachment. It is unimportant
Hematoma: This results from rupture of the umbilical unless the attachment is fragile (Figs 23.8A and B).
vein and blood being collected into the cord. It is •• Velamentous insertion of the cord: The cord is inserted
also associated with umbilical vein puncture after into the membranes at a distance from the edge of the
diagnostic/therapeutic tap. main placenta. The umbilical vessels run through the
Cyst: It could be true or false according to their origin membranes between cord and the placenta. Mostly
of tissue. True cyst are small and may be derived seen in twins and always in triplet pregnancy (Fig. 23.9).
from remnants of the umbilical vesicles or allantois. •• Cord blood vessels abnormalities, e.g. two vessels only.
False cysts may vary in size; they occur as a result of Clinical significance: It may be associated with placenta
liquefaction of Wharton’s jelly. previa, a condition where the umbilical vessels are presen
Edema: Occurs usually associated with stillbirth. ting before the fetus.
A B
Figs 23.8A and B: A. Battledore (schematic representation); B. Battledore insertion of the cord (photograph)
uterine decompression or with history of supine

hypotension syndrome or smoking.
Long cord: True knots are common in long cords and
are more likely to prolapse through the cervix. Further,
the long cord may also cause entangling of the fetus
thus causing torsion and sometimes preventing its
descent and delivery.
Vasa previa: The velamentous insertion of the cord is
associated with vasa previa as some of the fetal vessels
in the membrane cross the region of the internal os
and occupy a position ahead of the presenting part. If
an artificial rupture of membrane (ARM) is done or if
membranes are ruptured this could be accompanied
by rupture of these vessels, which will exsanguinate the
fetus (as the blood lost is of fetal origin).
Fig. 23.9: Velamentous insertion of the cord Some found that abnormal umbilical cord coiling
detected at second trimester fetal ultrasound is
associated with a higher incidence of non reassuming
Clinical Importance of Cord Abnormalities
fetal status in labor.
The presence of a single umbilical artery raises suspicion
of an associated fetal congenital anomaly. ABNORMALITIES OF AMNIOTIC
Persistence of vitelline duct—Meckel’s diverticulum.

FLUID VOLUME
Remnant of the exocoelom in the anterior portion of
the cord may contain loops of intestine, which develop Polyhydraminos
outside the embryo. Although the loops are later with- Polyhydramnios or hydramnios is defined as a condition
drawn, the apex of the midgut loop retains it. Some- in which amniotic fluid is in excessive amount, i.e. more
times the intestinal loops are not withdrawn and this than 2 liters. But since quantitative assessment of liquor
presents as a congenital umbilical hernia. amnii is impractical, most commonly used definition is
A short cord causes fetal distress and may be the cause by ultrasound assessment, i.e. when amniotic fluid index
of uterine inversion or abruptio placentae and stillbirth, (AFI) is more than 25 cm or above or finding a pocket of
especially if associated with a sick placenta, a sudden fluid more than 8 cm or above in vertical diameter.
Grades of Polyhydramnios Placental causes

•• Chorioangioma of placenta due to excessive transu-
Mild hydramnios: When single deepest pocket mea-
suring between 8 and 11 cm in vertical dimension (seen dation of fluid from it.
in 80% cases). •• Circumvallate placenta.
Moderate hydramnios: When single deepest pocket

Clinical Types
measuring between 12 and 15 cm in vertical dimension
(seen in 15% cases). Depending upon rapidity of onset, polyhydramnios can
Severe hydramnios: When single deepest pocket mea- be (a) chronic (most common)—onset is insidious, taking
sures ≥ 16 cm (seen in 5% cases). few weeks, (b) acute (extremely rare)—onset is sudden,
within few days.
Incidence
Polyhydramnios is seen in approximately 0.4–1.5% of all Chronic Polyhydramnios
pregnancies, being more common in multiparas than It is a more common variety with gradual accumulation of
primigravidas. liquor over few weeks, such that the symptoms are not so
severe and patient is not so sick.
Causes
Symptoms: They are mainly from mechanical causes:
Polyhydramnios can be due to excess production of amni- Respiratory: Patient may complain of dyspnea or
otic fluid or due to defective absorption. Various causes are: orthopnea and may remain in the sitting position most
Idiopathic: In 66% (two-third) cases, the cause is
of the time for easier breathing
unknown.
Palpitation
Fetal causes:
Swelling of legs, vulva and abdominal wall
•• Anencephaly: Swallowing is reduced plus increased
Varicosities in legs or vulva due to compression of veins
transudation of cerebrospinal fluid (CSF) into
amniotic fluid due to absence of cranial vault by large uterus.
and increased urination due to inhibition of fetal Signs
antidiuretic hormone (ADH). Patient may be dyspneic in lying down position
Spinal deformities like meningocele, meningomy- Signs of pre-eclampsia (edema, hypertension and pro
elocele. Due to excessive transudation of fluid from teinuria) may be present.

exposed meninges.
•• Facial deformities and neck swellings like—cleft lip, Abdominal Examination
cleft palate, thyroid swelling, cystic hygroma. They Inspection
reduce swallowing of amniotic fluid. Abdomen is markedly enlarged with fullness at flanks
•• Esophageal or duodenal atresia or stenosis: Due to Abdominal skin is shiny and glistening.
impaired swallowing Palpation
•• Bowel obstruction
Height of uterus is more than period of amenorrhea
•• Congenital diaphragmatic hernia
Abdominal girth is more than normal
•• Fetal sacrococcygeal teratoma
Fluid thrill can be elicited due to excessive fluid
•• Erythroblastosis fetalis
Fetal parts, also the presentation and position are ill
•• Non-immune hydrops
•• Fetal infections like toxoplasma, rubella, syphilis
defined
External ballotment is easily demonstrated.
•• Multiple pregnancy: Due to big placenta. It is more
common in monochorionic twins and is associated
Auscultation Examination
with twin–twin transfusion syndrome (TTTS).
•• Fetal muscular dystrophy, Bartter syndrome. Fetal heart sound is not heard distinctly by stethoscope,
Maternal causes but can be picked up by Doppler ultrasound.
•• Diabetes: Maternal hyperglycemia leads to fetal
hyperglycemia causing fetal diuresis and hydramnios. Vaginal Examination
•• Cardiac diseases due to excessive transudation of fluid. Cervix may be pulled up or may be slightly dilated with
•• Renal diseases from large placenta. tense bulging membranes.
Investigations Severe polyhydramnios: In view of the risks involved, the

Ultrasound: It is helpful to detect: patient should be shifted in a hospital equipped to deal
•• AFI of more than 25 cm or single vertical pocket of
with high-risk patients.
Supportive therapy: Mother should rest in left lateral
more than 8 cm
•• Multiple pregnancy
position with adequate back rest and treatment of the
•• Fetal congenital malformations
associated conditions like pre-eclampsia or diabetes.
Investigation: USG to exclude fetal congenital malfor-
•• To note the lie and presentation
mation. Blood test to detect diabetes and Rh isoimmu-
Blood
nization (Flowchart 23.1).
•• ABO and Rh typing: Rhesus (Rh)-isoimmunization
can cause hydrops fetal ascites. Acute polyhydramnios: Acute hydramnios is extremely
•• Fasting and post prandial blood sugar or glucose
rare and the fluid accumulates within a few days. It usually
tolerance test to rule out diabetes. occurs before 20 weeks of pregnancy.
Symptoms: Patients present with acute abdomen
Amniotic fluid: Alfa feto-protein in amniotic fluid is
markedly elevated in fetuses with open neural tube defect. features like abdominal pain, nausea, vomiting.
Signs
Differential Diagnosis •• Patient appears sick

•• Edema of legs or presence of other associated
Multiple pregnancy
features of amenorrhea. Abdominal skin is tense and
Pregnancy with large ovarian cyst
Maternal ascites shiny.
•• Fluid thrill is present.
Complications •• Neither fetal parts are felt nor fetal heart sound is
audible.
Complications of polyhydramnios are grouped into:
•• Vaginal examination may show effacement and
Maternal
dilatation of cervix and even bulging membranes
Fetal
through os.
Maternal Ultrasound confirms the diagnosis of hydramnios and
may detect its etiology.

During pregnancy: There is increased incidence of:
Treatment: Usually spontaneous abortion occurs in cases
Pre-eclampsia (25%)
Malpresentation and persistence of floating head

of early hydramnios. Slow amnioreduction is done for
Premature rupture of membranes
maternal distress. Usually induction of labor is performed
Preterm labor
by controlled low amniotomy and oxytocin drip.
Accidental hemorrhage.
Oligohydramnios
During labor
Early rupture of membranes
Oligohydramnios is a condition in which the amount
Cord prolapse
of amniotic fluid is reduced to less than 200 mL at term.
Uterine inertia
Sonographically, it is defined when the maximum vertical
Increased operative delivery due to malpresentation
liquor pocket is less than 2 cm or when the AFI is less than
5 cm.
Retained placenta, PPH and shock.
During puerperium Incidence

Subinvolution
Puerperal sepsis.
Oligohydramnios is seen in approximately 4% of all
pregnancies.
Fetal
Increased perinatal mortality. Deaths are mostly due to Causes
prematurity and congenital abnormality. Maternal
•• Preterm premature rupture of membranes (PPROM)
Management (most common)
Mild polyhydramnios: Commonly found in mid trimester •• Uteroplacental insufficiency
and usually requires no treatment. •• Hypertensive disorders
Flowchart 23.1: Treatment for severe polyhydramnios
•• Postmaturity Fetal growth restriction (FGR) may be present (oligohy-

•• Idiopathic. dramnios with FGR is associated with increased chro-
Fetal mosomal abnormalities)
•• Fetal chromosomal or structural anomalies Ultrasonography: AFI will be less than 5 cm or single
•• Fetal growth restriction (FGR) vertical pocket less than 2 cm. Structural anomalies
•• Intrauterine death (IUD) may be difficult to rule out due to reduced fluid.
•• Post-term pregnancy
•• Renal agenesis Complications
•• Obstructed uropathy Fetal
•• Drugs like PG inhibitions, angiotensin converting Abortion
enzyme (ACE) inhibitions. Deformities (due to intra-amniotic adhesions or bands)
Placental: Amnion nodosum (failure of secretion by like amputation of digits, club foot, alteration in shape
cells of amnion covering the placenta). of skull, etc.
Potter facies: Low set ears, epicanthal folds, receeding
Diagnosis mandible and flattened nose are the sequelae of oligo-
Uterine size is much smaller than the period of amenor- hydramnios.
rhea. Pulmonary hypoplasia
Uterus is full of fetus because of scanty liquor Fetal growth restriction
Decreased fetal movements Cord compression
Malpresentation is common High fetal mortality.

Maternal Neural tube defects (NTD): Concentration of

Prolonged labor due to uterine inertia. α-fetoprotein, acetyl cholinesterase and the presence
Increased operative interference due to malpresentation. of rapidly adhering cells can be diagnostic of NTD.
Chromosomal abnormality: Fetal cells (fibroblasts) from
Treatment amniotic fluid are cultured and arrested in the metaphase
Isolated oligohydramnios in the third trimester with no stage. These can provide accurate chromosomal diagnosis.
congenital abnormality may be managed conservatively. Isoimmunization: The level of bilirubin in amniotic
Oral administration of water increases amniotic fluid volume. fluid at an optical density of 450 nm, a golden color of
If lethal anomaly like bilateral renal agenesis is diag- liquor denotes hemolysis due to Rh incompatibility and
nosed, the woman must be counseled and termination severity of fetal hemolysis.
must be suggested. In case of correctable anomalies like Lung maturity: The lacithin/sphingomyelin (L/S) ratio
posterior urethral valves, the options of in utero therapy or
is a good indicator of lung maturity and, should be more
early neonatal correction are to be discussed.
than 2. Sometimes a lecithin phosphatidyl glycerol ratio
Intrapartum: Cesarean section may have to be done in
may be required (especially in diabetic patients).
many situations especially when the fetus is compromized.
Infections: Amniocentesis is done to determine the
If vaginal delivery is possible, electronic fetal monitoring is
essential. presence of white cells and bacteria, which is diagnostic
Amnioinfusion by normal saline is advocated by some of chorioamnionitis.
obstetricians. It is again to be emphasized that placenta, cord and
membranes (with the vessels) should be examined
Amniocentesis meticulously after delivery and mentioned in the case
Access to amniotic fluid is made by performing amniocen- report. It may be examined by a pathologist in cases of
tesis, which is indicated in the following conditions: stillbirths, fetal growth abnormalities, etc.
1. Explain abnormalities of placenta.
2. Differentiate between abnormalities of placenta and abnormalities of cord.
3. True/False:
i. Placenta villi are abnormally attached to the myometrium due to partial or total absence of decidua basalis.
ii. Cyst can be true or false according to their tissue or origin.
Section 4
Normal Labor
Section Outline
24. Mechanism of Parturition and Labor
25. Onset and Stages of Parturition and Labor
26. Initial Assessment at Onset of Normal Labor
27. Conduct of Normal Labor
28. Induction of Labor
29. Obstetric Analgesia and Anesthesia
24
Sudha Salhan, Pratima Mittal, Niharika Dhiman, Divya Pandey
Mechanism of
Parturition and Labor
points in the pelvis of the mother. For example, if fetal

DEFINITION
occiput is the denominator (in vertex presentation) it
Labor is the process by which a fetus is delivered by the can lie anteriorly in occipitoanterior position (to right
vaginal route. or left of the ileopectineal eminence of mothers pelvis)
The series of changes in position and attitude that the and posteriorly in occipitoposterior position (to right left
presenting part has to make, during its passage through sacroiliac joint of mothers pelvis). The fetal sacrum is the
the maternal pelvis and pelvic floor during the course of denominator in breech presentation. Frontal eminence
labor, constitute the mechanism of labor. is the denominator in brow presentation. Mentum is the
Before discussing the mechanism of labor, knowledge denominator in face presentation and acromion is the
of certain terms are essential. denominator in shoulder presentation.
Fetal attitude: It is the relationship of various fetal parts to
each other or in other words, it is the posture in which the
LIE fetus attains in utero. There is formation of fetal ovoid in a
Lie is the relationship of the long axis of the fetus to the universal flexion posture. The back is convex, the head is
long axis of the uterus or the maternal spine. flexed (chin in contact with the chest), thighs are flexed at
Longitudinal 99.5% the hip and legs are flexed at the knee, arms are flexed at
}
Transverse
the shoulder and crossover the thorax. This attitude helps
the fetus to accommodate itself in the uterus. There may be
Oblique 0.5%
differences from this universal flexion, e.g. deflexed head
Unstable
or breech with extended legs, etc. These differences will
modify the progress of labor.
PRESENTATION
The part of the fetus, which occupies the lower pole of the POSITION
uterus (is first to reach the birth canal):
Relationship of the fetal presenting part to the maternal
Cephalic 96%
pelvis is termed as position (Fig. 24.2).
Breech 3.5%
For this purpose the maternal pelvis is divided into
Shoulder 0.4%
eight equal segments of 45° (eight positions):
Oblique 0.3%
1. Left occipitotransverse (LOT) 40%
Cephalic presentation in itself can be either:
2. Right occipitotransverse (ROT) 24%
• Vertex (sharply flexed) 96% (Fig. 24.1) 3. Left occipitoanterior (LOA) 13%
• Face (marked deflexion) 4. Right occipitoanterior (ROA) 10%
• Sinciput (slight flexion) 5. Right occipitoposterior (ROP) 7.1%
• Brow (slight deflexion). 6. Left occipitoposterior (LOP) 3%
Denominator: It is an arbitrary fixed bony fetal point 7. Occipitoanterior (OA) 2%
which lies in different pelvic quadrants against the fixed 8. Occipitoposterior (OP) 1%
R L R L R
P P P
S S S
LOP LOT ROP
Fig. 24.1: Vertex presentation
Abbreviations: P—Pubic symphysis; S—Sacrum; R—Right; L—Left; LOP—Left occipitoposterior; LOT—Left occipitotransverse; ROP—Right
occipitoposterior
Fetal Hypothalamic Pituitary Adrenal Axis

Fetal hypothalamic pituitary adrenal axis is thought to be
very important in the initiation of normal labor.
Fetal pituitary production of very high levels of
placental corticotropin-releasing hormone (CRH) makes
the fetal adrenal to produce dehydroepiandrosterone
sulfate (DHEAS) and cortisol which further increase
CRH production. CRH modulates contractility. Cortisol
A B makes the fetal membrane produce prostaglandins. More
estrogen is produced due to more substrate, i.e. DHEAS,
Figs 24.2A and B: Identifying the position of the fetus. A. Right
offsetting the estrogen-progesterone ratio in favor of
occipitoanterior: The sagittal suture is in the right oblique diameter
of the pelvis; B. Right occipitoposterior: The sagittal suture is in the estrogen. This decreases myometrial inactivity. In humans,
left oblique diameter of the pelvis there may be a special form of progesterone, absence of
which ends uterine relaxation. There may be a decrease in
the activity of the progesterone receptors in the uterus in
THEORIES OF ONSET OF LABOR late pregnancy. In some fetal anomalies viz anencephaly,
there is adrenal hypoplasia which prolongs pregnancy.
The exact cause for onset of labor is not known. A number
of theories have been proposed. Uterotonic Theory of the Initiation of Labor
The uterotonics so far incriminated are oxytocin, prosta
Stretching of the Uterus
glandin, serotonin, angiotensin II, etc. During late preg-
Stretching of the uterus by the mature fetus plays a role nancy oxytocin receptors in the myometrium increases
in the fetomaternal endocrine cascades. Twins usually in number (up to 50 fold). Oxytocin is synthesized in the
cause preterm labor because of early stretching to the decidua. Its role is important in the second stage of labor
optimum size of singleton fetus. The same is true in cases and puerperium. Prostaglandins are also produced directly
of hydramnios. from the myometrium and fetal membranes.
Mechanism of Parturition and Labor 223
The role of amnion and chorion is also important.

Prostaglandins are produced in both of them, but chorion
has enzyme prostaglandin dehydrogenase (PGDH) which
inactivate any prostaglandin produced. Progesterone
increases PGDH and cortisol decreases PGDH.
There is a decrease in enzyme placental 11β-hydroxys
teroid 2 (11β-HSD2) at the end of gestation in baboons.
The enzyme 11β-HSD2 in the placenta regulates the
corticoid levels in the fetus by converting maternal cortisol
to cortisone (relatively inactive). Mother’s plasma has
4-fold higher cortisol than the fetus plasma. At the end
of gestation 11β-HSD2 decreases, hence, less of maternal
cortisol is inactivated. This leads to elevated level of
cortisol in fetal plasma. As we have seen earlier, cortisol
decreases PGDH enzyme, thus preventing metabolism of
prostaglandins. This may initiate labor.
MECHANISM OF LABOR
The mechanism of labor is dictated by the pelvic dimen
sions and configuration (both bony and soft parts), the
size of the passenger and strength of the contractions.
Cardinal Movements (Fig. 24.3)

Cardinal movements, which constitute the mechanism of
labor, are designed to adapt the smallest possible diameter
of the presenting part to the contours and varying Fig. 24.3: Rotation of fetal head and it descends through the labor
diameters of the pelvic canal so that it encounters as little
resistance as possible.
It is customary to describe these movements as the (9.4 cm) is at or has passed the pelvic inlet (brim). This
provides a clear indication that the pelvic inlet is large
movements of the head (Figs 24.4A to D), but in reality the
enough to accommodate the widest portion of the fetal
head is only the index, while the trunk also participates
head and thus it is of adequate size. For an average fetal
in it and probably also initiates some movements. These
head, the linear distance between the occiput and the
movements are:
plane of the BPD is less than the distance between the
Engagement
pelvic inlet and the ischial spines. So when the occiput is
Descent
at ischial spines the BPD has usually passed the pelvic inlet
Flexion
and the vertex is therefore engaged.
Internal rotation
Primigravida: Engagement occurs late in pregnancy
Restitution usually at 38 weeks.
External rotation. Multigravida: Engagement occurs with the onset of
There is a mechanism for every presentation and labor (1st stage).
position, while delivering vaginally. The most common Anteroposterior (AP) diameter of the fetal skull at
positions are left or right occipitoanterior thus these will the time of engagement is either suboccipitobregmatic
be described here. The attitude is one of flexion and, (9.5 cm) in a well-flexed head or suboccipitofrontal (10 cm)
therefore, the denominator is the occiput. with slight deflexion of the head in the vertex presentation.
Asynclitism (Fig. 24.5): When the vertex engages in
Engagement the pelvic brim, owing to lateral inclination of the fetal
It is the mechanism by which the greatest transverse head, one parietal bone usually lies at a lower level than
diameter of the fetal head biparietal diameter (BPD) the other and as a result, the sagittal suture does not
L R
A B C D
Figs 24.4A to D: Cardinal movements in mechanism of labor and delivery in right occipitoanterior position. A. Head floating before
engagement; B. Engagement, descent and flexion; C. Further descent, internal rotation; D. Complete rotation
A B C
Figs 24.5A to C: Asynclitism. A. Anterior asynclitism Naegele’s obliquity; B. Normal asynclitism; C. Posterior asynclitism Litzmann’s
obliquity ear presentation
correspond precisely to either the transverse diameter or In some cases (about 25%), this lateral inclination is
the oblique diameter. The sagittal suture is either deflected absent and the sagittal suture does correspond to the
more anteriorly towards the symphysis or more posteriorly pelvic diameter. Slight deflection occurs commonly, but
towards the sacral promontory. This is called asynclitism severe deflection can cause cephalopelvic disproportion
or parietal obliquity. even in a normal sized pelvis.
Usually the head inclines towards the posterior- In left occipitoanterior position, the head engaged
shoulder (one nearer to the sacrum), the sagittal suture in right oblique diameter from right sarcoiliac joint
posteriorly to left iliopectineal eminence so that occiput
lies nearer to the promontory of the sacrum than to the
occupies left side of mothers pelvis anteriorly. Similary,
symphysis pubis. Thus in this position, the anterior parietal
in right occipitoanterior position the engagement is in left
bone is more easily felt. This is known as the anterior
oblique diameter so from the left sacroiliac joint to right
asynclitism/anterior parietal presentation/Naegele’s
iliopectineal eminence thus occiput occupies right side
obliquity. This is common in multigravida (Fig. 24.5A). of mother pelvis anteriorly. In case of occipitoposterior
Sometimes the sagittal suture lies nearer to the pubic position occiput is in right of pelvis posteriorly in right
symphysis and when the head enters brim, the posterior oblique diameter from right sacroiliac joint posteriorly to
parietal bone is lower than the anterior and is thus the left iliopectineal eminence. In left occipitoposterior,
better felt. This is called posterior asynclitism/posterior the engagement is in left oblique diameter.
parietal presentation/Litzmann’s obliquity (posterior
ear is easily palpated in this presentation) (Fig. 24.5C). This Descent
is common in primigravidas because of the relatively tense This is a continuous process throughout the first and
abdominal wall which tends to keep the uterus back and second stage of labor.
so prevents the body of the fetus from coming forward into In a grand multigravida, the fetal head may be engaged
the line of the axis of the brim. at the onset of labor, so only a slight descent may occur
during the first stage of labor. While in a primigravida, Short posterior arm extends from the fulcrum to the
descent starts with the engagement before the first stage of occiput.
labor. Long anterior arm extends from the fulcrum to the chin.
Factors resulting in descent are: As the fetus presses downwards—the short posterior
Pressure of the amniotic fluid arm meets with less resistance and thus occiput
Direct pressure of the uterine fundus with contractions descends more.
Bearing down efforts
Extension and straightening of the fetal ovoid.

Internal Rotation
This is defined as turning of the head in such a manner
Flexion that the occiput gradually moves anteriorly towards the
The head is already flexed to an extent at the time of symphysis pubis. This carries the long diameter of the head
engagement and further flexion occurs during the first into the anteroposterior diameter, i.e. the longest diameter
stage of labor. The descending head meets the resistance of the pelvic outlet from the previous occipitoanterior,
from the cervix, the walls of pelvis, pelvic floor and occipitolateral positions (in occipitoanterior, the head
thus the chin is brought into a more intimate contact rotates by one-eighth of a circle and in occipitotransverse,
with the chest. The shortest anteroposterior diameter, the head rotates through two-eighth of a circle forward).
suboccipitobregmatic (9.5 cm), is thus substituted for Internal rotation brings the occiput forwards under the
the longer suboccipitofrontal/occipitofrontal diameter. pubic arch. With this, there is a twist in the neck of the fetus.
When this flexion is deficient, the diameter of engagement The twist in the neck is through one-eighth of the circle
is longer and difficulties during the passage of head are in occipitoanterior position, two-eighth of the circle in
consequently greater. occipitotransverse and three-eighth of a circle in complete
Factors responsible for flexion are: internal rotation of occipitoposterior position. In internal
Shape of the head: The slope of the occipital region of
rotation, when the head rotates through one-eighth of a
the head is much steeper than that of the forehead, so circle, there is no movement of shoulders. The neck can
the occiput descends more. sustain only one-eighth of a circle twist. When the twist
Arm lever theory: During contractions, fetal axis
in the neck is two-eighth of a circle the shoulders rotate
pressure is generated—the head is a lever with the through one-eighth of a circle and if the twist is through
atlantooccipital joint as the fulcrum (Fig. 24.6). three-eighth of a circle the shoulder rotates through two-
eighth of a circle.
Factors responsible for internal rotation are:
Slope of pelvic floor: The levator ani are directed
downwards, forwards and inwards towards the mid-

line (leading to formation of a gutter). During each
contraction, the occiput stretches the muscles and with
each passing contraction, the elastic recoil brings the
occiput anteriorly (Hart’s rule).
Shape of pelvis: Forward inclination of pelvic side
walls, the narrow interspinous diameter and the long

anteroposterior diameter of outlet, favors movement of
the occiput anteriorly.
Deficient pelvic boundary anteriorly and wide
pubic arc: This anatomy leads to movement of occiput

anteriorly in the direction of least resistance.
• In left occipitotransverse position: Occiput rotates
by two-eighth of a circle (90º).
• Occipitoanterior position: Occiput rotates by one-
Fig. 24.6: Lever action producing flexion of the head; conversion eighth of a circle (45º).
from occipitofrontal to suboccipitobregmatic diameter typically • In left occipitoposterior position: Occiput rotates
reduces the anteroposterior diameter from nearly 12–15 cm by three-eighth of a circle (135º).
Internal rotation occurs at the level of ischial spines are engaged in right oblique diameter (opposite to
pelvic floor. vertex which engages in left oblique diameter) while
Pre-requisites for adequate rotation are: the shoulders are in the anteroposterior diameter in
Well-flexed head the occipitotransverse position. The occiput points to
Efficient uterine contraction the maternal thigh of the corresponding side to which it
Favorable shape at mid-pelvis. originally lies.
Sometimes forward rotation of the occiput fails to
occur and the head either rotates in the reverse direction, External Rotation (Fig. 24.7C)
bringing the occiput in the hollow of the sacrum or In the internal rotation of the shoulder the movement of
rotation fails more or less entirely and the head remains the shoulder is by one-eighth of a circle. The engaging
in the oblique or transverse diameter of the pelvic cavity. bisacromial diameter thus comes into relation with the
When this forward rotation fails to occur the condition is anteroposterior diameter of the pelvic outlet. This is visible
called persistent occipitoposterior position and will be externally by the movement of the head by one-eighth
discussed in the Chapter 32. of a circle, in a direction opposite to internal rotation.
This is external rotation of the head. It occurs in the
Extension (Fig. 24.7A) same direction as restitution. Now the shoulders are in
In the second stage of labor (when the cervix is fully dilated), anteroposterior axis. The anterior shoulder escapes under
two forces act on the head. Uterine contractions and the pubic arch, while the posterior shoulder sweeps over
abdominal muscles’ contractions exert downwards force the perineum.
while the pelvic floor muscles are exerting upward and After the delivery of the shoulders, the rest of the body
forward resistance. As a result of these counter forces, the is delivered spontaneously by lateral flexion (Figs 24.8A to
forward force acts to deliver the head by extension. The chin G).
slides over the edge of the perineum and becomes separated
from the chest wall, i.e. the head becomes extended. The Mechanism of Labor in Right Occipitoanterior
vaginal outlet is stretched and crowning occurs. With (Figs 24.8A to G)
progressive distension of the perineum the occiput gradually The fetal head engages in the left oblique diameter
appears first and the head is delivered by further extension (opposite oblique diameter) of the maternal pelvis. The
with the occiput, bregma, forehead, nose, mouth and finally sinciput faces the left sacroiliac joint and the occiput
the chin passing successively over the perineum. is near the right ileopectineal eminence. The engaging
diameter of the fetal head is the suboccipitobregmatic
Restitution (Fig. 24.7B) (9.5 cm) or suboccipitofrontal (10 cm) depending on its
The movement of de-twisting of the neck, to release flexion.
the torsion it attained during internal rotation is visible Descent is a continuous process.
externally as a movement of the head, in a direction Flexion of the fetal head: It may be increased during
opposite to that of the internal rotation (45°)—for example the passage through the birth canal. Finally, the chin is
in right occipitoanterior the shoulders (after restitution) in contact with the chest.
A B C
Figs 24.7A to C: A. Birth of head; B. Restitution; C. External rotation

A B C D
E F G
Figs 24.8A to G: Illustration of rotation of head and delivery of shoulder. A. Engagement of left occipitoanterior; B. Descent in
occipitoanterior position; C. Anterior rotation of head; D. Extension of head; E. External rotation of head; F. Delivery of anterior shoulder;
G. Delivery of posterior shoulder
Internal rotation: It occurs at the level of ischial anteriorposterior diameter of the pelvis. With this, the
spines at the pelvic floor. The head comes into the head (being free) also rotates through 45° (one-eighth of
anteroposterior diameter of the pelvis from the previous circle) in a direction opposite to that of internal rotation
occipitoanterior position. The rotation is through one- (Fig. 24.8E).
eighth of a circle. By this rotation, the head is twisted The shoulders are now delivered. The anterior shoulder
at the neck. The shoulders engage in the left oblique comes out from below the pubic arch and posterior
diameter. There is no movement of the shoulders.
through the posterior hollow of the outlet.
However, in case of occipitoposterior position there is
The rest of the body is delivered by lateral flexion.
internal rotation of the head through three-eighth of
a circle then the neck cannot sustain and in that case
shoulders also rotate through two-eighth of a circle and
Effects of Labor on the Fetal Head
lie in transverse diameter. Due to the action of compressive forces, the head under
Extension: In second stage of labor, the occiput is goes certain changes either in its shape or in the consistency
hinged under the pubic arch and uterine contractions of its soft tissues.
(along with voluntary pushing) and extension occurs.
The chin gets off from the chest and the vertex stretches Caput Succedaneum
the vaginal outlet and gets visible at the vaginal
Formation of swelling on the fetal scalp due to stagnation
outlet without receding back, even after the uterine
contraction is over. This is crowning of the fetal head. of fluid in the layers of the scalp beneath the girdle of
Thereafter, forehead, face and chin come out in that contact. The girdle of contact may be bony or the dilating
order. After the head, the neck is delivered. cervix or the rigid vulvar ring.
Restitution: The one-eighth twist in the neck due The swelling is boggy/diffuse/not limited by sutures of
to internal rotation is undone, turning the occiput, skull.

towards the mothers left thigh. Disappears within 24 hours.
External rotation: Bisacromial diameter of the shoulder Forms as a result of blockage of the lymphatics and
has internal rotation and the shoulder comes to lie in the venous return.
The caput indicates a static position of the head for a other. Physiological molding is harmless and disappears
long time. The location of the caput indicates the position after birth.
of head in the pelvis and the degree of flexion achieved. Grades of molding
In a well-flexed head the caput is placed more post Grade I: The two parietal bones are touching but not
eriorly. A marked caput is seen in obstructed labor. overlapping.

Grade II: The two parietal bones are overlapping but
Molding easily separable.
Molding is the alternation of shape of the forecoming head Grade III: The two parietal bones have fixed overlap-
while passing though the resistant birth passage during ping. This may be associated with fetal heart rate related
labor. It offers little alteration in size because skull bones are attributed to fetal asphyxia changes.
incompressible, but a small amount of plasticity does occur Slight molding is beneficial while marked molding as
in vertex presentation. The engaging suboccipitobregmatic in cephalopelvic disproportion (CPD) causes tearing of
diameter is compressed with compensatory elongation in the tentorium cerebelli resulting in a subdural hematoma
the plane at a right angle to it, i.e. the elongation of head in formation. But neurological sequelae could be due to
the mentovertical diameter. In a normal course of labor, two multiple factors like prolonged labor, fetal acidosis and
parietal bones overlap over adjacent bones and over each sepsis, etc.
1. Write short note on mechanism of labor.
2. Define:
i. Denominator
ii. Fetal attitude
iii. Asynclitism
3. Explain the factors responsible for internal rotation.
4. True/False:
i. Slight molding is beneficial while marked molding as in CPD is harmful.
ii. Formation of swelling on the fetal scalp is due to muscle contraction.
25
Pratima Mittal, Sudha Salhan, Divya Pandey
Onset and Stages of
Parturition and Labor
Phase 2 of Parturition
PARTURITION (Preparation of Labor)
The literal meaning of parturition is ‘process of giving Uterus breaks its quiescent and there is uterine awakening
birth’. There are certain physiological changes that occur or reactivation. This occurs during last 6–8 weeks of
in the uterus and cervix right from the conception, labor, pregnancy. There is increase in uterus response to uterotonic
delivery till the involution. agents due to increase in oxytocin receptors and increase in
number of gap junctions. Hydroxyprogesterone caproate
injection helps in tocolysis by decreasing the formation
PHASES OF PARTURITION of these gap junctions in myometrium, thus allaying the
chances of preterm labor. With the formation of lower
The parturition has four phases:
uterine segment (forms from isthmus), fetal head descends
1. Phase 1 of parturition: Uterine quiescence and cervical
through pelvic inlet which is termed as lightening.
softening Cervical ripening occurs in this phase and the transition
2. Phase 2 of parturition: Preparation of labor from softening to ripening starts a few days before the onset
3. Phase 3 of parturition: Labor of uterine contractions. The collagen fibrils dispersion
4. Phase 4 of parturition: Phase of involution. occurs by decrease in cross-linking, leading to loss of tissue
Here, we describe phases of parturition in brief. Labor integrity and increased tissue compliance. In addition to
which forms the third phase of parturition is described in this, there is inflammatory process within the cervix which
more detail. Fourth phase of parturition, i.e. the involution causes release of proteases which further leads to collagen
phase is described in detail in Chapter 34. and extracellular matrix degradation.
Phase 3 of Parturition
Phase 1 of Parturition (Labor)
(Uterine Quiescence and Cervical Softening)
This phase is synonymous with active labor, which is
Uterine myometrium becomes unresponsive and quies- characterized by uterine contractions that bring about
cent even before the implantation. It comprises of 95% changes in cervix causing its dilatation, effacement and,
of pregnancy. Simultaneously, there it prepares itself for hence, delivery of the fetus. It is the process of delivery of
the 3rd and very important phase of parturition which is the fetus from the uterus through the vaginal route. Labor
“Labor” by increasing sin size and vascularity. Although has been divided in four stages:
quiescent,some infrequent and low intensity contractions 1. First stage (stage of cervical dilatation and efface
which have no effect on cervical dilatation may be there. ment): The first stage starts from the onset of regular
These are confined to lower abdomen and groin region. uterine contractions accompanied by the start of
They are referred to as Braxton Hicks contractions or false effacement and dilatation of the cervix to a full dilatation
labor. Cervical softening occurs due to hypertrophy of of the cervix (10 cm).
stroma, hyperplasia and hypertrophy of glands, increased Average duration in nulliparas is 8–12 hours and in
vascularity and increase in extracellular matrix. multiparas is 3–8 hours.
2. Second stage (stage of fetal expulsion): Second stage He described the physiological aspect of each division
starts from full dilatation of the cervix and ends with as follows:
expulsion of the fetus from the birth canal. Average Preparatory division: This phase corresponds to the
duration in primigravidas is 1–2 hours and in multigrav- latent phase. Minimal dilatation of cervix takes place
idas it is 0.5–1 hours. during this phase, although there is considerable
3. Third stage (stage of placental separation and softening of the cervix.
Dilatation division: The cervix dilates at more rapid
expulsion): This stage starts after the delivery of the baby
rate and it corresponds to the active phase of labor.
to the delivery of placenta and membranes. The duration
Pelvic division: The onset of pelvic division is seldom
is 20–30 minutes/5–15 minutes, if actively managed in
identified. The phase commences with the deceleration
multigravidas/primigravidas, respectively. This stage of
phase of cervical dilatation. The principal cardinal
labor also includes the control of hemorrhage. movements of the fetus take place during this phase.
4. Fourth stage: This stage begins after the delivery of the (Figs 25.1A and B).
placenta and lasts upto 2 hours after delivery. This is a Three main physiological processes take place in the
crucial period when the women may die without proper first stage of labor—softening of the cervix, effacement of
observation of postpartum hemorrhage (from a relaxed the cervix, dilatation of the cervix.
uterus or trauma) or a hematoma which is increasing Uterine contractions are responsible for the effacement
in size (episiotomy or tear). The American Academy and dilatation of the cervix, and the descent and expulsion
of Pediatrics (AAP) and the American College of of fetus in labor.
Obstetricians and Gynecologists (ACOG) recommends
Softening of Cervix
taking of maternal blood pressure and pulse immediately
after delivery and every 15 minutes in the first hour after Although considerable amount of cervical softening
birth besides seeing the size of uterus and examining the has already occurred during phase 1 and phase 2 of
parturition, the process intensifies further during phase 3
perineum for any bleeding or swelling.
of parturition, i.e. during labor to make cervix an yielding
and compliant structure for dilatation. Collagen fibers are
Phase 4 of Parturition needed to keep the uterine contents intact by providing
(Phase of Involution)
a rigid support. In preparation for parturition, softening
This phase of parturition is also known as phase of involu- of cervix occurs. The exact mechanism is not known but
tion. It is a dynamic phase during which the physiological some observations are made. In the later half of the third
changes that have occurred during pregnancy resolve and trimester, there is an increase in the breakdown of collagen
the body returns to its non-pregnant state. This phase is bundles. There is an increased production of cytokines
dealt in detail in Chapter on Puerperium. may be due to inflammation and due to infiltration of
leukocytes which degrade collagen. This starts cervical
LABOR softening (also called cervical ripening). There may be
local decrease of progesterone levels at the cervix which
may cause cervical softening.
NORMAL DELIVERY Smooth muscles are lesser in the cervix as compared with
It is the spontaneous vaginal delivery of a full term the main uterus. They constitute 6–25% of the whole cervix.
live fetus (37–40 weeks) weighing 2.5 kg or more, by Extracellular matrix consists of glycosaminoglycans,
vertex presentation without any intervention, (except dermatan sulfate and hyaluronic acid. At the end of
episiotomy), within 24 hours of onset of labor and without pregnancy, there is a striking increase in hyaluronic acid. It
any complication to the mother and fetus. increases the water content of the cervix. Dermatan sulfate
decreases, which reduces collagen fiber cross-linking.
All these changes lead to cervical softening, thinning and
PHYSIOLOGY OF LABOR relaxation allowing the cervix to start dilatation.
First Stage of Labor Effacement of cervix (Figs 25.2A to F)
The progress of normal labor was first described by It may start in the last 2–3 weeks of the third trimester of
Friedman (1954). He classically described it as a sigmoid pregnancy, i.e. end of the second phase of parturition. This
pattern by plotting cervical dilatation against time. occurs as a result of changes in the solubility of collagen
Onset and Stages of Parturition and Labor 231
A B
Figs 25.1A and B: A. Labor course divided functionally on the basis of dilatation and descent curves into—(1) a preparatory division;
(2) a dilatational division, occupying the phase of maximum slope; (3) a pelvic division encompassing both deceleration phase and
second stage concurrent with the phase of maximum slope of descent; B. Composite of the average dilatation curve for nulliparous
labor. The first stage is divided into a relatively flat latent phase and a rapidly progressive active phase. In the active phase, there are three
identifiable component parts that include an acceleration phase, a phase of maximum slope and a deceleration phase
Dilatation of the Cervix or External os of the Cervix

Progressive dilatation of the external os uteri is a sign of
true labor. It is assessed in centimeters. When the external
os is dilated sufficiently to allow the fetal head to pass
A B C through (i.e. diameter of about 10 cm) it implies that a full
dilatation of the cervix has been achieved. Measurement of
the cervical diameter in centimeters is done during pelvic
examination through digital estimation of the diameter of
the cervical opening (usually 1 fingertip = 2 cm). In the first
stage of labor, the process of dilatation is solely the result of
involuntary uterine contractions and the process cannot
D E F
be expedited through maternal efforts such as bearing
Figs 25.2A to F: A. Cervix before labor in a primigravida; down. The woman should be discouraged from bearing
B. Beginning of effacement in a primigravida; C. Completely
down until the cervix is fully dilated because premature
effaced cervix in a primigravida; D. Cervix before labor in a
multigravida; E. Beginning of effacement in a multigravida; bearing down may exhaust her and causes the cervix to
F. Complete effacement in a multigravida become edematous.
Forces concerned in dilatation are not well understood,
present in cervical tissue. The cervix becomes shorter, though several factors appear to be involved. The muscle
dilates slightly, and then becomes funnel shaped as fibers which surround the cervix are so arranged that they
the internal os opens to form a part of the lower uterine pull on the edges and draw it open. Mechanical stretching
segment. Normally, the cervical canal is around 2–3 cm of the cervix intensifies uterine activity (Ferguson’s reflex).
in length and about 1 cm thick. When the length of the Release of endogenous progesterone and/or oxytocin may
cervix is reduced by one-half, it is called 50% effaced. It mediate this process.
progresses to a state in which the canal no longer exists at In primigravida women, effacement occurs first and is
all, except for a circular as with thin edges. This is a 100% followed by dilatation of the cervix, while in multigravida,
effaced cervix. effacement and dilatation go hand by hand.
Uterine Contractions
They are involuntary, intermittent, regular and painful.
As discussed earlier, uterine contractions are a result of
various neurohormonal changes in the uterine milieu.
During contractions, ischemia develops in the muscle fibers
resulting in the pain. Backache may accompany cervical
dilatation and is due to the stimulation of sensory fibers, A B C D
which passes via the sympathetic nerves to the sacral plexus.
Figs 25.4A to D: Retraction of the uterine muscle fibers. A. Relaxed;
Characteristics of Uterine Contractions B. contracted; C. relaxed but retracted; D. contracted but shorter
Coordination of contractions (Figs 25.3A to F): Uterine and thicker than those in B
contractions start from the cornua of the uterus and
pass in waves inwards and downwards. The intensity is uterine segment, diminishes due to contractions and
greatest in the upper segment (fundus) and lessens as retractions of the muscle fibers, the fetus is forced
contractions pass down to the uterus (isthmus). This down into the lower segment and the presenting part
is called fundal dominance. The upper segment of exerts pressure on the os uteri, which not only leads to
the uterus contracts and retracts powerfully, whereas dilatation but also causes a reflex release of oxytocin
the lower segment contracts only slightly and dilates. and promotes uterine contractions.
Between uterine contractions the uterus relaxes. The
coordinated uterine activity is a characteristic of normal Formation of Upper and Lower Segment
labor occurs as a result of near simultaneous contraction The actively contracting fundus and body of the uterus
of all myometrial cells. becomes thicker with advancing labor. But the lower part
Retraction (Figs 25.4A to D): Retraction is a state of or passive segment of the uterus is relatively inactive. This
permanent shortening of the muscle fibers which occurs lower part then gradually becomes thinner. The difference
with each contraction. The muscle fibers, therefore, between the upper thicker and the lower thinner portions
gradually becomes shorter and thicker, especially in increases with the progress of labor. This division becomes
the upper uterine segment, exerting a pull on the less more apparent as the upper segment contracts and retracts
active lower uterine segment, with the maximum pull (i.e. it does not go back to the original size but decreases in
being directed towards the weakest point, the cervix. size). Thus, it becomes smaller and pushes the fetus down
The cervix is gradually effaced and the upward pull towards lower segment causing stretching of the lower
then dilates the os uteri. As the space within the upper segment, which stretches more with each contraction.
By this progressive, thickening of the upper segment and
thinning of the lower segment occur. A boundary between
the two is formed. It is named the physiological retraction
ring (see Chapter 26).
Cervical effacement and dilatation: The lower segment
of uterus has less resistance. During contraction, a

A B C centrifugal pull acts on the cervix which stretches and
thus dilates. Once forceful contractions of the fundus
and body of the uterus start, it exerts a hydrostatic
pressure via the fetal membranes on the cervix and lower
uterine segment. This pressure dilates the cervical canal
like a wedge. But if the membranes are absent (ruptured
membranes), the presenting part of the fetus itself exert
pressure on the cervix and dilates it.
D E F Cervical effacement is the disappearance or taking
Figs 25.3A to F: Diagrams showing fundal dominance during up of the cervix. The cervix which is initially about 2
uterine contractions. A. Contraction starting; B and C. Contraction cm in length is finally reduced to a very thin edge only.
spreading; D. Height of contraction; E and F. Contraction fading The internal os muscle fibers are pulled upwards or
taken up into the lower uterine segment. This is due 2–3 minutes. The membranes often rupture during the early
to progressive retraction of the upper segment (i.e. part of this stage, if they have not already ruptured, with a
muscles do not regain their original size but become gush of amniotic fluid from the vagina.
shorter, after the contraction passes off ). As the fetal head or presenting part descends and
Polarity: The coordination between the upper and reaches perineal floor, it exerts a pressure on the sacral
lower segment is balanced and harmonious in a normal and obturator nerves causing the woman to feel an urge to
labor. The upper segment contracts powerfully and push and muscles of the abdomen are brought into play.
retracts, while the lower segment contracts only and In synchrony with the contractions, the woman is asked to
dilates. The rhythmical coordination between the upper bear down with all her strength. There is an intense pressure
and lower uterine segment is called polarity. in the area of the perineum and rectum and the urge to
Resting tone: The uterus is never completely relaxed bear down is beyond her control. When the fetal presenting
and in between the contractions a resting tone can be part distends the pelvic floor, the stretch receptors trigger
measured which is usually around 4–10 mm Hg. During the release of endogenous oxytocin thereby augmenting
contractions, the blood flow to the placenta is curtailed, the uterine contractions further. The urge to push is
thus the period of relaxation in between contractions, influenced by the station of the fetus rather than by the
when the uterus has a low resting tone it is essential for cervical dilatation. Pressure of the presenting part in the
adequate blood supply to both the placenta and fetus. vagina causes the anus to become patulous and everted
Uterine contractions cause a rise in the intrauterine and small amount of fecal material may be expelled from
pressure which can be measured by placing a catheter the rectum with each contraction. With each contraction
in the uterus. Each contraction rises rapidly to a the perineum bulges and the vulva increasingly dilates
peak and then slowly declines to a resting tone. In and distends. The vulval opening is gradually converted
early labor, the intensity of the contractions is about into an ovoid and lastly into a circle. With the cessation of
20 mm Hg and lasts for about 20–30 seconds, at inter each contraction, the opening becomes smaller and the
vals of all but 20 minutes. At the end of first stage, head recedes from it until it advances again with the next
the contractions become stronger, last longer and contraction. With an increasing intensity of contractions,
occur more frequently with an amplitude as high as the head becomes increasingly visible at the vulva, the vulva
60 mm Hg, lasting for at least 45–60 seconds and occuring is stretched further and encircles the largest diameter of the
every 2–3 minutes. This is plotted in a partograph. fetus’ head. This is known as crowning where the head does
Formation of the forewaters and hindwaters: As not recede with the passing off of the uterine contraction.
the lower uterine segment stretches and the cervix In a breech presentation, a similar phenomenon occurs
starts to efface, some chorion becomes detached from which is then termed as the climbing of the perineum. An
the decidua and forms, with the amnion a small bag episiotomy is given at this stage if required, accompanied by
containing amniotic fluid, which protrudes into the perineal support. Assisted delivery of the head is done. After
cervix. When the fetal head descends, it separates crowning, usually two or three contractions are enough to
the small bag in front (forewaters) from the rest of achieve birth.
the amniotic fluid (hindwaters). The forewaters aid
effacement and early dilatation of the cervix while the Third Stage of Labor
hindwaters equalize the pressure in the uterus during The third stage of labor is made up of two phases—
contractions and provide protection to the fetus and (1) placental separation and (2) placental expulsion.
placenta.
Placental Separation
Second Stage of Labor When the fetus is expelled the uterus suddenly reduces
Unlike the first stage of labor, where forces are limited to in its size and since the uterine contractions continue
only the uterine action, here in second stage of labor two at regular intervals despite its diminishing content, the
forces are essential—(1) involuntary uterine contractions area of placental attachment is greatly reduced. The great
and (2) voluntary intra-abdominal pressure brought disproportion between the reduced placental site and the
about by bearing down efforts of the woman. size of the placenta brings about a folding of the maternal
During the second stage of labor, the uterine contractions surface of the placenta and a separation takes place
increase in intensity, last for 50–70 seconds and occur every (shearing effect).
A B
Figs 25.5A and B: Expulsion of the placenta by. A. Schultze mechanism; B. Matthew Duncan mechanism
There are two methods, by which the placenta separates fills the lower uterine segment and part of vaginal and
from the uterine wall (Figs 25.5A and B): pushes the uterus up.
1. Schultze method: Evident in about 80% cases, placental There is true lengthening of the umbilical cord which
separation starts in the center of the placenta and this indicates that the placenta is descending.
part descends first. The fetal surface, therefore, appears Following separation of the placenta, bleeding from
at the vulva with the membranes trailing behind. The the large, torn maternal sinuses in the placental bed is
controlled by:
retroplacental clot is contained within the inverted sac;
Powerful contraction and retraction of the uterus,
thus there is minimal visible blood loss.
specially due to the contraction of the muscle fibers
2. Matthew Duncan method: This mechanism is seen
arranged as interlacing fibers, at times known as the
in about 20% cases. The separation starts at the lower living ligatures, which constrict the blood vessels
edge of the placenta. The placenta, therefore, slips running through the myometrium.
down sideways and the maternal surface appears first Pressure exerted on the placental site by the walls of the
at the vulva. This is associated with some amount of uterus. Once the placenta and membranes have been
visible blood loss as the blood from the placental site delivered, the walls of the uterus appose each other,
escapes immediately and a retroplacental clot is not thereby, the placental bed becomes firmly contracted.
formed. Since, there is no retroplacental clot to aid the The blood clots at the placental site, in the sinuses and
separation of the placenta, it takes longer to separate. torn blood vessels.

No clinical significance has been attached to either Placental Expulsion
mechanism. Meanwhile, hemorrhage occurs within these
When the placental separation is complete, the upper
placental folds, which expedites separation of the placenta
uterine segment contracts strongly, forcing the placenta into
and it sinks into the lower uterine segment or upper vagina the lower segment and then into the vagina. Detachment
as an unattached body. The signs of placental separation of membranes begins in the first stage of labor, when
occur within 5 minutes of placental separation. separation occurs around the internal os. By the third stage,
The shape of uterus becomes globular and it becomes a complete separation of the membranes take place assisted
more firmer. This is earliest sign of placental separation. by the weight of the descending placenta, which peels them
There is a sudden gush of blood. from the uterine wall.
The uterus rises in the abdomen slightly more than its Physiological changes of labor are summarized in the
previous position because the placenta separates and Table 25.1.
TABLE 25.1: Summary of physiological changes in labor

First stage Second stage Third stage
Completion of effacement of the cervix Contractions are strong and expulsive in Placental separation
and dilatation of the os caused by uterine nature
activity
Contd…
Contd…
First stage Second stage Third stage

Uterine activity Secondary powers, i.e. diaphragm and Expulsion of placenta
zz Contraction and retraction of uterine abdominal muscles, and the expulsive Uterus strongly contracts and retracts
muscle effort Control of bleeding due to contraction of
zz Fundal dominance, i.e. active upper Pelvic floor is displaced by the advancing uterine muscles
segment and passive lower segment fetus
zz Formation of physiological retraction The fetus is expelled, making a series
ring of passive movements leading to
zz Polarity of the uterus compression of vessels during delivery
zz Intensity or amplitude of contractions
constant
zz Resting tone in between contractions
Formation of the bag of forewaters and

hindwaters
1. Explain parturition and labor in brief.
2. Differentiate between stages of labor.
3. Write short note on physiological changes in labor.
26
Pratima Mittal, Ritu Sharma, Sudha Salhan, Renuka Sinha
Initial Assessment at
Onset of Normal Labor
and this blood mixes with the mucus creating a pink tinge.
INTRODUCTION
It should be differentiated from a substantial discharge of
The aims of care during labor are: blood which may indicate an obstetric complication.
Safe delivery for the mother
A live healthy baby

ONSET OF LABOR
A pleasurable and fulfilling experience of childbirth for
both the mother and her partner. Painful uterine contractions (regular, rhythmic uterine
For appropriate management of labor one has to first contractions lasting for about 45 seconds with a
recognize that labor has set in. frequency of at least 2 per 15 minutes)
The concept of separation of high-risk and low-risk Slight uterine hemorrhage—show
labor is being modified now. Obstetricians must be ready Commencing dilatation of the internal os
to manage any emergency in all deliveries. Effacement of the cervix
Formation of bag of waters
PREMONITORY SIGNS OF LABOR Spontaneous rupture of membranes.
Premonitory signs refer to symptoms experienced before
the onset of true labor. These are: TRUE VERSUS FALSE LABOR
Lightening or descent of the fetal head into the pelvis
False labor contraction may begin as early as 3 or 4 weeks
occurs about 10–14 days before birth especially in
before the actual delivery of the fetus. They are merely
primigravidas. In multigravida, it is more likely to occur
an exaggeration of the intermittent uterine contractions
after labor begins
(Braxton Hicks) that have occurred throughout the
Braxton Hicks contractions
Cervical softening, effacement and occasional dilatation

entire gestation but now they may be accompanied by
of the cervix from 1 to 2 cm discomfort. A distinction between the true and false labor
Increased vaginal discharge
should be made to identify true labor (Table 26.1).
Sciatic nerve pressure
Greater frequency of urination ADMISSION CRITERIA

Occasional rupture of the membrane.
Contraction pattern suggestive of an established labor
Ruptured membranes
SHOW Vaginal bleeding
The mucus plug in the cervical canal during pregnancy Decreased fetal movements
contains accumulated cervical secretions, and may Post-dated pregnancy. It is to be noted, that patients
be expelled when the cervix softens in the last days of with some high-risk factors, e.g. pre-eclamptic toxemia,
pregnancy. Pressure of the descending presenting part of may need to be admitted to the hospital even before the
the fetus causes minute capillaries in the cervix to rupture onset of labor.
Initial Assessment at Onset of Normal Labor 237
TABLE 26.1: Differences between false and true labor

False labor True labor
Discomfort especially in lower abdomen and groin Discomfort starts from the back and sweeps around the abdomen
Irregular contractions Regular contractions
Not associated with progressive increase in frequency, intensity, Progressive increase in frequency, intensity and duration of uterine
duration of contractions contractions
Interval between contractions remains long Interval between contractions gradually shortens
No or little change in cervix Progressive cervical dilatation and effacement
Pain does not coincide with uterine contractions Pain coincides with uterine contractions
Emptying of bowel may lead to relief of symptoms Emptying of bowel does not lead to relief of symptoms but
contractions may be augmented
CONFIRM ACTIVE LABOR BEFORE Investigations

Usually patient has all reports of investigations which are
ADMITTING
done during routine antenatal care (ANC).
If in doubt about active labor the woman should be Hemoglobin (Hb): A recent report within the last 2
admitted for observation. Patients who is not in labor months should be available. If not, a repeat hemoglobin
should be educated about signs of labor and should be test is done
assured that they can come back to the hospital when Blood group and Rh factor
there is excessive abnormal discharge (watery or blood Venereal Disease Research Laboratory (VDRL) test
stained), pain or a decrease in fetal movements, etc. Blood sugar
Hepatitis B surface antigen (HBsAg) and hepatitis C
INITIAL ASSESSMENT AT THE TIME OF Human immunodeficiency virus (HIV) I and II (after
ADMISSION counseling the patient)

Urine analysis for albumin and sugar.
It includes:
Ultrasonography (USG): Reports of all USG performed
History
in ANC should be checked. Reports of Doppler flow
General physical examination
studies, if any, should be recorded.
Abdominal examination
Pelvic examination. Examination

Initial assessment gives information regarding presence
Complete general physical examination
of any high-risk factor and fetomaternal condition. Assess the general nutritional status to look for any sign
and symptoms suggestive of any high risk factors

Comprehensive History
Observe the hydration of patient
Comprehensive history should be taken. The following Pallor, icterus, cyanosis
questions must be asked: Temperature
Period of gestation by asking date of last menstrual Pulse rate, blood pressure (BP)
period (LMP) Weight
Previous obstetrical history—note the indication for Edema feet, facial puffiness
cesarean section, if done Cardiovascular system (CVS) and chest examination is
History of obstetrical or gynecological complications performed and recorded.
Is there pain or contractions Abdominal examination
Is there any leaking or bleeding per vaginal (P/V) Fundal height
Does the patient feels an urge to defecate or desire to push Presentation, position and lie
Antenatal care (booked/unbooked, immunized/not) Engagement
Multiple births anticipated Approximate clinical assessment of fetal weight
Any history of dai handling or interference by another Fetal heart rate (FHR), watch for any post-contraction dip
doctor. Uterine contraction—frequency, duration and intensity.

Fetal presenting part, position and station of the

presenting part
Pelvic assessment.
CONSENT
Consent for treatment should be taken and counseling
done regarding:
Condition of the fetus
Condition of the mother
Incidence of complication anticipated
Incidence of operative delivery
Consent for delivery and intervention taken
Any immediate family planning method to be adopted.
AT THE TIME OF ADMISSION TO THE

LABOR ROOM
Fig. 26.1: Per vaginal examination
Patient’s clothes are changed to comfortable labor
gowns (Fig. 26.2). In Safdarjung hospital a delivery
Local examination of genitalia: Look for any vulval gown is designed by Dr Banashree Das which has a big
edema, varicose veins, leaking or bleeding. window with a flap at the position of abdomen. By this
Per vaginal examination (Fig. 26.1): It should be done abdominal examination can be done by lifting the flap
at the time of admission. Sterile gloves are worn. Under without exposing the perineum. The belongings are
all aseptic precautions, the perineum is cleaned from handed over to the relatives.
above downwards and once the anus is touched the swab Part preparation—normal (hair should be clipped
is discarded. A perineal sheet is placed in position. With short, shaving is not necessary).
the thumb and forefinger of the left hand the labia are Hb, HIV status and blood group of all patients should
separated. The index and second finger of the right hand be known.
(in a right handed person) are introduced into the vagina.
Avoid the anal region and do not remove the fingers ESTIMATION OF STATION OF
from the vagina before completion of the examination,
as reintroduction of fingers increases the chances of
PRESENTING PART (FIGS 26.3A AND B)
introduction of infection. Conventionally, a three station scale is used. American
Per vaginal examination is contraindicated in patients College of Obstetrics and Gynecology (ACOG) uses 5 cm
who present with history of bleeding per vaginam, scale. Where numerator denotes station and denominator
before the ultrasound to rule out placenta previa. Per
vaginal examination in active labor should be restricted
to a minimum of 4–6 hourly unless there is spontaneous
rupture of membranes, sudden deceleration of fetal heart
or if the patient starts bearing down. P/V examination
should also be restricted when signs and symptoms of
chorioamnionitis are present and in patients suffering
from heart disease and in HIV infected patients.
The following points are recorded during pelvic
examination:
Any leaking P/V and if present the color of the liquor
and the amount of leaking

Consistency of the cervix, effacement, position and
dilatation. Bishop’s scoring is done

Status of membranes, any prolapse of cord Fig. 26.2: Maternity gown
A B
Figs 26.3A and B: Stations of the fetal head in relation to ischial spine. A. Classic three station scale; B. ACOG scale
TABLE 26.2: Scales used for representing station of head TABLE 26.3: Modified Bishop score
Classic three station Cervical Pelvic Pelvic Pelvic Pelvic
scale ACOG scale Cranial position features score 0 score 1 score 2 score 3
}
–3 –5 Dilatation Closed 1–2 3–4 >4
–2 –4 (cms)
Pelvic inlet
–3
–1 Length (cms) 3 2 1 0
–1
0 Station –3 -2 –1/0 +1/+2
}
0
+1 +1 Consistency Firm Medium Soft –
+2
+2 Ischial spine (engagement) Position Posterior Mid Anterior –
+4
+3 +5 Score of 6 or more indicates favorable cervix.
shows that 5 cm and it is recorded as fraction, e.g. –2/5 Allows early detection of problems in labor like cepha-
scale has been used (Table 26.2). lopelvic disproportion (CPD), prolonged labor, fetal
Assessment of the pelvis is done to rule out cephalopelvic distress, etc.
disproportion (Table 26.3). Allows timely referral to higher center serving as an
Progress of labor—documentation of progress of labor early warning system
is carried out for each patient using a partogram starting Allows timely intervention like augmentation using
from admission. amniotomy or oxytocin, instrumental delivery, cesarean
section, etc.
PARTOGRAPH Decreases fetomaternal morbidity and mortality
It is the graphical record of progress of labor and fetoma Acts as an efficient training tool
ternal condition on a single sheet of paper. It also includes Provides medicolegal record.
any intervention done during labor. It is plotted once the
patient enters the active phase of labor, i.e. the cervix is
Limitations
> 4 cm dilated. Women with obstetrical problems requiring Frequency of examinations varies
special attention do not need a partogram. Deviation from 1 cm/hour dilatation rate may be normal.
A sample of modified WHO (World Health Organization)
Benefits partograph is shown in Figure 26.4. Various components
Ensures proper supervision of labor of partograph (from above downwards) and their inter
Avoids unnecessary interventions pretation is described in the Table 26.4.
Fig. 26.4: WHO modified partograph

TABLE 26.4: Description of modified WHO partograph

Component Description Interpretation and intervention
Personal information This includes name of the patient, her gravidity, parity, date Details about patient including obstetrical history are
and time of admission, admission number, time of ruptured available in this section
membranes
Fetal heart rate (FHR) It is plotted as a dot. Each rectangle on the vertical side There are two solid lines at 100 and 180 beats/minute
represents 10 beats/minute and on the horizontal line Immediate action for delivering the baby has to
represents 30 minutes time interval. It is recorded every be taken once the FHR crosses these lines as they
30 minutes or earlier if indicated represent severe bradycardia and severe tachycardia
respectively
Amniotic fluid Note the status of membranes each time pelvic examination The following codes are used:
is done (4 hourly or earlier); if ruptured note down the color I-Intact membranes
of amniotic fluid C-Clear liquor
M-Meconium stained
B-Blood stained
Thick meconium/absent liquor may indicate fetal
distress while blood stained liquor may represent
abruption, requiring strict vigilance
Molding It is the degree of overlapping of the bones of the skull. It is The following codes are used:
noted at the time of pelvic examination (4 hourly or earlier) 0 Bones separate, sutures felt easily
+ Bones just touching
++ Bones overlapping
+++ Severe overlapping
The more is the molding, the more severe is the
cephalopelvic disproportion (CPD) and intervention is
decided accordingly (instrumental delivery or cesarian)
Cervical dilatation It is plotted as X. Vertical side of each square represents Plotting of cervical dilatation remains on the alert line
1 cm dilatation while horizontal side represents 30 minutes or to the left of it in case of normal progress of labor.
time interval. There are two preplotted lines—alert line If it lies to the right of alert line, it indicates slow
and action line. Alert line begins at 4 cm and extends till progress (amniotomy may be done) and if it reaches
full dilatation at the rate of 1 cm/hour which is the slowest or crosses the action line, it indicates extremely
progress rate in a primigravida. Action line lies 4 hours to slow progress. Immediate action is recommended
the right of alert line and runs parallel to it. It is recorded (oxytocin infusion or cesarean section)
every 4 hourly or earlier. Cervical dilatation in active phase
on admission is recorded on the alert line
Descent of head It is plotted as O. It is plotted along the space from 5 to 0 as Full dilatation with no descent or arrest of descent
is used in dilatation. Vertical side of each square represents may indicate CPD and intervention is required
one-fifth of the head above pelvic brim. It is recorded every accordingly
4 hourly or earlier
Time The horizontal side of each rectangle in upper row represents
1 hour while lower row represents actual time
Contractions/10 We record the duration and frequency of contractions in 10 Frequency is represented by the number of shaded
minutes minutes. It is plotted every half hourly or earlier squares and appropriate shading represents duration
as shown below.
• • •••
• • • • • Dots-mild contractions < 20 seconds
• • •
Diagonal lines-moderate contractions
20–40 seconds
Solid color-strong contractions >40 seconds
If there is slow progress with associated poor

contractile activity, oxytocin infusion can be given
Contd…
Contd…
Component Description Interpretation and intervention
Oxytocin If inadequate uterine contractions are the cause for the Titration of dose of oxytocin can be done more
slow progress of labor, administer oxytocin. It is recorded precisely. Always do amniotomy before oxytocin
half hourly with concentration written in the upper row and infusion in active labor
number of drops in the lower row
Drugs and intravenous The name, time, dose and route of administration of each Detailed information about any drug administration
(IV) fluids drug is recorded is available for analysis
Maternal vital charting: Pulse is plotted every half hourly or earlier with a dot Overall view about the general condition of the
Maternal pulse joined by solid line mother is available and intervention can be done
Blood pressure Blood pressure charting is done every 4 hourly or earlier accordingly
Temperature and is plotted by two arrows joined together; the upper
Urine
arrow representing systolic and lower one representing
diastolic blood pressure
Temperature is recorded 4 hourly or earlier
Urine is tested for amount, proteins and acetone every
time patient passes urine
CASE 1 (FIG. 26.5) minute and regular. On pelvic examination, the cervix was 4
cm dilated, membranes were intact and there was no caput
Mrs B, 36-year-old, G3P2L2, hospital number–3314, got
or molding. Her pulse was monitored every half hourly
admitted on 12.09.15 at 9.00 AM in labor room with period
along with FHR and contractions. At 8.00 PM her pulse rate
of gestation 40 weeks 3 days with leaking since 8.00 AM.
was 90/minute, BP-120/80 mm Hg, temperature was 37°C
Her pulse rate was 90/min, BP-130/80 mm Hg, temperature
and urine output 400 mL which was negative for ketones,
was 36.5°C and urine output was 400 mL which was
sugar and albumin. On per abdominal examination, there
negative for albumin, sugar and ketone. On per abdominal
were three contractions/10 minutes each lasting for about
examination, there were three contractions/10 minutes
30 seconds, head was three-fifth palpable and FHR was
each lasting for about 30 seconds, head was three-fifth
136/minute and regular. On pelvic examination, the cervix
palpable, and FHR was 140/minute and regular. On pelvic
was 5 cm dilated, membranes were intact without any
examination, the cervix was 5 cm dilated, membranes
caput or molding. Amniotomy was done, liquor was clear
were absent, liquor was clear and there was no caput or
and labor was monitored cautiously as recommended. At
molding. Her pulse was monitored every half hourly along
12 AM, her pulse rate was 80/minutes, BP-120/70 mm Hg,
with FHR and contractions. At 1.00 PM her pulse rate was
temperature was 36.5°C and urine output 400 mL which
80/minutes, BP-120/80 mm Hg, temperature was 37°C
was negative for ketones, sugar and albumin. On per
and urine output 400 mL which was negative for ketones,
abdominal examination, there were three contractions/10
sugar and albumin. On per abdominal examination, there
minutes each lasting for about 30 seconds, head was three-
were four contractions/10 minutes each lasting for about
fifth palpable and FHR was 130/minute and regular. On
45 seconds, head was one-fifth palpable and FHR was 136/ pelvic examination, the cervix was 6 cm dilated without
minute and regular. On pelvic examination, the cervix was any caput or molding and liquor was clear. 2U oxytocin
fully dilated, liquor was clear and there was no caput or infusion was started at the rate of 30 drops/minute and
molding. Patient had spontaneous vaginal delivery of a augmentation was done titrated with contractions. Labor
male baby at 1.30 PM weighing 3 kg. was monitored vigorously. At 2 AM her pulse rate was 90/
minute, BP-130/70 mm Hg, temperature was 36.5°C and
CASE 2 (FIG. 26.6) urine output 500 mL which was negative for ketones, sugar
Mrs A, 26-year-old, primigravida, hospital number – 1224, and albumin. 2U oxytocin infusion was on flow at the rate
got admitted on 20.09.15 at 4.00 PM in labor room with of 60 drops/minute. On per abdominal examination, there
period of gestation 39 weeks 3 days. Her pulse rate was 80/ were four contractions/10 minutes each lasting for about
minute, BP-110/70 mm Hg, temperature was 36.5°C and 45 seconds, head was zero-fifth palpable and FHR was
urine output was 300 mL which was negative for albumin, 140/min and regular. On pelvic examination, the cervix
sugar and ketone. On per abdominal examination, there was fully dilated without any caput or molding and liquor
were two contractions/10 minutes each lasting for about 20 was clear. Patient had spontaneous vaginal delivery of
seconds, head was three-fifth palpable, and FHR was 140/ female baby at 2.30 AM weighing 3.2 kg.
Fig. 26.5: Partograph of case 1

Fig. 26.6: Partograph of case 2

1. Differentiate true and false labor.
2. Define per vaginal examination.
3. What is the initial assessment at the time of admission?
27
Pratima Mittal, Ritu Sharma, Sudha Salhan
Conduct of Normal Labor
Monitor progress of labor

FIRST STAGE OF LABOR
Detect any factor that may adversely affect the labor at

The first stage starts from the onset of labor to full the earliest.
dilatation of the cervix (diameter 10 cm). On an average in Noninterference means as far as possible, we let the
a primigravida patient, it lasts for around 8–12 hours while delivery occur by itself without actively interfering to
in a multigravida, for 3–8 hours. It is subdivided into: deliver a part or whole of the fetus.
All vital fetomaternal parameters have to be plotted on
Latent Phase of the First Stage
a single sheet—the partograph.
The latent phase commences with maternal perception of
regular contractions and slow cervical dilatation and ends Maternal Wellbeing
at a cervical dilatation of 4 cm. Here the progress of labor is
assessed with the Bishop score. The cervix should change This is ensured by observing the vital parameters such as
at a minimum of 1 Bishop score point an hour if the labor pulse, blood pressure (BP), temperature, respiratory rate,
is to end within a reasonable time. A score of 11 indicates etc. at frequent intervals. In active phase, pulse is monitored
the onset of active labor. every 30 minutes or earlier; BP and temperature are
monitored every 4 hourly or earlier. Hydration is maintained
Active Phase of the First Stage by allowing the patient to take sips of fluids like tea, fruit
It starts from a cervical dilatation of 4 cm to full cervical juice, soup in low risk-pregnancies; intravenous (IV) fluids
dilatation (10 cm). For a normal progress of labor, the rate are administered in cases where the labor is prolonged.
of cervical dilatation should be more than 1–1.2 cm/hour Solid foods are withheld in active labor because:
in nulliparous and more than 1.5 cm/hour in multiparous Emptying of the stomach is delayed
women. The active phase has an initial acceleration phase, Vomiting/aspiration may occur
then a phase of maximum slope and finally a deceleration If the need for an operative delivery arises, then the risk
phase. If the rate of progress is less than that of the normal, of aspiration and other post-operative complications
one should rule out: (Mendelson’s syndrome) has to be borne in mind.
Hypotonic uterine contractions Oral ranitidine 150 mg should be given 6 hourly to a
Cephalopelvic disproportion (CPD) woman in labor (if there is a chance that operative delivery
Excessive sedation is needed later on).
Fetal malpositions. During the early stages of labor, the mother is allowed to
Appropriate action according to the cause should be stay out of bed (move about) if membranes are intact, but
taken for labor to be successful. once the membranes are ruptured the mother’s movement
should be restricted. Bed rest in a lateral position is
Principles of Management preferred as it lifts the uterus away from the great vessels,
Noninterference thus preventing a compromise in the blood supply to the
Monitor maternal and fetal wellbeing fetus.
Conduct of Normal Labor 247
Per abdominal examination is done to monitor the Labor assessment is done to assess descent and rotation
uterine contractions, descent of the head, fetal heart sounds of the presenting part. If the patient is making appropriate
and any distension of the urinary bladder. Monitoring progress one can anticipate vaginal delivery. Fetal descent
of the uterine contractions is carried out by the palm of should be more than 1 cm per hour.
the hand lightly placed on the abdomen. Time of onset, Monitor the FHR every 5 minutes
duration and intensity of each uterine contraction is The patient should be lying down with legs half flexed at
noted. During a uterine contraction, the thumb cannot the time of bearing down and a dorsal lithotomy position
indent the uterus. Contractions are monitored every should be maintained (with or without stirrups) at the
30 minutes. Descent of head is monitored by fifths formula. time of delivery. Shoulders should be raised.
During first stage, fetal heart rate (FHR) is monitored An episiotomy should be given at the crowning of
every 30 minutes or earlier. The suprapubic region should head, if the doctor conducting delivery thinks that
be checked in every abdominal examination for bladder the perineum is likely to tear, especially in cases of
fullness. Bladder distension should be avoided. The nulliparous women and instrumental deliveries. For the
patient should be encouraged to pass urine at least every correct technique of giving an episiotomy (see Chapter
2 hours. Per vaginal (PV) examination is performed every 58). Local anesthesia using 1% lignocaine should be
4 hourly or earlier to check the progress of labor needless given.
to say, before a PV examination, the patient should be If the progress of labor is not adequate, evaluate:
explained about the procedure. Adequate pain relief in Uterine contractions
the form of parenteral analgesics or epidural analgesia can Fetal position (occipitotransverse or occipitoposterior)
be offered. However, one must bear in mind that reassurance Rule out CPD
is still one of the best analgesics. Relaxation techniques Evaluate fluid balance (correction of dehydration if any
taught during the antenatal period are of a great help. should be done).
Partograph is important to monitor the progress of Unless contraindicated, oxytocin augmentation for
labor and for early detection of any abnormality in the prolonged second stage is advocated. When the above
labor; thus enabling the prompt appropriate intervention measures fail, operative vaginal delivery including vacuum
to be taken. If there is slow progress, amniotomy is the first
extraction or forceps delivery should be considered unless
step to be taken before oxytocin infusion or any operative
contraindicated. Cesarean section should be considered
interference.
in cases of failed progress and non-descent of head.
Amniotomy offers the benefit of:
The partograph is still an essential tool for decision-
Rapid onset/augmentation of labor
making during labor.
Early detection of meconium stained liquor
Not to be advocated:
Scalp electrodes can be applied
Fundal pressure
Intrauterine pressure catheter can be applied.
Ironing or stretching of perineum.
Disadvantages are that of:
Risk of cord prolapse, if the head or other presenting part
Delivery of the Baby
is not well applied or if engagement has not occurred
Increased chance of infection.
With one hand pressure is given on the perineum just in
front of the crowning head and with the other hand
pressure is applied against the occiput keeping the head
SECOND STAGE OF LABOR flexed till the nape of the neck is visible (Ritgen’s maneuver)
The second stage starts from a full dilatation of the cervix to (Fig. 27.1).
the delivery of the baby. It last on an average for 1–2 hours This ensures flexion of the head and thus the smaller sub-
in primigravidas and in 0.5–1 hour in multigravidas. In the occipitofrontal diameter distends the outlet. Sub-occipital
absence of fetal compromise, maternal distress, rupture of region of the fetal head is held against the symphysis.
membranes or other indications for termination there is The head is delivered by extension towards the end of a
no urgency in delivering the patient. contraction or in between contractions.
Suction is contraindicated in babies who start breathing
Principles of Management on their own irrespective of meconium in liquor as it
Assist in maternal expulsion of the fetus can cause severe bradycardia and meconium aspiration
Prevent perineal injuries syndrome.
THIRD STAGE OF LABOR

The third stage starts after the delivery of the baby and lasts
up to the delivery of the placenta and the membranes. The
duration is usually of 5–15 minutes, if actively managed
but it can be as long as 15–20 minutes without interven-
tion, i.e. in expectant management. Nowadays there is no
role of expectant management as active management is
associated with the advantages of shortened duration of
third stage along with decreased blood loss.
Active Management of Third Stage of

Labor (AMTSL)
AMTSL has three components:
Fig. 27.1: Modified Ritgen’s maneuver 1. Prophylactic uterotonic after the delivery of baby
(oxytocin 10 U intramuscularly)
An index finger should now be used to check for a 2. Controlled cord traction
nuchal cord (cord round the neck). If present loosely 3. Uterine massage.
gentle unwrapping is advocated before the fetus delivers. Active management stimulates powerful uterine contrac
If unwrapping cannot be done then the cord should tions leading to early separation of placenta.
be clamped and cut at this time and completion of the The disadvantage is a slightly higher incidence of
delivery should be hastened. retained placenta (1–2%).
The delivery of the anterior shoulder should be assisted Following delivery of the baby, the placenta is expected
by a gentle downward traction on the head, followed by the to separate immediately and is delivered by controlled
delivery of the posterior shoulder by elevating the head. cord traction. Needless to say, after the delivery of one
The rest of the body is then delivered by lateral flexion. neonate one should exclude multiple pregnancies before
using these pharmacological measures.
Baby Should be Kept Below the
Level of the Perineum Modified Brandt-Andrews Technique
This position is maintained for about 20 seconds to allow (Controlled Cord Traction)
infusion of blood from the placenta to fetus. The cord is The fundus is pushed upwards and backwards during
clamped once the pulsations have ceased. An average of contraction and controlled cord traction is applied in
80 mL of blood may be shifted to the neonate through the downwards direction. Uterine elevation and not cord
cord. Early cord clamping should be done in cases of fetal traction assists in the expulsion (Figs 27.2A and B).
distress, preterm, intrauterine growth restriction (IUGR) Examination of the placenta and membrane (see Fig.
and rhesus (RH) incompatible babies. 33.1): Look for any abnormality, e.g. bilobed placenta (see
For cutting the cord, one clamp is placed about 8 inches Chapter 23), missing cotyledons, calcifications, size and
away from newborn and the second clamp about 2–3 weight of the placenta. Do not forget to examine the cord
inches further away from first clamp. Sterile scissors or especially for number of vessels.
scalpel should be used to cut the cord between these
two clamps. The ends of the cord should be inspected Episiotomy/Perineal Tear Repair
for bleeding and additional clamps should be applied if Suturing the perineum is done under local anesthesia
needed. The baby (especially the sex of the baby) is shown using chromic catgut no. 1–0 or vicryl rapide. Repair is done
to the mother if there is no need for active resuscitation. in three layers—mucosa by continuous suture, muscle
The baby is examined for any signs of distress and resusci and fascia by interrupted sutures. The skin is sutured by
tated if required (see Chapter 66). A quick examination is interrupted stitches or by subcuticular suture using a
done to rule out any major congenital abnormality. delayed absorbable suture such as vicryl.
A B
Figs 27.2A and B: A. Controlled cord traction; B. Brandt-Andrews maneuver (controlled cord traction). Traction is exerted on the cord
as the uterus is gently elevated. Blood pressure is sorted between the symphysis and the uterine fundus, forcing the uterus upward and
the placenta outward, as traction on the cord is continued
Put the baby on the breast as soon as possible. This will To provide effective analgesia during the period of labor.
also help in the prevention of postpartum hemorrhage To reduce the duration of labor and, hence, the suffering
(PPH) because of release of oxytocin. Nowadays initiation of of the patients.
breastfeeding on the delivery table itself is recommended. To cause fast yet smooth dilatation of the cervix, hence,
reduce the chances of cervical tear.

FOURTH STAGE OF LABOR To reduce the incidence of PPH during the third stage
of labor.
This stage extends from the delivery of the placenta upto To alleviate the pain during the repair of episiotomy
2 hours after delivery. As per the recommendations of wound.
American Academy of Pediatrics and the American College A patient is taken up for programed labor only after
of Obstetricians and Gynecologists, maternal blood pressure she enters the active phase of the first stage of labor. From
and pulse should be monitored immediately after delivery that point onwards all events in labor are documented on
and then every 15 minutes in the first hour after birth. a partogram. Labor is monitored by a skilled attendant.
Also palpate the fundus to look for the tone of the uterus All medications will follow a preconceived and accepted
and examine the perineum for any excessive bleeding or protocol of drug administration.
swelling. Enquiry is also made regarding voiding of urine
post delivery. Ensure Adequate Contractions
If the condition of the patient remains stable, she could Amniotomy and oxytocin infusion to ensure that the patient
be transferred to the ward 2 hours after her delivery. gets three sustained contractions/10 minutes, each lasting
35–45 seconds. The FHR pattern should be satisfactory
SUMMARY OF MANAGEMENT OF and the uterus should relax well between pains.
NORMAL LABOR (TABLE 27.1)
Ensure Pain Relief
Programed Labor Epidural may be used if available. Otherwise analgesic
It is a new concept advocated by Daftory and associates drugs can be gainfully employed to provide reasonable
(2003). It is a careful monitoring of the labor fulfilling the pain relief, freedom from anxiety and patient cooperation.
following aims and objectives: When the patient is in established labor and reaches
TABLE 27.1: Summary of management of normal labor

Features First stage Second stage Third stage Fourth stage
Pulse On admission and then every Every 30 minutes –
30 minutes
BP On admission and then 4 hourly 1 hourly – Pulse and BP—every 15 minutes
post delivery for 1 hour (transfer
the patient after 2 hours if stable)
Temperature On admission, then 4 hourly – – Every shift
Urine for proteins On admission, then 2 hourly – – –
If positive then analyze
Fetal heart rate Every 30 minutes. Listen at least 5 minutes – –
through one, preferably two
contractions and note accelerations
with contractions
Contractions: Assess and record every 30 minutes Assess and record – Note the tone every 15 minutes
Frequency every 15 minutes
Duration
Quality
Resting tone
P/V exam On admission, then 4 hourly or at Assist delivery at – –

rupture of membranes. Cervical crowning of head
dilatation should be at the rate of
1–1.2 cm/hour in nulliparous and
> 1.5 cm/hour in multiparous
Total duration Prolonged if > 20 hours in nullipara 1–2 hours in nullipara Not more –
and > 14 hours in multipara and 0.5–1 hours in than 30 minutes
Average 8–12 hours in nullipara and multipara
3–8 hours in multipara
Diet Sips of clear fluid intravenous fluids if – – Allowed to take fluids and soft diet
labor is lengthy when stable
Ambulation Early stages allow ambulation unless – – –
there is frank leaking
I and O Every shift Every shift Every shift Note first void
Encourage patient to pass urine
2 hourly
Fundus and lochia – – – First 15 minutes and then hourly
till patient is transferred (transfer
the patient after 2 hours, if
stable). Inspect episiotomy site for
hematoma
Abbreviations: BP—Blood pressure; P/V—Per vaginal; I and O—Input and output
to about 4 cm of cervical dilatation, the patient is is also administered. If the patient’s weight is over 60 kg,
closely observed in the labor ward, and partographic increase the dose to 1.0 mg/kg maternal body weight.
documentation implemented. Along with the tramadol, administer a smooth muscle
Set up an intravenous (IV) infusion line using Ringer’s relaxant (drotin, anafortan, buscopan, epidosin). The
lactate solution. Administer a small dose of 2 mg diazepam combined drug effect provides an excellent pain relief and
and 6 mg pentazocine diluted in 10 mL of saline, slow also facilitates cervical dilatation. The labor progresses
intravenously as a bolus for pain relief. This dose is satisfactorily until the head comes down upto the pelvic
so small that it does not affect the mother or the fetus floor. At this time, the cervix is close to full dilatation
adversely. Injection tramadol 50 mg intramuscular (IM) and the station of the presenting part in the lower pelvic
strait. Should the pains be strong and distressing, it is safe

UNDERWATER DELIVERY
to administer ketamine after a proper counseling. This
produces analgesia and amnesia. The drug is short acting It is a new concept in which labor, or delivery, or both
(20 minutes). Ketamine is reserved for those few cases allowed to occur in a birth pool filled with warm water.
who complain of excess pain during an advanced labor, Immersion in water during the first stage has shown
where the head has started stretching the pelvic floor and association with decreased pain, decreased use of
the cervix reaches a dilatation of 7 cm or more. The initial analgesia, decreased incidence of perineal tear, greater
dose is 0.5 mg per kg body weight IV. If further pain relief sense of wellbeing and control, and decreased duration of
is required a top up dose of half the initial loading dose labor without affecting the perinatal outcome. Immersion
may be repeated. It passes into the fetal circulation but is in water during the second stage is still in experimental
rapidly metabolized. However, ketamine is a drug to be stage without any established fetomaternal benefit.
used with caution because serious though rare side effects Complications include increased risk of infections and
exist, e.g. seizures, bronchospasm, etc. avulsion of umbilical cord. Immersion in water is also
After birth if the baby does not cry, ventilatory support associated with neonatal drowning or near drowning,
with bag and mask may be needed. hypothermia, asphyxia and seizures. The patients with
During the third stage of labor, active management is malpresentations, multiple gestations, prematurity,
required after expulsion of the placenta. Inspect the birth associated medical disorders, risk of infection and those
canal and perineum for injuries and repair the same. A requiring continuous monitoring should not be given this
single dose of ketamine after delivery permits an easy option. Institutes have to formulate their own protocols
examination of the birth canal and an easy repair of keeping in minutes not to compromise the patient care at
episiotomy/tear/lacerations. any step.
1. What is the active phase of the first stage of labor?
2. True/False:
i. Active management of third stage of labor has four components.
ii. Partograph is important to monitor the progress of labor and for early detection of any abnormality in the labor.
i. Brandt-Andrews Technique
ii. Underwater delivery.
28
Usha Gupta, Sudha Salhan, Deepali Garg
Induction of Labor
Chorioamnionitis
INTRODUCTION
Rhesus (Rh)-isoimmunization
Induction of labor is the artificial (with the help of Accidental hemorrhage
pharmacological or mechanical methods) initiation of Icterus gravidarum (cholestasis of pregnancy)
labor, after 28 weeks of gestation, before the spontaneous Intrauterine fetal demise
onset of labor, for the purpose to achieve normal vaginal Bad obstetric history.
delivery. It is generally done as a therapeutic option
when the benefits of expeditious delivery outweigh the Fetal Indications
risks of continuing the pregnancy to the life or wellbeing Fetal compromise (severe fetal growth restriction, Rh-
of either the mother or her unborn child or both. The isoimmunization, oligohydroamnios, hydrops fetalis)
benefits of induction of labor must be weighed against Post-maturity
the potential risks to the mother or to the fetus associated Hyperemesis with ketosis at term gestation
with this procedure. In developed countries, around 25% Intrauterine growth restriction (IUGR) at term
of all deliveries at term now involve labor induction. In Congenital malformations in the fetus which are
developing countries, the induction rates are generally incompatible with life
lower but in some countries they are as high as observed Suspected jeopardy to the fetus
in developed countries. Previous unexplained stillbirths/intrauterine fetal death
(IUD).
AUGMENTATION OF LABOR
For the Sake of Both Mother and Fetus
It is the intervention that is intended to enhance already Pre-eclampsia and eclampsia
existing spontaneous contractions that are considered Hypertension complicating pregnancy
inadequate because of failure of progression or slow Renal disease complicating pregnancy
progression of labor. Diabetes mellitus
Rh-isoimmunization.
INDICATIONS FOR INDUCTION OF
LABOR CONTRAINDICATIONS
Indications can be for the sake of mother, fetus or both. Major degrees of contracted pelvis leading to cephalo-
pelvic disproportion (CPD)
Maternal Indications Major degrees of placenta previa—types II B, III and IV.
Maternal medical conditions (e.g. diabetes mellitus, Vasa previa
renal disease, chronic pulmonary disease, chronic hyper Fetal malpresentations, e.g. transverse lie, breech presen
tention, antiphospholipid antibody syndrome) tation and oblique lie
Fulminating pre-eclampsia, eclampsia Fetal distress, umbilical cord presentation or cord prolapse
Premature rupture of membranes at term Tumors of cervix or bony pelvis
Induction of Labor 253
Previous scarred uterus like previous classical cesarean TABLE 28.1: Bishop’s cervical score
section, myomectomy scar, uteroplasty, previous two or Score 0 1 2 3
more lower segment cesarean section
Position of Posterior Mid position Anterior –
Previous difficult instrumental delivery cervix
Multiple gestation
Dilatation of Closed 1–2 3– 4 5+
Active herpes infection cervix (cm)
Tests of fetal wellbeing [nonstress test (NST), color Consistency Firm Medium Soft and –
Doppler] indicating fetal jeopardy before the onset of of cervix stretchable
labor. Such a fetus may not withstand labor pains Station of –3 –2 –1, –0 +1, +2
Pregnancy following repair of a vesicovaginal fistula the head
(VVF) Cervical 3 2 1 0
Any other contraindication for safe vaginal delivery. length (cm)
PREREQUISITES OF LABOR INDUCTION

The pre-labor ripening of the cervix is characterized by
There should be valid medical indication for labor important structural changes such as softening, shortening
induction and expected benefits outweigh its potential and opening of the cervical os and biochemical changes in
harms. the ground substance. These are associated with gradual
Consideration must be given to the actual conditions, dissociation and rearrangements of the rigid bundles of
wishes and preferences of the patient with due emphesis collagen by collagenases into loose fibers which allows
on cervical status, specific method of labor induction the tissue distensibility in the cervix. There are changes
and associated conditions like parity and rupture of in glycosaminoglycans (GAGs) and increased amount of
membranes. Take an informed consent from the patient hyluronic acid and decreased amount of dermatan sulfate
after explaining to her all the pros and cons of the increases water content of cervix so that cervix become
procedure. soft and pliable.
Facilities for maternal and fetal monitoring must be Several scoring methods are available to determine the
there, since, the procedure carries the risk of uterine success of induction. The most widely used system is the
hyperstimulation, uterine rupture, chorioamnionitis modified Bishop’s cervical score (Table 28.1).
and fetal distress. A Bishop score of 6 or less generally define an unfa
Facilities for emergency cesarean section must be there vorable cervix in most randomized controlled trials (RCTs).
round the clock. If the total score is more than 8 then probability of normal
Fetal lung maturity must be confirmed by all means as vaginal delivery is similar to that after spontaneous labor.
far as possible. This ideal may, however, not be fulfilled Other scoring methods are:
if the life of mother or fetus is at risk. Fields scoring index (1966)
The cervix must be ripe, if cervix is unripe then its Burnett scoring index (1966)
priming to be done before induction. Friedman scoring systems (1967)
The fetus should be able to withstand the hypoxic effect Lange scoring system (1982)
of labor pains. There should be no pre-existing fetal Dhall scoring system (1982).
hypoxia. Usually cervical ripening is followed by induction of

labor.
CERVICAL RIPENING/PRIMING Pre-induction Methods of Cervical Ripening
Cervical ripening is aimed to facilitate the process of There are so many mechanical as well as pharmacological
cervical softening, thinning and dialating with resultant methods available for cervical priming, the popular one
reduction in rate of induction failure and induction include the use of mechanical cervical dialators and
to delivery interval. Cervical remodelling is a critical synthetic prostaglandin E1 (PGE1) and PGE2 administration.
component of normal vaginal delivery. The success of any Mechanical methods include manual dialatation and
method of induction depends on the parity and the state of stripping of membrane. Mechanical dilators like osmotic/
the cervix before induction. hygroscopic dilators, swell by extracting water from
cervical tissue, gradually expands the cervical canal, drug are extensive and Food and Drug Administration (FDA)
e.g. Laminaria japonicum tents or Lamicel (synthetic has approved in 2002 a new lable on the use of misoprostol
tents impregnated with magnesium sulfate) Hypan and during pregnancy for cervical priming and labor induction.
Dilapan (a copolymer of polyacrylonitrile). Laminaria Usual doses are 25 or 50 microgram.
tents are associated with increased peripartum infections, PGE2 is available commercially in two preparations—
extra-amniotic Foley’s catheter (14–26 F) balloon inflation a gel available in a 2.5 mL syringe containing 0.5 mg of
with inflation volume of 30–80 mL, extra-amniotic saline dinoprostone and a vaginal insert having 10 mg of dino
infusion with infusion rate of 30–40 mL per hour, double prostone. Both are FDA approved for cervical ripening.
balloon devices (Atad Ripener device). The balloon of the Intracervical or intravaginal PGE2 is superior to placebo or
catheter is withdrawn gently till the level of the internal no therapy in inducing cervical ripening.
cervical os. The basic mechanism of cervical ripening Both intracervical and intravaginal routes are popular
by extra-amniotic balloon catheter seems to be direct as both are safe, efficacious and easy to administer.
pressure and over-stretching of the lower uterine segment Intracervical instillation is usually done. Intracervical PGE2
and cervix. Extra-amniotic infusion of saline separates 0.5 mg in viscous cellulose gel can be used thrice at 6–12
the chorioamnion and deciduas and possibly stimulates hours interval with a maximum cumulative dose of 1.5 mg
prostaglandin (PG) production. In a study conducted of dinoprostone within 24 hours period (Figs 28.1A and B).
in VM Medical College and Safdarjung Hospital, it was Intravaginal tablets of PGE2 in 2–5 mg as biodegradable
concluded that the Foley’s catheter with or without extra- vaginal pessaries are introduced into the posterior fornix
amniotic saline infusion is an efficacious method for pre- of vagina. The use of PGE2 is associated with increased
induction cervical ripening. More women achieved a incidences of uterine tachysystole with associated fetal
favorable Bishop score in a shorter time interval after the heart rate (FHR) changes more so with vaginal insert in
start of cervical ripening with Foley’s catheter as compared comparison to intracervical gel.
to PGE2 gel without increasing the cesarean rate, maternal Other topical agents: Estradiol in tylose gel, relaxin and
and neonatal morbidity. Other advantages of balloon RU 486 (mifepristone), glyceryl trinitrate, isosorbide
catheter include low cost, stability at room temperature, dinitrate (ISDN) have been used with varying success.
reduced risk of uterine tachysystole and uterine rupture.
For these reasons feto-maternal monitoring is required
less and, hence, a preferred in previous cesarean cases for METHODS OF INDUCTION OF LABOR
labor induction. All methods of cervical ripening also do Physical methods
labor induction as well. Surgical methods
Prostaglandins: PGE1 and PGE2 (dinoprostone) (Figs Pharmacological methods.
28.1A and B) have been used commonly via various routes.
PGE1 (misoprostol, a synthetic PGE1 analogue) is widely Physical Methods
used for cervical priming. It can be administered via oral/ Stimulation of nipple
sublingual/intravaginal route. Clinical experiences with this Giving hot bath
A B
Figs 28.1A and B: PGE2 cervical gel

part directly presses on the cervix making it to dilate. It is

an effective way to induce labor in carefully selected cases
with a high Bishop score. Once performed it commits the
obstetrician to delivering the patient, hence, it should
be performed when chances of success of induction of
labor are high. Amniotomy alone would result in vaginal
delivery in most women with good cervical score but with
an unfavorable cervical score it has to be combined with
oxytocic agents for good response. There are inadequate
evidences on safety and efficacy of amniotomy alone for
induction of labor.
Technique
Fig. 28.2: Extra-amniotic saline infusion
It should be properly timed. The patient should be
instructed to empty her bladder, then the abdominal
Castor oil enema findings confirmed and fetal heart sounds (FHS) checked.
Sweeping of membranes The lie should be longitudinal with cephalic presentation
Extra-amniotic balloon catheter inflation
and an adequate pelvis. Preferably the fetal head should
Extra-amniotic saline infusion
be fixed or if free, stabilized by an assistant. Make no effort
Laminaria.
to strip the membranes or to displace the head upward to
Sweeping of fetal membranes is digital separation
draw liquor. Rule out cord presentation. The forewaters
of chorioamniotic membranes from the lower uterine
are then ruptured with a Kocher’s forceps under aseptic
segment, which result in significant increase in phospho
precautions and the liquor drained out slowly. The color
lipase A2 activity and endogenous prostaglandins F2 alpha
of the liquor and the presence of any blood or meconium
levels. If the cervix is favorable and patient is near term,
is noted. The time of ARM is noted. FHS are again
she is likely to go into labor. However, with an unfavorable
checked and recorded after the procedure to rule out cord
cervix the response is poor with this method. Membrane
sweeping is recommended by WHO (World Health compression.
Organization) for reducing formal labor induction as it
increases the likelihood of spontaneous labor within 48
Contraindications
hours (moderate quality evidence, strong recommendation) Intrauterine device, unless the patient is in active labor
but sweeping alone is not recommended as method of High presenting part.
induction labor. Further stripping of membranes is not
routinely recommended by ACOG (American College of Disadvantages
Obstetricians and Gynecologists) as it has an unpredictable Failure of the technique especially if the cervix is unripe.
efficacy, is associated with the risk of maternal and fetal Fetal distress or fetal death due to the cord prolapse,
infection, can cause bleeding from unsuspected placenta injury to the fetus or rupture of vasa previa (causing
previa and membranes can be accidentally ruptured. In excessive fetal bleeding).
addition it cannot be done when the cervical os is closed. Risk of intrapartum chorioamnionitis in the mother
Among all mechanical methods, balloon catheter inflation and infection of the fetus causing neonatal septicemia
(Fig. 28.2) is recommended by WHO for labor induction or pneumonia with the potential of neonatal death due
(moderate quality evidence, strong recommendation). to prolonged rupture of membranes.
Evidence related to use of laminaria are low quality. Accidental hemorrhage can occur due to separation of
the placenta when there is sudden decompression of
Surgical Methods the uterus especially in patients with polyhydramnios.
Amniotomy Dry labor can occur due to the drainage of liquor.
Amniotomy or artificial rupture of the membranes (ARM) The uterus loses its expulsive efficacy, becomes more
induces labor by the release of prostaglandins from the irritable leading to a constriction ring and infection.
membranes, causing the cervix to dilate. The presenting This can result in fetal distress.
TABLE 28.2: Labor stimulation with oxytocin and fetal hypoxia. Once good contractions (50–60 mm Hg by
Starting dose Incremental internal monitor) for 40–60 seconds (by external monitor)
Regimen (mIU/mL) dose (mIU/mL) Interval (min) are achieved at 2.5–4 minutes interval, do not increase
Low dose 0.5–2 1–2 15–40 oxytocin concentration any further (Table 28.2).
High dose 6 3–6 15–40
Side Effects
Uterine tachysystole—when uterine contractions are
Pharmacological Methods

occurring at a frequency of more than 5 contractions

Oxytocin in 10 minutes, averaged over a 30 minutes window. It
It is the most widely used pharmacologic agent for should always be qualified as to the absence or presence
induction of labor. It can be used by the intravenous route, of fetal heart rate decelerations. This may be due to an
as a nasal spray or as buccal tablets. The most commonly excess dose of oxytocin or to an inherent increased
used method is the intravenous infusion and as there myometrial susceptibility to it. The half-life of oxytocin
are considerable variations in the sensitivities of the is only 3–4 minutes, hence, hyperstimulation can be
individuals to oxytocin, its dose is titrated according to the corrected by decreasing or stopping the oxytocin drip.
uterine contractions. The ACOG recommends any of the low Additional measures include maternal posture change
or high dose oxytocin regimen as shown in Table 28.2. High to left lateral, oxygen inhalation, intravenous fluids and
dose regimen shows shorter induction-delivery interval sometime tocolysis is required.
as compared to low dose, delivery is faster and decreased Rupture of the uterus due to injudicious use of oxytocin.
chances of chorioamnionitis and cesarean section for Antidiuresis can be induced at high dose usually in
dystocia but increased incidences of uterine tachysystole excess of 40 mIU/min. This can cause water intoxication
associated with FHR changes. Oxytocin generally is diluted characterized by nausea, vomiting, confusion, convul
10 units in 1000 mL of an isotonic solution to form a solution sions and coma.
10 mIU/mL concentration. This solution is administered Amniotic fluid embolism: This is rare but often this
preferably by an microinfusion pump (Fig. 28.3). Escalating fatal complication can occur when strong uterine con
dose of oxytocin is increased periodically till satisfactory tractions squeeze the amniotic fluid into the maternal
uterine contractions are established and escalating dose of circulation.
oxytocin is maintained. The dose escalation may be done Fetal compromise (distress): Due to tetanic contrac
by the arithmetic method or by the geometric method. In tions of the uterus. In such cases, the oxytocin drip is
the former, the dose is increased more slowly at a fixed rate stopped immediately.
but in the latter the dose is doubled every 30 minutes till Neonatal hyperbilirubinemia: This risk is small if the
adequate uterine activity is attained. The geometric method total dose of oxytocin does not exceed 20 units.
is associated with a higher incidence of uterine tachysystole Psychological effects may occur due to fear and anxiety
especially if induction is prolonged and difficult.
Increased chances of postpartum hemorrhage due to
oxytocin receptor downregulation.
Hypotension following rapid intravenous infusion.
Prostaglandins
PGE1 (misoprostol) can be given orally/sublingually/
intravaginally 25 or 50 microgram tablet can be used 3–6
hourly. In cases of less gestational period like before 28
weeks, misoprostol by vaginal route is the most efficient
agent for inducing labor irrespective of cervical score.
Also in cases of IUFD of less than 28 weeks of gestation
vaginal misoprostol is most effective in labor induction
and the doses are 200–400 mcg every 4–12 hours. It should
be avoided in cases of scarred uterus, as incidences of
Fig. 28.3: Microinfusion pump ruptured uterus are increased. PGE2 is effective by the oral
route and causes less nausea and vomiting. In a typical Flowchart 28.1: Induction of labor
regimen, oral PGE2 is started in a dose of 0.5 mg/hour. The
dose is increased every 4 hours by 0.5 mg till 1.5–2 mg/
hour. This treatment is continued till labor is established.
Further dose is adjusted according to the uterine activity
and cervical dilatation. With an unfavorable cervix, two
PGE2 vaginal pessaries inserted 4–6 hours apart followed
by induction with amniotomy/oxytocin gives good results.
Vaginal application of 0.5 mg of PGE2 has become very
popular due to ease of administration and high efficacy.
Dinoprostone comes pre-packed in a single dose syringe
containing 0.5 mg PGE2 in 2.5 mL of a viscous gel of colloidal
silicon dioxide in triacetin. It is applied intracervically/
intravaginally at a dosage interval of 6–12 hours. Maximum Abbreviation: PGE2—Prostaglandin E2
1.5 mg dinoprostone can be given in 24 hours.
If hyperstimulation occurs following induction with Per vaginal examination:
prostaglandins, it can be reversed by using tocolytics like • Pelvis adequate. If pelvis is inadequate—consider
terbutaline in a dose of 0.25 mg in 5 mL of saline given lower segment cesarean section (LSCS).
intravenously over 5 minutes. • Assess the cervical score for induction (Flowchart 28.1).
The uterotonic action of prostaglandins is more
physiological than oxytocin. The initiation of labor is slow MONITORING OF LABOR
to occur but once it is established its progress is smooth
and uninterrupted. The uterine contractions increase in
DURING INDUCTION
intensity, frequency and duration and the uterine tone Induction of labor demands intensive maternal and fetal
is not elevated and the uterine blood supply is preserved monitoring as it deals with pregnancy at risk. Its successful
during the relaxation phase. outcome depends on the state of the cervix, the ability to
achieve effective uterine contractions and the prevention
Side Effects of fetal hypoxia and maternal distress. In addition
Uterine hypertonus. It occurs in 0.5–2.0% of cases. Uterine facilities for blood transfusion and operative intervention,
rupture. anesthesia and special nursing care should be available.
Gastrointestinal symptoms—nausea, vomiting and Monitoring and precise control of parturition can be
diarrhea. achieved by keeping a partogram and inductogram. In
Flushing, headache and fever. this the details of maternal vital statistics, uterine activity,
descent of presenting part, FHR, cervical dilatation and
Relaxin effacement and station of the presenting part of the fetus
Relaxin is a polypeptide hormone produced in human are recorded at periodic intervals. A record is also kept of
corpus luteum, decidua and chorion. Purified protein the input and output chart and of the various drugs like
relaxin 2 mg in tylose gel, is given either vaginally or intra oxytocic agents or analgesics given to the patient. Narcotic
cervically. Cervical ripening occurs in 80% of cases, labor analgesics when judiciously used keep the patient sedated,
starts within 12 hours. cooperative and prevent premature expulsive efforts and
assist in delivery. One should keep in mind that if narcotics
are given to the mother it can cause respiratory depression
PROTOCOL FOR INDUCTION OF LABOR in the neonate and the pediatrician should be informed
Need for induction—an indication well in advance.
Proper selection of patient Fetal wellbeing can be ascertained by intermittent
Take informed consent auscultation of the FHS or by continuous electronic FHR
History monitoring and by the study of fetal acid-base status by
General physical examination using fetal scalp blood sampling (if available). ARM or
Systemic examination amniotomy is done when the cervix is 4 cm dilated. See
Abdominal palpation—confirm lie and presentation also the color of liquor, and check FHS after ARM.
Uterine rupture
RISKS AND COMPLICATIONS

Antepartum hemorrhage (APH) from undiagnosed

OF INDUCTION OF LABOR placenta previa/rupture of vasa previa.
Iatrogenic prematurity of fetus—an accurate deter Complications specific to each method are discussed above.
mination of gestational age of fetus is mandatory
Precipitate labor may result FAILURE OF INDUCTION
During amniotomy injury/compression/prolapse of
cord may occur accidently Implies those cases in which the uterus failed to establish
Injudious administration or inadequate observation of adequate uterine contractions along with progressive
pharmacological agents during induction could lead to cervical changes despite using a method of labor induction
fetal distress or even fetal death in utero or delivery of a correctly along with adequate waiting period. Failed
baby with poor Apgar score induction does not necessarily indicate cesarean section.
Increased incidences of operative interference (instru Sometime, if one method fails the other method may be
mental vaginal deliveries/cesarean section) used taking care of maternal as well as fetal conditions.
Uterine tachysystole with or without associated FHR Induction-delivery interval is a good indicator of the
changes success of induction. It is the time between the start of
Increased chances of chorioamnionitis (more with induction and the time of delivery. As this interval increases
mechanical methods) chances of failure increases. Those methods which have
Increased incidences of postpartum hemorrhage short average induction-delivery interval show low rate of
Abruptio placentae induction failure.
1. What is the method of induction of labor?
2. Explain monitoring of labor during induction?
i. ____________ is a critical component of normal vaginal delivery.
ii. Dry labor can occur due to the ____________ of liquor.
iii. Mechanical methods include ____________ dialatation and stripping of ____________.
iv. Antidiuresis can cause ____________ characterized by nausea, vomiting, confusion, convulsions and coma.
29
PK Verma
Obstetric
Analgesia and Anesthesia
labor), decrease in uterine blood flow, fetal asphyxia,

GENERAL OBJECTIVES
detrimental changes in the fetal cardiovascular system
The purpose of this chapter is to prime the students about and acid-base status. Effective pain relief by various
the management of pain in labor and of anesthesia for the means have been shown to attenuate elevations of these
delivery of the fetus. While the students are not expected hormones, and to decrease the detrimental effects of these
to practice various techniques of labor analgesia or to hormones on the mother and the fetus.
administer anesthesia, a comprehensive knowledge about
these can allow them to understand the indications, merits, LABOR PAIN IS UNIQUE
demerits, degree of acceptance and various complications
of these techniques. Moreover, they should understand The relief of pain in labor (as compared to a non-pregnant
the importance of supine hypotension (aortocaval patient) presents a few unique problems, which include:
compression) syndrome, aspiration pneumonitis In a non-pregnant patient undergoing surgery, only
(Mendelson syndrome), and maintaining oxygenation in one patient is there for consideration, but during labor,
a pregnant patient. This will help them to approach these one need to care about fetus-infant also, who is highly
patients with confidence and prepare them optimally sensitive to various sedatives and anesthetic drugs.
before these techniques/procedures can be administered/ Duration of anesthesia for a surgical procedure is
performed. The students should also know how the generally short (1–4 hours) but analgesia for labor may
management of a cardiac arrest in a pregnant woman is last upto 12–14 hours.
different from a nonpregnant adult patient. Very often, there is either less time or no time to prepare
these patients. They are, by the very nature of the pregnant

WHY TREAT LABOR PAIN? state, more prone to gastric aspiration and increased
Very often cinema scenes of women clutching at bedposts morbidity and mortality during obstetric anesthesia. This
and emitting blood-curdling screams, plus discussion is because there is delay in gastric emptying and relaxed
with those who have given birth, are among the sources esophagogastric (cardiac) opening.
The various agents used for analgesia and anesthesia
of the nullipara’s expectations about labor pain. In
fact, this may be the only pain which is considered should not affect the progress of labor or cause relax-
physiological. Labor may subject the nulliparous woman ation of the uterus giving rise to an increased incidence
to the most severe pain and stress that she has ever of postpartum hemorrhage (PPH).
experienced. It is associated with (same responses as Although anesthesia is mandatory for a major surgery, it
for other types of pain, surgical stress or even hypoxia) is not for a normal vaginal delivery. In fact, the primary
prolonged increase in plasma cortisol levels in early labor concern of every parturient is a healthy infant, even if it
and increase in adrenocorticotropic hormone (ACTH), is at the cost of some discomfort.
cortisol, epinephrine, nor epinephrine and β-endorphins Therefore, the agent/technique used should be comp
throughout labor. These hormones in turn produce various letely harmless, safe and should cover not only labor
effect which include relaxation of the uterus (prolonged (analgesia) but also delivery (anesthesia). Unfortunately,
there is no single agent/technique which meets all the

requirements. Therefore, very often a combination of
various modalities is used.
HOW DID LABOR ANALGESIA AND

ANESTHESIA START
The knowledge that it is possible to alleviate the pain
of labor dates far back to early Chinese writings. The
first recognized obstetric anesthesia, using ether, was
administered by Dr James Young Simpson in 1847, but
perhaps it was not until John Snow in 1853 administered
chloroform to Queen Victoria for the birth of Prince
Leopold that obstetric anesthesia and analgesia gained
popularity and respectability.
ANALGESIA AND ANESTHESIA

Analgesia refers to the loss or modulation of pain
perception and could be local, affecting only a small area of
the body; regional, affecting a larger portion; or systemic.
Anesthesia refers to the total loss of sensory perception,
and may include loss of consciousness. In obstetrics,
regional anesthesia is accomplished with local anesthetic
techniques (epidural, spinal). General anesthesia is given, Fig. 29.1: Anatomy of pain during labor
with systemic medication and endotracheal intubation.
Since the word ‘anesthesia’ includes various compo Pattern of Labor Pain (Fig. 29.2)
nents like analgesia, amnesia, muscle relaxation, and loss
of reflex response to pain, analgesia can be regarded as In an average normal labor, contractions usually become
one of the components of anesthesia. painful when the cervix is dilated 3–4 cm, and the intensity
of the pain increases as cervical dilatation proceeds. The
last quarter of the first stage may be accompanied by severe
ANATOMY OF PAIN (FIG. 29.1) pain. After full dilatation of the cervix, the pain changes in
Pain in the first stage of labor is because of the ischemia character. The distention and stretching of the perineal
of the uterus during contractions as well as dilatation and tissue, due to the descending of the presenting part causes
effacement of the cervix. Sensory pathways that convey sensation of pressure and pain, and an intense urge to
nociceptive impulses of this stage are the uterine plexus, bear down with contractions. The patient feels the pain of
the inferior, middle, and superior hypogastric plexus, the intense contractions not in the uterus but as a colicky pain
lumbar, and lower thoracic sympathetic chain, and the across the lower abdomen. It is also frequently referred
T10–L1 spinal segments.
to the back and sometimes radiates down the thighs. The
Pain in the second stage of labor is produced by the
factors that influence the severity of labor pain are:
distension of the pelvic floor, vagina and perineum by the
Physical, e.g. intensity and duration of uterine contra
presenting part of the fetus. Sensory pathways from these
areas are conveyed mainly by branches of the pudendal ctions, resistance of the cervix to dilatation, the resis
nerve via the dorsal nerve of the clitoris, the labial nerves, tance to distension of perineal tissues, presence of any
and the inferior hemorrhoidal nerves. These major sensory cephalopelvic disproportion, and occipitoposterior
branches to perineum convey pain along nerve roots position of the fetal head, which can produce a most
S2–S4. Other nerves like the ilioinguinal nerves, the genital distressing backache and the patient’s tolerance of pain.
branches of the genitofemoral nerves, and the perineal Psychological factors, e.g. cultural patterns and customs
branches of the posterior femoral cutaneous nerves may (a noisy patient may not necessarily be having more
also plays a role in some patients. pain), education and emotional preparedness for labor
Obstetric Analgesia and Anesthesia 261
Fig. 29.2: Pattern of labor pain
(fear, apprehension, ignorance, and loneliness lower percentage of patients and are time consuming. Further,
the tolerance), and the attitude of the doctors, nurses, some additional measures for pain relief are required in
and attending staff towards the patients. the late stages of labor and during childbirth. Hypnosis
refers to a state of altered consciousness in which the
LABOR ANALGESIA profound concentration causes reduced awareness of
the pain of labor. It is time consuming and results are not
While providing pain relief, the technique chosen should encouraging. Acupuncture and transcutaneous electrical
be simple and safe, both for the mother and the fetus. The nerve stimulation (TENS) are other techniques which
patient should be closely monitored throughout the labor. have been used to provide pain relief. These are of limited
value in labor pain.
Non-Pharmacological Means of
Providing Pain Relief Injectable Pharmacological Agents
Fear of the unknown potentiates pain. Various techniques Parenterally injected agents raise the patient’s pain
have been developed that aim at reducing anxiety, tension threshold, produce amnesia, sedation, or reduce
and fear. These techniques also aim at educating/helping apprehension and anxiety. The ideal drug should have
the parturient about/understand the various physiological an optimal beneficial effect on the mother with no or a
changes occurring during labor and delivery. In addition, minimal depressant effect on the fetus-neonate. None
they provide an opportunity for closer understanding of the available narcotic/sedative drugs have a selective
and communication between the patient and her mate, effect on the mother. Usually sedatives, tranquilizers and
who may be an important source of comfort to her analgesics are given by intramuscular (IM) injection.
during the stressful period of childbirth. Such techniques Sometimes, the intravenous (IV) route is preferred. The
include “natural childbirth” developed by Grantly Dick- advantages of intravenous administration are prompt
Read in the early 1930’s, and psychoprophylaxis, initially onset of effect and ability to titrate the dose to response,
developed by Velvovski in Russia in 1950 and later on thereby avoiding the peak effect of an intramuscular
introduced in France by Lamaze in 1970. These techniques bolus. The disadvantage of an intravenous route is the
provide variable amount of pain relief with effectiveness depressant effect of an overdosage, but the use of smaller
ranging from 10 to 20% to as high as 70–80% in a small doses at more frequent intervals can overcome this
disadvantage. A number of drugs like opioids (morphine, particularly in early labor, has been demonstrated. It is
fentanyl) can also be administered by patient controlled used for patient-controlled analgesia in the bolus dose
infusion. The advantages of this method include the sense of 0.2–0.8 µg/kg, low dose initially, the titrated to effect;
of autonomy, which patients appreciate, more consistent however, common side effects (i.e. maternal sedation,
effect, and the reduced dosages of the drugs required. respiratory depression) warrant vigilance during use.
Sedatives, anxiolytics and tranquilizers—benzodiaze-
Narcotic Analgesics pines (diazepam, midazolam, lorazepam) and phenothia
Morphine, 2–3 mg IV, 5–10 mg IM; Pethidine, 25–50 mg zines (promethazine and barbiturates) are used.
IV, 50–75 mg IM; Fentanyl 25–50 mg IV, 50–100 mg IM; These agents do not possess analgesic properties. They
Butorphanol 1–2 mg IV, 1–2 mg IM; Tramadol 50–100 mg cross the placenta freely, and except for benzodiazepines,
IV, 50–100 mg IM, remifentanil. do not have known antagonists. They are most often used
All these agents produce good pain relief with a sense in early labor to relieve anxiety or to augment the analgesic
of euphoria for a variable period of time usually lasting properties and reduce the nausea associated with narcotic
1–4 hours. However, these agents also produce respiratory analgesics.
depression in both the mother and the newborn. The
degree of respiratory depression is usually comparable for Benzodiazepines
equipotent analgesic doses. These drugs also frequently Because diazepam causes fetal hypotonia, hypothermia,
cause sedation or nausea and occasionally, an acute and a loss of beat-to-beat variability in the fetal heart rate,
state of confusion. Nevertheless, when used judiciously it is rarely used during labor. Midazolam, a shorter-acting
and appropriately, they can be safe and effective. In drug, appears to be devoid of these effects and is more
general longer-acting agents (morphine, pethidine) are rapidly cleared. Its exact place in labor pain relief is yet to
more appropriate in early first stage of labor, since pain be established.
relief is needed for longer periods of time and delivery
is distant. Shorter acting agents (e.g. fentanyl) may be Phenothiazines
more appropriate during transitional labor when the Promethazine (12.5–25 mg IM) is perhaps the most widely
need for pain relief is brief and delivery is imminent. used phenothiazine and when given in small doses in
Fentanyl is usually administered as an infusion or with combination with an opioid, does not seem to produce
a patient-controlled device. Its rapid onset (peak effect, additional neonatal depression. However, larger doses
2–4 minutes), short duration of action (30–600 minutes), should be avoided.
and lack of active metabolites make it attractive for labor
analgesia. Fentanyl causes less neonatal depression than Barbiturates
pethidine. If any respiratory depression is seen in the Because of their effect on the fetus causing central nervous
newborn, it can be reversed using naloxone. system depression, periodic apnea and even abolition of all
Tramadol has lower efficacy and more side effects than movements, and because of their anti-analgesic properties,
with pethidine. their use for obstetric analgesia is no longer recommended.
In general, the efficacy of systemic opioid analgesia and
the incidence of side effects are largely dose dependent Inhalational Analgesia
rather than drug dependent. It involves administration of the analgesic gases or
Remifentanil is a synthetic drug with selective activity volatile agents in subanesthetic concentrations via a mask
at µ-opioid receptor, low lipid solubility, and a low volume held by the patient to relieve the pain associated with
of distribution. Remifentanil undergoes rapid hydrolysis uterine contractions. Various agents (trichloroethylene,
by nonspecific plasma and tissue esterases to an inactive methoxyflurane) have been used in the past, but are
metabolite, resulting in short elimination half-life of not available presently. Nitrous oxide, an inhalational
approximately 9.5 minutes. The effective analgesia half- anesthetic, is an analgesic at low concentrations and is
life is 6 minutes, thus allowing effective analgesia for available as the 50:50 prepared mixture of nitrous oxide with
consecutive uterine contractions. The rapid elimination oxygen (Entonox). Entonox can produce acceptable levels
of remifentanil also reduces the propensity for neonatal of analgesia of approximately the same order as pethidine.
respiratory depression compared to that with longer- However, experience is needed to use this drug safely, as
acting opioids. The analgesic efficacy of remifentanil, pregnant patients are sensitive to its anesthetic effects.
Other agents that have been tried in the recent years total dose of anesthetic, (2) decreased motor blockade, (3)
are the volatile anesthetic agents sevoflurane (Sevox) reduced shivering, and (4) greater patient satisfaction.
isoflurane and enflurane. Sevoflurane appears to be
the best suited inhalational agent for labor analgesia, Caudal Analgesia
because of its short onset and offset of action and can be It refers to the introduction of local anesthetic solution into
administered as patient-controlled inhalational analgesia the epidural space through the sacrococcygeal membrane
in the concentration of 0.8% with oxygen. Routine use (as compared to through the space between two adjacent
of inhalational analgesia may be limited by the need vertebral spines in epidural analgesia). It is rarely used for
for specialized equipment, concern for environmental labor analgesia because of the high rate of complications.
pollution, and the potential for maternal amnesia and the Lumbar epidural analgesia is considered a safer alternative.
loss of protective airway reflexes.
Spinal Analgesia
LOCAL ANALGESIA It refers to injection of local anesthetic solution into
It refers to infiltration or deposition of a dilute solution of a subarachnoid space and has been and is being used
local anesthetic agent to achieve analgesic effect in a small widely for anesthesia in the second stage of labor. Its use
area, e.g. local infiltration of the perineum, or pudendal for analgesia in the first stage of labor is limited by the fact
nerve block. Advantages of local analgesia include: that it is usually a single injection and therefore, of limited
Simplicity of administration, duration. It provides good anesthesia for operative vaginal
No interference with uterine contractions, delivery or removal of retained placenta.
Minimal toxic effects, and These blocks can be tailored to the individual’s needs
When used optimally, no increase in maternal and fetal and expectations, the stage of labor (by titrating the
morbidity and mortality. concentration, and volume of local anesthetic, and the
However, it cannot be used to treat the pain of the first position of the patient), the degree of pain and the need
stage of labor. It is used mainly to perform an episiotomy for operative delivery. Recent modifications with these
or for simple outlet forceps delivery, or after delivery, into techniques include ambulatory epidurals, combined
the site of lacerations to be repaired. spinal-epidurals, continuous intrathecal opiates and
patient-controlled analgesia.
REGIONAL ANALGESIA (OR NEURAXIAL Recent advances in neuraxial analgesia are tabulated in
Table 29.1.
ANALGESIA)
Regional analgesia includes epidural, caudal and spinal Disadvantages
analgesia. Although epidural or combined spinal-epidural analgesia
is considered by many to be the ideal analgesia technique,
Epidural Analgesia there are many disadvantages also. These include
It refers to the introduction of a local anesthetic solution hypotension, local anesthetic toxicity, high or total spinal
into the epidural space (outside the dura) which lies anesthesia, neurologic injury, spinal headache and allergic
between the ligamentum flavum and the dura mater. Once reaction. Administration of local anesthetic agent must be
deposited in the epidural space, the local anesthetic agent followed by appropriate monitoring for adverse reactions,
penetrates the dural cuffs surrounding the nerves and and equipment and personnel to manage these reactions
blocks the fully formed spinal nerves. This route can be must be immediately available. Steps to prevent various
used both for labor analgesia and for providing anesthesia complications include infusion of 500 to 1000 mL of a
during operative delivery. Presently, opioids especially balanced salt solution before performing the block, taking
fentanyl, are added to the local anesthetic solution to all aseptic precautions while performing the block. In cases
increase the effectiveness of the block and to decrease the of hypertensive disorders using small gauge, Whitacre
dose of local anesthetic agent. spinal needle and avoiding multiple punctures, use of as
Epidural labor analgesia is usually initiated with the little dose as possible of local anesthetic agent, avoiding
bolus injection of a local anesthetic combined with a lipid- intravascular injection of the drug, preventing completely
soluble opioid. The advantage of the addition of an opioid supine position, and use of ephedrine to treat hypotension
to an epidural solution of local anesthetic include (1) lower at an early stage. Fluid infused must be monitored properly.
TABLE 29.1: Recent advances in neuraxial analgesia recommended doses, and these should not be exceeded.
In fact, the correct dose of any local anesthetic agent is
Technical advances
zz Combined spinal epidural analgesia
the smallest quantity of drug in the greatest dilution that
zz Continuous spinal analgesia using microcatheters will provide adequate analgesia. Also important to keep in
zz Ambulatory epidurals concept of minimum local anesthetic mind that injection of drug into a highly vascular area will
volume (MLAV) and minimum local anesthetic doses (MLAD)*, result in more rapid systemic absorption than, for example,
low dose and ultra low dose epidurals.
injection into the skin. To prevent too rapid absorption,
Pharmacological advances epinephrine in a final concentration of 1:200,000 is added
zz Ropivacaine, levobupivacaine**
which act by producing local vasoconstriction.
zz Newer opioids: Sufentanil, fentnyl**, remifentanil
zz Adjuvants: Clonidine and neostigmine***

To sum up, phase I (early labor) of stage I should be
managed by simple reassurance and verbal commentary
Technological advances
zz Availibility of ultrasound to facilitate localization of epidural
if the patient has been educated in the antepartum period.
space, minimizing failures Options available to manage phase II of stage I include
zz Patient-controlled epidural analgesia regimes segmental epidural block, a sedative—hypnotic, a narcotic
* With the emerging concept of low dose and MLAV and KLAD; all
or a tranquilizer drug and continued reassurance. The
present-day labor epidurals are low-dose epidurals, resulting in accentuated phase of labor (phase III of stage I) may be
reduced total dose of local anesthetic and side effects, such as handled by segmental epidural block, a combination of
motor blockade. tranquilizer and analgesic or a caudal epidural block with
** There are no clinically significant difference among the three
continued reassurance. During the second stage of labor,
commonly used long-acting amide local anesthetics (bupivacaine,
ropivacaine, levobupivacaine) nor between fentanyl and sufentanil. either spinal block can be used or if epidural technique is
*** Adjuvants such as clonidine may prove useful in selected patients, already utilized for first stage pain relief, top up of the drug
but they currently do not offer any significant advantage to low- may be given through the indwelling catheter to cover the
dose local anesthetic/lipid-soluble opioid combination.
second stage of labor.
Use of diazepam, or thiopentone to treat convulsions, ANESTHESIA FOR CESREAN SECTION

administration of oxygen or assistance to respiration may
be required in case of local anesthetic toxicity. The choice of anesthesia for cesarean section depends
on the reason for the operation, the degree of urgency,
and the desire of the patient and as anesthesiologist.
LOCAL ANESTHETIC AGENTS (TABLE 29.2)
Epidural or spinal anesthesia for caesarean section allows
These agents inhibit the transient increase in permeability the mother to be awake, minimizes or completely avoids
of excitable membranes to sodium ions, thereby producing the problem of maternal aspiration, and avoids neonatal
a temporary inability of the nerve fibers to transmit the drug depression from general anesthesia. Statistics show
nerve impulse. Conduction of all types of axons is blocked, that spinal/epidural anesthesia is preferred by many
but fibers of small diameter are usually more susceptible anesthesiologists over general anesthesia for cesarean
to local anesthetics and are slower to recover than fibers section. In pre-eclampsia, eclampsia there may be edema
of larger diameter. All local anesthetics have maximal of the glottis causing difficulty in intubation.
TABLE 29.2: Local anesthetic agents commonly used in obstetrics

Anesthetic agent Usual concentration (%) Onset Average duration (min) Toxic dose (mg/kg) Clinical use
Xylocaine 0.5 Rapid 30–60 Plain (3–4) Local infiltration or
2 60–90 With epinephrine pudendal block
5 45–60 (6–7) Epidural for cesarean
Spinal for cesarean
or puerperal tubal
ligation
Bupivacaine 0.5 Slow 90–150 1.5 Epidural for cesarean
0.0125, 0.25 60–90 Epidural for labor
0.5 60–120 Spinal for cesarean
In contrast to regional (epidural/spinal) anesthesia, Aspiration of gastric contents (Pulmonary aspiration,

general anesthesia has the advantages of a more rapid Mendelson’s syndrome): Acid pulmonary aspiration
induction, less associated hypotension and cardiovascular should be suspected in any patient who presents with
instability and better control of the airway and ventilation. symptoms similar to those of an acute asthmatic attack
General anesthesia may be preferable in patients with with cyanosis, tachycardia, tachypnea, hypotension,
acute severe fetal distress (with epidural catheter not in hypoxia, with wheezes, rales, and rhonchi heard over the
situ), relative or absolute contraindication to regional affected areas of the lungs. Recommended therapy for
anesthesia (e.g. hemodynamic instability, co-existing symptomatic aspiration includes:
maternal cardiac disease, coagulopathy, or infections), Intubation and positive pressure ventilation with
or in those patients who refuse regional anesthesia or are positive end-expiratory pressure (PEEP).
terrified of needles in the back. Oxygen supplementation to maintain oxygen saturation
above 90%.
Maintaining fluid balance and use of vasopressors in
HIGH-RISK CASES case of hypotension.
Whichever type of anesthetic is used for whatever proce- Bronchoscopy only if needed to clear food from the
dure, there are some basic points in maternal preparation airway.

that are common to all anesthesia techniques. Rigid maintenance of asepsis.
There is no role of bronchial lavage, prophylactic anti

Maternal Starvation and Antacid Therapy biotics and steroids.
All patients in the labor ward should be considered as
having full stomach and at high-risk of aspiration. Factors Aortocaval Compression
contributing to this are raised progesterone levels delaying (Supine Hypotension Syndrome)
gastric emptying and the term uterus causing an increase (Figs 29.3A and B)
in intra-abdominal pressure. It has been traditional for Compression of the inferior vena cava and the aorta by
mothers in labor to be kept starved just in case they the abdominal contents occurs rarely in non-pregnant
should require an anesthetic. However, current practices patients but almost universally among parturients. The
allow the intake of clear fluid throughout labor. It is also a inferior vena cava is an easily collapsible blood vessel that
universal practice that prior to an anesthetic, be it general frequently gets caught between a rock (the gravid uterus)
or regional, something should be given to reduce the and a hard place (the maternal vertebral bodies). Various
volume and the pH of the gastric contents. Gastric acid factors which increase the incidence and severity of aorto-
production can be eliminated by giving an H2 receptor caval compression are supine position, hypovolemia,
antagonist (ranitidine). Sodium citrate 30 mL of a 0.3 M spinal or epidural anesthesia (induce a form of distributive
solution should be administered less than 30 minutes hypovolemia) and uterine contractions. It is routinely
before induction of anesthesia in order to decrease the avoided by ensuring that the mother is never allowed to
acidity of gastric contents rendering them less damaging lie flat on her back, but is always kept in a lateral or tilted
to the pulmonary alveolar lining. Metoclopramide is also position (by inserting a wedge under the hip) prior to
recommended to improve gastric emptying, increase and during surgery and by infusion of balanced salt or
gastroesophageal junction pressure and decrease colloid solution intravenously. Leg wrappings and use of
intraoperative nausea and vomiting. In cases where general vasopressors may also be required in an emergency.
anesthesia is necessary, additional prophylaxis includes
rapid sequence induction with cricoid pressure, preceded Intravenous Access
by pre-oxygenation. Cricoid pressure (Sellick’s maneuvre) Massive hemorrhage in obstetrics often occurs with very
should be maintained by an assistant from the time of little warning and the importance of inserting a large bore
induction until an endotracheal tube has been inserted intravenous cannula (16G) before starting any form of
and the cuff inflated. Pressure on the cricoid cartilage will anesthetic cannot be overstressed.
compress the esophagus and prevent passive regurgitation
of gastric contents. This method is only to be used on a Postoperative Period
paralyzed patient. The patient should be extubated only The extensive intraoperative monitoring should continue in
when protective airway reflexes have returned and should the immediate postoperative period with special emphasis
be nursed in the lateral position postoperatively. on the management of pain, fluid balance and oxygenation.
A B
Figs 29.3A and B: A. Inferior vena cava (IVC) and aorta (Ao) compressed by the enlarged uterus when the gravida lies supine;
B. Lack of IVC and Ao compression with a wedge under the gravida’s hip
Bretylium is the drug of choice when dealing with ven-

CARDIAC ARREST
tricular tachycardia/fibrillation caused by bupivacaine

Management of cardiac arrest in a pregnant patient is overdose. The dose is 5 mg/kg intravenously every
slightly different from that in a non-pregnant patient in a 30 seconds to a maximum dose of 30 mg/kg.
Defibrillation paddles are best placed in the anterior-
number of ways.
posterior (not apex-sternum) position in the left lateral-
Prevention of any aortocaval compression is of great
tilted term patient with a large gravid uterus with
importance. pendulous breasts.
Arterial hypoxemia develops much more rapidly. The infant must be delivered expeditiously by cesarean
There is high-risk of pulmonary aspiration. section if advanced life-support resuscitation is not
Securing the airway can be much more difficult. rapidly successful.
1. Define the pattern of labor pain.
2. What is the anesthesia for cesarean section?
3. True/False:
i. Pain in the second stage of labor is produced by the distension of the pelvic floor, vagina and perineum.
ii. Spinal analgesia refers to introduction of local anesthetic solution into epidural space through the sacrococcygeal
membrane.
Section 5
Abnormal Labor
Section Outline
30. Abnormalities of the Passage
31. Malpositions and Malpresentations
32. Labor Dystocia: Dysfunctional Labor
33. Complications of Third Stage of Labor
30
Abnormalities of the Passage
The importance of the shape of the pelvis is that it

CAUSES OF ABNORMALITIES
influences the mechanism of labor. However, in the
Abnormalities of the obstetric passage may lead to diffi presence of even minor contraction in any of the three
culties in delivery. nongynecoid pelvis the labor can be adversely affected.
These can be due to the following causes:
Bony abnormalities (pelvic dystocia) or pelvic contraction Gynecoid Pelvis (Fig. 30.1)
Obstruction of the birth canal by soft tissue abnor
The gynecoid pelvis has a rounded inlet with a sacral
malities
angle more than 90° (sacrum is concave). The anterior and
Abnormalities of placental location.
posterior segments are almost equally spacious. The sacro-
sciatic notches are wide and the side walls are straight.
CONTRACTION OF PELVIS The ischial spines are not prominent. The sub-pubic angle
Pelvic contraction is reduction in one or more diameters of (arch) is wide. It is seen in 50% of women.
the pelvis to such an extent that the normal mechanism of This pelvis is the most favorable for uncomplicated
labor is adversely affected. vaginal delivery. However, even a round gynecoid pelvis
The contraction of the pelvis can be due to: can be contracted if the dimensions are small. This is then
Developmental variations in the size and shape of the
known as a generally contracted pelvis.
pelvis
Diseases affecting the skeletal system as a whole
Anthropoid Pelvis (Inlet is Oval) (Fig. 30.2)
Diseases affecting the spine
The anthropoid pelvis has an anteroposterior diameter of
Diseases affecting the lower limb and hip joint
the inlet, which is greater than the transverse diameter.
Injuries and diseases of the pelvis.
Developmental Variations of the Pelvis

Variations in Shape
Anatomical and radiological studies have shown that the
shape of the female pelvis can be divided into four groups
(Caldwell and Moloy):
1. Gynecoid (50%)
2. Anthropoid (25%)
3. Android (20%)
4. Platypelloid (5%).
However, most of the pelves are not pure but mixed
with characteristics of two parent types. For example, an
androgynecoid pelvis has a forepelvis which has gynecoid
features and a hind pelvis has android features. Fig. 30.1: Gynecoid pelvis
Fig. 30.2: Anthropoid pelvis Fig. 30.3: Android pelvis
Pelvic side walls are divergent and the sacrum is inclined

posteriorly. This type of pelvis usually tends to be deep
because the sacrum usually has six segments (high
assimilation pelvis-sacralization of lumbar vertebra). If this
pelvis is contracted it discourages transverse engagement
of the head. The head then engages in the occipito-anterior
or posterior position. If it engages in the occipitoposterior
position, then the long interval rotation does not take
place and delivery will be face to pubes (persistent
occipitoposterior).
Android Pelvis (Fig. 30.3)

Fig. 30.4: Platypelloid pelvis
The android pelvis is the one, which is most detrimental
to normal labor. The inlet is wedge (triangle) shaped. The
flattened in the upper portion with a sharp curve forwards
ischial spines are prominent, the sub-pubic angle (arch)
near its tip. If contracted it becomes similar to a rickety flat
is narrow and the sacrum is inclined anteriorly (sacral
pelvis. Deep transverse arrest is seen in this type of pelvis.
angle is less than 90°) in its lower third. The sacrosciatic
The engagement of head is difficult and direct pressure is
notches are narrow and deep and the side walls are
put on the bladder neck during a difficult engagement,
convergent. The outlet tends to be small with a short bi-
which can lead to vesico-vaginal fistula.
tuberous diameter. This type of pelvis is funnel-shaped
Besides these types the configuration of pelvis can be
with a diameter which decreases from above downwards.
disrupted by trauma (accidents) diseases (ricket, osteo
Persistent occipitoposterior and deep transverse arrest
malacia and tumors).
occur if not supervised. The posterior sagittal diameter
at the inlet is much shorter than the anterior one, which
limits the posterior space available to the fetal head.
Diseases Affecting the Skeletal System
Normal vaginal delivery is not possible. Hence, cesarean In this group the most important diseases are rickets and
section is done and because of this vesico-vaginal fistula is osteomalacia.
rare in android pelvis.
Rickets
Platypelloid Pelvis (Fig. 30.4) Rickets is a disease of early childhood when the bones are
The platypelloid pelvis is the rarest of all types. It has an soft. The child has a stunted growth and there is a general
inlet which is transversely oval and the transverse diameter contraction of the pelvis. There is flattening of the inlet and
is much bigger than the anteroposterior diameter. The the sacral promontary bulges forward giving a ‘reniform’
cavity is roomy and side walls are divergent. The sacrum is shape to the inlet.
Abnormalities of the Passage 271
Fig. 30.6: Scoliosis

Fig. 30.5: Kyphosis
Osteomalacia Injuries and Diseases of the Pelvis

The deficiency of calcium and vitamin D causes osteomalacia. Deformities of obstetrical significance may result from pel
This is more commonly seen in grand multiparas having poor vic fractures, chondroma, osteoma, chondrodystrophic
nutrition and following repeated pregnancies and lactation. pelvis, kyphotic and scoliotic pelvis, triradiate pelvis, exos
The sacral promontary is pushed downwards and toses and bony neoplasms (Figs 30.7 and 30.8).
forwards and the lateral pelvic walls inwards causing the To complete the list there are two pelves of historical
anterior wall to project like a beak. The shape of the pelvic interest. First is the Naegele’s pelvis. In this the sacral ala is
inlet becomes like a three cornered hat. not properly developed leading to asymmetry of the pelvis
(Fig. 30.9).
Diseases Affecting the Spine The second is Robert’s pelvis in which both the sacral
Kyphosis (Fig. 30.5) ala are absent (Fig. 30.10).
The site of the disease is important. A high dorsal kyphosis
is offset by a compensatory lordosis so that pelvic shape VARIATIONS IN SIZE
is unaltered. A low kyphosis encourages a pendulous The size of the pelvis is of utmost importance. If adequate,
abdomen with a tendency for outlet contraction. There is it will allow easy passage of the average fetal head whatever
extreme funneling of the pelvis in this case. is the shape of the pelvis. The contractions can be:
At the level of inlet
Scoliosis Mid-pelvis
Scoliosis can lead to pelvic asymmetry due to displacement Outlet of the pelvis
of acetabulum inwards on the weight-bearing side (Fig. Generally contracted pelvis.
30.6).
Inlet Contractions
Diseases Affecting the Lower Limb and Hip Joint The pelvic inlet is contracted if the obstetric conjugate, that
The diseases affecting the lower limb and hip joint can is the shortest anteroposterior diameter of the inlet, is less
be either congenital or acquired in childhood. Some of than 10 cm and transverse diameter is less than 12 cm or
the diseases which can lead to a contracted pelvis are both. This is because a fetus at term has a bi-parietal diameter
poliomyelitis, congenital dislocation of hip and tuberculous ranging from 9.5 to 9.8 cm. Clinically the inlet contraction
arthritis of the hip joint. is diagnosed by measuring the diagonal conjugate. If this is
Fig. 30.7: Triradiate pelvis Fig. 30.8: Tumor of bone causing deformity
Fig. 30.9: Naegele’s pelvis Fig. 30.10: Robert’s pelvis
less than 11.5 cm then inlet contraction is suspected. The 10.5 cm and the anterior-posterior diameter from the
patient with inlet contraction will have non-engagement lower border of the symphisis pubis to the junction of the
of head, slow progress of labor or secondary arrest. There fourth and fifth sacral vertebra which averages 11.5 cm.
is often early spontaneous rupture of membranes. The If the interspinous diameter is less than 10 cm then
inlet contraction is also associated with a high incidence of a contracted mid-pelvis is suspected, if less than 8 cm a
abnormal presentations, considerable molding of the fetal contracted mid-pelvis is diagnosed. The anterior sagittal
head, caput succedaneum formation and cord prolapse. diameter is 11.5 cm and posterior sagittal diameter is
5 cm. Mid-pelvis contraction is diagnosed on manual
Mid-pelvis Contraction examination. On pelvic examination mid-pelvis contraction
The important diameter of the mid-pelvis are the transverse is present if the ischial spines are prominent, the side walls
diameter, that is, the interspinous diameter which is about are convergent and if the sacrosciatic notches are narrow.
Abnormalities of the Passage 273
However, several factors together determine the successful Elective section is also indicated in moderate contraction
passage of the fetal head through the mid-pelvis. These associated with a risk factor, e.g. elderly primigravida, post-
are the shape of the pelvis, the degree of contraction of the maturity, malpresentation, pre-eclampsia and medical
mid-pelvis, the size of the fetal head and the frequency and disorders.
amplitude of the uterine contractions. Ultimately, it is the
fetal head, which is the best pelvimeter. Trial of Labor
Mid-pelvis contraction may present as prolonged second Trial of labor is the conduct of spontaneous onset labor
stage, persistent occipitoposterior position or deep transverse in cases of mild to moderate degree of pelvic contraction.
arrest. Molding and formation of caput succedaneum are The trial is conducted with the hope that normal vaginal
common. delivery will take place but should be abandoned at
If prolonged labor is neglected uterine rupture can the earliest evidence of maternal or fetal distress. It is
occur and VVF (vesico-vaginal fistula) may be a late sequel. conducted in a well-equipped adequately staffed hospital.
The onset of labor is spontaneous and not induced.
Pelvic Outlet Contraction The trial begins only after rupture of membranes. The
The inter-ischial tuberous diameter is reduced to less progress of labor is recorded carefully and the progressive
than 8 cm in the case of outlet contraction. The diameter descent of the head and dilatation of the cervix are noted.
divides the outlet into anterior and posterior triangles. If A successful trial is when the baby is born vaginally and
the posterior triangle is roomy, delivery of the fetal head both the mother and the baby are in good condition.
is possible even if the inter-tuberous diameter is less than The advantage of a trial of labor is that it avoids
8 cm. Outlet contraction is rarely seen in isolation. It is unnecessary cesarean sections and assures the woman of
often associated with a mid-pelvic contraction. her future obstetric performance.
Android pelvis high assimilated pelvis, anthropoid It is contraindicated in:
pelvis and the pelvis of patients with kyphoscoliosis have a Elderly primigravida
tendency for outlet contraction. Malpresentation
Outlet contraction
Management of Contracted Pelvis In presence of other complications:
The diagnosis of contracted pelvis should ideally be made • Cardiac disease

before labor starts. Ultrasound, magnetic resonance • Pulmonary disease
imaging (MRI) and X-rays are used to investigate doubtful • Pre-eclampsia
shapes and sizes of the pelvis. The Colcher-Sussman system • Hypertension
can be used. It sees the average and lower limits of anterior- If there is history of failure of trial of labor in previous
posterior and transverse diameter of the pelvis but this pregnancy.
system is not commonly used. Clinical pelvimetry is useful
in evaluation of pelvis for the feasibility of vaginal breech OBSTRUCTION OF BIRTH CANAL BY
delivery and in assessing gross bony distortion in patients
SOFT TISSUE ABNORMALITIES
with previous pelvic fracture or other deformities. The
choices are an elective cesarean section or a trial of labor. Some anatomical abnormalities of the reproductive tract
may cause dystocia. Soft tissue dystocia may be caused by
Elective Cesarean Section uterine or vaginal congenital abnormalities, scarring of the
Elective cesarean section is indicated in all cases where birth canal and pelvic masses.
there is a gross pelvic contraction. Any pelvis with a true Abnormalities of placental location and even low implan
conjugate of less than 9 cm is severely contracted. tation of the placenta can cause difficulty during labor.
1. Name the diseases affecting the spine.
2. Name the four shapes of the female pelvis.
3. Explain the injuries and diseases of the pelvis.
4. Define pelvic outlet contraction.
31 Malpositions and
Malpresentations
Rekha Bharti, Sudha Salhan, Harsha Gaikwad, Sunita Malik, Mahua Maiti, PK Shah, NS Sardeshpande
MALPOSITION AND MALPRESENTATION Etiology

Mostly unexplained (idiopathic)
It is found that adopting the cephalic position is an active Others etiological factors are as follows:
process being the best fit. • Shape of the pelvis:
A normal fetus frequently changes positions in the uterus Anthropoid or android pelvis: Associated with >
till term. The malposition and malpresentations seen are: 50% occipitoposterior position as the wide occiput
Occipitoposterior (OP) position can be easily placed in the wider posterior segment
Face presentation of the pelvis.
Brow presentation • Deflexion of fetal head due to:
Transverse lie –– High pelvic inclinations
Compound presentation. –– Attachment of the placenta on the anterior wall
of the uterus
OCCIPITOPOSTERIOR POSITION –– Primary brachycephaly
–– Baby’s spine is juxtaposed to the mother’s spine.
Occipitoposterior position is a cephalic presentation Hence, fundal pressure along the baby’s spine is
where the occiput (the denominator for the head) is more likely to extend the head instead of flexing.
placed posteriorly over the sacroiliac joint (right or left
• Abnormal uterine contractions: The uterine contra
occipitoposterior) or directly over the sacrum (direct
ctions (Braxton Hicks) may not be strong enough to
occipitoposterior). It is not an abnormal presentation, but
push the head into the brim and make it flex prior
an abnormal position.
to the onset of labor. As the head remains extended
it presents an oblong-shaped outline to the lower
Incidence segment thus the stimulus for fundal contraction
Twenty-five percent of all labors, to begin with, are in may be irregular and ineffective.
occipitoposterior position, in 80–90% of these cases rota- • As the head is presenting its largest transverse
tion occurs, leaving only 10–20% cases in which some diameter in the occiput it fits poorly into the space
intervention is required because of persisting occipitopos- between the sacral promontory and pectineal line,
terior position. the cervix is not stimulated correctly by the oblong
surface presented by the extended head. When the
Types occiput touches the pelvic floor it may fail to rotate
Occipitoposterior position can be divided into: anteriorly partly due to long circle three-eighth
Primary (occipitoposterior): When position occurs (135°) and also the posterior shoulder is caught
before onset of labor and during antenatal period. in the mother’s sacral promontory. If it rotates
Secondary (occipitoposterior): When it develops during through 45°C it becomes transverse position. If
early labor. 45°C posterior rotation occurs it acquires the direct
Malpositions and Malpresentations 275
The anterior shoulder lies far away from the midline.

On auscultation—fetal heart sounds (FHS) is heard
on the flank with difficulty. In direct occipitoposterior,
FHS is heard directly anteriorly or out in the flanks and
distinctly heard in the midline.
Uterine action may be in-coordinate.
On per vaginal examination in early labor:
Elongated bag of membranes is felt which is likely to
rupture during examination.

Sagittal suture occupies any of the oblique diameters
A B
(right or left) of the pelvis.
Posterior fontanelle is felt near the sacroiliac joint.
Anterior fontanelle is more easily felt because the
head is deflexed and at times at a lower level than the

posterior one.
If FHS is heard on the left side with the back on left side
and sagittal sutures in the left oblique diameter, it is the

left OP position and vice versa when FHS is on right side.
Assessment during pelvic examination is very important.
Degree of deflexion of fetal head is noted. Assess the
C D bony pelvis and elasticity of maternal soft tissues and
whether the cervix is applied well to the presenting part
Figs 31.1A to D: Area of fetal head engagement and molding or not particularly during a contraction. If membranes are
ruptured see the color of the amniotic fluid.
occipitoposterior position. In the last it can deliver
as face to pubes. In late labor:
Diagnosis is often difficult because of caput formation,
• Hypotonus in the uterus prevent the normal flexed
attitude in utero. which obliterates the sutures and fontanelles. Location
• Position of the trunk, shape and size of the fetal head of the fetal ear is important and the unfolded pinna
(Figs 31.1A to D). points towards the occiput.
Repeat pelvic assessment to rule out CPD.
Diagnosis Hanging cervix, which is not well-applied.
On history: There is slow progress of the active phase of labor. First

History of early rupture of membranes. stage may be prolonged because of non-rotation and
History of backache. non-descent and delayed engagement. Second stage
Bladder fills too frequently.
is also prolonged. On an average labor is prolonged
Possibility of associated cephalopelvic disproportion by 3–4 hours in primigravidas and about 1–2 hours in
(CPD) is to be ruled out on per abdomen examination:
multigravidas.
The abdominal contour has a sharp fall down to the
Patients start bearing down early, as the head is pushed
xiphisternum.
posteriorly and backache occurs.
The abdominal contour below the umbilicus upto the
pubic symphysis is flattened or concave (scaphoid). Mechanism of Labor
Limbs are felt with unusual ease on both sides of the
abdomen very prominently.

(Figs 31.2A to H and 31.3A to G)
The back is difficult to locate. Right occipitoposterior The engagement occur in the same oblique diameter. That
being more common, the back is usually felt on right side. means if the occiput is towards the right sacroiliac joint it is
The head feels smaller as the sinciput is anterior and the right OP position (in right oblique diameter) and vice versa
back is difficult to feel. in left OP position.
As the head is deflexed, occiput and sinciput are at the Most often (90%), OP positions undergo spontaneous
same level. This is one of the most common causes of a anterior rotation through three-eighth of a circle (Fig.
high head at term. 31.2). The rest 10% may either rotate posteriorly (Fig. 31.3)
A B
C D
E F
G H
Figs 31.2A to H: Mechanism of labor in left occipitoposterior position (LOP) long arc rotation (three-eighth of circle). A. Onset of labor;
B. Descent and flexion; C. Internal rotation to left occipitotransverse; D. Internal rotation left occipitotransverse to right occipitoanterior;
E. Internal rotation to occipitoanterior (OA); F. Extension; G. Restitution OA to right occipitoanterior; H. External rotation left
occipitoanterior to left occipitotransverse
Keys: 1—Pubic symphysis; 2—Anterior fontanel; 3—Coccyx; 4—Posterior fontanel; 5—Ischial tuberosities
A B
C D
E F
G
Figs 31.3A to G: Mechanism of labor in left occipitoposterior position (LOP) short arc rotation (one-eighth of circle). A. Onset of labor;
B. Descent and flexion; C. Internal rotation (left occipitoposterior to OP), direct; D. Birth by flexion; E. Head falls back in extension
(face to pubes); F. Restitution OP to left occipitoposterior; G. External rotation left occipitoposterior to left occipitotransverse
(occipito-sacral) or anteriorly through one-eighth of a Vacuum Extraction

circle (occipitotransverse). The exact reason for failure to After liberal episiotomy, the largest possible metal cup
rotate forward is not known but transverse narrowing of should be used and should be placed as far posteriorly as
the mid-pelvis is a contributory factor. There may be hypo- can be reached. Traction is applied at right angles to the
tonic uterine contractions (spontaneous or due to analge- cup along with the uterine contractions.
sia).
Manual Rotation
Management (Flowchart 31.1)
It is done under general anesthesia. After fulfilling the
Maintain sedation, hydration and nourishment of the pre-requisites manual rotation of the head is done by half
patient hand or full hand method. Pronated right hand can be
Monitor maternal and fetal wellbeing and await sponta-
used for the right position and pronated left hand for the
neous rotation and delivery left position. Rotation of the occiput anteriorly is achieved
Only judicious interventions are required. Sometimes by supination. After rotation, the head is extracted with
change of position to lateral, may help. the help of forceps (mid-cavity) by applying the right blade
Little needs to be done until it becomes evident during first. Please note that this is one of the rare indications for
the second stage of labor that the occiput is not rotating the application of the right blade first.
forward, in spite of good uterine contractions and none of
the complicating factors co-exist. Forceps
Algorithm for management of occipitoposterior is as Direct occipitoposterior: Liberal episiotomy is given.
follows. Long axis traction forceps are used, pelvic application is
Flowchart 31.1: The management of occipitoposterior position labor

made with the blades correctly gripping the sides of the Cesarean section in deep transverse arrest is often
head. Traction is made in a horizontal direction until the technically difficult and there are greater chances of
forehead is under the symphysis, then the handles are infection. Disimpaction and pushing at the head is done by
gradually elevated to bring the occiput slowly over the an assistant with the hand in the vagina. Difficult forceps
perineal margin. The handles are then depressed to bring delivery is not performed nowadays.
the forehead and face out. Face to pubes delivery occurs.
Occipitotransverse: It is sometimes a transient position;
later it rotates to the occipitoanterior position. Persistent
FACE PRESENTATION
occipitotransverse is seen in pelvic dystocia, uterine It is a rare variety of cephalic presentation where the
dystocia and platypelloid or android pelvis. In these cases presenting part is face. There is complete extension of the
treatment is like that in persistent OP position. head so that the occiput is in contact with the fetal back.
Kielland’s forceps The denominator is the chin (mentum). The chin can be
Scanzoni’s maneuver (double application of forceps) anterior (mentoanterior) or posterior (mentoposterior)
Vacuum extraction. relative to the mother’s symphysis pubis.
Deep transverse arrest: This occurs in neglected cases of Right and left mentoanterior or right and left mento-
OP position. At the level of the inlet the descent of the fetal posterior are also possible.
head is arrested in the transverse diameter. The cervix is Left mentoanterior is the most common position in
fully dilated. There is well-marked caput succedaneum face presentation (Figs 31.5 and 31.6A to C). The right
and molding is pronounced thus falsely indicating lower oblique diameter in the left mentoanterior and left oblique
descent and position of head (Figs 31.4A to C). diameter in right mentoanterior. Diameter of engagement
Etiology: This is specially seen in a pelvis which narrows of the head in face presentation submentobregmatic in
down from above downwards (funnel pelvis). There may be completely extended head. The engagement occur in
flattening of the sacral curve, or forward position of the sacral
the opposite oblique diameter of the pelvis. The right
tip so that the posterior sagittal measurements of the cavity
mentoanterior position in the left oblique diameter and
and outlet are reduced or the transverse diameter is reduced:
vice versa for the left mentoanterior position.
Projecting ischial spine or
Narrow pubic arch. Incidence

More than one pelvic abnormality is seen together. This is
One in 500 births. It occurs more commonly in multiparae
a serious condition for both the mother and the fetus.
(70%).
Prevention is important. A close watch on the progress
It is rare during pregnancy, but the fetus attains this
of labor in the OP position is required. Any undue delay
position after the onset of labor.
in progress must alert the obstetrician (if partograph is
maintained it is detected early). Exclude any CPD. Do not Etiology
let this condition develop. Decide in favor of cesarean early.
Labor is usually far advanced (as mentioned earlier, the Maternal
cervix is fully dilated). At this point, the general condition Maternal causes include:
of mother is reassessed. The amount of liquor is estimated. Multiparity with pendulous abdomen, back of the fetus
If possible, a liberal episiotomy and a ventouse delivery is sags forward

attempted. Lateral obliquity of the uterus
A B C
Figs 31.4A to C: Deep transverse arrest. A. Onset of labor; B. Descent and flexion; C. Internal rotation to left occipitotransverse
Fetal
Congenital malformation (15%), e.g. anencephaly, con-
genital goiter, dolichocephalic head, congenital bron-
chocele, macrosomia, hydrocephalus
Prematurity
Nuchal cord
Increased tone of the extensor group of neck muscles.
Diagnosis
Inspection
No visible bulging of the flanks because of ‘s’ shaped spine.
Palpation
Head seems big and not engaged (high and deflexed).
The cephalic prominence is to the side towards which
the back lies with a sharp angulation.
Fig. 31.5: Face presentation—right mentoposterior Groove between head and back is prominent in mento-
posterior position.
On Per Vaginal Examination

Mouth and malar eminences are not in line. This helps
to differentiate it from a breech presentation in which
the ischial tuberosities and anal orifice are in a straight
line.
Mentum and mouth are clearly identified to rule out
brow presentation.
One can feel the nose and two orbital hollows.
A B Biting effect of mouth, hard gum margins and absence
of meconium on examining finger excludes anus (in
breech presentation).
Elongated bag of membrane.
Look for cord prolapse (if membranes rupture).
Mechanism of Labor
In mentoanterior position, there is flexion of the head and
C in typical mentoanterior position, vaginal delivery occurs as
the submentobregmatic diameter is the engaging diameter.
Figs 31.6A to C: A. Left mentoposterior; B. Mentoanterior;
C. Right mentotransverse But some difficulty is expected because the facial bones do
not mold as much as the parietal bones.
An association is seen with contracted pelvis (40%). A Course of Labor

flat pelvis favors face presentation Early rupture of membranes.
Pelvic mass Cord prolapse due to ill-fitting presenting part.
Advanced maternal age Chances of taking greater time for anterior rotation.
Multiple gestation Delay in labor at all stages because of:

Polyhydramnios Weak uterine contractions
Cornual implantation of placenta Absence of molding of the facial bones
Placenta previa and Delayed engagement
Premature rupture of membranes. Late internal rotation/arrest.

Mentoanterior (Chin is Anterior) On pelvic examination:

One can feel root of the nose and two orbital ridges and
Wait for spontaneous delivery. Oxytocin augmentation
anterior fontanel at the pelvic inlet.
may be considered in arrest of labor after CPD is ruled
Neither mouth nor chin is felt.
out.
There is no mechanism of labor of brow presentation.
Perineum should be protected with liberal medio-
lateral episiotomy. In case of delay, forceps is applied, Management
cesarean section may be needed. The head may flex converting into face presentation in
Mentoposterior (Chin is Posterior) early labor. Some time may be spent in expecting it to flex
In uncomplicated cases, wait for spontaneous anterior to face or vertex, if the baby is small, the pelvis is roomy
and there are strong uterine contractions. If any one of
rotation of chin and proceed as for mentoanterior position.
these conditions is lacking a cesarean is indicated (in live
In incomplete or malrotations, early decision for the
fetus) immediately. Thorn’s maneuver is done to turn the
method of delivery is to be taken soon after full dilatation
brow into vertex position by walking the fingers over the
of the cervix. The following methods may be employed to
head. An experienced obstetrician is required for this. If the
expedite the delivery: presenting part is engaged it can be flexed with a vacuum
Early decision for lower segment cesarean section
cup placed as posteriorly as possible or an experienced
(LSCS) should be taken soon after full dilation. There are obstetrician can rotate it to the occipitoanterior position with
chances of impaction of the head in the pelvis if rotation Kielland’s forceps and delivery. These procedures can only
fails to occur. Cesarean should be decided early in labor. be tried in a patient who refuses cesarean section. Oxytocin
Manual rotation and extraction—as in occipitoposterior is not indicated as uterine inertia is due to dystocia. Even if
position this is usually performed by expert obstetricians the fetus is dead cesarean section is generally preferred to
only hence not commonly done. craniotomy and forceful delivery (Fig. 31.8).
Forceps rotation and extraction using Kielland’s forceps—
not usually performed nowadays. TRANSVERSE LIE

Craniotomy: In case of dead baby.
When the long axis of the fetus lies perpendicular to the
BROW PRESENTATION (FIG. 31.7) maternal spine or the centralized uterine axis, it is called
transverse lie. However more commonly the fetus lies
Hyperextension of the fetal head leads rarely to brow obliquely (an acute angle with the long axis) and is then
presentation. It is usually a transient fetal presentation known as oblique lie. In oblique lie if the head is situated
and is mostly converted to face or vertex. above the umbilicus, the presentation can change to
breech. This is called an unstable lie. If the shoulder is over
the pelvic inlet it is called right or left acromial position.
The back may be anterior or posterior, therefore, called
dorsoanterior or dorsoposterior (Figs 31.9A and B).
Incidence
The incidence is 2% in the early third trimester and
spontaneous resolution occur in 80–90% of cases before
delivery. The incidence at term is 0.3%. Dorsoanterior is the
most common (60%). In dorsoposterior position, the chance
of fetal extension is common with the risk of arm prolapse.
According to the position of the head, the fetal position is
termed left or right dorsoanterior or dorsoposterior.
It is common in premature and macerated fetuses and
5 times more common in multiparae than primigravidae.
Position
Fig. 31.7: Brow presentation The back is the denominator.
Fig. 31.8: Thorn’s maneuver
On lateral grip—head and breech are felt. If the back is

anterior it is easily felt but in the dorsoposterior position
irregular small parts are felt (limbs).
Pelvic grip—the lower pole is empty and this may be
occupied by shoulder in labor.
Auscultation
FHS is heard much below the umbilicus (dorsoanterior)
or located at a higher level and often indistinct in the
dorsoposterior position.
Ultrasound is done to exclude any abnormalities men-
A B tioned above and placenta previa.
Figs 31.9A and B: A. Dorsoposterior; B. Dorsoanterior
Per Vaginal Examination
It is done only if placenta previa is excluded by ultra
Etiology sound.
During pregnancy: Some soft parts can be felt. Side of
Multiparity—lax and pendulous abdomen, imperfect the thorax may be palpated as a ‘grid iron’ feel of the ribs.
uterine tone, and extreme uterine obliquity with four or During labor: Elongated bag of membranes (BOM)
more deliveries (ten times more common). can be felt. When dilatation increases, the scapula and
Prematurity clavicle may be felt. In late labor the hand may prolapse.
Twins The shoulder can be confused with breech hence, an
Hydramnios ultrasound examination is important. Shoulder, arm,
Contracted pelvis leg and loop of cord may be palpated.
Placenta previa
Leiomyoma uterus Management during Antenatal Period
Pelvic tumors, e.g. ovarian tumor An external version can be tried at 32 weeks, if ultrasound
Arcuate/subseptate uterus shows no abnormality. This external version can be repeated
Intrautenine fetal demise. at 37 weeks of pregnancy but may not be successful because
of less amniotic fluid. The patient is admitted at 37 weeks,
Diagnosis and one of the following three modes of managements are
chosen:
Inspection
Conservative
The uterus looks broader and often asymmetrical, not Stabilizing induction
maintaining the pyriform shape. Elective cesarean section.
Palpation Mechanism of Labor

The fundal height is less than period of amenorrhea. There is no mechanism of labor in transverse lie. If the fetus
Fundal and pelvic grip are empty. is dead and small in size it can deliver doubled up vaginally.
Clinical Course of Labor be tried because the cervix may appear fully dilated, but
It can be summarized in Flowchart 31.2. once internal version is performed and membranes are
ruptured the uterus will clamp down on the fetus and the
Management cervix will be seen only 6–7 cm dilated. Hence, internal
Vaginal delivery is allowed in a dead or congenitally mal podalic version is allowed only for the second twin.
formed fetus provided no other contraindication exists. If the baby is dead, decapitation or evisceration can be
Labor is allowed till full dilatation of cervix, followed by done. Alternatively, cesarean section is safer in hands of
internal version or destructive operation. those who are not experienced with destructive operations.
In twins, after the delivery of the first child, when the
second twin is transverse, the membranes have recently Unstable Lie
ruptured and there is adequate amniotic fluid, an internal After 36 weeks period of gestation, the lie of the baby
podalic version is carried out. Oxytocin is started and should have stabilized; but in this condition, the position
routine breech delivery is conducted. Otherwise, in a of the fetus is constantly changing even beyond 36 weeks
singleton pregnancy internal podalic version should not period of gestation.
Flowchart 31.2: Outcome in transverse lie

Stabilizing Induction of Labor hand and the rarest is head with foot. It is an uncommon
Rule out placenta previa, fetal abnormalities and CPD. presentation. As the fit of the presenting part with the
The presentation is checked and external cephalic version pelvis is not complete, umbilical cord prolapse may occurs
(ECV) is performed and the fetus is made to present by (in 11–20%), breech with hands is rarely seen.
head. Oxytocin drip is started and titrated till effective
uterine contractions occur. The urinary bladder is kept Incidence
empty. After about 1 hour per vaginal examination is carried One in 600 to 1000 pregnancies.
out to rule out cord prolapse and low artificial rupture
of membranes (ARM) is performed. Labor is expected to Etiology
continue normally if the fetus remains longitudinal. Prematurity (about 50% of compound presentation)
Spontaneous onset of labor can be awaited but acciden- CPD
tal cord prolapse may occur which nullifies the advantages Grand multiparity
of early admission. Pelvic tumors
If stabilizing induction fails, do not wait for long. Do a Multiple pregnancy—mostly with second twin
cesarean section early. Increased perinatal mortality is due Macerated fetus
to cord prolapse, prematurity and vaginal manipulative High head with premature/early rupture of membrane
delivery. Hydramnios.
COMPOUND PRESENTATION (FIG. 31.10) Diagnosis

Compound presentation is suspected when there is poor
This is defined as a presentation where when a cephalic
progress of labor, especially when the presenting part fails
presentation is complicated by the presence of a hand
to engage during active labor.
or a foot or both. Alongside the head there is presence of
On per vaginam examination when the cervix is
one or both hands or feet. The most common is head with
sufficiently dilated palpation of a fetal extremity (hand
or foot) adjacent to the presenting part.
Premature rupture of membrane (PROM)/early ROM
is associated in one-third cases and the diagnosis

becomes clearer. Ultrasound may help before rupture
of membranes.
Rule out cord prolapse (10–20%).
Management
Depends on the period of gestation and the type of
compound presentation. If the fetus is less than 24 weeks
of gestation and in labor, the labor is permitted vaginally
because of the small-sized fetus.
Elevation of the prolapsed limb with descent of the
presenting part usually occurs spontaneously. Umbilical
cord prolapse is to be prevented, if possible. Otherwise
continuous fetal heart rate (FHR) monitoring and immediate
delivery is essential. Cesarean section is performed for
maternal or fetal indications. Other indications for cesarean
section are failure to progress, non-reassuring FHR pattern
and persistent compound presentation with a term size
fetus. Fetal malformations also lead to dystocia.
Resist the temptation to replace the limbs early as it is
not only unnecessary but carries maternal and fetal risks.
Fig. 31.10: Compound presentation A slight pull on the limb will lead to retraction by the fetus.
CORD PROLAPSE
UMBILICAL CORD PROLAPSE

Umbilical cord prolapse remains one of the true
emergencies in modern obstetrics. Its incidence ranges
from 0.08–0.9% and it has been associated with a perinatal
mortality of 50% and an unknown incidence of permanent
brain injury. As a result, cord prolapse continues to be a
common cause of medical malpractice litigation. There
are three clinical types of abnormal descent of cord by the
side of presenting part: Fig. 31.11: Incidence of cord prolapse according to fetal
1. Occult prolapse: The cord is placed by the side of the presentation
presenting part and is not felt by fingers on internal
examination.
2. Cord presentation: The cord has slipped below the
presenting part and is felt lying in the intact bag of
membranes.
3. Cord prolapse: The cord is lying inside or outside the
vagina following rupture of membranes.
Cord presentation and cord prolapse are not synony
mous and it is not a must that all cord presentations
should end in cord prolapse. In one study, cord presenta
tion was seen in 0.16% cases and out of these only 23% has
persistent cord presentation on repeat scan. Therefore,
Fig. 31.12: Incidence of cord prolapse related to different types
repeat assessment should be done intrapartum to decide of breech
the mode of delivery.
Etiology (Figs 31.11 and 31.12) Multiple pregnancy

Descent of cord is more likely to occur when the presenting Hydramnios
Pelvic tumor
part imperfectly fits the pelvic brim and lower uterine
CPD
segment, leaving space for the cord to prolapse. Thus, cord
Placental factors and umbilical cord causes
prolapse is associated with the following conditions:
• Placenta previa
Malpresentation
• Marginal insertion of cord
• Breech presentation
• Long cord.
–– Extended—0.5%
Iatrogenic causes account for 47% of all cases of cord
–– Flexed—5%
prolapse. These may be due to:
–– Footling—15–18%
• Ill timed ARM
• Brow presentation, compound presentation, face
• Manual rotation of head
presentation and transverse lie, OP position of the • External cephalic version (ECV)
head. • Scalp electrode application
Unstable lie • Intrauterine catheter insertion
Contracted pelvis: A malfitting head leaves space for • Expectant management of preterm PROM.
the cord to slip below Length of umbilical cord is important. Cord prolapse is
Prematurity and intrauterine growth restriction (IUGR) not seen when the umbilical cord is less than 35 cm. The
Grand multiparity (more than 5 pregnancies) incidence of this accident is 4–6% when the cord is 80 cm
PROM before engagement of the presenting part or longer.
Fig. 31.13: Occult prolapse Fig. 31.14: Cord presentation
Diagnosis
Occult Prolapse (Fig. 31.13)
It is difficult to diagnose. However, the possibility is sus-
pected while doing electronic fetal monitoring when there
is:
Persistent profound variable decelerations in an other
wise normal labor.

Sustained bradycardia—irregular compression of the
cord.
Persistent fetal souffle with irregular fetal heart sound
and confirmed by ultrasonography. It can be seen after

ARM.
Cord Presentation (Fig. 31.14)

On feeling of pulsation of cord through intact membranes
while doing routine vaginal examination.
The possibility of cord (funic) presentation should always
be kept in cases of malpresentation, unengaged head,
Fig. 31.15: Cord prolapse (no membranes)
hydramnios, etc. In such high-risk cases as mentioned in the
etiology, a clinician should always consider an ultrasound
evaluation using a vaginal probe with color flow Doppler, if These pulsations may disappear during uterine con-
available. Abdominal scan can also indicate the presence of traction, however, return after the contraction passes off.
cord astride neck. So one should always listen to FHS even in the absence of
Few conditions simulate a cord presentation, like tips of cord pulsations before declaring the fetus dead.
fingers and toes, but they move away from the examining
fingers. Note if pulsations in the cord can be felt. Prognosis
Prolapse of the umbilical cord below or at the level of
Cord Prolapse (Fig. 31.15) the presenting part exposes the umbilical cord to the
About half of the cases of cord prolapse occur in the second atmosphere, which may cause irritation and cooling
stage of labor. One can actually see the cord and feel the leading to vasospasm in cord vessels and fetal compromise.
pulsations if the fetus is alive. Another important factor is compression of the umbilical
cord between the presenting past and pelvic inlet, cervix or is prolapsed in the second stage (30%) than when it
vaginal canal. This compromises fetal circulation leading to prolapses in the first stage (70%).
fetal hypoxia, brain damage and death. Perinatal mortality Fetal reserve, e.g. growth restricted baby cannot with
is increased. Besides the cause of prolapse, prematurity, if stand cord compression for even a few minutes.
associated, also causes perinatal loss. Experience and expertize of obstetrician.
Perinatal mortality is mainly because of occlusion of Emergency operation theater (OT) and neonatal
blood flow due to mechanical compression by presenting resuscitation facilities.
part especially vertex against incompletely dilated cervix Cord handling and exposure to cold.
and pelvic wall or vasospasm due to exposure to cold.
Maternal morbidity is also increased as a consequence Prevention
of operative delivery with associated risk of anesthesia, Patients with predisposing factors should be treated as
blood transfusion, infection and the direct trauma of high-risk for cord prolapse. An ultrasound examination,
instruments. before labor or at the start of labor is done to find the
The fetal prognosis depends on the following factors: lie of the fetus and the position of the umbilical cord.
Duration of cord compression: It cannot be stated Cord prolapse occurs mostly during labor. Hence, one
exactly how long a fetus can survive after it has been should continuously monitor these high-risk patients for
deprived of oxygen. Survival for about 10 minutes can abnormality of FHR. Avoid artificial rupture of membranes
be anticipated when the deprivation has been sudden till the presenting part is well-applied to the cervix. If the
in onset. It is possible that compression of cord can membranes rupture spontaneously immediate pelvic
last as long as 20 minutes before the fetus dies from examination is done to see for prolapse of the cord. If
asphyxia. Overall perinatal mortality rate is 50%, which drainage of amniotic fluid is needed in an unengaged
can be improved to 10% if the delivery can be conducted presenting part aspiration by a needle and syringe can be
within half an hour. done.
Status of membranes: Cord presentation (membranes
infact) has 100% survival rate for the fetus, if diagnosed Management (Flowchart 31.3)
in time. Principles of Management
Parity (nulliparity v/s multiparity): The risk is less in
In cord presentation:
a multigravida because the labor is usually short.
• Once a diagnosis is made no attempt should be
Exact position of cord in pelvis: The position of the
made to replace the cord.
prolapsed cord in the pelvis chiefly depends on the • If immediate vaginal delivery is not possible or
position of fetus, i.e. on the side where abdomen of fetus contraindicated, cesarean section is the best. During
is facing. As this is directed more posteriorly, the cord preparation for this the patient is kept in exaggerated
lies near one of the sacroiliac joints and thus entirely Sim’s position or knee-chest position to minimize
escapes compression. In OP position of the vertex and cord compression (Figs 31.16 and 31.17).
dorsoposterior presentation, it will be found in the • Rarely, watchful expectancy may be done in a mul-
neighborhood of one or other iliopectineal eminence tiparous woman with longitudinal lie, having good
where it will be compressed between the head and the uterine contractions, cervix ≥ 8 cm dilated without
cervix or the anterior pelvic wall. any evidence of fetal distress, till full dilatation of
Fetal presentation: The dangers are greater in vertex cervix, when the delivery can be accomplished with
than breech presentation. Also the conditions which forceps or vacuum.
favor cord prolapse prevent early engagement of head; Once prolapse of the cord has occurred urgent action is
the cord often escapes pressure in early stage of labor. needed.
With a flat pelvis the cord may be little pressed upon Immediate pelvic examination is to be done to find
until the head is in the pelvis, because it slips into one dilatation and effacement of cervix:
or other bay to either side of the promontory. With • To relieve pressure on the cord.
shoulder presentation similarly the pressure on the • To find out if the fetus is alive or dead, strength of
cord is less in early labor. pulsations of the cord. Repeated cord palpation for
Stage of labor: The average fetal mortality except in pulsation also induces spasm hence, listening to
skilled hands, is 50%. The risk is less when the cord fetal heart is a better alternative.
Flowchart 31.3: The management of cord prolapse
Abbreviations: CS—Cesarean section; NA—Not available
• To expedite delivery, if alive. • The end of bed may be elevated. High Trendelenburg
• To await spontaneous delivery if dead and the pelvis and knee-chest position traditionally mentioned is
and presentation are favorable. very tiring and irksome to the patient but may be
In cord prolapse—first look for: tried (Figs 31.16 and 31.17).
• Viability of the fetus • A technique of keeping the presenting part above the
• Maturity of the fetus brim is to distend the urinary bladder with 500–600
• Associated complicating factors mL normal saline through a Foley’s catheter.
• Dilatation of the cervix. • Tocolytic drugs such as a IV drip of ritrodine 50 mg
If the Fetus is Alive in 1 unit of 5% glucose or Terbutaline 0.25 mg SC or
Immediate vaginal delivery not possible or contra-
indicated: First aid is to minimize pressure on cord as
long as the patient can be transferred or prepared for
assisted delivery. Give oxygen to the mother:
• To lift the presenting part off the cord by the gloved
fingers into the vagina and keep there till definitive
treatment can be done. Amnioinfusion may be done
in an attempt to decrease pressure on umbilical cord.
• Keep the patient in exaggerated elevated Sim’s
position with pillow under the buttocks. Fig. 31.16: High Trendelenburg position
Exclude cord presentation or occult prolapse in unex-

plained fetal distress during labor.
Routine antenatal Doppler examination should be
done in all high-risk cases.

Things not to do:
Pulling down the cord loop for visualization.
Unnecessary handling of the cord.
Rupturing the membranes with cord presentation.
Declaring the fetus dead even before listening to FHS.

Fig. 31.17: Knee-chest position
Trying to replace the cord in cord presentation as it
inevitably leads to cord prolapse.

IV salbutamol 0.5 mL slowly over 2 minutes will relax
the uterus, delay the descent and enable a live baby Management
to be delivered by a LSCS.
Management protocol is as above.
• In case the cord is hanging outside, gently replace it
in the vagina to minimize vasospasm due to cold or
irritation. BREECH PRESENTATION
Definitive Treatment
Cesarean section when the baby is sufficiently mature DEFINITION
enough to survive and the cervix is not fully dilated. This is a malpresentation where the podalic pole (fetal
Listen to FHS just prior to giving an abdominal incision
buttocks or the lower extremity) presents at the pelvic inlet.
to avoid a section on dead baby.
The lie is longitudinal and the denominator is sacrum. The
Baby may be delivered by ventouse in term fetus if the
cervix is > 7–8 cm dilated. various positions are as follows (Fig. 31.18).
Reposition of cord: This procedure carries high fetal
risk but may be done if immediate cesarean section is Anterior
not possible or the baby is too premature. The cervix RSA—Right sacroanterior
must be half dilated, the cord is wrapped in sterile roller SA—Sacroanterior
gauze and manually pushed above the presenting part LSA—Left sacroanterior
under general anesthesia.
Cervix is fully dilated and immediate safe delivery is Posterior
possible. RSP—Right sacroposterior
If head is engaged, complete the delivery by forceps or
SP—Sacroposterior
ventouse (pressure can be safely built quickly).
LSP—Left sacroposterior
In breech presentation—do a breech extraction.
In transverse lie—do an internal podalic version and
Right sacroanterior is the common position due to the
breech extraction under anesthesia, if possible. presence of maternal sigmoid color in the left quadrant of
In twins with second baby, head not engaged and the maternal pelvis.
cord prolapse, do internal podalic version and breech
extraction. INCIDENCE
Fetus Dead The incidence of breech presentation varies from 2.2
Labor is allowed to continue awaiting spontaneous delivery. to 3.7% at term to 14% between 29 and 32 weeks. Prior to
Sometimes destructive operation may be required. 28 weeks, the incidence may be as high as 25%. In USA,
Things to do: the incidence of breech delivery is about 4.8%.
Conduct an internal examination whenever the mem-
branes rupture during labor in all cases of malpresen- TYPES OF BREECH
tation and free head.
Surgical induction (ARM) should be performed in the There are 4 types of breech (Fig. 31.19):
OT with everything ready for cesarean section especially 1. Complete (5–12%): Flexion at the hip and knees (‘can-
with unengaged head. nonball’ appearance).
Fig. 31.18: Positions of breech presentation
A B C
Figs 31.19A to C: Types of breech

2. Footling (10–30%): This may be double or single with anencephalic babies and those with meningomyelocele
extension at the hip and knee of both limbs or only one presenting as breech, and 50% of trisomic babies and
limb. The foot is the presenting part. babies afflicted with the Prader-Willi syndrome presenting
3. Frank breech (48–73%): Extension at the hip and knees as breech. Fetuses with ascites and sacrococcygeal
(‘pike’ appearance). The feet of the baby are in contact teratomas have been known to present as breech.
with the head at the fundus of the uterus. Prematurity is the most common cause
Large baby
4. Kneeling: This may be single or double with extension
Postdatism
at the hip and flexion at the knee of one limb or both
Intrauterine fetal death
limbs.
Fetal aneuploidy.
Breech fetuses show reduced fetoplacental ratios and

ETIOLOGY increased head circumference and are small for gestation
Factors predisposing to breech presentation relate to one age. These differences persist till 18 months of life and
of the three causes, i.e. abnormal uterine shape, excessive disappear at 4 years of age.
fetal mobility or interference in fetopelvic relationships. An association between increased risk of recurrent
breech presentation and extended fetal legs has been
Maternal Factors noted indicating a genetic predisposition to this posture.
Cephalopelvic disproportion at the pelvic inlet. Habitual breech is an entity where, in a particular
Soft tissue dystocia, e.g. fibroid in the lower uterine woman, all her fetuses are delivered as breech.
segment. But in more than half of the cases the cause of breech
Congenital uterine anomalies like septate and unicor- presentation is not known.
nuate uterus. Septate uterus usually gives rise to a trans-
verse lie. If the knees are extended and hips flexed along DIAGNOSIS OF BREECH PRESENTATION
with reduced space in the uterine cavity, the larger vol- (FIGS 31.20A AND B)
ume of the head and feet fits into the fundus of the uterus
and the breech into the lower pole. Clifford White states that ‘to confuse the breech (in a vaginal
In grand multiparae, poor muscular tone predisposes to examination) with the face is the traditional mistake,
an unstable lie leading to a breech presentation by chance. but a more dangerous mistake is that of diagnosing the
Anticonvulsants and maternal alcohol intake, by presenting part as the breech when it is really the shoulder.’
causing fetal neurological dysfunction and reduced On abdominal examination, the lie is longitudinal.
fetal movements predispose to a breech presentation. The fundal grip reveals a smooth, hard and ballotable
structure (the fetal head). Lateral grips reveal the firm,
Placenta, Liquor and Cord Factors uniform, board like fetal back on one side and the soft fetal
limbs on the other. In sacroanterior position the back may
Placenta previa reduces space in the lower uterine
be felt close to the midline or away from it in sacroposterior
segment and thus prevents engagement of fetal head. presentation.
One study found that cornufundal implantation of The pelvic grip reveals the irregular soft and non-
placenta was seen in 73% of breech presentations as ballotable breech which is usually floating. The FHS is
opposed to only 5% of vertex presentations. heard just above the umbilicus of the mother varying from
Polyhydramnios predisposes to an unstable lie. close to the midline (sacroanterior position) to away from
Oligohydramnios may trap the baby in breech presen it (sacroposterior position).
tation by reducing mobility. On vaginal examination, one finds a broad soft rounded
Very long or very short cord. mass. THe task is to differentiate the anterior buttock of
breech from the fetal shoulder, the skull of an anencephalic
Fetal Factors fetus, the face or the brow, and a vertex covered with a
Multiple gestation: The second twin commonly pres- thick caput succedaneum. This can be done by seeking the
ents as breech. four cardinal points.
Congenital anomalies: Fetal anomalies have been The fetal sacrum—a well-defined area of bony resistance
observed in 18% of preterm breech, and 4–8% of term shaped like a Crusader’s shield with a roughened convex
breech delivers. Central nervous system (CNS) anomalies surface and 3 to 4 small sacral spinous processes in a
are the most common with 50% of hydrocephalic, straight line.
A B
Figs 31.20A and B: A. Diagnosis of breech; B. Landmarks during diagnosis of breech
The spinous processes, when followed downwards, Delivery of Lower Limbs and Buttocks
lead to the sharp point of the coccyx beyond which is an (Figs 31.21A to F)
abrupt deep depression—the anal cleft.
Engagement: The bitrochanteric diameter (9.5 cm)
Overhanging the anal cleft and parallel to the anal
passes through the inlet in the oblique diameter.
orifice are the ischial tuberosities which are felt as two
Descent: This is slow as the breech is a less efficient
bony ridges to the right and left of the anal cleft. The dilator of the cervix than the head. The breech may
ischial tuberosities and the anal cleft lie in a straight remain high in the pelvis and descend quickly after full
line (in face presentation, the malar prominences and cervical dilatation. In a frank breech, the legs may act as a
the mouth form a triangle). There is no sucking of the splint along the body of the fetus causing prolong descent.
finger at the anus (unlike the mouth in face presentation, Flexion: Once the breech touches the pelvic floor, there
sharp jaw edge is felt in mouth) and meconium may be is lateral flexion at the waist.
demonstrated (on the examining finger in breech). Internal rotation: The anterior hip rotates through
When breech presentation cannot be excluded by 45°. The bitrochanteric diameter comes to lie in the
careful abdominal and vaginal examination, near term, anteroposterior diameter of the pelvis. The sacrum
an ultrasonography is indicated. This diagnosis should comes to the transverse pelvic diameter.
be suspected when there is an obstetric history of a Birth of buttocks: After the anterior hip hinges under
previous breech presentation. Twenty percent of patients the pubic symphysis, the posterior hip delivers over
give such a history. Ultrasound is also useful for fetal the perineum by lateral flexion and drops down. The
weight estimation, excluding fetal abnormalities and anterior hip slips out under the symphysis pubis
hyperextension of the head. followed by the lower limbs.
Delivery of Shoulder and Arms (Figs 31.22A to C)

MECHANISM OF LABOR
The sacrum, after delivery, rotates by 45° opposite to
This is divided into: internal rotation to undo the torsion at the waist.
Delivery of lower limbs and buttocks Engagement: The bisacromial diameter (12 cm) engages
Delivery of shoulders and arms in the right oblique diameter of the pelvis.
Delivery of aftercoming head. Descent continues.
The most common position adopted is the right Internal rotation: On touching the pelvic floor, the
sacroanterior position due to the reason explained earlier. anterior shoulder rotates 45° so that the bisacromial
A B
C D
E F
Figs 31.21A to F: A. Engagement of breech; B. Onset of labor; C. Internal rotation of breech; D. Birth of buttocks: Breech crowning;
E. Birth of buttocks: Delivery of posterior buttock; F. Birth of buttocks: Delivery of anterior buttock
diameter lies in the anteroposterior diameter of the Birth of Aftercoming Head (Figs 31.23A to C)
midpelvis, along with 45° external rotation of the sacrum. Engagement: The head (suboccipitofrontal diameter
Birth of shoulders: The anterior shoulder impinges 10.5 cm or suboccipitobregmatic diameter 9.5 cm)
under the pubic symphysis and the posterior shoulder engages in the left oblique diameter.
and arm are born over the perineum. The anterior Descent
shoulder then delivers under the pubic symphysis. Flexion: This often is maintained by contractions aided
Restitution: After delivery of the shoulders rotates— by suprapubic pressure.
through 45° to assume a right oblique position to undo Internal rotation: When the head touches the pelvic
the torsion on the neck. floor, it rotates by 45° so that the sagittal sutures lies in
A B
Figs 31.22A to C: A. Engagement of shoulders; B. Internal rotation

C of shoulders; C. Delivery of shoulders
the anteroposterior pelvic diameter, the occiput lies If the head is deflexed or extended, the chin impinging
anteriorly and brow lies in the hollow of the sacrum. below the pubic symphysis promotes further extension.
Birth of the head: The nape of the neck impinges This requires manual rotation of the body along with the
against the pubic symphysis and the chin, mouth, head to occipitoanterior position and suprapubic pressure
nose, forehead, bregma and occiput are born over the along with other maneuvers to aid delivery.
perineum by flexion.
Molding
MECHANISM OF LABOR IN OTHER As the head passes rapidly through the pelvis, molding
does not occur. This may be potentially dangerous.
POSITIONS
Sacroposterior Position MANAGEMENT OF BREECH
In rare cases, the sacrum and the head rotate posteriorly so
PRESENTATION
that the occiput is in the hollow of the sacrum and the face Investigations
is behind the pubic symphysis. Routine antenatal investigations
If the head is flexed, it may deliver in the occipito Ultrasound
posterior position. The nasion pivots under the pubic sym- • Presence of fetal anomalies
physis and the nape of the neck, occiput and vertex deliver • Fetal head extension
over the perineum followed by the face from behind the • Fetal maturity
symphysis pubis. • Site and grade of placenta
A B
Figs 31.23A to C: A. Descent of head; B. Internal rotation of

C head; C. Delivery of head
• Adequacy of liquor The breech score of Zatuchni and Andros is a numerical

• Ruling out multiple gestation summary of several important parameters and may help
• Confirming fetal presentation. in decision-making. Similarly, other scoring systems
X-ray abdomen (done rarely and only for specific have also been devised. In the Zatuchni-Andros score, a
indications) score of 3 or less is associated with a high degree of fetal
• Skeletal congenital anomalies in the fetus morbidity, prolonged labor and increased rates of cesarean
• Fetal maturity delivery. Higher scores, although they do not guarantee
• Pelvimetry a safe vaginal delivery, suggest a trial of labor with close
• Ruling out multiple gestation. monitoring (Table 31.1).
Ultrasound may guide decision-making by giving an
MANAGEMENT DURING PREGNANCY idea of the estimated fetal weight. Neck hyperextension
is an important cause of spinal cord or brain injuries at
Version is an operation by which the fetus is turned in delivery.
utero for the purpose of changing the presentation.
During ultrasound one can measure the craniospinal
Version was first done by Celsus in 13 AD on a dead
angle by measuring a sagittal view of the fetus, visualizing
fetus. Soranus, 100 years later, performed it on a live fetus.
the orbital ridge and the occipital eminence along with
After years of disuse, Ambroise Paré revived it in the
the spine in the same plane. A line is drawn between the
16th century.
orbital ridge and occipital eminence and the angle formed
with the second line which passes through the cervical
MANAGEMENT IN LABOR
and thoracic vertebrae is measured. Majority cases where
At the time of admission of the patient, a decision should the angle was greater than 90° delivered vaginally, but
be made regarding trial of labor or cesarean delivery. some suffered damage to cervical cord. Hence, perform
TABLE 31.1: Zatuchini and Andros score In a footling breech, due to smaller diameter of breech,
entrapment of head in an incompletely dilated cervix
0 Point 1 Point 2 Points
may occur.
Parity Primigravida Multiple
Premature baby (see Chapter 19).
Gestational 39 weeks or 38 weeks 37 weeks or Breech score of 3 or less.
age more Previous cesarean delivery has been debated.
Estimated fetal > 8 lb 7-8 lb < 7 lb Chronic fetal compromise/intrauterine growth restriction
weight 3690 g 3176-3630 g < 3176 g (IUGR).
Previous breech None 1 2 or more Fetal biparietal diameter (BPD) >9.5 cm.
> 2500 g Factors like elderly primigravida, history of primary
Cervical 2 cm or less 3 cm 4 cm or more infertility and bad obstetric history are not indications
dilatation on for cesarean delivery.
admission by
vaginal Indications for Trial of Labor
examination
Frank breech
Station on –3 or higher –2 – 1 or lower
admission Gestational age 36 to 42 weeks
Estimated fetal weight 1500 to 3900 grams
Flexed fetal BPD <9.5 cm
cesarean delivery if the craniospinal angle greater than Adequate maternal pelvis
90°. Breech score of 4 or more.
X-ray pelvimetry or CT (computed tomography) pel-
vimetry, which uses less radiation, have been advocated First Stage of Labor
for pelvic assessment. Along with routine preparation like simple enema and
The criteria for a vaginal delivery suggested: clipping of hair over the private parts, blood should be
Inlet: Transverse diameter >11.5 cm and antero-
kept typed and cross matched in anticipation of a cesarean
posterior diameter >10.5 cm. delivery. The maternal and fetal condition should be
Midpelvis: Transverse diameter >10 cm and anteropos-
monitored, and adequate hydration and nourishment of
terior diameter >11.5 cm. the mother maintained. The membranes should be kept
Vaginal breech delivery can be: intact as long as possible as they act as a dilating wedge
Spontaneous breech delivery: The entire infant is and prevent overt cord prolapse.
expelled by the natural forces of the mother, with no A partogram should be maintained. Oxytocin induction
assistance other than support of the baby as it is being and augmentation has its share of detractors as it is feared
born. This method of delivery is now obsolete. that nonphysiological contractions may lead to head
Assisted breech delivery: The infant is delivered by entrapment in an incompletely dilated cervix. Continuous
natural forces upto the umbilicus while the delivery of electronic fetal monitoring is used, when available.
the remainder of the baby is assisted by the obstetrician. An anesthetist should be kept ready if anesthesia has to
This is the ideal method. be given for management of complications. A pediatrician
Total breech extraction: The entire body of the infant should be notified in view of the increased risk of neonatal
is extracted by the obstetrician. This method is not depression and unrecognized fetal anomalies.
recommended except in breech presenting second twin The patient should be resting, fasting and should not
just after the delivery of the first twin (vertex) when the bear down until full cervical dilatation.
cervix is fully dilated. Epidural analgesia may be beneficial in reducing the
patient’s pain, anxiety and premature bearing down and
Indications for Elective Cesarean Delivery relaxing the pelvic musculature to accommodate the
Contracted, borderline or abnormal pelvis. unmolded fetal head.
Placenta previa of any degree.
Large baby with ultrasound estimated weight of 4 kg or Second Stage of Labor
more allowing for a 15% error in ultrasound estimation A liberal mediolateral episiotomy must be given during
of weight at term. ‘crowning’ (climbing of breech over perineum), even in
Hyperextension of fetal head. multiparas, to overcome soft tissue resistance.
The posterior buttock is hooked by a finger and delivered in the oblique diameter and the posterior leg
delivered. The anterior buttock is also hooked out. Allow hooked out after pressing the popliteal fossa—the leg
descent upto the umbilicus with uterine contractions. comes down followed by the anterior leg (Figs 31.24A
The back is always kept anterior. and B).
Wrap the baby in a warm towel (Savage’s maneuver). If the baby is dead, single or double groin traction may
This reduces vasospasm of the umbilical vessels due to be used.
atmospheric temperature, prevents stimulation of fetal If a frank breech prevents descent, the patient is
respiration and aspiration of vaginal secretions, and anesthetized. One hand is introduced into the uterus
makes it easier to hold the baby. along the baby’s leg. The middle finger exerts pressure
Once the body is delivered upto the umbilicus, push over the popliteal fossa. This flexes the knee joint and the
the cord to one side to minimize the traction and leg drops into the accoucheur’s (obstetrician’s) hand.
compression if it is caught between the fetal body or The limb is extracted by holding the ankle in a cigarette
head and the pelvic wall. holding fashion. The same procedure is repeated
If the bitrochanteric diameter is large and cannot be with the other leg. This is called Pinard’s maneuver
delivered in the anteroposterior pelvic diameter, it is (Figs 31.25A and B).
A B
Figs 31.24A and B: Assisted delivery of lower limbs
A B
Figs 31.25A and B: Pinard maneuver

A B
C Figs 31.26A to C: Assisted delivery of shoulders and upper limbs
Delivery of shoulders (Figs 31.26A to C): The body is

depressed and delivered upto the scapula so that the
anterior shoulder comes under the pubic symphysis.
To deliver the anterior arm, the accoucheur passes his
hand up the baby’s back, over the shoulder and down
the chest, sweeping the arm and hand in front of the face
under the pubis with his finger. The baby is then raised
such that the posterior scapula and the posterior arm
are born over the perineum by the same maneuver (Figs
31.26A to C).
If the bisacromial diameter is large and cannot be
delivered through the anteroposterior diameter of
the outlet, the baby is rotated by 45° into the oblique
diameter of the pelvis. The shoulders are then hooked
out and delivered.
If the arms are extended than there are two possibilities:
1. Extended arms: Arms above the head with extension Fig. 31.27: Nuchal arms presentation
at both shoulder and elbow joint.
2. Nuchal arms: Extension of shoulder and flexion Hook the arm by flexing it at the elbow and shoulder,
at elbow with the arms extending behind the head and then sweep it over the chest in case of extended arm
(Fig. 31.27). (Fig. 31.28).
If rotation fails, the clavicle is broken at the junction of

medial one-third and lateral two-thirds with cleidotomy
scissors. This reduces the engaging diameter and delivery
is effected.
Sometimes, one shoulder remains in the false pelvis,
while the other lies at the inlet. The bisacromial diameter is
now at an angle to the inlet. The baby is held at the buttocks
and back (femoro–pelvic grip), and rotated keeping the
back anterior. This brings the anterior shoulder from
above the inlet into the hollow of the sacrum. One more
180º rotation helps it to deliver below the pubic symphysis.
The other shoulder is delivered subsequently. This is called
the Loveset’s maneuver. The advantage of this maneuver
is that all manipulation is external and in one smooth
Fig. 31.28: Delivery of nuchal arms
movement. Anesthesia is not required (Figs 31.29A to C).
DELIVERY OF THE AFTERCOMING HEAD

If the above method fails and the arm is nuchal and
fixed behind the head, the baby is rotated in the direction Most of the babies who present as breech require the
to which the thumb is pointing. Due to friction between Kristellar’s maneuver, i.e. continuous suprapubic pres
the fetal arm, fetal face and maternal soft tissues, the arm sure to maintain flexion of the head, and to deliver it.
gets dislodged and then can be hooked out. If arrest occurs, the accoucheur has only 3 minutes to
If both the arms are nuchal, the baby is rotated in one deliver the head, after which the brain of the fetus suffers
direction to free one arm and in the opposite direction to hypoxia.
free the other arm. The following maneuvers can be employed.
A B
Figs 31.29A to C: Loveset’s maneuver

C Abbreviations: A—Anterior; P—Posterior
A B
Figs 31.30A and B: Bracht’s or Burns Marshall maneuver
Bracht’s Maneuver/Burns Marshall Maneuver

(Figs 31.30A and B)
Erich Bracht in 1935, noted that the conventional ‘assisted’
breech delivery interferes with the normal mechanism of
labor and proposed a new technique permitting spontaneous
delivery of the infant. In this method, the principal role of
the accoucheur is to support the infant’s body against the
force of gravity during birth, without traction, expulsion
being accomplished by the force of the contracting uterus,
augmented if necessary by suprapubic pressure.
The breech is allowed to deliver spontaneously
upto the umbilicus without any interference. The body
and extended legs are held together with both hands
maintaining the upward and anterior rotation of the body.
When the anterior rotation is nearly complete (back comes Fig. 31.31: Wigand-Martin maneuver
anteriorly), the baby is held, not pressed, against the pubic
symphysis. The force applied should be equivalent to the
gravitational force or the weight of that part of the baby The finger in the mouth maintains flexion of the head.
already delivered. Maintenance of this position, with or A continuous suprapubic pressure is exerted. Traction is
without suprapubic pressure (moderate), is sufficient to then exerted along the pelvic axis by the index and ring
accomplish delivery by swinging the legs towards mother's fingers to effect delivery.
abdomen, perineal support is required.
Mauriceau-Smellie-Veit Maneuver (Fig. 31.32)
Wigand-Martin Maneuver (Fig. 31.31) Mauriceau, in the third edition of his book “Trait Des
The body of the baby is placed on the accoucheur’s arm. Maladies des Femme Grosses” in 1881, mentioned this
The middle finger of the hand of that arm is placed in the maneuver, which was subsequently modified by a number
baby’s mouth and the index and ring fingers of the same of obstetricians including Smellie, Levret, Clifford,
hand are placed on the malar bones. Lachapelle, Veit, Wigand, Martin and Van Winkel.
OCCIPITOPOSTERIOR POSITION
OF HEAD
Rarely, the chin of the baby rotates anteriorly and the back
rotates posteriorly. This is managed by substituting deep
anesthesia, ceasing all traction, digitally dislodging the
chin from behind the pubic symphysis, rotating the face
posteriorly, flexing the chin, and delivering by suprapubic
pressure and Mauriceau-Smellie-Veit maneuver or by a
Piper’s forceps.
If this technique fails, the Prague maneuver is used. The
fingers of the accoucheur are placed on the baby’s shoulder,
an outward and upward traction is applied. The legs are
grasped with the other hand and the body is swung over
the mother’s abdomen through 360° along with suprapubic
Fig. 31.32: Mauriceau-Smellie-Veit maneuver pressure. The occiput is born over the perineum. This
method carries the danger of overstretching, dislocating or
Its principal features consist of turning the infant so that breaking the cervical spine of the infant.
it faces posteriorly away from the pubic symphysis and
inserting one or two fingers into its mouth to aid flexion TOTAL BREECH EXTRACTION
of the head and provide gentle traction for delivery with
the index and ring fingers placed on the malar bones. This is the immediate vaginal extraction of the fetus, when
Now the finger is placed on the chin and not in the mouth. signs of fetal distress demand rapid delivery of the fetus.
The second hand's middle finger is placed on the occiput
to assist flexion and index and ring fingers on both side Pre-requisites
shoulders. The assistant maintains constant suprapubic There should be no fetopelvic disproportion.
pressure. The cervix must be fully dilated.
The bladder and rectum should be empty.
Forceps Delivery (Figs 31.33A to D) Anesthesia is essential.
Though it was sometimes practices in 18th century but early Good assistance is mandatory.
in the 20th century, only interest was renewed in forceps A pediatrician must be available.
assistance in head of the fetus breech deliveries.
The blades of the forceps have flat pelvic side and long Procedure
shank. The patient is placed in a lithotomy position, anesthetized
The chief purpose of the instrument (forceps) is flexion and catheterized. The feet are pulled down (complete
not traction. It controls the exit of the brow across the perineal breech) or Pinard’s maneuver performed (frank breech).
edge and protects the perineum from lacerations. The maneuvers for delivery of shoulders, arms and head
Piper advised only one gentle effort to deliver the head are the same as those described earlier. Traction from
with the Wigand or Mauriceau-Smellie-Veit method and, below is substituted for uterine contractions from above.
in the event of failure, to pass at once to the use of forceps.
Application, the baby’s arms are kept close to the trunk
and a towel is passed over the chest and arms forming a
HYPEREXTENSION OF THE
sling (Savage’s maneuver). The baby is gently raised. The FETAL HEAD (FIGS 31.34A AND B)
left blade of the forceps is held in the left hand and is
passed over the right hand placed in the vagina to the left Etiology
side of the maternal pelvis over the right side of the fetal Spasm or congenital shortening of the extensor muscles
head. The right blade is inserted on the opposite side and of the neck
the blades locked so that they sit along the occipitomental Umbilical cord looped around the neck
diameter, one over each ear. After locking the blades the Congenital tumors of the fetal neck, e.g. teratomas or
head is gently delivered. cystic hygromas
A B
C D
Figs 31.33A to D: A. Piper’s forceps—right blade application; B. Piper’s forceps–left blade application; C. Traction and delivery of the
aftercoming head by Piper’s forceps; D. Lateral view of Piper’s forceps applied to the fetal head
Uterine anomalies Dangers involved during Delivery

Placental tumors.
There is a risk of spinal cord damage by:
Diagnosis Excessive longitudinal stretching of the spinal cord
X-ray appearance is classically called “star gazing fetus.” Extreme flexion of the neck during delivery
Ultrasound measurement of the craniospinal angle. Marked torsion.

A B
Figs 31.34A and B: Arrest of after coming head in the occipitoposterior (face to pubis) position
Dural or epidural hemorrhage may occur. Dislocation delivery with subsequent stretching and tearing of
or fracture of cervical vertebrae is rare. Sudden flexion of intracranial ligaments and vasculature.
the fetal head may result in vaginal lacerations. Fractures of the skull bones.
Brain dysfunction: In a long-term study of term infants
PROGNOSIS FOR BREECH undergoing breech delivery, the incidence of serious
perinatal morbidity was 2.8% (0.5% in controls). Hence,
PRESENTATION
it is suggested that planned vaginal delivery remains
Maternal Prognosis an option for selected term breech patients. The
Genital tract lacerations and hemorrhage may occur due to difficulties noted included those in reading, writing,
rapid and forceful delivery of the baby through a pelvis that and disturbances in hearing, sight and speech.
is too small or where the soft parts have not been dilated.
Prematurity
Krebs and Langhoff-Roos, in their study of 15,441
primigravidas with breech presentation concluded that 94.1% of breech stillbirths and neonatal deaths involve
elective cesarean delivery was associated with lower rates fetuses with birth weight ≤ 2500 grams.
of puerperal fever and pelvic infection [relative risk (RR):
0.81; 95% confidence interval (CI): 0.70–0.92], hemorrhage
Congenital Anomalies
and anemia (RR: 0.91; 95% CI: 0.84–0.97), and operation Congenital anomalies are more common in breech
for wound infection (RR: 0.69; 95% CI: 0.57–0.83). Women presentations and account for 35.3% of breech stillbirths
with elective cesarean delivery more often underwent and neonatal deaths. Common anomalies are congenital
elective cesarean delivery in their second pregnancy dislocation of hip, hydrocephaly, anencephaly and
(RR: 1.25; 95% CI: 1.21–1.29). Thromboembolic disease meningomyelocele.
occurred the 0.1% of operated patients and anal sphincter
defects in 1.7% of vaginal deliveries. Birth Asphyxia
It may occur due to:
Fetal Prognosis Prolonged compression of the umbilical cord between
Breech deliveries accounted for around 25.5% of all the pelvis and aftercoming head
stillbirths, and 25.8% of neonatal deaths. Fetal mortality in Cord prolapse
breech presentations is three times higher than in cephalic Aspiration of liquor and vaginal secretion due to
presentation. It is highest in double footling breech and premature breathing efforts

lowest in frank breech. Prolonged labor.
Injury to the Brain and Skull Fetal Injuries

Intracranial hemorrhage: Due to sudden compres- The injuries noted are:
sion—decompression of the unmolded head during Fracture of fetal neck, humerus, clavicle or femur
Cervical and brachial plexus palsies a traumatic delivery is anticipated. However, their results
Hepatic rupture do not support use of tocolytics for routine cesarean
Splenic lacerations breech delivery.
Fetal adrenal gland rupture
Pharyngeal injures during Mauriceau-Smellie-Veit PRETERM BREECH DELIVERY
maneuver.
Twenty to eighty percent of preterm fetues are in breech
presentation. Frank breeches (67%) are more common
THE TERM BREECH TRIAL than incomplete or footling breeches. Labor carries the
In 2001, ACOG (American College of Obstetricians and risk of cord prolapse, and decreased potential of the
Gynecologists) recommended that obstetricians continue fetus to withstand acidosis. There is increased risk of intra-
their efforts to reduce breech presentations in singleton ventricular hemorrhage from the fragile capillary choroid
gestations through application of external cephalic version plexus which can be worsened by hypoxia and acidosis,
wherever possible and that patients with persistent breech 6–18% of preterm breech fetuses have congenital anoma-
presentation at term in a singleton gestation undergo a lies.
planned cesarean delivery.
Birth Weight 1500–2500 Grams
The SOGC (Society of Obstetricians and Gynecology
Footling breech presentation should be managed by
of Canada) interim position paper on the management of
elective cesarean delivery as cord prolapse can occur in
term breech states:
18% of these presentations.
Interim analysis indicates outcome is better in the
If the ultrasound estimated fetal weight is more than
cesarean delivery group when compared to planned
2000 grams (even a 20% error assumes a lower limit of 1500
vaginal delivery group.
grams) and the craniospinal angle is less than 90, vaginal
The physician should inform all patients with term
delivery can be attempted.
breech presentations of the results of the interim
Continuous fetal monitoring is essential. The membranes
analysis of the term breech trial study.
are kept intact as long as possible. Epidural analgesia can
Individual physicians should address their own
be used liberally. A liberal episiotomy is given in the second
expertise and skills in the management of the term
stage allowing upto 3.5 minutes for delivery of the fetal head
breech.
Decisions about the method of delivery of the term
breech should be made on an individual basis after full

disclosure of the risks and benefits.
CESAREAN SECTION FOR BREECH

PRESENTATION
Entrapment of the fetal head can occur if the uterus con-
tracts down after delivery of the body even in an adequate
appearing lower uterine segment. Many authors advocate
a low vertical incision for a preterm breech presentation.
This often extends into the upper segment necessitating
cesarean delivery in subsequent pregnancies.
The principle of delivery of a breech is to avoid trauma
to the fragile fetal head. A low transverse incision is made
keeping the membranes intact and the breech is quickly
extracted. Instead of a T-shaped incision in case of difficult
delivery, the incision may be curved upwards to avoid
traumatizing the uterine vessels. Some authors suggest
that ritodrine and nitroglycerine are safe agents to use at
cesarean breech delivery along with epidural or spinal
anesthesia, and may be considered for uterine relaxation if Fig. 31.35: Prague maneuver
without compromising the Apgar score. Routine use of by cesarean section), neonatal deaths or average age of
forceps has not been found to be advantageous. discharge (121 days for both groups).
Birth Weight Less than 1500 Grams Entrapment of Fetal Head (Fig. 31.35)
It has been suggested that fetuses weighing between 750
and 1500 g be delivered by cesarean section. The survival This may occur in preterm fetuses or with footling presen-
rate of fetuses between 750 and 1500 g is 89% and those tation, where the largest diameter (fetal head) delivers last
between 500 and 750 g is 22%, hence, cesarean delivery of and gets trapped above the incompletely dilated cervix.
fetuses less than 750 g is not advisable. Management is by deep anesthesia to relax the cervix,
During cesarean delivery, a splint technique with pushing the cervix over the head which is gripped and
forearm inserted into the uterus to splint the torso with the delivered by the Mariceau–Smellie–Veit maneuver (shoe-
head supported in the palm has been advocated. horn method) or by Dührssen’s incisions on the cervix
There are also recommended delivering preterm breech as a final measure when other attempts fail. All these
presentations with membranes intact (in caul). There was procedures along with extraction of the head needs to be
no difference in Apgar score (6 in vaginal delivery and 5.5 accomplished in less those 3.5 minutes. Fetal morbidity
by cesarean section), pH (7.41 by vaginal delivery and 7.32 and mortality is, however, extremely high.
1. What do you understand about malposition and malpresentation?
2. Define:
i. Brow presentation
ii. Vacuum extraction
iii. Cord presentation
iv. Wigand-Martin maneuver
i. Baby may be delivered by ___________ in term fetus if the cervix is > 7–8 cm dilated.
ii. ___________ is lying inside or outside the vagina following rupture of membrane.
iii. ___________ position occurs before onset of labor and during antenatal period.
iv. The anterior shoulder impinges under the pubic symphysis and the ___________ and ___________ are born over the
perineum.
v. As the head passes rapidly through the ___________, molding does not occur.
4. What are indications for trial of labor in breech presentation?
5. Explain the term forceps delivery in breech presentation.
6. Name the types of breech presentation.
7. Explain Thorn's maneuver.
32
Labor Dystocia:
Dysfunctional Labor
to 75 mmHg above a baseline of 5 to 20 mmHg. Uterine work

INTRODUCTION
can be expressed as montevideo (MV) units. Most women in
An abnormal or difficult labor or childbirth is usually spontaneous labor will have 3 contractions in 10 minutes and
termed as dysfunctional labor or dystocia. Dysfunctional will produce approximately 100–200 MV units power in the
labor occurs in 8 to 10% of all deliveries and is the number second stage of labor. THe uterine work is complemented by
one cause of cesarean deliveries. As we have seen, in maternal expulsive efforts that become an important part of
normal labor dystocia occurs due to a combination of the power required to achieve vaginal delivery.
abnormalities. Ineffective uterine activity may be primary or secondary
Management of labor based on evidence and best due to the following conditions:
practices can significantly reduce the incidence of dystocia. Overweight
The criteria of effective uterine contractions is progressive Short stature
dilatation of the cervix with descent of the presenting part Prior version
within the specified time limit. Congenitally abnormal uterus
Failure to progress—it is defined as no progress of cervical Overdistended uterus as in multiple pregnancy and
dilatation for 2–4 hours, with adequate uterine contractions polyhydramnios

and after cervical dilatation of 3 cm or more. American Collage Malpresentations
Fetopelvic disproportion
of Obstetricians and Gynecologists (ACOG) recommend that
Overstimulation of uterus with oxytocin
the diagnosis of latent arrest disorders are not made until the
Dehydration and electrolyte imbalance
cervix is atleast 4 cm dilated. It is postulated that it is probable
Administration of an analgesic too early in labor or use
that most of them were not in active labor at the time of the
of continuous epidural anesthesia
decision to do a cesarean section. Recently, there is a more to
Extreme maternal fear or anxiety causing the adrenal
define active labor only after 6 cm of cervical dilatation.
medulla to secrete catecholamines that interfere with
uterine contractility.
ETIOLOGY
Dystocia can result from several distinct abnormalities
CLASSIFICATION OF DYSTOCIA
involving the cervix, uterus, fetus, maternal bony pelvis or
other obstructions in the birth canal. These abnormalities One of the most thorough evaluations of the first stage of
have been simplified by ACOG into three categories (3 P’s): labor is that by Friedman. He divided the first stage of labor
1. Abnormalities of power into the latent phase, and the active phase (Fig. 32.1).
2. Abnormalities of passage The active phase consisting of acceleration phase, phase
3. Abnormalities of passenger. of maximum slope and deceleration phase. Since then
numerous studies have been done which indicate that the
Abnormalities of Power or Uterine Contractions pattern of labor curve is different from what was observed
During normal labor the uterus contracts every 3 to 4 minutes in the 1950’s. Differences include a gradual rather than
and each contraction increases the intrauterine pressure by 25 an abrupt transition from latent to active phase of labor
Labor Dystocia: Dysfunctional Labor 307
TABLE 32.1: Abnormal labor patterns and diagnostic criteria

Diagnostic criteria
Labor pattern Nullipara Multipara
Latent phase > 20 hour > 14 hour
Prolongation disorder
(prolonged latent
phase)
Active phase
Protraction disorders slow progress
Protracted active Rate of cervical < 1.5 cm/
phase dilatation < 1.2 cm/ hour
hour
Protracted descent Rate of descent of < 2 cm/hour
presenting part < 1
cm/hour
Fig. 32.1: Phases of normal labor Arrest disorders no >3 hour >1 hour
progress
(5.5 hours rather than 2.5 hours described by Friedman),
Prolonged > 2 hour or more >2 hour or
no deceleration phase, the common occurrence of at deceleration phase more
least 2 hours elapsing in the active phase without cervical Secondary arrest of > 1 hour > 1 hour
dilatation and the 5th percentile of rate of dilatation being dilatation
less than 1 cm/hour.
The abnormalities of labor may be classified according to
Arrest of descent
Failure of descent
} No descent in
deceleration phase or
second stage
the period of labor in which they occur. In first stage of labor, Precipitate labor
the latent phase has only one abnormality, i.e. prolonged Dilatation > 5 cm/hour >10 cm/hour
latent phase. The abnormalities of the active phase are: Descent > 5 cm/hour >10 cm/hour
Protracted active phase
Secondary arrest of dilatation
Prolonged deceleration phase.
The abnormalities of the second stage of labor are:

Failure of descent
Protracted descent and arrest of descent
Finally the labor may be too fast, known as precipitate
labor (Table 32.1).
Prolonged Latent Phase

Latent phase is the period from the onset of regular Fig. 32.2: Prolonged latent phase. Dotted lines depict normal
uterine contractions to the beginning of the active phase. time and cervical dilatation
A prolonged latent phase occurs when regular painful
uterine contractions are present for an extended period of Causes of prolonged latent phase may be:
Excessive sedation or sedation before start of active
time without entering the active phase of labor (Fig. 32.2).
In a nulliparous woman the limit is 20 hours (6.4 hours phase
Prematurely administered epidural anesthesia before
normal) and in a multiparous woman it should not
exceed 14 hours (4.8 hours normal). Before labeling this start of active phase of labor
entity one should always rule out false labor. True labor in Unfavorable cervical status
nulliparous woman is manifested by cervical effacement Myometrial dysfunction, e.g. weak, irregular, ineffective
followed by cervical dilatation, show and regular, painful and incoordinated uterine contraction
uterine contractions. Conversely in the multiparous Cephalopelvic disproportion (CPD).
woman the initial stage of labor is often characterized by Consequences of prolonged latent phase are:
cervical dilatation followed by effacement. The amniotic Increased risk of subsequent labor abnormalities
membranes may or may not be intact. Cesarean delivery

Flowchart 32.1: Management of labor dystocia
Low Apgar score of the neonate runs the risk of prolonging a potentially dysfunctional
Need for neonatal resuscitation. labor. Also with oxytocin there is less time available to
correct fluid and electrolyte imbalance and to meet the
Management (Flowchart 32.1) patient’s psychologic needs. There is no opportunity to
Management consists of two steps: identify patients who are in false labor. If immediate
1. One is to provide supportive measures including delivery is required for clinical reasons (e.g. severe
intravenous hydration, rest and narcotic pain relief for pre-eclampsia or amnionitis), oxytocin infusion is
6 to 12 hours. 85% of these women begin spontaneous the treatment of choice with strong sedatives. Either
active labor. Another 10% cease contracting and thus option is acceptable and the decision requires obstetric
had false labor. They are discharged with the instruction judgment and a motivated informed patient.
to come in active labor. Only 5% experience recurrence
of an abnormal latent phase. Protraction Disorders
2. Other approach is to manage aggressively with amnio A protracted active phase is defined as a slow rate of
tomy and oxytocin infusion mostly the 5% resistant cases. dilatation or descent of the head in the active phase of labor.
But some obstetricians use this in all cases (active man The rate of dilatation in this disorder for nulliparous women
agement of labor). is 1.2 cm or more and for multiparous women it is 1.5 cm or
The latter course of management runs the risk of more per hour. For descent of the fetal head the rate is 1.0
performing an induction of labor with an attendant cm/hour or more for nullipara; for multipara it should be 2
higher risk of cesarean delivery whereas the former cm/hour or more as seen in the following graph (Fig. 32.3).
Fig. 32.3: Protracted active phase dotted lines show normal course Fig. 32.4: Arrest disorder
Causes of a dominant myometrial pacemaker, with several pace

Main causes of protraction disorders are: makers firing independently without coordinated uterine
CPD in about a third of the cases contractions (incoordinate uterine action). Oxytocin
Excessive sedation usually corrects the underlying problem.
Fetal malposition, e.g. occipitoposterior position
Use of conduction anesthesia (above T10 dermatome) Arrest of Descent

Pelvic tumors obstructing the birth canal. Arrest of descent may be due to inadequate uterine
contractions, CPD, malposition of the fetus, asynclitism
Treatment of the fetal head. A thorough evaluation of the pelvis and
Treatment depends on the presence or absence of fetopelvic fetus is essential. If there is any fetopelvic disproportion
disproportion, adequate uterine contractions and the a cesarean section is required. If not so, oxytocin can be
fetal status. Reassess the pelvis for adequacy. Cesarean used or operative vaginal delivery may help.
delivery is indicated in the presence of confirmed fetopelvic Management depends on the underlying cause and
disproportion. In other cases conservative management includes oxytocin/operative vaginal delivery/cesarean
consisting of support and close observation, carries a good section. The choice is guided by the fetal status, station of
prognosis for vaginal delivery if continued progress occurs the fetal head and maternal status.
and there is no fetal compromise. Uterine contractions can Using labor progression guidelines based on the slower
be enhanced by oxytocin in the absence of other indications labor curves characteristic of parturients. Rouse and
for cesarean section. The fetus is closely monitored. colleagues (1999) demonstrated the effectiveness of a new
protocol to treat arrest disorders, which has 3 principal
Arrest Disorders elements:
1. An intent to achieve a sustained uterine contraction
Arrest disorders are defined as the cessation of either
of greater than 200 MV units as measured by an
cervical dilatation or the descent of the fetal head in the
intrauterine pressure catheter (of cardiotocometer) or at
active phase of labor. In their pure form arrest disorders
least 3 contractions in 10 minutes and each contraction
differ from protraction disorders in that prior to the arrest,
lasting for 30 to 40 seconds (charted on partograph).
the rate of cervical dilatation or descent of the fetal head
2. A minimum of 4 hours of oxytocin augmented labor
was normal as is seen in partograph (Fig. 32.4).
arrest with a contraction pattern of greater than 200 MV
units is mandatory before proceeding to abdominal
Etiology
delivery for active phase arrest, which is more liberal
About half of arrest disorders have cephalopelvic dispro than the original (Friedman 1978) cutoff of 2 hours.
portion. Other causes are fetal malposition (e.g. occipito 3. For patients who cannot sustain a uterine contraction
posterior, occipitotransverse, face or brow) inappropriate pattern of 200 MV units, administration of a minimum
sedation or anesthesia. of 6 hours of oxytocin augmentation before proceeding
to cesarean delivery for active phase labor arrest.
Arrest of Dilatation With these guidelines, the researchers could achieve a
It may be due to ineffective uterine activity (hypotonia) 92% vaginal delivery rate with no serious adverse maternal
or uterine contractions may be noted to stop due to loss or perinatal effects. The only side effect was an increased
risk of maternal infection. The risk was proportional to the

time elapsed. Close fetal monitoring is very important.
Prolonged Deceleration Phase

It is the slow progress of labor beyond 8 cms of cervical dil
atation. Some authorities argue that there is no decelera
tion phase of active labor and if it appears, is an ominous
sign and a cue for close monitoring of both the mother
and the fetus. Uterine contractions become dysfunction Fig. 32.5: Precipitate labor (dotted lines are normal)
al and are not corrected by oxytocin, the cervix becomes
edematous and fetal caput and molding occur. The cause Causes
may be fetal malposition, deflexed occipitoposterior (OP)
Extremely strong uterine contractions may be due to
or occipitoanterior (OA) position at a high station or true
oxytocin administration
CPD. Cesarean section is the only management left in such
Low birth canal resistance.
cases and must be resorted to early.
Prolonged Second Stage Complications

The normal second stage lasts for 20 minutes in multiparous The maternal complications are rare if the cervix and
and 50 minutes in nulliparous women. The second stage birth canal are relaxed but if it is rigid, chances of uterine
may be prolonged due to arrest of descent or rotation. rupture and lacerations of the birth canal are greater.
Previously when the second stage lasted more than one It is also known antecedent of maternal amniotic fluid
hour in multiparous women and two hours in nulliparous embolism.
women and two and three hours respectively under May accompany abruptio placentae.
anesthesia it was considered a prolonged second stage. Higher incidence of postpartum hemorrhage as the
Currently based on many trials, some obstetricians think uterus which is hypertonic in labor tends to be come
that as long as there is no serious fetal heart rate abnormality suddenly hypotonic postpartum.
and the fetus is tolerating the stress of the second stage well;
the mother is well hydrated and reasonably comfortable; Fetal Complications in Precipitate Labor
there is some progress of descent or rotation of fetal head, Perinatal mortality is high because of:
there is no need of terminating the second stage early Hypoxia due to decreased uteroplacental blood flow due
regardless of the cumulative time of pushing efforts. However, to more frequent and more severe uterine contractions
there is usually increased maternal blood loss probably due and increased basal uterine tone.
to increased surgical interventions, e.g. blood may be lost Possible intracranial hemorrhage due to presenting part
due to trickling of blood from an episiotomy incision while
literally serving as a battering ram against unyielding
the obstetrician waits for labor to progress. This generally
maternal tissue and may sustain trauma.
happens with epidural analgesia. Management consists of
Unattended delivery may result in direct injury from ill
operative vaginal delivery or cesarean section depending
directed efforts and resuscitation may not be available.
upon maternal and fetal status and the decision of attending
obstetrician.
Treatment
Precipitate Labor Disorders Oxytocin may be stopped if that is the cause of hypertonic
A labor is called precipitate when the combined duration uterine contractions. Once it is stopped the effect is seen
of the first and second stage of labor is less than two hours. within 5 minutes.
According to the partograph, precipitate dilatation in a The patient is put in lateral position to prevent pres
nullipara is a maximum slope of 5 cm or more per hour and sure on inferior vena cava. If there are fetal heart rate
in a multipara a maximum slope of 10 cm or more per hour. abnormalities caused by excessive uterine contractions
Precipitate descent for a nullipara is the descent of the fetal then besides discontinuation of oxytocin retrodrine
presenting part of 5 cm or more per hour and for multiparas can be used in the drip slowly (if there is no contrain
as descent of 10 cms or more per hour (Fig. 32.5). dication). Other drugs, e.g. betamimetics epinephrine,
magnesium sulfate and various tocolytic agents have Causes

been recommended but they are not of much use. Bony pelvis: Any contraction of the pelvic diameter at
Anesthesia, analgesia and any physical attempt to the level of inlet, midpelvis or outlet or a combination
retard delivery are absolutely contraindicated. of these can cause obstructed labor.
• Inlet: Anteroposterior diameter < 10.0 cm
PREVENTION OF DYSTOCIA Transverse diameter < 12.0 cm.
• Midpelvis: Inter-ischial spinous diameter (ISD) < 10 cm
There are certain factors in the antenatal and intranatal
–– Sum of ISD (10.5) cm + posterior sagittal diameter
period, which help in reducing the incidence of dystocia.
– (5 cm) = < 13.5 cm.
Careful monitoring of labor can prevent most of the –– Outlet: Inter-ischial tuberous diameter also called
dystocia. transverse diameter of the outlet (TDO) < 8 cm.
Timely diagnosis of CPD, malpresentation and malpo
Rickets or osteomalacia cause specific pelvic def
sition. ormities.
Action to be taken according to partogram for LSCS or
Soft tissue and bony obstruction
instrumental delivery depending on the maternal and • Cervical fibroid
fetal condition. • Ovarian tumor below the presenting part
Training of midwives to detect prolonged labor and • Tumor of pelvic bone, rectum or bladder
timely referral to a higher center. • Pelvic kidney
• Vaginal atresia or stenosis either congenital or due to
EFFECTS OF DYSTOCIA previous surgery
• Cervical stenosis due to previous surgery (e.g.
Mother and fetus both are adversely affected whenever Manchester repair)
the labor is prolonged with serious consequences. These • Constriction ring of uterus.
effects are: Fetal abnormalities
Intrapartum infection • Large baby (macrosomia)
Obstructed labor • Hydrocephalus
Rupture of the uterus • Fetal ascites
Pelvic floor injury. • Conjoined twins
• Locked twins
Intrapartum Infection • Monster baby
The incidence of chorioamnionitis is increased in • Occipitoposterior position combined with minor
prolonged labor especially in the setting of ruptured pelvic deformities causing deflexed head
membranes. Bacteria from the vagina ascend into the uterus • Breech presentation with large fetus
and invade the decidua and chorionic vessels leading to • Mentoposterior position of face
• Brow presentation
maternal and fetal bacteremia and sepsis with consequent
• Transverse or oblique lie
maternal and perinatal morbidity and mortality. If the fetus
• Compound presentation.
is born alive, it may suffer from pneumonia due to aspiration
of infected amniotic fluid. Pathology
Obstructed Labor Normally the upper uterine segment is an active segment
with fundal dominance of myometrial contractility and
Obstructed labor is a prolongation of labor almost with the lower uterine segment is a passive segment, which is
fully dilated cervix where further progress is impossible stretched as the fetus descends (Fig. 32.6).
without assistance despite good uterine contractions. The junction between the two is known as the retraction
The arrest is most often due to mechanical obstruction ring. Whenever there is an obstruction to the descent of the
(cephalopelvic disproportion). In developing countries we fetus the upper uterine segment manifests by progressively
still receive referred patients admitted with the diagnosis strong uterine contractions and retractions. With time this
of obstructed labor, especially in rural areas where skilled segment becomes thick while the lower uterine segment
supervision is lacking. becomes thin, stretched and over distended, resulting in
Fig. 32.6: Changes in the upper and lower uterine segment and Fig. 32.7: Changes in the upper and lower uterine segment
formation of retraction ring in normal labor and formation of pathological retraction ring (Bandl’s Ring) in
obstructed labor
formation of a pathological retraction ring (Bandl’s ring) Diagnosis

which can be seen as a groove between the symphysis and History of prolonged labor is present.
the umbilicus (Fig. 32.7). General examination
Primigravidae generally responds to obstruction by The patient is examined for general condition, presenta
developing hypotonic uterine intertia and non progress tion and position and condition of the fetus and assess
of labor while the multiparous women continue having ment of the pelvis.
progressively stronger uterine contractions leading to Early rupture of membranes due to non-application of
rupture of the uterus and fetal demise. The urinary bladder presenting part to the cervix.
is distended due to obstruction and compression of the Labor pains become severe, frequent, prolonged with
vesicourethral junction by the presenting part. In prolonged bearing down effect. This phase may be followed by sudden
obstruction this part may suffer ischemia leading onto cessation of pains in a nulliparous woman due to uterine
fistula formation later on. inertia and rupture uterus in a multiparous woman.
Formation of caput succedaneum is due to collection The patient is exhausted and anxious-looking with fever
of fluid on the most dependent part of the fetal head. In and dehydration. The tongue is coated, with a foul smell
obstructed labor this caput becomes so large as to reach in breath. Pulse rate and respiratory rate are high.
upto the pelvic floor although the head is still not engaged. Abdominal examination
In such a setting an inexperienced obstetrician may make Tense, tender, tonically contracted uterus, firm to hard
premature and unwise attempts at instrumental delivery. to feel.
Excessive fetal head molding, i.e. overlapping of cranial The round ligaments are taut and very tender.
plates at the major sutures may occur due to strong uterine The lower uterine segment feels thin and overstretched
contractions. This may lead to tentorial tears, laceration of with appearance of Bandl’s ring. Distended bladder is
fetal blood vessels and intracranial hemorrhage. seen as a suprapubic swelling with a transverse depression
Characteristic pressure marks may form upon the between the fundus and lower uterine segment (Fig. 32.8).
scalp, covering the portion of head that passes over the Fetal parts cannot be palpated and there is evidence of
promontary of the sacrum. fetal bradycardia or absent fetal heart sounds (FHS).
Skull fractures may be found occasionally, especially, if Vaginal examination
some one tries to deliver forcibly, ignoring the signs of The vulva is swollen and edematous (because of repeated
obstructed labor. These fractures are either a shallow per vaginal examinations)
groove or a spoon-shaped depression just posterior to the The vagina is hot and dry with purulent discharge
coronal suture. The cervix is generally fully dilated
The mother may have dehydration due to increased Large caput succedaneum is felt reaching almost upto
muscular activity and inadequate fluid intake. There may be the introitus
metabolic acidosis due to fat metabolism in the absence of Extreme molding of head and impacted fetal presenting
adequate carbohydrate intake. Electrolyte imbalance may part in the pelvis while the major diameter of presenting
lead to muscular hypotonia and consequent postpartum part may still be lying above the brim
hemorrhage. It is very difficult to negotiate a sterile catheter in the
Repeated internal examination may cause features of bladder due to jammed presenting part
chorioamnionitis leading on to septicemia. Rupture of the uterus should always be excluded.
period. Previous history of prolonged or difficult labor and

history of big babies in the last pregnancy may be elicited. At
term failure of engagement of head and abnormal position
may give indication for cephalopelvic disproportion.
Anticipation in labor—abnormal uterine activity may
be obvious.
Management of labor should be done with charting
on a partograph so that any anomaly of the active phase
and the second stage can be detected in time and tackled
promptly. Abnormality of prolonged labor and arrest are
to be dealt with actively. Reassesment and management
according to results and findings is essential.
Curative Treatment
General Measures
Fig. 32.8: Bandl’s ring Start intravenous infusion to correct dehydration and
electrolyte imbalance.
Maternal Morbidity and Mortality Bladder may be catheterized to monitor urinary output
and examine the urine with a self retaining catheter. It
Causes may be:
should be kept for 10 to 14 days post delivery to prevent
Ruptured uterus
subsequent genitourinary fistula.
Operative procedures
Blood transfusion may be arranged according to the
Anesthetic complications
general condition of the patient and hemoglobin level.
Postpartum hemorrhage
Broad-spectrum antibiotics should be administered to
Puerperal sepsis.
combat infection immediately and later on modified
Perinatal Morbidity and Mortality according to culture and sensitivity report of the vaginal
It may be due to fetal hypoxia subsequent to: swab, which should be taken immediately.
Tonic uterine contractions
Injection morphine sulfate 15 mg IM or injection
Cord prolapse
pethidine 100 mg IM to reduce uterine activity and allay
Rupture uterus
pain and anxiety should be given.
Fetal acidosis.
Specific Measures
Intracranial Hemorrhage Always rule out uterine rupture, as it requires immediate
Tentorial tear laparotomy.
Traumatic delivery Cesarean section is the procedure of choice in cases
Intranatal sepsis. of threatened rupture of the uterus even with a dead
fetus and in most cases of alive fetus, preferably under
Management of Obstructed Labor general anesthesia. Lower segment cesarean section is
The outcome depends on the general condition of patient, generally performed, however there is always a risk of
duration of obstructed labor, facilities at the treating lateral extension due to thinning of the lower segment
center and availability of transport in time, if in a remote and jammed presenting part. Assistance may be needed
peripheral area. from the vaginal side to push the head up or take out the
breech first or use Patwardhan technique.
Prevention Destructive operations can be done by trained obste
All women with high-risk factors for obstructed labor should tricians (see Chapter 60) in case of a dead fetus.
be referred in the antenatal period itself and delivered in a Make arrangements for prevention and management
hospital with facilities of anesthesia and blood transfusion. of subsequent postpartum hemorrhage in the form of
Women with short height are to be suspected in the antenatal oxytocin and blood for transfusion.
Classification and Etiology

Rupture of uterus may occur during the pregnancy or
labor which in turn may be spontaneous of traumatic—
(a) rupture during pregnancy and (b) rupture during labor.
Rupture during Pregnancy

Spontaneous rupture of the uterus may occur during
pregnancy due to previous trauma:
• Cesarean section (mainly classical) and closure in a
single layer
• Previous repaired uterine rupture
• Previous myomectomy incision (which went through
or up to the endometrium)
• Deep cornual resection of the interstitial portion of
A B
the fallopian tube in a previous ectopic pregnancy
Figs 32.9A and B: Ruptured uterus • Metroplasty
• Abortion with instrumentation—currette, dilator
• Sharp or blunt trauma—hit with bull’s horn, accidents,
Rupture of Uterus (Figs 32.9A and B)
bullets, knives
Rupture of the uterus is one of the serious complications • Silent rupture in previous pregnancy
that may occur during pregnancy or labor. The incidence • Manual removal of placenta especially in placenta
varies among different institutions with a wide range of accreta may damage the underlying muscles.
1:500 in referral hospitals catering to rural areas to 1:18, in Rupture of intact uterus—rupture during pregnancy
the developed world. Although the frequency of uterine with intact uterus is very rare but may occur in the
rupture from all causes has probably not decreased following conditions:
remarkably during the past several decades, the etiology • Pregnancy in underdeveloped uterine horn of a
of rupture has changed appreciably and the outcome has bicornuate uterus
improved significantly due to availability of better referral • Placenta increta or percreta
system, transport, blood transfusion and antibiotics. • Gestational trophoblastic neoplasia
• Adenomyosis
Definitions • Sacculation of entrapped retroverted uterus.
Traumatic rupture of uterus in pregnancy is rare and
Rupture of the uterus may be complete or incomplete
Complete: Rupture of the uterus may communicate
most often is due to blunt trauma by falls, accidents and
directly with the peritoneal cavity. There is full thickness external version or sharp trauma with bullet or knife
and even the horn of a bull (one case was seen our hos
uterine separation including peritoneum and there
pital in recent years).
may be fetal extrusion.
Traumatic rupture during labor generally occurs in the
Incomplete: Visceral peritoneum is still intact over the
lower uterine segment. The various causes may be:
uterus or the broad ligament.
Internal version
Dehiscence: Generally used for a previous cesarean
Difficult forceps delivery
section scar in which the fetal membranes are not Breech extraction
ruptured and the fetus is not extruded into the peritoneal Destructive operations
cavity. The peritoneum overlying the defect is also intact Vigorous uterine pressure during delivery
while in rupture of the scar there is separation of the Difficult manual removal of placenta
old uterine incision throughout most of its length with Perforation by intrauterine pressure catheter
rupture of the fetal membranes and communication of Sharp or blunt trauma
the uterine and peritoneal cavity. The whole of the fetus Rupture of the uterus with a previous cesarean section
may be lying in the peritoneal cavity outside the uterus. shorter intercesarean interval.
Rupture of a previous cesarean section scar obliquely. It may involve the cervix and vagina or even the
In the present era, more than 50% of ruptures of the uterus bladder or extend upwards into the upper uterine segment.
are associated with previous cesarean section. During The fetus is expelled complete into the peritoneal
pregnancy, it is the classical cesarean section scar that cavity with intraperitoneal hemorrhage or partially if
gives way more often (4%) than the lower segment one the presenting part is firmly engaged in the pelvis. In
(0.4%), maybe because of defective healing (as the upper incomplete rupture the hemorrhage frequently extends
segment keeps contracting during puerperium hence no into the broad ligament and may result in a retroperitoneal
rest) or because the placenta may be situated over it. There hematoma which may extend even up to the renal area.
may also be incomplete hemostasis and infection during
healing of last operation. There is increasing evidence Clinical Features
of a four-fold higher risk of uterine rupture in previous Rupture during pregnancy is difficult to diagnose and
cesarean delivery with single layer closure as compared to mimics concealed accidental hemorrhage or other
double layer closure. causes of acute abdomen. So attention should be paid
The process is insidious and signs and symptoms are to any abdominal pain complained by a patient with
misleading so it may appear as silent rupture. The scar previous scarred uterus. The patient may even have
generally gives way between 34 and 38 weeks of pregnancy referred chest pain from diaphragmatic irritability due to
when the uterine distension reaches its maximum although hemoperitoneum. One may even think of pulmonary or
uterine rupture as early as 24 weeks is also reported. In amniotic fluid embolism in such cases.
silent cases the fetal sac herniates through the scar and the The clinical picture is in accordance with the amount
uterus retracts thereafter. There is little or no bleeding in of hemorrhage and time taken to diagnose the condition.
this process. These ruptures are almost always complete. In case of protracted labor there will be all the signs and
If the placenta is implanted on the scar, rupture is more symptoms of a long and difficult labor, i.e.
common with poor prognosis as bleeding is profuse due Severe pain due to strong uterine contractions with
to perforation by the placenta. Lower segment scar on the distended bladder and Bandl’s ring (threatened rupture
other hand usually ruptures during labor and most of the of uterus)
times it is only a dehiscence. With complete rupture there is feeling of giving way and
Ultrasonography is helpful in early diagnosis of such
temporary relief
cases. With prior cesarean delivery the American College
Collapse due to hemorrhage and shock with little or no
of Obstetricians and Gynecologists (ACOG) cite the
vaginal bleeding
following figures for uterine rupture associated with a trial
Irregularity of fetal heart rate is the earliest sign. When
of labor—1 to 7% with low vertical incision, 4 to 9% with
the baby is removed within 20 minutes of this sign the
T-shaped and classical scar, 0.5% with low transverse scar.
chances of survival are good
Because of the risk of subsequent scar rupture the
Fetal parts are easily palpable
selection criteria for vaginal birth after cesarean section
A contracted hard uterus is felt separate from fetus
(VBAC) should be stringent, i.e. hospital delivery should
Receding of the presenting part which was earlier in the
be mandatory where a physician capable of monitoring
pelvis
labor and performing an emergency cesarean section
Absence of fetal heart
delivery is available throughout active labor. In our
Hematuria may be present
institution we allow VBAC in previous one low transverse
On per vaginal examination, the cervix hangs loose with
cesarean section and a clinically adequate pelvis with
no other uterine scar or previous rupture, under close presenting part high up.
supervision as long as at least three years have elapsed Appearance of blood at the vulva in a case of obstructed
since the previous cesarean section. labor usually indicate rupture of the uterus. But if the
presenting part is firmly impacted, bleeding may not be
Rupture during Labor seen. In patients seen late after rupture there is tenderness
Rupture during labor usually occurs after a protracted all over the abdomen. A fluid thrill or shifting dullness can
labor. The upper uterine segment contracts and retracts be elicited per abdomen and needle aspiration reveals
while the lower uterine segment distends and stretches thin blood. Fetal limbs becomes abnormally easy to feel. The
with formation of a pathological retraction ring (Bandl’s). presenting part is seen high up in the pelvis and the mostly
So the rupture usually involves the lower segment in the empty uterus is concealed behind the fetus but it may
immediate vicinity of the cervix extending transversally or sometimes be felt.
In cases of previous lower segment cesarean section may be: Antibiotics—third generation cephalosporins and
Suprapubic pain and bladder tenesmus gentamycin to cover gram-positive and gram-negative
Hematuria bacteria along with an adequate cover for anaerobes
Severe variable decelerations or clinical evidence of with an appropriate antibiotic (metronidazole)
fetal distress Foley’s catheter is inserted to monitor the output
Scar tenderness Arrangement for immediate laparotomy.
Diffuse fluctuant swelling over the anterior and antero
lateral aspect of the lower segment Specific Measures

Ever increasing pain followed by collapse in complete Immediate laparotomy should be performed in all cases
rupture. of rupture of the uterus. Do not attempt to deliver the baby
Sometimes the rupture may be detected after the vaginally.
delivery. So, following all intrauterine manipulations one After delivering the fetus and placenta look for the
should examine the uterus thoroughly for any associated site of damage. In cases of previous cesarean section in
rupture. In cases of previous cesarean section it is our policy the lower segment one may repair the scar if the tear is
not to explore the scar unless there is evident hemorrhage small; the edges are not ragged and infected and there is a
outside or the uterus fails to contract or the patient collapses. strong reason to preserve the uterus (e.g. no living issue).
Therefore, such patients should be carefully monitored in Concomitant tubal sterilization may be done if the patient
the fourth stage of labor. has the desired number of children. The anterior wall is
most commonly involved. Sometimes the bladder is also
Prognosis torn and the rupture tear may extend downward into the
vagina and laterally into the broad ligament. Posterior
Maternal morbidity and mortality depends on the type
rupture of the lower segment occurs in cases of traction on
of rupture, time taken to come to the facility, amount
a high head with forceps or on a high after coming head.
of bleeding, time taken to diagnose the condition and
In all other cases with ragged unrepairable tears hys
efficiency of management. It is much better to diagnose
terectomy should be done. Speed is essential in all such
uterine rupture too readily, than to miss it as any delay
cases. If the patient can stand it and in cases of associated
gravely impairs the patients’ and the neonate’s chances of
colporrhexis, total hysterectomy is the best procedure.
survival. Speed and effectiveness of resuscitation is critical
Otherwise subtotal hysterectomy may be done with ampu
especially a large quantity of blood transfusion. A competent
tation till the site of rupture. If the bladder is also involved,
surgeon and anesthetist is vital. The fetus is generally dead
repair the rent in 2 layers and keep a Foley’s catheter for
unless rupture is diagnosed at the time of dehiscence.
continuous drainage for two weeks.
Otherwise, hypoxia from placental separation and maternal
In case of broad ligament hematoma: Do not try to clamp
hypovolemia will lead invariably to fetal death. Even after
and ligate as the uterine artery may have retracted. First
the diagnosis, the prognosis depends on the time taken
identify the bladder and ureter and then ligate the bleeding
to operate, availability of blood and antibiotics to combat
vessels. If one cannot identify the retracted uterine artery
infection. The main causes of maternal mortality are:
and there is peristent oozing in the field, internal iliac
Hemorrhage
artery may be ligated on one or both sides.
Shock
In some women, pelvic vessel bleeding may continue
Sepsis
even after internal iliac artery ligation. In such cases if the
Complications of anesthesia
facilities are available, angiographically directed arterial
Obstetric anuria.
embolization may be done, otherwise pack with gauze and
Mortality is highest in rupture following dystocia and remove it after 48–72 hours.
lowest after rupture of a cesarean scar. Treatment if seen late after rupture: Prognosis is very
poor as apart form hemorrhage, infection has also set in,
Management
leading to abdominal distension. Since the patient has sur
General Measures vived the initial hemorrhage, try to rally the patient round
Resuscitation with intravenous fluids with morphia, warmth and rapid, large blood transfusion
Arrange for blood transfusion to bring the BP to 90-100 mmHg before laparotomy. But do
Strong sedation and information to the anesthetist not wait too long and proceed with hysterectomy.
Rupture diagnosed after delivery: Needs the same Pelvic Floor Injury
treatment as the one diagnosed before. During childbirth the pelvic floor is exposed to direct
Postoperatively the first few hours after operation are compression from the fetal head and downward pressure
very important to complete the correction of shock (cor from maternal expulsive efforts resulting in functional and
rection with liberal blood transfusion). Electrolyte imbal anatomic alternation in muscles, nerves and connective
ance and ketoacidosis caused by preceding obstructed tissues. All these come back to normal (like the uterus and
labor is to be dealt with judiciously. An overload is to be other organs) during puerperium. However, in neglected
avoided. A Ryle’s tube maybe needed in a neglected rup cases of dystocia varying degree of injuries are seen. The
ture till bowel sounds return. types of injury varies from perineal tears, urinary and anal
Continue with intravenous fluids, blood transfusion incontinence to genital prolapse.
and antibiotics. Look for any evidence of sepsis. Keep the All injuries must be meticulously repaired immediately
Foley’s catheter for at least 2 weeks if rupture has occurred preferably under anesthesia after proper exposure to
after obstructed labor or a bladder rent has been repaired. complete the surgery.
1. What are preventions of dystocia?
2. What are the abnormalities of the active phase?
i. Ruptured uterus
ii. Arrest disorders
iii. Pelvic floor injury
i. Management consists of operative vaginal delivery or cesarean section depending upon ____________ and ____________
status and decision of attending obstetrician.
ii. ____________ peritoneum is still intact over the uterus or the broad ligament.
33
Reva Tripathy, Sudha Salhan
Complications of
Third Stage of Labor
woman can tolerate blood loss, which is fatal for an

DEFINITION anemic patient.
The third stage of labor starts after the delivery of the fetus Slow bleeding for a prolonged period may add up and
and ends at the delivery of the placenta and membranes. cause significant blood loss (e.g. from an unstitched
Some people define a fourth stage as the stage following episiotomy), which may not be recognized and cause
the delivery of placenta. These are crucial periods during sudden shock.
which disaster in the form of maternal morbidity and Sudden bleeding can occur even after a normal delivery.
mortality can be caused by the unwary practitioner. In many serious cases of concealed bleeding (retained
The complications of third stage are: clot behind the placenta or inside myometrium in
Postpartum hemorrhage (PPH)
placental abruption, in broad ligament and peritoneal
Retained placenta
cavity in rupture uterus and paravaginal and para-
Adherent placenta
vulval tissue spaces) the amount of revealed bleeding
Puerperal hematoma
may be insignificant and deceptively low. Therefore, it is
better to over diagnoses than under diagnose PPH.
Uterine inversion.
Blood loss during the first 24 hours after delivery is
early PPH and that between 24 hours and 6 weeks after
POSTPARTUM HEMORRHAGE delivery is late or secondary PPH.
It is one of the most common obstetric complications and Hence, PPH can be defined as the blood loss after the
one of the major causes of maternal mortality. Prompt delivery of the fetus which causes collapse of the mother
diagnosis and management is essential. and it can be less than the 500 mL (vaginal delivery) or
The classic definition of PPH is blood loss greater than 1000 mL (cesarean section).
Most often the uterine bleeding occurs primarily from
500 mL after vaginal delivery. It can occur before, during
the placental site. It is controlled initially by the contrac
and after delivery of the placenta. More than 1000 mL
tion of the interlocking uterine muscle fibers (biological
blood loss after cesarean section and twin vaginal delivery
ligature) (see Chapter 2, Fig. 2.12) and later by platelet
is also postpartum hemorrhage. This definition is not
aggregation and formation of fibrin thrombi in the decidual
always realistic because of the following reasons: spiral arteries and veins. Failure of uterine contractions is
In clinical practice, PPH is a diagnosis visually made
usually due to myometrial dysfunction (uterine atony) and
in the delivery room when the amount of the bleeding retained placenta.
exceeds the practitioner’s estimate of “normal”. Hence The causative factors are—uterine atony, genital tract
most of the time it is arbitrary calculation and usually trauma, clotting disorders. This can be summarized with
underestimated by 30–50%. the 4T’s–tone, trauma, tissue and thrombin.
The patient’s ability to withstand bleeding is very impor- 1. T-uterine atony
tant. A severely anemic patient may collapse with a loss 2. T-obstetric lacerations (trauma)
of as little as 100 mL of blood. Hence, the importance of 3. T-retained placental tissue
volume varies with the woman’s hemoglobin. A normal 4. T-coagulation defects (thrombin).
Complications of Third Stage of Labor 319
TABLE 33.1: Factors predisposing to atonic uterus

Past history of postpartum hemorrhage (PPH)
Retained placenta or cotyledon (bleeding from the placental site and partly contracted uterus)
Halothane anesthesia (uterus does not contract promptly)
Large placental site (twins, severe rhesus disease, large baby)
Low lying placenta (lower segment is less muscular and has less biological ligature effect)
Overdistended uterus (polyhydramnios, twins)
Placental abruption (blood in between uterine muscles and hence they are less efficient in contracting)
Uterine malformations
Prolonged labor (uterine exhaustion)
Anemia
Poor second stage uterine contractions
Elderly woman
Multiparity
In oxytocin stimulated labor—the drip must be continued beyond the third stage of labor otherwise reflex relaxation may occur, causing
PPH
Previous cesarean section
Amnionitis
Obesity
Known coagulation disorders
Precipitate labor
Fibroid uterus due to mechanical interference with uterine contractions. Also if the placenta is located at the fibroid site there may be
adhesions (because decidual reactions is less complete here)
Presence of clot in the uterus hampers its contractions.
PPH is responsible for 1,25,000 maternal deaths corrected before (prenatal) or during pregnancy. The
worldwide per year. The rate of blood flow to the uterus obstetrician can predict (from previous or recent obstetric
and the placenta is upto 600 mL/minute at term. Hence, history-table above) those who will have PPH. A history of
failure of the myometrium to contract even for a very short PPH in previous delivery or a history of retained placenta
period can rapidly result in significant blood loss. or placental adherence (all grades increta, percreta, etc.) in
Certain risk factors predispose to uterine atony are given a previous delivery must alert the obstetrician. Twin, large
in Table 33.1. PPH must be anticipated in these conditions. baby, polyhydramnios, low-lying placenta and placental
In antenatal period prevent/treat anemia, keep blood ready abruption in the current pregnancy are candidates for
and active management of the third stage is required. PPH. In high-risks cases blood is booked in the antenatal
Placental causes period itself (get blood donated in antenatal period only).
At the time of onset of labor: A vein is secured and blood
Retained placenta (partial or complete)
is kept ready. Precautions are to be taken in the second stage
Adherent placenta (partial or complete).
of labor. The baby’s trunk is delivered gently and slowly.
Traumatic causes Active management of third stage of labor is to be done.
Trauma to uterus, cervix, vagina and perineum Injection of 10 units of oxytocin after the delivery of the baby
Not stitching episiotomy in time. is given, controlled cord traction and uterine message is
Coagulation defects done (see Figs 27.2A and B). This reduces both postpartum
Intrauterine death causing coagulation disorder blood loss and the incidence of manual removal of placenta.
Pre-eclampsia, eclampsia, infection causing derangement The obstetrician should ensure that the uterus is well
of coagulation factors. contracted. All these women must be closely monitored to
prevent, detect and promptly manage PPH, if it at all occurs.
If the placenta is retained for 30 minutes or more and is
PREVENTION not delivered with controlled cord traction injection of the
Prepregnancy correction of anemia is very important. In umbilical cord with saline or oxytocin may help. However,
antenatal period, assessing risks in the antenatal period no time is wasted if there is bleeding and urgent manual
and correcting prevents PPH. Anemia is diagnosed and removal of placenta is to be done under anesthesia.
Spontaneous delivery of the placenta after administra-

tion of oxytocin leads to less blood loss during cesarean
section. There is reduction of blood loss (30%) and endo-
metritis (seven-folds) compared to manual removal of pla-
centa. Sometimes, PPH may be unpredictable and needs
to be identified and managed immediately.
Management: PPH is an emergency and must be promptly
managed. Do a rapid general assessment and examination
of the uterus and perineum. Evaluate signs of hypovolemia
(tachycardia and hypotension), any injury (lacerations,
hematoma) uterine tone (relaxed or contracted), uterine
size (large with retained placenta, etc.) and uterine
tenderness. Look for the source of bleeding. The broad
principles include:
Set up intravenous (IV) line
Assess for uterine atony and look for trauma
If atony is detected, give ergometrine 0.2 mg IV and star
oxytocin infusion
Arrange and cross-matched blood
Give high flow of oxygen Fig. 33.1: Checking the completeness of membranes
Empty the bladder
Monitor pulse, blood pressure (BP), and urine output.
If in shock give IV fluids until systolic BP > 100 mm

Hg and urine flows at > 30 mL/min. Rapid infusion of
Ringer’ lactate or normal saline is life-saving till blood for
transfusion is obtained. Oxytocin is given from another
venous channel.
Whenever PPH occurs it is essential to decide whether
bleeding is of placental or extraplacental in origin. This
must be done as soon as possible because after initial
emergency measures, subsequent management will
depend on this fact. As a rule of thumb, if the uterus is well
contracted the bleeding is unlikely to be uterine in nature,
i.e. it is from a laceration in the cervix or vagina or other
traumatic causes, whereas if the uterus is flabby, bleeding
is generally from the placental site.
If the placenta is delivered, it must be checked for
completeness. If incomplete, explore the uterus (Fig. 33.1).
If the placenta is complete, look for membranes. If Fig. 33.2: Uterine bimanual massage
complete then check the uterus for atony.
Mechanical compression by uterine bimanual massage
(Fig. 33.2) combined with brisk infusion of dilute to uterine atony. Its routine use is contraindicated in
oxytocin will correct most cases of uterine atony within hypertension and heart disease.
a few minutes. If bleeding is not controlled, can give PGF2α 250 mg
The most effective dose of oxytocin is 100–500 mU/min; deep intramuscular (IM) or misoprostol 600 µg per
this is achieved by adding 20–40 units of oxytocin to 1L rectal. It controls bleeding in 88% of cases. Ensure that
of crystalloid and infusing at 10–15 mL/min. the uterus is empty by exploration and if the bleeding
Give methylergometrine 0.2 mg IV, produces a tetanic is from the site of placenta previa hemostatic sutures in
contraction and this is effective in treating PPH due the area may help (during cesarean or after laparotomy).
• Firm uterine packing is no longer advocated.

• Pressure occlusion of the aorta may help us to gain
time. It can be done per abdominally or during
laparotomy. In the young and otherwise healthy patient
pressure occlusion can be maintained for several
minutes without permanent damage (Fig. 33.3).
Downward pressure with a closed fist over the
abdominal aorta, directly or through the abdominal
wall, just above the umbilicus and slightly to the left,
(after feeling the aortic pulsation) is applied.
With the other hand, palpate the femoral pulse to
check the adequacy of compression (Fig. 33.3). If the
pulse is palpated during compression, the pressure
exerted by the fist is not enough. If the femoral pulse Fig. 33.4: B-Lynch suture
is not palpable the pressure exerted is adequate.
Maintain compression till things are ready for
laparotomy, should bleeding recur. Uterine balloon tamponade
If the bleeding continues despite all the above, check
B-Lynch sutures (Fig. 33.4)
the coagulation profile bleeding time, clotting time, Stamp sutures.
platelets count, prothrombin time, kaolin clotting time, If all the measures fail, hysterectomy may be needed.
fibrin degradation products whichever is possible.
Persistent hemorrhage despite a firmly contracted PLACENTAL CAUSES
uterus necessitates a more thorough examination with
If the placenta has not been delivered but has separated
adequate exposure for injuries.
attempt to deliver it by controlled cord traction. If the
Explore the vulva, vagina, cervix for tears and the uterus
placenta has not separated after 30 minutes of delivery
for possible rupture.
of the baby, (and there is no bleeding) shift the patient to
Insert an indwelling catheter in urinary bladder to
operation theater (OT) and do manual removal of placenta
measure urine output and keep bladder empty.
under general anesthesia. But if there is bleeding do the
Conservative surgical options include (see Chapter 59).
manual removal quickly.
Stepwise vessel ligation (uterine, ovarian, hypogastric)
Angiographic embolization
RETAINED PLACENTA
Physiologically, the duration of the third stage is 30
minutes. With the use of oxytoxic drugs during delivery
and controlled cord traction, i.e. active management, the
third stage is complete in 10 minutes in 97% of labors. A
placenta not delivered by 30 minutes will probably not
be expelled spontaneously. The danger with retained
placenta is hemorrhage. This problem may occur in cases
with previous retained placenta; previous uterine surgery,
preterm delivery; maternal age > 35 years; placental weight
< 600 g; pethidine use in labor; induced labor; parity > 5.
Management: This depends on whether there is bleeding
or not. If there is no bleeding and the placenta does not
separate readily, avoid excessive cord traction the cord
may snap or the uterus may invert. Check that the placenta
is not in the vagina. One can inject saline or oxytocin in the
cord and wait. If the patient is bleeding and the placenta
Fig. 33.3: Compression of abdominal aorta and palpation of has not separated completely manual removal of placenta
femoral pulse (MRP) (see Figs 59.17A and B) under general anesthesia is
done immediately as delay may precipitate PPH. After MRP TABLE 33.2: Risk factors associated with placenta accreta
give oxytocic drugs, antibiotics and blood (if required).
Previous cesarean section (35%)
Uterine artery ligation: Uterine artery supplies 90 percent Parity (2–3%)
of the blood to the uterus. Direct ligation at laparotomy Placenta praevia (14%)
may control hemorrhage in 75–90% of cases. Previous history of curettage (18–60%)
Bilateral utero ovarian ligation: Bilateral internal artery Previously treated Asherman’s syndrome (15%)
ligation can be done. Prior manual removal of placenta
B-Lynch brace sutures: Brace sutures are place to compress Prior history of postpartum hemorrhage
the uterus and stop bleeding especially for stopping lower Endometritis
segment bleeding (Fig. 33.4).
Stamp sutures are applied to approximate uterine ultrasound examination, if there is lack of sonolucent area
musculature and stop bleeding. beneath the placenta site. Doppler imaging and MRI may
Radiographic embolization of pelvic vessels is done by be helpful, if there is suspicion.
trained interventional radiologists. It is helpful in both Most of the time the diagnosis is made after delivery of
atonic and traumatic PPH. Adequate recanalization of the fetus. Almost half of patients having placenta accreta
the blood vessels occurs in due course of time. present with PPH. In the acute setting the diagnosis is
Balloon occlusion of the internal iliac artery may be done. usually made clinically. An abnormally adherent placenta,
with no plane of cleavage with or without bleeding, may
ADHERENT PLACENTA suggest accreta and will often require manual extraction,
resulting in fragmentation and piecemeal removal.
Placenta Accreta, Increta and Percreta
Examination of placenta following manual removal may
The normal mechanism of the third stage of labor involves reveal missing cotyledons (see Chapter 23).
the development of a plane of cleavage in the spongy layer Once a postpartum clinical diagnosis of abnormally
of the decidua basalis underlying the placenta. Sometimes adherent placenta has been made, usually by the inability
this fails to occur. Most often a manual extraction of the to locate a plane of cleavage between uterus and placenta
placenta should be performed if spontaneous delivery has an important decision must be made between conservative
not occurred within a reasonable period of time (typically (which would ensure uterus preserving) versus more
30 minutes). radical treatment (where hysterectomy may be required).
It is exactly at this point that the operator should be To persist in trying to find a plane where none exists invites
accurately aware of the various forms of abnormally disaster; it is in this setting that hemorrhage is greatest. If
adherent placenta that may be encountered. Accreta there is no bleeding methotrexate may be given and a part
(villi adhere superficially to myometrium), increta (villi of placenta can be left in uterus, which will gradually get
invading the myometrium), and percreta (villi invading absorbed. We have done this in a couple of cases where
the full thickiness of myometrium and hence beneath or there is no bleeding by tying the cord an near the placenta
even through the uterine serosa) (see Chapter 23.) Each as possible and giving methotraxate with satisfactory
of these entities may be focal, partial, or total. In focal results. The patient is kept under observation; removal of
a single cotyledon may be involved. In partial one or totally adherent placenta may be dangerous. Pressure on
several cotyledons are involved and in total adherence the aorta may be beneficial.
entire placenta is involved. The pathological hallmark is Stepwise vessel ligation (uterine, ovarian and hypogas-
the absence of the decidua basalis; the fibrinoid layer of tric).
Nitabuch’s is often absent as well. Balloon occlusion of internal artery may help. Angio-
graphic embolism can be done, if available.

Incidence and Risk Factors Hysterectomy is clearly indicated if blood loss is
The incidence of placenta accreta has been reported in excessive or preservation of fertility is not an issue.
several large studies to range from 1/2,000 to 1/3,750. Risk
factors reported to be associated with placenta accreta are
listed in Table 33.2.
TRAUMATIC PPH
The sites of trauma may be vulval, perineal, cervical,
Presentation/Diagnosis uterine and broad ligament. The vulva, perineum, vagina
Antenatal: It can be suspected antenatally when there is and cervix should be carefully inspected immediately after
history of the risk factors reported above. On antenatal delivery of placenta with adequate lighting and assistance.
LACERATION OF THE VAGINA AND Repair of First and Second Degree Perineal Tear
Repair of the perineal tears should be done in and by
PERINEUM proper visualization in good light, requisite surgical instru
These are most often preventable if adequate perineal ments and suture material should be available, adequate
support is given during delivery of the baby. anesthesia should be used.
Many first degree tears may close spontaneously if
Predisposing Factors for Perineal Tears not bleeding. Before suturing explain to the patient the
Large babies (more than 4 kg) requirement of repair and get necessary consent. Place the
Malposition, e.g. persistent occipitoposterior patient in a lithotomy position. Apply antiseptic solution
Anesthesia-epidural to area around the tear. Local infiltration with lignocaine
should be done beneath the vaginal mucosa, the skin of
Most of them primigravida
the perineum and deeply into the perineal muscle using
Second stage-prolonged
about 10 mL 0.5% lignocaine solution; ensure that no
Shoulder dystocia
vessel has been penetrated (slightly by with drawing the
Midline episiotomy
plunger of the syringe). Pudendal block may also be used.
Delivery with instruments By placing a gloved finger in the anus and gently lift the
finger and identify the sphincter. If the sphincter is not
Classification of Perineal Tears injured, proceed with repair.
Injury to skin of the perineum, vagina and connective First and second degree laceration repair is easy.
tissue—first degree. Episiotomy or any minor perineal tears are quickly repaired
First degree plus perineal muscle injury not involving after massage has produced a contracted uterus. Begin the
anal sphincter—second degree. vaginal mucosa repair above the highest-extent of laceration
Perineal injury involving anal sphincter—third degree. to prevent retraction of blood vessels from the laceration
It is further divided as follows: or episiotomy site. These lacerations may bleed a lot and
• Less than 50% tear of external anal sphinctor (EAS) jeopardize the woman’s life. Hence, early repair is life saving.
(Fig. 33.5A) Approximation of layers by continuous sutures. If
• More than 50% tear of external anal sphinctor (EAS) the tip is beyond reach start as anchoring suture and
• Both EAS and IAS (internal anal sphinctor) are torn gradually reach the tip. Perineal muscles are next stitched
(Fig. 33.5B) by interupted stitches, if the tear is deep a second layer of
Perineal injury involving anal sphincter complex (both EAS
stitching is done. Repair of the skin may be done either
and IAS) with rectal mucosa—fourth degree (Fig. 33.6). by using interrupted suture or subcutaneous 2-0 suture
It is better to classify to the higher degree, when in starting from above downwards. Now see that rectum has
doubt. no stich by doing per rectal examination.
A B
Figs 33.5A and B: Perineal tears

Fig. 33.6: Complete perineal tear Fig. 33.7: Cervical stitching
Repair of Third and Fourth Degree Perineal Tear • The use of postoperative stool softeners and laxatives
like lactulose for postoperative wound dehiscence
In cases of mediolateral episiotomy the incidence of these
for about 7–10 days.
tears is 0.6–0.9% (Fig. 33.6). But hidden anal sphincter
Indwelling urinary catheter is generally required.
injuries do occur in 36% of deliveries (recognized by endo
Inspection of the cervix for any injury: In good light,
anal ultrasound). The repair is to be done in the operation
the posterior vaginal wall is retraced with Sim’s retractor.
theatre with appropriate instruments under regioWnal/
Three sponge holders W taken and the cervix is inspected
general anesthesia performed by experience obstetrician
meticulously all around. If a laceration is seen, it is to be
preferably with all aseptic precautions. Adequate light stitched (Fig. 33.7). Take the first stitch above the tear.
and assistance, with relaxed sphincter help to retrieve Place interrupted stitches.
the retracted torn ends of the anal sphincter and ease of A cervical or vaginal laceration extending into the
bringing them together. broad ligament is to be repaired by laparotomy. Evacuate
the resultant hematoma and obliterate the cavity with
Essential Steps Involve hemostatic sutures (something the tears are so extensive
Two methods are used overlap method or end to end that hysterectomy is required).
method. Basic steps are as follows:
Approximate the torn edges of the anal sphincter by
UTERINE RUPTURE
interrupted stitches 0.5 cm apart
Muscle layers are stitched and then covered with a layer of
If possible, simple hemostatic repair of a ruptured uterus
fascia. Rectal mucosa is stitched with continuous sutures with or without tubal ligation in a woman of high parity on in
poor condition is preferred if bleeding is stopped (Fig. 33.8).
The fascial sheath of the rectal sphincter is then reap-
However, if the tears in the uterus are extensive, irregular
proximated end to end.
and the patient continues to bleed a hysterectomy is life
saving. Depending on the general condition of the patient
Postoperative Care subtotal (cervix left behind) or total hysterectomy is done.
Analgesics for 24 hours Rapid fluid and blood replacement is vital in saving the
The use of broad-spectrum antibiotics is recommended patient. It may be necessary to insert a second large bore
• Pack is removed after 24 hours intravenous canula. In patients with severe hemorrhage,
• Advised to wash the perineum after micturition with massive transfusion may be needed. Packed cells, platelets,
antiseptic solution. fresh frozen plasma and cryoprecipitate are given whenever
and individual bleeding vessels ligated. More often, only

a diffuse oozing will be identified. A multi-layered clossure
should help to secure hemostasis and eliminate dead
space. A vaginal pack can be left in place at the discretion
of the operator for 12–18 hours. We advocate the use of
broad-spectrum antibiotics in this setting and transfusion
as indicated.
UTERINE INVERSION
It is the prolapse of the fundus to or through the cervix
so that the uterus is in effect turned inside out. It is an
Fig. 33.8: Rupture of uterus obstetric emergency. Inversion of the uterus is rare. It may
be due to the mismanagement of the third stage, e.g. with
indicated. Delay of transfusion may contribute to the cord traction in an atonic uterus with a fundal insertion
development of disseminated intravascular coagulation of the placenta. Precipitate labor may cause inversion
(DIC). Hence, prompt replacement is essential. of uterus (before separation of the placenta). It may be
completely revealed, or partial when the uterus remains
HEMATOMAS within the vagina. Even without hemorrhage the mother
may collapse, as there is a major component of neurogenic
Puerperal hematomas may be associated with significant shock.
hemorrhage, both immediately after delivery and later
Degree of inversion-incomplete inversion: Uterus is
in the postpartum course. Prompt recognition and
inverted but does not protrude through the cervix (Fig. 33.9).
appropriate management can minimize morbidity.
Complete inversion: The fundus has come out of the
The majority of hematomas following vaginal delivery
cervix and is even seen at vagina.
are vulvovaginal combinations involving the posterior tri-
It is also classified on the basis of duration of inversion:
angle. The most common factor associated with puerperal
Acute inversion: Immediately after delivery before the
hematomas is improperly stitched episiotomy (leaving
behind bleeding vessels), which is reported in 85–93% cases. cervix constricts.
Subacute inversion: Once the cervix constricts.
Chronic inversion: It is seen more than 4 weeks after

PRESENTATION delivery. It is important to recognize and treat all cases
The presenting symptom is usually unremitting pain of acute inversion immediately after delivery.
not responding to any analgesics. Further the clinical
manifestations in these cases are due to blood loss. Most
hematomas will present within 24 hours of delivery.
The perivaginal space and ischiorectal fossa are both
limited by soft tissue. A significant amount of blood can
accumulate in these spaces before signs or symptoms
develop. Therefore, blood loss is often underestimated.
MANAGEMENT
Some authors suggest only observation for small
hematomas, particularly those less than 3 cm in diameter,
and we would agree. In rest the operation is done under
anesthesia after taking informed written consent and
arranging blood. Larger hematomas or those seen to
be increasing in size should be widely incised and clots
evacuated. Next, the area involved should be irrigated Fig. 33.9: Incomplete inversion
Prevention: Majority of the cases are due to mismanage uterus. If it is not possible try under general anesthesia
ment of third stage of labor. Hence avoid: to provide uterine reduction. Tocolytics may be used as
Excessive traction on the umbilical cord anesthesia is being administered. A fist is placed on the
Excessive fundal pressure (Credé’s maneuver) uterine fundus and it is gradually pushed back through the
Excessive intra-abdominal pressure dilated cervix. Once the uterus is reposited in its position
Excessive vigorous manual removal of placenta. anesthesia and tocolysis is discontinued. Now infusion
Diagnosis: There is considerable pain. Shock is out of proof oxytocin or IM methylergometrine PGF2α is given to
portion to the bleeding due to neurological components. start effective uterine contractions. Bimanual uterine
A dark red blue bleeding mass is seen at the perineum or compression and massage are maintained until the uterus
palpated per vaginum. The uterine fundus is not palpable is well contracted. Now remove the placenta. Never try to
on abdominal examination. remove the placenta in an inverted uterus. Oxytocin are
Management: Success in treatment depends on imme- continued for at least 24 hours. There are more chances of
diate identification and treatment. Hypovolemia should endometritis hence antibiotics are given.
be vigorously treated with blood and fluid. The ease with Surgical reposition (Fig. 33.11) is life saving and is
which the uterus is replaced depends on the amount of needed when the patient reports late. It may be rarely
time elapsed since inversion. With an inversion noted ear- required. Laparotomy is done. Posterior vertical incision
ly before shock sets in, replacement by hand might be pos- is given in the lower segment of the uterus. The uterus is
sible. If shock has ensued set up a fast IV line and infuse
colloid or blood. Summon expert help.
Reposition: It can be hydrostatic, manual or surgical.
Under hydrostatic reposition halothane anesthesia is
given to relax the uterus. Hold the uterus in the vagina
with one hand. Run 2 L of warm 0.9% saline fast into the
vagina through cystoscopy tubing (or with funnel and
tube) with an assistant holding the labia encircled tightly
around the operator’s arm to prevent the fluid getting
expelled. Running fluid through silastic ventouse cup held
in the vagina improves the ‘vaginal seal’. The hydrostatic
pressure of the water should reduce the uterus. Once the
inversion has been corrected, give ergometrine to contract
the uterus and prevent recurrence.
Manual reposition (Figs 33.10A to C): The inverted
fundus along with the placenta (if it is still attached) is
slowly and steadily pushed upwards in the axis of the Fig. 33.11: Combined manual and surgical reposition
A B C
Figs 33.10A to C: Manual reposition

reposited by pulling from above or rarely pushing from ultrasound or MRI or a tender uterus with an open os,
below. The incision is closed. then exploration is required. Cross match 2 units of blood
If inversion occurs before placental expulsion then first pre-operatively. Give antibiotics (e.g. ampicillin 500 mg/6
the uterus must be reposited and then the placenta removed hourly, gentamicin 80 mg 8 hourly, metronidazole 1g/12
as a contracted uterus is much more difficult to repository. hourly) and evacuate the uterus very carefully as it is
easily perforated at this stage. Send curetting for histology,
which will also exclude choriocarcinoma. This is a risky
SECONDARY PPH procedure and, hence, must be done very cautiously.
This is exclusive blood loss from the genital tract after Oxytocin IV drip, or 15 methyl PGF2α, 2.5 mg IM every
24 hours of delivery. It occurs between 5 and 12 days 2 hours or methylergometrine every 6 hours for a least
48 hours is given.
and is due to retained placental tissue or clot. Secondary
infection is the most common feature. Uterine involution
may be incomplete. Do a complete blood count to CONCLUSION
determine the degree of anemia and obtain the WBC Proper management of PPH requires a well-versed prac-
count. A vaginal or abdominal ultrasound or an MRI titioner and available resources, including a blood bank,
will give the diagnosis of retained placenta tissues. If antibiotics, and anesthesia. Only when the practitioner is
bleeding is slight and there is no sign of infection it may aware of all the causes of the hemorrhage can this problem
be managed conservatively. However, if there is more than be managed appropriately otherwise it could have disas-
slight bleeding or the suggestion of retained products on trous consequences including maternal mortality.
1. What do you understand by the term postpartum hemorrhage?
2. What is the risk factors of placenta accreta?
3. How do you explain uterine inversion?
i. ____________ are place to compress the uterus and stop bleeding especially for stopping lower segment bleeding.
ii. Slow bleeding for a prolonged period may add up and cause significant ____________, which may not be recognized and
cause sudden shock.
Section 6
Puerperium
Section Outline
34. Normal Puerperium
35. Abnormal Puerperium
34
Sudha Salhan, Meetu Salhan, Sugandha Arya, Padmabati Rath
Normal Puerperium
INTRODUCTION
Puerperium or the postpartum period is from placental
expulsion to 6 weeks after delivery. During this priod there
is readjustment in anatomical and physiological changes
of pregnancy in the woman to almost prepregnancy
level. However, some cardiovascular and psychological
alterations may take many months to return to the non-
pregnancy level.
This period can be divided, for the purpose of a proper
management, into an immediate puerperium, early
puerperium and remote puerperium.
Immediate Puerperium
It is the first 24 hours after delivery when acute postpartum
or postanesthetic (if given) complications can occur which Fig. 34.1: Involution changes in the size of uterus during the first
may be life-threatening like postpartum hemorrhage ten days of puerperium
(PPH), acute inversion of uterus, Mendelson syndrome,
etc. the umbilicus (about 20 weeks pregnancy size). During
the first week (postpartum), there is approximately 31%
Early Puerperium
decrease in uterine size and it involutes upto the level of
It includes first week after parturition. pubic symphysis (2 cm per day). The involuting uterus
produce contractions which may be painful (first few
Remote Puerperium days after delivery). These are known as after pains and
The period from second to six weeks after delivery. may need analgesics to give relief. By the second week the
During this time involution of uterus and adnexa, return uterus becomes a pelvic organ. The uterine size decreases
of menstrual period (if the patient is not exclusive breast by 48% and 18% after third week because of reduction in
feeding) and reversal of changes in cardiovascular system overall size of uterine muscles.
(CVS) and other systems, take place. After delivery the uterus is tonically contraced in
primipara and contracts in waves in multipara.
POSTPARTUM CHANGES Control of bleeding after delivery of the placenta is
achieved by arterial smooth muscle contractions and the
Involution of Uterus (Fig. 34.1) living ligatures (Fig. 34.2) of uterine muscles around them.
The weight of the non pregnant uterus is 50–100 g. Im- If the baby is put to the breast immediately after delivery
mediately after delivery it weighs 1,000 g and comes upto it also helps in reducing bleeding by releasing oxytocin.
of leukocytes, a few red blood cells (RBCs), placental

wound exudates, cervical mucus and bacteria (need not
pathological). Lochia alba is white and has fishy odor. Its
contents are decidual cells, leukocytes, mucus crystals,
granular epithelial cells and bacteria.
Initally it is alkaline but turn acidic at the end. Amount
is about 250 mL per day at the start but can be more in
multiple gestation, hydramnios and big babies. It is scanty
in preterm deliveries. Vulval pad should be inspected daily
to watch for amount of discharge an offensive odor.
Lochial discharge lasts for 4 to 8 weeks after delivery. Use
of oxytocics beyond control of third stage bleeding, neither
reduce blood loss nor helps in involution of the uterus.
In patients where there is scanty lochia, lochiometra or
pyometra should be rule out. If it is prolonged, then it is a
sign of subinvolution of the uterus. If lochia alba persists,
rule out local lesions.
Fig. 34.2: Living ligatures arrangement of blood vessels and
muscle fibers in myometrium Offensive odor of lochia: A pelvic examination is done to
rule out any swab or tampon left inside the vagina.
Later on, the blood vessels at the placental site develop Subinvolution: The rate of involution of the uterus may be
thrombosis, hyalinization and the arteries develop an delayed and is called subinvolution. In this the bleeding
obliterative fibrinoid endarteritis. and lochial discharge continous beyond 4–8 weeks. Early
After delivery, the average size of the placental site diagnosis and treatment may nip it early.
on the endometrial surface decreases from 18 cm at term
to 9 cm. Within 3 days of parturition the placental site Changes in Cervix
endometrium and superficial myometrium are infiltrated During pregnancy there is an increase in the vascularity of
with granulocytes and mononuclear cells, presumably the cervix beside an increase in the thickness of the cervical
forming an anti-inflammatory barrier. These are signs epithelium, hyperplasia and hypertrophy of the cervical
of a recent pregnancy. This infiltration is reduced by the glands. Cervical epithelium becomes thin within 4 days of
tenth day though plasma cells and lymphocytes persist for delivery and by one week cervical swelling and bleeding
several months. The endometrium also starts reforming are reduced to a great extent. By the end of six weeks a
and is fully-developed by the sixteenth postpartum day. majority of the changes, except round cell infiltration and
The decidua starts to undergo a necrotic process from some swelling, are reversed.
day one and within a week it can be perceived separately The cervix closes slowly and by seven days after delivery
from the non-necrotic area above the endometrium it is about 1 cm open. After a vaginal delivery the external os
on ultrasound. The latter were previously endometrial becomes transverse in shape instead of the circular shape
connective tissue cells and they now take part in the (Figs 34.3A and B) which is present in the nulliparous
reconstruction of the endometrium. There are no decidual state; but remains round in shape in case the patient
cells seen at 6 weeks postpartum. delivers by cesarean section. Colposcopic examination
immediately after delivery shows ulceration, ecchymosis
Lochia and laceration. Complete re-epithelialization takes
This is the discharge from the reproductive tract during 6–12 weeks. But the site of a tear, if substantial, remains as
initial 3–4 weeks of puerperium. Its contents are blood and a scarred notch if not immediately stitched.
sloughed decidua, etc. It is of 3 types viz. rubra (first 3–4
days), serosa (5–9 days) and alba (10–15 days). Vagina
Lochia rubra is red in color due to blood, decidua, fetal Around the third week, its distention is slowly reduced.
membranes, vernix caseosa, epithelial cells, bacteria and But in a lactating mother the estrogenic changes like
meconium. Lubra serosa is yellow to brown. It consists thickening of the mucosa, cervical mucus production, etc.
Normal Puerperium 333
muscles of pelvis and other pelvic supports slowly

regain their tone (6–7 weeks) after delivery. Tearing and
overstretching of the musculature or fascia during delivery
may cause genital hernias (prolapsed). Hence, advise for
exercises after proper involution of muscles and ligaments.
Loss of Weight
During pregnancy approximately 10 to 15 kg weight is
gained. Immediately after delivery about 5 kg is lost (fetus,
placenta, amniotic fluid and blood loss). About 2L is lost in
first week due to fluid excretion and 1.5L in next 5 weeks
of delivery (about 4 kg) due to loss of extracellular fluid.
This loss of salt and water is greater in patients with pre-
eclampsia and eclampsia.
Breastfeeding has no effect on this process. If the diet is
A B controlled and aerobic exercises are done the weight loss
is uniform. Cellular breakdown can cause an increased K+
Figs 34.3A and B: A. Nulliparous cervix; B. Parous cervix
level. Increased Na+ can also occur due to decrease in the
aldosterone antagonists because of a low progesterone
are delayed. The carunculae myrtiformes, in the form level. Hence, osmolarity is increased by 7 mOsm/L by the
of fibrosed nodules, result from the healing of the torn end of the first week.
hymen.
Cardiovascular System
Fallopian Tubes
During pregnancy, the total blood volume increases
Because of the high levels of estrogen and progesterone gradually to around 35% above the prepregnancy level.
during conception, fallopian tubes develop an increased Plasma volume expands approximately by 1200 mL and
number of tall nonciliated cells. After delivery these red cell volume by around 250 mL. The blood loss in
hormones are absent or very low. Thus, the nonciliated cells
vaginal delivery is approximately 500 mL, around 1000 mL
nuclei extrude and the cellular layer thins. Inflammatory
in a cesarean section and about 1,500 mL in a cesarean
changes may be seen.
hysterectomy. This decreases blood volume.
Ovaries On the third day post delivery, there is a shift of
In lactating women, there is anovulation because of extracellular fluid into intravascular compartment of
elevated prolactin levels. Otherwise ovulation can occur as 900–1200 mL. This change occurs irrespective of vaginal
early as 27 days postpartum (mean of 70–75 days) in mixed or cesarean delivery. It is established that a patient who
feeding and non-lactating mother and menstruation starts delivers vaginally has a 5% rise in hematocrit and those who
after 7–9 weeks of delivery. The amenorrhea may last have cesarean section have a 6% decrease in hemoglobin.
longer in women who exclusively breastfeed. In them, the In a patient suffering from pre-eclampsia or eclam
incidence of ovulation in the first 6 months postpartum psia peripheral vasoconstriction occurs and excess extra
is as low as 1–5%. Level of follicular stimulating hormone cellular fluid released may cause a moderate increase in
(FSH) is same irrespective of lactation practices but it the amount of expansion of vascular volume by the third
cannot stimulate ovulation in presence of high prolactin postpartum day. Plasma levels of atrial natriuretic peptide
levels (during lactation). Women who undergo medical almost double on the first postpartum day due to the
termination of pregnancy (MTP) or after treatment of an stretching of arteries by an increased blood volume. This is
ectopic pregnancy may ovulate as early as 14 days. important in post delivery natriuresis and diuresis.
The red cell volume returns to prepregnancy level within
Pelvic Changes 8 weeks of delivery. There is stimulation of reticulocytes
In normal vaginal delivery, for easy passage of the fetus, (maximum on fourth day of delivery) and a moderate
there is widening of the symphysis pubis and the sacroiliac increase in erythropoietin due to rapid loss of blood at
joints occasionally can be seen as gap. The voluntary delivery bone marrow becomes hyperactive with a marked
leucocytosis during delivery and early puerperium upto Metabolic Changes

25,000/µL consisting especially of granulocytes. It may Pregnancy increase of fatty acids come down by second
be due to the stress of labor. Prolactin also stimulates the day of delivery. There is a slow fall of plasma triglyceride
bone marrow. (6–7 weeks) lactation has no effect on fatty acid levels. The
In the early puerperium, the serum iron levels are hyperlipidemia can be controlled by diet after delivery.
decreased which return to normal by the second week Hypoglycemia is seen on second and third day after
postpartum. delivery due to renal threshold changes. There is increase
in free plasma amino acids.
Hemodynamic Readjustment
Cardiac output increases in labor with uterine contractions, Coagulation Mechanism
there is an increase in the central venous pressure, arterial As the placenta separates, platelet count decreases. An
pressure and stroke volume and a decrease in the pulse rate. increase in their adhesiveness and secondary increase can
These changes are more when the patient is lying supine occur later. The plasma fibrinogen concentration decreases
than if the patient is lying on her side. All these changes after delivery of placental bed which has a large deposit of
revert to the prepregnancy state in early puerperium. fibrin from where a continuous release of fibrin breakdown
After reduction of blood volume there is decrease in products occur. A secondary increase occur after a few
size of deep veins, return of venous tone and increase in days. The pregnancy increase of clotting factors are proving
venous flow velocity in lower limbs. a reserve for their rapid consumption during delivery and
Blood pressure is slightly increased in the first 5 days after help in achieving hemostasis after delivery. Patients with
delivery due to an increase in uterine vascular resistance a congenital deficiency of antithrombin III have recurrent
and increase in the plasma volume. Ventricular hypertrophy venous thrombotic disease and a hypercoagulable state.
of pregnancy resolves in about one year. Lactation has no Maternal plasma fibrinolytic activity is decreased to a
effect on the resolution in hemodynamics. great extent in the last month of pregnancy but it increases
rapidly after delivery. There is an increase in the tissue
Urinary System plasminogen activator (TPA), a slight increase in the
prothrombin time, a decrease in plasminogen activator
The increased fluid of pregnancy is excreated by diuresis. inhibitors and a remarkable increment in the fibrin split
The mucosa of the urinary bladder is edematous due products. Protein S which acts as a cofactor in the activity
to labor and delivery. The capacity of the bladder is also of protein C (an important coagulation inhibitor that
increased. Therefore, after delivery there is a common is present in both as a free form and as a complex). This
problem of bladder over distension and incomplete protein S (both total and free) level is high on the first day
emptying with a significant amount of residual urine. The after delivery and slowly returns to normal, in about seven
recovery is slightly retarded (during first 1 or 2 days) in days thereafter.
cases of prolonged labor and epidural anesthesia. During However, during delivery, the excessive coagulation
immediate postpartum, there may be a mild proteinuria activity, with decreased activity, infection or trauma
which is normal. The collection system, which was also during parturition may predispose to thromboembolic
dilated during pregnancy, comes back to the prepregnancy complication. A secondary increment in the level of
size by 6 weeks in most women. However, some stasis of fibrinogen, factor VIII and platelets, can also be seen which
urine may continue till 12 weeks after delivery. In the latter is highest in first week after delivery. All this do increase
there are more chances of urinary tract infection (UTI). thrombosis susceptibility during puerperium. But an
Obvious renal enlargement may persist for many weeks immediate reversion to normal fibrinolytic activity after
postpartum. The 5% increase of glomerular filtration rate parturition prevent this mishap. Some puerperal women
(GFR) during pregnancy comes to normal by 8 weeks have a reduced fibrinolytic activity after parturition and
after delivery but the 25% increase of renal plasma flow are thus at an increased risk of developing postpartum
of pregnancy may take a longer time to remit, sometimes thromboembolic episodes.
as long as upto 24 months. Pregnancy induced glycosuria
disappears after delivery. Blood urea increases slightly by Respiratory Changes
the first week after delivery (it is from, 15–20 mg/dL) but After delivery the diaphragm comes down to its normal
soon reverts to normal. position due to a decrease in the size of the uterus. The
residual volume of the lungs increases while the inspiratory 100 ng/mL. Thus, frequent feeds help in maintain high
capacities decrease. In pregnancy, respiratory alkalosis prolactin levels.
and compensated metabolic acidosis is present. Labor is a If a baby is breastfed more than 6 times in a day (including
transition period. From the end of the first stage of labor to at night) the increased level of serum prolactin may even
the start of puerperium, there is a rise in the blood lactate persist for more than one year. However, if the breastfeeding
levels a fall in the pH and hypocapnea (pCO2< 30 mm Hg). is done only 1–3 times in 24 hours, the serum prolactin
Normal non pregnant values of pCO2 of 35–40 mm Hg levels return to normal within 6 months of delivery.
occur within 3 weeks after delivery. The normal non pregnant night time peak levels of
The resting oxygen cosumption is increased during prolactin are absent during pregnancy but are restored
pregnancy and upto 7–14 days after delivery (depending within one week of delivery in women who are not
on the duration and severity of the second stage of labor). breastfeeding their infants.
Later, the basal metabolic rate may be elevated due to lac-
tation, mild anemia and psychologic factors. FSH and LH
Serum FSH and LH levels 10–12 days after delivery are
Hormonal Changes very low with or without lactation. The follicular phase
As the placenta is expelled, its hormone levels fall rapidly. concentration is seen by third week postpartum. The rise
Human placental lactogen (hPL) disappear on first day in LH concentration during sleep disappears once normal
after delivery (half life 20 minutes). Human chorionic ovulatory cycles are established. This is like pre-pubertal
gonadotrophin (hCG) has a half life of 9 hours. Hence cycles. There is a change from post-delivery amenorrhea
its level is below 1000 mU/mL at 48 hours, less than 100 to cyclic changes. In puberty too gonadotropin secretion
mu/minutes after 7 days postpartum and no harmone by increases during sleep. Reduced gonadotropin-releasing
11–16 days. This pattern is slower in first trimester abor hormone (GnRH) during pregnancy and early puerperium
tions, especially in those treated with suction curettage for is responsible for low levels of follicle-stimulating hormone
molar pregnancy. (FSH) and luteinizing hormone (LH). During pregnancy
there is increased endogenous opioids activity because of
Plasma 17 β-Estradiol high estrogen and progesterone concentration, the latter
may suppress GnRH levels during pregnancy and early
Plasma 17 b-estradiol starts falling within 3 hours of
puerperium.
expulsion of placenta (10% fall) and after 7 days the levels
are lowest. In non lactating mother >50 pg/mL (follicular Resumption of Menses
phase level) is reached by 19–21 days and in lactating
The ovaries are relatively non-responsive to exogenous
mother 60–80 days post delivery. In the latter the estrogen
gonadotropin stimulation in both lactating and non-
level are less than 10 pg/mL (lactational amenorrhea)
lactating women. High prolactin levels play a partial role in
causing breast engorgement on 3–4 days after delivery
ovulation suppression because bromocriptine treatment
(reverse of the fact that high estrogen levels cause lactation
can reduce prolactin level but not the inhibition of GnRH
supression).
secretion. As ovaries resume functioning after weaning, it
Progestrone is supposed that either the suckling stimulus itself or the
raised levels of prolactin cause suppression of pulsatile
Level are very low (>1 ng/mL) on third day of delivery GnRH secretion.
because short half life of a few minutes.
Oxytocin and Endogenous Opioids
Prolactin
Oxytocin and endogenous opioids present during suckling
In the nine months of confinement the prolactin level may also inhibit the pulsatile release of GnRH.
rises upto 200 ng/mL or more. In women who do not Nourishment of the woman also has an important role.
breastfeed after delivery, the level of prolactin falls to non If the woman is healthy, her menstruation may return
pregnant level, i.e. less than 20 ng/mL by the third week. earlier. If she is malnourished, the infertility may be
But the prolactin levels in those mothers who breastfeed prolonged to as long as 1–2 years.
their babies remains above the prepregnancy level and There is a failure rate of about 2% in lactational amen
with each suckling episode the level of prolactin rises upto orrhea as a method of family planning.
Pituitary Gland investigation for ovarian function should be done to rule out
The pituitary gland increases in weight by 30–100% during any ovarian pathology.
pregnancy (about 0.08 mm/week). This trend continues Renin and angiotensin concentration decrease to non
till the first week after delivery. After that it starts to regress pregnant level within 2 hours of delivery pointing to its
to normal size. The increase is greater in the lactotrophic fetoplacental origin.
cells than in the somatotrophic cells. The growth hormone
is less in the second half of pregnancy and the early MANAGEMENT
postpartum period. But the insulin-like growth hormone The observation is started just after delivery. Examinations
(IGF-1) is increased throughout pregnancy because to be done every 15 minutes in the first hour after delivery
of the production of growth hormone by the placenta. (4th stage of labor).
Increased somatostatin secretions may be responsible for Pulse
insensitivity of the pituitary to growth hormone releasing Blood pressure (BP)
hormone (GHRH) and insulin stimulation during preg Per abdomen (P/A) size of the uterus and bladder
nancy and early puerperium. Per vaginal (P/V) any bleeding, hematoma.
Because hPL declines rapidly after delivery and the Ideally, 2–4 days of hospitalization after delivery are
levels of growth hormone are also reduced there is a relative needed to observe for difficulties in breastfeeding, urinary
deficiency of anti-insulin factors just after parturition. or fecal incontinence, urinary infection, episiotomy pain or
Hence, the requirement of insulin therapy in gestational swelling, examination of umbilical stump of the neonate,
diabetic mothers is reduced after delivery. By 6–8 weeks of etc. However, due to lack of beds and overcrowding in
puerperium the insulin and glucose levels come to normal. Government hospitals, patients are discharged 24 hours
The fasting glucagon levels also fall. after normal vaginal delivery, after examining the mother,
her neonate and after ensuring that the infant has passed
Thyroid Hormones
urine and stools.
Hyperthyroidism or hypothyroidism due to autoimmune Check tetanus toxoid (TT) immunization status. If the
thyroid diseases which may become suppressed during status is unknown give TT 0.5 mL intramuscular (IM) in
pregnancy (due to immunosuppression of pregnancy), the upper arm. Also give 200,000 IU vitamin A capsule
may resurface after delivery. In hypothyroid mothers there after delivery or within six weeks of delivery. It helps the
may be a failure of establishment of lactation. In the rare patient to recover better and the baby receives the vitamin
cases of Sheehan’s syndrome (due to excessive postpartum through the breast milk. Also give iron and folic acid (WHO
hemorrhage) puerperal cachexia and myxedema can 2003) besides calcium and vitamin D.
occur. Examination on rounds: Ask for any complaints. Then
enquire whether the patient is passing enough urine
Total and Free Adrenocorticotropic
without pain, look for her general condition, and record
Hormone (ACTH)
pulse, BP, respiratory rate. See the breasts, height of uterus,
Plasma cortisol and immunoreactive corticotropin- lochia and amount of bleeding. If an episiotomy was given
releasing hormone (CRH) and β-endorphins increase examine for any swelling, infection or hematoma. Examine
during pregnancy and labor. They all fall after delivery the legs for thrombophlebitis.
and their normal prepregnancy levels are achieved Daily examination
within 24 hours. The placenta may be the source of CRH Pulse
because dexamethasone is not able to suppress ACTH in BP
pregnancy. But by vasopressin maternal control of ACTH Breasts
production is intact to allow normal response to stress. P/A for involution at the rate of 2 cm/day
Post-delivery, mood changes may be due to peripartum Perineum for lochia and healing of episiotomy
cortisol and β-endorphins levels. Calf muscles tenderness.
17-Ketosteroid levels in urine are elevated in late
pregnancy and during labor due to an increased production
of androgenic precursors from the placenta and ovaries
BREASTFEEDING
and return to the non pregnant level by the end of the first All studies have found breast milk to be the best milk for
postpartum week. If the levels remain high after this time an a baby. It is species and age specific. It is estimated that
over one million children die in the world each year from infection, bacterial meningitis and urinary infection are
diarrhea, respiratory and other infections because they are minimal compared to non lactating infant. Necrotizing
either not given breast milk or are given mixed feed (both enterocolitis especially in preterm neonates is far less
breast and other feeds). All neonates must be put to breast in breastfed infant due to epidermal growth factor in
within half hour of birth. Here, we will learn advantages of breast milk (American Academy of Pediatrics).
breastfeeding, breastfeeding technique, common problems They also recover faster than non breastfed babies.
in breastfeeding and techniques to express breast milk. The breastfed children are protected against allergies
Types of neonatal feedings: including asthma.
Exclusive breastfeeding: The baby should be exclusively Mother–child bondage and emotional security is more
breastfed (i.e. no prelactal or other feeds, even water is hence, breastfed babies are psychologically more stable
prohibited), the mother should feed the baby frequently, than their bottlefed counterparts.
both day and night and till the menstrual period has Babies fed on mothers milk have higher IQ.
not started (only vitamins and essential medicine are They have less chances of sudden infant death.
allowed). Breastfed children have a lesser incidence of developing
Mixed feeding hypertension, diabetes mellitus, coronary heart disease,
Only top feeding. liver diseases, ulcerative colitis, lymphoma, appendicitis
and even cancer in later life besides higher cognitive
Advantages of Breastfeeding development.
Benefits to the Baby Bedwetting is seen less often in breastfed children.
It is safe as it is not contaminated. Thus, there is increased
Breast milk is perfect for the neonate.
chances of survival.
It is complete nutrition (has exact nutrients for optimum
growth) for the baby upto 6 months of age. Calcium Benefits to the Mother
in breast milk is readily absorbed high contents of
lactose and galactose in breast milk (component of Breastfeeding reduces the chances of postpartum
galactocerebroside) are required for neonatal brain hemorrhage by secreting oxytocin. Hence, the beneficial
development. Taurine and cysteine (amino acids) of practise of putting to breast immediately after delivery.
breast milk are important neurotransmitters. Similarly The process of involution is accelerated.
polyunsaturated fatty acids in mothers milk are used in Natural contraception if the mother is practising exclusive
myelination of central nervous system. Intestinal tract breastfeeding.
gets hormones and epidermal growth factors for its It also lowers the risk of breast and epithelial ovarian
maturation. cancer in the mother who had breastfed their offspring.
The breast milk proteins are mostly lactalbumin and
The work required to prepare feeds is not there (lessen
lactoglobulin (more than 60%) that form a soft curd and mothers burden) leaving utensils, boiling milk etc.
has exactare easy to digest. The enzyme lipase, in the It helps in better mother-infant bonding.
breast milk, helps in the digestion of fats. Easy digestion Postpartum healing of surgical wounds (episiotomy/
ensures its proper utilization for baby’s growth. cesarean) is faster in breastfeeding mothers.
Breast milk contains all vitamins except vitamin K.
Breastfeeding mothers have a lesser chance of post
Breastfeeding helps recovery from illness not only
partum psychosis.
because sick babies usually lose their appetite for all There is better bone health in mother in later life.
except breast milk but also due to an early protection
given to a baby against infections. The protective factors Benefits to the Family and the Society
in breast milk include IgA, macrophages, lymphocytes, Breastfeeding is more economical than artificial feeding.
bifidus factor, unsaturated lactoferrin, lysozyme, It saves the cost of buying formula milk, bottles, teat,
comple ment and interferon, etc. Hence, breastfed sterilization and refrigeration. The baby does not fall ill
neonate are less likely to develop infections. A breastfed often and, hence, save money on healthcare and work
baby is 14.2 times less likely to die of diarrhea and 3.6 days lost.
times less likely to die of respiratory infections. They are Family planning automatically occurs in exclusive breast
less prone to Escherichia coli to rotavirus infection. The feeding.
incidence and severity of diarrhea, respiratory and ear Less infant morbidity and mortality.
Box 34.1: Comparison of breast milk and cow’s milk

Components Human Cow
Protein 1%–1.5% (40% casein) 3.3% (80% casein)
Carbohydrate 7% 4.5%
Fat 4% 4%
Minerals 0.2% 0.75%
Composition of Breast Milk

It varies in first feeds (colostrum), beginning and end of
a feed, according to the age of the child and in different
times of the day.
Colostrum: It is produced during first few days of delivery. Fig. 34.4: Internal breast structure
It is thick and yellow in color and the amount is less. It
is richer in antibiotics, anti-infective proteins and white
blood cells then milk produced after first week of delivery.
All these protect the newborn from most initial infections
encounters after delivery. It may also help in prevention of
allergies. It also causes purgation getting rid of meconium
and bilirubin (thus prevent jaundice by decreasing
enterohepatic circulation).
Mature milk is produced late in first week of life. It is
enough in amount and thin in consistency. The mik milk
produced at the start of a feed (fore milk) is full of protein,
lactose (provide nutrition) and water and is thinner.
The end feed milk from a breast (hind milk) is full of fats
(provide energy) and is thicker. It produces satiety.
It is important to remember that baby must drink milk
Fig. 34.5: Prolactin reflex
from one breast till it is empty (both fore and hind milk).
The breast milk contains the adequate amount of water,
vitamins and minerals according to requirement for first Physiological function of breast: Prolactin make breast
6 months of life (Box 34.1). produce milk under the stimulation of suckling by the
baby [prolactin reflux/milk secretion reflux (Fig. 34.5)].
Breastfeeding Advise Night feeding is important as more prolactin is secreted at
Put newborn to breast within ½–1 hour of birth. night. This prolactin produces milk for the next feed. Milk
National guidelines on infant and young child feeding production is directly related to the amount of suckling.
advocate that exclusive breastfeeding should be given If two children (twins) are sucking, enough milk will be
for first 6 months of life. Complimentary feeding produced for both of them.
starting after 6 months. Though continue breastfeeding The second important hormone is lactation is oxytocin.
till 2 years or beyond. It makes the myoepithelium around the milk secreting
Feed on demand from one breast till he leaves the breast glands of the breast to contract thus ejecting milk into milk
himself. Night feed is a must. ducts leading to the nipple, hence, oxtocin produces milk
Do not give the baby water, honey, gutty, gripe water, for the current feed. Oxytocin reflex (Fig. 34.6) is initiated
tea of any other liquid feeds. by thought, sight or sound of the child and by suckling.
Oxytocin: This hormone also help mothers uterus to
ANATOMY AND PHYSIOLOGY OF
contract preventing PPH.
BREAST (FIG. 34.4) The infant takes the whole nipple, along with areola in his
Breast consists of glands (surrounded by myoepithelium, a mouth and presses it against the hard palate and squeezes
thin muscle) tubules, supporting tissue and fat. the milk by the tongue from before backwards (Fig. 34.7).
Fig. 34.6: Oxytocin reflex Fig. 34.7: Reflexes in the baby
Fig. 34.8: Position of mother and child Fig. 34.9: Good attachment
Baby who just sucks the nipple bad attachment is not

BREASTFEEDING TECHNIQUE
properly fed and the mother develops sore nipple because
Breastfeeding may need help in the form of positioning of vigorous sucking damage by baby’s gums.
and attachment.
Positioning (Fig. 34.8) DIFFICULTIES IN BREASTFEEDING

This requires: (1) Face baby towards the mother so that Inverted nipple: It is to be detected during antenatal visit.
their abdomen are in contect. (2) Support whole of baby, It hampers lactation. Nipples are to be pulled up by fingers
keeping head, neck and trunk in the same plane. many times. Syringe suction can also be tried (Fig. 34.10).
Soreness of nipple: Besides wrong attachment it could
Attachment (Fig. 34.9) also be due to candial infection.
For this we look for wide open mouth of the child, his/ Treatment is keeping nipple clean and to correct attach
her lower lip turned outward, chin of the child touching ment. Hind milk application after the feed accelerates
mothers breast and baby’s mouth has most of the areola. healing.
segment of the breast form an abscess. There may be

high fever and raised leukocyte count in mother.
Treatment: Mother is given antibiotics and analgesics.
Breast abscess is incised and breastfeeding is continued
from the other breast.
Inadequate formation of milk is complained by some
mothers. If the weight gain of the child is alright, is
pasing urine 6-8 times and is sleeping 2–3 hours after
each feed assure mother that the milk production is
enough. Less milk production is due to not feeding often
and adequately (hurried and short feeds), improper
position and attachment engorged breast, mastitis,
poor oxytocin reflex, etc. are the causes.
Management
True stimulation for lactation is brestfeeding, more the
child sucks more milk is produced. Proper counseling for
Fig. 34.10: Syringing suction for retracted nipple
exclusive breastfeeding is essential. Primiparas often get
exhausted. If time is given for feeding it gets established.
To allow healing in between feeds use of nipple shield Proper rest and diet is essential. Feeding more frequently
to prevent further trauma. Massage cream or placental also a night helps. Back massage facilitates (Fig. 34.11).
extract may also help healing but wash them off before Expression of breast milk is needed in the following
starting feeding. circumstances:
In mothers of the premature, sick, low birth weight babies
Suppression of lactation: There is no absolute
indication. We have seen in the mechanism of milk who cannot directly breastfeed for sometimes so the milk
production continues.
production that the amount of milk synthesized is
When mothers go for work, the expressed milk is
directly proportionate to the amount of milk suckled
kept for feeding the baby with feeding cup or paladai
by the baby. If the breastfeeding is more (e.g. twins)
(Fig. 34.12).
more milk is secreted, if the breastfeeding is less then In cases of breast engorgement.
less milk is produced. When the mother is not lactating
(stillbirth or neonatal death HIV infection, etc.) milk
production automatically stops. So, tight breast support
and not handling the breast stops milk production and
there is no need to give any drug.
Engorgement of breasts occurs on second or third day
of birth when either the baby’s positioning is not correct
or milk produced is not optimally utilized. The alveoli
are full of milk and breasts are swollen, hard and tender.
Treatment: Breast engorgement is prevented by correct
attachment and frequent feeding. Once developed the
treatment is cold packs locally right breast support,
analgesics (paracetamol) to the mother and gentle
expression of milk is essential. Sometimes injection
oxytocin is given intramuscularly (5–10 units) will make
acini to contract and expel the accumulated milk.
Abscess of breast: It develops when infected cracked
nipple, engorged breasts, blocked ducts or mastitis
is not treated or inadequately treated. The infected Fig. 34.11: Back massage
Box 34.2: Drugs having deleterious effects on lactation

Amantadine Carbimazole Lithium
Amiodarone Cascara Phenindione
Anthraquinone Chloramphenicol Primidone
Antineoplastics Ephedrine Radioactive agents
Atropine Ergotamine Streptomycin
Fig. 34.12: Paladai or feeding cup
Barbiturates Iodine Sulphonamides
Benzodiazepines Kanamycin Thiouracil
Bromides
Contraindications of Breastfeeding
Absolute Contraindications
Use of addictive drugs, e.g. cocaine or excess alcohol advice for herself. In cases of delivery by cesarean section
consumption the patient can be sent home after 7 days (after suture
HIV infection in developed countries removal) or if the obstetrician feels that the mother and
Certain drugs: Bromocriptine, doxorubucin, lithium, the child are doing well, on the third postoperative day of
phenindione cesarean section. In that case she is advised to come back
Breast cancer on the 7th or 8th postoperative day for suture removal.
Human T-cell virus type infection Early discharge may lead to readmission of the neonate for
Active herpes simplex infection of the breast infection or jaundice. Emotional and physical support by
Mother on anticancer drugs the partner and other family members is very important.
Phenylketonuria or galactosemia in the neonate.
Maternal Nutrition during Lactation
Relative Contraindications She can eat as soon as the effect of analgesia and anesthesia
Active pulmonary tuberculosis of the mother. (if any) is worn off. A hygienically prepared balanced diet is
However, Indian Academy of Pediatrics (IAP) does not advised. Enough water and roughage is needed to prevent
recommend discontinuation of breastfeeding even in constipation.
this scenario (see Chapter 43). During the first six months of lactation, the energy
Mothers with HIV infection (in developing countries). requirements have been fixed at +550 Kcal/day, protein
Mothers with cystic fibrosis (milk is high in sodium). at +25 g/day and fat at a total of 45 gm/day. Calcium
Clinical varicella of the mother, till the baby receive its remains constant at 1000 mg/day as during pregnancy.
vaccine and the mother’s skin lesions have healed. Iron requirement is 30 mg/day. Vitamin A, B, C and B12
If the neonate develop jaundice from breast milk. In requirement increases during lactation as indicated by
such a situation, breastfeeding can be discontinued for the figures in the Table 34.1 while folic acid requirement
a short while. The serum bilirubin will rapidly fall and is decreased.
on restarting breastfeeding will not rise to the previous During lactation, as during pregnancy, the mother
high levels. requires sufficient nutrient intake and stores to suggest
Cytomegalovirus infection of the mother with a preterm both the infant’s growth and her own health. If she does
neonate. not eat well throughout pregnancy and lactation, her
health may be compromised—in some instances, to a
Drugs which have Deleterious
Effects on Lactation (Box 34.2) TABLE 34.1: Daily dietary intake of lactating women
Advise at discharge to exclusively breastfeed the baby for Dietary requirement Actual Recommended
at least 6 months and to take care of the perineal wound. Calories (Kcal) 1970 2425
Instructions are given about her diet and care of the infant. Protein (g) 47 75
A home visit by a nursing personnel from 5th to 7th day
Iron (mg) 14.6 30
will be perfect, if available. The woman is advised to report
Calcium (mg) 408 1000
to the hospital if she or her infant has any problem.
Otherwise she is instructed to come after 6 weeks Vitamin A or retinol (mg) 304 950
for immunization of the child and for family planning Source: National nutrition monitoring bureau (NNMB) 2002
greater extent than that of her child. In addition, lactation

is likely to be unsuccessful.
Water
Water is the major nutrient in breast milk. Total milk
volume varies with infant age, but not with maternal fluid
intake, as might be expected. But to prevent dehydration
she must drink a glass of milk, water or juice at each meal
and each time she nurses her baby.
Energy and Energy Nutrients

Energy from maternal diet and tissue reserves supports
both lactation and maternal health and activities on an
average about 25 ounces of milk per day by a lactating
mother. Severe energy restriction, however, hinders milk
production. Atleast 1800 Kcal/day is needed for proper
lactation.
Carbohydrate: The breast milk carbohydrate is always Fig. 34.13: Comparisons of energy and nutrient recommenda-
lactose, and the concentration is always about 70 g per liter tions for non pregnant, pregnant and lactating women
but it does not reflect maternal carbohydrate intake.
Protein: Maternal nutrition may have no effect on breast by well nourished mothers. To maintain maternal vitamin
milk protein, either. In general, the protein concentration A stores and sufficient concentrations in breast milk,
of breast milk in malnourished women is similar to that of women need an extra 400 to 500 mg vitamin A daily.
well-nourished women. Vitamin D is essential as maternal level correlates directly
Lipids: Maternal dietary intake alters the fatty acid com- with breast milk concentration. Vitamin E in breast milk
position of breast milk, but not the total fat concentration also varies directly with maternal intake and stores. The
or milk volumes. recommended dietary allowance (RDA) increases slightly
during lactation to account for the vitamin E in breast milk.
Vitamins and Minerals Breast milk vitamin K concentrations are insufficient to
Lactating mother (even if she herself is malnurised) produce meet the infant’s needs, even when the maternal diet is
milk with sufficient protein, carbohydrates, fats and most adequate. Consequently the RDA does not change during
minerals at the expense of her nutrition. The daily dietary lactation.
intake of women during lactation is discussed in Table 34.1.
Figure 34.13 shows the average intake and the recommend- Water Soluble Vitamins
ed dietary intake for a pregnant and lactating mother. The breast milk water soluble vitamins reflect maternal
Therefore, it is essential to ensure that dietary intake intake to varying extents. Marginal deficiencies and daily
does not fall below the habitual levels. Providing simple fluctuations have little, if any, influence on breast milk
technologies to reduce physical activity in these women composition, but severely vitamin deficient mothers
and providing contraceptive care are two non-nutritional produce vitamin deficient breast milk. For example, lactating
measures that might go a long way in preventing deteriora women who consume a strict vegetarian diet produce
tion in maternal nutritional status in lactating women and vitamin B12 deficient milk. The RDA for most of the vitamins
preventing the next pregnancy. are greater during lactation than during pregnancy; the
RDA for vitamin B12 remain at their pregnancy level during
Fat Soluble Vitamins lactation; the RDA for vitamin B6 and folate are lower during
Breast milk composition may change with maternal dietary lactations than during pregnancy.
excesses and deficiencies of the fat-soluble vitamins,
depending on the vitamin. The vitamin A concentration Minerals
in breast milk reflects the mother’s intakes and stores. In general, maternal dietary intake of minerals does
Therefore, vitamin A deficiency is rare in infant’s breastfed not influence their concentrations in milk. This is most
apparent in the calcium, phosphorus, and magnesium

contents of breast milk, which is important, however,
because a low calcium intake promotes mobilization of
calcium from maternal bone stores. A lactating woman
whose daily diet lacks calcium rich foods may find herself
later in life with weakened bones.
Breast milk iron concentration also remains fairly
constant whether the mother takes an iron supplement
or suffers iron deficiency anemia. The mother’s body is
designed to deliver iron to the infant, no matter as what
cost to her health.
POSTNATAL EXERCISES
The relaxation of ligaments and connective tissues of
pelvis (stretched during pregnancy by supporting parous
uterus with all its contents) remains for four to five months Fig. 34.15: Deep breathing exercises (yoga) are helpful for relaxation
postpartum. Similarly abdominal musculature is also
loose. A split of varying length can be seen between the
two recti abdominis muscles (diastasis or divarication of
recti) (Figs 34.14A and B). Hence, the entire abdominal
wall is weakened. Incorrect posture in doing heavy work
may lead to back muscle injury.
Extensive bruising and edema may be there in perineum
besides stretching and tears or episotomy. There may be
some neurological damage during delivery leading to
temporary (short or long duration) or permanent damage
to sensations and muscles. Hemorrhoids may cause
discomfort. Similarly legs may be swollen on paining just
after delivery.
There is overcrowding in hospitals in developing countries.
Therefore, patients are discharged 24–48 hours after delivery.
Hence, postnatal nutrition, postures and exercises are to be
learned for proper puerperal rehabilitation.
Fig. 34.16: Proper sitting posture
Initial Postnatal Exercises (Fig. 34.15)

The patient is taught to breath in, breath out, tuck in her
abdomen and then relax. This is done more comfortably
when she is lying on her side and when she is sitting.
Pelvic tilting is to be done on side lying and crook
lying. She holds the abdomen muscle, tilts then relaxes
and repeats the cycle. Also teach her proper postures to
prevent backache.
A B Sitting (Fig. 34.16)

Figs 34.14A and B: A. Abdominal muscles in a nullipara; The patient should go to the end of the bed or chair with
B. Divarication of recti (muscles) after delivery pillows supporting the perineum and back.
Feeding While changing the soiled clothes of the newborn, the

The woman should sit upright with her back applied to the mother must not bend her back (Figs 34.18A to D).
back of the chair with a pillow each under the perineum The mother may carry the child in a hammock while
and the back. A foot rest to support the legs is useful. One doing household work.
pillow is kept below the baby to prevent her from stooping. At the time of discharge she is advised as follows:
While lying down or sitting in bed too she must have pillow She is asked to take a daily walk with the baby in a sling
supports so that she need not bend forward (Figs 34.17A (Figs 34.19A and B).
to C). She should continue her pelvic floor exercises.
A B C
Figs 34.17A to C: Positions for feeding and looking after the newborn
A B
C D
Figs 34.18A to D: Positions while nappy changing
A B
Figs 34.19A and B: Carrying the child Fig. 34.20: A supported coughing position in cesarean section patient
She can do side flexion and rotation exercises and

exercises of curling down half way from the crook
sitting, stop in this position for a few seconds and return
to upright position (curl downs).
During coughing (Fig. 34.20), getting in and out of bed,
or simply moving around when caring for the baby,
assuming the proper position is very important.
Transcutaneous Nerve Stimulation (TNS)

(Fig. 34.21)
Mothers are often handicapped in their efforts to care
for their newborn baby by postoperative pain, which can
be intense. TNS has successfully been used for analgesia
following surgery by many practitioners. TNS may be
used for post cesarean section pain and frequently gives
the mother an additional source of comfort without the
disorientating narcotic effects of conventional invasive Fig. 34.21: Transcutaneous nerve stimulation electrodes for pain
postoperative analgesia. TNS has been seen to decrease relief above the cesarean wound
the amount of narcotic analgesia required in post cesarean
section women; this also reduces the amount of drugs inguinal ligaments. The obstetric pulsar can be used, and
passing to the babies of breastfeeding mothers. Two allows the mother to choose both the amplitude and mode
electrodes can be placed at either end of a suprapubic of stimulation best suited to her needs.
Pfannenstiel incision or parallel to a vertical paramedian
incision. The electrodes should be positioned over the Abdominal Wall Weakness
site of pain, or else they can extend from just below the An assessment for abdominal wall laxity is important.
anterior superior iliac spine above and parallel to the The patient is asked to sit up. If the divarication of rectus
muscle is less than 2 fingers in width, abdominal exercises The site of pain in the back after delivery may be:
may ameliorate it rapidly. But if the divarication is more Coccygeal
than 2 fingers, rotation and side flexion exercise should be Lumbar
delayed until the gap is reduced by abdominal exercises. Sacroiliac
The patient is asked to lie down, cross her hand over her Thoracic
abdomen with fingers outside the lateral borders of the Sometimes cervical (neck).
recti muscles and then oppose them as she raises her head A complete check up is to be done. Active treatment
and shoulder above the pillows. As soon as the peeking of in the form of analgesic and rest will help. In addition the
abdomen starts, she should stop rising but should stay at following measures are also required.
that position for 4–6 seconds and then lower down slowly.
This exercise is continued till the divarication of recti is no In low Backache
longer there. Lying on the face well supported by pillows may help.
The patient is asked to always keep the abdominal Specific supports for the sacroiliac, lumbar or lumbosacral
muscles in mind during performing all day to day work. regions may give relief.
She is asked to retract them whenever she can. Pain in the thoracic region is mitigated by using the
Pelvic tilting exercises are taught if the rectal divarication correct position while feeding the baby.
is less than 2 fingers. These are taught in crook and side
lying, sitting and standing position. Coccydynia
It is a painful and incapacitating condition at the site of the
Pelvic Floor Exercise coccyx in the early postpartum period especially during
Repeated contraction and relaxation of the pelvic floor sitting. The cause is mostly damaged ligaments associated
muscles are done. It can be done in any position but it is with displacement of the coccyx, but it can occur even
more comfortable in stride crook lying, prone lying and without displacement. There may be a history of injury
stride standing. She is asked to pull her pelvic floor in and to the coccyx in the past, which is aggravated during
hold for sometime and to then let go. This can be done for pregnancy. There are incidences of spontaneous fracture
2–3 sessions per day increasing the number of contractions of the coccyx during the second stage of labor.
and relaxations per sessions as days pass by. These exercises Analgesics are prescribed. Ultrasound, ice or hot packs
can be done in a variety of situations, e.g. while queuing, locally are helpful. Ask the patient to lie on her face. TNS
telephoning, driving, watching television, cooking, etc. administered locally cures the pain. This condition can be
present for a long duration.
Infrared Irradiation Pain at the symphysis pubis is felt by some patients
postpartum. It is most often seen in traumatic deliveries.
These are delivered by infrared lamps. The patient lies in
The patient is not able to walk without support and it is a
bed with legs apart and supported on pillows. The infrared
very painful condition. It can occur in a less severe form
irradiation is now administered. It causes relief of pain in
3 days after delivery due to the swelling inside the intact
from episiotomy wounds, stitched tears. The lamp is kept at a
fibrous tissue confines of the joint. Bed rest, a firm support
distance of 50–70 cm and irradiation is given upto 20 minutes. and drugs to prevent pain are indicated in the first 2–3
These are also useful on cesarean scars and other days. Then gradual mobilization is started. The knees
painful conditions after cesarean section. should be flexed and slightly adducted when moving
in bed. Ultrasound and ice packs applied locally relieve
BACKACHE edema and help healing.
Backache may be felt starting from the antenatal period
or may be first noticed after delivery. During delivery the
CARPAL TUNNEL SYNDROME
passage of the fetus through the pelvis results in stretching Carpal tunnel syndrome occurring in pregnancy usually
and movement of previously lax joints. This may be the resolves shortly after delivery. It can, however, develop in
cause of pain. The position during delivery may also have the puerperium and appears then to be closely associated
some effect. The positions adopted during feeding, lifting with breastfeeding. It may develop after an average three
and other work are very important. Tiredness and stress and a half weeks following delivery. Complete resolution
add to the backache. of the condition does not take place until breastfeeding has
been totally stopped. Improvement begins approximately Ask her to urinate frequently to keep the urinary bladder
14 days following the beginning of weaning. empty. A difficult or obstructed labor may inflict some
Wrist splints, reassurance, diuretics, non-steroidal anti- damage to the bladder base and catheterization should be
inflammatory drugs and steroid injections have been used liberally used to prevent distension of bladder and urinary
to treat the condition with varying results. The obstetric tract fistula.
physiotherapist who encounters carpal tunnel syndrome In cases of episiotomy there is pain in the perineum,
in the postpartum period could use exercise, elevation, which is sometimes precipitated by constipation. Taking a
positioning, ultrasound or use of ice bath as soon as she feels is advised. Sitz bath is beneficial
for vaginal and perineal wound healing. Cold sitz bath may
WHEN TO REPORT IMMEDIATELY provide relief from edema and pain by vasoconstriction
(by decreasing the excitability of nerve endings and nerve
AFTER DISCHARGE
conduction) hematoma, and reduce muscle irritability and
For Mother spasm. Ultraviolet light may help hasten repair. However,
Fever vaginal douching is dangerous. Analgesia by nonsteroidal
Excessive bleeding anti-inflammatory agents may be needed to combat pain
Excessive pain in the abdomen for a day or so, the repaired area is to be seen daily on
Dyspnea rounds.
Complaints of breast swelling or pain If the pain persists for more than 2–3 days a per vaginal
Burning micturition or pain during micturition and per rectal examination is needed to rule out hematoma
Excessive or foul smelling lochia or perineal infection. In rare case the sutures are removed,
Weeping or depression attacks. hematoma or infection (collection of pus) drained and
resutured. Antibiotics (ampicillin 500 mg QID) are given.
For Neonate Sitz bath (warm) are needed.
Fever
Diarrhea EMOTIONAL SUPPORT
Convulsions Community support for breastfeeding is essential. Baby
Dyspnea friendly hospitals encourage breastfeeding practice. Infor
Not taking feeds ming about breastfeeding in childbirth and antenatal visits
Bleeding or pus discharge from umbilicus is also important rooming in (keeping the child with the
Yellowness of eyes or body. mother) is helpful. Involving husband in support give
encouraging results. Breastfeeding breaks for working
AMBULATION women is recommended.
Rooming in, i.e. the newborn is kept in the same room
The woman is asked to move about as soon as she can. It as the mother (in a cradle kept near mothers bed or in
instills a sense of wellbeing in her, the uterine drainage is mothers bed) is a vital step in building attachments,
improved, involution of uterus is helped and there are less between the mother and her child. The baby is to be put
chances of thrombophlebitis. But adequate rest and sleep to breast within half an hour of birth. She may experience
are needed after delivery. As β-endorphins are released tearfulness, anxiety, restlessness, etc. They constitute
during lactation, night feedings are not tiring. Other maternity blues and are short-lasting.
recommendations can be individualized. Slow start of As stated before, psychological and physical support
exercise is important. These do not interfere with lactation of the partner and other family members is of paramount
and the infant’s weight gain. importance.
SEXUAL ACTIVITY FAMILY PLANNING ADVICE

Sexual activity is safe when the perineal wound is healed Advice about family planning is essential. Breastfeeding
and lochial discharge has stopped or reduced. On an is a very good natural method of contraception. The
average a 6 weeks period of abstinence is sufficient. It pregnancy rate is very close to those of barrier methods of
depends on perineal and vaginal healing. contraception. Yet it is often overlooked, poorly understood
or misrepresented by healthcare workers who are not well-

educated in this aspect patient is receptive at this time.
EXAMINATION AND INSTRUCTIONS AT
Lactational amenorrhea method has 1% failure rate at THE TIME OF DISCHARGE
1 year after delivery. This is an opportunity to examine the woman, as she may
Post Placental Copper T (380 A) can be inserted imme not come to you later. Ask for any complaints and ask if she
diately after birth [postpartum intrauterine contraceptive is passing urine and stools normally. Anemia and jaundice
device (PPIUCD)].
are ruled out. The breasts and abdomen are examined. How
Non-lactating mother, if not desirous of further preg
much involution of the uterus is there is documented. If
nancy may be offered, besides PPIUCD, barrier methods like
there is a complaint of any pain, it is elicited. Lochia is seen.
spermicidal agents, condoms, etc. (failure upto 21/100 women
The episiotomy site is observed for healing. If there is no
years). It is difficult to fit a diaphragm as involution is taking
significant complaint pelvic examination is deferred. Look
time. If used, is should be in combination with spermicidal
nonoxynol-9 preparations. The non-lactating mothers can be for calf tenderness. Hemoglobin estimation must be done.
offered combined pills 2 to 3 weeks postpartum. Instructions are given about nutrition and hygiene. They
Lactating mothers can take progesterone only pills to pre- are advised proper rest and sleep and asked not to start
vent compromise on quantity and quality of milk production. household work for 6 weeks, if possible. The government
Depot medroxyprogestrone acetate (DMPA) 150 mg of India gives six months leave to the mother and fifteen
(for 90 days) or norethindrone acetate 200 mg (for 60 days) days paternity leave for the father for the first two births.
can also be given intramascularly to lactating mothers The mother is advised to note her temperature on a
after establishment of lactation or 6 weeks postpartum. notebook. She must report to the hospital if there is fever,
These two drugs do not have an effect on milk volume, milk bleeding from the vagina or backache. She is made to
production or thromboembolism as compared to combined understand that her discharge from the vagina will gradually
pill or combined injections. But they do cause amenorrhea decrease till the fifth week after delivery. If everything is
or irregular bleeding, lipid metabolism changes and normal she is advised to come after 6 weeks.
reduction in bone density (which is reversible). Implants
of single mode (implanon) were available for research. POSTPARTUM VISIT AT 6 WEEKS
Counseling plays a very important role in continuation of
any method. Intrauterine contraceptive devices (IUCD) are Her blood pressure is taken and her weight recorded.
inserted after 6 weeks after delivery when the mother visits Hemoglobin estimation is also done. The breast must be
the hospital. Copper T (380 A) is available in government examined for any cracks in nipple. Ask for any suckling
hospitals. Progesterone-releasing (progestasert) or levonor difficulties. The episiotomy scar is examined, the cervix
gestrel impregnated, IUCD—Mirena are highly effective (< is examined and one may take a pap smear, if facilities
2-3 pregnancies/100 women years). Tubal sterilization is are available. Bimanual examination is carried out and
the most common method used in India. It is performed adenexae are palpated. Asymptomatic retroversion is of no
with cesarean section or within 24–48 hours after a normal significance. If any prolapse is seen she is advised pelvic
vaginal delivery. Failure rate is less than 1%. Six to eight floor exercises and asked to come after 3 months for review.
weeks after delivery the women can be sterilized by The infant is sent for examination and immunization.
laparoscopic method. The mother is offered contraceptive measures. She is also
Vasectomy in the husband is suggested but there are given the knowledge of emergency contraception, in case of
few takers. failure of contraception or an unprotected sexual act.
1. Described postpartum changes in a woman.
2. What is the difference between nulliparous cervix and parous cervix.
3. True/False:
i. In lactating women, there is anovulation because of elevated prolactin levels.
ii. As the placenta separates platelet count increases.
35
Sudha Salhan, Nivedita Sarda, Divya Pandey
Abnormal Puerperium
Genital tract infection is to be considered as the cause

INTRODUCTION
for puerperal pyrexia unless proved otherwise. The advent
Puerperium is a period of rapid physical, physiological and of antibiotics has led to the decline in the number of
gynecological readjustments. A normal healthy woman in puerperal pyrexia cases. Routine following of 5 C’s delivery
a congenial (healthy and supportive) environment will practices defined and recommended by World Health
have an uneventful puerperium. But this may not always Organization (WHO), by the health personnels can further
be the case and abnormalities develop in the puerperium. decrease the incidence further. These 5 C’s denote 5 cleans,
Besides the general ailments, puerperal abnormalities are
i.e. Clean hands, Clean perineum, Clean delivery surface,
considered under the following headings:
Clean cord cutting instruments and Clean cord ties.
Infections
In general, causes of puerperal fever may be placed in
Secondary postpartum hemorrhage
the following headings:
Subinvolution of the uterus
Puerperal uterine infection, e.g. endometritis and
Difficulties in breastfeeding
retained products of conception
Endocrine disorders
Perineal infection, including cellulitis
Pshychiatric problems
Postsurgical wound infections
Postpartum neuritis
Breast infection—mastitis
Postpartum emergencies, e.g. pulmonary embolism.
Thrombophlebitis
Urinary tract infection (UTI)

INFECTIONS
Respiratory complications after anesthesia
The placental site in the uterus is like a wound in the body, Other incidental infections:
which is exposed to infections after delivery. Besides,
• Tuberculosis
the cervix is open for the infection to travel in fast. The
• Malaria
blood in uterus is a good medium allowing any injection
• Typhoid
to multiple fact. Hence, meticulous asepsis is essential.
• Chest infections, e.g. pneumonia, bronchitis
Taking all precautions to prevent infection during and after
• Human immunodeficiency virus (HIV)/acquired
delivery and proper instruction of hygiene to the patient
immune deficiency syndrome (AIDS).
are an absolute must. These include using clean pads,
washing the perineal wound after defecation and cleaning
Puerperal Sepsis
from before backward only, etc. Puerperal infections can
manifest as puerperal pyrexia and puerperal sepsis. Puerperal sepsis is defined as the infection of the genital
tract at any time between delivery of the fetus till 42 days
Puerperal Pyrexia (Fever) after delivery. Two or more of the following features need
It is defined as a temperature of 38°C (100.4°F) or more to be present before labelling the condition as puerperal
lasting more than 24 hours (first 24 hours after delivery sepsis:
are excluded) recorded twice or more, within 10 days Fever of 38.5°C or 100.4°F on any one occasion
following delivery. Abnormal vaginal discharge, e.g. discharge of pus

Foul odor/abnormal smell of the discharge Twin delivery

Pelvic pain Low socioeconomic status.
Delay in involution of the uterus (subinvolution), i.e.
less than 2 cm/day during the first 8 days after delivery. Organisms
Many microorganisms are involved and include
Endometritis (also called Metritis or Escherichia coli, β-haemolytic streptococci, facultative
Endoparametritis) organisms (Streptococcus faecalis and Peptostreptococcus,
Infection of the uterine endometrial lining is the most Bacteroides and Prevotella). These causative organisms
common infection following delivery, more so after can be divided into 4 groups:
cesarean section than after vaginal delivery. With vaginal 1. Aerobic gram-negative bacilli
delivery, the incidence is 1–3% and with elective cesarean 2. Aerobic gram-positive bacilli
section, it is 5–15%. It is 30–35% in emergency cesarean 3. Aerobic Streptococcus, and
section, performed after prolonged labor and rupture 4. Anaerobic gram-positive cocci.
of membranes without antibiotics. With antibiotic Common symptoms are fever with chills, headache, lower
prophylaxis, the incidence of endometritis in emergency abdominal pain, malodorous lochia, more then normal
cesarean section reduces to 15–20%. In high-risk patients vaginal bleeding. There may be anorexia and malaise.
(diabetic, anemic and obese, etc.) these rates get doubled. One must elicit the history of risk factors like pre-existing
Myometrium and parametrium are also involved. Use of anemia, prolonged labor, prolonged leaking, MRP, retained
prophylactic antibiotics after cesarean section reduces products of conception, instrumental delivery or cesarean
the incidence considerably. The raw placental site in the section, number of vaginal examinations in labor, etc.
uterus is the initial site of infection (Flowchart 35.1). Physical examination needed includes a record of
Risk factors include: vital signs, examination of the breast, auscultation of the
Prolonged ruptured of membranes
lungs to exclude atelectasis, per vaginal examination and
Antepartum hemorrhage
examination of the lower extremities (thrombosis of deep
Placental site near exterior (placenta previa) veins) to exclude other causes of fever in puerperium.
Cesarean delivery, especially emergency cesarean delivery Abdominal examination is a must and should be thorough
Pre-existing chorioamnionitis to rule out subinvolution, any organomegaly or presence
Bacterial vaginosis of any sign of peritonitis. Apart from this, the condition of
Anemia, obesity, diabetes mellitus stitchline (cesarean or episiotomy) should be assessed.
Multiple vaginal examinations during labor A patient with endometritis, typically has a fever of 38°C,
Manipulation in delivery and trauma tachycardia and fundal tenderness. Pallor may be present.
Poor surgical technique during operative delivery Some may develop mucopurulent vaginal discharge.
Prolonged labor
Pre-existing infection of the lower genital tract

Investigations
Manual removal of placenta (MRP) Laboratory tests include:
Postpartum hemorrhage Complete blood count with differential white blood cell
Placement of intrauterine catheter (WBC) count

Immunosuppressive states like HIV/AIDS or patients Urine analysis
with renal transplant, etc. are highly conducive to the Cultures of urine, cervical and vaginal discharge. Blood
growth of microorganisms cultures in immunocompromised and febrile patients.
Flowchart 35.1: Flowchart showing development of endometritis

Abnormal Puerperium 351
High vaginal and endocervical swabs are taken for 8 hourly) and clindamycin (900 mg every 8 hours) is
anaerobic and aerobic cultures. preferred. Any placenta bits or membranes left in the
Chest X-ray [posterior-anterior (PA) view] to rule uterus are evacuated.
out pneumonitis, pulmonary Koch’s reactivation or A third antibiotic is added if fever persists after
atelectasis. excluding other causes of fever. Broad-spectrum second
Ultrasound of abdomen and pelvis to rule out retained and third generation cephalosporines, broad-spectrum
products of conception/peritoneal abscess/pelvic abscess. penicillins and combination of beta-lactamase inhibitors
Color Doppler ultrasound of lower limbs to rule out with penicillins can be given. Prophylactic Antibiotics use
deep venous thrombosis. in cesarean deliveries reduces the incidence of infections
by 70–80% [American Collage of Obstetricians and
Morbidity and Mortality Gynecologist (ACOG), Evidence level Ia].
Following 48–72 hours of intravenous antibiotic therapy, Management
90% of women recover. Less than 2% develop serious life-
Surgical Treatment
threatening complications like:
Parametritis
Any tear or injury is repaired immediately. If infected,
Peritonitis
it should be resutured after infection control by
Septic shock
serial dressings and antibiotic coverage. One should
Pelvic abscess
specifically, look for wound infection and other causes
of infection and treat accordingly.
Pelvic vein thrombosis.
Culdocentesis (aspiration of pus from pouch of Douglas)
Differential Diagnosis of Puerperal Sepsis or posterior colpotomy (incision and drainage via
pouch of douglas) can be needed for pelvic abscesses
Urinary tract infection (see procedures in Chapter 58).
Acute pyelonephritis Residual products of conception (POC) evacuation is
Lower genital tract infection done after 24 hours of intravenous antibiotic cover.
Wound infection (episiotomy or cesarean section) Laparotomy is done for antibiotic resistant peritonitis
Atelectasis or tubo-ovarian abscess or peritoneal abscess.
Pneumonia Hysterectomy is done rarely only in case of gangrene/
Thrombophlebitis rupture or multiple abscess.
Mastitis
Appendicitis. Supportive Treatment
Along with parenteral antibiotics other supportive therapy,
Prevention e.g. vitamin C and blood transfusion are given if needed.
Preventing and treating anemia in the antenatal period. This is done till the patient’s symptoms resolve, starts
Avoiding sexual intercourse in the last month of accepting orally and is afebrile for 48 hours. Thereafter,
pregnancy. patient is switched to oral antibiotics, and other supportive
Limiting the number of per vaginal examinations after treatment like vitamin C and balanced diet is continued.
rupture of membrane during labor. Heparin is added in pelvic vein thrombosis.
Maintaining a partograph to manage labor, detecting
slow labor early and taking timely action, e.g. augmen- CRITERIA FOR PATIENT’S DISCHARGE
tation of labor are important preventive measures. This should be considered when patient has been switched
Gross inspection of the placenta and membranes for to oral antibiotics and has been afebrile for 48 hours. Then
completeness in all deliveries is essential. oral antibiotics can be given and she is discharged.
Prophylactic antibiotics (mostly triple antibiotics viz If all symptoms do not respond to the above therapy,
capsule ampicillin, injection gentamicin and metroni she should be shifted for intensive care unit (ICU) care.
dazole) in high-risk cases avoids the associated Persistent puerperal fever can be due to:
mortality and morbidity. In mild cases of endometritis Drug-resistant organisms
oral antibiotics will help. However, if the symptoms Wound infection
are severe then intravenous or parenteral combination Mastitis
of gentamicin 120 mg loading dose (80 mg every Drug fever

Septic pelvic vein thrombosis Toxic Shock Syndrome

Pelvic abscess This condition is due to the exotoxin produced by
Recurrence of connective tissue disease Staphylococcus aureus. It presents with usual sign and
Extragenital causes (those mentioned under differential sympyoms of puerperal sepsis. There may be even multiorgan
diagnosis). failure in form of renal or hepatic failure, disseminated
Wound Infection intravascular coagulation (DIC) and or shock. Management
includes volume resuscitation and maintainence by
The incidence depends on the general condition of the
appropriate intravenous fluids or blood blood product
patient at the time of episiotomy or cesarean section.
transfusion and broad-spectrum antibiotics. Respiratory and
Corticosteroid therapy increases the incidence. There
is erythema, induration and pain along the margin of dialysis support may be needed.
the wound. Slight pressure may cause serous or purulent
discharge.
Pelvic Abscess
In patients who undergo cesarean section, the incidence Fortunately, with the use of modern antibiotics the
is 3–5% (Duff 1983). Appropriate chemotherapy is started. incidence of pelvic abscess is less than 1%. The collection of
A few stitches are removed and the wound is inspected pus is seen mostly in the pouch of Douglas (POD) or broad
to see whether it is superficial or deep. If superficial, ligament. There is persistent fever in spite of antibiotic. The
antiseptic dressing is done. It may be dehiscent and may patient has malaise, tachycardia, lower abdominal pain; a
need resuturing. When infection clears up, resuturing is palpable pelvic mass is found on per vaginal examination.
done which will shorten the healing time. Total leucocytic count (TLC) is increased and an ultrasound
usually diagnoses the condition. Sometimes computed
Wound Dehiscence (Burst Abdomen) tomography (CT) and magnetic resonance imaging (MRI)
Though uncommon, it is seen in cases with high risk for may be needed. Culdocentesis is done by introducing
wound infection (obesity, anemia, diabetes mellitus, a needle in the POD and pus is aspirated. Colpotomy
etc.). There is separation of the wound involving all fascial drainage is then done in the operation theatre and a drain
layers. There is profuse serosanguinous discharge around is placed (see procedures of Culdocentesis and Colpotomy
the fifth postoperative day indicating impending wound in Chapter 58).
dehiscence. It is a serious complication. The patient is The pus drained is sent for culture and drug sensitivity.
taken to the operation theater. Under general or regional Antibiotics given are penicillin (5 million unit IV every
anesthesia debridement is done and fascial closure is 6 hours) or ampicillin (2 gm IV every 6 hours) with
done with non-absorbable sutures with or without tension gentamicin (1.5 mg/kg IV every 8 hours or 7 mg/kg of ideal
suturing. For prevention of this condition, first the high risk weight every 24 hours) and clindamycin (900 mg IV every
patients are to be identified. Their nutritional status and hour) or metronidazole (500 mg IV every 12 hours). If renal
anemia should be improved by appropriate medications functions are not normal gentamicin is replaced by other
and blood transfusion as indicated. The rectus sheath
antibiotics.
closure is done using non absorbable sutures. It has been
After drainage of pelvic abscess the symptoms subside
suggested that in these high risk cases every third or fourth
within 24–48 hours. Then antibiotics can be given orally
stitch is to be locked. Infection prevention is done by
and the drain is removed when pus discharge stops.
appropriate antibiotic prophylaxis.
Necrotizing Fasciitis Septic Pelvic Vein Thrombosis

This is a very serious but fortunately less common It is also an uncommon condition, thanks to antibiotic
complication of abdominal and episiotomy wounds. use. The incidence is about 1% of puerperal endometritis.
Patients with diabetes mellitus, or those on immuno- It occurs in two forms.
suppressive therapy or malignancy are more prone to 1. The more common form is acute thrombosis of one
develop this complication. The wound margins are dis (right) or both ovarian veins.
colored and no sensation is perceived. Subcutaneous 2. The second is enigmatic fever having symptoms of
tissues are also involved. Aggressive treatment is life- endometritis. Even after antibiotics the temperature
saving. Broad-spectrum intravenous antibiotics are given. does not settle down. It is to be differentiated from
Electrolyte balance is maintained. The wound is debrided drug fever, viral infection, pelvic abscess and collagen
of all necrotic tissue. vascular disease.
Abnormal Puerperium 353
A vascular surgeon is consulted color Doppler, CT scan or warm bath. If patient fails to void over next two hours
or MRI are diagnostic. In addition to antibiotic, heparin or the voided volume is less than 200 mL, evacuation
is added to the treatment. The dose is titrated to keep the by indwelling catheter is required. If residual volume is
activated partial thromboplastin time (APTT) to about > 150 mL, indwelling catheter is kept for atleast 48 hours
2 times normal. The heparin level in serum should be till bladder tone is restored the catheter sample is also sent
around 0.2 to 0.7 IU/mL. This treatment is given for 7 to for culture and sensitivity examination. Along with urinary
10 days. Within 48 to 72 hours the symptoms must start antiseptics and drugs like flavoxate may be used. If the
regressing. If they persist then surgery, e.g. ligation of the voided urine volume is > 200 mL, non invasive methods
affected vessel(s) or embolectomy should be done, as the are continued (maintaining hydration and measures to
case may be. If there is a well-defined abscess, excision of evoke bladder emptying).
infected vessels and adnexa with or without the uterus is
considered according to the severity. Urinary Incontinence
Rare complications of septic vein thrombosis are: It can be due to overflow incontinence due to loss of
Pulmonary embolism (see Chapter 43)
bladder tone. Stress urinary incontinence (SUI) or true
Thrombosis of leg veins
incontinence is due to weakness of bladder neck support.
Phlegmasia nigra dolens
Overflow incontinence can be managed as described
Phlegmasia alba dolens (white leg)
above to regain the bladder tone by using drugs and
Neurological complications.
indwelling catheterization. SUI can be managed by Kegel’s
pelvic floor exercises.
URINARY PROBLEMS
Urinary Tract Infection SECONDARY POSTPARTUM
Urinary tract infections occur in 3–34% of patients depen HEMORRHAGE
ding on their general condition. The organisms isolated are Occurs after 24 hours of delivery. It is due to infection
E. coli, group B streptococci, Staphylococcus saprophyticus, (retained products, etc.) and is managed with antibiotic
E. faecalis, Proteus and K. pneumoniae. treatment and removal of retained products of conception
This is to be differentiated from acute cystitis and acute (placental bits or membranes) if present.
pyelonephritis. Urine is sent for culture and sensitivity.
Treating with appropriate antibiotics for 7 days will suffice.
Drugs commonly used are—trimethoprim/sulfamethoxa-
SUBINVOLUTION OF UTERUS
zole, ciprofloxacin, norfloxacin and amoxicillin. (PARTIAL INVOLUTION)
It is defined as absent or delayed uterine involution
Urinary Retention
during the postpartum period. The causes of subinvolu-
This is an immediate puerperium problem. Risk factors tion are retained products of conception (placental bits
for this condition are prolonged/difficult labor, prolonged or membranes) if present, uterine fibromyomas, infection
second stage, operative delivery (cesarean or vaginal), and conditions with over distended uterus like polyhy-
epidural analgesia, bladder over distension immediately dramnios or multiple gestation. The symptoms are heavy
after childbirth and good size baby. This is due to bruising and prolonged bleeding post delivery. On abdominal
and edema of bladder neck especially during operative examination, a larger and softer uterus (for that particu-
vaginal delivery. It may also be due to pain from local/ lar postpartum day). Treatment includes methylergome
vaginal or paraurethral trauma or tears. trine orally for 3 days. Antibiotics should be prescribed in
Overt urinary retention: It refers to symptomatic case of any infection. The hemoglobin is also evaluated,
inability to pass urine spontaneously within six hours of accordingly oral or parenteral iron is given. A follow-
delivery or after removal of urinary catheter. After first up examination is done after 2 weeks.
four hours, management includes ensuring hydration.
Providing privacy and pain relief measures help in most
cases. Psychological treatment in the form initiating
PROBLEMS OF BREASTFEEDING
bladder reflex bladder voiding by the sound of running They are discussed in detail in breastfeeding (see Chapter
tapwater or sprinkling lukewarm water over perineum 34). Some common problems are as follows.
Lactation Mastitis ENDOCRINE DISORDERS

There is fever (39–40°C) followed by redness and tender Endocrine disorders can occur in puerperium. They are
ness in the affected breast. Continue breastfeeding to rare but the following are to be kept in mind:
facilitate drainage. Supportive care viz rest analgesics, Postpartum thyroiditis
hot compresses, breast support and an increased fluid Postpartum Graves’ disease
intake will help. It is not infective and will subside by itself. Sheehan’s syndrome.
Cloxacillin is the drug of choice for these cases as they may The first two are described in detail see Chapter 46.
lead to breast abscess if not treated adequately.
Complications occur if not treated in time. Cracked Sheehan’s Syndrome
nipple is a painful condition caused mostly by faulty This condition merits special mention. It is caused by pituitary
application of the child to the breast. If the child takes the hypofunction due to massive intrapartum or postpartum
whole of nipple and areola in his mouth there are lesser hemorrhage. Most of the endocrine glands of the body—
chances of developing cracked nipple. thyroid, adrenal, ovaries, etc. suffer in their functions due to
The nipple is kept clean. The hind milk (last part of the less blood supply. There is failure of lactation, amenorrhea,
feed) if applied to cracked nipple, will help in healing (it is breast atrophy, loss of pubic and axillary hair.
rich in fats). Adequate replacement of the hormones is advised. This
Application of emollients or lanolin cream after feed condition is very uncommon nowadays.
and cleaning it off before start of lactation may help. Use
of nipple shield (a plastic device with rubber nipple) can PSYCHIATRIC DISORDERS
provide rest to the nipple and help in healing. Failure They are seen in puerperium. Postpartum blues is a mild-
to establish lactation is seen in hypothyroid patients, form however, postpartum depression and psychosis may
patients suffering from Sheehan’s syndrome, etc. develop. They are dealt with in Chapter 53.
Postpartum emergencies, e.g. embolism are dealt with
Breast Abscess in the Chapter 43 and 45.
In mastitis, if the fever does not subside within 48–72
hours or a palpable mass is felt one should suspect breast POSTPARTUM NEURITIS
abscess. Ultrasound examination will help in making the They are also known as postpartum traumatic neuritis or
diagnosis. Surgical drainage is carried out under adequate postpartum dysfunction of lumbosacral nerves is fairly
anesthesia. The incision is made corresponding to the common. The most common nerve involved is peroneal
skin lines in the most dependent fluctuant portion of the nerve leading to foot drop. Risk factors are short statured
breast. Septa and loculi are broken with fingers. The cavity primigravidas, operative vaginal deliveries especially
is packed with gauze, which is replaced by a smaller pack forceps, occipitoposterior position, narrow pelvis and big fetal
after 24 hours. head. Treatment is physiotherapy and orthotics if required.
Ultrasound guided needle aspiration is another option.
Pus should be sent for culture and sensitivity. Antibiotics PULMONARY EMBOLISM
can be changed according to the culture report. It has been dealt in detail in (see Chapter 43).
1. What is Sheehan’s syndrome?
2. Define risk factors of endometritis.
3. True/False:
i. The placental site in the uterus is like a wound in the body.
ii. The incidence is about 10% of puerperal endometritis.
iii. A products of conception (POC) evacuation is done after 24 hours of intravenous antibiotic cover.
iv. SUI can be managed by Kegel’s pelvic floor exercises.
Section 7
Medical Disorders in Pregnancy
Section Outline
36. Preconceptional Counseling
37. Anemia in Obstetrics
38. Pregnancy and Heart Disease
39. Diabetes and other Endocrine Disorders in Pregnancy
40. Hypertension in Pregnancy
41. Renal Disorders Complicating Pregnancy
42. Liver and Pancreatic Diseases in Pregnancy
43. Respiratory Disorders in Pregnancy
44. Rh Isoimmunization in Pregnancy
45. Alteration of Hemostatic System and Coagulation Disorders in Pregnancy
46. Thyroid Disease in Pregnancy
47. Neurological Disorders in Pregnancy
36
Sudha Salhan, Meetu Salhan, Meenakshi Bhatt
Preconceptional Counseling
Examination of a woman before the couple embarks on veneral disease research laboratory (VDRL), hepatitis B,
pregnancy is a very important preventive measure. human immunodeficiency virus (HIV), hepatitis C, sexually
transmitted diseases (STDs), etc. According to the family
DEFINITION history, screening for specific genetic disorders can be done.
Titers of rubella antibody if available and if required are
Preconceptional counseling is defined as identifying measured. Urine analysis to rule out urinary tract infection
factors (social, familial, obstetric, medical or lifestyle) (UTI) and pap smear are also carried out.
which affect pregnancy. These factors when appropriately Counseling will include evaluation of:
modified can reduce the pregnancy risks and improve both Medical disorders
the maternal and fetal outcome and also determine risks Genetic disorders
which are severe enough to advise against pregnancy (e.g.
Previous obstetric outcome
complicated aortic coarctation, Marfan’s syndrome, etc.) It
Drugs and vaccination
provides prospective parents with a series of options which
Nutrition
may not be available once pregnancy occurs. This concept
The process begins with taking a good history and doing
has been around for less than 30 years unlike antenatal
a thorough physical examination. The risk to the mother
care which has more than 100 years of standing. Although
and fetus are high in some diseases. Women should
pregnancy for some will be unplanned, but the majority of
conceive only when their disease is under remission or
couples who are planning pregnancy will be benefitted by
this notion. proper control by treatment (e.g. heart disease).
It is the most appropriate preventive technique for a
couple (especially the woman) planning pregnancy. We
Medical Disorders
can imagine it to be similar to getting our vehicle tested Anemia: Anemia is the second greatest killer during
before going on a long journey in order to ensure a smooth pregnancy in our country. It is the cause of 20% direct
ride with as little inconvenience as possible. It helps and 20% indirect maternal deaths. The woman, if
women to embark on a vital venture (pregnancy) with the anemic, should be appropriately investigated and the
least possible risks or complications. underlying causes treated by medications (iron therapy,
antihelminthics, etc.) and with dietary modifications.
Heart disease: The woman should be evaluated for her
PATIENT EVALUATION
cardiac functional status so that if possible the severity

The patient’s general condition, height, weight, body mass of the disease can be reduced and complications
index (BMI), blood pressure (BP) and other systemic (pulmonary edema, congestive heart failure and
evaluations are done to detect any abnormalities. The arryhthmias) can be prevented with medications prior
laboratory investigations will include a baseline hemoglobin to pregnancy. If any surgical correction is needed, it
level, peripheral smear for type of anemia and electrophoresis should also be planned such that she enters pregnancy
for patient suspected with hemoglobinopathies. A baseline in a stable condition. This decreases maternal mortality
blood sugar analysis and tests to rule out infections like and morbidity to a great extent.
Diabetes mellitus: It has been seen by several Drugs and Vaccinations

investigators that if the blood sugar is controlled for Drugs
at least 2–3 months before pregnancy with insulin
(monitored by HbA1C), the incidence of congenital The number of medicines and their dosage is to be kept
malformations are significantly reduced. The pregnant to a minimum. Unsafe drugs during pregnancy (class-X)
mother should be guided to maintain a diabetic diet. should be stopped before conception. In several cases of
She should also be taught self monitoring of blood congenital abnormalities in previous pregnancies, this is
glucose and how to recognize signs of hypoglycemia/ the time to advise folic acid intake to prevent recurrence. In
hyperglycemia and ketoacidosis and how to take fact, folic acid should be regularly advised to all women for
appropriate first aid measures. In the presence of those 2–3 months preconceptionally, as it remarkably decreases
danger signs she should immediately report to a health the incidence of neural tube defects (NTDs). Any addictive
facility for appropriate treatment. Vasculopathies, if drug, is to be discontinued before conception (e.g.
present, should be brought under adequate control cocaine). Smoking and the consumption of alcohol should
before conception. also be stopped.
Seizure: The management of the epileptic patient
Chronic hypertension: Blood pressure should be well
controlled. Hypertension is often associated with other should be in consultation with a neurologist. Some
systemic complications (renal and cardiac). These drugs could either be discontinued (if using multiple
should be evaluated and appropriately treated. drugs) or changed so that the least harmful or
Renal insufficiency: If the disease is severe enough, renal teratogenic drugs are selected. Monotherapy, with the
transplantation may be required. Successful pregnancies lowest possible effective dosage, is the ideal mode of
after renal transplantation have been reported. treatment. If there is a history of previous NTDs, then
Thyroid disorders: A euthyroid state should be achieved folic acid supplementation (5 mg) 2–3 months prior to
before pregnancy. conception is advisable to prevent recurrences.
Tuberculosis: Treatment of tuberculosis is essential
If the HIV status is known before pregnancy, the woman
for the wellbeing of both the mother and her fetus.
can be counselled about its effect on the fetus. The mother
Therefore, the therapy should be continued according
should also be informed about measures which can be
to the regimen and drug sensitivity. Though some drugs
taken to reduce HIV transmission to the fetus. Ongoing
are contraindicated in pregnancy, e.g. streptomycin,
counseling for psychological support is also important.
kanamycin and capreomycin (due to their ototoxicity)
Genital tract malignancy: It may be treated according
and pyrazinamide (due to inadequate availability of
to the stage of the disease. Pregnancy may not be
safety profile) other drug regimens must continue.
possible after complete treatment except in cases of
Hypertension: Blood pressure should be controlled
carcinoma—in situ of cervix (which is treated by wedge
with a drug regimen which is safe in pregnancy (e.g.
resection) and choriocarcinoma (medical treatment).
α-methyldopa, nifedipine). Angiotensin converting
Sexually transmitted diseases (STDs): Both partners
enzyme (ACE) inhibitors should be discontinued and
should be adequately treated.
replaced by safer drugs. Diuretics are contraindicated.
If there is a risk of pre-eclampsia, calcium supplements
Genetic Disorders
can be started.
If there is a history of maternal, paternal or familial genetic Diabetes: Two to three months before conception, the
or inheritable disorders, further evaluation should be therapy is shifted from oral hypoglycemic agents to
offered (e.g. thalassemia, inborn errors of metabolism, insulin (as they can cause fetal hyperinsulinemia and
previous congenital or chromosomal abnormalities even congenital malformations). Insulin crosses the
and previous X-linked disorders) in the form of genetic placenta, but at a very slow rate. Glyburide therapy and
mapping of both partners. metformin (used in polycystic ovarian disease) have also
been shown to be effective with no apparent neonatal
Previous Obstetric Outcome complication. The continuation of metformin (once
Patients with a bad obstetric history (e.g. preterm labor, pregnancy is proved) is still debatable. In addition, folic
miscarriage, still birth, Rh blood group isoimmunization, acid therapy should be started to prevent NTDs.
etc.) need to be investigated further to find out the Heart disease: Prophylactic penicillin therapy in patients
causative factor so that it can be appropriately treated and with rheumatic heart disease is continued or started
recurrences can be prevented. for endocarditis prophylaxis. In addition, prophylaxis
Preconceptional Counseling 359
during gastrointestinal (GI), dental and genitourinary Vaccination: Immunological status (antibody titer) of the
procedures is administered. If the patient is on warfarin woman for rubella and hepatitis B should be assessed as
(as in vulvectomy), it should be replaced by heparin. rubella can cause lethal congenital abnormalities in the
Complications such as congestive cardiac failure, fetus and hepatitis B can be vertically transmitted to the
pulmonary edema and arrhythmias must be corrected fetus. If the antibodies are absent then vaccinations against
with medications or other means. Conditions which may them are recommended. However, pregnancy should be
worsen the cardiac status (anemia, thyrotoxicosis and avoided for 1 months after rubella immunization.
infections, etc.) should be kept in check.
Oral contraception: It should be stopped at least Nutrition
3 months and preferably 6 months prior to planning Obesity can lead to both maternal and fetal complications
a pregnancy to allow for the resumption of natural such as:
hormone regulation and ovulation. Oral contraceptive Pre-eclampsia
pills are associated with vitamin (deficiency of folic Hypertension
acid, B complex and vitamin C and high vitamin A) and Gestational diabetes
mineral imbalance (raised copper and low-zinc level). Labor abnormalities
Other forms of contraception like barrier methods can Increased operative interventions
be used during this interval. Preterm deliveries
Substance abuse: Smoking, alcoholism, intake of Increased risk of late fetal deaths
addictive drugs (e.g. marijuana, cocaine, heroin, etc.) Congenital malformations.
should be stopped as they severely affect the fetal Hence, weight reduction before pregnancy is beneficial.
outcome like miscarriage, preterm labor, low birth Malnutrition may also affect the pregnancy outcome by:
weight, stillbirth and abnormalities. Premature labor
Malignancy: All antineoplastic drugs are teratogenic, Intrauterine fetal growth restrictions (IUGR)
thus, female patients should be advised against Intrauterine fetal demise
conception during therapy. Accidental hemorrhage.
Unless corrected or stabilized before pregnancy, the Thus, a balanced healthy diet is advised and the body
following conditions are contraindicated for pregnancy weight should be maintained within normal limits prior to
because of very high incidence of maternal mortality. pregnancy.
• Marfan’s syndrome Avoidance of alcohol and caffeine is important. Adequate
• Aortic aneurysm time is given for explanation, clarifying misconceptions and
• Pulmonary hypertension answering questions. Most of the ailments can be cured or
• Cardiomyopathy treated, others are reduced in intensity by therapy. By doing
• Coarctation of aorta these, we reduce the danger to the mother and the fetus.
• Decompensated heart failure Thus, preconceptional counseling is very important
• Advanced renal failure for the final outcome of a healthy mother with a normal
• Advanced hepatic failure healthy baby.
1. Among the following medical disorders, which is the second greatest killer causing maternal deaths during pregnancy in our
country?
i. Anemia
ii. Heart disease
iii. Diabetes mellitus
iv. Hypertension.
2. Avoidance of smoking and alcoholism is beneficial as they affect the fetal outcome like low birthweight, preterm labor. State
True or False.
3. Immunological status of the woman for rubella should be assessed, as rubella enters the placenta and causes _____________.
4. The folic acid supplementation 2–3 months prior to conception is beneficial, if there is any prior history of neural tube defects.
State True or False.
37
Sudha Salhan, JB Sharma, Divya Pandey, HP Anand
Anemia in Obstetrics
MAGNITUDE OF THE PROBLEM DEFINITION OF ANEMIA

Anemia is a global problem having a wide range of Statistical definition: A condition of low hemoglobin
prevalence, severity and etiology in various countries. concentration in circulation, two standards deviation
It is especially challenging for the obstetricians as it is below the median of healthy population of similar stage
responsible for a major chunk of maternal mortality of pregnancy and age.
(40–60%). It causes direct and indirect deaths due to WHO definition: Hemoglobin concentration of less
hemorrhage, infection, cardiac failure, pre-eclampsia. than 11 g/dL (7.45 mmol 1/L) and a hematocrit of less
There is also danger to the fetus and newborn. Above than 33%.
25% of the people in the World are anemic, the cause of Centers for disease control (CDC), USA definition:
more than half of it is iron deficiency. The magnitude of Hemoglobin less than 11 g% in first and third trimester
affection is more in pregnant women. More than 85% of and less than 10.5 g% in second trimester of pregnancy.
the absolute anemia burden of the World is shared by Asia
and Africa.
Classifications
WHO Classification of Anemia (Degree)
INDIAN SCENARIO Mild anemia Hb =10 g% and less.
Moderate anemia =7.1-9 g%
It is a major health problem in our country. World Health Severe anemia=less than 7 g%
Organization (WHO) estimates 74.3% of Indian population Indian Council of Medical Research (ICMR) categorizes
is anemic, almost 58% of pregnant women in India have one more group—very severe anemia/ decompensation =
anemia, which is also the underlying cause for 40% (20% less than 4 g%
direct and 20% indirect) maternal deaths. That means By etiology of anemia in pregnancy
that, if we wipe out anemia from India almost half of our Physiological: Pregnancy
pregnant women will not die. This task does not require Nutritional: Iron, folate, vitamin B , vitamin A defici-
12
any major technical input. Diet and supplementation is all ency (dietary deficiency)
that is needed. The National Family Health Survey-3 has Hemorrhagic:
shown that anemia is widely present in all age groups, but • Acute: Miscarriages, antepartum hemorrhage (APH),
is particularly high among the most vulnerable group, i.e. postpartum hemorrhage (PPH)
pregnant women (58%), non-pregnant and non-lactating • Chronic: Bleeding, hemorrhoids, hookworm or
(50%) women and adolescent girls (56%). other parasitic infestations
In India, anemia antedating pregnancy is aggravated by Acute or chronic infections: Malaria, tuberculosis,
increased demand of mother and fetus in pregnancy and urinary tract infection (UTI), etc.
bleeding at the time of delivery. Sepsis in antenatal and Hemolytic anemia:
postnatal periods and early advent of the next pregnancy • Congenital: Glucose-6-phosphate dehydrogenase
perpetuates it. (G-6PD) deficiency, hereditary spherocytosis
Anemia in Obstetrics 361
• Acquired: Microangiopathic hemolytic anemia, Two forms of iron are present in our diet viz. heme
immune hemolytic anemia and non-heme. Heme iron is absorbed more readily. Non
Hemoglobinopathies: Sickle cell trait, sickle cell dis- heme iron is in insoluble ferric form. It is to be converted
ease, thalassemia to ferrous iron (in the stomach by hydrochloric acid (HCl)
Aplastic anemia. at the brush border by a ferrireductase enzyme) which is
Based on red cell Indices soluble and can be absorbed.
Microcytic hypochromic anemia Ferrous form of iron is taken up by intestinal mucosa’s
• Mean corpuscular volume (MCV) < 80 fl luminal cells. Divalent metal transporters (DMT1)—a general
• Mean corpuscular hemoglobin concentration cation transporter, helps transport ferrous iron across the
(MCHC) < 27 pg cell membrane. Here, it combines with apoferritin to form
Seen in iron deficiency anemia (IDA), thalassemias ferritin. Absorption of ferrous iron continues till apoferritin is
Normocytic normochromic anemia
fully saturated with iron (around 2–3 g of iron).
• MCV, 80–95 fl After that, no further iron is absorbed at that point of
• MCHC, 27–34 pg time (mucosal block). Once in the cells of the intestines,
Seen in acute blood loss, hemolytic anemia or bone this iron is either stored as ferritin in the cells only (if the
marrow failure body has enough iron) or transported through membrane-
Macrocytic anemia
embedded iron exporter–ferroprotein. After coming out of
the cell iron interacts with hephaestin (HEPH,a ferroxidase)
• MCV > 95 fl
and is oxidized into ferric state for binding to transferrin.
• MCHC > 35 pg
This combination travels with its receptor through blood
Seen in megaloblastic anemia and indicates folate or
and releases iron in reticuloendothelial system (RES) in the
vitamin B12 deficiency
bone marrow, spleen and liver to form RBC—erythropoiesis.
Dimorphic anemia
When in erythroid cells, iron form hemoglobin.
Both iron deficiency and folic acid and vitamin B12
Similarly, the iron released from RBCs at the end of its life
deficiency.
(approximately 120 days) is transported to RES. Excess iron
in RES is stored in macrophages as ferritin to be used when
ABSORPTION OF IRON required for erythropoiesis.
Heme iron is absorbed without ascorbic acid and HCl
Iron Deficiency Anemia (IDA) help in the cells. Inside the cell, iron comes out of the
It is most common type of anemia in women. Iron is a heme moeity and similarly utilized.
metal which is precious for human body. Its total amount
in an adult is around 4 grams. It is normally not excreted Iron Requirements in Pregnancy
(always bound with protein) and is reutilized at once [e.g. Iron needs vary with the pre-pregnancy hemoglobin, body
after breakdown of red blood cells (RBCs)] . weight of the mother, and the size and maturity of the
The iron is mostly absorbed by mucosal cells (of fetus. In an average singleton pregnancy following are the
duodenum and jejunum) which has a protein apoferritin requirements (Table 37.1).
under the influence of hepcidin—the iron regulatory There is conservation of 240–480 mg of iron due to
hormone of liver. amenorrhea and thus 700–1200 (average 1000 mg) of iron
The absorption of iron varies according to the need of is required during pregnancy.
the body (mucosal block). Normally, 10% of dietary iron
is absorbed, but if there are very low iron stores in the body
the absorption of dietary iron may rise upto 20% or even TABLE 37.1: Need of iron in singleton pregnancy
30–40%. Similarly, if the iron stores are full, no food iron Increase in RBCs 570 mg
may be absorbed. In a normal hemogloboin level, pregnant Day-to-day loss 270 g
woman’s iron absorption depends on type of food and iron Requirement of fetus 200–350 mg
bioavailability. Some food articles like phytates, tannins, Placenta and umbilical cord 50–150 mg
tea, coffee, milk, calcium, etc. hamper absorption of iron.
Loss during delivery 100–250 mg
In diet which has meat, fish and citrus fruits has more
iron absorption. Absorption also depends on whether it is Lactation requirement 100–180 mg
taken before meals (absorption is maximum) or during or Approximate total need of iron 1200–1600 mg
after meals. during pregnancy
Hence, daily iron requirement is 4 mg/day (on an Clinical history is taken in chronological order. Pre-
average) throughout pregnancy varying from 2.5 mg/ senting complaints, systemic history, social history, past
day in early pregnancy, in mid pregnancy it is 5.5 mg and and family history should be noted.
6.6 mg from 32 weeks of gestation onwards. The presenting complaints may be the common symp
The absorption of iron is 10% which requires 40–60 mg of toms like tiredness, lassitude, getting fatigued easily,
iron to be available in the diet to achieve 4–6 mg of absorption muscular weakness of the body. Ask questions to exclude
daily. This is not available in the average Indian diet hence, heart disease and other causes of these symptoms.
there is the need to supplement. 100 tablets containing Enquire about the onset of the symptoms; if the
100 mg iron and 0.5 mg folic acid, each one tablet daily symptoms are sudden (acute bleeding) or gradual [uterine
from second trimester onwards during normal pregnancy is or gastrointestinal (GI-bleed)].
given (Government of India’s Anemia Prevention Program). In reproductive system, ask age of menarche, menstrual
In cases where the pregnant woman is anemic, double dose cycle regularity, duration, and amount of bleeding. History
of prevention program (i.e. 200 tablets) is recommended of previous pregnancy (if any)—interval (less than 3
in the National Program. years), was supervised by antenatal care (ANC) check-
ups, any iron folic acid (IFA), supplement taken and
Reasons for High Incidence
history of diarrhea. History should be recorded in terms
Main causes of IDA are as follows: of any abortion, amount of bleeding during abortion or
Dietary habits
pregnancy, APH and PPH. History of blood transfusion in
• Consumption of low bioavailability diets (cereals
previous conception should also be taken.
and tubers) like maize, rice, beans, whole wheat and
To rule our GI-bleed, ask about symptoms of peptic
negligible meat, fish, poultry and ascorbic acid
ulcer, piles, history of intake of analgesics. History of
• Food fads (restriction of specific foods in pregnancy)
chronic diarrhea may cause megaloblastic anemia or even
• Phytates, tannates and calcium in tea, coffee, herbal
drinks in the diet impair absorption of iron iron deficiency anemia.
Defective absorption
Urinary system—polyuria at night, bacteriuria, hema
• Worm infestations (hookworms), amoebiasis, giar- turia or chronic renal disease may cause anemia. Bone
diasis, celiac disease, tropical sprue pains, marrow replacement in malignancies and bleeding
Low iron stores and iron loss
tendencies are important in history.
• Low baseline reserves Drug ingestion, e.g. analgesics for chronic headache
• Multiple pregnancies and short intervals between or arthritis. History of taking anti malarial in endemic
two births area points to anemia due to malaria. Any other illness—
• Menorrhagia autoimmune disease, AIDS, etc. Dietary history is to be
• Excessive sweating in the tropics taken in detail. Socioeconomic status is documented.
• Schistosomiasis, malaria and hookworms Personal history of any chronic illness, alcohol con-
Vitamin A deficiency sumption or other drug addictions. Past history of anemia,
• Dietary deficiency. blood transfusion, history of jaundice (congenital hemo-
lytic anemia) or any hereditary anemia.
Factors Affecting Iron Absorption
Inhibitors of absorption: Clinical Features
• Tea, coffee, milk, egg Mild anemia: No adverse effect
• Phytates, zinc, calcium rich foods Moderate anemia: Fatigue, weakness, lassitude, exhaus
• Antacids, calcium phosphate herbal drinks tion, anorexia, indigestion, dyspnea, giddiness
Enhancers of absorption Severe anemia: Tachycardia, dyspnea, palpitations,
• Heme iron, proteins fermentation products, meat, increased cardiac output, congestive heart failure, gene
fish ralized anasarca, pulmonary edema.
• Ascorbic acid, citric acid
• Tartaric acid, gastric acidity Examination
• Iron deficiency Do complete general examination. Look for fever and
• Increased erythropoeisis occurs at high altitude pallor on face and skin. Also see the nails changes
• After hemolysis and bleeding (depressed nails koilonychia) (Fig. 37.1) gums, oral cavity,
RBC count (normal 4.0–5.2 million/mm3): Total and

differential leukocyte count and platelet count help to
differentiate anemia due to general bone marrow defects
(hypoplasia, infiltration and infection) from other causes
(pure anemia and pancytopenia). In populations with
a high prevalence of beta thalassemia trait, red cell
distribution width (RDW) which is high in nutritional
anemias helps to differentiate from thalassemias where
it is normal. (normal 60 mg–120 mg/dL).
Reticulocyte count and peripheral blood smear
(Figs 37.2A and B): A microcytic hypochromic picture is
seen in IDA with anisocytosis and poikilocytosis. Malarial
parasites may be seen. Free erythrocyte protoporphyrin
(FEP) rises with a defective iron supply to developing
red cells and takes 2–3 weeks to become abnormal after
Fig 37.1: Depressed nails (Koilonychia) depletion of iron stores (more than 50 mg/dL).
Hematocrit (normal 32–36%): IDA (< 30%).
Red cell indices.
and lips for pallor, cheilosis, glossitis. Look for edema on
legs and tenderness of bones. Laboratory Iron Studies
Cardiovascular system (CVS) shows palpitation, Total iron binding capacity (normal 300–350 mg/
murmur (hemic or due to heart disease or both), hyper dL): In IDA, it is increased.
tension may develop due to renal insufficiency. There may Serum iron (normal 50–150 mg/dL): Affected by recent
be congestive cardiac failure, splenomegaly, enlarged iron ingestion, has diurnal variation. Iron deficiency
and tender liver (decompensated anemia), edema, has low serum iron of less than 50 mg/dL.
hyperdynamic circulation as evidenced by a short and soft Serum ferritin level indicates iron stores of tissues
systolic murmur, signs of congestive heart failure . (normal 50–150 mg/L): In IDA, it may be less than 15
Renal: Any hematuria or UTI mg/L. It rises in inflammation upto three-folds and is
Respiratory system: Crypts, rhonchi, etc. not affected by recent ingestion of iron. However, its
Any discharge or bleeding per vaginum. levels fall in pregnancy due to hemodilution.
Transferrin saturation decreases to less than 15% in
Investigations IDA.
Hemoglobin measurement: Measurement by colorim- Transferrin receptor concentration: It shows tissue
eter by cyanmethemoglobin is the most accurate. Tallquist iron status. This is not influenced by pregnancy,
method and sahli’s method have less accurate results. chronic disease or acute infection. It is increased in iron
A B
Figs 37.2A and B: Hypochromic microcytic anemia. A. Reticulocyte count; B. Peripheral blood smear
deficiency anemia (normal 4–9 mg/L by immunoassay). TABLE 37.3: Hematological indices
It is a good marker of iron deficiency in pregnancy.
Normal Iron deficiency anemia
Free erythrocyte protoporphyrin (FEP) indicates
MCV 75-95 fl <75 fl
supply of iron to developing RBCs.
It is increased in IDA, but it is normal in thalassemia. MCH 26-31 pg <25 pg
This test is indicated if the iron status of the woman MCHC 30–35 gm/dL <30 gm/dL
cannot be assessed accurately (like inflammation) or if no Abbreviations: MCV—Mean corpuscular volume; MCH—Mean cor-
response occurs in anemia in 4 weeks of therapy. In the puscular hemoglobin; MCHC—Mean corpuscular hemoglobin concen-
tration
absence of supplementation, more than 80% of women
at term have no detectable stainable iron. Bone marrow Effect
examination can also diagnose kala azar by detecting Consequences of IDA can be seen both in the pregnant
Leishman donovan (LD) bodies. woman and the fetus specially in moderate and severe
Other investigations to know the etiology of the anemia anemia.
include:
Three subsequent stool examination (ova and cysts)
Effects on Mother
Urine examination (for any infection, microscopic
Pre-eclampsia, preterm labor, cardiac failure, PPH, puer
hematuria and for schistosomes in endemic areas)
peral sepsis, sub-involution of uterus, failure of lactation,
Urine culture (asymptomatic bacteriuria)
Sputum examination
puerperal venous thrombosis etc.
Chest X-ray
Renal function tests

Effect on Fetus and Neonate
Liver function tests with serum proteins (for hypo Low birthweight, intrauterine death, iron deficiency in
proteinemia). the fetus , minimal iron stores of iron in neonate, neonatal
Bone marrow stores evaluation (Table 37.2). cognitive and affective dysfunction.
Thus, if hemoglobin is low with a microcytic, hypo
chromic picture and a low MCV, MCH and MCHC IDA Management
can be suspected (Table 37.3). Serum ferritin is measured Prevention Strategies
which if less than 15 mg/L, confirmative of IDA. When
The management starts from the cradle. Female neonates
in doubtful range (12–50 mg/L), transferrin receptor
concentration can clinch the diagnosis. Bone marrow of iron deficient mothers show normal hemoglobin at
examination can be performed to confirm the diagnosis birth, but have poor iron stores. Hence, iron therapy must
(rarely needed). There are three stages of iron deficiency. be started as early as possible. Prevent IDA in adolescent
1. Stage I: Iron stores are low shown by low-level of serum females. Prenatal check-up is necessary to cure anemia
ferritin before embarking on pregnancy. Personal hygiene to be
2. Stage II: There is rise in total iron binding capacity taught to children as early as possible it prevent infection
due to fall in serum iron which is not sufficient for and anemia.
erythropoiesis Dietary modifications: Eating iron rich food, e.g.
3. Stage III: Hemoglobin synthesis does not occur and green vegetables (like spinach, mustard leaves, green
IDA becomes obvious clinically. turnip), jaggery, cereals, sprouted pulses
TABLE 37.2: Various parameters in iron deficiency anemia

Normal Negative iron balance Iron deficient erythropoiesis Iron deficiency anemia
Marrow stores 1–3+ 0-1+ 0 0
Serum ferritin (mg/L) 50–200 <20 <15 <15
TIBC 300–360 >360 >380 >400
Serum iron (mg/L) 50–150 NL <50 <30
Saturation % 30–50 NL <20 <10
Morphology Normal Normal Normal Microcytic hypochromic
Abbreviation: TIBC—Total iron binding capacity
• Cooking food in iron utensils Newer Strategies

• Avoidance of excessive tea and coffee and of over Schools in Delhi are giving iron supplements to all adoles-
cooking of food. cent girls along with their deworming.
Iron supplementation with folic acid to adolescent and Intermittent supplementation (weekly and biweekly
reproductive age women in between pregnancies supplementation) based on mucosal block theory of iron
Treatment of hookworm infection by albendazole/ supplementation has been suggested for better results and
mebendazole to all anemic pregnant women after first good compliance.
trimester of pregnancy
Iron supplementation in pregnant women Treatment
• WHO recommends universal supplementation for Diet rich in iron, proteins, vitamins and ascorbic acid to
6 months in countries with a prevalence of anemia be prescribed
<40% and for additional 3 months postpartum Elimination of septic foci
(prevalence >40%) Checking compliance to therapy.
• Ministry of Health and Family Welfare (GOI) in anemia
prevention program recommend and distributes free Specific
one hundred tablets containing 100 mg of elementary Choice of therapy would depend on:
iron and 0.5 mg folic acid to pregnant women from Gestational age
second trimester onwards for prevention of anemia Severity of anemia (to know the time we have for
(and double the dose for treatment of anemia) correction).
• Routine supplementation is considered cost effective
in developing countries like India as serum ferritin Differential Diagnosis
screening is costly and most women have depleted IDA is to be differentiated from chronic inflammation or
iron stores who are likely to benefit from it with little malignancy, thalassemia, sideroblastic anemia in resistant
problem of overload cases (Table 37.4).
Food fortification: Fortification of cereals, sugar, curry Treatment of anemia based on the period of gestation.
powder with ferrous salts or chelated iron compounds Flowchart 37.1 below outlines the strategy of treatment
has been tried. Fortification of common salt with iron depending on period of gestation
has also been successfully done in some countries The method of anemia correction depends on the time
Prenatal assessment and correction available before delivery. In general, there should be at
Antenatal care started at the earliest for early recognition least ten weeks time provided the anemia is not severe or
and prompt treatment of deficiency. very severe. Here, satisfactory result can be achieved by
TABLE 37.4: Differential diagnosis of microcytic anemia includes

Iron deficiency Chronic inflammation or malignancy Thalassemias Sideroblastic anemia
MCV All reduced in relation Low normal or mild reduction All reduced, very low for Very low in congenital,
MCH to severity of anemia degree of anemia raised MCV in acquired
MCHC
Serum iron Reduced Reduced Normal Raised
TIBC Raised Reduced Normal Normal
Serum ferritin Reduced Normal Normal Raised
Bone
Iron Reduced Present Present Present
Stores
Erythroblast iron Hb Absent Absent Present Ring forms
Electrophoresis Normal Normal HbA2 raised in beta form Normal
Abbreviations: MCV—Mean corpuscular volume; MCH—Mean corpuscular hemoglobin; MCHC—Mean corpuscular hemoglobin concentration;
Hb— Hemoglobin; TIBC—Total iron binding capacity
Flowchart 37.1: Strategy of treatment of anemia depending on the period of gestation
Abbreviations: IV—Intravenous; IM—Intramuscular; Hb—Hemoglobin
oral formulations. Parenteral preparations are needed in acid, gluconic acid, glutamic acid, lactic acid and trace
case of iron intolerance, inflammatory bowel disease or elements (Cu, Co, Mn).
non/poor response to oral iron therapy. Blood transfusion Newer preparations like Iron polymaltose complex, iron
should be reserved for severely anemic cases during the polysucrose complex and carbonyl iron are available
last 4 weeks period of pregnancy. with better GI tolerance, but are more expensive.
Both Iron (II) [Fe2+ (ferrous)] and Iron (III) [Fe3+
Iron Preparations (ferric)] salts are available, but ferrous compounds are
The gold standard of treatment of mild to moderate IDA is better tolerated due to higher bioavailability in contrast
oral iron therapy. Iron is given in the dose of 180–200 mg to lower bioavailability of ferric salts due to formation of
of elemental iron per day. It is prescribed along with folic insoluble complexes. Different preparations are available,
acid, Vitamin C which acts as cofactor along with protein but all are similar in context of pharmacokinetics and
rich diet. pharmacodynamics (Table 37.4). Ferrous sulfate (Fig.
Preparations commonly available are as follows: 37.3) is the most common preparation available and is free
Ferrous salt: e.g. ferrous sulfate, ferrous succinate, of cost available in hospitals through Government supply.
ferrous glycine sulfate, ferrous fumarate The reference iron which has been used to evaluate
Ferric salts: e.g. carboxymaltose. They are slow to be bioavailability of other oral iron preparations is ferrous
absorbed ascorbate. It has been suggested as the most favorable iron
Iron preparations in combination: Iron is combined preparation for oral iron therapy in Indians where diet has
with some compounds to enhance absorption by high amounts of iron absorption inhibitor. Moreover, due
forming chelates which keep the divalent iron available. to the presence of its ascorbate part which is a potent anti-
It is combined with succinic acid, ascorbic acid, fumaric oxidant, ferrous salts can not undergo oxidation to ferric form.
TABLE 37.4: Amount of elemental iron in different iron preparations

Amount (mg) Elemental Iron (mg)
Ferrous sulfate (7H2O) 300 60
Ferrous gluconate 300 35
Ferrous fumarate 200 65
Ferrous sulfate, anhydrous 200 65
(dried)
Ferrous sulfate, exsciccated 200 60
(1H2O)
Ferrous glycine sulfate 225 45
Ferrous succinate 100 35
Fig. 37.3: Ferrous sulfate tablet
Ferrous glycine sulfate is the only available iron prepa- sequestrants like cholestyramine. It should be taken
ration in chelated form with amino acid.This chelation preferably an hour before meal along with vitamin C or
leads to high bioavailability even in presence of dietary with fruit juice. It should never be taken with tea/coffee,
iron absorption inhibitors by inhibiting iron binding to cereal based/legume based or vegetable diet containg
these dietary inhibitors. phytates which interfere with the absorption. Along with
Sustained release preparations such as iron hydroxide this, ingestion of high protein diet and heme iron like
polysucrose complex and polymaltose complex contain meat, poultry and fish should be stressed upon.
nonionic iron in a stable form, thus has better bioavailabitity
Side Effects
and fewer side effects. The polymaltose complex are
a slow release formulation where polymaltose encase The common dose limiting GI side effects are constipation,
the iron leading to its slow release. Another form of oral heartburn and nausea observed in about one third of the
iron preparation is carbonyl iron. It comes in modified patients. These lead to non-compliance and response
release preparation where the pentavalent carbonyl iron is failure. In case of intolerable side effects, the dose needs to
be reduced or switching over to different preparation may
processed to microfine particles of less than 5 microns which
be needed. The side effects can also be reduced by taking
have better absorption and lesser side effects. But, of all
iron after meals or by prescribing newer formulations.
preparations available, ferrous sulfate and ferrous ascorbate
should be preferred while iron therapy prescription. To Goal of Treatment
increase the compliance of patient which is the most
The goal of treatment is to achieve serum ferritin of
common cause of nonresponse to therapy, the preparation
50 mgm/L, transferrin saturation of 35%. Once hemoglobin
which is available in hospital supply, i.e. the ferrous sulfate is achieved, the treatment is continued for 3–6 months to
should be given. In case of IDA, for therapeutic effect, replenish the stores. Effective iron replacement is reflected
2 tablets of ferrous sulfate per day are required. as reticulocytosis which starts as early as 3–5 days and
hemoglobin rise is 0.1–0.2 g/dL/day or 2 g/dL in 3 weeks.
Drug Interactions As per National Anemia Control Program, the dose of
Due to potential drug interactions proper advice on 100 mg of elemental iron along with 500 mgm of folic acid
how to take iron medication should be stressed upon is given per day till Hb is normal, followed by continuation
the antenatal women while prescribing iron. It should of the same dose for next 12 weeks.
not be prescribed with calcium which is an important
supplement in pregnancy. Reasons of Failure
Various common reasons for failure of oral iron therapy are
How to Prescribe Oral Iron Therapy? incorrect diagnosis, non-compliance, GI disease (Crohn’s,
Other drugs which can decrease the absorption are ulcerative colitis), malabsorption (e.g. celiac disease),
antacids, proton pump inhibitors, L-thyroxine, bile acid various infections (decrease erythropoiesis), comorbid
conditions like renal failure, or ongoing blood loss (GI- Parenteral Iron Preparations
bleed/parasitic manifestation) and drug suppressing
They are classified under 3 groups based on pharmacoki-
erythropoiesis like cytotoxic drugs. netics, complex stability, molecular mass, toxicity and side
effects
Parenteral Iron Therapy
1. Type I complexes
Indications 2. Type II complexes
The indications for parenteral iron therapy are inadequate 3. Type III complexes.
or lack of response or intolerance to oral iron, non-
compliant patient, inadequate oral iron absorption due to Type I Complexes
intestinal disease and in combination with recombinant This group has high molecular weight and thus more
human erythropoetin (rhEPO) (for prevention of functional stable. Allergic reactions are common (more with dextran
Fe deficiency). It is also indicated in females with severe (DT) formation of biological polymers), e.g. iron dextrin,
anemia after 32 weeks since, its compliance is 100%. iron dextran. Commonly used preparation is imferon.
Iron dextran: It has high molecular weight. It can be
Advantages
administered via both IM and IV routes. A small dose
The advantage of parenteral iron therapy is that it bypasses of 0.5 cc is given IM or a test dose of 0.5 mL (25 mg) in
the enteral mechanisms thus the side effects associated 50 mL normal saline can be infused over 10–15 minutes.
with oral formulations are avoided. Moreover, the compli- After one hour, if there is no sign and symptoms of any
ance is a surity so there is a certainty of administration and reaction and then, full dose is given either by deep IM route
uptake and replenishment of iron stores. However, as it through Z technique or as total dose infusion (TDI) IV
allows free iron (non-protein bound) in circulation, it over 2–4 hours (total dose diluted in 0.9% normal saline).
should be prescribed only in proven IDA as free iron can Anaphylaxis and other hypersensitivity reactions have
lead to free radical cell damage. been reported after uneventful test dose and therapeutic
doses of iron dextran injection. Thus, administration
Rate of Hb Rise of subsequent test doses should be considered during
The rate of rise of hemoglobin after iron therapy is same as therapy. Immediate resuscitation measures should be
in oral iron therapy i.e. 0.7–1.0 g/dL per week. handy in case of reaction. Adrenaline should be kept
immediately available in event of acute hypersensitivity
Caution reaction (0.5 mL of 1:1000 solution). Due to this
It should only be given in patients with proven iron disadvantage, iron dextran has been replaced almost
deficiency to prevent free radical damage. completely by iron sucrose in current clinical practice.
It has 60–70% bioavailability. Thirty percent of the dose
Calculation of Iron Requirement administered gets blocked in muscles. The disadvantages
This is an important step while prescribing parenteral iron and side effects include repeated painful injections, skin
therapy so as to decrease the side effects and risks of iron discoloration, lymphadenopathy, headache, nausea,
overload. Elemental iron dose in mg is calculated by any abscess formation and joint pain. The incidence of side
one of the following formulae: effects is greater with TDI.
It is available as 50 mg/mL of elemental iron in 2 mL
Total iron requirement (mg) = Body weight (kg) × Hb
ampoules. It takes about 200 mg of elemental iron to raise
deficit (normal Hb-patient’s actual Hb in g%) × 2.21
the hemoglobin by 1 g%.
+ 1000 mg, normal Hb = 14 g/dL, 2.21 = standard
coefficient, 1000 mg is added for the iron stores Type II Complexes
Total iron requirement (mg) = Body weight (lbs) × Hb
This group preparation has medium stability. The max-
deficit (Normal Hb-patient’s actual Hb in g%) × 0.3 imum plasma concentration is reached within 10 minutes
In this formula, 0.3 is the standard coefficient and 50% after bolus adminstration. They are extremely safe for rou-
is added to the calculated dose for the stores tine use as there is no biological polymer formation. Thus,
Total iron requirement (mg) = 250 × Hb deficit minimal chance of anaphylaxis. The general side effects
Accordingly the dose can be calculated and again 50% are metallic taste, nausea, local irritation and dizziness,
of the calculated dose is added for the stores. e.g. iron hydroxide-sucrose complex.
Iron hydroxide-sucrose complex: This is the most common of 50–150 m/kg subcutaneously (SC) twice or thrice a week.
type of parenteral iron in current clinical practice for anemic However, some recent studies have shown that even 150–
antenatal women. The test dose is not required which 300 m/kg single IV dose may suffice. Its advantages are:
makes it superior to other iron preparations where allergic It can be used in nonresponding cases to parenteral iron
reactions may be there. Iron sucrose is given undiluted as Used in treatment of moderate to severe IDA as an
a bolus (over 5–10 minutes) or diluted in 100 mL normal alternative to blood transfusion
saline as short infusion (over 20 minutes). The maximum Leads to rapid anemia correction in severe anemia
dose that can be given in single sitting is 200 mg. Maximum within 2 weeks
of three such doses can be administered in a week (i.e. 600 Used in conditions where patient is on drug suppressing
mg/week) to reach target Hb-11 g%. Oral iron needs to erythropoiesis (cytotoxic drug).
be stopped before IV iron therapy to prevent receptor site
saturation. Place of Blood Transfusion
Indicated in severe anemia near term or in labor
Type III Complexes Partial exchange transfusion has a great role in the
They are unstable, labile forms with low molecular weight. prevention of pulmonary edema in patients with severe
The stability is less than sucrose and dextrans. The protein anemia with cardiac failure as it does not cause overload.
binding is less so free iron is released in short term. It is practised in Safdarjung hospital
Moreover, they have less side effects like iron sucrose. Severe anemia first seen after 36 weeks of pregnancy
Other, e.g. iron gluconate, iron ammonium citrate, iron Anemia due to blood loss or PPH
hydroxide sorbitol complex. It has low molecular weight. Associated infection.
It is given by only IM route. Being a small molecule, it gets Packed cells are preferred for transfusion to prevent
rapidly absorbed. Sixty percent of the drug is absorbed volume overload. Blood transfusion should be managed
within 3 hours from site of injection. Complete absorption with extreme care as transfusion reactions, preterm labor
occurs over next 10 days in contrast to 3–4 weeks taken by and overloading of heart could be precipitated. To prevent
iron dextran. Because of its small molecule, it combines with overload of heart partial exchange has great success.
transferrin causing more toxicity so, not given by IV route.
Test dose of 0.5 mL (25 mg) is given at the site where Partial Exchange Transfusion (Figs 37.4A to C)
full dose is to be given. After one hour, in absence of any A study was carried out in the Department of Obstetrics
adverse reaction complete dose is injected. The injection and Gynecology, VMM College and Safdarjung Hospital.
is deep IM with 20–22 gauge needle using Z technique, i.e. Analysis was carried out for changes in the outcome
pulling the skin laterally while inserting the needle so as to parameter. The following conclusions were drawn:
avoid staining. The site should not be rubbed. It is available Partial exchange blood transfusion produces significant
as 50 mg/mL of elemental iron in 2 mL ampoules. improvement in all the 5 parameters namely:
Dosage: For IM iron 100 mg/day till total dose; maximum 1. Hemoglobin
dose 200 mg/day can be given. For IV—1000 mg can be 2. Packed cell volume (PCV)
given in one sitting as total infusion drip. 3. Pulse rate
Diagnosis of IDA should be confirmed before parental 4. Respiratory rate
therapy 5. Pulse pressure in the patients within the test group.
Z-shaped deep IM injection given to avoid skin staining Better improvement in the vitals as compared to whole
Oral therapy to be suspended 48 hours before parenteral blood transfusion without exchange with absence of
therapy to avoid toxicity cardiac decompensation.
Emergency measures to be kept ready before test dose
is given. Management of Labor in Patients with Anemia

Adequate sedation and pain relief should be provided.
Role of Erythryopoetin Propped up position should be used in severe anemia
The EPO is similar to human erythropoetin. It is a selective Intermittent oxygen therapy should be available
growth factor for erythroid series. Traditionally it has been Beta-mimetics and steroids should be used with
used for treatment of anemia due to renal disease. Its use extreme caution to arrest preterm labor due to the risk
has been extended in obstetrics, where it is given in dose of pulmonary edema
A B
Figs 37.4A to C: A. Withdrawal of blood; B. Trans-

fusion of packed cells (two pints); C. Transfusion of
C RBCs of self
Vaginal delivery should be aimed at Iron and folate supplementation to be continued for at
Antibiotic prophylaxis should be provided least 3 months
Strict asepsis should be maintained Encourage and initiate effective contraception
Forceps and ventouse should be used to cut short the Maternal mortality in severe anemia is most likely to
second stage occur at the following periods:
Active management of the third stage of labor (AMTSL) • At term pregnancy
Vigorous management of PPH is mandatory. • During labor
• Immediately after delivery
Puerperium • During puerperium.
Adequate rest
Treatment of septic foci, if any MEGALOBLASTIC ANEMIA
Watch for signs of puerperal sepsis, failing lactation, This is a disorder caused by impaired deoxyribonucleic
sub involution, thromboembolism acid (DNA) synthesis affecting hematopoietic precursors
and GI epithelial cells. Megaloblastic cells, with increased On examination, varying degrees of pallor with glossitis,
ribonucleic acid (RNA) to DNA ratio, are formed as a hemorrhagic patches under the skin and conjunctiva,
result of the slow cell division which cannot pace with the hepatosplenomegaly, polyneuropathy.
ongoing normal cytoplasmic development. Megaloblastic
erythroid precursors get destroyed in the bone marrow Effect on Pregnancy
leading to ineffective erythropoiesis. Most cases of Anemia during pregnancy has shown increased incidence
megaloblastic anemia are due to the deficiency of folic of abortion, fetal growth restriction, abruptio placentae,
acid and/or cyanocobalamin (Vitamin B12).
pre-eclampsia, etc.
Folic Acid Deficiency Effect on Fetus

To meet the demands of the growing fetus, placenta,
Neural tube defects can be prevented in most cases by
uterine enlargement and expanded maternal red cell
periconceptional folic acid in dose of 400 mg/day in low-
volume, folate requirements are increased during the
risk cases and 5 mg/day in high-risk women. There is an
pregnancy. In developing countries, folate deficiency
increased incidence of abortion, premature babies, small
may complicate upto 30% of all pregnancies, being more
for date babies and neonatal folate deficiency.
prevalent multiple pregnancies.
Etiology Investigations
Hemoglobin below 10 g/dL
Dietary lack—food deficient in green vegetables, fruits,
Macrocytosis refers to MCV more than 100 fl. Macro
liver, kidney with prolonged cooking of food
cytosis is masked by concurrent iron deficiency or
Goat’s milk anemia
thalassemia. MCH is more than 33 pg and MCHC is
Hyperemesis gravidarum
normal. Macrocytosis is also seen in patients with liver
Malabsorption syndromes—tropical sprue, celiac
disorders, alcoholism, hemolysis, hypothyroidism and
disease
Drugs—anticonvulsant therapy, pyrimethamine, trime aplastic anemia
thoprim Reticulocyte count, leukocyte and platelet count are low
Excess utilization: Peripheral smear (Fig. 37.5) anisocytosis, poikilocytosis
• Physiological—pregnancy and lactation
with macroovalocytes, basophilic stippling, hyperseg-
• Pathological—hemolytic anemias, malignancies
mented neutrophils (nucleus > 6 lobes)
Inflammatory conditions like Crohn’s disease, Serum folate < 3 mg/mL and red cell folate < 150 mg/mL
tuberculosis, rheumatoid arthritis, psoriasis, exfoliative is diagnostic of folate deficiency. Red cell folate does
dermatitis not change due to short-term fluctuations. Thus, it is a
Hemorrhagic states like peptic ulcer, hookworm infesta better indicator
tion, hemorrhoids and hemolytic states such as chronic Deoxyuridine supression test distinguishes folate from
malaria, sickle cell anemia and thalassemia lead to vitamin B12 deficiency
increased erythropoiesis
Excess urine folate loss, active liver disease, congestive
heart failure
Iron deficiency anemia—it not only conceals morpho-
logical evidence of megaloblastic anemia, but treatment
with iron would lead to a hyperplastic marrow which in-
creases the need for folic acid and thus, precipitates its
deficiency producing ineffective erythropoiesis.
Clinical Features
Insidious onset
Vomiting, diarrhea, constitutional symptoms like unex-
plained fever Fig. 37.5: Peripheral smear showing macrocytic anemia
Hypercellular bone marrow with increased myeloid/ Clinical Features

erythroid ratio and abundant stainable iron is there. Hematologic manifestations are a result of anemia and
Nuclear cytoplasmic asynchrony is present sometimes purpura results due to thrombocytopenia.
Serum iron is normal or high GI manifestations include sore tongue, anorexia, diarrhea.
Increased formiminoglutamic acid in urine following Neurological manifestations begin with demyelination
a loading dose of histidine is found in folate deficiency followed by axonal degeneration and finally neuronal
Serum lactate dehydrogenase (LDH) and homocysteine death. There can be numbness, paraesthesia, weakness,
levels are elevated in folate deficiency. ataxia, etc.
Prophylaxis Investigations
Routine prophylaxis is recommended by WHO as folic acid Findings are the same as in folate deficiency. The normal
400 mgm/day. Pregnant women should eat more green range of serum vitamin B12 is 200–900 pg/mL. In clinically
leafy vegetables (spinach, brocolli) and excessive cooking significant deficiency, value can go down to less than 100
should be avoided. pg/mL.
Shilling’s test delineates the pathogenesis of cobalamin
Treatment
deficiency. In first step, the radioactive cobalamin is
5 mg/day of folate is recommended to be continued for administered orally, followed shortly by an IM injection of
at least 4 weeks in puerperium. A response is indicated unlabelled cobalamin. Urine over next 24 hours is analyzed
by a fall in LDH levels within 3–4 days and increase in to measure the proportion of radioactive cobalamine. In
reticulocyte count in 5–8 days. In case of gastric intolerance, the second step, the patient is given labelled cobalamin
malabsorption syndromes or late in pregnancy, parenteral bound to intrinsic factor which will be absorbed normally
folate is indicated. Associated iron deficiency should be if the patient has pernicious anemia.
corrected. Serum methylmalonic acid and homocysteine levels
are raised and thus useful in diagnosis of B12 deficiency.
Cyanocobalamin Deficiency (Vitamin B12)
Homocysteine levels are also elevated in folate deficiency.
Vitamin B12 is a complex organometallic compound in
which a cobalt atom is situated within a corrin ring. As Treatment
it cannot be synthesized in the human body, it needs Specific therapy for underlying disorders
supplementation through the diet. The source of vitamin Replacement therapy—since the defect is mainly always
B12 are meat, fish, eggs and dairy foods. The daily diet malabsorption, parenteral treatment in the form of IM
contains average 5–30 mgm of vitamin B12 of which cyanocobalamin is recommended.
1–5 mg is absorbed. Daily requirement of vitamin B12 is only IM injection of Vitamin B12 (Fig. 37.6) or cyanocobalamin
3 mgm which is easily met with a normal diet. Only strict in the dose of 1000 mg per weeks, 8 weeks is administered
vegetarians need supplementation during pregnancy. followed by 100 mg IM every month for the rest of the life.
Folate alone cannot correct megaloblastic anemia of
Etiology
cobalamin deficiency and does not alter the neurological
Inadequate diet abnormalities. The folate therapy alone can even aggravate
• Strict vegetarians the neurological manifestations.
Malabsorption
• Defective release of cobalamin from food (gastric
achlorhydria, partial gastrectomy)
DIMORPHIC ANEMIA
• Inadequate production of intrinsic factor It is the most common type of anemia encountered in
• Pernicious anemia, total gastrectomy tropical countries where deficiency of both iron and folate
• Disorder of terminal ileum is present with findings of both anemias, but dominance of
• Regional enteritis, non-tropical and tropical sprue, one. The blood film may show macrocytic or normocytic
intestinal reaction or hypochromic pictures. The bone marrow is usually
• Fish tapeworm disease (Diphyllobothrium latum) megaloblastic. The treatment is prescription of both folate
• Blind loop syndrome. and iron in therapeutic doses.
Fig. 37.7: Peripheral smear showing hemolytic picture showing

early forms of RBCs (red arrow) and schistocytes (broken RBCs);
(black arrows)
Pregnancy Induced Hemolytic Anemia

It is a rare entity, develops early in pregnancy and resolves
within months after delivery. It responds to treatment with
glucocorticoids.
Fig. 37.6: Multidose vial of injection cyanocobalamin
Paroxysmal Nocturnal Hemoglobinuria
It is a serious and unpredictable disease and associated
ANEMIA FROM ACUTE BLOOD LOSS pregnancy may be dangerous. Postpartum, half the
Antepartum hemorrhage (APH) due to abruptio placentae women develop deep venous thrombosis (DVT) including
and placenta previa can lead to serious blood loss. Budd-Chiari syndrome or cerebral vein thrombosis (CVT).
Acute blood loss due to abortion, ectopic pregnancy Successful outcomes are possible with close supervision.
and hydatidiform mole can lead to anemia in early
trimester. A massive hemorrhage demands immediate
Other Acquired Anemias
treatment by blood transfusion to restore and maintain Overt fragmentation (microangiopathic) hemolysis with
perfusion of vital organs. Residual anemia would need visible hemoglobinemia infrequently complicates pre-
iron replacement. If hemoglobin is more than 7 g/dL in eclampsia/eclampsia and is called HELLP syndrome
a patient whose condition is stable with no risk of further (hemolysis elevated liver enzymes and low platelet count).
serious hemorrhage and ambulation is possible without The most fulminant acquired hemolytic anemia
adverse symptoms, iron therapy for at least 3 months encountered during pregnancy is caused by the exotoxin
rather than blood transfusion is the best treatment. of Clostridium perfringens and may prove fatal.
Gram-negative bacterial endotoxin or lipopoly sac
HEMOLYTIC ANEMIAS charide, especially with severe acute pyelonephritis
during pregnancy may be accompanied by evidence of
Acquired Hemolytic Anemia hemolysis and mild to moderate anemia.
Autoimmune: This is caused by either warm active
autoantibodies (80–90%), or cold autoantibodies or a Hemoglobinopathies
combination. It could be classified as primary or idiopathic Structural abnormalities in globin chain synthesis
or secondary autoimmune (lymphomas, leukemias, Reduced globin chain synthesis.
connective tissues disorders, some infections, chronic
inflammatory disease or drug induced).
Sickle Cell Anemia
Both direct and indirect antiglobin (Coombs) tests are Hemoglobin S results from a single substitution of glutamic
positive. Spherocytosis and reticulocytosis are charact- acid by valine in the beta-chain because of an A for T
eristically seen on the peripheral blood smear (Fig. 37.7). substitution of the beta globin gene at the chromosome 6.
There may be a marked acceleration of the hemolytic Sickle cell anemia (SS disease), sickle cell hemoglobin
process during pregnancy for which glucocorticoids are disease (SC disease) and sickle cell beta-thalassemia
effective. Cold agglutinin disease may be induced by disease (S-beta α-thalassemia) are the most common of
Mycoplasma pneumoniae or infectious mononucleosis. sickle hemoglobinopathies.
Fig. 37.8: Positve for sickle cell by sodium metabisulphite method, Fig. 37.9: Sickle cells (arrow) in peripheral smear (Leishman stain
wet mount x 100 x 100)
Courtesy: Bhilai Steel Plant Hospital
The hallmark is the period of sickling episodes during

which there is ischemia and infarction within various
organs which produces pain (sickle crisis). This is due
to sickle shaped cells (Figs 37.8 and 37.9) blocking
microcirculation due to their rigid structure. This sickling
(HbS in deoxygenated state) is precipitated by infection,
acidosis, dehydration and hypoxia.
Sickle Cell Trait

Sickle cell trait is the result of inheritance of gene coding for
hemoglobin S from one parent and that for hemoglobin A
from other. The amount of HbS (38–45%) is less than HbA.
It does not influence unfavorably the incidence of
abortion, perinatal mortality, low birth weight and
pregnancy induced hypertension. Urinary infection and
asymptomatic bacteriuria occurs twice as common in sickle
cell trait and so is asymptomatic bacteriuria. It should not Fig. 37.10: Solubility test for sickle cell screen
be considered as a deterrent to pregnancy on the basis of Courtesy: Bhilai Steel Plant Hospital
increased risk to the mother. The probability of serious sickle
cell hemoglobinopathy in her offspring is 1 in 4 wherever
the father carries a gene for an abnormal hemoglobin. surveillance is recommended at 32–34 weeks along
with serial ultrasonography to monitor fetal growth and
Sickle Cell Disease amniotic fluid volume (AFV).
It is genetically inherited and transmitted equally by males The acute painful sickling crisis during pregnancy should
and females. The diagnosis is by refractory hypochromic be differentiated from acute conditions like acute ectopic,
anemia, high fasting serum iron levels, identification by abruptio placentae, acute pyelonephritis, acute appendicitis,
sickling test (Fig. 37.10) and identification of the type of acute cholecystitis and other serious obstetrical or medical
hemoglobin by electrophoresis. problems causing pain, anemia or both.
In the absence of infection or nutritional deficiency, the
Effect on Pregnancy and Fetus hemoglobin concentration does not fall below 7 g/dL. Folate
Increased incidence of abortion, fetal growth restriction supplementation is required. There is increased incidence
and prematurity have been seen. Routine antepartum of bacteriuria and pyelonephritis which can further
precipitate red cell destruction. Cardiac dysfunction is seen

THALASSEMIA SYNDROMES
in most of the women. Pre-eclampsia is also increased.
They are inherited hemoglobinopathies due to disorder in
Effect of Disease biosynthesis of alpha and beta globin chain of hemoglobin.
Sickling may occur acutely specially late in late third The reduced supply of globin thus decreases hemoglobin
trimester, intrapartum and in early postpartum period. tetramers leading to microcytic hypochromic anemia.
There is an disproportionate accumulation of alpha and
Management beta subunits as the synthesis of unaffected globin goes on
Preconceptional Counseling at a normal rate.
Prenatal identification of homozygous state of the disorder
Alpha-thalassemia Syndromes
is an indication for early termination. In utero stem cell
therapy (with normal hemoglobin A stem cells) may be These syndromes are found in South East Asia and China,
done. and people of African descent. Alpha-thalassemia minor is
found in 2%, HbH is rare, HbBarts is unreported.
Pregnancy Alpha-thalassemia—2 Trait—one of the four globin loci
Antenatal surveillance with fetal monitoring affected

Alpha-thalassemia—1 Trait—two loci are deleted
Folate supplementation
Hemoglobin should be kept above 25% (Prophylactic [Resembles beta thalassemia minor) (—/α) or - α / - α)
HbH disease—3 loci are deleted (—/-α)
red cell transfusions) and concentration of HbS should
HbBarts—all 4 loci are deleted (—/—).
be kept under 60%. The blood used is negative for Kell,
Duffy, Kidd antigens, washed and buffy coat poor Offspring doubly heterozygous for alpha-thalassemia-2
Iron supplementation is provided only in proven cases and alpha-thalassemia-1 show a more severe phenotype
of iron deficiency. called HbH disease. HbA production is only 25–30% of
normal. Unpaired beta chains accumulate and are soluble
Labor enough to form beta-4 tetramers called HbH. The patients
Labor should be managed the same way as for cardiac have moderately severe hemolytic anemia. The neonate
disease is well at birth, but develops hemolytic anemia in early
Over sedation should be avoided infancy. Survival into mid adult life without multiple
Epidural analgesia is suited for labor and delivery. Some transfusions is common (5–30% of hemoglobin is H).
recommend elective cesarean section at 36 weeks after Disease severity may be similar to beta-thalassemia major.
partial exchange transfusion Anemia is worsened during pregnancy.
Avoidance of dehydration and acidosis
Compatible blood should be kept available
HbBarts (Gamma 4)
Circulatory over load is to be avoided. In this condition physiologically active hemoglobin fails
to develop beyond the embryonic stage. Tetramers called
Contraception HbBarts are formed due to excessive deletion of globin
Barrier method is recommended as oral contraception forms. The fetus has tissue hypoxia, hydrops fetalis,
would predispose to thromboembolism. Sterilization is congestive heart failure and even intrauterine death. It is
advocated at a young age in parous women due to short a common cause of stillbirths in South East Asia. It may
life span. Intrauterine contraceptive device (IUCD) is cause severe pre-eclampsia in the mother. A large fetus and
contraindicated due to the risk of infection. very bulky placenta may cause difficult vaginal delivery.
Experimental Therapy Alpha-thalassemia Minor

Introduction of HbF by stimulating gamma chain Alpha-thalassemia minor is due to deletion of two genes.
synthesis appears to be a promising form of treatment Mild to moderate hypochromic microcytic anemia charac-
for sickling and some thalassemia syndromes as they terizes this clinical condition. It goes unrecognized because
inhibit polymerization of hemoglobin S. Hydroxy urea, there is no associated clinical abnormality. Hemoglobin
azacytidine as well as recombinant erythropoietin increase Barts is present at birth, but as it dissipates, it is not replaced
fetal hemoglobin and decrease sickling. by HbH. These women tolerate pregnancy quite well.
Beta-thalassemia there is no thalassemia. If it is hazy, it signifies thalassemia.

The sensitivity is 94.4% and a negative predictive value
This is the result of impaired beta globin chains’ production
of 97.6%. It costs about ` 10 per test. It is used in mass
and the molecular pathology for the defective production
screening as in an antenatal clinic. Patients positive for
involves nearly 100 point mutations in the beta-globin
this test are subjected to electrophoresis.
gene. The transcription and translation of beta globin RNA
is affected by deletional and non-deletional mutations. The pregnant woman testing positive for the
The delta-gamma-beta gene cluster is on chromosome thalassemia trait needs her partner to be tested for the
eleven. Hypochromasia along with microcytosis due to same. If he is also positive, there is a need of prenatal
decreased amounts of hemoglobin tetramers is present in diagnosis as there is a 25% chance of homozygous state in
all β-thalassemia forms. the fetus. If both parents are positive, do confirmatory test
followed by genetic testing of the fetus by chorionic villous
Beta-thalassemia Minor biopsy or amniocentesis before 18 weeks of pregnancy.
The termination of pregnancy is advised, if the fetus is
There is severe hypochromasia and microcytosis along with
homozygous.
target cells but only minimal or mild anemia on complete
The most common methods for screening and diag-
blood count (CBC) and periphral smear examination.
nosis are:
MSV is seldom > 75 fl
CBC and peripheral smear: It shows a low level of
Hematocrit rarely < 30–33%
hemoglobin and reduced MCV. The smear shows
Elevated HbA (3.5–7.5%)
microcytic, hypochromic and anisopoikilocytosis. In
Serum iron and TIBC are normal.
addition, target cells and basophilic stippling can be
The hemoglobin concentration is typically 8–10 g/dL seen in beta–thalassemia
late in the second trimester. For beta-thalassemia minor Nestroft: This test has been used as a screening method
during pregnancy, there is no specific treatment and the Hemoglobin electrophoresis or Hb high performance
fetomaternal outcomes are satisfactory. Blood transfusions liquid chromatography (HPLC): It helps in confirmation
are seldom indicated except for hemorrhage. Prophylactic and assessment of severity of the condition. Manual
iron and folate are adminstered in daily doses of 60 mg and 1 HPLC has been replaced by automated HPLC nowadays
mg respectively. Parenteral iron therapy is contraindicated.
and can give result in as less as in 12 minutes. HbA2 is
elevated to > 3.5% in beta-thalassemia trait. However,
Thalassemia Major
alpha-thalassemia cannot be diagnozed by Hb electro
There is decreased production of beta chains and excess phoresis or HPLC.
alpha chains precipitate to cause cell membrane damage. Molecular genetic testing—however, alpha-thalassemia
There is failure to thrive in the infant with the fall of HbF cannot be diagnozed by Hb electrophoresis or HPLC.
level leading to severe anemia. Multiple transfusion It requires molecular genetic testing for detection of
programs make the child survive till the first decade. alpha globin gene deletion.
Females who survive beyond childhood are usually sterile Prenatal diagnosis is done by amniocentesis, chorionic
and the life expectancy is short. Pregnancy is rare. villus sampling (CVS) or cordocentesis. Ultrasonography
can be an auxillary aid in diagnosis of alpha-thalassemia
NESTROFT (NAKED EYE SINGLE TUBE severe forms, but not helpful for beta-thalassemia
RED CELL OSMOTIC FRAGILITY TEST) cases. Hydrops fetalis, cardiomegaly, placentomegaly
and forward flow velocities in ductus venosus (DV) and
Disproportionately higher RBC count for a given hemoglo- middle cerebral artery (MCA) can be seen.
bin concentration indicates beta-thalassemia trait. Mean
corpuscular hemoglobin < 80 in pregnancy, and MCH < 25
PREVENTION
rules out beta thalassemia.
NESTROFT is the test used for screening of patients for Thalassemia syndrome of fetus can be easily detected
thalassemia (in hospitals) based on the fact that red cells prenatally. Fetal DNA can be retrieved by amniocentesis,
with large surface area and volume ratio resist lysis in CVS or cordocentesis. It is amplified by polymerase chain
hypotonic saline indicating lower red cell osmotic fragility, reaction (PCR) followed by hybridization to allele specific
suggesting thalassemia trait. If the tube contents are clear, oligonucleotide probes to reach the diagnosis.
1. ____________ is the result of inheritance of gene coding for hemoglobin S from one parent and that for hemoglobin A from
other.
2. ____________ is a disorder caused by impaired DNA synthesis affecting hematopoietic precursors and gastrointestinal epithelial
cells.
3. Two forms of iron are present in our diet where heme iron is absorbed more readily and non-heme iron is insoluble ferric form.
State True or False.
4. Tallquist and Sahli’s method is used for hemoglobin measurement and have less accurate results. State True or False.
38 Pregnancy and Heart Disease
Dheeraj Deo Bhatt, Sudha Salhan, Manjula Sharma
The incidence of heart disease in pregnancy in the Western vascular resistance, and cardiac output return to their
population ranges from 0.2–4%. There congenital heart pre-pregnancy levels over the course of 4–12 weeks.
disease predominates, but in India, rheumatic heart All these changes in maternal hemodynamics are well
disease comprises the majority of cardiovascular diseases tolerated by a normal pregnant woman, but can cause
during pregnancy. decompensation in a diseased cardiovascular system.
Hemodynamic alterations in pregnancy and labor
put stress on the maternal cardiovascular system. Often PRE-CONCEPTION COUNSELING
the diagnosis of heart disease is made for the first time Ideally a woman of childbearing age who has a heart
during pregnancy. Many of the symptoms associated with disease should discuss with the cardiologist and obste
cardiovascular diseases like fatigue, palpitation, swelling trician about the effect of pregnancy on her heart disease.
of legs may also be present in a normal pregnancy. A high The discussion should include possible risks for the mother
index of suspicion is therefore required to diagnose heart and the fetus in continuing the pregnancy, need for any
disease in pregnancy. intervention before conception or during pregnancy,
It is important to understand the physiological changes contraception and genetic counseling when appropriate.
during normal pregnancy, to understand how pregnancy
affects a patient with cardiovascular disease. Risk Assessment and Stratification
Some of the physiological changes seen during a normal In one multicenter study of 562 consecutive pregnant
pregnancy are as follows: patients with heart disease, 13% pregnancies were
Blood volume and cardiac output increase in the first complicated by primary cardiac events, with 55% occurring
two trimesters. Blood volume reaches a plateau of in the pre-partum period. Prior cardiac events or
140–150% of the pre-pregnancy level around 32 weeks arrhythmia, poor functional class or cyanosis, left heart
and cardiac output increases till 25 weeks’ of gestation obstruction, and left ventricular systolic dysfunction
There is a fall in systemic vascular resistance. This leads independently predicted maternal cardiac complications.
to a fall in blood pressure. There is a larger proportional These predictors of risk were incorporated in a revised risk
fall in the diastolic pressure and hence an increase in score with 1 point assigned to each factor. The estimated
pulse pressure risk of a cardiac event in pregnancies with 0, 1, and >1
During labor, each uterine contraction results in points found were 5%, 27%, and 75% respectively.
redistribution of about 500 mL of blood to the central The European Society of Cardiology recommends
circulation from the uterus. that maternal risk assessment be done according to the
Immediately after delivery, approximately 500 mL of modified World Health Organization (WHO) classification.
blood from the uterus and placenta is returned to the Table 38.1 describes the principles of classification of risk.
maternal circulation (like autotransfusion). Along, with Table 38.2 show the practical application of the WHO
release of pressure on inferior vena cava (IVC). Thus, risk stratification according to the individual lesions.
leading to 10–20% increase in cardiac output. The prospective mother should be told about the risk of
In postpartum period, extra vascular fluid is mobilized transmission of the maternal heart disease to the fetus if any.
and diuresis occurs. The blood volume, peripheral Risk of heart disease in a newborn in general population is
Pregnancy and Heart Disease 379
TABLE 38.1: Modified WHO classification of maternal cardiovascular risk principles

Risk class Risk of pregnancy by medical condition
I No detectable increased risk of maternal mortality and no/mild increase in morbidity
II Small increased risk of maternal mortality or moderate increase in morbidity
III Significantly increased risk of maternal mortality or severe morbidity. Expert counseling is required. If pregnancy is decided
upon, intensive specialist cardiac and obstetric monitoring needed throughout pregnancy, childbirth, and the puerperium
IV Extremely high risk of maternal mortality or severe morbidity; pregnancy contraindicated. If pregnancy occurs, termination
should be discussed. If pregnancy continues, care as for class III
TABLE 38.2: Modified WHO classification of maternal 0.4–0.6%. This risk increases when a pregnant mother has
cardiovascular risk application heart disease. Generally women with congenital heart
WHO risk I disease give birth to congenital heart disease (CHD)
Uncomplicated, small or mild suffering offspring approximately 5–6%, whereas 2–3% in
Pulmonary stenosis case of men suffering from the same. If the maternal disease
Ventricular septal defect is autosomal dominant, it has 50% risk of transmission to
Patent ductus arteriosus the fetus. Genetic counseling, should be offered to patients
Mitral valve prolapse with no more than trivial mitral regurgitation
having syndromic disease or other relatives having heart
Successfully repaired simple lesions, e.g.
disease. All pregnant females, with heart disease should
Ostium secundum atrial septal defect
also undergo fetal echocardiography to assess the fetus for
Ventricular septal defect
Patent ductus arteriosus

heart disease.
Total anomalous pulmonary venous drainage
Isolated ventricular extra systoles and atrial ectopic beats MANAGEMENT OF HEART DISEASE
WHO II; if otherwise well and uncomplicated Management of heart disease during pregnancy is a complex
Unoperated atrial or ventricular septal defect and evolving specialty requiring multi-disciplinary specialist
Repaired tetralogy of Fallot care. Co-ordination between the obstetrician and other
Most arrhythmias
specialists (cardiologist, cardiac surgeons, neonatologist and
WHO II and III; depending on individual
anesthesiologist) is of utmost importance in the management
Mild left ventricular impairment
of these patients.
Hypertrophic cardiomyopathy
Native or tissue valvular heart disease not considered in WHO I or IV Antenatal Care at First Visit
Marfan syndrome without aortic dilatation
Aorta <45 mm in aortic disease associated with bicuspid aortic valve Taking a proper history is very important. Breathlessness is
Repaired coarctation the most frequent symptom. Ask if she had this symptom
WHO III before pregnancy. History of palpitation is important.
Mechanical valve History of syncope is present in severe aortic stenosis,
Systemic right ventricle hypertrophic cardiomyopathy, Fallot’s tetralogy and
Fontan circulation Eisenmenger syndrome, though it may be seen in a normal
Cyanotic heart disease (CHD) (unrepaired) and other complex pregnancy. Chest pain may be seen in a case of hypertrophic
CHD cardiomyopathy and severe aortic stenosis.
Aortic dilatation 40–45 mm in Marfan syndrome
Aortic dilatation 45–50 mm in aortic disease associated with Physical Examination
bicuspid aortic valve
Any other murmur, besides a haemic murmur due to
WHO IV
anemia and hyperdynamic circulation of pregnancy must
Pulmonary arterial hypertension of any cause
be investigated. Look for cyanosis and clubbing of fingers.
Severe systemic ventricular dysfunction
Pulse deficit is an important sign. In endocarditis splinter
NYHA III–IV or LVEF 30%
Previous peripartum cardiomyopathy with any residual hemorrhages are seen.
impairment of left ventricular function
Severe left heart obstruction
Special Investigation
Marfan syndrome with aorta dilated 40 mm Chest radiography is done after shielding the abdomen.
Abbreviations: LVEF—Left ventricular ejection fraction; NYHA—New Cardiomegaly and increased pulmonary vascular
York Heart Association markings are seen.
Electrocardiography is more helpful to diagnose MANAGEMENT IN LABOR

dysrhythmias. A team comprising an obstetrician, a
cardiologist and if possible a geneticist (in inheritable The delivery should be carried out at tertiary centers with a
heart diseases) and a cardiac dietician is ideal. multidisciplinary team for monitoring and management
Avoidance of risk factors for heart failure is very of high risk pregnancy.
important (UTI, hypertension, obesity, anemia, etc.). A team comprising of an obstetrician, an anaesthetist a
paediatrician and a cardiologist is ideal.
At Subsequent Visits
At each ANC visit, the patient has to be reclassified Induction of Labor
(WHO classes). As such there is no place of induction of labor in such patients
The patient is asked to avoid excess work, avoid stress but it can be done by PGE2 in some patients, (because usually
and have a home help. patients go in spontaneous premature labor). Caesarean
Avoid infections such as influenza and avoid-contact section is solely done for absolute obstetric causes, e.g.
with persons having respiratory infections. Pneumococ- cephalopelvic disproportion (CPD), contracted pelvis, etc.
cal and influenza subunit vaccines are recommended. Labor should be conducted in the left lateral position.
Dental hygiene has to be looked into at each ANC visit. IV fluids should be restricted to 75 mL/hour. If possible,
Frequent urine cultures, to rule out UTI should be done. use central catheterisation (Swan-Ganz technique) to
Benzathine penicillin prophylaxis (1.2 mega units I/M) measure right arterial pressure, wedge pressure and
three weekly should be given to patients of rheumatic cardiac output. A woman entering labor with 14 mmHg
heart disease (RHD). In case the patient is sensitive to wedge pressure will not develop pulmonary edema.
penicillin she can be put on erythromycin daily (250 Intranasal oxygen should be given at a rate of 5-6 L/min.
mgs BD). Pain relief is a to be provided with epidural anesthesia
Early detection and correction of anemia is necessary (contraindicated in Eisenmenger’s syndrome and hyper
in these patients. tensive cardiomyopathy) for these patients. Pudendal
block and parenteral pethidine may be needed.
Follow-up Visits If on anticoagulant, get APTT before inserting an
With class 1 or 2 see every 2-4 weeks till 24 weeks and then epidural catheter.
every 1–2 weeks. Class 3 patients should be seen every 1–2 CVP line is needed in case of class 3 and 4 patients.
weeks. Patients with class 4 are hospitalised as soon as Bacterial endocarditis prophylaxis is a must.
they are diagnosed. Class 3 and 4 need foetal testing. Frequent monitoring of vitals to detect any untoward
At each ANC visit pulse, BP, respiratory rate, weight gain, complication and watching for signs and symptoms of
status of jugular venous pressure (JVP), auscultation cardiac failure throughout labor, which are as follows:
of lung bases and signs of failure if present, are noted. • Pulse > 110/min
Pulse rate greater than 100 per minute or rapid weight • Breathlessness
gain may point to impending heart failure and needs • Raised JVP
immediate admission in the hospital. Urine culture is • Basal crepitations
done at each visit. • Edema of feet
The patients have to be counselled to avoid alcohol and • Cyanosis.
stop cigarette smoking, and illicit drug intake. Anticoagulants are stopped at the time of delivery
Salt restriction is advised. Long induction time should be avoided. Delivery may
At 24 weeks a foetal echo is recommended. be assisted by low forceps or vacuum. Vaginal delivery
In case of class 1 and 2, the patient should be admitted is the preferred mode and cesarean delivery is generally
at about 37 weeks unless there are signs and symptoms indicated for obstetric reasons only. However, cesarean
of cardiac failure. delivery should be considered in the following situations:
In case of class 3 and 4, the patient should be admitted Patient with preterm labor who is on oral anticoagulant
as soon as a diagnosis is made and should remain in the Marfan syndrome with aortic diameter > 40–45 mm
hospital till delivery. Acute or chronic aortic dissection
If the patient is on digitalis then frequent serum electro Patient in intractable heart failure.
lyte study is required. It can also be considered in patients with severe aortic
Echocardiography is to be done to rule out endocarditis. stenosis and severe pulmonary hypertension.
Fluid restriction and judicious use of diuretics can tide

LABOR AND DELIVERY
over the crisis in less critical lesions. Heart rate controlling
Valvular Heart Disease agents, are beneficial by prolonging the diastolic filling.
These lesions fall in modified WHO risk class II or III Metoprolol is the preferred beta-blocker in pregnancy as it
depending on the presence of symptoms, left ventricular causes less intrauterine growth restriction in the fetus. Non
dysfunction or prosthetic valves. In the developing count invasive ventilation may be tried in those who continue to
ries, rheumatic heart disease (RHD) is the most common have symptoms despite the above measures.
cause of valvular heart disease. The physiological prob Balloon mitral valvotomy (BMV) is indicated if the
lems imposed by valvular lesions (either acquired or patient is found to have severe mitral stenosis with or with
congenital) are stenosis, regurgitation or a combination of out symptoms (valve area < 1.5 cm) before conception.
both. Regurgitant lesions are better tolerated than stenotic However, during pregnancy, indication for valvotomy is
ones. severe symptomatic mitral stenosis (with NYHA class III/
Among the four cardiac valves the most common valves IV symptoms) despite medical therapy in a valve with
resulting in problems during pregnancy are mitral and favorable morphology. Significant subvalvular involvement,
aortic valves. Rarely pulmonary or tricuspid valvular lesions calcification, more than moderate mitral regurgitation
are also seen. Pregnancy in the presence of prosthetic heart and left atrial clot are contraindication for BMV. In these
valve is a separate topic which needs to be discussed. situations and in the presence of NYHA class IV symptoms,
Sometimes patients present with severe valvular mitral valve replacement is indicated.
disease and significant symptoms requiring percutaneous Patients with atrial fibrillation in the presence of mitral
or surgical intervention during pregnancy. As per the stenosis should receive anticoagulants to prevent throm-
American Heart Association guidelines on valvular heart boemboli. However, risk and benefit of anticoagulants
disease there is no ideal timing for cardiac intervention during pregnancy are needed to be discussed with the pa-
during pregnancy. However, if necessary it should be done tients.
in the second trimester of pregnancy. In the first trimester,
there is risk of fetal malformation and in the third trimester Aortic Stenosis
there is a risk of preterm delivery. During cardiac surgery Unlike mitral stenosis which is mostly rheumatic in origin,
in pregnancy maternal mortality is similar to that in non- aortic stenosis in females of reproductive age may be due to
pregnant females (3%), but the fetal mortality remains congenital lesion of the aortic valve or a result of RHD. The
high (19%). High pump flow (>2.5 L/min/m2), perfusion most common CHD leading to aortic stenosis is bicuspid
pressure >70 mm Hg, normorthermic perfusion and aortic valve. Patients may have prior knowledge of their
minimal pump time should be used. Valve repair should heart disease and might have undergone balloon aortic
be preferred over replacement. However, as most valvular valvotomy in childhood. It is important to evaluate the
lesions in the developing countries are due to rheumatic aorta in these patients as they may have dilated ascending
heart disease, repair is often not an option. Penicillin aorta which predisposes them to aortic dissection.
prophylaxis should continue as before pregnancy. There is Aortic stenosis, causes less than expected elevation
no role of infective endocarditis prophylaxis in the current of cardiac output in the face of increased demand of
American Heart Association guidelines and local data. pregnancy. Patient may complain of fatigue, dizziness,
Therefore, it is the discretion of the treating physician. chest pain or syncope especially during exertion. These
are the manifestation of inadequate cardiac output. As the
Stenotic Lesions severity of obstruction increases there is also an elevation
Mitral Stenosis of pulmonary capillary wedge pressure which manifests
The most common cause of mitral stenosis in females of as dyspnoea. Unlike aortic stenosis due to bicuspid aortic
reproductive age group is RHD. The elevation of maternal valve, rheumatic aortic stenosis is usually associated with
blood volume and reduction of systemic vascular resist other lesions, especially of the mitral valve and is usually
ance that occurs normally during pregnancy results in not amenable to balloon valvotomy.
increased pulmonary wedge pressure as the stenotic mitral Severe symptomatic aortic stenosis (valve area < 1.0
orifice cannot accommodate the increased cardiac output. cm 2, and mean gradient > 40 mmHg) requires operative
Therefore, there is worsening of symptoms of dyspnoea as intervention to relieve stenosis irrespective of pregnancy.
pregnancy progresses. In asymptomatic patients with severe aortic stenosis
exercise testing should be considered before pregnancy to heart valves should be discussed with the patient in pre
evaluate whether they are truly asymptomatic. pregnancy counseling.
Ideally, warfarin needs to be stopped during the period
Regurgitant Lesions of organogenesis (first trimester) to prevent embryopathy.
Mitral and aortic regurgitation are common regurgitant Warfarin embryopathy is characterized by hypoplasia of
valvular lesions. Regurgitant lesions are relatively well nasal bridge, laryngomalacia, pectus carinatum, congenital
tolerated because of normal decrease in systemic vascular heart defects, ventriculomegaly, agenesis of the corpus
resistance during pregnancy which causes a fall in after callosum, stippled epiphyses and growth retardation.
load, leading to efficient cardiac output. An important In the first trimester there are three choices for anti
cause of mitral regurgitation in the developed countries coagulation. There are no randomized control trials com
is mitral valve prolapse. In these patients the presence of paring the efficacy of one regimen with another. These
severe regurgitation-valve repair may be considered even 3 choices are as follows:
in the absence of symptoms before pregnancy. Continue warfarin (with INR monitoring) this option is
In patients with severe symptomatic regurgitant used only if daily warfarin dose is less than 5 mg per day
Dose adjusted Low molecular weight heparin twice
valvular lesion and those with left ventricular systolic
function, there is a high risk of developing heart failure daily subcutaneous (with anti-Xa level monitoring)
Dose adjusted continuous infusion of unfractionated
during pregnancy. Any decision to do valve replacement
prior to pregnancy should be done only after a detailed heparin ( with aPTT monitoring)
discussion, regarding prosthetic valves, anticoagulants Warfarin higher than 5 mg per day is associated with
and involve a multidisciplinary team of obstetricians, >8% risk of embryopathy as compared to doses less than
anesthesiologists, cardiologists and cardiac surgeons. 5 mg which is associated with 3% risk, therefore higher
Surgery during pregnancy should be reserved for those dose is not used in first trimester.
with symptoms of intractable heart failure. Low molecular weight heparin has ease of admin-
istration and can be given in twice daily subcutaneous
Prosthetic Valve injections. However, the exact dose needs to be titrated
according to anti factor Xa enzyme assay which should be
There are two types of prosthetic valves, bio-prosthetic and
0.8–1.2 U/mL 4–6 hours after the last dose. Unfortunately
mechanical prosthetic valves. Bio-prosthetic valves have
this test is not readily available in India. Even after titrat-
shorter lifespan than mechanical valves but do not require
ing with factor anti-Xa levels its anticoagulant there are
anticoagulation. It is not clear, however, whether their
cases of valve thrombosis reported. Standard heparin has
deterioration is hastened by pregnancy. Echocardiography
to be given as a continuous intravenous infusion because
should be done in patients with prosthetic valves to assess
of its short half life. It requires frequent monitoring of aPTT
the baseline function of valves and gradients across the (keeping it twice the normal) to titrate its dosage. It is a
valves. difficult task to give prolonged intravenous heparin. Long
Pregnancy in the presence of mechanical valve falls term intravenous heparin is associated with intravenous
under risk class III of the modified WHO risk classification line infection, osteoporosis and thrombocytopenia.
(Table 38.2). Patients in this group have significantly Warfarin is the drug of choice for anticoagulation in the
increased risk of maternal mortality or severe morbidity— second and third trimester. Along with anticoagulant, aspirin
multidisciplinary specialist care is required during and 75–100 mg/day should also be given to all women with
after delivery. Mechanical prosthetic valves require oral prosthetic aortic valves in the second and third trimester.
anticoagulation to prevent valve thrombosis. Since, Before planned delivery, the patient must be admitted
pregnancy itself is a pro-thrombotic state, pregnant and switched to unfractionated heparin before delivery
patients with mechanical valves should be followed up because warfarin is transmitted across the placenta and
in a tertiary care center. Use of oral anticoagulants in first can cause intracranial bleeding of fetus during vaginal
trimester of pregnancy is associated with embryopathy, risk delivery. Heparin can be stopped once labor starts.
of miscarriage and bleeding. Without anticoagulation there In the absence of bleeding heparin should restarted
is high risk of maternal mortality and thromboembolism. 4–6 hours after delivery and also restart oral warfarin. It
There should be frequent monitoring of international takes 3–4 days to achieve therapeutic INR after starting
normalized ratio (INR) during pregnancy. The risks of warfarin and heparin should be continued till therapeutic
continuing pregnancy in the presence of mechanical INR is achieved.
Congenital Heart Disease maternal oxygen saturation.Live birth rate is 12% with
Acyanotic and Obstructive Lesions less than 85% oxygen saturation and 92% with 90% oxygen
saturation.
Most common CHD associated with pregnancy are
repaired or unrepaired acyanotic diseases with left to right Pulmonary Hypertension
shunts like atrial septal defect, ventricular septal defect
and patent ductus arteriousus. Most of these patients fall in These patients fall in WHO risk class IV and pregnancy is
the risk class I or II of modified WHO risk classification and contraindicated. Eisenmenger syndrome is the end result of
usually do not pose significant problem during pregnancy. uncorrected large left to right shunts, leading to irreversible
Large defects with significant left to right shunts can cause and severe pulmonary hypertension. Patients with
heart failure due to fluid overload but the effect of volume pulmonary hypertension due to Eisenmenger syndrome or
overload is offset by decrease in peripheral vascular other causes have very high risk of pregnancy with maternal
resistance during pregnancy. Some of them might require mortality ranging from 30–56%. Due to this pregnancy
judicious use of diuretics. is contraindicated and termination is the safest option.
Patients with corrected coarctation have chances of Patients should be given advice about contraception.
developing hypertension during pregnancy. They should
be evaluated for the presence of aneurysm at the site of
Repaired Cyanotic Heart Disease
repair and magnetic resonance imaging (MRI) should be In general, in these patients, maternal mortality is low but
done pre-pregnancy. Those with unrepaired coarctation there is a possibility of increased maternal morbidity and
may have upper body hypertension and medication given adverse fetal outcomes. Risks related to pregnancy cannot
to control blood pressure may cause hypoperfusion in be generalized and needed to be individualized even after
lower limbs and placenta leading to intrauterine growth repair.
restriction of the fetus. Repaired tetralogy of fallot (TOF) may be low, medium,
Dissection of aorta is also reported in pregnancy without or high risk depending on the residual ventricular septal
other known associated conditions. Probably it is related defeat (VSD), ventricular function, and valvar function.
to hormonal and hemodynamic changes associated with Surgical scar might be substrates of arrhythmias. Case
pregnancy. Marfan syndrome, bicuspid aortic valve, series of patient with repaired TOF have shown that
coarctation of aorta, Ehler-danlos, Loeys-Dietz syndromes pregnancy is overall well tolerated but severe pulmonary
are all associated with aortopathy which might lead to regurgitation can cause decompensation. In repaired TOF
dissection of aorta. with preserved ventricular function and those without
In patients with Marfan syndrome aortic root diameter significant pulmonary regurgitation, pregnancy is well
> 40 mm is a contraindication for pregnancy. Beta blockers tolerated.
are usually given to patients with Marfan syndrome in the Case series of patients with transposition of great
hope of preventing dissection of aorta, though there are no arteries who have undergone atrial switch repair in
trials to document its effectiveness in this situation. childhood indicate that there are frequent but manageable
cardiac complications, a high incidence of serious obstetric
Unrepaired Cyanotic Heart Diseases complications and high mortality in the offspring in these
Unrepaired cyanotic CHD are high risk groups (WHO patients. These patients should be carefully monitored
risk class III) for pregnancy. The most common group of during pregnancy. Increasing number of patients with
patients reaching adulthood and pregnancy would be transposition of great arteries (TGA) who have undergone
those with Tetralogy of Fallot (TOF) physiology. Classic arterial switch are also reaching child-bearing age. Case
TOF and other cyanotic heart diseases with TOF physiology series have shown that a significant proportion of them
are characterized by cyanosis due to decreased pulmonary have sequelae that can cause adverse cardiac events in
blood flow. Women with cyanotic CHD can go through pregnancy and therefore these pregnancies must be very
pregnancy with a relatively low risk to themselves provided carefully monitored.
they do not have pulmonary hypertension. The main risk Fontan surgery is used to correct a variety of complex
is related to ventricular dysfunction, bleeding, paradoxical CHD characterized by single functional ventricle. They
embolism and heart failure. Fetal complications are high fall in the modified WHO risk class III and require
and include miscarriage, premature births, and low birth multidisciplinary specialist care. Whatever, limited data
weights. Fetal complications are highly dependent on we have regarding pregnancy in these patients suggests
that though maternal mortality is uncommon, maternal fraction (EF) is nearly always reduced below 45%. Though
morbidity like arrhythmia and congestive heart failure is exact cause is not clear, oxidative stress and generation of
common. Since there is sluggish flow through the atrial cardiotoxic sub fragment of prolactin is believed to play a
and pulmonary circuit, theoretically there is high risk of key role in its pathophysiology. Mostly after 4 months of
thrombosis and pulmonary embolism but most patients are parturition they present to the doctor with symptoms and
also on anticoagulation. There is also risk of miscarriages around 10% only are seen one month before delivery. It
and preterm labor but, if pregnancy is sustained beyond requires a high index of suspicion for diagnosis because
14 weeks, fetal outcome is usually good. Therefore, each symptoms are non-specific and may be seen in normal
patient must be counseled before pregnancy and decision pregnancy. Management is not different from that of other
regarding pregnancy should be individualized. causes of heart failure. Prognosis is different from that of
idiopathic dilated cardiomyopathy, with a significant
Other Cardiac Conditions During Pregnancy proportion (almost 50%) improving or normalizing their left
Coronary Artery Disease ventricular function over the first 6 months after diagnosis.
Coronary artery disease is rare during pregnancy. The Retrospective studies suggest that recurrence of
main differential diagnosis of acute coronary syndrome cardiomyopathy and heart failure is high in subsequent
(ACS) in pregnancy are pre-eclampsia, acute pulmonary pregnancy, especially if ejection fraction is less than 25%
embolism, and aortic dissection wave inversion in ECG may or if it has not normalized. Patients should be counseled
occur in otherwise normal pregnancy. Cardiac troponin against pregnancy in this subset. In those whose ejection
and echocardiography are safe and helpful for diagnosis. fraction has normalized, they should be told about the
Coronary angiography and percutaneous revascularization possibility of relapse which may occur despite termination
are the best options for diagnosis and management of ACS of pregnancy. Appropriate counseling about contraception
in pregnancy. Coronary dissection is most common cause should be given as risk posed by a subsequent pregnancy
of ACS in pregnant females than in other group of patients. may not be mitigated even by termination of pregnancy.
Standard medications can be given except ACE inhibitors, Anticoagulation is not contraindicated in pregnancy
aldosterone antagonist and statins. with artificial heart valves and in breastfeeding.
Bioprosthetic valves do not require anticoagulant and
Tachyarrhythmias hence, are the best choice during the reproductive life.
Supra-ventricular tachycardia (SVT) may be encountered But they mechanically deteriorate during pregnancy,
in a pregnant female and is usually not life threatening. especially the mitral ones. Heparin given in patients with
Carotid sinus massage, intravenous adenosine, beta mechanical valve replacement should achieve the goal of
blocker or cardioversion can be used to treat SVT. Careful atleast doubling the partial thromboplastin time. It should
evaluation for structural heart disease is important as replace warfarin before pregnancy. After delivery both
sometimes arrhythmias may be the first manifestation warfarin and heparin are given for about 5 days and then
the underlying disease. In the presence of structural heart warfarin is continued. Warfarin is not contraindicated in
disease atrial fibrillation, flutter or atrial tachycardia may breastfeeding as insignificant quantities are secreted in
be encountered. Anticoagulation may also be required milk. But phenindione is contraindicated in breastfeedeing
to prevent thromboembolism in such a scenario. In the
presence of repaired CHD ventricular tachycardia may Contraception
be encountered. Acute management with procainamide, Advice regarding contraception should be individualized
amiodarone, sotalol or other beta blocker may be done. according to the clinical condition.
Cardioversion may be done if required. For patients who have high risk related to pregnancy
barrier contraception is good option in view of their high
Peripartum Cardiomyopathy failure rate.
Peripartum cardiomyopathy is an idiopathic cardiomy Combined estrogen and progesten contraceptive pills
opathy presenting with heart failure (HF) secondary to predispose to both arterial and venous thrombosis. They are
left ventricular (LV) systolic dysfunction towards the end not good options in those with history of thromboembolism,
of pregnancy or in the months following delivery, where stroke, cyanotic heart disease, Eisenmenger physiology,
no other cause of heart faliure is found. It is a diagnosis mechanical valves, Fontan circulation, sustained arrhy
of exclusion. The LV may not be dilated but the ejection thmias, or significant ventricular dysfunction.
Intramuscular medroxyprogesterone acetate and sub

FETAL OUTCOME
cutaneous implants are highly effective and also good
options for those with heart disease but pose a small risk According to NYHA, foetal mortality varies from none in
of hematoma in patients taking anticoagulant. class I to 30 per cent in class IV. In RHD, foetal outcome
Intrauterine devices are also highly effective and safe is usually good. However, babies are likely to be lighter
for patients with heart disease once they are inserted. (small for date). In CHD, there is no excess foetal mortality
However, they may be associated with bacteremia or except in the cyanotic group, with or without pulmonary
rarely vasovasgal syncope during insertion both of which hypertension. Foetal losses, including abortion, may be
may be dangerous in patients with Fontan circulation or as high as 45 per cent. The majority of these babies are
growth restricted due to an inadequate oxygen supply.
pulmonary hypertension.
The placental exchange cannot compensate because of
Puerperium the maternal systemic hypoxemia. Risk of CHD in infants
of these mothers is about 2–4% and the defect is usually
Close observation for 24 hours is necessary. The patient concordant, i.e. of the same nature as that in the mother.
should be confined to bed with limb movements The incidence varies from 3–14% compared to 1% in the
allowed. Pain relief is provided. Hourly vital charting is general population. Congenital heart disease in the father
done. has less profound effects
The patient is kept in the hospital in bed for at least Patients with cyanotic heart disease have abortion,
10 days. Limb movements are allowed and breathing preterm delivery and IUGR. Otherwise sometimes babies
exercises are encouraged. may have IUGR or are preterm. More important is the
Breastfeeding is contraindicated only in the presence of prevalence of congenital heart disease in the infants of
failure. mothers with congenital heart disease.
1. What are prosthetic heart values? Define with appropriate examples.
2. What are congenital heart diseases? Explain with appropriate examples.
i. For patients who have high risk related to pregnancy ____________ and ____________ are not good options for
contraception.
ii. ____________ surgery is used to correct variety of complex CHD.
iii. Mechanical prosthetic value require ____________ to prevent value thrombosis
iv. SVT stands for ____________.
Diabetes and other
39
Smiti Nanda, Meenakshi Bhatt, Ritu Sharma, Meenakshi B Chauhan
Endocrine Disorders
in Pregnancy
Increased food consumption and static life style are

DIABETES MELLITUS
other factors responsible for hyperglycemic state in preg-
Diabetes mellitus is a common medical condition compli- nancy.
cating pregnancy and its prevalence is rising continuously.
The world prevalence was around 6.4% in 2010 and has Classification of Diabetes Mellitus
been estimated to increase up to 7.7% by 2030. Abnormal According to International Association of Diabetes and
maternal regulation is observed in 3–10% of pregnancies. Pregnancy Study Group (IADPSG) diabetes detected first
Though advances in management of diabetes and its time in pregnancy can be classified into overt diabetes or
complications have occurred, the maternal and perinatal gestational diabetes.
complications still pose an increased burden in pregnant According to American Diabetes Association (ADA), it
women. can be classified as follows:
Pregnancy is itself a diabetogenic condition. The Insulin dependent or type I diabetes
diabetogenic state of pregnancy is attributed to following Insulin independent or type II diabetes
causes: Gestational diabetes mellitus (GDM).
Insulin resistance: It is due to the following factors:
Severity of pregestational diabetes can be categorized
• Placental production of human placental lactogen,
according to White’s classification (Table 39.1). American
placental growth hormone, and placental insulinase Congress of Obstetricians and Gynecologists (ACOG)
all of which have anti-insulin action. further utilizes a single classification based on the presence
• Increased production of cortisol, estriol, progesterone
or absence of maternal vasculopathy. Patients with diabetic
and prolactin.
vasculopathy require more aggressive management.
• Increased insulin destruction by the kidney and
placenta. Complications of Diabetes Mellitus in
• Resistin, a placental hormone, plays a part in insulin
Pregnancy
sensitivity imposed by other hormones during preg
nancy and thus is a potential important mediator of Maternal complications are:
Acute: These occur mainly due to fluctuation in blood
insulin resistance.
• Cytokine—TNF-α (Tumor necrosis factor-α) and leptin glucose levels. There can be severe hyperglycemia with
from the placenta also increase insulin resistance. ketoacidosis or hyperosmolar coma or hypoglycaemia.
• Increased body weight and calorie intake during Chronic: These complications are due to long standing
pregnancy also aggravate the insulin resistance. hyperglycaemic state leading to angiopathy and include
Accelerated Lipolysis: Maternal fat stores are broken- progression of maternal diabetic retinopathy, worsening
down for caloric requirement to save glucose for fetal of nephropathy and cardiomyopathy.
needs. The complications peculiar to pregnancy can be listed as
Changes in gluconeogenesis: Alamine and other follows:
amino acids are preferentially used by fetus depriving During pregnancy
the mother of a major store for gluconeogenesis. • Spontaneous abortions

Diabetes and other Endocrine Disorders in Pregnancy 387
TABLE 39.1: Classification of Diabetes Complicating Pregnancy (Cunningham et al. 2010)

Class Onset Fasting 2-hour Postprandial Therapy
A1 Gestational < 105 mg/dL < 120 mg/dL Diet
A2 Gestational > 105 mg/dL > 120 mg/dL Oral agent or insulin
Class Age of onset (yr) Duration (yr) Vascular Disease Therapy
B* ≥ 20 < 10 None Insulin
C* 10–19 10–19 None Insulin
D* Before 10 > 20 Benign retinopathy Insulin
F Any Any Nephropathy* Insulin
R Any Any Proliferative retinopathy Insulin
H Any Any Heart Insulin
* Single criteria required for diagnosis: age of onset, duration or vascular disease
* Diagnosed when 500 mg or more proteinuria per 24 hours measured before 20 weeks’ gestation.
• Urinary tract infections (UTIs) Cardiac:

• Candidal vaginitis • Transposition of great vessels
• Pre-eclampsia • Atrial septal defect
• Polyhydramnios • Ventricular septal defect (incidence is increased by
During delivery 5 folds)
• Preterm labor (infection, polyhydramnios may be • Aortic coarctation
the cause) • Patent ductus arteriosus
• Shoulder dystocia • Cardiomegaly
• Prolonged labor Renal:
• Increase incidence of operative or instrumental deliveries • Renal atresia/agenesis

• Trauma to maternal genital tract and fetus • Ureteral duplication
• Postpartum hemorrhage—traumatic (due to instru- • Hydronephrosis

• Cystic kidneys
mental delivery, extension of episiotomy)/atonic
Retinal anomalies
(due to uterine over distension)
Gastrointestinal tract:
Post delivery
• Anal atresia
• Postpartum sepsis
• Duodenal atresia
• Subinvolution of uterus
• Small left colon syndrome
Delayed: May develop diabetes mellitus and cardiovas-
• Single umbilical artery
cular diseases in later life (1/3rd).
• Tracheoesophageal fistula
Skeletal and spine: Caudal regression syndrome (sacral
Fetal and Neonatal Complications
agenesis) is the most common defect and a unique
Congenital Anomalies: The incidence of major malforma- anomaly.
tions is increased four-fold in the offspring of women with Fetal macrosomia: Incidence is about 30–40%. Patho
overt diabetes. Incidence of congenital malformation is genesis can be explained by Pederson hypothesis.
directly proportion to glycosylated hemoglobin (HbA1C); According to this hypothesis, maternal hyperglycmia
incidence being very high if levels are > 10%. Common leads to fetal hyperglycemia which causes fetal pancreatic
fetal malformation include: beta cell stimulation resulting in hyperinsulinemia and
Central nervous system: excessive somatic growth and lipid accumulation. Insulin
• Spina bifida like growth factors, maternal obesity and increased transfer
• Anencephaly of free fatty acids to fetus are other factors contributing to
• Encephalocele macrosomia.
• Hydrocephalus Fetal growth restriction
• Microcephaly Intrauterine fetal death—Hypoxia and lactic acidosis
• Holoprosencephaly are the ultimate responsible factors

• Meningomyelocele Birth trauma
Birth asphyxia cerned, initial screening should be done in first trimester

Neonatal hyperviscosity syndrome or the first antenatal visit. If it is negative, then retest should
Neonatal hypoglycemia be done at 24–28 weeks and at 32–34 weeks of gestation.
Neonatal hypocalcemia ACOG recommends two step approach to diagnose
Neonatal hyperbilirubinemia gestational diabetes which includes—50 grams oral
Neonatal polycythemia glucose challenge test (GCT) and plasma glucose level of
Respiratory distress syndrome: Research has shown that 140 mg/dL at 1 hour is taken as cut off value. Screening
hyperglycemia and hyperinsulinemia interfere with of positive patients then would proceed to the second
the surfactant biosynthesis and thus delay pulmonary step; oral glucose tolerance test (OGTT) with 100 grams
maturation glucose. Plasma glucose is estimated at 0, 1, 2 and 3 hours.
Cardiomyopathy Gestational Diabetes Mellitus is diagnosed (Carpenter
Long-term complications: and Coustan criteria) if > 2 values meet or exceed—Fasting
• Obesity > 95 mg/dL, 1 hour > 180 mg/dL, 2 hour > 155 mg/dL and
• Diabetes 3 hour > 140 mg/dL.
• Neuropsychological defects and breast cancer. Now one step approach using 75 grams 2 hour oral GTT
Risk factors for gestatational diabetes as per National recommended by World Health Organization (WHO),
Institute for Health and Clinical Excellence (NICE) guide Federation of Obstetric and Gynecological Societies of
lines (2015) are: India (FOGSI) and Diabetes in Pregnancy Study Group
Obese or overweight women (>15% of non-pregnant
of India (DIPSI) has become popular due to its simplicity
ideal body weight or weight > 200 pounds) and advantages over the two step approach (Table
Thirty years old or more
39.2). GDM is diagnosed if 2 hour plasma glucose is
Diabetes mellitus in last conception
≥ 140 mg/dL. This single step approach is both screening
History of diabetes in family members (sibling/parents)
as well as diagnostic. It can be done irrespective of fasting
Unexplained prior miscarriages or stillbirths
status. As single sample is required, it eliminates the need
Prior history of unexpected neonatal death
of multiple visits. Thus this test is economical, simple and
Bad obstetric history (> 3 spontaneous abortions in the
acceptable. This approach eliminates the confusion among
first or second trimester) the service providers regarding the different approaches
Prior macrosomia of 9 lb or more (or > 4.5 kg)
with different cut off values in pregnant and non pregnant
women as the cut off values in both the groups here are
History of traumatic delivery with associated neurolo
similar. Again > 140 mg/dL cut off has been set up taking
gical disorders in the infant
fetal prognosis into consideration. If the 2 hour plasma
Prior baby with congenital anomalies
glucose is > 200 mg/dL in the early weeks of pregnancy,
Hypertension and/or hyperlipidemia
she may be a case of overt diabetes mellitus and HbA1c of
History of pre-eclampsia
> 6.5% or fasting blood sugar > 126 is confirmatory.
Repeated infections (especially urinary tract infections,
IADPSG and ADA also utilizes 75g OGTT but the cut off
severe moniliasis) and development of chorioamnion-
values are different as shown in the Table below 39.3. GDM
itis in pregnancy
is diagnosed when > one value is abnormal.
Polyhydramnios
Polycystic ovarian syndrome (PCOS). Management

Screening: There is no uniform approach for diagnosis of Aims of Management
gestational diabetes mellitus (GDM). Recent recommen- Achieving a euglycemic state similar to a non-diabetic
dation is on universal screening. As far as timing is con- pregnant patient and its maintenance.
TABLE 39.2: 75 grams 2 hour OGTT (WHO, FOGSI, DIPSI)

2 hour Blood sugar values (mg/dL) Pregnant Non pregnant
<120 Normal Normal
120–139 GGI (Gestational glucose intolerance) Normal
140–199 GDM (Gestational diabetes mellitus ) IGT (Impaired glucose tolerance)
> 200 Diabetes Diabetes
Abbreviations: OGTT—Oral glucose tolerance test; WHO— World Health Organization; FOGSI— Federation of Obstetric and Gynecological
Societies of India; DIPSI— Diabetes in Pregnancy Study Group of India
TABLE 39.3: Different cut offs adopted in 75 g OGTT blood urea nitrogen to rule out diabetic nephropathy, fundus
Plasma glucose WHO IADPSG, ADA examination to rule out diabetic retinopathy and recording
Fasting >125 mg/dL >92 mg/dL of blood pressure, electrocardiogram, echocardiography
(>6.9 mmol/L) (>5.1 mmol/L) and stress test in case coronary artery disease.
1 hour – >180 mg/dL The couple is explained the need to plan pregnancy
(>10 mmol/L) with good glycemic control so as to minimize the risk of
2 hour >140 mg/dL >153 mg/dL congenital anomalies. HbA1c level should be in the normal
(>7.8 mmol/L) (>8.5 mmol/L)
range, i.e. 4—6.5%. The blood glucose targets as per ADA are
Abbreviations: IADPSG— International Association of Diabetes and
Pregnancy Study Group; ADA—American Diabetes Association same in both pregnant and non pregnant. Patient should
try to achieve them by lifestyle modifications in form of
Avoiding iatrogenic prematurity. weight management, daily exercise, cessation of smoking
Monitoring for intrauterine fetal jeopardy. and reduced alcohol intake. Folic acid supplementation
Eliminating maternal complications.
5 g daily is prescribed for three months prior to conception.
Multidisciplinary team approach consisting of obstetri-
Insulin should be substituted in place of oral hypoglycemic
cian, dietician, endocrinologist and a pediatrician should
agents in preconception period and in pregnancy due
be involved. The management should be initiated from the
to concerns regarding teratogenicity and hypoglycemia.
preconception period and continued to the postpartum
Although ongoing research has shown increasing evidence
period, as explained is Flowchart 39.1
regarding safety of metformin and glyburide in diabetes in
Preconceptional Counseling pregnancy, most of the organizations do not recommend
It includes emphasis on fact that pregnancy with diabetes their routine use during pregnancy. One has to weigh the
is a high risk pregnancy, so need for regular follow-up and likely benefits against the harms if these drugs are to be given
compliance to treatment is a must. Evaluation of end organ or continued. Isophane insulin is the first choice in pregnancy;
damage should be done before embarking on pregnancy. however, newer rapid acting insulin analogues (aspart and
Investigations that are advised for end organ evaluation lispro) with associated advantages can be considered. Newer
include, 24 hours urinary protein, serum creatinine, and long acting insulin G-largine is under trial.
Flowchart 39.1: Management of pregnancy with diabetes mellitus
Abbreviation: CPD—Cephalopelvic disproportion

Antepartum Management unsaturated fats and 20% of proteins. Avoid alcohol and
Patient should be registered as early as possible and advised to non-sucrose sweeteners.
attend antenatal clinic regularly. End organ evaluation, if not
Exercise
done, should be carried out. Self monitoring of blood sugar
is encouraged. Monitoring is done weekly or twice weekly Regular physical exercise of upper body muscles within a
depending on control of blood sugar levels. Fetomaternal tolerable limit should be encouraged. Thirty minutes of walk
surveillance is very important throughout pregnancy. after meals is also beneficial. Always assess the autonomic
Glycemic control can be achieved by modification of diet, nervous system. Signs and symptoms of hypoglycemia
daily exercise and insulin. The intervention required is along with its management requires discussion with the
recommended as shown in the Table 39.4. patient.
Therapeutic targets as per ADA include a fasting blood
sugar level of < 95 mg/dL (5.3 mmol/L), 1 hour value < Insulin Therapy
140 mg/dL (7.8 mmol/L) and 2 hour value < 120 mg/dL If lifestyle modifications fail to achieve optimum control
(6.7 mmol/L). in 2 weeks, insulin therapy is initiated. The insulin used in
pregnancy is mostly biosynthetic human insulin. Initial
Medical Nutrition Therapy (MNT) daily dose required is calculated as 1.1 U/kg ideal body
All women with GDM should receive nutritional counsel- weight and should not exceed 60U/day. Two-third of daily
ing. Dietary intervention should be individualized. Calorie dose of insulin is given in the morning (70% as intermediate
requirement is calculated depending on body mass index acting and 30% as a short acting) and remaining one-third
(BMI) as shown in the Table 39.5. before the evening meal, (50% given as intermediate acting
In obese patients, calorie restricted diet without and 50% as short acting). Approximately 1 unit of insulin is
causing ketosis is recommended. Extra 300 Kcal is to be required for every 30 mg/dL rise in blood glucose above the
added especially in third trimester. Diet is divided into normal expected level. A two hours post meal monitoring
three meals and three snacks or three meals and one bed is preferable for assessing the blood sugar control. Self
time snack. Calorie distribution in breakfast, lunch, dinner monitoring of blood glucose seven times a day should
and snacks should be 10–20%, 20–30%, 30–40% and 30% ideally be advised. Although frequency of blood glucose
of total calorie requirement respectively. As per ADA the monitoring is variable as per different recommendations,
diet should consist of 40–50% of carbohydrates which usually it is done in every 2–3 days till recommended levels
should include complex sugars and dietary fibers, 40% of are achieved. Signs and symptoms of hypoglycemia should
be explained. Blood sugar levels in patient on insulin should
be maintained >70 mg/dL (4 mmol/L). Further adjustment
TABLE 39.4: Interventions recommended in diabetes in pregnancy
if required is done in 5U steps.
Intervention Indication Insulin requirement in type 1 diabetes is increased in
Life style modification FBS < 126 mg/dL (< 7 mmol/L) pregnancy depending upon gestational age as shown in
(Diet, Exercise) the Table 39.6.
Life style modification FBS > 126 mg/dL (>7 mmol/L)
+ Insulin FBS 105–125 mg/dL (6–6.9 m mol/L) Fetomaternal Surveillance
+ complications (e.g. Hydramnios,
macrosomia) Maternal surveillance includes frequent estimation of blood
Target levels not achieved with diet sugar profile (weekly or twice weekly), HbA1c estimation
and exercise within 2 weeks in every trimester, urine examination, urine culture and
Abbreviation: FBS—Fasting blood sugar investigations for evaluating end organ status. Fetal
TABLE 39.5: Calorie requirement in diabetes in pregnancy TABLE 39.6: Insulin requirement in type I diabetes mellitus
Insulin requirement
BMI (kg/m )2
Calorie requirement (kcal/kg)
Gestational age (U/kg body weight/ day)
20 –≤ 25 (normal weight) 30 6–18 weeks 0.7
25–34 (overweight/obese) 25 18–26 weeks 0.8
>34 (morbidly obese) < 20 26–36 weeks 0.9
Abbreviation: BMI—Body mass index 36–40 weeks 1
surveillance starts at 11 weeks with early anomaly scan and TABLE 39.7: Insulin administration in labor
dual marker test. At 16–20 weeks quadruple screening, level Blood Glucose Insulin Dosage I/V Fluids
II ultrasonography and fetal echocardiography (ECG) are Level (mg/dL) (U/hr) (125 mL/hr)
recommended. Obstetrical ultrasound is recommended, < 100 0 D5 RL
4 week every from 28 weeks, onwards till 36 weeks to 100–140 1.0 D5 RL
diagnose fetal growth restriction, macrosomia and oligo 141–180 1.5 NS
hydramnios. Color Doppler studies, nonstress test (NST) 181–220 2.0 NS
and biophysical profile are recommended, if there is > 220 2.5 NS
associated FGR or other associated high risk factors.
Delivery biotics are administered. Sedatives are avoided. Epidural

analgesia is preferred. The progress of labor is monitored
Timing of Delivery
carefully with the help of a partogram. Liberal episiotomy
Women with well controlled uncomplicated diabetes may should be given to prevent genital tract injury. One should
be allowed to go in spontaneous labor till 40+6 weeks; be well prepared to tackle shoulder dystocia if encoun-
otherwise labor has to be induced or cesarean has to be tered. Examine placenta and umbilical cord to detect any
done (if indicated). In complicated cases (associated fetal abnormalities like single umbilical artery.
complications like IUGR, macrsomia or maternal complic- Indications of elective cesarean section
ations like hypertensive disorders, vascular disease, Macrosomic fetus weighing > 4.5 kg
uncontrolled diabetes) delivery at 38 weeks or earlier is Bad obstetrical history
indicated. Unstable diabetes
In preterm labor, antenatal steroids for fetal lung matu Obstetrical indications.
ration and tocolysis can be prescribed; however strict The elective cesarean in the woman with diabetes
monitoring is required and additional insulin may be mellitus should be done as the first case in the operation
needed. Betamimetics should not be used for tocolysis as theater. The usual dose of insulin is given in the night prior
they aggravate hyperglycemia and precipitate ketoacido- to surgery, and the morning dose is omitted. The woman is
sis. Magnesium sulphate is the drug of choice. Calcium kept fasting since midnight. Fasting blood sugar and serum
channel blockers can also be used. electrolytes are sent preoperatively; fluids and insulin given
Mode of Delivery accordingly. Regional anesthesia preferred as an awake
patient can report symptoms suggestive of hypoglycemia.
Vaginal delivery can be attempted if the following criteria
are fulfilled:
Postpartum Care
Longitudinal lie with vertex presentation
Adequate intrapartum fetal monitoring

In the postpartum period, insulin requirement dramati-
No cephalopelvic disproportion (CPD)
cally falls to half to two-third than that in antenatal period
No evidence of intrauterine jeopardy.
due to loss of insulin resistance. Blood sugar examinations
should be done and insulin given accordingly. In patients
Glycemic Control During Labor with pregestational diabetes, once the patient begins a
A strict glycemic control during labor is important to regular diet, the prepregnant insulin dose or oral hypo-
prevent neonatal hypoglycemia. Omit the morning dose of glycemics can be started. Antibiotics are continued in the
long acting insulin on the day of termination of pregnancy postpartum period. Breastfeeding should be encouraged.
or if the woman goes in to spontaneous labor. The morning
fasting blood glucose sample is sent and the intravenous Neonatal Care
fluids and insulin are administered as per the blood sugar Neonates should be kept under observation for 48 hours
levels given in Table 39.7. Blood glucose is monitored every and their blood glucose level should be maintained at
1–2 hourly. Urinary ketones and serum electrolytes are a value of > 47 mg% (> 2mmol/L) to prevent neonatal
done 4 hourly. The aim is to maintain the blood glucose hypoglycemia. Early breastfeeding (within 30 min to 1
between 80–110 mg/dL (4–7 mmol/L). Insulin should hour) should be encouraged and should be continued
preferably be administered with an infusion pump. every 3-4 hourly. Congenital malformations and other
Strict asepsis is maintained and per vaginum exami- neonatal complications if any should be detected in this
nations are limited to avoid infection. Prophylactic anti- period and managed. Blood tests should also be done to
TABLE 39.8: 75 gm Postpartum OGTT patient desires. Hormone IUCDs can be used with careful
follow up only. Women with completed families should
Fasting Plasma 2 hour Plasma
glucose (mg/dL) glucose (mg/dL) Interpretation undergo sterilization.
Diabetes with end organ damage (like retinopathy and
<110 <140 Normal
nephropathy) is a relative contraindication to pregnancy
110-125 140–199 Impaired glucose
as pregnancy can worsen the vasculopathy thus shortening
tolerance (IGT)
the life span of the mother apart from increasing fetal
>126 >200 Overt Diabetes
mortality and morbidity.
detect hypocalcemia, hypomagnesemia, polycythemia

Management of Complications
and hyperbilirubinemia. Echocardiography should be Diabetic Ketocidosis
done if heart disease is suspected. One percent of pregnant patients are affected by this
medical emergency characterized by hyperglycemia
Postpartum Follow-up (>250 mg/dL), ketosis (ketonemia and ketonuria) and
Postpartum follow-up is essential to diagnose overt metabolic acidosis (pH <7.3, bicarbonates <15 meq/L).
diabetes and the risk for the same. Patient usually present in altered conscious state with
ADA recommends 75 g 2 hour OGTT in patients with abdominal pain, nausea, vomiting, hypotension, rapid and
gestational diabetes between 6 and 12 weeks of delivery deep respiration. In 50% of patients, the cause is infection
(or later) to assess risk for overt diabetes and intervention and in rest, the cause can be dietary, non-compliance,
advised accordingly (Table 39.8). steroids and beta sympathomimetics administration,
As per recent amendment in NICE guidelines (2015) hyperemesis gravidarum and idiopathic. Insulin deficiency
only fasting plasma glucose test is recommended between and effect of counter regulatory harmones is responsible
6–13 weeks postpartum in women with gestational for the pathogenesis. The condition is associated with high
diabetes; if delayed do fasting plasma glucose test or fetomaternal mortality. Management includes estimation
HbA1c. The management that is recommended is shown of blood sugar values every hourly; estimation of ketone
in Table 39.9. bodies in blood, serum electrolytes, arterial blood gas
Follow-up with annual HbA1c test is recommended in analysis every 4 hourly along with estimation of glycosuria
women who were diagnosed with gestational diabetes, but and ketonuria 4 hourly. Complete blood count (CBC),
had a negative postnatal test for diabetes. ECG and chest X-ray have to be done.
To correct dehydration, one liter of normal saline is
Postpartum Contraceptive Advice
given in the first hour followed by 250 mL/hour. To correct
Barrier contraception used to be the best method for hyperglycemia insulin is given in bolus dose of 0.2U/kg
spacing. Now newer low dose oral contraceptive selection body weight intravenously followed by 0.1 U/kg/hour in 5%
(OCP’s) with minimal metabolic effects can be prescribed dextrose. Glucose should decrease by 70–100 mg/dL/hour
after assessing the individual case. Copper-T can be used if using this regimen and dose can be adjusted accordingly.
Change the fluid to dextrose normal saline (DNS) once the
TABLE 39.9: Postpartum screening blood sugar level reaches 250 mg/dL. If levels are less than
Fasting plasma Risk for overt 150, decrease the dose of insulin. Correct hypokalemia,
glucose HbA1c Diabetes Intervention if present, by infusing 20–40 meq of potassium as soon as
< 6 mmol/L < 5.7% Low risk Continue life possible preferably within first hour of insulin therapy. If pH
(<105 mg/dL) style changes <7.1 sodium bicarbonate (0.3 × body wt in kg × Base deficit)
6–6.9 mmol/L 5.7–6.4% High risk Life style every 2 hourly is given till pH rises to normal. Antibiotics are
(105–125 mg/dL) changes + started and strict vital monitoring is recommended. Once
Pharmacological she is able to take orally, the usual insulin regimen is started.
Intervention
≥ 7 mmol/L ≥ 6.5% Likely to have Diagnostic test
type 2 Diabetes (75 grams 2 hour
INFANT OF DIABETIC MOTHER
(≥ 126 mg/mL)
OGTT ) The outcome in both mother and child has improved as
Abbreviation: OGTT—Oral glucose tolerance test diabetes mellitus is controlled by insulin. However, the
neonatal mortality in infants of diabetic mothers (IDMs) shoulder dystocia and birth trauma (Erb’s palsy, clavicular
is five times that of neonates of mothers who do not suffer fracture, etc.) The rate of cesarean delivery is 4–5 times
from diabetes. greater than in non-diabetic women.
In this section, we will discuss some problems that The increased size is due to increase in both fatty and
commonly occur in IDMs, their pathogenesis and their non-fatty tissue (involves all, excluding the brain). Fat
management. deposition is mainly in the shoulders and the interscapular
area. The head appears small, as the brain growth is normal
Complications in IDM for the age.
Commonly occurring complications in IDMs include: The pathogenesis involved include excess synthesis of
Immediate glycogen, fat and protein due to hyperinsulinemia, Pederson
• Congenital anomalies hypothesis, increase in insulin like growth factors in IDMs
• Macrosomia and excess circulating fatty acids and glucose in the maternal
• Prematurity plasma. The genetic response of the fetus is also a factor.
• Hypoxia of the fetus and neonate Macrosomia correlates best with poorly controlled
• Hypoglycemia diabetes in the last trimester and can be avoided by a tight
• Hypocalcemia control of maternal serum glucose. Macrosomic neonates
• Hyperbilirubinemia are more prone to congenital anomalies.
• Polycythemia However, even intrauterine growth restriction is seen if
• Respiratory distress the mother is suffering from vascular disease which leads
• Poor feeding to placental insufficiency.
• Myocardial dysfunction
• Renal vein thrombosis Prematurity
Long term There is a higher risk of premature delivery in diabetic
• Obesity mothers. Also, there is a greater incidence of premature
• Diabetes delivery induced for fetal wellbeing when the intrauterine
• Neuropsychological effects environment is no longer conducive for fetal survival.
• Cardiovascular disease
• Breast cancer Hypoxia of the Fetus and Neonate
Hyperglycemia increases oxygen consumption by the
Congenital Anomalies fetoplacental unit. Vascular disease may compromise
The incidence is three to four times higher in IDMs than in vascular supply to the fetus. Glycosylated hemoglobin
the normal population (6–9% vs 2%). The anomalies usually has increased affinity for oxygen and this may be another
involve the nervous system (anencephaly, meningocele, contributor to fetal and neonatal hypoxia.
holoprosencephaly), heart (VSD or ASD, transposition Diabetic pregnancies need to be closely monitored for
of great vessels, truncus arteriosus, etc.) and also include fetal wellbeing and the pediatrician attending the delivery
hydronephrosis, renal agenesis, dyplasia, double ureter, should be adequately prepared for resuscitation of the
duodenal or anorectal atresia, small left colon syndrome, newborn.
skeletal anomalies and caudal regression syndrome.
Although caudal regression syndrome occurs almost Hypoglycemia
exclusively in IDMs, no anomaly is specific for IDMs. It is defined as a blood glucose of <45 mg/dL regardless
High sugar levels have been found to have a toxic effect of the presence or absence of symptoms. It occurs in
on the growth of cultured cells. Preconception and first 25–50% IDMs in the first 24 hours after birth and especially
trimester control of diabetes can help in reducing the so among macrosomic infants.
incidence of congenital anomalies in IDMs. Hypoglycemia is multifactorial. Pederson’s maternal
hyperglycemia, fetal hyperinsulinemia hypothesis, explains
Macrosomia how maternal hyperglycemia due to an increase in the
It is generally defined as birth weight higher than the 90th number of beta cells in the islets of the pancreas causes
percentile for gestational age or more than 4000 g. Macro fetal hyperglycemia and resultant fetal hyperinsulinemia.
somic infants carry a higher risk of cesarean delivery, Decreased catecholamine, glucagon secretion, diminished
hepatic gluconeogenesis and fatty acid oxidation also recommended. Instead a sample to test serum calcium
contribute to hypoglycemia. should be drawn in a neonate with symptoms suggestive of
Hypoglycemic neonates may be symptomatic or asymp- hypocalcemia, e.g. jitteriness and seizures. After drawing
tomatic. Lethargy is commonly seen. Other signs include the sample, a bolus of 2 mL/kg of calcium gluconate
apnea, tachypnea, cyanosis, respiratory distress, hyperten- diluted 1:1 with saline or distilled water is administered as
sion, shock, seizures and poor sucking. The risk of sequelae is slow IV bolus under continuous cardiac monitoring.
greater if symptoms are present but brain damage may occur If hypomagnesemia co-exists it will need correction
even in the absence of symptoms. This makes prevention and with a 50% solution of magnesium sulphate at a dose of
prompt treatment of hypoglycemia essential.
0.25 mg/kg.
Prevention
Good glycemic control throughout pregnancy
Polycythemia
Avoiding high intrapartum maternal blood glucose 30 min Insulin causes increased erythropoiesis. Upto 20% of
to 1 hour IDMs suffer from polycythemia. This predisposes them
Early feeding, at least within the first hour to hyperbilirubinemia, hyperviscosity and hypoglycemia.
Monitoring of blood glucose Hematocrit levels are checked when clinical appearance is
Blood glucose should be measured at 2, 6, 12, 36 and suggestive of polycythemia.
48 hours of life and if indicated, at 72 hours of life by Treatment involves increasing the daily IV or oral fluid
glucose measurement strips. A value of < 45 mg/dL should intake or partial exchange transfusion depending on the
be confirmed by laboratory estimation of blood glucose. hematocrit and the symptoms exhibited by the neonate.
However, treatment should be instituted immediately and
the laboratory value should not be waited for. Hyperbilirubinemia
More frequent monitoring is required if the infant is
The cause for this can be an increased red blood cell
symptomatic, if low blood glucose level is detected and to
(RBC) mass, less deformable RBC membranes due to
see the response to therapy.
glycosylation of the cell membrane proteins, or breakdown
Management of blood in bruises or hematomas formed intrapartum.
Immediate feeding Prematurity may also be a contributor.
Re-testing of blood glucose half hour after feed Lactation may take time to be established in the diabetic
Symptomatic hypoglycemia mother and the resulting dehydration may exacerbate the
2 mL/kg blous of 10% dextrose is given over 2–3 minutes jaundice.
(slow IV push) Therapy is the same as all other causes of neonatal
A maintenance glucose infusion of 6 mg/kg/min is started jaundice via phototherapy or exchange transfusion based
Frequent blood glucose monitoring is required so that on gestation and age appropriate bilirubin charts.
glucose infusion may be slowly tapered
If hypoglycemia is difficult to control, hydrocortisone Respiratory Distress
5 mg/kg/day may be required. IDMs have a high risk of hyaline membrane disease because
insulin interferes with production of lecithin, which is an
Hypocalcemia
ingredient of surfactant. Other causes of respiratory distress
The incidence is 10–20% in IDMs. The mechanism is not very
include transient tachypnea of the newborn, hypoglycemia,
clear. It probably occurs due to low serum parathormone,
polycythemia, cardiac failure and birth asphyxia.
maternal hypomagnesaemia (due to increased urinary
losses), leading to neonatal hypomagnesaemia. This
Poor Feeding
interferes with the action of the parathyroid hormone.
The clinical features include jitteriness, lethargy or It may be due to prematurity, respiratory distress and poor
seizures. maternal milk let down.
Management Myocardial Dysfunction

Routine testing for hypocalcemia or routine supplemen This can be due to post-asphyxia cardiomyopathy or
tation of calcium in intravenous fluids is no longer transient hypertrophy of the ventricular septum.
Renal vein Thrombosis and continued throughout pregnancy. If treatment for a

The presentation of renal vein thrombosis is with hema- few days does not show improvement, dexamethasone 4
turia, flank mass and hypertension. It is probably due to mg, 6 hourly is indicated. If there is no response even with
hyperviscosity, though it may occur even with a normal the above then, surgery is necessary.
hematocrit. Management is conservative. Radiation therapy is seldom indicated. Its only indica
tion is post surgical residual cases in order to prevent
Long term Risks recurrences.
The incidence of diabetes mellitus in infants is increased Breastfeeding is not contraindicated in patients with
in IDMs as compared to the general population. This is prolactinomas. The patient should be evaluated for any
because, both the parents have diabetes. Macrosomia may tumor growth and bromocriptine therapy is re-started if
predispose to childhood obesity and this risk may persist there is persistent hyperprolactinemia.
into adult life.
Nevertheless, a diabetic who maintains a strict control Acromegaly
of blood glucose during pregnancy has a 95% chance of Acromegaly is caused by an excess of growth hormone,
having a healthy child. As a result, the need for preconcep- which may be from an acidophilic or chromophilic pituitary
tion counseling of known diabetics, early diagnosis of adenoma. Pregnancy is rare in acromegalic woman.
diabetes in pregnancy, and strict control of glucose during Symptoms may be due to local expansion of the tumor,
pregnancy cannot be over-emphasized. headache, visual field disturbances, and facial changes.
The diagnosis in pregnant state is difficult, however in
OTHER ENDOCRINE DISORDERS AND non pregnant state it is diagnosed with the presence
of increased growth hormones and insulin like growth
PREGNANCY factor-1. These patients are more susceptible to develop
Pituitary Diseases gestational diabetes in pregnancy.
In non-pregnant patients, the management includes
Normally, the pituitary increases in weight by about 30%
surgery and/or radiation or medical therapy with soma
in the first pregnancy and by about 50% in subsequent
pregnancies. The number of lactotrophs is increased tostatic analogues. The newer agents Octreotide and
while the number of growth hormone and gonadotrophin Lanreotide, inhibit the production of growth hormone
secreting cells is reduced. (GH), glucagon and insulin. In the event of pregnancy,
Pituitary adenomas are benign neoplasms, and may the drug is discontinued. The patient is monitored with
secrete prolactin or ACTH. According to their size, they visual field examination in each trimester or as clinically
are divided into microadenomas (less than 10 mm) or indicated with headache or visual disturbances. If enlar
macroadenomas. They are also classified according to gement is detected, medical therapy is reinstituted.
the hormone they secrete, the ‘Prolactinomas’ being
the most common. The symptoms may be amenorrhoea, Diabetes Insipidus (DI)
galactorrhea, hirsutism, headache or visual field defects. It is a rare complication of pregnancy and is characterized
The diagnosis is confirmed by MRI or CT imaging. clinically by polyuria and polydipsia due to the deficiency
Several types of treatment modalities are available, of antidiuretic hormone (central) or due to the peripheral
medical, surgical or radiation therapy. The choice depends antidiuretic hormone resistance (nephrogenic).
upon the symptoms, size of tumor, patient’s age and desire Fifty per cent of cases are considered to be idiopathic in
to continue pregnancy. origin. The cause may be, invasion of neurohypophysis by
Medical therapy with bromocriptine decreases pro- tumors or metastatic lesions, including breast cancer.
lactin levels in about 90% of patients. Though, it is not a The presenting symptoms are generally acute and out
known teratogenic agent, the drug is discontinued as soon put may be 4–15 L per day.
as conception occurs. In patients with large tumors, the The diagnosis is confirmed by water deprivation test.
drug should be given for at least 1 year. The drug of choice in confirmed cases is Desmopressin
Since the normal pituitary enlarges during pregnancy, DDAVP (1-desamino-8-D-arginine-vasopressin). Plasma
the possibility of enlargement of adenoma exists. In the electrolytes, fluid intake and urinary output should be
event of any definitive evidence of tumor enlargement monitored. There are no adverse fetal effects and the drug
during pregnancy, bromocriptine therapy is re-started is safe during breast feeding.
Labour and delivery are generally uneventful in patients Treatment is intravenous hydrocortisone 100 mg 6
with DI. Occasionally, however, uterine atony may develop. hourly, initially. Long-term replacement consists of 12-15
mg/m2 per day of hydrocortisone, fludrocortisone acetate
Diseases of Adrenal Glands 100 g per day for mineralocorticoid activity. Additional
In a normal pregnancy the adrenal gland does not enlarge cortisol replacement is recommended during periods of
but there is an increase in the width of the zona fasciculata. major stress, e.g. surgery.
Progesterone has anti-glucocorticoid effect. Both the
plasma total and unbound cortisol, as well as cortisol Congenital Adrenal Hyperplasia (CAH)
binding globulin levels rise during pregnancy. The aldo CAH is a hereditary disorder, resulting from, one of sev-
sterone secretion also increases during pregnancy. eral enzyme defects in cortisol synthesis, 21-hydroxylation
(CYP21A2) defect being the most common. Others are
Cushing Syndrome β-hydroxylase or 18 hydroxy steroid dehydrogenase defi-
It is the result of long-term exposure to excessive levels ciency.
of glucocorticoids and it may be ACTH dependent or Since, the enzymes are responsible for synthesis of corti-
independent. In childbearing years, the most common sol, their deficiency will directly lead to cortisol deficiency.
cause in women is bilateral adrenal hyperplasia (75%). Then a vicious cycle will start resulting in stimulation of
Other causes may be an adrenal tumor, or ectopic ACTH ACTH synthesis, increased androgenic cortisol precursors,
production. In pregnancy however, adrenal adenoma is and a decreased aldosterone production. The increased
seen in more than 50% cases. androgenic steroids are responsible for virilization of
Clinically, patient presents as amenorrhea/oligomenor- female fetus.
rhea, hirsutism, weight gain personality changes or muscle The diagnosis of CAH in the fetus can be done by
weakeness. Pregnancy in such women is uncommon. The
chorionic villus sampling or amniocyte cytology. fetal
clinical diagnosis is difficult during pregnancy because
treatment can be initiated with maternal intake of dexa
of similarity of symptoms, e.g. striae, weight gain or
methasone.
hypertension. Maternal complications like, hypertension,
In the neonate, ambiguous genitalia in the female
diabetes mellitus and heart failure are common during
or penile enlargement in the male occurs. This requires
pregnancy resulting in abortions, preterm labour and hence
rapid diagnosis and treatment. Karyotyping, electrolytes,
increased fetal morbidity and mortality. These patients have
β-hydroxyprogesterone, urinary 17-ketosteroids should be
elevated plasma cortisol without diurnal variation, which
tested.
is not suppressed with dexamethasone. CT scan may be
required if adrenal cancer is suspected. Determination of 24
Pheochromocytoma
hours urinary free cortisol is the best screening test to rule
out Cushing syndrome in pregnancy. It is a rare chromaffin tumor that secretes catecholamines.
Medical therapy is usually unsatisfactory. During It presents as hypertension which is paroxysmal but may
pregnancy, the etiology and the period of gestation, be sustained. Other symptoms may be headache, tremors,
determine the management. Adrenal surgery in the presence palpitations anxiety or seizures, chest pain, flushing
of tumor (adrenal, pituitary) in the 1st and 2nd trimester nausea or vomiting.
may be attempted. In the third trimester, drug therapy with Pheochromocytoma associated with pregnancy is
ketoconazole or metyrapone should be considered. uncommon, but when present, it is life-threatening for
both the mother and the baby.
Addison’s Disease/Primary Adrenal Insufficiency The diagnosis is made by 24 hr urinary catecholamine,
The disease results when at least 90% destruction of vanillylmandelic acid (VMA) or metanephrines. The
adrenal cortex has taken place and is very rare. The causes tumor should be localized by CT scan.
may be autoimmune, granulomatous lesions like TB, other As soon as the diagnosis is confirmed α-blockers
infections, bilateral adrenalectomy, metastatic tumors etc. should be started. Phenoxybenzamine 10 mg daily is used
Secondary adrenal insufficiency is the result of pituitary to control blood pressure, and it should be increased, as
insufficiency. per requirement.
The signs and symptoms include fatigue, pigmentation β-blockers may be added if palpitation is present or
and weight loss. A plasma cortisol level of less than tachycardia develops. Propranolol 10 mg 3 or 4 time a day
20 mg/L is consistent with Addison disease. is commonly used. Labetalol should not be used.
After 1–2 weeks of medical therapy the patient should be In symptomatic disease, surgery is indicated which
taken up for surgical removal of the tumor. Multispecialty should preferably be done in the second trimester. Medical
management of the patient is advised including care from therapy with oral phosphates is indicated only when the
an internist and a surgeon in addition to an obstetrician. patient is unfit for surgery.
Diseases of Parathyroid Gland There is an increase in perinatal morbidity and mortality.
1,25 dihydroxyvitamin D regulates calcium and phosphate During pregnancy, if a diagnosis is made proper treatment
metabolism in kidneys and its own synthesis is under the should be instituted. Surgery for an adenoma is indicated.
effect of parathyroid hormone (PTH). Serum PTH levels Neonatal tetany or seizures due to hypocalcemia may be
gradually increase during pregnancy, resulting in an the first indication of maternal hyperparathyroidism.
increased transfer of calcium to the fetus. Hypoparathyroidism needs to be differentiated from
Primary hyperparathyroidism is a rare condition. It pseudohypoparathyroidism in which PTH is normal but
may be caused by an insignificant parathyroid adenoma. end organs do not respond to PTH.
Symptoms in pregnancy are those of prolonged nausea of Symptoms are those of decreased serum ionized
vomiting, or abdominal pain. Serum calcium levels though
calcium level and increased neuromuscular irritability.
are diagnostic, but there may be physiological changes in
The most common cause is surgical removal of the
pregnancy. Levels more than 12 mg/dL are diagnostic of
hyperparathyroidism. gland during thyroidectomy or irradiation. Diagnosis is by
Management guidelines for primary hyperparathyroi persistent low calcium, and high phosphorus levels.
tism in pregnancy are not uniform. In an asymptomatic Treatment is with calcitriol (1,25 dihydroxyvitamin D)
patient with serum calcium below 11 mg/dL, conservative dihydrotachysters/large doses of vitamin D, calcium and
management and monitoring may be done. low dietary phosphates.
1. What are the classification of diabetes mellitus?
2. How to manage the pregnancy with diabetes mellitus?
i. ____________ should done to defect hypocalcemia, hypoglycemia and polycythemia.
ii. In ____________ antenatal steroids for fetal lung retortion and tocolysis can be prescribed.
iii. Self monitoring of blood sugar is ____________.
40
Banashree Das, HP Anand, Sudha Salhan
Hypertension in Pregnancy
Hypertension associated with pregnancy, whether it is The arm is at the level of heart
pre-existent or developed during pregnancy, is one of the The cuff of the instrument is of appropriate size for the
most common conditions encountered by obstetricians. arm. Length should be 1.5 times of circumference of
Hypertension increases both maternal and fetal mortality the arm. Average size available is 12.5–13 cm width and
and morbidity, as it virtually involves every organ and 35 cm in length
system in the body. The manometer should be at the level of the heart.
Korotkoff phase V (disappearance of sounds) is now

INCIDENCE universally accepted for measurement of diastolic pressure.
Incidence of hypertension in pregnancy varies from 5–10% Phase IV or muffling is to be considered only if sound are
worldwide. There is a widespread geographical variation. heard till 0 mmHg pereseure. The use of Korotkoff phase V
Incidence is higher in developing countries. reduces the intra and interobserver variations in the blood
Mortality from pre-eclampsia may be as high as 0.4% pressure measurement and is closer to the arterial pressure.
whereas in case of eclampsia it varies from 6.1% in develo
ping countries and about 1.8% in UK.
CLASSIFICATION OF HYPERTENSION
DEFINITION IN PREGNANCY
Hypertension in pregnancy is defined as systolic blood If a pregnant woman is found to be having an elevated
pressure measurement of more than or equal to 140 mmHg blood pressure, as per these criteria, she may be suffering
or diastolic blood pressure more than or equal to from one of the following 4 entities:
90 mmHg ,taken on two occasions, at least 4 hours apart, 1. Gestational hypertension
but within one week [American college of Obstetrician 2. Pre-eclampsia/eclampsia
and Gynecologist 2014 (ACOG 2014)]
3. Chronic hypertension
The previous diagnostic criteria—30 mmHg rise of
4. Pre-eclampsia superimposed on chronic hypertension.
systolic or 15 mmHg rise of diastolic from previous
reading are no longer recommended for the diagnosis
of hypertension in pregnancy but a close observation of Diagnostic Criteria of Gestational Hypertension
these patients is warranted. It is characterized by elevation of blood pressure alone
for the first time, after 20 weeks of pregnancy or in early
MEASUREMENT OF BLOOD PRESSURE puerperium. High blood pressure reverts back to normal
within twelve weeks of delivery. Sometimes final diagnosis
Special attention is necessary for measurement of blood
is possible only in postpartum period.
pressure of pregnant women. Posture of the woman is
an important consideration. The recommended position
is sitting position in the outpatient setting and lateral Pre-eclampsia and Eclampsia
recumbence, if more convenient, in a hospitalized gravida. A disorder which involves many systems of the body
Whatever the posture, care should be taken to see that: and occurs in pregnant women only. It is defined as
Hypertension in Pregnancy 399
elevation of blood pressure after 20 weeks of gestation the mother’s response to abnormal placentation.
associated with proteinuria or any of the severe feature, Abnormal placental development and placental damage
i.e. thrombocytopenia, impaired liver function, new due to diffuse microthrombosis is found to be the main
development of renal insufficiency, pulmonary edema cause of this disorder.
or new onset visual or cerebral disturbances. Patient with At present, following theories have been put forwarded
hydatidiform mole may develop pre-eclampsia before as the probable cause of pre-eclampsia:
20 weeks of gestation. When pre-eclampsia is associated Abnormal trophoblastic invasion of uterine vessels.
with tonic clonic convulsion it is called eclampsia. In pre-eclampsia, vascular changes of normal pregnancy
Diagnosis of pre-eclampsia is no longer dependent on is affected. Uterine vascular changes in normal pregnancy
the presence of proteinuria. If any of the severe features occur in the following order. The low pressure-placental
are present, even in absence of proteinura, then patient to bed spiral arteries are first invaded by cytotrophoblast
be treated as severe pre-eclampsia. and it breaks down the endothelial layer, internal elastic
Previously a classic triad of hypertension, proteinuria lamina and muscular coat by the end of the first trimester.
and edema was defined as pre-eclampsia. Now, it is They are then invaded by a secondary wave of endovas-
universally accepted that edema is a common finding in cular trophoblast beyond the deciduo-myometrial junc-
many normal pregnancies, and one-third of eclamptic tion. This destroys the smooth muscle wall of the arterioles
women (serious convulsive stage of pre-eclampsia) do not which changes the high pressure-low flow system to a low
have edema. So, the presence of edema is not a feature for pressure-high flow system to meet the needs of the fetus.
the diagnosis of pre-eclampsia. Nevertheless, generalized (Figs 40.1A and B). These changes are going on throughout
edema or sudden gain in weight of at least 5 lb in a week is pregnancy.
ominous. There is also a suggestion that interstitial cytotrophoblast
produces vasoactive mediators and they causes vascular
Chronic Hypertension dilatation before invasion of the spiral arteries by endo
When hypertension predates pregnancy, detected before vascular trophoblast.
20 weeks of pregnancy or persists beyond 84 days In pre-eclampsia, these changes are affected and only
(12 weeks) after delivery, is labelled as chronic hyper half to two-thirds of spiral arteries of the decidua undergo
tension. this physiological change of primary invasion and the
secondary wave is absent or is limited. All these lead to
Pre-eclampsia or Eclampsia Superimposed restricted blood flow through the placenta. It worsens
on Chronic Hypertension with increasing gestation as demand increases. Since, the
muscle coat of vessels is maintained, they remain sensitive
Pregnant women with pre-existent chronic hypertension
to vasomotor stimuli. Magnitude of defective invasion of
may develop pre-eclampsia and eclampsia. The diagnosis
spiral arteries is proportional to severity of pre-eclampsia.
should not be based solely on increase in blood pressure.
There is endothelial damage, insudation of plasma
The criteria include new onset or marked increase in
constituents into vessel walls, proliferation of myointimal
proteinuria, hyperuricemia and/or thrombocytopenia
cells. There is evidence of lipid accumulation in the
and convulsions in the case of eclampsia.
myointimal cells. All this reduces blood flow. Less blood
Out of these four entities chronic hypertension is a
coincidental finding while the other three entities are
peculiar to pregnancy and have a pregnancy-related cause.
Etiology
The exact cause of development of pre-eclampsia is
not known, but causes can be multifactorial. Delivery
of placenta leads to resolution of symptoms of pre-
eclampsia leading to the confirmation of the theory that
placenta plays an important role in pathophysiology of
its development. Exposure for the first time or excess
A B
exposure to chorionic villi is found to be associated with
development of hypertension in pregnancy. It represents Figs 40.1A and B: A. Normotension; B. Pre-eclampsia
flow causes infarcts, patchy necrosis of placenta. Placental necrosis factor (TNFa), interleukin (IL-6, IL-1a and IL-1b)],
hypoperfusion, is the starting point for tilting the balance lipid peroxides and reactive oxygen intermediates. All these
of prostanoid secretion towards a vasospastic state which are implicated for endothelial cell injury. Endothelial cell
leads to pre-eclampsia syndrome. damage is associated with microvascular coagulation and
increased capillary permeability. It may explain the fact
Immune Response Factor that pre-eclampsia is found more commonly in patients
According to this most recent theory, there is inadequate with pre-existing metabolic, renal, vascular disorders and
maternal antibody response to the fetal allograft causing connective tissue disorders.
vascular damage from circulating immune complexes. Various maternal system involved are central nervous
This is thought to be autoimmune in nature. Seminal system (CNS), hepatic, pulmonary, renal and hematological
vesicle derived transforming growth factor-1 (TGF-1) initi system. Endothelial damage may lead to pathological
ates an inflammatory reaction towards paternal antigens capillary leak which may present as rapid weight gain,
leading to maternal-fetal (paternal) immune maladapta- non-dependant edema and pulmonary edema. Placental
pathology leads to decreased uteroplacental circulation
tion. The primary defect is failure of transformation of
which in turn causes oligohydromnios, fetal growth
spiral arteries. Some combinations of fetal human leucko-
restriction, etc. The triggering factor is not certain, but it
cytes antigen-C (HLA-C) and maternal natural killer (NK)
may be due to the paternal or fetal genotype triggering the
cells receptor– killer immunoglobulin like receptors (KIR)
immunological response in pregnant women.
may result in inadequate trophoblastic invasion. Level of
helper T lymphocyte is found to be low in second trimester Nutritional Factors
in patients destined to develop pre-eclampsia. Previous Some studies have shown relationship between pre-
exposure to the placenta and fetal cells (paternal antigen) eclampsia and dietary deficiencies. Supplementation of
is protective. This theory is substantiated by the occurrence various micronutrients like zinc, magnesium and calcium
of hypertension in first pregnancies. It is postulated that a were found to decrease the incidence of pre-eclampsia.
long period of regular exposure to sperms of the husband There are few studies which reported that diet rich
(exposure before pregnancy) is protective. This theory is in fruits and vegetables which are good source of
justifies by the fact that the incidence of pre-eclampsia antioxidants, were found to reduce the incidence of pre-
and eclampsia is more in primigravida and cases of sperm eclampsia. However, role of diet is not proven.
donated pregnancies.
RISK FACTORS
Genetic Influence in Development of
Pre-eclampsia Various risk factors for development of hypertension in
pregnancy are as follows:
Antigenic imbalance found in pre-eclampsia may be
Age—pregnancy in extreme of ages, teenage pregnancy
influenced by genetic factor. Genetic etiology of pre-
or advanced maternal age (>35 years)
eclampsia gets its importance due to evidence that
Parity—nulliparous women
women with family history of pre-eclampsia in mother
History of hypertension during previous pregnancy or
and maternal grandmother are more susceptible to get
chronic hypertension
pre-eclampsia. Women with a fetus with trisomy 13 Family history of pre-eclampsia and eclampsia
found to have higher incidence of pre-eclampsia. Besides especially in first degree relative
maternal genotype, paternal genotype may also contribute Women born small for gestational age
in development of pre-eclampsia. Man who was born of a Multiple pregnancy (twins, etc.)
pregnancy complicated by pre-eclampsia is more likely to Associated gestational trophoblastic disease (hydati-
father, a pre-eclampsia pregnancy. diform mole, etc.)
Pregnancy following oocyte or sperm donation
Vasculopathy and Inflammatory Changes Diabetes mellitus
According to this theory, eclampsia is due to generalized Renal disease
vasculopathy. Imbalance between prostacyclin and Chronic hypertension
thromboxane leads to hypoperfusion of placenta. Placen Central obesity
tal hypoperfusion in turn lead to accumulation of nitric Congenital or acquired thrombophilia like anti
oxide, cellular fibronactin, inflammatory cytokines [tumor phospholipid syndrome

Collagen vascular disease of red cells, hyaline and granular casts in the urine. As the
Hyperthyroidism glomerular filtration decreases, it will cause oliguria (less
Low-socioeconomic status than 500 mL/24 hr) and may lead to acute tubular necrosis
Environmental factors. (rare).
PATHOPHYSIOLOGY Liver
Damage includes hemorrhage, periportal fibrin deposition
Pre-eclampsia is a multisystem disorder. Spectrum varies and areas of infarction and necrosis. These changes may
from very mild which may be unnoticeable to severe be secondary to vasospasm and intravascular coagulation,
changes that can be life threatening to both mother and endothelial damage and vasoconstriction. The liver
her fetus. It may affect maternal organ systems or fetal necrosis (centrilobular and mid-zonal portion of lobules)
systems or both. Various maternal system involved are is found in fatal cases of eclampsia thought to be due
CNS, hepatic, pulmonary, renal and hematological system. to hypoxia. Liver damage lead to release of enzymes
(transaminases and γ-glutamyl transferase) and plasma
CHANGES IN PLACENTA bilirubin are increased. Subcapsular hematoma (causing
stretching of Glisson’s capsule) and hepatic rupture
Currently genetic, immunological and inflammatory factors
(causing pain in shoulder tip) sometimes occur. Hepatic
alone or in combination are thought to be responsible for
dysfunction is an independent risk factor for maternal and
failure of secondary trophoblastic invasion, which initiates
fetal outcome HELLP (hemolysis elevated liver enzymes
spasm of uteroplacental vessels. This leads to intrauterine
low platelet count) syndrome has liver damage as one
growth restriction (IUGR), abruptio placentae, placental
component. Involvement of liver is found in only 10% of
infraction and premature delivery. Direct assessment of
patients with severe pre-eclampsia (mostty centrilobular
human maternal and placental blood flow is difficult to
and mid-zonal).
measure, but indirect assessment can be done by assessing
the blood flow by Doppler study. There is evidence of Brain
increase resistance to vascular flow on Doppler study in
Headache and visual disturbance is the most common
patients with pre-eclampsia.
symptoms of severe features of pre-eclampsia. The brain
has the capability of autoregulation of blood flow. However,
CHANGES IN MATERNAL SYSTEMS the level of autoregulation has individual variations. In
pre-eclampsia and eclampsia, autoregulation fails when
Kidneys blood pressure increases above a threshold level. In that
Due to reduced plasma volume, there is reduced renal case, the endothelial junctions open, thereby red blood
perfusion which leads to mild to moderately diminished cells and plasma leak into the extravascular space. This
glomerular filtration rate (GFR). This is evident by doubling causes cerebral edema, petechial hemorrhages, even
of plasma creatinine level over normal pregnancy. In gross intracranial bleeding or infarcts in the cortex and
severe cases, glomerular capillary endotheliosis develops subcortical areas. In eclampsia, the mechanism of brain
specific to pre-eclampsia. In this condition, the glomeruli damage is not clear. There may be coagulopathy, vasospasm
enlarge because of swelling and lipid vacuolation of and fibrinoid changes in the wall of the vessels. All these
glomerular capillary endothelium and mesangial cells. changes are widespread throughout the brain especially
The cytoplasm of endothelial cells of capillary loops may in the posterior hemisphere (visual disturbances) but
bulge into proximal tubules which reduces the lumen. unlike hypertensive encephalopathy the brainstem is not
This leads to reduced GFR. Thus, blood urea and serum much influenced. Gross hemorrhage due to rupture of
creatinine increase and there is proteinuria. The latter vessels is mostly seen in women with underlying chronic
may be because of loss of the strong negative charge that hypertension.
repels proteins from the glomerular basement membrane Computed tomography (CT) scans in eclampsia show
in normal pregnancies. Tubular dysfunction is seen as hypodense areas in the cortex which corresponds to
hyperuricemia due to increased reabsorption of uric petechial hemorrhage and infarction. Clinical symptoms
acid (coupled with tubular sodium reabsorption). Both and severity of symptoms depends on size and location of
glomerular and tubular damage is evident by the presence involvement. Extensive occipital lobe edema is evident in
CT and magnetic resonance imaging (MRI) in patient with high afterload causing pulmonary edema. There may
blindness following eclampsia. Diffuse arterial venous be scattered alveolar hemorrhages in the lungs. Various
constriction is seen in cerebral angiography in patients types of pneumonias, ranging from patchy pneumonitis to
suffering from eclampsia. adult respiratory distress syndrome (ARDS), may develop.
Pulmonary complication is one of the important causes of
Eye morbidity and even mortality in these women.
Retinal artery spasm is associated with visual disturbances. Aspiration of the stomach contents is most feared
Serious retinal detachment and cortical blindness can during eclamptic convulsion. This may lead to death
occur. This may be due to generalized vasoconstriction or from asphyxia (due to blockage of major airways by food
capillary leak. All changes slowly return to normal within particles) or lead to chemical pneumonia because of
6 weeks postpartum. Sudden blindness may occur in about hydrochloric acid (HCL) of the stomach.
half of the patients, but the usual visual disturbances seen
are scotoma and blurring of vision. GESTATIONAL HYPERTENSION
Cardiovascular System It is hypertension occurring after 20 weeks of pregnancy
(earlier in hydatidiform mole) without any other feature
Unlike normal pregnancy, where plasma volume is
of pre-eclampsia. Out of all spectrums of hypertension in
increased, in pre-eclampsia there is contracted plasma
volume and hemoconcentration. There is increase pregnancy, it is the mildest form. It is the most common
systemic vascular resistance, normal or reduced cardiac cause of hypertension in pregnancy. Its incidence ranges
output and higher cardiac after load. There is increased from 6–18% in nulliparous and 6–8% in multiparous
sensitivity to angiotensin-II (A-II) in women with pre- women. Patients with gestational hypertension, especially
eclampsia in contrast to normal pregnancy. There are when diagnosed at an earlier gestational age, are at
reduced levels of prostacyclin and nitric oxide. Both are an increased risk of developing severe hypertension,
consistent with epithelial damage and vasoconstriction pre-eclampsia and eclampsia. Woman who develops
and increased peripheral resistance. Central venous gestational hypertension in successive pregnancy is at
pressure and pulmonary wedge pressure are decreased. high-risk of developing chronic hypertension in the future.
Blood Coagulation Management

Pre-eclampsia and eclampsia patients mostly have a The goal of treatment of gestational hypertension is to
normal clotting process. The abnormalities found are eliminate the effect of hypertension on the mother and the
isolated thrombocytopenia (most common), increased fetus and to prolong pregnancy to prevent prematurity.
blood viscosity and hemoconcentration. Microangiopathic At the onset, patents should be reassessed to determine
hemolytic anemia and disseminated intravascular presence or absence of high risk factors for development
coagulation (DIC) may develop in severe cases. A low of pre-eclampsia. It is possible to prolong the pregnancy
thrombocyte level is the most common finding. Fibrinogen by conservative management with constant evaluation.
levels are elevated. Low levels of fibrinogen are seen in Patients with gestational hypertension are classified
abruptio placentae or intrauterine fetal death. Increased into two groups—mild and severe, depending on the
levels of fibrin split products are also seen in some. The blood pressure level.
balance between blood coagulation and fibrinolysis is
disturbed and there are changes in a number of clotting Mild Gestational Hypertension
factors. Factor VIII clotting activity is reduced, so there is Patient with blood pressure less than 160 systolic and
increased consumption of factor VIII in pre-eclampsia. less than 110 mmHg diastolic is grouped under mild
Plasma antithrombin III is decreased and is directly related gestational hypertension. This group of patients need
to the clinical severity of the condition. close supervision, as they may progress any time to severe
gestational hypertension, pre-eclampsia and eclampsia.
Respiratory System Management to be done by qualified obstetrician in a
Pulmonary edema may develop in some cases of pre- tertiary care center. If blood pressure is below 150/100
eclampsia and eclampsia. This is due to increased mmHg, patient can be treated as outpatient provided
capillary permeability and reduced oncotic pressure. patients is compliant and understand and follow all
If there is a severe rise in blood pressure there can be instruction diligently. Patients should be educated about
signs and symptoms of pre-eclampsia and should be When it is associated with tonic contraction of muscle it
asked to report immediately in case any symptoms of pre- is called eclampsia.
eclampsia evolve. Maternal evaluation should be done Pre-eclampsia used to be classified in to mild and
every week. Blood pressure measurement should be done severe depending on the severity. Recently, ACOG has
at home daily. ACOG task force (2013) recommends at recommended changing of this nomenclature to pre-
least twice weekly measurement of blood pressure. If Blood eclampsia without severe feature and pre-eclampsia
pressure is more than 150/100 mmHg, patient should be with severe features in view of the fact that it is a dynamic
put on antihypertensive treatment. (NICE guideline 2010). process. Mild disease may changes to severe any time.
Drug preferred is labetalol. Other drugs can be used are
methyldopa and nifedepin. Aim of treatment is to maintain Pre-eclampsia without Severe Feature
diastolic blood pressure between 80 and 90 and systolic New onset hypertension more than or equal to 140/90
blood pressure below 150 mmHg. Blood pressure should mmHg, but less than 160/110 mmHg after 20 weeks gesta-
be measured twice a day. Urine protein should be tested tion and proteinuria more than or equal to 300 mg/24 hour
daily. Weekly blood investigation for total count, kidney or 1+ by dipstick method and absence of severe features.
function test, and liver function test should be carried out.
In these patients, pregnancy can be allowed to continue Pre-eclampsia with Severe Features
till term, but should not allow beyond 40 weeks of gestation.
Blood pressure 160/110 mmHg or more with any of the
Patients should be assessed at 37 weeks and pregnancy
following features:
terminated if pelvic examination findings are favorable.
Thrombocytopenia (Platelet count less than 100,000/
Severe Gestational Hypertension mm3)

Impaired liver functions (elevated serum transaminases
When systolic blood pressure is more than or equal to
twice of normal value. Severe persistent right upper
160 mmHg and/or diastolic blood pressure is more than
quadrant or epigastric pain not responding to
or equal to 110 mmHg it is called severe gestational
medication and not explainable by any other diagnosis
hypertension. Patients with severe gestational hyper
or both)
tension should be admitted to the hospital and put on
Renal insufficiency (serum creatinine greater than
antihypertensive agents to control the blood pressure
1.1 mg/dL or doubling of previous value)
to safer levels. They need intensive monitoring. Blood
Pulmonary edema
pressure should be checked four times daily. Urine should
Cerebral or visual symptoms.
be examined for protein daily and blood investigation
According to this recommendation massive proteinuria
including platelet count, liver function test, and kidney
(>5 g/24 hours) is no longer used for consideration of
function test carried out weekly fundal examination done.
severe pre-eclampsia. Treatment should not be deferred
They should be closely monitored to detect any signs of
even if there is no massive proteinuria. Twenty percent of
onset of pre-eclampsia. The pregnancy is to be terminated
women who develop eclampsia may not have proteinuria.
at 34 weeks of gestation. (ACOG recommendation)
But in patient with massive proteinuria, one should
exclude signs of chronic renal disease such as nephrotic
PRE-ECLAMPSIA AND ECLAMPSIA syndrome, hyperlipidemia, diabetes nephropathy and
Pre-eclampsia is defined as hypertension (blood pressure lupus erythematosus. A follow-up after delivery for
more than or equal to 140/90 mmHg) and proteinuria proteinuria is very important. Fetal growth restriction is
(more than or equal to 300 mg/dL in 24 hours) or presence also no longer included in findings indicative of severe
of any severe features described below, after 20 weeks of pre-eclampsia.
pregnancy. Severe features of pre-eclampsia are:
Thrombocytopenia (platelet count less than 1,00000/mm )
3
Biochemical Abnormalities in Pre-eclampsia
Impaired liver functions (elevated serum transaminases
twice of normal value)

Renal Function
Renal insufficiency (serum creatinine greater than Uric acid is commonly elevated
1.1 mg/dL or doubling of previous value) Serum creatinine is rarely increased
Pulmonary edema More than 4.5 mg% of serum uric acid level is diagnostic
Cerebral or visual symptoms of pre-eclampsia.
Hepatic Function Maternal Complications

Transaminase level is commonly slightly elevated Accidental hemorrhage
In pre-eclampsia, bilirubin (mostly indirect) is some- Preterm labor
times increased, but jaundice is infrequent. Oliguria and anuria, renal failure
Eclampsia which can develop during pregnancy, during
Hematological Changes labor or during early puerperium
Hematocrit is raised due to hemoconcentration HELLP syndrome and hepatic rupture
Most frequently seen abnormality is thrombocytopenia Diminished vision and even blindness
Low fibrinogen level Cerebrovascular accident
Prothrombin time—should be evaluated. Increased operative delivery
Postpartum hemorrhage (PPH), which may be due to
Prediction of Pre-eclampsia atony of the uterus or coagulations failure
Numerous clinical tests has been done to establish a Hypovolemic shock occurs as there is already reduced
reliable method to predict pre-eclampsia but none of them intravascular volume and even slight loss of blood can
has been accepted as useful. Some important tests are: lead to shock
If average mean arterial pressure (MAP) in the second
Sepsis which is due to increased incidence of induction,
trimester is equal to or more than 85–90 mmHg
operative interference and low resistance
Rollover test at 28–32 weeks. This test was designed
DIC and its complications
to detect disorder of vascular responsiveness, which
Death.
occurs in pre-eclampsia. In this test blood pressure
is measured in the left lateral position and then again
Fetal Complications
in the supine position. A 20 mmHg or more rises in
diastolic pressure, when patient is placed in the supine Growth restriction
position is thought to predict pre-eclampsia Intrauterine asphyxia
Isometric exercise test done at 28–32 weeks Oligohydramnios
Angiotensin II infusion test at 26–28 weeks Placental infarction
Doppler velocimetry of uterine vessels at 24 weeks. Intrauterine death (IVD) due to varying degree of utero
Detection of diastolic notch at 24 weeks of pregnancy placental insuffiency. Intrauterine fetal death also may
predicts future development of pre-eclampsia be due to accidental hemorrhage. (Another common
Maternal serum uric acid level (higher level at 12 weeks complication of pre-eclampsia)
in cases who develop pre-eclampsia) Prematurity which is either due to spontaneous onset
Maternal serum alpha fetoprotein and β-human of labor or due to accidental hemorrhage or due to
chorionic gonadotropin (β-hCG) level increased in induction of labor (iatrogenic). There is 25% chance of
second trimester developing pre-eclampsia in next pregnancy.
Plasma fibronectin level increased
Urinary calcium excretion decreased

HELLP Syndrome (of Weinstein)
Sex hormone binding globulin (SHBG) decreased
It is a multisystem disease and a severe form of pre-
Increased level of lipid peroxidases. Homocysteine
level (elevated) eclampsia, in which women exhibit common laboratory

Serum level of placental peptide placental [PIGF (Phos-
markers for a syndrome of:
Hemolysis (H): Abnormal peripheral smear/ increased
phatidylinositol-glycan biosynthesis class F protein)
and SFLT1] in first trimester. Bilirubin level.
These tests alone or in combination may be of some use Elevated liver enzymes (EL): Serum transaminase > or
in women with known high risk factors for development of equal to 72 IU/L and increased lactic dehydrogenase
pre-eclampsia. However, best way to prevent complication 600 IU/L)
Low platelet count (LP): Platelets < 100,000/mm ).
3
of pre-eclampsia is to detect early and to manage efficiently.
Women with HELLP presents with variety of symptoms
Complications of Pre-eclampsia like malaise, epigastric or right upper quadrant pain
Various complications can occur in the mother and in the (90%), nausea and vomiting (50%). It usually develops in
fetus during pregnancy, during delivery and also in the the late second trimester or early third trimester. About
postpartum period. 20% of women with severe pre-eclampsia and eclampsia
may present with HELLP. It may be associated with wall and vulva. Serious symptoms may develop acutely
placental abruption, acute renal failure, subcapsular liver which include:
hematoma and even pulmonary edema. Recurrence Headache (usually frontal or occipital)
of HELLP syndrome in subsequent pregnancies is Epigastric pain or pain in right hypochondria

documented. As the presenting symptoms of these Blurring of vision or rarely sudden blindness
cases are usually non-obstetric, so the diagnosis may be Respiratory difficulty
delayed leading to a delay in treatment and increased Less urine output
maternal and fetal mortality. Therefore, a high index of Severe pain abdomen
suspicion should be maintained. Vaginal bleeding.
Differential Diagnosis of HELLP Syndrome Signs

Viral hepatitis General physical examination may reveal:
Gallbladder disease Edema of feet, abdominal wall and/or edema of vulva
Gastroenteritis or generalized edema
Kidney stones
Lungs: basal crepitation
Peptic ulcer
Increased blood pressure
Idiopathic thrombocytopenia
Obstetrical examination may reveal signs of IUGR, or
Thrombotic thrombocytopenic purpura
signs of accidental hemorrhage.
Hemolytic uremic syndrome
Acute glomerulonephritis
Management of Pre-eclampsia
Encephalopathy
Definitive treatment of pre-eclampsia is delivery of the
Acute fatty liver of pregnancy
fetus. Delivery time depends on:
Appendicitis
Severity of the disease
Pancreatitis.
Fetal maturity
Assessment and management of this syndrome is the
Maternal condition
same as in severe pre-eclampsia. Depending on severity,
Fetal condition
there are 3 classes of HELLP syndrome (Mississippi
Bishop score of the cervix.
classification)
1. Class 1: Below 50,000/mm platelet count. Aspartate Objectives in management of pre-eclampsia are:
transaminases (AST) or transaminases (ALT) >70 IU/L, Prevention of accidental hemorrhage, pulmonary
LDH >600 IU/L edema, renal failure, cardiovascular accidents in the

2. Class 2: Between 50,000 and 100,000/mm3 platelet mother
count. AST or ALT >70 IU/L, LDH >600 IU/L Prevention of eclampsia (as it is 10 times more lethal to
3. Class 3: Between 100,000 and 150,000/mm3 platelet the mother and dangerous for fetus and neonate)
count. AST or ALT >40 IU/L, LDH >600 IU/L Minimise maternal and neonatal morbidity.
They are useful in finding the rate of recovery, mother Management of patient with pre-eclampsia without
and fetal effect and requirement for plasmapheresis. severe feature.
Management should be in a tertiary care center with
Clinical Features of Pre-eclampsia neonatal care facility as patient may develop severe
Onset of this disease is insidious. Through in some cases features at any time. Management depends on the period
it may develop rapidly. It is more common in patients of gestation at the time of diagnosis.
with high risk factors as described above. Detailed history Period of gestation more than or equal to 37 weeks.
taking to identify high risk factors is important. Hospitalize the patient, evaluate thoroughly and
terminate the pregnancy if the cervix is favorable.
Symptoms Pregnancy should not be allowed to continue beyond
In early cases, there may not be any symptoms and 40 weeks.
diagnosed on routine antenatal examination. Patients Pregnancy is less than 37 weeks of gestation.
may complain of swelling of legs or tightening of ring in • Hospitalize the patient

the morning. In advanced cases, patient may complain • Advised to take rest, in the left lateral position. But
of excessive swelling of whole body including abdominal complete bed rest is not recommended
• Both maternal and fetal conditions to be monitored Fundal height and abdominal girth should be measured
carefully weekly.
• Salt restriction is not recommended. Ultrasonography (USG) scanning is done at least once
Once patient complete 37 weeks of gestation, delivery in every two weeks

rather than continued observation is suggested. (ACOG ) Nonstress test (NST) should be done twice weekly or
If there is no obstetrical indication for cesarean delivery, earlier, if necessary

patient to be allowed for vaginal delivery. If Bishop’s score Weekly estimation of biophysical profile may be neces-
is unfavorable pregnancy may be continued but should sary in selected cases.

not be allowed to go beyond 40 weeks. If the patient’s blood pressure remains stable and not
more than 100 mmHg diastolic and the patient does not
Monitoring of Maternal Condition in Hospitalized have any sign of worsening of the condition, then she can
Patients be discharged from the hospital. She should be advised to
Blood pressure monitoring should be done at least three take rest at home (not absolute bed rest) and to keep fetal
times daily. Antihypertensive treatment (described movement count. She should also be explained about other
later) to be started if BP is more than or equal to 150/100 symptoms of worsening of the condition (severe features of
mm HG. pre-eclampsia), i.e. persistent and severe headache, visual
Monitoring should be done for signs and symptoms of changes (changes in vision due to retinal detachment),
severe features of pre-eclampsia like headache, visual epigastrium pain (due to liver capsule stretch) vomiting,
disturbance, epigastric pain and decreased urine out- bleeding per vaginum (accidental hemorrhage), etc. and
put, signs of CNS irritability in the form of clonus and to report to the hospital at the earliest with any of these
exaggerated knee jerk. indication. Blood pressure recording should be done every
Maternal weight recording should be done twice alternate day. The patient is evaluated every week for
weekly. maternal and fetal wellbeing.
Total protein in 24 hours urine to be done. Quantification At any time during the monitoring, if the condition
need not be repeated. deteriorates and there is sign of severe features of pre-
Ophthalmic examination (examination of the fundus) eclampsia, the patient should be admitted and managed
should be done to exclude retinal changes (Table 40.1). accordingly.
Hemoglobin with platelet count, liver function tests, Management of patients with pre-eclampsia with severe
and kidney function tests should be done twice weekly. feature.
When blood pressure is more than or equal to 150/100 The patient is to be admitted. Definitive management
mmHg, then all these should be repeated thrice a week. of pre-eclampsia with severe feature is termination of
Routine antenatal investigations [blood group and Rh pregnancy. Whatever the period of gestation, termination
type, HbSAg, HIV, venereal disease research laboratory of pregnancy is advisable as the incidence of both maternal
(VDRL) Blood sugar], if not done before. and fetal complication are very high in these patients.
The retinal changes (hypertensive retinopathy) were Again management should be done in a tertiary care
graded according to Keith Wagener classification into 4 center, where multidisciplinary management with well-
grades (Table 40.1) equipped nursery facility is available.
Management of this group of patients needs a fine
Monitoring of Fetal Condition balancing of maternal and fetal wellbeing. Therefore, it
depends on the period of gestation at which severe pre-
The patient is advised to keep daily fetal movement
eclampsia is diagnosed and the fetal parameters at that time.
count
Before proceeding for delivery, blood pressure should
be controled by appropriate antihypertensive drugs.
TABLE 40.1: Hypertensive retinal changes
Prophylactic anticonvulsants should be started. Loading
Grade I Mild generalized arterial attenuation, particularly of dose of anticonvulsant may not be necessary unless the
small branches
patient has signs and symptoms of impending eclampsia.
Grade II More severe grade I + focal arteriolar attenuation
Stabilization and termination of pregnancy is advised
Grade III Grade II + hemorrhages, hard exudates, cotton wool as prolongation of pregnancy to achieve fetal maturity in
spots
this group of patients will markedly increase the maternal
Grade IV Grade III + optic disc swelling (papilledema).
morbidity and mortality.
Pregnancy More than or Equal to Ultrasound weekly for amniotic fluid volume (AFV)
34 weeks of Gestation Ultrasound with Doppler every two weeks for fetal
growth and wellbeing
Termination of pregnancy is the choice of treatment in
Watch for symptoms and signs of eclampsia.
all patients of pre-eclampsia with severe feature once
Indication for delivery of these patients will be:
pregnancy reached 34 completed weeks as fetal outcome
BP persistently more than or equal to 160/110 despite
is good and no need to increase maternal morbidity by
treatment
continuation of pregnancy. Give cortisone, stabilize blood
Urine output 500 mL or less per 24 hours
pressure and induce labor Serum creatinine increasing
Persistent severe headache or visual changes

Pregnancy Less than or 28 weeks of Gestation
Abnormal or progressively deteriorating LFTs, lactic
Termination of pregnancy is advised in this group of dehydrogenase (LDH) > 1000 IU/L
patients as continuation of pregnancy for prolonged Mother complaining of decreased fetal movements
period to achieve good fetal outcome highly increases On color Doppler there is reversed umbilical blood flow
maternal morbidity and mortality. In this case, also give Severe IUGR and oligohydramnios
cortisone, stabilize blood pressure and induce labor. Any signs of coagulation disorder
Abnormal NST—fetal condition nonreassuring

Pregnancy between 28 and Abruptio placentae
34 weeks of Gestation Pulmonary edema
Management of this group of patients is to be individualized Development of eclampsia
according to case and to be taken for termination or for HELLP syndrome
conservative management. Emphasis should be that Fetal death
termination of pregnancy is the only definitive treatment. Attainment of 34 weeks of gestation
Risk to the mother and to the fetus due to continuation of Preterm labor.
pregnancy should be explained. If conservative manage

ment is planned, the patient will need intensive maternal Prevention of Pre-eclampsia
and fetal care in a high dependency unit (HDU) of a There is no definite method to prevent or reduce the
tertiary care hospital. Corticosteroid injection should be incidence of pre-eclampsia as the etiology is not well
administered to enhance the lung maturity of the fetus known. The high-risk factors, e.g. obesity, family history,
which significantly benefits preterm newborn. Appropriate etc. may alert the obstetrician. A combination of clinical
antihypertensive treatment should be started. Prophylactic and biochemical markers are also of not much help.
anticonvulsant therapy should brgin. Monitoring of the The most helpful test is Doppler ultrasound to look for
patient should be more frequent but on the line described persisting uterine artery notching at 22 weeks of pregnancy.
in the monitoring of mild pre-eclampsia patients before Different workers have tried a number of methods to
37 weeks of pregnancy. For example, biophysical profile correct theoretical abnormalities. Some of these include
three times a week, weekly ultrasound with Doppler nutritional supplementation like antioxidants ( vitamin C
examination for fetal growth. and E), minerals like calcium, magnesium, zinc others like
Expectant management of pre-eclampsia with severe fish and evening primrose oil and low-dose aspirin.
Features—Less than 34 Weeks Some normal patients develop pre-eclampsia even
Rest in bed with regular antenatal care (within 0–28 days of last visit).
Blood pressure monitoring 6 hourly. Evaluate for signs Therefore, making the patient aware of adverse symptoms is
and symptom for impending eclampsia very important so that the patient may report immediately.
Measuring weight daily Continuous education of medical and midwifery staff is also
Examination of fundus of the eyes essential. It will help in early detection and prompt referral.
Drugs to control hypertension
Corticosteroid administration Role of Corticosteroids

Liver function test (LFT), renal function test (RFT), It is a safe and effective drug for preventing respiratory
hematological evaluations on alternate days distress syndrome. Maximum benefit is achieved when an
Daily fetal movement count appropriate dose is administered and the last dose is given
Daily NST at least 24 hours before delivery. The preferred choice of
corticosteroid is betamethasone 12 mg as soon as possible pressure in a gradual manner. Sudden hypotension will
and to be repeated 24 hours later. Only one course is lead to acute reduction of placental blood flow. The drug
advised. should reverse vasospasm induced by the hypertensive
Prophylactic anticonvulsant treatment is stared in pre- disease process. The duration of action should be less so
eclampsia with severe features. that the sudden hypotensive effect can be controled. It
Anticonvulsants are found to reduce the incidence should also reduce uterine vascular resistance (causing
of eclampsia when used prophylactically. The preferred increased uterine flow and hence increasing blood
anticonvulsant is magnesium sulfate. Prophylactic anti flow to the placenta and the fetus). However, there is no
convulsant should be started if patient is planned to such drug available at present. Most widely used drug
deliver within 24 hours or if patient is in labor and if it is is methyldopa. It is central acting, a-2 agonist. Safety of
diagnosed within 24 hours of delivery. It decreases cerebral this drug is well-tested as it is being used for last almost
vasospasm and ischemia reduces incidence of eclampsia. 40 years. Only drawback is that BP control is gradual, takes
6–8 hours. It is central acting sympathetic nervous system
Antihypertensive Treatment inhibitor. Peripherally acting agents like lebetalol, calcium
channel blocker are preferred for its rapid action. List of
An antihypertensive drug for treatment of blood pressure
the drugs commonly used and dose is given in Table 40.2.
is used when blood pressure is equal to or more than
In severe hypertension nitrotriglycerine drip is given
150/ 100 mmHg to prevent maternal vascular accident. The
under strict control.
goal of treatment is to reduce the diastolic blood pressure
to 90 mmHg. At that level, the risk of cerebrovascular Other Drug used Nitric Oxide Donor
accidents is very low. Women in the second trimester of Transdermal patch or sublingual isosorbide dinitrate
pregnancy, even with lower blood pressure need to be (ISDN)—200 mg over 24 hours daily till delivery, signifi-
treated because the magnitude and rate of increase is more cantly suppresses blood pressure, reduces pulsatility index
closely related to adverse events than the absolute level of in the uterine and the umbilical arteries. The amniotic
arterial pressure. Too much lowering of blood pressure is fluid pocket size is increased several fold after treatment.
also harmful as it reduces placental perfusion and increase
the incidence of IUGR and fetal demise. Intravenous (IV) Fluid
The ideal drug for the treatment of severe hypertension In patients of pre-eclampsia and eclampsia, the volume
should be one which acts quickly but reduces blood of IV fluid should be monitored carefully preferably
TABLE 40.2: Antihypertensive drug in pregnancy

Drugs (category) Dose and route Onset of action Maternal side effects Fetal side effects
Methyldopa 0.5 g to 2 g orally in 3–4 6–8 hours Decreased mental alertness Considered safe (category B)
divided doses gradual impaired sleep, depression
Labetalol 20 mg IV than 20–80 mg 5 min Flushing headache, nausea, Fetal and neonatal bradycardia and
every 20–30 min, total dose peak 30 min vomiting hypoglycemia
upto 300 mg or continuous Contraindicated in women
infusion of 1–2 mg/min with asthma and first degree
till desired effect or 300mg heart block
then switch to oral.
Orally 100 mg 8 hourly,
may increase to 800 mg/day
Nifedipine 5–10 mg orally, repeat after 10 mins Flushing, headache, Fetal safety not yet
30 mins if necessary, then 10– peak 30 min tachycardia, established
20 mg every 3–6 hours (not nausea and inhibition
to be given sublingually) of labor
Hydralazine 5 mg IV/IM, 5 mg every IV-5 min Nausea, vomiting, flushing, Decreased variability
20–40 min or continuous peak 30 min headache, CNS depression
infusion of 0.5–10 mg/hours
Orally 100 mg/day in 4
divided doses.
by a central venous line (CVP) line and output should Following delivery, the patient should be closely observed
be measured by an indwelling Foley’s catheter and for 24 hours and continue magnesium sulfate as eclampsia
monitoring hourly urine output. If CVP is >4 mmHg and can develop.
there is no pulmonary edema management is expectant
but a fluid challenge can be given. Ringer lactate solution Anesthesia in Severe Pre-eclampsia
is normally administered 100–125 mL/hour. Excess fluid Epidural, spinal, and combined epidural and spinal anes-
may lead in the mother to pulmonary edema and ARDS, thesia with meticulous attention to technique and volume
which may be fatal. expansion is preferred. Endotracheal intubations in gene
If the CVP is >8 mmHg, one should look for pulmonary ral anesthesia may be difficult because of the presence
edema (basal crepitation). If present, frusemide 20 mg IV is of laryngeal edema and may cause a sudden increase in
administered and if no response is seen 40 mg IV is given. blood pressure and tachycardia leading to cerebral com-
If there is still no response, despite volume expansion a plications.
dopamine infusion (1 mg/kg/min upto 5 mg/kg/min)
is given to enhance renal perfusion. Urea and creatinine Maternal and Perinatal Outcome
are to be monitored. In case of any deterioration, a in Pre-eclampsia
nephrologist is to be consulted.
Maternal and perinatal outcome depends on the time
Delivery is expedited, if coagulopathy complicates the
of onset of the disease, presence or absence of any other
situation. It is corrected by delivery and by administering
underlying disease like hypertension or kidney disease,
platelet concentrates and fresh frozen plasma.
fetal maturity and presence or absence of any fetal
Management of Labor in Patient with complication. In pre-eclampsia without severe feature near
Pre-eclampsia term, perinatal outcome is similar to those of normotensive
women. In patients of pre-eclampsia with severe features,
The most suitable route to expedite delivery depends on
perinatal outcome will be favorable, if disease develops
obstetric parameters.
after 34 weeks of gestation. The prognosis is worse, if disease
If the patient is in spontaneous labor, close monitoring
develops before 28 weeks of gestation.
of labor is necessary. If available, continuous electrical
After delivery, the antihypertensive treatment may
monitoring of the fetal heart and uterine activity should
need to be continued. Methyldopa should be stopped as it
be carried out. If necessary, augmentation of labor is done
by IV oxytocin. Oxytocin infusion by infusion pump is may cause psychological changes. Angiotensin-converting
preferable to IV drip to prevent fluid overload. enzyme(ACE) inhibitors can be used after delivery. Strict
Induction of labor when indicated is carried out by blood pressure monitoring should be continued for at least
cervical ripening by prostaglandin gel (PGE2 500 mg) 72 hours. The blood pressure may increase and eclampsia
followed by oxytocin infusion by infusion pump (if is known to develop in the first week after delivery,
available). There is no advantage of cesarean delivery over therefore, vigil is essential. Hypertension usually resolves
vaginal delivery. Termination of pregnancy is done by lower within 6 weeks postpartum.
segment cesarean section only for obstetric indication.
Application of forceps to cut short the second stage in Postnatal Assessment
case of vaginal delivery is unnecessary, but second stage The patient should be assessed for proteinuria and
should not be prolonged. hypertension 6 weeks after delivery and if it is still persists,
At delivery, blood loss may be more than normal. If should be evaluated for associated disease. The next
patient was on magnesium sulfate, it may further prevent pregnancy should be advised only if the patient’s renal
uterine contraction leading to increased blood loss. Due status and blood pressure return to normal. The patient
to the already contracted blood volume, patients with can be advised steroidal contraception and intrauterine
severe pre-eclampsia and eclampsia cannot tolerate contraceptive device (IUCD). Postpartum ligation should
even moderate blood loss. So, blood should always be be avoided as the risk of anesthesia and risk of other
grouped, cross matched and kept ready once the patient complications are high at that time. Interval sterilization
goes into labor. For prevention of PPH oxytocin 5-10 is advised when blood pressure revert back to normal.
units intramuscular (IM) should be used. Ergometrine The patient should be advised to report to the doctor or
preparations are avoided as it can worsen hypertension hospital as soon as she conceives again.
Recurrence: The risk of recurrence is high. Women who Cerebral hemorrhage and cerebral edema: May cause
develop pre-eclampsia early in pregnancy or had pre- irritation
eclampsia with severe features, or had underlying disease Cerebral dysrhythmia: Due to hypoxia and edema
(chronic hypertension, renal disease, etc.) and where there DIC in cerebral microcirculation. The level of blood pres-
is fetal contribution (multiple pregnancy or hydatidiform sure does not correlate with the development of seizures.
mole) in previous pregnancy on development of pre- Eclamptic convulsions are not due to hypertensive ence
eclampsia, these patients have more chance of recurrence phalopathy as they are not commonly associated with
in subsequent pregnancies. retinal hemorrhage, exudates and papilledema.
ECLAMPSIA Clinical Presentations

History
Eclampsia is defined as the occurrence of tonic, clonic
convulsions or coma in patients with pre-eclampsia, which Patient is most commonly young primigravida with pre-
is not attributable to any cause other than pregnancy. There eclampsia presents with convulsions. Characteristic
is functional derangement of multiple organ systems. of convulsion are very specific. Convulsive movement
The degree derangement depends on medical factors, usually starts as—(a) facial twisting which lasts for few
obstetric factors and the time taken to treat eclampsia. seconds, (b) This is followed by generalized body muscle
Blood pressure may be only slightly elevated above the contraction making the whole body rigid. This phase lasts
non-pregnant values. Proteinuria (> 2+ on dipstick) may for 15–20 seconds, (c) This is followed by sudden violent
or may not be present. opening and closing of jaws which often lead to biting of
It is one of the few conditions with a very high maternal tongue, (d) Following this, there is an alternate contraction
and the neonatal mortality, if not treated promptly. and relaxation of all muscle in rapid succession for about a
Depending on time of onset of the disease in relation to minute. Gradually, these movement become less frequent
stages of pregnancy, it can be classified into: and patient become listless for moments and (e) During
Antepartum (50%): Seizure occurs before the onset of
all these period, respiration is halted. As convulsion stops,
labor patient takes a long deep inhalation and breathing starts
Intrapartum (30%): Seizure occurs for the first time
again. Around 80% cases of eclampsia have prodromal
during labor signs in the form of:
Postpartum (20%): Seizure occurs for the first time Severe and persistent headache (in about 80% of cases)
in puerperium usually within 48 hours of delivery. A Epigastric or right upper quadrant pain (in roughly 20%
seizure occurring beyond 7 days reasonably rules out cases)

eclampsia. Photophobia or blurred vision (in around 40–50% cases).
Hyperactive deep tendon reflexes.
Atypical Eclampsia Delay may lead to multiple organ dysfunction which is

Eclampsia occurring before 20th week of gestation or often fatal. On examination high blood pressure is recorded
more than 48 hours postpartum is exceedingly rare and in most of the patient. Proteinuria (>2+ on dipstick) may
is known as atypical eclampsia. Incidence varies, largely or may not be present. Generalized edema is seen only in
depends on availability of antenatal care: about 20% cases of eclampsia.
1 in 1000 in developing countries Differential diagnosis: Since eclampsia shows a wide
1 in 2000 in developed countries. variety of signs and symptoms it sometimes needs to be

Risk factors are the same as for gestational hypertension differentiated from the following conditions:
and pre-eclampsia. • Cerebrovascular accident (e.g. hemorrhage or
thrombosis)
Causes of Convulsions • Epilepsy (mostly normotensive)
A number of mechanism for the onset of convulsions have • Hypertensive disorders (e.g. hypertensive encephal-
been postulated. The main ones are as follows: opathy, rarely pheochromocytoma)
Hypoxia: Spasm of cerebral vessels due to hypertension • Infections (e.g. meningitis, encephalitis)
– Increased vascular resistance—fall in oxygen supply – • Metabolic diseases (e.g. hypoglycemia, water intoxi-
hypoxia cation)
• Thrombotic thrombocytopenic purpura The patient is placed in the left lateral position
• Hysteria Side supports of the bed should be there to prevent the
• Poisoning. patient from falling
Mouth gag or padded tongue blade is inserted to
Laboratory Findings prevent biting of the tongue
Investigations required are hemoglobin, platelet count, Secretions are removed by suction
coagulation profile, LFT, kidney function test (KFT), CT Oxygen is given by a face mask
and MRI scans are optional. An IV access is established
Hematological and biochemical abnormality expected Monitor heart rate, blood pressure, respiratory rate half
are same as that of pre-eclampsia with severe features. Due hourly

to hemoconcentration, the hemoglobin level increases. Monitor the fetal heart rate
The platelet count is usually normal or low. Only if treat- The patient is catheterized by indwelling catheter to
ment is delayed or accidental hemorrhage occurs than monitor hourly urine output
coagulation abnormalities may be present. Derangement A complete examination is done after convulsion is
of liver functions is more frequent in patients who com- controled.

plain of pain in the upper abdomen. There is an increase Once the patient is stable labor is induced because
in serum transaminases, LDHs and sometimes bilirubin, delivery is the only treatment of eclampsia. Oxytocin can
but jaundice is an infrequent finding. HELLP syndrome of be used in all patients preferably by an infusion pump.
Weinstein is seen in about one-tenth of eclamptic patients. Management outline is shown in Flowchart 40.1.
Cerebral abnormalities are seen only on postmortem
examination of eclamptic patients. Electroencephalo Control of Convulsions
graphy (EEG) changes are similar to those seen in hypoxia. Simultaneously, anticonvulsant drugs are administered
A CT scan can be done. MRI is useful only to differentiate by another doctor or nurse. Most preferred drug used is
from other cause of convulsions. There are no permanent magnesium sulfate. Other two drugs used are phenytoin
or long-term neurologic defects. and diazepam.
Management Magnesium Sulfate (MgSO4)

Prevention: Appropriate antenatal supervision and prompt It has combined action as a vasodilator and a membrane
treatment of pre-eclampsia can prevent majority cases of stabilizer. The first dose should be given immediately
eclampsia. However, all cases still cannot be prevented. even at the primary health care facility without worrying
Prompt diagnosis and management is essential to about toxicity. The patient is then transferred to a better
prevent maternal and perinatal mortality and serious facility with provision of cesarean section and a neonatal
morbidity. Management of eclamptic convulsion requires nursery. Care should be taken that patient is stabilized
emergency measures. The principles of treatment are to before transfer and a skilled person should accompany
Keep the airway clear and maintain vitals of the patient the patient to prevent hypoxia and to prevent aspiration
Avoid injury—(1) Bed side rails, (2) Tongue blade and while transferring. Many lives can be saved by this simple
(3) Physical restraints intervention especially in developing countries like India.
Avoid aspiration by keeping in lateral position Mechanism of action: The exact mechanism of action
Control convulsions is not known yet. It is found to have a peripheral action

Treat hypertension at the neuromuscular junction. It does not cross the
Monitor to prevent hypoxia blood-brain barrier, but it does relax cerebral vessels
Maintain fluid balance in eclampsia. It does not cause maternal or neonatal
Deliver the women safely as soon as possible sedation. Eclampsia trial collaboration group has amply
Prevent recurrence of convulsions demonstrated the superiority of magnesium sulfate
Treat the complications. over diazepam and phenytoin (which are considered the
The immediate treatment should be started to prevent second line drugs for treatment of convulsion). It is found
maternal injury, maintain adequate oxygenation and mini to be safe and effective. At present, World over magnesium
mization of the risk aspiration. Patient should be treated in sulfate is the drug of choice for treatment of eclampsia. It
an environment where there is no or very minimum noise. can be given by one of the following protocols.
Flowchart 40.1: Management of eclampsia
Abbreviations: ARM—Artificial rupture of membranes; CS—Cesarean section
Pritchard regimen: Magnesium sulfate 4 g, as 20 mL If possible, serum level of magnesium should be moni-
of 20% solution given IV slowly over 3–4 minutes, tored.
immediately, followed by IM injection of 5 g MgSO4, Antidote for magnesium toxicity is calcium gluconate.
as 10 mL of 50% solution given in each buttock (total Ten percent calcium gluconate, 10 mL slow IV (1 g)
14 gms). Followed by—5 g IM in alternate buttock 4 should be given over 3 minutes. If respiratory difficulty
hourly. 10 mL Im injections is very painful, give it with develops mechanical ventilatory support should be
local xylocaine. Injection should be continued for 24 provided. In case of recurrent seizures—2 g magnesium
hours after delivery. sulfate can be repeated IV.
After first administration and before giving next dose of If seizures continue unabated—intubation may be
drug following monitoring is required to avoid magnesium necessary. Further seizures are managed by muscle
toxicity. relaxant and intermittent positive pressure ventilation
Knee jerk (should be present) with the help of anesthetists.
Urine output (> 100 mL in 4 hours) Zuspan regimen: In this regimen, loading dose of 4 g
Respiratory rate (> 16/min). magnesium of IV is followed by IV infusion of 1 g/hour.

Therapeutic level of magnesium sulfate is 4–7 mEq/L It is to be continued till 24 hours after delivery.
Depression of patellar reflex is earliest sign of magne Sibai regimen: Magnesium sulfate 6 g IV is followed by
sium toxicity. Respiratory depression correlate with serum 1 g/hour infusion. This also needs to be continued for
level of 10–12 mg/L. Cardiac arrest occurs at serum level 24 hours after the last seizure.
of 30–35 mg/L. The patient may complain of double vision Dhaka regimen: Keeping in mind that Southeast Asian
and slurred speech. women have smaller body , this regimen was introduced
with lower dose. This should prevent magnesium and left ventricular failure. Crystalloids provide the
toxicity. In this regimen loading dose is 10 g slow IV in mainstay of management. IV fluids should be given at
contrast to 14 g of Pritchard regimen. This is followed by rate of 1 mL/kg/hour or can be calculated as the previ-
2.5 g IM 4 hourly for 24 hours after delivery. ous hours urine output + 30 mL.
IV magnesium sulfate injection has the drawback of
uneven absorption due to vasospasm and also may lead to Complication
gluteal abscess. IV injection has the advantage of uniform Due to convulsions—injuries, e.g. tongue bite, fall from
absorption but need very strict monitoring. Preferably it bed
should be infused with infusion pump. • Aspiration of vomitus
Antihypertensive nifedepine should not be combined • Exhaustion
with magnesium sulfate. If unavoidable than should be given Acute left ventricular failure—due to hypoxia and
under careful vigilance as it causes sudden hypotension. severe hypertension
Pulmonary edema/embolism
Phenytoin Pneumonia
It is normally used as second line treatment and it is pre Anuria
ferable in patients where diagnosis is in doubt. It inhibits Postpartum shock—dehydration and ketoacidosis
spread of abnormal activity from seizure foci to the motor Hepatic necrosis
cortex. The loading dose is 15–25 mg/kg IV. Psychosis
In general, the dose used is 1 gm IV loading dose diluted Peripheral sepsis
in 200 mL of normal saline given by slow infusion over 20 min Eye complications
followed by 100 mg 6 hourly. Common side effects are— DIC
cardiac toxicity, nystagmus, hypotension, ataxia and lethargy Renal failure
Diazepam (Lean Regimen): This drug is not preferred ARDS
because it causes lethargy and apnea of newborn. Dose Death.
regimen is as follows. A loading dose of 10 mg IV over
2 min is followed by IV infusion of 40 mg in 500 mL Prognosis
normal saline for 24 hours. During the next 24 hours—20 Prompt diagnosis and treatment may help the mother, but
mg of diazepam is infused in 500 mL of normal saline. fetal prognosis is often grim.
Krishna Menon Regimen (Lytic Cocktail Regimen): Maternal prognosis is ominous if
This regimen was popular about three decades back. Long interval between the onset of fit and commence-
Now it is obsolete. Combination of chlorpromazine, ment of treatment

promethazine and pethidine was used in that regimen. Antepartum eclampsia with long delivery interval
Number of seizures more than 10

Antihypertensive Therapy Coma because of convulsions
The addition of antihypertensive treatment is to lower the Uncontroled severe hypertension
BP to avoid cerebrovascular accident. Aim of treatment is Associated hyperpyrexia
to maintain diastolic blood pressure between 90 and 105 Oliguria
mmHg and MAP between 105 and 125 mmHg. Preferred Non-response to treatment
first line antihypertensive drug is Labetalol or nifedipine Jaundice.
because of its rapid action. Remote effect: Recurrence is 30%.

Postnatal management: Patient should be closely
monitored for at least till 24 hours of delivery, because Fetal Prognosis

convulsions are sometimes precipitated. ACE inhibitors Perinatal mortality is very high (30–50%) due to prema-
can be introduced as antihypertensives postpartum, turity and intrauterine hypoxia. Morbidity is also high due
as they are not contraindicated in breastfeeding. As to effects of drugs used in eclampsia and due to trauma
mentioned earlier, avoid methyldopa because it may during operative delivery.
cause depression, magnesium sulfate is continued for The patient is followed-up until normal BP is achieved.
at least 24 hours after the last seizure. If normal BP is not achieved even 6 weeks postpartum, the
Fluid management: Careful input/output charting patient should be investigated for an underlying cause or
should be maintained to prevent pulmonary edema for essential hypertension.
–– SLE
CHRONIC HYPERTENSION WITH –– Polyarteritis nodosa
PREGNANCY –– Polycystic kidney disease
–– Renal artery stenosis
Diagnosis –– Chronic renal failure on dialysis
It is the hypertension that predates pregnancy or persists –– Renal transplant
beyond 42 days after delivery. It is to be differentiated from • Gross increase in BMR
pre-eclampsia (Table 40.3). Most of the cases diagnosis is • Endocrine disease
made by the fact that hypertension is detected before 20 –– Cushing’s disease and syndrome
weeks of gestation (when pregnancy is not complicated by –– Primary hyperaldosteronism
hydatidiform mole or nonimmune hydrops fetalis). Other –– Thyrotoxicosis
findings suggestive of chronic hypertension are: –– Pheochromocytoma
Retinal changes found on fundus examination –– Acromegaly
Evidence of cardiac enlargement • Coarctation of the aorta.
Evidence of renal disease Depending on the degree of rise in blood pressure, chronic
Associated medical disorder like systemic lupus erythe- hypertension is divided to mild and severe. The criteria for
matosis (SLE), pheochromocytoma, scleroderma, peri- this classification are the same as in pre-eclampsia.
arteritis nodosa, etc.
Evaluation of Patient
Classification of Chronic Hypertension Evaluation of a patient with chronic hypertension with
Chronic hypertension associated with pregnancy may be pregnancy includes a thorough history and a complete
Primary hypertension or essential hypertension: This examination to find the presence or absence of and status
is most common. In these patients, no other cause of of the associated disease if present. In the childbearing
hypertension can be found. age, cardiac, cerebrovascular or renal complications are
Secondary hypertension: When there is some under unusual. Nevertheless, one should always look for these
lying pathology which is the cause of hypertension, than complications, as they cause very high maternal and fetal
it is labelled as secondary hypertension. Most common mortality and morbidity.
causes are:
• Renal disease Laboratory Investigation
–– Acute and chronic glomerulonephritis (including Laboratory investigation are required to establish the
diabetic) presence or absence of other associated causes of hyper-
TABLE 40.3: Difference between pre-eclampsia and chronic hypertension

Pre-eclampsia Chronic hypertension
Age Extremes of reproductive age Mostly older women
Parity Usually nulliparous Usually multiparous women
Period of gestation Rarely before 20 weeks Before 20 weeks of gestation
History Negative Positive, often history of hypertension in previous pregnancy
Cardiac status Usually normal Ventricular hypertrophy, if disease is long standing
Deep tendon reflexes Hyperactive Normal
Hemoglobin/Hematocrit Increased value support diagnosis Unchanged
Platelet count Decreased count Unchanged
Serum creatinine Abnormal or rising levels, suggest May be elevated in long standing cases
severe pre-eclampsia
Proteinuria Increased Absent or minimum in essential hypertension
Uric acid Frequently elevated Often normal
Liver function Pain and tenderness in right upper Normal
quadrant/elevated liver enzymes
tension. Urine analysis, serum creatinine, potassium and Methyldopa: It is the drug of choice for the treatment of
calcium levels, baseline determination of platelet count chronic hypertension in pregnancy. Safety for mother
and uric acid are done as changes in these parameters and fetus (after first trimester) is well documented.
may be helpful in distinguishing between superimposed Dose is 500–2000 mg in divided doses. The drug is
pre-eclampsia and exacerbation of chronic hypertension. tolerated better when started in lower doses. Onset of
Based on initial assessment patients are divided into; action is within 6 hours and the full effect is seen in
low-risk chronic hypertension and high-risk chronic 2–3 days.
hypertension. Labetalol: It is a mixed antagonist (alpha-1 and non
selective beta-receptor antagonist). Its sympatho-

Management mimetic activity is largely confined to beta 2-adrenergic
The primary objective of treatment is to decrease maternal receptor. The onset of action is within 2–4 hours. The
and perinatal morbidity and mortality. Pre-conception dose 200–1200 mg in 2–3 divided doses. It can be started
counseling and evaluation is very important. The patient as orally. Efficacy and short-term safety appears equal
should be counseled before pregnancy regarding potential to that of methyldopa.
risk of pregnancy with chronic hypertension and the effect Beta-adrenergic-receptor inhibitors: Used preferable
of antihypertensive treatment on the fetus. They should only in the third trimester. These agents cross the pla-
be also counseled regarding the need for close antenatal cental barrier. The dose depends on specific agent used.
monitoring in a well-equipped center. Atenolol should not be used for a prolonged duration
In mild chronic hypertension patients, one may be able because it causes IUGR. Atenolol is given 50–100 mg/
to reduce the dose, or to stop the drugs before conception daily. The duration of action is more than 24 hours. It
and also during the first trimester. In women with severe also may cause fetal bradycardia and impaired fetal
hypertension, who are already on ACE inhibitor or ANG II response to hypoxia. These drugs are to be used only if
other drugs fail to control blood pressure.
receptor blockers, the drug has to be changed.
Nifedipine: It is a calcium channel blocker. It is more
Uncomplicated low-risk patients will have good
extensively used for treatment of acute hypertension.
perinatal outcome. In this group, start antihypertensive
Its dose varies from 30–120 mg in 4 divided doses
treatment if BP exceeds 150 mmHg systolic and 100 mmHg
depending of the preparation used. It can inhibit labor
diastolic. We need to keep diastolic BP below 100 mmHg.
and may have synergistic effect with magnesium sulfate.
The pregnancy is allowed to continue till term. If chronic
Hydralazine: Its main action is that of a vasodilator.
hypertension is superimposed on eclampsia or there are
This drug is also most commonly used for treatment of
signs of the development of fetal growth restriction, these
acute hypertension. The dose varies from 50–100 mg
patients are treated as cases of pre-eclampsia.
in 2–4 divided doses. When given orally, it is weak
Patient with chronic hypertension in pregnancy with antihypertensives and has to be given with other
high-risk factors like elderly, known hypertensive for antihypertensives like methyldopa or beta blocker.
more than 15 years, severe hypertension, renal disease, No serious side effects are documented. Neonatal
cardiomyopathy, coarctation of aorta and previous preg thrombocytopenia may occur.
nancy with perinatal loss, etc. should be hospitalized Diuretics and sodium restriction: Diuretics are only
for evaluation. Antihypertensive drugs are continued to recommended in cases with pulmonary edema and/
keep the systolic blood pressure between 140 and 160 or left ventricular failure. Sodium restriction is also not
mmHg and diastolic blood pressure between 90 and 100 recommended because of adverse effects reported.
mmHg. Early and frequent prenatal care is important Effect of chronic hypertension on mother and the
and the patient may need multiple hospitalizations. Fetal fetus: Maternal complications include cerebrovascular
evaluation should be started at 28 weeks of gestation. accident, deterioration of renal function, congestive
Superimposed pre-eclampsia is an indication of hospital heart failure, and hemorrhage secondary to placental
admission. Chronic hypertension patient associated with abruption. Fetal and neonatal complications include
superimposed pre-eclampsia with severe feature should IUGR, prematurity and perinatal mortality.
be treated as patient of pre-eclampsia with severe feature. These complications are very low in patients with mild
Following are the drug used in cases of chronic hyper uncomplicated disease. Maternal and perinatal complica-
tension. tions are mostly seen in patients with severe secondary
hypertension and in patients with superimposed hyper- Management of Pregnant Women with
tension. Secondary Causes of Hypertension
Chronic Hypertension with Superimposed Though the incidence is very low, it is important to
recognize those patients. The management depends on
Pre-eclampsia individual cases. Pheochromocytoma is associated with
Chronic hypertension with superimposed pre-eclampsia 50% maternal mortality if not recognized before the onset
is diagnosed on the basis of exacerbation of hyperte- of labor. Coarctation of aorta is accompanied by increased
nsion (systolic >30 mmHg or diastolic >15 mmHg) risk of aortic dissection or rupture during pregnancy.
and development of other signs and symptoms of pre- In case of renal vascular hypertension, management
eclampsia. If the patient is on antihypertensive medication, depends on the level of maternal hypertension and
then elevation of blood pressure is less. In such cases renal function rather than the actual lesion. If markedly
diagnosis will be based on new onset proteinuria and elevated blood pressure is present in the first trimester,
abnormal laboratory tests or symptoms of pre-eclampsia. then therapeutic termination may be recommended. In
Management of patients with superimposed pre-eclampsia women, where pregnancy is continued, drug therapy is
will be similar to that of patients with pre-eclampsia as the treatment of choice. If hypertension is unresponsive,
discussed earlier. balloon angioplasty of renal artery stenosis may be done.
1. Name the classification of hypertension in pregnancy?
2. What is the full form of HELLP syndrome?
3. What are the changes in maternal status in eyes?
i. Patients with gestational hypertension are classified into two groups ____________ and ____________.
ii. Normal range of blood pressure is ____________.
iii. Chronic hypertension associated with pregnancy may be ____________ or ____________.
4. True/False
i. Methyldopa is the drug of choice for treatment of chronic hypertension in pregnancy.
ii. The patient should not be assessed for proteinuria and hypertension 6 weeks after delivery.
41
Sudha Salhan
Renal Disorders
Complicating Pregnancy
INTRODUCTION URINARY INFECTIONS AND

Anatomical changes, like increased capacity of the dilated ASYMPTOMATIC BACTERIURIA
renal collecting system (physiologic hydronephrosis of Urinary infection in pregnancy is easily acquired due to the
pregnancy) are seen more on the right side. Inhibition of above mentioned changes in urinary tract. The incidence
ureteral peristalsis and mechanical obstruction (by the is greater in the low socioeconomic group, patient with
gravid uterus) are also known to occur during pregnancy. diabetes or sickle cell trait or disease. If untreated, it can
progress to pyelonephritis in about 30% of cases.
Small muscle relaxation due to progesterone contributes
Half of the women with bacteriuria (more than 10,000
to an increased incidence of vesicoureteral reflux. There organism/mL of urine) do not have any symptoms
is 75% increase in renal blood flow by second trimester. (asymptomatic bacteriuria). Hence, screening by urine
Glomerular filtration is increased by 50%. Serum culture and microscopy atleast on the first visit is essential,
creatinine and blood urea nitrogen levels are decreased. as there are chances of fetal and maternal morbidity.
Plasma osmolarity is decreased due to a low concentration Urinary infections even if asymptomatic, should be treated
of sodium because of increased glomerular filtration rate according to the sensitivity of the organism for 10–14 days.
(GFR). Some glucosuria and aminoaciduria also aids Urine culture is repeated after 1 week of completion of
bacterial growth. Pregnancy may also induce polyuria and therapy to detect recurrence.
stress incontinence.
These changes predispose pregnant women to urinary
CYSTITIS AND PYELONEPHRITIS
tract stasis and infection. Besides, with the improvement Cystitis is easier to eradicate and has a lower recurrence
of medical care, women having renal disease, diabetes rate than asymptomatic bacteriuria. Culture of the
urine is done in all gravidas on the first antenatal unit.
mellitus and hypertension become pregnant. Women with
Pyelonephritis is usually caused by aerobic bacteria.
renal transplantation also conceive and need extra care Treatment with appropriate antibiotic for 7–10 days is
during the antenatal, natal and postnatal period. Renal essential. The tolerance of the body to these infections
disease can become a significant risk factor for adverse is decreased in pregnancy. Hence, patients with acute
pregnancy outcome (miscarriage, preterm labor). pyelonephritis in pregnancy are more prone to shock,
Pregnancy may have a deleterious effect on pre- respiratory distress syndrome and various liver function
existing renal ailments . Urinary infection can even lead to and hemolytic abnormalities. In the fetus, there may be a
septicemia in pregnancy. Hence, preconceptional check- higher incidence of congenital abnormalities, miscarriages
premature birth, fetal growth restriction and intrauterine
up is very important before embarking on the pregnancy.
fetal demise. There may be marked decrease in GFR
A complete urine check-up, to exclude and if present treat,
though recovery is common. The patient is admitted in the
asymptomatic bacteriuria may go a long way in preventing hospital. Hydration and appropriate antibiotics are given
maternal morbidity (pyelonephritis) and prematurity. for 3–5 weeks with suppressive treatment for 6 months or
Common urinary diseases in pregnancy are discussed close surveillance by repeated urine cultures. These cases
below. may be investigated after delivery too.
If 24 hours urinary excretion of proteins is greater than sparing the medulla. It is seen in late pregnancy, mostly
2 gm, it is suggestive of a glomerular damage. Tubular after abruption and pre-eclampsia. It can rarely be seen
damage causes less proteinuria. Hematuria greater than with prolonged intrauterine death (IUD) too.
one or two red blood cells (RBCs) per high power field There is prolonged and selective renal vasospasm.
of urine sediment is due to an organic cause; strenous Some of the patients are elderly who may have pre-existing
exercise and acute febrile illness may be the culprit. nephrosclerosis. Amniotic fluid embolism may be a cause.
Presence of proteinuria, red cell casts or dysmorphic RBC The anuria lasts longer than in ATN. These changes are
(irregularly shaped) points to glomerulonephritis. Pre- more easily produced in pregnant women. Acute fatty
eclampsia does not produce hematuria. Hence, a patient
liver of pregnancy can cause nausea and vomiting causing
of pre-eclampsia who develops hematuria is probably
anuria. Dialysis is rarely needed.
suffering from renal pathology. If glomerulonephritis is
Idiopathic postpartum renal failure is seen after
progressing, renal biopsy is indicated. Otherwise biopsy is
an uneventful gestation. Its onset is between day one and
postponed to postpartum period.
several weeks after delivery. There is oliguria which may
lead to anuria and azotemia and consumptive coagulo
ACUTE RENAL FAILURE
pathy. Peripheral blood smear shows schistocytes and
Acute renal failure (ARF) is not common. There is a burr cells.
sudden decrease in renal function with oliguria over Extra renal manifestations include cardiac dilatation,
a period of hours or days. Non-oliguric ARF can also congestive heart failure (CHF), lethargy and convulsions
occur. The plasma creatinine level rises by atleast central nervous system (CNS). The cause is not known but
0.5 mg/dL/day and urine output is below 400 mL/24 hours.
some hypothesis are put forward:
This condition may need dialysis.
Retained placental fragments
In pregnancy, it can be due to acute tubular necrosis
An antecedent urinary infection
(ATN), renal cortical necrosis or postpartum ARF. Renal
Drugs like ergotamine, oxytocic agents
failure can be prerenal (hypoperfusion) renal (parenchy-
Hypocomplementemia is seen in some suggesting an
mal disease and nephrotoxins) and post-renal (obstructive
uropathy). immune mechanism
Deficient prostaglandin production
ACUTE TUBULAR NECROSIS Decreased antithrombin III level
Deficiency of endothelial derived relaxing factor

In pregnancy, this is commonly associated with sepsis leading to endothelial dysfunction
(septic miscarriage and puerperal sepsis) or hyper- A variety of thrombotic microangiopathies
tension. Rarely, it is caused by exposure to nephrotoxins
Renal pathology—lesions seen are due to changes in the
drugs like antibiotics (aminoglycosides) acetaminophen,
glomerular capillary like hemolytic uremic syndrome
hemoproteins. First trimester septic miscarriage is the
Arteriolar lesions.
most usual cause. The infection may be due to Escherichia
coli. In late pregnancy pre-eclampsia or bleeding of
Management
abruptio placentae or hemolysis elevated liver enzymes
low platelet count (HELLP) syndrome may lead to ATN. The patient is admitted to the hospital. General supportive
Severe and prolonged volume depletion as in hyperemesis measure like intravenous fluid are started. The patient
gravidarum, rarely may be the cause. needs intensive care. Blood pressure needs to be controled.
Acute fatty liver of pregnancy is an uncommon reason. An ultrasound examination to find any retained product
There is an abrupt rise of temperature with vomiting and of conception is carried out dilatation and evacuation
diarrhea. Urine examination may be normal or show renal (D&E) is done to remove them if found. Replace blood if
tubular cells and brown pigmented casts. there is revealed or concealed hemorrhage. Peritoneal
The progression of shock may be rapid. Mild jaundice dialysis or hemodialysis is performed if needed. The aim is
(secondary to hemolysis) cyanosis and pallor may be seen. to maintain blood urea nitrogen below 50 mg/dL.
Most of the patients respond to vigorous antibiotics and
If the patient has not delivered, consider delivery once
volume resuscitation usually in an intensive care unit (ICU).
she has stabilized.
All acute renal diseases have an adverse effect on the
RENAL CORTICAL NECROSIS fetus in the form of spontaneous abortion, stillbirth,
Most of the causes of ATN also lead to renal patchy cortical intrauterine growth restriction (IUGR), neonatal death
necrosis. There is tissue death throughout the cortex and prematurity.
Renal Disorders Complicating Pregnancy 419
capillary pressure and harmful cytokine production. This

CHRONIC RENAL DISEASE
restriction is not to be followed after conception. The patient
Previously women with chronic renal disease were not is managed in a tertiary care center. Fortnightly visits are
able to conceive. But now pregnancy does occur in chronic important till 32 weeks. Then, the patient is seen weekly.
renal disease patients. The prognosis rests on the degree of Serum creatinine, 24 hours urea clearance and serum
renal insufficiency at conception. electrolytes are tested. Serum albumin, triglyceride level,
Women with normal blood pressure and mild renal uric dehydrogenase and platelet count estimations are
disease (serum creatinine < 1.4 mL/dL) do well and performed. Judicious use of (e.g. in diabetic nephropathy)
there are a few or no adverse effects. However, the cortisone may help. Prophylactic anticoagulation (low
presence of hypertension before pregnancy increases dose heparin) may be administred to select patients at risk
the risk to the mother and the fetus, even if the renal of thrombosis, e.g. those on long period of bed rest.
functions are preserved Dialysis is to be initiated early and more frequently when
If renal function is moderately impaired (serum creati serum creatinine levels are 5–7 mg/dL or urea nitrogen
nine 1.5–3 mL/dL) before conception the condition level are 60 mg/dL or higher. The aim is to maintain blood
deteriorates urea nitrogen level at 50 mg/dL, avoid fluctuation of BP,
With severe renal disease (serum creatinine ≥ 3 mg/dL) rapid volume changes and electrolyte imbalance.
women are usually infertile. If conception occurs, there Dialysis may induce uterine contractions, hence mag-
is a substantial maternal and fetal risk. There is a higher nesium sulfate can be given. The dose of heparin needs to
incidence of pre-eclampsia preterm delivery and IUGR. be increased. Special nutrition supplements are needed
to replace potassium, other minerals and proteins lost in
COLLAGEN VASCULAR DISORDERS dialysis. Erythropoietin may be given to correct resistent
anemia.
In pregnant women with lupus nephropathy, there is
exacerbation during pregnancy and puerperium. Renal Renal Transplantation
sclerosis and polyarteritis nodosa have a poor prognosis
Reports of successful pregnancy in renal transplant
during pregnancy.
patient are present in literature. Pre-conception check-up
is essential. Patients with renal transplants should wait for
DIABETIC NEPHROPATHY 2 years before attempting pregnancy.
With moderate to greater dysfunction before pregnancy, it Stable renal function with plasma creatinine < 2 mL/dL,
deteriorates rapidly after conception. preferably 1.5 mL/dL should be achieved. There must not
be any hypertension. The medications received should
MANAGEMENT FOR RENAL DISORDERS be reduced to minimum possible, i.e. prednisone < 15
mg/day, azathioprine < 2 mg/kg/day, cyclosporine (safe
IN PREGNANCY dose not known) below 5 mg/kg/day. Very close prenatal
Counseling before and during pregnancy is important. and intranatal care is needed. Infection control is very
A protein restricted diet before pregnancy is advised. It important. Cesarean section is to be done for obstetric
prevents hyperfilteration, decrease in intraglomerular indications only.
1. Acute tubular necrosis is commonly associated with sepsis or hypertension. State True or False.
2. ____________ is a sudden decrease in renal function with oliguria over a period of hours a days in pregnancy, it can be due to
acute tubular necrosis.
3. Chronic kidney disease is identified by a blood test for ____________ , which is a breakdown product of muscle metabolism.
4. The most common recognized cause of chronic kidney disease from the following is:
i. Diabetes mellitus
ii. Acute fatty liver
iii. Lupus nephritis
iv. Hypotension.
42
Liver and Pancreatic
Diseases in Pregnancy
TYPES OF THE LIVER DISEASES DISEASES SPECIFIC TO PREGNANCY

The liver is a unique organ because it is the main site of
metabolism in the body. Its diseases during pregnancy are
Intrahepatic Cholestasis of Pregnancy
as follows: This hepatic disorder specific to pregnancy is found
Diseases specific to pregnancy mostly in the third trimester. It is also called cholestatic
• Intrahepatic cholestasis of pregnancy (IHCP) hepatosis, icterus gravidarum and recurrent jaundice
• Acute fatty liver of pregnancy (AFLP) of pregnancy.
• Liver damage due to severe pre-eclampsia, eclampsia
• Hepatic damage in hyperemesis gravidarum. Incidence
Diseases coincidental to pregnancy Its incidence is different in different regions. The recur-
• Acute viral hepatitis rence is upto 20.9% in twins.
• Drug induced hepatic injury.
Chronic liver diseases that antedates pregnancy Etiology
• Pregnancy in a case of The exact etiology is uncertain.
–– Chronic hepatitis Genetic and environmental: Recent evidence suggests
–– Autoimmune hepatitis that a polygenic inheritance along with an environ-

–– Cirrhosis mental influence has a role in the development of IHCP.
Hormonal: The hormonal etiology is based on the fact
–– Liver transplantation
that there is an increased incidence in women taking
Diseases of gallbladder
oral contraceptives and in twin pregnancies (associated
• Cholelithiasis and cholecystitis
with higher estrogen levels).
Diseases of pancreas during pregnancy
However, evidence against this hormonal hypothesis are
• Pancreatitis
also available:
• Pancreatic transplantation.
Patients occasionally acquire the disease in the first
trimester or continue symptoms even upto 8 weeks after

Physiological Changes delivery when the hormone levels are usually not elevated.
Pregnancy normally alters the hepatic functions. The enzyme Some patients improve before delivery when the levels
alkaline phosphatase (ALP) is markedly increased. Serum of the hormones are the highest.
albumin is decreased, globulin is slightly increased, and Not all patients who develop the disease have recur-
hormone binding proteins and transferrin are elevated. rence with estrogen administration after delivery.
Triglycerides and cholesterol are elevated. The clotting factors
VII, VIII, X and fibrinogen are elevated. Palmar erythema and Clinical Features
spider angiomas can be seen. Now we will discuss some of Pruritus and mild jaundice are usually the only presenting
the above pathological entities in greater detail. symptoms. Generalized, pruritus of insidious onset
Liver and Pancreatic Diseases in Pregnancy 421
mainly in late second or third trimester (particularly on is administered at the dose of 14–16 mg/kg/day. Other
palms and soles) is the dominant (70% of cases) and the drugs used are cholestyramine 8–16 g/day in 3–4 divided
most disturbing clinical feature while jaundice is usually doses, aluminium containing antacids, guar gum and
mildoccurring in only a few patients (presenting with phenobarbitone upto 90 mg/day. If no respite is obtained
dark urine/light-colored stools). There can be associated with these, then dexamethasone 12 mg once daily (OD × 7
malaise, nausea and vomiting and steatorrhea. days can be used). Injection vitamin K should be admini
stered intramuscular (IM) to decrease risk of postpartum
Investigations hemorrhage (PPH).
Serum ALP levels are increased 5–10 fold; most of it is Due to adverse effects on pregnancy (stillbirth and fetal
hepatic in origin distress), continuous fetal monitoring is essential. Once
Bilirubin is increased upto 5 mg/dL lung maturity occurs, induction of labor and intrapartum
Vitamin K level is decreased surveillance is advised and the patient is kept under close
Serum transaminase [aspartate aminotransferase (AST) observation because of an increased risk of PPH and to
and alanine aminotransferase (ALT)] levels are normal monitor the requirement of cesarean section in case of
or moderately increased fetal distress.
Serum triglyceride and cholesterol levels are markedly Post delivery, LFTs return to normal by 6 weeks. However
increased since it can recur with combined oral contraceptive (COC)
Selenium levels are low and copper levels are high in pills, same should be avoided.
the patients
Serum prothrombin time is usually normal. Acute Fatty Liver of Pregnancy (AFLP)
To clinch the diagnosis fasting serum bile acids (SBA) It is a rare and potentially fatal disease complicating
should be at least 3 times the normal (value 2–10 µmol/L) a normal pregnancy in the third trimester with high
along with pruritus and jaundice. Rise in the bile acids perinatal and maternal morbidity and mortality.
(10–100 fold) is the earliest and the most consistent finding.
SBA value more than 40 µmol/L are associated with fetal Incidence
complications. The incidence is 1 in 10,000 pregnancies.
Alteration in the estrogen metabolism (decreased
excretion of estriol glucuronide or increased excretion of Etiology
estriol sulfate in the urine) due to marked reduction in the A recessive inheritance of defective mitochondrial enzymes
bile excretion of estriol may also occur. leading to abnormalities of fatty acid oxidation is the
Ultrasonography (USG) may show some atrophy and supposed cause. This is due to mutation of chromosome
destruction of microvilli of the bile canaliculi. On histology, 2 genes, coding for long chain 3-hydroxyacyl-CoA
the centrilobular area shows dilated bile canaliculi and it dehydrogenase (LCHAD). This chromosomal mutation
may contain bile plugs without inflammatory cells. in females can pose them to risk of AFLP in pregnancy.
However, homozygous LCHAD deficient fetus aggravates
Effect on Pregnancy the condition in its mother (Sims and co-workers 1995).
There is increased incidence of preterm labor (19–60%),
fetal growth restriction (FGR), meconium staining of liquor Clinical Features
(MSL) (27%), intrapartum cardiotocographic abnormalities It is more common in primigravida with a male fetus or with
and even sudden intrauterine death (IUD). multiple gestation. It presents mostly in third trimester or
sometimes in late second trimester. Almost 50% of these
Treatment patients have hypertension and pre-eclampsia. It starts
The women should be counseled about the associated with malaise, anorexia, nausea, vomiting, right upper
risks and hence, the importance of regular antenatal quadrant and epigastric pain and progressive jaundice.
follow-up. Liver function tests (LFTs) and serum bile Half of these patients have hypertension and pre-
acids should be monitored during the antenatal period. eclampsia. Liver is not enlarged.
Treatment is directed towards reducing the disturbing
pruritus. S-adenylmethionine (SAM) and ursodeoxy- Investigations
cholic acid (UDCA) in combination is effective. UDCA Leukocytosis is seen
There is hyperbilirubinemia with levels upto 10 mg/dL recur in the subsequent pregnancy, the symptoms may be
Serum transaminase levels are elevated upto 300–500 quite mild or sometimes absent in a later pregnancy.
U/L
Hypofibrinogenemia with abnormal coagulation prolo Treatment
nged, e.g. prolonged clotting time is seen It is a disease with a high fatality rate leading to multiorgan
Cholestatic enzymes such as gamma glutamyl trans- failure; thus mandates a multidisciplinary care involving
peptidase (GGTP) are also elevated along with the obstetrician, physician (hepatologist preferably) and
prothrombin time anesthetist. Termination of pregnancy (preferably through
Ammonia and uric acid are increased and these findings
vaginal route) is required and if needed, cesarean section
are suggestive of true hepatic failure can be done under epidural anesthesia subject to normal
Hemolysis may be observed
coagulation profile.
Hypoglycemia is frequent finding
Intensive supportive measures for the wellbeing of the
Ultrasound and computed tomography (CT) are not
mother should also be undertaken, e.g. adequate intra
sensitive and usually confirm the diagnosis in retro-
venous (IV) glucose to prevent hypoglycemia.
spect after recovery from the disease
Complete recovery following delivery usually occurs.
Magnetic resonance imaging (MRI) with T2 weighted
Transfusion of fresh frozen plasma, cryoprecipitate, platelets
gradient echosequences helps in diagnosis (Siegelmen
are given, as per need. If liver functions have not resumed
1997)
after delivery, liver transplantation may be needed.
Liver biopsy is confirmative, but should be done
cautiously after obtaining a normal coagulation study,

Liver Disease in Pre-eclampsia and Eclampsia
especially in the setting of pre-eclampsia (coincidental
hemolysis elevated liver enzymes low platelet count Hepatic abnormalities increase in severity with increasing
(HELLP) syndrome and liver rupture]. Histology shows severity of pre-eclampsia and eclampsia. The liver lesions
swollen hepatocytes with propensity of microvesicular are periportal hemorrhage, fibrin deposition along with
fat in their cytoplasm; the nucleus remains central. mild steatosis (fatty infiltration) and, may be, necrosis
There is minimum hepatocellular necrosis (as seen in liver biopsy which should as far as possible be
Special investigations like toluidine blue staining of the avoided) caused by ischemia.
fat droplets and mitochondrial changes followed by
microscopic examination may be required to differentiate Clinical Features and Investigations
it from ballooning of cells as seen in viral hepatitis. The patient complains of epigastric or right upper quadrant
The disease worsens rapidly with marked hypoglyce- pain with a tender, but normal-sized liver.
mia and coma, coagulopathy and even renal failure. Fetal Serum AST levels rise upto 500 IU/L. Serum bilirubin may
demise occurs in severe cases. Thus, early diagnosis and be slightly increased or even normal at times. Prothrombin
delivery is important and sometimes intensive manage- time and fibrinogen levels are usually normal unless the
ment like liver transplantation may be required. condition is complicated by disseminated intervascular
coagulation (DIC). In severe cases, subcapsular hemor
Differential Diagnosis rhages are seen. Once such case was operated for acute
It is also difficult to differentiate from Reye’s syndrome, abdomen at 36 weeks of pregnancy in our hospital.
which also shows a mitochondrial dysfunction along Liver lesions are part of HELLP syndrome having
with a deficiency of medium chain acetyl coenzyme-A hemolysis (H) (usually sub-clinical, evident only as
dehydrogenase. Over half of the patients develop diabetes abnormal red blood cells (RBCs) on the peripheral
insipidus, thus diuresis in the affected patients should not smear), elevated liver enzymes (EL) and low platelets (LP)
be neglected. (<100, 000/mm3) and occurring usually in the third trimester.
The recurrence rate ranges between 2% and 19%. It is
Course and Prognosis classified into three categories using the as per Mississippi
The disease is usually self-limiting. Symptoms begin to classification system it is classified in three categories.
subside immediately after delivery and completely recover 1. Class I (characterized by severe thrombocytopenia):
over 24 hours to several days postpartum (though some Platelet count < 50,000/mm3
biochemical parameters may remain elevated for upto 2. Class II (characterized by moderate thrombocytopenia):
6 months). Though, the disease has a rare tendency to Platelet count between 50,000/mm3 and 100,000/mm3
3. Class III (characterized by mild thrombocytopenia):

Platelet count between 100,000/mm3 and 150,000/mm3
DISEASES COINCIDENTAL TO
Prompt delivery will normalize the patient. PREGNANCY
Acute Viral Hepatitis
Severe Form of HELLP
It is common in pregnancy. There are six viral agents
Spontaneous hepatic rupture and hematoma present with causing—1. Hepatitis A (HAV), 2. Hepatitis B (HBV), 3.
features of shock and peritonitis (if the capsule is ruptured Hepatitis C (HCV), 4. Hepatitis D (Hepatitis B associated
leading to hemoperitoneum), abdominal distension and delta agent), 5. Hepatitis E (HEV) and 6. Hepatitis G (HGV).
symptoms due to stretching or irritation of the hepatic They are all ribonucleic acid (RNA) viruses except hepatitis
capsule (due to hepatic hematoma). Ultrasound and B, which is a deoxyribonucleic acid (DNA) virus. These
CT/MRI may be required for diagnosis (as liver biopsy is hepatotropic viruses are not hepatotoxic perse, but lead
contraindicated in these cases). The treatment includes to hepatocellular necrosis as a result of host’s immune
immediate delivery along with aggressive management reponse. Besides, viral hepatitis can also be caused by
of liver trauma and maintenance of the patient’s general Ebstein-Barr Virus (EBV), Echovirus and Yellow Fever
condition. Virus.
Another clinical presentation in pre-eclampsia and
Hepatitis A Virus
HELLP could be hepatic infarction (large, punched out
devascularised areas on CT with necrotic tissue on aspi- The incubation period is 2–7 weeks. It is transmitted mostly
ration). The condition has been dealt in greater detail in by fecal and oral route. Acute symptoms are low grade fever,
nausea, vomiting, anorexia and bodyache. The diagnosis is
Chapter 41.
achieved by anti-HAV IgM (immunoglobulin M) antibody
detection in serum. The course is self-limiting and
Differential Diagnosis
progression to liver failure is rare. Neonatal transmission
AFLP: Unlike AFLP (from which it is difficult to differ
risk is due to intrapartum fecal contamination. Treatment
entiate, due to its association with pre-eclampsia and is symptomatic with rest, hydration and balanced diet.
eclampsia) true hepatic failure and coagulopathy are Hospitalization may be needed till the improvement
absent of appetite. The risk of preterm delivery is increased.
Acute viral hepatitis: Differentiation from this condi- Prophylaxis with Igs can be given perinatally.
tion requires a complete history of risk factors and sero-
logical investigations Hepatitis B Virus
Thrombotic thrombocytopenic purpura (absence of The incubation period is 6 weeks to 6 months. The
hypertension) is unrelated to pregnancy infection is seen in IV drug abusers, homosexuals, health
Gestational thrombocytopenia (platelet count <70,000/ care workers and recepients of blood and blood products.
mm3 without pre-eclampsia): This is a benign condition Sexual and vertical transmission along with transmission
and other features of pre-eclampsia are absent. through breast milk is also possible. Although most
patients are asymptomatic and diagnosed incidently
Hyperemesis Gravidarum during antenatal screening, in acute phase, they may have
flu like symptoms, nausea, vomiting, anorexia and jaundice
There is excessive nausea and vomiting which are prolon
in rare cases. It can lead to serious sequelae like chronic
ged and occur throughout the day. It is mostly associated
hepatitis, liver cirrhosis or even hepatocellular carcinoma
with primigravida, multiple gestation, obesity, non- (HCC). One percent of HBsAg positive mothers may
smokers, molar gestation and female fetuses. There may progress to fulminant hepatitis which can lead to maternal
be weight loss and dehydration. Ketosis, mild jaundice and mortality. Universal screening of all pregnant women should
hypothyroidism may develop. Serum amino-transferases be done by testing for serum HbsAg (surface antigen). If this
may be raised upto 250 IU/L. It is more common in young is positive, the patient is tested for HBeAg antigen which
mothers (under 20 years), in obese women and in non- is an indicator of vertical (mother to child) transmission
smokers. Liver biopsy may be normal though some fatty (80–90%). Diagnosis is confirmed by HBsAg, HBeAg
changes are observed. The condition has been dealt in (indicator of infective status) and HBcAg (Hepatitis B core
greater detail in Chapter 13. antigen). Chronic carrier state shows presence of HBsAg,
HbeAg with anti HBcAb, 6 months after initial infection. Clinical Course of Viral Hepatitis in Pregnancy
LFT is deranged with high transaminase levels (40–40,000 It has a broad spectrum in pregnancy. Most are asympto
IU/L) in initial phase of infection. matic, but some do develop a fatal fulminant disease.
The disease course usually commences with prodromal
Treatment is Supportive
symptoms like general malaise, myalgia, fatigue, anorexia,
In case of an HBsAg positive mother, the newborn is given nausea and vomiting, right upper quadrant pain and low-
Hepatitis B vaccine and 0.5 mL Ig just after birth. It is grade fever. Mild but tender hepatomegaly is seen. Jaundice
imperative to give the Ig as soon as possible after delivery appears 1–2 weeks later along with clay-colored stools
because the efficacy declines with time. Two booster doses with deep color urine. White blood cells are depressed.
of the vaccine at 1–6 month of age are also recommended. Serum transaminases (AST, ALT), bilirubin and ALP are
This is 85–95% effective in preventing vertical transmission. elevated. Prothrombin time (PT) and activated partial
Breastfeeding is not infectious as long as the infant has thromboplastin time (APTT) may be prolonged.
been immunized. In our hospital, all the newborns are Acute illness mostly resolves rapidly in 2–3 weeks. Ten
immunized against hepatitis B just after birth. percent of cases of hepatitis B and C become chronic.
About 1–3% develop acute fulminate hepatitis.
Hepatitis C
It is most common cause of non A, non B hepatitis. The Diagnosis
transmission is blood borne mainly, sexual and feco-oral The diagnosis is clinched by the respective serological
(rarely). Thus it is seen in IV drug abusers, hemophiliacs markers of each specific virus viz. anti-HAVIgM, HbsAg,
(who receive repeated blood transfusions) and women anti-HBcIgM, HCV polymerase chain reaction (PCR),
with high-risk sexual behavior. Two-third of the patients HDV PCR, anti-HEVIgM and anti-HGVIgM. Biopsy of the
show chronic active hepatitis and 20–30% may progress liver may show massive hepatocellular injury and inflam-
to cirrhosis. Donor screening for HCV has become matory infiltration.
mandatory in blood banks to reduce incidence of post
transfusion hepatitis. Treatment of Viral Hepatitis
High maternal viremia, infantile hypoxia and intrapartum Hospitalization is indicated in severe cases. Restriction
exposure to viral contaminated maternal blood increases of physical activities and a high caloric diet are required.
the transmission to the fetus. Antenatal screening in high risk If vomiting persists, IV feeding is needed. Gloves should
categories had been recommended (ACOG 2007). Vertical be worn when handling bedpans or fecal material of
transmission occurs in 3–6% of fetuses. Breastfeeding is not hepatitis A and E patients and while taking blood samples
contraindicated. There is a need to screen every pregnancy. in hepatitis B and C patients. Hand washing is very impor
tant. Fetal assessment and surveillance is required to
Hepatitis D prevent premature delivery and stillbirth. Gamma globulin
The virus exists as a coinfection with hepatitis B virus. prophylaxis should be given to pregnant patients within
A combination of B and D infection is a more serious disease, 2 weeks of exposure to hepatitis.
as chance of cirrhosis are much greater than with hepatitis B Hepatitis A vaccine is also now available, though not
infection alone. This virus is also transmitted vertically. in common use. In an HbsAg negative patient, hepatitis B
Vaccination against hepatitis B prevents this hepatitis. vaccine can be given before pregnancy.
Hepatitis E Fulminant Hepatitis

It is water-borne and is spread via the oral fecal route. If It is mostly seen with hepatitis B, D and E infections.
acquired late in pregnancy it is more severe and may lead Clinically, the patient is confused and disorientated and
to fulminant hepatic failure. may develop encephalopathy or go into coma. One of the
earliest symptoms of encephalopathy is a reversal of the
Hepatitis G sleep-wake cycle with excessive daytime sleepiness. The
It is blood-borne and is a coinfection with hepatitis B liver is usually small. If the prothrombin time is excessively
and C in patients with a history of IV drug abuse. Vertical prolonged, the patient may have DIC. Serum bilirubin
transmission has been noted. rises rapidly. Ascites and generalized edema may develop.
Cerebral edema, brainstem compression, gastrointestinal Liver Transplantation

(GI) bleeding, sepsis, respiratory failure, cardiovascular It is becoming more frequent. Associated pregnancy may
collapse, and renal failure may develop. The mortality is be complicated by hypertension, anemia and preterm
very high. Liver transplantation may be life-saving. The delivery. In cases of hepatic transplantation, pregnancy is
use of interferon therapy should be considered with close to be avoided for at least 2 year post transplantation so that
monitoring in hepatitis B and C. viability of the graft is assessed and immunosuppressive
drugs are stabilized at minimum maintenance dose.
Toxic Hepatitis Spontaneous miscarriages are not increased. The rate of
Direct or indirect injury to the liver by medications like rejection of the graft is also unaltered by pregnancy.
sulpha drugs, chlorpromazine, tetracycline, isoniazid
(INH), phenytoin, acetaminophen, azathioprine (following DISEASES OF THE GALLBLADDER
organ transplant) or some anesthetic agents like halothane
Cholelithiasis and cholecystitis during pregnancy—
is the cause. It causes nausea, vomiting, abdominal pain, pregnancy increases the risk of gallstones as incomplete
mild jaundice or even hepatic failure. emptying causes retention of cholesterol crystals. Though,
The treatment involves stopping the causative agent and conservative treatment is recommended, surgery may be
supportive care. Amoebic hepatitis is rare in pregnancy. needed in some of required, elective surgery during the
second trimester is the best option.
CHRONIC LIVER DISEASE THAT
ANTEDATES PREGNANCY DISEASES OF THE PANCREAS
DURING PREGNANCY
The physiological changes of pregnancy and pre-existing
liver disease affect the health of a pregnant woman. Acute pancreatitis, more common in advanced gestation,
is potentially serious yet rare complication taking place
during pregnancy with incidence of 1/4450 pregnancies
Chronic Hepatitis
(Hernandez et al, 2007). The main etiology is pancreatic
Pregnancy is rare in chronic progressive liver disease. If it duct blockade. Pancreatic duct blockade can lead to
does occur, there may be transient hepatic failure, variceal autodigestion and inflammation of the gland triggered
hemorrhage, stillbirths, prematurity and LBW babies. by pancreatic hyperstimulation causing release of
There are chances of PPH in patients with cirrhosis. pancreatic enzymes within the acinar cells, leading to
acute pancreatitis. Pregnancy is a high risk state for biliary
Cirrhosis sludge formation and risk of cholelithiasis. This is due to
In pregnancy, most common cause of cirhossis is post physiological changes during pregnancy like decreased
enterohepatic circulation, increased bile acid pool
necrotic cirrhosis after chronic hepatitis B and C. Clinical
and stasis of bile, decreased gallbladder motility under
features include jaundice, edema, coagulation failure,
effect of progesterone, increased cholesterol secretion
metabolic derangements, portal hypertension with
under estrogen influence and increased pressure due
gastroesophageal varices and splenomegaly. Deep vein to enlarged gravid uterus in third trimester leading to
thrombosis (DVT) incidence increases in these cases. The raised pressure on biliary ducts. Cholelithiasis is the most
prognosis is very grave. common etiolgical factor followed by hyperlipidemia,
hypertriglyceridemia, hyperparathyroidism, autoimmune
Autoimmune Hepatitis pancreatitis and congenital ductal anomalies. However,
It undergoes remission during pregnancy, but after delivery occasional development of non-biliary pancreatitis is
there is a rebound and clinicians should be aware of it due to viral infection,drug-induced, associated trauma or
(Izumi and associates 2002). Esophageal varices may be postoperative state.
seen with or without cirrhosis, but it is serious, if associated
with the latter. Pregnancy increases the risk of bleeding Clinical Features
from esophageal varies. Beta-blockers (e.g. propranolol), It usually presents with symptoms of cholecystitis with
endoscopic band ligation or endoscopic sclerotherapy are similar history in pre-pregnant state for the first time
used according to the severity. in pregnancy. There is sharp stabbing pain of sudden
onset in epigastrium radiating to back, flank, scapula or of safer procedures (i.e. EUSG or MRCP). ERCP is used
shoulder along with features of peritonitis in severe cases. only as a therapeutic modality in selected cases with
Besides pain,nausea,vomiting, low grade fever, dyspepsia confirmed CBD calculi.
and intolerance to fatty food may be there. In severe cases,
in response to systemic inflammation, acute respiratory Management
distress syndrome may ensue. Maternal electrolyte and Mild cases can be treated with supportive treatment while
acid base imbalance may lead to acute fetal hypoxia and severe cases needs hospitalization with intensive care
even IUD. The specific physical findings like jaundice in along with analgesics, oxygen, hydration, total parenteral
biliary cause, spider angioma in alcoholic and xanthomas nutrition (TPN) and enteral nutrition to decrease pancreatic
in hyperlipidemia associated pancreatitis may be seen. secretion. ERCP is used for biliary pancreatitis and
sphincterotomy. In gallbladder disease, cholecystectomy
Effect on Pregnancy is done once acute inflammation subsides. However,
severe necrotizing pancreatitis needs laparotomy and
Preterm delivery rates have been reported to as high as in
debridement. Laparoscopic cholecystectomy can be
30% cases. Early recognition due to increased diagnostic
undertaken preferably in second trimester. Thus, it calls
modalities and thus, better and early management has led
for a multidisciplinary approach by gastroenterologist, GI
to decline in maternal mortality rates to less than 50%.
surgeon, radiologist and obstetrician in the treatment and
Investigations follow-up of these patients.
Serum amylase and lipase levels may raise to more than Pancreatic Transplantation
three-fold. Psuedopancreatic cysts and dilated pancreatic
With rising incidence of diabetes mellitus, pancreas
ducts canbe diagnosed with abdominal USG. Endoscopic transplantation is being done increasingly. The 5 year
ultrasound (EUSG) is the best imaging modality for survival rate in pancreatic transplant is 80%. The survival
common bile duct (CBD), but is expensive, needs IV rate is still better when combined transplantation of
sedation and needs skill. It is better than magnetic pancreas and kidneys is done in DM-Type I and renal
resonance cholangiopancreatography (MRCP). MRCP failure. The incidence of pre-eclampsia, preterm delivery
is indicated in pregnancy only, if other non-ionizing and FGR is high during pregnancy in transplantation
forms of diagnostic imaging modalities are inadequate. cases. Successful pregnancy outcome after pancreatic
Endoscopic retrograde cholangiopancreatography (ERCP) autotransplantation following pancreatectomy is known
as diagnostic procedure is no more used due to availability through few reported cases.
1. Icterus gravidarum is a hepatic disorder specific to pregnancy and is found mostly in ____________ trimester.
2. The mutation of chromosome 2 genes, coding for long chain b-hydroxy acyl-CoA dehydrogenase in females can pose risk of
____________ in pregnancy.
3. There are six viral agents causing acute viral hepatitis in pregnancy, where hepatitis B is a DNA virus. State True or False.
4. Name the disease which is water-borne and spread by orofecal route. It is acquired late in pregnancy and may lead to fulminant
hepatic failure.
i. Hepatitis A
ii. Hepatitis B
iii. Hepatitis E
iv. Hepatitis C.
43
Ruchi Arora Sachdeva, Sudha Salhan
Respiratory Disorders
in Pregnancy
morbidity about four folds, while the risk of preterm labor

TUBERCULOSIS
may be increased nine folds.
Tuberculosis (TB) constitutes a major global health hazard.
In 2013, 9 million people fell ill with TB and 1.5 million Effect of Pregnancy on Tuberculosis
died from the disease. It is a curable and preventable Till 14th century, it was believed that pregnancy will slow
communicable disease and is the seventh leading cause the progression of TB as pulmonary cavities result from
of death worldwide. Over 95% of TB deaths occur in low TB were believed to collapse as a result of increase intra
and middle income countries and it is among the top five abdominal pressure associated with pregnancy. But in
causes of death for women aged 15–44 years. early 20th century, it was believed that pregnancy favors
India’s TB problem is further compounded by poverty, the progression of tuberculosis, as in pregnancy there is
malnutrition, human immunodeficiency virus (HIV) and shift of cell mediated TH1 (T helper) response towards TH2
multidrug resistance cases. response. As TH1 mediated immune response are essential
Standard diagnostic and treatment protocols are avai to protective cell mediated immunity in TB and TH2 are
lable with highly effective drugs, based on scientific antagonistic to such protection.
principles and years of research. However, large section of However, researcher have demonstrated no net benefit
medical community has neglected there basic principles or adverse effect of pregnancy on TB. Frequent pregnancies
and lead to the emergence of more number of drug resis may have negative effect , as they may cause reactivation of
tance cases. latent TB.
Effect of Tuberculosis on Pregnancy and Diaganosis

Neonate The presenting complaints of patient suffering from
Study from India shows that there is no difference in tuberculosis are same in pregnant and non-pregnant
pregnancy complications and pregnancy outcomes women. The diagnosis of TB in pregnancy is often
in women diagnosed and treated for TB in pregnancy delayed due to non specific nature of early symptoms of
compared to matched controls of pregnant women who infection such as malaise, fatigue which are also present
had no TB. Treatment outcomes—sputum conversion, in pregnancy and thus, do not raise suspicious of TB
disease stabilization and rates of relapse were similar in the during routine antenatal care. Pulmonary TB is the most
two groups. The problem arises only when TB treatment common form of disease. Extra pulmonary TB occurs in
is started late in pregnancy, it leads to increase neonatal 5–10% of pregnant patients suffering from tuberculosis.
mortality and prematurity. Other obstetric complications History of contact with TB patients is important with
reported are—higher rate of spontaneous abortion, small complaint of cough for 2 week or more. Other symptoms
for date fetus, suboptimal weight gain in pregnancy. include evening rise of temperature, anorexia, weight loss,
Others includes preterm labor, low birth weight (LBW) and breathlessness or hemoptysis. Pregnant patient presenting
increase neonatal, morbidity and mortality. Late diagnosis with these symptoms should get sputum examination
is an independent factor, which may increase obstetric done to see acid-fast bacilli (AFB) by Ziehl-Neelsen (ZN)
staining method; as per revised national tuberculosis TABLE 43.1: Dosage and adverse effects of 1st line antitubercular
control program (RNTCP) it is the preferred method for drugs
diagnosing pulmonary tuberculosis (PTB). Chest-X-ray is Dose mg/ Daily adult
done (with shielding the abdomen) if two sputum smears Drug kg/BW dose (mg) Adverse effects
are negative for AFB, and symptoms persist despite giving Isoniazid 05 300 Hepatitis, raised liver
antibiotics for 1–2 weeks. enzymes, peripheral
Extra pulmonary disease will lead to symptoms specific neuritis
to the organ affected. Abdominal tuberculosis will present Rifampicin 10 450–600 Orange discoloration
as abdominal pain, swelling of the abdomen and altered of secretions, nausea,
bowel habits. Persistent back pain may be an indication of vomiting, febrile
reactions hepatitis,
tuberculosis of the spine and enlarged lymph nodes may purpura
be due to tuberculosis of the lymph nodes.
Pyrazinamide 30 1500–2000 Hyperuricemia
When a pregnant woman is admitted with headache, loss hepatotoxicity
of consciousness and convulsions, tuberculosis meningitis
Ethambutol 12–35 750–1000 Optic neuritis, skin
has to be kept in mind. Early diagnosis and prompt treatment rash
is very important to reduce the mortality in such cases.
Streptomycin 20 Ototoxicity,
Tuberculo mastitis is a very rare entity, but it deserves (not nephrotoxicity
special mention because it is almost exclusively confined recommended
to women of the reproductive age group. in pregnancy)
For diagnosing case of extrapulmonary TB (EPTB)
with pregnancy, tuberculin skin test along with site
specific investigations are done. For a case of multiple well by most of pregnant patients (Table 43.1). However,
lymphadenopathy, fine needle aspiration cytology (FNAC) if an individual is having intolerable side effects with
and biopsy are done, for a case of pleural, pericardial and any particular drug, it may be modified (drug dosage) or
ascitic fluid, tapping of the fluid for investigation [cytology, changed. Currently intermittent regimen, (thrice weekly)
biochemistry, AFB, adenosine deaminase (ADA) is done]. under directly observed treatment strategy (DOTS) of
For a case of TB meningitis, lumbar puncture is done. RNTCP is being increasingly used worldwide for the
Tuberculin skin test is suggestive of infection and not pregnant women having TB.
disease, so it is important that patient should have clinical Table 43.2 indicates the treatment regimen, types of
features suggestive of TB along with tuberculine sensitivity patient and regimen prescribed.
test (TST) positive.
Pregnancy with Multi Drug Resistant TB
Treatment (Mdr-Tb)
Patient diagnosed of having PTB or EPTB with pregnancy Multidrug resistant-TB (MDR-TB) is defined a Myco-
should be started with antitubercular treatment (ATT) bacterium tuberculosis bacteria resistant to isoniazid
immediately, to avoid the serious effect of disease on (INH) and rifampicin with or without resistant to other
mother and fetus and also to make mother noninfectious. drugs.
Regimen of ATT are same in pregnant and nonpregnant There is lack of experience in treating pregnant women
status except for withholding streptomycin. As strepto- with MDR-TB. Teratogenicity has been reported with some
mycin has teratogenic side effects in first trimester of second line drugs.
pregnancy. Streptomycin is ototoxic and nephrotoxic to All the patients diagnosed as MDR suspect or MDR-TB
fetus. Quinolones should be avoided in pregnancy, as they patient with pregnancy should be evaluated in consultant
impair growth and can produced injury to the growing with obstetrician taking into account (risk and benefit
cartilage. Pyridoxine (50 mg per day) should be given to of MDR-TB treatment, severity of MDR-TB, gestational
prevent neurotoxicity in mother (peripheral neuropathy) age, potential risk to the fetus). Management of MDR-TB
and newborn (neonatal seizures). Rifampicin is a potent patients who are pregnant prior to initiation of treatment
inducer of oral contraceptive pills may be decreased, so or while on treatment are based on duration of pregnancy.
either use some alternative anti-contraception method If the duration of pregnancy <20 week patient should
or use pills containing higher doses of estrogens. All other be advised to opt for medical termination of pregnancy
first line antitubercular drugs (H, R, Z, E ) are tolerated (MTP) in view of severe risk to both mother and fetus.
Respiratory Disorders in Pregnancy 429
TABLE 43.2: Type of patients and prescribed treatment regimen For patients who are unwilling for MTP or have
Regimen1 pregnancy > 20 week. (Making them ineligible for MTP)
Treatment Intensive Continuation The risk to mother and fetus needs to be explained
groups Types of patient phase (IP) phase (CP) clearly and modified MDR-TB treatment (Flowchart
New* Sputum smear- 2H3R3Z3E3 4H3R3 43.1) to be started pregnancy (1st trimester) <12 week—
positive
kanamycin and ethionamide are omitted from the regimen
Sputum smear-
negative and paraaminosalicylic acid (PAS) is added.

Others More than 12 week—kanamycin is replaced with PAS.
Previously Smear-positive 2H3R3Z3E3S3 5H3R3E3 postpartum PAS may be replaced with kanamycin and
treated** relapse /1H3R3Z3E3 continued until the end of intensive phase.
Smear-positive
This regimen for MDR-TB comprises of 6 drugs without
failure
Smear-positive
pregnancy —1. Kanamycin (Km), 2. Levofloxacin (LVx), 3.
treatment after Ethionamide (Eto), 4. Pyrazinamide (Z), 5. Ethambutol (E)
default and 6. Cycloserine (Cs) during 6–9 months of the intensive
Others
2
phase and 4 drugs are:
1. The number before the letters refers to he number of months of LVx, Eto, E and Cs during the 18 months of the
treatment. The subscript after the letters refers to the number of
doses per week. The dosage strengths are as follows: Isoniazid (H) 600 continuation phase.
mg, rifampicin (R) 450 mg, pyrazinamide (Z) 1500 mg, ethambutol (E) All drugs should be given in a single daily dosage under
1200 mg, streptomycin (S) 750 mg.
• Patients who weight 60 kg or more receive additional rifampicin DOT by a DOT Provider. All patients will receive drugs
150 mg. under direct observation on 6 days of the week. On Sunday,
• Patients who are more than 50-years-old receive streptomycin the oral drugs will be administered unsupervised whereas
500 mg. Patients who weight less than 30 kg, receive drugs as per
pediatric weight band boxes according to body weight. injection. Kanamycin will be omitted. If intolerance occurs
2. In rare and exceptional cases, patients who are sputum smear- to the drugs, Eto, Cs and PAS may be split into two dosages.
negative or who have extrapulmonary disease can have recurrence The morning dose administered under DOT and the
non-response. This diagnosis in all such cases should always be
made by an MO and should be supported by culture or histological evening dose will be self-administered. The empty blister
evidence of current, active TB. In these cases, the patient should be packs of the self-administered doses will be checked
typed as Others and given treatment regimen for previously treated.
* New includes former categories. in the next morning during DOT. Pyridoxine should be
** Previously treated is former category II. administered to all patients on regimen for MDR-TB.
Flowchart 43.1: Management of MDR tuberculosis in pregnancy
Abbreviations: MTP—Medical termination of pregnancy; PAS—Para aminosalicylic acid

RNTCP Regimen for MDR TB: 6 (9) Km Lvx Eto Cs Z pregnancy in second trimester. There is only small increase
E/18 Lvx Eto Cs E risk to the babies of asthmatic mothers, but this risk is
(Reserve/Substitute drugs: PAS, Mfx, Cm) small in actively managed patients and can be minimized
by maintaining good asthma control throughout preg
Breastfeeding and Neonate Chemoprophylaxis
nancy. Females with intermittent or mild bronchial
Breastfeeding for all the newborn is recommended asthma do not have much problem during pregnancy,
irrespective of TB status of the mother by RNTCP and
however, those with severe asthma have greater risk of
American Academy of Pediatrics. Separation of mother
worsening symptoms during late pregnancy. Progesterone
and child is not required. Even, if mother is HIV infected
increase during pregnancy causes bronchodilatation and
breastfeeding is encouraged, the risk of transmission of TB
increase serum free cortisol levels and thus, improvement
through breast milk is negligible. First line ATT cross into
of asthma symptoms. Many asthmatic patients stop or
breast milk in small amounts and have no adverse effects,
reduce their medication due to fear about its safety, this
and this does not contribute to the development of drug
causes worsening of their symptoms.
resistance.
Chemoprophylaxis Maternal and Fetal Outcomes of

A child born to mother diagnosed to have TB in pregnancy Asthma and Pregnancy
should receive chemoprophylaxis with INH 10 mg/day A prospective case-control study performed over 12 years
for 6 months provided congenital TB has been ruled out. in one institute demonstrated no differences in rates of
Bacillus Calmette-guerin (BCG) vaccination to be given at pre-eclampsia, perinatal mortality, LBW or congenital
birth, even if (INH) chemoprophylaxis is planned. malformations, except for a discharge diagnosis of neonatal
sepsis and an increased maternal cesarean section rate in
HIV, TB and Pregnancy women with moderate or severe asthma.
In HIV, there is suppression of cell mediated immune
response which increases the risk and severity of TB, and Treatment
also TB accelerates the progression of HIV disease. This The successful treatment of asthma during pregnancy
synergestic effect contributes to high maternal mortality
requires a cooperation approach between obstetricians,
in coinfected women.
chest specialist, midwives , nurse specialist and the patient
As the diagnosis of TB with HIV with pregnancy is
herself. The goals and principles of managing bronchial
made. ATT should be started immediately followed by
asthma are same in pregnant and non-pregnant patients.
antiretroviral therapy to prevent the progression of the
Allergen avoidance by environmental control measures,
disease and adverse obstetric outcome.
avoidance of cigarette smoke and avoidance of other spe
cific triggers in individual patients should be identified and
ASTHMA IN PREGNANCY controled. Objective measurement of bronchial asthma by
spirometry should be done in order to stage the severity
Epidemiology of bronchial asthma. Based on history and forced expira
1–4% of pregnancies are complicated by bronchial asthma tory volume (FEV) in first second, it is accessed whether
national association of environmental professional asthma is controled, partially controled or uncontroled.
(NAEP). Ten percent of pregnant asthmatic patients have Although, there is general concern about any medi
exacerbation of bronchial asthma during labor and status cation use in pregnancy, the advantages of actively treating
asthmaticus is present in 0.2% of pregnancies. asthma in pregnancy markedly outweigh any potential risk
of usual controler and reliever medications. Use of inhaled
Effect of Pregnancy on Bronchial Asthma corticosteroids (ICS), beta-2 agonist, montelukast or theo
Studies of asthma symptoms is reported by pregnant phylline is not associated with an increase incidence of
women. twenty-two percent had worsening symptoms, fetal abnormalities.
29% reported improvement, 22% had no change. NAEP A stepwise approach is now followed to control
working group came to conclusion that course of asthma in symptoms and minimize future risk. For intermittent
pregnancy was better in one-third, worse in one-third and bronchial asthma as needed short acting beta-2 agonist
unchanged in one-third. Exacerbations are common in (SABA) is the treatment of choice. Asthma that causes
more than occasional symptoms should be treated daily opiates as analgesics should be avoided. If required,
with anti-inflammatory therapy using either ICS or sodium epidural anesthesia is preferred to general anesthesia
cromolyn. Frequent need for beta-2 agonist should be (may cause chest infection and atelectasis besides
prescribed for symptomatic relief in all grades of asthma. difficulty in intubation). Ergometrine, especially with
Use of sustained release theophylline or long acting beta-2 general anesthesia, may cause bronchospasm. Instead,
agonist (LABA) along with ICS is appropriate for persistant oxytocin can be used to prevent postpartum hemorrhage
asthma in patients already taking the first two agents (ICS, (PPH). Postoperative analgesia needs to be administered
SABA). Further, if symptoms persist then short course of after enquiring about any aspirin or nonsteroidal anti-
oral corticosteroid is added to the above drugs (LABA, inflammatory drug (NSAID) allergy.
SABA, ICS). Similarly, if symptoms are controled then step Women using inhaled drugs, oral cortisone and methylx
down approach is to be followed. The inhaler technique anthines can safely breastfeed her child. In addition, breast
should be checked and a chart recording peak expiratory feeding reduces atopy and other allergies in the child.
flow-rate should be maintained. A self management Status asthmaticus: If the mother is exhausted, her PCO2
plan should be agreed upon. Theophylline is considered is above 40 mmHg, or PO2 less than 60 mmHg or O2 satura
safe in pregnancy, therapeutic range in plasma should tion is less than 90 mmHg, endotracheal intubation needs
be adjusted to 8–12 µgm/mL. It crosses placenta, but to be carried out and she should be kept in intensive care
newborn rarely shows sign of theophylline toxicity, when unit. Humidified oxygen and continuous positive airway
blood levels are high. It is also passed in breast milk, only pressure is used. A team of physician and anesthetist need
1% of dose reaches infant. to be present.
Leukotriene inhibitor zafirlukast, montlukast are safe in
pregnancy. Zileuton should not be used in pregnancy. Breastfeeding
Oral corticosteroids—some animal studies shows
All women with bronchial asthma should be encouraged
increase incidence of cleft palate with oral corticosteroid.
for breastfeeding. This risk of atopic disease in child is 1
They have also been reported to cause intrauterine growth
in 3 if both parents are atopic. This risk can be reduced by
restriction (IUGR), if given in first trimester. The maternal
breastfeeding.
side effect from steroid therapy include increase risk of
infections, reduced glucose tolerance and increase in
gestational diabetes. The rare, but important psychiatric PULMONARY EDEMA
side effect of oral steroids should be remembered. Increase
risk of pregnancy induce hypertension and pre-eclampsia
Cardiogenic Pulmonary Edema
have been reported in asthmatic women on steroid. Patient with underlying cardiac disorder (stenotic lesions)
Addition of systemic corticosteroid to control develop pulmonary edema during gestation and postpartum.
exacerbation of asthma is appropriate, and must not Perturbations induced by pregnancy alter fractional shunts,
be withheld if current medicines are inadequate. Chest induce hypoxemia and precipitate pulmonary edema. Peri
X-ray, if clinically indicated must be done with abdominal partum cardiomyopathy that develops in 1 of 1300–15000
shielding, it causes minimal exposure of fetus to ionizing deliveries presents with congestive heart failure (CHF) and
radiation and must never be withhold just because patient can develop pulmonary and systemic emboli during last
is pregnant. month of pregnancy and for upto 5 months thereafter.
Management of Asthma During Labor Tocolysis Induced Pulmonary Edema

The normal medication, oral or inhalational, should be Administration of beta-2 agonist to retard premature labor
continued throughout labor, as scheduled. If the patient is associated with 0–4.4% incidence of pulmonary edema.
was on steroids for maintenance or therapy for more than Simple discontinuation of beta-2 agonist results in rapid
2 weeks before the onset of labor, she should be given improvement, along with diuretics.
parentral hydrocorticosone 100 mg till oral therapy is
restarted. Prostaglandin F2α is not recommended, as it
Pulmonary Edema Associated with
may cause bronchospasm but prostaglandin E2 can be Pre-eclampsia
used for cervical ripening, because it is bronchodilator. An 2.9% of patients with pre-eclampsia or eclampsia develop
acute asthmatic attack is rare, but in cases where it occurs pulmonary edema. Hemodynamic changes are—left
ventricular preload is normal or low, afterload is high anesthesia and delivery poses a severe risk to women
and cardiac output is normal or low, systolic and diastolic suffering from primary and secondary PAH. Maternal
function impaired. Low colloid oncotic pressure and mortality in this is from 30–56%. Recent studies have
abnormal vascular permeability also contribute pulmonary documented successful use of IV or inhaled epoprostenol,
edema commonly present in postpartum period. sildenafil in PAH, however, long term effect and overall
pregnancy related mortality is not known.
Pulmonary Embolism
It is an important cause of maternal mortality. Rate of 0.5– Bronchiectasis
1.3 per 1000, with increasing incidence in age over 35 year. This is an irreversible bronchial dilatation associated with
Various risk factor for pulmonary embolus are: chronic productive cough with recurrent infections. Usually,
Venous stasis (uterus compresses inferior vena cava
pregnancy does not cause much change with underlying
and left iliac vein). bronchiectasis. But cases with deteriorating pulmonary
Increase coagulation factors (V, VIII, X and von
functions and LBW or intrauterine death (IUD) of the fetus
Willebrand factor antigen) and fall in protein S. have been reported.
Injury to pelvic veins at delivery
Treatment goals include removal of any identifiable
Other factors which increase the chance of pulmonary underlying cause, clearance of tracheobronchial secretion
embolism are women taking oral contraceptive pills (usually requiring bronchodilators and proper positioning
(OCPs), bed rest, complicated or cesarean delivery, age of the patient) which also aids in improving any reversible
and inherited coagulation defects (deficiency of factor S, airway obstruction and control of infections. Nutrition
C, antithrombin III or the presence of antiphospholipid status of mother is to be maintained. Correction of
antibodies, factor V leiden and prothrombin 920210A. hypoxemia (it may cause IUGR). At first sign of infection,
Diagnosis give appropriate antibiotics. Obstructive defect is to be
corrected with bronchodilator.
Tachypnea, peripheral edema on examination
Echocardiography, arterial blood gas (ABG) chest X-ray Adult Respiratory Distress Syndrome (ARDS)
Duplex ultrasonography (combined real time B mode
compression ultrasonography plus Doppler venous It is a severe form of lung disease of acute onset. Charac
ultrasonography). In patient with high clinical suspicious terized by dyspnea, hypoxemia, nonpliable (stiff ) lungs
repeat test at 5–7 days and diffuse infiltration on chest radiography, mimick
Venography (gold standard) ing pulmonary edema. The patient develops mechanical
Ventilation perfusion scanning and CT angiography. respiratory failure and requires mechanical ventilation,
positive end-expiratory pressure (PEEP) and reduction of
Treatment left atrial filling pressures by a strict fluid control. Death
Low molecular weight heparin (LMWH) is safe in preg may be caused by multisystem organ failure which usually
nancy and lactation. Warfarin crosses placenta and cause occurs due to the same predisposing factors which cause
nasal, ophthalmologic and central nervous system (CNS) ARDS.
abnormalities. Unfractionated heparin causes thrombocy Besides infection (sepsis or primary pulmonary
topenia and osteoporosis. infection), amniotic fluid embolism, pulmonary edema
Safe regime is LMWH in first trimester, during second (due to excessive tocolytic drugs) and aspiraton of gastric
and third trimester. LMWH is to be replaced with warfarin contents, pre-eclampsia, eclampsia, seizures, massive
after delivery. The dose of unfractionated and LMWH blood transfusion, hemorrhage and coagulopathy are
may be reduced during delivery to prophylactic dose some of the predisposing factors of ARDS. Lungs functional
even through risk of maternal hemorrhage during vaginal capacity decreases and shunting and hypoxemia develop.
delivery is minimal. Treatment should be continued for Physiological changes in the mother aggravate ARDS.
3 months. Unless there is history of previous thrombo
embolism, when life long treatment may be necessary. Cystic Fibrosis
With increase in medical care facilities, life span of
Pulmonary Artery Hypertension (PAH) cystic fibrosis patients has increased. In patients with
The cardiovascular and hemodynamic change (i.e, increase stable cystic fibrosis, pregnancy has no or little effect on
cardiac output, blood volume) associated with pregnancy, them, whereas those with severe disease they have poor
outcomes. Therefore pre-pregnancy counseling explaining It is one of the causes of ARDS of pregnancy. Amniotic
maternal and fetal risk forms an important component in fluid enters into the maternal circulation reaching up to
pregnant patient with severe cystic fibrosis. FEV1 below the pulmonary vasculature, causing embolization. The
60% and presence of pulmonary hypertension are poor contents could include amniotic fluid, fetal squamous
prognostic factor for both mother and infant. MTP should cells coated with white blood cells (WBCs), vernix, lanugo
be recommended to those with poor functional status. hair, meconium, fat, bile, mucin and granular debris.
For stable cystic fibrosis patients, bronchodilators, chest Various mediators in response to foreign substances are
physiotherapy, treating chest infection with antibiotics, released and they enter the circulation. They are leuko
treating hemoptysis, pneumothorax, to be managed jointly trienes, histamine, proteolytic enzymes, complement,
by obstetrician and respiratory physician. biogenic amines, (e.g. serotonin, bradykinin, prostaglandin,
etc). They may cause anaphylactoid syndrome of pregnancy.
Sleep Disorders Systemic hypotension and hypoxia develop and lead to
cardiopulmonary collapse, renal insufficiency, liver failure,
Snoring is increased in pregnancy. Increase estrogen results
seizure and coma.
in hyperemia, upper airway narrowing. Progesterone results
In humans, the effect may be biphasic. First intense
in increase respiratory drive along with decrease functional
vasospasm, severe pulmonary hypertension and hypoxia
residual capacity (FRC) and compliance. All these hormonal
develop. This leads to a significantly high maternal mortality
change result in alteration in sleep during pregnancy. Noc
in the first hour itself. The pulmonary hypertension is
turnal hypoxemia effects fetal growth. Although prevalence
difficult to diagnose. Predisposing factors that are postulated
of sleep disorder during pregnancy is not known. However
for amniotic fluid embolism are:
females who develop pre-eclampsia, pregnancy induce Hectic labors (e.g. precipitate labor or tetanic uterine
hypertension, symptoms of sleep disorder should be evalu contractions)
ated with polysomnogram and treated with [nasal continu Induction of labor using uterine stimulants, though
ous positive airway pressure (CPAP)]. their role is not uniformly accepted
Meconium stained amniotic fluid
Interstitial Lung Disease Primigravida
Patients with interstitial lung disease (ILD) have restric Multiparity
tive lung disease, along with reduced diffusion capacity. In High cervical laceration
pregnancy, there is increase oxygen consumption require Increased permeability and friability of fetal membranes
ment, thus along with ILD, patient will have increase exer in intrauterine fetal death.
tional dyspnea and hypoxia. Patients with vital capacity less Clinically, it is a form of ARDS and there is respiratory
than 1L and along with pulmonary hypertension should distress, cardiovascular failure, and disseminated intra
avoid pregnancy. Lymphangiomyomatosis and systemic muscular coagulation (DIC) in association with labor or
lupus erythematosus (SLE) worsen with pregnancy. after delivery. The diagnosis is made clinically. It may
present as:
Pleural Diseases • Respiratory distress and cyanosis in 51%
Small asymptomatic pleural effusion may develop post • Bleeding diathesis in 37–54%
partum in normal pregnancies, or in pre-eclampsia and • Hypertension in 27%
choriocarcinoma. Nothing needs to be done. Patient with • Seizure.
symptoms of chest pain, dyspnea, moderate to severe
pleural effusion needs full clinical evaluation. Patients
Laboratory Findings
with underlying obstructive airway disease may develop Arterial blood oxygen tension is reduced. This hypoxemia
spontaneous pneumothorax and pneumomediastinum may be due to: (a) ventilation-perfusion imbalance,
following delivery. (b) atelectasis and (c) pulmonary edema. Bleeding disorder
is manifested in:
Amniotic Fluid Embolism Microangiopathic hemolysis
Though not common (1: 8,000–1: 80,000 pregnancies) its Hypofibrinogenemia
importance lies in the very high mortality rate making up Prolonged clotting time (CT) and bleeding time (BT)
to 10–15% of maternal deaths. Increased fibrin split products

X-ray chest may show pulmonary edema Pulmonary aspiration shows tachycardia, shock, respi-
CT lung also shows—edema ratory distress and frothy pink sputum but there is
ECG—manifests tachycardia, ST and T wave changes bronchospasm and wheezing too
Air embolism
representing right ventricular strain pattern. If blood
Myocardial infarction
can be drawn from pulmonary arteries, one can see
Anaphylactic shock
cytological components.
Placental abruption
Eclampsia
Differential Diagnosis of
Rupture of uterus
Amniotic Fluid Embolism
Transfusion reaction
Pulmonary thromboembolism—severe hypoxemia and Drug reaction due to drugs used in anesthesia in 10%.
pulmonary edema. Chest pain is common Treatment involves supportive treatment for DIC,
Congestive cardiac failure—due to fluid overload or respiratory failure, left ventricular failure (LVF). If the
previous heart disease. These patients show cardio- fetus survives initial insult, it should be delivered. In
pulmonary compromise case of maternal death, emergency postmortem or peri
Hypotension due to various causes like septic chorio- resusitation cesarean section is done or cardiopulmonary
amnionitis, PPH resuscitation (CPR) in pregnancy.
1. Patient diagnosed of having pulmonary tuberculosis with pregnancy should be started with anti-tubercular treatment to avoid
serious effect on mother and fetus. State True or False.
2. ____________ is defined as Mycobacterium tuberculosis bacteria resistant to isoniazid and refampicin with or without resistant
to other drugs.
3. Amniotic fluid embolism causes ____________ because amniotic fluid enters the maternal circulation reaching upto the
pulmonary vasculature causing embolization.
44
Sudha Salhan, Meenakshi Bhatt, Banashree Das
Rh-Isoimmunization
in Pregnancy
INTRODUCTION ISOIMMUNIZATION
Role of Rhesus Blood Group in Pregnancy It is the production of immune antibodies in an individual
in response to antigen derived from another individual of
As other characteristics, the fetus acquires blood group
the same species, provided the first one lacks the antigen.
from both parents.
For Rh-isoimmunization three conditions must exist:
Rhesus (Rh) blood group system has an antibody
directed toward red blood cells (RBC) surface antigen 1. The fetus must have Rh-positive RBCs and mother must
called Rhesus (Rh) factor. This Rh factor has five major have Rh-negative RBCs
identifiable viz. Cc, D0, e and E. No ‘d’ antigen has 2. A sufficient number of fetal RBCs must gain access to
been identified, hence instead of d zero (0) is donated. the maternal circulation
According to Fisher race concept, Rh-antigen complex 3. The mother must have immunogenic capacity to produce
is the final expression of these five possible antigens, of antibody directed against D antigen.
which the D antigen is the most potent and accounts for
95% of damages due to Rh blood groups and its absence Incidence
or presence denotes an individual to be Rh-negative or It is 15–17% in European and American whites whereas
positive (Flowchart 44.1). 1–2% in India.
But nowadays, all Rh-negative women who deliver Rh-
positive neonates are given anti-D antibodies (as prophy- Pathogenesis
laxis). Therefore, now we rarely see Rh-isoimmunization. Fetomaternal hemorrhage results in the passage of fetal
RBC’s into the maternal circulation and a maternal
response is evoked. It can occur during pregnancy (6.7% in
first trimester, 15.9% in second trimester and 28.9% in third
Flowchart 44.1: Rhesus factor inheritance trimester) or during delivery (15–50%) (Fig. 44.1A to E).
Factors Predisposing to Fetomaternal Leak

Spontaneous or induced miscarriage
Chorionic villus sampling (CVS)
Amniocentesis
External cephalic version
Manual removal of placenta
Abdominal trauma
Placenta previa
Accidental hemorrhage
Abruption of placenta
ABO incompatibility exerts a protective effect in the

following way:
• If along with Rh incompatibility, there is ABO
incomptability the fetal RBCs are rapidly cleared
from circulation because ABO antibodies already
exist in mother, so that trapping of antigen occurs
A B C in the spleen (where sensitization occur) and Rh-
immunization does not take place.
• The presence of antibodies against A or B along with
Rh incompatibility destroy fetal Rh-antigen quickly
as it enters into mothers circulation and is no longer
immunogenic. This is seen at its maximum with
mother type O and father type, B or AB. Hence, ABO
D E
incompatibility is protective.
Figs 44.1A to E: A. Rh-negative women before pregnancy; Difference between ABO Incompatibility and CDE
B. Pregnancy occurs with Rh-positive fetus; C. Placenta separates Incompatibility?
after delivery; D. After delivery Rh-immunization occurs in mother, ABO antigens and their isoagglutinins are present at
she develops antibodies to Rh-positive antigen; E. Next pregnancy
with Rh-positive fetus, maternal antibodies cross placenta, enter
birth. Therefore, this incompatibility is seen even in the
fetal blood, attach to Rh-positive RBCs causing hemolysis first born
Most A, B, O antigens are IgM and do not cross the
placenta and fetal RBCs have only few A, B, O antigens

Intrauterine death (IUD) of the fetus
and do not evoke immunogenic response or mild
Cesarean section.
disease
Very small amount (even 0.1 mL) of Rh-positive
ABO incompatibility rarely gets progressively worse in
fetal blood after traversing the placenta can sensitize
subsequent pregnancies.
an Rh-negative mother. The maternal response to Rh Screening: On first antenatal visit, blood group and Rh
sensitization is the production of IgM (immunoglobulin typing of the pregnant woman is advised. If she is Rh-
M) (high molecular weight) antibody which cannot cross negative, her husband’s blood group and Rh typing is
the placenta. Within 6–30 weeks, an IgG response is ordered. When the husband is Rh-negative, no further
produced which is able to cross the placenta and attack the investigation in this segment is required as all offsprings will
Rh-antigen on the fetal RBCs and destroy them, causing be Rh-negative, but if he is Rh-positive, paternal zygosity
fetal anemia. This stimulates the fetal bone marrow and is done (if possible) as in homozygous (DD) father, 100%
extra modularly hematopoietic sites (liver, spleen, etc.) fetuses will be affected but in heterozygous (D0) father
and immature RBC appear in the circulation. Excessive only 50% offsprings are affected. Fetal deoxyribonucleic
destruction of RBC’s cause release of bilirubin in blood, acid (DNA) (to know fetal Rh-type) in maternal plasma is
these are passed into maternal circulation by the placenta a new noninvasive test. Invasive tests like chorionic villus
where they are metabolized. biopsy, amniocentesis or fetal blood sampling (umbilical
Severe anemia in the fetus leads to hydrops or eryth blood) also find out fetal Rh-type but have danger of
roblastosis (Fig. 44.2) fetalis, characterized by: isoimmunization besides other complications. Antibody
Severe anemia level test (indirect Coombs test) are ordered when father
Extramedullary hematopoiesis (liver and spleen is Rh-positive at 28 weeks of pregnancy or earlier, if there is
enlargement) a history of Rh-isoimmunization in a previous pregnancy.
Heart failure
Edema and ascites

Manifestation of Hemolytic Disease
Pericardial effusion. Maternal
Why does isoimmunization not occur in all Rh-negative Increased incidence of pre-eclampsia, polyhydramnios,
mothers? large sized baby
Thirty percent Rh-negative individuals do not respond Increased incidence of postpartum hemorrhage (PPH)
immunologically due to a large placenta and coagulopathy
Rh-Isoimmunization in Pregnancy 437
Mirror syndrome—caused by vascular changes in Indirect Coombs test (mother)—positive

the placenta. The mother develops pre-eclampsia and Ultrasonography (USG)—edematous skin of scalp,
edema similar to the fetus pleural and pericardial effusion
Grandmother therapy—rarely the D-negative female Placenta is large, boggy, pale and edematous
fetus is exposed to D antigen from the mother and Doppler ultrasound will show fetal anemia (middle
sensitized as a result. If such a sensitized female
cerebral artery flow)
child grows-up to bear an Rh-positive fetus, the fetus
X-ray abdomen—buddha position with a halo around
is jeopardized by antibodies initially provoked by
its grandmother’s blood. As this is very rare, anti-D the head.
prophylaxis is not recommended Icterus gravis neonatorum—the baby is born active
Anamnestic response—presence of an antibody titre without any evidence of jaundice but it soon develops it
in the mother need not necessarily depict the fetal within 24 hours of birth.
wellbeing. Previously, sensitized women may have a Congenital anemia of newborn—even in the mildest
higher load during subsequent pregnancies even if the form of the disease, the destruction of RBCs continues till 6
present fetus is D-negative. weeks after birth (after which no more maternal antibodies
are available).
Fetal and Neonatal Manifestation
Varying degrees of anemia leading to immune hydrops MANAGEMENT (FLOWCHART 44.2)
(the presence of abnormal fluid in two or more sites
Management of Unsensitized Rh-Negative
such as thorax, abdomen or skin, Fig. 44.2)
Heart failure
Pregnant Women
Intrauterine fetal demise At 28 weeks of pregnancy, if the indirect Coombs test
Neonatal jaundice and kernicterus. is negative the mother is given 300 mg of anti-D (IgD)
injection. Her indirect Coombs test (ICT) is tested every
Theories month. If it remains negative, she is delivered at term
Heart failure from prolonged anemia (do not allow her to go postterm) and the cord’s blood is
Hypoxia with severe anemia causes severe leakage collected for different tests. If the newborn is Rh-positive,
Parenchymal disruption by extramedullary hemato 300 mg of immunoglobin serum (anti-D) is to be given
poiesis due to portal and umbilical venous hypertension to the mother within 72 hours of birth to neutralize any
Liver dysfunction causes hypoproteinemia leads to antibodies formed (protection for next birth). If the
lower colloid osmotic pressure. neonate is Rh-negative, nothing need to be done. If ICT is
positive, it means that the patient has been sensitised. Rh-
Diagnosis isoimmunization was major cause of perinatal mortality
Pregnant mother is Rh-negative with Rh-positive father in the previous four decades. Once ICT is positive fetal
wellbeing is to be assessed. This is done by amniocentesis,
cordocentesis and Doppler ultrasound.
Bilirubin in amniotic fluid is an indirect marker of
fetal hemolytic disease. Amniotic fluid is seen at ∆ optical
density 450 (delta OD 450) and amount is calculated. This
is charted against weeks’ of gestation in Liley’s graph
(Fig. 44.3) on a semi-logarithmic paper. The graph is
divided into three zones. Zone 1 indicates an unaffected
fetus. Zone 2 is a mild to moderately affected fetus
and Zone 3 indicates a severely affected fetus with an
imminent risk of intrauterine death (IUD). Follow-up with
amniocentesis at 2–3 weeks is needed in Zone 1. In Zone
2, amniocentesis is repeated after 2 weeks. If the trend of
OD 450 is decreasing we only observe and repeat the test
Fig. 44.2: Hydrops fetalis for 37 weeks and then induce labor. If the OD 450 trend is
Flowchart 44.2: Management of unsensitized pregnancy gives an indication of the degree of fetal involvement and
helps further management.
Calculation of the amount of fetomaternal bleed:
number of fetal RBCs
Fetal blood (mL) = ______________________ × 5000
1000 maternal RBCs
5000 is the maternal blood volume in pregnancy.
If there are 80 fetal RBC in 50 low power field in maternal
peripheral blood film—it represents transplacental hemor
rhage to the extent of 4 mL of fetal blood.
Roughly, 100 mg of anti-D is required for neutralization
of 5 mL of fetal Rh-positive cells. But if the load is more than
15 mL (i.e. 300 mg of anti-D) than more anti-D globulin
(IgG) is to be given.
PREVENTION
Prevent or Minimize Fetomaternal Leak
During cesarean—prevent blood spillage into the peritoneal
cavity and manual removal of placenta should not be done as
a routine. If needed, it should be performed gently.
Prophylactic ergometrine with of anterior shoulder
should be withheld
Amniocentesis should be done under sonographic
localization of the placenta to prevent injury to it

Forcible attempts to perform an external cephalic
version should be avoided

Abbreviation: ICT—Indirect Coombs test Avoid giving Rh-positive blood to an Rh-negative female
from her birth to menopause

Giving anti-D therapy after the birth of an Rh-positive
increasing then, the gestation of the fetus is the deciding
infant.
factor. If the fetus is mature (37 weeks or more), delivery
Critical titre: When anti-D levels are above a critical
is immediately indicated. If not mature, intrauterine
level, a substational proportion of fetuses are significantly
transfusion is indicated and the fetus is delivered after
anemic. This level varies from laboratory to laboratory. ICT
maturity. In Zone 3, give an intrauterine transfusion and
is done on the mother’s blood at 28 weeks’ of pregnancy
deliver. Queenan curve or extrapolation of Liley’s curve is
(earlier if there is previous history of an isoimmunized
used in some previous pregnancy erythroblastosis cases.
fetus). It measures the antibody (anti-D) levels in the
It is used in the second trimester and has four outcome
zones. Trend is more important than a single reading. maternal serum. (The cut-off values are 1:16 in AIIMS
Doppler ultrasound: Level of anemia in these fetuses is and 1:8 in Safdarjung Hospital). These critical titres of ICT
diagnosed by doing peak systolic velocity in fetal middle guide further management, i.e. amniocentesis.
cerebral arteries (MCA) for amount of RBCs. In severe CE antibodies of Rhesus are less immunogenic; the
cases is performed every 2 weeks. If the MCA, Doppler critical titre is 1:32 or higher. The critical titre for anti Kell
is more than 1.5 MoM cordocentesis for fetal blood is antibodies is 1:8.
performed.
Management of Rh Sensitized (Immunized)
Cordocentesis is ultrasound guided direct sampling
of fetal blood from the umbilical cord for testing of fetal Pregnancy (Flowchart 44.3)
hematocrit (less than 30%) hemoglobin level, serum These patients are managed according to Liley’s graph as
bilirubin and direct Coombs test (DCT) fetal Rh type. This explained under non-immunized pregnancy.
Fig. 44.3: Liley’s Graph
Do not let her become post mature hours of birth of Rh-positive infant. If this is not possible,
Care during delivery there will be some advantage even when given within 9–10
• Careful monitoring of follicle-stimulating hormone days of delivery. The longer prophylaxis is delayed, the
(FHS) lesser is the protection but some times benefit is seen as
• Prophylactic methergine to be withheld late as 28 days after delivery it is for the next pregnancy.
• Gentle handling of the uterus in the 3rd stage
• Watch for PPH
Mode of Action
• Cord blood to be taken for fetal hemoglobin, fetal Antibody binds to D antigen on the cell membrane of the
blood bilirubin, fetal blood group Rh and direct fetal RBCs in mothers blood, so that they cannot excite
coomb’s test (DCT) immune competent cells in the maternal system.
• Early clamping of cord: The cord should be kept
Dose
15–20 cm long (for further exchange transfusion, if
20 mg of anti-D per mL of fetal RBC’s
need be)
10 mg of anti-D per mL of fetal whole blood
Cesarean delivery
• 1st trimester spontaneously or induced abortion, give
• Avoid spillage of blood into the peritoneal cavity
50 mg
• Routine manual removal of placenta to be avoided.
• 1st trimester chorionic villus sampling, give 50 mg.
• Ectopic pregnancy and evacuation of partial mole
Prevention –– Prior to 12 weeks –50 mg (250 IU)
Rh (anti-D) immunoglobulin has prevented a major cause –– After 12 weeks – 300 mg (1500 IU)
of perinatal mortality (Rh-isoimmunization) in the last • Amniocentesis/CVS or any other invasive procedure,
4 decades. 300 mg
• Also give 300 mg in antepartum hemorrhage (APH)
ACTIVE IMMUNIZATION in cases of heavy repeated bleeding with abdominal

pain (monitor with ICT test)
Rh (anti-D) immunoglobulin is administered intra- • In all these, give 300 mg Rh-anti D.
muscularly (IM) into the deltoid region of the upper arm • External cephalic version
(for better absorption) in Rh-negative patient within 72 • Closed abdominal injury
Flowchart 44.3: Management of sensitized (Rh-immunized) pregnancy
Abbreviations: ICD—Indirect Coombs test; USG—Ultrasonography; OD—Optical density; IV—Intravenous
Any procedure in the second trimester 15 mL of fetomaternal bleeding is neutralized. However,

Abdominal trauma or fetal death about 0.3% of women have greater than 15 mL of
fetomaternal bleeding. In them, the amount of this bleeding
Amount of Fetomaternal Bleed is to be assessed. The methods for the same are as follows:
Rosette test is a simple test but is only for screening and
In 99% of cases, fetomaternal hemorrhage is less than 4 mL is used to calculate the number of fetal RBCs per 50 lower
after delivery. By giving 300 mg of Rh (anti-D) immunoglobin power fields
By Kleihauer count using acid elution of D-positive fetal High dose intravenous immunoglobin (IVIG): Exact
RBCs in maternal blood (based on the fact that fetal mechanism of action not known—may blocks fetal cell
HbF is more resistant to acid than adult HbA) mediated antibody and placental antigen blockage or
Flow cytometry is more accurate. blockage at bone marrow level. It inhibits hemolysis
specially in early cases
Collection of Cord Blood in all Dose 100 mg/kg every 3–4 weeks from 14–18 weeks.
Rh-Negative Patients It is reserved for the cases where MCA shows fetal
Cord blood is taken from the placental end of the cord anemia. It reduces transfusion.
The cord should not be squeezed to avoid contamination On experimental basis the research on animals by
with Wharton’s jelly father’s white cells immunization is in progress.
Collect 5 mL of blood Rhesus C, E antigens and other red cell antigens also
2 mL oxalated blood for—hemoglobin estimation, contributes to fetal and neonatal isoimmunization. Anti-C
peripheral smear for hemolysis isoimmunization is mostly due to previous pregnancy, but
3 mL clotted for—blood group, Rh typing DCT and serum can also be due to blood transfusion (clinical significance
bilirubin. It is a useful guide to correct fetal anemia to is almost equal to anti-D).
improve oxygenation thus reducing extramedullary
hematopoiesis, thus causing a fall in portal venous MINOR BLOOD GROUPS
pressure and improving liver function.
Sensitization caused by minor blood group antigens is
becoming more common. These include:
INTRAUTERINE TRANSFUSION Kell group
• K
Intrauterine transfusion is of 3 types:
• Ko
1. Intravascular (into umbilical vein)
• Kpa
2. Intraperitoneal
• Kpb
3. Combined.
Duffy system
O negative (O–), leukocyte poor, packed RBCs cross
• Fya -most immunogenic
matched with the maternal serum are used.
• Fyb
The amount of blood given—(gestational age in weeks –
• Jka
20) × 10 mL (Table 44.1).
Kidd system
Other Therapies • Jkb

Lenu’s
Plasmapheresis: Reduces the level of maternal anti-D
MNS antigen system
transiently
Lutheran system
Diego
TABLE 44.1: Difference between intraperitoneal and intravascular XG
transfusion
P antigen system.
Inraperitoneal transfusion Intravascular transfusion Antibody to Kell system is also common; it results in
Blood transfused into the Blood transfused into the
more rapid and more severe anemia and only a mild
peritoneal cavity and RBCs umbilical vein
taken up by sub diaphragmatic increase in bilirubin. Anti-Kell antibodies attack on fetal
Advantages
lymphatics Higher survival rate
RBCs precursors directly in the bone marrow, which
Advantages Direct estimation of prevents hemopoietic response to anemia. Hence, it
Easier to perform hematocrit can be done is more dangerous. As few RBCs are produced, lesser
Disadvantages Significant reduction in low hemolysis and lesser bilirubin is produced despite severe
Fetal distress apgar score, cesarean delivery anemia. Therefore, intervention is required earlier when
PROM Disadvantages
Infection
maternal anti-Kell titre is 1:8 or greater. As fetal anemia is
Fetal bradycardia
Trauma to other organs Risk of fetomaternal

out of proportion to amniotic fluid evidence of hemolysis,
hemorrhage cordocentesis is requirement for initial evaluation.
Volume overload ABO incompatibility: It is seen in A or B group infants
Abbreviation: PROM—Premature rupture of membranes with group O mothers. Group ‘O’ individuals produce IgG
anti-A and anti-B antibodies. These cross the placenta, but may be drawn while the mother’s blood group analysis is
no harm is done during pregnancy. This problem is seen awaited and can be sent for evaluation if she turns out to
only after birth with early onset of jaundice (within 24 be Rh-negative.
hours). Unlike, Rh incompatibility kernicterus and anemia Subsequently, serial monitoring of heel stick/venous
are rare. Hence, bilirubin monitoring, phototherapy and TSB/ transcutaneous bilirubin is required in infants at
exchange transfusion are not widely needed. risk to pick-up jaundice early, so that treatment may be
Platelet alloimmunization may be seen. instituted without delay.
NEONATAL JAUNDICE Complications

The most important complication of neonatal jaundice is
Neonatal jaundice occurs in upto 50% of term neonates bilirubin encephalopathy (kernicterus), which is divided
and even more often in preterm. The neonate appears
into stages based on the temporal sequence of appearance
icteric at a bilirubin level of ≥ 7 mg/dL. The causes and
of symptoms and signs.
treatment of hyperbilirubinemia in the neonate are very
different from those in adults. Treatment
Common Causes The two main modalities of treatment are phototherapy
and exchange transfusion. Drugs may sometimes be
Physiologic jaundice—it occurs after the first day
used. However, exposing the neonate to sunlight is not
of life, peaks by day 5 and 7 with peak values of total
advised since, it may cause hyperthermia.
serum bilirubin (TSB) not more than 12 and 15 mg/dL Phototherapy (Figs 44.4A and B): Exposure of the
in terms and preterm neonates respectively. This is the neonate with unconjugated hyperbilirubinemia to special
most common cause of jaundice in neonates blue light with peak output between 425 and 475 mm
Pathologic jaundice—this may have several causes. causes structural isomerization of bilirubin to lumirubin.
Some of the common ones are listed below: This stable compound is excreted rapidly. The eyes should
• ABO or Rh incompatibility
be covered with an opaque bandage to prevent retinal
• Polycythemia [Intrauterine growth restriction
damage and the genitalia in males should also be shielded.
(IUGR), twin-to-twin transfusion, delayed clamping All other clothes should be removed and the baby’s
of cord, etc.] phototherapy should be interrupted only for feeding
• Birth trauma causing bruises, cephalhematoma, etc.
purposes. Temperature of the baby should be monitored
• Infants of diabetic mothers
to prevent hypothermia and hyperthermia.
• Birth asphyxia
Exchange transfusion: This procedure involves removing
• Prematurity
a precalculated volume of the baby‘s blood in small
• Glucose-6-phosphate dehydrogenase (G-6-PD) def-
aliquots and replacing it with donor’s blood in aliquots of
iciency.
the same volume. The level of bilirubin at which exchange
transfusion is performed, is decided based on birth weight
Clinical Assessment
and hours/days of life (standard charts are available for
Jaundice, first appears on the face and spreads caudad. the same).
Any neonate with jaundice within the first 24 hours of life Drugs: Phenobarbitone or metalloporphyrins have been
has pathological jaundice. In term, good weight babies rarely used.
which having yellow staining of soles is a very rough guide
to starting phototherapy. However, this is needed to be Prevention
confirmed by serum bilirubin measurement. Though neonatal jaundice cannot be and need not be
prevented, the severity can sometimes be decreased by
Investigation avoiding dehydration (regular, adequate breast feeds).
In a mother with known or suspected Rh incompatibility, This should be especially emphasized in babies in whom
it is important to take a cord blood sample for assessment jaundice is anticipated (vide supra). In premature/IUGR,
of the blood group, DCT, bilirubin and hemoglobin. This babies delayed clamping of cord should be avoided.
also holds true for a mother with poor or no antenatal In addition, it is possible to prevent the serious
care whose blood group is unknown. A cord blood sample sequelae of bilirubin excess (bilirubin encephalopathy)
A B
Figs 44.4A and B: Phototherapy machine A. Single and B. Double
by regular monitoring of serum bilirubin in neonates The parents of a neonate with hyperbilirubinemia
and timely and effective phototherapy and/or exchange should be informed about the nature and manifestation of
transfusion. hemolytic disease.
1. How to calculate the amount of fetomaternal bleeding?
2. What are the common causes of neonatal jaundice?
i. Intrauterine transfusion is of three types ___________, ___________ and ___________.
ii. ___________ test is a simple test but is only for screening and is used to calculate the number of fetal RBCs per 50 lower
power fields.
iii. The most important complication of neonatal jaundice is ___________.
iv. Jaundice first appears on face and spreads ___________.
Alteration of Hemostatic
45
Achla Batra, Sudha Salhan, Harsha Gaikwad
System and Coagulation
Disorders in Pregnancy
Flowchart 45.1: Extrinsic and intrinsic system of coagulation

INTRODUCTION
Hemostasis is responsible for stoppage of blood flow from
the injured vessels. Components of hemostatic system
are platelets, coagulation factors and vessel wall and
fibrinolytic system.
The initial response to injury is constriction of vessels
and formation of a platelet plug which is stabilized by fibrin.
Under normal circumstances, the aggregation of platelets
and fibrin formation takes place simultaneously at the site
of vessel injury. In large blood vessels, platelets may be
unable to seal a defect on their own and homeostasis will
depend largely on effective vasoconstriction and fibrin
formation.
The formation of fibrin from fibrinogen is the end
product of a complex series of reactions of soluble plasma
protein. There are two parallel mechanisms, which are
integral to normal hemostasis, the extrinsic and intrinsic
system (Flowchart 45.1) of coagulation. The intrinsic dothelium in vivo. This contact initiates a cascade (series)
pathway is slower than the extrinsic pathway. of reactions. The key contact is factor XII which gets
activated to XIIa. This in turn activates factor XI to XIa,
which cleaves factor IX to give the active molecule IXa.
INTRINSIC PATHWAY IXa complexes with VIIIa and calcium on phospholipids
All the factors responsible in the intrinsic system are within produced by blood platelets. This complex acts on factor
the blood and can be divided in three groups: X to activate it to Xa. Deficiency of factor VIII and IX can
1. Contact group—XI and XII give rise to classic hemophilia and Christmas disease
2. Prothrombin or vitamin K-dependent group—contains respectively.
the vitamin K-dependent coagulation factors II, VII, IX,
and X. These factors are synthesized in the liver in the EXTRINSIC PATHWAY
presence of vitamin K, which acts as a cofactor
3. Fibrinogen group includes fibrinogen (factor I) and It is so called because some of its key factors lie outside
factors V, VIII, and XIII. These are found in platelets the blood. The vital element is tissue factor which reacts
except factor XIII and factor VIIIc. with plasma factor VII in the presence of calcium ions
The contact group is adsorbed by contact with a and activates it to VIIa which in turn activates the factor
negatively charged surface such as collagen or the suben- X to Xa. Thus, both the extrinsic and intrinsic pathway
Alteration of Hemostatic System and Coagulation Disorders in Pregnancy 445
ultimately lead to the formation of active factor X which Flowchart 45.2: Fibrinolytic system
enters a final common pathway. In the extrinsic system,
there is a powerful feedback mechanism and Xa further,
activates VII to form VIIa, which accelerates the final
common pathway. Therefore, formation of fibrin, in the
extrinsic pathway is much faster. The prothrombin time
(PT) test is used to evaluates the extrinsic system.
In the final common pathway, factor X, calcium, factor
V and phospholipids activate prothrombin by proteolytic
cleavage to form an active enzyme thrombin. Thrombin is
a powerful platelet aggregator and forms fibrin monomers
from fibrinogen over the irreversible platelet aggregates.
Thrombin also activates factor XIII which makes fibrin
soluble. The fibrin monomers polymerize to form a
soluble fibrin clot. Both extrinsic and intrinsic pathways
are occurring side by side and there is a cross reaction
between the two systems. Plasminogen Activators
A failure of fibrin formation may result from a Plasminogen activator activity is mainly centered around
number of factors. There may be: the wall of blood vessels and is greater in veins than in
� Insufficient fibrinogen for conversion to fibrin.
arteries. The plasminogen activators originating from
However, for isolated fibrinogen deficiency to cause within the blood and from tissues, are called tissue
bleeding, the levels have to be very low plasminogen activators (TPA). The organs rich in TPA
� There may be a deficiency of one or more clotting
are the uterus, the prostate and the lungs. Urokinase
factors leading to defective thrombin formation as in like plasminogen activators are also present in plasma
hemophilia and Christmas disease. In these cases, urokinase-type plasminogen activators (UPA).
the response to the hemostatic challenge, may be
insufficient and bleeding may result
Fibrinolytic Inhibitors
� Finally, a failure of normal fibrin stabilization leads to Plasmin can digest a variety of substrates, therefore, it is
the formation of loose clots which are not able to secure essential that its activity is restricted to the dissolution of
hemostasis. Fibrin degradation products (FDPs) also fibrin clots. There are powerful inhibitors of plasminogen
interfere with fibrin stabilization and add to coagulation activator and plasmin in the circulation to prevent and
failure. neutralize free plasmin activity.
Usually, there are multiple factors operating to interfere The two main antiplasmin are:
with the hemostatic mechanism when there are bleeding 1. a2 macroglobulin, which reacts quickly and reversibly
problems in obstetrics. with plasmin
2. a1 antitrypsin, which reacts more slowly but firmly to
produce an inactive complex. If plasmin spills into the
FIBRINOLYTIC SYSTEM (FLOWCHART 45.2) circulation, it is quickly acted upon by antiplasmin in
There has to be a system to stop the formation of clot after plasma. If there is a excessive generation of plasmin,
the hemostasis is achieved. The fibrinolytic system helps to antiplasmins may be overwhelmed and free plasmin
maintain the patency of the vascular tree by removal of fibrin appears in the circulation.
and restoration of vascular patency. Its component include A variety of plasminogen activator inhibitors (PAI) have
plasminogen, its activators and inhibitors. Plasminogen is also been identified. The most important ones are found in
the inactive form of the proteolytic enzyme, plasmin which endothelium and platelets.
is a powerful proteolytic enzyme. Plasmin breaks down
fibrin to FDPs. Deficient production of plasminogen by Coagulation Inhibitors
the liver as in cirrhosis and premature infants is associated Naturally occurring anticoagulant mechanisms are
with the thrombotic state. Dysplasminogenemia is also present in the body to prevent inadvertent activation of the
presents as a familial disorder. clotting process. The various inhibitors are anti-thrombin
III, protein S, a2 macroglobulin, a1 antitrypsin and heparin TABLE 45.1: Common tests for integrity of hemostatic mechanism
cofactor II. The most important of these is antithrombin
III, which is an inhibitor of both thrombin and activated Entity Level of
Test Measured Normal value action if
factor IX, X, XI and XII.
Deficiency of any of these coagulation inhibitors is Platelet count Platelet 1.5–4 lac/dL < 50, 000 /dL
function
associated with a thrombotic tendency and is defined as
thrombophilia. Bleeding time Platelet 2–8 minutes > 8 minutes
function
Hemostatic Changes in Pregnancy APTT (activated Intrinsic 28–30 sec > 40 sec
Pregnancy is associated with major changes in all aspects partial thrombo- pathway
plastin time)
of hemostasis, platelet coagulation, fibrinolytic and anti-
fibrinolytic components, such that the balance is shifted PT (Prothrombin Extrinsic 1.0–1.3 > 1.3
towards hypercoagulability to meet the hemostatic chal- time) system
lenge of delivery. Thrombin time Factor I and II 16–20 sec > 20 sec
There is an increase in all coagulation factors with the Fibrinogen level Fibrinogen 300–600 mg/dL < 100 mg/dL
exception of factor XI. Fibrinogen levels increase almost
two folds by term. There is no change or increase in D-Dimer Fibrinolytic <0.05 mg/L >0.05 mg/L
activity
antithrombin III activity, protein C (activated) shows a rise
postpartum. Protein S is reduced during pregnancy but
comes to normal post-delivery. related disorders are responsible for as high as 50% cases
The fibrinolytic activity is impaired during pregnancy of DIC.
and returns to normal rapidly following delivery. Though
the concentration of plasminogen and its activator Pathogenesis
increases in pregnancy, the concentration of PAI is
DIC is a paradox in which blood coagulation, clot
increased five-fold and an additional PAI-2 is produced
by the placenta. These two PAI depress fibrinolytic activity dissolution and bleeding, all take place at the same time.
during pregnancy. The basic pathology is that, a clot promoting agent gains
Pregnancy is a hypercoagulable state. Immediately entrance into the circulation ,then it induces a widespread
following delivery, there is evidence of contact system formation of fibrin monomers as well as activation
activation and platelet consumption. Increase in of fibrinolytic proteases. As a result, consumption of
fibrinogen, factor VIII and platelets also occurs a few days hemostatic factors occurs. That is why, DIC is also known
later. These changes lead to an increased risk of thrombosis as a type of consumptive coagulopathy. The pathological
at this time. To counter act this, following placental sequence results in a combined threat of thrombosis and
separation of maternal plasma fibrinolytic activity also bleeding, overwhelming the normal anticoagulant control.
increases rapidly. The coagulation and fibrinolytic system The thrombin which is generated cleaves fibrinopeptin from
revert to normal levels, 6 weeks after delivery. the fibrinogen and fibrin monomers are formed. The fibrin
Common tests for integrity of hemostatic mechanism monomers polymerize to form a clot or they polymerize
are listed in Table 45.1. with fibrinogen in FDPs. The activated fibrinolytic system
Disorders of coagulation and thrombosis are signifi- and FDPs, further impair the hemostatic mechanism in
cantly important to maternal morbidity and mortality. The plasma. The platelet count also decreases due to utilization
spectrum of coagulation disorders in pregnancy ranges of platelets in platelet thrombi, platelet aggregation and
from thrombotic coagulation disorders such as venous subsequent removal from the circulation. The low platelet
thromboembolism (VTE) to disseminated intravascular count further contributes to DIC. The ultimate outcome
coagulation (DIC). depends on the condition of the case, its speed and the
capacity of the host to generate clotting factor.
DISSEMINATED INTRAVASCULAR
Etiology
COAGULATION (DIC) Various disorders of pregnancy can manifest as DIC by
DIC is not a unique disease but can be an intermediate producing a clot promoting agent or causing endothelial
mechanism in many well-defined diseases. Pregnancy damage.
Abruptio placentae: It is the most common obstetrical Management

cause of DIC and it is present in 20% of women with The most important factor to remember in the management
abruptio. Decidual fragment and serum containing of DIC is that it is always a secondary phenomenon.
activated coagulation factors and other substances from Removal of the initiating stimulus is the mainstay of
the placental site enter in the venous circulation due to treatment along with support of maternal circulation
rupture of basal decidual plate. and replacement of blood components. If the patient is
Amniotic fluid embolism: In this, the relatively weak in shock due to bleeding, the initial treatment is started
thromboplastin that increases in potency with increasing with crystalloids. They should given in an amount of
the gestational age together with other substances which 2–3 times, the estimated blood loss and should be followed
activate factor X directly enter the circulation suddenly. by colloids till blood is available.
Intrauterine death (IUD): Chronic DIC occur in 35% Fresh whole blood not more than 36 hours old or packed
of patient who retain a dead fetus for more than3–4 cell with fresh frozen plasma (15 mL/kg) are infused as
they contain most of the coagulation factors. Platelet rich
weeks. Thromboplastin from the dead fetus is slowly but
plasma should be used. Platelet count, PT, activated partial
continuously absorbed and then, chronic progressive DIC
thromboplastin time (aPTT) fibrinogen level and FDP are
results.
done to assess the severity of DIC in every 4 hours.
Septicemia: Septicemia causes DIC as a result of bacteria
that possess potent endotoxin which produces several
effects such as activation of factor XII, platelet aggregation, VENOUS THROMBOEMBOLISM (VTE)
inhibition of fibrinolysis, leukocyte aggregation, direct VTE is a rare but potentially life-threatening condition that
endothelial injury and impairment of compensatory affects the pregnant women five times more frequently
mechanisms. than non-pregnant women of similar age. It is reported
Pre-eclampsia: Overt DIC is uncommon in pre-eclampsia to occur in 1:2000–1:20000 pregnancies but the true rate
but subclinical consumptive coagulopathy is present. may be 3–4 times higher. VTE occur more frequently in the
Abortion with saline and urea: Fleeting DIC often postpartum period and the period of maximum risk is the
first 7 days postpartum followed by the next 7 days. The two
accompanies saline or urea induced miscarriage with no
manifestations of VTE are deep venous thrombosis (DVT)
clinical consequences.
and pulmonary embolism (PE). DVT is approximately 3
times more common than PE in pregnancy.
Clinical Features
Once it sets in, DIC result in a self propagating vicious Pathophysiology
cycle manifesting as hemorrhage, shock and multiple Venous thrombosis are intravascular deposits composed
organ failure. Shock, further aggravate the problem. The of fibrin and red cell, with a variable platelet and leukocyte
spectrum of severity can be divided into three stages: component. They usually form in the region of slow or
Stage I: Low grade compensated DIC as seen in retained disturbed flow in large venous sinuses and valve cusp
dead fetus or pre-eclampsia. Laboratory test show an pockets in the deep veins of the calf or in venous segments
increase in FDP and fibrinogen and platelets are normal. that have been exposed to direct trauma. The factors
There is an increase in soluble fibrin complexes and an traditionally blamed in the pathogenesis of venous
increased ratio of von Willebrand factor to factor VIII. thrombosis are activation of blood coagulation, venous
stasis and vascular injury. All the three are operative
Stage II: Uncompensated DIC is present but no hemostatic
during pregnancy. The procoagulant factors increase in
failure is seen. This scenario is seen in small abruption,
pregnancy with decrease in inhibitors. There is a reduction
severe pre-eclampsia. Fibrinogen as well as platelets are
in fibrinolytic activity. Decreased venous tone and venous
decreased. There is a decrease in factor V, VII and FDP are
flow in the lower extremeties occurs in pregnancy due to
increased. the effect of progesterone. In addition, venous outflow
Stage III: Severe DIC with hemostatic failure is present obstruction may occur as a consequences of obstruction
in this stage, there is severe thrombocytopenia with gross of the inferior vena cava and the left iliac vein by the gravid
depletion of coagulation factors specially fibrinogen. There uterus. Passage of the fetal head through the birth canal
is an increase in FDP levels. This is seen in large abruptio also cause trauma to the pelvic veins. This trauma is further
and amniotic fluid embolism. increased in operative delivery.
Risk Factors pulses may be decreased or absent and signs of motor

The most important risk factor for a women experiencing weakness and sensory loss may occur.
pregnancy-related VTE is prior personal history of VTE,
Clinical Diagnosis
which increases the risk of VTE 3-fold to 5-fold. The next
most common risk factor is thrombophilia, which is It is non-specific because none of the signs and symptoms
present in 20–50% of women with VTE in pregnancy. Other are unique to the disease and all can be caused by non-
common risk factors include cesarean delivery, which thrombotic disease.
conveys twice the risk of VTE as vaginal delivery, obesity,
Differential Diagnosis
maternal cardiac disease, premature delivery and smoking.
It include cellulities, arthritis, lipoderma, lymphedema,
Diagnosis sciatic nerve compression, tendonitis, primary varicose
veins and superficial thrombophlebitis. Objective tests
The majority of women with VTE in pregnancy have have to be done to confirm the diagnosis of DVT. Once
clinical symptoms. The symptoms and signs of DVT DVT has been excluded by objective tests, then other
include leg pain and swelling (usually unilateral) and differential diagnoses such as Baker’s cyst, leg trauma,
lower abdominal pain (reflecting extension of thrombus postphlebitis syndrome and physiological swelling of leg
into the pelvic vessels and/or development of a collateral of pregnancy have to be considered.
circulation) and the symptoms of PE include dyspnea, A number of bedside maneuvers are used to illicit
chest pain, hemoptysis and collapse. tenderness in patients with suspected DVT.
Any woman with symptoms and/or signs suggestive of Lewenberg’ sign: This sign is illicited by wrapping a
VTE should have objective testing performed expeditiously sphygmomanometer cuff around each calf and then
and treatment with low-molecular weight heparin (LMWH) inflating both simultaneously. In DVT, pain occur in the
given until the diagnosis is excluded by objective testing, affected calf at a lower pressure then on the other side.
unless treatment is strongly contraindicated. Homan’s sign: It is performed by first flexing the patient’s
knee to approximately 30º and then suddenly partially
dorsiflexing the ankle. It causes squeezing of the relaxed
DEEP VENOUS THROMBOSIS (DVT) calf muscle from side-to-side and is painful.
It is an elusive illness that can result in suffering and death Measuring the leg: A difference of 2 cm or more in leg
if not recognized and treated effectively. Death can occur diameter on the same point above the medial malleolus is
when venous thrombi break off and form pulmonary of considerable significance.
emboli which can then obstruct the arteries of the lung. The subjective clinical assessment of DVT is unrealible
In non-fatal cases, DVT can become a chronic disease in and less than half of the women with clinically suspected
patients who survive the initial episode. These patients DVT have the diagnosis confirmed when objective testing
are prone to chronic swelling of the leg and pain due to is performed.
damage of valves of veins. In addition, these patients are Compression duplex ultrasound should be undertaken
more prone to recurrent episodes of thromboembolism. where there is clinical suspicion of DVT. If ultrasound is
negative and there is a low level of clinical suspicion,
Clinical Features anticoagulant treatment can be discontinued. If ultrasound
is negative and a high level of clinical suspicion exists,
The clinical manifestations of DVT are protean but the
anticoagulant treatment should be discontinued but the
characteristic symptoms consist of pain, swelling and
ultrasound should be repeated on days 3 and 7.
warmth of the lower extremity. These symptoms occur due
to venous outflow obstruction and inflammation of the Management
vessel wall and surrounding tissue.
Guidelines for management of venous thromboembolism
in pregnancy are listed in Table 45.2.
Phlegmasia Cerulea Dolens
It is a rare manifestation of DVT and is seen in 1% of cases.
The cause is extensive deep vein thrombosis of iliac and
PULMONARY EMBOLISM (PE)
femoral veins. There is massive swelling of legs with severe Women presenting with symptoms and signs of an acute
pain and tenderness. The skin on the leg is stretched tight PE should have an electrocardiogram (ECG) and a chest
and shining with mottled cyanosis. Peripheral arterial X-ray (CXR) performed.
TABLE 45.2: Evidence-based clinical practice guidelines for antithrombotic therapy for venous thromboembolism pregnancy
Risk factor Recommendations
Women with a single episode of VTE associated with a transient risk Clinical surveillance and anticoagulant prophylaxis postpartum
factor that is no longer present
Women with a single episode of VTE and thrombophilia (confirmed Prophylactic or intermediate-dose LMWH or UFH, plus postpartum
laboratory abnormality) and a strong family history of thrombosis who anticoagulation for at least 6 weeks (for a total minimum duration
are not receiving long-term anticoagulants of therapy of 6 months)
Women with antithrombin deficiency and no previous VTE Antepartum and postpartum prophylaxis
Women with thrombophilia (other than antithrombin deficiency) and Clinical surveillance or prophylactic LMWH or UFH and anticoagulant
no previous VTE prophylaxis postpartum
Women with multiple (≥ 2) episodes of VTE who are not receiving long- Prophylactic, intermediate-dose or adjusted-dose UFH or adjusted-
term anticoagulants dose LMWH followed by long-term anticoagulation postpartum
Women with multiple (≥ 2) episodes of VTE who are receiving long-term Adjusted-dose UFH or LMWH followed by resumption of long-term
anticoagulants anticoagulation postpartum
All women with previous DVT, antenatal and postpartum Use of graduated elastic compression stockings
Women with antiphospholipid antibody syndrome and a history of Antepartum aspirin plus prophylactic or intermediate-dose UFH or
multiple (≥ 2) early pregnancy losses or ≥ 1 late pregnancy losses, pre- LMWH
eclampsia, IUGR, or abruption
Abbreviations: VTE—Venous thromboembolism; DVT—Deep venous thrombosis; LMWH—Low-molecular-weight heparin; UFH—Unfractionated
heparin; IUGR— Intrauterine growth retardation
In women with suspected PE who also have symptoms absence of contraindications. The common classes of anti-
and signs of DVT, compression duplex ultrasound should coagulation drugs are as follows:
be performed. If compression ultrasonography confirms � Indirect thrombin inhibitors: These include unfrac
the presence of DVT, no further investigation is necessary tionated heparin and LMWH (enoxaparin), as well as
and treatment for VTE should continue. synthetic heparin pentasaccharides (fondaparinux)
In women with suspected PE without symptoms and and the new orally administered factor Xa inhibitors
signs of DVT, a ventilation/perfusion (V/Q) lung scan or a (rivaroxaban)
� Direct thrombin inhibitors: These include argatroban,
computerized tomography pulmonary angiogram (CTPA)
lepirudin, and bivalirudin
should be performed.
� Vitamin K antagonist: This includes warfarin.
When the chest X-ray is abnormal and there is a clinical
Heparin (both unfractionated and low molecular
suspicion of PE, CTPA should be performed in preference
weight) is the preferred drugs for management of VTE in
to a V/Q scan. Alternative or repeat testing should be
pregnancy. Unfractionated heparin (UFH) is listed as a
carried out where V/Q scan or CTPA is normal but the category C drug in pregnancy and LMWH is category B.
clinical suspicion of PE remains. Anticoagulant treatment Both are large molecular weight molecules and neither
should be continued until PE is definitively excluded. crosses the placenta.
Treatment with therapeutic doses of subcutaneous
Treatment LMWH should be employed during the remainder of the
Once the diagnosis of VTE (Table 45.2) is suspected, pregnancy and for at least 6 weeks postnatally and until at
therapeutic anticoagulation should be initiated in the least 3 months of treatment has been given in total.
1. Define the term fibrinolytic system.
2. What are common classes of anticoagulation drugs?
i. ______________ sign is illicited by wrapping a sphygmomanometer cuff around each calf and then inflating both
simultaneously.
ii. There are two parallel mechanisms, which are integral to normal hemostasis ______________ and ______________ system
of coagulation.
iii. ______________ is approximately 3 times more common than PE in pregnancy.
iv. The most important factor to remember in the ______________ of ______________ is that always secondary phenomenon.
46 Thyroid Disease in Pregnancy
Sudha Salhan, Divya Pandey, Sunita Seth, Meenakshi Bhatt
BACKGROUND TABLE 46.1: Changes in maternal thyroid physiology

Physiological changes
Thyroid disorders account for the second most common in pregnancy Response in thyroid function
endocrine disorders affecting the women of reproductive
Raised estrogen Raised serum TBG
period. Besides adversely affecting fertility, it can also
Raised serum TBG Raised bound form
effect fetal growth and development.
Raised total T4 and T3
For optimum thyroid function assessment during
Raised hCG Raised FT4
pregnancy, due consideration needs to be given on clinical
Reduced TSH
symptomatology along with thyroid-stimulating hormone Raised dietary iodine requirement
(TSH) levels and free thyroxine (T4) (not total T4) should
Raised GFR and renal Raised renal clearance of Iodide
be done. plasma flow Reduced PBI
Raised iodine clearance Raised thyroid hormone production
CHANGES IN THYROID PHYSIOLOGY in endemic zone
Raised goiter formation
DURING PREGNANCY
Raised type III deiodinase Raised T3 and T4 metabolism

During Pregnancy enzyme Raised demand for T4 and T3
Increased thyroid Raised thyroglobulin
Estrogen induces increase in synthesis and simul
hormone demand Raised thyroid volume (30%)
taneous decreased hepatic clearance of thyroid binding
Raised goiter in endemic zones
globulin (TBG).
Abbreviations: TBG—Thyroid-binding globulin; hCG—Human chorionic
Level of deviodinase II and III enzymes in placental
gonadotropin; GFR—Glomerular filtration rate; T4—Thyroxine; T3—Trii-
tissues during pregnancy is raised, which consequently odothyronine; FT4—Free thyroxine; TSH—Thyroid-stimulating hormone;
leads to increase RT3 (reverse triiodothyroxine), which PBI—Plasma bound iodide
is biologically inactive form.
Fifty percent increase in glomerular filtration rate (GFR)
and renal plasma flow increase the renal clearance fetus is entirely dependent on maternal levothyroxine (LT4)
of plasma bound iodide (PBI) thus, decompensates for brain and neurodevelopment. Thus, any abnormality
women due to pre-existing or borderline iodine defici in maternal thyroid physiology especially in first trimester
ency leading to goiter. can adversely affect the fetus.
Thus, the changes depicted in the Table 46.1 and 46.2
should be considered during evaluation of thyroid function UNIVERSAL SCREENING FOR
during pregnancy.
THYROID DISEASE
Changes in Thyroid Function in Fetus The American College of Obstetricians and Gynecologists
Fetal thyroid becomes mature and functional by the end of (ACOG), the American Association of Clinical Endocrino
first trimester, i.e. around 12 weeks. Before this period, the logists (AACE) and the American Endocrine Society, do not
Thyroid Disease in Pregnancy 451
TABLE 46.2: Thyroid function changes in normal pregnancy and in thyroid surgery raise the risk of fetal and neonatal hyperthy-
thyroid disease in pregnancy roidism and goiter which is not seen with antithyroid medi-
TSH (Thyroid- cation, which reaches fetus transplacentally and blocks the
Free T4 stimulating action of thyrotropin receptor antibodies. The importance
Clinical condition (thyroxine) hormone) of achieving euthyroidism in hyperthyroid females should
Pregnancy Unchanged Variable* be stressed upon as it leads to rise in rates of congenital mal-
Subclinical hypothyroidism Unchanged Increased formations in fetus.
Overt hypothyroidism Decreased Increased
Subclinical Unchanged Decreased HYPOTHYROIDISM
hyperthyroidism
Overt hyperthyroidism Increased Decreased The overall incidence of hypothyroidism is 0.3–3% of
*First trimester: Thyrotropic effect of human chorionic gonadotropin which overt hypothyroidism account for 0.3–0.5% while
(hCG) leads to weak TSH rector stimulation leading to decrease in TSH subclinical hypothyroidism accounts for 2–5%.
levels till first 12 weeks of pregnancy. After first trimester, with decline
in hCG levels, TSH levels return to baseline levels. Subclinical Hypothyroidism
Source: American College of Obstetricians and Gynecologists
Practice (ACOGP) Bulletin number 148. Thyroid April 2015; Volume It refers to biochemical derangement of thyroid profile
125, number 4, April 2015:996-1004. (raised TSH with normal FT4 level) in a clinically asympto
matic individual. Currently, there is no evidence that
identification and treatment of subclinical hypothyroidism
recommend universal screening for the thyroid disease in
during pregnancy improves adverse pregnancy outcomes
pregnancy (level A evidence).
(ACOG, level I evidence).
However, screening should be extended to females who
are at increased risk of overt hypothyroidism (either sign or Overt Hypothyroidism
symptoms of hypothyroidism or personal history of thyroid
It is characterized by raised level of TSH and decreased
disorder). Even asymptomatic individuals with mildly
free T4 (Table 46.2).
enlarged thyroid do not warrant thyroid testing, as upto
30%, thyroid enlargement can be seen during pregnancy. Causes
The first-line screening test for assessment of thyroid
The most common cause of hypothyroidism in pregnancy
dysfunction during pregnancy is TSH measurement
in iodine sufficient areas is autoimmune, i.e. Hashimoto’s
(ACOG, level A evidence) (ACOG 2015) (Table 46.3).
thyroiditis, where antithyroid antibodies (anti-thyroglobulin
and antithyroid peroxidase) are present which lead to
ROLE OF PRECONCEPTION COUNSELING thyroid destruction. In endemic zones, however, the most
Importance of attaining euthyroid status before concep common cause is iodine deficiency.
tion should be a part of preconception counseling while
dealing such women. Clinical Presentation
In case of hypothyroid women, who are stable on The clinical symptoms of this clinical condition are often
thyroid hormone supplementation should be counseled indifferentiable from common pregnancy symptoms
to notify their physician to increase the dose of thyroid like fatigue, muscular cramps, weight gain, constipation,
medication by 30% after first missed period or positive edema and loss of hair and skin dryness. Additional sign
urine pregnancy test. can be a prolongation of relaxation phase of deep tendon
On the other hand, women with known hyperthyroidism reflexes (DTR).
must be counseled about the available treatment, their
adverse effects and impact on future pregnancies. Anti Effect on Pregnancy (Table 46.3)
thyroid treatment available are antithyroid medica tion, Adverse pregnancy outcomes like raised incidence of mis-
radioactive iodine (RAI) ablation and thyroidectomy. All carriage, preterm labor, abruptio placentae, pre-eclamp-
side effects of antithyroid drugs like congenital abnormali- sia and even intrauterine death (IUD) are known to occur.
ties and neonatal hypothyroidism should be explained. The There is no recommendation for termination of pregnancy
patients who have RAI ablation should defer the conception even if the woman is found to be severely hypothyroid at
for 6 months after the complete therapeutic dose. RAI and any stage of pregnancy.
TABLE 46.3 : Indications of thyroid screening in pregnancy are needed for patients who had low thyroid levels, post-
Presently on thyroid � Presence of goiter thyroidectomy or post radioiodine ablation. Post-delivery,
medication � History of neck irradiation the dose should be reduced to pre-pregnancy level and
Family history of autoimmune � Autoimmune disease dose readjustment to be checked by serum TSH.
thyroid disorder
History of
Prevention of Maternal Iodine Deficiency
� Thyroid dysfunction in
postpartum period It should be ensured that expectant mothers especially from

� Previous neonate with endemic regions should have the recommended amount
thyroid disease of iodine which is 220 µg/day for pregnant females and
� On antithyroid medication
290 µg/day in case of lactating females.
� Diabetes mellitus type 1
Source: The American Thyroid Association task force on thyroid disease

during pregnancy and postpartum. Stagnaro-Green A, Abalovich M, et HYPERTHYROIDISM
al. Guidelines of the American Thyroid Association for the diagnosis and
management of thyroid disease during pregnancy and postpartum.
The overall incidence of hyperthyroidism is 0.2% which
Thyroid 2011;21(10):1081-1125. doi:10.1089/thy. 2011.0087 is less than hypothyroidism. Grave’s disease is the most
common cause of this condition.
Subclinical hyperthyroidism: It refers to very low serum
Effect on Neonate
TSH with normal free T4 levels (Table 46.2). The incidence
There is rise in incidence of low birth weight and impaired is 1.7%. Subclinical condition has not been associated
neurocognitive development of the newborn. However,
with unfavorable pregnancy outcomes. Treatment of
maternal autoantibodies rarely cross placental barrier to
subclinical hyperthyroidism is not required as the anti
cause fetal hypothyroidism, which is estimated to be only
thyroid medication gets transferred through placenta and
1 in 180,000 neonates.
can adversely affect the fetus.
Overt hyperthyroidism: It is characterized by raised level
Diagnosis
of FT4 and low TSH reference range FT4: 0.8–1.8 mg/dL
Serum TSH is the most sensitive and reliable marker.
(Table 46.2).
Trimester wise TSH reference range recommended by
American Thyroid Association is as follows: Causes
First trimester 0.1–2.5 mIU/L
In 95% cases, the cause of hyperthyroidism in pregnancy is
Second trimester 0.2–3 mIU/L
Grave’s disease. Other causes are gestational trophoblastic
Third trimester 0.3–3 mIU/L
diseases, solitary toxic adenoma, viral thyroiditis, nodular
Free T4 level should be measured in case TSH is goiter and pituitary or ovary tumors. Thyrotropic effect
abnormally low. Routine testing of antithyroid antibodies of hCG in Hyperemesis gravidarum can lead to transient
in all cases of hypothyroidism is not recommended hyperthyroidism.
(ACOG, 2015).
Clinical Presentation
Treatment The clinical symptoms include tremors, palpitations,
Levothyroxine is mainstay of the treatment. The starting weight loss, goiter, insomnia, intolerance to heat, exces-
dose is 1–2 µg/kg/day or approximately 100 microgram/day. sive sweating, proximal muscle weakness, hypertension,
Levothyroxine should be taken empty stomach. Milk, iron, nervousness and frequent bowel movements.
calcium and proton pump inhibitors should be avoided
within 4 hours of ingestion. Patients who are known Effect on Pregnancy
hypothyroid controlled on thyroid supplementation, The course of disease in pregnancy is variable depending
need dose increment by 30% (2 additional tablet/week i.e. on the etiology. Grave’s disease being an autoimmune
9 tablets/week instead of 7) as soon as urine pregnancy disease has initial exacerbation of symptoms in first
test is positive. The goal of treatment is to maintain the trimester due to thyrotropic action of hCG. Improvement
TSH level less than 2.5 mIU/L and the dose is increased is seen in second trimester onwards, the symptoms
by 25–50 microgram/day to reach this target. Serum TSH improve but the disease recurs in postpartum period.
level is to be measured every 4–6 weeks. Higher doses During pregnancy adverse events like congestive heart
failure (CHF), abruption placenta, preterm labor and pre- divided dose. Once thyrotoxicosis is controlled, PTU dose
eclampsia is common. Uncontrolled hyperthyroidism at should be decreased and patient should be kept on lowest
the time of conception is known to cause fetal congenital possible dose preferable < 100 mg/day. Dry should be
malformations. continued during lactation.
Transient leukopenia can occur in 10% cases with the
Effect on Neonate thionamide therapy but this does not call for stopping
There is rise in incidence of low birth weight, prematurity, the treatment. Agranulocytosis, which occurs in less than
small for gestational age, stillbirth, fetal and neonatal 1% patients, however, mandates stopping the treatment.
goiter, and fetal thyroid dysfunction even fetal hydrops. Routine liver function test (LFT) and total leucocyte count
There can be fetal hyperthyroidism or hypothyroidism due (TLC) is not done in patients on thionamide medication.
to transplacental shift of maternal antibodies like thyroid- But patient is properly instructed to stop the drug and get
stimulating immunoglobulin (TSI) and TSH binding TLC done, in case of sore throat. RAI is contraindicated in
inhibitory immunoglobulins. pregnancy and patient should conceive after 3 months of
completion of therapy.
Diagnosis
In addition to changes in thyroid profile, (Table 46.2), Contraception
antithyroid antibodies can be helpful in diagnosis. RAI Patients with thyroid disorders (goiter, hypothyroid or
uptake scan used for diagnosis of hyperthyroidism is hyperthyroid) fall under category 1(i.e. can be prescribed
contraindicated in pregnancy. without any risk) as per world health organization (WHO)
Medical Eligibility Criteria formulated for hormonal
Antepartum Fetal Surveillance contraception. Intrauterine contraceptive devices (IUCDs)
Antepartum surveillance can be started at 32 weeks can also be prescribed.
onwards for patients with well controlled hyperthyroidism Role of subtotal thyroidectomy: It has to be done
as for other low-risk pregnancies. However, patients with preferably in second trimester and is indicated if patient
poorly controlled hyperthyroidism fall in the high risk has adverse reaction to antithyroid drugs (ATD), or requi
group and need earlier fetal surveillance (ACOG Practice ring persistently high dose of ATD (>450 mg/day of MMI)
Bulletin no. 145, July 2014). or having uncontrolled hyperthyroidism.
Treatment Thyroid Nodule in Pregnancy (Fig. 46.1)

Previously, propylthiouracil (PTU), a thionamide which If recognized for the first time in pregnancy and patient
inhibits thyroid biosynthesis and peripheral conversion of is not hyperthyroid, an ultrasonography (USG) and fine
T4 to T3 had been the drug of choice for hyperthyroidism needle aspiration cytology (FNAC) is recommended to
in pregnancy. Methimazole (MMI), another thionamide rule out malignancy.
was not used due to Methimazole induced embryopathy
which is characterized by choanal or esophageal atresia Endemic Goiter
and aplasia cutis. The endemic zones for iodine deficiency are the Andes,
PTU use, however, has been associated with hepato- Sub Himalayan belt, Southeast Asia and Central Africa.
toxicity. Later in 2009, United States Food and Drug Although, frank hypo or hyperthyroidism is not present
Administration (USFDA) issued a safety alert regarding
PTU induced hepatotoxicity (seen in 0.1–0.2%
cases). After this the recommended treatment, during
pregnancy is PTU during first trimester followed by switch
over to methimazole therapy from second trimester.
Dose of antithyroid medication is adjusted with the
goal of maintaining FT4 at or just above the upper limit
of non pregnant reference range so as to avoid fetal
hypothyroidism. TSH and FT4 are to be measured every
2–4 weeks initially and then every 4–6 weeks. The dose are
as follows—PUT 100–150 mg every 8 hours, MMI 20 mg in Fig. 46.1: Thyroid nodule in pregnancy
yet pregnancy outcome is adversely affected. The abortion Thionamides, PTU is administered 600–800 mg orally stat
rate is seen in about one-third of the patients with followed by 150–200 mg every 4–6 hourly. After 1–2 hours
hypothyroidism. Even those who are euthyroid, iodine of PTU administration, saturated solution of potassium
deficiency in first trimester can lead to serious effects on iodide is given 2–5 drops orally, every 8 hours. Besides
fetal central nervous system (CNG) leading to nuerological this, Lugol’s solution or lithium carbonate can also be
cretinism. The baby is usually clinically euthyroid but may given. Bronchodilators are given for bronchospasm
be biochemically hypothyroid, have goiter with mental and phenobarbital for extreme restlessness. Supportive
retardation, deafness and spasticity. This condition does measures include oxygen, intravenous (IV) fluids,
not respond to any kind of treatment. electrolyte correction and antipyretics. Termination of
When iodine deficiency leads to fetal hypothyroidism pregnancy should be reserved for fetal indications that
in the second and third trimesters, the baby is born as outweigh maternal risks.
a hypothyroid cretin. The baby is lethargic, has a large
tongue, a hoarse cry, dry skin, a pot belly and sometimes POSTPARTUM THYROID (PPT)
an umbilical hernia. Goiter is seen less commonly than
neurological cretinism. This type of cretinism responds to DISORDERS
iodine replacement or to thyroid hormone replacement. The Postpartum Thyroiditis
prognosis is directly related to how soon the replacement is
PPT usually occurs during first postpartum year with
started. Both forms of cretinism and the effects of maternal
prevalence of 1–17% of females and 25% women with
hypothyroidism are prevented by treatment with iodine
type 2 diabetes mellitus (DM). It is autoimmune in nature
before pregnancy occurs (preconceptional).
due to antithyroid peroxidase (anti-TPO) antibodies
Carcinoma Thyroid and lead to transient exacerbation of underlying silent
Normal thyroid profile in presence of irregularly enlarged thyroiditis. There is cytotoxic T cell and antithyroid
thyroid gland calls for ruling out malignancy. Differentiated antibodies mediated thyroid gland destruction leading
carcinoma of thyroid is one of the most common tumors to rapid release of thyroid hormones. It can present as
occurring in the young females, thus needs to be excluded. hypothyroidism, hyperthyroidism and/or hyperthyroidism
In case, it is diagnosed during first trimester, surgery can followed by hypothyroidism in first year postpartum
be safely scheduled during the second trimester but if without overt thyroid disease before pregnancy. It may
diagnosed in later trimester, surgery can be deferred till occur in cases of Grave’s disease who may become
6 weeks postpartum. Natural history of any thyroid cancer euthyroid during pregnancy. Patients with established
remains unaltered by pregnancy. but mild Hashimoto’s disease may also experience
PPT. In fact postpartum silent thyroiditis may occur and
mask the development of postpartum Grave’s disease.
THYROID STORM If the patient is asymptomatic no therapy is required
Thyroid storm and CHF due to thyrotoxicosis are medical and the patient is seen every 4 weeks because of the risk
emergencies. Although rare, occurring in 1–2% of pregnant of subsequent hypothyroidism. Initial hyperthyroidism
females, thyroid storm can cause potential complication (1–4 months) is followed by hypothyroidism (5–8
of CHF and pulmonary hypertension leading to maternal months). If the patient is symptomatic, a brief course of
morbidity and mortality. This hypermetabolic state is propranolol (10–20 mg qid) may be used. Prophylaxis
characterized signs and symptoms like palpitations, fever, with steroids in mothers with elevated first trimester
tremors, nervousness, cardiac arrhythmias and CNS antithyroid antibodies is contraindicated because of the
dysfunction due to involvement of thermoregulation, low morbidity and excellent response of PPT to timely
cardiovascular and CNS leading ultimately to multiorgan treatment. Thionamides are not recommended because
failure and death. the resolution or progression to hypothyroidism occurs
When suspected or anticipated, evaluation of FT3, spontaneously and theoretically they would have little
FT4 and TSH levels should be done but the treatment effect on a gland undergoing destruction and inactivation
should not be withheld due to pending investigations as of organification mechanisms. Postpartum depression or
this is an emergency. Treatment include intensive care psychosis is more common in these women and must be
unit (ICU) admission. Beta-blockers like propanolol are treated. Postpartum thyroiditis may recur in subsequent
given in treatment and prophylaxis of this condition. pregnancies.
Postpartum Grave’s Disease Hypothyroidism with thyroid tissue present: There

The symptoms occur 3–5 months postdelivery and RAI may be an iodine transport defect. Defects in the steps
uptake is elevated. This condition may become transient of biosynthesis are inherited as autosomal recessive
or permanent. A thyroid ultrasound may be done if the traits. A family history of goitrous cretinism must alert
mother is lactating and a radioactive thyroid scan if she is the physician. At birth the thyroid may be of normal size
not lactating to exclude toxic uni or multinodular goiter. because of in utero supply of the mother’s hormone.
Treatment is by PTU but if the patient does not respond, The development of the central nervous system is
surgery/destructive therapy with RAI is recommended. dependent on thyroid hormone from the early fetal life.
In lactating mothers a low dose PTU is preferred because If the mother’s hypothyroidism is not treated there can
of its poor concentration in breast milk as compared to be irreversible brain damage.
methimazole. As there is risk of neonatal hypothyroidism, In babies of mothers with past or current Graves’
the newborn should be regularly tested for thyroid functions. disease, transient neonatal hypothyroidism is seen. It is
Autoimmune thyroid diseases like other autoimmune due to the transplacental transmission of PTU. However,
diseases, e.g. rheumatoid arthritis and systemic lupus transient athyrosis is observed secondary to blocking
erythematosus (SLE) undergo spontaneous remission by thyrotrophin binding inhibitory immunoglobulins.
during the later half of pregnancy because of the suppression There may also be suppression of the fetal and neonatal
of humoral and cell mediated immunity (CMI). Relapse of thyroid by excess T4 from the thyrotoxic mother or due
these diseases in the postpartum period is due to regain of to TSI (Connor and Styne 1986).
cell mediated and humoral immunity. Approximately, 95% Neonatal screening and the start of aggressive treat
of the cases of postpartum hyperthyroidism are accounted ment within 2 weeks of birth generally restores the IQ. There
for by the early phase of postpartum thyroiditis (70–80%) may be association with Down syndrome. The mother’s
and the onset of recurrence of authentic postpartum hormones may mask the signs and symptoms at birth, except
Graves’ disease (PGD) (10–15%). sometimes when goiter is seen. These children may be large
for dates. Feeding and respiratory difficulties (mostly due to
CONGENITAL HYPOTHYROIDISM goiter) may be seen. Distension of the abdomen, vomiting,
prolonged jaundice, hypotonia, hypothermia, large post
Congenital hypothyroidism is seen in approximately 1 in erior fontanel, hoarse cry, dry skin, coarse facies with
4000 births (Fisher 1997) twice as often in females as in macroglossia, umbilical hernia, constipation and anemia
males. may be seen.
Causes for congenital hypothyroidism can be clubbed Differentiation from Down syndrome is done by the fact
into groups as follows.
that babies with Down syndrome are more active neonates
Primary hypothyroidism, thyroid agenesis, due to
with typical stigmata of the syndrome. X-ray of bones
muta
tions in the TSH-receptor, PAX-8 or TTF-2. It
shows delayed ossification in hypothyroidism. Distal and
has a hereditary predisposition. A small amount of
proximal tibial non-ossification reflects thyroid hormone
thyroid tissue may be present. Rarely, there can be
deficiency in utero. Once diagnosed a thyroid scan is done
maternal and fetal pituitary deficiency. Antithyroid
to know the size of the gland (whether normal or small).
drugs or iodine ingested by the mother affect thyroid
function. PTU taken by pregnant women may lead to Screening is also done to see increased TSH level (>80
the birth of a newborn with a small goiter and transient mg/mL) in neonatal blood. There may be low thyroxine
hypothyroidism in 1 in 100 cases. Large doses of iodine level (<6 mg/mL) as well. We may miss the rare congenital
ingested by a pregnant woman in chronic lung disease pituitary hypothyroidism. These children are referred to an
is another cause. As little as 12 mg iodine daily may endocrinologist.
cause goiter in the neonate. The antiarrhythmic drug Treatment must be started vigorously as soon as
amiodarone (containing 75 mg iodine per 200 mg possible. Normal IQ can be restored but there may remain
capsule) may cause goiter in some fetuses. Ultrasound speech disorders or non-coordination of fine motor
examination may delineate a large goiter in utero. movements.
After delivery there may be difficulty in maintaining Visualization of the fetal goiter by ultrasound in the
an adequate airway and immediate surgery may antenatal period or ultrasound guided umbilical blood
be necessary if there is a huge goiter. Hypothyroidism sampling can diagnose fetal hypothyroidism. In these
may be temporary but mental retardation may occur. cases a trial of intra-amniotic or intramuscular injection of
T4 into the fetal buttocks is under trial as in utero therapy levels are five times the upper limit of normal fetal and
(Nicolini and co-workers 1996). neonatal hyperthyroidism is to be suspected.
The condition is more or less self-limiting as maternal
NEONATAL HYPERTHYROIDISM immunoglobins disappear within 6 weeks.
Breastfeeding: If the mother is receiving less than 15 mg
This is rarely seen. The cause is more often thyroid
carbimazole per day and propylthiouracil (PTU) of less
stimulating immunoglobulins (TSI) in Graves’ disease or
than 150 mg/per day, then breastfeeding is allowed.
rarely Hashimoto’s disease being transferred to the fetus
But PTU is highly protein bound and hence, excretion
through the placenta.
in milk is very little (0.025–0.077%) than carbimazole.
Neonatal thyrotoxicosis is temporary till the mother’s TSI
Therefore, PTU in preferred in lactating mothers. Except
are cleared from the newborn’s circulation. It persists when
the newborn dominantly inherits the disease and there is the mildest biochemical hyperthyroidism, all neonatal
no maternal autoimmunity. There may be fluctuations in thyrotoxicoses are to be treated. Short-term treatment is
TSH receptors and stimulation of protein, e.g. McCune- life-saving. However, hypothyroidism is to be prevented
Albright syndrome. Here, more than two generations have and this requires close monitoring. Thionamides (both
thyrotoxicosis or first-degree relatives are involved. The PTU and carbimazole) block the organification of iodine
occurrence of neonatal hyperthyroidism depends on the and the coupling of iodothyronine residues, thus blocking
control of the mother’s condition especially in the second- the thyroid hormone synthesis. PTU also inhibits the
half of pregnancy. The incidence may be as high as 22% in peripheral tissues deiodination of T4 to T3 (which is more
newborns of these mothers. The complications can be heart active). Hence, PTU is the preferred drug. A dose of 5–10
failure, tracheal compression (due to goiter), infections and mg/kg/day of PTU TDS or 0.5–1.5 mg/kg/day carbimazole
thrombocytopenia. Tachycardia is common. There may be once daily are given. However, because only synthesis of
arrhythmia, systemic and pulmonary hypertension. There the hormone is prevented the stored hormones continue
can be growth retardation due to hyperthyroidism and also to be released till these stores are exhausted. Hence, the
pre-eclampsia in the mother. Intrauterine fetal death occurs response will not be seen till then. If iodine solution is
in 5–7% of treated mothers and 24% of untreated mothers. given along with thionamides it will inhibit the release
Preterm delivery is seen in 4–11% in treated women and if thyroid hormone. Saturated potassium iodide (KI) as
53% in untreated ones. Nonimmune hydrops is seen one drop daily or Lugol’s solution (5% KI, 8 mg iodine/
because of cardiac failure. drop) 1–3 drops/day is given. Ioponoic acid and sodium
CNS signs are irritability, restlessness and jitteriness. ioponate are also used 0.5 g every 3 days.
Periorbital edema, lid retraction and exophthalmos may
To control adrenergic effects, β-blockers are given.
be seen.
Propranolol in a does of 0.27-0.75 mg/kg TDS can be given
Hypermetabolism is seen as diarrhea, sweating,
but needs close monitoring for serious hypoglycemia,
flushing, increased appetite and later weight loss.
bradycardia and hypotension. For cardiac failure digoxin
Hepato splenomegaly, acrocyanosis, lymphadenopathy,
and diuretics are used. Cortisone, prednisolone 2 mg/
enlargement of the thymus, thrombocytopenia causing
kg/day is used in severe neonatal hyperthyrotoxicosis to
bruising and petechial hemorrhages, advanced bone age,
craniosynostosis, hyperviscosity and microcephaly can be suppress deiodination of T4 to T3 and to replace hyper-
seen in the fetus and the neonate. catabolism of endogenous glucocorticoid by thyroid
There is very little data on the long-term effects of hyper hormones. Irritability and restlessness can be controlled
thyroidism in the infants and after infancy. No adverse by sedatives.
effects are seen due to the mother taking antithyroid drugs Exchange transfusion may be needed to reduce TSH
during pregnancy. levels and to treat non-immune hydrops. Weekly review is
Management consist of testing for TSH and T4 levels carried out till the child becomes stable. It may require 4–8
after birth. A high index of suspicion should be maintained weeks. However if there is thyrotoxicosis due to activated
in babies who show an evidence of thyrotoxicosis in utero. mutations of the TSH receptor then ablative surgery is
They are kept for a longer time in the hospital and closely performed. Neurological follow-up is required for a long
observed. The mother’s TSH levels are measured. If the period.
1. What do you understand by the term hypothyroidism?
2. Can low thyroid levels increase a baby’s risk of low IQ?
3. State True/False:
i. In case of hypothyroid women, who are stable on thyroid hormone supplementation should not be counseled to notify their
physician to increase the dose of thyroid medication.
ii. Grave’s disease being an autoimmune disease has initial exacerbation of symptoms in first trimester due to thyrotropic
action of hCG.
47
Neurological Disorders
in Pregnancy
Estrogens probably stimulate the seizure.

SEIZURE
Increased plasma clearance of the anticonvulsants in

Seizure disorders are the most common central nervous pregnancy leads to sub-therapeutic drug levels. This is
ailment seen in pregnancy. Besides, seizure disorders due to physiological changes during pregnancy such as:
in pregnancy, we will discuss certain other uncommon •• Increased nausea and vomiting
neurological problems that can be encountered during •• Increased blood volume
pregnancy. •• Increase in glomerular filtration rate (GFR)
Seizure is defined as paroxysmal disorder of the central •• Altered gastric motility.
nervous system (CNS) characterized by abnormal neuro Other factors:
nal discharge and muscle contractions involving a group •• Use of antacids
of muscles or generalized with or without loss of con •• Non-compliance in the drug intake
sciousness. •• Sleep deprivation
•• Hypoventilation during labor.
EPILEPSY Drug interactions: Induction of hepatic, plasma and
placental microsomal enzymes by the drugs leading to
This is a defect characterized by a tendency for two or their rapid clearance from the blood.
more recurrent seizures unprovoked by any known insult.
Affecting approximately 0.5–1% of the general popula
Effect of Epilepsy on Pregnancy
tion, seizure disorders are the most common neurologic
disorder encountered in antenatal period. Multidisci Besides increase in the incidence of congenital malforma-
plinary care by both obstetrician and neurologist is tions in the fetus, there are increased risks of abortion, fetal
needed for optimum maternal and fetal outcome. growth restriction, oligohydramnios and even intrauterine
death.
Effect of Pregnancy on Epilepsy
While the seizure frequency increases in about one-third Effect of Anticonvulsant Medications on the
patients during pregnancy, it remains unchanged in about Fetus
two–thirds of them. Poorly controlled epilepsy during pre-
Antiepileptic medications are associated with major con
pregnancy state suffers deterioration and even experience
genital malformations. This is true even more in context to
exacerbation during pregnancy.
However, it may be static or even show improvement in a those patients who are on polytherapy, sodium valproate
compliant patient kept under close supervision. There may or topiramate monotherapy. Orofacial clefts are the most
be an alteration in the drug levels due to decrease in the common major malformations. Specific fetal hydantoin
protein-binding and thus, an increased free concentration syndromes have been well characterized and include
of the drugs. mild to moderate mental retardation, microcephaly,
The increase in seizure activity during pregnancy may developmental delay, pre and postnatal growth retarda
be due to variations in the blood concentration of drugs. tion, facial clefts and dysmorphism, nail hypoplasia and
This is due to following reasons: hypertelorism.
Neurological Disorders in Pregnancy 459
TABLE 47.1: Dosage and side effects of common antiepileptics

Congenital
Drug rate Maternal effects Fetal effects malformation Usual dose
Phenytoin Megaloblastic anemia, Fetal hydantoin syndrome, 3–7% 150–300 mg/day in divided
ginigival hyperplasia, craniofacial defects, fetal growth dose
hirsutism, nystagmus, restriction
ataxia
Carbamazepine Drowsiness, Possible craniofacial and neural 3–6% 600–1200 mg/day in divided
leukopenia, ataxia, tube defects dose
mild hepatotoxicity
Valproic acid Thrombocytopenia, Neural tube defects and possibly 5–11% 500–2 gm/day
ataxia, alopecia in divided dose craniofacial and
drowsiness skeletal defects
Trimethadione Growth delays, cardiac and 300–500 mg/day
ocular defects microcephaly,
hypospadias, low set ears palatal
abnormalities, incompatible
with pregnancy, 2/3 have major
congenital defects
Lamotrigine Rashes Cleft lip and palate 2–3% 300–500 mg/day
Levetiracetam – – 0.6–2% 1000–3000 mg/day
Patients treated with a single anticonvulsant and the Newer antiepileptic drugs like gabapentin, that work at
lowest concentration of the drug have infants with a lower neurotransmitter level like GABA (gamma aminobutyric
rate of anomalies than women on a multiple drug regimens acid) and sodium channel blockade are under trial At
(Tables 47.1 and 47.2). present a number of studies of its safety in pregnancy are
Neural tube defects (NTDs) are associated with valpro available. Topiramate given in the dose of 100–400 mg/day,
ate exposure in utero. A 1.5% risk has been reported with interferes with the oral contaceptive pills. While tiagabine
valproate exposure in the first trimester. The congenital given in the usual dose of 8–56 mg/day does not interfere
malformation rate is as high as 8–16% with polytherapy with oral contaceptive pills.
including valproate.
Carbamazepine, which was once considered to be
Pathophysiology of Effect of
safer than other antiepileptics during pregnancy, has Drugs on the Fetus
been seen to be associated with minor craniofacial The exact mechanism is not known. Few hypothesis
defects, finger nail hypoplasia, spina bifida (1%) and even advocated are as follows:
developmental delays. Barbiturate withdrawal syndrome Hydroxylase deficiency in the epileptic female can
is also sometimes seen in neonates in the first week of life, shift the anticonvulsant metabolism to a potentially
in cases where mothers were stabilized on barbiturates. teratogenic pathway.
TABLE 47.2: Anticonvulsants commonly used during pregnancy

Drug Therapeutic level mg/L Usual non pregnant dose Half-life
Carbamazepine 4–10 600–1,200 mg/day in three or divides doses (two doses if Initially 36 h, chronic therapy 16 h
extended—release forms are used)
Phenobarbital 15–40 90–180 mg/day in two or three divided doses 100 h
Phenytoin 5–15 300–500 mg/day in three divided doses Average 24 h
Primidone* 50–500 750–1,500 mg/day in three divided doses 8h
Valproic acid 550–2, 000 mg/day in three divided doses Average 13 h
* If a total dose of more than 300 mg is needed, dividing the dose will result in a more stable serum concentration.
Toxic effect of phenytoin is due to conversion to epoxide of pregnancy (MTP) in epileptic patient]. Hence, advise
molecule rather than interference with folic acid other methods of contraception till epilepsy is controlled.
metabolism.
Change in vitamin K production can lead to an increase Management of the Patient during Pregnancy
in fetal and neonatal hemorrhage. Early start of antenatal care is very important (as early as
Folic acid malabsorption. possible). Accurate dating of pregnancy by ensuring last
Withdrawal symptoms after cessation of drug within menstrual period (LMP) reliability and first trimester dating
one week of exposure and can transiently retard fetal scan, is important for prediction of fetal growth restriction
growth. (FGR). Consider early genetic counseling. MSAFP (maternal
serum alpha fetoprotein) levels and TIFFA (targeted imaging
Effect of Epilepsy on the Fetus or Neonate for fetal anomalies) scan should be done between 16 and 20
The patient may get injured during the attack leading to weeks. Amniocentesis should be done for acetylcholinesterase
abruption of the placenta. There are genetic effects also. and alpha-fetoprotein should be considered(especially if she
� Hereditary inheritance of seizure disorder. is taking valproate and carbamazepine).
Teratogenic and toxic effects of antiepileptic drugs: The total and free drug levels of antiepileptic drugs
•• Congenital malformations should be monitored so as to titrate the minimum possible
•• Withdrawal symptoms drug level to keep her seizure free. Longer periods of
Seizures per se cause
control imply better prognosis. During hyperemesis of first
•• Injuries
trimester the drug levels are erratic and must be monitored
closely to prevent precipitation of a convulsion.
•• Abruption
Serial fetal growth scans are recommended to detect
•• Intrauterine growth restriction
FGR as the risk for FGR is increased in fetuses in utero
•• Intrauterine fetal demise
exposure to anticonvulsants. Folic acid supplementation
Effect during breastfeeding by transmission of the drug
should be prescribed to prevent NTDs. Women taking
through milk. phenytoin should be advised to consider taking 10 mg
vitamin K orally each day during the last 1 to 2 months
Preconceptional Counseling of pregnancy. Alternatively, the newborn infants can be
It is very important in an epileptic patient. The patient given intramuscular vitamin K immediately after birth
should be informed about the fetal anomalies associated (phytonadione 1 mg).
with antiepileptic drugs and taking an informed consent is
advisable. Compliance of the female should be reinforced. Differential Diagnosis
Consider switching to anti-epileptic medication with least Other causes of convulsions include:
congenital malformation rate and to decrease it to the least Trauma
possible dose for seizure prophylaxis. In those who are Alcohol and drug-induced withdrawal syndromes
Brain tumors
seizure free for 2–5 years, even complete drug withdrawal
Arteriovenous malformations
can be considered. If patient is on polytherapy, try to switch
Non-cerebrovascular causes e.g. electrolyte imbalances,
to monotherapy. Those who are on drug with minimal
protein-binding like lamotrigine and carbamazepine hypoglycemia, hypocalcemia, hyponatremia, etc.
need dose increment by 25% and 50% respectively to Labor and Delivery
ensure therapeutic levels of drug (due to increased
In antenatal patients with seizure disorder, vaginal
GFR). Preconceptional prescription of folic acid 5 mg is delivery remains the route of choice. Cesarean section is
advisable to prevent congenital malformations (as this is done for obstetric indication, after stabilization. Transient
the dose available in the market, though a dose 0.4–1 mg is fetal bradycardia may be seen in case of seizures during
adequate in these women while a dose of 5 mg is reserved labor. Administration of anticonvulsant medication
for women with a family history of NTDs and it should during a prolonged labor is a challenge. This is because,
continue throughout pregnancy or at least during the first during labor absorption of drug through oral route remains
trimester of pregnancy. Carbamazepine, phenobarbital erratic. In case of vomiting, dose needs to be repeated or
and phenytoin being enzyme inducers leading to a rapid to be given by parenteral route. Phenobarbital is available
clearance of oral contraceptive hormones leading to as intramuscular preparation while intravenous form of
contraceptive failure and pregnancy [medical termination phenytoin is available. Parenteral form of carbamazepine
is not available although extended-release formulations Investigations

are available.
Rule out other causes of convulsions
Prophylactic oral administration can be given, but in
•• Skull X-rays
patients with seizures or a pre-seizure aura, loading dose
of phenytoin can be given. The usual loading dose is 10–15 •• Magnetic resonance imaging (MRI)
mg/kg administered intravenously at a rate no faster than •• Electroencephalogram (EEG)
50 mg/min. Relief of pain during labor is very important •• Arteriography
because hyperventilation with pain may lead to respiratory •• Serum electrolytes
alkalosis which may lower the seizure threshold and •• Lumbar puncture
precipitate a convulsion. Fetal monitoring is done by •• Screening for toxic substances
intermittent ausculatation or electronic fetal monitoring Rule out congenital malformations
as per the availability.
•• Ultrasound (especially in the second trimester)
New Onset of Seizures in Pregnancy and the congenital defects such as cardiac and craniofacial)
Puerperium •• Amniocentesis (to diagnose NTDs)
Sometimes seizures will be diagnosed for the first time •• Triple marker screening (α-fetoprotein, estradiol and
during pregnancy and may present a diagnostic dilemma β-human chorionic gonadotrophins)
(Table 47.3). Tests of fetal wellbeing.
Table 47.3: Differential diagnosis of peripartum seizures

S. No. Blood pressure Proteinuria Seizures timing CSF Other features
1. Eclampsia ↓ +++ +++ Second trimester Early: RBC 0–1000, Platelets RBC normal
>20 weeks/ protein, 50–150 mg/dL or decreased
third trimester/ Late: grossly bloody
intrapartum/
postpartum
2. Epilepsy Normal Normal Any trimester Normal Low level
anticonvulsant
3. Subarachnoid + to +++ 0 to + Any trimester Grossly bloody
Hemorrhage (labile)
4. Thrombotic Normal ++ Third trimester RBC 0–100 Platelets ↓↓
Thrombocytopenic to ++ +++ RBC–fragmented
Purpura (TTP)
5. Amniotic Fluid Embolism Shock – Intrapartum Normal Hypoxia, cyanosis
platelets, RBC normal
6. Cerebral Vein Thrombosis + – Postpartum Normal Headache occasional-
pelvic phlebitis
7. Water intoxication Normal – Intrapartum Normal Oxytocin infusion rate
> 45 mU/min serum
NA < 124 mEq/L
8. Pheochromocytoma +++ (labile) + Any trimester Normal Neurofibromatosis
9. Autonomic stress +++ with labor – Intrapartum Normal Cardiac arrhythmia
syndrome of paraplegics pains
10. Toxicity of local Variable – Intrapartum Normal –
anesthetics
11. Pseudoseizures – Any trimester Normal No postictal state
no bladder/bowel
incontinence
hysterical attack
hyperventillation
Postpartum Period and Breastfeeding In case of respiratory depression—endotracheal intuba

In cases where the drug dosage was increased during tion and intermittent positive pressure ventilation along
with oxygen administration may be required
pregnancy, reduce the dose postdelivery to pre-pregnancy
Uncontrolled seizures may require neuromuscular
levels. Although anticonvulsant drugs are known to be
blockade/general anesthesia with intubation (with
secreted in breast milk, their use is not a contraindication
midazolam)
to breastfeeding. The American Academy of Pediatricians
Cerebral edema (if occurs)—dexamethasone and/or
considers carbamazepine (milk: plasma ratio—0.25:0.69),
mannitol is to be given
to be compatible with breastfeeding.
After control of seizures—continuous infusion of
Phenytoin, valproic acid and its metabolites are excreted
diazepam/lorazepam should be started
minimally in the breast milk and thus produce no toxicity in
Throughout the control, continuous monitoring of
the infant. Therefore, they can also be used in a breastfeeding
maternal vital signs, electrocardiography (ECG) and
epileptic patient. fetal well-being should be done.
Phenobarbitone accumulates in the neonatal serum
thus neonatal levels may even exceed those in the plasma,
OTHER MISCELLANEOUS NEUROLOGI-
causing sedation in the neonate.
CAL PROBLEMS DURING PREGNANCY
Contraception Multiple Sclerosis (MS)
Oral contraception and progestins implants are associated It is an autoimmune disorder involving central nervous
with contraceptive failure in women taking antiepileptic system (CNS) due to axonal damage and demyelination
drugs as these drugs induce hepatic P450 microsomal enzymes in CNS and is characterized by stages of relapse and
and thus lead to increased clearance of the contraceptive remission. Common presentation includes dysarthria,
hormones. However, the use of oral contraceptive with bladder dysfunction, hyperreflexia, muscular weakness,
50 mg estrogen will not evoke a convulsion. ataxia and features of optic neuritis (diplopia and
Barrier methods and intrauterine devices can be blindness). Pregnancy does not increase the course of
advised to these women, as their efficacy is not affected by MS in pregnancy rather may have a protective effect.
the antiepileptic drugs. But relapses are more common in puerperium. There is
Depo-provera is the drug of choice in women with a tendency of easy fatigability and urinary tract infections
poorly controlled seizure disorder as it has been noted that (UTIs) due to bladder dysfuntion.
not only are the circulating hormone levels much higher Treatment should be individualized as per the
as compared to oral contraceptives but it has been found presentation of the patient. High dose prednisolone
to decrease the seizure frequency in many patient. through intravenous route is given during severe relapses
followed by oral steroids. Urinary urgency can be treated
STATUS EPILEPTICUS by using imipramine. Anticonvulsant drugs are needed for
epilepsy. To reduce the relapse rates and the development
It can complicate pregnancy by causing maternal hypoxia, of brain lesions. Beta-interferon, azathioprine and cyclo
acidosis, hyperthermia, fractures, rhabdomyolysis, hypo phosphamide can also be used.
tension, arrhythmias and respiratory depression and fetal Cesarean delivery is done for obstetric indication or in
hypoxia and arrhythmias. Thus, it is an emergency and cases where vaginal delivery is practically difficult due to
immediate seizure control is important. serious disability. Breastfeeding is contraindicated during
interferon therapy.
Management
Immediate control of convulsions—diazepam 2 mg Myasthenia Gravis
(minimum) to 20 mg (maximum) or phenytoin 50 mg It is a neuromuscular disorder characterized by immuno-
(minimum) to 180 mg (maximum) globulin G (IgG) mediated destruction of post-synaptic
Rule out precipitating factors such as—hypoglycemia, acetylcholine receptors in striated muscle. This disease is
electrolyte imbalance, infection, failure to monitor also characterized by periods of remissions and exacer
serum levels and non-compliance bations, exacerbations being precipitated by systemic
Maintain the temperature of the patient illness and infection. The common presentation is
Suction of secretions marked fatiguability of facial, extraocular, oropharyngeal
and limb muscles. Thymic hyperplasia and thymoma is formations should be given multidisciplinary care invol
seen in 75% women and should be treated by thymectomy. ving obstetrician and neurosurgeon. Those with large
First line treatment is with long acting acetyl- AV-malformations must undergo corrective surgeries
cholinesterase inhibitors such as neostigmine and pyrido before planning pregnancy.
stigmine and can be given during pregnancy. Steroids,
zathioprine and methotrexate are second line treatment Ischemic Stroke
while plasmapheresis and intravenous immunoglobulin Risk factors for ischemic stroke are history of previous
infusion is reserved for serious exacerbations. Pregnancy unprovoked thrombosis, known thrombophillias [antipho
does not affect the course of the disease. Acetylcholine sphalipid antibody syndrome (ALPA) in particular] and
receptor IgG antibodies present in the maternal serum, in those having mechanical heart valve. Management
can cross the placenta leading to feeble cry, poor suckling include aspirin and anticoagulants like heparin and war
and respiratory depression. farin. Both are considered safe in lactating females. Those
The management should be done in association with the on anticoagulants should have planned delivery and
neurologist. Vaginal delivery can be achieved and epidural cesarean section is reserved for obstetric indications.
analgesia can be given. Operative vaginal delivery may Aspirin should be prescribed to all high risk women as a
be needed in case of skeletal muscle fatigue. Magnesium secondary prevention method to prevent stroke.
sulfate is contraindicated for treatment of eclampsia in
these women. Breastfeeding is done with caution in case Cerebral Vein and Sinus Thrombosis
where mother is on anticholinesterase drugs. Cerebral venous thrombosis (CVT) occurring during
pregnancy is associated with high mortality and morbidity.
STROKE Its incidence is as high as 11.6 per 1000,000 deliveries.
During pregnancy most common type of stroke is The risk factors are infection, dehydration, anemia,
hemorrahgic stroke in contrast to ischemic stroke which is raised homocysteine levels and thrombophillias. Signs
most common. In nonpregnant population the alteration and symptoms are similar to those in stroke like raised
in physiology during pregnancy plays a key role in intracranial pressure, headache, vomiting, photophobia
increasing the risk of stroke during pregnancy (Table 47.4) with or without fever. Etiopathogenesis involves an inter
Though a rare event during pregnancy, post stroke play between the raised hypercoaguability in pregnancy
mortality has been higher in pregnant individuals than in and endothelium microtrauma leading to formation
nonpregnant ones. of thrombus. Investigation of choice is venography
(MRI/V). Management includes, maintaining hydration
Hemmorhagic Stroke anticoagulants and symptomatic treatment.
Hypertension is the most important treatable risk factor
for hemorrhagic stroke during pregnancy. Blood pressure Migraine
should be kept below 160/110 mmHg. Low dose aspirin This disease is characterized by episodes of severe
(70 mg) prescribed as a method of prevention of pre- headache and autonomic nervous system dysfunction. It
eclampsia, does not increase the chance of hemorrhagic can be with or without aura. Aura is characterized by visual
stroke. Pregnant females having arterivenous (AV) mal hallucinations and scotomas. Although no direct effect
on pregnancy is seen, but it is associated with fetal limb
TABLE 47.4: Physiological changes in pregnancy increasing the reduction defects and increased incidence of pre-eclampsia.
risk of cerebrovascular accidents Simple analgesics help in mild migraine while severe
Blood changes Increase in factor-VIII, IX, X and fibrinogen migraine calls for maintenance of hydration, intravenous
Decrease in antithrombin and protein S levels
antiemetics and opioidan algesics Ergotamine medications
Cardiac Raised cardiac output
are to be avoided. Sumatriptan can be given in pregnancy.
Decreased venous return hypertension and
vasospasm in hypertensive conditions of

pregnancy, increased vessel compliance, higher Neuropathies
incidence of arrhythmias The incidence of entrapment neuropathies increase during
Endocrine Increase in estrogen mediated cholesterol
pregnancy. Of them, carpal tunnel syndrome (CTS) is the
Raised diabetogenic potential during pregnancy
most common effecting about 2% of antenatal females and
Surgical Cesarean section or other surgical intervention
is characterized by pain and numbness or paresthesia of
the index and long fingers and the adjoining thumb and Bell’s palsy (unilateral lower motor neuron palsy
ring finger. It is due to median nerve compression within involving facial nerve) is seen more commonly during
the carpal tunnel. Treatment is simple analgesics with pregnancy. Symptoms and prognosis are same as those
wrist splinting in some cases. In severe cases local steroid in non-pregnant females. Steroid (prednisolone) is safe
injection can be given. in pregnancy and helps in recovery and reducing severity
In postpartum females, most common neuropathy enco of symptoms if given within 48 hours; in more than 90%
untered is due to dysfunction of lumbosacral plexus nerves. cases, condition resolves spontaneously over months.
The risk factors for this are forceps delivery, narrow pelvis, However, Ramsay Hunt syndrome (RHS) must be ruled
big fetal head, occipitoposterior position, short stature out before giving steroids.
primigravidas. Among these most common nerve getting
affected is peroneal nerve leading to foot drop. Management Pshychiatric Disorders
includes physiotherapy and orthotics or boots. These are dealt in detail in Chapter 53.
1. What are the effects of epilepsy on pregnancy?
2. Write the management of :
i. Hemorrhagic stroke in pregnancy
ii. Multiple sclerosis in pregnancy
iii. Migraine in pregnancy
Section 8
Infections in Pregnancy
Section Outline
48. HIV in Pregnancy
49. Malaria in Pregnancy
50. Other Infections in Pregnancy
48
Sudha Salhan
HIV in Pregnancy
women and 30,000 children get infected every year (Tables

INTRODUCTION 48.2 to 48.4). Since the country is vast, the overall number
The breakthrough discovery of human immunodeficiency of infected individuals is also substantial and must make
virus (HIV) by French researcher Francoise Barré Sinoussi us sit up and think. In India women account for one million
and Luc Montagnier solved the mystery of acquired HIV positive patients out of a total 2.1 million (Table 48.1).
immunodeficiency syndrome (AIDS) first detected in a According to National AIDS Control Organization
patient in 1981, though they were awarded Nobel Prize in (NACO) total HIV patients are around 51% males. In
2008. First case in India was diagnosed in Chennai. It was India. Hence, from an exclusive male disease HIV/AIDS
considered a disease of males (more in men having sex is now equally distributed in both sexes. Majority of HIV
with men). Gradually it was acquired by women. Now in infected children have acquired their infection because of
new cases of HIV, women are equally affected if not more transmission from their parents. Around 500,000 infants
per year acquire HIV infection about 0.1 million; children
than men.
below 15 years registered for ART (antiretroviral therapy)
After infecting, the HIV virus produces reverse
or OI (opportune infection) treatment (Table 48.2). Hence,
transcriptase (a diploid double stranded DNA provirus).
prevention of PTCT is very important for reducing the
This provirus attack DNA of host cells. Transcription and
incidence of pediatric HIV infection.
translation occur, allowing assembly of viral proteins With about 27 million births occur in India per year
necessary for the production of virions that are released and 1% seropositive women and a 30% transmission rate
after the death of host cell to infect other cells. There are (without any treatment), we have 75,000 HIV infected
two types of HIV viruses viz. HIV-1 and HIV-2. HIV-1 is newborns every year. But only 8.83 million avail the
associated with higher parent to child transmission (PTCT)
rate (20–35%) compared with 0.4% with HIV-2. This is most
probably because there is a lower concentration of HIV-2 TABLE 48.1: Magnitude of the problem
in cervicovaginal secretions. Total people living with AIDS worldwide (WHO): 37 millions
Total HIV patients (in India): 2.1 million
This rapid spread of HIV in women especially in the
Males: 51%
child bearing age makes the prevention of PTCT of HIV Females: 49%
more difficult in third countries. As these women get Children below 15 years registered for ART: 0.1 million
infected from their husband, hence, in India mother to
Source: National AIDS Control Organization of India (NACO) Data 2011
child transmission (MTCT) is renamed as PTCT.
TABLE 48.2: Age distribution with percentage of HIV patients in

MAGNITUDE OF PROBLEM India (NACO)
Due to under recognition, the actual HIV epidemic Age group Percentage
burden is probably greater than reported (Table 48.1). It is < 15 years 3.8
estimated that in our country 2 adults get infected every 15–49 years 88.7
minute and more than 0.5 million young people, 2,30,000 > 50 years 7.5
facility of HIV counseling and testing. We have to bring TABLE 48.3: Routes of infection in children
maximum pregnant women (27 million per year) under No. of cases Percentage
direct supervision so that they are tested for HIV and ART Sexual 95941 85.96
given to positive patients to prevent pediatric HIV in our Perinatal transmission 4059 3.64
country. Blood and blood products 2231 2.00
Recently, India has surpassed South Africa as being the Injection drug users 2672 2.39
country with the largest HIV-infected population. Others (not specified) 6705 6.01
Total 111608 100.00
RISK FACTORS IN FEMALES Source: NACO
Due to the under recognition of HIV in women, the actual
male to female transmission more efficient than vice versa
epidemic burden is probably greater that reported. The
(2–17 times higher). Sex during menstruation and anal
special risk factors in females are given in Box 48.1.
sex (single layer linning) also favors more male to female
Routes of infection in Females (Table 48.3) transmission.
Unprotected heterosexual exposure is the primary factor. Child prostitutes and young women suffering sexual
More than four-fifth of all infected women get the virus abuse contribute to increase in the female population
from a male sex partner. infected from this disease at a younger age. India is a
The remainder become infected from a blood trans country of young population.
fusion, etc.
More and more adolescent and younger females
Economically
are becoming victims of HIV by injecting drugs with Women are mostly dependent on males. Hence, they can-
contaminated needles. not have a say in sex, violence and treatment of diseases.
Being often less educated they are not aware of the
Risk Factors in Females (Box 48.1) disease and its consequences.
Biological Disadvantages Migration, poverty and gender inequality increases the
As we know, girls are married off at a younger age in our rate of HIV infection in women.
country (before 18–20 years of age). At this age the vagina is It is the fifth leading cause of death in the age group
lined by only a single layer of columnar epithelium which of 25–44 year population.
offer minimal protection against HIV and other infections Previous reproductive tract infection (RTI) and sexually
compared with the multilayered non cornified stratified transmitted infections (STIs) causing ulcers and discharge
squamous epithelium lining the vagina in females of 20 increasing the chances of HIV transmission. Females mostly
years or more in age. The immature cervix (with cervical have few symptoms in RTI/STI infections and no felt need
ectopy) of these younger women has relatively low for treatment.
mucous production, hence, less barrier to HIV making
them biologically more susceptible to infections. HIV IN CHILDREN
Compared to men, in women surface area of cervix Almost all cases of HIV infection in children (91%) are
and vagina exposed to HIV infected secretion of the sex acquired by PTCT. About 7% of total HIV infection in India.
partner is larger and these secretions stay longer in the As on March 2013, 0.1 million children are registered in
area. Moreover, infected semen has more concentration of ART program in India and 38579 are receiving free ART
HIV than female secretions. Some abrasion in vagina and (Table 48.4) .
perineum may occur during intercourse. All this makes
TABLE 48.4: Sex of HIV infected population
Box 48.1: Risk factors in females
Age group Male Female Total
Younger women married to older men more likely having HIV/AIDS
Economic dependence
0–15 years 2860 1994 4854
Male to female transmission more efficient 15–29 years 21782 14405 36187
Unrecognized reproductive tract infections (RTI) and sexually
30–49 years 48342 14508 62850
transmitted infections (STI) is mostly symptomless
> 50 years 6057 1660 7717
Illicit drug use and cigarette smoking
More frequent transfusion of blood in females Total 79041 32567 111608

Teenage population indulging in unsafe sexual practices.
Source: NACO
HIV in Pregnancy 469
Diagnosis of HIV serostatus in early pregnancy in starting of ART in all pregnant women irrespective of her
women is of paramount importance, because this can disease status, to prevent PTCT of HIV in children.
prevent the HIV transmission in the child by proper
management.
Concurrent RTI/STI and Other Infections
These are also strongly associated with vertical perinatal
Definition of Perinatal Transmission HIV transmission, e.g. syphilis infection. Evidence is
It is vertical transmission of HIV from mother to child during accumulating to suggest that malaria, tuberculosis,
pregnancy, labor, delivery or breastfeeding. Transmission parasitic infestation (hookworm, etc.), bacterial vaginosis
from parent can be prevented if the disease is detected in and chlamydia trichomatis in pregnant women is
associated with more PTCT of HIV. Hepatitis C with HIV in
time. Not all fetuses of HIV positive mothers acquire the
pregnancy doubles the PTCT of HIV. It disturbs dynamics
infection. The incidence varies from 15 to 48%. Hence, it is
of immune transmission. HIV and Hepatitis B increase the
important to know the factors which enhance the PTCT of
transmission from 16 to 26%. Herpes simplex virus (HSV)
HIV. The main determinants are given in Box 48.2.
is also associated with more PTCT of HIV.
Viral Load (Box 48.2) Unprotected Sexual Intercourse
Viral load in the mother is maximal immediately after Though transmission through a single sexual act is small,
infection and in the advanced stage of the disease. the frequency of the act is high. Sexual act is very frequently
Measurement of plasma HIV-1 and quantitative culture, done even in pregnancy. Hence, the commutative effect
especially the former, is a better predictor of vertical makes it the most common route of infection of HIV.
transmission. Data from studies shows that neonatal
infection of HIV is below 5% with less than 1000 copies/mL Maternal CD4 and Lymphocyte Count
of plasma viral burden and over 40% with levels greater than It is an independent predictor of prenatal transmission
100,000 copies/mL. In the current era of potent antiviral risk. A lesser concentration causes greater transmission as
therapy these studies provide a scientific rationale for they have less immunity.
measuring viral load in pregnant women both to predict
risk of transmission and to monitor antiviral therapy HIV-
Mother’s Neutralizing Antibody
2 has less transmission (0–4%) than HIV-1 (25–40% which Monoclonal HIV-3-
is commonly seen in India). New guidlines of WHO require This mostly protect from acquiring infection.
Nutritional Status
Box 48.2: Factors determining vertical transmission Inadequate nutrition enhance mother’s and fetal factor
Maternal for vertical transmission. Deficiency of micronutrients like
Viral load
zinc, reduce systemic immune response and epithelial integ-
Biological prototype of virus
rity of placenta, and genital tract increasing vertical trans-
Unprotected sex during pregnancy
Smoking and illicit drug use in mother

mission. It causes decreased number of T lymphocytes.
Maternal level of CD4 and lymphocyte count
Also low vitamin A levels in mother enhance HIV transmis-
Low maternal zinc, vitamin A level sion to the fetus.
Presence of RTI/STI in mother
Time of rupture of membranes and chorioamnionitis more than

Rupture of Membranes
4 hours Time between rupture of membranes and PTCT is
Episiotomy and operative vaginal delivery
significant, if it is more than 4 hours(14–25%).
Presence and amount of virus in genital tract.
Fetal Type of Virus

Preterm fetus
Fetal ingestion of the virus

T cell tropic type virus are transmitted less than monocyte-
Fetal scalp electrode, scalp blood sampling and umbilical blood
macrophage type (M tropic)
sampling
Duration of exposure to maternal secretions (first twin)
Placental Barrier
Via breast milk depending on the immune response of the Breaks in placental barrier will cause maternal and fetal
newborn and period of breastfeeding and infectivity of mother. blood mixing leading to enhanced transmission. This
condition is more in maternal cigarette smoking or using

ilicit drugs. Also in chorioamnionitis.
Presence and Amount of Virus in the

Genital Tract
Presence of large amount of virus in the genital tract is a
factor in PTCT.
Smoking and Illicit Drug Use

Maternal use of illicit drug (cocaine and heroin) may
increase the risk three fold. Cigarette smoking during
pregnancy also increases vertical transmission of HIV.
Fetal Factors
Fetal cells have genetic different factor in susceptibility
to HIV and may vary with gestational period because Fig. 48.1: Intrauterine transmission
of development. It has been reported that there is a 3.7
times relative risk for intrapartum HIV transmission during
Transmission during pregnancy: (Fig 48.1) is confirmed
preterm delivery, perhaps because the newborn’s immune
by finding the virus in the placenta,amniotic fluid, and fetal
mechanism is immature.
Intensive exposure of the infant’s thin skin and mucosal blood. Around 20% of transmission occurs before 36 weeks,
surfaces to maternal blood and secretions during the 50% before delivery, 30% during delivery. Postpartum
birth process could provide a significant route for viral transmission through breast milk is upto 30%.
transmission. In most of the cases, however, transmission occurs
Consistent with a possible route of HIV-1 transmission during birth.
by oral exposure, in one study, HIV-1 was detected in During delivery (Fig. 48.2): The baby is infected from
the gastric aspirate form 2 of 4 newborns who were cervicovaginal secretions and exposure to mother’s blood
subsequently shown to be infected. (more with episiotomy). As first twin remains in maternal
Invasive procedures that breach the infant’s skin passage more time it is more prone to PTCT than the second
barriers could provide another mechanism for viral entry twin. Hence, protection at all levels is essential to prevent
(e.g. fetal scalp electrode, scalp blood sampling, chorionic PTCT of HIV.
villus sampling, amniocentesis, cordocentesis). External
cephalic version, episiotomy and operative vaginal Breastfeeding (Fig. 48.3)
delivery also increase intrapartum transmission to the During breastfeeding virus is transmitted via milk to the
fetus. infant by the infected mother or from an infected wet
It is observed that there is a more than two-fold risk nurses.
of infection of the first-born twin as compared to second There is evidence that breastfeeding increases postnatal
(26% versus 13% respectively). These data suggest that the HIV-1 transmission by as high as 30–40%. Breastfeeding
greater risk of infection in the first born may be related to transmission appears to result from the coexistence of
more prolonged exposure of the presenting first twin to HIV-1 and an inadequate humoral response to milk.
infectious secretions in the genital tract during the later Hence, complete avoidance of breastfeeding is the surest
stages of pregnancy and delivery. As first twin stays longer way to avoid PTCT of HIV through breastfeeding. Despite
in the maternal passage. this, in underdeveloped countries, formula feeding may
be impractical and associated with an increased mortality
Timing of Vertical Transmission from diarrhea and respiratory infection. WHO has
Precious timing of PTCT is not known but fetus can get reported a six-fold increase in the risk of mortality from
infected in the uterus during early and late pregnancy. diarrhea in children of the developing world who are
Some are infected during delivery and other after delivery not breastfed in the first 6 months of life and around
by breast milk by lactating mother. a two-fold increased risk of mortality from respiratory
Fig. 48.2: Transmission during delivery Fig. 48.3: Breastfeeding
diseases. WHO recommended exclusive breastfeeding, as Cesarean Delivery

malnutrition is the primary cause of infant death in many There is evidence that intrapartum (during delivery)
developing countries. The mother is counseled about rise
transmission is the highest. This gave rise to the idea of
of breastfeeding.
carrying out a cesarean section in all HIV positive patients.
The risk of transmission varies with:
But there are some doubts of it being the best method to
Duration of breastfeeding
reduce PTCT.
Maternal HIV load
Because the antiviral therapy decreases the PTCT risk to
HIV disease status (more infections in early or terminal
less than 2%. Hence, if the mother is on ART, perform LSCS
disease)
only if obstetrically indicated. If the viral load is more than
Associated breast abscess
1000 copies/mL indication for elective LSCS is there to
Cracks in nipple
prevent PTCT, at 38 weeks before rupture of membranes.
Whether exclusive breastfeeding or mixed feeding.
It was found that breastfeeding beyond 15 months was

Newborn Immune Response
associated with a 1.9 fold increased risk of infection. 32%
of HIV infection was attributed to breastfeeding beyond 15 The immune response to HIV infection in the newborn can
months. It was calculated that the risk of HIV-1 transmission prevent and clear PTCT.
exceeded the potential benefits of breastfeeding after 6
months of age. Hence, it is recommended to exclusively MANAGEMENT OF HIV POSITIVE
breastfeed the baby for 6 months only. Associated breast PREGNANT WOMEN
abscess or cracks in the nipple lead to more PTCT of HIV.
Exclusive breastfeeding is to be stressed as mixed feeding It is a team approach comprising a counseler, obstetrician,
(both breastfeeding and top feeding) is more harmful. physician, psychiatrist and pediatrician.
The newborn’s immature gastrointestinal tract (GIT) The primary step to diagnose HIV in pregnant woman
may facilitate transmission; gastric acidity is diminished in is done by investigating HIV serostatus after counselling.
the newborn and the mucosa and microvilli are thin with Obstetricians are to be involve in primary care of HIV–
a deficiency of IgA secreting cells. However, an immature positive pregnant woman as soon as she comes for antenatal
GIT is not a requirement, because transmission has been care. Give her choice (if she comes in early pregnancy) of
reported in infants beginning breastfeeding after the MTP or continuation of pregnancy. If she wants MTP provide
neonatal period. her safe services. If she wants to continue this pregnancy.
Pasteurization of expressed milk and then feeding is She comes under the fold of antenatal care (ANC) routinely
also offered. practised in a pregnant women.
She is advised not to use ilicit drugs,smoking and alcohol. Box 48.3: Interventions aimed at decreasing the risk of PTCT
Proper sleep is required. She is prone to opportunistic Antenatal Care
infections (OI) if her CD4 counts falls below 200/mm3. Her Counseling and knowing the HIV status (preferably before
obstetricians must be vigilant for the signs and symptoms pregnancy)

of opportunistic infections (as CD4 count is a costly affair in Choice of MTP or continuation of pregnancy
Correct diet and anemia

underdeveloped countries) and must initiate appropriate
Discontinue smoking and illicit drugs
prophylactic therapies (trimethoprim-sulphamethoxazole
Regular check-up
or pentamidine). CD4 counts ≤ 100/mm3 may invite Treat RTI/STI
Toxoplasma gondii infection and at counts ≤ 50/mm3 Detect and treat opportunistic infection
MAC (Mycobacterium avium complex) and perhaps CMV Delivery in hospital
(Cytomegalovirus) conjunctivitis can occur. Screening for Antiretroviral drugs
Do not do amniotomy, fetal scalp electrode monitoring, fetal

tuberculosis is to be done. Appropriate prophylaxis should
scalp blood sample or umbilical blood sampling
be started and may need modification. US Public Health Avoid episiotomy and vaginal operative delivery (if possible)
Service instructed to do a CD4 and a T-lymphocyte count Systematic cleaning of birth canal immunotherapy
in every trimester (if possible). These tests show the effect Immediate bath to baby
of treatment and provide an indication as to when to start Antiretroviral therapy.
treatment of opportunistic infections (OI). Test for viral

load is to be performed (if feasible) near term to decide the
Prong 4: Provide care, support and treatment to women
route of delivery (vaginal or cesarean section).
living with HIV, her children and family in women in child
Using harm-reducing strategies like needle exchange
bearing age.
program reduces HIV transmission and finally targeting
interventions to the vulnerable groups is very helpful. Primary Prevention (Proving Testing and
Obstetric management (i.e. decisions regarding moni- Counseling to HIV-negative Pregnant Women)
toring obstetric problems and choosing candidates for
timing of induced delivery) is uninfluenced by a woman’s Global preventive initiatives target young people by giving
serostatus. messages of safe sexual behavior, promotion of condom
Controversy exists regarding vaccination because the use (male and female), teaching negotiation skills, dual
associated viremia during pregnancy poses the theoretical protection and diagnosis and treatment of STI and RTI.
Prevention of unintended pregnancy is a very impor
risk of increasing the rate of antepartum transmission of
tant primary preventive measure for PPTCT.
HIV. Nevertheless, tetanus prophylaxis is essential.
Secondary Prevention
INTERVENTIONS AIMED AT
The prevention of the vertical transmission of HIV from
DECREASING THE RISK OF PTCT OF HIV mother to child can be done by following the broad
INFECTION (BOX 48.3) principles.
The Goals of the PPTCT Program Counseling

In line with WHO standards for a comprehensive strategy, Counseling is mandatory for the HIV-positive woman.
the National prevention of parent-to-child transmission This is preferable early in pregnancy (prenatal) and if she
(PPTCT) program recognises the four elements integral to chooses to continue pregnancy (natal), ongoing counseling
preventing HIV transmission among women and children. for psychological support is important. Because of the
These are: devastating consequences of this infection if untreated, a
Prong 1: Primary prevention of HIV, especially among shift has occurred from exclusive protection of the fetus
women of child bearing age. by drugs to treatment of the mother and fetal protection
Prong 2: Preventing unintended pregnancies among from HIV infection. Now post delivery care of the HIV
women living with HIV. infected mother is part of the treatment. If counseling and
Prong 3: Prevent HIV transmission from pregnant women HIV testing is not possible during pregnancy (as about half
infected with HIV to their child. of our patients are unbooked with no antenatal care) this
must be done immediately at admission for delivery or Box 48.4: ART eligibility in pregnant women
after delivery (rapid test). This is an important entry point Initiate lifelong ART in all pregnant women with confirmed HIV
to prevent PTCT by giving chemotherapy. infection regardless of WHO clinical stage or CD4 cell count.
TDF + 3TC + EFV is recommended as first-line ART in pregnant
General Measures and breastfeeding women, (including pregnant women in the
The mother should be kept in good health. Treating first trimester of pregnancy and women of childbearing age).
malnutrition in pregnant mothers helps in reducing ART shall be initiated only at ART center as care, to prevent HIV
transmission during breastfeeding is important.
PTCT. Testing for other sexually transmitted diseases and
for tuberculosis is carried out. If detected they are to be
treated vigorously. They must have early glucose tolerance for initiating ART in HIV positive pregnant women are as
screening besides all routine testing and follow-up of shown in Box 48.4.
normal pregnancy (see Chapter 12). All HIV positive pregnant women are to be at ART
clinics on priority basis.
Immunological This treatment serves two key purposes:
Immunological approaches are based on the assumption 1. Improves health and prolongs survival of the mother.
that greater transmission occurs at or around the time 2. Reduces the risk of HIV transmission from mother-to
of delivery and that a combination of passive and active child during pregnancy, labor, delivery, and throughout
immunization will be effective in the transmission. At this the breastfeeding period.
stage, however, vaccine is a concept rather than a reality Start ART as soon as possible and continue ART
under research (active immunization). Passive protection throughout pregnancy, delivery, breastfeeding period
using HIV IgG is presently under investigation (ATGT, 185). and thereafter lifelong.
Use of hyperimmune anti-HIV immunoglobulin given The recommended first-line regimen is Tenofovir
IV to the baby alone or also to the mother may reduce (TDF) (300 mgs) + Lamuvidine (3TC) (300 mg) + Efavirenz
perinatal HIV transmission. Protocols to test neutralizing (EFV) (600 mg) once daily.
monoclonal antibodies are in the developmental stage. Even if the pregnant women presents very late in
Early umbilical cord clamping is thought to decrease pregnancy (including those who present after 36 weeks of
the chance of blood containing HIV crossing over to the gestation), ART should be initiated promptly.
fetus. A few examples of conditions seen in a pregnant woman
are given below.
Antiretroviral Drugs Ideally HIV testing is done before embarking on
WHO new guidelines (June 2013) recommend two options: pregnancy (preconceptionally). If she is HIV negative at
1. Providing lifelong ART to all the pregnant and breast antenatal clinic give her preventive counseling.
feeding women living with HIV regardless of CD4 count Pregnant women who are already receiving ART for
or clinical stage. their own health, should continue to receive the same
2. Providing ART [antiretroviral (ARV) drugs] for pregnant regimen throughout pregnancy, labor, breastfeeding
and breastfeeding women with HIV during the mother to period and thereafter life-long. If a woman is on an
child transmission risk period and then continuing life- EFV based regimen, there is no need to substitute with
long ART for those women eligible for treatment for their nevirapine. She must continue on whatever regimen
own health. Register them in ART clinics and care. All she is stabilized on and is responding to adequately.
HIV infected pregnant women (irrespective of CD4 count/ HIV infected pregnant women who have had previous
clinical stage) should receive lifelong ART clinic care. exposure to Sd NVP or EFV for PPTCT prophylaxis in
prior pregnancies, an NNRTI-based ART regimen such
Criteria for ART Initiation as TDF + 3TC + EFV may not be fully effective due to
Initiation of ART in pregnant women needs to be done at persistence of archived mutation to NNRTIs. Thus,
the earliest and after adequate treatment preparedness for these women will require a protease-inhibitor based
adherence to maintain her own health and also to prevent ART regimen viz:
HIV virus transmission to the unborn baby. TDF + 3TC + LPV/r (Lopinavir/ritonavir).
In HIV infected pregnant women the dictum should The dose will be TDF + 3TC (1 tablet daily) + LPV (200
be “do not delay ART initiation”. The eligibility criteria mg)/r (50 mg) (2 tablets BD).
She is coming in the first trimester and is diagnosed If positive counsel her to meticulously follow the
HIV positive. Refer her to ART clinic for starting ART medicines for her child and her own welfare. On discharge
and evaluating her condition. accompany her to ART center for further treatment.
She has first reported at 36 weeks of pregnancy in the Counsel and advise for exclusive breast-feeding for first
outpatient department (OPD) and is tested positive. 6 months, if she has already started breastfeeds. If not she
She is sent to ART clinic for HIV treatment. must be counseled on option for breast vs replacement
There is a significant percentage of pregnant women feeding but must adhere to either exclusive breastfeeding
or exclusive replacement feeding for first six months. No
with unknown HIV status presenting directly in labor
Mixed Feeding.
for delivery (unbooked cases). Any pregnant woman
HIV-infected pregnant women with active tuberculosis.
who presents in active labor with unknown HIV status The tuberculosis treatment should be started first.
should be offered the routine screening of HIV, with opt- Followed by ART as soon as feasible (usually after 2
out option as per National Guidelines. Screening using weeks). Refer HIV infected pregnant mother to ART
Whole Blood Finger Prick Test in the delivery/labor ward center for CD4 test, TB screening and clinical staging.
should be undertaken (Rapid test). If found positive Ensure all referred pregnant women actually reach the
initiated on ART (TDF + 3TC + EFV) immediately. The ART center and are started on ART without delay as wating
next day the Counselor should visit the post-natal ward for CD4 and other laboratory tests. The recommended
offer pre-test counseling, get her HIV testing. Laboratory clinical and laboratory follow-up schedule for pregnant
technition (lab tech) will confirm the HIV status by 3 women is similar to that for adult non pregnant women.
rapid anti-body tests. Blood sample for CD4 testing shall
Precautions
be drawn of all HIV confirmed cases by lab tech and S/
Precautions taken during MTP or delivery of HIV-positive
he will personally carry the sample to CD4 lab and bring
women (Figs 48.4A and B).
the report along with a month’s supply of ART taking
her spouse or buddy alongwith her/him under extreme Obstetric Measures
circumstances when the postpartum mother is unable They are very important. Follow universal precautions
to reach the ART center within the next 2 days for Pre- during labor. Prevent chorioamnionitis by not doing
ART registration and adherence counseling. However, repeated per vaginal examinations. Avoid rupture of
she should be motivated and followed-up for ensuring membranes as far as possible. Start antibiotic therapy early
that she reports to the ART Center within 30 days if required.
A B
Figs. 48.4A and B: Items to be kept available in labor room and OT as a part of universal precautions
Some obstetricians,do birth canal cleaning by Benzal- During Delivery

konium chloride, Chlorhexidine, Nonoxynol-9, betadine, Precautions by obstetrician
etc. vaginal gels, which kill the HIV virus are under Universal precaution
research. Gloves
Do not do placement of fetal scalp electrode or Gown
fetal scalp blood sampling, umbilical cord sampling Mask
like invasive procedures during labor. Do not give Boots
episiotomy or operative vaginal delilvery if feasible. Eye glasses eye protection shield
Baby should be bathed just after birth with soap and Mucus trap automatic water tap.
water to prevent the virus to get foot hold on the skin of Precaution by person who cleans labor room
the newborn. Universal precautions
HIV infected pregnant women require joint manage Pour 0.5% bleach solution on labor table for half an hour
ment from both the HIV care team (for her HIV condition) Clean with bleach solution
and the obstetric team (for successful outcomes of Blood and liquor on the floor be flooded with 0.5%
pregnancy). HIV infected pregnant women require all bleach solution for half hour and then clean it
Dip dirty linen in 0.5% bleach solution for half hour
components of good antenatal care, including iron-folate
supplementation, anemia management, baseline CD4 before sending for laundry
Put placenta in yellow bag and send for incineration
count, screening of TB, prevention and management of OIs,
or for burial with bleaching powder in the bag.
STI treatment, special obstetric practices especially during
Precaution during MTP or cesarean section
labor and delivery, ART initiation and its continuation
Universal precautions
counseling for infant feeding options, postnatal care,
Double gloves
follow-up, family planning and contraception. Postpartum
Gown
care and follow-up for the wellbeing of mother and infant, Boot
as well as adherence to ART. Eye glasses eye protection shield.
Barrier
EFFECT OF PREGNANCY ON HIV DISEASE
Use of barriers to prevent PTCT and safety of the obstetri-
cians–wearing of gloves after hand washing and wearing According to CDC, maternal morbidity and mortality are
special gown. Wear cap, mask, eye glass shield and long not increased by pregnancy in seropositive but otherwise
rubber boots. The baby’s mouth may be sucked by wall suc- asymptomatic women. Acquiring HIV during pregnancy
is higher and this may be due to hormonal influence or
tion with mucus trap in between with a pressure less than
pregnancy related immunosuppression.
140 mmHg to prevent gut damage.
Disinfectant Solution EFFECT OF HIV ON PREGNANCY

Cleaning by disinfectant solution as follows: This depends on the CD4 count of the mother. Lesser the
The labor table soiled floor cleaned with 0.5% bleach CD4 count, there may be premature births. In a CD4 count
solution. of less than 14%. IUGR are seen in one fourth of the points.
Soiled linen is immersed in 1% bleach solution for 30 There is increased stillbirths with maternal HIV infection.
minutes before washing. Spontaneous abortions and ectopic pregnancies are also
Placenta and attached membranes are put in yellow
reported more often. In the cases RTI/STI of genital ulcers
bags for incineration or burial with bleach powder. disease,warts at external genitalia or positive VDRL test and
endometriosis, low CD4 count will cause all these effects.
Precaution during Operation
Use puncture-resistant gloves (if available) or use HIV-EXPOSED NEWBORN
double gloves. Upto 18 months after birth, mother’s antibodies are
Special gown ,eye glasses and boots are used. present in the child hence his/her HIV status cannot
Try to lift tissues with instruments and not with hands. be obtained with precision. True picture is obtained by
polymerase chain reaction (PCR), viral culture and p 24 prepartum and postpartum HIV transmission, in
antigen analysis which are not available everywhere and addition to the protection received from the mother’s
are costly. A newborn who is PCR test positive (within ART regimen. Infant ARV prophylaxis provides added
48 hours of delivery) is supposed to have acquired the protection from early postpartum transmission,
infection during pregnancy (intrauterine). However, the Particularly in situations where women started ART late
child is negative by PCR with 48 hours of life but become in pregnancy, have less than optimal adherence to ART
positive after 7–90 days of birth had acquired infection and have not achieved full HIV viral suppression.
during delivery (if he is not breastfed). An HIV exposed The infant ARV prophylaxis where mothers are
newborn must be kept under Laboratory surveillance upto receiving ART is daily NVP for 6 weeks (i.e. till the first
18 months of age. No live vaccine should be given. The immunization visit for the infant), regardless of whether
child is protected from infections. Using general hygiene
the infant is exclusively breastfed or receives exclusive
and non exposure to infection.
replacement feeding.
HIV-EXPOSED INFANT (HEI) CONTRACEPTION AND HIV

The principles of infant feeding options for HIV infected
In HIV-infected women, there is dual risk of sexually
pregnant women and their infants are:
transmitted diseases (STDs) (including HIV/AIDS) and
•• All HIV infected pregnant women should have
unwanted pregnancy. These women may face a heightened
PPTCT interventions provided early in pregnancy as
risk of HIV transmission depending upon their choice of
far as possible.
contraceptive method.
•• Exclusive breastfeeding is the recommended infant
feeding choice in the first 6 months, irrespective
Copper T and other Intrauterine Contraceptive
of the fact that mother is on ART early or infant is
provided with ARV prophylaxis for 6 weeks. Devices
•• Mixed feeding should not be done at any cost HIV positive woman is at risk of getting pregnant and
within the first 6 months. (Feeding breastfeeds acquiring reproductive tract infections (RTIs, STIs and HIV).
and replacement feeds simultaneously in the first 6 She should use dual protection as all contaceptives do not
months). Exclusive breastfeeds up to 6 months and provide safety from RTI/STI and though condom provide
continued breastfeeds in addition to complementary this safety .It is not totally safe against unwanted pregnancy
feeds after 6 months up to 1 year for early infant (high failure rate). Therefore, she must always insist on
diagnosis (EID) negative babies and up to 2 years for condom use. Women on highly active antiretroviral therapy
EID positive babies who receive pediatric ART. (HAART) can use IUCD.
Postpartum ARV prophylaxis for infant for minimum
6 weeks. Barrier and Spermicide
Early infant diagnosis at 6 weeks of age; repeat testing Barrier contraceptions condom (both male and female) is
at 6 months, 12 months and 6 weeks after cessation of
to be used as continuous second method.
breastfeeds.
Co-trimoxazole prophylaxis from 6 weeks of age. Oral Contraception
HIV care and pediatric ART for infants and children
diagnosed as HIV positive through EID. There is drug interactions between ethinyl estradiol and
Growth and nutrition monitoring. ritonavir (one of the antiretroviral drugs use in HIV/AIDS).
Immunizations and routine infant care. Besides combine pill cause ectopy of the cervix which
Gradual weaning after 6 months and introduction of may increase access to virus in the body. Cell mediated
complementary feeds from 6 months onwards along immunity is impaired by estrogen suppressing plasma cells
with continuation of breastfeeding for at least 1 year for in the mucosa by decreasing IgA or by changing function
adequate growth and development of the child. of T cells. Hence, combined oral pills are not much helpful.
Confirmation of HIV status of all babies at 18 months Depo-medroxyprogesterone acetate (DPMA) and other
using all three antibody (rapid) tests. Infant ARV progesterone only contraceptive injections can be used for
prophylaxis is required for all infants born to HIV spacing. Psychological support, appropriate chemotherapy
infected women receiving ART to further reduce and follow-up is essential after delivery.
Permanent methods viz. tubal ligation and vasectomy Couple has safe sex counselling and HIV testing of
can be offered if the family is complete. The advantages of spouse and other living children
the use of two methods at the same time must be made Linkage to ART services
clearer in public campaigns. This may increase their use. ART is given to all gravidus regardless of clinical stage
and CD4 count

ETHICS AND HIV DISEASE IN WOMEN Nutrition counseling and linkages to Government/
other nutrition programs

Before testing for HIV, pretest counseling must be carried Family planning services
out, after taking an informed written consent and ensuring Exclusive breastfeeding (EBF) reinforcement/infant
complete confidentiality. A pregnant woman is concerned feeding support through home visits
about her unborn child. Hence, while framing the HIV testing Psychosocial support through follow-up counseling,
policy of a country we must keep HIV-positive pregnant home visits etc.
women in mind. She has the right to information as to her The essential package of PPTCT services includes:
HIV status and the effect on her unborn child, influence of Routine offer of HIV counseling (group/individual
breastfeeding and even the effect of antiretroviral therapy.
counseling) and testing to all pregnant women attend-
She must know the side effects of these drugs.
ing antenatal care, with ‘opt out’ option.
To reduce the vulnerability of women to HIV
Ensure involvement of spouse and other family members
infection it is important to ensure support from men
and move from an “ANC centric” to a “family centric”
at all levels. Educational programs must focus on the
approach.
media and other means of dissemination of knowledge
Provide ART to all HIV infected pregnant women
about how HIV spreads and how it can be prevented.
regardless of WHO staging and CD4 count results.
The responsibility of men and women in preventing
Preferred regimen is TDF + 3TC + EFV.
transmission by engaging in safer sex practices should
Promote institutional delivery for all HIV infected preg-
be given wide coverage. Increasing the age of marriage,
nant women auxiliary nurse midwives (ANMs)/ASHAs,
and providing economic independence to woman are
community workers to accompany to institutions; reduc-
important steps.
tion of stigma and discrimination amongst healthcare
All pregnant woman be offered HIV counseling
testing facilities. providers through sensitization and capacity building).
Provision of care for associated conditions (STI/RTI, TB
HIV Negative Women and other OIs).

Provide nutrition counseling and psychosocial support
Safe sex counseling
for HIV infected pregnant women (linkages with ANM,
Couple counseling
ASHAs, community outreach workers, DLNs to advise
Linkages to family planning services
them on the right foods to take and to go to anganwadi
Free condoms
Behavior change communication (BCC) for high risk centers for nutritional support and to the district level
women and her partner network of positive people for peer counseling and
Repeat HIV testing, considering window period if psychosocial support).
Provide counseling and support for initiation of
spouse is positive or s/he have high risk behavior
Infant feeding and nutrition counseling. exclusive breastfeeds within an hour of delivery as
the preferred option and continue for 6 months. After
HIV Infected Pregnant Women 6 months, complementary feeding should be given
Antenatal care (ensure at least four visits) along with breastfeeds. A small number of babies born
Counseling on choices of continuation or MTP to to HIV infected mothers who have serious illness or
undertake with in the first 3 months of pregnancy only have died and a few reluctant mothers (who at their own
Screening for tuberculosis (TB) (40 GeneXpert testing risk despite counseling) may decide not to breastfeed
sites is being launched shortly) and other OIs but adopt exclusive replacement feeding (ERF).
Screening and treatment for STIs Provide antiretroviral prophylaxis to infants from birth
WHO clinical staging and CD4 testing up to a minimum period of 6 weeks.

Counseling on positive living, safe delivery, birth- Integrate follow-up of HIV-exposed infants (HEIs) into
planning and infant feeding options routine healthcare services including immunization.
Ensure initiation of cotrimoxazole prophylactic therapy Strengthen follow-up and outreach through ANMs, ASHAs
(CPT) and EID using HIV DNA PCR at 6 weeks of age and district level networks and other outreach workers to
onwards as per the EID guidelines. support HIV infected pregnant women and their family.
1. Define the terms:
i. Sexually transmitted infections
ii. Perinatal transmission
iii. Oral contraception
2. What are the effects of HIV on pregnancy?
3. What are the risk of transmission of infection?
49
Sudha Salhan
Malaria in Pregnancy
Malaria affects one million people in India annually. It is Pregnancy is a hypoimmune state and, hence, more
endemic in our country. Therefore, malaria is often seen prone.
in pregnant ladies here. It can seriously affect the health There is increased cortisol level in pregnancy associ-
of the pregnant woman, her fetus and subsequently the ated with increased risk.
neonate. Its effect depends on the epidemiological pattern Age: Younger age pregnant women more prone.
in the area. If malaria is stable in the community, i.e. Parity: Primigravida more susuptible.
there is constantly repeated infections (holoendemic), Duration of pregnancy: More seen in second and third
epidemics do not occur and the population has a high trimesters.
degree of immunity. Unstable malaria is seen in areas They exhale more and their abdominal temperature is
where transmission is intermittent, communal immunity
more than nonpregnant women hence easily detected
is poor and it is here that epidemics may be seen. The
by the mosquitos.
degree of immunity possessed by an individual is the sum
Have polyurea, hence, go out of security circle in the
total of phylogenetic or racial immunity (natural selection
open and hence more exposed to mosquito attack.
over ages), passive immunity (as seen upto the first month
P. falciparum infected red blood cells (RBCs) in a
after birth) and active immunity. Active immunity is
acquired by reticuloendothelial macrophages fixed in the pregnant woman bind to chondroitin sulfate A (CSA)
liver and in the circulation by lymphocytes (phagocytosis and get collected in placenta. These RBCs do not bind to
of parasites). Parasitemia also stimulates specific antibody other two receptors viz. CD36 and intracellular adhesion
development. molecule (ICAM 1) which are used in nonpregnant
Hence, it is obvious that history of previous malaria state. The antigen on infected RBCs in pregnancy is
infection has wide differences in the effect of malaria in the called variant surface antigen 2-chondroitin sulfate A
course of pregnancy. If there is no previous immunity, e.g. (VAR2CSA). It is not found in men. The level of anti-
immigrants from a nonendemic area to an endemic area, VAR2CSA specific IgG increase with parity and, hence,
the pregnant mother is highly susceptible. An immune protect multigravida from acquiring malaria.
pregnant woman can control her malarial infection
(though not able to cure it). EFFECT OF PREGNANCY ON
Malaria is a protozoan infection caused by four
MALARIAL COURSE
species of Plasmodium viz. P. vivax, P. malarial, P. ovale
and P. falciparum. Besides acquiring from the bite of The stress of pregnancy may breakdown acquired
infected female Anopheles mosquito it can be acquired immunity to malaria in the individual. If the dietary intake
through blood transfusion, organ transplantation, use of of protein is insufficient in a pregnant woman, the protein is
contaminated needle, etc. diverted from the immune system for the growth of the fetus
Why are pregnant women more susuptable to malaria and other changes. Therefore, immunity declines, hence,
than nonpregnant? inability to limit parasitemia. The factors responsible are not
The exact mechanism is not known but following totally understood but it may be because of changes in cell
hypothesis are put forward: mediated immunity and antibody production. Hence, both
parasite rate and parasite density are higher in pregnancy. As placental changes are seen where parasites are present. In
pregnancy advances this effect is manifested more severely. chronic infection (starting from first trimester), parasites
Attacks of fever are more frequent in the third trimester and malarial pigment (hemozoin) are present. The placenta
than in the first trimester. It may cause intrauterine growth in women infected with malaria act like the spleen.
restriction (IUGR) and premature labor. If the area has a Parasites (in varying number) and macrophages pack the
higher incidence of pernicious malaria, cerebral malaria intervillous spaces. This is mostly seen in the second half
can develop. of pregnancy more so with P. falciparum infection and in
the first pregnancy. This interferes with the circulation of
EFFECTS OF MALARIA ON PREGNANCY maternal blood through intervillous spaces impairing fetal
growth. The infant’s weight is significantly lower than that
This depends on degree of acquired immunity and dose of infants with no placental infection. These infants are
of infection. It can cause deviation from the course of sometimes called low birth weight tropical neonates. The
pregnancy (miscarriage, premature labor, IUGR) and situation is further complicated by prematurity thereby
affect the health of the mother. Thus malaria can result in
significantly increasing infant mortality rate. This placental
maternal morbidity and mortality and infant morbidity
infection can be prevented by chemotherapy.
and mortality. In endemic countries (e.g. Africa, Asian
countries including India), primigravidas are more
susceptible with a higher rate of parasitemia compared to EFFECT OF MATERNAL MALARIA
multigravidas or nonpregnant females. The primigravidas ON NEONATE
may be recently shifted from a nonendemic area to an
These are low birth weight, prematurity, congenital malaria,
endemic area after marriage, therefore have probably not
developed immunity towards Plasmodium and breakdown increased infant morbidity and mortality.
of maternal immunity is most marked in them. In addition,
primigravidas may be very young with lower immunity CONGENITAL MALARIA
besides other unresolved causes. Multigravidas are affected
Occurrence of congenital malaria ranges from 0.1 to 12%.
too but the severity is less. The most important influence
of the disease on maternal health is indirect, by causing Congenital malaria is seen in infants of unprotected
hemolysis of even non parasitized RBCs. Hence, the anemia susceptible women. The antimalarial antibodies readily
is mostly out of proportion of parasitemia. It is assumed traverse the placental barrier and reach the fetus. The
that parasitized RBCs become antigenic and produce parasites may reach the neonatal circulation. Maternofetal
auto-antibodies against RBCs and lead to intravascular transfusion during labor transfers a degree of immunity by
hemolysis causing severe anemia. The effect of excessive the mother and this is possessed by the neonate at birth. This
destruction of red cells is also more serious in pregnancy depends on the immunity possessed by the mother. Hence,
when immunity is reduced. The hematopoiesis is to be congenital malaria occurs only if the level of immunity
accelerated. This require folic acid which is usually not passively transferred (by gamma-globulins) was low. How
sufficient. Megaloblastic changes are seen in the bone the parasites cross the placenta is not fully understood. They
marrow. Therefore, both types of anemia-microcytic (due perhaps travel to the fetal circulation through the damaged
to red cell destruction) and megaloblastic (due to folic acid portion of the placenta. This may not be the cause of
deficiency) are seen. This anemia may progress rapidly and intrauterine death. It is the hyperpyrexia which causes fetal
may be very severe causing substantial maternal and fetal demise. Thus, congenital malaria can cause neonatal death
mortality. Cerebral malaria is usually uncommon in adults. if not diagnosed and treated. Neonatal death may also occur
But during pregnancy it can be seen P. falciparum infection because of anemia, prematurity, IUGR.
is also called malignant malaria due to grave complications.
Miscarrige before 16 weeks or premature labor, and
intrauterine death may be precipitated by hyperpyrexia
CLINICAL PRESENTATION
in susceptible women, unprotected by chemotherapy. Pyrexia is the main symptom and its frequency depends
But miscarriage can occur in afebrile pregnant women on the species of Plasmodium involved. However, fever
due to anemia and tumor necrosis factor (TNF) alpha or may even be continuous. Signs of intravascular hemolysis
interleukin 10 as major risk factors. There may be fetal like hepatomegaly, splenomegaly, anemia or thrombo-
growth restriction even leading to intrauterine death. cytopenia may be present. Severe malaria is more com-
Transplacental infection occurs. In acute infection, mon in primigravidas in second or third trimester and
Malaria in Pregnancy 481
TABLE 49.1: Differential diagnosis of cerebral malaria vs eclampsia

Features Eclampsia Cerebral malaria
High BP +++ –
Massive proteinurea +++ +
Repeated epileptiform + –
convulsions with coma
in between
Coma without fits – +
Hyperpyrexia + +++
Blood film
Showing MP – ++ Fig. 49.2: Schizont stage of Plasmodium vivax
Incidence Common Uncommon Courtesy: Dr Diwan, Safdarjung Hospital, Delhi
Relief with quinine – +
antigen. Results are available within 20 minutes. National
Abbreviations: BP—Blood pressure; MP—Malarial parasite
Vector Borne Disease Control Program (NVBDCP)
recommends only antigen-based bivalent RDTs
may have lung edema, severe anemia and hypoglycemia.
(P. falciparum and P. vivax) for diagnosis of malaria.
Malaria may mimic other common diseases like typhoid,
Polymerase chain reaction (PCR) can detect parasitic
etc. and delay treatment leading to an increase in mortality
nucleic acid. It require designated laboratory, it is
and morbidity of both the mother and the fetus. Cerebral
costly, not available everywhere and results take time. It
malaria is a rare entity but sometimes it is difficult to
distinguish from eclampsia. Both conditions have con- is useful in confirm species of malaria parasite once the
vulsions, coma, pyrexia and proteinuria (Table 49.1). diagnosis is made by slide test or RDT.
Serology: Antigen antibody tests are done. Indirect
immunofluoresence assay (IFA) and enzyme linked
INVESTIGATIONS immunosorbent assay (ELISA).
A thick peripheral blood smear especially during fever Detection of iron crystal biproduct of hemoglobin is
will detect the parasite. One thin film is also made as seen only in RBC infested with malarial parasites.
this helps in detection of species. It is the cheapest and After delivery can do placental histology.
best method (Figs 49.1 and 49.2). Placental blood and
cord blood smear can also be made during delivery. PREVENTION
Rapid diagnostic test (RDT): It is done where
experienced laboratory staff are not available. Finger Use of long-lasting insecticide-treated nets (LLINs) is a
prick or venous blood is taken. The test detect parasitic very useful habit. Outdoor and indoor spray and use of
larvivorous fish beside other methods to avoid insect bite.
Intermittent preventive treatment in pregnancy: WHO
prescribe the sulfadoxine-pyrimethamine (SP) at least twice
in second and third trimester of pregnancy irrespective of
malaria infection in endemic areas. Mefloquine (MQ) is an
alternative as has a long half-life.
In India we, have NVBDCP to eradicate this disease.
A vaccine (undertrial) would best be administered
before pregnancy.
TREATMENT
Once maternal malarial infection is confirmed, treatment
Fig. 49.1: Infection with gamete of Plasmodium falciparum must commence promptly to prevent further morbidity of
Courtesy: Dr Diwan, Safdarjung Hospital, Delhi mother and fetus and further spread by mosquito bite.
Artemisinin are relatively safe in first trimester of eliminate remaining parasite preventing reinfection and
pregnancy. Chloroquine can be used for treatment of act as post treatment prophylaxis but there safety is under
P. vivax, P. malariae and P. ovale infections. Four tablets research. WHO recommends intermittent preventive
of chloroquine phosphate (Lariago) 150 mg each are given treatment with sulfadoxine-pyrimethamine in endemic
initially with cold sweetened milk. Then two tablets are areas as part of antenatal care.
given after 6 hours. After that one tablet twice a day for Severe malaria: Prompt artesunate/quinine parental can
2 days to make a total of 10 tablets for a pregnant woman of
be given depending upon the availability but the former is
about 50 kg of weight will suffice. The above dose does not
life-saving. Exchange transfusion is helpful in some cases.
harm the fetus. Quinine, clindamycin and proguanil can
Recently mefloquine is being used in chloroquine
also be used depending on the availability. A combination
resistant cases. It can be given in the second and third
of quinine and clindamycin for 7 days can be prescribed.
Malaria in second and third trimester of pregnancy can trimester. It is considered safe. Tetracycline is also active
be treated with artemisinin. A combination of artesunate against chloroquine resistant malaria but it can cause
and clindamycin for 7 days or quinine and clindamycin maternal hepatotoxicity and fetal dental discoloration and
for 7 days is prescribed. Amodiquine (AQ) can be given in dysplasia.
P. falciparum malaria. Recently longer actin partner Therefore, keeping malarial infection in mind helps
drugs with artemisinin (lumefenitrine, piperaquine, etc.) treat the disease early, saving many mothers and neonates.
1. What are the effects of malaria during pregnancy on mother and fetus?
i. ____________ is the main symptoms and its frequency depends on the species of Plasmodium involved.
ii. Malaria in second and third trimester of pregnancy can be treated with ____________.
iii. The effects of maternal malaria on neonates are ____________, ____________, ____________ increased infant morbidity
and mortality.
iv. Malaria is a protozoan infection caused by ____________ species.
50
Sudha Salhan
Other Infections in Pregnancy
The sites of infection are choriodecidual space and

MATERNAL INFECTION
chorioamniotic space (Figs 50.1A and B).
Infections of the mother during pregnancy may be the
cause of abortions, preterm birth and even cerebral palsy Mechanism of Action
and chronic lung diseases in the neonate. Some infections Bacteria or its lipopolysaccharide activate macrophages.
are vertically transmitted to the fetus like human immuno Macrophages secrete cytokines (pro-inflammatory),
deficiency (HIV), hepatitis B, etc. In our country, prenatal interleukin 1 and 6 (IL-1 and IL-6) and tumor necrosis
examination and universal antenatal checkup are not factor alpha (TNF-α), etc. Human deciduas also
100% practiced. Therefore, these infections play a vital manufacture IL-1 and TNF-α in cases of infection. TNF-α,
role in maternal morbidity, maternal mortality, perinatal IL-1 and IL-6 stimulate prostaglandin (PG) production
morbidity and mortality. from the myometrium, decidua and amnion. In amniotic
Role of maternal infection in preterm labor studies of fluid testing, IL-6 level is the most sensitive and specific
amniotic fluid and placenta of premature infants revealed marker to detect intrauterine infection and is said to
infection in 70% of cases. The common organisms isolated predict fetuses at risk of significant neonatal morbidity. It
are mycoplasmas (Mycoplasma hominis and Ureaplasma is better than amniotic fluid culture results as it predicts
urealyticum) and group B streptococcus. Even systemic infection in the uterine cavity. Phospholipase A and C
infections like pneumonia, pyelonephritis, typhoid fever, from invading bacteria also stimulate PG production from
malaria, periodontal infection, etc. may lead to preterm human amnion, chorion and decidua.
delivery (Flowchart 50.1). Macrophages in response to infection produce cycloox
ygenase-2 (COX-2). COX-2 directly increases prostaglan
Flowchart 50.1: Role of infection in preterm labor din production. Uterine activity and cervical effacement,
PG induced myometrial contractions and changes in
cervical extracellular matrix causing its ripening. 15-
hydroxy prostaglandin dehydrogenase (15-OH-PGDH)
enzyme is present in chorio-trophoblastic cells. It quickly
degrades PG produced by the amnion and chorion, thus
preventing it from reaching the myometrium to produce
uterine contractions.
Hence, there is a fair balance of PG and PGDH to prevent
premature labor. Intrauterine infections may produce
excess PG so much so that PGDH is not able to cope.
Role of Maternal Infection in Intraventricular

Hemorrhage (IVH) of the Newborn
Abbreviations: IL—Interleukin; TNF—Tumor necrosis factors;
COX—Cyclooxygenase; PGDH—Prostaglandin dehydrogenase; Prematurity is the major cause of intraventricular
PG—Prostaglandin hemorrhage (IVH) of the neonate. Infections have a major
A B
Figs 50.1A and B: Sites of bacterial infection in the uterus
role in preterm births. Besides this, fetuses of mothers Flowchart 50.2: Flowchart showing genesis of intraventricular
having inflamed cerebral coverings (dura mater, etc.) and hemorrhage
increased IL-6 in amniotic fluid show 3–4 fold greater risk
of IVH than fetuses whose mother do not have inflamed
membranes. This pro-inflammatory cytokines explain
the association of infection with IVH. TNF-α causes vaso-
dilation, more permeability by blood vessels lead to heart
muscle depression and even shock. This causes circulatory
changes growing fetal brain. The germinal matrix has fragile
blood vessels (without muscle). Due to variation of blood
supply to fetal brain (e.g. due to TNF-α), this matrix zone is
liable to ischemia and hemorrhage. This may rupture one
layered of blood vessels between lateral ventricle and thus
lead to IVH. Intrathecal TNF-α levels correlate with damage
to the blood-brain barrier. Due to IVH, size of cerebral
ventricles increases. This compresses nearly periventricular
capillaries leading to ischemia and matter of the fetal brain
is damage (Flowchart 50.2).
CEREBRAL PALSY (CP) AND

MATERNAL INFECTION
Recent epidemiologic, clinical and animal experiments
have negated the long held belief that cerebral palsy is
due to antepartum and intrapartum events. A great role is Abbreviations: IL—Interleukin; TNF—Tumor neurosis factor
Other Infections in Pregnancy 485
Flowchart 50.3: Flowchart showing genesis of cerebral palsy Flowchart 50.4: Flowchart showing genesis of bronchopulmonary
dysplasia
Abbreviations: CMV—Cytomegalovirus; IL—Interleukin;

WBC—White blood cells
after birth tracheal aspiration shows that high levels of

cytokines preceded the neutrophil influx in neonates who
are destined to develop bronchopulmonary dysplasia.
There is very high umbilical blood level of IL-6 in these
newborns. This is even more true in preterm neonates.
Researchers suggest that these cytokines either initiate
the acute inflammatory process in the lung or they are
early risk markers of BPD. These infants have more
Abbreviations: TNF—Tumor necrosis factor; IVH—Interventricular
hemorrhage frequent respiratory infections and they thrive poorly,
neurodevelopmental delay and cardiovascular disease are
more commonly seen in them (Flowchart 50.4).
played by infection or inflammation in the pathogenesis of
cerebral palsy. Preterm infants with choriamnionitis in the
mother are at a greater risk of periventricular leukomalacia
TORCHS INFECTION
(PVL) or necrosis (cystic echolucent or hypoechoic Besides these infections there are some specific infections
cerebral white matter on neurosonography) and IVH. which may adversely influence the fetus or the neonate.
The role of central nervous system (CNS) trauma in the They come under the acronym toxoplasma, others, rubella,
etiology of CP is also doubtful. PVL is a precursor lesion of cytomegalovirus and herpes infection, syphilis (TORCHS)
CP (Flowchart 50.3). Cytokine and TNF-α released during (Box 50.1).
infection may cause circulatory collapse and exert a direct
toxic effect on oligodendrocytes. There exists a correlation Toxoplasmosis
between finding interlukin 1, 6 and 8 and TNF-α in the It is caused by Toxoplasma gondii, an obligatory intra
amniotic fluid culture and blood of umbilical cord and cellular protozoan. It is acquired by (a) eating uncooked
PVL development. Infections also cause preterm labor as or undercooked meat (b) drinking non-pasteurized milk
seen in Flowchart 50.1. from an animal with active infection (c) transplacental
spread to the fetus (d) rarely by blood and blood products
BRONCHOPULMONARY DYSPLASIA and organ transplantation.
Acute maternal toxoplasmosis during pregnancy
(BPD) AND INTRAUTERINE INFECTIONS causes more miscarriage and intrauterine deaths. Infec
It is a chronic lung disease occurring in upto 20% of tion during in the first trimester causes abortion and
preterm babies. The inciting events may be intrauterine severe neurological damage. Congenital toxoplasmosis is
exposure to infection by mycoplasmas, U. urealyticum manifested in 15% of cases it causes blindness, chorioretinitis,
and cytomegalovirus (CMV). M. hominis and its antigen deafness, hydrocephalus small head, hepatosplenomegaly,
stimulate production of pro-inflammatory cytokines. Soon pneumonia and coagulopathy jaundice.
Box 50.1: Classification of TORCH infections

T O R C H S
Toxoplasma Others Rubella Cytomegalovirus Herpes Syphilis
Bacterial vaginosis HIV
Gonorrhea Hepatitis B
Trichomonas vaginitis Hepatitis C
Group B streptococcus Human papillomavirus
Escherichia coli Human parvovirus
Ureaplasma urealyticum
Chlamydia trachomatis
Hemophilus influenzae
Varicella zoster
Listeria monocytogenes
Malaria
Tuberculosis
The mother is mostly asymptomatic. Hence, a pre- Chlamydial Infection

conceptional testing is necessary. Acute phase specific Chalmydia trachomatis is an obligatory intracellular
immunoglobulin M (IgM) antibody is taken as diagnostic. bacterium. Infection is usually asymptomatic but urethritis
Polymerase chain reaction (PCR) testing of amniotic fluid and mucopurulent cervicitis (may be due to gonorrhea)
confirms the diagnosis in the fetus. After birth IgM antibody may occur. It may cause neonatal conjunctivitis and
signifies congenital infection. IgG titre which are declining pneumonia. It is the most common cause of preventable
denotes only passive transfer of maternal antibodies. blindness in children in developing countries. Postpartum
If the mother is diagnosed to be suffering from toxo infections may manifest two to three weeks after delivery.
plasmosis, she should be treated 6 weeks before becoming Target screening of high-risk women can be carried
pregnant and throughout pregnancy. This reduces the out. Treatment for the pregnant woman is erythromycin
incidence of congenital toxoplasmosis by around 60%. 500 mg QID for 7 days. The sexual partner should also be
Spiramycin 3 MIU/day orally in two divided doses treated. It also causes lymphogranuloma venereum. In
throughout the pregnancy is advocated. Pyrimethamine this disease erythromycin is given for 21 days. Here too,
(25 mg) in combination with sulfadiazine (1 g QID) has treat the sexual partner also.
a better effect but is teratogenic. Hence, this therapy
is given only after 14 weeks of pregnancy and then too Chickenpox
with folic acid (5 mg TDS). Sulfonamides are not given It is caused by varicella zoster virus (a DNA virus). If it
near term in order to avoid kernicterus. Both spiramycin occurs in first 20 weeks of pregnancy the fetal congenital
and pyremethamine sulfate in combination are giving malformations are chorioretinitis, cerebral cortical atro
better results. Triple therapy for 3 weeks alternating with phy, hydronephrosis, cutaneous and bony defects. The
spiramycin, pyrimethamine, sulfadiazine for 3 weeks is highest risk is between 13 and 20 weeks of gestation. After
given if the mother is infected before 28 weeks of gestation. 20 weeks of pregnancy there is minimal evidence of fetal
If she is infected after that spiramycin alone is enough. infection. If the maternal infection occurs in the last week
Termination of pregnancy is considered if there is of pregnancy (when maternal antibodies are not enough to
documentation of infection in the first trimester of pregnancy. protect the fetus) severe and even fatal infection can occur
In congenital toxoplasmosis give treatment to the child in the neonate. In these cases, administration of varicella
for 6 months with pyrimethamine, sulfadiazine and folic zoster immunoglobin to the newborn is mandatory and
acid and next 6 months with spiramycin. may be life-saving.
Prevention of Toxoplasmosis Gonorrhea

Thoroughly cooking meat, and after working with raw It is caused by gram-negative intracellular diplococcus
meat, wash hand properly wash fruits and vegetables Neisseria gonorrhoeae. It is mainly transmitted through
before eating. Avoid contact with cats and their excreta. sexual intercourse. The newborn acquires it during birth,
in utero or in postpartum period. Conjunctivitis in the Ongoing cellular destruction or immunopathologic

neonate is called ophthalmia neonatorum. Most preg damage to tissue
nant patients suffering from gonorrhea are asymptomatic. Formation of circulating antigen antibody complexes
Symptoms of dysuria, proctitis and pharyngitis may be with deposition into certain tissues.
seen. Disseminated infection through blood born spread The fatal consequences of rubella relate directly to
my involve faints and other organs may occur in the preg gestational timing of infection.
nant. There is some evidence that blood borne spread lead
ing to disseminated infection with involvement of joints Congenital Rubella Syndrome
and other systems is more common in pregnant women. Maternal viremia infects the placenta and through it the
Infection during delivery may lead to endometritis, pelvic virus reach the fetus. Infection during the first trimester
infection and secondary sterility occur if she is infected of pregnancy may cause abortion, preterm labor, stillbirth
during delivery. Diagnosis is by smear and culture. and fetal malformations. The greatest risk to the fetus is in
Treatment of uncomplicated gonorrhea is by giving the first trimester but fetal infection is possible throughout
cefixime—orally 400 mg once dose or infection of ceft pregnancy. The risk again increases near term.
riaxone once 250 mg can also give azithromycin 2g single Grigg’s triad is cardiovascular defects, eye defects and
dose. For gonococcal endocarditis treatment is for 4 weeks. deafness.
Gonococcal meningitis is to be treated for 10 to 14 days. Congenital anomalies of the fetus in congenital rubella
Also treat the sex partner. syndrome are (Box 50.2):
Infants are given prophylaxis against eye infection with
Congenital heart defects
25–50 mg/kg ceftriaxone IM or intravenous (IV) as a single
Hearing loss
dose.
Cataract or glaucoma
If ophthalmia neonatorum has developed, hospita
Chorioretinits
lization and evaluation for disseminated infection is
advised. Topical drugs do not help. Neurologic disorders and mental retardation
Extended rubella syndrome has progressive panen

Rubella cephalitis too. Other fetal effects of rubella infection of the
Congenital defects can be caused by rubella contracted pregnant woman are:
by the mother during pregnancy. Now it is proven that Fetal growth restriction
German measles (rubella) infection in pregnancy can Microcephaly
have devastating effects on the fetus (Table 50.1). This viral

infection is spread by direct contact or droplet infection. Box 50.2: Major categories of congenital rubella syndrome
About half of all infections are asymptomatic. There may Transient form: Small for date, enlarged liver and, spleen. Low platelet
be fever, lymphadenopathy and maculopapular rash count and purpura, osteal pathology, encephlomeningitus, liverinfection,
hemolytic anemia, enlargement of lymph nodes, pneumonia.
(16–21 days after infection).
Permanent lesions: Impairment of hearing, heart lesion (stenosis of
Mechanisms of teratogenesis are: pulmonary tree, PDA, septal defect of ventricle), ophthalmic defect
Direct cellular destruction, causing altered formation (cataract, retinal damage, small eyes, giaucoma and myomia).
or function of developing tissues Development/delayed: Hearing defect, developmental defect of
Blood vessel obliteration with resultant hypoxic damage brain, diabeties mellitus and thyroid disorders etc. are seen at 20 or
Chromosomal injury
30 years of age
TABLE 50.1: Risk of rubella during pregnancy and management

Risk of congenital
Duration of pregnancy abnormality Affection Management
0–12 weeks 40–60% 100% risk of fetus being congenitally infected Termination of pregnancy
resulting in major congenital abnormality
13–16 weeks 30–35% Deafness and retinopathy, 15%; spontaneous Conservative treatment, amniocentesis and
abortion, 20% fetal blood monitoring
After 16 weeks 10% Normal conservative development, slight risk
of deafness and retinopathy
Hepatosplenomegaly Chorioretinitis
Thrombocytopenic purpura Sensorineural deafness
Radiolucent bone disease Mostly seen in primigravida without the development
Behavioral changes. of protective antibodies.
Infants with multiple congenital defects have high Most maternal infections are not recognized until after
mortality in infancy. delivery when the neonate is diagnosed with congenital
In cases with delayed expression, hypothyroidism CMV. Around 95% of congenitally CMV infected neonates
(chronic lymphocytic thyroiditis) diabetes mellitus, bile have no apparent abnormality. Hence, treatment during
duct atresia and cirrhosis may occur. pregnancy is not possible and not recommended.
Amelioration of symptoms can be done by CMV immune
Diagnosis globulin. The infection is prevented by giving the use of
Isolation of the virus from the nasopharynx, urine and seronegative or filtered blood products for transfusion.
cerebrospinal fluid (CSF) upto first 6 months of life. Recombinant glycoprotein B vaccine is under study.
Rubella IgM in cord blood or neonatal serum. Though the maternal antibodies do not prevent fetal
Prevention: Measles, mumps, rubella (MMR) vaccine is infection, they appears to decrease the likelihood of severe
given at 9 months of age. All adolescent girls must have fetal consequences to some extent. A vaccine administered
rubella vaccination; can give this vaccine recently married to women seronegative for CMV in the preconception
women who are not vaccinated or who are showing no period may decrease the risk of congenital CMV by 69%.
IgG against varicella also to vaccinated and after this must Newborns younger than 30 weeks of gestation and birth
avoid pregnant for 1 month. weight less than 1000 gm are at an exceptionally greater
No vaccination is given to a pregnant woman (as it risk of acquiring CMV by breast milk. Sterilizing milk
is a live vaccine). Nonimmune pregnant women are before feeding may help. Ganciclovir is the treatment of
advised to stay away from known cases of rubella. Give CMV. Antibodies to CMV infection is also being tried.
immunoglobulin 20 mL IM within 72 hours of exposure it There is no risk in future pregnancy as the mother
may reduce but not eliminate the risk of infection. develops antibodies.
Cytomegalovirus (CMV) Herpes Simplex Virus

Cytomegalovirus infection is usually sub-clinical and Two types of virus HSV I and HSV II are known. They can
self-limiting. Symptoms are also nonspecific. Besides cause primary infection, non-primary first episode and
close contact it is transmitted sexually, through saliva, recurrent infection. Acyclovir appears to be safe for use in
transfusion of blood and transplantation of organs or pregnant women.
tissues. It is also transmitted in utero, during birth or after Late pregnancy primary infection can cause preterm
birth. Infections during the first two trimesters have more labor. Newborn may have disseminated involvement
severe effects on the fetus. Upto 40,000 babies die with this of major viscera, or localized effect on CNS, eye, skin or
infection every year in USA. Manifestations of congenital mucosa. The newborn may even be asymptomatic.
CMV infection are: The infection is acquired by the fetus during vaginal
Hepatosplenomegaly delivery. Hence, elective cesarean section is done to
Jaundice prevent transmission to the fetus. The neonate should be
Petechial rash isolated from other babies. Breastfeeding is allowed. The
Thrombocytopenia infant should not be kissed by orally infected relatives.
Intracranial calcification
Chorioretinitis Syphilis
Deafness It is caused by the spirochaete Treponema pallidum. It is
Microcephaly primarily transmitted through sexual contact or transpla
Intrauterine death (upto 20% die before or soon after centally.
birth). The clinical course of syphilis is the same as in non-
Long-term consequence include: pregnant woman. Syphilis should be kept in mind if the
Psychomotor retardation pregnant woman has a genital lesion or skin rash especially
Microcephaly in palms and soles.
Screening in done in pregnancy by doing a Venereal acquired by pregnant women. It is caused by eating
Disease Research Laboratory (VDRL) test in both the unpasteurized milk and its products, raw or less cooked
partners. If positive, one can do specific treponemal tests meat and fish etc.
to confirm the diagnosis. In pregnant women there may be miscarriage, premature
Dark ground illumination test, T. Pallidum hemag delivery, intrauterine fetal death, and neonatal sepsis.
glutination test, or immobilization tests can be carried out. Symptomatic patients need antibiotic therapy.
The primary aim of screening is to prevent transmission to
the fetus. Infection of the fetus can occur from 6 weeks of SWINE FLU IN PREGNANCY
pregnancy onwards.
Congenital infection can cause: Swine flu is caused by a new strain of Influenza A (HINI
Spontaneous abortion virus). It is RNA virus. Spread is directly from pigs to human
Intrauterine growth restriction (IUGR) and vice versa. Between humans the spread is mostly
Premature delivery through droplet infection. Hand washing is an important
Non-immune hydrops preventive measure.
Perinatal loss. It presents as fever, cough, nasal discharge, malaise etc.
Rarely rapid progression present as dyspnoea, tachypnoea
Kassowitz Law and CNS involvement etc..
There is a sequence of premature stillbirth, full term still Diagnosis is confirmed by rapid influenza antigen(RT
birth, live birth with congenital syphilis, normal nonin PCR) of the nasopharengial swab.
fected newborn. However, this is not always seen.
Most of the neonates with congenital syphilis appear Complications
normal. Rhinitis (snuffles) can be seen. The rash, osteo
In first trimester, miscarriage can occur. If there is high fever
chondritis and perichondritis are common. More severely
during this time there may be congenital abnormalities
infected fetus may show jaundice, hepato-splenomegaly,
like neural tube defects.
generalized lymphadenopathy and anemia.
If infection is acquired in third trimester, premature
Penicillin is used in all stages of syphilis. In primary, sec
rupture of membrane and preterm labor may be seen.
ondary and early late stage, 2.4 mega units of penicillin after
test dose followed by 1.2 mega unit in each buttock as single Fetal tachycardia leads to more cesarean births. High
dose is given. Treatment of the sexual partner is essential. fever during labor may cause neonatal encephalopathy,
In cases of late, latent or of unknown duration 2.4 mega cerebral palsy, neonatal seizures and even neonatal death.
unit is given in 3 doses at 1 week interval. The cause of these complications is not known but high
Tertiary syphilis (gumma or cardiovascular) 2.4 million fever may be the culprit rather the virus directly.
IM 3 doses at 1 week interval is the treatment.
Tertiary syphilis IV (neurosyphilis) penicillin 18–24 Management
mu/day 3–4 mu IV every 4 hours after test dose for 10– Admit in the hospital if report with signs of pneumonia
14 days or procaine penicillin 24 mega unit IV after test especially during epidemics. Third trimester is the most
dose with probenicid 500 mg orally QID daily for 10–14 vulnerable period for higher risk of serious complications.
days. The partner is to be treated in all the above stages. Frequent hand washing is very important. Rest, proper
Congenital syphilis: Aqueous crystalline penicillin G nutritional supplements are needed. Enough fluids is
100,000–150,000 µ/kg/day after test dose 50, 000 IU/kg/ essential. High fever is to be brought down. The drugs
dose IV BD × 1st 7 days of life and then TDS for next used in this disease are of category C and proper data
10 days or procaine penicilline G 50, 000 unit/kg/day about their safety is not known. These antiviral drugs are
after TD IM OD × 10 days. oselnivir and zanamivir. Paracetamol can be used for fever
Syphilis positive pregnant women should be tested to and other symptoms but NSAIDS are to be avoided.
look for other sexually transmitted diseases (STDs) includ After delivery the newborn is separated from the infected
ing HIV.
mother. This mother is given antiviral drugs for at least 48
hours. After that she can breastfeed with a mask on her face.
LISTRRIOSIS During epidemics inactivated influenza vaccine can
It is a bacterial (Listeria) infection causing mild symptoms be given to pregnant women [Advisary Committee on
(pain in the body and tiredness).This infection is readily Immunization Practices-(ACIP)].
ZIKA VIRUS DISEASE IN PREGNANCY Diagnosis

It is done by genetic testing. Blood test is not possible as
The Zika virus disease is known since 1947. But its impor
the virus stays there only for one week.
tance in pregnant women has recently come to light.
There is no specific medicine. General measures like
This disease is caused by the virus spread by aedes
rest, proper diet and paracetamol is needed to make the
aegypti mosquito. WHO traced its spread to 21 countries,
pregnant women comfortable.
Brazil being the worst hit (around 4000 babies affected in
a year).
There is mild fever, conjectivitis and headache.
GROUP B STREPTOCOCCAL BACTERIAL
INFECTION IN PREGNANCY
Infection During Pregnancy It is to be tested in the third trimester and treated vigorously,
Maximum damage occur during first trimester. It causes if positive, to prevent fatal neonatal sepsis.
microcephaly in the fetus (head size less than 31.5 cm) and
hence the brain is not fully developed (Fig. 50.2). RABIES IN PREGNANCY
About 30,000 people die yearly due to this disease in India.
The incidence in pregnancy is the same as in general
public. Tissue culture derived rabies vaccine, human or
equine rabies immunoglobin should be given to rabies
exposed pregnant women promptly and in the same
manner as to others after proper toiletting of the wound.
Tissue culture derived rabies vaccine is safe in pregnancy.
Purified vaccines has shown no adverse effect, hence need
not be withheld in pregnancy.
CHOLERA
It is caused by vibrio cholera bacteria causing loose stools
and pain abdomen plenty of fluids and proper antibiotics
cures.
Tuberculosis HIV malaria in pregnancy are discussed in
Fig. 50.2: Microcephaly (due to Zika virus) respective chapters.
1. Describe the types of maternal infections.
2. ‘TORCH’ stand for?
i. ____________ is caused by vibrio cholera bacteria.
ii. Neisseria gonorrhoeae is a ____________ bacteria.
iii. Toxoplasmosis is caused by ____________.
iv. ____________ is caused by varicella zoster virus.
Section 9
Special Conditions
Section Outline
51. Dermatological Problems in Pregnancy
52. Care of Pregnant Patient with Previous Cesarean Section
53. Psychiatric Disorders in Pregnancy and Puerperium
54. Gynecological and Surgical Disorders Associated with Pregnancy
55. High-risk Pregnancies
56. Obstetrical Collapse
57. Asepsis and Antisepsis in Operation Theater
51
Sudha Salhan
Dermatological Problems
in Pregnancy
During pregnancy, besides the increased activity of the

pituitary, adrenal and thyroid gland, a new endocrine
gland—the placenta develops. Increased hormone secre
tions from all these glands have a significant effect on the
skin of the mother.
PIGMENTATION
Hyperpigmentation of the areola (secondary areola)
(Fig. 51.1), perineum, abdomen, linea nigra, and face
(chloasma or melasma) develop which may not completely
regress after delivery. The process of pigmentation is most
probably initiated by increased levels of estrogen and
progesterone and continued by placental corticotropin-
releasing hormone and pro-opiomelanocortin derived
Fig. 51.2: Chloasma or mask of pregnancy
peptides, such as adrenocorticotropic hormone (ACTH),
α-melanocyte-stimulating hormone (a-MSH), β-MSH
and β-endorphin. hydrocortisone powder getting a final concentration of
The chloasma or mask of pregnancy is seen on both 0.5% used once a day for 6 to 12 weeks along with a sun
cheeks, above eyebrows, mid forehead, above upper lip blocking cream with sun protecting factor (SPF). The lotion
and on chin; it progresses throughout the pregnancy may cause irritation. Chemical peels and laser ablation
(Fig. 51.2). This can also be seen in oral contraceptive pill can also be used with caution.
users. Treatment after delivery is with a mixture containing
equal part of 0.05% tretinoin, 4% hydroquinone cream and BLOOD VESSELS
Neovascularization is a part of pregnancy changes. The
placental angiogenesis factor, has been identified as basic
fibroblast growth factor (BFGF) besides other hormones,
which increase in the mother’s body (Morgioris, et al.
1988) during pregnancy.
This formation of new vessels is also responsible for the
earliest signs of pregnancy (Jacquemier-Chadwick sign) a
purplish discoloration of the vulvar vestibule and vagina.
Vascular spider nevi and palmar erythema which are
also seen in chronic liver disease can also be seen.
By the 7th week after delivery most of these changes
Fig. 51.1: Secondary areola regress.
A B
Figs 51.3A and B: Vulval and lower limb varicosities in pregnancy
VARICOSITIES
These are seen on the legs, vulva and rectum (Figs 51.3A
and B). They can be ascribed to the compression of the
pelvic plexus by the enlarged gravid uterus and a weakness
of the vessel walls in pregnancy. There may be discomfort
or pain in the legs or the vulva. The hemorrhoids may give
rise to pain and bleeding. Deep vein thrombosis is rare.
Treatment
Conservative: Avoid prolonged standing and carrying out
frequent leg elevation and avoid tight clothes. Sleeping in Fig. 51.4: Striae gravidarum
Trendelenburg (leg elevated) or lateral decubitus position
may also help. Support of varicose veins while standing which can cause a decrease in the number of fibroblasts
by elastic bandage or stockings can be practised but care in the dermis and reduction in collagen synthesis. Similar
should be taken that these do not cause constriction. striae are also seen in Cushing’s disease or in patients
on steroidal therapy (the reason being the same high
Drug corticosteroids).
For residual large varicosities persisting 6 weeks after Applying creams like topical tretinoin may help in
delivery other options of treatment are surgery or reducing the mild itching experienced by some patients.
injection of hypertonic saline or other sclerosing agents. After delivery, the discoloration fades in due course of
Hemorrhoidectomy may be necessary for persistent non- time and striae become less prominent.
regressing hemorrhoids 3 months postpartum.
SKIN TAGS OR MOLLUSCUM
STRIAE GRAVIDARUM (FIG. 51.4) FIBROSUM GRAVIDARUM
These are linear patches of dermal and epidermal atrophy These are slightly hyperpigmed polypoidal lesions in the
on the abdomen, breasts, buttocks and thighs. They are neck, axilla, groin, intramammary and other regions. They
partly due to increased stretching of the skin (due to an appear in the second half of the pregnancy and may cause
enlarging uterus and fat deposition) but mainly due to irritation. They can be treated snipping them off or by
high levels of glucocorticoids associated with pregnancy electrocautery under local anesthesia.
Dermatological Problems in Pregnancy 495
There may be an associated increased incidence of

GINGIVITIS prematurity and intrauterine growth restriction (IUGR).
This is of varying degrees and is seen in some patients. Recurrence is seen in subsequent pregnancies. Topical
The gums may bleed easily. Some of the lesions may be in corticoid and anti-histaminics may help. Skin biopsy
the form of epulis, a highly vascular tumor, which regress shows subepithelial blisters. Direct immunofluorescence
completely after delivery (highly vascular angiogenesis shows immunoglobin G (IgG) and complement along the
of pregnancy). Treatment is maintenance of good dental basement membrane.
hygiene. Removal may be needed in pregnancy but it
recurs. OTHER SKIN DISEASES
Acne
PRURITIC CONDITIONS These are increased because of increased sebaceous gland
Pruritic conditions occur in: activity. Topical antibiotics and oral erythromycin may help.
Intrahepatic cholestasis of pregnancy
Pemphigoid (herpes gestationis) Prurigo of Pregnancy

Liver involvement is seen by occasional mild jaundice This causes itchy papules on the abdomen and extensor
and a mild elevation of transaminase level. Total serum surface of the body and is usually seen during the third
bile acid are elevated and may produce pruritis trimester and even after delivery. No specific treatment is
Intrahepatic cholestasis of pregnancy causes intense required. Recurrences are seen.
itching in late pregnancy even in the absence of any
skin disease Psoriasis (Fig. 51.5)
A genetic predisposition is suggested More than half of the patients suffering from psoriasis
Hormonal influence of estrogen is possible as it recurs show a decrease in the disease during pregnancy but flare
in subsequent pregnancies up within 4 months after delivery. During pregnancy use
One must rule out environmental factors. topical corticosteroids, dithranol and ultraviolet light.
Treatment Atopic Eczema

It is relieved after delivery. Calamine lotion or other It may decrease during pregnancy. But if there is itching
soothing lotions may decrease the intensity of itching. around the nipple, use topical corticoid and chlorpheni
Emollient and body oils may sometimes help. The use of ramine.
ursodeoxycholic acid (UDCA) decreases total bile acid and
Erythema Multiforme
hence reduce itching. Fetal distress and premature birth
can occur. However, the newborn is otherwise healthy. Erythema multiforme has herpes simplex virus as etio
logical agent. During pregnancy, acute eruption may need
Polymorphic Eruption in Pregnancy only symptomatic treatment. Repeated episodes may need
It is commonly seen in pregnancy, mainly in the last
trimester of primigravida but may be seen in the early
postpartum period. The periumbilical area is spared.
Itchy urticarial papules are seen on the striae. Topical
corticosteroids and antihistamines may help.
Pemphigoid (Herpes Gestationis)

This is a rare entity. It present with intense itching and
pleomorphic eruptions starting in the second or third
trimester and immediately postpartum. The lesions begin
from the umbilicus. Urticaria and erythema and bullae are
seen and mucous membranes are spared. It is associated
with hydatidiform mole and usually occurs in the first
pregnancy. Fig. 51.5: Psoriasis in pregnancy
acyclovir therapy. There is no increase in the risk to either

the fetus or the mother.
Lupus Erythematosus
There is some evidence that in patients with systemic lupus
erythematosus (SLE), the skin eruption can flare up with
pregnancy. Offspring may have a congenital heart block
or lesions of subacute cutaneous lupus erythematosus
(SCLE). Treatment includes skin protection, topical
steroids. Hydroxychloroquine may be needed.
Warts in Pregnancy
Warts are mostly seen in the perineal area (Fig. 51.6).
Cryocautery is used. Imiquimod is to be used cautiously. Do
not use podophyllin. Cesarean section is done in these cases. Fig. 51.6: Warts at perineal area in pregnancy
1. What do you understand by the term psoriasis?
2. True/False:
i. Striae gravidarum are linear patches of dermal and epidermal atrophy on the abdomen, breasts, buttocks and thighs during
pregnancy.
ii. Hemorrhoidectomy may not be necessary for persistent non-regressing hemorrhoids 3 months postpartum.
52
Sudha Salhan
Care of Pregnant Patient with
Previous Cesarean Section
INTRODUCTION traindicated for VBAC. Lower vertical is also considered

for VBAC by some obstetricians.
Cragin had given the dictum of ‘once a cesarean always If there is a history suggestive of postoperative infection
a cesarean’. In those days cesarean sections (CS) were leading to poorly healed scar viz. history of fever, foul
performed by the classical upper segment route; and smelling discharge or whether the abdominal scar
anesthetic agents and antibiotics were given in the primitive was resutured, vaginal delivery is not allowed because
stage. Then in 1960, it was found by various investigators that there is a three-fold increase in the risk of rupture of the
vaginal birth after cesarean (VBAC) is feasible and safe. This uterus.
is because of good antibiotics, safe anesthesia, availability If the uterus was stitched in a single layer, there is
of blood transfusion and lower segment cesarean section four-fold greater chances of rupture than double layer
(LSCS). suturing.
Women with previous CS are high-risk patients, i.e. they If there is a period of less than 18 months in between
have an increased risk regardless of the mode of delivery. two pregnancies we do not allow vaginal delivery, as
Selection of patients for VBAC, the following points are there is three-fold increase in the incidence of uterine
kept in mind of the previous cesarean: scar rupture.
Indication of cesarean: Elective cesarean section
If there are more than one scars or a history of previous
(ECS) is done if the indication for previous cesarean rupture, we prefer ECS. Previous myomectomy in which
is recurrent like cephalopelvic disproportion, failure uterine cavity was opened is a high-risk suture line.
of progress of labor or dystocia, repair of vesicovaginal Others: Factors to be considered are as follow:
fistula. In these cases vaginal delivery is not allowed. • If the patient is admitted in labor her Bishop score is
If the indication is non-recurrent like breech, fetal determined.
compromise (fetal distress), placenta previa, abruptio • If there is any doubt of pelvic inadequacy, we prefer
placentae or cord prolapse the patient can be considered ECS.
for VBAC. • If the age of the patient is more than 30 years, we
Place of operation (facility) and intraoperative advise ECS.
complications: When the technical skills of the • When the estimated weight of the baby is more than
surgeon are doubtful, as in the cases of CS done in 4 kg, an ECS is preferred.
remote areas or if there were technical difficulties • Place of delivery is important. If there is a provision
during surgery found on discharge slip (tear, extension of an operation theater within 20 to 30 minutes, we
of scar) then vaginal delivery is not allowed. allow vaginal delivery (needed in cases of rupture
Type of scar: One should keep in mind whether the uterus).
uterine scar is in the upper segment or the lower seg- • If there is a normal delivery before and after the CS,
ment. In the lower segment it may be transverse or we safely allow vaginal delivery.
lower vertical. Only if it is a lower segment transverse • Twins (if combined weight is 4 kg or more) and
scar then vaginal delivery is allowed. Inverted T and J polyhydramnios, an ECS is preferred.
shaped incision. Scar’s integrity is doubtful hence con- • Length of gestation beyond 40 weeks need a CS.
SCAR THICKNESS COUNSELING

There are no clear cut guidelines about scar thickness by Counseling of the patient is very important. The obstetrician
ultrasound. A scar less than 8 mm is considered a weak scar. should start counseling early about the feasibility and the
Scar dehiscence (2%) is defined as an asymptomatic safety of vaginal delivery during antenatal visits in this
disruption of previous uterine scar but the peritoneum pregnancy (if she fulfils the criteria of VBAC). Check for
is intact. It is discovered incidentally at the time of scar thickness, if possible, by ultrasound examination.
laparotomy or by digital examination of the uterus after She must know the maternal fetal and anesthetist in both
vaginal delivery. types of deliveries. VBAC avoids abdominal surgery, less
infection, less days in the hospital, etc. Repeat ECS has
SCAR RUPTURE more maternal morbidity and mortality. Chances of
hysterectomy are more, more blood is to be transfused. But
Scar rupture is when all layers of the uterus, including the the neonate may have slightly more respiratory problems.
peritoneum open at the site of previous uterine scar. It is A proper written consent is taken after the counseling.
an acute emergency and require immediate laparotomy. After proper selection, patients have a 60–80% chance
The incidence of scar rupture in different situations are of a successful vaginal delivery. Ideally the patient is
as follows: admitted at 38 weeks of pregnancy. But if satisfied with her
condition she can be advised to come at term or when she
Classical scar rupture 4–9%
T-shaped incision 4–9%
start having labor pains, leaking or any other abnormality.
Low vertical 1–7% At that time she is admitted and assessed.
Low transverse 0.1–1.5%
Previous rupture in lower segment 6% INTRAPARTUM MANAGEMENT
Previous rupture in upper segment 32%
Intrapartum management in the labor room:
Intravenous (IV) access is established.
Features of Impending Scar Rupture Blood is sent for grouping and cross-matching.
Suprapubic pain persisting in between contraction Bishops score is determined and if unfavorable pros-
Vaginal bleeding taglandin E2 (PGE2) gel can be given for cervical ripening.
Bladder tenesmus (hematuria can be seen if catherized) Vital charting is done every 15 minutes.
Unexplained tachycardia The patient is put on CTG, there is no role of intermittent
Maternal hypotension auscultation.
Tenderness over the uterine scar Only oxytocin is allowed for augmentation of labor
Ballooning of the lower uterine segment (maximum dose 20–30 mU/minute). Prostaglandin of
Cardiotocography (CTG) shows hypercontractility any brand is contraindicated for this purpose. If any
(increased frequency or intensity of contractions) and tachysystole occurs with oxytocin, stop the IV drug and
abnormal fetal heart sounds (FHS) (prolonged, late or give subcutaneous terbutaline 0.25 mg and oxygen.
variable decelerations) Analgesics are given at the appropriate time.
Failure of progress of labor without any cause. The pediatrician should be available at the time of delivery.
In CTG, note the type of contraction. Any demonstration

PLACENTA PREVIA of hyperactivity (increased frequency or intensity)
The incidence of placenta previa increases with each or abnormality of FHS (prolonged, late or variable
operation. decelerations) must alert the obstetrician. If in this case
the cervix is not fully dilated, a CS should be performed
Normal incidence 4% immediately (within 30 minute) to prevent impending
One cesarean section 10–35%
Multiple cesarean sections 65% rupture.
We can also measure intrauterine pressure by monitoring
To diagnose abnormalities of placental insertion, with a catheter (when available). Any loss of intrauterine
e.g. percreta, increta, etc. (an MRI is more accurate, if pressure is an indication of uterine rupture and immediate
available). laparotomy is indicated.
Care of Pregnant Patient with Previous Cesarean Section 499
Nowadays, intrauterine exploration of the uterine scar necessary. Otherwise, close observation of vital signs and
after vaginal delivery is not routinely done. However, serial hematocrit determination is needed.
if there is active bleeding, laparotomy may become Thus, we can say that the dictum now should be, ‘once a
cesarean always a hospital delivery’.
1. What are the features of impending scar rupture?
2. Define scar dehiscence.
i. Full form of VBAC is ____________.
ii. ____________ is allowed for augmentation of labor.
53
Rajesh Rastogi, Anukriti Verma
Psychiatric Disorders in
Pregnancy and Puerperium
diagnosed during pregnancy. Screening tests like

PSYCHIATRIC DISORDERS
Edinburgh Postnatal Depression Scale (EPDS) are validated
DURING PREGNANCY for detecting depression in both pregnant and postnatal
Pregnancy is the most cherished goal of almost all married women.
women. It is itself a very significant life event for any Women who have past or family history of depression
woman which involves a continuous process of change, both are at greater risk and so are those with psychosocial
physiologically and psychologically. Both, the hormonal stressors like unwanted pregnancy, poverty or relationship
changes and the realization of increased responsibility issues.
and lifestyle changes may act as a stressor. An expectant
mother may adapt well to these changes or she may develop Treatment
symptoms of anxiety, depression or dysphoria. Pregnancy No clear consensus exists about the safety of use of
may well be the stressor precipitating a de novo psychiatric psychotropic medication during pregnancy (Table 53.1).
disorder or may mark the worsening of a previously The potential risks of adverse effects of medication must
developed psychiatric syndrome, especially if previously be carefully weighed against the potential hazards of
prescribed psychiatric medication is stopped. psychiatric disorders. In mild illness, non pharmaco
Psychiatric problems during pregnancy are known to logical approaches like counseling, reassurance and
adversely effect course of pregnancy by causing obstetric psychotherapy are advisable. In more serious cases anti
complications like pre-eclampsia, preterm delivery and
placental abnormalities and also effect normal fetal
TABLE 53.1: Food and drug administration rating of drug safety in
growth, development and cause low birth weight or fetal pregnancy
distress. Category Definition Drug examples
A No fetal risks in controlled Iron
Depression during Pregnancy human studies
Depression occurs commonly during pregnancy. The B Animal studies show no fetal Acetaminophen
symptoms of depression effect 20% of pregnant women. risk, but controlled studies
Some studies shows that the rates at which depression have not been done in
occurs are more at 32 weeks of pregnancy than at 8 human studies
weeks of postpartum. Despite its common prevalence, C Adverse fetal effects in Haloperidol,
animals and no human data chlorpromazine,
depression frequently goes undetected and untreated
available aspirin
during pregnancy.
D Human fetal risk seen (may Tetracycline,
be used in life-threatening ethanol, lithium
Clinical Features and Risk Factors situation)
Depression shares some features common to pregnancy X Proved fetal risk in humans Valproic acid,
itself like easy fatigue, sleep and appetite changes and (no indication for use, even in thalidomide
irritable mood and this contributes to it being under- life-threatening situations)
Psychiatric Disorders in Pregnancy and Puerperium 501
depressants selective serotonin reuptake inhibitors (SSRIs) TABLE 53.2: Puerperal mood disorders
may be tried. Although no clear evidence of teratogenic Maternity Postpartum Postpartum
effects of SSRIs exists, however, their absolute safety Features blues depression psychosis
cannot be guaranteed especially if prescribed during first Incidence 30–75% 10–15% 0.2%
trimester. Exposure to SSRIs in third trimester may lead Onset after 3–10 days 3 weeks 2 weeks
to a transient mild perinatal syndrome with symptoms of childbirth
hypotonia, hypoglycemia, weak cry, breathing difficulties Management Support Brief cognitive Admission,
or sometimes seizures in some cases. In utero late exposure and therapy, education,
education counseling antidepressants,
to SSRIs may also increase the chances of the neonate
and/or mood stabilizers,
developing persistent pulmonary hypertension. Patients
antidepres- antipsychotics,
not responding to or poorly tolerating drugs may require sants ECT
to be given electroconvulsive therapy (ECT).
Abbreviation: ECT—Electroconvulsive therapy
PSYCHIATRIC DISORDERS IN
Treatment includes counseling, psychoeducation and
PUERPERIUM reassurance.
Psychiatric disorders are common during the postpartum
period. A combination of endocrinal, metabolic and Postpartum Depression
psychological factors play a major role. Maternal sleep The prevalence of postpartum depression is about 10–15%.
deprivation, round the clock responsibility of the newborn, First 3 months after delivery are a period of high- risk for
drastic changes in lifestyle and added costs all contribute developing depression.
to the stress of the mother. Risk factors are as follows:
There is an increased risk in those who have had Previous postpartum depression
previous history of psychiatric disorders, particularly History of depression
during previous pregnancies or postpartum periods. Those Family history of mood disorders
with family histories of psychiatric disorders (especially Stressful life events
mood disorders) are also predisposed. Increased risk of Poor social support
mood disorders with those who have had bipolar illness as Low self esteem
compared to unipolar illness. Elevated mid pregnancy levels of placental corticotropin-
releasing hormone.
Classification Neuroreceptor downregulation following delivery may
In International Classification of Diseases, Tenth Edition also contribute to the depression.
(ICD-10), clinicians are discouraged from categorizing
psychiatric disorders during the postpartum period as Clinical Features
separate from other affective disorders. Postpartum Depressed mood, weight changes, anxiety and insomnia
depression is coded as a subtype of major depressive for a period of atleast 2 weeks. Somatic complaints are also
disorder in DSM–5. common. In its most severe form, postpartum depression
For simplicity, the postpartum puerperal mood disorders may result in profound dysfunction. Suicidal ideation is
are classified as in Table 53.2. frequently reported, however, suicide rates appear to be
relatively low.
Postpartum Blues/Maternity (Baby) Blues
Baby blues are the most common psychiatric disorder in Treatment
the immediate postpartum period (with prevalence of The non-pharmacological therapies such as inter-
50–80%) with onset typically on day 3 of post-delivery personal psychotherapy and cognitive behavioral therapies
and spontaneous resolution by day 10. Symptoms are are effective interventions in many patients. Availability of
characterized by irritability, tearfulness, mood swings, support is important.
anxiety, sleep disturbances, decreased appetite and The pharmacological treatment of postpartum depres-
fatigue. This is a transient disorder which rarely transform sion is not well researched due to the potential risks
into a full blown depressive episode in 20–25% cases. associated with transmitting the drugs to the newborn via
lactation. However, studies claim that SSRI and Tricyclic Clinical Features
antidepressants (TCAs) are relatively safe. Escitalopram Delusions, hallucinations, depression, suicidal and
10–20 mg, fluoxetine 20–60 mg or sertraline 50–200 mg infanticidal ideation are characteristic features. Symptoms
may be prescribed. Careful monitoring of the breastfed
begin with insomnia, fatigue, restlessness, irritability,
infant of such mothers is advisable for potential harmful
mood swings. These are followed by suspiciousness,
effects. Anxiolytics such as benzodiazepines (clonazepam
incoherent speech, violence, there may be delusions about
0.5 mg or lorazepam 1 mg) may be prescribed in addition
the baby being evil, dead or defective. Patient may believe
for insomnia and anxiety.
she is virginal and has not delivered. May hear voices
Women must be cautioned that these medications are
commanding her to harm/kill herself or the baby. The
secreted in the breast milk. In cases of severe postpartum
mother would stop caring for the baby and may instead be
depression and patients who are at risk of suicide may
trying to harm him.
need hospitalization.
Electroconvulsive therapy (ECT) is generally regarded Risk factors include complications of pregnancy,
as a safe and effective treatment in postpartum women. family history of mood disorder. In 50–60% cases it is in the
ECT may be particularly useful in women who are first delivery of the lady. One such episode of postpartum
strongly suicidal or homicidal, or who are reluctant to take predisposes to further similar episodes in future deliveries.
medication while breastfeeding. They are given six to eight
treatments on a twice/thrice weekly schedule. Treatment
Postpartum psychosis is a psychiatric emergency as it
Postpartum Psychosis entails a significant risk both to mother and child. The
Psychosis may have its onset in the postpartum period patient frequently needs hospitalization and her contact
between 2 to 8 weeks after delivery (sometimes even upto with her child needs to be strictly supervised.
5 months). Its prevalence is about 0.1 to 0.2%. Postpartum Drug treatment includes use of antipsychotics like
psychosis is the most severe form of puerperal mood olanzapine/risperidone along with mood stabilizer like
disorders with significant risk for both the mother and lithium and possibly antidepressant (if not in mania)
child. It needs prompt diagnosis and treatment. along with benzodiazepines for short duration. Care
Recent literature suggests postpartum psychosis is essen should be taken to prevent lactational transmittance of
tially an episode of bipolar mood disorder which is likely these drugs to the infant. Counseling and psychotherapy
to recur later. In the recent edition of DSM-5, postpartum forms the integral part of the therapy. A few cases that are
psychosis is categorized as a subtype of bipolar disorder. very agitated or suicidal may require ECT.
1. Discuss maternity blues and its treatment.
2. Discuss the severe form of puerperal mood disorder.
i. Name the screening test for detecting depression in pregnant women ____________.
ii. Antidepressants for treatment of depression in pregnant women are ____________.
iii. ____________ depression is subtypes of major depressive disorder is DSM–5.
Gynecological
54
Sudha Salhan
and Surgical Disorders
Associated with Pregnancy
INTRODUCTION (oophorectomy or ovarian cystectomy depending upon

the case). Tumor markers are of no help in pregnancy.
Pregnancy is a normal physiological condition of the The ovary is sent for histopathology and further treatment
body. However, the pregnant woman may have some depends on whether it is benign or malignant.
gynecological (e.g. ovarian tumor) or surgical illnesses
(appendicitis) before or during conception and they
may influence the health of the mother. Some common UTERINE LEIOMYOMA ASSOCIATED
gynecological and surgical disorders seen with pregnancy WITH PREGNANCY
are described further.
Uterine myomas are situated at different sites in the uterus.
OVARIAN TUMORS Effect of Myoma on Pregnancy

Ovarian tumors of various types may complicate It is observed that myomas greater than 3 cm in diameter
conception; the average incidence being 1 in 200 has significantly increased rates of preterm labor, placenta
pregnancies. Mostly they are cystic tumors. Because of the abruption, pelvic pain and cesarean delivery as they may
availability of ultrasound they are more often diagnosed. cause obstructed labor. Tumors less than 3 cm in size are
There may be torsion (first trimester), the tumor may lead of no clinical importance. The incidence of abortion is
to obstruction during labor or may rupture during labor or only increased if the placenta is near or implanted on the
at the time of surgical removal. Torsion also occurs after myoma. In this case there is also a chance of postpartum
delivery when there is much space in abdomen. hemorrhage (PPH). PPH is not common but if it occurs
it is massive, not controlled with medical treatment and
Management mostly corrected by hysterectomy. Multiple myomas may
The ultrasound characteristics of the tumor must be lead to fetal malposition, e.g. breech, etc.
evaluated. With septa or solid areas tumors between
5 to 10 cm and all tumors more than 10 cm in size are to
Effect of Pregnancy on Myoma
be removed. Masses less than 5 cm are to be observed. The hormones and growth factors that support normal
If there is an increase in the size or there is pain and the uterine growth during pregnancy also help myomas to grow.
tumor persists after 16 weeks of pregnancy, surgery is Increase in the size of the myoma occurs in the first trimester
to be carried out after 16 weeks of pregnancy or in the of pregnancy. However, accurate prediction of growth of a
early second trimester. Early removal may jeopardize the myoma in pregnancy cannot be made. During pregnancy
pregnancy as the corpus luteum of pregnancy may be and occasionally in puerperium, myomas undergo red or
removed with the tumor. If removal is delayed till the onset hemorrhagic degeneration. There is pain and tenderness
of severe symptoms, the outcome of pregnancy will suffer. on palpation and low grade fever. Moderate leukocytosis is
Usually laparotomy is performed but recently laparoscopic seen. This should be differentiated from ureteric calculus or
removal has been started. An ovarian mass seen for the first pyelonephritis. The management is conservative, rest and
time during a cesarean section (CS) should be removed analgesics, mostly non-steroidal, are very good.
After abortion or delivery, myomas may get infected. is asked to lie prone, as much as possible. Appropriate
Antibiotic treatment and sometimes hysterectomy may urinary antibiotics are given. In due course of time,
be needed. If myomas are seen during CS they are not the uterus becomes an abdominal organ and urinary
to be removed except for pedunculated myomas. This retention is no longer occurs. The catheter is removed and
is because there may be life-threatening hemorrhage the patient is discharged.
leading to hysterectomy. These myomas mostly regress
after delivery in due course of time and eliminating the PREGNANCY WITH PROLAPSE OF
indication for myomectomy.
UTERUS
Ultrasound is a very important tool to detect and
follow-up these myomas. If available, magnetic resonance This condition is not often seen. Temporary reduction
imaging (MRI) is superior in these cases. Pregnancy by pessary will tide over the situation. After the uterus
after myomectomy carries a high-risk because there is a becomes an abdominal organ, the pessary is removed.
significant risk of uterine rupture even early in pregnancy
remote from labor particularly if the uterine cavity was SURGICAL CONDITIONS DURING
entered during myomectomy. In the latter case, it is to be PREGNANCY
treated as a post cesarean pregnancy.
There are changed anatomical relations because of the
gravid uterus. There is an inability to palpate non-uterine
CARCINOMA masses and symptoms are altered (e.g. severity is less so
Carcinoma of the cervix complicating pregnancy causes these symptoms may be passed as normal discomforts of
difficulty in staging. On examination, the stage of pregnancy) and there may be difficulty in differentiating
carcinoma appears about one stage higher than it actually obstetrical and surgical conditions.
is. Because of all the above factors, the diagnosis of acute
abdominal (surgical) conditions becomes difficult.
Effect of Pregnancy Spontaneous abortion may occur if surgery is perfor
The survival rate of cervical cancer is not altered. Treatment med before 14 weeks of pregnancy but when indicated,
varies according to the stage and duration of pregnancy. In emergency surgery is carried out to save mother’s life. The
early pregnancy, immediate treatment is offered. Radical approach in pregnancy or in a delivered patient is as same
hysterectomy with pelvic lymph node resection with as in the non pregnant state. If unnecessary manipulation
the fetus in utero is carried out. Delayed treatment after of the uterus and adnexa is avoided, the results are
greater fetal maturity is allowed, if the patient insists, if comparable.
the lesion is less bulky (less than stage IIB) and gestation Difficulty in anesthesia: Occurs because of the effect
is more than 20 weeks. In our department, we first deliver of progesterone gastric emptying is delayed and may
the fetus by hysterotomy or classical CS. The uterine scar lead to aspiration (Mendelson’s syndrome) if proper
is then stitched in one layer. This is followed by radical precautions (antacids and if needed Ryle’s tube suction)
hysterectomy with pelvic lymph node dissection. Ovaries are not taken. There may be hyperemia causing narrowing
can be preserved in these young patients. Vaginal delivery of the upper airway (difficult intubation). Decreased
is not allowed. lung capacity, uterine compression of large vessels and
In extensive cancer in early pregnancy, external hypercoagulability are other hurdles.
radiotherapy can be given. Evacuation may be done
if abortion has not occurred. One week after abortion ACUTE APPENDICITIS
intracavity radiation is given or surgery is done after external
The incidence of acute appendicitis is not increased
radiation.
in pregnancy, because pregnancy does not effect its
occurrence but the chances of rupture are increased.
RETROVERTED GRAVID UTERUS This is most probably because of delay in the diagnosis
Retroverted uterus in pregnancy mostly causes retention and operation thus increasing both the maternal and the
of urine in early pregnancy. The patient is admitted in the perinatal morbidity and mortality. The complications of
hospital. An indwelling catheter is introduced. The patient peritonitis is dangerous to both mother and the fetus.
Gynecological and Surgical Disorders Associated with Pregnancy 505
ACUTE CHOLECYSTITIS AND

CHOLELITHIASIS
Pregnancy increases the risk of gallstones formation. This
may be due to high progesterone levels inhibiting smooth
muscle contractions. The volume of the gallbladder
increases with stasis of cholesterol thus helping gallstone
formation. There may be obstruction of the cystic duct.
Low grade fever epigastric and right scapular or left
upper quadrant pain are signs of biliary colic. It is acute
in onset and triggered by a meal. Increased leukocytic
count with immature forms are seen. Increase in aspartate
aminotransferase (AST)/serum glutamic oxaloacetic
transaminase (SGOT) and alanine aminotransferase
(ALT)/serum glutamic pyruvic transaminase (SGPT) are
Fig. 54.1: Position of appendix according to gestation period seen when liver function tests are performed. Alkaline
phosphatase and bilirubin are elevated on the first day of
the attack. Ultrasound reveals stones in the gallbladder,
The pain is in the right lower or middle quadrant
dilated common bile duct and swelling in the pancreas.
depending on the period of gestation. This is because there
is an upward displacement of the appendix as gestation Differential Diagnoses
progresses (Fig. 54.1). The pain is usually vague. Muscle
They are HELLP (hemolysis elevated liver enzyme and low
guarding and rebound tenderness cannot be demonstrated platelet count) syndrome, acute fatty liver of pregnancy,
because of the gravid uterus. Nausea and vomiting are severe pre-eclampsia and acute hepatitis.
present but are confused with normal symptoms of Treatment consists of bowel rest (nil orally, may be by
pregnancy. Fever is not a permanent sign. The relative Ryle’s tube suction), intravenous (IV) hydration, correction of
leukocytosis of pregnancy masks the infection. There may electrolyte imbalance, IV antibiotics and antispasmodics. If
be pyuria and hematuria. All these make the diagnosis symptoms do not disappear with medical treatment surgery
difficult and delayed. Now ultrasound and abdominal MRI is carried out, preferably in the second trimester (to prevent
have made the diagnosis easy. fetal loss in the first trimester). Nowadays, laparoscopic
cholecystectomy has made the operation easy in pregnant
Differential Diagnosis women too. The outcome for mother and fetus following
uncomplicated gallbladder surgery is very good. In fact,
Pyelonephritis is a differential diagnosis as like ruptured
delaying surgery may be harmful.
ectopic pregnancy, torsion of the right adnexa, red
degeneration of myoma, diverticulitis, etc.
ACUTE PANCREATITIS
A liberal view towards surgery is life saving. Nowadays,
laparoscopic appendectomies in pregnancy (especially Acute pancreatitis occurs mostly in the third trimester and
the puerperium. Mortality is greater because there is a
early pregnancy) have started. The treatment of non-
delay in diagnosis. It is precipitated by cholelithiasis. Some
perforated acute appendicitis is laparotomy followed
believe that pregnancy induced hypertension may also
by appendectomy. In the first half of pregnancy, some
lead to pancreatitis. Other causes are alcohol consumption,
surgeons do use a laparoscope. In the late second and third trauma, some drugs and hypertriglyceridemia. There is
trimester, a muscle splitting incision around the center severe, steady epigastric pain, and this pain may radiate
of the site of maximum pain is given. Only the appendix to the back. The pain is increased by food intake and
is removed and the uterus is not touched. Sometimes sometimes there may be nausea, vomiting and anorexia.
a negative laparotomy may be performed, i.e. no Usually, no physical findings are seen. However, a low
appendicitis is found on operation though the symptoms grade fever, tachycardia and postural hypotension may be
were suggestive. Cesarean section is not indicated at the seen. If there is hemorrhage, Cullen’s sign (periumbilical
time of appendectomy. A recent abdominal scar does not ecchymosis) and Turner’s sign (flank ecchymosis) may be
present any problem during normal labor. seen.
Serum amylase is increased (normal 100 U/mL and 200

ACUTE INTESTINAL OBSTRUCTION
U/mL in the first and second trimester). The level of serum
lipase, a pancreatic specific enzyme is important. There The incidence of this condition is not increased in
pregnancy. It is not commonly seen in pregnant women.
may be hypocalcemia in several cases. Ultrasound shows
It is usually seen in the third trimester. Adhesions due
an enlarged pancreas with a blunted contour, peritoneal or to prior abdominal or pelvic surgery may be the cause.
peripancreatic fluid and abscess or pseudocyst formation. Volvulus, ileus, intussusception and hernia are other
It also shows cholelithiasis. Ultrasound should also be etiological factors. Abdominal pain, nausea, vomiting and
done to rule out ectopic pregnancy. constipation are the main symptoms. Later, fever, oliguria
and shock may occur. Plain abdominal X-ray may be
Differential Diagnosis required to document airfluid levels.
It is to be differentiated from hyperemesis gravidarum, Treatment
ruptured ectopic pregnancy, pre-eclampsia, perforated
Treatment consists of IV hydration and correction of
peptic ulcer, intestinal obstruction, cholecystitis, ruptured eletrolytes, gastric suction, antibiotics and nil orally.
spleen, liver abscess, perinephric abscess. Sepsis and shock causes maternal and fetal death. If
conservative treatment is not effective, timely surgery
Treatment is advisable (within 6–8 hours). Delayed surgery may
The patient is admitted to the hospital. Treatment is lead to bowel necrosis and perforation. Tocolysis may be
primarily supportive and medical. Bowel rest, nasogastric needed during the operative and postoperative period.
suction, IV fluid, electrolyte replacement and analgesics After delivery pseudo-obstruction of the colon may occur
(Ogilvie syndrome). This is caused by adynamic colonic
are the mainstay of treatment. If there is evidence of
ileus. There is massive abdominal distention due to cecal
acute infection one can give antibiotics. Pregnancy does
dilatation. Decompression may help otherwise surgery is
not alter the course of the disease. Removal of gallstones indicated.
may be considered after the infection subsides. Surgery
is also indicated in cases of pancreatic abscess, ruptured HEMORRHOIDS
pseudocyst or severe hemorrhagic pancreatitis.
It is a common finding in pregnancy due to venous
Maternal mortality is high. Respiratory failure, need of congestion. This is secondary to straining in constipation
massive fluid replacement and severe hypocalcemia are (progesterone effect), increased venous pressure and
indicators of severity. Preterm labor may supervene. increased intra-abdominal pressure (gravid uterus).
Adding fruits and raw vegetables (fibers) to the diet will
PEPTIC ULCER DISEASE help in mild cases. Banding and hemorroidectomy are
indicated in severe cases.
It is very uncommon in pregnancy as 90% of women with Spontaneous splenic rupture in enlarged spleens (due
known peptic ulcer are relieved during pregnancy. This to hypervolemia and anemia) may occur. Splenic artery
occurs because of reduced gastric secretion and motility, aneurysm rupture is rare but may cause acute abdomen in
and increased mucus secretion in pregnancy. Dyspepsia pregnancy. Hyperactive peristalsis is seen.
should be treated with dietary and lifestyle changes along In this chapter, we have learnt that keeping the various
with antacids. causes of acute abdomen in mind will save many lives.
1. What are the reason for postpartum hemorrhage?
2. Explain the effect of myoma on pregnancy.
i. Full form of HELLP is ____________.
ii. Postpartum hemorrhage occurs if placenta is ____________ or ___________ on the myoma.
iii. During pregnancy myomas undergoes ____________ or ____________ degeneration.
iv. Retroverted uterus in pregnancy causes____________ in early pregnancy.
55
Sudha Salhan, Rajesh Kumari, Sonia Ghumman
High-risk Pregnancies
Duration of labor and history of precipitate and

INTRODUCTION
prolonged labor is significant, any injury to her or the
High-risk pregnancies are the cases where the obstetric future newborn, weight and condition of the newborn, any
is likely to be affected by the present features, e.g. teenage or history of retained placenta, details of the management
elderly primipara, less height or weight of the pregnant patient also play a major role. How long after the birth of the child,
in the pregnancy or previous obstetric mishaps or conditions.
the placenta was delivered? Delivery of the placenta was
Conditions in present pregnancy
done by simple maneuvers or under anesthesia?
Extremes of ages
In case of if neonatal death, weight of the neonate,
Low height
Lower and higher than normal weight

duration of gestation, fresh or macerated, any deformity, etc.
Hypertension
are to be elicited. Prematurity can recur in next pregnancy
Diabetes mellitus with all the risks leading to perinatal mortality. Similarly,
Epilepsy postmaturity does recur. The weight of the newborn and
Heart disease type of delivery are important points to be elicited.
Infections. Once congenital abnormalities occur, its recurrence
Conditions in previous pregnancies is increased. Hence, parental karyotyping and use of
Stillbirth or fresh/macerated folic acid in preconception and perinatal period is to be
Neonatal death considered.
Congenital abnormalities
Indication for CS and procedural complications and
Third stage accidents, e.g. adherent placenta, retained
postoperative complications are important points to be
placenta, postpartum hemorrhage (PPH)
asked in history.
Prematurity
Rhesus (RH) incompatibility, though less common,
Postmaturity
are still seen. Besides, fear of the previous disaster being
Intrauterine growth restriction (IUGR)
Multiple pregnancy
repeated make the patient anxious. Hence, an emphathetic
Pre-eclampsia and eclampsia
attitude is essential. Exclusion of causes of recurrence is
Obstructed labor and injuries to rectum or bladder very important. A detail discussion with the patient and
Effect of pregnancy and delivery in cardiac case her partner will go a long way in allaying their fears.
Miscarriage All these cases are considered high-risk. They require
Previous cesarean section (CS) adequate antenatal care and mandatory hospital delivery.
Cholestasis of pregnancy The important ones are either discussed in separate
Psychological changes. chapters or in this chapter as follows.
Death of the child after delivery due to infections,
accidents, etc. are not included.
ELDERLY PRIMIGRAVIDAE
History details of previous pregnancies is very impor-
tant. Antenatal details of any complication, e.g. bleeding, Women having their first pregnancy at or above the age
high blood pressure, tests performed. of 30 years are called elderly primigravidae. The age limit
is arbitrary and at some places the cut off is taken as Postpartum

35 years. It has been seen that the outcome of pregnancy is
Increased morbidity due to operative interference.
adversely affected beyond this specified age limit. At some
Failed lactation.
places, this group of females are referred to as mature
primigravidae. Perinatal
Elderly primigravidae includes two groups of patients:
1. High fecundity: Women married late but conceives Increased mortality rate was found in some studies
soon after. while in others modern perinatal management was
2. Low fecundity: Women married early but conceive long very effective and allowed normal fetal outcome.
after marriage. The latter group is more unfavorable as Increased neonatal morbidity—18%.
far as obstetric outcome is concerned. Increased incidence of small for dates infants—11%.
Increased stillbirths.
Complications Increased congenital malformations—12 v/s 1.28%
Maternal (Down syndrome).
During the antenatal period there is an increased
Management
incidence of:
Miscarriage
Considering the risks involved in pregnancy and later,
Chronic hypertension and pre-eclampsia are the most
(intrapartum, postpartum, perinatal) these patients are
common complications seen in 24.3% women considered to be ‘high-risk’. THey need to be watched more
Impaired glucose tolerance and gestational diabetes mellitus
closely in their first pregnancies and deliveries. Meticulous
Antepartum hemorrhage (APH) and abruptio placentae
antenatal supervision and mandatory hospital delivery is
because of pre-eclampsia and folic acid deficiency needed. Ultrasonography should be carried out to exclude
(19.6 v/s 2.5%) congenital malformations of the fetus. Complications
Uterine fibroid and ovarian cyst (7.69 v/s 1.92%)
should be timely and accurately diagnosed so as to lead
Organic heart disease
to a favorable outcome. Labor should be judiciously
Preterm labor
monitored. Cesarean section is a preferred alternatively if
Premature rupture of membranes (PROM) (16 v/s 8%)
induction of labor fails.
in general population The neonate should be managed by an expert neonatologist.
Post-term pregnancy
IUGR TEENAGE PREGNANCY

Malpresentations: The incidence of breech present-
These are the pregnancies which occur at a younger age,
ation was found to be higher in elderly primigravidae as
i.e. from the age of menarche to nineteen years. Pregnancy
compared to younger primigravidae
can sometimes occur even when ovulated before first
Multiple gestation (as they frequently undergo induc-
menstrual period. Hence, before engaging in sexual
tion of ovulation).
practice the teenagers must understand the reproductive
Intrapartum physiology. Their body itself is growing and the need to
There is an increased incidence of: support the growth of the fetus exposes them to additional
Prolonged labor—due to uterine inertia and malposi- physiological, physical and emotional challenges.
tions like occipitoposterior position
Failed induction—higher oxytocin use
Incidence
Maternal and fetal distress Eleven percent of US births were in teenage mothers.
Instrumental vaginal delivery Around 78% of teen pregnancies are unplanned. One-
Cesarean section rate—31.3 v/s 13.5%. The higher rate of fourth of teenage mothers have a second child within
CS in elderly primigravidae is mainly due to the higher 2 years of their first birth. In our country, early marriage
rate of obstetric complications such as pre-eclampsia, is very common leading to a higher incidence which can
malpresentations and prolonged labor being the most never be ascertained, but approximately it is 18–20%.
common indications for abdominal delivery. In our country, teenage marriages does take place and
Retained placentae—due to uterine atony and increased pregnancy usually occur fast after marriage, despite a law
association of fibroid. against early marriage.
High-risk Pregnancies 509
Social Risk Factors Medical cover as early as possible is advised and is life-
saving in many. Diagnose and treat sexually transmitted
The most important factor is poverty
diseases (STDs) including human immunodeficiency virus
Early marriage
(HIV)/acquired immune deficiency syndrome (AIDS).
Low academic interest and achievement
Try to find her social environment and advise about diet,
Depression and stress rest and frequency of hospital visits. Closely follow her
Violence (domestic and sexual) for common complications. Educate her of emergency
Trouble in school or with the in-laws conditions. Tell her symptoms of early labor and where to
Limited job opportunities report in emergency.
Social isolation In American teenage population, there is an increase
A previous unplanned teenage pregnancy in STDs including HIV/AIDS. There is also more chronic
Single parent homes pelvic pain, ectopic pregnancies and cervical dysplasia.
Addictions and high-risk habits like substance abuse, Single parent motherhood is slowly coming up in our
alcohol use and smoking, etc. society also.
Delinquency. Preventive education: Education in schools and
colleges can help in taking decision about age of starting
Diagnosis sex life and ways of preventing STDs and pregnancy. This
A urine pregnancy test is required when a teenage girl comes under family life counseling.
reports to a doctor with a history of delayed, irregular
Counseling
periods or amenorrhea. This is essential for helping the
teenager emotionally, physically and medically. Because Contraceptive counseling is extremely essential to prevent
repeated unwanted pregnancies and induced miscarriages
early antenatal care is life-saving in them preventing many
leading to chronic ill health. Post placental intrauterine
conditions given below.
contraceptive device (IUCD) as a long acting contraceptive
Medical Risks to Teenage Mothers is very useful. Injectable progesterone, e.g. depot
medroxyprogesterone acetate (DMPA) can be given. But
In our country only 28.2% are delivered by a doctor. The it is important to stress the need to prevent STDs by using
teenage pregnant patient is at a much higher risk for the barrier contraceptives (male or female condom). Double
following: duck method: They must have knowledge of emergency
Very low hemoglobin contraception. Always discuss abstinence.
Miscarriage
Prematurity: 21% as compared to 9% at the age of 30 to Antenatal Period

34 years. This is also due to lower genital tract infection Look closely and prevent anemia. Detect and control
because of below optimum hygiene habits in them. hypertension.
Hypertension (gestational hypertension, pre-eclampsia
and eclampsia). More CS rate due to cephalopelvic dis- Labor

proportion (CPD) (mother pelvis is not fully developed Pelvic assessment—routinely
and child body does not fit in it), hypertensive disorders Presentation and position to be checked
and fetal distress, etc. Careful watch for progression of labor. Undue delay in
The newborn or infant may be premature, or even progress should be viewed with concern
at fullterm may be with low birth weight, with no iron To remain vigilant againsts PPH
stores, may lack full immunization can be seen with Postpartum—encourage lactation. Give advice about
developmental delays, may have behavior problems and limiting the family.
sometimes suffer domestic violence, accidental trauma
and poisoning, etc. and may die of sudden infant death.
GRAND MULTIPARITY
Delayed effects of teenage pregnancies include low
education, limited job outlets, poverty, domestic violence, A grand multipara is a pregnant mother who has had four
poor knowledge of bringing up children (more children), or more viable births.
use of illicit drugs, depression and other medical Extreme grand multiparity is defined as mothers having
ailments, etc. ten or more previous viable pregnancies.
Magnitude of Problem During Labor

It constitutes about one-tenth of the hospital population There is an increased incidence of:
and account for one-third of maternal deaths in developing Cord prolapse: Due to malpresentation and high-
countries. floating head at onset of labor

Cephalopelvic disproportion due to:
Complications • Increasing size of fetus.
During pregnancy there is an increased incidence of • Secondary contracted pelvic due to malnutrition.
(i) Miscarriage (spontaneous and induced) (ii) Obstetric • Forward projection of sacrum due to subluxation of
hazards viz. sacroiliac joints, thus diminishing diagonal conjugate.
Malpresentation: Resulting from associated pendulous Obstructed labor: Due to malpresentation, malposi-
abdomen and increased pelvic inclination. tion, CPD.

Placenta previa, abruptio placentae. Rupture uterus: Uncared obstructed labor.
Medical disorders: Increased incidence of anemia, Postpartum hemorrhage: Due to atonic uterus or
hypertension, cardiac disability, exaggerated mani- increased association of adherent placenta or due to
festation of hemorrhage and varicose veins. increased collagen deposition in between muscle fibers.
Prematurity. Shock due to hemorrhage and rupture.
In cases of extreme grand multiparity besides diabetes Increased operative interference.
mellitus and macrosomia much of the other list of

complications is a reflection of socioeconomic and Puerperium
environmental factors rather than biological limits on the Increased morbidity due to intranatal hazards
capacity of reproduction. Excellent medical care and good Subinvolution
health in these patients prevented complications. Failing lactation.
1. Explain the term early primigravidae.
2. Define grand multiparity and complications related to it.
i. Early primigravidae includes two groups ____________ and ____________.
ii. ____________ are the pregnancies which occur at a younger age, i.e. from the age of menarche to nineteen years.
56
Sudha Salhan, Divya Pandey, Pinkee Saxena
Obstetrical Collapse
INTRODUCTION HEMORRHAGIC SHOCK

Collapse or shock is a condition of decreased tissue It is due to excessive blood loss.
perfusion which leads to cellular hypoxia which in turn can Early pregnancy: Causes abortion, ectopic pregnancy,
lead to irreversible tissue damage, if not treated in time. gestational trophoblastic disease.
If not managed timely, there is multisystem involvement. Antepartum hemorrhage: Causes placenta previa or
There may be an overall decrease in tissue perfusion abruptio placenta.
throughout the body or poor blood distribution as in Rupture uterus
septic shock. This diminished perfusion leads to inability Postpartum hemorrhage.
to fulfill the metabolic demands of tissues thereby leading Clinical Features
to cellular hypoxia which in turn leads to reversible or Patients usually present with pallor, cold and clammy
irreversible organ damage. extremities, rapid thready pulse, low blood pressure, air
Collapse during pregnancy is one of the most crucial hunger, diminution of vision, oliguria and anuria.
and difficult problems faced by an obstetrician. Ninety
percent of hemorrhage in obstetrics is due to placental Classification
abnormalities or uterine atony. Rest 10% are associated A 500 mL of blood loss in normal vaginal delivery and a
with trauma related to the birth canal. The amount of blood loss of more than 1 liter during cesarean section
morbidity in patients depends on the duration of shock (CS) is normally tolerated by a healthy pregnant woman
(i.e. duration of cellular hypoxia). This calls for timely due to physiological changes in cardiovascular and hema
initiation of resuscitative measures and appropriate tological system.
management for shock even before the identification of Depending upon the amount of hemorrhage shock, it is
the underlying cause. classified as following phases:
Phase of compensation
Phase of decompensation
TYPES AND CAUSES OF COLLAPSE IN Phase of cellular damage
OBSTETRICS
Phase of Compensation
Hemorrhagic shock: Due to hypovolemia.
Mild: Blood loss is less than 15%. No changes in vital signs
Endotoxic shock: Due to release of toxins which causes are seen. Postural hypotension is noted.
generalized vascular disturbance. Sympathetic stimulation: Sympathetic system is stimu
Cardiogenic shock: Due to inefficient pumping by lated as first response to blood loss leading to peripheral
heart, leading to circulatory collapse. vasoconstriction so as to maintain blood supply to vital
Neurogenic shock organs.
Anaphylactic shock: Due to hypersensitivity reaction. Clinical features: Increased perspiration, pallor, incre
Other causes (embolism): Amniotic fluid, air or ased pulse rate, increased respiratory rate but blood
thrombus. pressure remains normal.
Phase of Decompensation available, by whole blood preferably packed cells. If

Moderate: Blood loss is 20–35%. There are changes in vital cross match from same group is not available, Group
signs and is associated with cold and clammy extremity, O –ve blood or group specific blood may be given as a
increased pulse rate, increased respiratory rate, pulse life-saving measure. Insert an indwelling catheter in the
pressure less than 30 mmHg, low systolic pressure and urinary bladder.
delayed capillary filling.
Drug Therapy
This phase can be present if blood loss exceeds 1,000
mL in normal patient or less than 1 liter in presence of Analgesics: 10–15 mg morphine IV if there is pain,
underlying anemia. tissue damage or irritability.
Clinical feature: It is the classic clinical picture of Corticosteroids: Hydrocortisone 1 g or dexametha-sone
shock. 20 mg slowly IV. Its mode of action is controversial; it

Appropriate and timely management till this phase can decreases peripheral resistance and potentiate cardiac
improve the clinical condition without residual morbidity. response thus improving tissue perfusion.
Sodium bicarbonate: 100 mEq IV in presence of
Phase of Cellular Damage and Danger of Death metabolic acidosis.

Vasopressors: To maintain renal perfusion by increasing
Severe: Blood loss is more than 40%. It is associated with
profound hypotension with only the carotid pulse being the blood pressure.
palpable. Oliguria and anuria is noted. • Dopamine: 2.5 mg/kg/minute IV is the drug of
Inadequately treated hemorrhagic shock results in choice.
prolonged and profound tissue hypoxia and damage with • b-adrenergic stimulant: Isoprenaline 1 mg in 500 mL
the following effects: 5% glucose slow IV infusion.
Metabolic acidosis: This is due to anaerobic metabolism As this management is being done, simultaneously
in absence of oxygen. ultrasound examination is carried out to find out the cause
Arteriolar dilatation: The acidic pH and formation of of blood loss and assess the fetus in antenatal patients.
anaerobic metabolites leads to capillary blood pooling Monitoring is done by assessment of central venous
and stagnation, thereby leading to fluid leakage into the pressure (CVP), pulse rate, blood pressure, urine output,
tissues. pulmonary capillary wedge pressure and by clinical
Disseminated intravascular coagulation: It is caused improvement in the pallor, cyanosis, air hunger, sweating
by thromboplastin release from the damaged tissues. and consciousness.
Cardiac failure: It is due to decreased coronary blood In addition to medical management, surgical inter-
flow. vention depending upon the cause of hemorrhage like
In this phase death is imminent, transfusion alone evacuation of products of conception, laparotomy, emer
is not sufficient and even if recovery from acute phase gency cesarean or in extreme cases internal iliac ligation or
occurs, there is residual tissue damage due to renal and/or hysterectomy may be required.
pituitary necrosis.
Complications
Management Acute renal failure
Immediate resuscitative measures should be taken which Pituitary necrosis (Sheehan’s syndrome)
include: Disseminated intravascular coagulation.
Establishment of one or preferably two wide bore intra
venous (IV) lines with collection of blood sample for ENDOTOXIC SHOCK (SEPTIC OR
grouping and cross-matching and baseline investigations. BACTEREMIA)
Establishment of an airway and oxygen therapy.
Elevation of the lower limbs increases venous return. Infection caused by gram-positive or negative bacteria,
Volume replacement which is done initially by viruses or fungi leads to septic shock during pregnancy.
crystalloid solutions like ringer lactate at approximately
three times the estimated blood loss (3:1 ratio) and Causative Organisms
colloid solutions like dextran 40 or 70 (1:1 ratio), plasma Gram-negative bacilli (Escherichia coli, proteus,
protein fraction or fresh frozen plasma and later, when Klebsiella, pseudomonas and bacteroides). They produce
Obstetrical Collapse 513
endotoxin which is a phospholipid polysaccharide Management

released by lysis of the cell envelope. Main aim is the restoration of circulatory function and
b-hemolytic streptococci, anaerobic streptococci and oxygenation.
Clostridia produce exotoxin which can lead to septic shock. • Replacement of blood loss should be done by
whole blood transfusion. If blood is not available,
Pathology infusion is started with colloids or crystalloids. The
Endotoxins released by microorganisms lead to initiation CVP measurement is essential to check against
of inflammatory cascade due to activation of complement circulatory overload.
system and cytokines. This releases sepsis mediators • Corticosteroids: Hydrocortisone 1 gm IV 6 hours or,
which bring about changes like vasodilatation, decreased dexamethasone 20 mg initially followed by 200 mg/
peripheral resistance, decreased blood pressure, increased day by IV infusion.
tissue permeability leading to leakage of intracellular fluid • Vasoactive drug like isoprenaline cause arteriolar
from intravascular compartment to extracellular spaces. dilatation, increase heart rate, stroke volume and
This leads to fluid collection in lung parenchyma leading improving tissue perfusion. But blood volume must
to noncardiogenic low pulmonary pressure, pulmonary be normal prior to its administration. Epinephrine,
edema, hence causing adult respiratory disease syndrome alpha and beta agonist, may be preferred in patients
with acute hypotension during pregnancy.
(ARDS). Futhermore, poor blood redistribution results
Maintain adequate tissue oxygenation. Patients with
in inadequate perfusion of multiple organs leading to
severe hypoxemia may need to be intubated and
multiorgan dysfunction and ultimately failure due to
mechanically-ventillated.
cellular damage because of hypoxia.
Bronchospasm can be overcome using aminophylline.
Identification of cause and eradication of infection:

Causes
Cultures of sputum, blood, urine and swabs from infective
Septic abortion source are taken for antibiotic sensitivity.
Chorioamnionitis Empirical antibiotic therapy is started immediately by IV
Puerperal sepsis route. Later, the antibiotic therapy is reviewed according to
Retained products of conception the patient’s response to therapy and the results of culture
Instrumentation of genitourinary tract and sensitivity. The antibiotic therapy should cover a wide
Severe acute pyelonephritis range of organisms (Table 56.1).
Respiratory tract infections. Surgical intervention is indicated in case of presence
of retained infected tissues as in septic abortion. Digital
Clinical Features evacuation, suction evacuation or hysterectomy should
Endotoxic shock has two stages—reversible and irreversible.
Reversible stage: It has two phases: TABLE 56.1: Antibiotic therapy in shock
1. Early (warm) phase is associated with fever with rigors, Antibiotic Actions/upon Dose
hypotension, tachycardia, tachypnea and flushed skin. Regimen 1 Ampicillin or Aerobic gram 500–1000 mg/
The patient is alert. cephalosporins +ve organisms 6 hours
2. Late (cold) phase: Patient has cold and clammy skin, and gram –ve
cocci
cyanosis, jaundice and bradycardia. There is progressive
mental confusion and coma. Gentamicin Aerobic gram 80 mg/8 hours
–ve bacilli
Irreversible stage: Metabolic acidosis, acute renal failure,
Metronidazole Anaerobic 500 mg/8 hours
cardiovascular failure, pulmonary edema, adrenal failure
Regimen 2 Clindamycin Aerobic gram 600 mg/6 hours
and ultimately death may ensue because of irreversible
+ve organisms
damage due to prolonged cellular hypoxia. gram –ve cocci +
Anaerobic
Differential Diagnosis organisms
Amniotic fluid embolism, pulmonary embolism, ARDS Gentamicin Aerobic 80 mg/8 hours
and myocardial infarction. gram –ve bacilli
be done to remove the infected tissue, with the start of Airway: Clear the airway of vomitus, blood, teeth
antibiotic therapy and resuscitative measures. and foreign body. Mandible and tongue should be
Disseminated intravascular coagulation (DIC): As a pulled forward and an airway inserted. Endotracheal
prophylactic measure heparin therapy is started. DIC intubation should be done as soon as possible.
profile is sent. If there is active bleeding it is best treated by Breathing: Mouth to mouth artificial respiration
fresh blood transfusion. should be given or after inserting a cuffed endotracheal

tube intermittent positive pressure using 100% oxygen
should be given.
CARDIOGENIC SHOCK
Cardiac massage: Put the patient on a firm surface,
It is defined as circulatory collapse caused by sudden and using the heel of one hand, with the other on top,
failure of the heart to pump the blood adequately. and with the arms extended, apply pressure to the
lower sternum using full body weight. A compression-
Causes ventilation ratio of 30:2 is recommended.
Failure of left ventricular ejection is due to: Drugs
Cardiac arrest (asystole/ventricular fibrillation) • Sodium bicarbonate 8.4% solution to counteract

Myocardial infarction. metabolic acidosis. Give 100 mL initially and a further
10 mL for each subsequent minute of inadequate
Failure of Ventricular Filling circulation.
Cardiac tamponade • Cardiac stimulants can be given IV or intracardiac,
Pulmonary embolism. e.g. adrenaline 0.5–1.0 mg, atropine 0.6 mg, isopren
The major cause of cardiogenic shock during pregnancy is aline 4 mg in 500 mL solution.
• Direct current (DC) defibrillator is used if required.
severe valvular disease.
Any reason for obstetric shock can result in cardiac Electrical cardioversion during pregnancy has been
arrest. In addition, septic shock is often associated with described and appears to be safe for the fetus.
myocardial dysfunction. If cardiac arrest is not reverted immediately (4–5 minutes)
by basic and advanced life support, emergency cesarean
Clinical Features delivery should be performed to save the fetus after the age
of viability. The best survival rate are there for a fetus more
Patient presents with distended neck veins, dyspnea,
than 24 weeks, if delivered within 5 minutes of cardiac
tachypnea, presence of third heart sound, cardiac murmurs
arrest.
and generalized edema. This may be followed by sudden
collapse with loss of consciousness, absence of pulse
including the carotid and femoral pulse, apnea, cyanosis of NEUROGENIC SHOCK
variable degree and fixed dilatation of the pupils. It maybe due to painful conditions like:
Acute uterine inversion
Management Rapid evacuation of the uterine contents as in pre
The following ABC (airway, breathing, circulation) steps cipitate labor and rupture of membranes in polyhy
are carried out. In case of cardiac arrest in pregnancy, dramnios. This leads to rapid accumulation of blood
cardiopulmonary resuscitation is started with CAB in the splanchnic area due to sudden relief of pressure
(circulation, airway, breathing) instead of ABC. Call an (splanchnic shock).
anesthetist for help. In case of pregnancy, keep the patient Management includes fluid replacement, correction of
in left lateral position, ventilate with 100% oxygen establish acidosis, vasoactive drugs, corticosteroids, ventilation and
IV access and administer fluids through upper extremity elimination of the source of neurogenic stimulus.
veins. For amniotic fluid embolism (see Chapter 43).
1. What are the types and causes of collapse in obstetric?
2. Name few drugs used for the treatment of cardiogenic shock.
3. Hemorrhagic shock is classified as ____________, ____________ and ____________.
57
Asepsis and Antisepsis in
Operation Theater
Asepsis and antisepsis in the operation theater (OT) The air in the OT can be kept free of contamination
are very critical compenents of patient care. Most of by maintaining a laminar flow under positive pressure.
the postoperative infections have their origin in the Further, using air asepticizer and ultraviolet (UV) lamps,
intraoperative period. A proper operative technique with the air in the OT can be made germ free. Air asepticizer
meticulous attention to details of the OT protocols goes a and UV equipment can be fixed (Fig. 57.1) or mobile
long way in preventing this morbidity in patients who are (Fig. 57.2). The fixed ones are equipped with an UV source
undergoing elective and emergency surgery. (UV 30L90) which emits radiation in the germicidal band
at a wavelength of 2537 Å. The mobile device disinfects
and deodorize rooms upto 100 m3 in OT. A fan coupled
NEED FOR ASEPSIS IN
to an electric heating element (2 Kw) blows warm air over
OPERATION THEATER one evaporation unit where one 500 mL container has
The OT is a place where one is deliberately cutting or bactericidal solution.
opening the protective barrier of skin during a surgical Atomizers and vaporizers can create plasma of an
procedure creating a potential portal for infection. Further, antiseptic material (e.g. formalin) which percolates through
at the end of procedure one will be leaving behind foreign the nooks and corners of immobile structures of the OT
bodies in the form of suture materials and some devitalized sterilizing/disinfecting them.
tissue creating a stage for setting up of infection. In this
Instruments
scenario any implantation of a potential infective organism
in these tissues will trigger the onset of a well established The surgical instruments come in close contact with the
infection, resulting in postoperative morbidity. Sometimes surgical wound and could be a potential source of infection,
even mortality may occur. if not sterilized before use and is not handled properly.
The possible sources of this infection could be from:
Environment
Instruments
Patient
Medical personnel.
Environment
The environment of the OT can contaminate the surgical
wound. This includes:
Air
Immobile structures like the walls, OT tables, etc.
The floor and walls of the OT must be wet mopped rather

than swept. Door handles and other surfaces which are
frequently touched, to be cleaned by wet antiseptic solution. Fig. 57.1: Fixed air asepticizer
preparation in the form of a high cleansing enema or

a bowel wash using ‘polyethylene glycol’ may help in
preventing surgical infection.
Finally on the OT table a routine protocol of skin/vaginal
cleaning of the patient with antiseptic solutions such as
savlon, dry swab, iodine—spirit solution in this order is
to be done. Start from the proposed incision site and go
laterally (Fig. 57.3). Never come back from farthest point
to the operation site. In case of the abdominal surgery
clear the umbilicus last of all. In case of iodine, sqeeze the
solution from the swab and do the cleaning. Never let it
trickle behind the abdomen, it will form painful burns. Take
care to wipe out the iodine solution with the spirit. Now
drape the surgical area with sterile drapes. This also helps in
prevention of surgical infection.
Fig. 57.2: Mobile air asepticizer
Medical Personnel
They are best sterilized using steam sterilization through The operating team could be a source of infection through:
Clothes
autoclaving after decontamination in bleech solution and
Droplet infection
washing with water.
Falling hair
However, some of the equipments especially plastics
Sweat and body contamination
and rubber may not withstand autoclaving and may need
Infection on hands (Fig. 57.4).
to be treated with ethylene oxide or gamma radiations to
make them sterile. Some of the modern sterilizers use the
nascent oxygen produced from H2O2 for sterilization of
delicate equipments like endoscopes.
Various chemicals like glutaraldehyde, lysol, carbolic
acid have been used as disinfectant, to disinfect the
instrument by soaking them overnight.
In an emergency, instruments can be sterilized by
flaming, i.e. by pouring alcohol over them and setting it
aflame, for a fast and quick sterilization.
The Patient
The patient herself can be a source of infection for her
surgical wound. The microorganisms normally inhabiting
her skin or the vaginal flora can contaminate the surgical
wound.
Shaving causes cuts which invite infection. Clipping of
the hairs over the operative site and a thorough scrubbing
bath on the day prior to surgery may mechanically reduce
the bacterial load from these sites.
Vaginal preparations in the form of antiseptic douche,
painting with antiseptic solutions or placement of vaginal
pessaries overnight may protect the surgical wound from
contamination by the vaginal flora.
Fig. 57.3: Technique of cleaning and painting the abdomen,
Whenever, there is a possibility of accidental encro- (1) Nipple to mid thigh; (2) Laterally up to mid axillary line;
achment into the bowel during surgery (e.g. dense (3) Center to periphery: (max time spent at clearing umbilicus) a
adhesions or in ovarian malignancy), a thorough bowel peri-incsional area; (4) Perineum: A perianal area in the end
Asepsis and Antisepsis in Operation Theater 517
projecting out. Long hair needs bunching up to be kept

under the cap.
Sweat and Body Contamination

The other possible point of contamination of surgical
wound is from the body sweat of the surgical team. The
sterile gown worn will be impervious to bacteria as long
as it remains dry. A plastic apron worn underneath will
ensure this. It should be made certain that the front of the
plastic apron is dry before putting on the sterile gown.
Hands Washing
Surgical Scrub (Figs 57.5 to 57.18)
Hands washing is the simplest and a very important way to
control infection. It is required:
Fig. 57.4: Infected areas of the hands To remove microorganisms and dirt from nails, hands
and forearms.
It decreases the count of resident microorganisms.
The OT personnel must maintain personal hygiene.
Prevent rapid rebound growth of microorganisms.
They must take a thorough bath and wear clean clothes
before coming to the OT. Techniques of hands washing
Clothes The nails must be cut short. There must not be cuts or
wounds on the hands. Remove all jewelery (rings, watch,
By adhering to the following protocol regarding the clothes
bracelets, etc).
in which the OT personnel enter the OT, the postoperative
Wash hands upto elbow thoroughly from clean part
infection can be minimized to a great extent.
(hands) to less clean part (arms). A systematic and
Never enter the OT in a street wear
effective approach is followed to ensure proper cleansing.
Never go out in the wards with OT wear including
While scrubing remember each finger has four surfaces
slippers
and not just two. The scrubbing should be thorough and
The OT dress should be made up of materials which will
systematic and each sequence of scrub and wash should
not carry static electricity, hence, the dust and bacteria
last from 3 to 5 minutes. The sequence should be repeated
along with and are preferably of cotton
two to three times.
It must be clean
Change footwear before entering the OT room.
Droplet Infection
Wearing a mask will prevent the droplets from spilling onto
the operative site as well as in the OT environment. The
mask should be made of sufficiently impervious material
to prevent droplet infection but still comfortable to breathe
in. It should cover the nose and mouth completely and
should be in position all the time when the person is inside
the OT area. Provision of a nose clip built in the mask will
help maintaining the mask in the proper position over the
nose and mouth.
Falling Hair
A cap over the head will prevent the hairs from falling
onto the operative field. Caps should be sufficiently large
to cover the head completely without any part of the hair Fig. 57.5: Proper cleaning of nails
A B
Figs 57.6A and B: Palm to palm
Fig. 57.7: Right palm over left dorsum Fig. 57.8: Rotational rubbing
A B
Figs 57.9A and B: A. Interplace fingers of right hand over left. Change hands and repeat; B. Rotational rubbing backwards
A B
Figs 57.10A and B: Cleaning of thumb
A B
Figs 57.11A and B: A. Back of fingers to opposing palm with fingers interlocked; B. Washing off soap with water
Fig. 57.12: Rub both wrists in a rotating manner. Rinse and dry Fig. 57.13: Back of fingers
thoroughly
Fig. 57.14: Front of fingers Fig. 57.15: Final rinse with water
Fig. 57.16: Position of hand in final rinse Fig. 57.17: Position of arm after final rinse
Rubbing with a brush is going into disfavor as it may

produce microscopic or macroscopic cuts which may end
up harboring infection and very hot water is harder on skin
and uncomfortable for washing for the stipulated time and
cold water does not produce lather and hence germs are
not properly washed away.
Procedure for a cycle of 5 minutes of scrub is as follow:
Time the act
Clean areas below the nails.
Clean all sides of each finger and between fingers and
front and back of hands for 2 minutes.

Now wash arms, always keep the hands higher then
arms so that soap mixed with water and germs do not

contaminate the hands. Wash all sides of both arms
Fig. 57.18: Position before wearing gown till elbow for 1 minute keeping hands above elbows
A B
C D
Figs 57.19A to D: Proper techniques of wearing a sterile gown
all times. If the hand touches anything at anytime, the secures the gown from behind (Fig. 57.19). Always keep
scrub must be lengthened by 1 minute for the area that the hands high or docked in front. Do not touch any
has been contaminated. part of the gown.
If the hands appear dirty, the scrub time is to be increased.
Do not scrub vigorously it may abrade the skin and Wearing of Surgical Gloves (Figs 57.20A to H)
harbor germs.
The principle is that the outside of the sterile gloves
Rinse hands and arms by passing them through the
which come in direct contact with the surgical wound is
water in one direction only, from fingertips to elbow.
Do not move the arm back and forth through the water. never touched with bare ungloved hands.
Repeat the whole sequence two to three times. First one glove is worn holding the inside of its cuff with
Walk to drapping section theater holding hands poin the other hand.
ting upwards. Now put the gloved hand into the cuff of the second
Dry with a sterilized dry towel from hands down to glove and manipulates it onto the hand and finally on
elbow viz. hands first and elbow last and discard the the cuff of the gown.
towel (protocol). The plastic apron is wiped dry with Now the surgeons hand are totally dedicated for the
sterile towel by the circulating nurse.
patient use and he cannot use it for his own use, till the
After this you wear a sterilized gown and gloves.
procedure is completed or till he/she is willing to go
Wearing of Surgical Gowns (Figs 57.19A to D) through the whole rituals of scrubbing and wearing of
The sterile gowns are provided with their outside surface gown and gloves again.
folded in, exposing the inside surface for handling. One can conclude that by strict adherence to such basic
The arms are slid into the sleeves of the gown touching protocols one can considerably reduce the infection in
only its inner part. The scrub nurse or an assistant surgical patients, making the surgical procedures safe.
A B C
D E F
G H
Figs 57.20A to H: Method of wearing gloves. A. to C. Ungloved hand touching the inside of the sterile glove; D. and E. Gloved hand
touching the outside of the sterile glove. If both hands are with gloves, one can now do final adjustment of the gloves over the gown
cuff; F. to H. Wearing of sterile gloves, hands not touching the outside of the gloves
antibiotic cover given as a single dose approximately

PROPHYLACTIC ANTIBIOTICS 1–2 hours prior to beginning of the surgery and may be
Antibiotics cannot substitute for the aseptic precautions repeated if the operation lasts more than 3 hours or if
and complete hemostasis and gentle handling of tissues blood loss is more than 1,500 mL.
by the surgeon. Contaminated cases which are already infected even
A clean surgical wound where vagina and bowel has not before the beginning of the surgery requires a full course
been transgressed does not require any antibiotic coverage. of antibiotics.
A clean contaminated wound where the vagina or the The choice of antibiotic should be based on sensitivity
bowel has been transgressed requires only a prophylactic studies and the hospital policy.
1. Possible sources of infection in operation theater are from ____________, ____________, ____________ and ____________.
2. Air asepticizer can be ____________ or ____________.
3. Name chemicals for disinfecting instruments used in operation theater.
4. What are the steps of wearing surgical gowns?
Section 10
Operative Obstetrics
Section Outline
58. Minor Obstetric Procedures
59. Female Sterilization, Cesarean Delivery and other Emergency Obstetric Operations
60. Destructive Operations
61. Interpreting Arterial Blood Gas Sample
58 Minor Obstetric Procedures
Sudha Salhan, Anshula Gupta, Harsha Gaikwad, Indira Ganeshan
Most of the times the patients are not used to hospital

environment. The surgery is quite frightening to the patient
POSTOPERATIVE CARE
and her relatives. Therefore, explaining in detail and Vital signs: Temperature should be taken 6 hourly on the
counseling is essential in obstetric cases where surgery is day of operation. Pulse, blood pressure (BP) and respiration
contemplated. rate to be taken frequently on the day of operation.
Recording of day’s input and output is maintained.
PREOPERATIVE CARE Care of tubes and drains (urinary catheter, etc.).
Nothing is given for at least 4 hours after general

Detail history is taken to exclude any acute or chronic
anesthesia.
illness, any drug allergy, any previous surgery or any
She may vomit. Keep her face on one side and let her
ongoing medications.
vomit. It is noted in the case sheet and orders given.
Before performing any operative procedure, whether
Movements of limbs are allowed as early as possible.
it is a minor or a major one, the patient and her relatives
Follow the universal precautions before every procedure.
are informed about the procedure to be performed, the
indication, risk, complications of the procedure and the
anesthesia with its consequent problems. A fully-informed, Checklist for Universal Precautions
written consent is taken. The consent is to be signed by the Hands are appropriately washed to prevent cross-
patient as well as by a close relative if the patient is more than infection.
18 years of age. The guardian/guardians are asked to sign Soap and water to be available.
the consent if the patient is a minor or mentally challenged. Clean towels/tissue papers must be available.
Patient should have an empty stomach. Injection tetanus Random check of the staff to observe hand washing
toxoid (TT) is given before the procedure. practices (after contact with body fluid, removal of
gloves and contact with patients).
Procedures A protective barrier is worn to prevent exposure to
Operation Notes blood. The following barriers are available for use by staff
These are written under the following headings: depending on the clinical area and risk of exposure.
Date Disposable sterilized gloves for every procedure
Name of the operation Masks
Indication Gowns and plastic aprons
Anesthesia Protective eye wears (goggles)
Surgeon’s name Gum boots.
Assistant doctor and/or nurse name
Name of the operation theater (OT)
Steps
PROCEDURES
Operative findings The following procedures are generally done in obstetric
Postoperative orders. practice.
Normal 5 cm, 22 or 24 G needle is attached to 10–20 mL

syringe and 0.5% lignocaine is taken.
Slight traction is applied on tenaculum to help and
identify the area between the smooth cervical epithelium
and the vaginal tissue. This is the site for insertion of the
needle around the cervix.
Insert the needle just under the epithelium. Injections
are given at 2 o’clock and 10 o’clock position or 5 o’clock
and 7 o’clock while some obstetricians advised 3 o’clock
and 9 o’clock position.
After inserting the needle, aspirate to be sure that no
vessel has been penetrated. If the blood come into
syringe, then remove the needle and recheck the
position and try again. Never inject if blood is aspirated,
it can lead to convulsions and even death.
Inject 2 mL of lignocaine just under the epithelium not
deeper than 3 mm. When correctly placed swelling and
blanching of the tissue can be noted.
Fig. 58.1: Paracervical block Wait for 2–5 minutes then pinch the cervix with forceps
to check the effect of anesthesia.
Paracervical Block (Fig. 58.1)
Dangerous Effects of Lignocaine
Indications Hypersensitivity or anaphylactic response
Dilatation and curettage Twitching of muscles
Manual vacuum aspiration (MVA) Convulsions
Dilatation and evacuation
Severe hypotension
Pain relief during first stage of labor.
Bradycardia
Contraindication: Any known allergies to lignocaine. Cardiovascular collapse
Requirements Respiratory collapse.
Tenaculum Management
Sponge holder
If the above signs and symptoms develop, do the following:
Sim’s speculum
Ask somebody to call anesthetist and ask for assistant
Anterior vaginal wall retractor
doctor
22 G needle
Put intravenous (IV) access
0–20 mL syringes
Start oxygen
Injection lignocaine 0.5% without adrenaline.
Control convulsion by injection of diazepam/thio-
Procedure pentone slowly

Immediate intubation is required
Bladder is evacuated.
Patient put in lithotomy position. Artificial ventilation may be required and maintain with
Do aseptic ritual and draping. 100% oxygen and relaxation

Posterior vaginal wall is retracted with Sim’s speculum. If cardiovascular collapse occurs, then vasopressors
Anterior vaginal wall is retracted with anterior vaginal and IV fluid are indicated.
wall retractor. The support of respiration and cardiovascular activity
One mL of 0.5% lignocaine solution is injected into will be required to be maintained for the duration of
anterior lip of the cervix where we are going to use action of the drug (for lignocaine it is 45 minutes). The
tenaculum. maximum cumulative safe dose for adult is
Anterior lip of cervix held with tenaculum or sponge • 0.5–1% lidocaine 4 mg/kg
holder (in case of pregnant patient). • 0.5–1% lidocaine + adrenaline 7 mg/kg.
Minor Obstetric Procedures 527
Pudendal Block Anesthesia in the vagina and advanced towards the ischial spine. The
needle inserted through this guide pierces the vaginal
Indications
mucosa and sacrospinous ligament to get into the exact
Instrumental (forceps ventouse) delivery position. Rest of the procedure is same as above.
Breech delivery At the end of the procedure, wait for a few minutes
Episiotomy before starting for the anesthetic effect to take place.
Repair of perineal tears
Before destructive operations, e.g. craniotomy, etc. Dilatation and Evacuation (D&E)
The operation consists of dilatation of the cervix and evacu-
Requirements
ation of the products of conception from the uterine cavity.
Sponge holder
22 G needle Indications
10–20 mL syringe
Incomplete abortion
Injection lignocaine without adrenaline
Inevitable abortion
30–40 mL of 0.5% lignocaine without adrenaline is used as
Missed abortion
the anesthetic agent for the block. The aim is to infiltrate Hydatidiform mole in the process of expulsion
about 15–20 mL of this solution around the pudendal Medical termination of pregnancy (MTP) (first
nerve as it passes through the lesser sciatic notch around trimester).
the ischial spine. The procedure is carried out using Anesthesia: Either general or local anesthesia with
sterile technique. Two approaches are described: sedation.
1. Transperineal
2. Transvaginal. Procedure (Fig. 58.3)
In the transperineal approach (Fig. 58.2A), the needle Patient is put in lithotomy position after voiding urine. The
pierces the perineal skin on either side of the vagina medial part of perineum along with lower abdomen and thighs are
to ischial tuberosity. Two fingers in the vagina guide the cleaned first with savlon, then iodine and finally spirit. The
needle tip towards ischial spines. The tip is slightly carried cleaning is started from the part to be operated and then go
beyond the sacrospinous ligament and after confirming laterally. Do not clean with strokes from clean part to unclean
that it is not in a vessel by aspiration, about 15 mL of the part and back to clean part. Now clean vagina by savlon and
lignocaine solution is injected. The same procedure is then iodine. Now drape with autoclaved, cut perineal sheet.
repeated on the other side. Procedure is done under aseptic conditions, bimanual
In the transvaginal procedure (Fig. 58.2B), a special examination is done to access the size and position of
pudendal needle guide (trumpet) is inserted (if available) the uterus, any findings in the fornices.
A B
Figs 58.2A and B: Pudendal block. A. Transperineal approach; B. Transvaginal approach

The products of conception or the material obtained is

sent for histopathological examination.
Prophylactic antibiotics may be given after the operation.
Postoperative Orders
Nil orally for 2 hours
Half-hourly pulse/BP/respiration check for first 2 hours
Observe the pad
Antibiotics—mostly ampicillin is given but if patient
comes with incomplete abortion metrogyl may be added

Mala N is given to regulate the pituitary ovarian axis for
3 months for contraception.

In some cases, this procedure is done in two stages.
In first stage, cervix is only dilated by either tents or
intravaginal prostaglandin E2 pessary or gel or misoprostol
tablets.
In second stage, further dilatation by metal dilator is
Fig. 58.3: Dilatation of cervix done and evacuation of uterus is carried out.
Posterior vaginal wall is retracted by Sim’s speculum.

Complications
Cervix is visualized. Anterior lip of cervix is grasped Excessive hemorrhage
by sponge holding forceps (in gravid uterus) with Cervical laceration
tenaculum in early pregnancy. Uterine perforation
Apply iodine to the cervix twice. Late complications: Pelvic inflammation, infertility,
The cervix is dilated gently upto the desired extent by the cervical incompetence, uterine synechiae.
graduated metal dilator. The tip of the dilator should go Instructions at discharge: If everything is normal, to
just beyond internal os and the cervix should be dilated report after 6 weeks for collecting histopathology report.
enough to admit the index finger of the operator easily. Investigations to find the cause may then be carried out.
Report immediately if there is excessive vomiting, pain,
Closed ovum forceps is passed into the uterine cavity. The
fever or bleeding.
blades of the ovum forceps are opened and detached pieces
• Take medicines as prescribed
of products of conception are grasped with the blades,
• Avoid sex till next period, which may start after 1
close the blades and removed them. The ovum forceps
month to 6 weeks
may be rotated through a right angle before withdrawing
• Avoid pregnancy for 6 months.
it from the uterine cavity. This ensures better grasp on the
material held with the forceps. The ovum forceps may have Suction Evacuation
to be passed many times in the uterine cavity.
It is a procedure in which the products of conception are
When all the products of conception have been
sucked out from the uterus with the help of a cannula fitted
removed, a blunt curette is passed into the uterine
to a suction apparatus or MVA syringes (Fig. 58.4).
cavity and gentle scrapping of all the walls of the uterus
is done till the typical grating sensation is felt. Indications
Injection methergine 0.2 mg is to be administered IV MTP (first trimester)
during the procedure. Inevitable abortion
The Sim’s speculum is removed and with the two Recent incomplete abortion
fingers in the anterior fornix and the other hand on the Hydatidiform mole.
abdomen, the uterus is massaged to expel any clots left
in the uterus. A final bimanual examination is done. Procedure
After being satisfied that the uterus is remaining firm and The steps followed are the same as adopted for D&E.
the bleeding is minimal, the vagina and the perineum The procedure may be done under IV sedation supple-
are toileted dried and a sterile vulval pad is placed. mented with paracervical block.
normal cycle when the presence of an early pregnancy

cannot be diagnosed accurately.
The operation is done as an outdoor procedure and in
apprehensive patients; paracervical block anesthesia may
be given. A 4–5 mm flexible plastic cannula is introduced
into the uterine cavity and employing suction with the
50 mL plastic syringe, the endometrium is sucked out. The
sucked out material should be sent for histology.
The procedure is contraindicated in pregnancy for
more than 44 days and in the presence of local pelvic
inflammation. There is risk of continuation of pregnancy
(0.5%) and as such, it is advisable to report, if the
menstruation fails to resume after 1 month.
Manual Vacuum Aspiration (Fig. 58.4)

Fig. 58.4: Manual vacuum aspiration syringes The apparatus is handy where these is no electricity. It is
efficient method of such on evacuation as described above.
See in Textbook of Gynecology by the same author.
The cervix is dilated with graduated metal dilators or
Karman’s cannula in MVA upto one size less than that Hysterotomy
of suction cannula.
It is an operative procedure of extracting the products of
The appropriate suction cannula is fitted to the suction
conception out of the womb upto 20th week by cutting
apparatus or MVA syringes. The cannula is then
through the anterior wall of the uterus. It is a miniature
introduced into the uterus, the tip is to be placed in the
cesarean section (CS).
mid uterine cavity.
The pressure of the suction is raised to 400–600 mm Hg.

Indications
The cannula is moved up and down and rotated within
the uterine cavity. The suction bottle is inspected for the MTP (midtrimester)—methods of termination have
products of conception and blood loss. failed or are contraindicated. This is to be done upto 20
The endpoint of suction is denoted by: weeks only.
• No more material is being suctioned out In selected cases of molar evacuation, when suction
• Gripping of the cannula by the contracting uterus curettage cannot be used for some reason and the uterus
• Grating sensation has to be conserved.
• Appearance of the bubbles in the cannula Painless vaginal bleeding in midtrimester pregnancy with
The vacuum should be broken before withdrawing the cervix remaining unfavorable. The bleeding is mostly due
cannula down through the cervical canal to prevent to low-lying placenta.
injury to the internal os. In preterm prolonged rupture of membranes, when
The procedure is completed as described above for signs of chorioamnionitis set in without evidence of
D&E. vaginal delivery.
Complications Preoperative
Excessive hemorrhage but it is much less than in D&E Injection TT 0.5 mL intramuscular (IM) is given before
Cervical laceration operation and informed written consent is taken from the
Uterine perforation. patient and one relative. Preoperative investigation and
Late complications: Pelvic inflammation, infertility, cervical preanesthetic checkup is done.
incompetence, uterine synechiae.
Steps
Menstrual Regulation Technique is similar to the one employed in CS. The
Menstrual regulation is the aspiration of the endometrial incision in the abdomen and uterine walls in hysterotomy
cavity within 14 days of the missed period in a previously are smaller. If further child bearing is desired, smallest
uterine incision that will allow removal of fetus and

placenta should be made, away from the fundus, and the
uterine wound should be carefully repaired (transverse
incision is preferred, if feasible).
Abdomen is cleaned with savlon, dried, then with
iodine and finally with spirit. Abdomen is drapped.

Abdomen is opened by a Pfannenstiel incision and
peritoneal cavity is entered.

Uterovesical fold of peritoneum is incised transversely and
the bladder is pushed down. Doyen’s retractor is inserted.

The uterine incision may be:
• Transverse incision as low as possible.

• Low vertical in the region of the lower uterine segment.
The incision is deepened till the amniotic sac bulges out
through it. The right index finger is introduced along the Fig. 58.5: Scar endometriosis
sac to separate it out from the wall completely.
Uterus is compressed and the amniotic sac pops out of Episiotomy (Perineotomy)
the wound. Fetus and placenta are also removed in the
It is the most common operation in obstetrics. It is a
similar fashion.
surgically-planned incision on the perineum and the
Uterine incision is closed in two layers, the deep muscular
posterior vaginal wall during the second stage of labor. It
and superficial seromuscular by number 1 chromic catgut
should not be performed routinely.
or number 1 vicryl. It is deliberate inflicted second degree perineal injury
The uterovesicular peritoneum is advanced, so as
under local anesthesia and the structures cut are:
to cover the uterine scar completely, after obtaining Fourchette
hemostasis, by 0 chromic catgut. Posterior vaginal wall
Peritoneal toilet is done and the abdomen is closed in
Superficial and deep transverse perineal muscles, bul-
layers. First abdominal peritoneum is closed by 0 chronic bospongiosus and part of levator ani and pubococ-
catgut continuous sutures it (is optional). In the second cygeus muscles
layer, the rectus sheet is stitched with either number 1 Bulbocavernous gland
chromic catgut or with number 1 vicryl by continuous Fascia covering the muscles
sutures. If the amount of subcutaneous fat is more it is Transverse perineal branches of pudendal nerve
stitched in separate layer by interrupted number 0 plain Subcutaneous tissue and skin.
catgut. Skin is stitched by interrupted mattress sutures of It causes a neat straight incision instead of the ragged
silk or stapled or by subcutaneous sutures (which need lacerations and hence easy to repair.
not be removed); skin stitches or staples are removed on
7th day of operation. Indications
To prevent perineal tears in cases of primigravida, face
Complications to pubes or face delivery, big baby or narrow pubic arch.
Immediate Rigidity of perineum as in elderly primigravida or old
• Uterine bleeding perineal scar of episiotomy.
• Injuries to other viscera like bladder, intestines, etc. Before operative or manipulative delivery such as vac-
• Peritonitis uum extraction (not always), forceps, breech extraction
• Intestinal obstruction procedures or internal version.
• Anesthetic hazards To cut short the second stage as in heart disease, severe
Remote pre-eclampsia or eclampsia, postcesarean cases, etc.
• Menstrual abnormality—menorrhagia or irregular In cases of premature delivery: The head of the premature
periods baby, though small cannot stand compression at perineum.
• Scar endometriosis (1%) (Fig. 58.5) During breech delivery, to minimize sudden com-
• Scar rupture in subsequent pregnancy. pression and decompression of head at the vulva.
Merits: Least blood loss, easy repair, minimum post

operative discomfort, superior healing, decreased
chances of wound disruption.
Demerits: Extension, if occurs, may involve the rectum.
3. Lateral (least popular): Incision starts from about 1
cm away from center of fourchette and extends laterally.
It causes more bleeding and may damage the Bartholin’s
duct or gland.
4. J-shaped: Incision begins in the center of fourchette
and is directed posteriorly along the midline for about
1.5 cm and then directed downwards and outwards
along 5 or 7 o’clock position to avoid anal sphincter.
Disadvantage: Apposition is not perfect and the
repaired wound tends to be puckered.
Timing of Repair
Just after delivery of the placenta. Because episiotomy
repair is not interrupted or disrupted by obvious necessity
of delivering the placenta especially in some cases of
manual removal of placenta.
Fig. 58.6: Technique of infiltration of local anesthetics
Technique (Mediolateral Episiotomy)
Episiotomy is to be performed when absolutely necessary. (Figs 58.7A to D)
Ensure that the patient is immunized against tetanus and a
Anesthesia (Fig. 58.6) written consent is taken. The basic principle is to obtain the
Local infiltration with or without pudendal block. Anesth- hemostasis and anatomical restoration without excessive
etize the area early to provide sufficient time for effect. suturing. Avoid placing knots near the hymen ring and
perineal skin it will reduce the discomfort and dyspareunia.
Timing of Episiotomy The perineum is thoroughly swabbed with antiseptic
Bulging thinned perineum during contraction just prior to lotion and draped.
crowning is the ideal time. Early episiotomy will cause loss The perineum is infiltrated with 10 mL of 0.5%
of precious blood from bleeding and may be dangerous for lignocaine in the line of proposed incision.
an anemic patient. The index and middle finger of left hand are put into
the vagina with palmar surface towards the perineum

Types to expose the vaginal skin fourchette and perineal body
Four types of episiotomies can be given: and to protect the baby’s head.
1. Mediolateral (most common): Incision starts from the The episiotomy scissors are introduced between the
midpoint of the fourchette and is directed diagonally in fingers and the perineum is cut at the height of uterine
a straight line (either to left or right) which runs about contraction (incision and structures cut are described
2.5 cm away from the anus. above) under vision.
Merits: Extension will not involve anal sphincter. If The repair is done in three layers:
necessary, the incision can be safely extended. 1. Vaginal mucosa and submucosal tissue in a conti
Demerits: There is an increased blood loss from incision nuous suture starting beyond the apex of mucosal
of the pubococcygeus and bulbocavernosus muscles. incision; by number 0 chromic catgut.
Apposition of tissues is not very good and blood loss 2. Perineal muscles—interrupted sutures by number 1
is a little more. Postoperative discomfort is also more. chromic catgut.
Relatively increased incidence of wound disruption 3. Skin and subcutaneous tissue—interrupted sutures
and dyspareunia. of number 1/0 chromic catgut or subcuticular stitches
2. Median: Incision extends from the center of the four- of number 2/0 chromic catgut. Polyglycolic sutures
chette and extends posteriorly along midline for 2.5 cm. are better for their tensile strength, nonallergic
A B
C D
Figs 58.7A to D: A. Sites of median and mediolateral episiotomy; B. Stitching vaginal mucosa; C. Repair of muscle layer; D. Stitching skin
properties and lower probability of infections After delivery for first 1 hour the episiotomy is watched
complication and breakdown of episiotomy. See that along with general condition of the mother such as
no swab is left behind as it is very important step. pulse, uterine size and firmness and for any postpartum
Episiotomy is inspected for the first hour in the recovery hemorrhage (PPH). Any hematoma is specially looked for
room every 15 minutes and during ward rounds. and written notes are put every 15 minutes.
Internal version: The entire hand is introduced into the

uterine cavity and the other hand is on the abdomen.
Bipolar (Braxton Hicks): The conversion is done
introducing one or two fingers through the cervix and
the other hand on the abdomen.
EXTERNAL CEPHALIC VERSION (ECV)

ECV was first described by Hippocrates in the 4th century
AD. Initially popular in the 1960s and 1970s, ECV fall into
disrepute due to reports of death following the procedure.
Reintroduced in the US, it became increasingly popular in
the 1990s.
Time of Version
Fig. 58.8: Vulval hematoma after episiotomy In the past it was believed that the best time to do version
was between 32–34 weeks. Since then it has been suggested
During postoperative period, the episiotomy should be that ECV should not be preferred on preterm breeches as
washed from above down each time following urination they are more likely to spontaneously convert to vertex
and defecation, and local application of antiseptic cream and also may revert to breech (50%) following version.
Advantages of early version:
is done after each perineal wash.
• Fetus is small.
Complications • Liquor is abundant.
Extension of incision to involve the rectum. • May be easier to carry out.

Disadvantages of early version:
Excessive bleeding if not stitched promptly.
Vulval hematoma: Open, drain and resutures under • After successful version, there is a greater chance of
anesthesia (Fig 58.8). the fetus reverting to breech spontaneously due to
Infection: Open and drain and do debridement. large amount of amniotic fluid.
Breakdown of episiotomy: Secondary suturing will be • There is good chance that the fetus may spon t
done when no infection after antibiotic therapy and aneously change to cephalic presentation in future.
keeping the wound clean. Advantages of version at term:
Remote complication include dyspareunia, scar endo- • After successful version, the fetus is unlikely to revert
metriosis. to breech due to its large size, reduced liquor and
Recently the practice of episiotomy is dwindling due to irritability of the myometrium.
more parent-to-child transmission (PTCT) of HIV. • Contraindications to ECV such as intrauterine
growth restriction (IUGR) may manifest in the third
Version trimester.
It is an operation by which the fetus is turned in utero for • In case of fetal complications, immediate delivery of
the purpose of changing the presentation and to bring a functionally mature fetus may be carried out.
the comparatively favorable pole to the lower part of the • The fetus is allowed to convert to vertex spont
uterus and facilitate normal vaginal delivery. aneously.
Disadvantages of version at term: In case the patient
Types goes into preterm labor, the opportunity of performing
According to whether the head or breech is the presenting version may be missed by deciding to wait till 37 weeks.
part, the operation is designated cephalic or podalic
version. It is also named according to the method by which Contraindications
it is done: This includes contraindications to vaginal delivery like her-
External version: The maneuver is done solely through pes simplex infection and placenta previa. Polyhydram-
anterior abdominal wall. nios, oligohydramnios, IUGR, uterine malformations and
fetal anomalies are relative contraindications. Ultrasound The patient should be kept in steep head low, slight
estimated fetal weight and abdominal circumference lateral tilt or Trendelenburg position for 15–20 minutes
greater than 20% of that expected for gestational age, any to dislodge the presenting past. Then the patient is made
single amniotic fluid pocket less than 2 cm, sacroanterior supine with a pillow under her shoulders, abdomen
position, although known to reduce the success of ECV, are exposed and limbs flexed at the hips and knees to relax
not contraindicated for performing the procedure. Gesta- the abdominal wall. The abdomen may be powdered
tional age and head circumference have not been found to with talcum powder.
affect the success rates of ECV according to recent studies.
Uterine scars have been traditionally considered as a Procedure (Figs 58.9A and B)
contraindication in performing ECV. The obstetrician stands on the patient’s right side.
The fetal heart rate (FHR) is to be auscultated every
Prerequisites 2 minutes and the procedure abandoned in case of
There must be a singleton pregnancy. gross abnormality.
Accurate diagnosis of fetal position is of prime importance. The doctor’s left hand grips the head and the right hand
Fetopelvic disproportion should be always ruled out. grips the breech. The head is moved towards the pelvis
The presenting part should not be deeply engaged. and breech towards the fundus to achieve a transverse
Fetus should be freely mobile. lie. If any FHR abnormality is noted, the fetus is to be
Membranes should be intact. turned back to its original position.
Uterus must be relaxed. Now, the doctor’s left hand grips the breech and the
An ultrasound (USG) and a non-stress test (NST) right hand the head, and the fetus is moved into vertex
should be performed prior to the procedure and the presentation. If the heart rate is normal after completion
NST should be repeated after the procedure. of version, the head can be pushed into the pelvis to
prevent reversion to breech.
Success Rate Any attempt at version should not last for more than 5
The success rate of ECV varies from 35 to 86%. Cesarean minutes. Do not perform a forced version. If the procedure
delivery rates were reduced by 50% for breech presentation. cannot be performed easily and gently, abandon it.
In the forward, somersault method of ECV, the face
Dangers of the fetus leads the way. However, the head may get
Unexplained intrauterine death after version. deflexed or extended if flexion is not maintained. In the
Transient bradycardia due to head compression has backward somersault technique, the occiput leads the
been noted (40%). The heart rate almost always comes way. Although flexion is better maintained, there is the
to normal within 3 minutes. risk of getting the lower limbs entangled in the cord and
Premature separation of the placenta and fetomaternal trauma to the placenta.
hemorrhage (0–5%).
Premature rupture of membranes. External Cephalic Version under Anesthesia
Umbilical cord prolapse, cord compression and cord Regional anesthesia has the advantage of relaxing the anterior
entanglement (<1.5%). abdominal wall, making palpation and manipulation of the
Fetal injury, e.g. fractured bones and ruptured viscera fetus easier, and eliminates pain and bearing down or tensing
have been noted. of muscles. In addition, at term, labor may be induced with
epidural analgesia offering pain relief after successful version.
Technique If necessary, cesarean delivery may be carried out rapidly if
Preparation complications develop. However, regional anesthesia has
Written, informed consent from the patient and relative. its own risks and lack of pain may lead to inadvertent use of
Bladder should be empty. excessive force by the doctor.
Injection anti-D (300 µg) should be given to Rhesus
(Rh) negative mothers. External Cephalic Version with Fetal Acoustic
USG and NST should be performed. Stimulation
Serum electrolytes and blood sugar should be per Fetal acoustic stimulation causes shift of fetal spine to lateral
formed if tocolysis is being considered. aspect and increases success in midline spine presentation.
A B
Figs 58.9A and B: External cephalic version
External Cephalic Version with Tocolysis Spontaneous version may be aided by a full bladder,
The tocolytics used for ECV are: manual disengagement of the fetal head and postural change,
10 µg of hexoprenaline IV over 1 minute.
knee-chest position for 10 minutes daily, and elevation of
0.25 mg terbutaline in 5 mL normal saline IV over
pelvis abduction of the high and relaxed breathing.
5 minutes.
Internal Version
0.25 to 0.50 mg/minute terbutaline IV over 15–20 minutes.
0.2 µg/minute ritodrine IV for 20 minutes.

It is always a podalic version and is completed with the
Antepartum abdominal amnioinfusion has also been extraction of the fetus.
used to facilitate version.
Indication
Spontaneous Version Transverse lie and in the case of second baby of twins
Spontaneous version to vertex may occur in as many (Figs 58.10A to C).
as 57% of pregnancies after 32 weeks and 25% after 36
weeks especially in nulliparous. Hence, the presentation Prerequisites
should always be confirmed prior to a cesarean delivery by Written informed consent:
ultrasound if necessary. Fully, dilated cervix
A B C
Figs 58.10A to C: Internal version

Adequate liquor amnii for intrauterine fetal manipulation coming out it is pelvis abscess, send the pus for culture. If it is
Fetus must be living. non- clotting blood rupture ectopic pregnancy is suspected.
Contraindications: Neglected obstructed labor even if If blood is aspirated which clots a vein or artery may have
the fetus is living. been injured. Remove the needle and reinsert and aspirate.
Procedure
COLPOTOMY
It is done under general anesthesia. One hand is introduced
into the uterus in a cone-shaped manner. If the podalic It is cutting open pouch of Douglas (POD).
pole of the fetus is on the left side of the mother, the right Indication: Pelvic abscess (Fig. 58.12).
hand is to be introduced and vice-versa. Traction is given The procedure is explained to the patient and consent is
to the leg while it is gripped in a cigarette holding fashion taken. The patient is taken into the OT after emptying uri
and simultaneously the other hand pushes up the head nary bladder. She is asked to lie in the lithotomy position.
externally. The delivery is completed by breech extraction.
Sedation is given. Perineum is cleaned and drapped. The
Routine exploration of the uterovaginal canal is done to
cervix is exposed by Sim’s speculum and anterior vaginal
exclude rupture of the uterus or any other injury.
wall retractor. Posterior lip of the cervix is caught by a
tenaculum or vulsellum. Vagina below the cervix is grasped
CULDOCENTESIS (FIG. 58.11) between two Allis forceps. The middle part of vagina is cut
This is done in cases of fluid (blood or pus) in pouch of by a pair of scissors. Pus will come out send after culture
Douglas (POD). The procedure is explained to the patient and sensitivity. A drain is put so that the drainage of pus
and a written, informed consent of the patient is taken. continues. On second or third day when pus discharge
Ask her to lie in lithotomy position after passing urine. stops the drain is removed.
Perineum is cleaned and drapped cervix is exposed by If the abscess is situated anterior or lateral to the
either Sims posterior vaginal wall speculum or Cusco’s uterus, drainage may be performed by ultrasound guided
bivalve speculum. Posterior lip of the cervix is caught by placement of catheter drain. When the abscess cannot be
a tenaculum or vulsellum. A long needle or spinal needle reached by any of the above methods an open laparotomy
with 20 mL syringe is introduced in POD just below the is carried out. Pus is removed, pelvic cavity is irrigated and
posterior lip of the cervix and aspiration is done. If pus is a drain is kept for a day or two.
Fig. 58.11: Culdocentesis Fig. 58.12: Colpotomy

1. Discuss indications, contraindication and procedure of paracervical block.
i. The operation of dilatation and evacuation consist of ____________ of cervix and ____________ products of conception.
ii. Two approaches is pudendal block anesthesia are ____________ and ____________.
iii. Complications of pudendal block anesthesia are ____________, ____________, ____________ and ____________.
Female Sterilization, Cesarean
59 Delivery and other Emergency

Obstetric Operations
Sudha Salhan, Harsha Gaikwad, PK Verma, Puja Jain, Indira Ganeshan
FEMALE STERILIZATION Laparoscopic sterilization is not permitted with second

trimester abortion and in postpartum (within 6 weeks of
Female sterilization or tubectomy is the most common
delivery). This is because fallopian tubes being thicker get
family planning method practised throughout the world.
torn more often and recanalyzes easily (failure). In these
This operation was first performed in 1823 in London by
cases male sterilization or minilaparotomy procedure is
Dr J Blundell. By 1950 and 1960, it was initiated in several
countries. Since 1970 its use has rapidly grown. According allowed by the Government of India.
to World Health Organization (WHO) (1994) data, 202
Eligibility Criteria for Female Sterilization
million (female and male) sterilization are done worldwide
with 163 million women sterilization. It can be performed (Case Selection)
per abdominally (minilaparotomy or laparoscopically) (Government of India, Ministry of Health and Family
and per vaginally. Welfare)
The patient should be married (including ever married).
Methods used Per Abdominally Age above 22 years and below 49 years. Husband should
After a postpartum or puerperal waiting period of be below 60 years.

24 hours for rest after delivery, the operation can be The couple should have at least one child more than
performed upto 7 days after parturition. 1 year of age.

Cesarean section (CS): There is an indication to do CS. The client or her spouse must not have undergone
Ligation itself is not an indication for CS. sterilization in the past (not applicable in cases of
With medical termination of pregnancy (MTP) or failure of previous sterilization) unless sterilization is
evacuation of incomplete abortion in the same sitting. medically indicated.
With gynecological operations of Manchester repair, The client must be in a sound state of mind so as to
vesicovaginal fistula (VVF) repair. understand the full implications of sterilization.
Interval sterilization (in between two pregnancies) Mentally ill clients must be certified by a psychiatrist
preferably atleast 6 weeks after delivery and beyond.
regarding the soundness of the client’s state of mind and
Do it within 7 to 10 days of onset of menstrual period to
consent should be given by the legal guardian spouse.
prevent any chances of pregnancy.
Vaginal Sterilization WHO Eligibility Criteria for

Vaginal sterilization as such alone or with Manchester Female Sterilization (2004)
repair or MTP. Contraindications: Absolute contraindications are not
there. But caution (C), delay (D) and special (S) conditions
Laparoscopic Sterilization are considered.
With MTP (first trimester) Known to have or suspected to have pregnancy (wanted)
With surgical procedures: Manchester repair and VVF Active pelvic infections (pelvic peritonitis)
repair Acute systemic infection
Alone as interval surgical procedure. Active liver disease

Female Sterilization, Cesarean Delivery and other Emergency Obstetric Operations 539
Skin infection at the proposed operation site Side effects and potential complications of surgery are
Sexually transmitted disease (STD) also told in a clear, balanced way.
Severe anemia (less than 8 gm/dL) Information given about sterilization: Practically it is
Acute respiratory disease a safe, surgical permanent method for stopping future
Current cardiovascular or coronary heart disease pregnancies. Though surgery has its inherent risk. It
Malignant trophoblastic disease does not influence client’s strength, her ability to do her
Any other temporary operative risk routine works or her ability to perform and enjoy sex. But
Any psychiatric condition that may impair decision- this operation does not protect against reproductive tract
making. infection (RTI)/sexually transmitted infection (STI) along
Following pregnancy conditions to be treated and with human immunodeficiency virus (HIV)/acquired
resolved before operation: immune deficiency syndrome (AIDS). A small numbers
Puerperal sepsis do fail. If need be a reversal operation can be performed,
Prolonged rupture of membrane (24 hours or more) which is a major surgery, but the success is not certain
Pregnancy with persistent hypertension (100%). She is free to clarify doubts. It is not compulsory or
Antepartum hemorrhage (APH) and postpartum hemor binding. It is voluntary.
rhage (PPH) The woman’s informed consent is taken which is
Severe trauma to the genital tract voluntary. It is not taken when the woman is sedated or
Postpartum psychosis under stress. A printed consent form is provided by the
Unhealthy newborn/stillbirth Government. The husband’s consent is not essential.
Recent septic abortion
Severe postabortal hemorrhage Preoperatively

Delay should be atleast 6 weeks after delivery or abortion. Before surgery the client is assessed by taking history,
Conditions where reference to center with facilities for physical examination and hemoglobin and urine analysis
general anesthesia and other medical support is mandatory. (reducing substance and protein). Tetanus toxoid (TT) is
Conditions increasing anesthetic risk are: given (if not previously immunized). Informed written
Postcardiovascular disease consent is taken. The hemoglobin must be 8 g or more.
Chronic respiratory problem
Hypertension [blood pressure (BP) > 160/100 mmHg] Who can Perform
Hyperthyroidism
Minilaparotomy can be performed by a trained MBBS
Diabetes with vascular disease
doctor. Laproscopic sterilization is allowed by a gynecologist
Moderate anemia (> 7–10 gm/dL)
(DGO/MD/MS) or a trained laparoscopic surgeon (MS).
Severe chronic liver disease.
Timing of surgical procedure: 24 hours after delivery
In these conditions, experienced medical staff are
and upto 7th postpartum day concurrently with MTP and
required to perform the procedure.
cesarean section is preformed concurrently.
Conditions that increase surgical difficulties and risks:
Premedication/anesthesia/analgesia: Tablet alprazolam
Endometriosis
(0.25–0.50 mg) or tablet diazepam (5–10 mg) a night before
Past pelvic infection
surgery is given. An intravenous (IV) line is secured. General
Past complicated abdominal or pelvic surgery
or spinal anesthesia is given in postpartum sterilization.
Marked obesity
Umbilical hernia
Coagulation disorders.
Techniques
The surgeon must see that enough tube is left for recana-
Counseling lization (if the need arises) and ligation is not carried out too
Counseling in a language understood well by the client close to the cornua. The following methods are mostly used.
is very important in helping her, make an informed and
Pomeroy’s Method (Figs 59.1A and B and
voluntary decision about her fertility. All family planning
methods are explained to the client and is told about this see 77.29A to G)
method being permanent (recanalization is not 100% The patient is kept fasting overnight. She is given sedation.
successful). Local, spinal or general anesthesia is then given. The part
A B
Figs 59.1A and B: Pomeroy‘s method
is cleaned and draped. The laparotomy is performed by Irving method Ligating and burying the proximal tubal end in
intra-umbilical route. The size of incision depends on the serosa of the posterior uterine wall
the uterine size. In postpartum sterilization, the uterine (Figs 59.2A to D)
Uchida method The medial tied end of the fallopian tube is retracted
size is big and the incision is given below the height of
into the mesosalpinx after tying and cutting it
uterus (3–4 cm) but in interval ligation it is 2.5 cm above Parkland method The tube is tied at two ends after making a
the symphysis pubis. The tube is identified, always look window in an avascular portion of the meso-
for the fimbrial end. Use no. 1 chromic catgut. In modified salpinx and cut in between (Figs 59.3A to C)
Pomeroy use one zero plain catgut. A loop is made about Fimbriectomy
Coagulation Bipolar coagulation (Figs 59.4A to C)
4 cm lateral to the fundus and ligated twice by catgut. The methods Unipolar coagulation
loop above the ligature is cut and the surgeon should look
for any hemorrhage. Same procedure is done by second Advantages
fallopian tube. The abdomen closed in layers. Cut tubes A safe, effective, convenient method.
are sent for histopathological examination. Can be done as outpatient department (OPD) procedures.
After the catgut is absorbed, the ends retract and hence Can be performed by a junior doctor at primary health
the tube cannot recanalize spontaneously (see Fig. 77.29G). centers or camps.
The failure rate is 1:300:400. Complications are mostly minor.
No special equipment or training is needed (compared
Minilaparotomy to laparoscopic sterilization).
Can be performed soon after childbirth, abortion or as
This can be done under general anesthesia or local anesthe-
interval sterilization.
sia (0.5% lignocaine) and sedation. The patient empties her
urinary bladder. Cleaning and draping is done. Local anes- Drawbacks
thesia is given. A uterine elevator is passed from the vagina. Infection of wound can occur.
A 2.5 cm incision is given midway between the pubic The scar is larger.
symphysis and the umbilicus.
In interval ligation the incision is given above the Laproscopic Ligation
symphysis pubis. The abdomen is opened. Both tubes are It is done by a subumbilical incision Veress needle is passed
ligated and cut one by one. into the abdomen (tested by easy passing normal saline).
Identification of the tube is very important. It is caught Pneumoperitoneal is created by carbon dioxide gas
with Babcock’s forceps and the fimbrial end is identified (non-inflmmable, easily absorbed). Incision is slightly
always safely away from the cornua. Usually Pomeroy’s increased and 10 mm trochar with cannula in inserted
technique is used in most of the hospitals in India. in the abdomen. Cannula is removed and laproscope
Other methods of female sterilization by laparotomy loaded with Fallop’s rings (Fig. 59.5) inserted in the
are shown in the box: abdomen. Pelvic manipulation bring one fallopian tube in
A B
C D
Figs 59.2A to D: Irving method
A B C
Figs 59.3A to C: Parkland method
view (recognize by fimbrial end) catch one fallopian tube operations (Manchester repair). It can be done as an
shoot fallops ring watch for blanching. Similar treatment interval procedure.
is done to other tube. Remove laparoscope than deflate After anesthesia the patient is put in a lithotomy
abdomen of CO2. Insert cannula, remove trochar stitch the position. The part is cleaned and draped. The lower lip of
the cervix is secured by vulsellum and colpotomy is done.
skin incision, remove vaginal instruments.
The tubes are ligated and cut one after the other. In all
sterilization operations both fallopian tubes are to be sent
Vaginal Tubal Ligation
for histological profile (in medicolegal cases it is helpful).
This method was in vogue in the 1970s. But because of a In both abdominal and vaginal ligation analgesics and
greater risk of infection it is not commonly used. It can be antibiotics are prescribed for 3 days. In vaginal ligation
combined with MTP and gynecologic pelvic correction intercourse is to be avoided for at least 3 weeks.
A B C
Figs 59.4A to C: Types of methods of female sterilization. A. Bipolar cautery method; B. Silicone band method (laparoscopy); C. Spring
clip method (laparoscopy)
CESAREAN DELIVERY
This is performed for abdominal delivery of the fetus after
28 weeks of pregnancy (before that it is called hysterotomy)
excluding rupture of uterus.
Cesarean birth and cesarean delivery are preferable terms.
Incidence
There has been an increased incidence of cesarean section
(CS) during the last two or three decades to the extent
of about 10% or ever more amongst hospital deliveries.
Incidence in Safdarjung hospital is around 10%. Apart
from increased safety of the operation due to improved
Fig. 59.5: Fallops rings used in laproscopic sterilization
anesthesia, availability of blood transfusion and antibiotics,
the other responsible factors are:
Because around 50% of pregnant women are first time
TABLE 59.1: Postpartum complications
pregnant hence the indications are the conditions
Immediate complications Complications commonly encountered in nulliparas.
Anesthesia hazard Anesthesia use Advancing age increase the frequency of the operation.
Bowel and bladder injures Route (abdominal or vaginal) The frequency of CS also inceases with more use of
Tube and ovaries injuries in association with MTP or electronic fetal monitoring.
Broad ligament injuries sterilization
Nowadays most of the breech presentations are

Hematoma at incision site Age

Place of operation
delivered by CS.
Uterine perforation
New American College of Obstetricians and Gyne
Selection of patient
Technique cologist (ACOG) guidelines discourage vaginal delive
ries for above mid pelvis presentations. Hence more
Abbreviation: MTP—Medical termination or pregnancy
operative abdominal deliveries.
Due to frequent litigations obstetricians resort to CS sooner.
Postoperative complications depend on the method of With adoption of small family size and carefully
sterilization shown in Table 59.1. planned pregnancies neither the obstetricians, nor the
Wound infection: This is the most common complication. patients desire to take even the slightest extra fetal risk
Sometimes hematoma formation and subsequent infec of abnormal vaginal delivery.
tion can occur. Intraperitoneal hemorrhage, bowel and
bladder injuries are rarely seen. Ectopic pregnancy is an Indications
uncommon complication In general, CS is done when normal vaginal delivery
Client is monitored for postoperative care. is contraindicated or it may lead to unsafe outcome in
TABLE 59.2: Common indications for cesarean delivery employed selectively, include the following—‘significant’
Fetal
nonremediable and nonreassuring fetal heart rate (FHR)
patterns, especially when associated with progressive loss
Nonreassuring FHR
of variability, various categories of breech presentation at
Breech presentation (mostly primigravidae)
LBW with IUGR
risk for head entrapment and/or cord prolapse, the very
Conjoined twins low birth weight (VLBW) fetus and active genital herpes.
Maternal fetal The decision to employ cesarean delivery may be selective,
Cephalopelvic disproportion based on the results of ultrasound or cordocentesis studies
Contracted pelvis (and major fetal congenital anomalies such as hydrocep-
Failure to progress halus, gastroschisis or omphalocele).
Placental abruption
Placental previa Maternal Fetal Indications
Maternal Placental abnormalities such as placenta previa or placental
Obstructive benign and malignant tumors abruption in which hemorrhage poses a significant risk to
Large vulvar condyloma
both mother and fetus, as well as labor dystocia, failed to
Cervical cerclage (abdominal)
progress (FTP), relative cephalopelvic disproportion (CPD)
Previous genital fistula (repaired)
Herpes simplex virus infection/HIV
and absolute contracted pelvis on the rare occasion when
Carcinoma of cervix the latter can be diagnosed. Some include failed inductions
Abbreviations: FHR—Fetal heart rate; LBW—Low birth weight; under this designation.
IUGR—Intrauterine growth restriction; HIV—Human immunodefi-
ciency virus Maternal Indications
There are only a few indications for cesarean delivery that
the mother and the fetus. Although it is not possible to are solely maternal. They include mechanical obstructions
catalogue comprehensively all appropriate indications for of the vagina from large vulvovaginal condylomata,
cesarean delivery, most are performed because of: advanced lower genital tract malignancy repair urogenital
Prior cesarean (for recurring cause)
fistula and placement of a permanent abdominal cerclage
Labor dystocia
with a desire for future pregnancies.
Fetal compromise (distress)
Preoperative preparation is done, informed written
Malpresentations (breech, face, brow, transverse).
consent is to be taken. Hemoglobin and urine routine and
Indications for cesarean delivery can be categorized in microscopic test is carried out.
several ways (Table 59.2). Some indications strictly benefit
the fetus, whereas others are largely done for maternal When to Perform Cesarean Section
benefit to avoid maternal hemorrhage, reduce the potential Elective CS is performed as a pre-planned procedure
spread of malignancy, avoid the repeated need for additional during late pregnancy after definitely ascertaining fetal
procedures such as abdominal cerclage in future pregnancies maturity at ≥39 weeks, e.g. repeat CS, high-risk pregnancy.
and prevent uterine rupture. Some indications will benefit Emergency CS: When CS is done on an emergency
both the mother and the fetus. Some indications are well basis irrespective of duration of pregnancy or time of
accepted even though selectively applied on a subjective the day for a patient in labor in the interest of either the
basis. Placenta previa or conjoined twins are universally mother or the fetus.
accepted as indications for cesarean birth. On the other How to time elective CS at 39 weeks: At least one of
hand, several indications such as a breech presentation or a these criteria must be met in a woman if she had normal
very low birth weight (VLBW) fetus are controversial. cycle and had not taken hormonal contraceptive before
this pregnancy.
Fetal Indications • Detection of fetal heart sound (FHS) by Doppler at
Fetal indications for cesarean birth are in large part designed 20 weeks
to minimize neonatal morbidity and possibility of long- • 36 weeks after positive pregnancy test
term consequences of profound intrapartum metabolic • An ultrasound for crown rump length (CRL) at 6–11
or mixed metabolic acidemia and/or delivery related weeks
trauma (including significant fetal thrombocytopenia) • Ultrasound at 18–20 weeks for fetal wellbeing
or transmission of infection. Accepted indications, often • Early clinical examination.
Types of Cesarean Section hemorrhage is reduced. The abdominal wall is opened by

an appropriate incision and two large abdominal gauze
Lower segment cesarean section (LSCS)—99.8%
swabs are used to pack off the intestines and omentum
Classical or upper segment—0.02%
in the recesses of the wound. Free swabs should never be
Cesarean hysterectomy—0.18%
used, as they can be easily lost in the blood that collects
Extraperitoneal lower segment operation.
in the recesses at the sides of the uterus. Dextrorotation of
Technique for Cesarean Delivery the uterus should be corrected before incising the uterine
peritoneum. A Doyen’s retractor is used to visualize the
Abdominal Incision
lower segment. The loose peritoneum covering the LUS is
Vertical incision: Below umbilicus (midline or parame- lifted up, snipped with scissors and the bladder is gently
dian) separated from the underlying myometrium but not more
than 5 cm in depth. The uterus is then opened through the
Transverse Incision
LUS about 1 cm below the upper margin of the peritoneal
Pfannenstiel incision is used which is at the level of pubic reflection (Kerr incision).
symphysis slightly rectus abdominus muscles lateral border
made at the level of the pubic hairline and is extended Delivery of the Infant
somewhat beyond the lateral borders of the rectus muscles. In cephalic presentations, a hand is slipped into the uterine
Exposure of the pregnant uterus is not as good as with a cavity between the symphysis and fetal head, and the head
vertical incision and reentry through a Pfannenstiel incision is gently elevated with the fingers and palm through the
is likely to be more time consuming because of scarring. incision aided by modest transabdominal fundal pressure.
However, it has fewer postoperative complications besides To minimize aspiration by the fetus of amniotic fluid and
an esthetic advantage of not being visible. its contents, the exposed nares and mouth are aspirated
with a bulb syringe before the thorax is delivered. The
Uterine Incision
shoulders then are delivered using gentle traction plus
Classical cesarean incision, which is seldom used today fundal pressure. The rest of the body readily follows.
involves a vertical incision into the body of the uterus As soon as the shoulders are delivered, an IV infusion
above the lower uterine segment (LUS) and reaching the containing about 20 units of oxytocin per liter is started for
uterine fundus. satisfactory contraction of the uterus. The cord is clamped
Nowadays the incision is mostly made in the LUS trans- with the infant held at the level of the abdominal wall, and
versely or less often, vertically. For a cephalic presenta- the infant is handed over to the pediatric resuscitative team.
tion, a transverse incision through the LUS is most often The placenta is then removed as it separates spont
the uterine incision of choice, because it: aneously and its delivery is hastened by fundal massage.
Requires only modest dissection of the bladder from Inspect the uterine cavity and wipe out the cavity of avulsed
the underlying myometrium. fetal membranes, vernix, clots her debris or by a gauge pack.
Is easier to repair.
Is located at a site least likely to rupture with extrusion of Uterine Repair

the fetus into the abdominal cavity during a subsequent Both angles of uterine incision are inspected for bleeding
pregnancy. and caught by Green Armitage or sponge holding forceps.
Does not promote adherence of bowel or omentum to
Check for cervical os to prevent suturing anterior wall
the incisional line. with the posterior uterine wall. Re-approximation of the
lower uterine incision may be performed in two layers
Technique for Transverse Cesarean Incision using no. 2 chromic catgut or similar absorbable synthetic
The patient is encouraged to pass urine before anesthesia. suture such as vicryl, the second layer inverting the first.
In cases of repeat cesarean or where duration of operation The initial suture should be placed lateral to the angle of
time is expected to be more, the bladder is emptied by a transverse incision or inferior to the lower margin of a
a catheter, which is left in position until the operation vertical incision. Subsequent stitches of the peritoneal
is completed. The patient should be positioned with a fold may be run in a continuous or continuous-locking
left lateral tilt, using a firm pillow or sandbags. In this manner to the opposite end of the incision. Single layer
way, a fall in the cardiac output and placental perfusion closure cause more ruptures in next pregnancy compared
(supine hypertension) is avoided and uterine venous to double layer closure (Fig. 59.6).
oxytocin/methylergometrine/prostaglandin uterine
arteries and hypogastric artery ligation, ovarian artery
ligation and hysterectomy.
Placenta increta and percreta in cases of anterior
placenta in previous CS is a very common indication

for hysterectomy.
Anesthetic complications—anaphylaxis, aspiration
pneumonitis.
Lower uterine incision of Kerr is associated with fewer
incidences of excessive maternal blood loss, parametrial
hematoma, transfusion and emergency hysterectomy
than classical fundal incision.
Fig. 59.6: Technique of closure in classical cesarean section Postoperative Complications

Maternal morbidity and mortality: The major sources
of morbidity and associated mortality are related to
Abdominal Closure anethesia, PPH, maternal infection, thromboembolism,
Before peritoneal closure the operating team should etc.
confirm that the needle and sponge counts are correct. The Endomyometritis: Primary cesarean delivery is the
visceral and parietal peritoneum may be reapproximated greatest risk factor for endomyometritis with rates upto
with a running 2-0 or 3-0 chromic or similar absorbable 20-fold than associated with vaginal delivery.
suture. Alternatively, they may be left unrepaired as the Wound complications: Identifiable medical risk factors
mesothelial surfaces spontaneously reapproximate within that increase the likelihood of poor wound healing
48 hours and demonstrate healing with no scar formation include diabetes mellitus and malnutrition. Surgical
at 5 days. The rectus fascia is stitched using synthetic risk factors to be considered are the duration of
braided sutures (e.g. vicryl, dexona) which maintain tensile surgery, the use of drains, the suture material chosen
strength thoughout fascial healing (either interrupted and the closure technique employed. Postoperative
or non-locking continuous stitches). If the patient is at factors include asthma, pulmonary complications and
risk of wound breakdown, delayed absorbable materials associated coughing and vomiting.
such as polydioxanone (PDS) or polyglyconate (Maxon) Urinary complications: Urinary tract infections (UTI)
or permanent material such as nylon or polypropylene are second only to endomyometritis as a cause of post
(prolene) may be used. cesarean febrile morbidity.
Thromboembolic disorders: The risk of thrombosis
Intraoperative Complications increases during pregnancy because of both higher levels
The patient undergoing cesarean delivery is at risk of many of coagulation factors and diminished fibrinolysis. These
complications which are not faced by a patient undergoing changes peak near term and immediately after delivery.
a vaginal delivery.
In a macrosomic fetus or a noncephalic presentation
Remote Complications
lower segment uterine lacerations are more common. Gynecological: Menstrual disorders (menorrhagia,
The lateral apex of the extension should be identified amenorrhea) chronic pelvic pain, scar endometriosis
and the suture placed just lateral to that point. (Fig. 59.7), vesicovaginal fistula.
Bladder and ureteral injuries: Injury to the bladder Incisional hernia or adhesions causing intestinal
or ureter are infrequent but recognized complication of obstruction.
cesarean delivery. Obstetric: Scar rupture in future pregnancy.
Gastrointestinal injury: Injuries to the bowel are also Others: Failing lactation.
rare, but reported prior abdominal surgery and pelvic/
abdominal infection leading to adhesion formation are
Classical Cesarean Section
common risk factors. Indications
Uterine atony: Initial efforts to control uterine atony Where the urinary bladder is densely adherent in LUS
include uterine massage and medical therapy with (repeat cesarean)
should compress the myometrium on each side of

the incision medially during placing and ligating the
sutures.
The serosa should be sutured with continuous suture
with no. 2–0 chromic catgut.

The rest of the abdomen is closed as done in LSCS.
Note: The low vertical incision can be extended upto the

fundus if more surgical space is required.
Perimortem Cesarean Section

The operation of CS was supposed to be started by a
Roman law Lex Regis stated that no mother can be buried
with a fetus inside also called Lex Cesare. This was in the
Fig. 59.7: Scar endometriosis hope of obtaining a living child when the mother was dead
or so near death that maternal survival was not a practical
Lower segment fibroid consideration. A prior written permission from relative
Invasive carcinoma of the cervix is required before carrying out such a procedure in the
In some cases of transverse lie with macrosomic babies, current scenario.
with hand prolapse It is rarely done nowadays. Perinatal outcome is
Some case of anterior placenta previa according to interval of time from maternal death to
Previous classical scar delivery of the child, age of gestation, the nature of the
Fetal malformations maternal injury and the availability of neonatal intensive
Urgent obstetric problems, e.g. cord prolapse and severe care facilities.
acute hypertension In general if the fetus is less than 28 weeks or less than
In placenta percreta in lower segment if diagnosed 1000 g the survival is unlikely. If the CS is performed
antenatally by ultrasound examination. within 5 minutes of the death of the mother the outcome
is excellent, within 5–10 minutes fetal survival is good,
Steps of Upper Segment CS within 10–15 minutes it is fair but poor if the operation is
Bladder is evacuated. performed within 15 –20 minutes of the mother’s death. If
Aseptic ritual and draping done. there is a sudden death of previously healthy mother, the
Laparotomy is done by a midline or right paramedian prognosis is excellent for the baby. It is not so good if there
incision. was prolonged or debilitating illness of mother, e.g. pre-
A vertical midline incision above the LUS is given in the eclampsia or eclampsia, etc.
uterus. This incision is extended till the surgeon gets The operation is to be done by the most experienced
enough room to deliver the baby. personnel present preferably an obstetrician. A neonato
The incision bleeds profusely as there are plenty of large logist is also called for providing appropriate care to the
vessels in the uterine incision and the muscle walls are baby.
thicker and is not stretched and thinned out as in lower A vertical incision extending from the uterine fundus
segment. These vessels have to be ligated as soon as the to the symphysis is made by cutting through the skin
baby is delivered. and abdominal wall structures, open peritoneal cavity.
Repair of uterine incision is usually done in two Avoid fetal injury. Vertical incision is given in the uterus
layers as the thickness of upper segment is more. The cephalic to bladder until amniotic fluid is obtained or the
approximation has to be done carefully so as not to leave uterine cavity is entered. The incision can be extended till
any dead space. The first layer is a continuous layer with the fundus and infant is gently delivered. Suction of the
suture no. 1 or 1–0 chromic catgut, some people prefer mouth and nose is done and the cord is clamped and cut
using vicryl no. 1. This takes care of the inner half of the down. Prompt resuscitation (wrapping clothes in winter)
incision. is immediately done and the newborn is transferred to the
The outer layer is closed with same suture, by figure of nursery. The uterus is stitched in one layer and the same is
eight or continuous layer. While doing this the assistant done for the abdomen.
Repair of Ruptured Uterus (see Fig. 33.8) A defective scar

In this case do laparotomy and examine the tears. If it is Ruptured uterus (not amenable to repair)
a clean cut tear it is repaired with continuous locking Placenta accreta, percreta or increta (more common
stitches by 0 no. chromic catgut or polyglycolic. To obtain now due to increase in cesarean deliveries).
complete homeostasis a second layer of suturing is done.
Ragged tears can be trimmed and stitched. If the patient
Technique
has completed her family, tubal sterilization can be done. Supracervical (subtotal) hysterectomy: The body of
If the tear is ragged and too extensive, total or subtotal the uterus is removed only till this level. The remaining
hysterectomy is done according to the general condition of cervical portion is repaired by interrupted chromic
the patient. catgut sutures no. 1 or 2.
The abdomen is closed in layers and routine post Both uterus and cervix are removed in total hysterectomy.
operative care is given. Proper rest is important for smooth
convalescence. The patient must start doing household Steps
chores after 6 weeks–2 months later. After the delivery of fetus and placenta, the bleeders in
the uterine segment are ligated.
PERIPARTUM HYSTERECTOMY Clamp, cut and doubly ligate the round ligament close
to the uterus. The visceral peritoneum is opened. Clamp
(FIGS 59.8A TO C) the utero-ovarian ligament tying the ovarian vessels and
Too much time must not be wasted on deciding for hyster- fallopian tubes, cut and doubly ligate near the uterus.
ectomy as urgent action is required to prevent morbidity The bladder is mobilized in the midline and laterally.
and mortality. In the casesheet one must explain in detail This will make the bladder and ureter go down and
the discussion with the patient or their relatives about the when it is retracted, will prevent laceration or other
risks and indications of the hysterectomy. kinds of injury when clamps are applied in the cervix or
at the vaginal angles.
Indications Bilaterally ligate, cut and doubly tie the uterine vessels
Major atonic PPH not responding to conservative approach (Figs 59.9A and B), care is taken so as not to injure the
Severe cervical dysplasia, carcinoma cervix (if known ureter which passes below the uterine vessels at this
before a planned Wertheim hysterectomy is done) stage.
A B C
Figs 59.8A to C: Steps in cesarean hysterectomy. A. Line of amputation in subtotal hysterectomy; B. Dividing the round ligaments;
C. Dividing the tube and ovarian ligaments
A B
Figs 59.9A and B: A. Ligating uterine arteries; B. Dividing and ligating uterosacrals and cardinal ligaments
The uterosacral and cardinal ligaments are clamped, Diagnosis

incised and ligated, vaginal injury is repaired. A severe hemorrhage during the third stage, when the
Hemostasis is achieved.
uterus is firmly contracted. Cervical exploration is needed
The peritoneum can be sutured or can be left alone after
(Figs 59.10A to D).
doing counts of instruments and swabs. The abdomen The vagina is carefully retracted with 2 Sim’s speculum,
is then closed in layers. right angle retractor can also be used.
Subtotal hysterectomy does not appear to be associated Four sponge or ring forceps are taken.
with increased morbidity and should be considered when These forceps are applied to the lip of cervix. The
emergency peripartum hysterectomy is required. obstetrician carefully looks for any tear or bleeder while
Postoperative care: Replace the blood loss as soon as rotating the sponge holders and examining the entire
possible. Delaying replacement may cause the patient’s circumference of the cervix.
condition to deteriorate and may lead to disseminated The assistant is asked to push the uterus slightly from
intravascular coagulation (DIC). Input and output is above, and slight traction is also applied on the sponge
strictly recorded. Other postoperative measures are taken. holder. The cervix is again examined now for any tear or
In cases of uterine rupture with broad ligament hematoma, any profuse bleeding from anywhere.
the broad ligament is opened after clamping and cutting Sometimes the lateral tear can be so extensive, so as to
the round ligament. The hematoma is drained. involve the uterine vessels and tear even goes through
Inspect the uterine artery and ureter, ligate any bleeder the peritoneum. In these case wherein a lower segment
and obliterate the cavity created. or peritoneal perforation is suspected, laparotomy
should be considered.
REPAIR OF CERVICAL TEAR
Treatment
Etiology Once the tear is confirmed, the repair has to be done.
Application of forceps or vacuum and traction on an Blood is arranged if the bleeding is profuse. Informed
undilated cervix. written consent is taken before repair.
Sometimes seen in spontaneous vaginal delivery.
A cervical tear less than 2 cm, if not bleeding, needs no Sutures used for Repair
active intervention as such tears heal rapidly on their own. Chromic catgut no. 2–0 on small half circle needle is used.
‘Bucket handle’ tears occur in 2% of cases. After carefully exposing the cervix, the first stitch is placed
A B
C D
Figs 59.10A to D: Cervical exploration
above the apex of the tear in an outward direction towards Second degree: The skin, superficial muscles and deep
the repairing surgeon. muscles of the pelvic floor are involved.
The sutures are either continuous running or inter Third degree: The skin, superficial muscles, the deep
rupted, but the muscle and elastic tissue of the cervix have muscles, the anal sphincters are involved.
a tendency to retract and ordinary stitching inevitably Fourth degree: Here the anal canal is also opened up by
results in rolling in of the edges of the cervical laceration. the tear (this term is used only by some).
This might lead to poor healing. Interrupted mattress type
Repair
suture is used to achieve optimum approximation of the
Good exposure and illumination of the vagina is
edges.
required to identify the other associated vaginal tears,
extension and hematoma.
PERINEAL TEAR (SEE CHAPTER 33) Good analgesia/anesthesia, atleast a pudendal block
Conditions predisposing to perineal tear are: should be given to make the patient comfortable.
All actively bleeding vessels should be ligated properly-
Delivery of a large (macrocosmic) baby
hemostasis should be achieved, to make the repair
Malpresentation and malpositions
comfortable.
Narrow outlet
Upper vagina can be packed if required.
Faulty instrumental delivery
If the tear cannot be seen or if it is high up, a stay suture
Precipitate labor
should be placed on the lateral side or the apex should be
Spontaneous delivery without any assistance. caught if possible with forceps and slight traction should
Defect of perineal tear is classified into four degrees: be applied before attempting to place the sutures beyond
First degree: The tear is limited to vaginal and perineal its position. The repair of first and second degree perineal
skin and superficial muscles. tears are same as that of episiotomy repair.
Third Degree and Fourth Degree Tears The patient is given stool softener (e.g. liquid paraffin
The repair is done by senior faculty and not by a junior 15 mL twice a day) after the procedure.
doctor as it is very important for the patient’s future The patient is started on semisolid after 48 hours taking
wellbeing. It could lead to rectovaginal fistula or anal care to keep it low on fiber.
incontinence, if not properly stitched.
The first step is to identify and pull out the anal sphincter. POSTPARTUM HEMORRHAGE
These appear as thick muscle projecting as an irregular tag
The following operative procedures can be used to control
on one side and as a dimple on the other side. Allis forceps
PPH (also see Chapter 33).
is used to grasp the retracted end, they are crossed across
Uterine artery ligation
each other and a little finger of the assistant is inserted to
Internal (hypogastric) artery ligation
see whether tightening occurs and now sutures are taken 2
Lynch brace suture
in number with no. 1 Vicryl and held with small mosquito
Stamp sutures in the LUS
forceps. Never hold the cut ends of anal sphincter with
Selective arterial embolization.
artery forceps as it leads to ischemia and later poor healing
of the same. Uterine Artery Ligation (Fig. 59.11)
This is followed by the approximation of the muscle
wall of the rectum and anal canal. These are closed by Since most of the uterine blood is supplied by the uterine
interrupted or continuous chromic catgut no. 2-0 sutures. arteries, their ligation can control PPH especially during
The suturing above the level of perineal body, where the LSCS. The collateral supply is sufficient to maintain the
vagina and rectum lie in close approximation should be viability of the organ. It is useful in the treatment of PPH.
performed with very secure stitches without any dead
Technique
space otherwise a rectovaginal fistula may be formed. Care
should be taken to separate out by simple dissection, the A proper informed consent is taken. After anesthetizing
rectal and vaginal walls for atleast 1.5 cm above the upper the patient, the abdomen is cleaned and draped. The
limit of the tear. The rectal sutures should be made with 2-0 abdomen is opened by a subumbilical right paramedian
chromic catgut; nowadays it is not mandatory to keep the incision. The uterus is lifted upwards and opposite to the
knot on the inner side of rectum. Some doctors prefer to side to be ligated. Uterine artery is palpated at isthmus. At
take sutures through the levator ani muscle thus supporting this site pass a suture at the site of lower segment incision
the perineum further. This is followed by tightening of the around the ascending uterine artery and vein with 0 or
anal sphincter sutures, which were previously taken. These 1 no. chromic catgut. On one side a suture passing through
are closed in the form of a figure of 8. At the same time the the myometrium 2–4 cm medial to the vessel and through
assistant puts his little finger into the anal orifice to feel the the avascular area of the broad ligament. The myometrium
tightening of the sphincter. is included to fix the suture and avoiding tearing of the
After closing the rectal mucosa, the rectal muscle wall vessels. Placing the stitch close to uterus spares ureter. Tie
and vaginal wall are repaired the same way as an extended the knot. Do not cut the vessel. If it done, control bleeding.
episiotomy. As previously mentioned, one must carefully During CS the sutures are placed just below the uterine
obliterate the dead space.
Postoperative Management of Third Degree

and Fourth Degree Tear Repair
The most important part of the treatment which influences
the outcome is the postoperative management.
The patient is kept on only fluid diet, which is low on the
residue for 48 hours.

The patient is given adequate antibiotic, antiinflam
matory and analgesic cover.

Perineal care, sitz bath and infrared rays are used to
decrease the tissue edema and increase the vascular

supply to the affected area. Fig. 59.11: Uterine and utero-ovarian artery ligation
incision under the bladder flap. Observe for amount of Technique

bleeding. Mostly the abdomen is opened in order to surgically control
Sometimes bilateral utero-ovarian artery ligation PPH. The round ligament is cut between two clamps. The
is done with chromic catgut no. 0 or 1 near the point of peritoneum in between is separated and incised upwards
anastomoses between the ovarian artery and the ascending and downward. The area is cleared by blunt dissection. The
uterine artery at the utero-ovarian ligament (stepwise next step is to identify the ureter and then look for the site
ligation). The vessels are ligated but not divided. The uterus of common iliac artery bifurcation. Identify the internal
becomes blanched with a pink hue and bleeding subsides. iliac artery. It is isolated and doubly ligated by silk at its
Recanalization takes place in most cases. Subsequent origin from the common iliac artery. It is not cut but only
menstruation and pregnancy are unaffected. Inadvertent ligated. Adjacent veins must be protected from tearing.
ligation of the ureters should be avoided. Blood flow distally (to the uterus, cervix, upper vagina) is
The abdomen is closed after ensuring that there is no not occluded but pulse pressure is sufficiently reduced to
abnormal bleeding. allow hemostasis to occur by in situ thrombosis.
Subsequent pregnancies are not compromised.
Postoperative Care
Replace blood as early as possible to ensure better recovery Lynch Brace Suture (Figs 59.13A to C)
and prevention of DIC. Input and output documentation It is used to compress the uterus in cases of diffuse bleeding
is very important. in PPH. It avoids hysterectomy (see Fig. 33.4).
Internal (Hypogastric) Artery Ligation (Fig. 59.12) Technique

Indication: To control PPH. After proper counseling and informed consent a
laparotomy is done. Uterus is opened by lower segment
transverse incision. The bladder is pushed down. The
uterus is brought out of the abdominal incision. If by
compressing the uterus manually the bleeding is reduced,
this method will succeed. Suture used is chromic catgut
no. 2 needle is inserted 3 cm from right lower edge
3 cm from right edge and come out 3 cm above the
incision. The needle is now passed posteriorly to include
uterine wall posteriorly. Compress the uterine walls
manually and the sutures are tightened. The suture is now
passed posteriorly on the left side over the fundus of the
uterus and tied similarly. The uterine incision in the lower
segment is closed in layers as in CS.
Stamp Sutures in the Lower Uterine Segment

These sutures help stop bleeding.
Selective Arterial Embolization

It is a therapeutic option in obstetric hemorrhage. A
Fig. 59.12: Internal artery ligation close working relationship between the obstetricians and
A B C
Figs 59.13A to C: Lynch brace sutures

radiologist is needed. The role of the obstetrician is to specific complications occur is less than 10% of cases. A
identify the patient at high-risk life-threatening bleeding. more serious complication (though uncommon) is reflux
of embolic material to nontargeted pelvic structures.
Technique Prophylactic catheterization of anterior division of
Under local anesthesia a catheter is directed to the aorta internal iliac artery is done under fluoroscopy in less than
and to the bleeding vessel under fluoroscopy guidance. 10 minutes. The radiation exposure is of 2 rads per minute.
This technique can be used instead of, or after failure of In antepartum hemorrhage if the fetus is not delivered,
hysterectomy or ligation of the internal iliac artery or the fetal risk as compared to the risk of life-threatening
uterine artery for the treatment of pelvic hemorrhage. bleeding is explained to the patient.
Under radiologic angiographic control, a polyethylene
catheter is introduced into the aorta via the femoral artery. Bladder Injury and its Repair
Each internal iliac artery is catheterized and occluded with The incidence of bladder injury at the time of cesarean
small (2–3 mm) fragments of gelfoam. Other materials, operation is 1.4 per 1000. The vesicocervical space is
which can be used are polyvinyl alcohol, glue, or coils. normally filled with loose areolar tissue, which allows the
In situations of pelvic hemorrhage other than that are bladder to expand and empty for its ordinary function.
caused by uterine atony the specific bleeding vessel can Still the bladder separation from the uterus during CS
be identified and selectively embolized. The procedure should be done with careful sharp dissection with scissors,
can be carried out in less than 1 hour but requires trained particularly in patients who have undergone previous
and experienced interventionists. The procedure imposes CS. Blunt dissection may result in inadvertent injury. To
little morbidity and no mortality. It has an advantage confirm the injury during surgery methylene blue dye or
over internal iliac ligation in that the distal blood vessels sterile milk can be filled through a urethral catheter to
are occluded, so that bleeding from reconstituted, distal delineate the area.
vessels are rare. In addition, the uterus is retained and To rule out injury to the ureteric opening look for the
further child bearing is possible. extend of injury in relation to the trigone of urinary
The embolization material is sterile, nonantigenic and bladder.
remains in vessels for 20–50 days and forms the fibrin Urinary bladder is separated from the LUS by sharp
mesh framework upon which a blood clot may develop. Its (scissors) or blunt (sponge on holder) dissection.
immediate effect is to obstruct the distal artery or arteriole Free about 2 cm of urinary bladder tissue around the
and reduce the pulse pressure in the bleeding vessel thus tear.
allowing clot formation and cessation of bleeding. Repair is done with a no. 3-0 delayed absorbable suture
Complications are minor and transient examples as follows:
being pelvic pain and fever because of local ischemia and • The bladder mucosa and bladder muscle is sutured
cellulitis. in continuous stitches.
• The outer layer is inverted over the first layer.
Advantage over Surgical Methods • Trigone area is not to be sutures.
Anesthetic risk is less. Bladder peritoneum may be sutured on it. A watertight
Surgical risk is reduced. closure is tested by filling 200 cc of methylene blue dye. If a
As a specific vessel is identified and selectively occluded, leak is present and sutures are reinserted. Again test till no
hysterectomy can be avoided. leak is seen. Postoperatively an indwelling transurethral
catheter should be left in place for 7–10 days. Encourage
Indications the woman to ingest plenty of liquids. Tissue healing
Placenta accreta is enhanced by the accurate placement of the correct
PPH from atony or injury number of sutures that will approximate the bladder
Bleeding from pelvic vessel laceration wall correctly and not interfere with its blood supply.
Post cesarean hemorrhage Continuous drainage is the mainstay in healing. One
Bleeding from extrauterine pregnancy (cervical preg hourly urine output chart is essential. The bladder is kept
nancy, abdominal pregnancy, etc.) empty so that it heals. Ampicillin, gentamycin and metron-
In the absence of coagulopathy, the success rate of idazole are to be given postoperatively. Urine examination
arterial embolization is greater than 90%. Procedure for microscopy and culture is done on alternate days and
appropriate antibiotics may be given. Never apply a clamp precautions. Two fingers (lubricated with antiseptic) are
on the catheter. The bladder will distend and the stitch line introduced into the vagina gently, the status of the cervix,
will open up. position and presentation of the fetus are confirmed and
pelvic assessment is done. The index finger is advanced
Cervical Encirclage through the cervical canal beyond the internal os. A long
This procedure is used in cases of incompetent os. The artery forceps (Kocher’s) is introduced with blades closed
diagnosis can be made in between pregnancies by Hager along the palmar aspect of the fingers facing upwards.
test or ultrasound examination. One can also look for After reaching the membranes the blades of Kocher’s are
cervical incompetence in a pregnant woman with repeated opened by the free hand and membranes are pinched with
second trimester abortions by ultrasound examination. the tip of the instrument and gently twisted. One can see
The operation can be carried out in the non pregnant state the liquor coming out at this stage. The color, consistency
by a per abdominal operation otherwise, during pregnancy and amount of liquor is noted. If the presenting part is not
the per vaginal route is preferred. engaged, an assistant fixes the presenting part to prevent
cord prolapse and excessive flow of liquor. The hand with
OTHER PROCEDURES USED IN the instrument is removed. FHS are noted immediately
OBSTETRIC PRACTICE after the procedure. A sterile pad is applied.
Amniotomy or Artificial Rupture of Complications
Membranes (ARM) Cord prolapse
It is also referred to as surgical induction and is commonly Sudden decompression of the uterus can lead to
done to induce or augment labor. The other indications are: abruptio placentae in cases of polyhydramnios
Elective amniotomy to hasten spontaneous labor or
Injury to pelvic tissues or the presenting part
detect meconium Rupture of vasa previa leading to fetal blood loss
Abruptio placentae (to reduce intrauterine pressure
Amnionitis
and reduce bleeding) Rarely amniotic fluid embolism.
Polyhydramnios
Severe pre-eclampsia Urethral Catheterization

Eclampsia
It is an important step in any obstetric examination and
Internal electronic FHR monitoring.
procedure. It helps in draining the bladder continuously while
Intrauterine assessment of contractions when labor has
performing all abdominal procedures and vaginal surgeries. It
been unsatisfactory.
also facilitates filling of the bladder as required for:
Contraindications Pelvic ultrasound
Cord prolapse cases till cesarean section is performed

Intrauterine death (IUD) of the fetus
To check for bladder trauma during surgeries
Cord presentation.
For cystoscopy, etc.
Prerequisites Owing to the anatomical location and size of the

Soft, effaced cervix admitting at least one finger. It is urethra (4 cm) the urinary system in females is more prone
effective if the cervix is favorable and the presenting to infections. To prevent infections catheterization is to
part is low in the pelvis. ARM causes separation of the be done with all aseptic precautions and with the utmost
membranes, release of prostaglandins further enhancing care. Urinary catheters are:
he uterine activity and thus augmenting labor. Red rubber catheter—for short duration use
Latex self retaining catheter (Foley’s catheter)—for

Procedure longer duration.
Hear FHS before ARM informed written consent is taken.
The procedure requires no anesthesia. It can be done Procedure
during routine per vaginal examination while following The patient, if conscious, is asked to lie down in the dorsal
strict aseptic measures. lithotomy position. The surgeon wears a mask and a
The patient is placed in lithotomy position. The part is cap, scrubs the hands thoroughly and puts on gloves (all
cleaned and draped. The operator must follow all universal universal precautions must be followed). The patient is
informed about the procedure. The perineum is cleaned

from medial to lateral side and up to mid thighs on both
sides and draped. The patency of catheter is to be checked,
(if it is a red rubber catheter). The urethra is exposed
gently with the left hand. The external urethral meatus
is cleaned from above downwards with dettol/savlon
swabs. The catheter is held in the right hand at least 5 to 6
cm away from the tip. The catheter is coated in xylocaine
jelly (local anesthetic). Take care not to touch the tip
of the catheter with your hands or the thighs or vagina.
The catheter is introduce slowly through the urethra and Fig. 59.14: Dinoprostone instillation
advanced further till urine starts flowing out. Wait till
urine stops flowing. Once there is no urine seen coming
out, the catheter is further advanced slightly and left there. Relative Contraindications
If it is a self retaining catheter, the other end is connected Patient with hypersensitivity to prostaglandins
to the collecting bag and the balloon is inflated with
Patient with previous uterine scars
20–30 mL of fluid and the catheter is gently pulled out till
Grand multipara
the obstruction of the internal urethral meatus is felt. If it
Patients with ruptured membranes
is a red rubber catheter the other end is fixed to the medial
Patient with asthma
aspect of the thigh with a strip of leukoplast.
Patient with glaucoma or increased intraocular pressure.
Red rubber catheter can be removed immediately after
the operative procedure is over. For example following a Absolute Contraindications
cesarean section without complications. The self retaining
catheter is to be kept in place for about 2–21 days depending Patient with major degree of CPD.
upon the operation performed, e.g. bladder repair along with Patient with acute fetal distress (compromise) with a
CS, hysterectomy for uterine rupture. In retroverted gravid closed cervix.
uterus with urinary retention the self retaining catheter Patients with transverse lie or non vertex presentation.
is to be kept as a therapeutic measure in first trimester Patients with difficult or traumatic labor.
of pregnancy and can be removed once retroversion is Where vaginal delivery is a contraindication.
corrected which may need about 2 weeks time.
Prophylactic urinary antibiotics are to be started, e.g. Adverse Reactions
ampicillin, cloxacillin, norfloxacin. No serious effects are seen. Some patients may complain
In self retaining catheterization, the patency of the of nausea, vomiting and diarrhea.
catheter is to be checked periodically. If it is blocked
then the catheter should be changed. Dosage
The periurethral area is to be kept clean by washing. It comes in a packaging containing 0.5 mg dinoprostone
Urine sample is sent for routine examination and per 2.5 mL in a prefilled syringe with a plastic catheter for
culture after 48 hours or earlier if indicated. endocervical application.
If prolonged catheterization is required the patient is
asked to drink plenty of liquids and a urinary alkalinizer Prerequisites

is prescribed (if allowed orally). Confirm the gestational age
Confirm the presentation
Dinoprostone Gel Instillation (Fig. 59.14)

Confirm the indication

Indications Rule out all contraindications
It is used for preinduction cervical ripening and cervical FHS to be auscultated per abdominally.
dilatation in patients with term pregnancy specially in
patients with poor Bishop score. Steps
It is used prior to MTP, dilatation and evacuation (D&E) The patient put in lithotomy position after evacuating
or other procedures, which require dilatation of the the urinary bladder.
cervix (for cervical softening). Aseptic scrubbing and draping of perineum is done.
The dinoprostone gel syringe is to be assembled as arrange cross match blood (2 units). Call the anesthetist
shown in Figures 59.15 and 59.16 after the surgeon and obtain consent of the patient and her relatives. The
scrubs and wear sterile gloves. procedure can be performed under epidural if it is in situ.
A Cusco’s speculum is inserted into the vagina and the Halothane assists by relaxing the uterus. With the patient in
external os is identified. the lithotomy position, using aseptic technique, place one
The gel with the catheter is inserted into the endo hand on the abdomen to stabilize the uterus. Introduce
cervical canal and the drug is deposited there. In some
the second hand into the uterus. The fingers must follow
cases, like in patients with ruptured membrane, the gel
the cord, which assists in finding the placenta. Once cord
is deposited in posterior vaginal fornices. The speculum
attachment to the placenta is reached the periphery of the
is taken out, and the fetal heart is auscultated to rule
out fetal distess. The uterine activity, cervical dilatation placenta is approached. The operator must gently work
and effacement is monitored to detect any hypertonic round the placental edge separating it from the uterus
uterine contractions. using the ulnar border of the hand. When separated it
The patient is asked to lie on the couch for 30 minutes. should be possible to remove it by cord traction. Once
removed check that it is complete and no uterine damage
Manual Removal of Placenta has occurred. Give oxytoxic drugs and start antibiotics.
(Figs 59.17A and B) Rarely, the placenta will not separate (placenta accreta
Informed written consent is taken. This operation is or percreta) and hysterectomy may be necessary—by a
carried out in the operation theater (OT). Set up IV line and senior obstetrician if bleeding.
Fig. 59.15: Dinoprostone gel kit Fig. 59.16: Package
A B
Figs 59.17A and B: Manual removal of placenta

A B C
Figs 59.18A to C: Venesection
Venesection (Figs 59.18A to C)

It is required in moribund patients:
Palpate and locate the saphenous vein
Inject local anesthetic around it
Incise trasversly (2 cm)
Expose the vein
Insert sutures loosely under proximal and distal end of
the vein and tie distal suture

Make a small incision in vein
Expose the vein and insert cannula
Tie upper suture to secure cannula
Close the wound
Secure cannula with suture.
Indications
To collect blood
To inject medications
To give transfusions/infusions. Fig. 59.19: Technique of venepuncture
Venepuncture of the vein into the subcutaneous tissues with the bevel
Sites: Median cubital vein in the cubital fossa is commonly facing upwards. The needle is advanced till it pierces the
used for collection of blood and giving medications/ vein (felt as a characteristic ‘give in’). As counter puncture
infusions (Fig. 59.19). can occur as blood comes into the syringe do not push
If the superficial veins are collapsed then femoral vein is the needle any further. Pull the piston out and collect the
punctured 1 cm distal to the inguinal ligament. The femoral required amount of blood. Ask the patient to loosen the fist
artery is first felt at the midpoint of the inguinal ligament and and remove the tourniquet. Take out the needle and press
the needle can be introduced medial to it. Keep all the vials for the site with spirit swab for one minute. The swab is to be
blood collection or the medicine to be given, ready (Fig. 59.20). thrown in yellow/red bag.
The doctor must wash his/her hands, put on sterile For giving IV medication, rotate the needle and syringe
gloves, clean the skin with spirit. For making the vein by 180° so that the bevel faces opposite to the operator and
prominent tie a rubber tourniquet proximal to the vene then inject the drug. If it is to be given continuously either
puncture site or ask an assistant to compress at that point in the infusion pump, or IV line, hang the bottle by the
with a hand. Ask the patient to close the fist. Pull the skin at tripod drip stand. The exact rate of drug therapy or infusion
the puncture site and then introduce the needle by the side is set and written in the instructions in the casesheet.
Increased venous return

Increased intrathoracic pressure
Decreased ability of the right heart to move blood.
Causes of decreased CVP include the following:

Inadequate circulating blood volume (hypovolemia)
Decreased intrathoracic pressure
Placement of the transducer or zero level of the water
manometer above the patient’s right atrial level

Air bubbles or leaks in the pressure line.
CVP Catheters and Insertion Sites

CVP catheters (single-lumen or multi-lumen) are positi
oned in the superior vena cava (Fig. 59.21) via the
subclavian or internal and external jugular or antecubital
veins (and rarely via general veins). The internal jugular
vein has become the most popular site because of the ease
of insertion, low risk of pneumothorax and good visibility
if hematomas forms.
Care of CVP Line

Insert CVP catheters under all aseptic conditions. Migration
of bacteria from the skin surface along the subcutaneous
tract to the blood stream has been designated as the
primary mechanism in the pathogenesis of catheter–
related septicemia. A sterile pad is put and dressed. It is to
be assessed every 2–4 hours and as necessary and should
Fig. 59.20: Femoral vein puncture
be replaced when it is wet, loose or soiled.
Complications CVP Monitoring

Counter puncture and hematoma formation CVP may be obtained using a transducer system or a water
Thrombophlebitis manometer. Water manometer measures pressure in centi
Extravasation meters of water whereas a transducer shows pressure in
Inadvertent injection into an artery mm of mercury (mmHg).
Air embolism if the fluid bottle is empty. For measuring CVP using a water manometer system,
proceed in steps, as described below:
CENTRAL VENOUS PRESSURE (CVP) Wash hands
Confirm the position of CVP catheter—for confirmation,

It is the pressure of blood in right atrium or the superior look for the following:
vena cava, where the blood is returned to the heart from • Free–flowing IV fluid
the venous system. Because the tricuspid valve is opened • Ability to easily aspirate a blood sample from the
between the right atrium and the right ventricle during CVP catheter
diastole (ventricular filling), right atrial pressure or CVP • A rapidly falling water column when the pressure is
also represents the right ventricle end-diastolic pressure obtained
(RVEDP) and reflects preload for the right ventricle. • Oscillations at the top of the water column accruing
with respiration
Clinical Significance • X-ray verification of the tip of the catheter (if possible).
A balance between hearts ability to pump blood from right Position the bed so that the patient is supine with the
atrium and returned blood amount to the heart regulates head of the bed flat or elevated no more than 60°.
CVP. Normal CVP is between 3–12 cm H2O. CVP may be Locate the atrial reference point. It is at the mid-chest
elevated under the following conditions: level at the fourth intercostal space (Fig. 59.21B).
A B C
Figs 59.21A to C: Central venous pressure (CVP)
Use a carpenter’s level or spirit level to match the zero the catheter has become occluded or malpositioned or the
level of the manometer with the atrial reference point. patient has developed a catheter—related infection. While
Turn the water manometer stopcock open to the IV fluid removing the CVP line, following steps should be followed.
bag and open the IV tubing roller clamp so that fluid Remove the catheter dressing and discard.
flows from the IV fluid bag into the water manometer Change gloves, clean the area with alcohol or povidone-
(Fig. 59.21A). iodine.

Close the roller clamp on the IV tubing. Turn the water Ensure that the head of the bed is flat, remove the pillow
manometer stopcock open to the patient and closed to and have the patient turn his/her head away from the
the IV solution (Fig. 59.21B). catheter.
Measure the CVP at end-expiration. Carefully cut the suture and pull the suture through the
Turn the water manometer stopcock open to the IV skin.
fluid bag and to the patient (Fig. 59.21C). Grasp the catheter by hand and remove the cather
Wash hands. slowly. With other hand, quickly apply pressure over
the puncture site with a sterile gauge.
CVP Line Removal Maintain pressure for 2–5 minutes until hemostasis has
Central venous catheters are removed when therapy is been achieved. Apply an occlusive, sterile dressing over
completed, or a mechanical malfunction has occured, or the site.
1. What do you understand by the term female sterilization?
2. Explain the types of cesarean section.
3. What are the conditions of perineal tear?
3. Fill in the blanks.
i. Defect of perineal tear is classified into ____________ degrees.
ii. ____________ method was in vogue in the 1970s.
iii. ____________ is used to compress the uterus in cases of diffuse bleeding in PPH.
iv. Halothane assists by ____________ the uterus.
v. CVP is the pressure of blood in ____________ or the superior vena cava.
60
Rahul Manchanda, SK Sen, Sudha Salhan
Destructive Operations
have failed to deliver them. At this stage, the problem for

INTRODUCTION the clinicians is not to save the fetus, which is mostly dead
We firmly believe that destructive operations have a or badly damaged, but how best to save the mother after
definite place, especially in developing countries, like emptying the uterus quickly, preferably by vaginal route.
India, where a lot of areas are still untouched by the It may also happen that patients and her relatives may not
advanced medical and surgical practice, that we take for give consent for delivery of the dead fetus by CS. This may
granted in developed countries. also be due to religious beliefs of some communities. The
obstetrician, in such a case, has no choice but to deliver the
DEFINITION fetus through the vaginal route by destructive operations.
Most of these cases being grossly infected, maternal
These are defined as a group of operations that aim at morbidity and mortality is greater following CS than
reducing the size of the head, shoulder, girdle or trunk of following vaginal delivery by destructive operations, as
the dead fetus in order to allow for its vaginal delivery. observed by many obstetricians. They are safer for mothers
as the general peritoneum is not contaminated with uterine
SCOPE OF DESTRUCTIVE OPERATIONS contents, which is unavoidable if cesarean delivery is
The scope of destructive operations has been narrowed undertaken.
down following better obstetric care to the expectant Hence, the indications for destructive operations are as
mothers through availability of latest diagnostic modalities, follows:
superior antibiotics and anesthetic drugs, greater If the labor is prolonged and neglected and the fetus is
availability and use of transfusion facilities and better dead.

operative technique. These have indeed tilted the balance Skill staff is not available to carry out CS immediately.
towards cesarean delivery in difficult and neglected cases Risk of overwhelming infection
of obstructed labor, especially in developed countries. The patient or relatives insist on a vaginal delivery, and
However, there still is and will be occasions where do not give consent for CS.
destructive operations will be considered as the procedure There will be no skilled supervision in the subsequent
of choice because it simplifies vaginal delivery, minimizes pregnancy hence, she does not want a cesarean.
maternal trauma and obviates necessity for cesarean Decompression of gross hydrocephalus.
section (CS) with all its hazards in cases of neglected
obstructive labor particularly in remote and rural areas.
TYPES OF DESTRUCTIVE OPERATIONS
Obstructed labor is still prevalent amongst rural mothers
in developing countries. Anemic, malnourished mothers Decompression of hydrocephalic head
with frequent coexisting toxemia, and evidences of sepsis, Craniotomy
are rushed to distant hospitals in a very poor condition. Most Decapitation
of them are unbooked cases, brought in late labor several Evisceration
hours after the rupture of membranes, infected and in a Cleidotomy
state of threatened uterine rupture after unskilled attendants Spondylotomy.
First three are more commonly required and these are the septa and brain substance. Kocher’s forceps are used to
emphasized here. clamp the lip of the incised scalp. The legs of the patient are
removed from the stirrups. Bandages are passed through
Decompression of Hydrocephalic Head the two Kocher’s forceps and the other end is attached to a
In a hydrocephalic fetus presenting by head, cerebrospinal hanging weight. Some surgeons use Simpson’s perforator
fluid (CSF) is drained (before full dilatation) by the most for entering the skull.
accessible presenting part per vaginam. At the fontanel a The fetus is easily delivered. Crushing instruments like
needle can do the job. But at any other place craniotomy cranioclast and cephalotribe are obsolete now. The urinary
is needed. If the fetus presents by breech, the CSF can be bladder is continuously drained for 5–10 days. Antibiotics,
drained via the spinal canal. If spina bifida is present, then mostly triple (ampicillin, gentamycin and metrogyl) are
a needle or catheter introduced there, will help in draining given.
the CSF. Decompression of hydrocephalus can be done Debdas’s cranial perforator, which is like a mechanical
trans abdominally after emptying the bladder. Once the drill, can be used and is less traumatic and safer to use and
head collapses it can be delivered per vaginally, after the has the added advantage of the entry point need not be at
cervix is fully dilated. the fontanel.
After coming head (breech presentation) is perforated
Craniotomy through the occiput. The perforator is passed through
It literally means opening of the cranium (head) of the a subcutaneous tunnel. The dead fetus’s body is pulled
fetus. This is done in order to decompress the head and down by the assistant. An incision is given in the skin over
diminish the bulk of the head of the fetus (by removing the cervical spine. The sharp pointed scissors or perforator
accumulated fluid and brain matter) with the objective are passed to perforate the skull. Septa are broken and
to permit easy delivery of the dead fetus through the brain tissue is extruded, reducing the size of the head.
parturient canal. This operation is still being practiced and
is one of the easiest to perform. It is used for delivery of
Evisceration
a dead fetus mostly in obstructed labor. It is difficult and In this operation, the dead fetus’s abdomen or thorax or
dangerous if the head is more than three-fifth above the both are opened up, usually by an embryotomy scissors,
pelvic brim or is mobile. Hence, it is contraindicated in at the most accessible site and the viscera of the fetus are
such conditions. removed piecemeal so that the fetus may diminish in bulk
A simple and safe method of craniotomy needs the and be delivered easily by vaginal route. In all operations,
following instruments: the operators’ non-dominant hand is introduced into the
Sim’s speculum birth canal and protects the maternal tissues and guides
Sharp pointed scissors the dominant hand, which performs the actual operation.
Kocher’s forceps The overlying skin of the most-dependant part is
Sponge holder incised with scissors first. This is followed by the division
Swabs, lotion. of the ribs of the chest wall or the back, or the muscles
After confirming intrauterine death and excluding of the abdominal wall (as the case may be) by the same
rupture of the uterus, the patient is given a suitable scissors. Thus the chest cavity or the abdominal cavity is
sedation, and put in the lithotomy position. The perineum opened and then the organs are delivered out piecemeal,
is cleaned and draped. The urinary bladder is catheterized. slowly and carefully. For an experienced operator, it is
The fetal caput is incised (3 cm) in the posterior aspect by not difficult to do the procedure blindly by assessing the
the scissors. The index finger is inserted in this incision to condition following careful vaginal examination and
trace the posterior fornix. The left hand finger is kept there having a clear mental picture about the status of the lower
and with the other hand the scissors are directed along the uterine segment and the fetus inside.
palmer surface of the left hand till the scissors touches the
fontanel. The scissors is pushed through the fontanel into Decapitation (Fig. 60.1)
the skull. It is opened in one direction, then closed and It can be performed when the head gets stuck in cases of
rotated through 90° and opened again (cruciate opening breech or impacted shoulder presentation in a dead fetus
in the skull). The closed scissors or perforator is inserted not responding to other maneuvers. This procedure can also
deep into the skull, opened and briskly rotated to break up be practiced in neglected transverse lie with hand prolapse.
Destructive Operations 561
Fig. 60.1: Decapitation Fig. 60.2: Blond-Heidler Decapitation Saw
The patient is put in the lithotomy position. The perineum is sufficient alone to deliver a dead fetus. In this operation
is cleaned and draped. A very gentle pelvic examination enlargement of the pelvis by dividing the symphysis pubis
is done to locate the neck. The arm is pulled down by an is done.
assistant. In a small fetus the neck can be easily severed by
stout scissors. In a slightly bigger fetus the Blond-Heidler INDICATIONS
Decapitation Saw is safest (Fig. 60.2). The saw is threaded
Hydrocephalus where the fetus is not salvageable
around the neck to severe it. The trunk is delivered and the
Obstructed labor with a dead fetus
head is grasped with vulsellum and delivered.
Shoulder dystocia with a dead baby
In most destructive operations, two Sim’s speculums,
Transverse lie with a dead fetus
one anteriorly and one posteriorly, should be used for
Conjoined twins (non-viable)/fetal monstrosities
better exposure of parts. This will also protect the urinary
Fetal ascites
bladder in front and the rectum behind. Hydrothorax
Cystic kidneys/liver ailments
Cleidotomy Sacrococcygeal teratoma
It involves cutting of the clavicles in order to decrease the Abdominal/thoracic tumors.
inter shoulder distance in cases of shoulder dystocia to
deliver the dead fetus. A stout scissors first cuts the most PREREQUISITES
accessible clavicle.
It is probably the only destructive operation which may The fetus must be dead or grossly malformed, with the
still be acceptable in live babies in very rare circumstances. malformations being incompatible with life.
The pelvis should not be grossly contracted. True
This is justified because though it is a traumatic operation,
conjugate (conjugate vera) should be more than
the clavicles heal very well in children and at times this
5.5 cm. The maternal pelvis must have sufficient room to
procedure can be life-saving to both the mother and her
accommodate the destructive instruments, permitting
fetus.
their application and manipulation and allowing
extraction of the body of the fetus.
Spondylotomy Cervix more than three-fourth dilated (the more dilated
It involves fracturing and cutting the spine and may be used the cervix, the safer the operation). However, in cases
in conjunction with any of the other operations in order of gross hydrocephalus, the uterus ruptures before full
to deliver the dead fetus. It is practiced with evisceration dilatation of cervix.
in cases where the back is the presenting part in a case of There should not be any pathological lesion of the
transverse lie. cervix (carcinoma).
Symphysiotomy can be combined with a destructive There should not be any obstructing pelvic tumor
operation to increase the pelvic dimensions. Sometimes it (fibromyoma, ovarian tumor)
Figs 60.3A to G: A. Sim’s vaginal speculum; B. Simpson’s perforator; C. Embryotomy scissors; D. Decapitation hook; E. Sharp-pointed,
straight scissors; F. Vulsellum forceps; G. Sponge holding forceps
Do proper explanation of the procedure to the patient be foul smelling. The bladder is often distended. So, the
and her relatives. A written consent for the operation is following steps need to be taken:
taken from the patient and her relatives. A general physical examination is to be done to assess
the condition of the patient (pulse, BP, respiratory

INSTRUMENTS rate, temperature, pallor, edema, cyanosis, chest and
cardiovascular system). A central venous pressure (CVP)
Most of the textbooks on instruments give a detailed line may be put in.
description of the heavy and unsightly instruments that Per abdominal examination (to rule out obstruction) is
have been described by pioneers. We propagate doing
carried out and ruptured uterus is excluded.
these very operations with regular instruments being used
Resuscitation of the patient with intravenous (IV) fluids
in surgery, a list of which is given below (Figs 60.3A to G).
is done to correct dehydration, electrolyte imbalance
Sim’s vaginal speculum
and acidosis by 5–10% dextrose followed by dextrose
Simpson’s perforator
Embryotomy scissors
saline and ringer lactate solution.
Sedation is given by injection of morphine sulphate
Decapitation hook
Sharp-pointed straight scissors

15 mg intramuscularly (IM) or pethidine and phenergan.
Broad spectrum IV antibiotics are started after taking
Vulsellum forceps
Sponge holding forceps.

samples for vaginal swabs and blood culture, if such
facilities are available.
The urinary bladder is emptied, by Foley’s indwelling
PREOPERATIVE MEASURES catheter.
Preoperative assessment and resuscitation is to be done. An adequate amount of compatible blood is arranged.
Many patients who are referred to tertiary hospitals may be Per vaginal examination is done for proper diagnosis
in labor for 2 or more days. Depending on the duration of and to confirm the feasibility of a destructive operation,
the labor, the patient may be dehydrated, anxious, febrile, e.g. cervix being dilated greater than or equal to 7 cm.
tachycardiac, ketotic and exhausted. The fetal heart sound Ryle’s tube aspiration and instillation of an antacid is done.
is not heard. The vagina and cervix may be edematous; Laboratory investigations—hemoglobin, blood group,
the vagina may be dry and hot. Liquor, if still present, may urine routine, microscopy examination and ketones
Destructive Operations 563
is carried out. Vaginal swab and blood for culture and • Hypovolemic
sensitivity are taken as mentioned. • Neurogenic
Ultrasonography is carried out to confirm fetal status (if Puerperal sepsis
available and possible). Subinvolution of the uterus
Prolonged ill health.
Anesthesia
In less traumatic operations like hydrocephalic drainage, CONCLUSION
a pethidine and phenergan cocktail is supplemented, if
Destructive operations are not as difficult as usually
required by midazolam IV and this may be adequate to
thought of, but have a definitive learning curve.
carry out the procedure unhindered and comfortably.
Whenever such operations are performed it is wise to
In order to relax a tonically contracted uterus, general
be prepared for the treatment of shock, postpartum
anesthesia is always preferred. A general anesthetic is also
hemorrhage and puerperal infection.
preferred in evisceration. A skillful anesthetist makes the
Maternal tissue must be carefully protected from the
operators work easy.
instruments and fetal bones while extraction.
Routine exploration of the uterus following any
COMPLICATIONS OF DESTRUCTIVE destructive operation is mandatory to detect rupture of
OPERATION uterus. The cervix, vagina and perineum should also be
When the cases are carefully selected, complications carefully examined to detect any injury.
A self-retaining catheter can be kept in situ for 7–14 days
should be very few. The genital tract and rectum are to
be carefully examined after the procedure. A continuous to prevent the development of a VVF in severe cases due
urinary bladder drainage for 7–14 days is very important. to pressure necrosis.
A written consent for destructive operations should be
Nevertheless, a few complication can occur.
Vaginal and cervical lacerations taken after explaining exact nature of the operation.
Uterine rupture (generally lower uterine segment) Like the art of breech delivery, the authors feel this art is
Injury to adjacent viscera: also dying and needs to be kept alive within perspective.
• Urinary bladder—vesicovaginal fistula (VVF) formation It should be a part of every obstetrician’s armoury. One
• Rectal wall—rectovaginal fistula (RVF) formation must not forget those procedures that have stood us
Postpartum hemorrhage in good stead in tough conditions saving many lives
• Traumatic (ironically and despite the name given to them).
• Atonic Avoiding a CS for obstructed labor and a dead baby
Shock (unless vaginal delivery is dangerous) should be the aim of
• Hemorrhagic all obstetricians.
1. True/False:
i. Craniotomy is a type of destructive disorder.
ii. Resuscitation of the patient is done with IV fluid to correct dehydration and acidosis.
2. Fill in the blanks.
i. ____________ is supplemented in hydrophobic drainage.
ii. Compression of hydrocephalus head is done by ____________.
61
PK Verma, Ruchi Kapoor
Interpreting
Arterial Blood Gas Sample
INTRODUCTION of partial pressure of oxygen (PaO2) when patient inhales

room air is over 90 mm Hg; normal partial pressure of
Arterial blood gas (ABG) analysis is a single most useful carbon dioxide (PaCO2) value: 35–45 mm Hg.
laboratory test for wellbeing as it can be safely and easily
obtained and furnishes rapid and accurate information
on how well the lungs and kidneys are working. Moreover, pH SCALE
clinical signs of tachypnea and cyanosis are not objective The concentration of hydrogen ions (H+) in blood is expressed
and do not give accurate assessment of the partial pressures in terms pH which is the logarithmic function of H+ ions. The
of carbon dioxide and the oxygen content of blood for normal pH of an arterial blood sample is between 7.36 and
which mandates the accurate measurement of the partial 7.44 and this is equivalent to a H+ ion concentration of 44–
pressure of oxygen. The ABG provides the most important 36 nmol/L respectively. The pH values of 6.8–7.8 is the pH
way of making a diagnostic assessment of the nature, range usually considered compatible with life.
progression, and severity of a respiratory disturbance.
It is important to have a clear understanding of what is Acidemia
meant by the commonly used terms in blood gas analysis
Acidemia refers to an arterial pH below 7.35.
and acid-base balance.
Alkalemia
PARTIAL PRESSURE Alkalemia refers to an arterial pH above 7.45.
The pressure of any gas is the sum total of the molecules
in the gas colliding with the walls of the container. If the Acidosis
gas is a mixture (such as air) then the total pressure is the A physiologic process that occurs alone leads to an acidosis.
sum of all the individual partial pressures of the gases. The Common clinical causes include low-perfusion states
pressure of individual gas is known as partial pressure. (metabolic acidosis) and hypoventilation (respiratory
When a gas mixture is in contact with a liquid, some of acidosis).
the gas will dissolve in the liquid and the volume that
dissolves depends on the partial pressure exerted by the Alkalosis
the individual gas molecules into the liquid and the ease
A physiologic process that occurring alone leads to an
of the individual gas molecules to get into the liquid (that
is, its solubility). In time, provided the gas and solution alkalemia. Common clinical causes include diuretic therapy
are left undisturbed, an equilibrium will develop whereby (metabolic alkalosis) and hyperventilation (respiratory
the number of gas molecules leaving the liquid will be alkalosis).
equal to the number entering the liquid. At this point, the
partial pressure of each individual gas molecule within Buffers
the liquid will be equal to the partial pressure of the same A buffer is defined as a compound which opposes changes
gas molecule in contact with the liquid. Partial pressures in H+. Physiological buffers consist of a weak acid in equili-
are measured in either mm Hg or kPa. The normal values brium with its conjugate base:
Interpreting Arterial Blood Gas Sample 565
Acid H+ Conjugate base– + H+ Heparin: A heparinized syringe (to prevent the sample
Ka = ([H+] × [Conjugate base–])/[acid]. from clotting) is used to take an ABG sample. PaCO2
Where Ka is the dissociation constant. H+ added to this and HCO3– show an inverse relationship to the volume
system will combine with the conjugate base to form the of heparin used, especially if the volume is greater than
undissociated acid (lowering the [H+]. If [H+] falls, the acid 10% of the sample volume. Heparin 5000 IU/mL is
will dissociate to generate more H+. The body’s main buffer acidic and may influence [H+] reading.
systems are (1) intracellular (protein, phosphate, and Air bubbles more than 0.5–1% of the sample volume
hemoglobin) and (2) extracellular (bicarbonate). will introduce error.
Any sample that cannot be measured in less than
Standard Bicarbonate 10 minutes must be sealed, packed in ice and measured
This is plasma concentration of the bicarbonate (HCO3–) within 1 hour.
that has been fully equilibrated with a normal PaCO2 at
standard temperature and pressure and thus reflects only
Interpretation of a Blood Gas Sample
non-respiratory (i.e. metabolic) effects. Normal value is Before attempting to interpret, it is useful to take a moment
21–27 mmol/L. to confirm whether the sample represents arterial blood.
The interpretation of ABG should always be based on the
Actual Bicarbonate background of clinical history and physical examination of
the patient. While interpreting, it is advisable to proceed
The concentration of HCO3– that is measured in a sample
in steps.
without any corrections as mentioned for standard
bicarbonate is the actual bicarbonate concentration.
Step 1: Is there an Acidemia or Alkalemia?
Therefore, the actual bicarbonate reflects the contribution
of both the respiratory and metabolic components of Though pH is used as a guideline to diagnose acidemia
the body’s acid-base balance and not the metabolic or alakalemia, a normal pH still does not rule out
component in isolation of HCO3– will fall with respiratory acid-base disturbances. The normal value could be
alkalosis. Normal value 21 to 28 mmol/L. due to compensation by the body for a single acid-
base disturbance or due to presence of more than one
Base Excess disturbance counteracting each other’s effect on pH. A
pH less than 7.35 denotes acidemia and more than 7.45
Base excess is the amount of strong acid that would have
denotes alkalemia. In most of the acute situations, when
to be added per unit volume of whole blood to titrate it to
pH 7.4 while at 37°C and at a carbon dioxide pressure of the body has had no time to compensate completely for
40 mm Hg. It depicts the deviation from normal of the the alteration in H+, the altered pH reflects the primary
buffering capacity of the body. A deficiency of buffer base or acid-base problem.
negative base excess implies a nonrespiratory (metabolic) Patient’s clinical condition and examination, and
acidosis; a positive base excess implies metabolic alkalosis. knowledge of underlying pathology may help one to have
Base excess (negative or positive) takes into account all the an idea about which of these options is true. To confirm,
buffers in the blood sample and is, therefore considered a however, one needs to go to the next step.
more accurate assessment of the metabolic component of
the patient’s acid-base status. Normal base excess value is Step 2: Look at the PaCO2 and HCO3–
± 2 mmol/L. In a patient with acidemia, an increase in PaCO2 level
indicates primary respiratory acidosis and a decrease in
ARTERIAL BLOOD GAS SAMPLING: bicarbonate level indicates primary metabolic acidosis.
Similarly, in a patient with alkalemia, a decrease in the
CLINICAL CONSIDERATIONS PaCO2 level indicates primary respiratory alkalosis and
While taking an ABG sample, the following points should an increase in the level of bicarbonate suggests primary
be considered: metabolic alkalosis.
Is ABG machine working and has it been calibrated? However, there may be situations where, for example,
Date and time of sample the pH is low and the PaCO2, standard bicarbonate, and
Fraction of oxygen in inspired air (FiO )
2
base excess concentrations are all high. The most likely
Ventilatory status reason for this is a respiratory acidosis that has persisted
TABLE 61.1: Primary examples

Standard HCO3–
pH PaCO2 and base excess Likely causes
Low High Low Acidemia due to combined primary respiratory and metabolic acidosis
Low Low Low Acidemia due to either a primary metabolic acidosis with incomplete respiratory compensation or
a primary metabolic acidosis with a primary respiratory alkalosis
High Low High Alkalemia due to a combined primary (1°) respiratory and metabolic alkalosis
High Low Low Alkalemia due to either a primary respiratory alkalosis with incomplete metabolic compensation or
a primary respiratory alkalosis with a primary metabolic acidosis
High High High Alkalemia due to either a primary metabolic alkalosis with incomplete respiratory compensation or
a 1° metabolic alkalosis with a 1° respiratory acidosis
Normal High High Combined respiratory acidosis and metabolic alkalosis that are cancelling out each other’s pH
changes. Both can be 1° disturbance or one could be completely compensating for the other
Normal Low Low Combined respiratory alkalosis and metabolic acidosis that are cancelling out each other’s pH
changes. Both can be 1° disturbances or one could be completely compensating for the other.
long enough to enable some metabolic compensation TABLE 61.2: Expected changes for acid-base disturbance
to occur or it could be because of primary respiratory
Acute respiratory acidosis A 10 mm Hg rise in PaCO2
acidosis and combined primary metabolic alkalosis. A few
produces 1.0 mmol/L rise in actual
more examples, as given in Table 61.1, can make the point bicarbonate
clear.
Chronic respiratory acidosis A 10 mm Hg rise in PaCO2 produces
As one observes from the above table, there are more
3.5–4.0 mmol/L rise in actual
than one possible causes for the changes in pH, PaCO2, bicarbonate
bicarbonate and base excess.
Acute respiratory alkalosis A 10 mm Hg fall in PaCO2
produces 2.0 mmol/L fall in actual
Step 3: Compare with the Expected Changes bicarbonate
To clarify the matter, one needs to quantify the changes in Respiratory alkalosis A 10 mm Hg fall in PaCO2
PaCO2, actual bicarbonate, and base excess and compare produces 5.0 mmol/L fall in actual
these with the expected changes appropriate for a single bicarbonate
acid-base disturbance (Table 61.2). Metabolic acidosis A 1.0 mmol/L fall in actual
When the observed values lie beyond the expected bicarbonate produces a 1.0–.3 mm
range of changes, as derived by calculation, then there is a Hg fall in PaCO2
possibility of more than one acid-base disturbance in the Metabolic alkalosis A 1.0 mmol/L rise in actual
patient. bicarbonate produces a 0.6 mm Hg
rise in PaCO2.
Step 4: Look at the PaO2 and FiO2
Finally, one needs to look at the PaO2 value. Low partial
PaO2 indicates less uptake of oxygen leading to hypoxia. 760/100 = 380 mm Hg (that is, half the normal atmospheric
Hypoxia in turn causes anaerobic metabolism and lactic pressure). This would mean the expected PaCO2 would be
acid formation leading to metabolic acidosis. However, at least 380 – 75 = 305 mm Hg.
simply looking at PaO2 is not enough, it should be evaluated
with reference to the fraction of FiO2. By knowing the FiO2, Step 5: Integrate the Clinical Findings and
it is possible to have a rough idea of what the PaO2 should ABG Data
be if patient is ventilating normally. A difference between Finally, it is important to integrate the clinical findings and
FiO2 and PaO2 of more than 75 mm Hg would imply that ABG data to efficiently manage the patient, simply using
there is a defect in the uptake of oxygen. For example, an the ABG data in isolation increases the chances of missing
inspired oxygen of 50% will have a partial pressure of 50 × a coexisting acid-base disturbance.
Interpreting Arterial Blood Gas Sample 567
1. Define partial pressure.
2. Explain the term base excess.
i. Acidemia is condition in which arterial pH is below ____________.
ii. Buffer is compound which changes in ____________ ion.
iii. Normal range of standard bicarbonate in blood is ____________ to ____________.
Section 11
Routine and
Special Investigations
Section Outline
62. Ultrasound, Doppler, MRI, CT-scan and X-ray in Obstetrics
63. Prenatal Diagnosis and Fetal Therapy
64. Antepartum Fetal Surveillance
65. Intrapartum Fetal Monitoring
62 Ultrasound, Doppler, MRI,
CT-scan and X-ray in Obstetrics
Rajesh Uppal, Ashok Khurana, Sudha Salhan, Sangeeta Tripathi
1. Early first trimester 6–10 weeks

ULTRASOUND IN OBSTETRICS* 2. Late first trimester 11–14 weeks
Since the introduction of ultrasound, obstetric manage- 3. Anomly scans 18–23 weeks
ment has undergone a revolution—a pre-ultrasound era 4. Growth scans Third trimester
versus a post-ultrasound era. 5. Doppler and fetal wellbeing Late third trimester.
Detailed explanation of the technique and abnormali-
ties are beyond the limits of a textbook of obstetrics. New
information in Doppler 3D and 4D imaging are adding
EARLY FIRST TRIMESTER
more understanding of fetal health and disease. Indications
This chapter will deal with the basic ultrasound infor-
To establish the site of pregnancy—intrauterine or
mation for obstetric practice.
extrauterine.
To confirm the age of gestation (Table 62.1) (Figs 62.1
PHYSICS
and 62.2).
Crystals like barium titanate and lead zirconate generate To confirm the number of fetuses (Figs 62.3 and 62.4).
high frequency waves on application of electric current. To confirm fetal viability (Fig. 62.5).
These sound waves are projected into the area of interest To evaluate complications—missed abortion, incomplete
and are absorbed, attenuated and reflected depending on abortion, molar pregnancy, choriomyometrial separation,
the tissue characteristics. The reflected waves are analyzed
etc.
by converting them into images.
TABLE 62.1: Gestational age and ultrasound findings
TRANSDUCERS Gestation age Beta hCG
Transducers come in various shapes and in various (From date of LMP) Ultrasound findings level Units
frequencies. The usual median frequency in transabdo- 4 weeks No change 30 IU
minal scanning is 3.5 MHz. At this frequency, the near 4–5 weeks Small hypoechoic complex 300 IU
organs are poorly evaluated. To see superficial organs, we thickened endometrium,
need a higher frequency. Transvaginal probes use a range Double decidual sign
of 5–7 MHz. Still higher frequencies (7–12 MHz) are used 5–6 weeks Sac measures approx 10 1000 IU
in linear probes for scan superficial organs. (Figs 62.3 and 62.4) mm,
Instruments have rapidly evolved in the last few decades Yolk sac is seen,
from static scanners with low frame rates to scanner with Fetal pole is seen
high resolution and real time images. 6–7 weeks (Fig. 62.5) Fetal cardiac activity detected, 3000 IU
Fetal pole approx 10 mm
INDICATIONS 8 weeks CRL of approx 14–21 mm,
Broadly one can divide ultrasound application in obstetrics Yolk sac decreases
in five categories: Abbreviations: IU—International units; CRL—Crown rump length
* Ultrasound in obstetrics is contributed by Dr Rajesh Uppal
Fig. 62.1: 5 weeks intrauterine sac Fig. 62.2: 6 weeks sac with fetal pole and yolk sac
Fig. 62.3: Twin—dichorionic diamniotic Fig. 62.4: Twins—monochorionic
Complications
Complications usually encountered in the first trimester of
pregnancy are:
Anembryonic pregnancy (Fig. 62.6)
Missed abortion (Fig. 62.7)
Incomplete abortion
Molar change (Fig. 62.8)
Sub-chorionic bleed (Fig. 62.9)
Ectopic pregnancy (Figs 62.10 to 62.14)
Ectopic Pregnancy
With the advances in ultrasound and better availability of
beta-human chorionic gonadotropin (hCG) levels, detec
tion test, diagnosis of ecotopic pregnancy is more frequently
Fig. 62.5: 6 weeks fetus with cardiac activity made at earlier stages.
Ultrasound, Doppler, MRI, CT-scan and X-ray in Obstetrics 573
Fig. 62.6: Anembryonic sac Fig. 62.7: Missed abortion
Fig. 62.8: Molar change—hydatidiform mole Fig. 62.9: Subchorionic bleed
Fig. 62.10: Ectopic as a mixed echogenic mass—unruptured Fig. 62.11: Ectopic as echogenic mass with central sac
Fig. 62.12: Complex adnexal mass—ectopic ruptured Fig. 62.13: Ectopic with fetus
Large irregular mass with fluid in the pelvis

Rarely, heterotopic pregnancy (both intrauterine ecto
pic pregnancy) may be seen.
Chronic ectopic pregnancy: Result from organization of
the ectopic tissue and the surrounding hematoma (Fig.
62.14).
LATE FIRST TRIMESTER

[11–14 Weeks Scan/Nuchal Translucency/(NT) Scan]
A late first trimester scan should be offered as a routine to
all cases.
Advantages
Approximately 40% of all anomalies can be detected
including anencephaly, encephaloceles, body stalk
Fig. 62.14: Chronic ectopic with bone elements
defects, major limb defects, early hydrops, abdominal
wall defects. Detailed scanning can reveal many defects
Clinical features conventionally believed to be seen in an older fetus.
Period of amenorrhea Nuchal translucency evaluation gives an opportunity
Pain in the lower abdomen to suspect chromosomal defects (Down’s, Turner’s,
Abnormal vaginal bleeding Trisomy 18, Trisomy 13, Noonans), heart defects and is
Collapse of the patient. used as an adjuvant in dual screening. Traditionally, a
Ultrasound findings value of 2.5 mm or more is significant.
Absence of intrauterine pregnancy alerts to an ectopic Absense of intracranical lucency raises the suspicion of
gestation. Pseudosac or endomterial thickening may be open neural tube defect.

seen Uterine artery Doppler: High resistance is predictive
Adnexal mass with variable morphology of development of pregnancy-induced hypertension

Well-defined rounded hyperechoic adnexal mass (PIH), pre-eclamptic toxemia (PET).
Presence of cystic area suggestive of sac with or without However, the NT scan is the most abused scan in obstetric
fetal pole practice. It is urged that each obstetrician is familiar with
Heterogenous mass separated from the uterus and the ovary the images and insists on correct documentation.
Increased Nuchal Translucency Advantages

To evaluate for structural defects. Almost 40% of ad-
Causes
ditional defects can be assessed at 18–20 weeks and

Chromosomal aberrations additional 15% at 23 weeks.
Down’s syndrome, Trisomy 18, Trisomy 13, Turner’s, For fetal biometry
Noonan syndrome. Placenta
Cardiac defect Cervical evaluation
Metabolic diseases
Amniotic fluid evaluation-eclampsia
Uterine artery resistance for pre-eclampsia screening.
Fetal akinesia syndrome
Ideal value of NT should be correlated with the crown Normal Fetal Anatomy (Figs 62.20 to 62.33)
rump length (CRL). A thumb rule is that a value of 2.5 mm Details of fetal morphology are very sophisticated. However,
is abnormal (Figs 62.15 to 62.19). the scan should cover the following features:
Head: Vault and intracranial structures including
Anomaly Scan ventricles.
It is done during 18–23 weeks of gestation. Face: Orbits, lips, palate, nasal bones
Fig. 62.15: 12 weeks fetus with nuchal translucency 1.4 mm Fig. 62.16: Nuchal translucency seen in prone position
Fig. 62.17: Nuchal translucency and intracranial lucency in first Fig. 62.18: Increased nuchal translucency
trimester—normal
Fig. 62.19: Diffuse increase in cutaneous fluid Fig. 62.20: Axial section of head
Fig. 62.21: Posterior structures in fetal head Fig. 62.22: Fetal orbits
Fig. 62.23: Sagittal section with nasal bone and cranium Fig. 62.24: Lips
Fig. 62.25: Spine Fig. 62.26: Four chamber view of heart
Fig. 62.27: Color Doppler 4 chamber view Fig. 62.28: Fetal stomach
Fig. 62.29: Urinary bladder with two umbilical arteries Fig. 62.30: Femur length
Fig. 62.31: Fetal leg Fig. 62.32: Bilateral feet
Right subclavian artery: Aberrant course is a marker

of Down’s syndrome
Choroid plexus cysts
Pelvicaliectasis
Hyperechoic bowel loops
Echogenic intracardiac focus
Clinodactyly
Short long bones
Effusions
Single umbilical artery.
Detailed anomaly description merits a full length text

and a snapshot of images of some anomalies is provided
(Figs 62.34 to 62.50):
CNS: Anencephaly, ventriculomegaly,
meningomyelocele
Fig. 62.33: Fetal hand
Heart: Structural defects
Abdominal wall: Omphalocele, gastroschisis
Spine: Continuity and completeness Renal: Pelvicaliectasis, multicystic dysplastic
Situs: Thoracic and abdominal
kidneys
Heart: Four chamber and outflow tracts
Limbs: Club feet, bony dysplasia
Stomach, bowel loops, kidneys, bladder
Face: Cleft lip.
Anterior abdominal wall and cord
Lower limbs: Thighs, legs, feet
Upper limbs: Arms, forearms, hands

THIRD TRIMESTER
Soft markers: Nuchal fold, nasal bone, right subclavian Fetal biometry: Head circumference (HC), abdominal
artery. circumference (AC), femur length (FL)
Detailed evaluation of the above structures is manda Amniotic fluid evaluation
tory. Minor aberrations should be documented as they can Fetal presentation viability
be markers of aneuploidies. Placental localization and maturity
A few of the markers are listed below: Doppler evaluation: Uterine artery, middle cerebral
Nuchal fold thickness: Thickness of 6 mm or more artery, umbilical artery flows. Doppler evaluation is an
Nasal bone: Absence is a soft marker integral component of third trimester scans.
Fig. 62.34: Absence of head at cranial end of spine—anencephaly Fig. 62.35: Occipital encephalocele
Fig. 62.36: Ventriculomegaly Fig. 62.37: Cystic defect in the spine
Fig. 62.38: Transverse view of spine with spinal dysraphism Fig. 62.39: Asymmetrical cardiac chambers
Fig. 62.40: Asymmetrical chambers on color Doppler Fig. 62.41: Large omphalocele
Fig. 62.42: Gastroschisis—free-floating bowel loops Fig. 62.43: Multicystic dysplastic kidney
Fig. 62.44: Bilateral kidneys with pelvicaliectasis Fig. 62.45: Club foot
Fig. 62.46: Club foot on 3D view Fig. 62.47: Shortening of all long bones
Fig. 62.48: Shortening of all long bones Fig. 62.49: Unilateral cleft lip
Placenta
By 10–12 weeks’ of gestation, the diffused granular mor-
phology of the placenta can be seen. By the third month,
placental septa are developed. Later, the placenta shows a
heterogenous morphology.
Placenta scoring 0,I,II,III stages are mentioned later in
this chapter.
Placenta Previa
Location of the placenta in relation to the internal os
(location) is always noted during the routine scans. Low
lying placenta, is graded as I, II (low lying reaching till the
os), III (reaching till the os and covering the os) and IV
(central). Note that this is different from placenta maturity
Fig. 62.50: Cleft lip on 3D view grading.
Retroplacental Hemorrhage Crown Rump Length (CRL)

Retroplacental bleeding is another important cause of Highly accurate for estimation of fetal age in the early
antepartum hemorrhage (APH). A collection may be seen pregnancy, CRL measurements should be correlated in all
in the retroplacental region (as a mass), intraplacentally (as subsequent scans, if available.
a diffused or a localized change) or as a submembranous
collection separate from the placenta. Head Circumference (HC)
Historically the head measurements were extensively
Placenta Calcification used to date fetuses. HC performs better than biparietal
Placental calcification occurs as a maturing process during diameter (BPD), is highy accurate between 14 and 25
pregnancy. During the first 6 months, the deposition is weeks. In case of abnormal shape of the fetal head, values
microscopic. Large plaques appear in the third trimester. should be disregarded.
Most placentae show calcification after 33 weeks. There
is no evidence to link calcification with any pathological Head Circumference and Femur Length
process or clinical significance. No increase in calcification They are excellent parameters, particularly in the third
is seen post-maturity. trimester.
Placental calcification is seen commonly in the third
trimester. It represents calcium in the basal plate and the Abdominal Circumference (AC)
septae and is likely to be related to maternal serum calcium Measure at the level of the portal vein. This parameter is
level. not useful for calculation of gestation age, but is useful in
Historical placental grading has been linked to fetal assessment of intrauterine growth restrictions (IUGR).
growth restriction. However, no correlation exists in this Intrauterine growth restrictions
respect.
IUGR as seen on ultrasound is indication of low weight
Placenta grading (Grannum ‘s Grading) percentile. However, a large number of small of dates
fetuses are only genetically ‘small’ and not at risk of increase
GRADE 0: Homogenous placenta.
perinatal problems.
Straight line of chorionic plate.
A quarter of the IUGR fetuses show growth restraints
GRADE I: Undulated chorionic plate.
due to uteroplacental insufficiency. This subgroup is at
Scattered bright placenta echoes.
GRADE II: Linear bright echoes parallel to basal plate. risk of prenatal complications.
Confluent stippled echoes within placenta. A small percentage of fetuses are affected due to chromo
GRADE III: Calcified intercotyledonary septae. somal aberration, intrinsic defects (e.g. renal failure) or
extrinsic influence [e.g. TORCH (toxoplasmosis other rubella,
Fetal Biometry cytomegalovirus and herpes) infections].
Fetal biometry is important since in the third trimester
Fetal Biophysical Profile
fetal growth can be charted by fetal biometry alone. Fetal
measurements are compared to normal biometric values . Balancing the fetal risk versus the neonatal risk is the
crux of the issue in evaluation of fetus in last trimester of
Principles of Fetal Biometry pregnancy. A fetus with IUGR and impending compromise
Gestational age accuracy is conversely related to the requires urgent intervention. Conversely, an immature
period of amenorrhea. Accuracy of assessment of IUGR fetus with normal functions can be considered for
gestation age is very high in early pregnancy and varies conservative management rather than urgent delivery.
widely in the third trimester. A scoring system widely in use is authored by Manning.
Optimal parameters vary with the gestational age It evaluates 5 parameters in 30 minutes period. Scores of
First trimester: CRL 0–2 are allotted for each parameter and the total is added
Second trimester: HC up for the score. A decreasing score denotes greater risk.
Third trimester: FL Movement: At least 3 discrete movements in 30 minutes.
In the third trimester, serial measurements are more Respiration: At least 1 episode of 30 seconds in 30 minutes.
useful than isolated values. Tone: Active extension with return to flexion.
Fetal heart: At least 2 episodes of acceleration of at least 15 method of mapping is known as the Doppler spectrum
beats/minute for 15 seconds along with fetal movements which consists of a graph showing flow characteristics as a
(nonstress test-NST). waveform. These can then be quantified as velocities, ratios
Amniotic fluid: At least one pocket, measuring 2 cm × and indices. The Doppler spectrum has an equivalent
2 cm. simultaneous audio signal as well which one learns to
assess and analyze with increasing experience.
COLOR DOPPLER APPLICATIONS IN Power Doppler is a newer form of flow imaging. It uses
OBSTETRICS amplitude of scatter rather than a frequency shift to make
a map of tissue flow. It is by its inherent nature far more
The color Doppler technique is as established as a yardstick sensitive to slow flow and, therefore, proving to be useful
of pathophysiology as is 2D Real Time Grey Scale Ultrasound
in placental angiogenesis studies and in the vascular
as that of morbid anatomy.
evaluation of some fetal malformations.
The following discussion outlines the increased accuracy
and diagnostic confidence when color Doppler techniques
are used in obstetric situations, thereby ensuring rational EARLY PREGNANCY AND ECTOPIC
treatment protocols and actually saving on costs. PREGNANCY
The term M-mode refers to a motion mode in B-mode
studies. This is currently employed in obstetrics to assess fetal The earliest sign of a pregnancy event is a persistence of
cardiac motion to assess heart rate and rhythm as well as for a vascularized corpus luteum beyond day 28 (Fig. 62.51).
Corpus luteum vascularization. Note the extensive
studying the excursions of the valves and the myocardium.
The term Doppler is loosely used to indicate the vascularization in the wall of the corpus luteum. The
blood flow information. It is based on the Doppler effect flow velocity waveform shows a low impedance flow
wherein the returning frequency of waves is altered by with a resistive index (RI) of less than 0.55.
the movement of a target. The moving target is red blood This appears as a cystic, hypoechoic, isoechoic or echo
cells (RBCs) in the blood vessels in the region of interest. genic area in the active ovary and this area shows intense
The returning signal is mapped in two ways. A map of the peripheral flow signals on color flow mapping and power
vessels can be obtained which can be superimposed on Doppler studies. On spectral Doppler analysis, the flow
the grey scale image. This is known as color flow mapping. velocity waveform shows a low impedance flow with a
This indicates direction and velocity of flow. The other RI of 0.55 or less. Several studies have investigated the
Fig. 62.51: Corpus luteum vascularization

Fig. 62.52: Corpus luteum vascularization in the wall
relationship of corpus luteum blood flow and pregnancy trophoblastic signal in the endometrium is, however,
outcome. Corpora lutea with an increased impedance well-described and consistently demonstrable using
to flow (RI greater than 0.56) are associated with a color Doppler or power Doppler techniques.
higher incidence of spontaneous and missed abortions. Hypertrophy of a single spiral artery is often the first
Supporting these patients with exogenous progesterone clue to intrauterine implantation of a gestational sac.
seems to improve pregnancy salvage. Color Doppler is It can be seen considerably earlier than the gestational
also useful in delineating an isoechoic (hemorrhagic) sac itself. The vessel has a low impedance flow velocity
corpus luteum (Fig. 62.52). waveform (Fig. 62.53).
Corpora lutea are not infrequently hemorrhagic and are The normal ongoing pregnancy shows occasional
then isoechoic with the ovarian parenchyma. The only peritrophoblastic vascular signals (Fig. 62.54). Note the
way to identify them in this situation is to locate them scant vascular signals around the sac.
with a color flow or power Doppler window that shows The abnormal sac shows arterial and venous hyperemia
the vascularization in the wall. Failure to utilize the and an overtly vascular myometrium (Fig. 62.55).
technique erroneously results in failure to identify the A variably thin-walled gestational sac is seen with a
corpus luteum and consequentially unnecessary shrunken embryo and peritrophoblastic hyperemia.
progesterone supplementation. Power Doppler studies enhance the diagnostic confi
The gestational sac can first be seen implanted in one dence in this situation and hasten appropriate decision
of the walls of the endometrium between 4 weeks and making.
1 day to 4 weeks and 3 days of gestation (counted from In a complete abortion the uterus reverts to being poorly
the first day of the last menstrual period) by transvaginal vascular but may show some increase in the number of
scanning (TVS) and by 5 weeks on transabdominal venous signals.
scans (TAS) done on high quality equipment. Prior to In the absence of a recognizable sac as in an incomplete
the visualization of the gestational sac, a focal distortion abortion, arterial hyperemia and a low impedance
or focal increased echogenicity of the endometrium ‘trophoblastic signal’ may be evident (Fig. 62.56).
has been described on TVS and 3D studies but is not The endometrium is inhomogeneous but shows no sac.
very reliable. A focal high velocity low impedance Power Doppler shows a high-velocity low impedance
Fig. 62.53: Hypertrophy of a single spiral artery Fig. 62.54: Gestational sac with a normal peritrophoblastic flow
Fig. 62.55: Thin-walled gestational sac with a shrunken embryo Fig. 62.56: Incomplete abortion
pattern which is a trophoblastic signature. Curettage In an ectopic pregnancy, the uterus may be cold or
confirms villi. warm and shows no trophoblastic signal. A variably
The trophoblastic signal is mimicked by other conditions
vascular corpus luteum is evident. Trophoblastic flow
including endometritis and a degenerating submucous may or may not be classical in an extraovarian adnexal
fibroid. A pseudosac of an ectopic gestation can also be mass and the flow pattern may be bizarre. If, however,
confirmed by the absence of peripheral flow. the mass shows trophoblastic low impedance flow, then
Fig. 62.57: Right adnexal ectopic gestation
the diagnostic confidence in a diagnosis of an ectopic normal renal artery (on the side of the observed kidney)
gestation is enhanced (Fig. 62.57). This figure shows a and a unilateral renal agenesis with no renal artery on
right adnexal ectopic gestation. 3D reconstruction the side of the missing kidney.
studies with power Doppler confirm a right adnexal The other conditions which can be diagnosed by color
mass in this clinically high-risk patient. Flow can be Doppler include single umbilical artery, absent renal
quantified with 3D studies and used elegantly to identify arteries anomalous pulmonary venous connections,
decreased flow in ectopic pregnancies being observed pulmonary sequestration (Fig. 62.59), vein of Galen
for spontaneous resolution and in those patients on aneurysms, arteriovenous shunts in hemangiomas and
methotrexate treatment. endotheliomas of the liver and in sacrococcygeal tera-
This information is proving remarkably useful in the tomas, agenesis of the corpus callosum and, of course,
non-surgical management of ectopic gestations as well the delineation of abnormal cardiac configuration, con-
as in the follow-up evaluation of those on methotrexate nections, their functional significance and progression.
therapy. Figure 62.59 shows a 19 weeks fetus with a chest mass
The findings in molar pregnancies depend on the size of
that is triangular, echogenic, homogeneous and basal.
the vesicles and may present as numerous cystic spaces
When 3D power Doppler studies were carried out to
in the cavity that may extend into the myometrium when
confirm a pulmonary sequestration, the mass was
invasive, or a diffusely echogenic picture. Vascularity is
seen to have no supply from the aorta as expected for a
usually scant except in recurrences and invasion.
sequestration. The entire supply was from the pulmonary
circuit. A postnatal computed tomography (CT) scan
FETAL DEVELOPMENTAL ANOMALIES confirmed a congenital cystic adenomatoid malformation.
Several developmental anomalies lend themselves to a
more detailed and accurate diagnostic evaluation by color UTERINE ARTERY FLOW VELOCITY
Doppler.
WAVEFORMS
Figure 62.58 shows a power Doppler evaluation of
the aorta in a fetus where one kidney could not be Color flow mapping and pulsed wave Doppler evaluation
identified. Studies confirmed a normal aorta, only one of the uterine arteries is now an accepted, reliable method
Fig. 62.58: Doppler evaluation of the aorta
Fig. 62.59: Congenital cystic adenomatoid malformation
of evaluating the low-risk mother for prediction of a 62.60 shows the right and left uterine artery flow velocity
hypertensive disorder in pregnancy and high-risk mother waveforms in a patient with the onset of pregnancy induced
for prediction of perinatal morbidity and mortality. It hypertension at 30 weeks of gestation. The upper tracing
is imperative to obtain right and left uterine artery flow shows a low impedance pattern with a RI of 0.44 and no
velocity waveforms in the terminal portion of the arterial notch in early diastole. This is the normal pattern after
course, distal to the origin of the tubal branch and proximal 22–24 weeks of gestation. The lower tracing shows a high
to the fanning out of arcuate arteries. Indices used to impedance flow with a notch in early diastole and a high
predict adverse outcome should be deployed after 24–26 RI (0.88).
weeks of pregnancy. The variables include a Resistive The uterine artery flow velocity waveform is more sen-
Index of > 0.56, a systolic/diastolic ratio of > 2.60, a notch sitive and specific for pregnancy outcome than the blood
in early diastole, systolic notch and a large difference of pressure, fundal height evaluation, creatinine clearance
the right and left sides of the uterine circulation. Figure and serum uric acid levels.
or quantifying a clear cut off level in these parameters is

especially relevant in the premature small for gestational
age fetus where the neonatal course can be drastically
different for an asphyxiated mature fetus compared to a
mildly premature non-asphyxiated fetus.
The duration of the time interval from the onset of
absent end-diastolic flow in the umbilical artery to
abnormal fetal heart rate (FHR) pattern can vary from
0–7 weeks. Obstetric decision-making will be erroneous
if based on this Doppler parameter alone. Middle
cerebral artery flow velocity waveforms in the hypoxic
fetus initially shows increased end diastolic velocities.
In the deteriorating fetus, this progresses to an inability
for compensation that is shown by a reduced flow
representing fetal brain edema. An isolated assessment of
Fig. 62.60: Uterine artery flow velocity waveforms
this vessel is unable to predict or identify this occurrence.
Flow alterations in the inferior vena cava have been
identified by some authors as correlating well with fetal
FETAL HYPOXIA AND ACIDOSIS acidemia. However, there is no firm association between
quantified venous pulsatility and blood gases. This is
In the fetus deprived of energy substrate, oxygen supply, or
probably because there is no standard landmark to place
both, there is a shift of metabolism to the anerobic lactate
sample volumes in the inferior vena cava and the length of
pathway. Hypoxemia, hypoxia, acidemia and acidosis are
this vessel between the renal vein and the hepatic veins is
the common end-points, irrespective of cause. Surviving
fairly long. The ductus venosus systolic/atrial ratio of 4.5
IUG-restricted fetuses shows a significant relationship
is the value below which the high-risk fetus is unlikely to
between neurodevelopmental scores and the presence of
be compromized. Resorting to such an analysis can greatly
acidemia at cordocentesis.
improve perinatal outcomes by postponing obstetric
The negative predictive value of normal biometry and a
intervention in non-critically ill hypoxic fetuses.
normal amniotic fluid index (AFI) is high for the absence
of growth restriction. The specificity of various parameters
for growth restriction is low except a decreased AFI, a MULTIPLE GESTATIONS
decreased abdominal perimeter and an elevated head Twins with an abnormal umbilical artery flow velocity
perimeter/abdominal perimeter ratio. It is wise, therefore, waveform tend to be born 3–4 weeks earlier, show a higher
to base a firm diagnosis of growth restriction only on the incidence of stillbirths and dysmorphic developmental
latter. anomalies, as well as greater morbidity when compared
Whereas conventional ultrasound is able to identify with fetuses with normal color Doppler. The availability of
abnormal fetal growth, quantify liquor amnii and assess color flow data decreases perinatal morbidity and mortality
fetal biophysical parameters, it fails to identify where in and a reduction in the number of infants requiring
the hypoxia cascade the fetus lies and, therefore, what is intensive nursery care. The diagnosis of discordant twins
the ideal time for obstetric intervention. is made mainly by ultrasound using derived fetal weight,
Doppler ultrasound studies of the fetal circulation in fetal biometry and a difference in the systolic/diastolic
IUGR and other hypoxic states have shown increased resis ratio of the twin cords in the region of 0.4 or more.
tance to flow in the umbilical arteries and redistribution
of fetal cardiac output to favor the cranial circulation
and the myocardium and to restrict or deprive the flow
CONCLUSION
to abdominal viscera and extremities. In conjunction It is apparent from this review that color Doppler studies,
with ultrasound evaluation of fetal size and maturity, are here to stay, because of their inherent ability to offer
quantification of liquor amnii and assessment of the fetal physiological and pathophysiological information, indis-
biophysical profile, abnormal Doppler velocimetry is now pensible for the practicing obstetrician. It is hoped that in
used extensively to identify the fetus at risk for death or the future all ultrasound scanners will offer color Doppler
hypoxic damage in utero. The need for reliably identifying capabilities for an acceptable price tag.
Once sure about the diagnosis of gestational trophoblastic

MRI IN OBSTETRICS

tumor, we can do MRI to find out viable portion of the

tumor and to detect arteriovenous abnormalities.
INDICATIONS Though MRI is avoided in first trimester, it may be used
Ultrasound results are not always sufficient in obstetric in early suspected ovarian ectopic pregnancy.
diagnosis. Magnetic resonance imaging (MRI), (Figs 62.61A In cases of unequivocal ultrasound report, fast MRI is
and B) do not use ionizing radiation and (hence, not harming helpful to diagnose congenital abnormalities of brain,
the fetus) is sometimes used in detail studies. A powerful spine, skeletal and miscellaneous regions of the body.
magnetic field is passed through the body. Hydrogen atoms In cases of first convulsive fit in pregnancy, an MRI of
of the body are thus aligned. The proton in the hydrogen ion the brain is indicated.
gives out small radio signals. These proton densities mapped
in different sections of the body. Nowadays, there is no need COMPUTED TOMOGRAPHY IN OBSTETRICS
to sedate the fetus.
In some obstetrical conditions more accurate diagnosis Computed tomography (CT) is an imaging technology that
can be obtained by MRI. In pregnancy the use of contrast enables cross-sectional imaging in which there are display
media is contraindicated. The indications are as follows: of different sections the body, using X-ray absorption
Acute conditions in pregnancy, (e.g. acute fatty liver of measurements. It is not advised in pregnancy due to its
pregnancy), pulmonary embolism, etc. radiation hazards. CT has no role in obstetrics.
The placenta, its edge and the cervical canal are clearly
seen at MRI. This helps in localization of placenta previa ROLE OF X-RAY IN PREGNANCY
and in cases of previous cesarean section diagnosing of
placenta accreta, increta and percreta. Nowadays, ultrasound is the choice of investigation for
Red degeneration of a uterine leiomyoma with pregnancy.
pregnant woman. In some cases, as it has no adverse effect
More detailed characterization of ovarian cysts and
neither on fetus nor on mother.
pelvic tumors in a pregnant woman. Occasionally, X-ray and X-ray procedures during preg-
Complications in postpartum period like hematoma, nancy are used for the treatment of particular medical
abscess and ovarian vein thrombosis can be better problems. It is also occasionally used for obstetrical
differentiated. purpose.
In pregnancy, we can do urography by MRI to localize According to the American College of Radiology, no
the site of obstruction (in cases of hydronephrosis). single diagnostic X-ray procedure results in radiation
In the case of breech presentation, we can do pelvimetry exposure to a degree that would threaten the wellbeing of the
by MRI to plan type of delivery (vaginal/cesarean). developing pre-embryo, embryo or the fetus. The exposure
A B
Figs 62.61A and B: MRI machine: The patient lies in the magnetic field of strong magnets. The radio frequency transmitter coils send
waves into the patient’s body and the same coil receives signals from patient (tissue). These signals are then calculated and displayed as
images
to a single X-ray during pregnancy is not an indication for Intravenous pyelography (IVP) More than or equal to
therapeutic abortion. A plain X-ray generally exposes the 1 rad (exposure
fetus to a very small amounts of radiation, as generally depands on the no.
the uterus is shielded for non-pelvic procedures. Most of of films
the fluoroscopic examinations result in fetal exposure of Barium enema or small 2–4 rads
milirads (mrads). X-ray of the torso, abdomen, pelvis, lower bowel series
back, stomach have greater chance of exposure then uterus. Dental X-ray of mother 0.01 mrad
If the doctor feels X-ray is needed for particular medical Generally it is rare for any X-ray to be stronger than
examination, the amount of radiation that fetus receives is 5 rads.
likely to be well within the safe range. But make sure that
the radiologist and radiographer know that the patient is GENERAL USES OF X-RAYS IN
pregnant so that they will shield her properly. X-ray should
OBSTETRICS
only be done when the benefits outweighs the risks.
Exposing a fetus to more than 10 rads shows the X-rays of fetus during pregnancy is used to diagnose:
increase risk of learning disabilities and eye problems. But Multiple pregnancies (Fig. 62.62)
it is rare for any X-ray to be stronger than 5 rads. A fetus Other conditions such as pseudocyesis
gets 290 mrads for an abdominal X-ray and 800 mrads Age of the fetus
for a CT scan. During pregnancy, the fetus is exposed to Fetal death (to be put)
100 mrads of natural radiation from sun. Higher doses of Fetal abnormalities of fetal development, example
X-ray on fetus can cause birth defects—such as physical anencephaly (Fig. 62.63).
and mental developmental problems. X-ray can cause To know the secondaries of trophoblastic tumor
childhood cancers if the fetus is exposed to X-rays at high Roentgen pelvimetry and antepartum fetometry were
doses, for example leukemias. used to predermine a difficult or impossible labor.
Estimated fetal exposure from some common radiologic
procedures are as follows: Multiple Pregnancies
Procedure Fetal exposure If ultrasound shows more than two fetuses X-ray abdomen
Chest X-ray (2 views) 60 mrad is required to know the exact number of fetuses.
Abdomen X-ray (single view) 100–290 mrads Multiple pregnancies—generally multiplicity of fetal
Hip film (single view) 7–20 mrad parts are seen which make the diagnosis obvious.
Fig. 62.62: X-ray showing multiple pregnancy Fig. 62.63: X-ray showing intrauterine fetal death
Plain film of the abdomen is useful for confirming the the midpelvis and outlet with a minimum of outside
diagnosis of pseudocyesis in obese women with large pen- assistance. Previously, Thoms devised fetal cephelometry
dulous abdomen who frequently have episodes of amen- by which size and weight of the fetus can be calculated at
orrhea. 36 weeks’ of gestation.
Fetal age by observation of various fetal ossification
centers. The appearance of distal epiphysis of the femur GUIDELINES
implies that fetus has reached at least 8 months’ of
gestation. The proximal epiphysis of tibia if seen, according Single diagnostic procedure does not give harmful fetal
to Homles and Ruggles, the fetus is considered to be at term effects, especially exposure to less than 5 rad has not
or about 40 weeks’ of gestation. Occipitofrontal diameter of been associated with an increase in fetal anomalies or
11.5 cm or more represents that maturity was followed fetal loss. This should be explained to the women.
earlier by Clifford’s graph. X-rays should be done when the benefits outweighs
Overlapping of cranial sutures (patient not in labor), the risk. X-rays can give patients’ healthcare provider
unusal definition of fetal parts, (due to lack of movement important and even life-saving information about
eliminating the fuzziness about the bones), peculiar numerous medical conditions.
angulations of fetal spine, collapse of thoracic cage (late During pregnancy, other imaging processes not associ
sign) and decrease of fetal cranial contents, etc. are ated with ionizing radiation, for example ultrasono
considered as signs of fetal death. graphy (USG) and MRI should be considered instead of
To know the secondaries of trophoblastic tumors see X-rays, when appropriate.
Figure 16.8. Consultation with an expert in dosimetry calculation
may be helpful in calculating the estimated fetal dose
ABNORMALITIES OF FETAL in a pregnant patient when multiple diagnostic X-rays
are performed.
DEVELOPMENT USG and MRI are not associated with known adverse
Earlier, X-rays were helpful in cases of abnormalities in fetal effects.
fetal development. If there is such suspicion on clinical Radiopaque and paramagnetic contrast agents may be
examination of fetal death or anencephly nowadays there of diagnostic benefits but should be used in pregnancy
is no requirement of X-ray in case of availability of usg (Fig. only if the potential benefits justifies the potential risks
62.63). to the fetus. Mostly contraindicated in pregnancy.
Earlier, X-ray pelvimetry was used to estimate whether Use of radioactive isotope of iodine is contraindicated
a particular head could enter the pelvis inlet, pass through for therapeutic use during pregnancy.
1. What do you understand by the term MRI and also explain its uses in obstetric?
2. How MRI works? Explain with the help of labelled diagram.
3. What are the merits and demerits of X-Ray during pregnancy?
63
Sudha Salhan, Sunita Seth, Indira Ganeshan
Prenatal Diagnosis
and Fetal Therapy
nucleic acid integrity or function, lack of normal precursors

PRENATAL DIAGNOSIS or substrates, change in membrane characteristics, osmolar
Having a normal child developing into a healthy adult imbalance, altered energy sources and enzyme inhibition.
is the dream of all parents. A malformed child is a great The effect of teratogens depends on the timing of exposure
psychological trauma. Minor or structural abnormalities (maximum effect if exposed between second and eights
are seen in 0.5–2% of cases. These are mainly due to weeks of development), the critical stage of development and
abnormal morphogenesis. the dose of the teratogen.
TERATOLOGY TYPES OF BIRTH DEFECTS

The study of abnormalities in the fetus is called teratology. Anomaly: A structure feature which is not normal.
The abnormal development of the fertilized ovum is called Malformation: It is an abnormality in structure, as a result
teratogenesis. Its research is directed at understanding of an abnormality in morphogenesis.
the causes and mechanism of maldevelopment. The agent Deformation: It is a genetically normal fetus in an abnor
causing the abnormality is called a teratogen or teratogenic mal environment causing structural changes, e.g. club foot
agent. A teratogenic agent can be a drug (thalidomide, in oligohydramnios (Flowchart 63.1).
valproic acid), chemical agents, (mercury, lead, nitrates Disruption: A genetically normal fetus, suffers an insult
and nitrate-fertilizers), anesthetic gases, physical agents resulting in disruption of normal development, e.g.
(ionizing radiation), diet (blighted potato), genetic influence amniotic bands which cause limb reduction defects.
(hemophilia, muscular dystrophy) and viruses (rubella) So, an identical appearing anomaly may have varying
zika, etc. A teratogen acts by one or more of the following etiologies making the diagnose difficult.
mechanisms, i.e. gene mutation, chromosomal abnormalities Syndrome: Multiple anomalies in a single fetus due to one
(e.g. breaks or non-disjunction), mitotic interference, altered cause, e.g. trisomy 18.
Flowchart 63.1: Types of birth defects

Prenatal Diagnosis and Fetal Therapy 593
Sequence: All abnormalities occurring sequentially as a can be treated in utero or postnatally. Therefore, early
result of one insult, for, e.g. oligohydramnios leading to diagnosis can facilitate decision-making regarding mode
pulmonary hypoplasia and limb defects and facial defects. and place of delivery especially if neonatal resuscitation
Association: These anomalies may occur together and immediate surgery is required.
frequently, but do not seem be linked etiologically, e.g. The Royal College of Obstetrician and Gynecologists
Colboma, Heart defects, Atresia choanae, Retardation (RCOG) recommends routine ultrasound at 18–20 weeks.
(mental), Growth deficiency and Ear anomalies (CHARGE). If fetal abnormalities are detected at this stage, second
trimester termination may be necessary. Second trimester
termination is associated with marked psychological
ETIOLOGY OF MALFORMATIONS sequelae because in the second trimester, pregnancy may
Genetic defects be visible abdominally. It also has greater morbidity and
Teratogenic/environmental forces mortality than first trimester termination. Considering all
Unknown factors (60%). these points, this chapter will focus on first and second
trimester screening of congenital anomalies. Third
CONGENITAL ABNORMALITIES trimester detection of birth defects for unbooked patients
shall also be discussed for patients who come to the
(FLOWCHART 63.2)
hospital for the first time in third trimester or in early labor.
The obstetrician’s role in providing routine antenatal A very important role of obstetrician is to identify
care is to reduce maternal and perinatal morbidity and patients at high-risk for genetic disease. The obstetrician
mortality while preserving maternal satisfaction with should discuss with such patients implications of
pregnancy. Congenital anomalies can contribute upto the problem, technology available for diagnosis and
15% of perinatal deaths. While fetal anomalies are more alternatives available if a genetic disease is found. This is
common in certain high-risk groups, the vast majority called genetic counseling.
of anomalies will not be anticipated. It is, therefore, To facilitate identification of patients at risk, it is useful
important to screen for fetal abnormalities in the general to incorporate into the antenatal records, a genetic
obstetric population (screen all pregnant women). screening questionnaire suggested by the American
Prenatal diagnosis has a profound impact on the antenatal College of Obstetricians and Gynecologists (ACOG)
and intrapartum management. Certain manifestations (see Chapter 6).
Flowchart 63.2: Causes of congenital abnormalities

Hence, genetic counseling is a communication process Certain single gene disorders (Marfan syndrome achond
which deals with the occurrence or risk of occurrence of roplasia, etc.) are more common when the father is of an
a genetic disorder in a family. This is to be provided by all older age.
obstetricians. It is the obstetrician’s discreation to refer the
patient to specialized center. Chromosome Constitution
In the parents who have had a child with neural tube
High-risk Factors defects, the recurrence risk is 4% with one child and 10%
Advanced age of the parents: Risk of having a child with a with two previous children with the defect.
congenital anomaly is 1:526 at the age of 20 and 1:18 at the Environmental factor: An association is found between
age of 45. One common defect is Down syndrome (trisomy occupational lead exposure of the mother and increased
21), although trisomy 18 and 13 is also found. Therefore, risk of low birth weight (LBW) and neural tube defects
genetic diagnostic procedures are routinely offered to babies. In parents who have had a child with congenital
women who are 35 years or older. Unfortunately, even heart disease, the recurrence risk is 2–4%.
with generalized use of genetic diagnostic techniques in Monozygosity in twins is a high-risk factor for congenital
pregnant women of 35 years or older, only a maximum abnormalities.
of 25% of all fetuses with chromosomal abnormalities
are identified before birth. The majority of pregnancies
occuring in younger women (amounting to over 50%
PRE-IMPLANTATION GENETIC
genetic abnormalities) are not being screened. This has DIAGNOSIS (PGD)
stimulated researchers to design and conduct trials of The technique of PGD was developed more than two decade
biochemical markers to identify patients at risk. If either ago. It was intended to weed out genetically defective
parent has a balanced 21/21 translocation, the risk of human embryos before they have a chance to develop. The
having an affected child in future is 100% (Table 63.1). first ‘PGD baby’ was born in 1989. This method is used for
patients who have a genetic disorder or a genetically based
disease and have a high-risk (25–50%) of transmission to
TABLE 63.1: Types of chromosomal anomalies their offspring. Typically one or both the partners have
Affected Child Father Mother Risk to offspring been genetically screened previously and have been
Trisomy 21 Normal Normal found to be carriers. These tests give results for only a few
Female 2–3% genetic disorders, they are expensive and require invasive
< 30 years procedures to obtain specimens for testing. There can be
in present risks to the fetus. During genetic counseling these points
pregnancy
must be stressed. It must be understood that a negative
Female Female age test only indicates a fetus unaffected by the condition in
> 30 years had + 1%
baby with question and does not guarantee a total normal pregnancy
outcome.
Down’s at
< 30 years The procedure is technically complex with a few experts
Female Mothers age
available. Patients are required to go through a standard
> 30 years had in vitro fertilization (IVF) procedure, so that embryos
baby with can be generated. The woman is given drugs to produce
Down’s at superovulation, multiple oocytes are then aspirated and
> 30 years placed in a dish to be fertilized by the partner’s sperms.
Translocation About three days after fertilization when the embryo has
14/21, 15/21 Normal Carrier 12% divided to the 7–8 cell level, a biopsy is performed.
Translocation
Biopsy
13/21, 21/21 Carrier Normal 2–3%
Three stages at which cells can be removed from the pre-
Translocation Normal Carrier 100%
implanted embryo are:
21/21 Carrier Normal 100%
1. Polar bodies from the oocyte or zygote. (Polar body
Mosaic Normal Normal 2–3%
biopsy) (Fig. 63.1)
Beta-thalassemia
Cystic fibrosis
Hemophilia A and B
Myotonic dystrophy
Retinitis pigmentosa
Neurofibromatosis
Achondroplasia
Huntington’s disease
Sickle cell disease
Retinoblastoma.
Female ova can be also checked for a gene that increases

the propensity to develop breast cancer or muscular
dystrophy. Some genetic disorders are sex-linked, even
if such diseases cannot be directly detected. We can
completely eliminate all embryos of that particular sex
Fig. 63.1: Polar body biopsy and only embryos of the opposite sex are transferred to the
uterus for implantation thus, preventing the transmission
of the disease. PGD is a useful technique, as it is able to
detect a defect before implantation unlike chorionic
biopsy and amniocentesis, which is performed later in
gestation and may need termination of pregnancy.
Screeening in First Trimester

This shall be discussed in detail in Chapter 12
Screening in Second Trimester

Seventeen percent of fetal anomalies can only be
detected in the second trimester, e.g. some cases of spina
Fig. 63.2: Blastocyst biopsy for PGD
bifida, heart defects (Fig. 63.3) and limb abnormalities.
Sometimes the patient also comes late for checkup (Figs
2. Blastomeres from cleavage stage embryo (Cleavage 63.4A and B). Second trimester screening is then needed.
stage biopsy) Details of screening is given in Chapter 12.
3. Trophectoderm cells from the blastocyst (Blastocyst
biopsy) (Fig. 63.2).
Procedure
One or two cells are removed and subjected to a molecular
analysis. This requires removal of the genetic material—
DNA (deoxyribonucleic acid). This DNA is amplified by
a polymerase chain reaction (PCR). The copies are then
subjected to a molecular analysis that assists in identifying
the sequence (code) that will determine the inheritance of
the gene in question. If genetic defects are found, then that
embryo is destroyed and not implanted in the uterus, only
healthy embryos are selected and transferred to the uterus
for implantation. If the embryo fails to implant, the patient
goes through the same procedure again in subsequent
cycle.
The following are some of the diseases for which PGD is
recommended: Fig. 63.3: Acardiac fetus
A B
Figs 63.4A and B: Serum markers. A. Normal; B. Abnormal
Screeening in Third Trimester be carried out depending on the gestation and the tissue
Sometimes the pregnant woman report late in third sample required.
Fetal cells in maternal circulation
trimester. Her screening is given in Chapter 12. If any
defect is visualized then one should hunt for any associated Fetal cells in endocervical mucus
chromosomal and genetic syndrome and other invasive Chorionic villus sampling (CVS)
techniques, if required, may be combined with routine Amniocentesis
investigations for evaluation of the fetus. Cordocentesis (percutaneous umbilical cord blood
Ultrasound is very useful in detecting anatomical errors. sampling—PUBS)

It should be performed only by experienced doctor. Aspiration of fetal urine and pleural fluid
Once there is suspicion in screening in pregnancy, the Fetal tissue biopsy
couple and the family members are counseled about the Placental biopsy
doubt of congenital anomaly (structural, chromosomal Fetal reduction in 4 or more pregnancies/selective
and biochemical) and methods of confirming the termination
diagnosis. If they give the consent (as most of them are Fetal therapy.
invasive procedures), then only we proceed further. The
procedures are discussed below. Fetal Cells in Maternal Circulation
It has been proved that virtually all women have at least a
INVASIVE TECHNIQUES OF PRENATAL small number of fetal cells in their blood stream. Fetal cells
DIAGNOSIS AND THERAPY can be isolated from maternal blood by density gradient,
Fetal interventions have made prenatal diagnosis and protein separation technique, fluorescence activated cell
intrauterine treatment easy. The following procedures can sorting, magnetic activated cell sorting, etc. It is very useful in
screening of aneuploidy of embryo/fetus because their count into the endocervical canal and advanced towards the
in mother’s blood increases upto six-fold. Using fluorescence chorion frondosum. The catheter should be inserted
in situ hybridization (FISH) technique, many single gene parallel to the chorion frondosum and the tip of the
defects can be detected with remarkable accuracy. The catheter should be near its end before a sample is
technique of studying fetal cells in the maternal circulation obtained. Once the tip of the catheter is in the desired
is still under research and once well developed will replace position, the obturator is removed, a syringe with a
invasive diagnostic procedures in the fetus. small amount of cell culture medium is connected to the
Fetal cells can be obtained from endocervical mucus in catheter and negative pressure is applied while catheter
50–70% of cases. This method is also in the experimental is slowly removed. An adequate sample consist of
stage. 10–20 mg of placental tissue. A sample of tissue obtained
is analyzed under a microscope.
Chorionic Villus Sampling (CVS) Transabdominal CVS (Fig. 63.6): If transcervical
It can be performed both transvaginally or transabdo CVS is contraindicated, the transabdominal route may
minally under ultrasound guidance. Indications include be used. Transcervical CVS is not done when there
finding chromosomal abnormality like aneuploidy in is a positive Neisseria gonorrhoea culture of cervical
elderly gravida, detection of inborn errors of metabolism, secretions, active genital herpes, active bleeding,
in cases with a history of previous child with genetic or maternal coagulopathy, cervical stenosis, cervicitis
sex-linked disorders or detection of thalassemia (where and intrauterine death (IUD). An 18 gauge needle is
maternal screening is done). inserted (under ultrasound guidance) into the chorion
CVS is performed between 10 and 12 weeks. CVS avoids frondosum. The stylet of the needle is then removed
problems associated with traditional amniocentesis. and a 20 gauge needle, 1.5 cm longer than first one is
Transcervical CVS (Fig. 63.5) starts with ultrasound inserted though the first needle. The stylet of the second
examination to look for number of gestational sacs, needle is removed and connected to a 20 mL syringe
gestational age, presence of fetal heart activity and containing 2–5 mL of culture medium. The syringe is
localization of chorion frondosum. The one person attached to an aspiration device to facilitate suction.
does the sonographic evaluation and second carries out The advantage of using 2 needles is that if the amount of
the sampling. A sterile polyethylene catheter (1.5 mm tissue is inadequate, re-sampling can be done easily as
diameter) with malleable metal obturator is inserted first needle is still in place.
Fig. 63.5: Transcervical chorionic villus sampling Fig. 63.6: Transabdominal chorionic villus sampling
Complications of CVS are:

Miscarriage occur in 0.8%.
Limb reduction defects (specially transverse digital
deficiency), especially if done before the 9th week of

gestation. Hence, this test is only performed after 10
weeks of gestation.
Amniocentesis (Fig. 63.7)

Traditionally, amniocentesis is performed at 16–18 weeks
of pregnancy but recently early genetic amniocentesis
between 12 and 14 weeks is becoming increasingly popu-
lar. The procedure can be performed as early as 10 weeks
and is easily carried out after 12 weeks.
It is done under ultrasound guidance using an 18–22
G needle. The needle tip is to be continuously visualized
and 20 mL of amniotic fluid is removed. Umbilical vessels
are to be avoided. It has many indications, both diagnostic Fig. 63.8: Fluroscein staining for trisomy 21
and therapeutic.
• Bilirubin level by estimating level at D450 in Rh-
Diagnostic Indications isoimmunization of the fetus
Assessment of severity of Rh-isoimmunization • For fetal lung maturity [Lecithin/sphingomyelin
Diagnosis of chromosomal anomalies (Fig. 63.8) (L/S) ratio].
Diagnosis of genetic disorders
Diagnosis of infection viral culture and PCR Therapeutic Indications
Biochemical analysis Polyhydramnios—to remove small amounts of amniotic
• Alpha-fetoprotein estimation fluid by amniocentesis when patient is in distress
• Acetylcholinesterase level estimation Amnioinfusion in oligohydramnios
Injection of drugs for reduction of fetal number if four
or more fetuses
Treatment in hypothyroidism and other drug therapies
Fetal blood transfusion in severe anemia.
Karyotyping requires viable cells for diagnosis. These are

cultured and the cell division is arrested during metaphase.
The metaphase spread is then stained with various dyes and
several structural defects can thus be picked up. Cell culture
and karyotype analysis usually takes 12–21 days.
Fluorescent in situ hybridization (FISH) is a technique
which can be used even on non dividing cells. It is not
a technique to pick up several kinds of defects in a single
test (unlike karyotyping). Instead a single DNA probe for a
known defective target DNA sequence is used. The probe is
radiolabelled. If that particular abnormality is present in the
genome the radiolabelled probe will bind to it and can be
picked up as fluorescence. It has been used in the diagnosis
of fragile X syndrome, Prader Willi syndrome, etc.
PCR is a rapid technique by which the gene sequence of
interest can be amplified several fold (105–106) using a heat
Fig. 63.7: Amniocentesis stable polymerase enzyme.
Human leukocyte antigen (HLA) Class I and II typing pancuronium (IM). If the fetus is less than 20 weeks, about
of cultured amniotic fluid cells or chorionic villi cells are 1 mL of blood can be collected. If the fetus is more than 20
used nowadays to diagnose prenatally congenital adrenal weeks, upto 5 mL of blood can be collected. FISH analysis
hyperplasia (CAH) due to 21-hydroxylase deficiency. of fetal blood can be done within 24–48 hours hence this
This is because CyP21A, (gene encoding 21-hydroxylase procedure is rapid in giving results. A whole range of
enzyme) is closely linked to HLA system. hematological, immunological and biochemical tests can
be performed.
Complications of Amniocentesis
Miscarriage—about 0.5% (more in cases of neural tube Post-Procedure
defects if performed before 14 weeks)
Watch for any bleeding
Preterm labor
Observe the fetus for any signs of fetal distress
IUD
Pain relief with nonsteroidal anti-inflammatory drugs
Isoimmunization
(NSAIDs) is provided if needed
Fetal trauma (fetal talipes, if done before 14 weeks)
Anti-D prophylaxis is administered in Rh-negative
Respiratory distress
pregnancy
Postural deformities—like talipes
Prior to discharge from the hospital, a cardiotocography
Amniotic fluid leak
(CTG) is performed.
Infection.
Indications
Cordocentesis (Percutaneous Umbilical Cord
Blood Sampling—PUBS) (Fig. 63.9) It can be diagnostic and therapeutic.
This technique is usually performed after 18 weeks under Diagnostic Indications

ultrasound guidance. In PUBS, umbilical vein puncture
Assessing the severity of Rh-isoimmunization
(cordocentesis) is done. The umbilical vessel is tapped at
Analysis of non immune hydrops
or near its placental origin with a 25 G spinal needle under
For detection of chromosomal anomalies
ultrasound guidance. Now, even fetal heart blood contents
Gene anomalies
and sampling from intrahepatic vessels are also possible.
For hematologic studies, e.g. thalassemia, thrombocy-
If needed, the fetus can be made immobile by injection of
topenia
Metabolic studies
Acid-base analysis of an intrauterine growth restriction
(IUGR) fetus
Viral culture, PCR, etc.
Immunological studies, IgM, etc.
CAH diagnosis.
Therapeutic
Blood transfusion in severe anemia (Rh- isoimmuniza-
tion)
Platelet transfusion in thrombocytopenia
Drug infusion—fetal therapy
PUBS can be harmful to the fetus hence, the indication

must have definite benefit for the fetus and the mother. It is
to be performed by an experienced obstetrician only. The
complications can be fetal or maternal.
Fetal complications include
Bleeding at the puncture site, hematoma formation and
fetomaternal hemorrhage
Deceleration of fetal heart sound (FHS) (as umbilical
Fig. 63.9: Percutaneous umbilical cord blood sampling—PUBS vessels go into spasm)
Chorioamnionitis They are rapidly cleared after delivery. While DNA is the
Premature rupture of membranes (PROM) genetic blueprint, mRNA provides information about which
Accidental hemorrhage gene are actually being expressed. Many diseases, genetic
Preterm labor or otherwise might be associated with abnormalities in RNA
Miscarriage expression. Till date, mRNA encoding of human placental
IUD. lactogen (hPL) and human chorionic gonadotropin (hCG)
The morbidity and mortality in the fetus—depends on is being carried out. This has a considerable potential for
the condition of the fetus at the time of the procedure, e.g. non-invasive prenatal screening and diagnosis.
less with healthy fetus but more with severely compromized
fetuses with erythroblastosis or severe IUGR. FETAL THERAPY
Overall fetal loss is 3–5%.
Fetal therapy can be indirect or direct.
Maternal complications are
Isoimmunization
Indirect fetal therapy is the treatment given to the
Chorioamnionitis
mother and direct is treatment given to the fetus. Its scope
Trauma to the intestines, etc.
has recently increased.
May need emergency lower segmentation cesarean
The indications are:
Maternal therapy for treatment of fetal condition
section (LSCS).
Fetal transfusion
Aspiration of Fetal Fluids Intervention in twin-to-twin transfusion
For therapy or fetal medication, e.g. in fetal hyper

Aspiration of fetal urine is done to analyse it biochemi
thyroidism, fetal cardiac arrhythmia
cally. It is performed under ultrasound guidance and helps
Fetal surgery—mostly experimental.
in the management of obstructive uropathy. Aspiration of
pleural fluid can be done. If leukocytes are increased in
aspirated pleural fluid (done under ultrasound observa- MATERNAL THERAPY
tion) of the fetus it is diagnostic of chylothorax. Direct treatment is given to mother [Syphilis gonorrhea,
toxoplasmosis and human immunodeficiency virus
Fetal Tissue Biopsy (HIV)] to prevent or cure fetal infection. Administration of
This can be done under ultrasound guidance for specific zidovudine or nevirapine to HIV positive mothers helps in
tissues like skin, liver, muscle, etc. for diagnosis of pathological reduction in fetal HIV infection. Giving corticosteroids in
conditions (e.g. muscle dystrophies, mitochondrial preterm labor help lung maturity in the fetus. In Grave’s
myopathy, epidermolysis bullosa lethalis and ornithine disease, the IgG thyroid stimulating antibodies reach the
transcarbamylase deficiency, etc.) It was used to be done by fetus through the placenta and cause fetal thyrotoxicosis. In
fetoscopy in the past. such cases, treatment of the mother with propylthiouracil
Complications include a high incidence of miscarriage helps the fetus. In CAH, the mother is given corticosteroids
and preterm delivery. Fetal tissue biopsy is done only in to prevent fetal masculinization. In cases of sustained
specialized centers, as expertise of the operator is very tachyarrhythmia of the fetus, the mother is administered
important in obtaining a good biopsy with minimal digoxin, verapamil, quinidine, etc. Recently, the adminis
complications (prophylactic antibiotics are to be given tration of hyperimmune serum for cytomegalovirus (CMV)
according to the fetal gestation period). to mother has been found to help in remission of fetal
CMV infection. Indomethacin for 5–7 days to reduce urine
Placental Biopsy production in idiopathic polyhydramnios.
This procedure can be performed transvaginally upto 13 weeks
and then per abdominally after 13 weeks under ultrasound MEDICAL THERAPY TO THE FETUS
guidance. The most common indication for placental biopsy Some medications can be directly introduced into the
is the diagnosis of chromosomal abnormalities. amniotic fluid or given intramuscularly (injection of digoxin
The placenta is an important source of fetal nucleic acid into fetal buttocks in severely affected arrhythmic fetus) or
release into maternal plasma. Hence, detection of mRNA into the umbilical cord under ultrasound guidance.
(messenger ribonucleic acid) transcripts from placental Interventions in twin-to-twin transfusion could be
expressed genes are readily detectable in maternal plasma. carried out after 24 weeks of pregnancy—removal of
amniotic fluid from a hydramniotic fetus, or the deliberate Rare hemoglobinopathies

creation of an opening in amnion between two fetuses Severe alloimmune thrombocytopenia, some obstetri-
thus amniotic fluid will move in both sacs, these two cians have tried platelet transfusion.
interventions aim to equalize the pressure in both sacs and Fetal blood transfusion can be given intraperitone-
prevent over perfusion of one of the fetuses. Other options ally and intraumbilically. In intraperitoneal transfusion,
are more drastic like endoscopic laser separation of placenta ultrasound guided insertion of a large-bore (22 gauge)
into two halves or selective feticide of the donor twin. These needle is used and blood is transfused into the peritone-
two options can even lead to the death of both twins. al cavity of the fetus. This is slowly absorbed by the sub-
diaphragmatic lymphatics. Sometimes in severe hydrops
Injections into the Amniotic Fluid even this may not be life saving. For these moribund cases,
Thyroid hormone in fetal hypothyroid goiter, intraperi ultrasound guided direct blood transfusions into the fetal
toneal antiarrhythmic drugs. umbilical cord, the hepatic part of the umbilical cord or in
the fetal heart can be carried out using a 22 gauge needle.
Fetal Blood Transfusion (Fig. 63.10) Furosemide can also be given directly with blood.
Rh-isoimmunization Fetal Reduction
Severe anemia
It was observed that in pregnancies with four or more fetuses,
Non immune hydrops
embryo reduction to twins is associated with a decrease in
Severe fetomaternal hemorrhage
the risk of miscarriage and perinatal death. The procedure
is done after counseling and obtaining written consent of
the prospective parent. Injection of potassium chloride into
the fetal thorax or heart by a transabdominal or transvaginal
route under ultrasound guidance is carried out.
Fetal Surgery
Fetal surgery is still in its infancy. Ultrasound and laparo
scopy have helped in the progress of this intervention. As
already emphasized, counseling and written consent of the
expectant parent is essential. The most important criterion
for fetal surgery is that this surgery should substantially
improve the chances of a healthy fetus. This is because
these procedures have a great operative risk to the fetus.
The natural history of the disease with and without these
surgeries must be known. These procedures require a highly
technically competent surgical team.
Certain corrective surgeries can be performed in utero
in case of bladder obstruction due to posterior urethral
valves (PUV). This will prevent hydronephrosis, renal
failure, pulmonary hypoplasia and limb defects which
may be seen if surgery is not carried out in time.
Different Fetal Surgeries Include

Urinary shunts: These are carried out only after a proper
evaluation and exclusion of any other major abnormalities
like renal agenesis or cystic dysplasia, etc. This surgery is use-
ful in PUV, urethral atresia and obstruction at the ureteropel-
vic junction. A double-pigtail catheter is placed in situ and
fetal urine can be shunted to the amniotic fluid. Use of percu-
Fig. 63.10: Fetal blood transfusion taneous fetal cystoscopy is also tried.
Congenital diaphragmatic hernia: May cause upto fetus is reposited back in the uterus which is stitched and
80% perinatal mortality. The cases for surgery have to be abdomen closed. It is practised in giant fetal neck mass
carefully selected, e.g. an isolated defect and with inter- (lympho pharyngeoma) and cervical teratoma.
mittent or late left sided herniation. The trachea is banded
or plugged in the fetus with the hernia by fetoscopy. Open Stem Cell Transplantation and Gene Transfer
surgery is also being performed. Research work is going on in therapeutic bone marrow
Sacrococcygeal teratoma: Debulking of the tumor by transplantation in the human fetus for thalassemia,
endoscopic or open surgery is being performed at some immunodeficiency syndrome, etc. The basis of this therapy
centers with good results. This is followed by total excision is that till 18 weeks of gestation the fetus can tolerate foreign
of the tumor after birth. Recently, use of laser has came into antigen because of non-developing immunocompetence
practice to occlude selection feeding vessels of the tumor. till then. These bone marrow cells can also act as a delivery
Neural tube defects: Both opening and endoscopic closure vehicle for gene transfer. The latter is in its experimental
of a defect is practiced at some hospitals. stage and many ethical issues need to be resolved before
Thoracic shunts: For tumors are carried out, but results making it practically applicable.
are still not good. Thus, we see that pre-implantation and fetal interven
In a fetus with congenital cystic: Malformations or pulmo tion is a very rapidly developing and interesting field but it
nary sequestration, where these are rapidly increasing, serial is still in early stages of research.
cystic drainage or open surgical resection does improve
the survival. Thoracic amniotic shunting may be done.
Gene Therapy
It is the integration of a foreign DNA in the fetus. It will be
Ex Utero Intrapartum Surgery (EXIT Procedures) useful in life threatening diseases like α-thalassemia and
It include partial delivery of fetus at laparotomy, doing severe combined immunodeficiency disorders (adenosine
a fast operation in relaxed uterus. After operation the deaminase deficiency).
1. Write a short note on CVS.
2. Explain stem cell transplantation and gene transfer.
3. True/False:
i. PGD stands for postpartum gestational diagnostic.
ii. Fetal therapy can be direct or indirect.
iii. FISH is a technique which can be used even on non dividing cells.
64 Antepartum Fetal Surveillance
Nivedita Sarda, Jyotsna Suri, Sudha Salhan
As we are aware, the first aim of obstetricians was to for uteroplacental insufficiency and hence, should be
prevent maternal morbidity and mortality. Now, with more actively monitored.
knowledge and tools available, we try to save the fetus as
well, as far as possible, to reduce perinatal mortality rate. To TIME OF STARTING ANTENATAL
achieve this goal of prevention of fetal death, antepartum SURVEILLANCE
fetal surveillance has come into being.
The antepartum fetal surveillance should be initiated as
soon as the risk to the fetus is identified. It need not be
INTRODUCTION carried out before the period of viability of the fetus as at this
Antepartum fetal surveillance is defined as the assess stage, no intervention will be possible. The period of viability
ment of in utero fetal wellbeing prior to the onset of is generally considered to be about 26 weeks though it can
labor. The causes of fetal compromise are mostly due to be as early as 24 weeks in some parts of the world.
uteroplacental insufficiency. Once diagnosed, prompt Therefore, the time of starting antenatal surveillance
interventions prevent fetal loss in many cases. depends largely on the past history and the severity of
Antepartum fetal assessment is done in pregnancy maternal and fetal condition. In the majority of high-risk
to reduce perinatal morbidity and mortality. This helps pregnancies (Table 64.1), antenatal testing is begun from
to identify fetuses in whom physiological adaptation 32–34 weeks onwards as these conditions jeopardize the
is deranged. Early detection and management prevent fetus more in the late 3rd trimester; in cases where risk
further deterioration. By this, we also find out normal fetus is identified earlier, for example, growth restriction at
and avoid harmful unwarranted interventions. 28 weeks or past history of intrauterine death (IUD) at 30
The methods of antepartum fetal surveillance are: weeks, the monitoring should be initiated earlier. It can be
Daily fetal movement count repeated weekly or more often depending on the risk.
Nonstress test (NST) To summarize, antepartum surveillance in normal
CST (contraction stress test) pregnancy should begin at 36 weeks. At least, fetal
Vibroacoustic stimulation test movement count should begin at 32 weeks in high-risk
Nipple stimulation test cases. However, in case of severe disease, surveillance can
Biophysical profile (BPP) be started at 26–28 weeks.
Doppler study
Fetal lung maturation test. INDICATIONS FOR ANTEPARTUM

Who should undergo antepartum fetal surveillance? FETAL SURVEILLANCE
It is not possible to predict intrauterine fetal death (IUFD)
or poor fetal outcome in most cases, e.g. cord prolapse, Maternal Factors
rupture uterus and accidental hemorrhage. However, Chronic hypertension, diabetes mellitus, chronic kidney
there are a group of high-risk pregnancies who need to disease, antiphospholipid syndrome, poorly controlled
be subjected to fetal surveillance. These can be classified hyperthyroidism, hemoglobinopathies such as hemoglo
according to the maternal, fetal and pregnancy-specific bin SS, SC or S-thalassemia, cyanotic heart disease, sys
factors (Table 64.1). These pregnancies are at higher risk temic lupus erythematosus (SLE), etc.
TABLE 64.1: High-risk conditions with poor fetal outcome

Maternal factors Fetal factors Pregnancy-specific factors
Chronic hypertension IUGR Poorly controlled gestational diabetes
Collagen-vascular diseases Congenital anomalies Multiple gestations
Sickle cell anemia Fetal cardiac arrhythmias Pregnancy-induced hypertension
Current substance abuse Isoimmunization Renal disease with pregnancy
Impaired renal function Hydrops fetalis Cholestasis of pregnancy
Asthma Fetal infections such as parvovirus, Premature rupture of membranes
Pneumonia coxsackie virus B, syphilis, toxoplasmosis (preterm)

Significant cardiac disease Unexplained elevated with pregnancy
Seizure disorders MSAF polyhydramnios and
Diabetes oligohydramnios
Acute febrile illnesses Placental abruption
Significant anemia (hematocrit < 26%) Abnormal placentation
Postdate pregnancy decreased fetal
movements
Unexplained stillbirth in a previous
pregnancy
SLE
Abbreviations: IUGR—Intrauterine growth restriction; MSAF—Meconium-stained amniotic fluid; SLE—Systemic lupus erythematosus
Pregnancy-specific Factors Methods of Assessment of Fetal Movement

Pre-eclampsia, gestational hypertension, oligohydram The mother is asked to lie down in the left lateral position
nios, polyhydramnios, intrauterine growth restriction and concentrate on any fetal movement, 2–3 times every
(IUGR), post-term pregnancy, moderate to severe iso day for 30–60 minutes. Less than 3 movements per hour
immunization, previous fetal demise (unexplained or on 2 consecutive days or less than 10 movements in 3
recurrent risk), multiple gestation with significant growth hours of 60 minutes, each requires further evaluation.
discrepancy, decreased fetal movement. Cardiff Count-to-10.
Sherer and associates (1996), observed decreased fetal The mother is asked start counting the fetal movements
activity with diminished amniotic volume. in the morning and record the time at which the tenth
movement occurs. More than 10 movements per 12 hours
Fetal Factors
are normal.
IUGR, isoimmunization and hydrops fetalis. Perception of fetal movement may be decreased in:
Obesity
TECHNIQUES OF ANTEPARTUM FETAL Anterior placenta
SURVEILLANCE Hydramnios
Congenital abnormalities,
Fetal Movement Counts by the Mother
Maternal activity
The fetal movement count which is perceived by the mother
Maternal medications, e.g. narcotics and barbiturates.
is a universally accepted method of fetal surveillance
which is non-invasive and has no cost. This method is Maternal Assessment of Fetal Activity
useful in singleton pregnancies.
The principle behind this is that the fetuses with Maximum movements are between 9 pm and 1 am.
hypoxemia are sluggish in movements. The patient is Movements increase with maternal hypoglycemia.
instructed to count the fetal movements over a one hour Fetal movement (as is commonly perceived) does not
period. Three to five movements in an hour are considered increase after meals.
reassuring. The other methods are the Cardiff Count- Periods of active fetal movement are often cyclic lasting
to-Ten chart, wherein the patient records fetal movements for about 40 minutes with intervening non active
while performing her usual daily activity. A period of periods of 20 minutes.
12 hours without at least 10 perceived movements requires Presence of fetal activity is a reassuring sign.
further evaluation in the form of a NST. Absence of fetal activity requires further evaluation.
Antepartum Fetal Surveillance 605
The fetus has four stages of behavior in the uterus. Stage

1F is quiet sleep (quiescent stage); stage 2F has frequent
eye movements, gross body movements and accelerated
heart rate; stage 3F is defined by no accelerations of heart
rate along with absent body movement and continuous
eye movements; stage 4F is vigorous eye movements, body
movements along with acceleration of heart rate.
Further evaluation, if daily fetal movement record
Fig. 64.1: Reactive nonstress test
(DFMR) is decreased.
Abbreviations: UA—Uterine activity; FM—Fetal movement
Nonstress Test (NST)

The principle of the NST rests on the fact that the autonomic
system comprising of sympathetic and parasympathetic
system that controls the fetal heart rate (FHR), which
in response to fetal movement shows a temporary
acceleration of the FHR, in normal fetuses (reactive
NST). However, when the fetus is hypoxic or acidotic, this
acceleration of heart rate will be absent, i.e. nonreactive
NST. The other reasons for a nonreactive NST may be, fetal Fig. 64.2: A non reactive nonstress test
sleep cycle, immaturity of the fetus, maternal smoking Abbreviations: UA—Uterine activity; FM—Fetal movement
prior to test, cardiac or neurologic anomalies in the fetus
and ingestion of drugs by mother who have cardiac effects,
Nonreactive (nonreassuring): Absence of the accelera-
e.g. β-blockers.
tions as described above is considered as nonreactive NST
The equipment required to conduct the test is a Doppler
(Fig. 64.2) and is nonreassuring.
ultrasound transducer and a tocodynamometer that
NST is only a screening test. Once nonreactive, further
record the fetal heart along with the uterine contractions.
tests are done to find fetal wellbeing.
The fetal movements are also recorded by the patient who
If extended NST is nonreactive, consider repeat test
presses a button whenever a movement is perceived.
between 9 pm and 1 am.
Besides the accelerations, the baseline variability
should also be studied in the fetal heart tracing. A good Advantage: Easy to use and interpret, non-invasive.
variability signifies a healthy fetus whereas if the FHR Disadvantage: High false-positive and-negative rate.
tracing is almost flat with no change over a 10 minute
period, it indicates depressed central nervous system Vibroacoustic or Fetal Acoustic
(CNS) of the fetus and is nonreassuring. Stimulation Test (VAS)
The reactivity of the FHR is dependent on the gestational The principle is to startle the fetus with a loud sound.
age of the fetus. It is absent before 24 weeks and generally Vibroacoustic stimulators are artificial larynxes or an
starts after 28 weeks. Hence, interpretation in the preterm electric tooth brush that is held briefly to the maternal
fetuses may have different criteria. abdomen near the fetal head. The advantage of this test
is that it may shorten the time taken for NST and also
Interpretation of the NST arouse the baby from its sleep cycle. The stimulus can
Reactive (reassuring): In a fetus from 33 weeks to term- be given after about 5 minutes of starting the NST. A
acceleration of the fetal heart by 15 beats per minute for at Cochrane review in 2014 found that performing VAS test
least 15 seconds in a 20 minute period (Fig. 64.1). It can be decreases the time taken for NST by 7 minutes. It has been
extended upto 40 minutes if reactivity is not demonstrated recommended that the stimulus should be given through
in 20 minutes (extended NST). Reactive NST is a reassuring the maternal abdomen for 1–2 seconds (ACOG practice
finding. bulletin 145, 2014). If the response is not seen then upto
In gestations less than 32 weeks, it is suggested that 3 repeat stimuli for longer periods of up to 3 seconds
2 accelerations of 10 beats per minute over 10 seconds may be given. An absence of response with VAS warrants
should be considered reactive (Macones et al. 2008). further evaluation.
Contraction Stress Test (CST)

The aim of the test is to study the FHR pattern under the
stress of labor which may lead to hypoxia in a compro-
mized fetus. For achieving this, it is required to have at
least 3 uterine contractions over a 10 minute period. The
contractions can be induced by oxytocin infusion, nipple
stimulation or may be spontaneous. In a compromized
fetus, the FHR may dip just after the nadir of contraction
Fig. 64.3: A negative CST. There are no late decelerations
also known as late deceleration. It is a more cumbersome
Abbreviations: FM—Fetal movement; UA—Uterine activity
test compared to NST and also is contraindicated in
several conditions which are actually a contraindications
for normal delivery. These are as follows:
Placenta previa, vasa previa
Previous classical cesarean section or extensive past
uterine surgery
Women at risk of preterm labor
Preterm premature rupture of membranes (PPROM).
CST Procedure
The patient is made to rest in a semi fowler position,
with a slight tilt to the left to avoid supine hypotension. Fig. 64.4: A positive CST. Late decelerations are observed
Blood pressure (BP) is recorded every 5–10 minutes. Abbreviations: FM—Fetal movement; UA—Uterine activity
Baseline FHR and uterine tone are recorded on a
cardiotocograph (CTG) for 10–20 minutes. with contractions more frequently than every 2 minutes or
The test requires 3 uterine contractions lasting 40–60 lasting longer than 90 seconds.
seconds over 10 minutes. Note: A late deceleration is defined as a decrease in FHR
Oxytocin is administered by an infusion pump at after the peak of the uterine contraction which persists
0.5 mU/min. even after the contraction has stopped. A late deceleration
The infusion rate is doubled every 20 minutes till is ominous and indicates fetal hypoxia; a variable
required contractions occur (maximum 10 mU/min). deceleration is termed when the drop in FHR has no fixed
relationship with the uterine contraction. The main cause of
Interpretation of CST variable deceleration is cord compression and oligoamnios.
Interpretation of the CST is made according to the absence
or presence of late decelerations in the FHR which reach Nipple Stimulation Test
their nadir after the peak of the contraction and persist Apply a warm moist towel to each breast for 5 minutes. If
after the contraction ceases. no uterine contractions occur then massage one nipple
The ACOG practice bulletin (145, 2014) defines the with palmar surface of fingers through her clothes for
following terms for interpretation of CST: 2 minutes, stop for 5 minutes and repeat if required. The time
Negative: A negative test is considered as reassuring— required is approximately 45 minutes. Hyperstimulation is
there are no late decelerations or any significant variable avoided by intermittent stimulation. Contraindications and
decelerations (Fig. 64.3). interpretations are the same as for oxytocin stress test (OCT).
Positive: Positive or nonreassuring test is one in which
there are late decelerations after at least ≥50% of Biophysical Profile (BPP)
contractions. It is considered positive even if there are less The BPP combines the NST along with certain fetal
than 3 contractions in 10 minutes (Fig. 64.4). parameters which are assessed by ultrasonography. A
Equivocal: An equivocal or suspicious test is when there numerical score is given to each of the 5 parameters which
are significant variable decelerations or intermittent are tested—NST, gross body movements, fetal tone, fetal
late decelerations, whereas an equivocal-tachysystole breathing movements and amniotic fluid volume (AFV). A
(hyperstimulation) is defined if there are decelerations normal test has a maximum of 10 points.
It is hence possible to assess acute and chronic indicators Clinically Significant Points
of hypoxia with this test. AFV is reduced in chronic hypoxia Do not perform BPP within 48–96 hours of corticosteroids
whereas all the other parameters are deranged in acute because they decrease the BPP. These changes are transient
hypoxia. The derangement of the parameters is reverse of the and return to normal by 48–96 hours after steroid treatment.
acquisition of these neuro-developmental characteristics as NST is an indicator of present fetal condition and is
seen below. the first one to be affected in BPP. This is followed by fetal
Timing of Fetal Neurodevelopment breathing movements and then gross fetal movements.
Fetal tone is the last to be affected. Amniotic fluid index
Tone appears the earliest at 7.5–8.5 weeks
(AFI) is a marker of long-term fetal status.
Body movements follow at 9 weeks
Breathing is seen at 20–21 weeks Interpretation of BPP (Table 64.2)
FHR reactivity appears at 24 weeks.
The BPP has to be interpreted in the background of the
Sequence of Fetal Deterioration clinical features. For instance, in a case of 26 weeks’
gestational age fetus with PPROM, there may be a low
Cardiac reactivity in NST decreases or is absent (Fig. 64.4)
score of 6 points because of oligohydramnios (because of
followed by fetal breathing deterioration
drained liquor and not because of chronic hypoxia) and no
Absent/diminished fetal movement
reactivity of fetal heart because of immaturity. However,
Decrease in fetal tone
despite the low score, the baby may not be compromized.
Amniotic fluid decreases (chronic hypoxia).
Further, there are times when the baby may be in the sleep
Technique of Manning’s Biophysical cycle or the mother may be sedated, in which case clinical
Profile (MBPP) Scoring judgment is important.
Sensitivity, specificity and false-positive rates for the
Fetal breathing movements
NST, CST and BPP are shown in Table 64.3.
• Normal is (score 2), when there is at least movements
one episode of > 30 seconds in 30 minutes of
Modified Biophysical Profile
observation.
• Abnormal (score 0), is absence of/no episode of >30
Modified biophysical profile (MBPP) is an alternative to the
seconds breathing movement in 30 minutes. BPP, which combines the NST and assessment of AFV on
Gross body movements
• Normal is (score 2), when there are at least 3 move TABLE 64.2: Illustration of interpretation BPP score
ments discrete body/limb movements in a period of If score is 10 The infant is normal. Repeat test weekly. In diabetics
30 minutes. and prolonged gestation repeat twice weekly
• Abnormal (0), upto 2 movements in 30 minutes. If score is 8 Low-risk of chronic asphyxia. Oligohydramnios is a
Fetal tone indication for delivery, otherwise repeat weekly
• Normal (2), there is at least 1 episode of active If score is 6 Suspect chronic asphyxia. If >36 weeks and
conditions favorable then deliver
extension followed by flexion of fetal limb/trunk or
If repeat is < 6 Deliver
opening and closing of hand.
If score is 4 Suspect chronic asphyxia. If >36 weeks then
• Abnormal (0), slow extension which comes to partial
deliver. For others, repeat test same day. If still < 6
flexion or movement in full extension or an absence then deliver
of fetal movement. Score is 0–2 Certain fetal asphyxia. Deliver
Reactive NST
• Normal (2), are when there are at least 2 episodes of TABLE 64.3: Statistical measures of tests for antepartum fetal
acceleration > or = to 15 bpm lasting for at least 15 surveillance
seconds in 30 minutes. Statistical measure NST CST BPP
• Abnormal (0), fewer than 2 accelerations or <15 bpm Sensitivity Poor Average High
in 30 minutes. Specificity High High High
Amniotic fluid False-positive rate High High High
• Normal (2), minimum one pocket of AFV on ultra False-negative rate Low Low Average
sound which measures 2 cm. Abbreviations: NST—Nonstress test; CST—Contraction stress test;
• Abnormal (0), no amniotic fluid detected/pocket < 2 cm. BPP—Biophysical profile
ultrasound. The NST is an indicator of the acute oxygenation The umbilical artery systolic/diastolic (S/D) ratio > 95
and the AFI of long term oxygenation of the fetus. Hence, a the percentile for gestational age is abnormal.
combination of these two is often used instead of BPP, as it An absent or reverse flow is of value only in cases of
decreases the testing time tremendously. IUGR. Even reverse flow is not an indication for delivery
In a fetus who is hypoxemic, the blood flow is but merits other tests.
preferentially diverted to vital organs like brain and heart Reverse flow in the ductus venosus is an ominous sign
resulting in lesser blood supply to the kidneys, leading and predicts IUD within 7 days. Hence, in these cases
to low urine output and consequent oligoamnios, over very close watch is essential.
a period of time. There are two methods to assess the
amniotic fluid on ultrasound—the measurement of a single Fetal Lung Maturation Tests
deepest pocket and measuring the AFI. Both the methods They are essential in high-risk pregnancies (especially
have got almost similar values for predicting adverse fetal when premature) to predict the chances of developing
outcomes. The AFI is more commonly used. It is calculated respiratory distress syndrome (RDS). The methods used
by the sum of the single deepest pocket, which is cord free, can involve quantitative assessment of surfactant Lecithin/
in all the four quadrants of the abdomen. A minimum of 5 sphingomyelin (L/S) ratio, measure the function of surfactant
cm is considered as normal. Hence, if NST is reactive and (shake test) or can evaluate the amniotic fluid turbidity.
the AFI is more than 5, it is considered reassuring. If either Test for fetal lung maturity: (if the amount of pooling is
of the parameters is abnormal a full BPP is indicated. large) by evaluating
It has been seen with both BPP and MBPP that their L/S ratio
false positive rates are high though their false negative Phosphatidylglycerol (PG) level
rates are low. So, if these tests are normal there is very little Shake test: This is a semiquantitative measure of the
probability of occurrence of a stillbirth in a week after the surfactant present in a sample of amniotic fluid. In this
test. test, the fluid is mixed with ethanol in the necessary
amounts to achieve concentrations of 44–50%. The risk
Umbilical Artery and Ductus Venous Doppler of RDS is 73% when the test is negative and no bubbles
Velocimetry are formed at 44% of alcohol. The chances of developing
Doppler ultrasonography is used to assess the hemo RDS is 0.35% if bubbles are produced when the ethanol
dynamic components of vascular impedance (by a non- concentration is 47%.
invasive method), in the umbilical artery in high-risk How often should antepartum surveillance be per
pregnancies only. Doppler flow velocimetry is being formed?
used as a fetal surveillance technique because it has Antepartum testing has been advocated by most authors
been seen that flow velocity waveforms in the umbilical at weekly intervals. However, the frequency of the tests
artery of fetuses with normal growth parameters is guided by the maternal high-risk condition and the
are different from those of fetuses with IUGR. The clinical setting under which these tests are performed.
umbilical flow velocity waveform of a normally growing More frequent testing is indicated in conditions such as
fetus has high-velocity diastolic flow, whereas when preterm rupture of the membranes, severe IUGR with
60–70% of the uteroplacental circulation is compromized, oligohydramnios and severe, acute maternal illness. Many
the umbilical artery diastolic flow is diminished, resulting studies have shown improved outcomes with twice-weekly
in growth restriction. As the severity of the pathology testing, particularly when the NST is used as the primary
increases, the flow in the umbilical artery may become screening. General guidelines for antepartum testing
absent or even reversed. There is a high chance of poor are given in Table 64.4. It is important that the testing is
fetal outcome among such pregnancies. These findings individualized according to the patients’ requirement.
can also predict congenital abnormalities.
Blood flow through ductus venosus also gives good MANAGEMENT
results. The patient who has an abnormal screening tests should
be followed by a more sensitive and specific test, to avoid
Doppler Ultrasound acting on a false-positive result. For example, a patient
This technique is not beneficial for routine fetal surveil with decreased fetal movement should be advised a NST;
lance. Its main role is in cases of IUGR. if this is also nonreassuring, a CST or BPP should follow.
TABLE 64.4: Initiation and frequency for antepartum testing in to accelerate fetal lung, brain and gut maturity, as long as
high-risk conditions maternal and fetal conditions are monitored closely.
Condition Initiation Frequency Antepartum surveillance in normal pregnancy should
begin at 36 weeks. In high-risk cases it should begin at 32
Post-term pregnancy 41 weeks Twice a week
weeks. However, in case of severe disease start surveillance
PPROM At onset Daily at 28 weeks.
APH 26 weeks or at onset Twice a week
Oligoamnios 26 weeks or at onset Twice a week SUMMARY AND RECOMMENDATIONS
Diabetes The testing should be at 32–34 weeks of gestation for
Class A1 (well- controlled 36 weeks Weekly most pregnancies that are at increased risk of stillbirth.
and no complications) In pregnancies with multiple or serious high-risk
Class A2 and B (well- conditions, testing may be initiated as early as 26–28
controlled and no 32 weeks Twice a week weeks of gestation.
complications)
Women at high-risk for stillbirth should be advised
Class A or B with poor
control, Class C-R 28 weeks Weekly
antepartum fetal monitoring using the NST, CST, BPP
or MBPP.
Pregnancy- induced/ 28 Weeks Weekly
In cases, where the clinical condition that prompted
chronic hypertension
testing persists, a reassuring test should be repeated
Collagen-vascular 28 Weeks Weekly weekly or, depending on the test used and the presence
disease/antiphospholipid
antibody syndrome
of certain high-risk conditions, twice weekly until
delivery. Any significant deterioration in the clinical
Thyroid disease 32 weeks Weekly
picture requires fetal reevaluation, regardless of the
Maternal heart disease 28 weeks Weekly amount of time that has elapsed since the last test.
(NYHA class III or IV) When a NST or NBPP is nonreassuring, it should be
Cholestasis of 32 weeks Weekly further followed by a CST or a full BPP. Subsequent
pregnancy management should be decided according to the results of
Prior history of stillbirth At 2 weeks before Weekly the CST or BPP, the gestational age, the degree of oligohyd-
prior ramnios (if assessed) and the overall maternal condition.
fetal death Oligohydramnios, which is defined as no vertical pocket
Multiple gestation 32 weeks Weekly of amniotic fluid greater than 2 cm or an AFI of 5 cm or
Isoimmunization 26 weeks Twice a week less, as assessed ultrasonographically, requires (depen-
ding on the severity of oligohydramnios, the gestational
Fetal growth 26 weeks or at onset Twice a week
age of the fetus and the maternal clinical condition)
restriction
delivery, or close maternal or fetal surveillance.
Decreased fetal At time of complaint Once If there are no obstetric contraindications, delivery
movement
of the fetus with an abnormal test may be attempted
Abbreviations: PPROM—Preterm premature rupture of membranes; by induction of labor with continuous monitoring
APH—Antepartum hemorrhage; NYHA—New York Heart association of the FHR and contractions. In case, repetitive late
decelerations are seen, cesarean delivery is advisable.
Secondly, a test with equivocal or suspicious results should Recent, normal antepartum fetal test results are not enough
either be acted on (i.e. with delivery if at term) or repeated to preclude the use of intrapartum fetal monitoring.
same day but never ignored. Umbilical artery Doppler velocimetry may benefit
Once a decision is made to proceed to delivery, the only pregnancies with IUGR. If used in this setting,
route and exact timing depend on other obstetric factors. decisions regarding timing of delivery should be made
Induction of labor is to be judiously conducted under using a combination of information from the Doppler
electronic surveillance, when the antepartum tests suggest ultrasonography and other tests of fetal wellbeing, along
utero-placental insufficiency. Delivery can often be safely with monitoring of maternal status. Middle cerebral
delayed while the medical condition of the patient is stabilized artery Doppler velocimetry may also be considered as
(e.g. control of hypertension or correction of metabolic another investigational approach to antepartum fetal
abnormalities) or while corticosteroids are administered surveillance.
1. What do you understand by the term antepartum fetal surveillance?
2. Differentiate between biophysical profile and modified biophysical profile.
3. Write a short note on:
i. Nonstress test (NST)
ii. Contraction stress test (CST)
iii. Nipple stimulation test.
65 Intrapartum Fetal Monitoring
Sudha Salhan, Divya Pandey, Indira Ganeshan
INTRODUCTION INTRAPARTUM FETAL MONITORING

Fetal monitoring (surveillance) in labor is crucial. The It is done to detect fetal hypoxia promptly and manage it
fetus is inaccessible to direct evaluation of its wellbeing. rapidly. The method which is noninvasive and acceptable to
Oxygenation of the fetus is considered as a very important the mother and has high specificity and sensitivity is ideal.
indicator of fetal health. Hence, in intrapartum fetal However, such method is not developed yet. Fetal heart rate
monitoring, we try to detect the severity and time of fetal (FHR) is considered for fetal monitoring. It depends on many
oxygen lack and acidosis. stimuli reaching the brain like chemoreceptors, pressure-
receptors and metabolic changes in brain. If FHR is normal,
Causes of less oxygen supply (and thus perfusion) to the
we assume proper oxygen supply to the fetus. Abnormal FHR
fetus during labor signifies hypoxia or other factors affecting FHR.
Longer and stronger uterine contractions
Fetal surveillance during labor includes the following
Supine position in labor methods:
Regional anesthesia Intermittent fetal heart auscultation (FHA) by Pinard’s
Maternal hemorrhage (antepartum) stethoscope, stethoscope or simple heart Doppler are
Poor uteroplacental perfusion in gestational hyperten- traditional methods of fetal surveillance
sion, pre-eclampsia, eclampsia, diabetic vasculopathy, Meconium stained liquor
collagen vascular diseases and post maturity, etc. Electronic fetal monitoring—cardiotocography (CTG)
recording
Computer assistant interpretation of CTG
FETAL RESPONSE TO REDUCED
Fetal acoustic stimulation test (FAST)
OXYGEN DELIVERY Assessment of amniotic fluid volume
Umbilical artery Doppler Velocimetry for intrapartum

Fetal Chemoreceptors monitoring
Fetal chemoreceptors are situated in the neck along the Fetal blood sampling
sides of the carotid artery. They are sensitive to fetal blood Fetal scalp stimulation test
oxygen content. They respond to a change in arterial Intrapartum monitoring with fetal electrocardiography
oxygen content, rather than to a given level of oxygen in (ECG) wave form analysis
the blood, i.e. oxygen delivery to the mother rather than Fetal pulse oximetry
the absolute level of fetal arterial oxygen. Near infrared spectroscopy (NIRS).
Fetal Catecholamines Secretion Intermittent Auscultation of FHS (IA)

Adrenal glands are stimulated only if the oxygen delivery (Table 65.1)
to the fetus is rendered less for a longer period or a severe Auscultation should be performed for full one minute, with
fall in fetal oxygenation occurs. This causes significant rise 30–45 seconds following uterine contractions (to note any
in catecholamine levels. post contraction dip).
TABLE 65.1: Fetal heart auscultation (FHA) there is any stress on the fetus during contractions, it will
Low-risk cases Frequency of IA
reduce the placental perfusion. If the FHR is maintained
and no change is observed, the trace is normal and labelled
1st stage Every half hour/30 minutes
reassuring. The chances of fetal hypoxemia other than due
2nd stage Every 5 minutes to acute events are unlikely in the next few hours of labor.
High-risk cases
1st stage Once every 15 minutes Duration of Recording
2nd stage Every 5 minutes It is usually for 20 minutes, but can be as short as 5–10
minutes if the baseline rate, baseline variability, two
Abbreviations: IA—Intermittent auscultation
accelerations and two contractions with no FHR change
can be identified.
Auscultation must also be done:
Before amniotomy Advantage over FHR Auscultation
Administration of medication/analgesia
The features of reduced baseline variability and shallow
After amniotomy
deceleration are recorded on paper; these are suggestive of
Abnormal uterine activity.
fetal hypoxia. The results of AT with or without FAST may
Technique of Auscultation be a good predictor of the fetal condition at the time of
admission and the next few hours in a term fetus at low risk.
Perform Leopold’s maneuvers
When AT is reactive (reassuring)—intermittent electronic
Place Doppler/fetoscope/stethoscope over fetal back
fetal monitor (EFM) for 10–20 minutes every 2–3 hours, or
Feel mothers pulse and calculate difference from FHR
auscultation 20–30 minutes may suffice.
Palpate uterine contractions during FHR auscultation
The CTG findings can be interpreted by computer also.
Count FHR before, during and after contraction for
atleast 60 seconds. Fetal or Vibroacoustic Stimulation
Normal Findings Test (FAST/VAST)
Fetal heart sound (FHS) 120–160 beats/minute An artificial larynx is used to produce sounds and stimulate
With accelerations. the fetus. The response is noted on CTG.
The sensitivity of AT is increased by combining it with
Abnormal Findings FAST after a 15–20 minutes AT, FHR acceleration is elicited
Clear FHS not heard by Vibroacoustic stimulator.
Bradycardia (below 120/minute) Response: A fetus which is not hypoxic, would exhibit
Tachycardia (above 160/minute) two accelerations, more than 15 beats for 15 seconds or a
No accelerations heard, especially with fetal movement sustained acceleration lasting more than 3 minutes.
Deceleration of FHR. Type 1A: Prolonged period of acceleration or tachycardia
more than 15 beats above the baseline for 3 minutes.
Limitations
Type 1B: Two accelerations more than 15 beats for 15
Baseline variability, accelerations and decelerations are seconds or single acceleration of more than 1 minute.
difficult to quantify. Type 2: A biphasic response with acceleration followed by
Color of the Liquor deceleration usually more than 60 beats from the baseline
lasting more than 60 seconds.
Hypoxia in fetus is depicted as meconium staining.
Type 3: No acceleration or accelerations less than 15 beats
However, nowadays intrapartum meconium as a sign of
from baseline rates.
fetal hypoxia is not that important.
Type 1A and Type 1B are normal, type 2 and type 3 are
Cardiotocography Recording abnormal.
Admission Test (AT) Amniotic Fluid Volume Assessment

This is done to know the fetal status in early labor. Liquor amnii is an important indicator of fetal wellbeing
In this test, the FHR is recorded electronically for a and also is an important predictor for perinatal outcome.
period of 20 minutes on admission. If during this time Decreased amniotic fluid index (AFI) is associated with
Intrapartum Fetal Monitoring 613
increase mortality and morbidity of the baby and an Bradycardia can be mild (100–110 bpm), moderate
increased rate of operative delivery of the mother. (80–100 bpm) or severe bradycardia (less than 80/min).
Count for continuous 3 minutes.
Electronic Fetal Monitoring (EFM) Causes of bradycardia
The predictive value of EFM is better in: Fetal head compression during labor (physiological)
High-risk pregnancy
Fetal hypoxemia
Thick meconium stained (dark green) and tenacious
Fetal congenital heart block
liquor. Maternal hypothermia.
Limitations Tachycardia means baseline FHR more than 160/

min. It can be mild tachycardia (160–180 bpm) and severe
Nonspecific for diagnosis of fetal wellbeing.
Shortage of experienced trained personnel. (≥ 180 bpm).
Intrapartum CTG is not a sensitive index of fetal Causes of tachycardia
wellbeing. There is a poor correlation with cord arterial Maternal infection (chorioamnionitis)
blood pH and Apgar at birth. The interpretation of intra Maternal hyperthermia
partum CTG is a major problem. Fetal compromise
Fetal cardiac arrhythmias

Advantages of EFM Maternal medications (atropine, terbutaline and ritodrine).
Online documentation
Easy application of equipment Beat-to-Beat Variability
Accuracy of picking up FHR signals
This is regulated by the autonomic nervous system via the
Information on uterine contractions
sinoatrial node which mediates movement to movement
Reduced cost of equipment.
or beat to beat changes of baseline FHR. Variability can be
There are two types of continuous fetal heart monitoring: short term and long term. The alteration of FHR from one
1. Internal monitoring: Internal fetal scalp electrodes
beat to the next (R wave) is short-term variability whereas,
are applied to get electric fetal cardiac signals which
the alteration of FHR over one minute causing waviness of
are fed into a cardiotocometer for FHR calculation. The
the baseline is long-term variability. Normal frequency is
fetal ECG complex is also shown on the recordings. This
method is more invasive but precise. 3–5 cycles/min.
2. External monitoring: Doppler principle is used to get FHR
Deceleration
through the maternal abdominal wall. Ultrasound signals
are edited before they are printed on bedside monitoring It is divided into early, late or variable deceleration
tracing paper. Usually 3 cm per minute and 30 beats per depending on its onset compared with the corresponding
cm is the usual speed of the graph tracing of FHR. uterine contraction.
Early deceleration of FHR implies with uterine con-
Indications for EFM tractions, there is slow decrease and return to baseline.
High-risk pregnancy—preterm and postterm pregnancy, Late deceleration is a slow reduction of FHR starting at
intrauterine growth restriction (IUGR), small for date or or after peak of uterine contraction and coming back to
maternal diseases baseline only after the contraction is over.
Inaudible or nonreassuring finding on intermitted Variable deceleration is the most common deceleration
auscultation pattern encountered during labor. There is sudden

Meconium-stained amniotic fluid (MSAF) decrease in FHR. Deceleration varies with successive
Inadequate progress of labor contractions.
During oxytocic administration Fetal health is marked by accelerations and normal
With epidural anesthesia baseline variables.
Breech presentation. Intrapartum CTG trace are classified as follows:
Normal: Fetal baseline heart rate of 110–150/minute with a
FHR on CTG variability of 10–25 beats/minute and two accelerations in
Bradycardia means baseline FHR less than 110/minute. 20 minutes and no decelerations.
Fetal head compression also causes bradycardia but the Indeterminate: Absent acceleration in any of the following
fetal heart picks up soon after contraction. is suspicious.
Baseline FHR less than 110 bpm or more than 150 bpm They are strong predictor of normal fetal acid-base
Baseline variability less than 10/min (less than 5/min, status. They should be monitored and no specific action is
needs urgent attention) or more than 40/min required.
Variable decelerations not accompanied by ominous
Category II FHR Tracings (indeterminate): They include
features. all FHR tracings, not categorized as I or III. Examples may
Abnormal: Absent acceleration in any of the following is include any of the following:
abnormal.
Baseline rate
Baseline rate and variability less than 5 or greater than
• Bradycardia not accompanied by absent baseline
40/min
Ominous features with variable deceleration
variability
Repeated late decelerations.
• Tachycardia.
Baseline FHR variability
Ominous Features • Minimal baseline variability (amplitude <5 beats/
Persisting > 60 seconds minute)
Beat loss > 60 bpm • Absent baseline variability with no recurrent decel-
Late recovery component of late deceleration erations (amplitude range undetectable)
Poor baseline variability between and/or during decel-
• Marked baseline variability (amplitude>25 beats/
erations. minute).
Other specific CTG patterns categorized as abnormal
Accelerations
are:
• Absence of accelerations after fetal stimulation.
Sinusoidal pattern
Periodic or episodic decelerations
Prolonged bradycardia (below 100 bpm) for > 3 minutes
Shallow decelerations in the presence of markedly

• Recurrent variable decelerations accompanied by
reduced baseline variability below 5 bpm in a non- minimal or moderate baseline variability
reactive trace. • Prolonged deceleration more than 2 minutes but
Meta-analyses of the trials of the liberal use of less than 10 minutes
intrapartum EFM versus IA shows that EFM is associated • Recurrent late decelerations with moderate baseline
with increased operative delivery for fetal distress, without variability
an associated improved neonatal wellbeing. There is • Variable decelerations with other characteristics such
a lack of knowledge, among the obstetricians, about as slow return to baseline, overshoots or shoulder.
interpretation of uterine tracing. Hence, Doppler training
They are not strong predictive of abnormal fetal acid-
is essential, velocimetry of umbilical vessels is more
base status, but they require evaluation and continuous
accurate. Cesarean section (CS) rate is more in view of
medico-legal implications, e.g. Consumer Act, but there is fetal surveillance and reevaluation.
no decrease in perinatal mortality. If the EFM findings are Category III FHR Tracings(abnormal): They include:
normal there is no danger to the fetus. But abnormal EFM Sinusoidal pattern (visually apparent, smooth, sine
findings do not necessarily means a compromized fetus. wave like undulating pattern in FHR baseline with a
Its negative predictive value is greater than its positive cycle frequency of 3–5 per minute which persists for
predictive value. 20 minutes or more)
Recently, a three tiered system for categorization of Absent baseline FHR variability with any of the following
FHR pattern has been described. It has to be kept in mind • Recurrent late decelerations
that any particular fetal heart pattern tells only about the • Recurrent variable decelerations
current acid-base status of fetus. • Bradycardia.
Category I FHR tracings (normal): They include all of the
They are associated with abnormal fetal acid-base
following:
status at the time of observation. They require prompt
Baseline rate: 110–160 beats/minute
Baseline FHR variability: Moderate (normal) i.e.

evaluation and treatment with maternal oxygenation,
amplitude range 6–25 beats/minute change of posture, treatment of maternal hypotension and
Late or variable decelerations should be absent tachysystole (> 5 contractions in 10 minutes) with FHR
Early decelerations may be present or absent changes and stopping of labor stimulation. If unresolved,
Accelerations may be present or absent. delivery should be expedited.
Fetal Scalp Blood Sampling

It may be useful (when available) when fetal monitoring
patterns are non-interpretable or nonreassuring. Fetal
blood pH more than 7.25 needs repeating the sample, if
CTG abnormalities persists. If the fetal pH is between 7.21
and 7.24, take another sample in half an hour if the reading
falling deliver as early as possible. If it is less than 7.20,
immediate delivery is mandatory.
Disadvantage
Needs special instrument (blood gas analyzer) which
requires expert hands.
Measures the fetal blood pH at a particular time only
and it takes time for analysis. By the, time the results
are available the condition of the fetus may deteriorate
or improve. It does not depict the fluctuations that are
constantly occurring. Fig. 65.1: Fetal pulse oximetry sensor placement
Repeated tests only give a picture of the fetal condition.
It is an invasive procedure (to be repeated again and
Intrapartum Monitoring with Fetal ECG
again).
Waveform Analysis—Fetal ECG ST Segment
Fetal Scalp Stimulation Test (Fig. 65.2)
When the scalp is stimulated by a painful stimulus by ST wave form analysis is a well-established stress test for
pinching with an Allis’s forceps, if acceleration is present, adults. Fetal ECG can be obtained from a conventional
it is unlikely that the scalp blood pH is below 7.20. This is fetal scalp electrode of CTG monitor. It measures the fetal
a good test to rule out those who are not at risk of acidosis stress in labor.
The PR interval correlates negatively with the FHR
but not those who are likely to be acidotic.
ST waveform: It is analyzed by a computer. The fetal ST
Fetal Pulse Oximetry (Fig. 65.1) changes correlate well with oxygen saturation of fetal
blood. It reflects the fetal heart and brain sensitivity to
In this, a technology similar to adult pulse oximetry is
oxygen in the fetal blood. It is used when the gestational
used. A pad like sensor of fetal pulse oximetry is inserted
age is more than 36 weeks. It is carried out along with
transcervically and placed between wall of uterus and fetal
face. The sensor is then connected to a light source. The
reflections are split and transmitted to an electronic sensor
and a low voltage microprocessor-based monitor. There
are light emitting diodes (which are light sources) and two
photodetector diodes (one emitting red light of wavelength
735 nm and infrared light of wavelength 890 nm). When
these light waves pass via the tissues of the fetus at the site of
sensor placement, a fraction of the light waves is absorbed
and rest reflected back and is measured. The absorbed part
reflects oxygen saturation at each arterial pulse.
Disadvantages
The sensor may change its position and altered cutaneous
blood flow may change the results. Further research is Fig. 65.2: Bipolar electrode attached to fetal scalp for detection of
needed in this direction. fetal QRS complex and ST wave
CTG monitoring. If a fetus with previously normal ECG Signs of fetal distress
or ST waveform shows any abnormality during second Abnormal FHR pattern
stage of labor, the delivery should be undertaken Meconium-staining of the liquor
immediately. Thus, this modality helps in preventing Abnormal pH < 7.20
intrauterine fetal demise. Further research is going on, Low Apgar score at 1 minute.
in cases of fetal growth restriction and prematurity, etc. Fetal response to hypoxia will depend on:
Disadvantages: It is an invasive procedure and hence, Acuteness of hypoxia
contraindicated in human immunodeficiency virus Severity of hypoxia
(HIV) positive and hepatitis B infected mothers. Duration of insult.
• It may cause scalp injury Acute hypoxia will cause an initial fall in FHR due to
• Cervical dilation must be adequate. chemical receptor-mediated stimulation and later due to
To avoid the invasive aspect, some obstetrician are myocardial hypoxia leading to respiratory acidosis. If not
using 12 abdominal electrode to do the test, though this relieved, it leads to metabolic acidosis, decrease in pH and
needs further refining. increase in base deficit.
If labor is progressing rapidly and FHR changes are Total sudden cessation of oxygenation will affect the
gradual, only therapeutic measures to increase oxygen pontine region and cause sudden fetal death.
supply and the use of forceps at full dilatation of the cervix Graded hypoxia causes necrosis of basal ganglia and
will suffice. hypoxemic encephalopathy. Antepartum surveillance in
But if the progress is slow and FHR is rapidly changing normal pregnancy should begin at 36 weeks. In high-risk
for the worse, a CS must be performed. The presence of cases, it should begin at 32 weeks. However, in cases of
other risk factors are also important, e.g. IUGR, positron severe disease, starts surveillance at 28 weeks.
emission tomography (PET) and meconium-staining of
the liquor. Definition of Nonreassuring FHR
Near Infrared Spectroscopy (NIRS) Variable deceleration: These are non-uniform and
periodic decreases in FHR from the baseline rate
Here, NIRS detectors are placed on the fetal head. Light is unrelated to uterine contractions.
passed through the detector. It will be reflected back depend- Severe variable deceleration: FHR of less than 70 bpm
ing on the oxygenation and the amount of blood flow through with duration of more than 60 seconds.
the fetal head near the detectors. This can be monitored Persistent severe variable deceleration: These are
continuously during labor. This method is still evolving. severe variable decelerations persisting for more than
30 minutes.
FETAL DISTRESS (FETAL COMPROMISE, Late decelerations: Decrease in FHR from the baseline
NONREASSURING FETUS STATUS) rate with a lag time of greater than 20 seconds from
the peak of the contractions to the nadir of FHR
Fetal compromise is a syndrome complex of intrauterine
deceleration.
fetal jeopardy and is a result of intrauterine fetal hypoxia.
Persistent and non-remediable late deceleration:
It can either occur in the antepartum period or during
Late decelerations refers to dips in FHR which are non
labor (that is, intrapartum). Seventy percent of fetal deaths
reponsive to the usual obstetrical interventions and
occur in early labor or before the onset of labor. Hence,
occur repeatedly over a period of 10–15 minutes.
the importance of both antepartum and intrapartum fetal
Severe bradycardia: FHR less than 80 bpm.
surveillance. The aim of fetal surveillance is to predict
Persistent severe bradycardia: Severe bradycardia
the potential adverse events by detecting warning signs
that lasts for more than 5 minutes.
and accordingly take best possible timely intervention
to prevent fetal demise. The term fetal distress can be
Management of Fetal Distress
replaced by nonreassuring fetal status (NRFS). This
includes alteration of FHR. For detecting, NRFS apart from Intrauterine Fetal Resuscitation
meconium-staining, one or more of the following must be Re-position the patient especially if under epidural
present: anesthesia. Shift the patient to the lateral position to
Persistent severe variable deceleration increase fetal placental perfusion. Variable decelerations
Persistent and non-remedial late decelerations due to cord compression as in oligohydramnios may
Persistent severe bradycardia. disappear by changing position.
Stop oxytocin or other uterine stimulants if on-flow. The patient should be oxygenated and hydrated before
Hydration: 180–200 mL ringer lactate solution per hour the procedure.
should be given unless contraindicated. Inadequate In case the mother has a high-risk for anesthesia or
uteroplacental perfusion in most of the cases is operative delivery then the condition of the mother takes
responsible for fetal hypoxia and acidosis. precedence over the fetal condition.
Oxygen by mask at the rate of 5–6 L/min. (Oxygen
should not be given in a chronically asphyxiated fetus.) Meconium

There is no role of oxygen if decelerations persist in Meconium is the tenacious, odorless, viscid, green-brown
spite of oxygen. material, first seen in the fetal intestines at 10–12 weeks of
Cord prolapse is ruled out by doing per vaginal exami-
gestation. At term 60–200 gm of meconium is present in
nation. the fetal intestine.
Intravenous (IV) dextrose (5%) at 180–200 mL per hour
Contents: Meconium is the first feces of a fetus or the
may benefit a normoglycemic fetus. However, in a newborn infant. It primarily contain water (70–89%)
growth restricted fetus who cannot surmount insulin derived from the fetal swallowing of the amniotic fluid.
response to hyperglycemia, Dextrose infusion induced The composition of meconium is undigested debris
hyperglycemia can block cellular glucose uptake thereby from products of fetal lung secretions like phospholipid
leading to anerobic metabolism and hence, fetal distress.
and glycerol, desquamated squamous cells, swallowed
Ensure presence of qualified personnel for resuscitation
amniotic fluid, lanugo, scalp hair and vernix, bile acids,
of newborn.
salts, proteins, lipids, cholesterol, steroid precursors
Tocolysis can be considered if there is abnormal uterine
enzymes and mucopolysaccharides and pigment biliverdin
activity and the operation theater (OT) is not immediately
and bilirubin (the last one gives the color to meconium).
available. Bolus dose of Terbutaline 0.25 mg SC or IM can
Although, it is an excellent culture medium, meconium
be given. It causes maternal tachycardia and increases
is normally sterile. After birth, the passage of meconium
placental perfusion. It also decreases uterine contraction
occurs within 24 hours in 95% of term infants. But the
leading to increased placental perfusion. A small dose of
passage of meconium before birth has always generated
nitroglycerine (60–180 mg) IV is also tried.
Consider amnioinfusion for variable decelerations.
great concern among the obstetricians.
Do a per-vaginal examination to assess the cervical Meconium passage may predispose the neonate to
dilatation, effacement and station of the presenting part. meconium aspiration syndrome (MAS). It is caused by
If the pre-requisite for instrumental delivery is fulfilled aspiration of meconium by the newborn during or just
the baby should be delivered soon in the presence of a after delivery leads to this condition.
pediatrician. Otherwise, if delivery is not imminent within Meconium passage can occur as a normal peristalsis in
30 minutes then patient should be taken up for lower a mature fetus or as a result of vagal stimulation as in cord
segment cesarean section (LSCS) immediately. When a compression, hypoxia stimulating arginine vasopressin
diagnosis of fetal distress is made, consider performing a release from the fetal pituitary, which causes contraction of
pathologic examination of placenta. the smooth muscle of the colon resulting in intraamniotic
defecation (increased peristalsis, sphincter relaxation and
Prior to LSCS meconium passage). Meconium-staining of the amniotic
Initiate preoperative routine including a written fluid during labor is a very important marker of increased
informed consent. Explain fetal prognosis. perinatal risk in 2 ways.
Inform the pediatrician and the neonatal intensive care 1. It may reflect underlying uteroplacental insufficiency
unit (ICU). and oligohydramnios.
The patient should be shifted to OT urgently. 2. Meconium passage may predispose the neonate to
Ensure presence of qualified personnel for resuscitation meconium aspiration and MAS.
of the baby.
Monitor FHR before abdominal preparation. Predisposing Factors
Repeat per vaginal examination before painting the In general, intrauterine passage of meconium is considered
abdomen to rule out imminent delivery. a sign of fetal distress. The inciting event can be acute
Be gentle while scrubbing the abdomen to avoid or chronic, as intrapartum cord compression and pre-
aggravation of fetal bradycardia. eclampsia, respectively. The passage of meconium during
the final stages of delivery denotes moderate distress. If it trickle down, gets trapped in small airways, leading to ball
happens in utero, it reflects more severe or chronic distress. valve type of gas trapping. In most cases, the meconium
It is seen more commonly in post-mature fetuses. It gets gradually eliminated from the respiratory tract by
is rarely seen in fetuses less than 36 weeks of pregnancy. means of phagocytosis, thereby returning the pulmonary
Staining of the amniotic membranes is obvious within function to normal over a week. However, in more severe
1–3 hours after passage of meconium. Intrapartum and cases, MAS may lead to respiratory failure and even death
perinatal risk is increased in prolonged pregnancies may ensue in spite of aggressive intervention.
when meconium is present. Meconium is found in more Finding thick meconium in the amniotic fluid is
than a fourth of post-term pregnancies and results in worrisome. The viscosity is due to lack of liquid and so
MAS oligohydramnios along with cord compression, is oligohydramnios. Aspiration of thick meconium may
significantly increased (27%). cause severe pulmonary dysfunction and neonatal death.
Unfortunately pathological meconium aspiration The likelihood of successful vaginal delivery is reduced
cannot be predicted. for the nulliparous woman with thick meconium stained
MSAF is one of the major challenges in obstetrician liquor in early labor. Strong consideration should be given
faces while conducting labor. Perinatal outcome is similar to prompt CS especially when cephalopelvic disproportion
with thin meconium stained and clear amniotic fluid. Thick (CPD) is suspected or labor is becoming dysfunctional.
MSAF is associated with MAS. Thick meconium signifies Some obstetricians choose to avoid oxytocin in these
oligohydramnios (sign of chronic hypoxia to the fetus). cases. Maternal intranasal oxygen with left lateral position
Thorough search for potential causes should be initiated. of the mother is preferred.
Obstetric emergencies (umbilical cord prolapse, placental
abruption, uterine rupture, uterine hyper stimulation)
Amnioinfusion
should be excluded. Injections of fluid into the amniotic fluid are consi
If the abnormal FHR tracing (absence of acceleration, dered a life saving measure in fetal compromise by
loss of variability, fetal tachycardia, repetitive late or some obstetricians. They demonstrated the utility of
severe variable decelerations) persist, immediate delivery, amnioinfusion for relief of variable decelerations in labor
depending upon the dilatation of cervix, is indicated. in monkeys. The same technique was applied to human
With saline amnioinfusion, many obstetricians reported fetuses experiencing variable heart rate decelerations in
a significant decline in the incidence of fetal distress and labor. It was then suggested that amnioinfusion might also
MAS. prevent meconium aspiration because fetal gasping would
There has been an increasing interest in the obstetrics be less likely with reduced variable decelerations from cord
and pediatrics management of MSAF and newer therapies compression. Amnioinfusion significantly lowered the
are being used in an attempt to prevent and treat the incidence of MAS (or 0.30), meconium beneath the vocal
disorder. cords (or 0.18), and neonatal acidemia. Amnioinfusion for
meconium may be beneficial only when the meconium is
Incidence thick and there are recurrent variable decelerations that
The incidence of meconium staining as a significant could provoke aspiration. Finally, it will not benefit fetuses
indicator of fetal distress is in 10–20% of all deliveries. in whom meconium aspiration has occurred well before
MAS occur in 2–4% of all deliveries and about 20–25% of the onset of labor.
deliveries with meconium stained liquor. For infants, who are depressed or those who have
The neonatal mortality is 3.3%. The incidence of fetal passed thick meconium, after placing them on the radiant
acidemia is greater as compared to fetus with clear liquor. warmer, suctioning of hypopharynx is done under direct
visualization to remove the residual meconium. The
Management and Outcome of MAS trachea is then intubated and intratracheal meconium
Meconium, owing to its high protein and lipid-rich suction is done. The stomach is emptied to avoid the
content, is an highly irritant material for mucous possibility of further meconium aspiration. It remains
membranes of the distal airways, with potential to cause controversial whether a vigorous infant with thinly
chemical pneumonitis. Dissolved meconium may reach meconium stained fluid requires tracheal suctioning as
the lower respiratory tract and inactivates pulmonary there is no documentation of their long-term morbidity
surfactant causing a functional surfactant deficiency and mortality. However, in the current guidelines for
state. More the particulate meconium which cannot the management of a neonate born through meconium
stained liquor there is no difference in management of Prevention

thick meconium stained liquor. Only a neonate who is not MAS can be prevented by oropharyngeal suctioning of
vigorous needs active resuscitation. the infant following delivery of the chest but cannot be
In a study conducted at Safdarjung Hospital, Delhi on eliminated totally. Some studies present an evidence that
the same topic, it was found that the maximum number development of newborn pulmonary hypertension with
of cases with MAS was beyond 38 weeks (26%), while 38% MAS depended on a chronic or recurring antenatal insult,
were at 40 weeks or more. which in turn would cause abnormal vascularization of the
FHR abnormalities in the form of variable or late interacinar arteries beginning well before birth and thus
decelerations were found in 24% of the fetuses with MAS would be unaffected by maneuvres at delivery. Chronic
while in the control cases without MAS it was 5.7%. The antepartum asphyxia causes pathophysiological damage,
time interval between detection of MSAF and delivery pulmonary hypertension and persistent fetal circulation .
either by LSCS or vaginal route was as follows: There is no sufficient data available on management
Hours MAS% practices, outcome of pregnancy, morbidity and mortality
< 2 47.4 of MAS babies in India. The most recent Cochrane library
2–4 34 review concluded that until further evidence is available,
>4 18.5 endotracheal suctioning for meconium should be reserved
for those infants who are depressed or have respiratory
Hours % of control cases
difficulties.
< 2 55
2–4 46 Role of Amnioinfusion
> 4 16.5
Indications
The delivery outcome was early neonatal deaths with
MAS as compared to none in the control cases. Variable decelerations in case of oligohydramnios
In case of meconium stained liquor to decrease incidence
Meconium amniotic syndrome (MAS): This often causes
of chorioamnionitis
morbidity and mortality in prolonged pregnancy and IUGR
Transabdominally before external cephalic version if
infants. The cause is gasping in utero. Meconium acts as a
liquor is reduced.
foreign body and not only obstructs the flow of air into the
pulmonary alveoli but may set up aspiration pneumonia Absolute Contraindications
and inactivate pulmonary surfactant. The nasopharynx Active maternal herpes genitalis
and oropharynx should be cleared up with suction as soon Decreased FHR variability
as the fetal head is born. The use of amnioinfusion before Fetal scalp pH < 7.20
birth can significantly reduce this problem. Late decelerations in FHR (will further compromise
uteroplacental flow)
Management of MAS Placenta previa
Immediate suction of oropharynx and intubation and Abruptio placentae.
suction of larynx prior to the first breath of the neonate
is ideal Relative Contraindications
High frequency ventilation Impending delivery
Nitric oxide inhalation Multiple gestation
Extracorporeal membrane oxygen (ECMO). Previous LSCS.
1. Explain the term—intrapartum fetal monitoring.
2. Write a short note on:
i. Cardiotocography recording
ii. Electronic fetal monitoring
iii. Fetal pulse oximetry.
Section 12
Neonatology
Section Outline
66. Neonatal Resuscitation
67. Newborn Examination and Common Early Neonatal Problems
68. Care of Premature Newborn
66
Harish Chellani, Sugandha Arya
Neonatal Resuscitation
Birth asphyxia accounts for about 20% of the approximately reversed with stimulation and assisted ventilation must be
five million neonatal deaths that occur each year, provided.
worldwide. Of the 26 million infants born in our country, When faced with an apneic infant at birth, since it is not
3.5% experience asphyxia at birth. Perinatal asphyxia results possible to distinguish between primary and secondary
from conditions that interfere with maternal transport of apnea, one must assume that apnea in newborn at birth is
oxygen to the placenta, placental/fetal gas exchange and secondary apnea and begin assisted ventilation if there is
transport of oxygen from the placenta to the fetal tissues. no response to tactile stimulation given twice.
It is usually accompanied by hypercapnia and results in
hypoxia and metabolic acidosis. This suggests that the PREPARATION FOR DELIVERY
outcome of more than one million newborns each year can
be improved by using the correct resuscitation techniques. At every birth, the doctor should be prepared to resuscitate
Most newborn babies are vigorous at birth and a newborn because the need for resuscitation can come as
make a smooth transition from intrauterine lives to the a complete surprise. Three important questions need to be
extrauterine environment. About 10% of babies require answered while preparing for resuscitation:
some assistance at birth; however, the absolute number 1. What are the risk factors associated with this pregnancy?
becomes more due to the large number of births in our 2. What personnel should be present at the delivery?
country. Only about 1% need extensive resuscitative 3. Which equipment should be made available?
techniques including chest compression and medications.
Risk Factors
All babies born to mothers with risk factors have more
PHYSIOLOGY OF ASPHYXIA
chances of needing resuscitation and these babies also
Although fetal lungs are expanded in utero, the alveoli are require postnatal care in a specialized center. If these
fluid filled. At birth, the fluid in the alveoli is absorbed into facilities are not available at your hospital, arrange for in
lung tissue and is replaced by air. utero transportation of the baby (i.e. mother) to a nearby
In utero, the blood vessels in fetal lungs are markedly referral center with all facilities and personnels.
constricted. Exposure to oxygen after birth causes the
pulmonary arterioles to relax, permitting a dramatic High-Risk Factors
increase in pulmonary blood flow. The blood absorbs Mother with high blood pressure, diabetes or severe
oxygen from the air in the alveoli, and the oxygen-enriched anemia
blood is pumped into the tissues throughout the body. Bleeding in the second or the third trimester
But when a fetus/newborn becomes deprived of Previous fetal or neonatal death
oxygen, an initial period of rapid breathing is followed History of a premature or low birth weight (LBW) baby
by primary apnea. Primary apnea can be resolved by Age of the mother less than 16 years or more than
tactile stimulation. If oxygen deprivation continues, 35 years
secondary apnea ensues. The heart rate continues to fall, Breech or other abnormal presentation
and the blood pressure falls. Secondary apnea cannot be Multiple pregnancies, etc.
Personnel by wiping the baby’s nose and mouth. After 1–3 minutes,
A person who has the skill of basic resuscitation must be the cord can be cut and the baby is placed on the mother’s
present at every birth. The individual must be a doctor chest. Breastfeeding can be initiated. Ongoing breathing
or a nurse who knows the initial steps and techniques and activity can be observed with the baby on the mother’s
of positive pressure ventilation (PPV). This person must chest.
be present physically and not only be on call because Initial assessment, performed within a few seconds,
evidence suggests that problems can arise at the time of determines whether resuscitation is required for the new
labor in a number of low-risk cases too. When resuscitation born. The three questions to be answered are:
is anticipated, additional personnel should be present in 1. Is the baby breathing or crying?
the delivery room to assist in the resuscitation procedures. 2. Is there good muscle tone?
3. Was the baby born at term?
Equipment If the answer is ‘Yes’ to all questions, i.e. the baby is term,
Before delivery one must check the following equipment, spontaneously breathing or crying, and having good muscle
which should be in working conditions: tone, give ‘routine care’ to these babies as already described.
Radiant warmer
If the answer is ‘No’ to any of these questions, i.e. if the
A minimum of two clean dry sheets for each newborn baby is having poor respiratory effort, is preterm or he/
Oxygen supply she is flaccid, then cut the cord immediately and begin the
Self-inflating bag (250–500 mL) with face masks of three initial steps of resuscitation.
different sizes
Laryngoscopes with endotracheal tubes of different INITIAL STEPS OF RESUSCITATION
sizes along with spare batteries
Drugs—epinephrine, normal saline Provision of warmth
Suction catheters 12 and 14 F Positioning
Tape, scissors Clearing of the airway
Sterile gloves. Physical stimulation.
1. Warmth is provided by placing the baby under the

THE PRINCIPLES OF RESUSCITATION radiant warmer. Then the body and head should be
quickly dried with a pre–warmed sheet after removing
The cardinal principles of resuscitation are: the wet sheet, wrap the baby in a pre–warmed sheet.
A. Ensure an open AIRWAY through proper positioning 2. Position the baby by placing a small towel folded and
and clearing the passage of any secretions. kept under the baby’s shoulder to raise it about 2–2.5
B. To initiate BREATHING by tactile stimulation and PPV cm above the mattress thereby slightly extending the
when necessary. neck. Care should be taken to prevent hyperextension or
C. To maintain CIRCULATION with chest compressions flexion of the neck since either may decrease air entry.
and medication. 3. Clearing the airway: The appropriate method of
T. Newborn babies are wet following birth and heat loss clearing the airway depends on the presence or
by evaporation is great. It is, therefore, important to absence of meconium and the baby’s level of activity.
maintain body temperature. No meconium: Secretions are removed from the airway
Hence, modifying ‘ABC’ to ‘TABC’ for the neonate with a suction catheter (12 or 14 F). If the secretions
would be more appropriate. are copious turn the head to one side. Secretions are
aspirated from the oral cavity first and then the nose.
ROUTINE CARE Never put suction, in the nose first as this may initiate a
Nearly 90% newborns are vigorous term babies with no risk gasp and the secretions in the mouth may be aspirated.
factors and clear amniotic fluid. These babies do not need Avoid vigorous suctioning and stimulation of the
to be separated from their mothers to receive the initial posterior pharyngeal wall as both these may stimulate
care. Temperature can be maintained by placing the baby the vagus nerve and cause bradycardia or apnea. The
directly on the mother’s abdomen without cutting the cord suction pressure should not exceed 80–100 mmHg.
and covering with dry linen. Warmth is provided by direct Meconium present: (a) If the baby is vigorous after
skin to skin contact. Just clearing of the airway can be done birth (vigorous is defined as a newborn with strong
Neonatal Resuscitation 625
respiratory efforts, good muscle tone and a heart rate TABLE 66.1: Harmful action and their consequences of physical
greater than 100 bpm), continue with the remainder stimulation
of the initial steps, i.e. clearing the airway, drying and Harmful Actions Consequences
physical stimulation. Intrapartum nasopharyngeal and
Slapping the back Bruising
oral suction of meconium practiced earlier is no longer
Squeezing the rib cage Fractures, pneumothorax, death
recommended. (b) Meconium present and infant
is depressed: However, if the baby is depressed, then Forcing thighs onto abdomen Rupture of liver or spleen
after delivery, when the infant has been placed under a Dilating anal sphincter Tearing of anal sphincter
warmer, residual meconium in the hypopharynx should
be removed by suctioning under direct vision using
a laryngoscope. Intubate trachea and do meconium connecting a pulse oximeter to the right hand wrist of
suction from the lower airway. Drying the baby provides the baby to assess oxygenation as cyanosis in the baby at
physical stimulation and initiates respiration, thereby birth is a poor indicator of the adequacy of oxygenation.
causing meconium to travel down the alveoli causing If the baby has adequate breathing efforts, heart
‘meconium aspiration syndrome (MAS)’. Tracheal rate greater than 100 beats/min and has respiratory
suctioning is best done by applying suction directly to distress, connect a pulse oximeter to the right wrist of the
an endotracheal (ET) tube. Once the ET tube has been baby to assess oxygenation and provide supplementary
inserted, continuous suction is applied to the tube as oxygen titrated to the target oxygen saturations for
it is withdrawn. Suction pressure should not exceed the age of the baby as shown in flowchart, by using
100 mmHg. Reintubation followed by suctioning may an oxygen blender and adjusting the inspired oxygen
be repeated once or twice until return is nearly free concentration (FiO2). If the newborn is a preterm infant,
of meconium. To minimise hypoxia when suctioning and the facilities are available, then continous positive
under direct vision, free flow oxygen should be provided
airway pressure (CPAP) may be initiated in the delivery
by oxygen tubing.
room before transfer to neonatal intensive care unit
4. Tactile stimulation: If the baby fails to establish
(NICU).
spontaneous and effective respiration even after drying,
positioning and suctioning, tactile stimulation must
be given. Safe and appropriate method of providing POSITIVE PRESSURE VENTILATION
additional tactile stimulation includes either slapping/ Indications:
flicking the sole of the feet or gently rubbing the back Apnea/gasping respiration after initial steps, or
of the newborn. Each of these methods is done once Heart rate below 100 per min after the initial steps, or
or twice and if no response occurs, it is discontinued
Persistent cyanosis or low target oxygen saturation,
because such a baby requires PPV. Always remember
despite free flow oxygen increased to 100%.
that continued use of tactile stimulation in an infant
who does not respond is not warranted and may be Bag and Mask
harmful, since valuable time is being wasted. Certain
actions of physical stimulation can harm the baby and Self-inflating bag is designed to inflate automatically as
should not be used (Table 66.1). you release your grip on the bag. It does not require a
compressed gas source to fill. It has the following parts—
air inlet, oxygen inlet, patient outlet, valve assembly and
ASSESSMENT OF BABY pressure release valve (Fig. 66.1).
The baby’s breathing and heart rate should be assessed after
provision of initial steps. If the baby has good breathing
efforts and the heart rate is more than 100 beats/minute
(assessed by auscultation of heart beats and counting for
6 seconds and multiplying by 10 to get beats/minute),
continue providing routine care as described above.
If the baby has poor breathing efforts/is apneic or
has a heart rate less than 100 beats/minute, one must

initiate PPV with bag and mask. One must also consider Fig. 66.1: Self-inflating bag
An oxygen reservoir is an appliance that can be placed In term babies, PPV should be initiated with room air
over the bag’s air inlet. The advantage of a reservoir is and then titrated based on oximetry readings. In preterm
that it helps to deliver 90–100% oxygen at the baby’s babies too, it is advisable to initiate PPV with room air and
inlet as compared to only 40% without a reservoir. then subsequently titrate with pulse oximetry readings.
The pressure release valve is also called a pop-off valve. The baby should be assessed for effectiveness of PPV after
If a pressure greater than 30–40 cm H2O is generated 5–10 inflations.
as the bag is compressed the valve opens, limiting the Effectiveness of ventilation is indicated by following signs:
Increasing heart rate
pressure being transmitted to the lungs of the infant.
Spontaneous breathing
The ideal size of the bag for neonates has a capacity
Improvement in color and muscle tone.
250–500 mL.
Select the appropriate sized mask. The mask should Increasing heart rate is most important indicator of
effective ventilation.
cover the mouth, nose and tip of the chin but not the
If ventilation is not effective and heart rate is not increas-
eyes. It should be cushioned and round.
ing, it is possible that chest is not expanding adequately.
Procedure of PPV (Fig. 66.2) Poor chest expansion is due to inadequate seal, blocked
airway (wrong position secretions) or ventilating with inad-
Position yourself at the side or the head of the baby to use
equate pressure. If these corrective measures fail, consider
the bag effectively and to view baby’s chest for rise and fall.
ET intubation.
The mask should be applied with slight pressure to avoid
After 30 seconds of effective PPV reassess the baby for
leakage and should be held with the thumb, the index heart rate. You will come across one of the following three
and the middle finger of the left hand; while supporting possible situations:
the chin with the ring and the little finger. 1. Adequate respiration heart rate above 100% minute—
The bag is squeezed to cause a visible chest expansion.
stop PPV and monitor oxygen saturation
The best guide to adequate pressure during bag and 2. Heart rate between 60 and 100/minute—continue PPV
mask ventilation is an easy rise and fall of the chest with and recheck for chest expansion.
each breath. 3. Heart rate below 60% minute—continue PPV and start
The rate of PPV should be 40–60/min. While applying
chest compression.
pressure say ‘squeeze, two three … squeeze, two, three Bag and mask ventilation causes abdominal expansion as
… squeeze, two, three’ to maintain this rate. Release the air/oxygen not only enters the lungs but also escapes into the
pressure while counting ‘…two, three’ This sequence stomach via the esophagus. A distended stomach presses on
will give a rate of 40–60 breaths/minute. the diaphragm and compromise ventilation. Therefore, if bag
and mask ventilation continues for more than 2 minutes, an
orogastric tube (feeding tube size 6-8 Fr) should be inserted
and left open to decompress the stomach.
CHEST COMPRESSION
The heart circulates blood throughout the body, delivering
oxygen to the vital organs. When an infant becomes
hypoxic, the heart rate slows and myocardial contractility
decreases. As a result, there is diminished flow of blood
and oxygen to the vital organs. The decreased supply of
oxygen can lead to irreversible damage to the brain, heart,
kidneys and bowel.
Chest compression must always be accompanied
by ventilation with 100% oxygen. Ventilation must be
performed to ensure that the blood circulated during
chest compression gets oxygenated. If the baby has not
been intubated, one should consider ET intubation before
Fig. 66.2: Bag and mask ventilation initiating chest compressions.
ENDOTRACHEAL INTUBATION
Most of the babies are managed by the initial steps of
resuscitation and PPV. Only about 1% of newborns need
chest compression and/or endotracheal intubation.
Intubation is relatively difficult skill to master and it requires
frequent practice to master and maintain this skill.
Indications
Meconium stained liquor limped child and/or apneic
Suspected congenital diaphragmatic hernia
Fig. 66.3: Technique of chest compression Non-response to bag and mask ventilation
Prolonged PPV is required.
Indications
Heart rate below 60 beats/minute after 30 seconds of PPV
Technique of Intubation
with 100% oxygen. Select the correct sized ET tube and obtain straight
blade laryngoscope of size zero for preterm and size
Technique one for term neonates. The appropriate size of the tubes
For chest compression two trained personnel are needed: for different babies based on their birth weight is given
One for assisted ventilation and the other for chest com- in the Table 66.2.
pression (Fig. 66.3). With the help of the laryngoscope, introduce the ET
There are two ways of chest compression: Thumb tube to a level such that the vocal cord guide is placed at
technique and finger technique. The thumb technique the level of the vocal cords. This usually positions the tip
is better than finger technique. of the tube above the bifurcation of the trachea.
Thumbs of both hands are placed either side by side or Confirm the tube placement by ventilating the infant.
one over the other with fingers encircling the rib cage. With a correctly placed tube, air entry is heard equally
Chest compression is used to temporarily increase both sides of the chest and not audible entering the
circulation and oxygen delivery. stomach.
The site of chest compression is the lower one-third of After confirmation of correct tube position, the ET tube
sternum (the area just below the inter nipple line and is cut so that the length outside mouth is around 4 cm.
above the xiphisternum).
The depth of compression should be one-third of the
DRUGS
antero-posterior diameter of the chest.
The rate of chest compression should be coordinated The role of drugs in neonatal resuscitation is very limited.
with ventilatory support, i.e. three chest compressions In few infants, who fail to improve with ventilation and
and one breath. ‘1 and 2 and 3 and squeeze’, should be chest compression, medications become necessary. Only
the sequence of chest compressions and PPV. the following drugs are required in the labor room.
Evaluate the neonate again after 60 secs of chest Volume expanders (normal saline)
compression and PPV. Make your decision on the basis These are indicated if baby is in shock with evidence of
of the heart rate. acute blood loss [as in antepartum hemorrhage (APH)].
Chest compression is discontinued once the heart rate Normal saline or Ringer lactate (RL) can be used in
is above 60/min whereas PPV should be continued dose of 10 mL/kg.
till the heart rate is above 100/min and the infant is
breathing spontaneously. TABLE 66.2: Tube size and weight of the neonate
Over zealous chest compression can cause trauma to Tube size inner diameter (mm) Weight (g)
the infant. Two vital organs lie within the rib cage; the 2.5 < 1000
heart and the lungs. The liver lies partially under the 3.0 1000–2000
ribs although it is in the abdominal cavity. Pressure over
3.5 2000–3000
the ribs and xiphoid can lead to broken ribs, laceration
4.0 > 3000
of the liver and pneumothorax.
It should be noted that naloxone, atropine, dexameth- TABLE 66.3: Apgar scoring system
asone, calcium, dextrose, etc. are not indicated for 0 1 2
resuscitation in the delivery room.
Respiration Nil Slow, gasping Crying
Epinephrine: It is indicated when the heart rate is below
Heart rate/min Nil Upto 100 More than 100
60 per min despite chest compressions and PPV for 60
secs. It is given through intravenous (IV) or intratracheal Muscle tone Flaccid In-between Flexed
route but never through intracardiac route. Give 0.1 Reflex response Nil Grimace Cry
to 0.3 mL per Kg of 1:10,000 dilution intravenously. Color Pale or Peripheral Pink
Intravenous route is preferred over IV route. blue cyanosis
WHEN TO TERMINATE RESUSCITATION take place at 1st and 5th minute of age and should be
continued every 5 minutes until the score is more than 7.
If the heart rate is zero for 10 minutes despite giving
A low Apgar score is not synomyms with asphyxia.
chest compressions, you may stop resuscitation as by
Other non-asphyxial factors that depress the Apgar score
this time brain death would have occurred.
include low gestational age, maternal medications, infec-
The prognosis of such children must be discussed with
tion, neonatal respiratory diseases and congenital neuro-
the parents before discontinuing resuscitation.
logic or neuromuscular disease.
Resuscitation should not be started at all in the
following cases:
Birth weight below 400 g and gestation < 23 weeks
CONCLUSION
Anencephaly The Guidelines on Neonatal Resuscitation have been
Confirmed trisomy 13 or trisomy 18 modified in the year 2010 and they are now more evidence
Remember in all so-called ‘stillbirths’ the resuscitation based. There is a need to anticipate high-risk deliveries
efforts must be continued for 10–15 minutes. The data and transfer these babies in utero to specialities where
suggests that in fresh stillbirths prognosis is not all that neonatal services are available. The necessary equipment
bad. Approximately, 60–65% term babies can be revived must be available and in working order before the delivery.
with good outcome in so-called stillbirths. Every one posted in the labor room must learn the basic
skills of resuscitation (initial steps and bag and mask
ROLE OF APGAR SCORING (TABLE 66.3) ventilation steps).
The outcome in most of the cases is good, if the steps
Apgar scoring is a qualitative tool of assessing the infant’s are followed in the correct sequence. Data suggests that
respiratory, circulatory and neurological status. It does morbidity and mortality can be reduced by 80% just by
not guide the need for initiating resuscitative efforts as it learning and following the steps of basic resuscitation
is taken on 1,5,10 minutes. By one minute the initial steps correctly.
and 30 seconds of the PPV have already been completed.
However, poor Apgar score does suggest poor neurological ALGORITHM FOR RESUSCITATION OF
outcome later it provides the objective measure of the
newborn’s condition and is most useful for assessing the
THE NEWLY BORN INFANT
effectiveness of the resuscitative efforts. Scoring should Flowchart 66.1
Flowchart 66.1: Neonatal Resuscitation Program 2010
Abbreviations: IV—Intravenous; HR—Heart rate; PPV—Positive pressure ventilation; CPAP—Continous positive airway pressure
1. What do you understand by the term neonatal resuscitation?
2. Explain the procedure and types of chest compression.
3. Write a short note on principles of resuscitation?
Newborn Examination
67
Sugandha Arya, Harish Chellani
and Common Early
Neonatal Problems
cooperation of the baby during the examination, the

NEWBORN EXAMINATION examiner’s hands must be warm and dry.
Newborn examination requires patience, gentleness The physical examination of the baby should be conducted
and flexibility of routine. Overall visual and auditory soon after birth. This first examination is done to determine:
appraisal of the naked newborn offers more information Whether the baby has any congenital abnormalities.
than careful organ examination. Baby should be naked (Figs 67.1A to C).
To categorize the baby in the birth weight and gesta-
particularly during initial examination but should not be
kept uncovered for more than a minute or two as they may tional age groups to determine the level of care needed.
To detect any other disorder which may affect the
easily become hypothermic particularly in colder months.
neonatal course and which may require urgent attention.
The baby should preferably be under in a warming device
Following the initial examination, a detailed physical
or the room temperature maintained at about 28–30°C.
examination of the newborn should be conducted at
The examination of newborn should preferably be carried 24 hours of age as by this time, most infants have recovered
out in the mother’s presence as it helps in allaying her from the physical stress of labor and can withstand greater
doubts and anxiety about the infant. handling. A further physical examination is desirable
Adequate information during systemic examination before the baby is discharged from the hospital.
is best obtained when the infant is asleep or in a state
of quiet wakefulness, the crying infant can often be General Examination
quietened by placing on the mother’s lap and conducting Initial Observation
further examination in that position. To ensure, continued The initial observations of the neonate should include:
B C
Figs 67.1A to C: A and B. Baby with six digits; C. Evisceration

Newborn Examination and Common Early Neonatal Problems 631
Posture of the baby: The full-term infant lies in an attitude

of flexion similar to the position assumed in utero. The
preterm infant usually lies in extended position.
Color: Pallor may represent anemia, shock or anoxia.
Peripheral cyanosis may be present for a short while
after birth even in normal neonates which disappear
once the child’s temperature is stabilized. The presence
of jaundice should also be noted.
Cry of a term neonate is vigorous. Feeble, soft or high
pitched shrieking cry is abnormal.
Alertness and spontaneous movements: These will be
discussed along with neurologic examination.
Fig. 67.2: Recording weight of newborn on electronic weighing
Vitals scale
Temperature, respiratory rate, heart rate and CRT should
be recorded in all newborns as abnormality in these may
indicate an underlying illness:
Temperature: Routine temperature recording should
be done by the axillary method. It is recorded by placing

the bulb of thermometer against the roof of the dry
axilla, free from moisture. The baby’s arm is held close
to the chest of the baby to keep the thermometer in
place. The temperature is read after 3 minutes. Normal
axillary temperature is 36.5–37.5°C. Rectal temperature
recording is not done routinely. However, it is the best Fig. 67.3: Recording length of newborn on infantometer
guide for core temperature in cold sick neonates. The
baby’s temperature can be reliably assessed by human
Gestational Assessment
touch. The warm and pink feet of the baby indicate that
the baby is in thermal comfort. Gestational assessment by physical and neurologic criteria
Respiratory rate, heart rate and CRT—will be discussed
should be carried out in all babies particularly in babies
along with the examination of cardiorespiratory system. where the date of the last menstrual period of the mother
is not known or unreliable. Soon after birth, assessment of
Anthropometry gestation is to be made by using physical criteria as the
All neonates should have the following anthropometric newborn may not be in an optimal state for neurologic
measurements recorded: examination. The following features in a newborn suggest
Weight: If recorded on a beam balance, record weight prematurity (i.e. gestation period of less than 37 weeks):
to the nearest 20 g after zero error correction. Weight Deep sole creases are absent or limited to anterior one-
may be recorded on electronic weighing scale. Babies third of the sole.

weighing < 2.5 kg are called low birth weight (LBW) Genitalia: Testes are at the external ring. Scrotum is
babies. Term babies weighing more than 3.8 kg are small with few rugosities. Labia in female infants are
called macrosomic/large for date (Fig. 67.2). widely separated.
Length should be measured on an infantometer taking Breast nodule is less than 5 mm in diameter or not
care that knees are fully extended and the feet are perceptible. It may also be small in terms of growth
perpendicular to the horizontal. The term neonate at retarded babies.
birth is about 50 cm long (Fig. 67.3). Ear cartilage is deficient and has poor elastic recoil.
Head circumference: This is measured at the level of the Skin is smooth, pink with visible veins. Fuzzy or wooly
supraorbital ridges and maximal parietal prominences. hair called lanugo may be present.
The head circumference of term newborn is about After 24 hours of age, as baby stabilizes, detailed gesta
33–38 cm. tional assessment using both physical and neurological
TABLE 67.1: Expanded New Ballard Score for gestation assessment

Neuromuscular Maturity
Physical Maturity
Skin Sticky, friable, Gelatinous, Smooth, pink Superficial Cracking, Parchment, Leathery,
transparent red, visible veins peeling and/or pale areas; deep cracking; cracked, wrinkled
translucent rash; few veins rare veins no vessels
Lanugo None Sparse Abundant Thinning Bald area Mostly bald Score Weeks
Heel-toe >50mm, no Faint red marks Anterior Creases Creases over –10 20
Plantar 40-50 mm:-1 crease transverse anterior 2/3 entire sole –5 22
surface < 40 mm:-2 crease only
0 24
Imperceptible Barely Flat areola no Stippled Raised areola Full areola, 5 26
Breast perceptible bud areola, 1–2 3–4 mm bud 5–10 mm bud
mm bud 10 28
15 30
Lids fused lids open; Slightly curved Well curved Formed and Thick cartilage
Eye/ear loosely: -1 pinna flat; pinna; soft; slow pinna; soft but firm instant ear stiff 20 32
Tightly: - 2 stays folded recoil ready recoil recoil 25 34
Genitals Scrotum flat, Scrotum Testes in upper Testes Testes down, Testes 30 36
(male) smooth empty, faint canal, rare descending rugosities pendulous, 35 38
rugae rugae few rugae deep rugae 40 40
Genitals Clitoris Clitoris Majora and Majora large, Majora large, Majora cover 45 42
(female) prominent, labia prominent, minora equally minora small minora small minora
50 44
flat small labia prominent
minora
criteria can be done by various scoring methods, e.g. Skull

Ballard scoring, Dubowitz scoring. Expanded New Ballard The skull should be examined for abnormal shape (as in
scoring (Table 67.1) is widely used in practice and its video craniosynostosis), sutural separation (for hydrocephalus)
demonstration is available at www.ballardscore.com. (Fig. 67.4) and abnormal swellings (e.g. cephalhematoma,
Fig. 67.4: Photograph of a case of hydrocephalus showing large Fig. 67.5: A neonate with unruptured meningomyelocele in the
head and prominent veins lumbar region with a tuft of hair
encephalocele). Look for size of the anterior fontanel of the hip (CDH). Incomplete abduction at the hip will detect
(normal size is 20 ± 10 mm). CDH. Abnormal intrauterine posture can result in what
appears to be a talipes deformity. If feet can be dorsiflexed
Eyes to the extent that dorsum of foot touches the tibial skin,
Attempts to force open the eyelids of a newborn are likely this excludes a pathological talipes equinovarus deformity.
to result in failure. Gentle tilting of the head back and Count the fingers and toes for any abnormality (Fig. 67.1)
forth (Doll’s eye maneuvre) will succeed in opening the
newborn’s eyes. The eyes should be carefully examined for Spine
icterus, subconjunctival hemorrhage, iris abnormalities, The spine must be examined for presence of tuft of hair,
cataract or any other corneal abnormality. Red reflex pigmentation, lipoma or hemangioma (as these may indi-
should always be looked for. cate an occult spina bifida), meningocele—or meningo-
Mouth myelocele or a pilonidal sinus (Fig. 67.5).
The mouth should be examined for cleft palate, deciduous Systemic Examination
teeth and cysts.
Cardiorespiratory System
Ears The respiratory rate: The respiratory rate of a newborn
Evidence of external ear malformations may be a marker is normally between 40 and 60 breath/minute. Auscul-
of associated renal anomalies. tation and percussion of chest are of limited diagnostic
value in a newborn. As a general rule, if the infant has
Skin good color and no respiratory distress, there is unlikely
The skin of a preterm neonate is thin and pink unlike that to be a major cardiorespiratory problem. The severity
of a term neonate in whom it is paler. Loose wrinkled of respiratory distress may be assessed by the presence
skin with peeling suggests intrauterine malnutrition or or absence of tachypnea (RR >60/min) or by the pres-
post-maturity. Parchment like skin with peeling may be ence or absence of use of accessory muscles and nasal
seen in congenital ichthyosis. An extraordinary division flaring. There are different scoring systems to assess
of the body from forehead to pubis into red and pale the respiratory distress in a newborn Silverman Score,
halves is harlequin color change, a transient and harmless Downe’s Score, ACoRN score (Table 67.2).
condition. A score of more than 8 indicates need for ventilatory
assistance.
Extremities Note for any abnormal bulge in either hemithorax
It should be checked for their mobility at joints, particularly or in the supraclavicular region. If associated with a
for hyperextensibility at knees and congenital dislocation shift of heart, there may either be a pneumothorax or
TABLE 67.2: ACoRN scoring system for respiratory distress in newborn

Score Respiratory rate Cyanosis Air entry Grunt Retraction Prematurity
0 <60/min Nil Normal None Nil ≥34 weeks
1 60–80/min In room air Mild decrease Audible with stethoscope Mild 30 – 34 weeks
2 >80/min In >40% FiO2 Marked decrease Audible with unaided ear Moderate <30 weeks
a diaphragmatic hernia. In case of a diaphragmatic umbilical hernia, granuloma or evidence of infection

hernia, the abdomen is usually scaphoid and bowel (erythema, induration or seropurulent discharge).
sounds may be auscultated in the chest. The liver in the newborn is normally about 2–2.5 cm
The heart rate in a newborn may vary normally from below the right costal margin. The tip of the spleen
120/min in relaxed sleep to 160/min during activity. The may be palpable. Remember, that there may be situs
femoral pulses should always be palpated to exclude inversus.
coarctation of aorta. Both kidneys are usually palpable during the first
Murmurs heard in the newborn period may be transient 2 days of life. Large palpable kidneys may be due to
while significant heart disease may exist in the absence cystic or hydronephrotic changes or a tumor (e.g.
of murmur. neuroblastoma).
Blood pressure needs to be recorded only in sick Genitalia: Phimosis is invariably present in newborn
neonates. It may be recorded by auscultatory method
males and is normal. A hydrocele in the newborn
if stethoscope head is small enough. Doppler method,
mostly disappears spontaneously. The testes should be
using a transducer in the cuff can accurately measure
palpated for their presence in the scrotal sac. In females,
systolic and diastolic pressure. Non-invasive blood
the labia must be parted and examined for imperforate
pressure monitors based on oscillometry also give
hymen or vaginal cysts.
accurate results. Palpatory and flush methods only
The anus and rectum should be checked for patency.
give systolic pressure. The normal blood pressure in
a neonate has wide range of systolic 50–80 mmHg,
diastolic 25–50 mmHg. Neurologic Examination
Capillary refill time—good perfusion signifies adequacy Probably, the most reliable information that can be
of circulation. Poor perfusion indicates hypotension. A obtained is while handling the baby during the preceding
simple and reliable clinical indicator of perfusion is CRT. physical examination. Symmetry of movements, body
The skin over the mid-sternum or forehead is pressed tone, posture and response to handling can be evaluated
with a finger for 5 seconds so that it blanches. The finger while examining the other organs. To reliably interpret,
is then lifted and time taken for refilling of the capillaries the results of a newborn neurologic examination, the
and return to original skin color is noted. Normal CRT baby should be more than 24 hours of age and should
is 3 seconds or less. CRT may also be prolonged due to be examined about 1 hour after a feed when he is likely
hypothermia because of peripheral vasoconstriction. to be in an appropriate state of quiet wakefulness.
Alertness and spontaneous movements: The neonate’s
Abdomen state of alertness—sleeping, quiet wakefulness or
The abdominal shape may offer important clues to crying should be noted. Absence of spontaneous
underlying problems. A scaphoid abdomen suggests movements in one or more limbs should prompt further
the presence of diaphragmatic hernia, a fullness in the examination, e.g. Erb’s palsy usually revealed by lack of
flank may indicate a renal mass and a tense distended motion of the shoulder and arm; the arm will lie beside
abdomen at birth may indicate intrauterine intestinal the body in response rather than being normally flexed
perforation (commonly due to meconium ileus). with fist near mouth.
The umbilicus should be examined soon after birth for Cry: A newborn’s cry is probably one of the most
the presence of two umbilical arteries and one umbilical sensitive indicators of neurologic wellbeing. The
vein. A single umbilical artery is usually associated intensity and pitch should be noted. A high-pitched cry
with other congenital malformation. In subsequent may suggest raised intracranial pressure seen in babies
examinations of the umbilicus, one should look for with severe birth asphyxia or meningitis. Seventh nerve
Fig. 67.6: Eliciting rooting reflex Fig. 67.7: Moro’s reflex
palsy can also be detected (mouth drawn to one side) and/or abdominal distension, check for anal patency
while the baby is crying. by passing a nasogastric tube into the anal canal if not
Neonatal reflexes: A number of primitive neonatal done at birth. Investigate for anorectal anomalies and
reflexes can be elicited in healthy term neonate. Absence intestinal obstruction. It should be remembered that
of reflex response indicates general depression, central some babies might have passed urine and/or stool
or peripheral motor dysfunction. in labor room immediately after delivery but mother
• Sucking, rooting and swallowing reflexes: When the might not be aware. Also, delayed passage of meconium
nipple of breast or finger is brought into contact with may normally be seen in the preterm babies due to
infant’s cheek, he seeks the nipple or finger (rooting functional immaturity of the bowel.
reflex) (Fig. 67.6). Stimulation of the upper and lower Passage of urine: Most of the newborns (93%) void urine
lips produces movement of the lip and tongue in the by 24 hours of age and almost all (98%) void by 48 hours.
direction of the stimulus (sucking reflex). Sucking The rate of urine formation varies from 0.5–5.0 mL/kg/
reflex is feeble in the sick and preterm infants. hour at all gestational ages. Common causes of delay in
• Moro’s reflex: The infant should be held supine voiding are perinatal asphyxia, limited fluid intake due
over the examiner’s right hand and arm. The head to poor feeding, increased fluid losses due to radiant
is flexed by 30° and then it is allowed to drop. A warmers and increased environmental temperature. If
positive response consists of sudden abduction of there is failure to pass urine for 48 hours, investigate for
the arms at the shoulder and extension of arms at the renal function tests and abdominal sonography. Assess
elbow. This is followed by adduction of the arms and for presence and size of kidneys and to rule out any
flexion of the forearm. There is complete opening of genitourinary malformation.
hands (Fig. 67.7). Infants with cerebral damage have Regurgitation of milk: Most of the neonates take out
exaggerated or absent response. An asymmetric small amount of curdled milk soon after feed. Child
response is seen in Erb’s palsy, spastic hemiplegia is usually active and vomitus is never yellow or green
and fracture of the humerus or clavicle.
colored and baby looks healthy. To decrease the
If the above neurological screening is normal, there is
problem, mother should be advised regarding burping
rarely a need for detailed neurologic examination of the
after feed and reassured regarding benign nature of the
newborn.
problem.
Transitional stools: It is the transition from meconium
COMMON EARLY NEONATAL PROBLEMS (sticky thick green or black stools passed during first
Most mothers do observe their babies carefully and are 2–3 days of life) to the yellow homogenous stool of a
often worried about minor physical peculiarities and breastfed infant and is physiological. It starts on the 3rd
problems, which are of no serious consequence. She must or 4th day of life, is yellowish green and may be watery
be adequately informed and appropriately advised regarding and contains some mucus. The frequency of stools is
minor problems to prevent undue anxiety of the mother. increased (upto 10–15/day) and usually decreases by
Passage of meconium: Most of the neonates (94%) 10th day of life.
pass meconium by 24 hours of age. If meconium is not • It must be differentiated from diarrhea as it causes:
passed by 24 hours and/or has associated vomiting –– No pathological weight loss
–– No dehydration than a week, although at times it can last several weeks.

–– No foul smelling stools. Advise mother not to compress or manipulate breasts,
• Transitional stools require no treatment except since they will not reduce the swelling but can cause
parental reassurance. infection.
Erythema toxicum Neonatal jaundice
• The rash usually appears on the second or third day • Jaundice is a common physical finding (manifesting
of life. It is a scattering of erythematous macules, as yellowness of the skin of the face when the serum
papules and even vesicles. It occurs commonly bilirubin level exceeds 5 mg/dL) during first week of
over the trunk, face and extremities while palms life.
and soles are spared. It is to be differentiated from • Common causes of neonatal jaundice are:
pyoderma in the vesicular stage. Microscopy reveals –– Physiological
eosinophils in erythema toxicum and cultures of –– Blood group incompatability
vesicular fluid are sterile. –– Glucose-6-phosphate dehydrogenase (G-6-PD)
• The rash disappears spontaneously in 1–3 days. deficiency
Reassurance of parents is all the treatment that is –– Bruising and cephalhematoma
required. –– Intrauterine and postnatal infections
–– Breast milk jaundice.
Mongolian spots: They are pigmented lesions found
• As the degree of jaundice increases, there is a cepha-
at birth in more than 50% of black native American or
lopedal progression of jaundice. Yellow Coloration
Asian infants and occasionally in white ones. The area
of trunk indicates the serum bilirubin to be in range
most commonly involved is the lumbosacral region
between 10 and 12 mg/dL, whereas staining of palms
but occasionally in the upper back, shoulders, arms,
and soles is ominous as it indicates a serum bilirubin
buttock and legs may be involved. The lesions may be
of more than 15 mg/dL.
small or large, grayish-blue or bluish black in color,
• More than 90% of all neonatal jaundice is physio
irregularly shaped and always macular. The lesions
logical and does not need any specific therapy.
need no treatment except reassurance to parents as
It is recognized by its characteristic timetable—
they tend to disappear within first year of life. jaundice appears between 24 and 72 hours of age,
Vaginal discharge and bleeding its maximum intensity (peak serum bilirubin always
• White, glairy vaginal discharge on second or third below 15 mg/dL) is seen on the 4th to 5th day of life
day of life and disappearing by two weeks of life is and usually disappears before 14th day of life.
physiological. • About 5–10% of newborn babies develop pathological
• Vaginal bleeding in term of babies on about 3–7 jaundice or hyperbilirubinemia. It should be consid-
days of life is physiological. It is a form of withdrawal ered a medical emergency as it may cause bilirubin
bleeding due to the removal of maternal estrogen encephalopathy or kernicterus when unconjugated
influence. It needs no treatment other than parental bilirubin exceeds 20 mg/dL (term baby) or at lower
reassurance as it is self limiting in 4–5 days. levels in (preterm). Pathological jaundice is recog-
Breast engorgement: Full-term babies of both sexes nized by any of these features. Jaundice appearing
may develop engorgement of breasts on the third or within 24 hours of age, serum bilirubin levels exceed-
fourth day of life. A white or creamy white liquid may also ing 15 mg/dL, direct component of serum biliru-
ooze from the nipples. It is attributed to transplacentally bin more than 2 mg/dL and persistence of jaundice
acquired maternal hormones. It normally lasts less beyond two weeks of age (see Chapter 44).
1. List common neonatal problems.
2. Asphyxia is a common cause of death and long-term disability. Explain.
3. Write down all the common causes of a jaundice in a neonate and the age when jaundice will appear?
68
Meenakshi Bhatt
Care of Premature Newborn
Care of the premature newborn is best entrusted to a 34 weeks, if the suck is strong and there is no respiratory
pediatrician. However, it is important for the obstetrician distress or danger signs, breastfeeding should be started
to be able to provide basic supportive care for the first few within half an hour of birth. The initial feeds should be
minutes of life and to be aware of danger signs which will two hourly.
make intervention necessary. If the child manifest any of the following signs, the
pediatrician should be immediately informed.
Respiratory: Respiratory rate more than 60/minute,
BASIC CARE nasal flare, chest retractions, cyanosis, grunt and apnea.
Cardiovascular: Bradycardia less than 100/minute, tachy-
The principles of drying and providing warmth apply
cardia > 200/minute, absent femoral pulse and cyanosis.
to premature babies, too. These babies due to their larger
Nervous system: Shrill cry, seizure, paucity of movement
surface area, weight ratio, thinner skin and very poor energy
and inability to suck.
stores are very prone to hypothermia. Since, evaporative
Gastrointestinal: Continuous frothing from mouth
heat loss is an important cause of hypothermia in a wet (esophageal atresia), absence of an anal orifice.
newborn, quickly drying and then wrapping in a dry, In the end, it is important to stress the involvement of
pre-warmed clean cloth is mandatory. Subsequently, the a pediatrician in the care of a premature neonates as early
child should be clothed in pre-washed and clean clothes as possible. It is best that a pediatrician should be present
(including cap and socks) or wrapped in clean cotton if right at the time of delivery as special care is needed from
these are not available. Special attention should be paid to the very beginning. Though he/she should be present at
the extremities. Cool extremities imply ‘cold stress’. A cold- every preterm delivery, where this may not be possible, the
stressed child is wasting vital energy in keeping himself presence of a pediatrician should be ensured at least at the
warm. Heaters can be used for providing warmth. They delivery of a newborn less than 34 weeks of gestation. This
are not kept very close to the child (to prevent burns). is because older children can often breastfeed and are less
Rod heaters should be avoided as they pose a fire hazard. likely to suffer from respiratory distress syndrome (RDS).
Needless, to say, the baby should be handed over to However, even these babies should get a pediatricians care
mother if he is stable, as rooming in will promote mother within an hour or two of birth, even if there are no danger
and child bonding and the mother’s body temperature will signs.
be an additional source of warmth. In addition, premature deliveries with known compli
The next important step is feeding. Feeding in neonates cating factors, e.g. Rh-isoimmunization, fetal distress,
twin deliveries pose a greater challenge and should not be
less than 30 weeks of gestation or those with danger
managed by obstetricians alone.
signs (vide infra) should be started with intravenous (IV)
fluids and feeds should be gradually introduced and
then increased. In neonates, between 30 and 34 weeks
PRETERM INFANTS ARE AT A GREATER
of gestation, feeding should be via orogastric tube. Feed RISK FOR
intolerance should be monitored by measuring abdominal RDS
girth at the level of the umbilicus before each feed. Beyond Intraventricular hemorrhage (IVH)
Bronchopulmonary dysplasia (BPD) LONG-TERM MORBIDITY

Patient ductus arteriosus (PDA) Preterm children have a higher rate of cerebral palsy, severe
Necrotising enterocolitis (NEC) visual impairment, abnormal cognitive, academic, visual
Sepsis motor, gross motor, adaptive performance and chronic lung
Apnea disease. Like mortality, morbidity is inversely related to
gestational age and weight at birth. If weight is 1000–1500 g
Retinopathy of prematurity (ROP)
the survival is better than in infants with a weight 1000 g or
Sudden infant death syndrome. less. Care of intrauterine growth restriction (IUGR) newborn
These are more common at earlier gestations. (see Chapter 20).
1. What are the basic care that a premature baby requires? Do these differ from a mature child?
2. Explain the procedure of feeding in premature neonates.
3. What are the different signs and symptoms in which a pediatrician should be consulted?
Section 13
Contemporary Issues in
Obstetrics
Section Outline
69. Medicolegal, PCPNDT and Bioethics
70. Reproductive Morbidity and Maternal Mortality
71. Government Programs for Reproductive and Child Health
72. Biomedical Waste Management
69
Sudha Salhan, Sanjay Gupte, Vasantha Muthuswamy
Medicolegal,
PCPNDT and Bioethics
on the doctor as they are in a more advantageous position

MEDICOLEGAL ASPECT OF OBSTETRICS
as regards the patient. This negligence can be civil or
Consumer Protection Act (CPA) was passed in 1991 and criminal. When medical negligence is a civil wrong it
since then litigations against doctors have increased pro attracts the provisions of the law of Torts.
pensity. This Act has made the doctors to act defensively. Most often when there is death of a patient, the relatives
Besides, the doctor-patient relationship is no longer cor lodge a complain at the police station under criminal law.
dial. The cases against obstetricians are maximum because Hence, the patient or her relatives can sue the doctor
two lives are at stake. The fetus cannot be examined under any or all of the three laws:
directly and any pregnancy and labor can turn to high- 1. Consumer Protection Act
risk anytime without any warning. To overcome this, the 2. The civil law
doctors are to be knowledgeable on legal concepts of her/ 3. The criminal law.
his specialty. The causes of litigation can be ignorance of In obstetrics, some of the examples of negligence:
concern laws, noncommunication, incomplete records, Surgery/sterilization without consent (life-saving
misinterpretation and even negligence.
surgery is an exception under section 92 IPC).
In the event of an unexpected obstetric, complication
• Follow-up instructions may not given, especially in
occurs during the medical practice, the patient most com
cases of failure of sterilization
monly wants to sue the doctor for ‘negligence’. Negligence
• Careless operation leading to bleeding and death
is defined by the Supreme Court as failure to act in accor
• Leaving sponge, instruments, etc. in cesarean
dance with the standards of reasonable competence at the
operation.
time. But you must not find him negligent simply because
In cases of medical termination of pregnancy
something happens to go wrong; if, for instance, one of
the risks inherent in an operation actually takes away the (MTP): The procedure done by unqualified person at
benefits that were hoped for, or if in a matter of opinion unrecognized place, and one with improper consent or
he makes an error of judgment. You should only find him complications which are not recognized and not treated
guilty of negligence when he falls short of the standard by all invite litigation.
In antenatal checkup, causes for litigation are
of a reasonably skillful medical man, in short, when he is
deserving of censure for negligence, e.g. careless operation failure to diagnose pregnancy, using drugs which are
leading to bleeding and death. harmful to fetus (teratogenic), omitting to carry out the
Following the decision of the Supreme Court in Indian screening tests for detection of congenital abnormalities
Medical Association (IMA) vs VP Shantha, the doctor (biochemical tests and ultrasound), unable to recognize
is considered as a service provider and the patient as a complications [intrauterine growth restriction (IUGR),
consumer. Therefore, a suit will lie in the jurisdiction of hypertension, etc].
the consumer forum. The doctor-patient relationship is In cases of lower section cesarean section (LSCS),
based on a contract and hence, the principles of Indian improper indication, timing, maternal and fetal morbid
Contract Act I become applicable but the courts tend to ity and mortality, complications of the procedure or the
look at it as ‘fiduciary’ contracts which puts more liability anesthesia and complications may invite court cases.
Similarly other operative deliveries like forceps and attending the patient may deteriorate the condition of the
ventouse can lead to Medicolegal situation. patient and invite litigation. Never show indifference to
To avoid Medicolegal problems, proper communi- the complains of the patient. Our communication with the
cation and documentation are the two most important patient and her attendants is important. Do not be rude.
aspects, which need to be remembered. Be empathetic. Inform her and her relatives the facts about
To make it easy to remember, the author would like to her disease and the treatment require. Answer as many
put our guidelines in the following way: of their queries as possible, honestly. The hospital staff
In India, the Indian Penal Code (IPC) and Criminal should speak in one voice and never give contradictory
Procedure Code (CrPC) deal with the criminal law. Most statements to the patient and her attendants. In private
often, when there is death of a patient, the relatives practice do reasonable charging. If you ask for exuberant
are likely to lodge a complaint against the doctor. The fees you may be sued.
complaint is lodged at the police station under the section Updating our professional knowledge with newer
304A of IPC. developments is essential. Do only relevant investigations.
Consent has an important place in patient-care. Pre Equip your hospital with all the essential ornamentations
ferably written informal consent. (blood pressure apparatus, oxygen cylinder, etc.) which
Let us understand the basic concepts of these laws to are in a working conditions.
realize that how complaints are made and how defence is Proper documentation of patient’s records help
planned. Under the Contract Act (in CPA, it is considered us during litigations. Take written consent before any
as contract between the doctor and the patient) the intervention. Do correct and complete documentation
consent carries a great value. A good informed consent is in chronicle order. Make-up records are held as criminal
an important aspect of defence. forgery. Sometimes, certificates (for rest, maternity leave,
With regards to the law of negligence, it is important etc.) of the patients are important documents. Give only
that the patient should prove these points: true certificates, never change the facts, it will invite
The doctor was legally bound to give the treatment criminal proceedings.
The actual damage has been caused to the patient,
which can be proved THE PRECONCEPTION (PC) AND PRENATAL

The doctor’s treatment has been the proximate cause of DIAGNOSTIC TECHNIQUES (PNDT)
the damage (Causa causans)
(PROHIBITION OF SEX SELECTION) ACT
The treatment of the doctor was below the accepted
standard of care at that time. Adverse Child Sex Ratio In India

The doctor could contest the above, stating that: Sex ratio is the number of females per thousand males.
The damage was not due to his or her treatment
Declining trend in sex ratio has been a matter of concern
The patient was also negligent and if he/she not been
for all in our country. Sex ratio in India has declined
negligent, the damage could have been mitigated. The over the century from 972 in 1901 to 927 in 1991. The sex
most common example not following the advice of the ratio has since gone up to 933 in 2001 and 940 in 2011
doctor called as contributory negligence (Table 69.1 and Fig. 69.1). The sociocultural practices
The said complication is Vis major (Act of God) and not in India are predominantly biased against females. The
due to negligence of the doctor encouraging trend in the sex ratio during 1991–2011
The treatment of the doctor was well within the current was marred by the decline of 18 points in the sex ratio of
standards which established in the field. children aged 6 years or below, like 945 (1991), 927 (2001),
These concepts must be employed in day-to-day 919 (2011) (Fig. 69.2). Some of the reasons commonly put
obstetric practice. Meticulous record keeping with this forward to explain the consistently low levels of sex ratio
insight of law can do wonders while contesting cases of are son or boy preference, neglect girl child resulting in
medical negligence. higher mortality at younger age, female feticide, female
infanticide, higher maternal mortality and male bias in
Avoidance of Medicolegal Problems enumeration of population. Easy availability of the sex
Always be aware of chances of litigation especially in determination tests and abortion services may also be
cases of mishaps (miscarriage, fetal loss, complication proving to be catalyst in the process, which may be further
of surgery, etc.). Prompt attention is essential. Delay in stimulated by preconception sex selection facilities.
Medicolegal, PCPNDT and Bioethics 643
TABLE 69.1: Sex ratio in India over the years Sex determination techniques have been use in India
Year Sex ratio
since 1975 primarily for the determination of genetic
abnormalities. However, these techniques were widely
1901 972
misused to determine the sex of the fetus and subsequent
1911 964
induced abortions if the fetus was found to be female.
1921 955 Approximately, 2000 females feticide occur per day in
1931 950 India, more so in urban areas. To curb this practice and in
1941 945 order to check the female feticide, the prenatal diagnostic
1951 946 techniques (regulation and prevention of misuse) Act,
1961 941 1994, was brought into operation from 1st January, 1996.
1971 930 This technique has been amended to make it more com
1981 934
prehensive. The amended Act and rules came into force
with effect from 14th february, 2003 and the PNDT Act has
1991 927
been renamed—preconception and prenatal diagnos-
2001 933
tic techniques (PCPNDT) (prohibition of sex selection)
2011 940 Act 1994. The Act provides the prohibition of sex selection
Fig. 69.1: Child sex ratio (0–6 years) in states of India

Fig. 69.2: Sex ratio in India over the years
before (preconception) and after conception (prenatal) Three types of clinics are considered in this act and all
and for regulation of prenatal diagnostic techniques. The to be registered with the District Medical officers. These
purpose of detecting genetic abnormalities or metabolic are:
disorders, or chromosomal abnormalities or certain con Genetic counseling center
genital malformations, or sex-linked disorders and for the Genetic laboratory
prevention of their misuse for sex determination leading Genetic clinic (ultrasound clinic/imaging center).
to female feticide and for matters which are connected
therewith or incidental thereto. This Act extends to whole Genetic Counseling Center (CGC)
of India except the state of Jammu and Kashmir. It is both A geneticist, gynecologist or pediatrician who has 6 months
prohibitory and regulatory in nature and its violation is a experience or 4 weeks training in genetic counseling or a
punishable offence. The technique of preconception sex medical geneticists can run this clinic. Equipments include
selection has been brought within the ambit of this act so educational charts, models, etc. Space must be adequate.
as to pre-empt the use of such technologies, which signifi
A medical geneticist possesses a degree or a diploma in
cantly contribute to the declining sex ratio. Use of ultra
genetic science.
sound machines has also been brought within the purview
of this act more explicitly so as to curb their misuse for de Genetic Laboratory
tection and disclosure of sex of the fetus leading to female
feticide. Genetic laboratories with the prescribed equipments
Preconception prenatal diagnostic procedures include are needed. A degree or diploma holder of medical
all gynecological or obstetric or medical procedure such as laboratory course and medical geneticist with at least
prenatal diagnostic test means ultrasonography or any test, 1 year experience in the field of sex selection and prenatal
blood, any tissue or fluid of a pregnant woman or fetoscopy, diagnostic techniques or has experience of not less than
taking or removing the samples of amniotic fluid, chorionic 2 years in any of these fields after obtaining any one of
villi sampling, embryo, blood or any other tissue or fluid of the medical qualification recognized under the Indian
a man or a woman before or after conception, being sent Medical Council (IMC) Act 1956 or a postgraduate degree
(genetic laboratory or genetic clinic) for a conducting or in a biological sciences, chorionic biopsy, amniotic fluid
any type of analysis or for the selection of sex before or aspiration ,umbilical blood aspiration and tissues of the
after conception. Conceptus conducted to detect genetic fetus extraction and analysis.
or metabolic disorders, chromosomal abnormalities or
congenital anomalies, hemoglobinopathies or sex-linked Genetic Clinic (Ultrasound Clinic and
diseased. Imaging Center)
Sex selection includes any procedure, technique, test or A registered dedicated ultrasound machine and a
administration, prescription or provision of anything for sonologist are the requirements.
the purpose of ensuring or increasing the probability that Central supervisory board (CSB) constituted under
an embryo will be of a particular sex. It is a determination the chairmanship of Minister of health and Family
of the sex of unborn child and eliminate it, if found to be a Welfare has been further empowered for monitoring the
female. implementation of the Act.
State level supervisory (SLS) board in the line of the seminars, workshops, training/orientation programs for
CSB constituted at the center has been introduced for public meetings, debates, essay competitions, nukkad
monitoring and reviewing the implementation of the Act nataks, stage shows, etc.
in the states/union territories (UTs). Medical audit of all the ultrasound clinics in the country,
The state/UT level appropriate authority (AA) has been so as to catch the violators of the Act by scrutinizing
made a multi-member body for better implementation and the “Form F’ which is filled in respect of all pregnant
monitoring of the Act at the state district/sub-district level. women by the clinics.
More stringent punishments are prescribed under the Act Changing AAs: In place of Chief Medical Officer/District
so as to serve as a deterrent for minimizing violations of Health Officer, now District Collectors/District Magistrates
the act. AAs are empowered with the powers of civil court have been placed as district AAs to strengthen them in the
for search, seizure and sealing the machines, equipments implementation of the Act at the ground level.
and records of the violators of law including sealing of Proposed amendments to PC and PNDT Act.
premises and commissioning of witness. Sensitization of Funding to the state through reproductive and child
AA through training and workshop. health (RCH-II).
It has been made mandatory to maintain proper Inclusion of the issue under national rural health
records in respect to the use of the ultrasound machines mission (NRHM).
and other equipments capable of detection of sex of the Constitution of national inspection and monitoring
fetus and also in respect of test and procedures that committee (NMC).
may lead to preconception selection of sex. The sale of Constitution of national support and monitoring (NSMC).
ultrasound machines has been regulated through laying Meeting with the manufacturers of ultrasound machines.
down the condition of sale, only to the bodies registered Sensitizing and training of judiciary and setting up
under the Act. Manufacturers of ultrasound machines are designated courts to hear cases of violation of the act
required to send report to the AA, giving details of clinics for faster conviction rates.
Annual report on implemntation of the PNDT Act
and doctors to whom they sold ultrasound machines.
(Fig. 69.3) shows number of cases of violation of the Act.
Punishment Under the Act Designated toll free number 1800110500 for complaints.
Frequently asked questions are framed.
The punishments prescribed are imprisonment upto
Awareness Generation: It nevertheless recognizes that
3 years and fine up to ` 10,000. For any subsequent
mere legislation is not enough to deal with this problem
offences, he/she may be imprisoned upto 5 years and fined
that has roots in social behavior and prejudices. Various
upto ` 50,000–100,000. The name of the registered medical
activities have been undertaken to create awareness
practitioner is reported by the AA to the state medical
against the practice of prenatal determination of sex
council concerned for taking necessary action including
and female feticide through radio, television and print
suspension of the registration if the charges are framed by
the court and till the case is disposed off. Government of
India is contemplating a longer jail sentence along with
higher monitoring penalty upto 1 lakh. Ministry of Health
and Family Welfare has taken a number of steps for the
implementation of the Act.
The major steps taken are as follows:
Meeting of the central supervisory board (CSB): PC
and PNDT act are being held regularly every 6 months

under the chairmanship of Union Minister of Health
and Family Welfare.
Sensitization through members of parliament: An
amount of ` 5 lac each, has been given to 126 members

of Parliament (Lok sabha and rajya sabha) from states of
Chandigarh, Delhi, Gujarat, Haryana, Himachal pradesh,
Punjab and Rajasthan to create public awarness on sex Fig. 69.3: Percentage distribution of ongoing cases of violation
selection and declining sex ratio by organizing exhibition, under PC and PNDT act by the type of violation (as on March, 2006)
media units. Workshops and seminars are also organized The AA acknowledges the receipt.
through voluntary organization at state/regional/ The AA inspects the venue, see the requirement and
district/block levels to create awareness against the social present the application with the findings before the
evil. Cooperation has also been sought from religious/ advisory committee.
spiritual leaders as well as medical fraternity to curb this • All within prescribed requirement registration is
practice. The Government of India has launched save granted on Form B.
the girl child campaign with a view to lessen the son • If all requirements are not fulfilled in the application,
preference by highlighting the achievements of young is rejected on Form C citing the deficiencies. After
girls. fulfilling all the requirement he/she can reapply
No prenatal diagnostic techniques shall be conducted within 90 days. The certificate of registration is non-
except for detection of: transferable. If the owner is changed, the certificate
Chromosomal abnormalities
must be surrendered. The new owner will apply
Genetic metabolic diseases
a fresh registration. Any addition or deletion of
Hemoglobinopathies
the instruments, etc. (like ultrasound machine)
Sex-linked genital disease
or employee (as sonologist) must be informed.
Congenital anomalies
Registration is for 5 years. Then, it is to be renewed.
Any other abnormalities or diseases as may be specified
Minimum requirements are specific for all 3 types of
by the CSB. centers.
No prenatal diagnostic techniques shall be conducted Maintenance of records
Genetic counseling center will fill the record in Form D
unless the person qualifies to do so and is satisfied for
and genetic laboratory fill in Form E. Genetic clinic keeps
reasons to be recorded in writing that any of the following
the record in Form F. Consent of the patient is taken in
conditions are fulfilled:
Form G in her language. A declaration, by the person
Age of the pregnant woman is above 35 years
conducting the procedure, is given that sex of the fetus is
The pregnant woman has undergone 2 or more sponta
neither detected nor disclosed. The patient also declares
neous abortions or fetal loss
in the Form H (that she does not want to know the sex of
The pregnant woman has been exposed to potentially
the fetus) which is a permanent record to be maintained
teratogenic agents such as drugs, radiation, infection or
as a register in the custody of the AA and after that all filled
chemicals forms to be sent to the AA.
The pregnant woman or her spouse has a family history
Cancellation of suspension of registration: AA on its
of mental retardation or physical deformities such as, own or on a complaint by anyone can issue a show cause
spasticity, or any other genital disease notice, as to why its registration should not be cancelled or
Any other conditions as may be specified by the CSB.
suspended for breach of any provision of the PC and PNDT
Written consent of the pregnant woman is taken and Act or the rules. Appeal may be put by the center.
all known side effects of the procedure are explained
to her. Sex of the baby is not to be told to the pregnant
BIOETHICS IN THE PRACTICE OF
woman or her relative or any other person. A board telling
that detection of sex is illegal and punishable and in OBSTETRICS
this clinic, sex determination is not done is displayed Bioethics is the study of the ethical and moral implication
prominently at the clinic. of medical practice and research. This involves teaching-
Registration of genetic counseling centers, genetic training of medical healthcare personnel in ethical issues
laboratories and genetic clinic is done as follows: around patient-care and biomedical research.
An application for registration shall be made to the The ethical code of conduct for medical professionals
AA in duplicate in Form A with an affidavit that the and physicians existed since time immemorial, the most
(i) center/laboratory/or clinic will not conduct any test ancient reference being found in the Charaka Samhita
for sex determination, (ii) will display prominently a of Ayurveda (1st–2nd century AD), which describes
notice that they do not conduct any technique, test or the physician’s duties towards his patients and others in
procedure, etc. by whatever name called, for detection the profession. However, the most well known code for
of sex of the fetus or for selection of sex before or after medical professionals is the Hippocratic Oath (600 AD)
conception, (iii) an application fees. of the greek-roman period. All these and other such codes
have stemmed from the basic concept of nonmaleficence, skill. From the beginning, medicine physicians knew that
i.e. Do no harm which was the driving principle for all treatment which is successful in prior cases might fail in a
physicians in their handling of their patients resulting in a present case. In desperate moments of illness, previously
fiduciary relationship between the two. untried remedies were attempted, sometimes with
Most of the Medical Councils around the world have unexpected success. However, the Hippocratic maxim,
thus prescribed the codes for the respective countries. benefit and do no harm urged physicians to maintain a
The Medical Council of India which is the statutory body constant intent to cure.
established under an Act of Parliament vested with the The worst scientific experiments came to light
power of regulating standards of medical education and following the Second World War at the Doctors’ trial in
medical practice, promulgated the Code of Ethics in 1956 Nuremberg where innumerable atrocities were committed
which is to be honored by all registered medical practitional on the prisoners by the Nazi physicians in the name of
of the country. Any violation of the Code may lead to medical research and shocked the entire world. This
penalties, including cancellation of registration. Every was followed by proclamation of Nuremberg Code on
medical student on completion of the course is required to Experimentation in human subjects in 1947, marking a
take the oath to adhere to the following declaration: new era of code of ethics for medical research, which drew
I solemnly pledge myself to consecrate my life to the
unprecedented attention from public, professionals and
service of humanity. policy makers. Thus, a new beginning was made in the
Even under threat, I will not use my medical knowledge
moral traditions of medicine and laid the foundation for
contrary to the laws of humanity. the new discipline of Biomedical ethics or research ethics
I will maintain the utmost respect for human life from
as a part of bioethics.
the time of conception.
The four cardinal virtues of a health professional are
I will not permit consideration of religion, nationality,
compassion, discernment, trustworthiness and integrity.
race, party politics or social standing to intervene
Ten basic principles for medical research have been
between my duty and my patient.
delineated in the Nuremberg Code that should be adhered
I will practice my profession with conscience and dignity.
to satisfy moral and legal concept. Subjects (human) give
The health of my patient will be my first consideration.
a voluntary consent, subjects, experimental results to
I will respect the secrets which are confined in me.
bring good to the society, prior experiments with animals,
I will give to my teachers respect and gratitude which is
avoidance of unnecessary physical and mental suffering,
their due.
prior assurance that no death or disability will result,
I will maintain by all the means in my power the honor
the scientific qualification of researchers, evaluation by
and noble traditions of the medical profession.
My colleagues will be my brothers. I make these
subjects rights and researcher’s duty to terminate harmful
promises solemnly, freely and upon my honor. experiments are the major principles of this Code which
The above declaration describes the decorum, duties holds good till date. The World Medical Association (WMA)
and social ethics of physicians and prescribes the also brought out the Helsinki Declaration in 1964 to guide
standards of conduct appropriate to a good physician. the treating physicians about the norms to be followed in
Such a professional decorum surrounded by an aura therapeutic as well as non-therapeutic research.
of scientific knowledge related to health and diseases
Evidence-based Reproductive Medicine (EBRM)
satisfied the public for centuries that doctors were decent,
responsible, competent and trustworthy. The prestige that It is the conscientious, explicit and judicious use of
this profession enjoys in the eyes of the society is related current best evidence in making decisions about care of
to its contributions to the wellbeing of the society and the the individual patients (David Sachett, the God Father
quality of performance by its members in adhering to the of evidence-based medicine). Evidence-based medical
laid down principles of doing no harm, relieving pain and practice and clinical research and is graded into 3
suffering, maintaining confidentiality, being trustworthy categories.
and fair in their dealings. Grade I randmomized control trials (RCTs), Grade
II-1 cont-rolled trials without randomization, Grade II-2
Biomedical Research Ethics cohort or case control studies and Grade II-3 comparison
The ancient codes of ethics directed physicians that they between time/place with or without intervention. Grade
have a moral obligation to attain a new knowledge and III clinical experience. EBRM tries to integrate the best
literature evidence with clinical expertise. The treatment research is needed for therapeutic surgeries and diag-
is tailored to individual patient. It requires a fresh outlook nostic tests. EBRM separates facts from fantasy in clinical
towards apparently well-known problems. This is all for practice. There is no place for reference. It is not ethical to
better care of the patients without wasting valuable time on promote certain treatment without a proper clinical trial.
unnecessary procedure and drugs (minimizes redundant For EBRM, constant updating of knowledge and keeping
procedures). It is an emerging paradigm for medical up with the many meta-analyses results and research
practice and teachings. More and more RCT are required outcomes is essential. All these improve patient-care
in both undergraduate and postgraduate curriculum for (which is our main goal).
better patient-care. Now, for any medical research worth patient-care
Now, virtually no drug enters into the clinical practice and publication needs to get sanctioned through ethical
without clinical trial of safety and efficacy. Similarly, committee of the institution.
1. Enumerate types of Medicolegal cases which you deal with in your practice.
2. What are the main causes of complaints of negligence against doctors in your opinion?
3. Which diagnostic techniques are covered by the PC and PNDT Act (1994)?
4. Write a short note on evidence-based reproductive medicine?
70
Sudha Salhan, Matthews Mathai, BD Hasija
Reproductive Morbidity
and Maternal Mortality
REPRODUCTIVE HEALTH WOMEN’S MORBIDITY

Health of women, reproductive health in particular, is Women’s morbidity refers to all types of diseases in women.
receiving considerable attention in the current trend of This is a broad issue.
healthcare practices. There is enough data on reproductive
deaths (mortality), but not on morbidities. It is estimated REPRODUCTIVE MORBIDITY
that for each maternal mortality there are about 20 cases Reproductive morbidity refers to diseases that affects the
of morbidity, which can even stretch beyond reproductive reproductive system, although not necessarily as a con-
years (e.g. prolapse uterus). sequences of reproduction. It can go beyond reproductive
The heavy burden of reproductive disease plays a very years. Reproductive morbidity has several different aspects.
important role in the economic development of any nation An example is given by the following case. Mrs.Seema
(World Bank 1993). The project Global Burden of Disease (name changed), aged 22 years came to antenatal clinic.
and Injury (GBDI) undertaken by the World Health She is a third gravida with seven month pregnancy with
Organization (WHO), Harv ard School of Public Health hemoglobin of 4.5 g%. She was married at the age of 17
and the World Bank has estimated the years lived with years as the family was poor and hence, she got inadequate
disability (YLD). They thus quantify the total impact of nutrition. Her first pregnancy occurred immediately
diseases and injuries in global and regional populations. thereafter. No antenatal checkup was done. She was
WHO has done this by assessing the burden of sexual and anemic at that time. She delivered a 7 month preterm
reproductive ill health by calculating disability adjusted male child at home and had excessive bleeding during
life years (DALYs). All these help in assessing the need of delivery. The child died within one month due to diarrhea.
the community and region and these data are useful for She conceived again after one year with no checkup or
planning and investment in various health interactions treatment in between. She had a normal delivery (male
especially in countries like India, where the resources are child) at home, who was breastfed for 2 years, further
limited. The subject of morbidity has not been tackled till depleting her iron’s reservoir besides her other nutrients.
recently. There is a massive burden of these morbidities This time she complained of breathlessness, tiredness and
(more so in country with high adolescent fertility), which was brought to the antenatal clinic.
can undermine the quality of women’s life for long. All this reflects early marriage, lack of preconception
These problems are, almost always, preventable. Hence, and postconceptional checkup and improper dietary and
providing adequate quality services during pregnancy, family planning advice. The anemia became progressively
abortion, delivery, etc. will go a long way in reducing these severe due to lack of quality care.
disabilities. Hence, if neglected, it may prove fatal besides causing
Reproductive health was defined in the 1994 United severe morbidity.
Nations Cairo Conference on Population Development as
a ‘state of complete mental, physical and social wellbeing Duration
in all matters related to the reproductive system and to its Some obstetric morbidities are short lived. The patient may
functions and processes.’ die or survive without permanent sequel [e.g. postpartum
hemorrhage (PPH) when handled properly]. But some Complications of Pregnancy and Childbirth
obstetric morbidities may have long-term sequels (e.g.
These are the leading causes of death (mortality) and
obstructed labor causing obstetric fistulas).
disability (morbidity) among women of reproductive age
(15–45 years) in less developed countries like India. Around
Time of Onset
27 million births occur in our country per year. About half
At a particular lifespan, the incidence of some specific of them experience some complications (acute morbidity)
morbidities are seen to have an increased incidence. For
and from 10 to 12 million develop disabilities (chronic
women between 15 and 45 years the cluster of diseases is
morbidity). Hence, maternal morbidity can be classified as:
called reproductive diseases. Some reproductive events
Acute
cause morbidity in later life (uterine prolapse, fistulae,
Chronic.
cervical cancer).
Acute maternal morbidity
Accumulation These are antepartum hemorrhage (APH), PPH, obstruc
ted labor, sepsis, etc.
Some morbidities accumulate over time and grow pro-
Chronic maternal morbidity
gressively worse because of:
It is seen as genital prolapse, obstetric fistula, urinary
Continued exposure of the disease causing agent like
stress incontinence, pelvic inflammatory disease (PID),
human papillomavirus (HPV) and cancer of the cervix,
dysfunctional uterine bleeding (DUB), Sheehan’s syndrome,
repeated childbirth and uterovaginal prolapse.
secondary infertility, choriocarcinoma and carcinoma of
Lack of exposure to disease preventing agent (presence
the cervix, etc. The incidence of Sheehan’s syndrome is not
of iron in the diet).
well documented. It can cause chronic weakness, premature
Combination of both.
aging, amenorrhea, mental apathy and confusion, etc.
Sequel Our country has highest adolescent fertility (almost
one-third births occur in women between 15 and 19
Some morbidities have sequels occurring with varying
years). Hence, the burden of reproductive disabilities
frequency. The sequelae may be even more life threatening
(morbidities) is expected to be very high.
than the original morbidity (e.g. choriocarcinoma
Reproductive morbidity refers to diseases that affect
following molar pregnancy). Mrs Rekha (name changed)
the reproductive system although not necessarily as a
came to us with bleeding per vaginum for 2 months. There
consequences of reproduction. YLD estimates suggest
was no history of preceding amenorrhea. She had delivered
that a substantial number of women may be affected for
a male child normally 4 years back and had an abortion
6 months earlier. On examination, she was anemic. Her many years beyond their reproductive age. Reproductive
per vaginal examination showed a bulky uterus. Her chest morbidity is divided into the following subcategories:
Obstetric (or maternal) morbidity
radiograph showed secondaries in the lungs. The liver and
Gynecologic morbidity
skull computed tomography (CT) were clear. Her serum
Contraceptive morbidity
human chorionic gonadotropin (β-hCG) was 2,50,000 IU/
Sexual morbidity.
mL. She was diagnosed to have choriocarcinoma and was
given appropriate chemotherapy and was declared cured
after 3 negative β-hCG reports. Obstetric Maternal Morbidity
Appropriate treatment of the original morbidity may It refers to morbidity that is a consequence of pregnancy
prevent sequelae (early cesarean section for obstructed or childbirth or the consequence of treatment received
labor can prevent obstetric fistulae). during pregnancy or childbirth. It refers to conditions that
occur to women who are pregnant, in labor or in the puer-
Social perium. This category also includes conditions that persist
Social content of the disease as cause and consequences beyond the puerperium. Obstetric morbidities are further
is very important. A resource deficient household cannot subdivided into:
invest in medical care of the pregnant member of their Direct obstetric morbidity
family. The power to make personal decisions relating to Indirect obstetric morbidity
health, including sexual behavior and reproduction has an Psychological morbidity
important bearing on reproductive (and women’s) health. Non-obstetric morbidity.

Reproductive Morbidity and Maternal Mortality 651
Direct Obstetric Morbidity placing it on the national and international policy agenda.
These are the conditions, which arise due to pregnancy These morbidities undermine the quality of a woman’s
or labor (hence not seen in non-pregnant women), e.g. life, and have a far-reaching effect on the economy of
hemorrhage (antepartum and postpartum), puerperal any nation. Most of these can be reduced by quality care
before pregnancy, during pregnancy, during delivery,
sepsis. Hypertensive disorder of pregnancy may lead
miscarriages and contraceptive prescriptions.
to chronic hypertension, renal failure and neurological
disorders. This subgroup also includes obstetric morbi
dities caused from the treatment of direct obstetric morbi MATERNAL MORTALITY AND
dities, e.g. a woman with obstructed labor who undergoes APPROACH TO ITS REVIEW
a cesarean section develops wound infection.
While pregnancy and childbirth should be an occasion
Mostly these direct obstetric morbidities are short- lived.
for rejoicing, life-threatening complications may occur,
The women suffer and then either recover or die. Sometimes, which, if inappropriately managed, could lead to maternal
they may have long lasting sequelae. Hemorrhage may death or disability. Developing countries have a large
lead to Sheehan’s syndrome. Choriocarcinoma, is a direct share of these mortalities (99%). In these countries every
result of a preceding pregnancy (abortion, molar pregnancy minute one maternal death occurs. About 1600 women die
or normal pregnancy). It can be easily treated to begin per day in India. Throughout the world around over half a
with. If not treated it is always fatal. Obstetric fistulae and million deaths are recorded per year during pregnancy and
uterovaginal prolapse also are long-term morbidities. childbirth and beyond. Biggest number of maternal deaths
take place in Asia, particularly in India, Bangladesh, Nepal
Indirect Obstetric Morbidity and Indonesia.
The morbidity in this case is not caused by pregnancy but is
made worse by it. It may be due to compromized immune MATERNAL DEATHS
function, which occurs in pregnancy. Hence, several infec
tions, e.g. malaria, tuberculosis, hepatitis, etc are more Definition
serious during pregnancy. Some chronic diseases may be Maternal mortality ratio (MMR)—(not a rate), as the
exacerbated by pregnancy, e.g. rheumatic heart disease denominator does not include all pregnancies, only live
(RHD), chronic hypertension, sickle cell anemia. Breast births. MMR also measures the risk of women dying from
cancer also progress more rapidly during pregnancy. ‘puerperal causes’ and is defined as:
Total number of maternal deaths due to complica-
Psychological Disorders tions of pregnancy, childbirth or within 42 days of
It is present because of the stress due to the hormonal delivery from puerperal causes in an area during a
year × 100,000
changes in pregnancy. MMR =
Total number of live births in the same area and year
Non-obstetric Morbidity MMR is highest in Africa and Asia with the largest
These are conditions which occur during pregnancy, population staying in these places. In Africa, the lifetime risk
delivery or puerperium but appears to be unrelated to of maternal mortality is 1 in 16,1 in 58 in Asia whereas 1 in
pregnancy. The relation sometimes is not that clear, e.g. 4000 to 10,000 in industrialized countries. This is perhaps
attempted suicide or homicide in an unmarried pregnant the index with the greatest disparity between developed
girl. Pregnant woman are more prone to burn accidents and developing countries.
because of their unstable position. There is growing Maternal death can be categorized as direct maternal
acceptance of defining such deaths and morbidities being death or indirect maternal death.
included in maternal mortality and morbidity.
Gynecological morbidity, contraceptive morbidity and Direct Maternal Deaths
sexual morbidity are dealt with in detail in the Textbook These are 80% of these mortality. They are the deaths caused
of Gynecology by the same author. by conditions during pregnancy, delivery and puerperium
We have a massive burden of reproductive morbidity in and their management, omission and incorrect treatment.
our country. This is a highly neglected issue and there is an It includes deaths from abortion, ectopic gestation, APH,
urgent need for awareness of reproductive morbidities and PPH, pre-eclampsia, eclampsia and puerperal sepsis.
Indirect Maternal Deaths TABLE 70.1: Maternal mortality in selected countries (2013)
They are because of pre-existing diseases that alter their Maternal mortality (per
course during pregnancy which were exaggerated by Country 100,000 live births)
physiological alterations of pregnancy and labor and are India 190

not directly related to pregnancy, but which may worsen Sri Lanka 29
during and/or following pregnancy and childbirth. These Bangladesh 170
are anemia, cardiac diseases, diabetes mellitus, thyroid Nepal 190
disease and viral hepatitis, etc. of which anemia is the Myanmar 200
most important single cause in the developing countries. Thailand 26
An example of indirect maternal death is death from RHD China 32
in pregnancy; physiological changes in pregnancy worsen Japan 06
already existing cardiac dysfunction. In most developed Singapore 06
countries, maternal mortality due to direct causes has UK 08
declined and the majority of maternal death occur due to USA 28
indirect causes. Switzerland 06
Iceland 04
Incidence (Table 70.1 ) Russian Fedration 28
Source: WHO, UNICEF, UNFPA, World Bank and United Nations
In developed countries, MMR varies from 4 to 40 per 100,000
Population Divison Maternal Mortality Estimation Interagency Group
live births. In the developing countries, it varies from (1990–2013)
100 to 700, with India having about 190 per 100,000 live
births. Therefore, 99 % of maternal mortalities occur in
developing countries, being the leading excuse for death Factors Affecting Maternal Mortality
of women of reproductive age group in many parts of the Age: In very young adolescent, pregnancy carries a higher
world. risk due to pre-eclampsia, cephalopelvic disproportion
Most maternal deaths and pregnancy complications (CPD) and lack of antenatal care (ANC). In women aged
can be prevented by providing good quality maternity 35 years or above, there is a 3–4 times higher risk because
services. Reduction of maternal mortality is included in of hypertension, diabetes and CPD.
Millennium Development Goal 5 (MDG5). Estimates Parity: Risk is lowest in the second pregnancy, slightly
of maternal mortality in some countries are given in more in primigravida but it increases to 3 times in
Table 70.1. woman with 5th pregnancy and above due to PPH,
India is among those countries which have high maternal malpresentations and rupture uterus.
mortality rate because of domestic deliveries conducted by Antenatal care: The most significant factor affecting
untrained personnel and lack of proper referral system to maternal mortality is availability of quality ANC facilities
well-equipped facilities for emergency obstetric care. and their utilization by the community. Due to lack of
The MMR in India was 190, as estimated by the WHO in education in patients of low socioeconomic status there
2013. However, there are wide variations in MMR among is higher fertility and under utilization of these services
the various states. Among the larger states, the lowest and thus a higher rate of maternal mortality. There is
MMR is in Kerala, while MMR in Bihar, Madhya Pradesh, lack of felt need.
Uttar Pradesh, Rajasthan and Orissa are well above the Socioeconomic strata: Maternal mortality ratio are
national average. higher in women belonging to low socioeconomic
status, as they are less privileged in education, nutrition,
Why Do Mothers Die? housing and approach to healthcare facilities.
Most common cause is hemorrhage (25%). Other direct Social factors: Low status of women in the society
causes include high blood pressure, abnormal labor, e.g. coupled with their low literacy levels prevents women
dystocia, illegal abortions and sepsis. However, while it is from taking full advantage of maternity services
possible to attribute a medical cause for every maternal available in the community.
death, it is equally important to look at non-medical Most deliveries are conducted by untrained personnel
causes for maternal deaths. at home, which leads to higher maternal mortality. Other
A maternal death is the end result of inadequately or

inappropriately managed complications arising during
pregnancy and childbirth. The reason for inadequate or
inappropriate management could be traced backwards to
the health seeking behavior of the woman, her family and
her community, the access that she had to healthcare, her
health status, her socioeconomic status, and ultimately, to
her status in the society. Poverty and low status of women
in society are limiting factors in seeking healthcare, even in
an emergency. Also, a poor malnourished woman cannot
withstand complications in pregnancy and childbirth as a
better nourished, healthy woman. The status of women in
Fig. 70.1: Causes of maternal deaths society plays a major role in their survival; maternal survival
is best in communities where women are educated, are
social factors are short interval between 2 pregnancies aware of their rights and have an equal status in society as
(less than 3 years), number of members of the family, lack men.
of proper nutrition, low income, illiteracy, ignorance, prej-
udices, unhygienic environment, bad roads, poor methods Three Delays
of transport, etc. Delays may occur between the time a woman develops
Figure 70.1 shows that about 80% maternal mortalities a life-threatening complication to the time she receives
are due to direct causes. Twenty per cent are because of appropriate treatment. These delays may occur at one or
indirect conditions like anemia, malaria and heart disease, more levels. The first delay is when complications arise; the
etc. woman and her family may not recognize the significance
Hemorrhage: Hemorrhage is responsible for 25% of
of the problem. Even when the problem is recognized,
maternal death and is mostly due to PPH, retained pla- there may be other factors, which delay further decisions
centa, abruptio placentae, placenta previa, abortion to seek care. Once she decides to go to a doctor, there is a
and ectopic pregnancy.
delay in arriving at a facility where care can be provided.
Sepsis: Sepsis accounts for 15% of maternal mortality.
This second delay may be related to the distance between
Puerperal infections are due to poor hygiene during
the woman’s home and the appropriate health facility,
delivery and untreated reproductive tract infections
lack of transport, difficult access due to lack or damaged
(RTIs).
roads, floods, etc. Finally, even after the woman reaches
Hypertensive disorders in pregnancy: About 12%
the facility, for various reasons, there may be delay in her
death occur because of pre-eclampsia and eclampsia
receiving appropriate care (third delay).
and are mostly preventable with good ANC.
Prolonged and obstructed labor: About 7% deaths
Interventions to Prevent Maternal Deaths
occur as a result of prolonged and obstructed labor.
Around 8% of maternal deaths are due to ectopic preg-
The following measures are to be taken to decrease
nancy, embolism and anesthesia related complications MMR:
and 13% are due to unsafe abortions. Promotion of family planning services to reduce
Indirect causes: These causes are responsible for about unwanted pregnancies and illegal septic abortions. No
20% of maternal mortality viz. Pre-existing diseases are unwanted pregnancy and hence, no associated maternal
extenuated by physiological effect of pregnancy—most morbidity.
signified is anemia. In 15–20% of all maternal deaths, Preconception checkup. Both partners must get checkup
anemia is usually a contributing factor. About 40% of done and get any deficiency or disease corrected
obstetric patients in developing countries suffer from or controlled to prevent major complication during
anemia and may die during pregnancy or labor due to pregnancy, labor and puerperium (see Chapter 36).
congestive cardiac failure. Early registration of pregnancy should be done. At
• Infective hepatitis is a significant cause least three antenatal checkups should be done. First
• Cardiovascular diseases by second trimester (16–20 weeks), second visit at 32
• Diseases of the endocrine and metabolic system. weeks and third visit at 36 weeks. Identification of high-
risk cases should be done and they should be referred Most conditions leading to maternal death cannot be
to better health facilities. Provision of ANC is a must adequately prevented by ANC alone. Over 60% maternal
and it is important in reducing a significant amount of mortalities happen in immediately after birth of the
maternal deaths. neonate due to PPH and sepsis. PPH can kill an otherwise
Dietary supplementations and prophylaxis for anemia healthy woman within 2 hours of onset of bleeding. While
to be given to every pregnant women. Tetanus toxoid 50% women in developing countries like India receive
prophylaxis to be given. some form of ANC the proportion of women having
Essential obstetric care should be provided at the appropriate quality intrapartum and postpartum care
doorstep of the pregnant women, i.e. at first referral is only 30%. Besides essential obstetric care emergency
level hospitals. obstetric care is also essential.
• In India, about 60% of rural mothers deliver at home However, this does not mean that ANC has no benefits.
and these deliveries are conducted by untrained Good ANC can reduce the number of anemic women in
dais. A large number of maternal deaths can be the community, prevent maternal tetanus and provide
prevented with the help of trained local dais and appropriate advice to women on the place of delivery and
female health workers for the delivery at hospitals. on being prepared for complications, if they arise.
• In case of emergencies, transport facilities should be
Preventing Unwanted and Unsafe Abortions
provided for referral to better health facilities.
Medical disorders of pregnancies particularly anemia,
Over 75 million women globally have unwanted preg
diabetes, hypertension and cardiac disease, which are nancies. Many of these end up in unsafe, induced
important indirect causes of maternal deaths should abortions. A large proportion of women live in countries
be managed by joint consultation of specialists in the where abortion is illegal. Even in places where abortion is
tertiary hospital. legal (as in India), many women continue to have unsafe
There should be provisions for good anesthetic facilities,
abortions, endangering their lives. Effective contraception
blood bank, specialist services in the labor room of the will prevent pregnancy, the prerequisite condition for
maternal death. Reduction in the number of pregnancies
hospital.
will effectively reduce the risk of death that a woman faces
Maternal mortality review should be conducted regard-
during her lifetime. Better access to effective contraception,
ing the cause of death and any avoidable factors and
[including emergency contraception (EC)], safe abortion
remedial measures should be taken time-to-time to
and postabortion care, providing appropriate education,
reduce maternal deaths in the future.
counseling and involvement of the male partner in
Training courses for training of health workers, traditional
responsible parenthood should help to reduce maternal
dais and private practitioners should be arranged which
deaths due to unsafe abortion.
will greatly help reducing the maternal mortality.
Several interventions have been proposed and tried Training Traditional Birth Attendants
out to reduce maternal mortality. Only a few have been
In India, the majority of women are delivered at home,
successful.
outside a health facility. In these situations, women are
delivered by members of their family or by traditional birth
Antenatal Care and the at-Risk Approach
attendants (TBAs). There have been many attempts to train
Antenatal care is often referred to as an intervention TBAs in conducting safe delivery. Unfortunately, these
to reduce maternal mortality. For many years, the attempts have been, by and large, unsuccessful in reducing
‘at-risk’ approach was promoted as an effective inter- maternal mortality significantly. It has been estimated
vention. The principle of ‘something for all, but more for that only 3% of maternal deaths can be prevented by TBA
those in greater need’ makes sense when resources are training. Most TBA training has concentrated on teaching
limited. Unfortunately, life-threatening complications clean delivery techniques—clean hands, clean surface for
do occur in low-risk pregnancies also. Numerically there delivery, cord tie, blade to cut the cord, cloths to receive
are many more low-risk pregnancies in the population. the newborn, etc. However, a TBA is unlikely to recognize
Therefore, although ‘high-risk’ has more complication in and appropriately manage PPH, eclampsia or puerperal
absolute numbers (percentage wise), but more complica- sepsis. There is also concern that the number of deliveries
tions occur in low-risk women because they are greater in conducted by a TBA every year is usually less than the
number. number required to retain key skills.
Ensuring Skilled Attendant at Birth INSTITUTING MATERNAL DEATH REVIEWS

The intervention of ensuring a skill birth attendant at each
parturition is very crucial in reducing maternal mortality While MMR indicates the level of care or lack of it, does
Skilled birth attendant is a person with midwifery not indicate the reasons for mother’s death. It is important
education and training in the skills to manage normal for everyone concerned with maternal health to go
labor deliveries and recognize, any complications arising beyond these numbers and to identify the reasons for
during parturition and supervize for interventions not every maternal death. Medical causes are only part of the
possible at their facility (this includes doctors and nurses reason. It is at least equally important to understand the
with midwifery training). non-medical causes for her death. These may be within
A skilled attendant can prevent PPH (by active the family, the community or health system.
management of third stage of labor), eclampsia by early Various approaches have been used to study maternal
detection and proper management of pre-eclampsia, death.
Verbal autopsies for deaths occurring in the community
obstructed labor by using partograph, and puerperal sepsis
Hospital based death reviews (facility-based maternal
by meticulously observing aseptic techniques. If these
complications arise, a skilled birth attendant can manage death review)
Confidential reviews of all maternal deaths in the state
(a) PPH by use of oxytocics, uterine massage, manual
Clinical audit
removal of placenta, fluids and blood; (b) eclampsia with
For every maternal death, there are at least 20 cases
magnesium sulfate, antihypertensives and delivery; (c)
obstructed labor by cesarean section or symphysiotomy; of significant maternal morbidity. Some of these may
and (d) puerperal sepsis by instituting antibiotic therapy have ended in maternal deaths had it not been for some
and removal of infected material. intervention (near misses).
There are ample evidences from observational studies Reviews of these ‘near misses’ also provide valuable
on the role of skilled attendant at birth in reducing maternal information, which can be used to prevent further
mortality. The maternal mortality ratio in Sweden, where maternal mortality and morbidity.
midwives who conducted deliveries at home were allowed It is important to learn lessons from every maternal
to perform postpartum uterine massage and manual death and ‘near miss’ and to institute changes in practices
removal of retained placenta, had fallen to about 100 by that aim to prevent similar complications and deaths from
the end of the 18th century. This level of MMR reached happening again. Every maternal death is a tragedy can be
well before antibiotics, blood transfusions, safe cesarean greater when we fail to know how a pregnant women died.
delivery and universal ANC became available. MMR is Maternal mortality reflects the status of women in a
inversely correlated to the percentage of skilled birth community or a country. Meticulous study of each death
attendants; the higher the percentage of skilled birth is essential. This gives the insight into the conditions
attendants, the lower the MMR. The examples of Kerala prevailing in the community and healthcare facilities. This
and Sri Lanka, where nearly 100% of deliveries are attended review guides health personnel for possible interventions
by skilled attendants are in contrast to the high mortality in to prevent repeating the same deficiency, as far as possible.
those states and countries where women do not have this The following approaches are used to review maternal
help at childbirth. deaths.
The presence of a skilled attendant alone may not
be enough. Drugs, supplies and a functioning referral
Verbal Autopsies for Deaths Occurring in the
system are essential in ensuring maternal survival. If a Community
complication arise that is beyond the managerial capability By this method we try to find out personal, family and
of this attendant or beyond what is available in the given community factors responsible for a maternal death
circumstances, the attendant should be able to refer to occurring outside and even inside a medical facility,
a facility which can provide comprehensive emergency by interviewing persons knowing about the event of
obstetric care, including cesarean section, laparotomy maternal death and circumstances leading to the mortality
and blood transfusions. With skilled birth attendants and (family members, neighbours and TBAs etc). This is also
a functional referral system, approximately 60–75% of sometimes used to find factors contri buting to death
maternal deaths can be prevented. within a healthcare facility.
Prerequisites It is less costly as is done by the staff positioned in the

The family members of the deceased woman. hospital.
This facility-based maternal mortality review provides a
The interviewer must have sensitivity while finding the
circumstances of death. good learning experience to all staff members.
It helps to develop standards and formation of protocols
Advantages in that facility.
While most of the maternal mortality occur at home, verbal Disadvantages

autopsies guide one to find medical factors of demise.
These are less systematic than clinical audit. The large
There is exploration of both non-medical and medical
amount of information collected is difficult to formulate
factors in analyzing the events leading to maternal
and synthesized.
mortality in that community.
To do the process and proceed with constructive changes
It gives an opportunity to improve health services
we need committed and skill persons.
for the pregnant women by incorporating family’s and
No information can be gathered in cases of maternal
community’s view on the quality and quantity of healthcare. mortality happening in the community (brought dead
cases).
Disadvantages Support of hospital managers and administrators is
The details are given differently and medical causes must.
obtained are not exact. If a visit to a community can be arranged it may be
A large number of elements influence finding the avoi difficult to trace the family of the dead women as they
dable factors (subjective judgement). The lay informers may have moved out of that place because of her death.
account is not developed in accordance with the one
which is written in the death certificate. Confidential Enquiries of the Maternal Deaths
Under-reporting especially in early pregnancy deaths It is confidential (anonymous) multidisciplinary inves-
from indirect causes, and even over reporting too may tigation or a representive sample of maternal mortalities
be a problem. occurring in a demographic place (a nation, state, district,
taluka, etc.). The numbers of death, reasons, preventable
Facility-based Maternal Death Review factors and lesson learnt from every maternal death by
It investigates in depth the circumstances leading to the meticulous data is collected. Thus, pinpointing the prob-
maternal death which happened in the medical facility lematic area. It helps in finding the cause of every maternal
(hospital). It also take note of the factors in the community mortality and highlighting the important areas that needs
which lead to this death and finding avoidable factors to updated guidelines for improving clinical outcomes.
prevent further similar mortality. These enquiries are usually published.
Prerequisites
Prerequisite
There must be a pre-existing and functional system at a place
Cooperation and willingness of doctors and nurses who in the hospital for vital records, statistical analysis of birth
were involved in the care of the decease is essential. If and deaths, persons employed (statistical infrastucture)
needed, they are also interviewed. they have designated faculty who will regularly report any
maternal death to the enquiry committe.
Advantages
It may be going on in one form or the other in most of Advantages
the hospitals. Hence, approval to support by the higher More general policy recommendation can be made
authority is easy to obtain. than only facility specific ones.
As the process is going on in some form or the other in Better picture of maternal mortality and deaths in
most of the facilities it is easy to introduce changes to projected.
make it slightly more precise. The quality of maternal care improves as the findings of
This gives whole circumstances leading to the death by the enquiry are widely published.
finding the avoidable and non-avoidable factors in the It also given the lessons learnt are also given a mass
hospital and if possible in the community. dissemination for public consumption.
Regional and national health departments are involved It can be started at a place (hospital) and by analysis we
indicating the commitment of the government. In can get local and immediately changeable data.
some states, the Chief Minister takes personal interest Problems in record keeping and maintaining can be
in causes of each maternal death thus improvement highlighted and corrected.
in healthcare and less maternal deaths. This also
culminate in close liason among the policy makers and Disadvantages
serving personnel (doctors and nurses, etc.).
Community issues cannot be dealt with. Only that
As a representative sample is taken, the limited number
hospital care is accounted and corrected.
enables in depth investigation.
All maternal mortalities are not completly studied, but
Disadvantages reasons of death at a particular period are addressed.
Workshops are needed to familiarize and reassure the
Only information on maternal death (numerator date)
doctors and nurses about evidence-based practices.
is available. But characteristics of all delivering women
A set of local or standard criteria and protocols are to be
is not provided.
developed.
Committed participation and resource intensive
Non-medical audit assistance (staff of record section)
reviews are required and hence, it may not be possible
are required to locate patient records and get informa
everywhere.
tion from them.
Analysis of all maternal deaths is complex. Hence, only
a representative sample is taken. There may be lack of willingness to complete the audit
The socioeconomic factors (poverty, under nutrition, loop.
geographic locations) are not adequately covered.
Surveys of Severe Morbidity (Near Miss)
Clinical Audit Definition
Definition When severe complications are treated in a woman who
A process of quality improvement to enhance patient’s is pregnant, a recently delivered or one who suffered a
care by systematic review of maternal mortality cases miscarriage is saved because of hospital care; she was
against clear criteria (protocol, standards, etc.) and imple- provided in a near miss otherwise she would have died.
mentation of the changes needed.
Prerequisites
Prerequisites
Medical record section must be good. Life-threatening
Protocols, standards or explicit criteria are essential to events management must be discussed freely without
be in place against which each case is judged, pointing punitive threat.
the weak point. The committed clinical staff and management must be
Identify relevant cases from hospital registers and retrieve
in the committee.
notes.
The management of mortality cases must be discussed Advantages
freely and suggest and revise protocols, whenever, required
by the healthcare personnel. Cases of severe morbidity are seen more often than
deaths. This allows quantification of available factors.
Advantages As the woman has survived serious complications the
Improvement in the patient care is brought about by the study will be less threatening to the health providers.
participatory elements of clinical audit. The woman herself can be interviewed about the first
It is an excellent educational tool when properly hand report rather than proxy by family members (as in
executed in a non-punishment mode. cases of verbal autopsy).
A realistic feedback is provided to the care givers on Severe morbidity case reviews gives a good record of the
practises and performance helping them to find out standard of care in that hospital.
means of improvements. If audit recommendations are addressed adequately, it
It is less expensive because in-service personnel can do prevents life-threatening events and recurrences lead
data retrieving. ing to a death can be greatly reduced
Disadvantages Factors Related to Transportation and

Near miss analysis can be done only in healthcare Primary Aid—Case Report
facilities. Heera (name changed) had a full term normal delivery at
Clear definition and sophisticated tools are required to a private nursing home. She was referred to the hospital
identify near miss cases. after suffering from PPH due to extensive cervical tears.
A concentrated effort by all providers is needed to She traveled in a private transport. No primary aid was
define life-threatening severe obstetric morbidity as administered. She was already in shock due to hypovolemia
they are not easy to define. by the time she is brought to the hospital. She had cardiac
Large number of registers and case sheets are to be arrest on way to operation theater and died. A few inter
screened to find the cases. vention like tight vaginal packing, fluid resuscitation and
For this study, selection criteria are needed to do oxygen during transportation could have averted this
indepth review of all cases, e.g. paying attention on a outcome.
particular type of complication (say obstructed labor)
Importance of Antenatal Checks
or night time events.
Consent from the patient should taken before inter Forty-four of the seventy nine unbooked cases did not
undergo antenatal checkup (56%).
viewing her.
This points towards a broader policy issue of raising
awareness about the importance of antenatal checkup and
OPERATIONALIZING THE REVIEW its components.
The facility-based review involves assessment at two levels. Importance of Antenatal Check—Case Report
The first level of assessment is done by the specialist and
Maya (name changed) was the resident of a village from
consultant of the concerned unit after going through
the neighboring district. She was admitted with severe
the case records and maternal death. Notification forms
pregnancy-induced hypertension resulting in eclampsia
are to be filled by the senior resident on duty.
and cerebrovascular accident. At the time of admission
The second level of assessment is done by the members
in the hospital she was in labor. She did not undergo any
of the faculty from all units which form the maternal antenatal checkup. As a result, she missed warning signs
death review committe. The assessor control sheet of hypertension, proteinuria and edema that preceded the
is filled after a thorough review of the case and after convulsions by a few days (as per the description provided
performing the required interviews with the doctors by the relatives). With an active management of labor,
and other staff. she delivered a live baby of 2.3 kg within four hours of her
arrival at the hospital. However, despite all the efforts she
LESSONS LEARNT could not be saved.
In the Department of Obstetric and Gynecology in Need for Skilled Birth Attendant
Safdarjung Hospital, New Delhi facility-based maternal Almost 15% of the deliveries were conducted by unskilled
death is being done. A few examples of lesson learnt and birth attendants. This underlines the need of the delivery
steps taken to improve maternal care are discussed later. by skilled birth attendant.
Some factors have been found common to several
Case Report
deaths analyzed in the facility–based maternal mortality
review at Safdarjung Hospital: Madhu (name changed) was fourth gravida and third para.
She had not undergone any antenatal checkup. She had a
home delivery assisted by a dai. She developed distension
Factors Related to Transportation and
of abdomen and fever after delivery and was admitted to
Primary Aid the hospital after 6 days of delivery. She was diagnosed
When patients are referred from other hospitals they are as puerperal sepsis with pyoperitonitis. Following a
transported in private vehicles without any life support. laparotomy, 2 liters of pus was drained. Despite all
Lack of adequate details in the referral card/slip leads to treatments there was no relief from fever. Madhu died on
further loss of critical time. after few days in the hospital.
Need for Safe Abortion early labor with severe anemia (hemoglobin of 2 g%)
Abortion related deaths accounted for almost 12% of our and cardiac failure. In the labor, room the patient was
cases. This accounts the importance of safe abortions. propped up and oxygen mask was administered. She was
given injection furosemide 40 mg IV. This was followed by
Case Report partial exchange transfusion (a procedure started for the
Neela (name changed) had got an medical termination last 4 years for the treatment of severe anemia in patients
of pregnancy (MTP) done from a private clinic in a in our department). Approximately 350 mL blood was
neighboring district. She was referred to the hospital after removed slowly. Two units of packed hemoglobin cells
6–7 days of MTP when she developed fever and distension were transfused in the next 6 hours. The cell component
of the abdomen. On arrival, she was already in septicemia. of the blood that was removed initially from Rita was also
Despite immediate laparotomy and all efforts to treat retransfused. This process saved the patient.
septicemia she could not be saved.
Case 2
Family Related Factors Shweta (name changed), a para 1, had a delivery two
Family related factors include sensitization of family months ago. She was referred to our hospital as a case
members on issues pertaining to the family. of cardiac failure and severe anemia. On examination,
The lack of awareness becomes a major impediment her general condition was critical. There was abdominal
particularly when there is need for blood donation. distension. Paracentesis revealed frank blood. A diagnosis
of a ruptured ectopic was made and the patient was
Case Report immediately taken to the OT after resuscitating her and
Geeta (name changed) was admitted in our hospital in a arranging 6 units of blood. Timely availability of blood and
critical condition. She was diagnosed as molar pregnancy, quick laparotomy saved the patient.
severe anemia and respiratory distress. She had no
antenatal checkup. The treatment planned for her was Actions Taken after Instituting
blood transfusion along with suction evacuation. However, Facility-based Review
no relative was willing to donate blood. Neither the patient, Increased stress on post-delivery and postoperative
nor her husband gave consent for surgery despite repeated monitoring
counseling. The patient started bleeding profusely. After • Improving availability of blood
sometime, despite blood transfusion she could not be saved. • Doctors in emergency department were sensitized
to ask for date of last menstrual period from all acute
Medical Service Factors cases in reproductive age group females. This led to
Non-availability of blood or delay in its provision: diagnostic and saving of lives of 3 ectopic pregnancy
Institutional delay in treatment cases.
Inappropriate treatment • Advocacy at institutional level for more infrastructure.
Poor post-delivery and postoperative monitoring. Coordination with other departments
Development of protocols.
Near Miss Cases All these measures, saved many lives.
The department has witnessed maternal deaths, experience
has also led to saving lives. This is illustrated by these 2 cases. CONCLUSION
Case 1 Introspection along with little progress every day can
Rita (name changed) 34 years old, unbooked G5P4L2 lead to big results and help us achieve our goal of safe
came to the our emergency room, as term pregnancy in motherhood.
1. What do you understand by the term morbidity and mortality?
2. What do you understand by the term maternal mortality? Also discuss about different factors affecting maternal mortality.
3. What are the benefits of having skilled labor attendants?
4. How can you prevent unsafe and unwanted abortions?
71
Government Programs for
Reproductive and Child Health
ignored. This specific contraceptive targets and incentives

INTRODUCTION
were replaced by reproductive health indicators.
‘Within the framework of World Health Organization Thus in April 1996, Target Free Approach was adopted
(WHO), the definition of health is as a state of complete by ‘National Family Welfare Program’ and it was appro-
physical, mental and social wellbeing, and not merely priately renamed in September, 1995 as Community Needs
the absence of disease, and infirmity, in the stages of life’. Assessment Approach (CNAA). CNAA refers to client-
Reproductive health, therefore, implies that ‘people are
oriented, target free approach, ensuring reproductive child
able to have a responsible, satisfying and safe sex life and
health services to the clients-based on community needs
that they have the capability to reproduce and the freedom
to decide if, when and how often to do so.’ given through decentralized planning. This was in contrast
to earlier centralized approach where contraceptive
National Family Planning (NFP) program was launched
for the first time in the World, in India in 1952 with an targets were set at the center.
aim of population stabilization by decreasing the birth RCH was launched in October 1997. It covered four
rate. With this aim, subsequent five year plans witnessed programs and services merged together, i.e. CSSM, family
implementation of variety of population stabilizing welfare program, management of RTIs (reproductive tract
strategies and ensuring optimum health of mother and infections) and STIs (sexually transmitted infections) and
child. Under eighth plan, in August 1992, Child Survival adolescent reproductive health.
and Safe Motherhood (CSSM) program was launched. Thus, the emphasis was on lifecycle approach, i.e. a
Initial focus was on decreasing birth rate also known healthy female gives birth to a healthy baby, who in turns
as fertility reduction. In 1994, International Conference grows up in a healthy adolescent. A healthy adolscent
on Population Development was held at Cairo and it also leads to a healthy reproductive years thereby a healthy
focused on ‘Reproductive and Child Health approach’ pregnancy and hence, ensuring a healthy newborn. This
(RCH approach) and fertility regulation. was the first phase of RCH program.
RCH approach is defined as ‘people have the ability
The RCH phase II was launched in April 2005. The main
to reproduce and regulate their fertility. Women are able
features of RCH phase II were decentralized planning and
to go through the pregnancy and childbirth safely. The
outcome of pregnancies is successful in terms of maternal CNAA approach. The CNAA approach has been renamed
and infant survival and wellbeing, and couples are able to as Community Needs Assessment and Monitoring
have sexual relations free from fear from pregnancy and Approach (CNAMA).
contracting disease’. Emergency obstetric care (EmOC) is generally char-
In 1994–95, National Family Welfare Program was acterized as basic EmOC (BEmOC) and comprehensive
reviewed. It showed that introduction of concept of EmOC (CEmOC).
specific contraceptive targets and incentives led to rise Basic emergency obstetric care is provided by skilled
in performance figures, omitted neglect of client’s needs birth attendants. It is based on antenatal care (ANC):
and quality of services. There are some fallacies like, major Risk scoring in good ANC
stress was on sterilization and many important factors like Social mobilization
male participation and spacing in young couples were Management by skilled health personnel
Government Programs for Reproductive and Child Health 661
Parenteral antibiotics Improve coverage, equity and quality of ANC:

Parenteral oxytocic drugs • ANC is important for the mother and the newborn.
Parenteral anticonvulsants • RCH-II aims to raise the proportion of pregnant
Manual removal of placenta and assisted vaginal delivery women receiving 3 ANC checks to 80% from the
Good referral system. present level of 44%.
Comprehensive EmOC is delivered by skilled health • Make special efforts to reach women of below
personnel who can provide full Basic EmOC plus medical poverty live (BPL), scheduled caste (SC)/scheduled
doctor‘s services viz. tribe (ST) and other marginalized groups, targeting
Surgical services (cesarean section) by skilled obstetrician primigravida and adolescents.
Safe blood transfusion services • Ensure fixed day ANC services in the community and
Anesthetic services. facilities and involve AWWs, women’s group, TBAs
and other community partners to reach out to each
STRATEGIES IN RCH-II pregnant woman, especially the above mentioned
groups.
Increasing number of facilities offering safe delivery,
• Improve quality of ANC by ensuring: first checkup
EmOC and demand for services.
in the first trimester, total 3 checkups or more, two
Ensuring access to safe blood at all district hospitals
doses of TT and ingestion of 100 tablets of iron folic
and first referral units (FRUs).
acid (IFA).
Highest priority for RCH II. Two level of institutions
• Improve counseling at ANC sessions.
were targeted:
• Care of newborn, immediate and exclusive breast
• Primary health center (PHC) and community health
feeding, drying/wrapping and delaying bath.
center (CHC) for BEmOC
Strengthen postpartum care in the community.
• FRU for CEmOC.
• Focusing on the home, even the mothers who deliver
Training MBBS Medical Officers, in cesarean section.
Anesthesia training for MBBS Medical Officers. in institutions are likely to be discharged within a
Specialists (obstetricians/anesthetists/pediatricians day or so.
• AWWs will visit neonates and mothers on days 1, 2,
were transferred from dispensaries and PHCs to FRUs
and CHCs, where they can contribute to emergency 7, 14 and 28 with particular emphasis on the first two
care of women and children. Involved general surgeons visits.
in providing EmOC. • The key messages for the mothers will include:
Provide RTIs/STIs treatment. danger signs, nutrition, IFA tablets, birth spacing
Use telecommunication system to improve referral and newborn care.
system. Provide skilled care to pregnant women at the community
Provide safe abortion services at PHC onwards and level.
encourage the use of manual vacuum aspiration (MVA). • Promote deliveries by skilled birth attendants at
Provide incentives to doctors and other staff to work at subcenter and in the community.
PHCs/CHCs/FRUs. • Encourage more ANMs to provide skilled care in
Provide impress money to doctor and other staff to these settings. States will be encouraged to include
work at PHCs/CHCs/FRUs for transport, etc. subcenter strengthening for deliveries as a priority.
Encourage establishment of maternity hospitals/nursing • A new cadre of community-skilled birth attendants
homes in small towns. (C-SBAs) will be introduced. After a training of one-
Coordinated activities to raise awareness of danger year, a C-SBA will provide midwifery care as in the
signs in pregnancy, labor and postpartum period. community.
Social mobilization with help of panchayati raj institu- • Extend role of ANMs to administer obstetrics
tions, opinion leaders, non-government organizations first-aid. At present, ANMs are not permitted to
(NGOs), anganwadi worker (AWW), link volunteers, administer injectable oxytocics, tablet misoprostol,
auxillary nurse midwife (ANM) and other stakeholders. magnesium sulfate (MgSO4) injection or antibiotics,
Promote referral transport for routine deliveries and all of which can be life-saving. Sanction from the
EmOC. Make transport funds available with AWW/ drug controller of India has been taken for all these
ANM. drugs to be administered by ANM.
It is recommended that ANMs permitted to use these Increased facilities for medical termination of pregnancy
drugs after proper training. (MTP).
Conditional cash incentives for promotion of institu
tional deliveries by programs such as: Package for Newborn and Child Health
Janani suraksha yojana (JSY): This scheme aims to Newborn care facilities
reduce maternal and neonatal mortality by providing Home-based newborn care
cash incentives to beneficiaries going for institutional Infant and young child feeding
deliveries and for referral, transport and escort services. Integrated management of neonatal and childhood
JSY is the modified version of National Maternity illness (IMNCI) for common childhood illnesses
Benefit Scheme (NMBS). The maternity benefit for poor Vitamin A and folic acid supplementation
pregnant women BPL is provided after 19 years of age. Universal immunization
Pregnant women belonging to BPL will be eligible. Management of diarrhea
Pregnant women choosing institutional deliveries will Nutrition rehabilitation centers
receive financial assistance (more for the girl child). Folic acid supplementation in periconception period
Cash assistance (` 1500) will be provided for cesarean Preconception and prenatal diagnostic techniques act,
delivery. implementation to prevent female feticide
Transport assistance (` 150) will be provided to a rural Early initiation of breastfeeding and promotion of
woman for travel to a health center for delivery (variable). exclusive breastfeeding, timely addition of complimentary
Transport money will be reembursed by the ANM. Under feeding
JSY, a women who belongs to BPL can avoid transport Child welfare programs.
changes when referred to any facility (government or • Navjat shishu suraksha karyakarm (NSSK): It is
non-government). A woman who does not belong to a two day training program for doctors, ANMs and
BPL can avail JSY transport facility, if she is referred to a nurses about basic newborn care and resuscitation.
government hospital. • Janani shishu suraksha karyakram (JSSK): It pro-
Trained birth attendants (TBAs) who mobilize women vides for free referral transport of newborns to health
for ANC, institutional delivery and PNC will be provided facility, free drugs, free diagnostics and treatment.
with financial incentive. • Rashtriya bal swasthya karyakram (RBSK): It is
The newest strategy is RMNCH + A-Approach (Reprod- a new program aimed at early detection and thus,
uctive, Maternal, Newborn, Child plus Adolescent Health) early management for children from birth to 18 years
which emphasizes on continuum of care. to cover 4 ‘D’s’, i.e. ‘Defects at birth, Deficiencies,
RMNCH + A-Approach: To achieve the Millennium Diseases and Developmental delays including
Development Goals (MDG), maternal and child health Disability’. This ultimately lead to reduction in
approach has been now focussed on RMNCH + mortality, morbidity and disability.
A-Approach. It further reiterates that maternal and • Intensified newborn action plan: This has been
child health are mutually linked to each other and should launched recently under RMNCH + A framework
not be addressed in isolation. to reduce mortality among children within 28 days
of birth. Its goal is to bring down neonatal mortality
RMNCH + A-PACKAGE OF SERVICES rates to 24, 21 and 15 per 1,000 by 2017, 2020 and
2025, respectively.
Maternal Package
Early registration Services for Adolescents
ANC—four or more visits Adolescent nutrition, IFA supplementation
Anemia prophylaxis and treatment Adolescent friendly health services
Tetanus immunization Information and counseling on adolescent sexual
Institutional deliveries and deliveries by skilled birth reproductive health and other health issues
attendants Preventive health checkups and screening for diseases,
Referrals to FRUs for obstetric emergencies deficiency and disability in children
Home-based postnatal care Mental health, substance abuse, injuries, violence, non-
Counseling for birth spacing and limiting births communicable disease
Government Programs for Reproductive and Child Health 663
Facility-based adolescent reproductive and sexual cable only BPL families. The couple where girl is at
health services (adolescent health clinics) least 19 years at marriage,and who plan to bear the
Information and counseling on adolescent sexual first child after at least 2 years of marriage will get an
reproductive health and other health issues award of ` 5000 (boy child)/` 7,000 (girl child).
Adolescent welfare programs: • Santushti: It is a scheme of jansankhya sthirata kosh
• Menstrual hygiene scheme (MHS): It has been started (JSK) for highly populated states where gynecologists
to promote menstrual hygiene among adolescent and vasectomy surgeons from private sector are
girls in rural India by providing sanitory napkin. accredited by government to conduct sterilization.
• Rashtriya kishore swasthya karyakarm (RKSK): • National Helpline: Toll free (1800-11-6555): This is a
This was launched on 7 January, 2014 with aim to national helpline number in India to provide reliable
improve the health of adolescents (10–19 years) who information on reproductive health, sexual health,
comprise 21% of country’s population. This is an effort contraception, pregnancy, child health and related
to move away from a doctor driven effort towards a issues specially for adolescents, newly married and
holistic and participative program. The program about to get married persons.
emphasizes on seven ‘C’s’: Coverage, Content,
Communities, Communication, Counseling, Clinics
Other Services
and Convergences. Increased choice and availability of family planning
services
Reproductive Tract and Sexually Transmitted Gender sensitization and gender equality
Infections (RTIs/STIs) Safe MTP services
Screening and treatment of cancer
Promote recognition and referral of women and their
New interventions are:
partners with suspected RTIs/STIs.
• Mother and child protection (MCP) card: A joint
Strengthen services for diagnosis and treatment at
MCP card of Ministry of Health and Family Welfare
PHCs, CHCs, FRUs and district hospitals
and Ministry of Women and Child Development is
Strengthen synergy with National AIDS Control Organi
being used by all states as a tool for monitoring and
zation (NACO) activities.
improvement of quality of maternal and child health
(MCH) and nutrition interventions.
Family Planning Services
• Maternal death review (MDR): This has been
Home delivery of contraceptives to improve access: institutionalized across the country to identify not
This is done through accredited social health activist only the medical causes but also the sociocultural-
(ASHA) workers who deliver contraceptives at the door- economic determinants and gaps in the system
step of beneficiaries at a nominal amount, i.e., ` 1 for a leading to maternal deaths. The main aim is to
pack of 3 condoms, ` 1 for a cycle of oral contraceptive identify the corrective actions so as to improve the
pills (OCPs) and ` 2 for a pack of one tablet of emer- quality of obstetric care.
gency contraception (EC). • Web enabled mother and child tracking system
Ensuring spacing at birth(ESB): ASHA is paid incentive (MCTS): This has been implemented to register and
for counseling newly married couples to ensure spacing track every antenatal woman, neonate, infant and
of 2 years after marriage and couples with 1 child to have child by name so as to ensure a quality antenatal
spacing of 3 years after the birth of first child. care, intranatal care, postnatal care, family planning
Several programs launched with this aim, are: and immunization services.
• Prerna (Resposible childhood strategy): It is • JSY
launched in seven states viz, Bihar, UP, MP, Chhat- • JSSK
tisgarh, Jharkhand, Odisha and Rajasthan and appli- • Indira Gandhi matritva sahyog yojana (IGMSY)
Important demographic, fertility and mortality indicators

Indicators Current Status
Crude birth rate 21.4 (2013)
Crude death rate 7.0 (2013)
Natural growth rate (%) 1.44 (2013)
Infant mortality rate 40 (2013)
Neonatal mortality rate 29 (2012)
Postneonatal mortality rate 13 (2012)
Stillbirth rate 5 (2012)
Perinatal mortality rate 28 (2012)
Child (0–4) mortality rate 11.5 (2012)
Under-5 mortality rate 52 (2012)
Maternal mortality ratio 178 (2010–12)
Total fertility rate 2.4 (2012)
Life expectancy at birth (years)
Male 62.6 (2002–6)
Female 64.2 (2002-6)
i. RCH–II
ii. RMNCH + A-approach
iii. Intensified newborn action plan.
2. What are the main components of basic emergency obstetric care (BEmOC) and comprehensive emergency obstetrics care
(CEmOC)?
72
Sudha Salhan
Biomedical Waste Management
Protection Act 1986. It is applicable on all persons who

INTRODUCTION
create or generate, handle, collect, receive, store, transport,
Our household, the fields, industries, health centers and put them in place (dispose off ), treat the biomedical waste
commercial establishments, etc. generate waste. Waste is in in whichever form. This is generated in the diagnostic
the form of solid and liquid. Then there is radiation waste. laboratories, immunization clinics, in research laboratories
Hospitals, dental clinics, diagnostic laboratories, blood etc. This also includes other wastes like cytotoxic drugs
banks, etc. where patients with their attendants, generate (discarded), chemical waste and ashes from incineration.
different types of wastes which need to be segregated and All hospitals, dispensaries, nursing homes, clinics, dental
disposed off regularly to prevent their piling up and causing establishments, pathology laboratories, blood banks,
harm to the patients, health workers (doctors, paramedicals veterinary institutions, animal house must make sure that
and other hospital staff) and the environment. this biological waste do not adversely affect the health of
The main health hazards of biomedical waste in the the persons around and the environment.
hospital are mostly infections, viz. hepatitis B and C, The seven steps used to minimize the risk to health
human immunodeficiency virus (HIV), measles, mumps, and environment in biomedical waste management are
pneumonia, tuberculosis (most of the time multidrug handling, segregation, disinfection, storage, transport,
resistant type) dermatitis, etc. There can be accidental treatment, and disposal.
injuries from the sharp edges, from leakage of gases, The waste generated in the health center includes
formaldehyde fumes, etc. waste papers and packing material, dirty clothes, dressing
material, plaster of paris cast, soiled swabs (after taking
GUIDELINES ON BIOMEDICAL WASTE blood samples), body parts, placenta, etc. used items
(plastic bottles of intravenous (IV) fluid, plastic syringes),
MANAGEMENT FOR HOSPITAL STAFF cannulas, catheters, needles, blades, drugs, chemicals and
Hospital waste management has emerged as an important radioactive substances.
area of concern in recent times due to its ramifications on There are six schedules in the rule:
health facilities. Biomedical waste management in a new Schedule I of the biomedical waste (management and
Government Policy, is legal binding under the Biomedical handling, rule 1998) is categorization of biomedical wastes.
Act (Handling and Management), July 1998. Schedule II gives guidelines for color coding (type of
All hospital staff must be aware of these guidelines. It container) for disposal of biomedical wastes.
has a very important role in reproductive child health Schedule III gives instructions for labels for biomedical
(RCH) II. waste containers (bags), etc. (Fig. 72.1).
Schedule IV labels for the transport of biomedical
BIOMEDICAL WASTE MANAGEMENT wastes containers/bags.
The date, time, waste class, sender’s name and address,
AND HANDLING RULES receiver’s name and address with contact person is recorded.
This rule was gazetted on July 27th, 1998 and came into Schedule V standards for treatment and disposal of
force on the same date. This rule is part of Environment biomedical wastes.
labeled (Table 72.1). Then they are transported in covered

trolleys to waste treatment site within 48 hours.
Categories are mentioned in Schedule I of the rules
(Table 72.2).
Waste collection—should be taken care of transport
inside the facility (hospital) a fully covered labeled vehicle
(wheelbarrow) (Fig. 72.2).
If there is spillage of mercury (broken thermometer or
from blood pressure apparatus) use cardboard sheet and
collect all beads of mercury together with gloved hands,
suck in a syringe and place it in a container with some
water. Put all (cardboard, syringes, gloves) in a large plastic
bag, label it as mercury waste, transfer it to a second bag
Fig. 72.1: Biomedical waste container and label it. It is disposed off in a hazardous waste facility
or should be given to a mercury equipment manufacturer.
Schedule VI for time limit to installation of facilities like Radioactive waste is handled according to Bhabha
incinerator, autoclave/microwave system. Atomic Research Center (BARC), Mumbai guidelines.
The rules were amended and named as Biomedical Some of the equipments used for biomedical waste
Waste Management and Handling (Amendment Rules management and handling are as follows:
2003).
Needle Destroyer
Segregation, Packing, Transport and Storage It is an electrically operated machine where the needle is
The waste generated in the hospital is enormous. Approxi burnt after use (Fig. 72.3).
mately 0.43 kg of waste is generated daily from each
Incinerator (Figs 72.4 and 72.5)
hospital bed. Treatment of this amount of waste will cost
a lot. Hence, it is segregated into non-infected (requiring Objects intended for the incinerator are not disinfected.
ordinary disposal) and infected (needs special treatment). The yellow bags go for incineration. The temperature rises
Non-infected waste forms 85% of the hospital waste. above 850°C by dry heat. Initially red bags were sent for
Therefore, infected waste is only 15% of the total and needs incineration. But they produced toxic fumes and polluted
special treatment. This 15% cannot be kept untreated the atmosphere. They are no longer in use; only yellow
for more than 48 hours. The container is labeled. It is bags are used.
transported only in authorized vehicles. Here, the waste is destroyed by dry oxidizing heat.
The prescribed authority for enforcement of the The organic biomedical waste (e.g. placenta, parts of the
provision of these rules is the State Pollution Control human body removed during operation, etc.) is converted
Board. In the armed forces under the Ministry of Defense to a small volume of inorganic waste. The emission from
the prescribed authority is the Director General, Armed these incinerator is to be controlled according to emission
Forces Medical Sciences. Implementation of the rules is standards to minimize pollution.
carried out by the prescribed authority.
An advisory committee is made and it advises the Shredding (Fig. 72.6)
government, regarding issues related to biomedical waste. It is done for plastic IV bottles, plastic syringes, etc. (after
Annual reports are sent to the authority in a special disinfection). The waste is cut into smaller pieces to prevent
form (Form II) by the 31st of January every year. unauthorized recycline of syringes, etc. (which is a very
Every authorized person in the facility (hospital) hazardous practice). The shredded plastic is sold off.
shall maintain a record related to genesis, collection,
reception, storage, transport, treatment, disposal and/or Autoclave
any form of handling of biomedical waste. These records This uses sterilization by direct steam penetration with a
can be inspected and verified anytime. temperature range of 121–135°C to kill microorganisms
The biomedical wastes are kept in bags or containers and spores. Portable solar powered autoclaves are under
at the point of generation (in wards, laboratory, etc.) and research in Sydney.
Biomedical Waste Management 667
TABLE 72.1: Color coding and type of container for disposal of biomedical wastes
Color coding Type of container Waste category Treatment options as per schedule I
Yellow Plastic bag Category (1, 2, 3 and 6) Incineration/deep burial
Black Plastic bag Category (5, 9 and 10) (solid) ordinary Disposed in secured landfill (Municipal)
waste
Blue Plastic bags or puncture proof container Plastic and bottles category 4 Shredding and sold off
TABLE 72.2: Categories of biomedical waste

Option Waste Category Treatment and disposal
Category 1 Human anatomical waste (human tissues, organs, body parts) Incineration/deep burial
Category 2 Animal waste (animal tissues, organs, body parts, carcasses, Incineration/deep burial
bleeding parts, fluids, blood and experimental animals used
in research, waste generated by veterinary hospitals, colleges,
discharge from hospital animal houses)
Category 3 Microbiology and biotechnology waste (wastes from laboratory Local autoclaving/microwaving/incineration
cultures, stocks or specimen of microorganisms, live or attenuated
vaccines, human and animal cell cultures used in research,
infectious agents from research and industrial laboratories, waste
from production of biological, toxins, dishes and devices used for
transfer of cultures)
Category 4 Waste sharps (needles, syringes, scalpels, blades, glass, etc. Disinfection (chemical treatment/ autoclaving/
that may cause puncture and cuts. This includes both used and microwaving and mutilation/shredding)
unused sharps).
Category 5 Discarded medicines and cytotoxic drugs (waste comprising of Incineration/destruction and drugs disposal in secured
outdated, contaminated and discarded medicines) landfills
Category 6 Soiled waste (items contaminated with blood and body fluids Incineration/autoclaving/microwaving
including cotton dressing, soiled plaster casts, linen beddings,
other material contaminated with blood)
Category 7 Solid waste (waste generated from disposal items, other than Disinfection by chemical treatment/autoclaving micro
the waste shapers such as tubing, catheter, intravenous sets, etc.) waving and mutilation/shredding
Category 8 Liquid waste (waste generated from laboratory and washing, Disinfection by chemical treatment and discharges into
cleaning, housekeeping and disinfection activities) drains.
Category 9 Incineration ash (ash from incineration of any biomedical waste) Disposal in municipal landfill
Category 10 Chemical waste (chemical used in production of biologicals, Chemical treatment and discharge into drains for liquids
chemicals insecticides used in disinfection etc.) and secured landfill for solids
Hydroclave 2400–300,00 MHz and its wavelength is of 12.24 cm. The

fluid content of the waste is quickly heated.
It is a type of autoclave. Here, the temperature reaches
Personnel handling waste must wear gloves (heavy
between 350°C and 750°C. The biomedical waste is put
duty rubber gloves), aprons, mask, boots, etc. to protect
in a double sheeted layered cylinder where it is kept
themselves. Mobile hospital waste management systems
in movement during the process. It is heated by steam
for small healthcare units are on the anvil.
produced in a boiler. This steam passes between the two
layers of the cylinder and does not come in direct contact
SOME COMMON PROCEDURES IN THE
with the waste.
HOSPITAL
Microwave I will be taking examples from some common procedures
Microwave technique is like a household microwave oven. done in our department to give an idea as to how waste
The frequency of electromagnetic radiation is around segregation is to be done.
Fig. 72.2: Transporting Fig. 72.3: Needle destroyer
Fig. 72.4: Incinerator (outer view) Fig. 72.5: Incinerator (inner view)
I will start from the entry of the patient in the gynecology sodium hypochlorite (bleach) solution. Wash hands with
receiving room (GRR) or outpatient department (OPD). soap and water immediately after removing the gloves.
To examine a fresh case, one would use a pair of gloves, a All metal instruments (speculum in this case) should be
savlon swab, and a speculum. Please note that the color removed from bleach solution after 10 minutes, washed
of the plastic bag at the foot end of the examining table is thoroughly with lukewarm water and detergent and
red or yellow. Please do not use it as a waste paper basket. then sent for autoclaving. Other items like gloves are
When gloves are worn, the glove wrapping paper goes into soaked for at least half an hour, after which they are also
the black bag. The savlon swab used for examination and cleaned by water and sent for autoclaving. This treatment
any biological tissue removed during examination (for of articles in 1% sodium hypochlorite solution is called
example clots or products of conception) are discarded decontamination or pretreatment and whenever I refer
into the red/yellow bag. After examination, the speculum to ‘decontamination’ it means submersion of the object in
and gloves are immersed in a bucket containing 10% a solution of 1% sodium hypochlorite.
Fig. 72.6: Shredder Fig. 72.7: Hypochlorite solution
In the ward, during the conduct of preoperative

investigation, blood samples have to be drawn. No
sampling or insertion of IV catheter should ever be done
without wearing sterile gloves (protection of the doctor).
Collecting blood samples is the most common
procedure in the wards. Always wear gloves. Ask all
patients to press the puncture site with a swab after
collection of the blood sample. After drawing the last blood
sample, with the same gloved hands collect the soiled
swabs from all patients by doing a reverse round. Throw
them in the yellow bag. The used syringe and is dipped in
hypochlorite solution (Fig. 72.7) after filling the syringe
with the solution. The needle tip is put in puncture proof
container (Fig. 72.8) after mutilating the needle in needle
destroyer. The syringe is washed and sent for autoclaving
(if a glass syringe) or put in a blue bag for shredding
(if of plastic). Discard gloves in bleach solution container
Fig. 72.8: Sharp container (puncture proof )
and wash hands with soap and water. Keep requisition
forms away from samples. Do not soil them with blood by
keeping the vial on them. in the red or yellow bag for incineration and the container
Another common waste in the ward are the returned vial can be autoclaved and used for blood samples.
blood samples from the laboratory which are often Gloves are not required while giving intra muscular
thrown into the nearest bag without thinking. The blood (IM) injections, but they should always be worn while
should first be decontaminated by adding the sodium drawing blood samples or starting IV lines. When an IV
hypochlorite solution into the vial and leaving it there for at catheter is inserted, the wrapping paper is thrown in the
least half an hour. After that the blood can be poured down black bag, the plastic part of the wrapping in the blue bag,
the drain and the vial cleaned via autoclave and recycled the needle inside the catheter is thrown into the sharp
for more samples. At times, there are outdated medicines decontamination unit, the savlon swab into the red or
to be discarded. Drugs including cytotoxic drugs are kept yellow bag. Never leave it on the bed. Put the polythene
cover of the drip set into the black bag, the cap of the IV Ensure that the solution in the bowls is changed in every
bottle in the blue bag and the gloves are placed into the shift of a nurse. The broken ampules and the metal cap of
sodium hypochlorite solution. Hands are always washed the vial are non-infectious and can be put directly into the
with soap and water after removal of gloves. puncture-proof box.
When an injection is used, the sterile wrapping of both
syringe and needle are thrown into the black bag. The plastic
OPERATION THEATER
cap of the needle is thrown into the blue bag. The needle
is removed without touching the tip. After the injection, After entering OT, change clothes, wearing cap, mask and
all used syringes and needles are to be decontaminated goggles is prescribed. Thorough handwashing should be
in 1% sodium hypochlorite solution before final disposal. done, followed by wearing gown and gloves in the proper
Two bowls filled with this solution are going to be provided manner (see Chapter 57).
at each required site, one for syringes and other for sharp Cleaning of the part to b operated generates swabs
instrument. with savlon and other chemicals. During operation, soiled
When putting the syringe for decontamination, draw swabs are generated, IV drips are used and drugs are
some of the fluid left into the syringe for decontamintion injected (via syringes and needles). Anesthetization by
and ensure that it is submerged completely. The glass intubation generates swab, plastic disposables and mouth
syringes are also placed in the bowl of sodium hypochlorite. piece. Use a kidney tray to keep sharps, e.g. scissors and
The sharp deconta mination unit may contain a sieve needles. The surgeon will pick them up herself/himself.
inside a puncture proof bowl, and is meant for sharp Do not pass sharps by hand, to prevent injury.
wastes like injections needle, suture needle and blades. The decontamination unit for the surgical instruments
After the instruments have been soaked for minimum of is similar to the sharp decontamination unit but larger
30 minutes, the sieve is lifted to drain the fluid and the in size. If a large sieve is not available, the bucket can be
contents are emptied into a puncture proof box without lined with a large gauze. Immediately after use, all the
manual handling of the sharp objects. instruments are to be placed in this unit. They should be
Do not recap, bend or break needle before disposal. taken out within 10 minutes by lifting the sieve or gauze
To prevent unauthorized reuse of the needle it can be and washed with lukewarm water and detergent as
mutilated with a needle destroyer (Fig. 72.3). chlorine corrodes metal. Those instruments, which receive
One more commonly performed procedure is wound chemical disinfection, e.g. Kochers and obstetric forceps,
dressing in the ward. Gloves and masks are adequate should be dried before insertion into cidex to prevent
precautions for self-protection. The soiled gauze with dilution of cidex.
sticking plaster, any removed stitches, savlon and spirit All plastic waste is placed in the blue bag. The non-
swabs are all thrown in the yellow or red bag. If a rubber infectious one like IV bottle and drip sets can be kept
drain or Foley catheter is removed, they are soaked directly and the potentially infectious one like plastic
in sodium hypochlorite solution for half an hour for syringes are placed in the blue bag after decontamination;
decontamination, mutilated and discarded in the black they are sent for shredding.
bag. We feel that if there is left-over blood in the bag The unsoiled linen (bed sheet, etc.) can be sent straight
(due to death of the patient or a reaction or for any other to the washing place where the soiled linen is soaked in a
reason) the contents can be emptied into the drain—the drum of sodium hypochlorite for 10 minutes before being
bag itself is to be cut from the center for mutilation, soaked washed.
into the hypochlorite solution along with the syringes and If there is a spillage of blood or liquor on the mattress
placed into the blue bag. Similarly the urine bag is emptied or floor, please ensure that it is taken care of immediately.
of its contents, mutilated, decontaminated and sent in the Sodium hypochlorite is poured over the area and left for
blue bags. If a stitch has been removed, the surgical blade 10 minutes after which, it is mopped by a cloth/gauze.
is placed in the sharp decontamination unit, the same The types of waste generated in all the major surgeries
one as for needles. Tooth forceps, scissors or any other are more or less the same. When the bottle in the suction
instruments used, are decontaminated for 10 minutes, apparatus is nearly full, it is decontaminated by adding
in bleach solution, then they are washed and sent for the sodium hypochlorite solution. After half an hour, the
autoclaving; the used gloves are decontaminated for half suction bottles are carefully emptied of their contents in
an hour. the drain. Alternately, the sodium hypochlorite solution
can be placed in the bottle at the very beginning, before Use gloves during all invasive procedures, handling
starting any procedure. If disposable gloves are used, they and labeling of patient’s blood, body fluids and tissues
are decontaminated for half an hour, mutilated by cutting containing blood.
with a pair of scissors and placed in the black bag. Similarly, After removal of gloves (disposable and non-disposable)
other disposable rubber items like Foley’s catheter are to dip it in 1% sodium hypochlorite solution or bleach
be decontaminated, mutilated, and placed in the black solution kept in a plastic container in sister’s duty room
bag. Rubber cannot be recycled so it cannot be put in for at least half an hour.
the blue bag, and it cannot be incinerated, so it cannot Recyclable gloves will be sent for autoclaving and
be placed in the red or yellow bag. Mutilation is safer to disposable gloves will be mutilated by cutting with
do with scissors rather than blade to prevent injury to the scissors and will be kept in black bag to be carried away by
worker. Red rubber catheter is decontaminated, cleaned
Municipal Corporation of Delhi (MCD) truck for land
and sent for autoclave. In the minor operation theater
filling.
(OT), the Kelly’s pad should be cleaned with hypochlorite
Used needles and syringes, (both glass and plastic)
solution after every procedure.
should be dipped in 1% sodium hypochlorite solution.
The plastic apron can be decontaminated, the linen—
cleaned and reused or discarded after mutilation into the Leave the syringes and needles after drawing out from
black bag. The used cap and mask are discarded in the 10% sodium hypochlorite solution in the duty room of
black bag. the ward for at least 30 minutes. After that contaminated
glass syringes are sent for autoclaving and plastic
syringes are sent for shredding.
KEY POINTS TO HIGHLIGHT Dispose off human anatomical waste, blood and tissue
Always take appropriate precautions for self-protection fluid soaked cotton swabs, gauze and dressing in red or
Whenever discarding an object, pause, think and cat yellow bags provided in the dressing trolley. These bags
egorize the kind of waste and discard it into appropriate will be sent for incineration as final disposal.
container. Blood or body fluid soaked linen must be kept separately
Segregation of waste is the responsibility of the person from unspoiled linen. Soiled linen bed sheets, etc.
generating it (e.g. doctor who is taking blood sample is should be kept in 1% sodium hypochlorite solution kept
responsible for the waste generated viz. swabs, syringe, in a plastic bucket for 30 minutes before it is sent to the
needle and gloves). laundry.
Yellow or red bags are for infectious biological non- Use color-coded bags for different types of wastes.
sharp solid waste. Items placed in this bag should not
Black polythene garbage bags will be used for non-
be decontaminated [rubber and polyvinyl chloride
infectious waste like paper, left out food, peel of fruits,
(PVC) containing plastic should not been thrown into
vegetables, unsoiled gauze, bandages, etc.
the red and yellow bag]. Rubber, PVC and chlorine emit
toxic fumes when incinerated.
The blue bag is for plastic waste which goes for shredding
Dont’s
The black bag is for non-infections household wastes Never throw used cotton swabs on the patient’s bed or
like paper, left-over food and discarded disposable the floor.
rubber items after they have been rendered safe in Never pass sharps, like needles or blades from one
the sodium hypochlorite solution, unsoiled dressing person to another person.

(gauze, cotton), etc. Never recap, bend or break disposable needles. Needles
can be destroyed by needle destroyer.

Do’s For guiding sutures never use fingers. Always use tissue
Any person who is generating biomedical waste is forceps.

responsible for safe disposal of that waste. Do not mix hazardous and non-hazardous waste.
Segregation of different wastes is required to be Never mix soiled and unsoiled linen.
carried out at the site of generation (ward, OPD etc.) If A zero waste idea is to be the final goal.
segregation is done by medical, paramedical and staff If the waste management is proper, there will be less
involved in patient healthcare then 90% of the manage hospital acquired infections to the patient, less exposure
ment problem is solved. Segregation is a key factor in to hazard for hospital employees and protection of
the management of biomedical waste. community and environment.
Handling of sharps: Use a kidney tray to keep sharps

UNIVERSAL (WORK PLACE)
(blade, scissors and needle); the surgeon will pick up

PRECAUTIONS these things from there. Do not pass sharps by hand. It
These precautions are now called work place precautions. can cause cuts.
They are the precautions observed as a preventive Needles are not to be recapped after taking blood
measure against communicable diseases which have been or giving injections. After passing through a needle
standardized by the World Health Organization (WHO). destroyer put them in puncture proof container.
They are to be followed strictly in each healthcare setting Do not handle patients if you are having skin lesion on
irrespective of whether the patient is HIV/HbsAg positive your hands.
or not. This is in addition to the waste management and All injuries from sharps (blade, needles) are to be
stops spreading of infection. reported to the authorities in the hospital (e.g. casualty
These precautions, are to be taken while examining medical officer) for consideration of post-exposure
prophylaxis.
the patient, handling blood, body fluids (cerebrospinal
In case when accidental prick with a contaminated
fluid, pleural fluid, pericardial fluid) and all body tissues
needle takes place, the following steps to be followed:
containing visible blood.
• Step I: The wound should be encouraged to bleed
These precautions include:
• Step II: Clean with soap and water thoroughly
Handwashing with soap and water before and after
• Step III: Cover the cut part with waterproof dressing.
examining the patient, before putting on gloves, after
In case of splashes over mouth or eyes, with patients
removing gloves, etc.
blood or body fluid, e.g. rupture of membranes in normal
Gloves are to be worn during internal examination per
delivery or laparotomy or during postmortem: Rinse and
vaginal, per rectal, etc. drawing blood or body fluids.
splash thoroughly with plenty of running water.
Wash hands before wearing gloves and removing gloves
All healthcare workers should be protected against
after each examination. Gloves are also to be worn Hepatitis B and tetanus by active immunization.
while starting an intravenous line and for washing used
instruments, after operation.
Aprons and gowns are worn to protect the wearer from
PUNISHMENT
infection. The institutional head or the person who generates
Goggles are used to protect eyes from splashes of the waste, (e.g. doctor collecting blood) and does not
infected fluids (liquor amnii, blood, etc.) properly dispose, the cotton swabs (in yellow bag), needles
Masks are used to protect the patient from being and syringe in 10% bleach solution, etc. will be punished
infected. The nasal opening and mouth should be with an imprisonment of 5 years or a fine of one lac rupees
covered properly. or both.
1. Describe the procedures for decontamination.
2. Write a short note on universal precautions.
3. Describe the process of incineration.
Section 14
Pharmacotherapeutics in
Obstetrics
Section Outline
73. Clinical Pharmacology in Obstetrics
73 Clinical Pharmacology
Pikee Saxena, Sudha Salhan, Meenakshi Bhatt, Ipsita Ray, Ritu Sharma
in Obstetrics
INTRODUCTION So, iron supplementation is required in pregnancy (see

Chapter 37).
The importance of drugs in the field of obstetrics cannot
be over emphasized. The last few decades have shown Folic Acid
profound changes in the field of both obstetrics and Folic acid is given prophylactically in the periconcep-
pharmacology. We will try to highlight briefly the current tional period to avoid congenital anomalies like neural
therapies, possible adverse effects and practical problems tube defects, etc. It also prevent abortions and premature
faced by the clinicians in this field. deliveries during pregnancy. It is the drug of choice in
Pharmacokinetics of drugs is altered during pregnancy megaloblastic anemia.
due to variations in metabolism and excretion. The potential Daily administration of 5 mg of folic acid leads to
transfer of drugs across the placenta is crucial as these drugs reticulocytosis within one week which is a sign of bone
may harm the fetus. The insult to the fetus varies depending marrow response. It can be administered parenterally in
on the period of gestation (POG) of pregnancy and the cases of malabsorption syndrome. The intramuscular (IM)
teratogenic potential of the drug. Even the drugs administered vitamin B12, 100 mg can be given daily or on alternate day in
during labor, may affect the newborn. Herbal or homeopathic the second trimester of pregnancy.
medicines taken during pregnancy might also be harmful to
the fetus. So, during pregnancy no drugs should be prescribed Calcium
until their safety and benefits are well established. Avoid
Calcium is required to keep bones and teeth healthy in
drugs with questionable efficacy. Also, avoid drug intake in
mother as well as in fetus. Calcium supplementation of
postovulatory period of unprotected cycle. The dose, duration
1500–2000 mg daily in the second trimester onwards has
and number of drugs should be kept to a minimum.
shown association with the decreased incidence of pre-
However, pharmacological treatment should not be
eclampsia, preterm deliveries, low birthweight babies and
withheld during pregnancy in cases where the disease
cesarean section.
process per se might seriously affect the maternal or fetal
The plasma concentration of calcium is maintained
condition, if the treatment is not started in time.
by parathyroid hormone, calcitonin and vitamin D. The
physiological effects are exerted by ionic calcium.
NUTRITIONAL SUPPLEMENTS IN
PREGNANCY UTERINE STIMULANTS OR OXYTOCICS
Iron Oxytocics are drugs that increase the uterine contractions.
To meet the fetal-maternal requirements, the demand of These are as follows:
iron doubles up in pregnancy. Diet contains iron either Posterior pituitary hormone (oxytocin)
in heme or inorganic form. Heme iron is absorbed more Ergot alkaloids (ergometrine, ergonovine, methyl-
easily (about 33%) than the inorganic form (about 5%) ergonovine)
whose absorption is hindered by several other dietary Prostaglandins [PGE2, PGF2α, 15-methyl-PGF2α, miso
factors. Diet alone cannot meet the increased demand. prostol (PGE1 analog)].
Oxytocin
Oxytocin is a cyclic nonapeptide hormone synthesized
in the paraventricular and supraoptic nuclei of the
hypothalamus and secreted by the posterior pituitary in
response to cervical and vaginal stimulation, suckling,
dehydration, hypovolemia, hemorrhage and pain.
Physiological Roles of Oxytocin

On uterus: Oxytocin increases both the force and frequency
of uterine contractions. Estrogen sensitizes the uterus to
the effect of oxytocin, with uterine sensitivity increasing
progressively in pregnancy.
On breast: It stimulates myoepithelial cells of the breast
to cause milk ejection. Oxytocin responsible for the milk
ejection in response to suckling or mechanical manipulation
Fig. 73.1: Infusion pump
of the breast by contractions of periacinar muscles (let-
down reflex).
Cardiovascular effect: Bolus intravenous (IV) injection of Adverse Effects
oxytocin causes the uterus to contract tetanically. It causes Hypertonic contractions.
severe hypotension, there is a transient marked fall of Water intoxication may occur if large amounts of
arterial blood pressure that is followed by increase in the hypotonic fluids are infused along with oxytocin. This
cardiac output. Therefore, a bolus IV injection of oxytocin effect is enhanced by the vasopressin-like effect of
is contraindicated. oxytocin.
Hypotension and reflex tachycardia can occur at higher
Pharmacokinetics doses due to vasodilatation.
Oxytocin is inactive orally as it is a protein in nature and so Desamino-oxytocin: It is a buccal formulation of oxytocin,
is administered by IM or IV routes or as buccal tablets or as which can be used for all the indications of parenteral
intranasal spray. Due to rapid metabolism of oxytocin in the oxytocin.
liver and kidney by oxytocinase the half-life of IV oxytocin is
approximately 3 minutes and the duration of action is short. Ergot Derivatives: Ergonovine and
Methylergonovine
Uses
Ergot alkaloids have positive effect on uterine contractions
Induction of labor: May be needed in cases of prema-
with respect to their frequency, duration and intensity.
ture rupture of membranes (PROM), intrauterine growth
At higher doses, they can increase the resting tone of the
restriction (IUGR), placental insufficiency, isoimmuniza-
myometrium and even cause sustained contractions. The
tion, etc.
gravid uterus is more sensitive especially at term and in
Augmentation of labor: Oxytocin may be used to aug-
early puerperium. Thus, ergonovine and methylergonovine
ment uterine contractions when they are not progressing
are used to prevent and treat postpartum hemorrhage
satisfactorily during dysfunctional labor. It can be given
(PPH). They are also used to ensure normal involution
IV in the bottle or by an infusion pump (Fig. 73.1).
after delivery or abortion but routine use for this indication
Management of 3rd stage of labor and puerperium:
is not justified.
Oxytocin is used in active management of third stage of
labor.
Contraindications
Breast engorgement: Buccal oxytocin or intranasal
spray may be used before suckling if the milk ejection Labor, labor induction, hypertensive disorders, sepsis,
reflex is inefficient. severe liver, heart and renal diseases.
Oxytocin challenge test: To detect uteroplacental
insufficiency and assess the fetal wellbeing in high-risk
Side Effects
pregnancies (maternal diabetes mellitus and maternal Gastrointestinal (GI) symptoms (nausea, vomiting), ves-
hypertension). tibular symptoms (tinnitus, dizziness, headache), breath-
Clinical Pharmacology in Obstetrics 677
lessness, palpitations, sudden onset chest pain, stroke, Absolute Contraindications

myocardial infarction and pulmonary edema. Unexplained vaginal bleeding, hypersensitivity and all
contraindication of induction of labor.
Prostaglandins
Prostaglandins have been accorded a number of roles in Side Effects
conception, labor and in the pathogenesis of dysmenorrhea.
GI symptoms, shivering, fever, uterine rupture, sudden
They find use in obstetrics and gynecology as they have
onset chest pain, myocardial infarction.
been found to increase the tone and amplitude of uterine
contractions throughout pregnancy. Prostaglandins also
Misoprostol
soften the cervix and make it more compliant. They are used
for: It is a synthetic 15-deoxy-16-hydroxy-16-methyl analog
of naturally occurring PGE1. Originally, it was used
Uses for prevention and treatment of nonsteroidal anti-
Abortion inflammatory drugs (NSAIDs) induced peptic ulcers. Now,
First trimester abortions it is being used in obstetrics and gynecology for various
Misoprostol (PGE1 analog) in combination with
indications like ripening of cervix, induction of labor,
mifepristone (an antiprogesterone agent) is highly medical termination of pregnancy (MTP), PPH, before
effective in the termination of early pregnancy by drugs. endometrial biopsy and hysteroscopy.
Intravaginal PGE2 pessary, inserted 3 hours before
attempting dilatation, can be used to minimize the Advantages

trauma to the cervix in surgical termination. Vaginal administration of misoprostol acts as depot prepa-
For mid-term abortions, missed abortion and molar ration with more and long lasting efficacy as compared to
gestation: Vaginal suppository containing PGE2, oral oral administration. Cost effectiveness, stability at room
and sublingual or vaginal misoprostol and injection of temperature, easy administration and relatively few sys-
15-methyl-PGF2α are used for the induction of therapeutic temic side effects are the other advantages.
mid-trimester abortion. First trimester medical abortion: Misoprostol in
combination with mifepristone (RU 486) is approved

Induction/Augmentation of Labor for medical abortion upto 49 days.
PGE2 and misoprostol can be used for induction/augmen- Preoperative cervical ripening: It used before endo
tation of labor. However, there are wide variations in metrial biopsy, hysteroscopy and surgical abortion.
responses to these agents. Labor induction in third trimester: For cervical ripening
and labor induction, 25 mg of misoprostol is given orally

Cervical Ripening or vaginally, every 4–6 hours though not approved for
PGE2 or dinoprostone, applied as cervical gel, can be used this use till now by food and drug administration (FDA).
for cervical ripening. Postpartum hemorrhage: For prophylactic use, 600 mg
orally can be given but for treating PPH 1000 µg rectally

Postpartum Hemorrhage or 600 mg sublingually is the recommended dose.
15-methyl-PGF2α (carboprost) injected IM or intrarectal/
sublingual/oral misoprostol may be used in patients UTERINE RELAXANTS (TOCOLYTICS)
resistant to oxytocin and ergot alkaloids.
b2 agonists—ritodrine, salbutamol, terbutaline, isoxsu-
Dinoprostone prine
This is a form of prostaglandin, which provides 0.5 mg of PGE2 Magnesium sulfate
for application in the cervical canal as gel. This instillation can Calcium channel blockers—nifedipine
result in hyperstimulation (hypertonus) of the uterus. Others—prostaglandin synthesis inhibitors, ethyl alcohol,
progesterone injections, dermal nitroglycerine patch.

Relative Contraindications Use: To delay or postpone premature labor for cortisone
Obstructive lung disease, glaucoma, local vaginal and therapy to be effective and gaining time for in utero transfer
cervical infection. of the preterm fetus to a well-equipped facility.
Beta-agonists Flowchart 73.1: Mode of action MgSO4 as tocolytic
Salbutamol, ritodrine and terbutaline are most commonly

used tocolytic agents.
These agents act as tocolytics by reducing intracellular
calcium concentration through extrusion. Isoxsuprine is a
widely used drug for the treatment of threatened abortion
but efficacy is doubtful.
Adverse Effects
These include maternal hypotension, tachycardia, hypo-
kalemia, arrhythmias, pulmonary edema, hyperglycemia,
hyperinsulinemia, anxiety, restlessness and headache.
The neonate may develop hypoglycemia and paralytic
ileus.
Ritodrine and Terbutaline

These can be used to delay the labor upto a maximum of
7 days. Among the two, only ritodrine is FDA approved.
Caution: They should be administered via controlled
infusion device in titrated doses until there is cessation of
contractions or pulse rate exceeds to 120. The maximum
dose for ritodrine is 350 µg/min. Once the contractions
cease, the dose is tapered gradually. Monitoring of
maternal pulse, BP, input and output, auscultation of lung
fields and serum electrolytes is strictly recommended as
their use is associated with fluid overload. Abbreviation: ATP—Adenosine triphosphate
Magnesium Salts Prostaglandin Synthesis Inhibitors

Aspirin, ibuprofen and indomethacin can delay labor before
Magnesium salts have been used as a tocolytic since 1969 it has started. However, they can lead to various maternal
and are considered quite safe. But it should not be use as and fetal side effects, most common being premature
tocolytics in very small birth fetuses as it may contribute to closure of ductus arteriosus.
cerebral palsy in the infant. So, these should not be used for this indication routinely
The mode of action of MgSO4 as tocolytic is given in (can be used for maximum 5–7 days). They are also used
Flowchart 73.1. for a limited time in polyhydramnios.
Nifedipine/Nicardipine Ethyl Alcohol

Ethyl alcohol was given by IV infusion as 10% solution. As
They inhibit the intracellular entry of calcium ions. These
it causes marked maternal and fetal side effects, it is not
should be given orally and never be given sublingually.
being used now. There is an inverse relationship between
With oral administration, they have long duration of action
frontal brain size and maternal alcohol consumption.
of about 6 hours.
17-alpha-hydroxyprogesterone caproate (Makena):
FDA approved 17-alpha-hydroxyprogesterone caproate
Oxytocin Inhibitors/Antagonists (Makena) injection to reduce the risk of preterm delivery
Atosiban is a nonapeptide oxytocin antagonist with few before 37 weeks. Progesterone supplementation for
GI side effects. It is given orally. Adverse effects include asymptomatic women with an incidentally identified very
muscle paralysis, cardiac arrhythmias, maternal and fetal short cervical length (< 15 mm) may be considered (ACOG
respiratory and central nervous system (CNS) depression. Committee Opinion 2008). Multiple gestations or other
risk factors for preterm birth are contraindications for its chemoreceptor trigger zone and is metabolized in kidneys.
use. It stimulates intestinal motility.
Dose: 250 mg (1 mL) IM in the buttocks once weekly Dose: 10 mg orally QID, 100 mg daily IV/IM every 6 hourly,
beginning between 16 and 21 weeks of pregnancy and (30 min before meals and at bedtime).
continued till 36 weeks.
Pyridoxine (Vitamin B6)
Dermal Nitroglycerine Patch Some obstetricians prefer to use pyridoxine.
Its use as a tocolytic which has been found to be effective Dose: 10–20 mg orally 6 hourly for 3 weeks or 10 mg IV
but due to the inadequate large randomized controlled 4 hourly.
studies it is not used routinely.
Thiamine (Vitamin B1)
Maternal Corticosteroid It is used in cases of confirmed thiamine deficiency
including Wernicke’s encephalopathy syndrome.
Betamethasone is administered as 2 doses of 12 mg given
Dose: 100 mg daily IV/IM for upto 2 weeks.
24 hours apart IM whereas dexamethasone is administered
6 mg hourly for 4 doses IM. Betamethasone has proved to
be better alternative. Ideally, the delivery if possible should
ASTHMA IN PREGNANCY
be planned between 24 hours and 7 days after the start of Medications
treatment. This dose is given only once. They increase the Patients with acute asthma are given inhaled short-
efficacy of surfactant and decrease the risk of neonatal acting beta-agonists. For long-term control inhaled
death, intraventricular hemorrhage (IVH) and necrotising corticosteroids alone or in combination with inhaled long-
enterocolitis. acting beta-agonists are prescribed daily.
Inhaled steroids: For asthma, beclomethasone 2–5 puffs
HYPEREMESIS GRAVIDARUM 6–12 hourly; for allergic rhinitis, 2 sprays in each nostril
12 hourly.
Antiemetics Oral steroids: Prednisone, 40 mg/day in single or divided
Promethazine doses for 1 week and the dose is then tapered off in another
week. Long-term therapy is associated with side effects;
This is an antidopaminergic antiemetic agent.
Dose: It is given by parentral route (IV or IM) in the dose of so, in prolonged therapy single morning dose is given on
25 mg and orally in the dose of 12.5 mg, 8 hourly. alternate days.
Cromolyn sodium: For asthma, 2 puffs 6 hourly; for
Prochlorperazine allergic rhinitis 2 sprays in each nostril 6–12 hourly.
This is an antidopaminergic antiemetic drug which also Inhaled beta-agonists: 2 puffs 4 hourly
depresses the reticular activating system. Theophylline: Target is to achieve a serum level of
Dose: 5–10 mg orally 6–8 hourly, not to exceed 40 mg/day; 8–12 mg/mL using sustained release oral preparations.
2.5–10 mg IV 8 hourly, maximum dose is 40 mg/day. Antihistamines: Chlorpheniramine 4 mg 6 hourly or
8–12 mg sustained release preparation 12 hourly.
Ondansetron Decongestants: Pseudoephedrine 60 mg 6 hourly or 120 mg
This is a central and peripheral selective 5-HT3-receptor sustained release preparation 12 hourly; for rhinosinusitis
antagonist metabolized by P450 mechanism in liver. use oxymetazoline intranasal spray or drops upto 5 days.
Dose: 2–4 mg IV 6–8 hourly. Cough medications: Guaifenesin given in the dose
of 2 teaspoons 6 hourly alone or in combination with
Droperidol dextromethorphan.
This neuroleptic agent blocks stimulation of dopamine at
chemoreceptor trigger zone.
HYPERPROLACTINEMIA IN
Dose: 1.25–2.5 mg IV/IM 3–4 hourly. PREGNANCY
Dopamine agonists like bromocriptine and cabergoline are
Metoclopramide effective in a majority of women. Bromocriptine use during
This drug is used when symptoms are not controlled pregnancy has been found to be safe for the developing
by other drugs. It blocks the dopamine receptors at the fetus till 4–6 weeks after conception. Also, preliminary
evidences by research studies done on cabergoline does Phenobarbital

not show increase in adverse fetal effects. Although its use has not been found to be associated with
the increased risk of congenital malformations, it is not a
Dose preferred drug.
Bromocriptine is started at 1.25 mg at bedtime for a week Dose: 60 mg 1–3 times a day.
after which its dose is gradually increased upto 5 mg 12 Patients on carbamazepine, valproic acid and phenytoin
hourly. can breastfeed their infants as the drug concentration
Cabergoline is started at 0.25 mg twice a week for 4 weeks. in breast milk is very small. However, breastfeeding is
The dose can be gradually increased in 0.5 mg increments to contraindicated if the mother is on phenobarbital.
reach the lowest effective dose. If there is no lactation or a
still born baby there is no/need for milk suppression as an ANTICOAGULANTS IN PREGNANCY
suckling is occuring,no milk formation will occur.
Though all anticoagulants are not without fetal risk, their
use in life-threatening conditions, has more benefits to the
ANTIEPILEPTICS IN PREGNANCY mother as compared to fetal harms.
Most of the first line antiepileptics are associated with
certain degree of fetal risk but the benefits to the mother Warfarin
outweigh the fetal risks. The dose of antiepileptic drugs Due to the fact that warfarin can cross the placenta, its use
may have to be increased with advancing POG especially in first trimester is associated with warfarin embryopathy
if other high-risk factors like hypertension, hyponatremia (< 10%) along with increased risk of spontaneous abortion,
and hypoalbuminemia are associated. prematurity and stillbirth. Its use is contraindicated in first
trimester.
Valproic Acid Maternal effects of warfarin sodium can be reversed by
Associated adverse fetal effects include neural tube defects giving fresh frozen plasma but the fetus requires 1–2 weeks
(2%) and limb deformities; however, the evidence for the after discontinuation to reverse anticoagulant effect. So,
latter is limited. It acts by prolonged inactivation of sodium a woman on warfarin therapy is switched over to heparin
channels and also by increasing the concentration of the during the first 12 weeks and after 36 weeks of gestation.
inhibitory substance gamma-aminobutyric acid (GABA).
Dose: 200 mg 3 times a day, which can be increased
Heparin
gradually to a maximum of 800 mg 8 hourly. Heparin is considered safe, as it does not cross the
placental barrier. High-risk women can be continued with
Carbamazepine heparin IV even after first trimester and transition to oral
During pregnancy, carbamezapine is considered to be anticoagulant warfarin can be done later.
The patient on heparin will have normal clotting, 4–6
the drug of choice for epilepsy although the risk of neural
hours after discontinuing the medication.
tube defect is about 1%. It acts by prolonged inactivation
of sodium channels, but the profile of action on neurons in
brain is different. ANTIHYPERTENSIVES IN PREGNANCY
Dose: 200–400 mg 3 times a day. The commonly used drugs can be classified as:
I. Sympatholytics
Phenytoin
Central sympatholytics Methyldopa, clonidine
This drug is thought to act by decreasing folate absorption.
Beta-adrenergic blockers Propranolol, metoprolol, atenolol
Folate replacement in a dose of 4 mg/day is recommended.
Alpha-adrenergic blockers Prazosin, phentolamine
Fetal hydantoin syndrome (craniofacial anomalies like
broad and flat nasal bridge, cleft lip and palate, epicanthic Alpha and beta-adrenergic Labetalol
blockers
folds, hypertelorism, wide mouth, congenital heart
II. Vasodilators
diseases, growth restriction, mental retardation and limb
defects) is seen in < 10% of infants. Arteriolar Hydralazine, diazoxide
Dose: 100 mg 12 hourly to a maximum of 400 mg/day. Contd…
Contd… Vasodilators
Arteriolar + venous Sodium nitroprusside Hydralazine
III. Diuretics It acts on the smooth muscles of arterial vasculature
Not used in pregnancy as Furosemide (for the latter leading to vasodilatation. Hydralazine increases cardiac
antihypertensives but are indication) output by vasodilatation. If administered orally, peak
used selectively in some action occurs by 3–4 hours. The action of hydralazine lasts
patients with pulmonary
edema or congestive heart for 6–12 hours. Its side effects include headache, anxiety,
failure. nausea, flushing, and epigastric pain, lupus like syndrome.
IV. Calcium channel Nifedipine, verapamil Dose: 40–200 mg twice a day.
blockers
Calcium Channel Blockers
Alpha Methyldopa These drugs act by decreasing peripheral resistance
Alpha methyldopa is the front line antihypertensive drug without compromising the cardiac output. These agents
in pregnancy as it has been found to be safe in pregnancy cause relaxation of vascular smooth muscles by preventing
over the past several year of use. It leads to dilatation of influx of calcium ions.
both arteries and veins, which increases IV volume. It also They also relax the uterus and can be used for tocolysis
maintains renal blood flow. After oral administration, less as their use does not lead to any major side effects to the
than one-third of the dose is absorbed. Its antihypertensive mother or the fetus.
effect develops over 4–6 hours and lasts for 12–24 hours. Nifedipine can also be used in cases of fulminating pre-
This drug crosses the placenta and is excreted at low eclampsia to obtain a quick reduction in blood pressure
concentration in human breast milk, but no neonatal levels, by the oral route. Sublingual administration should
side effect has been associated with its use. It acts on the be avoided as it may lead to unpredictable absorption
brainstem as an alpha-agonist to reduce sympathetic resulting in sudden decrease in uteroplacental circulation
outflow activity. and fetal compromise and a sudden fall in maternal blood
Side effects—are mild depression, sedation and postural pressure, which might compromise the maternal cerebral
hypotension. It might lead to a problem during cross circulation.
matching of blood as methyldopa treatment causes a Side effects—are mild in the form of flushes, headache, GI
positive direct Coombs test. It can cause intestinal ileus in upset, ischemic pain.
fetus. Dose: Nifedipine 30–60 mg once daily or 10 mg 2–3 times/
Dose: 250 mg BD or TDS, gradually increasing as required day verapamil 80 mg 4 times a day.
over a period of 2 days to a maximum of 2 gm/day.
Contraindications to alpha methyldopa are hepatic
ANTIHYPERTENSIVES IN ACUTE CRISIS
disorders, psychiatric ailments, congestive cardiac failure
(CCF), etc. Intavenous antihypertensives are required in case where
Alpha methyldopa should be stopped after delivery and systolic BP is > 160–180 mmHg or diastolic BP is > 110
one can give beta-blockers because it causes depression. mmHg as a prophylaxis against cerebral hemorrhage. Do
not decrease the BP rapidly as this can lead to dercrease in
Beta-blockers uteroplacental circulation resulting in fetal distress. Aim is
Beta-blockers acts upon both the heart and peripheral to keep the systolic BP between 120 and 140 mmHg and
vasculature in order to lower the blood pressure. These diastolic BP between 90 and 100 mmHg.
drugs compete with endogenous catecholamines for beta- Hydralazine and labetalol can be used for control of
adrenergic receptors. Their hypotensive response develops blood pressure, parenterally.
slowly, although their effect lasts for 24 hours with a single
daily dose. These drugs are contraindicated in patients Hydralazine
with bronchial asthma, renal insufficiency and diabetes. It is the drug of choice.
Dose: Labetalol: 400–800 mg/day in divided doses Dose: 10 mg IV over 2 minute given at 15–20 minutes
Oxprenalol: 80–160 mg/day in divided doses. interval till adequate response is obtained.
Labetalol Diazepam (Valium)

It is also a first line drug. Useful for treatment of seizures resistant to magnesium
Dose: Start with 10–20 mmHg IV over 2 min. If no response sulfate. It causes depression at all levels of CNS, possibly
is there in 10 min give 40 mg IV; if still no response in by increasing the activity of gamma aminobenzoic acid.
another 10 min, give 80 mg IV and repeat the dose every Dose: 10 mg at a rate of 1 mg/min.
10 min, if required. Maximum permissible dose is 300 mg.
VACCINES
Diuretics
Two doses of tetanus toxoid are given in the second
Diuretic use in pregnancy should be avoided. However, it trimester at least 4 weeks apart.
may be used with caution in cases of pregnancy induced Rabies tissue culture vaccine is safe in pregnancy.
hypertension with massive edema or pulmonary edema in Rubella vaccine, which is a live virus vaccine which can
cases of severe anemia with heart failure. cause infection of both the placenta and the developing
Angiotensin Converting Enzyme Inhibitor fetus. Thus it is contraindicated in pregnancy. Infact, a
woman of child-bearing age who receives this vaccine
These agents are strictly contraindicated in pregnancy as should avoid pregnancy for one month.
they might cause renal failure or teratogenesis in the fetus. Live virus vaccines, e.g. measles, mumps, polio,
chickenpox and yellow fever are given to a pregnant patient
DRUGS TO TERMINATE SEIZURES only if she is at a substantial risk of becoming infected with
one of these organisms.
Magnesium Sulfate
Magnesium sulfate is now the drug of choice for ANTITHYROID DRUGS
prophylaxis and treatment of eclampsia with lower risk
Radioactive iodine is not given to pregnant women to treat
of recurrence and perinatal mortality and morbidity. The
hyperthyroidism as it can cross the placenta and destroy
drug does not increase troponin 1 in umbilical cord which
the fetal thyroid gland, if exposure occurs after 12 weeks
is a marker for fetal myocardial damage indicating that it
of pregnancy. Before this, the fetal thyroid is incapable of
does not have a toxic effect on fetal heart. Usually, seizures
concentrating thyroxine. Antithyroid drugs, propylthiouracil
terminate with loading dose of magnesium sulfate only; if
(PTU) and methimazole, can cross the placenta leading
they recur, benzodiazepines are the drug of choice.
to goitre in the fetus. The hyperthyroidism in the mother
Magnesium ions block neuromuscular transmission
should, therefore, be slightly under corrected.
by blocking the release of acetylcholine from the nerve
endings. MgSO4 may also have some central action. It
Drugs for Toxoplasmosis
relaxes smooth muscles by competing with calcium ions.
It can be given by the IV/IM route for seizure prophylaxis Spiramycin is non-teratogenic and hence, prescribed.
in severe pre-eclampsia. MgSO4 may cause hyporeflexia, A combination of pyrimethamine and sulfadiazine has
respiratory depression and bradycardia. Its antidote is better effects but is teratogenic and hence, given only after
calcium gluconate 10% solution which can be given as 14 weeks of pregnancy (if required).
10–20 mL IV as an antidote for clinically significant hyper-
magnesemia. ANTIANXIETY DRUGS
Phenytoin No proof of teratogenicity of benzodiazepines forth-
coming because alcohol and its substance abuse often
Phenytoin is an antiepileptic drug, used to control several
accompany their use. However, the diazepam, midazolam
types of seizure.
or lorazepam use in the perinatal period can cause
Dose: 20 mg/kg at a maximum rate of 50 mg/min IV. One
hypotonia, hypothermia and respiratory depression.
must remember not to infuse it in dextrose containing
fluids as it precipitates in them.
ANTIDEPRESSANTS
Lytic Cocktail Therapy Fluoxetine and tricyclic antidepressants do not cause fetal
This used to be given in eclampsia. malformations.
LITHIUM TABLE 73.1: Radiation to ovary with different radiologic procedures

Procedure Exposure in rads
Earlier reports stating that the use of lithium causes X-ray chest 8
Ebstein’s anomaly have been refuted by recent studies.
Cholecystography 300
Still, it is better avoided in pregnancy.
Intravenous pyelography (IVP) 407
Barium enema 805
ANTIBIOTICS Pelvic X-ray 41
Antibacterial penicillins, cephalosporins, aztreonam, Abdomen X-ray 289
imipenem, erythromycin, chloramphenicol, quinolones Lumbar X-ray 275
all have not been observed to cause congenital anomalies.
Penicillins are the safest of these. Antitubercular drugs—
rifampicin, isoniazid and ethambutol are also safe. ANTIHISTAMINES
Nitrofurantoin is used to treat acute urinary tract infec Chlorpheniramine and astemizole do not have teratogenic
tion (UTI) and for preventing recurrent UTI in pregnancy potential.
but it is actively transported into human milk, (5 times
higher concentration than mother and hence, should not HORMONES
be prescribed to lactating mothers and infants under the
age of 1 month). Oral contraceptive pills (OCPs) do not cause fetal genital
malformations even after the first trimester exposure.
ANTIPARASITIC Diethylstilbestrol (DES)
Chloroquine, mefloquine, pyrimethamine, metro- Exposure in utero increases the risk of vaginal adenocarci-
nidazole, spiramycin and mebendazole have been proven noma, ectropion, adenosis, hypoplastic T-shaped uterine
safe in several studies. Quinine and quinidine should be cavity, etc.
used in patients with chloroquine-resistant malaria, and
in severely ill-women. ISOTRETINOIN
This derivative of retinoic acid is used for the treatment of
ANTIVIRAL cystic acne and is a potent human teratogen with a high
In first trimester, zidovudine exposure does not increase rate of fetal loss and malformation, if exposure occurs in
the incidence of birth defects. the first trimester.
ANTICANCER DRUGS TERATOGEN

Chemotherapy taken in the childhood (of the pregnant (Greek, teras=monster) A substance that causes fetal
lady) does not appear to effect this pregnancy. But prior malformations. The main manifestations are malformations,
pelvic irradiation (before this pregnancy) has a small, but growth retardation, functional disorders and death. There
significant, adverse effect on birthweight. If, anticancer could be a miscarriage in extreme cases. The mechanism
drugs are started in the present pregnancy after the first to cause teratogenesis are mutations, chromosomal
trimester the adverse effect are low, if any. disruptions, alteration in mitosis, nucleic acid integrity or
function, osmolar balances, energy sources and membrane
character.
X-RAY THERAPY
The dilemma of prescribing in pregnancy is a cause of
The effect of X-ray therapy depends on the dosage and the concern to the obstetricians. Very few drugs are considered
pelvic field exposed. No serious risk to the fetus occurs upto safe during pregnancy. This is because it is not possible to
an absorbed dose of 10 rads. Larger doses, to the pregnant conduct a trial of any drug in pregnant and breastfeeding
woman cause microcephaly and mental retardation in the women.
fetus. Shielding of abdomen may help in chest X-ray, etc. Factors that influence teratogenicity include:
IUGR is seen in some cases (Table 73.1). Genotype of mother and fetus
Embryonic stage at the time of exposure—during 0–17 FDA Categories of Drugs as Teratogen
days post-fertilization leads to death of embryo and Category A No fetal risk disclosed by well controlled
abortion; exposure during 18–56 days (organogenesis) human studies
leads to teratogenesis and during 56 days to term, Category B No fetal risk disclosed by animal studies; or
affects development some risk suggested which is not confirmed
Dose and duration of exposure by controlled human studies; or inadequate
Nature of the agent human studies
Mechanism by which it causes a defect Category C Adverse fetal effects disclosed by animal
Simultaneous exposure to other drugs or environmental studies; inadequate controlled studies on
agents that may affect potential abnormalities human beings
Maternal and fetal metabolism of the drug Category D Some fetal risks revealed but benefits may
Extent to which the drug crosses the placenta. outweigh risks (e.g. life-threatening illness,
The drugs according to FDA are divided into five no safer effective drug)
categories depending on their teratogenic potential and as Category X Fetal abnormalities revealed by animal and
per law the drug label must give the relevant information human studies; risks outweigh benefits.
regarding the teratogenic potential of the drug. Contraindicated in pregnancy (Table 73.2)
TABLE: 73.2: Drugs with proven teratogenic and adverse effect on fetus
Agents Effects
Thalidomide Multiple especially limb defects
Angiotensin-converting-enzyme (ACE ) Renal damage in the fetus especially during 2nd and 3rd trimester
inhibitors
Cocaine Contraindicated in all trimesters. It can lead to various congenital anomalies
Carbamazepine Neural tube defects if given in first trimester
Phenytoin Cleft lip and palate cardiovascular abnormalities, skeletal abnormalities
Valproic acid Neural tube defect
Tetracycline Bone abnormalities
Aminoglycosides Deafness
Quinine Congenital deafness, optic nerve hypoplasia
Glucocorticoids Cleft lip
Alcohol Cleft lip and palate cardiovascular abnormalities, skeletal abnormalities
Cytotoxic drugs Multiple congenital abnormalities
Iodine Congenital goitre (hypothyroidism)
Pseudoephedrine Gastroschisis
Isotretinoin Hydrocephalus, small ears, facial bones abnormalities, aplasia of thymus, cardiovascular
abnormalities
Warfarin Central nervous system abnormalities, chondrodysplasia, hypoplasia of nasal bones
Lithium Cardiovascular abnormalities
Irridation Thyroid carcinoma, leukemia
Diethylstilbestrol (DES) Vaginal carcinoma and vaginal adenosis T-shaped uterus in young women
Opioids Neonatal drug dependence
Benzodiazepines Neonatal drug dependence
Barbiturates Neonatal drug dependence
Chlorpropamide Prolonged neonatal hypoglycemia
Nonsteroidal anti-inflammatory drugs Premature closure of ductus arteriosus
(NSAIDs)
Antithyroid drugs-like propylthiouracil Congenital goiter
(PTU)
gastric emptying time is increased, especially during

THALIDOMIDE
labor.
Thalidomide was introduced in 1957 as a nontoxic sedative Total body water increased by 8 liters, so drug distri
and tranquilizer, but in 1961 it was implicated as a cause bution is affected.
of an epidemic of congenital limb defects. Following this, Overall absorption of drug is increased because of
the drug was withdrawn. The mechanism of embryopathy reduced intestinal motility.
is not understood. However, it was discovered to be Plasma binding of drugs is decreased—plasma albumin
effective in the treatment of erythema nodosum leprosum is reduced in pregnancy. Renal plasma flow and
(ENL). Thalidomide has been found useful in aphthous glomerular filteration is increased hence increased in
stomatitis and Behçet’s disease. In addition, it possesses the clearance of water-soluble drugs.
antiangiogenic properties due to which it is finding use in Liver enzymes are increased in pregnancy, so there is
patients of advanced multiple myeloma. In 1998, the FDA increased metabolism of drugs which are metabolized
granted marketing approval to thalidomide. by liver enzymes.
Increased fat stores in pregnancy leads to larger
GENERAL ASPECTS OF reservoir for lipid-soluble drugs.
Increased half-life of lipid-soluble drugs.
PHARMACOLOGY IN PREGNANCY
The fetus has more sensitivity for carcinogenic drugs as

Effect of orally administered drug is very slow because compared to adults.
1. What is the importance of folic acid in pregnancy?
2. What are the commonly used drugs in antihypertensives in pregnancy?
3. Write doses of each drugs:
i. Hydralazine
ii. Carbamazepine
i. A drug ending in suffix (azole) is considered as _____________.
ii. Potassium sparing diuretics have the primary effect upon the _____________ found in the kidney.
Section 15
Practical in Obstetrics
Section Outline
74. Obstetrics Instruments
75. Obstetrics Forceps and Ventouse
76. Specimens in Obstetrics
77. Contraception
74
Obstetrics Instruments
OBSTETRICS FORCEPS
(SEE CHAPTER 75)
Obstetrics forceps are stainless steel forceps having two
independent branches, with each branch comprising of a
blade, a handle and an intervening shank. Both the branches
can be locked together. The lock is essential for holding the
two branches together, otherwise it may cause damage.
English lock, has a notch on each branch and on locking one
notch fits into opposite branch notch. French lock has either
a detachable or semi-fixed screw about which the opposite
branch can rotate. German lock is mixture of both an English
and French lock with an additional lock across the handles.
The blade has a tip, body and base which may be
fenestrated or pseudo-fenestrated. The blade has two
curves; the cephalic curve for accommodating fetal head
and pelvic curve for maternal pelvis adjustment. These
curves are perpendicular to each other. The length of the
shank varies depending on the length of forceps, more
the length, more the leverage, more the force exerted and
Fig. 74.1: Wrigley’s forceps
more the chances of trauma.
There are various types of obstetrics forceps like the
Wrigley’s forceps, Simpson’s long forceps, Simpson’s short Shanks are 6.25 cm long, parallel, diverging rapidly from the
forceps, Haig Ferguson’s forceps, etc. English lock, so that, the distension of maternal perineum
is marked. Blades are relatively longer, measuring 12.5 cm.
Wrigley’s Forceps (Fig. 74.1)
It is a light weight, 27.3 cm long forceps having an English Simpson’s Short Forceps (Fig. 74.3)
lock. It is used for low and outlet forceps delivery and has It is as long as Wrigley’s forceps, (27.5 cm) having a short
more pronounced cephalic curve with a normal pelvic shank, small handles and with identical blades. There is
curve. It can also be used during cesarean section (CS) for no pelvic curve present. Like Wrigley’s forceps, Simpson’s
extraction of head. short forceps also has an English lock. Usage is also similar
to Wrigley’s forceps.
Simpson’s Long Forceps (Fig. 74.2)
It is 35 cm long and the maximum distance between Haig Ferguson’s Forceps (Fig. 74.4)
blades is 8.5 cm. It has a shallow cephalic curve, with 11.25 It is a forcep, with traction rod. Traction handle is hooked
cm radius while the radius of the pelvic curve is 17.5 cm. over the shanks. The perforations in the blades were
Fig. 74.2: Simpson’s long forceps Fig. 74.3: Simpson’s short forceps
Fig. 74.4: Haig Ferguson’s forceps Fig. 74.5: KN Das’ forceps
originally intended for the accommodation of long tapes, Kielland’s Forceps (Fig. 74.6)
but are not used now. This is a modified axis traction forcep.
Pelvic curve is almost obliterated, enabling a correct
Joints in the handle and traction rod allows mobility in
cephalic grip. It is useful in delivering arrest of head in
both horizontal and vertical planes.
transverse diameter. The lock is of sliding nature which
KN Das’ Forceps (Fig. 74.5) allows a better adjustment of the blades, if the head
Kedarnath Das of Calcutta designed this forceps according is asynclitic. During traction, the shanks are made to
to Indian women pelvic measurement. It is of axis traction depress the perineum for better axis traction. It is used in
rod variety. It is available without traction rod also. Milne deep transverse arrest for rotating the head and then for
Murray forceps has great similarities. extraction of head.
Obstetrics Instruments 691
Fig. 74.6: Kielland’s forceps Fig. 74.7: Piper’s forceps
Total length is 40 cm, handles, shanks and blades are

12,13 and 15 cm respectively. Blades are 4 cm wide slightly
thicker due to beveled edges for better grip on fetal head.
Its application needs great expertise.
Piper’s Forceps (Fig. 74.7)

It is a light weight forceps used for the delivery of after-
coming head in breech presentation. It is the longest
forcep measuring 44.5 cm, with 12 cm long hollow handle
and English lock blades, which are fenestrated with a length
of 17.5 cm and 5 cm wide. It has a slight pelvic curve, while
its perineal curve makes handle at lower level than the
blades to facilitate delivery of head in breech presentation.
OTHER INSTRUMENTS USED IN

OBSTETRICS PRACTICE
Fig. 74.8: Sponge holding forceps
Sponge Holding Forceps (Fig. 74.8)
It is a long instrument made up of stainless steel used to
catch the anterior up of the cervix in minor procedures (2, 5). They can be either straight or curved. Kocher’s
during early pregnancy for example, evacuation of uterus forceps has a tooth at its tip, for a better grip on tissues, it is
in incomplete abortion, encirclage operation in cervical used in doing artificial rupture of membranes for induction
incompetence (Shirodhkar, McDonald). It is also used in of labor. Artery forceps are used to catch bleeding blood
inspecting cervix for any tear after delivery. It is routinely vessels.
used for holding swab, for cleaning local area. It also has a
lock. In the absence of Green Armytage forceps, it is used Abdominal Retractor
to catch cut uterine ends in CS.
Deaver’s Retractor (Fig. 74.10)
Artery Forceps (Fig. 74.9) It is used during CS for retracting bladder. It is available in
There are different varieties of artery forceps like, Mosquito three sizes: small, medium and large. It can also be used in
(3, 4), Spencer Wells (1, 6) and Kocher’s artery forceps laparotomy and other gynecological surgeries.
Fig. 74.9: Artery forceps: Mosquito (3, 4); Spencer Wells (1, 6); Fig. 74.10: Deaver’s retractor
Kocher’s (2, 5)
Fig. 74.11: Balfour abdominal retractor Fig. 74.12: Green Armytage clamp
Balfour Abdominal Retractor (Fig. 74.11) Green Armytage Uterine Clamp (Fig. 74.12)
It is a self-retaining abdominal retractor. It has two side It is a clamp with wide ends, which have transverse ridges
blades, which are adjustable on a rod. There is a central on inner side. It is used for controlling hemorrhage from
blade for retracting bladder, which can also be screwed on sinuses on the uterine incision during CS. It is atraumatic.
to the rod connecting the two lateral blades. The two sided Episiotomy Cutting Scissors (Fig. 74.13)
blades, retract abdominal wall. It gives good exposure of It has a suitable curvature for cutting episiotomy. It is
the abdominal cavity. angled on one side and one blade is sharply pointed than
Fig. 74.13: Episiotomy scissors Fig. 74.14: Umbilical cord cutting scissors
the other. Thin blade is kept outside on the vulva and the
thick blade goes inside.
Umbilical Cord Cutting Scissors (Fig. 74.14)

It is sturdy scissor for cutting umbilical cord. It is 10.5 cm
long. It has long and curved blades for a better grip on
umbilical cord. Normal scissors can also be used for cutting
umbilical cord, but the cord may slip. Surgical blade can
also be used for cutting umbilical cord.
Vacuum Extractor (Figs 74.15 to 74.17)

(see Chapter 75)
It is used for extraction of fetal head. It consists of a suction
cup (Figs 74.16A to D) (which may be made up of silastic
or metals like stainless steel or brass) and the suction
machine (Figs 74.15 to 74.17).
Cups are available in 3 sizes, with diameter of 30, 50 Fig. 74.15: Vacuum extractor (manual)
and 60 mm respectively. Metallic cup has a small knob
to indicate occiput of fetus. There is a metal plate inside electric suction (Fig. 74.17). Pressure builds up slowly from
the cup, with a metal chain fitted to the plate. The chain 0.1 kg/cm2 to 0.8 kg/cm2 in 8–10 minutes. It can be raised
passes out through a short piece of metal tubing, fitted on rapidly also. This pressure is corresponding to 688 mmHg.
the back surface of the cup. This chain then passes through Although it can be applied at 8 cm dilatation of cervix,
a piece of rubber tubing and terminates in the handle. The yet it is recommended that it should be applied only on fully
cup is 20 mm deep with its open end fitting on the fetal dilated cervix. Traction on undilated cervix may predispose
head, the other end being connected to the tube. Silastic
to prolapse uterus.
cups are very pliable.
Traction Handle Advantages of Ventouse Over Forceps

It is fitted at the distal end of the rubber tube, attached to Lesser traction is required
the suction cup by means of a lock pin. The other end of It can be used in unrotated malrotated head
traction handle is either connected to manual suction or It can be applied even through incompletely dilated cervix.
A B
C D
Figs 74.16A to D: A and B. Metal cup; C and D. Silastic Cup
A B
Figs 74.17A and B: A. Electric vacuum extractor; B. Manual vacuum extractor

Advantages of Forceps Over Ventouse

It can quickly expedite delivery in cases of fetal distress
Safer in premature babies
It can be applied in mentoanterior position after coming
head of the fetus.
Causes of Failure
Improper selection of case—cephalopelvic dispropor-
tion (CPD), thick cervix
Instrumental defect—failure to develop required Fig. 74.19: Cephalotribe
pressure, due to leakage from the tubes
Faulty technique—wrong size of the cup, pulling too vault or the base of the skull, it can be used for extraction
hard or too soft, pulling in wrong direction and trapping of the head by traction.
of vagina in or cervix the cup.
Cephalotribe (Fig. 74.19) (German word:
Complications kephale, the head; tribo, to bruise)
Injury to the fetal scalp Forcep like instrument, with a screw handle, used to crush
Intracranial hemorrhage the head of a dead fetus. This instrument has three strong
Cervical/vaginal lacerations or tears blades. One central and two laterals marked 1 and 2. The
central blade is serrated on one side and has a screw shaped
tip. It is passed through the perforation hole in the skull and
INSTRUMENTS FOR DESTRUCTIVE screwed into the base of the skull. Blade marked 1, is passed
OBSTETRICS OPERATION over the face fixed in position by using the butterfly nut. Thus,
These instruments are designed to facilitate delivery of a crushing anterior part of the head. Blades marked 2 are then
dead or grossly abnormal fetus, (incompetent to survive) passed over the occiput, which is crushed in a similar way.
Both the blades are fixed with latch to the central part. After
by crushing or pulling. In present era, these destructive
crushing, the head is extracted, like forceps.
instruments have a limited role to play and are of antique
value. The common ones are cranioclast, cephalotribe, Indication
hook and perforator etc.
Dead fetus with obstructed labor in:
• Vertex presentation with contracted pelvis
Cranioclast (Fig. 74.18) (German word: kranion,
• Persistent brow
skull; klao, to break in pieces) • Impacted mentoposterior
A sturdy forcep used for crushing and extracting the fetal • Deep transverse arrest
head after perforation. • Arrested after-coming head in breech
It consists of two blades, i.e. concave–convex. Convex Hydrocephalus.
blade, is pushed in through the opening in the skull and
the concave blade is applied on the outside, preferably over Crochet (Fig. 74.20) (French word: croche, hook)
face. Both the blades face in the same direction. The head A hooked instrument, used for removing a dead fetus.
is firmly grasped and partially crushed. After crushing the It is passed into the cranial cavity after the perforation.
Fig. 74.18: Cranioclast Fig. 74.20: Crochet

is withdrawn slightly, turned through a right angle,

pushed in up to the shoulder again and reopened. It
creates a cruciate wound. The instrument is pushed well
inside the skull—the brain and medulla are destroyed by
stirring them up. The contents are washed out by curette
or a rubber catheter.
Blond-Heidler Decapitation Saw (Fig. 74.22)

It is used to decapitate a dead fetus, mostly in obstructed
Fig. 74.21: Perforator
labor.
Debdas Cranial Perforator

Traction is applied after hooking it over the orbit or the
All these instruments are decontaminated by placing in
mandible. It is used for:
bleech solution before washing and autoclaving.
Applying groin traction in breech with extended legs in
a dead fetus Pinard’s Fetoscope (Figs 74.23A and B)

Extracting the decapitated head
It is a one piece monaural instrument used to hear fetal
Extracting a perforated after-coming head in a dead
heart sound.
fetus
Extracting a hydrocephalus head. Doptone (Figs 74.24A and B)
It helps in detection of fetal heart sounds. Doptone is
Perforator (Fig. 74.21) a hand-held, battery operated device. It works on the
It is an instrument for reducing the size of the dead is fetal principle of ultrasound. When we are not able to hear fetal
skull by perforating cranium to make its extraction easy heart sound by stethoscope or fetoscope, doptone is very
in a dead fetus. It has two blades, which have a triangular useful.
sharp pointed end with cutting sides 2.5 cm long. There is
shoulder at the base of the tip to prevent it from slipping Cardiotocograph (Fig. 74.25)
out of the fetal head after craniotomy. When the handles Cardiotocograph makes a record of fetal heart rate in relation
are pressed together the cutting edges of the tip are forced to fetal movements (nonstress) and uterine contractions
apart. Under anesthesia and sterile condition the tip of (stress) both before and during labor. The ultrasound
the perforator is guided along the palm of the hand in the transducer is straped on mothers lower abdomen. In twin
vagina to the point selected for perforation. pregnancies, two transducers are available.
For vertex presentation—the anterior or presenting
parietal bone
For face—palate or orbit
For brow—the frontal bone
For after-coming head of breech—the occiput.
Technique of Perforation
In perforating the parietal bone, the perforation should
be near to the anterior fontanel, so that the blades of
crushing instrument are easily fitted over the face and
occiput. Perforation of the skull is done by a slight jabbing
movement, followed by a rotary movement, keeping the
point of the instrument at right angles to the skull. The
instrument is pushed inside the skull up to the shoulder
and the blades are separated by pressing the handles
together, then the blades are closed again. The instrument Fig. 74.22: Blond-Heidler decapitation saw
A B
Figs 74.23A and B: Pinard’s fetoscope
A B
Fig. 74.24A and B: Doptone
Fig. 74.25: Cardiotocography (CTG) machine
1. What are the different instruments used in destructive obstetrics?
i. Vacuum extractor
ii. Doptone
75
Obstetrics
Forceps and Ventouse
OBSTETRICS FORCEPS curve, which are in two different planes of the blade at right
angles to each other. The cephalic curve is in the horizontal
‘If one resorts to lower segment cesarean section (LSCS) plane of the assembled forceps and is structured, so as
easily for the slightest problems of labor, it would make to give a firm grip on the fetal head without excessively
only midwives and surgeons out of the members of compressing it.
our specialty and we will be left with nobody called an The pelvic curve of the blade is in the vertical plane
obstetrician’. Hence, learning the art of forceps and and accommodates to the maternal pelvic curvature.
ventouse application is essential in obstetrics. This curve makes the forceps grasp the fetal head more
anteriorly in the pelvis, so that forces of traction does not
Definition cause extension of fetal head while extraction (Fig. 75.2).
An instrument designed to assist in the extraction of fetal
head. Shank
The shanks add length to the forceps blades and allow
Instruments for easy locking of the blades at a distance outside the
An obstetrics forceps (Fig. 75.1) consists of a pair of blades introitus.
which are designated as right and left. Each blade has a:
Blade portion Lock
Shank The most common type of lock used in forceps are the
Lock British type of lock (Fig. 75.3). Normally, the lock is located
Handle. on the left blade, which necessitates its application first
in the pelvis. The lock closed when both the blades are
Blade Portion interlocked. The other type of lock are the French type of
The blades are fenestrated to make them light and easily locks (found in cephalotribes) and the sliding lock (found
maneuverable. Each blade has a cephalic and a pelvic in Kielland forceps).
Fig. 75.1: Obstetrics forceps Fig. 75.2: Pelvic curve

Obstetrics Forceps and Ventouse 699
regional anesthesia in primi (in parous women, it is 2

hours and 1 hour respectively).
Parity With regional anesthesia Without regional anesthesia
Primi 3 hours 2 hours
Multi 2 hours 1 hour
Contraindications of Forceps Delivery

Unengaged fetal head
Non-willing patient
Known osteogenesis imperfecta (OI) or bleeding dis
orders of the fetus
Position of fetal head is not certain.
Types of Forceps Application (Fig. 75.4)

Outlet Forceps
Fig. 75.3: British lock
The diameter of engagement of the presenting part is in
Handle the obstetrical outlet.
This facilitates to provide a firm grip on the forceps by the Fetal head is on the perineum.
Fetal head is visible at the introitus without separation of

operator.
labia.
Indications for Forceps Delivery Sagittal sutures is in the anteroposterior (AP) diameter.
Fetal Indication Low Forceps

Appearance of fetal, compromise in the second stage of The diameter of engagement of the presenting part is at in
labor when prospects of vaginal delivery are safe, cord the inlet of the obstetrical outlet. These types of forceps are
prolapse. most commonly used.
Maternal Indications
Maternal exhaustion
Pre-eclampsia, eclampsia
Heart disease
Severe anemia
Sedated patient
Prolapse of umbilical cord with a complete dilatation of
the cervix
Pulmonary injury or compromise
Ocular ailment contraindicating pushing
Note: In all these cases, the delivery is expedited to

minimize the distress of labor for the mother. However,
it is only safe to cut short the second stage in these
situations through a simple outlet forceps delivery
and not through a complicated and risky delivery from
higher stations like mid high forceps
Also applied to after-coming head of the fetus in breech
delivery (Piper forceps).
Prolonged Second Stage

Failure of satisfactory advancement of head for a period
of more than 3 hours with anesthesia and 2 hours without Fig. 75.4: Types of forceps applications
Head at +3 to +4 station (of + 5 system) If good uterine contractions are not present, start
Criteria for outlet, not met oxytocin drip.
Sagittal sutures less than 45° from AP diameter. Patient should be in a lithotomy position with appro-
(If it is more than 45° but less than 90°, it will still be priate preparations and drapes.
a low forceps with the other criteria being met with, but Bladder must be emptied.
delivery involves a higher risk). Pelvic examination is performed to know the position
and presentation.
Mid Forceps Appropriate anesthesia should be in effect (best carried
The diameter of engagement of the presenting part is in the out with pudendal block and perineal infiltration).
pelvic cavity between the pelvic brim and the obstetrical Ensure that uterus should be preferably contracting and
relaxing as a safeguard against postpartum hemorrhage
outlet. Head is engaged and leading point of head is above
(PPH).
+3 or +4 station.
Select the appropriate forceps for the application
High Forceps (Wrigley’s for outlet and Simpson’s for low forceps).
A generous mediolateral episiotomy is performed.
The diameter of engagement of the presenting part is
An assistant and pediatrician should be present before
above the brim and is unengaged.
commencing the procedure.
Pelvic versus Cephalic Application
Pudendal Block Anesthesia
In a cephalic application, the blades are applied along
(see Chapter 58).
the sides of the head grasping the biparietal diameter
(BPD) in between the widest part of the blades. The long Application Procedure (Figs 75.5A to D)
axis of blades corresponds to the occipitomental plane
For outlet application with the sagittal suture in AP
of fetal head. It is the ideal method of application and all
diameter:
application should be made in this way, so as to cause the
Blades are identified as right and left, after holding
least compression on the cranium.
them locked with the pelvic curve directed towards
In a pelvic application, the blades are applied on the
the patient in the position in which they will be, when
lateral pelvic wall ignoring the position of the head. In finally applied (Ghosting).
an unrotated head, this type of application puts serious Grasp the left blade handle with the left hand then
compression effect on the fetal skull and hence should be blade is inserted into the left side of the pelvis into the
avoided in a live fetus. sacral bay in front of the left ear of the fetus. The shank
Conditions to be fulfilled before the application of is allowed to drop on to the perineum and the assistant
forceps: is asked to stabilize the blade in this position.
Head must be engaged (modern obstetricians. pre-
Procedure is repeated on the right-side grasping the
scribes only outlet and low midcavity applications). handle with the right hand.
The presentation and position of the fetal head must be
Blades are locked in position (Fig. 75.6).
precisely known and suitable for safe forceps applica Correctness of the cephalic application is checked by
tion. Figure 75.7.
Cervix must be fully-dilated. First check: Post-fontanel should be located at midway
Membranes must be ruptured. between the sides of the blade and one finger-breadth
There should be no cephalopelvic disproportion (CPD). above the plane of the shank.
Explain the procedure to the patient. Second check: Sagittal suture should be perpendicular
to the plane of the shank throughout its length.

Technique of Forceps Application Third check: The fenestration of the blade should be
Preliminaries barely felt, if at all. Not more than the tip of a finger should
Ensure the indication for application a written, and be able to be inserted between them and the head.
informed consent from the patient for the procedure Unless these conditions are fulfilled, the application is
has been seen. not cephalic and blades need readjustment.
A B
C D
Figs 75.5A to D: Application of forcep. A. Assembling (Ghosting); B. Applying the left blade; C. Left blade applied; D. Application
complete
Fig. 75.6: Correct application of forceps Fig. 75.7: Check for cephalic application
Readjustment of blades Trial of Forceps Versus Failed Forceps

Post-fontanel (a) more than one finger-breadth above
An unsuccessful full-hearted effort at an extraction of
plane of shank, unlock the handles, elevate them one baby using forceps without anticipating any difficulties
at a time to the required level and relock them; (b) if in delivery can cause serious damage to both the fetus
less than a finger-breadth or even below the plane of and the maternal passage. Such a situation is termed as
the shank, depress the handle one at a time against the failed forceps.
perineum after unlocking, until the shanks are at the But anticipating the possibility of a failure, an attempted
desired level. forceps delivery and its abandonment in favor of
When sagittal suture runs obliquely to the plane of the cesarean section (CS), before a full effort at vaginal
shank, it suggests a brow-mastoid application. The delivery, is less injurious to both the mother and fetus.
blades are unlocked, and adjusted without removing This is called trial of forceps. All forceps applications
them one at a time. The handle is moved away from should be taken up as only a trial of forceps delivery and
the midline to move the tip of the blade, away from the not as a commitment for vaginal delivery at any cost.
head. Then, the blades are manipulated around the If need be abandoning forceps delivery is very important
head in opposite direction till the plane of the shank for the safety of mother and baby should always be kept in
is perpendicular to the sagittal suture before they are mind.
locked again.
If more than half inch of fenestration is felt below the
Causes of Difficulty in Forceps Application
head, it signifies a short application with the toe of the Application of Blades
blade not well-anchored beyond the malar eminence. If Incompletely dilated cervix
traction is applied, there is a real danger of forceps slip- Unrotated or unengaged head
ping and coming off the head, causing deep laceration. Locking
Blades are unlocked and are carried up one at a time • Application on an unrotated head
further into the pelvis till the fenestration cannot be felt • Improper insertion of blades—short application
• Failure to depress the handle against the perineum
below the head and it is then locked again.
• Entanglement of cord or fetal parts in the fenestra of
After the final check of the application, traction is
blades.
applied in a downward and backward direction with
Traction
proper perineal support to effect the delivery of the
• Undiagnosed occipitoposterior positions
head.
• Faulty cephalic application
For low forceps application with sagittal suture in • Wrong direction of traction
oblique diameter • Pelvic contraction
Here, in order to get a proper cephalic application the • Constriction ring
blades are to be applied as anterior and posterior ones, Slipping of blades
at an angle to the AP diameter of the outlet. • Blades are not introduced far enough—short applica
In all left anterior and right posterior positions, the tion.
left blade will occupy a posterior position and applied
Complications
first.
Watch out for any of the following complications in mother
In all right anterior and left posterior positions, the right
and baby or fetal:
blade will occupy a posterior position and applied first
Mother:
(Since, the standard lock is on the shank of left blade it
• Vaginal and cervical lacerations
involves the crossing of the left handle under that of the • Extension of episiotomy wound and 3rd degree peri-
right before they can be locked). neal tear
The corresponding anterior blade is introduced more • PPH.
anteriorly so that its tip goes beyond the brow and Fetal:
lies adjacent to the anterior frontal bone. This blade is • Laceration or bruising of fetal skull
manipulated to align with the posterior blade before • Intracranial hemorrhage (ICH), tentorial tears
they are locked in position. • Laceration and injury to scalp
After checking the correctness of cephalic application, • Neurological injury in the form of facial palsy, Erb’s
traction is applied to effect delivery during contractions. palsy
• Cephalhematoma Contd…
• Skull fracture
was easy (mention the detail of difficulty, if any encountered). Baby
• Any newborn baby with brachial plexus injury, must
cried immediately (mentioned if asphyxiated). Placenta and mem-
have an X-ray cervical and upper thoracic vertebra branes expelled completely. No PPH. No cervical tear or lacerations.
because a cervical rib predisposes to brachial No extension of episiotomy wound which was sutured in layers.
plexus injury with neck flexion and traction and/or Baby notes Maternal condition immediate
comprehension of the shoulder girdle against the � Sex post-delivery:
spine. � Time of Birth (TOB) � BP
� Birth Weight � Pulse
Medicolegal Aspects � Apgar � Bleeding PV—amount
In order to safeguard oneself from legal litigations, stress Shifted with Mother/nursery (reason for shifting)
Injury (details if present)

should be laid on the following points for documentation
Molding
of the case record:
Comment on placenta and membranes and liquor amnii.
Indication for forceps delivery should be outlined to
the patient and written in the record.

Informed consent of the patient with signatures of
witnesses should be recorded in the case-sheet.

Pertinent factors of pre and post-delivery fetal status,
VENTOUSE (VACUUM EXTRACTOR)
details of station, position and presentation at the Definition
time of application of forceps, instrument and the type
A traction devise used to assist in the delivery of the head
of procedure used as well as the details of the degree
that is attached to fetal scalp by suction forces.
of difficulty encountered in the procedure should be
recorded in delivery notes.
Instruments
Use the laboratory facilities to the full wherever
necessary and available, like scalp pH, cord blood pH, There are two components:
pathological examination of placenta. 1. Suction cups
Do not reapply the forceps if once failed.
2. Suction machine.
Model of Case Record Suction Cups

Consent form Metal cups: (see Figs 74.16A and B) Bairds modification
type, traction chain is attached at the center, a separate
I have been explained the need for the procedure and the suction hose is attached at the rim or at the side (in
risk involved in forceps extraction of my baby, which I have OP cup), edges of the cup are inverted to facilitate the
comprehended fully. I hereby consent, for the delivery of my baby expansion of chignon, the artificial caput into the cup
by forceps extraction, at my own risk.
to give a firmer grip. Three sizes of cups are available:
Signature of the patient
Signature of witnesses 1. 6 cm–should be the first choice in all application;
Signature of Husband/Relative being the largest cup.
Delivery Notes 2. 5 cm–best suited as OP cup in occipitoposterior
(A model-effect, suitable changes as per the situation) position applications.
Operation: Outlet/low midcavity forceps delivery/ventouse 3. 3 cm–not used in extraction of fetal head.
delivery
Metal cups are suitable in cases where rotation is
Indication: (Mention the indication)
Anesthesia: Pudendal block with/local perineal infiltration
needed.
Silastic cups: (see Figs 74.16C and D) These are soft
Surgeon: (Name)
Procedure: cups made of silastic, the edges are straight or everted
PV findings (at the time of application) (thus, no chignon effect). Traction and suction ports
FHS record (at the time of application) are integrated into the centre of the cup causing higher
A mediolateral episiotomy was given. A live boy/girl baby was incidence of cup pop-off from lateral traction. Two sizes
delivered by outlet/low forceps extraction on at by vertex (face to
are available—6 cm and 5 cm.
pubes/face). Application of forceps blades, locking and traction
Note: Always try to use the largest possible cup as it gives a
Contd… better traction with lesser chances of cup pop-off.
Silastic cups are best used for outlet applications that

do not require any rotation of the head. Low applications
requiring some degree of rotational movement which are
better addressed by using a metallic cup.
Suction Machine (see Figs 74.17A and B)

It can be operated mechanically, manually or by electricity.
Electrical suction machines are preferred which create
a vacuum of about 0.8 kg/cm2. They have fine regulatory
switch that can precisely control the vacuum with small
increments.
Indications
Same as that of forceps applications. Exception is, in case of
2nd of twin where the maternal passage is already prepared Fig. 75.8: Application of ventouse cup
and dilated by the first twin, one can take up a high ventouse
application even with the head in mid cavity. It can also Asymmetrical placement relative to sagittal suture will
be applied before full-dilatation of the cervix and it is also aggravate asynclitism.
useful when the vertex is not fully-rotated. Proper cup placement with vertex in outlet position and
occipitoanterior position is quite easy. For other situation,
Contraindications metal cups may be preferred as they are easier to place in
the optimal position. Episiotomy is not always required.
Non-vertex presentation
Fetal coagulopathies (suspect in case of mothers with Creation of Vacuum
coagulopathies or low-platelets-count) After placement of cup confirm that no maternal tissue
Following recent scalp blood sampling is incarcerated between the cup and fetal scalp by
Unengaged head running a finger around.
Inexperienced operator Cup is connected to the suction machine and an initial
Known macrosomia vacuum of about 0.15 kg/cm2 is created. A repeat check
Extreme prematurity. is made to ensure that no maternal tissue is trapped
Ventouse is likely to spread herpes in some cases. Evidence inside the cup.
for spread of hepatitis B virus (HBV) are not present yet. Next, the vacuum is raised in a single step to the target
level of 0.8 kg/cm2 within a minute.

Procedure of Ventouse Extraction Previously, slow suction was advised but it is not
Prerequisites, preliminaries are the same as for forceps required. Rapid suction causes no extra harm.
application.
Traction
In ventouse, it is more important that the patient is
having good uterine contraction along with the effective Traction is exerted intermittently coordinating with the
bearing down efforts from the mother. uterine contraction and maternal expulsive efforts.
As the cup occupies less space, the procedure can be It is initiated by using a two-hand technique—fingers of
carried out under local perineal infiltration anesthesia. the passive hand are placed against the edge of the cup
The largest available cup size is selected. pressing it against the scalp, while the active hand grasps
the traction rod of the instrument. The fingers of the passive
hand can feel for any signs of impending dislodgement of
Application of the Cup (Fig. 75.8)
cup, so that the traction force can be readjusted.
Proper cup placement is the most important determinant Manual torque should never be applied to the cup
in the success of the application. for rotating the head. The head undergoes into auto
The centre of the cup should be over the sagittal suture rotation with traction automatically.
and 2–3 cm in front of post-fontanel—(flexion point). Neither data nor consensus are available on the number
Anterior placement nearer the anterior fontanel will of pulls required to effect delivery or the total duration
aggravate deflexion. of the procedure.
The procedure should always be considered as trial, and

SKILLS AND RESPONSIBILITIES
if no early and clear evidence of descent towards delivery
consideration for alternative approach is advisable. A junior resident can apply an outlet forceps only
under the supervision of a senior resident after having
Cup Pop-off received adequate training in this application.
If it is due to the technical failure or wrong or suboptimal Only a senior resident should carry out low forceps
placement of cup—may merit additional attempts at delivery, as it demands higher skills and experience on
placement and delivery. the part of the operator.
On the other hand with optimal placement of cup, the A ventouse application being simple, tends to be
cup pop-off indicates relative or absolute disproportion overused resulting in its injudicious use. Senior resident
or asynclitism requiring excessive traction forces. In should validate appropriates of the procedure.
such circumstances, it may be prudent to abandon the A senior resident, not trained or experienced in low
procedure in favor of an alternate method of delivery. forceps application or ventouse, should seek the help of
When to abandon—when the cup slips twice and if a faculty member and perform a few applications under
there is no descent with 3 contractions or even with 30 their supervision before carrying it out on their own.
minutes of application, the baby is not delivered.
Complications
PREREQUISITES OF FORCEPS AND
Look for the following complications in the mother and
VENTOUSE DELIVERY
newborn or fetal: F – Favorable vertex position, fetal weight and mat
Mother urity
Vaginal and cervical laceration, cervical avulsion O – Os to be sufficiently open for ventouse and fully-
Vaginal hematoma dilated for forceps delivery
Third degree perineal tear. R – Ruptured membranes
Newborn or fetal C – Consent
Scalp injury – Contracting uterus
Cephalhematoma E – Empty bladder, head engaged episiotomy (if
Subaponeurotic hematoma required) epidural anesthesia (or local)
Intracranial hemorrhage P – Pediatrician to be present, prepare for CS, if
Retinal hemorrhage. needed.
1. Discuss the indications and complications of forceps and ventouse delivery.
i. Trial of forceps
ii. Failed forceps
3. True/False:
i. Metal cups are suitable in cases where rotation is not required.
ii. Asymmetrical placement relative to sagittal suture will aggravate asynclitism.
76
Specimens in Obstetrics
ANENCEPHALY (FIG. 76.1) brainstem and cerebellum may seem to be well

developed or with various degrees of malformation.
1. Describe the below specimen? 2. What may be other associated abnormalities?
Ans. This is a specimen of anencephaly fetus. In this Ans. Spinal defects may be associated like spina bifida in
case, the upper or cephalic part of neural tube does 26% of cases, cleft lip in 11% of cases, omphalocele in
not close, hence, there is absence of major portion 6% and cardiac abnormalities in 5% of cases.
of the brain, skull and scalp. There may be absence
3. Can this fetus be viable at or near term?
of the central nervous system and at the lower end,
Ans. Usually, it is a stillborn child. When born alive the
there is absence of both cerebral hemispheres. The
newborn may be deaf or blind or unconscious and
absence of cranial vault gives the eyes appearance
of protrusion. Facial features are ugly. Neck may insensitive to pain. As there is no functioning cere-
be short or absent due to malformation of cervical brum the neonate will not be conscious. Incidence is
vertebrae. The pituitary gland is absent in 50% about 1 in 1,000 pregnancies.
cases and sella turcica cannot be identified. When 4. How can this condition be diagnosed during ante-
the pituitary gland is there only anterior lobe is natal period?
present. Eyes shows absence or degeneration Ans. It can be diagnosed by ultrasound in any trimester
of ganglion cells of retina. Optic nerve has only of pregnancy. In first trimester, an ultrasound can
glial cells and there is absence of nerve fibers. diagnose it earliest at 10.5–16 weeks of pregnancy.
Adrenal glands are either hypoplastic or absent. At 16–18 weeks of gestation besides ultrasound
Thyroid gland is large and well developed. The elevated maternal serum alpha fetoprotein clinches
the diagnosis. In second trimester, and thereafter,
head is not palpable on clinical examination. It
may be associated with polyhydramnios or/and
abnormal presentation.
5. Are there any associated pre-existing clinical
conditions associated with anencephaly?
Ans. Dietary deficiency of folic acid is the most common
etiological factor. Congenital abnormality is more
common in mothers with diabetes mellitus, rubella,
multiple pregnancy, hypervitaminosis A, hyper-
thermia (102° or more), environmental pollution,
genetic (Waardenburg syndrome) and certain
ethinic groups, etc.
6. What is the outcome of the neonate after delivery?
Ans. Either it is stillbirth or will not survive (die within a few
Fig. 76.1: Anencephaly hours to a few days) as the brainstem is rudimentary.
Specimens in Obstetrics 707
7. What is the incidence? of interstitial edema of cytotrophoblastic and

Ans. It is 1 in 1000 pregnancy. Risk of recurrence is 5% syncytiotrophoblast. There is absence of fetal vessels
after one affected child and 13% after two affected in villous stroma and lack of trophoblastic stromal
children. invasion. A complete mole produces human chorionic
8. What are the complications associated with gonadotropin (hCG). Karyotype: These are diploid
anencephaly? (90% are 46XX and 10% have 46XY). Mitochondria
Ans. Obstetric complications associated with anencephaly comes from mother but chromosomes are totally from
are polyhydramnios, malpresentation, postdatism, father. It appears that a complete mole arises when an
shoulder dystocia and obstructed labor due to empty-ovum is fertilized by self duplicated haploid
simultaneous engagement of head and shoulder sperm (homozygous monospermic androgenic
because of short neck. fertilization) or by two haploid sperms with fusion and
replication (heterozygotic dispermic diandrogenetic
9. Is there any role of pre-conceptional counseling?
fertilization) partial hydatidiform mole
Ans. There is a essential role of counseling in women who
The partial mole, in contrast to the complete mole,
are at high-risk for anencephaly or with a history
has the presence of identifiable embryonic or fetal
of neural tube defects in herself or in the family.
tissues Gross examination of the placenta shows
Prescribe folic acid 0.4–1 mg daily should be taken
both normal and hydropic villi. There is variation in
3 months prior to conception and continued through
the size of the chorionic villi and the microscopic
the first trimester in a daily dose of 0.4–1 mg/day. It
examination shows focal swelling, cavitations and
reduces the incidence of neural tube defect by 70%. trophoblastic hyperplasia along with normal villi. A
normal amniotic membrane is seen. Trophoblastic
HYDATIDIFORM MOLE (FIG. 76.2) stromal invasion is present. Scalloping of the hy-
dropic villi may be seen. Fetal vessels are often seen.
10. Identify the below specimen.
There may be nucleated fetal red blood cells (RBCs)
Ans. This is a specimen showing grape-like vesicles. It is
in these vessels The fetus in partial mole has growth
a case of hydatidiform mole as a result of hydropic
restriction and shows multiple congenital abnormal-
swelling of chorionic villi. ities. hCG is produced.
11. What is the pathology?
12. Give common symptoms and signs associated
Ans. Complete mole occur with abnormal conception
with this condition?
which do not have recognizable embryonic and
Ans. It may be having any or all of the following symptoms
fetal tissue on microscopic examination. Gross
and signs:
examination shows grape-like vesicles of 1–3 cm in
Symptoms: Besides amenorrhea there is bleeding per
diameter (hydropic villi).
vaginal with sometimes history of expelling grape like
On microscopic examination, there is hydropic
structures, hyperemesis, pre-eclampsia, and no
swelling of chorionic villi and diffuse hyperplasia
fetal movement. In partial mole, there is addition fetal
movement. It can be like missed or incomplete abortion.
Signs: Uterine size is usually more than period of
gestation (POG). Then there are signs of hypereme
sis, pre-eclampsia (hypertension, proteinurea), con
vulsions may occur even before 20 weeks of gestation.
The uterus is more than period of amenorrhea in
sigh which is doughy in consistency. Fetal parts are
felt in partial mole.
On ultrasound, snowstorm appearance in complete
mole. In partial mole, fetal parts can be seen. Ovaries
may show theca lutein cysts.
13. Is there any risk factor associated with it?
Ans. No particular risk factors can be pinpointed. But
deficiency of carotene and animal fats is associated
Fig. 76.2: Hydatidiform mole by some workers.
14. How is the condition diagnosed?

Ans. It can be diagnosed by the signs and symptoms
discussed earlier. It is confirmed by ultrasound
examination and quantitative serum, beta-hCG.
15. Is there any treatment option once it has been
diagnosed?
Ans. After confirming, the condition patient is hospitalized
in a place where blood transfusion facilities are
available.
–– Stabilize her, correct hypertension, anemia and
any coagulopathy, if present. Suction evacuation
is the treatment of choice. Start a plain drip for
access to a vein. Keep blood in operation theater
(OT) before evacuation. Only after evacuation,
give uterotonics (e.g. syntocinon infusion) to
prevent trophoblastic embolism.
–– Repeat evacuation after one week, is not warranted.
She is followed by β-hCG levels in blood. Fig. 76.3: Lateral uterine rupture in the lower segment, involving
16. Describe follow-up of patient after evacuation? cervix and opening into the broad ligament
Ans. Weekly hCG levels are tested in woman’s serum till
3 consequent normal levels. No pregnany for one is corresponding to about 18–20 weeks size of
year is essential. pregnancy. It is showing lateral uterine rupture in
17. What can be the complications during suction the lower segment, involving cervix and opening into
evacuation? the broad ligament. The uterus has been removed
Ans. Complications include hemorrhage, perforation, because of rupture of the uterus. It is present in
disseminated intravascular coagulation (DIC), trop anterior surface of uterus. Complete rupture of uterus
hoblastic embolization and malignant transforma- is involving in all the layers of uterine wall including
tion, etc. serosa resulting in communication between uterine
18. What is the prognosis? cavity and peritoneal cavity. The lower segment
Ans. It depends on many factors: rupture is oblique. It is in the both anterior and
If diagnosed early and effectively treated, it is posterior wall. It is due to upward extension of
curable (100%). Trophoblastic malignancy develops cervical tear extending into broad ligament.
in 20% of cases of complete mole. It is not certain 21. Is it same as scar dehiscence?
who will develop malignancy, but it may depend in Ans. It is different from scar dehiscence, which is the
cases of advance age of the patient, high level of hCG partial separation of previous cesarean scar with
(more than 100,000 mIU/mL), reflecting degree of intact peritoneum and fetal membranes. It has
trophoblastic proliferation, hyperthyroidism, theca minimal bleeding. Incomplete rupture is a defect in
lutein cysts, etc. uterine wall, contained by visceral peritoneum or
broad ligament.
19. What advice is given to the patient?
22. What are the causes of uterine rupture during
Ans. As there is a chance of developing malignancy which
pregnancy?
can be cured with drugs, it is essential to do meticu-
lous follow-up for one year. Use contraception for Ans. Causes of uterine rupture during pregnancy are:
Previous classical cesarean section
this period to avoid confusion of developing malig-
Previous hysterotomy
nancy (elevated beta-hCG).
History of uterine perforation during D&C/medi-
cal termination of pregnancy (MTP)

RUPTURE UTERUS (FIG. 76.3) Injudicious use of oxytocin/prostaglandin
20. Identify the above specimen. Corneal resection
Ans. This is a specimen of uterus which is removed Uterine surgery like resection of septum, myomec-
by cesarean hysterectomy. The size of the uterus tomy, adhesiolysis
Specimens in Obstetrics 709
Placenta percreta 26. Describe the specimen.

Trauma Ans. This is a placenta of twin gestation. It shows single
Grand multiparity placenta with two cords and two separate amniotic
Obstructed labor sacs. It is from diamniotic pregnancy.
Over-distended uterus due to hydramnios, multi 27. What is the incidence of multiple pregnancies?
parity Ans. It is 3–4%, but it is more in the cases of being treated
Manual removal of placenta by ovulation induction.
Neglected shoulder presentation. 28. What are predisposing conditions for twins
23. What are the symptoms and signs of rupture pregnancy?
uterus? Ans. � High parity
Ans. Symptoms and signs: Advanced maternal age
In impending rupture of uterus, there may be Family history of twins
tachycardia initially Ovulation induction drug like clomiphene, gona
It may be associated with pain in abdomen and, dotropins, gonadotropin releasing hormone
on palpation there may be tenderness (GnRH) analogs
Patient is uncomfortable, restless In vitro fertilization (IVF); transfer of multiple
There may be scar tenderness in a case of previous blastomeres

cesarean case Race.
Fetal distress signs are present in early stage and 29. What is differential diagnosis of multiple gesta-
later it may become absent tions? (Fig. 76.4)
Uterine contour may be lost Ans. � Full bladder
Uterine contractions disappear Wrong dates
Vaginal bleeding may be present Hydramnios
Hematuria may be present Pregnancy with fibroid uterus
Abdominal paracentesis in flank will show hemo- Gestational diabetes
peritoneum Hydatidiform mole.
Sometimes postpartum shock or hemorrhage 30. What complications can occur?

Distension of abdomen. Ans. Maternal complication:
24. What is differential diagnosis of rupture uterus? Anemia
Hypertension
Ans. Differential diagnosis are:
Antepartum hemorrhage (APH)
Abruptio placentae
Postpartum hemorrhage (PPH)
Secondary abdominal pregnancy
Co-existing ovarian tumor and fibroid
Rupture of liver.
25. How is rupture uterus managed?

Ans. � Resuscitate the patient immediately
Put intravenous (IV) line and send blood sample for
arranging the required amount of cross matched

blood
Immediate laparotomy is undertaking and shock
if present, is simultaneously managed

After removing, baby extent of trauma to uterus is
assessed and if possible repair is done

If patient has completed her family simultaneous-
tubectomy is done after proper consent

Hysterectomy is done, if it is not possible to repair
rupture uterus
There is a danger of repeat rupture in 4–10% of
subsequent pregnancy. Fig. 76.4: Placenta of twin pregnancy

Fetal complications: Fetal death

Prematurity Asphyxia.
Hydramnios 31. What are the causes of low birth weight in twins?
Entanglement of twins Ans. � Discordance due to unequal placentation
Twin-to-twin transfusion in monoamniotic twins Large fetal body weight due to multiplicity
Intrauterine growth restriction (IUGR) Relative placental insufficiency
Congenital malformation Umbilical cord abnormality
Umbilical cord problem Unequal distribution of blastomeres in monocho-
Malpresentations rionic twins.

77
Sudha Salhan
Contraception
Benefit to the society and country: We all see countries

INTRODUCTION
who have risen from ashes after 2nd World War and now
Contraception is prevention of pregnancy. The methods they have one child (China ) or small family (Japan) norm.
used help in planning the size of family desired by the couple. Many family planning methods have non-contraceptive
India was one of the first countries to start a family planning health benefit, e.g. oral contraceptives pills (OCPs) are also
program in 1952. Our country’s economical advantages used to treat abnormal uterine bleeding (AUB) and hence,
get diluted by uncontrolled increase in population unlike curb anemia. Condom prevents sexually transmitted
countries strictly preventing population explosion (China). diseases (STDs) including human immunodeficiency
Contraception has the following advantages: virus/acquired immune deficiency syndrome (HIV)/
Controlling the population explosion (AIDS). Many cancers like ovarian, and endometrial
Better maternal health cancers are prevented by OCPs. The constant morbid fear
• It helps in increase the intervals between children of pregnancy is no longer there, thus reducing her stress.
• There is reduction in obstetrics morbidities and
mortalities, both by childbirth and induced unsafe
abortions DEFINITIONS
• There are fewer multiparty and high-risk pregnancies,
World Health Organization (WHO) defines family
decreasing maternal morbidity and mortality planning as a way of living and thinking that is adopted
• Contraception is a big step towards emancipation of
voluntarily upon the basis of individuals and couples in
the woman. By contraception, she has good health
order to promote the health and welfare of the family and
and has time to invest in herself besides looking after
thus, contribute effectively to the social development of a
the family affairs and children. She can channelize
country. It is now considered as a human right.
her energies towards better household management,
Eligible couple: Currently married couple wherein the
personal development and community welfare.
wife is in the reproductive age (15–45 years). There are
Spacing by contraception gives her time to improve
150/180 such couples per 1000 population in India.
her education level, thus getting better jobs and
spend more time on her health and hobbies. Couple protection rate: Defined as the percent of the
Benefit to children: By assaying a gap of 3 years or
eligible couples effectively protected against unwanted
more between two children, there is an investment in childbirth by one or the other methods of contraception.
the health of the children, they get more undivided Pearl index: The pregnancy rate per 100 woman years (HWY).
care thus they grow healthier and more intelligent. Pregnancy rate per HWY = Total accidental pregnancy × 12
Unwanted feeling has a long-term impact on the child’s Total months of exposure to unintended pregnancy
health, so a child must be born when he or she wanted. Total fertility rate (TFR): The average number of children
Benefit to the family: It there is a small size of the a woman would potentially have
family, the family income per person becomes more, Contraceptive prevalence rate (CPR): Proportion of
i.e. prosperity of the family. That means better health, population practicing contraception at some defined
food, education and family ties. point of time among the number of married woman of
reproductive age group. Every 2.4% point increase in

contraceptive prevalence is associated with a one point
decline in the birth rate. CPR in India is 45%.
METHODS OF CONTRACEPTION
They can be broadly divided into spacing (temporary)
and permanent methods.
Spacing methods
Natural methods
Barrier methods
Intrauterine contraceptive devices (IUCDs)
Oral contraceptive
Injectable contraceptive
Implants
Vaginal rings
Transdermal patches
Injection of chemicals and insertion of devices in
fallopian tubes and vas deferens

Contraceptive vaccine A
Emergency contraception (EC).
Permanent methods
Female sterilization
Male sterilization.
WHO medical eligibility criteria of contraception use

In this document, there are recommendations for the
safety of various methods of contraception with certain
diseases in the client as in India’s context. It is represented
by a wheel.
This wheel contains the medical eligibility criteria for
starting use of contraceptive methods, based on Medical
eligibility criteria for contraceptive use, 5th edition (2015),
one of WHO evidence-based guidelines (Figs 77.1A and B).
It guides family planning providers in recommending
safe and effective contraception methods for woman with
medical conditions or medically-relevant characteristics.
The wheel includes recommendations on initiating the
use of 9 common types of contraceptive methods:
1. Combined pills, COC (low-dose combined oral contra B
ceptives, with ≤ 35 μg ethinyl estradiol)
Figs 77.1A and B: WHO medical eligibility criteria wheel for
2. Combined contraceptive patch (P)
contraceptive use 2015
3. Combined contraceptive vaginal ring (CVR)
4. Combined injectable contraceptives (CIC) 8. Levonorgestrel-releasing intrautrine device (LNG-IUCD)
5. Progestogen-only pills (POP) 9. Copper-bearing intrauterine device (Cu-IUCD).
6. Progestogen-only injectables (POI) DMPA (IM or SC)/ The wheel has 2 sides.
NET-EN (depot medroxyprogesterone acetate (intramu- The eligibility for a contraceptive method in each case given
scular or subcutaneous)/(norethisterone enanthate, intra- after going through 3 categories of conditions as below:
muscular) 1. There is no restriction for the use of contraceptive method
7. Progestogen-only implants, LNG/ETG (levonorgestrel 2. The proven or theoretical risks generally overweigh the
or etonogestrel) advantages of using the method
Contraception 713
3. There is unacceptable health-risk, if this contraceptive Privacy is maintained. There is no side effect as no outside
method is utilized. agency (drugs, devices, etc.) is involved. Date of last
First and second category permits use while third menstrual period must be known. This method includes
category do not permit the use of that particular method. the following:
With few exceptions, all woman can use EC, barrier and Withdrawal and coitus interrupts method
natural methods including lactation amenorrhea method Rhythm method
(LAM). Basal body temperature (BBT) method
Sometimes, these categories differ for initiation and Standard day method
continuation. For example, if a client is having pelvic
Cervical mucus method
infection category 3 is applied and she is advised against
Symptothermal method (SDM)
the use of initiation of IUCDs. But, if she already has an
Lactational amenorrhea method (LAM)
IUCD placed in her uterus, treatment for the infection is
Commercial ovulation detection (do it yourself methods)
given and IUCD is not removed (details can be accessed at
http://www.int/reproductivehealth/en/). are coming up.
Counseling is crucial while prescribing the family Failure rate of NFP method: If these methods are used
planning methods. Privacy is ensured. The client is given with precision, the failure rate can be as small as 1–9 per
relevant knowledge of all the methods of contraception. 100 woman years. If natural methods are used with barrier
(Basket approach) It will help the couple to make choices method, the efficacy will be higher.
and ensure to follow them. Counseling helps in longer The methods are as follows:
use of method of contraception. For any method to be
effective, very good counseling is an essential prerequisite. Withdrawal and Coitus Interrupts Method
Use GATHER Approach (see Chapter 7) By this method, no sperms are deposited in the vagina. It
No method is 100% efficient and there are some side is one of the oldest family planning methods. Here, during
effects in all the methods except natural methods. Except the process of sexual act the male partner withdraws his
condoms (both male and female), no contraceptive organ from the vagina and discharges the ejaculation
method prevents STDs including HIV/AIDS. outside the female genitalia.
TEMPORARY OR SPACING METHODS Advantages

No expense is involved
By temporary family planning method, we establish a gap
of 3–5 years between two children. If the mother delivers No harm is done
at short intervals, her health suffers. The health of the last No infection.
born also suffers a lot. Hence, if all children are born at
Disadvantages
least 3 years apart, 3–4 million deaths under-5 years can be
prevented. It provides better life for both mother and child Great motivation and self-control is needed in the male
and hence, the family. partner. Psychological effect on both the partners is seen
When these methods are discontinued, the fertility in some couples.
returns after a reasonable gap of time. Temporary methods Efficacy: Failure rate 6.7 per 100 woman years.
Coitus intercurtis: The coitus performed in between
are also used when either partner is ill or unfit for safe
pregnancy and delivery. Pregnancy can be temporarily the thighs of the female
Coitus reservatus (Carezza): There is no movement
postponed when the couple is not financially, mentally and
physically able to support a child, e.g. too early marriage, during the act hence, ejaculation does not occur
extramarital or premarital sex, etc. Coitus saxonicus: The act continues till ejaculation, then
male perineum is stroked, thereby the spermatozoas go

Natural Methods of Contraception into urinary bladder instead of coming out
Natural family planning (NFP) methods are defined by Extra vaginal sex: Oral and anal sex.
WHO as methods of planning or preventing pregnancy by

observations of natural symptoms and signs of fertile or Rhythm Method or Calendar Method
infertile phase of menstrual cycle like temperature chart, This method avoids sexual intercourse during fertile
etc. This is practiced with abstinence during fertile period phase. This is also called Periodic abstinence or fertility
without use of any drugs and device. No money is spent. awareness-based method or safe period method.
As known, that ovulation occurs 14 ± 2 days before next Three days after the rise of temperature the couple is
period. The Safe Period (Ogino-Knaus theory) depends allowed to have sexual contact. In between, if sex is to be
on the length of the cycle. Ovum remains fertilizable for practiced then barrier methods can be used.
24 hours after ovulation. A sperm can fertilize the ovum Disadvantages: Sometimes the temperature rises slowly
within 3 days (WHO). This NFP method is based on the for several days. The rise may occur twice. During fever
assumption that if coitus can be avoided during the fertile and other illness, the records is not helpful.
or unsafe period, there will be no conception.
With a 28 ± 2 days cycle, the safe period days are; (i) the Standard Day Method (SDM)
menstrual flow days (4–6 days), (ii) 3 days after menses This natural method of contraception highlights from 8th
and (iii) 9 days before periods. If the period is short, the day of period upto 19th day of menstrual period (cycle
safe period days are less and if it is longer than 28 days of 26–32 days) as the fertile window. Avoid unprotective
cycle, the safe period days are more. sexual contact during these days. One year failure rate is
To be more accurate, a record of 6 cycles are made. The 4.8%.
longest and shortest cycles are to be noted. By subtracting
Method of uses: This method uses a beaded circle (Fig.
18 from her shortest period, she can know her first day of
77.3). The beads denote a day of the menstrual period. On
fertile period. From the longest period minus 11, she can,
the first day of bleeding put black ring on the red bead.
calculate the last fertile day. For example, in a 26–32 day
She moves it forward, one bead each day in a clockwise
cycles, 26–18 = 8th day is first fertile day; 32–11, i.e. 21st
direction. Brown beads denote safe period but when
day is the last fertile day. Thus, from 8th to 21st day no
the black ring is on white beads, the couple must avoid
sexual intercourse is to be done to avoid pregnancy.
unprotected intercourse.
Disadvantages: It is not applicable in irregular cycle.
Sometimes, ovulation can occur with sexual intercourse.
Cervical Mucus (Billing’s) Method
Efficacy: The failure rate of this method is 10 per 100
woman years. But, if the fertile period is not strictly avoided This method includes recognizing the changes occurring in
then pregnancy rate increases. the cervical mucus at different stages of the menstrual cycle.
The cervical mucus is opaque, sticking, scanty and thick in
Basal Body Temperature (BBT) Methods (Fig. 77.2) pre-ovulatory period of the cycle. Just before and at the time
After ovulation, progesterone levels rises and this increases of ovulation the cervical mucus becomes clear, copious and
0.5–0.8°F or 0.2–0.4°C of body temperature. There may can be stretched easily between the fingers. During these
sometimes be a visible drop (0.2°F) before this rise. days, unprotected sex is to be avoided (Fig. 77.4).
Every day the woman records her oral temperature She is instructed to wash her hands with soap and water.
(keeping the thermometer for 3–5 min under the tongue) Wipe dry. She can collect the discharge at vaginal outlet by
as soon as she wakes-up, before leaving the bed and a finger inserted in the vagina and the discharge collected
taking any fluids or food and before washing, etc. Special is wiped on paper. The stickiness, consistency and amount
thermometers with 36–38°C marking are easier to read. is observed daily and carefully recorded.
The temperature is recorded on temperature chart and If she can stretch the cervical mucus between thumb
special BBT charts are also available. and index finger, it is fertile period.
Fig. 77.2: Days of menstrual cycle

Contraception 715
Fig. 77.3: Standard day method (SDM) beaded circle Fig. 77.4: Cervical mucus method
Disadvantages: If there is a vaginal infection, the discharge

will not follow the normal physiological process. Cervical
surgery will also modify the normal observations.
Efficacy: Failure rate is 3 pregnancies per 100 woman
years.
Symptothermal Method
This is a combined method using BBT, Billing’s method and
other factors of ovulation like midcycle pain, spotting or
bleeding in midcycle and breast tenderness. The woman can
also feel the cervix by clean hands inserted in the vagina. The
cervix becomes soft and os is slightly open during ovulation.
There is a special chart (symptothermal chart devised by
WHO.
Efficacy: Failure rate is 2 pregnancies per 100 woman years.
Lactational Amenorrhea Method (LAM) (Fig. 77.5)

There are certain pre-requisitions to ensure the optimum
Fig. 77.5: Lactating mother
results.
The child is exclusively breastfed, i.e. breastfeeding in
This prevents from life-threatening conditions in the
both during day and night. No other feed (even water)
child like diarrhea, pneumonia, etc.
is given to the child
Help to develop a mother and a child bonding
There is amenorrhea
This can be started immediately after birth
It is useful for first 6 months of life.
No effect of weight and smoking status of the mother
If any of these 3 conditions is not fulfilled, another
No other precaution is to be taken to prevent pregnancy
family planning method is to be started.
during intercourse No cost is engaged for using this
Advantages family planning method
This is a very good temporary method. Mother is protected from postpartum hemorrhage
Besides family planning, baby’s health is taken care in (PPH) and subinvolution of uterus, cancer of the breast,
the form of adequate nutrition the mother’s milk. etc. Wounds heal faster in these woman
Psychological support to both mother and child Kits for planning the sexual act accordingly is also
No hormonal and other side effects available in the market. They give LH levels and can find
Disadvantages: No protection from STDs including out exact time of ovulation.
HIV/AIDS for both mother and child (if the mother is
HIV positive) Barrier Methods
Frequent breastfeeding may be difficult for working
These methods achieve avoidance of pregnancy by pre-
woman.
venting the sperm and ovum to come together.
Mechanism of action The methods used are:
Condoms, both male and female
Prolactin levels fall immediately after delivery. If the
Spermicides
mother is not exclusively breastfeeding, this level is not
high enough to produce anovulation and amenorrhea. By Occlusive vaginal devices
10–15 weeks postpartum, the ovulation and menstruation Vaginal diaphragm
is resumed. But if the woman is exclusively breastfeeding, Cervical caps
she maintains high blood levels of prolactin which inhibits Vault cap
luteinizing hormone (LH) and also prevent the effect of Vimule cap.
follicle-stimulating hormone (FSH) and LH on ovaries.
Hence, very little estrogen and progesterone are produced Male Condoms
preventing ovulation and menstruation.
Male condoms are being used for a long time. It is made
In these woman, amenorrhea may lasts for 5–9 months
of fine latex rubber of various colors. The precise use is
and anovulation upto 6–10 months.
This method is effective upto 6 months after childbirth. important to prevent failures. Hence, good counseling and
Because after 6 months the child is initiated to other feeds instructions for correct use are essential.
(weaned) and hence, prolactin levels start coming down. Government hospitals provide Nirodh at family planni
Therefore, after 6 months LAM is to be supplement with ng clinics, free of cost. One can purchase it from chemist
other NFP methods. shops, grocery shops, pan shops and by vending machines.
Efficacy: 2 pregnancies per100 woman years.
Instructions for use
Advantages of NFP methods Put the condom on erect penis before touching vagina
Menstrual cycle is not altered Open the pack by tearing the ribbed edge. The rolled
No financial cost rim is to face away from the penis
No physical side effects of drug devices or surgery The foreskin is to be pulled back in uncircumcised penis
No effect of smoking Put the condom on tip of the penis and then unroll
Cooperation of the husband is required, it improves Nirodh towards base. If it is difficult to unroll then
marital relationship discard this condom and use a new one
This can be used by woman of any constitution, thin or fat No lubricant with oil is to be used. It will damage the
There is no resistance from the society and the religion condom and hence, cause failure. But, can use water or
There is no setback, when the supply is cut or erratic
water-based lubricants like spermicides, etc.
compared to other methods
The rim of Nirodh is pinched at the base after ejaculation
Privacy is maintained
to prevent slipping off. He may be advised to pull out of
This can be taught to uneducated couples also
vagina before losing the erection.
There is no increased risk of chromosomal or congenital
• Removal—slip it off without soiling the vaginal
abnormalities.
opening with semen
Disadvantages Disposal—cover it with a paper and then dispose off
If not used correctly, the failure rate increases in a dustbin or can burn or bury it
More failure rate than other methods of contraception • It is to be used only one time.
Protection against sexually transmitted infections In case of breaking, insert spermicide in the vagina (if
(STIs) including HIV/AIDS is not there handy). Emergency contraception (EC) can be used to
Non-cooperation of the husband will not bring out the prevent pregnancy. Immediately washing the penis and
desired level of results douching the vagina will reduce STDs risk.
Contraception 717
Storage: Keep it in a cool dark corner. Handle carefully as Used in the formation of vaginal mold in the operation
finger nails and rings can tear it. See the manufacturing of vaginoplasty
date. Use can be upto 5 years from manufacturing date. During ultrasound examination of a female, it is used to
Return to health facility if, cover the vaginal probe.
Need more condoms
Symptoms of STDs develop (sore genitalia, dysuria or

Female Condom (Reality Condom, Femidom)
discharge) (Figs 77.6A to E)
Allergic to condom material Consists of a soft loose polyurethane sheath (15–7 cm) with 2
Condoms break—(for supply of EC, if not available) flexible rings. One ring covers the vulva and the second one
Any other problem—advise for other methods. covers the cervix internally like a diaphragm. It is introduced
like a tampon. Inserted before intercourse. It is pre-
Advantages lubricated with a silicone-based lubricant (dimethicone). It
The most harmless method of contraception. is to be removed after 8 hours and not more than 24 hours
It can be used just after delivery
after intercourse. It is disposable like male condom.
No side effects of hormones
It has the advantage of being a woman—controlled
No prescription is required for procurement
method of family planning and for protection against
No daily keep-up is needed
STDs including HIV/AIDS.
Any age is eligible to use
Disadvantage: It is expensive; supply must be handy.
Easy to obtain from health facility and market
Efficacy: Used correctly and consistently, 5 pregnancies
per 100 woman years.
Prevent STDs including HIV/AIDS
It can be stop at any time Spermicides

No previous health check-up is needed
These are chemical agents capable of destroying sperms and
Making men feel responsible
are incorporated with an inert base. They are introduced in
Use in late pregnancy can prevent amniotic infection.
vagina before intercourse. The base may be gelatin, glycerin
If used for more than 5 years, it reduces the chances or wax which melt at the body temperature. They are to
of developing severe cervical dysplasia and cancer cervix be inserted 30 minutes before the act. No douching is to
and does reverse dysplasia. be done within 8 hours. Spermicide alone, are not a very
efficient spacing method. They are used with other methods
Disadvantages
like condom, diaphragm, etc. They are marketed in various
May cause allergy in some males forms viz. dispersible tablets (Today tablets) (Fig. 77.7), films,
Privacy is needed aerosol and sponge (Today sponge). Mostly Nonoxynol 9 is
Ready supply must always available
chemicaly used. Foaming tablets with suppositories utilize a
Man’s cooperation is needed
chemical base, which releases carbon dioxide (CO2) which
Buying may cause embarrassment
helps in the distribution of spermicidal agent throughout the
Some complain, decrease in sensation upper vagina. A spermicidal film that can be used vaginally
It may break during the act. or over the penis. It is a small sheet of material that dissolves
Recently, polyurethane condoms are also being made. in the vagina and is used in South Korea, Malaysia, Spain, etc.
Besides other attractions it is less susceptible to deteriora- It is designed to prolong release of Nonoxynol 9 after
tion during storage. There is also introducing of spermici- single vaginal application in polycarbophil base. Best
dal coated condoms (using Nonoxynol 9) it increases the example of sponge containing 1 g of Nonoxynol 9 to release
efficacy. 125–150 mg. It is inserted after wetting with water. Remove 6
Efficacy: 3 pregnancies per 100 woman years, if used hours after the act of intercourse by pulling its loop attached
correctly and consistently. at the bottom. It is not to be used during menstrual period
Contraindication—only severe allergy to latex rubber, and after childbirth. Other spermicidal chemicals under
can change brand or use recent polyurethane condom. trial are zinc acetate, Magainin G, Magainin A, etc.
Non-contraceptive uses Advantages

Prevent STIs/HIV/AIDS Easily available and easy to use
Used as condom catheter in the treatment of PPH No gross medical side effects.
A B C
D E
Figs 77.6A to E: Method of inserting female condom
Disadvantages
It is messy and not liked by some
It cannot be used alone as efficacy is not good.
Efficacy: 21% failure rate. When used with condom it gives
very good efficacy.
Vaginal Diaphragm (Fig. 77.8)

It consists of a thin, nearly hemispherical dome
shaped rubber or latex structure. The periphery has
metal spring ring. They are of different sizes and are of two
types—coil spring type and flat spring type. It is not much
used now.
Cervical Cap (Fig. 77.9)

They are smaller rubber appliance. They are dome-shaped
and cover the cervix and remain in place by suction.
Fig. 77.7: Dispersible tablets Different sizes are available.
Contraception 719
Fig. 77.8: Vaginal diaphragm Fig. 77.9: Cervical cap
Vault Cap These are as follows:

Lippes loop
Rubber or plastic cap fitting in the vaginal vault covering the
Copper T-250, 380A devices
cervix. No metal spring in the rim is there.
Multiload
Vimule Cap Frameless devices
Hormonal IUCDs like mirena

It made of rubber with string attached. In woman with
Under research IUCDs.
cystocele, where diaphragm does not fit, it can be used.
Contraindication: Prolapse of uterus—vesico vaginal They are becoming an increasingly popular method
fistula, recotovaginal fistula. and are used worldwide for contraception among eligible
Motivation and teaching the method of insertion is woman in reproductive age group. It has been in use more
essential. It is to be inserted 2 hours before intercourse. than 50 years, being safe, effective, convenient, reversible,
These devices are removed 6–8 hours after intercourse. long-acting contraceptive method used by more than 100
Do not leave them inside vagina for more than 8 hours. million woman in the world. Nearly 40% of woman are in
Remove and clean with soap and water and then dried. China. IUCDs usage in developed countries is about 6%.
Talcum powder is applied and is kept in air-tight container. Studies show that nearly 6 out of 10 woman use the pill
incorrectly. IUCDs generally avoid the problem of incorrect
Advantages use hence, IUCDs are superior to use effectiveness to
Harmless OCPs. Because user has to return to the health care facility
Fitted before and removed after sexual act, hence do for discontinuation, hence continuation rate is higher in
not interfere in the act IUCD in contrast to OCP which can be discontinued easily
Woman friendly device. without return visit.
National family planning program of government of
Disadvantages India and IUCD
Privacy is needed Lippes Loop was first introduced in the year 1965. After the
Rubber allergy can occur results of clinical trials in 1972 conducted by the Indians
If kept longer in the vagina, it can cause infection Council of Medical Research (ICMR), Copper T-200B was
Does not prevent HIV/AIDS included in this program in 1975 and Copper T-380A in
May cause urinary tract infections (UTIs). 2002.
Efficacy: 18–28% failure rate. Decreases to 6% if used with
spermicides. History of IUCDs
There are fascinating stories available in history, regarding
Intrauterine Contraceptive Devices (IUCDs) the first use of contraceptive devices in animals and humans.
They are placed inside the uterus. Various IUCDs are To prevent pregnancy in animals in caravans, man insert-
available. ed pebbles into their uterus during long journeys. In 1909,
A B A B C
Figs 77.10A and B: A. Lippes Loop; B. Safety coil Figs 77.11A to C: A. CuT-200; B. Cu7; C. Multiload
Richter in Germany described the first genuine IUCD.

Grafenberg (1928–30) used a sillk device, he is considered
pioneer in IUCDs. Ohta ring later came in use. In 1960,
Lippes Loop and margulies spiral (of polyethylene) were
invented. In the year 1962, population council organized
first International Conference on IUCDs in New York,
where marguiles rings and lippes loop were presented.
In 1964, the second conference on IUCDs was held and
many devices of different shapes were presented. The first
medicated devices were developed in 1969 using copper.
In 1970, a USA company developed a Dalkon shield which
had a faulty design and caused severe infections, some-
Fig. 77.12: CuT-380A
times fatal, this led to many lawsuits and removal from the
market.
CuT-220C/Nova-T: They are made up of polyethylene to
The Modern IUCDs which barium sulfate is added. Copper (200 mm2) is in
seven sleeves—two on the arms and five on the stem.
The IUCDs development continued and many improve
CuT-380A, CuT-380Ag, CuT-380 Slimline (CuT-380 S):
ments have been taken place to reduce the unpleasant
It is made up of polyethylene to which barium sulfate is
side effects of cramping and bleeding.
added so as to make it visible on X-rays. It has copper wire
Types of IUCDs 314 mm2 on its stem and 2 solid copper sleeves of 33 mm2
on each transverse arms (hence A in the name). CuT-380
First Generation IUCDs Ag, the wire has a silver core.
Lippes loop, spirals, coils, rings and bows (Figs 77.10A and The length of vertical stem is 36 mm and of horizontal
B) of A, B, C, D sizes. limb is 32 mm.
Multiload–250, Multiload-375 (MLCu-250 with 250 mm2
Second Generation IUCDs copper wire and MLCu-375 with 375 mm2 of copper wire )
Copper 7, Copper T-200 (Figs 77.11A and B). Multiload Cu- have 2 flexible arms having spurs with 3 sizes.
250 and 375, and NOVAt (Fig. 77.11C).
Newer Variants: Copper T-200B, CuT-380A (at present Third Generation IUCDs
provided by NFP program) CuT-380Ag, (Fig. 77.12) These are hormonal progesterone releasing contraceptive
CuT-380 Slimline, CuT-220C. system.
CuT-200, CuT-200B, CuT-200Ag: They are made up of Progestasert: T-shaped device of copolymer ethylene vinyl
polyethylene to which barium sulfate is added. In copper acetate (EVA) storing 38 mg of progesterone (releasing 65
T-200, copper wire of 200 mm2 is wrapped around the µg/24 hours) the stem also has barium sulfate in silicone-
stem. In CuT-200Ag, the wire has a silver core. oil base.
Contraception 721
Fig. 77.13: Mirena
LNG-20 (Mirena) (Fig. 77.13): Levonorgestrel releasing very effective, have intermediate failure rates of 1–3 per
contraceptive system is more potent. A T-shaped device 100 woman years whereas IUCDs releasing progesterone
arm containing in its vertical limb LNG (52 mg) and with a failure rate of 0.2 per 100 woman years at first year
polydimethylsiloxane releasing 20 mg of LNG daily (daily and 0.1 per 100 woman years in subsequent years.
blood level 150–200 mg in serum). Familia slim is thinner Efficacy: CuT-380 has a failure rate in first year which is
in size than mirena. 0.3–0.8% (equal to female sterilization).
Other IUCDs How IUCDs act?

Copper-bearing IUCDs
Copper SAFE-300, IUCD has more flexible plastic and is
smaller than CuT-380 A Preventing fertilization as the copper ions alter the
uterine and tubal fluid environment. This fluid contains
Sof-T available only in Switzerland
leukocytes, copper ions, enzymes and prostaglandins.
Future IUCDs: Flexiguard, gynefix, cu-fix, fibroplant—for
Copper is toxic to sperms hence, decreases the sperm
perimenopausal woman.
motility and function thereby, preventing sperms to
Frameless IUCDs: Several copper cylinders strung toge
reach the fallopian tube at time to fertilize the ovum.
ther are anchored into the uterus.
In the endometrium, copper produces a sterile inflam-
Copper fix is a new frameless IUCDs. It is highly effective
mation which prevents implantation as it releases the
against pregnancy but has more expulsion rate than CuT- macrophages which engulfs sperms and fertilized ovum.
380A. LNG-IUCDs produce atrophy of endometrial glands by
progestational effect and further development of ovum
Approved Life-span of IUCDs
is inhibited. Hence, uterine endometrial lining is a poor
The inert IUCDs can be used indefinitely. The medicated place for a fertilized egg to implant and grow. Progesterone
devices are approved for different lengths of time in increases thickening of cervical mucus, reducing sperm
different countries. This is called approved life-span. The transport. The hormones in the LNG-IUCDs also reduce
approved life-span of CuT-380 is 10 years whereas that of menstrual bleeding and cramping.
CuT-200 is 4 years, CuT 380Ag is 4 years and CuT-380 S is According to WHO eligibility criteria, a woman with
2.5 years. CuT-220C has an effective span of 3 years and pelvic inflammatory disease (PID) is not a candidate for
Nova-T is estimated to be effective for 5 years. MLCu- IUCD (category 4). She is to be treated to become eligible
250 has a life-span of 3 years and that of MLCu-375 is for IUCD. But a client who has IUCD in position, develops
5 years. The approved life-span of progestasert is 1 year PID is category 2. The IUCD is not removed but the
only whereas that of LNG-20 (Mirena) is 5 years. infection has to be treated.
Effectiveness: The IUCD is an extremely effective method
of contraception. The copper-bearing IUCDs, with the Side Effects
largest surface area of copper (CuT-380A and MLCu-375) Side effects of IUCDs are mostly minor and resolve a few
has a failure rate of 0.5–0.6 per 100 woman years and are months after insertion. Therefore, for the continuation,
proper counseling is essential. Some common symptoms of insertion, insertion procedure, and effective life. Post-
are as follows: insertion counseling and follow-up counseling should
Menstrual changes: There may be an increase in uterine include information regarding the warning signs that
bleeding, either a prolonged cycle or heavy menstrual necessitate medical attention.
bleeding or intermenstrual spotting for initial few days Client assessment: The objective of client assessment is
or months. They are controlled by nonsteroidal anti- done to know the eligibility, general history, menstrual and
inflammatory drugs (NSAIDs). In hormonal IUCDs, there obstetric history, reproductive history including history
is spotting and intermenstrual bleeding in initial few of (H/O) PID, STIs or a high individual risk of exposure
months. to reproductive tract infections (RTIs)/(STIs) should be
Dysmenorrhea/cramps at insertion for a few days may clearly brought out. Limited general physical examination
go away itself or sometimes an antispasmotic or NSAIDs is necessary. Pelvic examination is performed to exclude
agents may be necessary. any genital tract infection and to assess for uterine size,
shape, position any adnexal pathology.
Concerns, Myths and Misconceptions
Regarding IUCDs Timing of the Insertion
IUCD and infection (PID), infertility: There is minimal IUCDs can be inserted any day of the menstrual cycle
risk (less than 1%) and occurs within the first 3 weeks of provided, she is reasonably sure of being not pregnant
insertion and after that the risk is same as in a woman who It may also be inserted immediately (postplacental
is not using an IUCD. It needs an accomplice (chlamydia, insertion) after delivery or within 48 hours of delivery by
gonorrhea) to cause infection The risk is not due to IUCD trained person using special insertion forceps (Kelley’s)
itself, but from non-sterile insertion technique. Using It can also be inserted more than 4–6 weeks, postpartum.
recommended infection prevention practices including
IUCD can be inserted along with first trimester of
loading of CuT in its sterile package (no-touch technique)
medical termination of pregnancy (MTP)
and smearing the cervix twice with povidone iodine before
Provided there is no infection, IUCD can be inserted
insertion can further minimize the risk.
IUCDs and risk of ectopic pregnancy: The WHO after first menstrual period following second trimester
multicenter study concluded that copper-IUCDs produce miscarriage (spontaneous or MTP)
very good protection against both intrauterine and ectopic In a woman in lactational amenorrhea, after ruling out
pregnancies (91% less chances of ectopic pregnancy than pregnancy
a non-contraceptive user). But if a pregnancy occurs in a It can be used as EC within 5 days of unprotected sex.
copper-IUCD user, the chance of that pregnancy being an It will be continued where long-term contraception is
ectopic is very high. desired.
IUCDs and risk of expulsion: The chances of spontaneous
expulsion vary between 2 and 8%, common during men- Technique of Insertion
struation in the initial 3 months. More so, in a nulliparous Prepare the client and ask her to lie on the table
client or one who has menorrhagia or after second trimes- Do per vaginum examination
ter abortion.
Loading the IUCD in the sterile package (Figs 77.14A to
IUCDs and risk of perforation: The risk of uterine
E). When correct procedure, i.e. NO TOUCH technique
perforation is rare. It occur during insertion due to wrong
is adopted and the infection prevention precautions are
abandon method, the procedure immediately will prevent
any harm. followed, for inserting an IUCD, there is minimum risk
IUCDs and HIV/AIDS: The IUCD do not protect. of post-insertion infection, perforation and expulsion
Insert the vaginal speculum and catch the hold of
Prerequisites of IUCDs Insertion anterior lip of cervix with a vulsellum
Counseling: Counseling plays a vital role in increasing Clean the cervix thoroughly with iodine solution twice
the acceptance of any family planning method. If a Insert uterine sound in the uterus to know the size and
client chooses an IUCD, it is essential to provide specific direction (anteverted or retroverted). Note the size
information about the advantages, disadvantages including The sound and the loaded IUCD must not touch the
the side effects and possible complications along with their vaginal walls or blades of the speculum or pass through
management. The counseling should also include timing the cervix more than once
Contraception 723
A B C
D E
Figs 77.14A to E: Steps of loading IUCD with NO TOUCH technique. A. Partially open package till 1/3rd of flap; B. Placing white
plunger rod into tube; C. Push the card (Measurement insert) upto seal end of packet; D. Inserting folded IUCD arms into insertion tube;
E. CuT-380A ready for insertion
Insert the loaded IUCD after adjusting with uterine size.

Advance the loaded IUCD till the blue length gauge
reaches the cervix or resistance is felt
Keep the plunger rod stationary with one hand and
withdraw the insertion tube downwards with the other

hand, till it touches the grip of plunger tube (thus
releasing the Copper T in the uterus)—withdrawal
technique—to prevent perforation
The insertion tube is kept stable and white plunger tube
is removed to prevent the thread to be caught between

the two and displacing IUCD
Gently push the insertion tube up towards the fundus till
resistance is felt (to ensure high position of Copper T in Fig. 77.15: Instruments of postplacental insertion of CuT
uterus—to prevent expulsion). Remove insertion tube
Cut the thread (3–4 cm from the cervix) with a sterile forceps) to place the device at the fundus. The instruments
scissors required are shown in (Fig. 77.15). There is special method
Remove vulsellum and look for any bleeding from its grip of holding CuT (Fig. 77.16).
site. If no bleeding from cervix, also remove the speculum.
Put both instruments in 0.5% chlorine solution for atleast Copper-IUCDs—advantages
10 minutes (decontamination) before washing and send- Gives a long-term contraception which is reversible and
ing for sterilization highly effective immediately after insertion. It is also an EC.
Client is allowed to rest for sometime. It can be replaced as many times as needed without any
Immediately, after delivery (postplacental) and imme- gap in ones reproductive life. There is no special attention
diate postpartum (within 24 hours of delivery), insertion needed during sexual act or on day-to-day basis. Unlike,
of copper T requires a special long instrument (Kelley’s OCPs which are to be taken daily, IUCDs insertion is a one
Steps for Mirena Insertion (Figs 77.17A to E)

When to Remove an IUCDs
Client wants it to be removed. Replacement after the
designated time
Want another child (tell her the importance of antennal,
intranatal and postnatal care)

Started another method of contraception (say tubectomy)
Heavy bleeding not able to control by medicines (rare).

Menopause
Fig. 77.16: Postplacental insertion of CuT (method of catching Evidence of IUCD displacement.
CuT in Kelley’s clamp) Advantages of hormonal IUCDs over copper-bearing
devices:
time procedure. It is available free of charge by government. It is more effective than Cu-bearing IUCDs
It is cheap even when it is purchased from the market. It Hormonal IUCDs decrease the amount of bleeding, can
can be used by breastfeeding mothers. It has no interaction be used in woman with AUB and improves hematocrit
with any medication being consumed by the client. She can It also reduces the pain and cramps in dysmenorrhea
promptly conceive after removal of the IUCDs. and endometriosis. There is a beneficial effect on fibroids
A B C
D E
Figs 77.17A to E: Pictorial representation of important steps of Mirena insertion

Contraception 725
Disadvantages of hormonal IUCDs: They are very

expensive and may not be affordable for many. Oligo-
menorrhea or amenorrhea may not be acceptable to all
woman. Sometimes, they can cause irregular bleeding or
spotting. Insertion requires a special technique.
Complications and their Management

Pregnancy with IUCDs: Failures are also seen with this
effective method of contraception. If a client reports of
having missed her period and pregnancy is suspected, do
urine pregnancy test and exclude ectopic pregnancy, If
she does not wants this pregnancy (due to contraceptive
failure) offer her MTP within 20 weeks of pregnancy. But
if she wants to continue this pregnancy remove the IUCD
Fig. 77.18: CuT removal hook
immediately if strings are visible (it will slightly increase
the chances of miscarriage). However, if the IUCD is not
removed it can cause infection, second trimester abortion
or preterm delivery. Pregnancy with IUCD in situ does not
increase the risk of congenital anomalies in the baby.
Missing strings: Missing, shorter, or longer strings may
be due to IUCD expulsion, malposition or uterine
perforation. The partner may be bothered by short thread
during sexual act. In case of a problem, like missing thread
first rule out pregnancy then try to locate the thread in the
cervical canal by sterile long artery forceps and pull them
out gently. If the strings are not located or cannot be drawn
out, by the use of a uterine sound try to locate the IUCD
(sounding), carefully without injuring the uterus. An X-ray
(using a sound in uterus) or ultrasound is done to see the
position of IUCD in the uterus or it is expelled.
Misplaced IUCD: It can be removed from the uterus by Fig. 77.19: USG showing IUCD within uterus
IUCD hook (Fig. 77.18). Courtesy: Dr Rajesh Uppal, Uppal Diagnostics, Delhi
If the IUCD is intrauterine and removal is not easily
possible, direct visualization with USG (Fig. 77.19) or
hysteroscopy can be tried. A forcep may be used to extract
IUCD under ultrasonic visualization. If still not successful
then hysteroscopic removal can be done.
If the IUCD is in the abdominal cavity, it should be
removed by operative laparoscopy or laparotomy under
anesthesia, as copper can form adhesions in the abdominal
cavity. If an IUCD has partially perforated, the myometrium
both routes, i.e. hysterolaparoscopy may be useful.
Perforation (Fig. 77.20): Perforation of uterus is very
rare and only occur when standard insertion procedure
(withdrawal method) is not followed because of unskilled
provider.
If perforation is detected late, i.e. missing strings,
unexplained or persistent pain/pregnancy, confirm the Fig. 77.20: USG showing perforation
diagnosis by USG/X-ray. Courtesy: Dr Rajesh Uppal, Uppal Diagnostics, Delhi
Expulsion: Symptoms like irregular bleeding, dyspareunia, Change in cervical mucus which becomes thick and
abnormal vaginal discharge may points to complete or viscous (progesterone effect) impairing sperm passage.
partial expulsion of IUCD but sometimes there may be no Increase fallopian tube peristalsis and making the ovum
complains. Longer or missing thread or missed menstrual or the fertilized ovum to reach earlier to the uterus
period are other possible presentations. Expelled IUCD which is not prepared to receive it.
may be seen by the client (complete expulsion) or felt in Alteration of endometrium: There is an exhaustion
the vagina (partial expulsion). and atrophy of endometrial glands and thinning of
endometrium. Decidua does not form and hence, no
Under Research IUCDs implantation can occur.
Progesterone receptor modulator (CDB-2914) to be used Methods of use is to be explained. Start with first
as IUCD. 5 days of last menstrual period. If taken at night, there is
less chances of nausea. If the pill is taken at the same time
Oral Contraceptives each day, it maintains hormone concentration in blood at
This is the method under the control of woman. OCPs are optimum level and make her more compliant.
very effective method of contraception and prolong use In event of missed pill:
If one pill is missed, take when you remember it and
do not cause any harm. Fertility returns within 3 months
today’s pill is taken at its stipulated time.
of discontinuation. It is freely available at all government
If started the packet late by 2 or more days or missed
outlets free of cost. But it does not protect from STIs
2–4 pills during 1–7 days of menstrual cycle, then she
including HIV. The common available OCP are:
can continue taking one pill per day and use another
• Combined oral contraceptive (COC)
contraceptive method for 7 days.
• Progesterone-only pill (POP)
If missed 2–4 pills during 15–21 days of the cycle, finish
• Multiphasic pills
all white pill (one per day), do not eat iron pills and start
• Centchroman
a new pack.
• Combined non-estrogen POP pill and under research
Newer concept-extended cycles: Woman takes mono-
OCPs
phasic pill for more than one month without a break.
• Male pills.
Though there is not much information for long-term safety.
Combined Oral Contraceptive It is also more expensive. Two types of pills are available:
1. Seasonale: It has ethinyl estradiol 30 mcg and 150 mcg.
Monophasic pills: They contain estrogen and progesterone
LNG in each 84 tablets with 7 non-hormonal pills. Its
in the same amount in 21 tablets. Last 7 pills contain no
pearl index is 0.78.
hormone, only iron tablets. They are simple to use, do not
2. Lybrel: It has ethinyl estradiol 20 mcg and 0.09 mcg
interfere in sexual act. The monophasic pills contents are
LNG in each 365 tablets.
as follows:
The last has pearl index of 0.09 with newer progestins, Advantages
desogestrel. There is no increase in the body weight, no Lesser days of bleeding, reducing overall blood loss
premenstrual symptoms, dysmenorrhea and acne. Advantages for the patients with menorrhagia.
Mechanism of action of COC pills are:
Inhibition of ovulation by suppressing gonadotropin
Progesterone-only Pill (Fig. 77.21)
releasing hormone (GnRH) and in turn FSH and LH. It is useful in lactating mothers (as quality and quantity of
There is no LH surge and ovulation does not occur. milk is not affected by progesterone). They act by thickening
Drug Estrogen Progestogen

Enovid Mestranol (150 mcg) Norethynodrel (9.85 mg)
Mala D Ethinyl estradiol (30 µ) Norgestrel (0.15 mg)
(Available in market @ ` 3/pkt)
Mala N 30 µ Levonorgestrel (0.15 mg) (Available at Government health facilities, free)
Marvelon 30 µ Desogestrel (1.50 mg)
Loestrin –1/20 20 µ Norethindrone (1 gm)
Crisanta/Yasmin/Rasmin 30 µ Drospirenone (3 mg)
Dronis –20 20 µ Drospirenone (3 mg), 24/4 days off
Contraception 727
Non-contraceptive advantages of oral contraception

Cycle stabilized
Lesser premenstrual tension
Lesser dysmenorrhea
Menorrhagia is cured—there is less blood loss and
hence, anemia is reduced

Protection against endometrial cancer. Even shorter use
(as small as one year) reduces the chances upto 50% and
the effect lasts for 15 years (by reducing cell division)
Epithelial ovarian cancer is prevented. This effect is due
to prevention of ovulation
Protection against benign breast diseases, e.g. fibroade-
nomous disease, colorectal cancer

Protection against functional ovarian cyst
Protection against PID, endometriosis, acne, hirsutism
and ectopic pregnancy

Fig. 77.21: Progesterone-only pill Third generation progestin increases high density
lipoprotein (HDL)/low density lipoprotein (LDL) ratio.

of cervical mucus decreasing sperm penetration. Affects Side effects: Minor ones are:
To avoid nausea and vomiting (due to estrogenic effect
endometrial maturation preventing implantation of
fertilized ovum. Also interfere with corpus luteal function. passes off in 2–3 weeks time), use the pill at night
Headache
There is erratic suppression of ovulation.
Acne and oily skin
Side effect: Staining in between periods.
Failure rate of POP: 1.3 pregnancy/100 woman years. Menstrual irregularities—breakthrough bleeding, hypo-
Available in India are: Cerazette/ZeroGen (contain menorrhea, amenorrhea.

desogestrel 0.075 mg per tablet). Newer POP with 4 mg Major adverse effects:
(24/4). Drospirenone and desogestrel only pill are recently Cardiovascular system (CVS)—hypertension (due to water
introduced with less bleeding . retention by estrogens)

Vascular effects—venous thromboembolism (VTE)
Multiphasic Pill • Arterial thromboembolism

They reduce the total progesterone intake per month Liver—increase cholestasis
with similar efficacy of monophasic pill. They have less Neoplasia—increase of hepatocellular adenoma
amenorrhea, breakhtrough bleeding and acne. • Increase of risk of breast cancer

Triphasic pill (triquilar): The dose of ethinyl estradiol is • Increase risk of dysplasia, cancer in situ of cervix and
0.03 mg is same in all pills.. The concentration of progesto- invasive cancer cervix by causing ectopy.
gen varies as follows:
LNG, 0.05 mg for first 6 days, 0.075 mg for next 5 days and Centchroman (Saheli) (Fig. 77.22)
0.125 mg in last 10 days. It is a non-hormonal pill. Its active component is ormel-
It is not commonly used. Main disadvantage is break- oxifene (non-steroidal). It is an Indian product, developed
through bleeding. by Central Drug Research Institute (CDRI), Lucknow.
Four-phasic pill (Qlaira): In this pill, for first two days it
contains estradiol valerate (E2) 3 mg and dienogest (DNG) Mechanism of Action
2 mg. Next 5 days pills have E2, 2 mg and DNG, 2 mg. Next It has a potent antiestrogenic and weak estrogenic action
17 days has E2, 2 mg and DNG, 3 mg, last 2 days pill contain It slightly increases the speed of movement of zygote
E2, 1 mg and DNG, 3 mg. through the fallopian tubes
• Blastocyst formation is accelerated
Disadvantages • Uterine endometrial proliferation is suppressed and
There is failure due to error in taking dated pills. It cannot formation of deciduous is defective (uterine epithe-
postpone menstrual dates when needed. lial tissue mitosis is blocked).
Progesterones—reduce spermatogenesis but also cause

loss of libido and potency.
Long-acting androgens—cause serious metabolic side
effects.
Antiandrogenic drugs like cyproterone acetate and fluta
mide reduce spermatogenesis and causes decreased
libido and gynecomastia.
Under trail is oral Desogestrel, 75–300 mg daily with SC
testosterone pellets, this suppresses the gonadotropin
secretion profoundly, and within 8 weeks some men in
300 mg group are azoospermic. HDL cholestrol does
not change.
Other drug under trial is prolactin. It inhibits sperm
atogenesis in dogs. Exact mechanism of action is under
investigation. It may become future Male Pill.
Nofertyl pill—low dose gossypol
Mifepristone—disable sperms by acting on sperm
Fig. 77.22: Centchroman (Saheli)
membrane
Extract from tripterygium—wilfordii and triptolide—is
All these effects are combined to prevent implantation a male pill in China.
because of in-coordination between endometrial matura-
tion and zygote development. Injectable Contraceptive (Fig. 77.23)
Method of use (30 mg): First tablet on first day of the Efficacy of all preprations are more or less same viz. 0.0–0.3
cycle, then one tablet twice a week at the same time for per 100 woman years.
2 months then once a week. No side effects of hormonal Depot medroxyprogesterone acetate (DMPA)
contraceptives are there. There is doubtful association of Norethisterone enanthate
benign ovarian cyst with its use which is being investigated. Cyclofem
Failure rate: 1–4/100 woman years. Mesigyna
Any deviation may lead to pregnancy. If period is Lunelle
delayed beyond 15 days, she must consult the physician.
Deladroxate
Other similar drug which acts on embryogenesis and pre-
GnRH antagonist
implantation is under trial.
Under research injectable hormonal contraceptives
Male injectable contraceptives.

Non-estrogen Combined Pill and other Under
research oral Pills Under injectable contraception, the most popular are
DMPA—150 mg, pregnancy rate is 0.04/100 woman year.
The widely used RU 486 (mifepristone) delays folliculo-
It is given in every 3 months by IM route.
genesis and luteinization. This property is under investi-
gation to design a non-estrogen combined pill.
First 15 days RU 486 (mifepristone) 5 mg/day is taken,
next 13 days, medroxyprogesterone acetate (MPA) 10 mg/
day be used.
It does not inhibit ovulation but retarded the endome-
trial maturation and hence, prevent implantation. Conse-
quences of long-term therapy is under study.
Other antiprogestins under trail are ZK 98, 734, ZK 78
and 299, HPR 2000.
Male Pills
They have not been successful so far with Mala pill. Various
drugs are tried. Fig. 77.23: DMPA and NET-EN injections
Contraception 729
NET-EN—200 mg (two monthly). The salt is norethisterone out affecting libido. In another trial, intranasal NET-EN
enanthate. First injection is given within seven days of was administered daily—number of sperms was con-
beginning of period (so as to be sure that injection is given siderably reduced. These changes are reversible on dis-
in non-pregnant period). Immediately after abortion and continuation of drug
six weeks after delivery. It has been seen to be harmless, Inj testosterone undecanoate combined with testoster-
if given early after well-establishment of lactation. Side one and progesterone preparation for contraceptive
effects—are mainly episodes of irregular bleeding. Hence, effect by augmentary suppression of gonadotropins
proper selection of patients and counseling is essential. Combined etonogestrel implant with testosterone
Other side effects are bone density loss and delayed return (Implanon rod with testosterone pellets)
of fertility which are reversible. Combination of cyproterone acetate with testosterone.
Depo-subQ provera 104—has 104 mg of MPA in 0.65 mL Non-contraceptive benefits of progesterone injections
given as SC injection which is effective for 3 months. It Protect against endometrial cancer
causes fewer side effects, such as weight gain. Estrogen Protects against PID
is added and irregular bleeding, only progesterone Reduces incidence of anemia by reducing blood loss
injection stops. The CIC available are injection Cyclofem— Reduces dysmenorrhea
previously called cyclo provera has 25 mg of DMPA and 5 mg Reduces acute sickle cell crisis
of estradiol cypionate. Injection Mesigyna contain 50 mg Reduces ovarian cysts
NET-EN and 5 mg estradiol valerate. Lunelle has 25 mg MPA Decreases pain associated with ovulation.
and 5 mg estradiol cypionate. Deladroxate contain 150 mg
dihydroxyprogesterone acetophenide and 10 mg estradiol Implants
enanthate. These injections are given after every 30 days. Norplant
GnRH antagonist—is particularly useful for woman over Jadelle
35 years of age. A third generation compound antide (Nal- Implanon
Lys GnRH antagonist) is developed which is well-tolerated Planon
and is of sufficient potency. It is under trial for both Biodegradable and other implants under research
males and females. It acts by direct competitive (receptor Under research male implant.
saturation), inhibition to suppress FSH/LH secretion. It They are inserted (SC) and removed by a minor
needs a long-term delivery system to achieve and sustain procedure performed under local anesthesia. Pregnancy
higher serum levels (Depo delivery in the form of IM rate is less than 1/100 woman years. Although a irregular
microsphere or SC implants is under trial). Under research bleeding is commonly reported by users, it is a very effective
hormonal contraceptives. Three monthly injectable LNG method. The rate of ectopic pregnancy is very low. There is
butanoate (5–10 mg). no incidence of neoplastic and cardiovascular disease. The
Male injectable contraceptive: They are under trial. most important implants are as follows:
They are testosterone enanthate/testosterone undecanoate Norplant (Fig. 77.24) is a first generation implant
weekly, testosterone buciclate 3 monthly. These suppresses system. It is a subdermal implant containing LNG with
hypothalamic GnRH and pituitary gonadotropins. There six non-biodegradable silicon capsules. It gives 5 years
is less LH causing low-levels of testosterone, low-FSH of effective and convenient contraception.
levels, produce sertoli cell malfunction. Testosterone enan- Norplant-2 or Jadelle which consist of two silastine
thate gel + DMPA injection/daily. Testosterone enanthate covered rods releasing levonogestrel. Its use is upto
injection + LNG oral. Injections GnRH per day with weekly 5 years.
testoterone enanthate injections Implanon (Fig. 77.25) which consists of EVA containing
Inhibin and prolactin injections are also under trial. 68 mg in one rod releasing 3 etonogestrel and have
Inhibin is peptide hormone found in gonads. It only a contraceptive efficacy of 3 years are classed as 2nd
suppresses the release of FSH from pituitary and thus generation implant systems.
could prevent sperm production without affecting Planon: It is a single rod 4 cm x 5 mm, made up of EVA
the production of testosterone. Prolactin injection copolymer with barium sulfate (to detect it by X-rays).
suppresses spermatogenesis in dogs. It promises to be It contain etonogestrel 68 mg. Initial release per day is
the future male contraceptive injection 70 mcg to 25–30 mcg/day by the end of its life (3 years).
A WHO study showed that long-acting androgen, when Biodergradable implants are under trial such as,
given by injection cause reversible oligospermia with- capronor, norethindrone pellet and microspheres.
Fig. 77.24: Norplant Fig. 77.25: Implanon
These implants deliver progestin from a carrier to be

inserted and do not need to be removed and may cost
less to manufacture.
Capronor has LNG. It provides effective contraception
for one and a half year. 17-a 19-norgesterone implants
for males.
Pellet contains NET-EN with cholesterol in 4 pellets,
each size of a grain of rice. It provides highly effective
contraception for one year. A B
Microspheres consist of a biodegradable copolymer Figs 77.26A and B: Contraceptive vaginal rings
similar to one used in synthetic absorbable surgical
suture and steroid hormone. They utilize ortho pH new
54 mm and 4 mm in cross section). Four designs are there
progestin—norgestimate which is less androgenic.
of which shell is most common. Combined one releases
A large clinical trial of 90 days NET-EN microsphere
ethinyl estradiol 15 mcg and 120 mcg of etonogestrel per day
system is currently under trial.
for 3 weeks. During this period, never keep it out of vagina
Luteinizing hormone receptor (LHR) antagonist pellet
for more than 3 hours; remove for a week (withdrawal).
is under trial.
Failure rate is 0.1–0.3 per 100 woman years.
Nestorone releasing single rod implant (release 100 Only progesterone containing vaginal ring: The vaginal
mcg/day). ring contain 2 gm micronized progesterone (used for 3
Male implant containing 7-a methyl 19 norgesterone. months). It is releasing 10 mg per day.
Male implant consists of LNG with testosterone Under research contraceptive rings are:
undecanoate injection every 8 weeks. Male implant of Ethinyl estradiol rings for once a year (Nestorone). Ring
testosterone enanthate with DMPA. showing dual action ring having protection pregnancy
and HIV infection. Progesterone receptor modulator ring
Contraceptive Vaginal Rings and
(CDB-2914).
Nova Ring (Figs 77.26A and B)
Offer an easy option for administration of contraceptive Transdermal Patches
steroid which is under control of woman. It is easy to insert Three-level patch (inner layer removed on insertion, 2nd
and removed by the woman. It delivers effective contra- layer is medicated layer, 3rd layer is protective polyester
ceptive dosage of steroid into the circulation by absorp- layer).
tion through the vaginal epithelium. It avoids the necessity A patch is 20 cm in size. During first 3 weeks of the cycle,
of remembering to ingest a pill daily and it bypasses liver, one patch is applied every week and then one week is patch
gives more uniform hormone levels. free. Areas used are lower abdomen, buttocks upper torso,
They are made of non-toxic silicon (ethylene vinyl upper outer arm but not on breasts (mostly non-hairy area).
copolymer). The release of hormones is proportionate to New patch is applied to a different area of skin on the same
their surface area and inversely proportional to the thickness day of week as previous patch. A combined medicated
of the outer wall (most common has outer 4 ring diameter, patch (Orth Evra) contain ethinyl estradiol (600 mcg) and
Contraception 731
norelgestromin-metabolite of norgestimate (6000 mcg)

release 20 mcg and 150 mcg of each drug respectively.
When to start first patch—started on any day after
excluding pregnancy within first 5 days of period.
If patch gets detached, apply within 24 hour at the same
body location and use backup method for 7 days.
Side effects: Skin irritation can be seen. Other side effects A B
are same as OCP pill. Not effective in obese patients (more
Figs 77.27A and B: Essure
than 198 lbs) does not protect against STIs/HIV. Perfect
use gives 0.3–0.7/ woman years is the failure rate.
Silicon rubber
Under Research Transdermal Contraceptions CuT with silastic ball at tip of the arm.
Gels and sprays are also modes of delivery of contraceptive Most commonly practiced is Essure (Figs 77.27A and
drugs. B)—it is non-incisional alternative to tubal ligation. A soft
Nestorone containing gel: This progestin mainly inhibit flexible microinsert is placed in each fallopian tube through
ovulation. Apply for 21 days (daily 2–3 mg per day). hysteroscope. It can be inserted after exclusion of pregnancy
Nestorone transdermal spray: 2–3 mg, once a day for and on any day of her cycle. It is taken as permanent method
21 days per month. of contraception because removal needs surgery and
there are no results yet on future functioning of tubes. The
Injection of Chemicals in Fallopian Tubes and patient must use an alternative method for contraception
Vas Deferens till hystrosalpingography (HSG) performed after 3 months
showing satisfactory results.
Injection in Fallopian Tubes
Quinacrine (QC) injection: Pellets or injection at the Intravasal Contraceptive Device (IVCD)
fallopian opening went into disrepute for improper (Male Contraception)
selection of patients but has reemerged .
These are under trial like intratubal contraceptive devices.
Injection in Vas Deferens (Male Contraception) Researchers are trying to put some foreign body in the vas
Reversible inhibition of sperm under guidance (RISUG). deferens in males to produce temporary blockage leading
This method is developed in India. to contraception. The methods under trials are:
RISUG: Styrene maleic anhydride (5 mg) injected intra- Thick nylon thread
vasa deferens it coats its lining with a clear polymer gel Vas valves
having positive and negative electric charges. The difference Bayeux
of charges with the sperm, rupture its cell membrane as it Brigid end tube valves
passes through the vas deferens and its journey is stopped Reversible intravasal occlusive device (RIOD). It does not
before it reaches the ovum. Surrounding tissues are not protect against STIs/HIV. Use some other contraceptive
affected as they have no charge. method for first 3 months, the period in which growth of
A single injection has long lasting contraceptive effect tissue results in vas obstruction. One year failure rate is
(10 years). 0.2/100 woman years.
Insertion of Devices in Fallopian Tubes Contraceptive Vaccine (CV)

These are under trial. Temporary plugging of fallopian If we want success in population control, active immuni
tubes is done through hysteroscope. Various methods zation is the procedure of choice for this large scale
under research are as follows: family planning program in our country. Keeping in
Tubal blocking plug mind immunization against polio and other diseases the
Essure (flexible microinsert) (Figs 77.27A and B) contraceptive vaccine holds many attractive attributes,
Crafts ceramic plug confirms long-term effective reversible protection against
Hossemian polyethylene plug pregnancy, follow a single or a couple (booster) of injec-
Preformed silicone plug tions, (i) no side effects of drugs which are seen with other
Nylon intratubal device—hamou methods of contraception, (ii) no device (IUCD) or implant
to be inserted, (iii) effective even if the client has no active provides a second chance of protection against unwanted
involvement after immunization (e.g. taking oral drugs or pregnancy for woman who experience contraceptive
injection), (iv) it covers many clients in a shorter period failure (e.g. condom ruptures), woman not using any
of time, (v) inexpensive and (vi) acceptable, thus fulfilling methods and who have unplanned sex (including rape).
properties of an ideal contraceptive. These methods of EC intercept pregnancy at ovulation,
The active immunization depends on generation of an fertilization or implementation depending upon the time
immune response directly against the target antigens in the of unprotective sexual act. There are two methods:
reproductive tract. In contraceptive vaccine, three types 1. Postcoital drug use
of antigen are targeted in 3 different stages of development 2. Insertion of IUCD.
of human reproduction cycle. They are: These 2 methods prevent pregnancy in 75% and 99%
1. Production of the gamete cases respectively. Though the usual and recommended
2. Function of the gamete practice is to seek assurance that a woman has not been
3. Outcome of the gamete. sexually exposed at the time of insertion. IUCDs have been
The research was started by Dr G P Talwar in National deliberately inserted on an experimental basis, immedi-
Institute of Immunology (NII), Delhi. ately after unprotected intercourse, when a woman might
The vaccines so far tested are: become pregnant, so as to prevent or interrupt the implan-
β-hCG linked with tetanus toxoid injection
tation of a fertilized ovum in the uterus. This procedure
β-hCG linked with DPT vaccine
shows no morbidity.
β-hCG linked with LH
Vaccine against LHRH (Luteinizing hormone releasing Oral Emergency Contraceptive

hormone).
The most commonly used drug is norgestrel 1.5 mg as
Other immunologic methods under trial are:
single dose taken as early as possible after unprotected
Induction of mucosal immunity in the genital tract
exposure. It will prevent pregnancy upto 120 hours for
along oral vaccine: It appears that uterus does not have
that unprotected act. Various mechanisms of action,
a significant secretory immunoglobulin (IgA) defense
according to the time of menstrual cycle are
system, but is permeable to systemic IgG. Hence, this site
• If exposure was before ovulation there is prevention
can be manipulated by systemic oral vaccine. The local
genital tract (cervix + vagina) has strong local secretory of ovulation or delay in ovulation beyond the period
immunity and thus local immunity can be induced of sperm survival
at these sites. Therefore, in both females and males, • Thickening of cervical mucus preventing sperm
a primary oral immunization followed by repeated movement

local (vaginal or rectal) boosters by self-administered • Endometrium development is altered, preventing
suppositories at regular intervals would appear to have implantation of fertilized ovum due to altered hor-
best chance of being successful. Hence, a contraceptive monal pattern
vaccine will find its way into family planning practice in • Fallopian tube mobility is altered hence, alters the
near future. transport of sperm, ovum and fertilized ovum
Intrauterine neem oil instillation: Neem oil generate • It may cause absent or subnormal LH surge hence,
local cell mediated immune response against pregnancy. ovulation dysfunction
Neem seed oil was instilled into the uterine cavity— • Corpus luteal function is impaired.
cytokines are generated which kills spermatozoa or Hence, there is action on ovulation, fertilization (affecting
embryo hindering pregnancy. sperm mobility) and implantation of fertilized ovum.
Thus, with more choice of contraceptive methods with Other drugs used for EC are:
less and less complications, doctors can have a method of High dose estrogen—they produce many side effects
choice for different individuals as far as possible and thus like vomiting.
helps in reduce the population explosion. Yuzpe regimen uses 50 µg ethinyl estradiol and 0.5
mg norgestrel 2 tablets twice 12 hours apart and it will

Emergency Contraception (EC) (Morning after protect upto 72 hours. Though side effects were less but
pill or Postcoital contraceptive) they were still there. She can use 4 tablets of COC pill
Unintended pregnancy has many social, personal and (30 mg ethinyl estradiol and 0.03 mg norgestrel) twice
financial consequences besides dangerous to health. EC at an interval of 12 hours.
Contraception 733
PERMANENT METHODS
Female sterilization
Male sterilization
Female Sterilization
It is the most common method of contraception in India.
It was first performed in 1823 in London by Dr J Blundell.
By 1950 and 1960, it was initiated in several countries. It
can be performed per abdominally (minilaparotomy or
laparoscopically) and per vaginally.
Methods Per Abdomen

After a postpartum or puerperal waiting period of
Fig. 77.28: E-Pill 24 hours for rest after delivery, the operation can be
performed upto 7 days after parturition
Mifepristone (RU 486)—antiprogestogen 10 mg dose Ligation itself is not an indication for cesarean section,
as soon as possible. It is anti-implantation in action. concomitance with CS
Menstrual disturbances are seen. With MTP or evacuation of incomplete abortion in the
Danazol, 400 mg twice at an interval of 12 hours. It is same setting
luteolytic in action. With gynecological operations of Manchester repair,
Centchroman—two 50 mg tablets given twice at 12 vesicovaginal fistula (VVF) repair
interval within 72 hours of exposure. It is still under trial Interval sterilization (in between two pregnancies)
for this indication. preferably at least 6 weeks after delivery and beyond.
Ulipristal—an orally active synthetic progesterone Do it within 7–10 days of onset of menstrual period to
receptor modulator. It inhibits or delays ovulation. The prevent any chances of pregnancy.
dose is 30 mg stat. Vaginal sterilization—as such alone or with
E-Pill is available free of cost by Government of India as Manchester repair or MTP.
an emergency contraceptive (Fig. 77.28).
Advantages of EC pills: Prevent unwanted pregnancy Laparoscopic Sterilization
and illegal abortion, thus improve health of woman in With MTP
reproductive age group. With surgical procedures—Manchester repair and VVF
repair
Intrauterine Contraceptive Devices (IUCDs) Alone as interval surgical procedure.
Copper-containing IUCDs can be used as a very Government of India, Ministry of Health and Family
effective postcoital contraceptive if used within 5 days of Welfare prohibit laparoscopic sterilization after second
unprotective sex (98%) even if multiple exposures. The trimester miscarriage and just after delivery. In these
incidence of ectopic pregnancy does not change and EC cases, male sterilization or minilaparotomy procedure is
does not impair future fertility. It is specially suitable for allowed. This is because fallopian tubes being larger get
woman who want to continue to use it as regular method. torn more often and recanalize easily (failure).
Eligibility criteria for female sterilization (case selection)
Advantages (see Chapter 59).
Pregnancy rate is <1%
Continued contraception
Counseling (see Chapter 59)
Subsequent intercourses protected. Information given about sterilization are:
It is a safe and simple procedure
Disadvantages It is a permanent method and reversal is not 100%.(that
Infrastructure and training required also require a major surgery). The surgery has its own
After checking and ruling out PID. complications.
Sexual pleasure is not interfered with and can perform Advantages of Female Sterilization
day-to-day activities as usual. A safe, effective, convenient method. After proper training,
There is a small chance of failure
an MBBS doctor can perform this operation. Complications
There is no protection from STIs/HIV or AIDS
are mostly minor. When performed according to accepted
She is encouraged to ask questions to clarify doubts
medical standards (Government of India Manual). No
She is told that she has the option of deciding against
special equipment or training is needed (compared to
the procedure without sacrificing her right to other laparoscopic sterilization). It can be performed soon after
reproductive health services childbirth, abortion or as interval sterilization. It is once only
It is not compulsory or binding. It is voluntary. It is not procedures. There is no need for long-term contraceptive
taken when the woman is sedated or under stress. A supplies.
printed consent form is provided by the Government
The husband’s consent is not essential. Complications
Preoperatively: Medical history is taken. Do physical 1.8% major and 14% of minor complications are reported .
examination and tests of hemoglobin and sugar and Wound infection: This is the most common complication.
albumin in urine are carried out. Tetanus toxoid is given (if Sometimes hematoma formation and subsequent infection
not previously immunized). Informed written consent is can occur. Intraperitoneal hemorrhage, bowel and bladder
taken. The hemoglobin must be 8 g or more. (Government of injuries are rarely seen. Ectopic pregnancy is an uncommon
India manual on standards for female and male sterilization complication.
service, 2006). Female sterilization gives no protection against STDs
Who can perform: Female sterilization by mini-laparotomy. including HIV/AIDS.
Only a trained MBBS doctor can do this operation. However,
laproscopic sterilization is to be performed by a trained Male Sterilization
gynecologist (DGO/MD) or a trained surgeon with a MS Male permanent method: It is called vasectomy. It can be
degree. performed under local anesthesia.
Premedication/Anesthesia/Analgesia tablet alprazolam The scrotum is cleaned and drapped. The vas deferens
(0.25–0.50 mg) or tablets Diazepam (5–10 mg), a night is stabilized between the fingers and local lignocaine
before is given. An IV line is secured. General or spinal is injected. After giving time for the anesthesia to act an
anesthesia is given in postpartum sterilization. incision is given over the vas and it is brought out. It is
ligated and cut. The procedure is repeated on the other
Techniques of Operation (see Chapter 59) side through the same skin incision. The vas is deposited
Pomeroy’s method, modified Pomeroy’s method (Figs back and skin incision is stitched. Scrotal support is given.
77.29A to G) and minilaparotomy (see Chapter 59). Both cut pieces of vas deferens are sent for histological
Other methods of female sterilization by laparotomy are: examination.
Irving method (see Figs 59.2A to D). Nowadays, non scalpel vasectomy (NSV) is done. Here,
Uchida method: The medical tied end of the fallopian scalpel is not used to incise the scrotal skin. Instead, a
tubes is retracted into the mesosalpinx after tying and special sharp pointed artery forceps is used to pierce the
cutting it. skin and it is dilated and the procedure of vasectomy is
Parkland method: The tube is tied at two ends after making carried out as given above. An alternative method of family
a window in an avascular portion of the mesosalpinx and planning is used till 3 months/when semen examination
cut in between (see Figs 59.3A to C). shows no sperms.
Complications are mostly local viz. hematoma formation
Coagulation Methods (immediate) and local infection.
Bipolar coagulation Failure rate are comparable to female sterilization.
Unipolar coagulation. Advantages of vasectomy are:
Bipolar cautery method (see Fig. 59.4A): Here, the tube is The procedure is very simple and can be easily learned
cauterized by electric cautery at 2 points. by an MBBS doctor.

Fimbriectomy: The fimbrial ends are cut and tied. Abdomen is never opened hence, major complications
Vaginal tubal ligation: (see Chapter 59). are not seen.

Contraception 735
A B C
D E F
Figs 77.29A to G: Female sterilization (by modified Pomeroy’s technique).

G Female sterilization (Final result)
1. Will the pill cause birth defects if a woman wants to become pregnant in the future?
2. Can a woman use emergency contraceptive (EC) pills as a regular method of family planing?
3. Will using an injectable contraceptives increase a woman’s risk of contracting HIV?
4. If a man uses a condom, will he be able to have an erection?
i. Oral contraceptives
ii. IUCDs
iii. Male pills
iv. Sterilization
i. Beside the condom, the another barrier method of birth control is ____________.
ii. ____________ method is called natural family planning.
Index
Page numbers followed by f refer to figure and t refer to table, respectively.
A Adenosine deaminase 428 Amodiquine 482

Adequate response to treatment 154 Ampulla 15
Abdominal aorta 21, 321f Adherent placenta 318, 319, 322 Anal sphincter
Abdominal circumference 192, 206, 578, Adnexa 151 external 323
582 Adrenal gland diseases of 396 internal 323
Abdominal ectopic pregnancy 143f Adrenocorticotropic hormone 65, 259, 336, Analgesia 260
Abdominal enlargement 92 493 Anamnestic response 437
Abdominal examination 122, 126, 186, 196, Adult respiratory Anaphylactic shock 511
206, 214, 237, 291, 312 disease syndrome 402, 432, 513 Anastomoses 21, 22
Abdominal incision 544 failure 161 Anchoring villi 61
Abdominal muscles in nullipara 343f Ageing of placenta 65 Androgen excess 121
Abdominal pregnancy 77f, 143 Agglutination tests 92 Android pelvis 270, 270f, 274
Abdominal retractor 691 Alanine aminotransferase 421, 505 Andros score 296t
Abdominal ultrasound 183 Alanine transaminase 154 Anembryonic sac 573f
Abdominal wall 78, 578 Alfa-fetoprotein 97 Anemia 319, 357, 360, 373
weakness 345 Alkalemia 564, 565 in obstetrics 360
ABO incompatibility 441 Alkaline phosphatase 170, 182, 420 mild 362
Abortion 677 Alkalosis 564 moderate 362
first trimester 677 Allantois 68 physiological 79
incomplete 584, 585f Allogenic lymphocyte immunization 131 severe 362
mid-term 677 Alloimmune factors 129 signs of severe 45
missed 677 Alpha methyldopa 681 Anencephaly 214, 579f, 706, 706f
preventing unwanted 654 Alpha-thalassemia Anesthesia 260, 527, 563
safe 659 minor 375 difficulty in 504
unsafe 653, 654 syndromes 375 for cesarean section 264
with saline 447 Amenorrhea 90, 715 in severe pre-eclampsia 409
with urea 447 period of 122 Anesthetic complications 545
Abruptio placentae 162, 167t, 447 Amniocentesis 72, 97, 183, 187, 217, 598, Anganwadi worker 661
Acardiac fetus 595f 598f Angiotensin converting enzyme inhibitor
Accelerated lipolysis 386 complications of 599 216, 358, 682
Accidental hemorrhage 162, 162f, 163, 164t Amniogenic cells 70 Antacid therapy 265
Accoucheur’s arm 300 Amnioinfusion Antedates pregnancy 425
Accredited social health activist 663 role of 619 Antenatal
Achordia 69 Amnion care 43, 94, 237, 322, 362, 379, 471, 472,
Acid base development of 70, 70f 508, 652, 654, 660
balance 81 epithelial cells 70 exercises 94, 101
disturbance 566t mesenchymal cells 70 period 173, 282, 319, 509
Acid-fast bacilli 427 Amniotic cavity 55 surveillance 603
Acidemia 564, 565 Amniotic fluid 71, 186, 188, 215, 583, 601, Antepartum fetal surveillance 453, 603, 604
Acidosis 588 607 tests for 607t
Acne 495 amount of 71 Antepartum hemorrhage 158, 166, 171, 181,
Acquired immune deficiency syndrome composition of 71 191, 210, 211, 258, 360, 373, 439, 508, 511,
188, 349, 467, 509, 539 cytokine 182 539, 582, 627
Acquired anemias 373 embolism 256, 433, 434, 447 Anterior asynclitism 224
Acquired defects of uterus 128 examination 183 Anterior parietal presentation 224
Acquired hemolytic anemia 373 index 160, 172, 189, 192, 213, 588, 607, Anteroposterior diameter 29
Acromegaly 395 612 Anthropoid pelvis 269, 270f
Acrosin 53 volume 175, 183, 193, 374, 407, 606, 612 Anthropometry 631
Activated partial thromboplastin time 81, 424 abnormalities of 209, 213 Antianxiety drugs 682
Acupuncture 109 Amniotomy 255, 553 Anticancer drugs 683
Acyanotic lesions 383 artificial rupture of membrane, Anticardiolipin antibodies 200
Addison’s disease 396 advantage of 165 Anticonvulsant medications on fetus 458
Antidepressants 682 Aspiration Biomedical waste 665

Antidiuretic hormone 78, 124, 194, 214 cytology 428 categories of 667t
Antidote 412 of fetal fluids 600 container 666f
Antiemetics 679 of gastric contents 265 management 665
Antiepileptic Asthma 430 and handling rules 665
dosage of 459t in pregnancy 430, 679 Biophysical profile 188, 607
in pregnancy 680 labor, management of 431 Biopsy 594
side effects of 459t Asymmetric intrauterine growth Birth
Antihistamines 679, 683 restriction 191 asphyxia 303
Antihypertensive Asymptomatic bacteriuria 417 attendants 662
drug in pregnancy 408t Asynclitism 223, 224, 224f defects, types of 592
in acute crisis 681 posterior 224 of aftercoming head 293
in pregnancy 680 Atonic uterus 319t of baby with anomaly 40
therapy 413 Atopic eczema 495 of buttocks 292, 293f
Atosiban 185 of head 226f, 294
treatment 408
Atresia choanae 593 of shoulders 293
Antinuclear antibody 128, 129
Atrial natriuretic peptide 193 Bishop’s cervical score 253, 253t
Antiparasitic 683
Atypical eclampsia 410 Bispinous or transverse diameter 28
Antiphospholipid 128
Autoimmune hepatitis 425 Bladder injury 545, 552
antibody 200 Autosomal trisomy 127 repair 552
syndrome 609 Auxiliary nurse midwives 94, 477, 661 Blade portion 698
Antiretroviral 473 Azygos 22 Blades, application of 702
drugs 473 Blastocyst biopsy 595
therapy 467, 476
initiation 473 B Blighted ovum 126
Blocking antibodies 87
Antisepsis in operation theater 515 Bacillus Calmette-Guerin 430 Blond-Heidler decapitation saw 561f, 696,
Antithyroid drugs 453, 682 Backache 104f, 346
696f
Antitubercular drugs 428t Bacteremia 512
Blunt curette 528
Antitubercular treatment 428 Bacterial infection in uterus 484f
B-lynch
Antiviral 683 Bacteriostatic 71
brace sutures 322
Aortocaval compression 265 Bacteroides 350, 512
suture 321f
Apgar scoring fragilis 185
Bolus intravenous 676
role of 628 b-adrenergic stimulant 512
Bony pelvis 19, 20, 24, 311
system 628t Bag and mask 625
Brachial plexus palsies 304
Aplastic anemia 361 ventilation 626f
Bracht’s maneuver 300
Apnea 637, 638 Bag of membranes 282
Brandt-Andrews
primary 623 Balfour abdominal retractor 692, 692f
maneuver 249f
secondary 623 Ball of fire 135 technique 248
Apocrine glands 8 Balloon mitral valvotomy 381 Braxton Hicks contractions 74, 75, 92
Appendicitis, acute 504 Balloon occlusion 322 Breast 77f, 78, 676
Appetite, abnormal 90 Bandl’s ring 312, 312f, 313f abscess of 91, 340, 354
Arbor vitae 13 Barbiturates 262 anatomy of 338
Arcuate uterus 282 Barker hypothesis 194 care of 101
Arcus tendinei 20 Bartholin’s cyst 9, 9f changes in pregnancy 91f
Areola tubercles 77f Bartholin’s gland 7, 9, 9f discomfort 90
Arm lever theory 225 Basal body temperature method 713, 714 engorgement of 340, 636, 676
Aromatherapist 109 Battledore insertion of cord 212 examination 100
Arrest disorder 309, 309f Benzodiazepines 262 function of 338
Artemisinin 482 Beta-adrenergic-receptor inhibitors 415 milk 338t
Arterial blood gas 432, 564 Beta-agonists 678 composition of 338
sample 564, 565 Beta-blockers 681 expression of 340
Arterial embolization 155, 551 Beta-human chorionic gonadotropin 90, 204 nodule 631
Artery forceps 691 Beta-thalassemia 376 physiology of 338
mosquito 962f minor 376 structure, internal 338f
Artery ligation, internal 551, 551f Bicornuate uterus at laparotomy 128f Breastfeeding 336, 338, 430, 431, 456, 470, 471f
Artificial rupture of membrane 72, 161, Bile duct 426 advantages of 337
165, 166, 207, 213, 255, 284, 553 Billing’s method 714 contraindications of 341
Asepsis in operation theater 515 Binovular twin 169 difficulties in 339
Asherman’s syndrome 128 Biodergradable implants 729 exclusive 477
Aspartate aminotransferase 421, 505 Bioethics problems of 353
Asphyxia, physiology of 623 in obstetrics 646 technique 339
Index 739
Breech Carezza 713 Cervix 12, 13, 75, 231, 279

diagnosis of 292f Carneous mole 126 before labor in primigravida 231
engagement of 293f Carpal tunnel syndrome 346, 463 changes in 92, 332
types of 285f, 289, 290f Carunculae myrtiformes 10, 333 condition of 50
Breech crowning 293f Caudal analgesia 263 dilatation of 528f
Breech delivery 296 Centchroman 727, 728f effacement of 230
Breech presentation 49f, 285, 289, 290f, 291 Central tendon of perineum 12 in primigravida 231
management of 294 Central venous pressure 165, 512, 557, incompetence of 181
prognosis for 303 softening of 230
558f, 562
Cesarean delivery 296, 307, 471, 538, 542,
Breech trial 304 catheters 557
543t, 544
British lock 699f line removal 558 Cesarean hysterectomy, steps in 547f
Broad ligament 20, 151, 324 monitoring 557 Cesarean in twin
hematoma 316 Cephalhematoma 632 pregnancy 177
Bronchial asthma 430 Cephalic application 700, 701f Cesarean section 161, 178, 273, 497, 503,
Bronchiectasis 432 curve 698 529, 538, 542, 559, 614, 689, 702
Bronchopulmonary dysplasia 485, 638 presentation 50f for breech presentation 304
Brow 50f Cephalic version in placenta previa 161
presentation 281, 281f, 285 external 177, 178, 284, 285, 533, 535f types of 544
Bulbocavernosus muscle 12, 20 under anesthesia 534 Chadwick’s sign 91
Bulbourethral glands 9 with fetal acoustic stimulation 534 CHAMOCA 154
Burns Marshall maneuver 300, 300f with tocolysis 535 Chest
Burst abdomen 352 Cephalopelvic disproportion 100, 228, 239, compression 626, 627f
246, 252, 275, 307, 311, 380, 391, 509, 510, retractions 637
C 543, 618, 652, 695, 700 X-ray 448
Chickenpox 486
Cesarean, indication of 497 Cephalosporines 351
Cephalotribe 695, 695f Chignon 703
Calcitonin gene-related peptide 80
Cerebral Child
Calcium 111, 675
channel blockers 185, 681 dysrhythmia 410 health 660
Camper’s fascia 8 edema 410 mortality rate 664
Canal of Nuck 8 hemorrhage 410 sex ratio 643f
Candida albicans 76 malaria vs eclampsia, diagnosis of 481t in India 642
Capillary refill time 634 palsy 484, 638 survival and safe motherhood 660
Caput succedaneum 36, 36f, 227, 312 pathology 173 Childbirth, complications of 650
Car belt position 106f vein 463 Childhood illness, management of 662
Carbamazepine 680 thrombosis 373, 463 Children, benefit to 711
Carcinoembryonic antigen 149 Cerebrospinal fluid 32, 150, 214, 488, 560 Chlamydia trachomatis 144, 98, 121, 133,
Carcinoma 504 Cervical 181, 183, 185, 486
cervix 120 canal 75 Chlamydial infection 486
thyroid 454 cancer 650 Chloasma 78f, 493
Cardiac cap 718, 719f Chlorambucil 154
arrest 266 dilatation 307f Chloroquine 482
conditions during pregnancy 384 ectopic pregnancy 142, 142f Cholecystitis, acute 505
disease 273, 652 Cholelithiasis 505
encirclage 553
failure 512, 659 Cholestasis of pregnancy 507
exploration 549f
massage 514 Chondroitin sulfate A 479
fibroid 311
ligaments 548f Chorioadenoma detruens 147
gel 254f
Cardinal movements 223, 224f Chorioamnionitis 200
incompetence 128, 131
Cardinal virtues 647
index 131 signs of 188t
Cardiogenic pulmonary edema 431
length 182 Choriocarcinoma 148, 148f, 149f, 156, 650
Cardiogenic shock 511, 514
motion tenderness 135 Chorion laevae 62
Cardiopulmonary resuscitation 434
mucus 76, 714 Chorion, development of 70f
Cardiorespiratory system 633
Cardiotocograph 177, 204, 498, 599, 606, method 715f Chorionic
611, 696 palsies 304 adenocorticotrophins 67
Cardiotocography polyp 120 frondosum 62
monitoring 190 ripening 230, 677 gonadotropins in
machine 697f score 176 serum 92
recording 612 softening 229, 230 urine 92
diseases 653 stenosis 311 thyrotropin 67
effect 676 stitching 324f villus sampling 96, 97, 376, 435,
system 171, 237, 331, 333, 363, 402, 727 tear 548 596, 597
in labor 80 weakness 181 complications of 598
Chromosomal anemia of newborn 437 Corticotropin releasing hormone 83, 182,

abnormalities 72, 95, 96, 191, 217 anomalies 173, 291, 303, 387, 393 205, 222, 336, 478
anomalies 121 cystic adenomatoid malformation 587f Cotyledon 61, 63, 64, 64f, 319
types of 594t defects of uterus 128 Couple protection rate 711
Chronic ectopic diaphragmatic hernia 602 Couvelaire uterus 165, 166f
pregnancy 574 heart disease 191, 199, 379, 383 Cowper’s glands 9
with bone elements 574f hypothyroidism 455 Cracked nipple 354
Chronic fetal compromise 296 malaria 480 Cranioclast 695, 695f
Chronic hepatitis 425 malformations 170, 199 Craniopagus 170
Chronic hypertension 358, 399, 414t, 609 Rubella syndrome 487, 487t Craniosynostosis 632
with pre-eclampsia 416 syphilis 489 Craniotomy 155, 281, 560
with pregnancy 414 Congestive heart failure 418, 431, 452 Cranium 576f
Chronic infections 360 Conjoined twins 179f, 311 C-reactive protein 183, 188
Chronic intertwin transfusion 172 Contraception 156, 169, 375, 384, 476, 711 Cretinism 112
Chronic liver disease 425, 493 advantages of 711 Crista dividens 58
Chronic maternal morbidity 650 natural methods of 713 Crochet 695, 695f
Chronic polyhydramnios 214 Contraceptive Cromolyn sodium 679
Chronic renal disease 419 prevalence rate 711 Crook lying 106f
Cilia 15, 133 vaccine 731 Crown rump length 57, 93, 96, 199, 543,
Circummarginate placenta 210 vaginal rings 730, 730f 575, 582
Circumvallate placenta 210, 211f Contraction stress test 193, 603, 606, 610 Crowning 233
Cirrhosis 425 procedure 606 of fetal head 227
Cisterna chyli 23 Convulsions Cruciate 560
Classical cesarean section 545, 545f causes of 410 Crude birth rate 664
Cleidotomy 561 control of 411 Crude fetal kick 5
Clitoris 7, 9 Coomb’s test 437-439 Crura 9
Clostridia 513 Copper T 476 Cry 631, 634
Clostridium perfringens 373 Copper-bearing Culdocentesis 11, 12f, 135, 135f, 352, 536, 536f
Clostridium welchii 203 devices 724 Cullen’s sign 138, 505
Clot retraction time 126 IUCDs 721 Cup pop-off 705
Clotting time 126, 164, 201 advantages of 723 Curve of Carus 30
Clubfoot 580f, 581f Cord abnormalities 200, 209, 212, 213 Cushing’s disease 494
Coagulation changes 81 Cord blood, collection of 441 Cushing’s syndrome 396
Coagulation disorders 200 Cord coiling 212 Cyanocobalamin deficiency 372
in pregnancy 444 Cord compression 287 Cyanosis 637
Coccydynia 346 Cord entanglement 173 Cyanotic heart disease 383
Coccygeus muscle 20 Cord in pelvis 287 Cyclic adenosine monophosphate 53
Coitus Cord presentation 285, 286, 286f Cyclofem 729
intercurtis 713 Cord prolapse 285, 286, 286f, 510 Cyclophosphamide 154
interrupts method 713 Cord traction 248, 249f Cyst 212
reservatus 713 Cord, insertion of 212 Cystic defect in spine 579
saxonicus 713 Cordocentesis 438, 599 Cystic fibrosis 432
Colboma 593 Cornified vaginal wall 11f Cystitis and pyelonephritis 417
Collagen-vascular disorders 419, 609 Cornua 15 Cytomegalovirus 121, 191, 485, 488
Collapse in obstetrics Coronal suture 31 Cytotrophoblast 60
causes of 511 Coronary artery disease 384 Cytotrophoblastic shell 61
types of 511 Coronary syndrome, acute 384
Colles’ fascia 8 Corpora cavernosa 9
Colostrum 338 Corpus albicans 15, 16f
D
Colpotomy 12f, 352, 536, 536f Corpus luteal Dactinomycin 154
Complete hydatidiform mole 145 cyst 16f Daily fetal movement record 605
Complete miscarriage 125 hematoma 136 Dais 654
Complete perineal tear 324f Corpus luteum 16f Dead fetus 695
Complex adnexal mass 574f of pregnancy 76 Deaver’s retractor 691, 692f
Concealed accidental hemorrhage 163f vascularization 583, 583f Debdas’s cranial perforator 560, 696
Concealed hemorrhage 162 in wall 584f Decidua 62, 74
Condom 717 Corpuscular hemoglobin concentration 361 basalis 62, 211f
Congenital Corpuscular volume 361 capsularis 62
abnormalities 212, 593 Corticosteroid-binding globulin 83 changes in 87
of uterus 181 Corticosteroids 512, 513 of pregnancy 62f
adrenal hyperplasia 99, 396, 599 role of 407 parietalis 62
Index 741
spongiosum 64 mellitus 127, 196, 200, 358, 386, 507, 652 Early neonatal problems 635
vera 62 classification of 386 Early version, advantages of 533
Decidual reaction 62 in pregnancy, complications of 386 EC pills, advantages of 733
Decidual/placental bleeding 42 type I 390t Eclampsia 398, 399, 403, 410, 422
Deciduate 63 Diabetic ketocidosis 392 management of 412
Decongestants 679 Diabetic nephropathy 419 Ectocervix 14f
Deep circumflex artery 21 Diamniotic-dichorionic fused 169f Ectoderm 56
Deep sole creases 631 Diamniotic-monochorionic placenta with Ectopic pregnancy 133, 135, 136f, 137, 138, 572,
Deep transverse arrest 279, 279f cords 170f 583, 585, 722
Deep venous thrombosis 373, 425, 447, 448 Diazepam 413, 682 anatomy of 134
Deflexed head 50f Dichorionic diamniotic 572f diagnosis of 137
Deflexed occipitoposterior 310 placentae 178f fate of 137
Dehydroepiandrosterone sulfate 121, 127, 222 Dietary in fallopian tube 140f
Deladroxate 729 habits 45 treatment of 139
Delivery 381, 391, 460, 475, 619 intake of lactating women 341t Ectopic ruptured 574f
care during 193 modifications 364 Ectopic with fetus 574f
decision for 165 Diethylstilbestrol 121, 133, 683 Edinburgh postnatal depression scale 500
estimated date of 43 Dimorphic anemia 372 Effacement in primigravida 231
in abruptio placenta 166 Dinoprostone 677 Electronic fetal 5
involved during 302 gel instillation 554 monitor 612, 613
mode of 391 gel kit 555f Embryo
normal 230 instillation 554f development of 55, 55f, 56f
of aftercoming head 299 Discordant twins 172 Embryonal plate evolution 56
of anterior buttock 293f Disinfectant solution 475 Embryonic
of arms 292 Disposable gloves 671 disc 55
Disposal of biomedical wastes 667t plate 55
of baby 247
Disseminated coagulation intravascular stage 56
of head 295f
161, 165, 166, 325, 352, 402, 422, 433, Emergency contraception 654, 663, 712, 732
of infant 544
446, 512, 514, 548, 708 Emergency obstetric care 654, 660
of lower limbs 292, 297f
Diuretics 415, 682 Empty-ovum 145, 707
of nuchal arms 299f
Dizygotic twin 169 Encephalocele 633
of posterior
Doderlein’s bacilli 11, 12 Endemic goiter 453
arm 198
Doll’s eye maneuver 633 Endocervical
buttock 293f
Dopamine 512 canal 555
of shoulder 292, 294f, 298, 298f
Doppler evaluation 578 length 131
of upper limbs 298f
of aorta 587f mucus 597
place of 497 Endocervix 14f
Doppler machine 49f
preparation for 623 Endocrine disorders 354, 395
Doppler spectrum 583
surface, clean 349 in pregnancy 386
Doppler ultrasound 438, 608
timing of 391 Endocrine
Doptone 696, 697f
Depo-medroxyprogesterone acetate 476, factors 127
Dorsoanterior 282f
509, 728 function of placenta 65
Down syndrome 508
Depression 501 glands 83
Droperidol 679
during pregnancy 500 pregnancy 395
Droplet infection 517
Dermal nitroglycerine patch 679 Endoderm 56
Ductus arteriosus 58
Dermatological problems in pregnancy 493 Endogenous opioids 335
Ductus venosus 58, 193, 376, 588
Desamino-oxytocin 676 Duffy system 441 Endometritis 350
Desogestrel 728 Dührssen’s incisions 305 development of 350
Destructive operation 559, 563 Duodenal atresia 214 Endometrium 13
complications of 563 Dysfunctional labor 306 alteration of 726
types of 559 Dysfunctional uterine bleeding 650 attachment to 88
Detrusor muscle 18 Dystocia matrix metalloproteinases 88
Dextran 368 classification of 306 Endomyometritis 545
Dextrorotation 74 effects of 311 Endoparametritis 350
Dextrose normal saline 392 prevention of 311 Endoscopic retrograde
Dhaka regimen 412 cholangiopancreatography 426
Diabetes 214, 358, 386, 609 Endotoxic shock 511, 512
complicating pregnancy, classification E Endotracheal 625
of 387t Ear 633 intubation 627
in pregnancy 388, 390t anomalies 593 Energy nutrients 342
insipidus 395 cartilage 631 during pregnancy 110
Environmental toxins 122 Female condom 717, 718f compromise 256, 616
Enzyme immunoassay 183 Female genital organs 7, 8f, 12, 16f condition 67, 406
Enzyme linked immunosorbent assay Female pelvis with death 199, 591
(ELISA) 481 false pelvis 25f late 199
Epidural analgesia 263 true pelvis 25f demise 200
Epilepsy 458 Female sterilization 538, 733, 735f deterioration 607
on fetus 460 advantages of 734 development 56, 68f
on pregnancy 458 eligibility criteria for 538, 733 abnormalities of 591
E-pill 733f Femidom 717 anomalies 586
Episiotomy 248, 530 Femoral artery 21 in weeks of gestation 57f
breakdown of 533 Femoral length 192 distress 616
cutting scissors 692 Femoral nodes 23 management of 616
median 532f Femoral pulse, palpation of 321f signs of 616
mediolateral 532f Femoral vein puncture 557f effects 591
scissors 693f Femoro-pelvic grip 299 exposure 590
Episodic decelerations 614 Femur length 206, 577f, 578, 582 factors 470, 604
Epithelioid trophoblastic tumor 156 Fenestrated placenta 210, 210f causing preterm labor 182
Epoophoron 16 Ferguson’s reflex 75 fibronectin 183
Epstein-Barr virus 423 Ferning 186, 187f growth 170
Ergonovine 676 Ferric salts 366 disproportional 191
Ergot alkaloids 675 Ferrous form of iron 361 restriction 112, 191, 216, 421,
Ergot derivatives 676 Ferrous salt 366 460
Erythema multiforme 495 Fertile day 714 hand 31, 578f
Erythema nodosum leprosum 685 Fertile window 714 head
Erythema toxicum 636 Fertility engagement of 33
Erythroblastosis 436 awareness-based method 713 entrapment of 305
Erythryopoetin, role of 369 indicators 664 extension 294
Escherichia coli 127, 337, 353, 512 influence on 143 flexion of 226
Esophageal atresia 637 reduction 660 structures in 576f
Essential hypertension 414 regulation 660 heart 146, 583
Ethyl alcohol 678 regulatory methods 134 auscultation 611, 612t
Etoposide 154 Fertilization 53, 59 rate 160, 177, 183, 237, 247, 284,
Evisceration 560 Fetal 167, 185, 188, 195, 206, 215, 216, 280, 534, 588, 605, 611
Ex utero intrapartum surgery 602 469t sound 93, 98, 126, 160, 166, 177,
Extra-amniotic saline infusion 255f abnormalities 97t, 311 186, 201, 275, 312, 498,
Extracellular matrix 230 acidosis 313 543, 599
Extrachorial placenta 210 acoustic stimulation test 611 hypothalamic pituitary adrenal axis 222
Extracorporeal membrane oxygen 619 activity, maternal assessment of 604 hypoxia 588
Extrapulmonary TB 428 adrenal subsequent 313
gland rupture 304 indications 252, 543, 699
hypoplasia 68 injuries 303
F age 591 leg 578f
Face 32, 48, 50f, 280f, 575, 578 anatomy 575 lobule 65f
to pubis position 303f anomalies 205 lung
Falling hair 517 presence of 294 maturation tests 608
Fallopian tube 7, 12, 13, 15, 15f, 76, 133, 134, ascites 311 maturity, test for 608
333, 731 attitude 221 macrosomia 387
injection in 731 biometry 578, 582 manifestation 437
Fallops rings 542f principles of 582 maturity 188, 294
Familia slim 721 biophysical profile 582 membranes 60, 69, 70f
Family planning 711 biparietal diameter 296 nasal bone 96
advice 347 blood transfusion 601, 601f neurodevelopment 607
services 663 breathing movements 607 nutrition 110
Fascia ligaments 19, 20 catecholamines secretion 611 orbits 576f
Fas-fas ligand system 88 causes 191, 199, 214 outcome, poor 604t
Fat 111 cells in ovoid 50, 221
soluble vitamins 342 maternal circulation 596 presentation 285f
Fatty liver of pregnancy, acute 420, 421 mother 97 prognosis 287, 303, 413
Feeding 344 chemoreceptors 611 pulse oximetry 615
cup 341f circulation 58, 58f, 59 sensor placement 615f
exclusive replacement 477 complication 173, 195, 196, 387, 404, 599 reduction 601
poor 394 in precipitate labor 310 reserve 287
Index 743
sacrum 291 causes of difficulty in 702 Gestational age 188, 194, 571t
scalp blood sampling 615 technique of 700 determine 187
scalp stimulation test 615 types of 699, 699f neonate 194
sex 170 Forceps delivery 301, 699 Gestational assessment 631
skull 31, 31f, 32f, 33, 33f, 34f, 34t contraindications of 699 Gestational diabetes 95
during labor 33 Forceps over ventouse, advantages of 695 mellitus 95, 386, 388
parts of 32 Forewaters 233 Gestational hypertension 398, 402
stillbirth 202f Fossa navicularis 8 mild 402
stomach 577f Fourchette 8 severe 403
surface 64, 64f Four-phasic pill 727 Gestational sac 585f
surgery 601 Frank breech 291, 296 Gestational thrombocytopenia 423
surveillance 193 Free-floating bowel loops 580f Gestational trophoblastic
therapy 600 Frenulum 8 disease 68, 145, 150, 151
tissue biopsy 600 Fundal dominance 232 treatment of 152
tone 607 Fundal grip 47, 47f tumor 151, 151t, 153
urine 600 Fundal pressure 197f Gingivitis 495
Fetomaternal bleed, amount of 440 Fundus 12 Glairy 636
Fetomaternal leak 435 Funic 286 Glands of cervix 75
Fetomaternal surveillance 390 souffle 49 Glans 9
Fetus 31 Funnel pelvis 279 Glomerular filtration rate 79, 171, 334, 401, 417,
adverse effect on 684t 450, 458
and fetopelvic relations 31
assess 165 G Glucocorticosteroid treatment 68
Gluconeogenesis 386
chronic hypertension on 415 Gallbladder 82 Glucose
dead 289 diseases of 425 challenge test 95, 388
development of 55 Gamma glutamyl transpeptidase 422 tolerance test 127, 196
during labor 611 Gamma-aminobutyric acid 680 transport 194
during pregnancy 590 Gartner’s cysts 11 Glycemic control during labor 391
effect on 117, 364, 371, 374 Gartner’s duct 16 Glycosaminoglycans 253
teratogenic on 684t Gastroschisis 580f
with molar tissue 147f Gonadotropin-releasing hormone 130,
Gene 131t, 335
with nuchal translucency 575f therapy 602
Fibrin antagonist 729
transfer 602 Gonorrhea 486
clot 445 Genesis of
degradation products 163, 445 Graafian follicle 15f
cerebral palsy 485 Gram-negative bacilli 512
formation 445
intraventricular hemorrhage 484 Grandmother therapy 437
stabilization 445
Genetic Grannum’s grading 582
Fibrinolytic inhibitors 445
abnormalities 127 Granulocyte colony stimulating factor 88,
Fibrinolytic system 445
counseling 593 176
Fibroid 128
center 644 Granulocyte macrophage colony
Fibronectin 182
Fiduciary 641 diagnosis, pre-implantation 594 stimulating factor 88
Fimbria ovarica 15 disorders 358 Granulocytes 87
Fimbrial end 15 history 44 Graves’ disease 455
Fimbriectomy 734 influence 400 Gravid uterus 506
Fine needle aspiration cytology 453 laboratory 644 Gravida’s hip 266f
First pelvic grip 48f metabolic diseases 646 Green armytage
First trimester Genital clamp 692f
invasive techniques in 96 organs, internal 7 uterine 692
miscarriages 124 structures 151 Group B streptococcal 177
Fistula 650 tract bacterial infection in pregnancy 490
Fluorescent in situ hybridization (FISH) 598 infections 185 Growth hormone 395
Fluoride 112 involvement 151 Growth restriction 172
Fluroscein staining for trisomy 21 598f malignancy 358 Gynecoid pelvis 269, 269f
Folic acid 110f, 675 Genitalia 631, 634
deficiency 371 local examination of 238
Follicle-stimulating hormone 66, 83, 130, Germinal epithelium 15 H
333, 335, 439, 716 Gestation 67f Habitual miscarriage 126
Food fortification 365 age 191 Haig Ferguson’s forceps 689, 690f
Foot exercises 104 assessment 632t Halothane anesthesia 319
Foramen ovale 58 of pregnancy, period of 675 Hand
Forcep, application of 701f period of 186, 193, 505f, 707 clean 349
in final rinse, position of 520f High density lipoprotein 727 Hyperpigmentation of areola 493
infected areas of 517f High-risk pregnancies 507 Hyperplacentosis 160
washing 517, 672 Hippocratic oath 646 Hyperprolactinemia in pregnancy 679
techniques of 517 Hirsutism 77f Hypertension 358
Hartman’s sign 90 Histocompatibility complex 87 causes of 416
Head 150 Histogenesis of amniotic cells 70 classification of chronic 414
anterior rotation of 227f HIV positive pregnant women, in pregnancy 398
circumference 578, 582, 631 management of 471 classification of 398
descent of 295f Homan’s sign 448 proteinurea 707
extension of 227f Hormonal IUCDs, secondary 414
external rotation of 227f advantages of 724 Hypertensive disorders 200
flexion of 225f disadvantages of 725 in pregnancy 162, 653
in occipitoposterior position 303f Hormone 55, 683 Hypertensive retinal changes 406t
shape of 225 Human chorionic Hyperthyroidism 146, 451, 452
Hypnosis 109
Hearing fetal heart sound 49f gonadotropin 65, 66, 96, 136, 139, 148,
Hypocalcemia 394
with fetoscope 48f 163, 335, 572, 600
Hypochlorite solution 669f
Heart 578 thyrotropin 66
Hypochromic microcytic anemia 363f
and blood vessel changes 80 Human growth hormone 67
Hypogastric artery 22, 551
defects 593 Human immunodeficiency virus 44, 94, 121,
Hypothalamic-like releasing hormones 67
disease 357, 358, 378, 507 237, 349, 357, 427, 467, 476, 483, 509, 539, Hypothyroidism 451
management of 379 600, 616, 665, 711, 722 primary 455
failure 384 disease in women 477 with thyroid tissue 455
rate 629, 634 exposed infant 476, 477 Hypotonus 275
controlling agents 381 exposed newborn 475 Hypoxia 410
Heartburn 81 in children 468 in fetus 393, 612
Hegar’s sign 91, 92f infected pregnant women 477 of neonate 393
Helicobacter pylori 82 infection 472 Hysterectomy 153, 155
HELLP syndrome 404, 405 negative pregnant women 472 Hysterosalpingography 130
Hematological indices 364t negative women 477 Hysteroscope 731
Hematoma 212, 325 on pregnancy 475 Hysterotomy 529
Hematuria 316 patients in India 467t Hystrosalpingography 731
Hemmorhagic stroke 463 testing for 95
Hemodynamic effects of exercise 102 transmission to unborn baby 473
Hemodynamic readjustment 334 Human leucocyte antigen 87, 129, 400, 599
I
Hemoglobin 94, 100, 130, 161, 237 Human papillomavirus 650 Icterus gravis neonatorum 437
measurement 363 Human placental Identical twins 169
Hemoglobinopathies 361, 373, 646 lactogen 65, 67, 84, 136, 148, 335 Iliac arteries 21
Hemolysis 404 trophoblastic 145 external 21
Hemolytic anemia 360, 373 Human sex ratio 59 Iliac branches, internal 21
Hemolytic disease, manifestation of 436 Hyaluronidase 53 Iliac group, internal 23
Hemorrhagic shock 165, 511 Hydatidiform mole 145, 146f, 147, 152, 573f, Iliac lymph nodes 23
external 23
Hemorrhoids 101, 506 707, 707f
internal 23
Hemostatic changes in pregnancy 446 Hydralazine 415, 681
Illicit drug 470
Heparan sulphate proteoglycan 55 Hydramnios 282
Immediate delivery 187
Hepatic mild 214
Immune cells 88
function 404 moderate 214
Immune tolerance 85, 88
metastasis 150 severe 214 in pregnancy 86, 86f
resection 155 Hydrocephalic head, decompression of 560 Immunity against self 128
rupture 304 Hydrocephalus 311, 632 Immunization 101
Hepatitis Hydroclave 667 Immunoassay
B antigen 95 Hydroxyprogesterone caproate 678 card test 66f, 92f
surface antigen 95, 237 Hymen 7, 10 with radioisotopes 93
virus 704 Hyperandrogenism 131 without radioisotopes 92
C virus 94 Hyperbilirubinemia 394 Immunofluoresence assay 481
E antigen 95 Hypercoagulability 446 Immunoglobulin 129
fulminant 424 Hypercoagulable state 81 G 128
Herpes gestationis 495 Hyperemesis 146 M 486
Herpes infection 485 gravidarum 117, 118t, 423, 679 Immunological function 65
Herpes simplex virus 488 Hyperextension of fetal head 301 Immunology of normal pregnancy 85
Heterotopic ectopic pregnancy 141 Hyperglycosylated hCG 150 Imperforate hymen 10, 10f
Index 745
Implantation bleeding 120 Intrauterine 136 Jaundice

In situ hybridization 597 contraceptive device 121, 134, 348, pathologic 442
In vitro fertilization 128, 131t, 134, 594 375, 409, 453, 476, 509, 712, 719, 733 physiologic 442
Infant mortality rate 664 death 40, 173, 182, 193, 199, 216, 404, Jugular venous pressure 380
Infant of diabetic mother 392, 393 421, 436, 437, 447, 451, 553, 597, 603
Infection 121, 127, 191, 199, 200, 203, 217, devices 162 K
349, 533 fetal death 167, 199, 202f, 252, 590f, 603 Karyotype 145, 147, 598, 707
acute 360 management of 202 Kassowitz law 489
ascending 127 fetal demise 282 Kelley’s clamp 724f
during pregnancy 490 of one twin 172 Kidd system 441
in children, routes of 468t fetal growth restriction 170, 359
Kidney 401
in females, routes of 468 fetal resuscitation 616
function test 411
in preterm labor, role of 483 growth restriction 94, 123, 161, 172, 182,
Kielland’s forceps 279, 690, 691f
postoperative 497 191, 201, 210, 248, 252, 285, 296, 401, 418,
Killer immunoglobulin like receptors 400
with gamete of Plasmodium falciparum 431, 442, 480, 489, 495, 507, 533, 582, 599,
Klebsiella 512
481f 613, 638, 676, 710
KN Das’ forceps 690, 690f
Infertility 722 infections 485
Koilonychia 363f
period(s) of 44 Neem oil instillation 732
Krishna Menon regimen 5, 413
treatment of 43 transfusion 441, 470f
Kristellar’s maneuver 299
Intravasal contraceptive device 731
Infrared irradiation 346 Kyphosis 271, 271f
Intravascular extravillous
Infrared spectroscopy 611, 616
cytotrophoblast 63
Infusion pump 676f
Intravascular transfusion 441t
L
Inhalational analgesia 262 Labetalol 415, 682
Intravenous access 265
Inhaled beta-agonists 679 Labia majora 7, 8
Intravenous fluid 408
Inhaled corticosteroids 430 Labia minora 7, 8
Intravenous immunoglobulin 131t, 441
Inhaled steroids 679 Labor 82, 173, 204, 206, 215, 229, 230, 236,
Intravenous pyelography 590
Injectable contraceptive 728 Intraventricular hemorrhage 184, 193, 483, 375, 381, 460, 510
Insulin 637, 679 abnormalities of 307
resistance 386 Invasive mole 147 analgesia 260, 261
therapy 390 Invasive mole, complications of 148 anticipation in 313
Insulin-like growth hormone 336 Inversion, duration of 325 assessment 247
Intact membranes 286 Inversion-incomplete inversion 325 augmentation of 252, 676, 677
Intelligence quotient 194 Iodine 112 course of 280, 283
Interischial spinous diameter 311 Iron 111, 675 during induction 257
Interleukin 136 absorption of 361, 362 dystocia 306
Internal iliac deficiency 360 management of 308
artery 22 anemia 361, 364t false 237t
branch of 22 dextran 368 first stage of 107f, 108f, 177, 246, 296
Internal podalic version 177 folic acid 362, 661 in right occipitoanterior 226
Internal rotation of hydroxide-sucrose complex 369 induction of 203, 253, 380, 252, 257, 676
breech 293f in singleton pregnancy 361t in third trimester 677
head 295f preparations 366, 367t management during 190
shoulders 294f in combination 366 management in 295, 380
Interstitial extravillous cytotrophoblast 62 requirement 368 management of third stage of 248, 319,
Intertwin transfusion, acute 172 in pregnancy 361 370
Intestinal obstruction, acute 506 stores of tissues 363 mechanism of 221, 223, 292
Intra-amniotic injection 187 supplements 113 normal 246, 250t
Intracellular adhesion molecule 479 Ischemic stroke 463 on fetal head, effects of 227
Intracranial hemorrhage 303, 313, 702 Ischial spine 17, 28 onset of 279f, 293f
Intracranial lucency in first trimester 575f Ischial tuberosities 280 outcome, exercise in 102
Intracranial status of fetal head 32 Ischiopagus 170 pain 259, 260, 261f
Intraembryonic mesoderm 55 Isoimmunization 72, 217, 435, 609 phases of normal 307f
Intrahepatic cholestasis of pregnancy 420 Isoniazid 425, 428 physiology of 230
Intranatal sepsis 313 Isotretinoin 683 premonitory signs of 236
Intraoperative complications 545 Isoxsuprine 184 preparation of 229
Intrapartum Isthmus 12, 75 prolonged 653
asphyxia 200 room 474f
fetal monitoring 611 J admission to 238
infection 311 Jacquemier’s sign 91 second stage of 247, 296
management 177 Jacquemier-Chadwick sign 493 stage of 287
stimulation with oxytocin 256t Low fecundity 508 cardiovascular risk, classification of 379t
trial of 273, 296 Low forceps 699 causes 192, 214
true 237t Low inclination 26 complications 173, 195, 404, 600
with anemia, management of 369 Low lying 160 condition 703
with pre-eclampsia, management of 409 Low molecular weight heparin 432 corticosteroid 679
Lactate dehydrogenase 372 Low platelet count 404, 505 death 651, 652, 656, 663
Lactating mother 715f Lower segment causes of 653f
Lactation amenorrhea method 713, 348, 715 cesarean section 44, 99, 166, 281, 497, prevent 653
Lactation mastitis 354 544, 617, 600 698 exhaustion 699
Lactobacillus 12 uterine lacerations 545 factors 603
Langhan’s layer 60 Lower uterine segment 158, 544, 551 causing preterm labor 181
Laparoscopic electrocautery of ovarian Lubra serosa 332 fetal indications 543
surface 131 Lumbar plexus 22 heart disease 609
Laparoscopic salpingostomy 140f Lung hyperandrogenicity 127
Laparoscopic sterilization 538, 733 disease 433 hypoxia 192
Laparotomy 137 function tests 83t immune rejection 87
Laproscopic ligation 540 maturity 72, 217 indications 252, 543, 699
Laproscopic sterilization 542f parameters during pregnancy 83t infection 483, 484
Leg Lupus anticoagulant 200 in preterm labor, role of 483
cramps 101 Lupus erythematosus 496 iodine deficiency 452
exercises 104 Luteal phase defect 127, 130 legs hyperflexed 197f
Leiomyoma uterus 282 Lutein ovarian cysts 146 malaria on neonate 480
Leishman donovan 364 Luteinizing hormone 66, 83, 121, 335, 716 morbidity 287, 545
Leukocyte count 130, 141, 154, 183 receptor antagonist 730 severe 40
Levator ani 19, 20 Lymph nodes 23 mortality 40, 161, 313, 506, 545, 651,
Levothyroxine 450 Lymphatic drainage of female pelvis 7, 23, 652, 652t
Lewenberg’ sign 448 23t ratio 651, 664
Ligament 76 Lynch brace suture 551, 551f nutrition during lactation 341
round 20 Lytic cocktail parameters 189
Ligating uterine arteries 548f regimen 413 pelvis 24
Ligating uterosacrals 548f therapy 682
Lignocaine, effects of 526 prognosis 303
Liley’s graph 439f renal disease 68
Lip of cervix, posterior 536
M serum 67f
Lippes loop 720f Macerated stillbirth 199f, 201f alpha-fetoprotein 97
Liquor Macrocytic anemia 371f starvation 265
amnii 71, 612 Macrosomia 194, 393 surface 63, 64f
color of 612 Macrosomic fetuses 194, 631 systems 401
Listeria monocytogenes 121, 191 Magnesium 112 therapy 600
Listeriosis 489 salts 678 thyroid physiology 450t
Lithium 683 sulfate 184, 411, 682 weight gain during pregnancy 98
Litmus paper 186 Magnetic resonance wellbeing 246
Litzmann’s obliquity 224 cholangiopancreatography 426 Matthew Duncan method 234
Live fetus 700 Malaria Mature milk 338
Liver 401, 420 in pregnancy 479 Mature placenta with
disease 422 on pregnancy, effects of 480 membranes 64f
types of 420 severe 480, 482 umbilical cord 64f
enzymes 404 Male Mauriceau-Smellie-Veit maneuver 300,
function test 141, 154, 201, 407, 421, 453 condoms 716 301f, 304
transplantation 425 contraception 731 Mcafee Johnson regimen 161
Living ligatures 74f, 234, 332f injectable contraceptive 729 McRoberts maneuver 197
Local analgesia 263 permanent method 734 Measles 488
Local anesthetic agents 264, 264t pills 728 Meconium 617
Lochia 332 sterilization 734 amniotic syndrome 619
alba 332 Malformation 592 aspiration syndrome 617, 625
rubra 332 etiology of 593 present 624, 625
Loveset’s maneuver 299, 299f Manchester repair 311 stained amniotic fluid 613
Low backache 346 Manning’s biophysical profile 607 staining of liquor 421
Low birth weight 101, 123, 172, 181, 192, 427, Maternal Medical abortion, first trimester 677
543, 594, 623, 631 and child health 663 causes 117
Low density lipoprotein ratio 727 blood flow 65f disorders 121, 357, 510
Index 747
nutrition therapy 390 Mimicked 585 Multiple sclerosis 462

risks to teenage mothers 509 Minilaparotomy 540 Mumps 488
service factors 659 Mirena 721f Myasthenia gravis 462
termination of pregnancy 72, 97, insertion, steps for 724 Mycobacterium avium 472
128, 133, 333, 527, 538, 542t, 641, 659, Mirror syndrome 437 Mycobacterium tuberculosis 428
662, 677, 708 Miscarriage 43, 120, 598 Mycoplasma hominis 121, 127, 483, 485
Medicolegal problems 642 incomplete 125, 125f Mycoplasma pneumoniae 373
Medroxyprogesterone acetate 728 inevitable 123, 123f Myocardial dysfunction 394
Mefloquine 481 of early pregnancy 136 Myoma, effect of 503
Megaloblastic anemia 370 threatened 122, 122f Myometrium 13
Melasma 493 Misoprostol 677
Missed abortion 573f
Membranes
Missed miscarriage 125, 126
N
completeness of 320f
complications of 72, 209 Missed pill 726 Naegele’s obliquity 224, 224f
rupture of 98, 469 Missing strings 725 Naegele’s pelvis 272
Membranous placenta 210 Mitral stenosis 381 Naegele’s rule 42
Mendelson’s syndrome 265, 504 Mixed hemorrhage 162 Nails
Meningocele 633 Mobile air asepticizer 516f depressed 363f
Meningomyelocele 633 Molar gestation 677 proper cleaning of 517f
Menopause 15 Molar pregnancies 146f, 586, 650 Narcotic analgesics 262
Menses, resumption of 335 Mole, partial 147f Nasal
Menstrual Molluscum fibrosum gravidarum 494 bone 576f, 578
changes 722 Mongolian spots 636 flare 637
cycle 714f Monoamniotic-monochorionic twins 170f National AIDS Control Organization 467, 663
history 42 Monochorionic 572f National Family Planning Program 660, 719
hygiene scheme 663 Monochorionic-monozygotic 178f National Maternity Benefit Scheme 662
period 42, 186, 192, 205, 237, 460 Monophasic pills 726 National Nutrition Monitoring Bureau 110
regulation 529 Monosomy X 127 National Tuberculosis Control Program 428
Mentum 32 Monozygosity 594 National Vector Borne Disease Control
Mercury 666 Mons pubis 7, 8 Program 481
Mesenteric branch, inferior 21 Mons veneris 7, 8 Natural family planning 713
Mesigyna 729 Montgomery’s tubercles 45, 45f, 77f, 78 Nausea 100, 119, 506
Mesoderm 56 Morning after pill 732 causes of 117
Metabolic acidosis 512 Moro’s reflex 635, 635f in pregnancy 117
Metal cups 703 Mother Navicular cells 76
Metastases in trophoblastic neoplasia 152t and child Necrotizing fasciitis 352
Metastatic disease protection card 663 Neisseria gonorrhoea 98, 121, 181, 185, 486,
role of 155 tracking system 663 597
surgery in 155 and fetus, temperature of 102 Neonatal
Metastatic gestational trophoblastic benefits to 337 care unit 176, 391
disease 149 chronic hypertension on 415 complications 387
Methimazole 453 effects on 118, 364 hyperbilirubinemia 256
Methotrexate 154 to child transmission 95, 467 hyperthyroidism 456
Methyldopa 415 Mucosal block 361 illness, management of 662
Methylergonovine 676 Mucosal immunity in genital tract 732 intensive care unit 207, 625
Metoclopramide 679 Mülllerian ducts 11 jaundice 442, 636
Metritis 350 Multiagent chemotherapy 154 mortality rate 664
Microinfusion pump 256f Multicystic dysplastic kidney 580f reflexes 635
Microspheres 730 Multidose vial of injection resuscitation 623
Micturition, frequency of 90 cyanocobalamin 373f facilities 287
Midampullary ectopic 139 Multidrug resistant-TB 428 program 2010 629
Midampullary pregnancy, removal of 139 Multifetal Neonate
Middle cerebral artery 193, 376, 588 delivery 179 chemoprophylaxis 430
Middle rectal artery 22 gestation 168 effect on 364, 452, 453
Middle sacral 21 pregnancy 168 epilepsy on 460
Midpelvis 271, 296, 311 reduction 176 with unruptured meningomyelocele 633f
contraction 272 Multigravida 43, 223 Nerve supply 75
Migraine 463 Multiload 720f of pelvis 7, 22, 22t
Milk, formation of 340 Multiphasic pill 727 Nestorone containing gel 731
Milking of tube 139 Multiple gestation 291, 588, 609 Nestorone transdermal spray 731
Millennium development goals 662 Multiple pregnancy 214, 590, 590f Neural tube defects 72, 217, 358, 459, 602
Neuraxial analgesia 263, 264t instruments 689 inhibitors 678

Neurogenic shock 511, 514 measures 474 reflex 338, 339f
Neurologic examination 634 medicolegal aspect of 641 roles of 676
Neurological operation 538 stress test 606
changes 77 destructive 695
disorders in pregnancy 458
Neuromuscular maturity 632
outcome 358 P
pharmacology in 675
Neuropathies 463 practice 553 Packed cell volume 161, 195, 369
NFP methods procedures, minor 525 Page’s classification 164t
advantages of 716 specimens in 706 Pain 163
Nicardipine 678 ultrasound in 571 after 331
Nifedipine 415, 678, 681 ventouse 698 anatomy of 260
Nile blue sulfate test 186 Obstetrical during labor, anatomy of 260f
Nipple of cervical excision 135
collapse 511
soreness of 339 relief 104, 249
examination 45
stimulation test 606 Pancreatic diseases in pregnancy 420
significance of cavity 28
Nitabuch’s layer 61 Pancreatic transplantation 426
transverse 27
Nitrazine paper test 186 Pancreatitis, acute 505
Nitric oxide donor 185, 408 Obstructed labor 311, 510
management of 313 Papanicolaou smear 98
Non-gestational trophoblastic disease 145
Obstructive lesions 383 Paracervical block 526, 526f
Non-obstetric causes of bleeding in first
Occipital Parametrium 76
trimester 120
bone 31 Parasympathetic nerves 22
Non-obstetric morbidity 651
Non-reactive nonstress test 605f encephalocele 579f Parathyroid gland, diseases of 397
Nonreassuring fetus status 616 Occipitoposterior 278 Parathyroid hormone 397
Nonsteroidal anti-inflammatory drugs position 225, 226, 274 related protein 66, 67
599, 677, 722 of head 301 Paraurethral
Nonstress test 176, 253, 391, 406, 534, 603, Odor of lochia 332 gland 9
605, 610 Oligohydramnios 71, 206, 215, 609 pouches 9
Non-verbal communication 38, 38f Omphalocele 580f Parenteral
Norgestimate 730 Oocyte 594 antibiotics 661
Normotension 399f Operative anticonvulsants 661
Nova ring 730 deliveries 642 iron 368
Nuchal arms 298 obstetrics 523 oxytocic drugs 661
presentation 298f Ophthalmia neonatorum 487 Parent-to-child transmission 467, 472, 533
Nuchal fold 96 Opportunistic infections 472 Parietal bone
thickness 578 Oral middle of 36
Nuchal translucency 96, 574, 575f contraception 169, 359, 476 left 36
Nulligravida 43 contraceptive 169, 421, 726 right 36
Nullipara 43 pills 432, 663, 683 Parietal presentation, posterior 224
Nulliparous cervix 333f selection 392 Parous cervix 333f
during lactation 109 emergency contraceptive 732 Paroxysmal nocturnal hemoglobinuria 373
during pregnancy 94, 109 Partial hydatidiform mole 148t
glucose tolerance test 388
of mother 110 Parturition phase 229
iron therapy 367
Nutritional status 130, 469 Parvovirus B19 121
steroids 679
Nutritional supplements in pregnancy 675
vaccine 732 Past obstetric history 43, 44
Nutritive functions of placenta 65, 66f
Osiander’s sign 91 Patent ductus arteriosus 184, 638
Nymphae 7, 8
Osteogenesis imperfecta 699 Patient-doctor communication 37
Osteomalacia 270, 271 Pawlik’s grip 47, 48f
O Ovarian Pelvic
Obstetric 264t, 545, 590 ectopic pregnancy 142 abscess 352
analgesia 259 ligament 20 application 700
anesthesia 259 pregnancy 143 colon 7, 19
anuria 316 torsion 136 contraction 269
care 654, 660 tumor 282, 503 curve 698, 698f
causes of bleeding in first trimester 120 vein 21 diaphragm 20
computed tomography in 589 Ovary 7, 15, 15f, 16f, 76, 333 dimension 27, 28
fistula 650 Oxytocics 675 division 230
forceps 689, 698, 698f Oxytocin 256, 335, 338, 675, 676 dystocia 269
grips 47 challenge test 676 examination 50, 124, 125, 126, 281
history, present 43 drip 165 floor 76, 104
Index 749
exercise 346 Pharyngeal injures 304 perfusion 64

injury 317 Phenothiazines 262 products 65
repair 17 Phenytoin 413, 680, 682 separation 233
slope of 225 Pheochromocytoma 396 signs of 234
grip 282 Phlegmasia cerulea dolens 448 Placental septa 64
inflammatory disease 137, 650, 721 Phosphatidylglycerol 183, 608 Placental sign 90
inlet 26, 26f Pilonidal sinus 633 Placental site 332
kidney 311 Pinard’s fetoscope 696, 697f trophoblastic tumor 145, 149, 151, 156
mass 280 maneuver 297, 297f tumors 151
organs Piper 301 Placental sulfatase deficiency 68
arterial supply of 21t forceps 302f, 691, 691f, 699 Placental transfer 65, 110
internal 13f Pituitary Placentation, abnormal 129, 131
peritoneum 19 diseases 395 Plasmapheresis 441
plane 27, 28 gland 83, 336 Plasmin 445
segments 29f hormone, posterior 675 breaks down 445
soft tissues 4 Placenta 60, 64f, 87, 170, 211, 211f, 248, 326, Plasminogen 445
tilting exercises 104 581 activator 445
tumors 282, 284 abnormalities of 209 inhibitors 445
Pelvis 25, 150, 271 accreta 211, 211f, 322, 322t Plasmodium 479, 480
contraction of 269, 282, 285 anatomy of 63, 209 falciparum 479, 480, 482
diameter of mid 28 bipartite 209, 210f malariae 479, 482
diseases of 271 calcification 582 ovale 479, 482
false 24 changes in 401 vivax 479, 482
lower true 24 decidua basalis intervenes 211f Platelet alloimmunization 442
mid 28 development of 60 Platypelloid 269
shape of 225 diffusa 210 pelvis 270, 270f
variations of 269 documentation of 178 Plicae palmatae 13
vertex in relation to 50f duplex 209 Podalic version 177
Pelvi-ureteric junction 99 examination of 203 external 178
Pemphigoid 495 expulsion of 234f internal 178
Polar body 594
Pendulous abdomen 282 functional subunits of 63
biopsy 595f
Peptic ulcer disease 506 functions of 65 Polycystic ovarian disease 127, 131t
Peptostreptococcus 350 grading 582 tests 131
Percutaneous umbilical cord blood in triplet pregnancy 177f Polycystic ovary syndrome 121, 388
sampling 596, 599, 599f increta 211, 211f, 314 Polycythemia 394
Perimortem cesarean section 546 manual removal of 321, 350, 555, 555f Polydioxanone 545
Perinatal mortality 171, 287, 313 marginal attachment of 212f Polyhydraminos 71, 213, 280
rate 664 maternal part of 62 acute 215
transmission 469 of twin pregnancy 709f grades of 214
Perineal body 12 percreta 211 mild 215
tear 323, 323f, 549 previa 158, 159f, 166, 167t, 211, 498, 581 severe 215
classification of 323 complications of 161t treatment for 216f
Polymerase chain reaction 376, 424, 481,
repair 248 type of 161
486, 595
Perineotomy 530 with hemorrhage 162 Polymorphic eruption in pregnancy 495
Perineum 7 without hemorrhage 161 Pomeroy’s method 540f, 539
clean 349 retained 318, 319, 321 technique 735f
climbing of 233 triplex 209 Positive airway pressure 629
laceration of 323 Placental amnion 71 Postcoital contraceptive 732
level of 248 barrier 62 Postmaturity syndrome 205
Peripartum biopsy 600 Postnatal
cardiomyopathy 384 causes 192, 214, 321 assessment 409
hysterectomy 547 circulation 64f exercises 343
seizures 461t estrogen synthesis 68 management 413
Peripheral NK cells 87 Postneonatal mortality rate 664
expulsion 234
Postpartum 179, 410
Peritrophoblastic flow 585f factors 285 blues 501
Periventricular leukomalacia 485 hormones 67 care 391
Peroxisome proliferator-activated infarcts 211 changes 331
receptors 55 lobule 61 complications 542t
Per-speculum examination 186 membrane 62 contraceptive advice 392
pH scale 564 migration 160 depression 40, 501
emergencies 354 on exercise, influence of 102 Prolactin 335, 728

Grave’s disease 455 on HIV disease, effect of 475 reflex 338f
hemorrhage 165, 168, 204, 209, 259, on malarial course, effect of 479 Promethazine 679
318, 319, 331, 360, 404, 421, 436, on myoma, effect of 503 Prominent veins 633f
503, 507, 510, 532, 539, 550, 649, on tuberculosis, effect of 427 Prophylactic antibiotics 522
676, 677, 700, 715 Prophylaxis 372
persistent ectopic 142
prevent 13, 74, 431 Propylthiouracil 453, 456, 682
pharmacology in 685
secondary 353 Prostaglandin 254, 256, 677
physiological changes in 73
intrauterine contraceptive device 348 dehydrogenase 223
positive signs of 93
neuritis 354 synthesis inhibitors 678
prevention of unintended 472
period and breastfeeding 462 Prosthetic valve 382
probable signs of 91
psychosis 502 Proteus 353, 512
renal failure 418 prolonged 205
role of X-ray in 589 Prothrombin time 81, 164, 424, 445
thyroid disorders 454 Protraction disorders 308
thyroiditis 454 seizures in 461
Prurigo of pregnancy 495
Post-term pregnancy 200, 609 signs 93
Pruritic conditions 495
causes of 205 specific factors 604
Pseudomonas 512
management of 207 specific β-glycoprotein 65
Pshychiatric disorders 464
Postures in early labor 108f symptoms of 93
Pshycological support 203
Potter facies 216 test 135
Psoriasis 495
Pouch of Douglas 11, 76, 135, 352, 536, 583 treatment in 481
in pregnancy 495f
Prague maneuver 304f weight gain during 78t Psychiatric disorders 354
Precipitate labor 307, 310f with diabetes mellitus, management of during pregnancy 500
disorders 310 389 in pregnancy 500
Preconception counseling 357, 375, 378, with multi drug resistant TB 428 in puerperium 500, 501
389, 460 with plasma protein A 192, 204 Psychological disorders 651
role of 451 with protein 66 Pubocervical
Pre-eclampsia 146, 398, 399, 399f, 403, 405, Premature fascia 19, 20
414t, 422, 447 baby 296 ligament 20
complications of 404 delivery 530 Pubourethrovaginal ligaments 20
development of 400 labor 181 Pudenda 7
management of 405 newborn, care of 637 Pudendal block 527f
prevention of 407 ovarian failure 127 anesthesia 527, 700
screening for 97 rupture of membrane 163, 171, 181, Puerperal fever 4
toxemia 574 185, 284, 508, 600, 676 hematoma 318
Pre-embryo development 55 Prenatal mood disorders 501t
Pre-existing diseases 653 diagnosis and therapy 596 pyrexia 349
Pregnancy 44, 117, 206, 215, 375, 378, 430, diagnostic test 644 sepsis 313, 351, 513
450, 609, 619 Pressure ventilation, positive 624, 629 Puerperium 44, 173, 215, 331, 370, 385, 510
anticoagulants in 680 Preterm birth abnormal 349
complications of 650 normal 331
prevention of 182
conditions in present 507 seizures in 461
breech delivery 304
diagnosis of 90 Pulmonary
infants 637
diseases angiogram 449
labor 161, 181, 182
coincidental to 423 artery hypertension 432
management of 183
specific to 420 aspiration 265
prevention of 176
disorders with 503 disease 273
duration of 479 Preterm premature rupture of membranes
185, 215, 606 edema 431
early 511, 583 with pre-eclampsia 431
effect on 371, 374, 421, 426, 430, 451, Preterm rupture of membranes 102, 161
embolism 354, 432, 447, 448
452, 503, 504 Primary adrenal insufficiency 396
hypertension 383
exercises in 103 Primary hypertension 414
metastasis 149, 149f
induced hemolytic anemia 373 Primigravida 43, 223
tuberculosis 428
induced hypertension 574 elderly 507
Pulsatility index 177
infections in 483 Prochlorperazine 679 Pygopagus 170
loss, management of recurrent 131t Progesterone 68, 335 Pyridoxine 679
management of unsensitized 438 deficiency 121, 127
mask of 78f, 493 effect 506
minor ailments of 100 only pill 726, 727f Q
normal 51 receptor gene 88 Quad screening 97
on epilepsy, effect of 458 with endometrial protein 130 Quadruplets with mother 168f
Index 751
Queen Charlotte’s hospital 4 Retention of urine 504 invasive techniques in 97

Quinacrine injection 731 Retinopathy of prematurity 638 miscarriages 124
Quintuplets 168 Retroplacental hemorrhage 582 Septic 349, 512, 638, 653
Retroverted gravid uterus 504 abortion 513
R Rhesus 94, 248, 435, 534 miscarriage 126
antibodies 95 pelvic vein thrombosis 352
Rabies 682 blood group in pregnancy, role of 435 Septicemia 447
in pregnancy 490 factor inheritance 435 Septum 10
Racket handle attachment 212 incompatibility 199 Serology 481
Radical salpingectomy 139 isoimmunization in pregnancy 435 Serotonin reuptake inhibitors 501
Radioactive negative patients 441 Serum
iodine 451 negative pregnant women, bile acids 421
waste 666 management of 437 FSH and LH levels 335
Radioimmunoassay 93 negative women before pregnancy 436f glutamic oxaloacetic transaminase 141,
Rapid diagnostic test 481 positive fetus 436f 505
Reactive nonstress test 605f sensitized, management of 438 glutamic pyruvic transaminase 141, 505
Recombinant human erythropoetin 368 Rheumatic heart disease 380, 381, 651 iron 363
Rectal arteries, superior 21 Right adnexal ectopic gestation 586, 586f normal 596f
Recti after delivery, divarication of 343f cornual ectopic pregnancy 136f progesterone level 136
Rectouterine pouch of Douglas 10 mentoposterior 280f Sex hormone binding globulin 404
Rectovaginal occipitoanterior 221 Sex-linked genital disease 646
fistula 563 occipitotransverse 221 Sextuplets 168
septum 10, 20 palm over left dorsum 518f Sexually transmitted
Rectum 7, 19 sacroanterior 289 disease 44, 357, 476, 539, 711
Red cell indices 361 sacroposterior 289 infection 182, 468, 539, 663
Reflexes in baby 339 subclavian artery 578 Shake test 189, 608
Regional analgesia 263 ventricle end-diastolic pressure 557 Sheehan’s syndrome 354, 512, 650, 651
Regurgitant lesions 382 Ring-shaped placenta 209 Sher’s clinical grades 164t
Relaxation exercises 104 Ritodrine 184, 678 Shoulder
Relaxin 67, 257 delivery of anterior 227
Robert’s pelvis 271, 272f
Remnants of extrauterine life 59t dystocia 196, 197
Rooting reflex 635, 635f engagement of 294f
Renal 363, 387, 578 Rubella 121, 485, 487, 488 Shrill cry 637
cortical necrosis 418 during management 487t Shrunken embryo 585f
disorders during pregnancy 487t Siamese twins 170
complicating pregnancy 417 syndrome 487 Sibai regimen 412
in pregnancy 419 vaccine 682 Sickle cell 374f
failure, acute 418, 512 Rubin maneuver 197 anemia 373
function 403 Rugae of vagina 11f disease 374
test 201, 407 Ruptured uterus 547 in peripheral smear 374f
insufficiency 358 Ryle’s tube 504, 505 screen, test for 374f
transplantation 419 trait 374
vein thrombosis 395 Silastic cups 703
Reproductive S Simpson’s for low forceps 700
long forceps 689, 690f
child health 665 Sacral flexure, concavity of 19
short forceps 689, 690f
diseases 650 Sacral promontory 27 Sinciput 32, 48
health 649, 660 Sacrococcygeal teratoma 602 Skeletal system 76
immunology 85 Sacrosciatic pain 107f diseases affecting 270
medicine 647 Safe delivery 289 Skene’s tubules 9, 18
morbidity 649 Safety coil 720f Skin 77, 631, 633
technique 168 Saheli 727, 728f changes 91
tract infection 181, 468, 539, 653 Saling’s technique 5 diseases 8, 495
Respiratory disorders in pregnancy 427 Salivary estriol 182 peeling of 201f
Respiratory distress 394 Salpingitis 136 tags 494
in newborn, system for 634t Salpingo-oophorectomy 139 Skull 632
circumferences of 33
syndrome 184, 608, 637 Scanzoni’s maneuver 279
cranium 31
function 65 Scarpa’s fascia of abdomen 8 diameters of 33
rate 633 Schizont stage of plasmodium vivax 481f injury to 303
system 363, 402 Schultze method 234 Sleep disorders 433
in pregnancy 82 Scoliosis 271, 271f Smoking 470
Restitution 226f Sebaceous cysts 8 Sodium metabisulfite method 374f
Resuscitation, steps of 624 Second trimester Sodium restriction 415
Soranus’ gynecology 3 Syphilis 95, 121, 485, 488 Tocolytic drugs 184
Sore nipple 339 Systemic lupus erythematosus 121, 200, therapy 184
Souffle 49 433, 455, 496, 603 Tocolytics 677
Speculum examination 122, 124, 125, 126, Tonic uterine contractions 313
130, 183
Spencer wells 692f T TORCH infection 485
classification of 486t
Sperm penetration 53 Tachyarrhythmias 384 Torsion 212
Spermatozoon, structure of 53f Tachycardia, causes of 613 of pedunculated fibroid 136
Spermicides 717 Tactile stimulation 625 Tortuous blood supply 75f
Sphenoid 31 Taenia coli 19 Total breech extraction 296, 301
Sphincteric structures 7 Tears
Spiegelberg criteria 143 dose infusion 368
fourth degree 550 fertility rate 711
Spinal analgesia 263
Spine 577f, 578, 633 third degree 550 iron binding capacity 363
diseases affecting 271 Teenage pregnancy 508 leucocyte count 130, 183, 352, 453
with spinal dysraphism 579f Temkin’s edition 3 parenteral nutrition 426
Spiral artery 62, 63f Temporal bones 31 serum bilirubin 442
single 584 Tendon reflexes 451 Toxic hepatitis 425
Splenic lacerations 304 Tenofovir 473 Toxic shock syndrome 352
Spondylotomy 561 Tentorial tear 313 Toxoplasma 485
Sponge holding forceps 691, 691f Teratogen 592, 683 gondii 121, 472, 485
Spontaneous breech delivery 296 Terbutaline 184, 678 Toxoplasmosis 121, 485
miscarriage 120, 122 Terminate resuscitation 628 prevention of 486
types of 122 Tertiary syphilis 489 Trabeculae 60
movements 631, 634 Tetanus toxoid 43, 101, 124, 336, 525, 539, 682 Traction handle 693
splenic rupture 506 Tetralogy of Fallot 383 Traditional birth attendants 654
Stalworthy’s sign 160 Thalassemia
Staphylococcus saprophyticus 353 Transabdominal chorionic villus
major 376 sampling 597f
Star gazing fetus 302 syndromes 375
State Pollution Control Board 666 Transcervical chorionic villus sampling 597f
Thalidomide 685 Transcutaneous electrical nerve
Status asthmaticus 431 Theophylline 679
epilepticus 462 stimulation 109, 109f, 261
Thiamine 679
membranes of 287 Transcutaneous nerve stimulation 345
Third stage of labor, complications of 318
Stem cell transplantation 602 electrodes 345
Third trimester 93, 578
Stillbirth 40, 176 Transdermal contraceptions 731
rate 664 screening 99
patches 730
Streptococcus agalactiae 121 villi 65
Transferrin receptor concentration 363
Streptococcus faecalis 350 Thoracopagus 170
Transferrin saturation 363
Stress urinary incontinence 353 Thorn’s maneuver 281, 282f
Transient fetal 281
Striae gravidarum 78, 494, 494f Thrombin inhibitors 449
Thromboembolic disorders 545 Transitional epithelium 17
Subacute cutaneous lupus erythematosus
Thrombophilia 446 stools 635
496
Thromboplastin time 353 zone 14
Subacute inversion 325
Subclinical hyperthyroidism 451, 452 Thrombosis, acute 352 Transperitoneal migration 139
Subcutaneous symphysiotomy 198 Thrombotic thrombocytopenic purpura 423 Transplacental supply of nutrients 110
Subseptate uterus 282 Thyroid 83 Transportation and primary aid 658
Substance abuse 181, 359 binding globulin 450 Transverse cesarean incision 544
Subtotal thyroidectomy, role of 453 disease 450, 609, 652 Trauma 121, 318
Succenturiate placenta 209, 210f in pregnancy 450 to uterus 319
Sucking 635 disorders 358 Traumatic delivery 313
Suction cups 703 function Trendelenburg position 288f
evacuation 152, 528 abnormalities 127 Treponema pallidum 488
machines 704 Trichomonas vaginalis 185, 186
in fetus 450
Sun protecting factor 493 Tricyclic antidepressants 502
hormones 336
Supine hypotension syndrome 265 Tripartite placenta 209
nodule in pregnancy 453, 453f
Suprapubic catheterization 18
physiology during pregnancy 450 Triphasic pill 727
pressure 197, 197f
screening in pregnancy 452t Triploidy 127
Supraventricular tachycardia 384
Surgical gloves, wearing of 521 stimulating hormone 66, 83, 94, 450 Triradiate pelvis 272f
Swallowing reflexes 635 stimulating immunoglobulin 453, 456 Trophoblast 60
Swine flu in pregnancy 489 storm 454 differentiation of 61
Symphysis pubis 346 Thyrotropin-releasing hormone 184 Trophoblastic invasion, abnormal 399
Symptothermal method 713, 715 Thyroxine 450 Trophoblastic signal 584
Syncytium 60 Tocolysis induced pulmonary edema 431 Tubal abortion 138t
Syntocinon infusion 708 Tocolysis, contraindications for 185 Tubal rupture 138t
Index 753
Tuberculine sensitivity test 428 Urine 187, 635 Vaccum aspiration 124, 526, 529, 661
Tuberculosis 358, 427, 477, 665 examination 183, 187 syringes 529f
on neonate, effect of 427 pregnancy test 122, 123, 126 extraction 278, 279, 693, 693f
on pregnancy, effect of 427 Urogenital diaphragm 20 extractor 703
Tubular necrosis, acute 418 Urokinase-type plasminogen activators 445 electric 694f
Tuft of hair 633f Ursodeoxycholic acid 421, 495 manual 694f
Tumor 270 Uterine 550f Vagina 7, 10, 76, 151, 332
artery 22, 574 laceration of 323
necrosis factor 193, 480
flow velocity waveforms 586, 588f normal 10f
alpha 483 opening of 11
of bone causing deformity 272f ligation 322, 550
Vaginal artery 22
of pelvic bone 311 scores 176
Vaginal birth after cesarean 497
secondary 156 atony 318, 545
section 315
Turner’s sign 505 awakening 229 Vaginal bleeding 120, 145, 498, 636
Twin 282, 572f bimanual massage 320f in third trimester of pregnancy, causes
during labor, management of 177 bleeding, abnormal 711 of 158
pregnancy 168 changes in diaphragm 718, 719f
complications of 178 shape 91 discharge 636
on mother 171 size 91 entrance 7, 10
reversed arterial perfusion 170 softness 91 examination 27f, 122, 130, 177, 183,
to twin transfusion 600 contractions 232, 232f, 306 214, 238, 238f, 280, 282, 312
syndrome 170, 172, 200, 214 abnormal 274 inclusion cysts 12
types of 169 curettage 136 infection 182
horns on hysterosalpingography 128f metastatic 150, 150f
incision 544 ring 730
U inversion 325 sex 713
leiomyoma with pregnancy 503 sterilization 538, 733
Uchida method 734
muscle 211f tubal ligation 541, 734
Umbilical amnion 71
criss-cross spiral fashion of 13f walls 11
Umbilical arteries 577f, 608 Vaginitis 186
Umbilical cord 60, 68, 68f fibers 232f
Valium 682
causes 285 musculature 73, 211f
Valproic acid 680
cutting scissors 693, 693f quiescence 229
Valvotomy 381
development 56 receptivity 55 Valvular heart disease 381
prolapse 285 relaxants 677 Vanillylmandelic acid 396
Umbilicus 297 repair 544 Vanishing twin 171
Underwater delivery 251 rupture 324 Varicella-zoster 121
Unilateral cleft lip 581f in lower segment 708f Varicosities 100, 494
Uniovular twins 169 segment of vulva 100f
Unprotected sexual intercourse 469 lower 312f Vas deferens 731
Ureaplasma urealyticum 121, 127, 483, 485 upper 312f injection in 731
Ureter 7, 16, 17f souffle 49 Vasa previa 162, 213
route of 17f sound 12 Vascular endothelial growth factor 88
stimulants 675 Vascular spider nevi 493
Ureteral injuries 545
vessels 399 Vasectomy
Ureteric canal 17
wall 211f advantages of 734
Urethra 7, 9, 18
Utero-ovarian
Urethral Vasoactive drugs 514
artery ligation 550f
catheterization 553 Velamentous insertion of cord 212, 213f
ligation 322
labia 9 Vena cava
Uteroplacental vessels in placental bed 63f
meatus, external 9 inferior 58, 74, 266f, 378, 588
Uterosacral ligament 19, 20
valves, posterior 601 superior 58
Uterotonic theory of initiation of labor 222
Urinary Venepuncture, technique of 556f
Uterus 7, 12, 20, 73, 676, 725f
bladder 7, 17, 18, 18f, 577f Veneral disease 94, 125, 161, 201, 202f, 237,
abnormalities of 121, 128
complications 545 357, 406, 489
anteversion of 108f
frequency 101 Venous thromboembolism 446, 447, 727
involution of 331
incontinence 186, 353 rupture of 313, 314, 314f, 325f, 510, 708 pregnancy 449t
infections 417 stretching of 222 Ventouse 703
problems 353 subinvolution of 353 cup, application of 704f
retention 353 delivery 705
shunts 601 extraction 704
system 81, 334 V over forceps, advantages of 693
tract infection 101, 137, 334, 349, 353, Vaccinations 358 Ventricular septal defeat 383
357, 360, 387, 683, 545, 719 Vaccines 682 Verbal autopsies 655
Vertex 50f Vitelline duct 55 Wound

Vesicovaginal Vomiting 100 complications 545
fascia 10 in pregnancy 117, 119 dehiscence 352
fistula 4, 18, 253, 273, 538, 563, 733 early 117 dressing 670
Vestibular bulb 7, 9f, 10 late 117 infection 352, 542, 734
Vibroacoustic stimulation test 612 mechanism of 118 Wrigley’s forceps 689, 689f
Villous trophoblast 60 still persists 119
Vincristine 154 to pregnancy 117
Viral Vulva 7, 76
X
hepatitis 652 Vulval Xiphisternum 275
acute 423 boil 8f
in pregnancy 424 hematoma 533, 533f Y
treatment of 424 varicosities in pregnancy 77f
load 469 Yoga 107f, 343f
Vital capacity 82
W
Vitamin 342 Z
A 112, 342 Waddling gait 77
B 111 Warfarin 680 Zatuchini score 296t
B1 679 Warning bleed 160 Zavanelli maneuver 198
B12 372, 675 Warts in pregnancy 496 Zika virus 490f
B6 679 Waste space of morris 29, 29f disease 490
C 112 Wearing sterile gown, techniques of 521f Zinc 111
D 112, 342 Wernicke’s encephalopathy 118 Zona-pellucida 53
E 112, 342 Wigand-Martin maneuver 300, 300f Zuspan regimen 412
K 342 William smellie 4 Zygosity, determination of 170
K antagonist 449 Wood’s maneuver 197, 198f Zygote 594

Textbook of Obstetrics

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The Health Sciences Publisher

BD Hasija Jyotsna Suri

Deepali Garg Kavita N Singh

Dheeraj Deo Bhatt Mahua Maiti

Divya Pandey Manjula Sharma

Matthews Mathai PK Shah

Pikee Saxena Rajesh Uppal

Renuka Sinha Smiti Nanda

Section 2 Normal Pregnancy

Section 3 Abnormal Pregnancy

20. Disproportional Fetal Growth............................................................................................................................................................................................191

Section 4 Normal Labor

Section 5 Abnormal Labor

Section 7 Medical Disorders in Pregnancy

39. Diabetes and other Endocrine Disorders in Pregnancy............................................................................................................................................386

Section 8 Infections in Pregnancy

Section 9 Special Conditions

Section 10 Operative Obstetrics

60. Destructive Operations........................................................................................................................................................................................................559

Section 11 Routine and Special Investigations

Section 13 Contemporary Issues in Obstetrics

Section 14 Pharmacotherapeutics in Obstetrics

Section 15 Practical in Obstetrics

various illustrated positions of the fetus in Temkin's edition

Figs 2.6A and B: A. Normal vagina—10x; B. Histopathology of vagina

1 cm and 2.5 cm respectively, from its lower end. The

Fig. 2.9: Culdocentesis Fig. 2.10: Colpotomy

The cavity is shaped like an inverted triangle. It

Applied Anatomy Histopathology

Fig. 2.14: Histology of ectocervix Fig. 2.15: Histology of endocervix

Figs 2.16A to C: A. Transitional zone (T-zone) junction; B. Histo-

this is termed as anteversion. The uterus is also flexed

separated by the uterovesical pouch of peritoneum.

colon and upper rectum. Laterally, the broad ligaments

abdominal and pelvic parts. There are slight constrictions

continue as the anal canal. The peritoneum covers it on •• Ovarian ligament.

The maternal pelvis is made up

True Pelvis Plane

fetal head is delayed and occipitoposterior positions are

pelvic dimensions; otherwise it forms a wedge posteriorly

Obstetrical Significance of Cavity

 Plane: It is represented by a line joining the lower

 Plane: It is the same as the plane of least pelvic

•• Transverse or bispinous diameter (10.5 cm): It is

THE PASSENGER (THE FETUS)

FETAL HEAD (SKULL CRANIUM)

–– Position of occiput in relation to the pelvis

along with supraorbital ridges and the junction of the

Fig. 4.4: Anteroposterior diameters of fetal skull

TABLE 4.1: Anteroposterior diameters of fetal skull

TABLE 4.2: Transverse diameters of fetal skull

Thus, the edges of frontal bones anteriorly, occipital bones

 LOP—middle of right parietal bone.

INTRODUCTION LISTENING AND LEARNING SKILLS

INTRODUCTION Identification and Demographic Data

Kartik November (during puerperium).

 Reduced fetal movements 4. Product

have disorders like Down syndrome, neural tube defects,

Plane: It is represented by a line joining the lower

Plane: It is the same as the plane of least pelvic

LOP—middle of right parietal bone.

Reduced fetal movements 4. Product

as compared to multiparas. In the early weeks the Palpation

The patient should be examined from the right side.

The hands should be warm especially in cold weather

Souffle is a soft blowing sound heard on auscultation

Engaged: The largest transverse diameter of the head,

brim. Adequacy of pelvis.

In case of non-fertilization, the ovum degenerates in

The entering pole of the late stage blastocyst is at the site

Umbilical Cord Development 11th day – Implantation completed

Low Levels of hCG are Found in Anti-insulin action.

Amnion: The amnion has following layers:

Interstitial collagenase In conclusion, it must be appreciated that implantation