The Diagnosis and Management of The Acute Abdomen in Pregnancy-Greenspan, Peter, Springer Verlag (2017)

The Diagnosis and
Management of
the Acute Abdomen
in Pregnancy
Peter Bogach Greenspan

Editor
123
The Diagnosis and Management
of the Acute Abdomen in Pregnancy
Editor
The Diagnosis and

Management of the Acute
Abdomen in Pregnancy
Editor
Department of Obstetrics and Gynecology
University of Missouri – Kansas City School of Medicine
Kansas City, MO, USA
Obstetrical and Gynecological Services
Truman Medical Center Lakewood
ISBN 978-3-319-62282-8 ISBN 978-3-319-62283-5 (eBook)

DOI 10.1007/978-3-319-62283-5
Library of Congress Control Number: 2017952195
© Springer International Publishing AG 2018

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This textbook is dedicated to the memories of the late
Lt. Col. Reynold S. Greenspan, DO, MS, USAF, my
dad, and the late James P. Youngblood, MD, FACOG,
my other dad.
Foreword
Dr. Greenspan is the author of an excellent textbook on an important subject that has
had very little recent update. It comprises 14 sections covering important and current
information that very accurately involves the diagnosis of the acute abdomen. Each
section by Dr. Greenspan, and by physicians with special interests and expertise in
various components, is well organized and has helpful information for those involved
in the practice of obstetrics.
This textbook is well written and easily readable. It provides prompt access to
information on a subject that may at times require expedited action.
UMKC School of Medicine, Obstetrics Harry S. Jonas, MD, FACOG

and Gynecology,
University of Missouri Kansas City
Lee’s Summit, MO, USA
vii
Preface
An acute abdomen is defined as “an abnormal condition characterized by the acute

onset of severe pain within the abdominal cavity” [1]. Although rare, it represents a
potentially life-threatening emergency that necessitates immediate diagnosis and
competent intervention. The management, however, can be highly challenging as
acute abdominal pain is multi-etiologic and can originate from any of the multiple
intraabdominal organs. Acute abdomen in pregnancy elevates these challenges to a
higher level of complexity. Thus, the pregnancy-induced maternal physiological
and anatomical changes, the considerations for two patients – the mother and the
fetus – and the addition of obstetrical sources of an abdominal emergency com-
pound the diagnostic and therapeutic challenges in a pregnant mother. Ensuring an
optimal maternal and fetal outcome would necessarily require an integrated multi-
disciplinary expertise. Responding to a dearth of any practical up-to-date single
reference source for managing this life-threatening condition, Dr. Peter Greenspan
has assembled a team of extraordinarily talented and accomplished contributors to
address the various aspects of managing an acute abdomen in pregnancy in this
practical and highly useful textbook.
A spectrum of chapters deals comprehensively with the various aspects of the
subject. The initial chapters discuss the relevant aspects of maternal anatomical and
physiological changes in pregnancy, fetal development, general diagnostic principles
of the acute abdomen, and the diagnostic imaging and laboratory investigations.
Subsequent chapters present state-of-the-art reviews on the management of specific
etiologies – obstetrical, gynecological, cardiopulmonary, gastrointestinal, urologi-
cal, and trauma. The concluding chapters discuss the surgical and gynecological
principles in managing a pregnant patient and the relevant liability considerations.
As evident, the book admirably fulfils its promise.
Dr. Greenspan should be congratulated for this worthy undertaking. As a distin-
guished academic obstetrician gynecologist in excellent standing with years of
expertise and experience as a practitioner and a teacher, he certainly has the
ix
x Preface
appropriate credentials. I am highly confident that the book will be well received
and highly valued by all who are involved in providing professional care for preg-
nant mothers afflicted with this dire emergency.
Reference
1. Mosby’s Medical Dictionary. 9th ed. Elsevier; 2009.
Kansas City, MO, USA Dev Maulik, MD, PhD, FACOG

Acknowledgments
The daunting task of editing and contributing to a medical textbook is a humbling

experience. Such an undertaking would not have been possible without the advice,
assistance, encouragement, and patience of numerous individuals.
I owe an enormous amount of gratitude to Gwen Sprague, MLS, our medical
librarian at Truman Medical Center who, while undergoing radiation and chemo-
therapy, gave me excellent support and counsel. Gwen was always available for me
to discuss graphics, tables, and copyright issues and to assist me in organizing and
optimizing the chapters. At the time of this writing, Gwen is cured and stronger than
ever.
I am very grateful for the advice and suggestions of a dear friend, colleague, and
mentor, Roger P. Smith, MD, FACOG, the author of over 40 books on topics from
obstetrics and gynecology to gumball machine collecting. Dr. Smith referred me to
Bonita Allen and Jennifer Jones, of Elsevier, who were instrumental in assisting me
in obtaining many of the graphical materials used in this textbook.
The foreword and introduction were written by Harry S. Jonas, MD, FACOG,
and Dev Maulik, MD, PhD, FACOG, FRCOG, respectively, who have been my col-
leagues and mentors for my entire career. Their guidance in this project is greatly
appreciated.
Many thanks to Glenn Talboy, MD, FACS, a close friend and colleague, to whom
I am indebted for his advice and clinical acumen.
I thank Johan P. Suyderhoud, MD, and Kara Settles, MD, of the UMKC School
of Medicine Department of Anesthesia, for providing assistance in enlisting con-
tributors for the project.
Richard Hruska, the executive editor of this textbook for Springer US, has been
very patient with our production delays but has always been gracious and welcom-
ing ever since he approached me to edit this work. Colton Coreschi, his assistant,
has been diligent in moving the project continually toward publication.
Connie Walsh, however, deserves particularly special gratitude, as the develop-
mental editor. Her involvement, on a daily basis with advising, suggesting, and
hand-holding, as this textbook went from the outline stage to the finished project,
has been quintessential. Without her encouragement and patience, this textbook
would never have been concluded.
I am greatly indebted to my professional associates and personal friends, Kristin
J. Kruse, MD, FACOG, and Sarah E. Sudduth, MD, FACOG, for their forbearance
xi
xii Acknowledgments
and cooperation over the period of time that my favorite excuse for any reason was
“sorry, I have to work on the book.”
Additionally, I would be remiss if I didn’t extend my sincerest appreciation to
Joy Hobick, our administrative assistant, without whom, the three of us would be
helpless in the day-to-day operation of our clinical and academic services.
Lastly, I want to acknowledge my ever-encouraging and enthusiastic children for
their support, but my deepest appreciation and the most thanks go to my soul mate and
pilot, the love of my life, Kim Greenspan, who has been an endless source of sugges-
tions, encouragement, support, and sacrifice during the entirety of the enterprise of
creating this textbook.
Contents
1 Maternal Anatomical and Physiological Adaption to Pregnancy�� 1

2 Overview of the Normal Development of the Human Embryo
and Fetus�� 25
David C. Mundy and Gustavo Vilchez
3 General Principles in the Diagnosis of the Acute Abdomen�� 41
4 Imaging the Gravid Female�� 49
Stephanie Anne Scott and Justin Stowell
5 Laboratory Studies�� 99
Kamani M. Lankachandra
6 Obstetrical Etiologies of Abdominal Pain�� 107
7 Gynecologic Etiologies of Abdominal Pain in Pregnancy�� 141
Layan Alrahmani, Paul M. Magtibay III, Javier F. Magrina,
and Paul M. Magtibay
8 Gastrointestinal Etiologies of Abdominal Pain in Pregnancy�� 165
Farzad Alemi, Teisha Shiozaki, Alexis Graham-Stephenson,
and Alexandra Bors
9 Urological Etiologies of Abdominal Pain �� 193
Joshua A. Broghammer and Marcus Austenfeld
10 Trauma During Pregnancy �� 209
Stanley M. Augustin, Maxwell Almenoff, and Aaron Sparks
11 Surgical Principles in the Gravid Female�� 217
12 Principles and Practice of Anesthetic Management
in the Gravid Patient Undergoing Abdominal Surgery�� 227
Tibor G. Mohácsi and Kathleen A. Leavitt
xiii
xiv Contents
13 Postoperative Care Issues�� 237

14 Legal Concerns in Complicated Obstetrical Cases�� 241
Marilyn M. Pesto, Janet I. Mittenfelner, and Andrew Spaedy
Index�� 269
Contributors
Farzad Alemi, MD, MS Department of Surgery, University of Missouri Kansas

City School of Medicine, Truman Medical Centers, Kansas City, MO, USA
Maxwell Almenoff, MD Department of Surgery, University of Missouri Kansas
City School of Medicine, Kansas City, MO, USA
Layan Alrahmani, MD Department of Obstetrics and Gynecology, Division of
Maternal Fetal Medicine, Mayo Clinic, Rochester, MN, USA
Stanley M. Augustin, MD, FACS Department of Surgery, University of Missouri
Kansas City School of Medicine, Truman Medical Centers, Kansas City, MO, USA
Marcus Austenfeld, MD Department of Urology, University of Kansas Medical
Center, Kansas City, KS, USA
Alexandra Bors, MD Department of Surgery, University of Missouri Kansas City
School of Medicine, Truman Medical Centers, Kansas City, MO, USA
Joshua A. Broghammer, MD, FACS Department of Urology, University of
Kansas Medical Center, Kansas City, KS, USA
Alexis Graham-Stephenson, MD Department of Surgery, University of Missouri
Kansas City School of Medicine, Truman Medical Centers, Kansas City, MO, USA
Peter Bogach Greenspan, DO, FACOG, FACS Department of Obstetrics and
Gynecology, University of Missouri – Kansas City School of Medicine, Kansas
City, MO, USA
Obstetrical and Gynecological Services, Truman Medical Center Lakewood, Kansas
City, MO, USA
Harry S. Jonas, MD, FACOG Department of Obstetrics and Gynecology,
University of Missouri Kansas City School of Medicine, Lee’s Summit, MD, USA
Kamani M. Lankachandra, MD, FACP Department of Pathology, University of
Missouri School of Medicine, Truman Medical Centers, Kansas City, MO, USA
xv
xvi Contributors
Kathleen A. Leavitt, MD Department of Anesthesiology, University of Missouri

Kansas City School of Medicine, Kansas City, MO, USA
Javier F. Magrina, MD, FACOG, FACS Department of Obstetrics and
Gynecology and Gynecologic Oncology, Mayo Clinic Graduate School of Medicine
and Biomedical Sciences, Mayo Clinic Arizona, Phoenix, AZ, USA
Paul M. Magtibay, MD, FACOG, FACS Department of Obstetrics and
Gynecology and Gynecologic Oncology, Mayo Clinic Graduate School of Medicine
and Biomedical Sciences, Mayo Clinic, Phoenix, AZ, USA
Paul M. Magtibay III, MD Department of Obstetrics and Gynecology and
Gynecologic Oncology, Mayo Clinic Graduate School of Medicine and Biomedical
Sciences, Mayo Clinic, Phoenix, AZ, USA
Janet I. Mittenfelner, JD, MHSA Office of General Counsel, Litigation Counsel,
TMC Professional and General Liability Trust, Truman Medical Centers, Kansas
City, MO, USA
Tibor G. Mohácsi, MD Department of Anesthesiology, University of Missouri
Kansas City School of Medicine, Saint Luke’s Hospital, Kansas City, MO, USA
David C. Mundy, MD, FACOG Department of Obstetrics and Gynecology,
Division of Maternal Fetal Medicine, University of Missouri Kansas City School of
Medicine, Truman Medical Centers, Kansas City, MO, USA
Marilyn M. Pesto, JD, MSN, BSN Medical Humanities & Social Sciences,
Sirridge Office of Medical Humanities and Bioethics, University of Missouri
Kansas City School of Medicine, Kansas City, MO, USA
Stephanie Anne Scott, MD Department of Radiology, University of Missouri
Kansas City School of Medicine, Truman Medical Center, Kansas City, MO, USA
Teisha Shiozaki, MD Department of Surgery, University of Missouri Kansas City
School of Medicine, Truman Medical Centers, Kansas City, MO, USA
Andrew Spaedy University of Missouri Kansas City School of Medicine, Kansas
City, MO, USA
Aaron Sparks, DO Department of Surgery, University of Missouri Kansas City
School of Medicine, Kansas City, MO, USA
Justin Stowell, MD Department of Radiology, University of Missouri Kansas City
School of Medicine, Kansas City, MO, USA
Gustavo Vilchez, MD Department of Obstetrics and Gynecology, Division of
Maternal Fetal Medicine, University of Missouri Kansas City School of Medicine,
Truman Medical Centers, Kansas City, MO, USA
Maternal Anatomical and Physiological
Adaption to Pregnancy 1
Anatomical Changes
Introduction
Pregnancy is not a pathological state. However, maternal and/or fetal diseases can
rapidly transform a normal pregnancy into a serious condition, requiring meticulous
diagnosis and management to avoid catastrophes to the mother, the fetus, or both.
Conditions that arise in pregnancy are often associated with the acute abdomen.
Several of these conditions can be managed medically, while other conditions
require surgical intervention. Pregnant women are also subject to serious traumatic
injuries, such as may occur in vehicular accidents or violent crimes, among other
causes.
The modern practice of medicine and surgery allows the caregivers of sick and
injured pregnant women to vastly improve maternal and fetal outcome with inter-
ventions that are safe for both.
The diagnosis and management of disease and injury in pregnancy are compli-
cated by several factors such as changes in maternal anatomy and physiology as
well length of gestation and consideration of the trimesters of pregnancy, which
may inform the provider as to what options are available for the safest outcome in
each case.
When confronted with a gravid female who presents to the clinic or the labor
suite with signs and symptoms of an acute abdomen, the clinician must be well
P.B. Greenspan, DO, FACOG, FACS (*)

Department of Obstetrics and Gynecology, University of Missouri – Kansas City School
of Medicine, Kansas City, MO, USA
Obstetrical and Gynecological Services, Truman Medical Center Lakewood,
e-mail: [email protected]
© Springer International Publishing AG 2018 1

P.B. Greenspan (ed.), The Diagnosis and Management of the Acute Abdomen
in Pregnancy, DOI 10.1007/978-3-319-62283-5_1
2 P.B. Greenspan
educated in the anatomical and physiological adaptations and alterations that occur
normally in pregnancy to be able to make the most accurate diagnosis.
Uterine Enlargement
The implantation of a gestation produces physiological effects on the uterine mus-

culature that allows for the myometrium to soften and expand. These changes are
palpable to the examiner by 5–6 weeks of pregnancy. The nonpregnant uterus is
located in the pelvic cavity between the bladder anteriorly and the rectum posteri-
orly [1].
Usually, the gravid uterus is not palpable above the pubic ramus until about
12 weeks of gestation. The inferior portion of the anterior uterine wall, called the
lower uterine segment, is united to the posterior wall of the bladder by a well-
defined loose connective tissue layer – the vesicouterine peritoneum. During cesar-
ean delivery, the peritoneum of the vesicouterine pouch is often sharply incised, and
the vesicouterine space is entered. This is referred to as the bladder flap.
The majority of the uterus, with the exception of the cervix, is muscle. The inner
surfaces of the anterior and posterior walls are closely approximated, and the cavity
between these walls forms a mere slit. The nulligravid uterus measures 6–8 cm in
length compared with 9–10 cm in multiparous women. The uterus averages 60 g
and typically weighs more in parous women [2, 3].
A gestation stimulates remarkable uterine growth due to hypertrophy of the mus-
cle fiber. The uterine fundus, a previously flattened convexity between tubal inser-
tions, now becomes dome shaped. Furthermore, the round ligaments appear to insert
at the junction of the middle and upper thirds of the organ. The fallopian tubes
elongate, but the ovaries grossly remain the same.
The growth of the uterus is initially cephalad, but by 14–16 weeks of gestation,
the fundus also protrudes anteriorly thus creating a visible bulge in the abdominal
wall. In healthy gravidas, the fundus is at the level of the umbilicus by 20 weeks of
gestation.
In normal pregnancy, the fundus grows at a rate of about 1 cm per week and can
be documented as “MacDonald’s Measurement.” Deviation in expected growth,
either less or more than expected, should arouse suspicion in the examiner of poten-
tial maternal/fetal problems.
As the gravid uterus expands, it naturally displaces other viscera. Furthermore,
the expansion may produce compression of surrounding organs, which in turn, may
compromise the functions of those structures. This accounts for increased urinary
frequency in pregnancy, as well as constipation. In the latter third trimester, the
displacement of the intestines and stomach often encroach on the diaphragm of the
gravid woman, often producing shortness of air and difficulty with breathing.
Palpitations are also common, as the abdominal viscera push up on the diaphragm,
allowing the gravida to sense her beating heart. Gastrointestinal reflux and nausea
are often associated with compression of the stomach. Biliary function may be com-
promised, as well. Upward displacement of the appendix can make the diagnosis of
1 Maternal Anatomical and Physiological Adaption to Pregnancy 3
appendicitis very difficult. Uterine enlargement combined with other natural physi-
ological alterations in pregnancy must be understood to accurately evaluate and
treat the acute abdomen in the pregnant woman.
Physiological Changes
Cardiovascular System
Gestation produces significant physiological changes in the cardiovascular system.

Several adaptive mechanisms are initiated as early as 5 weeks’ gestation to maxi-
mize oxygen delivery to maternal and fetal tissues [4].
Most pregnant women tolerate these physiological changes. In cardiac diseases,
however, maternal morbidity and even mortality may occur.
Heart
Displacement of the diaphragm and the effect of pregnancy on the shape of the rib
cage shift the heart cephalad and to the left. In addition, the heart rotates on its long
axis, moving the apex somewhat laterally, causing an increased cardiac silhouette
on radiographic studies, without an actual change in the cardiothoracic ratio. Other
radiographic findings include an apparent straightening of the border of the left side
of the heart and increased prominence of the pulmonary conus. Diagnosis of cardio-
megaly by chest x-ray should be confirmed by echocardiogram if clinically appro-
priate [5].
Actual cardiomegaly in pregnancy is rare; however, physiological myocardial
hypertrophy of the heart is observed as a result of expanded blood volume in the first
half of the pregnancy and progressively increasing afterload in the latter part of the
pregnancy. These structural changes in the heart are similar to the findings in
response to exercise and result in eccentric hypertrophy as opposed to concentric
hypertrophy that is observed with disease states such as hypertension or aortic ste-
nosis. The eccentric hypertrophy facilitates enhanced pumping capacity in response
to increased demand, producing greater mechanical efficiency [6, 7].
These physiological alterations commence early in the first trimester and peak by
30–34 weeks’ gestation. Left ventricular end-diastolic dimension increases 12%
over preconceptional values by M-mode echocardiography. Concurrently, left ven-
tricular wall mass increases by 52% (mild myocardial hypertrophy), and atrial
diameters increase bilaterally, peaking at 40% above nonpregnant values [7].
Pulmonary capillary wedge pressures are stable, as a result of a combination of
decreased pulmonary vascular resistance and increased blood volume. Multiple
gestations increase myocardial hypertrophy, atrial dilation, and end-diastolic ven-
tricular measurements even further [8]. Following delivery, the pregnant heart
slowly regresses in size and may take up to 6 months to return to prepregnant
dimensions [9].
Evaluation of left ventricular contractility is difficult in pregnancy because it is
strongly influenced by changes in heart rate (HR), preload, and afterload. Despite
4 P.B. Greenspan
the increase in stroke volume (SV) and cardiac output (CO), normal pregnancy is
not associated with hyperdynamic left ventricular function during the third trimes-
ter, as measured by ejection fraction, left ventricular stroke work index, or fractional
shortening of the left ventricle. However, some studies have shown that contractility
might be slightly increased in the first two trimesters, whereas other literature
reports no change throughout the pregnancy, and some report a decline toward term
[7]. A recent study demonstrated that in the third trimester, the cardiac systolic func-
tion declines as demonstrated by a decrease in the ejection fraction and the systolic
myocardial velocities compared with the first trimester. The study results are consis-
tent with impaired contraction and relaxation of the left ventricle at the end of preg-
nancy suggesting that a decline in cardiac function at term is normal in pregnancy
and that an exaggeration of this decline may explain the etiology for peripartum
cardiomyopathy [10].
Clinicians and researchers have concentrated on abnormalities of diastolic func-
tion as significant contributors to cardiac disease and symptom severity, especially
in the setting of normal or near-normal systolic function [11].
One review noted that diastolic dysfunction was highlighted as a leading cause
of cardiac failure in pregnancy [12].
The effects of pregnancy on diastolic function have been exhaustively investi-
gated using pulsed-wave Doppler echocardiography [7].
In young healthy women, the left ventricle is elastic; therefore, diastolic relax-
ation is swift, and ventricular filling occurs almost completely by early diastole with
minimal contribution from the atrial kick. The E/A ratio compares the peak mitral
flow velocity in early diastole (E) to the peak atrial kick velocity (A); although both
velocities increase in pregnancy, the overall ratio falls because of a greater rise in
the A-wave velocity. The rise in the A value, which begins in the second trimester
and increases throughout the third trimester, indicates the increased importance of
the atrial contraction in left ventricular filling during pregnancy [7].
Veille et al. found that in healthy women, pregnancy did not adversely affect
baseline diastolic function, however at maximal exercise, diastolic function was
impaired. This impairment was attributed to increased left ventricular wall stiffness.
The authors also speculated that this change may be the limiting factor for exercise
in pregnancy [13].
Cardiac Output
The tremendous increase in CO is one of the most remarkable changes in preg-
nancy. Van Oppen and coworkers performed a meta-analysis of 33 cross-sectional
and 19 longitudinal studies and found greatly divergent results on when CO peaked,
the magnitude of the rise in CO before labor, and the effect of the third trimester on
CO [14].
All of the studies agreed that CO increased significantly beginning in early preg-
nancy, peaking in between 30% and 50% above preconceptional values. In a longi-
tudinal study by Robson and associates using Doppler echocardiography, CO
increased by 50% at 34 weeks from a prepregnancy value of 4.88–7.34 L/min [15,
16] (Fig. 1.1).
Fig. 1.1 Cardiac output in pregnancy. Increase in cardiac output, stroke volume, and heart rate
from the nonpregnant state throughout pregnancy (From Gabbe [17]. Reprinted with permission
from Elsevier)
6 P.B. Greenspan
The CO in twin gestations incrementally increases an additional 20% greater

than that of singleton pregnancies [8]. Robson et al. showed that by 5 weeks’ gesta-
tion, CO has already risen by more than 10%. At 12 weeks, the rise in output is
34–39% above nongravid levels, accounting for about 75% of the total increase in
CO during pregnancy. There is no literature consensus as to the exact gestation
when CO peaks, but most studies point to a range between 25 and 30 weeks [18].
The data on whether the CO continues to increase in the third trimester are very
divergent, with equal numbers of good longitudinal studies showing a mild decrease,
a slight increase, or no change [14].
These study discrepancies are not explained by differences in investigative tech-
niques, position of the women during measurements, or study design. This apparent
discrepancy appears to be explained by the small number of individuals in each
study and the probability that the course of CO during the third trimester is deter-
mined by factors specific to the individual [14].
Desai and coworkers reported that CO in the third trimester is significantly cor-
related with fetal birthweight and maternal height and weight [19].
Increases in CO are mostly directed to the uterus, placenta, and breasts. The
uterus receives 2–3% of CO in the first trimester as well as in the nongravid
state. The breasts receive 1%. CO going to the kidneys (20%), skin (10%), brain
(10%), and coronary arteries (5%) remains at similar nonpregnant percentages.
However, because of the overall increase in CO, this results in an increase in
absolute blood flow of about 50% [15]. At term, the uterus receives 17% (450–
650 mL/min) and the breasts 2%, mostly at the expense of a reduction of the
fraction of the CO going to the splanchnic bed and skeletal muscle. The absolute
blood flow to the liver is not changed, but the overall percentage of CO is sig-
nificantly decreased.
CO is the product of SV and HR (CO = SV × HR). Both are increased during
pregnancy and contribute to the overall rise in CO. Maternal HR initially rises at
5 weeks’ gestation and peaks at 32 weeks’ gestation at 15–20 beats above the non-
gravid rate, an increase of 17%. The SV starts to rise by 8 weeks’ gestation reaching
its maximum at about 20 weeks, which is 20–30% above nonpregnant values. In the
third trimester, it is primarily variations in the SV that determine whether CO
increases, decreases, or remains stable, as described earlier.
Maternal position influences CO in pregnancy. One study in 10 normal gravid
women in the third trimester, using pulmonary artery catheterization, CO was
noted to be highest in the knee–chest position and lateral recumbent position at
6.6–6.9 L/min. CO decreased by 2.2–5.4 L/min in the standing position. The
decrease in CO in the supine position compared with the lateral recumbent position
is 10–30%. In both the standing and the supine positions, decreased CO results
from a fall in SV secondary to decreased blood return to the heart. The enlarged
uterus compresses the inferior vena cava in the supine position, reducing venous
return. However, this effect is not observed before 24 weeks. Importantly, in late
pregnancy, the inferior vena cava is completely occluded in the supine position,
with venous return from the lower extremities occurring through the dilated para-
vertebral collateral circulation [16].
Most supine women are not hypotensive or symptomatic because of the compen-
sated rise in systemic vascular resistance (SVR), despite decreased CO. However,
5–10% of gravidas experience supine hypotension with symptoms of dizziness,
lightheadedness, nausea, and occasional syncope. The women who are symptom-
atic have a greater decrease in CO and blood pressure (BP) and a greater increase in
HR when in the supine position than do asymptomatic women [20]. It has been
proposed that the determination of whether women become symptomatic depends
on the development of an adequate paravertebral collateral circulation. Interestingly,
with engagement of the fetal head, less of an effect on CO is seen [16].
Maintaining a normal BP in the supine position may be lost during epidural or
spinal anesthesia because of the inability to increase SVR. The clinical significance
of the effects of maternal position on CO are especially important when the gravida
is clinically hypotensive or in the setting of a category II or III fetal heart rate trac-
ing. The observation of decreased birthweight and placental infarctions in working
women who stand for prolonged periods may be associated with findings of a
decreased CO in the standing position.
rterial Blood Pressure and Systemic Vascular Resistance

A
Blood Pressure (BP) is the product of CO and resistance (BP = CO × SVR). Even
with the large increase in CO, typically the maternal BP is decreased until later in
pregnancy because of a decrease in SVR that peaks in midpregnancy, followed by a
gradual rise until term. The SVR remains 21% lower than prepregnancy values in
pregnancies not affected by gestational hypertension or preeclampsia, even at full
term. Progesterone-mediated smooth muscle relaxation is the most obvious cause
for the decreased SVR. However, the precise mechanism for the fall in SVR is not
well understood. Increased nitric oxide (NO) also contributes to decreased vascular
resistance by direct actions and by blunting the vascular responsiveness to vasocon-
strictors such as angiotensin II and norepinephrine. During conception, the expres-
sion and activity of NO synthase is elevated and the plasma level of cyclic guanosine
monophosphate, a second messenger of NO and a mediator of vascular smooth
muscle relaxation, is also increased [21]. Consequently, despite the overall increase
in the renin–angiotensin–aldosterone system (RAAS), the normal gravida is resis-
tant to the vasoconstrictive effects of angiotensin II. Gant et al. showed that nullipa-
rous women who developed preeclamptic continue to respond to angiotensin II
before the appearance of clinical signs of preeclampsia [22].
Initial decreases in BP manifest at 8 weeks’ gestation or earlier paralleling the
falling SVR. Current studies did not include preconception BP or frequent first-
trimester BP sampling and, therefore, cannot determine the exact time course of
hemodynamic alterations. Menstruation causes fluctuations in BP, which is decreased
in the luteal phase. Therefore, it seems reasonable that BP drops immediately in early
pregnancy. The diastolic BP and the mean arterial pressure [MAP = (2 × diastolic
BP + systolic BP)/3] decrease more than the systolic BP (Fig. 1.2).
The diastolic BP and the MAP reach their peaks at midpregnancy. By term, they
both return to prepregnancy levels and rarely exceed prepregnancy or postpartum
values. However, some investigators have reported that at term, the BP is greater
8 P.B. Greenspan
Fig. 1.2 Blood pressure in pregnancy. Blood pressure trends (sitting and lying) during pregnancy.
Postnatal measures performed 6 weeks postpartum (From Gabbe [17]. Reprinted with permission
from Elsevier)
than in matched nonpregnant controls and believe that in the third trimester, the BP
is higher than prepregnant values. These studies are very limited by the absence of
preconceptional values for comparison within individual patients.
Positioning and Korotkoff sounds are important when the BP is taken to deter-
mine the diastolic BP. BP is lowest in the lateral recumbent position, and the BP of
the superior arm in this position is 10–12 mm Hg lower than the inferior arm.
Clinically, BP should be taken in the sitting position and the Korotkoff 5 sound
should be used. This is the diastolic BP when the sound disappears as opposed to the
Korotkoff 4, when there is a muffling of the sound. One study of 250 gravidas
showed that the Korotkoff 4 sound could only be identified in 48% of patients,
whereas the Korotkoff 5 sound could always be determined. The Korotkoff 4 should
only be used when the Korotkoff 5 occurs at 0 mm Hg [23].
When compared with mercury sphygmomanometry during pregnancy, auto-
mated BP monitors tended to overestimate the diastolic BP. However, the overall
results were similar in normotensive women. Automated monitors appear increas-
ingly inaccurate at higher BPs in women with preeclampsia.
Venous Pressure
Venous pressure in the upper extremities remains unchanged in pregnancy but rises
progressively in the lower extremities. Femoral venous pressure increases from val-
ues near 10 cmH2O at 10 weeks’ gestation to 25 cmH2O near term [24]. Clinically,
the increase in venous pressure, as well as the obstruction of the inferior vena cava
by the enlarging uterus, leads to the development of edema, varicose veins, and
hemorrhoids, and increases the risk for developing deep venous thrombosis.
Pulmonary System
Upper Respiratory Tract

Pregnancy causes the mucosa of the nasopharynx to become hyperemic and edema-
tous with hypersecretion of mucus due to increased estrogen. Marked nasal stuffi-
ness is the result of these changes; epistaxis is also common. Insertion of nasogastric
tubes may cause excessive bleeding if adequate lubrication is not used [25].
Polyposis of the nose and nasal sinuses develop in some individuals, which regress
postpartum. Because of these changes, many pregnant women complain of chronic
cold symptoms; however, the temptation to use nasal decongestants should be
avoided because of the risk for hypertension and rebound congestion.
Mechanical Changes
The anatomic configuration of the thorax changes early in pregnancy, much earlier
than can be explained by mechanical pressure from the enlarging uterus. Relaxation
of the ligaments between the ribs and sternum may be responsible for these configu-
rations. The subcostal angle increases from 68° to 103°, the transverse diameter of
the chest expands by 2 cm, and the chest circumference expands by 5–7 cm. As
pregnancy progresses, the diaphragm rises 4 cm; however, diaphragmatic excursion
is not impeded and actually increases 1–2 cm. Respiratory muscle function is not
affected by pregnancy, and maximal inspiratory and expiratory pressures are
unchanged [26].
ung Volume and Pulmonary Function

L
The anatomic changes in chest wall configuration and the diaphragm lead to changes
in static lung volumes. In a review of studies with at least 15 subjects compared with
nonpregnant controls, Crapo found significant changes [25] (Fig. 1.3 and Table 1.1).
The elevation of the diaphragm decreases the volume of the lungs in the resting
state, thereby reducing total lung capacity and the functional residual capacity
(FRC). The FRC can be subdivided into expiratory reserve volume and residual
volume, and both decrease.
Spirometric measurements evaluating bronchial flow are unchanged in preg-
nancy. The forced expiratory volume in 1 second (FEV1) and the ratio of FEV1 to
forced vital capacity are both unchanged, implying that airway function remains
stable. Additionally, peak expiratory flow rates measured using a peak flow meter
seem to be unaltered in pregnancy at rates of 450 ± 16 L/min [28]. Harirah and
associates performed a longitudinal study of the peak flow in 38 women from the
first trimester until 6 weeks postpartum [29]. They reported that the peak flows had
a statistically significant decrease as the pregnancy progressed; however, the amount
of the decrease was minimal enough to be of questionable clinical significance.
Similarly, a small decrease in the peak flow was noted in the supine position versus
the standing or sitting position. Therefore, during gestation, both spirometry and
peak flow meters can be used in diagnosing and managing respiratory illnesses, but
the clinician should ensure that measurements are performed in the same maternal
position [29].
10 P.B. Greenspan
Fig. 1.3 Lung volumes in pregnant and nonpregnant women. ERV expiratory reserve, FRC func-
tional residual capacity, IC inspiratory capacity, IRV inspiratory reserve, RV residual volume, TLC
total lung capacity, TV tidal volume, VC vital capacity (From Gabbe [27]. Reprinted with permis-
sion from Elsevier)
Table 1.1 Lung functions in pregnancy

Lung volumes and capacities in pregnancy
Change in
Measurement Definition pregnancy
Respiratory race (RR) Number of breaths per minute Unchanged
Vital capacity (VC) Maximal amount of air that can be forcibly Unchanged
expired after maximal inspiration (IC + ERV)
Inspiratory capacity Maximal amount of air that can be inspired Increased 5–10%
(IC) from resting expiratory level (TV + IRV)
Tidal volume (TV) Amount of air inspired and expired with a Increased
normal breath 30–40%
Inspiratory reserve Maximal amount of air that can be inspired at Unchanged
volume (IRV) end of normal inspiration
Functional residual Amount of air in lungs at resting expiratory Decreased 20%
capacity (FRC) level (ERV + RV)
Expiratory reserve Maximal amount of air that can be expired Decreased
volume (ERV) from resting expiratory level 15–20%
Residual volume (RV) Amount of air in lungs after maximal Decreased
expiration 20–25%
Total lung capacity Total amount of air in lungs at maximal Decreased 5%
(TLC) inspiration (VC + RV)
From Cruickshank et al. [27], Gabbe [17]. Reprinted with permission from Elsevier
Gas Exchange
Rising progesterone levels drive a state of chronic hyperventilation, as noted by a
30–50% increase in tidal volume by 8 weeks’ gestation. In turn, increased tidal
volume results in an overall parallel rise in minute ventilation, regardless of a stable
respiratory rate (minute ventilation = tidal volume × respiratory rate). The rise in
minute ventilation, combined with a decrease in FRC, leads to a larger than expected
increase in alveolar ventilation (50–70%). Chronic mild hyperventilation produces
an increase in alveolar oxygen (PaO2) and a decrease in arterial carbon dioxide
(PaCO2) from normal levels (Table 1.2).
The drop in the PaCO2 is extremely important because it drives a more favorable
carbon dioxide (CO2) gradient between the fetus and mother, facilitating CO2 trans-
fer. The low maternal PaCO2 results in a chronic respiratory alkalosis. The increased
excretion of bicarbonate, as a result of partial renal compensation, helps maintain
the pH between 7.4 and 7.45 and lowers the serum bicarbonate levels. In early preg-
nancy, the arterial oxygen (PaO2) increases (106–108 mm Hg) as the PaCO2
decreases; however, by the third trimester, a slight decrease in the PaO2 (101–
104 mm Hg) occurs as a result of the expanding uterus. This decrease in the PaO2
late in pregnancy is even more pronounced in the supine position, with a further
drop of 5–10 mm Hg and an increase in the alveolar-to-arterial gradient to 26 mm
Hg, and up to 25% of women exhibit a PaO2 of less than 90 mm Hg [25, 32].
A simultaneous but smaller increase in oxygen uptake and consumption occurs
as the minute ventilation increases. Most investigators have found maternal oxygen
consumption to be 20–40% above nonpregnant levels. This increase is a result of the
oxygen requirements of the fetus, the placenta, and the increased oxygen require-
ment of maternal organs. With exercise or during labor, an even greater rise in both
minute ventilation and oxygen consumption takes place [25]. Oxygen consumption
can triple during contractions. Increased oxygen consumption and decreased FRC
results in a lowering of the maternal oxygen reserve. Therefore, pregnant women
are more susceptible to the effects of apnea, for example, during intubation when a
more rapid onset of hypoxia, hypercapnia, and respiratory acidosis is seen.
Table 1.2 Lung volumes in pregnant and non-pregnant women

Blood gas values in third trimester of pregnancy
Pregnant Nonpregnant
Pao2 (mm Hg)a 101.8 ± 1 93.4 ± 2.04
Arterial Hgb saturation (%)b 98.5 ± 0.7% 98 ± 0.8%
Paco2 (mm hg)a 30.4 ± 0.6 40 ± 2.5
pHa 7.43 ± 0.006 7.43 ± 0.02
Serum bicarbonate (Hco3) (mmol/L) 21.7 ± 1.6 25.3 ± 1.2
Base deficit (mmol/L)a 3.1 ± 0.2 1.06 ± 0.6
Alveolar-arterial gradient [P(a-a)o2 (mm Hg)]a 16.1 ± 0.9 15.7 ± 0.6
Data from Templeton and Kelman [30]. Data present as mean ± SEM
a
b
Data from McAuliffe et al. [31]. Data presented as mean ± SD
From Gabbe [17]. Reprinted with permission from Elsevier
12 P.B. Greenspan
Gastrointestinal System
Appetite
The appetite of most women increases throughout pregnancy. At the end of the first
trimester, food intake increases by about 200 kcal/day, in the absence of nausea. An
additional 300 kcal/day is recommended, but the majority of gravidas compensate
for this by decreasing their activity. Depending on the population being studied,
energy requirements vary. More active women and teenagers show a greater increase
in the need for calories. Cultural folklore about dietary cravings and aversions dur-
ing gestation abound. These may be the result of an individual’s perception of which
foods aggravate or ameliorate symptoms such as nausea and heartburn. Some
women experience a decrease in taste thus producing an increased desire for highly
seasoned food. Bizarre cravings for strange foods, Pica, are relatively common
among gravidas. Women with anemia or poor weight gain should be evaluated for a
history of pica. Pica examples include the consumption of clay, starch, toothpaste,
and ice [33].
Mouth
The pH and the production of saliva remain unchanged during gestation. Ptyalism,
considered an unusual complication of pregnancy, usually occurs in women suffer-
ing from nausea. Women with ptyalism may secrete 1–2 L of saliva per day. Many
experts believe that ptyalism actually represents an inability of the nauseated woman
to swallow normal amounts of saliva as opposed to a true increase in the saliva pro-
duction. Decreasing the ingestion of starchy foods may help to lower the amount of
saliva. There is no evidence to support that pregnancy produces or accelerates dental
caries. The gums, however, swell and may bleed after tooth brushing, thus causing
“gingivitis of pregnancy”. Tumorous gingivitis may occur occasionally, presenting
as a violaceous pedunculated lesion at the gum line that may bleed profusely. This
is called epulis gravidarum or pyogenic granulomas. These lesions consist of granu-
lation tissue and an inflammatory infiltrate [33].
Stomach
The tone and motility of the stomach are decreased because of the smooth muscle–
relaxing effects of progesterone and estrogen. The scientific evidence regarding
delayed gastric emptying, however, is inconclusive [34]. Macfie et al. studied acet-
aminophen absorption as an indirect measure of gastric emptying. But they were
unable to demonstrate a delay in gastric emptying when comparing 15 nonpregnant
controls with 15 women in each trimester [34]. Additionally, a recent study showed
no delay in gastric emptying in parturients at term who ingested 300 mL of water
following an overnight fast [35]. However, an increased delay was seen in labor,
with the etiology being ascribed to the pain and stress of parturition.
A decrease in peptic ulcer disease is observed in pregnancy. However, gastro-
esophageal reflux and dyspepsia increases by 30–50% [36]. This may be explained,
in part, by physiological changes of the stomach and lower esophagus. Gestational
hormones causing esophageal dysmotility play a role in gastroesophageal reflux
disease. Other factors include gastric compression from the enlarged uterus and a
decrease in the pressure of the gastroesophageal sphincter. Progesterone causes the
decrease in the tone of the gastroesophageal sphincter, while estrogen may be attrib-
uted to increased reflux of stomach acids into the esophagus. This may be the pre-
dominant cause of reflux symptoms. The decreased incidence of peptic ulcer disease,
in theory, includes increased placental histaminase synthesis with lower maternal
histamine levels, increased gastric mucin production leading to protection of the gas-
tric mucosa, reduced gastric acid secretion, and enhanced immunologic tolerance of
Helicobacter pylori, the infectious agent that causes peptic ulcer disease [36].
Intestines
Alterations in the motility of the small intestines and colon are common in preg-
nancy, thus causing an increased incidence of constipation in some and diarrhea in
others. One study noted up to 34% of women experienced an increased frequency
of bowel movements, possibly associated with increased levels of prostaglandin
synthesis [37]. The incidence of constipation seems to be higher in early pregnancy,
with 35–39% of women having constipation in the first and second trimester and
only 21% in the last trimester [38]. Small intestines motility is reduced in preg-
nancy, with increased oral–cecal transit times. Progesterone has been thought to be
the primary cause of the decrease in gastrointestinal motility, but newer studies
showed that the actual etiology may be due to estrogen. Estrogen affects the
increased release of NO from nerves in the gastrointestinal tract that subsequently
cause relaxation of the gastrointestinal tract musculature. Absorption of nutrients
from the small bowel is unchanged aside from the exception of increased iron and
calcium absorption, but the increased transit time provides more efficient absorp-
tion. Parry and colleagues documented an increase in both water and sodium absorp-
tion in the colon [39].
The enlarging uterus produces intestinal displacement, and most importantly, the
position of the appendix changes. Thus, the management of appendicitis regarding
presentation, physical signs, and type of surgical incision are affected. An increase
in portal venous pressure leads to dilation wherever there is portosystemic venous
anastomosis such as at the gastroesophageal junction and the hemorrhoidal veins
resulting in the common complaint of hemorrhoids.
Gallbladder
Gallbladder function is markedly altered because of the effects of progesterone.
Starting in the second trimester, the fasting and residual volumes are double, and the
rate of gallbladder emptying is much slower. Furthermore, the biliary cholesterol
saturation is increased, and the chenodeoxycholic acid level is decreased [40]. As a
result of this change, the composition of the bile fluid favors the formation of cho-
lesterol crystals, and with incomplete emptying of the gallbladder, the crystals are
retained, and enhanced gallstone formation ensues. One third of pregnant women
develop biliary sludge. At the time of delivery, 10–12% of women have gallstones
on ultrasonographic examination. Postpartum, biliary sludge disappears in essen-
tially all women, but only about one third of small stones disappear.
14 P.B. Greenspan
Liver
Pregnancy does not change the size or the histology of the liver. There are, however,
many clinical and laboratory signs present that may be associated with liver disease.
Spider angiomata and palmar erythema, resulting from elevated estrogen levels, are
normal and resolve at the conclusion of the gestation. The serum albumin and total
protein levels fall progressively during pregnancy. Albumin levels are 25% lower
than nonpregnant levels at term. Hemodilution causes a decrease in total protein and
albumin concentrations despite an overall increase in total body protein. Furthermore,
serum alkaline phosphatase levels rise during the third trimester to that of two to
four times those of nongravid women. This increase is explained by placental pro-
duction of the heat-stable isoenzyme and not from the liver [41]. Many protein
serum concentrations produced by the liver increase. Other elevations occur in
serum fibrinogen, ceruloplasmin, transferrin, and the binding proteins for cortico-
steroids, sex steroids, and thyroid hormones [41].
Other “liver function tests” remain unchanged by pregnancy, including serum
levels of bilirubin, aspartate aminotransferase (AST), alanine aminotransferase
(ALT), γ-glutamyltransferase, 5′-nucleotidase, creatinine phosphokinase, and lac-
tate dehydrogenase, with the exception of alkaline phosphatase. The mean levels of
ALT and AST are often mildly elevated but still within normal values [42]. Creatinine
phosphokinase and lactate dehydrogenase levels can increase during labor. Further,
pregnancy may cause some changes in the production and secretion of bile acid.
Pregnancy may be associated with mild subclinical cholestasis resulting from the
high concentrations of estrogen. Reports differ on serum bile acid concentrations,
with some studies showing an increase and others no change. The fasting levels are
unchanged. The measurement of a fasting level appears to be the best test for diag-
nosing cholestasis of pregnancy [42]. Cholestasis is caused by elevated levels of bile
acids and is associated with significant pruritus. It is also noted to produce mild
increases of ALT/AST and an increased risk for poor fetal outcomes.
ausea and Vomiting of Pregnancy

N
Seventy percent of pregnancies are complicated by nausea and vomiting, or “morn-
ing sickness.” Usually, the onset is between 4 and 8 weeks’ gestation. Most women
improve before 16 weeks. As many as 10–25% of women still experience symptoms
at 20–22 weeks’ gestation, and some women experience symptoms throughout the
gestation [43]. In most patients, simple morning sickness rarely leads to significant
weight loss, ketonemia, or electrolyte disturbances. In very few pregnant women,
pernicious nausea and vomiting can be life-threatening. The cause is still poorly
understood, although relaxation of the smooth muscle of the stomach probably
plays a role. Elevated levels of human chorionic gonadotropin (hCG) have been
implicated, although a good correlation between maternal hCG concentrations and
the degree of nausea and vomiting has yet to be demonstrated. Correspondingly,
little data exist to confirm that the etiology is related to higher levels of estrogen or
progesterone. It has been observed that pregnancies complicated by nausea and
vomiting generally have a more favorable outcome than do those without such
symptoms [43]. Management is generally supportive, consisting of reassurance,
avoidance of foods found to prompt nausea, and consuming frequent small meals.
Ingesting dry toast or crackers before getting out of bed may be helpful. The
American College of Obstetricians and Gynecologists has endorsed the use of either
vitamin B6 alone or in combination with doxylamine (Unisom) as a safe and effec-
tive treatment and should be considered a first line of medical treatment. A recent
review of alternative therapies to antiemetic drugs found that acupressure, wrist-
bands, or treatment with ginger root may be helpful.
Hyperemesis gravidarum is a form of nausea and vomiting that is more perni-
cious and is associated with weight loss, ketonemia, electrolyte imbalance, and
dehydration. It affects 1–3% of women, with persistence often throughout preg-
nancy. Rarely does it result in significant complications, but may include Wernicke
encephalopathy, rhabdomyolysis, acute renal failure, and esophageal rupture. The
clinician must rule out other pathologies such as pancreatitis, cholecystitis, hepati-
tis, and psychiatric disease. In some cases, hospitalization with intravenous replace-
ment of fluids and electrolytes is needed. Several options of antiemetics include the
phenothiazines: promethazine (Phenergan), chlorpromazine (Thorazine), and pro-
chlorperazine (Compazine) or metoclopramide (Reglan), or ondansetron (Zofran)
[44]. When hospital admission is inevitable, the patient should be given intravenous
hydration and treated with one of the aforementioned medications (intravenously or
intramuscularly initially). The clinician should not combine the phenothiazines with
metoclopramide because of the additive risks for causing extrapyramidal reactions
(tardive dyskinesia). Chlorpromazine given rectally (25–50 mg every 8 h) may be
highly effective in the more refractory patients. The use of oral methylprednisolone,
16 mg three times daily for 3 days and then tapered over 2 weeks, has been shown
to be more effective than promethazine, but several subsequent trials did not dem-
onstrate benefit from the use of steroids [44].
There is currently no single therapy that works in all women. Occasionally, multiple
different medications must be tried prior to having effective success. There are poten-
tial risks of parenteral caloric replacement, and this option should only be used as a last
resort following multiple antiemetic treatments and attempts at enteral tube feedings.
Musculoskeletal System
Calcium Metabolism
In the past, pregnancy was believed to be a state of “physiologic hyperparathyroid-
ism” with maternal skeletal calcium loss occurring to supply calcium to the fetus. It
was also thought that this could produce long-term maternal bone loss. Now it is
known that the majority of fetal calcium needs are provided by a series of physio-
logical changes in calcium metabolism devoid of long-term consequences to the
maternal skeleton [45]. This allows the fetus to accumulate 21 grams (g) (range
13–33 g) of calcium, 80% of this amount during the third trimester, when fetal skel-
etal mineralization is at its peak. Calcium is actively transported across the placenta.
Interestingly, calcium is excreted in larger amounts by the maternal kidneys so that,
by term, calciuria doubles.
16 P.B. Greenspan
There is a decline of maternal total calcium levels throughout pregnancy.

Reduced serum albumin levels cause the fall of total calcium that result in a decrease
in the albumin-bound fraction of calcium. However, the physiologically important
fraction, serum ionized calcium, is unchanged and constant [45] (Fig. 1.4).
Consequently, maternal serum calcium levels are maintained, and the fetal cal-
cium needs are met largely through increased intestinal calcium absorption. Calcium
absorption occurs in the small intestines, and its absorption doubles by 12 weeks
gestation; maximal absorption occurring in the third trimester [45, 46]. The early
increase in absorption possibly allows the maternal skeleton to accumulate calcium
in advance of the peak third-trimester fetal demands. Although the majority of fetal
calcium needs are met by increased absorption of calcium, accumulating data con-
firm that at least some calcium resorption from maternal bone occurs to assist in
meeting the increased fetal demands in the third trimester. These data are compati-
ble with the hypothesis that physiological mechanisms exist to ensure an adequate
supply of calcium for fetal growth and milk production without sole reliance on the
maternal diet [46]. In similar fashion, maternal serum phosphate levels are
unchanged [45].
In five recent prospective studies of maternal parathyroid hormone (PTH) levels,
all using modern assays, maternal levels of PTH were not elevated and essentially
remained in the low-normal range throughout gestation [45]. Hence, pregnancy is
not concomitant with relative hyperparathyroidism.
The prohormone vitamin D is derived from cholesterol and occurs in two main
nutritional forms: D3 (cholecalciferol), which is produced in the skin, and D2 (ergo-
calciferol), which is derived from plants and absorbed in the gut. Serum levels of
25-hydroxyvitamin D (25[OH]D) increase in proportion to vitamin D synthesis and
intake. The best indicator of vitamin D status is levels of 25[OH]D. 25[OH]D is
further metabolized to 1,25-dihydroxyvitamin D or active vitamin D. Levels of
1,25-dihydroxyvitamin D increase overall in pregnancy, with prepregnancy levels
doubling in the first trimester and peaking in the third trimester [47]. Unless vitamin
D intake or synthesis is changed, levels of 25[OH]D do not change in pregnancy.
Increases in 1,25-dihydroxyvitamin D are secondary to increased production by the
maternal kidneys and potentially the fetoplacental unit and is independent of PTH
control. The increase in 1,25-dihydroxyvitamin D is directly responsible for most of
the increase in intestinal calcium absorption [45]. The prevalence of vitamin D defi-
ciency in pregnancy is 5–50%, which has recently created a great deal of interest.
The recommendations to introduce universal screening during pregnancy by mea-
suring serum levels of 25[OH]D are controversial. Levels less than 32 ng/mL indi-
cate vitamin D deficiency. It is recommended to increase vitamin D supplementation
should a deficiency be diagnosed [47]. Calcitonin levels also rise by 20% and may
help protect the maternal skeleton from excess bone loss [45].
keletal and Postural Changes

S
The effect of pregnancy on bone metabolism is complex. The evidence of mater-
nal bone loss during pregnancy has been inconsistent, with various studies report-
ing bone loss, no change, and even gain. A critical question is whether pregnancy
Fig. 1.4 Calcium in pregnancy. The longitudinal changes in calcium and calcitropic hormone
levels that occur during human pregnancy. Normal adult ranges are indicated by the shaded areas.
1,25-D 1,25-dihydroxyvitamin D, PTH parathyroid hormone (From Gabbe [17]. Reprinted with
permission from Elsevier)
18 P.B. Greenspan
and lactation have a long-term risk for causing osteoporosis later in life [48]. A
recent review of 23 studies, by Ensom and colleagues, determined that pregnancy
is a state of high bone turnover and remodeling. Pregnancy and lactation can
cause reversible bone loss; the loss being increased in women who breastfeed for
longer intervals [48]. There is no support of an association between parity and
osteoporosis later in life. Furthermore, in a comparison of female twins discordant
for parity, pregnancy and lactation were found to have no detrimental effect on
long-term bone loss.
Bone turnover is apparently low in the first half of gestation, but then it increases
in the third trimester, corresponding to the peak rate of fetal calcium needs, and may
represent turnover of previously stored skeletal calcium [45]. Markers of both bone
resorption (hydroxyproline and tartrate-resistant acid phosphatase) and bone forma-
tion (alkaline phosphatase and procollagen peptides) are increased during gestation
[46]. Shahtaheri and associates, in the only study of bone biopsies performed during
pregnancy, noted a change in the microarchitectural pattern of bone; however, no
change in overall bone mass was elucidated. This change in the microarchitectural
pattern seems to result in a framework more resistant to the bending forces and
biomechanical stresses needed to carry a growing fetus [49]. Multiple recent studies
that support these findings have shown that bone loss occurs only in the trabecular
bone and not cortical bone. Promislow et al., measured bone mineral density twice
during pregnancies using dual-energy x-ray absorptiometry and showed the mean
loss of trabecular bone was 1.9% per 20 weeks’ gestation [50]. However, women
placed on bed rest had significantly greater bone loss. In comparison, the mean bone
loss in postmenopausal women rarely exceeds 2% per year. There are previous
reports that indicate that the cortical bone thickness of long bones may even increase
with pregnancy.
Osteoporosis during or soon after pregnancy is rare, despite the bone loss that
occurs. It remains controversial whether additional calcium intake during pregnancy
and lactation prevents bone loss. More recent studies indicate that calcium supple-
mentation does not decrease the amount of bone loss, but Promislow and associates
found that maternal intake of 2 g per day or greater was modestly protective [50].
This exceeds the recommended dietary allowance of 1000–1300 mg/day during
pregnancy and lactation [46].
Progressively increasing anterior convexity of the lumbar spine (lordosis) occurs
in pregnancy. This is a compensatory mechanism that keeps the woman’s center of
gravity over her legs and prevents the enlarging uterus from shifting the center of
gravity anteriorly. Low back pain in two thirds of women is an unfortunate side
effect of this compensation. In one third of the women, this pain is described as
severe. Ligaments that support the pubic symphysis and sacroiliac joints loosen,
assumed to be from the effects of the hormone relaxin. Relaxin levels increase ten-
fold in pregnancy. Marked widening of the pubic symphysis occurs by 28–32 weeks’
gestation, with the width increasing from 3–4 mm to 7.7–7.9 mm. As a result, pain
is referred down the inner thigh with standing and may result in a disturbing sensa-
tion of snapping or movement of the bones with walking.
Renal System
One of the most significant adaptations of pregnancy is the increase in total body
water of 6.5–8.5 L by the end of gestation. The fetus, placenta, and amniotic fluid
at term account for approximately 3.5 L of water content. Additional water is
accounted for by expansion of the maternal blood volume by 1500–1600 mL,
plasma volume by 1200–1300 mL, and red blood cells by 300–400 mL. The bal-
ance is attributed to extravascular fluid, intracellular fluid in the uterus and breasts,
and expanded adipose tissue. Consequently, pregnancy produces chronic volume
overload with active sodium and water retention secondary to changes in the
osmoregulation and the renin–angiotensin system. The increase in body water
content contributes to maternal weight gain, hemodilution, physiological anemia
of pregnancy, and the elevation in maternal cardiac output. Inadequate plasma
volume expansion has been associated with increased risks for preeclampsia and
fetal growth restriction [33].
Osmoregulation
Shortly after conception, expansion in plasma volume begins, mediated partially
by a change in maternal osmoregulation through altered secretion of arginine
vasopressin (AVP) by the posterior pituitary. Water retention exceeds sodium
retention despite an additional 900 mEq of sodium being retained during preg-
nancy, and serum levels of sodium decrease by 3–4 mmol/L. This is reflected by
decreased overall plasma osmolality of 8–10 mOsm/kg, a change that is in place
by 10 weeks’ gestation and continues through 1–2 weeks postpartum [51].
Correspondingly, the threshold for thirst and vasopressin release changes early in
pregnancy; during gestational weeks 5–8, an increase in water intake occurs and
results in a transient increase in urinary volume but a net increase in total body
water. Initial changes in AVP regulation may be due to placental signals involv-
ing NO and the hormone relaxin [52]. Following the 8th week of gestation, the
new steady state for osmolality has been established with little subsequent change
in water turnover, resulting in decreased polyuria. Pregnant women discern fluid
challenges or dehydration normally with changes in thirst and AVP secretion, but
at a new, lower “osmostat” [52].
The levels of plasma AVP remain relatively unchanged despite heightened pro-
duction because of the threefold to fourfold increase in the metabolic clearance.
Increased clearance results from a circulating vasopressinase produced by the pla-
centa that rapidly inactivates both AVP and oxytocin. This enzyme increases about
300–1000-fold over the course of gestation proportional to fetal weight, with the
highest concentrations occurring in multiple gestations. Increased AVP clearance
can unmask subclinical forms of diabetes insipidus, presumably because of an
insufficient pituitary AVP reserveand causes transient diabetes insipidus with an
incidence of 2–6 per 1000. Typically presenting with polydipsia and polyuria,
hyperosmolality is usually mild unless the thirst mechanism is abnormal or access
to water is limited [53].
20 P.B. Greenspan
Salt Metabolism
Sodium metabolism is carefully balanced, facilitating a net accumulation of about
900 mEq of sodium. The fetoplacental unit contains 60% of the additional sodium
(including amniotic fluid) and is lost at delivery. By 2 months postpartum, the serum
sodium returns to preconceptional levels. Pregnancy increases the preference for
sodium intake and is explained primarily by enhanced tubular sodium reabsorption.
Increased glomerular filtration raises the total filtered sodium load from 20,000 to
about 30,000 mmol/day; sodium reabsorption must increase to prevent sodium loss.
However, the adaptive rise in tubular reabsorption surpasses the increase in filtered
load, resulting in an additional 2–6 mEq of sodium reabsorption per day. Alterations
in sodium handling signify the largest renal adjustment that occurs in gestation [54].
Hormonal control of sodium balance is under the opposing actions of the Renin–
Angiotensin–Aldosterone System and the natriuretic peptides; both being modified
during pregnancy [33].
Renin–Angiotensin–Aldosterone System
Normal pregnancy is typified by a significant increase in all components of the
Renin–Angiotensin–Aldosterone System (RAAS) system. In early gestation,
reduced systemic vascular tone (attributed to gestational hormones and increased
NO production) results in decreased mean arterial pressure (MAP). As a result,
decreased MAP activates adaptations to preserve intravascular volume through
sodium retention [4]. Plasma renin activity, renin substrate (angiotensinogen), and
angiotensin levels are all increased a minimum of fourfold to fivefold over nonpreg-
nant levels. Activation of these components of RAAS leads to twofold elevated
levels of aldosterone by the third trimester, increasing sodium reabsorption and pre-
venting sodium loss. Regardless of the elevated aldosterone levels in late pregnancy,
normal homeostatic responses still occur to changes in salt balance, fluid loss, and
postural stimuli. In addition to aldosterone, other hormones that may contribute to
increased tubular sodium retention include deoxycorticosterone and estrogen.
trial and Brain Natriuretic Peptide

A
Circulatory hemostasis is maintained by neuropeptides that are released in the myo-
cardium. Atrial natriuretic peptide (ANP) is secreted primarily by the atrial myo-
cytes in response to dilation, and in response to end-diastolic pressure and volume,
the ventricles secrete brain natriuretic peptide (BNP). Both peptides have similar
physiological actions, acting as diuretics, natriuretics, vasorelaxants, and overall
antagonists to the RAAS. Elevated levels of ANP and BNP are found in both physi-
ological and pathological conditions of volume overload and can be used to screen
for congestive heart failure outside of pregnancy in symptomatic patients. As gravi-
das frequently present with shortness of air and many of the physiological effects of
conception mimic heart disease, it is clinically significant whether pregnancy affects
the levels of these hormones. Gestational alterations in ANP are controversial
because some authors have reported higher plasma levels during different stages of
pregnancy, whereas others have reported no change. In a meta-analysis by Castro
and colleagues, ANP levels were 40% higher during gestation and 150% higher dur-
ing the first postpartum week [55].
The circulating concentration of BNP is 20% less than that of ANP in normal
individuals and noted to be more useful in the diagnosis of congestive heart failure.
Levels of BNP are reported to increase largely in the third trimester of pregnancy
compared with first-trimester levels (21.5 ± 8 pg/mL vs. 15.2 ± 5 pg/mL) and are
highest in pregnancies complicated by preeclampsia (37.1 ± 10 pg/mL). The levels
throughout pregnancy have been found to be higher than in nonpregnant controls.
Preeclamptic pregnancies demonstrate higher levels of BNP, which are associated
with echocardiographic evidence of left ventricular enlargement [56]. Although the
levels of BNP are increased during pregnancy and with preeclampsia, the mean
values are still lower than the levels used to screen for cardiac dysfunction (>75–
100 pg/mL) and, therefore, can be used to screen for congestive heart failure [57].
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Overview of the Normal Development
of the Human Embryo and Fetus 2
David C. Mundy and Gustavo Vilchez
Introduction
Although the complex mechanisms controlling human development have not yet
been fully delineated, science and technology have advanced the understanding of
these processes. Fertilization of the ovum by the spermatozoa initiates a transfigura-
tion resulting in a fully formed infant, whose development continues long after the
day of delivery. During gestation, numerous changes occur at the cellular level,
including cell division, migration, differentiation, rearrangement, transportation,
growth, and apoptosis [1]. This chapter will provide an overview of early pregnancy
events and review the development of major fetal organ systems. When discussing
the developing human, confusion may exist because of the differences in embry-
onic, fetal, and gestational age. Unless otherwise stated, gestational age will be the
primary measure in this chapter.
Periods of Antenatal Human Development
By convention, human antenatal development is typically divided into two phases

(Fig. 2.1) [1]:
(a) Embryonic development phase: The embryonic phase starts with fertilization
and continues until the 10th week of gestation. Totipotent cells, which form the
embryo, and extraembryonic tissue are present during the first few cell divisions
D.C. Mundy, MD, FACOG (*) • G. Vilchez, MD

Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine,
University of Missouri Kansas City School of Medicine, Truman Medical Centers,

in Pregnancy, DOI 10.1007/978-3-319-62283-5_2
26 D.C. Mundy and G. Vilchez
Fig. 2.1 Phases of antenatal human development (Image used under license from Shutterstock.
com)
and give way to pluripotent cells that differentiate into the cells forming all
components of the body.
( b) Fetal development phase: The fetal phase begins during the 10th gestational
week and ends on the day of delivery. This period is characterized by organ dif-
ferentiation and growth [1, 2].
The Embryonic Period
First Postconceptional Week

Week 1 begins at conception and typically occurs approximately 14 days after the
onset of the last menstrual period. Embryonic age at week 1 therefore correlates
with a gestational age of 3 weeks. Fertilization normally takes place in the ampulla
of the fallopian tube (Fig. 2.2) [2, 3]. The sperm penetrates the corona radiata of the
ovum, binds to, and then penetrates the zona pellucida. It then enters the oocyte
membrane, fuses to the oocyte, and forms a highly specialized totipotent cell called
the zygote [1]. After its formation, the zygote undergoes cleavage, which is charac-
terized by a sequence of mitotic cell divisions into daughter cells called blastomeres
[1, 2].
Cleavage starts approximately 30 h after fertilization. The mass of the blasto-
meres does not increase during these divisions, so the entire embryo maintains its
size [2, 4].
2 Overview of the Normal Development of the Human Embryo and Fetus
27
Fig. 2.2 First postconceptional week of embryonic development (Image used under license from Shutterstock.com)
Three days after fertilization the conceptus consists of 12–32 blastomeres and
becomes the morula [1]. The morula enters the uterus approximately 4 days after
fertilization [5]. Fluid accumulates within the morula and forms a cavity [4, 6]. At
this point, the developing human is called the blastocyst. This cavity separates the
conceptus into two parts (Fig. 2.2):
(a) The trophoblast: the thin outer cell layer formed by 53 cells [4, 5] that gives rise
to the placenta, and
(b) The embryoblast: a group of five centrally located pluripotent cells [4, 5] that
gives rise to the embryo.
Approximately 4 days after fertilization, the zona pellucida degenerates. Six to

seven days after fertilization (day 20 after the first day of the last menstrual period),
the blastocyst attaches to the endometrium and implantation begins [1].
Implantation typically occurs at the posterior and superior portion of the uterus,
in the functional layer of the endometrium during the secretory phase of the men-
strual cycle. As the blastocyst attaches to the endometrium, the trophoblast will
differentiate into the cytotrophoblast and the syncytiotrophoblast [7].
Second Postconceptional Week

The process of implantation occurring during the second week can be divided into
four stages: lysis or “hatching” of the surrounding zona pellucida; apposition of
trophoblast cells into the decidua of endometrium; adhesion; and invasion [8]. At
implantation (Fig. 2.2), the embryoblast undergoes cellular proliferation and dif-
ferentiation into two layers:
(a) The epiblast: a dorsal layer formed by columnar cells, and

(b) The hypoblast: a ventral layer formed by cuboid cells.
These two layers form the primordial bilaminar embryonic disc, which will give
rise to the three germ cell layers that will form all the body’s tissues and organs
(Fig. 2.3).
Upon implantation of the blastocyst, the syncytiotrophoblast produces human
chorionic gonadotropin (hCG). Secreted hCG enters the maternal blood via the
lacunae, which are small blood-filled spaces that form in the syncytiotrophoblast.
These lacunae will form a primitive uteroplacental circulation to pass oxygen and
provide nutrients to the embryonic disc. Production of hCG is sufficient by the end
of the second week to yield a positive pregnancy test [9].
Within the epiblast, small clefts develop that subsequently coalesce and form the
primordium of the amniotic cavity [2]. This primordial amniotic cavity becomes
lined by a thin layer of cells from the epiblast to form the amnion [10].
Hypoblast cells migrate and line the inner surface of the cytotrophoblast to form
the exocoelomic membrane, which delimits the former blastocyst cavity and forms
the primary umbilical vesicle.
Connective tissue from the epiblast surrounds the amnion and umbilical vesicle,
filling the space between the exocoelomic membrane and the cytotrophoblast, form-
ing the extraembryonic mesoderm.
2 Overview of the Normal Development of the Human Embryo and Fetus 29
Fig. 2.3 Origin of the three germ cell layers and their derivatives
Fluid-filled spaces then appear in the extraembryonic mesoderm. These spaces

will form the extraembryonic coelom or chorionic cavity surrounding the amnion
and umbilical vesicle. The remaining of mesoderm, called the connecting stalk, is
the structure that maintains the embryonic attachment to the trophoblast. The extra-
embryonic coelom divides the extraembryonic mesoderm into somatic and splanch-
nic layers. The somatic mesoderm will merge with the trophoblast to form the
chorionic sac.
Third Postconceptional Week

During the third week, the bilaminar embryonic disc is converted into a trilaminar
disc by gastrulation. These three germ layers will give rise to all the tissues and
organs of the human body.
Fig. 2.4 Third postconceptional week of embryonic development (Image used under license from
Shutterstock.com)
Gastrulation begins with the formation of the primitive streak, which is an inden-
tation of the epiblastic surface in the caudal portion of the embryo (Fig. 2.4). From
this primitive streak, epiblast cells migrate ventrally, laterally, and cranially between
the epiblast and hypoblast. Subsequently, the epiblast transforms into embryonic
ectoderm. Some epiblast cells also displace the hypoblast and form embryonic
endoderm (Fig. 2.4). Mesenchymal cells occupy the area between ectoderm and
endoderm, and form the intraembryonic mesoderm [11]. All three germ cell layers
are derived from the epiblast [8]. These mesenchymal cells migrate between the
ectoderm and mesoderm to form the intraembryonic mesoderm:
(a) The first cells that travel toward the cephalic end will form the prechordal plate.
(b) Mesenchymal cells that migrate cranially from the primitive node form a
median cellular cord called the notochordal process. This notochordal process
will merge with cells from the hypoblast to form the notochord. This structure
extends from the primitive node to the prechordal plate.
(c) Mesodermal cells that migrate to the embryonic disc edges will join the extra-
embryonic mesoderm surrounding the amnion and umbilical vesicle.
(d) The paraxial mesoderm, a thick plate of mesoderm located at each side of the
midline, will form the somites.
(e) The lateral mesoderm is a thin plate of mesoderm located along the lateral sides
of the embryo, which develops into the intraembryonic coelom.
(f) Mesoderm cells traveling to the cranial end to a horseshoe-shaped region called
the cardiogenic region will form the future heart.
The notochord is the primordium of the vertebral column. The notochord induces
a thickening in the embryonic ectoderm called the neural plate. A groove along the
neural plate forms the neural folds (Fig. 2.4). The neural folds fuse with the neural
plate to form the neural tube, which is the progenitor of the central nervous system
(CNS) [9]. The neural crest is formed between the surface ectoderm and neural
tube. Mesoderm on each side of the notochord forms longitudinal columns of par-
axial mesoderm that will give rise to the somites.
The heart and great vessels are formed from mesenchymal cells in the cardio-
genic area. Endocardial heart tubes fuse to form the primordial heart tube. These
tubes join with the formed blood vessels to form the primordial cardiovascular
system [9].
ourth to Eighth Postconceptional Weeks

F
During this period, the three germ layers differentiate into various tissues that will
form the primordia of most of the major organs and systems of the body [2].
Exposure to teratogens during this period may cause malformations [10].
At this stage of development, the uteroplacental circulation alone is no longer
sufficient to satisfy the increasing nutritional needs of the embryo. Development of
the cardiovascular system to supplement nutritional needs is critical for survival.
Differential growth rates cause the flat embryo to develop curves and folds com-
mencing on day 22. Due to the growth of the neural tube and the amnion in the
median plane (craniocaudal folding), the enlarging sheet of the embryo pushes out
and over the rim of the umbilical vesicle [2]. At the cranial end, the neural tube
forms, the buccopharyngeal membrane (Fig. 2.4) is positioned where the mouth will
develop, and the cells that will form the heart tube are positioned in what will be the
future thorax. At the caudal end, the connecting stalk is in the region of the future
umbilical cord, and the cloacal membrane is positioned more caudally (Fig. 2.4).
Due to the growth of the somites, the amnion and the lateral body walls, the left
and right flanks of the embryonic disc extend and curl around and underneath the
embryo, squeezing the sides of the umbilical vesicle (lateral folding). The flanks
meet in the midline ventrally, and the germ cell layers of both flanks fuse. The
umbilical vesicle is converted to a slender vitelline duct [2]. The ectoderm fuses
and forms the external surface of the embryo. The endoderm forms the primitive
gut, from the buccopharyngeal membrane cranially and the cloacal membrane
caudally [10].
Because of median and lateral folding, the initial trilaminar embryonic disc is
converted to a c-shaped, cylindrical embryo. By the end of the eighth week, the
embryo has recognizable human morphology [10]. Major organ systems have begun
development even though functionality may be minimal.
The Fetal Period
The fetal period, beginning at a gestational age of 11 weeks and continuing to deliv-
ery, is characterized development that involves rapid corporeal growth and differen-
tiation of tissues, organs, and systems (Fig. 2.1) [4]. As most of the organs are
already developed, the fetus is less vulnerable to teratogens during this period.
However, some agents may still interfere with growth and functional development.
There is a relative slowing in the growth of the head compared with the growth
of the rest of the body [7]. By the 11th week, the face is broad, eyes are widely sepa-
rated, eyelids are fused, and ears are low set. By the 12th week, swallowing can be
visualized, and fingernail development commences.
By the 14th week, primary ossification centers appear in the cranium and long
bones. The neck is well defined. The upper limbs have almost reached their maxi-
mum length in relation to the body. The fingers and toes have become differentiated.
The liver is the major site of erythropoiesis. The intestines rotate into the abdomen
[4]. Urine formation begins and is discharged through the urethra into the amniotic
cavity. The external genitalia become identifiable. The fetus can be observed mak-
ing spontaneous movements [12].
By 15 weeks, fetal growth accelerates. The fetal head continues to grow, but at a
rate less than the fetal corpus. The fetal head measures about half the size of the
fetus [4]. Scalp hair may be visualized. The position of the eyes is more anterior and
no longer anterolateral. The external ears approximate to their position at term.
Lower limbs lengthen, and their movements become coordinated and visible during
ultrasonography. Primary ossification centers are active and developing bones are
visible on ultrasound. Ovaries are differentiated and contain primordial ovarian fol-
licles. Genitalia can be recognized [13]. Respiratory movements can be seen by
16 weeks. By the 16th–18th week, eye movement begins, coinciding with midbrain
maturation [12].
By the 21st week, lanugo and head hair appear, and the skin is less transparent
and coated with vernix caseosa. Substantial weight gain occurs, and the fetus
becomes better proportioned [13]. Fetal movements are clearly recognized by the
mother, and the fetus is active 30% of the time [12]. The skin is pink, wrinkled, and
more translucent. Rapid eye movements and blinking commence. Fingernails start
apparent. Type II pneumocytes begin to secrete surfactant. Fetuses born at this ges-
tational period are usually capable of extrauterine existence, mainly because of the
maturity of its respiratory system, but it will require intensive care unit care [13].
Cochlear function develops by 22nd–25th weeks [12]. Sucking movements can be
seen by 24 weeks [4].
By 26 weeks, the eyes begin to open, and lanugo and head hair are well devel-
oped. Toenails are visible, and considerable subcutaneous fat develops under the
skin, giving the fetus a smooth, healthy appearance [13]. The CNS is able to direct
rhythmic breathing movements and control body temperature, and some sounds can
be perceived by the fetus [4]. Lungs and pulmonary vasculature have developed suf-
ficiently to provide adequate gas exchange. The neural pain system is developed
[12]. The fetal spleen is an important site of erythropoiesis up to 28 weeks, and then
the bone marrow becomes the major site of erythropoiesis [13]. By 28 weeks, eyes
may be wide open and are sensitive to light [4].
By 30 weeks, the pupillary reflex develops. The limbs develop a chubby appear-
ance [13]. In males, the testicles begin to descend.
By 35 weeks, there is a decrease in the growth rate as the time of birth approaches.
Fetus adds 14 g of fat per day during these last weeks, being most of the time plump,
and can reach 360 mm of height and 3400 grams [13]. The nervous system is mature,
and the fetus can carry out some integrative functions, such us firm grasp and orien-
tation to light. The thorax is prominent and the breasts protrude [13]. The testicles
are usually descended in full-term male neonates [13].
Important Aspects of Specific Fetal Systems Development
Nervous System
The process of formation of the neural tube is called neurulation [14]. The noto-
chord and paraxial mesenchyme induce the thickening of ectoderm, called the neu-
ral plate, which gives rise to the CNS [15]. The neural plate invaginates to form a
neural groove with neural folds on each side. The neural folds fuse and the neural
tube is formed during the fourth week. The neural tube is initially open at each end
(rostral and caudal neuropores) and communicates with the amniotic cavity through
these neuropores. The anterior neuropore will close by day 25 and will become the
lamina terminalis. The posterior neuropore will close by day 27 [11]. The notochord
will form the nucleus pulposus of the intervertebral disk [14].
The neural tube has a broad cephalic portion and a long caudal portion [4]. The
portion of the neural tube forming the primordial brain undergoes flexion at three
points: mesencephalic flexure; cervical flexure; and pontine flexure. The first two
flexures are ventral; the third flexion is dorsal [2]. Three primary brain vesicles
develop during week 4 in the cranial end of the neural tube: the forebrain; the mid-
brain; and the hindbrain (Fig. 2.5). During week 6, five secondary brain vesicles
will form. The forebrain splits into the telencephalon and diencephalon. The dorsal
telencephalon will form the cerebral cortex; the ventral telencephalon will become
the basal ganglia. The diencephalon will form the optic cup and stalk, the pituitary
gland, thalamus, hypothalamus, and pineal body. The mesencephalon does not sub-
divide and becomes the adult midbrain (Fig. 2.5) [4].
The hindbrain divides into the metencephalon and myelencephalon. The meten-
cephalon will form the pons ventrally and the cerebellum dorsally [8]. The myelen-
cephalon will form the medulla oblongata. The caudal end of the neural tube
continues to elongate and forms the spinal cord [11]. The neural canal (neurocele)
forms by 9 week and differentiates into the ventricles of the brain and the central
canal of the medulla and spinal cord [8]. The walls of the neural tube thicken by
neuroepithelial cellular proliferation, and give rise to all nerve and macroglial cells
in the CNS (Fig. 2.5). The microglia differentiates from mesenchymal cells that
enter the CNS with the blood vessels [11].
Cardiovascular System
The heart and vascular systems develop from the splanchnic mesoderm by the third
week after fertilization [16]. Heart progenitor cells migrate through the primitive
streak to a position cranial to the neural folds where they form a horseshoe-shaped
Fig. 2.5 Primordium of the nervous system and its derivatives. Sections of the primitive neural
tube, vesicles, and adult derivatives (Image used under license from Shutterstock.com)
region [4]. Blood islands appear in this region and split the mesoderm into somatic
and splanchnic layers, forming the pericardiac cavity [8]. As folding of the embryo
occurs, the heart-forming regions fuse at midline and form a continuous sheet of
mesoderm. Vascular channels form within this sheet of mesoderm, remodeling into
a single endocardial tube. Progenitor cells migrate from the epiblast to become
myoblasts and surround the endocardial tube. The primordial heart starts beating
during the fourth week [7].
The heart primordium consists of four chambers: the bulbus cordis; primitive
ventricle; primitive atrium; and sinus venosus [7]. The truncus arteriosus (primor-
dium of the ascending aorta and pulmonary trunk) is continuous caudally with the
bulbus cordis, which becomes part of the ventricles. These chambers, by looping,
folding, remodeling, and partitioning [16], will give rise to the main structures of
the adult heart (Fig. 2.6). As the heart grows, it starts to bend at 23 days to the right
undergoing an S-shaped looping and soon acquires the general external appearance
of the heart. The heart becomes partitioned into four chambers between the fourth
and seventh weeks.
The critical period of heart development is from day 20 to day 50 after fertiliza-
tion [7]. Numerous events occur during cardiac development, and deviation from
the normal pattern at any time may produce one or more congenital defects.
Fig. 2.6 Dilations of the heart primordium and definitive structures. Vesicles of the primitive heart
and derivative structures
Respiratory System
The development of the fetal lung is divided into four stages (Table 2.1): pseudo-
glandular (6–16 weeks); canalicular (16–26 weeks); terminal sac (26 weeks to
birth); and alveolar (32 weeks to birth). By the fourth week, a laryngotracheal diver-
ticulum develops from the floor of the primordial pharynx at the ventral wall of the
developing gut. This diverticulum becomes separated from the foregut by tracheo-
esophageal folds that fuse to form a tracheoesophageal septum [17]. This septum
results in the formation of the esophagus and laryngotracheal tube.
The endoderm of the laryngotracheal bud gives rise to the lower respiratory
organs and tracheobronchial gland epithelium. The splanchnic mesenchyme that
surrounds this respiratory bud will form connective tissue, cartilage, muscle, blood,
and lymphatic vessels [8]. Pharyngeal arch mesenchyme forms the epiglottis and
connective tissue of the larynx. Mesenchyma from the caudal pharyngeal arches
will form the laryngeal muscles. The laryngeal cartilages are derived from neural
crest cells [17].
Table 2.1 Stages in the development of the respiratory system

Stage Time Events during development
Embryonic 3–5 weeks Initial bud (respiratory diverticulum)
Initial three rounds of branching to form the
primordia of lungs, lobes, and segments
Diverticulum stem forms the trachea and larynx
Pseudoglandular 5–16 weeks Respiratory tree branching
Formation of terminal bronchioles
No respiratory bronchioles or alveoli are present yet
Canalicular 16–26 weeks Terminal bronchiole divides into respiratory
bronchioles
Respiratory vasculatory begins to develop
Differentiation of respiratory epithelium
Saccular 26 weeks to term Respiratory bronchioles divide to produce terminal
sacs
Capillaries establish close contact with terminal
sacs
Alveolar 8 months to Mature alveoli with well-developed blood–air
childhood barrier
During the fifth week, the distal end of the laryngotracheal diverticulum divides
into two bronchial buds. Each bronchial bud enlarges to form a main bronchus, and
then the main bronchus subdivides to form lobar, segmental, and subsegmental
branches. Each tertiary bronchial bud with the surrounding mesenchyme represents
the primordium of each bronchopulmonary segment [17].
Canals of tubes branch out from the terminal bronchioles, and each tube forms
an acinus comprising the terminal bronchiole, an alveolar duct and a terminal sac,
which forms the primitive alveolus. By 20–22 weeks, type II pneumocytes begin to
secrete pulmonary surfactant [17]. Growth of the lungs will continue until and after
birth.
Gastrointestinal System
The primordial gut forms from the dorsal part of the umbilical vesicle after it rotates
into the embryo during lateral folding [8]. Endoderm will form the lining of the
primordial gut, except at the cranial and caudal parts, which are derived from ecto-
derm of the buccopharyngeal membrane and cloacal membrane, respectively [10].
The primordial gut remains in contact with the umbilical vesicle through the
vitelline duct. The cranial end of the primordial gut is sealed by the buccopharyn-
geal membrane, which will deteriorate during the fourth week and become the
mouth. The caudal end is sealed by the cloacal membrane, which will deteriorate
during the seventh week and become the anus. This opening will further connect the
primordial gut with the umbilical vesicle. The mesenchyme surrounding the primor-
dial gut gives rise to the muscular and connective tissue of the gastrointestinal track.
Buds develop along the length of the tube that will form gastrointestinal and respira-
tory structures.
The gut is divided into three portions: the foregut; the midgut; and the hindgut.
The foregut develops into the pharynx, lower respiratory system, esophagus, stom-
ach, proximal part of the duodenum, liver, pancreas, and biliary system. The lower
foregut begins to dilate by the fourth week; the dorsal side grows faster than the
ventral side until the sixth week, then after that it will become the stomach [18].
An outgrowth of the endodermal epithelial lining of the foregut gives rise to the
hepatic diverticulum, primordium of the liver, gallbladder, and biliary duct system
[10]. The hepatic diverticulum forms epithelial cords that become the septum trans-
versum. Primordial cells between the layers of the ventral mesentery derived from
the septum transversum differentiate into hepatic tissues and linings of the ducts of
the biliary system. The endodermal lining of the foregut forms the ventral and dor-
sal pancreatic buds [10].
When the duodenum rotates to the right, the pancreatic bud fuses to give rise to
the pancreas. The ventral bud forms the head of the pancreas and the uncinate pro-
cess. The dorsal pancreatic bud forms the remainder of the pancreas.
The midgut gives rise to the duodenum, jejunum, ileum, cecum, appendix,
ascending colon, and right transverse colon. It forms a U-shaped umbilical loop of
intestine that herniates into the umbilical cord during the sixth week because there
is no room for it in the abdomen. While in the umbilical cord, the midgut loop
rotates counterclockwise 90°. During the 10th week, the intestines return to the
abdomen, rotating a further 180° [10].
The hindgut becomes the left transverse colon, the descending and sigmoid
colon, the rectum, and the superior part of the anal canal. The anal pit gives rise to
the inferior part of the anal canal. The caudal part of the hindgut divides the cloaca
into the urogenital sinus anteriorly and the anorectal canal posteriorly. The urogeni-
tal sinus gives rise to the urinary bladder and urethra [10]. The rectum and superior
part of the anal canal are separated from the exterior by the cloacal membrane,
which will break down by the end of the eighth week, opening the gut to the amni-
otic cavity.
Urinary System
Production of urine by the fetus is important for maintenance of amniotic fluid vol-
ume and composition [16]. The urinary system arises from the intermediate meso-
derm [18]. At the level of the abdomen, this intermediate mesoderm forms a
condensation of cells called the urogenital ridge. This ridge contains the nephro-
genic cord and the gonadal ridge [8].
By the fourth week, the cloaca is split by the urorectal septum into the urogenital
sinus (ventrally) and the anal canal (dorsally). The top portion of the urogenital
sinus, the allantois, and the surrounding splanchic mesenchyme give rise to the
bladder. The middle and lower portions of the urogenital sinus will form the
urethra.
The nephrogenic cord evolves into three kidney components: the pronephros; the
mesonephros; and the metanephros.
The first system called the pronephros appears by the third week at the level of
the embryo neck. It is a transitory, nonfunctional structure that disappears by the
fifth week.
The second phase of renal development, called the mesonephros, appears by the
fourth week. This system develops caudally to the pronephros by differentiation of
the mesoderm in a craniocaudal sequence that forms pairs of mesonephric ducts
(Wolffian ducts) and mesonephric tubules. It is a partially transitory structure, as the
tubules regress, but the ducts persist and open into the urogenital sinus.
The third phase of renal development is the metanephros (primordia of the per-
manent kidney) and begins to form by the fifth week caudal to the mesonephros
[12]. It develops from an outgrowth of the mesonephric duct to form the ureteric
bud, as well as from a condensation of mesoderm within the nephrogenic cord
called the metanephric blastema, and will finally become the newborn kidney.
The ureteric buds branch and give rise to the ureter, renal pelvis, calices, and col-
lecting tubules [8]. The metanephrogenic blastema, metanephric diverticulum, and
growing vascular endothelial cells within the developing metanephros will give rise
to the nephrons [17]. Capillaries grow into Bowman’s capsule from the dorsal aor-
tae and convolute to form the glomeruli. The ureters insert into the posterior bladder
wall. This functional renal unit will produce urine from week 12 onwards and will
continue to form throughout fetal life [18].
The intricate and complex process of embryonic and fetal development informs
the clinician that stresses such as diseases and conditions that may produce abdom-
inal pain in the gravid female could easily disrupt pregnancy, yet in most cases,
they do not.
Other influences such as anesthetics, radiation from imaging, and mechanical
manipulations during surgery also can interfere with the developing fetus, but, sur-
prisingly, usually do not.
Nonetheless, clinicians must appreciate the developmental process of the fetus
when considering any issue that involves the patient in whom the fetus resides.
References
1. Moore KL, Persaud TVN, Torchia MG. Introduction to human development. In: Moore KL,
Persaud TVN, Torchia MG, editors. The developing human clinically oriented embryology.
London: Elsevier Health Sciences; 2015. p. 1 online resource (681 p.).
2. Schoenwolf GC, et al. Gametogenesis, fertilization, and first week. In: Schoenwolf GC, et al.,
editors. Larsen’s human embryology. Philadelphia: Elsevier Churchill Livingstone; 2015.
p. 14–42.
3. Sadler TW, Langman J. Langman’s medical embryology. 11th ed. Philadelphia: Wolters
Kluwer Health/Lippincott William & Wilkins; 2010. ix, 385 pages, 3 unnumbered pages of
plates.
4. Sadler TW, Sadler-Redmond SL, Tosney K. Langman’s medical embryology. 13th ed.
Philadelphia: Wolters Kluwer; 2015. xiii, 407 pages.
5. Creasy RK, et al. Normal early development. In: Creasy RK, et al., editors. Creasy and
Resnik’s maternal-fetal medicine principles and practice. Philadelphia: Elsevier/Saunders;
2014. p. 37–46.
6. Sadler TW, Langman J. First week of development: ovulation to implantation. In: Sadler TW,
Langman J, editors. Langman’s medical embryology. Philadelphia: Wolters Kluwer Health/
Lippincott Williams & Wilkins; 2012. p. 34–48.
7. Moore KL, Persaud TVN, Torchia MG. Fetal Period. In: Moore KL, Persaud TVN, Torchia
MG, editors. The developing human clinically oriented embryology. London: Elsevier Health
Sciences; 2015. p. 1 online resource (681 p.).
8. Webster S, Corporation E. Embryology at a glance. Place of publication not identified: John
Wiley & Sons; 2016. p. 1 online resource.
9. Moore KL, Persaud TVN, Torchia MG. Cardiovascular system. In: Moore KL, Persaud TVN,
Torchia MG, editors. The developing human clinically oriented embryology. London: Elsevier
Health Sciences; 2015. p. 1 online resource (681 p.).
10. Moore KL, Persaud TVN, Torchia MG. Alimentary system. In: Moore KL, Persaud TVN,
Torchia MG, editors. The developing human clinically oriented embryology. London: Elsevier
Health Sciences; 2015. p. 1 online resource (681 p.).
11. Moore KL, Persaud TVN, Torchia MG. Third week of human development. In: Moore KL,
12. Cunningham FG, Williams JW. Embryogenesis and fetal morphological development.

In: Cunningham FG, Williams JW, editors. Williams Obstetrics: 24rd edition. New York:
McGraw-Hill Medical; 2014. p. 127–53.
13. Moore KL, Persaud TVN, Torchia MG. Second week of human development. In: Moore KL,
14. Dudek RW. High-yield embryology. 2nd ed. Philadelphia: Lippincott Williams & Wilkins;
2001. xi, 151 pages.
15. Moore KL, Nervous system. In: Moore KL, Persaud TVN, Torchia MG, editors. The devel-
oping human: clinically oriented embryology. London: Elsevier Health Sciences; 2015. p. 1
online resource (681 p.).
16. Ross M, Ervin M. Fetal Development and Physiology. In: Gabbe S. Obstetrics: Normal and
Problem Pregnancies. Philadelphia: Elsevier, 2017.
17. Moore KL, Persaud TVN, Torchia MG. Respiratory system. In: The developing human clini-
cally oriented embryology. London: Elsevier Health Sciences; 2015. p. 1 online resource
(681 p.).
18. Carlson BM. Urogenital System. In: Carlson BM, editor. Human embryology and develop-
mental biology. Philadelphia: Elsevier/Saunders; 2014. p. xiii, 506 pages.
General Principles in the Diagnosis
of the Acute Abdomen 3
Introduction
The overall antenatal hospitalization rate is approximately 10.1 per 100 deliveries
[1]. One third is for nonobstetrical conditions that includes renal, pulmonary, and
infectious diseases. One in every 635 pregnant women will undergo a nonobstetrical
surgical procedure [2, 3].
The obstetrician may be qualified to manage many nonobstetrical disorders.
Other conditions will require consultation, and others still may require a multidisci-
plinary team. Consultants may include maternal–fetal medicine specialists, inter-
nists and medical subspecialists, surgeons, anesthesiologists, and numerous other
disciplines [4]. Obstetricians should have knowledge of a wide range of surgical
disorders frequently diagnosed in women of childbearing age. Consequently, non-
obstetricians who care for these women and their unborn fetuses need to be familiar
with pregnancy-induced physiological changes that occur in the gravida as well as
special fetal considerations. Often normal pregnancy distresses have clinically sig-
nificant effects on various diseases and may cause aberrant changes in routine labo-
ratory values.
It is obvious that a woman should never be punished because she is pregnant.
Gravid women are susceptible to any of the medical and surgical maladies that can


in Pregnancy, DOI 10.1007/978-3-319-62283-5_3
42 P.B. Greenspan
affect women of childbearing age. A number of questions should be addressed to

assure appropriate evaluation and management:
• Would a different management plan be recommended if the woman was not

pregnant?
• If the management plan is different because the woman is pregnant, can this be
justified?
• What are the risks versus benefits to the mother and her fetus, and are they coun-
ter to each other?
• Are there individualized management plans that balance the benefits versus risks
of any alterations?
This approach allows individualization of care for women with most surgical
disorders complicating pregnancy. This may be specifically helpful for consider-
ation by nonobstetrical consultants.
History
The foundation of the diagnostic process is the patient’s history. Skilled history tak-
ing is acquired with experience and the utilization of the examiners’ senses. An
understanding of body language often significantly contributes to the history-taking
process.
Aside from patients who are unconscious, obtaining a coherent, accurate history
is often challenging. Language barriers, educational disparities, and cultural differ-
ences among other things can make obtaining a clear history very difficult. At times,
even with a conscious patient, getting a coherent history is all but impossible.
Often, an emergency is pending and time for history taking can be severely cur-
tailed. In such cases, the most essential information to be obtained includes the
patients’ allergies, medications, major prior medical and surgical problems, etc.
When the clinical setting allows for more time, then a general history should be
ascertained on all patients with whom the examiner is otherwise, unfamiliar. This is
essential in the determination of the type and urgency of the proposed surgery, if
that is warranted.
The interview typically begins with the elicitation of a chief complaint from
which the examiner develops the history of the present illness. Often, there is more
than one chief complaint; therefore, each one should be explored, as well. In some
instances, multiple complaints can be coalesced into a single history.
One should be cautious not to develop the notion of a “routine” history as each
patient is entirely unique. Observation of the patient while questioning them is
critical.
The examiner should sit while interviewing the patient affording him or her enor-
mous amounts of information. Furthermore, this usually makes the suffering patient
feel more at ease.
3 General Principles in the Diagnosis of the Acute Abdomen 43
Observations of the patients’ position in the bed, facial expressions, degree of

stillness versus movement (such as rocking back and forth) provides very useful
clues to the clinician [5, page 19].
Determining the acuteness of onset of the pain provides clues to its severity.
Determination of what the patient was doing when the pain began is very useful.
Was the gravida asleep and awakened by the pain? Was she standing, sitting, or
lying down when the pain began? Was she walking, running, exercising, etc.? Did
the pain begin during or after sexual intercourse?
Rarely, patients will develop sudden-onset severe pain that will cause them to fall
down or faint. However, in pregnant women, fainting or collapse is associated with
ovarian torsion and rupture of an ectopic pregnancy [5, page 21].
Characterization of pain regarding onset and distribution is greatly important.
Pain that is felt throughout the abdomen is associated with sudden exposure of the
peritoneum to fluids such as blood, pus, or succus entericus. When generalized pain
can be further characterized to specific locations in the abdomen, this aids the clini-
cian in focusing on the likely source. For example, if a pregnant patient has general-
ized abdominal pain but the greatest intensity is in the left lower quadrant, then the
most likely explanation is ovarian, sigmoid or rectal pathology and not appendix or
ileocecal disease.
Pain associated with small bowel obstruction or colic is first noted in the epigas-
trium and periumbilical regions, which corresponds to the innervation by the ninth
and tenth thoracic nerves. These nerves also supply the appendix; hence, early
appendicitis pain is often felt in the epigastrium. Typically, the pain from large
bowel pathologies is felt in the hypogastrium [5, page 22].
An accurate description of the pain regarding severity or quality is often an indi-
cation of the seriousness of the underlying cause. For example, burning is used to
describe pain from gastric ulcer, whereas pancreatitis may cause agonizing pain.
Colicky pain is sharp and constricting, whereas tearing pain may be described in an
aortic dissecting aneurysm, albeit rare in pregnant women. Obstructions of the
bowel may be described as gripping pain, but appendicitis may produce dull aching.
Pelvic abscess may also be described as dull pain as well [5, page 22].
Pain that radiates or travels along the area of distribution of the nerves from that
segment of the spinal cord often provides valuable diagnostic information. The pain
of biliary colic, fairly common in gravidas, typically radiates or is referred to the tip
of the inferior angle of the right scapula. The pain caused by renal lithiasis is often
perceived in the patients’ labia.
Pain that worsens with inspiration is associated with pleuritic inflammation;
however, this may also be of a musculoskeletal origin, devoid of any organic pathol-
ogy [5, page 23].
Patients with an acute abdomen often present with vomiting. If the patient does
not have gastritis, then the vomiting is typically due to one of the following:
1 . Peritoneal or mesenteric nerve irritation

2. Luminal obstructions of a ureter, bile duct, endocervical canal, or intestines
44 P.B. Greenspan
Any irritation of the peritoneum from blood, gastric secretions, or inflammation

of an organ will stimulate sympathetic nerves, which produce persistent vomiting.
Similarly, as smooth muscles are stretched as in cases of torsion or bowel obstruc-
tion, this will result in vomiting.
Determining the relationship of the vomiting to the onset of the pain is very critical.
The more sudden and/or severe the stimulation to the peritoneum, the earlier the vom-
iting occurs. Duct obstructions from renal calculi, gallstones, or pancreatic duct ranu-
lae produce early-onset, sudden, and severe vomiting. Vomiting from small intestinal
obstructions generally follow the pain onset by 4 or more hours. Large bowel obstruc-
tions do not feature vomiting in many cases, but are associated with nausea.
Pain that is produced by appendicitis usually precedes the onset of vomiting by
3–4 h or longer. It is unusual for the vomiting and pain to coincide or that the vomit-
ing precedes pain development [5, page 21].
Vomiting frequency is variable and is often directly correlated to the severity of
the underlying cause for the pain. Beware that there are numerous serious abdomi-
nal pathologies that produce minimal or no vomiting.
Whenever observable, the character of the emesis may provide clues to the cau-
sation of the pain. Simple gastritis generates undigested stomach contents with little
or no bile. Bilious vomit is a sign of bile duct obstruction. Intestinal obstruction may
produce various materials, but feculent emesis is pathognomonic of bowel obstruc-
tion in the later stages of the process [5, Page 22].
Anorexia that is acute in onset is significant and raises the suspicion of appendi-
citis. However, the loss of appetite may or may not be associated with vomiting.
Other questions regarding the patients’ pain may include exploration of their
bowel habits. Recent changes that include constipation or diarrhea provide impor-
tant clues in diagnosing the pain. Gravidas with hypogastric pain and diarrhea fol-
lowed by tenderness and constipation may have a pelvic abscess [5, Page 23]. The
finding of frank blood and mucus in the rectum is often a sign of intussusception.
The pain presentation might include the O-P-Q-R-S-T mnemonic.
O-onset: When did the pain begin or first become noticeable?

P-Provocation/Palliation: What makes the pain worse? What improves the
pain?
Q-Quantity: Clinicians usually offer a scale of 1–10. Observation by the
examiner may render a different assessment of the pain quantity versus the
patient’s subjective description.
R-Radiation: Does the pain travel elsewhere or is it referred to another
location?
S-Severity: How does the patient describe the pain, that is, severe, burning,
sharp, shooting, etc.? How does the patient rate the pain relative to a score
(1–10, etc.)?
T-Temporality: Is there a time relationship accompanying the pain, that is,
morning, afternoon, only while having a bowel movement, etc.?
Other details of the history should include past surgical history, prior hospitaliza-
tions, trauma, family medical history, and prior obstetrical and gynecological prob-
lems. Social history is essential, as well, addressing nicotine use, past and present,
alcohol and illicit drug consumption, and if pertinent, sexual practices. Information
regarding a patient’s social history helps the examiner to be alert for problems in the
perioperative period such as drug or alcohol withdrawal. A history of any substance
abuse including nicotine provides essential information that may have significant
impact on the intraoperative and postoperative course. This is especially of concern
in the gravid patient. The effects of substances on the fetus must be given appropri-
ate consideration.
Though it is often uncomfortable for some examiners to question the patient’s
sexual history, there are many times, especially in the evaluation of a pain com-
plaint, that sexual practices play a significant role in the etiology of the pain.
Furthermore, sexual abuse and trauma can produce significant but unapparent inter-
nal injuries that manifest as an acute abdomen in a gravid woman.
Low-risk procedures may not need further evaluation even in the highest risk
patient. Emergency surgeries should not be delayed for “medical clearance”
when the risk of the procedure outweighs the benefit of postponing the interven-
tion [6].
There are instances when clearance would be appropriate particularly in the
assessment of cardiovascular and pulmonary risks. If the history warrants it and
time allows for it, then “medical clearance” is a valuable undertaking to avoid sig-
nificant morbidity and mortality [6]. Rudimentary screening for history of deep
venous thrombosis or pulmonary embolism is preferable, and appropriate precau-
tions and interventions should be implemented if indicated. A full coagulation panel
is not necessary in a patient with a negative history of coagulopathy as these tests do
not predict bleeding risk [6].
Physical Examination
A thorough, comprehensive physical examination is always preferable; however,

there are instances when an emergency requires a limited exam, focusing on the
problem area. In pregnant women, a digital vaginal exam may be pertinent to ascer-
tain cervical change associated with labor, which may or may not be associated with
the patient’s complaint.
The general examination includes an assessment of vital signs, mental status,
cardiopulmonary findings, and a minimal neurological evaluation.
The focused physical assessment, particularly in pregnant patients with abdomi-
nal pain, can be challenging due to the presence of the gravid uterus. The enlarging
uterus displaces the viscera, which may render confusing findings. The examiner
should consider that any pathology or condition that occurs in nonpregnant women
can occur in the pregnant state, as well.
46 P.B. Greenspan
Observation
As was addressed in the section on History, observation of the patient is the initial
step in the physical examination. In what position is the patient when you first greet
her? Is the patient lying down, sitting up, curled into the fetal position? How easily
can the patient communicate? Is there an emesis basin nearby? Has intravenous
access been started by other providers? Facial expression may provide clues as to
the severity of the patients’ pain in many but not all cases. Grimacing and sweating
can indicate greater degrees of suffering. Pallor may raise the suspicion of intra-
abdominal hemorrhage. The simple application of the examiners’ palm on the
patients’ forehead may provide clues about fever. Answers to these and other ques-
tions provide clues to the examiner about the patient’s condition and disposition.
Auscultation
Auscultation of the undisturbed abdomen can provide significant clues in diagnos-

ing the patient with an acute abdomen. The presence and quality versus the absence
of bowel sounds can be correlated to many diagnoses, including bowel obstruction,
appendicitis, etc. Furthermore, as one listens to the abdomen with a stethoscope, the
examiner can alternate pressure with the head of the stethoscope placed on the vari-
ous quadrants to see if that elicits guarding or utterances of pain from the patient.
Bowel sounds are variable and may be absent in many patients with other signs and
symptoms of a peritonitis.
Rarely observed, a succusion splash may suggest a bowel obstruction.
Palpation
Pregnant women with abdominal pain may be difficult to palpate due to the pres-
ence of the gravid uterus. Bear in mind, however, that the cause of abdominal pain
is often directly related to the gravid uterus, itself, so care should be taken to evalu-
ate the uterus systematically, including the use of Leopold’s Maneuvers for fetal
positioning.
When the patient has localized pain, it is helpful to ask her to point with a single
finger to the area of maximal pain intensity. This helps to narrow the examiners area
of exploration. Typically, one would palpate all other regions and quadrants of the
abdomen prior to palpating the affected area last.
Gentle pressure is imperative; a hard compression of the painful site will usually
elicit guarding and unnecessary discomfort for the patient. Rebound tenderness is
addressed under a separate heading.
Palpation may reveal nonpain-related important findings such as masses, organo-
megaly, pulsatility of major vessels, etc. Such findings may or may not be related to
the diagnosis.
Percussion of the abdomen has limited value, but it may help to demonstrate a
fluid wave. This should also be implemented with gentleness, as the tapping over
areas of peritonitis may elicit unnecessary exacerbation of the pain. In gravid

women, this technique rarely yields useful information.
The Pelvic Examination
The pelvic examination of a pregnant woman includes variously a speculum evaluation

of the vaginal vault and cervix, and a bimanual digital examination of the vagina to
palpate the cervix, uterine fundus, and adnexa. Adding a digital rectal exam may be
warranted, especially when considering the diagnosis of appendicitis. Rectal exami-
nation, albeit generally uncomfortable to the patient, allows the examiner access to the
lower pelvic peritoneum, which is cases of appendicitis or pelvic abscess will elicit
significant pain on palpation. The individual components or any combination thereof
depends on the clinical presentation. Evaluation of vaginal discharge is often indi-
cated in pain assessments, as well as the collection of secretions for screening of sexu-
ally transmitted infections and to rule out rupture of membranes.
Cervical dilatation and the station of the presenting part are relevant if preterm or
term labor is a concern. Furthermore, the patient with a presentation of abdominal
pain may simply be in labor and should thus be managed accordingly.
Supplemental Examinations
Other examinations that complement the physical examination are addressed else-
where in this text. These include laboratory studies and imaging options.
One must be cautioned, however to use discretion and experience when relying
on evaluation technologies other than the classic history and physical examination.
Hayward [7] proposed a condition described as V.O.M.I.T. syndrome. This stands
for Victims Of Modern Imaging Technology. His point is worth heeding. Many
times, the clinician is apt to make major decisions on the basis of a finding on CT
scan or sonogram, without considering the limitations of these tools. As much as
modern imaging technology has vastly contributed to the practice of medicine and
surgery over the past several decades, they should not be considered a substitute for
sound clinical judgment and experience.
The Use of Rebound Tenderness (Commentary)
This author agrees with the sentiments of the Late Sir Zachary Cope [8], one of the
greatest surgical diagnosticians of the twentieth century:
If the fingers be pressed gently but deeply over an inflamed focus within the abdomen and
then the pressure be suddenly released, the patient may experience sudden, sometimes
severe pain on the ‘rebound’. We do not recommend the performance of this test for it elicits
no more than can be ascertained by careful gentle pressure and may cause unexpected and
unnecessary pain.
48 P.B. Greenspan
References
1. Gazmararian JA, Petersen R, Jamieson DJ, et al. Hospitalizations during pregnancy among
managed care enrollees. Obstet Gynecol. 2002;100:94.
2. Corneille MG, Gallup TM, Bening T, et al. The use of laparoscopic surgery in pregnancy:
evaluation of safety and efficacy. Am J Surg. 2010;200:363.
3. Kizer NT, Powell MA. Surgery in the pregnant patient. Clin Obstet Gynecol. 2011;54(4):633–41.
4. American College of Obstetricians and Gynecologists: nonobstetric surgery in pregnancy.
Committee Opinion No. 474. Feb 2011, Reaffirmed 2013.
5. Silen MD. William, Cope’s early diagnosis of the acute abdomen. 21st ed. Oxford: Oxford
University Press; 2005. p. 19–23.
6. LeBlond RF, Brown DD, Suneja M, Szot JF. DeGowin’s diagnostic examination. 10th ed.
New York: McGraw-Hill Education; 2015.
7. Hayward R. VOMIT (victims of modern imaging technology) – an acronym for our time. BMJ.
2003;326:1273.
8. Cope SZ. The early diagnosis of the acute abdomen. 14th ed. Oxford: Oxford University
Press; 1972.
Imaging the Gravid Female
4
Stephanie Anne Scott and Justin Stowell
Abbreviations
ACOG American College of Obstetrics and Gynecology

ACR American College of Radiology
ADC Apparent diffusion coefficient
AFLP Acute fatty liver of pregnancy
ART Assisted reproductive technology
β-hCG Serum human chorionic gonadotropin
C-section Caesarian section
CT Computed tomography
dB Decibel
DWI Diffusion-weighted imaging
FAST Focused abdominal sonography for trauma
FDA Food and Drug Administration
GS Gestational sac
Gy Gray
hCG Human chorionic gonadotropin
HEELP Hemolysis, elevated liver enzymes, low platelets
IBD Inflammatory bowel disease
IUP Intrauterine pregnancy
kV Kilovolt
mAS Milliampere-second
S.A. Scott, MD (*)

Department of Radiology, University of Missouri Kansas City School of Medicine,
Truman Medical Center, Kansas City, MO, USA
J. Stowell, MD
Department of Radiology, University of Missouri Kansas City School of Medicine,

in Pregnancy, DOI 10.1007/978-3-319-62283-5_4
50 S.A. Scott and J. Stowell
mGy Milligray
MR Magnetic resonance
MRCP Magnetic resonance cholangiopancreatography
MRI Magnetic resonance imaging
MRU Magnetic resonance urography
mSV Millisievert
mW/cm2 Milliwatt per square centimeter
OHSS Ovarian hyperstimulation syndrome
PID Pelvic inflammatory disease
RI Resistive index
SAR Specific absorption rate
SSFP Single-shot fast spin-echo
TOA Tubo-ovarian abscess
TV Transvaginal
US Ultrasound
W/kg Watt per kilogram
YS Yolk sac
Introduction and Background
Imaging is frequently employed in the initial workup of patients presenting with

acute abdominal or pelvic complaints. As discussed, signs and symptoms of
expected benign physiological changes in pregnancy often masquerade with more
ominous features of an acute abdomen, leading to diagnostic uncertainty. Rapid and
accurate diagnosis of the cause of the acute abdomen in pregnant patients can be
achieved with the help of imaging, preventing a delay in diagnosis, and allowing for
the timely initiation of appropriate treatment thereby reducing morbidity and mor-
tality for both the patient and her developing fetus.
Utilization and selection of appropriate imaging in gravid patients present unique
challenges to the clinician. The risk-to-benefit ratio, balancing the need for precise
diagnostic imaging and avoiding undue risks to the patient and the fetus, must be
carefully considered. Uncertainty as to the best choice of imaging modality in vari-
ous clinical scenarios is common. Ultrasound (US) and magnetic resonance imag-
ing (MR, or MRI) are preferred for the pregnant patient, as they do not expose the
fetus or patient to ionizing radiation [1, 2]. Nonetheless, fear of exposure of the
fetus to ionizing radiation should not delay the diagnostic workup in some critical
patients, which might require the use of radiography or computed tomography (CT)
[1–3]. Condition-specific imaging algorithms can be developed by individual
healthcare institutions as part of a collaboration between clinicians and radiologists
to help guide appropriate use of imaging [1, 3, 4].
4 Imaging the Gravid Female 51
Ionizing Radiation and Risks
In recent years, the use of radiological examinations in pregnant women has more
than doubled, with the greatest increase in utilization of examinations associated
with ionizing radiation (particularly CT) [5, 6]. Despite issuance of practice guide-
lines for the use of imaging in pregnant patients by the American College of
Radiology (ACR) and American College of Obstetricians and Gynecologists
(ACOG) [1, 2], generalized lack of familiarity among referring providers about the
risks of radiation and inconsistent adherence to these guidelines among radiology
departments exists [7–10]. As such, a working understanding of the inherent risks of
ionizing radiation associated with radiography and CT is paramount for clinicians
and radiologists involved in the care of pregnant patients to ensure safe and judi-
cious use of imaging.
Two categories of radiation effects—deterministic or stochastic—are used to
describe the types of biological damage incurred as a function of radiation dose and
time from exposure [1, 5, 11]. Deterministic effects manifest as cell death that
occurs progressively in proportion to the absorbed radiation dose at or above a
threshold level, and are not encountered at doses below these tissue-specific thresh-
olds [1]. An example of a deterministic effect is skin erythema that occurs at doses
of 2–5 gray (Gy). Stochastic effects are less predictable and may occur at any dose.
In other words, there is no threshold dose limit below which stochastic effects can-
not occur, and unlike deterministic effects, the severity of the radiation damage is
not dose dependent [1]. Stochastic effects represent sequelae of damaged chromo-
somal material which may lead to mutations or some malignancies [1, 12, 13]. Fetal
effects of radiation (either deterministic or stochastic) take the form of radiation-
induced teratogenesis or carcinogenesis, respectively.
Radiation and the Developing Fetus
Absorbed radiation dose (measured as milligray [mGy]) and gestational age are two
of the primary factors which determine the potential effects of radiation on fetal
development [1, 12, 13] (Table 4.1). Fetuses exposed at earlier gestational ages
exhibit the highest risk of detrimental deterministic effects, attributable to relative
genetic susceptibility of rapidly dividing tissues to X-ray damage during early peri-
ods of organogenesis (4th through 10th weeks) [1] (Table 4.1). Effects of radiation
exposure range in severity, such as embryonic death, malformation, growth restric-
tion, and carcinogenesis [11–13].
Teratogenic effects from radiation exposures during this period generally mani-
fest with radiation-induced malformations and general growth restriction. The cen-
tral nervous system is particularly sensitive to ionizing radiation during this period
and extending to the 15th week of pregnancy, as neuronal stem cells with high
mitotic activity migrate along their pathways from the ventricular zones to the corti-
cal mantle [1, 12]. This probably explains the relative frequency of diminished IQ,
mental restriction, and microcephaly found in patients exposed to sufficient fetal
Table 4.1 Threshold radiation dose limits incurring teratogenesis throughout gestation
Dose range
Developmental period (mGy) Teratogenic effects
Any <50 None
Preimplantation 50–100 All-or-none effect resulting in either embryonic
(0–2 weeks after demise or no effect
conception)
Organogenesis (2–8 weeks) 200–250 Congenital anomalies and growth restriction
Fetal period: 8–15 weeks 60–310 High risk for neurological deficits (microcephaly,
intellectual deficit, or severe intellectual disability)
related to accelerated neuronal proliferation and
migration during this period
Fetal period: 16–25 weeks 250–280 Lower risk for severe intellectual disability as
neurons become progressively neuroresistant
Data from [1, 2, 4]
doses during susceptible developmental periods. Cells of the central nervous system
become progressively more radioresistant beyond the 25th week of gestation, after
which there are very little, if any, neurological effects. As these malformations are
deterministic effects, the threshold dose necessary to induce these effects ranges
from 100 to over 200 mGy [1].
Examinations in which the fetus is positioned directly within the radiation field
(e.g., abdominopelvic CT) warrant consideration of the potential risks of fetal expo-
sure (Table 4.2), whereas CT examinations where the fetus is not directly irradiated
(i.e., scatter radiation from chest, head, or neck CT) pose less of a risk [1, 14]. Direct
measurement of fetal dose is not possible due to variations in beam attenuation
related to maternal size (anteroposterior dimension), fetal depth, the scanned region,
and CT scanner parameters (filtration, tube voltage [kV, kilovolt], current [mAs,
milliampere-second], pitch, rotation time, detector configuration, and number of
acquisitions) [4, 14, 15]. Estimates of absorbed fetal dose are derived from phantom
models [15, 16]. Based on these and a few clinical models, estimated fetal doses
from single-acquisition abdominopelvic CT have ranged from 10 to 15 mGy, well
below the threshold dose associated with fetal malformations [14].
Stochastic effects of in utero exposures (namely carcinogenesis) are probably of
higher concern for the patient and clinician, as these are not predictable and may
occur at any dose or gestational age, with increasing probability with higher or more
frequent exposures [1, 11, 12]. The risk of developing childhood cancer from in
utero exposure varies from negligible to low depending on whether the exposure
was a one-time, high-dose event or repeated low-dose (≥10 mGy) exposures.
Comparing the lifetime risk of development of childhood malignancy (e.g., leuke-
mia) in exposed fetuses to unexposed controls (rate 0.2–0.3%), the relative increase
in risk of developing radiation-induced cancer was minimal (rate 0.3–0.7%) [1, 13].
Table 4.2 Estimated maternal and fetal exposures to ionizing radiation during abdominal and
pelvic imaging
Fetal dose Maternal dose
Modality (mGy) (mSv)
Radiography
Abdominal 0.1–0.3 0.01–1.1
Pelvis 1.1–4
Fluoroscopy
Intravenous pyelography 5–10 0.7–3.7
Small bowel follow-through 1.0–20 2.0–18.0
Barium enema (double contrast) 7 3.0–7.8
CT
Abdomen 1.3–35 3.5–25
Pelvis 10–50 3.3–10
Abdomen & Pelvis without contrast (renal stone 10–11 3–10
protocol)
Abdomen & Pelvis with contrast 13–25 3–45
Nuclear medicine
99m
Tc DTPA 0.35–9 1.39–3.79
99m
Tc MAG3 0.58–13.5 1.32–9.0
99m
Tc MDP 1.8–7.87 1.8–4.7
99m
Tc RBC in vivo 2.51–5.95 2.5–6.0
Data from [5, 13, 18, 19]
Tc technetium 99 m, DTPA diethlenetriaminepentacetate, MAG3 mercaptoacetyltriglycine,
99m
MDP methylene diphosphonate, RBC red blood cell
adiography, Fluoroscopy, Interventional Radiology

R
and Nuclear Medicine
Although radiography remains the most common radiation-producing imaging

examination performed in pregnant patients, the total average absorbed fetal dose
from this modality is far less than that of CT [6]. If exposure of the fetus to radiation
from a fluoroscopic or interventional radiology procedure is necessary, ultrasonog-
raphy should be used for guidance, when possible, and dose-minimizing techniques
employed by the operator, including optimization of patient positioning and shield-
ing, limiting fluoroscopic time, reducing the number of images, utilizing last-image
hold technique, lowering the frame rate, applying tight collimation, and limiting use
of magnification [5, 17].
In general, most nuclear medicine procedures may be delayed until the postpar-
tum period. However, most achieve radiation exposures much below threshold
doses believed to induce fetal harm [5, 13, 18, 19] (Table 4.2) For example, techne-
tium 99 m used for most procedures delivers less than 5 mGy to the fetus. Adequate
hydration and bladder catheterization may be useful to expedite the renal excretion
of radiotracers, thereby limiting fetal exposures [5].
Ultrasonography
Ultrasonography has long been established as a safe modality for the first-line eval-
uation of both fetal and maternal wellbeing. It is preferred in the evaluation of preg-
nant patients as it avoids the use of ionizing radiation, is inexpensive, and easily
accessible. However, limitations of ultrasonography relate to the skill of the opera-
tor (sonographer) and patient body habitus [20]. Ultrasonography operates on depo-
sition of energy in the form of sound waves though tissues, measuring tissue
composition and movement as reflections and attenuation of the sound beam.
Mechanical and thermal energy produced by the ultrasound pulse waves may theo-
retically affect the developing fetus, although no deleterious effects have been docu-
mented in humans. Nonetheless, the Food and Drug Administration (FDA) has
established limits for mechanical and thermal indices of less than 1 and energy
exposure to less than 94 mW/cm2 (milliwatts per square centimeter) [5, 20, 21]. As
color, power, and spectral Doppler techniques utilize higher intensity acoustic out-
put, these modalities are generally used only when needed throughout pregnancy
and avoided in the early 1st trimester. Fetal heart rate is instead evaluated with lower
energy M-mode ultrasonography [5, 21].
Computerized Tomography
In general, CT is to be avoided in pregnancy, as scans of the abdomen and pelvis

deliver the most radiation to the fetus. Nevertheless, its use in pregnancy is increasing
at a rate more than twice that of other imaging modalities [6, 22]. Despite the contin-
ued increase in abdominopelvic CT utilization in pregnancy, the percentage of scans
positive for acute pathology has not changed [6]. The benefits of information obtained
from a scan must outweigh the inherent risks to the fetus. However, these perceived
fetal risks should not deter a clinician from using CT as a diagnostic tool should acqui-
sition of adequate information about potentially life-threatening diagnoses be delayed
or suboptimal by other means [1, 2, 12, 23]. CT offers the added benefit of detecting
unanticipated masquerading causes of acute abdominal pain [21]. It is generally pre-
ferred to exhaust nonionizing imaging modalities (US and MR) before CT or radiog-
raphy when possible. Uniquely, CT is considered a first-line modality in the evaluation
of pregnant trauma patients, following initial rapid triage with focused abdominal
sonography for trauma (FAST) scan to evaluate for free intraperitoneal fluid, pleural
effusions, and pericardial fluid [3, 5, 21, 23, 24].
Magnetic Resonance Imaging
MRI offers the diagnostic benefits of nonionizing, cross-sectional, high soft tissue
resolution evaluation of abdominopelvic pathology. MR imaging at ≤3 tesla strength
is possible and safe at all stages of development [1, 2, 5]. To date, no studies have
demonstrated harmful effects to the fetus from MR. However, theoretical risks to
the fetus exist related to inherent properties of the magnet. These include the static
magnetic field strength, applied gradient magnetic fields, and radio frequency (RF)
pulses. High magnetic field strengths are hypothesized to affect fetal neuronal
migration and proliferation during early pregnancy but remain theoretical [5].
Energy deposition in tissues from the RF pulses may lead to tissue heating. This
is known as the specific absorption rate (SAR) and is quantified as watts per kilo-
gram (W/kg), with federally mandated and internally monitored upper limit of 4 W/
kg. This limit is associated with a 0.6 °C increase in maternal body temperatures
after 20–30 min of imaging [5]. Fetal injury may occur with maternal temperature
elevations of 2–2.5 °C for 30–60 min, but the maximum SAR is deposited in the
maternal surface tissues with fetal heating considerably less than the proposed det-
rimental levels [5, 25].
MR sequences that employ rapid gradient switching (particularly in single-shot
fast spin-echo [SSFP] sequences commonly utilized in fetal imaging) lead to higher
energy deposition, as well as acoustic noise in the scanner. Use of such sequences
should be kept brief, as theoretical damage to the developing fetal ear may result
exposure to ≥90 dB (decibel) [5].
Utilization of Intravenous Contrast in Pregnancy
In addition to the risks of ionizing radiation, intravenous contrast material utilized

in diagnostic imaging poses additional risks to fetal wellbeing. Both iodine- and
gadolinium-based contrast agents are known to cross the blood–placenta barrier and
enter the fetoamniotic circulation [26].
Iodinated Contrast
To date, no adverse fetal or neonatal effects have been documented from administra-
tion of low-osmolality iodinated contrast media (e.g., iodinated contrast used in CT)
and are thus classified by the United States FDA as Category B (no adverse effects
in animal studies but controlled studies in pregnant patients do not exist) [5]. The
American College of Radiologists (ACR), therefore, recommends against withhold-
ing iodinated contrast agents in pregnant patients if it is necessary for diagnosis
[26]. Concerns over fetal and neonatal hypothyroidism after in utero exposure to
iodinated contrast have not been validated, and neonates are generally screened for
hypothyroidism at birth if there is a pertinent history [5, 26].
Gadolinium-Based Contrast
Gadolinium-based contrast agents have been labeled as Category C medications by

the FDA because of documented fetal demise and malformations associated with in
utero exposure in animal studies, yet these effects have not been documented in
retrospective human studies [5]. Therefore, these agents should be administered

with caution in pregnant patients, and their use is generally avoided [2, 26]. The
ACR does indicate that use of gadolinium-based contrast in pregnancy should occur
only after carefully documented consensus decision by the radiologist, clinician,
and patient, when the information obtained from its use outweighs the purported
risks to the fetus from exposure to free gadolinium ions [2, 5, 26, 27]. In such cases,
agents with tightly bound gadolinium-chelate complexes are advised, administered
at the lowest dose, including gadobenate dimeglumine (MultiHance; Bracco
Diagnostics, Monroe Township, NJ) or gadoteridol (ProHance; Bracco Diagnostics)
[5]. Informed consent should be obtained from the patient and documented in the
medical record prior to gadolinium administration.
Allergic Reactions
Pretreatment and treatment of allergic reactions to contrast media should follow

established guidelines from the ACR, such as oral and intravenous diphenhydr-
amine and corticosteroids (prednisone or dexamethasone) [5, 26].
Screening for Pregnancy
In allowable clinical settings, all women of potential childbearing age (defined as

ages 12 through 50 years) should undergo a full determination of pregnancy status
to include menstrual and surgical history (tubal ligation or hysterectomy), contra-
ceptive use, and qualitative urine human chorionic gonadotropin (hCG) or quantita-
tive serum human chorionic gonadotropin (β-hCG) testing, prior to the use of direct
ionizing radiation [1, 2, 21]. In some patients, pelvic US may be indicated to assess
the status of the pregnancy. Pregnancy status can be assessed by interview of the
patient as to her likelihood of pregnancy (e.g., not sexually active, on effective birth
control, or biologically incapable of pregnancy) or that she has recently completed
her menstrual period within the last 4 weeks prior to imaging [1]. Pregnancy test
results should not be the sole screening measure, and patients must undergo the
standard interview procedure, as negative pregnancy tests do not necessarily exclude
recent conception [5]. A positive pregnancy test will prompt the imaging technolo-
gist to follow appropriate pregnancy-tailored protocols. For procedures expected to
deliver high doses of radiation to the uterus (e.g., pelvic interventional procedures),
a pregnancy test should be obtained within 72 h proceeding [1]. The ACR and
ACOG both emphasize that when pregnancy status cannot be verified in the emer-
gent setting, a waiver should be included in the patient’s medical record document-
ing the critical need for the study [1, 2].
Counseling the Pregnant Patient About Imaging Procedures
Patients may report anxiety surrounding the exposure of their fetuses to ionizing
radiation and must be appropriately counseled. It should be emphasized in a positive
light that for most imaging modalities, the risk of pregnancy loss, birth defects,
mental restriction, and subsequent childhood malignancy are small [1, 21]. The risk
of incurring detrimental effects from exposure to ionizing radiation of imaging
examinations must be considered in light of generalized background risks associ-
ated with pregnancy, such as birth defects (3%), miscarriage (15%), prematurity
(4%), growth restriction (4%), and mental restriction or neurological deficits (1%)
[1, 2, 20, 22]. At the relatively low fetal doses encountered in abdomen and pelvic
imaging (10–35 mGy for abdominopelvic CT), threshold limits are extremely
unlikely to be met to cause deterministic effects. The main concerns therefore are
those of carcinogenesis in later life, which, for examinations involving less than
50 mGy fetal exposures, are less than 0.8% with attributable lifetime risk of approx-
imately 2% [1, 2, 5]. More clearly stated, there is a 98–99% likelihood that the fetus
will be unaffected by the radiation. Useful comparisons with background radiation
may highlight that differences in topographic elevation between women in Denver,
Colorado, and those living at sea level result in a slight relative excess exposure to
radiation levels (about 0.6 mSv, millisievert), which only theoretically place fetuses
at risk for an additional attributable cancer in every 5000 births [1]. Average back-
ground radiation is estimated at 1.0–2.5 mGy. There exists no single, wellmonitored
diagnostic radiology procedure which will result in a radiation dose significant
enough to affect the wellbeing of the fetus. Therefore, pregnancy termination is not
justified for fetal exposures to a single examination (< 100 mGy) [1, 2, 5, 11].
Nongynecological Causes of Abdominal Pain
Appendicitis
Acute appendicitis is the leading cause of acute abdominal pain in pregnancy requir-
ing surgical intervention and complicates 1 in 2000 pregnancies [3, 21, 28, 29].
First-line imaging of the pregnant patient with right lower quadrant pain is ultra-
sound with graded compression. However, despite being the first-line modality for
the evaluation of appendicitis, ultrasonography has a low yield, allowing visualiza-
tion of the appendix only 1/3 of the time. Another study showed that the sensitivity
and specificity of US in the assessment of appendicitis is only up to 78% and 83%,
respectively [20]. Knowledge of variation in appendiceal location in the gravid
abdomen may increase diagnostic yield. Detection of a blind-ending, tubular, non-
peristaltic, noncompressible structure arising from the cecal base, with luminal
diameter > 6 mm establishes the imaging diagnosis (Fig. 4.1). Use of color Doppler
may reveal associated hyperemia and surrounding inflammation of the periappendi-
ceal fat [20, 21, 28, 30]. In the setting of acute appendicitis, the patient is often
exquisitely tender with direct transducer pressure over the appendix, which can help
Fig. 4.1 US of acute appendicitis: acute appendicitis in a 31 y/o pregnant patient at 21 weeks’
with right lower quadrant abdominal pain. (a) Gray scale image of the right lower quadrant dem-
onstrates a longitudinal view of a dilated, blind ending tubular structure arising from the cecum
consistent with the appendix (arrows). Echogenic, shadowing appendicolith (arrowhead) is seen
within the lumen toward the base. Gray scale transverse images through the appendix without (b)
and with compression (c) demonstrate an appendiceal diameter of 10 mm with no change with
compression. Appendicitis was confirmed at surgery
confirm the diagnosis. When these findings are variably present, equivocal, or when
the appendix is not discretely visualized, imaging with other modalities is typically
warranted.
Delay in diagnosis and surgical management may lead to perforation, which is
associated with up to 30% fetal loss, and occurs most frequently in later stages of
pregnancy when sonographic evaluation of the appendix is technically difficult
from progressive displacement of the appendix by the gravid uterus [28]. MR is a
highly sensitive (100%) and specific (94%) modality for the diagnosis of appendi-
citis in pregnancy after targeted ultrasound examinations fail to demonstrate a nor-
mal appendix [25, 27, 31, 32]. The extremely high negative predictive value of MR
(100%) is helpful in triaging patients who may potentially have a surgical abdomen
[31]. As with the other modalities, the variable position of the appendix may com-
plicate interpretation. A normal appendix is defined as one with a luminal diameter
of ≤6 mm, or an air- or contrast-filled lumen (using either rectal saline or oral feru-
moxil oral suspension admixed with barium sulfate) [31]. A positive exam demon-
strates an enlarged, thickened appendix (>7 mm) with fluid-filled lumen with or
without periappendiceal inflammation, most apparent on T2-weighted images as
ill-defined increased signal in the periappendiceal fat (Fig. 4.2). Indeterminate
results include luminal size between 6 and 7 mm and no surrounding inflammation
[27, 31]. MR also offers the added benefit of detecting potential alternate diagnoses
for the patient’s complaints [32].
If ultrasonography and MRI are inconclusive or in the absence of available MRI,
abdominopelvic CT with contrast may be used to evaluate for appendicitis [3].
However, dose reduction techniques should be considered [8]. Lazarus and col-
leagues reported CT to have a 92% sensitivity and 99% specificity for the diagnosis
of appendicitis, with overall negative predictive value of 94% [29]. Furthermore,
CT can detect additional pertinent diagnostic information, such as small bowel
obstruction and urinary calculi, among others [29].
Fig. 4.2 MRI of acute appendicitis: acute appendicitis in a 29 y/o pregnant patient at 31 weeks’
with right lower quadrant abdominal pain. Axial (a) and coronal (b) T2 HASTE images demon-
strate a dilated, thick walled, fluid-filled appendix (arrows) measuring 9 mm in diameter with
periappendiceal inflammation. Appendicitis was confirmed at surgery
Urolithiasis and Urinary Tract
Urolithiasis and urinary tract infections constitute the most common painful nonob-
stetric causes of abdominal or pelvic pain in pregnancy [21]. Urolithiasis affects as
many as 1 in every 1500 pregnancies, and coexisting pyelonephritis or urinary tract
infection frequently leads to hospitalization. Ultrasound is the first-line modality for
evaluation of suspected renal colic in pregnancy [3, 5, 21, 22, 28, 33]. Renal sonog-
raphy readily detects the presence of hydronephrosis, but a distinction must be
determined between physiological hydronephrosis of pregnancy (more commonly
right sided and a result of mechanical compression of the gravid uterus and hormone-
related ureteral relaxation) and obstructive urolithiasis (more frequent in pregnancy
due to increased urine production and stasis) [21, 28, 33]. Renal pelvis diameter
measuring up to 25 mm on the right and 10 mm on the left up to 40 weeks of gesta-
tion may be physiological [34]. Smooth tapering of the distal ureter as it enters the
pelvis and the absence of luminal filling defects help confirm the diagnosis.
Ultrasonography is highly sensitive and specific (90% and 98%, respectively) for
hydronephrosis, increased in the presence of a stone [33].
Ultrasonographic sensitivity for detection of stones is highly variable, ranging
from 34–95% [35, 36]. Renal or ureteral stones manifest as foci of hyperecho-
genicity often with accompanying acoustic shadowing (Fig. 4.3). When color
Doppler is applied, a “twinkling artifact” may result (up to 86% of urinary calculi),
increasing diagnostic confidence [30, 34]. When possible, imaging should be per-
formed with a distended bladder to better evaluate distal ureters. Transvaginal (TV)
ultrasound can be performed to evaluate the presence of distal ureteral stones, distal
ureteral dilatation, and ureteral jets in patients with inconclusive transabdominal
examinations. In late pregnancy, ureteral jets may not be visualized, and their
absence does not necessarily indicate obstructive urolithiasis. Reimaging the patient
Fig. 4.3 US of obstructive uropathy: 35 y/o pregnant patient at 33 weeks’ with right flank pain.
(a) Longitudinal gray scale image of the right kidney (arrows) demonstrates moderate right hydro-
nephrosis (asterisk). (b) Gray scale image at the level of the distal right ureter and bladder (aster-
isk) shows an echogenic shadowing calculus (arrow) in the distal right ureter at the ureterovesicular
junction. This initially was not seen when the patient had a decompressed bladder. After hydration
and reimaging, the calculus was able to be visualized. The patient was admitted and passed the
stone the following day
in the contralateral decubitus position may elicit a ureteral jet or confirm its absence
[33]. Despite conflicting evidence, differences in renal vascular resistive indices
(RI) between each kidney can help to differentiate these entities, with no difference
in RI between the kidneys in physiological hydronephrosis whereas RI greater than
0.70 suggests obstructive pathology, particularly if unilateral [33]. The rate of spon-
taneous passage of urinary stones in pregnant women reportedly ranges from 48%
to 81% and persistent obstructive stones although conservative management may
undergo further treatment with nephrostomy tube placement or ureteral stent place-
ment [33]. Nephrostomy tube placement may be accomplished with ultrasound
guidance to further limit exposure of the patient and fetus to fluoroscopy [17].
Low-dose noncontrast CT is a sensitive and specific test for detection of obstruc-
tive uropathy in the pregnant patient and should be considered if ultrasound is
inconclusive [36, 37]. The likelihood of spontaneous stone passage is dependent on
stone width, with decreasing likelihood of passage above 5 mm and a more proxi-
mal ureteral location [38]. Stone size can be readily measured by CT and is less
reliable on MRI. Retained or impacted stones place the patient at risk for pyelone-
phritis and pyonephrosis, which can lead to untoward pregnancy complications.
Thus, low-dose, noncontrast CT should be used in the setting of suspected obstruc-
tive uropathy, even in pregnant patients [37].
MR and MR urography (MRU) utilizing heavily T2-weighted images may serve
as helpful adjunct modalities in evaluation of suspected urolithiasis, especially
when coexistent physiological hydronephrosis and hydroureter confound US find-
ings in the third trimester [20, 21, 25, 35, 39] (Fig. 4.4). Although, when compared
to low-dose CT, MRU suffers from poor spatial resolution and lower sensitivity for
detecting calcified stones, with an overall sensitivity of 80% [20, 39]. Flow-related
Fig. 4.4 MRI of obstructive uropathy: 28 y/o pregnant patient at 29 weeks’ with right flank pain
and hematuria. Renal US demonstrated right hydronephrosis but no obvious ureteral calculus (not
shown). (a) Axial T2-weighted MR image of the abdomen demonstrates mild right hydronephro-
sis, perinephric-free fluid (arrowheads), and a 4 mm hypointense filling defect in the proximal
ureter compatible with ureteropelvic junction calculus (arrow). Partial visualization of IUP anteri-
orly (asterisk). (b) Coronal T2 FIESTA fat-saturated image through the abdomen demonstrates
mild right-sided hydronephrosis (asterisk), perinephric-free fluid (arrowhead), and filling defect in
the proximal ureter compatible with ureteral calculus (arrow). Right nephroureteral stent was
placed after stone extraction
artifacts may mimic calculi, resulting in false positive examinations [21]. Findings
of obstructive uropathy on MR include renal enlargement, increased signal (edema)
in the renal parenchyma on T2-weighted images, and perirenal fluid [25, 35, 39].
Calculi appear as focal filling defects within the ureteral lumen, usually at a point of
abrupt caliber change. MRU may identify distal ureteral calculi and manifest the
“double-kink sign” – a column of urine in the distal ureter in association with ure-
teral constriction at the pelvic brim and vesicoureteral junction [35].
Biliary Disease
Hormones of pregnancy lead to hypersecretion of biliary cholesterol and gallblad-

der stasis, predisposing a patient to cholelithiasis and subsequent risk for acute cho-
lecystitis, the second-most common surgical abdominal emergency affecting
pregnant women [25, 28]. Ultrasonography is routinely used as a first-line evalua-
tion of acute right upper quadrant pain and suspected hepatobiliary pathology. The
presence of shadowing gallstones (95% sensitivity), gallbladder wall thickening
(>3 mm), distention (>5 cm transverse diameter), pericholecystic fluid, and the
presence of a sonographic Murphy sign may be used to diagnoses acute cholecysti-
tis [28] (Fig. 4.5). Dilation of the biliary tree may suggest the presence of choledo-
cholithiasis. However, direct detection of common bile duct stones may be possible
in as few as 20% of cases, as bowel gas may obscure the distal duct and 10% of
stones may not produce characteristic shadowing [20].
Findings of acute cholecystitis on MRI reflect those of US, with gallbladder wall
thickening and edema (increased signal on T2-weighted images), pericholecystic
fluid, and low signal filling defects within the lumen of the gallbladder reflecting
gallstones [25, 40]. In addition, choledocholithiasis is well evaluated by MR
Fig. 4.5 US of acute cholecystitis: acute cholecystitis in a 26 y/o pregnant patient at 19 weeks’
with right upper quadrant pain. Longitudinal (a) and transverse (b) images through the gallbladder
demonstrating a distended gallbladder with echogenic intraluminal sludge (asterisks), small layer-
ing shadowing echogenic gallstones (arrows) and gallbladder wall thickening (5 mm). Gangrenous
cholecystitis was found at time of surgery and confirmed at pathology
Fig. 4.6 MRI of choledocholithiasis: Choledocholithaisis in a 19 y/o pregnant patient at 25 weeks’

with epigastric pain and elevated bilirubin. (a) Coronal T2 HASTE image demonstrates a dilated
common bile duct (arrow), which measured up to 14 mm, and intrauterine pregnancy (asterisk).
(b) Coronal oblique T2 HASTE fat-saturated image from MRCP demonstrates an intraductal-
rounded T2 hypointense filling defect in the distal common bile duct measuring 4 mm compatible
with choledocholith (arrow). Patient subsequently underwent ERCP with stone removal and stent
placement
cholangiopancreatography (MRCP) [40]. The positive predictive value of MR is

100% for diagnosis of biliary obstruction. Thin-section (1 mm) overlapping MRCP
images depict small-rounded hypointense filling defects in T2-hyperintense lumen
of the biliary tree, indicating choledocholiths (Fig. 4.6). Common bile duct dilation
is present when the distance between the outer walls of the common bile duct mea-
sures greater than 7 mm [41].
Although US and MRI are the preferred modalities for evaluation of the biliary
system, CT with dose reduction techniques may be utilized when there are contra-
indications to MRI or when other means for rapid diagnosis are not available [40].
Despite being slightly less sensitive than MR for detecting small noncalcified
stones, CT has similar performance to even noncontrast MR in detecting the pres-
ence of biliary ductal dilation and choledocholithiasis [42].
Pancreatitis
Pancreatitis is a rare cause of abdominal pain in pregnancy, occurring most fre-

quently in the third trimester and usually as a result of gallstones [43]. Pancreatitis
may affect 1 in every 3300 pregnancies [20, 28]. Ultrasonography is limited in the
evaluation of the pancreas in the acute setting, as inflammation contributes to gen-
eralized ileus, causing bowel loops to interdigitate between the transducer and the
pancreatic parenchyma, obscuring its evaluation though bowel gas shadowing [43].
However, US is frequently used as first-line imaging to evaluate for the presence of
gallstones. When seen by US, the pancreas may appear enlarged and hypoechoic
(edematous), with or without peripancreatic fluid, which may become organized
into a collection [34].
As in nonpregnant patients, contrast-enhanced CT depicts changes of pancreatic

parenchymal edema, peripancreatic inflammation and fluid, and associated compli-
cations such as pancreatic necrosis (parenchymal nonenhancement), peripancreatic
fluid collections, ductal dilation, or vascular complications (pseudoaneurysm,
venous thrombosis, or hemorrhage) [44]. In general, CT evaluation of pancreatitis
requires multiphasic technique, which would subject the patient and fetus to high
doses of radiation. Therefore, noncontrast MR is typically utilized in the evaluation
of acute pancreatitis in pregnancy, discussed subsequently.
MR findings of acute pancreatitis include parenchymal edema and peripancreatic
fluid with or without pancreatic ductal dilation. Complicated pancreatitis may result
in peripancreatic fluid collections, which manifest as variable signal on T2-weighted
images. As gadolinium-based contrast is typically contraindicated in pregnancy,
evaluation for pancreatic necrosis or vascular complications may be limited but can
manifest as fluid signal areas surrounding the pancreas on T2-weighted images in
the former and lack of flow voids in the setting of splenic vein thrombosis [44].
Diffusion-weighted sequences: diffusion-weighted imaging (DWI) and apparent
diffusion coefficient (ADC), are highly sensitive for early pancreatic inflammation.
Furthermore, the presence of hemorrhage may be suggested as heterogenous areas
of T1-hyperintense signal within the pancreatic bed [34]. MRCP may be helpful in
evaluation of the pancreatic and biliary ductal system, identifying obstructive
lesions or variant anatomy [44].
Hepatic Disease
HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) occurs in
up to 12% of pregnant patients with severe hypertension. Findings on ultrasound
may be the first signs of the disease, occurring even before biochemical changes,
such as hepatic edema (hypertrophy, periportal hypoechoic “halos,” a “starry sky”
appearance of the liver with echogenic portal triads admixed among the edematous
parenchyma, capsular thickening, or scattered areas of increased echogenicity) [44].
The syndrome may result in hepatic hemorrhage, rupture, or infarction. US diagno-
sis of hemorrhage can be made by visualization of a heterogeneously echogenic,
nonvascular, complex cystic mass with or without lacy internal echoes representing
fibrin strands. Serial US examinations should document progressive involution of
the hematoma and exclude an underlying mass. Both adenomas and hemangiomas
can enlarge during pregnancy, with increased risk of hemorrhage [44]. Although
these findings are nonspecific, other causes of hepatic hematoma must be excluded,
such as hemorrhagic adenoma, trauma, or intrahepatic vascular abnormalities [20].
Hepatic infarcts manifest as peripheral, geographic, or wedge- shaped hypoechoic
areas with diminished vascularity [40].
Pregnancy induces a hypercoagulable state, which predisposes patients to throm-
bosis [20]. Budd-Chiari syndrome, manifesting clinically as portal hypertension
and liver failure, may result from thrombosis of hepatic venules, veins, or the infe-
rior vena cava. Depending on the age of thrombus, venous thrombus may appear
hypo- or hyperechoic, with associated expansion of the affected vessel and lack of
color signal on color Doppler imaging [45]. A thin fibrotic echogenic cord may be
seen within a retracted vessel lumen with chronic occlusion, or as treatment resolves
the clot. Color Doppler may also depict extrahepatic or intrahepatic collateral ves-
sels, an indirect, though specific sign of Budd-Chiari syndrome. Hepatic congestion
leads to portal hypertension, with dampened or reversal of flow within the portal
veins with color and spectral Doppler. A secondary sign of portal hypertension is
ascites, visualized on US as simple peritoneal free fluid [45].
Magnetic resonance findings in HELLP syndrome reflect those of sonography.
The areas of increased echogenicity on US may demonstrate increased signal on
T2-weighted images, indicating edema and early hepatic necrosis [25, 40]. MR
appearance of hepatic hematomas varies on the acuity of the blood products but will
appear heterogeneous on T1 and T2-weighted images, causing mass effect, with or
without capsular rupture, manifest as focal irregularity of the capsule and adjacent
sentinel clot [40].
Acute fatty liver of pregnancy (AFLP) most often manifests in the third trimester
of nulliparous women with a diffusely hyperechoic hepatic parenchyma on US, a
nonspecific qualitative finding [20, 40]. Acute fatty liver of pregnancy on MR
appears as hepatomegaly with diffuse increased signal on T1-weighted in-phase
images with signal dropout on opposed phase images (representing intracellular
triglycerides), or signal dropout on fat-saturated images (revealing the presence of
macroscopic hepatic fat) [25].
Budd-Chiari syndrome may manifest on MR as morphological changes in liver
contour with subacute and chronic stages (particularly caudate lobe hypertrophy)
but diffuse hepatomegaly with smooth contours in the acute stage [45]. Evaluation
of hepatic venous patency may be suboptimal without contrast. However, a filling
defect within the hepatic vein or inferior vena cava flow voids may suggest the pres-
ence of a thrombus. On contrast-enhanced examinations, variations in hepatic per-
fusion are a prominent feature in Budd-Chiari syndrome, a manifestation of
intrahepatic and extrahepatic collateralization. MR may reveal the presence of mul-
tiple 1–4 cm regenerative nodules with iso- to hyperintense signal on T1 sequences
and iso- to hypointense signal on T2-weighted images, with arterial enhancement
and retention of contrast on the portal venous phase [40, 45]. However, given the
contraindication of gadolinium in pregnancy, the imager may have to rely on non-
contrast features.
Gastrointestinal Disease
Bowel obstruction is another leading cause of abdominal pain, during pregnancy,

most often occurring in the second or third trimester [28]. Intestinal obstruction
represents the third leading cause for surgical intervention for acute abdominal pain
in pregnancy [44]. Most commonly, the obstruction is due to adhesions, which gen-
erally cannot be visualized on imaging. Following initial examination with abdomi-
nal radiography, CT is typically the next modality utilized in the evaluation of
suspected intestinal obstruction in the nonpregnant patient. However, this algorithm

is often altered in pregnancy to avoid the use of ionizing radiation by utilizing US
or MRI.
The use of sonography has been advocated as a first-line modality for the evalu-
ation of suspected small bowel obstruction in pregnant patients, both because of the
lack of ionizing radiation, and targeted evaluation of the bowel, when a gravid
uterus in the third trimester may displace the bowel, making typical patterns of
bowel obstruction on radiography less reliable [34, 44]. US findings include dilated
(>3 cm), hyperperistaltic bowel loops with swirling of intraluminal contents involv-
ing long segments (>10 cm) of bowel [46]. Identification of these findings should
prompt further evaluation with MRI or CT to identify the transition point and asso-
ciated complications of obstruction [34].
Findings of small bowel obstruction on CT and MRI include the presence of
dilated fluid-filled bowel loops measuring >2.5–3.0 cm in diameter, intraluminal
air-fluid levels, “fecalization” of bowel contents from delayed small bowel transit,
mesenteric fluid and haziness, and decompressed bowel distal to the site of obstruc-
tion indicated by “beaking” of the stenosed bowel segment [25, 34, 47, 48]. Closed-
loop obstructions manifest with clustered small bowel loops tethered in one quadrant
of the abdomen and twisting of mesenteric vessels. Bowel wall thickening, mesen-
teric edema, and hypoperfusion of bowel segments (seen on contrast-enhanced CT
as hypoenhancing bowel walls) suggest strangulation [47, 48].
Other etiologies of intestinal obstruction in pregnancy may be secondary to
underlying inflammation or fibrosis from active or chronic changes of inflammatory
bowel disease (IBD), particularly Crohn’s disease or less likely ulcerative colitis
[44]. Although fluoroscopic examinations (namely small bowel follow through)
have been traditionally used for evaluation of the small bowel, cross-sectional imag-
ing with CT or MRI is typically preferred as it offers evaluation of extramural dis-
ease extent [44]. CT (and particularly CT enterography) findings include mural
thickening and enhancement, luminal narrowing, mesenteric or mural inflamma-
tion, and fibrofatty proliferation of chronically affected segments [20]. Other com-
plications of IBD are readily depicted on CT and include abscess, fistula, and sinus
tract formation. Typically, however, pregnant patients with IBD are imaged with
MRI [34].
MR and MR enterography findings mirror those of CT, with increased sensitivity
of depicting early bowel wall inflammation in the setting of IBD as increased signal
on T2-weighted images. Sensitivity and specificity of MR for detecting these fea-
tures may be as high as 98% and 100%, respectively [20].
Vascular
Various vascular complications of pregnancy may occur. Pregnant patients are pre-
disposed to ovarian venous thrombusthat is believed to be secondary to the relative
hypercoagulable state of pregnancy and venous stasis from compression of the
gonadal vein at the pelvic brim by the gravid uterus. As a rare complication of preg-
nancy, affecting nearly 0.2% of pregnancies, mortality may exceed 60%. [34]. The
retroperitoneal location of the ovarian vein often precludes complete visualization
by US. The reported sensitivity of US for depicting ovarian venous thrombosis is
just over 50% [34, 49].
MR venography (with time-of-flight sequencing) may offer the highest sensitiv-
ity and specificity (100%) for diagnosis of ovarian venous thrombosis, manifesting
as an area of signal void within the vein. T1- and T2-weighted sequences may reveal
intermediate to high signal of the intraluminal clot, depending on the acuity [25, 34,
49]. Therefore, noncontrast MR venography is recommended as the next-line evalu-
ation for patients with inconclusive findings at US [49].
Contrast-enhanced CT with adequate bolus timing and opacification of the
gonadal veins may depict the low-attenuation intraluminal filling defects within
dilated retroperitoneal tubular structures, indicating thrombus [49].
Splenic artery aneurysms affect approximately 10% of the general population,
exhibit a distinct association with pregnancy, and may be complicated by rupture in
up to 25% of cases [34, 50]. Several risk factors exist for splenic artery aneurysms,
including pregnancy itself. Splenic artery aneurysms may be diagnosed using gray
scale and spectral Doppler US as hypo- or anechoic dilations of the native artery
near the splenic hilum and a weak, turbulent pulsatile flow pattern. In the presence
of mural thrombus or calcification, no flow may be seen.
CT may show a peripherally calcified mass in association with the splenic vessels,
most frequently near the splenic hilum. Most measure less than 2.5 cm in size [34].
Aneurysm rupture may be noted as dense fluid in the region of the spleen. MR of
splenic aneurysms may show a rounded dark flow void next to the splenic hilum in the
presence of flow. Otherwise, thrombosed or calcified aneurysms would appear as iso-
to hyperintense masses on T1- or T2-weighted images, near the native vessel [34].
Physiological adaptations to pregnancy include increased circulating blood vol-
ume and hormonal changes of the aortic wall, which may predispose to aortic dis-
section, particularly in the third trimester [51]. Underlying connective tissue
disorders, such as in the Marfan syndrome, contribute to inherent weakness of the
aortic media, making these patients particularly susceptible to aortic dissection with
a fivefold increased risk (4.4%) [52]. Older patient age (>32 years) and ascending
aortic lumen diameter > 4.2 cm are both associated with increased risk of dissection
and rupture [52, 53]. Contrast-enhanced CT angiography is first employed in the
setting of suspected acute aortic dissection, as it is rapid and the extent of the dis-
section and associated complications can be readily defined. CT findings include
the presence of a displaced intimomedial flap which divides the true and false
lumens [54]. Complications of branch vessel occlusion, thrombosis, or vessel rup-
ture may also be detected. While not typically used in the acute setting, MRI may
provide not only structural information of abdominal aortic aneurysms, but also
dynamic and flow-related information [55].
Trauma
Rapid and accurate assessment of the maternal abdomen, placenta, and fetus for
traumatic injury is imperative. FAST exams are rapid bedside procedures used by
initial responders and physicians as a screening tool for the presence of pericardial,
pleural, and peritoneal blood. Their sensitivity may be low for detecting small
bleeds, but a positive exam allows for rapid triage of the patient for appropriate
treatment algorithms. Placental abruption is the most common cause of fetal mortal-
ity in trauma followed by maternal visceral (splenic and liver) injury [20, 21, 23, 30,
56]. In many centers, the FAST examination is first performed to assess maternal
wellbeing, and once stabilized, a fetal US is performed [23]. In a large review,
Meisinger et al. concluded that FAST examinations (with extended examination of
the kidneys, liver, spleen, placenta, amniotic fluid volume, and limited fetal evalua-
tion including M-mode interrogation of fetal heart rate) in pregnant patients who
sustained blunt abdominal trauma, were 85.7% sensitive and 99.7% specific, which
is similar to that of abdominopelvic CT [24]. Richards et al. reported similar sensi-
tivity (64%) and specificity (94.4%) which were highest in the first trimester [57].
The sensitivity of US tends to decrease with increasing gestational age, and osseous,
retroperitoneal, and hollow viscus injury may be missed by US [3].
Hesitation over the perceived risk of radiation exposure should not delay the use
of contrast-enhanced CT in the evaluation of the pregnant patient who sustains
abdominal or pelvic trauma [1, 21, 23]. CT has important implications for clinical
management, allowing for the rapid diagnosis of immediate life-threatening condi-
tions and permitting appropriate patient triage [23]. Injury patterns in pregnant
patients favor the abdomen and pelvis relative to other body regions, especially
when compared with those of nonpregnant trauma patients, thought to be related to
physiological and anatomical changes of pregnancy [23, 58]. Especially in the third
trimester, the gravid uterus will displace the liver and spleen, making them prone to
injury from overlying ribs [23, 58]. Solid organ injury is depicted as peripheral lin-
ear or wedge-shaped areas of hypoattenuation, indicating laceration or fracture.
Physiological hydronephrosis of pregnancy may predispose the renal collecting sys-
tems to blunt or sheer injury, leading to calyceal rupture, and may be best visualized
on delay scanning as spillage of contrast material from the collecting system [23].
Low-dose CT cystogram should be considered in the presence of pelvic fractures to
exclude bladder injury, as the displaced urinary bladder is at the higher risk for
injury in pregnancy. Pelvic and acetabular fractures are associated with high mater-
nal and fetal mortality [23, 58] (Fig. 4.7). Placental injury is the most common
pregnancy-related injury in the setting of blunt abdominal trauma, followed by uter-
ine rupture and direct fetal injury [20, 23]. Placental abruption manifests as large
confluent areas of hypoattenuation and hypoenhancement that may be retroplacen-
tal or extend through the entirety of the placental thickness [58, 59]. Hyperdense
amniotic fluid may further suggest the diagnosis, indicating hemorrhage within the
amniotic fluid [58]. However, the CT findings of placental abruption vary signifi-
cantly and may be hard to detect, likely from lack of data available on the normal
appearance of the placenta as well as pathology mimics (e.g., myometrial
Fig. 4.7 CT of a pregnant trauma patient: 30 y/o pregnant patient at 30 weeks was an unrestrained
driver in a high-speed MVC. Axial CT through the pelvis demonstrates a comminuted left acetabu-
lar fracture (arrows) and pelvic hematoma (asterisk). Partial visualization of fetal skull (arrow-
heads). Acute traumatic aortic injury of the thoracic aorta was identified in the chest (not shown).
Intrauterine fetal demise was noted at time of arrival to the trauma bay. Upon delivery of the fetus,
multiple fetal skull fractures were noted. The patient expired in the operating room
contraction) [59]. Uterine rupture manifests as decreased enhancement in the

affected uterine wall extending though a variable thickness and rarely an empty
uterus with a free-floating fetus within the maternal abdomen [58].
MR imaging is typically reserved for follow-up examinations after the patient
has been clinically stabilized, as the length of the MR exam and difficulty in patient
monitoring would place undue risk to the patient and fetus in the acute care setting
[21, 23, 56].
Gynecological Causes of Abdominal Pain
Adnexal Masses
The increased utilization of routine obstetric ultrasound has resulted in the more
common detection of adnexal masses during pregnancy. Etiologies are variable,
ranging from the frequently encountered physiologic, hormonally influenced cyst to
the rarely encountered malignant ovarian neoplasm. Most adnexal masses in preg-
nancy are asymptomatic and incidentally visualized on imaging. However, adnexal
masses can be a source of acute pain in pregnancy, particularly in the first trimester
[60, 61].
Ultrasound is the initial imaging modality of choice for the evaluation of pelvic
pain in pregnancy and for characterization of pelvic masses [61, 62]. This character-
ization helps guide clinical management by determining those masses likely to
spontaneously regress with progression of pregnancy from those that place the
patient at increased risk for future complications such as torsion or preterm labor or
those that have features that raise concerns for malignancy [61].
Functional Cysts
The corpus luteum of pregnancy and other hormonally responsive cysts are the most
commonly encountered adnexal masses of pregnancy. Although the majority of
these physiological structures resolve by 14–16 weeks of gestation [60], they can be
a source of pelvic pain. Symptoms typically are located on the ipsilateral side of the
lesion and can be secondary to size (from compression of or by adjacent structures),
internal hemorrhage, or rupture [61, 62]. In addition, as with any of the following
adnexal masses, there is a predisposition for ovarian torsion leading to acute pelvic
pain (particularly in lesions >5 cm), which will be discussed later [63].
Corpus Luteum
The physiological corpus luteum is responsible for the maintenance of early preg-
nancy until the development of the placenta and is a common cause of pain in the
first trimester [60, 62]. Familiarity with the variable sonographic appearances of the
corpus luteum is key; these cysts can be confused with an ectopic pregnancy or
suspicious mass. The corpus luteum may appear as a simple cystic structure with
variable wall thickness or as a complex cystic lesion [60]. When complex, the cor-
pus luteum may appear as an isoechoic or hypoechoic solid-appearing structure due
to wall thickening or internal hemorrhage [64]. The thickened wall is typically
hypoechoic with pronounced peripheral vascularity noted on color or power Doppler
producing a “ring of fire” appearance [60, 64]. This is not to be confused with the
“ring of fire” seen in ectopic pregnancies (which often demonstrate hyperechoic
walls), which will be discussed later. In the absence of hemorrhage, corpus lutea are
centrally anechoic. In the presence of internal hemorrhage, internal debris is noted
with the appearance dependent on the acuity and extent of bleeding and paralleling
the internal appearance of other hemorrhagic cysts, discussed below [62]. In the
setting of rupture, patients can present with acute onset pelvic pain with free fluid,
either simple or containing internal echoes reflecting hemoperitoneum [62]. With
corpus luteum rupture, the walls may appear partially collapsed.
Simple Cysts
Simple cysts are anechoic, rounded structures with a thin, smooth wall, and no inter-
nal septations or solid components. While most are commonly asymptomatic, when
large (greater than 5 cm), simple cysts can produce symptoms due to compression
and have a higher propensity to persist throughout pregnancy [61, 65]. Larger cysts
should, therefore, be followed on serial ultrasounds. On MRI, simple cysts appear
as round, circumscribed lesions with high signal on T2-weighted images and low to
intermediate signal on T1-weighted images [25].
Hemorrhagic Cysts
Hemorrhagic cysts demonstrate a variable appearance depending on the duration
and degree of internal blood products. However, classic patterns of internal hemor-
rhage include internal reticular echoes from fibrin strands that produce a lacy or
fishnet appearance (not to be confused with thicker septations) or more solid appear-
ing hypoechoic internal echoes, which can be diffuse or focal. Lack of internal
blood flow as well as concave margins and angularity (seen with retracting clot)
within these more solid appearing areas as well as increased through transmission
help to distinguish internal hemorrhage from a true solid mass or solid mural nodu-
larity [60, 64]. Evolution of the findings over serial ultrasounds also helps to con-
firm the diagnosis and exclude a more worrisome mass. Acutely, hemorrhagic cysts
can be centrally hyperechoic relative to ovarian tissue or centrally heterogenous [60,
65]. On MRI, hemorrhagic cysts typically demonstrate high signal on T1-weighted
images and variable signal on T2-weighted images [25].
Adnexal Masses Unique to Pregnancy
yperstimulated Ovaries and Ovarian Hyperstimulation Syndrome

H
Several entities involving the adnexa which are unique to pregnancy can be a source
of pelvic pain and have a classic ultrasound appearance. Hyperstimulated ovaries
can occasionally be seen in unassisted pregnancies but are more commonly observed
in the setting of ovulation induction [60, 65]. Ultrasound shows enlarged bilateral
ovaries with multiple predominantly peripherally located cysts of variable sizes
(most commonly simple but can be complicated by hemorrhage) with thin interven-
ing cyst walls appearing like echogenic intervening septa and echogenic ovarian
stroma centrally producing a classic “spoke wheel” appearance [60, 66]. A poten-
tially severe complication of ovarian induction which can be seen in early preg-
nancy is ovarian hyperstimulation syndrome (OHSS), which is associated with the
above ovarian findings (often with massively enlarged ovaries > 12 cm in severe
cases) in combination with fluid shift out of the intravascular space, visualized on
US as ascites [66]. Pleural effusions can also be seen with more severe cases. The
increased ovarian volumes significantly increase the risk of ovarian torsion, with an
incidence of 7.5% in patients with OHSS [66]. These findings typically resolve over
the course of pregnancy on serial ultrasounds. The appearance of hyperstimulated
ovaries with apparent septations due to abutting thin cyst walls should not be con-
fused with a multiseptate cystic ovarian neoplasm. Key distinguishing features
include lack of solid components or mural nodules and visualization of central ovar-
ian stroma [66].
MRI features of ovarian hyperstimulation parallel the ultrasound findings, with
enlarged bilateral ovaries with multiple T1 hypointense and T2 hyperintense cysts
seen in the characteristic peripheral distribution with ovarian stroma centrally.
When cysts are complicated with hemorrhage, increased T1 signal and variable T2
signal are noted [66]. If ascites is present, it is most commonly simple, with T2
hyperintense, T1 hypointense-free fluid visualized.
yperreactio Luteinalis and Theca Lutein Cysts

H
In nonassisted reproduction, an abnormal, hypersensitivity of the ovary to circulat-
ing levels of hCG can lead to a similar but less pronounced appearance of hyper-
stimulated ovaries. This is referred to as hyperreactio luteinalis and can be seen in
the setting of normal serum β-hCG levels or in elevated levels as seen with multiple
gestations or fetal hydrops [60, 65]. This entity is more commonly observed in the
3rd trimester. A similar ultrasound appearance can also be seen with theca lutein
cysts, which develop in the setting of gestational trophoblastic disease (molar preg-
nancies) in response to markedly elevated levels of serum β-hCG. Ultrasound will
demonstrate enlarged ovaries with multiple prominent anechoic cysts [62, 65]
(Fig. 4.8).
Endometriomas
Endometriomas are an infrequent cause of abdominal pain in pregnancy and account
for approximately 4% of adnexal masses in pregnancy [67]. The classic ultrasound
appearance of an endometrioma is that of a complex cyst with diffuse low-level or
medium-level internal echoes (ground glass appearance) with no internal flow [64,
68] (Fig. 4.9). Depending on the stage of internal hemorrhage, a hemorrhagic cyst
can sometimes demonstrate a similar appearance. Small echogenic foci in the cyst
Fig. 4.8 US of theca lutein cysts: 33 y/o pregnant patient at 14 weeks’ with partial molar preg-
nancy and β-hCG >200,000. Longitudinal and transverse gray scale images of the left ovary dem-
onstrate ovarian enlargement with numerous anechoic cystic structures predominantly in the
periphery with echogenic central ovarian stroma producing a “spoke wheel pattern”. The ovary
measured up to 7 cm
Fig. 4.9 US of an
incidental endometrioma:
36 y/o pregnant patient at
5 weeks’ presented with
vaginal bleeding. Gray
scale image of the left
ovary demonstrates a
hypoechoic cyst with
homogenous low-level
internal echoes classic of
an endometrioma
(arrowheads). See adjacent
ovarian tissue with follicles
(arrows)
walls thought to represent cholesterol crystals have also been described with endo-
metriomas [64, 68].
On MRI, endometriomas classically demonstrate high signal on T1-weighted
images and signal lower than simple fluid on T2-weighted images, which has been
coined “T2 shading” [69]. Fat saturated T1-weighted sequences can help distin-
guish endometriomas (which will remain T1 hyperintense) from fat containing der-
moid cysts (which will decrease in signal) [69].
Decidualization of an endometrioma during pregnancy is a recognized entity that
can mimic ovarian neoplasm. In this process, mural nodules or papillary excres-
cences with vascularity develop in ectopic endometrial stroma in response to
increased circulating progesterone, paralleling the response of the normal endome-
trium as it becomes the decidual lining of pregnancy. While these findings can
appear worrisome on ultrasound and MRI and overlap with malignancy, a key fea-
ture described on MRI can help distinguish this entity. The nodules of a decidual-
ized endometrioma have been described to demonstrate similar T2 signal
hyperintensity to that of the decidualized endometrium [68–70].
Ovarian Neoplasms
Mature Cystic Teratoma

The most common benign ovarian neoplasm in pregnancy is the mature cystic tera-
toma or dermoid cyst [25]. Although often asymptomatic and diagnosed inciden-
tally on a routine screening ultrasound, these, like other ovarian masses, predispose
the ovary to torsion and can be a source of acute abdominal pain. Dermoid cysts
have a complex appearance on ultrasound, but key characteristic findings help con-
firm the diagnosis. Hyperechoic areas with pronounced posterior shadowing result
in a “tip of the iceberg sign”; a hyperechoic nodule in a background of complicated
cyst described as the Rokitansky nodule or “dermoid plug,” and multiple hyper-
echoic lines and dots, so called “dermoid mesh” or “dot-dash” appearance (which
represents floating hair in sebum) are classic features. Additional findings are calci-
fications (often due to bone or teeth) and fluid-fluid levels with hyperechoic floating
fat and more hypoechoic dependent echoes [60, 64, 71]. Two or more of these fea-
tures allow for the diagnosis of a dermoid cyst with a high degree of accuracy [60].
In indeterminate lesions, MRI can be utilized to evaluate for the presence of fat. The
sebaceous components of dermoid cysts demonstrate high signal on T1-weighted
images with signal dropout on fat-saturated sequences [71] (Fig. 4.10). Despite its
specificity for detecting fat and calcification within dermoid cysts, which can con-
firm the diagnosis, CT is typically avoided in pregnancy due to the ionizing
radiation.
Fig. 4.10 MRI and US of a dermoid cyst. 35 y/o pregnant patient at 25 weeks’ with an incidental
dermoid cyst. (a) T1-weighted axial MRI of the upper abdomen superior to a gravid uterus dem-
onstrates a rounded, lobulated predominantly T1 hyperintense mass (arrows). (b) Fat-saturated
T1-weighted image at the same level demonstrates signal drop out (dark signal) within a majority
of the mass (arrows), compatible with internal fat. (c) Gray scale US of the upper abdomen supe-
rior to the uterus containing IUP (asterisk) demonstrates a complex mass (between calipers) with
multiple hyperechoic lines and dots suggestive of dermoid mesh (arrowhead) and rounded echo-
genic component suggestive of Rokitansky nodule (arrow) classic of a dermoid cyst. The ovary
was displaced superiorly in the abdomen by the gravid uterus
Epithelial Neoplasms
Epithelial neoplasms include benign cystadenomas, tumors of low malignant poten-
tial, and malignant cystadenocarcinomas. As mentioned with other masses, these
entities are often detected incidentally on routine imaging but increase the risk of
torsion by acting as a lead point and can present in the acute setting. In addition,
advanced ovarian malignancy may be symptomatic due to size or metastases. After
teratomas, cystadenomas (serous and mucinous), are the next most common benign
ovarian neoplasms of pregnancy [25, 67]. Serous cystadenomas are characteristi-
cally unilocular, simple appearing cystic structures with or without thin septations
which persist or grow throughout pregnancy and are typically larger than functional
cysts [60]. Mucinous cystadenomas can be indistinguishable on ultrasound from
serous cystadenomas; however, more commonly contain multiple septations and
low-level internal echoes [60].
An estimated 1% of adnexal masses detected during pregnancy are malignant
[25]. Features that increase the suspicion for malignancy include solid components
with vascular flow, papillary projections (> 3 mm), thick, irregular walls, and mul-
tiple thick septations (> 2–3 mm) with vascular flow [60, 64] (Fig. 4.11). Ascites is
an indirect finding seen with malignancy, usually as the result of peritoneal metas-
tasis [60, 64] but by itself is a nonspecific finding. MRI can be used as an adjunct in
indeterminate masses on US, or for further staging. MRI features of malignant
masses reflect the US features, including solid components, mural nodules, papil-
lary excrescences, and thick septations. Because gadolinium is avoided in preg-
nancy, evaluation for internal enhancement is not possible. MRI also allows for
additional imaging information, including evaluation for adenopathy, peritoneal or
omental implants, ascites, and distant metastases [72].
ther Ovarian Neoplasms

O
Other ovarian neoplasms such as sex cord stromal tumors are rare, but if detected by
ultrasound, can be further characterized with MRI [60].
Limited Role of CT
In general, CT is of limited benefit in the characterization of adnexal masses [64],

particularly during pregnancy due to the risk of ionizing radiation. There is much
overlap in the CT appearances of benign ovarian masses, and ultrasound and MRI
are far superior at demonstrating the internal characteristics of the masses.
Macroscopic fat and calcifications can be easily demonstrated on CT to reliably
diagnose a dermoid cyst. However, when these features are absent, CT is of little
benefit in distinguishing dermoid cysts from other lesions [64]. Although MRI is
preferred in the setting of pregnancy, CT can be useful in the staging of malignancy
and for evaluation for metastatic disease if MRI is inconclusive.
Fig. 4.11 US and MRI of ovarian cancer. 29 y/o pregnant patient presented at 7 weeks’ with left-
sided pelvic pain. (a) Gray scale image of the pelvis demonstrates a large complex cystic mass with
large central solid nodule (arrow) along a septation, small mural nodules along the periphery
(arrowheads) and solid component (asterisk). Internal blood flow was present in the solid compo-
nents (not shown). (b) Gray scale image of the right upper quadrant shows moderate abdominal
ascites (asterisk). (c) Coronal oblique T2-weighted MR mage of the pelvis demonstrates a large
complex cystic mass (arrowheads) with solid central mural nodule along a septation (arrow) and
heterogenous solid component inferiorly (asterisk). Ascites is also present. The patient underwent
exploratory laparotomy with debulking surgery at 10 weeks due to increasing distension and short-
ness of air. Seven liters of ascites was found along with a 15 cm right ovarian mass with papillary
frond like projections and diffuse carcinomatosis. Pathology revealed high-grade papillary serous
carcinoma. The patient received chemotherapy during pregnancy and delivered a viable neonate at
39 weeks
Ovarian Torsion
Ovarian or adnexal torsion has an increased incidence in pregnancy, estimated at

1:1800 [67] and most commonly occurs during the mid to late 1st trimester [62].
The increased incidence is thought to be due to increased laxity of supporting liga-
mentous structures, the increased movement of the ovaries and adnexa during rapid
enlargement of the uterus, and the increased incidence of masses during pregnancy
which can serve as pathological lead points [60, 61, 73]. An estimated 7% of
ovarian masses in pregnancy are complicated by torsion [25, 61]. However, torsion
can still occur in the absence of an underlying ovarian mass, in which case it more
commonly occurs on the right [61].
Torsion results from a twisting of either the ovary (and/or fallopian tube) and its
vascular pedicle in its suspensory ligament, first compromising low-pressure venous
outflow, then later, the higher pressure arterial inflow. This leads to thrombosis,
progressive ischemia, and eventual hemorrhagic infarction [73]. Ultrasound is the
imaging modality of choice to evaluate suspected ovarian torsion. Characteristic
gray scale findings include a unilaterally enlarged ovary, abnormally positioned
ovary (often midline or on the contralateral side), multiple peripherally displaced
follicles, and heterogenous, edematous central ovarian stroma [60, 73]. A coexisting
dominant cyst or mass may be seen, which serves as the lead point, but is not a
necessity. A specific sign, when seen, is the twisted vascular pedicle adjacent to the
ovary resulting in a “whirlpool sign” which can be detected using a combination of
gray scale and color Doppler [73].
Doppler findings in torsion are variable and depend on the degree or extent or
duration of torsion. The absence of blood flow to an enlarged ovary on the ipsilateral
side of pain is the most specific Doppler finding on ultrasound. However, a critical
point to note is that the presence of blood flow (either arterial or venous) does not
exclude the diagnosis of torsion, and the presence of ovarian blood flow in the set-
ting of a classic clinical history and the aforementioned gray scale findings should
not dissuade one from the diagnosis. The ovary has a dual blood supply, receiving
arterial blood flow from ovarian and uterine branches, which can preserve arterial
flow. Torsion can be incomplete or intermittent, which can also preserve blood flow
[60, 65]. Free pelvic fluid with echoes suggesting hemoperitoneum may be observed
as a secondary finding.
MRI features of ovarian torsion parallel those of US and are best visualized on
T2 weighted as increased ovarian volume with increased T2 signal within central
edematous ovarian stroma and multiple peripherally located T2 hyperintense folli-
cles. With progressive torsion and internal hemorrhage, increased signal on
T1-weighted images can be seen. A T1 hyperintense rim has been described as a
finding associated with ovarian torsion relating to subacute hemorrhage [73]. A
dominant mass acting as lead point may or may not be seen. Use of multiplanar
reformatted images can increase the detection of a twisted vascular pedicle and
associated thickened fallopian tube.
CT is typically not indicated for the diagnosis of torsion given the superiority of
US and MRI; however, similar findings to those previously described can be seen on
CT. The most common finding on CT is a unilaterally enlarged ovary, sometimes in
an atypical location. A twisted vascular pedicle, peripherally located follicles, and
areas of nonenhancement are better seen in the presence of IV contrast. However,
like Doppler, the presence of ovarian enhancement does not exclude the diagnosis
of torsion. Heterogenous increased attenuation can be seen in the setting of internal
hemorrhage and an underlying mass may or may not be detected [73].
Massive Ovarian Edema
Massive ovarian edema is a rare condition that results from vascular congestion of
the ovary, thought to be due to intermittent or partial ovarian torsion or compression
of the vascular pedicle between the gravid uterus and adjacent stationary pelvic
structures. This most commonly occurs in the 2nd and 3rd trimesters. Venous and
lymphatic obstruction causes progressive accumulation of fluid within ovarian
stroma resulting in a massively enlarged, edematous ovary with peripherally dis-
placed follicles [74, 75]. This is usually unilateral. Imaging findings are often indis-
tinguishable from torsion. Ultrasound demonstrates an enlarged ovary with
peripherally located follicles with some internal blood flow [74]. MRI demonstrates
asymmetric ovarian enlargement and a classic “teardrop” configuration, stromal T2
hyperintensity, peripheral T2 bright follicles, and variable T2 and T1 hyperintensity
depending on the presence of hemorrhagic congestion [75].
Leiomyomas
Leiomyomas (also known as fibroids) are detected in 1–4% of pregnancies [65, 67]
and are considered the most common solid masses in pregnancy [65]. Fibroids can
be intramural, submucosal, and subserosal (in which case they may be pedunculated
and mimic an ovarian mass). Fibroids can produce acute pain due to internal degen-
eration, hemorrhagic infarction, or torsion (if pedunculated).
Fibroids can have a variable sonographic appearance but often appear as round,
heterogenous hypoechoic masses. Uterine contractions can mimic a fibroid but can
be distinguished by the lack of persistence during the scan. During pregnancy,
fibroids can enlarge, decrease in size, or remain stable [60, 61, 67]. When fibroids
enlarge during pregnancy as a result of hormonal influence, they can outgrow their
blood supply and undergo hemorrhagic infarction, so called “red degeneration
[62].” Ultrasonographically, this is manifested as internal cystic spaces or heterog-
enous echogenicity within fibroids [61, 65] (Fig. 4.12). Pain elicited with the trans-
ducer directly over the degenerating fibroid can confirm this as the etiology of the
patient’s symptoms [61].
A torsioned, pedunculated fibroid can demonstrate a similar sonographic appear-
ance and can also be “probed” by the transducer to confirm this is the cause of the
patient’s pain. A variable internal flow pattern can be noted with Doppler interroga-
tion due to the twisted stalk [60], including the absence of flow. Detection of a con-
necting stalk of the fibroid to the uterus should be sought to exclude a solid adnexal
mass. When not able to be visualized, MRI can be helpful to confidently distinguish
a pedunculated fibroid from adnexal mass [65]. On MRI, fibroids with red degen-
eration demonstrate peripheral or diffuse increased T1 signal and a variable appear-
ance on T2-weighted images, often with a low T2 signal rim [61].
Fig. 4.12 US of cystic degeneration of a fibroid: 29 y/o pregnant patient at 35 weeks’ presenting
at follow-up US. (a) Gray scale image through the right lower uterus demonstrates a lobulated
mass (arrows) compatible with fibroid with internal cystic (asterisk) and hypoechoic solid appear-
ing areas (arrowhead) compatible with fibroid with cystic degeneration. (b) Gray scale image of
the same area 3 months prior demonstrating the fibroid (arrows) was previously solid throughout
with heterogenous echogenicity. Adjacent IUP (asterisk)
Pelvic Inflammatory Disease
Patients with pelvic inflammatory disease (PID) often present with fever and non-
specific abdominal or pelvic pain. Ultrasound is the diagnostic imaging modality of
choice for the evaluation of suspected PID. Findings of early PID are difficult to
detect on US but include the subtle findings of increased echogenicity of peritoneal
fat surrounding the uterus and adnexa as well as indistinctness of the uterine serosal
surface [76]. More advanced PID is more easily depicted on US. Inflamed fallopian
tubes appear as dilated, fluid-filled, tubular structures with thickened, hyperemic
walls, and thickened endosalpingeal folds (cogwheel sign). Often, the internal fluid
is echogenic, owing to pyosalpinx. If inflammation extends beyond the fallopian
tube, but a distinct ovary is still visualized separately, a tubo-ovarian complex is
described. If the normal ovarian architecture is no longer visualized, then the term
tubo-ovarian abscess (TOA) is used [60, 76]. TOAs can have a variable appearance
but often appear as heterogeneous, complex adnexal masses with hypervascularity,
unilocular or multilocular cystic spaces, and variable solid appearing areas [64].
In the nonpregnant patient, CT can be useful as an adjunct to US to document the
extent of disease and involvement of any adjacent structures. However, MRI is pre-
ferred with pregnancy to avoid ionizing radiation. MRI findings in PID parallel the
US findings, with dilated, tubular structures in the adnexa with thickened walls
reflecting pyosalpinx. An ill-defined, heterogeneous adnexal mass with thick, irreg-
ular walls and variable signal fluid components suggest TOA. The signal of the fluid
in TOA can be variable, ranging from low to intermediate to high signal on
T1-weighted imaging and heterogenous or high on T2-weighted imaging [77].
Diffusion-weighted imaging (DWI) can improve the accuracy of MRI detection of
PID. On DWI, abscess cavities and pyosalpinx can demonstrate high signal and cor-
responding low apparent diffusion coefficient (ADC) values [78].
Obstetric Causes of Abdominal Pain
First Trimester Causes

Common causes of pregnancy-related abdominal and pelvic pain in the first trimes-
ter include early pregnancy failure and ectopic pregnancy. However, early viable
pregnancies can also present with mild symptoms including crampy abdominal pain
and can be concerning enough for a gravida to seek medical attention [62].
Recognition of the early signs of an intrauterine pregnancy is important to be able
to distinguish a normal early intrauterine pregnancy (IUP) from abnormal findings.
arly Normal Pregnancy

E
Ultrasound is the diagnostic imaging modality of choice for pregnant patients who
present with acute pelvic pain. Evidence of an IUP can be visualized as early as
4–4.5 weeks’ on transvaginal (TV) US. The earliest ultrasound finding is the visu-
alization of the gestational sac (GS), and an “intradecidual sac sign” helps distin-
guish the GS from potential mimickers. The intradecidual sac sign occurs with
visualization of a small, discrete fluid collection with echogenic rim eccentrically
positioned in the endometrium (renamed the decidua during pregnancy) [62, 79]
(Fig. 4.13). This structure should not change in appearance during the scan and
should be visualized in two planes to document precise location embedded within
the endometrium. This should not be confused with a pseudogestational sac, which
is anechoic or hypoechoic fluid most often representing blood products, located
centrally within the endometrial cavity – a finding associated with approximately
10% of ectopic pregnancies [62, 79, 80]. This endometrial fluid of a pseudogesta-
tional sac can also be noted to move during real-time scanning. In addition, the
intradecidual sac sign should be distinguished from decidual cysts – small, thin-
walled simple appearing cysts in the endometrium, typically located at the endome-
trial–myometrial junction (Fig. 4.14). Decidual cysts are often multiple and occur in
both ectopic pregnancies and early IUPs. The lack of an echogenic rim helps distin-
guish these from an early GS. However, at times, differentiation is not possible and
short-term follow-up is advised.
Around 5 weeks’ gestation, a “double decidual sac sign” is briefly seen as the GS
is surrounded by the decidua capsularis and decidua parietalis with a small interven-
ing crescentic focus of fluid sometimes visualized in the endometrial cavity [81]. A
secondary yolk sac (YS) is visualized within the GS at approximately 5.5 weeks’
and confirms the presence of an IUP, although viability cannot be assessed until an
embryo is visualized at around 6 weeks’ gestation [79]. Cardiac activity is observed
shortly after formation of the embryo, also at approximately 6 weeks’, and can be
detected in embryos as small as 1–2 mm [81].
Fig. 4.13 US of intradecidual sac sign: US of a 25 y/o pregnant patient with cramping and pink
discharge and β-hCG of 471. Transverse (a) and longitudinal (b) gray scale images through the
uterus demonstrate a tiny sac-like structure with echogenic rim (arrows) eccentrically positioned
in the endometrium compatible with the intradecidual sac sign. The adjacent echogenic linear
interface of the endometrial walls is visualized (arrowheads). (c) Follow-up US performed 2 weeks
later demonstrates a 6 week IUP with gestational sac, yolk sac, and embryo (arrow)
arly Pregnancy Failure

E
Approximately 12% of first trimester pregnancies result in spontaneous abortion
[82]. Most commonly, patients present with pain and vaginal bleeding and are eval-
uated with ultrasound to determine the presence and viability of an IUP as well as
features suggestive of active spontaneous abortion or early pregnancy failure.
Recently, generous thresholds for absolute criteria for diagnosing nonviable preg-
nancy have been recommended and are being adopted to prevent any potentially
dreadful surgical or medical action from being taken on a potentially viable early
pregnancy [83]. The goal in the diagnosis of nonviable pregnancies is a specificity
of as close to 100% as possible, to prevent any false positive results (or a pregnancy
that is potentially viable deemed nonviable) [83]. The higher measurements are in
part to account for interobserver variability in measurements and differing ultra-
sound equipment. Based on these guidelines, findings diagnostic of pregnancy fail-
ure include a crown-rump length (CRL) of an embryo ≥7 mm and no heartbeat, a
mean sac diameter of the GS ≥ 25 mm and no embryo, as well as follow-up ultra-
sound demonstrating no embryo with heartbeat ≥2 weeks after a scan that showed
Fig. 4.14 US of decidual cysts and early gestational sac: 19 y/o pregnant patient with quantitative
β-hCG of 2967 and abdominal pain. (a) Longitudinal gray scale image through the uterus demon-
strates a thickened endometrium with numerous tiny thin-walled anechoic foci suggestive of
decidual cysts predominantly in the periphery of the endometrium. (b) Transverse gray scale
image through the uterus demonstrate a larger dominant cystic structure with echogenic rim
(arrows) suspicious for early gestational sac with surrounding decidual reaction. No yolk sac or
embryo was seen, expected given mean sac diameter of 5 mm. (c) Follow-up US 18 days later
shows an early IUP. Decidual cysts can be seen with early intrauterine pregnancy, early pregnancy
failure or ectopic pregnancy
a GS without a YS or ≥11 days after a scan that showed a GS with a YS. Additional

features suspicious for but not diagnostic of early pregnancy failure include an
enlarged YS (> 7 mm), small GS in relation to the embryo (< 5 mm difference
between GS and CRL), and CRL < 7 mm with no heartbeat, among others [83].
These measurements are all based on a TV exam. Ultrasounds with findings suspi-
cious for early pregnancy failure should have short-term ultrasound follow-up [81].
Ectopic Pregnancy
Ectopic pregnancy is estimated to occur in approximately 2% of all pregnancies

[79]. However, the incidence is even higher with the use of assisted reproductive
technology (ART), which is becoming increasingly utilized with greater than 1% of
all births now involving ART [66]. Risk factors for ectopic pregnancy include a his-
tory of previous pelvic inflammatory disease or sexually transmitted disease, previ-
ous personal history of ectopic pregnancy, previous tubal surgery, endometriosis,
and ART, among others [61, 80]. Patients often present with pelvic pain and vaginal
bleeding, and ultrasound is the first-line imaging modality to evaluate a suspected
ectopic pregnancy. Timely diagnosis is crucial as ectopic pregnancy remains the
leading cause of obstetric related death in the first trimester [80].
Serum β-hCG levels are helpful in the final interpretation of the ultrasound exam
and for follow-up recommendations; however, ultrasound scanning should not be
delayed in a patient suspected of having an ectopic pregnancy to await the results. A
delay in scanning could be catastrophic in the setting of a ruptured ectopic preg-
nancy. An intrauterine GS is usually able to be visualized with a β-hCG of 1000–
2000 or greater [82]. The β-hCG levels in ectopic pregnancies can be highly variable
and are often lower (less than 1000) [83]. Therefore, a certain β-hCG level should
never preclude an ultrasound exam in the setting of a positive pregnancy test and
clinical suspicion of ectopic pregnancy [83]. On the other hand, it is also extremely
important to not “overcall” the diagnosis of ectopic pregnancy based solely on dis-
criminatory levels, as this would lead to a catastrophic early termination of a poten-
tially viable but occult IUP. While higher β-hCG levels and an empty uterus increase
the likelihood of an ectopic pregnancy, at a β-hCG level of >3000, there is still a
0.5% chance of a viable IUP [81].
Transabdominal ultrasound exam should be performed first for an initial evalua-
tion of the uterus and adnexa and to evaluate for the presence of free fluid. Rarely, a
transabdominally detected ectopic pregnancy may not be visualized on TV exam if
obscured by leiomyomas or other pelvic masses [79]. In addition, if free fluid is
detected in the pelvis, the upper abdomen (particularly Morrison’s pouch between
the liver and right kidney) should be evaluated to document the extent of free fluid.
In the vast majority of cases, a TV scan will also be required for better visualization
and characterization of the uterus and adnexa. In the presence of a large amount of
free fluid suggestive of hemoperitoneum, the ultrasound exam should be expedited
to facilitate rapid patient treatment.
ubal Ectopic Pregnancy

T
Approximately 95% of ectopic pregnancies occur within the fallopian tube with the
remaining rare sites accounting for less than 5% of ectopic pregnancies [84]. The
most common ultrasound finding in tubal ectopic pregnancy is an adnexal mass
separate from the ovary. The mass can be of variable sonographic appearance, rang-
ing from a sac-like structure to an amorphous complex solid and cystic mass, com-
monly seen with rupture or surrounding tubal hemorrhage (Fig. 4.15). The “tubal
ring sign” manifests as an a sac-like structure in the adnexa representing the GS
with surrounding echogenic rim and often demonstrates a “ring of fire” pattern of
pronounced peripheral vascularity on color or power Doppler [61, 79, 82] (Fig. 4.16).
Specificity of ectopic pregnancy increases with the visualization of an internal YS
or embryo. When an extrauterine live embryo is detected in the adnexa, diagnosis of
an ectopic pregnancy is made with certainty. A thorough evaluation of the uterus for
Fig. 4.15 US of tubal ectopic pregnancy: US of a 25 y/o pregnant patient with right-sided abdom-
inal pain and quantitative β-hCG of 2757. (a) Gray scale image of the right adnexa demonstrates a
large amorphous mass (arrows) with small central sac-like structure containing yolk sac (arrow-
head). Tiny embyro with heartbeat was also present (not shown). Small amount of adjacent free
fluid present (asterisk). (b) Gray scale image of the left adnexa demonstrates complex-free pelvic
fluid (asterisk) compatible with hemoperitoneum. Surgery confirmed right tubal ectopic pregnancy
with swollen tube and adherent clot adjacent to the tube
coexisting IUP should be performed to exclude the rare heterotopic pregnancy (dis-
cussed later) [61, 82] (Fig. 4.17). Intra-ovarian ectopics are rare. The mass must be
demonstrated to be separate from the ovary, thus, increasing specificity. Gentle pres-
sure applied on the TV probe can confirm an extra-ovarian location of the mass by
demonstrating movement of the mass separate from the ovary [80]. The size of the
mass should be documented as this has implications for management. The presence
of complex-free fluid (suggesting hemoperitoneum) in the setting of a positive preg-
nancy test and no visualized IUP increases the likelihood of ectopic pregnancy, even
when an adnexal mass is not visualized [80]. However, hemoperitoneum alone is
nonspecific and can be seen with a ruptured hemorrhagic cyst.
Up to 12–35% of ectopic pregnancies may not manifest as an adnexal mass on
ultrasound, and in these cases, the diagnosis cannot be excluded by imaging [66,
80]. In these situations, if the patient is hemodynamically stable, follow-up of serial
β–hCG levels (to evaluate for appropriate or inappropriate doubling time) and short-
term follow-up US are indicated until the location of pregnancy is confirmed. This
scenario (in which no IUP is seen and the remaining pelvic ultrasound is normal)
has been recently termed “pregnancy of unknown location” to emphasize that the
differential considerations include both IUP and ectopic pregnancy [81].
The endometrium can have a variable appearance in the setting of ectopic preg-
nancy. A “pseudogestational sac” can be seen in up to 10% of ectopic pregnancies
as anechoic or hypoechoic fluid centrally positioned in the endometrial cavity (as
opposed to the eccentric location of a GS). A trilaminar appearance of the endome-
trium can also be visualized, which is typically seen in the late proliferative phase
of the menstrual cycle as opposed to the usual hyperechoic appearance of
Fig. 4.16 US of a corpus luteum and tubal ectopic pregnancy: US of a 30 y/o pregnant patient
with quantitative β-hCG of 266 with cramping and vaginal bleeding. (a) Gray scale image of the
right ovary demonstrates a thick-walled cystic structure with hypoechoic wall (arrows) compatible
with typical appearance of a corpus luteum. (b) Color Doppler demonstrates pronounced periph-
eral flow producing a so-called “ring of fire” pattern. (c) Gray scale image of the right adnexa
demonstrates an echogenic thick walled cystic structure compatible with “tubal ring sign” (arrows)
in the right adnexa adjacent to and separate from the right ovary. Contrast the echogenic wall of the
tubal ectopic with the hypoechoic wall of the corpus luteum (arrowheads). (d) Color Doppler
demonstrates significant peripheral vascularity in a “ring of fire” pattern
pregnancy. Decidual cysts or small, thin-walled cystic foci can also be seen.
However, these can be present in both normal and ectopic pregnancies [80].
ess Frequent Sites of Ectopic Pregnancy

L
Less common sites of ectopic pregnancy account for <5% of ectopic pregnancies
but can have very strong clinical implications, with increased maternal morbidity
and mortality [80].
I nterstitial Ectopic Pregnancy

Interstitial ectopic pregnancies, estimated at 2–4% of ectopic pregnancies, occur in
the interstitial or intramyometrial portion of the fallopian tube. Due to the proximity
Fig. 4.17 US of living right adnexal ectopic pregnancy: 33 y/o pregnant patient presented at
9 weeks’ for a routine dating ultrasound. (a) Gray scale transverse image through the superior
uterus and right adnexa demonstrate an extrauterine right adnexal pregnancy (arrows) with embryo
(arrowhead). Embyronic heart beat was present (not shown). (b) Gray scale image of Morrison’s
pouch in the RUQ demonstrates free fluid (arrows) compatible with large volume hemoperito-
neum. 1500 ml hemoperitoneum was noted at time of surgery
of the implantation site to prominent vasculature, massive hemorrhage can occur

with interstitial ectopic rupture leading to increased maternal mortality of up to 15
times that of tubal ectopics [84]. The term cornual ectopic pregnancy has been used
interchangeably to describe this entity. However, cornual pregnancy more accu-
rately describes pregnancy occurring in the horn of a bicornuate or unicornuate
uterus. These gestations are located in the endometrial cavity, albeit in an ectopic
location.
Ultrasound findings in interstitial ectopic pregnancy include a far high and lateral
location of the GS within the uterine fundus surrounded by a thin rim of myome-
trium measuring <5 mm [79, 84] (Fig. 4.18). An “interstitial line sign” refers to
visualization a thin echogenic line extending from the lateral endometrial cavity
through the myometrium to the GS, which represents visualization of the interstitial
portion of the fallopian tube. Bulging of the outer lateral fundal uterine contour can
also be seen [84].
ervical Ectopic Pregnancy

C
Cervical ectopic pregnancies account for less than 1% of ectopics. They are defined
by implantation within the cervix below the internal OS. Gray scale ultrasound find-
ings include a GS with or without embryo within the cervix. Doppler interrogation
often demonstrates peritrophoblastic blood flow, but flow can be variable. Related
to the expansion and enlargement of the cervix, the uterus may take on an hourglass
or figure-of-eight configuration [66]. The main differential diagnosis is a spontane-
ous abortion in progress, in which case a sac can also be seen in the endocervical
canal. However, the sac is often more irregular in a spontaneous abortion compared
with the rounded sac of a cervical ectopic and peripheral flow is usually absent due
Fig. 4.18 US of interstitial ectopic pregnancy: US of a 38 y/o pregnant patient with lower pelvic
pain and spotting with β-hCG of 16,060. (a) Gray scale image of the left superior uterus demon-
strates a very high and laterally located sac-like structure with thick echogenic rim (arrow). Only
a thin rim of surrounding myometrium surrounds the sac measuring 3 mm (arrowheads). (b)
Image with Color Doppler demonstrates marked peripheral vascularity compatible with peritro-
phoblastic flow. (c) Additional transverse image through the superior uterus demonstrates the
endometrium (asterisk) separate from the gestational sac (arrow) which contains a yolk sac
(arrowhead). Embryo with heartbeat was also present (not shown). Interstitial ectopic pregnancy
was confirmed at surgery. Resection of the ectopic and cornu of the uterus was performed
to detachment from the site of implantation [84]. Another potentially helpful distin-
guishing feature is the mobility of an abortion in progress which can occasionally
be elicited with gentle pressure applied with the TV probe, distinguishing it from
the nonmobile, fixed cervical ectopic. An open cervix with blood products in the
endometrial cavity can also be seen with miscarriage [84]. If the diagnosis is unclear
and the patient is hemodynamically stable, a short-term follow-up US in 2–3 days
can help to differentiate the two entities. An abortion in progress would be expected
to change position, though a cervical ectopic will remain fixed and demonstrate
growth. Recognition of a cervical ectopic pregnancy and alerting the referring phy-
sician to the diagnosis are critical due to the increased risk of massive hemorrhage
with dilatation and curettage [79, 84].
aesarian Scar Ectopic Pregnancy

C
Caesarian-section (C-section) scar ectopics account for <1% of ectopics and are
defined as implantation of the embryo into the scar of a prior C-section [66]. US
shows a GS embedded in the anterior lower uterine segment myometrium at the site
of the scar, which is best visualized on longitudinal views through the uterus. An
echogenic rim and peritrophoblastic vascularity can also be observed. Scar ectopic
pregnancies pose a high risk for uterine rupture and massive hemorrhage. Thus,
detection is critical [66].
varian Ectopic Pregnancy

O
Ovarian ectopic pregnancies are extremely rare. Ultrasound findings include an
echogenic, thick walled cystic structure with or without internal YS or embryo
inseparable from ovarian parenchyma [62]. A “ring of fire” pattern of vascularity is
commonly seen. However, distinguishing an intraovarian ectopic pregnancy from a
corpus luteum (which also characteristically demonstrates a “ring of fire”) can be
challenging. In general, the wall of a corpus luteum is typically lower echogenicity
than that of an ectopic. In addition, the vast majority of thick-walled cysts with
peripheral flow will be corpus lutea because intraovarian ectopic pregnancies are so
uncommon. If the diagnosis is unclear and the patient is clinically stable, short-term
follow-up US and repeat β-hCG levels are advised [84].
bdominal Ectopic Pregnancy

A
Abdominal ectopic pregnancies are exceedingly rare. On ultrasound, the pregnancy
is visualized separate from the uterus and not associated with the ovaries or adnexa.
Abdominal ectopics most commonly implant in the broad ligament. However,
implantation may occur anywhere along the peritoneal surface or abdominal viscera
[62]. MRI can provide useful management implications by identifying sites of pla-
cental implantation [85].
Heterotopic Pregnancy
Heterotopic pregnancy is defined by the coexistence of an IUP and ectopic preg-
nancy and is exceedingly rare in unassisted, spontaneous conceptions (estimated
between 1:21,000 and 30,000) [84, 85]. However, the incidence is much higher
(1–3%) in the setting of ART [61, 66, 84, 85]. When an IUP is documented by ultra-
sound, a thorough evaluation of the adnexa and entire pelvis must be conducted to
avoid a “satisfaction of search” and exclude this life-threatening entity. Particularly
if hemoperitoneum is visualized in the setting of an IUP, a careful search for a con-
comitant ectopic pregnancy should be performed (Fig. 4.19).
ole of MRI in the Diagnosis of Ectopic Pregnancy

R
Although most ectopic pregnancies are diagnosed by ultrasound, MRI can be a use-
ful adjunct in certain situations and has the potential to diagnose clinically unsus-
pected ectopic pregnancies with the increased utilization of MRI in the evaluation
of abdominal pain in the pregnant patient. MRI is particularly useful for further
characterization of the uncommon types of ectopic pregnancy previously discussed,
Fig. 4.19 US and CT in heterotopic pregnancy: (a) Gray scale image of a 34 y/o pregnant patient
with mild low back pain and abdominal pain demonstrates an early IUP with gestational sac and
yolk sac (arrow) at 6 weeks’ (embryo with heartbeat was also present, not shown). No free fluid
was seen, and bilateral ovaries were normal in appearance (not shown). The patient returned the
following day with severe pain, syncope, and hypotension. (b) Axial contrast-enhanced CT through
the upper abdomen demonstrates complex-free fluid compatible with hemoperitoneum (asterisks).
(c) Axial CT through the pelvis demonstrates an ill-defined focus of hyperattenuation in the right
adnexa suggestive of active bleeding (arrow) and areas of intermediate attenuation clotted blood
(asterisks). Ruptured right tubal ectopic pregnancy with active bleeding was found at surgery. The
patient went on to deliver the intrauterine pregnancy at 40 weeks
such as interstitial, scar, cervical, ovarian, and intraabdominal, due to the larger field
of view and high soft tissue contrast with this modality. A key feature will be the
absence of an IUP in the vast majority of cases, keeping in mind the rare heterotopic
pregnancy will be an exception.
As in ultrasound, hemoperitoneum raises suspicion for ectopic pregnancy in the
absence of a documented IUP and is most often visualized on MRI as iso- to
hyperintense-free fluid on T1-weighted images. The T2 signal of the fluid is often
variable or heterogeneous [85]. Tubal ectopic pregnancy on MRI may manifest as a
thick-walled, cystic structure with increased signal on T2-weighted images and
variable amounts of acute hemorrhage, depicted on MRI as intermediate or
hyperintense signal on T1-weighted images. At times, a heterogeneous predomi-

nantly high T2 signal mass-like adnexal structure will be seen without a discrete
GS. Hematosalpinx, visualized as a dilated tubular structure with high signal inten-
sity fluid on T1-weighted images, is highly concerning for ectopic pregnancy in the
absence of an IUP, even when a discrete adnexal mass is not visualized [85].
On MRI, interstitial ectopic pregnancies appear as heterogeneous, predomi-
nantly high T2 signal masses in the lateral uterine fundus which are contiguous with
the myometrium. A location lateral to an intact junctional zone can help distinguish
these from eccentrically positioned IUPs [85]. In the setting of scar ectopics, MRI
can be useful to evaluate for adjacent organ invasion (i.e., urinary bladder). As men-
tioned previously, MRI can help delineate placental implantation sites in the setting
of an abdominal pregnancy [85].
Placental Abruption
Placental abruption is a rare complication of pregnancy, occurring in less than 1%

of all pregnancies but associated with significantly increased fetal mortality and
increased risk of preterm labor [86, 87]. Classically, patients present with vaginal
bleeding and abdominal pain. Sonography is the initial modality of choice to evalu-
ate for this diagnosis, although sensitivity for its detection is low with US, with a
reported sensitivity of only 25% [86]. The detection of hemorrhage deep to the
placenta or deep to the chorion suggests the diagnosis of placental abruption on
ultrasound (Fig. 4.20). Hemorrhagic collections can have a variable sonographic
appearance depending on acuity, ranging from iso- to hyperechoic in acute to sub-
acute hematomas to hypoechoic in subacute to chronic hematomas [61]. In the acute
setting, abruption commonly manifests as an apparently thickened placenta, with
the hemorrhage deep to the placenta isoechoic to and difficult to delineate from the
placenta (Fig. 4.21). Comparison with the appearance of the placenta on previous
ultrasounds can help confirm this finding as a true abnormality. Cases not detectable
by US are felt likely due to hemorrhage from the placental separation passing
through the cervix and not forming a discrete hematoma deep to the chorion or
placenta [61, 86]. When present, sonographic findings of placental abruption have a
high positive predictive value and portend a worse clinical prognosis [61, 86]. MRI
can be used as a problem-solving tool, yet should not delay clinical management.
On MRI, hematoma will demonstrate increased signal on T1-weighted images com-
pared with the lower signal intensity placenta [61].
Uterine Rupture
Uterine rupture is a rare, life-threatening complication of pregnancy associated with

high fetal and maternal morbidity and is considered a true surgical emergency. The
diagnosis is often suspected clinically, and thus, imaging is not routinely performed.
Risk factors for uterine rupture include previous uterine surgery (including cesarean
Fig. 4.20 US of marginal placental abruption: US of a 35 y/o pregnant patient at 34 weeks’ with
irregular contractions and decreased fetal movement. (a, b) Transverse gray scale images through
uterus demonstrate a large, heterogenous mixed isoechoic and hypoechoic collection with small
retroplacental component (arrows) and larger subchorionic component (asterisks) without internal
flow with Doppler (c) compatible with placental abruption. Patient underwent emergent C-section
with delivery of a viable neonate
section or myomectomy), trauma, abnormal placentation (placenta percreta), and

ectopic pregnancy (particularly interstitial and scar ectopics) [61, 84, 88]. Complete
uterine rupture involves disruption of all layers of the uterus surrounding the fetus
with incomplete rupture only involving the myometrium [89]. Rupture can occur dur-
ing or shortly after delivery, or well before delivery in the setting of ectopic pregnan-
cies [61, 90]. Imaging will demonstrate disruption of the uterine wall with possible
herniation of the GS contents and fetus beyond the uterus. Hemoperitoneum is usually
present. Contrast-enhanced CT will show a full thickness defect within the uterine
wall, which is typically low density compared with adjacent normally enhancing
myometrium [23, 88]. Hemoperitoneum will invariably be present as intermediate to
high density-free fluid, and one should carefully search for active extravasation. In
severe cases, the fetus will be seen extruding into the abdomen [23].
Fig. 4.21 US of retroplacental placental abruption: US of a 40 y/o pregnant patient at 38 weeks’

with decreased fetal movement. (a) Gray scale image of the uterine fundus demonstrates an appar-
ent markedly thickened placenta (asterisk) and IUP (arrowhead). (b) Image with color Doppler
demonstrates no internal flow. (c) This represented a significant change from previous US of the
placenta (asterisk) performed 2 weeks prior. Findings are compatible with massive retroplacental
abruption with the hemorrhage isoechoic to and unable to be delineated from the placenta.
Intrauterine fetal demise was noted at the time of the scan (not shown). 800 ml of blood clot was
noted at delivery
Conclusion
Imaging the pregnant patient with acute abdominal and pelvic complaints presents
a unique challenge to the clinician and radiologist. Patients should be adequately
informed about the imaging procedures proposed for their care, particularly the
risks of radiation exposure, contrast administration, as well as the potential benefits
of the information obtained. Accurate and timely imaging is requisite as clinical and
laboratory examinations may be nonspecific or misleading. Imaging serves a vital
role in directing treatment algorithms, avoiding underdiagnoses, diagnostic delay,
or unnecessary interventions. When possible, imaging algorithms should be directed
toward the use of imaging modalities that avoid ionizing radiation, reserving CT for
specific clinical scenarios. As in all instances of medical imaging including ionizing

and nonionizing procedures, the principle standard of “as low as reasonably achiev-
able (ALARA)” should be routinely applied.
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Laboratory Studies
5
Kamani M. Lankachandra
The acute abdomen in pregnancy is a diagnostic challenge due to the presences of

the gravid uterus obscuring meaningful clinical evaluation and changes in most of
the laboratory parameters during pregnancy. For example, leukocytosis is a normal
occurrence in pregnancy, and C-reactive protein values are already elevated through-
out all semesters. Many clotting factors including fibrinogen, factors VII, VIII, IX,
and XII continue to rise throughout the pregnancy and reach their peak at term [1].
One should not rely heavily on laboratory testing to make a diagnosis of an acute
abdomen. However, with an adequate knowledge of the physiological and biochem-
ical variations that occur during pregnancy, the clinician can use these studies to aid
and/or confirm already established diagnoses or help narrow down a differential
diagnosis. A list of commonly used laboratory tests and their variations during preg-
nancy are listed at the end of this chapter.
The acute abdomen in pregnancy may result in etiologies that are pregnancy
related and/or unrelated. Diagnosis of some of the conditions may not require labo-
ratory studies. The following are the important etiological considerations for an
acute abdomen in pregnancy and laboratory tests that help confirm the diagnoses.
Pregnancy-Related Conditions
• Extrauterine pregnancy including simultaneous intrauterine and tubal/abdominal

pregnancy
• Premature separation of placenta (Placental Abruption)
• Chorioamnionitis
• HELLP syndrome
K.M. Lankachandra, MD, FACP (*)

Department of Pathology, University of Missouri School of Medicine,

in Pregnancy, DOI 10.1007/978-3-319-62283-5_5
100 K.M. Lankachandra
Causes Unrelated to Pregnancy
• Appendicitis
• Cholecystitis
• Bowel obstruction
• Acute Pancreatitis
• Nephrolithiasis
he Following Nonabdominal Conditions May Present

T
as Acute Abdomen
• Myocardial infarction
• Pulmonary embolism
• Pneumonia
• Sickle cell crisis
• Porphyria
Useful Laboratory Tests for Pregnancy-Related Conditions
Extrauterine Pregnancy
A positive urine pregnancy test without evidence of intrauterine pregnancy should

immediately raise the suspicion of extrauterine gestation.
Premature Separation of Placenta Causing Abruption
Disseminated intravascular coagulation (DIC) and massive hemorrhage are the

most serious complications of abruption.
Helpful Laboratory Tests

• Complete blood count with platelet count
• D-dimer assay
• prothrombin time (PT)
• partial thromboplastin time (PTT)
• Fibrinogen levels
Thrombocytopenia, prolonged PT and PTT, elevated D-dimer levels, and low

fibrinogen levels support the diagnosis of disseminated intravascular coagulation.
Of these, the D-dimer assay is the most sensitive laboratory test (95% sensitivity).
A scoring system has been developed by the International Society of Thrombosis
and Hemostasis for the diagnosis of DIC [2].
5 Laboratory Studies 101
Chorioamnionitis
Chorioamnionitis can present as an acute abdomen and when severe, carries a sig-
nificant maternal and neonatal risk of morbidity. The following laboratory tests are
useful in establishing the diagnosis.
• CBC: Elevated white cell count with bandemia is often seen in

chorioamnionitis.
• Amniotic fluid: Amniotic fluid culture has a limited use in the diagnosis of acute
chorioamnionitis due to the long turnaround time (usually 2–3 days). Amniotic
fluid culture will isolate the causative pathogen; however, clinical usefulness of
this exercise is limited [3].
• Placental histology: Histological examination of the placenta can detect clinical
as well as subclinical chorioamnionitis. However, one should not wait for pla-
cental histology to diagnose acute chorioamnionitis. This should only be the con-
firmatory finding of the clinical diagnosis after the fetus is delivered.
ELLP Syndrome (Hemolysis, Elevated Liver Enzymes and low

H
Platelet Count)
The three most important laboratory diagnostic criteria are as follows:
• Elevated liver enzymes: Marked elevation of serum transaminase levels up to

4000 U/L has been reported, but moderate elevation is common.
• Evidence of hemolysis: Low hemoglobin, the presence of schistocytes, frag-
mented red cells, and nucleated red cells in the peripheral smear are strong evi-
dence of hemolysis.
• Low platelet count: Any pregnant women with a significant drop in the platelet
count during the antenatal period should be suspected as having a potential risk
of developing HELLP syndrome.
Based on the platelet count, HELLP syndrome can be divided into three
subclasses.
• Class I – Platelet count >50,000 per mm3

• Class II – Platelet count 50,000–100,000 per mm3
• Class III – Platelet count 100,000–150,000 per mm3
Women with the diagnosis of Class I HELLP carry a higher morbidity and
mortality.
Coagulation tests are normal in patients with HELLP syndrome unless compli-
cated by disseminated intravascular coagulation (DIC). Low fibrinogen (less than
300 mg/dL) is a strong indicator that the patient also has DIC.
ommon Conditions Unrelated to Pregnancy that Can Present

C
as Acute Abdomen
Appendicitis
This is the most common cause for nonobstetrical surgical intervention in preg-
nancy [1, 4]. The laboratory test that can support the diagnosis is leukocytosis with
bandemia. Note that leukocytosis is common in normal pregnancy, and acute appen-
dicitis may not always show leukocytosis. However, in the proper clinical setting,
leukocytosis with bandemia favors acute appendicitis. The serum procalcitonin
level is not a useful test for uncomplicated appendicitis, but elevated procalcitonin
levels are of diagnostic use in appendiceal perforation with abscess formation and/
or peritonitis.
Small Bowel Obstruction
Small bowel obstruction can produce symptoms that are nonspecific such as nausea
and vomiting; symptoms that are commonly associated with pregnancy. Delay in
diagnosis can be devastating to the fetus and the mother.
Blood gas analysis will yield abnormal results including base excess and ele-
vated serum lactate levels. However, the specificity of these tests is low [5].
Furthermore, blood gas analysis may be normal in the early stages of intestinal
obstruction [2, 6].
Cholecystitis
Laboratory tests are not commonly used in the diagnosis of acute cholecystitis
although an elevated white blood cell count with bandemia is often present. Elevated
liver enzyme levels and direct bilirubin levels have been observed in acute cholecys-
titis. The clinical challenge is to rule out HELLP syndrome in this setting.
Acute Pancreatitis
Elevations of pancreatic amylase and lipase are the most important laboratory find-
ings that help make the correct diagnosis of acute pancreatitis. Moderate elevation
of the white blood cell count is also commonly observed in acute pancreatitis.
Elevation of the serum procalcitonin level is useful in the diagnosis of pancreatitis
and peritonitis. This disease is very serious, in general, and particularly in gravid
women.
Nephrolithiasis
Urinalysis may reveal red blood cells (75–95%), but this is not diagnostic of renal
calculi. If there is a clinical suspicion of urinary tract infection, urine culture should
be performed. There are other studies that will support this diagnosis in pregnancy,
such as a variety of imaging options.
Myocardial Infarction
Serial cardiac troponin tests should be performed in suspected myocardial infarc-

tion. It is important to be familiarized with the laboratory method of the clinician’s
institution, and the reference ranges for accurate interpretation of troponin levels.
Consultation with the cardiology team is helpful for their expert opinion in difficult
and ambiguous cases.
Sickle Cell Crisis
Although rare, sickle cell crisis, particularly in a patient with undiagnosed sickle
cell disease, may present with acute abdominal symptoms. The sickling test, CBC,
and hemoglobin electrophoresis assist the clinician at arriving at the correct
diagnosis.
Porphyria
Acute intermittent porphyria, the most common inherited form of porphyria should
be considered in the differential diagnosis of the acute abdomen. Patient may pres-
ent with acute abdominal symptoms, vomiting, and leukocytosis. The diagnostic
laboratory findings include increased urinary porphobilinogen and acute and tran-
sient elevation of alkaline phosphatase and bilirubin.
omplete Blood Count with Peripheral Smear Recommended

C
for Initial Evaluation of the Gravid Female Presenting
with an Acute Abdomen
Red Blood Cells
Red cell morphology can be useful in the diagnosis and management of diseases
causing microangiopathic hemolytic anemia (MAHA), thrombotic thrombocytope-
nic purpura (TTP) and HELLP syndrome. Many fragmented cells, schistocytes, and
nucleated red cells are present in the peripheral blood as a result of hemolysis.
Table 5.1 Laboratory reference values in pregnancy [7]

Nonpregnant Second Third
adult First trimester trimester trimester
Hematology
Hemoglobin (g/dL) 12–15.8 11.6–13.9 9.7–14.8 9.5–15.0
Hematocrit (%) 35.4–44.4 31.0–41.0 30.0–39.0 28.0–40.0
Mean corpuscular hemoglobin 27–32 30–32 30–33 29–32
(pg/cell)
Mean corpuscular volume (m3) 79–93 81–96 82–97 81–99
Platelets (×10 6/L) 165–415 174–391 155–409 146–429
WBC (×10 3/mm 3) 3.5–9.1 5.7–13.6 5.6–14.8 5.9–16.9
Neutrophils (×10 3/mm 3) 1.4–4.6 3.6–10.1 3.8–12.3 1.0–3.6
Coagulation
PT (sec) 12.7–15.4 9.7–13.5 9.5–13.4 9.6–12.9
PTT (sec) 26.3–39.4 24.3–38.9 24.2–38.1 24.7–35.0
D-dimer (mug/mL) 0.22–0.74 0.05–0.95 0.32–1.29 0.13–1.7
Blood chemical constituents
Alanine transaminase (U/L) 7–41 3–30 2–33 2–25
Aspartate transaminase (U/L) 12–38 3–23 3–33 4–32
Alkaline phosphatase (U/L) 33–96 17–88 25–126 38–229
Amylase (U/L) 20–96 24–83 16–73 15–81
Lipase (U/L) 3–43 21–76 26–100 41–112
LDH (U/L) 115–221 78–433 80–447 82–524
Bilirubin total (mg/dL) 0.3–1.3 0.1–0.4 0.1–0.8 0.1–1.1
Bilirubin unconjugated (mg/ 0.2–0.9 0.1–0.5 0.1–0.4 0.1–0.5
dL)
Bilirubin conjugated (mg/dL) 0.1–0.4 0–0.1 0–0.1 0–0.1
C-reactive protein (mg/dL) 0.2–3.0 Not reported 0.4–20.3 0.4–8.1
Data from: Abbassi-Ghanavati et al. [7]
WBC
Increased white cell count with neutrophilia is seen in infections including appendi-
citis, cholecystitis, and urinary tract infections and pyelonephritis. A Neutrophil
series often shows a left shift with band forms in the peripheral blood. Note that a
normal white blood cell count does not exclude any of the aforementioned condi-
tions. Clinical history, positive physical examination signs, and radiographic evi-
dence should lead to the correct diagnosis rather than relying on laboratory results.
More severe life-threatening conditions including sepsis, peritonitis, and acute pan-
creatitis can present with high white count and neutrophilia.
Platelet Count
Low platelet counts are often associated with severe sepsis leading in to dissemi-
nated intravascular coagulation as well as a feature of TTP andHELLP syndrome.
References
1. KilpatricK CC, Monga M. Approach to the acute abdomen in pregnancy. Obstet Gynecol Clin
N Am. 2007;34:389.
2. Wang L, Matsunaga S, Mikami Y, Takai Y, Terui K, Seki H. Pre-delivery fibrinogen predicts
adverse maternal or neonatal outcomes in patients with placental abruption. J Obstet Gynaecol
Res. 2016;42(7):796–802.
3. Tita AT, Andrews W. Diagnosis and management of clinical corioamnionitis. Clin Perinatol.
2010;37(2):339–54.
4. Mourad J, Elliot JP, Erickson L, Lisboa L. Appendicitis in pregnancy: new information that
contradicts long-held clinical beliefs. Am J Obstet Gynecol. 2000;182(5):1027–9.
5. Mayumi T, Yoshida M, et al. Practice guidelines for primary care of acute abdomen 2015.
J Hepatobiliary Pancreat Sci. 2016;23:3–36.
6. Van Den Heijkant TC, Aerts B, Teijink JA, Buurman WA, Luver M. Challenges in diagnosing
mesenteric ischemia. World J Gastroenterol. 2013;19(9):1338–41.
7. Abbassi-Ghanavati M, Greer LG, Cunningham FG. Pregnancy and laboratory studies: a refer-
ence table for clinicians. Obstet Gynecol. 2009;114(6):1326–31.
Suggested Reading
8. Bilir F, Akdemir N, Ozden S, Cevrioglu AS, Bilir C. Increase serum procalcitonin levels in
pregnant patients with asymptomatic bacteriuria. Ann Clin Microbiol Antimicrob. 2013;12:25.
9. Cartwright SL, Knudson MP. Evaluation of acute abdominal pain in adults. Am Fam Physician.
2008;77(7):971–8.
10. HELLP syndrome. BMJ Best Practice. Jun 02 2016. Accessed online: bestpractice.bmj.com/
best-practice/monograph/1000/treatment/step-by-step.html.
11. Kobayashi T. Obstetrical disseminated intravascular coagulation score. J Obstet Gynaecol Res.
2014;40(6):1500–6.
12. Masselli G, Derchi L, McHugo J, Rockall A, Vock P, Weston M, Spencer J. Acute abdominal
and pelvic pain in pregnancy: ESUR recommendations. Eur Roadiol. 2013;23:3485–500.
Obstetrical Etiologies of Abdominal Pain
6
First-Trimester Spontaneous Abortion
Spontaneous pregnancy loss in the first 12 weeks of gestation is ubiquitous. The

spontaneous or induced termination of pregnancy before fetal viability is the defini-
tion of abortion. The term miscarriage and abortion are used interchangeably. Many
individuals prefer miscarriage for spontaneous fetal loss. The widespread use of
sonography and human chorionic gonadotropin (hCG) measurements that identify
extremely early pregnancies has resulted in new terminologies that include early
pregnancy loss, wastage, or failure.
Abortion that occurs naturally is of clinical importance since spontaneous abor-
tion can produce abdominal and pelvic pain, thus presenting a challenge to the clini-
cian who is evaluating a pregnant woman who presents with pain.
Spontaneous abortion includes subclassifications such as threatened, inevitable,
incomplete, complete, and missed abortion. When any of these variations in preg-
nancy loss result in infection, then the term septic abortion is applicable.
Spontaneous abortions occurring within the first 12 weeks of gestation account
for >80% of pregnancy losses. It appears that embryonic or fetal death almost
always precedes the spontaneous expulsion of the products of conception.
Hemorrhage into the decidua basalis occurs as a result of this death. The adjacent
tissue necrosis stimulates uterine contractions and expulsion of the products of con-
ception. Inspection of the gestational sac demonstrates that it is fluid-filled and may
or may not contain an embryo or fetus [1] (Fig. 6.1).

e-mail: [email protected]; [email protected]

in Pregnancy, DOI 10.1007/978-3-319-62283-5_6
108 P.B. Greenspan
Threatened abortion Inevitable abortion
Expelled products of
complete abortion
Incomplete abortion Missed abortion
Fig. 6.1 Spontaneous abortion (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com.
Used with permission)
6 Obstetrical Etiologies of Abdominal Pain 109
Diagnosis
The spontaneous loss of an intrauterine pregnancy (IUP) prior to 20 weeks of gesta-

tion is diagnostic of abortion. This is accompanied by low or falling levels of Human
Chorionic Gonadotropin (hCG), bleeding and/or midline cramping pain, open cer-
vical os, and the complete or partial expulsion of the products of conception.
Nearly 20% of clinically diagnosed pregnancies terminate in spontaneous
abortion.
Greater than 60% of spontaneous abortions result from chromosomal defects.
Another 15% of losses are associated with maternal trauma, infection, dietary
deficiency, diabetes mellitus, hypothyroidism, the lupus anticoagulant-
anticardiolipin-antiphospholipid antibody syndrome, and anatomic malformations.
Evidence suggests that psychic stimuli such as severe fright, grief, anger, or anxi-
ety can induce pregnancy loss. However, there is no evidence that electromagnetic
fields are associated with an increased risk of abortion.
Women with the diagnosis of incompetent cervix should be distinguished from
more typical early abortion, premature labor, or rupture of the membranes [1, 2].
Symptoms and Signs
Incompetent cervix typically presents as “silent” cervical dilation (without contrac-

tions) between weeks 16 and 28 of gestation. An antecedent history is valuable in
such patients. A “threatened abortion” is any bleeding in the first half of pregnancy.
There may or may not be cramping noted and evaluation with imaging, etc., dem-
onstrates that the pregnancy is intact. There is no cervical dilation noted in cases of
threatened abortion [1] (Fig. 6.2).
Inevitable abortion implies that the process has begun towards eventual preg-
nancy loss. The cervix in this case is dilated and the fetal membranes can have
undergone rupture. There has been no passage of the products of conception but if
visible at the cervical os, then abortion would be inevitable [1].
Complete abortion is defined as the passage of intact products of conception usu-
ally accompanied by the alleviation of cramping and pain, with or without persistent
spotting and bleeding. The patient’s cervical os can already have closed upon visual
inspection [1].
Incomplete abortion describes the passage of partial products of conception
while a portion thus remains in the uterus. The patient can have mild cramps and can
experience bleeding which is persistent and at times presents as hemorrhage.
Missed abortion is a term used to describe a pregnancy that has ceased to develop,
but the products of conception have not been expelled. This diagnosis is usually
made sonographically. The gravida can note brownish vaginal discharge but gener-
ally there is no active bleeding. Often, both the subjective and objective signs and
symptoms of pregnancy disappear, often rather abruptly [1].
The pregnant patient who is experiencing abdominal and pelvic pain in the first
half of pregnancy must be considered for the evaluation of a pregnancy loss.
110 P.B. Greenspan
Bulging membranes
Dilated
cervical
canal
Fetal expulsion Ruptured

membranes
Cervical insufficiency becomes If left untreated, the dilated cervical

manifest in second trimester as canal may result in rupture of
dilation of cervical canal membranes and/or fetal expulsion
Surgical management of cervical insufficiency (cerclage)
Suture
Dilated cervical canal
Cervix
Purse-string (cerclage)
suture prior to tying
Suture tied
Narrowed cervical canal
Suture pulled taut

and tied, narrowing
cervical canal
Nonabsorbable purse-string suture placed

around cervix at level of internal os
Fig. 6.2 (a) Cervical insufficiency. (b) Cerclage for surgical management of cervical insuffi-
ciency (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com. Used with permission)
Other diagnoses that should be closely considered include ectopic pregnancy,

hydatidiform mole, anovulatory bleeding in a nonpregnant women, cervical neo-
plasm, and other uterine pathologies.
The diagnosis of spontaneous abortion is rarely challenging or confusing, espe-
cially when accurate laboratory studies and imaging are readily available.
Simple measurement of the serum hCG will demonstrate declining levels. If
there is considerable blood loss, a complete blood count should be obtained imme-
diately. It is critical to ascertain the Rh type and Rho (D) Ig should be administered
if the maternal blood type is Rh negative. Failure to do so can result in Rh isoim-
munization. Any passed tissue should be assessed by a pathologist, as this can pro-
vide clues to other processes such as choriocarcinoma or hydatidiform mole.
Transvaginal sonography (TVS) can identify a gestational sac 5–6 weeks from the
first day of the last menstrual period, a fetal pole by 6 weeks, and fetal cardiac activ-
ity at 6–7 weeks. A small, irregular sac without a fetal pole is usually diagnostic of
an abnormal pregnancy [1, 2].
Management
Antibiotics should not be routinely administered unless there is evidence of infec-

tion. The use of Misoprostol, 200–800 μg orally or vaginally once, combined with
an antiprogesterone (i.e., mifepristone, 600 mg orally once) has afforded a nonsur-
gical option in the treatment of early pregnancy loss; however, if there is excessive
bleeding, a surgical procedure can be required.
Incomplete or inevitable abortions are treated with prompt removal of any
remaining products of conception to stop bleeding and prevent infection.
Threatened abortion is managed with conservative observation. Whether bed rest
reduces the incidence of pregnancy loss has never been substantiated in any studies
to date. The recommendation of abstinence from coitus and douching is also unsub-
stantiated but seems to make sense.
When the pregnancy loss is inevitable or in cases of missed abortion, medically
induced first-trimester treatment with prostaglandins (i.e., misoprostol given vagi-
nally or orally in a dose of 200–800 μg) combined with an antiprogesterone (i.e.,
mifepristone 600 mg orally) has been shown to be safe, effective, less invasive, and
more private than surgical intervention. However, if this approach is unsuccessful or
if bleeding is excessive, then a surgical procedure (dilation and curettage, suction
curettage) can still be needed [1, 2].
Midtrimester Abortion
Midtrimester fetal loss ranges from 12 weeks until the fetus weighs ≥500 g or ges-
tational age reaches 20 weeks. A gestational age of 22–23 weeks is more accurate.
The etiology of midtrimester pregnancy loss can be more readily explained if a
careful evaluation is undertaken.
112 P.B. Greenspan
Incidence and Etiology
By the end of the first trimester, spontaneous abortion becomes much less common
and continues to decline as the pregnancy progresses. Spontaneous loss in the sec-
ond trimester is estimated at 1.5–3%. After 16 weeks, the incidence is about 1% [3,
4]. Bleeding in the first trimester increases the incidence of second-trimester loss by
a factor of two [5, 6]. Unlike first-trimester abortions that commonly are caused by
chromosomal aneuploidies, midtrimester fetal losses are the result of a multitude of
causes. The accurate estimate of the incidences of these various causes has no sup-
portive data.
Race, ethnicity, prior poor obstetrical outcomes, and extremes of maternal age
are risk factors for second-trimester abortion. There is speculation that first-trimester
bleeding has been cited as a potent risk factor [5]. Edlow et al. found that 27% of
women with such a loss in the index pregnancy had a recurrent second-trimester
loss in their next pregnancy. Furthermore, one-third of these women had a subse-
quent preterm birth [7].
The clinical presentation of second-trimester abortion is much like first-trimester
loss. The gravida can present with pain and cramping in the lower abdomen, in the
midline. Multigravid women who have experienced labor may report that their
symptoms are very similar to labor contractions. Membrane rupture and/or vaginal
bleeding are significant, ominous signs. When evaluated for their symptoms, cervi-
cal dilatation can be advanced and delivery of a nonviable fetus can be inevitable.
Other diagnoses need consideration if the patient is having pain, but does not
seem to be contracting or is not bleeding. The differential diagnosis should include
torsion of an adnexa, degeneration of uterine leiomyomata, urinary tract infection or
calculi, and any number of gastrointestinal disorders including bowel obstruction.
Concealed placental abruption should also be considered.
Ectopic Pregnancy
Normally, the blastocyst implants in the endometrial lining of the uterine cavity fol-
lowing fertilization and fallopian tube transit. Implantation anywhere other than that
is considered an ectopic location. Ectopic pregnancies comprise 1–2% of all first-
trimester pregnancies in the United States. Nonetheless, this disproportionally
accounts for 6% of all pregnancy-related deaths [8, 9]. Furthermore, subsequent
successful pregnancy likelihood is reduced after an ectopic pregnancy.
Urine and serum human chorionic gonadotropin (hCG) assays and transvaginal
sonography have facilitated early diagnosis and treatment. Consequently, maternal
survival and conservation of reproductive capability has improved (Fig. 6.3).
Approximately 95% of ectopic pregnancies occur in the fallopian tube giving
rise to fimbrial, ampullary, isthmic, or interstitial tubal pregnancies [10, 11]. The
ampulla is the most frequent site, followed by the isthmus. Five percent of non-
fallopian tube ectopic pregnancies implant in the ovary, peritoneal cavity, cervix, or
prior cesarean scar. Rarely, a twin pregnancy occurs with one conceptus in the
Diagnosis of Ectopic Pregnancy

Isthmic
Ovarian
Interstitial
Ampullary
Cervical
Abdominal
Ectopic implantation sites
Sonogram of empty uterine cavity
Laparoscopy may be used to confirm

diagnosis of ectopic pregnancy Sonogram of gestational sac
Pregnancy monitoring with serial sonograms and b-HCG determinations
Absence of sac Sac without Sac with Fetus and heart

fetal pole fetal pole movement
Intrauterine gestational
sac is rarely visualized
on sonogram before
25 days after LMP.
Normal sac should be
visible if b -HGC level
is 6,000 mlU/ml
100,000
50,000
b-HCG (mlU/ml)
25,000
10,000
5,000
2,500
1,000
500
250
100
1 2 3 4 5 6 7 8
Weeks since last menstrual period (LMP)
Fig. 6.3 Ectopic pregnancy (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com.
114 P.B. Greenspan
uterus and the other one implanted ectopically. This “heterotopic” pregnancy rate is
approximately 1 per 30,000 pregnancies. Conversely, the development of assisted
reproductive technologies (ARTs) has increased their incidence to 1 in 7000 overall,
and following ovulation induction, it can be as high as 0.5–1% [12]. Twin tubal
pregnancy with both embryos in the same tube or with one in each tube has been
reported [13, 14]. The admiration of immunoglobulin G (IgG) anti-D immunoglob-
ulin should be given to D-negative (Rh negative) women with ectopic pregnancies
(Fig. 6.4).
Risks
The underlying cause of many tubal ectopic pregnancies is abnormal fallopian tube
anatomy. Previous surgeries for prior tubal pregnancy, fertility restoration, or for
sterilization render the highest risk of tubal implantation. After one previous ectopic
pregnancy, the chance of another approximates 10% [15, 16]. History of sexually
transmitted disease or other tubal infection, which can alter normal tubal anatomy,
is a common risk factor. One episode of salpingitis can result in a subsequent ecto-
pic pregnancy in up to 9% of women [17]. Peritubal adhesions consequent of salpin-
gitis, appendicitis, or endometriosis can further increase the risk of tubal pregnancy.
Salpingitis isthmica nodosa, a condition in which epithelium-lined diverticula pro-
trude into a hypertrophied muscularis layer of the uterus, additionally poses an
increased risk [18]. Congenital fallopian tube anomalies, especially those secondary
to in utero diethylstilbestrol exposure (extremely rare today), can result in anoma-
lous tubes and higher ectopic rates [19].
A number of ectopic pregnancies spontaneously fail and are therefore spontane-
ously reabsorbed. Sensitive hCG assays permit this to be documented more regu-
larly (Fig. 6.5).
Clinical Manifestations
In modern practice, ectopic pregnancies rarely rupture. This is due to earlier patient
presentation and more precise diagnostic technology. Early on, symptoms and signs
of ectopic pregnancy are typically subtle or even absent. The gravida has no suspi-
cion of tubal pregnancy and assumes that she has a normal early pregnancy or is
experiencing a miscarriage.
A “classic” presentation is typified by the triad of delayed menstruation, pain,
and vaginal bleeding or spotting. When rupture ensues, there is usually severe lower
abdominal and pelvic pain that is commonly described as sharp, stabbing, or tear-
ing. Tenderness is elicited during abdominal palpation. Bimanual pelvic examina-
tion causes exquisite pain. Cervical motion tenderness is often present. The posterior
vaginal fornix can bulge from blood in the rectouterine cul-de-sac, or a tender,
boggy mass can be felt to one side of the uterus. The uterus can be displaced to one
side by an ectopic mass. The uterus can also be somewhat enlarged due to hormonal
Sites of ectopic implantation

Interstitial Tubal (isthmic) Abdominal
Tubal (ampullar)
Infundibular (ostial)
Ovarian
Cervical
Unruptured tubal pregnancy
Section through tubal pregnancy

Chorion
Villi invading tubular wall
Fetus Amnion
Amnion Hemorrhage
Chorion in tubal wall
Lumen of tube
Ultrasonographic view of adnexa
116 P.B. Greenspan
Interstitial pregnancy
Uterus
Uterine tube
Abdominal pregnancy
Placenta on the body wall,

liver, stomach, and intestines
Ovarian pregnancy
Pubic symphysis
Urinary bladder
Uterus Vagina Rectum
stimulation. Shoulder or neck pain, a result of diaphragmatic irritation, is observed

in about half of patients with significant hemoperitoneum.
Vaginal spotting or bleeding is reported by 60–80% of women with tubal preg-
nancy. Occasionally, there is profuse vaginal bleeding which is suggestive of an incom-
plete abortion. Furthermore, ectopic pregnancy can lead to profound intraabdominal
hemorrhage. Moderate bleeding can induce no change in vital signs, a slight rise in
blood pressure, or a vasovagal response with bradycardia and hypotension. Birkhahn
and colleagues observed that in 25 gravidas with ruptured ectopic pregnancy, the
majority at presentation had a heart rate <100 beats per minute and a systolic blood
pressure >100 mm Hg [20]. Blood pressure will fall and pulse will rise only if bleeding
persists and hypovolemia becomes significant. Vertigo or syncope can develop.
Hemoglobin or hematocrit readings can at first show only a slight reduction even
with significant hemoperitoneum. Therefore, following an acute hemorrhage, a
decrease in hemoglobin or hematocrit level over several hours is a more valuable
index of blood loss than is the initial level. In roughly half of women with a ruptured
ectopic pregnancy, a leukocytosis of up to 30,000/μL can be found.
Endometrium that is hormonally prepared for pregnancy is called decidua, and the
degree to which the endometrium is converted with ectopic pregnancy is variable.
Consequently, along with bleeding, women with ectopic tubal pregnancy can pass a
decidual cast. This is the sloughed endometrium that takes the form of the endometrial
cavity (Fig. 6.6). Significantly, decidual sloughing can occur with uterine abortion.
This tissue should be evaluated and then submitted to pathology for evidence of a con-
ceptus. If there is no clear gestational sac or if no chorionic villi are identified histologi-
cally, then consideration of ectopic pregnancy must be entertained by the clinician.
Fig. 6.6 Decidual cast (© McGraw-Hill Inc. All rights reserved. Williams’ Textbook of Obstetrics,
24th ed. Used with permission)
118 P.B. Greenspan
Abdominal pain in the pregnant patient creates an extensive differential diagno-

sis. Uterine conditions such as miscarriage, infection, degenerating or enlarging
leiomyomata, molar pregnancy, or round-ligament pain are all under consideration.
Adnexal pathology includes ectopic pregnancy; hemorrhagic, ruptured, or torsioned
ovarian masses; salpingitis; or tuboovarian abscess. Furthermore, appendicitis, cys-
titis, renal stone, or gastroenteritis are nongynecologic sources of lower abdominal
pain in early pregnancy.
Several algorithms have been proposed to diagnose ectopic pregnancy. The
majority includes these crucial components: physical findings, transvaginal sonog-
raphy (TVS), and serum hCG level measurement (the initial and the consequent
pattern of rise or decline) and diagnostic surgery. Surgical options include uterine
curettage, laparoscopy, and, occasionally, laparotomy. Women with presumed or
obvious rupture should undergo urgent surgical intervention. When evaluating a
suspected unruptured ectopic pregnancy, care must be taken to avoid the interrup-
tion of a normal pregnancy. However, strategies that reduce the potential for normal
pregnancy interruption can postpone the diagnosis of an ectopic pregnancy.
Beta Human Chorionic Gonadotropin
The diagnosis of ectopic gestation requires a rapid and accurate determination of

pregnancy. Available serum and urine pregnancy tests utilizing enzyme-linked
immunosorbent assays (ELISAs) for hCG are sensitive to levels of 10–20 mIU/mL
and are positive in >99% of ectopic pregnancies [21]. Ectopic pregnancies with
negative hCG levels are rare.
Patients who present with bleeding or pain as well as a positive pregnancy test
result should undergo initial transvaginal sonography (TVS) to identify the location
of the gestation. Diagnosis is ascertained if a yolk sac, embryo, or fetus is identified
within the uterus or the adnexa. However, often a TVS is nondiagnostic, and tubal
pregnancy remains possible. When neither intrauterine nor extrauterine pregnancy
is identified, the term “pregnancy of unknown location” (PUL) is applied until addi-
tional clinical findings allow determination of pregnancy location.
evels Above the Discriminatory Zone

L
Several investigators have elucidated discriminatory hCG levels above which non-
visualization of an intrauterine pregnancy (IUP) indicates that the pregnancy is
either nonviable or is ectopic. Barnhart et al. found that an empty uterus with a
serum hCG concentration ≥1500 mIU/mL was 100% accurate in ruling out a live
uterine pregnancy [22]. There are several institutions that set their discriminatory
threshold higher at ≥2000 mIU/mL. Moreover, Connolly and colleagues stated that
there is evidence to suggest an even higher threshold. They posited that with a via-
ble uterine pregnancy, a gestational sac was seen 99% of the time with a discrimina-
tory level of 3510 mIU/mL [23].
When initial hCG level surpasses the set discriminatory level and there is no
evidence for a uterine pregnancy observed with TVS, then the diagnosis is attributed
to a failed uterine pregnancy, completed abortion, or an ectopic pregnancy. However,

early multifetal gestation should be considered. If in a stable patient that a PUL that
could still have a normal pregnancy, it is judicious to continue expectant manage-
ment with serial hCG level assessment to prevent aborting an early normal preg-
nancy. The serial hCG levels will drop rapidly when the patient history or extruded
tissue suggests a completed abortion. Curettage will differentiate an ectopic from a
nonviable uterine pregnancy. Barnhart and colleagues do not recommend diagnostic
curettage as it results in unnecessary surgical therapy [24]. This can be countered by
concern for methotrexate toxicity if it is administered inappropriately to patients
with a presumed ectopic pregnancy.
evels Below the Discriminatory Zone

L
When the initial hCG level falls below the set discriminatory value, the location of
the pregnancy may not be technically discernible with TVS. With cases of PUL,
serial hCG level assays are repeated to identify patterns that specify either a grow-
ing or failing uterine pregnancy. Results that rise or fall outside these expected
ranges increase the concern for ectopic pregnancy. Therefore, women with a sus-
pected ectopic pregnancy, but whose initial hCG level is below the discriminatory
threshold, are reevaluated at 2 days intervals. First, with early normally progressing
uterine pregnancies, Kadar and Romero noted that the mean doubling time for
serum hCG levels was approximately 48 h [25]. The lowest normal value for this
increase was 66%. Barnhart et al. reported a rise of 53% within 48-h with a 24-h
minimum rise of 24% [26]. Seeber and associates proposed a more conservative
35% 48-h rise [27]. Silva and colleagues advise that one-third of women with an
ectopic pregnancy experience a 53% rise at 48 h. Furthermore, they reported that no
single pattern characterizes ectopic pregnancy and that approximately 50% of ecto-
pic pregnancies are found to have decreasing hCG levels, whereas the other half will
have increasing levels [28].
Failing intrauterine pregnancies also show patterns of hCG level decline as well.
Decline rates ranging between 21% and 35% are typical.
In pregnancies without these expected rises or falls in hCG levels, distinction
between a nonliving intrauterine and an ectopic pregnancy can be aided by repeat
hCG level evaluation [29]. Uterine curettage can be performed as well. Barnhart and
coworkers concluded that endometrial biopsy was less sensitive than curettage [30].
Prior to curettage, a repeat TVS examination can reveal new informative findings.
Serum Progesterone
Serum progesterone determinations can clarify the diagnosis in a few patients [31,
32]. A value of 25 ng/mL or higher eliminates the likelihood of ectopic pregnancy
with 92.5% sensitivity [33, 34]. Values <5 ng/mL are found in only 0.3% of normal
pregnancies [35]. Therefore, values <5 ng/mL indicate either a nonviable uterine
pregnancy or an ectopic pregnancy. Ectopic pregnancies typically demonstrate pro-
gesterone levels ranging between 10 and 25 ng/mL; therefore, the clinical utility of
120 P.B. Greenspan
progesterone is limited [36]. One exception is that pregnancy conceived via ART
can be associated with higher than usual progesterone levels [37].
Transvaginal Sonography
Endometrial Findings
Patients with an ectopic pregnancy require TVS to find evidence of a uterine preg-
nancy or an ectopic gestation. An intrauterine gestational sac is typically observable
between 4½ and 5 weeks. The yolk sac appears between 5 and 6 weeks, and a fetal
pole with cardiac activity is first detected at 5½ to 6 weeks. These structures are
visualized slightly later with transabdominal sonography.
In patients with an ectopic pregnancy, a trilaminar endometrial pattern can be
diagnostic (Fig. 6.7). However, its specificity is 94%, but with a sensitivity of only
38% [38]. In addition, Moschos and Twickler found that in women with PUL at
presentation, no normal pregnancies had a stripe thickness <8 mm [39].
Collections of anechoic fluid, often observed normally with an early intrauterine
gestational sac, can possibly be seen with ectopic pregnancy. Two features observed
include pseudogestational sac and decidual cyst. A pseudosac is a fluid collection
between the endometrial layers and conforms to the cavity shape. Finding a pseudo-
sac increases the risk of ectopic pregnancy [40, 41]. Secondly, a decidual cyst is an
anechoic area within the endometrium but distant from the canal and often at the
endometrial-myometrial border. Ackerman et al. proposed that this finding signifies
early decidual breakdown and leads to decidual cast formation [42].
These findings are dissimilar to the intradecidual sign seen with intrauterine
pregnancy, that being an early gestational sac and is eccentrically located within one
of the endometrial stripe layers [43]. The American College of Obstetricians and
Fig. 6.7 Trilaminar sonographic pattern associated with ectopic gestation (© McGraw-Hill Inc.
All rights reserved. Williams’ Textbook of Obstetrics, 24th ed. Used with permission)
Gynecologists recommends restraint in diagnosing a uterine pregnancy when a defi-

nite yolk sac or embryo is absent [44].
Adnexal Findings
The sonographic evidence of ectopic pregnancy depends on visualization of an
adnexal mass separate from the ovary. An ectopic pregnancy is clearly confirmed if
fallopian tubes and ovaries are seen and an extrauterine yolk sac, embryo, or fetus
is identified. There are cases in which a hyperechoic halo or tubal ring surrounding
an anechoic sac can be imaged. Alternatively, an inhomogeneous complex adnexal
mass is usually the result of hemorrhage inside the ectopic sac or by an ectopic
gestation that has ruptured into the tube. Generally, roughly 60% of ectopic preg-
nancies are seen as an inhomogeneous mass next to the ovary; 20% appear as a
hyperechoic ring; and 13% have an obvious gestational sac with a fetal pole [45]. It
is important to note that not all adnexal masses are ectopic pregnancies, and correla-
tion of sonographic findings with other clinical information is essential in making
an accurate diagnosis.
There is a color Doppler image referred to as “the ring of fire” which represents
placental blood flow within the periphery of the complex adnexal mass. Though this
can assist in the diagnosis, this finding also appears with a corpus luteum of preg-
nancy; therefore, differentiation can be challenging.
Hemoperitoneum
Evaluation for hemoperitoneum can add valuable clinical information in women

suspected of having an ectopic pregnancy. Usually, this is detected with sonography.
However, this can also be diagnosed by culdocentesis, a valuable diagnostic test that
is utilized less and less today.
The sonographic fluid noted in cases of hemoperitoneum is anechoic or
hypoechoic. Blood accumulates initially in the dependent retrouterine cul-de-sac,
and then surrounds the uterus as it fills the pelvis (Fig. 6.8). Fifty milliliters can be
imaged in the cul-de-sac using TVS, and transabdominal imaging improves the
assessment of the extent of hemoperitoneum. Significant intraabdominal hemor-
rhage results in blood tracking up the pericolic gutters to fill Morison’s pouch near
the liver. Free fluid in this pouch is usually not apparent until accumulated blood
reaches 400–700 mL [46–48]. Peritoneal fluid in conjunction with an adnexal mass
is highly predictive of ectopic pregnancy [49]. A small amount of peritoneal fluid is
physiologically normal.
Culdocentesis is a simple technique. It was used frequently in the past to diag-
nose hemoperitoneum. The cervix is grasped with a tenaculum and pulled outward
and upward toward the symphysis. A syringe with a long 18-gauge needle is used to
penetrate the posterior vaginal fornix into the retrouterine cul-de-sac. If fluid such
as blood or pus is present, it can be aspirated. Failure to obtain fluid, however, is
interpreted as an unsatisfactory entry into the cul-de-sac and does not rule out ecto-
pic pregnancy. When fluid is obtained and contains fragments of old clots or frank
122 P.B. Greenspan
Fig. 6.8 (a) Sonographic evidence of hemoperitoneum. (b) Culdocentesis (© McGraw-Hill Inc.

All rights reserved. Williams’ Textbook of Obstetrics, 24th ed. Used with permission)
nonclotting blood, this finding is compatible with the diagnosis of hemoperitoneum.

Conversely, if the blood sample clots, it might have been drawn directly from an
adjacent blood vessel or from a briskly bleeding ectopic pregnancy. A number of
studies have challenged its usefulness, and culdocentesis has been largely replaced
by TVS [50, 51]. This author appreciates the advances in imaging in the diagnosis
of ectopic gestation, however, continues to train residents in the technique of culdo-
centesis so that if one encounters a patient with a suspected ectopic pregnancy and
reliable imaging is unavailable, a simple diagnostic test can help to establish the
diagnosis.
Pelviscopy
Minimally invasive, endoscopic procedures afford direct visualization of the fallo-

pian tubes and pelvis. Pelviscopy affords a reliable diagnosis in the vast majority of
cases of suspected ectopic pregnancy. Furthermore, pelviscopy is therapeutic in
many instances, since the ectopic pregnancy can be managed with this technique.
Interstitial Pregnancy
Diagnosis
Interstitial pregnancies are lodged in the proximal tubal segment that lies within the
muscular uterine wall. Sometimes, they are inaccurately called cornual pregnancies;
however, cornual pregnancies describe a conception that develops in the rudimen-
tary horn of a uterus with a müllerian anomaly. Risk factors are similar to others
mentioned for tubal ectopic pregnancy; however, previous ipsilateral salpingectomy
is a specific risk factor for interstitial pregnancy [51]. Interstitial pregnancies tend to
rupture later than more distal tubal ectopic pregnancies, between 8 and 16 weeks of
amenorrhea. This is consequent to greater distensibility of the myometrium cover-

ing the interstitial fallopian tube segment. Ruptures of interstitial gestations are
associated with an increased risk of mortality; as high as 2.5% because of the prox-
imity of these pregnancies to the uterine and ovarian arteries, thus producing severe
hemorrhage [52].
Interstitial pregnancy can be detected early in many cases utilizing TVS and
serum hCG assays, but diagnosis can still be challenging. At times, these pregnan-
cies appear sonographically comparable to an eccentrically implanted intrauterine
pregnancy, more so in a uterus with a müllerian anomaly. Differentiation includes
an empty uterus, a gestational sac seen separate from the endometrium and >1 cm
away from the most lateral edge of the uterine cavity, and a thin, <5-mm myometrial
mantle surrounding the sac [53]. Furthermore, an echogenic line, referred to as the
“interstitial line sign,” extending from the gestational sac to the endometrial cavity
most likely represents the interstitial portion of the fallopian tube and is highly sen-
sitive and specific [54]. Occasionally, three-dimensional sonography, magnetic
resonance imaging (MRI), or diagnostic pelviscopy can also provide clarification
[55, 56]. Pelviscopically, an enlarged protuberance lying outside the round ligament
coexistent with normal distal fallopian tubes and ovaries is observed (Fig. 6.9).
Management
Surgical management with cornual resection or cornuostomy can be undertaken via

laparotomy or pelviscopy, depending on patient hemodynamic stability and surgeon
expertise [57, 58]. Whatever approach is chosen, intraoperative intramyometrial
vasopressin injection can decrease surgical blood loss. Postoperative hCG levels
should be obtained to exclude remnant trophoblast. Cornual resection excises the
gestational sac and surrounding cornual myometrium by means of a wedge resec-
tion, whereas cornuostomy involves incision of the cornua and suction or
Fig. 6.9 (a) Sonographic evidence of interstitial pregnancy. (b) Operative view of interstitial
pregnancy (© McGraw-Hill Inc. All rights reserved. Williams’ Textbook of Obstetrics, 24th ed.
124 P.B. Greenspan
instrument extraction of the pregnancy. The availability of computer-assisted pel-

viscopy in the hands of this author has considerably improved this operation.
Conservative medical management can be considered if the diagnosis is made
early on [59]. Consensus regarding methotrexate route or regimen is lacking
because of the low incidence of this ectopic gestation. Jermy and associates
reported a 94% success with systemic methotrexate using a dose of 50 mg/m2
BSA [60]. This, however, was a small series. Others have described direct metho-
trexate injection into the gestational sac [61]. Importantly, because these patients
usually have higher initial serum hCG levels at diagnosis, a longer period of sur-
veillance is usually needed.
It is not clear what risk of uterine rupture with subsequent pregnancies is follow-
ing either medical or conservative surgical management. Therefore, close observa-
tion of these patients during subsequent pregnancy, as well as the strong consideration
of elective cesarean delivery, is reasonable.
Different than interstitial pregnancy, the term angular pregnancy describes intra-
uterine implantation in one of the lateral angles of the uterus and medial to the
uterotubal junction and round ligament. This is relevant since angular pregnancies
sometimes can be carried to term attendant with an increased risk of abnormal pla-
centation and its consequences [62].
Abdominal Pregnancy (Fig. 6.5)
Diagnosis
Abdominal pregnancy, technically, is an implantation in the peritoneal cavity

exclusive of tubal, ovarian, or intraligamentous implantations. These pregnan-
cies are rare with an incidence of 1 in 10,000 to 25,000 live births [63, 64]. A
zygote can traverse the tube and implant primarily in the peritoneal cavity; how-
ever, the majority of abdominal pregnancies are assumed to follow early tubal
rupture or abortion with reimplantation. In the rare instance of advanced extra-
uterine pregnancy, it is common that the placenta is still at least partially attached
to the uterus or adnexa.
Diagnosis is challenging. There can be no or minimal symptoms. Laboratory
tests are usually normal; however, maternal serum α-fetoprotein (MSAFP) levels
can be elevated. Clinically, palpation can indicate an abnormal fetal position or the
cervix can be displaced [65]. Imaging of an abdominal pregnancy might not be
recognized, and the diagnosis is often overlooked [66]. Oligohydramnios is com-
mon but may or may not have significance. Other observations include a fetus seen
separate from the uterus or eccentrically positioned within the pelvis; lack of myo-
metrium between the fetus and the maternal anterior abdominal wall or bladder; and
extrauterine placental tissue [67]. MR imaging can provide additional anatomical
information and can be used to confirm the diagnosis and provide maximal details
regarding placental implantation [68, 69].
Ovarian Pregnancy (Fig. 6.5)
Ectopic gestations implanted in the ovary are rare. Diagnosis is confirmed if four
clinical criteria are met. These were outlined by Spiegelberg: (1) the ipsilateral tube
is intact and distinct from the ovary; (2) the ectopic pregnancy occupies the ovary;
(3) the ectopic pregnancy is connected by the uteroovarian ligament to the uterus;
and (4) ovarian tissue can be demonstrated histologically amid the placental tissue
[70]. Risk factors are like those for tubal pregnancies, but Assisted Reproductive
Technology or IUD failure appears to be disproportionately associated with this rar-
ity [71]. Presenting complaints and findings are identical to tubal ectopic pregnancy.
The ovary can accommodate the expanding pregnancy more easily than the fallo-
pian tube, but rupture early on is the usual consequence.
The availability of TVS has resulted in increased diagnosis of unruptured ovarian
pregnancies. Sonographically, an internal anechoic area is surrounded by a wide
echogenic ring, surrounded by ovarian cortex [72]. In their review of 49 cases, Choi
et al. observed that the diagnosis cannot be made until surgery since the majority of
cases are presumed to be tubal ectopic pregnancy [73]. Additionally, at surgery, an
early ovarian pregnancy can be thought to be a hemorrhagic corpus luteum cyst or
a bleeding corpus luteum.
Evidence-based management accrues mainly from case reports [74, 75]. The
classical management of ovarian pregnancies has been surgical. Smaller lesions can
be managed by ovarian wedge resection or cystectomy; however, larger lesions
require oophorectomy. Systemic or locally injected methotrexate has been used suc-
cessfully to treat small unruptured ovarian pregnancies [76]. Conservative surgery
or medical management mandates hCG levels be monitored to exclude remnant
trophoblast.
Cesarean Scar Pregnancy
Cesarean scar pregnancy (CSP) occurs when implantation of the gestation is within
the myometrium of a prior cesarean delivery scar. Its incidence approaches 1 in
2000 normal pregnancies and has increased in recent years commensurate with the
increased cesarean delivery rate [77, 78]. The pathogenesis of cesarean scar preg-
nancy has been equated to that of placenta accreta and carries similar risk of serious
hemorrhage [79]. Whether the incidence increases with multiple cesarean deliveries
or if it is affected by either one- or two-layer uterine incision closure is not known.
Pain and bleeding are common; thus, patients with CSP often present early on.
As much as 40% of women are asymptomatic and are diagnosed during routine
sonographic examination [78]. Rarely, early rupture can lead to an abdominal preg-
nancy [80].
The differentiation between a cervicoisthmic intrauterine pregnancy and CSP
can be difficult; several investigators have described sonographic findings [81, 82].
Godin et al. report that there are four sonographic criteria that should be met for the
diagnosis (Fig. 6.10) [83]. TVS is the usual first imaging tool; however, Magnetic
126 P.B. Greenspan
Fig. 6.10 (a) Sonographic evidence of uterine scar pregnancy. (b, c) Hysterectomy specimen with
uterine scar pregnancy (© McGraw-Hill Inc. All rights reserved. Williams’ Textbook of Obstetrics,
24th ed. Used with permission)
Resonance imaging is helpful when sonography is equivocal or inconclusive before

intervention [84].
There are currently no treatment standards for CSP. Several options are pro-
posed. Hysterectomy is a reasonable initial choice in those desiring sterilization. At
times, it is necessary to control heavy bleeding. If fertility preservation is desired,
then options include systemic or locally injected methotrexate, either alone or com-
bined with conservative surgery [85–87]. Surgical intervention includes visually
guided suction curettage or transvaginal aspiration, hysteroscopic removal, or isth-
mic excision. These are completed solely or usually with adjunctive methotrexate
[79, 88–92]. Preoperative uterine artery) embolization has been utilized to minimize
hemorrhage risk [93, 94].
Uterine Rupture (Figs. 6.11 and 6.12)
Classification
Uterine rupture is usually classified as either (1) complete when all layers of the
uterine wall are separated or (2) incomplete when the uterine muscle is separated
but the visceral peritoneum is intact. Uterine dehiscence is another term for
Intraperitoneal rupture of uterine tube
Uterus
Uterus
Ovarian ligament
Spontaneous tubal abortion
Dead,
Ovary calcified
embryo
in uterine tube
Lithopedion formation
Rupture into broad ligament
Fig. 6.11 Ectopic pregnancy 2 (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com.
128 P.B. Greenspan
Placenta accreta
Rupture through scar of classic cesarean section
Rupture of lower uterine segment into broad ligament
Fig. 6.12 Uterine rupture (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com.
incomplete rupture. Morbidity and mortality rates are considerably higher when
rupture is complete. Prior cesarean delivery is the greatest risk factor for either form
of rupture. Kieser and Baskett reported that 92% occurred in women with a prior
cesarean birth [95]. Holmgren et al. described 42 cases of rupture in gravidas with
a prior hysterotomy. Thirty-six patients were laboring at the time of rupture [96].
Diagnosis
Progress of labor in gravidas attempting Trial of Labor After Cesarean (TOLAC) is

similar to regular labor, and there is no specific pattern that signals uterine rupture
[97, 98]. Prior to the onset of hypovolemic shock, symptoms and signs in women
with uterine rupture can appear unusual unless the possibility of rupture is kept in
mind. Hemoperitoneum, for instance, as a result of ruptured uterus could cause
diaphragmatic irritation with pain referred to the chest steering the clinician toward
a diagnosis of pulmonary or amnionic fluid embolism instead of uterine rupture.
The most consistent sign of uterine rupture is a Category II or III fetal heart rate
pattern with variable heart rate decelerations that can progress into late decelera-
tions and bradycardia (Fig. 6.13) [99].
Of 36 cases of uterine rupture during a trial of labor reported by Holmgren et al.,
there were fetal signs in 24, maternal in eight, and both in three [96]. Most patients
do not experience cessation of contractions at the time of uterine rupture; therefore,
the use of intrauterine pressure catheters has not been shown to be effective in the
diagnosis [100].
The appearance of uterine rupture is identical to that of placental abruption in
some patients. The majority, however, shows remarkably little appreciable pain or
tenderness. Furthermore, since most gravidas in labor are managed for discomfort
Fig. 6.13 Category III fetal heart rate pattern associated with uterine rupture (© McGraw-Hill
Inc. All rights reserved. Williams’ Textbook of Obstetrics, 24th ed. Used with permission)
130 P.B. Greenspan
with either narcotics or epidural analgesia, pain and tenderness might not be obvi-
ous. Rupture is usually evident because of fetal intolerance signs and intermittently
because of maternal hypovolemia due to concealed hemorrhage.
Loss of station can be apparent by pelvic examination if the fetal presenting part
has entered the pelvis with labor. When the fetus is partially or totally extruded
through the uterine rupture site, abdominal palpation or vaginal examination can
help to identify the presenting part, which will have vacated the pelvic inlet. Firm
contractions can be felt alongside the fetus.
Uterine Incarceration
Uterine incarceration refers to a pregnant uterus that is entrapped in the pelvis

between the pubic symphysis and sacral promontory. It has been reported to occur
in 1 in 3000 to 10,000 pregnancies [101].
Uterine retroversion occurs in up to 20% of pregnant women [102]. Uterine
enlargement in the first trimester produces a rise of the fundus from the hollow of
the sacrum to an anterior ventral position. This spontaneously corrects the retrover-
sion. However, rarely, the fundus becomes wedged below the sacral promontory,
which displaces the bladder and cervix upward and anterior, and in turn, can pro-
duce urethral obstruction [103].
Risk factors that contribute to uterine incarceration include adhesions from prior
surgery, pelvic inflammatory disease, endometriosis, uterine leiomyomata, uterine
anomalies, and a deep sacral concavity with pronounced sacral promontory. Laxity
of the pelvic support architecture can also be involved in this process [104, 105]. In
some patients, there are no risk factors at all [106, 107].
Gravidas usually present at 14–16 weeks of gestation with symptoms, associated
with pressure on the anatomic structures adjacent to the enlarging uterus. The most
common symptoms are pain and progressive difficulty with voiding. The pain can
be abdominal, suprapubic, or in the lumbosacral spine; or can be limited to pelvic
discomfort or a feeling of pelvic fullness. Urinary complaints include frequency,
dysuria, sensation of incomplete bladder emptying, dribbling small volumes due to
overflow incontinence, and, often, urinary retention. Gastrointestinal symptoms
include rectal pressure, tenesmus, and worsening constipation due to compression
of the rectum [104, 105]. Vaginal bleeding has also been described. Symptoms can
be intermittent, resolving for a period of time and then returning weeks later.
The principal sign on physical examination is severe anterior displacement of the
cervix behind the pubic symphysis. The examiner may not be able to visualize the
cervix with a speculum or palpate the external os on pelvic examination [102].
Furthermore, the vagina is angulated anteriorly and a large, boggy, smooth, non-
tender mass (the incarcerated uterus) fills the cul-de-sac.
The bladder is displaced superiorly and elongated from compression by the cer-
vix and uterus. The fundus is located in the hollow of the sacrum; as a result, a
fundal placenta can be mistaken for a placenta previa. The fetus can be seen poste-
riorly against the sacrum deep in the pelvis.
Fig. 6.14 Uterine incarceration (Personal Image of Peter B. Greenspan, DO, FACOG, FACS)
Sonographic imaging can demonstrate a cervix which might be obscured or

appear thin and elongated, pulled anterior to the uterus [102]. Difficulty in identify-
ing the cervix should raise suspicion for uterine incarceration [108] (Fig. 6.14).
The incarcerated uterus can produce complications such as an obstructed urethra.
This can produce urinary retention to the point of hydronephrosis, urinary infection,
and rupture of the bladder [105].
Malposition of the uterus can possibly compromise uterine arterial blood flow,
which increases the risk of decidual bleeding, spontaneous abortion, oligohydram-
nios, fetal growth restriction, and fetal demise [109]. Second-trimester pregnancy
loss has been reported to be as high as 33% [103, 104]. Van Winter et al. report an
increased risk of premature rupture of membranes and preterm delivery [109].
Other complications described in case reports include uterine wall necrosis, uter-
ine rupture, development of a cervicovaginal fistula, and rectal gangrene [105].
Compression of pelvic veins can promote thrombosis, resulting in postpartum pul-
monary embolism in the absence of thrombosis in the deep veins of the lower limbs
[106]. Labor is inevitably complicated by dystocia.
Incarceration can be confused with other physical findings such as pelvic masses,
extrauterine pregnancy, adnexal torsion, leiomyomata, and uterine anomalies
including uterus didelphys or rudimentary uterine horn [110].
Intervention is essential for the successful management of an incarcerated uterus.
It is recommended to repeat a bimanual exam on any patient with a retroverted
132 P.B. Greenspan
uterus noted in the first trimester, at 16 weeks of gestation. If retroversion persists,

reduction in the retroverted fundus may be indicated [111].
Passive reduction requires maneuvers on the patients’ part in the knee-chest posi-
tion, for 10 min at least 3 times a day. This works well in patients who are
asymptomatic.
The use of manual reduction can be attempted without sedation or anesthesia, but
those modalities may need to be implemented for success [112].
A ring forceps can be applied to the cervix and gently pulled toward the introitus
to provide countertraction, while the fundus is being pushed cephalad. Use of sono-
graphic guidance during manipulation of the uterus can be helpful [113].
In rare instances, colonoscopy, pelviscopy, or laparotomy has been employed to
reduce uterine incarceration.
Recurrence is associated with persistence of predisposing factors mentioned
above [104, 114].
Placental Abruption
Placental abruption, or abruptio placenta, is the premature separation of a normally

implanted placenta from the uterus. Usually, abnormal maternal vessels in the
decidua basalis rupture and cause the separation. Rarely, the separation can be
caused by a disruption of the fetal-placental vessels [115]. The damaged vessels
cause bleeding, resulting in a decidual hematoma that can lead to placental separa-
tion, destruction of placental tissue, and a loss of maternal-fetal surface area for
nutrient and gas exchange.
Abruption is frequently associated with both acute and chronic processes.
Thrombin, which is released in response to decidual hemorrhage or hypoxia,
appears to play an active role in the pathogenesis of placental abruption [116].
Thrombin acts as a direct uterotonic, which augments the action of matrix metallo-
proteinases, and upregulates apoptosis genes, thus increasing the expression of
inflammatory cytokines [116, 117]. These thrombin-mediated events initiate a
cyclic pathway of vascular disruption, hemorrhage, inflammation, contractions, and
rupture of membranes [115].
Incidence
Placental abruption occurs once in 100 births; however, a range of 1 in 75 to 1 in 226
deliveries has been reported [115, 118]. The range in incidence possibly reflects
variable criteria for the diagnosis in addition to an increased recognition recently of
milder forms of abruption. About one-third of all antepartum bleeding can be attrib-
uted to placental abruption [118]. The peak incidence of placental abruption occurs
between 24 and 26 weeks of gestation [115]. The incidence has risen in the United
States because of the increased rates of gestational diabetes mellitus, preterm labor,
and umbilical cord abnormalities [119].
Clinical Manifestations
Various factors determine the clinical manifestations of placental abruption. These

include the temporal nature of the abruption (acute versus chronic), the clinical
presentation (overt versus concealed), and the severity [115]. An acute, frank abrup-
tion usually presents with sudden-onset vaginal bleeding, severe abdominal pain,
and uterine contractions. Worsening of the placental separation results in uterine
tenderness, tachysystole, non-reassuring fetal heart rate patterns, and fetal death can
occur [120]. There is a poor correlation between the amount of vaginal bleeding and
the extent of placental separation and its potential for fetal compromise. Concealed
abruption is reported in 10–20% of cases [121]. With severe abruptions, >50% of
the placental surface area separates [115]. In these clinical settings, maternal com-
promise in the form of consumptive coagulopathy can result from the triggering of
the clotting cascade by hemorrhage and extensive thrombin deposition [120, 122].
The presentation of chronic abruption can be insidious and is commonly associ-
ated with ischemic placental disease [123]. Typically, these gravidas present with
intermittent, light vaginal bleeding and evidence of chronic placental inflammation
and dysfunction, such as oligohydramnios, fetal growth restriction, preterm labor,
premature preterm rupture of membranes, and preeclampsia [124] (Fig. 6.15).
Risk Factors
Although the exact etiology of placental abruption is unclear, a variety of risk fac-
tors have been identified.
Placental abruption
Section through placenta

in premature separation
Obstruction of cervix by presenting part showing nodular ischemia
External bleeding Internal (concealed) bleeding and infarction above clots.
Placenta previa
Marginal placenta previa

Partial placenta previa Total (central) placenta previa
Fig. 6.15 Placental abruption, placenta previa (© 2016 Elsevier Inc. All rights reserved. www.
netterimages.com. Used with permission)
134 P.B. Greenspan
• Increasing parity and/or maternal age

• Cigarette smoking
• Cocaine abuse
• Trauma
• Maternal hypertension
• Preterm premature rupture of membranes
• Rapid uterine decompression associated with multiple gestation and
polyhydramnios
• Inherited or acquired thrombophilia
• Uterine malformations or fibroids
• Placental abnormalities or ischemia
• Prior abruption
Diagnosis
Placental abruption is usually a clinical diagnosis that is supported by imaging,

laboratory, and pathologic studies. Any gravida with findings of vaginal bleeding,
preterm labor, abdominal pain, or trauma should prompt an investigation of placen-
tal abruption [115].
Imaging
Detection rates of abruption by sonography in the past were abysmal; however,

recent advances in imaging have improved considerably. Hemorrhage in early ges-
tation is usually hyperechoic or isoechoic. Resolving hematomas are hypoechoic
within 1 week and sonolucent within 2 weeks of the abruption. Acute hemorrhage
can be misinterpreted as a thickened placenta or fibroid.
Sonography is able to identify three predominant locations for placental abrup-
tion. These include subchorionic (between the placenta and the membranes), retro-
placental (between the placenta and the myometrium), and preplacental (between
the placenta and the amniotic fluid).
Figure 6.13 illustrates the classification of hematomas in and around the pla-
centa. Figure 6.14 demonstrates a sonographic representation of a subchorionic
abruption.
The location and extent of the placental abruption identified on ultrasound exam-
ination are clinically significant (Fig. 6.16). The worse prognosis for fetal survival
is associated with retroplacental hematomas more so than subchorionic hemor-
rhage. Hemorrhage size is also predictive of fetal survival. Large retroplacental
hemorrhages (>60 mL) are associated with a 50% or greater fetal mortality, while
similarly sized subchorionic hemorrhages are associated with a 10% mortality risk
[125].
Magnetic resonance imaging (MRI) is useful in diagnosing placental abruption
when sonography is equivocal.
Fig. 6.16 Subchorionic hemorrhage (© McGraw-Hill Inc. All rights reserved. Williams’ Textbook
of Obstetrics, 24th ed. Used with permission)
Laboratory Findings
Few laboratory studies assist in the diagnosis of placental abruption.

Hypofibrinogenemia and evidence of consumptive coagulopathy are indicative of a
severe abruption; however, clinical correlation is necessary.
Abnormal serum markers early in pregnancy, such as an unexplained elevated
maternal serum α-fetoprotein (MSAFP) and hCG, have been associated with an
increased risk of subsequent placental abruption [115, 126].
Placenta Previa
Placenta previa is defined as the presence of placental tissue over or adjacent to the
cervical os. While placental abruption is associated with a cause for abdominal pain
in pregnancy, placenta previa is mentioned only in contradistinction to abruption,
because bleeding from placenta previa is classically painless (see Fig. 6.13).
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Gynecologic Etiologies of Abdominal
Pain in Pregnancy 7
Layan Alrahmani, Paul M. Magtibay III, Javier F. Magrina,
and Paul M. Magtibay
Adnexal Masses in Pregnancy
Introduction
The routine use of ultrasound in pregnancy, especially early pregnancy, has led to
more incidental diagnoses of adnexal masses in women who were otherwise asymp-
tomatic. The incidence of adnexal masses in pregnancy is 0.5–3.2% of live births,
and 3.6–6.8% of patients with persistent masses are malignant [1]. Ovarian torsion
is a gynecologic surgical emergency known to be increased in pregnancy. Of torsion
cases, 10–22% occurred in pregnancy in some series [2, 3]. The exact incidence is
unknown, but is estimated to be approximately 1 in 1800 [4].
Presentation
Most pregnant patients with adnexal masses are asymptomatic, with the diagnosis
being incidentally discovered during antenatal ultrasound or at the time of cesarean
delivery. The majority of symptomatic patients will present with nonspecific com-
plaints such as abdominal or pelvic pain, constipation, abdominal distension, or loss
of appetite, all of which are often attributed to pregnancy, thus unlikely to trigger a
diagnostic evaluation.
L. Alrahmani, MD (*)
Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine,
Mayo Clinic, Rochester, MN, USA
P.M. Magtibay III, MD, FACOG, FACS • J.F. Magrina, MD, FACOG, FACS
P.M. Magtibay, MD
Department of Obstetrics and Gynecology and Gynecologic Oncology, Mayo Clinic Graduate
School of Medicine and Biomedical Sciences, Mayo Clinic, Phoenix, AZ, USA

in Pregnancy, DOI 10.1007/978-3-319-62283-5_7
142 L. Alrahmani et al.
A small number of patients will present with acute abdominal pain, most com-
monly due to ovarian torsion or rupture of a mass. Most ovarian torsions occur in
the later part of the first to early second trimester [5].
Causes
The most common benign adnexal masses diagnosed in pregnancy are usually func-
tional simple cysts, being either follicular or corpus luteum cysts. Fibroids, mature
teratomas (teratomata), and cystadenomas (cystadenomata), serous and mucinous,
are other common benign cysts associated with pregnancy. Most pregnancy-
associated ovarian malignancies are either malignant germ cell tumors, sex cord-
stromal tumors, or epithelial tumors of low malignant potential (borderline tumors).
Differential diagnoses should also include nongynecologic causes such as gastroin-
testinal (e.g., diverticular abscess, appendiceal abscess or mucocele or colorectal
cancer) and urologic causes (e.g., pelvic kidney, or ureterocele).
Diagnosis
Diagnosis of an adnexal mass is generally made with ultrasound, which will usually
provide sufficient information to guide management. Most cystic masses will
resolve throughout the course of the pregnancy. Sonographic features of adnexal
masses that predict persistence include size greater than 5 cm and “complex” mor-
phology [6]. Adding color Doppler to ultrasound will increase specificity and sensi-
tivity of the diagnosis. If additional imaging is required, magnetic resonance
imaging (MRI) is the modality of choice (see Figs. 7.1 and 7.2).
Due to the quantitative increase in many tumor markers in normal pregnancy,
such as human chorionic gonadotropin hormone, CA-125, and alpha-fetoprotein,
these markers are not considered reliable for diagnosis or followed up in pregnancy
unless significant elevations are found. Also, one must be aware that certain condi-
tions in pregnancy may render the finding of even significant elevations not useful,
such as in cases of fetal aneuploidy, open neural tube defects, or preeclampsia [7].
One tumor marker, human epididymis protein 4 (HE-4), appears to be unaffected by
pregnancy [8]. It is currently used for treatment follow-up rather than screening of
ovarian cancer. However, note that the baseline normal reference values are changed
in pregnancy [9].
The diagnosis of ovarian torsion is made clinically and aided with Doppler ultra-
sound. Sonographic detection rates vary in different studies from 46% to 74% [10,
11]. A high index of suspicion is necessary for diagnosis of ovarian torsion in preg-
nant women as well as in nonpregnant women. Torsion should be suspected in all
patients with an acute onset of severe pelvic or abdominal pain, which may be
accompanied by fever or nausea, especially in the setting of an adnexal mass in the
first or second trimester (see Fig. 7.3).
7 Gynecologic Etiologies of Abdominal Pain in Pregnancy 143
Differential Diagnosis
Low-lying Distended
cecum bladder
Redundant
sigmoid
colon Pregnancy,
hydramnios,
hydatid mole,
hematometra,
pyometra
Bicornuate uterus
with pregnancy in
one horn, or interstitial
pregnancy
Appendiceal abscess
Desmoid;
urachal cyst
Paraovarian
cyst
D
Fibroids:
A. pedunculated
or parasitic
B. intraligamentous C B
C. of round ligament
Ectopic pregnancy D. cystic degeneration
with hematocele
Fig. 7.1 Pelvic masses that may present in pregnancy (© 2016 Elsevier Inc. All rights reserved.
www.netterimages.com. Used with permission)
Management
The definitive management of adnexal masses is surgery. However, because of the

low likelihood of malignancy and acute complications associated with surgery dur-
ing pregnancy, the risks of surgery frequently outweigh the benefits. Therefore,
Paraovarian cyst
(cyst of the epoöphoron)
Section of cyst lining
Cyst opened (unilocular

character and rugose lining)
Section through cyst wall (laminated

cuticula, parenchymal layer, and
daughter cysts containing scolices)
Hydatid (Echinococcus) cysts
Fig. 7.2 Para-ovarian cysts are often identified during routine obstetrical sonographic evaluations
(© 2016 Elsevier Inc. All rights reserved. www.netterimages.com. Used with permission)
Clinical Findings
Acute nausea and vomiting
Severe lower-quadrant abdominal pain,

may be confused with ruptured ovarian cyst
Benign cystic dermoid
Up to 50% of torsion cases may be associated

with a medium-sized (10–12 cm) mass
Mechanism of Torsion
Normal Torsion
Infundibulopelvic ligament
Ovarian branches with ovarian vessels
Ovarian of uterine vessels
ligament Torsion of ligaments and vessels
Torsion of ligaments
and vessels
Torsion of ovary causes twisting

of suspensory ligaments and
vascular pedicles resulting in venous
occlusion and congestion and, in severe Venous congestion
cases, arterial occlusion and ischemia and hemorrhage
Fig. 7.3 Ovarian torsion (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com. Used
with permission)
most adnexal masses in pregnancy can be managed expectantly and observed

through the postpartum period. With the appropriate patient selection, adverse out-
comes are not increased with conservative management [12]. Treatment should be
tailored to the nature, symptoms, and clinical suspicion of the mass. Should there be
a need for surgical excision, a minimally invasive approach in the early second tri-
mester (around 14–16 weeks’ gestation) will minimize the risks of preterm labor or
loss of the pregnancy.
Indications for surgery include suspicion for ovarian torsion or malignancy as
suggested by history, physical examination, or sonographic features. Laparoscopic
versus laparotomy approach should be individualized depending on size of mass,
gestational age, suspected malignancy, and expertise of the surgeon. More extensive
surgery may be indicated for ovarian malignancies. The extent of the surgery must
be tailored to the clinical situation such as gestational age, desire for retention of the
pregnancy, future fertility, histologic cell type, and extent of the disease. Some set-
tings may be managed via minimally invasive surgery, while others might require a
vertical skin incision, surgical staging, and cytoreduction [13].
The management of ovarian torsion is similar as that in nonpregnant patients,
consisting of laparoscopic detorsion with or without ovarian cystectomy or oopho-
rectomy. During the third trimester, the size of the gravid uterus may preclude a
minimally invasive approach.
Ovarian cyst rupture is usually a self-limited event. However, significant hemo-
peritoneum leading to hemodynamic instability requires surgical exploration and
source control of the bleeding.
Obstetrical Considerations
Generally, a vaginal delivery is not contraindicated unless the mass is fixed in the
pelvis resulting in pelvic outlet obstruction. Cesarean delivery should be reserved
for appropriate obstetrical indications. If a conservative approach is chosen, follow-
up is appropriate 6–12 weeks after delivery, which coincides with return to pre-
pregnancy physiology and resolution of most functional masses.
Uterine Fibroids in Pregnancy
Introduction
Uterine fibroids, or leiomyomata, are benign smooth muscle tumors of the uterus
(see Figs. 7.4, 7.5, and 7.6). The prevalence of fibroids in pregnancy has been sited
to be anywhere between 1.6% and 10% [14–16]. Fibroids are mainly asymptomatic
and usually discovered during routine fetal ultrasound. Most fibroids will remain
stable in size throughout pregnancy, while about 25% will increase and 10% will
decrease in size. Enlargement occurs most commonly in the first trimester, with an
average increase of approximately 12% [17, 18].
Presentation
Most fibroids are asymptomatic. Gravid patients may present with pelvic pain, pres-
sure, or vaginal bleeding. Acute abdominal pain can occur in rare situations, namely,
carneous degeneration, torsion, or prolapse through the cervix.
Degeneration occurs as a result of rapid growth of the fibroid subsequently out-
growing its blood supply, leading to ischemia and prostaglandin release, producing
significant pain [19]. Other signs and symptoms may include low-grade fever, ten-
derness to palpation, or peritoneal signs. Torsion presents the same way, and should
be suspected in the setting of a pedunculated or subserosal fibroid.
Histology of fibroid
Interstitial (intramural) Pedunculated, subserous

Subserous, displacing tube
Subserous
Pedunculated,
submucous
Submucous
Intraligamentary
Cervical
Pedunculated, submucous,
protruding through external os
Ultrasonographic appearance of fibroids
Fig. 7.4 Types of uterine leiomyomata (© 2016 Elsevier Inc. All rights reserved. www.netterim-
ages.com. Used with permission)
Calcification
Red degeneration of fibroid in gravid uterus
Sloughing fibroid (torsion of pedicle)
Inversion of uterus due to prolapse of submucous fibroid
Fig. 7.5 Consequences of uterine leiomyomata (© 2016 Elsevier Inc. All rights reserved. www.
netterimages.com. Used with permission)
Cystic degeneration
Incarceration
Fibroids retracted with cervix

permitting passage of child Incarcerated fibroid causing dystocia
Fig. 7.6 Uterine leiomyomata complicating pregnancy (© 2016 Elsevier Inc. All rights reserved.
www.netterimages.com. Used with permission)
Studies regarding the increased predisposition to placental abruption are incon-

sistent. Regardless, abruption may cause significant pain and should be ruled out
[20].
Diagnosis
Ultrasound is usually sufficient to establish the presence of fibroids. Important char-

acteristics to note are anatomic location, size, number, and blood supply. Torsion
can be identified in pedunculated fibroids using Doppler sonography of the stalk,
although this is not always possible [21]. Pelvic magnetic resonance imaging (MRI)
without contrast can also aid in diagnosis if it is unclear. Note that gadolinium has
been shown to be teratogenic in animal studies, thus it is considered contraindicated
in pregnancy unless absolutely necessary [22].
Although we recommend ultrasound or MRI for detecting fibroids, there is no
imaging modality that is perfectly sensitive or specific for detecting complications
of fibroids such as degeneration or torsion, and diagnosis therefore must rely on a
thorough history and physical examination. In rare select cases, a diagnostic lapa-
roscopy or laparotomy may be necessary.
Management
Pain from degeneration of fibroids can be managed conservatively with oral analge-
sics, such as acetaminophen, a short course of nonsteroidal anti-inflammatory drugs
(NSAIDs) such as ibuprofen or indomethacin prior to 32 weeks, or opioid analgesia.
Adverse fetal effects of NSAIDs when given after 32 weeks’ gestation include pre-
mature closure of the ductus arteriosus, neonatal pulmonary hypertension, oligohy-
dramnios, and fetal or neonatal platelet dysfunction and are best avoided [23]. Prior
to 32 weeks’ gestation, we suggest indomethacin dosing of 25 mg every 6 h for
48 h. Repeat courses can be administered as needed. Admission may be required for
parenteral pain control.
Excision of a fibroid prolapsed into the vagina should only be performed in case
of significant symptoms such as severe pain or bleeding, as intervention can lead to
significant hemorrhage, rupture of membranes, and even fetal loss [24, 25]. In these
cases, careful preoperative planning is crucial. Imaging to delineate the origin of
fibroid, adequate anesthesia, and a blood type and cross-match should be
available.
Torsion of a pedunculated fibroid is exceedingly rare. In a symptomatic patient,
management of torsion is surgical. A laparoscopic approach is preferable if feasible,
and it can be both diagnostic and therapeutic. In these cases, we recommend a myo-
mectomy be carried out as detorsion is not usually sufficient [26].
Obstetrical Implications
Obstetrical complications of fibroids include spontaneous abortion, preterm deliv-

ery, fetal growth restriction, fetal malpresentation, and abnormal placentation (pla-
centa previa or placental abruption) [20, 27–29]. In addition to counseling and
routine prenatal care, there are no specific recommendations regarding follow-up of
these patients. We recommend preemptive serial fetal growth ultrasounds in case of
substantial fibroids that interfere with fundal height measurements. Neonatal out-
comes are excellent overall. Poor outcomes are mainly related to prematurity.
Patients with fibroids are at increased risk for pre-labor cesarean delivery.
Common reasons for cesarean delivery include fetal malpresentation, abnormal pla-
centation, and presence of fibroid in the lower uterine segment. However, even after
adjusting for the aforementioned factors, these patients still had a higher rate of
cesarean delivery [30]. Gravid women with fibroids of any size may undergo a vagi-
nal delivery, and cesarean delivery should be reserved for appropriate obstetrical
indications. Patients should also be reassured that their likelihood of a successful
vaginal delivery does not differ from that of the general population.
Endometriosis (see Fig. 7.7)
The state of pregnancy will often improve or eliminate endometriosis lesions as

well as their associated symptoms. This is attributed to the altered hormonal envi-
ronment of pregnancy that results in decidualization of the endometriotic lesions
[31]. The decidualized lesions, however, may still be biologically active and pro-
duce symptoms and complications. There are reports in the literature that describe
intestinal perforation [32] hemoperitoneum [33–35], uroperitoneum [36, 37], acute
appendicitis [38, 39], and ruptured or infected ovarian endometrioma [40].
Endometriosis-induced complications that occur in pregnancy, albeit rare, may
be associated with the expanding uterus putting traction on adhesions, increased
friability of inflamed tissues, and alteration of vessel walls by decidualized lesions
[40].
The rarity of these complications in pregnancy does not warrant additional moni-
toring or interventions in gravid women with an endometriosis history.
A retrospective populations-based study of more than 82,000 singleton pregnan-
cies demonstrates a negative impact on pregnancy outcome in women with endome-
triosis. These adverse effects include an increased risk of preterm birth, preeclampsia,
and abdominal delivery when compared to gravidas without endometriosis [41].
Other studies have shown that endometriosis is associated with an increased risk of
spontaneous abortion, ectopic pregnancy, placenta previa, unexplained antepartum
hemorrhage, postpartum hemorrhage, and preterm delivery when compared with
unaffected women [42].
Other studies, however, report decreased or no change in risk of hypertensive
disorders of pregnancy in gravidas with endometriosis [43, 44]. There is no known
mechanism attributed to these problems and, again, closer scrutiny of pregnant
women with endometriosis is not warranted [40].
Endometriosis of
rectovaginal septum
and posterior fornix
Diffuse pelvic endometriosis: ruptured

endometrial (chocolate) cyst
Microscopic section through

lining of endometrial cyst
Hemisection of ovary with endometrial of ovary
cysts and corpus luteum
Ureter
Umbilicus
Small bowel
Cecum
Appendix Pelvic peritoneum
Laparotomy Fallopian tube
scar Sigmoid colon
Inguinal ring Ovary
Round Surface of uterus
ligament Myometrium (adenomyosis)
Bladder Uterosacral ligament
Uterovesical Rectovaginal septum
fold Cervix
Groin Vagina
Perineum
Vulva and
Bartholin’s
gland
Possible sites of distribution of endometriosis
Fig. 7.7 Endometriosis (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com. Used
with permission)
Ovarian Malignancy in Pregnancy
The incidence of ovarian malignancy during pregnancy is generally lower than that
of the general population, mainly because pregnancy occurs in a younger popula-
tion [1]. Currently, the most common ovarian malignancy in pregnancy is germ cell
tumors, and up to 30% of all ovarian malignancies are dysgerminomas.
Presentation for ovarian malignancy is generally similar to that of all

adnexal masses with some exceptions. Sex cord-stromal tumors, although rare
in pregnancy, can lead to evidence of hormonal excess (hyperestrogenism or
virilization). Advanced stage ovarian malignancy may lead to small bowel
obstruction.
When ovarian malignancy is suspected, the patient should be immediately
referred to a gynecologic oncologist. Ovarian cancer, like most gynecologic
malignancies, is surgically staged. During pregnancy, if discovered in the first
trimester, the best time for surgery is after 8-10 weeks, when placental function is
established and the corpus luteum has involuted, should there be a need for an
oophorectomy. Surgical staging during pregnancy usually entails a unilateral
salpingo-oophorectomy, omentectomy, peritoneal biopsies, lymphadenectomy,
and peritoneal washings. More comprehensive staging will include the aforemen-
tioned in addition to a total abdominal hysterectomy and bilateral salpingo-
oophorectomy. If the contralateral ovary appears normal, there is no need for
ovarian biopsies or resection on that side. If discovered in the third trimester, more
complete staging can be completed at the time of cesarean or after delivery.
Decisions regarding timing and choice of surgery as well as need for adjuvant or
neoadjuvant chemotherapy are made in consultation with a gynecologic oncolo-
gist. Note that pregnancy is not a contraindication to most chemotherapeutic
agents, especially after the first trimester.
Prognosis mainly depends on the stage of the disease at the time of diagnosis and
histologic tumor type, and is similar to that in nonpregnant patients.
Timing of delivery should be individualized. Things to consider are the stage and
type of cancer, timing in pregnancy, and patient wishes regarding treatment and
continuation of pregnancy especially before viability.
Cervical Intraepithelial Neoplasia and Cervical Cancer
Introduction
Although cervical cancer is the leading cause of gynecologic malignancy

worldwide, it is rather uncommon in the developed world due to the
Papanicolaou (Pap) smear. Cervical dysplasia, otherwise known as cervical
intraepithelial neoplasia (CIN), is a pre-cancerous lesion that is not infre-
quently diagnosed, especially in pregnancy when women tend to have the
most consistent medical care.
Presentation
CIN is usually asymptomatic, but may present with abnormal vaginal or postcoital
bleeding. Cervical malignancy is a rare cause of pain. However, advanced disease
with local invasion can lead to pelvic or lower back pain or pressure.
Diagnosis
Diagnosis is first suspected with a Pap smear and confirmed by directed colposcopic
biopsies.
For cervical dysplasia found on Pap smear, we recommend following the
American Society for Colposcopy and Cervical Pathology (ASCCP) guidelines.
This generally leads to observation without therapy, which is appropriate for preg-
nant women with cervical dysplasia if invasive cervical cancer has been excluded by
colposcopy with or without biopsies. Of note, endocervical curettage is contraindi-
cated in pregnancy, although the evidence that it adversely affects pregnancy is poor
[45].
Cervical cancer is the only gynecologic cancer that is clinically staged. Staging
in the nonpregnant woman includes physical examination and imaging, which con-
sists of chest and skeletal radiographs, intravenous pyelogram, and barium enema.
Other imaging studies may not be used for staging purposes. However, there are
limited recommendations for staging in the pregnant woman, and it should be indi-
vidualized [46]. Magnetic resonance imaging (MRI) and ultrasound may need to be
used in this situation to plan management approach and can be repeated during
pregnancy if necessary (see Table 7.1).
Management
Management generally depends on time of diagnosis, desire for pregnancy continu-

ation, and FIGO stage. As a rule, pregnancy termination is offered before 24 weeks
of pregnancy, and pregnancy continuation after 24 weeks due to fetal viability.
Pregnancy termination is subject to local laws, and treatment is as in the nongravid
patient. When pregnancy is continued, an early cesarean delivery is planned as soon
as fetal maturity is reached.
If pregnancy continuation is desired, MRI at diagnosis and at least one more time
later in pregnancy is recommended to determine tumor growth. As a rule, cervical
cancer growth during pregnancy is slow. Conization during pregnancy should be
avoided due to the risk for severe bleeding requiring blood transfusion, spontaneous
abortion, premature rupture of membranes, preterm delivery, infection, and fetal
loss [47]. Conization (cold knife or loop electrosurgical excision procedure) in the
operating room is an option only if absolutely necessary and thought to alter the
course of the treatment or delivery. Patients need to be counseled on the risks
involved.
In advanced stages, either expectant management until early cesarean delivery or
platinum-based neoadjuvant chemotherapy until cesarean delivery are adequate
options and depends on patient’s clinical condition and extent of disease [46]. The
effects of chemotherapy on pregnancy are agent, dose, and gestational age-dependent.
In the first 4 weeks of gestation, the pregnancy will result in loss or there will be no
effect at all, known as the “all or none” phenomenon. Between 4 and 12 weeks' ges-
tation , teratogenicity may occur depending on the agent used. Chemotherapy is
Table 7.1 FIGO staging of cervical cancer [57]

I Cervical carcinoma confined to the cervix
IA Invasive carcinoma diagnosed only by microscopy; stromal
invasion with a maximum depth of 5.0 mm measured from the
base of the epithelium and a horizontal spread of 7.0 mm or less;
vascular space involvement, venous or lymphatic, does not affect
classification
IA1 Measured stromal invasion ≤3.0 mm in depth and ≤7.0 mm in
horizontal spread
IA2 Measured stromal invasion >3.0 mm and ≤5.0 mm with a
horizontal spread ≤7.0 mm
IB Clinically visible lesion confined to the cervix or microscopic
lesion greater than IA2
IB1 Clinically visible lesion ≤4.0 cm in greatest dimension
IB2 Clinically visible lesion >4.0 cm in greatest dimension
II Cervical carcinoma invades beyond uterus but not to pelvic wall or
to lower third of vagina
IIA Tumor without parametrial invasion
IIA1 Clinically visible lesion ≤4.0 cm in greatest dimension
IIA2 Clinically visible lesion >4.0 cm in greatest dimension
IIB Tumor with parametrial invasion
III Tumor extends to pelvic wall and/or involves lower third of vagina
and/or causes hydronephrosis or nonfunctional kidney
IIIA Tumor involves lower third of vagina, no extension to pelvic wall
IIIB Tumor extends to pelvic wall and/or causes hydronephrosis or
nonfunctional kidney
IV Tumor invades mucosa of bladder or rectum and/or extends beyond
true pelvis
IVA Tumor invades mucosa of bladder or rectum
IVB Tumor extends beyond true pelvis
Used with permission of the American Joint Committee on Cancer (AJCC), Chicago, Illinois. The
original and primary source for this information is the AJCC Cancer Staging Manual, Eighth
Edition (2017) published by Springer International Publishing
generally thought to be safe after organogenesis is completed (after 15 weeks). One

meta-analysis reported healthy newborns in two-thirds of patients who received che-
motherapy for cervical cancer between 17 and 33 weeks of gestation [48].
Obstetrical Implications
No consensus has been reached regarding timing of delivery in those who desire
pregnancy preservation. Timing depends on gestational age as well as disease stage
at diagnosis. Optimally, a full-term pregnancy is desirable. However, this may not
always be feasible, and should be individualized.
In cases of early stage disease, mode of delivery should be as per routine obstetri-
cal indications. In case of macroscopic disease (FIGO stage IB1 or higher), cesar-
ean delivery is preferable due to risk of tumor seeding at episiotomy site, cervical
hemorrhage, infection, and obstruction of birth canal [49]. Definitive surgery for
cure may be attempted at time of cesarean delivery in select patients with a cesarean
radical hysterectomy.
elvic Infection (Pelvic Inflammatory Disease

P
and Tubo-Ovarian Abscess)
Introduction
Pelvic inflammatory disease (PID) is an infection of the upper female reproductive

tract, involving the uterus and/or adnexae (see Fig. 7.8). Tubo-ovarian abscess
(TOA) is a pelvic abscess that may result from untreated or mismanaged PID (see
Fig. 7.9). They are generally a result of a sexually transmitted infection. The inci-
dence of PID and TOA in pregnancy is unknown but exceedingly rare, limited to
case reports in the literature [50]. This is thought to be due to the cervical mucous
plug that prevents ascending cervical infection into the uterine cavity. Although the
initial culprit is commonly a cervicitis due to Chlamydia trachomatis and Neisseria
gonorrhoeae, the etiology of upper genital tract infections is usually polymicrobial
[51]. PID may occur in the first trimester before the development of the mucous
plug. Severe PID can cause tubo-ovarian abscess and/or sepsis (see Fig. 7.10).
Presentation
Patients with PID typically present with lower abdominal pain, with or without
fever, chills, nausea, dyspareunia, or vaginal spotting or bleeding. A ruptured tubo-
ovarian abscess (TOA) usually presents with severe acute abdominal pain and pos-
sibly peritonitis, but not always. Occasionally, right upper quadrant pain can occur
due to perihepatitis (Fitz-Hugh-Curtis syndrome).
Risk factors include young age (less than 25 years), multiple sexual partners,
personal history of sexually transmitted infections, or PID [52], as well as assisted
reproductive technology [50]. Pregnancy is a protective factor.
Diagnosis
PID is diagnosed clinically. The Center for Disease Control (CDC) diagnostic crite-
rion includes pelvic pain in a sexually active woman with either uterine, adnexal or
cervical motion tenderness, and other causes are ruled out [53]. Pelvic tenderness is
highly sensitive but not specific. Cervical inflammation may be apparent on specu-
lum exam, with friability and erythema as well as purulent discharge. Cervical
nucleic acid amplification test (NAAT) for gonorrhea or chlamydia should be per-
formed. A positive NAAT is useful but not necessary for diagnosis. Besides ruling
out other suspected etiologies, laboratory work-up is nonspecific and unnecessary.
Early acute salpingitis Cellular infiltration.

Chiefly polymorpho-
nuclear in early
acute salpingitis
Uterus
Fallopian tube
Ovary
More advanced
acute salpingitis
Large pyosalpinx
Plasma cell infiltration. Characteristic of

subacute and chronic salpingitis
Fig. 7.8 Pelvic inflammatory disease (© 2016 Elsevier Inc. All rights reserved. www.netterim-
ages.com. Used with permission)
Abscess has
progressed,
involving most
Fully developed of ovary
abscess
Pathogenesis of
tubo-ovarian abcess.
Adherence of tube and
infection of ruptured
follicle (corpus luteum)
Large tubo-ovarian cyst
Pseudofollicular
hydrosalpinx Wall of
hydrosalpinx
simplex
Small and
moderate sized
hydrosalpinx Large cystic
hydrosalpinx
Fig. 7.9 Tubo-ovarian abscess (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com.
Pathways of gonorrheal
and nongonorrheal
infection
Green — Gonorrheal
Red — Nongonorrheal
(generally puerperal,
postabortal, or traumatic)
Parametritis
with abscess
(dissection
from behind)
Parametritis
Nongonorrheal salpingitis.
Parametritis with abscess (dissection Infiltration chiefly in tubal wall
from above) showing extension laterally,
forward, and backward
Fig. 7.10 Pelvic abscess (© 2016 Elsevier Inc. All rights reserved. www.netterimages.com. Used
with permission)
Additional imaging is not necessary in the nongravid patient. However, due to the
rarity of this condition in pregnancy, we suggest a pelvic ultrasound for fetal assess-
ment as well as to rule out other etiologies. Direct confirmation during surgery is
rarely necessary for diagnosis, although has been used historically.
TOA can present the same way. A high index of suspicion is necessary, espe-
cially in patients who do not respond to antibiotic treatment for PID. Sonography is
first line for diagnosis of TOA. However, magnetic resonance imaging or computer
tomography may be necessary with advanced gestation and poor visualization of the
adnexa.
We recommend screening for other sexually transmitted infections once the
diagnosis is made.
Management
Treatment of PID is with antibiotics. The CDC recommends hospitalization and

parenteral treatment for all pregnant women [53]. Note that regimens including
doxycycline should be avoided in pregnancy due to its teratogenic effect on fetal
bones. Studies are lacking specifically addressing PID in pregnancy, but azithromy-
cin should be used as a substitute for doxycycline. One study showed high PID cure
rates in nongravid patients used azithromycin [54], and several randomized con-
trolled trials have shown effectiveness of azithromycin for cervical chlamydial
infection in pregnancy [55, 56]. The following outlines our suggested regimens of
initial antibiotic in treatment of PID in pregnancy, adapted from the original recom-
mendations of the CDC [53]:
1 . Cefotetan 2 g IV every 12 h plus azithromycin 1 g orally or IV every 24 h
2. Cefoxitin 2 g IV every 6 h plus azithromycin 1 g orally or IV every 24 h
3. Clindamycin 900 mg IV every 8 h plus gentamicin loading dose IV or IM (2 mg/
kg), followed by a maintenance dose (1.5 mg/kg) every 8 h. Single daily dosing
(3–5 mg/kg) can be substituted
Once clinical improvement is noted, the patient may be switched to an oral regi-
men to continue a total of 14 days of antibiotics, which consists of azithromycin 1 g
orally or IV every 24 h for 14 days, with or without metronidazole 500 mg orally
twice a day.
TOA can also be managed with antibiotic therapy alone on most occasions.
However, if clinical improvement is not seen within 48–72 h, surgical or radiologic
drainage of abscess may be necessary. A ruptured TOA needs surgical exploration.
The patient should be counseled on safe sexual practices prior to discharge. Male
sexual partners need to be evaluated and treated. Regardless of treatment of their
sexual partners, all women with positive chlamydia or gonorrhea should undergo a
test-of-cure 3–4 weeks after completion of treatment, preferably with NAAT [53].
Pregnancy Implications
Short- and long-term effects of PID and TOA have been well studied in the non-
gravid population, which include infertility, ectopic pregnancy, and chronic pelvic
pain. However, much less is known of these conditions in pregnancy, making it is
difficult to assess fetal risk. When treated promptly and appropriately, pregnancy
outcomes are thought to be good. As long as the patient is clinically stable, the fetus
should remain unaffected. A ruptured TOA is a surgical emergency. Sepsis can lead
to rapid deterioration of maternal and fetal conditions and preterm delivery.
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Gastrointestinal Etiologies of Abdominal
Pain in Pregnancy 8
Farzad Alemi, Teisha Shiozaki, Alexis Graham-Stephenson,
and Alexandra Bors
Introduction
While the etiologies of acute abdomen in pregnancy are varied and manifold, among the
most common include disorders of the gastroenteric and hepatopancreatobiliary sys-
tems (see Fig. 8.1). This chapter systematically reviews both the common and uncom-
mon causes of acute abdomen in the gravid patient due to intra-abdominal etiologies
typically evaluated by gastroenterologists and general, colorectal, and hepatobiliary sur-
geons. Unique considerations in the pregnant patient are explored with respect to diag-
nosis and management options to provide optimal care to both mother and fetus.
Gastroesophageal Reflux Disease
Background
In the nongravid patient, gastroesophageal reflux disease (GERD) affects close to

40% of patients; during pregnancy, approximately 30–50% of patients are affected
[1]. GERD symptoms, including heartburn and regurgitation, most frequently occur
in the third trimester of pregnancy [2], but the most important risk factor is pre-
existing GERD [1]. Interestingly, GERD symptoms can disappear after delivery,
and can recur with subsequent pregnancies [3]. This is, perhaps, due to the effects
of progesterone which mediates lower esophageal sphincter relaxation leading to a
decrease in muscle tone by approximately 33–50% by 36 weeks’ gestation [4, 5].
Recent studies have shown the significant impact of GERD on quality of life, with
F. Alemi, MD, MS (*) • T. Shiozaki, MD • A. Graham-Stephenson, MD • A. Bors, MD

Department of Surgery, University of Missouri Kansas City School of Medicine,

in Pregnancy, DOI 10.1007/978-3-319-62283-5_8
166 F. Alemi et al.
Traumatic rupture
Hepatic
Abscess Infarction
Pyogenic Abscess
Splenic
Acute cholecystitis Amebic Rupture
Hydrops Traumatic
Empyema Malarial
Biliary
Ruptured
Gastroesophageal reflux
Gastric
Free (bile peritonitis)
disease (GERD)
Abscess (pericholecystic)
Peptic ulcer
Biliary colic
Perforated
creatic
Gastroenteric Duodenal
Peptic ulcer
Pan-
Obstruction Pancreatitis
Rupture
Mesenteric
Blunt trauma Mesenteric lymphadenitis
Mesenteric thrombosis
Acute gastroenteritis
Food poisoning Nonspecific ulcerative colitis
Dietary indiscretion Fulminating
Chemical Toxic dilation
Perforation
Peritonitis Obstruction
Peritoneal
Primary diffuse (pneumococcus) Volvulus

Secondary to visceral pathology Sigmoid
Local (abscess) Cecal
Generalized “benign paroxysmal” Specific colitis
Large intestinal
Obstruction Amebic
Meckel’s diverticulum Bacillary
Inflammation Neoplasm
Obstruction
Small Intestinal
Torsion
Perforation Perforation
Traumatic Intussusception
Inflammatory Perforation
Due to strangulation Rupture
Intussusception Perforating injury
Ileocecal tuberculosis Appendicitis
Regional enteritis
Incarcerated hernia Foreign body
Fecal impaction
Rupture Rectally inserted
Spontaneous (in pregnancy) Ingested
Uterine
Instrumental
Ruptured follicular
Ovarian
Infection cyst or corpus luteum
Postabortal Torsion or cyst pedicle
Puerperal Ruptured endometrial cyst
Testicular
Ectopic gestation
urinary
Tubal
Testicular torsion Tubo-ovarian abscess

Renal/
Urinary tract infection

Renal calculi Acute salpingitis
Torsion of hydrosalpinx
Fig. 8.1 Causes of abdominal pain (© 2016 Elsevier Inc. All rights reserved. www.netterimages.
com. Used with permission)
more than 70% of gravid patients reporting heartburn and regurgitation which lead
to significant reductions in social and emotional functioning [1].
Diagnosis
Typical symptoms of GERD include heartburn and regurgitation, but it is also associ-
ated with nausea and vomiting. Extra-esophageal manifestations are oftentimes pres-
ent, including asthma (3.5%), chest pain (6%), and cough (1.2%) [6]. Usually the
diagnosis of GERD can be made clinically without the use of further imaging. If
necessary for intractable cases, endoscopy is the procedure of choice for diagnosis [7].
However, manometry and pH studies can also be performed safely if necessary [5].
Treatment
Lifestyle modifications are the primary modality employed to treat GERD during
pregnancy. This includes changes in meal sizes and frequency as well as timing.
8 Gastrointestinal Etiologies of Abdominal Pain in Pregnancy 167
Identification of foods which trigger symptoms is critical, and avoidance of those

foods is encouraged. If nighttime GERD is problematic, those patients should ele-
vate the head of the bed.
Medical management of GERD is used in conjunction with lifestyle modifica-
tions as first-line therapy and effective for most patients [8]. Mild-to-moderate cases
of GERD should be treated with H2 antagonists and antacids. All proton pump
inhibitors are classified as safe for consumption during pregnancy with no adverse
outcomes reported such as spontaneous abortion or congenital malformations [1].
Surgical management for GERD, such as laparoscopic fundoplication, has not
been reported in the gravid population owing to the efficacy of medical manage-
ment. In some instances, patients with underlying severe GERD have undergone
surgery prior to pregnancy, with good results [9].
Peptic Ulcer Disease
Background
The incidence of peptic ulcer disease (PUD) in pregnancy is low, occurring in 78

of 60,994 women with a medically diagnosed ulcer [10]. Peptic ulcer disease,
including ulceration of the stomach, duodenum or any combination thereof, often
presents with nausea, emesis, and dyspepsia and rarely can be asymptomatic
with gastrointestinal bleeding as the presenting symptom [1, 11]. Other condi-
tions that can present similarly include GERD, nonulcer dyspepsia, and hyper-
emesis gravidarum [12].
There is some thought that PUD improves during pregnancy [1]. Possible expla-
nations include increased prostaglandins and estrogens that offer protective effects
to the gastric and duodenal mucosa, immunologic tolerance from pregnancy, health-
ier lifestyle including reduction in tobacco and alcohol use, diet alterations, and
better medical care [1–3].
Diagnosis
Diagnosis of PUD in pregnancy is limited, due in part to self-treatment and decreased

reporting, hesitancy of physicians to recommend diagnostic workup during preg-
nancy, and misdiagnosis with similarly presenting conditions common in pregnancy
[3]. While esophagogastroduodenoscopy (EGD) is an accepted and studied diag-
nostic tool in pregnancy, the use of other studies for nausea and emesis which may
otherwise be used for diagnosis, such as the upper GI series, would be contraindi-
cated due to the risk of radiation exposure [3]. The most frequent indications for
EGD in pregnancy are refractory dyspepsia and GI hemorrhage [3]. A 2011
European study involving treatment for PUD found that only a small number of
those diagnosed with PUD have had an endoscopic exam for diagnosis and the
majority of those cases were self-diagnosed [1].
168 F. Alemi et al.
Diagnosis of a perforated peptic ulcer is typically clinical, with findings of peri-

tonitis and acute abdomen. Performance of a plain film to document free intraperi-
toneal air is critical and not contraindicated in pregnancy [13]. EGD, however, is
contraindicated when perforation is suspected.
Diagnosis of a bleeding ulcer is also clinical, with patients presenting with
melena, hematemesis, hematochezia, and hypotension. Initial diagnostic maneuvers
include performance of nasogastric lavage. Nasogastric decompression is also criti-
cal to prevent pulmonary aspiration during subsequent EGD [14].
Treatment
Once diagnosed, recommended treatment for ulcer disease first includes lifestyle mod-
ifications. This means smaller, more frequent meals, separate liquid intake from meals,
maintaining upright position postprandially, avoiding late night meals, and triggering
foods such as caffeine, fatty foods, and if applicable, tobacco, and alcohol [3].
If PUD is refractory to lifestyle modifications, then drug therapies are com-
monly recommended [1]. Frequently utilized medications include antacids, gas-
tric acid secretion inhibitors (H2 blocker), proton pump inhibitors, and
cytoprotective medications (carafate). Eradication of Helicobacter pylori, a
treatment option in the nonpregnancy population, should be deferred to the post-
partum period [3]). A 2011 European study failed to identify a higher occurrence
of congenital abnormalities in women with PUD or those who received drug
treatments during pregnancy [1]. Another European study of proton pump inhibi-
tors similarly did not show an increased risk of congenital abnormalities in those
exposed [15].
Perforation and bleeding are the two most frequent indications for surgical
intervention, and treatment in the gravid patient is the same as in the nongravid
patient. A perforated peptic ulcer necessitates emergent surgical intervention
with concurrent resuscitation and broad-spectrum antibiotics. Medical manage-
ment of perforated ulcers is associated with poor prognosis for both mother and
fetus, with mortality ranging between 60% and 100% [5]. In the operating room,
either Graham patch closure or partial gastrectomy is indicated depending on
clinical findings.
Should gastrointestinal bleeding be the presenting symptom, the patient should
be hospitalized, observed, and fluid resuscitated as indicated. The bleeding patient
should be placed in the left lateral decubitus position to improve venous return
through the vena cava and maintenance of uterine perfusion [16]. Endoscopic man-
agement with possible therapeutic intervention should be considered first to manage
hemorrhage [3]. Indications for surgery for PUD bleeding include failure of endo-
scopic management, hemodynamic instability, or continued hemorrhage after trans-
fusion of six or more units of red blood cells. As with perforated ulcers, surgical as
opposed to medical management of bleeding ulcer disease is associated with
improved maternal and fetal outcomes [5].
Hepatic Disease
Fortunately, the etiologies of acute abdomen secondary to hepatic pathology are

rare. However, owing to its rarity, the liver may be overlooked as a cause of abdomi-
nal pain and this may adversely impact maternal and fetal well-being. The major
causes of hepatically induced acute abdomen are hepatic rupture, abscess, and fatty
liver of pregnancy.
Hepatic Rupture
Hepatic rupture can occur spontaneously or after an inciting event, such as trauma.
The liver is a protected organ owing to its location adjacent to the ribs and dia-
phragm. Nevertheless, the liver parenchyma itself or lesions within the liver, such as
tumors or cysts, can rupture. In the gravid patient, there is an association between
pre-eclampsia, eclampsia, and HELLP syndrome (hemolysis, elevated liver
enzymes, and low platelets) with spontaneous hepatic rupture, with a case-to-
delivery ratio of 1:45,000 [17, 18]. In fact, the vast majority (approximately 80%)
of spontaneous ruptures are associated with pre-eclampsia [19].
Hepatic rupture usually occurs in the third trimester. In approximately 75% of
patients, intraparenchymal hemorrhage occurs in the right lobe; 11% of rupture
occurs within the left lobe; and in 14% of patients there is bilateral involvement
[20]. Intraparenchymal hemorrhage progresses to contained subcapsular hemor-
rhage. After the capsule ruptures, the tamponade effect is released, and in patients
who are thrombocytopenic, appropriate clotting will not contain progressive hemor-
rhage [21]. Maternal mortality remains high with this diagnosis, ranging from 25%
to 75% [1].
Other rare causes of hepatic rupture include hepatic cysts, which are relatively
common and occur in up to 5% of patients [22]. Intraperitoneal or extraperito-
neal hemorrhagic cyst rupture is rare, occurring in only 1% of patients. The risk
of rupture corresponds to the intracystic pressure and not to the intra-abdominal
pressure, so the resultant effects of pregnancy are not necessarily a risk factor
[23], and there have only been case reports of ruptured cysts in the gravid popula-
tion [24].
Diagnosis
Typically, a patient presenting with hepatic rupture is hemodynamically compro-
mised and exhibits peritonitis and abdominal distention on examination. Definitive
diagnosis must be made by imaging, usually ultrasound or CT.
Treatment
Hepatic rupture, if the cause is known (i.e., trauma), can sometimes be managed
conservatively. Invasive hemodynamic monitoring should be performed, and avail-
ability of large volumes of blood products is critical. Coagulopathy must be cor-
rected to prevent further exsanguination, and there have been reports of successful
170 F. Alemi et al.
use of recombinant Factor VIIa to assist with hemostasis, thus averting surgical
intervention [25, 26]. Additional trauma to the patient should be avoided (i.e.,
unnecessary bed transfers, palpation, emesis, etc.).
If conservative management is unsuccessful or the patient presents in extremis,
surgical intervention will be required to first control the hemorrhage, which can be
achieved with packing. The area of laceration or rupture can then be repaired expe-
ditiously; this may rarely require temporary occlusion of the hepatoduodenal liga-
ment (Pringle maneuver), hepatic artery ligation, or even hepatic resection. In rare
scenarios, the need for emergent liver transplant [2] is necessary to control hemor-
rhage and rupture.
Liver Abscess
Liver abscess is a serious condition which can result from a variety of intra-
abdominal processes, such as perforated viscus due to appendicitis or diverticu-
litis with resultant hematogenous spread to the liver [27]. Not surprisingly, then,
enteric bacteria including Bacteroides and Escherichia coli are the most preva-
lent causative organisms. In areas where endemic, amoebic liver abscesses
(Entamoeba histolytica) should also be considered. However, liver abscesses
can also occur from liver necrosis secondary to liver infarction resulting from
pre-eclampsia.
Diagnosis
Right upper quadrant pain and fever are the most common presenting clinical
symptoms. Laboratory analysis is relatively nonspecific, but elevated ALT and
thrombocytopenia in pregnancy have been reported [28]. Imaging is key to
diagnosis, with ultrasound being of primary consideration with a sensitivity of
86% [29]. In pregnancy, early diagnosis is critical given the high perinatal mor-
tality rate with untreated cases. Additionally, its delayed diagnosis and pro-
gression is associated with increased rates of fetal infection and preterm
delivery [30].
Treatment
Patients suspected of harboring a liver abscess need prompt resuscitation and com-
mencement of broad-spectrum antibiotics. Definitive aspiration and drainage of the
abscess is both diagnostic and therapeutic. This is typically achieved with ultra-
sound guided percutaneous drainage. It is critical to take cultures from the aspirate
to guide the antibiotic regimen.
If percutaneous drainage is unsuccessful or incomplete, surgical drainage may be
necessary. Surgical exploration is also necessary in the patient in whom ruptured
abscess is suspected; typically these patients will present with peritonitis and sepsis.
This intervention is critical for washout of the abdomen, as well as source control
and complete drainage of the abscess.
Cholecystitis and Biliary Tract Disease
Biliary Physiology in Pregnancy
Biliary disease is the second most common gastrointestinal disorder requiring sur-
gery during pregnancy [31]. Perhaps, this is due to the changes in biliary physiology
induced by the hormones of pregnancy. Increased serum estrogen and progesterone
during pregnancy induce metabolic changes in the synthetic and excretory physiol-
ogy of bile.
Bile, which is composed of bile salts derived from cholesterol, increases in viscos-
ity and volume with elevated estrogen [32]. This risks increased cholesterol crystal
aggregation and therefore gallstones. Increased progesterone has been shown to cause
relaxation within the smooth muscle of the gallbladder which leads to bile stasis [33].
Studies have widely demonstrated that gravid patients are at increased risk for biliary
tract disease, as more than 25% of postpartum patients were demonstrated to have
biliary sludge as a result of hormonal changes induced by pregnancy [34].
Cholecystitis
Among the most frequent causes of acute abdomen in pregnancy is acute cholecys-
titis. Its incidence ranges from between 0.2 and 0.5 per 1000 pregnancies [35]. In
the nongravid patient, this typically presents with right upper quadrant pain and
fevers, and treatment of cholecystitis can vary, ranging from medical therapy, endo-
scopic therapy, percutaneous drainage, or surgery depending on the patient’s under-
lying medical conditions and presentation. In the gravid patient, however, the
differential diagnosis for right upper pain is broad, and can include uterine contrac-
tions, fetal movement, adnexal torsion or rupture, liver hematoma, cholangitis, hep-
atitis, peptic ulcer, and pancreatitis. It is important then, to first accurately make the
diagnosis and then offer the appropriate treatments in a timely fashion.
Diagnosis
To accurately diagnose cholecystitis, it becomes important to “rule out” other con-
founding causes. Uterine and fetal monitoring should be routinely established to
determine maternal and fetal well-being as well as assessing for the possibility of
uterine contractions. Clinical history for cholelithiasis and cholecystitis is para-
mount. Suspicion should be increased in older patients who have a four times
increased prevalence of calculi in comparison to younger patients [36]. A previous
history of pregnancy is also a risk factor, as multiparous females have a 12-fold
increased risk of calculi when compared to nulliparous patients [37].
Otherwise, classic clinical symptoms of postprandial right upper quadrant pain
related to fatty foods are diagnostic of biliary colic. When coupled with fevers, chills,
nausea, and vomiting, the clinical suspicion for cholecystitis should be elevated.
Delays in diagnosis can ultimately lead to decompensation of the mother and
acute perforations of the gallbladder or biliary tree. The unfortunate result of
172 F. Alemi et al.
peritonitis or sepsis may contribute to increased risk of fetal abnormalities, maternal

mortality, preterm labor, fetal loss, and death [38, 39]. When suspected, then, proper
workup including laboratory analysis and radiographic imaging is critical.
Laboratory Analysis
Liver function tests are sometimes difficult to interpret, given the normal changes
seen in pregnancy. Typically, AST/ALT levels should remain normal throughout
pregnancy, though bilirubin levels tend to decrease and alkaline phosphatase
increases [40]. In addition, given the alterations seen in white blood count, the diag-
nosis of cholecystitis should not be based on laboratory anomalies alone, but rather
the entire clinical picture.
Radiographic Analysis
In gravid and nongravid patients, ultrasound remains the gold-standard diagnostic
imaging modality for cholecystitis and biliary tract disease. Its benefits of being
quick, noninvasive, and devoid of radiation risk are coupled with its superior sensi-
tivity and specificity for gallbladder disease (typically >97%) [15]. The entirety of
the gallbladder and biliary tree can be visualized by ultrasonography, to identify
calculi, obstructing stones, biliary sludge, and gallbladder wall thickening. An ultra-
sonographic Murphy’s sign is also highly sensitive for acute cholecystitis.
Treatment
Initial management of the patient with acute cholecystitis should include resuscita-
tion with intravenous fluids and commencement of broad-spectrum antibiotics. In
its acute presentation, laparoscopic cholecystectomy should be the standard treat-
ment for cholecystitis. Open cholecystectomy has been shown to result in a higher
rate of postoperative premature uterine contractions and use of tocolytic therapy
[41]. Laparoscopy has been proven to be quite safe during pregnancy, though care
should be taken to enter the abdomen and obtain pneumoperitoneum safely (typi-
cally, via Hasson open approach) [42]. Intraoperatively, fetal monitoring should be
employed. Pneumoperitoneum should be kept at a maximum of 15 mm Hg, though
this may need to be decreased in some instances given patient compliance.
The timing of cholecystectomy is important; in the nongravid patient, patients
either undergo operative removal of the gallbladder, percutaneous cholecystos-
tomy tube placement, or medical management with bowel rest and antibiotics. In
the pregnant patient, much debate has surrounded whether these approaches are
equivalent, especially with respect to the safety of laparoscopic cholecystectomy
during the first and third trimesters. Given these uncertainties, some have advo-
cated for temporizing measures such as percutaneous cholecystostomy tube
placement in the gravid patient who is not in the second trimester [43]. This
allows for safer performance of laparoscopic cholecystectomy during that safe
interval (if presenting in the first trimester) or postpartum (if presenting in the
third trimester). In nonemergent situations, however, guidelines for laparoscopic
treatment of biliary disease recommend elective operations to be performed
within the second trimester [27].
Operations performed, even in the second trimester, are not without risk. There
have been reports of spontaneous contractions, premature birth, and spontaneous
abortions associated with laparoscopic cholecystectomy in the second semester
[25, 44]. The alternative of nonoperative management, though, appears to be
worse. Collectively reviewed published reports have demonstrated a fetal demise
rate of 7% with nonoperative management of acute cholecystitis, compared to
2.2% with laparoscopic cholecystectomy [45]. Moreover, relapse rates of between
40% and 55% were demonstrated with nonoperative management. With this infor-
mation, decision-tree analysis demonstrates the superiority of operative manage-
ment in gravid patients with acute cholecystitis, especially in the first or second
trimester [30].
Biliary Tract Disease
The biliary tract can be prone to complications from benign and malignant condi-
tions which can cause an acute abdomen in the pregnant patient. The diagnosis and
treatment of these conditions should ultimately be undertaken with the health and
safety of the mother primarily, but modifications in workup and treatment strata-
gems can be considered to maximize the chance of successful pregnancy and mini-
mize harm to the fetus.
Choledocholithiasis
As discussed earlier, the pregnant patient is prone to develop gallstones given the
effects of hormones on bile stasis and cholesterol crystallization. When the stones
are passed into and retained within the common bile duct or common hepatic duct,
choledocholithiasis, and the more concerning sequela of cholangitis can result.
Choledocholithiasis, though rare, is estimated to affect 1 in 1200 pregnancies [46].
Others have identified that it can complicate up to 12% of pregnancies, and has an
increasing incidence with age [47]. Cholangitis is considered a surgical emergency
and rapid decompression of the biliary tract is necessary to prevent sepsis from
bacterial overgrowth.
Diagnosis
The diagnosis of biliary pathology during pregnancy can be difficult. The clinical
symptoms of choledocholithiasis can be nonspecific (nausea, vomiting, anorexia,
and pain) and can be masked by the pregnant state. Laboratory analysis, too, can be
masked by pregnancy as leukocytosis and elevated liver function tests (especially
alkaline phosphatase) can have a placental origin [48].
When suspected imaging becomes critical to rapid diagnosis and treatment.
Ultrasound remains the modality of choice given its noninvasiveness, ease of use,
and rapidity of results. However, despite its excellent sensitivity for cholelithiasis,
its diagnostic ability for choledocholithiasis is limited and sensitivity ranges
174 F. Alemi et al.
between 20% and 38% [49], likely a result of the inaccessibility of the common bile
duct by ultrasound given its location and presence of overlying bowel gas and the
gravid uterus.
When ultrasound is nondiagnostic, other noninvasive methods can be employed.
Cross-sectional imaging using computed tomography (CT) unfortunately has low
sensitivity for the diagnosis of common bile duct stones, and furthermore risks radi-
ation exposure to the fetus [50]. Magnetic resonance cholangiopancreatography
(MRCP) is an established method of fine detailed analysis of the biliary tree and is
routinely used in nongravid patients. It poses no risk to the fetus and has an accuracy
of close to 100% in diagnosing the presence and level of biliary obstruction [51].
When negative, it has the benefit of potentially excluding patients who would need
endoscopic management of choledocholithiasis, as well as sometimes obviating the
need for intraoperative cholangiography during cholecystectomy, thereby reducing
the risk of radiation in these patients.
Treatment
Endoscopic Therapy
Medical treatment with endoscopic therapy has become the standard of care to treat
choledocholithiasis. With endoscopic retrograde cholangiography, it becomes pos-
sible to both diagnose obstructing lesions within the biliary tree and treat them using
extraction and stenting techniques.
Endoscopic retrograde cholangiopancreatography (ERCP) does not come with-
out increased risk, however. The ability to visualize the biliary tree requires the use
of fluoroscopy, iodinated contrast, radiation, and sedation. In the first trimester, this
combination of factors can result in increased complications. Tang and colleagues
reported a lower rate of full-term pregnancy (73%), lower birth weight (21%), and
higher rate of preterm delivery (20%) in 65 patients who underwent ERCP in the
first trimester [30].
The radiation exposure risk from ERCP can be clinically significant. In the preg-
nant patient, the typical radiation doses using ERCP range from 3.4 mGy to
55.9 mGy [52]. Fortunately, the fetus lies outside the radiation beam during ERCP,
but there is potential to exceed the safe clinical radiation thresholds of 50 mGy
stipulated by ACOG guidelines [53]. Doses in excess of 100 mGy can result in sig-
nificant fetal complications, such as growth restrictions, mental retardation, fetal
malformations, and intrauterine death [54, 55]. Strategies to mitigate radiation
exposure include minimizing fluoroscopic time and performance of ERCP by an
experienced practitioner. Smith and colleagues demonstrated that when ERCP was
performed by a specialty biliary endoscopist with more than 500 cases yearly, the
estimated fetal radiation dose was less than 0.5 mGy [17].
Another strategy that can minimize radiation exposure is performance of endo-
scopic ultrasound (EUS) to visualize the biliary tree. Only after obstructing stones
are located and identified can ERCP and fluoroscopy be performed. Lee and
colleagues demonstrated that this approach led to fewer complications and allowed
for proper selection of patients which would benefit from ERCP [37].
Surgical Therapy
When a calculus within the common bile duct is unable to be retrieved endoscopi-
cally, a number of options exist. If the stone is partially obstructing, allowing the
passage of a plastic stent, that may be a temporizing measure to ensure proper flow
of bile. At some point, however, the patient will require removal of the offending
obstruction. This will need to be performed surgically in the form of a common bile
duct exploration, which can be performed laparoscopically or in an open fashion.
Typically, laparoscopic exploration is successful in 80–90% of patients, but does
require a skilled surgeon [56]. Laparoscopic exploration can be performed transcys-
tically when the stone burden is low (<5 stones), small (<0.8 cm), not located in the
common hepatic duct, and anatomy is favorable (i.e., cystic duct joins common bile
duct laterally and not medially) [57]. In cases where the stone is larger and more
impacted, a choledochotomy may be necessary to remove the stone [58]. Though
the number of laparoscopic common bile duct explorations is limited in the preg-
nant population, the case reports of such a technique have yielded successful out-
comes with no obstetric complications [43, 59].
Surgical Therapy After Endoscopy
The decision to operate after successful ERCP should be made on a case-by-case

basis. If ERCP was successful in stone removal and sphincterotomy was performed,
the necessity for emergent cholecystectomy to prevent future episodes may be mini-
mized. It seems more advantageous to delay cholecystectomy in this situation until
after delivery. On the other hand, if the patient seems to have continued symptoms
or develops acute cholecystitis, more immediate surgery should be performed [23].
Pancreatitis
Background
The incidence of pancreatitis in pregnancy varies between 1:882 and 1:4,449 preg-
nancies [60–64]. Despite the overall low number of cases in the literature, general
trends do arise. The most common causes of pancreatitis in pregnancy were related
to biliary etiology and hypertriglyceridemia. Acute pancreatitis related to a biliary
etiology was estimated 57–73% of the cases studied [46–49, 65]. A variety of less
common causes, including alcohol consumption, hypercalcemia, hyperparathyroid-
ism, trauma, anatomic variables, cystic fibrosis, medications, and idiopathic causes,
are also known to be causes [46, 49, 50]. There is a trend toward both mild and
176 F. Alemi et al.
severe pancreatitis presenting later in gestation [50], with 43–95% of cases in the
third, 5–33% in the second, and 0–24% in the first trimester [45, 46, 48, 50, 66, 67].
Several pregnancy-related risk factors have been identified which predispose one
to biliary pancreatitis. Weight gain and hormonal changes associated with preg-
nancy lead to increased biliary sludge and gallstone production [49, 68]. Hormonal
changes also lead to smooth muscle relaxation and bile stasis resulting in reduced
gallbladder motility [52]. It is thought that cholesterol secretion increases in the
second and third trimesters of pregnancy leading to saturated bile, and that while the
fasting and postprandial gallbladder volumes are greater, the emptying rate and vol-
ume are reduced [53]. After delivery with normalization of hormones, gallbladder
motility normalizes and the stones may disappear as biliary homeostasis is restored
[53].
Estrogen is believed to be related to increases in triglycerides during pregnancy,
with up to a fourfold increase in levels considered “physiological hyperlipidemia or
pregnancy” [69, 70]. Despite this rise, levels generally do not reach above 300 mg/
dL, and hypertriglyceridemia is more pronounced during the second and third tri-
mesters [55, 71]. Many cases of hypertriglyceridemic pancreatitis did not have pre-
gestational hyperlipidemia nor familial dyslipidemia [10]; however, an underlying
genetic predisposition, obesity, excessive weight gain, diabetes, alcohol consump-
tion, and some drugs may contribute to dyslipidemia [4, 6].
The overall majority of cases of acute pancreatitis were noted to be mild with
generally favorable maternal and fetal outcomes [45]. However, in cases of severe
acute pancreatitis more than 77% were caused by hypertriglyceridemia [51].
Nonbiliary pancreatitis was associated with more complications, worse outcomes
such as preterm delivery when compared to biliary pancreatitis as well [51, 54].
Others have reported biliary and idiopathic causes had better overall outcomes with
fewer incidences of organ failure and fetal mortality [50].
In patients with severe pancreatitis, despite the aggressive management
required—including mechanical ventilation, hemodialysis, percutaneous drainage,
chest drainage, and open necrosectomy—there are no maternal deaths reported
[54]. The organ systems most vulnerable to failure are respiratory, renal, and hepatic,
with renal and coagulation disorders denoting poor prognosis. Fetal death was more
likely when two or more organ systems were affected [50].
Diagnosis
The clinical presentation of acute pancreatitis often elicits complaints of epigastric,

right, or left upper quadrant pain, with associated nausea or emesis. The pain is
often constant with radiation to the back, chest, and flanks [72]. Despite the com-
mon complaints of nausea and emesis in pregnancy, any patient presenting with
prolonged nausea and emesis should elicit a pancreatitis workup [17]. Initial workup
begins with bloodwork including amylase, lipase, complete blood counts, metabolic
panel including liver function testing and a triglyceride level. Serum amylase and
lipase continue to be reliable markers during pregnancy, with lipase level unchanged
and amylase remaining normal or mildly elevated [53]. Elevation of serum lipase
and amylase to levels three times higher than normal has a good positive predictive
value [52]. Elevation of alanine aminotransferase to levels greater than three times
normal is a sensitive marker for a biliary etiology of pancreatitis [53]. Triglyceride
levels rise gradually and reach a peak during the third trimester, to almost twice
nonpregnant levels, then return to prepregnancy levels by 6 weeks postpartum [52].
Nonbiliary causes of pancreatitis have been found to produce worse outcomes and
thus screening for these etiologies is of particular importance [50, 55]. The use of
serum calcium and triglycerides, parathyroid levels, and discussions about alcohol
consumption allow for comprehensive assessment of etiology [46, 50, 55].
Abdominal ultrasonography is a safe and reliable way to diagnose biliary pancre-
atitis and identifies cholelithiasis or sludge in up to 70% of patients [48]. It can be
limited in detection of common bile duct stones; therefore, alternative imaging may
be considered when ultrasound or lab findings suggest choledocholithiasis despite
an inconclusive ultrasound [53]. Due to concerns of radiation exposure related to
computed tomography (CT) imaging and endoscopic retrograde cholangiopancrea-
tography (ERCP), magnetic resonance cholangiopancreatography (MRCP), and
endoscopic ultrasonography (EUS) should be considered for diagnosis [49, 52, 53].
Additionally, MRCP use can limit the use of ERCP to therapeutic procedures only
[53, 55], given concerns about radiation exposure to the fetus.
Treatment
Treatment of pancreatitis in pregnancy generally follows similar principles to that in

the nonpregnant population. Hospitalization is indicated for diagnosis, pain man-
agement, aggressive rehydration, electrolyte replacement, nasogastric decompres-
sion, and, in limited cases, hyperalimentation [17]. Following the American College
of Gastroenterology (ACG) guidelines, aggressive hydration is most beneficial and
of vital importance in the first 12–24 h [56], with lactated ringers as the choice crys-
talloid replacement fluid. Frequent reassessment within the first 48 h and use of
BUN, creatinine, and hematocrit as surrogate markers for successful rehydration are
standard means to follow the clinical course of pancreatitis.
Bowel rest is indicated though nutrition is of obvious importance to the pregnant
state. According to the ACG, bowel and pancreatic rest until complete resolution of
pancreatitis is no longer indicated. Current guidelines indicate that complete bowel
rest is associated with intestinal mucosal atrophy and increased infectious compli-
cations [56]. There is some suggestion that the frequency of maternal complications
secondary to central venous catheters is higher in the pregnant population [53].
While studies are limited in addressing this factor specifically during pregnancy,
general principles for the nonpregnant population recommend enteral feeding over
parenteral feeding when possible [56]. Enteral nutrition has recognized benefits
including maintenance of the gut flora and mucosal barriers, promoting of gut
immunity, and reduction of bacterial translocation [48, 54]. For patients with mild
pancreatitis, immediate refeeding with a soft, low-fat, low residual diet is safe and
178 F. Alemi et al.
may lead to shorter hospitalization than advancing through from the clear liquid diet
[56]. Early enteral nutrition (within 1–3 days) in severe pancreatitis was initiated in
a 2010 study where 18 of 69 cases were deemed severe, there were no maternal
deaths reported in the study nor feeding-related complications [54].
It is believed that early diagnosis, aggressive treatment and intervention, and
improvements in intensive care for both mother and fetus have played a role in the
decrease in morbidity and mortality associated with pancreatitis [55]. The main
causes of perinatal mortality were preterm delivery, while additional risks include
threatened preterm labor and in utero fetal death [52, 55]. Intensive fetal monitoring
has been suggested when recurrence or prolonged disease is encountered. This may
consist of nonstress testing and serial ultrasounds for fetal growth as well as bio-
physical profiles [17].
Biliary Etiologies
Definitive management of biliary pancreatitis includes the decision on timing of cho-
lecystectomy and disease management in the interim. Optimal timing of cholecystec-
tomy needs to be considered in the context of best outcomes for the mother and the
fetus, taking into account gestation age, recurrence rates, and pregnancy outcomes.
One-third of patients experienced between two and five recurrences during the same
pregnancy, with 50% of those in the biliary pancreatitis group who had been man-
aged conservatively experiencing recurrence [49]. Similar results were noted in other
studies which confirmed a higher relapse rate, as high as 55% [17, 47].
Given that recurrence of pancreatitis is more likely in patients with gallstone
pancreatitis [47], management strategies aimed at definitive intervention need to be
considered. The gestational age at which pancreatitis presents can assist with choice
of therapy [47]. As a surgical concept is it advisable to undertake surgical interven-
tion in the second trimester, when the fetus has completed the organogenesis of the
first trimester and while the uterus is still sufficiently small such as to avoid interfer-
ing within the surgical field. A simple algorithm devised by Swisher et al., suggests
that pancreatitis presenting in the first or third trimester be treated medically until
surgical intervention can be performed in the second trimester or postpartum period,
respectively; second trimester pancreatitis should be treated with surgical interven-
tion after initial resuscitation[47]. By this stratagem, there was no fetal or maternal
mortality attributed to surgical intervention, nor was there any difference in prema-
ture labor compared to the medically treated group.
ERCP with sphincterotomy and clearance of the bile duct offers an alternative
until surgical intervention is possible [52, 53]. A 2004 study on the safety of ERCP
during pregnancy with concurrent literature review concluded that with appropriate
monitoring and adjustments in technique to minimize fluoroscopy time, ERCP is
both safe and efficacious in pregnancy [73]. Other groups have reported an absence
of serious complications and a relative low (<5%) risk of fetal complications related
to ERCP [52]. The danger in not treating biliary pancreatitis surgically or endo-
scopically was highlighted by a 2008 study at 15 Midwestern hospitals, where
patients treated conservatively (without antepartum cholecystectomy or ERCP)
demonstrated significantly higher rates of fetal demise, preterm delivery, and recur-
rence of pancreatitis [46].
Delivery
Delivery has been suggested as a treatment option for severe pancreatitis, particu-
larly when organ failure in two or more systems was observed [50, 54]. With severe
disease serving as a surrogate for worse fetal outcomes, pregnancy termination may
improve maternal outcomes while allowing for enhanced fetal survival rates, by
removing the fetus from an environment with an increasingly mounting inflamma-
tory response [54]. It is thought that the state of hypovolemia, hypercoagulability,
and intimal inflammation may be associated with a decline in placental blood perfu-
sion, while pancreatitis may directly irritate the uterus leading to contractions [50].
Termination of pregnancy has been recommended in extreme cases when homeo-
static conditions cannot be achieved rapidly in the mother. While minimal discus-
sion exists regarding delivery methods during acute pancreatitis, it is suggested that
vaginal delivery is preferable to cesarean section where possible in order to limit the
risk of infection to any existing pancreatic necrosis [52].
Mesenteric Ischemia
Background
Mesenteric venous thrombosis (MVT) is the least common form of mesenteric isch-
emia, occurring in approximately 5% of the population, with an average age at
presentation of 45–60 years. However, in younger patients without cardiovascular
disease, it is the major cause of acute small bowel ischemia [74]. In a large percent-
age of patients with MVT, a previous history of deep vein thrombosis has been
reported, as well as underlying acquired and inherited risk factors that predispose
patients to the disorder. Local intraperitoneal inflammatory processes (i.e., pancre-
atitis, cirrhosis, and portal hypertension) and trauma generally affect the larger
veins, thereby increasing the risk of mesenteric thromboembolic complications,
while nephrotic syndrome, malignancy, and other systemic hypercoagulable states
generally affect the distal, smaller vessels. In pregnancy, high levels of factors VII-X
and fibrinogen reduced fibrinolytic activity, venous stasis, and blood pooling, and
other factors result in increased morbidity [58].
Underlying hereditary coagulopathies significantly increase the maternal risk of
thromboembolic episodes, including mesenteric and portal vein thromboses [75].
Additionally, repeated abdominal surgery, cesarean section, appendectomy, elective
laparoscopic cholecystectomy, inflammatory bowel disease (IBD), and continued
oral contraceptive use during gestation have all been associated with mesenteric
venous thrombosis in the absence of any heritable thrombophilia [58]. In the major-
ity of cases, MVT involves the distal small intestine (superior mesenteric venous
drainage) and rarely involves the colon, which drains through the inferior mesen-
teric vein.
180 F. Alemi et al.
Diagnosis
Early acute mesenteric venous thrombosis is characterized by the insidious onset of

diffuse, colicky abdominal pain that is out of proportion to physical examination.
Pain is often dull with a less sudden onset than other forms of acute mesenteric
ischemia, and 75% of patients with MVT report a least a 2-day history of symptoms
before pursuing medical care [76]. Nausea, vomiting, and abdominal distension are
common, and can be accompanied by gastrointestinal bleeding, diarrhea, and/or
leukocytosis, although the latter is a nonspecific finding in pregnancy and generally
does not aid in the diagnosis. In later stages, bowel edema, infarction, and necrosis
develop, and classic findings of peritonitis are observed.
Definitive diagnosis of mesenteric venous thrombosis is best seen with MR
venography, although CT with and without oral and IV contrast is the initial screen-
ing study of choice due to widespread availability. Findings suggestive of acute
mesenteric ischemia include the presence of venous filling defects or absent flow
in the mesenteric veins, severe bowel wall thickening (>3 mm) secondary to mural
edema and hemorrhage, and poor mucosal enhancement, suggesting infarction
[77]. Pneumatosis intestinalis, portal vein gas, and unexplained ascites may be
seen in patients with advanced ischemia. In pregnant patients with a nondiagnostic
CT and strong clinical suspicion of mesenteric vein thrombosis, CT angiography
with delayed imaging is recommended [58]. Suggestive findings on angiography
include late filling or thrombus in the superior mesenteric vein, arterial spasm, a
prolonged vascular blush, and reflux of IV contrast into the aorta due to resistance
to venous flow.
Treatment
Mesenteric venous thrombosis is generally managed conservatively, using systemic

anticoagulation, bowel rest, and serial abdominal exams [78]. Thrombolytics,
although used in nonpregnant patients, are not recommended during pregnancy
[79]. If mesenteric venous thrombosis without evidence of bowel infarction is con-
firmed or strongly suspected, therapeutic anticoagulation with low molecular weight
heparin (LMWH) or intravenous unfractionated heparin should be initiated imme-
diately. Initial dosing is weight based, with subsequent dose adjustments depending
on anti-factor-Xa levels and aPTT, respectively. Altered LMWH metabolism due to
the physiologic changes of pregnancy results in lower peak levels and a higher
clearance rate; thus, greater or more frequent doses may be required [63]. If heparin
is chosen as the initial agent, transition to therapeutic LMWH is appropriate after
several days. In patients with signs of bowel infarction or necrosis, surgical explora-
tion and resection of nonviable bowel are performed, with a goal of conserving as
much bowel as possible [80].
Therapeutic anticoagulation after an initial thrombotic event during gestation
should be maintained for at least 3 months. Postpartum, continued anticoagulation
is essential, as approximately one-third of thromboembolic events occur during the
puerperium until 6–12 weeks after delivery [58]. Transition to oral anticoagulants is

possible during this time. Although warfarin may appear in small amounts in breast
milk, it is considered compatible with breastfeeding and has not been associated
with adverse events in newborns [63]. In patients with a history of MVT or other
thromboembolic complication during pregnancy, hypercoagulable testing is recom-
mended for preconception management of subsequent pregnancies, including pro-
phylactic anticoagulation in certain high-risk populations.
Small Bowel Obstruction
Background
Small bowel obstruction (SBO) in pregnancy is the third most common cause of
acute abdomen in pregnancy, following acute appendicitis and acute cholecystitis
[81]. The incidence is estimated at 1:1500 to 1:16,000 [45]. The most common
cause is related to postsurgical adhesions, accounting for 50–60% of small bowel
obstruction [45, 82]. Other causes include volvulus, internal hernia, intussuscep-
tions, carcinoma, hernia, and appendicitis [45, 46, 83]. It is suggested by case stud-
ies that the majority of patients with small bowel obstruction have prior abdominal
or pelvic surgical history [84]. In patients who have had previous Roux-en-Y-gastric
bypass surgery, for instance, the majority of which are women of child-bearing age,
an internal hernia is a recognized complication. In a review of 46 cases of SBO in
pregnancy, 50% were found to be caused by adhesions, followed by volvulus 15%,
and internal hernia 13% [46].
A high index of suspicion is needed to diagnose bowel obstruction, as there is a
high rate of associated maternal morbidity, mortality, fetal loss, and premature
onset of labor, especially when diagnosis is delayed. The overall risk of fetal loss
is estimated to be as high as 17% [46]. It is estimated that only one-third of preg-
nant patients with bowel obstruction complete term pregnancies after operative
intervention [47].
Diagnosis
The most common presenting symptoms are the same as in nonpregnant patients,
including spasmodic abdominal pain, nausea and vomiting, abdominal distension,
and obstipation. A careful history and physical examination should be obtained
focusing on vital sign abnormalities, signs of sepsis, abdominal tenderness, and any
previous abdominal or pelvic surgeries, which will often point to a specific cause.
Abdominal wall laxity may delay peritoneal signs [85].
While the symptoms can be atypical, a pregnant patient with intractable vomit-
ing and new onset abdominal pain should be assessed with further imaging. A plain
abdominal radiograph will show dilated loops of bowel and air fluid levels [45, 86].
Abdominal ultrasound is often utilized for initial workup. Specific sonographic
182 F. Alemi et al.
findings include small bowel wall edema and diameter of >25 mm; a small bowel
transition point may also be visualized [87]. Ultrasound is thought to be more accu-
rate than X-ray; however, diagnosis is more difficult during pregnancy [88]. CT
scan may not be necessary for diagnosis, unless X-ray and ultrasound show no
abnormalities and clinical suspicion is still high. However, in patients with severe
abdominal pain, a CT scan should not be delayed if deemed necessary. MRI may
also be used and can help distinguish between adhesive disease and volvulus or
internal hernia which is more likely to require surgery [46].
Treatment
Treatment in the pregnant patient mirrors that of the nonpregnant patient with main-
stay conservative management of bowel rest, correcting fluid and metabolic derange-
ments, and nasogastric decompression. Treatment of hypovolemia and correction of
electrolyte abnormalities should also be prompt as fetal death from hypoxia second-
ary to maternal hypovolemia and shock has been reported [48]. Typically, if there
are no signs or symptoms of systemic illness to suggest impending bowel compro-
mise, then expectant management is initially undertaken. The decision to operate
will depend on patient clinical resolution of obstruction; those patients who fail to
resolve or worsen will necessitate surgical intervention.
However, in patients with signs of intestinal ischemia, peritonitis, worsening
pain, and imaging findings suggestive of bowel strangulation, urgent surgical explo-
ration is indicated. This is also especially true if peritonitis, closed loop obstruc-
tions, or volvulus is suspected. In these patients in whom bowel ischemia is
suspected, broad-spectrum antibiotics and resuscitation should immediately pre-
cede operative exploration.
The most common postoperative complication is premature labor [46]. In
patients with signs or symptoms of premature labor, tocolysis may be indicated
[48]. Early surgical intervention may decrease occurrence, as there is an association
between longer delays before surgery and premature labor [46]. Favorable fetal
outcomes are associated with early diagnosis, early surgical intervention when indi-
cated, and avoidance of maternal hypotension and hypoxia [48].
Hernias and Incarceration
Background
A hernia is a defect in the body wall and can occur through the body wall, dia-
phragm, pelvic floor, and through internal abdominal viscera [89]. Due to increases
in intra-abdominal pressure, abdominal wall hernias may become visible that are
not apparent in the nongravid state.
Inguinal hernias are rare in adult women, with a lifetime risk estimated at 3%,
and even more so in pregnant women, with prevalence estimated at 1:2000 [90, 91].
Umbilical hernias, caused by failure of closure of the umbilical ring, account for
about 10% of primary hernias in adults [92].
When hernias do occur in pregnant women, they present a unique challenge as
risk of incarceration could result in a high level of morbidity to the mother and fetus.
In a retrospective review, the occurrence of incarceration is exceedingly rare,
accounting for <5% of intestinal obstruction in pregnancy [93]. There have also
been reports of incisional hernias complicating pregnancy which can manifest as a
gravid uterus herniating through an incisional hernia [94].
Diagnosis
The diagnosis of inguinal hernia in pregnant women is made by the presence of

a new, symptomatic groin mass groin, which may or may not be reducible [90].
The differential diagnosis should include round ligament varicosities, lipoma,
vascular aneurysm, hematoma, and abscess [95]. Round ligament varicosities,
similar to inguinal hernia, can present with swelling and tenderness in the groin,
can be reducible, or nonreducible, and are more common in pregnancy due to
pelvic vein enlargement related to smooth muscle relaxation, increased venous
return, and pelvic venous obstruction from a gravid uterus; the diagnosis can be
confirmed with duplex ultrasound showing prominent venous plexus [96].
Patients are more likely to become symptomatic with groin or umbilical hernias
in the second trimester [56].
Treatment
Traditionally, hernia repair in pregnancy has been reserved for cases of strangula-
tion or incarceration. This has been supported by contemporary studies showing low
rates of incarceration with conservative measures, namely, weight loss, abdominal
binders, and stool softeners aimed at reducing intra-abdominal pressure [56]. In a
retrospective study of 12 gravid patients with hernia, a watchful waiting strategy is
supported for reducible groin masses, with a plan for postpartum herniorrhaphy.
This approach has been supported, as none of the patients followed had any periop-
erative or postoperative complications [56].
Colitis
Background
Inflammatory bowel disease(IBD) is among the most common causes of intestinal

inflammation in pregnancy. Two conditions, ulcerative colitis (UC) and Crohn’s
disease (CD), are the most common and their peak incidence occurs between ages
15 and 30, and therefore often affect women during pregnancy [97].
184 F. Alemi et al.
Compared to the general population, women with inflammatory bowel disease

are at risk for worse medical and pregnancy-related outcomes, such as preterm
birth, antepartum hemorrhage, and low birth weight infants. These patients should
be considered high-risk [98]. Active disease at the time of conception is associated
with an increased risk of active disease during gestation, contributing in part to
worse obstetric outcomes [99, 100]. The risk of relapse is highest in the first trimes-
ter, and up to one-third of patients with quiescent disease at conception relapse over
the course of their pregnancy and during the postpartum; this risk is especially high
among women with ulcerative colitis [101]. Preconception counseling should be
undertaken to identify risk factors and optimize control of disease activity, as well
as to discuss the potential risk of medications usage during pregnancy to maintain
remission.
Diagnosis
The diagnosis of IBD is typically made prior to pregnancy and is similar to those in
nonpregnant patients. During pregnancy, the gravid uterus makes physical examina-
tion difficult. Endoscopy may be indicated for the diagnosis of IBD or the manage-
ment of complications in patients with established disease. However, due to limited
evidence regarding safety and efficacy, it should generally be postponed until the
second trimester [102]. Similarly, limited evidence exists for colonoscopy in preg-
nant patients. Flexible sigmoidoscopy, however, is low risk in pregnancy in any tri-
mester, and can be done without colonic preparation or sedation.
Treatment
Ultimately, treatment depends on patient severity and disease process. Absolute

indications for surgery are the same as in nonpregnant patients, and include obstruc-
tion, perforation, severe hemorrhage, increasing transfusion requirements, acute
refractory colitis, and abscess formation. However, medical management should be
attempted whenever possible. Surgery in the gravid female has been associated with
higher rates of preterm labor and fetal loss (especially when peritonitis is present),
but there is limited data regarding the risk to pregnant patients with IBD [103].
In patients with fulminant colitis with or without toxic megacolon, prophylaxis
with broad-spectrum antibiotics is indicated in anticipation of perforation. High-
dose intravenous corticosteroids (hydrocortisone 400 mg/day or equivalent) should
be administered to treat the underlying inflammatory bowel disease, resulting in a
resolution of the majority of cases of fulminant colitis [85]. If colonic distension is
not resolved after 48 to 72 hours, colectomy is recommended before perforation
occurs. Other medications designed for treatment of ulcerative colitis or Crohn’s
disease should be avoided until the acute process has begun to resolve; even then,
their use may be limited in pregnancy due to adverse effects on the fetus. Patients
with symptomatic fistulas not amenable to bowel rest and spontaneous closure
should undergo resection of the affected intestine. In patients with colitis or colonic
hemorrhage requiring urgent or emergent surgery, subtotal colectomy with end-ile-
ostomy is the procedure of choice. Regardless of disease process, early surgical
consultation should be obtained to mitigate poor outcomes.
Diverticulitis
Background
Colonic diverticular disease represents a clinical condition often seen in developed

countries, although reports during pregnancy remain exceedingly rare [104, 105].
Generally seen in aging populations, its prevalence reaches about 75% in adults
over the age of 80 years. In young adults, diverticulosis is uncommon. As such, it is
not routinely considered in pregnant women with abdominal symptoms.
Small bowel diverticula are generally asymptomatic and found incidentally on
routine imaging studies. Like colonic diverticula, their incidence is increased with
age, and thus is rare in pregnancy. An exception in pregnant women is Meckel’s
diverticulum, which has been described in several case reports as a source of
abdominal symptoms [106].
Diagnosis
A very limited number of case reports have described right-sided colonic diverticu-
litis during gestation [89, 90]. Right-sided diverticula are more common in non-
Western countries, and most patients are younger compared to those with left-sided
disease. The majority are asymptomatic, likely due to increased fluid consistency of
stool in the right hemicolon. Decreased colonic motility in pregnancy can predis-
pose patients to constipation and diverticular inflammation, which most commonly
presents as localized abdominal pain in the right lower quadrant; other symptoms
include changes in bowel habits, nausea, anorexia, fever or chills, or urinary urgency
secondary to bladder irritation. Diagnosis is often difficult due to nonspecific symp-
toms, baseline elevation in white blood cell count during pregnancy, and decreased
peritoneal signs in the gravid female. Since right-sided diverticulitis mimics acute
appendicitis, accurate clinical diagnosis is difficult. Abdominal imaging with ultra-
sonography, computed tomography, or magnetic resonance imaging may be helpful,
and can be used in the pregnant patient.
Meckel’s diverticula are most commonly associated with gastrointestinal bleed-
ing due to the presence of ectopic gastric mucosa. Others remain asymptomatic or
may present with bowel obstruction secondary to torsion, incarceration, or peptic
ulceration. Obstruction and bacterial overgrowth can result in diverticular inflam-
mation, or perforation, with patients exhibiting symptoms similar to acute appendi-
citis with or without rupture. As with other causes of obstruction, abdominal
distension, nausea, vomiting, and obstipation are common presenting symptoms.
186 F. Alemi et al.
Abscesses and ectopic peptic ulceration, as well as Littre’s hernia—an incarcerated

Meckel’s diverticulum in an abdominal wall or internal hernia—can also occur.
Several imaging studies may be useful in establishing a diagnosis of Meckel’s
diverticulum. Similar to right-sided diverticula, Meckel’s can be found using ultra-
sonography followed by computed tomography or magnetic resonance of the abdo-
men and pelvis. Radionucleotide imaging with technetium 99 m (i.e., a Meckel’s
scan) can also be used during gestation, with whole fetal exposure doses of less than
0.5 rad, well within the known safe range of 0–5 rad throughout the course of preg-
nancy. Prior to performing the study, a nuclear medicine consultation should be
considered.
Treatment
Management of colonic diverticulitis depends on patient presentation, and ranges

from conservative antibiotic therapy to surgical resection. In the absence of frank
peritonitis or diffuse dissemination, conservative management (antibiotics and per-
cutaneous drainage) may be attempted, but data regarding outcomes are limited.
Surgical options include isolated diverticulectomy, ileocecal resection, or right
hemicolectomy. Concurrent appendectomy during surgical exploration is often rec-
ommended if the base of the appendix and cecum are not inflamed [107]. Abdominal
exploration and resection of the Meckel’s diverticulum is the treatment of choice.
Appendicitis
Background
Acute appendicitis is the most common cause of acute abdomen in pregnancy, and
the most common reason for nonobstetric surgical intervention [108]. The incidence
is estimated at 0.15–2.1 cases with appendicitis per 1000 pregnancies. Appendicitis
can occur at any time during pregnancy, though cohort studies suggest a preponder-
ance for the second trimester with reports of 40% of cases compared to 25% and
34% in the first and third trimesters, respectively [109, 110]. The perforation rate is
up to 25% higher if surgery is delayed, with rates reported of up to 65% when
delayed more than 24 h. In cases where the appendix is perforated, the rate of fetal
loss is up to 36% in comparison to 3–5% in cases of early diagnosis where the
appendix is nonperforated [53–55]. Therefore, early surgery is advisable to prevent
the morbidity associated with perforation.
Cohort studies have compared the rate of acute appendicitis during antepartum
and postpartum periods and have found pregnant women to be slightly less likely to
be diagnosed with acute appendicitis than nonpregnant women [111]. A case-
control of 53,000 age matched controls corroborated the inverse relationship
between pregnancy and appendicitis, especially in the third trimester [112].
Diagnosis
Appendicitis continues to be a diagnosis that is best made on clinical suspicion.

The most common presenting symptom is abdominal pain, which is located in
the right lower quadrant at McBurney’s point in the majority of cases, regardless
of trimester of pregnancy [113]. Abdominal guarding and percussion tenderness
may be more difficult to detect in the late stages of pregnancy due to abdominal
wall laxity [53]. The patient may also complain of nausea and vomiting; how-
ever, nausea by itself is common in normal pregnancy, especially during the first
trimester.
Attention has been given to diagnostic difficulties given the common atypical
presentation, and differentiating appendicitis among other common gastrointesti-
nal complaints of pregnancy. While a mild leukocytosis is common in pregnancy,
the mean WBC for patients with proven appendicitis is higher—16.4, compared
to 14 for patients without appendicitis [57]. Ultrasonography is often considered
a safe imaging modality in the workup of acute abdominal pain and can aid in the
differentiation of many gynecologic and nongynecologic intra-abdominal pro-
cesses. However, ultrasonography is often operator dependent, has a limited field
of view, and may delay diagnosis and treatment when inconclusive [114]. MRI
has the potential to give more diagnostic information, and simultaneously limit
radiation. Although ultrasound and MRI may be the primary imaging modalities
when evaluating pregnant patients with abdominal pain, when a rapid diagnosis is
necessary for a potentially lifesaving treatment, CT is the primary imaging tool as
it is rapidly available.
Treatment
The treatment of appendicitis is the same as in nonpregnant women, with prac-

tice guidelines supporting laparoscopy as safe and effective in any trimester of
pregnancy [115]. Access to the abdomen is based on the size of the uterus, with
both the use of the Hasson trocar and the Veress needle being supported as safe
approaches, although there have been reports of Veress placement into the
amniotic cavity resulting in fetal loss [116]. Historically, there has been con-
cern regarding the increase in intra-abdominal pressure during laparoscopy
resulting in decreased maternal cardiac output, as well as fetal acidosis from
carbon dioxide pneumoperitoneum. Current guidelines from the Society of
American Gastrointestinal and Endoscopic Surgeons report that routine blood
gas monitoring is sufficient and 10–15 mmHg intra-abdominal pressure should
be maintained. Intraoperative and perioperative fetal monitoring should be
used in pregnancies over 24 weeks. A normal appendix at the time of surgery
is an acceptable tradeoff given the high morbidity in pregnancy associated with
treatment delay.
188 F. Alemi et al.
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Urological Etiologies of Abdominal Pain
9
Joshua A. Broghammer and Marcus Austenfeld
Introduction
Urological causes of pain during pregnancy are common and can be caused by both
normal physiological changes of pregnancy and by newly acquired pathological
processes. Care of the pregnant patient must take into account the health of the
mother and the fetus. A firm understanding of the normal urological anatomical
changes during pregnancy will help with determining the etiology of the pain.
Imaging of the urinary tract must be done in a safe but efficient manner to minimize
the radiation exposure required to make the correct diagnosis. Finally, surgical
intervention can be performed when required with minimal risk to the mother and
fetus.
Physiological Changes to the Urinary Tract in Pregnancy
Lower Urinary Tract
Changes to the bladder are somewhat limited during the first trimester. As the preg-
nancy progresses, increased pelvic vascular congestion results in increased mucosal
vascularity. The bladder begins to change with a widening of the trigone, elevation
of the ureteral orifices, and compression of the bladder dome from the gravid uterus
[1]. Urodynamic studies during pregnancy reveal increased bladder pressures of up
to 20 cm H2O at term [2]. This increased pressure would normally result in episodes
of stress urinary incontinence, but there is a compensatory increase in urethral
length and urethral closure pressure as the pregnancy progresses [2]. In contrast,
J.A. Broghammer, MD, FACS (*) • M. Austenfeld, MD

Department of Urology, University of Kansas Medical Center, Kansas City, KS, USA

in Pregnancy, DOI 10.1007/978-3-319-62283-5_9
194 J.A. Broghammer and M. Austenfeld
those women who did experience more stress incontinence showed less overall
increase in urethral length and decreased urethral closing pressures [3].
Urinary frequency is considered normal during gestation and worsens as preg-
nancy progresses [1]. By the 12th week of gestation, urinary urgency and frequency
are at a high of 63% and 74%, respectively [4]. Nocturia occurs in over 90% of
women during gestation [5]. Lower urinary tract symptoms are common and quality
of life questionnaires indicate that nearly half of all women were generally dissatis-
fied with their urinary symptoms [6]. The majority of symptoms will resolve after
pregnancy but stress incontinence in early pregnancy and advanced maternal age
was predictive of stress incontinence a year after delivery. Urge incontinence was
found to be more predominant after Caesarean section [7]. Lower urinary tract
symptoms are commonplace during pregnancy and do not require treatment, but
other causes must be considered.
Upper Tract Changes
The kidney and collecting system undergo dynamic changes during gestation.
Pregnancy causes plasma volume expansion due to retention of sodium [8]. The
renal parenchyma begins to expand due to increased intravascular volume, and
uptake in renal perfusion contributes to an increase in renal length of 1 cm [9]. This
is not a true renal hypertrophy but rather an expansion of interstitial volume.
Pregnancy results in a state of renal hyperfiltration with a 80% increase renal plasma
flow by second trimester and an increase in glomerular filtration rate of 50% [10].
These changes result in an alteration in renal substrates and solutes processing.
The kidney is not the only genitourinary organ which increases in size. There is
a slow and steady dilation of the collecting system which occurs throughout
advancement of the pregnancy. The exact etiology for this is unclear. This is thought
to be due to several factors which are both mechanical and hormonal. Compression
of the ureters by the gravid uterus occurs above the pelvic brim, but the ureters
remain undilated distally, in the lower pelvis [11]. Interestingly, quadruped animals
do not develop hydronephrosis as the weight of the ureters is borne on the anterior
abdominal wall and is not seated in the pelvis. There is a more pronounced dilation
of the right side compared with the left side [12]. Many theories exist for this pref-
erential dilation including compression of the right ureter by the more dilated right
ovarian vein complex, dextro-rotation of the ureters, and cushioning of the left ure-
ter by the sigmoid colon [13, 14]. Progesterone likely plays a role as it stimulates
muscle atony in other organs during pregnancy. Van Wagenen et al. demonstrated
that the removal of a monkey fetus mid pregnancy with retention of the placenta
revealed continued ureteral dilation. This is not without controversy as the studies
were repeated by Roberts et al. Intraureteral pressure catheters were placed in rhe-
sus monkeys, and when upper tract ureteral pressures increased, laparotomy was
performed, the uterus was elevated off the ureters, and the pressure readings returned
to normal [15]. No matter what the etiology, hydronephrosis of pregnancy has
implications on clinical conditions causing pain in the pregnant patient.
9 Urological Etiologies of Abdominal Pain 195
Acute Urinary Retention
Acute urinary retention is rare among pregnant women. Patients present with the
inability to void, abdominal distention, and suprapubic pain. A population-based
study on Taiwanese women showed that the incidence of overall acute urinary reten-
tion (AUR) is 0.47% [16]. The peak risk of AUR occurred between the 9th and 16th
weeks. Preterm delivery posed the highest risks at 2.18% [16]. There have been
many case reports of a retroverted, incarcerated (impacted) uterus causing AUR
[17]. Physical exam findings include a low fundal height, fetal position deep in the
pelvis, and no detectable uterine cervix [18]. Ultrasound findings indicate that the
uterine fundus lies posterior to the cervix and the bladder is enlarged and distended
[19]. The mainstay of treatment is catheterization of the bladder and manual manip-
ulation of the uterus into its correct position. The use of a pessary has also been
described [17].
Infections of the Urinary Tract
Asymptomatic Bacteriuria
The incidence of asymptomatic bacteriuria (ASB) during pregnancy is roughly

2–7% [20, 21]. The definition of ASB is the development of 105 colony-forming
units of asingle bacterium on two consecutive voided cultures or alternatively, a
single catheterized specimen with 102 colony-forming units [22]. Women with dia-
betes mellitus and a previous history of urinary tract infection are at higher risk for
ASB [23] as well as those of lower socioeconomic status [24] and increased parity
[25]. The most common bacteria associated with ASB are coliform bacteria from
the gastrointestinal tract. Escherichia coli is the most common cause of ASB [26],
but other Gram-negative rods include Klebsiella, Enterobacter, Proteus, and
Pseudomonas are all associated [25, 26]. Group B Streptococci is the most common
Gram-positive bacteria) and is seen in up to 10% of ASB patients [25].
ASB has been associated with an increased risk of pyelonephritis in up to 30%
pregnant patients [27]. There is also an association with low birth weight and pre-
term labor [27]. Given these findings, both the United States Preventative Services
Task Force (USPTF) and the American College of Obstetricians and Gynecologists
(ACOG) recommend for the routine screening for ASB with a single urine culture
[28, 29]. The relationship between preterm labor and ASB is controversial and may
simply be a side effect of the increased risk of pyelonephritis with the associated
risk of systemic infection [25, 27]. A recent study in the Netherlands screened preg-
nant women in the 16th to 22nd week of pregnancy for ASB. Those with ASB were
randomized to treatment with nitrofurantoin versus placebo for 5 days. The authors
concluded that ASB did not create an increased risk for low birth weight, but the
study was underpowered to detect this difference. There was no difference in pre-
term labor rates between the groups. There was, however, a lower rate of
pyelonephritis in the treated cohort (0.6%) compared with the untreated, placebo
group (2.4%) [30].
Treatment of ASB is dependent on the organism detected during screening urine
culture and tailored to the safety in the current stage of pregnancy. Therefore, no
single agent can be recommended in all occurrences of ASB. The duration of treat-
ment is controversial, and many single dose regimens have been reported, but a
recent Cochrane database review suggests that a 7 day course of therapy is more
efficacious than shorter therapies. More studies are needed to determine actual cure
rates [31]. A repeat urine culture is recommended after a course of therapy to assure
clearance of the bacteria) [32]. Recurrent infections may suggest an anatomical
abnormality or other process, and thus, the recommendation is for a further urologi-
cal workup after delivery.
Acute Cystitis/Pyelonephritis
Acute cystitis is a symptomatic infection of the bladder. Symptoms are the same in
both pregnant and nonpregnant women and generally include dysuria, frequency,
and urgency. Systemic infections do not generally occur. Frequency is common dur-
ing pregnancy, and its presence alone should not be an indication of infection [1].
Dysuria is not a normal finding in pregnancy and as such should mandate an evalu-
ation. Microscopic hematuria is often positive on urinalysis. Gross hematuria may
be present in more severe cases of cystitis but is rare and necessitates a more exten-
sive urological workup including cystoscopy. A urinalysis with signs of pyuria indi-
cates an infection. All cases of cystitis can be treated with empirical therapy, but a
culture should be obtained to determine the causative bacteria. The duration of treat-
ment is similar to that of ASB and should be 7 days [31]. A repeat urine culture is
required after treatment to confirm clearance of the bacteria.
Pyelonephritis is associated with fever, flank pain, nausea, vomiting, and costo-
vertebral angle tenderness on examination. The incidence of pyelonephritis in preg-
nancy is 0.5% [33]. Women with pyelonephritis were more likely to be smokers,
present late for prenatal care, belong to African American and Hispanic populations,
and have less education [33]. Patients should be promptly evaluated, admitted to the
hospital, and administered intravenous antibiotics. A urine culture prior to initiating
antibiotic therapy is obtained. Parenteral antibiotics are continued until the patient
remains afebrile for 48 h. Transitioning to oral antibiotics can be performed once
culture-directed therapy is available. Twenty percent of patients will progress to
severe infections and develop septic shock [34]. Women with pyelonephritis suf-
fered more complications with their pregnancy including sepsis, anemia, acute
respiratory failure, acute renal failure, and preterm birth.
Those with complex urological histories such as renal stones, ureteropelvic junc-
tion obstructions, prior surgery on the urinary tract, and those not responding to
antibiotic therapy should be screened with upper tract imaging to rule out urinary
tract obstruction. Renal and bladder ultrasound serves as a safe baseline study that
poses minimal risk to the fetus. Cultures confirming clearance of bacteria should be
performed after treatment to reduce the risk of recurrence.
Hydronephrosis of Pregnancy
The ureters and renal pelvis undergo dilation in up to 80% of pregnant women [13].
This phenomenon is called hydroureter and hydronephrosis, respectively. The dila-
tion is more prominent on the right than the left. Ultrasonographic studies can dem-
onstrate these changes by the second trimester and may persist until 12 weeks
postpartum. The dilated ureters can retain as much as 200–300 mL of urine, produc-
ing stasis which can result in a bacterial reservoir, thus, contributing to an increased
risk of pyelonephritis during gestation.
Hydroureter and hydronephrosis in pregnancy may be a result of hormonal influ-
ences, physical compression, and intrinsic alterations in the walls of the ureters
[35]. In addition, high concentrations of progesterone reduce ureteral tone, peristal-
sis, and contraction pressure. The typical dextrorotation of the gravid uterus by the
sigmoid colon helps explain the more likely involvement of the right ureter. In some
cases, this effect can kink the right ureter as it passes over the right iliac artery.
Furthermore, the enlargement of the ovarian infudibulopelvic ligament vessels may
cause ureteral compression at the sacroiliac articulation. In addition, the gravid
uterus, as it enlarges, may produce elongations and tortuosity of the ureters, displac-
ing them more laterally. Albeit rare, these changes may produce maternal pain and
true urinary obstruction.
The connective tissue that surrounds the ureters (Waldeyer’s sheath) undergoes
hypertrophy which may have a protective effect of preventing hormone-induced
dilation below the pelvic brim [36]. Obstructive uropathy, from nephrolithiasis or
stricture, will produce ureteral dilation. This causes flank pain. Typically, it can be
distinguished from physiological hydronephrosis on imaging studies which may
identify a cause for obstruction.
Patients presenting with symptomatic hydronephrosis should be managed with
conservative measures including analgesics, hydration, and repositioning [37]. The
lateral decubitus position can help to unload the compressive weight of the gravid
uterus on the posterior pelvis and thus decompress the ureters. Multiple studies have
shown that conservative treatment is effective in over 90% of patients [38, 39].
Renal and bladder ultrasound is used to evaluate the severity of hydronephrosis and
the presence of obstruction. Ureteral jets are easily seen during pregnancy by per-
forming an ultrasound of the bladder [40]. The absence of a ureteral jet is consistent
with renal obstruction (Fig. 9.1). Color Doppler can aid in the diagnosis. A renal
arterial resistive index of >0.70 and a difference of 10% compared with the contra-
lateral kidney or reduced ureteral jet is indicative of ureteral obstruction [41].
Patients failing conservative treatment for symptomatic hydronephrosis and
demonstrating obstruction should be managed with the placement of an indwelling
ureteral stent [39], although this is not without controversy. One group reported that
the degree of hydronephrosis did not actually correlate with pain scores in patients
Fig. 9.1 Ultrasound of a pregnant patient presenting with flank pain, nausea, and vomiting with a
right-sided ureteral stone. Color Doppler indicates the loss of a right ureteral jet, consistent with
obstruction
presenting with flank pain [42]. Caution must be exercised in not underdiagnosing
obstructed patients with less severe forms of hydronephrosis. One case-controlled
study showed no difference between conservative treatment and ureteral stent place-
ment, noting that both had similar pain scores before therapy and a week after.
However, a randomized trial of conservative therapy or stent placement for symp-
tomatic hydronephrosis revealed that stent placement has a lower failure rate in
moderate to severe cases of hydronephrosis. The authors noted that 16% of patients
with ureteral stents complained of stent-related discomfort, and they felt that con-
servative management should be attempted first [43]. Rare cases of renal pelvis
rupture have been reported due to obstruction which can mimic normal symptom-
atic hydronephrosis of pregnancy [44]. This is also treated with ureteral stent
placement.
Pregnancy causes the bladder mucosa to become edematous and hyperemic.
High levels of progesterone cause bladder wall relaxation and increased bladder
capacity. However, the enlarging uterus displaces the bladder superiorly and anteri-
orly, thus, flattening it, and in effect, reducing capacity. The flaccidity of the bladder
may produce incompetence of the vesicoureteral valve. The combination of
increased intravesical and decreased intraureteral pressures may cause transient
vesicoureteral reflux [45, 46].
Nephrolithiasis
Symptomatic nephrolithiasis is a common nonobstetric cause of hospital admission

for pregnant patients [47]. Although the rates vary within the literature, roughly 1 in
1500 pregnancies is affected by stones, but the overall rate of symptomatic stones
remains the same between pregnant and nonpregnant women; 0.03–1% [48].
Presenting symptoms are similar to the general population: nausea, flank pain, uri-
nary frequency, microscopic, and even gross hematuria are common. The vast
majority of patients can be managed expectantly but cautiously; pregnant women
admitted for renal colic associated with kidney stones have a higher risk of preterm
delivery [49–51].
Beginning in the first trimester, gestational hydronephrosis is seen in 80% or
more of pregnant women and should resolve in the postpartum period [50]. The
right ureter is typically more dilated than the left, but symptomatic stone frequency
is the same bilaterally [52]. This is felt to be primarily the result of compression by
the dextrorotated uterus and dilation of the right ovarian vein, although serum pro-
gesterone levels may contribute to ureteric smooth muscle relaxation [53].
Hydronephrosis and resultant urinary stasis can produce a lithogenic environment.
Renal blood flow in pregnant women increases as does overall kidney size [54].
As the glomerular flow increases, the serum levels of creatinine, blood urea nitro-
gen, and uric acid decrease [55]. Pregnant women are at risk of stones due to this
increased urinary uric acid as well as increased calcium excretion, but the risk is
offset by excretion of other factors such as citrate and magnesium. Hypercalciuria
is secondary to the elevation of 1, 25-dihydroxyvitamin D in the maternal blood-
stream as the fetus removes calcium across the placenta; hypercalciuria is seen in all
trimesters but should return to normal levels after birth [56].
Although calcium oxalate stones are the most common type of kidney stone
regardless of age and gender, a greater proportion of women in childbearing years
develop calcium phosphate stones than at later ages. Studies of symptomatic preg-
nant women suggest that calcium phosphate stones are much more common than
calcium oxalate stones, at rates of 65–70% [57, 58]. The exact etiology behind this
difference is still under investigation, but it has been suggested that the increased
urinary calcium and slightly higher urine pH of pregnant women in the third and
second trimester, in addition to increased urinary stasis, may be linked.
The medical and surgical treatment of nephrolithiasis in the pregnant patient
should be coordinated between the urologist and obstetrician [59]. The rate of spon-
taneous passage of stones is high: from 64% to 81%, and pregnant women are often
able to pass stones at an increased rate compared with nonpregnant women [52, 58].
Due to the risks of anesthesia, conservative trials for passage with opiate pain medi-
cation are often recommended as a first-line intervention [59]. Tamsulosin, an
alpha-1a antagonist, is commonly prescribed as part of medical expulsive therapy;
in nonpregnant patients, it has been shown to decrease pain and decrease time to
stone passage [60]. It is rated as a pregnancy category B (no adequate and well-
controlled studies in pregnant women) by the Food and Drug Administration; thus,
its use in the pregnant population is controversial. Animal studies in rats and rabbits
demonstrated no evidence of fetal harm [61]. Data in pregnant women are sparse,
but Bailey et al. found that in a retrospective review of 27 women treated with
Tamsulosin for symptomatic stones, women on Tamsulosin had an increased rate of
spontaneous stone passage compared with controls without increased rates of
obstetric or perinatal complications [62]. The majority of women in the study had
symptomatic stones and subsequent Tamsulosin exposure in the second and third
trimester, consistent with usual stone presentation. While later use of Tamsulosin
would ideally prevent fetal exposure at the most vulnerable times of pregnancy,
Tamsulosin’s use for medical expulsive therapy in the pregnant patient is off-label
and must be associated with careful counseling between physician and patient, par-
ticularly before of the third trimester. The counseling must be accompanied by clear
documentation in the medical record.
Imaging options for the pregnant woman with flank pain and concern for stones
are often limited due to concern for fetal safety. Ultrasonography is a natural first-
line choice without any concern for side effects, although long durations of Doppler
signals can cause temperature elevations and should be limited during the first tri-
mester. Unfortunately, hydronephrosis is common in pregnant women and, espe-
cially in the late term, is not specific for nephrolithiasis and can have a sensitivity as
low as 34% in the detection of kidney stones [63]. The distal ureter can be evaluated
with transvaginal ultrasound; this is tolerable by patients and can complete the eval-
uation of the entire ureter; physiological compression of the ureter should not occur
below the pelvic brim in pregnancy [64]. Ureteric jets may be helpful in determin-
ing if a ureter is obstructed, although 15% of asymptomatic pregnant women may
not have detectable jets [65].
Noncontrast magnetic resonance imaging (MRI) avoids radiation exposure and
can help with stone identification as well. Although noncontrast computerized
tomography (CT) remains the most accurate imaging modality for stone identifica-
tion, MRI can detect a filling defect signifying a stone (Fig. 9.2) and also other
secondary signs that suggest the presence of nonphysiological obstruction [66]. A
standing column of urine within the ureter, ending at an abrupt transition point, is
indicative of obstruction (Fig. 9.3) [67]. Physiological obstruction is often more
tapered in shape and should not extend beyond the pelvic brim; perinephric and
periureteral edema, as well as pyelonephritis, can also be seen on MRI. In the mid-
dle of the night, however, on-call radiologists may not read MRI studies, and smaller
hospitals may not have MR imaging available. Gadolinium contrast increases the
specificity of MRI but is not recommended in pregnant patients; it is water soluble
and can cross the placenta into the fetal circulation. The risks to fetal exposure are
not known, but the American College of Obstetricians and Gynecologists recom-
mends against its use unless benefit clearly outweighs risk [68].
Noncontrast CT is an ideal method for imaging stones but exposes the fetus
directly to ionizing radiation. According to the ACOG guidelines, radiation expo-
sure through CT scans is much lower than the exposure associated with fetal harm,
and if the safety of the pregnant woman is in question, CT studies should not be
withheld from the patient. However, for routine imaging or equivocal cases where
ultrasound or MRI is possible, CT should be avoided. The American College of
Fig. 9.2 Magnetic resonance imaging (MRI) in a pregnant patient with a right-sided, symptom-
atic, obstructing stone. The arrow indicates a filling defect consistent with a proximal ureteral
stone
Radiology guidelines support these recommendations; the risks of fetal damage by

low-dose noncontrast CT are exceptionally low, particularly at doses of radiation
less than 100 mGy and/or after 15 weeks of conception [69].
Stone disease which is not responsive to hydration and analgesics requires surgi-
cal intervention [59]. Cystoscopy and stent placement rapidly relieve the ureteral
obstruction [37]. Likewise, those with obstruction and signs of urinary tract infec-
tion require emergent decompression via ureteral stenting. Septic patients with
hemodynamic instability should undergo percutaneous nephrostomy placement to
decompress the collecting system [70]. Percutaneous nephrostomy placement
avoids general anesthetic and can be performed under local analgesia. Ureteral stent
placement should be done using the ALARA (as low as reasonably achievable)
principles. Most urological cases can be performed with ultrasound guidance rather
than fluoroscopy [71–73]. In cases where fluoroscopy is required, it should be per-
formed with minimal fluoroscopy usage and lead shielding of the fetus (Fig. 9.4).
Once the stone is treated acutely, long-term management is dependent on the
risks associated with treatment and the stage of pregnancy. Ureteral stents placed to
Fig. 9.3 Reconstructed magnetic resonance imaging (MRI) in a pregnant patient with a right-
sided, symptomatic, proximal ureteral stone. The arrow indicates a fluid column in the right ureter
with an abrupt transition point and is indicative of obstruction
relieve the obstruction of stones typically last 3–6 months in a nonpregnant patient
before requiring replacement. In the pregnant patient, ureteral stent dwell times are
much shorter and may require frequent changes due to encrustation in a mere 4–6
weeks [59]. These stent changes lend themselves to increased exposure to both
anesthesia and radiation. A growing body of literature suggests that ureteroscopy
with holmium laser lithotripsy may be a safe and effective alternative to repetitive
stent changes [59, 74, 75]. Analytical models demonstrate that stone treatment with
ureteroscopy is more cost-effective than stent changes alone regardless of gesta-
tional age [76]. Ureteroscopic management should only be performed at centers
capable of providing specialty services and the ancillary equipment required to
handle pregnant stone patients [59].
Extracorporeal shock wave lithotripsy (ESWL) is commonplace in the treatment
of renal stones but is contraindicated in the pregnant patient. Larger stones in the
kidney which are not amenable to ureteroscopy should be managed expectantly
until after delivery in most cases. There are newer studies which indicate that percu-
taneous nephrolithotomy is feasible in the pregnant patient [70, 77]. Positioning of
Fig. 9.4 Lead shielding

placed over the mid and
lower abdomen during the
placement of a right
ureteral stent under
fluoroscopic guidance. The
arrow indicates a renal
stone
the patient in the prone position is difficult in the later stages of pregnancy. Complex
surgical intervention such as this should be left to centers of excellence familiar
with the technique and proper resources for both mother and fetus.
Summary
The genitourinary system undergoes extensive changes during pregnancy. Many

alterations of normal function such as infection, dilation, or obstruction of the uri-
nary tract, and formation of renal stones can all lead to abdominal pain in the preg-
nant patient. Imaging strategies use ultrasonography as the main modality with the
addition use of MRI when appropriate, minimizing fetal exposure to the risks of
ionizing radiation. Patient management is dependent on the stage of the pregnancy
and overall maternal health. Core principles include treatment of infection, drainage
of the collecting system, and treatment of the offending obstruction. The majority of
urological issues in the pregnant patient can be managed both safely and effectively
with minimal risk to both mother and child.
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Trauma During Pregnancy
10
Stanley M. Augustin, Maxwell Almenoff, and Aaron Sparks
Introduction
Trauma in pregnant women presents a unique problem. The addition of a second

patient adds a layer of complexity to management. Trauma is a significant cause of
morbidity and mortality to both the mother and fetus. Trauma represents the leading
cause of death in women under the age of 35 [1]. Six to seven percent of pregnancies
are complicated by trauma [2]. Common causes include motor vehicle collisions,
falls, and assaults. Trauma is a leading cause of death during pregnancy and is
related to 50% of maternal deaths [3]. The fetal death rate has been reported at 6.5
per 1000 live births [3]. The primary cause of fetal death is maternal death.
Trauma represents a significant burden to the pregnant patient and fetus. This
chapter will explore relevant anatomical and physiological changes, injury preven-
tion, injury patterns, initial and operative management, specific obstetrical compli-
cations, and outcomes.
In general, the initial management of pregnant trauma patients mirrors the man-
agement of nonpregnant trauma patients. The relevant differences and important
distinctions in the pregnant patient will be highlighted.
S.M. Augustin, MD, FACS (*)

M. Almenoff, MD • A. Sparks, DO

in Pregnancy, DOI 10.1007/978-3-319-62283-5_10
210 S.M. Augustin et al.
Anatomy and Physiology of Pregnancy
A complete discussion of the physiological changes in pregnancy is discussed else-

where. The relevant factors to the trauma patient are discussed here. The pregnant
patient can be expected to have increased minute ventilation. A study of the blood
gases will reflect the changes in ventilation. The pregnant trauma patient may have
an elevated diaphragm. Chest tube placement may need to be 1 to 2 intercostal
spaces higher in the pregnant patient. A decrease in lower esophageal sphincter
pressure increases the risk of aspiration. Early placement of a nasal or oral gastric
tube should be considered in those gravid patients who are without a protected
airway.
Cardiovascular vital signs are altered in the pregnant population. An increased
heart rate and altered blood pressures are considered to be normal physiological
alterations in gravid women. The blood pressure decreases in the first trimester and
reaches a low point in the second trimester. It returns to near normal in the third
trimester. However, attributing tachycardia and hypotension to normal physiology
represents a potential pitfall in the pregnant trauma patient. Plasma volume expands
and results in a relative anemia (RBC mass increases by a lesser value). Plasma
expansion increases the loss of blood volume necessary to cause clinical hypoten-
sion. A relatively “minor” blood loss results in shunting blood away from the pla-
centa. Thus, the fetus may be experiencing shock in a mother with normal or near
normal vital signs. The gravid uterus exerts pressure on the inferior vena cava and
decreases preload which can result in hypotension when supine.
Injury Prevention
Trauma represents a serious cause of morbidity and mortality in pregnancy. Simple

interventions, however, can protect both the mother and fetus. The utilization of a
seat belt is paramount in the pregnant patient. Correct placement and usage of both
the lap belt and the shoulder harness provide the best protection. The lap belt should
be placed under the abdomen and across the upper thigh. The shoulder harness is
placed between the woman’s breasts. Placing the lap belt across the abdomen may
result in injury to the uterus and fetus during motor vehicle collision. Nonuse of the
shoulder harness exposes the uterus to flexion/compression injuries and increases
risk of maternal injury. The greatest benefit of a seat belt is not being ejected from
the vehicle.
Domestic violence represents another source of trauma in the pregnant patient.
The incidence of domestic violence varies by study and may be as high as 30% [2].
The primary care physician, obstetrician, and trauma team have a duty to identify
and recognize warning signs (inconsistent injury/history, frequent hospital/ED/
office visits, substance abuse, depression, partner unwilling to leave during exami-
nation). Involvement of the appropriate agencies, interventions, and counseling pro-
vides safety to mother and fetus. In addition, substance abuse represents an increased
risk of trauma along with the additional negative side effects on the fetus. Screening
10 Trauma During Pregnancy 211
and intervention of at- risk individuals provide another opportunity to intervene

before a trauma occurs.
Injury Patterns
Pregnancy changes the patterns of injury in trauma. However, it does not affect the
morbidity or mortality. The changes in injury patterns include more severe abdomi-
nal injuries, higher percentage of extremity injuries, and less severe head injuries
[4]. Depending on the size of the uterus, the fetus may be more likely to be injured
than the mother. The incidence of trauma and the likelihood of injury to the fetus
increases with an increase in gestational age. Half of all traumas in the pregnant
population occur in the third trimester [5].
The most common cause of injury is blunt trauma as a result of motor vehicle
collisions, falls, assaults, automobile striking pedestrians, and domestic violence.
Penetrating injuries include stab wounds, gunshot wounds, and impalement.
Stabbing wounds are generally better tolerated than gunshot wounds [2]. Domestic
violence is common during pregnancy with a rate of 10–30% [3]; fetal death occurs
in 5% of these cases [3].
Imaging Issues
Trauma patients frequently require multiple imaging modalities. Exposure of the

fetus to ionizing radiation represents an obvious concern. However, the risk of ion-
izing radiation should not outweigh the benefits of imaging in pregnant trauma
patients. The imaging necessary to identify injury and treat the mother is obtained.
The threat of a missed or misdiagnosed injury represents great harm to the mother
and fetus. Despite the concern about ionizing radiation, routine imaging in pregnant
trauma patients presents a low risk to the fetus. The typical dose of ionizing radia-
tion to the fetus in a CT study of the abdomen and pelvis is 25 mGy [6]. The dose
may be lower with modern CT scanning and the use of automated exposure control
[6]. “In 1977, the National Council of Radiation Protection and Measurement issued
the following policy statement with regard to radiation and pregnancy: ‘The risk [of
abnormality] is considered to be negligible at 50 mGy or less…’” [6]. The American
College of Obstetricians and Gynecologists offered a similar statement in 2004:
“Women should be counseled that x-ray exposure from a single diagnostic proce-
dure does not result in harmful fetal effects. Specifically, exposure to less than 5 rad
[50 mGy] has not been associated with an increase in fetal anomalies or pregnancy
loss” [6]. Routine trauma imaging does not appear to increase the risk of radiation-
induced diseases. However, it is prudent to limit exposure without compromising
patient care. Shielding the uterus is appropriate, when possible, and limitation of the
number of nonessential radiographic studies is advisable.
Primary and Secondary Survey
The gravid uterus does not alter the primary survey of the injured patient. The
mother takes precedent over the fetus. Standard trauma resuscitation utilizes the
ABCDE’s to identify and treat life-threatening injuries. A patent airway is con-
firmed or secured based on the patient’s clinical status. Supplemental oxygen is
administered to prevent maternal and fetal hypoxia. Breath sounds are auscultated
bilaterally (and confirmed with a chest X-ray as an adjunct to the primary survey).
Pulses are palpated, and hemorrhage is controlled to confirm and protect cardiovas-
cular circulation. The liberal use of intravenous fluids and blood products should be
administered through large bore peripheral intravenous accesses. The physiological
volume expansion of pregnancy can obscure hypovolemia so a clinically high index
of suspicion is required to assess fluid status. The gravid patient should be placed on
their left side to avoid obstruction of the inferior vena cava. Alternatively, if the
patient must be maintained on a backboard due to concern for spinal injury, a wedge
can be placed under the patient’s right hip and flank. A rapid neurological assess-
ment provides a measure of disability. The patient is rolled and completely exposed
to identify further injury.
The secondary survey contains a head-to-toe physical examination as in the non-
pregnant patient. Injuries should be identified and addressed. The secondary survey
should contain a thorough obstetrical history and formal pelvic examination unless
vaginal bleeding is observed. An obstetrical consultant should be obtained and
remains readily available to the trauma team.
It is important to identify vaginal lacerations/bleeding, fluid indicating possible
rupture of membranes, early contractions/labor, placenta previa, placental abrup-
tion, prolapsed cord, and any fetal heart rate abnormalities. If available, sonography
of the abdomen should be liberally applied.
The initial fetal evaluation takes place after the mother’s primary survey and
stabilization. It is important to initially establish an estimation of the gestational
age. The gestational age addresses the important question of viability and dictates
management. Fetal heart rate auscultation, fundal height measurement, presence of
and frequency of contractions and sonographic evaluation of the placenta and fetus
are important aspects of the evaluation [1]. Early initiation of continuous electronic
fetal monitoring is important way to assess fetal distress [7].
The diagnostic workup for the mother should proceed in a manner to address her
injuries. Routine trauma lab studies should be obtained. In addition, Kleihauer-Betke
acid elution testing (KB) should be performed and Rho(D) immune globulin given if
appropriate. KB testing helps to identify those patients at higher risk of abruption and
preterm labor [5]. Radiographic imaging should be obtained as indicated by the
mother’s injury pattern, just as for a nonpregnant patient. Ultrasound can be used to
evaluate the fetal gestational age and injuries and assess amniotic fluid volume.
Continuous electronic fetal monitoring is the standard of care in patients with a via-
ble fetus. Monitoring should be a minimum of 6 h in the absence of no concerning
findings and up to 24–48 h with uterine contractions, nonreassuring fetal heart rate
patterns, vaginal bleeding, uterine tenderness, and rupture of membranes or with
serious maternal injury [5]. The setting for continuous fetal monitoring depends on
the mother’s injuries and may include the intensive care unit, operating room, and/or
obstetrical unit.
Operative Intervention
The operative indications are the same for the pregnant and nonpregnant trauma
patients. The presence of a gravid uterus should not alter the decision to proceed
with exploratory laparotomy. Penetrating abdominal trauma violating the peritoneal
cavity should proceed to the operating room. Some penetrating trauma (knife
wounds not penetrating peritoneum) may not need laparotomy. Blunt abdominal
trauma with a positive physical exam (peritonitis), hemodynamic instability, and
those patients requiring continuing resuscitation should proceed to laparotomy.
Specific findings on CT scan may dictate further management per trauma guide-
lines. The fetus should tolerate the operation well, if appropriately resuscitated [1].
It is paramount that the mother, and by extension the fetus, receive appropriate
resuscitation. The operation should proceed as in a nonpregnant patient. The tenets
for operative intervention include hemorrhage control, contamination control, iden-
tification of injuries, and repair/reconstruction. An important distinction includes
management of the injured uterus. In a viable pregnancy, abdominal delivery should
be considered in patients with an injured uterus and evidence of fetal intolerance to
the intrauterine environment [1]. The injured uterus can then be repaired or excised
if necessary. If the pregnancy is nonviable, the uterus can be repaired and managed
expectantly in many cases [1].
Obstetric Emergencies in Trauma
Abruption of the placenta is the 2nd most common cause of fetal death in trauma
patients [2]. Placental separation represents a cause of significant morbidity and mor-
tality to the fetus. The rate of placental abruption is 5% in minor injuries and increases
to 50% in patients with severe injuries [2]. The overall fetal mortality rate may be as
high as 60% [2]. Placental abruption, of clinical significance usually presents within
24–48 h after the initial trauma [2]. As in nontrauma patients, symptoms include pain-
ful vaginal bleeding. It can lead to premature labor and disseminated intravascular
coagulation. Continuous fetal monitoring is the most sensitive diagnostic test and
should be maintained for a minimum of 6 h per Eastern Association for the Surgery of
Trauma (EAST) guidelines [5]. In the absence of symptoms, monitoring can be
discontinued after 6 h [4]. Ultrasound can also aid in diagnosis but does not rule out
abruption in some cases secondary to low sensitivity [4].
Uterine rupture represents a rare event and occurs in less than 1% of traumas [4].
The most significant risk factor for rupture is a prior cesarean section [4]. It occurs
after direct abdominal trauma in the late second and third trimesters. The maternal
mortality rate approximates 10%, and the fetal morality approaches 100% [2].
Physical examination demonstrates abdominal tenderness, uterine irregularity, and

palpable fetal parts. Early recognition may increase maternal survival. The treat-
ment is emergency laparotomy and possible hysterectomy.
Fetal injury should be suspected when the uterus has sustained a penetrating
injury. The fetus is injured in 2/3 of cases with penetrating uterine trauma [1]. Fetal
skull and brain injury are common in pelvic fractures when the head is presenting at
the pelvic inlet and is engaged in the pelvis [1].
Umbilical cord prolapse into the vagina can occur with spontaneous rupture of
membranes when there are no fetal parts engaged in the pelvis. The potential
sequelae include fetal hypoxia and death. The treatment is emergent abdominal
delivery for viable gestations.
Urgent abdominal delivery is considered on an individualized basis. Abdominal
delivery should be considered in all patients over 26 weeks with fetal intolerance to
the intrauterine environment [2]. The risk of prematurity should be weighed against
the fetal compromise and need for delivery. Other indications for delivery include a
gravid uterus preventing repair of maternal injuries, unstable spinal injuries, and if
maternal demise is imminent [2]. In the event of maternal death or failure of resus-
citation, emergent abdominal delivery should be considered in all fetuses over
24 weeks [2]. The best results occur if the fetus is delivered within 4 min of maternal
demise [5].
Outcomes
Trauma is a leading cause of maternal death and accounts for over 5% of fetal
deaths. Interestingly, the overall morbidity rates are similar to those of nonpregnant
patients and the mortality rate of pregnant patients may actually be lower in the set-
ting of trauma [4, 7, 8]. Pregnancy-related morbidity occurs in approximately 25%
of trauma patients [9]. Maternal mortality is associated with amniotic fluid embo-
lism, deep vein thrombosis/pulmonary embolism, and infections [3]. Even pregnant
patients with minor traumatic injury have increased risk of preterm delivery and a
low birth weight infant [4]. Trauma patients should be monitored more closely
throughout their pregnancy as the associated risks are both short and long term [10].
The maternal injury severity score correlates well with adverse fetal outcomes. A
score of over 25 is associated with a 50% fetal mortality rate. Risk factors for fetal
death include maternal death, overall maternal injury, ejection from a motor vehicle,
pelvic fracture, severe abdominal injury, and hemorrhagic shock. Maternal shock is
associated with preterm labor and fetal intolerance to the intrauterine environment
resulting in an 80% fetal mortality [5].
The presence of disseminated intravascular coagulation represents a major pre-
dictor of fetal mortality and consideration should be given to imminent delivery of
a fetus with viable gestational age [4]. Additional factors associated with fetal mor-
tality include decreased Glasgow Coma Scale, maternal acidosis, decreased serum
bicarbonate, maternal hypoxia, fetal heart rate under 110 beats per minute, maternal
malperfusion, maternal death, pelvic fracture, ejection from a vehicle, direct utero-
placental injury, and severe maternal head injury [3, 4]. Composite morbidity mod-
els using third trimester trauma, hospital length of stay greater than 2 days,
abdominal trauma, an injury severity score of greater than 2, or a positive Kleihauer-
Betke test identifies those at risk for adverse perinatal outcomes [11]. Both major
and minor injury places the fetus at increased risk for fetal demise, premature
delivery, and low birth weight [12].
Summary
Trauma represents a significant cause of morbidity and mortality in pregnancy.

The presence of a second patient presents unique management challenges. However,
the initial management of a pregnant trauma patient is unchanged. The mother
should be treated as in a nongravid patient. A good outcome for the mother is the
best chance for fetal survival.
References
1. Grimes J, Rosenbaum F. Trauma in the pregnant patient. In: Eastman AL, Rosenbaum DA,
Thal E, editors. Parkland trauma handbook. 3rd ed. Philadelphia: Mosby; 2009. p. 403–9.
2. Tsuei BJ. Assessment of the pregnant trauma patient. Injury. 2006;37(5):367–73.
3. Petrone P. Trauma in pregnant patients. Curr Probl Surg. 2015;52(8):330–51.
4. Cusick SS, Tibbles CD. Trauma in pregnancy. Emerg Med Clin North Am. 2007;25(3):
861–72. xi
5. Barraco RD, Chiu WC, Clancy TV, Como JJ, et al. Injury, infection, and critical care: practice
management guidelines for the diagnosis and management of injury in the pregnant patient:
the EAST practice management guidelines work group. J Trauma. 2010;69(1):211–4.
6. Sadro C, Bernstein MP, Kanal KM. Imaging of trauma: part 2, abdominal trauma and
pregnancy – a radiologist's guide to doing what is best for the mother and baby. AJR Am
J Roentgenol. 2012;199(6):1207–19.
7. Shah AJ, Kilcline BA. Trauma in pregnancy. Emerg Med Clin North Am. 2003;21(3):615–29.
8. John PR, Shiozawa A, Haut E, Efron D, Haider A, Cornwell E. An assessment of the impact of
pregnancy on trauma mortality. Surgery. 2011;149(1):94–8.
9. Einav S. Management and outcomes of trauma during pregnancy. Anesthesiol Clin.
2013;31(1):56–141.
10. Melamed N, Aviram AW, Silver M, Peled Y, Wiznitzer AM, Blezerman MB, Yogev

Y. Pregnancy course and outcome following blunt trauma. J Matern Fetal Neonatal Med.
2012;25(9):1612–7.
11. Trivedi NN, Ylagan M, Moore TR, Bansal V, Wolfson T, Fortlage D, Coimbra R,

Kelly T. Predicting adverse outcomes following trauma in pregnancy. J Reprod Med.
2012;57(1-2):3–8.
12. Fischer PE, Zarzaur BL, Fabian TC, Magnotti LJ, Croce MA. Minor trauma is an unrecog-
nized contributor to poor fetal outcomes: a population-based study of 78,552 pregnancies.
J Trauma. 2011;71(1):90–3.
Recommended Reading
George ER, Vanderkwaak T, Scholten DJ. Factors influencing pregnancy outcome after trauma.
[Review], American Surgeon. 58(9):594–8.
Patrone P, Talving P, Browder T, Teixeira P, Fisher O, Lozornio A, Chan L. Abdominal injuries in
pregnancy: a 155 month study at two level 1 trauma centers. Injury. 2011;42(1):47–9.
Vladutiu CJ, Marshall SW, Poole C, Casteel C, Menard KM, Weiss HB. Adverse pregnancy
outcomes following motor vehicle collisions. Am J Prev Med. 2013;45(5):36–629.
Surgical Principles in the Gravid Female
11
Introduction
Surgical intervention in the gravid female does not appreciably result in adverse
outcome for the mother or the fetus. Risks may be increased, however, if complica-
tions arise. For example, peritonitis from a perforated appendix produces significant
maternal and fetal morbidity and mortality, despite appropriate anesthesia and sur-
gical intervention. Nonetheless, gravid women do not seem to have significant
untoward complications when compared with non-gravid women undergoing simi-
lar procedures [1].
General Principles
Nonobstetric surgery during pregnancy is a significant issue for providers who care
for women. Large-scale randomized clinical trials in this population are difficult to
perform; therefore, no data are available to allow for specific recommendations.
It is important for a provider to seek obstetrical consultation prior to performing
nonobstetric surgery and certain invasive procedures (e.g., cardiac catheterization or
colonoscopy) because obstetricians are uniquely qualified to discuss aspects of
maternal physiology and anatomy that may affect intraoperative maternal–fetal
well-being.


in Pregnancy, DOI 10.1007/978-3-319-62283-5_11
218 P.B. Greenspan
The following generalizations outlined in American College of Obstetricians and

Gynecologists (ACOG) Committee Opinion #696 may be helpful to guide
decision-making:
• No currently used anesthetic agents have been revealed to have any teratogenic
effects in humans when using standard concentrations at any gestational age.
• Fetal heart rate monitoring may assist in maternal positioning and cardiorespira-
tory management and may influence a decision to deliver the fetus [2].
The following recommendations represent the consensus of the ACOG

committee:
• A gravid woman should never be denied indicated surgery, regardless of

trimester.
• Elective surgery should be postponed until after delivery.
• Whenever possible, nonurgent surgery should be performed in the second tri-
mester when preterm contractions and spontaneous abortion are least likely [2].
When nonobstetric surgery is planned by a nonobstetric provider, an obstetric

care provider should be consulted, if possible. If such a health care provider is not
at the institution where surgery is to be performed, another obstetric care provider
with privileges at another institution should be involved.
If fetal monitoring is to be used, consider the following recommendations:
• Surgery should be done at an institution with neonatal and pediatric services.

• An obstetric care provider with cesarean delivery privileges should be readily
available.
• A qualified individual should be available to interpret the fetal heart rate
patterns.
General guidelines for fetal monitoring include the following:
• If the fetus is considered previable, it is usually sufficient to determine the fetal

heart rate by Doppler before and after the procedure.
• If the fetus is considered to be viable, simultaneous electronic fetal heart rate and
contraction monitoring should be performed before and after the procedure to
assess fetal well-being and the status of contractions.
Intraoperative electronic fetal monitoring may be appropriate when all of the fol-
lowing apply:
1 . The fetus is viable.

2. It is physically possible to perform intraoperative electronic fetal monitoring.
3. A health care provider with obstetric surgery privileges is accessible and willing
to intervene during the surgical procedure for fetal indications.
11 Surgical Principles in the Gravid Female 219
4. When possible, the gravida should be given informed consent for emergency
cesarean delivery.
5. The nature of the planned surgery will allow the safe interruption or alteration of
the procedure to provide access to perform emergency delivery.
In select circumstances, intraoperative fetal monitoring may be considered for

previable fetuses to facilitate positioning or oxygenation interventions.
The decision to use fetal monitoring should be individualized and, if used, should
be based on gestational age, type of surgery, and facilities available. Ultimately,
each case warrants a team approach (anesthesia and obstetric care providers, sur-
geons, pediatricians, and nurses) for optimal safety of the woman and the fetus.
Optimal Timing for Surgery
There are little data to support optimal timing for surgery in a gravid woman.
Modern surgical practice, combined with extremely safe anesthesia support and an
understanding of maternal and fetal physiology, allows for surgery to occur essen-
tially at any time during gestation.
Conventional wisdom and experience point to the optimal timing for nonemer-
gent surgery occurring between 16 and 20 weeks. This allows time for resolution of
benign cysts and reduces rates of preterm labor associated with surgery later during
pregnancy [3].
Consideration of Delivery of the Fetus
The delivery of the fetus in an acutely ill surgical patient is incumbent on multiple
factors. One important consideration is the morbidity that the condition is producing
in the gravid woman. The physiological alterations that result in the disease process
may impose physiological limitations on the mothers’ ability to oxygenate her fetus.
Hemodynamic status of the mother is an important consideration.
Proper positioning of the gravida during surgery is imperative. The operative
management of pregnant patients must include interventions that prevent maternal
hypotension, hypoglycemia, hypothermia, and hypoxia.
The Four H’s of surgery on pregnant patients:
1. Prevent maternal hypotension
2. Prevent maternal hypoglycemia
3. Prevent maternal hypothermia
4. Prevent maternal hypoxia
The patient should be positioned in a partial left lateral tilt to reduce pressure on
the vena cava and maintain adequate venous return. Reese and Willis determined
that a tilt at 27 degrees was optimal for cardiopulmonary resuscitation and would
also be sufficient for general operative procedures on patients beyond the first
220 P.B. Greenspan
trimester [4]. This concept is universally practiced in the abdominal delivery of

fetuses at term or otherwise, for any indication mandating delivery.
The Swedish Birth Registry as described by Mazze and Källén provides the most
extensive data regarding anesthetic and surgical risks to pregnant women [5]. The
analysis of the effects on pregnancy outcomes of 5405 nonobstetrical surgical pro-
cedures performed in 720,000 pregnant women from 1973 to 1981 was reported.
General anesthesia was administered for approximately half of these procedures
and frequently involved nitrous oxide supplemented by another inhalation agent or
intravenous medications. These procedures were performed on 41 percent of women
in the first trimester, 35 percent in the second, and 24 percent in the third (Fig. 11.1).
Twenty-five percent were abdominal operations, and 20 percent were gynecological
or urological procedures. The most frequently performed procedure was laparos-
copy, and appendectomy was the most common second-trimester procedure.
Increased perinatal morbidity related to nonobstetrical surgery is often attribut-
able to the underlying disease process rather than to adverse effects of surgery and
anesthesia. The Swedish Birth Registry again provides valuable data [5].
The incidence of newborns with congenital malformations or those stillborn
was not considerably different from that of nonexposed control neonates.
However, there were significantly increased incidences of low birth weight, pre-
term birth, and neonatal death in infants born to women who had undergone
surgery. Increased neonatal deaths were mainly due to preterm birth. These
investigators concluded that these adverse outcomes likely were due to a syner-
gistic effect of the maternal morbidity in conjunction with the surgical proce-
dures. Hong reported that there was an increased preterm delivery rate in 235
women undergoing adnexal mass surgery [6].
1st Trimester
800
2rd Trimester
700 3rd Trimester
600
500
400
300
200
3rd Trimester
100
0 2rd Trimester
Abdominal
GU/GY 1st Trimester
Laproscopic
Endscopy
Fig. 11.1 Percentage of surgical procedures by trimester

The Role of Minimally Invasive Technologies
Pelviscopy, originally termed laparoscopy, was considered to be absolutely contra-

indicated in pregnancy until 1990. Nezhat et al. reported the first pelviscopic cystec-
tomy in a gravid woman in 1991. Technology since then has led to the development
of myriad endoscopic procedures as the safety of the technique in the pregnant
population has been very widely appreciated [7].
Pelviscopy is now considered the standard of care in the management of much of
the pathology in the gynecologic and obstetric populations. Examples include total
pelviscopic hysterectomy, salpingectomy, oophorectomy, endometriosis resection,
ovarian cystectomy, appendectomy, bowel resection, and ovarian detorsion. Several
müllerian anomalies may be managed pelviscopically. Single-incision pelviscopy is
emerging as an even less invasive operative intervention in treating the array of
gynecological pathologies that afflict women.
Fatum et al. have shown that the benefits of pelviscopy in the nonpregnant patient
can be applied to the gravid woman [8]. The pelviscope affords a magnified,
improved, and wide view of the operative field. The smaller incisions for the ports
into the abdomen result in lesser postoperative pain and more rapid postoperative
recovery. Reduction in postoperative pain leads to a decreased postoperative nar-
cotic consumption, earlier ambulation, and a reduced risk of thromboembolism.
Fetal depression is also less likely with reduced maternal narcotic use. Bowel
manipulation is usually minimal during pelviscopy, which benefits a quicker return
to bowel function, and a possible diminution in postoperative adhesions, ileus, and
bowel obstruction [9–11]. The smaller scars from pelviscopy result in less inci-
sional hernias, lower the risk of wound complications, and create less opportunity
for wound dehiscence as the gravid uterus distends the abdomen. Women undergo-
ing pelviscopic procedures also experience shorter hospital stays and promptly
return to regular activities [12].
Visualization and performance of pelviscopic procedures require pneumoperito-
neum. The cardiovascular and respiratory adaptations observed with pneumoperito-
neum during laparoscopy are heightened in the pregnant patient compared with the
general population [13]. The combination of the enlarging uterus which mechanically
displaces the diaphragm together with pneumoperitoneum produces decreased com-
pliance of the thoracic cavity, a decrease in the functional reserve capacity, an increase
in peak airway pressure, ventilation–perfusion mismatching, increased alveolar–arte-
rial oxygen gradient, and increased pleural pressure. These changes are further accen-
tuated by the Trendelenburg position commonly employed in pelviscopy [9, 13, 14].
The arterial carbon dioxide partial pressure is increased with pneumoperitoneum
because of absorption of carbon dioxide from the peritoneal cavity. This increase and
the concomitant decrease in arterial pH is of concern in that it may adversely affect the
fetus because fetal arterial CO2 is directly related to maternal arterial CO2. Bhavani-
Shankar et al. investigated this in eight gravid women at 17–24 weeks’ gestation that
underwent pelviscopic surgery with carbon dioxide pneumoperitoneum [15]. The
minute ventilation was adjusted to keep the end tidal CO2 at 32 mmHg, and arterial
blood gas was measured at preinsufflation, insufflation, postinsufflation, and
222 P.B. Greenspan
postoperatively. There were no differences observed in the partial pressure of arterial

CO2 to end-tidal CO2 gradient, or the partial pressure of arterial CO2 and pH during
the different phases of monitoring. The investigators concluded that end-tidal CO2
correlated with arterial CO2 and that optimal maternal arterial CO2 could be main-
tained during pelviscopy by adjusting minute ventilation. Blood gas monitoring may
not be necessary in healthy patients undergoing pelviscopy [15].
Cardiovascular and hemodynamic changes that occur with pneumoperitoneum are
the result of a combination of the physiological effects of patient positioning, anesthe-
sia, and carbon dioxide absorption. Insufflation decreases cardiac output, with a con-
comitant increase in systemic and pulmonary vascular resistance and blood pressure
[13, 16]. The reverse Trendelenburg position has been shown to intensify the cardio-
vascular changes observed with general anesthesia and pneumoperitoneum with a
reduction in the cardiac index of up to 50%. Significant hypotension is also detected
resulting from aortocaval compression by the pregnant uterus in conjunction with the
other cardiovascular changes induced by pneumoperitoneum [13, 16]. After 15 min of
insufflation, a study investigating the hemodynamic changes in laparoscopic surgery
in pregnant women revealed that the cardiac index dropped to 21% below baseline.
Systolic blood pressure 20% below baseline was aggressively managed with intrave-
nous ephedrine to minimize any decrease in uterine perfusion [15]. Left uterine dis-
placement and limiting the intra-abdominal insufflation pressure to 12 to 15 mmHg
are essential to minimizing these cardiovascular changes [15].
Pelviscopy during pregnancy is not without controversy. Timing, the safest
method of abdominal cannulation, and appropriate fetal and maternal monitoring are
issues that have been raised over time. Pregnancy in the first trimester poses the least
technical challenges during abdominal and pelvic surgery. The first trimester uterus
is well below the point of initial trocar entry, and visualization of the pelvis and
adnexa is optimal. Teratogenesis risk, however, is greatest during this trimester.
Second trimester operations pose less risk to the fetus but are technically more dif-
ficult, requiring greater surgical skill. The third trimester is attendant with a greater
potential for preterm labor, and visualization difficulties are further pronounced by
the enlarging uterus. The safest interval for operative intervention for elective cases
is during the second trimester. This is explained by the decreased rate of spontaneous
abortion, and the risk of premature labor increases as the gestation progresses [9].
Trocar placement and insertion of the pelviscope are determined by uterine size
and gestational age. Many surgeons utilize the open Hasson technique when operat-
ing in the second and third trimesters; however, studies have shown that closed-
entry techniques are undertaken by others [17]. The left upper quadrant (Palmer’s
point) entry is frequently chosen for insertion of the Veress needle in the closed-
entry technique, beyond the first trimester. With this approach, the primary trocar is
placed in the midclavicular line, 2 cm below the ribcage. Ultrasound guidance has
been utilized to improve the safety of Veress needle and trocar insertion. Similarly,
a subxyphoid entry can be undertaken with the trocar placement 2–6 cm above the
umbilicus, varying with the fundal height. The additional trocars are then placed
under direct visualization. The use of vaginal instrumentation, cervical clamps, and
uterine manipulators is contraindicated in the pregnant patient [18].
Because there are a large number of physiological changes seen with gestation
and the cardiovascular and pulmonary changes induced by laparoscopic surgery,
optimal perioperative monitoring is unclear. The standard precautions that apply to
pregnant women undergoing surgery should be sustained in laparoscopic surgery.
End-tidal CO2 should be maintained between 32 and 34 mmHg when using CO2
insufflation by increasing respiratory rate and tidal volume and systolic blood pres-
sure should be kept within 20% of baseline [14].
There are surgeons who have reported the use the apneumatic approach due to
concerns as to the effects of CO2 pneumoperitoneum. With this technic, pelviscopy
is performed using epidural anesthesia, and abdominal access is achieved by
mechanical lifting of the abdominal wall with wire spokes [19, 20]. Because this
option eliminates the effects of carbon dioxide insufflation seen with general endo-
tracheal anesthesia and is an appealing option for patients with preexisting cardio-
pulmonary disease, further study is needed to validate its efficacy.
No intraoperative fetal heart rate abnormalities have been reported. When urgent
abdominal surgery is indicated during pregnancy, fetal monitoring is sufficient in
the preoperative and postoperative periods. There has been no increased fetal mor-
bidity reported using this approach [21].
The positioning of the patient is important in pelviscopic procedures. The bowel
and omentum, the gravid uterus, and maternal obesity can make visualization of
pelvic organs difficult. Trendelenburg positioning is essential for pelviscopic sur-
geries. The gravida should be placed in the supine position with a leftward tilt to
reduce further compression of the inferior vena cava by the uterus, thus, allowing
maximized venous return to the heart and uterine perfusion. Trendelenburg position
should be accomplished to reduce the effect on hemodynamic stability.
The Society of American Gastrointestinal Endoscopic Surgeons Guidelines for
Laparoscopic Surgery during Pregnancy recommends the following:
• Gravid patients should be placed in the left lateral decubitus position to minimize
compression of the vena cava.
• Initial abdominal access can be safely performed with an open (Hasson) tech-
nique, Veress needle, or optical trocar if the location is adjusted according to
fundal height and previous incisions.
• Intraoperative CO2 monitoring by capnography should be used during laparos-
copy in the pregnant patient.
• Intraoperative and postoperative pneumatic compression devices and early post-
operative ambulation are recommended prophylaxis for deep venous thrombosis
in the gravid patient.
• Fetal heart monitoring should occur preoperatively and postoperatively in the
setting of urgent abdominal surgery during pregnancy.
• Obstetric consultation can be obtained preoperatively and/or postoperatively
based on the severity of the patient’s disease and availability.
• Tocolytics should not be used prophylactically in pregnant women undergoing
surgery but should be considered perioperatively when signs of preterm labor are
present [22, 24].
224 P.B. Greenspan
Extrapolation of the success of pelviscopy in the pregnant population has been

hindered by the lack of prospective trials and understudied risks. Pelviscopic sur-
gery has been performed safely on gravid women for more than 30 years. There are
numerous examples of women suspected of having ectopic pregnancies with subse-
quent findings of normal first trimester pregnancies that underwent pelviscopy and
have progressed to normal gestation and birth. Rizzo studied the effects of pelvi-
scopic surgery during pregnancy with patient and child follow-up during a 1–8-year
period [23]. Eleven pregnant women underwent pelviscopic procedures with only 1
conversion to laparotomy. The surgeries were accomplished in the first through
third trimesters of pregnancy (10–28 weeks) for acute cholecystitis, chronic chole-
cystitis and biliary colic, appendicitis, and bowel obstruction. The operative proto-
col was similar for all patients. All patients received general anesthesia, an open
Hasson entry technique, end-tidal CO2 monitoring, insufflations pressure of
10 mmHg, and left lateral positioning. Operative time ranged from 25 to 90 min.
Postoperative fetal monitoring was performed for a total of 24 hours. There were no
cases of fetal intolerance to the intrauterine environment, need for tocolysis, or fetal
demise. The gravidas and their offspring were followed for 6 years. None of the
offspring failed to thrive or developed any medical issue [23].
At times, pregnancy is complicated by pathologies and diseases necessitating
surgical intervention. The evidence, thus, far indicates that pelviscopic surgery can
be safely performed with clear benefits for gravid women.
Antibiotic Prophylaxis, Glucocorticoids, and Tocolytics
Antibiotic prophylaxis at the time of surgery on a gravid female depends on the

specific procedure. Antibiotics that have a good safety profile in gravid women
include the cephalosporins, penicillins, erythromycin (except the estolate), azithro-
mycin, and clindamycin. Aminoglycosides are relatively safe, but there remains the
risk of fetal (and maternal) ototoxicity and nephrotoxicity. Doxycycline is contrain-
dicated and should be avoided during pregnancy. Other tetracyclines have been
proven to cause transient suppression of bone growth and staining of developing
teeth, although available data do not implicate teratogenic effects from doxycycline.
Trimethoprim and nitrofurantoin are not recommended in the first trimester because
of a potential increased incidence of congenital malformations. Fluoroquinolones
are toxic to developing cartilage in experimental animal studies and are, therefore,
usually avoided during pregnancy and lactation. However, these adverse effects on
cartilage or an increase in congenital malformations from utilization during human
gestation has not been documented.
The standard practice of administration of antenatal glucocorticoids 24–48 h
prior to surgery between 24 and 34 weeks of gestation can reduce perinatal mor-
bidity/mortality if preterm birth occurs. However, the American College of
Obstetricians and Gynecologists recently published a Practice Advisory entitled
“Antenatal Corticosteroid Administration in the Late Preterm Period.” This advi-
sory proposes that with new data and until further guidance is released,
administration of betamethasone may be considered in woman with a singleton

pregnancy between 34 0/7 and 36 6/7 weeks at imminent risk of preterm birth
within 7 days [25]. Utilization depends upon the urgency of the surgery, and the
provider’s estimate of whether the gravida is at increased risk of preterm birth
due to the underlying disease or the planned procedure. Although there are poten-
tial benefits to the fetus, however, antenatal glucocorticoids should be avoided if
there is evidence of systemic infection (such as sepsis or a ruptured appendix),
because the steroids may impair the ability of the maternal immune system to
contain the infection.
The routine administration of prophylactic perioperative tocolytic therapy has no
proven benefit. Tocolytics are indicated for treatment of preterm labor until resolu-
tion of the underlying, self-limited condition that may have caused the
contractions.
Minimizing uterine manipulation may reduce the risk of development of uterine
contractions and preterm labor.
Thromboprophylaxis
The increase in the majority of coagulation factors and the decrease in protein S
levels during gestation result in a hypercoagulable state. This effect safeguards
against excessive blood loss at delivery but contributes to the risk of a thromboem-
bolic event in the postoperative period [16].
Randomized trials on the use of unfractionated or low molecular weight heparin
or intermittent pneumatic compression for venous thromboembolism prophylaxis in
pregnant patients undergoing pelviscopy provide no data at this time.
The Society of American Gastrointestinal and Endoscopic Surgeons (SAGES)
recommends applying pneumatic compression devices on the lower limbs of gravid
women undergoing pelviscopic procedures for surgical problems [17].
The 2012 American College of Chest Physicians (ACCP) clinical practice guide-
line on prevention and treatment of thrombosis recommends mechanical or pharma-
cological thromboprophylaxis for pregnant patients undergoing surgery [26]. For
any pelviscopic operation likely to take more than 45 min, the use of low molecular
weight heparin is recommended; mechanical thromboprophylaxis is a practical
alternative for shorter procedures.
Wound Care
The management of surgical wounds in gravid patients does not differ from that
which is administered to non-gravidas. The general principles of wound care such
as meticulous hemostasis and prevention of infection are universal. Closure of oper-
ative wounds is usually left to the discretion of the operator; however, the routine
use of sterile surgical staples in no longer advised. Furthermore, the routine place-
ment of surgical drains is discouraged.
226 P.B. Greenspan
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Committee Opinion No. 696, February 2011, Reaffirmed April, 2017.
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review. Int J Obstet Anesth. 2006;15:212.
7. Nezhat F, Nezhat C, Silfen SL, et al. Laparoscopic ovarian cystectomy during pregnancy.
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9. Conron RW Jr, Abbruzzi K, Cochrane SO, et al. Laparoscopic procedures in pregnancy. Am
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Principles and Practice of Anesthetic
Management in the Gravid Patient 12
Undergoing Abdominal Surgery
Tibor G. Mohácsi and Kathleen A. Leavitt
Maternal Physiologic Considerations
Physiologic adaptations to pregnancy are described in detail in Chap. 1. Table 12.1

summarizes the physiological alterations that have specific implications with respect
to anesthesia. They include the following:
The maternal airway, nasopharynx, and laryngeal structures are more edema-
tous, and the mucus membranes are more friable than in the nonpregnant state,
especially near term. Typically a smaller sized endotracheal tube (6.5–7.0 mm) is
used for endotracheal intubation. Extreme caution is used if placing anything
through the nares. The nares should be treated with a nasal decongestant spray prior
to inserting a nasogastric tube, especially if one is deemed necessary prior to intuba-
tion. Likewise, nasotracheal intubation is fraught with the potential for significant
epistaxis in the pregnant patient. Pregnant patients have higher incidence of difficult
intubation because enlarged breasts and excess soft tissue can make insertion of the
laryngoscope into the oropharynx, and visualization of the glottis difficult. A short-
handled laryngoscope and video laryngoscopy should be readily available. In the
obese patient, it is important to “ramp” them by placing several blankets underneath
the back and neck, placing the operating room table in reverse Trendelenburg posi-
tion, and asking an assistant to retract the breasts downward during laryngoscopy.
Respiratory changes in the parturient include a higher minute ventilation and a
significant reduction in functional residual capacity (FRC), or oxygen reserve. In
addition, the maternal “set point” with respect to normal PaCO2 is lowered to
T.G. Mohácsi, M.D. (*)

Assistant Professor, Department of Anesthesiology, University of Missouri Kansas City
School of Medicine, Saint Luke’s Hospital, Kansas City, MO, USA
K.A. Leavitt, M.D.
Assistant Professor, Director of Obstetric Anesthesia, Department of Anesthesiology,
University of Missouri Kansas City School of Medicine, Kansas City, MO, USA

in Pregnancy, DOI 10.1007/978-3-319-62283-5_12
228 T.G. Mohácsi and K.A. Leavitt
Table 12.1 Physiologic alterations of pregnancy and anesthetic implications

System Maternal physiologic alterations Anesthetic management
Airway Mucous membranes are more Use smaller sized ETT
edematous and friable (6.0–7.0 mm)
Breasts are enlarged Use short-handled laryngoscope or
video laryngoscopy
Pretreat with nasal decongestant
before placing anything through the
nares
Use ramp and/or Reverse
Trendelenburg position
Ask an assistant to retract the
breasts downward
Respiratory Lower FRC and higher oxygen Preoxygenate prior to induction of
consumption leads to rapid GETA with three vital capacity
desaturation breaths or 3 min of tidal breathing
“Normal” maternal PaCO2 is of 100% FIO2
30–32 mmHg With controlled ventilation, use
higher minute ventilation with target
ETCO2 of 25–28 mmHg
Cardiovascular 40% increase in cardiac output Decreased vascular responsiveness
by 28 weeks gestation to vasopressors
Higher maternal HR Ephedrine and phenylephrine first
Lower SVR line therapy for hypotension
Lower baseline MAP Norepinephrine also acceptable to
Aortocaval compression in the use
supine position Maintain left uterine displacement
after 20 weeks gestation
Gastrointestinal Increased gastric acid production Rapid sequence induction of GETA
Decreased lower esophageal should be performed on all
sphincter tone parturients after 16 weeks.
Upward displacement of the Consider NG tube placement prior
stomach by the gravid uterus to induction in the presence of
Volume of gastric content may be significant gastric volume.
difficult to assess
Hematologic Dilutional anemia from increased Blood transfusion should be guided
plasma volume relative to red cell by knowledge of lower baseline
mass maternal Hb.
“Normal” maternal Hb value DVT prophylaxis with pneumatic
10–12 mg/dL compression stockings, SQ heparin
Hypercoagulable from increased or enoxaparin.
synthesis of clotting factors
Renal/Hepatic Increased renal blood flow Drugs that are excreted by the
Decreased hepatic synthesis of kidney will undergo rapid
albumin and glycoproteins elimination.
Increased hepatic synthesis of Elevation of “free” fraction of drugs
coagulation factors that are protein bound will occur
Neurologic Endogenous endorphins, MAC is lowered
progesterone, and estrogen cause Use smaller doses of sedatives and
increased sensitivity to anesthetic narcotics
agents. Local anesthetic dose should be
Nerves are more sensitive to decreased by 25%
blockade by local anesthetics Emotional support is essential in the
Increased emotional lability setting of emergency surgery
12 Principles and Practice of Anesthetic Management in the Gravid Patient… 229
30–32 mmHg. Reduced FRC, combined with the high oxygen consumption of the
fetal-placental unit, results in rapid maternal desaturation during periods of apnea or
hypoventilation. It is extremely important to provide adequate preoxygenation prior
to induction of anesthesia using 3-4 vital capacity breaths or 3 min of normal tidal
breathing of 100% oxygen by mask. Mechanical ventilation requires both a larger
tidal volume and respiratory rate than in the nonpregnant state, with the target end-
tidal pCO2 value of 25–28 mmHg.
Gastroesophageal changes make ALL parturients after 16 weeks gestation at
higher risk of pulmonary aspiration and “full stomach” precautions should be initi-
ated regardless of NPO status. Decreased lower esophageal sphincter tone, higher
gastric acid production, and upward displacement of the stomach by the gravid
uterus all contribute to this phenomenon. In the presence of an “acute abdominal”
process, administration of narcotic pain medications, administration of oral contrast
during the diagnostic workup, delayed gastric emptying, and overt bowel obstruc-
tion significantly exacerbate the risk of pulmonary aspiration. The degree of gastric
distention may not be apparent on physical exam due to the presence of a gravid
uterus. The practitioner should review the CT/MRI results and consult with the
surgeon prior to induction of anesthesia to better approximate the volume of gastric
contents. If significant gastric content is present, placement of a nasogastric tube
and decompression of the stomach should strongly be considered before proceeding
with induction of general anesthesia. The nares should be treated with a nasal
decongestant spray prior to placement of a nasogastric tube, as mentioned above.
Cardiovascular changes in the parturient include a higher cardiac output and
circulatory volume by approximately 40% above baseline at 28 weeks gestation.
The pregnant state is characterized by increased heart rate, increased stoke volume,
and decreased systemic vascular resistance. Elevated heart rate and low systemic
vascular resistance would be easy to misinterpret as a manifestation of sepsis, if the
practitioner did not have an understanding of what constitutes “normal values” dur-
ing pregnancy. Because of hormonal changes, the parturient also exhibits decreased
responsiveness to vasopressors and requires larger doses for therapeutic effect.
Both indirect acting (ephedrine) and direct acting vasopressors (phenylephrine)
administered to treat hypotension and maintain uteroplacental perfusion are consid-
ered safe to use in pregnancy. Because the gravid uterus can cause aortocaval com-
pression by about 20 weeks of gestation, it is imperative to perform left uterine
displacement preoperatively, intraoperatively, and postoperatively to ensure ade-
quate maternal venous return from the lower half of the body to maintain maternal
blood pressure and uteroplacental perfusion.
Hematological adaptations to pregnancy include an increased plasma volume
relative to the increase in red cell mass, resulting in a dilutional anemia. Normal
maternal hemoglobin values range from 10–12 mg/dL. Maternal dehydration should
be suspected when the hemoglobin level is in a “normal” physiological range. In
addition, if surgery involves significant blood loss, blood transfusion should be
guided by the knowledge that the pregnant woman has a lower hemoglobin level at
baseline. Increased hepatic synthesis of coagulation factors renders pregnancy a
“hypercoagulable state,” making the parturient high risk for developing deep vein
thrombosis and pulmonary embolism. Pneumatic compression stockings should

always be applied during surgery and continued well into the postoperative period.
Subcutaneous heparin or low molecular weight heparin should be administered in
the perioperative period to patients confined to bed. Other hematological findings in
the parturient include increased concentration of fibrin degradation products and
plasminogen, suggesting that systemic fibrinolysis is occurring to some extent.
During pregnancy, the diagnosis of disseminated intravascular coagulation should
not be based on these lab values alone.
Renal blood flow is dramatically increased during pregnancy causing drugs that
are primarily excreted by the kidney to undergo rapid elimination. Hepatic synthesis
of serum proteins, especially albumin and glycoproteins, is diminished. This causes
a slight decrease in maternal colloid osmotic pressure. More importantly, elevated
free fractions of drugs that are highly protein bound will exist in the serum, increas-
ing their potential for toxicity.
Finally, neurological changes that occur include increased emotional lability
which, especially in the setting of impending emergency surgery, can lead to hyste-
ria, inability to cooperate, and irrational behavior. Minimum alveolar concentration
(MAC) is thought to be reduced by 40% due to hormonal changes (estrogen, pro-
gesterone) and increased levels of endorphins. Sensitivity of nerves to local anes-
thetic blockade is enhanced, and the dosages of all anesthetic agents should be
adjusted accordingly.
Fetal Considerations
Several different types of drugs will most likely be administered to a pregnant

patient with an acute abdomen should surgery become necessary. Multiple concerns
arise with respect to the fetus at this point.
• Do anesthetic agents have harmful effects on fetal growth and development?

• How might they affect the fetal status during emergency abdominal surgery?
• Are there any particular anesthetics or medications that should be avoided?
• How should we monitor the fetal status during surgery?
The potential for teratogenic effects of anesthetic agents on the developing fetus
has long been a concern. Teratogenicity depends on dosage, duration of exposure to
the agent, the susceptibility of the species studied, and the timing of exposure with
respect to organogenesis. In humans, organogenesis is generally during the first
trimester, approximately 15–60 days post conception. It is essentially impossible to
conduct controlled, randomized studies in humans due to ethical concerns, and thus,
available data are derived from animal studies and from retrospective human stud-
ies. Since 1979, the FDA has used a letter risk classification system (A, B, C, D, and
X) to categorize the teratogenic risk of medications (see Table 12.2). In 2015, that
system was abandoned and replaced by a narrative risk summary contained in the
Pregnancy and Lactation Labeling Rule (PLLR) [1]. However, most clinicians
Table 12.2 United States food and drug administration category ratings of drugs during
pregnancy
Risk Category during Pregnancy Outcome
A Controlled studies show no risks
B No evidence of risks in humans
C Risk cannot be ruled out
D Positive evidence of risk
X Contraindicated in pregnancy
PDR [5]
continue to use the letter categories as a quick reference. In animal models, MOST
anesthetic agents have been found to be teratogenic, though the doses used clini-
cally are MUCH lower, and thus, the data are of limited value for the anesthesia
practitioner (Tables 50.2 and 50.4 in [2]).
With the exception of muscle relaxants, most anesthetic agents, including vola-
tile anesthetics, readily cross the placenta and are present in the fetal bloodstream.
Suggested to be teratogenic in animal models with prolonged use (greater than 24 h)
is nitrous oxide. The associated teratogenicity of nitrous oxide was thought to be a
result of oxidation of vitamin B12 and the subsequent dysfunction as a coenzyme
for DNA synthesis (decreased methionine synthase and thus decreased tetrahydro-
folate production) leading to neurological and hematological symptoms. More
recent evidence suggests a more complex and multifactorial etiology, including pos-
tulated mechanism of decrease in uterine blood flow and overstimulation of certain
membrane signal pathways. Despite the fact that nitrous oxide has not been found
to be associated with congenital anomalies in humans, most clinicians avoid its use
especially during the first and second trimesters.
Intravenous opioids easily cross the placenta and may cause decreased heart rate
variability if fetal monitoring is being used during surgery or in the perioperative
period. If delivery of the fetus occurs after opioid administration to the mother, sig-
nificant respiratory depression may be observed in the newborn for several hours.
The respiratory-depressant effects are variable and depend upon the narcotic used.
Long-acting opioids such as morphine result in more significant respiratory depres-
sion than shorter acting opioids such as fentanyl. Opioids administered by the neur-
axial route (epidural or spinal) have little effect on the newborn.
Induction agents which include propofol, etomidate, and ketamine cross the pla-
centa and are present in the fetal circulation. Although ketamine has been shown to
cause a dose-dependent increase in uterine tone in vitro, all these induction agents
are considered safe to use in the fetus.
Therapy with benzodiazepines is controversial. Several studies reported a cor-
relation of maternal diazepam administration and infants with cleft lip. In one study,
278 mothers whose infants had major malformations, diazepam ingestion was four
times more common among mothers of infants with oral clefts than mothers of
infants with other defects [3]. Other studies have failed to show a correlation.
Although the consensus is that diazepam is not a proven human teratogen, the risk/
benefit ratio should be considered before starting chronic benzodiazepine during the
first trimester.
Due to their molecular size and ionized state, muscle relaxants DO NOT cross
the placenta to an appreciable extent. Placental transfer of local anesthetics depends
on several factors; route of metabolism, degree of protein binding, pKa, and mater-
nal and fetal acid base status. Because chloroprocaine undergoes rapid metabolism
by maternal plasma cholinesterase, minimal fetal transfer occurs. Highly protein
bound local anesthetics (bupivacaine and ropivacaine) undergo less fetal transfer
than local anesthetics that are less protein bound such as lidocaine. However, keep
in mind that serum protein levels are decreased in pregnancy, which can potentially
lead to increased concentrations of “free”, unbound drug in the maternal circulation.
This may result in enhanced fetal transfer of local anesthetics. Once these drugs
cross the placenta and enter the fetal circulation, they can potentially be converted
into an ionized form in the presence of fetal acidosis and remain “trapped” in the
fetal circulation, thus, increasing the potential for toxic effects.
Other medications that may be used when caring for a parturient undergoing
emergency abdominal surgery include medications with cardiovascular effects.
Vasopressors, beta-blockers, vasodilators, and atropine all cross the placenta.
However, glycopyrolate, a quaternary ammonium compound, does not. Expect to
see fetal heart rate effects when drugs that have the potential to cross the placenta
are administered to the parturient.
Finally, the use of ketorolac and other nonsteroidal anti-inflammatory agents are
generally avoided during pregnancy, especially during the third trimester due to the
concern about premature closure of the fetal ductus arteriosus.
Should the fetus be continually monitored during emergency abdominal surgery?
This decision should be made in consultation with the Obstetrician caring for the
parturient and the surgeon performing the surgery. ACOG states “The decision to
use intraoperative fetal monitoring should be individualized and, if used, should be
based on gestational age, type of surgery, and facilities available” [4]. It is unlikely
to be of benefit and not possible to do before 18 weeks gestation. It requires the
presence of personnel trained in interpretation of fetal monitoring, such as the
obstetrician or labor and delivery nurse. It also requires a plan in place for emer-
gency cesarean section should fetal compromise be detected. Proponents of con-
tinuous intraoperative fetal monitoring feel that it allows for optimization of the
fetal status should heart rate abnormalities be detected. Maternal blood pressure,
hemoglobin, and oxygen concentrations can be augmented to improve uteroplacen-
tal perfusion. When perioperative fetal heart rate monitoring is performed, clini-
cians should have a thorough understanding of the fetal effects of maternally
administered medications.
Anesthetic Recommendations
Regional Versus General Anesthesia
The type of anesthetic chosen will depend upon several factors: the site and nature
of the surgery, maternal factors, and patient preference. The use of regional anesthe-
sia (spinal, epidural, or peripheral nerve block) will almost always be the preferred
method in a pregnant patient, EXCEPT when presenting for acute abdominal sur-
gery. However, a strong argument may be made that a spinal or epidural anesthetic
COULD be performed in a handful of cases provided that there was not significant
bowel obstruction present. Examples might include
• Open repair of incarcerated inguinal hernia

• Open repair of incarcerated umbilical hernia
• Open repair of a ventral hernia
• Open appendectomy
Contraindications to regional anesthesia would include
• Patient refusal
• Coagulopathy
• Maternal hypotension, hypovolemia, and sepsis
• Evidence of significant bowel obstruction or bowel infarction
• Potential for significant blood loss
When spinal or epidural anesthesia is chosen for these procedures, keep in mind
that the abdominal viscera is innervated by nerve fibers that enter the spinal cord
and travel cephalad, synapsing within the sympathetic ganglia in the high or mid-
thoracic region. Thus, to truly provide adequate intraoperative anesthesia, the level
of epidural or spinal blockade must reach the T4-T6 dermatomes. This CAN be
accomplished using either a hyperbaric spinal anesthetic or an epidural anesthetic,
much like what is done when performing anesthesia for cesarean section. However,
high spinal blockade will increase the risk of pulmonary aspiration of gastric con-
tents in the setting of acute abdominal surgery. In addition, if maternal hypovolemia
or sepsis is present, significant hypotension would result from the sympathectomy
caused by this level of neural blockade and would therefore be contraindicated.
The vast majority of operations involving the abdomen and viscera will require
the use of general endotracheal anesthesia. The following are specific recommenda-
tions for the perioperative care of the parturient and her fetus.
Preoperative Preparation
Regardless of the type of anesthetic used, all patients undergoing surgery for an acute
abdominal procedure should undergo a thorough history and physical examination.
In addition to gestational age, history of prior medical problems such as asthma,
hypertension, or diabetes should be elicited, as well as medication allergies, or prob-
lems with prior anesthetics. Physical examination should focus on the patient’s air-
way, heart, and lungs, and estimation of gastric content. Fetal heart tones should be
documented and a decision should be made whether intraoperative continuous fetal
heart rate monitoring is feasible. ALL parturients should receive a 30 ml dose of a
nonparticulate antacid, such as sodium citrate, within 30 min of induction. In addi-
tion, a promotility agent such as metoclopramide, an H2 receptor antagonist such as
famotidine, or proton pump inhibitor such as pantoprazole should be administered

intravenously 30–60 min prior to induction in patients with increased risk of pulmo-
nary aspiration. A small dose of a short-acting benzodiazepine such as midazolam is
considered safe to use as a premedication to allay anxiety. Anti-emetic prophylaxis
with 4 mg of dexamethasone should also be administered preoperatively, as well as
4 mg of ondansetron prior to emergence from anesthesia.
Intraoperative Management
Standard monitors should include electrocardiography, pulse oximetry, noninva-

sive blood pressure measurement, capnography, as well as temperature and neu-
romuscular blockade monitoring. Invasive blood pressure measurement in the
setting of hypovolemia or sepsis is considered. Continuous fetal heart monitoring
should be utilized when feasible according to ACOG guidelines. Left uterine dis-
placement (after 20 weeks gestation) and pneumatic compression stockings
should be applied and maintained throughout the postoperative period.
Preoxygenation followed by rapid sequence induction of general endotracheal
anesthesia should be performed on all patients beyond 16 weeks of gestation and
in all patients with evidence of increased gastric content, regardless of gestational
age. Propofol is the most common agent used for induction, but using etomidate
or ketamine with preexisting hypotension or hypovolemia is considered. Despite
a lower plasma pseudocholinesterase concentration in pregnancy, a smaller induc-
tion dose of succinylcholine should not be used because clinical prolongation of
neuromuscular blockade rarely occurs. Anesthesia using volatile agents, narcot-
ics, and nondepolarizing muscle relaxants is maintained, keeping in mind that
MAC is reduced by 20–40% during pregnancy. An inspired oxygen concentration
greater than 50% is used, and nitrous oxide during abdominal surgery is avoided.
The fetal heart rate tracing will likely exhibit decreased beat-to-beat variability
due to the effects of narcotics and volatile agents. However, if persistent fetal
heart rate decelerations occur, every attempt to optimize the fetal status by increas-
ing maternal blood pressure and oxygenation is made.
Because many of these acute abdominal surgeries will be performed laparo-
scopically, it is important to anticipate the cardiorespiratory changes that are likely
to occur. Hypotension and decreased uteroplacental perfusion from increased
intra-abdominal pressure caused by carbon dioxide insufflation are common. The
reverse Trendelenburg position will enhance venous pooling and worsen maternal
hypotension. Carbon dioxide insufflation will also cause increased peak airway
pressures, decreased lung compliance, and decreased functional residual capacity.
Respiratory changes will be exacerbated in the Trendelenburg position, with obe-
sity, and with advanced gestational age. It is important to support maternal blood
pressure with appropriate fluid therapy and vasopressors and to attempt to maintain
end-tidal carbon dioxide between 32 and 36 mm HG. At the end of the procedure,
the patient must be fully conscious before extubation to ensure return of protective
airway reflexes.
Table 12.3 Summary of Anesthetic Recommendations

Postoperative
Preoperative preparation Intraoperative management management
Perform thorough history Monitors to include standard ASA; Monitor FHR and
and physical pulse oximetry, EKG, NIBP, observe for signs of
examination, paying capnography, temperature, increased uterine
close attention to the neuromuscular blockade, and FHR activity
airway and estimation of monitoring according to ACOG
gastric contents guidelines.
Document fetal heart Preoxygenation followed by RSI and Provide postop
tones and determine if GETA analgesia using
continuous fetal heart neuraxial and/or TAP
rate monitoring is blocks
feasible
Consider aspiration Maintain anesthesia with volatile agent, Consider multimodal
prophylaxis with any/all muscle relaxants, and narcotics, keeping analgesics such as
of the in mind that MAC is reduced by acetaminophen and
following: 30 ml 20–40% gabapentin administered
sodium bicitrate within Aggressively treat hypotension/ on a scheduled basis
30 min of induction hypovolemia to maintain uteroplacental Use reduced doses of
Metoclopramide perfusion narcotics and sedatives
10 mg IV Decreased FHR variability will likely be Avoid NSAID’s during
Famotidine 20 mg IV observed secondary to anesthetic agents. the third trimester
Pantoprazole 40 mg Institute DVT
IV prophylaxis
Postoperative Management
In addition to maternal vital signs, fetal heart tones and uterine activity should be
monitored for several days during the postoperative period. The risk of preterm
labor is increased after abdominal surgery, irrespective of anesthetic technique.
Nevertheless, prophylactic tocolytic agents are not routinely administered (see
Chap. 13). Postoperative analgesia in patients who have undergone laparotomy can
be provided by TAP blocks or thoracic epidural analgesia using a dilute infusion of
local anesthetic with fentanyl. Oral and parenteral opioids, as well as acetamino-
phen, usually provide adequate analgesia after laparoscopic procedures. Nonsteroidal
anti-inflammatory agents should be avoided during the second half of pregnancy
due to concerns of premature closure of the fetal ductus arteriosus. Pneumatic com-
pression stockings should be continued well into the postoperative period and
thromboprophylaxis with subcutaneous heparin or enoxaparin should be instituted
as soon as possible. Table 12.3 presents a summary of anesthetic recommendations
to follow when providing general anesthesia to a parturient and her fetus.
References

1. Federal Register. The Daily Journal of the United States Government. Content and
Format of Labeling for Human Prescription Drug and Biological Products; Requirements
for Pregnancy and Lactation Labeling. [internet] https://www.federalregister.gov/arti-
cles/2014/12/04/2014-28241/content-and-format-of-labeling-for-human-prescription-drug-
and-biological-products-requirements-for. Accessed 11 April, 2017.
2. Suresh M, editor. Shnider and Levinson’s anesthesia for obstetrics. 5th ed. Philadelphia:
Lippincott Williams & Wilkins; 2013.
3. Safra MJ, Oakley GP. Association between cleft lip with or without cleft palate and prenatal
exposure to diazepam. Lancet. 1975;2(7933):478–80.
4. American College of Obstetricians and Gynecologists. Nonobstetric surgery during pregnancy.
ACOG Committee opinion no 474. Obstet Gynecol. 2011;117:420–1.
5. PDR. Physicians’ desk reference. 64th ed. Montvale: PDR Network, LLC; 2013. p. 211.
Recommended Reading
Butterworth J, editor. Morgan & Mikhail’s clinical anesthesiology. 5th ed. New York: McGraw
Hill; 2013.
Chestnut D, editor. Chestnut’s obstetric anesthesia principles and practice. 5th ed. Philadelphia:
Saunders; 2014.
Postoperative Care Issues
13
Monitoring the Fetus and Timing of Delivery
Monitoring the fetus of a gravida who is undergoing surgery is addressed in the

ACOG Committee Opinion No. 696 on Nonobstetrical Surgery during Pregnancy
[1]. The status of the fetus is important in the postanesthesia care unit as well.
Depending on the fetal gestational age, the monitoring may only entail intermittent
fetal heart tone documentation or the fetus may require continuous electronic moni-
toring, especially in the later stages of pregnancy.
Pre-viable fetuses generally tolerate anesthetics and surgery very well; however,
if the fetal heart tones indicate fetal compromise, little can be done to manage that
other than correction of respiratory and metabolic problems in the gravida.
Viable fetuses that are demonstrating persistent intolerance to the intrauterine
environment may require intervention including interruption of the pregnancy, if the
offense causing the intolerance is irreversible with intrauterine resuscitative
measures.
It is preferable to have an obstetrical provider with surgical privileges available
in the postoperative period to intervene with emergent delivery if need be.

e-mail: [email protected]; [email protected]

in Pregnancy, DOI 10.1007/978-3-319-62283-5_13
238 P.B. Greenspan
Route of Delivery
The determination of delivery route is entirely dependent upon the urgency to

remove the fetus from a hostile intrauterine environment. In most cases, albeit rare,
the most expeditious route of delivery is abdominal, hence subjecting the gravida to
another surgical procedure. In rare instances, the delivery of the fetus coincides with
the surgical procedure being performed for the pathology that is causing the indica-
tion for surgery. In that case, the delivery of the fetus via Cesarean section, if indi-
cated, can be expedited through the same incision.
When continuation of the pregnancy is warranted, then the patient can be fol-
lowed for the pregnancy as she recovers from her surgery, until such time that a fetal
and/or maternal indication for delivery arises or the patient’s gestation reaches term
status.
General Postoperative Principles [2, 3]
Immediate postoperative care in most patients, pregnant or otherwise, is supportive

care with the goal of emerging the patient from the anesthetic that was provided for
the surgery. This includes maintenance of the patients’ airway with supplemental
oxygen, as needed.
The first 24–72 h of the postoperative period are the most critical. During this
time, monitoring of the patient for complications is essential.
The gravidas’ hemoglobin and hematocrit should be followed, most importantly
when the surgery was indicated for acute blood loss, such as trauma or abruption.
Maintenance of the intravascular volume may require replacement of blood prod-
ucts by transfusion, etc. The clinical presentation of the patients’ hemodynamic
status will determine what treatment is required.
The evaluation of fluids and electrolytes should be carefully considered espe-
cially when the procedure is lengthy and/or if there was a considerable preoperative
or intraoperative blood loss. Fluid management may also be a part of the nonsurgi-
cal care of the patient.
Care should be taken postoperatively to avoid emesis. In some cases, intraopera-
tive and postoperative gastrointestinal decompression with nasogastric suction may
be warranted. Once the gravida is alert and able to swallow, and any nausea and/or
vomiting has resolved, then nasogastric suction should be discontinued, as it is very
uncomfortable and may be of limited value in the prevention of postoperative ileus.
Indwelling Foley catheterization is helpful during and immediately following a
procedure to monitor urinary output and to assist the patient in emptying her bladder
until such time that she is stable and can void spontaneously on her own. The more
critically ill gravida who has undergone surgery may require bladder drainage for
longer periods of time. Furthermore, a catheter may prove to be useful since the
gravid uterus may predispose the patient to urinary retention.
13 Postoperative Care Issues 239
Postoperative antibiotic therapy is appropriate in select patients who are preop-

eratively infected, but the use of prophylactic antibiotics in the postoperative phase
of recovery is not indicated.
The implementation of a protocol for the prevention of venous thromboembo-
lism is very important especially in gravid women. Most institutions have order sets
or electronic medical record prompts that assist the clinician in choosing what type
of prophylaxis to implement. In almost all cases, the use of sequential compression
devices is appropriate.
Incentive spirometry and other forms of pulmonary support are recommended in
the postoperative gravid patient as would be in any other patient. These measures
are vital in the deterrence of atelectasis and pneumonia.
Early postoperative ambulation is encouraged if the gravida and her fetus are
otherwise found to be stable.
Very rarely is it necessary for a gravid postoperative patient to receive total par-
enteral nutrition. Parenteral nutrition requires expertise in multiple fields. Most cli-
nicians would obtain consultation from other specialists if this were warranted.
Wound care in pregnant women does not differ from that in nonpregnant patients.
References
1. American College of Obstetricians and Gynecologists, nonobstetrical surgery during preg-
nancy, Committee Opinion Number 696 (replaces No. 284, August 2003, Reaffirmed 2015).
April, 2017.
2. Barber HRK, Graber EA. Surgical diseases in pregnancy. Philadelphia: W.B. Saunders
Company; 1974.
3. Thompson JD, Rock JA. Te Linde’s operative gynecology. 7th ed. Philadelphia: J.P. Lippincott
Company; 1992.
Legal Concerns in Complicated
Obstetrical Cases 14
Marilyn M. Pesto, Janet I. Mittenfelner,
and Andrew Spaedy
Abbreviations
EHR Electronic Health Record

EMTALA Emergency Medical Treatment and Labor Act
FCA False Claims Act
HIPAA Health Insurance Portability and Accountability Act
OCR Office of Civil Rights
PSDA Patient Self-Determination Act
PVS Persistent Vegetative State
Introduction
The last thing healthcare providers want to think about is the legal implications of
practicing medicine. Most practitioners are attracted to the art and science of medi-
cine, and they are motivated by the altruistic notion that the long, hard years they
devote to the study and practice of medicine will improve the health and well-being
of their patients. In a perfect world, healthcare providers would go about their day
doing what they do best, without the worry of being sued for malpractice,
M.M. Pesto, JD, MSN, BSN (*)

Medical Humanities & Social Sciences, Sirridge Office of Medical Humanities and Bioethics,
J.I. Mittenfelner, JD, MHSA
Office of General Counsel, Litigation Counsel, TMC Professional and General Liability
Trust, Truman Medical Centers, Kansas City, MO, USA
A. Spaedy

in Pregnancy, DOI 10.1007/978-3-319-62283-5_14
242 M.M. Pesto et al.
committing a HIPAA violation, or otherwise being held legally liable. Unfortunately,

medicine is not practiced in a perfect world. Legal and regulatory issues in the
healthcare arena continue to expand and evolve, making the environment in which
patient care is provided ever more complex and cumbersome.
The objective of this chapter is to educate and empower the healthcare provider
by highlighting some of the legal issues one can expect to encounter when caring for
the gravid patient with acute abdominal pain. The risks are particularly high when
the gravid patient presents because there are two patients instead of one and, whether
realistic or not, patients have a near universal expectation of a perfect outcome with
the birth of their child. Obstetrics is a lightning rod for litigation and accounts for a
large percentage of all medical malpractice lawsuits. Ob/Gyns and surgeons are the
most likely to be sued among all physicians [1, 2]. A survey conducted in 2015
revealed that 85% of Ob/Gyns and 83% of general surgeons have been sued at some
point in their career [3]. By extension, the various settings in which care is provided
to the gravid patient with acute abdominal issues expose the practitioner to a higher
level of risk.
The number one rule of any practitioner is simple: always practice good medical
care. But just as litigators lose some trials they never should have lost, healthcare
providers lose some patients they never expected to lose or their patients experience
less than optimal outcomes, despite the best efforts of the provider. Unanticipated
outcomes are an inevitable fact of life from which no healthcare practitioner is
immune. It does not necessarily mean the practitioner was wrong, but poor out-
comes, regardless of fault, often lead to litigation. Similarly, a well-meaning practi-
tioner can unintentionally commit a regulatory infraction, but still be held legally
liable. With such high stakes associated with caring for the gravid patient, it is pru-
dent for practitioners in the various settings described in this book to arm them-
selves with the basic legal knowledge necessary to avoid legal pitfalls. The ultimate
goal is to provide the highest quality care to the patient while simultaneously pro-
tecting oneself from legal liability, both civil and criminal.
Professional Negligence
The legal concept with which healthcare providers are most familiar, and which cre-
ates the most dread, is professional negligence, also known as medical malpractice.
No practitioner sets out to harm a patient, so the prospect of being sued for a poor
outcome is difficult to accept as an occupational hazard. Yet it makes sense to hold
professionals with specialized training and knowledge to a high standard of profes-
sional practice. Without such standards there would be no protection of patients from
medical error or unreasonable risk of harm. Indeed, as a form of self-policing of sorts,
physicians serve as expert witnesses against other practicing physicians in order to
establish the necessary legal elements of a medical malpractice case. While no practi-
tioner should be crippled by a concern of being sued, familiarity with the elements of
professional negligence and knowledge of how to minimize the risk of malpractice are
essential components of the healthcare provider’s professional toolbox.
14 Legal Concerns in Complicated Obstetrical Cases 243
Elements of Medical Negligence
Negligence is what is known in the law as a type of tort. This is a wrongful act or
failure to act, by a party, for which the injured party is entitled to compensation. In
order for the injured party (known as a plaintiff in a lawsuit) to obtain a judgment in
their favor, they must establish four essential elements of negligence: duty, breach,
causation of injury, and resulting damages.
Elements of Medical Negligence

1. Duty
Obligation owed by a healthcare provider to the patient to provide that
degree of medical care which a reasonably prudent provider would exer-
cise in the same or similar circumstances.
Also known as the standard of care.
2. Breach
Violation of the duty owed to the patient. The healthcare provider failed
to meet the standard of care.
3. Causation
The causal link between the patient’s injury and the healthcare provid-
er’s action. “But for” the negligence of the healthcare provider, the patient
would not have been injured.
4. Damages
Economic or noneconomic harm arising from the injury to the patient.
Damages can be monetary or nonmonetary (pain and suffering).
The plaintiff has what is known as the burden of proof. In other words, the
defendant does not have to prove that these elements do not exist; the plaintiff has
to prove that they do. In the context of medical negligence, duty is the obligation
owed by a healthcare provider to his or her patient to provide that degree of medi-
cal care which a reasonably prudent provider would exercise in the same or simi-
lar circumstance. This is also known as “the standard of care.” By virtue of
entering into a healthcare provider-patient relationship, a duty to the patient is
created. If a provider’s treatment falls below the standard of care, it is considered
a breach of that duty. If the breach causes injury to the patient resulting in dam-
ages, then the four elements of medical negligence have been established.
Physician expert testimony about the standard of care must be entered into evi-
dence for the jury to render an opinion.
Not all breaches of the standard of care cause injury to the patient. For instance,
a provider may fail to respond to critical lab values in a gravid patient, but if neither
the mother nor the baby suffers any harm from that failure to respond, the four ele-
ments of negligence have not been established. While the elements of duty and
breach are present in that example, the breach did not cause an injury. Similarly, if
a provider fails to recognize a placental abruption on an ultrasound, but it can be
proven that the baby’s demise was due to a nuchal cord which preceded the
abruption, then there is no causation between the breach of the standard of care and
the poor outcome for the baby. In that example the elements of duty and breach
exist, but the elements of causation of injury and damages are missing because the
breach did not cause the harm suffered by the baby. While both examples represent
suboptimal practice, neither can be proven as medical malpractice in a court of law,
and thus, are not compensable. In other words, whatever the practitioner did or
failed to do caused no impact.
In medical malpractice cases, expert witnesses are utilized to establish standard
of care and causation. Practitioners in a same or similar field as the defendant offer
opinion testimony about whether or not the defendant breached the standard of care
and whether the injury was a direct result of the breach. The burden of proof for the
plaintiff is “more probable than not” or, stated another way, “to a reasonable degree
of medical probability.” The reason expert testimony is used is because most jurors
do not have the knowledge of complex medical concepts presented at trial in order
to draw conclusions about liability. The exception to that rule is when the evidence
is so common that even a lay person would understand the medical issues in the
case. The most common example in the context of a medical malpractice case is
when a foreign object, such as a sponge or instrument, is unintentionally left in a
patient after surgery. Even a lay person, with no medical knowledge or training, can
conclude that such an error is below the standard of care. Proving a breach of the
standard of care in that example does not require expert opinion testimony. This
concept is known in the law as res ipsa loquitur, which is Latin for “the thing speaks
for itself.”
Implicit in its definition, the standard of care will always evolve because the
practice of medicine is always evolving. With advances in drugs, procedures, diag-
nostic tools, and knowledge about disease processes, the standard of care for treat-
ing a pregnant woman 5 or 10 years ago is not the same as today. It is essential that
practitioners stay current in their field via continuing education because what a
reasonably prudent provider would do yesterday is not necessarily the same as what
one would do today or tomorrow. For example, until recently it was completely
within the standard of care to routinely perform an episiotomy during a delivery, but
today that practice has changed due to studies showing episiotomies can, under
certain circumstances, increase the risk of perineal lacerations as opposed to pro-
tecting against lacerations. The importance of evidence-based practice cannot be
overstated when it comes to a practitioner guarding against future lawsuits where it
will be alleged that the standard of care was breached.
Types of Torts
The tort of medical negligence described above is only one of several torts for which
a healthcare provider might be responsible. Other types of torts include intentional
torts and strict liability.
Types of Torts
1. Intentional Tort – an overt act which is done intentionally and causes harm.
2. Negligence – a breach of the duty of care owed to another that occurs with
factual and proximate cause and creates damages.
3. Strict Liability – liability that arises from certain actions without a showing
of actual negligence. Fault is not an issue.
An intentional tort is an overt act which is committed deliberately and causes

harm to another. In other words, it must be shown that the person committing the
tort, also known as the tortfeasor, intended to commit the act. Examples include
assault, battery, false imprisonment, abandonment, defamation, deceit, fraud, and
misrepresentation.
Intentional Torts
• Assault
• Battery
• False Imprisonment
• Abandonment
• Defamation
• Deceit
• Fraud and Misrepresentation
Assault is the threat to cause harm to another without any actual contact or harm
taking place. Battery is the intentional touching of another without that person’s
consent. A common example of battery in the medical context is performing a pro-
cedure on a patient without their consent, or going further with the procedure than
what the consent authorized, such as removing both an ovary and a fallopian tube
when the patient only consented to a salpingectomy. Abandonment is another tort
which often arises in the context of providing healthcare. When a physician-patient
relationship has been established, and the physician unilaterally terminates that
relationship without the patient’s consent and without giving reasonable notice to
the patient, and the patient is somehow harmed, the physician can be held liable for
abandonment.
The tort of strict liability is liability that arises from certain actions without a
showing of fault or actual negligence. This type of tort is more likely to arise in the
context of consumer products such as medical equipment or drugs where the manu-
facturer is held strictly liable for some kind of defect in the product, or for a lack of
warning about the dangers of the product, if the user suffered harm caused by the
product.
Damages
Damages are what an injured party can recover as compensation for their loss. Basic
types of damages include nominal damages, compensatory damages, and punitive
damages.
Types of Damages in Medical Negligence

1. Nominal Damages
A slight or token payment to demonstrate that, while there may not have
been any physical harm done, the patient’s legal rights were violated.
2. Compensatory Damages
Special compensatory is for actual economic loss.
General compensatory is for noneconomic loss such as pain and
suffering.
3. Punitive Damages
Damages awarded to punish the defendant and to serve as a deterrent.
Nominal damages are simply a small or token payment made to a litigant, often
to demonstrate that, while there may not have been any physical harm done; the
patient’s legal rights were violated. Alternatively, nominal damages are sometimes
paid in an effort to resolve a lawsuit where the defendant may have a good defense,
but the cost or inconvenience of litigating the case is higher than the value of the
case, so a token or nominal payment is offered to settle out of court. This is fre-
quently referred to as the “cost of defense.”
In a medical negligence claim, there are a wide variety of compensatory damages
that can be paid which fall into two main categories: special compensatory and
general compensatory damages. The former relates to actual economic loss, such as
past and future medical bills or lost wages, whereas the latter relates to noneco-
nomic loss, such as pain and suffering experienced due to a medical injury. In a trial
the plaintiff must introduce evidence of actual economic loss in order for a jury to
award money to compensate for those special damages. However, a jury is free to
award whatever amount they see fit to compensate for noneconomic loss based on
the plaintiff’s testimony about the pain and suffering they experienced. Because the
jury is not confined to a particular dollar amount with noneconomic damages, and
because jurors can be easily influenced by emotion, there is the potential to get a
“runaway jury” which awards an amount far beyond what may seem as reasonable
compensation. In an obstetrical case, the most costly claim frequently involves a
neurologically impaired infant. In such a case, both special and general compensa-
tory damages can be very high because the damages may cover the entire life span
of the child (calculated by creating a life care plan) and because juries tend to be
sympathetic toward an injured baby and its family.
Punitive damages are awarded for the purpose of punishing a defendant and to
serve as a deterrent of future behavior. In order for a plaintiff to be awarded punitive
damages, they must demonstrate that the behavior of the defendant was so egre-
gious as to warrant punishing him or her with a monetary sanction. The standard of
proof varies throughout the country but typically involves a showing of reckless,
wanton or malicious behavior which has a high likelihood of resulting in substantial
harm, or behavior which shows complete disregard for the health and safety of the
injured party. This standard of proof goes well beyond ordinary negligence or fail-
ure of a healthcare provider to meet the standard of care in a medical malpractice
case. An example would be a provider conducting a cesarean section while under
the influence of alcohol or drugs. Depending on the circumstances, the plaintiff
might be able to establish that such behavior showed a complete disregard for the
health and safety of the patient. Punitive damages are serious because, as they are
typically excluded from professional liability coverage, they place the provider at
risk of personal liability exposure. If a jury awarded punitive damages to a plaintiff,
which frequently are higher than other damages in a case, the provider would per-
sonally be responsible for paying those out of his or her own assets.
Professional Liability Cost
The cost associated with professional liability is a topic well known to most health-
care providers as it is frequently in the news and is the subject of much debate about
the rising cost of liability insurance and healthcare. In 2015, the total medical mal-
practice payout in the United States was $3,954,339,750, which represents an
increase of 1.68% over the prior year. Per capita by state, New York had the highest
payout and Wisconsin had the lowest. The most severe outcome as a result of medi-
cal malpractice in 2015 was death, constituting 30% of the cases and resulting in an
average payout of $374,944. The outcomes of quadriplegia, brain damage, and life-
long care constituted 16% of the cases, and resulted in an average payout of
$1,086,711, which was the highest average payout for all outcomes [4].
In an effort to control the cost of professional liability awards and the resultant
effect on medical malpractice insurance premiums, many states have passed tort
reform legislation which caps noneconomic damages at a certain dollar amount.
However, such caps do not limit what a plaintiff can be compensated for economic
damages.
Disclosure of Adverse Outcomes
Some literature advocates that disclosure of adverse events has benefits for the
patient and the physician [5] and that a patient is less likely to pursue litigation if
they perceive that the event was honestly disclosed. A formal Sentinel Event Policy
was adopted by The Joint Commission on Hospital Accreditation in 1996. The pol-
icy was developed to help hospitals improve patient safety, prevent further harm,
and learn from sentinel events (adverse outcomes). A sentinel event is a Patient
Safety Event that reaches a patient and results in:
1. Death
2. Permanent harm, or
3. Severe temporary harm and intervention is required to sustain life [6]
The AMA Code of Ethics states, “The physician is ethically required to inform
the patient of all the facts necessary to ensure an understanding of what has occurred”
[7]. Although studies show that disclosure of adverse events promote patient-
physician trust, there are many barriers to disclosure. A culture of blame, fear of
retribution, and fear of lawsuits have caused physicians great concerns [5]. Some
states have enacted legislation to provide protection from liability if the physician
offers acknowledgment of the patient suffering, expressions of sympathy or empa-
thy, or if appropriate, an apology.
Sample State Statute

Certain Statements, Writings, and Benevolent Gestures Inadmissible
Missouri Revised Statutes, Chapter 538, Tort Actions Based on Improper
Health Care
Section 538.229. August 28, 2016
538.229. Certain statements, writings, and benevolent gestures inad-
missible, when--definitions.
1. The portion of statements, writings, or benevolent gestures expressing
sympathy or a general sense of benevolence relating to the pain, suffering,
or death of a person and made to that person or to the family of that person
shall be inadmissible as evidence of an admission of liability in a civil
action. However, nothing in this section shall prohibit admission of a state-
ment of fault.
2. For the purposes of this section, the following terms mean:
(1) “Benevolent gestures,” actions which convey a sense of compassion or
commiseration emanating from humane impulses;
(2) “Family,” the spouse, parent, grandparent, stepmother, stepfather,

child, grandchild, brother, sister, half brother, half sister, adopted chil-
dren of a parent, or spouse’s parents of an injured party.
(L. 2005 H.B. 393)
Medical Records and Associated Topics
Documentation
In a legal context, the medical record can be considered a “silent witness” [8].
How care is documented can be the best defense should a legal action arise
because it is rare that a healthcare provider will have an independent recollection
of the details surrounding the care of a patient by the time a lawsuit is eventually
filed. More often than not, providers do not even remember the patient, let alone
what was said and done to the patient. Thus, the medical record is typically the
key evidence upon which a legal defense is built. On the other hand, the medical
record can also be the best witness for the plaintiff, particularly when there is a
failure to document [8]. Plaintiff attorneys love to assert that “if it wasn’t docu-
mented it wasn’t done.” While technically this is not true because it is unneces-
sary, impractical, and impossible to document every single thing that is done for a
patient, the reality is that if key information is missing from the record it will typi-
cally work to the plaintiff’s advantage and against the healthcare provider. The
jury may presume that if something was omitted from the record, it should have
been done but was not. A healthcare provider’s testimony that he or she has a
custom and practice of doing things, regardless of whether it is written down, can
be used as evidence in a lawsuit, but it is always best to preserve the key aspects
of patient care by making a written record.
Take, for example, the case where the provider allows his patient to be removed
from the fetal monitor because she needs to go to the bathroom and after 10 min
she returns to her bed. The monitoring is resumed with the strip suddenly indicat-
ing late decelerations, but there is nothing in the medical record documenting the
patient’s trip to the bathroom. Several years hence when a lawsuit is filed because
of fetal demise, the defendant healthcare provider and his attorney will attempt to
piece together what happened, but there will be no explanation in the medical
record for why the patient was off the monitor for 10 min. Unless the provider
specifically remembers the incident, there can only be speculation as to why there
is a gap in the fetal monitoring. The plaintiff’s attorney will assert that the patient
was experiencing late decelerations during the time she was off the monitor, and
he will argue that the defendant was negligent because, had there been continuous
monitoring, the fetal compromise would have been caught sooner and more timely
intrauterine resuscitation would have saved the baby’s life. A simple entry by a
provider about why the patient was off the monitor for 10 min would save a lot of
headache down the road.
Practice Tips for Documentation

Documentation serves the dual purpose of making a record of a patient’s health-
care while communicating important details to other providers, so there is conti-
nuity of care for the patient. Given the importance of medical record
documentation, it is helpful to cultivate good practice habits for documentation
which will serve a provider well over time. The acronym CART, which stands for
complete, accurate, rationale, and timely, is a useful tool when documenting in a
patient record.
Complete A good patient record is comprehensive in order to be complete, but it

should also be concise. The goal is to cover everything pertinent to a particular
exam, treatment, or consultation in a format that is easily and readily reviewed by
subsequent providers without getting bogged down in superfluous information.
Accurate Accuracy should go without saying in medical record documentation,

yet far too often in litigation a patient’s chart contains inaccuracies. Sometimes
those inaccuracies are ultimately not relevant to the issue in the case, yet they create
a poor image in the mind of the jury. If a provider or facility seems sloppy in its
documentation, then were they sloppy in their care? To be accurate, the medical
record needs to conform to the facts of the patient’s care and be as free from error
as possible.
Rationale A provider’s rationale should be apparent when reading the medical

record. In order to illustrate that the standard of care was met when caring for a
patient, the provider should document the logic behind his or her diagnosis and plan
of care. Unfortunately, when a medical record is reviewed down the road, it can be
difficult to understand the justification for a particular treatment or course of action.
Setting forth the reasons for a plan of care demonstrates that a provider took into
account the objective and subjective information in a patient’s case and drew logical
conclusions from that information.
Timely The general rule with documentation is that the closer in time it is done with
the care provided the more accurate and complete it will be. Documenting contem-
poraneously can be difficult in the busy life of a healthcare provider who is under
tremendous pressure in an increasingly complex healthcare environment. However,
making a habit of quickly capturing what has been done with a patient will pay off in
both the short run and the long run. In the short run, it saves the provider time by not
having to reconstruct what was done with a patient when the facts are not fresh in
one’s mind, and in the long run it creates a reliable record for future reference.
Sometimes it is necessary to make a late entry in a record. This situation often
occurs when an emergency arises, such as a caesarean section, and there is no time
to document contemporaneously. Obviously, patient care takes priority over chart-
ing, so “hands on the patient, not on the computer” is always a good rule for provid-
ing excellent and safe patient care. But those are exactly the kind of circumstances
where it is essential to have complete and accurate documentation which explains
the rationale behind the patient care. Regardless of the reason for the late entry, be
it an emergency or simply forgetting to put something in the chart, always indicate
that a late entry is being made as opposed to making it appear that the entry was
contemporaneous or made at some time other than the actual time it is being made.
Most entries in the electronic record have an internal time and date stamp associated
with them which will contradict an entry that is purposefully timed or dated differ-
ently. In the legal context, it is always easier to explain why a late entry was made
rather than explain why an entry was dated and/or timed inaccurately.
Liability Issues with Medical Records
Tampering with medical records, such as falsification or spoliation, can expose the
healthcare provider to civil or criminal liability. Spoliation is “the destruction or
significant alteration of evidence” [9]. Spoliation of evidence is usually done solely,

or primarily, to deprive an opposing party of its use. Spoliation can take many forms
but in a medical legal context it usually involves destroying a document or record or
the alteration of a record. However, spoliation can also take the form of concealment
of physical evidence or tampering with witnesses. A classic example is set forth in
the film, The Verdict, where a doctor ordered a nurse to change a 1 to a 9 in order to
bring the doctor’s actions within the standard of care for that particular case.
While most states refuse to recognize a claim for intentional spoliation, there
are a few that do allow the claim as a separate cause of action. However, even if
it is not recognized as a separate cause of action, it is condemned in every juris-
diction in the United States. Most states utilize jury instruction and negative
inferences to address the issue if a case is being tried. Spoliation is an all too
frequent occurrence. It has been estimated that as many as 50% of medical mal-
practice cases involve altered records [10]. The most common actions involve
altering the records, adding to the record at a later time, deletion and/or substitu-
tion, insertion of false information, and destruction or loss of X-rays, lab reports,
or other physical evidence.
Historically there have been two remedies for spoliation. First, and most com-
mon, is the court directs a jury to infer that the altered or missing evidence was
legally harmful to the spoliator. This inference only applies where the spoliator is a
party or its agent. The second remedy is monetary or nonmonetary discovery sanc-
tions imposed by the court during the discovery phase of a lawsuit. Monetary sanc-
tions include compensating the injured party for discovery costs, the cost of
reconstructing evidence, and attorney’s fees. Nonmonetary sanctions include pre-
cluding the evidence from being used [11], deeming certain facts established [12],
dismissing the action [13], entering a default judgment against the party who com-
mitted the spoliation [13], and holding the offending party in contempt [14].
Additionally, spoliation can cause the burden of proof to shift from the plaintiff to
the defendant.
Electronic Health Record Issues
With the advent of the electronic health record (EHR), there has been an unfortunate
tendency for healthcare providers to “copy and paste” from other providers’ notes
into their own notes in an effort to save time. This is frequently seen when a provider
is writing a progress note or consultation and they copy information from a prior
progress note, or history and physical, into their own note. While there is nothing
inherently wrong with repeating information already documented by another pro-
vider, a problem arises when the copied material contains information about the
patient that is no longer pertinent to their current status, or was mistaken when origi-
nally written. For example, if a physician is creating a progress note on day three of
a pregnant patient’s admission for contractions, which have now subsided due to
treatment with terbutaline, and he copies and pastes some of the patient’s history
from a prior day’s progress note without noticing that it states the patient is still
experiencing contractions, then his current progress note is immediately inaccurate

because it is inconsistent with the patient’s status. Not only is this dangerous in
terms of potential mistreatment of the patient due to a mistaken record, it is also a
legal liability should a lawsuit be filed down the road. You can be sure a jury will see
an exhibit comparing the two progress notes word for word, often including the
exact same typos or misplaced punctuation, and they will conclude that the copying
physician was lazy and sloppy, either because he did not bother to read the original
note to ensure its current applicability, or he did not bother to conduct his own com-
plete assessment of the patient, or both. Regardless of whether the copying physi-
cian met the standard of care in the underlying issue of the case, the jury will develop
an unfavorable view of that physician, or worse, question his credibility, which can
be fatal when it comes to returning a favorable verdict.
Another example of how copying and pasting can be risky is when one
provider documents an inaccurate assumption about a patient, such as assum-
ing the patient is a recreational drug user, or otherwise makes an error in his
documentation, such as transposing two digits of a lab value, and a subsequent
provider copies and pastes that information into her own note. It is not uncom-
mon to see the same error repeated over and over again in the patient’s chart
by numerous providers because nobody is actually making the effort to ensure
the copied information is accurate. Rather, they skim the record for a conve-
nient summary of the patient’s history, so they do not have to recreate it on
their own, and then copy it verbatim into their own note. Again, not only is this
unsafe for patient care, it can be embarrassing and damaging in subsequent
litigation.
While traditional documentation in the paper medical record had its own inher-
ent issues such as illegibility, the EHR has risks associated with it. Some exam-
ples are:
1. Inadequate training on use may lead to upcoding

2. Over-documentation or “note bloat”
3. Unauthorized prescribing and ordering
4. Lack of access to all patient data
5. Inaccurate time and date stamping
6. Pop-up reminder fatigue
7. Computer crashes and power outages
8. Vulnerable security
9. Errors caused by misuse of copy and paste (cloning)
10. Automatic coding features
Unfortunately, auto-coding, record cloning, and software prompts have made it

easy to achieve inflated upper-level coding and additional payment for services.
Billing and coding errors, whether intentional or unintentional, have led to a sub-
stantial attack on providers for healthcare fraud.
Those involved in healthcare fraud are vigorously pursued by The Department of
Justice- Health and Human Services Medicare Fraud Strike Force. This
multiagency team of federal, state, and local investigators was designed to combat
Medicare fraud. The False Claims Act (FCA) prohibits individuals from submitting,
or causing someone else to submit a false or fraudulent claim for payment, to the
government. It applies to all government programs including Medicare. The two
most common violations of the FCA are the fabrication of records to get a false
claim paid and the submission of false claims to the government. The False Claims
Act is discussed later in this chapter.
Privacy and Protection of Health Information
Medical records and medical information are protected by a multitude of laws

including the Health Insurance Portability and Accountability Act (HIPAA).
HIPAA ensures (1) privacy and (2) protection of health information that is indi-
vidually identifiable health information maintained or transmitted in any form.
Required disclosures under HIPAA are limited to (1) disclosures to the individ-
ual who is the subject of the information and (2) disclosures to the Office of Civil
Rights (OCR) to determine compliance. All other uses and disclosures are
permissive.
The patient’s rights under HIPAA include [15]:
1 . Right to inspect and copy protected health information

2. Right to amend the record
3. Right to an accounting of disclosures
4. Right to have reasonable requests for confidential information accommodated
5. Right to file a complaint with the OCR or with a covered entity
6. Right to written notice of information practices from providers and health plans
HIPAA has placed additional burdens on healthcare providers and institutions to

safeguard the confidentiality of medical records and has created civil and criminal
penalties for violations. The OCR is responsible for administering, investigating,
and enforcing the HIPAA privacy standards. The American Recovery and
Reinvestment Act created a tiered penalty configuration for HIPAA violations. But
the OCR determines the amount of each penalty, and it is dependent upon the nature
and extent of harm that results from a breach (see Table 14.1).
Table 14.1 Tiered penalties Category Fine range

for HIPAA violations Did not know of breach $100–50,000
Had reasonable cause to $1000–50,000
know
Willful neglect, corrected $10,000–50,000
Willful neglect, not corrected $50,000
Informed Consent
Informed consent is a doctrine that recognizes the right of a patient to be fully

informed of the risks, benefits, and alternatives to treatment before undergoing any
such treatment. A long line of legal cases in the twentieth century helped shape the
law of informed consent including the concept that treating a patient without con-
sent is a violation of the patient’s bodily integrity for which a physician can be liable
for assault and battery. The responsibility of informed consent typically falls
squarely on the shoulders of the physician because he or she has the necessary train-
ing, education, and expertise to understand what information should be provided to
the patient to enable them to give informed consent. In the context of the acute
abdomen in the pregnant patient, extra consideration should be given by the health-
care provider to informed consent because with most treatments and procedures
there are risks, benefits, and alternatives which may impact both the mother and
fetus, and often times those conflict with each other. For instance, a medication that
is indicated for the mother may involve severe risks to the unborn fetus. Likewise,
treatment that could improve the condition of the fetus might compromise the health
of the mother.
Elements
There are three main elements of informed consent which should be considered
when discussing treatment with a patient: (1) threshold elements, (2) information
elements, and (3) decision and authorization.
Elements of Informed Consent

Threshold Elements
• Capacity
• Voluntariness
Information Elements
• Disclosure
• Recommendation
• Understanding
Consent
• Decision
• Authorization
hreshold Elements (Capacity and Voluntariness)

T
Threshold elements of informed consent take into account whether a patient has the
ability to comprehend the treatment being discussed and whether the patient is giv-
ing consent voluntarily. The first threshold element to consider is whether the patient
has capacity to give consent. Capacity refers to an individual’s actual ability to
understand or form an intention with regard to some act such as consenting to treat-
ment. The provider needs to evaluate if the patient has an adequate level of attention
during the informed consent discussion, whether their judgment is sufficiently
intact, and whether they are able to comprehend relevant instructions. The age of the
patient, her cognitive capabilities, and her mental status are examples of factors
which might prevent her from being able to give informed consent. If a patient lacks
capacity to understand the information provided about the proposed treatment, then
she is not capable of giving informed consent. Physicians regularly make determi-
nations of capacity. When a patient lacks capacity, informed consent must be
obtained from next of kin, a guardian, or some other person who can consent on the
patient’s behalf.

Who May Give Consent
Missouri Revised Statutes, Chapter 431
General Provisions as to Contracts
431.061. Consent to surgical or medical treatment, who may give,
when.
1. In addition to such other persons as may be so authorized and empowered,

any one of the following persons if otherwise competent to contract, is
authorized and empowered to consent, either orally or otherwise, to any
surgical, medical, or other treatment or procedures, including immuniza-
tions, not prohibited by law:
(1) Any adult 18 years of age or older for himself;
(2) Any parent for his minor child in his legal custody;
(3) Any minor who has been lawfully married and any minor parent or
legal custodian of a child for himself, his child and any child in his
legal custody;
(4) Any minor for himself in case of:
(a) Pregnancy, but excluding abortions;
(b) Venereal disease;
(c) Drug or substance abuse including those referred to in chapter
195;
(5) Any adult standing in loco parentis, whether serving formally or not,
for his minor charge in case of emergency as defined in section
431.063;
(continued)
( 6) Any guardian of the person for his ward;

(7) Any relative caregiver of a minor child as provided for under section
431.058
2. The provisions of sections 431.061 and 431.063 shall be liberally con-
strued, and all relationships set forth in subsection 1 of this section shall
include the adoptive and step-relationship as well as the natural relation-
ship and the relationship by the half-blood as well as by the whole blood.
3. A consent by one person so authorized and empowered shall be sufficient
notwithstanding that there are other persons so authorized and empowered
or that such other persons shall refuse or decline to consent or shall protest
against the proposed surgical, medical, or other treatment or procedures.
4. Any person acting in good faith and not having been put on notice to the
contrary shall be justified in relying on the representations of any person
purporting to give such consent, including, but not limited to, his identity,
his age, his marital status, and his relationship to any other person for
whom the consent is purportedly given.
(L. 1971 H.B. 73 § 1, A.L. 1977 S.B. 48, A.L. 2014 S.B. 532)
It is important to recognize that capacity can be a moving target because it can

vary over time and with different circumstances. A patient who has current capacity
to consent to a procedure today may be disoriented later in the evening, and thus not
able to partake in a different informed consent discussion. Likewise, a patient with
a behavioral health disorder may not have capacity to consent to something as com-
plex and serious as surgery, but still be able to consent to having an IV started,
because they have the cognitive abilities to understand the latter.
Capacity is sometimes confused with the concept of competence, and the terms
are often used interchangeably, but they are not interchangeable from a legal per-
spective. They each have unique definitions. Competence refers to one’s legal status
as a decision-maker. Competence is a vague and ambiguous term because it is a
broad concept that encompasses many different legal issues and contexts. In gen-
eral, competence refers to some minimal cognitive or behavioral ability, trait, or
required capability.
Competence in the civil context is commonly raised in two situations, legal age
of majority, and mental disability. With some exceptions the age of majority is 18
and persons of this age are presumed to be competent. Incapacity secondary to men-
tal disability may be slightly more nuanced depending on the context. In the discus-
sion of consent to medical treatment, competency to consent might be questioned if
the person is mentally ill, under the influence of drugs or alcohol, has a brain injury,
or suffers from some other medical condition which causes mental disability such
as Alzheimer’s disease. The question of competency and determination of incompe-
tency can only be judicially determined. A person is presumed competent unless
adjudicated incompetent. There is no established set of criteria, nor a single test, for
determining a person’s competence. Rather, a judge weighs the evidence presented

at a hearing which typically includes evaluations of decisional capacity by profes-
sionals such as physicians, psychologists, and social workers. The fact that a patient
may be deemed incompetent or has been appointed a guardian does not meant they
lack capacity to participate meaningfully in certain treatment decisions, or that their
wishes should be ignored. To the degree that they are able to participate, there is a
moral obligation to allow them to do so.
Capacity and competence do not always coincide. Minors are incompetent to
make most healthcare decisions, yet as a matter of public policy they may have
decisional capacity in certain circumstances such as pregnancy, sexually transmitted
infections, and drug or substance abuse. To encourage minors to seek treatment
under those circumstances, most states have granted minors, via minor treatment
statutes, the ability to make certain healthcare decisions. Similarly, certain minors
who are emancipated or married are considered mature minors who are recognized
as competent decision-makers and may consent to treatment on their own behalf, or
for their children (see above Sample State Statute: Who May Give Consent).
Voluntariness requires freedom of choice and freedom from controlling influ-
ence by others. Undue pressure from family members, clinicians, religious groups,
ethnic custom, or others may invalidate a consent. Physicians need to preserve
patient voluntariness.
I nformation Elements (Disclosure, Recommendation,

and Understanding)
Information elements of informed consent include disclosure, recommendation, and
understanding. Disclosure refers to the key pieces of information that must be made
known to the patient and understood by the patient. These include the nature of the
therapy, purpose, risks and consequences, benefits, probability of success, feasible
alternatives, and prognosis with no therapy.
Informed Consent Disclosure

• Nature of the therapy
• Purpose
• Risks and consequences
• Benefits
• Probability of success
• Feasible alternatives
• Prognosis with no therapy
Once that information is disclosed, a recommendation is made by the physician

based on his or her expertise. Recommendations are often meaningful to the patient
because without one, the patient may feel lost or overwhelmed. However, the final
decision obviously rests with the patient. It is the physician’s responsibility to make
sure the patient understands what has been discussed and to avoid confusing medi-
cal jargon. Asking a patient to describe in their own words their understanding of
the proposed treatment is a helpful way to verify comprehension, as opposed to

asking close-ended questions, such as “Do you understand?”
onsent (Decision and Authorization)

C
Most patients follow a recommended treatment plan, but ultimately it is their right
to choose how to proceed. If they decide to undergo the treatment, they must pro-
vide authorization of their consent. If they decide not to undergo treatment, although
uncommon in pregnant patients, their right to refuse treatment is still a common law
right guaranteed by the 14th Amendment. Regardless of the patient’s decision, it is
important for the physician to document the informed consent discussion so that the
record reflects the patient made a well-informed decision. Sometimes refusal to
treat involves an end of life issue. There is further discussion of this issue in section
“Persistent Vegetative State and End of Life Medical Matters” where the Self
Determination Act is addressed.
Exceptions to Informed Consent
There are five situations in which informed consent is not required: emergencies,
therapeutic privilege, patient knowingly yields right to informed consent, incompe-
tency, and national/state waivers (in the case of the military).
Informed Consent Exceptions

1. Emergencies
In an emergency the patient may be unable to give consent or will incur
greater harm if time is taken to explain medical interventions.
2. Therapeutic Privilege
The withholding of information by the physician based on the judgment
that disclosure would be harmful to the patient.
3. Patient knowingly yields right to informed consent
When patients voluntarily and purposefully give up their rights to dis-
closure and autonomous decision-making
4. Incompetency
In the context of medical decisions “incompetency” is a legal term to
describe the condition of a person lacking legal capacity to make certain
decisions concerning his/her medical care. Legal incompetency must be
determined by a court in a legal proceeding.
5. National/State Waivers (military)
Where a service member is required to undergo physical, psychiatric, or
other types of medical care to determine fitness for duty
In an emergency, the patient may be unable to give consent or will incur

greater harm if time is taken to explain medical interventions. The most common
example is an unconscious or incapacitated patient who comes to the emergency
department as a result of a motor vehicle accident or a shooting. Often the pro-

viders are faced with needing to perform life-saving measures or are faced with
tremendous blood loss and do not have time to obtain informed consent for treat-
ment. Under these circumstances, the consent of the patient is presumed and it is
not necessary to obtain consent to treat the patient. Therapeutic privilege is the
withholding of information by the physician based on his or her judgment that
disclosure would be harmful to the patient. While it should only be invoked on
rare occasions, an example would be not immediately telling a suicidal patient
that she has lost her baby for fear that it would provoke a suicidal act on her part.
A patient knowingly yielding their right to informed consent is when they volun-
tarily and purposefully give up their rights to disclosure and autonomous deci-
sion-making. This could arise in the context of a medical research study where
the patient has agreed they will not be told whether they are receiving a placebo
or the actual study drug.
Incompetence, discussed earlier, is an exception to informed consent and it is a
legal term to describe where a person lacks legal capacity to make certain decisions
concerning his or her medical care. Legal incompetency must be determined by a
court in a legal proceeding. Unlike capacity, it is not a medical judgment. Before a
provider should decide that informed consent is not necessary due to incompetency,
they should have documentation from a court which has made that legal determina-
tion. Typically when a patient has been declared legally incompetent they have been
appointed a legal guardian from whom informed consent must be obtained when
treating the patient. The final exception to informed consent is in the context of mili-
tary service where a service member can be required to undergo physical, psychiat-
ric, or other types of medical care to determine fitness for duty, or required to have
certain vaccinations.
Immunity and Good Samaritan Law
The five exceptions to informed consent discussed above protect a healthcare

provider against an allegation that treatment was provided without informed
consent. Somewhat similar to the emergency exception for informed consent,
but extended to liability for negligence, most states grant immunity to health-
care professionals under what is typically referred to as Good Samaritan laws.
These statutes vary from state to state, but they typically protect providers
responding to an emergency situation from liability if they did so voluntarily
and without expectation of pay. The public policy behind these statutes is to
encourage trained medical providers to respond to the scene of an emergency
and offer aid to people suffering from serious bodily injury or life-threatening
situations.

Good Samaritan Law
Missouri Revised Statutes, Chapter 537
Torts and Actions for Damages
537.037. Emergency care, no civil liability, exceptions (Good Samaritan law).
1. Any physician or surgeon, registered professional nurse or licensed practi-
cal nurse licensed to practice in this state under the provisions of chapter
334 or 335, or licensed to practice under the equivalent laws of any other
state and any person licensed as a mobile emergency medical technician
under the provisions of chapter 190, may:
(1) In good faith render emergency care or assistance, without compensa-
tion, at the scene of an emergency or accident, and shall not be liable
for any civil damages for acts or omissions other than damages occa-
sioned by gross negligence or by willful or wanton acts or omissions
by such person in rendering such emergency care.
(2) In good faith render emergency care or assistance, without compensa-
tion, to any minor involved in an accident, or in competitive sports, or
other emergency at the scene of an accident, without first obtaining the
consent of the parent or guardian of the minor, and shall not be liable
for any civil damages other than damages occasioned by gross negli-
gence or by willful or wanton acts or omissions by such person in
rendering the emergency care.
2. Any other person who has been trained to provide first aid in a standard recog-
nized training program may, without compensation, render emergency care or
assistance to the level for which he or she has been trained, at the scene of an
emergency or accident, and shall not be liable for civil damages for acts or
omissions other than damages occasioned by gross negligence or by willful or
wanton acts or omissions by such person in rendering such emergency care.
3. Any mental health professional, as defined in section 632.005, or qualified
counselor, as defined in section 631.005, or any practicing medical, osteo-
pathic, or chiropractic physician, or certified nurse practitioner, or physi-
cians’ assistant may in good faith render suicide prevention interventions
at the scene of a threatened suicide and shall not be liable for any civil
damages for acts or omissions other than damages occasioned by gross
negligence or by willful or wanton acts or omissions by such person in
rendering such suicide prevention interventions.
4. Any other person may, without compensation, render suicide prevention
interventions at the scene of a threatened suicide and shall not be liable for
civil damages for acts or omissions other than damages occasioned by
gross negligence or by willful or wanton acts or omissions by such person
in rendering such suicide prevention interventions.
(L. 1979 H.B. 445 § 1, A.L. 1983 1st Ex. Sess. H.B. 8, A.L. 1986 H.B. 860,
A.L. 2005 H.B. 462 & 463, A.L. 2008 S.B. 1081)
EMTALA
The Emergency Medical Treatment and Active Labor Act (EMTALA) was enacted
in 1986 to ensure that all patients in a medical crisis were appropriately treated. It
was created to address the problem of hospital emergency departments turning
away patients who could not pay [16]. The fact that it specifically covers patients in
active labor makes it particularly relevant to the subject of this textbook. If a preg-
nant patient cannot reach her doctor and presents to the emergency department with
abdominal pain, or other abdominal issues, the healthcare provider should have a
thorough understanding of how to comply with the Act and the ramifications of fail-
ing to do so. To comply with EMTALA, a hospital must follow three basic require-
ments [17]:
1 . Screen patients to determine whether a medical emergency exists

2. Stabilize patients with medical emergencies
3. Restrict transfer of nonstabilized patients to two circumstances, described in
more detail below
As for requirement 1, the emergency department must provide a medical screen-

ing exam to any patient who requests treatment, regardless of ability to pay, in order
to determine whether a medical emergency exists. An emergency medical condition
is considered to be the presence of acute symptoms of such severity that the absence
of immediate medical attention could reasonably be expected to result in placing an
individual’s health in serious jeopardy, serious impairment to bodily functions or
serious dysfunction of any bodily organ or part. The medical screening exam should
be comparable to an exam performed on another patient who presents with the same
or similar symptoms. With respect to a pregnant woman who is having contractions,
an emergency medical condition is one in which there is inadequate time for safe
transfer to another hospital before delivery, or one in which transfer may pose a
threat to the health or safety of the woman or unborn child.
As for requirement 2, if the patient has an emergency medical condition, the
hospital must provide treatment until the patient is stabilized, then transfer the
patient to a medical facility that is better able to provide the necessary treatment.
The transferring hospital must try to minimize the risk of transfer, obtain the
patient’s written consent for transfer, provide a signed certificate of transfer, assure
that the transfer takes place with qualified personnel and equipment, and send cop-
ies of medical records related to the emergency condition to the receiving hospital.
The receiving hospital is obligated to have available space and qualified personnel
to treat the patient, agree to accept the transfer, and provide appropriate medical
treatment. Regional referral centers and hospitals with specialized capabilities can-
not refuse to accept an appropriate transfer it they have the capacity.
As for requirement 3, nonstabilized patients may be transferred only if the patient
(or someone acting on the patient’s behalf) requests a transfer in writing after being
informed of the risks involved and the hospital’s duty to treat under EMTALA, or a
physician certifies that the medical benefits expected from transfer outweigh the
risks involved in the transfer.
Triaging abdominal pain in pregnancy can be difficult. The healthcare provider

should carefully discern whether the abdominal pain is attributable to labor or
another abdominal condition. Failure to make a timely and accurate diagnosis can
delay treatment and may lead to an increased risk of adverse events. A real life
example illustrates this point: a pregnant patient presented to the Emergency
Department with abdominal pain and inability to void. The ED nurse evaluated the
patient and contacted the obstetrician by phone, who ordered observation for several
hours. After 2 h of observation the nurse discharged the patient. Four hours later the
patient returned with worsening abdominal pain and vaginal bleeding. An ultra-
sound confirmed an intrauterine fetal demise secondary to placental abruption.
Setting aside professional liability issues, the patient was allowed to proceed with a
claim for an EMTALA violation because of the lack of compliance with hospital
policy which required a patient in active labor to be examined by an obstetrician or
other physician before discharge [18].
There are two courses of action for violations of EMTALA: private civil suits
against the hospital (but not the physician) and a Health and Human Services (HHS)
penalty which fines the hospital, the physician, or both. HHS may fine and penalize
a physician who fails to respond to an emergency while on call, fails to perform a
screening exam, fails to inform emergency patients of the risks and benefits of trans-
fer, or signs a transfer certification when he or she can reasonably be expected to
know that the risks outweigh the benefits of the transfer.
An Overview of EMTALA Fines and Penalties for EMTALA Violations [19]

Fines and penalties for violations of the EMTALA statute are as follows:
• Hospitals may be fined $50,000 per violation ($25,000 for hospitals with
<100 beds).
• Physicians may be fined $50,000 per violation.
• The hospital or physician’s Medicare provider agreement may be
terminated.
• The hospital may be sued by the patient in civil court for an EMTALA
violation.
• A receiving hospital can bring suit against a transferring hospital for its
EMTALA violation.
• More than one violation can result from a single patient encounter.
Healthcare Fraud and Abuse
There are many state and federal laws which govern physician practices and
which are enforced by government entities including the Centers for Medicaid
and Medicare Services, the Office of Inspector General, the Department of Justice
and the Department of Health and Human Services. The five main areas of fraud
and abuse include the False Claims Act (FCA), the Anti-Kickback Statute, the
Physician Self-Referral Act (Stark), and the Exclusion Statute and the Civil
Monetary Penalty Law [20]. For purposes of this chapter, the focus will be only
on the FCA in order to stress the importance of handling coding and billing prop-
erly in order to avoid liability.
As alluded to earlier in this chapter, auto-coding and record cloning sometimes
causes inflated upper level coding and additional payment. The FCA permits
recovery of funds from anyone who knowingly presents or causes to be presented
a fraudulent claim for payment to the government. To establish FCA liability, it
must be proven that a defendant knowingly submitted or caused to be submitted a
false claim for reimbursement of services. The claim need not be entirely fraudu-
lent in order to violate the FCA. Rather, the FCA prohibits use of any false state-
ment or document in support of a claim for government funds. Apart from
traditional claims, liability under the FCA also attaches to anyone who acts
improperly to avoid having to pay money to the government (known as “reverse”
false claims).
Common examples of healthcare fraud include [21]:
1. Billing for services not rendered

2. Falsifying a patient’s diagnosis to justify tests, surgeries, or other procedures
3. Misrepresenting procedures performed to obtain payment for noncovered
services
4. Billing for a more costly service than the one performed (upcoding services)
5. Billing for more expensive equipment that was delivered to patient (upcoding
medical supplies)
6. Billing each stage of a procedure as if it were a separate procedure
(unbundling)
7. Billing for services not medically necessary
8. Accepting kickbacks for patient referrals
9. Waiving patient copays or deductibles
10. Overbilling the insurance carrier or benefit plan
Financial recovery against a defendant under the FCA can be devastating, with
penalties of $5500–11,000 per claim plus three times the government’s damages. In
the context of Medicare billing, the potential exists for a catastrophic judgment
based on the number of claims at issue. Individuals may be held responsible if found
to have acted willfully, recklessly, or with deliberate ignorance in making or causing
the submission of false claims. Those responsible may even face criminal charges in
extreme cases. The very potential for imposition of individual liability and/or crimi-
nal sanctions allows the government to aggressively and effectively leverage settle-
ments when armed with FCA allegations. Further, liability under the FCA is
allowable for violations of the Stark Law and the Anti-kickback Statute.
Persistent Vegetative State and End of Life Medical Matters
atient Self-Determination Act, DPOA Issues, Advance Directives,

P
PVS, Brain Damage
The incidence of encountering end of life medical and legal issues is low in the
context of pregnant women, but awareness of possible issues is important, neverthe-
less. The Patient Self-Determination Act (PSDA) of 1990 encourages all people to
make choices now about the types of and extent of medical care they want to accept
or refuse should they become unable to make those decisions due to illness or inca-
pacitation. Compliance with this federal law is mandatory. All healthcare agencies
(hospitals, long-term care facilities, and home health agencies) receiving Medicare
and Medicaid reimbursement are required to recognize living wills, advanced direc-
tives, and durable powers of healthcare.
The PSDA does not create new rights but affirms the common law right of self-
determination as guaranteed by the due process clause of the 14th Amendment.
Healthcare agencies must ask the patient whether they have an advance directive,
and if they do not, must provide information about it if requested. This written noti-
fication of the patient’s right to refuse or consent to medical treatment is an impor-
tant vehicle to improving the healthcare decision-making process. Complex issues
such as irreversible maternal brain injury during pregnancy, persistent vegetative
state (PVS), and brain death in contemporary healthcare practice can be navigated
more successfully with advance consideration. The literature documents several
cases of maternal brain death in pregnancy as well as cases of PVS associated with
irreversible brain injury [22]. Feldman et al. described a case of a pregnant mother
who sustained irreversible brain damage. The family chose to maintain the preg-
nancy via aggressive life support of the mother. After a lengthy hospital course, a
viable infant was delivered by cesarean section followed by successful organ har-
vesting from the mother [22]. A protocol for managing such patients was created by
Feldman et al. Fig. 14.1 is an adaptation of that protocol.
These are examples of rare but tragic and complex cases a provider may confront
when caring for the pregnant patient. Prior to current medical technology, fetuses in
utero historically died with the mother. Now women who have experienced a CVA
or other brain injury leave the provider to deal with issues of self-determination vis-
à-vis the fetus in utero.
Conclusion
This chapter has highlighted a variety of medico-legal issues the healthcare provider
may encounter, but it is by no means comprehensive. The legal issue typically most
worrisome to the practitioner is medical negligence. To protect oneself from liabil-
ity, the practitioner must stay abreast of the standard of care and strive to provide the
best care possible. Complete, accurate documentation which supports the rationale
for the care provided, and is entered in the medical record in a timely manner, will
Fig. 14.1 Algorithm for management of maternal brain death [22]

go a long way in protecting against liability. Likewise, ensuring that informed con-
sent discussions cover all necessary components, including risks, benefits, and alter-
natives; and are thoroughly documented in the medical record, will help establish
that the patient understood and voluntarily made a well-informed treatment choice.
Familiarity with regulatory issues such as EMTALA and HIPAA, as well as end
of life matters, is essential for the provider in today’s complex healthcare environ-
ment to avoid legal and ethical pitfalls. Not every legal issue can be anticipated in
the healthcare arena, but the practitioner armed with basic legal knowledge will
navigate the medico-legal waters more confidently and successfully.
References
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www.nejm.org/doi/full/10.1056/NEJMsa1012370#t=article 10.1056/NEJMsa1012370.
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get sued; 2015 .[cited 2017 Mar 28] Available from: http://www.medscape.com/features/
slideshow/public/malpractice-report-2015#page=1
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the-standard/2016-medical-malpractice-payout-analysis/.
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mission.org/sentinel_event_policy_and_procedures/.
7. The AMA code of medical ethics’ opinions on patient safety. AMA J Ethics. 2011;13(9):626–8.
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Neonatal Med. 2005;10(1):3–9.
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11. Federal Rules of Civil Procedure: Rule 37(b)(2)(B) (2016).
12. Federal Rules of Civil Procedure: Rule 37(b)(2)(A) (2016).
13. Federal Rules of Civil Procedure: Rule 37(b)(2)(C).
14. Federal Rules of Civil Procedure: Rule 37(b)(2)(D).
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www.cms.gov/regulations-and-guidance/legislation/emtala/.
17. 42 U.S.C. Sec. 1395dd. Examination and treatment for emergency medical conditions and
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1 8. Williamson v. Roth, 120 F. Supp. 2d 1327 (M.D. Fla. 2000).

19. The Consolidated Omnibus Budget Reconciliation Act of 1985, Pub L No. 99272, Sec. 9121,
100 Stat 82 (1986).
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news/aaosnow/aug11/advocacy3.asp
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Index
A functional cysts, 70
Abdominal and pelvic pain, 45–48 pregnancy failure, 81, 82
bilious vomit, 44 Abortion, 107–124, 126–130, 132
bowel habits, 44 abdominal pregnancy, 124
cardiovascular and pulmonary risks, 45 CSP, 125, 126
characterization, 43 ectopic (see Ectopic pregnancy)
clinical setting, 42 first-trimester spontaneous abortion
diagnosis, 193 (see First-trimester spontaneous
duct obstructions, 44 abortion)
emergency, 42 interstitial pregnancy (see Interstitial
evaluation and management, 42 pregnancy)
gastric ulcer, 43 midtrimester (see Midtrimester abortion)
history-taking process, 42 ovarian pregnancy, 125
low-risk procedures, 45 placenta previa, 135
medical clearance, 45 placental abruption (see Placental
musculoskeletal origin, 43 abruption)
nonobstetrical surgical procedure, 41 rupture, uterine (see Uterine rupture)
obstetricians, 41 uterine incarceration, 130–132
O-P-Q-R-S-T mnemonic, 44 Abruption, 100
patient’s history, 42, 45 Acute abdomen in pregnancy, 99, 100, 103, 104
patients’ position, 43 blood count, red blood cells, 103–104
pelvic abscess, 43 causes (see Causes unrelated to pregnancy)
physical examination (see Physical clinical evaluation and changes, 99
examination) laboratory reference values, 104
pregnancy-induced physiological laboratory testing, 99
changes, 41 nonabdominal conditions, 100
sexual intercourse, 43 related conditions (see Pregnancy-related
small bowel obstruction, 43 conditions)
social history, 45 Acute cystitis, 196
surgical disorders, 42 Acute fatty liver of pregnancy (AFLP), 65
urological anatomical changes, 193 Acute pancreatitis, 102
vomiting, 43 Acute urinary retention (AUR), 195
Abdominal ectopic pregnancies, 88, 124 Adnexal mass
Abdominal trauma acute abdominal pain, 142
adnexal masses, 69, 70 asymptomatic, 141
corpus luteum, 70 causes, 142
cysts, 70 cesarean delivery, 146
early normal pregnancy, 80 diagnosis, 142
first trimester causes, 80 incidence, 141

in Pregnancy, DOI 10.1007/978-3-319-62283-5
270 Index
Adnexal mass (cont.) in pregnancy, 57, 59, 186

management, 143 sensitivity, 57
symptomatic, 141 specificity, 57
ultrasound, 141 surgical management, 59
AMA Code of Ethics, 248 treatment, 187
American College of Chest Physicians ultrasonography, 59
(ACCP), 225 As low as reasonably achievable (ALARA), 92
American College of Obstetricians and Assisted reproductive technology (ART), 82
Gynecologists (ACOG), 51, 195 Asymptomatic bacteriuria (ASB), 195, 196
American College of Radiology (ACR), 51, 55 Atrial natriuretic peptide (ANP), 20
American Society for Colposcopy and Auscultation, 46
Cervical Pathology (ASCCP)
guidelines, 154
Anatomical changes, pregnancy B
conditions, 1 Benzodiazepines, 231, 234
developments, maternal and fetal Biliary tract disease, 62, 63
outcome, 1 benign and malignant conditions, 173
diagnosis and management, disease and diagnosis, 173, 174
injury, 1 surgical therapy, 175
signs and symptoms, 1 Blastocyst
uterine enlargement, 2, 3 cavity, 28
Anesthetic considerations, acute abdomen differentiation, cytotrophoblast and
bowel obstruction, 233 syncytiotrophoblast, 28
endotracheal anesthesia, 233 embryoblast, 28
factors, 232 endometrium and implantation, 28
physiologic alterations, 228 implantation, 28
regional anesthesia, 233 trophoblast, 28
spinal/epidural anesthesia, 233 Blood pressure (BP), 7, 8
T4-T6 dermatomes, 233 arterial BP and SVR
Anorexia, 44 CO and resistance, 7
ANP. See Atrial natriuretic peptide (ANP) diastolic BP and MAP, 7
Antenatal human development, 26–31 luteal phase, 7
detal development phase, 26 mercury sphygmomanometry, 8
embryonic development phase, 25 NO synthase, 7
embryonic period 8 weeks’ gestation, 7
first postconceptional week, 26–28 postnatal measures, 8
fourth to eighth postconceptional Blunt, 211, 213
weeks, 31 BNP. See Brain natriuretic peptide (BNP)
second postconceptional week, 28, 29 Bowel obstruction
third postconceptional week, 29–31 diagnosis, 181
fetal period, 31, 32 maternal morbidity, 181
phases, 26 in pregnancy, 181
Antibiotics treatment, 182
prophylaxis, 224, 225 Brain natriuretic peptide (BNP), 20
spontaneous abortion, 111 Budd-Chiari syndrome, 64, 65
Anti-Kickback Statute, 263
Apparent diffusion coefficient (ADC), 64
Appendicitis, 102 C
abdominal pain, 58 Caesarian-section (C-section) scar, 88
air-/contrast-filled lumen, 59 Calcium metabolism
cohort studies, 186 absorption, 16
diagnosis, 59, 187 activity, 15
MRI, 59 albumin-bound fraction, 16
oral ferumoxil oral suspension, 59 calcitropic hormone levels, 16, 17
Index 271
loss, 15 acute abdomen, 171

parathyroid hormone, 16 biliary disease, 171
physiologic hyperparathyroidism, 15 diagnosis, 171
vitamin D, 16 laboratory analysis, 102, 172
Carcinogenesis, 51 radiographic analysis, 172
Cardiac output (CO) treatment, 172, 173
and BP, 7 Choledocholithiasis, 62, 173
early pregnancy, 4 Cholestasis, 14
fetal birthweight and maternal height and Chorioamnionitis, 101
weight, 6 Colitis
fetal HR tracing, 7 diagnosis, 184
gestations, 6 treatment, 184
investigative techniques, 6 UC and CD, 183
maternal position influences, 6 Computerized tomography (CT)
pregnancy, 5 adnexal masses, 75
SV and HR, 6 macroscopic fat, 75
systemic vascular resistance (SVR), 7 in pregnancy, 54
trimester, 6 radiography, 54
uterus, placenta and breasts, 6 Consent
Cardiovascular system, 3–7 elements, 254
arterial BP and SVR, 7, 8 exceptions, 258, 259
CO (see Cardiac output (CO)) immunity, 259, 260
fetal development, 33, 34 legal cases, 254
heart (see Heart) Corticosteroid administration, 224
maternal morbidity, 3
oxygen delivery, 3
venous pressure, 8 D
Causes unrelated to pregnancy, 102 Delivery, 219, 220
acute pancreatitis, 102 Dermoid cyst, 74
appendicitis, 102 Diffusion-weighted imaging
cholecystitis, 102 (DWI), 64
diagnosis, 100 Disseminated intravascular coagulation (DIC),
myocardial infarction, 103 100, 101
nephrolithiasis, 103 Diverticulitis
porphyria, 103 bowel diverticula, 185
sickle cell crisis, 103 diagnosis, 185, 186
small bowel obstruction, 102 treatment, 186
Cervical cancer Doppler echocardiography
diagnosis, 154 CO, 4
FIGO staging, 155 diastolic function, 4
management, 154 Doxycycline, 224, 225
Papanicolaou (Pap) smear, 153 DPOA issues, 264
pelvic/lower back pain/pressure, 153
Cervical ectopic pregnancies, 86, 87
Cervical intraepithelial neoplasia (CIN) E
asymptomatic, 153 Ectopic pregnancy, 115, 116, 118–121, 127
diagnosis, 154 abdominal pain, 88, 118
malignancy, 153 beta human chorionic gonadotropin
management, 154 diagnosis, 118
obstetrical implications, 155–156 levels above the discriminatory zone,
pre-cancerous lesion, 153 118–119
Cesarean scar pregnancy (CSP), 125, 126 levels below the discriminatory zone,
Chloroprocaine, 232 119
Cholecystitis, 62 TVS, 118
272 Index
Ectopic pregnancy (cont.) cellular proliferation and

bimanual pelvic examination, 114 differentiation, 28
blastocyst implants, 112 clefts development, 28
cervical, 86, 87 formation, extraembryonic mesoderm, 28
components, 118 hCG, 28
C-section, 88 hypoblast cells migration, 28
decidual cast, 117 implantation, 28
delayed menstruation, pain and vaginal third postconceptional week, 30
bleeding/spotting, 114, 117 bilaminar embryonic disc, 29
diagnosis, 83, 112, 114 gastrulation, 30
fallopian tube, 112 heart and great vessels formation, 31
hemoglobin, 117 mesenchymal cells, 30
hemoperitoneum, 121, 122 notochord, 30
hyperintense signal, 90 The Emergency Medical Treatment and Active
interstitial, 85, 86 Labor Act (EMTALA), 261, 262
morbidity, 85 Endometriomas, 72, 73
mortality, 85 Endometriosis, 151, 152
MRI, 88 Endoscopic retrograde cholangiopancreatography
ovarian, 88 (ERCP), 174, 177
pelviscopy, 122 Epistaxis, 9
placental implantation, 90 Epithelial neoplasms, 75
pregnancy-related deaths, 112 Extracorporeal shock wave lithotripsy
reproductive capability, 113 (ESWL), 202
risk factors, 83, 114 Extrauterine pregnancy, 99, 100
serum β-hCG levels, 83
serum progesterone, 119–120
transabdominal ultrasound exam, 83 F
transvaginal sonography False Claims Act (FCA), 263
adnexal, 121 Fecalization, 66
endometrial, 120, 121 Fetal development
trilaminar sonographic pattern, 120 cardiovascular system, 33, 34
twin pregnancy, 112 gastrointestinal system, 36, 37
Electrolytes, 238 nervous system, 33, 34
Electronic health record (EHR), 251–253 respiratory system, 35, 36
Embryology, 25–33 urinary system, 37, 38
fertilization, 25 Fetal effects, 51
gestation, 25 Fetal lung development, 35, 36
periods, antenatal human development Fetal monitoring during surgery
(see Antenatal human development) ACOG, 232
Embryonic period, 26, 28–31 benzodiazepines, 231
first postconceptional week, 27 classification system, 230
blastocyst, 28 diazepam, 231
blastomeres, 28 DNA synthesis, 231
cleavage, 26 induction agents, 231
fertilization, ampulla of fallopian tube, 26 ketorolac, 232
implantation, 28 medications, 232
sperm penetration, 26 molecular size, 232
zona pellucida, 28 muscle relaxants, 231
fourth to eighth postconceptional week nonobstetrical surgery, 237
differtiation, germ layers, 31 obstetrical provider, 237
growth, 31 pre-viable, 237
uteroplacental circulation, 31 teratogenic effects, 230
second postconceptional week types, 230
blastocyst, 28 Fetal period, 31–33
Index 273
Fetal positioning, 46 CIN (see Cervical intraepithelial neoplasia

Fetus, 51, 52 (CIN))
in gestational age, 211 endometriosis, 151
ionizing radiation, 211 ovarian malignancy, 152
mortality, 214 PID (see Pelvic inflammatory disease (PID))
mother, 209 TOA (see Tubo-ovarian abscess (TOA))
side effects, 210 uterine fibroids (see Uterine fibroids in
supplemental oxygen, 212 pregnancy)
vital signs, 210
First-trimester spontaneous abortion, 108
abdominal and pelvic pain, 107 H
cervical insufficiency, 110 Healthcare fraud, 262, 263
diagnosis, 109 Health Insurance Portability and
embryonic/fetal death, 107 Accountability Act (HIPAA), 253
fetal loss, 107 disclosures, 253
first 12 weeks of gestation, 107 penalties, 253
hCG measurements, 107 privacy standards, 253
management, 111 violation, 242
subclassifications, 107 Heart
symptoms and signs, 109–111 actual cardiomegaly, 3
Fluoroscopy, 53 diaphragm displacement and effects, 3
Focused abdominal sonography for trauma diastolic function, 4
(FAST), 54 E/A ratio, 4
Foley catheterization, 238 left ventricular contractility, 3
Food and Drug Administration (FDA), 54, 231 pulmonary capillary wedge pressures, 3
“Full stomach” precautions, 229 systolic function, 4
Functional residual capacity (FRC), 227 Helicobacter pylori, 168
Hemolysis, elevated liver enzymes, and low
platelets (HELLP) syndrome, 64,
G 65, 99, 101–103
Gadolinium-based contrast, 55 Hemorrhagic cysts, 71
Gallbladder function, 13 Hepatic disease
Gas exchange, 11 cysts, 169
Gastroesophageal reflux (GERD) diagnosis, 169
diagnosis, 166 intracystic pressure, 169
heartburn, 166 intraparenchymal hemorrhage, 169
quality of life, 165 trauma, 169
symptoms, 165 treatment, 169
treatment, 166, 167 Hernias
Gastrointestinal system adult women, 182
appetite, 12 diagnosis, 183
diseases, 65, 66 treatment, 183
fetal development, 36, 37 Heterotopic pregnancy, 88, 89
gallbladder function, 13 Human chorionic gonadotropin (β-hCG), 56
intestines, 13 Hydronephrosis, 197, 198
liver, 14 and hydroureter, 61
mouth, 12 physiological hydronephrosis, 60
nausea and vomiting, 14, 15 pregnancy, 68
stomach, 12, 13 stone, 60
Glucocorticoids, 224, 225 Hypercalciuria, 199
Gynecologic causes, abdominal pain in Hypercoagulable state, 229
pregnancy, 141–151, 153–156 Hyperemesis gravidarum, 15
adnexal masses (see Adnexal masses) Hyperreactio luteinalis, 72
cervical cancer (see Cervical cancer) Hypersecretion, 62
274 Index
Hyperstimulated ovaries, 71 Liver functions, 10, 14

Hypoglycemia, 219 Lung volumes in pregnant and non-pregnant
Hypotension, 219, 222 women, 10, 11
Hypothermia, 219
Hypoxia, 219
M
MacDonald’s measurement, uterine
I enlargement, 2
Imaging Magnetic resonance cholangiopancreatography
abdominal/pelvic complaints, 50 (MRCP), 62–63
counseling, 56 Magnetic resonance imaging (MRI)
maternal and fetal exposures, 53 energy deposition, 55
in pregnant patients, 50 fetus, 54
risk-to-benefit ratio, 50 MR sequences, 55
Implantation pregnant patient, 50
blastocyst, 28 Magnetic resonance urography
posterior and superior portion, uterus, 28 (MRU), 61
second postconceptional week, 28 Malpractice, 241, 242, 244
Incentive spirometry, 239 Massive ovarian edema, 78
Inflammatory bowel disease (IBD), 183 Maternal physiological adaptations to
Information elements, 257, 258 pregnancy
Injury airway, nasopharynx and laryngeal
patterns, 211 structures, 227
prevention, 210 anesthesia, 227
Intentional torts, 245 cardiovascular changes, 229
Interstitial ectopic pregnancies, 85–87 gastroesophageal changes, 229
Interstitial pregnancy hematological adaptations, 229
abnormal placentation, 124 neurological changes, 230
conservative medical management, 124 renal blood flow, 230
cornual pregnancies, 122 respiratory changes, 227, 229
detection, 123 Mature cystic teratoma, 73
proximal tubal segment, 122 Medical record documentation
risk factors, 122 accuracy, 250
ruptures, 123 complete, 250
sonography, 123 fetal monitor, 249
surgical management, 123 liability issues, 250
Interventional radiology, 53 rationale, 250
Intestines motility, 13 recollection, 248
Intraoperative management, 234 time, 250
Intravenous opioids, 231 tips, 249
Iodinated contrast, 55 Mesenteric ischemia
diagnosis, 180
distal small intestine, 179
K hereditary coagulopathies, 179
Kidney stone, 199, 200 inherited risk factors, 179
treatment, 180, 181
Mesenteric venous thrombosis (MVT), 179
L Midtrimester abortion
Leiomyomas, 78 (see also Uterine fibroids in after 16 weeks, 112
pregnancy) bleeding, 112
Liver abscess differential diagnosis, 112
diagnosis, 170 pain, 112
intra-abdominal processes, 170 risk factors, 112
treatment, 170 22–23 weeks, 111
Index 275
Minimally invasive surgery physiological obstruction, 200

abdominal cannulation, 222 prone position, 203
abdominal surgery, 223 renal blood flow, 199
aortocaval compression, 222 stone disease, 201
apneumatic approach, 223 symptoms, 199
arterial carbon dioxide, 221 ureteroscopy, 202
cardiovascular and hemodynamic Nervous system, 33, 34
changes, 222 Neural tube
extrapolation, 224 broad cephalic and long caudal portion, 33
nonpregnant patient, 221 buccopharyngeal membrane, 31
pelviscopic cystectomy, 221 CNS, 31
pelviscopic procedures, 223 formation, 31
pneumoperitoneum, 221 growth, 31
precautions, 223 neural plate, 33
second and third trimester, 222 neurulation, 33
Society of American Gastrointestinal rostral and caudal neuropores, 33
Endoscopic Surgeons Guidelines, 223 walls, 33
surgical intervention, 224 Neurulation, 33
trimesters of pregnancy, 224 Nonobstetrical disorders, 41
trocar placement, 222 Nuclear medicine, 53
ultrasound guidance, 222
ventilation, 222
wound complications, 221 O
Mother Obstructive uropathy, 60
and fetus, 209, 210 Osmoregulation, 19
injury pattern, 212 Osteoporosis, 18
life-threatening injuries, 212 Ovarian/adnexal torsion, 76, 77, 141, 142,
primary survey, 212 145, 146
vital signs, 210 Ovarian cancer, 76, 142, 153
Mouth, pregnancy, 12 Ovarian ectopic pregnancies, 88
Myocardial infarction, 103 Ovarian hyperstimulation syndrome, 71
Ovarian malignancy in pregnancy, 125, 152, 153
N
Nausea and vomiting of pregnancy, 14, 15 P
Negligence Palpation, 46, 47
adverse events, 247, 249 Pancreatitis, 63, 64
damages, 246 biliary etiologies, 178
elements, 243, 244 delivery, 179
legal concept, 242 diagnosis, 176
professional liability, 247 estrogen, 176
Nephrolithiasis hypertriglyceridemia, 175
anesthesia, 199 mechanical ventilation, 176
calcium oxalate stones, 199 pregnancy-related risk factors, 176
distal ureter, 200 Para-ovarian cysts, 144
first trimester, 199 Parenteral nutrition, 239
imaging options, 200 The Patient Self-Determination Act
lab tests, 103 (PSDA), 264
long-term management, 201 Pelvic abscess, 43, 159
magnetic resonance imaging (MRI), 200 Pelvic examination, 47
medical and surgical treatment, 199 Pelvic inflammatory disease (PID), 79, 157
nephrostomy placement, 201 diagnoses, 156
noncontrast CT, 200 infection, 156
nonobstetric cause, 199 lower abdominal pain, 156
276 Index
Pelvic inflammatory disease (PID) (cont.) MRI, 134

pregnancy implications, 161 placenta previa, 133
risk factors, 156 risk factors, 133–134
treatment, 160 separation, 132
uterine cavity, 156 sonography, 134
Pelvic masses, 143 thrombin, 132
Pelviscopy ultrasound examination, 134
bowel manipulation, 221 Placenta previa, 135
epidural anesthesia, 223 Pleuritic inflammation, 43
incisional hernias, 221 Pneumoperitoneum
laparoscopy, 221 CO2, 223
nonpregnant patient, 221 diaphragm, 221
pathology, 221 pelviscopic surgery and procedures, 221
pregnancy, 222 physiological effects, 222
pregnant population, 224 Porphyria, 103
single-incision, 221 Postoperative analgesia, 235
Trendelenburg position, 221 Postoperative care
Penetration fetal/maternal indication, 238
abdominal trauma, 213 gravidas’ hemoglobin, 238
fetus, 214 hostile intrauterine environment, 238
gunshot wounds, 211 parenteral nutrition, 239
injury, 214 protocol, 239
stab wounds, 211 spirometry, 239
uterine trauma, 214 Pregnancy and Lactation Labeling Rule
Peptic ulcer disease (PUD) (PLLR), 230
diagnosis, 167 Pregnancy related conditions, 100, 101
in pregnancy, 167 allergic reactions, 56
treatment, 168 counseling, 56, 57
Percussion, 46 diagnoses, 99
Persistent vegetative state (PVS), 264 gadolinium-based contrast, 55
Physical examination hyperreactio luteinalis, 72
auscultation, 46 hyperstimulated ovaries, 71
observation, 45, 46 iodinated contrast, 55
palpation, 46, 47 lab tests
pelvic, 47 abruption, 100
supplemental examinations, 47 chorioamnionitis, 101
Physiological changes, 3–8, 12–21 extrauterine gestation, 100
cardiovascular (see Cardiovascular system) HELLP Syndrome, 101
gastrointestinal (see Gastrointestinal ovarian hyperstimulation syndrome
system) (OHSS), 71
musculoskeletal system screening, 56
calcium metabolism, 15, 16 vascular complications, 66, 67
skeletal and postural changes, 16–18 Premature separation of placenta, 100
renal (see Renal system) Preoperative assessment and preparation, 233
Pica, 12 Primordial gut, 36
Placental abruption, 90 Primordial heart tube, 31
acute and chronic processes, 132 Professional liability, 247
clinical manifestations, 133 Pseudogestational sac, 84
detection rates, 134 Pulmonary capillary wedge pressures, 3
diagnosis, 134 Pulmonary system
hematomas, 134 gas exchange, 11
hemorrhage, 134 lung volume, 9
incidence, 132 mechanical changes, 9
laboratory tests, 135 upper respiratory tract, 9
Index 277
Pyelonephritis ACOG committee, 218

ASB, 195 appendix, 217
bladder infection, 196 decision-making, 218
gestation, 197 fetal monitoring, 218
microscopic hematuria, 196 fetal morbidity, 217
perinephric and periureteral edema, 200 gestational age, 219
in pregnancy, 196 nonemergent surgery, 219
risk of systemic infection, 195 nonobstetric surgery, 217, 218
urine culture, 196 obstetric surgery, 218
urological histories, 196 optimal timing, 219
R T
RAAS. See Renin–Angiotensin–Aldosterone Tamsulosin, 200
System (RAAS) Teratogenesis, 52
Radiation exposure Threshold elements, 255–257
fetus, 51, 52 Thromboprophylaxis, 225
imaging modalities, 211 Tocolytics, 224, 225
ionizing, 51 Torts
and pregnancy, 211 medical negligence, 244
Radiation-induced teratogenesis, 51 types, 245
Radio frequency (RF), 55 Transvaginal sonography (TVS), 118
Radiography, 53 Transvaginal (TV) ultrasound, 60
Renal colic, 60 Trauma, 68, 69
Renal system anatomy, 210
ANP and BNP, 20, 21 death, 209
fetus, placenta and amniotic fluid, 19 imaging issues, 211
osmoregulation, 19 injury patterns, 211
RAAS, 20 injury prevention, 210
sodium metabolism, 20 morbidity and mortality, 209
Renin–Angiotensin–Aldosterone System obstetric emergencies, 213, 214
(RAAS), 20 operative indications, 213
Resistive indices (RI), 61 physiology, 210
Respiratory system, 35, 36 pregnant patient, 209
Retroplacental placental abruption, 92 primary and secondary survey, 212
Tubal ectopic pregnancy, 83, 84
Tubo-ovarian abscess (TOA), 158
S diagnosis, 160
Salt metabolism, 20 management, 160
Sentinel Event Policy, 247 peritonitis, 156
Sickle cell crisis, 103 pregnancy implications, 156, 161
Single-incision pelviscopy, 221 severe acute abdominal pain, 156
Skin erythema, 51
Small bowel obstruction, 102
Society of American Gastrointestinal and U
Endoscopic Surgeons (SAGES), Ultrasonography, 54
225 Ultrasound (US), 50
Specific absorption rate (SAR), 55 United States Preventative Services Task Force
Splenic artery aneurysms, 67 (USPTF), 195
Stomach, gastrointestinal effects, pregnancy, Ureteral stone, 198
12, 13 Urinary system, fetal development, 37, 38
Stroke volume (SV), 4, 5 Urinary tract
Subchorionic hemorrhage, 135 ASB, 195, 196
Surgical intervention first trimester, 193
278 Index
Urinary tract (cont.) prevalence, 146

frequency, 194 torsion, 146
infections, 60–62 Uterine incarceration, 130–132
pregnancy progresses, 193 Uterine leiomyomata, 148, 149
retention, 194, 195 Uterine rupture, 90, 128, 129
upper tract, 194 classification, 126–129
Urolithiasis, 60–62 diagnosis, 129, 130
Uterine enlargement Uterine scar pregnancy, 126
cervix, 2
cesarean delivery, 2
fundus, 2 V
gastrointestinal reflux and Venous pressure, pregnancy, 8
nausea, 2 Victims Of Modern Imaging Technology
gestation, 2 (V.O.M.I.T. syndrome), 47
gravid uterus, 2 Vomiting, 43
hypertrophy, muscle fiber, 2
intestines, 2
palpitations, 2 W
Uterine fibroids in pregnancy Wound care, 225
asymptomatic, 146
diagnosis, 150
growth, 146 Z
management, 150 Zygote
obstetrical complications, 151 cleavage, 26
pain, 150 totipotent cell, 26

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The Diagnosis and

Peter Bogach Greenspan

The Diagnosis and

ISBN 978-3-319-62282-8 ISBN 978-3-319-62283-5 (eBook)

Library of Congress Control Number: 2017952195

© Springer International Publishing AG 2018

Printed on acid-free paper

This Springer imprint is published by Springer Nature

UMKC School of Medicine, Obstetrics Harry S. Jonas, MD, FACOG

An acute abdomen is defined as “an abnormal condition characterized by the acute

Kansas City, MO, USA Dev Maulik, MD, PhD, FACOG

The daunting task of editing and contributing to a medical textbook is a humbling

1 Maternal Anatomical and Physiological Adaption to Pregnancy������������ 1

13 Postoperative Care Issues������������������������������������������������������������������������ 237

Farzad Alemi, MD, MS Department of Surgery, University of Missouri Kansas

Kathleen A. Leavitt, MD Department of Anesthesiology, University of Missouri

P.B. Greenspan, DO, FACOG, FACS (*)

© Springer International Publishing AG 2018 1

The implantation of a gestation produces physiological effects on the uterine mus-

Gestation produces significant physiological changes in the cardiovascular system.

The CO in twin gestations incrementally increases an additional 20% greater

 rterial Blood Pressure and Systemic Vascular Resistance

Upper Respiratory Tract

 ung Volume and Pulmonary Function

Table 1.1 Lung functions in pregnancy

Table 1.2 Lung volumes in pregnant and non-pregnant women

 ausea and Vomiting of Pregnancy

There is a decline of maternal total calcium levels throughout pregnancy.

 keletal and Postural Changes

 trial and Brain Natriuretic Peptide

19. Desai K, Moodley J, Naidoo D. Echocardiographic hemodynamics in normal pregnancy.

Periods of Antenatal Human Development

By convention, human antenatal development is typically divided into two phases

D.C. Mundy, MD, FACOG (*) • G. Vilchez, MD

© Springer International Publishing AG 2018 25

The Embryonic Period

First Postconceptional Week

Approximately 4 days after fertilization, the zona pellucida degenerates. Six to

Second Postconceptional Week

(a) The epiblast: a dorsal layer formed by columnar cells, and

Fluid-filled spaces then appear in the extraembryonic mesoderm. These spaces

Third Postconceptional Week

 ourth to Eighth Postconceptional Weeks

The Fetal Period

Important Aspects of Specific Fetal Systems Development

Table 2.1 Stages in the development of the respiratory system

P.B. Greenspan, DO, FACOG, FACS (*)

© Springer International Publishing AG 2018 41

affect women of childbearing age. A number of questions should be addressed to

• Would a different management plan be recommended if the woman was not

Observations of the patients’ position in the bed, facial expressions, degree of

1 . Peritoneal or mesenteric nerve irritation

Any irritation of the peritoneum from blood, gastric secretions, or inflammation

O-onset: When did the pain begin or first become noticeable?

A thorough, comprehensive physical examination is always preferable; however,

Kansas City, MO, USA Dev Maulik, MD, PhD, FACOG

1 Maternal Anatomical and Physiological Adaption to Pregnancy�� 1

13 Postoperative Care Issues�� 237

rterial Blood Pressure and Systemic Vascular Resistance

Upper Respiratory Tract

ung Volume and Pulmonary Function

ausea and Vomiting of Pregnancy

keletal and Postural Changes

trial and Brain Natriuretic Peptide

Periods of Antenatal Human Development

The Embryonic Period

First Postconceptional Week

Second Postconceptional Week

Third Postconceptional Week

ourth to Eighth Postconceptional Weeks

The Fetal Period

Important Aspects of Specific Fetal Systems Development

The Pelvic Examination

The Use of Rebound Tenderness (Commentary)

Ionizing Radiation and Risks

Radiation and the Developing Fetus

adiography, Fluoroscopy, Interventional Radiology

Magnetic Resonance Imaging

Utilization of Intravenous Contrast in Pregnancy

Counseling the Pregnant Patient About Imaging Procedures

Nongynecological Causes of Abdominal Pain

Urolithiasis and Urinary Tract

Gynecological Causes of Abdominal Pain

Adnexal Masses Unique to Pregnancy

yperstimulated Ovaries and Ovarian Hyperstimulation Syndrome

yperreactio Luteinalis and Theca Lutein Cysts

Mature Cystic Teratoma

ther Ovarian Neoplasms

Limited Role of CT

Massive Ovarian Edema

Pelvic Inflammatory Disease

Obstetric Causes of Abdominal Pain

First Trimester Causes

arly Normal Pregnancy

arly Pregnancy Failure

ubal Ectopic Pregnancy

ess Frequent Sites of Ectopic Pregnancy

I nterstitial Ectopic Pregnancy

ervical Ectopic Pregnancy

aesarian Scar Ectopic Pregnancy

varian Ectopic Pregnancy

bdominal Ectopic Pregnancy

ole of MRI in the Diagnosis of Ectopic Pregnancy

Causes Unrelated to Pregnancy