Pedia Platinum (1st Edition)
Pedia Platinum (1st Edition)
Pedia Platinum (1st Edition)
PEDIA
PLATI
F
NUM
PLATINUM
IR S T E
FIRST D IT IO N
EDITION
2020
PEDIA
PLATINUM
FIRST EDITION
2 0 2 0
EDITOR
VICTORS. DOCTOR, MD
The printing of Pedia Platinum is financed by Top Practice Medical Publishing
Corporation, Manila, Philippines. Proceeds from the purchase of this book will
fund the development and improvement of future editions of this book.
Book design and layout by Manuel S. Vidal, Jr. All rights reserved. No part of this publication may
be reproduced, stored in a retrieval system, or transmitted, in any form by any means without
prior permission from Top Practice Medical Publishing Corporation.
Published by:
Top Practice Medical Publishing Corporation
No. 27 Mercury Street, Fairview, Quezon City
ISBN 978-621-95388-4-8
ii
CONTRIBUTING
AUTHORS
Justine Iris C. Yap, MD, FPPS, FPCC, FEACVI
Jerry V. Pua, RMT,MD, DPPS
Romana Marie M. Vila, MD, FPCR, FCTMRISP
Diosemyl L. Leyson-Guzman, MD, DPPS, DPSN,DPNSP
ILLUSTRATOR
Joerelle V. Mojica, MD, FPCP, FPCC
LAYOUT
EDITOR
Manuel S. Vidal, Jr., RCh
V
NOTICE
The information in this book has been reviewed and verified with
reliable sources, and the approaches to management have been utilized
in clinical practice. Howevet~ medicine is an ever-changing science. New
research, changes in guidelines, and human error occul'. The authors,
editor, and publisher are not responsible for errors or omissions or
for any untoward outcomes from application of data in this book. The
authors, edito1; publishe1; and other parties who have been involved in
the preparation of this book make no warranty, expressed or implied,
with respect to the completeness, accuracy, or being up-to-date of all
the information contained in this publication. The authors, edito1; and
publisher encourage the readers to confirm the information herein
with other sources, and to exercise critical thinking based on the clinical
presentation of the patient in making decisions for management.
vi
PREFACE
As a practicing pediatrician dealing with emergencies for the past 15 years, I find it highly
gratifying, and of utmost importance that I am able to share my clinical experiences with the
medical students and residents. Through those years as a teacher in Pediatrics, an inner desire
to provide the medical students a compendium for recapitulating what is necessary in this
subject stirred in me. This dream slowly took form as I became part of the faculty of Topnotch
Medical Board Prep since its inception. Topnotch Medical Board Prep has definitely gained a
renowned and prestigious reputation in the field and has taken essential steps in aiding the
medical students to realize their dream of becoming licensed physicians. The success of the first
two books, IM Platinum and Surgery Platinum with the publication of Medical Jurisprudence,
were testimonies of its quest for providing high quality review books.
There has been a dearth of review books in Pediatrics in the home front hence, we envisioned
to provide one for you. It is heartwarming to receive initial feedback that pediatric residents
in training as well as our other colleagues in the medical field who have been practicing for
some time have also expressed their anticipation of this book. At this digital era, one cannot
deny the instantaneous and expeditious access of a learner to journals, latest research, and
medical textbooks. But many of you may agree that all of this information can be overwhelming
as well. Thus, our team spearheaded by Dr. Enrico Paolo Banzuela sat down exactly two years
ago (January 2018) and discussed the birth of Pedia Platinum.
Our two-year trek has been spiced with trials both on a personal and professional level. The lulls in our
momentum have been due to conflicts in schedule, falling ill, fulfilling graduate school requirements,
welcoming babies in the family, dealing with loss of a loved one, and other professional commitments.
But we still forged to move forward as we were all fueled to come up with our dream review book
We came up with a total of21 chapters mirroring the subspecialties in Pediatrics, each carefully
scrutinized and dissected as if we were the ones who were going to read it. Will this topic
be useful for the board exam and for the usual rounds? Is this topic a "must know" category
versus something that is least likely to be discussed? All of these questions were disputed and
settled with our sense of humor intact. I believe my colleagues would agree with me that the
most challenging chapter was that of fluids and electrolytes as we argued on which guidelines
to put in the book. It is not a hidden truth that most of what we learn in medical school can be
challenged and unlearned during internship and residency training because of "hand me down"
information and local practices. To resolve this, we did an extensive research particularly on
the computation of fluids and electrolytes and cited references accordingly. You will also note
that after each presentation of a certain guideline, we included a statement explaining that such
guidelines may vary from one local institution to another.
In the end, we were highly satisfied that the product of our hard work gave rise to a very practical,
useful, and comprehensive review book in Pediatrics. I would like to give my eternal gratitude
to Dr. Enrico Paolo Banzuela, a visionary himself, who has painstakingly led us in accomplishing
this book; to my colleagues in Pediatrics Dr. Ana Marie Morelos, Dr. Adrian De Vera, and Dr. Carol
Tan-Lim whose dedication and tenacity are worth emulating; to Dr. Marc Denver Tiongson (for
his valuable contribution and leadership) and Dr. Jaime Aherrera (with his uncanny skill in
transforming texts into tables as well as his leadership) who have been highly instrumental in
the completion of this book; Manuel Vidal, an upcoming bright physician with his skills in laying
out the book; Dr. Mark Louis Mann for taking extra special care of handling the promotion of
the book; and to all the contributing authors. Special thanks to our beloved Dr. Victor S. Doctor,
past president the Philippine Pediatric Society and a pillar in pediatric nephrology, for being
our editor. Thank you to our Almighty God for His guidance and unending grace. This is a dream
team indeed!
This is our passion ...this is our legacy ...and we are sharing this with pride and joy to all of you ...
vii
FOREWORD
This book, PEDIA PLATINUM, symbolizes knowledge that does not rust, a source of light when
memory dims, sometimes, and a reminder that knowledge is indeed power. It is one of your
resources to strengthen your knowledge, skills, and confidence as a medical practitioner. It
is a handy reference to spark back your memory of Pediatrics.
The authors take pride in the production of a compact medical literature of the pediatric
specialties that should consolidate to a strong foundation. The men and women behind:
They put up their best efforts and interests to synthesize local and international literature
with proper acknowledgements. We dedicate this publication to all medical practitioners,
especially to our younger colleagues.
With the FIRST EDITION of PEDIA PLATINUM, we hope to accommodate the rush of
developments that impact pediatric practice. Ultimately, all of these will translate to
comprehensive patient care.
Find time to internalize what this book can offer for your professional growth. Love your
profession!
viii
ACKNOWLEDGEMENT
We would like to offer our utmost gratitude:
To our families, for their unfailing love, support and inspiration: The Punongbayan Family
especially to Miss Amelita Punongbayan; Mrs. Eladia Bautista Ramirez, Mr. Juan Paolo, Ms.
Maria Angelica Beatriz & Mr. Edilberto Lorenzo Morelos; Mr. Archie & Mstr. Chase Stephen
Lim; Mr. Manuel, Dr. Bonaleth & Atty. Jo Franz de Vera, & Mrs. Diana, Ms. Adriana & Mstr.
Nicolo de Vera; Capt. Jaime Julian & Mrs. Ma. Rosario Aherrera; Mrs. Maria Cristina Tiongson,
Dr. Lalaine & Mstr. Matthew Damian Tiongson, Atty. Virgilio, Mrs. Marilyn, Mr. Patrick Jeanne
& Ms. Patricia Meryl Tiongson, & Mr. Dennis, Mrs. Maita, Ms. Maiden Kristine & Mr. Andrei
Nikolai Tiongson; and Mrs. Arabella Chiong Banzuela, Dr. Nifia Banzuela-Cruz, Dr. Rocky Lim
& Ms. Arabella Aurora Lim Banzuela;
To all our mentors, Dr. Ramon L. Arcadia, Dr. Carmencita Padilla, Dr. Lulu Bravo, Dr. Salvacion
Gatchalian, Dr. Juliet Sia-Aguilar, Dr. Lorna Abad, Dr. Bernadette Madrid, Dr. Marysia Recto,
Dr. Mary Anne Castor, Dr. Agnes Mejia, Dr. Rody Sy, Dr. John Afionuevo, Dr. Madeleine Sosa,
Dr. Sandra Litao, Dr. Maria Concellene Laforteza, Dr. Jose Fernando Fontanilla, Dr. Maria
Luz Querubin, and Dr. Erlyn Sana, Dr. Rose Anna Banal, Dr. Robert Arias, Dr. Pacifico Eric
Calderon, Dr. Eric Calderon Jr., & Dr. Mark Louie Mann; Dr. Julius Lecciones, Dr. Michael
Resurreccion, Dr. Sonia Gonzales, Dr. Florentina Uy-Ty, Dr. Victoria Ribaya, Dr. Jonathan Cu,
Dr. Cristan Cabanilla, Dr. Amel Jiao, Dr. Maria Beatrice Gepte, Dr. Reynaldo de Castro Jr, Dr.
Sheila Ann Masangkay, and Dr. Cecile Gan for their invaluable guidance and wisdom;
To all our colleagues and friends from the Chinese General Hospital and Medical Center,
Pamantasan ng Lungsod ng Maynila College of Medicine, Ospital ng Maynila, Philippine
Children's Medical Center, St. Luke's Medical Center Quezon City, UP College of Medicine, UP-
Philippine General Hospital Department of Pediatrics, for helping us bring the best in us and
help us become the doctors we are today;
To our fellow teachers and bosses from San Beda University College of Medicine, Ateneo
School of Medicine and Public Health, De La Salle Medical and Health Science Institute, Bica!
University College of Medicine, New Era University College of Medicine, for enabling us to
undertake this endeavor; to our students, for inspiring us to be better educators every day;
To all main authors, contributing writers of the IM Platinum, Surgery Platinum and Philippine
Medical Jurisprudence, thank you very much for all your help in making the Platinum Series
Dream come true;
To our patients especially the Filipino Children, our greatest teachers, to whom the essence
and soul of this book is rooted on. This book is for you first and foremost.
This book is lovingly dedicated to Mr. Eduardo Punongbayant, Mrs. Clarita Punongbayant,
Dr. Miguel L Noche, Jr.t, Justice Pedro Alaras Ramirezt, Dr. Edilberto Torres Morelost,
Atty. Virgilio Tiongsont, and Mrs. Paula Chuat.
ix
DEDICATION
To my parents ...
To the medical students for making me embrace the love for teaching ...
Ruby
X
THE
AUTHORS
Ruby L. Punongbayan, MD, FPPS, MA
Dr. Punongbayan graduated from Pamantasan ng Lungsod ng Maynila College of Medicine with full academic
scholarship. She took her fellowship in Ambulatory Pediatrics in the University of the Philippines ·Philippine
General Hospital and then proceeded to take Master of Arts in Clinical Psychology in Pamantasan ng Lungsod
ng Maynila Graduate School of Medicine. Dr Punongbayan also took the Basic Course in Health Professions
Education in the University of the Philippines •NTTC. To further help patients, she took Cognitive Behavioral
Therapy at Beck Institute, Pennsylvania, USA. lnspite being the Section Head of Pediatric Emergency
Medicine of St. Luke's Medical Center in Quezon City and Program Head of the Department of Pediatrics
of San Beda University College of Medicine, she is still an Active Consultant of the Institute of Pediatrics
and Child Health in St. Luke's Medical Center Quezon City, an Associate Professor in Pediatrics and a part
time clinical professor in the Department of Pediatrics of Pamantasan ng Lungsod ng Maynila and St. Luke's
College of Medicine. She also contributes her time to teach underboard physicians who will be taking the
physician licensure exam by reviewing them in Pediatrics at Topnotch Medical Board Prep. She is also an
Ambulatory Pediatrics consultant in Centre Medicale Internationale in Bonifacio Global City, Taguig City, a
Fellow of Philippine Pediatric Society and a member of the Philippine Ambulatory Pediatric Association. Dr
Ruby likes playing the piano, into abstract painting with acrylic as medium, singing, and is skilled at American
sign language. She also loves traveling, be it solo or by group, and explores the off-the-beaten paths.
xi
Adrian Salvador M. de Vera, MD, DPPS
Dr. De Vera graduated with a B.S. Biology degree from the Ateneo de Manila University in 2007. He then
attained his medical degree from the UP College of Medicine in 2012. He finished his Pediatrics Residency
program at the Philippine Children's Medical Center in 2016. At that same year, he was awarded the Dr. Joel
Elises Award for Excellence in Pediatrics in 2016, the highest award given to residents by the said institution.
His research on the use of peripheral veins to extract blood for monitoring dengue patients won several
awards locally and internationally. Today, he is a practicing pediatrician at De Vera Medical Center Inc. At the
same institution, he leads by serving as a member of the Board of Directors and as Training Officer of the
Nursing Professional Advancement and Development Program. His main advocacies include breastfeeding
and vaccination. He is also a professor at Topnotch Medical Board Prep since 2012, professional newborn
photographer at Nouveau Nee Photography, car racing and table tennis enthusiast. More than all these, he is
a loving husband to Diana Kibanoff-De Vera and father to Adriana and Nicolo.
xii
Enrico Paolo C. Banzuela, MD, DHPEd, MSEd, FPSP
Dr. Banzuela graduated with a B.S. Basic Medical Sciences degree (INTARMED) from UP Manila in 2002. He
obtained his medical degree from the UP College of Medicine in 2005. He finished his Masters in Educational
Entrepreneurship (MSEd) at the University of Pennsylvania in 2019. He obtained his Diploma in Health
Professions Education from the UP National Teacher Training Center for the Health Professions in 2018. He
also a graduate of the Management Development Program of the Asian Institute of Management in 2018.
He is currently taking a Masters in Health Professions Education at the University of Maastricht in the
Netherlands. At the same time he is also taking up a Postgraduate Certificate in Teaching Evidence-Based
Health Care at the University of Oxford in the United Kingdom. Upon passing the medical board exams in
2005, he served as a volunteer physician for the 2005 Manila Southeast Asian Games. He also worked as a
University Researcher for the UP National Institutes of Health under the Phil Health Research Study Group for
3 years. He co-authored a book entitled "Survival Guide for Doctors [and Non-Doctors Too) with Dr. Willie
Ong and Dr. Liza Ong. He is also a co-author of IM Platinum, Surgery Platinum and now Pedia Platinum.
Dr. Banzuela is the Chair of the Section of Medical Physiology (Associate Professor 11) at the San Beda
University College of Medicine and has been a faculty member since 2005. he has also served as lecturer for
Biochemistry, Neurology, Family and Community Medicine at the same institution. He is a guest lecturer for
Biochemistry at the Ateneo School of Medicine and Public Health. He currently serves as Vice-President of the
Philippine Society of Physiologists. He is the President of Topnotch Medical Board Prep where he also teaches
Physiology. Dr. Banzuela has always been involved with preparing doctors for the medical board exams since
2005, having written guides, given orientation talks, created school-specific board exam programs and
lectured subjects at various hospitals and institutions. He enjoys fishing, driving, playing basketball, listening
to audiophile setups, film photography, and going on food trips with his family.
THE
EDITOR
Victor S. Doctor, MD, FPPS, FPNSP, FPSN
Dr. Doctor as he is currently called by his colleagues pursued his medical career in the University of the East
-Ramon Magsaysay Medical Center, Inc. and his Residency in Pediatrics in the same institution. He went to
Georgetown University, Washington DC to pursue his subspecialty in Pediatric Nephrology. He is a fellow of
the following institutions: Philippine Pediatric Society, Inc. (PPS), Philippine Society of Nephrology (PSN),
and the Pediatric Nephrology Society of the Philippines (PNSP). He also has a passion for teaching and was
a professor at UERMMMCI (Retired November 2012), Professor Ill Pamantasan ng Lungsod ng Maynila
(Retired November 2012), Professorial Lecturer Ill Pamantasan ng Lungsod ng Maynila (December 1, 2012-
Present) Professorial Lecturer UERMMMCI. He also serves as a Nephrology Consultant at UERMMMCI -
Department of Pediatric, Cardinal Santos Medical Center and Amang Rodriguez Medical Center, Marikina. He
served as President in the prestigious Philippine Pediatric Society, Inc., Pediatric Nephrology Society of the
Philippines and Philippine Society of Nephrology [PSN) 2016-2017. In his spare time, he enjoys singing and
playing the guitar.
xiii
CONTRIBUTING
AUTHORS
Justine Iris C. Yap, MD, FPPS, FPCC, FEACVI
Dr. Yap earned her medical degree in 2005 and has completed her post graduate internship in 2006 in the University
of the Philippines• Philippine General Hospital. After passing the physician's licensure examination, she then pursued
her residency and fellowship training in General Pediatrics and Pediatric Cardiology in the University of the Philippines
- Philippine General Hospital, which commenced in 2010 and 2014 respectively. Majorly inspired by her professors
and mentors in the department, and with her enthusiasm to lead the trainees for more learning opportunities and
broaden the network amongst inter- national colleagues, she pioneered the international clinical attachment of pediatric
cardiology trainees as part of the curriculum in the Division of Pediatric Cardiology in UP-PGH which supported trainees
attached in different international training centres of their choice in their field of interest. Her inclination in the field
of advanced cardiac imaging was magnified when she went to lnstitut ]antung Negara in Kuala Lumpur Malaysia,
under the mentorship of Dr. Haifa Abdul Latiff in 2014 who was then already specialising in fetal echocardiography
and cardiac CT angiogram. Dr. Yap then subsequently joined the Division of Pediatric Cardiology in UP-PGH thereafter
performing non-invasive cardiac imaging which included transthoracic, transesophageal and fetal echocardiogram which
helped obtained more volume of congenital heart diseases carefully selected for heart surgeries and those amenable
with minimal interventional procedures to correct heart defects. Seeing hmv valuable multi modality imaging is in
congenital and structural heart diseases, she then further trained in advanced cardiac imaging which included advanced
echocardiography, cardiac CT and MRI in Birmingham Children's Hospital and was an honorary fellow in Evelina
London Children's Hospital from 2018to2019. Her main goal is to continue teaching and training our young cardiology
enthusiasts whilst strengthening the core of multi modality imaging in congenital and structural heart diseases both
pediatric and adult population. At present. she is a clinical associate professor and a consultant pediatric cardiologist in
the University of the Philippines• Philippine General Hospital. She is a Diplomate in Philippine Pediatric Society, Fellow
in Philippine College of Cardiology, Fellow of European Cardiovascular Imaging, a member of Society of Cardiovascular
Computed Tomography and Society of Cardiac Magnetic Resonance with Level Ill Accreditation.
ILLUSTRATOR
Joerelle V. Mojica, MD, FPCP, FPCC
Or. Joey Mojica completed her degree in B.S. Occupational Therapy at University of the Philippines · Manila in 2006,
Doctor of Medicine al the University of the East Ramon Magsaysay Memorial Medical Center in 2010, Internal Medicine
residency at Manila Doctors Hospital in 2014, Cardiology fellowship at Philippine General Hospital in 2018. and
Cardiac Electrophysiology and Pacing fellowship at St. Luke's Medical Center • Global City in 2019. She is currently
training for Cardiac EP in Universitair Ziekenhuis in Brussels, Belgium under Dr. Pedro Brugada. Joey enjoys watching
movies, eating out \.vith family and friends, and teaching Medicine to her younger sister, Chris. She's thrilled to be part
of something that cultivates the learning, this time, of many.
LAYOUT
EDITOR
Manuel S. Vidal, Jr., RCh
Mavi graduated with a BS Biochemistry degree, magna cum laude, valedictorian, from the De La Salle University- Manila
under the Star Scholarship Program, with several other awards: Excellence in Chemistry, Most Outstanding Thesis, and
Dr. Jose Rizal Honors Society inductee. He ranked second in the Chemistly Licensure Examinations in 2013. Currently,
he is an intern at the Philippine General Hospital under the MD-PhD Program, and aspires to be a future OBGYN
practitioner. On a personal note, his interests span current events, music, cookery, sports, and fragrances. He is very
grateful for the opportunity to be included in this ground-breaking work.
xiv
TABLE
OFCONTENTS
Preface vii
Foreword viii
Acknowledgment ix
Dedication X
Authors xi· xii
Editor xiii
Contributing Authors, Illustrator, Layout Editor xiv
CHAPTER 1:INTRODUCTION
TOPEDIATRICS
Section 1: History Taking and Physical Examination
1. History Taking in a Pediatric Patient 3
2. Sample History ofa Pediatric Patient 4
3. Vital Signs 5
4. Physical Examination of the Pediatric Patient 8
5. FRICHMOND Method of Endorsement 9
Section 2: Admitting Orders and Daily Rounds
1. Writing Admitting Orders 10
2. Tips on Doing Daily Rounds and Documenting Orders 10
CHAPTER
2:FLUIDSAND ELECTROLYTES
Section 1: Physiology ofBody Fluids 13
Section 2: Fluid Therapy 14
Section 3: Specific Electrolyte Disorders
1. Hypernatremia 21
2. Hyponatremia 23
3. Hyperkalemia 25
4. Hypokalemia 28
5. Hypocalcemia 30
6. Hypercalcemia 31
Section 4: Drips, Blood Transfusion, and Glucose Infusion 33
CHAPTER
4:INTERPRETATION
OFCOMMON
DIAGNOSTIC
TESTS
Section 1: Electrocardiogram
1. ECGWaves and Segments 69
2. Differences Between Pediatric and Adult ECG 70
3. Steps in Pediatric ECG Interpretation 72
4. Common ECGAbnormalities 80
Section 2: Arterial Blood Gas (ABG) Interpretation
1. Overview of Arterial Blood Gas (ABG) 83
2. Basic Steps in ABG Interpretation 83
Section 3: Reading Chest Radiographs
1. Overview ofRadiographs 91
2. Steps in Reading Radiographs 92
3. Common Pathologies and Findings 96
xv
CHAPTER
5:BASIC
PROCEDURES
Foley Catheter Insertion 101
Intravenous Line Insertion 103
Nasogastric/Orogastric Tube Insertion 104
Capillary Blood Sampling 106
Arterial Blood Sampling 107
lntraosseous Infusion 108
Umbilical Vein Catheterization 110
Lumbar Puncture 112
Needle Aspiration 113
Endotrachea\ Intubation via Direct Laryngoscope Technique 114
Mantoux Test and Interpretation (Tuberculin Skin Test) 116
CHAPTER
6:GROWTH
ANODEVELOPMENT
Section 1: Anthropometric Measurements
1. Overview of Anthropometric Measurements 119
2. Interpretation of Anthropometric Measurements 125
Section 2: Development
1. Introduction 130
2. Developmental Milestones 131
3. Second Year to Middle Childhood 133
4. Adolescence 133
Section 3: Common Behavioral Disorders
1. Autism Spectrum Disorder (ASD) 137
2. Attention-Deficit/Hyperactivity Disorder 138
CHAPTER
7:PREVENTIVE
PEDIATRICS
Section 1: Immunization
1. Overview of Immunization 141
2. Principles of Immunization 142
3. 2019 Childhood Immunization Schedule 143
4. Vaccines for Special Groups 146
Section 2: Preventive Pediatrics and Anticipatory Care
1. Screening Tests 149
2. Dental Care 150
3. Red Flags for Child Maltreatment 150
4. Infant and Child Nutrition 152
5. Deworming 153
CHAPTER
8:NEONATOLOGV
Section 1: Evaluating the Newborn 157
Section 2:Essential lntrapartum and Newborn Care 170
Section 3: Neonatal Resuscitation 173
Section 4: Breastfeeding 175
Section 5: Approach to Problems of the Newborn
1. Approach to Apnea 179
2. Approach to Bloody Stool 180
3. Approach to Abnormal Stool Patterns 181
4. Approach to Respiratory Distress 182
5. Approach to Oliguria and Anuria 183
6. Approach to Neonatal Seizures 184
7. Approach to Cyanosis 184
8. Approach to Jaundice 186
9. Approach to Eye Discharge 191
Section 6: Other Issues of the Newborn
1. Retinopathy of Prematurity 193
2. Multiple Gestation 193
3. Intrauterine Growth Restriction 194
CHAPTER9:INFECTIOUS
DISEASES
Section 1: Approach to Fever 199
Section 2: Infections in the Neonate
I. Neonatal Sepsis 202
2. Necrotizing Enterocolitis 204
3. Transplacental Infections 206
xvi
Section 3: Viral Infections
1. Influenza 209
2. Herpes Simplex Virus [HSY) 210
3. Mumps 211
4. Viral Exanthems 212
5. Poliomyelitis 214
6. Dengue Fever 215
7. Rabies 221
8. Human Immunodeficiency Virus (HIV) 222
Section 4: Bacterial Infections
1. Streptococcal Infections 224
2. Staphylococcal Infections 226
3. Escherichia coli 227
4. Typhoid Fever 228
5. Meningococcemia 229
6. Pertussis 231
7. Tetanus 232
8. Tuberculosis 233
9. Leptospirosis 234
10. Bacterial Skin Infections 236
11. Other Bacterial Infections 237
Section 5: Fungal and Parasitic Infections 239
Section 6: Clinical Syndromes 240
CHAPTER
10:GASTROENTEROLOGY
Section 1: Approach to Gastrointestinal Complaints 247
Section 2: Gastrointestinal Disorders of the Neonate
1. Esophageal Atresia (EA)and Tracheoesophageal Fistula (TEF) 249
2. Hypertrophic Pyloric Stenosis 250
3. Hirschsprung Disease (HD) 251
4. Other Disorders Encountered in the Neonate 252
Section 3: Diarrhea and Gastroenteritis 254
Section 4: Disorders of the Gastrointestinal Tract
1. Gastroesophageal Reflux Disease (GERO) 259
2. Peptic Ulcer Disease (PUD) 260
Section 5: Obstruction in the Gastrointestinal Tract
1. Intestinal Obstruction 261
2. Some Causes of Intestinal Obstruction 262
Section 5: Disorders of the Liver and Pancreas
1. Overview of Viral Hepatitis (Hepatitis A-E) 264
2. Hepatitis B 265
3. Acute Pancreatitis (AP) 267
Section 6: Nutrition and Related Disorders
1. Severe Childhood Undernutrition (SCU) 268
2. Micronutrient Deficiency 269
CHAPTER
11:HEMATOLOGY
ANO
ONCOLOGY
Section 1: The Anemia
1. General Approach to Anemia 273
2. Anemias of Inadequate Production 273
3. Hemolytic Anemias 276
Section 2: Bleeding Disorders
l. GeneralApproachto Bleeding 279
2. Overview of Bleeding Disorders 279
3. Immune Thrombocytopenia (ITP) 280
4. Thrombotic Thrombocyt.openic Purpura 280
5. Hemophilia 281
6. Von Willebrand Disease 282
Section 3: Oncology
1.Leukemias 283
2. Lymphoma 285
3. Brain Tumor 286
4. Musculoskeletal Tumors 286
5. Abdominal Tumors 287
xvii
12:PULMONOLOGY
CHAPTER
Section 1: Approach to Common Complaints 291
Section 2: Pulmonary Disorders of the Neonate
I. Respiratory Distress Syndrome (Hyaline Membrane Disease) 293
2. TransientTachypnea of the Newbron (TTN) 294
3. Persistent Pulmonary Hypertension of the Newborn (PPHN) 295
4. Meconium Aspiration Syndrome (MAS) 296
S. Bronchopulmonary Dysplasia (Neonatal Chronic Lung Disease) 298
6. Congenital Diaphragmatic Hernia (CDH) 299
7. Choanal Atresia 300
Section 3: Disorders of the Upper Respiratory Tract
1. Rhinitis (The Common Cold) 301
2. Sinusitis 302
3. Acute Pharyngitis 303
4. Peritonsillar Abscess 304
S. Retropharyngeal Abscess 305
6. Laryngotracheobronchitis (Viral Croup) 306
7. Acute Epiglotittis (supraglotittis) 307
8. Summary Table for Epiglotittis vs Croup 308
9. Bacterial Tracheitis 308
Section 4: Disorders of the Lower Respiratory Tract
1. Bronchiolitis 309
2. Acute Bronchitis 310
3. Pneumonia 310
4. Pulmonary Tuberculosis 313
S. Bronchial Asthma 318
6. Exacerbation of Bronchial Asthma 324
Section S: Disorders of the Pleura
1. Pleural Effusion 326
2. Pneurnothorax 329
CHAPTER
14:RHEUMATDLDGY
Section 1: Approach to Rheumatologic Diseases
1. Overview of Rheumatologic Diseases 351
2. Approach to Musculoskeletal Pain/Swelling 352
Section 2: Disorders in Rheumatology
1. Juvenile Idiopathic Arthritis (JIA) 353
2. Systemic Lupus Erythematosus (SLE) 355
3. Reactive and Post-infectious Arthritis 357
4. juvenile Derrnatomyositis 358
5. Vasculitis Syndromes 360
6. Other Rheumatologic Disorders 361
CHAPTER 15:CARDIOLOGY
Section 1: Overview of the Circulatory System
1. Fetal Circulation 365
2. Transition at Delivery 366
Section 2: Approach to Common Cardiac Complaints
1. Approach to Chest Pain 367
2. Approach to Cyanosis 367
3. Approach to Common Pediatric Cardiac Murmurs 368
Section 3: Congenital Heart Diseases
1. Overview of Congenital Heart Diseases 369
2. Congenital Acyanotic Heart Diseases 370
3. Congenital Cyanotic Heart Diseases 375
xviii
4. Obstructive Lesions 378
Section 4: Acquired Heart Diseases
1. Rheumatic Fever 382
2. Valvular Heart Disease 385
3. Infective Endocarditis 386
4. Kawasaki Disease 389
CHAPTER
16:NEPHROLOGY
Section 1: Approach to Hematuria
1. Overview of Hematuria 393
2. Glomerulonephritis 394
3. Evaluating a Patient with Gross Hematuria 397
Section 2: Approach to Proteinuria
1. Overview of Proteinuria 398
2. Nephrotic Syndrome 399
Section 3: Approach to Azotemia
1. Glomerular Filtration Rate (GFR) 402
2. Renal Failure 402
Section 4: Specific Disorders in Nephrology
1. Acute Poststreptococcal Glomerulonephritis (PSGN) 404
2. lgA Nephropathy or Berger Disease 405
3. Hemolytic-Uremic Syndrome (HUS) 405
4. Autosomal Recessive Polycystic Kidney Disease (ARPKD) 407
5. Urinary Tract Infection 407
6. Renal Tubular Acidosis 409
CHAPTER 17:ENDOCRINOLOGY
Section 1: Disorders of the Hypothalamus and Pituitary Gland
1. Overview of the Pituitary Hormones 413
2. Hypopituitarism 413
3. Hyperpituitarism 415
4 .. Diabetes lnsipidus (DI) 415
5. Precocious Puberty 417
Section 2: Disorders oft he Thyroid Gland
1. Overview of the Thyroid, Parathyroid.and Related Hormones 418
2. Hyperthyroidism 418
3. Hypothyroidism 420
Section 3: Disorders of the Adrenal Gland and Gonads
1. Congenital Adrenal Hyperplasia (CAH) 422
2. Addison Disease 423
3. Cushing Syndrome 424
4. Pheochromocytoma 425
5. Genetic Causes ofHypertrophic Hypogonadism 426
Section 4: Diabetes Mellitus
1. Diabetes Mellitus (DM) 427
2. Diabetic Ketoacidosis 428
CHAPTER 18:NEUROLOGY
Section 1: Approach to Neurologic Complaints
1. Neurologic Examination 433
2. Special Diagnostic Tests 436
Section 2: Congenital Anomalies in Neurology
1. Spinal Cord Malformation 438
2. Hydrocephalus 439
Section 3: Migraine and Headache
1. Approach to Headache in Children 441
2. Migraine 442
Section 4: Seizures and Epilepsy
1. Approach to Seizures 444
2. Seizures and Epilepsy 445
3. Febrile Seizures 448
4. Status Epilipticus 449
Section 5: Neurocutaneous Syndromes
1. Tuberous Sclerosis 450
2. Neurofibromatosis 451
xix
Section 6: CNS Infections
1. Tuberculous (TB) Meningitis 452
2. Viral Meningitis 453
3. Bacterial Meningitis 453
4. Brain Abscess 455
Section 7: Neuromuscular Disorders
1. Guillain-Barre Syndrome 456
2. Cerebral Palsy (CP) 457
CHAPTER 19:ACUTECARE
Section 1: Pediatric Basic Life Support 461
Section 2: Pediatric Advanced Life Support and Arrhythmias
1. Bradyarrhythmias 463
2. Tachyarrhythmias 464
Section 3: Shock 467
Section 4: Foreign Bodies
1. Foreign Bodies in the External Auditory Canal [EAC) 471
2. Foreign Bodies in the Nose 471
3. Foreign Bodies in the Gastrointestinal Tract 472
4. Caustic Ingestions 473
Section 5: Burns and Electrical Injuries
1. Burns 475
2. Assessment of Extent ofBurns by Body Surface Area [BSA) 476
3. Electrical Injury 477
Section 6: Head Trauma 479
Section 7: Toxicology 481
CHAPTER20:ESSENTIALS INPEDIATRICS
Section 1: Examination of the Pediatric Patient
1. Vital Signs 485
2. Glasgow Coma Scale 485
3. Growth and Development 485
Section 2: Immunization Schedule 488
Section 3: Neonatology 489
Section 4: Fluids and Electrolytes 491
Section 5: Measurement of Commonly Used Equipment
1. Nasogastric Tube 495
2. Foley Catheter 495
3. Endotracheal Tube 495
Section 6: Laboratory Reference Values
1. Complete Blood Count 496
2. Blood Chemistry 497
CHAPTER21:BOARD
CORRELATES
Fluids, ECG,ABC, Chest Radiographs sos
Basic Bedside Procedures in Pediatrics sos
Preventive Pediatrics 506
Neonatology 507
Infectious Diseases 508
Gastroenterology 512
Hematology and Oncology 514
Pulmonology 516
Immunology 517
Rheumatology 518
Cardiology 519
Nephrology 519
Endocrinology 520
Neurology 522
Acute Care 523
xx
INTRODUCTION
TOPEDIATRICS
3
• Important during infancy and childhood and in dealing with
problems of delayed development & behavioral disturbances
Growth and • Physical growth: actual ( or approximate) weight and height at birth
developmental
history and at 1, 2, 5 and 10 years, history of any slow or rapid gains or
losses, tooth eruption and loss pattern
• Developmental milestones
• Concerns in nutritional status contributing to the present illness
• Important during first 2 years of life & in dealing with problems of
Nutritional
under- and overnutrition
(feeding) history
• Breastfeeding, artificial feeding, preparation of milk, micronutrient
supplements, complementary feeding, and childhood eating habits
Immunization • Specific dates of administration of each vaccine
Source:BickleyLS,el al. Bales'guidelo physicalexamination andhistorylaking.6th ed.Philadelphia;
2007
Katzenellenbogen R. HEADSS:the reviewof systemsfor adolescents. VirtualMentor;2005
AthreyaB, et al. Pediatricphysicaldiagnosis.2nded.AnshanPublishers;2010
COMPONENT REMARKS
Juana De Leon, 3 year-old female, Filipino, Roman Catholic, born in Laguna
General data and presently residing in Tonda, Manila, was admitted for the first time at
(name of hospital) on July 1, 2019 at Sam.
Chief complaint Cough
The patient was apparently well until 2 days prior to admission (PTA), when
she developed productive cough and fever, with a maximum temperature of
39°C, relieved by intake of paracetamol at 10 mg/kg/dose every 4-6 hours.
History of 12 hours PTA,while aforementioned symptoms persisted, the patient experienced
present illness difficulty of breathing described by the parents as fast breathing with chest
indrawing. There was no cyanosis, convulsions, irritability or lethargy.
Due to persistence of symptoms, the parents decided to consult at the
emergency room where the child was subsequently advised admission
The patient has no changes in sensorium, rashes, jaundice, eye redness or
Review of discharge, naso-aural discharge, epistaxis, vomiting, diarrhea, constipation,
systems changes in urination, easy bruising, limitation of motion, edema, weakness,
or loss of consciousness
Past medical Patient has had no similar illness in the past, no previous hospitalizations and
history no previous surgery. She has no history of allergy.
The father has bronchial asthma and her maternal grandmother has
Family history hypertension. There are no other diseases in the family. No heredofamilial
diseases were reported. There is no family history of TB, hepatitis A or B,
nor are there any other chronic infectious conditions existing in their family.
Juana is the first child of Roberto and Sally. Her father works as a security
guard while the mother is a housewife. She has a 3-month old sister and
Personal and they live in a one-storey 2-bedroom house with adequate ventilation. Water
social history supply comes from Maynilad & distilled water is used for drinking. The
mother cooks the food eaten by Juana. Juana is able to feed herself. Their
toilet is flush type and garbage is collected by a dump truck 3 times a week.
The patient was born full term to a then 28 year-old GlPO mother at a local
hospital. The mother had no history of illness, alcohol intake, bleeding nor
exposure to infections or radiation during pregnancy. She had regular prenatal
Birth and consults with an 08-GYN. The mother did not take any medications during
maternal pregnancy aside from multivitamins.
history She was delivered by spontaneous vaginal delivery. She had good cry and
activity at birth with no meconium staining. Birth weight was 3 kg, length
was 50 cm and pediatric aging was 39 weeks, thus she was appropriate for
gestational age. She was immediately roomed-in a few hours after birth.
4
Gross Motor: Rolled Over ; 4 months, Sat alone ; 8 months, Ran well ; 2
years, at present able to ride tricycle
I
.
Fine Motor: Hands not fisted; 3 months, Reached and pulled objects; 6
months, Linear scr·ibbles; 8 months, At present, draws circles
Growth and
developmental Language: Turned to sound ; 4 months, Babbled ; 7 months, First word
history "dada"; 12 months, Spoke in 2-word phrases; 2 years, At present, states
full name, age and sex
Personal / Social: Smiled responsively ; 3 months, Held and bit cracker;
6 months, Interactive games; 15 months, At present, removes garments,
engages in pretend play
Patient was fully breastfed and then shifted to Enfalac at 1:1 dilution at
3 months old. Enfapro A+ at the same dilution was started as follow-on
formula at 12 months. At 24 months, she was weaned from the bottle and
Nutritional
shifted to Nido 1+ at 4 scoops per glass. Complementary feeding was started
(feeding)
at 6 months. At 12 months, she was started on regular table food. Presently,
history
she eats a variety of food with preference for chicken, soup, fruits. Feeding
schedule comprises 3 main meals of about a cup full of rice, fish or chicken,
and fruits for dessert. Morning and afternoon snacks are given.
Juana was given BCG vaccine at birth. She has received 3 doses each of
hepatitis B, hemophilus influenza B, DPT, inactivated polio vaccine (6-in-1
Immunization
vaccine) at 6, 10 and 14 weeks. She received measles vaccine at 9 months of
history
age. She has not received pneumococcal, flu, MMR, hepatitis A, and varicella
vaccines.
VITAL SIGNS
The following table serves as a guide to check if the obtained vital signs are within normal range.
Howeve,; the range of normal values may va,y depending on the reference you use. Always
correlate the obtained measurements cli11ical/y.
AGE
Premature
l"=
..~1-1~
{beats/min)
120-170
(bre::min)
5
I. RESPIRATORYRATE
• Based on WHO, the following values serve as the cut-off values per age for tachypnea
• These values are more commonly used in the clinical setting
AGE GROUP DEFINITION
Newborn >60 breaths/min
2-12 months >SO breaths/min
1-5 years >40 breaths/min
>5 years >30 breaths/min
Source:Haz1nsk1
MF.Manualof PediatricCnl1cal Care(1sted.).Elsevier,1999
BloomfieldD, et al. Tachypnea.
PediatricsIn Review;2002
II. BLOODPRESSURE(BP)
Determine the Blood Pressure using the Following Steps:
Taking the Blood Pressure using the Upper Extremities
• Child should be seated 3-5 minutes before measurement
• Right arm is usually recommended for standardization (since there is a possibility of
having false low readings in the left arm if there is coarctation of the aorta)
• Use the correct cuff size:
, Bladder length ;,BO% of the upper arm circumference
'Bladder width ;,40% of the upper arm circumference
• The lower part of the cuff is placed 2-3 cm above the antecubital fossa
• The bell of the stethoscope is then placed over the brachia! artery
• The cuff is inflated 20-30 mm Hg above the point at which the radial pulse disappears and
is then deflated at a rate of 2-3 mmHg per second
• The first and last Korotkoff sounds are measured and recorded with measurements read
to the nearest 2 mm Hg
Taking the Blood Pressure using the Lower Extremities
• Patient should be placed in prone position
• The cuff is placed at the midthigh and the stethoscope is placed over the popliteal artery
• Systolic BP in the legs is 10-20% higher than the arms
• Check the BP of all extremities to rule out diseases like coarctation of aorta
A. Detection of Hypertension
The following steps describe the ideal method for interpretation of blood pressure to detect
hypertension (table in previous page is only an approximation)
After determining the blood pressure as described above, follow the steps below:
Step 1. Determine where the Systolic and Diastolic BP Percentile Falls
Using the BP levels for age and height percentile, determine where the BP percentile falls
If the height fallsexactly in between two percentiles, choose the lower percentile cut-off
The BP percentile table is freely downloadable online
Step 2. Interpret the BP using the following table (Definitions of BP Categories & Stages)
INTERPRETATION* ----------~
I AGE
I 1 to <13 Years Old , _ 13 Years Old
Normal • <90'h percentile • <120/80 mmHg
• ;,90"" to <95'" percentile, or • 120/80 to 129/80 mrnHg
Elevated BP or
• 120/80 mmHg to< 95"'
Pre hypertension
percentile (whichever is lower)
• ;,95,h percentile to <95'" • 130/80 to 139/89mrnHg
Stage 1 percentile+ 12 mmHg, or
hypertension • 130/80 to 139/89 mmHg
(whichever is lower)
Stage 2 • ;, 95'" percentile+ 12 mmHg, or • ;,140/90 mmHg
hypertension • ;,140/90 (whichever is lower)
'Hypertensionis presentifchildmeets abovecriteriaon 3 or moreseparate occasions(differentclinicvisits)
6
Sample Case 1: An 8 year old male with a height of 141 cm sought consult for a general check-
up. BP on three separate determinations was 115/74 mmHg.
I
.
ARelyl SPP,recn:de
95th
"
107
$
,os
~
'"
ffl
110
~
Ill
~
112
100
112
"' "'
"'
112
"' '"
'"
115
127
116
128
117
"'
1 table from standard
BP P~n:cnhle 09PfrnmH51
charts or tables A)iC !~I
l"e15rithn!
Hc1&IIIf~ml
·~
-H!
l21J
""'
.?~6
ins
1te1gritPerun:11eorMeasurtdHe1~nt
'ZS%
So
127
,,.
s~
'"19
,s...
1.SSI
...
S.is
"" +u1
95~
555
.,
,.,
""" 57
"
57
" "n 60
""
70
""
70
,Slh
"" "" "" " "
9:Sth•lJrnmllli;
" 81 87 81
Sample Case 2: An 8 year old male with a height of 141 cm sought consult for a general check-
up. BP on three separate determinations was 120/80.
,..
S%
'"' "~ ""' "~ 95%
Ht,ght!Cfftl
~O!h
so:11
121 ~
95
IOi
,.
-,---ikililifit-,1----,1s·--4g-;---!IO--sis--~n-···--S'l""r-~
12.s;
10,
"'
" " "''
100
Ut
!Ill
110
13'>1
99
112
+1~1
,oo
,,.
112 112 '"
"' "'
~5th Ill
'" 10li
~H
25%
"" "~
532 '"" "~
"'"
,-----Ht~ihn) ti6 !U6
..,,
~. 8 :;5$
Hc1ghtCcml
50th
121 ~ 12J.5
57 '"., 1351
s,
1.!88 ♦ 141
90th
51
",, 70 "
70
"
60
95th
" 7J
a; " " "" 75 "
75
9Sth•12rnmll)1:
" " 87
" "
• Patient's BP falls between 95th percentile and 95th + 12 mmHg
2 Interpret
• This is therefore interpreted as Stage 1 Hypertension
Sample Case 3: An Byear old male with a height of 141 cm sought consult for a general check-
up. BP on three separate determinations was 140/90 mm Hg.
7
B. Detection of Hypotension
To determine if patient is hypotensive, the following cut-offs are used in practice (the values in
the above table derived from Nelson is only a quick reference)
AGE SYSTOLIC BLOOD PRESSURE (SBP)*
Term neonates (0-28 days) <60 mm Hg
Infants (1-12 months) <70 mm Hg
Children 1 to 10 years <70 + (age in years x 2) mmHg
Children >10 years <90 mm Hg
Source:Hazinski
MF.Manualof Pediatric
CriticalCare(1sted.).Elsevier:
1999
• A blood pressure of80/50 mm Hg is considered hypotensive for the 8 year old patient
since the SBP is <86 mm Hg
8
• Inspection: no masses or lesions, deformities or defects on chest
wall, no lagging of respiratory movement, with regular and
symmetrical breathing, no retractions
I
.
9
SECTION TWO
ADMITTING ORDERS AND DAILY ROUNDS
• Admit under the service of ____________ (state name of attending physician or if using
HMO, under the name of the HMO coordinator first then state the name of the attending
MD who will actually manage and do the rounds of the patient)
• Admit to _________(room of choice: regular private room, or pedia ICU, or neonatal ICU,
or intermediate medical care unit - IMCU, or ward and bed number)
• How the patient should feed (NPO, full diet for age, state restrictions/known allergies
if present)
• IV fluids needed at the moment, the need for the patient to be re-assessed after fluid
resuscitation, if applicable, so that follow-up fluids could be carefully decided on)
• Diagnostics: include all laboratory exams and imaging modalities that need to be done
for the patient
• Therapeutics: all medications with properly computed doses, frequency, route of
administration (use only standard and universally accepted abbreviations; better to
spell out millileters and milligrams to avoid confusion)
• Frequency of monitoring vital signs, fluid input and urine output/stool output (e.g.,
monitor vital signs every 4 hours; monitor neurologic vital signs every 4 hours;
monitor urine output every 8 hours)
• Oxygen support, if needed (e.g., nasal cannula at 2 liters per minute)
• Watch out for: indicate pertinent signs of deterioration or signs of persistent
problematic symptoms (this should be specific and appropriate to the current clinical
condition of the patient)
• Inform pediatrics resident or pediatrics hospitalist or junior consultant of admission
(whichever is appropriate)
• If applicable, state whether there are other services that will be on board for the care of
the patient (e.g., refer to Surgery [and state name of attending MD if known at this time]
for further evaluation and management of abdominal pain)
• Refer accordingly
REFERENCES
1. Antia AU,MaxwellSR,GoughA, and Ayeni0. (1978). Position of the apex beat. Arch DisChild,53(7), 585-589.
2. Athreya 8, Pearlman SA,Zitelli 8 (2010). Pediatric physical diagnosis. 2nd ed. Anshan Publishers
3. Bickley LS,Szilagyi PG,& Bates 8. (2007). Bates' guide to physical examination and histo1y
taking. 6th ed. Philadelphia: Lippincott Williams & Wilkins.
4. Katzenellenbogen R. (ZOOS).HEADSS:the review of systems for adolescents. Virtual Ment01;
7(3):231- 233.
5. WolfADand LavineJE.(2000). Hepatomegalyin neonates and children. Pediatrics in Review,21(9), 303-310.
10
FLUIDS
ANDELECTROLYTES
0 FLUID THERAPY
BASIC PHYSIOLOGY
PHYSIOLOGY OF BODY FLUIDS I
I. COMPOSITION OF BODY FLUIDS
• Total body water (TBW) percentages varies with age
75% of birth weight for term infant (higher in preterm infants)
0 By the 1st year of life, TBW decreases to adult values of 60%
0 Newborn extracellular fluid (ECF) is higher than the intracellular (ICF)
Hydrostatic and oncotic pressure maintain equilibrium between intravascular fluid and
interstitial fluid
lntravascular volume is crucial for tissue perfusion
OSMOLALITY
• ICF and ECF compartments are in osmotic equilibrium
• Osmotic pressure differences cause water movement between the ICF and ECF to equalize
the osmolality
• Na: in mmol/L
= 2(Na') +Glucose+ BUN • Glucose and BUN: in mg/dL
-- • Normal value= 285-295 mOsm/kg
18 2.8
Hyperglycemia causes increased osmolality which causes movement of water from ICF to
ECF and dilutes Na•
Source:KliegmanR, et al. Nelsontextbookof pediatrics(21sted.). Philadelphia:Elsevier:2020
PhilippinePediatricSociety,Inc.Consensusstatements.:2017
13
SECTION TWO
FLUID THERAPY
Calculations for maintenance and deficit therapy stated in this book are simply guidelines
and not absolute requirements. Clinical and/or laboratory assessment are more important
in determining the appropriate fluid therapy
I. INDICATIONSFORSTARTINGINTRAVENOUSFLUIDS (IVF):
• Acute volume expansion
• Correction of fluid and electrolyte imbalances
• Compensation for ongoing problems that may affect fluid and electrolyte levels
• Maintenance therapy for patients who cannot be fed enterally to prevent dehydration,
electrolyte disorders, ketoacidosis, protein degradation
1) MAINTENANCE THERAPY
• Requirement depends on the age and clinical status of the patient
Healthy adolescents can tolerate nothing per orem (NPO) for 12-18 hours
Infants & children must be started on maintenance therapy ifNPO duration exceeds 8 hours
0
14
B. Ludan Method (Basal Caloric Expenditure-based)
Widely used in the Philippines, but not internationally
° Closer to basal caloric expenditure
WEIGHT
0-10 kg • 100 mL/kg
MAINTENANCE THERAPY FOR 24 HOURS
accepted
I
10-20 kg • 75 mL/kg
20-30 kg • 50-60 mL/kg
30-60kg • 40-50 mL/kg
IVF RATE
COMPUTATION OF (Total amount/
METHOD
MAINTENANCE THERAPY number of hours
infused)
First 10 kg = 1,000 mL
Holliday-
6kgx50mL/kg = 300 mL 54 mL/hour
Segar Method
Total = 1,300 mL in 24 hours
Ludan
16 kg x 75 mL/kg = 1,200 mL in 24 hours SOmL/hour
Method
BSA= ✓[(16 kg x 103 cm)/3600]
Crawford = 0.68 m 2 43 mL/hour
Method
1,500 mL/m' x 0.68 1112 = 1020 mL in 24 hours
Note the differences in results depending on the method used. This highlights the importance of
individualizingfluid requirements
15
II. MAINTENANCE ELECTROLYTE REQUIREMENTS
• Depends on the patients' weight and clinical condition
• The water and electrolyte requirements of patients dictate the appropriate fluid to be used
Recommended Electrolyte Requirements
Na (Na•) • 2-3 mEq/kg/day
Potassium (K•J • 1-2 mEq/kg/day
Chloride (Cl") • 2-4 mEq/kg/day
• 0.5-1 mmol/kg/day (200-500 mg/kg/day Ca2·gluconate, maximum
Calcium (Ca2 •J
2 g/day in infants and 3-4 g/day in older children)
Magnesium (Mg'•) • 0.25 mEq/kg/day
Phosphate' • 2 mEq/kg/ day
Sources:Avner,E.,et al. PediatricNephrology (7thed.).London:Springer;2016
KliegmanR, et al. Nelsontextbookof pediatrics(21thed.).Philadelphia:
Elsevier;2020
Fluids
Sample case: A 2 year-old boy was admitted for diarrhea of 2 days. His pre-illness weight
is 11 kg and on admission he weighed 10 kg. Calculate the fluid deficit:
18
IV. STEPS IN INTRAVENOUS(IV) MANAGEMENTOF FLUID DEFICIT
• Oral rehydration is still the safest and preferred method to correct fluid deficit
• The table below summarizes the steps in IV management of fluid deficit
STEP 4: REPLACEONGOINGLOSSES
• Given to patients in addition to the maintenance therapy in cases of ongoing fluid losses
• Refer to "replacement therapy" on the next page (see below)
"'Push-pull" method: where fluidsare intermittentlydrawn into a syringe from an infusionbag and manually
administered to the patient
Sample Case:
A 4 year-old male, weighing 15 kg, was brought in for 5 days history of diarrhea and
vomiting. On assessment, BP is palpatory 80 mm Hg, lethargic, sunken eyeballs, dry lips,
with poor skin turgor.
19
Continuation of the Case: After the first bolus, the patient is out of shock. Proceed with
computing for the 24-hour fluid requirements
First step is to compute for the Maintenance and Deficit
• Maintenance fluid requirement (using Holliday-Segar)
= 1250 mL
• Fluid deficit (for severe dehydration)
= 90 mL/kg x 15 = 1350 mL
Next is to compute for the 24-hour fluid requirement:
3)REPLACEMENTTHERAPY
• Given in addition to maintenance therapy in cases of ongoing fluid losses (e.g., from GIT)
• For previously healthy and well-nourished patients, 1·eplacement of ongoing losses with
reduced osmolarity ORS is preferred (glucose 75 mmol/L, Na+ 75 mmol/L, K+ 20 mmol/L,
Cl- 65 mmol/L, citrate 10 mmol/L)
• Replace losses volume per volume every 1-4 hours
IV replacements are usually infused for 30 minutes to 1 hour (given at a slower rate for
those with congestion, fluid overload, and in malnourished patients)
Presented below are the specific recommended fluids depending on the type of losses
I
TYPES OF FLUID APPROACH TO REPLACEMENT***
• Reduced osmolarity ORS is the replacement fluid of choice
Diarrhea* • Options for those who cannot tolerate ORS: pLR or D5LR
(advantage of preventing hypoglycemia)
Emesis or nasogastric
• NSS + 10 mEq/L KC!
losses**
Surgical drains and chest tube • NSS or LR
Third space losses (burns) • NSS or LR or 5% albumin
II. MANIFESTATIONS
• Dehydration
• Doughy feel of skin during abdominal skin pinch
CNS manifestations: irritability, restlessness, weakness, lethargy, seizures, coma
• Fever
Hyperglycemia and hypocalcemia
• Most dreaded complication is brain hemorrhage
III. MANAGEMENT
A. Address the Underlying Cause
ETIOLOGY MANAGEMENT
Mild/moderate dehydration in AGE • Oral rehydration
• Priority is restoration of intravascular volume
Hypernatremic dehydration by giving isotonic boluses 10-20 mL/kg
• Fluid of choice: pNSS
Central diabetes insipidus • Desmopressin
Nephrogenic diabetes insipidus • Thiazide diuretic
Iatrogenic hypernatremia • Decrease or stop sodium infusion
21
IV. SAMPLESTRATEGYFOR TREATMENT OF HYPERNATREMIA
Step 1: Restore intravascular volume in patients who are severely dehydrated
May give pNSS 20 mL/kg over 5-20 minutes via "push-pull" technique
May repeat as necessary, usually up to 3 boluses
145-157 24
158-170 48
171-183 72
184-196 96
Step 3: Compute for amount of fluid to be given and determine IVF rate
Maintenance fluid+ 30-50 mL/kg given over desired correction time
• If boluses are given in Step 1, subtract it from the total fluid to be given
• If sodium is to be corrected in 48 hours, maintenance fluid is computed for 48 hours
• Example: the rnaintenance fluid of a 15 kg child is 1250 rnL for 24 hours, 2500 mL for
48 hours, 3750 mL for 72 hours and so forth
Initial fluid: D5 1/2NS +/- 20mEq KCL
Do not give KCL unless patient has established adequate urine output
Sample Case: A 15 kg male carne in due to vorniting and diarrhea for 5 days. BP 90/60
rnrnHg. He is awake, responsive, has sunken eyeballs & dry lips. Sodium level is 160
mEq/L. How would you manage this case?
Sodium(Na·)<135mEq/L
Checkosmolality
.~-------~.--------_
~ :
:_Pseudohyponatremia , Hyperglycemia , I TrueHyponatremiaj
: Mannitoladministration:
·--------------------· IAssessvolumestatus
Euvolemia Hypovolemia
6 Hypervolernia
1
Spot UrineNa· >20mEq/l
,~
__________
L_________SIAOH<
SpotUrineNa·< 10 mEq/l I ~tUrineNa'>20mEq/L I SpotUrincNa'<lOmEq/l
Source:
Kliegman
R,etal.Nelson
textbook
of pediatrics
(21sted.).Philadelphia:
Elsevier;
2020
PhadkeK.etal.Manualof Pediatric
Nephrology.London:
Springer:
2014
23
IV. MANAGEMENT
A. Management based on Underlying Pathophysiology
PATHOPHYSlOLOGY MANAGEMENT
• Restore intravascular volume with isotonic saline
Hypovolemic hyponatremia
• Restoration of intravascular volume takes priority
Hypervolemic hyponatremia • Water and sodium restriction
B. Specific Management
Sample Case: A 3 year old, 15 kg patient came in due to 3 day history of vomiting and LBM
>10 episodes per day, in active seizures. BP= 90/60 mm Hg, HR= 110 bpm, RR =30/min. He
had dry lips & sunken eyeballs. Hgt= 90 mg/dL. Na= 120 mEq/L
24
HYPERKALEMIA
I. ETIOPATHOGENESIS
• Defined as serum K+ >6 mEq/L in newborn and >5.5 mEq/L in older children
• Refer to essentials chapter for normal range of potassium levels depending on age group
I
MECHANISM MANAGEMENT
Spurious laboratory values • Hemolysis, tissue ischemia, thrombocytosis, leukocytosis
Increased intake ofK+ • Iatrogenic, blood transfusions
• Acidosis, rhabdomyolysis, tumor lysis syndrome,
Transcellular shifts of K+ exercise, beta-adrenergic blockers, insulin deficiency,
hyperkalemic periodic paralysis
• Renal failure, Addison Disease, congenital adrenal
hyperplasia, Hyporeninemic Hypoaldosteronism, Renal
Decreased excretion of K+
tubular disease, medications (ACEi,ARBs, potassium-
sparing diuretics, NSAIDs,heparin, drospirenone)
II. MANIFESTATIONS
• Most importantly affects membrane potential and the cardiac conduction system
• Some patients manifest with paresthesia, fasciculation, weakness and ascending paralysis
However, cardiac toxicity usually precedes these above manifestations
Tall peaked
Twave
8.0
Loss of P waves, =·"'
P wave
widening of QRS
~
\
9.0
10
ST-segment
depression, further
widening of QRS
JvC
Bradycardia, sine wave QRS-T, first degree AV block,
ventricular arrhythmia
Source:EngornB, et al. TheHamelLaneHandbcok(20thed.).Ph1ladelph1a:
Elsevier;2015
25
III. APPROACH TO DIAGNOSIS
• Cause is olten evident on good clinical history
• Laboratory tests:
Serum K+ level (request for plasma levels if with significant leukocytosis or thrombocytosis)
BUN, creatinine
0Blood gases
ECG to assess the urgency of the situation
Hyperkalemia
,----------------------
Acute kidney Injury Check aldosterone & renin levels
,___ Chronic kidney disease ___ ,
IV. MANAGEMENT
A. Management based on Potassium Level
26
B. Options in Management
RATIONALE
1. Calcium Glucanate
HOW TO ADMINISTER MAXIMUM DOSE
• Commonpractice is a max
I
• Most important step is to dose of 10-20 mL (10%
reverse membrane effects of • 10% Ca2 • gluconate calcium gluconate)
hyperkalemia (Ca2 • stabilizes 100 mg/kg/dose (1 mL/kg/ • Maximum IV rate
the membrane of cardiac dose) over 3-5 minutes (may • Push: 100 mg/min
cells to prevent arrhythmia) repeat in 10 mins) • Infusion:120-240mg/kg/hr
• Does not lower serum K' levels with max concentration of
50 mg/mL
2. Sodium Bicarbonate (NaHCO,)
• Administration: dilute 1 • Max dose 50-100 mEq
mEq/mL NaHC03 with
• Causes intracellular shift • Common practice is to infuse
sterile water or D5 water
ofK+ over 30 minutes to 1 hour
(1:1 dilution)
• Most efficacious in patients • May be repeated every
• 1-2 mEq/kg IV given over
with metabolic acidosis 5-10 minutes, at a rate no 5-10 minutes as needed to
greater than 10 mEq/min reverse ECGabnormalities
4. Salbutamol Nebu/ization
• Stimulation of beta-1
• 2.5 mg for children <25 kg • May be given every 1-2
receptors causes
• 5 mg for children >25 kg hours
intracellular shift of K·
S. Sodium polystyrene (Kayexelate)
• Potassium binders • 1 g/kg/dose every 4-6 hours mixed with 250 mL of water as
• Exchange resin retention enema
6. Loop Diuretic
Sample Case: A 1 year-old was admitted due to severe hyperkalemia. Weight 10 kg. K· = 8
mEq/L. How will you manage the patient's hyperkalemia?
• Calcium gluconate 10% 100 mg/kg or 1 mL/kg: 1 gram or 10 mL slow IV push over 10 minutes
• NaHC03 1 mEq/kg: 10 mEq + 10 mL D5W slow IV over 10 minutes
• Regular Insulin 0.1 u/kg + 2 mL/kg D5W: 1 unit+ 20 ml D5W to be given over 30 minutes
• Salbutamol 2.5 mg nebulization every 1-2 hours
• Sodium polystyrene 1 g/kg: 10 g every 4-6 hours mixed with 250 mL of water as retention enema
• Furosemide 1 mg/kg: 10 mg IV every 6 hours
• Dialysis
Depending on clinical situation and physician's judgement, some strategies may be utilized. Remember
that calcium gluconate is the most important management since it stabilizes cardiac cell membranes.
Source:EngornB, et al.TheHamelLaneHandbook Elsevier;2015
(20thed.l.Ph1ladelph1a:
Kliegman :t~~o~~ii~~d~~~~o\~~
R, et al;,_~r\'~~0£. Mfi ti~~~~::
.,intt~§~~ ~8ti
27
HYPOKALEMIA
I. ETIOPATHOGENESIS
• Defined as serum K· level <3.5 mEq/L
• Common etiologies include the following:
MECHANISM MANAGEMENT
Spurious • Increased WBC
Transcellular • Alkalosis, insulin, drugs/toxins, hypokalemic periodic paralysis,
shifts thyrotoxic periodic paralysis, refeeding syndrome
Decreased Intake • Anorexia
Extrarenal Loss • Diarrhea, laxative, kayexalate or clay ingestion
• RTAType 1 and 2, OKA,Gitelman Syndrome, Bartter Syndrome
Renal losses
• Loop/thiazide diuretics, hyperaldosteronism, licorice ingestion, emesis
Source:KllegmanR,et al. Nelsontextbookof ped,atncs(21sted). Ph1ladelph1a:
Elsevier:2020
II. MANIFESTATIONS
• Cardiac and skeletal muscles are vulnerable to hypokalemia
Muscle weakness and cramps, constipation, ileus, urinary retention
• Paralysis may occur at potassium levels <2.5 mEq/L and may cause respiratory compromise
• ECGchanges: flattened T wave, depressed ST segment, U waves, arrhythmias
III. DIAGNOSIS
• Etiology of hypokalemia is usually apparent from clinical history
• If etiology is uncertain, measure urinary K' to distinguish renal from extra-renal losses
If extra-renal loss: kidneys should conserve K· (i.e., low urinary K·)
0 Methods: 24 hour urine collection, spot K·:creatinine ratio, fractional excretion of K·
IV. MANAGEMENT
• There is no single strict formula for correcting potassium derangements
• Patients with impaired renal function should be treated cautiously to avoid hyperkalemia
ROUTE DOSE REMARKS
• Dose: 2-4 mEq/kg/day
• Preparations (varies depending on brand): • Max dose: 120-140 mEq/
Oral
° KC!syrup 5 mEq/5 rnL day in divided doses
° KC!tablets (1 tab= 10 mEq or 8 mEq K·)
• Maximum concentration of
IV • Dose: 2-4 mEq/kg/day K• incorporation:
Correction • Incorporate KCIinto the IV fluid 0 40 mEq/L in peripheral line
A Oral Correction:
0 Safest and is the preferred method (effective in 90% of cases)
Increase dietary intake ofK'-rich food (e.g. broccoli, tomato, squash, banana)
0
0
Hypomagnesemia is considered if hypokalemia is persistent or unresponsive to correction
IV MgSO4 25- 50 mg/kg/dose (max: 2 g) over 2 hours x 3-4 doses, q4-6 hours
° Common method is to mix MgSO4 with D5W to make a total volume of 30 mL to be
I
: ,
Sample Case 1: A 2 year-old female was rushed to the ER due to LBM of more than 10
episodes. Weight is 10 kg. On work-up, K' = 2 mEq/L and there are ECG changes. How will
you correct the hypokalemia?
IV "fast" correction
• Dose: 1 mEq/kg x 10 kg= 10 mEq
• Order: Give 10 mEq KCIplus D5W to make 100 mL to run for 1 hour
= 1 mEq/kg/hr
*KIR is the maximum recommended (0.5-1 mEq/kg/hr)
Reminder!
• IV "fast" correction should be done under close monitoring, ideally in an ICU setting
• Take note of the maximum KIR and concentration of potassium incorporated depending
on the site of infusion
Sample Case 2: A 1 year-old male was brought in due to diarrhea of3 days. Weight 10 kg.
Physical examination shows no signs of dehydration. Work-up shows hypokalemia K' = 3
mEq/L and patient cannot be fed enterally but is otherwise asymptomatic.
Strategy: Incorporate KCI in the maintenance IVF taking note of the maximum
concentration of KCI incorporation and maximum KIR.
IV incorporation
• Dose: 3 mEq/kg/day = 3 mEq x 10 kg= 30 mEq/day
• Compute for KCIto be incorporated: 30 mEq KCIin 1 liter offluid
• Order: incorporate 30 mEq KCIto 1 liter D5 ½ NS to run for 40 mL/hr
(delivering 3 mEq KCl/kg/day)
Reminder! Take note of fluids that already have potassium in them (LR, 1MB, NM, IES).
The amount of potassium in these fluids should be considered in the computation of the
amount of KC! incorporation and KIR.
Source:Engorn8, et al.TheHarrietlane Handbook
(20thed.).Ph1ladelph1a:
Elsevier;2015
29
Sample Case 3: A 1 year-old male was brought in due to diarrhea of3 days. Weight 10
kg. Physical examination shows no sign of dehydration. On work up K· = 3 mEq/L. He is
asymptomatic and can tolerate oral feeding. How will you correct patient's hypokalemia?
Oral correction
• Dose: 3 mEq/kg/day x 10 kg= 30 mEq/day
• Frequency: In three divided doses= 10 mEq/dose
• Order: Give KC)syrup 5 mEq/5 mL, 10 mL qB per orem. Re-check K· levels as needed
HYPOCALCEMIA
I. ETIOPATHOGENESlS
A. Review of Physiology
Calcium exists in three forms in plasma:
Calcium bound to protein, predominantly albumin (40%)
Ionized calcium (48%)
Calcium complexed with anions like phosphate, citrate and bicarbonate (12%)
B D f fH
SERUM CALCIUM IONIZED CALCIUM
Newborn • Refer to essentials section
C. Etiology of Hypocalcemia
ETIOLOGY EXAMPLE
Vitamin D deficiency • Nutritional, Vitamin D dependent rickets, CKD
• DiGeorge Syndrome
• CHARGE(Coloboma, heart anomaly, choanal atresia, mental
Hypoparathyroidism retardation, genital hypoplasia, ear anomalies) association
• Neck surgery, Thalassemia, Wilson disease, Iodine 131 therapy
II. MANIFESTATIONS
Often asymptomatic
• Most common presentation: tetany and seizures
Acute manifestations: neuromuscular irritability, prolonged QT interval, heart block
• Chronic manifestations: cataracts, basal ganglia calcifications, extrapyramidal symptoms,
enamel hypoplasia, papilledema, rickets
SIGN PROCEDURE RESULT
• Repeatedly tap
lateral cheek over • Twitching of the
the course of the corner of the mouth
Chvostek
facial nerve (-1 cm on the ipsilateral side
sign
over the zygomatic due to contractions of
process & 2 cm circumoral muscle
anteriorto earlobe)
30
III. DIAGNOSIS
• Serum calcium, phosphate, magnesium
• Serum albumin
Corrected Calcium
Change in serum albumin by 1 g/dL causes proportional change in serum Ca2 • by
I
0.8 mg/dL (0.2 mmol/L)
Corrected Ca2 • (mg/dL) = Serum Ca'' (mg/dL) + [0.8 x (4 -serum albumin (g/dL)))
Sample Case: A child sought consult. serum Ca 2' was 1.8 mg/dL and albumin 3.5 g/dL.
Compute for the corrected Ca''
Solution:
• 1.8 mg/dL + (0.8 x (4 - 3.5)] = 2.2 mg/dL
IV. MANAGEMENT
A. Symptomatic Hypocalcemia
Calcium gluconate 10% at 100-200 mg/kg/dose (1-2 mL/kg/dose) + equal diluent
given IV at a rate not more than 100 mg/min. Maximum adult dose is 3 g
Common practice is to give calcium gluconate infusion over 1 hour, at a maximum dose
of 1-2 g/dose (equivalent to 10-20 mL of calcium gluconate 10%)
0 Same dose is repeated every 6-8 hours until asymptomatic
, Hook patient to cardiac monitor while ongoing calcium infusion to monitor for arrhythmia
8. Asymptomatic Hypocalcemia
, Oral supplements at 50-100 mg/kg/day of elemental calcium in 4 divided doses
Source:PhadkeK, et al. Manualof PediatricNephrology. London:Springer:2014
Engorn8, et al. TheHarrietLaneHandbook(20thed.).Philadelphia: Elsevier:2015
KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Philadelphia:
Elsevier:2020
HYPERCALCEMIA
I. ETIOPATHOGENESIS
A. Definition of Hypercalcemia
0 Serum Ca2 '>12 mg/dL (>3 mmol/L)
0 Severe hypercalcemia = serum Ca'' >15 mg/dL (>3.75 mmol/L)
B. Etiology
ETIOLOGY EXAMPLE
• Adenoma, Multiple endocrine neoplasia, secondary and
Hyperparathyroidism
tertiary hyperparathyroidism from CKD
Excess vitamin D • Hypervitaminosis D, Sarcoidosis, Cat-scratch disease, TB
Ca'' release from bone • Thyrotoxicosis, immobilization, malignancy, SLE
• Idiopathic infantile hypercalcemia, Phosphate depletion in
Others
preterm newborns, Addison disease, Cushing disease
31
II. MANIFESTATIONS
EARLY SIGNS OF HYPERCALCEMIA PROLONGED HYPERCALCEMIA
IV. MANAGEMENT
A.Goals:
0Decrease intestinal calcium absorption
0Increase urinary calcium excretion
Decrease bone resorption
0Remove excess calcium through dialysis
B. Specific Management
TREATMENT EXAMPLE
• 3000 mL/m 2 /day of isotonic saline
Hydration
• Renal function must be normal
Loop diuretics • Furosemide 1 mg/kg/dose every 6 hours
• 1 mg/kg/dose every 6 hours
Hydrocortisone • F'or vitamin D intoxication, granulomatous disease,
paraneoplastic syndrome
• Pamidronate
Bisphosphonates • Mild hypercalcemia: 0.5-1 mg/kg/dose IV
• Severe hypercalcemia: 1.5-2 mg/kg/dose
• 4 IU/kg every 12-24 hours IM or SC
Calcitonin
• May increase up to 8 JU/kg every 6-12 hours
Dialysis • Done if with renal failure or if above measures fail
Surgical subtotal • For primary or tertiary hyperparathyroidism
parathyroidectomy
32
SECTION FOUR
COMMON DRIPS, BLOOD TRANSFUSION,
GLUCOSE INFUSION
I
INTRAVENOUS DRIPS
There are many methods in compt1ting for the rate and concentration ofintravenot1s drips.
Familiarizeyot1rselfwith the method that is easiest for yot1 to remember.
I. METHOD 1:
STEP 1. Determine the concentration of the drug based on the preparation of the drug and
amount of diluent used.
Concentration _ Volumeof drug (mL)x Preparation of drug (mg/mL) x 1000 (if desired dose is in mcg)
(mcg/m L) - Total volume of preparation (mL)
Sample Case: For a 10 kg patient, administer dopamine via drip at a dose of 5 mcg/kg/
min. The available dopamine ampule has a preparation of 200mg/5mL, 5 mL per ampule.
A user defined desired total volume of 50 mL (5 mL of dopamine+ 45mL D5W diluent).
Desired total volume is set by user. 50 mL is a commonly used volume since most syringe
pumps for inotropes have a maximum of 50 mL volume.
Order: Start dopamine drip as follows: Dopamine (200mg/5mL) 5mL + 45mL D5water to
run at 0.75mL/hour (delivering 5 mcg/kg/min)
II. METHOD 2
Determine the total volume of the preparation based on the preparation of the drug and
desired drip rate
33
Sample Case: A 10 kg patient, compute how to give dopamine drip at a dose of 5 mcg/kg/
min. The available dopamine ampule has a preparation of200mg/5mL, 5 mL per ampule.
Your desired drip rate is 1 mL/hour
1 mL/hour = 10kg x 5 mcg/kg/min x 60min/hour x total volume
200,000 mcg
(this is 200 mg converted to mcg)
Total volume= 67 mL
Order: Start dopamine drip as follows: Dopamine 200mg/5mL ampule, 1 ampule+ enough
D5W to make a total volume of 67 mL, to run at 1 mL hour (delivering 5 mcg/kg/min)
III. METHOD 3:
20 mL of • 2.5-15 mcg/kg/min
Dobutamine
dobutamine 5000
250mg/20mL • Max:40 mcg/kg/min
+ 30 mL of diluent
Epinephrine 5 mL of epinephrine
250 • 0.1-1 mcg/kg/min
lmg/mL + 15 mL of diluent
3 mL ofmidazolam
300
Midazolam + 47 mL of diluent
• 1-2 mcg/kg/min
Smg/mL 6 mL of midazolam
600
+ 44 mL of diluent
34
BLOOD TRANSFUSION
I. PACKED RED BLOOD CELLS (pRBC)
• 1 unit= approximately 250 mL
• Transfuse properly typed and cross-matched blood product whenever possible
• Blood type 0- may be used if transfusion is emergent
I
.,
A. Indications
CHILDREN > 4 MONTHS OLD INFANTS S4 MONTHS OLD
1. Hb < 7.0 g/dL and patient is in the l. Hb < 7.0 g/dL and patient has
perioperative period, with symptomatic symptomatic anemia or is in the
chronic anemia, or with marrow failure postoperative period
2. Hb < 12.0 g/dL and patient has severe 2. Hb < 10.0 g/dL and patient has moderate
cardiopulmonary disease or is on pulmonary disease, preoperative period, or
extracorporeal membrane oxygenation undergoing major surgery
(ECMO)
3. Hb < 12.0 g/dL and patient has severe
3. Acute loss of >25% of circulating volume cardiopulmonary disease or is on ECMO
B.Volume: There are 3 common methods to com ute the needed volume for transfusion
Method 1 (Empiric)
Volume of PRBC= 10-15 ml/kg
'This increases Hb by about 2-3 g/dL
Method 2 (Harriet Lane)
Volume of PRBC (mL) = EBVx (desired Hct- actual Hct) x Hctof PRBC
Where
• Desired Hct is usually 35%-45%
• Hct of PRBC is 55%-70%
• EBV is estimated blood volume
C.Administration
Transfuse at a rate no faster than 2-3 mL/kg/hour (generally equivalent to 10-15 mL/kg
over 4 hours)
° For severe compensated anemia, transfuse slowly to avoid congestion. The general rule
is to transfuse a maximum amount in mL/kg equivalent to patients Hb level in g/dL
(e.g., if patient's hemoglobin is 5.0 g/dL, transfuse 5 mL/kg PRBC over 4 hours)
35
Sample Case: Compute for PRBC transfusion for a symptomatic 1 year old child diagnosed with
acute leukemia, weighing 10 kg with Hct 25% and Hb of 6.8 g/dL
Compute for desired volume of PRBC using the any of the formulas mentioned above.
Reminder
• Take note of the maximum amount to be transfused for this patient (based on the Hb level:
approximately 6.8 mL/kg). Since our target volume to transfuse is around 100 mL based
on method #s 1 and 3:
0 Order transfusion as follows: Transfuse PRBC properly typed and cross-matched, 2
aliquots at SO mL/aliquot each to run for 4 hours, given 6 hours apart
0 After transfusion of 2 aliquots, we have given a total volume of 100ml PRBC which is our
computed target for this patient
• Common clinical practice is to transfuse the amount of PRBC for 2-4 hours, 6 hours apart
(this is acceptable as long as we take note of the maximum infusion rate of 2-3 mL/kg/hour)
• CBC is then repeated after 6 hours to check for increase in Hb and HCT
A. Indications
36
B. Dose (common clinical practice):
0 1 unit per 10 kg or 4 units per m2 (body surface area)
10 mL/kg (neonate)
° Common clinical practice for patients beyond neonatal period
mL of platelet concentrate= weight (in kg) x 7
• usually rounded based on unit volume of platelet concentrate
I
.
C. Administration
0 Given as fast drip because it adheres to tubings
0 Exception: given for 1 hour in neonates
Sample Case: A 4 year-old patient diagnosed with ALL was found to have a platelet count of
10 on routine CBC.Weight is 20 kg patient. Compute for platelet transfusion.
Amount to be transfused= lunit/lOkg = 2 units
OR mL of platelet concentrate= 20 x 7 = 140 m L = 2 or 3 units can be given
Order:
• Prepare type-specific platelet concentrate 50ml/unit
• Transfuse 2 units as fast drip one after the other
• Repeat CBC 6 hours post-transfusion
A. Indications
Severe clotting factor deficiencies with active bleeding or with invasive procedure
0 Reversal of effects ofwarfarin
0 Disseminated intravascular coagulopathy (DIC)
, Liver disease
0 Dilutional coagulopathy and bleeding (seen in massive transfusion)
B. Dose
0 10-15 mL/kg infused as rapidly as tolerated by patient
Common clinical practice is to infuse FFP over 2 hours (sometimes over 4 hours if
patient is prone to volume overload)
IV. CRYOSUPERNATANT
• Contains unmeasurable amount of Factor VIII and Fibrinogen
• Standard dosing: 10-15 mL/kg
The volume transfused will depend on the clinical situation and patient size
• Indications: Thrombotic Thrombocytopenic Purpura (TTP) or Hemolytic Uremic
Syndrome (HUS)
V. CRYOPRECIPITATE
• Sometimes called Cryoprecipitated Antihemophilic Factor
• Each unit (around 10-15 rnL) provides Fibrinogen, Factor VIII, von Willebrand Factor, and
Factor XIII
• Each unit contain minimum of 150 mg Fibrinogen and 80 IU of Factor VIII
• Indications:
Hemophilia as emergency back up when factor concentrates are not available
0 Von Willebrand Disease as a reserve treatment
0 Hypofibrinogenernia secondary to massive transfusion
Afribrinogenemia
DIC and Uremic Bleeding Tendency
Sources:EngornB,et al. TheHarrietLaneHandbook (20thed.).Philadelphia:
Elsevier;2015
OrkinS, et al. NathanandOski'shematology of infancyandchildhood(7thed.).SaundersElsevier:2009
HillyerC, et al. Handbook of PediatricTransfusionMedicine(1sted.).SanDiego:Elsevier:2004
HillyerC. Bloodbankingandtransfusion medicine.Philadelphia,PA:ChurchillLivingstone/Elsevier:
2007
Ktiegman R, et al. Nelsontextbookor pediatrics(21sted.).Philadelphia:
Elsevier:2020
37
GLUCOSE INFUSION
I. FOR SYMPTOMATIC HYPOGLYCEMIA
• Give D10 water (Dl0W) 2 mL/kg for neonates OR 5 mL/kg for older infants and children
• Re-check glucose levels after 30 minutes
• May give another bolus of Dl0W and adjust glucose infusion accordingly
General Formula:
IV rate (mL/hr) x dextrose concentration (g/dL) x 1000 (mg/g)
Weight (kg) x 60 (min/hr) x 100 (mL/dL)
Sample Case. A 10 kg child was placed on NPO due to vomiting. IV fluids started is DSLR
at maintenance rate using Holliday-Segar formula. Calculate for the G!R
= 1000 mL/day
!VF rate
= 42 mL/hour
= IV rate x dextrose concentration x 0.167
Weight
GIR = 42 X 5 X 0.167
10
= 3.5 mg/kg/min
38
FORMULAS FOR ADJUSTING DEXTROSITY/DEXTROSE CONCENTRATION
• Computations for increasing and decreasing dextrosity are important to be able to
concoct desired dextrose concentration using readily available stock preparations.
• In general, the maximum dextrose concentration for peripheral lines is 12.5% (e.g., D12.5) I
I. INCREASING DEXTROSITY
Sample Case. Concoct a final mixture of 1LD101MB using 051MB and D50 Water (D50W)
Step 1. Determine
stock preparations D5 1MB and DSOW
tobeused
Factor= Desired dextrosity - actual dextrosity
Highest dextrosity- lowest dextrosity
In our example:
Step 2. Compute • Desired dextrosity = 10 (we want to make D10 1MB)
for Factor • Actual dextrosity = 5 (we are making the solution from D5 1MB)
• Highest dextrosity = 50, lowest dextrosity = 5
(we are mixing 051MB and DSOW)
Factor = 10 - 5 = 0.11
--
50 - 5
Step 3. Compute
for amount of Amount of D50W = factor x total volume offinal product (i.e. 1000 mL)
D50Wto be = 0.11 x 1000 = llOmL
added
Step 4. Concoct Prepare D10 1MB as follows: OS 1MB 890 rnL + D50W 110 mL = lL
the fluid D10 1MB
39
REFERENCES
1. Avnet; E., Harmon, W.,Niaudet, P.,Yoshikawa, N.,Emma, F.,& Goldstein, S. Pediatric Nephrology
7th ed. 2016; London: Springer
2. Cloherty, )., Eichenwald, E., Hansen, A., & Stark, A. Manual of Neonatal Care 7th ed. 2012.
Philadelphia: Lippincott Williams & Wilkins.
3. Crawford,)., Terry, M., & Rourke, G. Simplification of drug dosage calculation by application of
the surface area principle. Pediatrics, 1950, 5(783)
4. Del Mundo, Fe. Textbook of Pediatrics and Child Health. )MC Press Inc; 1947
5. Engorn, B., and Flerlage, J. The Harriet Lane Handbook 20th ed. 2015, Philadelphia:
Elsevier.
6. Feld, L., and Kaskel, F.Fluid and Electrolytes in Pediatrics. 2010, New York: Humana Press.
7. Friedman JN, Goldman RD, Srivastava R, Parkin PC. Development of a clinical dehydration
scale for use in children between 1 and 36 months of age. J Pediat,: 2004;145(2):201-207.
8. Glucose Infusion Rate. Retrieved from
9. http://www-users.med.cornell.edu/~spon/picu/calc/glucinfrhtm. Accessed: November 10, 2018.
10. Gillis HC, et al. Rapid fluid administration: an evaluation of two techniques. Medical
Devices: evidence and Research; 2018
11. Hall, j. Guyton and Hall textbook of medical physiology 13th ed., 2006. Philadelphia: Elsevier·.
12. Hillyer, CD, Strauss Sand Luban, N. Handbook of Pediatric Transfusion Medicine. 2004. San
Diego: Elsevier
13. Hillyet; CD, Silbersfein LE, Ness PM et al., Blood banking and transfusion medicine. 2007.
Philadelphia, PA: Churchill Livingstone/Elsevier.
14. Holliday, M., and Segat; W. The maintenance need for water in parenteral fluid therapy.
Pediatrics, 1957; 19.
15. Kliegman, R., ST GEME Ill,)., Blum, N., Shah, S., Tasker, R., Wilson, K., & Behrman, R. Nelson
Textbook of Pediatrics 21st ed. 2020. Philadelphia: Elsevier.
16. Koeppen, B. M., Stanton, B. A. Berne & Levy Physiology. 2010, Philadelphia, PA: Mosby/
Elsevier.
17. Ludan AC. Pediatric fluid and electrolyte therapy. In Del Mundo, et al. Textbook of Pediatrics
and Child Health, 1st Ed, 1974. Quezon City: )MC Press Inc
18. Malbrain, M., Maria, P., Witters, I., Cordemans, C., Kirkpatrick, A., Roberts, D., & Van
Regenmortel, N. Fluid overload, de-resuscitation, and outcomes in critically ill or injured
patients: a systematic review with suggestions for clinical practice. Anaesthesiology
Intensive Therapy, 2014, 46(5), 361-380.
19. National Institute for Health and Clinical Excellence. Diarrhoea and vomiting caused by
gastroenteritis diagnosis, assessment and management in children younger than 5 years.
2019 London: RCOGPress.
20. National Institute for Health and Care Excellence. Intravenous fluid therapy in children
and young people. Available from: https://www.nice.org.uk/guidance/ng29. Published
2015. Accessed: November 15, 2018.
21. Phadke, K.,Goodye1; P.,& Bitzan, M. Manual of Pediatric Nephrology. 2014, London: Springe1:
22. Philippine Pediatric Society, Inc. Consensus statements on parenteral fluid therapy in
infants, children and adolescents, 2017; Philippine Pediatric Society, Inc.; Philippines
23. Orkin, SH and Nathan NG. Nathan and Oski's hematology of infancy and childhood (7th ed.)
2009. Saunders Elsevier
24. World Health Organization. The treatment of diarrhoea. Geneva: World Health Organization; 2005
Available from: https:/ /apps.who.int/iris/bitstream/handle/10665/ 43209 /9241593180.
pdf;jsessionid= 6 BF5 24 B8A D49C4Cl E439 D18C5 E3 D7717?seq uence= 1
40
COMMONMEDICATIONS
INPEDIATRICS
SECTION ONE
INTRODUCTION TO PRESCRIPTION WRITING
1 drop () 1/20 mL
(or 0.05 mL)
1 minim
1 teaspoonful
~ 5 mL 1 dram
1 tablespoonful
1 15 mL 1/2 fluid ounce
1 wine glassful
2 60 mL 2 fluid ounces
□
1 glassful 250 mL 8 fluid ounces
Example Prescription
PART DESCRIPTION
Superscription Patient X; 1/M March 5, 2020
Alabang, Muntinlupa
Rx
Inscription (body) Paracetamol Syrup 250 mg/5mL
Subscription Dispense 1 Bottle (60 mL)
Sign a/label Sig: Take 5 ml every 6 hours for 3 days
Prescriber's data Juan Aherrera MD
License No. 123456
PTR No. 345678
Example for drugs computed as milligram per kilogram per dose (mkdose):
Case: You want to prescribe a child (with a weight o/25 kg) paracetamol syrup ata dose of 10
mkdose for 3 days. The available paracetamol preparation is 250mg/5ml syrup.
Compute for the dose Dose = (Desired Dosage x Weight)/ Preparation
= (10 mkdose x 25 kg)/ (250 mg/ 5 mL)
= 5 mL per dose
Compute for the dispense Dispense Number= 5 mL X 4 doses per day x 3 days
number
=60mL
Dispense 1 bottle (60 mL)
Sample Signatura Take 5 mL every 6 hours for 3 days
44
Example for drugs computed as milligram per kilogram per day (mkday):
Case: You want to prescribe a child (with a weight of 25 kg) amoxici/lin syrup at a dose of 30
mkday qB hours for 7 days. The preparation of amoxicillin is 250mg/5ml syrup
Compute for the dose Dose = (Desired dose x weight)/ Preparation
= (30 mkday x 25 kg)/ (250 mg/ SmL)
= 15 mL per day
I
Convert to "per dose": 15 mLperday / 3 doses per day= 5 mL per dose
Compute for the dispense Dispense Number= 5 mL X 3 doses per day x 7 days
number
= 105 mL
Dispense 1 bottle (120 mL)
Sample Signatura Take 5 mL every 8 hours for 7 days
Example for drugs computed as milligram per kilogram per dose (mkdose)
Case: You want to prescribe a child (with a weightof50 kg) paracetamol tablet at a dose oflO
mkdose for 3 days. The available paracetamol preparation is 500 mg/tablet
Compute for the dose Dose = (Desired Dosage x Weight)/ Preparation
= (10 mkdose x 50 kg)/ 500 mg/tab
= 1 tablet per dose
Compute for the dispense Dispense Number= 1 tablet X 4 doses per day x 3 days
number
= 12 tablets
Sample Signatura Take 1 tablet every 6 hours for 3 days
Example for drugs computed as milligram per kilogram per day (mkday)
Case: You want to prescribe a child (with a weight of 50 kg) amoxicillin ata dose of30 mkday
qBfor 7 days. The preparation of amoxicil/in is 500 mg/capsule
Compute for the dose Dose = (Desired dose x weight)/ Preparation
= (30 mkday x 50 kg)/ 500 mg/cap
= 3 capsules per day
45
SECTION TWO
COMMON DRUGS USED IN PEDIATRICS
ANTIBIOTICS
MAXIMUM DOSE/
DRUG INDICATION/DOSE PREPARATIONS
REMARKS
• Max: initial 1.5 g/
day, then monitor
• 100 mg/amp
• 15-22.5 mkday IV/IM levels
• 200 mg/amp
Amikacin q8, or • WOF: ototoxicity,
• 250 mg/amp
• 15-20 mkday IV/IM OD nephrotoxicity,
• 500 mg/amp
neuromuscular
blockade, rash
• Standard dose: 25-50 • 250 mg cap
mkday PO q8/q12 • 500 mg cap • Max: 2-3 g/day
Amoxicillin • High dose {resistant S. • 100 mg/mL drops • WOF: rash,
pneumoniae): 80-90 • 125 mg/5mL syr diarrhea
mkday PO q12 • 250 mg/5mL syr
• 250/125 mg tab
• Q8 dosing: 20-40 • Max: 2 g PO q12
• 500/125 mg tab
mkday PO • 125/31.25mg/5mL syr • WOF: rash,
Amoxicillin- • 250/62.5 mg/5mL syr diarrhea
Clavulanic • Dosage based
Acid • 875/125 mg tab on amoxicillin
• Q12 dosing: 25-45 • 200/28.5 mg/SmL syr component
mkdayPO • 400/57 mg/5mL syr
• 600/42.9 mg/5mL syr
• Max: 12 g/day
• Mild-moderate infection • Usual meningitic
• 250 mg vial
100-200 mkday IV/IM q6 dose is 200mkday
• 500 mg vial
Ampicillin • Severe • WOF: rash, diarrhea,
• 1 gvial
200-400 mkday IV/IM interstitial nephritis,
q4/q6 pseudo membranous
enterocolitis
46
, Maxfor 5 day regimen:
, 5 day regimen ( otitis
500 mg/day day 1,
media, PCAP,pertussis}
250 mg/day days 2-5
10 mkday PO OD day 1,
, Maxfor 3 day regimen:
Azithromycin
5 mkday PO OD days 2-5
, 3 day regimen (otitis
media, acute sinusitis)
10 mkday PO OD
• 1 day regimen {otitis
• 250 mg tab
• 500 mg tab
• 200 mg/5mL syr
500mg/day
• Maxfor 1 day regimen:
1500 mg/day
• Max for pharyngitis/
I
tonsillitis:500 mg/day
media): 30 mkday PO OD • WOF: transaminitis,
, Pharyngitis/tonsillitis:
cholestatic jaundice,
12 mkday PO ODx 5 days GI discomfort
• 50-100 mkday IV/IM , Max dose: 6 g/day,
• 250 mg vial
q6/q8 prophylaxis 1 g/dose
Cefazolin • 500 mg vial
, IEprophylaxis , WOF: leukopenia,
(1st gen) • 1 g vial
SOmkdose IV/IM 30 mins thrombocytopenia,
before procedure transaminitis
, 25-100 mkday PO q6
• 250 mg cap
(q8/q12 for , Max dose: 4 g/day;
• 500 mg cap
Cephalexin uncomplicated infections) prophylaxis 2 g/dose
• 100 mg/mL drops
(1" gen) • IE prophylaxis • WOF: GI discomfort
• 125 mg/5mL syr
SOmkdose PO 1 hour
• 250 mg/5mL syr
before procedure
• 250 mg cap • Max dose: 2 g/day
, 375 mg ER tab , WOF: increased
Cefaclor • 500 mg cap hepatic enzymes,
, 20-40 mkday PO q8
(2 nd gen) • 50 mg/mL drops bone marrow
, 125 mg/5mL syr suppression,
• 250 mg/5mL syr moniliasis
• 250 mg vial • Max dose: 9 g/day
• IV/IM:
• 750 mg vial • WOF: GI discomfort,
75-150 mkday qB
• 1.5 g vial thrombophlebitis
Cefuroxime
(2 nd gen) • 250 mg tab • Max dose: 1 g/day
• PO: • 500 mg tab
• WOF: GI discomfort
20-30 mkday q12 • 125 mg/SmL syr
• 250 mg/5mL syr
47
• Max dose:
• Usual dose
• 500 mg vial usual dose 4 g/day,
100 mkday IV/IM q12
Cefepime • 1 g vial 6 g/day
meningiticdose:
• Meningitis, neutropenia,
(4 th gen) • 2 g vial • WOF: GI discomfort,
serious infection
thrombophlebitis,
150 mkday IV/IM q8
transaminitis
• Max dose: 4 g/day
• WOF: marrow
• Usual dose • 250 mg cap suppression, Gray
50-75 mkday IVor PO q6 • 500 mg cap baby syndrome
Chloramphenicol
• Meningitic dose • 125 mg/5mL syr • Use with caution
75-100 mkday IV q6 • 1 g/vial in G6PD deficiency,
renal or hepatic
dysfunction
• Max dose: 1 g/day
• 125 mg tab
• WOF: diarrhea,
• 250 mg tab
abnormal taste,
Clarithromycin • 15 mkday PO q12 • 500 mg tab
abdominal pain,
• 125 mg/5mL syr
QT prolongation,
• 250 mg/5mL syr
arrhythmias
• Max dose: 4.8 g/ day
• WOF:diarrhea, rash,
pseudomembranous
• IV/IM: • 150 mg/mL amp colitis, Steven-
Johnson syndrome,
25-40 mkday q6/q8 • 150 mg/2 mL amp granulocytopenia,
thrombocytopenia,
sterile abscess at
injection site
Clindamycin • Max dose: 1.8 g/day,
prophylaxis
• PO: 10-30 mkday q6/q8 600 mg/dose
• 75 mg cap
• Bacterial endocarditis • WOF:diarrhea, rash,
• 150 mg cap
prophylaxis: pseudo membranous
• 300 mg cap
20 mkdose PO 1 hour colitis, Steven-
• 75 mg/SmL syr
before procedure Johnson syndrome,
granulocytopenia,
thrombocytopenia
• Mild-moderate infection:
• 500 mg cap • Max dose: 2 g/day
12.5-50 mkday PO q6
Cloxacillin • 125 mg/SmL syr • WOF: nausea,
• Severe
• 250 mg/SmL syr vomiting, diarrhea
50-100 mkday PO q6
• 250 mg tab • Max dose: 2 g/day
• 500 mg tab • WOF:nausea,vomiting,
• 30-50 mkday PO q6/q8
• 100 mg/mL drops abdominal cramps,
• RF prophylaxis
• 100 mg/2.5 mL drops CYP450drug
Erythromycin 500 mg/day PO q12
• 125 mg/5 mLsyr interactions,
• Pertussis
• 200 mg/5 mL syr hypertrophic
SOmkday POq6 x 14 days
• 250 mg/5 mL syr pyloric stenosis in
• 400 mg/5 mL syr neonates
• WOF: ototoxicity,
Gentamicin • 7.5 mkday IV/IM q8 • 40 mg/mL vial
nephrotoxicity
48
• Max for skin &
subcutaneous
tissue infection:
1.5 g/day
Meropenem
• Skin and subcutaneous
tissue infection
30 mkday IV q8
• Intra-abdominal,
mild-moderate infection
• 500 mg vial
• 1 g vial
• Max for intra-
abdominal, mild-
moderate infection:
3 g/day
I
• Max for meningitis,
60 mkday IV q8
severe infection:
• Meningitis, severe
6 g/day
infection
• WOF: diarrhea,
120 mkday IV q8
rash, nausea, oral
moniliasis,glossitis,
headache, pain at
injection site
• Anaerobic infection
30 mkday IV/PO q6
• Bacterial vaginosis • Max for anaerobic
(adolescent) infection: 4 g/day
500 mg PO q12 x 7 days, • Max for giardiasis
750 mg PO OD x 7 days 750 mg/day
(if extended release tab) • Max for C.difficile:
• Trichomoniasis 500 mg/dose
° Child • Max for H. pylori:
• 250 mg/tab
15 mkday PO q8 x 7 days 500 mg/dose
• 500 mg/tab
0 Adolescent • WOF: nausea,
• 125mg/5 mL
Metronidazole 2 g PO x 1 dose, or 250 diarrhea, urticaria,
suspension
mg PO q8 x 7 days or dry mouth,
• 500 mg/vial
375 mg PO q12 x 7 days leukopenia,
• Ciardiasis vertigo, metallic
15 mkday PO q8 x 5 days taste, peripheral
• C.difficile infection neuropathy,
30 mkday IV/PO q6 disulfiram-type
x 10 days (IV less reaction with
efficacious) alcohol ingestion
• H. pylori infection
15-20 mkday PO q12 x
4 weeks
• Max dose: 12 g/day
• 100-200 mkday IV/IM
Oxacillin • 500 mg vial • WOF: rash, GI
q4/q6
disturbances
• Max dose: 4 g IV q6
• WOF: rash, diarrhea,
• <6 months: headache, fever,
• 2/0.25 g vial
Piperacillin- 150-300 mkday IVq6/q8 thrombophlebitis,
• 4/0.S g vial
Tazobactam • 2:6 months: injection site pain,
300-400 mkday IVq6/q8 • Dosage based
on piperacillin
component
49
• Max dose: 24
million u/day
• 100,000-400,000
• WOF: anaphylaxis,
ukday IV/IM q4/q6 • 1 million u vial
Penicillin G - urticaria, hemolytic
• Neurosyphilis • 5 million u vial
aqueous anemia, interstitial
200,000-300,000ukday IV
nephritis, Jarisch-
q4/q6 x 10-14 days
Herxheimer
reaction (syphilis)
Group A streptococci
• <27 kg:
600,000 u/dose IMx 1
• "?.27kg:
1.2 million u/dose IMxl
• Max dose for
RF prophylaxis syphilis: 2.4 million
• <27 kg: 600,000 u/dose
Penicillin G · u/dose IMq3 weeks • WOF: same as pen
• 1.2 million u vial
benzathine • "?.27kg: 1.2 million G-aqueous
u/dose IMq3 weeks • Do not administer
IV
Syphilis
• Early acquired
50,000 ukdose IM xl
• > 1 year duration
50,000 ukdose IM q7
days x 3 doses
Usual Dose
• Child:
25-50 mkday PO q6/q8
• Adolescent: 125-500
mg/dose PO q6/q8
Group A strep
pharyngitis
• <27 kg: 250 mg PO • 250 mg cap • Max dose: 3 g/day
Penicillin VK • 500 mg cap • WOF: same as pen
q8/q12 x 10 days
• "?.27kg: 500 mg PO G-aqueous
q8/q12 x 10 days
RF prophylaxis:
• 2 months-<3 years:
125 mg PO q12
• "?.3years:
250 mg PO q12
50
• Mild-moderate
infection: 2 g/day
• Mild-moderate infection • Severe infection: 4
40-45 mkday IV q6/q8 • 500 mg vial g/day
Vaneomycin
• Severe infection
45-60 mkday IV q6/q8
• 1 g vial • WOF: Red man
syndrome,
ototoxicity,
nephrotoxicity
I
ANTITUBERCULOUS AGENTS
INDICATION/ MAXIMUM DOSE I
DRUG PREPARATION
DOSE REMARKS
• 300 mg tab
• 200 mg H/
10 mg pyridoxine/ • Max dose: 300 mg/day
5 mLsyr • WOF: peripheral neuropathy,
lsoniazid • 10 (10-15J • 200 mg H/ hepatic side effects
(HJ mkday PO OD 12 mg pyridoxine/
5 mL • Supplemental pyridoxine
• 200 mg H/ (1-2mkday) is recommended
20 mg pyridoxine/
5 mL
51
ANTIBIOTICS FOR TOPICAL/OPHTHALMIC/OTIC USE
INDICATION/ MAXIMUM DOSE/
DRUG PREPARATION
DOSE REMARKS
52
ANTIPARASITIC AGENTS
MAXIMUM DOSE/
DRUG INDICATION/DOSE PREPARATION
REMARKS
• Uncomplicated Malaria
10 mg base/kg PO then
6, 24, & 48 hours: 5 mg
base/kg PO; total dose:
• Max dose for prophylaxis:
300 mg/dose
• WOF: nausea, vomiting,
ECGabnormalities, QT
prolongation, blurred
I
2 5 mg base /kg • 250 mg/tab
Chloroquine vision,headache,confusion,
• Malaria prophylaxis (150 mg base)
skeletal muscle
5 mkdose PO q7 days
weakness,
(start 1 week prior &
increased liver
continue for 4 weeks
enzymes, hair
after exposure)
depigmentation
• Pinworm
l00mgPOxl
• Hookworm, roundworm,
whipworm • 500 mg tab • WOF: rash, headache,
Mebendazole 100 mg PO q12 x 3 days • 20 mg/mL syr diarrhea, abdominal
• Capillariasis • 50 mg/mL syr cramping
200 mg PO q12 x 20 days
• Toxocariasis
100-200mg POq12 x 5 days
Pediculus capitis
• Saturate hair and scalp
with shampoo. Leave for
10 mins then wash off.
May repeat in 9-10 days.
• WOF: pruritus,
• Shampoo, hypersensitivity,
Permethrin Scabies lotion burning, stinging,
• Apply lotion from neck erythema, rash
to toe (head to toe for
infants and toddlers).
Wash off in 8-14 hrs. May
repeat in 7 days.
53
ANALGESICS/ANTIPYRETICS
54
ANTIFUNGAL AGENTS
MAXIMUM DOSE/
DRUG INDICATION/DOSE PREPARATION
REMARKS
Amphotericin B
• Initial dose
0.5-1 mkday
• Maintenance dose
0.5-1 mkday IV OD or 1.5
• 50 mg vial
• Max dose: 1.5 mkday
• WOF: feve1;chills,
headache, hypotension,
vomiting, hypercalciuria,
hypoK- hyp0Mg 2 ·, RTA,
I
mkdose every other day
renaljliver failure
• Apply to affected areas • Cream, powder, • WOF: erythema,
Clotrimazole
q8-12 x 2-8 weeks topical solution blistering, urticaria
• Oropharyngea/ • Maxfororopharyngeal
candidiasis & esophageal
LO 6 mkdose IV/PO, candidiasis: 400 mg/day
MD 3 mkday IV/PO OD • Max for systemic
• Esophageal candidiasis • 50 mg cap candidiasis/cryptococcal
LO 12 mkdose IV/PO, • 150 mg cap meningitis: 800 mg/day
Fluconazole
MD 6 mkday IV/PO OD • 200 mg cap • WOF: nausea, headache,
• Cryptocaccal meningitis • 200 mg vial rash, vomiting, diarrhea
or invasive systemic abdominal pain,
candidiasis hepatitis, cholestasis
LO 12 mkdose IV/PO, • Begin MD 24 hours
MD 6-12 mkday IV/PO OD after LD
• Topical cream: 1-2
applications/day • WOF: local burning
• Cream,
Ketoconazole • Shampoo: 2x weekly sensation, itching,
shampoo
with at least 3 days contact dermatitis
between applications
• 100,000 IU/ml
Nystatin • 4-6 mL swish & swallow q6 • WOF: GI side effects
suspension
ANTIVIRAL AGENTS
IVfor HSV encephalitis
• 3 months-<12 years:
60 mkday q8 x 14-21 days • WOF: renal
• ~12 years: impairment [adequate
30 mkday q8 x 14-21 days hydration and slow
• 250 mg vial
IVfor Varicella IV administration to
• 2:2years: prevent crystallization
Acyclovir in renal tubules)
30 mkday q8 or
1500 mg/m 2 /day q8
x 7-10 days
• 200 mg tab • Max dose: 800 kg/dose
POfor Varicel/a
• 400 mg tab
• 2:2years: or 3200 mg/day
• 800 mg tab
20 mkdose q6 x 5 days • WOF: renal impairment
• 200 mg/SmL syr
Influenza treatment (S days)
• <3 mos: 12 mg PO q12
• 3-5 mos: 20 mg PO q12
• 6-11 mos: 25 mg PO q12
Oseltamivir • 2'1 year & ,;;15kg: 30mg • 75mgcap • WOF: nausea, vomiting
PO q12
• >15-23 kg: 45mg PO q12
• >23-40 kg: 60mg PO q12
• >40 kg: 75 mg PO q12
55
DRUGS USED FOR ALLERGY AND ASTHMA
I. ANTIHISTAMINES
MAXIMUM DOSE/
DRUG INDICATION/DOSE !"REPARATION
REMARKS
• 6-12 months:
2.5 mg PO OD
• 12-23 months: • 10 mg tab • WOF:sedation,
2.5 mg PO OD or q12 • 2.5 mg/mL drops headache,
Cetirizine • 2-5 years: • 10 mg/mL drops sore throat, GI
2.5 mg PO OD or • 1 mg/mL syr symptoms,
5 mg/day PO OD or q12 • 5 mg/SmL syr dry mouth
• ;;,6years:
5-10mg/dayPOODorq12
• 6-11 months:
• WOF: fatigue, dry
1 mg PO OD
mouth,
• 12 mo-5 years: • 5 mg tab
headache, diarrhea,
Desloratadine 1.25 mg PO OD • 2.5 mg/SmL syr
fever,
• 6-11 years:
insomnia,
2.5 mg PO OD
hypersensitivity
• ;;,12years: 5 mg PO OD
• Max dose: SO mg/
• 25 mg tab
dose, 300 mg/day
• 1-2mkdoselV/lM/ • SO mg cap
Diphenhydramine • WOF: sedation,
POq6 • 12.5 mg/SmL syr
nausea, vomiting, dry
• SO mg amp
mouth, blurred vision
• 6 months-<2 years:
15 mg PO q12
• WOF: drowsiness,
• 2-llyears: • 60 mg tab
fatigue, headache,
Fexofenadine 30 mg PO q12 • 120 mg tab
dyspepsia, nausea,
• ;;,12 years: • 180 mg tab
dysmenorrhea
60 mg PO q12 or
180 mg PO OD
• WOF: somnolence,
• 6 months-5 years: • 5 mg tab
dry mouth, cough,
1.25mgPOOD • 10 mg tab
headache, fatigue,
Levocetirizine • 6-11 years: • 2.5 mg/SmL syr
nasopharyngitis,
2.5 mg PO OD • 500 mcg/mL syr
pharyngitis, pyrexia,
• ;;e12years: 5 mg PO OD • 5 mg/mL syr
epistaxis, rhinitis
• 2-5 years:
5 mg PO OD • 10 mg tab • WOF: drowsiness,
Loratadine • ;;,6 years: • 5 mg/SmL syr fatigue, dry mouth,
lOmgPOODor headache,nausea
SmgPOq12
56
II. DRUGSFORASTHMA
MAXIMUM DOSE/
DRUG INDICATION/DOSE PREPARATION REMARKS
Ipratropium
bromide
• Nebulization for <12 yr:
250 mcg/dose q6/q8
• Nebulization for 2:12 yr:
250-500 mcg/dose q6/q8
• 500mcg/2mL
neb
• Salbutamol +
ipratropium
500mcg/ 2.5mg/
• WOF: anxiety,
dizziness, headache,
GI discomfort, cough
I
2.5mL neb
• 6 months-5 years:
• WOF: headache,
4 mg PO OD at night • 4 mg granules
abdominal pain,
• 6-14 years: • 5 mg tab
Montelukast dyspepsia, fatigue,
5 mg PO OD at night • 10 mg tab
dizziness, cough,
• >14 years:
elevated liver enzymes
10 mg PO OD at night
Nebulization: • WOF: tachycardia,
• <l years: palpitations,
0.05-0.15 mkdose q4-6 tremo1~insomnia,
• l mg/mL neb
• 1-5 years: nervousness, nausea,
• 2 mg/mL neb
1.25-2.S mg/dose q4-6 headache
• 2.5 mg/2.SmL neb
• 5-12 years: • Oral dose is discouraged
Salbutamol 2.5 mg/dose q4-6 due to increased side
• >12 years: effects & decreased
2.5-5 mg/dose q4-8 efficacy
• MDI: 100 mcg/
Inhaler
actuation • WOF: same as in
• 2 puffs q4-6 prn
• Inhalation powder nebulization
cap: 200 mcg
Ill. STEROID-CONTAININGDRUGS
MAXIMUM DOSE/
DRUG INDICATION/DOSE PREPARATION
REMARKS
• Betamethasone
di propionate • Max dose: 14daysAND
• Topical
cream or ointment • Cream and ointment:
Betamethasone Apply to affected areas
• Betamethasone 45g/week
q12 or OD
valerate cream, • Lotion: 50mljweek
lotion or ointment
Nebulized
• No prior steroid use: • Maxif no p1iorsteroiduse:
0.5 mg/day q12 or OD 0.5 mg/day
• 250 mcg/mL neb
• Prior inhaled steroid use: • Max if with prior
• 500 mcg/mL neb
0.5 mg/day q12 or OD inhaled/ oral steroid use:
• Prior oral steroid use: 1 mg/day
Budesonide 1 mg/day q12 or OD
• Max dose: 4
Oral inhaler DP!: inhalations/day
• 2:6years: 1 inhalation q12, • 200 mcg/ • WOF:pha1yngitis,cough,
may increase as needed metered dose HPA-axis suppression
• Rinse mouth after use
57
5-11 years:
• 2 inhalations q12 of
80/4.5 mcg inhaler • Maxdose for 5-11 years:
;,,12 years: 2 inhalations of
• No prior inhaledsteroid use 80/4.5 mcg q12
2 inhalations q12 of MDI: • Max dose for ;,,12 years:
80/4.5 mcg OR 160/4.5 • 80/4.5 mcg 2 inhalations of
mcg inhaler depending inhaler 160/4.5 mcg q12
Budesonide +
on severity • 160/4.5 mcg • WOF: pharyngitis,
Formoterol
• Prior low-medium doses inhaler cough, HPA-axis
of inhaled steroid use • 320/9 mcg suppression,
2 inhalations q12 of inhaler abdominal pain,
80/4.5 mcg inhaler nausea, dyspepsia,
• Prior medium-high doses tremor
of inhaled steroid use
2 inhalations q12 of
160/4.5 mcg inhaler
Intranasal
• 2-llyears
Nasal spray:
(fluticasonefuroate):
• 27.5 mcg/
1 spray each nostril OD
actuation • Maxdose: 2 sprays per
• 4-11 years
(fluticasone nostril/day
(fluticasone propionate):
furoate) • WOF: epistaxis, nasal
1 spray each nostril OD
• SO mcg/ irritation
• ;,,12 years:
actuation
2 sprays each nostril OD,
(fluticasone
may reduce to 1 spray
propionate)
Fluticasone each nostril OD once
controlled
Inhaler
• 1-4 years: 100 mcg q12 MDI:
• >4 years: 50-100 mcg • SO mcg/
q12 if well-controlled actuation
• WOF: oral candidiasis,
asthma, 200 mcg q12 if • 125 mcg/
hoarseness
insufficient control actuation
• > 16 years: 100-1000 (fluticasone
mcg q12 (depends on propionate)
severity of asthma)
• Max dose: 2
inhalations q12 of MDI
250/10 mcg
• WOF: insomnia,
MDI: headache, tremor,
Fluticasone + • ;,,12 years: 2 • 50/5 mcg dizziness, palpitations,
formoterol inhalations q12 • 125/5 mcg, ventricular
• 250/10 mcg extrasystoles,
dysphonia, throat
irritation, dry mouth,
rash, peripheral
edema
58
MDI
• >4 years: 2 inhalations
MDI:
q12 of 50/25 mcg
• 50/25 mcg • Max dose: 1
• ;,12 years: 2
Fluticasone +
salmeterol
inhalations q12 of
50/25 mcg, 125/25
mcg, or 250/25 mcg
DP!
• 125/25 mcg
• 250/25 mcg
inhalation q12 of
DP! 500/50mcg, or 2
inhalations q12 of MDI
250/25 mcg
I
.
• 5 mg tab
• 20 mg tab
• See prednisone • WOF: same as
Prednisolone • 1 mg/mL drops
(equivalent dosing) prednisone
• 15 mg/SmL syr
• 20 mg/SmLsyr
59
• Max: 60-80 mg/day
• Acute asthma • WOF: mood
2 mkday PO q12 or OD changes, seizures,
• 5 mg tab
x 5-7 days hyperglycemia,
• 20 mg tab
• Anti-inflammatory diarrhea, nausea,
Prednisone • 10 mg/5mL syr
0.5-2 mkday PO q12 abdominal distention,
• 20 mg/5mL syr
or OD GI bleeding, HPA
• Nephrotic syndrome axis suppression,
2 mkday PO q8-24 osteopenia, cushingoid
effects, cataracts
ANTICONVULSANTS
MAXIMUM DOSE/
DRUG INDICATION/DOSE PREPARATION
REMARKS
• <6 years: 10-20 • Max for <6 years:
mkday PO q8/q12, 35 mkday
titrate q5-7 days • Max for 6-12 years:
• 6-12 years: initial initial dose 100 mg/
dose 10 mkday PO dose q12, maintenance
q12, titrate by 100 dose 1000 mg/day
mg/day weekly, • Max for 12-15 years:
• 200 mg tab
maintenance dose lOOOmg/day
Carbamazepine
• 400 mg tab
20-30 mkday PO • Max for >15 years:
• 100 mg/5mL syr
q6-12 1200 mg/day
• > 12 years: initial • WOF: sedation,
dose 200 mg PO ql2, dizziness, diplopia,
titrate by 200 aplastic anemia,
mg/day weekly, neutropenia, urinary
maintenance dose retention, nausea,
800-1200 mg/day SIADH,Stevens-Johnson
PO q6-12 syndrome
• Max for sedation:
0.6 mg/kg
within 8 hours
• Max total dose for
• Sedation
seizures <5 years:
0.04-0.2 mkdose IV/
5 mg, may repeat dosing
IM q2-4 hour
in 2-4 hours as needed
Diazepam • Seizllre • 10 mg amp
• Max total dose for
0.2-0.5 mkdose IV
seizures 2:5years:
q15-30 mins
10 mg, may repeat dosing
in 2-4 hours as needed
• WOF: hypotension,
respiratory depression
• Do not mix with IV J/llids
• 4-15years: • Max for <16 years:
10 mkdose PO q12, 30 mkdose PO q12
may increase by • 250 mg tab • Max for 2:16 years:
10 mkdose q12 • 500 mg tab 1500 mg PO q12
Levetiracetam every 2 weeks • 750 mg tab • WOF: loss of
• 2:16years: • 1000 mg tab appetite, vomiting,
500 mg PO q12, titrate • 100 mg/mL syr dizziness,headache,
by 500 mg/dose q12 somnolence, agitation,
every 2 weeks depression, mood swings
60
LD
• 15-20 mkdose IV
MD
• Neonate:
3-5 mkday IV/PO
q12 or OD
• Infant:
5-6 mkday IV/PO q12
•
•
15 mg tab
30 mg tab
• Max LO: 40 mg/kg IV
• WOF: drowsiness,
cognitive impairment,
ataxia, hypotension,
I
or OD • 60 mg tab
Phenobarbital hepatitis, skin rash,
• l-5years: • 90 mg tab
respiratory depression,
6-8 mkday IV/PO q12 • 130 mg/mL amp
apnea, megaloblastic
or OD anemia
• 6-12 years:
4-6 mkday IV/PO q12
or OD
• > 12 years:
1-3 mkday IV/PO q12
or OD
LD
• 15-20 mkdose IV • Max LO: 1500 mg/day
• WOF:gingival hyperplasia,
MD • 100 mg cap hirsutism, dermatitis,
• Start with 5 mkday • 30 mg/SmL syr blood dyscrasia, ataxia,
IV/PO q8/q12, usual • 125 mg/5mL syr lupus-like syndrome,
Phenytoin
dose range: • 100 mg amp Stevens-Johnsonsyndrome,
• 6 months-3 years: • 250 mg amp lymphadenopathy, liver
8-10 mkday damage, nystagmus
• 4-6 years: 7.5-9 mkday • IVpush/infusionrate NOT
• 7-9 years: 7-8 mkday to exceedlmgjkg/min
• 10-16years: 6-7mkday
• Max dose: 60 mkday
PO • WOF: GI, liver, blood
• 125 mg tab
• Initial and CNS toxicity,
• 200 mg tab
10-15 mkday q8-24 weight gain, transient
• 250 mg tab
• Increment alopecia, pancreatitis,
• 500 mg tab
5-10 mkday weekly nausea, sedation,
• 200 mg/5mL syr
Valproic acid • MD vomiting, headache,
• 250 mg/5mL syr
30-60 mkday q8/q12 thrombocytopenia, rash,
hyperammonemia
IV
• Same as PO dose but • WOF: same as PO
• 500 mg/5mL vial
give q6, use only when valproic acid
PO is not possible
61
ANTI HYPERTENSIVES
Esomeprazole
• 1-11 years:
10 mg PO OD
• ;o,12years:
20-40 mg PO OD
• Cap: 20 mg, 40 mg
• Powder for oral
suspension:
10 mg
• WOF: GI disturbances,
headache
I
• 1-12 years: • Max dose: 40 mg/day
0.6-0.8 mkday IV qB-12 • WOF: headache,
Famotidine • 20 mg tab
• >12 years: constipation, diarrhea,
20 mg IV q12 drowsiness
• <6 years: 1 infant
suppository • WOF: rectal irritation,
• Pediatric 1.9 g
Glycerin PR q12 or OD prn abdominal pain,
• Adult 2.5 g
• ;,6 years: 1 suppository bloating, dizziness
PR q12 or OD prn
• <1 year: 2.5 ml q12
• 1-5 years: 5 ml q12 • Max dose: 60 mlfday
Lactulose • 5-10 years: 10 ml q12 • 3.3 g/5mL syr • WOF: GI discomfort,
• >10 years: 15-30 ml/ diarrhea
day q12 or OD
• Max for GER: 0.8
• GER
mkday, 15 mg/dose
0.1-0.2 mkdose IV/IM/PO
• Max for post-op
up to q6
nausea and vomiting:
• Post-op nausea/ • 5 mg/5mL syr
10 mg/dose
Metoclopramide vomiting • 10 mg amp
• WOF: Sedation,
,;14 years: 0.1-0.2
0
headache, anxiety,
mkdose IV q6/q8 prn
depression, leukopenia,
>14 years:
0
diarrhea, extrapyramidal
10 mg IV q6/q8 prn
symptoms at high doses
63
OTHER MEDICATIONS IN PEDIATRICS
• 250 mg tab
(elemental Fe 75
mg)
• 310mgtab • Max dose: 60 mg
(elementalFe100 elemental Fe q6
• Iron deficiency anemia
Ferrous mg) • WOF: constipation,
3-6 mkday (elemental Fe)
sulfate • 125 mg/mL drops dark stool, nausea,
PO qS-24
(elemental Fe epigastric pain
25 mg/mL)
• 150mg/5mL syr
(elemental Fe
30mg/5mL)
• Max dose:
• Initial: 0.5-1 gkdose IV
• Mannitol (20%) 100 ml IVq4
MannitoI • MD: 0.25-0.5 gkdose
20 g/lOOmL • WOF: hypovolemia,
1Vq4-6
headache, polydipsia
64
Sedation for procedures
• 6 months-5 years: Max total dose
0.05-0.1 mkdose IV for sedation for
q2-3 mins prn
I
procedures:
• 6-12 years: 0.025-0.05 • 6 months-5 years: 6
mkdose IV q2-3 mins prn mg, 0.6 mg/kg
• >12 years: 0.5-2 mg/ • S mg amp • 6-12 years: 10 mg,
Midazolam dose IV q2-3 mins prn • 15 mg amp 0.4 mg/kg
• >12 years: 10mg
Sedation with
mechanical ventilation • WOF: respiratory
• 0.05-0.15 mkdose IV depression,
ql-2 hours prn, or hypotension,
• 1-2 mcg/kg/min bradycardia
continuous IV infusion
titrated to effect
• Nasal spray
2-6 sprays per nostril • 0.65% nasal
Sodium q2 prn spray • WOF: stinging of nose,
chloride -
• Drops • 0.65% nasal transient sneezing
inhaled
2-6 drops per nostril drops
q2 prn
IV/IM/SC
• Child: 2-3 mg/day OD or
1-2 mg/dose x 1 dose • WOF: flushing,
• 10 mg amp
• Adolescent: 5-10 mg/ dizziness, anaphylaxis,
day OD or 10 mg/dose hypotension, cardiac/
Vitamin K xl dose respiratory arrest
PO • IV injection rate not to
• Child: 2-3 mg/day OD exceed 1 mg/min
or 2.5-5 mg/day • 10 mg/mL
• Adolescent: 5-10 mg/day
OD or 2.5-25 mg/day
REFERENCES
1. Department of Health. (2014) National Tuberculosis Control Program Manual of Procedures
(5th ed.). Manila: Department of Health.
2. Kimberlin OW, Brady MT,Jackson MA, Long SS. (Eds.) (2015). American Academy of Pediatrics.
Red book: 2015 report of the Committee on Infectious Diseases (30th ed.). Elk Grove Village,
IL: American Academy of Pediatrics
3. Kliegman RM, Stanton BF, St Geme )W, Schor NF. (Eds.) (2020) Nelson Textbook of Pediatrics.
Philadelphia, PA: Elseviel'.
4. MIMS Drug Reference Philippines (151" ed.). (2017) Alexandra Technopark, Singapore: MIMS
Pte Ltd.
5. Sanden, E and Fleriage J (eds) (2015). The Harriet Lane handbook: a manual for pediatric
.house officers (20'" ed.). Philadelphia. PA: Mosby Elsevier.
65
INTERPRETATION
OFCOMMON
DIAGNOSTIC
TESTS
SECTION ONE
ELECTROCARDIOGRAM
ECG WAVES AND SEGMENT
---------~--......,
RR lnterv~"l
.•••.•..•..•
.
..'. .. ..
.
. . ... .
. . .. .
,R.
P?ln~I
....... .
... ..... .-. .
: .........
. :•R••·••·
I
.
.. . .......
. . ,.
.......................................
. . .
.. . . . . ..
.,
I
.
.
•
.
................... .
.
. ~ •
I
.
.
. • •
. '• ll •
.........
•
. .
• •
. .......
..
• • •
. ..
o •
.
..
,.
• • ♦
.
• • • • •
"•
: • ~p~ 5:~: :f:
S~grr~• : ~ • • ~ •: •: •: •: • ~ . : ' • • : · : . ~ '
OT ln(erval
r
ECG STANDARDIZATION
Smm=
0.5 mV
l~
0.1 mV
'--1--+--+-~1--+---1
.,..._,.__,.__,..._..,._-t
Figure 2. In the standardrecordingspeed
(25 mm/sec)in thehorizontalaxis(time),one
small box (1 mm)is equivalentto 0.04 sec-
ondsor40 msec;andonebigbox(5mm)rep-
resents0.2 secondsor 200msec. In thever-
tical axis (amplitude),one small box (1 mm)
is equivalentto 0.1 mV amplitude;and one
L
big box(5 mm)represents0.5 mVamplitude.
A standardmarkeris usuallyinscribedon the
leftof thetracingas an uprightrectangle,with
a heightof 10 mm (10 smallboxes= 1 mV)
Speed: 25 mm/sec
1 mm= 0.04 sec or 40 msec
5 mm= 0.2 sec or 200 msec
25 mm= 1 sec
69
DIFFERENCES BETWEEN PEDIATRIC AND ADULT ECG
aVR aVL
,v,
Figures 3 and 4. Overview of the 15 Lead ECG in Pediatrics. The figure on the left is a representation of the
hexaxial reference system. The figure on the right shows the precordial leads.
• Vl: 4•h JCS, right parasternal border • V7: lateral to V6 at posterior axillary line
• V2: 4'h JCS, left parasternal border • VS: level ofV7 at the mid-scapular line
• V4: S'h !CS, left midclavicular line • V9: level of VS at the paravertebral line
• V6: S'h !CS, left mid-axillary line (left posterior thorax, midway from spine
• V7: s•h !CS, left posterior axillary line to VS)
• V3R & V4R: mirror images ofV3 & V4
respectively
70
2. Adult type R/S progression in precordial leads is rarely seen during first month of life
• Usual R/S progression in adults: deep S waves in Vl & V2 and tall R waves in VS & V6
• These findings may vary in pediatric patients:
By 3 years of age
• Partial reversal of this progression is seen with dominant R wave in
Vl-V2 and in VS-V6
Figure5. ECGof a 1 week old infant. Notethe tall R waves in V1-V2and the deep S waves in V5-V6
aVR V1
v~
_J_A_ -r- ~
II aVL
V2~~ V5~
+- T
I~ av~ V3+V6J__
Figure6. ECGof a normaladult. Notethe deep S waves in V1-V2and the typicalR wave progressionto tall R
waves in V5-V6
71
STEPS IN PEDIATRIC ECG INTERPRETATION
72
STEP 2: RATE AND RHYTHM
A. Rate (varies with age)
HR greater than the upper limit of normal is termed tachycardia, while HR less than
the lower limit of normal is termed bradycardia
0 Rate is calculated by measuring either the P-P (atrial rate) or R-R interval (ventricular rate)
Lead II is commonly used to calculate the rate
21 small boxes
between R-R
I
1500
Heart Rate= 71 bpm
21
Figure 7. In this example, the HR is equal to 1500 divided by 21 small boxes or 71 beats/minute (bpm)
10 2 150
15 3 100
20 4 75
25 5 60
For rapid calculation, the number of large boxes between two consecutive R-R intervals is
measured. Applying this short-cut in the example above, the R-R value is approximately 20
small boxes or 4 big boxes. The estimated heart rate is 75 bpm.
Heart rate=# ofR waves within 30 large boxes x 10 (if using 6 second strip)
Heart rate=# of R waves within 50 large boxes x 6 (if using 10 second strip)
10 11 12 13
A. P Wave Axis
Mean vector of atrial depolarization
Electrical activity generated is moving from the high RA to low septa! RA and generally
moving from the right side of the heart to a leftward direction
A sinus P wave will appear positive in leads I, II, and avF and negative in lead avR (this
generates an axis ofO to +90 degrees)
B.QRS Axis
0 Mean vector of ventricular depolarization
0 Right sided forces dominate in the newborn
0 Axis will shift and will be predominantly left sided over time
Figure9. Illustration
of thedifferentinterpretations
of axes + 90°
74
Steps in Determining the Axis
1. Locate a Quadrant using Leads I and a VF
Axis Lead I Lead aVF Quadrant
.,..
0° to +90°
l l ·-EB.
I .,..
..-EB.
.,..
0° to -90°
l I .,..
+90° to :t:180°
j l ·-©·
....
..t9.
• goo
-90° to :t:180°
j I .,..
2. Among the remaining four limb leads, find the equiphasic QRS (wherein the R wave is
equal to the S wave). The QRS axis is perpendicular to that lead.
_L T
aVL
I~
+
II~ av~:
Step 1. Lead I has positivedeflection& lead aVF has a positivedeflection.Thereforethe axis fallssomewhere
in the leftinferiorquadrant
0° to +90°
~ _L ..~.
.so-
'-
75
tep2. In thetracingbelow,theequiphasicQRSis in leadaVL(ie., theamplitudeof theR waveof aVLapproximates
he S wave)- therefore,the QRSaxisis perpendicular to aVL. Basedon thehexaxialsystem,axisis+ 60 degrees
-90
+90
aVF
-·I+
·Lead II
Right Atrial
Enlargement • Tall, peaked P waves;;, 3mm
(RAE)
Lead II
~
• Wide and notched P waves
• Duration in lead II:
0 >0.08 sec in infants
Left Atrial
Enlargement
(LAE)
V1
~
• Biphasic with prolonged
negative segment in lead Vl
Bia trial
Enlargement
• Combination of increased
amplitude and duration
76
+
8. P-R Interval
Bestassessedinleadll
° Calculated by measuring from the beginning of P wave to the first deflection of the QRS
( negative deflection if a Q wave or positive if an R wave)
I
0
Phi
' 'PR/
PATHOLOGIC
LOWER LIMIT OF PR INTERVAL (in seconds)
INTERVAL
• Myocarditis (rheumatic fever, viral, diphtheria), digitalis
P.-olonged PR or quinidine toxicity, congenital heart disease (endocardial
interval ( or first cushion defect, ASD,Ebstein anomaly), myocardial
degree AV block) dysfunction, hyperkalemia
• Normal heart with vagal stimulation
• Wolff-Parkinson-White(WPW), Lown-Ganong-Levine
syndrome, myocardiopathies, Friedrich Ataxia, Duchenne
Short PR interval
Muscular Dystrophy, Pheochromocytoma
• May be normal in children
• Wandering atrial pacemaker
Variable PR interval
• Mobitz Type 1 second degree AVblock (Wenckebach)
77
STEP 5. INTERVENTRICULARCONDUCTION
A.Q Waves
Represents left to right depolarization of the ventricular septum
Can be considered benign finding in children
Normal Q waves are small and narrow and usually less than one small box (1mm) wide
and no more than two small boxes (2mm) deep
B. QRS Complex
, R wave is an upward/positive infliction from the baseline
, S wave is a downward/negative deflection from the baseline that occurs after the R wave
Causes of Prolonged QRS Complexes {see conduction disturbance & arrhythmias section)
CAUSES EXAMPLES
• RBBB or LBBB
Ventricular • WPW preexcitation
Conduction
Disturbances • lntraventricular blocks (e.g., hyperkalemia, procainamide or
qunidine toxicity, myocardial dysfunction)
• Premature ventricular contraction (PVC)
Ventricular
• Ventricular tachycardia
Arrhythmias
• Implanted ventricular pacemaker
C. QT Interval
The QT interval varies with HR
, Compute for corrected QT (QTc) using Bazett formula
78
D Check for ST and T wave Abnormalities
• Changes are rare in children
ST Segment • Normally isoelectric
• May have elevation or depression up to 2 mm in the limb leads
• Peaked T waves seen in hyperkalemia and LVH
Twaves • Flat or low T waves may be normal in newborns or seen in
hypothyroidism, hypokalemia, pericarditis, myocarditis, ischemia
Examples:
V41~L
~L-LJJ'-av:,y~r--T-v1nT_
+~-lr-aVL~V2t--rrV5jj:~
1
Tl!•VFTTT VITT V6UL
Figure10.Tracingshowingdeep S wavesinV1(arrows)and largeR wavesinV6(arrows)consistentwithLVH.
+-H--
~aV~~ V1_Jf--.--J.-----J~
V4
aVLT----rT
-"1~--y'-- v2_+,-+~~
V51~r,
~aVF..,._,~ V3~ V6_,°Y~
Figure11.Rhythmis sinuswithrightaxisdeviation
(axis=+ 150degrees).
TheRwavesin leadsII & aVRandS wavesin I & V6are
beyondupperlimit.R/Sratioin V1or V2aregreaterthanupperlimitandin V6is lessthanlowerlimit.Tracingconsistent
withRVH.
79
COMMON ECG ABNORMALITIES
I. RHYTHMS ORIGINATING FROM THE SINUS NODE
Sinus Tachycardia or Bradycardia
• Both are considered "sinus" (because impulse originates in the sinus node
• Tachycardia (upper image): rate faster than upper limit for age (but usually <200 bpm)
• Bradycardia (lower image): rate slower than normal limit for age
·········• ·············•··:··· ······:·······
Sinus Arrhythmia
• Sinus rhythm is maintained
• Some children have phasic variation in heart rate: heart rate increases slightly during
inspiration and decreases slightly during expiration
Inspiration
Atrial Tachycardia
• Narrow QRS complex tachycardia in the absence of aberrancy or bundle branch block
• P waves occur at rapid rate
• P axis is different from sinus rhythm
• Usual heart rate is 110-160 bpm (but may reach 300 bpm
80
Atrial Flutter
• F wave with sawtooth configuration
• The heart rate may be around 240-360 bpm
• QRS complexes are normal
• Ventricular response may have varying degrees of block (e.g., 2:1, 3:1, 4:1)
Normal ORS
Atrial Fibrillation
I
• Extremely fast atrial rate (F wave rate of 350-600 bpm)
• Irregularly irregular ventricular response with normal QRS
Rapid Ventricular Response
Ventricular Fibrillation
• Bizarre QRS complexes of varying sizes and configuration
• Rate is rapid and irregular
81
IV. ATRIOVENTRICULAR BLOCKS
First Degree AV Block
• Prolonged PR interval for age and HR
• PR interval is usually >0.2 seconds
pp pp pp pp PP pp
82
SECTION TWO
ARTE-RIAL BLOOD GAS INTERPRETATION
OVERVIEW OF ARTERIAL BLOOD GAS (ABG)
• Diagnostic exam that determines arterial oxygen (Pa0 2 ), carbon dioxide (pCO,), acidity
(pH), oxygen saturation (Sa0 2 ) and bicarbonate (HC0 3 )
• Venous blood gas (VBG) may be a suitable alternative and correlates with pH, CO, and
bicarbonate levels of ABG, but oxygenation correlates poorly with VBG -
I
._.
• Refer to Chapter 5 for indications, contraindications, and steps in performing ABG
Check pH
~_P"~, '"""l;.;,
. I PRIMARY
DISORDER
CHECK
Check pH PRIMARY DISORDER
6pCO 2 and 6HCO 3
Metabolic Acidosis
pC0 2 should decrease pC0 2 =(1.5 x HC03 ) + 8 ± 2
(low pH+ low HC03 )
Sources:
Kliegman
R.etal.Nelson
Textbook
ofPediatrics
(21sted).Elsevier;
2020
84
STEP 3. CHECK FOR SECONDARY ACID-BASE DISORDER OR MIXED ACID BASE DISORDER
• Mixed acid-base disorders are defined as independently coexisting disorders (not merely
compensatory responses)
• Example: A patient with metabolic acidosis from diabetic ketoacidosis may develop an
independent respiratory disturbance (acidosis or alkalosis) from pneumonia
Metabolic
Acidosis
Actual reduction ofpCO, from baseline
is GREATER than that of predicted/
calculated compensation
Actual reduction ofpC0 2 from baseline
Secondary RESPIRATORY
ALKALOSISis present I
Secondary RESPIRATORY
is LESS than that of predicted/
ACIDOSISis present
calculated compensation
Actual increase of pC0 2 from baseline
Secondary RESPIRATORY
is GREATER than that of predicted/
ACIDOSISis present
Metabolic calculated compensation
Alkalosis Actual increase of pC0 2 from baseline is
Secondary RESPIRATORY
LESS than that of predicted/calculated
ALKALOSISis present
compensation
Actual increase of HC0 3 from baseline
Secondary METABOLIC
is GREATER than that of predicted/
ALKALOSIS is present
Respiratory calculated compensation
Acidosis Actual increase ofHC0 3 from baseline
Secondary METABOLIC
is LESS than that of predicted/
ACIDOSIS is present
calculated compensation
Actual decrease of HC0 3 from baseline
Secondary METABOLIC
is GREATER than that of predicted/
ACIDOSIS is present
Respiratory calculated compensation
Alkalosis Actual decrease ofHC0 3 from baseline
Secondary METABOLIC
is LESS than that of predicted/
ALKALOSIS is present
calculated compensation
85
STEP 4. CHECKFORANION GAP AND t,/t-.
A.. Anion Gap formula
I. MEASURES OF OXYGENATION
• The partial pressure of oxygen in arterial blood or Pa0 2 is a measure of dissolved oxygen
in arterial blood plasma
• Hypoxemia is defined as a low Pa 0 2 , which can be obtained by blood gas analysis
• A reduced PaO, is a non-specific finding (i.e. it only signifies a disturbance of gas exchange)
• Pao, is differerit from Sa0 2, which describes the amount of oxygen bound to hemoglobin
SaO, can also be measured via blood gas analysis
• When Sa0 2 is measured using pulse oximetry, the more appropriate term then becomes Sp0 2
86
B. Determination of Fi0 2 in Patients with Nasal Cannula or a Simple Face Mask
° Fraction of inspired oxygen (Fi0 2) is the concentration ofoxygen (expressed in percent)
that a person inhales
0 Ambient or room air is made up of 21 % oxygen, hence Fi0 2 of room air= 21 %
0 When you give supplemental 0 2, you are raising the patient's Fi0 2 to a level over 21 %
(ranges from 22-100%)
° For every 1 LPM, there is an estimated increase of 4% in Fi0 2
C. Related Formulas
87
II. PaO,-FiO, RATIO (Carrico Index or the PF Ratio)
• It is the ratio of arterial oxygen partial pressure (Pa0 2) to fraction of inspired oxygen (Fi0 2)
• Serves as a clinical indicator of hvooxemia
Pa0 2 : arterial oxygen partial pressure; obtained from ABG
Fi0 2 : fraction of inspired 0 2 (in decimal) at the time the ABGwas drawn
Normal PFR value on room air (at sea level) is 100 mm Hg / 0.21 = 476
mm Hg (or more)
PFR = Pao,
Fi0 1 For patients on non-invasive mechanical ventilation, Pediatric Acute
Respiratory Distress Syndrome (PARDS) can be diagnosed with a PFR,; 300
Samole Cases:
Case 1. 2 year old male is intubated for severe pneumonia and sepsis. Work-up showed:
pH= 7.25; pC0 2 = 50 mm Hg, HC0 3 20 mEq/L, pa0 2 = 90 mm Hg
Mechanical ventilator setting Fi0 2 - 40% Na·= 140 mmol/L, Cl= 105 mmol/L
• Since pH< 7.4 the primary disorder is ACIDOSIS
• In this scenario pC0 2 is increased while HC03 is decreased. This
suggests both metabolic and respiratory acidosis is present
Step 1: • To determine whether it is primarily respiratory or metabolic
Determine the
primary disorder acidosis see which has a higher change from baseline
0 tipC0
2 = (50-40)/40 = 0.25
0 tiHC0
3 = (24-20)/24 = 0.17
0 The tipC0
2 > tiHC0 3 , therefore it is primarily respiratory acidosis
Step 2: Determine
• pH and HC0 3 suggests acidosis therefore this is primarily
METABOLICACIDOSIS
• pC0 2 = 1.5 x HC03 + 8 ± 2
• pCO, = 1.5 x 15 + 8 ± 2 = 28.5-32.5 mmHg
I
appropriateness of
• Our patient's CO2 is 30 mm Hg which falls within the expected
compensation
value, the physiologic compensation is adequate
Step 3: Check for • The patient's CO2 falls within the expected value
secondary acid base
disorder • This is no secondary acid-base disorder
(15-11)/(24-15) = 0.44
0
Step 5: Check • Patient is breathing room air and has a pa0 2 of 90 mm Hg which
oxygenation status is considered normal
• High anion and normal anion gap metabolic acidosis
Interpretation • Patient has severe dehydration. Lactic acidosis can explain the
HAGMA(diarrhea can account for the NAGMA)
Case 3. 4 year old female post surgery is intubated in the recovery room. Mechanical
ventilator setting of Fi02 60% and RR of 50 breaths per minute.
89
Case 4. 1 year old female is admitted for severe pediatric community acquired pneumonia.
Patient is tachypneic and has signs of dehydration from poor oral intake.
ABG pH= 7.45; pC0 2 = 25 mm Hg; HC0 3 = 18 mEq/L; pa0 2 = 65 mmHg at room air
Na= 140 mmol/L, Cl= 105 mmol/L
• pH of 7.45 is ALKALOTIC(within normal value but greater than
mean of7.4)
Step 1: Determine • pCO, suggests ALKALOSIS
the primary • HC0 3 suggests ACIDOSIS
disorder • pH and pC0 2 suggests ALKALOSIStherfore the primary disorder
is RESPIRATORYALKALOSIS
0 Respiratory alkalosis probably secondary to the tachypnea
• i 11HC03 = 2 x 11pC02/10 = 2 x [( 40-25)/10] = 3 mEq/L
Step 2: Determine • Expected HC0 3 is 24 mEq/L- 3 mEq/L = 21 mEq/L
appropriateness of • Patient's HC0 3 decreased more than the expected compensation.
compensation It is therfore compensated but also suggestive that there is a
secondary acid-base disorder
Step 3: Check for • The HC0 3 falls more than the expected compensation
secondary acid base • This suggests a CONCOMITANTMETABOLICACIDOSIS
disorder 0 Probably secondary to the dehydration
• Anion gap= [Na•] - [CJ·]- [HCO;J = 140-105-18= 17
• Our patient has HAGMA
Step 4: Anion gap • Compute for Ii/ Ii for HAGMA
and 11/11when
0 /iAnion Gap/ /iHC0
needed 3
0 (17-11)/(24-18) =1
• 11/11=1 suggests pure HAGMA
• Patient is breathing room air and has a pa02 of 65 mm Hg
= mild hypoxemia
• Compute for the desired Fi0 2
Step 5: Check
= (current Fi0 2 x desired pa0 2) / (current pa0 2) = 21x100/65 =
oxygenation status
32%
0 Patient should be given supplemental oxygen of at least 3LPM
via nasal cannula
• Compensated respiratory alkalosis with concomitant high anion
Interpretation
gap metabolic acidosis with mild hypoxemia
90
SECTION THREE
READING CHEST RADIOGRAPHS
OVERVIEW OF RADIOGRAPHS
I. PRINCIPLES OF EVALUATING RADIOGRAPHS
A. Densities of Structure Determine Opacity (high density structures appear white)
Bone Soft Tissues Fat Air I
92
Step 3: ASSESS THE QUALITY OF THE FILM
ASPECT QUALITY INDICATOR
• Good visualization is characterized by inclusion of entire thoracic cage
• Lung apices and first ribs caudally
Visualization
• Edges of ribs laterally
• Reported as: "good visualization"
Inspiratory
Effort
• Chest x-ray are conventionally taken while patients are in the
inspiratory phase of respiratory cycle
• One should count 6-8 anterior ribs, 9-11 posterior ribs
• Diaphragm should be intersected by the 6th rib in the midclavicular line
I
• Inadequate inspiration leads to crowding of structures
• Reported as: "good inspiratory effort"
• Of no value in infants
• This pertains to the degree to which x-rays have passed through the body
• A well-penetrated/exposed chest x-ray is one where the upper four thoracic
ve1tebrae and ve1tebrae behind the heart are just visible
• Reported as: "good exposure/penetration"
- p::
Exposure/
Penetration
Figure 011 the left displays an overexposed film (since >T4 are exposed)
Figure 011 the right displays an underexposed film, since <T4 are exposed)
• The spinous processes should be in the midline and should be
Obliquity/ equidistant from medial ends of the clavicle
Rotation • Rotation may lead to misinterpretation of structures
• Reported as: "no obliquity or significant rotation"
Presence of • Artifacts may be due to radiographic technique, patient factors (e.g.,
artifacts poor cooperation, obesity)or non-anatomical objects (e.g., devices)
2. Normal Mediastinum
The mediastinum contains the heart, great vessels (middle mediastinum) and
potential spaces anterior to the heart (anterior mediastinum), posterior to the heart
(posterior mediastinum) and above the heart (superior mediastinum)
Thymus increases in size from birth to puberty, but as the child grows, the thymus
appears smaller
3. Cardiothoracic Ratio (CTR) of the Heart
Size of heart is assessed by CTR (increased CTR suggests cardiomegaly)
Calculated by getting the ratio between the cardiac size and the thoracic width:
Cardiac size is measured by drawing vertical parallel lines down the most lateral
points on each side of the heart, and measuring between them
Thoracic width is measured by vertical parallel lines down the inner aspect of the
widest points of the rib cage & measuring between them (above the diaphragms)
Normal CTR measured in PAview
Since AP view causes magnification of heart size, the normal pediatric CTR varies
AGE MEAN CT RATIO RANGE
0-3 weeks 0.55 0.45-0.65
4-7weeks 0.58 0.49-0.70
1 year 0.53 0.45-0.61
1-2 years 0.49 0.39-0.60
2-6 years 0.45 0.40-0.52
>7 years <0.5 0.40-0.50
D. Other Structures
• Trachea is at the center (or slightly to the right) as an area of
Airways radiolucency
• It eventually branches at the carina into the two main bronchi
• Lung roots at the hila are occupied by major bronchi & pulmonary vessels
Hilar
• The left hilum is often higher than the right (both should be of similar
Structures
density and overall size)
Costophrenic • Created by the dome of each hemidiaphragm and the lateral chest walls
Angles • On frontal chest x-ray, costophrenic angles should form sharp acute angles
• Well-defined domed structures occupying the caudal end of the film
• Right hemidiaphragm is slightly higher than the left because of the liver
Berni-
below it pushes it cranially
diaphragm
• Below the left hemidiaphragm, a round area of lucency is occasionally
found (gastric bubble)
94
Step 5: DETERMINETHE PRESENCEOF ABNORMALITIES
A. Lungs
• Appear as areas which are whiter than surrounding structures
Increased density
• Area may be filled with exudates, transudates, blood and
in lung zones
malignant cells
Decreased density • Appear in areas which are darker than the surrounding structures
I
in lung areas • Area may be filled with air
Displacement of • Volume changes within a certain lung lobe/zone may lead to
lung fissures pushing or pulling of fissure
Lung
• >10 posterior ribs visualized in the lung parenchyma
hyperexpansion
Pleural thickening • Seen in asbestosis, mesothelioma
Prominence of
pleural spaces • Air may be trapped in pleural space (pneumothorax)
C. Heart
Left Ventricular
• Apex displaced inferiorly and laterally (drooping apex)
Enlargement
Right Ventricular
Enlargement • Apex displaced superiorly and laterally (e.g., uplifted apex)
D.Others
• Anything that increases volume or pressure in one hemithorax will
Tracheal push the trachea (and medastinum) towards contralateral side
displacement • If it causes volume loss, it will pull the trachea towards the
ipsilateral side
• Obscured hemidiaphragm may be due to adjacent lung disease
Diaphragmatic
• Displaced may be due to air /viscus underneath, phrenic nerve
abnormalities
palsy, or hernia
95
COMMON PATHOLOGIES & CHEST RADIOGRAPH FINDINGS
Pneumonia Consolidation
• Left lower lobe pneumonia showing • Inhomogeneous opacities with prominent
opacification in the lung field air bronchogram
96
Pneumothorax Pleural Effusion
• Lung collapse do to air in pleural space • Blunting of costophrenic sulci
• Absence of lung markings • Meniscus sign
• In massive effusion, there may be
shifting of the mediastinal structures to
the contra lateral side
97
BASIC
PROCEDURES
FOLEY CATHETER INSERTION
INTRAOSSEUS INFUSION
LUMBAR PUNCTURE
NEEDLE ASPIRATION
ENDOTRACHEAL INTUBATION
I
CONTRAINDICATIONS
Indications • Foley catheter (appropriate size)
• Collection of urine for analysis and culture • Urine bag
• Management of urina,y retention and • Drapes
obstruction • 10 cc syringe
• Accurate monitoring of urine output • 1 vial sterile water
• Drainageof bladder p1im;dwing, or after surge1y • Clean (non-sterile) gloves
• Neurogenic bladder • Sterile gloves
• Cotton
Contraindications • Rubbing alcohol
• Presence of urethral trauma • Povidone-iodine
• Presence of acute pelvic fracture • Sterile lubricant and/or Xylocaine jelly
• Careful consideration should be given in syringe (plain sterile lubricant for infants)
patients with the following: • Micropore or Foley catheter holder
0Recent genitourinary surgery • Sterile specimen bottles (if for urine
0Genital abnormality collection)
METHODS
1. Observe hand hygiene and prepare materials using aseptic technique
2. Provide as much privacy as possible
3. Position patient properly and comfortably
° For males: supine position
0 For females: supine position with knees bent and hips flexed
4. Clean genital area if soiling is evident
5. Open foley catheter package, put aside but maintain sterile zone around foley catheter
6. Wear clean gloves
7. Expose the urethral meatus
0 For males: lift the penis and retract foreskin. Be careful when retracting the foreskin
because it may lead to complications such as paraphimosis and infection. The foreskin
should not be retracted beyond the point where it has naturally separated. A safer method
of catheterization is to do it without retracting the foreskin (see illustration on next page)
° For females: spread the labia
8. Clean urethral opening and surrounding tissue aseptically
° For males: circular motion from the urethral opening to the base of the penis
° For females: from above the urethral opening down towards the rectum
9. Change to sterile gloves
10. Lubricate the tip of the catheter generously
11. Insert the catheter into the urethral opening until the "Y" of the catheter
° For males: extend the penile shaft so that it is perpendicular to the abdomen
° For females: upward at approximately 30-degree angle
12. Observe for urine flow
13. Inflate the balloon slowly using sterile water. If the catheter has a guide wire (in very
small caliber catheters) remove the guide wire
14. Withdraw the catheter until resistance is met
15. Attach the end of the catheter to the urine bag
16. Secure the catheter to the upper leg with the Foley catheter holder or tape
17. Place urine bag below the level of the bladder
18. Dry patient's perineum
19. Instruct patient on catheter care
101
Technique for catheterization without retraction: the thumb is used to stablize the penis,
while the index and middle fingers are used to occlude the preputial space and guide the
catheter through the preputial opening into the urethral meatus
102
INTRAVENOUS LINE INSERTION
INDICATIONS AND MATERIALS NEEDED
CONTRAINDICATIONS
Indications • IV cannula
• Administration of the following: • Microset/lV tubing
0 IV fluids • IV trolley
0 IV medications • Clean (non-sterile) gloves
0 IV chemotherapy • Tourniquet
0 IV nutritional support • Cotton
0 Radiologic contrast agents
• Blood sampling for laboratory tests
Contraindications
• Alcohol
• Antiseptic solution (2% chlorhexidine in
70% isopropyl alcohol)
• Micropore or Zinc Oxide Tape (usually
more appropriate because it adheres to
I
• Presence of injury, infection, or burns in
the extremity the skin better. Example is Leukoplast)
• Saline solution
• 2 mL syringes (2)
• Dressing pack
• Splint (optional)
METHODS
1. Hand hygiene and prepare materials needed
2. Wear clean gloves
3. Select position/site ofvenipuncture. A strong penlight may be used as an improvised vein
finder. The light is placed under the hand of the patient. If done inside a dim room, the
veins maybe visualized.
4. Draw up saline solution into 2-mL syringes (2)
5. Prime cannula and assembled equipment with saline solution
6. Swab puncture site with antiseptic solution and allow to air-dry
7. Apply tourniquet
8. Stretch the skin and stabilize the selected vein
9. Insert the needle bevel up
10. Observe for blood backflow
11. Remove the needle while pushing cannula further into the vein
12. Release tourniquet
13. Flush with saline solution to check patency
14. Use tape around the end of the hub of the cannula (without touching the insertion site)
15. Attach extension tubing and secure with tape
16. Apply splint
17. Instruct the patient on care of IV site
103
NASOGASTRIC/OROGASTRIC TUBE INSERTION
INDICATIONS AND MATERIALS NEEDED
CONTRAINDICATIONS
Indications • Nasogastric/orogastric tube (appropriate
• Disorders of oral feeding for intended purpose and size appropriate
• Increased nutrient or metabolic requirement to patient)
• Nutritional support/ feeding administration 0 OGT is used for neonates because
• Medication administration neonates are preferential nasal
• Bowel decompression in gastrointestinal breathers. Beyond the neonatal period,
obstruction common clinical practice is to use OGT
• Evaluation of upper GI bleeding when the patient has no erupted tooth/
• Aspiration of gastric fluid content from teeth yet, otherwise NGT is used.
recent ingestion of toxic material • Water-soluble lubricant
• Administration of radiographic contrast • Oral syringe or luer-lock syringe with
to GI tract syringe adapter (appropriate to type of
tube used)
Contraindications • Suction tubing and container
• Problems with the GI function • Clean (non-sterile) gloves
• Intestinal perforation • Zinc oxide tape
• Severe maxillofacial (midface) trauma • 2% viscous lidocaine ( 54mg/kg)
• Basilar skull fracture • Stethoscope
• Coagulation abnormality • pH strips
• Esophageal varices • Glass of water with straw
• Acid/alkaline ingestion
METHODS
1. Wear clean gloves
2. If patient is able to follow commands, instill 10 mL of lidocaine down nostril with the head
tilted backwards and ask patient to sniff and swallow
3. Ensure that the patient's vital signs and indicators of adequate oxygenation and
ventilation are monitored
4. Position the patient properly (supine)
5. Approximate length of insertion by measuring the distance from the tip of the nose to the
earlobe, then from the earlobe to the midpoint between the xiphoid and the umbilicus
(mark this point on the NGT/OGT)
6. Lubricate the distal tip of the tube
7. Gently and steadily insert tube through either the nostril or mouth to previously identified mark
(if patient cannot follow instructions, gently advance the tube. Do not force against resistance)
° For NGT: insert the tube into a nostril, aiming posterior and parallel to the nasal septum.
When the tube touches the pharynx, flex patient's head forward and ask patient to
swallow. Advance the tube as the patient swallows.
0 For OGT: position the end of the tube downward and insert the tube into the oral cavity
over the tongue. Aim the tube back and down towards the pharynx. When the tube
touches the pharynx, flex the head forward. Ask patient to take sips of water through a
straw while tube is advanced.
8. Verify tube placement by injecting 2-5 mL of air using oral syringe or luer-lock syringe
with syringe adapter (for high-risk patients: radiographic confirmation of placement)
9. lfph strip is a available, aspirate gastric content and test for pH reading (should be 56)
10. Once placement of tube is confirmed, secure the tube using zinc oxide tape
11. Loop the tube and cover the tip by partially inserting a part of the tube to the opening
(or keep open if used for decompression)
12. Instruct the patient and relatives on care of NGT/OGT
104
Selection of NGT/OGT Size based on Weight and Age
105
CAPILLARY BLOOD SAMPLING
INDICATIONS AND MATERIALS NEEDED
CONTRAINDICATIONS
Indications • Lancet or automated disposable incision
• Blood sampling for laboratory tests (e.g., device
CBC,glucose, newborn screening) • Blood collection tubes (capillary tubes or
Microtainers)
Contraindications • Cotton
• Presence of local inflammation or hematoma • Alcohol
• Recent puncture in the same site • Clean (non-sterile) gloves
• Micropore
METHODS
1. Assemble equipment and supplies
2. Perform hand hygiene
3. Put on well-fitting, non-sterile gloves
4. Select the site and apply 70% isopropyl alcohol & allow to air dry
5. Puncture the skin with one quick, continuous, and deliberate stroke
6. Wipe away the first drop of blood and allow a second drop to form
7. Place the capillary tube in the drop of blood and invert the proximal end of the tube to fill
the capillary tube until blood reaches the demarcation line (avoid squeezing too tightly)
8. Dispose used sharps in an appropriate container
9. Dispose other used supplies in an appropriate container
10. Perform hand hygiene
TIP for heel-prick: allow the foot of the baby to "refill" by observing for capillary refill
(i.e. foot turns back to red) before pressing/squeezing it from time to time. Continuous
vigorous squeezing without waiting for refill will less likely lead to good flow of blood.
106
Conditions influencing the Choice of Heel or Finger-Prick (for capillary blood sampling)
CONDITION HEEL-PRICK FINGER-PRICK
Age 0 -'6 months Over 6 months
Weight 3 -10 kg Greater than 10 kg
On the side of the ball of the finger
Placement of On the medial or lateral
perpendicular to the lines of the
lancet plantar surface
fingerprint
Recommended Second and third finger (i.e. middle
I
. Not applicable
finger and ring finger)
METHODS
1. Position patient properly (supine) and comfortably and restrain the child if needed
2. Locate radial artery by performing an Allen test for collateral circulation
3. Disinfect sampling site with antiseptic solution and allow to air-dry
4. Penetrate skin at a 30- to 45-degree angle. Neonates have arteries that are more shallowly
located. Therefore, the needle is inserted at a lesser angle (i.e. more parallel to the skin).
5. Advance the needle slowly until radial artery is punctured or resistance (bone) is met
6. Observe for blood flashback
7. Provide continuous but gentle suction with the plunger of the syringe
8. Allow syringe to fill to the appropriate level
9. Withdraw the needle and syringe
10. Place gauze or cotton over puncture site and apply pressure to stop bleeding
11. Expel air bubbles, cap syringe, and roll specimen between the hands to gently mix it
12. Cap the syringe, label and send specimen to laboratory immediately
NOTE: A common clinical practice is to extract arterial blood using the "fountain" method
wherein a bare needle is used instead of a syringe. Blood is then allowed to drip from the needle
and collected. The reason for such practice is that a bare needle is less likely to be dislodged as
compared to a needle with a syringe attached to it. This procedure is NOT ideal.
107
INTRAOSSEOUS INFUSION
INDICATIONS AND MATERIALS NEEDED
CONTRAINDICATIONS
Indications • Chlorhexidine or povidone iodine
• Vascular access emergently needed but not • Surgical mask
immediately available via peripheral vein • Latex-free sterile gloves
• Emergency administration of medications • Eye protection
and fluids • 10 mL syringe
• Syringe with saline flush
Contraindications • 10 needle and/or device (e.g. manual
• Bone fracture IO needle). If IO needle is not readily
• Recent 10 attempt in same insertion site available, an alternative would be a
• Osteogenesis imperfecta regular gauge 16/18 needle.
• Osteopetrosis • 1% lidocaine (awake patients) in small-
• Overlying infection, cellulitis, burns, or volume syringe
osteomyelitis at proposed insertion site • Micropore
• Dressing
METHODS
1. Wear surgical mask, eye protection, and sterile gloves
2. Prepare the injection site with an antiseptic
3. If patient is awake, infiltrate the skin, subcutaneous tissue, and periosteum with 1 %
lidocaine
4. Place the leg with knee extended in neutral position and then slightly externally rotate at
the hip to expose the flat part of the tibial surface, and externally rotate the foot
5. Check the needle to ensure that the bevels of the outer needle and the internal stylet are
properly aligned
6. Grasp the leg distally and lateral to the insertion site with the palm and fingers of the non-
dominant hand to brace the leg against the force of IO placement and to prevent distal leg
movement during the procedure
7. Palpate the landmarks to identify the flat surface of the tibia approximately 1 to 2 cm
below and slightly (up to 1 cm) medial to the tibial tuberosity, and insert the IO needle
through the skin
8. Direct the IO needle perpendicular to the entry site 01; in skeletally immature children, at
a slight angle (10 to 15 degrees) from vertical (caudad for the proximal tibia); cephalad
for the distal tibia or femur
9. Apply pressure with a twisting motion
10. Unscrew the needle cap and remove the stylet
11. Confirm correct needle placement by aspirating blood
12. Once proper placement is confirmed, flush the needle with 10 mL of normal saline and
connect it to conventional IV tubing
13. Secure the bone marrow needle with tape and a dressing that does not obscure the
needle placement site so that infiltration can be rapidly detected
14. Remove the needle by grasping the shaft and pulling up with a slight rotary motion
15. Apply pressure to IO site
16. Dress site using aseptic technique
17. Provide analgesia, as needed and depending upon patient status
108
INTRAOSSEOUS NEEDLE INSERTION SITE
Altcrnato
SIio
Femur
lntraosseous needle insertion sites in older Distal tibia intraosseous needle insertion
children and adolescents site in older children and adolescents
1 2
Position and stabilize the leg Insert the needle at a 90° angle and apply
pressure with a twisting motion
109
UMBILICAL VESSEL CATHETERIZATION
INDICATIONS AND MATERIALS NEEDED
CONTRAINDICATIONS
Indications • Umbilical catheter
Umbilical Artery Catheterization 0 Less than 3.5 kg: Fr 5
• For frequent sampling of arterial blood 0 More than or equal to 3.5 kg Fr 8
gas, continuous monitoring of arterial • Antiseptic solution (e.g. Povidone-iodine)
blood pressure and route for infusion of • Sterile gloves
parenteral fluid • Medical tape
• Reserved for seriously ill infant because of • Scalpel
high rates of complications; blanching of • Mosquito
extremity, infection, thrombosis, etc.
• CDCrecommends a maximum of? days
Umbilical Vein Catheterization
• For early and emergency vascular access
in neonates
Contraindications
• Omphalitis
• Omphalocele
• Peritonitis
• Necrotizing enterocolitis
• For umbilical artery (UA): evidence of
ischemia in lower extremities
• For umbilical vein: pmtal venous hypertension
METHODS
1. Determine catheter length
2. Hand hygiene and aseptic technique
3. Place infant in a supine position
4. Tie the base of the umbilicus using a firm half knot that will help control bleeding while
allowing the passage of the catheter
5. Cut the cord approximately 2 cm above skin
6. Identify the vein (located at the 12 o'clock position, thin-walled) or artery (thick-walled)
7. Hold the base of the umbilicus and insert the pre-flushed umbilical catheter
8. Observe the blood to flow through the catheter
9. Once adequate placement confirmed, secure the catheter using a tie or adhesive medical tape
110
IDENTIFYING THE UMBILICAL VESSELS
1 2
I
VERIFYING THE CATHETER POSITION
AP View showing UAC initially coursing down in contrast to the UVC extending
superiorly
Lateral view showing the course of the umbilical catheters (UAC versus UVC)
111
LUMBAR PUNCTURE
INDICATIONS AND MATERIALS NEEDED
CONTRAINDICATIONS
Indications • Spinal Needle
• Diagnosis of • Sterile Gloves
Suspected CNS infection
0 • Drapes
Suspected subarachnoid hemorrhage
0 • Antiseptic solution (Povidone-iodine)
• Introduce contrast agents into the CSF for • Specimen bottles
diagnostic purposes • Syringe
• Measure pH, enzymes, neurotransmitters • Lidocaine
and trace constituents
• Measure and fractionate CSF proteins in
suspected immunologic disease especially
Multiple Sclerosis or Guillain-Barre
syndrome
• Identify neoplastic invasion or seeding
of the subarachnoid space by gliomas,
carcinomas, leukemias, lymphomas
Contraindications
• Suspected mass lesion in the brain
(especially posterior fossa or
supratentorial lesions with midline shift)
• Impending cerebral herniation
• Critical illness/unstable condition
• Skin infection
• Thrombocytopenia < 20 xl0 9 /L
METHODS
l. Prepare materials
2. Positioning: Position an acutely ill patient on the side with the legs drawn up and the
spine flexed to increase the distance between the processes and lamina of the adjacent
vertebrae
3. Palpate the iliac crest and slide down to L4 to LS
4. Needle Insertion and manometry:
Scrub skin with antiseptic
0
Insert needle in the interspace between the dorsal processes of vertebra L4-L5 or LS-Sl
0
Once the back flow of CSF is constant, remove sty let and attach to manometry tube
0
5. Collection of the CSF:collect 10-lSmL of CSF by allowing several mL to drip into the tubes
0 1: Gram stain, culture and sensitivity
4: Special studies
0
1 2
112
NEEDLE ASPIRATION
INDICATIONS AND MATERIALS NEEDED
CONTRAINDICATIONS
Indications • Large-bore intravenous catheter (Gauge
• Urgent management of tension 14or 16)
pneumothorax or primary spontaneous • Syringe
pneumothorax • Three way stopcock
• Sterile gloves
Contraindications (Relative) • Povidone-iodine
• Anticoagulation, coagulopathy and
bleeding diathesis
METHODS
•
•
•
Sterile gloves
Cotton
Micropore I
1. Prep the site with povidone-iodine
2. Locate the site at the second intercostal space superior to the third rib at the
midclavicular line
3. Hold the needle that is connected to a syringe via a 3-way stopcock perpendicular to the
chest wall
4. Puncture the site in the middle third to minimize the risk of injury to the internal
mammary artery
5. Place the catheter just above the cephalad border of the rib
6. Remove the needle leaving the cannula in place
7. Air is withdrawn manually until no more can be aspirated
8. If no further air can be aspirated, close the stopcock
9. Send patient for tube thoracostomy
113
ENDOTRACHEAL INTUBATION VIA DIRECT LARYNGOSCOPIC TECHNIQUE
INDICATIONS ANO MATERIALS NEEDED
CONTRAINDICATIONS
Indications • Endotracheal tube of appropriate length
• Acute respiratory failure • Stylet
• Airway protection • Sterile lubricant
• Preoperative setting in patients requiring • Laryngoscope
general anesthesia • Zinc oxide tape
• Advance airway in patients suffering from • Sterile gloves
cardiac arrest • Oxygen tubings
• Bag valve mask
Contraindications • Suction device
• Trauma to upper airway • Lidocaine spray
• Pulse oximeter
• Cardiac monitors
• Sedative medication
• 10 cc syringe
• Stethoscope
METHODS
1. Obtain assistance
2. Prepare materials
3. Wear gloves
4. Assess, preoxygenate and position patient
5. If properly trained with Rapid Sequence Intubation, may administer medications for RSI.
Otherwise, skip this step.
6. Open the patient's mouth and carefully position the laryngoscope
7. Deflect the tongue and soft tissue to the left side of the mouth with the flange
8. Identify and locate the epiglottis
9. Improve view by using bimanual laryngoscopy, head elevation, and lower neck flexion
(not done when there is suspected neck trauma/injury)
10. Insert the endotracheal tube through the vocal cords into the trachea under direct vision
11. Remove the stylet and inflate balloon
Note: It is a common clinical practice to use uncuffed ET in neonates and children.
Cuffed is mostly used for adolescents and adults. Howevet; literature states that both
cuffed and uncuffed are acceptable for intubating infants and children.
12. Confirm positioning of the tube within the trachea through visualization, auscultation,
and CO2 detection
13. Check for any secretions/output from the ET tube
14. Secure the tracheal tube
15. Hook to mechanical ventilator
16. Provide sedation and analgesia
17. Send specimens for culture studies (ETA GS/CS, ETAAFB, ETAGeneXpert)
18. Send for post-intubation AP films to confirm tube placement and adjustment
19. Send for post-intubation blood gases to check oxygenation and gas exchange as well as
to guide adjustment of mechanical ventilator settings
114
DIRECT LARYNGOSCOPIC TECHNIQUE
I
2
REFERENCES
1. Pediatric Advanced Life Support. Circulation 2005;112;1V-167-IV-187
2. Kliegman, R., ST GEME Ill,)., Blum, N., Shah, S., Taske1; R., Wilson, K., & Behrman, R. (2020).
Nelson Textbook of Pediatrics (21st ed.). Philadelphia: Elsevier
3. Cloherty, J.,Eichenwald, E., Hansen, A., & Stark, A. (2012). Manual of Neonatal Care (7th ed.).
Philadelphia: Lippincott Williams & Wilkins.
4. Center for disease control and prevention. Targeted tuberculin testing and treatment for
latent tuberculosis infection. 2005
5. Carmack.A.,& Milos, M. (2017). Catheterization without foreskin retraction. Canadian Family
Physician, 36.
116
GROWTH
AND
DEVELOPMENT
SECTION ONE
ANTHROPOMETRIC MEASUREMENTS
I. AVERAGEBIRTH MEASUREMENTS
The following values approximate the average weight, length, and head circumference of
I
a Filipino infant at birth and at 1 year of age. It serves as a quick guide to assess an infant's
anthropometric measurements, but the ideal method is to check appropriate growth charts.
EXPECTED VALUES BY THE FIRST
PARAMETER AT BIRTH
BIRTHDAY
Weight 3000 g 3x the birth weight - 9-10 kg
Length 50cm 50% increase from birth length ~ 75cm
Head 35 cm
Circumference (32-37 cm)
Increase by 10 cm ~ 45 cm
Source:KliegmanR.et al. NelsonTextbookof Pediatrics
(21sted.).Elsevier;2020
Competency-Based
of Pediatrics
NavarroX, et al. Fundamentals 2014
(1sted.).C & E Publishing;
II.WEIGHT
The average weight of a Filipino newborn is 3000 g. The following are used to approximate
the average weight of a Filipino child and to quickly assess a child's weight if it is within
normal range. Growth charts are still the ideal method for assessment of nutritional status.
Sample cases
1. A full term baby is delivered with a birth weight of 3000 g. On the 5"' day of
life, his weight is 2800 g. Is this normal?
• During the first week of life, a normal full-term infant is expected to lose
approximately 10% of the birth weight (10% of 3000 g is 300 g)
• The loss of 200 g by the patient is still within physiologic levels
2. What is the expected weight at 4 months and 1 year of age if a baby was born
with a weight of2500 g?
119
B. Formulas to Estimate Weight
AGE
Sample cases
1. What is the expected weight of a 5 month old with a birth weight of 3000 g?
• Weight in grams= Age in months x 600 + Birth Weight in grams
= 5 months x 600 + 3000 g
= 6000 g
• At 5 months old, the expected weight of the infant with a birth weight of 3000g is 6000 g
lll. LENGTH
A. Expected Changes in Length or Height
The following formulas are used to approximate the average length/height of a Filipino
~r
child and to quickly assess a child's length/height if it is within normal range
Howevet; growth charts are still the ideal method for assessment
".~};;~~::-••_Fo~
0
AGE 'st!•"';.
Birth to 3
+9cm 3 cm per month
months
3-6 months +8cm 2.67 cm per month
6-9 months +5cm 1.67 cm per month
9-12 months + 3 cm 1 cm per month
2-12 years old Height in cm= Age in years x 6 + 77
120
B. Proper Measurement of Length
For Children < 2 Years Old: measure the recumbent length
Movableheadboard Ltngthboard Filedheadboard
• Use a length board or infantometer placed
on a flat surface
• Ideally taken with child's clothing and
footwear removed
• Place the child on his/her back with the
head against the fixed headboard
121
Sample cases
1. What is the expected length of a 3 month old baby who was born with a length of SO cm?
• Expected length gain from birth to 3 months is 9 cm
0 Length= 50 cm+ 9 cm= 59 cm
0 By 3 months, the expected length of a baby with a birth length of 50 cm is 59 cm
2. What is the expected height of a S year old?
0 Height in cm = Age in years x 6 + 77
0 Height in cm= 5 x 6 +77 = 107 cm
0 The expected height of an average 5 year old is 107 cm
AGE
r~~:-: CIRCUMFERENCE
----------
Expected
I ge increase in HC
1 to 4 months + 2 Inches • 1/2 inch per month
4 to 12 months + 2 Inches • 1/4 inch per month
1 to 3 years + 2 inches • 1 Inch/year
3 to 6 years + 1.5 Inches • 1/2 inch per year
6 to 20 years + 1.5 inches • 1/2 inch per 5 years
andChildHealth.4thed.JMCPress:20C0
of Pediatrics
Source:DelMundoF el al.Textbook
122
8. Using Growth Charts
0 To interpret if measured head circumference is within normal, refer to growth charts
' Aside from WHO growth charts, this head circumference chart is commonly used in:
60 I I I
I
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64
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. r-r: ~--
,.. I
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46
rr-r
1 ·-:::;;_~,t::±
71,--1~-+::;;
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:;-.
-
1 1:::!l=1i- .tlj:;:.::1.:t
1-1::.t,,1•~-.:1:.t• 1J,jtt.:tj•'
9
~
I /'
I , _•.-
,,,,,
~--,
.........-i
l .... -· I
~---'r-r-·'
1 ,
i I
I
,
f
I I
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17
} '%,_/-r ,
42 •'' ~ , .. , I I
1 l : , : ,,: '
I I I
I
16
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:~/, I i : I ! I : : I
3,ll j I 1 I I '. I
I
I
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I I I
12
10 12 14 16 18 8 10 12 14 16 18
B-------- MO: THS --------i------YEARS -----
Source:MenkesJ, el al.ChildNeurology
(7thed).Lippincott
Williams& Wilkins;2006
123
V. MID-UPPERARM CIRCUMFERENCE
(MUAC)
Measuring the Mid-Upper Arm Circumference
• In infants 6-59 months old, MUACis an alternative method
commonly used to determine wasting (acute malnutrition)
• Procedure
0 Place measuring tape from the tip of shoulder to the elbow
0 Mark the mid-point between the shoulder and the elbow
0 Measure the circumference at this mid-point, making sure that
correct tape tension is placed (not too tight and not too loose)
0 Record and interpret MUAC
• Interpretation ofMUAC
0 115 to <125 mm= moderate acute malnutrition
0 <115 mm = severe acute malnutrition
Source:MwangomeM,et al. BulletinOfTheWorldHealthOrganization;2012
WHO,Management of severeacutemalnutrition
in infantsandchildren
WHO,Supplementary
foodsfor the management of moderateacutemalnutrition
Sample cases
Using the formulas described above, compute for the estimated weight and length/height
Case 1: A 3 year old with a birth weight of 3 kg and birth length of 50 cm
• Weight
0 Weight in kg= Age in years x 2 + 8
0 Weight = 3 x 2 + 8
, Weight= 14 kg
• Height
0 Height in cm= Age in years x 6 + 77
0 Height= 3 x 6 + 77
0 Height= 95 cm
• Conclusion: At 3 years old, the patient's expected weight is 14 kg and expected height is 95 cm
• Weight
0 Weight in grams = Age in months x 500 + Birth Weight in grams
0 Weight= (7 x 500) + 3000
0 Weight= 6500 grams
• Length
0 Birth to 3 months=+ 9 cm
0 3 to 6 months = + 8 cm
0 6 to 7 months=+ 1.67 cm
0 Total gain in length= 18.67 cm
0 Length= 50cm + 18.67cm = 68.67 cm
• Conclusion: At 7 months old, the expected weight is 6500 g and the expected length is
68.67 cm
124
INTERPRETATION OF ANTHROPOMETRIC MEASUREMENTS
• Interpretation of anthropometric measurements using the WHO Growth Charts are discussed
in this section (this is the ideal method of interpreting a child's weight & height/length)
• The step-by-step approach for interpretation is illustrated through the sample cases
provided below (please see WHOgrowth charts available 011/ine:www.who.int/
childgrowth/standards/en)
Z Score INTERPRETATION*
Between 1 to -1 • 0 (median)
Between 1 to 2 • Above 1 (Z-score >l)
Between 2 to 3 • Above 2 (Z-score >2)
Higher than 3 • Above 3 (Z-score >3)
Between -1 to -2 • Below -1 (Z-score < -1)
Between -2 to -3 • Below -2 (Z-score <-2)
Lower than -3 • Below -3 (Z-score <-3)
*If the point is exactly on a z-score, it is interpreted in the less severe category (e.g., plotted
point falls exactly on -3, interpret as below -2)
125
STEP 4: Interpret
• Interpret the Z-score using the table below
• Note that wasting is the most appropriate measure of severe acute malnutrition
PARAMETERS INTERPRETATION
Normal • 0 to below -1
• Above 1 (better assessed with
Risk for Overweight
Weight for age weight for length/height or BMI)
Underweight • Below-2
Severely underweight • Below-3
Normal • Below -1 to above 2
Source:PPSPreventive
PediatricHealthCareHandbook
2018
~fl -Id~l"_J!
Hf-:L__
T_:r_-__l~J_1
~ ; ~ ~-: '
-J_L : -~
-r L
The given weight of 10 kg intersects with the given age of 14 months, yielding a z-score of 0
(median). This means he has a normal weight in relation to his age.
126
Length-for-age for Boys: Birth to 2 years (Z-score)
I 1
-·r-i-r-~ i 1
i
i
, I
.
r -,.
.
•
t
II
t
-{- -~
' I
The given length of 75 cm intersects with the given age of 14 months, yielding a z-score of 0
(median). This means he has a normal length in relation to his age.
-·-~t-
__ ,·'.-:f-=r-
•
, ·-·--•--~
♦ • • :
. -
~
.2
3
• 1
0
-1
·,2
.:~:=:
.··
......
,·
-3
I .
- ... .L.... .. .. . . ·- . 1 -
:r:;' . '
~ r· · I
The given weight of 10 kg intersects with the given length of 75 cm, yielding a z-score of 0
(median). This means he has a normal weight in relation to his length.
Source:TheWHOChildGrowthStandards.Retrievedfromhltp:l/www.who.inV
WorldHeallhOrganization.
TrainingCourseon ChildGrowthAssessmentGeneva,WHO,2008.
127
Sample Case 2: A 2 year old male was brought to your clinic for a general check-up.
Weight= 7 kg Length= 85 cm
STEP 4: Interpret
• Interpret the Z-score using the table shown above
Weight for age: Z-score < -3 (interpretation: severely underweight)
• Length for age: Z-score O = median (interpretation: normal)
• Weight for length: Z-score < -3 (interpretation: severely wasted)
• Based on the growth charts, the child is severely wasted. His length is within normal range.
i .
t j.
i ;
! -···-
I-+t i~-
--f-!-'--'-
i TT-'.
The given weight of 7 kg, with the given age of 2 years, yields a z-score below -3.
This means he is severely underweight for his age.
128
length-for-age for Boys: Birth to 2 years (Z-score)
I
The given length of 85 cm with the given age of 2 years yields a z-score between O and -2,
which still falls within the median (see table under Step 3). This means he has a normal
length in relation to his age.
The given weight of7 kg with the given length of85 cm yields a z-score below-3.
This means he has severe wasting (see table under Step 4).
Source:TheWHOChildGrowthSlandards. Retrieved
fromhttp://www.who.in1/
WorldHealthOrganization.
TrainingCourseon ChildGrowthAssessment.Geneva,WHO,2008.
129
SECTION TWO
DEVELOPMENT
INTRODUCTION
I. PRINCIPLESOF DEVELOPMENT
• Development is a continuous process of reaching maturity with increase in function and skills
• Developmental sequence is orderly and predictable
0 Progresses in a cephalocaudal manner and proximodistal pattern
0 Responses proceed from generalized reflexes to discrete voluntary actions
• Rate varies from child to child and is affected by biologic and psychosocial factors
II. DEVELOPMENTALDOMAINS
• The developmental domains consist of gross motor, fine motot; social, and language
(expressive and receptive)
• Developmental milestones are present in each domain that serve as criteria in deciding
whether a child is developing accordingly
Developmental delay refers to a slower than acceptable rate of development in at least 1
of the domains
• Concrete • Formaloperations
• Preoperational
(abstract thinking,
[symbolic operations
• Sensorimotor (thinking is tied deductive
thinking; able ( use of logic
to immediate sensations) reasoning&
to form mental and inductive hypothetical
images) reasoning) thinking)
3) Erikson (Psychosocial development)
• Trust • Autonomy • Industry • Identity versus
• Initiative
versus versus shame versus role diffusion
versus guilt
mistrust and doubt inferiority
4) Koh/berg (Moral Development)
• Preconventional
• Conventional • Conventional • Postconventional:
(stage 1 & 2):avoid
(stage 3): (stage 4): law moral
punishment/
conformity and order principles
obtain rewards
Source:KliegmanR.el al NelsonTextbookof Pediatrics(21sted}.Elsevier:2020
NavarroX, et al. Fundamentals
of PediatricsCompetency-based (1sted}.C&EPublishing: 2014
130
DEVELOPMENTAL MILESTONES
• The actual age at which a milestone is achieved by a normal child may range within 2
months of this age level in the first year of life to 4 months from the second year onwards
Fine motor
Language
• Presence of grasp reflex
• Hands remain fisted
• Sweeping movements towards object are observed
•Crying/ whimpering (expressive language)
I
"
3 months • Coo
Personal-social 6 months • Babble
9 months • Say "mama/papa" but non-specific
12 months • Speak single words with meaning
Source:KliegmanR,et al NelsonTextbook
of Pediatrics
(21sted).Elsevier:2020
NavarroX et al. Fundamentals
of Pediatrics
Competency-based (1sted).C & E Publishing:
2014
131
III. DEVELOPMENTAL MILESTONES FROM TODDLERHOOD TO SCHOOL-AGE
DOMAIN AGE SKILLS
15 months • Run, pivot, walk backwards, and crawl upstairs
18 months • Walk upstairs with rails and run stifny
24 months • Jump with both feet and run well; climb on furniture; walk up
and down the stairs 1 step at a time
4 years • Hop; throws ball overhead; use scissors to cut out pictures
5 yea,·s • Skip
7 years • Climb and run
15 months • Scribble spontaneously; make tower of 3 cubes
18 months • Imitate stroke on paper; make tower of 4 cubes
24 months • Imitate vertical lines; make tower of 7 cubes
• Draw circle with series of perseverating lines; make tower of
30 months
9 cubes
Fine motor 3 years • Draw circle and a person with 2 body parts; make tower of 10 cubes
3.5-4 years • Draw a cross
132
SECOND YEAR OF LIFE TO MIDDLE CHILDHOOD
3-5 YEARS OLD 6-11 YEARS OLD
2YEARSOLD
(PRESCHOOL YEARS) (MIDDLE CHILDHOOD)
Growth
• Growth rate slows • Gain of 3-3.5 kg and 6-7 cm per year
down by the end of • Head grows only 2-3 cm during
the first year • Weight gain of about 2 this period
• 2"'1 year of life kg per year • Dentition:
0 3-5 lbs weight gain • Growth of about 6-8 0 6 years old: loss of deciduous teeth
0 10-12 cm increase cm per year 0 9 years old: 8 permanent
in height incisors & 4 permanent molars
0 90% of adult head
size attained
Other Aspects
• Appetite declines
0 11-12 years old: pre-molars erupt
'
• Interest in sexuality
(physiologic anorexia) • Muscle strength, coordination, and
(may play with their
• Myelination ofd1e brain stamina increase progressively
genitals as a sign of
is most rapid & dramatic • Issues of overweight from
normal curiosity)
• Protuberant abdomen, sedentary habits
• Make-believe games
baby fat, lordosis • Social:
• May make up stories
• Emotional: temper 0 Attachment to parents decrease &
• Encourage child to
tantrums; seeks to peer increase by 7 years of age
sleep in own bed
independence but still 0 Reliance on peer groups
• Teach the child not to
relies on parental ties 0 Group loyalty, commitment to
talk to strangers
for confidence best friends by 9 years old
Source.KltegmanR, et al NelsonTextbookof Ped1atncs (21sted). Elsevier,2020
NavarroX el al. Fundamentals
of PediatricsCompetency-based (1st ed). C & E Publishing;2014
ADOLESCENCE
I. GENERAL
• Adolescence is the transition from childhood to adulthood
• Rapid physical and sexual changes:
Growth spurt
Sexual maturation (appearance of secondary sex characteristics)
Menarche (event to indicate fertility)
Ejaculation (comparative indicator of reproductive potential)
B. Bone Age
0 An index of physiological maturation
Radiographs of the hand, wrist, or knee are compared to the standards of maturation
in a normal population
Any value >2 SD above or below the mean for age is considered abnormal
133
• Increases (to 25% of body
Adipose tissue • Decreases
weight)
Average gain in height • 28 cm • 25 cm
• Increases from 80 to 90% • Decreases from 80 to 75%
Muscle mass
of body weight of body weight
Peak height velocity • 13.S years • 11.S years
• Occurs with peak height • Occurs 6 months after
Peak weight velocity
velocity (13.S years) peak height velocity
Rate of linear growth • 9-10 cm per year • 8-9 cm per year
III. SEXUALMATURITYRATING
SMR
ILLUSTRATION PUBIC HAIR PENIS TESTES 0
STAGE
1 y J
• None • Preadolescent • Preadolescent
2
y J
• Scanty, long
• Slightly
pigmented
• Slight
enlargement
• Enlarged
scrotum
• Pink texture
altered
3
y !
• Darker
• Starts to curl
• Small amount
• Longer • Larger
4 y !
• Resembles
adult type
but less in
quantity
• Coarse, curly
• Larger
• Glans and
breadth
increases in
size
• Larger
• Scrotum dark
y
• Adult
distribution
• Spread to
5 • Adult • Adult
the medial
! surface of
thighs
134
SMR
ILLUSTRATION PUBIC HAIR BREAST
STAGE
1
(y);f~(0 • Preadolescent • Preadolescent
2
(y)ft~ (0 • Lightly
pigmented
• Straight
• Medial border
oflabia
papilla elevated
as small mound
• Areolar
diameter
increased
I
\y/;t~((/
• Darker • Breast
• Beginning to and areola
3 curl enlarged
• Increased • No contour
amount separation
lr/A{O
• Coarse, curly • Areola and
• Abundant but papilla form
4
amount less secondary
than in adult mound
• Mature
ITIW<~~
• Adult feminine
• Nipple
triangle spread
projects
5 to the medial
• Areola part of
surface of
general breast
thighs
contour
Source:KhegmanR. et al NelsonTextbookof Ped,atncs
(21sted).EIsevier·
_ , 2020
Navarrox et al. Fundamentals
of PediatricsCompetency-based (1sted).C & E Pubhsh,ng;2014
BOYS GIRLS
• Sequence of pubertal events: thelarche,
adrenarche, peak height velocity,
• Complete sexual maturity is usually
continued breast and hair development,
achieved by 17-18 years old
menarche, completion of puberty
Sequence of pubertal events: testicular
, Average duration of completion of
enlargement, adrenarche, continued
puberty is 4 years
testicular and penile enlargement, peak
• Menarche is achieved by 90% of girls
height velocity with peak weight velocity
during SMR breast 4
• Gynecomastia is seen in about 60% of
, Filipino girls' average age of menarche
boys and is noted at SMR 2-4
is 13.3 years and cycles may be
• Ejaculation usually occurs at SMR 3
anovulatory for 2 years after menarche
• Voice change noted between SMR 3-4
Full fertility usually reached within 2
• Fertility is usually established at SMR 4
years of menarche (average age
between 14-15 years)
135
IV. CHARACTERISTIC BEHAVIORS OF ADOLESCENTS
EARLY ADOLESCENCE MIDDLE ADOLESCENCE LATE ADOLESCENCE
(10-13 Years Old} (14-17 Years Old) (18-21 Years Old}
1)Autonomy
• Argumentative, disobedient,
and tends to challenge family
and authority • Shows ambivalence on
• Emancipation (college, work,
• May have mood swings; emerging independence
vocations, adopts an adult
daydreams which may lead to family
lifestyle)
• Rejects things of childhood conflicts
• Displays a growing need for
privacy
2) Body Image
• Critical of and preoccupied
• Increased interest in making
with physical appearance
body image more attractive
and changes • Usually comfortable with
• Excessive physical activity
• May be anxious about wet body image
alternating with lethargy can
dreams, masturbation,
be shown
breast or penis size
3) Cognitive Development
• Focuses thinking on "here • Emergence of formal
and now" because of a operations that lead to
• Emergence of abstract
lack of understanding effective planning
reasoning
of consequence despite • Understands better the
• Able to compromise as they
concrete thinking consequences of behavior
are able to engage with their
• Need for instant gratification • Feelings of omnipotence
conscience
and a lack of impulse control, and immortality are present
• Able to delay gratification
thus engages in risk-taking which may lead to risk-
behavior taking behaviors
4) Identity Development
SJ Peer Group
• Formation of strong peer • Makes decisions and
allegiances maintains values as they are
• Development of intense
• Susceptible to peer pressure less influenced by peers
friendships with the same sex
• Fad behavior • Relaxes to individuals more
• Contact with opposite sex in
• Emerging sexual drives lead than to peer group
peer groups
to exploration and ability to • Selects partner based on
attract a partner individual preference
6) Vocation
• Resets priorities for social
• Able to set more realistic • Pursues realistic academic/
life rather than study
academic or vocational goals vocational goals with
• May have unrealistic
• Begins to realize strengths training or actual
academic goals and
and limitations employment
frequently changes them
136
SECTION THREE
BEHAVIORAL DISORDERS
II. MANIFESTATIONS
• Symptoms are typically recognized and observed during the second year of life
• Deficits in 2 core domains: social communication/social interaction AND restricted
repetitive patterns ofbehaviot; interests, and activities
I
Ill. DIAGNOSTIC CRITERIA
137
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER
I. ETIOPATHOGENESIS
• Characterized by difficulty paying attention, excessive activity, and acting without regards
to consequences, which are otherwise not appropriate for a person's age
• Males are more commonly affected than females
• Exact cause us unknown in the majority
II. DIAGNOSTICCRITERIA
A. Persistent pattern of inattention and/or hyperactivity-impulsivity
1. Inattention & disorganization: ~6 of the following persisting for at least 6 months
Fails to give close attention to details or makes careless mistakes in school
Difficulty sustaining attention in tasks or play activities
Does not seem to listen when spoken to directly
Does not follow through on instructions and fails to finish schoolwork
Difficulty in organizing tasks
Avoids, dislikes or is reluctant to engage in tasks that require sustained mental effort
Loses things necessary for tasks
Easily distracted by external stimuli
Forgetful in daily activities
2. Hyperactivity-impulsivity: ~6 of the following persisting for at least 6 months
Fidgets with hands or feet or squirms in seat
Leaves seat in classroom
Runs about or climbs excessively
Difficulty playing or engaging in leisure activities quietly
"On the go"
Talks excessively
Blurts out answers before questions have been completed
Difficulty awaiting turn
Interrupts or intrudes on others
B. Symptoms are present prior to age 12 years
C. Symptoms are present in ~2 settings (e.g., at home, school, or work; with friends or
relatives; in other activities)
D.Symptoms interfere with, or reduce the quality of, social, academic, or occupational functioning.
E. The symptoms do not occur exclusively during the course of schizophrenia or another
psychotic disorder and are not better explained by another mental disorder
Source:APADiagnosticandStatisticalManualof MentalDisorders,
5th Ed.AmericanPsychiatric
Association;
2013
REFERENCES
1. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders,
Fifth Edition. Arlington, VA,American Psychiatric Association, 2013.
2. Engorn, B., and Flerlage, J. The Harriet Lane Handbook 20th ed. 2015. Philadelphia: Elsevier.
3. Hazinski, MF. Manual of Pediatric Critical Care 1st ed. 2009. Elsevier.
4. Hazinski, MF. Nursing Care of the Critically Ill Child 3rd ed. 2013. Elsevier.
5. Kliegman, R.,Stanton, B.,St. Geme,J., Schor, N.,and Behrman, R..Nelson Textbook of Pediatrics
21st ed. 2020. Canada: Elsevier.
6. Mwangome, M.,Fegan, G.,Fulford, T.,Prentice.A., and Berkley,). Mid-upper arm circumference
at age of routine infant vaccination to identify infants at elevated risk of death: a retrospective
cohortstudyin the Gambia. Bulletin OfThe World Health Organization, 2012 90(12), 887-894.
doi: 10.2471/blt.12.109009
7. Navarro,X., Bauzon,A.,AguilatJ., and Malanyaon, 0. Fundamentals of Pediatrics Competency-
based 1st ed. 2014. Quezon City: C and E Publishing, Inc.
8. Parthasarathy A, Menon PSN, Agarwal RN, Choudhury P,Thacker NC,Ugra D.!AP textbook of
pediatrics 4th ed. 2009. New Delhi: Jaypee Brothers
9. World Health Organization. Training Course on Child Growth Assessment. Geneva, WHO,2008.
10. The WHOChildGrowth Standards. Retrieved from http:j /www.who.int/childgrowth/standards/en/
138
PEDIATRICS
PREVENTIVE
SECTION ONE
IMMUNIZATION
OVERVIEW OF IMMUNIZATION
• Ultimate goal: eradication of disease
• Immediate goal: prevention of disease
Definitions
• Natural: person contracted the
disease and the immune system
creates antibodies
• Artificial: all or part of the
• Natural: transfer of maternal antibodies
to the fetus via the placenta
141
III. IMPORTANTPOINTS TO REMEMBER
• For IM injections. the choice of site is based on the volume of the injected material and the
muscle mass
• In children younger than 1 year of age, the anterolateral aspect of the thigh is the
preferred site.
• In children older than 1 year, the deltoid muscle is usually large enough for IM injection.
• The upper, outer aspect of the buttocks should not be used
Source:KliegmanR, el al NelsonTextbook
of Pediatrics
{21st ed).Elsevier:2020
Kimberlin
DW.et al. ReportoftheCommittee
on Infectious Diseases.
American Academy of Pediatrics:
2018
PRINCIPLES OF IMMUNIZATION
I. SIMULTANEOUSADMINISTRATIONOF MULTIPLEVACCINES
• Most vaccines can be safely and effectively given simultaneously
• Use separate syringes and sites
• Exception is yellow fever and cholera vaccine (separate by at least 3 weeks)
• If vaccines are not given simultaneously, the recommended minimum interval varies
depending on type of vaccine:
V. PRE-EXPOSUREVERSUS POST-EXPOSUREPROPHYLAXIS
• Consists of a course of vaccination given prior to an
Pre-Exposure Prophylaxis (PrEP)
exposure
142
2019 CHILDHOODIMMUNIZATIONSCHEDULEOF THE PHILIPPINES
MINIMUM TIMING OF
VACCINE ROUTE DOSE/NOTES
AGE ADMINISTRATION
• Birth (or preferably
within first 2 months)
• Healthy >2 months old,
PPD prior to BCGnot
necessary
• PPD is needed prior to
Bacillus • 0.05 mL <12 months
BCGif any is present:
Calmette- ID Birth • 0.1 mL >12 months
congenital TB, history
Guerin (BCG)
of close contract to
known cases, and
clinical symptoms
suggestive of TB
I
and/or chest. X ray
suggestive ofTB
• Birth, 6-10-14 weeks
• See discussion on
Hepatitis B IM Birth • Booster may be given
succeedingpages
based on titers
• 5 th dose not needed
if 4'" dose given at 4
• Primary series: 6-10-
years old or older
14 weeks
• DTwP-Hib-Hep B
DTwP-Hib-HepB • Boosters given at 12-
(given usually in health
or IM 6 weeks 18 months (interval
DTaP-Hib-lPV centers; "w" in DTP
between 3 rd and 4 1h
stands for whole cell)
dose is 6 months) and
• DTaP-Hib-lPV (in
at 4-6 years old
institutions / clinics;
"a" stands for acellular)
• Given if pentavalent
• Primary series: 6-10- vaccine DTwP-Hib-
Oral Polio
Oral 6 weeks 14 weeks HepB was used
Vaccine
• Booster at 4 years old • IPV is given with
3rd OPV dose
• Healthy children 2-5
years old without
Pneumococcal • Primary series: 6-10-
previous vaccine may
conjugate 14 weeks
be given 1 dose PCV
vaccine IM 6 weeks • Booster 6 months
(PCV13 or 13 or 2 doses PCV 10
after the 3,d dose
PCVl0) 8 weeks apart
• Not routinely given
>5 years old
• Monovalent (RVl):
2 doses 6-10 weeks • Maximum age: 32
Rotavirus weeks old
Oral 6 weeks • Pentavalent human
vaccine • Do not begin in older
bovine vaccine (RVS): than 15 weeks old
3 doses 6-10-14weeks
• 6 months to 8 years old:
2 doses with interval
• 0.25 mL for 6-35
of 4 weeks if receiving
Influenza months
IM 6 months vaccine for the is1 time
vaccine • 0.5 mL for 36
then annually thereafter
months-18 years old
• 9-18 years old:
1 dose annually
143
MINIMUM TIMING OF
VACCINE ROUTE DOSE/NOTES
AGE ADMINISTRATION
• May be given as
Measles • 9 months old
SC 9 months early as 6 months
vaccine • Booster given as MMR
during outbreaks
• 9 months to 17
years old: 2°• dose
Japanese given 12-24 months
encephalitis SC 9 months
(IE) vaccine after 1st dose
• Single dose
for =1:18years old
• Children <12
Measles • 2 doses at least 4 months given any
Mumps weeks apart measles containing
SC 12 months
Rubella • 2"' dose usually at vaccine should
(MMR) vaccine 4-6 years old receive additional 2
doses ofMMR
• <13 years old:
interval between
2 doses ideally
• 2 doses
Varicella at least 3 months
SC 12 months • 2°• dose
vaccine (but 4 weeks is
at 4-6 years old
acceptable)
• =1:13years old:
4 weeks interval
Hepatitis A • 2 doses • See discussion on
IM 12 months
vaccine 6 months apart succeeding pages
• History of sexual
abuse: begin series
• 9-14 years old:
at 9 years old
Human 0 and 6 months
• lmmunocompromised
Papilloma (2 doses)
Virus (HPV) IM 9 years old 9-26 years old: 3
• 15 years and older:
vaccine doses (0, 1-2, 6
0, 2, 6 months
months)
(3 doses)
• Pregnancy: not
recommended
• Primary series:
6-10-14 weeks
• Not routinely given
Hib vaccine IM 6 weeks • Booster at 12-15
>5 years old
months (6 months
from the 3rd dose)
• For fully immunized 7-18 years old (received 5 doses of DTP
or 4 doses of DTPif 4th dose was given =1:4 years of age): 1 dose
Tdap then Td booster every 10 years
Tetanus- • For unvaccinated 7-18 years old: 3 doses at 0,1,6 months,
reduced with Tdap as the first dose and Td for the remaining doses
diphtheria- • For incompletely vaccinated 7-18 years old: 1 dose Tdap
acellular
IM
then Td for the remaining dose at least 1 month after
pertussis • Fully immunized pregnant adolescent: give 1 dose Tdap any
(Tdap) time after 20 weeks AOG
• Unimmunized pregnant adolescent: give 3 dose Td
containing vaccine (Td/Tdap) following 0-1-6 month schedule.
Tdap should replace Td preferably after 20 weeks AOG
144
(")
AGE IN BIRTH WEEKS MONTHS YEARS :t
0 2 4 6 8 10 12 14 16 18 20 22 6 8 10 12 14 16 18 20 2 4 6 8 10 12 14 16 18 r
C
:t
Legend: 0
Rangeof Recommended
Age BCG ,BJ 0
C
Hep B HJB ~
I
Hep B• Hep B•
s:
C
Catchup immunization (DTwP-Hib-
I I I Hep B• .. : z
~
Hep B) and
other DTaP
c,,.......
p,.,.. DTwP•/OTap•
I I I l I I I I I
NOTE:Forthe latest
ChildhoodImmunization Schedule
combo
IPV/OPV
'0~1
.•~
II
OPV•/IPV
.I
OTwP•/oTap•
I !l I
OTaP
IPV
HiB
DT•P..
OPV
Tdap/Td
6
z
I I OPV•/IPV en
(usuallyupdatedeveryFebruary) ..- -
visit www.philvaccine.org. PCV
PCV pcv• I I --l
I PCV• l l I !
(")
:t
I I
I I i I I
PCV m
C
RV
Influenza
RV Series•
I
I 11 II III Influenza Yearly
·,-,
C
r
m
I I I
...
N
I I I II I !
0
I
Measles Measles
1· (0
JE Vaccine
I I I JEV
I I I
. I I I I I I I I i I I I I
MMR MMR MMR
I I I I I I !, ! I
Varicella j llrh:ell:.
I
Varicella
I I I I I I I I I
Hep A Hep A Series
'·'"'
I I I I
IIII
I
HPV
I I I
HPVScries
I I I I
-
Source:ChildhoodImmunization
Scheduleby PediatricInfectiousDiseaseSocietyof the Philippines,PPPS,andPhilippineFoundationfor Vaccination:
2019.
Accessedat www.philvaccine.org
.
I. HEPATITIS B VACCINE
• Administration of a 4th dose is permitted when a combination vaccine containing Hep B
is used after the birth dose (as in the case of our EPI).
• Minimum age for the final dose is 24 weeks old (if 3 dose series is used)
• If 3rd dose is given earlier, give 4th dose at least 4 weeks from the 3rd dose
146
II. RABIES VACCINE
A. Post-Exposure Prophylaxis
CATEGORY I CATEGORY II CATEGORY Ill
(No exposure) (Exposure) (Severe exposure)
• Transdermal bites
(puncture wounds,
lacerations, or
avulsions), scratches
• Feeding/ touching
or abrasions with
an animal
spontaneous bleeding
• Licking of intact • Nibbling of
• Licks on broken skin
skin uncovered skin with
or mucous membrane
• Sharing of eating or or without bruising
• Exposure to a rabies
drinking utensils or hematoma
patient through bites,
with a person with • Minor or superficial
Description contamination of
rabies scratches /abrasions
mucous membranes,
I
• Casual contact and without bleeding,
or open skin lesions
routine delive1y including those
with body fluids
of health care to induced to bleed
• Unprotected handling
patients with signs
of infected carcass
and symptoms of
• Ingestion of raw
rabies
infected meat
• Exposure to bats
• AllcategoryIIexposures
on the head and neck
Management
• Immediate vaccination
using any of the
following schedules
regardless of the status
• No vaccine or rabies of the biting animal • Immediate
immunoglobulin 0 2-sites ID vaccination using
For (RIG) needed on days 0, 3, 7 any of the schedules
immunologically • Pre-exposure 0 1-site IM suggested in Category
naive patients prophylaxis may be on days 0, 3, 7 and II exposure
considered for high- between day 14-28 • RIGadministration
risk persons 0 2-sites IM on day 0
and 1 site IM on
days7,21
• Rabiesimmunogiobulin
(RIG) is not indicated
• Immediate vaccination using ANY of the following:
0 1-site ID on days 0,3
For previously
• No vaccine or rabies 0 4-sites ID on day 0
immunized
immunoglobulin 0 1-site IM on days 0,3
(i.e. received
(RIG) needed • Immediate vaccination not needed if complete
PrEP or PEP)
PEP received <3 months prior
• RIGnot indicated
Notes:
• Forall categories,exposedskinshouldbe washed immediately withsoap and water
• Vaccinationregimenin BOLD text are the ones commonlyused in localpractice
Rabiesimmunoglobulin (RIG)
0ERIG(equine)40 units/kgor HRIG(human)20 units/kgIM
02018WHOguidelinessuggest that maximuminfiltration of RIGintoand aroundthe woundis effective
0Benefitof IMadministrationof remainingRIGis likelyto be verylimited(WHOno longerrecommendsthis)
0RIGshouldnot be givenafter7 days followingthe firstrabiesvaccinedose
0Skintestingis not recommended
147
8. Pre-Exposure Prophylaxis (PrEP)
0 WHO recommends PrEP for individuals at high risk of exposure and in populations
living in rabies endemic areas (dog bite incidence >5% per year or vampire bat rabies
is known to be present)
0 Pre-exposure Prophylaxis Anti-Rabies Act 2007: for children ages 5-14 years old (high
incidence: >2.5 human rabies/million population)
0 Latest recommendations (2018) for schedule of PrEP as follows:
Two-site intradermal vaccine 0.1 mL on days O and 7
• One-site intramuscular vaccine 0.5 mL or 1 mL (depending on manufacturer) on days O& 7
C.Antibiotics
0 Given for all Category Ill wounds and all frankly infected wounds
0 Drug of choice: Co-amoxiclav 40-50 mg/kg/day in 2-3 divided doses for 7 days
0 Alternative: Clindamycin 20-30 mg/kg/day in 4 divided doses
WorldHealthOrganization.
Sources: WHOposition
Rabiesvaccines: 2018
paper.Vaccine;
MP committee oninfectious 2018
diseases.Pediatrics;
RobinsonC. el al. MMWR.MorbidityAndMortalityWeeklyReport:2018
PPS/ PIDSP/ PFVChildhoodImmunization Schedule2019
III. TYPHOID FEVERVACCINE
• Recommended for travelers to areas where there is risk of exposure & for persons with
frequent exposure to 5. typhi
• Single IM dose may be given as early as 2 years old
Revaccination every 2-3 years if there is continued exposure to S. typhi
In spite of vaccine availability, sanitation and good hygiene remain the best preventive measures
Two available forms
0 Live oral for 6 years old and above: 4-dose schedule at 0, 2, 4, 6 days
0 Inactivated polysaccharide vaccine: 1 dose IM every 2 years
IV. PNEUMOCOCCALPOLYSACCHARIDEVACCINE
Minimum age: 2 years old
• Given for high risk population
• Give 1 dose at least 8 weeks after final dose of PCV to high-risk children 2 years and older
• Congenital immunodeficiencies
• Chronic heart disease, heart failure, and
• HIV infection
cardiomyopathies
• Chronic renal failure or nephrotic syndrome
• Chronic lung disease (COPD, asthma,
• Leukemia or lymphoma
emphysema)
• Generalized malignancy
• Diabetes mellitus
• Solid organ transplant
• CSF leaks
• Multiple myeloma
• Cochlear implant
• Iatrogenic immunosuppression
• Alcoholism
(treatment with immunosuppressive drugs,
• Chronic liver disease
radiation therapy)
V. POSTEXPOSUREPROPHYLAXISFORCOMMONVIRAL EXANTHEMS
SCREENING TESTS
I. RECOMMENDEDSCREENINGTESTS
AGE GROUP TEST
Infancy • Developmental surveillance and screening
• Developmental surveillance and screening
Childhood
• Done at 9 months, 18 months, 30 months, and every year thereafter
• Screening for alcohol and drug use
0 14 to 21 years old, at every health encounter
DENTAL CARE
I. DENTAL VISITS (Recommendation from Philippine Pediatric Dental Society, Inc)
• First dental visit should be done at the time of eruption of the first tooth and no later than
12 months of age
• Follow-up dental visits at 18 months through 6 years old and every year thereafter
• Adult supervision on oral hygiene is recommended until 6-8 years old
150
II. SIGNS AND RED FLAGS
Source:PediatricPreventiveHealthCare Handbook2018
151
INFANT & CHILD NUTRITION
• Proper nutrition is crucial to optimal growth and development
• Rapid growth rates in children are accompanied by high maintenance needs
II. MICRONUTRIENTSUPPLEMENTATION
AGE PREPARATION DOSE/ DURATION
1) Iron Supplementation*
For low birth weight • Drops with 15 mg elemental • 0.3 mL once a day to start at 2
(1,500-2,499 grams) iron per 0.6 mL months old until 6 months old
Infants • Drops with 15 mg elemental • 0.6 mL once a day for 3
6-11 months old iron per 0.6 mL months
• 5 mL once a day for 3 months
• Syrup with 30 mg elemental or 30 mg once a week for
1-5 years old
iron per 5 mL 6 months with supervised
administration
• Tablet with 60 mg elemental
Adolescent females
iron with 400 mcg folic acid • One tablet once a day
10-19 years old
(coated)
2) Vitamin A Supplementation
• One dose only (one capsule is
given anytime between 6-11
Infants 6-11 months
• 100,000 1.U. months old, but usually given
old
at 9 months old during the
measles immunization)
Children 12-71
• 200,000 1.U. • One capsule every 6 months
months old
'Recommendationfromthe PhilippineSocietyof PediatricHematology:a CBCto screen for anemiaat least once
betweenthe time intervalsfor those at risk:6-24 monthsold,2-6 years old, 10-19years old.The Societyof Adoles-
cent Medicineof the Philippinesrecommendsat least once at each stage of adolescence.
Source:DOHPhilippines.
UpdatedGuidelineson Micronutrient
Supplementation. DOH:2013
KliegmanR.et al NelsonTextbook
of Pediatrics(21sted).Elsevier:2020
152
DEWORMING
I. INDICATIONS& CONTRAINDICATIONS
INDICATIONS CONTRAINDICATIONS
• Severe malnutrition
• High-grade fever
• Profuse diarrhea
• Dewonning for children 1-12 years old • Abdominal pain
• Serious illness
• Previous hypersensitivity to
anti-helminthic drug
II. REGIMENS
DRUG* AGE GROUP** DOSE FREQUENCY
• 12-23 months old • 200 mg • Single dose, every 6 months
Albendazole
Mebendazole
• 24 months and above
• 500 mg
• Single dose, every 6 months
Source:
DOHRevised
Guidelines
onMassDrugAdministration
& Management
ofAdverse
EventsFollowing
Deworming
REFERENCES
1. AAP Committee on infectious diseases. Recommended Childhood and Adolescent
Immunization Schedules: United States, 2018. Pediatrics. 2018;141(3): e20180083
2. ClinicalPractice Guideline on "The Routine Eye Examination as a Screening Tool for Retinoblastoma"
3. Department of Health. DOH Philippines Administrative Order No.119 s. 2003. "Updated Guidelines
on Micronutrient Supplementation (Vitamin A, Iron and Iodine)."Available from< https:/ /ww2.fda.gov.ph/>
4. Department of Health. DOH Administrative Order 2015-0054 Revised Guidelines on Mass
Drug Administration and Management of Adverse Events Following Deworming and Serious
Adverse Events. Available from <l1ttps://www.doh.gov.ph>
5. Department of Health. Updated Guidelines on Micronutrient Supplementation. DOH; 2013.
Available from <https:/ /www.doh.gov.ph>
6. Kimberlin DW, Brady MT.Jackson MA, Long SS, eds. Red Book: 2018 Report of the Committee
on Infectious Diseases. 31st ed. Itasca, IL: American Academy of Pediatrics; 2018
7. Kliegman, R., Stanton, B., St. Geme, J., Scho1; N., and Behrman, R.. Nelson Textbook of
Pediatrics 21st ed. 2020. Canada: Elsevie1:
8. Navarro, X., Bauzon, A., Aguila 1:)., and Malanyaon, 0. Fundamentals of Pediatrics
Competency-based 1st ed. 2014. Quezon City: C & E Publishing, Inc.
9. Pediatric Preventive Health Care Handbook 2018. Philippine Pediatric Society. Philippines, 2018
IO.Pediatric Infectious Disease Society of the Philippines, Philippine Pediatric Society and
Philippine Foundation for Vaccination. Childhood Immunization Schedule 2019. Available
from < http://www.phitvaccine.org/>
11.Republic of the Philippine Congress. Republic Act No. 7610 - Special Protection of Children Against
Child Abuse, Exploitation, and Discrimination Act. Available from< https:/ /pcw.gov.ph/law /
republic-act-7610>
12.Richerson JE, Simon GR,Abularrage JJ,et al., Committee On Practice And Ambulato1y Medicine; Bright
Futures Periodicity Schedule Workgroup. 2017 Recommendations for Preventive Pediatric Health
Care. Pediatrics. 2017 Apr;139(4). pii: e20170254. doi: 10.1542/peds.2017-0254. Epub 2017 Feb 17.
13.Robinson, C.,Romero,)., Kempe, A., Pellegrini, C.,& Szilagyi, P. (2018). Advisory Committee on
Immunization Practices Recommended Immunization Schedule for Children and Adolescents
Aged 18 Years or Younger- United States, 2018. MMWR. Morbidity And Mortality Weekly Report,
67(5), 156-157. doi: 10.15585/mmwr.mm6705e2
14.World Health Organization. (2018). Rabies vaccines: WHO position paper, April 2018 -
Recommendations. Vaccine, 36(37), 5500-5503. doi: 10.1016/j.vaccine.2018.06.061
153
154
NEONATOLOGY
SECTION ONE
EVALUATING THE NEWBORN
DEFINITION OF TERMS
I. PERIODS OF DEVELOPMENT
PERIOD DURATION
Perinatal Period • 28'h week of gestation to 7'" day after birth
• First 28 days after birth
• Further subdivided into:
Neonatal Period 0Very early: birth to < 24 hours
0Early: birth to 7 days
0Late: 8 days to 28 days
Infancy
II. GESTATIONALAGE
• Birth to 1 year
157
• Age of gestation upon delivery
• Was the delivery induced and reason for induction
• Mode of delivery (spontaneous vaginal, cesarean, forceps,
vacuum assisted, anesthesia or sedation)
• Total duration oflabor and delivery
• Oligohydramnios / polyhydramnios
Peripartum • Premature rupture of membranes (PROM) defined as rupture
> 18 hours prior to delivery
• Place of delivery
• Attendant during the delivery (OB, midwife, traditional birth
attendant)
• Appearance of the cord and the placenta
• Presence of complications
Source:KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Elsevier:2020
GleasonC, et al. Avery'sdiseasesof the newborn(10thed.).Elsevie:2017
II. VITALSIGNS
PARAMETER NORMAL VALUES/REMARKS
Respiratory Rate (RR) • 30-60 counts per minute (cpm)
Heart Rate (HR) • 120-160 beats per minute (bpm)
Core Temperature • 36.5° - 37.5° C
• Not routinely taken in newborns unless there are signs and
Blood Pressure (BP)
predisposing factors associated with circulatory problems
158
Ill. APGAR SCORE
• Taken at 1 and 5 minutes after birth
• May be repeated at 5-minute intervals for infants with 5 minute scores <7
• It is used as method of reporting the status of the newborn and the response to resuscitation
• However, it is important to note the following:
0 Several factors may affect the APGARscore (e.g., prematurity, sedative drugs,
congenital anomalies, neuropathies)
0 There is no consistent data on the significance of APGARscore on preterm infants
It is not used to established asphyxia
It does not predict specific neurologic outcomes
• A low 1-minute score does not correlate with outcome; but the 5-minute score is a valid
predictor of neonatal mortality
G rimace
(reflex irritability)*
• Absent
• No response
• < 100 bpm
• Grimace
•>l00bpm
• Cough or sneeze
• Pulls away, crying
I
A ppearance • Body pink,
(skin color) • Blue, pale • Completely pink
extremities blue
Interpretationof theAPGARScore:
• 7-10 points:goodcardiopulmonary adaptation,newbornwilldo well
• 4-6 points:needforresuscitation,
especiallyventilatory
support,& medicalintervention
• 0-3 points:needforimmediateresuscitationand mayneed NICUcare
Source:ApgarV.A Proposalfor a NewMethodof Evaluationof the NewbornInfant.Anesthesia& Analgesia:1953
KliegmanR. et al. NelsonTextbookof Pediatrics(21sted.). Elsevier:2020
GleasonC, et al.Avery'sdiseasesof the newborn(10thed.). Elsevie:2017
Case: At the 1" minute of life, a newborn was noted to have acrocyanosis, HR of 130 bpm
grimaces to stimulation, good respiration, and with active movement of extremities. What
is the APGAR score at this time?
A= 2 (active movement)
P = 2 (HR> 100)
G = 1 (grimace)
A= 1 (acrocyanotic)
R = 2 (regular respiration)
SCORE= 8
159
IV. BALLARDSCORINGSYSTEM (MATURITY RATING)
• Used for maturational assessment of gestational age
• Accuracy is +/- 2 weeks the actual gestational age
• High risk for mmtality or morbidity if a discrepancy exists between the estimation of gestational
age by examination, the mother's estimated date of her LMP,and fetal ultrasound evaluation
• Full term infants are scored as early as possible and may be reliably scored within 72
hours of birth
• Extremely preterm infants should be scored within the first 12 hours of life
• Divided into two groups of scoring system:
0 Physical maturity
0 Neurologic maturity
• The physical and neurologic scores are added, the sum of which calculates gestational age
A. Physical Maturity
I -1 I 0 1 2 3 4 5
Smooth. Superiicial Parchment
Sticky, Gelatinous. Cracking. Leathery,
Pink peeling deep
SKIN friable. red. pale areas, cracked
visible and/or rash cracking
transparent translucent rare veins Wrinkled
veins few veins No vessels
Stripped Raised
Barely Flat areola, Full areola.
BREAST Imperceptible areola, areaola.
perceptible no bud 5-10mm bud
1-2mm bud 3-4mm bud
Slightly Well-curved
Lids fused: lids open, Formed and Thick
curved pinna. soft
EYE/EAR loosely (-1). pinna flat. firm. instant cartilage, ear
pinna: sett. but ready
tightly (-2) stays folded recoil stiff
slow recoil recoil
Scrotum Testes in Testes Testes Testes
GENITALS Scrotum flat.
empty. faint upper canal. descending, down, good pendulous.
MALE smooth
rugae rare rugae few rugae rugae deep rugrae
Prominent Prominent Majera and
Clitoris Majera Majera
GENITALS clitoris. clitoris, minora
prominent. large, cover clitoris
FEMALE small labia enlarging equally
labia flat minora small and minora
minora minora prminent
8. Neurologic Maturity
-1 0 1 2 3 4 5
Posture ~ ~ o¢=c ~ ~
Square
Window
(Wrist) r r r
>90° go• 60°
~
45°
~
30°
I
o•
Arm Recoil
~180°
11'-i}- ½
140-180° 110-140° 90-110°
{}
<90°
c6 ~ ~
Popliteal
Angle ~ ~ ~ c6
180° 160° 140° 120° 100° goo <90°
Scarf Sign
tr ~ & ~ ~ §
Heel to Ear GE:=) ci=:3 CC3 ~ CX:B ~
--------------- . ···--·--·----- ----- I
160
PARAMETER INSTRUCTIONS ILLUSTRATION
Square window
• Straighten the infant's
fingers and apply gentle
pressure on the dorsum of the
hand, close to the fingers
I
• With the infant lying supine,
the examiner places one
hand beneath the elbow for
support.
• Elbow is then placed into
flexion then momentarily
extends the arm before
Arm recoil
releasing the hand.
• The angle of recoil to which
the forearm springs back to
flexion is noted
• A score of 4 is when there is
contact between the infant's
fist and face
161
• With the infant lying supine
and head in the midline,
the examiner supports the
infant's hand across the
upper chest with one hand
Scarf sign
• Thumb of the examiner's
other hand is placed on the
infant's elbow
• Elbow is nudged across the
chest until resistance is felt
• Infant is placed in supine
position & the flexed lower
extremity is brought to rest
on mattress alongside the
trunk of the infant
• Other hand is used to hold
Heel to ear
foot at the side & to pull it
toward the ipsilateral ear
• Location of heel where a
significant resistance to
extension of the posterior
pelvic girdle flexors is noted
V. ANTHROPOMETRICS
• Birth weight, birth length, head circumference and chest circumference are plotted
against gestational age on standard growth curves shown on next page {Lubchenco Chart)
• A different chart is used for premature infants (Fenton Chart)
162
B. Classification based on Birth Weight versus Gestational Age (using the Lubchenco Chart)
Small for gestational age: birth weight below 10'" percentile
0 Appropriate for gestational age: birth weight between 10'" to 90'" percentile
Large for gestational age: birth weight above 90'"-percentile
PRETERM TERM
GM I I I
4250 WEIGHT
I
-
4000
3750 90 %
3500
3250
3000
.,.i...- - - I
·50 %
~ ,
2750 ,
2500 , ,, ,,. -i- 10 %
2250
2000
,,
,J,,
, V
, I'
1750 .,,,. ,
---,,,,.-~, /
- --
1500
/
1250
1000
750 ·i
500
'""1'""
I
I
250
o
24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43
CM
53 90%
52 ~LENGTH
51
49
48
47
45 10%
44
43
42
40
39
38
37
35
34
33
31
30
29
28
26
25
26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42
CM
39
39 HEAD CIRCUMFERENCE
38
37
90%
36
35
50%
H~~
31
10%
31
30
29
28
27
26
~~ ii
22
21
20 Source:
LubchencoL.,etal.Journal
ofPed,ilrics;
1966
26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 F.,etal.
Battagl,i Journal
ofPed@lrics;
1967
WEEK OF GESTATION LowdermilkDL,etal.SLLouis;
2007
163
VI. SPECIFICEXAMINATIONOF THE NEWBORN
ASPECT DESCRIPTION
1) Genera IAppearance
'
• Assess overall appearance/color
Observe infant
• Assess respiratory effort and any signs of distress
in a resting non-
stimulated state • Assess position/posture & movement/activity ( e.g., asleep, alert)
• Assess quality of cry /suck
i) SRin II " ~ -c
164
Caput • Edema of scalp skin
succedaneum • Crosses suture line
• Minimal bleeding
• Resolves in 2-3 days
Cephalhematoma • Subperibsteal in location
• No edema or discoloration of the scalp
• Does not cross the suture line
• Bleeding is rarely severe
• Resolves in 2-3 weeks
Subgaleal • Beneath epicranial aponeurosis
hemorrhage • May extend to orbits (racoon eyes) & nape
• Bleeding may be massive
Check for Trauma • Resolves in 2-3 weeks
I
Skm
Gal:::~eE:r~s1s
....
•··. ....•····
... ..
Penosteum ···· ··
Skull
Dura
4J Eyes
• Often open spontaneously if the infant is held up and tipped gently
General Findings forward and backward
• Pupillary reflexes present after 28-30 weeks AOG
• White pupillary reflex (warrants immediate ophthalmologic consult)
Leukocoria
• Suggests cataracts, tumor, chorioretinitis, retinopathy of prematurity
Subconjunctival • Regresses spontaneously (85% resolve by 2 weeks of age; in all
Hemorrhage infants by 4 weeks; no treatment needed)
• Congenital malformation of the eye causing defects in the iris, lens,
Coloboma
or retina (small notch to a large cleft)
Aniridia • Absence of the iris
Congenital
• Tearing, photophobia, and cornea > 1 cm in diameter
Glaucoma
5) Ears
Skin tags, pits,
malformed ears • Associated with hearing and other anomalies
165
• Presence of teeth at birth
Natal teeth
• Should be removed by a dentist to prevent the risk of aspiration
• Examine closely the throat and check for palatal or uvular clefts
Throat • Contour of the palate must be noted if the arch is excessively high
or the uvula is bifid
,.
7) N·ose ~r -
General Findings • Newborns are obligate nose breathers
Choanal atresia • Inability to pass a feeding tube through the nares
C
8) Neck ., lJ
Branchial cleft • Incomplete closure of branchial clefts
cysts • Found lateral and anterior to the sternocleidomastoid muscle
Thyroglossal duct
• Cystic dilatation of thyroglossal duct remnants seen in the midline
cysts
Congenital
• Head turned toward and the face turns away from the affected side
torticollis
Redundant skin
• Suggests Turner syndrome if in females
or webbing of neck
9) Chest I~ ;,,
I
Females covers labia minora
• Blood tinged discharge is due to withdrawal from maternal estrogen
• Inspect phallus, retract prepuce to view the urethral orifice
• Hypospadia: urethral orifice located on the glans or ventral surface
of the shaft
• Chordee: caudal curvature of the penis due to incomplete
development of the foreskin
Males • Testes: commonly palpable in the scrotum, may be retractable
• Persistence of processus vaginalis:
0 Inguinal hernia: opening at the inguinal ring allows extrusion of
the abdominal viscera with increased intra-abdominal pressure
0 Hydrocele: narrow opening at the inguinal ring allows peritoneal
3) Placing/Stepping Reflex
• Stimulating dorsum of
the foot against the edge
of the examining table • 37 weeks AOG • 4-5 111onths
• Response: infant lifts
leg on the table
168
5) Tonic Neck (Fencing) Reflex
• Placing pressure on
the palm of the sole
• Response: similar • 11 weeks AOG • 7-9 months
response as the palmar
grasp reflex but weaker
7) Landau Reflex
I
• Examiner lifts the
infant with one hand
under the trunk
facing downward • Covered up by
• 3 months
• Response: extension voluntary action
of the vertebral
column causing the
infant to lift head
8) Parachute Reflex
• Examiner supports
the infant's trunk and
suddenly lowers the
• Covered up by
infant as if he/she • 4-9 months
voluntary action
were falling
• Response: the arms
extend to break the fall
9) Crawling Reflex
• If baby is placed on
stomach, he/she will
pull legs under the
body & kick them out
in a crawling motion
• Disappears after
• When babies are • 28 weeks AOG
just a few weeks
placed on mother's
stomach, they are
able to crawl up to the
breasts and start
suckling
Source:KliegmanR.et al. Nelsontextbookof pediatrics(21sted.).Canada:Elsevier;2020
MenkesJ, et al. ChildNeurology(7thed.).LippincottWilliams& Wilkins;2006
169
SECTION TWO
ES.SENTIAL INTRAPARTUM AND.NEWBORN.CARE
I. EINC CORESTEPS
STEPS MANAGEMENT
• Immediately dry the baby to stimulate breathing and to avoid hypothermia
for a full 30 seconds unless the infant is both floppy/limp and apneic
• Sequence of drying is as follows (5 seconds each): face, head, trunk, back,
Immediate arms, legs
and
1 • Hypothermia can lead to infection, coagulation defects, acidosis, delayed
Thorough
fetal to newborn circulatory adjustment, hyaline membrane disease, or
Drying
brain hemorrhage
• Routine suctioning of nose and mouth has no proven benefit unless
meconium stained and the baby is limp or apneic
• Place the baby on mother's chest or abdomen to provide warmth & allow the
"good bacteria" from the mother's skin to infiltrate the newborn
• Increases the duration of breastfeeding
• Technique (if breathing or crying):
• Position prone on the mother's abdomen or chest in between the breasts
• Cover the newborn
0 Dry linen for back
NEWBORN CARE
ASPECT MANAGEMENT
I
• For all infants, including those born by cesarean section
• To protect against gonococcal ophthalmia neonatorum
• Medications:
Eye prophylaxis
0Erythromycin ointment 0.5% or tetracycline ointment 1%
0Alternative is Crede's prophylaxis: 1% silver nitrate solution (can
lead to a transient chemical conjunctivitis in 10-20% of cases)
• Dose: 0.5-1.0 mg IMat anterolateral thigh
VitaminK
• To prevent hemorrhagic disease of the newbor
• Bacillus Calmette-Guerin (BCG):0.05 mL intradermally
• Hepatitis B vaccine (0.5 mL)
Vaccinations
• Hbig IM (0.5 mL) if mother is HBsAg-positive or if mother's HBsAg
status is unknown and birth weight is < 2 kg
Source:WHO.EarlyEssential
Newborn
CareClinicalPractice
Pocketguide.Geneva,Switzerland: WHO:2014
WHO.Newborncareuntil the firstweekof life. Geneva:WHO;2009
171
III. DISEASES SCREENED IN THE EXPANDED NEWBORN SCREENING
DISORDERS SPECIFIC DISEASES
• Congenital Hypothyroidism
Endocrine
• Congenital Adrenal Hyperplasia
• Homocystinuria
• Hypermethioninemia/Methionine
Amino acid • Adenosine Transferase Deficiency
disorders • Maple Syrup Urine Disease
• Phenylketonuria
• Tyrosinemia Type I, II, III
• Carnitine Palmioyltransferase I & II Deficiency
• Carnitine Uptake Deficiency Glutaric Acidemia Type II
Fatty acid
• Long Chain Hydroxyacyl-CoA Dehydrogenase Deficiency
disorders
• Medium and Very Long Chain-Acyl-CoA Dehydrogenase Deficiency
• Trifunctional Protein Deficiency
• 3-Methylcrotnyl CoA Carboxylase Deficiency
• Beta Ketothiolase Deficiency
• Glutaric Acidemia Type I
Organic Acids • lsovaleric Acidemia
• Methylmalonic Acidemia
• Multiple Carboxylase Deficiency
• Propionic Acidemia
• Citrullinemia
Urea cycle defects
• Argininosuccinic Aciduria
• Alpha & Beta Thalassemia
Hematologic • Hemoglobin C, Hemoglobin D, Hemoglobin E
• Sickle Cell Disease
• Galactosemia, Cystic Fibrosis Biotinidase Deficiency
Others
• Glucose-6-Phosphate Dehydrogenase Deficiency,
172
SECTION THREE
N'EONATAL RESUSCITATION
NEONATAL RESUSCITATION
• Done to prevent the morbidity /mortality associated with hypoxic-ischemic tissue injury
and to reestablish adequate spontaneous respiration and cardiac output
• At the delivery of a newborn, the first step is immediate thorough drying and quick
assessment for thirty seconds
• The most important initial question to ask is "ls the baby apneic/gasping or limp"? - this
will differentiate a baby who will receive EINCand those that will be needing resuscitation
• Preparation is important:
Assessment of intrapartum and antepartum risk factors
Preparation of materials and personnel knowledgeable in newborn resuscitation
Teamwork and communication during resuscitation
Birth
'-----'
U ~
I ...-:
I. Immediate
thorough
drying and
i quick
j
!
Apnea/
gasping or
limp
NO
Small baby?
I
I________________
'
assessment
:
YES
YES
j 1. Callfor help :
j 2. Changewet linen
: 3. Clamp and cut the cord
i 4. Transfertowarmer
! S. Position airway
: 6. Clear secretionsif needed
Stal
Labored breathing NO Post-resuscitation
Apnea / gasping or
or persistent care
HR<l00bpm
cyanosis Transport
Mask adjustment Team debriefing
Reposition Airway
Open mouth
Pressureincrease
Airway alternative
lmin: 60-65%
2min: 65-70% HR<60bpm
3min; 70-75%
4min:
Smin:
75-80%
80-85%
·--~Esi
14. IV epinephrine
lOmin:85-05% 15. Consider hypovolemia
16. Consider pneumothorax
Resuscitation
shouldproceedrapidly.Onehasapproximately30 seconds(or60secondsif chestcompressions)
to achievea response
fromonestepbeforedecidingwhetheryouneedto moveon to thenext. Evaluation anddecision-making
arebasedpnmarilyon
respiralions,
heartrate,andoxygenation
(bypulseoximetryprimanly;colorin previousprotocols)
173
RESUSCITATIVE EFFORTS
174
SECTION FOUR
BREASTFEEDING
OVERVIEW OF BREASTFEEDING
WHO/UNICEF global strategy on infant and young child feeding (2002) recommends
exclusive breastfeeding (i.e., no other food or drink, even water) for the first 6 months
• Breastmilk is the most appropriate nutrition for the infant. It is uniquely adapted for the
infant's needs for growth and development
I. ADVANTAGESOF BREASTFEEDING
• Most appropriate food for the infant
• No risk of contamination
• Cost-effective
• Protection against colic, atopic dermatitis, GI bleeding and other diseases
• Decreases incidence of diarrhea, UTI, respiratory tract infection, CNS infections, middle
ear infections, necrotizing enterocolitis, sepsis and botulism
II. BREASTMILKCOMPOSITION
175
IV. PHYSICALASPECTS
WITHIN A FEED REMARKS
• Curds are the semi-solid fraction which settles out when milk
is clotted, and whey is the clear fluid which remains. Curds are
made from the casein proteins.
Curds/whey • Human milk has low casein:whey ratio
10:90 in early milk
0
Bioactive Comp61!f;!lts
"'
} - ,.,,, .,,, .,~-. '"--"'
• Protection against specific
Maternal
secretory IgA antigens + -
Maternal WBC • For phagocytosis of pathogens
+ -
Lysozyme • Lysis of bacteria
+ -
• Inhibits binding of pathogens
Milk lipids to host cells and causes lysis
of enveloped pathogens
+ Less effective
Epidermal growth
factor
• Promotes maturation of gut
+ -
• Mediators necessary to mount
Cytokines an antibody defense against
foreign organisms
+ -
176
Bile salt
stimulated lipase
(BSSL)
• For fat digestion +
• Palmitic acid, Oleic acid,
Linolenic acid,
Docosahexaenoic acid (DHA), Complete
Essential fatty Fewer and less
Linoleic Acid, Arachidonic acid and highly
acids bioavailable
• Wide function of activity such bioavailable
as CNS development and
retina development
177
• Refrain from breastfeeding and infant contact until treated
Tuberculosis
• No longer considered contagious after 2 weeks of treatment
Herpetic lesions on the • Avoid breastfeeding until active lesions have resolved
breast • Vaginal herpes is NOT a contraindication
• Express milk until lesions are crusted over. Administer varicella
Varicella
immunoglobulin to infant
• If safer alternatives are available, HIV infected mothers should not
breastfeed
Human
• WHO recommends breastfeeding in HIVinfection endemic areas
immunodeficiency
unless safe infant formula is readily available. The risks associated
virus (HIV)
with formula feeding in developing countries is greater than the risk
of acquiring HIVinfection with breastfeeding
Use of illicit drugs • Absolute contraindication
• Seek specialty consultation
Cancer chemotherapy
• Generally contraindicated for the duration of treatment
or radiation treatment
• Expressed breastmilk should be discarded during this time
Source:
Andreas
N, et al. Humanbreastmilk:A reviewonitscomposition andbioactivity.
EarlyHumanDevelopment; 2015
WuX, et al. HumanMilkNutrientComposition in the UnitedStates:CurrentDevelopmentsIn Nutrition;2018
GleasonC, et al.Avery'sDiseasesof the Newborn(9thed.).Elsevier;2012
Academyof Breastteeding Medicine.HumanMilkStoragelnfomnalion. BreastteedingMedicine;2018
CDC.ProperHandlingandStorageof HumanMilk;2015and2017
178
SECTION FIVE
APPROACH TO COMMON PROBLEMS OF THE NEWBORN
APPROACH TO APNEA
I. DEFINITION OF TERMS
TERM DEFINITION
• Normal respiratory pattern in neonates
Periodic breathing • Brief episodes of respiratory pauses 5-10 seconds followed by rapid
respirations 50-60 breaths/min lasting for 10-15 seconds
• Absence of the brainstem stimulus to breathe
Central apnea
• No respiratory effort
Severe apnea
apnea
179
III. DIAGNOSTICS
• ABGto rule out hypoxia and/or acidosis
• CBCwith differential count to check for infection, anemia, polycythemia
• Cultures
• Electrolytes: Na, Ca, Mg, glucose
• For inborn errors of metabolism: organic acid levels, amino acid profiles, ketones in urine
• Chest radiograph
• ECG
• Abdominal radiograph
• Ultrasonography of head if suspecting hypoxic ischemic encephalopathy
IV. MANAGEMENT
• See neonatal resuscitation
• Tactile stimulation with supplemental oxygen (1-2 LPM via
Emergency treatment nasal cannula)
• Bag-mask ventilation or intubation if necessary
• Once stabilized, work-up for suspected etiology
Determine cause • Rule out treatable causes before diagnosis and treatment of
of apnea & start
treatment if possible apnea of prematurity
180
APPROACH TO ABNORMAL STOOL PATTERNS
• 99% of term infants, 100% of post-term infants, and 76% of preterm infants should pass
stool in the first 24 hours of life
• Infants have a mean of 4 stools per day during the first week of life, which gradually
decreases to 1.7 per day at 2 years
• The first passage of meconium is a marker of normal gastrointestinal function
• Delayed meconium passage may occur due to gestational immaturity, severe illness, or
bowel obstruction (this may predispose the infant to bowel perforation)
I
disease pass out meconium
• If abnormal stools recur, rule
out Hirschsprung disease
2) Small Left Colon Syndrome
• Due to transient • Plain radiograph findings: • Contrast enema is diagnostic
dysmotility in descending 0 Dilated intestinal loops and therapeutic
colon among term infants 0 Air-fluid levels • Surgery is indicated for
• 50% have mothers with recurrence or perforation
diabetes mellitus
3) Hirschsprung Disease
• Delayed passage of • Barium Enema • Surgical correction
meconium • Rectalbiopsy (gold standard)
4) lmperforate Anus
• Delayed passage of • Radiographic studies • Insert double-lumen NG
meconium oflumbosacral spine, tube for decompression
• Intestinal obstruction urinary tract • Rule out other congenital
• Spinal UTZ/MRIto rule out anomalies
tethered cord syndrome • Pediatric surgical consultation
5) Duodenal Atresia
• Bilious vomiting usually • Double bubble sign on • Decompression
noted on the 1st day of life plain radiograph • Surgical repair
• No abdominal distention
6) lieus
• Signs of infection • Septic/metabolic work up • Antibiotics
• Electrolyte derangement • Radiographs • Treat and correct causes
7) Other Causes of Abnormal Stool Pattern
• Prematurity /low birth weight: due to immature colon • Identify and treat causes
and delayed first feeding • Prematurity: conservative
• Electrolyte abnormalities: hypokalemia, hyponatremia, treatment for infants not
hypercalcemia and hypermagnesemia vomiting. Low osmolality
• Maternal medications: magnesium sulfate, opiates,
water-soluble contrast
neuroleptics, antidepressants
enema for passage of stool
• Drugs: theophylline, opiates, narcotic analgesic therapy
• Hypothyroidism
181
APPROACH TO RESPIRATORY DISTRESS
{details discussed in Pulmonology Chapter)
• Pulmonary
• Deficiency in • Disorder resulting
hypertension that • Aspiration of
surfactant, leading from delayed
causes hypoxemia meconium-stained
to respiratory clearance of fetal
from right to left amniotic fluid
distress alveolar fluid
shunting of blood
Profile and Manifestations
• Progressive
worsening of
cyanosis & dyspnea • Recovers rapidly
• Unpredictable course
• Symptoms peak within 3 days
within three days
then improves
Chest Radiograph Findings
• Surfactant
replacement • Oxygen
• Positive pressure supplementation,
• Treat underlying
ventilation ( e.g., • Supplemental intubation, and
cause
CPAP,mechanical oxygen support suctioning
• Supportive care
ventilation) • Supportive care
• Prevent with
antenatal steroids
Source:KliegmanR, et at NelsonTextbookof Pediatrics(21sted.).Philadelphia:
2020
ClohertyJ. et al. Manualof NeonatalCare(7thed.).Philadelphia:
2012
182
APPROACH TO ANURIAAND OLIGURIA
• All healthy preterm, full-term and post-term infants void by 24 hours of age
• Oliguria: urine output <l mL/kg/hour for 24 hours
• Anuria: absence of urine output by 48 hours of age
Maternal diabetes
mellitus
• ACEinhibitors & NSAIDs interfere with fetal nephrogenesis and result in
renal tubular dysgenesis and acute kidney injury in neonates
8.lmaging
IMAGING FINDINGS
• Evaluate urinary tract obstruction, congenital disorders or
Renal
vascular abnormalities
ultrasonography with
• Doppler examination of renal blood flow: may suggest renal
doppler flow studies
vascular thrombosis
Abdominal radiographs • Can suggest ascites or possible masses
Radionuclide renal
• Evaluate kidney function
scanning
183
Ill. MANAGEMENT
• Bladder catheterization
• Fluid challenge for diagnosis and initial management in infant
without evidence of heart failure or volume overload:
Initial evaluation 0 10-20 mL/kg NSS IV over 1-2 hours. Repeat once ifno response.
of suspected renal 0Increase in urine output 2:l ml/kg/hour indicates prerenal cause
failure • Discontinue or restrict potassium in IV fluids
• Evaluate medications, adjust dose if necessary, discontinue
nephrotoxic medications
• Strict I &O monitoring, weigh infant every 12 hours
Management • Depends on etiology of oliguria/anuria
Source:GomellaTL. et al. Neonatology
7th Edition.McGraw-Hill; 2013
AveryGB.et al.Avery'sneonatology 7th Edition.2016
APPROACH TO CYANOSIS
CLUES POSSIBLE ETIOLOGY
Signs of respiratory distress • Pulmonary etiology
• Transposition of the great vessels
Cyanosis at birth
and tricuspid atresia
Cyanosis in the perinatal period • Truncus arteriosus, TOF
Cyanosis with feeding • Esophageal atresia
Cyanosis that disappears with crying • Choanal atresia
Cyanosis improved by crying • Pulmonary
Cyanosis worsened by crying • Cardiac
Cyanosis with normal pulse oximeter reading • Methemoglobinemia
184
III. COMMONETIOLOGIES
A. Perinatal Asphyxia
• Most common cause of neonatal seizures
• Occur within the first 24 hours of life
• Persistence leads to progressive hypoxemia and hypercapnea, and eventually to
hypoxic-ischemic encephalopathy (HIE)
• Commonly presents as generalized tonic clonic seizure in preterms and multifocal
clonic type in fullterms
2. Management
Prophylactic use of anticonvulsant therapy may reduce the occurrence of death and
I·:
neurodevelopmental disability
Phenobarbital (with therapeutic hypothermia, if indicated) to reduce clinical seizures
IV, DIAGNOSIS
DIAGNOSTICS REMARKS
Complete blood count • Rule out infection and polycythemia
Serum chemistries • Glucose, calcium, sodium, BUN,magnesium, blood gases
CSFfluid analysis • As needed if suspecting infectious etiology of seizures
Imaging • Cranial ultrasonography, CT scan or MRI
• EEG
Others • Blood ammonia levels
• Amino acids
185
V. MANAGEMENT
MANAGEMENT REMARKS
• Initial drug of choice
Phenobarbital* • LD:15-20 mg/kg in single or divided doses (not to exceed 1 mg/kg/min)
• After 12-24 hours, begin maintenance: 3-4 mg/kg/day PO or IVonce daily
• LD: 15-20 mg/kg IVat a slow rate not to exceed 0.5 mg/kg/min
Phenytoin* • After 12 hours, begin maintenance: 4-8 mg/kg/day PO or IV divided
every 12 hours
• 0.2-0.5 mg/kg/dose IVas needed for seizures
Diazepam
• 0.3 mg/kg/hour as continuous infusion considered if seizures persist
• Correct underlying etiology
• Trial of pyridoxine (B6) if seizures still persist: 50-100 mg IV with
Others
EEGmonitoring
• Therapeutic hypothermia
therapy(phenobarbital
•Anticonvulsant loadingdosescontrol85%ofneonatalseizures)
and phenytoin
2013
71hEdition.McGraw-Hill;
Source:GomellaTl, el al. Neonalology
(21sted.).Elsevier;2020
of Pediatrics
KliegmanR. el al. NelsonTextbook
2016
71hEdition.Philadelphia;
AveryGB,el al.Avery'sneonalology
Engorn,8., & Flerlage,J. (2015).TheHarrie!lane Handbook Elsevier
(20lhed.).Philadelphia:
APPROACH TO JAUNDICE
I. OVERVIEW OF JAUNDICE
• Jaundice is the accumulation of yellow-orange pigment bilirubin in the skin, sclera & mucosa
• It is the most common transitional finding in the newborn period (60-70% oftenn &
80% of preterm infants)
• Becomes clinically apparent when serum bilirubin concentration is.: 5mg/dL
• Neonatal hyperbilirubinemia in infants ;,35 weeks gestational age is defined as total
serum or plasma bilirubin (TB) >95th percentile on the hour-specific Bhutani nomogram
40th Percentile
75th Percentile
97th Percentile
- -- ---
.--- ----
20 342
High ,
-
t11gnI ~termeu1;,te
::r
~
.S,10
15
,'/
, .-
, ,-
~
- ~
~
Lowi ~termedi Me
257
171
~
0
E
e
'1//
- -~ ~"
----
Ill
I-
C/)
Low
5 85
0 0
0 12 24 48 72 96 120 144
186
II. PATHOPHYSIOLOGY
• Bilirubin is the end product of heme catabolism derived primarily from the breakdown of
red blood cell hemoglobin
• Physiologic jaundice is the most common cause of jaundice in healthy infants
• There are two forms of circulating bilirubin: unconjugated bilirubin and conjugated bilirubin
FORM REMARKS
• Water-soluble (does not cross blood-brain barrier)
Conjugated • Elevated levels are always pathologic
Bilirubin • Conjugated bilirubin is considered elevated if it is:
(Direct) 0>l mg/dL for total bilirubin levels ~5 mg/dL, or
0>20% of the total bilirubin for total bilirubin levels >5 mg/dL
• Lipid soluble (may cross blood brain barrier) & predominantly bound
to albumin
Unconjugated • Kernicterus or bilirubin encephalopathy (clinical diagnosis):
Bilirubin 0 Most dreaded complication of unconjugated hyperbilirubinemia
(Indirect) ° Caused by the accumulation of unconjugated bilirubin in the basal
ganglia and brainstem nuclei
0 Rare in healthy children with bilirubin levels <20 mg/dL
187
IV. DIFFERENTIAL DIAGNOSIS FOR JAUNDICE
Hyperbilirubinemia
Direct Indirect
.J
CholestaticJaundice
"
INCREASEDHb Normal/Low Hb
...........
i...........
.
Polycythemia
Infant of diabetic mother
Increased Reticulocytes Normal Reticulocytes
SGA
Delayed cord clamping
Twin transfusion/
Characteristic RBC
Maternal-fetal transfusion
Morphology
.........
J
Spherocytosis
Elliptocytosis
Source:Taeusch
HW,et al. SchafferandAvery'sdiseasesof thenewborn.
Philadelphia;
1991
188
B. Hemolytic Anemia from ABO and Rh Incompatibility
ABO INCOMPATIBILITY Rh INCOMPATIBILITY
• Occurs when Rh(+) blood is
infused to a Rh(-) women
• Most common cause of hemolytic • Rarely occurs in first pregnancy
disease of the newborn because transfusion of Rh(+)
Description
• Mother is type O and baby is fetal blood occurs near the time
either A or B of delive1y which does not give
enough time for sensitization
• Majority is triggered by the D-antigen
• Most cases are mild • Mild hemolysis (15%) to
• Jaundice usually during first 24 severe anemia
Presentation
hours of life • Jaundice is usually evident on the
• Mild hepatosplenomegaly 1st day of life
• Presumptive diagnosis in the
• Direct Coombs test positive
presence of:
• Anemia is generally present
0 ABO incompatibility
• Increased reticulocyte count with
Weakly to moderately positive
I
0
polychromasia
Diagnostic direct Coombs test
• Definitive diagnosis:
findings 0 Spherocytes in blood smear
demonstration of blood
• Hemoglobin is usually normal
group incompatibility and
• Increased reticulocyte count
corresponding antibody bound to
• Extensivepolychromasia& increased
the infant's RBCs
numbers of nucleated RBCs
Management • See management ofunconjugated hyperbilirubinemia below
V. DIAGNOSIS
DIAGNOSTICS REMARKS
Bilirubin levels
• Total bilirubin level is plotted in the Bhutani chart
(Total, Direct, Indirect)
Blood type and Rh status • Rule out ABO and Rh incompatibility
of mother and infant • Cord blood can be sent for routine blood typing of the newborn
• Detects antibodies bound to the surface of RBCs
Direct Coombs test
• Positive in hemolytic disease as a result of isoimmunization
• Anemia suggests hemolytic process
CBCand blood smear • Polycythemia increases risk for jaundice
• RBC morphology: spherocytes suggest ABO incompatibility
Reticulocytes • Elevation suggests hemolytic disease, occult or ove,t hemorrhage
• Assess fraction ofbilirubin unbound to albumin in the circulation
Serum albumin
• Useful in determination of exchange transfusion
189
VI. MANAGEMENTOF UNCONCONJUGATED
HYPERBILIRUBINEMIA
• The goal of management is to prevent acute bilirubin encephalopathy
• The mainstay in management is phototherapy
MANAGEMENT POSSIBLE
REMARKS
COMPLICATIONS
• Phototherapy converts bilirubin • Bronze baby syndrome
into byproducts that are less toxic (bronze color of urine & skin)
& more easily excreted (process is with photodestruction of
Phototherapy
called photoisomerization) copper porphyrins, causing
• Recommended distance is 20 cm retinal degeneration ( eye
between infant and light source shields must be used)
• Metabolic acidosis
• Electrolyte derangement
• A double volume exchange • Hypoglycemia
replaces 85% of circulating RBC • Hypocalcemia
• Thrombocytopenia
Exchange and decreases bilirubin to half
• Volume overload
transfusion the pre-exchange value
• Arrhythmia
• See discussion below for • NEC
indications • Infection
• Graft-vs-host disease
• Death
A. Phototherapy
Should be initiated when the Serum Total Bilirubin (STB) exceeds the cut-off line for
each risk category in relation to the age of the infant at the time of blood extraction
22
. . .....
342
16.5 257
:r ..I
~ ---
0
171 E
Cl
.§.11 e
tll 0
1-
(/) ~
5.5 V° 85
0 0
Birth 12 24 48 72 96 120 144
Postnatalage (hours}
Source:AAPSubcommittee
on Hyperbilirubinemia.
Pediatrics:
2004
190
8. Exchange Transfusion
Should be done when the STB exceeds the cut-off line for each risk category in
relation to the age of the infant at the time of blood extraction.
Should be done in:
Evidence of ongoing hemolysis and TB fails to decline despite 4-6 hours of
intensive phototherapy
Rate of increase in TB indicates that the level will reach 25 mg/dL within 48 hours
Early signs ofbilirubin encephalopathy (e.g., hypertonia, arching, torticollis,
opisthotonus, feve1; high-pitched cry)
There is hemolysis causing anemia and hydrops fetalis
- Infants at higher risk (35-37 6/7 wk + risk Factors)
- - Infants at medium risk(> or= 38 weeks + risk factors or 35-37 sn weeks and well)
· · Infants at lower risk ::-38 weeks and well)
30 513
26 445
14./ 291
10 171
Birth 24 48 72 96 120 144
• Isolate patient
• Obtain viral cultures: blood, CSF,eyes, stool,
urine, mouth, nasopharynx
• Topical ophthalmic therapy: 3% vidarabine
• Suspect if not responding to
ointment, 1% trifluridine, or 0.1%
antibiotics
iododeoxyuridine every 2 hours for 14 days
• Acyclovir 60 mg/kg/day IVdivided into 3 doses for
14 days (21 days if disseminated/CNS infection)
• Consult with ophthalmologist
192
SECTION SEVEN
OTHER ISSUES IN THE NEWBORN
I
vascular and avascular retina
Stage Ill • New blood vessels grow along the ridge & often extend into the vitreous
• Partial retinal detachment:
Stage IV 0 IV-A:excludes the macula
0 IV-8: includes the macula
Stage V • Total retinal detachment
II. DIAGNOSIS
• Examination by binocular indirect ophthalmoscopy confirms the diagnosis
• Infants weighing <1500 g or those <30 weeks AOG should have dilated eye examinations
at 4-6 weeks of age or 31-33 weeks postmenstrual age, and continued examination every
2-3 weeks until retinal maturity
• Infants with ROP or very immature vessels should be examined every 1-2 weeks
MULTIPLE GESTATION
I. ETIOPATHOGENESIS
A. Placental Classification
° Classified according to the placental disk (single, fused or separate), number of
chorions (mono or dichorionic) and number of amnions (mono or diamniotic)
Heterosexual (dizygotic) twins always have a dichorionic placenta
0 Monochorionic twins are always of the same sex and monozygotic
B. Placental Complications:
0 Increased frequency of anomalies of the placenta and adnexa (i.e. single umbilical artery)
0 Umbilical cord is more susceptible to thrombosis when compression or twisting
occurs, resulting in intrapartum fetal distress
C. Perinatal Complications
0 Prematurity and uteroplacental insufficiency are major contributors to perinatal complications
0 Intrauterine growth restriction (incidence of LBW among twins at 50-60%)
° Congenital anomalies
193
II. TWIN-TWIN TRANSFUSION SYNDROME
• Vascular anastomoses seen among monochorionic placentas, wherein the donor fetus
pumps blood into the recipient's circulation)
• Twins have a hemoglobin difference of >5 g/dL and weight discordance >20%
MANIFESTATIONS MANAGEMENT
• Pale/anemic
• Low birth weight • Requires volume expansion and/
Donor twin
• Oligohydramnios or RBCtransfusion
• Hypoglycemia
• Plethoric
• High birth weight
• Polyhydramnios • May require partial exchange
Recipient twin
• Polycythemia transfusion
• Hyperviscosity / hypervolemia
• Hyperbilirubinemia
194
II. MANIFESTATIONSAND DIAGNOSIS
A. General Features of IUGR
° Fetus responds to compromised nutrient supply by reducing its overall size,
preserving brain growth, accelerating lung maturation, and increasing RBC production
Wasted appearance of the infant (because total body fat, lean mass, and bone mineral
content are reduced)
Risk of mortality and morbidity is increased in IUGR
B. Classification of IUGR
ASYMMETRIC IUGR SYMMETRIC IUGR
• Weight affected more than • Weight, length and head
Presentation
length circumference equally affected
• Poor maternal nutrition or • Genetic and metabolic
Predisposing
exacerbation of maternal conditions that affect fetal cell
condition
vascular disease number
Timing of • Fetus affected late in the • Fetus affected early in
insult gestation gestation, usually <18 weeks
Prognosis
C. Signs of IUGR
• Good catch-up growth (brain
growth is spared)
III. MANAGEMENT
ASPECT MANAGEMENT
• Monitoring of fetal wellbeing
• IUGRinfants have worse outcomes when delivered before
Delivery and
28-30 weeks
resuscitation
• Cesarean section delivery when lungs are mature or when
there is fetal distress
• Prevent hypothermia
• Monitor blood glucose levels & treat hypoglycemia promptly
Supportive
• Hematocrit readings to detect polycythemia
management
• Screen for congenital infections
• Screen for genetic anomalies
IV. PROGNOSIS
• Neurodevelopmental morbidities is seen 5-lOx more often in IUGR
• Smaller head circumference is associated with cognitive, psychomotor and behavioral delays
• Prete rm IUGR: higher incidence of abnormalities than the general population having been
subjected to both the risks of prematurity and IUGR
195
REFERENCES
1. Kliegman, R., ST GEME 111,)., Blum, N., Shah, S., Taske1; R., Wilson, K.. & Behrman, R. (2020). Nelson
Textbook of Pediatrics (21st ed.). Philadelphia: Elsevier.
3. Gleason, C.,& Juul, S. (2017). Ave1y's diseases of the newborn (10th ed.). Philadelphia: Elsevier.
4. Apgar, V.(1953). A Proposal for a New Method of Evaluation of the Newborn Infant. Anesthesia & Analgesia, 32(1).
5. The Apgar Score, American Academy of Pediatric, Committee on Fetus and Newborn, American College
of Obstetricians and Gynecologists and Committee on Obstetric Practice. Pediatrics 2006; 117; 1444
6. Ballard ]L, Khou1y JC, Wedig K, et al: New Ballard Score, expanded to include extremely
premature infants.] Pediatrics 1991; 119:417-423.
7. Lowdermilk, D.L. and Perry, S.E.: Maternity & women's health care [9th ed.]. St. Louis, 2007, Elsevier
Mosby; modified from Lubchenco, L., Hansman, C., Boyd, E.: Intrauterine growth in length and head
circumference as estimated from live births at gestational ages from 26 to 42 weeks. Journal of
Pediatrics, 37:403, 1966; Battaglia, F. and Lubchenco, L.: A practical classification of newborn infants by
weight and gestational age. Journal of Pediatrics, 71 [2]:159-163, 1967.
8. Fanaroff, A., Martin, R., & Walsh, M. (2015). Fanaroff and Martin's neonatal-perinatal medicine
(! 0th ed.). Philadelphia: Elsevier/Saunders.
9. World Health Organization. (2014). Early Essential Newborn Care Clinical Practice Pocket
guide. Geneva, Switzerland: WHO.
10. World Health Organization. (2009). Newborn care until the first week of life. Geneva: WHO.
11.American Academy of Pediatrics (AAP): Textbook of Neonatal Resuscitation; 6th Ed. Elk
Grove Village, IL; 2011
12.Perlman, ]., Wyllie,)., Kattwinkel. ]., Wyckoff, M.. Aziz, K., & Guinsburg, R. et al. (2015). Part 7: Neonatal
Resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Science With Treatment Recommendations [Reprint). Pediatrics 136[Supplement),
S120-S!66. doi: 10.1542/peds.2015-3373d
13. Wyckoff, M., Aziz, K., Escobedo, M., Kapadia, V., Kattwinkel, ).. & Perlman, ]. et al. (2015).
Part 13: Neonatal Resuscitation: 2015 American Heart Association Guidelines Update for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (Reprint).
PEDIATRICS,136(Supplement), Sl 96-S218. doi: 10.1542/peds.2015-3373g
14.Republic of The Philippines, Department of Health. (2009). Universal Hearing Screening
and Intervention act of 2009.
15.Andreas, N., Kampmann, 8., & Mehring Le-Doare, K. (2015). Human breast milk: A review
on its composition and bioactivity. Early Human Development, 91 (11), 629-635. doi:
l 0.1016/j.earlhumdev.2015.08.013
16. Wu, X., Jackson, R., Khan, S., Ahuja, )., & Pehrsson, P. (2018). Human Milk Nutrient
Composition in the United States: Current Knowledge, Challenges, and Research Needs.
Current Developments In Nutrition, 2(7). doi: 10.1093/cdn/nzy025
17.Academy of Breastfeeding Medicine. (2017) Clinical Protocol Number #8: Human Milk
Storage Information for Home Use for Healthy Full Term Infants. Breastfeeding Medicine,
12(7), 390-395.
18.Centers for Disease Control and Prevention (CDC). (2015). Breastfeeding: Frequently
Asked Questions. Retrieved from https://www.cdc.gov/breastfeeding/faq/index.htm
19.Centers for Disease Control and Prevention (CDC). (2017). Proper Handling and Storage of
Human Milk. Retrieved from https://www.cdc.gov/breastfeeding/recommendations/
handling_breastmilk.htm
20.Gomella TL, et al. Neonatology 7th Edition. McGraw-Hill; 2013
21.Cloherty, ]., Eichenwald, E., Hansen, A., & Stark, A. (2012). Manual of Neonatal Care (7th
ed.). Philadelphia: Lippincott Williams & Wilkins.
22.Sharma, V., Berkelhamer, S., & Lakshminrusimha, S. (2015). Persistent pulmonary
hypertension of the newborn. Maternal Health, Neonatology And Perinatology, 1(1).
doi: 10.1186/s40748-015-0015-4 Modified from 2015 Red Book Report of the Committee
on Infectious Diseases, 30th ed
23.Ave,y GB, et al. Avery's neonatology 7th Edition. Philadelphia; 2016
24. Engorn, 8., & Flerlage, ]. (2015). The Harriet Lane Handbook (20th ed.). Philadelphia: Elsevier
25.Bhutani VK, Johnson L, Sivieri EM: Predictive ability of a predischarge hour-specific
serum bilirubin for subsequent significant hyperbilirubinemia in healthy term and near-
term newborns, Pediatrics 103:6-14,
26.0ski FA: Differential diagnosis of jaundice. In Taeusch HW, Ballard RA. Avery MA. editors:
Schaffer and Avery's diseases of the newborn, ed 6, Philadelphia, 1991. Saunders
27.American Academy of Pediatrics Subcommittee on Hyperbilirubinemia: Management of
hyperbilirubinemia in the newborn infant 35 or more weeks of gestation, Pediatrics
114:297-316, 2004
28.International Committee for Classification of Retinopathy of Prematurity. The International
Classification of Retinopathy of Prematurity revisited. Arch Ophthalmol 2005; 123: 991
196
DISEASES
INFECTIOUS
SECTION ONE
APPROACH TO FEVER
OVERVIEW OF FEVER
I. DEFINITION OF FEVER
• Fever is a normal response to a variety of conditions, usually from an infection
• Controlled increase in body temperature of c,l °C above normal values at the following sites:
SITE TEMPERATURE
Rectal "38.0 °C
Oral ;,, 37.6 °C
Axilla ;,, 37.4 °C
Tympanic "37.6 °C
Source:KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Philadelphia;
2020
Undulant • Gradual increase in temperature that remains high for a few days then
fever gradually decreases to normal temperature levels
Septic/ • Large differences between peak and trough temperatures
Hectic fever
Source:KliegmanR.et al. NelsonTextbookof Pediatrics(21sted.).Philadelphia;
2020
199
GENERAL CLASSIFICATION OF FEVER
I. FEVER WITH LOCALIZING SIGNS
An acute illness with the focus of infection readily identified
• Management is directed toward the underlying cause
200
B. Fever of Unknown Origin (FUO)
0 Documented fever for which the cause could not be identified after 3 weeks of
evaluation as outpatient or after 1 week of evaluation in the hospital
HEALTHCARE- IMMUNE-
HIV-RELATED
FEATURE CLASSIC FUO ASSOCIATED DEFICIENT
FUO
FUO FUO
• >3 weeks as
Duration of outpatient
evaluation & • >l week • >l week
fever • >3 weeks as • >l week as
outpatient inpatient
• >2 visits
• >l week as
inpatient
• Not present • Negative
Other • HIV infection
or incubating cultures after
Aspects confirmed
on admission 48hrs
• HIV primary
I
infection
• Typical and
atypical
• Healthcare- • Majority are Mycabacteria
• Cancer
associated caused by • CMV
• Infections
infections infections, • Lymphoma
Causes • Inflammation
• Postoperative documented • Toxoplasmosis
• Hyperthermia
complications only in • Cyptococcosis
• Undiagnosed
• Drug fever 40-60% • Immune
reconstitution
inflammatory
syndrome
(IRIS)
201
SECTION TWO
INFECTIONS IN THE NEONATE
NEONATAL SEPSIS
• Clinical syndrome of systemic illness accompanied by bacteremia occurring in the first
month of life
I. ETIOPATHOGENESIS
EARLY-ONSET SEPSIS LATE-ONSET SEPSIS
Onset • Birth to 7th day of life • 8th to 30th day of life
• Transplacental • Vertical transmission: acquired
• From the maternal genital after birth from the maternal
tract during the antepartum or genital tract
How intrapartum period • Horizontal transmission or
organism is
acquired • Ascent of pathogens after rupture from contact with contaminated
of amniotic membrane leading to equipment, environmental
chmioamnionitis& fetalcolonization/ sources, or healthcare workers
aspiration of amniotic fluid • Hematogenous route
Most common • GBS • GBS
bacterial
agents • E. coli • S. aureus
II. MANIFESTATIONS
REMARKS
Temperature
instability • Hypothermia/hyperthermia
202
III. DIAGNOSIS
DIAGNOSTICS REMARKS
• Neutropenia (better specificity than leukocytosis)
CBC
• Decreased platelet count: late sign of sepsis and very nonspecific
Acute phase
• Increased CRP
reactants
Chest
• Done if with respiratory manifestation
radiograph
Blood culture • Required for all neonates with suspected sepsis
Urine culture • Not part of routine workup
Urinary tract • Ultrasound, renal scan, voiding cystourethrogram
imaging • If sepsis is accompanied by UT!
• Indications include:
Lumbar tap for 0 Positive blood culture
CSFstudies 0 Suspected meningitis
0 Non-responsive to antibiotics
IV. MANAGEMENT
ASPECT
Prevention
MANAGEMENT
• GBS prophylaxis with penicillin/ampicillin/cefazolin during labor or
rupture of membranes among those screened at 35-37 weeks AOGto be:
I
0Positive for vaginal and rectal GBScolonization
0With GBS isolated in the urine (>10,000 cfu/ml)
Empiric • Early-onset: Ampicillin + Aminoglycoside or 3"' generation Cephalosporin
treatment • Late-onset: Vancomycin + Aminoglycoside or 3"' generation Cephalosporin
Limited evaluation
Maternal Chorioamnionitis?
Antibiotic therapy
No
No
203
NECROTIZING ENTEROCOLITIS
• lschemic and inflammatory necrosis of the bowel after initiation of enteral feeding
• Most common life threatening emergency of the GIT in neonates
I. ETIOPATHOGENESIS
A. Pathophysiology
0 Multi factorial cause: prematurity, formula milk, ischemia and bacterial colonization
0 Triad of NEC: Intestinal ischemia (injury), enteral nutrition (metabolic substrate),
pathogenic organisms (bacterial translocation)
Increase in incidence & case fatality rates in decreasing birth weight and gestational age
0 Most commonly involved area: distal ileum & proximal colon
° Characteristic histologic finding: coagulation necrosis
8. Risk Factors
0 Prematurity (most important risk factor due to immature mucosa! barrier)
• Microbial colonization
0 Enteral feeding
• Circulatory instability (blood is diverted away from splanchnic circulation)
0 Others: maternal cigarette smoking, congenital heart disease (hypoxemia from cardiac
failure), and polycythemia & hyperviscosity syndromes
II. MANIFESTATIONS
• May be insidious or acute
• Usually occurs in the z,•
or 3•• week of life to as late as 3 months old for the very low
birth weight (VLBW) infants
Age of onset is inversely proportional to gestational age
III. DIAGNOSIS
DIAGNOSTIC REMARKS
• CBC with differential count and platelets
• CRP
Laboratory
• Blood & stool culture
Tests
• Electrolytes, ABG
• Coagulation studies
204
Modified Bell Staging Criteria for NECin Neonates (for evaluation of disease severity)
STAGE& RADIOGRAPHIC
SYSTEMIC SIGNS ABDOMINAL SIGNS
CLASSIFICATION SIGNS
IIIA
Advanced,
severely ill,
• Hypotension,
bradycardia,
severe apnea,
combined
• Same as above, plus
• Signs of peritonitis,
marked tenderness,
and abdominal
• Same as above,
plus
• Ascites
I
intact bowel respiratory
distention
and metabolic
acidosis, DIC,
neutropenia
• Exclusive breastfeeding
Prevention • Minimal enteral feeds followed by judicious volume advancement
• Probiotics
• Systemic antibiotics (with gram positive, gram negative, and
Antibiotics anaerobic coverage) after blood is drawn for cultures
• Usually given for 10-14 days
• Cessation of feeding
• Bowel decompression
Supportive Care
• IV fluids and monitor fluid intake/output
• Monitor hemodynamics, coagulation profile, electrolytes, acid-base status
• Evidence of perforation on abdominal radiograph
• Abdominal paracentesis shows stool or organism on Gram stain
Indications for • Failure of medical management
surgery • Single fixed bowel loop on X-ray
• Abdominal wall erythema
• Palpable mass
Source:Khegman
R, et al. NelsonTextbookof Ped,atncs
(21sted.).Ph1ladelph1a;
2020
GomellaTL,et al. Neonatology7thEdition.McGraw-Hill;
2013
205
TRANSPLACENTAL INFECTIONS
2) Rubella
• IUGR • Cultures may be done up to 1 year
N
• Mental retardation, of illness (nasopharyngeal swabs,
0
• Spread by respiratory secretions,
• "Blueberry muffin" rash conjunctiva! scrapings, urine, CSF)
stool, urine and cervical secretions • No specific treatment
"' • Earlier infection (1-12 weeks AOG)
• Cataracts • Serologic studies: rubella specific lgM
• Prevent with maternal rubella vaccination
• Microphthalmos in serum or oral fluid taken before 3
carries higher incidence of congenital prior to pregnancy
• Retinopathy months of age
defects and greater effects on the fetus
• Congenital heart disease (e.g., PDA) • Rubella virus PCR
• Sensorineural deafness • CSF examination: encephalitis with
• Speech and language delay increased protein and cell count
3) Cytomegalovirus
• Prenatal ultrasonography
• Ganciclovir for infants with symptomatic
• Pregnant women develop • Gold standard: urine or saliva Clllture
• Most common congenital infection disease
mononucleosis-like illness obtained before 3 weeks of age
• Transmitted through secretions • Symptomatic infants have a mortality rate
• Triad of congenital CMV: • PCR for CMV DNA of blood
• Penetrates placental and blood brain of 20-30% (sepsis like illness)
chorioretinitis, microcephaly, • Serology: lgM detection
barrier • Leading cause of deafness
periventricular calcifications • CBC, liver function tests, CSF analysis
• Teratogenic potential in the fetus • Late complications: intellectual or
• Other findings:hepatosplenomegaly, and culture
during the first trimester developmental impairment, IUGR,
petechial rashes, jaundice • Cranial UTZ or CT scan demonstrate
microcephaly
periventricular calcification
PATHOGENESIS MANIFESTATION DIAGNOSIS MANAGEMENT
4) Herpes Simplex
• Viral cultures of skin or
• For mothers with genital lesions, do surface
mucocutancous membrane lesions/
• Three patterns of disease: cultures of infant at 12-24 hours of age and
surface
0 Disease localized to the skin, eyes, treat if symptoms develop or if cultures are
• Most are due to HSV-2 • PCR of CSF and blood
or mouth positive
• Acquired intrauterine, • Immunologic assays: HSV antigen
0 Encephalitis with or without skin, • Acyclovir IV 60 mg/kg/day every 8 hours
intrapartum or postnatal • Imaging: CT or MRI of brain
eyes, and mouth disease 0 14 days for skin, eyes and mouth disease
• 85% are ascending infection reveals parenchyrnal brain edema,
0 Disseminated infection involving 0 21 days for disseminated or CNS disease
hemorrhage and destructive lesions in
multiple organs • Acyclovir PO 300 mg/m' /dose thrice a day for 6
the temporal lobe
months after treatment as suppressive therapy
• EEG for infants with CNS involvement
N
0
5) Varicella (Fetal Varicella Syndrome)
___,
• Mother: VZIG or !VIG given within 72-96 hours
of exposure
• Cicatricial scars and skin loss • Maternal varicella
• Acyclovir if chicken pox is diagnosed during
• CNS:microcephaly, seizures, encephalitis, • Presence of congenital skin lesions in
pregnancy
cortical & spinal cord atrophy, mental dermatomal distribution
• Develops when mother is exposed • Infant:
retardation, cerebral calcifications • Proof of intrauterine VZVinfection by:
during first half of pregnancy 0 Supportive care because of profound
• Ocular: microphthalmia, 0 Detection of viral DNA in infant by
(8th-20th week) neurologic impairment
chorioretinitis, cataracts, optic atrophy, PCR (fetal blood and amniotic fluid)
• Virus spreads to all fetal organs 0 Acyclovir to stop progression of eye disease
nystagmus, Horner syndrome (ptosis, 0 VZVspecific IgM
hematogenously or to treat shingles, which is common during
miosis, enophthalmos) 0 VZV specific IgG beyond 7 months
the first 2 years of life
• Limb hypoplasia 0 Ultrasonography for typical VZV
• 30% die in the first 4 months
• Prematurity and IUGR anomalies
• High risk of developing zoster in the first 2
years
-
PATHOGENESIS MANIFESTATION DIAGNOSIS MANAGEMENT
6) Congenital Varicella Infection
• Centripetal rash that spares the • VZV DNA PCR of vesicular fluid or scabs,
• Occurs when mother suffers from extremities biopsies, amniotic nuid • IVIG400mg/kg as soon as possible, not later
infection during the last 3 weeks of • Macules that progress to vesicles and • Viral culture and direct fluorescent than 10 days
pregnancy or within first few days encrustation antibody assay • Acyclovir: lSmg/kg/dose every 8 hours for
postpartum (when rash appears 5 days • Staphylococcal and streptococcal • Serum testing ofVZV antibody: lgM 7 days for post exposure prophylaxis and as
before delivery & 2 days post partum) superinfectionare the main complicatons detected as soon as 3 days after treatment of symptomatic neonates
• May develop varicella pneumonia appearance of symptoms
7) Chlamydia trachomatis
• Conjunctivitis: discharge, redness, • Gold standard: culture of the organism
swelling, corneal opacification, chemosis, from tarsal conjunctivae or from the
• Most common cause of sexually • Erythromycin SO mg/kg/day divided in 4
pseudomernbrane formation nasopharyngealaspiration
transmitted genital infections doses for 14 days OR Azithromycin 20 mg/kg
• Trachoma: chronicfollirularkeratoconjunctivitis • NucleicAcid Amplification tests
single daily dose for 3 doses
• Causes conjunctivitis and pneumonia whichcauses scaningandneovdSrulaiii.ationof • Antigen detection tests:direct fluorescent
• Note: reported associationof erythromycin
N in infants the cornea resulting in blindness antibody and enzyme immunoassay
0 with the development of infantile
00 • Neonate acquires infection through • Pneumonia:presentsat 3-11 weeks of • Serum anti-chlamydia! antibody (lgM)
hypertrophic pyloric stenosis (IHPS) in infants
vaginal delivery (infected cervix) life, majority are afebrile concentration
< 6weeks
• Paroxysmal, staccato cough that • Pneumonia:WBC is normal but with
interferes with sleepingand eating eosinophilia in 70%
8) Neisseria gonorrhea
• Non-disseminatedinfections (including
• Ophthalrnianeonatorum
• Gram stain of any exudate ophthalmia neonatorum):
• Gonococcalarthritis (common in knees
• Transmitted via contact with cervical • Culture of eye discharge, nasopharynx, Ceftriaxoneor Ceoftaxime single dose
& ankles)
orogastricor anorectalarea • Arthritis and septicemia:
canal during delivery or with • Amniotic nuid syndrome when there
• Blood r.:ulture Ceftriaxoneor Cefotc1xi111e for 7 days
contaminated amniotic fluid is premature rupture of membranes,
• Lumbar puncture with spinal fluid • Meningitis:
• Co-infection with Chlamydia is inflammation of the placenta and
studies Ceftriaxone or Cefotaxime for 10-14 days
common umbilical cord
• Culture for concomitantChlamydia • All infants with gonococcalinfection:contact
• Sepsisand meningitis
trachomatis isolation until effective parenteral antibiotic
• Scalpabscess
therapy given for 24 hours
Source:KliegmanR.et al. NelsonTextbookof Ped,atncs(21sted.). Phrladelphra;
2020
GomellaTL,et al. Neonatology7th Edition.McGraw-Hill;2013
NeuN,et al. Clinicsin Perinatology.
Elsevier;2015
SECTION THREE
VIRAL INFECTIONS
INFLUENZA
I. ETIOPATHOGENESIS
A. Influenza Virus (Types A, B, and C)
RNA virus, orthomyxovirus
, Antigenic drift: minor antigenic variations may occur within types A & B that result in
new strains leading to seasonal epidemics
0 Antigenic shift: major antigenic changes in influenza A viruses resulting in new HA or
NA which can result in pandemics
• Causes epidemics
• Has an animal host
Influenza Type A
• Subtypes (based on surface antigens Hemagglutinin and
Neuraminidase): H & N
• Causes epidemics
Influenza Type B
• Has no animal host
Influenza Type C • Causes sporadic mild influenza-like illness
B. Transmission
• Respiratory droplets
• Contact with respiratory tract droplet-contaminated surfaces
I
Mode of
followed by autoinoculation
Transmission
• Viral shedding in nasal secretions peak on first 3 days of illness
and cease within 7 days
Incubation Period • 1-4 days
II. MANIFESTATIONS
• Abrupt onset of high grade fever, coryza, conjunctivitis, pharyngitis, dry cough, myalgia,
malaise & headache
• Majority recover fully after 3-7 days
• Complications include:
Otitis media
0 Pneumonia
° Febrile seizures to encephalopathy /encephalitis
Reye syndrome with intake of aspirin
0 Myocarditis
Invasive secondary bacterial infections
Ill. DIAGNOSIS
• May be confirmed serologically by hemagglutination inhibition test (during acute and
convalescent stages), viral culture, reverse transcriptase-PCR
IV. MANAGEMENT
209
HERPES SIMPLEX VIRUS (HSV)
I. ETIOPATHOGENESIS
A. Etiologic Agent
HSVTYPE 1 HSVTYPE2
• Affects the face & skin above • Affects the genitalia & skin
Infection
the waist below the waist
Incubation Period • 2-12 days • 2-12 days
• Direct contact with virus
Mode of • Direct contact with infected
shed from genital lesions or
Transmission secretions or orolabial lesions
secretions duting sexual activity
II. MANIFESTATIONS
MANIFESTATION DESCRIPTION
• Most commonly affects 6 months to 5 years old
• Drooling, high-grade fever, refusal to eat or drink, and painful
Herpetic
ulcers on the tongue, gums, lips
gingivostomatitis
• Hallmark: skin vesicles and shallow ulcers that are more
extensively distributed than herpangina
IV. MANAGEMENT
ANTI-VIRAL AGENT INDICATIONS
• Severe mucocutaneous and disseminated infections in
immunocompromised patients
IV acyclovir
• CNS infection
• Perinatal infection
• Gingivostomatitis
Oral acyclovir or
• Herpes labialis
valacyclovir
• Genital herpes
Source:KliegmanR.et al. NelsonTextbook
of Pediatrics
(21sted.).Philadelphia;
2020
Redbook.Reportof theCommittee on InfectiousDiseases,31sted;2018
MUMPS
I. ETIOPATHOGENESIS
• Due to RNAvirus of the family Paramyxoviridae and the genus
Etiology
Mode of Transmission
Period of
Communicability
Rubulavirus
• Respiratory droplets from person to person
II, MANIFESTATIONS
• Presents with 1-2 days prodrome of fever, headache, vomiting then parotitis appears
• Parotid swelling and tenderness, peaks in 3 days then gradually subsides over 7 days,
occurs bilaterally in 70% of cases
• Angleof the jaw is obscured as swelling ensues and the earlobe may be lifted upward and outward
• Edema over the sternum may occur due to lymphatic obstruction
III. DIAGNOSIS
• Enzyme immunoassay for mumps lgM
• Serum lgG from acute and convalescent serum specimens
• Virus isolated from upper respiratory tract secretions, urine, or CSF during the acute
illness through cell culture, immunofluorescence, reverse transcriptase PCR
IV. MANAGEMENT
• Supportive: antipyretics, pain relief, adequate hydration
V. COMPLICATIONS
• High-grade revcr with cough, conjunctivitis and colds • Most common: otitis media
• Airborne • Most common cause of
(3-5 days) and photophobia
• Viable virus may he mortJlity: pneumonia
• Enanthcm: Kuplik spots (grayish white dots with red
found up to 1 hour in • Warthin- • Subacu1·c sdcrosing
border opposite lower molars) appear before the rash • Supportive
air and up to 2 hours Finkeldey panencephalitis (ratal
• Paramyxovirus • Rashes usually appear at the height of fever • Vitamin A oral OD
on contnct surfaces giant cells degenerative disease from
• 1P8-12days • Cranioan1d.ildissemination:1naculopapularrashbeginsin face lor2 days
• Communicability: 4 (rusion or persistent infection 7-l Oyears
• Rash fades downward in the same sequence in which it
days before to 4 days infected cells) after natural measles infection)
dcsqunmation), disappears i117-10 days
appeared (b1c11111y • Final common pathway to a
after onset or rash
• If uncomplicated, symptoms subside rapidly & fover fatal outcome: bronchiolitis
abates as rashes appe;,1rs on the legs & feet obliterans
N
2) German Measles (Rubella or 3-day Measles)
......
N
• Most characteristic sign: retroauricular, posterior
• Thrombocytopenia 2 weeks
cervical & postoccipital symmetrical lymphadenopathy • Droplet or
• fourfold after rash
(begins 24 hours before the rash & remains for 1 week) transplacenta\ • Arthritis of the snrnll joints
• Enanthem: Forschcimcr spots fdiscrete rose spots on increase in
• Togavirus • Communicability: 7 of the hands (adult women)
• IP 14-21 days . the soft palate) appear at the same time as rash
No photophobia
• Feverwitl1decrease in temperature on 3"14 th day as rashes appear
clays before to 6-7 clays
after onset of rash
lgM and lgG
antibody is
• Supportive
within 1 week of rash
• Encephalitis (postinfoctious
diagnostic syndrome or a rare progressive
• Maculopapular rash begins at face and neck and
panencephalitis)
spreads centrifugally as discrete maculcs
3) Roseola lnfantum
. Most often among <3 years old, peak at 6-15 mos old
• Fever for 3-5 days with fussiness • Probably acquired from
• HHV-6
• Excellent with no obvious
serology, l'CR,
• Human Herpes • Rash appears within 12-24 hours of fever resolution: the saliva or healthy sequelae
virus culture
virus (l·IHV) discrete, small pink lesions on the trunk, spreads in a persons, enters host • Hl·IV-6can suppress all cellular
• LowWllC • Supportive
6&7 centripetal pattern, fades in 1-3 days through mucosa lineages within the bone
count,
• 11'9-l0days • Ulcers in uvulopalatoglossal junction (Nagayama spots) • Communicability: marrow
neutrophils,
• Bulging of anterior fontanelle unknown
• Convulsions lymphocytes
ETIOLOGY & TRANSMISSION
INCUBATION MANIFESTATION & PERIOD OF DIAGNOSIS MANAGEMENT COMPLICATIONS
PERIOD (IP) COMMUNICABILITY
4) Chickenpox (Varicella)
• Varicella zoster • IV Acyclovir: for
• Fever then pruritic exanthem • Direct contact or
antibody titers severe disease and • Secondary bacterial
• All stages of rash are present simultaneously airborne spread
• Leukopenia immunocompromised infection
• Varicclla·Zoster • Rash often appear first on the scalp, face, or trunk, then • Communicability: 1-2
during the 1st • Oral acyclovir best • Encephalitis or meningitis
Virus (VZV) spread to other parts of the body days before the onset
3 days after started on JS1 day • Pneumonia
• IP 10-21 days • Intensely pruritic red macules, become pa pules, then of the rash until all the
onset of rash, of illness to reduce • Reye syndrome
vesicles (rapid progression) lesions have crusted
followed by number of lesions & • Glomerular nephritis
• Ulcers also common in oropharynx and vagina
lymphocytosis shorten course
6) Hand-Foot-Mouth Disease
• Commonly affects <l Oyears of age • Fecal-oral and
• Viral culture • More severe disease
• 1-2 days fever then enanthem (vesicles & ulcerations in respiratory routes
[gold standard) with enterovirus 71:
• Coxsackie A 16 the oral cavity) followed by exanthem • Communicability:
• Serotype neurologic disease,
• Enterovirus 71 • Exanthem: tender vesicular skin lesions with Viral shedding from the • Supportive
identification encephalomyelitis,
• IP 4-6 days surrounding erythema on the hands (more than feet), respiratorytrnct1-3weeks
for outbreak pulmonary edema,
buttocks, groin & fecalshedclingupto 7-11
investigation hemorrhage
• Vesicles resolve by absorption of nuid in ~1 week weeks post-infection
Source:KhegmanR, et al. NelsonTextbook
of Ped,atncs(21sted.).Ph1ladelphra;
2020
Redbook.Reportofthe Committee on Infectious
Diseases,31sted; 2018
Ill
POLIOMYELITIS
I. ETIOPATHOGENESIS
• Polio virus is an Enterovirus from Picornaviridae family
Etiology (coxsackie, echovirus, polio) with 3 antigenically distinct
serotypes (1. 2, and 3)
Mode of Transmission • Fecal-oral
• Shortly before & after the onset of clinical illness
Period of
• Virus persists in the throat until a week after onset & excreted
Communicability
in the feces for 3-4 weeks
Incubation Period • 7-21 days
II. DIAGNOSIS
DIAGNOSTIC REMARKS
• Blood (end of 1st week)
• Throat (end of 2nd week)
Isolation of virus
• Feces (end of 3rd week)
• CSF
• Pleocytosis with early predominance of PMNs followed by a
CSF analysis shift to mononuclear cells
• Normal glucose, increased protein
Source:KliegmanR. et at NelsonTextbook
of Pediatrics
(21sted.).Philadelphia:
2020
Redbook.Reportof the Committeeon InfectiousDiseases.31sted: 2018
214
DENGUE FEVER
I. ETIOPATHOGENESIS
A. Dengue Virus
0 Refers to four serotypes of RNAviruses from the genus Flaviridae (DENV-1, 2, 3, and 4)
0 Transmitted to humans through the bite of infected Aedes aegypti mosquito
0 Infection with one DENVtype produces life-long immunity against that type and a very
short period of protection against the other three serotypes - thereafte1; infection with
a different strain may predispose to more severe disease
8. Transmission
II. MANIFESTATIONS
A. Characteristic Rash
0 Transient, macula,; generalized rash that blanches under pressure seen during the
first 24-48 hours of fever
1-2 days after defervescence, a generalized maculopapular rash appears which spares
the palms & soles; this disappears in 1-5 days and may desquamate (Hermann rash)
I
B. Phases of Dengue Infection
Days of illness 2 3 4 5. 6 7 8 9 10
Temperature
40'
Laboratory changes
Dehydration
-
Organ impairment
' ......................
.
Reabsorption
Fluid overload
Platelet
Hematocrit
Serology and virology
Viraemia
215
PHASE MANIFESTATIONS COMPLICATIONS
• Sudden high-grade fever &
• Anorexia, nausea, and vomiting
• Facial flushing, skin erythema, generalized rash • Dehydration
• Generalized body ache, myalgia, arthralgia • High fever may
Febrile Phase ("back-break fever" or "breakbone fever") cause neurologic
(3-7 days) • Retroorbital eye pain, photophobia, headache disturbances and
• Petechiae, mucosa) membrane bleeding, easy febrile seizures in
bruising, and bleeding may be present young children
• Enlarged and tender liver
• Leukopenia on CBC
• Not all pass through this phase
• Warning signs mark the onset of this phase as
a result of plasma leakage
• Weak pulses, cold clammy extremities, and
Critical Phase prolonged capillary refill time • Shock from plasma
(24-48 hours • Easy bruising and bleeding leakage
after fever • Shock may result in metabolic acidosis, • Severe hemorrhage
defervesence) progressive organ impairment, and • Organ impairment
disseminated intravascular coagulopathy (DIC)
• Progressive leukopenia followed by
thrombocytopenia & increasing hematocrit
(hemoconcentration)
• Gradual reabsorption of extravascular
compartment fluid • Hypervolemia and
• May have bradycardia, stabilization of acute pulmonary
Recovery hematocrit, or hemodilution edema (if IV fluid
Phase • Improvement of well-being & return of appetite therapy was
• Hemodynamic status stabilized & diuresis ensues excessive or extended
• Hermann's rash ("isles of white in a sea of into this period)
red") & may have generalized pruritus
V. DIAGNOSIS
A. Diagnostics
DIAGNOSTIC REMARKS
Dengue NS-1 Antigen • Useful from day 1 until day 3 of the illness
217
B.The "ABCS"of Dengue
0 Suggested laboratory investigations for patients who do not respond well with
adequate volume replacement (both shock and non-shock)
INVESTIGATION REMARKS
• Seen in profound shock
• Blood gas
A: Acidosis • Work up for organ involvement: liver
(venous or capillary)
function, BUN,Crea
• An increase in hematocrit suggests
hemoconcentration
• A decrease in hematocrit with improving
B: Bleeding • Hematocrit clinical condition suggests that volume
resuscitation is working
• A drop in hematocrit with worsening clinical
condition suggests occult bleeding
• Hypocalcemia in almost all cases of DHF
C: Calcium • Electrolye (Ca2 ·J
• Usually asymptomatic
• Factors that contribute to hypoglycemia:
S: Blood sugar • Blood sugar
decreased intake, vomiting, hepatic impairment
VI. MANAGEMENT
• Not all cases should be admitted
• Supportive therapy is the main management of dengue fever
Anti-pyretic: paracetamol (ibuprofen and NSAIDsare generally avoided)
0
• Those with warning signs and complications (e.g., severe dengue, DHF
and DSS) should be admitted
• Maintenance of the cardiovascular and circulatory status is a priority
especially during the critical phase
• Fluid therapy is critical in the management of dengue because the main
pathophysiology is plasma leakage
• Isotonic fluids are preferred (e.g.,PNSS,PLR,IES-isotonic electrolyte solution)
• Fluids are adjusted based on:
0Hematocrit determination
Fluid
° Clinicalstatus: BP (watch out for narrowed pulse pressure & hypotension),
Therapy
sensorium, capillary refill time, extremities (cold & clammy), pulses
0Urine output (maintain a minimum of 1 mL/kg/hr in children and
0.5 mL/kg/hr in adolescents)
• After the critical phase, fluids should be tapered off or withheld to
prevent fluid overload (for specific guidelines, see algorithm below)
• Prophylactic transfusion of blood products, especially platelets and
plasma (FFP and cryoprecipitate) is not recommended (no proven
benefit & may contribute to fluid overload and adverse reactions)
• Whole blood or PRBCtransfusion is indicated for profuse bleeding or
Blood clinical deterioration that does not respond to fluid resuscitation
Transfusion • FFP and cryoprecipitate are indicated for bleeding that does not respond
to whole blood or prbc transfusion OR in cases of DIC
• Platelet transfusion is indicated if:
0Platelet :,:10,000/mm 3 with bleeding, or
0Prolonged shock with bleeding not responsive to red cell & plasma products
• Afebrile for at least 24-48 hours
Criteria for • Good well being
discharge • Stable hematocrit without !VF and increasing platelet trend
• At least 2-3 days from the last episode of shock
218
A. Fluid therapy for Patients Who are NOT Admitted or Patients NOT in Shock
Ifwithovert/occultbleeding(at any time, transfuse fresh whole blood20 ml/kg or PRBC10 ml/kg
• If patient improves,proceed to STEPB
• If patient does not improve,consider inotropes and refer to tertiarycenter
219
2. Hypotensive Shock
Defined as hypotension for age
• In BOLDtext are the key differences from compensated shock
STEP MANAGEMENT
• Obtain baseline hematocrit (HCT)
• Give isotonic crystalloid or colloid 20 ml/kg over 15 minutes via
"push-pull" method
A
• If with improvement, go to STEP B
• If without improvement, go to STEP C
• Reduce fluids as follows (as long as clinical and laboratory status are stable)
0 10 ml/kg/hour for 1 hour
B 0 5-7 mL/kg/hour
0 3-5 mL/kg/hour
for 2-4 hours
for 2-4 hours
0 2-3 mL/kg/hour for 2-4 hours
• Second bolus offluid (colloid) 10-20 ml/kg/hour in½ to 1 hour
0 If patient improves and HCT decreases, reduce IVF to 7-10 ml/kg/hour
for 1-2 hours and if patient remains stable proceed to STEP B
C 0 If patient does not improve, give 3rd bolus offluid (crystalloid/colloid)
10-20 mL/kg/hour in 1 hour
If patient improves, proceed to STEP B
• If patient does not improve, consider inotropes and refer to tertiary center
If withovert/occultbleeding (at anytime, transfuse fresh whole blood 20 mUkg or PRBC10 mUkg
• If patient improves, proceed to STEPB
• If patient does not improve,consider inotropes and refer to tertiarycenter
Source:WHO.Guidelinesforprevention
andcontrolofdengueanddenguehaemorrhagic fever.WHO:2011
WHO.Dengue:guidelines
fordiagnosis,
treatment.
preventionandcontrol
-- Newedition.Geneva:WHO:2009
Administrative
OrderNo. 2012-0006.DOHRevisedDengueClinicalCaseManagement Guidelines2011
220
RABIES
I. ETIOPATHOGENESIS
A. Transmission
B. Pathophysiology
, Rabies virus inoculation begins with an animal bite and local tissue replication in the
muscle and skin
, The virus attaches to nicotinic acetylcholine receptors and gains access into the
peripheral nervous system. It then moves centripetally eventually reaching the spinal
cord and the brain, salivary, and lacrimal glands.
Virus causes neuronal destruction in the brainstem & medulla
Negri bodies (pathognomonic): rabies specific eosinophilic inclusions within the
I
neuronal cytoplasm
II. MANIFESTATIONS
A. Prodrome (2-10 days)
Pain, pruritus, paresthesia, myoclonic jerking at the site of the wound/inoculation
' Fever, malaise, anorexia, dysphagia, changes in behavior, sleep patterns and emotions
III. DIAGNOSIS
• CBCreveals polymorphonucleosis
• CSF revelas mononuclear cells with increased protein
• Isolation of virus from saliva or CSF
• Detection of antibody in serum & CSF
• Postmortem diagnosis: fluorescent microscopy of brain & salivary glands
• Animal brain: Negri bodies
V. PROGNOSIS
• Rabies is generally fatal
• Neither rabies immunoglobulin nor rabies vaccine provides benefit once symptomatic
221
HUMAN IMMUNODEFICIENCY VIRUS (HIV) INFECTION
I. ETIOPATHOGENESIS
A. The Human Immunodeficiency Virus (from Retroviridae family)
B.Transmission
• Sexual contact
• Percutaneous blood exposure from contaminated needles and sharp
Modes of instruments
Transmission • Transfusion of contaminated blood products
• Vertical transmission can occur before (intrauterine), during
(intrapartum), or after delivery (through breastfeeding)
Incubation • 12-18 months for perinatally infected infants
Period • Some children are asymptomatic for >S years
C. Pathogenesis of HIV/AIDS
0 Depletion of CD4+ T cells leads to immunodeficiency
0 HIV infection ultimately leads to the impairment of every arm of the immune system
II. MANIFESTATIONS
A. Progression of Untreated HIV through 4 Clinical Phases
PHASE DESCRIPTION
Acute retroviral
• Flu-like syndrome
syndrome
• HIV DNA integrates into CD4+ cells
Latent infection
• Declining CD4+ counts
• Inability of immune system to contain viral replication
• Manifestations may include:
0 Generalized lymphadenopathy
0 Hepatosplenomegaly
° Failure to thrive
Symptomatic HIV ° Chronic or recurrent diarrhea
0 Interstitial pneumonia
0 Oral thrush
0 Recurrent bacterial infections
0 Lymphocytic interstitial pneumonitis
0 Early onset of progressive neurologic deterioration
• CD4 count <200 cel!s/uL
AIDS • Patient succumbs to opportunistic infection within 2 years
of developing AIDS
222
B. HIVClassification
CATEGORY REMARKS
• At least 2 mild symptoms: lymphadenopathy, parotitis,
A Mild Symptoms hepatosplenomegaly, dermatitis, persistent or
recurrent sinusitis or otitis media
• Any of the following: oropharyngeal thrush persisting
for >2 months, recurrent or chronic diarrhea, persistent
Moderate
B fever for> 1 month, hepatitis, recurrent herpetic
Symptoms
gingivostomatitis, pneumonitis, disseminated varicella
with visceral involvement, cardiomegaly
• Two of the following serious bacterial infections:
sepsis, meningitis, pneumonia in a 2-year period,
C Severe Symptoms lower respiratory tract candidiasis, cryptococcosis,
encephalopathy, malignancies, disseminated
mycobacterial infection, pneumocystis carinii pneumonia
III. DIAGNOSIS
• Demonstration of lgG to HIV by a repeatedly reactive enzyme
immunoassay & confirmatory test (Western immunoblot or
I
IF assay) establishes the diagnosis of HIV infection
• Some viral detection assays:
Any child >18 months
HIV DNA or RNA by PCR
0
HIV culture
0
HIV p24Ag
0
IV. MANAGEMENT
• Initiating antiretroviral treatment for pediatric HIV-infected patients are based on:
Magnitude of viral replication
° CD4+ count & percentage
° Clinical condition
• HIV-infected children with symptoms (clinical category A, B, C) or with evidence of
immune dysfunction should be treated with antiretrovirals regardless of age or viral load
• In general, the best single prognostic indicator is the plasma viral load
ANTIRETROVIRAL REMARKS
THERAPY
• Either nucleoside (NRTI) or non-nucleoside reverse
Reverse transcriptase inhibitors (NNRTI)
transcriptase 0 NRTI: Didanosine, Abacavi1; Stavudine, Lamivudine,
inhibitors Zidovudine
0 NNRTI: Delaviridine, Efavirenz, Nevirapine
• Prevent packaging of infectious virions before they leave the
infected cells
Protease inhibitors
• Examples include Indinavi1; Amprenavir, Nelfinavil; Ritonavir,
Saquinavir
223
SECTION FOUR
BACTERIAL INFE'CT.IONS
STREPTOCOCCAL INFECTIONS
224
III. GROUP-ASTREPTOCOCCALINFECTIONS(GAS)
• Streptococcus pyogenes is the most common & only clinically significant GASorganism
which infects children & adolescents (it causes a wide range of infections)
• Most common site of infection is the pharynx (followed by skin infections such as
pyoderma, impetigo)
Non-suppurative complications include:
0 Acute rheumatic fever (sequela of pharyngitis, NOT skin infections)
0 Acute glomerulonephritis (sequela of pharyngitis OR skin infections)
A.Acute Pharyngitis
• Contact with respiratory tract secretions
Transmission • Communicability highest during acute infection
• Children become non-contagious 24 hours after antibiotic initiation
Incubation • 2-5 days
• Feve1;sore throat, tonsillar inflammation ("beefy red tonsils") with
exudate, tender cervical lymphadenopathy
Manifestations
• Most often associated with scarlet fever (e.g., strawberry tongue,
erythematous sandpaper-like rash due to an erythrogenic exotoxin)
• Throat swab culture: 95% sensitivity to detect GAS
Diagnosis • Rapid antigen detection test: more expensive but yields fast results
(a negative rapid test does not exclude GAS)
Management
• Penicillin or amoxicillin is the drug of choice given for 10 days
, Oral Penicillin-V (Phenoxymethylpenicillin):
0
250 mg/dose 2-3 times a day if< 60 lbs
500 mg/dose 2-3x a day if >60 lbs
Amoxicillin 50 mg/kg/day in divided doses x 10 days
I
• For penicillin-allergic patients: oral clindamycin or oral macrolide
(e.g., erythromycin, clarithromycin, or azithromycin)
B. Impetigo (Pyoderma)
Incubation • 7-10 days
• Nonbullous impetigo (more common, 70%)
0 Staphylococcus aureus is the predominant cause ofnonbullous
impetigo
, Superficial infection: discrete papulovesicular lesion with
localized erythema that become purulent & covered with a thick,
confluent, amber-colored crust
0 Most common on the face and extremities
225
STAPHYLOCOCCAL INFECTIONS
• Gram-positive aerobic bacteria that grow in pairs and clusters
• Coagulase positive: Staphylococcus aureus (most common cause ofpyogenic infection of
the skin and soft tissues)
• Coagulase negative: S. epidermidis, S. saprophyticus, S. haemolyticus
• Clinical spectrum: osteomyelitis, suppurative arthritis, abscesses, pyomyositis, empyema, IE
• Toxin-mediated: scarlet fever, food poisoning, scalded skin syndrome, toxic shock syndrome
226
ESCHERICHIA COLI (E. coli)
I. ETIOPATHOGENESIS
• Person to person transmission
Mode of Transmission
• Fecal-oral route (contaminated food & water)
Incubation Period • 10 hours to 6 days
Infectious period • As long as the person excretes the bacteria (1-4 weeks)
II. MANIFESTATIONS
• Most fecal E.coli are nonpathogens
• Six major groups of pathogenic£. coli:
AGE GROUP TYPE OF OTHER
PATHOGENESIS MANIFESTATIONS
AT RISK DIARRHEA
I
Ill. DIAGNOSIS
• Clinical features of illness are seldom distinctive
• Routine laboratory tests are of very limited value
• Serotype O157:H?: suggested by isolation of£. coli that fails to ferment sorbitol on
MacConkey sobitol medium
• For the others: tissue cultures or identification of specific virulence factors of the bacteria
227
IV. MANAGEMENT
ASPECT MANAGEMENT
• Fluid and electrolyte therapy
Supportive
• Early refeeding (within 6-8 hours of initiation of rehydration)
• Specific antimicrobial therapy is problematic due to difficulty of
making a diagnosis & unpredictability of antibiotic susceptibilities
• Antibiotics should not be given for STEC or EHEC infection due to
Antimicrobials
increased risk of HUS
• Antibiotics may be useful for severe watery diarrhea in a traveler
coming from a developing country (ETEC responds to co-trimoxazole)
Zinc supplements • For malnourished children to hasten recovery
Prevention • Proper food and water handling procedures, handwashing
Source:KliegmanR. et al. NelsonTextbookof Pediatrics(21sted.). Philadelphia:2020
KimberlinDW,et al.AmericanAcademyof Pediatrics.Redbook:2015
TYPHOID FEVER
I. ETIOPATHOGENESIS
• Salmonella enterica serovar Typhi
Etiology
• Salmonella Paratyphi A, Band C (causes less severe disease)
• Most common: ingestion of food/water contaminated from human feces
• Shellfish and vegetable grown in sewage contaminated water
Transmission
• Communicable as long as the infected person excretes S. typhi (after
the 1" week of illness up to convalescence)
Incubation • 7-14 days, range of3-30 days
II. MANIFESTATIONS
A. Symptoms/Signs
• High-grade fevet; malaise, myalgia, abdominal pain, anorexia,
hepatosplenomegaly, diarrhea/ constipation
• Temperature pattern: rises in small increments then reaches 40°C
Symptoms
by the end of the 1" week
• Fever is remittent and rises to peak every afternoon
• Diarrhea (greenish pea soup) follows fever on the 2"d week
• Maculopapular rashes (rose spots): visible on day 7-10 of illness on
the lower chest or abdomen and lasts 2-3 days (seen in 25% only)
Signs
• Relative bradycardia, neurologic manifestations, and GI bleeding
are rare in children, but relatively common in adults
228
III. DIAGNOSIS
DIAGNOSTIC REMARKS
• Mainstay of diagnosis: blood culture (positive in 40-60% of
patients early in the disease course)
Cultures
• Stool and urine cultures become positive after the 1st week
• Bone marrow cultures
• Widal test (become positive in 7-10 days)
Typhoid Tests
• Typhidot lgM and lgG
• Leukopenia (leukocytosis in younger children), thrombocytopenia
Other Tests
• Deranged liver function tests
Multidrug-
Resistant
• Ceftriaxone OR Ciprofloxacin OR Azithromycin
• Ciprofloxacin
Guidelines2017
Source::NationalAnt1b1ot1c
I
V. PREVENTION
• Central chlorination and domestic water purification
• Avoid consumption of street food
• Typhoid vaccine for high risk populations Source:CDCandPrevention. Salmonella.
Veeraraghavan
8, et al.Typhoidfever;FutureSciOA;2018
WHOGuidelines forTyphoidFever.2011.
MENINGOCOCCEMIA
I. ETIOPATHOGENESIS
A Etiology
Etiologic agent • Neisseria meningitidis
Incubation
• 3-4 days (range of2-10 days)
period
• Close contact through aerosol droplets or contact with respiratory
Transmission secretions
• Humans are the only natural reservoir
B. Epidemiology
Sero groups A, B, C, W, Y: responsible for almost all cases of disease
Highest rate of disease occurs in infants <l year old
• Carriage of bacteria peaks during adolescence and young adulthood
C. Risk Factors
Respiratory viral infections (especially influenza)
Male gender
• Smoking, marijuana use, binge drinking
• Crowded living conditions (living in dormitories)
Underlying chronic diseases
• Low socioeconomic status
CDCandPrevention.Meningococcal Disease
HarrisonLH,et al. PediatrInfectDisJ; 2018
229
II. MANIFESTATIONS
• Most deaths occur within 48 hours of hospitalization
• Case fatality rate for invasive meningococcal disease is 5-10%
A. Different Presentations
PRESENTATION ANTIBIOTIC
Occult
meningococcal • Fever with or without associated symptoms
bacteremia
• Rare
Chronic
• Fever, arthralgia, headache, splenomegaly, maculopapular or
meningococcemia
petechial rash, lasting for 6-8 weeks
B p .
POOR PROGNOSTIC FACTORS POORER PROGNOSTIC FACTORS
• Hypothermia or hyperpyrexia
• Presence ofpetechiae <12 hrs before
• Hypotension or shock, seizures
admission
• Purpura fulminans
• Absence of meningitis
• Leukopenia, thrombocytopenia, acidosis
• Low or normal ESR
• High levels of endotoxin and TNF-alpha
Ill. DIAGNOSIS
• Identification of meningococci from blood, CSF,joint fluid or skin lesions
IV. MANAGEMENT
• Empiric antimicrobial therapy: third-generation cephalosporin
• Drug of choice for meningococcemia:
0 Penicillin G 300,000 units/kg/day IV in 4-6 divided doses
° Ceftriaxone 100 mg/kg/day IM or IV 1-2x/day
° Cefotaxime 200-300 mg/kg/day IM or IV every 6 or 8 hours
• Treatment duration: 5-7 days
V. PREVENTION
• Household, school or day care contacts during the 7 days before onset of illness should
receive antibiotic prophylaxis
• Prophylaxis not routinely recommended for medical personnel except those with
intimate exposure (intubation, suctioning, mouth to-mouth resuscitation):
0 Rifampicin 10 mg/kg PO every 12 hrs for a total of 4 doses (max 600 mg/dose);
5 mg/kg/dose for <l month old
° Ceftriaxone 125 mg single dose IM for <15 yrs old, 250 mg single dose IM for 2:15 years old
° Ciprofloxacin 500 mg PO as a single dose 2: 18 years old
• Meningococcal vaccination for high risk population
230
PERTUSSIS
I. ETIOPATHOGENESIS
• Bordetella pertussis
Etiologic agent
• Bordete/la parapertussis
Incubation
• 7-10 days (range of4-21 days)
period
• Aerosol droplets
Transmission • Extremely congatious [attack rates as high as 100% in susceptible
individuals)
II. MANIFESTATIONS
STAGES* REMARKS
• Non-specific symptoms of low-grade feve1; colds, congestion, sneezing,
Catarrhal stage (1-2
lacrimation, conjunctiva! suffusion
weeks)
• Patients are most infectious during this period
• Coughing marks the onset (starts as dry, intermittent and irritative
hack)
• Cough evolves into paroxysms of 5-10 rapid coughs ending in a high-
pitched whoop (forceful inspiratory gasp), described as "whooping
Paroxysmal stage
(2-6 weeks)
cough"
• Cyanosis during paroxysmal coughing, posttussive vomiting and
exhaustion, conjunctiva! hemorrhage, and petechiae on upper body is
common
• In between paroxyms, child may look well
I
Convalescent stage
• Number, severity, and duration of cough episodes diminish
(>2 weeks)
'Infants <3 months old may not manifestwiththe classic 3 stages (apnea with or withoutcough may be the
presenting symptom)
III. DIAGNOSIS
Clinical case
• Cough lasting ;,14 days, with paroxysmal cough, inspiratory whoop or vomiting
definition
Laboratory • Culture or PCR (specimen obtained through posterior nasopharyngeal swab)
confirmation • Paired serology
IV. MANAGEMENT
• Macrolides: drug of choice
• Infants <l month old should be treated with azithromycin due to higher risk of
developing infantile hypertrophic pyloric stenosis with erythromycin & clarithromycin
ANTIBIOTIC REMARKS
V. PREVENTION
• Household contacts should be treated with macro!ides (same dose as in management)
• Ensure complete immunization of children, adolescents and pregnant women (refer to
preventive pediatrics chapter)
231
TETANUS
• Acute spastic paralytic illness due to tetanus toxin (tetanospasmin)
• Favorable prognosis: long incubation period, absence of fever, localized disease
• Unfavorable prognosis: onset oftrismus <7 days after injury, generalized tetanic spasms
occuring <3 days after onset oftrismus, cephalic tetanus
I. ETIOPATHOGENESIS
Etiologic agent • Clostridium tetani
Incubation • 2-14 days, but may occur months after an injury
• Associated with traumatic injury(penetrating wound from a dirty object)
Transmission
• Introduced spores germinate, and produce tetanus toxin
II. MANIFESTATIONS
TYPES REMARKS
Neonatal or • Occurs within 3-12 days of birth
umbilical
tetanus (most
• Progressive difficulty in feeding
common form) • Hunger, crying, paralysis, stiffness and rigidity to touch, spasms
III. MANAGEMENT
• Human tetanus immunoglobulin 500 U single IM dose neutralizes
tetanus toxin
Vaccination
• lfTIG unavailable: human !Vig,equine or bovine-derived tetanus antitoxin
• Upon discharge, give tetanus toxoid
Antibiotics
• Metronidazole PO/IV is the drug of choice
• Penicillin G (erythromycin and tetracycline if penicillin-allergic)
• Wound excision & debridement
• For generalized tetanus: muscle relaxants and neuromuscular blockers
Supportive
• Intubation to prevent aspiration, early tracheostomy in severe cases
• Quiet, dark, secluded setting
IV. PREVENTION
• Vaccination with DTaP,Tdap and Td
• Pregnant women should receive 1 dose of Tdap during each pregnancy, at 27-36 weeks AOG
• Tetanus prophylaxis in wound management:
° Clean minor wounds and <3 doses ofTd: Tdap or Td
• Clean minor wounds and ,;:3 doses ofTd within the past 10 years: No need for toxoid
All other wounds and <3 doses ofTd: Tdap or Td and TIG
All other wounds and ;;;3doses ofTd within the past 5 years: No need for toxoid/TIG
Source:CDCandPrevention.
Tetanus;
2019
232
TUBERCULOSIS (TB)
I. ETIOPATHOGENESIS
Etiologic agent • Mycobacterium tuberculosis
• Inhalation of airborne mucus droplet nuclei
Mode of
• Factors increasing transmission:·extensive upper lobe infiltrate or cavity,
Transmission
copious sputum production, severe and forceful cough, poor air circulation
Incubation • 3 months to 2 years
• Aerosol droplets
Transmission
• Extremely congatious
Gastrointestinal
TB
• Most common form is pericarditis (e.g., chest pain, friction rub)
• May manifest as painless ulcer in the oral mucosa, TB peritonitis
(abdominal pain, ascites, anorexia, fever), or TB enteritis (abdominal
pain, diarrhea or constipation, weight loss, fever)
I
Renal TB {Rare) • Sterile pyuria, hematuria, dysuria, flank or abdominal pain
• Congenital transmission via hematogenous or transplacental spread
from an infected mother or during the postnatal period via inhalation
of airborne droplet nuclei
• Any infant with TB lesions & 1 or more of the following (Cantwell
Congenital
Tuberculosis Criteria, 1994):
0 Present within the first week of life
0 A primary hepatic complex or caseating hepatic granuloma
0 TB infection of placenta or endometrial TB in mother; or exclusion of the
possibility of postnatal transmission by excluding TB in other contacts
Ill. DIAGNOSIS
DIAGNOSTIC REMARKS
233
IV. MANAGEMENT
LEPTOSPIROSIS
I. ETIOPATHOGENESIS
Etiology • Nine pathogenic species of spirochetes from the genus leptospira
• Zoonotic disease: infection mostly results from exposure to water or
soil contaminated with rat urine
Transmission
• Other animal reservoirs: dogs, cats, livestock, wild mammals
• Incubation period: 7-12 days
• Leptospires enter humans through abraded skin, mucous membranes,
or ingestion
Pathogenesis • Leptospires circulate in the bloodstream and cause damage to the
endothelial lining of small blood vessels, resulting in ischemic damage
to the liver, kidneys, meninges & muscles
234
II. MANIFESTATIONS
• Lasts 2-7 days
• Abrupt onset of fever, chills, severe headache, malaise, nausea
• Severe myalgia most prominent in the lower extremities,
Initial or lumbosacral spine and abdomen
septicemic
phase • Conjunctiva! suffusion with photophobia & orbital pain,
without chemosis & purulent exudate
Anicteric • Hepatosplenomegaly, generalized lymphadenopathy
Leptospirosis • Transient e1ythematous maculopapular rash
• Lasts several weeks
Second or • Follows a brief asymptomatic interlude with recurrence of
immune fever (biphasic fever)
phase • Aseptic meningitis: CNS symptoms usually resolve
spontaneously within 1 week
• Severe form affecting < 10% of cases
• Initial or septicemic phase: similar to anicteric leptospirosis
• Immune phase:
Icteric Leptospirosis • Jaundice, RUQ pain, hepatomegaly, increased liver
(Weil's syndrome) enzymes, hyperbilirubinemia
• Renal failure (principal cause of death)
• Thrombocytopenia
III. DIAGNOSIS
• Hemorrhage & cardiovascular collapse
IV. MANAGEMENT
ASPECTS MANAGEMENT
• Penicillin G 6-8 million U/m2/day every 4 hours for 7 days**
Antibiotics* • Alternative: doxycycline (not for children <8 years old),
azithromycin
• Doxycycline 4mg/kg single dose (max 200mg): in children
Prophylaxis <8 years, dose and duration unlikely to cause dental staining
• Alternatives: Azithromycin OR Amoxicillin
• Rodent control measures
Prevention • Use protective clothing to avoid contaminated water and soil
• Immunization of livestock and domestic dogs
'Initiationof treatmentbeforethe 7th day may shorten the clinicalcourse and decrease the severityof infection
"Jarisch-Herxheimer reaction may develop after initiationof penicillintherapy
Sources:KliegmanRM,etal. NelsonTextbook
of Pediatrics
(21sted.).Elsevier;
2020
ChirathawomC,et al.AsianPacJ TropBiomed; 2014
Kimberlin
OW,et al.American
Academy of Pediatrics.
Redbook;2015
TheLeptospirosis
TaskForce(PSMID, PSN,PCP)Philippine CPG;2010
235
COMMON BACTERIAL SKIN INFECTIONS
2) Cellulitis
• Penicilinase·resistant penicillin
• Infection of loose connective tissue
[cloxacillin) or first generation
with limited dermal involvement
cephalosporin (cephalexin)
and sparing of the epidermis
• Parenteral therapy should be
• Staphylococcus • Area of edema, warmth, erythema,
initiated if (e.g., oxacillin):
aureus and tenderness with indistinct
• Disease progresses significantly
• Streptococcus margins
within 1-2 days of antibiotics
pyogenes • Cellulitis from S. aureus: more 0 No improvement noted on oral
localized
antibiotics
• Cellulitis from S. pyogenes: more
• With feve1; lymphadenopathy or
rapid and cause lymphangitis
constitutional signs
236
OTHER BACTERIAL INFECTIONS
-
Kimberlin
OW,et al.AmericanAcademyof Pediatrics.Redbook.American Academyof Pediatrics;
2015
GomellaTL,et al. Neonalology 7thEdition.McGraw-Hill;
201
ETIOLOGY MANIFESTATION TRANSMISSION DIAGNOSTICS MANAGEMENT CONTROL MEASURES
3) Shigellosis (Shigella dysenteriae)
• For bloody diarrhea,
• Bacillary dysentery: bloody diarrhea with feve1; • Presumptive regardless of age:
abdominal cramps, rectal pain and mucoicl stools
• Most common • Personto person diagnosis: fecal Ciprofloxacin 20-30
• Severe abdominal pain, cmesis, anorexia,
in 2-3 years transmission leukocytes, mg/kg/day in 2 • Proper handwashing
generalized toxicity, painful defecation (tenesmus)
old (fecal-oral route) fecal blood and divided doses techniques when preparing
• Abdominal distention & tenderness, hyperactive
• Incubation • Requires very low leukocytosis • Other antibiotics: food, using the toilet, or
bowel sounds, tender rectum on digital exam
period: 12 hrs inocula to cause • Definitive ° Cefixime changing diapers
• Neurologic manifestations (40%) are the most
to 7 days illness diagnosis: cultu,·e ° Ceftriaxone
common extraintestinal manifestation
0 Azithromycin
• Dehydration is the most common complication of stooljrectal swab
• Duration: 5 days
Diaper dermatitis
• Most common infection caused by
Candida
Candida
albicans
• Confluent erythematous rash with • Topical nystatin
satellite pustules • Miconazole
Vu!vovaginitis • Clotrimazole
• Pubertal & postpube1tal females
2) Tinea Versicolor
• Pain or itching, dysuria, vulvar or
vaginal erythema, opaque white or
cheesy exudate I
• Reddish brown macules (in fair-
• Topical selenium sulfide
skined children) or hypopigmented/
2.5% shampoo 10 minutes
hyperpigmented macules (in dark-
• Malassezia daily for 2 weeks, then once a
skinned children)
globose week (for several months) to
• Macules are covered with fine scales,
• Malassezia prevent relapse
beginning in a perifollicular location
sympodialis • Other topical agents:
and merging to form patches, with
• Malassezia ketoconazole shampoo,
little to no pruritus
restricta terbinafine, clotrimazole
• Most commonly found on neck, upper
• Malassezia • For severe/recurrent
chest, back & upper arms
furfur disease or if topical therapy
• Potassium hydroxide [KOH) scrapings
failed: oral ketoconazole,
show short curved hyphae & circular
fluconazole, or itraconazole
spores ("spaghetti & meatballs")
3)Scabies
239
SECTION SIX
CLINICAL SYNDROMES
Z) Eyelids
Blepharitis • S. aureus, S. epidermidis • Etythromycin or Bacitracin ointment
Hordeolum • S. aureus • Warm compress
• Clindamycin, plus
Neonates • S. aureus, GroupB streptococci,HiB
• Cefotaxime or ceftriaxone
240
INFECTIONS OF THE PULMONARY SYSTEM
I. UPPER RESPIRATORY TRACT INFECTIONS
INFECTION ETIOLOGY EMPIRIC ANTIMICROBIAL
• S. a11re11s,
Streptococcus, Gram (-) • Oxacillin or Clindamycin, plus
1) Parotitis
organisms, anaerobes aminoglycoside
• H. influenzae, S. pyogenes, S.
2) Epigfottitis • Ceftriaxone or Cefotaxime
aureus, S. pneumoniae
Neonate
• Group B streptococcus,
Gram-negative bacilli
• S. p11e11mo11iae,
H. i11f/11e11zae,
• Penicillin G or Ampicillin, plus
• Aminoglycoside
• Mild illness: Amoxicillin PO
• Moderate or serious illness: 2 nd
I
Infant to 5 yrs old
S. aureus or 3"1 generation cephalosporins
or Ampicillin-sulbactam
241
GENITOURINARY TRACT
INFECTION ETIOLOGY EMPIRIC ANTIMICROBIAL
1) Bacterial Vaginosis • Gardnerella,anaerobes • Metronidazole PO or vaginal gel
3) Gonococcal Infections
• Children <45 kg: Ceftriaxone IM
Uncomplicated
cervicitis, urethritis, • Adolescents: Ceftriaxone or Cefixime
vaginitis
• N. gonorrhea + regimen effective for Chlamydia
7) Syphilis
Congenital • Aqueous Penicillin G
• S.saprophyticus,Streptacoccus,
• Azithromycin or Doxycycline
Enterobacteriaceae,G.vaginalis
8) Non-Gonococcal • <8 years old: Erythromycin,
Urethritis Azithromycin
• Chlamydia trachomatis
• >8 years old: Azithromycin or
Doxycycline
MUSCULOSKELETAL INFECTIONS
INFECTION ETIOLOGY EMPIRIC ANTIMICROBIAL
1) Osteomyelitis
• S. aureus,gram negativebacilli, • Oxacillin, plus
Infants <4 months
Group B streptococcus • Ceftazidime
242
GASTROINTESTINAL TRACT
• Ampicillin, plus
2}Acute • Gram negative enteric aero bes • Metronidazole or Clindamycin,
Appendicitis and anaerobes plus
• Aminoglycoside
• 3 rd generation cephalosporin
3) Acute Cholangitis • E. coli, Klebsiel/a, Enterococcus, (except Ceftriaxone), plus
Cholecystitis Bacteroides • Metronidazole, plus
4) Peritonitis
Primary
• S. pneumoniae, S.pyogenes,
S. aureus, E. coli
• Aminoglycoside
• Penicillin G
I
• Ampicillin, plus
• Enteric gram negative aerobes,
Secondary • Metronidazole or Clindamycin,
anaerobes (8. fragilis)
plus Aminoglycoside
• S. aureus, Streptococcus, Gram • Clindamycin or
SJ Pyogenic Liver negative aerobic and anaerobic Oxacillin+Metronidazole, plus
Abscess
organisms • Aminoglycoside
Souce:Handbook
of PediatricInfectious
Diseases,2014
NationalAntibioticGuidelines
2017
243
REFERENCES
1. American Academy of Ped1atncs Kimberlin OW, Brady MT, Jackson MA, Long SS, eds Red
Book: 2015 Report of the Committee on Infectious Diseases 30th ed Elk G1ove Village, IL·
American Academy of Pediatrics; 2015.
2. American Academy of Pediatrics. Kimberlin OW, Brady MT, Jackson MA, Long SS, eds.
RedBook: 2018 Report of the Committee on Infectious Diseases. 31st ed. Itasca ,IL: American
Academy of Pediatrics 2018
3. Behr MA, et al. Revisiting the timetable of tuberculosis. BM) 2018;362:k2738.
4. Cantwell, M., Shehab, Z., Costello, A., Sands, L., Green, W., & Ewing, E. et al. (1994). Congenital
Tuberculosis. New England Journal Of Medicine, 330(15), 1051-1054
5. Centers for Disease Control and P1·evention. Meningococcal Disease. https://www.cdc.gov/
vaccines/pubs/pinkbook/mening.html. Accessed February 25, 2019.
6. Centers for Disease Control and Prevention. Recommended Antimicrobial Agents for the
Treatment and Postexposure Prophylaxis of Pertussis: 2005 CDC Guidelines. MMWR,
54(RR14), 1-16.
7. Centers for Disease Control and Prevention. Salmonella. https://www.cdc.gov/salmonella/
general/technical.ht111l. Accessed February 25, 2019.
8. Centers for Disease Control and Prevention. Tetanus. https://www.cdc.gov/tetanus/
clinicians.ht111l. Accessed February 25, 2019.
9. Department of Health. National Tuberculosis Control Program Manual of Procedures. (5th
ed.). Manila: Depart111ent of Health; 2014
10.Edwards, M. Clinical Features, Evaluation, Diagnosis of Sepsis in Term and Late Preterm
Infants. UpToDate20l 9.http://www.uptpdate.com. Accessed March 21, 2019
11.Edwards, M. Management and Outcome of Sepsis in Term and Late Preterm Infants.
UpToDate20l 9.http://www.uptodate.com Accessed March 21, 2019
12.French P. Syphilis. BM) 2007 334(7585), 143-147
13.Gappy C, et al. Orbital Cellulitis. https://www.uptodate.com/contents/orbital-cellulitis; 2019
14.Gappy C, et al. P1-eseptal Cellulitis. https://www.uptodate.com/contents/preseptal-
cellulitis; 2019
15.Gomella TL, et al. Neonatolgy 7th Edition. McGraw-Hill; 2013.
16.Harrison LH, Kreiner CJ, Shutt KA, Messonnier NE, O'Leary M, Stefonek KR, et al. (2008).
Risk factors for meningococcal disease in students in grades 9-12. Pediatr Infect Dis ],
27(3), 193-199.
I ?.Kimberlin DW, Brady Ml'. Jackson MA, Long SS. (Eds.) (2015). American Academy of
Pediatrics. Red book: 2015 report of the Committee on Infectious Diseases (30th ed.). Elk
Grove Village, IL: American Academy of Pediatrics.
18.Kliegman, R., ST GEME 111,)., Blum, N., Shah, S., Tasker, R., Wilson, K., & Behrman, R. (2020).
Nelson Textbook of Pediatrics (21st ed.). Philadelphia: Elsevie1c
I 9.Mandell GL, Bennett, JE and Dolin R. editors: Mandell, Douglas and Bennett's Principles
and Practice of Infectious Diseases, ed 7, Philadelphia, 2010,Elsevier
20.Natalie, N; Duchon, J; and Zachai-iah, P. Clinics in Perinatology, 2015-03-01, Volume 42,
Issue 1, Pages 77-103. 2015 Elsevier
21.National Antibiotic Guidelines Committee. National Antibiotic Guidelines 2017.
Department of Health Quezon City Philippines. 2017. Available from <https://drive.google.
com/file/d/1 lyc20ggVkTAim3fNG7rgmyEloHanQKnR/view>
22.National Dengue Prevention and Control Program. Revised Dengue Clinical Case
Management Guidelines 2011. Department of Health Manila Philippines. Available from <
thefilipinodoctor.com/cpm_pdf/CPM15th%20DENGUE%20FEVER%20(DOH).pdf>
23.Neu J. Necrotizing enterocolitis: the search for a unifying pathogenic theory leading to
prevention. Pediatr Clin North Am 1996; 43:409.
24.Patterson Mj and Davies JD. Syphilis (Treponema pallidum). In: Kliegman RM, Stanton BF,
St Geme JW, Schor NF. (Eds.) (2016} Nelson Textbook of Pediatrics (20th ed.). Philadelphia,
PA: Elsevier.
ZS.Philippine Pediatric Society. Handbook of Pediatric Infectious Disease 2014 Edition.
Philippine Pediatric Society Inc. 2014
26.The Leptospirosis Task Force (PSMID, PSN, PCP) Philippine Clinical P,·actice Guidelines on
the Diagnosis, Management and Prevention of Leptospirosis 2010
27.Veeraraghavan B, Pragasam AK, Bakthavatchalam TD, and Ralph R. (2018). Typhoid fever:
issues in laboratory detection, treatment options and concerns in management in
developing countries. Future Sci OA, 4(6), FS)312.
28.World Health Organization. Comprehensive guidelines for prevention and control of
dengue and dengue haemorrhagic fever. Revised and expanded edition .. New Delhi: World
Health Organization, Regional Office for South-East Asia 2011. Available from <http://
a pps.searo. who.int/pds_docs/B4 7 51.pdf>
29.World Health Organization. Dengue: guidelines for diagnosis, treatment, prevention
and control -- New edition. Geneva: WHO 2009. Available from < https://www.who.int/
tdr /publications/ documents/ dengue-diagnosis.pd f>
30.World Health Organization. Guidelines for Typhoid Fever July 2011. Available from <
http://apps.who.int/medicinedocs/documents/s20994en/s20994en.pdf>
31.Yip WCL. Dengue haemorrhagic fever: current approaches to management. Medical
Progress; 1980; 7(13):201-209
244
GASTROENTERO
SECTION ONE
APPROACH TO COMMON GASTROINESTINAL COMPLAINTS
247
• In neonates: Hirschsprung
disease, intestinal
pseudoobstruction,
• Definition is relative and hypothyroidism
depends on stool consistency • Fecal impaction
and frequency as well as • Functional constipation
Constipation difficulty in passing the stool • Spina bifida
• Hard stool passed with • Imperforate anus
difficulty every 3rd day is • Developmental delay
considered constipation • Dehydration
• Medications: narcotics
• Lead poisoning
• Botulism
• Functional abdominal pain
• Considerable variation • Irritable bowel syndrome
among children in their • Constipation
perception and tolerance for • Lactose intolerance
abdominal pain • Esophagitis
• Distinguish organic* and • Intestinal parasitism
nonorganic (functional) • Inflammatory bowel disease
causes of abdominal pain (IBD)
• Visceral pain: dull and • Cholelithiasis
Abdominal pain aching pain felt in the • Choledochal cyst
dennatome from which the • Pancreatitis
organ receives innervation • Appendicitis
• Somatic pain: intense • Inguinal or abdominal hernia
and well localized (e.g. • Intestinal obstruction
peritonitis) • Non-GI causes (e.g., renal colic,
• Referred pain: pain from pneumonia, pelvic inflammatory
other organs disease, sexual abuse,
psycho logic causes, HSP,
anaphylaxis)
• Hematemesis: originates • Erosive damage
from esophagus, stomach, or (most common cause)
duodenum • Bacterial enteritis
• Hematochezia: red blood in • Milk protein allergy
the stools; distal bleeding • lntussusception
Gastrointestinal site or massive bleeding • Anal fissure
hemorrhage above the distal ileum • Lymphonodular hyperplasia
• Melena: blackened stools of • Peptic ulcer/gastritis
tarry consistency; from mild • Swallowed epistaxis
to moderate bleeding above • Prolapse gastropathy
the distal ileum • Mallory-Weiss syndrome
I • Colonic polyps
• Ascites
• Distention results from
• Solid masses (Wilms
diminished tone of the wall
tumor, hydronephrosis,
Abdominal musculature or increased
neuroblastoma,
distention abdominal content
hepatoblastoma, lymphoma,
• If with as cites, fluid analysis
teratoma, mesenteric cyst)
aids in determining etiology
• Pregnancy
'Consider organicetiologyof abdominalpain ifwithfever,weightloss, biliousemesis,jaundice,hepatosplenomega-
ly,back or flankpain, awakenschildfromsleep, referredpain to shoulder,groinor back, elevatedESR,WBCcount,
CRP,anemia,edema, hematochezia,or withstrong historyof IBD
248
SECTION TWO
GASTROINTESTINAL DISORDERS OF THE NEONATE
I.ETIOPATHOGENESIS
TYPES OF TEF ILLUSTRATION DESCRIPTION
• Isolated EA
Type A (8%) • Pure esophageal atresia without
a TEF
I
• EA with distal TEF
• Most common type
• Esophagus ends blindly 10-20 cm
Type C (87%)
from the nares
• The distal esophagus communicates
with the posterior trachea
II. MANIFESTATIONS
• Infant is unable to handle secretions with subsequent excess salivation and aspiration of
pharyngeal contents due to the esophageal obstruction, requires frequent suctioning
• Feeding usually exacerbates the symptoms, causes regurgitation & precipitates aspiration
249
III. DIAGNOSIS
• Inability to pass an NGT or OGT in the newborn is suggestive especially in the setting of
early-onset respiratory distress
• Plain radiographic films may show coiled NGT/OGT tube in the esophageal pouch
• 50% have associated anomalies (VATER/VACTERL):
Vertebral • Esophagus
• Anorectal Renal
• Cardiac Radial
• Trachea • Limb syndrome
IV. MANAGEMENT
• Maintain a patent airway
• Pre-operative proximal pouch decompression to prevent aspiration of secretions
Supportive
• Antibiotic therapy for consequent pneumonia
• Prone positioning to reduce regurgitation & esophageal suctioning
• Current standard surgical approach: surgical ligation of the TEF & primary
Surgery
end-to-end anastomosis of the esophagus via right-sided thoracotomy
Sources:DunkleyM, et al. InternationalSurgery:2014
ClohertyJ, et al. Manualof NeonatalCare(7thed.).LippincottWilliams& Wilkins:2012
GomellaTl, et al. Neonatology
7th Edition.McGraw-Hill:2013
II. MANIFESTATIONS
• Postprandial, nonbilious vomiting is the initial symptom that usually starts
at 3 weeks of age
Symptoms
• Non-bloody, nonbilious emesis increasing over the course despite small
frequent feedings
• Firm, movable, olive-shaped mass, easily palpable after vomiting
Signs
• Visible gastric peristaltic wave after feeding may be seen
III. DIAGNOSIS
REMARKS/FINDINGS
• Persistent muscle thickness in the presence of functional gastric outlet
obstruction
Ultrasound • Confirmatory findings:
• Pyloric thickness 3-4 mm
• Overall pyloric length 15-19 mm
• Pyloric diameter 10-14 mm
IV. MANAGEMENT
• Correcting fluid, acid-base, and electrolyte losses
• Surgical procedure: Ramstedt pyloromyotomy
Source:KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Canada:Elsevier:2020
GomellaTL, et al. Neonatolgy7th Edition.McGraw-Hill:
2013
250
HIRSCHSPRUNG DISEASE (HD)
• Congenital aganglionic megacolon causing loss of ability of the muscles in the bowels to
move stool through the intestine
• Most common cause of lower intestinal obstruction in neonates
I. ETIOPATHOGENESIS
• More common in males
• Due to arrest of neuroblast migration from the proximal to distal bowel, leading to
absence of ganglion cells in the bowel wall beginning in the internal anal sphincter
• Absence of Meissner & Auerbach plexus and hypertrophied bundles with high
concentrations of acetylcholinesterase between the muscular & sub mucosa layers leads to:
0 Decreased motility in the affected bowel segment
0 Lack of propagation of peristaltic waves into the aganglionic colon
0 Abnormal or absent relaxation of this segment and of the internal anal sphincter
II. MANIFESTATIONS
• Distended abdomen, failure to pass meconium, bilious emesis or
aspirates, feeding intolerance
Symptoms • Suspected in any full-term infant with delayed passage of stool (no
meconium output> 48 hours of life)
• Some present with history of chronic constipation
• Tympanitic and distended abdomen
Signs • Large fecal mass palpable in the left lower quadrant
• Pellet-like or ribbon-like stool or with fluid consistency
I
Rectal • Rectum usually empty of feces on exam with normal anal tone
Examination • May have an explosive discharge ("gush of air") once finger is removed
Ill. DIAGNOSIS
DIAGNOSTIC REMARKS/FINDINGS
Rectal suction
biopsy • Gold standard (easy and reliable J
• Transition zone between normal dilated proximal colon and the
Abdominal smaller-caliber obstructed distal colon due to nonrelaxation of the
X-ray with
aganglionic bowel
contrast
enema • A rectal diameter that is the same as or smaller than the sigmoid colon
is suggestive
IV. MANAGEMENT
• Operative repair with surgical options/ techniques: Swenson, Duhamel, Soave
• Currently, many infants undergo primary pull-through procedure unless there is
associated enterocolitis or other complications
251
OTHER DISORDERS ENCOUNTERED IN THE NEONATE
I. DUODENALATRESIA
• Due to failure to recanalize the lumen during the 4th-5th week of gestation
Etiopathogenesis • Obstruction usually distal to the ampulla of Vater
• More common in preterm infants
III. IMPERFORATEANUS
Etiopathogenesis • Absence ofan anal opening of proper location and size
Alimentation
• High association with
congenital anomalies/
chromosomal abnormalities
• Normal
• Volvulus
• Atresia
• Delayed
I
Surgical • Not urgent with intact
management • Urgent
membrane
• Total parenteral nutrition
• Total parenteral nutrition
• Hydration
• Hydration
• Ruptured omphalocele: similar
• Prevent evap.orative heat loss by
management to gastroschisis
Other Supportive decompression and wrapping
• Intact sac: timing of repair
Ma11agement with moist clean dressing
depends on size of defect,
• Nasogastric decompression
gestational age and co-morbid
• Broad spectrum antibiotics as
conditions
indicated
• P:ntibiotics as indicated
253
SECTION THREE
DIARRHEA AND GASTROENTERITIS
ACUTE GASTROENTERITIS
I.ETJOPATHOGENESIS
• Acute diarrhea (less than 14 days) must be differentiated from chronic or persistent
diarrhea (more than 14 days duration)
• Majority are foodborne illnesses
• Viruses are one of the most common causes of acute diarrhea in children
A. Etiology of Acute Diarrhea
• C.jejuni, C. difficile, EIEC (Enteroinvasive £. coli), Salmonella,
Inflammatory
Shigella, Yersinia
• EPEC (Enteropathogenic £. co/1), ETEC (Enterotoxigenic E. coh),
Noninflammatory
V.cholera
Viral • Rotavirus, Adenovirus, Astrovirus, Norwalk, Calicivirus
Parasitic • G.lomblia, E. histolytica, B. coli, Strongyloides, spore-forming protozoa
C. Mechanisms of Diarrhea
OSMOTIC DIARRHEA SECRETORY DIARRHEA
• Presence of nonabsorbable • Activation of intracellular
solutes in the GITas a result of: mediators (e.g., cAMP,
• Intestinal damage cGMP) that stimulate active
• Reduced absorptive surface chloride secretion & inhibit
area (e.g., active celiac disease)
Pathogenesis the neutral coupled NaCl
• Defective digestive enzyme (e.g.,
lactose intolerance) absorption
0 Decreased intestinal transit time • Toxin-mediated injury to the
• Nutrient overload (e.g., tight junctions
overfeeding.sorbitol in fruit juice) • Results in extremely watery stool
254
D. Stool Output in Infants/Children contains approximately per liter (average composition of diarrhea):
55 mEq of Na+
25 mEq of K+
15 mEq of HCO-
III. DIAGNOSIS
• Diagnosis is based on clinical recognition, evaluating severity by rapid assessment
• For most cases, no laboratory tests are required except for epidemiologic purposes
DIAGNOSTICS REMARKS/FINDINGS
• Examine for mucus, blood, and leukocytes
Stool exam • Fecal leukocytes indicate bacterial invasion of colonic mucosa, or early
Stool culture
infection by Shigella, Shiga toxin-producing£. coli, or£. histo/ytica
• Usually done in the following cases:
0
0
Hemolytic Uremic Syndrome (HUS) is suspected
Bloody diarrhea
I
0Stool with fecal leukocytes
0During outbreaks
0Immunocompromised patients
IV. MANAGEMENT
• Management of dehydration is the cornerstone
Rehydration
• Rehydration with replacement of losses during the first 4-6 hours
• Reintroduce food once rehydration is complete
• Continued enteral feeding in diarrhea aids in recovery
Feeding
• Zinc supplementation reduces duration & severity of diarrhea and
prevents recurrence
Anti-diarrheals • Generally not recommended
• Generally not administered
• Antibiotics may be necessary for some infectious causes to reduce the
Antibiotics fluid requirements and limit the excretion of organism:
0 Shigella: Ciprofloxacin
255
APPROACH TO MANAGEMENT OF ACUTE GASTROENTERITIS (AGE)
• Assess the degree of dehydration & provide fluid & electrolyte replacement
Prevent spread of the enteropathogen
• Determine etiologic agent in selected cases & provide specific therapy if indicated
PARAMETER• 1-.~~~D~
DEH~git~
General Lethargic***,
Alert Irritable Unconscious
condition
Eyes•• Normal Sunken Sunken
Drinks poorly, not
Thirst None Drinks eagerly able to drink
Skin
Quick Slow Very slow
retraction ••
Glucose 75
Sodium 75
Chloride 65
Potassium 20
Citrate 10
Osmolarity 245
Source:Kliegman R.el al. NelsonTextbookof Pedialncs(21sted.).Philadelphia:
Elsevier:
2020
WorldHealthOrganization.Thetreatment of diarrhea.Geneva;
2005
LongS,et al. Pnnciples
andpracticeof pediatncinfectious
diseases(4thed.).Saunders Elsevier:
2012
Practical Tips: For patients with vomiting it is better to administer ORS slowly via
dropper, with few minutes of rest in between, instead of drinking it from a cup or bottle.
If patient remains to vomit ORS despite the above strategy, it can be given in smaller
volume with longer interval in between. For example: give a teaspoonful every 1-2 minutes.
If the child vomits, wait 5-10 minutes then continue ORS administration more slowly
256
III. COMPOSITION OF COMMONLYUSED FLUIDS
• Fruit juice, soda, sports drinks, and commercially prepared soup a,·e not recommended since
their electrolyte composition & osmolarity does not match physiologic replacement of losses
• WHO recommends the use of reduced osmolarity ORS (applicable for patients without
severe malnutrition)
• For those with severe malnutrition
In hospital management and referral to a specialist is recommended
° Full strength ORSshould not be used for oral rehydration Q1alfstrength ORSis recommended)
I
0
0May be repeated if some signs of dehydration are still present after 4 hours
• The following table may be used to approximate amount of ORS from patient's
age if the weight is unknown
---~---....-----....-------.--------,,------,
<4 mos 4-11 mos 12-23 mos 2-4 yrs 5-14 yrs 2:15 yrs
PlanB
<5 5-7.9 8-10.9 11-15.9 16-29.9 ~30
257
Case 2. A 4 year-old female, weight of15 kg, was brought to the OPDdue to 4 day history
of LBMwith several episodes of vomiting. BP= 90/60 HR=120 RR= 20. Patient is awake,
drinks eagerly, with sunken eyeballs and poor skin turgor.
Assessment • Some signs of dehydration
• Treatment Plan B
, 75 mL/kg x 15 = 1.125 mL ofORS to be given within 4 hours
Plan
' If ORS is tolerated and patient has no signs of dehydration after 4 hours.
may send patient home on treatment plan A
Case 3. A 4 year-old male was brought in the ER due to 3 days of LBM. Patient is
lethargic, does not drink fluids, sunken eyeballs with a BP of90/60
Assessment • Severe dehydration
• Treatment plan C
Plan , pLR 450 mL IV for 30 minutes, then 1,050 mL to run for 2 ½ hours
, Reassess patient after 3 hours & manage accordingly (Plan A, B or C)
Watery or
Bloody • Escherichia coli • See IDS chapter for details
CHRONIC DIARRHEA
I. ETIOPATHOGENESIS
• Increased total daily stool output with increased stool water content lasting <!4weeks
• Persistent diarrhea lasts 14 days or more. In clinical practice this is equivalent to loose or
watery stool more than 3 times per day
• Results from altered intestinal water and electrolyte transport
II. MANAGEMENT
• General supportive measures
• Nutritional rehabilitation
• Elimination diet
• Medications as indicated (for specific etiologies)
258
SECTION FOUR
DISORDERS O.F THE GASTROINTESTINAL TRACT
I.ETIOPATHOGENESIS
• Most common esophageal disorder in children of all ages
• GER is considered a physiologic process
• GERO is pathologic: frequent or persistent episodes and with complications (esophagitis,
respiratory symptoms, failure to thrive, feeding refusal)
A. Pathophysiology:
LES is supported by the crura of diaphragm at the gastro-esophageal (GE) junction
which has valve-like functions & forms the anti-reflux barrier
Transient LES relaxation (TLESR) is the major mechanism allowing reflux to occur
Gastric distention is the main stimulus for TLESR (straining, coughing, large volume or
hyperosmolar meals)
B. Epidemiology
Infant reflux evident at first few months of life, peaks at 4 months, resolves mostly at
12 months & nearly all at 24 months old
Genetic predisposition: autosomal dominant (locus GERDl in chromosome 13q14)
II. MANIFESTATIONS
AGE GROUP MANIFESTATIONS BASED ON AGE GROUP
• Regurgitation, excessive crying/irritability, vomiting, food refusal
I
Infants
• Persistent hiccups, abnormal posturing, impaired quality of life
• Impaired quality oflife, vomiting, esophagitis
Children • Peristent/chronic cough, aspiration pneumonia, wheezing
• Ear infections, stridor, heartburn
Adolescents • Impaired quality of life, esophagi tis, dysphagia
and adults • Heartburn, epigastric pain, chest pain
Source:KllegmanR. et al. NelsonTextbookof Ped,atncs(21sted.).Canada:Elsevier;2020
Ill. DIAGNOSIS
A. Clinical Diagnosis
Thorough history and PE suffice initially to reach diagnosis
No single test to definitely diagnose GERO
Empirical anti-reflux therapy using a trial of high-dose proton pump inhibitors (PPI)
may be done [if responsive, then it is virtually diagnostic of GERO)
Bo· :
DIAGNOSTIC REMARKS
Barium study of
the upper GIT
• To rule out anatomic causes of vomiting
Gastroesophageal
• To scan for reflux using 99mTc-labeled markers
scintigraphy
259
IV. MANAGEMENT
ASPECT MANAGEMENT
• Lifestyle modification is the foundation of GERO therapy
Conservative
• Maintain on prone or upright carried position (avoid prone position
therapy
for infants who are asleep J
• Thickening of formula by adding up to 1 tablespoon of dry rice cereal per 1
Dietary
oz of formula or using commercially thickened formula for full term infants
measures
• Avoid acidic/spicy foods, juices, alcohol, caffeinated & carbonated drinks
• Proton pump inhibitors (PPI): current standard of care (e.g.,
Medical omeprazole, lansoprazole, esomeprazole)
• Others: Antacids, HZ Receptor antagonists, prokinetic agents
• May be an option for intractable GERO, refractory esophagitis &
Fundoplication
strictures, with morbidities from chronic pulmonary disease
Source:KliegmanR. et al. NelsonTextbook
of Pediatrics(21sted.).Canada:Elsevier:2020
LightdaleJ. et al. Pediatrics:2013
II. MANIFESTATIONS
• Majority present with poorly localized dull or aching abdominal pain, which may be
relieved after antacids in some
• Classic symptom: epigastric pain relieved by food intake (seen only in minority of children)
• Hematemesis or melena is reported in 50%
School-age children and adolescents: dyspepsia, abdominal fullness, epigastric pain, nausea
Infants and younger children: feeding difficulty, vomiting, irritability
Ill. DIAGNOSIS
• Esophagogastroduodenoscopy: method of choice
• Diagnostic tests for H.pylori
IV. MANAGEMENT
• First line drugs for treatment of PUD in children are PP ls and HZ receptor antagonists
• Cytoprotective agents (sucralfate 40-80 mg/kg/day) can also be used as adjunct in the
presence of mucosa I lesions
• Management should be based on H.pylori susceptibility studies
Children infrequently develop complications from H.pylori infection (compared to adults)
Majority of H.pylori-infected children are asymptomatic
For treatment failures, refer to specialist
260
SECTION FOUR
OBSTRUCTION IN THE GASTROINTESTINAL TRACT
INTESTINAL OBSTRUCTION
I.ETIOPATHOGENESIS
• Accumulation of food, gas, and intestinal secretions proximal to the point of obstruction
causes bowel distention
• Distention leads to decreased intestinal absorption, increased fluid & electrolyte
secretion, and isotonic intravascular depletion
• Intestinal contractions initially increase, then hypoactive bowel sounds persist
• Classified as either intrinsic (atresia, stenosis, meconium ileus, aganglionic megacolon) or
extrinsic (malrotation, constricting bands, intra-abdominal hernias, duplications)
• Definition of terms:
0 Atresia: complete obstruction of the bowel lumen
0 Stenosis: partial block ofluminal contents
II. MANIFESTATIONS
ASPECT MANIFESTATIONS
• Nausea & vomiting
Classic
• Abdominal distention
symptoms
• Obstipation
High • Large volume, frequent, bilious emesis
I
obstruction • Intermittent pain in epigastrium or periumbilical area, relieved by vomiting
Low • Moderate/marked distention with emesis that is progressively feculent
obstruction • Diffuse pain over the entire abdomen
III. DIAGNOSIS
DIAGNOSTIC REMARKS/FINDINGS
• Essential X-ray views in intestinal obstruction
0 Plain supine/upright/decubitus X-rays
° Cross-table lateral view: distended bowel above the obstruction with fluid
level and gas in the distended loops
• Abdominal X-ray findings in obstruction:
0 Poor gas distribution or gasless
0 Smooth bowel walls like sausages/hose
Radiograph 0 Preferential dilatation of the bowel proximal to the obstruction
• Many dilated air fluid levels in a given loop at different heights (candy canes)
0 Dilated loops in "stepladder" fashion
• Pneumoperitoneum may be seen in perforation (free air in the subphrenic
area or over the liver in the left lateral decubitus position)
• Ground-glass appearance in the RLQ with trapped air bubbles seen in
meconium ileus
Ultrasound • Identifies stenosis, malrotation, volvulus, intussusception
'
Contrast • Used when plain films or sonograms fail to identify source of obstruction
studies
IV. MANAGEMENT
• Fluid resuscitation
• Nasogastric decompression
• Cultures and antibiotics
• Surgery for strangulation
• Conservative measures for adhesions or strictures
• Water-soluble contrast enemas: useful in malrotation, meconium ileus/plug,
intussusception (diagnostic and therapeutic)
261
SOME CAUSES OF INTESTINAL OBSTRUCTION
I. MECKEL DIVERTICULUM
• It is a remnant of the omphalomesenteric duct which connects the yolk sac to the gut in
the embryo & provides nutrition
• Most common congenital GI tract anomaly
A. EtionathoQenesis: "Rule of 2's"
• Present in ~2% of the general population
• Usually located 2 feet proximal to the ileocecal valve
• Approximately 2 inches in length
• Can contain 2 types of ectopic tissue (gastric or pancreatic)
• Generally present before 2 years old
• Female to male ratio: 2:1
II. INTUSSUSCEPTION
• Occurs when a portion of the alimentary tract is telescoped into an adjacent segment
(most often ileocolic)
• Upper portion of bowel (intussusceptum) invaginates into the lower part
(intussuscipiens) dragging its mesentery along with it into the enveloping loop
• Mesentery constricts and obstructs venous return
• lntussusceptum engorges leading to edema & bleeding from the mucosa
A. Etiopathogenesis
Most common cause of intestinal obstruction between 5 months to 3 years; M > F
Most common abdominal emergency in children< 2 years
Idiopathic in 90% of cases with some degree of correlation with adenovirus
B. Manifestations
• Pain
Classic Triad
• Palpable sausage-shaped abdominal mass (in RUQ)
(in 30%)
• Currant-jelly stool
• Severe paroxysmal colicky pain that recurs at frequent intervals
• Child usually has straining efforts with legs and knees flexed & loud crying
• Infant may initially be comfortable and play normally between
paroxysms, becoming progressively lethargic
Symptoms
• If not reduced, a shock-like state, with fever and peritonitis, can
develop
• Vomiting is usually present in the early phase and later on becomes
bile-stained
262
C Dia0. nosis
DIAGNOSTIC REMARKS/FINDINGS
• Preferred screening tool (98-100% sensitive and 98% specific)
Ultrasound • Tubular mass in the longitudinal view
• Doughnut or target sign in transverse view
X-ray (plain • Vague and non-specific findings
abdominal) • A density may be seen in the area of intussusception
Barium • Coiled-spring sign (thin rim of barium trapped around the
enema invaginating part within the intussuscipiens)
Pathogenesis
around its mesenteric
attachment site which may occur
at various parts of the GIT
• Sigmoid & cecum more
commonly affected
the intestine during fetal
development which is completed
by 3 months of gestation
• Most common type involves
failure of the cecum to move into
I
the RLQ
• *Triad ofvolvulus ("S+R"): • Majority present within the 1st
• Sudden onset of severe year oflife with symptoms of
epigastric pain
Manifestations acute or chronic obstruction
• Inability to pass a tube into
• Vomiting is the most common
the stomach
• Retching with emesis symptom in this age group
• Findings on UGIS:*
• Findings on Abdominal X-ray: • Corkscrew sign: the distal
• Dilated stomach duodenum and proximal
• Inverted U sign (distended jejunum do not cross the
sigmoid loop) midline and instead take an
Diagnosis*
• Coffee bean sign (a midline inferior direction (loops twist
crease corresponding to the on a small bowel mesentery)
mesenteric root in a greatly • Bird's beak appearance of the
distended sigmoid) duodenum as it encounters
the volvulated loop
• Derotation & decompression
by barium enema or with
• Surgery (Ladd procedure) for
rectal tube, sigmoidoscope,
any patient with a significant
Management colonoscope if no signs of bowel
rotational abnormality
ischemia or perforation
regardless ofage
• Laparoscopic derotation or
laparotomy + /- bowel resection
'UpperGISeries (UGIS)is the imagingtest of choice& the goldstandardin the diagnosisof malrotation& volvulus
263
SECTION SIX
DISORDERS OF THE LIVER AND PANCREAS
Spread
Fecal-oral Yes No No No Yes
Blood/Blood No
Rare Yes Yes Yes
Product
Vertical/ No
No Yes Rare Yes
Perinatal
Etiopathogenesis
Incubation Variable* 21-63 days
15-19 days 60-180 days 14-160 days
period
Fulminant
Rare Yes Rare Yes Yes
Disease
1-2%
Mortality
<0.5% <1% <1% <1% (if pregnant:
(Acute)
10-20%)
264
HEPATITISA HEPATITIS B HEPATITIS C HEPATITIS D HEPATITIS E
(HAV) (HBV) (HCV) (HDV) (HEV)
Immunization
lmmuno-
globulin
Passive HBlg No No Yes
0.04-0.06
mL/kg
HBVaccine
Active Vaccine Vaccine No to prevent Vaccine
coinfection
(similarto HBC)
and60-180daysfor coinfection
·incubationperiodfor HepatitisD: 2-8weeksfor HOVsuperinfection
inimmunosuppressed
··chronichepatitis
2020
(21sted.).Philadelphia;
Source:KliegmanR. et al. NelsonTextbookof Pediatrics
Redbook.Reportof theCommittee on InfectiousDiseases.31sted;2018
Principles
Mandell.DouglasandBennett·s 2010
andPracticeof InfectiousDiseases;Philadelphia.
HEPATITIS-B
I. MODEOF TRANSMISSION
• Infected blood or body fluids: serum, semen, vaginal secretions, CSF,synovial, pleural,
pericardia!, peritoneal and amniotic fluid (most infectious)
• Percutaneous and permucosal exposure to fluids
• Sharing unsterilized needles, syringes, or glucose monitoring equipment
• Sharing inanimate objects such as razors and toothbrush
• Sexual contact with an infected person
• Risk of transmission is greatest if mother is also HbeAg-positive (up to 90% of these
infants become chronically infected if untreated)
I
• Perinatal exposure to infected mother: in utero, during labor and delivery:
Infants born to HBsAg ( +), HBeAg ( +) mothers: 70-90% risk of HBV
0Infants born to HBsAg ( +), HBeAg (·) mothers: 5-20% risk of HBV
265
Prodrome Convalesce11ce
Incubation Acute Disease Earty Late
Important diagnostic tests HBsAg HBsAg (Anti-HBC) Anll-HBc Anti-HBs (Anli-HBc)
Symptoms
SGPT(ALT)
....-........
.........
DNA polymerase ,,
H8Vparticle
, Core windows
.. • .... • •Ant1-H8c
'
Level of detection
Hepatitis B Profile
Relative concentration of reactants
Never infected - - - -
Incubation period + - - +
Acute Infection + - +IgM +
Window period - - +lgM -
Complete recovery - + +IgG -
Chronic carrier + - +lgG -
Chronic active + - +IgG +
Vaccinated
- + - -
IV.MANAGEMENTOF HBV
• Acute infection: no specific therapy available (i.e., supportive)
• Chronic infection: treatment to prevent cirrhosis, hepatic failure, & hepatocellular carcinoma
• Treatment for patients in the immune-active form of the disease as shown by increased
levels of liver function tests, those with fibrosis on liver biopsy:
lnterferon-a2b
0
Lamivudine
Adefovi1; Entecavi1; Tenofovir
Source:Kliegman
R. el al. NelsonTexlbookof Pediatrics
(21sted.).Canada:Elsevier; 2020
DavisonS, et al. BMJ;2014
Redbook. Reportof theCommitteeon lnfecliousDiseases, 31sted;2018
266
ACUTE PANCREATITIS (AP)
I.ETIOPATHOGENESIS
• Most common pancreatic disorder in children
• Following an insult, trypsinogen is prematurely activated to trypsin within the acinar cell,
activating other pancreatic proenzymes, leading to autodigestion
• Common causes:
Blunt abdominal injury
Multisystem diseases (e.g. HUS and IBD)
Biliary stones and microlithiasis
0Drugs (valproic acid, L-asparaginase, 6-mercaptopurine, azathioprine)
II. MANIFESTATIONS
III. DIAGNOSIS
A. Diagnostic Criteria (2 out of 3 of the following are needed)
0
Abdominal pain
Serum amylase AND/OR lipase 3 times elevated (compared to upper normal limit)
Imaging findings characteristic or compatible with pancreatitis
I
B. Diagnostics
DIAGNOSTIC REMARKS/FINDINGS
• Serum amylase level typically elevated for up to 4 days
• Serum lipase (test of choice) is more specific than amylase):
Lipase or amylase
rises by 4-8 hours, peaks at 24-48 hours, remains elevated 8-14
days longer than serum amylase
• Hemoconcentration, coagulopathy, leukocytosis, hyperglycemia,
Laboratory
hyperbilirubinemia
findings
• High gamma-g!utamyl transpeptidase
• 20% of children may have normal findings
Abdominal • Findings include: pancreatic enlargement, pancreatic masses,
Ultrasound and fluid collections, abscess
CT scan • CT scan: has a major role in the diagnosis and follow-up of
children with acute pancreatitis
267
SECTION SEVEN
NUTRITION & RELATED DISORDERS
SEVERE CHILDHOOD UNDERNUTRITION (SCU)
• Spectrum of conditions
• Most severe forms:
0 Marasmus: non-edematous SCU with severe wasting
° Kwashiorkor: edematous
I.ETIOPATHOGENESIS
A. Reductive Adaptation - adaptive responses to inadequate energy /protein intake
Mobilization of fat stores
0 Once fat is depleted, protein catabolism takes place to maintain basal metabolism
Energy conserved by reducing activity and growth, basal metabolism, functional
reserve of organs, inflammatory and immune response
II. MANIFESTATIONS
III. DIAGNOSIS
• Decreased serum albumin: most characteristic change
• Other findings include hypoglycemia, low plasma amino acid, low serum cholesterol,
decreased pancreatic & liver enzymes, anemia, delayed bone growth
268
IV. MANAGEMENT
A. Indications for Admission
THE FOLLOWING SHOULD BE THE FOLLOWING MAY BE
ADMITTED MANAGED AS OUTPATIENT
Severe edema or mid-upper arm circumference Edema or MUAC >115 mm and all of the
(MUAC) <115 mm and any of the following: following:
• Anorexia • Good appetite
• Clinically unwell • Clinically well
• Not alert • Alert
B.Aspects in Management
Immediate management of acute problems
Give appropriate antibiotics for bacterial infections
Correct dehydration, electrolyte abnormalities, hypothermia and hypoglycemia
° Correct micronutrient deficiencies
Cautious feeding and catch up growth
Co-management with GI specialist for caloric catch-up and nutritional support
Source:KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Canada:Elsevier;2020
WHO.Guidelines
fortheinpatient
treatment of severelymalnourishedchildren.
Geneva:WHO;2013
MICRONUTRIENT DEFICIENCY
VITAMIN IMPORTANCE MANIFESTATIONS OF DEFICIENCY
1) Water Soluble Vitamins
• Beri-beri
Thiamine
(Bl)
Riboflavin
• Coenzyme in ketoacid
decarboxylation
• FAD coenzyme in
•
•
•
•
•
Polyneuropathy
Calf tenderness
Heart failure
Mucositis
Cheilosis
I
oxidation-reduction
(B2) • Anemia
reactions • Nasolabial seborrhea
• NAO coenzyme in
Niacin (B3) • Pellagra: dermatitis, diarrhea, dementia
oxidation-reduction reactions
• Microcytic anemia
Pyridoxine • Cofactor in amino acid • Cheilosis
(B6) metabolism • Glossitis
• Dermatitis
• Scurvy
, Early symptoms: fever, irritability,
tachypnea, anorexia, generalized
• Maintains integrity of tenderness especially in the legs
0 Pseudoparalysis with hips & knees semi-
intracellular material
flexed & the feet rotated outward
Vitamin C • Facilitates absorption of 0 "Scorbutic rosary" at the costochondral
iron and conversion of
junction & depression of the sternum
folic acid to folinic acid 0 Bluish,purple spongy swellings of the mucous
membranes especiallyover the upper incisors
, Perifollicular hemorrhages, hyperkeratosis
of hair follicles, "corkscrew hair"
269
VITAMIN IMPORTANCE MANIFESTATIONS OF DEFICIENCY
2) Fat Soluble Vitamins
• Component of retinal • Nyctalopia, photophobia, xerophthalmia,
pigments keratomalacia, faulty epiphyseal bone
Vitamin A
• Role in bone, tooth, and formation, defective tooth enamel, impaired
epithelial development resistance to infection, Bitot spot
REFERENCES
1. Abu-El-Haija, M., Kuma1; S., Quiros, J., Balalaishnan, K, et al. Management of Acute Pancreatitis in tl1e Pediatric
Population: A Clinical Report From the Nortl1 American Society for Pediatric Gastroenterology, Hepatology and
Nutrition Pancreas Committee. JPGN,2018 66(1), 159-176.
2. American Academy of Pediatrics. Kimberlin DW, Brady MT. Jackson MA, Long SS, eds. Red Book: 2018 Repo,~ of
the Committee on Infectious Diseases. 31st ed. Itasca,IL:American Academy of Pediatrics2018
3. Christison-LagayER,Keller,CMand Langer,JC.Neonatal abdominal wall defects. Semin Fetal Neonatal Med. 16(3), 2011
4. Clohe1~, J., Eichenwald, E., Hansen, A., and Stark, A. Manual of Neonatal Care 7th ed. 2012. Philadelphia:
LippincottWilliams and Wilkins
5. Davison, S. and Strasser, S. Ordering and interpreting hepatitis B serology. BM); 2014
6, Dunkley, M., Zalewska, K, Shi, E,, & Stalewski, H, Management of Esophageal Atresia and Tracheoesophageal
Fistula in North Queensland. International Surgery, 2014: 99(3), 276-279.
7. Eherer; A, & Fordtran, J.Fecal osmotic gap and pH in experimental diarrhea of various causes. Gastroenterology,
1992, 103(2), 545-551. doi: 10.1016/0016-5085(92)90845-p
8. Gamba P and Midrio P. Abdominal wall defects: prenatal diagnosis, newborn management, and long-term
outcomes. Semin Pediatr Surg 2014, 23(5):283-90
9. Gomella TL, Cunningham, Mand Eyal F..Neonatolgy 7th Edition. 2013. McGraw-Hill.
10. Holcomb, G.,and Murphy, J. Ashcralt's Pediatric Surge,y 5th ed. 2010, Philadelphia: Saunders Elsevier.
11. Jones, N., Koletzko, S., Goodman, K., et al. Joint ESPGHAN/NASPGHAN Guidelines for the Management of
Helicobacter pylori in Children and Adolescents (Update 2016), JPGN,64(6), 991-1003.
12. Kliegman, R., Stanton, B., St. Geme, J., Scho1; N., & Behrman, R.. Nelson Textbook of Pediatrics 21st ed. 2020.
Philadelphia: Elseviei:
13. Ledbetter DJ: Congenital abdominal wall defects and reconstruction in pediatric surgery: gastroschisis and
omphalocele, Surg Clin Notth Am, 2012, 92(3):713-27, 2012
14. Lightdale, J., & Gremse, D, Gastroesophageal Reflux: Management Guidance for the Pediao•ician. Pediatrics, 2012
131(5), e1684-e1695. doi: 10.1542/peds.2013-0421
15. Long, S.,Probe,; C.,& Fischet; M,P1inciples and practice of pediatric infectious diseases 4th ed. 2012, Saunders Elseviei:
16. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases; Philadelphia, 2010
17. NeuJ.Necrotizingenterocolitis:the search fora unifyingpathogenictheol}' leadingto prevention Pedian·ClinNorth Arn 1996
18, Prefumo Fetal: Fetal abdominal wall defects, Best Pract Res Clin ObstetGynaecol. 28(3):391-402, 2014, Table 1
19. Reshetnyak, V.,Karlovich, T.,& llchenko, L.Hepatitis G Virus. World J Gastroenterol, 2008 14(30), 4725-4734.
20. Walther AE et al: Newborn abdominal wall defects. In: Wyllie R et al, eds: Pediatric Gastrointestinal and Liver
Disease, 5th ed. Philadelphia, PA: Elsevier: 2016:654-65,e4, Table 58-1
21. World Health Organization. Guidelines for the inpatient treatment of severely malnourished children. 2013
Geneva: WHO. Available from< https://www.who.int/nuo·ition/publications/guide_inpatient_text.pdf>
22. World Health Organization, The treatment of diarrhea. Geneva: 2005 Wyllie, R., and Hyams, J. Pedian·ic
gastrointestinal and liver disease 3rd ed. 2006. Philadelphia: Elsevier,
23. Zella, G.,and Israel, E. Chronic Diarrhea in Children. 2012 Pedian·ics In Review, 33(5), 207-218
270
HEMATOLOGY
AND
ONCOLOGY
SECTION ONE
THE ANEMIAS
... J
Iron Deficiency Anemia Drugs
Thalassemia Reticulocyte Vitamin 812/Folate
Sideroblastic Anemia Immune Hemolytic
Count
Anemia of Chronic Disease Diamond-Blackfan
Yes
(e.g.,jaundice, indirect hyperbifirubinemia, high
LOH. decreased hopcoglobon)
No
I
Hereditary spherocytosis Hemorrhage
Hereditary el!iptocytosis
G6PD
Sickle Cell Disease
HUS/TTP
I. IRON DEFICIENCYANEMIA
• Insufficient total body iron to maintain normal physiologic functions
• Most common nutritional deficiency in children
A. Etiopathogenesis (Risk Factors)
INFANTS AND TODDLERS OLDER CHILDREN AND ADOLESCENTS
• Low birth weight infants • Increased requirements (e.g., growth spurt,
• Prematurity pregnancy)
• Perinatal blood loss • Occult/chronic blood loss (e.g., peptic ulcer,
• Early cord clamping polyp, hemangioma)
• Excessive consumption of cow's • Menstrual blood loss
milk (cow's milk is low in iron) • Infection with intestinal hookworm, Tricht1ris,
Plasmodium, Helicobacter pylori, Giardia lamblia
273
B. Manifestations
• Most patients with mild to moderate anemia are asymptomatic
• Hgb 6-10 g/dL: mild irritability
General
Manifestations • Hgb 7-8 g/dL: pallor (most important clinical sign)
• Hgb <5 g/dL: lethargy, anorexia, easy fatigability, systolic flow
murmurs, and high-output cardiac failure
• Koilonychia: spoon nails
• Pica: desire to eat non-nutritive substances
Other Signs
• Pagophagia: desire to ingest ice
• Irreversible neurocognitive effects
Co· !
DIAGNOSTIC REMARKS
• Low RBC,MCV,reticulocyte count
CBC • Increased red cell distribution width (versus Thalassemia,
which has a normal ROW)
Peripheral blood • Microcytic, hypochromic RBCs (due to decreased hemoglobin
smear production or faulty function)
• Low serum iron & ferritin
Other tests • High total iron binding capacity (versus anemia of chronic
disease, which has low iron and low TIBC)
D.Management
• Look for cause of iron deficiency & address underlying problem
• Dietary counselling if anemia is due to a nutritional cause:
General Aspects
Delay introduction of cow's milk until at least 1 year of age
0
2. Follow-Up
Repeat CBC4 weeks after iron therapy (at this time, the hemoglobin has usually
risen by at least 1-2 g/dL and is often within normal levels)
If the anemia is severe, check for reticulocytosis within 2-3 days of therapy
Consider other causes of anemia when there is poor response to iron therapy
274
II. APLASTIC ANEMIA
• Life-threatening bone marrow failure
• Hallmark is peripheral pancytopenia with marrow hypoplasia or aplasia
A. Etiopathogenesis
Due to defect of hernatopoietic stem cells, defect in the rnicroenvironrnent of the
hematopoietic cells, or antibody-mediated mechanisms
• May be inherited (e.g. Fanconi anemia, Shwachrnan-Diarnond syndrome,
dyskeratosis congenital or acquired
Majority of cases are idiopathic
ACQUIRED ETIOLOGY CAUSES
Cytotoxic drugs and • Chemotherapy
radiation • Radiation therapy
• Anti-seizure agents (carbamazepine, phenytoin)
• Antibiotics (sulfonamides, chloramphenicol)
Drug/chemical reaction • NSAIDs[indornethacin, phenylbutazone)
• Anti-thyroid drugs (methimazole, propylthiouracyl)
• Others: gold, arsenicals, benzene
• Epstein-Barr virus
Viral infections • Seronegative hepatitis
• Others: HIV,Herpes viruses
• Eosinophilic fasciitis
Immune disorders • Systemic lupus erythernatosus
• Graft-versus-host disease
• Paroxysmal nocturnal hemoglobinuria
Others
• Thymoma, pregnancy, anorexia nervosa
I
8. Manifestations
Recurrent episodes of infection due to leukopenia
• Mucosa! hemorrhage or rnenorrhagia due to thrombocytopenia
• Pallor and easy fatigability due to anemia
C. Diagnosis
1. Diagnostics
DIAGNOSTIC FINDINGS/REMARKS
CBC&PBS • Pancytopenia (anemia, leukopenia, thrornbocytopenia)
• Required to establish diagnosis
Bone Marrow
• Hypocellular marrow with a decrease in all cell components,
Aspiration Biopsy
composed mostly of fat cells and marrow stroma
2 S f AI I A
MODERATE APLASTIC SEVERE APLASTIC
ANEMIA ANEMIA
Absolute Neutrophil 5OO-1OOO/rnm' <5OO/mm'
Count (ANC)
D. Management
Allogeneic hernatopoietic stern cell transplant (treatment of choice)
lmrnunosuppressive therapy with horse anti-thyrnocyte globulin and cyclosporine
(treatment of choice if without HLA-rnatched sibling or donor)
RBC and platelet transfusion
• Granulocyte colony-stimulating factor (G-CSF) or granulocyte-macrophage colony-
stimulating factor (GM-CSF)
• Withdrawal of any toxic causative agent
275
III. CONGENITALANEMIAS
ETIOPATHOGENESIS DIAGNOSIS MANAGEMENT
Fanconi Anemia
• Most common inherited • Allogenic hematopoietic bone
a plastic anemia • Based on physical marrow transplantation is the
• Cells cannot properly manifestations and only established curative therapy
repair DNA damage cytogenetic analysis • Androgen therapy to improve
known as interstrand blood counts
crosslinks • Blood transfusion, G-CSF
Shwachman-Diamond Syndrome
• Autosomal recessive • Oral pancreatic enzyme
inherited aplastic • Based on bone marrow replacement
anemia dysfunction and exocrine • Fat-soluble vitamins
• Genetic mutation affecting pancreatic dysfunction • Blood transfusion, G-CSF
1ibosome synthesis • Hematopoieticstem cell transplant
Diamond-Blackfan Syndrome
• Criteria (all should be met):
0 Age <1 year
• >90% diagnosed • Steroids: mainstay of therapy
0 Macrocytic anemia with
within 1 year old • Blood transfusion for those
no other cytopenias
• Genetic mutations who do not respond to or
0 Reticulocytopenia
affecting ribosome tolerate steroids
0 Normal marrow
synthesis
cellularity with a paucity
of erythroid precursors
HEMOLYTIC ANEMIAS
I. GLUCOSE-6-PHOSPHATEDEHYDROGENASE(G6PD) DEFICIENCY
A. Etiopathogenesis
Most common inherited enzymatic disorder
• Genetic defect in the red blood cell glucose-6-phosphate dehydrogenase
• Lack of this enzyme causes hemolytic anemia when exposed to oxidative stress
• Methylene blue
• Antibacterial: nitrofurantoin, • Arsine
furazolidone, nitrofurazone • Phenylhydrazine
• Analgesic/antipyretic: acetanilid, • Toluidine blue
aspirin • Trinitrotoluene
• Antihelminthic: B-napththol, • Aniline dye
niridazole, stibophan FOOD AND DRINKS
• Antimalarials: chloroquine,
primaquine, pentaquine, pamaquine • Fava beans
• Sulfonamides: TMP-SMX,sulfonylureas •Redwine
• Legumes
• Miscellaneous
• Blueberry
0 Aceytylphenylhydrazine
• Soya food
0 Dimercaprol
° Flutamide (anti-androgen) OTHERS
• lsobutyl nitrite
• Menthol (alaxan gel, efficascent oil,
0 Mepacrine (antiprotozoal) Listerine mouthwash, omega pain kille1;
• Phenazopyridine mentopas medicated plaster)
0 Probenecid ( uricosuric drug) • Camphor
0 Thiazolesulfone (lupus vulgaris) • Naphthalene (moth balls)
• Rasburicase (uricolytic agent) • Henna
• Some herbs
276
B. Manifestations
0 Most are asymptomatic unless triggered by precipitants
0 Hemolysis develops in 24-48 hours after exposure to precipitant
C. Diagnostics
0 G6PD Assay
° CBCwith PBS - low hemoglobin, Heinz bodies, anisopoikilocytosis, bite cells
D. Management
0 Avoidance of precipitants
0 Acute hemolytic episode
0Identify and remove the culprit agent
Hydration and transfusion for severe anemia
Source:Bolton-Maggs PH,et al. BrJ Haemalol2012
KliegmanR. et al. NelsonTextbookof Pediatrics (21sted.).Elsevier;2020
MichlilschJ. et al. PediatrBloodCancer;2009
II. THALASSEMIA
• Disorders wherein the alpha and globin chains are disrupted due to disease-causing
variant in one or more globin genes
ALPHA THALASSEMIA BETA THALASSEMIA
• Highly prevalent in Southern • Highly prevalent in Africa followed
China, Malaysia, and Thailand
by Asia
• Caused by gene deletions in one
• Caused by mutations in one or both
Pathogenesis or more genes encoding for alpha
of the beta globin genes
globin chain
• Severity correlates with the
• Vary depending on numbers of
gene deletion amount of Beta-globin production
• Severe
• Hydrops • B-Thalassemia microcytic
• Severe
11
Fetalis with Major (both beta anemia with
microcytic
Barts Hgb globin genes target cells
anemia • Transfusion
(4 Foci deleted) mutated)
dependent
277
III. OTHER HEMOLYTICANEMIAS
HEREDITARY
SICKLE CELL DISEASE
SPHEROCYTOSIS
• Most common cause of
hemolytic anemia due to a red • Autosomal recessive disorder
cell membrane defect • Develops at around 6 months of
Pathogenesis
• Due to abnormalities of ankyrin age when sickle cell hemoglobin
and spectrin (proteins involved replaces HbF
in RBCcytoskeleton)
• Clinical hallmarks: vasoocclusive
phenomena & hemolysis
• Pallor, jaundice • Recurrent painful episodes from
• Splenomegaly hypoxic tissue injury
Manifestations • Susceptibility to a plastic crisis • Organ-system complications
(when infected by certain (e.g., a plastic crisis, splenic
viruses like Parvovirus Bl 9) sequestration, priapism, stroke,
avascular necrosis, acute chest
syndrome)
• High performance liquid
• Osmotic fragility test: confirms
chromatography
presence of fragile sphere-shaped
(preferred method of diagnosis)
RBCs
• Hemoglobin electrophoresis
Diagnosis • CBCreveals high MCHC,normal
• Peripheral blood smear - Howell
MCV,high reticulocyte count
Jolly Bodies and sickle cells
• Peripheral smear: spherocytes
• "Crew cut" or "hair on end"
• Increased indirect bilirubin level
appearance on skull radiographs
• Splenectomy is curative and
recommended for:
0 Transfusion-dependent • Analgesia and hydration for acute
patients crises
0 Severe disease • Hydroxyurea to promote production
Management 0 Moderate disease with offetal hemoglobin
frequent hypoplastic or • Vaccinations against encapsulated
aplastic crises, poor growth, organisms
or cardiomegaly • Folate supplementation
• Folate supplementation may also
be useful
278
SECTION TWO
B.LEEDING DISORDERS
Bleeding
i Cti·o·n·
o·ecrea
~·e
·Prc;d·u - 'vWD
• Aplastic anemia i Factor XIII deficiency
: Platelet function disorders
Increased Destruction I Vascular abnormalities
• ITP,DIC,TTP
PT abnormal
I
PT normal PT abnormal
PTT normal PTT abnormal PTT abnormal
Sources:NathanandOski'sHematology
andOncologyof InfancyandChildhood(8thed).Philadelphia:
2015
RapaportSI. Introduction
to Hematology.
Philadelphia;
1987
279
IMMUNE THROMBOCYTOPENIA (ITP)
I. ETIOPATHOGENESIS
• Previously called Idiopathic Thrombocytopenic Purpura
• Most common cause of thrombocytopenia in childhood
• Immune-mediated disorder which can be triggered by viral infection, immunologic, or
environmental trigger
• Peak age: 1-4 years old
II. MANIFESTATIONS
• Classic presentation is previously healthy 1-4-year-old child with sudden onset of
generalized petechiae and purpura
• Recent history of viral illness in 50-65%
• Variable severity of bleeding
Mild: bruising and petechiae
0 Moderate: more severe skin and mucosa I lesions, troublesome epistaxis, and menorrhagia
0 Severe: bleeding episodes requiring transfusion or hospitalization
III. DIAGNOSIS
DIAGNOSTIC REMARKS
• Common finding: severe thrombocytopenia ( <20,000/uL)
CBC
• Normal Hgb, WBC count
Peripheral blood smear • Large platelets
• Indications: abnormal WBC count, unexplained anemia
Bone marrow aspiration
• Normal or increased megakaryocytes
biopsy
• Normal erythroid and myeloid precursors
IV. MANAGEMENT
• No treatment for mild and moderate symptoms
• Intravenous immunoglobulin 0.8-1 g/kg
• Prednisone 1-4 mg/kg/day
• Splenectomy for:
0 Life-threatening hemorrhage (intracranial bleed)
° Children ;,,4 years old with chronic ITP lasting> 1 year
° Children whose symptoms are difficult to control
II. MANIFESTATIONS
• Characterized by platelet rich thrombi in small vessels causing microangiopathic
hemolytic anemia and thrombocytopenia
• Five cardinal symptoms (FAT RN):
Fever
0 Anemia (microangiopathic, hemolytic type)
0 T hrombocytopenia
0 Renal dysfunction
Nervous system changes (changes in affect or orientation; aphasia, blindness, seizures)
III. DIAGNOSTICS
• Microangiopathichemolytic anemia (schistocytes, spherocytes, helmet cells)
CBCwith PBS • Elevated reticulocyte count
• Thrombocytopenia
Blood Chemistry • Elevated BUNand creatinine
IV. MANAGEMENT
• Plasmapheresis (to reverse platelet consumption) effective in 80-95% of cases
• Rituximab, steroids, and splenectomy are for refractory cases
280
HEMOPHILIA
• Hereditary, sex-linked hematologic disorder occurring almost exclusively in males
• Marked by delayed clotting of the blood caused by a deficiency of clotting factors
I. ETIOPATHOGENESIS
Three types
Hemophilia A or Factor VIII deficiency
• Hemophilia B or Factor IXdeficiency
• Hemophilia C or Factor XI deficiency
• Hemophilia A and Bare X-linked recessive, hemophilia C is autosomal recessive
• Hemophilia A more common and more severe than hemophilia Band C
INTRINSIC PATHWAY EXTRINSIC PATHWAY
I Contact Activation I
I
~-~
~
Tissue Factor
~~Xa PF-3
VIII
Tlla
•~
r---::-7 ,..ca++ ~
~ • •L_'.'.~
~-~~-~
!! Prothrombin Thrombin
Coagulation
Extrinsic
intrinsic
cascadeshowingthe Intrinsic,
and CommonPathways.Note
thatHemophiliaA,BandCare foundinthe
pathway.
Fibrinogen
Xllla
Soluble Fibrin
Insoluble Fibrin
I
II. MANIFESTATIONS
• First sign of early joint hemorrhage: warm, tingling sensation in the joint
Symptoms
• Easy bruising
• Hallmark of hemophilia: hemarthrosis
• Most common earliest joint involved: ankle
Signs • Older children and adolescents: knees and elbows
• Intramuscular hematomas
• Mucosa) bleeding is rare
III. DIAGNOSTICS
DIAGNOSTICS FINDINGS/REMARKS
Bleeding time • Normal
281
IV. MANAGEMENT
• Factor replacement during bleeding or as prophylaxis before surgical and dental procedures
• For mild/moderate bleeding: factor VIII or factor IXvalues must be raised to ~35-50% levels
• For major hemorrhages: the doses of factors VIII or IXshould achieve levels of 100% activity
• Factor VIII transfusion
Hemophilia A
• Alternatives: Cryoprecipitate, FFP,Emicizumab
• Factor IXtransfusion
Hemophilia B
• Alternatives: Cryosupernate, FFP
• Factor XI transfusion
Hemophilia C
• Alternatives: Cryosupernate, FFP
II. MANIFESTATIONS
• Disturbs both primary and secondary hemostasis
• Increased bleeding time causing mucous membrane bleeding, petechiae, purpura
• Often have a family history of bleeding
III. DIAGNOSTICS
• Decreased vWF levels
• Decreased Factor VIII
• Prolonged bleeding time
• Abnormal platelet adhesion
• Increased PTT
• Ristocetin cofactor assay (measures vWF antigen levels and activity)
IV. MANAGEMENT
• Desmopressin: increases amount of circulating vWF by release from storage
• Replacement therapy
• Antifibrinolytics
• Hormonal treatment with estrogen in women
282
SECTION THREE
ONCOLOGY
LEUKEMIAS
• Most common form of cancer in children
• Types of leukemias and frequency:
• Acute lymphoblastic leukemia [ALL): most common
• Acute myelogenous leukemia (AML)
• Chronic myelogenous leukemia (CML)
Juvenile myelomonocytic leukemia (JMML)
B. Manifestations
Acute onset (<4 weeks duration of symptoms)
Most common presentation are non-specific (e.g., anorexia, irritability, lethargy)
Signs of marrow failure (e.g., anemia, bleeding, purpuric/petechial lesions, low-grade fever)
Signs of infiltration (e.g., bone pain, lymphadenopathy, hepatosplenomegaly)
C. Diagnosis
DIAGNOSTICS FINDINGS/REMARKS
Bone marrow aspiration
biopsy
CBC
• >25% of the bone marrow cells are a homogenous
population of lymphoblasts
• Anemia, thrombocytopenia
• Atypical lymphocytes
I
• Some with hyperleukocytosis (WBC > 100xl0 9 /L)
Peripheral blood smear • Presence of blasts
Chest radiograph • Mediastinal mass (usually in T cell immunophenotype)
CSF • May contain lymphoblasts [if with CNS involvement)
Age • >l year old & <10 years old • <l year old & >10 years old
WBC at diagnosis • <50xl0 9 /L • > 50 x 10 9 /L
Immunophenotype • Pre B Cell • T Cell, mature B, Biphenotypic
CNS involvement • Negative • Positive
E. Management
• The single most important prognostic factor for ALL is receiving treatment
• Standard treatment: chemotherapy for 2-3 years with a goal of eradicating detectable
leukemia cells or remission:
BMA blast count <5%
Return of neutrophil and platelet counts to near-normal levels
283
l. Phases of Chemotherapy:
PHASE REMARKS
Remission induction • Eradicate leukemic cells from the bone marrow
• Focuses on intensive CNS therapy in combination with
Consolidation
continued intensive systemic therapy
• Phase of aggressive treatment as well as relatively non-
Intensification
toxic phase of treatment depending on risk stratification
Maintenance • Given to maintain patient on remission
• Associated with
Philadelphia
• Relative frequency
chromosomal • Typically affects <2
Pathogenesis of AML increases in
translocation (t(9;12)) years of age
adolescence
resulting in BCR-ABL
fusion protein gene
• Signs of marrow • Nonspecific symptoms
failure • Splenomegaly
• Subcutaneous • Initial chronic phase
nodules or (3-4 years) with
• Rashes,
"blueberry muffin" mild anemia and
lymphadenopathy,
Manifestations lesions thrombocytosis
splenomegaly,
• Gingival infiltration • Alter chronic phase,
hemorrhage
• Disseminated moves into accelerated
intravascular or blast crisis phase
coagulation with course similar to
• Chloromas acute leukemia
• Leukocytosis
• High WBC count
with increased
• >20% of bone with myeloid cells
monocytes
marrow cells at all stages of
• Thrombocytopenia
consist of differentiation in the
Diagnosis • Anemia with
homogeneous PBS and bone marrow
erythroblasts
population of blast (usually the same
• Myelodysplastic
cells appearance under the
pattern in bone
microscope)
marrow
• lmatinib, dasatinib
• Chemotherapy
(BCR-ABLtyrosine • Stem cell
Management • Stem cell
kinase inhibitor) transplantation
transplantation
• Hydroxyurea
284
LYMPHOMAS
• Neoplasms of lymphoid cells (lymphocytes, histiocytes & their precursors) - 6% of
childhood cancers
• Two types: Hodgkin and Non-Hodgkin Lymphoma
Diffuse extra-lymphatic
CNS or bone marrow
IV site involvement (usually IV involvement
bone marrow, CNS, liver)
285
BRAIN TUMORS
• Most common solid tumor in children
• Most common:
Pilocytic
astrocytoma • Second most common • Solid or solid-cystic
• Classic site of posterior fossa tumor tumors arising
occurrence: of childhood from remnants of
Pathogenesis
cerebellum • Most common Rathke pouch of the
• Most common malignant brain pituitary stalk in the
posterior fossa tumor of childhood suprasellar region
tumor: Cerebellar
astrocytoma
• Subacute • Increased intracranial
• Visual deficits that
progressive pressure because of
can be secondary to
neurologic signs obstruction of the 4th
compression on the
and symptoms ventricle (headache,
optic chiasm
(headache, nausea, vomiting,
• Direct damage to
Manifestations seizure, weakness, altered mental status,
structures can cause
memory loss, hypertension)
endocrine abnormalities
motor weakness, • Cerebellar
such deficiency of
visual symptoms, dysfunction (gait
growth hormone,
personality ataxia, dysmetria,
TSH, ACTH, ADH
changes) poor balance)
• MRI
• PET (to determine • MRI of brain & spine
metabolically active • Skeletal survey • MRI or CT scan
Diagnosis parts of the tumor)
• CSF cytology • Endocrine studies
• Biopsy for
malignancies not • Liver function tests
amenable to surge1y
• Surgical resection • Surgical resection
Management
• Radiotherapy and chemotherapy • Radiotherapy
MUSCULOSKELETAL TUMORS
OSTEOSARCOMA EWING SARCOMA
• Chemotherapy
• Chemotherapy
Management • Radiation
• Surgery
• Surgery
286
ABDOMINAL TUMORS
NEUROBLASTOMA WILMSTUMOR HEPATOBLASTOMA
I
subcutaneous
nodules
• Systemic symptoms
(fever & weight loss)
• Abdominal CTscan
• Abdominal UTZ, CT
• 24-hour urine
homovanillic scan or MRI
• Abdominal UTZ, CT
acid [HVA)and • Electrolytes, renal
scan or MRI
vanillylmandelic function tests
• Liver biopsy
Diagnosis acid (VMA) • Chest X ray or
• Bone marrow • Tumor marker: alpha
CT scan to check
showing fetoprotein
for pulmonary
myelophthisic metastasis
marrow
• Biopsy
• Surgery • Surgery
Management • Chemotherapy • Chemotherapy
• Radiation • Liver transplant
REFERENCES
I. Abrams SA, O'Brien KO. Wen J,et al. Absorption by 1-year-old children of an iron supplement given with cow's
milk or juice. Pediatr Res 1996; 39: 171.
2. Alter BP,Young NS. The Bone Marrow Failure Syndromes. In: Nathan and Oski's Hematology of Infancy and
Childhood, Nathan DG,Orkin SH (Eds), W.8. Saunders Company, 1998, p.237.
3. American Academy of Pediatrics. Iron. In: Pediatric Nutrition, 7th, Kleinman RE, Greer FR (Eds), American
Academy of Pediatrics, Elk Grove Village 2011. p.449
4. Beutler E. G6PD deficiency. Blood 1994; 84:3613.
5. Bolton-Maggs PH, Langer JC, lolascon A, et al. Guidelines for the diagnosis and management of hereditary
spherocytosis--2011 update. Br J Haematol 2012; 156:37.
6. Brancaleoni V, Di Pic1To E, Motta I, Cappellini MD. Laboratory diagnosis of thalassemia. Int J Lab Hematol 2016
7. Brodeur GM, Hogarty MD, Mosse YP, Maris JM.Neuroblastorna. In: Principles and Practice of Pediatric Oncology,
Pizzo PA, Poplack DG (Eds), Lippincott Williams & Wilkins, Philadelphia 2011. p.886.
8. Brodeur GM, Pritchard J,Berthold F, et al. Revisions of the international criteria for neuroblastoma diagnosis,
staging, and response to treatment. J Clin Oneal 1993; 11: 1466.
9. Brodsky RA, Jones RJ.Aplastic anaemia. Lancet 2005; 365: 1647.
10. Brugnara C, Oski FA, Nathan DG. Diagnostic approach to the anemic patient. In: Natlian and Oski's Hematology and
287
Oncology of Infancy and Childhood [8th ed), Orkin SH, Fisher DE,Ginsburg D,eta! [Eds). WB Saunders, Philadelphia; 2015
11. Carcao MD. The diagnosis and management of congenital hemophilia. Semin Thromb Hemost 2012; 38:727.
12. Cappellini MD, Fiorelli G. Glucose-6-phosphate dehydrogenase deficiency. Lancet 2008; 371:64.
13. Clarke RT,Van den Brue] A, Bankhead C, et al. Clinical presentation of childhood leukaemia: a systematic review
and meta-analysis. Arch Dis Child 2016; 101:894.
14. Dix DB, Fernandez CV, Chi YY, et al. Augmentation of therapy for favorable-histology Wilms Tumor with combined
loss of heterozygosity of chromosomes lp and 16q: A report from the Children's Oncology Group studies. J Clin
Oncol 2015
15. Eberhart CG, Kepner JL, Goldthwaite PT, et al. Histopathologic grading of medulloblastomas: a Pediatric
Oncology Group study. Cancer 2002; 94:552.
16. Esche rich G, Horstmann MA, Zimmermann M, et al. Cooperative study group for childhood acute lymphoblastic
leukaemia (COALLJ: long-term results of trials 82,85,89,92 and 97. Leukemia 2010; 24:298.
17. Fucharoen S,Viprakasit V.Hb H disease: clinicalcourse and disease modifiers. HematologyAm Soc Hematol Educ Program 2009
18. G6PD deficiency favism association website: http://www.g6pd.org/en/G6PDDeficiency/SafeUnsafe/DaEvitare_lSS
19. Glader 8. Hereditary hemolytic anemias due to red blood cell enzyme disorders. In: Wintrobe's Clinical Hematology,
13th edition, Greer JP.Arber D,Glader 8, et al (Eds), Wolters Kluwer/Lippincott Williams & Wilkins, Philadelphia
2014. p.728.
20. George JN. Congenital thrombotic thrombocytopenic purpura: Lessons for recognition and management of rare
syndromes. Pediatr Blood Cancer 2008; 50:947.
21. Gobbi PC,CavalliC, Gendarini A, et al. Reevaluationof prognosticsignificanceof symptoms in Hodgkin'sdisease.Cancer 1985;
22. Halperin DS,FreedmanMH. Diamond-blackfananemia:etiology,patJ10physiology,and treannent Am f PediatrHematol Oncol1989
23. Howard SC, Jones DP, Pui CH. The tumor lysis syndrome. N Engl J Med. 2011;364[19):1844-1854.
24. Howlader N, Noone AM, Krapcho M, Garshell), Miller D, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tata Jovich Z,
Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2012, National
Cancer Institute. Bethesda, MD, based on November 2014 SEER data submission, posted to the SEER web site,
April 2015. Available at:http://seercancer.gov/csr/1975_2012/results_merged/sect_29_childhood_cancer_iccc.
pdf Nelsons Pediatrics
25.https://www.fda.gov/downloads/drugs/guidances/ucm459987.pdf
26. Huvos A. Bone Tumors: Diagnosis, Treatment, Prognosis, 2nd, WB Saunders, Philadelphia 1991.
27. Jane JA Jr, Laws ER. Craniopharyngioma. Pituitary 2006; 9:323.
28. Kassebaum NJ,Jasrasaria R,NaghaviM,etal A systematicanalysis of globalanemia burden from 1990 to 2010. Blood 2014; 123:615.
29. Kiihne T, Berch told W, Michaels LA, et al. Newly diagnosed immune thrombocytopenia in children and adults:
a comparative prospective observational registry of the Intercontinental Cooperative Immune
Thrombocytopenia Study Group. Haematologica 2011;
30. Kliegman R, et al. Nelson Textbook of Pediatrics (21st ed.). Canada: Elsevier; 2020
31. Lawlor ER, Lim JF,Tao W, et al. The Ewing tumor family of peripheral primitive neuroectodermal tumors
expresses human gastrin-releasing peptide. Cancer Res 1998; 58:2469.
32. Martin A, Thompson AA. Thalassemias. Pediatr Clin North Am 2013; 60:1383.
33. Mason PJ, Bautista JM, Gilsanz F.C6PD deficiency: the genotype-phenotype association. Blood Rev 2007; 21:267.
34. Mc Lendon RE, Friedman HS, Fuchs HE, et al. Diagnostic markers in paediatric medulloblastoma: a Paediatric
Oncology Group Study. Histopathology 1999; 34:154.
35. Michlitsch ], Azimi M, Hoppe C, et al. Newborn screening for hemoglobinopathies in California. Pediatr Blood
Cancer 2009; 52:486
36. Mitchell C, Richards S, Harrison CJ,Eden T. Long-term follow-up of the United Kingdom medical research council
protocols for childhood acute lymphoblastic leukaemia, 1980-2001. Leukemia 2010; 24:406.
37. Narla J, Mohandas N. Red cell membrane disorders. Int J Lab Hema to! 2017; 39 Suppl 1:47.
38. Nkhoma ET, Poole C, Vannappagari V, et al. The global prevalence of glucose-6-phosphate dehydrogenase
deficiency: a systematic review and meta-analysis. Blood Cells Mo! Dis 2009; 42:267.
39. Orkin S,Natl1anD,Ginsburg D,LookA, Fisher D,LuxS.Nathan and Oski's Hematology of Infancyand Childhood.7tl1ed. 2009: 276
40. Petito CK, DeCirolami U, Earle KM. Craniopharyngiomas: a clinical and pathological review. Cancer 1976;
37:1944.
41. Provan D, Stasi R, Newland AC, et al. International consensus report on the investigation and management of
primary immune thrombocytopenia. Blood 2010; 115:168.
42. Rapaport SI. Diagnosis of anemia. In: Introduction to hematology, JB Lippincott, Philadelphia, 1987
43. Rees DC,Williams TN, Gladwin MT. Sickle-cell disease. Lancet 2010; 376:2018.
44. Rodeghiero F, Stasi R, Gernsheimer T, et al. Standardization of terminology, definitions and outcome criteria
in immune thrombocytopenic purpura of adults and children: report from an international working group.
Blood 2009
45. Sadler JE, Mannucci PM, Berntorp E, et al. Impact, diagnosis and treatment ofvon Willebrand disease. Thromb
Haemost 2000
46. Scott RH, Stiller CA, Walker L,et al Syndromes & constitutional chromosomal abnormalities associated with
Wilms tumour. J Med Genet 2006
47. Ward E, DeSantis C, Robbins A, et al. Childhood and adolescent cancer statistics, 2014. CA Cancer J Clin 2014; 64:83.
48. World Health Organization. Serum ferritin concentrations for the assessment of iron status and iron deficiency
in populations. Vitamin and Mineral Nutrition Information System. Geneva: World Health Organization; 2011
49. Schein berg P,Young NS. How I treat acquired aplastic anemia. Blood 2012; 120:1185.
SO.Shimamura A, Alter BP. Patho physiology and management of inherited bone marrow failure syndromes. Blood
Rev. 2010;24(3):101. Epub 2010 Apr 24.
51. Venkateswaran L, Wilimas JA, Jones DJ, Nuss R. Mild hemophilia in children: prevalence, complications, and
treatment. J Pediatr Hematol Oncol 1998; 20:32.
52. Vlachos A, Ball S, Dahl N, et al. Diagnosing and treating Diamond Blackfan anaemia: results of an international
clinical consensus conference. Br J Haematol 2008; 142:859.
53. Ward E, Desantis C, Robbins A, et al. Childhood and adolescent cancer statistics, 2014. CA Cancer J Clin 2014;
64:83.
54. WHO Classification ofTumours of the Central Nervous System, 4th ed, Louis DN, Ohgaki H, Wiestler OD, Cavenee
WK (Eds), !ARC, Lyon 2016.
55. World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Swerdlow SH,
Campo E, Harris NL, et al. [Eds), IARC Press, Lyon 2008
56. Young NS. Acquired a plastic anemia. Ann Intern Med. 2002;136(7):534.
57. Young NS, Scheinberg P, Calado RT.Aplastic anemia. Curr Opin Hematol 2008; 15:162.
288
PULMONOLOGY
'
SECTION ONE
APPROACH TO COMMON COMPLAINTS
RESPIRATORY DIFFERENTIALS
MANIFESTATIONS
PROBLEMS
• Tachypnea
• Wheezing (usually expiratory)
Signs of lower airway • Bronchiolitis
• Prolonged expiratory phase
obstruction • Asthma
with increased expiratory effort
• Cough
• Variable or irregular RR
and pattern (i.e., tachypnea
alternating with bradypnea)
• Toxins
I
• Variable respiratory effort • Neuromuscular disease
Signs of disordered • Shallow breathing with • Metabolic
controlofbreathing inadequate effort • Drug overdose
• Central apnea (apnea without • Increased ICP
respiratory effort)
• Normal or decreased air
movement
Source:AHAandAAPPediatricAdvancedLifeSupport2016
291
APPROACH TO COUGH
• Cough is defined as a reflex response of the lower respiratory tract to stimulation of
irritant or cough receptors in the airway mucosa.
CHARACTER OF
CONSIDERATION
COUGH
• Atypical infections like Chlamydia and Mycoplasma, pertussis,
Staccato, paroxysmal
foreign body, cystic fibrosis
Whooping • Pertussis
All day, never during
• Habit cough
sleep
Barking, brassy • Croup, habit cough, tracheitis, tracheomalacia, epiglottitis
Hoarseness • Laryngeal involvement
Acute onset • Foreign body, pulmonary embolism
After exercise • Reactive airway disease
Accompanies eating, • Gastroesophageal reflux (GER), tracheoesophageal fistula,
drinking aspiration
Throat clearing • Postnasal drip, vocal tic
Productive (wet cough) • Infection, bronchiectasis, cystic fibrosis
Nocturnal • Asthma, reactive airway disease, GER, sinusitis
Seasonal • Allergic rhinitis, reactive airway disease
lmmunosuppressed • Bacterial pneumonia, Mycobocterium tuberculosis, M. avium,
patients cytomegalovirus, Pneumocystis jiroveci pneumonia
• Chlamydia psitacci (birds), Yersinia pestis (rodents), Francisel/a
Animal exposure tularensis (rabbits), hantavirus (rodents), histoplasmosis
(pigeons), Q fever ( cattle, sheep)
Workdays with
• Occupational exposure
clearing on days off
Source:KhegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Elsevier:2020
KliegmanR. el al. PracticalStrategiesin PediatricDiagnosisandTherapy(2nded.):2004
• Upper airway
Stridor • lnspiratory • Continuous
obstruction
• Lower airway
Wheeze • Expiratory • Continuous • High
obstruction
• Lower airway
Rhonchi obstruction
• Either • Continuous • Low
or lung tissue
disease
Source:KliegmanR. et al. NelsonTextbookof Pediatrics(21sted.).Elsevier:2020
American HeanAssociation Pediatric
Advanced LifeSupport Manual
292
SECTION TWO
PULMONARY DISORDERS IN THE NEONATE
I. ETIOPATHOGENESIS
• Deficiency or immaturity of surfactant, complicated by an overly compliant chest wall
• Effects of surfactant deficiency:
Increased surface tension causing alveolar collapse
, Progressive atelectasis, V/Q mismatch & hypoxia
' Leads to failure to develop an effective functional residual capacity (FRC)
• Incidence is inversely proportional to gestational age (e.g., highest incidence in those
delivered <28 weeks AOG)
II. MANIFESTATIONS
• Respiratory distress soon after birth: tachypnea, prominent grunting, intercostal/
subcostal retractions, nasal flaring, cyanosis
• Breath sounds may be normal or decreased with a harsh tubular quality
• Fine crackles on deep inspiration
III. DIAGNOSIS
DIAGNOSTIC REMARKS/FINDINGS
• Shows characteristic "ground-glass" pattern or fine reticular
granularity of the parenchyma
Chest radiograph
• Low lung volumes and air bronchograms within the first 24 hours of
life may be present
Arterial blood gas • Findings may include hypoxemia, hypercarbia, metabolic acidosis
Other tests
• Sepsis workup (early-onset sepsis can be indistinguishable from
RDS clinically)
• 20 echocardiography to exclude possible cardiac pathology
• Rule out other causes of respiratory distress (e.g.,electrolyte imbalance)
I
IV. MANAGEMENT
ASPECT MANAGEMENT
• Recommended within 15 min of birth to infants <26 weeks AOG
• For all preterm with RDS who require delivery room intubation for
stabilization
Surfactant
• Technique INSURE:Intubate-Surfactant-Extubate to CPAP(Intubate,
replacement
administer surfactant intratracheally through ET tube, connect to
CPAP)reduces the need for mechanical ventilation and development
of bronchopulmonary dysplasia (BPD)
• Most cases of mild RDS are self-limited
• CPAPis increasingly becoming the mainstay therapy for RDS
• Mechanical ventilation only for severe RDS, respiratory failure, or
Supportive care
persistent apnea
• Fluid and nutritional support
• Antibiotic therapy to cover for the most common neonatal infections
• Obstetric measures to prevent preterm delivery
Prevention • Antenatal corticosteroids (dexamethasone or betamethasone) for
mothers at risk of preterm delivery
Source:GomellaTL.et al. Neonatolgy 7thEdition.McGraw-Hill;2013.
KliegmanR,et al. NelsonTextbook of Pediatrics
(21sted.).Elsevier;2020
ClohertyJ, et al. Manualof Neonatal
Care(7thed.).Philadelphia;
2012
293
TRANSIENT TACHYPNEA OF THE NEWBORN (TTN)
Benign, self-limited respiratory distress syndrome of term and late preterm infants
related to delayed clearance of lung fluid
• Most common perinatal respiratory disorder ( 40% of respiratory distress after birth)
I. ETIOPATHOGENESIS
• Central mechanism: delayed fluid resorption
• Lung fluid inhibits gas exchange leading to increased work of breathing and
compensatory tachypnea
• Hypoxia develops due to poorly ventilated alveoli
• Infants born by elective cesarean section have a higher risk for TTN because they are not
exposed to the stress (lack of catecholamine surge & active Na· reabsorption in lung) and
absence of uterine contractions (contractions result in high transpulmonary pressure
leading to lung fluid efflux)
II. MANIFESTATIONS
• Early onset of tachypnea soon a~er birth or within the first 6 hours after delivery
Retractions, nasal flaring, expiratory grunting, or cyanosis relieved by 0, supplementation
Barrel chest due to increased A-P diameter (hyperinflation) ·
• Crackles on auscultation
Liver & spleen may be palpable due to hyperinflation
III. DIAGNOSIS
DIAGNOSTIC REMARKS/FINDINGS
• Mild to moderate hypoxemia
Arterial blood gas
• Normal partial CO2 due to tachypnea
• Hyperinflation/over aeration, prominent perihilar streaking
( engorged lymphatics)
• Flattened diaphragm on lateral view
Chest radiograph
• Fluid in the intralobar fissures 01; rarely, small pleural effusions
• Prominent pulmonary vascular markings: "fuzzy vessels"
sunburst pattern, peripheral air trapping
• Double lung point
Lung 0 Diagnostic
comet-tail a1tifacts
IV. MANAGEMENT
ASPECT MANAGEMENT
• Oxygenation & thermoregulation
Supportive • Monitor fluids and electrolytes
Management • Beta agonists (e.g., salbutamol)
• Most cases resolve in 3-5 days
• Elective cesarean section (CS) scheduled at gestational age of
39 weeks or later
Prevention • Vaginal birth
• Establish fetal maturity prior to CS
• Antenatal betamethasone prior to elective CS at term
Source:GomellaTL,el al. Neonalolgy
7thEdition.McGraw-Hill:2013
KliegmanR, el al. NelsonTextbook
of Pediatrics
(21sted.).Elsevier;2020
294
PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN (PPHN)
• Marked pulmonary hypertension resulting from elevated pulmonary vascular resistance
and altered pulmonary vasoreactivity, leading to right to left extrapulmonary shunting of
blood across the foramen ovale and the ductus arteriosus
• Also referred to as Persistent Fetal Circulation
I. ETIOPATHOGENESIS
Failure of the normal circulatory transition after birth, due to high pulmonary vascular
resistance, secondary to:
Maladaptation from an acute injury
, Remodeling of pulmonary vasculature with vascular wall thickening and smooth
muscle hyperplasia
Pulmonary hypoplasia
Obstruction or any anomalies or abnormalities of pulmonary vessels
With inadequate pulmonary perfusion, neonates are at risk for developing refractory
hypoxemia, respiratory distress, and acidosis
Congenital heart
disease
•
•
•
•
Total anomalous venous return
Hypoplastic left heart
Coarctation of the aorta
Enclocardial cushion defects
I
• Transposition of the great arteries
• Aortic stenosis
• Asphyxia
Perinatal factors • Perinatal hypoxia
• Maternal ingestion of aspirin or indomethacin
II. MANIFESTATIONS
Respiratory distress with cyanosis (hypoxemia) despite adequate ventilation
Marked !ability in oxygenation
Significant decrease in pulse oximetry with routine nursing care or minor stress
• Signs of heart failure
Ill. DIAGNOSIS
DIAGNOSTIC REMARKS/FINDINGS
Chest radiograph • May be normal (depends on comorbid conditions)
• Gold standard to confirm the diagnosis of PPHN
• Useful in identifying sites of extrapulmonary shunting
2D-echocardiography
and assessing right and left ventricular function (to guide
appropriate vasodilator therapy)
295
IV. MANAGEMENT
ASPECT MANAGEMENT
• Reduces pulmonary vascular resistance
Inhaled • Improves oxygenation by directing blood to better aerated distal air
Nitric Oxide spaces
• Improves V/Q mismatch
• Mechanical ventilation to ensure adequate oxygenation
Initial
Management
• Presser agents (e.g., dopamine) to maintain normal blood pressure and
increase cardiac output
• Careful and intensive monitoring
• Prevent aggravation of left to right shunting through adequate hydration
• Maintain normal serum glucose and calcium
Supportive
• Thermoregulation
• Avoid acidosis
• Sedation to address !ability with minor stress
• Adequate resuscitation and support from birth may prevent or
Prevention
ameliorate PPHN
Source:GomellaTL, et al. Neonatolgy 7thEdition.McGraw-Hill;2013.
KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Philadelphia;
2020
I. ETIOPATHOGENESIS
• After in utero passage of meconium (affected by fetal distress & vagal stimulation), deep
irregular respiration/gasping can cause aspiration of MSAF
• Distal progression into the airways of meconium stained fluid occurs in conjunction with
reabsorption of lung fluid
• Early consequences include:
Airway obstruction
° Chemical pneumonitis
Release of inflammatory mediators
Surfactant dysfunction
Increase in pulmonary vascular resistance and pulmonary hypertension
II. MANIFESTATIONS
• Mild to severe respiratory distress with cardiopulmonary failure
General
• Early onset respiratory distress in an infant with MSAF
• Proportional to length of meconium exposure & meconium concentration:
Meconium 0 Stained umbilical cord: 15 minutes exposure to thick MSAF or 1 hour
staining of exposure to lightly stained fluid
skin 0 Yellow stained nails: indicate 4-6 hours exposure
0 Stained vernix caseosa: indicate 12 hours exposure
296
III. DIAGNOSIS
DIAGNOSTIC REMARKS/FINDINGS
• Hypoxemia
• Respiratory acidosis due to airway obstruction/atelectasis/
Arterial blood gas pneumonitis
• Combined respiratory and metabolic acidosis seen in
concomitant perinatal asphyxia
• Hyperexpansion of the lungs with flat diaphragms and widened
rib spaces
• Widespread, coarse, asymmetric, and patchy infiltrates
• Areas of lung atelectasis (complete obstruction) flanked by
Chest radiograph
irregular areas of overexpansion (partial obstruction)
• Diffuse homogeneous ground-glass lung density (similar to
that seen in respiratory distress syndrome)
• Others: pneumothorax, pleural effusion
IV. MANAGEMENT
ASPECT MANAGEMENT
• Routine intubation to aspirate the lungs of vigorous infants is
not effective in reducing MAS
General measures • Depressed infants may benefit from endotracheal intubation
and suctioning to remove meconium in the airway before the
first breath (however, data for this is inconclusive)
• Administer oxygen for respiratory distress or decreasing
oxygen saturation
• Endotracheal intubation with assisted ventilation for moderate
to severe MAS
I
• Sedation for infants on mechanical ventilation (pain
Supportive
precipitates hypoxia and right-to-left shunting)
• Antibiotic coverage: meconium (though sterile) inhibits the
normally bacteriostatic quality of amniotic fluid
• ECMO (Extracorporeal membrane oxygenation) as final rescue
therapy
• Mild disease requires <40% oxygen for up to 48 hours
Oxygen • Moderate disease requires >40% oxygen for >48 hours
administration • Severe disease requires assisted ventilation for >48 hours
(associated with PPHN)
Source: GornellaTL, et al, Neonalolgy7th Edition.McGraw-Hill;2013.
KliegrnanR. et al. NelsonTextbookof Pediatrics(21sted.). Philadelphia:2020
297
BRONCHOPULMONARY DYSPLASIA (NEONATALCHRONIC LUNG DISEASE)
• Form of chronic lung disease that affects newborns (mostly premature) and infants resulting
from damage to the lungs caused by mechanical ventilation and long-term use of oxygen
• Persistent oxygen dependency up to 28 days of life
• Incidence is influenced by lung maturity (increased incidence with lower birth weight)
I. ETIOPATHOGENESIS
• Exaggerated inflammatory response
• Volutrauma/barotrauma during mechanical ventilation
• Hyperoxia due to prolonged exposure (>150 hours) to FiO2 >60%
II. MANIFESTATIONS
• Worsening respiratory status with increased work of breathing
• Increased oxygen requirement
• Apnea
• May have manifestations of heart failure
SEVERITY DESCRIPTION
Mild BPD • Infants who have been weaned from any supplemental oxygen
Moderate BPD • Infants who continue to need up to 30% oxygen
• Infants who need >30% oxygen or require CPAP/mechanical
Severe BPD
ventilation
III. DIAGNOSIS
DIAGNOSTIC REMARKS/FINDINGS
• CO2 retention
Arterial blood gas
• pH derangements
• Shows diffuse haziness and lung hypoinflation among pre-
matures with persistent oxygen requirements
Chest radio graph • Streaky interstitial markings, patchy atelectasis intermingled
with cystic areas, severe lung hyperinflation
• "Bubbly lungs"
• Done for non-improving or worsening BPD
ECGand 2D echo
• To detect car pulmonale and/or pulmonary hypertension
• Electrolyte abnormalities from chronic CO2 retention, diuretic
Laboratory
examination therapy, fluid restriction
• CBC:to rule out infection
IV. MANAGEMENT
ASPECT MANAGEMENT
• Ventilatory and nutritional support
• Control of infection
Supportive
• Diuretic therapy, fluid restriction
• Bronchodilators, corticosteroids, pulmonary vasodilators
• There remains a lack of effective intervention that prevents BPD
• Strategies include:
0 Early use of nasal CPAP (nCPAP)
298
CONGENITAL DIAPHRAGMATIC HERNIA (CDH)
I. ETIOPATHOGENESIS
A. Two Types
TYPE DESCRIPTION
B. Pathophysiology
• At 10-12 weeks AOG,the abnormal communication between
the peritoneal and pleural cavities allows herniation of
Prenatal period intestine into the pleural space
• This results to underdevelopment (pulmonary atresia/
hypoplasia) of the lungs due to compression
• After delivery, the anomaly contributes to pulmonary
Postnatal period
parenchymal insufficiency
lll. MANAGEMENT
ASPECT
• Shift of mediastinal structures to the other side
MANAGEMENT
I
• Intubation with positive pressure ventilation
• Replacement surfactant therapy
• Nasogastric tube to lessen gaseous distention of the stomach
Supportive
and intestine
• Positive pressure ventilation (e.g., CPAP) is avoided for CDHas
added pressure in the stomach further compresses the lungs
• Surgical correction to reduce intrathoracic intestine and closure
Surgery
of the diaphragm
Source:GomellaTL, et al. Neonatolgy7th Edition.McGraw-Hill; 2013.
KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Philadelphia;
2020
299
CHOANAL ATRESIA
• Choana (i.e., back of the nasal passage) is blocked by an abnormal bony (90%) or
membranous septum (10%) due to failed recanalization of the nasal fossae
I. ETIOPATHOGENESIS
• Most common congenital anomaly of the nose with unknown pathogenesis (theoretically
due to the persistence of the buccopharyngeal membranes or failure of the oronasal
membrane to rupture)
• More common in females
Most have other congenital anomalies, such as:
CHARGEsyndrome (most common)
VACTERLsyndrome
Treacher-Collins syndrome
° Kallman syndrome
II. MANIFESTATIONS
• Difficulty with mouth breathing (e.g., they would suck in their
lips and may develop cyanosis)
Bilateral choanal
• Those able to breathe through their mouths may have difficulty
atresia (40%)
sucking and swallowing at the same time (e.g., as they attempt
to feed, they may develop cyanosis)
Unilateral choanal • Presents with unilateral purulent nasal discharge and obstruction
atresia (60%) • History of chronic sinusitis
III. DIAGNOSIS
DIAGNOSTIC REMARKS
• Diagnosis is established by inability to pass a firm catheter
Clinical
through each nostril 3-4 cm into the nasopharynx
Fiberoptic rhinoscopy • Atretic plate may be seen directly
High-resolution CTscan • Can best evaluate the anatomical abnormalities
IV. MANAGEMENT
ASPECT MANAGEMENT
• Prompt placement of an oral airway, maintain the mouth in an
Initial treatment open position, or intubation
• Bilateral cases: intubation or tracheotomy may be indicated
• Trans-nasal repair: operative intervention for neonates without
other serious medical problems
Surgery • Tracheotomy: for those with bilateral atresia and other
potentially life-threatening problems
• Elective surgery: for those with unilateral obstruction
Source:KliegmanR.et al. Nelsontextbookof pediatrics(21sted.).Canada:Elsevier
AndaloraC el al. ChoanalAtresia.In:Sta!Pearls;
2018
300
SECTION THREE
DISORDERS OF THE UPPER RESPIRATORY TRACT
II. MANIFESTATIONS
• Predominant in infants: nasal discharge and fever
• Sore throat, sneezing, nasal obstruction, rhinorrhea, irritability, decreased
appetite
• Cough usually begins after the onset of nasal symptoms and may persist for
Symptoms another 1-2 weeks after resolution of other symptoms
• Fever is more likely with influenza virus, RSV,human metapneumovirus,
and adenovirus
• Colds usually persist for 1 week
I
• Onset of symptoms typically occurs 1-3 days after viral infection
• Swollen, erythematous nasal turbinates
• Abnormal middle ear pressure
Signs • Anterior cervical lymphadenopathy or conjunctiva! injection
• Change in color of nasal secretion may indicate accumulation of
inflammatory cells and not necessarily bacterial superinfection
III.DIAGNOSIS
• Usually a clinical diagnosis
• Exclude conditions that are potentially more serious (e.g., sinusitis, foreign body)
IV. MANAGEMENT
• Supportive: topical nasal saline or saline nasal irrigation to reduce the symptoms
• Non-prescription cough & cold products should not be used for children <6 years old
• Complications: otitis media, sinusitis, pneumonia
301
SINUSITIS
I. ETIOPATHOGENESIS
A. Etiology
S. pnewnoniae (30%)
Nontypeable H. inf/llenzae (20%)
0 M. catarrhalis (20%)
Anaerobes and Staphy/ococcl/s aureus [uncommon)
8. Pathophysiology
0 Anything that impairs mucociliary transport or causes nasal obstruction
predisposes to sinusitis (e.g., viral URTI, allergic rhinitis, cigarette smoke exposure)
C. Classification of Sinusitis
CLASSIFICATION DURATION
Acute sinusitis • < 30 days
II MANIFESTATIONS
• Nasal congestion, purulent nasal discharge, feve1;and cough
• Maxilla1y tooth discomfort and pain or pressure exacerbated by bending
Symptoms
forward
• Headache and facial pain are rare in children
• Erythema and swelling of the nasal mucosa with purulent nasal
discharge
Signs
• Sinus tenderness detectable in adolescents
• Transillumination shows an opaque sinus that transmits light poorly
• Periorbital cellulitis
• Orbital cellulitis (proptosis, chemosis, decreased visual acuity,
diplopia, impaired EOMs, eye pain)
• Meningitis
Complications • Cavernous sinus thrombosis
• Brain abscess
• Pott puffy tumor [osteomyelitis of the frontal bone)
• Mucoceles (chronic inflammatory lesions in the frontal sinuses that
expand and displace the eye)
Source:KliegmanR.el al. Nelsontextbookof pediatrics(21sted.).Canada:Elsevier
MorcomS. et al. Sinusitis.AustFamPhysician:
2016
III. DIAGNOSIS
• Clinical diagnosis is based on histo1y:
0 Persistent nasal discharge & cough >10 days without improvement
Clinical
0 Temperature of at least 39°C
0 Purulent nasal discharge for 3-4 consecutive days
• Findings (not diagnostic):
0 Air-fluid levels
302
IV. MANAGEMENT
ASPECT MANAGEMENT
• Indicated for acute bacterial sinusitis with severe onset or a
worsening course
• Promotes resolution of symptoms & prevent suppurative complications
• Uncomplicated mild/moderate acute sinusitis: amoxicillin 45 mg/
kg/day BID for 10 days (or 7 days after resolution of symptoms)
• Alternatives if allergic to penicillin: cefuroxime, cefixime
Antibiotics • Amoxicillin-clavulanate 80-90 mg/kg/day for children with the
following risk factors:
0 Previous antibiotic treatment (past 1-3 months)
0 Daycare attendance
ACUTE PHARYNGITIS
I. ETIOPATHOGENESIS
• Inflammation of pharynx manifesting as erythema, edema, exudates, or enanthem
• Most of the pathogens are listed below
VIRUSES BACTERIA
• Adenovirus • Group A beta-hemolytic streptococcus or GABHS
• Coronavi rus (Strep. pyogenes): most common bacterial pathogen
• Cytomegalovirus • Fusobacterium necrophorum
•
•
•
Enterovirus
Epstein-Barr virus
Rhinovirus
• Corynebacterium diphtheriae
• Chlamydia trachomatis
• Chlamydophila pneumoniae
Source:Kliegman
R, et al. Nelsontextbook
of pediatrics
(21sted.).Canada:Elsevier
I
II. MANIFESTATIONS
VIRAL BACTERIA (due to GABHS)
• Gradual onset • Sore throat and fever
• Moderate throat pain • Headache, vomiting, abdominal pain
• Symptoms of viral URTI (e.g., • No URTI symptoms
conjunctivitis, coryza, cough) • Palatal petechiae
• Contacts with cold symptoms • Tonsillar exudate
• Vesicles and ulcers (HSV) • Scarlatiniform rash
• Conjunctivitis (adenovirus) • Swollen, tender anterior cervical nodes
Source:Shaikhet al. Journalof Pediatrics:2012
III. DIAGNOSIS
DIAGNOSTIC REMARKS
Throat culture • Gold standard for diagnosing GABHS pharyngitis
303
IV. MANAGEMENT
ASPECT MANAGEMENT
• Amoxicillin SO mg/kg PO x 10 days
• Penicillin or amoxicillin
• Penicillin 250 mg (if <27 kg) or 500 mg
for 10 days
(if;,27 kg) PO twice a day x 10 days
• Erythromycin 40 mg/kg/day PO twice a
day x 10 days (max: 1 g/day)
• Azithromycin 12 mg/kg on day 1; then 6
mg/kg on days 2-5 PO once a day (max:
• Treatment options if
500 mg/day)
allergic to penicillin
Antibiotics for • Clarithromycin 15 mg/kg/day twice a day
GABHS x 10 days (max: 500 mg/day)
• Clindamycin 20 mg/kg/day PO thrice a
day x 10 days (max: 1.8 g/ day)
• With a clinical diagnosis of scarlet fever
• With a household contact with
• Start antibiotics
documented Streptococcal Pharyngitis
immediately even
• With a past histmy of acute rheumatic fever
without culture if
• With a recent history of acute rheumatic
fever in a family member
• Considered for recurrent streptococcal pharyngitis, defined as culture
positive streptococcal pharyngitis that has been severe and frequent
(Paradise Criteria):
Tonsillectomy 0 ;,7 episodes in the previous year, or
0 ;,5 episodes in each of the preceding 2 years, or
0 ;,3 episodes in each of the preceding 3 years
V. COMPLICATIONSOF GABHS:
• Rheumatic fever
• Post-streptococcal glomerulonephritis
• Peritonsillar / retropharyngeal abscess
Sources:KliegmanR, et al. Nelsontextbookof pediatrics(21sted.).Canada:Elsevier
Shaikhet al. Journalof Pediatrics;2012
CDC& Prevention. GroupA Streptococcal (GAS)Disease
PERITONSILLAR ABSCESS
I. ETIOPATHOGENESIS
• Bacterial invasion through the capsule of the tonsils
• Usually affects adolescents
• Etiology: Group A streptococcus and mixed anaerobes
II. MANIFESTATIONS
• Fever, sore throat, dysphagia, odynophagia, drooling, trismus
• Asymmetric tonsillar bulge with a displaced uvula (diagnostic PE finding)
Ill. DIAGNOSIS
• Diagnosis is mainly clinical
• CT scan: helpful for showing the abscess
IV. MANAGEMENT
• Majority resolve after surgical drainage (I & Dor needle aspiration) and antibiotics
• Consider tonsillectomy when:
° Failure to improve within 24 hours of antibiotics and I & D
0 History of recurrent tonsillitis
° Complications from peritonsillar abscess
B. Pathophysiology
The retropharyngeal space is located between the pharynx & the cervical vertebrae
& extending down into the superior mediastinum
Infection of the retropharyngeal nodes usually occurs due to extension of a localized
infection of the oropharynx
° Can also result from penetrating trauma to the oropharynx, dental infection, and
vertebral osteomyelitis
C. Etiology
Group A streptococcus
Anaerobes
0 Staphylococcus aureus
Others: Klebsiella and Haemophi/us influenza
II. MANIFESTATIONS
• Fevet; irritability, decreased oral intake, drooling
• Neck stiffness or refusal to move the neck
• Limitation of neck extension, bulging of the posterior pharyngeal wall, muffled voice,
strider, respiratory distress
Ill. DIAGNOSIS
DIAGNOSTIC REMARKS
• Incision & drainage and culture of an abscessed node provides
Culture
I
the definitive diagnosis
• Can accurately identify abscess formation in majority of cases
• Findings include:
CT scan with contrast ° Central lucency
0 Ring enhancement
IV. MANAGEMENT
ASPECT MANAGEMENT
• IV antibiotics with or without surgical drainage
Antibiotic Therapy • 3" 1 generation cephalosporin with ampicillin-sulbactam or
clindamycin
• Drainage is necessary in patients with respiratory distress or
Drainage
failure to improve with IV antibiotics
305
LARYNGOTRACHEOBRONCHITIS (VIRAL CROUP)
I. ETIOPATHOGENESIS
• Acute inflammatory disease of the larynx (within the subglottic space)
Most common etiology is parainfluenza virus
• Affects children 3 months to 5 years old (peak incidence at 2 years old)
• More common in males
• Most common form of acute upper respiratory obstruction in children
II MANIFESTATIONS
• URTI and fever 1-3 days prior to upper airway obstruction
• "Barking cough"
Symptoms
• Hoarse voice
• Symptoms worse at night
• Coryza & rhinorrhea
• Normal to moderately inflamed pharynx
Signs
• Slight tachypnea
• lnspiratory stridor
III. DIAGNOSIS
A. Westley Croup Score (diagnosis of croup is mainly clinical)
SIGN DEGREE SCORE
• None 0
Stridor • At rest on auscultation 1
• At rest without auscultation 2
• None 0
• Mild 1
Chest wall retractions
• Moderate 2
• Severe 3
• Normal 0
Air entry • Decreased 1
• Severely decreased 2
• None 0
Cyanosis • With agitation 4
• At rest 5
• Normal 0
Consciousness level
• Altered 5
Interpretation of Results (total score can be 0-17 points):
• Mild: :s2
• Moderate: 3-7
• Severe: equal or >8
• Impending respiratory failure: equal or >12
Source:WoodsC. et al. Croup:Clinicalfeatures,evaluation,
anddiagnosis.
UpToDate:
2018
IV. MANAGEMENT
• No stridor at rest
• Severe disease: poor air entry, altered
• Normal oxygen saturation
consciousness
• Good air exchange
• Deterioration even after initial medical management
• No cyanosis
• Severe dehydration
• Normal level of consciousness
• Features suggesting secondary bacterial infection
• Able to tolerate fluids by mouth
306
B. Management of Croup based on Severity
SEVERITY INTERVENTION*
Mild • Dexamethasone 0.6 mg/kg/dose PO/IV /IM (max dose: 16 mg)
• Dexamethasone 0.6 mg/kg IV/IM
• Humidified oxygen (if02 saturation <92%)
Moderate to
• Give nothing by mouth
Severe
• Nebulize epinephrine over 15 minutes (0.5 mL/kg/dose, max 5 mL,
using 1:1000 dilution)
II. MANIFESTATIONS
Signs
to maintain the airway, muffled voice, "sniffing dog" or "tripod" position
• Direct visualization of inflamed cherry-red epiglottis under double set-up
( examine the throat only under double set-up because of risk for airway
obstruction and respiratory arrest)
I
III. DIAGNOSIS
DIAGNOSTIC REMARKS
• Blood, epiglottic surface, CSF (in some cases)
Cultures
• Done once airway is stabilized
Lateral neck
• Findings: "thumb" or "leaf" sign
radiograph
Fiberoptic
• Provides direct visualization of inflamed cherry-red epiglottis
laryngoscopy
IV. MANAGEMENT
• Secure airway (intubation or tracheostomy) under double set-up
• IV antibiotics (cefotaxime, ceftriaxone, or meropenem) for 7-10 days
V. PROPHYLAXIS:
• Indications for rifampicin prophylaxis (20 mg/kg orally once a day for 4 days with
maximum dose of600 mg/dose) for all household members with:
Any contact <4 years old who is incompletely immunized
Any contact <12 months old who has not received the primary vaccination series
0 An immunocompromised child in the household
Source:GuerraAM,et al. Epiglottitis.In: StatPearls.
Fl: StatPea~sPublishing;
2018
307
SUMMARY TABLE FOR EPIGLOTTITIS VS CROUP
BACTERIAL TRACHEITIS
• Most common cause is S. aureus
• Others:
• MRSA
0 S. pneumoniae
Etiopathogenesis 0 S. pyogenes
• M. catarrhalis
• Nontypeable H. influenza
0 Anaerobes
• Often follows a viral respiratory infection
• Brassy cough
• High fever and "toxicity" can occur immediately or after a few days
Manifestations of apparent improvement
• Can lie flat, does not drool, no dysphagia
• Mucosa I swelling at the level of the cricoid cartilage with copious,
thick, purulent secretions
• Based on bacterial upper airway disease (high fever, purulent airway
secretions, absence of classic findings of epiglottitis)
Diagnosis
• Neck radiograph: ragged tracheal air column, pseudomembrane
detachment in the trachea (lateral view)
Management • Vancomycin or clindamycin and a 3"' generation cephalosporin
Source:KliegmanR. el al. Nelsontextbookof pediatrics(21sted.).Canada:Elsevier
308
SECTION FOUR
DISORDERS OF THE LOWER RESPIRATORY TRACT
BRONCHIOLITIS
I. ETIOPATHOGENESIS
• Acute inflammation of the small airways in children <2 years old resulting in bronchiolar
obstruction with edema, mucus, and cellular debris
• Most commonly caused by RSV
• More common in:
Boys
Those who have not been breastfed
Those who live in crowded conditions
Infants with mothers who smoked during pregnancy
II. MANIFESTATIONS
• Child with coryzal prodrome lasting 1-3 days followed by persistent cough,
Symptoms tachypnea, and presence of wheezing/crackles
• Low-grade fever, rhinorrhea, cough
• Tachypnea, wheeze/crackles
Signs • Hyperresonance to percussion
• Prolonged expiratory phase
III. DIAGNOSIS
• Routine tests are not necessary
• Chest radiograph (not routinely indicated in uncomplicated cases): shows hyperinflation
with patchy atelectasis
IV. MANAGEMENT
A Management Based on Severity
SEVERITY
Mild
• May be managed at home
• Increase fluids
MANAGEMENT*
C. Prevention
Palivizumab (IM monoclonal antibody) for children <2 years with congenital heart
disease (CHD) and chronic lung disease (CLD), and history of prematurity
0 Hand hygiene practices
Exclusive breastfeeding for at least 6 months
Sources:NICEGuidelines
on Bronchiolitis
2015
AAPBronchiolitis
Guidelines2014
309
ACUTE BRONCHITIS
I. ETIOPATHOGENESIS
Inflammation of the large and medium-sized airways of the lungs
Tracheobronchial epithelium is invaded by the infectious agent that leads to activation of
inflammatory cells and release of cytokines
• Often follows a viral upper respiratory tract infection
II. MANIFESTATIONS
• Nonspecific URTI symptoms
Natural History • After 3-4 days, frequent dry, hacking cough
(entire course • Aher several days, sputum becomes purulent from leukocyte migration
lasts ~2-3 weeks) • Chest pain exacerbated by coughing may be prominent in older children
• Mucus gradually thins within 5-10 days and cough abates
• Early signs: low-grade feve1; nasopharyngitis, conjunctivitis, rhinitis
Signs
• Late signs: coarse breath sounds with crackles & scattered wheezing
IV.MANAGEMENT
• No specific treatment and it is self-limited
• Antibiotics do not hasten improvement
• Use of humidifiers do not shorten the course
Source:KliegmanR, et al. Nelsontexlbookof pediatrics(21sted.).Canada:Elsevier
SinghA. et al. AculeBronchilis.In: StatPearls.FL: SlalPearlsPublishing
PNEUMONIA
I. ETIOPATHOGENESIS
• Inflammation of the lung parenchyma
• Most commonly viral etiology in childhood
A.Etiology
AGE GROUP FREQUENT PATHOGENS (in order of frequency)
• Group B streptococcus
•£.coli
Neonates
• Listeria
(0-28 days)
• S. pneumoniae
• H. influenzae*
• Respiratory syncytial virus (RSV)
• Parainfluenza
• Chlamydia
3 weeks to
• Mycoplasma pneumoniae
3 months
• S. pneumoniae
• H. influenzae
• S. aureus
• RSV and other viruses
4 months to • S. pneumaniae
4 years • H. influenzae type b
• Mycoplasma pneumoniae
• Mycoplasma pneumoniae
5 to 15 years • S. pneumonia
• Chlamydaphila pneumoniae
'H. influenzae
typebis uncommon
withroutineH.inftuenzae
typeb immunization
• Themostcommoncauseof pneumonia acrossall agegroupsareviruses
• S. pneumoniaeis the mostcommonbacterialcauseof pneumoniaacrossall agegroup
310
B. Classification of Pneumonia According to Location
CLASSIFICATION DESCRIPTION
Pneumonitis • Inflammation of the interstitium
Lobar pneumonia • With consolidation of one or more lobes
Bronchopneumonia • Inflammation of the bronchioles with mucopurulent exudate
Source:KliegmanR.el al. Nelsonlextbookof pediatrics(21sled.).Canada:Elsevier
II. MANIFESTATIONS
A Overview of the Manifestations
• Clinical triad: feve,; cough, and tachypnea
Symptoms
• Abdominal pain is common in lower lobe pneumonia
• Tachypnea is the most consistent clinical manifestation
• Early: diminished breath sounds, scattered crackles and rhonchi
• Later: dullness on percussion & lag in respiratory excursion on
Signs
affected side (from consolidation and/or pleural effusion)
• Signs of respiratoty failure in severe cases: retractions, head
bobbing, cyanosis, grunting, apnea, and changes in sensorium
• "Staccato"
• Cough cough of
• Cough • High fever • Less ill-looking insidious
Manifestations • Wheezing • Dyspnea • Non-productive onset
• Stridor
• WBC normal
• Dullness to
percussion
cough • Maternal
history of
infection
• WBCusually
I
• WBC count
or mildly • Leukocytosis normal
CBC usually
elevated • Neutrophilia • Eosinophilia
normal
• Lyrnphocytosis
• Pneumococcal:
confluent lobar
consolidation
• Hyperinflation • Staphylococcal: • Interstitial
• Bilateral irregularareas infiltrates • Hype1inflation
Chest interstitial of cavitation lead • Most • Interstitial
Radiograph infiltrates to pneumatocele, common in infiltrates
• Peribronchial empyema, or lower lobes
cuffing bro11d1opulmonary
fistula
• Large pleural
effusion
• SeePCAP • Erythromycin
Management • Supportive management • Clarithromycin
below • Azithromycin
Source:KliegmanR. et al. Nelsontexlbookof pedialrics(21sted.).Canada:Elsevier
PuljizI. et al. ChlamydiapneumoniaeandMycoplasma pneumoniae pneumonia. Epidemiollnfecl:2006
311
III. CLASSIFICATION BASED ON PAPP (2016) AND WHO GUIDELINES
I
PAPP Classification* I PCAPA I
PCAP BI PCAPC PCAPD
I
Signs of failure:
• Retraction None IC/SC Supraclavicular/lC/SC
• Head bobbing None Present Present
• Cyanosis None Present Present
• Grunting None None Present
• Apnea None None Present
• Sensorium None Irritable Lethargic/com a tose
Diagnostic Aids
Management
312
IV. MANAGEMENT
CLASS MANAGEMENT*
• For those without previous • Oral amoxicillin 40-50 mg/kg/day in 3
antibiotic regardless of doses for 7 days (max 1500 mg/day); but
immunization status against may be given for a minimum of 3 days, or
Hib or S. pneumoniae in 2 divided dose for a minimum of 5 days)
PCAPA&
• Azithromycin 10 mg/kg/day OD for 3 days
PCAP B • If with known
(max: 500 mg/day) or 10 mg/kg/day on
hypersensitivity to
day 1 then 5 mg/kg/day on days 2-5
amoxicillin or suspicion of
(max: 500 mg/day)
atypical organisms especially
• Clarithromycin 15 mg/kg/day in 2 doses
Mycoplasma pneumoniae
for 7 days (max: 1000 mg/day)
• No previous antibiotic use
• Penicillin G 100,000 units/kg/day every
requiring hospitalization &
6 hours
with complete HiB vaccination
• With incomplete or unknown
• Ampicillin 100 mg/kg/day every 6 hours
PCAPC status of HiB vaccination
• IV non-antipseudomonal beta-lactam
(beta-lactam with beta-lactamase inhibitor,
• lf>l5 years old, can be cephalosporin, or carbapenem) plus
treated as adult extended macrolide or fluoroquinolone
• Example: Ceftriaxone 2 g IV OD for 7 days
plus Azithromycin 500 mg OD 3-Sdays
PCAPD • Refer to a specialist
'For patientssuspectedto have MRSA:startvancomycinand referto specialist
'If withoutclinicalresponsewithin72 hours,re-evaluateand considershiftingof antibiotics
Source:2016PAPPGuidelines
on PCAP
I
PhilippineCPG:Diagnosis,EmpincManagement
andPrevention
of CAPin lmmunocompetent
Adults2016Update.
313
II. MANIFESTATIONSOF PTB DISEASE
• Refers to the initial stage in children who inhale the
Mycobacterium tubeculosis bacilli
• The following three elements are present:
Ghan focus
0
Primary disease
Lymphadenitis
0
Lymphangitis
0
B. Classification of PTB
Bacteriologically- • Biological specimen is positive by smear microscopy, culture,
Confirmed or rapid diagnostic tests (such as Gene Xpert MTB/RIF)
• Child has been diagnosed with active TB by a medical
Clinically- practitioner who has decided to give the patient a full
Diagnosed course of TB medications, but does not fulfill the criteria for
bacteriologic confirmation
314
C. Presumptive Tuberculosis
Refers to any person with signs & symptoms suggestive of TB (whether pulmonary
or extra pulmonary), or those with radiographic findings suggestive of active TB
, Identification of "Presumptive TB" is summarized in the table below
1) For patients 15 years old and above, a presumptive TB has any of the following:
a. Cough of at least 2 weeks duration with or without the following symptoms:
' Significant and unintentional weight loss
' Fever
' Bloody sputum
' Chest/ back pains not referable to any musculoskeletal disorder
' Easy fatigability or malaise
' Night sweats
' Shortness of breath or difficulty of breathing
2) For patients below 15 years old, a presumptive TB has any of the following:
a. At least 3 of the following clinical criteria:
' Coughing/ wheezing of2 weeks or more, especially if unexplained
' Unexplained fever of 2 weeks or more after common causes have been excluded
' Loss of weight/ failure to gain weight/ weight faltering/ loss of appetite
' Failure to respond to 2 weeks of appropriate antibiotic therapy for lower
respiratory tract infection
' Failure to regain previous state of health 2 weeks after a viral infection or exanthem
' Fatigue, reduced playfulness, or lethargy
b. Any one (1) of the above in a child who is a close contact of a known active TB case
315
IV. MANAGEMENT
C P reventive Th erapy
• Prevent development of infection among exposed contacts:
primary prophylaxis
Aims
• Prevent progression of latent TB infection to disease: secondary
prophylaxis
I
• Disruption of • Nausea, vomiting • Discontinue if AST/ ALT is
membrane energy • Most common cause of more than 3-Sx the normal
metabolism hepatotoxicity in regimens also values
containing H & R • Requires dose adjustment in
• Hypersensitivity reactions renal failure
• Polyarthralgia
Note that dosing for children is higher compared to adults due to Jaster metabolism in children
Source:DOH.Manualof Procedures
of theNationalTuberculosis
ControlProgram.
5thed.2014
CDC.CoreCurnculum onTuberculosis.WhattheClinicianShouldKnow.6th
ed;2013
317
BRONCHIAL ASTHMA
I. ETIOPATHOGENESIS
• A reversible obstructive airway disease involving both the small & large airways with
increased residual lung volumes and a decreased FEVl/FVC ratio .
• Three components of an asthma attack: bronchospasm, airway edema, and increased
mucus production
II. MANIFESTATIONS
• Wheezing, shortness of breath, chest tightness, cough
• Symptoms worsen with certain "triggers" (e.g., viral infection, weather changes, exercise,
allergens, emotions, stress)
• Responds to therapy with bronchodilators
• Commonly with family history of asthma or atopy
III. DIAGNOSIS
A. Diagnosis in Children >5 years old (there are two main features for diagnosing asthma):
l. History of variable respiratory symptoms
Wheeze, shortness of breath, chest tightness, cough
Vary over time and intensity
Often occur or are worse at night or on waking
Often triggered by exercise, laughter, allergens, cold ai1; viral infections
318
C. Classification Based on Severity (For Initial Diagnosis)*
PERSISTENT
INTERMITTENT
MILD MODERATE SEVERE
c:80% c:80%
FEV1 60-79% < 60%
predicted predicted
'Higherseverity
ofclassification
takesprecendence
(e.g.onefeatureofsevereclassifies
a patient
assevere)
Interpretation of Control:
• Well-controlled:
• Uncontrolled:
nonepresent
• Partlycontrolled:1-2present
3-4 present
I
Source:GINA2019updatefor adultsandchildrenolderthan5 years
GINA2015updatefor children5 yearsandyounger
319
V. PHARMACOLOGJC THERAPY FOR ASTHMA
DRUG CLASS EXAMPLES USES & MECHANISM CAUTION
Chromones • Cromolyn sodium • Inhibit mast cell and • Very short duration
• Nedocromil sensory nerve activation of action needing
sodium frequent dosing
• Favorable safety
profile
Long-Acting • Tiotropium • Blocks acetylcholine's • Not for children
Muscarinic effect on muscarinic < 12 years old
Antagonists (LAMA) receptors • Dry mouth
• Tiotropium as mist
inhaler is an add on
treatment for patients
with history of
exacerbations (Step 4)
Anti-lgE • Omalizumab • Inhibits lgE-mediated • Not for children
reactions ,;5 years old
• Limited to patients
with elevated
serum IgE levels
320
Anti-I LS • Mepolizumab • Add-on therapy for • Not for children
• Benralizumab severe eosinophilic <12 years old
asthma • Headache, local
injection site
reactions
Reliever Medications
(for as-needed relief of breakthrough symptoms & prevention of exercise-induced asthma)
Short-Acting B2 • Salbutamol • Stimulates adenylyl • No effect on chronic
Agonists (SABAJ • Procaterol cyclase thus increasing inflammation
• Terbutaline cAMP levels and • May cause
• Albuterol causing bronchodilation tremors,
• Rapid onset of tachycardia, and
bronchodilation and a small fall in
best used for symptom potassium
relief
Short-Acting • lpratropium • Muscarinic receptor • Provide additional
Anticholinergics antagonists benefit when used
• Inhibit only the in combination
I
cholinergic reflex with SABAin those
components and with more severe
thereby less effective symptoms
than 82-agonists • Adverse effect:
dry mouth
(most common],
urinary retention,
glaucoma
321
VII. STEPWISE APPROACHTO CONTROLSYMPTOMS AND MINIMIZEFUTURE RISK
• Asthma treatment is a continuous cycle: assess, adjust treatment, and review response
• A~er starting initial controlle1; review response after 2-3 months (or according to urgency)
° Consider stepping up if: uncontrolled symptoms, exacerbations or risks (but also
assess adherence to medications, correct inhaler technique, and persistent
exposure to triggers)
° Consider stepping down if: symptoms controlled for 3 months, low risk for
exacerbations
• Find the patient's lowest treatment that controls both symptoms and exacerbations
sTEP~
LTRA
STEPZ Low-dose !CS
Intermittent !CS
As needed
STEP3 Double 'low-dose' !CS Low-dose lCS+ LTRA SABA
Add LTRA
STEP4 Refer to specialist lncreaselCSfrequency
Add intermittent JCS
SABA:shortactingB2-agonist LTRA:Leukotrienereceptorantagonist
ICS:inhaledcorticosteroid OCS:oralcorticosteroid
"Low-doseICS/formoterol
is the relievermedication
for thoseprescribed
withlow-dosebudesonide/formoterol
or
low-dosebeclometasonelformoterolmaintenancetherapy
Source:GINA2019updatefor adultsandchildrenolderthan5 years
GINA2015updatefor children5 yearsandyounger
322
A. Dose of Commonly used Inhaled Corticosteroids for Children :5 5 years
DRUG LOWTOTALDAILYDOSE
Budesonide pMDI + spacer • 200 mcg
Budesonide nebulized • 500 mcg
Fluticasone proprionate
(HFA: hydroflouroalkane propellant) • 100 mcg
Beclometasone dipropionate
• 100 mcg
(HFA: hydroflouroalkane propellant)
Ciclesonide • 160 mcg
Mometasone furoate • Not studied in <4 years old
Triamcinolone acetonide • Not studied in this age group
GINA2015updatefor children5 yearsandyounger
B. Dose of Inhaled Corticosteroid (mcg) in Children >5 Years, Adults & Adolescents
RS OLD
DRUG
jHIGH
Beclometasone
dipropionate 200-500 500-1000 > 1000 100-200 200-400 >400
(CFC)
Beclometasone
di propionate 100-200 200-400 >400 50-100 100-200 >200
(HFA)
Budesonide 200-400 >400
200-400 400-800 >800 100-200
(DPI)
Budesonide
nebule
Ciclesonide
(HFA)
80-160 160-320 >320
250-500
80
500-1000
80-160
>1000
>160
I
Fluticasone
propionate 200-400 >400
(DPI)
100-250 250-500 >500 100-200
Fluticasone
propionate 200-500 >500
(HFA)
Mometasone 110-220 220-440 >440 110 220-440 >440
furoate
Triamcinolone >2000 400-800 800-1200 >1200
400-1000 1000-2000
acetonide
CFC-chlorofluorocarbon
propellant
DPI- drypowderinhaler
HFA-hydrofluroalkane
propellant
323
EXACERBATION OF BRONCHIAL ASTHMA
I. DEFINITION
• Acute or subacute deterioration in symptom control that is sufficient to cause distress or
risk to health
• Manifests as any of the following:
• Increase in wheeze or shortness of breath
• Increase in coughing, especially at night
0 Lethargy or reduced exercise tolerance
• Impairment of daily activities
Poor response to reliever medication
Respiratory
• Fast • >30/min
rate • Drowsy, confused
Use ofaccessory • Silent chest
• No retractions • Yes
muscles
Pulse rate • 100-120bpm • >120 bpm
0 2 saturations • 90-95% • <90%
PEF • >50% predicted or best • $SO%predicted or best
Source:GINA2018
updateforadultsandchildren
olderthan5 years
GINA2019updateioradultsandchildren
olderthan5 years
324
III. MANAGEMENTOF EXACERBATIONS,,;5 YEARS OLD
MILD OR SEVERE OR
MODERATE LIFE THREATENING
Assess the Patient for Severity of Exacerbation
• Talks in words
• Confused, drowsy
• Talks in phrases
• Unable to speak or drink
Manifestations • Breathless, agitated
• Central cyanosis
• Markedsubcostalor subglotticreactions
• Silent chest on auscultation
• ,;200 bpm (,;3 years old) or • >200 bpm (,;3 years old) or
Pulse rate
,;180 bpm (4-5 years old) >180 bpm (4-5 years old)
0 2 saturations • ~92% • <92%
• SABA(2 puffs by pMDI + spacer or
2.5 mg by nebulizer q20 mins for
1 hour)
• Transfer to high level care (ICU)
• Oxygen (target sats 94-98%)
• Give inhaled SABAand
• Prednisolone 1-2mg/kg PO x 3-5
Management ipratropium bromide, 0 2 support,
days (max: 20 mg for <2 years,
and systemic corticosteroids
30 mg for 2-5 years) - if with
• Consider referral to specialists
recurrence of symptoms in 3-4 hours
• If worsening at 1 hour, transfer to
high level care (ICU)
• If continuing deterioration, treat as severe and admit to ICU
Monitoring • Consider referral to specialists
• See disposition or discharge planning below
'Afterfirsthourof inhaledSABA,dosevariesfrom4-10puffsq3-4hoursupto 2-3puffsperhour
"TreatmentwithbothSABAandipratropium (short-acting
anticholinergic)
formoderate-severe
exacerbations
is betterthanSABAalone
Follow up
Source:GINA2019updateforadultsandchildrenolderthan5 years
325
SECTION FIVE
PATHOLOGIES OF THE PLEURA
PLEURAL EFFUSION
I. ETIOPATHOGENESIS
• Pleural fluid comes from the capillaries of the parietal pleura and is absorbed from the
pleural space via pleural stomas and lymphatics
• Only 4-12 mL of fluid is present in the pleural space and if formation exceeds clearance,
fluid will accumulate as pleural effusion
SEROFIBRINOUS OR
DRY OR PLASTIC EMPYEMA OR PURULENT
SEROSANGUINEOUS
EFFUSION EFFUSION
EFFUSION
Possible Etiologies
• Pneumonia due to
S.pneumoniae (most
• Lung infections common) and S.aureus
• Acute bacterial or viral • Inflammatory conditions (most common in
pulmonary infection of the abdomen/mediastinum developing countries)
• Acute URTI • Connective tissue diseases • Rupture of a lung abscess
• TB (e.g., SLE) into the pleural space
• Connective tissue disorders • Primary or metastatic • Contamination introduced
such as rheumatic fever neoplasms of the lung, from trauma or thoracic
pleura, or mediastinum surgery
• Mediastinitis or extension
ofintraabdominal abscesses
Pathophysiology
• Process limited to the • Fibrinous exudate on the • Accumulation of pus in the
visceral pleura pleural surface pleural space
• Small amounts of yellow • Exudative effusion of • Three Stages
serous fluid and adhesions serous fluid into the 0 Exudative stage:
between the pleural surface pleural cavity fibrinous exudate on the
• In TB: pleura is thickened pleural surface
& adhesions develop rapidly ° Fibrinopurulent stage:
formation of fibrinous
septa leading to
loculation of fluid and
thickening of parietal
pleura
0 Organizational stage:
fibroblast proliferation
(pockets of loculated
pus may develop into
thick-walled abscess
cavities)
326
II. MANIFESTATIONS
SEROFIBRINOUS OR
DRY OR PLASTIC EMPYEMAOR
SEROSANGUINEOUS
EFFUSION PURULENT EFFUSION
EFFUSION
Symptoms • Chest pain • Early manifestations • Feve1; respiratory
exaggerated by deep of dry pleurisy distress
breathing, coughing, • As fluid accumulates, • Ill-looking patient
and straining pleuritic pain • Complications:
• Patient often lies on disappears bronchopleural
the affected side to • Small effusion: fistula and
decrease respiratory manifestations related pyopneumothorax
excursions to underlying disorder with S. aureus,
• Large effusion: cough, purulent pericarditis,
dyspnea, retractions, lung abscess, peritonitis,
tachypnea,orthopnea, osteomyelitis of the
or cyanosis ribs, septicemia
Signs • Leathery, rough, • Dull to flat on • Similar to
biphasic friction rub percussion; serofibrinous
• Dullness to percussion decreased or absent pleural effusion
• Decreased breath breath sounds ( differentiated only
sounds • Decreased tactile by thoracentesis)
fremitus
• Shift of mediastinum
away from the
affected side
• Signs may shift with
changes in position
if the fluid is not
loculated
III. DIAGNOSIS
A. Basic Tests and Chest Imaging
DRY OR PLASTIC
EFFUSION
SEROFIBRINOUS OR
SEROSANGUINEOUS
EMPYEMAOR
PURULENT
I
EFFUSION EFFUSION
Chest • Diffuse haziness at • Homogenous density • Similar findings
Radiograph the pleural surface obliterating the with any pleural
(X-ray) • Dense, sharply normal lung markings effusion
demarcated shadow • If small effusion: • The absence of
obliterated fluid shift with
costophrenic or changes in
cardiophrenic angles position indicates
or widening of the a loculated
interlobar septa empyema
• Examine the patient
both in supine and
upright positions to
demonstrate a shift of
the effusion
Chest • If radiographs are • Helpful guide to thoracentesis if effusion is
Ultrasound negative, ultrasound loculated
or CT scan of the
chest may be done
'Othertestsfor empyema
or purulenteffusion:bloodculture,CBC,ESR
327
8. Pleural Fluid Analysis
° Culture for bacterial, fungal. mycobacterial organisms, gram stain
0Protein, lactic dehydrogenase and glucose (Glucose is <60 mg/dL in malignancy, TB,
and rheumatoid disease)
0Amylase
Specific gravity and pH
Total cell count and differential, cytologic examination (to reveal malignant cells)
IV. MANAGEMENT
Dry or Plastic • Treatment is directed at the underlying disorder
Effusion • Patients with pleurisy and pneumonia should always be screened
for tuberculosis
• Analgesia with NSAIDs may be helpful
Serofibrinous or • Treatment is directed at the underlying disorder
Serosanguineous • Therapeutic thoracentesis unless small effusion only
Effusion • Rapid removal of :;,1 liter of pleural fluid may be associated with
re-expansion pulmonary edema
• If underlying problem is adequately treated, further drainage is
usually unnecessary
• Tube drainage is done for:
° Fluid re-accumulation leading to respiratory compromise
0 Older children with parapneumonic effusion, and the pleural
fluid pH is <7.20 or pleural fluid glucose level is <SO mg/dL
Antibiotics • Choice of antibiotic is based on in vitro sensitivities
of the responsible organism
• Clinical response is slow even with antibiotics (may
have little improvement for as long as 2 weeks)
• For staphylococcal infections: treatment for 3-4 weeks
Chest Tube • Controlled by underwater seal and continuous suction
Empyema or Drainage • Usually continued for 5-7 days
Purulent Effusion • Fibrinolytic agents are instilled to promote
drainage, decrease fever, lessen need for surgical
intervention, and shorten hospitalization
Surgery • If patient remains febrile and dyspneic >72 hours
after systemic antibiotics and chest tube drainage,
surgical decortication via VATS
• lfVATSis ineffective, open decortication is performed
Source:KliegmanR,et al. Nelsontextbookof pediatrics
(21sted.).Canada:Elsevier
CashenK, et al. Pleuraleffusions
andpneumothoraces. PediatricsinReview;
2017
328
PNEUMOTHORAX
I. ETIOPATHOGENESIS
• Accumulation of extra pulmonary air in the intrapleural space
• Most commonly due to leakage of air within the lung
A. Primary versus Secondary Pneumothorax
0 Primary pneumothorax: occurs without trauma or underlying lung disease
0 Seconda1y pneumothorax: complication of an underlying lung disorder but without trauma
II. MANIFESTATIONS
• Onset is usually abrupt
Symptoms • Severity of symptoms depend on extent of lung collapse & pre-existing lung disease
• Dyspnea, pain, cyanosis
• Respiratory distress with retractions, decreased breath sounds, tympanitic
I
on percussion on the involved side
Signs • Larynx, trachea, and heart shift toward the unaffected side
• Gurgling sounds synchronous with respiration suggests an open fistula
(when fluid is present in the pleural cavity)
III. DIAGNOSIS
DIAGNOSTIC REMARKS
• Shows less lung collapse if taken early
• Expiratory view accentuates the contrast between lung markings and the
Chest
clear area of the pneumothorax
Radiograph
• Evidence of tension pneumothorax if with shift of mediastinal structures
away from the air leak
Ultrasound • Chest ultrasound may be used to establish the diagnosis
IV. MANAGEMENT
ASPECT MANAGEMENT
• 100% oxygen may hasten resolution
Supportive
• Analgesic if with pleural pain
330
IMMUNOLOGY
AND
ALLERGY
SECTION ONE
ALLERGOLOGY
OVERVIEW OF ALLERGY
I. ETIOPATHOGENESIS& MANIFESTATIONS
• Chronic condition involving an abnormal reaction to an allergen
• Allergic patients have altered state of reactivity to environmental and food antigens
Response to allergen exposure: expansion ofT helper type 2 (Th2) cells, which then
favors IgE synthesis & eosinophilia
A portion of the immune response induces proliferation ofThl cells which leads to
chronicity and the effector phase
• Strong familial predisposition with about 60% heritability (risk for allergic disease of a
child is 30-50% if 1 parent is allergic and 60-80% if both parents are allergic)
333
Ill. MANAGEMENT
A. General Management
0 Avoidance of allergens (most common indoor allergens include house dust mites, cat,
cockroach)
Pharmacologic therapy (discussed in detail per disease entity)
B. Allergen lmmunotherapy
INDICATIONS* CONTRAINDICATIONS
• Allergic rhinitis • Patients under beta-blocker therapy
• Asthma triggered by allergen exposures • Severe or uncontrolled asthma
• Insect venom sensitivity • Significant cardiovascular disease
• Atopic dermatitis with aeroallergen • Patients poorly compliant or unable to
sensitization communicate clearly with physicians
'Notrecommended for<5yearsoldbecause ofincreased
riskofsystemic reactions,
specialexpertiserequired
to
treatanaphylaxis
in thisagegroup,inabilityto communicateclearlyintheeventof allergicreaction
Source:KliegmanRM,et al. NelsonTextbookof Pediatrics(21sted). Elsevier;2020
LeungDYM.et al. Pediatricallergyprinciplesandpractice.Elsevier;2015'Cox L. et al. J AllergyClin lmmunol.2011
--
A. Classification
INTERMITTENT PERSISTENT
MILD MODERATE-TO-SEVERE
(ALL OF THE FOLLOWING) (AT LEAST 1)
• Normal sleep • Abnormal sleep
• Normal daily activities • lmpain11ent of daily activities, sport & leisure
• Normal work and school • Impaired work or school
• No troublesome symptoms • Troublesome symptoms
Source:KliegmanRM.et al. NelsonTextbookof Pediatrics(21sted). Elsevier:2020
BousquetJ. et al. AllergicRhinitisandits ImpactonAsthma(ARIA)2008update.Allergy:2008
II. MANIFESTATIONS
• Sneezing, rhinorrhea, nasal obstruction
Symptoms • Itching of the nose, palate, pharynx & ears
• Itching, redness & tearing of the eyes
• Allergic salute: upward rubbing of nose to relieve itching and blockage
• Transverse nasal crease
Signs • Allergic gape: continuous open-mouth breathing
• Chapped lips, dental malocclusion
• Allergic shiners: dark circles under eyes
334
III. DIAGNOSIS
DIAGNOSTIC REMARKS
• To avoid false-negative results, montelukast should be withheld
Skin tests for 1 day, sedating antihistamines for 3-4 days, and non-sedating
antihistamines for 5-7 days
• Provide a suitable alternative to skin tests in the following conditions:
0 Dermatographism or extensive dermatitis
Serum IgE 0 Intake of medications that interfere with mast cell degranulation
0 High risk for anaphylaxis
0 Uncooperative patients
IV. MANAGEMENT
A. Pharmacologic Therapy
CLASS REMARKS
• Oral or intranasal antihistamine or intranasal glucocorticoids
Mild
• May add leukotriene receptor antagonists (LTRA)if with asthma
Intermittent
• May add decongestant
• Intranasal glucocorticosteroids
Moderate- • May add oral or intranasal antihistamine (2"' generation preferred
over 1st generation oral antihistamine)
SevereOR
Persistent AR • May add LTRAinstead of antihistamine if with concomitant asthma
• Intranasal chromones
• Add intraocular antihistamine/chromones for ocular symptoms
I
• Desloratadine
Gen • Levocetirizine antihistamines due to less sedation
• Fexofenadine
• Oral decongestant
• Cetirizine +
• Not favored for use due to irritability,
pseudoephedrine
insomnia, link with infant mortality
• Chlorpheniramine
Decongestants maleate + • Oral decongestant
phenylephrine HCl
• Intranasal decongestant
• Should not be used >3 days and not
• Oxymetazoline
to be repeated> lx per month to
avoid rebound nasal congestion
335
C. Monitoring for Persistent Rhinitis (review after 2-4 weeks)
0 If improved: continue treatment for 1 month
Failure of treatment:
Review diagnosis, review compliance, query infections or other causes
Increase intranasal steroid dose
0 Add antihistamine if with itch/sneeze
Add ipratropium bromide if with rhinorrhea
Add intranasal decongestant if with blockage (not for use in infants & preschool children)
Give short-term oral steroids if with severe nasal or ocular symptoms
0 If persistent failure despite above regimen: surgical referral
D.Others
Avoidance of allergens
0 Immunotherapy if symptoms cannot be adequately controlled by avoidance & medication
II. MANIFESTATIONS
• Severely dry skin is a hallmark of AD
• Cardinal features: intense pruritus especially at night and cutaneous reactivity
• Based on chronicity of AD:
Acute: pruritic, erythematous papules
0 Subacute: erythematous, excoriated, scaling pa pules
° Chronic: lichenification and fibrotic papules
• Patients often goes into remission as they grow olde1; leaving adolescents and adults with
skin prone to itching and inflammation when exposed to exogenous irritants
III. DIAGNOSIS
A. Classification Based on Severity of Disease
336
B. Diagnostic Criteria (Hanifin and Rajka)
MAJOR FEATURES MINOR FEATURES
(AT LEAST 3) (AT LEAST 3)
• Xerosis
• lchthyosis/palmar hyperlinearity /keratosis pilaris
• Immediate skin reactivity (type I skin test reactivity)
• Elevated serum lgE
• Early age of onset
• Tendency toward cutaneous infections/impaired
• Pruritus cell-mediated immunity
• Typical morphology and • Tendency toward non-specific hand or foot dermatitis
distribution: • Nipple eczema
° Flexural lichenification or • Cheilitis
linearity in adults • Recurrent conjunctivitis
• Dennie-Morgan infraorbital fold
° Facial & extensor involvement
• Keratoconus
in infants & children • Anterior subcapsular cataracts
• Chronic or chronically- • Orbital darkening
relapsing dermatitis • Facial pallor /facial erythema
• Personal or family history of • Pityriasis alba
atopy • Anterior neck folds
• Itch when sweating
• Intolerance to wool and lipid solvents
• Perifollicular accentuation
• Food intolerance
• Course influenced by environmentaljemotional factors
• White dermographism/delayed blanch
I
cosmetics
• Prolonged or repetitive contact
with physical, chemical or
• Removal of stimulus
Irritant contact mechanical irritants
• Topical corticosteroids
dermatitis • Examples: saliva, urine, feces,
fragrance, detergents, dyes,
caterpillars, chafing
• Infants:
• Chronic inflammatory disease 0 Emollients, baby oil, gentle
that parallels the distribution shampoo, soft brush to
and activity of sebaceous glands remove scales
• Unknown cause, ° For persistent lesions:
Ma/assezia fwfur implicated as topical corticosteroids,
Seborrheic
causative agent topical antifungal,
dermatitis
• Greasy, scaly, erythematous antifungal shampoo
papular dermatitis involving
scalp (cradle cap), face, neck, • Children and adolescents:
retroauricular areas, axillae, 0Antifungal shampoo
umbilicus, diaper area (first-line)
0Topical corticosteroids
Skin infections • Includes scabies, dermatophytosis {see infectious disease chapter]
Source:KliegmanRM,et al. NelsonTextbookof Pediatrics(21sted).Elsevier;2020
LeungDYM,et al. Pediatricallergyprinciplesandpractice.Elsevier;2015
HanifinJM,et al. 1980;Schneideret al. 2013
337
IV. MANAGEMENT
A. Overview of Management
ASPECT IN
REMARKS
MANAGEMENT
• First-line therapy
• Lukewarm soaking baths for 15-20 minutes followed
Moisturizers immediately by application of moisturizer
• Hydration promotes trans-epidermal penetration of topical
glucocorticoids
• Cornerstone of anti-inflammatory treatment
• Applied 1-2 times daily
• Includes: hydrocortisone, fluocinolone, betamethasone,
mometasone
• Proactive therapy: intermittent topical steroid therapy (1-2
times per week) may be administered as maintenance therapy
Topical on areas that commonly flare/relapse after control of AD is
corticosteroids achieved
• Monitor for cutaneous side effects (striae, skin atrophy)
• Commonly used method for selection of steroids:
0 Low potency (Group 6 and 7) steroids may be used for face,
axilla and genitals
0 Mid-potency (Group 4 and 5) may be used for the trunk and
extremities
• Topical calcineurin inhibitors (pimecrolimus, tacrolimus)
• Tar preparations
• Antihistamine
• Phototherapy
Others
• Systemic immunomodulatory agents in severe, refractory cases:
systemic steroids, cyclosporine, azathioprine, methotrexate,
mycophenolate mofetil, interferon gamma
• Antimicrobial therapy for secondary bacterial or viral infection
Source:KliegmanRM,et al. NelsonTextbookof Pediatrics(21sted). Elsevier;2020
Guidelines of careforthemanagement of atopicdermatitis;
2014
338
C. Classification of Commonly Used Topical Corticosteroids
0 Other countries adopt different classification method, the one presented here is the
one commonly used in our setting
GROUP ADD ON THERAPY
• Clobetasol propionate 0.05% ointment/cream
Group 1
• Betamethasone di propionate 0.05% ointment/lotion/gel
(most potent)
• Fluocinonide 0.1 % cream
• Mometasone furoate 0.1 % ointment
• Halcinonide 0.1 % cream
Group 2 • Fluocinonide 0.05% ointment/cream
• Desoximetasone 0.25% ointment/cream
• Betamethasone dipropionate 0.05% cream
• Fluticasone propionate 0.005% ointment
Group 3 • Halcinonide 0.1% ointment
• Betamethasone valerate 0.1% ointment
• Mometasone furoate 0.1 % cream
Group4 • Triamcinolone acetonide 0.1% ointment/cream
• Fluocinolone acetonide 0.025% ointment
• Fluocinolone acetonide 0.025% cream
Group 5
• Hydrocortisone valerate 0.2% ointment
• Desonide 05% ointment/cream/lotion
Group 6
• Alclometasone dipropionate 0.05% ointment/cream
Group 7
• Hydrocortisone 2.5%, 1%, 0.5% ointment/cream/lotion
(least potent)
FOOD ALLERGY
I. DEFINITION OF TERMS
• Food hypersensitivity: adverse immunologic response due to lgE-mediated or cell-
mediated mechanisms
0 lgE-mediated responses are more common, with rapid onset of symptoms
° Cell-mediated or non lgE-mediated food allergy is less common, with later onset of
symptoms
• Food intolerance: adverse physiologic responses based on functional properties of food
I
II. ETIOPATHOGENESIS
A. Etiology
Egg, milk, peanuts, fish soy, wheat account for 90% of food allergies during childhood
Virtually all milk allergies develop by 12 months of age, all egg allergies by 18
months of age
0 Most children "outgrow" milk and egg allergies, with about 50% doing so by school age.
0 About 80-90% of children with peanut, nut, or seafood allergy retain their allergy for life
0 Delayed introduction of these foods increases risk of allergy
339
III. MANIFESTATIONS
SYSTEM MANIFESTATIONS
Source:Kliegman
RM.et al. NelsonTextbookof Pediatrics(21sted). Elsevier;2020
Kananiet al. 2011,Kaplan2008
IV. DIAGNOSIS
DIAGNOSTIC REMARKS
V. MANAGEMENT
• Elimination of food with periodic reevaluation (since most food allergies are outgrown)
• Self-injectable epinephrine in case of accidental ingestion
340
URTICARIA (HIVES) AND ANGIOEDEMA
I. DEFINITION OF TERMS
URTICARIA ANGIOEDEMA
• Transient, pruritic, erythematous, raised
• Edema involving deeper subcutaneous
wheals with flat tops and edema that may
tissues (eyelids, lips, tongue, genitals,
become tense and painful
dorsum of hands or feet, GI tract wall)
• Blanches with pressure
• Sometimes painful rather than pruritic
• Resolves without residual lesions
• Resolves without residual lesions
• Usually last 20 minutes to 3 hours, rarely
• Slower resolution (up to 3 days)
more than 24 hours
II. CLASSIFICATION
ACUTE URTICARIA/ CHRONIC URTICARIA/
ANGIOEDEMA ANGIOEDEMA
Duration • ,;6 weeks • >6 weeks
• Often caused by IgE-mediated
reaction, but may also be from
• Autoimmune, neoplastic,
non-IgE mediated stimulation of
physical* urticaria
mast cells
Etiology • Chronic spontaneous urticaria
• Most commonly from food,
(idiopathic) in approximately
drugs, insect stings, infection,
80%
transfusion, contact allergy
• Idiopathic in approximately 50%
• Primary clinical
• Primary clinical • CBC, ESR, antinuclear antibodies
Diagnosis • Skin prick tests (ANA), thyroid autoantibody
• Serum-specific IgE tests testing, liver function tests,
autologous serum skin tests (ASST)
• Avoidance of trigger
• Avoidance of trigger
• Non-sedating Hl antihistamine:
• Non-sedating Hl antihistamine:
mainstay of therapy
• If inadequate control after
2-4 weeks or symptoms
I
Management mainstay of therapy are intolerable, increase
• If severe: epinephrine IM, oral antihistamine dose up to 4x
corticosteroids • If still with inadequate control,
add omalizumab
• If still with inadequate control,
add cyclosporine
'Examples of physicalurticaria:dermatographism(abilityto writeon skin),cold urticaria(coldstimulus),heat contact
urtcaria(warmstimulus),cholinergicurticaria(exercise,hot showers,sweating,strong emotion),delayed pressure
urticaria(tightclothing,sitting),solar urticaria(sun exposure),aquagenicurticaria(waler),vibratoryurticaria
(vibrations)
341
ADVERSE REACTIONS TO DRUGS
I. ETIOPATHOGENESIS
A. Types of Drug Reactions
II. MANIFESTATIONS
• Most common form of adverse drug reaction: cutaneous
• Most commonly implicated drugs: ampicillin, amoxicillin, penicillin, trimethoprim-
sulfamethoxazole
Ill. ALLERGICREACTIONS
• Risk Factors: prior exposure, previous reactions, age (20-49 years), route of
administration (parenteral or topical), dose (high), dosing schedule (intermittent),
genetic predisposition (slow acetylators)
• Diagnosis: skin test (most rapid and sensitive method)
• Management: desensitization for drugs in whom an alternative drug is not appropriate
342
III NON I : E MEDIATED DRUG ERUPTIONS
CAUSATIVE MANAGEMENT
MANIFESTATIONS
AGENTS
1) Stevens-Johnson Syndrome (SJS)
• Discontinue offending drug
• Supportive treatment:
• Erythematous macules 0 Ophthalmic topical steroids
rapidly developing central 0 Mouthwashes and glycerin
necrosis to form vesicles,
swabs
subepidermal bullae and • Sulfonamides, 0 Topical anesthetics
areas of denudation anticonvulsants, some
o Antibiotic therapy for
• Involvement of 2 or more NSAIDs,allopurinol
secondary bacterial infection
mucosa! surfaces (eyes, • Also associated with
0 IV fluids
oral cavity, upper airway, M. pneumoniae
0 Nutritional support
esophagus, GI tract, infection
0 Sheepskin or air-fluid bedding
anogenital mucosa)
0 Daily saline or Burrow
• Affects <10% of body
solution compresses
surface area
0 Paraffin gauze or colloidal gel
dressing of denuded areas
2) Toxic Epidermal Necrolysis (TEN)
• Management similar to that of
severe burns
• Similar to SJS, but >30% • Narcotics
• Same as SJS
epidermal detachment • Still controversial but
with success: systemic
glucocorticosteroids, !Vig
3) Drug Hypersensitivity Syndrome (DHS) or
Drug Rash with Eosinophilia & Systemic Symptoms (DRESS) Syndrome
• Severe exanthematous rash
(could become edematous, • Anticonvulsants,
pustular, purpuric), sulfonamides,
• Withdrawal of offending drug
I
exfoliative dermatitis minocycline,
• Systemic steroids
• Mucosa! lesions are allopurinol
• Supportive care
infrequent • Also associated with
• Feve1; facial edema, HHV6 reactivation
eosinophilia, generalized
lymphadenopathy
4) Erythema Multiforme (EM)
• Classic lesion: doughnut-
shaped, target-like (iris or
• Supportive care
bull's eye) pa pules with • Most common
• Topical emollients, systemic
e1ythematous outer borde1; implicated etiology:
antihistamines, NSAIDs for
inner pale ring. dusky purple HSV infection
symptomatic relief
to necrotic center • Drug-related EM is
• Opioids for severe mucosa\
• Exhibits less necrosis less common ( <10%),
disease
compared to SJS/TEN associated with
• Prophylactic oral acyclovir
• Most commonly affecting NSAIDs, paracetamol,
to control recurrent HSV-
extensor upper extremities sulfonamides,
associa tee! EM
• Oral lesions may occu1; but antibiotics
other mucosa! surfaces are
spared
343
ANAPHYLAXIS
I. ETIOPATHOGENESIS
• Serious, life-threatening systemic hypersensitivity reaction
• Triggers:
• Food (most common trigger in children)
0 Stinging insects
• Medications (most commonly antibiotics, NSAIDs,neuromuscular blocking agents)
• Diagnostic agents (radiocontrast media, fluorescein)
• Occupational allergens (bee venom, latex)
• Infants: due to inability to describe symptoms
Age-related factor • Adolescents and youn1J/dults: increased risk-taking behaviors
• Labor and delivery: ris from medications
• Elderly: increased risk of fatality
• Asthma
Concomitant • Allergic rhinitis
diseases • Atopic dermatitis
• Others: cardiovascular /respiratory /psychiatric diseases, mastocytosis
• Exercise, emotional stress
Co-factors • Acute infection
• Disruption of routine
• Premenstrual status
II MANIFESTATIONS
General • Sensation of warmth, weakness, apprehension (sense of doom)
• Generalized urticaria or angioedema
Skin or mucosa!
• Oral, periocular, or cutaneous pruritus
tissue involvement
• Flushing, swollen lips/tongue/uvula
• Dyspnea, wheeze, stridor
Respiratory
• Reduced peak PEF
compromise
• Hypoxemia
Symptoms of end- • Hypotonia/collapse, hypotension
organ dysfunction • Syncope, incontinence
Gastrointestinal • Crampy abdominal pain
symptoms • Nausea and vomiting
CNSsymptoms • Headache, altered mental status, dizziness, confusion
344
IV. DIAGNOSIS
IV. MANAGEMENT
A. Pharmacologic Management
• First-line drug (the only medication that reduces hospitalization
and death)
• Dose: 0.01 mg/kg of a 1:1000 solution (max dose is 0.5 mg for
Epinephrine
adults and 0.3 mg for children <40 kg)
• Route: Intramuscular injection in mid-anterolateral thigh
• May be repeated every 5-15 minutes if necessary
• Diphenhydramine 1 mg/kg IV,max SO mg
Hi-antihistamine
• Chlorpheniramine 2.5-5 mg
• Ranitidine 1 mg/kg IV,max SO mg
HZ-antihistamine
• To decrease flushing, headache
• Potentially relieve protracted anaphylaxis symptoms and
prevent biphasic anaphylaxis
Corticosteroids
• Methylprednisolone 1 mg/kg IV,max SO mg
• Prednisone 1 mg/kg PO, max 75 mg
Beta 2-agonist • Salbutamol nebulization pm for bronchospasm
Source:SimonsFER,et al. WAOguidelines
forassessmentandmanagement of anaphylaxis.WAOJournal; 2011
KliegmanRM,et al. NelsonTextbook
of Pediatrics(21sted).Philadelphia:
2020
B. Non-Pharmacologic Management
Remove exposure to the trigger if possible
Place patient in supine position with elevated lower extremities if hypotensive
Establish IV access and give 20 cc/kg bolus of isotonic fluids (normal saline or lactated
0
Ringer) ifhypotensive
Oxygen support via face mask if with respiratory distress or shock
1=
Monitor patient frequently and provide a written plan for emergency management of
allergic symptoms
Patient education on avoidance of triggers, recognition of early signs of anaphylaxis,
early treatment of allergic symptoms to avoid anaphylaxis
Source:KliegmanRM,et al. NelsonTextbookof Pediatrics(21sted).Elsevier:2020
TschudyMM.et al. TheHarrietLanehandbook:Philadelphia: 2012
Chameides L. et al.AHA:2012
SimonsFER.et al. WAOguidelinesfor assessmentandmanagement of anaphylaxis.WAOJournal:2011
345
SECTION TWO
IMMUNOLOGY
IMMUNODEFICIENCY
I. EVALUATION OF SUSPECTED IMMUNODEFICIENCY
• Most cost-effective screening test: CBC, manual differential count, ESR
Warning signs for primary immunodeficiency disorders:
;,4 new ear infections within 1 year
;,2 serious sinus infections within 1 year
;,2 months on antibiotics with little effect
;,2 pneumonias within 1 year
Failure of an infant to gain weight or grow normally
Recurrent, deep skin or organ abscesses
0 Persistent thrush in mouth or skin fungal infection
0 Need for intravenous antibiotics to clear infections
0 ;,2 deep-seated infections including septicemia
Family history of primary immunodeficiency disorder
• After maternal
• Early onset (2-6
Onset antibodies diminish • Early onset • Any age
months)
(5-7 months)
• Fungal, viral, • Haemophilus,
• Staphylococcus, • Neisseria,
protozoa!, Streptococcus,
Pathogens Serratia, Haemophilus,
mycobacterial Pneumococcus,
Aspergillus Coccobacilli
(opportunistic) Enterococcus
• Extensive • Autoimmune
• Autoimmunity
mucocutaneous disorders
• Lymphoreticular • Prolonged
candidiasis • Meningitis,
malignancy attachment of
• Failure to thrive arthritis,
Features (lymphoma, umbilical cord
• Protracted diarrhea septicemia,
thymoma) • Poor wound
• Post-vaccination recurrent
• Post-vaccination healing
disseminated BCG sinopulmonary
paralytic polio
or varicella infections
Common variable
• Later age of onset of infections • !Vig administration
immunodeficiency
• Infections are less severe • Judicious antibiotic use
(CVID)
• Respiratory, GI, urogenital tract • !Vig is not indicated because
Selective IgA infections lgG production is normal in
deficiency • Infusions with blood products >99%, !Vig administration
containing lgA may cause anaphylaxis may result in anaphylaxis
3) Combined T-Cel/ and B-Cel/ Defect
• X-linked recessive • Bone marrow or cord blood
• Immunodeficiency with transplantation
Wiskott-Aldrich
thrombocytopenia and eczema • Supportive care (nutrition,
syndrome
• Bloody stools, prolonged bleeding !Vig, killed vaccines, platelet
from circumcision, atopic dermatitis transfusion, splenectomy)
Chediak-Higashi
• Delayed umbilical cord detachment,
leukocytosis, recurrent infection
• Oculocutaneous albinism,
progressive peripheral neuropathy,
increased susceptibility to infections,
• Stem cell transplantation
5) Complement Deficiencies
• Usually asymptomatic but with risk
CZ Deficiency
of septicemia
348
RH
EUMATO
LOGY
SECTION ONE
APPROACH TO RHEUMATOLOGIC DISEASES
I. SYMPTOMSSUGGESTIVEOF RHEUMATICDISEASES
• Joint pains, feve1; fatigue, rash
• Joint pains without physical findings of arthritis may indicate other clinical conditions
such as fibromyalgia, growing pains, and benign hypermobility syndrome
351
APPROACH TO PATIENTS WITH MUSCULOSKELETAL PAIN/SWELLING
I. REMINDERS IN EVALUATINGMUSCULOSKELETALPAIN/ SWELLING
Observe patient from front to back and sides
Observe patient walking on his or her heels and on tiptoes
Observe the hands showing straight in front of you
Observe patient pinch index finger and thumb finger together
Ask patient to touch tips of the fingers
Ask patient to put hands together palm to palm and back to back
Observe while patient is asked to reach up while hands are raised
Ask patient to put hands behind his or her neck
Ask patient to try and touch his shoulder with his ear
Ask patient to open his mouth wide and put three fingers in the mouth
Palpate the knee
Ask patient to extend and flex the knee
Perform passive movement of hip
Ask patient to bend forward and touch his or her toes
Acute Chronic
(< 6 weeks) (> 6 weeks)
Signs of Inflammation?
M.'.JnoarticularArthritis PolyartlcularArthritis
352
SECTION TWO
DISORDERS IN RHEUMATOLOGY
B. Pathogenesis:
0 Two events are considered necessary for it to occur:
0 lmmunogenetic susceptibility
0 An external environmental trigger (e.g.,rubella, parvovirus, Epstein-Barr virus, antibiotics)
0 HLA types found with increased frequency in affected children
0 HLA-DR4: polyarticular disease
0 HLA-DR8 & -DRS: pauciarticular disease
II. MANIFESTATIONS
MANIFESTATIONS DESCRIPTION
• lntraarticular swelling or the presence of at least 2 of the
following:
Arthritis, morning 0 Limited range of motion
stiffness
0 Tenderness or pain on motion
0 Warmth
• Joints of the lower extremities are commonly affected, associated
Pauciarticuiar
with chronic uveitis
• Involvement of both large & small joints, more severe if extensors
I
Polyarthritis
of elbows and Achilles tendon are involved
• Quotidian fever with daily temperature spikes of 39°C for
Systemic-onset 2 weeks, faint red macular rash over the trunk & proximal
extremities, visceral involvement
III. DIAGNOSIS
A. Diagnostic Criteria
0 Age of onset <16 years
Arthritis in "1 joint
Duration of disease ;;,6 weeks
0 Onset type defined by type of disease in first 6 months:
Polyarthritis: ;;,5 inflamed joints
0 Pauciarticular /oligoarthritis: <5 inflamed joints (usually knees & ankles)
0 Systemic arthritis with characteristic fever
0 Exclusion of other forms of juvenile arthritis
353
B. Classifications of Childhood Chronic Arthritis
ACR CLASSIFICATION ILAR CLASSIFICATION
PARAMETER
(1977) (1997)
• Juvenile rheumatoid • Juvenile idiopathic
Terminology
arthritis arthritis
Minimum duration • 2e6weeks • 2e6weeks
Age at onset • <16 years • <16 years
• Oligoarthritis
• Persistent: s4 joints for
s4 joints in 1st 6 months
• Pauciarticular course of disease
after presentation
• Extended: >4 joints
after 6 months
• Polyarticular Rheumatoid
>4 joints in 1st 6 months Factor (RF) negative
• Polyarticular
after presentation
• Polya1ticular RF positive
Presence of fever, rash,
• Systemic )RA • Systemic )IA
arthritis
• Psoriatic arthritis
Other categories
• Exclusion of other forms • Enthesitis-related a1thritis
included
• Undifferentiated
Inclusion ofpsoriatic
arthritis, inflammatory
• No • Yes
bowel disease,
ankylosing spondylitis
·ACR:AmericanCollegeof Rheumatology(ACR)
·1LR:InternationalLeagueofAssociationsfor Rheumatology(ILAR)
C. Diagnostics
DIAGNOSTIC FINDINGS/REMARKS
Markers of • Increased ESR & CRP
inflammation • Leukocytosis, thrombocytosis, anemia of chronic disease
Antinuclear antibodies
• Positive in 40-85% with pauci- and polyarticular JRA
(ANA}
• Associated with onset of the disease in an older child
Rheumatoid factor with polyarticular type
• Portends a poor prognosis
• Soft tissue swelling, osteoporosis, periostitis, narrowed
X-ray/MRI
cartilage space
IV. MANAGEMENT
• Depends on subtype, severity, specific manifestations of the illness, and response to therapy
• Mild to moderate disease (non-disabling symptoms): NSAIDs
• Moderate to severe disease (disabling symptoms): immunosuppressive agents and
disease-modifying anti rheumatic agents such as steroids, anakinra, cankinumab,
tocilizumab, and methotrexate
• Physical and occupational therapy
354
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
I. ETIOPATHOGENESIS
• Autoantibody production against self-antigens resulting in inflammatory damage to organs
• Incidence of31 per 100,000 Asian children with female predominance
• Median age of diagnosis: 11-12 years old
• Fibrinoid deposits found in blood vessel walls of affected organs, skin, joints, kidneys,
blood-forming cells, blood vessels, and CNS
1) Clinical Criteria
Discoid rash
• Erythematosus raised
patches with adherent
keratotic scaling and
follicular plugging
• Atrophic scarring may
Chronic
cutaneous
lupus
OR
lupus, lupus panniculitis
(profundus ), mucosa!
lupus, lupus erythematosus
tumidus, chilblains lupus
I
occur in older lesions • Discoid lupus/lichen planus
overlap
355
ACR CRITERIA FOR SLE SLICC CRITERIA FOR SLE
CRITERION DEFINITION CRITERION DEFINITION
• Pleuritis: history • Typical pleurisy for more
of pleuritic pain or than one day, pleural
rubbing heard by a effusions, or pleural rub
clinician or evidence of
OR
pleural effusion • Pericardial pain (pain with
Serositis Serositis
OR recumbency improved
• Pericarditis: by sitting forward) for> 1
documented by ECG, day, pericardial effusion,
rub, or evidence of pericardia I rub, or
pericardia! effusion pericarditis by ECG
• Seizures, psychosis,
• Seizures OR psychosis
mononeuritis multiplex,
in the absence of
Neurologic myelitis, peripheral or
offending drugs or Neurologic
disorder cranial neuropathy, OR
known metabolic
acute confusional state (in
derangements
absence of other causes)
OR
• Thrombocytopenia
• Thrombocytopenia Thrombocytopenia
<100,000/nun' at least once
<100,000/mm'
2) Immunologic Criteria
• Abnormal titer, in
the absence of drugs
ANA ANA • Abnormal titer
associated with "drug-
induced lupus"
Anti-dsDNA
• Anti-DNA • Abnormal titer
Anti-Sm
OR
• Anti-Sm • Positive lupus anticoagulant,
false-positive test result
Immunologic OR
for rapid plasma reagin,
disorders • Positive Antiphospholipid
abnormal serum level of
antiphospholipid
anticardiolipin antibody or
antibody (Ab)
anti-beta 2-glycoprotein I
(anticardiolipin
lgG or lgM, lupus Low • Low C3, low C4 OR low
anticoagulant, or false- complement CH50
positive serologic test
for syphilis) • Positive test in the absence
Direct Coombs'
of hemolytic anemia
SLICC:SystemicLupusInternational
Collaborating
Clinics ANA:antinuclear
antibodies
Anti-Sm:
anti-Smith
antibody Anti-dsDNA:
anti-double-stranded
DNA
356
II MNEMONIC FOR REMEMBERING MANIFESTATIONS OF SLE· SOAP BRAIN MD
P hotosensitivity I mmunologic
N eurologic manifestations
Source:HochbergMC.ACRrevisedcriteriafor SLE;ArthritisRheum1997
PetriM, et al. SLICCclassificationcriteriafor SLE.ArthritisRheum:2012
TanEM,et al. 1982revisedcriteriafor the classification
of SLE.ArthritisRheum1982
Ill. MANAGEMENT
• Depends on the affected target organs & disease severity
• Serologic markers are used as guide
• Most important management tool: meticulous and frequent re-evaluation
CRITERION DEFINITION DEFINITION
• Patients who do not • NSAIDs
Mild disease have renal or other life- • Hydroxycholoroquine *
threatening involvement • Low dose glucocorticoids**
IV. PROGNOSIS
• With progress in diagnosis and treatment, 5-year survival rate is >90%
• Mortality from infection, complications of glomerulonephritis, central nervous sytem
disease, pulmonary hemorrhage, myocardial infarction
Source:Bader-Meunier B, et al. J Pediatr:2005
HirakiLT,et al. J Pediatr:2008:PinelesD. et al. Lupus;2011 I
REACTIVE AND POST-INFECTIOUS ARTHRITIS
I. ETIOPATHOGENESIS
• Sterile inflammatory reaction in the joints following a recent infection
• Caused by generation and deposition of immune complexes and antibodies or T-cell
mediated cross-reactivity
TERM DEFINITION
• Occurs following enteropathic or urogenital infection (e.g.,
Reactive arthritis Salmonella, Shigella, Yersinia enterocolitica, Campylobacter
jejuni, Chlamydia trachomatis, E.coli, Clostridium difficile)
357
II. MANIFESTATIONS
• Symptoms begin 2-4 weeks following infection
• Triad of arthritis, urethritis, and conjunctivitis relatively uncommon in children
Usually oligoarticular, with predilection to the lower extremities
• Dactylitis and enthesitis is common
• Cutaneous manifestations: circinate balanitis, ulcerative vulvitis, oral lesions, erythema
nodosum, keratoderma blennorhagicum
Systemic symptoms: feve1; malaise, fatigue
• Patterns based on etiology
0 Rubella and hepatitis B affect small joints
0 Mumps and varicella affect large joints like the knee
III. DIAGNOSIS
• No specific diagnostic test
CBC,acute phase reactants, metabolic panel and urinalysis to exclude other etiologies
• Imaging findings usually non-specific or normal
Important to rule out other causes of arthritis such as septic arthritis
IV. MANAGEMENT
• Specific treatment is unnecessary for most cases
NSAIDs for pain and functional limitation
• Intra-articular steroid for refractory or severely involved joints [rule out acute infection first)
V. PROGNOSIS
Usually resolves without complications
• Reactive arthritis with C. trachomatis has potential to develop into chronic arthritis
[spondyloarthritis)
Source:KliegmanR, el al. NelsonTextbookof Pediatrics(21sted.).Philadelphia:Elsevier:2020
JUVENILE DERMATOMYOSITIS
I. ETIOPATHOGENESIS
• Most common inflammatory myositis in children
• Defined by proximal muscle weakness and characteristic rash
• Etiology is multifactorial
• HLA88, DRBl *0301, DQAl*0501 and DQAl*0301 are associated with increased susceptibility
• Pathology: inflammatory cell infiltrates result in vascular inflammation
II. MANIFESTATIONS
• Initial presentation is either rash, insidious onset of weakness, or both.
• Lipodystrophy and calcinosis associated with long-standing or untreated disease
RASHES MUSCLE WEAKNESS
• Extreme photosensitivity to ultraviolet
light (shawl sign)
• Erythema over knees and elbows
• Typically symmetric
• Heliotrope rash: blue-violet discoloration
• Proximal muscles are affected more
of eyelids
• Positive for Gower sign (use of hands on
• Facial erythema crossing nasolabial fold
thighs to stand from sitting position)
• Gottron pa pules: bright pink or pale, shiny,
• Esophageal and respiratory muscles may
thickened or atrophic plaques over the
be affected
proximal interphalangeal joints and distal
interphalangeal joints
• Periungual erythema and telangiectasia
358
III. DIAGNOSIS
AB oI1an an d Peter 1agnost1c Cnteria
Classic rash (heliotrope rash, Gottron papules) plus THREE of the following:
1. Weakness: symmetric, proximal
Aldolase
0
3. Electromyographic changes;
Short, small polyphasic motor unit potentials
0
° Fibrillations
Positive sharp waves
0
Insertional Irritability
0
4. Muscle biopsy
Necrosis
0
Inflammation
0
IV. MANAGEMENT
• Corticosteroids alter the course and lower mortality and morbidity
0Prednisone 2 mg/kg/day (max 60 mg daily)
0 High dose methylprednisolone for more severe cases
• Methotrexate is commonly used as a steroid-sparing agent
• Hydroxychloroquine
V. PROGNOSIS
• Around 1% mortality
• With more aggressive immunosuppressive therapy, period of active symptoms decreases
to <1.5 years
• Up to one third may need long term therapy to control symptoms
I
Source:KliegmanR, et al. Nelsontextbookof pediatrics(21sted.).Philadelphia:
Elsevier;2020
BohanA, el al. NewEnglandJournalOf Medicine;1975
359
VASCULITIS SYNDROMES
• The table below summarizes the common vasculitis syndromes encountered
• Kawasaki disease (a medium-vessel vasculitis) is discussed in Cardiology chapter
PATHOGENESIS MANIFESTATIONS DIAGNOSIS MANAGEMENT
1) Henoch Schonlein Purpura (HSP)
360
OTHER RHEUMATOLOGIC DISEASES
• Primary variable
vessel vasculitis -
involves any size
• Most frequent
initial symptom is
painful oral ulcer
• Genital ulcers
• Recurrent oral
ulceration PLUS 2
of the following:
Eye lesions
0
Skin lesions
0
• Topical sucralfate
or steroids for
ulcers
• Colchicine
for erythema
I
• Anterior uveitis
and type of vessel Positive pathergy
0 nodosum or
(blurred vision,
• Polygenic test (pustular arthritis
redness, pain and
autoinflammatory reaction 24-48 • Other modalities:
photophobia)
disorder hours after thalidomide,
• Skin lesions:
needle puncture sulfasalazine,
etythema nodosum,
or saline injection) anti tumor
papulopustular
necrosis factor,
acneiform lesions,
cyclophosphamide,
folliculitis, purpura
interferon
and ulcers
361
PATHOGENESIS MANIFESTATIONS DIAGNOSIS MANAGEMENT
4} Sjogren Syndrome
• Oral: recurrent
parotitis, dry
• Chronic mouth
inflammatory, • Ocular:
• Symptomatic
autoimmune disease xerophthalmia, • No established
treatment
• Progressive recurrent diagnostic criteria
• Artificial tears
lymphocytic conjunctivitis, as of the moment
• Oral lozenges
and plasma cell keratoconjunctivitis • Immunologic tests:
• Corticosteroids,
infiltration of the sicca • Anti-SSA
NSAlDs,
exocrine glands, • Other: recurrent • Anti-SSB
hydroxychloroquine,
especially salivary vaginitis • High titer ANA
methotrexate,
and lacrimal, with • Systemic: feve1; • RF
etanercept
potential for systemic non-inflammatory
manifestation arthralgia,
hypokalemic paralysis,
abdominal pain
REFERENCES
1. Kliegman, R., Stanton, B., St. Geme, J., Schor, N., & Behrman, R. (2016). Nelson textbook of pediatrics
(20th ed.). Canada: Elsevier.
2. Foster H, Kimura Y. Ensuring that all paediatricians and rheumatologists recognise significant
rheumatic diseases. Best Pract Res Clin Rheumatol. 2009 Oct:23(5):625-42.
3. Foster HE, Jandial S. pGALS-A Screening Examination of the Musculoskeletal System in School-Aged
Children. Reports on the Rheumatic Diseases (Series SJ, Hands On 15. Arthritis Research Campaign;
2008 June. Copyright© 2008 Arthritis Research Campaign.
4. Khubchandani, R., & D'Souza, S. (2002). Initial evaluation of a child with arthritis-An algorithmic
approach. The Indian Journal Of Pediatrics, 69(10), 875-880. doi: 10.1007 /bf02723712
5. Horton DB, Scott Fl, Haynes K, Putt ME, Rose CD, Lewis JD, Strom BL. Antibiotic Exposure and
juvenile idiopathic Arthritis: A Case-Control Study. Pediatrics. 2015 Aug;136(2):e333-43. Epub
2015 Jul 20.
6. Lehmann HW, Knoll A, Kuster RM, Modrow S. Lehmann HW, Knoll A, Keister RM, Modrow S. Arthritis
Rheum. 2003;48(6):1631.
7. Pritchard MH, Matthews N, Munro). Antibodies to influenza A in a cluster of children with juvenile
chronic arthritis. Br) Rheumatol. 1988;27(3):176.
8. Sullivan DB, Cassidy )T, Petty RE. Pathogenic implications of age of onset in juvenile rheumatoid
arthritis. Arthritis Rheum. 1975;18(3):251.
9. Bader-Meunier B, Armengaud )B, Haddad E, et al. Initial presentation of childhood-onset systemic
lupus erythematosus: a French multicenter study) Pediatr 2005; 146:648.
10.Hiraki LT, Benseler SM, Tyrrell PN, et al. Clinical and laboratory characteristics and long-term
outcome of pediatric systemic lupus erythematosus: a longitudinal study.) Pediatr 2008; 152:550
11.Hochberg MC. Updating the American College of Rheumatology revised criteria for the
classification of systemic lupus erythematosus (letter]. Arthritis Rheum 1997; 40:1725
12.Lupus. 2011 Oct;20(11):1187-92. Epub 2011 Jul 18. Pediatrics. 1989;83(2):235.
13.Petri M, Orbai AM, Alarcon GS, et al. Derivation and validation of the Systemic Lupus International
Collaborating Clinics classification criteria for systemic lupus erythematosus. Arthritis Rheum
2012; 64:2677.
14.Pineles D, Valente A, Warren B, Peterson MG, Lehman T), Moorthy LN. Worldwide incidence and
prevalence of pediatric onset systemic lupus erythematosus. Lupus. 2011 Oct;20(11):1187-92.
Epub 2011 Jul 18.
15.Tan EM, Cohen AS, Fries JF, et al. The 1982 revised criteria for the classification of systemic lupus
erythematosus. Arthritis Rheum 1982; 25:1271.
16.Bohan, A., & Peter, J. (1975). Polymyositis and Dermatomyositis. New England journal Of
Medicine, 292, 403-407.
362
CARDIOLOGY
QJ OVERVIEW OF THE CIRCULATORY SYSTEM
I. Fetal Circulation
II. Transition at Delivery
FETAL CIRCULATION
• Prior to delivery, the fetus depends on the placenta for gas/nutrient exchange
• The low vascular resistance of the placenta and the high vascular resistance of the fetal
lungs result in right-to-left shunts characteristic of the fetal circulation:
Foramen ovale: blood shunted from right atrium (RA) to left atrium (LA)
0 Ductus arteriosus: blood shunted from the pulmonary artery (PA) to the aorta
NormalFetalCirculation
Pulmon!ryartery\
/ Lungs
i
Rightjventricle Pulmon!ryveins DuctusAjrteriosus
Leftatrium
Ft°ramen
ovare teft ventricl!
Rightatrium Aorta
Inferiorv}na cava j
Ouctusvenosus
Umbilical
t
vein - Placenta- Umbilical
arteries
Flow of blood in the fetus. Blood is first oxygenatedin the placenta,then returnsto the fetus via the um-
bilicalvein. Somebloodgoes into the hepaticcirculation/liver (50%),while the rest bypassthe liver via the
ductusvenosusand entersthe inferiorvena cava (IVC)then the right atrium(RA). Fetalsuperiorvenacava
bloodalso drains into the RA. From the RA, most blood bypassesthe right ventricle(RV) via the foramen
ovaleto enter the LA, then the left ventricle(LV),then the aorta towardsthe fetal tissues(i.e., systemiccir-
culation). From the RA, some bloodmay enter the RV,then the pulmonarytrunk (PT). From the PT, some
blood may enter the lungs, but most would bypassthe lungs via the ductus arteriosus(DA), then to the
aorta & systemiccirculation. Deoxygenatedbloodgoes back to the placentavia the two umbilicalarteries.
I
II. FETAL CARDIAC OUTPUT
• The fetal heart is unable to increase stroke volume when the heart rate (HR) falls because
it has low compliance
• Thus, the fetal cardiac output (CO) depends on HR; when the HR drops, the result is a
serious fall in CO
365
III. STRUCTURES IMPORTANT TO MAINTAIN PARALLEL CIRCULATION
FORAMEN OVALE DUCTUS ARTERIOSUS
DUCTUS VENOSUS
(FO) (DA)
• Precardiac (venous) • Postcardiac (arterial)
Location • lntracardiac shunt
shunt shunt
• Between left • Between pulmonary
Anatomy • Between LA & RA
umbilical vein & IVC artery & aorta
• Pulmonary circuit is
• Blood from IVC
bypassed due to high
directly flows to LA
pulmonary vascular
due to valves in IVC
resistance (PVR)
• Bypasses portal • No mixing of
Physiology • Less oxygenated blood
circulation deoxygenated
in PA flows through the
blood from SVC
open DAto descending
• Most of SVCblood
aorta then to placenta for
goes to the RV
oxygenation
• Within 48 hours of birth
• During umbilical • During 1" breath, (10-15 hours in a normal
Functional cord clamping septum primum neonate)
closure • Removal of placenta is pressed against • Occurs by constriction of
results in its closure septum secundum medial smooth muscles in
the DA
• 15-20 days when • 1 yea1; when there
Anatomic • At 2-3 weeks when there
there is proliferation is fusion of 2
closure is intimal proliferation
of obliterating tissue apposed septa
Remnant • Ligamentum venosum • Fossa ovale • Ligamentum arteriosus
TRANSITION AT DELIVERY
• The neonate must rapidly make physiologic changes when the umbilical cord is clamped
at birth (transition from intrauterine to extra uterine life)
• Successful transition involves:
Alveolar fluid clearance
0 Lung expansion with the first effective breath
Increases in pulmonary perfusion and systemic pressure
° Closure of the right-to-left shunts of the fetal circulation
Non-Cardiac Etiology
APPROACH TO CYANOSIS
• Bluish purple discoloration of tissues due to an increased concentration
hemoglobin in the capillary bed
CENTRAL CYANOSIS
of deoxygenated
PERIPHERAL CYANOSIS
I
• Due to decreased 0 2 saturation
Mechanism • Due to diminution of blood flow
(<85%) or high deoxygenated Hgb
Area involved • Generalized (e.g., lips, conjunctiva) • Localized (e.g., distal extremities)
Response to
• No improvement • With improvement
warming
Clubbing • Usually present • Absent
Capillary refill • < 2 seconds • > 2 seconds
367
APPROACH TO COMMON PEDIATRIC CARDIAC MURMURS
• Murmurs are common in healthy children & most are not pathologic ("innocent murmurs")
• A murmur may also be the sole finding in children with structural heart disease
I. INNOCENT MURMURS
Result from normal patterns of blood flow through the heart and vessels
Seven S's of innocent murmurs:
Sensitive (changes with position or respiration)
Short duration (not holosystolic)
Single (no associated clicks or gallops)
Small (small area and nonradiating)
Soft
Sweet (not harsh)
Systolic (limited to systole)
MURMUR DESCRIPTION
Aortic systolic
• Systolic ejection murmur over the aortic valve
murmur
• High pitched systolic murmur (can extend into diastole) best heard
Mammary
along the anterior chest wall over the breast
artery souffle
• Caused by blood flow in arteries & veins leading to and from the breasts
Obstructive Lesions
• Weak femoral pulses
Coarctation • Primary re-anastomosis
• BP in arms higher than • Rib notching on CXR
of the aorta
I
or a patch aortoplasty
in the legs
ASD:Atrialseptaldefect VSD:Ventricular
septaldefect RNLA:RighUlett
atrium
PDA:Patentductusarteriosus TGA:Transposition
of thegreatarteries RVILV:RighVlett
ventricle
TOF:Tetralogyof Fallo! TAPVR:Totalanomalous pulmonaryvenousrelurn PA:Pulmonaryartery
Source:Kliegman
R, et al. NelsonTextbook of Pediatrics
(21sted.).Philadelphia:
Elsevier:
2020
Park.M.PediatricCardiology for Practitioners
(6thed.).Philadelphia:
MosbyElsevier;2014
369
ACYANOTIC CONGENITAL HEART DISEASES
I. ATRIALSEPTALDEFECT(ASD)
A. Etiopathogenesis
0 ASDs can occur in any portion of the atrial septum (secundum, primum, or sinus venosus)
More common in females
1. Effects of an ASD in the heart
In large defects, oxygenated blood flows from LA to RA, which is added to the usual
venous return to the RA and is pumped by the RVto the lungs
Enlargement of the right sided chambers of the heart (RA, RV,PA)
LA is usually not enlarged
Pulmonary vascular resistance may begin to increase in adulthood
2. Types of ASD
TYPE REMARKS
Ostium • Most common
secundum • Defect present at the site of fossa ovalis
• Defect situated in the lower portion of the atrial septum and overlies
Ostium the mitral & tricuspid valves
primum • AVsepta! defect (AVcanal defect or endocardial cushion defect): consists of
contiguous atrial and VSDs with markedly abnormal AVvalves
Sinus • Defect situated in the upper part of the atrial septum close to the
venosus entry of the SVCor IVC(more common at SVC)
370
Chest • Enlarged RV,RA, and PA
Radiograph • Increased pulmonary vascularity
• Volume overload of the RV
ECG
• Normal or right axis deviation of the QRS
• RVoverload:
0 Increased RVend-diastolic dimension
° Flattening or reversed (anterior) motion of the ventricular septum
2D-echo
• Location and size of atrial defect seen
• Transesophaeal echocardiogram: recommended imaging modality
to delineate more accurate measurement/size of the defect
I
Enlargement of the LA, LV,and main PA
Size of the VSD is a major determinant of the magnitude of the left-to-right shunt
TYPE REMARKS
• Small communication is present (usually <5 mm)
Restrictive VSD
• RVpressure is normal
Large • Usually >10 mm
nonrestrictive VSD • Right and left ventricular pressures are equalized
371
2 T ofVSD
TYPE REMARKS
• Beneath the aortic valve
Membranous
• Most common type is perimembranous VSD (70% of all VSDs)
Outlet • 5%-7% ofVSDs
(infundibular • Defect located within the outlet (canal) septum
or conal) • The aortic and pulmona1y annulus forms part of its rim
• 5%-8% ofVSDs
Inlet (AV canal) • Located posterior and inferior to the perimembranous defect,
beneath the septa I leaflet of the tricuspid valve
Outlet/Supracristal/Subpulmonic/
lnfundibular/Juxta-arterial VSD
Perimembranous/Paramembranous/
Conoventricular VSD
B. Manifestations
• Small VSD (most common): asymptomatic with normal growth &
development
Symptoms
• Moderate to large VSD: delayed growth & development, decreased
exercise tolerance, repeated pulmonary infections, heart failure
• Systolic regurgitant murmur at the LLSB
Signs • Intensity of P2 is increased with a large shunt
• S2 is loud and single in pulmonary hypertension
• Spontaneous closure occurs in 40-50% of membranous and 90% in
Natural
muscular VSD (especially with small defects)
Course
• Eisenmenger syndrome
372
C. Diagnosis
DIAGNOSTIC SMALL VSD LARGEVSD
• Usually normal
• Cardiomegaly with prominence of both
• May have minimal
Chest ventricles, LA,and pulmonary artery
cardiomegaly &
Radiograph • Increased pulmonary vascular markings
borderline increase in
• Frank pulmonary edema may be present
pulmonary vasculature
• Biventricular hypertrophy
• Generally normal, but • Notched or peaked P waves
ECG
may suggest LVH • Presence of RVHsuggests a larger VSD
with pulmonary hypertension
• Shows the position and size of the VSD
2D Echo • Measures degree of volume overload of the LAand LV
• Estimated pulmonary artery pressure may be obtained
• Normal right heart • Equal or nearly equal pulmonary and
Cardiac
pressures & pulmonary systemic systolic pressure
Catheterization
vascular resistance • Elevated pulmonary vascular resistance
• Visualizes flow, defect position & size, ventricular volume &
Cardiac MRI
function, and net shunt quantification (arterial flow)
D. Management ofVSD
l. Management Depending on the Size
• Parents are reassured of the relatively benign nature of the VSD
Small VSD • Surgical repair is not recommended
• Infective endocarditis prophylaxis
• Management goals: control symptoms of heart failure and
prevent development of pulmonary vascular disease
LargeVSD
• Severe pulmonary vascular disease nonresponsive to pulmonary
vasodilators is a contraindication to repair an uncorrected large VSD
2. Treatment Modalities
• Indications for surgical closure:
0 Patients at any age with large defects when symptoms & failure
to thrive cannot be controlled medically
Surgery
0 Infants 6-12 months of age with large VSD& pulmonary
hypertension, even if symptoms are controlled by medication
Transcatheter
Closure
0 Patients >24 months with a Qp:Qs ratio >2:1
• Most successful for muscular VSDs
• Small sized perimembranous type VSDs with no associated aortic
valvar pathology
I
373
III. PATENTDUCTUSARTERI0SUS (PDA)
A. Etiopathogenesis
0 Persistent patency of a normal fetal structure between left PA & descending aorta
° Common in premature infants
More common in females
Effects of a PDA on the heart:
Blood shunts left-to-right through the ductus due to a higher aortic pressure
0 Enlarged LA, LV,main PA
Enlarged aorta, which also handles an increased amount of blood flow
B. Manifestations
• Small PDA: usually asymptomatic
Symptoms
• Large PDA: heart failure, growth retardation
• Small PDA: normal peripheral pulses, normal sized heart
• Large PDA: bounding peripheral arterial pulse, wide pulse
Signs pressure, cardiomegaly, prominent apical impulse
• Tachycardia & dyspnea due to volume overload on LA & LV
• Continuous machinery-like murmur at 2"• left ICS or LSB
• Spontaneous closure of ductus after infancy is rare
Natural Course • Small PDA: few complications, but late manifestations may occur
• Large PDA: heart failure occurs early in infancy
C. Diagnosis
DIAGNOSTICS REMARKS/FINDINGS
• Prominent PA with increased pulmonary vasculature
Chest • Enlarged LA and LV(depending on degree of the shunt)
Radiograph
• Aortic knob may be normal or prominent
• Small PDA: normal ECG
ECG
• Large PDA: LVHor biventricular hypertrophy
• Small PDA: normal sized cardiac chambers
20
Echocardiography • Large PDA: enlarged LA and LV
• Direct visualization of PDA
R.et al.NelsonTextbook
Source:Kliegman of Pediatrics
(21sted.).Philadelphia:
Elsevier;
2020
Park,M. PediatricCardiology for Practitioners
(6thed.).Philadelphia:
MosbyElsevier;2014
M. Fogelet al. Principles
andPracticeof CMRin CHOForm.Function. andFlow:2010
374
CYANOTIC CONGENITAL HEART DISEASES
DECREASED PULMONARY BLOOD FLOW INCREASED PULMONARY BLOOD FLOW
• Tetra logy of Fallot (TOF) • D-Transposition of the great arteries
• Pulmonary atresia • Total anomalous pulmonary venous return
• Tricuspid atresia • Truncus arteriosus
• Aorta arises from the right ventricle (canying desaturated blood to the body)
Abnormality
• Pulmona1y a1te1y arises from the LV(canying oxygenated blood to the lungs)
• Complete separation of pulmonary & systemic circulations, leading to
hypoxemic blood circulating throughout the body & hyperoxemic blood
Effect circulating in the pulmonary circuit
• Defects that permit mixing of the two circulations (e.g., ASD, VSD, PDA)
are needed for survival
B. Manifestations
• Cyanosis from birth
Symptoms
• Signs ofCHF with dyspnea & feeding difficulties during newborn period
• Single & loud SZ
• No hea1t murmur is heard in infants with an intact ventricular septum
Signs
• Severe arterial hypoxemia with or without acidosis (hypoxemia
unresponsive to oxygen inhalation)
C. Diagnosis
DIAGNOSTICS REMARKS/FINDINGS
Chest • Egg-shaped cardiac silhouette with a narrow, superior mediastinum
Radiograph • May show cardiomegaly & normal to increased pulmonary blood flow
ECG • Usually normal, showing the neonatal right-sided dominant pattern
Echocardiography • Diagnostic and confirmatory
Hyperoxia test • Arterial PO2 is low & does not rise after breathing of 100% oxygen
• Indicated if noninvasive imaging is diagnostically inconclusive, if
Cardiac
Catheterization
D. Management
unusual coronary artery anomaly is suspected, or if emergency
balloon atrial septostomy (Rashkind procedure) is required
I
ASPECT MANAGEMENT
• Prostaglandin El infusion: to maintain patency of the ductus
arteriosus
Palliative
• Create interatrial communication by balloon atrial septostomy
(Rashkind procedure) or atrial septostomy (Blalock-Hanlon procedure)
• Surgically switch right- & left-sided blood at three levels:
0 Atrial level (Senning or Mustard)
Definitive
0 Ventricular level (Rastelli)
0 Great artery level (latene, the surgical treatment of choice)
375
II. TETRALOGY OF FALLOT(TOF)
A. Etiopathogenesis
1. Anatomic Findings Characteristic ofTOF [mnemonic: PROVe)
Pulmonary stenosis (PS) or obstruction to RV outflow
Right ventricular hypertrophy
Overriding aorta (deviation of the origin of the aorta to the right)
Ventricular septa! defect
2. Pathophysiology
• Primary defect: the infundibular septum (the muscular septum that separates the
aortic & pulmonary outflow tracts) is anteriorly & superiorly deviated, resulting in:
Defect in the ventricular septum
0 Pulmonary stenosis by blocking flow to the PA,which leads to increased pressure
on the right side of the heart & RVH
Right to left shunting is increased when pressures on the left are decreased
There is absence of pulmonary congestion due to severe PS and reduced pulmonary
venous return to the left side of the heart
8. Manifestations
• Varying degrees of cyanosis, tachypnea, clubbing
• Cyanosis is not often present at birth, but with increasing RVhypertrophy
Symptoms in the infundibulum, cyanosis occurs later in the 1" year of life
• Timing of onset of symptoms, severity of cyanosis, and the degree of
RVHis determined by the degree of RVoutflow obstruction
• RVtap along the left sternal border
Signs • Systolic thrill along the left sternal border in the 3••-4•hparasternal spaces
• Loud systolic ejection murmur at mid- & ULSBwith radiation to the back
• Activities that suddenly lower the systemic vascular resistance (e.g., crying,
feeding, or defecation) initiate the spell, leading to an increase in cyanosis
Hypoxic
• Sudden onset of tachycardia or hypovolemia can cause the spell
or
TetSpells • Paroxysm of hyperpnea, irritability, prolonged crying, & increasing cyanosis
• Decreased intensity of the murmur because flow across the right
ventricular outflow tract (RVOT)diminishes
• Polycythemia develops
Natural • Growth retardation if cyanosis is severe
Course • Brain abscess & cerebrovascular accident (due to cerebral thrombosis)
• Coagulopathy is a late complication
:
DIAGNOSTIC REMARKS/FINDINGS
Chest • Decreased pulmonary vascular markings
Radiograph • Concave main PAwith an upturned apex (boot-shaped heart)
• RAD,RVH,and RAE (tall and peaked P wave)
ECG
• Dominant R wave in the right precordial chest leads
Echocardiography • Establishes the main anatomy
• Helpful for coronary anomalies
Cardiac CT • Advantage is the ability to delineate major aortopulmonary
collateral arteries difficult to visualize in echocardiogram
Cardiac MRI • Highly reproducible quantification of RVvolumes
• Necessary in TOF patients with pulmonary atresia to image the
Cardiac
source of blood supply to and size of each lung segment
Catheterization
• Markedly decreased PA pressure
Source:KliegmanRM.et al. NelsonTextbook of Pediatrics(21sted);2020
Park,M. PediatricCardiologyfor Practitioners
(6thed.).Philadelphia:
MosbyElsevier:2014
ChelliahA, et al. CurrentCardiovascularImagingReports;2019
376
D Management
• Maintain good dental hygiene & antibiotic prophylaxis against
General subacute bacterial endocarditis (SBE)
Management
• Phlebotomy & volume replacement for symptomatic polycythemic patients
• Timing of surge1y
determined by presence
I
to the RA • RVvolume overload
or absence of pulmona1y
• Supracardiac type (drains to a • "Snowman sign" on CXR(for
venous obstruction
vertical vein connected to the supracardiac type TAVR)
• Common pulmonaty
SVCdraining to the RA) is most
venous trunk anastomosed
common
directly to the LA
3) Single Ventricle (Double-Inlet Ventricle, Univentricular Heart)
377
4) Hypoplastic Left Heart Syndrome
• Related anomalies that present • Early cyanosis or grayish- • Prostaglandin infusion to
with underdevelopment of the blue color of skin because of maintain patency of a1terial
left side of the heart cyanosis and poor perfusion duct before the surgery
• Inadequate maintenance of • Signs of poor systemic • Staged surgical
systemic circulation perfusion and shock reconstruction
5) Tricuspid Atresia {TA)
• No outlet from the RA to the • Cyanosis at birth • For severely cyanotic
RVis present (i.e., atretic or • Holosystolic murmur at the neonates, prostaglandin
missing tricuspid valve) left sternal border infusion is done until
• Entire systemic venous return • Single S2 surgical aortopulmonary
leaves RAand enters the • LADand LVHon ECG shunt can be done
left side of the heart via the ( combination of cyanosis & • Surgicalmanagement:
fora men ova le or an ASD LADis highly suggestive) bidirectional Glennshunt or
• 20 echo: hypoplastic RV modified Fontan operation
Source:KliegmanRM,et al. NelsonTextbook of Pediatrics(21sted);2020
Park,M. PediatricCardiology
for Practitioners(6thed.).Philadelphia:
MosbyElsevier;2014
ChelliahA, et al. CurrentCardiovascular
ImagingReports:2019
JonasR. Comprehensive Surgical Management forCongenitalHeartDiseases. 2004
OBSTRUCTIVE LESIONS
I. COARCTATION OF THE AORTA (CoA)
A. Etiopathogenesis
1. Epidemiology
More common in males and most are associated with bicuspid aortic valve
Chromosomal abnormality associated with this condition: Turner's syndrome ( 45 XO)
Lesion is in the descending aorta in 98% of cases ( distal to the origin of the left
subclavian artery)
2. Effects in the Heart
Pressure build-up in the proximal aorta and LV
• Disease course depends on the degree of obstruction, presence of collateral
circulation, and associated cardiac anomalies
B. Manifestations
Asymptomatic for mild CoA; symptoms ofCHF if with more significant narrowing
° Classic sign: disparity in pulsation and blood pressure in arms & legs (BP is elevated in
vessels proximal to the coarctation; i.e., higher in the arms than in the legs)
0 Weak, delayed, or absent femoral pulses
Co· :
DIAGNOSTIC REMARKS/FINDINGS
• Rib notching: due to pressure erosion from increased blood flow through
Chest interthoracic & intercostal vessels which serve as collateral circulation
Radiograph
• Cardiac enlargement and pulmonary congestion in severe coarctation
• Normal in young children
ECG
• LVHin older patients
• Can visualize the segment of coarctation
Echocardiography • Not sufficient for the quantification & morphologic characterization
of coarctation
• Preferred non-invasive technique to evaluate the anatomy of the
Cardiac CT
entire aorta
378
D. Management
• Prostaglandin El infusion for neonates with severe coarctation to
In Neonates reopen the ductus and reestablish adequate lower extremity blood flow
• Surgery is done once diagnosis is confirmed
• Surgical repair: treatment of choice
Older Children • Balloon angioplasty/stent placement in selected cases (usually
recurrent CoAand adolescent/adult)
Source:KliegmanRM,et at NelsonTextbook of Pediatrics(21sted);2020
Park,M. PediatricCardiologyfor Practitioners
(6thed.).Philadelphia:
MosbyElsevier;2014
II. PULMONICSTENOSIS
A. Etiopathogenesis
° Causes RVOTobstruction
0 Associated with congenital rubella, Noonan & William syndrome
1 E I 'd :
TYPE REMARKS/FINDINGS
Valvar PS • Isolated valvular PS is the most common
Subvalvular
• Caused by muscular or fibrous obstruction in the RVOT
(infundibular) PS
Supra valvular • Constrictions along the major branches of pulmonary arteries
or peripheral PS • High incidence in congenital rubella syndrome
2. Effects in the
Obstruction
• RV pressure
• PA pressure
Heart
of flow from RVOTto PA results in increased RV systolic pressure & RVH
may be higher than systemic arterial pressure in severe cases of PS
( distal to obstruction) is normal or decreased
I
B. Manifestations
Symptoms • Asymptomatic, unless severe
• RV heave/tap
• Ejection click and systolic thrill
Signs • Systolic ejection murmur at the LUSBwith radiation to the back
• Soft P,
• Signs of RV failure in severe PS (e.g., hepatomegaly, edema)
• Asymptomatic; progression unlikely
Natural Course • Easy fatigability & CHF if severe
• Others: chest pain, syncope, sudden death, arrhythmias, endocarditis
379
Co· :
DIAGNOSTICS REMARKS/FINDINGS
• Normal or RV cardiomegaly (uplifting of the apex)
Chest
• Pulmonary vascularity may be normal or decreased
Radiograph
• If post-stenotic dilatation, normal or dilated MPA
• Right axis deviation
• Tall, spiked P wave
ECG
• RVH (pure Rand upright Tin Vl)
• RBBB may be seen
• Valvar PS: thickened pulmonic valve with restricted systolic motion
Echocardiogram • lnfundibular PS: hypertrophy of the RVOTclose to pulmonic valve
or well below it
OM :
TYPE MANAGEMENT
• Balloon valvuloplasty (catheterization) for moderate/severe
isolated PS as the initial treatment of choice
Valvar PS
• Surgical valvotomy for severely thickened pulmonic valves (e.g.,
Noonan syndrome)
Infundibular PS • Surgical resection of hypertrophied infundibular muscle in RVOT
Peripheral PS • Surgery or catheter balloon dilation
Source:KliegmanR, et al. NelsonTextbooko Pediatrics(21st ed.). Philadelphia:Elsevier:2019
Park.M. PediatricCardiologyfor Practitioners(6th ed.). Philadelphia:MosbyElsevier:2014
1. Types of AS
TYPE REMARKS
• Most common form
• Leaflets are thickened and commissures are fused
Valvular AS
• Valve is usually thickened and bicuspid with fused commissmes
and eccentric orifice
Subvalvular
• Discrete fibromuscular shelf below the aortic valve
(Subaortic) AS
Supravalvular AS • Least common type
380
B. Manifestations
• Usually asymptomatic until the LVfails (symptoms depend on
Symptoms severity of AS)
• Syncope and sudden death may occur with exercise
• Mild AS: pulses, heart size, and apical impulse are normal
• More severe AS: diminished pulses, enlarged heart, LVapical
Signs thrust, diminished Sl, paradoxical splitting of S2, presence of S4
from decreased LVcompliance
• Early systolic ejection click at the apex and left sternal edge
• Neonates with critical AS: severe heart failure with rapid
deterioration from a low-output shock state (emergency surgery
or balloon valvuloplasty is lifesaving)
Natural Course
• AS is one of the causes of sudden cardiac death in pediatrics
• Older children with isolated bicuspid AV:increased risk for
developing dilation of ascending aorta
C. Diagnosis
DIAGNOSTICS REMARKS/FINDINGS
Chest • Prominent ascending aorta with a normal aortic knob
Radiograph • Normal heart size
• May be normal
ECG
• LVHand strain (inverted T waves in left precordial leads)
• Defines the site and severity of AS
Echocardiogram
• Number of valve leaflets and morphology will be defined
Cardiac • Performed in conjunction with aortic balloon valvuloplasty
Catheterization • Demonstrates magnitude of pressure gradient from LVto the aorta
Source:KliegmanRM.et al. NelsonTextbookof Pediatrics(21sted);2020
Park,M. PediatricCardiologyfor Practitioners
(6thed.).Philadelphia:
MosbyElsevier;2014
D. Management
TYPE MANAGEMENT
• Balloon valvuloplasty (treatment of choice) indicated for
moderate-severe valvular AS
Valvular AS
• Surgery reserved for dysplastic aortic valves that are not
amenable to balloon therapy
Subvalvar AS
Supravalvular AS
• Surgical resection of discrete subaortic AS
• Surge1y
Source:KliegmanR, et al. NelsonTextbooko PedIatncs(21sted.).Philadelphia:
Park,M. PediatricCardiologyfor Practitioners
(6thed.).Philadelphia:
Elsevier;2019
MosbyElsevier;2014
I
381
SECTION FOUR
ACQUIRED HEART DISEASES
II. MANIFESTATIONS
History of streptococcal pharyngitis 1-4 weeks before the onset of symptoms
• Other non-specific manifestations: pal lot; malaise, easy fatigability, abdominal pain
A. Major Manifestations
MANIFESTATIONS REMARKS
• Low-risk*: migratory polyarthritis
• Moderate/high risk: monoarthritis, polyarthritis, or
polyarthralgia
Arthritis
• Most often asymmetric and affecting large joints (ankles, wrists,
(70%)
knees, elbows)
• Highly responsive to salicylates and NSAIDs
• Generally runs a self-limited course lasting approximately 4 weeks
• Clinical OR subclinical carditis
• May be pancarditis involving the pericardium, myocardium, and
endocardium
0 Pericarditis: audible friction rub, pericardia! effusion on
echocardiography
Carditis 0 Myocarditis: unexplained heart failure (gallop, soft heart
(50%) sounds), or cardiomegaly
0 Endocarditis/valvulitis: apical holosystolic murmur of mitral
regurgitation or basal early diastolic murmur
• Hallmark is valvular damage (only valvulitisleads to pe1111anentdamage)
• Characteristic manifestation is mitral regurgitation
• Single most important prognostic factor in RF
• Evanescent, pink rash seen with pale centers and rounded
serpiginous margins
Erythema • Most prominent on the trunk and inner proximal portions of the
marginatum
extremities
(<10%)
• Does not occur in the face
• Disappears on exposure to cold and reappear after a hot shower
III. DIAGNOSIS
The Revised Jones Criteria for the Diagnosis of RF and Rheumatic Heart Disease (RHO)
DIAGNOSIS CRITERIA
• Evidence of preceding group-A streptococcal infection; PLUS:
Initial Rheumatic 0 2 major criteria, or
Fever
0 1 major+ 2 minor criteria
Recurrent Rheumatic
Fever
• With a reliable past history of ARF or established RHO,and in
the face of documented GASinfection:
0 2 major criteria, or;
• 1 major+ 2 minor, or;
I
• 3 minor manifestations
ofRFcanbe madewithout
whereina diagnosis
Threecircumstances strictadherencetoJonescriteria:
• Whenchoreaistheonlymajormanifestation
carditis
• Whenindolent uponfirstcheckup,monthsaftertheapparentonsetofARF
istheonlymanifestation
• ApparentARF numberofpatientswithrecurrences
ina limited populations
high-risk
ofARFinparticularty
Gewitz
Source: MH,el al.AHARevisionoftheJonescriteria;
2015
Bisno Rheumatic
Consultation:
A,etal.WHOExpert heartdisease;
feverandrheumatic 2004
383
IV. MANAGEMENT
A.Antibiotic Therapy
Once the diagnosis of acute RF has been made, give 10 days of oral Penicillin or
Erythromycin or a single IM injection ofbenzathine Penicillin to eradicate GASfrom
the upper respiratory tract
• After this initial course of antibiotics, patient should be started on long-term antibiotic
prophylaxis
Source:AHAScientific
Slalemenl.
AcuteStreptococcal 2009
Pharyngitis:
GewitzMH,el al.AHARevision
of theJonescriteria;2015
• Asymptomatic if mild
• Dyspnea, 01thopnea, nocturnal
• Most common valvular dyspnea in severe cases
involvement in adults • Increased RV impulse along • Dental hygiene & antibiotic
• Thickening of leaflets and left parasternal border prophylaxis
fusion of the commissures • Opening snap followed by • Closed mitral
results in calcification with a low-frequency diastolic commissurotomy for those
immobility of the valve rumble at the apex without calcification
• LA and right-sided heart • CXR:enlarged LA& RV, • Valve replacement if valves
chambers become dilated prominent main pulmonary are calcified
and hypertrophied a1te1y (MPA)and lung fields
show pulmona1yvenous
congestion (with Kerley 8 lines)
2) Mitra/ Regurgitation (MR)
• Asymptomatic in childhood
• Most common valvular • Hyperdynamic apical impulse • Dental hygiene & antibiotic
involvement in RHO is palpable in severe MR prophylaxis
• Shortened leaflets due to • S1 is normal or diminished • Afterload-reducing agents
fibrosis • Systolic regurgitant to maintain forward cardiac
• Dilated LA & LVwith dilated murmur at the apex with output
MV ring transmission to the left axilla • Diuretics & digoxin for CHF
• Short, low-frequency • MV repair or replacement
diastolic rumble at the apex
3) Mitra/ Valve Prolapse (MVP)
• Identified by auscultation
in asymptomatic patients or
incidentally through 2D echo
• Major complications include: • Most common
• Asymptomatic patients
endocarditis, severe MR, complaint: palpitation
do not need treatment or
cerebrovascular ischemic from supraventricular
restriction of activity
events arrhythmias
• Systolic click: due to sudden
A. Etiology
0 Viridans-type streptococci (alpha-hemolytic strep) and Staphylococcus aureus
0 Other common causes: group D strep, Enterococws, S. bovis, S. faeca/is, etc.
0 ~6% of cases: blood cultures are negative
II. MANIFESTATIONS
A. Acute versus Subacute Endocarditis
B. Manifestations of IE
MANIFESTATION DESCRIPTION
Cardiac • Murmur is common, which may be indicative of valvular damage in IE
manifestations • Others: gallop, arrhythmias, pericardia! rub
Janeway lesions • Non-tender, slightly raised hemorrhages on the palms and soles
Osier's nodes • Tender; raised nodules on the pads of the fingers or toes
Splinter • Painless dark red linear lesions in the proximal nail bed that
hemorrhages may coalesce
Roth spots • Retinal hemorrhages with small, clear centers
386
Ill. DIAGNOSIS
A Major and Minor Criteria
MAJOR CRITERIA MINOR CRITERIA
1) Positive blood culture
• Typical organisms for IE from ;;;:2cultures:
• OR, Persistently positive cultures,
defined as: • Predisposing heart condition (valvular
0 At least 2 blood cultures drawn >12 disease with stenos is or regurgitation,
hours apart, or prosthetic valves, congenital heart
0 All of 3 or a majority of ;;,4 separate defects, prior endocarditis, hypertrophic
cultures with first and last drawn at cardiomyopathy) or injection drug use
least 1 hour apart
• OR, Single positive blood culture for
• Fever ;,3B.0°C
Coxiella burnetii or phase 1 lgG antibody
titer of ;el:800
• Vascular phenomena: major arterial
emboli, septic pulmona1y infarcts,
Note: If cultures remain negative after mycotic aneurysms, intracranial
48-72 hours, 2-3 additional blood culture hemorrhage, conjunctiva! hemorrhages,
sets should be obtained. Antimicrobial Janeway lesions
pretreatment reduces the yield of blood
culture to 50-60%
• Immunologic phenomena:
2) Evidence of endocardial involvement: glomerulonephritis, Osier's nodes, Roth's
• Positive echocardiogram for IE*: spots, rheumatoid factor
0Oscillating intracardiac mass on valves
or supporting structures • Microbiologic evidence: positive blood
0Abscess, or culture but not meeting major criterion or
0New dehiscence of prosthetic valve serologic evidence of active infection with
0New valvular regurgitation** organism consistent with IE
I
B.Duke Clinical Criteria for Diagnosis
DIAGNOSIS CLINICAL DEFINITION
• Two major criteria; OR
Definite
• One major criterion and three minor criteria; OR
Endocarditis
• Five minor criteria
Possible • 1 major and 1 minor criterion, OR
Endocarditis • 3 minor criteria
387
IV. MANAGEMENT
• Treatment is generally 4-6 weeks (referral to infectious disease specialist is recommended)
• Longer theapy may be required for recurrent endocarditis, prosthetic valve endocarditis,
and uncommon organisms
• Empirical therapy for patients without a prosthetic valve and at high risk of S. aureus,
enterococcus, and viridans-type streptococci: Vancomycin plus Gentamicin
ORGANISM REGIMEN
Unknown Agent
• Ampicillin/sulbactam plus gentamicin
Native valve or "late" prosthetic valve
• With or without vancomycin
infection (>l year after surgery)
• Add rifampin for prosthetic valve endocarditis
Nosocomial endocarditis associated • Vancomycin PLUS gentamicin
with vascular cannulae or "early"
• With or without rifampin if with prosthetic material
prostethic valve endocarditis
('.SIyear after surgery) • PLUS cefepime or ceftazidime
Streptococcus
Highly susceptible to penicillin G • Penicillin G or ceftriaxone
• Penicillin G (or ampicillin) PLUS gentamicin
Relatively resistant to penicillin
(for first 2 weeks, or whole course for enterococci)
Staphylococcus (S.aureus or Coagulase-Negative Staphylococci)
Susceptible to penicillin G (rare) • Penicillin G
Resistant to 0.1 ug/mL of penicillin G • Oxacillin OR nafcillin ± gentamicin x 3-5 days
MRSA • Vancomycin
Vancomycin resistant or intolerant • Daptomycin
If prosthetic material is present • PLUS rifampin PLUS gentamicin (for first 2 weeks)
Other Specific Therapy
• Ceftazidime, cefepime, cefotaxime, or ceftriaxone
Gram-negative enteric bacilli plus gentamicin (or tobramycin or amikacin,
depending on susceptibility)
• Ceftriaxone OR Cefotaxime OR
HACEK
• Ampicillin-sulbactam
Fungi: Candidaspp, Aspergillusspp • Amphotericin B or Flucytosine
388
KAWASAKI DISEASE (KD)
• Acute non-specific systemic vasculitis (medium-sized arteries)
• Vessels lose its structural integrity and weakens, resulting in dilatation and saccular or
fusiform aneurysm formation
I. ETIOPATHOGENESIS
A. Epidemiology
Most affected children are Asians although it occurs worldwide
0 More common in boys (1.5:1)
0 80% of patients are <5 years old
0 Unknown cause
B. Pathology
0 Arteritis is frequently observed in the coronary arteries and iliac arteries
0 Interstitial myocarditis, pericarditis, inflammation of the SA node and atrioventricular
conduction system, endocarditis and valvulitis may also be present
II. MANIFESTATIONS
PHASE DESCRIPTION
Acute febrile • Last 1-2 weeks
phase • Fever and other acute signs of illness
• Begins when fever & other acute signs have abated
Subacute • Associated with desquamation, thrombocytosis, coronary aneurysms
phase (highest risk of sudden death in those who have developed aneurysms)
• Lasts until the 4th week
Convalescent • Begins when all clinical signs have disappeared
phase • Continues until ESR & CRP return to normal ~6-8 weeks after onset
III. DIAGNOSIS
A. Diagnostic Criteria
Fever (spiking up to 40°C and persisting for 5 days or more, remittent, unresponsive
to antibiotics), plus presence of at least 4 features:
Fever plus less than four out of five remaining criteria or the presence of coronary lesions
(proven by echocardiogram or angiography) may still be diagnostic. In the presence of four
or more principal clinical features, especially when redness & swelling of the hands and feet
are present, the diagnosis can be made with 4 days of fever.
I
Incomplete or Atypical Kawasaki Disease is considered in any infant or child with prolonged
unexplained fever with fewer than 4 of the principal clinical features AND compatible
laboratory or echocardiographic findings
B. Diagnostics
DIAGNOSTIC REMARKS/FINDINGS
• Anemia and leukocytosis may be present
• Platelet count usually normal in the 1" week of illness but
Laboratory Tests
rapidly increases in the 2"'-3'' week
• Elevated ESR, CRP for 4-6 weeks
• Should be performed when diagnosis of KD is considered
Echocardiography
• Should be repeated within 1-2 weeks & 4-6 weeks after treatment
389
IV. MANAGEMENT
PHASE MANAGEMENT
• !VIG2 g/kg as single IV infusion within 10 days of illness onset but as
soon as possible after diagnosis
• May give !VIGto children after the 10th day of illness if they have either:
0Persistent fever without other explanation. or
Acute phase
° Coronary artery abnormalities with elevated ESR or CRP
• Aspirin as moderate- (30-50 mg/kg/day) to high-dose (80-100 mg/kg/
day) every 6 hours is reasonable until patient is afebrile (but there is no
evidence that it reduces coronary artery aneurysms)
• When high-dose ASA is discontinued, low-dose ASA (3-5 mg/kg/day)
Convalescent
is begun and continued until the patient has no evidence of coronary
phase
changes by 6-8 weeks after onset of illness
Long-term • For children who develop coronary abnormalities, ASA may be
therapy for
continued indefinitely
coronary
abnormalities • Aspirin 3-5 mg/kg once daily +/-clopidogrel 1 mg/kg/day (max 75 mg/day)
REFERENCES
I. Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Tleyjeh IM, Rybak MJ, et al. AHA Scientific Statement. Infective
Endocarditis in Adults: Oi;1gnosis, Antimicrobial Therapy. and Management of Complications: A Scientific Statement
for Healthcare Professionc1ls from the American Heart Association. Circulation. 2015;132(15): 1435·86.
2. Baltimore RS,Gewitz M,Baddour LM,Beerman LB.JacksonMA Lockhar1PB, Pahl E,Schutze GE,Shulman Sl'.Willoughby RJr:
on behalf of the American Hea1tAssociation Rheumatic Feve1;Enclocarditis,and Ka1,,vasaki
Disease Committee of the Council
on Cardiovascular Disease in the Young and the Council on Cardiovascular and Stroke Nursing. Infective endocarditis in
childhood: 2015 update: a scientific statement from the American Heait Association. Circulation.2015; 132: 1487-1515.
3. Bisno A. Butchart EG, Ganguly NK, Ghebrehiwer T, Lue HC, Kaplan EL, et al. World Health Organization Expert
Consultation: Rheumatic fever and rheumatic heart disease. WHO Library Cataloguing-in-Publication Data; 2004.
4. Chelliah A, et al. Cardiovascular CT in Cyanotic Congenital Heart Disease. Current Cardiovascular Imaging Repmts. July 2019.
5. Crain EF.Gershel]Cand Cunningham SJ(eds). ClinicalManual of Emergency Pediatrics 5th ed. 2011.Camb,idge UniversityPress
6. Fernandes CJ.Weisman LE, Kim MS.Physiologic transition from intrauterine to extrauterine life UpToDate: 2019
7. FogelM(eel).Principlesand Praa::iceof
Ca,tliacMagneticResonanceinCongenitalHea1tDise.:1.Se
Fonn,Function.andFlow2010,Wiley-Black\vell
8. Frank JE,Jacobe KM.Evaluation and management of heart murmurs in children. Am Fam Physician 84(7):793-800; 20 I 1
9. Gerber M. Baltimore RS, Eaton CB,Gewitz M, Rowley AH, Shulman ST, et al. Ame1ican Hea,t Association scientific stalemem:
Preventionof rheumatic feverand diagnosisand treatment of acute streptococcalphmyngitis.Circulation.2009; 119( 11):1541-155I.
CA,Shulmans-r,
I 0. GewitzMH,BaltimoreRS,Tani LY.Sable Carapetisj, RemenyiB,Taube1tKA,BolgerAF,Beennan L,MayosiBM,Beaton
A.Pandian NG,Kaplan EL;on behalfof the Ame1icanHea1tAssociationCommitteeon Rheumatic Fever,Endocarditis,and Km-vasaki
Diseaseofthe Councilon CardiovascularDiseasein the Young.Revisionof the Jonesaitetia for the diagnosisofacute rheumatic feverin
the era of Dopplerechocardiography:a scientificst,llement from the Ame1icanHea,t Association.Circulation.2015;131:1806-·1818
11. Gewitz MH,Baltimore RS,Tani LYet al. Revision of the Jones Criteria for the diagnosis of acute rheumatic fever in the eraof
doppler echocardiography: a scientific statement from the american hea1t association. Circulation 2015;131:1806-18.
12. Habib G. Lanccllotti, P,J\ntuncs, M et al.2015 ESCGuidelines for the management of infective endocarditis: The Task
Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC) Endorsed by:
European Association for Cardio•Thoracic Surgery (EJ\CTS), the European Association of Nuclear Medicine (EANM).
European Heart Journal, Volume 36, Issue 44, 21 November 20 I 5. Pages 3075-3128
13. jonas R. Comprehensive Surgical Management for Congenital Heart Diseases.2nd ed. 2004. CRCPress
14. Kliegman RM,Stanton BF,St Geme JW,Schor NF.Nelson Textbook of Pediatrics 21st ed. 2020. Philadelphia, PA:Elsevie1:
l 5. Li JS, Sexton DJ, Mick N, Nettles R, Fowler VG J1~Ryan T, et al. Proposed modifications to the Duke criteria for the
diagnosis of infective endocarditis. Clin Infect Dis. 2000;30( 4):633-638
I 6. McCrindle, 8.W. et al. Diagnosis, Treatment. and Long-Term Management of
Kawasaki Disease. A Scientific Statement for Health Professionals from the American Heart Association. 2017.
17. Ntsinjana H, Hughes, M, and Taylor A. The Role of Cardiovascular Magnetic Resonance.
Cardiovasc Magn Reson.2011; 13{1): 51.
18. Park, M. Pediatric Cardiology for Practitioners 6th ed. 2014. Philadelphia
390
NEPHROLOGY
SECTION ONE
APPROACH TO HEMATURIA
HEMATURIA
I. DEFINITION
• General definition of hematuria is the presence of at least 5 RBC per high-power field in
urine microscopy
• 10-50 RBCs/uL in microscopy may suggest underlying pathology
. No deposits
• No immune
deposits
• No deposits
I
• 95% resolve • Slow • 75% stabilize . 75% stabilize
Prognosis spontaneously progression in or improve if or improve if
• 5% RPGN 25-50% treated early treated early
PSGN:Poststreptococcal
glomerulonephritis
RPGN:
Rapidly progressive
glomerulonephritis
Source:Kliegman
R,et al.NelsonTextbook
ofPediatrics
(21sted).Elsevier:
2020
PhadkeK,et al.Manual
ofPediatric
Nephrology.Springer:
2014
393
III. CAUSES OF RED URINE
ORIGIN CHARACTERISTICS
GLOMERULONEPHRITIS
I. MANIFESTATIONS OF GLOMERULONEPHRITIS
• Tea- or cola-colored urine
• Facial or body edema
• Hypertension
• Oliguria
394
MANIFESTATIONS DIAGNOSTICS RENAL BIOPSY MANAGEMENT
2) IgA Nephropathy or Berger Disease
• Acute nephritis
with proteinuria
or nephrotic
• Identify cause of
RPGN
• Crescents in 50%
or more in the
glomeruli; no
• High-dose
corticosteroid and
cyclophosphamide
I
syndrome immune deposits • Poor prognosis if
• Rapid loss of renal • IF and pattern with a majority of
function of deposits to crescents on renal
• Renal failure/ identify underlying biopsy
insufficiency cause • End-stage renal
• May be primary or • Remember, disease in most
secondary to other "crescent" is an patients
conditions ( e.g., ominous sign
lgA nephropathy,
HSP nephritis,
PSGN, SLE)
395
MANIFESTATIONS DIAGNOSTICS RENAL BIOPSY MANAGEMENT
6) Henoch-Schonlein Purpura (HSP) or IgA vasculitis
• Idiopathic • 50% have renal • Deposition of • Urinalysis done
systemic immune manifestations: polymeric lgA in weekly during
complex-mediated asymptomatic the glomeruli the period of
vasculitis with lgA microscopic • Glomerular active disease
deposits in small hematuria to findings and then once a
blood vessel walls severe progressive indistinguishable month for up to 6
• Preceded by URTI glomerulonephritis from lgA months (if all are
• Any mucosa! • Skin biopsy: Nephropathy normal, nephritis
infection or leukocytoclastic is unlikely to
food antigen vascultis with develop)
may trigger lgA C3, and fibrin • Mild disease:
the increased deposition resolves
production of spontaneously
pathogenic lgA 1 • Moderate to severe
• Tetrad of HSP: disease: steroids
0 Palpable (e.g., prednisone
purpuric 1 mg/kg/day for
rashes on the 3 months with
dependent parts ACE inhibitors)
of the body followed by
0 Arthritis or azathioprine or
arthralgia mycophenolate if
0 Abdominal pain severity persists
0 Renal disease • Consult a specialist
if proteinuria,
renal insufficiency,
or hypertension
develops
• 2-5% risk of
developing CKD
7) Hemolytic-Uremic Syndrome (HUS)
• Triad of HUS: • PBS results: • Renal biopsy • Supportive therapy
0 Microangiopathic microangiopathic rarely performed & hydration
hemolytic anemia hemolytic anemia • Glomerular • PRBC transfusion
0TimJmbocytopenia • CBC results: thickening of • Correction
0 Renal anemia, capillary walls of electrolyte
insufficiency thrombocytopenia • Narrowing of abnormalities
• History of bloody (20,000-100,000) capillary lumen • Control of
gastroenteritis • Coombs test • Platelet-fibrin hypertension
within the usually negative thrombi in • Dialysis
preceding 3 weeks • Renal: elevation glomerular • Platelet
• Most common ofBUN and capillaries transfusion
form is due to creatinine, acute • Thrombi in generally not
Shiga toxin- renal failure afferent arterioles administered
producing and small arteries • Antibiotics may
Escherichia coli with fibrinoid precipitate toxin
0157:H7 (STEC) necrosis release
'Indications
forRenalBiopsy
inG!omerulonephritis:
Acuterenalfailure,Nephrolic
syndrome,Absence
ofevidence
ofstreptococcal
infection,
Normalcomplementlevel,Hematuria
andproteinuria,
Diminished renalfunction,
LowC3 >2 months
396
EVALUATING A PATIENT WITH GROSS HEMATURIA
Glomerular Hematuria No
(:!: hypertension, oliguria and edema) Non-glomerula r Hematuria
(work up as indicated)
397
SECTION TWO
APPROACH TO PROTEINURIA
PROTEINURIA
I. DIFFERENTIALS FOR PROTEINURIA
REMARKS POSSIBLE ETIOLOGIES
• Negative evaluation on repeated • Fever >38.3 °c
Transient dipstick • Exercise/stress, dehydration
proteinuria • Usually not >l-2+ on dipstick • Cold exposure
• Normal quantified urinary protein • Heart failure, seizures
• Upright position increases proteinuria
10-fold up to 1,000 mg/24h
• Normal or minimal proteinuria in
the supine position
Orthostatic • No hematuria, hypertension, edema, • It is the most common cause of
or Postural hypoalbuminemia, & renal dysfunction persistent proteinuria in school
proteinuria • Confirmation: absence of proteinuria age children
in 3 consecutive first morning void
0 Bladder is emptied before sleeping
0 Dipstick is negative or trace
0 UPCR <0.2
• Glomerular proteinuria
0MCD, FSGS, MPGN, MN
0Diabetic nephropathy
• Definition (on 3 separate occasions): 0Others: PSGN, lgA nephropathy,
Fixed 0 ;,+l on dipstick with SG >l.015, SLE, HSP,Alport syndrome
Proteinuria or
0 UPCR;, 0.2 • Tubular proteinuria
° Fanconi Syndrome
0 X-Linked tubular syndrome
0 Dent disease
398
3) Spot Urine for Protein/Creatinine Ratio (UPCR}
• Semiquantitative • Normal: • Easier collection
assessment of 0 <0.2 mg protein/mg creatinine in >2 yrs old • Use first morning void
proteinuria 0 <0.5 mg protein/mg creatinine in 6-24 mos • Less accurate than
• Nephrotic range: >2 mg protein/mg creatinine 24hr urine collection
• Not readily available
4) Microalbuminuria
• Assess risk of • Normal: <30 mg of urine albumin per gram of creatinine on first
progressive morning void
glomerulopathy
Source:KliegmanR.et al. NelsonTextbookof Pediatrics(21sted). Elsevier:2020
I. ETIOPATHOGENESIS
• More common in males
• Most common cause in children is minimal change disease & most respond to steroids
• Among those nonresponsive to corticosteroids, 80% would be FSGS
II. MANIFESTATIONS
• Generalized edema (including genitals), anorexia, irritability, abdominal pain
• Hypertension and gross hematuria are uncommon
399
I~-,
Ill. OVERVIEW OF THE TYPES OF NEPHROTIC SYNDROME
I I Membranoproliferative Glomerulonephritis
Focal Segmental I
Minimal Change
Glomerulosclerosis I Membranous Nephropathy I (MPGN)
-- ---~---
Disease (MCD) (MN) 1~· ~-
i
I I
(FSGS) I
I I
-,.y--;e Type II
V. MANAGEMENT
A. Steroids
If onset at 1-8 years old: likely steroid-responsive minimal change form (steroids may
be initiated without renal biopsy)
0 Prednisone 60 mg/m 2/day OR 2 mg/kg/day (max dose 60 mg daily) for 4-6 weeks
Taper prednisone after 4 weeks to alternate day therapy (starting at 40 mg/m' /day or
1.5 mg/kg/day) for 8 weeks to 5 months
DESCRIPTION
Response • Remission attained during first 4 weeks of steroid therapy
Remission • UPCR <0.2 or dipstick <l for 3 consecutive days
Relapse • UPCR >2 or dipstick ;,3+ for 3 consecutive days
Steroid • Two consecutive relapses during corticosteroid therapy or within 14
Dependent days of ceasing therapy
Steroid • Failure to achieve complete remission after 8 weeks of steroid therapy
Resistant • Requires renal biopsy and referral to specialist
Fluid
Balance
•
•
•
•
Fluid restriction and low sodium diet
Diuretics: furosemide 1 mg/kg/dose IV
Intravenous 25% human albumin 0.5 g/kg
Monitor volume status, serum electrolytes, renal function
I
• Pneumococcal vaccine (ideally when in remission and off daily steroids)
• Varicella vaccine (defer live vaccines until the prednisone dose is below
Vaccination
either 1 mg/kg daily or 2 mg/kg on alternate days)
• Influenza vaccine
VI. COMPLICATIONS
• Infection :major complication of NS (e.g., spontaneous bacterial peritonitis/SBP, bacteremia)
• Organisms: Streptococcus pneumoniae (most common in children) and E.coli
• Peritoneal leukocyte counts of>250 cells/uL highly suggestive ofSBP
VII. PROGNOSIS
• If steroid-resistant, FSGSis the usual form and has a much poorer prognosis
• If in remission, they are considered normal and may have unrestricted diet and activity
Source:KDOQIclinicalpracticeguidelines for CKD:AmJ Kidney:2002
KliegmanR, et al. NelsonTextbookof Pediatrics(21sted).Elsevier:2020
401
SECTION THREE
APPROACH TO AZOTEMIA
Height in cm x 36.5
eGFR=
Creatinine in mmol/l
OR
Height in cm x 0.413
eGFR=
Creatinine in mg/dl
RENAL FAILURE
I. ACUTE KIDNEYINJURY
• Abrupt loss of kidney function which leads to a rapid decline in the GFR, accumulation
of waste products, and dysregulation of extracellular volume and electrolyte homeostasis
Source:KDIGOClinicalPracticeGuidelineforAcuteKidneyInjury.Kidneyinter.,Suppl:2012
402
B. Indications for Dialysis in Acute Kidney Injury:
Anuria/oliguria
Volume overload with hypertension/pulmonary edema refractory to diuretics
Persistent hyperkalemia
Severe metabolic acidosis unresponsive to therapy
Uremia (encephalopathy, pericarditis, neuropathy)
Blood urea nitrogen >100-150 mg/dL (or lower if rapidly rising)
Calcium:Phosphorus imbalance, with tetany that cannot be controlled
0 Inability to provide adequate nutrition due to severe fluid restriction
2. GFR <60 ml/min/1.73111 2 for ;;,3 months, with or without the other signs of kidney
damage described above
403
SECTION FOUR
SPECIFIC DISORDERS IN NEPHROLOGY
II. MANIFESTATIONS
• Latency period: 1-2 weeks a~er throat infection and 3-6 weeks after pyodenna
• Nonspecific symptoms: malaise, lethargy, abdominal pain, or flank pain are common
• Gross hematuria, periorbital edema, hypertension, oliguria
• Complications:
0Encephalopathy (considered if with severe headache, altered mental status, or new seizures)
0Heart failure due to hypertension or hypervolemia
• Complete recovery is expected in >95% of cases
III. DIAGNOSIS
DIAGNOSTIC REMARKS/FINDINGS
Urinalysis • RBCs, often with RBC casts, proteinuria, and PMN leukocytes
CBC • May have mild normochromic anemia
• Low serum C3 in >90% of patients. C3 characteristically normalizes
Serum C3
in 6-8 weeks
• ASO for throat infection
Documentation
• DNAse-B Antigen for pyoderma
of GABHS infection
• Rising antibody titers to streptococcus-antigen
Renal biopsy • See findings at table under common causes of glomerulonephritis
IV. MANAGEMENT
ASPECT REMARKS
• Early systemic antibiotics do not eliminate the risk of GN
Antibiotics • Penicillin G x 10 days is recommended to limit spread of
nephritogenic strains
• Sodium restriction
• Diuresis (Furosemide 1-2 mg/kg/dose IV q 6-12 hours)
• Antihypertensives: ACE inhibitors, or CCBs,or vasodilators
Fluids
• Fluid restriction: 400 mL/BSA + urine output in 24 hours
• Strictly monitor input and output, weigh daily. Re-adjust fluid limit daily.
• Titrate diuretics accordingly based on the clinical status of the patient
• Microscopic hematuria can persist for 12-24 months after the initial
presentation
Monitoring • Hypertension usually normalizes 4-6 weeks after onset
• Acute phase generally resolves within 6-8 weeks
• C3 should normalize after 8 weeks
404
lgA NEPHROPATHY OR BERGER DISEASE
I. ETIOPATHOGENESIS
A. Epidemiology
0 Most common chronic glomerular disease worldwide
0 More common in males
B. Pathology
Immune complex disease that appears to be caused by abnormalities in the lgA
immune system
Predominance of lgA within mesangial deposits of the glomerulus in the absence of
systemic diseases
II. MANIFESTATIONS
• Gross and/or microscopic hematuria, associated with URTl or GI infection 1-2 days prior to
its onset
• May present as nephritic syndrome, nephrotic syndrome, or a combined nephritic-
nephrotic syndrome
III. DIAGNOSIS
• Normal serum C3 level
• Serum lgA has no diagnostic value (increased in only 15% of patients)
IV. MANAGEMENT
ASPECT REMARKS
ACE inhibitors
• Effective in managing hypertension and reducing proteinuria
&ARBs
Fish oil (omega-3
• May decrease the rate of renal progression
fatty acids)
• May be beneficial in some patients, if ACE inhibitors and ARBs are
Steroids
ineffective
V. PROGNOSIS
• Does not lead to significant kidney damage in most children
• Progressive disease in 20-30% of children at 15-20 years after onset
• Most children will not show progressive renal dysfunction until adulthood
• Poor prognosis if: persistent hypertension, renal dysfunction, heavy /prolonged proteinuria
A E.t10Iogy
Infection • Most common form of HUS is due to toxin-producing E.coli
B. Pathology
Toxin initiates endothelial cell injury which leads to microvascular injury
Microangiopathic anemia is due to mechanical damage to RBCs as they pass through
the altered vasculature
Thrombocytopenia is due to intra-renal platelet adhesion or damage
405
II. MANIFESTATIONS
• Most common in <4 years old
• Onset is usually preceded by gastroenteritis
• Sudden onset of pallor, irritability, weakness, lethargy, and oliguria
• Usually occurs 5-10 days after the initial illness
• Physical examination: dehydration, petechiae, hepatosplenomegaly, and marked irritability
III. DIAGNOSIS
A. Laboratory Criteria for Diagnosis of HUS
The following are both present at some time during the illness:
• Anemia (acute onset) with microangiopathic changes (schistocytes, burr cells, helmet cells)
on peripheral blood smear
• Acute renal injury: hematuria, proteinuria, elevated creatinine level (2el mg/dL in
<13 years old or >1.5 mg/dL in >13 years old or 2'50% increase over baseline)
B. Case Classification
CLASSIFICATION DESCRIPTION
• Meets the lab criteria but with no clear history of diarrhea in
the preceding 3 weeks, or
Probable
• Onset within 3 weeks of diarrhea, and meets the lab criteria
except that microangiopathic changes are not confirmed
Confirmed • Meets the laboratory criteria ANDbegan within 3 weeks of dian-hea
C 0th o· .
DIAGNOSTIC FINDINGS/REMARKS
• Leukocytosis, thrombocytopenia, anemia
CBCand peripheral
• Increased reticulocyte count
blood smear
• PBS findings: Helmet cells, burr cells, fragmented RBCs
• Negative Coombs test
• Hematuria & proteinuria
Others
• Normal PT & PTT
• Stool culture is often negative
IV. MANAGEMENT
• Correction of fluids & electrolytes derangements
• Aggressive nutrition
Supportive care • Early institution of peritoneal dialysis to decrease mortality
• BP control
• Red cell transfusion
• Not generally administered regardless of platelet count
Platelet
• Almost immediately consumed by active coagulation & can worsen
transfusion
the clinical course
Antibiotic
• No antibiotic therapy because this may lead to increased toxin release
therapy
• Complications (hypertension, chronic renal insufficiency, proteinuria)
Prognosis
may not be apparent for up to 20 years, long-term follow-up needed
406
AUTOSOMAL RECESSIVE POLYCYSTIC KIDNEY DISEASE (ARPKD)
I. ETIOPATHOGENESIS
• Infantile polycystic disease (1:10,000 - 1:40,000)
• Autosomal recessive
• The gene for autosomal recessive PKD (PKHDl) encodes fibrocystin, a large protein
• Both kidneys are markedly enlarged, grossly showing innumerable cysts
• Progressive interstitial fibrosis and tubular atrophy eventually leads to renal failure
II. MANIFESTATIONS
• Bilateral flank masses during the neonatal period or early infancy
• Associated with oligohydramnios, pulmonary hypoplasia, respiratory distress,
spontaneous pneumothorax in the neonatal period
• Oligohydramnios complex or Potter facies:
0 Low-set ears, micrognathia, flat nose, limb-positioning defects, growth deficiency
0 Hypertension, hyponatremia, impaired renal function, hepatic fibrosis
III. DIAGNOSIS
• Strongly suggested by:
° Clinical findings (bilateral palpable flank masses in an infant with pulmonary
hypoplasia, oligohydramnios, hypertension), with
0 Normal renal ultrasound of parents
• Renal ultrasound: enlarged and hyper-echogenic kidneys with poor cortico-medullary distinction
IV. MANAGEMENT
• Supportive: ventilatory support, control BP, fluid and electrolyte correction, osteopenia
management, management of clinical manifestations of renal insufficiency
B. Pathogenesis
0 Most UTls are ascending infections: bacteria arise from fecal flora and colonize the
perineum, and then enters the bladder via the urethra
Voiding dysfunction is a risk factor for UTI
C. Etiology
Caused mainly by colonic bacteria
0 In girls, 75-90% are due to Escherichia coli, followed by Klebsiellaand Protet1s
° For both sexes, Staphy/ococct1ssaprophyticus and Enterococcus
Clinical
FORM DESCRIPTION
• Characterized by (any or all) abdominal, flank, or back pain, fever
I
Pyelonephritis (may be the only manifestation), malaise, nausea/vomiting
• Indicates bladder involvement (more localized urinary signs and
symptoms)
• Gross hematuria and dysuria
Cystitis • Urgency, frequency, malodorous urine, incontinence, supra pubic pain
• May occur in response to chemical toxins (penicillins, dyes,
insecticides, cyclophosphamide ), viruses, radiation, idiopathic
• Usually resolves within 1 week
• (+)urine culture without any manifestations of infection
Asymptomatic
• Most common in girls; incidence declines with increasing age
Bacteriuria
• Benign and does not cause renal injury except in pregnant women
407
III. DIAGNOSIS
DIAGNOSTICS* DESCRIPTION
• Necessary for confirmation and appropriate therapy
• Positive culture:
0Suprapubic or cathterized sample: >50,000 colonies of a single
Urine culture
pathogen OR 10,000 colonies and the child is symptomatic
0In a bag/midstream urine sample: single organism cultured with
a colony count >100,000 AND (+)urinalysis AND symptomatic
• Pyuria (leukocytes in the urine) suggests infection, but may be
Urinalysis present without UTI ••
• Nitrites and leukocyte esterase are usually positive in infected urine
Imaging Studies
• To assess kidney size, detect hydronephrosis and ureteral dilation
• To evaluate bladder anatomy
Sonogram of • Indicated for:
kidneys and
bladder ° First UTI <6 months old
0 No response to antibiotic therapy within 24-48 hours
• If ultrasound is abnormal, DMSAor VCUGmay be done
Dimercaptosuccinic • To assess renal scarring and identify areas of acute pyelonephritic
acid (DMSA) scan involvement
Voiding
cystourethrogram • To assess for reflux
(VCUG)
'Note on obtainingappropriateurinesamples:
In toilet-trained
children.a midstream
sampleis usuallysatisfactory
Childrenwho are not toilet-trained:catheterizedurinesampleshouldbe obtained
IV. MANAGEMENT
TYPE DESCRIPTION
• <2 months: Cefotaxime + Amikacin for 10-14 days
• >2 months to 18 years old: Coamoxiclav, Cefuroxime, Ampicillin-
Sulbactam for 7-14 days
Acute • Nitrofurantoin can be given for adolescents (but ONLYfor acute
uncomplicated UTI:
Acute cystitis and cystitis)
pyelonephritis • Oral therapy is equally effective to IV therapy
• IV therapy preferred if seriously ill, cannot tolerate oral therapy
• Switch to oral therapy once afebrile for 24 hours and able to
tolerate oral therapy
Complicated UT!
• Refer to IDS, nephrologist and urologist
(catheter-related
or with co-morbids) • Ceftriaxone +/-Amikacin
408
RENAL TUBULAR ACIDOSIS
• Characterized by normal anion gap hyperchloremic metabolic acidosis in the setting of a
normal or near-normal GFR
I. ETIOPATHOGENESIS
TYPES PATHOGENESIS CLINICAL MANIFESTATIONS
• Inherited and persistent from birth or
occur transiently during infancy • Growth failure in the 1st year
• Usually occurs as a component of of life, polyuria, hyponatremic
Proximal (type
global proximal tubular dysfunction dehydration, anorexia,
II)RTA
(Fanconi syndrome: proteinuria, vomiting, constipation,
glycosuria, phosphaturia, hypotonia, hypokalemia
aminoaciduria, and proximal RTA)
• Sporadic or inherited
• Can occur as a complication of • Growth failure, hypokalemia,
inherited or acquired diseases of the nephrocalcinosis and
Distal (type I)
distal tubules hypercalciuria
RTA
• Results from impaired W ion • Absent phosphate and
excretion, so urine pH cannot be bicarbonate wasting
reduced to <5.5
• Due to impaired aldosterone production
(hypoaldosteronism) or impaired • Growth failure, hyperkalemia
renal responsiveness to aldosterone • Polyuria and dehydration from
(pseudohypoaldosteron ism) salt wasting are common
Hyperkalemic
• Aldosterone has a direct effect on • Urine may be alkaline or acidic
(type IV) RTA
hydrogen secretion & stimulates K" • High urinary sodium levels
secretion in the collecting tubule with inappropriately low
• Lack of aldosterone results in urinary K"
acidosis and hyperkalemia
• Associated with osteopetrosis
• Very rare, autosomal recessive or marble bone disease,
Combined • Due to inherited carbonic anhydrase cerebral calcification, and
proximal and
2 deficiency mental retardation
distal type
(type Ill) • Features of both proximal & distal RTA • Growth failure, bone fractures,
facial dysmorphism, conductive
hearing loss & blindness
II. DIAGNOSIS
FINDING
Urine pH with
PROXIMAL RTA
• <5.5
CLASSIC
DISTAL RTA
• >5.5
GENERALIZED
DISTAL
DYSFUNCTION
• <5.5 or >5.5
I
acidosis
Urine net charge • Negative • Positive • Positive
Fanconi lesion • Present • Absent • Absent
Fractional • >10-15% during
bicarbonate • 2-5% • 5-10%
excretion alkali therapy
Response to
• Least responsive • Responsive • Less responsive
therapy
Associated disease • Fanconi syndrome • Nephrocalcinosis • Renal insufficiency
Source:Kliegman
R,et al.NelsonTextbook
of Pedialrics(21sted).Elsevier;2020
409
III. MANAGEMENT& PROGNOSIS
• Bicarbonate replacement is the mainstay of therapy in all forms of RTA
0 Proximal RTAoften require bicarbonate ofup to 20 mEq/kg/day (e.g., sodium
bicarbonate or sodium citrate solution)
0 Distal RTAbase requirement is generally in the range of 2-4 mEq/kg/day and
requires monitoring for the development of hypercalciuria. Those with symptomatic
hypercalciuria, nephrocalcinosis, or nephrolithiasis may require thiazides to decrease
urine calcium excretion.
• Patients with Fanconi syndrome usually require phosphate supplementation
• Patients with type IV RTAcan require chronic treatment for hyperkalemia with sodium-
potassium exchange resin
• Prognosis of RTAlargely depends on the nature of any existing underlying disorder
• Those with treated isolated proximal or distal RTAgenerally show improvement in
growth as long as bicarbonate levels are maintained in the normal range
REFERENCES
1. Ammenti A, Cataldi L, Chimenz R, Fanos V, La Manna A, Marra G, et al., Italian Society of
Pediatric Nephrology. Febrile urinary tract infections in young children: recommendations for
the diagnosis, treatment and follow-up. Acta Paediatr 2012;101(5):45 le7.
2. Avner E, et al. Pediatric Nephrology 7th ed. 2016 Springer USA
3. Engorn, B., and Flerlage, j. The Harriet Lane Handbook 20th ed. 2015. Philadelphia: Elsevier.
4. Hemolytic Uremic Syndrome, Post-diarrheal I 1996 Case Definition. 2018. Available from
h ttps: / / wwwn .cdc.gov / nndss /conditions/hem o lyti c-u remi c-syn d ro me-post-diarrheal/
case-definition/1996/
5. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group.
KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2 :
1-138.
6. Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group. KDIGO
Clinical Practice Guideline for Glomerulonephritis. Kidney inter., Suppl. 2012; 2: 139-274.
7. Kliegman, R., Stanton, 8., St. Geme, j., Schor, N., and Behrman, R.. Nelson Textbook of Pediatrics
21st ed. 2020. Canada: Elsevier.
B. Kuma1; Vinay, Abu! K. Abbas, and Jon C.Aster. Robbins and Cotran Pathologic Basis of Disease.
Ninth edition. 2017 Philadelphia, PA: Elsevier/Saunders
9. Miliku, K.,Bakker, H., Dorresteijn, E., Crans berg, K., Franco, 0., Felix, j., and jaddoe, V.Childhood
Estimates ofGlomerular Filtration Rate Based on Creatinineand Cystatin C: Importance ofBody
Composition.American journal ofNephrology, 2017 45( 4), 320-326. doi: 10.1159/000463395
10.National Institute for Health and Care Excellence. Urinary tract infection in under 16s:
diagnosis and management. 2007. Available from: https://www.nice.org.uk/guidance/
cg54/ evidence/full-guideline-pdf-196566877
11.National Kidney Foundation: KDOQI clinical practice guidelines for chronic kidney disease:
evaluation, classification, and stratification, Am j Kidney Dis 39(2 Suppl 1):sl-s266, 2002.
12.Phadke, K., Goodyer, P., and Bitzan, M. (2014). Manual of Pediatric Nephrology. London:
Springer.
13.Consensus Statements on Parenteral Fluid Therapy in Infants, Children and Adolescents.
Task Force on Fluid and Electrolyte Therapy. Philippine Pediatric Society, Inc. 2017
14.Urinary Tract Infection: Clinical Practice Guideline for the Diagnosis and Management of
the Initial UTI in Febrile Infants and Children 2 to 24 Months .. PEDIATRICS, 2011, 128(3),
595-610. doi: 10.1542/peds.2011-1330
15.Weening, j. The Classification of Glomerulonephritis in Systemic Lupus Erythematosus
Revisited. journal of The American Society of Nephrology, 2004, 15(2), 241-250. doi:
10.1097 /Ol.asn.0000108969.21691.5d
16.Welch, T. An Approach to the Child with Acute Glomerulonephritis. International journal of
Pediatrics, 2012, 1-3. doi: 10.1155/2012/426192
410
ENDOCRINOLOGY
SECTION ONE
OISORDER'S OF THE HVPOTH·ALAMl)S & PITUITARY GLAND
HORMONES DESCRIPTION
Luteinizing hormone • Promotes luteinization of the ovary and Leydig cell function of
(LH) the testis
Follicle-stimulating • Stimulates follicular development in the ovary and
hormone (FSH) gametogenesis in the testis
HYPOPITUITARISM
I. ETIOPATHOGENESIS
• Deficiency of growth hormone with or without a deficiency of other pituitary hormones
• Congenital: if with severe defect of GH production or action, height will fall >4 SD below
the mean for length by 1 year old
• Acquired: child is normal initially and manifestations gradually appear and progress
II. MANIFESTATIONS
• Severe growth failure, tendency for hypoglycemia, micropenis, prolonged neonatal jaundice
• Short & broad face, prominent frontal bone, depressed nasal bridge, saddle-shaped nose,
underdeveloped mandible, short neck, high-pitched voice, well-proportioned extremities
I
but small hands & feet, delayed or absent sexual maturity
• Acquired: atrophy of adrenal cortex, thyroid & gonads result in weight loss, asthenia,
sensitivity to cold, and absence of sweating
413
DIFFERENTIALS FOR
SHORT STATURE DESCRIPTION
• Height is initially within normal range that starts falling off the
height curve over time
Pathologic Short • Delayed bone age
Stature • Possible causes: Prenatal onset (maternal infections and
undernutrition, chromosome defects) & postnatal onset (nutritional
deficiency, chronic systemic disease, psychosocial deprivation)
• Height is sustained at lower percentiles during childhood
• Hallmark finding: delayed pubertal growth spurt
Constitutional • Eventual normal final adult height is reached (catch-up growth
Growth Delay occurs late adolescence)
• Often with history of similar growth pattern with family members
• Delayed bone age (chronologic age > bone age)
• Stays parallel to the growth curve
Familial Short
• Significant number of family members who are short
Stature
• Bone age is not delayed (chronologic age = bone age)
Source:KliegmanRM,et al. NelsonTextbook of Pediatrics(21sted)Elsevier;2020
LifshitzF,el al. (5thEd.).PediatricEndocrinology.
lnformaHealthcare;2007
III. DIAGNOSIS
A. Examination
Diagnosis is suspected with severe postnatal growth failure defined as any of the following:
0 Height< 1st percentile for age and sex
0 Height> 2 SD below sex-adjusted mid-parental height
Height velocity is low relative to sex- and bone age-matched peers
See Growth and Development Chapter for proper height determination
B. Diagnostic Tests
• Absent or low levels of GH in response to stimulation or
provocative test (e.g., rapid administration of insulin, arginine,
clonidine, levodopa, or glucagon)
Definitive
Diagnosis • Always assess thyroid function prior to provocative GH test as it
is a prerequisite for normal GH synthesis
• Necessary to examine other pituitary functions (TSH, T3, T4,
cortisol, ACTH,gonadotropins, gonadal steroids)
• Delayed skeletal maturation / bone age
Radiologic
Findings • Small anterior pituitary gland
• Suprasellar calcification (if associated with craniopharyngioma)
Source:KliegmanRM,el al. NelsonTextbook
of Pediatrics
(21sted)Elsevier;2020
RogolAD,el al. J Pediatr;2014
IV. MANAGEMENT
Human Growth • Should be started as soon as diagnosis is made
Hormone (hGH) • Maximal response occurs in the 1" year of therapy with growth
Treatment Guide velocity usually above the 9S'h percentile for age
• Decision by the patient that he/she is tall enough
Criteria for stopping
treatment • Growth rate <l inch/year
• Bone age >14 years in girls & >16 years in boys
Source:RogolAD,et al. J Pediatr;2014
KliegmanRM,et al. NelsonTextbook
of Pediatrics
(21sted) Elsevier;2020
414
HYPERPITUITARISM
I. ETIOPATHOGENESIS
• Overproduction of GH leads to:
Gigantism if occurring among young patients with open epiphyses
0 Acromegaly if with closed epiphyses
II. MANIFESTATIONS
GlGANTlSM ACROMEGALY
IV. MANAGEMENT
• If with well-circumscribed pituitary adenomas: transsphenoidal surgery (complete
removal of the tumor)
• Pituitary irradiation if with local invasion, involvement of optic chiasm/nerve, or
unsuccessful surgery
• Octreotide (somatostatin analog) for GH suppression, pegvisomant [GH receptor antagonist)
Source:KliegmanRM,et al. NelsonTextbookof Pediatrics(21sted) Elsevier;2020
RootAW.PediatricEndocrinology; 2007
I
• Cardinal features: polyuria and polydipsia (exceeding 2 L/m 2 /24hr)
Request for the following:
, Serum osmolality
BUN, creatinine, Na', K·, Ca2 •
Glucose
Urine osmolality, specific gravity, urine glucose
• DI is established if serum osmolality is >300 mOsm/kg & urine osmolality <300 mOsm/kg
• For patients with serum osmolality >270 but <300 mOsm/kg, perform water deprivation
test to establish diagnosis and differentiate central from nephrogenic DI
415
III. DIFFERENTIAL DIAGNOSIS
SYNDROMEOF
INAPPAPROPRIATE
CEREBRAL
SALT NEPHROGENIC
PARAMETER ANTIDIURETIC CENTRAL DI
HORMONE
WASTING DI
SECRETION(SIADH)
(CSW)
• Congenital
• Congenital
• Hypercalcemia, hypokalemia
• Trauma (deceleration injury)
• Renal disease (polycystic kidney
• Tumors (craniopharyngioma,
disease, chronic renal failure,
lymphoma, leukemia)
acute tubular necrosis, obstructive
• Autoimmune
uropathy)
Etiology • Infection (meningitis, TB)
• Drugs (lithium, cisplatin,
• Drugs (ethanol, phenytoin,
methoxyflurane, demeclocycline)
opiate antagonists, alpha-
• Infiltrating lesions
adrenergic agents)
• Vascular (sickle cell anemia)
• Vascular (bleed or infarction)
• Solute diuresis (glucose, mannitol, Na.,
• Idiopathic in 10%
radiocontrast dyes)
• Treat underlying disorder
• Fluid therapy
• Thiazides (decrease overall urine
• Long-acting vasopressin
output by enhancing Na' excretion
analog DDAVP
at the expense of water & by causing
• Acute onset after
Management decrease in GFR)
neurosurgery: vasopressin
• Indomethacin and amiloride +/-
with total fluid intake
thiazides to further reduce polyuria
limited to 1 L/m 2/day during
• Ensure intake of adequate calories for
antidiuresis
growth & to avoid severe dehydration
Source:KliegmanRM,et al. NelsonTextbook of Pediatrics(21sted)Elsevier;2020
LifshitzF.et al. (5thEd.).PediatricEndocrinology.
lnformaHealthcare;
2007
JohnCA,et al. GritCareNurse;2012
416
PRECOCIOUS PUBERTY
I. ETIOPATHOGENESIS
• Onset of secondary sexual characteristics (breast development or testicular development)
before 8 years old in girls & 9 years old in boys
• Classification based on primary source of hormonal production:
I
• Infrequently may progress to precocious puberty
• Early appearance of pubic hair
Premature • Early increase in adrenal androgen production
pubarche/ • Increased prepubertal growth velocity but decreased pubertal
adrenarche growth, so adult height is not affected
• May herald disorders of androgen synthesis
HORMONES DESCRIPTION
• Increases oxygen consumption and basal metabolism
• Affects growth, differentiation, carbohydrate and lipid metabolism
Thyroid • Three forms:
hormones , Thyroxine (T4): prohormone
0 Triiodothyronine (T3): active form
, Reverse T3 (rT3): inactive form
• Secreted by the thyroid gland
Thyroxine (T4)
• ~70% is bound to thyroxine-binding globulin (TBG)
• Active form of thyroid hormone (3-4x more potent than T4)
Triiodothyronine
• Only 20% is secreted by the thyroid gland, majority is produced by
(T3)
deiodination ofT4 in the peripheral tissues
• Synthesized by the chief cells of the parathyroid gland
Parathyroid
• Stimulated by hypocalcemia
hormone (PTH)
• Increases serum Ca2 • and lowers serum PO4
• Promotes calcium & phosphate absorption from the small intestines,
VitaminD reabsorption from the kidneys and deposition to the bones
• Increases serum Ca2 ' and serum PO4
• Synthesized by the parafollicular cells of the thyroid gland
Calcitonin • Inhibits osteoclast activityleading to decreased resorption of Ca2' from bone
• Calcitonin levels increase in response to hypercalcemia
Source:KliegmanRM,et al. NelsonTextbookof Pediatrics(21sted) Elsevier:2020
KoeppenBM,Berne& LevyPhysiology. Mosby/Elsevier;2010
HYPERTHYROIDISM
• Excessive secretion of thyroid hormone
• During childhood, the most common cause is Graves disease (at least 95% of cases)
I. GRAVES DISEASE
A. Etiopathogenesis
0 Autoimmune disorder: production of thyrotropin receptor-stimulating antibody (TRSAb)
Females> males (5:1 ratio)
Most common cause of pediatric hyperthyroidism
B, Manifestations
SYMPTOMS SIGNS
418
C. Diagnosis
DIAGNOSTIC FINDINGS/REMARKS
D.Management
1 !
, ,
METHIMAZOLE /
DRUG PROPYLTHIOURACIL (PTU)
CARBIMAZOLE
3. Complications of Therapy
Radiofrequency ablation: might worsen ophthalmopathy
Thyroidectomy: recurrent laryngeal nerve damage, hypoparathyroidism
0
419
II. THYROID STORM
• Acute-life-threatening surge of thyroid hormone in the blood usually precipitated by
surgery, trauma, infection. or radioactive iodine treatment
• Fever, tachycardia, high output cardiac failure, gastrointestinal dysfunction (vomiting,
diarrhea, jaundice), neurologic changes (confusion, agitation, obtundation)
• With rapid progression to delirium, coma, and death
GOAL MANAGEMENT
• Propylthiouracil
Inhibition of thyroid • Saturated solution of potassium iodide (used only after
hormone formation and
secretion PTU has been administered to avoid potential increase in
thyroid hormone synthesis)
HYPOTHYROIDISM
• Due to deficient production of hormone or a defect in hormonal receptor activity
• May be congenital or acquired
I. CONGENITALHYPOTHYROIDISM
A. Etiopathogenesis
Thyroid dysgenesis (aplasia, hypoplasia, ectopia): most common cause of congenital
hypothyroidism
0 Dyshormonogenesis (defect in thyroid hormone synthesis)
TSH unresponsiveness
Endemic goiter (iodine deficiency)
0 Maternal antibodies: thyrotropin receptor-blocking antibody (TRBAb)
0 Maternal medications (e.g., PTU, methimazole, iodide, amiodarone, radioiodine)
B. Manifestations
SYMPTOMS SIGNS
C. Diagnosis
DIAGNOSTIC FINDINGS/REMARKS
• Elevated serum TSH
Serum TSH
• Used in screening tests
• Low serum T4 and free T4
SerumT4
• No need to measure T3 (normal in many patients with hypothyroidism)
• Thyroid scintigraphy can determine underlying cause and show
ectopic gland (this establishes need for lifelong treatment)
Thyroid
• Thyroid ultrasound documents absence or presence of an
imaging
anatomically normal gland
• Rarely needed, treatment should not be delayed to request for imaging
420
D.Management
• Treatment of choice: oral levothyroxine (10-15 mcg/kg/day once daily for 0-3 months old)
Normalization of thyroid function ideally within 2 weeks is vital in achieving optimal
neurodevelopmental outcome
• Regular monitoring of hormone levels: every 1-2 months in the 1st 6 months of life
then every 2-4 months between 6 months and 3 years of age
A. Etiopathogenesis
• Organ-specific autoimmune disease characterized histologically by lymphocytic
infiltration between the thyroid follicles and presence of lymphoid germinal centers
• Thyroid anti-peroxidase antibodies (TPO-Abs) & thyroglobulin antibodies (Tg-Abs) in 95%
More common in girls
8. Manifestations
• Most common manifestation: goiter (diffusely enlarged, firm, nontender thyroid) and
growth deceleration
• Most of the affected children are clinically euthyroid & asymptomatic
Variable clinical course
C. Diagnosis
DIAGNOSTIC FINDINGS/REMARKS
D.Management
May be self-limited (spontaneous regression) or may persist for years while the
patient remains euthyroid
If with thyrotoxicosis, address the thyroid tenderness with NSAIDs or a short course of
steroids if with severe pain; beta-blockers to alleviate palpitations I·-,_
0 Periodic re-evaluation every 6-8 weeks for early detection & treatment of hypothyroidism
CONDITION MANAGEMENT
If with evidence of
• Give levothyroxine ( age-specific dose)
hypothyroidism
If with subclinical • May give levothyroxine until growth and puberty are complete
hypothyroidism (still controversial)
421
SECTION THREE
DISORDERS OF THE ADRENAL GLAND AND GONADS
CONGENITAL ADRENAL HYPERPLASIA (CAH)
I. ETIOPATHOGENESIS
• Autosomal recessive disorders of cortisol synthesis leading to increased secretion of ACTH
(corticotropin) causing adrenocortical hyperplasia & overproduction of metabolites
• Deficiency of 21-hydroxylase accounts for 90% of affected patients
0 Lackof 21-hydroxylase causes excess substrates shunted towards synthesis of sex ho1111ones
II. MANIFESTATIONS
TYPES OF
21-HYDROXYLASE MANIFESTATIONS
DEFICIENCY
• 70% of patients with classic 21-hydroxylase deficiency
• Weight loss, anorexia, nausea, vomiting, weakness, salt craving
Salt-losing, classic • Dehydration, hypotension, skin hyperpigmentation
form • Hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis
• Symptoms appear at 10-14 days of age
• Signs of virilization (see below)
• 30% of patients with classic 21-hydroxylase deficiency
• Signs of virilization:
° Female infants: Ambiguous genitalia/masculinized external
Simple virilizing, genitalia (clitoral enlargement, labial fusion, urogenital sinus)
classic form 0Male infants: appear normal at birth. Postnatal signs of androgen
excess include rapid somatic growth, accelerated skeletal
maturation, stunting, pubic & axillary hair, acne, deep voice,
enlarged penis, scrotum & prostate but prepubertal testes
• Attenuated, late-onset form of adrenal hyperplasia
Non-classic form • May be asymptomatic, or may have precocious adrenarche,
hirsutism, acne, menstrual irregularity, infertility
III. DIAGNOSIS
DIAGNOSTIC FINDINGS/REMARKS
IV. MANAGEMENT
• Glucocorticoids inhibit excessive production of androgens & prevent progressive virilization
Hydrocortisone 15-20 mg/m2/day orally in 3 divided doses
0 Double or triple doses during periods of stress (surgery, infection)
Continued indefinitely in all patients with classic 21-hydroxylase deficiency
Monitor growth & hormonal levels
• Fludrocortisone as mineralocorticoid replacement+ NaClsupplementation for salt-losing disease
• Surgery for ambiguous genitals
II. MANIFESTATIONS
• Muscular weakness, malaise, anorexia, nausea, vomiting, weight loss, orthostatic
hypotension, salt craving
• Increased skin pigmentation more prominent in skin creases, mucosa and scars
• Acute decompensation (adrenal crisis) during relatively minor infectious illnesses
DIAGNOSTIC FINDINGS/REMARKS
Ill. MANAGEMENT
• D5 0.9 NSS IV:to correct hypoglycemia, hypovolemia, hyponatremia
• Hydrocortisone succinate:
For Acute 0 IVbolus, then divided doses every 6 hours for 1" 24 hours (SOmg/m 2 IV bolus
Adrenal then 25-100 mg/m 2/day as IVinfusion or in divided doses eve1y 6 hours), or
Insufficiency 0 As much as 10 mg for infants, 25 mg for toddlers, 50 mg for older children,
and 100 mg for adolescents administered as bolus, and similar amount in
divided doses every 6 hours for the first 24 hours
• Hydrocortisone 10 mg/m 2 /day in 3 divided doses, or equivalent doses of
prednisone twice daily
-. Fludrocortisone if with aldosterone insufficiency
Chronic
• Monitor ACTHlevels
Replacement
• Prevention of adrenal crisis:
Therapy
0 Increase hydrocortisone dose 2-3 fold during stress (infection/surgery)
423
CUSHING SYNDROME
I. ETIOPATHOGENESIS
• Result of abnormally high blood levels of cortisol or other glucocorticoids
• Most common cause: prolonged exogenous administration of glucocorticoid hormones
• In children >6 years old, endogenous Cushing syndrome is most commonly caused by
ACTH-secreting pituitary tumor (known as Cushing disease)
• In children <6 years old, adrenal causes are more common causes
II. MANIFESTATIONS
COMMON MANIFESTATIONS IN OLDER CHILDREN
• Rounded face
• Purplish striae on hips, abdomen & thighs
• Prominent cheeks
• Delayed puberty
• Moon facies
• Emotional !ability
• Buffalo hump
• Weakness
• Generalized obesity
• Headache
• Abnormal masculinization
• Hyperglycemia which may progress to diabetes
• Impaired growth
• Osteoporosis
• Hypertension
• Susceptibility to infection
Ill. DIAGNOSIS
DIAGNOSTIC FINDINGS/REMARKS
• Loss of circadian rhythm of cortisol (normally, serum cortisol levels are
highest at 8 am & decrease to <50% by midnight)
Cortisol Levels • Salivary cortisol screening test is a good outpatient screening test
0 Salivary cortisol levels reflect the unbound, biologically active serum cortisol
• Midnight cortisol levels >4.4 mcg/dL suggests diagnosis of Cushing syndrome
424
IV. MANAGEMENT
MODALITY REMARKS
Transsphenoidal
• Treatment of choice in Cushing disease
Pituitary Microsurgery
Adrenalectomy
.•• For pituitary adenomaunresponsive to treatment, aldosterone-
producing adenoma and ectopic ACTH-secreting metastatic tumor
PHEOCHROMOCYTOMA
I. ETIOPATHOGENESIS
• Catecholamine-secreting tumor arising from chromaffin cells
• Most common site of origin: adrenal medulla
• Tumors may develop anywhere along the abdominal sympathetic chain
• Tumors found more often on the right side, but bilateral in >20% affected children
• May be associated with genetic syndromes such as von Hippel-Lindau disease, neurofibromatosis,
MEN2Aand MEN28 syndromes, tuberous sclerosis, Sturge-Weber syndrome, ataxia-telangiectasia
II. MANIFESTATIONS
• Hypertension (more often sustained than paroxysmal in children)
• Headache, palpitations, abdominal pain, dizziness, pal lot; vomiting, sweating, convulsions
• May be symptom-free in-between attacks of hypertension
• Polyuria, polydipsia, growth failure
Severe disease: precordial pain radiating into arms, pulmona1y edema, cardiomegaly, hepatomegaly
III. DIAGNOSIS
DIAGNOSTIC FINDINGS/REMARKS
• Elevatedblood or rnina1y levels of catecholamines (e.g.,dopamine, norepinephrine,
epinephrine) & metabolites (e.g., normetanephrine, metanephrine)
• Predominant catecholamine excreted in urine among children is norepinephrine
Catecholamine
• Best sensitivity & specificity: measurement of plasma normetanephrine
levels
• Urinary excretion ofvanillylmandelic acid (VMA) is increased, but no
longer routinely used due to false-positive results from consumption of
I
vanilla-containing food
• CT,MRI, 123 !-metaiodobenzylguanidine: to localize tumor
Imaging • 85% of tumors are found in adrenal glands, 95% are within the abdomen
and pelvis
IV. MANAGEMENT
• Surgical removal of tumors
• Preoperative a & ~-adrenergic blockade and fluid loading
• Transabdominal exploration of all the usual sites because tumors are often multiple
NOONAN KLINEFELTER
PARAMETER TURNER SYNDROME
SYNDROME SYNDROME
426
SECTION FOUR
DIABETES MELLITUS
MATURITY-ONSET
TYPE TYPE 1 DM TYPE2 DM DIABETES OF THE
YOUNG (MODY)
• Adult-onset DM
Formerly • Insulin-dependent DM
• Non-insulin-
called • juvenile diabetes
dependent DM
• Insulin resistance
• Defect in insulin
atthe level of
secretion from
skeletal muscle,
• Autoimmune genetic mutations
liver, adipose tissue
Etiology destruction of involving
• Obesity is the most
pancreatic islet cells pancreatic/liver
important lifestyle
glucokinase or
factor associated
trans~ription factors
with T2DM
• Most common
endoc1ine-metabolic • Acanthosis • Autosomal
disorder in children nigricans (dark dominant
• Low or absent levels of pigmentation of inheritance
Characteristics
endogenous insulin skin crease at • Ketoacidosis is
• Dependence on nape) is a sign of rare
exogenous insulin to insulin resistance
prevent ketoacidosis
Family history • infrequent • Strong familyhistory • Strong familyhistory
• Peaks at 5-7 years old, • Incidence • Occurs before 25
Age at onset
puberty increases with age years of age
• Insulin therapy • Metformin: the
• Glucose monitoring only FDA approved
• Nutritional: 55% CHO, oral agent for • Depends on
I' 30% fat, 15% protein T2DM in children subtype
• Limit intake of sucrose • Lifestyle: low- • MODY3
& highly refined sugars calorie, low-fat (most common):
Management • Polyunsaturated: diet, physical sulfonylurea
saturated fat ratio ofl.2:1 activity 30-60 • MODY2(second
• <10% of calories from minutes, at least 5 most common):
1,
1,
saturated fats, up to 10%
from polyunsaturated
fats, the rest from
monounsaturated fats
times/week, and
limit screen time
1-2 hours/day
no treatment or
low dose insulin
I
II. MANIFESTATIONS
• Polydipsia, polyuria, nocturia
• Unexplained weight loss with glucosuria and ketonuria
• Monilial vaginitis among female patients from chronic glycosuria
Hyperphagia
• Weight loss
• Symptoms ofketoacidosis (see DKAsection below)
427
III. DIAGNOSIS
IMPAIRED FASTING
GLUCOSE (IFG)/ IMPAIRED DIABETES MELLITUS
GLUCOSE TOLERANCE (IGT)
• 100-125 mg/dL (5.6-7.0
Fasting Glucose • 2'126 mg/dL (7.0 mmol/L}
mmol/L}
2-hour Plasma • ;,140 mg/dL but <200 mg/dL
• 2'200 mg/dL (2'11.l mmol/L)
Glucose (OGTT) (2'7.8 but <11.1 mmol/L)
• Symptoms of DM + random
Others blood glucose 2'200 mg/dL
(2'11.1 mmol/L)
'Thesevaluesareusedtoclassify
prediabetes
amongadults.Itsutilityindiagnosing
prediabetes
amongchildren
isstillbeingstudied
II. MANIFESTATIONS
• Abdominal discomfort or pain, nausea, emesis
• Tachypnea, tachycardia
• Fruity breath odor (from acetone)
• Kussmaul respiration (deep, heavy, nonlabored rapid breathing)
• Polyuria, dehydration
• Diminished neurocognitive function, confusion, drowsiness, possible coma
• Progression of symptoms may be accelerated during illness or trauma
428
JII. DIAGNOSIS
A. Biochemical Criteria for Diagnosis of OKA
0 Hyperglycemia (blood glucose> 11 mmol/L or >200 mg/dL)
Venous pH <7.3 or serum bicarbonate <15 mmol/L
Ketonemia (blood beta-hydroxybuyrate 2:3 mmol/L) or moderate/large ketonuria (2:2+)
IV. MANAGEMENT
ASPECT MANAGEMENT
• Resuscitation fluids:
If volume depleted but not in shock: 10 mL/kg IVof0.9% saline over 30-
0
Bicarbonate
(HC03 )
Therapy
concurrent with insulin therapy
• Rarely neeeded (may even increase risk ofhypokalemia & cerebral edema)
• Administer (1-2 mmol/kg over 60 minutes) only if with:
Life-threatening hyperkalemia
0
I
Severe acidosis (venous pH <6.9)
0
429
• Vital signs, neurologic status, fluid input and output, capillary blood
Monitoring glucose hourly or more frequently as needed
• Electrolytes & blood gas every 2-4 hours or more frequently as needed
• Transition to oral intake & subcutaneous insulin upon resolution of OKA:
• HCO3>15 mEq/L
Transition
• pH >7.30
care
• Sodium 135-145 mEq/L
0 No emesis
Source:KliegmanRM.et al. NelsonTextbookof Pediatrics(21sted) Elsevier;2020
WolfsdortJI, et al. ISPAD,PediatrDiabetes;2018
REFERENCES
1. Abraham P, Avenell A, Park CM, Watson WA and Bevan JS. (2005). A systematic review of drug therapy for
Graves' hyperthyroidism. Eur J Endocrinol, 153, 489-498.
2. Ali 0. Hyperpituitarism, Tall Stature, and Overgrowth Syndromes. In Kliegman RM, Stanton BF, St Geme JW,
Schor NF. (Eds.) (2016) Nelson Textbook of Pediatrics (20th ed.). Philadelphia, PA: Elsevier.
3. American Diabetes Association Standards of Medical Care in Diabetes. (2016). Classification and diagnosis
of diabetes. Diabetes Care, 39(Suppl.1), S13-S22.
4. Breault OT and Majzoub JA. Diabetes lnsipidus. In Kliegman RM, Stanton BF, St Geme JW, Schor NF. (Eds.)
(2016) Nelson Textbook of Pediatrics (20th ed.). Philadelphia, PA: Elsevier.
5. Brook CGD,Brown RS.(2008) Handbook of Clinical Pediatric Endocrinology. Massachusetts: Blackwell Publishing.
6. Charmandari E, Nicolaides NC, and Chrousos GP. (2014). Adrenal insufficiency. Lancet, 383, 2152-2164.
7. Craig ME, Hattersley A and Donaghue KC.(2009). Definition, epidemiology and classification of diabetes in
children and adolescents. Pediatric Diabetes, lO(Suppl.12), 3-12.
8. John CA, Day MW. (2012). Central Neurogenic Diabetes lnsipidus, Syndrome of Inappropriate Secretion of
Antidiuretic Hormone, and Cerebral Salt-Wasting Syndrome in Traumatic Brain Injury. Crit Care Nurse, 32(2), el-e7.
9. Grim berg A and Lifshitz F. Worrisome Growth. In Lifshitz F. (Ed.) (2007) Pediatric Endocrinology. New York:
lnforma Healthcare.
10.Parks JS and Felnor El. Hypopituitarism. In Kliegman RM, Stanton BF, St Geme JW, Schor NF. (Eds.) (2019)
Nelson Textbook of Pediatrics (21st ed.). Philadelphia, PA: Elsevier:
11.Kliegman RM, Stanton BF, St Geme JW, Schor NF. (2020) Nelson Textbook of Pediatrics (21st ed.).
Philadelphia, PA: Elsevier.
12.Koeppen, B. M., Stanton, B. A. (2010). Berne & Levy Physiology. Philadelphia, PA: Mosby/Elsevier.
13. Leger J. Graves Disease in Children. In Szinnai G (Ed.) (2014) Paediatric Thyroidology. Endocr Dev. Basel: Karger.
14.Lietman SA, Germain-Lee EL, and Levine MA. (2010). Hypercalcemia in children and adolescents. Curr Opin
Pediatr, 22, 508-515.
15.Lee PA and Houk CP.Puberty and Its Disorders. In Lifshitz F. (Ed.) (2007) Pediatric Endocrinology. New York:
lnforma Healthcare.
16. Lifshitz F. (Ed.) (2007) Pediatric Endocrinology. New York: lnfonna Healthcare.
17.Lodish MB, Keil MF, Stratakis CA. (2018). Cushing's Syndrome in Pediatrics: An Update. Endocrinol Metab
Clin N Am, 47, 451-462.
18.Nowicka P, Santoro N, Liu H, et al. (2011). Utility of hemoglobin ale for diagnosing prediabetes and diabetes
in obese children and adolescents. Diabetes Care, 34(6), 1306-1311.
19.Rogol AD and Hayden GF. (2014). Etiologies and early diagnosis of short stature and growth failure in
children and adolescents.) Pediatr, 164(5), S l-S14.
20.Root AW, Diamond Jr FB. Disorders of mineral homeostasis in children and adolescents. In: Sperling MA.
(Ed.) (2014) Pediatric endocrinology. Philadelphia: Elsevier.
21.Svoren BM and Jospe N. Diabetes Mellitus. In Kliegman RM, Stanton BF,St Geme JW, Schor NF. (Eds.) (2016)
Nelson Textbook of Pediatrics (20th ed.). Philadelphia, PA: Elsevier.
22.Thanabalasingham G, Owen KR. (2011). Diagnosis and management of maturity onset diabetes of the young
(MODY]. BM), 343,838.
23.Tschudy MM, Arcara KM. (Eds.) (2012) The Harriet Lane handbook: a manual for pediatric house officers
(19th ed.). Philadelphia, PA: Mosby Elsevier:
24.Tsirlin A, Oo Y, Sharma R, Kansara A, Gliwa A, Banerji A. (2014). Pheochromocytoma: A review. Maturitas,
77, 229-238.
25.Vijayakumar P, Nelson RG, Hanson RL, et al. (2017). HbAlc and the prediction of type 2 diabetes in children
and adults. Diabetes Care, 40, 16-21.
26. White PC. Congenital Adrenal Hyperplasia and Related Disorders. In Kliegman RM, Stanton BF, St Geme )W,
Schor NF. (Eds.) (2016) Nelson Textbook of Pediatrics (20th ed). Philadelphia, PA: Elsevier:
27.Wolfsdorf JI, Glaser N, Agus M, Fritsch M, Hanas R, Rewers A, et al. (2018). Diabetic Ketoacidosis and
Hyperglycemic Hyperosmolar State: A Consensus Statement from the International Society for Pediatric and
Adolescent Diabetes. Pediatr Diabetes, doi: 10.1111/pedi.12701.
430
NEUROLOGY
SECTION ONE
APPROACH "FOPATIENTS WITH NEUROLOGIC COMPLAINTS
NEUROLOGIC EXAMINATION
I.HEAD
• Head circumference
0Serial monitoring to detect hydrocephalus or microcephaly
See Chapter 2 for measurement and interpretation of head circumference
0
• Fontanelles
Anterior fontanelle -- diamond-shaped, around 2x2 cm, and closes at 9-18 months
0Posterior fontanelle -- admits tip of finger and closes at 6-8 weeks (may be closed
at birth)
II. GLASGOWCOMASCALE
Sample Case
A 13 year-old boy was brought to the Emergency Room after sustaining injuries from a
bicycle accident. On assessment, he has eye opening when his name is called, responds
confusedly to questions, and localizes to pain. What is his GCS score?
• To compute for his GCSscore, identify the score for each of the 3 components
Eye opening (to voice)= 3 points
0
434
IV. MOTOREXAMINATION
A. General
Check for atrophy (decreased muscle bulk) or hypertrophy (increased muscle bulk)
° Check for abnormal movements such as fasciculations, tics, dystonia, chorea, athetosis
B. Muscle Tone
28 weeks: all 4 extremities are extended
0 32 weeks: flexor tone in lower extremities
36 weeks: flexor tone in upper extremities
Normal term: flexion of all 4 extremities
Neonates: postural tone
MUSCLE TONE REMARKS
• Examiner grasps infant's hands & pulls infant to sitting position
Traction
• Normal: head lags slightly behind body and then falls
Response
forward upon reaching sitting position
Postural • Examinerholds inrant by axillawithout grtppingthe thorax
Vertical
Tone in • Normal: infant remains suspended, lower extremity held in flexion
Suspension
Neonates • Hypotonic infant slips through the examiner's hands
• Examiner holds infant prone by placing hand under abdomen
Horizontal
• Normal: head rises, limbs flex
Suspension
• Hypotonic infant drapes over the hands and forms a U shape
• Initial resistance to passive motion followed by sudden release (clasp-knife
Spasticity phenomenon)
• Upper extremity flexors & lower extremity extensors usually affected
• Basal ganglia lesions
Rigidity
• Resistance to passive movement equal in flexor & extensors (lead pipe)
C. Muscle Strength
SCORE DESCRIPTION
0 • No contraction
5 • Normal power
V. SENSORYEXAMINATION
• Often difficult to perform in young children
• Isolated disorders of sensory system are less common in children
VI. REFLEXES
A. Deep Tendon Reflexes
Infants younger than 3 months can have 5-10 clonus
Older children can have 1-2 beats of clonus
1 + to 3+ reflex may be normal as long as symmetrical
Babinski: extension of great toe, fanning out of remaining toes
Weakness + +
Atrophy - +
Fasciculation - +
Reflex Increased Decreased
BC . CSF A
PRESSURE PROTEIN GLUCOSE LEUKOCYTES
(mmH2O) (mg/dL) (mg/dL) (mm')
1} Normal CSF(beyond the neonatal period)
• >50 mg/dL, or
• <5 mm3
• 50-80 mmH 2 0 • 20-45 mg/dL >75% of serum
• 75% lymphocytes
glucose
2) Bacterial Meningitis
• <40 mg/dL, or • Elevated (100 to
• Elevated (100-
• ;,100 mg/dL • <50% of >10,000 mm 3)
300 mmH 2 0)
serum glucose • PMN predominance
4) Viral Meningitis
• Rarely > 1,000 mm 3
• Normal to slightly • PMN predominance
• Commonly
elevated • 50-200 mg/dL early on, then
normal
(80-150 mmH 2 0) mononuclear through
most of the course
SJ Tuberculous Meningitis
• 10-500 mm 3
• Commonly • PMN predominance
• Commonly • Very high
decreased early on, then
elevated • 100-3,000 mg/dL
(<50 mg/dL) lymphocytes through
most of the course
Source:KliegmanR.et al. NelsonTextbookof Pediatrics(21sted). Elsevier:
2020
MenkesJ. et at ChildNeurology(7thed.).LippincottWilliams& Wilkins;2006
I
437
SECTION TWO
CONGENITAL ANOMALIES OF THE CNS
DIAGNOSTIC REMARKS
Ill. MANAGEMENT
• Prenatal screening of maternal serum for AFP in the 16th-18th week of gestation:
identifies pregnancies at risk for fetuses with neural tube defects (NTD) in utero
Prevention
• Maternal periconceptual use of folic acid (0.4 mg OD) reduces its incidence
{stmtedbeforeconceptionuntilat leastdie 12" weekofgestationwhenneu111lation
iscomplete)
• Immediate surgery is indicated for CSFleaks to prevent complications:
Surgery • Repair of myelomeningocele
• Shunting procedure for hydrocephalus
• With aggressive treatment, there is a 10-15% mortality rate
Prognosis
• 70% of survivors have normal intelligence
Sources:KliegmanR.et al. NelsonTextbook of Pediatrics
(21sted).Elsevier;2020
MenkesJ, et al. ChildNeurology(7thed.).LippincottWilliams& Wilkins;2006
FenichelG. et al. ClinicalPediatricNeurologyA signsandsymptoms approach(6thed).Elsevier;2009
WilliamsH, et al.Archivesof Diseasein Childhood• Education andPractice;2009
HYDROCEPHALUS
I. ETIOPATHOGENESIS
A. Physiology
CSF is produced in the choroid plexus epithelium within the cerebral ventricles
CSF is re-absorbed in the arachnoid villus cells (located in the superior sagittal
sinus) and returned to the bloodstream within vacuoles (via pinocytosis)
3rd ventricle
Foramen of Magendie
I
Central canal of the spinal cord
Flow ofCSF {Mnemonic:"ComeLet Me 71-ecrt Sisa For Lunch Maybe Somewhere in Ayala']: produced in the
Choroidplexus-> Lateral Ventricle•>fora men of Monroe ->Third Ventricle·>aqueduct of Sylvius -> Fourth
ventricle->Luschkaand Magendie->Subarachnoidspace where it is absorbed in the arachnoidgranulations
439
B. Types of Hydrocephalus and Pathophysiology
COMMUNICATING OR NONCOMMUNICATING
NONOBSTRUCTIVE OR OBSTRUCTIVE
HYDROCEPHALUS HYDROCEPHALUS
• Obliteration of subarachnoid
• Obstruction within the ventricular
Pathophysiology cisterns and/or malfunction
system
of arachnoid villi
• Achondroplasia • Aqueductal stenosis
• Basilar impression • Mitochondrial
• Benign enlargement of sub- • Autosomal recessive or dominant
arachnoid space • LlCAMmutations
Etiologies
• Choroid plexus papilloma • Chiari malformation
• Meningeal malignancy • Dandy-Walkermalformation'
• Meningitis • Klippel-Feilsyndrome"
• Posthemorrhagic • Mass lesionsc
a. Dandy-Walker malformation: triadof 1)agenesisof cerebellarvermis;2) cysticdilatationof the 4thventricle;
and 3) enlargementof the posteriorIossa
b. Klippel-Feil
syndrome:triadof 1) shortwebbedneck;2) decreasedrangeof motionofthe cervicalvertebrae;
and 3) lowposteriorhairlineaccompaniedby hydrocephalus
c. Masslesionsincludeabscess,hematoma,tumorsand neurocutaneous disorders,Veinof Galenmalformation,
Walker-Warburg syndrome(abnormalglycosylation of a-dystroglycan
causingcerebra-ocular dysgenesis)
Sources:KliegmanR, et al. NelsonTextbookof Pediatrics(21sted).Elsevier;2020
FenichelG. et al. ClinicalPediatricNeurology
A signsand symptomsapproach(6thed).Elsevier:2009
II. MANIFESTATIONS
• Infants: accelerated rate of head enlargement
Symptoms • Wide and bulging anterior fontanel
• Older children: headache is a prominent symptom
• Eyes may deviate downward due to impingement of the dilated suprapineal
recess on the tectum (setting-sun sign)
• Long-tract signs (brisk DTRs, spasticity, clonus, Babinski sign)
Signs • Percussion of skull produce a "cracked pot" sensation or Macewen sign
(separation of sutures)
• Foreshortened occiput may be seen in Chiari malformation
• Prominent occiput may be seen in Dandy-Walker malformation
III. DIAGNOSIS
DIAGNOSTIC REMARKS
IV. MANAGEMENT
• Depends on the etiology
• Acetazolamide & furosemide: provide temporary relief by reducing rate of CSFproduction
• Most cases will require extra-cranial shunts
• Most common complication of shunts: Staphylococcus epidermidis infection
440
SECTION THREE
MIGRAINE AND HEADACHE
MIGRAINE
I. ETIOPATHOGENESIS
• More common among females during adolescence
• More common in males among those younger than 10 years old
• >50% undergo spontaneous prolonged remission after the 10 11' birthday
• No one theory that can explain the exact pathogenesis of migraine
II. MANIFESTATIONS
• Episodic attacks moderate to severe in intensity, focal location, throbbing quality
• May be associated with nausea, vomiting, light sensitivity, sound sensitivity
TYPE DESCRIPTION
aura Vomiting
0
Pallor
0
Hemiplegic aura • Unilateral senso1y or motor signs that may persist for days
-·- -·
(migraine aura) • Good prognosis in an older child or adolescent
• Vasoconstriction of basilar and posterior cerebral arteries
• Vertigo, tinnitus, diplopia, scotoma, ataxia
Basilar-type
migraine • Altered consciousness with seizures
• Complete resolution after the attack
• Girls <4 years old at risk
Source:Headache
Classification
Committee
on lhe International
Headache
Society(HIS);2013
442
IV. MANAGEMENT
A. Three Components in the Management of Migraine
Acute treatment should be developed for stopping a headache attack on a consistent
basis with return to function within a maximum of 2 hours
Preventive treatment when headaches are frequent (;,,1 per week) and disabling
• Biobehavioral therapy
B. Acute Treatment
• NSAID for mild to moderate, restrict attack not more than 2-3 per week
• Add triptans if moderate-to-severe or NSAID fails
Restrict to not more than 4-6 attacks/month
• NSAIDS can be repeated q3-4h1; triptans q2hr
• Fluid hydration: important because vascular dilation is common feature of migraine
• Status migrainosus: persistent headache >3 days (refer to a specialist)
V. PHARMACOLOGIC OPTIONS FOR MIGRAINE
CLASS REMARKS REPRESENTATIVE DRUGS
• Paracetamol 15 mg/kg/dose q4-q6
• NSAIDSnot more than 2-3 times (max dose 90mg/kg/24h)
NSAIDs per week to avoid medication over- • Ibuprofen 7.5 mg/kg/dose q6-q8 (max
use headache dose 40mg/kg/24h)
• Aspirin as alternative for >15 years old
• For migraines uncontrolled by NSAIDs
• Side effects: tightness of jaw, chest,
• Almotriptan
Triptans fingers due to vascular constriction,
feeling of grogginess, and fatigue • Rizatriptan
due to central serotonin effect
• Due to antagonism of dopaminer-
gic neurotransmitter • Procholorperazine
Antiemetics
• Used if severe and unresponsive to • Metoclopramide
NSAIDand Triptans
B O t" p t" Tl
' '
DRUGS REMARKS
Amitriptyline
• Dose: 5 mg OD, increased after 10 months to 10 mg OD, with a month
off the drug every 4-6 months
Yes
t
Initial Seizure Recurrent Seizure
···---····················--·-·----
RBS,Ca1·, Metabolic : Consider and check the
Studies depending on ] following:
history and OE Drug compliance and
dosing
EEG? Metabolic disorder
Imaging? Structural lesion
CSF Examination 7 Drug Interaction
CNS degenerative
Follow up
.......... ,.....
Abnormal
Symptomatic seizures
Treat underlying cause
Anti-epileptic drug as
needed
I
---------
........................
...
111
No continuous
I
!'. ..
Normal
Isolated l5' seizure with normal EEG,
• drug treatment
nofamdyh1story
• Close observation
Follow up
i
=·_]
\
.
Normal except EEG
Consider drug therapy
I
Poor control
Regular follow up Consider hospitalization
Monitor drug levels and toxicity Re-adjustment of medication
.. E.E:(3.a~_!ri<;lic~jecJ Re-consider pathology
...Freguentf~llo.,v."P. ..
Source:KliegmanR.et al. NelsonTextbookof Pediatrics(21sted). Elsevier:2020
MenkesJ. et al. Child Neurology(7th ed). LippincottWilliams& Wilkins;2006
444
III. INITIAL MANAGEMENT
• Secure Airway, Breathing, and Circulation
ABCs • Position patient to avoid aspiration
• Provide 100% oxygen while ongoing seizure episode
• Diazepam IV 0.3 mg/kg/dose (max 5 mg for <S years, 10 mg >S years)
Initial • Rectal Diazepam 0.5 mg/kg/dose
anticonvulsant • Buccal Midazolam 0.3 mg/kg/dose
• Midazolam IV 0.2 mg/kg/dose
• Hypoglycemia
Correct • Electrolyte imbalance
underlying • Pyridoxine for lsoniazid toxicity
causes if any • May give trial 100 mg of Vitamin B6 (pyridoxine) for pyridoxine
responsive seizures
Breakthrough
• A single seizure lasting> 15 mins or a series of seizures without return
to baseline mental status between each episode
• Occurs in patients already being treated with anti epileptic drug but has
I
seizure achieved low drug levels
445
III. PATHOPHYSIOLOGY OF EPILEPSY
FOUR DISTINCT
MECHANISMS DESCRIPTION
PREVIOUS
NOMENCLATURE DEFINITION
TERMINOLOGY
Benign Rolandic • Usually begins between 3-13 years old; remits by 16 years old
Epilepsy • Single nocturnal seizure with clonic movement of the mouth and gurgling
(benignchildhood • Seizures resolve by 16 years
epilepsywith • Altered consciousness, postictal confusion, and aura are rare
centrotemporalspikes) • Oxcarbazepine, carbamazepine, levetiracetam, valproic acid
• Accounts for 70% of partial seizures
• Many have a prior history of febrile seizures or head trauma
Temporal Lobe
• Prodrome: lethargy
Epilepsy
• Oral or motor automatisms, altered consciousness, head & eye deviation,
contralateral twitching or tonic-clonic movements, posturing
• Sudden cessation of motor activity or speech with a blank facial
expression & flickering of the eyelids
• Uncommon before 5 years old
Absence seizures
• Never associated with an aura and rarely persist >30 seconds
• Not associated with a postictal state
• Patients do not lose body tone & usually resume activity after seizure
• Most common generalized motor seizures
• Can be primarily or secondarily generalized
• Usually starts with loss of consciousness or at times sudden cry
Generalized
Tonic-Clonic • Tonic phase: jaw snaps followed by 10-15 seconds or longer of tonic
spasms, apnea & cyanosis
• Clonic phase: 1-2 minutes of rhythmic generalized contractions
• Postictal state: vomiting, confusion, somnolence & intense headache
• Repetitive seizures consisting of brief, often symmetric muscular
Myoclonic
contractions with loss of body tone & falling or slumping forward
Infantile • Begin at 4-8 months
spasms (West • Brief symmetric contractions of neck, trunk, extremities
syndrome) • EEG shows hypsarrhythmia
VI. MANAGEMENT
• Different societies and institutions have different recommendations for AED therapy
• The table below are commonly used drug therapies for specific seizure types:
SEIZURE TYPE INITIAL DRUG THERAPY OF CHOICE
III. DIAGNOSIS
DIAGNOSTICS FINDINGS/REMARKS
• Indications:
• For all infants younger than <6 months, who present with fever & seizure
• If the child is ill-appearing
• At any age with clinical signs or symptoms of concern
Lumbar
• For children 6-12 months of age, LP is an option if:
puncture (LP)
• Simple febrile seizure and is deficient in Hib and streptococcal
immunization (or if with unknown immunization status]
• Pretreated with antibiotics
• PPS recommends LP for all <18 months of age with first febrile seizures
• Not done if first episode and is otherwise neurologically healthy
EEG
• Not predictive of future recurrence of febrile seizures or epilepsy
• Electrolytes & CBCare not routinely recommended for a first simple seizure
Serum studies • Blood glucose if with prolonged post-ictal obtundation of if with poor
oral intake (prolonged fasting)
• Not recommended after a first simple febrile seizure (no evidence)
Neuroimaging
• Workup of children with complex febrile seizure need to be individualized
IV. MANAGEMENT
General • Counseling and education on acute management and first aid
Aspects • Reassurance, emotional support, and allaying fears of the parents
• Given to address the fever and decrease the comfort
Antipyretics
• Does not reduce the risk of having a recurrent febrile seizure
• Can reduce the recurrence of febrile seizures
Anticonvulsants
• However, its adverse side effects do not warrant their use
5-20 minutes 0 Midazolam IV 10 mg for >40 kg, 5 mg for 13-40 kg; single dose
(initial therapy 0 Lorazepam IV 0.1 mg/kg/dose, max 4 mg/dose; may repeat dose once
phase) • If none of the 3 options above are available, choose ONE of the ff:
0 Rectal diazepam 0.2-0.5 mg/kg/dose, max 20 mg/dose; single close
0 Intranasal/buccal midazolam
0 Phenobarbital IV 15 mg/kg/dose; single dose
• If seizure stops, provide symptomatic care
• If seizure continues: there is no evidence-based preferred second
therapy of choice
20-40 minutes
• Choose one of the following second line options and give as a single dose:
(secondary
therapy phase)
0 Valproic acid IV 40 mg/kg, max 3000 mg/dose
0 Levetiracetam IV 60 mg/kg, max 4500 mg/close
40-60 minutes
• If none of the above options are available, give phenobarbital IV 15
mg/kg/dose; single dose (if not given already)
• If seizure stops, provide symptomatic care
• If seizure continues, there is no clear evidence to guide therapy in this
I
(third therapy phase. Choices include repeat of second-line therapy or anesthetic
phase) doses of either thiopental, midazolam, pentobarbital, or propofol (all
with continuous EEG monitoring)
Source:GlauserT,et al. Epilepsy
Curr.2016
449
SECTION FIVE
-------~-
TUBEROUS SCLEROSIS
NEUROCUTANEOUS SYNDROMES
I. ETIOPATHOGENESIS
Mode of inheritance: autosomal dominant
• Mutations: Tuberous sclerosis complex gene 1 and gene 2 (TSCl and TSC2) which
encodes for hamartin and tuberin respectively (both act as tumor suppressor genes)
III. DIAGNOSTICCRITERIA
• Careful examination of patient and parents is nearly as sensitive and much more cost
effective than imaging studies of another organ system
• Diagnosis should fulfill 2 Major OR 1 Major+ 2 Minor criteria
Skin lesions
• Facial angiofibromas
• Ungual or periungual fibromas
• Hypomelanotic maCLtles(>3)
• Cerebral white matter migration lines
• Shagreen patch
• Gingival fibromas
Brain lesions • Bone cysts
• Cortical tuber • Retinal achromatic patch
• Subependymal nodule • Confetti skin lesions
• Subependymal giant cell astrocytoma • Nonrenal hamartomas
Eye lesions • Multiple renal cysts
• Multiple retinal hamartomas • Hamartomatous rectal polyps
Tumors of other organs
• Cardiac rhabdomyoma
• Renal angiomyolipoma
• Pulmonary lymphangioleimyomatosis
IV. DIAGNOSTICS
• MRI of the brain reveals findings in most cases
• Echocardiography
• Imaging studies to locate hamartomatous lesions (e.g., ultrasound of kidneys)
• Genetic diagnosis has limited applications
V. MANAGEMENT
• No specific treatment
• Manage seizures
• Surgical management of tumors if warranted (e.g., ventricular obstruction)
450
NEUROFIBROMATOSIS
NEUROFIBROMATOSIS TYPE 1
DISEASE (VON RECKLINGHAUSEN NEUROFIBROMATOSIS TYPE 2
DISEASE)
Mode of • Both are autosomal dominant
Inheritance
• NF-1 gene mutation on • NF-2 gene mutation on
chromosome 17 q 11.2 chromosome 22ql.ll
Mutations
• Encodes for neurofibromin which • Encodes for merlin or
inhibits Ras oncogene schwannomin
• Progressive disease that can • Less common
affect almost every organ • Characterized by development
Clinical of CNS tumors, notably bilateral
• Most common skin lesion are
Manifestation
cafe-au-lait spots (light brown, vestibular schwannomas
well demarcated pigmentation)
NF-1 (most prevalent type) is NF-2 is diagnosed when 1 of the
diagnosed when any 2 of the following are present:
following are present: • Bilateral B'hnerve masses
• :e6 cafe au lait macules >5 mm in (acoustic neuroma)
diameter in prepubertals & >15 • Parent, sibling, or child with
mm in postpubertal individuals NF-2 & either unilateral B'" nerve
(predilection for the trunk & masses or any 2 of the following:
extremities with sparing of face) neurofibroma, meningioma,
• Axillary or inguinal freckling with glioma, schwannoma
multiple hyperpigmented areas
Diagnostic 2-3 mm in diameter
Criteria• • :e2iris Lischnodules (hamartomas
located within the iris)
• :e2 neurofibromas or one
plexiform neurofibroma (along
the skin, PNS, blood vessels &
within viscera)
• Distinctive osseous lesion
• Optic glioma
• 1" degree relative with NF-1
whose diagnosis was based on
the aforementioned criteria
• Symptomatic treatment
• Multidisciplinary approach
• Ophthalmologic examination
• Neurologic assessment
Management
• Blood pressure monitoring
• Scoliosis evaluation
• Developmental screening
• Genetic counseling
of criteriaimprovesas childgrowsolder.Diagnosiscannotbe madewithcertaintybefore1 yearofage in
·Reliability
almosthalfof childrenwitha negativefamilyhistory.DNAtestingis unnecessaryifdiagnosticcriteriaare met.
of Pediatrics(21sted).Elsevier;2020
Source:KliegmanR.et al. NelsonTextbook
(7thed).LippincottWilliams& Wilkins;2006
MenkesJ. et al. ChildNeurology
I
451
SECTION SIX
CNS INFECTIONS
TUBERCULOUS (TB) MENINGITIS
I. ETIOPATHOGENESIS
• From metastatic caseous lesion in the cerebral cortex or meninges that develop during
the lymphohematogenous dissemination of primary infection
Gelatinous exudates infiltrate the corticomeningeal blood vessels, which produces
inflammation, obstruction, and subsequent infarction of the cerebral cortex
• Brainstem is the site of greatest involvement, commonly affecting cranial nerves Ill, VI
and VII
• Exudates also interfere with the flow of CSF resulting in a communicating hydrocephalus
• Most common in children 6 months to 4 years of age
• Accompanies miliary tuberculosis in 50% of cases
II. MANIFESTATIONS
• More rapid progression in infants and young children
• Signs and symptoms: acute onset of hydrocephalus, seizures, and cerebral edema
• More commonly progresses over weeks in 3 stages
STAGE MANIFESTATION
• Lasts 1-2 weeks
• Non-specific signs and symptoms (e.g., feve1; headache, irritability,
1" stage
drowsiness and malaise)
• Infants may experience loss of developmental milestones
• Focal neurologic signs ( e.g., nuchal rigidity, seizures, positive Kernig and
Brudzinski, hypertonia, cranial nerve palsies)
2 nd stage
• Development of hydrocephalus, increased ICP and vasculitis
• Signs of encephalitis (disorientation, movement disorder or speech impairment)
3,d stage • Coma, hemiparaplegia, hypertension, deteriorating vital signs and death
Ill. DIAGNOSIS
IV. MANAGEMENT
II. MANIFESTATIONS
• Depends on etiologic agent
• May vary from mild illness to severe manifestations such as seizures, coma and death
• In general, viral meningitis have a more benign clinical course than bacterial meningitis
AGENTS PRESENTATION REMARKS
III. DIAGNOSIS
DIAGNOSTIC FINDINGS/ REMARKS
IV. MANAGEMENT
• Supportive
• Only HSV has a specific treatment: Acyclovir
BACTERIAL MENINGITIS
I. ETIOPATHOGENESIS
AGE GROUP COMMON ETIOLOGIC AGENT*
I
• Group B streptococcus
First 2 months of life • Gram negative enteric bacilli
• L. monocytogenes
• S. pneumoniae
2 months to 12 years old • H. influenzae
• N. meningitidis
Overall • Viral infections are more common
•Modeof transmissionis usuallyby hematogenousdisseminationof microorganism
froma distantsite of infection
453
II. MANIFESTATIONS
• Headache, nausea, vomiting, anorexia, restlessness, irritability, fever, neck pain & rigidity,
obtundation, coma, focal neurologic deficits (due to vascular occlusion)
• Nuchal rigidity secondary to inflammation of spinal nerves & roots produce meningeal
signs ofin·itation (Brudzinski and Kernig sign)
• 12-18 months old: Kernig and Brudzinski not consistently present
• Seizures due to cerebritis, infarction, or electrolyte losses (20-30% of patients)
III. DIAGNOSIS
DIAGNOSTIC FINDINGS/ REMARKS
• May see organisms on Gram stain and culture
Lumbar • If antibiotics started prior to LP: presumptive diagnosis of bacterial meningitis
puncture can be made despite negative cultures because pleocytosis, high CSFprotein
{LP) and CSF level, and low CSF sugar persist for several days even after antibiotics
GS/CS • If the LP is traumatic, it is prudent to rely on bacteriologic results because the
gram stain, culture, and glucose level may not be influenced by a traumatic LP
• Should be performed in all patients with suspected meningitis
Blood culture
• Reveals the responsible bacteria in up to 80-90% of cases of meningitis
High CRP,
ESR, and • Differentiates bacterial from viral causes of meningitis
procalcitonin
IV. MANAGEMENT
A. Antibiotics
• Ceftriaxone or cefotaxime
• Vancomycin if penicillin-resistant
Empiric Antibiotics
• Chloramphenicol for >l month old & allergic to penicillin
• Alternative: vancomycin + rifampin
• Penicillin G IV for 5-7 days
N. meningitidis • Alternative for penicillin allergic patients: meropenem or
vancomycin
• Vancomycin + 3" 1 generation Cephalosporin or Penicillin IV for
10-14 days
S. pneumoniae
• Vancomycin added for presumed S. p11eumo11iae meningitis
due to risk of resistance to penicillin, cefotaxime & ceftriaxone
Penicillin-resistant
• Vancomycin
isolates
• Ampicillin
L. monocytogenes
• Alternative: IV trimethoprim-sulfamethoxazole
Hib • Ampicillin for 7-10 days
454
V. COMPLICATIONS
• Hydrocephalus (communicating type): acute complication of meningitis
• Subdural effusions due to continued transudation (10-30% of patients)
• SIADH: may exacerbate cerebral edema and lead to hyponatremic seizures
Sources:KliegmanR.et al. NelsonTextbook
of Pediatrics
(21sted.).Canada:Elsevier;2020
MenkesJ, et al. ChildNeurology(7thed.).LippincottWilliams& Wilkins;2006
Kimberlin
OW,et al. 2018 Reportof theCommittee on Infectious
Diseases.Academyof Pediatrics: 2018
BRAIN ABSCESS
I. ETIOPATHOGENESIS
• Most common between 4-8 years old
• Etiology: embolization due to congenital heart disease with right to left shunts,
meningitis, chronic otitis media & mastoiditis, face & scalp infections, orbital cellulitis,
dental infections, penetrating head injuries, and VP shunt infections
Areas affected: cerebrum 80%; occipital lobe, cerebellum & brain stem 20%
• Majority are single abscess; 30% multiple
• Etiologic agents: S. aureus, streptococci, anaerobes, gram negative aerobic bacilli
(Proteus, Pseudomonas, Haemophi/us, Citrobacter)
II. MANIFESTATIONS
• Early stage: nonspecific symptoms: low-grade fever; headache, lethargy
• Vomiting, severe headache, seizures, focal neurologic signs (hemiparesis), papilledema,
and coma
Ill. DIAGNOSIS
• Positive blood culture in 10%
• CSF not done to avoid herniation
• Cranial CT scan & MRI (most reliable methods)
IV. MANAGEMENT
A. Empiric antibiotics
0 Duration of antibiotics: 4-6 weeks
' Depend on the probable pathogenesis & most likely organism
Unknown cause • 3rd generation Cephalosporin + Metronidazole
8. Surgery
Aspiration for encapsulated abscesses
, Indications for surgery:
0 With gas in the abscess
0 Multiloculated abscesses
0 Posterior fossa location
V. PROGNOSIS
, Fungal cause
0 Associated infections like mastoiditis, periorbital abscess, sinusitis
I
• High mortality: multiple abscesses, coma
• Long-term sequelae: behavior & learning problems, hydrocephalus, seizures, hemiparesis
455
SECTION SEVEN
NEUROMUSCULAR DISORDERS
GUILLAIN-BARRE SYNDROME
I. ETIOPATHOGENESIS
• Autoimmune disorder thought to be a post-infectious polyneuropathy (symmetric
ascending muscle weakness or paralysis)
• Etiology: autoimmune reaction that develops in response to a previous infection
leading to aberrant demyelination of peripheral nerves & ventral motor nerve roots
II. MANIFESTATIONS
• Initial symptoms include numbness and paresthesia followed by
progressive weakness and areflexia
Symptoms
• Weakness begins in the lower extremities & progressively involves the
trunk, upper limbs & bulbar muscles (Landry ascending paralysis)
• Cranial nerve deficits leading to dysphagia, dysa~thria, facial weakness,
papilledema, autonomic dysfunction, respiratory muscle paralysis
Signs
• Dysphagia and facial weakness: signs of impending respiratory failure
• Miller-Fisher syndrome: acute ophthalmoplegia, ataxia, areflexia
• Onset of weakness usually follows a nonspecific viral infection
(gastrointestinal or respiratory tract) by 10 days (Campylobacter
jejuni, H.pylori, Mycoplasma pneumonia, and Zika virus)
Course • Maximal severity of weakness is reached by 4 weeks after onset
• Benign clinical course with spontaneous recovery within 2-3 weeks
• Tendon reflexes usually the last function to recover & lower extremity
weakness last to resolve
• Three clinical features are predictive of poor outcome with sequela:
° Cranial nerve involvement
Prognosis
• Need for intubation
• Maximum disability at the time of presentation
III. DIAGNOSIS
IV. MANAGEMENT
456
CEREBRAL PALSY (CP)
I. ETIOPATHOGENESIS
• Group of permanent disorders of movement and posture causing activity limitation that
are due to non-progressive disturbances in the developing fetal or infant brain
Motor disorders are often accompanied by disturbances of sensation, perception, cognition,
communication, & behavior as well as by epilepsy and secondary musculoskeletal problems
A. Epidemiology:
More common in males
Major lesions that contribute to CP in preterm babies are:
lntracerebral hemorrhage
0
Periventricular leukomalacia
0
II. MANIFESTATIONS
• Arms more than legs (shows hand preference at a very early age)
• Decreased spontaneous movement on the affected side
Spastic • Delayed walking or walks on tiptoes
hemiplegia
• Circumductive gait
(25%)
• Spasticity apparent especially in the ankles
• Seizures (1/3 of patients) & cognitive impairment (25%)
• Bilateral spasticity of the legs (legs> arms)
• Damage to the immature white matter (during the 20-34'h week AOG)
• Commando crawl
Spastic diplegia
• Increased DTRs, (+) Babinski sign, and ankle clonus
(35%)
• Scissoring posture of extremities is seen when child is suspended by the axilla
• Normal intellect
• Periventricular leukomalacia (most common neuropathologic finding)
• Most severe form of CP due to marked motor impairment of all extremities
& high association with intellectual disabilities & seizures
Spastic • Swallowing difficulties due to supranuclear bulbar palsy
quadriplegia • Severe periventricular leukomalacia & multicystic encephalomalacia
(20%) (most common neuropathologic lesions)
• Increased tone and spasticity in all extremities, brisk reflexes and plantar
extensor responses
Ill. DIAGNOSTICS
• Baseline EEG & cranial MRI scan (to determine the extent and location of structural
I
lesions and associated congenital malformations)
• Hearing & visual function tests
Sources:KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.).Canada:Elsevier;2020
MenkesJ, et al. ChildNeurology(7thed.).LippincottWilliams& Wilkins;2006
457
IV. MANAGEMENT
• Multidisciplinary approach in the assessment & treatment
• For tight heel cord: tenotomy of Achilles tendon
• Drugs for spasticity:
Diazepam (oral): 0.01-0.3 mg/kg/day BID or QID
Baclofen: 0.2-2 mg/kg/day BID or TIO
0 Dantrolene: 0.5-10 mg/kg/day BID
Levodopa (for dystonia): 0.5-2 mg/kg/day
Reserpine or Tetrabenazine (for hyperkinetic movements)
Botulinum toxin
Deep brain stimulation
REFERENCES
1. Berg, A., Berkovic, S., Brodie, M., Buchhalter, J., Cross, J., and van Emde Boas, W. et al. Revised
terminology and concepts for organization of seizures and epilepsies: Report of the ILAE
Commission on Classification and Terminology, 2005-2009. Epilepsia 2010 51(4), 676-685
2. Dooley, ). The evaluation and management of paediatric headaches. Paediatrics and Child
Health, 2009, 14(1), 24-30. doi: 10.1093/pch/14.l.24
3. Febrile Seizures: Guideline for the Neurodiagnostic Evaluation of the Child with a Simple
Febrile Seizure. PEDIATRICS,2011, 127(2), 389-394
4. Fenichel, G. Clinical Pediatric Neurology A signs and symptoms approach 6th ed. 2009
Philadelphia: Saunders Elsevie1c
5. Glauser T, Shinnar S, Gloss D et al. Treatment of Convulsive Status Epilepticus in Children.
Epilepsy Cunc 2016 Jan-Feb; 16(1): 48-61.
6. Headache Classification Committee on the International Headache Society (HIS): The
International Classification of Headache Disorders, 3rd Ed. 2013 Cephalagia; 33(9):629-808
7. Jan, Mohammed and R Al-Buhairi, A and Baeesa, Saleh. Concise outline of the nervous system
examination for the generalist. Neurosciences 2001 (Riyadh, Saudi Arabia). 6. 16-22.
8. Kliegman, R., Stanton, B., St. Geme, J., Schor, N., and Behrman, R. Nelson Textbook of Pediatrics
21st ed. 2020. Canada: Elsevier
9. Menkes, J., Sarnat, H., and Maria, B. Child Neurology 7th ed. 2006 Philadelphia: Lippincott
Williams and Wilkins.
10.PedMIDAS Tool I Pediatric Migraine I Headache Cente1c 2018. Available from https://www.
cincinnatichildrens.org/service/h/headache-center/pedmidas
11.Pellock, J., Bourgeois, B., Dodson, W., Nordli, Jr, D., and Sankar, R. Pediatric Epilepsy Diagnosis
and Therapy 3rd ed. 2008. New York: Demos Medical Publishing.
12.Teasdale G, et al. Assessment of coma and impaired consciousness. Lancet; 1974
13.Trinka, E., Cock, H., Hesdorffer, D., Rossetti, A., Scheffer, I., and Shinnar, S. et al. A definition
and classification of status epilepticus - Report of the ILAE Task Force on Classification of
Status Epilepticus. Epilepsia, 2015 56(10), 1515-1523.
14.Van de Bos, F., Terken, M., Ypma, L., Kimpen, )., Ne!, E., and Schaaf, H. et al. Tuberculous
meningitis and miliary tuberculosis in young children. Tropical Medicine And International
Health, 2004 9(2), 309-313.
15.Williams, H. Spinal sinuses, dimples, pits and patches: what lies beneath. Archives of Disease
in Childhood-Education and Practice, 2006 91(3), ep75-ep80. doi: 10.l 136/adc.2006.105643
16.World Health Organization. Rapid Advice: Treatment of Tuberculosis in children. 2010
Geneva, Switzerland: WHO
17.Kimberlin OW, Brady MT,Jackson MA, Long SS, eds. Red Book: 2018 Report of the Committee
on Infectious Diseases. 31st ed. Itasca, IL: American Academy of Pediatrics; 2018
458
ACUTE
CARE
~ PEDIATRIC BASIC LIFE SUPPORT
~ SHOCK
~ HEAD TRAUMA
~ TOXICOLOGY
SECTION ONE
PEDIATRIC BASIC LIFE SUPPORT
------------------------------·
;
r············.
Establish scene safety
c •••••••••••••
:
l:}f!~~~~:i~:~~:~~~~~~~~~...
30 compressions/ 2 breaths
:
:
:·-··-·--···-·-··--·····-···•
Rhythm check:
Shockable rhythm?
Non•shockable Shockable
rhythm rhythm
·--------------
---·-·-··-
Immediately resume CPRfor 2 min : - Deliver single shock
Rhythm check every 2 min : . Immediately resume CPR for 2 min
Resume cycle until ALSprovider arrives, or victim i- Resume cycle until ALS provider arrives,
___begins to move -----------·--·-··- ···-·· ····-·-- ..• 1 i··-or victim begins to.move_·-·--·--------
Source:PediatricAdvancedLifeSupportbyAmericanHeartAssociation2016
RappA. The UllimaleBLSCheatsheet;2019
I
461
II. BASIC LIFESUPPORT FOR DOUBLERESCUER
Rhythm check:
Shockab!e rhythm?
Non-shockable Shockable
rhyth rhythm
Source:PediatricAdvancedLifeSupportby AmericanHeartAssociation2016
RappA. The UltimateBLSCheatsheet; 2019
462
SECTION TWO
PEDIATRIC ADVANCED LIFE SUPPORT AND
ARRHYTHMIAS
BRADYARRHYTHMIAS
• Defined as heart rate (HR) that is slow compared with the normal range for the child's
age, level of activity, and clinical condition
• Symptomatic bradycardia: heart rate slower than normal with associated hypotension,
altered sensorium, or signs of shock
I. CLASSIFICATIONOF BRADYCARDIA
ETIOLOGY EXAMPLES
• Congenital abnormality of the heart
• Congenital or acquired heart pacemaker or conduction system
conditions that result in slow • Surgical injury to the pacemaker or
Primary
spontaneous depolarization or slow conduction system
conduction through the system • Cardiomyopathy
• Myocarditis
• Hypoxia
• Acidosis
• Non-cardiac conditions that alter the
Secondary • Hypotension
normal function of the heart
• Hypothermia
• Effect of drugs
463
III. MANAGEMENT (Bradycardia with a Pulse and Poor Perfusion)
Support ABCs
Give oxygen
Observe
Bradycardia persists?
No
Consider expert consultation
Doses/Details
Source:PediatricAdvancedLife SupportbyAmericanHeartAssociation2016
KliegmanR, et al. NelsonTextbookof Pediatrics(21sted.). Elsevier;2020
Park,M. (2008).Pediatriccardiologyfor practitioners(5th ed.).Philadelphi:MosbyElsevier.
TACHYARRHYTHMIAS
• Rapid abnormal rhythms that originate from the atria or the ventricles
• Can be tolerated without symptoms for a variable period of time
• May manifest with palpitations, lightheadedness, syncope, or acute hemodynamic
compromise (shock or cardiac arrest)
• Infants may manifest with poor feeding, irritability, rapid breathing
464
II. SINUS TACHYCARDIAVERSUS SUPRAVENTRICULARTACHYCARDIA
SUPRAVENTRICULAR
PARAMETER SINUS TACHYCARDIA (ST)
TACHYCARDIA (SVT)
• Acute onset or acute termination,
• Gradual onset
• Infant: symptoms of congestive
• Signs of underlying cause of
Manifestations heart failure
ST can be identified such as
• Child: sudden onset of
fever, hypovolemia, anemia
palpitations
Usual heart rate
• <220/min • 2'220/min
(in infants)
Usual heart rate
• <180/min • ;;,180/min
(in children)
Source:PediatricAdvancedLifeSupportbyAmericanHeartAssociation
2016
YES I No
Search for and treat cause
.....L ..
Consider adenosine if
Doses/Details rhythm regular and
QRSmonomorphic
Synchronized Cardioversion
Begin with 0.5-1 J/kg, if not
effective, increase to 2 J/kg
Sedate if needed, but don't delay
cardioversion
Atropine 10/IV dose:
First dose: 0.01 mg/kg rapid bolus
( maximum 6mg)
Second dose: 0. 2mg/kg bolus
(Maximum seconddose: 12mg)
Amlodarone 10/IV dose:
Smg/kg over 30-60 minutes
or
Procainamide 10/IV dose:
lSmg/kg over 30-60 minutes
Do not routinely administer
amiodarone & procainamide
together
I
465
IV. PEDIATRIC TACHYCARDIAWITH A PULSEAND ADEQUATEPERFUSIONALGORITHM
2
Narrow (5:0.09 sec) Wide (2:_0.09sec)
Evaluate QRS duration
3 9
Evaluat~,hythm Evaluate rhythm
4
Probable Sinus Tachycardia Probable Supraventricular
10 ... C .....
.
, Possible Supraventricular
Probable Ventricular
Compatible histoz y consistent with known Tachycardia : Tachycardia
Tachycardia
cause Compatible history (vague, : . R·R interval regular
P waves present/normal nonspecific); histo1y of dbrupt rate : . Uniform QRS morphology
Variable R-R; constant PR
lnfanIs: rateusually<2.20/min
changes
P \·1aves absent/abnormal
l
Children: rate usually <1S0/min HR not variable l2 : . Expe,t consultation st,only :
6····················· 1 Infants: rate usually 2:220/min : recommended
~~~!? .l!J!-1.~~ly
...9~!1~r.~~.:. z:.1.~9/f!l.i!~
.. : • Search afor and treat reversible
Search for and treat cause , causes
: • Obtain 12·Iead ECG
: • Consider pharmacologic
cardioversion
► Amlodarone I0/IV dose: Smg/kg
over 30·60 minutes
7 o,
► Procalnam!de IO/IV dose:
Consider Vagal 15mg/kg over 30·60 minutes
Maneuvers :- ► Do not rou1inely administer
:............................. : amiodarone and procainamide
together
► May attempt adenosine if not
already administered
8
: • Consider electrical cardioverskm
:·:·Esia·bliSKV.iSCUia·r·acce·ss : ► Consult pediatric cardiologist
: • ConsidN adenoslne 0.1 mg/kg IV (maximum
• Attempt cardioversion with 0.5
first dose) May give second dose of 0.2mg/kg
to 11/kg (may incre.ise rn 2J/kg if
: IV (maximum second dose 12mg)
initial dose ineffective)
~:. ~~~~ .~~pj~I.~l.~I!~~
.1~.~1~!1.i9.1!~ • Seddtc bcfurc Cd1diove1 sion
·--------------------------·
SECTION THREE
SHOCK
OVERVIEW OF SHOCK
I. ETI0PATH0GENESIS
• Shock is defined as a state in which the delivery of oxygen is inadequate to meet the
metabolic demands of vital organs and tissues
• All types of shock can lead to impaired functioning of vital organs such as the brain and kidneys
2) Cardiogenic Shock
• Congenital heart disease • Decreased cardiac output due
• Signs of CHF (e.g.,
• Arrhythmia to abnormal cardiac function
crackles, jugular
• Cardiomyopathy • Compensatory mechanisms:
venous distention,
• Myocarditis tachycardia & increased
hepatomegaly)
• Myocardial injury or afterload
• Cyanosis
trauma • Pulmonary edema may occur
3) Septic Shock
• Fever, tachycardia, • High or low SVR that leads to
• Bacterial, viral, fungal tachypnea, maldistribution of blood flow
infections leukocytosis • Increased capillary permeability
• Focus of infection & decreased cardiac contractility
I
467
ETIOLOGY CLINICAL CLUES PHYSIOLOGY
4) Obstructive Shock
• History of trauma, sudden • Impaired blood flow
• Tension pneumothorax difficulty of breathing due to limited venous
• Pericardia! tamponade • Risk factors for return to the heart or
• Constriction of ductus pulmonary embolism limited pumping of blood
arteriosus in infants with are prolonged from the heart leads to
ductal-dependent lesions immobilization, decreased cardiac output
• Pulmonary embolism malignancy, and a compensatory
hypercoagulable states increase in SVR
5) Distributive Shock
• Acute onset of
hypotension, often • Vasodilation, increased
accompanied by wheals, capillary permeability,
• Anaphylaxis angioedema, pruritus, and pulmonary
dyspnea, wheezing, vasoconstriction lead to
abdominal pain, vomiting, reduced cardiac output
or loss of consciousness
• Loss of vascular tone leads
• History of trauma
• Spinal cord injury to severe vasodilation and
• Dysautonomia
hypotension
II. DIAGNOSIS
DIAGNOSTIC POSSIBLE FINDINGS
• May be normal
CBC
• Leukocytosis or leukopenia, thrombocytopenia, anemia
• Low K· due to failure of the energy-dependent transport mechanism
• Increased lactate due to metabolic acidosis associated with tissue
Blood Chemistry hypoxia & anaerobic metabolism (present in all forms of shock)
• Renal dysfunction ( elevated creatinine, BUN)
• Hepatic dysfunction (elevated ALT,AST)
• Hypoxemia, hypercarbia
ABG
• Acidosis
• Used to monitor adequacy of oxygen delivery
scvo 2 (Central • Normal value is 70-75% if arterial 0 2 saturation is 100%
Venous 0 2
Saturation) • About 25-30% below the arterial 0 2 saturation if the arterial 0 2
saturation is not normal
Hematologic • Prolonged prothrombin and partial thromboplastin time
abnormalities • Reduced serum fibrinogen level
Sources:Pediatric
Advanced life SupportbyAmericanHeartAssociation2016
Kliegrnan
R. et al. NelsonTextbook
of Pediatrics
(21sted.).Elsevier;2020
468
III. MANAGEMENT
A. General Approach to Shock
APPROACH REMARKS
• Responsive and stable child: put in the most comfortable position
Positioning
• Hypotensive child: place the child in a supine position
• Maintain a patent or open airway
Support airway, • Provide high concentration of o, to all with shock via high flow delivery
oxygenation, system (e.g. Non-rebreather mask at lOLPM)
and ventilation • Oxygenation & ventilatory support for patients with ineffective
respirations, altered sensorium, or increased work of breathing
• For compensated shock: peripheral venous cannulation
Establish
• For hypotensive shock: immediate vascular access through
vascular access
intraosseous route if peripheral IV access is NOT readily achieved
• For hypovolemic shock: isotonic crystalloid solution (NS/LR) should be
given as a 20 mL/kg bolus over 5-20 minutes
• For suspected cardiogenic shock: smaller boluses of isotonic crystalloid
fluid at 5-10 mL/kg given over 10-20 minutes
• For trauma and massive bleeding: give packed red blood cells
(10 mL/kg) if the child does not respond to isotonic crystalloid
Provide fluid • For neurogenic, anaphylactic, and obstructive shock
resuscitation (cardiac tamponade): 20 mL/kg isotonic crystalloid
• Reassess the following parameters and repeat fluid boluses as needed:
0 Heart rate
• Capillary refill time
• Urine output
• Level of consciousness
• For most, fluid boluses can be administered up to and over 60 mL/kg
• SpO2 and heart rate monitoring as soon as possible
• Mental status
• Temperature
• Ensure optimal urine output (may insert indwelling urina1y catheter):
Monitor the
• Infants and children: 1.5 to 2 mL/kg/hr
patient
• Older child and adolescent: 1 mL/kg/hr
• Ongoing fluid losses
• Manage hypoglycemia (<45 mg/dL for neonates & <60 mg/dL for the rest)
• Consider central venous or arterial catheterization
B. Pharmacologic Management
Vasoactive medications are indicated when shock persists despite adequate fluid
resuscitation (fluid refractory shock)
I
myocardium ( except vasopressin)
• Vasopressin
• Decreases SVR
Phosphodiesterase
• Milrinone • Improves contractility
inhibitors
• Improves coronary artery blood flow
469
C. Summary Table of Commonly Used lnotropic And Vasoactive Drugs
DRUG DOSE RECEPTOR INOTROPY HR SVR PVR
Norepinephrine 0.02-0.2
mcg/kg/
min al> Pl, P2 i i i i
Dopamine 2-5
mcg/kg/ DAl, DA2 +--t +--t +--t +--t
min
5-10
mcg/kg/
min Pl, P2 >al i i -,t +--t
>10
mcg/kg/
min
al> Pl, p2 i i i i
Dobutamine 2-20
mcg/kg/
min
Pl> p2, al i i t t
Milrinone Loading
dose 25-
100 mcg/ Phospho-
kg diesterase
Infusion
III
inhibitor/
i i t t
0.25-0.75 TcAMP
mcg/kg/
min
Nitroprusside 0.3-0.5
mcg/kg/
Vascular
min
(max of
myocyte,
TcGMP
+--t -,i t t
10 mcg/
kg/min)
Epinephrine 0.1-1
mcg/kg/
min
al> Pl, P2 i i i i
SVR:Systemic
Vascular
Resistance
PVR:Pulmonary
VascularResistance
Sources:
Pediatnc
Advanced LifeSupportbyAmericanHeartAssociation
2016
Kliegman
R, et al. NelsonTextbook
of Pediatncs
(21sted.).Elsevier.2020
470
SECTION FOUR
FOREIGN BODIES & CAUSTIC INGESTION
II. MANIFESTATIONS
• Frequently asymptomatic
• Common presentations include:
Witnessed by a parent/ caregiver that a foreign body was placed into the ear
Incidental finding during routine otoscopy
Decreased hearing or ear pain
0 Purulent or bloody ear drainage (rare)
Ill. DIAGNOSIS
Visualization of a foreign body in the EACon otoscopy
• Examine the other ear and nostrils for additional foreign bodies
IV. MANAGEMENT
A.Timing of Removal
Timing depends on type of foreign body
0 The following warrant urgent removal for the following reasons:
Button batteries: cause destruction due to strong electrical currents & pressure necrosis
0 Insects: live insect may damage tympanic membrane & middle ear (e.g., cockroach)
0 Penetrating foreign bodies: may penetrate middle ear structures
B. Elective Referral to an Otolaryngologist is warranted for asymptomatic patients with:
0 Spherical or other foreign body that is tightly wedged in the medial EAC (e.g., round
beads, paper, or rubber foam)
Foreign body that is pushed up against the tympanic membrane
° Foreign body that is not easily removed upon the first attempt
Uncooperative patients requiring sedation
C. Complications
0 Most common complication of foreign body removal: EACabrasion or laceration
0 Treatment consists of topical antibiotic ear drops
II. MANIFESTATIONS
• History of nasal foreign body insertion without symptoms (71-88%)
• Mucopurulent nasal discharge (17-24%)
• Others: foul odor (9%), epistaxis, nasal obstruction, mouth breathing
• Complications: septa! perforation with saddle nose deformity, nasal meatal stenosis,
inferior turbinate necrosis, collapse of the alar cartilage
III. DIAGNOSIS
• Visualization of the foreign body using a headlight or otoscope
• Some located high in nasal vault or posterior nasal cavity may require fiberoptic endoscopy
• Most nasal foreign bodies are radiolucent (radiographs are not routinely helpful)
• Plain radiographs are suggested when:
I
'
Positive • Soft nasal foreign • Have patient (generally >3 years old) blow
Pressure body that occludes his or her nose while occluding the nostril
Technique anterior nasal cavity that has no foreign body
• Apply topical anesthesia
• Nonocclusive foreign
Using • In young children & uncooperative patients,
bodies in the anterior
Instruments sedation may be needed (removal under
portion of the nose
general anesthesia is advised)
Magnet • When foreign body is • Grasp one magnet with a mosquito
removal a magnet hemostat & pull it away from other magnet
II. MANIFESTATIONS
• Esophageal foreign bodies tend to lodge in areas of physiologic narrowing
(upper esophageal sphincter, level of the aortic arch, lower sphincter)
• Dysphagia, drooling, gagging, substernal pain or irritation
Esophagus • Seconda,y airway symptoms (e.g.,wheezing/stridor) suggest tracheal compression
• If a sharp object perforated the esophagus, neck swelling, crepitus, or
pneumomediastinum may occur
• Acute lead toxicity present with lethargy and vomiting
• Objects that can pass safely into the stomach generally traverse the
Stomach& remainder of the GI tract without complications
intestines • Usually asymptomatic if objects reached the stomach
• If with gastric outlet obstruction: vomiting or feeding refusal
Ill. DIAGNOSIS
• Determining the presence of a foreign body requires an accurate history and often a
direct look down the airway
• Imaging can be used to confirm the findings and to localize the site of the foreign body
472
A. Radiographs
° Flat objects (e.g. coins or disc batteries) usually orient in the coronal plane and appear
as a circular object on an anteroposterior projection
0 Objects lodged in the trachea tend to orient in the sagittal plane and are best seen in
lateral projection
0 Not readily seen on plain films: plastic, wood, thin metal objects, and bones
• X ray of neck, chest, & abdomen ("wide" CXR) • Chest X ray ("wide" CXR that includes
• Soft tissue lateral neck esophagus and abdomen)
B. Imaging with
° CT/MRI suggested if: symptomatic, dangerous characteristics of foreign body (>2 cm
width, >S cm length, or sharp), or type of foreign body is not definitively known
0 Ultrasound: may identify location & nature of foreign bodies in esophagus or stomach
IV. MANAGEMENT
A. Timing of Intervention
Urgent intervention is indicated if any are present (warning signs):
• Ingested object is sharp, long, large, a superabsorbent polyme,; a corrosive foreign
body (disc or button battery), a high-powered magnet or lead-containing
• Disc battery is in the esophagus (and in some cases in the stomach)
• Signs of airway compromise
• Evidence of near-complete esophageal obstruction (e.g.,patient cannot swallow secretions)
• Symptoms suggesting inflammation or intestinal obstruction (e.g. feve,; pain, or vomiting)
• GI obstruction or perforation
• Objects lodged for >24 hours or for an unknown duration (after this period,
complications such as transmural erosion, perforation, & fistulae are more common)
Expectant management {observation for 12 -24 hours) for blunt foreign bodies without
the above characteristics that are lodged in the esophagus in an asymptomatic patient,
because spontaneous passage often occurs.
B. Procedure
Flexible endoscopy for most extractions in esophagus, stomach, or proximal duodenum
0 Rigid endoscopy or retrieval with Magill forceps for objects in the hypopharynx or
proximal esophagus
Source:GilgerM, et al. Foreignbodiesof the esophagusandgastrointestinal
tractin children.Uptodate;2018.
KtiegmanR.et al. NelsonTextbookof Pediatrics(21sted.).Elsevier;2020
CAUSTIC INGESTIONS
I. ETIOPATHOGENESIS
• Caustic substance: strong acids/alkali capable of corroding or burning organic tissue
• Caustic ingestions: most common in children 1-3 years old
• May cause acute severe injury and long-term complications such as esophageal strictures
• Most commonly ingested caustic substance: household bleach
ALKALI INGESTION ACID INGESTION
Type of Necrosis • Liquefaction necrosis • Coagulation necrosis
• Superficial penetration of tissues (coagulum
Layer Involved • Deep bowel mucosa that forms on the mucosa limit deeper
penetration of the caustic substance)
I
• Standard liquid household
, Low viscosity results in rapid transit to
Characteristics detergents and bleaches
the stomach leading to gastric injury
have pH of9-11
473
II. MANIFESTATIONS
• Upper airway injury: stridor, hoarseness, nasal flaring, retractions
• GI tract injury: dysphagia (most common symptom), drooling, retrosternal or abdominal
pain, hematemesis
III. DIAGNOSIS
• Timing of exposure and if witnessed or not
• Estimation of the amount of the substance ingested
• Exact type and brand of substance ingested
• pH determined from material safety data sheet or by the poison control center
• Rapid evaluation of vital signs, mental status, and pupils
History and
• Evaluate for respiratory compromise
Examination
• Drooling, refusal to eat or drink, and dysphagia suggest oropharyngeal or
esophageal injury
• Inspection oflips and oropharynx for plaques, circumferential ulcers, and
mucosa! sloughing
• Absence of lesions does not exclude significant esophagogastric injury
• Chest X ray in any patient with respiratory symptoms
• Signs of perforation: pneumomediastinum, mediastinal widening, subcutaneous
Imaging emphysema in the neck, pleural effusion, or subdiaphragmatic air
• Radiologic contrast studies generally are not valuable in the initial stage because
they are unreliable in detecting acute injury or in predicting stricture formation
IV. MANAGEMENT
A. Stabilization and Supportive Care
° Close observation with emphasis on prevention of vomiting, choking, or aspiration
0 Vomiting should not be induced
Diluting or neutralizing the caustic agent, administration of activated charcoal, or
doing gastric lavage is not recommended
B. Endoscopic Evaluation
Performed within 24 hours of ingestion to evaluate and stage the injury
Indications for endoscopy:
0 Definite history of caustic ingestion
0 Symptomatic patients
• Patients with oral lesions
Severity of esophageal injury is graded by endoscopic appearance of esophageal mucosa:
SEVERITY DESCRIPTION
Grade 0 • Normal mucosa
References:
Fishman.D. Causticesophageal injuryin children.Uptodate.Feb23,2018.
KliegmanR.et al. NelsonTextbookof Pediatrics(21sted.).Elsevier;2020
474
SECTION FIVE
BURNS & ELECTRICAL INJURY
BURNS
I. ETIOPATHOGENESIS
• The spectrum of burn injuries is immense, ranging from simple first-degree burns with
no sequela to third-degree burns with hypermetabolic response
Scalds, which account for the most common etiology of burn in patients <5 years of age,
are the second most common type of burn injury among all age groups
III. DIAGNOSIS
Obtain complete history surrounding the injury especially etiology (e.g., flame, scald,
electrical, chemical), time of exposure, whether the injury occurred in a closed space, and
the possibility of additional trauma
• Perform complete PE and look for head injuries, upper airway obstruction, cardiac
arrhythmias, eye and ear injuries, and circumferential burns (which can lead to extremity
compartment syndrome)
I
475
ASSESSMENT OF EXTENT OF BURNS BY BODY SURFACE AREA (BSA)
Front Back
2%
pi i 13%
IV. MANAGEMENT
A. Fluid Resuscitation
0 Burn injury may lead to a combination of hypovolemic and distributive shock
0 Monitor weight, serum electrolytes, urine output, and nasogastric losses
0 Maintain urine output >0.5 ml/kg/hr
476
B. Indications for Admission:
2"' degree burns: >5% TBSA in infants, 10% TBSA in children, 15% TBSA in adolescents
3'' degree burns: >2% TBSA
Significant electrical or chemical injury
Burns in critical areas such as face, hands, feet, perineum or joints
0 Suspicions of abuse or unsafe home environment
0 Patient with underlying chronic illness, multiple trauma
Evidence of significant inhalation injury
ELECTRICAL INJURY
I. ETIOPATHOGENESIS
• Injury can occur through a variety of mechanisms (e.g., lightning strikes, household outlets)
• Mechanisms of injury:
Direct effect of electrical current on body tissues
° Conversion of electrical energy to thermal energy resulting in superficial and deep burns
0 Blunt mechanical injury from lightning strike, muscle contraction, or fall after electrocution
• Tissues with higher resistance (skin, bone, fat) have a tendency to heat up and
coagulate, rather than transmit current
II. MANIFESTATIONS
(range from mild superficial burns to severe multi-organ dysfunction & death)
SYSTEM MANIFESTATIONS
Cardiac • Ventricular fibrillation (with AC)or asystole (usually with DCor lightning)
Renal • Acute kidney injury, rhabdomyolysis from massive tissue necrosis
Neurologic • Loss of consciousness, autonomic dysfunction, paralysis, sensory deficits
Skin
Musculoskeletal
• Partial thickness to full thickness thermal burns
• "Kissing burns" at flexor creases
• Osteonecrosis and periosteal burns
I
Vascular system • Acute compartment syndrome, delayed arterial thrombosis
477
III. CLASSIFICATIONOF ELECTRICALBURNS
DEGREE REMARKS
• Rarely cause significant tissue damage
Low voltage • Initial lab evaluations include creatine kinase (CK) levels, ECG
burns monitoring for 4-6 hours and urinalysis (to check for myoglobinuria)
(<1,000 volts) • If there is significant soft tissue damage or arrhythmia, they should
be admitted for telemetry monitoring for at least 24 hours
• Can cause massive amounts of tissue damage and fractures either
from fall or from contraction of major muscle groups
High-voltage • CK and CK-MBis often used to evaluate cardiac injury but there is a lack
burns
(>1,000 volts) of evidence supporting its use especially in the absence of ECGchanges
• Evaluate serum electrolytes, serum troponin, BUN and creatinine,
myoglobin in urine
• Lightning injury is a dramatic occurrence that many people believe
is uniformly fatal. However, because the electrical energy from a
lightning strike often flows over the surface of the body rather than
Very high- through it, the survival rate is 65% or higher
voltage burns • Cardiac standstill and paralysis of the respiratory center are the most
(10 million common reasons for sudden death
volts) • A seemingly lifeless victim should still be treated because of a rare
phenomenon known as keraunoparalysis, which is a transient
paralysis with extreme vasoconstriction and sensory disturbances of
one or more extremities
IV. MANAGEMENT
Prolonged CPR should be undertaken following electrical injury regardless of the initial
rhythm
• Patients can have spontaneous cardiac activity but have paralysis of the respiratory muscles
• Secure the airway to prevent secondary cardiac or neurologic dysfunction
• Trauma resuscitation, including cervical spine immobilization
• Fluid resuscitation:
• Aggressive IV fluid replacement often required with soft tissue injury from a severe
electrical burn
Less fluid volumes required in lightning injuries
Parkland formula is not used since surface burns may grossly underestimate the extent
of injury
V. DISPOSITION
• Severely injured patients are admitted to an ICU
• Those with significant electrical burns are transferred to a burn center when stable
• When exposure to high-voltage is suspected, cardiac monitoring for 12-24 hours is
prudent, especially when there is history of cardiac disease, chest pain, or arrhythmia
Patients with mild symptoms, minor skin burns, normal ECG and urinalysis can be
observed for a few hours and discharged with prompt follow up based on their wounds
• Asymptomatic patients after a low-voltage exposure with a normal PE do not require
ancillary tests and can be discharged
478
SECTION SIX
HEAD TRAUMA
APPROACH TO HEAD TRAUMA
I. ETIOPATHOGENESIS
• Most head trauma in childhood is minor; however, some who appear low risk may have a
clinically important traumatic brain injury
• The challenge for evaluating minor head trauma is to identify clinically important
traumatic brain injury (ciTBI) while limiting unnecessary imaging and radiation exposure
Neuroimaging (usually with a CT scan) is highly sensitive for identifying brain injury that
requires acute intervention
B. Concussion
From a direct blow to the head, face, neck or a blow elsewhere with an "impulsive"
force transmitted to the head
Results in rapid onset of short-lived impairment of neurologic function that resolves
spontaneously
Symptoms: headache, confusion/disorientation, difficulties with memory, blank stare
or "stunned" appearance, inattentiveness, slow or incoherent speech, dizziness, gait
abnormalities, vomiting, and emotional )ability ( e.g., inappropriate laughing or crying)
Ill. DIAGNOSIS
IMAGING REMARKS
• Most children with minor head trauma do not need head CT scans
Head CT
• Decision to obtain a head CT should be made using clinical predictors to
I
Scan
determine risk of ciTBI
479
IV. APPROACH TO CHILDREN <2 YEARS OLD
• GCSs14
• Palpable skull fracture
• Altered sensorium (agitation, • Normal mental status
somnolence, slow response) • No parietal, occipital or temporal scalp
• Loss of consciousness hematoma
• Severe mechanism of injury: • No loss of consciousness >S seconds
Motor vehicle collision with patient
0 • No evidence of skull fracture
ejection or death of another passenger • Normal behavior according to the
Rollover
0
routine caregiver
Pedestrian or cyclist without helmet
0
• No high-risk mechanism of injury
struck by motorized vehicle
Head struck by high-impact object
0
'Skullradiographs
mayoccasionally
beusefulto screenfor fracturein selectedasymptomatic
patients3-24monthsold
.. Donotperformneuroimaging
forchildrenat verylowriskforTBI.Thesechildrenshouldmeetall of theabovecriterialistedabove
Observation for 4-6 hours for those with GCS15 and no altered mental status, but
with anv of the followina:
• Occipital, parietal, or temporal scalp hematoma
• History of loss of consciousness ;,,S seconds
• Not acting normally according to parent
• Vomiting that is self-limited
CT scanis performed
forworsening
signsandsymptoms
during
observation
period;
consideration
ofparentpreference:
patientis
<3 monthsold;or unwitnessed
traumaofconcern
VI. DISCHARGEINSTRUCTIONS
• Caretakers of children with minor head trauma should be given instructions for
monitoring, when to seek medical help, and when to return for follow-up
Immediate medical attention is required when the following conditions are noted:
0 Inability to awaken the child as instructed
0 Persistent or worsening headache
Vomiting that begins or continues 4-6 hours after injury
Change in mental status or behavior
0 Unsteady gait, clumsiness or incoordination
0 Seizure
Source:Schutzman
S. Minorheadtraumain infants& children.UpToDate: 2016
McCroryP,
et al. ClinicalJournalOf SportMedicine:2013
480
SECTION TOXICOLOGY
TOXICOLOGY
COMMONLY ENCOUNTERED CASES IN TOXICOLOGY
ETIOLOGY MANIFESTATIONS INITIAL MANAGEMENT*
1) Paracetamol Toxicity
2) Iron Toxicity
3) /soniazid Toxicity
4) Kerosene Toxicity
I
• Give 0 2 via nasal cannula
• May be absorbed in the • CNS symptoms: initially may be • Do not induce emesis
GIT (optimal), through excited but seizures may follow • No benefit with using
inhalation or via the skin • Signs: respiratory distress, activated charcoal
(minimal) cyanosis, tachycardia, abdominal • Specific problems: gastritis,
• Can depress the CNS and tenderness, perianal burns, seizures, aspiration
lead to hypoxia altered sensorium pneumonia
481
ETIOLOGY MANIFESTATIONS INITIAL MANAGEMENT*
5) Or9anophosphate Toxicity
• Muscarinic (mild): • Ifpoison absorbed dennally,
Malaise, vomiting, diarrhea,
0
inhaled, or ingested then
• Organophosphates sweating, pain, salivation, miosis
vomited, provide oxygen,
inhibit the action of
remove the clothing and do
cholinesterase, the • Muscarinic & nicotinic (moderate):
Mild symptoms, plus sponge bath using alkaline soap
enzyme that breaks 0
REFERENCES
1. Allen, H., Shaddy, R, Penny, D., Fettes, T. and Cetta, F. Moss and Adams' Heart Disease in infants,
childrenand adolescents9th ed. 2016. Philadelphia:LippincottWilliams& Wilkins
2. AmericanHeart Association.PediatricAdvancedLifeSupport 2015.Availablefrom <https://ahajoumals.org>
3. CrainEF,GersheIJCandCwminghan1 SJ(eds).Clinical
ManualofEmergencyPediatJics
5thed.2011.Cambridge
University
Press
4. Dart, RC. Medical Toxicology 3rd ed. Philadelphia: Lippincott Williams and Williams. 2004
5. Fishman,D.Causticesophagealinjury in children.Uptodate.AccessedFebruary23, 2018.
6. Gilger, M, Jain, A, McOmbe,~ M. Foreign bodies of the esophagus and gastrointestinal tract in
children.Uptodate.AccessedFebruary 12, 2018.
7. HazinskiMF.NursingCareof the CriticallyIllChild.3rd ed; 2013. Elsevier
8. Hoffman,RSet al. Goldfrank'sManualofToxicologicEmergencies.9th ed. 2010 NewYork:McGraw-Hill. 2010
9. Joffe,M.EmergencyCareof Moderateand SevereThermal Burns in Children.Uptodate.AccessedJuly12, 2017
10. Kliegman, R., St. Geme, J., Blum, N., Shah, S., Taskei; R., and Wilson. Nelson textbook of
pediatrics 21st ed. 2020. Philadelphia:Elsevier
11. McCrory, P., Meeuwisse, W, Aubry, M., Cantu, 8., Dvorak, )., & Echemendia, R et al. (2013).
Consensus Statement on Concussion in Sport-the 4th International Conference on
Concussion in Sport Held in Zurich, November 2012. Clinical Journal Of Sport Medicine,
23(2), 89-117.doi: 10.1097/jsm.Ob013e31828b67cf
12. Minorhead trauma in infantsand childrenby Sara Schutzman,MD.UptoDate.AccessedJune4, 2016
13.Olson,KR Poisoningand DrugOverdose.6th ed. 2011 NewYork:McGraw-Hill.
14. Park,M.Pediatriccardiologyfor practitioners Sth ed. 2008. Philadelphia:MosbyElsevier
15. RappA. The UltimateBLSCheatsheet:2019 Availablefrom <https://emedce,t.com/blog/ultimate-bls-cheatsheet>
482
ESSENTIALS
INPEDIATRICS
SECTION ONE
EXAMINATION OF THE PEDIATRIC PATIENT
VITAL SIGNS
HEARTRATE RESPIRATORY
rsLOOD PRESSURE (BP)* I
AGE 1 I
(beats/min) (bre::min) s;;t~;i~-~~stolic BP r-~M;.~-
Head ~ 45cm
I
35 cm (32-37 cm) Increase by 10 cm
Circumference
NavarroX, et al. Fundamentals
of PediatricsCompetency-Based
(1sted.).C & E Publishing;
2014
485
II. WEIGHT & LENGTH
A. Formulas to Estimate Weight
EXPECTED/ESTIMATED WEIGHT
AGE
PARAMETER FORMULA
:56 months Weight in grams Age in months x 600 + Birth Weight in grams
6 to 11 months Weight in grams Age in months x 500 + Birth Weight in grams
1 to 6 years Weight in kg Age in years x 2 + 8
(Age in years x 7) - 5
7 to 12 years Weight in kg
2
V. SEXUALMATURITYRATINGFOR FEMALES
SMR
PUBIC HAIR BREASTS
STAGE
1 • None • Preadolescent
• Sparse, lightly pigmented • Breast and papilla elevated as small
2 • Straight mound
• Medial border of labia • Areolar diameter increased
• Darker
• Breast and areola enlarged
3 • Beginning to curl
• No contour separation
• Increased amount
• Coarse,curly • Areola and papilla form secondary
4
• Abundant but amount less than in adult mound
• Adult feminine triangle spread to the • Mature; nipple projects
5
medial surface of thighs • Areola part of general breast contour
Source:KliegmanR, et al NelsonTextbook
of Pediatrics
(21sted).Elsevier;2020
Source:NavarroX et al. Fundamentals
of Pediatrics
Competency-based (1sted).C & E Publishing;
2014
487
I
AGE IN BIRTH WEEKS MONTHS YEARS
0 2 4 6 8 10 12 14 16 18 20 22 6 8 10 12 14 16 18 20 2 4 6 8 10 12 14 16 18
Legend:
Rangeof Recommended
Age ...___, I
BCG ecc
I
Hep B He1 B
Catchup immunization HepB' Hep e• I I I I
(OTwP-Hib-
I [ I Hep e• .. '
Hep B) and
j I I I I I I I
I
DTwP• /DTap• [
other DTaP
NOTE:Forthe latest combo j DTwP• /DTap• DTaP
OT•P.
Tdap/Td
ChildhoodImmunizationSchedule
(usuallyupdatedeveryFebruary) IPV/OPV
OPV*/l~V-
I I
IIII
OPV•/IPV
IPV
HIB
,PV
visitwww.philvaccine.org.
PCV
PCV.- T-T 1·-, I I I [
.j>.
co I- I I 1 rev~ I
PCV
-·
co RV
Influenza
RV Serles•
1-T 11
Influenza Yearly
I
I I
Measles
JE Vaccine
Measles
I I I I I I 11 JEV
IIIII I
I I I I I I I I I I I I I
MMR MMR MMR
·f I I I I I ··I· ; I I
Vari eel la
I
a,lc:ell• Varlcella
I I I I I
..
Hep A
HPV
I reTTe•, 1
'
I l
HPV Serles
' >
I
I I
Pulse
• Absent • < 100 bpm • > 100 bpm
(heart rate)
Grimace
• No response • Grimace • Cough or sneeze
(reflex irritability)
-1 0 1 2 3 4 5
Smooth, Superficial Parchment
Sticky. Gelatinous, Cracking, Leathery,
Pink peeling deep
SKIN friable, red, pale areas, cracked
visible and/or rash cracking
transparent translucent rare veins Wrinkled
veins few veins No vessels
Stripped Raised
Barely Flat areola, Full areola,
BREAST Imperceptible areola, areaola.
perceptible no bud 5-10mm bud
1-2mm bud 3-4mm bud
Slightly Well-curved
Lids fused: Lids open, Formed and Thick
curved pinna, soft
EYE/EAR loosely (-1). pinna flat. firm, instant cartilage. ear
pinna: soft. but ready
tightly (-2) stays folded recoil stiff
slow recoil recoil
Scrotum Testes in Testes Testes Testes
GENITALS Scrotum flat.
empty, faint upper canal, descending. down, good pendulous.
MALE smooth
rugae rare rugae few rugae rugae deep rugrae
Prominent Prominent Majera and
Clitoris Majera Majera
GENITALS clitoris, clitoris. minora
prominent. large. cover clitoris
FEMALE small labia enlarging equally
labia flat minora small and minora
minora minora prminent
B. Neurological Maturity
-1 0 1 2 3 4 5
I
I
I
Posture Q¢):='. c¢::: c¢c ~ ~
Square
Window
(Wrist) r r r
>90° goo 60°
~
45°
~
30°
I
oo
I
I
Arm Recoil
~180°
iJ'
140-180°
i}-
110-140°
¾
90-110°
i}
<90°
I
I Popliteal
Angle ~ ~ ~ ~ ~ ~ ~
180° 160° 140° 120° 100° goo <90°
Scarf Sign
t ~ & ~ ~ § I
I
I
Heel to Ear Ge:::::3 ci=s CX3 CC9 CC9 cd
I -- -------· -----
490
SECTION FOUR
FLUID AND ELECTROLYTES
III. PRIMARYACID-BASEDISORDERS
491
I
IV. COMPOSITION OF INTRAVENOUS FLUIDS & COMPARISON WITH PLASMA
Fluids
• 1/2 NS, LR, NSS, JES with or • Patient on NPO for surgical
General use
without dextrose and K· procedures
For volume • Hypovolemic shock
• pNSS, pLR, p!ES
resuscitation • Severe dehydration
Significant
electrolyte • Custom-made or cocktail fluids
derangement
VI. OSMOLALITY
• Na·: in mmol/L
ECFosmolality = 2(Na) + G/ucose/18 +BUN/2.8 • Glucose and BUN: in mg/dL
• Normal value= 285-295 mOsm/kg
Corrected Sodium (Na•)
• RBS: in mg/dL
• For every increase of glucose by 100 mg/
Corrected Na·= Actual Na·+ 0.016 (RBS - 100)
dL above lOOmg/dL, Na+ is expected to
increase by 1.6 mEq/L
492
VII. COMMONLYUSED DRIPS
Concentration _ Volumeof drug (mL)x Preparationof drug (mg/mL) x 1000 (if desired dose is in mcg)
(mcg/mL) - Totalvolumeof preparation (mL)
EASY PREP
DRUG CONCENTRATION
(amount of drug + USUAL DOSE
(in mcg/ml)
diluent)
5 mL of dopamine
Dopamine
+ 45 m L of diluent= 4000
200mg/5mL
50 mL solution • 5-20 mcg/kg/min
Dopamine pre-mixed
No need for diluent 800
200mg/250ml
20 mL of
Dobutamine • 2.5-15 mcg/kg/min
dobutamine 5000
250mg/20mL • Max:40 mcg/kg/min
+ 30 mL of diluent
Epinephrine 5 mL of epinephrine
250 • 0.1- 1 mcg/kg/min
lmg/mL + 15 mL of diluent
PARAMETER
~;::~:i;oN--
General Lethargic,
Alert Irritable
condition Unconscious
Eyes Normal Sunken Sunken
Drinks poorly, not
Thirst None Drinks eagerly able to drink
Skin
Quick Slow Very slow
retraction
Weight loss% <5% 5-10% >10%
Does not fulfill
2:2 of the 4 moderate 2:2 of the 4 severe
Criteria criteria for some or
signs signs
severe dehydration
Fluid deficit
ml/kg
<SO mL/kg 50-100 mL/kg
Source:WorldHealthOrganization.
493
>100 mL/kg
Thetreatmentof diarrhea.Geneva;2005
I
IX. WHO-CDCPROTOCOLON REHYDRATIONFOR DIARRHEA
PLAN REMARKS
• Fluids: Give oral rehydrating solution (ORS) after every loose stool
0 <2 years: 50-100 mL per loose stool
Plan A
0 2-10 years: 100-200 mL per loose stool
0 >10 years: as much as tolerated
PlanB • Fluids: Give 75 cc/kg ORS per orem over 4 hours
• Give a total of 100 cc/kg (PLR or PNSS) IV as follows:
Plane ° First 30 cc/kg over 1 hour for infants ( <12 months) or 30 mins for children
0 Next 70 cc/kg over 5 hours for infants (<12months) or 2.5 hours for children
X. BLOODTRANSFUSION
BLOOD PRODUCT DOSE
Packed red blood cells • 10-15 mL/kg over 4 hours
Platelet • 1 unit/10 kg or 4 units/BSA as fast drip
Fresh frozen plasma • 10-15 mL/kg as rapidly as tolerated
Height in cm x 36.5
eGFR = Crea ti nine in mmol/l
OR
Height in cm x 0.413
eGFR = Creatinine in mg/dl
494
SECTION FIVE
MEASUREMENT OF COMMONLY USED EQUIPMENT
NASOGASTRIC TUBE: ESTIMATION OF TUBE SIZE (FORMULA)
(Patient's age+ 16)
Appropriate tube size (Fr)= 2
FOLEY CATHETER
CONDITIONS INFLUENCING THE SELECTION OF FOLEY CATHETER SIZE
AGE WEIGHT(kg) FOLEY (Fr)
< 1.2 3.5 umbilical catheter
Neonate 1.2 - 1.5 5 umbilical catheter
1.5 - 2.5 5 umbilical catheter or size 6 Nelaton
0-6 months 3.5-7 6
1 year old 10 6-8
2 years old 12 8
3 years old 14 8-10
5 years old 18 10
6 years old 21 12
8 years old 27 12
12 years old Varies 12-14
495
Length=
Age (Years) + 12
2
I
SECTION SIX
LABORATORY REFERENCE VALUES
The following section provides a guide for the normal reference values per age of common
laboratory examinations requested in pediatric patients.
496
ANALYTE AGE REFERENCE VALUE
BLOOD CHEMISTRY
I. CHEMISTRY GENERALLY USED IN NEPHR0L0GY
REFERENCE CONVENTIONAL
AGE SI UNITS
VALUES UNITS
Cord Blood 70-380 U/L 70-380 U/L
5-8 hours 214-1,175 U/L 214-1,175 U/L
Creatine kinase 24-33 hours 130-1,200 U/L 130-1,200 U/L
72-100 hours 87-725 U/L 87-725 U/L
Adult 5-130 U/L 5-130 U/L
0-4 years 0.03-0.50 mg/dL 2.65-44.2 umol/L
4-7 years 0.03-0.59 mg/dL 2.65-52.2 umol/L
Creatinine
7-10 years 0.22-0.59 mg/dL 19.4-52.2 umol/L
enzymatic
10-14 years 0.31-0.88 mg/dL 27.4-77.8 umol/L
>14 years 0.50-1.06 mg/dL 44.2-93.7 umol/L
Cord blood 21-40 mg/dL 7.5-14.3 mmol/L
Premature (1 week) 3-25 mg/dL 1.1-9.0 mmol/L
Urea Nitrogen Newborn 3-12 mg/dL 1.1-4.3 mmol/L
Infant or child 5-18 mg/dL 1.8-6.4 mmol/L
Thereafter
497
7-18 mg/dL 2.5-6.4 mmolfL
I
REFERENCE CONVENTIONAL
AGE SI UNITS
VALUES UNITS
Cord Blood 5.0-6.0 mg/dL 1.25-1.50 mmol/L
Newborn 3-24 hours 4.3-5.1 mg/dL 1.07-1.27 mmol/L
Calcium, Ionized
24-48 hours 4.0-4.7 mg/dL 1.00-1.17 mmol/L
Thereafter 4.8-4.92 mg/dL 1.12-1.23 mmol/L
Cord Blood 9.0-11.5 mg/dL 2.25-2.88 mmol/L
Newborn 3-24 hours 9.0-10.6 mg/dL 2.3-2.65 mmol/L
24-48 hours 7.0-12.0 mg/dL 1.75-3.00 mmol/L
Calcium, Total
4-7 days 9.0-10.9 mg/dL 2.25-2.73 mmol/L
Child 8.8-10.8 mg/dL 2.2-2.7 mmol/L
Thereafter 8.4-10.2 mg/dL 2.1-2.55 mmol/L
0-6 days 1.2-2.6 mg/dL 0.48-1.05 mmol/L
Magnesium 7 days - 2 years 1.6-2.6 mg/dL 0.65-1.05 mmol/L
2-14 years 1.5-2.3 mg/dL 0.60-0.95 mmol/L
0-5 days 4.8-8.2 mg/dL 1.55-2.65 mmol/L
1-3 years 3.8-6.5 mg/dL 1.25-2.1 mmol/L
Phosphorus,
Inorganic 4-11 years 3.7-5.6 mg/dL 1.20-1.80 mmol/L
12-15 years 2.9-5.4 mg/dL 0.95-1.75 mmol/L
16-19 years 2.7-4.7 mg/dL 0.90-1.50 mmol/L
0-1 week 3.2-5.5 mmol/L 3.2-5.5 mmol/L
1 week - 1 month 3.4-6.0 mmol/L 3.4-6.0 mmol/L
Potassium 1-6 months 3.5-5.6 mmol/L 3.5-5.6 mmol/L
6 months - 1 year 3.5-6.1 mmol/L 3.5-6.1 mmol/L
>l year 3.3-4.6 mmol/L 3.3-4.6 mmol/L
Newborn 133-146 mmol/L 133-146 mmol/L
Infant 134-144 mmol/L 134-144 mmol/L
Sodium
Child 134-143 mmol/L 134-143 mmol/L
Therafter 135-145 mmol/L 135-145 mmol/L
1-3 years 1.8-5.0 mg/dL 100-300 umol/L
4-6 years 2.2-4.7 mg/dL 130-280 umol/L
7-9 years 2.0-5.0 mg/dL 120-295 umol/L
498
II. CHEMISTRY GENERALLY USED IN GASTROENTEROLOGY
CONVENTIONAL SI
REFERENCE
AGE UNITS UNITS
VALUES
MALES FEMALES MALES FEMALES
0-7 days 6-40 U/L 6-40 U/L
Alanine
amino- 8-30 days 10-40 U/L 8-32 U/L 10-40 U/L 8-32 U/L
transferase 1-12 months 12-45 U/L 12-45 U/L
(ALT/SGPT)
1-19 years 5-45 U/L 5-45 U/L
Premature 1 day 1.8-3 g/dL 18-30 g/L
Fullterm <6 days 2.5-3.4 g/dL 25-34 g/L
Albumin 8 days to 1 year 1.9-4.9 g/dL 19-49 g/L
1-3 years 3.4-4.2 g/dL 34-42 g/L
4-19 years 3.5-5.6 g/dL 35-56 g/L
1-9 years 145- 420 U/L 145- 420 U/L
10-11 years 140-560 U/L 140-560 U/L
Alkaline 12-13 years 200-495 U/L 105-420 U/L 200-495 U/L 105-420 U/L
phospahatase
14-15 years 130-525 U/L 70-230 U/L 130-525 U/L 70-230 U/L
16-19 years 65-260 U/L 50-130 U/L 65-260 U/L 50-130 U/L
Ammonia 11-35 umol/L 11-35 umol/L
Amylase 1-19 years 30-100 U/L 30-100 U/L
0-7 days 30-100 U/L 24-95 U/L 30-100 U/L 24-95 U/L
8-30 days 22-71 U/L 22-71 U/L
499
I
III. CHEMISTRY GENERALLY USED IN ENDOCRINOLOGY
REFERENCE CONVENTIONAL SI UNITS
AGE
VALUES UNITS
Cord blood 45-96 mg/dL 2.5-5.3 mmol/L
Premature 20-60 mg/dL 1.1-3.3 mmol/L
Neonate 30-60 mg/dL 1.7-3.3 mmol/L
Glucose (serum) Newborn 1 day 40-60 mg/dL 2.2-3.3 mmol/L
Newborn >l day 50-90 mg/dL 2.8-5.0 11111101/L
Child 60-100 mg/dL 3.3-5.5 mmol/L
Adult 70-105 mg/dL 3.9-5.8 mmol/L
0-3 days 1.00-20.00 uIU/L 1.00-20.00 ulU/L
Thyroid 3-30 days 0.5-6.5 ulU/L 0.5-6.5 ulU/L
Stimulating
Hormone (TSH) 1-5 months 0.5-6.0 u!U/L 0.5-6.0 uIU/L
6 months - 18 years 0.5-4.5 ulU/L 0.5-4.5 ulU/L
0-3 days 2.00-5.00 ng/dL 25.7-64.3 pmol/L
Thyroxine, free 3-30 days 0.90-2.20 ng/dL 11.6-28.3 pmol/L
31 days -18 years 0.7-2.00 ng/dL 9.0-25.7 pmol/L
Cord blood 20-240 pg/dL 0.3-3.7 pmol/L
1-3 days 200-610 pg/dL 3.1-9.4 pmol/L
Triodothyronine,
free 6 weeks 240-560 pg/dL 3.7-8.6 pmol/L
Inflammatory markers
REFERENCE VALUES AGE UNIT
2-5 years < 120-160 Todd units
Antistreptolysin- 0 (ASO)
6-9 years < 240 Todd units
Titer
10-12 years < 320 Todd units
500
Evaluation of anemia
CONVENTIONAL SI
REFERENCE UNITS UNITS
AGE
VALUES
MALES FEMALES MALES FEMALES
0-6 weeks 0-400 ng/mL 0-400 ug/L
7 weeks to
10-95 ng/mL 10-95 ug/L
<1 year
Ferritin
1-9 years 10-60 ng/mL 10-60 ug/L
Iron
10-18 years
10-300
ng/mL I
22-184 ug/dL
10-70
ng/mL
10-300
ug/L I
4-33 umol/L
10-70
ug/L
REFERENCES
l. Bloomfield, D., and Adam, H. Tachypnea. Pediatrics In Review, 2002, 23(8), 294-295. doi:
10.1542/pir.23-8-294
2. Crawford, J., Terry, M., and Rourke, G. Simplification of drug dosage calculation by application
of the surface area principle. Pediatrics, 1950, 5(783)
3. Del Mundo Fetal. Textbook of Pediatrics and Child Health. 4th ed. 2000. )MC Press,166.
4. Engorn, B., and Flerlage, J. The Harriet Lane Handbook 20th ed. 2015. Philadelphia: Elsevier.
5. Flynn JT, Kaelber DC, Baker-Smith CM, et al; Subcommittee on Screening and Management of
high blood pressure in children. Clinical Practice Guideline for Screening and Management of
High Blood Pressure in Children and Adolescents. Pediatrics. 2017; 140(3):e20171904.
6. Hazinski, MF. Manual of Pediatric Critical Care 1st ed. 2009. Elsevier.
7. Hazinski, MF. Nursing Care of the Critically Ill Child 3rd ed. 2013. Elsevier.
8. Mwangome, M., Fegan, G., Fulford, T.,Prentice, A., and Berkley, J. Mid-upper arm circumference
at age of routine infant vaccination to identify infants at elevated risk of death: a retrospective
cohort study in the Gambia. Bulletin Of The World Health Organization, 2012, 90(12), 887-
894. doi: 10.2471/blt.12.109009
9. Kliegman, R., Stanton, B., St. Geme, )., Schm; N., and Behrman, R.. Nelson Textbook of Pediatrics
21st ed. 2020. Canada: Elsevier.
10.Navarro, X., Bauzon, A., Aguilar, )., and Malanyaon, 0. (2014). Fundamentals of Pediatrics
Competency-based (1st ed.). Quezon City: C and E Publishing, Inc.
11.Parthasarathy A, Menon PSN, Agarwal RN, Choudhury P, Thacker NC, Ugra D (2009). IAP
textbook of pediatrics (4th ed.). New Delhi: Jaypee Brothers
12.The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in
Children and Adolescents. PEDIATRICS, 2004, 114(2), 555-576. doi: 10.1542/
peds.114.2.sZ.555
13.The WHO Child Growth Standards. Retrieved from http://www.who.int/childgrowth/
standards/en/
14.World Health Organization. Management of severe acute malnutrition in infants and children.
Available from https://www.who.int/elena/titles/full_recommendations/sam_management/en/
15.World Health Organization. Supplementary foods for the management of moderate acute
malnutrition in children aged 6-59 months. Available from https://www.who.int/elena/
titles /food_child ren_mam/ en/
16.World Health Organization. Training Course on Child Growth Assessment. Geneva, WHO, 2008.
501
I
502
CORRELATES
BOARD
FLUIDS, ECG, ABG, CHEST RADIOGRAPHS
PREVENTIVE PEDIATRICS
NEONATOLOGY
INFECTIOUS DISEASES
GASTROENTEROLOGY
PULMONOLOGY
IMMUNOLOGY
RHEUMATOLOGY
CARDIOLOGY
NEPHROLOGY
ENDOCRINOLOGY
NEUROLOGY
ACUTE CARE
FLUIDS, ECG, ABG, AND CHEST RADIOGRAPHS: MOST COMMON
505
I
PREVENTIVE PEDIATRICS
Most common form of rape for victims • Acquaintance rape (by a person known to
16-24 years of age the victim)
• Anaphylactic reaction and encephalopathy
Permanent contraindications to
vaccination not due to another cause occurring within
7 days after pertussis vaccination
Vaccines given at birth • BCG& the 1" dose of hepatitis B vaccine
Prophylactic drug of choice for animal
bites category III • Co-amoxiclav for 7 days
506
• Recommended to be done at 9 months,
Developmental screening tests 18 months, 30 months old and every year
thereafter
Most common neurobehavioral disorder
of childhood • Attention-deficit/hyperactivity disorder
507
I
.
INFECTIOUS DISEASES· MOST COMMON
Source of postnatal infections in • Hand contamination of personnel
hospitalized newborns
Bacterial causes of neonatal meningitis • GBS,£. coli, and L. monocytogenes
Cause of neonatal sepsis • Group B streptococcus
Most common bacteria in intrapartum
• GBS and£. coli
and postpartum infections
Most common viruses in intrapartum
• CMV,HSV,enteroviruses, and HIV
and postpartum infections
Cause of hospital acquired infection,
• Coagulase-negative staphylococci (CoNS)
particularly in neonatal units
Vaccine-preventable disease occurring
among pediatric and adult travelers • Influenza
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Isolated organism in perichondritis and
chondritis • P aeruginosa
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Most common serotypes of Shiga Toxin- • E.coli 0157:H7, E.coli 0111:NM, and
Producing Escherichia coli (STEC) E.coli 026:Hll
Age group with TB among nonwhite • Young adults and children younger than 5
populations years of age
• Infiltrate or cavity in the apex of the upper
Form of reactivation TB
lobes
Symptoms of primary TB • Nonproductive cough & mild dyspnea
Form of cardiac tuberculosis • Pericarditis
Age group associated with military TB • Infants and young children
• Painless unilateral otorrhea, tinnitus,
Signs and symptoms of middle ear TB decreased hearing, facial paralysis, and a
perforated tympanic membrane
Form of extra pulmonary TB in children • Scrofula (TB of superficial lymph nodes)
• Basilar enhancement and communicating
Findings in TB meningitis hydrocephalus with signs of cerebral
edema or early focal ischemia
• Children between 6 months and 4 years
Age group in TB meningitis
of age
• Lower abdominal pain and dysmenorrhea
Symptoms of genital tract TB
or amenorrhea
Sequelae of female genital tract TB • Infertility
Organism associated with oral thrush • C.albicans
Opportunistic fungal infections in
patients with prolonged neutropenia • Candida spp. and Aspergillus spp.
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• Hemoconcentration (increase of >20% in
Hematologic abnormalities during hematocrit)
dengue hemorrhagic fever and dengue • Thrombocytopenia
shock syndrome • Prolonged bleeding time
• Moderately decreased prothrombin level
• Enteroviruses (coxsackieviruses,
echoviruses)
Viral causes of meningitis
• Arboviruses (La Crosse encephalitis virus
and equine encephalitis virus)
GASTROENTEROLOGY:MOSTCOMMON
Esophageal disorder in children of all ages • Gast1·oesophageal Reflux Disease (GERO)
Congenital anomaly of the esophagus • Esophageal atresia (EA)
• Type C (upper esophagus ends in blind pouch
Form ofEA
& TEF is connected to distal esophagus)
Encountered foregut duplications • Esophageal duplication cysts
Location for peptic strictures • Lower esophagus
Type of esophageal hiatal hernia • Sliding hiatal hernia
Oral lesion of GERO • Dental erosions
Ingested foreign bodies • Coins and small toy items
• Drain decloggers (especially since they are
Ingested caustic substance
tasteless unlike acidic agents)
Clinical association of pyloric stenos is • Hyperbilirubinemia
Location of gastric duplications • Greater curvature of stomach
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Surgical approach in gastric volvulus • Laparoscopic gastropexy
Symptom ofmalrotation in 1" year of life • Vomiting
• Failure of the cecum to move into the right
Type of malrotation
lower quadrant
Congenital anomaly of the GI tract • Meckel diverticulum
Cause oflower intestinal obstruction in • Congenital Aganglionic Megacolon
neonates (Hirschsprung Disease)
Cause of intestinal obstruction between
5 months & 3 years and most common • lntussusception
abdominal emergency in children <2 years
Time of onset of inflammatory bowel • Preadolescence, adolescence, young
disease adulthood
Hepatobiliary disease associated with IBD • Sclerosing cholangitis
Cause of exocrine pancreatic
• Cystic fibrosis
insufficiency in children
Form of malignant lymphomas of the
• Burkitt lymphoma
small intestines
Manifestations of gastroenteritis • Diarrhea and vomiting
Identifiable viral cause of
• Rotavirus infection
gastroenteritis in all children
Acute surgical condition in children and
• Acute appendicitis
a major cause of childhood morbidity
Misdiagnosis in child with appendicitis • Gastroenteritis
Cause of small bowel obstruction
in children without history of prior • "Missed" appendicitis
abdominal surgery
• Wound infections and intraabdominal
Complications of appendicitis
abscesses
Intestinal tumors of childhood • Hamartomatous polyps
Genetic polyposis syndrome • Familial adenomatous polyposis (FAP)
Primary GI carcinoma in children • Colorectal carcinoma
GI malignancy in the pediatric • Lymphoma (usually in the distal small
population bowel and ileocecal region)
Pancreatic disorder in children • Acute pancreatitis
• Palpable mass in 50%
Signs of pancreatic pseudocyst
• jaundice in 10%
Pancreatic neoplasm in young children • Pancreatoblastoma
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Transplantation-related infections • CMVand EBV infections
513
Cause ofacute hepatitis and jaundice
in the world; increased morbidity and • Hepatitis E virus (HEV) infection
mortality in pregnancy
Chronic liver disease in children • Nonalcoholic fatty liver disease (NAFLD)
Presentation of portal hypertension • Bleeding from esophageal varices
Causes of ascites • Hepatic and renal diseases
Cause of chylous ascites • Lymphatic malformation
Presentation of chylous ascites • Painless abdominal distention
Cause ofperiappendiceal and pelvic
abscesses • Perforated appendix
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• Cardiovascular defects involving right-
Hypoxic polycythemia to-left shunts and pulmonary diseases
interfering with proper oxygenation
Congenital coagulation factor • Hemophilia A (factor VIII deficiency) and
deficiencies hemophilia 8 (factor IXdeficiency)
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PULMONOLOGY: MOST COMMON
516
Causes ofparapneumonic effusions and
empyema • S. aureus, S. pneumoniae, and S. pyogenes
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RHEUMATOLOGY: MOST COMMON
Rheumatic disease in children • Juvenile idiopathic arthritis ()IA}
Subtype ofJIA • Oligoarthritis (40-50%)
Affected joints in Enthesitis-Related
• Knees, ankles, and hips
Arthritis
Presenting complaints of children with • Fever, fatigue, hematologic abnormalities,
SLE arthralgia, and arthritis
• Infection,complications of glomerulonephritis
Causes of death in individuals with SLE
and neuropsychiatric disease
Subtype of Juvenile Localized Scleroderma
• Linear scleroderma
(JLSor morphea)
Extracutaneous manifestation of JLS • Arthritis
Cause of death in Juvenile Systemic • Heart failure caused by myocardial and
Sclerosis pulmonary fibrosis
Manifestations of Sjogren syndrome in • Recurrent parotid gland enlargement and
children parotitis
• Sicca syndrome (dry mouth, painful
Manifestations of Sjogren Syndrome in
mucosa, sensitivity to spicy foods,
adults
halitosis, widespread dental caries)
• Periodic Fever, Aphthous Stoma ti tis,
Recurrent fever syndrome in children
Pharyngitis, and Adenitis (PFAPA)
Vessels affected in Kawasaki disease • Coronary arteries
Vasculitis of childhood • Henoch-Schiinlein purpura
Population group in Takayasu Arteritis (TA} • Asians
Aortic branches affected in TA • Subclavian, renal, and carotid arteries
• Patients with ulcerative colitis who
Population group associated with
ankylosing spondylitis have the human leukocyte antigen B27
phenotype
Presenting problem of children referred
to pediatric rheumatology clinics • Musculoskeletal pain
518
CARDIOLOGY: MOST COMMON
• Medium-pitched, vibratmy or "musical;'
Findings for innocent or functional
murmur relatively short systolic ejection murmur. heard
best along the left lower & midsternal border
Congenital heart defect • Ventricular septa! defect (VSD)
Form of atrial septal defect • Ostium secundum defect
Cause of death in adolescent athletes • Hypertrophic cardiomyopathy
Congenital defect associated with
sudden death in children • Valvar aortic stenos is
Form of acquired heart disease in all ages • Rheumatic Heart Disease (RHD)
Cause of serious morbidity in those with • Heart failure caused by vegetations
documented infective endocarditis involving the aortic or mitral valve
Form of cardiomyopathy in children • Dilated cardiomyopathy (DCM)
Etiology of DCM • Idiopathic
• Sharp, positional chest pain worse with
Symptom of acute pericarditis
inspiration & relieved by sitting upright
Pediatric cardiac tumors • Rhabdomyomas (myxomas in adults)
Diuretic in children with heart failure • Furosemide
Manifestation of target-organ damage
• Left ventricular hypertrophy (LVH)
in hypertensive children
NEPHROLOGY: MOST COMMON
Cause of gross hematuria • Bacterial urinary tract infection
Chronic glomerular disease in children • lgA nephropathy
Cause ofhypoalbuminemia in children • Renal disorder
Cause ofnephrotic syndrome worldwide • Membranous nephropathy from malaria
Cause of persistent proteinuria in
school-age children and adolescents • 01thostatic (postural) proteinuria
520
Clinical manifestations of chronic
lymphocytic thyroiditis • Goiter and growth retardation
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NEUROLOGY: MOST COMMON
522
ACUTECARE·MOSTCOMMON
• 0-4 years old: falls, nonaccidental trauma
Cause of traumatic brain injury
• > 14 years old: motor vehicle injury
REFERENCES
1. Kliegman, R., ST GEME Ill, j., Blum, N., Shah, S., Tasker, R., Wilson, K., & Behrman, R. (2020).
Nelson Textbook of Pediatrics (21st ed.). Philadelphia: Elsevier.
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