Neonatology for Primary Care Deborah E.

Campbell
install download

https://ebookmeta.com/product/neonatology-for-primary-care-
deborah-e-campbell/

Download more ebook from https://ebookmeta.com

We believe these products will be a great fit for you. Click
the link to download now, or visit ebookmeta.com
to discover even more!

Pediatric Primary Care 6th Edition Catherine E. Burns

(Editor)

https://ebookmeta.com/product/pediatric-primary-care-6th-edition-
catherine-e-burns-editor/

Dermatology for the Primary Care Provider Reid A.

Waldman

https://ebookmeta.com/product/dermatology-for-the-primary-care-
provider-reid-a-waldman/

Pediatric Psychopharmacology for Primary Care 3rd

Edition Mark A Riddle

https://ebookmeta.com/product/pediatric-psychopharmacology-for-
primary-care-3rd-edition-mark-a-riddle/

Comprehensive Clinical Approach to Diabetes During

Pregnancy Dimitrios G. Goulis

https://ebookmeta.com/product/comprehensive-clinical-approach-to-
diabetes-during-pregnancy-dimitrios-g-goulis/
DK How to Be Good at Math The simplest ever visual
guide Ages 7 11 Dorling Kindersley

https://ebookmeta.com/product/dk-how-to-be-good-at-math-the-
simplest-ever-visual-guide-ages-7-11-dorling-kindersley/

Introduction to Classical and Quantum Computing 1st

Edition Thomas Wong

https://ebookmeta.com/product/introduction-to-classical-and-
quantum-computing-1st-edition-thomas-wong/

Pearls gone wild Samantha Kidd Style Error Mystery 06

Diane Vallere Et El

https://ebookmeta.com/product/pearls-gone-wild-samantha-kidd-
style-error-mystery-06-diane-vallere-et-el/

Incarnate Earth Deep Incarnation and the Face of Christ

1st Edition Matthew Eaton

https://ebookmeta.com/product/incarnate-earth-deep-incarnation-
and-the-face-of-christ-1st-edition-matthew-eaton/

The AWK Programming Language Addison Wesley

Professional Computing Series 2nd Edition Alfred Aho

https://ebookmeta.com/product/the-awk-programming-language-
addison-wesley-professional-computing-series-2nd-edition-alfred-
aho/
RN Maternal Newborn Nursing REVIEW MODULE EDITION 11.0
Ati Nursing Education

https://ebookmeta.com/product/rn-maternal-newborn-nursing-review-
module-edition-11-0-ati-nursing-education/
 Neonatology for Primary Care
Neonatology

2nd Edition
for Primary Care Neonatology
2nd Edition
Editor: Deborah E. Campbell, MD, FAAP
The revised and updated second edition covers practical approaches to caring for healthy and
for Primary Care
high-risk newborns and infants. Topics covered include maternal and fetal health, care of the
newborn after delivery, breastfeeding, follow-up care, common congenital anomalies, the newborn
with a heart murmur or cyanosis, neurologic findings, primary care issues relating to newborns 2nd Edition
and infants requiring intensive care, and health and developmental outcomes.
The content covers the continuum of care from delivery through hospitalization and discharge
for the healthy term and late preterm newborn and infant, as well as the newborn who requires
specialized neonatal intensive care.
More than 40 chapters cover step-by-step recommendations on what to do, when to admit, and
when to refer. Detailed references and links to relevant American Academy of Pediatrics policies
are noted within each chapter.

New in the second edition

8 new chapters, including
• Prenatal Diagnosis • Balancing Safe Sleep and Other
• Fetal Interventions ­Recommendations for Newborns
• Optimizing Nutrition for the Preterm, • Vascular Anomalies
Very Low-Birth-Weight Infant After • Endocrine Disorders Manifesting in the
­Discharge From Neonatal Intensive Care Newborn Period
• Newborn Immunizations and Immune • Shared Decision Making Around Home
Prophylaxis Technologies

Comprehensive coverage includes

• Perinatal preventive care • Caring for the high-risk infant
• Routine care issues • Neonatal outcomes
• Assessment and physical examination • Medicolegal considerations
of the newborn • Support for families during perinatal
• Neonatal medical conditions illness and death

Neonatology for Primary Care, 2nd Edition, is an ideal resource for pediatricians, family physicians,
medical students, residents, residency program directors, physician assistants, pediatric nurse
practitioners, and nurses.

For other neonatal and pediatric resources, visit the American Academy of Pediatrics Editor: Deborah E. Campbell, MD, FAAP
at shop.aap.org.

AAP
Neonatology
for Primary Care
2nd Edition

Editor
Deborah E. Campbell, MD, FAAP
Professor of Pediatrics
Associate Professor of Obstetrics & Gynecology and Women’s Health
Albert Einstein College of Medicine
Chief, Division of Neonatology
Children’s Hospital at Montefiore
Bronx, NY
American Academy of Pediatrics Publishing Staff

Mary Lou White, Chief Product and Services Officer/SVP, Membership, Marketing, and
Publishing
Mark Grimes, Vice President, Publishing
Chris Wiberg, Senior Editor, Professional/Clinical Publishing
Theresa Wiener, Production Manager, Clinical and Professional Publications
Mary Louise Carr, MBA, Marketing Manager, Clinical Publications

Published by the American Academy of Pediatrics

345 Park Blvd
Itasca, IL 60143
Telephone: 630/626-6000
Facsimile: 847/434-8000
www.aap.org

The American Academy of Pediatrics is an organization of 67,000 primary care pediatricians,

pediatric medical subspecialists, and pediatric surgical specialists dedicated to the health,
safety, and well-being of infants, children, adolescents, and young adults.
The recommendations in this publication do not indicate an exclusive course of treatment or
serve as a standard of medical care. Variations, taking into account individual circumstances,
may be appropriate.
Any websites, brand names, products, or manufacturers are mentioned for informational and
identification purposes only and do not imply an endorsement by the American Academy of
Pediatrics (AAP). The AAP is not responsible for the content of external resources. Information
was current at the time of publication.
The publishers have made every effort to trace the copyright holders for borrowed material.
If they have inadvertently overlooked any, they will be pleased to make the necessary
arrangements at the first opportunity.
This publication has been developed by the American Academy of Pediatrics. The authors,
editors, and contributors are expert authorities in the field of pediatrics. No commercial
involvement of any kind has been solicited or accepted in the development of the content
of this publication. Disclosures: Dr Derrick (Ch 32) disclosed a family member’s consulting
relationship with Colgate. Dr Drzewiecki (Ch 32) disclosed a consulting relationship with
Astellas Pharma. Dr Kim (Ch 10) disclosed a consulting relationship with Medela and with
Astarte Medical, a shareholder relationship with Nicolette, and a principal investigator
relationship with Mallinckrodt. Dr Munjal (Ch 11) disclosed an employee and stockholder
relationship with Pfizer, Inc. Dr Schanler (Ch 9) disclosed a medical advisory board
relationship with Medela.
Every effort has been made to ensure that the drug selection and dosages set forth in this text
are in accordance with the current recommendations and practice at the time of publication.
It is the responsibility of the health care professional to check the package insert of each drug
for any change in indications and dosages and for added warnings and precautions.
Every effort is made to keep Neonatology for Primary Care consistent with the most recent
advice and information available from the American Academy of Pediatrics.
Special discounts are available for bulk purchases of this publication. Email Special Sales at
[email protected] for more information.
© 2020 American Academy of Pediatrics
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system,
or transmitted in any form or by any means—electronic, mechanical, photocopying, recording,
or otherwise—without prior written permission from the publisher (locate title at http://ebooks.
aappublications.org and click on © Get permissions; you may also fax the permissions editor
at 847/434-8780 or email [email protected]). First edition published 2015; fourth, 2020.

Printed in the United States of America

9-427/1219 1 2 3 4 5 6 7 8 9 10
MA0884
ISBN: 978-1-61002-224-8
eBook: 978-1-61002-225-5
Cover and publication design by Peg Mulcahy
Library of Congress Control Number: 2018932591
 Contributors

Mohamed Farooq Ahamed, MD, Albert Einstein College of

FAAP Medicine
Assistant Professor of Pediatrics Bronx, NY
Division of Neonatology 11. Newborn Immunizations and
Southern Illinois University- Immune Prophylaxis
School of Medicine
Springfield, IL Ada E. Aponte, MD, FAAP
34. Surgical Emergencies of the Assistant Professor, Albert
Chest and Abdomen in the Einstein College of Medicine
Newborn Newborn Nursery Hospitalist
The Children’s Hospital at
Neil Joseph B. Alviedo, MD Montefiore - Weiler Division
Assistant Professor Bronx, NY
Division of Neonatal-Perinatal 18. Physical Examination of the
Medicine Newborn
University of Florida
Jacksonville, FL Felix De Paz Bañadera, MD
29. Prenatal Drug Use: Neonatal Assistant Professor of Pediatrics
Effects and the Neonatal Neonatologist
Withdrawal Syndrome Division of Neonatology
University of Florida
Wyatt Andrasik, MD Jacksonville, FL
Resident, Dermatology 29. Prenatal Drug Use: Neonatal
Cleveland Clinic Foundation Effects and the Neonatal
Cleveland, OH Withdrawal Syndrome
20. Vascular Anomalies
Judy C. Bernbaum, MD, FAAP
Robert Angert, MD, FAAP Professor of Pediatrics
Attending Neonatologist The University of Pennsylvania
Assistant Professor of Pediatrics School of Medicine
Children’s Hospital at Montefiore Senior Attending Physician

iii
 CONTRIBUTORS
iv

Director, Neonatal Follow Up Chief, Division of Neonatology

Program Children’s Hospital at Montefiore
The Children’s Hospital of Bronx, NY
Philadelphia 7. Prenatal Pediatric Visit
Philadelphia, PA 38. Continuing Care of the Infant
40. Follow-up Care of the After Transfer From Neonatal
Graduate From Neonatal Intensive Care
Intensive Care 39. Discharge Planning for the
High-Risk Newborn Requiring
Diane E. Bloomfield, MD, FAAP Intensive Care
Assistant Professor 41. Health and Developmental
Division of Academic General Outcomes of Very Preterm and
Pediatrics Very Low-Birth-Weight Infants
The Children’s Hospital at 42. Health and Developmental
Montefiore Outcomes of Selected Medically
Albert Einstein College of Complex Neonates
Medicine 44. Support for Families Whose
Bronx, NY Infant Is Sick or Dying
8. Care of the Newborn After
Delivery Amy Y-Y. Chen, MD, FAAD
Assistant Professor of Dermatology
Luc P. Brion, MD, FAAP Department of Dermatology
Professor of Pediatrics University of Connecticut School
University of Texas Southwestern of Medicine
Medical Center Farmington, CT
Dallas, TX 19. Neonatal Skin
24. Neonatal Jaundice 20. Vascular Anomalies

Christie J. Bruno, DO, FAAP Charlie Tan Cheng, MD

Attending Neonatologist Research Assistant
Yale-New Haven Children’s Department of Pediatrics
Hospital Wayne State University
Assistant Professor of Pediatrics Detroit, MI
Yale School of Medicine 29. Prenatal Drug Use: Neonatal
New Haven, CT Effects and the Neonatal
2. Assisted Reproductive Withdrawal Syndrome
Technologies, Multiple Births,
and Pregnancy Outcomes Josef Cortez, MD, FAAP
Medical Director, Neonatal
Deborah E. Campbell, MD, Intensive Care Unit
FAAP Assistant Professor of Pediatrics
Professor of Pediatrics Division of Neonatology
Associate Professor of Obstetrics University of Florida College of
& Gynecology and Women’s Medicine - Jacksonville
Health Associate Neonatologist
Albert Einstein College of Wolfson Children’s Hospital
Medicine Jacksonville, FL
 CONTRIBUTORS
v

29. Prenatal Drug Use: Neonatal M. Catherine Driscoll, MD

Effects and the Neonatal Professor of Clinical Pediatrics
Withdrawal Syndrome Division of Pediatric
Hematology-Oncology
Lilia C. De Jesus, MD, FAAP Albert Einstein College of
Neonatologist Medicine
Benioff Children’s Hospital Bronx, NY
Oakland 28. The Newborn With
University of California San Hematologic Abnormalities
Francisco
San Francisco, CA Beth A. Drzewiecki, MD
29. Prenatal Drug Use: Neonatal Assistant Professor of Urology
Effects and the Neonatal Division of Pediatric Urology
Withdrawal Syndrome Children’s Hospital of Montefiore/
Albert Einstein College of
Sonia Dela Cruz-Rivera, MD Medicine
Assistant Professor of Pediatrics Bronx, NY
Division of Pediatrics 32. Endocrine Disorders
Montefiore Medical Center Manifesting in the Newborn
Bronx, NY Period
15. Hospital Discharge of the
Healthy Term and Late Preterm
Marian F. Earls, MD, MTS, FAAP
Infant
Clinical Professor of Pediatrics
University of North Carolina
Kristina M. Derrick, MD, ScM
School of Medicine
Assistant Professor of Pediatrics
Chapel Hill, NC
Division of Pediatric
Director of Pediatric Programs
Endocrinology
Community Care of North
Children’s Hospital at
Carolina
Montefiore/Albert Einstein
Raleigh, NC
College of Medicine
5. Maternal Depression
Bronx, NY
32. Endocrine Disorders
Manifesting in the Newborn Jonathan M. Fanaroff, MD, JD,
Period FAAP
Professor of Pediatrics
Elaine A. Dinolfo MD, MS, Case Western Reserve University
FAAP School of Medicine
Harlem Hospital Center Director, Rainbow Center for
Department of Pediatrics Pediatric Ethics
Assistant Clinical Professor of Co-Medical Director, Neonatal
Pediatrics Intensive Care Unit
Columbia University College of Rainbow Babies & Children’s
Physicians and Surgeons Hospital
New York, NY Cleveland, OH
8. Care of the Newborn After 6. Medicolegal Considerations in
Delivery the Care of Newborns
 CONTRIBUTORS
vi

John M. Fiascone, MD, FAAP Anna C. Ganster, MD

NICU Medical Director, South Clinical Assistant Professor of
Shore Hospital Pediatrics (Clinician Educator)
Lecturer in Pediatrics, Part time Fetal and Neonatal Institute,
Harvard Medical School Division of Neonatology
South Weymouth, MA Children’s Hospital Los Angeles,
30. Transient Metabolic Department of Pediatrics
Disturbances in the Newborn Keck School of Medicine,
University of Southern
Katie R. Forman, DO, FAAP California
Co-Director Neonatal Palliative Los Angeles, CA
Care Program 34. Surgical Emergencies of the
Assistant Professor of Pediatrics Chest and Abdomen in the
Albert Einstein College of Newborn
Medicine
The Children’s Hospital at Gina M. Geis, MD, FAAP
Montefiore Attending Neonatologist, Albany
Bronx, NY Medical Center
44. Support for Families Whose Associate Professor of Pediatrics
Infant Is Sick or Dying Associate Professor, Center for
Bioethics, Education and
Andrew L. Freedman, MD Research
Walter and Shirley Wang Chair in Chair, Hospital Ethics Committee,
Pediatric Surgery Albany Medical Center
Vice Chair for Pediatric Surgical Albany Medical College
Services Albany, NY
Director of Pediatric Urology 37. Care of the Sick or Preterm
Professor of Surgery Newborn Before Transport
Department of Surgery
Cedars-Sinai Medical Center Sarah Chambers Gurson, MD
Los Angeles, CA Pediatric Cardiology Associates, a
13. The Circumcision Decision MEDNAX affiliate
Fairfax, VA
Mamta Fuloria, MD, FAAP 42. Health and Developmental
Associate Professor, Pediatrics Outcomes of Selected Medically
Albert Einstein College of Complex Neonates
Medicine
Director, Neonatal-Perinatal Kendria C. Hall, MD, FAAP
Medicine Fellowship Training Assistant Professor of Pediatrics
Program Division of Neonatology
The Children’s Hospital at Albert Einstein College of
Montefiore Medicine
Bronx, NY Children’s Hospital at Montefiore
34. Surgical Emergencies of the Bronx, NY
Chest and Abdomen in the 17. Maternal Medical History
Newborn
 CONTRIBUTORS
vii

Nancy M. Hurst, RN, PhD, University of California San Diego

IBCLC San Diego, CA
Director, Women’s Support 24. Neonatal Jaundice
Services
Texas Children’s Hospital Pavilion Tamara Kalhan, MD
for Women Assistant Professor of
Assistant Professor of Pediatrics Pediatrics
Baylor College of Medicine Division of Neonatology
Houston, TX Children’s Hospital at Montefiore
10. Optimizing Nutrition for the Bronx, NY
Preterm, Very Low-Birth-Weight 11. Newborn Immunizations and
Infant After Discharge From Immune Prophylaxis
Neonatal Intensive Care
Harpreet Kaur, MD
Sonia O. Imaizumi, MD, FAAP Assistant Professor of Pediatrics
Medical Director, Independence Rutgers New Jersey Medical
Blue Cross School
Philadelphia, PA Newark, NJ
41. Health and Developmental 17. Maternal Medical History
Outcomes of Very Preterm and 18. Physical Examination of the
Very Low-Birth-Weight Infants Newborn

Abieyuwa Iyare, MD, FAAP Ann L. Kellams, MD, IBCLC,

Assistant Professor of Pediatrics FAAP, FABM
Division of Neonatology Associate Professor, Department
Albert Einstein College of Medicine of Pediatrics
Children’s Hospital of Montefiore Medical Director, Well Newborn
Bronx, NY and Breastfeeding Medicine
22. Postnatal Assessment of Services
Common Prenatal Sonographic University of Virginia
Findings Charlottesville, VA
12. Balancing Safe Sleep and
Yong-Hui Jiang, MD, PhD Other Recommendations for
Professor and Chief of Medical Newborns
Genetics
Department of Genetics Jae H. Kim, MD, PhD, FAAP
Yale University School of Professor of Pediatrics
Medicine Director, Division of Neonatology,
New Haven, CT Perinatal Institute
21. Common Congenital Cincinnati Children’s Hospital
Anomalies Medical Center
Cincinnati, OH
Kathryn A. Johnson, MD, FAAP 10. Optimizing Nutrition for
Associate Professor of Pediatrics the Preterm, Very Low-
Division of Academic General Birth-Weight Infant After
Pediatrics, Child Development, Discharge From Neonatal
and Community Health Intensive Care
 CONTRIBUTORS
viii

Tsoline Kojaoghlanian, MD, 21. Common Congenital

FAAP Anomalies
Director, Pediatric Infectious
Diseases Grace L. Lee, MD, FAAD
SBH Health System Assistant Professor of
Albert Einstein College of Medicine Dermatology and Pediatrics
Bronx, NY Texas Children’s Hospital
27. The Newborn at Risk of Baylor College of Medicine
Infection Houston, TX
20. Vascular Anomalies
Faye Kokotos, MD, FAAP
Assistant Professor of Pediatrics Bridget Leone, MD
Division of Academic General Montefiore Medical Center
Pediatrics Albert Einstein College of
Children’s Hospital at Montefiore Medicine
Albert Einstein College of Bronx, NY
Medicine 33. The Newborn With Neurologic
Bronx, NY Findings
8. Care of the Newborn After
Delivery George A. Little, MD, FAAP
Active Emeritus Professor of
Zuzanna Kubicka, MD Pediatrics
Boston Children’s Hospital Geisel School of Medicine
Boston, MA Dartmouth College
30. Transient Metabolic Hanover, NH
Disturbances in the Newborn 1. Perinatal Preventive Care: Fetal
Assessment
Leslie Lam, MD
Assistant Profess of Pediatrics Christina M. Long, DO
Interim Chief, Division of Associate Professor of Pediatrics
Pediatric Endocrine and Division of Neonatology
Diabetes University of Washington, Seattle
Children’s Hospital of Montefiore Children’s Hospital
Bronx, NY Seattle, WA
32. Endocrine Disorders 25. Respiratory Distress and
Manifesting in the Newborn Breathing Disorders in the
Period Newborn
39. Discharge Planning for the
M. Susan LaTuga, MD, MSPH, High-Risk Newborn Requiring
FAAP Intensive Care
Assistant Professor of Pediatrics
Division of Neonatology Deepa Manwani, MD
Albert Einstein College of Director, Pediatric Hematology
Medicine Program
The Children’s Hospital at Children’s Hospital at Montefiore
Montefiore Albert Einstein College of Medicine
Bronx, NY Bronx, NY
 CONTRIBUTORS
ix

28. The Newborn With Iona Munjal, MD

Hematologic Abnormalities Assistant Professor of Pediatrics
Montefiore Medical Center
Britni B. Maple, MD Bronx, NY
Fellow, Neonatal-Perinatal 11. Newborn Immunizations and
Medicine Immune Prophylaxis
University of Texas Southwestern
Medical Center Upender K. Munshi, MBBS,
Dallas, TX MD, FAAP
24. Neonatal Jaundice Professor of Pediatrics,
Neonatology Division
Nelly Maseda, MD, FAAP Albany Medical Center
Assistant Professor of Pediatrics Albany, NY
Albert Einstein School of Medicine 36. Identifying the Newborn Who
Pediatrician Requires Specialized Care
Children’s Hospital at Montefiore
Bronx, NY Suhas M. Nafday, MD, MRCP
7. Prenatal Pediatric Visit (Ire), DCH, FAAP
Associate Professor of Pediatrics
Teri Jo Mauch, MD, PhD, Albert Einstein College of
FAAP, FASN Medicine
Professor and Chief, Pediatric Director, Weiler Newborn
Nephrology Services, Neonatology
University of Nebraska Medical Chair, Neonatal Performance
Center and Omaha Children’s Improvement and Patient
Hospital Safety
Omaha, NE Children’s Hospital at Montefiore
22. Postnatal Assessment of Bronx, NY
Common Prenatal Sonographic 23. Abnormalities of Fetal Growth
Findings 25. Respiratory Distress and
Breathing Disorders in the
Rochelle R. Maxwell, MD Newborn
Instructor in Clinical
Investigation Sheri L. Nemerofsky, MD,
The Rockefeller University FAAP
New York, NY Associate Professor of Pediatrics
28. The Newborn With Division of Neonatology
Hematologic Abnormalities Albert Einstein College of
Medicine
Marie McDonald, MD Montefiore Medical Center
Division of Medical Genetics Bronx, NY
Department of Pediatrics 14. Care of the Late Preterm and
Duke University Early Term Infant
Durham, NC 22. Postnatal Assessment of
21. Common Congenital Common Prenatal Sonographic
Anomalies Findings
 CONTRIBUTORS
x

Sarah A. Nitka, DO, FAAP Geisel School of Medicine at

Assistant Professor of Pediatrics Dartmouth College
Division of Neonatology Hanover, NH
Albert Einstein College of 1. Perinatal Preventive Care: Fetal
Medicine Assessment
Children’s Hospital at Montefiore
Bronx, NY Alaina Pyle, MD, FAAP
14. Care of the Late Preterm and Assistant Professor of Pediatrics
Early Term Infant Connecticut Children’s Medical
Center
Enrique M. Ostrea Jr, MD Hartford, CT
Professor of Pediatrics 2. Assisted Reproductive
Wayne State University Technologies, Multiple Births,
Neonatologist and Pregnancy Outcomes
Hutzel Women’s Hospital
Children’s Hospital of Michigan Angel Rios, MD, FAAP
Detroit, MI Professor of Pediatrics
29. Prenatal Drug Use: Neonatal Director of Neonatology
Effects and the Neonatal Bernard and Millie Duker
Withdrawal Syndrome Children’s Hospital at the
Albany Medical Center
Jillian Parekh, MD, FAAP Albany, NY
Assistant Professor of Pediatrics 31. Specific Congenital Metabolic
Division of Academic General Diseases
Pediatrics
Children’s Hospital at Montefiore Richard J. Schanler, MD, FAAP
Bronx, NY Director, Neonatal Services
16. Follow-up Care of the Healthy Cohen Children’s Medical Center,
Newborn Northwell Health
Zucker School of Medicine at
Joaquim M. B. Pinheiro, MD, Hofstra/Northwell
MPH, FAAP New Hyde Park, NY
Professor of Pediatrics 9. Breastfeeding the Newborn
Director, Neonatology Fellowship
Program
Albany Medical Center Kathryn Scharbach, MD, MS
Albany, NY Assistant Professor of Pediatrics
35. Assessment and Stabilization Division of General Pediatrics
at Delivery Icahn School of Medicine at
Mount Sinai
E. Rebecca Pschirrer, MD, MPH New York, NY
Associate Professor of Obstetrics 39. Discharge Planning for the
& Gynecology, and Radiology High-Risk Newborn Requiring
Division of Maternal Fetal Intensive Care
Medicine 43. Shared Decision Making
Director of Obstetric Ultrasound Around Home Technologies
and Prenatal Diagnosis
 CONTRIBUTORS
xi

Natasha Shur, MD 3. Prenatal Diagnosis

Associate Professor of Pediatrics 4. Fetal Interventions
The George Washington
University Nicole J. Sutton, MD, FACC
Clinical Geneticist Associate Professor of Pediatrics
Rare Disease Institute Division of Pediatric Cardiology
Washington, DC Albert Einstein College of
31. Specific Congenital Metabolic Medicine
Diseases Bronx, NY
26. The Newborn With a Heart
Lisa M. Stellwagen, MD, FAAP Murmur or Cyanosis
Professor of Clinical Pediatrics
Director, Newborn Medicine Allison Taylor, MD, FAAP
Division of Academic General Assistant Professor of Pediatrics
Pediatrics Division of Academic Pediatrics
University of California, San Albert Einstein College of
Diego Medicine
San Diego, CA Montefiore Medical Center
9. Breastfeeding the Newborn Bronx, NY
10. Optimizing Nutrition for the 16. Follow-up Care of the Healthy
Preterm, Very Low-Birth-Weight Newborn
Infant After Discharge From
Neonatal Intensive Care Alecia Thompson-Branch, MD,
FAAP
Christina Kan Sullivan, MD Assistant Professor of Pediatrics
Assistant Clinical Professor of Division of Neonatology
Pediatrics Albert Einstein College of
Division of Academic General Medicine
Pediatrics Bronx, NY
Childrens Hospital at Montefiore 44. Support for Families Whose
Albert Einstein College of Infant Is Sick or Dying
Medicine
Bronx, NY Julian Trevino, MD, FAAD
15. Hospital Discharge of the Professor and Chair, Department
Healthy Term and Late Preterm of Dermatology
Infant Program Director, Dermatology
Residency Program
Barrie Suskin, MD, FACOG, Boonshoft School of Medicine
FACMG Wright State University
Assistant Professor of Obstetrics Fairborn, OH
and Gynecology 19. Neonatal Skin
Division of Ultrasound and Fetal 20. Vascular Anomalies
Medicine
Albert Einstein College of Robert Turbow, MD, JD, FAAP
Medicine Attending Neonatologist
Bronx, NY Chief Patient Safety Officer
 CONTRIBUTORS
xii

Marian Regional Medical Center Diana S. Wolfe, MD, MPH

Santa Maria, CA Associate Maternal Fetal
6. Medicolegal Considerations in Medicine Fellowship Director
the Care of Newborns Assistant Professor of Obstetrics
& Gynecology and Women’s
Lisa Underland, DO Health
Assistant Professor Albert Einstein College of
Children’s Hospital at Montefiore Medicine/Montefiore Medical
Bronx, NY Center
32. Endocrine Disorders Bronx, NY
Manifesting in the Newborn 3. Prenatal Diagnosis
Period
Karen S. Wood, MD, FAAP
Elizabeth Usedom, MD, MS Professor of Pediatrics
Drexel University College of Medical Director, Neonatal
Medicine Critical Care Center, UNC
Philadelphia, PA Hospitals
19. Neonatal Skin Medical Director, Pediatric
Transport, UNC AirCare
Joseph A. Vitterito II, MD and Ground Transportation
Chair, Department of Neonatology Services
Chief, Division of Neonatology Department of Pediatrics
St. Vincent’s Medical Center Division of Neonatal-Perinatal
Bridgeport, CT Medicine
Associate Professor of Pediatrics University of North Carolina
Frank Netter School of Medicine Hospitals, Chapel Hill, NC
North Haven, CT 37. Care of the Sick or Preterm
University of Connecticut School Newborn Before Transport
of Medicine
Farmington, CT Elissa Yozawitz, MD
44. Support for Families Whose Director, Neonatal Neurology
Infant Is Sick or Dying Associate Professor
Isabelle Rapin Division of Child
Christine A. Walsh, MD, FACC Neurology
Professor Emerita of the Saul R. Korey Department
Albert Einstein College of of Neurology
Medicine Montefiore Medical Center
Co-Director, Einstein-Montefiore Albert Einstein College of
Cardiogenetics Center Medicine
Division of Pediatric Cardiology Bronx, NY
Children’s Hospital at Montefiore 33. The Newborn With Neurologic
Bronx, NY Findings
26. The Newborn With a Heart
Murmur or Cyanosis
 American Academy of
Pediatrics Reviewers

Committee on Child Health Financing

Committee on Drugs
Committee on Fetus and Newborn
Committee on Infectious Diseases
Committee on Native American Child Health
Committee on Practice and Ambulatory Medicine
Council on Children With Disabilities
Disaster Preparedness Advisory Council
Family Partnerships Network
Infantile Hemangioma Clinical Practice Guideline Subcommittee
Section on Allergy and Immunology
Section on Breastfeeding
Section on Cardiology and Cardiac Surgery
Section on Endocrinology
Section on Gastroenterology, Hepatology, and Nutrition
Section on Hematology/Oncology
Section on Home Care
Section on Hospital Medicine
Section on Infectious Diseases
Section on Lesbian, Gay, Bisexual, and Transgender Health and
Wellness
Section on Minority Health, Equity, and Inclusion
Section on Neonatal-Perinatal Medicine
Section on Nephrology
Section on Neurology
Section on Ophthalmology
Section on Pediatric Pulmonology and Sleep Medicine
Section on Plastic Surgery
Section on Radiology
Section on Surgery
Section on Urology
Task Force on Sudden Infant Death Syndrome

xiii
 Contents

PREFACE..........................................................................................................................xxi

Part 1: Perinatal Health

1. PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT..................................... 3

E. Rebecca Pschirrer, MD, MPH
George A. Little, MD, FAAP

2. ASSISTED REPRODUCTIVE TECHNOLOGIES, MULTIPLE BIRTHS, AND

PREGNANCY OUTCOMES...................................................................................... 59
Christie J. Bruno, DO, FAAP
Alaina Pyle, MD, FAAP

3. PRENATAL DIAGNOSIS .......................................................................................... 77

Diana S. Wolfe, MD, MPH
Barrie Suskin, MD, FACOG, FACMG

4. FETAL INTERVENTIONS...................................................................................... 105

Barrie Suskin, MD, FACOG, FACMG

5. MATERNAL DEPRESSION .....................................................................................131

Marian F. Earls, MD, MTS, FAAP

Part 2: Routine Care Issues

6. MEDICOLEGAL CONSIDERATIONS IN THE CARE OF NEWBORNS................143

Jonathan M. Fanaroff, MD, JD, FAAP
Robert Turbow, MD, JD, FAAP

7. PRENATAL PEDIATRIC VISIT ............................................................................... 167

Nelly Maseda, MD, FAAP
Deborah E. Campbell, MD, FAAP

8. CARE OF THE NEWBORN AFTER DELIVERY ................................................... 175

Diane E. Bloomfield, MD, FAAP
Elaine A. Dinolfo, MD, MS, FAAP
Faye Kokotos, MD, FAAP

xv
 CONTENTS
xvi

9. BREASTFEEDING THE NEWBORN.....................................................................195

Lisa M. Stellwagen, MD, FAAP
Richard J. Schanler, MD, FAAP

10. OPTIMIZING NUTRITION FOR THE PRETERM, VERY LOW-BIRTH-WEIGHT

INFANT AFTER DISCHARGE FROM NEONATAL INTENSIVE CARE ...............235
Lisa M. Stellwagen, MD, FAAP
Jae H. Kim, MD, PhD, FAAP
Nancy M. Hurst, RN, PhD, IBCLC

11. NEWBORN IMMUNIZATIONS AND IMMUNE PROPHYLAXIS ......................... 263

Robert Angert, MD, FAAP
Iona Munjal, MD
Tamara Kalhan, MD

12. BALANCING SAFE SLEEP AND OTHER RECOMMENDATIONS FOR

NEWBORNS .......................................................................................................... 285
Ann L. Kellams, MD, IBCLC, FAAP, FABM

13. THE CIRCUMCISION DECISION ..........................................................................303

Andrew L. Freedman, MD

14. CARE OF THE LATE PRETERM AND EARLY TERM INFANT ............................315
Sheri L. Nemerofsky, MD, FAAP
Sarah A. Nitka, DO, FAAP

15. HOSPITAL DISCHARGE OF THE HEALTHY TERM AND LATE PRETERM

INFANT ....................................................................................................................341
Christina Kan Sullivan, MD
Sonia Dela Cruz-Rivera, MD

16. FOLLOW-UP CARE OF THE HEALTHY NEWBORN......................................... 365

Allison Taylor, MD, FAAP
Jillian Parekh, MD, FAAP

Part 3: Assessment and Physical Examination of the

Newborn

17. MATERNAL MEDICAL HISTORY ...........................................................................381

Harpreet Kaur, MD
Kendria C. Hall, MD, FAAP

18. PHYSICAL EXAMINATION OF THE NEWBORN................................................ 399

Harpreet Kaur, MD
Ada E. Aponte, MD, FAAP

19. NEONATAL SKIN....................................................................................................439

Julian Trevino, MD, FAAD
Elizabeth Usedom, MD, MS
Amy Y-Y. Chen, MD, FAAD

20. VASCULAR ANOMALIES.......................................................................................463

Grace L. Lee, MD, FAAD
Julian Trevino, MD, FAAD
 CONTENTS
xvii

Wyatt Andrasik, MD
Amy Y-Y. Chen, MD, FAAD

21. COMMON CONGENITAL ANOMALIES .................................................................491

M. Susan LaTuga, MD, MSPH, FAAP
Marie McDonald, MD
Yong-Hui Jiang, MD, PhD

22. POSTNATAL ASSESSMENT OF COMMON PRENATAL SONOGRAPHIC

FINDINGS ................................................................................................................513
Sheri L. Nemerofsky, MD, FAAP
Abieyuwa Iyare, MD, FAAP
Teri Jo Mauch, MD, PhD, FAAP, FASN

Part 4: Neonatal Medical Conditions

23. ABNORMALITIES OF FETAL GROWTH ............................................................. 539

Suhas M. Nafday, MD, MRCP (Ire), DCH, FAAP

24. NEONATAL JAUNDICE .......................................................................................... 565

Kathryn A. Johnson, MD, FAAP
Britni B. Maple, MD
Luc P. Brion, MD, FAAP

25. RESPIRATORY DISTRESS AND BREATHING DISORDERS

IN THE NEWBORN ............................................................................................... 595
Suhas M. Nafday, MD, MRCP (Ire), DCH, FAAP
Christina M. Long, DO

26. THE NEWBORN WITH A HEART MURMUR OR CYANOSIS ........................... 637

Nicole J. Sutton, MD, FACC
Christine A. Walsh, MD, FACC

27. THE NEWBORN AT RISK OF INFECTION ......................................................... 659

Tsoline Kojaoghlanian, MD, FAAP

28. THE NEWBORN WITH HEMATOLOGIC ABNORMALITIES .............................. 691

Rochelle R. Maxwell, MD
M. Catherine Driscoll, MD
Deepa Manwani, MD

29. PRENATAL DRUG USE: NEONATAL EFFECTS AND THE NEONATAL

WITHDRAWAL SYNDROME ................................................................................713
Enrique M. Ostrea Jr, MD
Josef Cortez, MD, FAAP
Neil Joseph B. Alviedo, MD
Felix De Paz Bañadera, MD
Lilia C. De Jesus, MD, FAAP
Charlie Tan Cheng, MD

30. TRANSIENT METABOLIC DISTURBANCES IN THE NEWBORN ..................... 753

Zuzanna Kubicka, MD
John M. Fiascone, MD, FAAP
 CONTENTS
xviii

31. SPECIFIC CONGENITAL METABOLIC DISEASES .............................................. 779

Angel Rios, MD, FAAP
Natasha Shur, MD

32. ENDOCRINE DISORDERS MANIFESTING IN THE NEWBORN PERIOD ........ 827

Leslie Lam, MD
Lisa Underland, DO
Kristina M. Derrick, MD, ScM
Beth A. Drzewiecki, MD

33. THE NEWBORN WITH NEUROLOGIC FINDINGS............................................. 853

Bridget Leone, MD
Elissa Yozawitz, MD

34. SURGICAL EMERGENCIES OF THE CHEST AND ABDOMEN

IN THE NEWBORN ................................................................................................ 871
Anna C. Ganster, MD
Mohamed Farooq Ahamed, MD, FAAP
Mamta Fuloria, MD, FAAP

Part 5: Perinatal Care: Caring for the High-Risk Infant

35. ASSESSMENT AND STABILIZATION AT DELIVERY ..........................................913

Joaquim M. B. Pinheiro, MD, MPH, FAAP

36. IDENTIFYING THE NEWBORN WHO REQUIRES SPECIALIZED CARE ........ 945
Upender K. Munshi, MBBS, MD, FAAP

37. CARE OF THE SICK OR PRETERM NEWBORN BEFORE TRANSPORT ........967

Gina M. Geis, MD, FAAP
Karen S. Wood, MD, FAAP

38. CONTINUING CARE OF THE INFANT AFTER TRANSFER FROM NEONATAL

INTENSIVE CARE.................................................................................................. 987
Deborah E. Campbell, MD, FAAP

39. DISCHARGE PLANNING FOR THE HIGH-RISK NEWBORN REQUIRING

INTENSIVE CARE................................................................................................ 1047
Christina M. Long, DO
Kathryn Scharbach, MD, MS
Deborah E. Campbell, MD, FAAP

40. FOLLOW-UP CARE OF THE GRADUATE FROM NEONATAL

INTENSIVE CARE................................................................................................ 1089
Judy C. Bernbaum, MD, FAAP

Part 6: Neonatal Outcomes

41. HEALTH AND DEVELOPMENTAL OUTCOMES OF VERY PRETERM AND VERY

LOW-BIRTH-WEIGHT INFANTS....................................................................... 1127
Deborah E. Campbell, MD, FAAP
Sonia O. Imaizumi, MD, FAAP
 CONTENTS
xix

42. HEALTH AND DEVELOPMENTAL OUTCOMES OF SELECTED MEDICALLY

COMPLEX NEONATES.......................................................................................... 1171
Sarah Chambers Gurson, MD
Deborah E. Campbell, MD, FAAP

Part 7: Supporting Families During Perinatal Illness and

Death

43. SHARED DECISION MAKING AROUND HOME TECHNOLOGIES .................. 1225

Kathryn Scharbach, MD, MS

44. SUPPORT FOR FAMILIES WHOSE INFANT IS SICK OR DYING ....................1235

Joseph A. Vitterito II, MD
Katie R. Forman, DO, FAAP
Alecia Thompson-Branch, MD, FAAP
Deborah E. Campbell, MD, FAAP

INDEX .............................................................................................................................1277
 Preface

The scope of pediatric primary care has expanded as advances in prena-

tal, neonatal, and pediatric specialty care have improved survival among
neonates whose births are complicated by prematurity, low birth weight,
congenital disorders and birth defects, and maternal conditions affecting
the newborn. Neonatology for Primary Care is a resource created specifi-
cally for the pediatric care professional (pediatrician, family physician,
nurse practitioner, and physician assistant) who treats newborns in the
hospital setting or provides pediatric primary care for both healthy and
medically complex infants. The content included covers the continuum
of care from delivery through the care needed during the hospitalization
and after discharge of the healthy term and late preterm infant, as well
as the neonate who requires specialized newborn or neonatal intensive
care because of the spectrum of conditions that can affect the health and
well-being of the neonate. Neonatology for Primary Care contains evidence-
based practice guidance and provides tools to support the in-hospital and
after-hospital community care for healthy and at-risk infants.
This second edition has been fully revised, updated, and rereviewed
to reflect the many new developments in neonatal care since the book’s
original publication in 2015. We have also added a number of new chapters
covering topics including safe sleep, newborn immunizations, prenatal
diagnosis, vascular anomalies, neonatal nutrition, and home technolo-
gies for the high-risk infant. We are pleased to have engaged more than a
dozen new expert physician authors to present these and other vital new
topics in newborn care.
In assembling this reference, we have capitalized on the unique
resources of the American Academy of Pediatrics (AAP). Each chapter
has been reviewed by experts from relevant AAP sections, committees,
and councils—more than 30 groups in total over the course of the book,
representing specialty perspectives ranging from genetics to neurology
to child health financing. The contributing authors and I are grateful for
these reviewers’ expertise and generous feedback.

xxi
 PREFACE
xxii

Primary care professionals are central to the care of the healthy as well
as the medically complex newborn, infant, and child. You are essential
partners with families in a child’s medical home and vital collaborators
with subspecialist colleagues and other health care professionals in the
effort to facilitate care, support families, and promote optimal outcomes.
Deborah E. Campbell, MD, FAAP
PART 1: PERINATAL HEALTH

1. PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT.............................3

E. Rebecca Pschirrer, MD, MPH
George A. Little, MD, FAAP

2. ASSISTED REPRODUCTIVE TECHNOLOGIES, MULTIPLE

BIRTHS, AND PREGNANCY OUTCOMES .....................................................59
Christie J. Bruno, DO, FAAP
Alaina Pyle, MD, FAAP

3. PRENATAL DIAGNOSIS .................................................................................. 77

Diana S. Wolfe, MD, MPH
Barrie Suskin, MD, FACOG, FACMG

4. FETAL INTERVENTIONS.............................................................................. 105

Barrie Suskin, MD, FACOG, FACMG

5. MATERNAL DEPRESSION ............................................................................ 131

Marian F. Earls, MD, MTS, FAAP

1
 Chapter 1

Perinatal Preventive Care:

Fetal Assessment
E. Rebecca Pschirrer, MD, MPH, and George A. Little, MD, FAAP

Pediatricians, as primary care physicians and as subspecialist neona-

tologists, consult and work collaboratively with obstetric providers in
preconception counseling, fetal risk identification, and peripartum deci-
sions. Historically, pediatricians first saw their newborn patients in the
nursery, but only after the events of pregnancy and delivery; today, their
initial interaction with the expectant mother may be during a prenatal
pediatric visit. In addition, pediatricians assume primary responsibility
for resuscitation, stabilization, and ongoing care of the neonate from the
moment of birth. Knowledge about fetal health includes appreciation of
the interaction of the fetus with the mother, her partner (if any), health
professionals, and society. Many examples exist of the capacity for health
professionals in the field of fetal medicine, as part of preconception and
prenatal care, to prevent or treat problems and improve outcomes.
Parents and health professionals have good reason to be concerned
about the immediate and long-term effects of agents or processes on the
fetus. Infections, such as rubella, can result in the loss of the fetus or
in multisystem disease. The magnitude and severity of manifestations
of maternal alcohol consumption, tobacco use, or substance use during
pregnancy may be evident in the infant’s physical appearance or behavior
in the neonatal period and throughout the child’s life course. Furthermore,
problems may not appear until a subsequent generation. The effects of
diethylstilbestrol, which historically was given to mothers to reduce the
risk of pregnancy complication or abortion, were not recognized until the
appearance of clear cell carcinoma of the vagina in female offspring 10
to 20 years later.1
Growth and development are as important to fetal medicine as they are
to pediatrics, of which study of the fetus is merely the first phase. Human
growth and development must be regarded as a continuum that begins
with conception. This chapter outlines some of the normal physical and
interactive aspects of fetal existence, and then discusses selected patho-
physiologic states that may adversely affect that existence.

3
 PART 1 : PERINATAL HEALTH
4

Maternal Conditions That Affect the Fetus and Newborn

Many authorities have pointed to socioeconomic status and social envi-
ronment as causes of fetal risk. Delineation of specific influences is dif-
ficult, but poverty is undoubtedly important, as are nutrition and hygiene.
Intrauterine infection is more frequent in mothers of lower socioeconomic
status. Emotional influences on fetal loss have been discussed; in addition,
the possibility that medical or socioeconomic deprivation contributes to
fetal loss cannot be discounted. Knowledge of a patient’s race, ethnicity,
and language and communication needs can assist in the provision of
patient-centered care, facilitate appropriate risk assessments, and improve
perinatal outcomes. Socioeconomic status, immigration, and health lit-
eracy may further moderate the effect of race, ethnicity, and language.
Quality maternity and perinatal care can be influenced by a health pro-
fessional’s identification and understanding of the cultural beliefs and
experiences of the pregnant woman and her family, and by the expression
and understanding of health care needs communicated by patients.2
The risk of adult health disorders, particularly obesity and metabolic
syndrome, can be markedly influenced by early life events, such as mater-
nal preexisting and pregnancy-related health conditions and environ-
mental exposures. These pregestational and gestational factors affect
both prenatal and neonatal growth trajectories. Alterations in embry-
onic and fetal nutrition as well as endocrine status during gestation can
result in developmental adaptations that produce permanent structural,
physiologic, metabolic, and epigenetic changes, thereby predisposing an
individual to adult cardiovascular, metabolic, and endocrine diseases,
particularly metabolic syndrome.

Maternal Nutrition
Maternal nutritional disorders, including situations in which gross depri-
vation is not apparent, represent a definite risk to the fetus. The supply
of substrate to the fetus for growth originates with the maternal circula-
tion and passes through an interface with fetal tissue at the placenta.
Placental insufficiency can result in fetal growth restriction (FGR) that
is not of maternal origin. The relationship between maternal and fetal
nutrition is complex. Maternal dietary changes usually do not directly or
rapidly influence fetal well-being; thus, the positive or negative effects of
changes in maternal nutrition are not easily recognized. Maternal weight
is an important concern.
Traditionally, 2 types of nutritional deficiency have been conceptualized:
general caloric or energy-related deficiency states and specific deficiencies.
Deprivation of maternal caloric intake to the point at which fetal growth
is markedly impaired also may be associated with specific deficiencies. If
maternal caloric deprivation is severe, fertility is decreased.
Women whose prepregnancy weight is below standard for height tend
to have babies whose weight is less than expected. Women with obesity
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
5

tend to have heavier babies. Problems such as hyperemesis gravidarum

can result in fetal caloric deprivation. The mother’s expression of eating
disorders, which often start during late childhood and adolescence, is a
possible fetal risk.
Specific deficiencies are well recognized; their risk to the fetus can
be reduced through public health and individual clinical interventions.
Vitamin deficiencies are of interest, and problems such as congenital
beriberi (lack of thiamine) and infant calcium disorders (lack of maternal
vitamin D) are of historical interest and decreasing incidence. Studies have
confirmed that the occurrence of neural tube defects can be reduced by
consuming folic acid, with the best protection achieved when 0.4 mg is
ingested from at least 1 month before conception through the first month
of pregnancy.3
Minerals are a major concern in pregnancy. Iodine deficiency is said to
be the most common cause of preventable mental deficiency in the world;
treatment during pregnancy protects the fetal brain, with later treatment
being much less beneficial to neurologic status.4 Zinc deficiency may also
be associated with anomalies. Maternal anemia caused by reduced avail-
ability of iron is well known; as a result, the fetus and infant can have
low iron stores, making the infant susceptible to iron deficiency if intake
after birth is inadequate.

Environmental Exposures
Adverse reproductive and developmental effects have been linked to envi-
ronmental exposures. Vulnerability to toxic insult varies with the rate of
cell division and with the developmental state of the exposed tissues; rap-
idly dividing cells, such as spermatocytes, neural stem cells, and embry-
onic cells, are especially susceptible. Adverse birth outcomes include
preterm birth and low birth weight, congenital malformation, spontane-
ous pregnancy loss, and neurodevelopmental impairment. Environmental
factors, such as radiation, chemicals, and drugs, affect people of all socio-
economic classes. A woman’s preconception or prenatal history should
include review of history of alcohol and smoking as well as secondhand
smoke exposure, illicit substance use, and other environmental exposures.
These environmental toxicant exposures include mercury intake through
fish consumption; well-water nitrate exposures; exposures to chemical,
physical, and/or biologic hazards in the workplace or community; and lead
and other toxicant exposures in the home. It is important to be aware that
men are also vulnerable to environmental toxin exposures. Male-linked
factors (referred to as male-mediated teratogens) that have been identi-
fied as having the potential to cause damage to offspring include cocaine,
alcohol, some pesticides and solvents (eg, dibromochloropropane and tri-
chloroethylene), and heavy metals such as lead and mercury. Reviewing
exposure and risk factors for potential exposure is important, particularly
for exposure to mercury, lead, pesticides, and endocrine disruptors, such
as phthalates, bisphenol A, and polybrominated diethyl ethers.5–7 Many
 PART 1 : PERINATAL HEALTH
6

excellent resources regarding environmental exposures are listed at the

end of this chapter. Radiation exposure in mammals causes fetal death,
growth restriction, and congenital malformation, with the central nervous
system (CNS) commonly affected. The relationship between embryonic
or fetal irradiation and carcinogenesis is unclear. Effects are both dose-
and rate-related. Death during the preimplantation period, malformation
during early organogenesis, and cell deletion and hypoplasia during fetal
life form a general pattern in animal studies. Guidelines exist for limiting
radiation to the embryo and fetus during occupational exposure or elective
diagnostic techniques; however, dilemmas often arise from lack of fore-
knowledge about pregnancy, nonelective medical evaluations, and emo-
tional factors. When necessary, a radiation physicist should be consulted.
Air pollution can originate from multiple sources, such as car exhaust,
power plants, factories, fires, and fumes from solvents. Of the many chemi-
cal components that constitute air pollution, 4 of the most dangerous
pollutants are sulfur dioxide, carbon monoxide, nitrogen oxides, and par-
ticulate matter. Exposure to air pollution early in pregnancy can affect fetal
development. Similarly, exposure to pesticides (organophosphates) and
herbicides through contact with contaminated air, food, and groundwater
can result in FGR and anomalies, such as limb reduction deformities and
urogenital and musculoskeletal defects. Neurotoxicity can result from
prenatal and postnatal exposure to lead and methylmercury, leading to
neurodevelopmental and cognitive impairments; cerebral palsy; sensory
deficits (blindness, deafness); and deficits in attention, fine motor func-
tion, language, visual-spatial abilities, and memory.
Chemicals in the environment are of natural and synthetic origin.
Certain substances, such as pesticides and mercury, have been the focus
of attention, although more study of other potential environmental toxins
is needed. Many agents are potentially more toxic to the embryo, fetus,
and neonate than to older children and adults. Perchlorate, which is both
a naturally occurring and a human-made contaminant increasingly found
in groundwater, surface water, and soil, is another environmental toxin
of increasing concern because of its interference with thyroid uptake of
iodide and potential to affect child health and development. Lead exposure
during pregnancy, at both low and high levels, has been associated with
adverse fetal and neonatal outcome. Appropriate maternal calcium intake
may decrease fetal lead exposure, resulting from decreased mobilization
of stored lead in maternal bone.8
Mercury exposure is a major issue in environmental health, in large
part because of its toxicity to the brain, especially the more susceptible
fetal brain. Mercury is common in the environment in small amounts
and occurs in 3 forms: the metallic element, inorganic salts, and organic
compounds. Predatory fish are the primary exposure, and local fish advi-
sory bans are available from the U.S. Environmental Protection Agency.9
Women planning pregnancy, women who are pregnant or breastfeeding,
and children younger than 15 years have been advised to avoid eating
swordfish, shark, mackerel, and orange roughy among others, and to limit
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
7

the amount of tuna eaten. Updates on information regarding the safety of

fish and shellfish, as well as resources for local health departments, may
be found through the U.S. Environmental Protection Agency.9 Research
has shown variable amounts of mercury during testing of different brands
of tuna.10 Thimerosal, a mercury-containing preservative used in some
vaccines, has been the subject of concern and controversy; as a result, it
is no longer used in vaccines, despite the lack of evidence of causality.11
(See Chapter 20, Newborn Immunizations and Immune Prophylaxis.)

Drugs and Other Substances

Drug use during pregnancy is epidemic and on the rise. Physicians must
be concerned about all types of drug use: legitimate (nonprescription
and prescription), social, illegal, and abusive. All health professionals,
especially the primary care physician, should recognize that the concept
of the placenta as an effective toxic substance barrier between maternal
and fetal circulation has been discarded.
The maternal-fetal pharmacologic mechanism is complex, with the
placenta serving as an organ of exchange (Figure 1-1). Placental diffusing

Mother Placenta Fetus

B Degradation

Metabolism
D
Metabolism
E

F Metabolism

FIGURE 1-1. Maternal-fetal transport patterns and the role of the placenta, a fetal organ with active metabolic
activity. A, Placental barrier with minimal uptake or transfer (eg, succinylcholine, highly charged quaternary
compounds). B, Active placental uptake and degradation without transfer, as seen with insulin. C, Placental
uptake and transfer without significant change, as with bilirubin. D, Placenta actively involved in uptake, partial
use, and transfer (oxygen, glucose, amino acids, free fatty acids). E, Uptake, partial metabolism, and transfer
(cyclosporine). F, Placenta actively modifies during transfer (25-hydroxyvitamin D3). G, Carrier-coupled uptake
occurs with release of ligand to the fetus and regeneration of carrier on the maternal side (transferrin-iron).
Reprinted with permission from Pridjian G. Fetomaternal interactions: placental physiology, the in utero envi-
ronment, and fetal determinants of adult health. In: MacDonald MG, Seshia MMK, eds. Avery’s Neonatology:
Pathophysiology and Management in the Newborn. 7th ed. Philadelphia, PA: Wolters Kluwer; 2016:134–146.
 PART 1 : PERINATAL HEALTH
8

capability or permeability of the simple variety operates for many sub-

stances; energy-utilizing transport is also important. Drugs in the mater-
nal circulation should be assumed to cross the placenta and should be
evaluated for potential teratogenesis. The risk to the fetus depends on
several factors, including concentration of the substance, length of expo-
sure, and when exposure occurs during gestation.
Therapeutic agents, both prescribed and nonprescribed, may be taken
before pregnancy is recognized, thereby placing the products of conception
at risk during the period of organogenesis in early gestation. An impor-
tant benefit of preconception or interconception care is the opportunity
to identify medication uses that are necessary (eg, anticonvulsant agents)
or desirable (eg, nonnarcotic analgesic agents) and to monitor or modify
exposure. Examples of problems include fetal hydantoin syndrome and the
potential effects of ibuprofen on the mother and fetus, such as disruption
of prostaglandin synthesis.
Many of the therapeutic agents indicated during the course of preg-
nancy and delivery require judicious use because of known and potential
risks. Antimicrobial therapy is often necessary when treating maternal
conditions, such as urinary tract or gynecologic infections, but must be
used with the knowledge that well-recognized fetal problems can result,
such as bone and dental dysplasias associated with fetal tetracycline
exposure and the potential hearing loss of fetal aminoglycoside toxicity.
Cardiovascular medications that cross the placenta readily, such as digi-
talis, can be used to treat the fetus or can cause fetal problems. Selective
serotonin reuptake inhibitors (SSRIs), such as commonly used antidepres-
sants, have been shown to cause mild neonatal abstinence syndrome. Of
note, poor neonatal adaptation has been found in the neonates of women
with untreated depression, as well.12 An increased rate of persistent pul-
monary hypertension of the newborn among infants who were exposed
as fetuses to SSRIs late in pregnancy has been reported; however, the
absolute risk is likely to be less than 1%. Furthermore, no significant rela-
tionship has been found between SSRI exposure and stillbirth, neonatal
death, or postneonatal death.13–15
Pediatricians need to know the effects of obstetric drugs on the fetus,
including narcotics, oxytocin, and magnesium sulfate, which can cause
depressed respiration, hyperbilirubinemia, and hypotonia, respectively.
Socially used and abused drugs are very well known to pediatricians for
their deleterious effect on the fetus, newborn, child, and adult. Mothers
who smoke have babies who are smaller than those of nonsmokers by an
average of 200 g. Varied active agents in tobacco smoke, such as carbon
monoxide and nicotine, have physiologic effects. Evidence suggests that
antenatal exposure to environmental tobacco smoke affects early child-
hood cognitive development. Exposure to tobacco smoke prenatally and
postnatally carries an increased risk of childhood asthma, respiratory
infections, otitis media, and sudden unexpected infant death, as well as
later behavioral problems and increased rates of adolescent smoking.16,17
The clear medical consensus is that smoking is a health hazard for the
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
9

fetus and newborn. Maternal alcohol consumption is associated with fetal

alcohol syndrome and should be discouraged during pregnancy in all
trimesters, although demonstrating deleterious effects is difficult when
small amounts are consumed.
Addictive drug use during pregnancy creates major medical and societal
problems. Many, if not most, users have lifestyles that include factors
such as poor nutrition or lack of prenatal care that present significant
background risk regardless of the addictive agent. Heroin is known to
reach the fetus soon after maternal use, with intrauterine dependency
and withdrawal recognized. Treatment programs that use methadone
or buprenorphine are preferable alternatives to continued illicit opioid
use, although neonatal withdrawal requires appropriate evaluation and
management.18 There is increasing evidence that neonatal outcomes are
better with buprenorphine than with methadone therapy. Regardless of
whether buprenorphine or methadone therapy is used, outcomes of women
and infants in treatment programs are significantly better than those of
women not undergoing treatment.19
Cocaine is considered to be responsible, directly or indirectly, for many
admissions to neonatal intensive care units. Cocaine use can result in
problems, such as placental abruption, that compromise the fetal and
neonatal cardiovascular and neurologic systems. Investigative efforts to
characterize and quantify long-term neurodevelopmental effects are ongo-
ing. (See Chapter 29, Prenatal Drug Use: Neonatal Effects and the Drug
Withdrawal Syndrome.)
Identification of environmental and lifestyle risks relies largely on the
maternal medical history. It is also important to investigate paternal history.
When specific factors such as radiation or chemical exposure are detected,
assessment of fetal well-being, especially its growth and morphology, may
be helpful. In many situations, however, decisions to continue or terminate
pregnancy are made based on possible fetal effects, involve parental emo-
tions and values, and require compassionate, nondirective counseling in
addition to the presentation of available scientific knowledge.

Dental Health
The relationship between periodontal disease and pregnancy outcome
is controversial. Some studies have shown that women with periodontal
disease are at increased risk of adverse perinatal events compared with
women without periodontal disease, whereas other studies have shown no
relationship. The increasing popularity of oral jewelry, including lip and
tongue piercing, has been associated with higher incidence of periodontal
disease.20 Women who are planning a pregnancy should pursue regular
dental care, with treatment of poor dentition and gingivitis.

Maternal Reproductive Capability and Health

Certain maternal factors result in fetal risk. Pregnancy can produce physi-
ologic changes in the mother that may complicate preexisting maternal
conditions, thereby jeopardizing the fetus. For example, mothers who
 PART 1 : PERINATAL HEALTH
10

have asymptomatic cardiac disease may decompensate when they become

pregnant.
Maternal biologic factors, such as age, weight, height, race, parity, and
previous obstetric history, directly affect fetal risk. Perinatal mortality
increases at the extremes of maternal age; the relative risk of stillbirth
increases with maternal age, regardless of medical comorbidity, parity, or
race and ethnicity.21 One large observational study determined the lowest
risk to be in the 16- to 19-year age range.22 However, such observations
should not be taken to encourage adolescent pregnancies; pregnancy
in those younger than 16 years has definite associated risks, and preg-
nancy throughout the teenage years is associated with medical and social
morbidity.23 Although adolescent pregnancy has declined in the United
States in recent years, there are significant ethnic, racial, geographic,
and socioeconomic disparities. Newborn weight and height are related
to maternal nutrition, socioeconomic status, and other variables, which
may jeopardize the fetus by increasing the incidence of prematurity or
intrapartum complications. Race is a complex factor that includes socio-
economic considerations; some congenital anomalies and medical condi-
tions may be racially predisposed. Congenital maternal reproductive tract
abnormalities are often associated with spontaneous abortion and with
prematurity. Cervical insufficiency occurs in 1 in 500 to 600 pregnancies
and can result in premature delivery. The interval between pregnancies
is an important contributor to the risk of low birth weight.
Maternal medical disorders carry a significant risk to both fetus and
mother. Cyanotic congenital heart disease in a mother is clearly related
to fetal problems, including FGR and prematurity. Termination of preg-
nancy should be considered if maternal cardiac decompensation later
in the pregnancy is anticipated. Asthma can threaten mother and fetus
but is commonly well controlled with medication. Tuberculosis demands
aggressive management of maternal disease with attention to potential
fetal exposure to drugs. Pregnancy in women with cystic fibrosis exposes
the fetus to a variety of medications, maternal pulmonary insufficiency,
and possible nutritional deficiency.
Preexisting and new-onset renal disease can complicate pregnancy.
Fetal risk increases markedly in the presence of maternal proteinuria,
impaired renal function, and hypertension. Hypertension can cause pla-
cental changes resulting in FGR. Adverse fetal outcome from urinary
tract infection relates primarily to the risk of premature birth. Successful
pregnancy is possible in women with kidney transplants, with the best
outcomes seen among women who have stable renal function, time since
transplantation of at least 2 years, and no evidence of rejection. Some
risks are associated with exposure to immunosuppressants, but they do
not prohibit a good outcome.
Maternal hematologic problems are common. In developing countries,
anemia has been demonstrated to correlate with low birth weight; the
effect of moderate maternal iron deficiency on the fetus is unclear. Some
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
11

hemoglobinopathies can profoundly increase fetal mortality and morbid-

ity as a result of either maternal health status or fetal disease. Pregnant
patients who have sickle cell disease require close attention. Immune
sensitization problems, such as Rh incompatibility and ABO incompat-
ibility, are discussed later in this chapter and in Chapter 17, Maternal
Medical History.
Maternal metabolic disorders can have a significant effect on the fetus.
The interaction of mother and fetus seems limitless: Compounds are
metabolized actively on both sides of the placenta; fetal organogenesis
and development may be affected; and fetal end organs may respond to
maternal abnormalities. Two conditions, diabetes and thyroid disorder,
deserve special mention.
Diabetes in pregnancy causes myriad fetal complications, including
stillbirth, increased frequency of congenital anomalies, macrosomia (a
large for gestational age state characterized by an increase in fat but not
in total body water), and conversely, growth restriction in a small num-
ber of infants. Evidence suggests that fetal pulmonary and neurologic
maturity may be delayed in these pregnancies. In addition, obstetric prob-
lems, including preeclampsia, hydramnios, and intrapartum complica-
tions resulting from excessive size, increase the risk further. Glucose is a
primary metabolite of the fetus. Pregnancies complicated by diabetes may
cause fluctuations in maternal-fetal glucose, with resultant fetal hyperin-
sulinism and hypoglycemia. The increase in pancreatic islet tissue leads
to fetal hyperinsulinism, which may be associated with a growth hormone
effect that results in macrosomia. Severe maternal diabetes, especially
when complicated by prepregnancy vascular disease, may result in small
fetuses rather than macrosomia because of placental insufficiency and
fetal nutritional deficit. Close control of maternal diabetes results in a
better overall perinatal outcome.24
Maternal thyroid disease is much less common than diabetes but also
has profound fetal effects. Fetal thyroid function appears by 12 weeks’
(12 0/7–12 6/7) gestation; thyroxine and triiodothyronine can cross the pla-
centa in small amounts in either direction. Classic cretinism, a reflection
of maternal and fetal hypothyroidism, includes obvious fetal neurodevel-
opmental problems and is a result of endemic iodine deficiency or auto-
immune maternal thyroiditis. Evidence is accumulating that maternal
hypothyroidism, even when subclinical, interferes with normal fetal brain
development and may be prevented by maternal screening and treat-
ment.25 Spontaneous loss, stillbirths, anomalies, and prematurity can be
associated with hypothyroidism. Increases in maternal thyroid replace-
ment hormone are generally necessary during pregnancy. Untreated
hyperthyroidism increases fetal loss. Its treatment, however, carries a
definite risk to the fetus because antithyroid drugs may affect the fetal
thyroid, and surgical intervention carries a surgical risk to fetus and
mother. Postoperative treatment with thyroid replacement therapy may
minimize fetal complications.
 PART 1 : PERINATAL HEALTH
12

Although seizure disorders are common, their course during pregnancy

is difficult to predict with certainty. The status of approximately one-half
of those affected is unchanged, and of the remaining number, one-half
improve and one-half worsen. Status epilepticus is an emergency for the
mother and fetus. Some anticonvulsant agents, such as trimethadione
and valproic acid, are clearly teratogenic. Carbamazepine is associated
with an increased risk of neural tube defect. Phenytoin has been linked to
fetal hydantoin syndrome, although the actual incidence is much debated.
Phenobarbital, carbamazepine, phenytoin, and other medications have a
broad-based effect on fetal enzymatic systems; they are associated with
vitamin K–dependent coagulation factor deficiency in neonates. Many
perinatologists suggest additional supplementation of vitamin K in the last
month of pregnancy. Women who have epilepsy have an approximately 1
in 40 chance that their children will develop the same condition.
Seizures that seem de novo in pregnancy must be thoroughly evaluated.
Eclampsia usually produces other signs and symptoms and is associated
with a high incidence of fetal and neonatal complications.
Maternal emotional status presents too complex a relationship with
physical and familial status to be used as a specific fetal risk factor in most
situations. Whether maternal emotional illness not related to pregnancy
can affect the fetus directly is unclear. Pregnancy-caused or pregnancy-
aggravated crises leading to abortion, substance use, or poor maternal
nutrition generate obvious fetal consequences.

Placenta and Membrane Disorders

The placenta and associated membranes are tissues on which the fetus
depends for respiration, nutrition, protection, and other functions.
Manifestations of placental disease are diverse and severe and include
fetal death, distress, hypoxia, shock, anemia, polycythemia, infection,
congenital anomalies, and neoplasia.
The implantation site is normally in the upper uterus but may be in the
lower segment, in the tubes, or, rarely, in the abdominal cavity. Maternal
anatomic factors may contribute to abnormal implantations. Abdominal
and tubal (ie, ectopic) pregnancies are potential disasters for both mother
and fetus; except for a rare surviving abdominal fetus, fetal loss is nearly
uniform, and maternal mortality and morbidity are common.
Placenta previa is associated with multiparity and places the fetus at
risk in the event of hemorrhage; premature delivery, usually by cesarean
section, is necessary. Abruption of the placenta often is associated with
maternal problems, including preeclampsia, hypertension, renal disease,
and multiparity. Sudden fetal death may occur after an extensive placental
separation; lesser degrees of separation can result in hypoxia and acute
fetal stress. Bleeding from placenta previa and abruption is usually mater-
nal but can be fetal and sufficient to cause fetal hypovolemia and anemia.
Cord abnormalities are unusual but may have severe consequences.
A short umbilical cord may be complicated by abruption. True knots are
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
13

unusual, but they do occur and can cause fetal stress. Prenatal ultra-
sonography (US) should be performed to evaluate for vasa previa and
velamentous cord insertion, because they can result in fetal compromise
or fetal exsanguination. A circumvallate placenta may be associated with
fetal growth restriction. Vascular abnormalities within the main placen-
tal structure are rare; fetal risk in monochorionic multiple pregnancies
includes the possibility of twin-to-twin transfusion syndrome, in which
arteriovenous vascular anastomoses result in blood flow between the
fetuses and in severe circulatory problems for recipient, donor, or both.
A vascular abnormality of the cord observed in 1% of pregnancies is
a 2-vessel cord with a single umbilical artery, rather than the normal 2
umbilical arteries. Evidence suggests that anomalies may be associated
with a 2-vessel cord.26,27 The risk of associated abnormalities, including
fetal growth restriction, renal abnormalities, and aneuploidy, is approxi-
mately 7%.
Premature rupture of membranes (PROM) is a major contributor to
perinatal mortality and morbidity. It is defined as rupture that occurs
before the onset of labor; it is usually spontaneous. Artificial rupture of
membranes may be accidental during an examination or may be used
to augment labor. Regardless of classification, the prenatal care team
must be aware that an inevitable process of increased fetal risk begins
soon after rupture and that prospective treatment protocols are desirable.
Most protocols stipulate evaluation and treatment in relation to the time
since rupture. Prolonged rupture of membranes, which most authorities
consider to be 18 hours after rupture, is the beginning of increased risk.
The primary cause of fetal and maternal morbidity and mortality in
prolonged rupture of membranes is sepsis. At term, labor occurs within
24 hours of rupture in 80% of pregnancies; in preterm pregnancies, labor
begins within 24 hours in less than 50%. The cause of preterm PROM is
often not clear, and except for entities such as an incompetent cervix or
history of a preterm delivery, no statistical correlation has been found
with prior risk factors.
The frequency and degree of inflammation of membranes, cord, or
fetus vary based on a direct relationship with time and onset of labor.
Infection apparently ascends to the fetus through the cervix, with labor
accelerating the process. Antibiotics given before delivery are of uncertain
value in providing effective maternal treatment, but they do prevent some
cases of sepsis in the fetus and newborn. Such is particularly the case
of chemoprophylaxis for prevention of group B streptococcal (GBS) infec-
tion. Current practice recommendations include culture of all pregnant
women for GBS infection between 35 and 37 weeks’ estimated gestational
age, with treatment at the time of labor with intravenous antibiotics in
women with a positive test result.28 Women with GBS urinary coloniza-
tion and women who have previously had an infant with invasive GBS
disease should receive intrapartum chemoprophylaxis; prenatal culture
screening is not necessary.
 PART 1 : PERINATAL HEALTH
14

A dilemma in fetal risk management occurs in the PROM pregnancy

that is significantly preterm. The fetus in this situation is at risk not only
from infection but also from premature birth and its complications, espe-
cially respiratory distress syndrome. Corticosteroids seem to accelerate
pulmonary maturity and improve postpartum status overall in certain
populations. The report from a year 2000 National Institutes of Health
Consensus Development Conference reiterates the previous recommenda-
tion for antenatal treatment with corticosteroids for fetuses between 24
and 32 weeks’ gestation that have preterm PROM.29 A single rescue course
of antenatal corticosteroids may be considered if the antecedent treatment
was given more than 2 weeks prior, the gestational age is less than 34
weeks, and the risk of delivery within 1 week is estimated to be high.30
There may be an increased risk of neurologic sequelae among babies
born prematurely after PROM. An increased incidence of periventricular
leukomalacia and cerebral palsy seems to be at least associated with, if
not caused by, intra-amniotic infection. Magnesium sulfate given before
anticipated early preterm birth, that is, less than 32 weeks’ gestation,
reduces the risk of cerebral palsy in surviving infants.31

Maternal-Fetal Unit
Fetal risk and poor perinatal outcomes are often associated with patho-
physiologic processes in which both mother and fetus play an integral
role. Causality in some situations is well understood, as in, for example,
alloimmunization, but causality for other situations, such as preeclamp-
sia, is not yet clear. A major factor in the risk of adverse neonatal outcome
relates to fetal age at the time of delivery. Currently, the mean gestational
age at delivery is 39 weeks both worldwide and specifically in the United
States. Infants delivered between 370/7 and 38 6/7 weeks of gestation are at
higher risk of neonatal morbidity and mortality than those born between
39 0/7 and 41 6/7 weeks of gestation.32 Neonatal mortality and morbidity
are higher after 42 0/7 weeks of gestation compared with 38 0/7 through
41 6/7 weeks of gestation, and they are also higher at 37 0/7 through 38 6/7
weeks of gestation than at 39 0/7 through 41 6/7 weeks of gestation. Infant
mortality is lowest for births at 39 0/7 through 41 0/7 weeks of gestation.33

Premature Birth
Prematurity and its complications are the prime contributors to perinatal
mortality and morbidity. The problems of prematurity and low birth weight
are similar but not identical.
The prevention and management of premature birth has been and
remains the primary objective of health professionals who provide peri-
natal care. Prematurity is multifactorial in origin, and its causes will
likely remain unclear for the foreseeable future, inasmuch as the precise
mechanisms that cause normal labor have yet to be elucidated. Many
factors that contribute to fetal risk precipitate adverse outcomes directly
or indirectly through premature birth.33
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
15

Pharmacologic Intervention
Tocolysis, or inhibition of uterine activity, is therapy directed at preventing
premature birth once labor has begun. Pharmacologic agents have been
used with this intent for years, with minimal success.
The theoretical basis for the use of β-mimetic drugs as tocolytics is their
inhibitory effect on uterine contractions through activation of β-adrenergic
receptors. β-Adrenergic receptors are subdivided into β1 and β2 groups,
with the latter dominant in blood vessels and the uterus. Isoxsuprine
hydrochloride (a derivative of catecholamine), ritodrine hydrochloride,
and terbutaline sulfate have been used and are thought to be effective in
depressing uterine contractions. A β-mimetic that has a narrow effect on
only the uterus has yet to be developed. Thus, maternal and fetal or neo-
natal side effects do occur, with documented cardiovascular, pulmonary,
and metabolic complications. For example, neonatal hypoglycemia is a
recognized complication of isoxsuprine therapy.
Calcium antagonists (eg, nifedipine) are now used as an adjunct for
tocolysis. Magnesium sulfate is no more effective than other agents but is
commonly used because of a better maternal side effect profile than the
β-adrenergic agents, as well as its efficacy as a neuroprotective agent.31
Prostaglandin synthetase inhibitors may have a future role, but currently
their use is limited because of their potential vasoactive effect on the fetus,
especially on the ductus arteriosus.
Tocolytic therapy can be beneficial between 24 and 33 weeks’ gesta-
tion. During that time, a relatively short delay of preterm delivery through
tocolysis or other interventions is long enough (24–48 hours) to allow
administration of corticosteroids for the enhancement of fetal lung matu-
rity and maternal antibiotics for GBS sepsis prophylaxis.

Prevention of Prematurity
Prevention of preterm birth is an area of ongoing research. Evaluation of
lifestyle factors associated with preterm delivery and the subsequent modi-
fication of identified risk factors have yielded mixed results. More recent
efforts have focused on cervical insufficiency and hormonal effects.34
The use of weekly progesterone to decrease the risk of recurrent
preterm birth in subsequent pregnancy seems promising because the
biggest risk factor for preterm delivery is a history of previous preterm
delivery.35
Physicians can play a major role in such preventive programs, because
physicians ensure that the need for intervention is documented and that
intervention occurs. In addition to management of specific medical prob-
lems, alterations in work and home environment may be necessary. Good
prenatal care and early work leave may be very important. Countries in
which such policies exist (eg, Sweden) have low prematurity rates, but
whether this circumstance is an association or a contributing factor is
currently unknown.
 PART 1 : PERINATAL HEALTH
16

Multiple Gestation
The incidence of multiple gestation has increased markedly because of the
application of newer reproductive technologies to treat infertility, and as
reproductive technology is refined, the incidence of higher-order multiple
gestation is decreasing.
Spontaneously occurring multiple gestation is also relatively common
(twins occur naturally in approximately 1 in 88 births). Regardless of the
source of multiple gestation, fetal risk is increased. These risks range from
those that are placental in origin, such as twin-to-twin transfusion, to rare
fetal malformations, as in conjoined twins, to the much more frequent
problems of prematurity and obstetric complications. Multiple gestation is
among the 3 most common causes of prematurity. Complications of labor
and delivery increase the risk of hypoxia or trauma, with the second-born
twin being more susceptible than the first.

Obstetric Complications
Obstetric complications jeopardize the fetus, with the most dire mani-
festation being intrapartum fetal death. Even the healthiest fetus is at
increased risk during labor and delivery. Stress to the fetus may be docu-
mented retrospectively by low Apgar scores, poor recovery after birth, and
subsequent complications. A fetus that undergoes chronic compromise
by adverse factors, such as diabetes in pregnancy, may be compromised
further by obstetric problems.
Abnormal presentations, such as breech and transverse lie, greatly
increase fetal risk, as does cephalopelvic disproportion (a mismatch
between the maternal pelvis and the fetal head). Malproportion can be
predominantly fetal, as in congenital hydrocephalus, or maternal when
congenital pelvic bone abnormalities exist.

Abnormal Growth and Gestation

Discrepancies between fetal growth and gestation are often manifestations
of an underlying disease process, but they may occur without apparent
cause. Regardless of cause, discrepancies in growth and gestation can
often result in such severe risk to the fetus as to be more worrisome than
the underlying problem. Postmaturity occurs much less often than prema-
turity, but it too places the fetus at increased risk. Continued growth in
utero increases the risk of macrosomia and birth trauma. Placental insuf-
ficiency may result in the development of hypoxia and acidosis before or
during labor that is characterized by non-reassuring fetal heart rate (FHR),
poor Apgar scores, and perinatal hypoxic encephalopathy. Meconium pas-
sage is common and poses a risk of meconium aspiration syndrome; it
may also signal peripartum infection.36
Deviations of growth and gestation can be cumulative for fetal risk. The
premature infant also affected by FGR has poor tolerance for intrauterine
stress, may exhibit respiratory distress syndrome or apnea after birth,
and is at risk of the development of hypoglycemia. New information is
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
17

emerging about the long-term effects of FGR. Fetal nutritional adapta-

tions to placental insufficiency may persist through adulthood; the risk
of coronary artery disease and chronic hypertension is increased among
adults who were born with FGR.37 The physician should appreciate that
evaluation of the fetus or newborn by birth weight and gestational age
can provide specific information that facilitates diagnosis and treatment.

Alloimmunization
Alloimmunization is a disease of the maternal-fetal unit that has decreased
in incidence because of successful efforts to prevent Rh disease with
Rh-globulin (RhoGAM). Passage into the maternal circulation of fetal red
cells, which possess antigens not present in the mother, stimulates pro-
duction of antibodies. Maternal antibodies of the immunoglobulin G (IgG)
class cross the placenta, resulting in a hemolytic process in the fetus that
can be severe. The initial alloimmunization can occur with blood transfu-
sions, with exposure resulting from shared needles during illicit injection
drug use, with spontaneous or induced abortion, or with the first or sub-
sequent pregnancy. Small amounts of red cell antigen contained in blood
measuring 1 mL or less (especially if repeated) can cause an antibody
response even in normal pregnancies. Sensitization risk is increased by
complications such as preeclampsia and cesarean delivery.
Rh incompatibility is associated with a variable but often severe sen-
sitization that can cause stillbirth, massive fetal erythropoiesis or eryth-
roblastosis, anemia, hydrops fetalis, and other systemic manifestations
The incidence of fetal Rh disease varies with the prevalence of Rh
negativity. This genetically determined state is not often documented in
Asian and Native American patients; however, it occurs in 15% of white
persons, resulting in the possibility of approximately 9% of these preg-
nancies involving an Rh-negative woman carrying an Rh-positive fetus.
Despite prophylaxis with RhoGAM for the D antigen, alloimmunization
still occurs in response to several other red cell antigens for which there is
no prophylaxis available, including c, C, e, E, Kell, Kidd, and Duffy. These
minor antigens can cause serious hemolysis. Some patients acquire more
than 1 hemolytic antibody, typically after blood transfusion; however, this
is also seen with illicit injection drug use.
Since the delineation of the cause of Rh sensitization, a wide range of
diagnostic and therapeutic methods have become available that make
Rh incompatibility treatment a paradigm for intensive perinatal care.
Currently used routine procedures for the disease include initial screen-
ing for the presence of alloimmunization and for Rh-negative women who
are still candidates for prevention with RhoGAM. If hemolytic antibody
is detected, maternal serum levels and amniotic fluid analysis can be
used to assess the possibility of severe fetal illness. Amniotic fluid can be
analyzed by polymerase chain reaction DNA analysis to determine fetal
blood type and the risk of hemolytic disease. Noninvasive methods of
diagnosis of fetal anemia have been developed that use US assessment
 PART 1 : PERINATAL HEALTH
18

of fetal cerebral blood flow in the middle cerebral artery. Peak systolic
velocity in the middle cerebral artery increases as anemia worsens. This
noninvasive option for monitoring results in decreased risk accrued with
serial amniocentesis, which can include infection, worsened sensitiza-
tion, and loss of pregnancy.38,39 When a high hemolytic risk is detected,
by either US or amniocentesis, fetal blood sampling by the percutaneous
umbilical route can be performed so that an accurate assessment can be
made and in utero blood transfusion may be administered. The timing of
delivery includes consideration of fetal health, the possibility of in utero
transfusion, and the degree of prematurity. Immediate, aggressive neona-
tal intensive care, including exchange transfusion and cardiopulmonary
support, may be indicated.
Incompatibilities of the ABO system result from the presence of mater-
nal anti-A or anti-B antibodies when fetal blood type is group A or B and
maternal blood type is group O. Severe hemolysis is much less common,
even though ABO incompatibility is potentially present in approximately
20% of pregnancies. Fetal erythrocytes seem to have fewer antigenic loci,
and maternal antibody appears in immunoglobulin A (IgA), immunoglobu-
lin M (IgM), and IgG forms, with only the latter crossing the placenta. These
facts may explain why ABO alloimmunization is usually of greater concern
in the newborn than in the fetus. Stillbirths and hydrops fetalis are rare,
but prolonged neonatal hyperbilirubinemia occurs often.

Gestational Hypertension
Hypertension of pregnancy is a major contributor to fetal risk. A group of
diseases seen only in pregnancy and presenting with acute and chronic
manifestations of hypertension, edema, and proteinuria may be grouped
together in this category. Preeclampsia is another term for the basic pro-
cess, which can be severe; when convulsions or coma occur, eclampsia is
present. Chronic hypertensive vascular disease with pregnancy is thought
by many to be a separate disease state that can have superimposed pre-
eclamptic manifestations. Low-dose aspirin has been shown to reduce
the risk of preeclampsia, and it is recommended by the U.S. Preventive
Services Task Force for use in women at high risk of developing preeclamp-
sia, beginning at 12 weeks of gestation.40
Premature birth may occur more frequently in cases of gestational
hypertension, because early delivery is often indicated as the result of
maternal or fetal need. As the severity of the disease increases, and par-
ticularly with the occurrence of eclampsia, stillbirth and maternal death
become much more frequent occurrences. Intrauterine growth restriction
is seen in one-third of perinatal deaths associated with preeclampsia. For
the fetus, this disease process presents a bleak perspective; fetal stress
is significant, and labor and delivery are often premature and timed
for maternal treatment. Neonatal complications are many and severe,
depending on gestational age and the presence or absence of growth
restriction.
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
19

Successful perinatal management of preeclampsia relies heavily on

early detection during prenatal care. When the process is discovered,
intensive perinatal care may be necessary; seizure prophylaxis with mag-
nesium sulfate is a mainstay of therapy. Preeclampsia with severe features
is a significant maternal threat and may require a decision to deliver a
premature baby. Proper expectant management requires careful maternal
and fetal surveillance, including assessment of fetal well-being by non-
stress testing, biophysical profile, amniotic fluid volume determinations,
Doppler studies of umbilical blood flow, and US studies of fetal growth.

Intrauterine Infections
The medical community’s understanding of the scope of the problem of
intrauterine infections and their fetal effects has broadened consider-
ably but is probably far from complete. Expression ranges from fetal loss
caused by spontaneous abortion and stillbirth through severely debili-
tating congenital anomalies resulting from teratogenic effects, to subtle
systemic manifestations, including those of the CNS, that are not detected
until later in childhood when problems with higher cerebral function and
behavior become apparent.
The important infectious agents include viruses, bacteria, spirochetes,
and protozoa. The route for infection varies by agent and can be transpla-
cental, ascending through the cervix, with or without the rupture of mem-
branes, which provide an imperfect protective cover, as well as through
direct contact with the fetus during passage through the vagina.
The pediatric physician must have a basic appreciation for the variety
of intrauterine infectious agents and the pathophysiologic processes and
clinical problems they invoke. Table 1-1 presents a modification of TORCH
infection (toxoplasmosis, other agents, rubella, cytomegalovirus, herpes
simplex), a schema that has served well for several decades.

HIV
Fetal, intrauterine, and peripartum considerations are but a small part
of the story of HIV (see also Chapter 17, Maternal Medical History, and
Chapter 27, The Newborn at Risk of Infection). Given the magnitude of
the HIV/AIDS problem and that of the 3 predominant modes of trans-
mission in the United States (sexual contact, percutaneous contact with
contaminated sharps, and fetal or infant contact with an infected mother),
2 involve reproduction, the pediatrician must know the specifics of trans-
mission and intervention. The ability to reduce the occurrence of vertical
transmission from mother to fetus makes universal screening of pregnant
women for HIV imperative. The fetus can be infected in utero, although
the exact timing is uncertain; other possibilities for transmission include
transplacental or peripartum, as well as postpartum (through breastfeed-
ing). The timing of the expression of disease in children is variable and is
thought to be determined by whether the infection was acquired before
delivery or during parturition. Without antiviral therapy, approximately
 PART 1 : PERINATAL HEALTH
20

Table 1-1. Maternal-Fetal Infections: TORCH

Infection Organism Transmission Comments
Toxoplas- Toxoplasma Transplacental Most common congenital parasitic infec-
mosis gondii tion in the United States
Domestic cat is primary host
Risk of infection is highest in third
trimester, but fetal effects are less
severe
Prenatal diagnosis by PCR or tissue
culture
Other Listeria Vertical or hori- Foodborne, gram-positive bacillus
agents monocyto- zontal (environ- Isolated from livestock and fowl
genes mental exposure) Outbreak related to consuming contami-
nated cheeses, raw vegetables, milk
Infection during first and second trimes-
ter associated with high rates of fetal
death
Diagnosis: positive body fluid cultures
Syphilis Transplacental Transmission at any stage of pregnancy
(Treponema Prevalence increasing in the United States
pallidum) Risk factors: young age, inadequate
prenatal care, substance use, multiple
partners, history of STIs, inadequate
treatment for prior infection
Maternal screening (VDRL, RPR) at entry
into prenatal care and at delivery is key
Varicella- Transplacental Varicella embryopathy caused by
zoster transmission during first 20 weeks of
gestation
Can cause limb deformities and cicatri-
cial skin scarring
Parvovirus Respiratory Typically, infection is more common in
B19 (fifth (most common), spring and summer.
disease) hematogenous Transmission risk is highest in the first
(transplacental), and second trimesters.
vertical Can cause fetal hydrops and increased
nuchal translucency in the first trimes-
ter.
Maternal testing for anti-parvovirus B19
IgM and IgG, amniotic fluid PCR.
Group B Streptococcus, gonococcus, HIV, mumps, enteroviruses, tuberculosis
Zika virus Transplacental Transmission at any stage in pregnancy
Risk of anomalies is poorly characterized
(may be as high as 8%–10%): micro-
cephaly, CNS anomalies, FGR, fetal loss
Prevention: avoidance of mosquito bites,
sexual transmission
 CHAPTER 1 : PERINATAL PREVENTIVE CARE: FETAL ASSESSMENT
21

Table 1-1. Maternal-Fetal Infections: TORCH—cont’d

Infection Organism Transmission Comments
Rubella Rubella virus Transplacental Rare in countries with universal rubella
vaccination
Fetal infection rates highest with expo-
sure in the first trimester
Diagnosis of maternal infection by testing
for rubella-specific IgM
Cyto- Human cyto- Congenital, trans- The most common congenital infection.
megalo- megalovirus placental Transmission more common in primary
virus (CMV, herpes 50% infected at maternal infection, resulting in 30%-
virus 5) birth 40% fetal infection.
Maternal disease typically is mild.
Infection risk increases with young
maternal age, single status, nonwhite
race, and exposure to young children.
Universal prenatal screening is not
routine.
Prenatal diagnosis: anti-HCMV IgM and
low avidity anti-HCMV IgG.
Herpes HSV 1 and 2 Intrapartum Neonatal infection usually results from
simplex Transplacental primary genital infection with HSV 2.
is rare The mother is often asymptomatic.
Neonatal disease is typically severe.
Diagnosis: HSV-PCR + HSV cultures.
Abbreviations: CNS, central nervous system; FGR, fetal growth restriction; HCMV, human cytomegalovi-
rus; HSV, herpes simplex virus; Ig, immunoglobulin; PCR, polymerase chain reaction; RPR, rapid plasma
reagin; STI, sexually transmitted infection; TORCH, toxoplasmosis, other agents, rubella, cytomegalovirus,
herpes simplex; VDRL, venereal disease research laboratory.

25% of babies born to HIV-infected women will become infected them-

selves. The use of antepartum, intrapartum, and postpartum multi-agent
antiretroviral prophylaxis may decrease the risk of congenital infection to
2%. Even further decreases in transmission may be associated with cesar-
ean delivery or vaginal delivery within 4 hours after rupture of membranes.
Whether cesarean delivery is protective for fetuses of women who have very
low or undetectable viral loads is uncertain.41 Newborns discovered to be
at risk should be continued on antiretroviral agents until their infective
status becomes clarified. In the United States, where safe artificial milk is
available, breastfeeding is contraindicated in HIV-infected women.

Rubella
Rubella virus is recognized as a potent teratogen. Infections during the first
trimester result in approximately 20% of fetuses being severely damaged
or malformed, with second-trimester involvement damaging 10%. Third-
trimester infection has presented few clinical problems. The expression of
rubella syndrome is variable. Manifestations of first-trimester fetal disease
 PART 1 : PERINATAL HEALTH
22

can be severe (eg, abortion, stillbirth, severe rubella syndrome). Severe

rubella syndrome includes growth restriction, eye defects (cataracts and
microphthalmia), congenital cardiac defects, deafness, thrombocytopenic
purpura, hepatosplenomegaly, bone lesions, pneumonitis, and cerebral
defects (microcephaly, encephalitis, intellectual disability, and spastic
quadriplegia). Infections in the second trimester are variable and tend to
be less severe.
The high fetal risk and potentially devastating consequences of intra-
uterine rubella have stimulated aggressive efforts to prevent maternal
rubella. Congenital rubella is a reportable disease. Vaccination of chil-
dren between ages 1 and 12 years is routine. Administration of vaccine
to women of childbearing age has been controversial because of concern
for possible vaccine effects on the developing fetus. However, a registry
of cases in which women received vaccine within 3 months of concep-
tion has found no cases of congenital rubella syndrome. Vaccine virus
was cultured from fetal and placental tissue, but teratogenic effects were
not seen. Preconception counseling should include rubella serotesting to
determine the need for vaccination prior to conception.

Cytomegalovirus Infections
The cytomegaloviruses (CMVs) are the most common cause of congenital
infection, occurring in 0.2% to 2.2% of neonates. This group of viruses is
widespread and produces various apparent and inapparent infections in
the general population: 58% of women of childbearing age are seropositive.
Among uninfected women, 1% to 4% will develop a primary CMV infection
during pregnancy, with approximately one-third of these women shed-
ding virus to their fetus transplacentally. Fetal infection usually occurs
through the placenta.
The fetal disease has been called cytomegalic inclusion disease
because of the large inclusion-bearing cells found in urine and many
organs. Severe cytomegalic inclusion disease includes hepatospleno-
megaly, microcephaly, cerebral calcifications, mental and motor mani-
festations, and chorioretinitis. It has been suggested that expression of
intrauterine infections is variable and that full recognition of incidence
is yet to come. Serologic tests for CMV are available and can provide
presumptive evidence for infection; however, reliability is not as good
as with rubella titers, and a vaccine is not available. Cytomegalovirus
antibody testing of infants reflects the maternal antibody status.
Consequently, congenital CMV infection cannot be diagnosed if the
infant is tested more than 2 to 3 weeks after birth. Urine CMV culture
is a good indicator of recent or active infection. Among infants born with
congenital CMV infection, approximately 80% are asymptomatic. One
in 750 infants with CMV infection will develop permanent CMV-related
sequelae. Cytomegalovirus is the most common cause of nonhereditary
hearing loss in children.
Discovering Diverse Content Through
Random Scribd Documents
[335]
Theodore Roosevelt, “A National Park Service,” Outlook, C (Feb.
3, 1912).

[336]
S. T. Mather’s “Report of The Director of The National Park
Service,” Report of the Department of the Interior 1918, pp. 842-
3.

[337]
Reports of the Secretary of the Interior 1918, pp. 842-3.

An interesting experiment, contrary to this principle, was an

attempt in 1906 to raise twelve Sequoia gigantea trees near the
arch at Gardiner entrance. All of the trees died.

[338]
James Bryce, “National Parks the Need of the Future,” The
Outlook, CII (December 14, 1912), 811.

[339]
Reports of the Secretary of the Interior 1918, pp. 813-4.

[340]
Ibid.

[341]
Ray S. Baker, “A Place of Marvels,” The Century Magazine, LXVI
(August, 1903), 487.

[342]
F. A. Boutelle, Report of the Acting Superintendent 1889
(Washington, D. C.: Government Printing Office, 1890), p. 148.

[343]
Report of the Secretary of the Interior 1937, p. 49.
[344]
Short terms of service were also held by Dr. Frank E. Thone,
1923, and Alfred H. Povah, 1931.

[345]
Editorial, “The Ranger Naturalist,” Nature Magazine, XVII (April,
1931), 219.

[346]
Exhibits were established at Rhyo-Travertine Gulch, Swan Lake
Flat, Beaver Dams, Nymph Lake, Tuff Cliff, and Firehole Canyon.

[347]
Report of the Secretary of the Interior 1938, p. 13.

[348]
Ibid., 1918, pp. 844-5.

[349]
George O. Smith, “The Nation’s Playgrounds,” Review of Reviews,
XL (July, 1909), 44.

[350]
Dwight L. Elmendorf, The Mentor, II (May 15, 1915), 13.

[351]
Earl of Dunraven, The Great Divide (London, 1876), p. XI.

The Scottish Earl of Dunraven visited the Park in 1874. A peak

and a pass commemorate his interest and service in informing
Europeans about Yellowstone.

[352]
The date of this communication was December 20, 1810.

[353]
Colter’s first sheet is readily identifiable, and part of another
sheet may be segregated with the use of imagination and
 understanding.

[354]
Many writers have failed to identify Gap and Sage as the same
creek. They also befuddle Wind and Shoshone rivers. There is no
evidence that Colter ever heard the name of Bighorn River.

[355]
The figure eight results from the fact that he went to the Yep-pe
camp, left it, came back, and left it again at the appropriate
angles.

[356]
The curious errors of the map are explained in Chapter II.

[357]
Lewis evidently complained to Biddle about the variations in
sheets because Clark stated in a letter to Biddle that these sheets
were all of the same scale. See Stallo Vinton, John Colter, p. 47.

[358]
This claim will be developed subsequently.

[359]
John D. Hicks, The Federal Union (New York: Houghton Mifflin
Co., 1937), p. 282.

[360]
The position of Henrys River, with reference to the Snake River
drainage, is almost wholly erroneous as shown on the Map of
1814. Wisers River is fictitious. The true and original Weiser River
lies three hundred miles west.

[361]
This hypothesis is based upon the findings of J. Neilson Barry of
Portland, Oregon. Mr. Barry is a profound student of Western
history and cartography. He has devoted years of intensive
research in correlating journals and geography.
[362]
There is a reasonable view that holds this lake to be the only real
feature upon this section of the map and identifies it as Brooks
Lake, but Colter never saw or knew of the main branch of the
Bighorn River or its source in Brooks Lake.

[363]
Clark named this mythical lake for William Eustis, who had been
representative to Congress from Massachusetts. About this time
he was Secretary of War in President Madison’s cabinet.

Whatever Colter drew was certainly lacking Lake Eustis, Lake

Biddle, and the Rio Grande, Arkansas, and Platte rivers. He was a
simple frontiersman who had probably never heard of Eustis or
Biddle and was not interested in mapping anything beyond his
own route. Had Lewis linked Eustis and Biddle-Riddle lakes
together, a possible approximation to Colter’s draft might have
appeared.

[364]
In 1941, Paul J. Shamp, a US. forester, reported the discovery of
numerous petrifications in the vicinity of Pass and Scatter creeks
in the Thorofare country. This is the line of Colter’s reconstructed
route.

It has been the author’s desire to make a search for this missing
link of evidence by actually going over the route. In 1947, he
made a partial exploration during a three day hike. It was enough
to suggest the size of the problem.

[365]
Colter may have reached Chicken Ridge by Fishhawk, Mountain,
or Lynx creeks or via Falcon, Mink, or Crooked streams. It must be
remembered that this map sheet has been much mussed up. It is
impossible to know what has been erased; yet, enough of Colter’s
map remains to provide a logical basis for the above itinerary. It is
relatively unimportant which creeks he negotiated to reach
 Chicken Ridge. The vitally important fact is that he drew a sketch
of South Arm from that angle which added to the Thumb makes
an accurate map of what a trapper would have seen of
Yellowstone Lake.

[366]
J. Neilson Barry has made the most intensive study of the Map of
1814. It is his opinion that Colter drew other map sheets besides
the one of the Buffalo Bill country. He also has hope that these
sheets may be discovered among the Lewis-Clark-Biddle papers.
310
 INDEX

A B C D E F G H I J K L M N O P Q R S T U
V W X Y Z

A
Absaroka Indians, 68, 74, 86
Absaroka Pass, 184, 298
Absaroka Range, 30, 42 ff., 96, 101, 104
Adams, Robert, Jr., 138
Albright, Supt. Horace M., 211, 270 ff.
Alder Gulch, 102;
gold found, 104, 161
Allard Bison Herd, 258
Allen, Dr. Eugene T., 264
Allen, G. N., 138
Alter, J. Cecil, 79
Alum Creek, 113, 181, 211
American Association for the Advancement of Science, 227
American Association of Museums, 272
American Fur Company, 94, 108
American Game Protective and Propagation Association, 225
American Journal of Science and Arts, 139
Amethyst Mountain, 104
Anderson, Capt. George S., 206, 210, 248, 260
Anderson, Ole, 216
Anthony, Sen. H. B., 140
Arbor Day, 229
Architectural Fountain Geyser, 139
Arickara Indians, 37, 61
Arnold, A. J., 172 ff.
Arthur, Pres. Chester A., 192 ff.
Ashley, Gen. William H., 81, 92
Astorians, 34
Atlantic Creek, 72, 296
Atwood, W. W., 270
Austin, ——, 103

B
Bach, E. W., 201
Baggley, George F., 273
Baker, Sergt. William, 121
Bannock Indians, 59;
description, 65, 86 ff.;
trail, 88;
defeat, 157
Barlow, Capt. J. W., survey, 137 ff.
Baronett, C. J., 105;
rescued Everts, 134;
bridge, 184;
road, 208
Bauer, Dr. C. Max, 270
Beaman, J. W., 138
Bear Paw Mountains, 187, 190
Bear River, 110
Beartooth Range, 30
“Beaver Dick” (Richard Leigh), 283
Bechler River, 27, 259
Beehive Geyser, 131, 197
Biddle, Lake, 292
Biddle, Nicholas, 50, 285, 290
Big Game Ridge, 47, 296
Big Hole, battle of, 170 ff., 180, 187
Bigfoot, Chief, 156
Bighorn Basin, 88, 112
Bighorn River, 32, 37, 42 ff., 55, 68, 290
Bison Peak, 261
Bitter Root Range, 67, 102, 170
Blackfeet Indians, 37;
attack Colter, 52 ff.;
description, 67, 74, 88, 98
Black Kettle’s village, 157
Blacks Fork of Green River, 108
Blaine, Sen. James G., 136 311
Bonaparte, Napoleon, 28
Bonneville, Capt. B. L. E., 99;
describes bison, 153; 232
Boone and Crockett Club, 235
Bottler, Frederick, 105;
stock range, 162;
ranch, 180
Boutelle, Capt. F. A., 268
Bowles, Samuel, 226
Bozeman, John, 158
Bozeman, Montana, 117, 138, 142, 176, 180, 205
Bozeman Pass, 55
Bozeman Trail, 161
Bradbury, John, 57
Brackenridge, Henry M., 37, 57 ff.
Bridger, James (Jim), 80, 98, 101;
ancestors, 106;
description, 106 ff.;
nicknames for, 110;
Indian wives, 110;
tall tales, 110 ff.;
death of, 115, 283
Brooks Lake, 44
Brothers, Henry J., 217
Bryant, Dr. Harold, 270
“Buckskin Charley,” (Charles Marble), 198, 283
Buffalo Ranch, 87
Bumpus, Dr. Hermon C., 270
Burgess, Felix, 247
Burlington Route, 202
Burns, A. E., 247

C
Cabeza de Vaca, description of bison, 153
Cache Creek, 104
California, 141;
climate of, 239;
University of, 270
Camas Creek, 94
Campfire Club of America, 235
Canyon Creek, Nez Percé fight Seventh Cavalry, 185, 186
Carnegie Geophysical Laboratory, 264
Carpenter, Frank, 172 ff.
Carpenter, Ida, 172
Carpenter, Robert E., 205, 244
Carrington, Campbell, 138, 139
Carrington, Henry B., 110
Carson, Kit, 285
Cassidy, “Butch,” 163
Castle Geyser, 131
Catholic Church, 174;
services, 217
Catlin, George, 144, 221 ff.
Cauliflower Geyser, 251
Cheyenne Indians, description, 70, 157, 187
Chicago Journal, 139
Chicken Ridge, 47, 296
Child, H. W., 201
Chittenden, Hiram M., 210
Chittenden Road, 210
Chivington, Col. J. M., 157
Cinnabar, 199 ff., 259
Civil War, 103, 120, 153, 157
Claggett, William H., 137;
sponsored Park Bill, 140 ff.
Clark, Dr. Dan E., 162
Clark, Capt. Philo, 193
Clark, William, 42 ff.;
Colter reports to, 50, 57, 285 ff.
Clarks Fork, 42, 50, 88, 184, 259, 286, 290, 298
Clearwater River, 35;
battle of, 169
Clematis Gulch, 182, 202
Cody, William F. “Buffalo Bill,” 151;
nickname, 153;
description, 233
Coffeen, Hon. Henry H., 208
Cole, Sen. Cornelius, 140
Colter, John, ancestors, 35 ff.;
joins Lisa, 37;
discovery of Park, 38 ff.;
attacked by Blackfeet, 52;
guide for Henry, 56;
reaches St. Louis, 57, 100;
route, 283 ff.
Colter Creek, 36
Colter’s Hell, 40, 45, 50, 291
Colter’s Peak, 58
Colville Reservation, 191
Community Chapel, 217
Condon, David de L., 270
Conger, Patrick A., 242
Conness, Sen. John, 225
Connor, Col. Patrick, 157 312
Conservation, 217 ff., 225;
Pres. Roosevelt’s Governor’s Conference, 229
Continental Divide, 25, 37, 45;
Colter crossed, 47, 99, 102, 118, 163, 259, 296
Cook, Charles W., 116, 118
Cooke, Montana, 208, 247, 259
Coronado, Francisco, 153
Cottage Hotel, 205
Counter, Hub, 196
Cowan, George F., 172 ff., 283
Cowan, Mrs. George F., describes Chief Joseph, 174
Crampton, Louis C., 211
Crazy Horse, Chief, 158, 162
Creamer, Phil, 106
Crook, Gen. George, 158
Crosby, Gov. John S., 193, 243
Crow Indians, 37, 54, 59, 86, 88, 104, 150, 184 ff., 240
Custer, Col. George A., 152, 157;
defeated, 158
Cougar Creek, 88

D
Davis, A. J., 162
Dawes, Chester M., 138
Dawes, Hon. Henry L., 138;
backed Park Bill, 141 ff.
Day, Dr. Arthur L., 264
Dead Indian Creek, 42, 50, 286, 298
Dedicatory Act, 144, 146, 202, 227, 230, 245
DeLacy, Walter W., 102 ff.;
his map, 121
Delano, Columbus, 139, 142
DeMaris Mineral Springs, 286
Devil’s Den, 122
Devil’s Hoof, 122
Devil’s Inkwell, 122
Devil’s Kitchen, 122
Devil’s Slide, 122
Diamond City, Montana, 116 ff.
Dickson, John, 35 ff.
Dietrich, Richard, 180 ff.
Dingee, William, 172 ff.
Dixon, George B., 138
Doane, Lieut. Gustavus C., 121;
 description of Old Faithful Geyser, 130;
with Hayden, 138, 164;
in pursuit of Nez Percé, 178 ff.
Dot Island, 207
Dragons Mouth, 45, 50, 124, 298
Driggs, Dr. Howard R., 144
Duncan, J. W., 138
Duncan, L., 180
Dunnell, Hon. Mark H., 141
Dunraven, Earl of, 80, 85, 151 ff.;
describes horse thieves, 164;
hunting, 233 ff.;
praises Park, 278
Dutcher, Mary, 234
Dutcher, Willard, 233

E
Eagle Blanket, Nez Percé, 168
Eagle Peak, 25
East Entrance, 202, 210
Eaton, Howard, 195;
trail, 195, 215
Ee-dah-how (Idaho), 27
Edmunds, Sen. George F., 140
Elk Thistle, 127;
see Everts Thistle, 128
Elk-Wapiti Creek, 47, 296
Elliott, Henry W., 137, 139
Emerald Pool, 131
Emerson, Ralph Waldo, 222, 223
Emigrant Gulch, 105
Ericson, Leif, 30
Eustis Lake, 292
Everts Thistle, 128
Everts, Truman C., 120 ff.;
lost in Park, 126 ff.;
 visit to Washington, D.C., 137, 283

F
Fairweather, William, 104
Falcon Creek, 296
Fall River, 259, 276
Fan Geyser, 131
Farcy, Sheriff, 193
Fee, Chester A., 177
Fergus, James, 162
Ferris, Warren A., 68; 313
describes geysers, 94, 100
Fetterman Massacre, 161
Firehole Basin, 98, 102, 129
Firehole Canyon, 210
Firehole Hotel, 204
Firehole River, 105, 118;
Nez Percé camp, 172, 200 ff., 227
Fisher, Capt. S. G., 177
Fishhawk Creek, 296,
Fishing Bridge, 26, 86, 87, 210;
museum, 273
Flat Mountain Arm, 47, 296
Flathead Indians, 59;
description, 66 ff.
Foller, August, 180 ff.
Folsom, David E., 116;
proposed park idea, 118, 142;
assistant superintendent, 240
Folsom-Cook-Peterson party, 30;
exploration, 116 ff.
Ford, R. S., 162
Forest fires, 253 ff.
Forest and Stream, 206, 242, 247 ff.
Forsyth, Lieut. William W., 247
Fort Bridger, 108
Fort Ellis, 121 ff., 138, 172
Fort Hall, 96, 99;
Bannock Reservation, 157
Fort Henry, founded, 32;
visited by Astorians, 34
Fort Laramie National Park, 83, 233
Fort Lisa (Manuel’s Fort, Fort Raymond), 37, 41 ff., 54 ff., 286
Fort Mandan, 31
Fort Yellowstone, 242, 266
Fossil, 296
Fountain Geyser, 205
Fountain House, 205
Freeman, L. M., 105

G
Gallatin Range, 30, 32, 88, 291
Gallatin River, 26, 52, 94, 291
Gallatin Valley, 100
Game Ranch, 87
Gap Creek, 286
Gardiner, Montana, 199, 200, 274
Gardner, Johnson, 98
Gardner Hole, 98
Gardner River, 67, 86 ff., 122, 138
Garfield, Thomas, 247
Garrison, L. A., 12, 274, 279
Gass, Patrick, 31
Gentian Pool, 131
George, James (“Yankee Jim”), 198, 283
Giant Geyser, 130
Giantess Geyser, 105, 130
Gibbon, Gen. John, 170
Gibbon Canyon, 210
Gibbon Falls, 210
Gibbon River, 131, 227
Gilbert, Col. Charles C., 178
Gillette, Warren C., 120
Glass, Hugh, 106
Goff, ——, 200
Golden Gate, 210
Gold seekers, 101
Good, James W., 211
Goodnight Bison Herd, 258
Gore, Sir George, 154
Graham and Klamer, 204
Grand Canyon National Park, 211, 268
Grand Geyser, 130 ff.
Grand Loop Highway, 127, 195, 210, 214
Grand Prismatic Spring, 98, 131
Grand Teton National Park, 83, 274
Grant, Brogan, and Lycan, 195
Grant, John, 162
Grant, Madison, 233
Grant, Pres. Ulysses S., 142
Great Salt Lake, 110
Green River, 45, 81, 163
Green River Valley, 66, 81
Gregory, Col. J. F., 193
Grinnell, George Bird, 242
Grizzly Lake, 261
Gros Ventre Indians, 69
Grotto Geyser, 130, 131
Guernsey Lake National Park, 83
Gunnison, Capt. J. W., 114

314

H
Hague, Dr. Arnold, 25
Hall, A. F., 270
Hamilton, Charles A., stores, 217
Hamilton, William, 104
Hancock, Forest, 35, 36
Harper’s Magazine, 120
Harrington, Ed., 163;
see Trafton, Edward
Harris, Moses (“Black”), 100
Harris, Capt. Moses, 246;
report of robbery, 250, 266
Harrison, Pres. Benjamin, 228
Hart Mountain, 184
Hauser, Samuel T., 120 ff., 137, 163
Hayden, Carl, 211
Hayden, Dr. Ferdinand V., 102 ff.;
praise of Bridger, 112;
hears Langford, 136 ff.;
expedition, 138 ff.
Hayden Valley, 26, 45, 50;
rendezvous, 81;
bison ranch, 258, 288, 298
Hayes Act, 246
Haynes, Frank Jay, 193, 200;
first studio, 216;
arrested poacher, 247
Haynes, Jack Ellis, 200, 241, 270
Heart Lake, 239
Hedges, Cornelius, 120 ff.;
quoted, 129;
proposed park idea, 132 ff., 142, 144
Hegley, C. DeV., 138
Helena, Montana, 102, 121, 184
Helena Daily Herald, 132, 136, 142
Helena Independent, 259
Helena tourists, 180 ff.
Hellbroth Springs, 122
Hell Roaring Mountain, 122
Hellroaring Creek, 261
Hells Half Acre, 122
Henderson, Bart, 105
Henderson, Walter L., 205
Henderson’s Ranch, 178
Henry, Major Andrew, 32 ff., 56, 92, 106, 291
Henrys Fork of Snake River, 88, 96, 291
Henrys Lake, 32, 88, 238
Hobart, C. T., 204
Hofer, Thomas Elwood, 198, 247
Hoffman, W., 201
Holm Transportation Company, 202
Hoodoo Creek region, 105, 240
Horseshow Cattle Company, 162
Hospital, 217
Hotels, 202 ff.
Hough, Emerson, 247
Hough, Franklin B., 228
Howard Eaton Trail, 195, 215
Howard, Gen. Oliver O., 166;
pursues Nez Percé, 169 ff.;
at Big Hole, 170;
at Henrys Lake, 178;
in Lamar Valley, 184 ff.
Howell, Ed, 247
Huntley, Child, and Bach, 201
Huntley, Silas S., 201
Huth, Dr. Hans, 226

I
Idaho, 102, 128, 160 ff.;
irrigation interests, 259;
entrance desired, 276
Improvement Company, 244
Index Peak, 104
Indian Creek, 86, 88
Innocents (Henry Plummer’s gang), 163
Irving, Washington, 40, 45
Isa Lake, 27

J
Jackson, “Teton,” 163
Jackson, William H., photographs, 139
Jackson Hole, 51, 96, 102, 202, 235
Jackson Lake, 44, 99, 210
Jacobs, John, 158
James, Thomas, 55 ff.
James, William, 250
Jamestown, 152
Jefferson, Pres. Thomas, 28, 221
Jefferson National Expansion Memorial, 83
Jefferson River, 26, 41, 52
Jenny, Indian wife of “Beaver Dick,” 238
Jones, W. A., 86 315
Jordan and Howell, 195
Joseph, Chief, 148 ff.;
promise to father, 165;
description, 166;
flight, 170 ff.;
surrender, 189;
death, 191, 283
Joseph, Old Chief, 165 ff.

K
Kenck, Charles, 180;
killed, 181;
buried, 182
Kent, Hon. William, 266
Kingman, Capt. D. C., 210
Kingsley, Mary, quoted, 233
Kipling, Rudyard, quoted, 241;
poem, 281 ff.
Kittams, Walter H., 235
Klamer, Henry E., 216
Kohrs, Conrad, 162

L
Lacey, John F., 233
Lacey Act, 246
Lake Biddle, 44
Lake Eustis, 45
Lake Hotel, 250
Lamar Creek, 86, 88
Lamar River, 27, 50, 86, 88, 117, 139;
Nez Percé flight, 184 ff., 238, 298
Lamar Unit or Buffalo Ranch, 258
Lamar Valley, 104
Lane, Franklin K., Secretary of the Interior, 264;
report of, 267
Langford, Nathaniel P., 118 ff.;
quoted, 129;
comment on Hedges’ remarks, 132;
lectures, 134;
advocacy of Park idea, 136 ff., 144, 164;
made superintendent of Park, 238
LaNoue, Francis D., 273
Lapwai, 36;
Indian Reservation, 166, 188
Larocque, Antoine, 31
Lava Creek, 86, 88, 296
Leigh, Richard (“Beaver Dick”), 238, 283
Leitner, William B., 138
Lewis and Clark, missed Yellowstone Park, 31 ff.; 41, 71, 165, 232;
journals, 285
Lewis Lake, 98, 102
Lewis, Meriwether, 35, 57
Lewis, Samuel, 285 ff.;
concealed map, 296
Libby, Rube, 104
Lincoln, Pres. Abraham, 225