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Pediatric
Dysphagia
Etiologies, Diagnosis, and Management
J.P.W.
C
Jay Paul Willging _ Claire Kane Miller _ Aliza P. Cohen
Pediatric Dysphagia: Etiologies, Diagnosis, and Management is a comprehensive professional
reference on the topic of pediatric feeding and swallowing disorders. Given that these disorders
derive from abnormalities in the function and/or structure of the airway and digestive systems,
multiple clinical specialists may be involved in the evaluation and management of affected children
at any given point in time. Therefore, this text includes significant contributions from a wide range of
experts in pediatric dysphagia, including members of the Interdisciplinary Feeding Team at Cincinnati
Children’s Medical Center. These experts present an in-depth description of their roles in the
diagnosis and management of dysphagic children, providing the reader with an understanding of why
a
multidisciplinary model of care is key to the optimization of outcomes.
Pediatric Dysphagia is divided into five parts. In Part I, readers are provided with an overview of the embryologic development of aerodigestive structures that relate to swallowing, an introduction to neural organization related to swallowing function and physiologic aspects of swallowing, a synopsis of oral motor development, a discussion of the various etiologic categories of feeding and swallowing disorders, and an overview of genetic disorders associated with feeding and swallowing issues. Part II covers the clinical and instrumental assessment of patients, including the interdisciplinary feeding team infrastructure and function, the roles of individual members of the feeding team, the specific diagnostic tests commonly used in the assessment of feeding and swallowing issues, the classification of neonatal intensive care units, and the assessment and management of feeding and swallowing issues encountered in the neonatal intensive care unit. Part III focuses on the management of pediatric dysphagia, covering a wide range of treatment strategies and interventions for children with various categories of feeding disorders. Part IV includes an introduction to the concept of evidence-based practice and the application of evidence-based strategies in the management of dysphagia. Part V presents a brief overview of the role of ethics in healthcare and ethical considerations in the treatment of dysphagic children.
In summary, the overall aim of this comprehensive text is to provide all pediatric professionals
involved in the care of dysphagic patients with a basic understanding of the complexity of this
disorder, the anatomic, neurologic, and physiologic components involved in this disorder, an overview
of the diverse population of children who suffer with this disorder, and with a wide range of
management approaches based on patient needs and capabilities. The authors also address clinical
problem solving and decision making, inspiring readers to develop multidisciplinary models of care at
their own institutions.
www.pluralpublishing.comJ.P.W.
C
Pediatric Dysphagia
Etiologies, Diagnosis, and Management
Willging
Miller
Cohen

Pediatric Dysphagia
Etiologies, Diagnosis, and Management

Pediatric Dysphagia
Etiologies, Diagnosis, and Management
Jay Paul Willging, MD
Claire Kane Miller, PhD, MHA, CCC-SLP, BCS-S
Aliza P. Cohen, MA

5521 Ruffin Road
San Diego, CA 92123
e-mail: [email protected]
Website: https://www.pluralpublishing.com
Copyright © 2020 by Plural Publishing, Inc.
Typeset in 10/12 Garamond Book by Flanagan’s Publishing Services, Inc.
Printed in the United States of America by Integrated Books International
All rights, including that of translation, 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, recording, or otherwise, including photocopying, recording,
taping, Web distribution, or information storage and retrieval systems without the prior
written consent of the publisher.
For permission to use material from this text, contact us by
Telephone: (866) 758-7251
Fax: (888) 758-7255
e-mail: [email protected]
Every attempt has been made to contact the copyright holders for material originally
printed in another source. If any have been inadvertently overlooked, the publishers will
gladly make the necessary arrangements at the first opportunity.
Library of Congress Cataloging-in-Publication Data:
Names: Willging, Jay Paul, author. | Miller, Claire Kane, author. | Cohen,
Aliza P., author.
Title: Pediatric dysphagia : etiologies, diagnosis, and management / Jay
Paul Willging, Claire Kane Miller, Aliza P. Cohen.
Description: San Diego, CA : Plural Publishing, Inc., [2020] | Includes
bibliographical references and index.
Identifiers: LCCN 2019035306 | ISBN 9781597568647 (paperback) | ISBN
1597568643 (paperback)
Subjects: MESH: Deglutition Disorders
— etiology | Deglutition
Disorders — diagnosis | Deglutition Disorders — therapy | Child
Classification: LCC RC815.2 | NLM WI 258 | DDC 616.3/23 — dc23
LC record available at https://lccn.loc.gov/2019035306
Disclaimer: Please note that ancillary content (such as documents, audio, and video,
etc.) may not be included as published in the original print version of this book.

v
Contents
Foreword by Robin T. Cotton xi
Pr
eface
xiii
About the Editors xv
A
cknowledgments
xvii
Contributors xix
Part I.
Foundations
Sec
tion 1.
Embryology
1 Embr 5
Relate to Swallowing
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
Section 2.
Neural Control of Swallowing
2 Neur 33
Claire Kane Miller, Lisa N. Kelchner, and Jay Paul Willging
3 Cr 41
Claire Kane Miller, Lisa N. Kelchner, and Jay Paul Willging
4 T 49
Claire Kane Miller, Lisa N. Kelchner, and Jay Paul Willging
5 R 53
Claire Kane Miller, Lisa N. Kelchner, and Jay Paul Willging
Section 3. Oral Motor Development
6 Or 61
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
Section 4. Etiologies
7 Syndromes, Sequences, and Associations 83
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
8 Neurologic Etiologies 93
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging

vi PediaDysphagia: Etiologies, Diagnosis, and Management
9 Str 105
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
10 R 119
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
11 Cardiac Conditions 123
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
12 Func 139
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
13 Func 143
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
14 Sensor 147
Claire Kane Miller, Jennifer Maybee, Aliza P. Cohen, and Jay Paul Willging
15 Meta 151
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
16 Psy 155
Claire Kane Miller, Lori Vincent, Aliza P. Cohen, and Jay Paul Willging
Section 5. Genetics
17 Genetic Syndromes and Disorders and Their Associated 161
Feeding Issues
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
Part II.
Clinical and Instrumental Assessment
Sec
tion 6.
Interdisciplinary Feeding Team
18 T 199
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
19 R 203
Jay Paul Willging
20 R 213
Dan T. Benscoter
21 R 231
Vincent Mukkada, Aliza P. Cohen, and Jay Paul Willging
22 R 241
Candace J. Hochstrasser
23 R 243
Candace J. Hochstrasser

Contents vii
24 R 249
Amy E. Reed
25 R 259
Claire Kane Miller
26 R 265
Elizabeth J. Kirby
27 R 271
Sarah M. Weller
28 Case Study Reflecting Interdisciplinary Feeding Team Approach 281
Claire Kane Miller
Section 7. Oral Motor Feeding Assessment
29 Clinical Oral Motor Feeding Assessment 289
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
Section 8. Instrumental Assessment
30 T 329
Claire Kane Miller, Steven J. Kraus, Aliza P. Cohen, and Jay Paul Willging
31 F 361
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
32 A 397
Pediatric Dysphagia
Charles M. Myer IV, Claire Kane Miller, Aliza P. Cohen,
and Jay Paul Willging
Section 9.
Assessment and Management of Feeding and
Swallowing Issues in the Neonatal Intensive Care Unit
33 Classif 415
Claire Kane Miller, Alison S. Riley, Brenda K. Thompson, and Ann Clonan
34 Selec 421
Care Unit
Claire Kane Miller, Alison S. Riley, Brenda K. Thompson, and Ann Clonan
35 T 435
Claire Kane Miller, Alison S. Riley, Brenda K. Thompson, and Ann Clonan
36 F 441
Care Unit
Claire Kane Miller, Alison S. Riley, Brenda K. Thompson, and Ann Clonan
37 T 449
Claire Kane Miller, Alison S. Riley, Brenda K. Thompson, and Ann Clonan

viii PediaDysphagia: Etiologies, Diagnosis, and Management
Part III. Management of Pediatric Dysphagia
Sec
tion 10.
Overview of Treatment Strategies
38 Ov 467
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
39 Management of Feeding Issues in Infants and Children with 491
Craniofacial Anomalies
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
40 Management of Dysphagia in Children with Underlying 519
Neurogenic Conditions
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging
Section 11.
Sensory Processing Disorders
41 Sensor 553
Affect Feeding
Claire Kane Miller and Jennifer Maybee
42 Inter 565
Claire Kane Miller and Jennifer Maybee
Section 12. Behavioral Feeding Disorders and
Intervention Strategies
43 Beha 581
Claire Kane Miller and Lori B. Vincent
44 Beha 587
Claire Kane Miller and Lori B. Vincent
45 Beha 593
Claire Kane Miller and Lori B. Vincent
Section 13. Management of Gagging, Retching, and
Tube Feeding Issues
46 Management of Gagging, Retching, and Tube Feeding Issues 617
Therese O’Flaherty, Aliza P. Cohen, and Jay Paul Willging
Part IV. Evidence-Based Practice
Sec
tion 14.
Evidence-Based Practice and Assessing Outcomes
in Pediatric Dysphagia
47 Le 633
Claire Kane Miller

Contents ix
48 Components of Evidence-Based Practice 637
Claire Kane Miller
49 Esta 647
Treatment Protocols
Claire Kane Miller
50 Integ 657
Treatment Plan
Claire Kane Miller
Part V.
Ethics in Pediatric Dysphagia
Sec
tion 15.
Ethics in Pediatric Dysphagia
51 Ethics in Pediatric Dysphagia 665
Candace Ganz and Claire Kane Miller
Index 685

xi
Foreword
It is indeed an honor to write this foreword
and to have personally been at the forefront
of the conceptual and clinical change that
transformed the model of care for children
with airway and swallowing issues. The tra-
ditional fragmented approach became one
in which all involved clinical specialists
evaluated the patient and together devel-
oped an integrated management plan
— an
interdisciplinar
y team approach. The inter-
disciplinary feeding team at Cincinnati Children’s Hospital Medical Center exem- plifies this holistic, cohesive model of care. The team began as a pilot project in 1987, with the mission of optimizing the well- being of children with complex feeding and swallowing issues. Since that time, we have become leaders of medical treatment offered in this format.
Given the remarkable advancements in
medical care that have been made over the past several decades, the number of children with complex syndromes and disorders pre-
senting to medical centers across the nation has dramatically increased. Many of these children experience difficulties with safe oral feeding and require input from clini- cians with special expertise in pediatric dys- phagia. Our interdisciplinary feeding team, along with other experts in various aspects of patient care, has written a comprehen- sive and unparalleled text designed to lay the foundation for an understanding of the embryologic, anatomic, neurogenic, cogni- tive, and behavioral components of dyspha- gia. They have also familiarized readers with the disorders and syndromes associated with dysphagia, the complexities of clini- cal decision making, the ethical issues often involved in patient care, and most impor-
tant, the need to strive for evidence-based approaches to treatment. In sum, they have shared their philosophy for collaborative care, their respect for the knowledge and skills of multiple clinical disciplines, and a willingness to learn from others.
Robin T. Cotton, MD, FRCS(C), FACS

xiii
Preface
Medical advancements in neonatal and pedi-
atric care over the past several decades have
led to the increased survival of infants and
children with a wide spectrum of congeni-
tal conditions, syndromes, and sequences,
many of which are associated with physio-
logic and anatomic abnormalities that result
in feeding and swallowing disorders. Given
the complexity of these patients, providing
optimal care requires a multidisciplinary
approach in which all involved health care
professionals must not only assess the
patient from the perspective of their own
discipline, but must understand and appre-
ciate the input and expertise of other team
members. Our book reflects this model of
care, including chapters written by mem-
bers of the Interdisciplinary Feeding Team
at Cincinnati Children’s Medical Center. We
cover the roles played by our medical sub-
specialists in otolaryngology, pulmonology,
and gastroenterology as well as the roles
of the nurse, advanced nurse practitioner,
dietitian, speech-language pathologist,
occupational therapist, psychologist, and
social worker.
Our book is divided into five parts. In
Part I, we provide readers with an overview
of the embryologic development of aerodi-
gestive structures that relate to swallowing,
an introduction to key structures involved
in the neural control of swallowing, a syn-
opsis of oral motor development, a discus-
sion of the various etiologic categories of
swallowing disorders, and an overview
of genetic disorders associated with feed-
ing and swallowing issues. Part II covers
the clinical and instrumental assessment
of patients, including the interdisciplinary
feeding team approach, the specific diag-
nostic tests commonly used in assessing
feeding issues, the classification of neona-
tal intensive care units, and the assessment
and management of feeding and swallow-
ing issues encountered in the neonatal
intensive care unit. Part III focuses on the
management of pediatric dysphagia, cov-
ering a wide range of treatment strategies
and interventions for children with various
categories of feeding disorders. In Part IV,
we present an introduction to the concept
of evidence-based medicine, an important
component of decision-making in regard to
treatment, and a topic that we have empha-
sized throughout the text. Part V presents a
brief overview of the role of ethics in health
care and in treating dysphagic children.
It is our hope that the information in
this text expands the knowledge of clini-
cians involved in the care of dysphagic
patients, assists them in clinical problem
solving and decision making, and inspires
them to develop multidisciplinary mod-
els of care at their own institutions. This
approach optimizes the outcomes of an
extremely diverse population of complex
patients, all of whom present with condi-
tions and accompanying dysphagia.
Jay Paul Willging
Claire Kane Miller
Aliza P. Cohen

xv
About the Editors
Jay Paul Willging, MD, is a Professor of
Otolaryngology–Head and Neck Surgery
at the University of Cincinnati College of
Medicine. He completed his fellowship in
pediatric otolaryngology at Cincinnati Chil-
dren’s Hospital Medical Center (CCHMC)
and has been a member of the Division
of Pediatric Otolaryngology–Head and
Neck Surgery at CCHMC since 1992. He is
the Director of the Pediatric Otolaryngol-
ogy Fellowship Training Program and also
the Director of Clinical Operations for the
Otolaryngology Division. He has served as
the Director of the Interdisciplinary Feed-
ing Team since 1999, and is also an active
participant in numerous other multidisci-
plinary programs, including the Aerodiges-
tive and Esophageal Center, the Craniofacial
Anomaly Team, the Fiberoptic Endoscopic
Evaluation of Swallowing Safety Clinic, and
the Velopharyngeal Insufficiency Clinic. Dr.
Willging has numerous peer-reviewed clini-
cal and research publications and has been
a longstanding contributor to textbooks on
a wide range of otolaryngology topics, par-
ticularly feeding and swallowing disorders.
Claire Kane Miller, PhD, MHA, CCC-SLP,
BCS-S, is the Program Director of the
Aerodigestive Center/Interdisciplinary Feeding Team at Cincinnati Children’s Hos- pital Medical Center, and holds a clinical and research position in the Division of
Speech-Language Pathology at Cincinnati Children’s. She is a field service associate affiliate professor in the Department of Oto- laryngology–Head and Neck Surgery at the University of Cincinnati College of Medicine and is also an assistant affiliate professor in the Department of Communication Sciences and Disorders at the University of Cincin- nati. Her research and clinical interests are predominantly in pediatric dysphagia. Throughout her career, she has focused on instrumental swallowing assessment and the clinical management of infants and children with congenital and acquired air-
way anomalies. She has authored numerous publications and has presented both nation- ally and internationally on diverse aspects of pediatric dysphagia.
Aliza P. Cohen, MA, is a medical and sci-
ence writer who joined the Division of Pediatric Otolaryngology–Head and Neck Surgery at Cincinnati Children's Hospi- tal Medical Center (CCHMC) in 2006. She has worked collaboratively with faculty and fellows in pediatric surgery, pediatric neu- rology, pediatric pulmonary and sleep medi-
cine, and pediatric otolaryngology. She has coauthored numerous articles and book chapters on a wide array of topics within these disciplines and has dedicated her efforts to mentoring fellows and faculty in the pursuit of excellence in writing.

xvii
Acknowledgments
We would like to express our gratitude to all
of the professionals on the Interdisciplinary
Feeding Team at Cincinnati Children’s Hos-
pital Medical Center (CCHMC) who have
taken the time to contribute to this text,
drawing from both their clinical expertise
and their years of experience in diagnos-
ing and caring for a wide array of com-
plex patients with feeding and swallowing
issues. We would also like to extend a spe-
cial thank you to other clinical specialists at
our institution and elsewhere who have col-
laborated with us in this endeavor, as well
as to partners and colleagues at CCHMC
who have provided guidance and support
over the years. In addition, a wholehearted
thank you to Joseph Alward for his invalu-
able assistance with all of the figures we
have included in our text and to Joseph P.
Willging for his artistic contributions. Lastly,
each of us would like to thank our families
for their enduring patience and unwaver-
ing support throughout this major project.
Without this support, we would not have
been able to bring our book to fruition.
Jay Paul Willging
Claire Kane Miller
Aliza P. Cohen

xix
Contributors
Dan T. Benscoter, DO
Division of Pulmonary Medicine, Cincinnati Children’s Hospital Medical Center
Assistant Professor, University of Cincinnati College of Medicine
Cincinnati, Ohio
Chapter 20
Ann Clonan, MEd, CCC-SLP
Division of Speech-Language Pathology, Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio
Chapters 33, 34, 35, 36, and 37
Aliza P. Cohen, MA
Medical Writer, Division of Pediatric Otolaryngology–Head and Neck Surgery, Cincinnati
Children's Hospital Medical Center
Cincinnati, Ohio
Chapters 1, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 21, 29, 30, 31, 32, 38, 39,
40, 46
Robin T. Cotton, MD, FRCS(C), FACS
Director, Aerodigestive and Esophageal Center, Cincinnati Children’s Hospital Medical
Center
Professor, University of Cincinnati College of Medicine
Cincinnati, Ohio
Foreword
Candace Ganz, EdD, CCC-SLP
Director, Division of Speech-Language Pathology, Cincinnati Children’s Hospital Medical
Center
Affiliate Associate Professor, Department of Communication Sciences and Disorders,
University of Cincinnati
Cincinnati, Ohio
Chapter 51
Candace J. Hochstrasser, MSN, APRN, FNP-BC, IBCLC
Division of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children’s Hospital
Medical Center
Cincinnati, Ohio
Chapters 22 and 23
Lisa N. Kelchner, PhD, CCC-SLP, BCS-S
Professor Emeritus, University of Cincinnati Department of Communication Sciences
and Disorders
Cincinnati, Ohio

xx PediaDysphagia: Etiologies, Diagnosis, and Management
Chapters 2, 3, 4, and 5
Elizabeth J. Kirby, OTR/L
Division of Occupational and Physical Therapy, Cincinnati Children’s Hospital Medical
Center
Cincinnati, Ohio
Chapter 26
Steven J. Kraus, MD, MS
Division Chief of Fluoroscopy, Department of Radiology and Medical Imaging,
Cincinnati Children’s Hospital Medical Center
Associate Professor of Radiology & Pediatrics Affiliated, University of Cincinnati College
of Medicine
Cincinnati, Ohio
Chapter 30
Jennifer Maybee, OTR, MA, CCC-SLP
Division of Speech-Language Pathology, Children’s Hospital Colorado
Boulder, Colorado
Chapters 41 and 42
Claire Kane Miller, PhD, MHA, CCC-SLP, BCS-S
Division of Speech-Language Pathology, Cincinnati Children’s Hospital Medical Center
Program Director, Aerodigestive and Esophageal Center/Interdisciplinary Feeding Team,
Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio
Chapters 1, 2, 3, 4, 5. 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 25, 28, 29, 30, 31, 32,
33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 47, 48, 49, 50, 51
Vincent Mukkada, MD
Division of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children’s Hospital
Medical Center
Associate Professor, University of Cincinnati College of Medicine
Cincinnati, Ohio
Chapter 21
Charles M. Myer IV, MD
Division of Pediatric Otolaryngology–Head and Neck Surgery, Cincinnati Children’s
Hospital Medical Center
Assistant Professor, University of Cincinnati College of Medicine
Cincinnati, Ohio
Chapter 32
Therese O’Flaherty, MS, RD, LD, CSP
Division of Nutrition Therapy, Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio
Chapter 46
Amy E. Reed, MS, RD, CSP, LD
Northeast Cincinnati Pediatric Associates

Contributors xxi
Cincinnati, Ohio
Chapter 24
Alison S. Riley, MA, CCC-SLP
Division of Speech-Language Pathology
Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio
Chapter 33, 34, 35, 36, and 37
Brenda K. Thompson, MA, CCC-SLP, BCS-S, CNT
Division of Speech-Language Pathology, Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio
Chapter 33, 34, 35, 36, and 37
Lori B. Vincent, PhD, BCBA-D
Division of Developmental and Behavioral Pediatrics, Cincinnati Children’s Hospital
Medical Center
Cincinnati, Ohio
Chapters 43, 44, and 45
Sarah M. Weller, MSW, LISW-S
Social Services, Cincinnati Children’s Hospital Medical Center
Cincinnati, Ohio
Chapter 27
Jay Paul Willging, MD
Division of Pediatric Otolaryngology–Head and Neck Surgery, Cincinnati Children’s
Hospital Medical Center
Medical Director, Interdisciplinary Feeding Team, Cincinnati Children’s Hospital Medical
Center
Professor, University of Cincinnati College of Medicine
Cincinnati, Ohio
Chapters 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 21, 29, 30, 31, 32,
38, 39, 40, 46

Part I
Foundations
Figure I. Branchial apparatus with the first arch defined.
Source:

Courtesy of Kathleen Sulik, PhD, Department of Cell Biol-
ogy and Physiology, University of North Carolina at Chapel Hill.

Section
1
Embryology

5
Chapter Outline
Overview
Prenatal Development
Neural Tube Development During the Embryonic Period
Pharyngeal Arches
The Pharyngeal Apparatus
Pharyngeal Clefts
Pharyngeal Pouches
Congenital Anomalies of the Pharyngeal Pouches
and Arches
Arteries, Muscles, Bones, and Cartilages Arising from the
Pharyngeal Arches
Development of the Skull
Development of the Face
Congenital Malformations of the Facial Skeleton
Development of the Palate
Cleft Lip and Palate
Lip Anomalies
Development of the Tongue
Congenital Malformations of the Tongue
Lingual Thyroid Gland
1
Embryologic Development
of Aerodigestive
Structures that Relate
to Swallowing
Claire Kane Miller, Aliza P. Cohen, and Jay Paul Willging

6 PediaDysphagia: Etiologies, Diagnosis, and Management
Overview
Embryology is a branch of science that
focuses on the formation, development, struc-
ture, and functional activities of embryos.
The first 8 weeks of the embryonic period
are critical, as it is during this period that
major organs and systems begin to form.
1

Interruptions or disturbances during this
time frame are the catalyst for major con-
genital anomalies, many of which have a
profoundly deleterious effect on the devel-
opment of the aerodigestive tract, and ulti-
mately adversely affect the normal feeding
and swallowing process. The congenital
lesions discussed in this chapter stem from
abnormal occurrences during develop-
ment, such as the lack of fusion between
two structures, the lack of separation of
two structures, the persistence of a struc-
ture that normally regresses, the trapping
of one tissue within another, or the failure
of a vital structure to form.
Prenatal
Development
The period of prenatal development is subdivided into (1) pre-embryonic devel- opment, which begins at fertilization and continues through cleavage (rapid cell divi- sion) and implantation of the fertilized egg to the wall of the uterus; (2) embryonic development, which extends from implan- tation to the end of the eighth developmen- tal week; and (3) fetal development, which begins with the ninth developmental week
and continues until birth. After week 9 of gestation, the embryo is referred to as a fetus, as its basic form has been acquired. The fetal period is characterized by rapid body growth and differentiation of the tis- sues and organs that have been formed dur-
ing the embryonic period.
Box 1–1 The gestational period is divided into three trimesters, each of which lasts for three months. The first trimester is criti- cal in that formation and development of the embryo (embryogenesis) takes place.
Three cell types differentiate in early em-
bryonic development as the embryo under-
goes an invagination (formation) process. The process of gastrulation (formation of embryo layers) leads to the development of organs and tissues. The outer germ layer is referred to as ectoderm, which gives rise to the epidermis, oral cavity, inner ear, and eye lens. The middle germ layer is referred to as the mesoderm. Its derivatives include muscle (skeletal, cardiac, smooth), skeleton, the circulatory system, gonads, and the kidneys. The derivatives of the endoderm (inner germ layer) include the digestive and respiratory systems.
Box 1–2 Invagination is a process of cellular migra-
tion. It is the initial step of gastrulation, which leads to a multilayered organism with three distinct germ cell layers
— ecto-
derm, mesoderm, and endoderm.
Congenital Malformations of the Oral Cavity
Development of the Gastrointestinal Tract
Congenital Anomalies of the Gastrointestinal Tract
Development of the Respiratory System
Congenital Anomalies of the Respiratory System
Questions Pertaining to Chapter

1. Embryologic Development of Aerodigestive Structures 7
Neural Tube Development
During the Embryonic Period
Prenatal development begins with fertil-
ization of the egg and the formation of a
zygote (fertilized ovum), which contains
the maternal and paternal chromosomes.
The zygote is transported to the uterus by
the ciliary action of the fallopian tube. By
week 3 of gestation, the central nervous
system (CNS) and the cardiovascular system
begin to form. The origin of the CNS is the
neural plate. This plate gives rise to the neu-
ral folds and the beginning of the formation
of the neural tube, from which the brain
and spinal cord form. As depicted in Fig-
ure 1–1, as the neural tube closes cranially
(toward the cranium), the spinal cord and
the major divisions of the brain develop.
These divisions include the prosencephalon
(forebrain), the mesencephalon (midbrain),
and the rhombencephalon (hindbrain). By
the end of week 3, further growth of the
neural tube gives rise to the first stages of
a recognizable face (frontal nasal process).
By the end of week 4, the primary organiza-
tion of the brain is identifiable.
If the neural tube does not develop and
close completely during the first 4 weeks
of gestation, defects in the brain, spinal
vertebrae, and/or spinal cord result. These
defects are referred to as neural tube defects,
and are the most common severe congenital
anomalies of the CNS.
2
Neural tube defects
may be open to the surface (open neural
tube defects) or closed, being covered with
skin (closed neural tube defects). Open
defects range from a complete opening
of the neural tube on the surface of the
skull and along the spine to only a local-
ized opening. Open neural tube defects are
considered to be the most severe.
3
The two most common neural tube
defects are anencephaly and spina bifida.
In infants with anencephaly, there is nor-
mal formation of the spinal cord, but failure
of neural tube closure for development of
the brain. These infants lack a functional
forebrain and cerebellum and typically sur-
vive for only a few weeks. In infants with
spina bifida, the spine does not grow nor-
mally over the spinal cord, causing expo-
sure of the spinal cord and the meninges
(Figure 1–2). In patients with meningocele
malformations, spinal fluid and meninges
(dura mater and arachnoid mater) protrude
Figure 1–1. This is a scanning electron
micr
ograph of the embryo dorsal view, show-
ing the neural tube closing, with open neuro-
pores and the paired somites visible through
the thin ectoderm.
Features: surface ecto-
derm, neural tube, cranial (anterior) neuro- pore, caudal (posterior) neuropore, somites, heart, cut edge of amnion, 24 days, 13 somite pairs. Source:
Courtesy of Kathleen Sulik, PhD,
Department of Cell Biology and Physiology,
University of North Carolina at Chapel Hill.

8 PediaDysphagia: Etiologies, Diagnosis, and Management
through an abnormal opening in the ver-
tebral column (Figure 1–3). Myelomenin-
gocele is the most severe form of spina
bifida. It is characterized by exposure of the
fetal spinal cord and the neural elements
through the opening in the spine, resulting
in complete or partial paralysis of the body
below the opening. Children with myelo-
meningocele are often unable to walk and
may have bowel and bladder dysfunction.
Closed neural tube defects (NTDs)
may be located at either the brain or spi-
nal levels, but are most often confined to
the spine. These defects are referred to as
spina bifida occulta. The most common
presentations of an NTD are an abnormal-
ity along the spine such as a tuft of hair
growing out of a dimple along the spine,
a pigmented nevus (mole), a lumbosacral
Figure 1–2. In cases of spina bifida, the neural tube does not close by the end of the first
month of pr
egnancy, leaving a small gap, the spina bifida defect, in the spinal cord. Source: Courtesy of the Midwest Fetal Care Center and Children’s Minnesota.
Box 1–3 The meninges are membranes that protect and cover the brain and spinal cord. They are composed of three pro- tective layers: (1) a tough outer layer (dura mater), (2) a delicate middle layer (arachnoid mater), and (3) an inner layer firmly attached to the surface of the brain (pia mater).

1. Embryologic Development of Aerodigestive Structures 9
vascular anomaly (hemangioma, port-wine
stain), a lipoma (skin doming caused by an
underlying mass of fatty tissue), or a dimple
in the lumbosacral region.
4
Encephaloceles occur when brain tis-
sue protrudes through gaps in the skull
secondary to the lack of bone fusion. The
portion of the brain that protrudes is cov-
ered by skin such that the protrusion is sac-
like in presentation. The protruding tissue
may occur on any part of the skull where
bone fusion did not occur (frontal, pari-
etal, occipital, and sphenoidal regions), but
most often affects the occipital region of the
skull. The effects of an encephalocele vary
between individuals, depending upon the
size, location (anterior or posterior), and
amount of brain tissue protruding from the
skull. Large, posteriorly located encephalo-
celes are likely to be associated with micro-
cephaly, and severely impact neurologic
function and survival. Small encephaloceles
located toward the front of the skull gener-
ally do not contain brain tissue and have a
more favorable prognosis.
2
A tethered spinal cord occurs as a
result of either an open or closed neural
tube defect. In this condition, the lower
end of the spinal cord is attached to the
skin, which restricts movement and causes stretching of the cord. This restriction and stretching may result in neurologic damage, requiring surgical intervention to release the cord.
Pharyngeal Arches
Human embryos have five pairs of pha- ryngeal arches (numbered in craniocaudal sequence) that give rise to the structures of the face, jaw, ear, and neck (Figure 1–4). These arches are also referred to as bran- chial arches. These arches surround the foregut (beginning of the digestive tract) of the embryo and are transiently present during days 20 to 35 of embryonic develop- ment. The arches are numbered 1, 2, 3, 4, and 6, as arch 5 either forms as a short-lived rudiment or does not form in humans (Fig- ure 1–5).
1
The development of the pharyn-
geal arches is regulated by HOX and other regulatory genes that control development of the embryo. Specific craniofacial defects may arise through the disruption of HOX gene expression as a result of a mutation or in response to a teratogen.
1
Figure 1–3. Types of spina bifida. Source: Courtesy of the Centers for Disease Control and
Prevention, National Center on Birth Defects and Developmental Disabilities.

10 PediaDysphagia: Etiologies, Diagnosis, and Management
The Pharyngeal Apparatus
The pharyngeal apparatus consists of the
paired pharyngeal arches, pharyngeal
pouches, and pharyngeal clefts (grooves).
The pouches and clefts separate the arches
(Figure 1–6). The intraluminal surface of
the pharyngeal apparatus is lined by endo-
derm. The pharyngeal clefts are located on
the external surface of the embryo and are
covered by ectoderm.
Each pharyngeal arch has identical
structures, including an internal pouch cov-
ered with endoderm, an external cleft cov-
ered with ectoderm, and a core of somatic
mesoderm and neural crest mesenchyme
between. The somatic mesoderm contributes
the artery, vein, and muscle associated with
a particular arch (Figure 1–7). The neural
crest mesenchyme develops into bone, car-
tilage, and/or connective tissue in each arch.
Each pharyngeal arch also has an associ-
ated cranial nerve with afferent and efferent
branches that innervate the structures of the
arch. The cranial nerve associated with each
arch maintains innervation of the muscula-
ture associated with that arch (Table 1–1).
Pharyngeal Clefts
Pharyngeal cleft 1 develops into the exter-
nal auditory canal. The corresponding
Figure 1–4. The first (A), second (B), third
(C), and fourth (D) arches are visible exter-
nally. The sixth arch does not form an exter-
nal elevation. Source: Courtesy of Kathleen
Sulik, PhD, Department of Cell Biology and
Physiology, University of North Carolina at
Chapel Hill.
Figure 1–5. The pharyngeal arches num-
ber
ed, and other structures identified. Source: Courtesy of Kathleen Sulik, PhD, Department
of Cell Biology and Physiology, University of
North Carolina at Chapel Hill.

11
Figure 1–6. Pharyngeal arches (A),
pouches (P), and clefts (C) are identi-
fied in this mouse, approximating
human age 29 days. The ectoderm
approximates the endoderm, separat- ing cleft from pouch.
The arch con-
sists of mesoderm. Source: Courtesy
of Kathleen Sulik, PhD, Department of
Cell Biology and Physiology, Univer-
sity of North Carolina at Chapel Hill.
Figure 1–7. Structural components of the pharyngeal arch. Source:
Courtesy of Loki austanfell. File licensed under Creative Commons
https://commons.wikimedia.org/wiki/File:PharyngealArchHuman.jpg.

12 PediaDysphagia: Etiologies, Diagnosis, and Management
pharyngeal pouch develops into the eusta-
chian tube, and the membrane formed at
the contact point between the invaginations
of the pouch and the cleft develops into
the tympanic membrane. Defects during
the development of pharyngeal arch 1 may
result in cysts or fistula tracts in the pre-
auricular area or can extend into the neck.
Pharyngeal clefts 2, 3, and 4 are engulfed
by the expansion of pharyngeal arch 2. The
remnants of these structures may appear as
cervical cysts or fistulae.
1
Pharyngeal Pouches
The pharyngeal pouches that form on the
inside of the pharynx between the arches
also give rise to structures. Pharyngeal
Ta Pharyngeal Arch Derivatives
Pharyngeal
ArchArteryNerve Muscles
Skeletal
Structures
1 Maxillary arteryTrigeminal
(CN V)
Muscles of
mastication;
mylohyoid,
anterior belly
of the digastric
muscle, tensor
tympani, tensor
veli palatini
Mandible,
maxilla, malleus,
incus, zygomatic
and temporal
bones
2
Stapedial
Corticotympanic
Facial (CN VII)Muscles of facial expression, stapedius, stylohyoid, posterior belly of the digastric muscleStapes, styloid
process, lesser cornu of the hyoid, upper part of the body of the hyoid bone
3
Common
carotid
Internal carotid
arteries
Glossopharyn-
geal (CN IX)
Hypoglossal
(CN XII)
Stylopharyngeus
4Aortic arch (left)
Right subclavian
artery
Vagus (CN X)
Superior
laryngeal nerve
Cricothyroid
Pharyngeal plexus
Laryngeal
cartilages: thyroid, cricoid, arytenoid, corniculate, and cuneiform cartilages
6 Pulmonary
artery (partial left and right)
Vagus (CN X)
Recurrent
laryngeal nerve
Intrinsic
muscles of the larynx, striated muscle of the esophagus; pharyngeal plexus
Laryngeal
cartilages: epiglottis, thyroid, cricoid, arytenoid, corniculate, and cuneiform cartilages
Source:
Adapted from information in Larsen’s Human Embryology, Schoenwolf, Bleyl, Brauer, Francis-
W
est, 2015.
1

1. Embryologic Development of Aerodigestive Structures 13
pouch 1 develops into the eustachian tube
and the majority of the middle ear cav-
ity. Pharyngeal pouch 2 forms the crypts
(infoldings) of the palatine tonsils, pha-
ryngeal pouch 3 divides into superior and
inferior portions that result in the thymus
gland and the inferior parathyroid glands,
and pharyngeal pouch 4 forms the superior
parathyroid glands.
Congenital Anomalies of the Pharyngeal
Pouches and Arches. Second pharyngeal
cleft and pouch anomalies are the most com- monly seen.
5
In that pharyngeal pouch 2
resides in the pharynx, developmental anomalies may present as masses in the oropharynx or as pharyngeal bands that cause obstruction of the upper aerodiges- tive tract. Fourth pharyngeal pouch anom- alies may present as cysts or recurrent abscesses in the neck, generally on the left side. There is often a fistula opening in the left pyriform sinus. First pharyngeal pouch cysts that result from errors in embryogen- esis may present in the lateral wall of the nasopharynx. Nasopharyngeal teratomas are solid masses of tissues derived from the embryonic ectoderm, mesoderm, and endo-
derm. Such teratomas may cause upper air-
way obstruction.
Arteries, Muscles, Bones,
and Cartilages Arising from
the Pharyngeal Arches
Each of the pharyngeal arches is associated with specific arteries, muscles, and bones or cartilage (see Table 1–1). The maxillary and mandibular prominences of pharyngeal arch 1 develop into the maxilla and man- dible. The derivatives of arch 1 include the maxillary artery, muscles of mastication, the mylohyoid muscle, the anterior belly of the digastric muscle, the tensor veli palatine muscle, and the tensor tympani muscle. The maxillary prominence of pharyngeal arch 1 gives rise to the maxilla, zygomatic bone, squamous temporal bone, palatine bone,
and the vomer. The mandibular prominence derivatives include the mandible, incus, and the malleus.
Pharyngeal arch 2, also known as the
hyoid arch, gives rise to the stapedial artery, muscles of facial expression, posterior belly of the digastric muscle, stylohyoid muscle, stapedius, the lesser horn of the hyoid and upper half of the body of the hyoid, the stapes, and the styloid process. Tissues from the first and second pharyngeal arches form the external ear.
Pharyngeal arch 3 is associated with
the common carotid artery and the proxi- mal internal carotid artery. The stylopharyn- geus muscle, as well as the greater horn of the hyoid and the lower half of the body of the hyoid emerge from pharyngeal arch 3.
Derivatives of pharyngeal arch 4 in-
clude the proximal right subclavian arch of the aorta, the muscles of the soft pal- ate (with the exception of the tensor veli palatine, which originates from arch 1), the muscles of the pharynx (with the excep- tion of the stylopharyngeus, which origi- nates from arch 3), the cricothyroid, and the cricopharyngeus. Pharyngeal arches 4 and 6 give rise to the thyroid cartilage, the cricoid cartilage, arytenoid cartilage, cor-
niculate cartilage, and cuneiform cartilage.
Lastly, pharyngeal arch 6 derivatives
include the ductus arteriosus and proximal pulmonary arteries, the intrinsic laryngeal muscles (with the exception of the cricothy- roid muscle, which originates from arch 4), the skeletal muscle of the esophagus, and the laryngeal cartilages in conjunction with pharyngeal arch 4.
Development of the Skull
The bones of the skull are divided into two portions: the neurocranium (surrounds and protects the brain and sensory organs) and the viscerocranium (bones of the lower face
and jaws). The bones of the infant skull are separated by fibrous connections called sutures, which meet at the fontanelles

14 PediaDysphagia: Etiologies, Diagnosis, and Management
(membranous areas) at the front and back
of the skull (Figure 1–8). The changes in
growth of a particular suture will affect
the growth pattern of adjacent sutures.
6

The metopic suture separates the frontal
bones from each other, the coronal suture
separates the two frontal bones from the
paired parietal bones posteriorly, the sagit-
tal suture separates the two parietal bones
from each other, and the lambdoid suture
separates the occipital bone from the two
parietal bones.
The fontanelles allow for expansion of
the cranium as the brain grows. The cranial
sutures remain open in infancy and typi-
cally begin to fuse as the child approaches 2
years of age; however, complete ossification
of the sutures does not occur until adult-
hood. The approximate time frames for
suture closure are summarized in Table 1–2.
Figure 1–8. The cranial suture lines and bones of the skull. Source:
Courtesy of Cincinnati Children’s Hospital Medical Center, Division of
Pediatric Otolaryngology–Head and Neck Surgery.
Ta Approximate Developmental Timeline
for Suture Closure in Humans
Suture TypeClosure Begins
Metopic 2 months
Sagittal 22 months, ossifies in adulthood
Coronal 24 months, ossifies in adulthood
Lambdoid 26 months, ossifies in adulthood
Source:
Adapted from UpToDate, 2018.

1. Embryologic Development of Aerodigestive Structures 15
Premature fusion of the sutures (cranio-
synostosis) may occur due to environmental
causes such as prenatal compression of the
infant head, teratogens, metabolic disorders,
gene mutations, or chromosomal abnormal-
ities. In other cases, there is no identifiable
causative agent. The premature closure of
the sutures can adversely affect the normal
growth of the brain and cause an abnor-
mal skull shape secondary to the pressure
of the growing brain against the skull. For
example, if the sagittal suture fuses prema-
turely (synostosis), the head appears long,
narrow, and “boat-shaped” (scaphocephaly)
(Figure 1–9). If the coronal suture fuses pre-
maturely, the forehead appears flattened
(anterior plagiocephaly) (Figure 1–10). If
the lambdoid suture closes prematurely,
flattening at the back of the skull occurs
(posterior plagiocephaly). Lastly, if prema-
ture fusion of the metopic suture occurs,
the head appears to be triangularly shaped
(trigonocephaly) in combination with a nar-
row forehead with a midline bony ridge and
closely positioned eyes.
In individuals with double suture syn-
ostosis, more than one suture is prematurely
fused. In those with bicoronal synosto-
sis, the skull appears wider than normal
(anterior brachycephaly). In bilambdoid
Figure 1–9. Sagittal craniosynostosis. Source: Courtesy of the Centers for Disease Control
and Pr
evention,
National Center on Birth Defects and Developmental Disabilities.

16 PediaDysphagia: Etiologies, Diagnosis, and Management
synostosis, the skull is wider than normal
(posterior brachycephaly), and in sagittal
plus metopic synostosis, the head appears
long and narrow (scaphocephaly). In com-
plex multisuture synostosis (bicoronal,
sagittal, metopic), the head appears short,
wide, and/or pointed. Multisuture synosto-
sis presents as a cloverleaf shaped skull.
Craniosynostosis may occur in association
with genetic syndromes such as Crouzon,
Apert, Pfeiffer, Muenke, and Saethre-Chot-
zen (see Chapter 7).
Chiari malformations are complex con-
genital structural abnormalities in the base
of the skull that occur during development
and that affect the structural relationships
between the cerebellum, brainstem, and the
cranial base.
7
The posterior fossa (cavity
near the base of the skull), which encloses
the cerebellum, is narrow and abnormally
small in comparison to the size of the cer-
ebellum. The relatively small posterior
fossa causes the developing cerebellum and
brainstem to be pushed inferiorly. The pos-
terior portions of the cerebellum (cerebellar
tonsils) protrude or herniate through the
foramen magnum and potentially interfere
with the normal circulation of cerebrospi-
nal fluid (CSF) (Figure 1–11). The malfor-
mation may cause increased CSF pressure
within the brain and produce hydrocepha-
lus caused by the accumulation of excessive
Figure 1–10. Unilateral coronal craniosynostosis. Source: Courtesy of the Centers for Dis-
ease Control and Prevention, National Center on Birth Defects and Developmental Disabilities.

1. Embryologic Development of Aerodigestive Structures 17
fluid in the brain. A fluid-filled cyst or cavity
(syrinx) filled with CFS can also develop
within the spinal cord (Figure 1–12).
Box 1–4 Chiari malformations are named after Professor Hans Chiari, the pathologist who first classified these malformations into types in 1891. Later, Julius Arnold, a colleague of Professor Chiari, made additional contributions to the defini-
tion of Chiari II malformation, hence the name Arnold–Chiari malformation.
8
Chiari I malformation is the least severe
of the spectrum. It is characterized by >5 mm descent of the caudal tip of the cerebellar ton- sils past the foramen magnum. Type II Chiari malformation is characterized by brainstem and fourth ventricle herniation and >5 mm descent of the caudal tip of the cerebel- lar tonsils past the foramen magnum, with spina bifida. Type II Chiari malformation is also often associated with myelomeningo- cele. Type III Chiari malformation is char-
F i g u r e 1–11. Chiari I malformation with herniation
of the cer
ebellar tonsils below the foramen magnum.
Source:
Courtesy of Cincinnati Children’s Hospital Medi-
cal Center, Department of Radiology.
Figure 1–12. Chiari malformation with an
associated syrinx of the spinal cor
d. Source: Reprinted with permission of the American
Syringomyelia and Chiari Alliance Project, Inc.

18 PediaDysphagia: Etiologies, Diagnosis, and Management
acterized by herniation of the cerebellum
with or without the brainstem through a
posterior encephalocele. Type IV Chiari
malformation is characterized by cerebellar
hypoplasia or aplasia, with normal poste-
rior fossa and no hindbrain herniation.
Development of the Face
The major development of the face is com- pleted between the fourth and tenth embry- onic weeks by the development and joining of five prominences: the frontonasal promi- nence, the two maxillary prominences, and the two mandibular prominences (Fig-
ure 1–13).
9
Early in the fourth week, the
forebrain enlarges and pushes the ectoderm anterior and laterally, creating the frontona-
sal process. Simultaneously, the two man- dibular prominences and the two maxillary prominences from the first pharyngeal arch grow anteriorly and medially during week 4 of gestation. As these processes grow and fuse, they create the stomodeum (precursor of the mouth), which is separated from the gastrointestinal tract by the oropharyngeal membrane.
Late in the fourth week, two nasal
placodes (paired ectodermal nasal plates) develop on the frontonasal prominence (Figure 1–14). Late in week 5, the lateral and medial nasal processes appear, forming the nasal pits between them. During week 5, rupture of the oropharyngeal membrane occurs to form the broad appearing slit- like embryonic mouth. Early in week 6, the oronasal membrane forms and the median nasal processes begin to form the nasal sep-
Figure 1–14. In the fifth week of human
gestation, the olfactory placodes line the

nasal pits (
NP). Medial (MNP) and lateral nasal
prominences (LNP) form around the nasal
pits. Pharyngeal arch I can be seen creating
the lower jaw. Source: Courtesy of Kathleen
Sulik, PhD, Department of Cell Biology and
Physiology, University of North Carolina at
Chapel Hill.
Figure 1–13. Following closure of the ante-
rior neur
opore, the ectoderm that will line
the nasal cavities (derived from the olfac-
tory placodes [
OP]) is located on the lateral
aspects of the frontonasal prominence. Pha- ryngeal arches 1 and 2 are also seen. Source:
Courtesy of Kathleen Sulik, PhD, Department
of Cell Biology and Physiology, University of
North Carolina at Chapel Hill.

1. Embryologic Development of Aerodigestive Structures 19
tum and primary palate. Late in the sixth
week, the lateral palatine processes and
external ears develop. The lips and gums
separate, the dental lamina appears, and the
future inferior turbinates begin to form.
Early in week 7, the philtrum and upper
lip are formed and further development of
the nasal septum occurs. By the end of the
seventh week, the external ear is fully devel-
oped, the palatal shelves elevate and fuse to
form the secondary palate, and fusion of the
maxillary and mandibular processes occurs.
The lateral nasal wall is well developed by
the eighth week of gestation.
Between weeks 9 and 10 of gestation,
the nasal septum grows down from the roof
of the nasal cavity to fuse with the upper
surface of the primary and secondary pal-
ates along the midline, and ossification
of the maxilla occurs. The nasal cavity is
divided into a left and right nasal passage
that open into the pharynx via the choanae
(posterior portion of the nasal cavity). The
mouth is reduced to its final width during
the second month of gestation, as fusion
of the lateral portions of the maxillary and
mandibular swellings creates the cheeks.
Macrostomia (a large mouth) occurs when
too little fusion occurs, and microstomia
(small mouth) occurs with too much fusion.
The derivatives of the frontonasal, lateral
nasal, medial nasal, maxillary, mandibular,
and mesenchyme in the facial prominences
are summarized in Table 1–3. Neural crest
cells give rise to the cartilage, bone, and
ligaments in the facial and oral regions. By
week 12, the ossification centers of all the
facial bones are present.
Congenital Malformations
of the Facial Skeleton
Holoprosencephaly occurs when the em-
bryonic forebrain (prosencephalon) does not divide into the right and left lobes of the cerebral hemispheres. This results in the
reduction of the midventral parts of the CNS as well as the reduction of midfacial struc- tures (skeletal and soft tissues). Affected infants may have facial deformities that affect the eyes, nose, and upper lip. For example, infants may present with a nar-
row forehead or hypotelorism (close-set eyes), or may lack a nose or philtrum. In extreme cases, only one eye may be present (cyclopia). There are three classifications of holoprosencephaly. These classifications include (1) alobar, characterized by severe facial features as a result of complete failure of brain division; (2) semilobar, in which the hemispheres have somewhat divided, resulting in a less severe form of the disor-
der; and (3) lobar, in which there is evidence of separate brain hemispheres; considered the least severe form of holoprosencephaly.
In normal development, the intermaxil-
lary process fuses with the lateral maxillary
Ta Derivatives of the Facial Prominences
Frontonasal prominenceForehead and the dorsum apex of the nose
Lateral nasal prominencesSides (alae) of the nose
Medial nasal prominencesNasal septum
Maxillary prominencesUpper cheek region, majority of upper lip
Mandibular prominencesChin, lower lip, lower cheek regions
Mesenchyme in the facial
prominences
Fleshy derivatives and bones

20 PediaDysphagia: Etiologies, Diagnosis, and Management
swellings to form the maxillary bones of
the upper jaw. Disruption of the develop-
ment of pharyngeal arches 1 and 2 leads to
underdevelopment of the lower face and
mandible, as seen in patients with Treacher
Collins syndrome (mandibulofacial dyso-
tosis). Disruption of pharyngeal arches 3
and 4 may result in DiGeorge syndrome
(22q11.2 deletion syndrome), which is char-
acterized by defects of the ear, palate, jaw,
agenesis of the thyroid and thymus glands,
and cardiovascular anomalies.
Development of the Palate
Palatal development occurs during the em- bryonic and the early fetal periods (Figure 1–15). The primary palate is formed by the maxillary components of the first pharyngeal arch and the frontonasal prominence, and
forms during the fifth to seventh week post- conception. The primary palate includes the medial portion of the upper lip and the pre-
maxilla. The premaxilla is a wedge-shaped mass of tissue containing the anterior pal- ate and the alveolar ridge. It contains the four central incisors and extends posteriorly to the incisive foramen (Figure 1–16). The incisive foramen is a small opening through which the nasopalatine nerve and the sphe- nopalatine artery pass to the oral mucosa of the hard palate. Embryologic fusion of the primary palate begins at the incisive fora- men and process anteriorly, toward the lip along the incisive suture lines.
During weeks 7 and 8 of gestation,
the maxillary processes produce the pala- tal processes that initially grow vertically downward, parallel to the lateral surfaces of the tongue. By the eighth week, the two ver-
tical shelves of bone lift and fuse in the mid- line; the fusion line is termed the median palatine suture or intermaxillary suture. The fused palatal processes form the secondary palate (Figure 1–17). The incisive foramen marks the central region where the primary and secondary palates meet. Growth and
Figure 1–15. The embryonic palate is complete by the
end of week 12 of gestation.
Source:
Courtesy of Kath-
leen Sulik, PhD, Department of Cell Biology and Physiol-
ogy, University of North Carolina at Chapel Hill.

1. Embryologic Development of Aerodigestive Structures 21
lowering of the mandibular (primordium)
is essential for the elevation of the palatal
shelves and the lowering of the tongue.
Cleft Lip and Palate
Each site where merging or fusion of tis- sue occurs during the embryologic develop- ment of the face and palate is a potential site for a cleft. A cleft may be complete or incomplete. A complete cleft has bone, and all soft tissues are missing from the site. An incomplete cleft lacks bone and muscle, but has skin bridging the cleft site.
There are different types and combina-
tions of clefts (Figure 1–18). Classification based on embryologic development divides these anomalies into clefts of the primary palate (anterior to incisive foramen, includ- ing the lip and alveolus) and clefts of the secondary palate (posterior to the incisive foramen, including the soft palate alone or in combination with the hard palate). Com- plete clefts refer to the maximum degree of clefting (eg, complete cleft of the secondary
palate or complete cleft of the lip, alveolar process, and the primary palate). Incom- plete clefts, such as an incomplete cleft of the soft palate, occur when some degree of fusion has taken place. A submucous cleft palate occurs when oral mucosal mem- brane covers or “hides” the underlying cleft. Although the palate may appear normal, there may be changes in muscle function as a result of the abnormal development.
During development, the mandibular
(primordium) grows, which allows the tongue to lower relative to the palatal shelves. If the first pharyngeal arch does not develop appropriately, the mandibular (primordium) will not grow, the tongue will not be lowered, and a physical obstruction to the palatal shelf elevation will result. In this circumstance, a cleft of the second- ary palate will occur in conjunction with micrognathia (small jaw), which results in glossoptosis (posterior displacement of the tongue). This circumstance is referred to as Pierre Robin sequence and is often associ- ated with syndromes such as Treacher Col- lins and Stickler.
Figure 1–16. Newborn with a complete
bilateral
cleft lip and palate.
The premaxilla
is seen between the two cleft sites. Source:
Reprinted with permission from Chandna
P, Adlakha VK, Singh N. Feeding obturator
appliance for an infant with cleft lip and
palate. J Indian Soc Pedod Prev Dent. 2011;
29(1):71-73.
F i gur e 1–17. The secondary palatal shelves
change their contours such that they initially approximate each other close to the mid- point, and fuse anteriorly and posteriorly from that point. Source:
Courtesy of Kath-
leen Sulik, PhD, Department of Cell Biology
and Physiology, University of North Carolina
at Chapel Hill.

22 PediaDysphagia: Etiologies, Diagnosis, and Management
Lip Anomalies
Joining of the medial nasal prominence with
the lateral nasal prominence and maxillary
prominence is necessary for normal devel-
opment of the upper lip, which is complex
in comparison to the development of the
lower lip, and occurs later in embryogen-
esis.
10
During the second and third months
of gestation, the upper lip divides into the
pars glabrosa and the pars villosa zones. The
pars villosa is an inner zone similar to the
mucosa of the oral cavity. The pars glabrosa
is the outer smooth zone close to the skin.
Hypertrophy of the pars villosa and the
persistence of a horizontal sulcus between
the pars glabrosa and the pars villosa give
the characteristic appearance of a double
lip.
11
Other congenital anomalies of the lip
include astomia, which is a rare condition
in which complete union of the upper and
lower lips occurs. The rudimentary oral
aperture that is associated with severe forms
of holoprosencephaly, trisomy 18, and Hall- ermann–Streiff syndrome is termed micro- stomia. A transverse facial cleft, known as macrostomia, occurs in association with Angelman, Noonan, Beckwith–Wiedemann, Treacher Collins, and Williams syndromes.
10

Congenital synechiae (adhesions) may occur between the hard palate and the floor of the mouth, tongue, or oropharynx. Synechiae may arise from the persistence of the buc- copharyngeal membrane that separates the mouth from the pharynx in the embryo, and typically require surgical division.
Development of the Tongue
The intrinsic and extrinsic musculature of the tongue is formed by the occipital somites, which are precursor populations of cells that differentiate into skeletal muscles, cartilage, tendons, vertebrae, and skin.
Figure 1–18. Types A. Unilateral left complete cleft of the lip
and primary palate. B. Bilateral complete cleft of the lip and primary palate. C. Unilateral left
complete cleft of the lip and palate. D. Bilateral complete cleft of the lip and palate. E. Cleft of
the secondary palate. Source: Adapted from Luciano Abreu Brito, Joanna Goes Castro Meira,
Gerson Shigeru Kobayashi, and Maria Rita Passos-Bueno, “Genetics and Management of the
Patient with Orofacial Cleft,” Plastic Surgery International, vol. 2012, Article ID 782821, 11
pages, 2012. https://doi.org/10.1155/2012/782821

1. Embryologic Development of Aerodigestive Structures 23
The mucosa covering the anterior two-
thirds of the tongue arises from median
and lateral tongue buds that originate from
the floor of pharyngeal arch 1. The first
pharyngeal arch forms the median tongue
bud (tuberculum impar) and two lateral
lingual swellings. As the two lingual swell-
ings grow and expand, they overgrow the
median tongue bud. Late in the fourth week
of gestation, the second pharyngeal arch
forms the copula and the third and fourth
arches form the hypopharyngeal eminence.
During the fifth and sixth weeks of gesta-
tion, the hypopharyngeal eminence con-
tinues to grow and the copula disappears.
The hypopharyngeal eminence forms the
mucosa of the posterior third of the tongue.
The anterior two-thirds of the tongue fuses
with the posterior one-third of the tongue
in a V-shaped line of fusion referred to as
the terminal sulcus. The foramen cecum is a
“pit” in the center of the terminal sulcus that
represents the origin of the thyroid gland
before its migration to the neck.
The nerves that supply pharyngeal
arches 1 to 4 contribute to the complex
innervation pattern of the tongue. The lin-
gual nerve (branch of CN V
3) supplies the
sensory innervation to the anterior two-thirds
of the tongue. The chorda tympani branch of
CN VII transmits taste information from the
anterior two-thirds of the tongue. The pos-
terior two-thirds of the tongue is formed pri-
marily from the third pharyngeal arch, and
therefore both taste and sensory information
are transmitted by CN IX (glossopharyngeal).
A portion of the posterior tongue mucosa is
formed by the fourth pharyngeal arch, and
therefore sensations are transmitted via the
superior laryngeal nerve (branch of CN X,
vagus). The musculature of the tongue is
innervated by CN XII (hypoglossal).
Congenital Malformations
of the Tongue
The most common malformations of the tongue are aglossia (complete absence of
the tongue), microglossia (small tongue), macroglossia (abnormally large tongue), and accessory tongue, which is also referred to as a cleft or bifid tongue.
12
Lingual Thyroid Gland
The thyroid gland derives from the fourth pouch and originates in the midline of the tongue base at the foramen cecum. The thy- roid gland normally descends into the neck with development. Occasionally, however, it fails to descend, resulting in a lingual thy- roid. A lingual thyroid mass presents as a mass in the tongue base that interferes with breathing and swallowing. Medications
to suppress the thyroid gland will lead to a reduction of its size and improve both breathing and swallowing.
Congenital Malformations
of the Oral Cavity
Errors in the embryonic fusion of the ante- rior tongue, tongue base, and the primor-
dial thyroid gland in the area of the foramen cecum may result in malformations of the oral cavity. Primitive foregut cysts may pres- ent in the floor of the mouth. A number of congenital tumors, including teratomas and epithelial choristomas (normal cells in an abnormal location), may arise in the oral cavity. Cysts and pseudocysts of the major and minor salivary glands are considered to be the most common soft tissue anomalies.
Development of the
Gastrointestinal Tract
The gastrointestinal tract arises during the process of gastrulation during the third week of gestation. The endodermal gut tube is created during the fourth week of gestation through a process of embryonic folding. This tube extends from the buc- copharyngeal membrane cranially to the

24 PediaDysphagia: Etiologies, Diagnosis, and Management
cloacal membrane caudally. It consists of
a cranial foregut (precursor of the phar-
ynx, esophagus, stomach, liver, gall blad-
der, pancreas, and the cranial portion of
the duodenum), midgut (origin of the cau-
dal portion of the duodenum, the jejunum,
ileum, ascending colon, and two-thirds of
the transverse colon, and hindgut (precur-
sor of the distal one-third of the transverse
colon, the descending colon, the rectum,
and the urogenital sinus). The primor-
dium of the primitive stomach is visible
by approximately week 4 of gestation. By
week 5, the thoracic and abdominal por-
tions of the foregut divide into the pharynx,
esophagus, stomach, and proximal duode-
num. Between gestational weeks 6 and 8,
the epithelium of the gut tube becomes
thickened and forms lumina that eventually
open into the gut lumen. Subsequently, the
villi (tiny finger-like structures that allow
for absorption of nutrients in the lumen)
are formed.
The neuromuscular structures asso-
ciated with the gastrointestinal tract are
formed by neural crest cell migration into
the rapidly growing alimentary tract. The
neural crest cells differentiate into three
separate layers of muscles that surround the
gut mucosa and the neural network. The
enteric nervous system controls and regu-
lates motor function of the gut. The stom-
ach is formed during gestational week 4 as
the foregut begins to expand. During ges-
tational weeks 7 and 8, the stomach under-
goes a 90 degree rotation in a clockwise
direction, causing the duodenum to acquire
a C-shaped loop.
Congenital Anomalies of
the Gastrointestinal Tract
Congenital anomalies of the gastrointestinal tract include esophageal atresia, intestinal malrotation, atresia in the jejunoileal region, atresia in the duodenum, and diaphragmatic hernia. Esophageal atresia is the most com-
mon malformation of the esophagus. The etiology of this anomaly is considered to be failure of the esophageal endoderm to pro- liferate in synchrony with the elongation of the embryo.
1
A failure in the formation of
the tubular esophagus thus occurs. Errors in forming the tracheoesophageal septa and/ or recanalization lead to tracheoesophageal fistulae and/or esophageal atresia. The fetus is unable to swallow, which results in poly- hydramnios (excessive amniotic fluid). This occurs because the amniotic fluid cannot pass into the intestines for return to the maternal circulation.
Lateralization in the developing embryo
refers to the positioning of organs during embryogenesis, resulting in a distinct left- right asymmetry. A number of abnormali- ties are related to errors of lateralization. In infants with situs inversus abdominis, the abdominal organs are located in the reverse of their normal position. If the midgut does not rotate normally as it retracts into the abdominal cavity, a malrotation of the mid- gut occurs, which causes intestinal obstruc- tion that typically becomes evident shortly after birth. Intestinal malrotation also pre- disposes the infant to volvulus of the mid- gut, whereby the intestines bind and twist around the mesentery (tissues that provide blood and nerve supply to the intestine and attach the intestines to the wall of the abdo- men). Volvulus interferes with the blood supply to the intestines and can result in necrosis (death) of the intestine. It is thus considered a surgical emergency.
Congenital hypertropic pyloric steno-
sis occurs when there is overgrowth of the longitudinal muscle fibers of the pylorus, creating a marked thickening of the pyloric outlet region of the stomach. The resulting stenosis of the pyloric canal obstructs pas- sage of food into the duodenum, and the newborn infant expels the contents of the stomach forcefully following a feeding (pro-
jectile vomiting). Omphalocele occurs when the midgut fails to retract into the abdomi- nal cavity during development, and at birth,

1. Embryologic Development of Aerodigestive Structures 25
the coils of intestine are covered only with
a transparent sac of amnion. An imperforate
anus occurs when the anal membrane fails
to break down prior to birth, necessitating
surgical reconstruction.
Development of the
Respiratory System
The development of the trachea, larynx, lungs, esophagus, and stomach from the fore- gut region is interrelated. Therefore, defects in the development of one of these organs often causes abnormalities to develop in other anatomic regions of the gastrointesti- nal or respiratory systems.
1
The development
of the lungs begins on day 22 of gesta- tion with the formation of the respiratory diverticulum (outpouching of the endoder-
mal foregut). The respiratory diverticulum undergoes bifurcation between days 26 to 28, dividing into the right and left bronchial buds. These buds are the progenitors of the right and left bronchi and lungs.
The proximal end of the respiratory
diverticulum forms the trachea and the lar-
ynx. The larynx opens into the pharynx via the glottis, which is formed at the original point of the outpouching of the respiratory diverticulum. The laryngotracheal opening is initially a slit. As the hyobranchial emi- nences and arytenoid swellings develop, the opening takes on a T shape. The hypo- branchial eminence gives rise to the epiglot-
tis. The lumen becomes obliterated as the lumen of the larynx fills with mesenchyme during weeks 5 to 7. At week 9, recanali- zation of the lumen occurs to reestablish communication through the larynx to the trachea below, and forms an oval lumen. The trachea develops during the second month of gestation, extending from the lar-
ynx to the primary bronchi. The cricoid ring is the only complete ring that forms. The remaining tracheal rings are incomplete and described as C-shaped, with the gap in
cartilage located posteriorly. The trachea is composed of cartilage anteriorly and a soft muscular tracheal membrane posteriorly.
During weeks 5 to 28, the primary
bronchial buds undergo repeated rounds of branching to form the respiratory tree of the lungs. The first round of bronchial bud branching produces the three second- ary bronchial buds on the right side of the embryo and two secondary bronchial buds on the left side. These secondary bronchial buds give rise to the lung lobes, with three buds in the right lung (upper, middle, lower) and two buds in the left lung (upper and lower). Further branching during week 6 of gestation produces the tertiary bronchial buds, which become the bronchopulmonary segments of the mature lung. By week 16, more branching occurs and the respiratory tree produces the termi- nal bronchioles, which further divide into the respiratory bronchioles. By week 28, the respiratory bronchioles sprout a final generation of stubby branches and a dense network of primitive alveoli is formed. Development of alveoli continues during lung maturation and is critical to the infant’s ability to breathe air and survive after birth. If the infant is born prematurely, the state of lung development is a primary determinant in survival.
Congenital Anomalies of
the Respiratory System
The total surface area for gas exchange in the lung depends on the number of alve- oli. In the weeks prior to birth, specific alveolar cells begin to secrete surfactant, which facilitates inflation of the alveoli by decreasing surface tension of the fluid coating the air sacs. In the absence of sur-
factant, the alveoli collapse, which is the primary cause of respiratory distress syn- drome in premature infants. Respiratory distress syndrome threatens infant survival and may cause immediate asphyxiation of

26 PediaDysphagia: Etiologies, Diagnosis, and Management
the infant. Mechanical ventilation, which
is often necessary to support respiration
in the premature infant, may damage the
delicate alveolar lining. Injury that leads to
detachment of the layers of cells within the
alveoli leads to hyaline membrane disease.
Bronchopulmonary disease, also referred to
as chronic lung disease, is characterized by
lung inflammation and scarring, thus com-
promising the ability to adequately oxygen-
ate the blood.
Box 1–5 Hyaline membrane disease (HMD), also known as infant respiratory dis- tress syndrome, is caused by the lack of surfactant in the lungs. HMD can be exacerbated by infection or trauma to the lungs. Dead cells and protein line the alveolar sacs, limiting gas exchange across the cell membranes.
The majority of lung anomalies result
from failure of the primitive lung bud to develop. The most severe congenital condi- tion is the unilateral or bilateral absence of lung tissue (pulmonary agenesis). Con- ditions that restrict lung growth such as oligohydramnios (insufficient amniotic fluid secondary to premature rupture of membranes or fetal kidney abnormalities), abnormalities of the thoracic cage struc- ture, and diaphragmatic hernia may cause pulmonary hypoplasia (reduced number of terminal air sacs). In infants with a congeni- tal diaphragmatic hernia, development of the abdominal (viscera) may bulge into the pleural cavity, stunting the development of the lungs. Diaphragmatic hernias are surgi-
cally corrected at birth, and in some set- tings, can be corrected in utero following identification.
Foregut duplications include broncho-
genic cysts and esophageal cysts. These cysts arise from an abnormal budding in the foregut and lead to the development of
benign mediastinal masses that may cause problems secondary to infection or com- pression of other structures. Bronchogenic cysts are filled with air or fluid and may cause infection, hemorrhage, or in rare cases malignancy. Compression of the trachea or bronchi may cause symptoms including stri- dor, dyspnea, and cyanotic spells following birth. Esophageal cysts lead to abdominal symptoms. Foregut duplication cysts are generally not detected prenatally.
Laryngeal clefts are caused by fail-
ure of the posterior cricoid lamina to fuse and may extend into the trachea if there is incomplete development of the tracheo- esophageal septum, as described in the Benjamin and Inglis classification system for laryngeal clefts (Figure 1–19). Failure of the recanalization process leads to laryn- geal atresia, laryngeal stenosis, or laryngeal webs, depending on the degree to which the airway lumen forms.
Congenital tracheal anomalies include
tracheal agenesis (complete absence of the trachea), tracheal atresia (incompletely formed trachea), tracheal webs, complete tracheal rings (encompassing a single ring, multiple rings, or the entire trachea), and congenital tracheomalacia. Tracheal atresia or total agenesis of the trachea is generally fatal at birth, unless there is a coexisting tracheoesophageal fistula for ventilation.
13

In this situation, airflow is possible through the pharynx to the trachea through the fis- tula into the distal trachea and the lungs. A tracheal web presents as a thin layer of tis- sue that extends across the tracheal lumen. There is no associated deformity or abnor-
mality of the underlying cartilaginous frame- work. The degree of respiratory symptoms correlates with the size of the available tra- cheal lumen. Treatment of tracheal obstruc- tion includes rupturing the web by dilation, laser surgery, or open surgical approaches. Complete tracheal rings occur when there is congenital absence of the posterior membra- nous portion of the ring. Complete tracheal

1. Embryologic Development of Aerodigestive Structures 27
rings are O-shaped ( compared to the nor-
mal C-shaped rings) and cause life-threat-
ening narrowing of the airway.
Primary tracheomalacia is defined as
softening of the tracheal wall due to an
abnormality of the cartilaginous rings and
hypotonia of the myoelastic elements.
Congenital tracheomalacia may occur in
isolation or in combination with vascular
abnormalities such as aortic arch abnor-
malities, innominate artery tracheal com-
pression syndrome, and pulmonary artery
slings. The most common types of vascular
rings that may compress the airway and/
or the esophagus are due to developmen-
tal anomalies of the aorta and its branches.
Fetal development of the aortic arch and
branches is shown in Figure 1–20. The per-
sistence of vascular structures that normally regress, or the regression of structures that normally persist, results in congenital anom- alies that can cause tracheal obstruction and abnormal arterial or venous circulation, all of which are potentially life-threatening and require surgical intervention.
Questions Pertaining
to
Chapter
Questions pertaining to the information presented in this chapter are provided in Appendix 1–1.
Figure 1–19. Benjamin and Inglis classification of laryngeal clefts.
Source:

Reprinted with permission from Benjamin B & Inglis A. Minor
Congenital Laryngeal Clefts: Diagnosis and Classification. Annals of
Otology, Rhinology & Laryngology. 1989;98(6).

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strong a hold upon me as I had upon him. I was satisfied of the
truth of what he had told me in regard to his own “coppers.” I had
inquired for myself, and I realized that he was making ten if not
fifteen thousand dollars by his operation.
I felt compelled to take the step he suggested. I owed my bank
three thousand dollars, and while Aunt Rachel was so feeble, I had
no hope of obtaining the amount from her. I must do something to
save myself from possible exposure. The brilliant example of
Cormorin loomed up before me. If he had made a large sum in
“coppers,” there was no reason why I should not do the same. It was
necessary that I should make the effort, and I gave him the five
thousand dollars he had just returned to me, to be invested in
Bustumups.
“It will be a safe operation, Glasswood,” continued Cormorin.
“Bustumups are sure to go up.”
I did not regard this last expression as one to be taken in the
metaphorical sense.
“You have looked into this matter, Cormorin, and of course you
understand it. As things now stand, you and I must hang together.”
“That’s so; count on me for anything you want.”
“Thank you. Now won’t you have a bottle of champagne with
me?”
“I am much obliged to you, Glasswood, but I can’t stop any
longer now. I must get your stock for you before four, or it will cost
you twenty-five to-morrow.”
“You are confident that this is a safe thing for me—are you not?”
“Oh, perfectly confident!” exclaimed he. “If you don’t believe in it,
don’t do it.”
“I rely upon your statements, and go in upon the assurance of
what you say.”
“Of course you must run your own risk. I can only advise you to
do what I would do myself.”
“That’s enough.”

He left me to procure the certificates of stock in the Bustumup
Company. I was to wait in the private room I had taken until his
return. I was alone, and when I began to think what I was doing, I
was appalled at the possibility of failure. I was in debt to the bank in
the sum of eight thousand dollars. If my investment should go wrong
I could not hope to make good the loss. I should be obliged to flee
from my wife and my home, and end my days in exile, if I should be
so fortunate as to escape without detection. A cold sweat stood on
my forehead as I thought of the possibility of discovery, of being
arrested even before I supposed any one suspected me, and of
being condemned to the State Prison for ten years or more.
I rang the bell, and ordered a bottle of champagne. I drank
several glasses of it, and the fumes went to my brain. I felt better.
My thoughts began to flow in another direction under the influence
of the sparkling fluid. Bustumups would advance every day. In a
week or two they would go up to a hundred dollars a share. If they
did this, I should make twenty thousand dollars, besides having my
capital returned to me. I should be able to pay off the bank, and
have seventeen thousand dollars left. My dream of future success
was colored with the pinkiest tint of the wine I drank.
I intended to be cautious. If, after my stock had gone up to fifty,
there were any signs of a reaction, I would sell, and still make ten
thousand dollars. Cormorin was sure the stock would be twenty-five
the next day. If it was, I should clear twelve hundred and fifty
dollars. But if it only went up to thirty-five in a week, it would enable
me to pay off what I owed the bank, and I should be content even
with that.
My new friend brought me the coveted shares, and helped me
finish the bottle of champagne before me. For some reason or other
he declined to punish a second one with me, and we separated. I
went home with my shares in my pocket. When the fumes of the
champagne passed off, I was uneasy again. I felt that I stood upon
the brink of a precipice. If Bustumups went down instead of going
up, I was ruined. There was no possible way for me to redeem
myself.

Though my uncle knew I was dealing in stocks—or rather took
my word for it—and was plunging into a sea of speculation, he did
not warn me against it. He had not a word of caution to utter, and
probably had no suspicion that I might be tempted to meddle with
the funds of the bank. If he had been as solicitous as he pretended
to be for my welfare, he would have warned me of the perils of my
course. For my own part, my uncle was a mystery to me.
Lilian with the black silk in prospect, was as happy as a queen. In
the evening Tom Flynn called. He was hardly seated before Mrs.
Oliphant and Bertha made us a call. “Dear ma” appeared to be cured
of her evil propensity, probably because another daughter, through
my indirect agency, was in a fair way of being disposed of. We had
sacred music, and a lively time generally. I was quite satisfied that
Tom would, at no distant day, make my wife’s sister his bride. This
prospect was quite enough to appease Mrs. Oliphant, and she really
looked quite amiable under the indications of this happy event.
Tom escorted Bertha and her mother home at ten o’clock, and
the next day the noble fellow told me with a blush, that he did not
leave the house on Tremont Street till the clock struck twelve. A
question or two from me brought out the fact that they were
engaged. I envied Tom—he was so happy. Why should he not be?
He owed the bank nothing. He had not soiled his soul by taking what
did not belong to him. He was a strictly moral and religious young
man. He would have gone without his dinner rather than stay away
from the evening prayer-meeting. I say I envied him. I did; and I
would have given all the world, had it been mine to give, for his
peace of mind.
I could not sleep that night when I went to bed. I got up and
drank nearly half a bottle of Smith’s old sherry, which stupefied my
brain, and gave me the needed rest from the goadings of conscience
and the terrors of the future. My fate depended upon the success of
the Bustumup Company. If that went down, I might be called at any
time to flee from my wife, and wander in fear and trembling as an
exile in some strange land. If I was in peril of exposure I could not
remain to face the blast of popular condemnation. My pride would

not permit me to live where any man could look down upon me with
either pity or contempt.
At twelve o’clock, when I run out for a lunch, I found that
Bustumups were quoted at twenty-five. This fact assured me, for
already I had practically paid off more than one-third of my debt.
The stock went a little higher before two o’clock, and my courage
was correspondingly increased. I was rather disturbed, however, at
the close of the bank, to see my uncle in close conversation with Mr.
Bristlebach. I fancied that I was the subject of their remarks,
especially as the president cast frequent glances at me. Captain
Halliard looked ugly.
I had shown him a portion of the certificates which Cormorin had
lent me. He was a shrewd business man, and though he had not
objected to the statement that I had saved half my salary, and
invested it in stocks, he might well have doubted the truth of it.
Perhaps he had been thinking over my affairs, and had come to the
conclusion that my assertions were doubtful. On two occasions he
had driven me up to the payment of money, and both times I had
met the demand.
Cormorin told me that he always ascertained when the directors
intended to make an examination. Captain Halliard meant mischief.
He intended, at least, to put me in condition to let Aunt Rachel
alone. I am confident he did not really believe that I had borrowed
any thing of the bank; but probably he wanted to satisfy himself that
I did not obtain my ready money from the drawer. As the
conversation continued I became alarmed. The President almost
invariably left the bank soon after two o’clock. To-day he remained.
As he had done once before since I occupied my position, he might
examine the condition of the cash department.
I meant to be on the sure side. I ran into the bank where
Cormorin was, and told him what I suspected. He promptly offered
to help me out, on the same terms that I had performed a similar
service for him.
“I want eight thousand,” I whispered. “I will return it to-morrow
morning.”

“Eight thousand!” exclaimed he. “Why, you are only five thousand
short.”
“Eight,” I replied, firmly.
“How’s that?”
“I was three thousand short when I made the little arrangement.”
“Thunder!” ejaculated he, impatiently. “Then you are the eagle
and I am the lamb.”
“We are both honest fellows, and mean to pay all we owe,” I
replied. “Do you suppose I would have accommodated you, the
other day, if I had not been in hot water myself? Of course if I go
down, you go with me.”
“But the security?” he asked.
“Two hundred and fifty shares of Bustumups.”
“They are worth only six thousand or so.”
“But will be worth more than eight in a few days; you shall have
your bills back to-morrow morning, without fail.”
I gave him my certificates and he handed me the money; but he
gnashed his teeth as he did so. If I fell, I should drag him down with
me.
“Is everything right in your drawer?” asked Heavyside, the
cashier, slyly, of me, when I returned.
“Certainly it is,” I replied. “Why do you ask?”
“Bristlebach is going to look over our accounts and cash this
afternoon.”
“All right,” I answered, carelessly.
I deposited the eight thousand in my drawer, balanced my cash,
and put the trunk into the safe. Paying no attention to any one, and
especially not to my uncle, I sauntered leisurely out of the bank.

B
CHAPTER XVIII.
BUSTUMUPS AT FIFTY.
Y the ruse in which Cormorin had instructed me, and for which he
had furnished the funds, I had provided against any exposure.
By this time I was fully satisfied that my uncle was working
against me; not that he intended to ruin me, but only to
maintain his own power and influence over me. There are men of this
stamp in the world, who will punish their best friends when they
refuse to be guided by them. Captain Halliard was as jealous of his
influence as he was of his money.
As my account with the bank was now square, I had no fear of the
investigation which was in progress. Mr. Heavyside, who had never
been suspected of even an irregularity, had been so kind as to inform
me of the proposed examination. I had in him a good friend, and a
mortgage on his future fidelity to me. I should defeat my uncle this
time, as I had before, but it was annoying to be subjected to his
espionage, though I could not afford to have a serious quarrel with
him.
I went home at about the usual hour. My Bustumups had done so
well that I was tolerably light-hearted. Lilian was as joyous as a
dream in June. Bertha had been with her all the forenoon, and I
heard much in praise of Tom Flynn. We dined, and then I proposed to
Lilian that we should ride out into the country. She was glad to go,
and we went. On my return home at six o’clock, Biddy handed me a
note from Mr. Bristlebach. I recognized his heavy hand-writing, and

my blood ceased to flow in its channels. I tore open the envelope. It
was simply a request to appear at the bank immediately.
What could it mean? My cash was all right. They could not have
discovered the truth. That was simply impossible. If there was any
trouble at the present time, Cormorin, and not myself, would be the
sufferer. If there had been a discovery of the whole truth, Mr.
Bristlebach was not the man to have sent a note to me; he would
have sent a constable. I decided to go at once to the bank, for I was
satisfied, from the manner in which the message had come, and by
the assurance that my cash was all right, that nothing very serious
could be charged upon me. I told Lilian I was going down town for an
hour, and she did not bother me with any troublesome questions.
On my arrival at the bank I found the president and my uncle in
the directors’ room. Both of them looked severe, but Captain Halliard
did not seem to be so much at his ease as usual. I knew him well
enough to be able to read his thoughts, and whatever mischief was
brewing he was at the bottom of it.
“Mr. Glasswood, of course you are aware that There is a deficiency
in your account?” said Mr. Bristlebach.
“No, sir, I am not aware of it,” I replied; and as I spoke the literal
truth, I answered with confidence.
“You are not?”
“No, sir.”
“Did you balance your cash to-day?”
“I did, sir; and at half-past two it was all right.”
“You put a bold face on the matter.”
“Certainly I do, sir. I am innocent of the charge, and I can afford
to speak the truth.”
“Nevertheless, your cash is short.”
“It was not short at half-past two to-day,” I replied, glancing at my
uncle.
He was uneasy, and did not confront me when I gazed at him.
“It is not a large deficiency,” added Mr. Bristlebach, “but large
enough to demand inquiry.”

“May I ask how much you found it short,” I inquired.
“Only three hundred dollars.”
“There may be some mistake—I hope there is,” suggested my
uncle.
“Who counted the cash?” I asked.
“We counted it together,” replied the president. “I wish to add that
I do not regard you as a defaulter or any thing of that sort. I sent for
you to enable you to explain the matter.”
“I have no further explanation to make. I left my cash all right to-
day,” I added, confidently.
“He is so sure, that I rather think some mistake has been made,”
added Captain Halliard.
“Probably there has been. Mr. Glasswood, I have had the utmost
confidence in you. When I suspected you before, a second
examination convinced me of your integrity. I have no doubt it will be
so this time.”
“I cannot undertake to keep my cash right, if other persons are
allowed to go to my drawer,” I continued, rather savagely.
“What!” exclaimed my uncle, springing to his feet.
“I said what I meant to say,” I replied.
The remark hit just where I intended it should. Mr. Bristlebach and
my uncle had been counting my cash. I had left it all right. If the
deficiency was insignificant, it was still enough to ruin me. I had
already made up my mind how my cash happened to be short. If the
president had made the examination himself there would have been
no deficiency. Of course I mean to say that Captain Halliard himself
had been the author of the mischief. In other words, he had either
taken three hundred dollars from my cash, or had falsely reported his
count.
Before I ventured to make this violent statement, I put my uncle
fairly on trial, and called up all the circumstances of our present
relations to testify against him. He was determined to maintain his
influence over me, and to prevent me from saying any thing to Aunt
Rachel about him. I had refused to give up my house at his bidding,

and prevented him from obliging his friend, Mr. Brentbone. I had
roundly reproached him for his conduct to me, and used language
which he could not tolerate in any one. I was satisfied that he had a
strong motive for desiring to obtain a hold upon me.
A strong motive, however, is not sufficient to explain so dastardly
an act as that in which I had dared to implicate my uncle. A man of
integrity, simply an honest man, would not be guilty of so vile a deed.
Was my uncle capable of such an act? He had procured my situation
for me by bringing up a charge against Tom Flynn which both he and
I knew was false—one which he himself had disproved as soon as his
purpose was accomplished. If he would do one mean thing, he would
not halt at another.
He had compelled me to pay the thousand dollars I owed Aunt
Rachel, out of sheer malice, and only to put me in a position where
he could control me. The mild speech of the president of the bank
assured me that I was not to be harshly dealt with; and my uncle
gently suggested that there might be a mistake.
“Be careful what you say, Mr. Glasswood,” said the president.
“Now I’m going out to get a cup of tea; when I come back we will
ascertain whether there is a mistake or not.”
Mr. Bristlebach left the room. My uncle looked embarrassed, thrust
his fingers into his vest pockets, and seemed to be feeling for
something. I was tempted to spring upon him, and throw out the
contents of those pockets, for I was satisfied that the deficiency in my
cash could be accounted for only in that way.
“Paley, you have been speculating in coppers,” said he.
“I have; but that is my business,” I replied, roughly.
“I propose to pay the bank the amount your cash is short, and to
hush the matter up where it is.”
“I don’t ask you to do any thing of the sort.”
“I am on your bond, and I must do it. No matter about that. I
expected, after you told me what you were doing in coppers, to find a
deficit of thousands. I was prepared to pay even that, for you are of
my own flesh and blood.”

“You are very affectionate!”
“I have succeeded in quieting Mr. Bristlebach.”
“I see you have.”
“You talk to me as though I had done you an injury instead of a
kindness,” added he, reproachfully.
“That is what you have done.”
“Your cash is three hundred short,” said he, putting his hands into
his vest pockets again.
Perhaps I was insane under the pressure of his implied charge; at
any rate, under the impulse of the moment, without consciously
determining to do it, I sprung upon him like a tiger; and having no
warning of my purpose myself, I gave him none. I thrust my hands
into his vest pockets, and drew from them whatever they contained. I
retreated into the farther corner of the room to examine my capture.
The deed was done so quick that Captain Halliard had no time to
resist, though he seized me by the shoulders. I was furious, and
shook him off like a child.
“What do you mean, you villain?” gasped he.
I paid no attention to him, but proceeded to examine my prize.
Among other things I found three bills, of one hundred dollars each.
“Do you mean to rob me, Paley?” demanded he; but, like Hamlet’s
ghost, he appeared to be “more in sorrow than in anger;” and more
in fear than in sorrow.
“Do you carry your money in your vest pockets, sir?” I demanded.
“Sometimes I do.”
“You took these bills from my trunk when you counted my cash.”
“Nonsense, Paley!”
“I can swear to one of them, at least,” I replied, holding up one of
the bills, on the face of which some clown had written a sentence
about depreciated currency, that had attracted my attention. “I left
this bill in my trunk in the vault at half-past two to-day; at half-past
six I find it in your pocket.”
“Do you think—”

“I know!” I interrupted, him, in the most savage manner. “If I can
find a policeman, I will put you on the track to the State Prison.”
“Don’t be absurd, Paley,” interposed my uncle; but I saw that
there was no heart in the remark. “There must have been a mistake
in the counting.”
“You stole this money from my trunk to get me into trouble.”
“Didn’t I tell the president that I would pay the deficit?” asked my
uncle. “Hush up! There comes Mr. Bristlebach! Not a word of this to
him.”
“You confess, then, that you took this money from my trunk?”
“By-and-by we will talk about it,” he replied, with much agitation.
I had proved my case. My uncle was a villain. He had taken three
hundred dollars from my cash—not enough to make me look like a
defaulter—for the purpose of maintaining his influence over me, and
to keep me from telling bad stories about him to Aunt Rachel. Guilty
as I was, I made myself believe that I was an innocent man, because
I was not guilty in the direction he accused me. Mr. Bristlebach
returned to the room.
“I am satisfied, from what Mr. Glasswood says, that there must
have been a mistake in our count,” said my uncle. “As I told you, I
was confident my nephew was honest, but I was fearful, when I
learned that he had been speculating in coppers. I thought, as I was
on his bond, we had better look into the matter. I am perfectly
satisfied now.”
This very consistent statement was assented to by the president,
but my cash was counted again, at the request of Captain Halliard. I
was in doubt whether to restore the three hundred I had wrested
from the conspirator, but I concluded that I could not afford to expose
him. We counted the cash, which was mostly in large bills, and of
course I was fully vindicated. The president was profuse in his
apologies, and my uncle was kind enough to take the burden of the
blunder on himself. He could even see where he had made the
mistake. I left the bank with him, and we walked up the street
together.
“That was an awkward mistake of mine,” said he.

“Very,” I replied, with a sneer.
“But I think I can explain it.”
“I don’t think you can.”
“You seem to have taken it into your head that I mean to injure
you.”
“I have.”
“You are mistaken. I am on your bond. Money is so plenty with
you, that I was afraid I might be called upon to pay the bond.
Bristlebach is so intimate with me that I could satisfy myself without
doing you any harm. That was all I intended.”
“And that’s the reason why you took three hundred dollars out of
my trunk, I suppose?”
“Mr. Bristlebach handed me that money himself. I wanted to pay
out that amount to-night, and I drew a check for it. I entirely forgot it
when we counted the cash, and that was the deficit. Here is the
check; as you put the money back, I took the check from your
drawer. That’s the whole story.”
“Why didn’t you explain it to Mr. Bristlebach, then?” I asked,
believing not a word he said.
“Because it was so stupid of me to forget that the check had been
paid out of your cash.”
“Very stupid, indeed!”
“I will tell him about it to-morrow,” added my uncle.
As I have said before, a man in my situation could not afford to
quarrel with one so powerful as Captain Halliard. I kept my own
counsel, not wholly certain that he would not yet be called upon to
pay the amount of his bond on my account. We parted in peace, and
I was abundantly pleased that I had been able to fight off the charge.
The next morning, when I went to the bank, I took the eight
thousand from the cash, which Cormorin had lent me, and returned it
to him. He was a happy man then. I doubt whether he slept a wink
the night before, for the idea of being responsible for my deficit, as
well as his own, could not have been very comforting to him.

I was all right at the bank, and my uncle treated me with
“distinguished consideration.” On several occasions he assured me he
should use his influence in my favor with Aunt Rachel. If I wished for
the money he had compelled me to pay—solely for my own good—he
would let me have it again. Indeed, if I was short at any time, he
would lend me a thousand dollars. I thought I might have occasion to
avail myself of his offer, and I was pleasant and pliable. I said nothing
more about the three hundred dollars.
For a week all was well with me. Ballyhacks went up to seventy-
five; but Bustumups were slower, and had only touched forty in the
same time. This figure satisfied me, inasmuch as it enabled me to pay
my debt at the bank. Yet I believed, with the utmost confidence, that
there was five or ten thousand more in the stock for me, and as long
as things were easy at the bank, I did not think of realizing.
Then I was sick for ten days, and was obliged to stay in the
house, but even while my brain was on fire with fever I went down
town one day. I dared not leave my deficit to be discovered by my
substitute. I compelled poor Cormorin to lend me the eight thousand
again, on the security of my Bustumups. They were worth nearly this
sum in the market by this time, and he did not object very
strenuously.
As soon as I was able to get out, I hastened back to the bank,
and took my place at the counter. Cormorin had sold his stock at
eighty. Bustumups were quoted at fifty, with a prospect of a further
advance. My friend had made thirteen thousand dollars. When I had
made him whole, he instantly resigned his place, fearful, I think, of
getting into trouble through my agency. He went to New York, to go
into business there. I did not care. My stocks at fifty paid my debt,
and left me forty-five hundred surplus. I was excited over the
prospect. I should be a rich man in a few weeks.
But everything did not turn out just as I anticipated.

I
CHAPTER XIX.
A CRASH IN COPPERS.
WAS worth forty-five hundred dollars while Bustumups were
quoted at fifty. Every day, while they hung at about this figure,
I debated with myself the policy of selling, paying my debt, and
investing my surplus in some other concern. Perhaps I should
have done so, if I had known of a company in which I could place
entire confidence. I missed Cormorin very much, for I needed his
advice; and I had come to regard him as an oracle in the matter of
coppers.
It looked like madness to sacrifice a stock which might go up to
eighty or a hundred, as the Ballyhack had, and though my debt
worried me, I could not make up my mind to let it go. If I could put
ten thousand dollars in my pocket, my fortune would be made, for
with this sum I could operate on a large scale. There was no danger
of another examination of my cash at present, and I was secure. But
Bustumups did not advance as rapidly as I wished. They hung at
about fifty. I was told that parties were investigating the condition of
the mine, and that as soon as they reported, the stock would go up
as rapidly as Ballyhack had done. I was willing to wait patiently for a
week or two, while the stock about held its own. Its trifling
fluctuations up and down troubled me, but the parties who worked it
convinced me that these were only accidental changes.

Though I saw my uncle every day, he did not allude to his own
villainy, and I was prudent enough to wait until I was out of the
woods before I did so. In the course of a couple of weeks, when I
had made my ten thousand dollars, I intended to resign my position,
and then I could afford to express my mind very freely to Captain
Halliard. With ten thousand dollars in my exchequer, I could go into
any business that suited me, and make money enough to support
me in a style becoming my abilities.
I still had strong hopes that the fortune of Aunt Rachel would be
mine. She was now apparently rapidly regaining her health, and I
determined to improve my chances as soon as I could. On the
following Saturday afternoon I took Lilian down to Springhaven with
me, and we both used our best efforts to win her regard. I took her
out to ride, I read to her, and the old lady seemed as fond of me as
when I was a boy. I was her only nephew, and it had been often
reported that I was to be her heir, though on what authority I did
not know. I invited her to spend a week or a month at my house in
Boston, and she promised to do so as soon as she was able.
A rumor that the parties who were investigating the condition of
the mine intended to make a favorable report sent Bustumups to
fifty-five, and I was very happy. I was worth nearly six thousand
dollars. At the end of another week the stock went up to sixty, and
the balance of worldly wealth in my favor was seven thousand
dollars. The game was becoming intensely exciting. Another week or
so would realize all my hopes. I should be free and safe.
While every thing was in this cheerful condition Aunt Rachel sent
for me, and I hastened to Springhaven, for I could not afford to
neglect her summons. She was ready to go home with me, and she
accompanied me to my house in Needham street. The old lady was
a little surprised to find that I lived in elegant style, as she was
pleased to express it; but then she regarded the salary I received,
which was double what her minister had, as princely in itself. Simple
as were her views of social economy, she did not accuse me of
extravagance. Lilian understood the matter perfectly, and was all
tenderness and devotion.

One morning, after she had been at our house three days, Aunt
Rachel asked me if I knew a certain Squire Townsend, a lawyer,
whom the old lady had been acquainted with in the early years of
her life. I had heard of him. He was an attorney of the old school,
and I hoped she intended to make her will while she was thus kindly
disposed towards me. She begged me to see the old gentleman, and
ask him to call upon her during the forenoon.
“Do you see much of Captain Halliard, Paley?” asked my aunt, as
I was going out.
“I see him nearly every day.”
“I wonder he has not been up to see me yet,” added the old lady.
I did not wonder. I had not taken the trouble to tell him that Aunt
Rachel was at my house.
“Do you wish to see him?” I asked.
“Not particularly. He has done considerable business for me.”
“I know it. He did some for you while you were sick.”
“Did he?”
“He made me pay the thousand dollars I borrowed of you.”
“What, Captain Halliard!” exclaimed the old lady.
“He did.”
“Why, I didn’t tell him to do that.”
“I know you didn’t, but he showed me a power of attorney from
you, and I couldn’t have helped myself if I had wished to do so; but
I paid it, and it’s of no consequence now.”
“I didn’t mean you should pay that money. I shouldn’t have cried
if you had never paid it. I’ll talk with Squire Townsend about it.
Couldn’t you take care of my property for me just as well as your
uncle?”
“Well, I suppose I could,” I replied, rather indifferently.
“I never liked your uncle very well. He is too sharp for me. I’ll see
what can be done.”
“I wouldn’t say anything about meddling with Captain Halliard, at
present,” I suggested, for I was somewhat afraid of him myself.

“I’ll see about it; but I didn’t mean he should trouble you about
that money. He’d no business to do it, and I shall tell him so when I
see him.”
I did not intend she should see him at present. I went to the
office of Squire Townsend, on my way down town, and left a
message for him to call upon my aunt. I was fully persuaded in my
own mind that she intended to make a will, and that she had come
up to Boston in order to have the instrument drawn up by her old
friend. Every thing looked rosy to me, for the old lady would
certainly leave me the larger portion, if not the whole, of her worldly
wealth.
When I went home in the afternoon I learned that Squire
Townsend had spent a couple of hours with Aunt Rachel, but Lilian
had not heard a word that passed between them. Then the squire
had called a carriage, and they had gone off together. I was not very
anxious to know where they had gone, though I concluded that it
was only to the office of her old friend for the purpose of having the
will properly signed and witnessed. Now, as always before, Aunt
Rachel kept her own counsel. She never told how much she was
worth, or what she intended to do with her property. She was true
to her antecedents, and during the remainder of her stay she never
mentioned the nature of her business with Squire Townsend, as she
invariably called him. She said a good deal about the worthy lawyer’s
history, and told stories about him at school. She was glad to meet
him once more before she left the world, but she did not hint that
she had special business with him.
The old lady staid her week out, and then said she must go
home. She did not think the city agreed with her. She did not sleep
as well nights as at Springhaven. Both Lilian and I pressed her to
remain longer, and promised to do every thing we could to make her
happy, but she was resolute, and I attended her home, a week to a
day from the time she arrived.
I never saw her again.
During the week that Aunt Rachel was with me, Bustumups
began to look a little shaky. From sixty the stock went down to fifty-

five in one day, but it immediately rallied, and those who managed it
assured me it was only because money was a little tight, and a
considerable portion of the stock had been forced upon the market.
I proposed to sell, as I had promised myself that I would on the first
appearance of a decline.
“Don’t do it,” said the operator. “Wait three days, and you can
take sixty, if not sixty-five, for your stock. If you crowd it upon the
market at once, you will drive it down, and cheat yourself out of
twelve hundred dollars.”
But it looks shaky,” I pleaded.
“The best stocks on the street go up and down by turns. Wait till
day after to-morrow, at least.”
I did wait, because I did not like to have twenty-five hundred
dollars taken out of my pocket at one swoop. Two days after, I was
in a fever of anxiety about my Bustumups. They had gone up and
down under the influence of various rumors, good and bad, and no
one could foresee the end. At noon Tom Flynn went out for his
lunch.
“The coppers are in a bad way,” said he, taking his place at the
counter on his return.
“What is the matter with them?” I inquired, with my heart in my
throat, for my very reputation rested upon the prosperity of the
coppers.
“Ballyhacks have dropped down from eighty to fifty,” added Tom.
“What?” I exclaimed.
“That’s what they say. Did you own any?”
“No, no; no Ballyhacks,” I replied, struggling to conceal my
emotion.
I had not told Tom I was speculating in coppers, and I think he
knew nothing about it, though he might have heard something of
the kind.
“Did you own any coppers?” he inquired, with a tone and look
that indicated the sympathy he felt for me.

“None of any consequence,” I replied.
I dared not talk with him about the matter lest I should expose
my emotion. With the stunning intelligence he had communicated to
me on my mind, it was simply impossible for me to discharge my
duties in the bank. I could hardly tell a hundred-dollar bill from a
thousand. I told the cashier that I was sick, and was fearful that I
should faint again if I did not get out in the air. He took my place,
and I staggered out into the street. There were people on the
sidewalk, but I could not see them. Every thing seemed to be
without form or shape. I was in a fearful agony of mind, and
dreaded lest I should drop senseless upon the pavement.
I went into a saloon and drank a glass of brandy. I sat down at
one of the little tables to gather up my shattered senses. Ruin stared
me in the face. If Ballyhacks had fallen from eighty to fifty, what
hope could there be for Bustumups? After all, the mischief might be
confined to this particular stock, and mine might be still on the top
of the wave. The brandy I had drank seemed to have no effect upon
me. I took another glass, and my courage began to rise a little. The
saloon was nearly filled with people, and there was a confused
jabber of tongues all around me. Men spoke to me, and called me by
name. I replied mechanically, but I could not have told a minute
later who had spoken to me.
“But they are a fraud,” said a gentleman, seating himself at the
table next to mine.
“Certainly they are,” replied the other. “The Ballyhack mine has
produced some copper; but they say there is not a particle of metal
on the Bustumup track—not an ounce! The managers of this affair
ought to be indicted and sent to the State Prison.”
“Merciful Heavens!” I ejaculated to myself, “I am ruined!”
“Ballyhack has gone down to forty within half an hour,” added
one of the gentlemen.
“I heard a man offer Bustumups just now for twenty, and people
laughed at him,” added the other. “I don’t believe they will bring
ten.”

“Probably not. There is not a dollar of value in them. The thing is
an unmitigated swindle.”
The whole of the savage truth was poured into my ears. A
moment later, I heard some one say that the managers of the
Bustumup Company had found it convenient to disappear. I was
almost a maniac. I cursed my folly because I had not sold my stock
when it began to look shaky. The villains who had comforted me and
made promises that I should sell at sixty were simply designing
knaves, who had fraudulently worked this stock up to sixty, while
there was not a penny of real value in it.
The first shock bore heavily upon me, but I soon recovered in
some measure from its effect. I went into the street, and inquired
for myself, in regard to the coppers. There were two or three
substantial companies which were actually producing metal and
paying handsome dividends. The other companies were swindles;
and Bustumup was the most egregious humbug of the whole. I tried
to get an offer for my stock, and found it would not bring a dollar a
share. Indeed, it could not be sold at any price. In a word, the five
thousand dollars I had borrowed from the bank was a total loss.
I will not attempt to describe the misery into which I was so
suddenly plunged. If I had sold my stock a week before, I might
have paid my debt and had five thousand dollars left. Now I was a
defaulter in the sum of eight thousand dollars. It was horrible to
think of. There was no possible way, that I could see, to escape the
consequences. What should I do?
I went back to the bank and told Mr. Heavyside that I was better.
I resumed my place at the counter, and did my work till the bank
closed, sustained by the brandy I had drank. I tried to devise some
plan by which I could conceal my deficit for a time. I could think of
nothing satisfactory. An examination of the affairs of the bank was
sure to betray me. I was tempted to commit suicide, as others have
done under the same pressure of guilt.
I thought of my wife, and my eyes filled with tears, as I pictured
the fall to which she would be subjected. It was ruin to her as well
as to me. What would she do, while I was thinking of her in my

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