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 Clinical Esophagology

Belafsky
Clinical Esophagology and Transnasal Esophagoscopy is a comprehensive book covering
the diagnosis and management of esophageal disorders for dysphagia clinicians. Nearly two thirds of
people with solid food dysphagia will have an esophageal contribution to their swallowing complaint.
One third of those with cervical dysphagia will have an esophageal etiology for their symptom. It
is essential that all dysphagia clinicians have an advanced knowledge of the esophageal phase and
Transnasal Esophagoscopy
of deglutition.

Some of the most common causes of solid food dysphagia include gastroesophageal reflux disease and
reflux esophagitis, esophageal webs and rings, allergic (eosinophilic) esophagitis, and hiatal hernia.

Clinical Esophagology and Transnasal Esophagoscopy

This book addresses the educational needs of otolaryngologists and speech-language pathologists and
will serve as a valuable resource for clinicians of all educational backgrounds and training levels.
Peter C. Belafsky

Peter C. Belafsky, MD, PhD, MPH, is Professor and Vice Chairman of the
Department of Otolaryngology/Head and Neck Surgery and the Director of the
Voice and Swallowing Center at the University of California, Davis. He holds a
joint appointment in the Department of Otolaryngology at the UC Davis School of
Medicine and the Department of Medicine and Epidemiology at the UC Davis School
of Veterinary Medicine. He is the recipient of numerous awards and grants and
was the lead investigator on the world’s second laryngeal transplantation. He has
authored over 150 peer-reviewed manuscripts, holds numerous patents, has edited
and authored five books, is the cofounder of two medical device startup companies, and is the past
president of the Dysphagia Research Society. Dr. Belafsky’s primary passion is the innovative treatment
of profound swallowing disorders. He has created a medical device that can manually control the upper
esophageal sphincter, is working on an innovative dilator for upper esophageal sphincter stenosis, is
developing a comprehensive swallow propulsion system, and is evaluating the use of muscle stem cells
for dysphagia rehabilitation. He has dedicated his career to improving the lives of people with profound
swallowing impairments.

www.pluralpublishing.com
 Clinical Esophagology
and
Transnasal Esophagoscopy
 Clinical Esophagology
and
Transnasal Esophagoscopy
Peter C. Belafsky, MD, MPH, PhD
5521 Ruffin Road
San Diego, CA 92123

e-mail: information@pluralpublishing.com
website: http://www.pluralpublishing.com

Copyright © 2019 by Plural Publishing, Inc.

Typeset in 11/13 Adobe Garamond by Flanagan’s Publishing Services, Inc.

Printed in the United States of America by McNaughton & Gunn, Inc.

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
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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.

NOTICE TO THE READER

Care has been taken to confirm the accuracy of the indications, procedures, drug dosages, and diagnosis and
remediation protocols presented in this book and to ensure that they conform to the practices of the general
medical and health services communities. However, the authors, editors, and publisher are not responsible
for errors or omissions or for any consequences from application of the information in this book and make
no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of
the publication. The diagnostic and remediation protocols and the medications described do not necessar-
ily have specific approval by the Food and Drug administration for use in the disorders and/or diseases and
dosages for which they are recommended. Application of this information in a particular situation remains
the professional responsibility of the practitioner. Because standards of practice and usage change, it is the
responsibility of the practitioner to keep abreast of revised recommendations, dosages, and procedures.

Library of Congress Cataloging-in-Publication Data

Names: Belafsky, Peter C., author.

Title: Clinical esophagology and transnasal esophagoscopy / Peter C. Belafsky.
Description: San Diego, CA : Plural Publishing, [2019] | Includes
bibliographical references and index.
Identifiers: LCCN 2018028890| ISBN 9781944883911 (alk. paper) | ISBN
1944883916 (alk. paper)
Subjects: | MESH: Esophageal Diseases — diagnostic imaging | Esophageal
Diseases--therapy | Esophagoscopy — methods
Classification: LCC RC815.7 | NLM WI 255 | DDC 616.3/20754 — dc23
LC record available at https://lccn.loc.gov/2018028890
 Contents

Preface vii

1 Esophageal Anatomy and Physiology 1

2 Transnasal Esophagoscopy (TNE) 15

3 The Videofluoroscopic Esophagram 29

4 High-Resolution Esophageal Manometry 49

5 Ambulatory pH and Impedance Monitoring 67

6 Esophagitis 79

7 Upper Esophageal Sphincter Dysfunction 91

8 Esophageal Webs and Rings and Diverticula 125

9 Esophageal Motility Disorders 141

10 Esophageal Stricture 159

11 Hiatal Hernia 177

12 Barrett’s Esophagus 189

13 Esophageal Neoplasia 201

Index 217

v
 Preface
The first bite of wedding cake. A champagne
toast. A lovingly prepared family meal. Just
a sip of water. From Sunday brunch to Sat-
urday dinner, one person’s joyful occasion
is another’s nightmare.
The ability to enjoy food and drink is
our common ground, our universal experi-
ence, one that is vital and cherished by all.
When our swallowing is jeopardized, what
was once mindless and festive becomes iso-
lating and painful.
Nearly two-thirds of people with solid
food dysphagia will have an esophageal
contribution to their swallowing complaint.
One-third of those with cervical dysphagia
will have an esophageal etiology for their
symptom. It is essential that all dysphagia
clinicians have an advanced knowledge of
the esophageal phase of deglutition.
This book has grown out of my passion
and dedication to improve the health and
wellness of every individual with swallowing
difficulty. It is my hope that it will serve as a
valuable resource for clinicians of all educa-
tional backgrounds and training levels.
vii
This work was supported by the endur-
ing conviction of my patients. Swallowing
disability is physically and emotionally
devastating. People, however, are resilient
and remarkably courageous in their fight
to restore dignity to a life that has been
radically altered. The physician-patient
relationship is an extraordinary bond, and
I dedicate this work to the patients whom
I have not been able to help. I would espe-
cially like to thank my mentors, my father,
and my loving wife. Without your guid-
ance, mentorship, and support, this would
not have been possible.
To our young clinicians and scientists —
the world needs you. Innovations in the
treatment of swallowing disorders are lim-
ited. For those of us who do battle in the
clinic, on the ward, in the operating room,
and in the laboratory, let us redouble our
efforts to innovate, raise awareness, and
make a difference. Vitalize your sense of
innovation and THINK BIG. The time is
now. Our patients are depending on you.
 1
Esophageal Anatomy and Physiology

Introduction cervical esophagus. There are many names

used to refer to the UEHPZ (Table 1–1).
The esophagus is a muscular tube approxi- The term upper esophageal sphincter (UES)
mately 25 cm long. It is guarded by two is typically used to refer to the anatomic
sphincters and withstands four anatomic
compressions. The length of the esophagus
and the distance from the nasal vestibule
and oral commissure to the level of each
compression are important for the clini-
cian to appreciate, as these distances serve
as essential landmarks when visualization
in the esophagus becomes obscured from
retained food and saliva, stricture, hernia,
or neoplasm. From cranial to caudal, the
compressions (and their approximate dis-
tance from the nasal vestibule and oral
commissure) are the cricoid cartilage and
cricopharyngeus muscle (17 cm), the aor-
tic arch (23 cm), the left mainstem bron-
chus (27 cm), and the diaphragmatic pinch
(39 cm) (Figures 1–1 to 1–3).

The Upper Esophageal

High-Pressure Zone

The upper esophageal high-pressure zone Figure 1–1. External compressions of the
(UEHPZ) is a 3-cm region of elevated pres- esophagus and the distances from the
sure that unites the hypopharynx with the nasal vestibule.

1
A B

C D

Figure 1–2. A. Endoscopic view of the esophageal compression caused by the dia-
phragm (diaphragmatic pinch, white arrows). Also seen is the squamocolumnar junc-
tion (black arrowheads) and gastric rugae (red arrowheads). The top of the gastric
fold is at the level of the squamocolumnar junction and demarcates the esophago-
gastric junction. The rugae extend approximately 1.5 cm above the diaphragm and
do not meet endoscopic criteria for diagnosis of hiatal hernia (>2 cm). B. Endoscopic
view of the esophageal compression from the left main stem bronchus (white arrows).
The compression is in a left anterior location. C. Endoscopic view of the esophageal
compression from the aortic arch (white arrows). The aortic compression is in the left
anterolateral location. D. Endoscopic view of the esophageal compression at the
pharyngoesophageal inlet (white arrows). The compression is primarily caused
by the elastic recoil of the laryngeal framework and cricoid cartilage against the cervi-
cal spine.

2
 1. Esophageal Anatomy and Physiology
3

Figure 1–3. Anterior-posterior fluoroscopic view displaying the 4 external compres-

sions of the esophagus. A. Pharyngoesophageal compression at the level of the cricoid
cartilage (blue arrow ) and aortic compression (red arrow ). B. Esophageal compres-
sion from the left main stem bronchus (blue arrow ) and diaphragm (red arrow ).

Table 1–1. Names Used to Describe the Upper Esophageal High-Pressure Zone

Name Description

Upper esophageal high-pressure 3-cm region of high pressure connecting the

zone (UEHPZ) hypopharynx to the cervical esophagus

Upper esophageal sphincter (UES) Manometric high-pressure zone connecting

the hypopharynx to the cervical esophagus

Pharyngoesophageal segment The anatomic components that contribute

(PES) to the upper esophageal high-pressure zone

Cricopharyngeus muscle (CPM) Striated muscle with tonic activity at rest

that contributes to the distal one-third of the
upper esophageal high-pressure zone

high-pressure zone appreciated with pha-
ryngoesophageal manometry (Figure 1–4).
Although the UES is used interchangeably
with the UEHPZ, a sphincter is technically
an “annular muscle capable of modulating
a body opening.”1 The numerous structures
that contribute to the UES do not meet the
definition of a sphincteric muscle, and the
term UEHPZ is more appropriate. The term
pharyngoesophageal segment (PES) is also syn-
onymous with the UES and UEHPZ and is
used to refer to the anatomic components
that contribute to the high-pressure zone
(Figure 1–5). The PES is made up of the
inferior pharyngeal constrictor (IPC), the
cricopharyngeus muscle (CPM), and the
most proximal cervical esophagus (see Fig-
ure 1–5). Also contributing to the pressure
Figure 1–4. Normal high-resolution manometry pressure topography plot. UES, upper
esophageal sphincter (larger black double arrow ); UES relaxation (small black double
arrow ); LES, lower esophageal sphincter (small red double arrow); LES relaxation (large
red double arrow ); esophageal body peristalsis (yellow arrow ).

Figure 1–5. The pharyngoesoph-

ageal segment (PES). (CPM, crico-
pharyngeus muscle; IPC, inferior
pharyngeal constrictor.) Source:
Gray, H., Anatomy of the Human
Body. Philadelphia, PA: Lea &
Febiger, 1918; Bartleby.com, 2000.

4
 1. Esophageal Anatomy and Physiology
of the UEHPZ is the elastic recoil of the
laryngeal framework against the cervical
spine. The elastic recoil of the thyroid and
cricoid cartilages against the anterior spine
makes up the majority of UEHPZ pres-
sure. The CPM only makes up the distal
one-third of the high-pressure zone and is
not synonymous with the UEHPZ, UES,
or PES.
The two functions of the UEHPZ are
to protect the proximal airway from regur-
gitated gastric and esophageal contents
and to prevent the swallowing of air (aero-
phagia) during respiration and phonation.
The UEHPZ maintains a consistent base-
line pressure at rest. Baseline UEHPZ rest-
ing pressure is variable and approximates
60–120 mm Hg. The valve reflexively
opens during deglutition, eructation (burp-
ing), and emesis. Esophageal distention and
acid exposure, emotional stress, and pha-
ryngeal stimulation all reflexively tighten
the UEHPZ.2 The CPM is the only aspect
of the UEHPZ that contracts and relaxes
during all reflex tasks. Thus, the CPM is
the only true sphincteric muscle.
Effective UEHPZ opening is essential
for safe and efficient bolus transit from
the pharynx into the esophagus. Open-
ing depends on elevation of the larynx
off of the cervical spine, intrinsic CPM
relaxation, and distention of the laryngeal
framework off of the spine afforded by the
pressure exerted on the advancing bolus
by the tongue and pharynx. Jacob et al
described five phases of UEHPZ opening
(Table 1–2).3
Phase I of UEHPZ opening involves
muscular relaxation of the tonically active
CPM (Figure 1–6). As the CPM relaxes, the
hyoid and larynx elevate off of the cervical
spine toward the mandible (Phase II, Figure
1–7). This brings the larynx forward under-
neath the base of the tongue and helps direct
the bolus posteriorly toward the hypo-
5
Table 1–2. Stages of Upper Esophageal
Sphincter High-Pressure Zone Opening
and Closing
Stage
I Muscular relaxation of the
CPM
II Elevation of the larynx off the
anterior cervical spine
III UEHPZ distention through
pressure exerted on the bolus
by the tongue and pharynx
IV Passive closure through
elastic recoil of the laryngeal
framework
V Active PES closure through
CPM contraction
Abbreviations: CPM, cricopharyngeus muscle;
PES, pharyngoesophageal segment; UEHPZ,
upper esophageal high-pressure zone.
pharynx. The laryngeal framework does
not actually distract off the spine to open
the UEHPZ in Phase II, but the region is
primed to accept the bolus in preparation
for definitive opening in Phase III. The
priming provided by hyolaryngeal eleva-
tion appears to be more important than
muscular inhibition of the CPM.4 This has
significant clinical implications, as degluti-
tion in individuals with good hyolaryngeal
elevation but poor CPM relaxation is pos-
sible and frequently encountered (CPM
bar, Figure 1–8). Safe and effective swal-
lowing in individuals who can intrinsically
relax their CPM but cannot elevate their
larynx has not been observed as the advanc-
ing bolus will reach a closed PES and follow
the path of least resistance into the airway.
Phase III of UEHPZ opening involves
distension of the PES through bolus size
and weight (see Figure 1–8). This phase
relies on pharyngeal and lingual peristalsis
Figure 1–6. Lateral fluoroscopic view depicting Phase I of
upper esophageal sphincter opening. The bolus (B) is in the
oral cavity. The hyoid bone (yellow arrow ) and thyroid carti-
lage (TC) remain low in the neck. The cricopharyngeus mus-
cle (red asterisk ) exhibits intrinsic relaxation.

Figure 1–7. Lateral fluoroscopic view depicting Phase II of

upper esophageal sphincter opening.The hyoid bone (green
arrowhead ) and thyroid cartilage (TC) are elevated anteriorly
away from the cervical spine toward the mandible as the
bolus (B) advances through the pharynx. The upper esopha-
geal sphincter (white arrows) is primed but remains closed.

6
 1. Esophageal Anatomy and Physiology
7

Figure 1–8. Lateral fluoroscopic view depicting Phase III of

upper esophageal sphincter opening. The hyoid bone and
thyroid cartilage remain elevated (Phase II). The intrabolus
pressure created by contraction of the tongue and pharynx
results in opening of the upper esophageal sphincter (red
asterisk ). There is incomplete relaxation of the cricopharyn-
geus muscle, which creates the fluoroscopic appearance of
a CP bar (white arrow ). The elevated pressure created by the
cricopharyngeus muscle dysfunction in this patient results
in pathologic dilation of the hypopharynx (green asterisk ).
There is penetration of barium to the level of the vocal folds
(blue arrowheads).

to propel the bolus past the expansive hypo-
pharynx, through the primed PES, behind
the elevating hyolaryngeal complex, and
into the cervical esophagus. The elasticity
of the elevating PES allows it to be opened
by the increasing pressure exerted by the
passing bolus. The elastic PES opens as lit-
tle as possible to accept the bolus. If there
is inadequate lingual and pharyngeal con-
traction, the bolus will not exert enough
pressure to open the PES, and the bolus
will again follow the path of least resistance
and threaten the airway. Phase IV of PES
opening involves passive collapse of the
elastic PES as the bolus passes and the lar-
ynx resumes its resting position against the
cervical spine (Figure 1–9). Phase V, the
final phase of UEHPZ opening, involves
PES closure through active contraction of
the CPM (Figure 1–10).
The Lower Esophageal
High-Pressure Zone
The lower esophageal high-pressure zone
(LEHPZ) is a 4-cm region of the distal
esophagus that functions as a valve with the
primary function of preventing the regurgi-
tation of gastric contents into the esopha-
gus. Although the valve must prevent gas-
troesophageal reflux (GER), it must also
Figure 1–9. Lateral fluoroscopic view depicting Phase IV of
upper esophageal sphincter opening. The elastic recoil of
the thyroid cartilage (TC) and cricoid cartilage (C) results in
closure of the upper esophageal sphincter (white arrow). The
bolus (B) has completely entered the esophagus.

Figure 1–10. Lateral fluoroscopic view depicting Phase V of

upper esophageal sphincter opening. The hyoid bone (red
arrowhead ) and thyroid cartilage (TC) remain in their resting
positions, and there is definitive UES closure through active
contraction of the cricopharyngeus muscle (green asterisk ).

8
 1. Esophageal Anatomy and Physiology
9

allow for the anterograde passage of food
and the retrograde venting of gas and food as
is required with belching and vomiting. The
lower high-pressure zone has a basal tone of
approximately 25 mm Hg and is composed
of the intrinsic lower esophageal sphincter
smooth muscle (LESM), the gastric sling
fibers and the angle of His, and the external
pressure exerted by the striated muscle of the
crural diaphragm (Figure 1–11).
The LESM is a 4-cm region of thickened
inner circular muscle layer. The LESM con-
tributes approximately 22 mm Hg (90%)
of the basal 25 mm Hg LEHPZ pressure.5
The histologic characteristics of the LESM
are no different than the outer longitudinal
and inner circular muscles of the remaining
esophagus. The intrinsic innervation of the
LESM contributes to the muscle’s thickness
and tone. When this tone is lost, the LESM
is difficult to differentiate from the rest of
the esophagus.6
The angle of His is essential to the pro-
tective mechanism of the LEHPZ. The
angle creates a barrier to prevent the regur-
gitation of gastric contents out of the gastric
fundus reservoir. With the development of
a hiatal hernia, this barrier is lost, and wors-
ening gastroesophageal reflux may ensue.
The crural diaphragm encloses the distal
2 cm of the LEHPZ. Although it provides
less than 10% of basal LEHPZ pressure,
the diaphragmatic contribution is essential
in preventing regurgitation during periods
of increased intragastric pressure as occurs
with inspiration and straining. The distal
esophagus is tethered to the diaphragm via
the phrenoesophageal ligaments (see Fig-
ure 1–11). When the ligaments become
lax, the gastric cardia herniates above the
diaphragm (hiatal hernia), the crural com-
ponent to the LEHPZ is lost, and the valve’s
ability to protect against “stress” reflux is
significantly altered.7

Figure 1–11. The lower esophageal high-pressure zone.

(Asterisk, gastroesophageal junction; HIS, angle of HIS; PEL,
phrenoesophageal ligament.)
 Clinical Esophagology and Transnasal Esophagoscopy
10

Esophageal Peristalsis 25-cm esophagus into the stomach. Once

Primary Esophageal Peristalsis
The esophagus is composed of inner circular
and outer longitudinal muscle layers. The
myenteric (Auerbach) plexus lies between
these layers and provides motor input to
both of these muscle groups. The proximal
esophagus is composed of skeletal muscle
that gradually transitions to smooth muscle
in the distal esophagus. This 2 to 3-cm tran-
sition zone, also referred to as the esopha-
geal dead zone, represents a manometric
low-pressure trough that may retain food
and liquid (Figure 1–12). Primary peristal-
sis initiates in the pharynx with the onset of
swallow. It is an essential mechanism that
transports food and liquid through the
the bolus traverses the UEHPZ, primary
peristalsis initiates the coordinated contrac-
tion of the esophageal inner circular muscle
to create a peristaltic wave and propel a
bolus along its length. The outer longitu-
dinal muscle of the esophagus is responsible
for esophageal shortening, and its precise
role in bolus propagation is uncertain. The
peristaltic wave travels through the esopha-
gus at an approximate velocity of 3 cm/s
with an amplitude of 35 to 70 mm Hg.
An unimpeded peristaltic wave should take
approximately 8 seconds to completely tra-
verse the esophagus. If a pharyngeal swal-
low is initiated prior to the completion of
the peristaltic wave, esophageal peristalsis is
centrally inhibited, and peristalsis is reiniti-
ated in the pharynx (deglutitive inhibition,

Figure 1–12. High-resolution manometry color topography plot displaying the low-
pressure upper esophageal transition zone (esophageal dead zone, double black
arrow). (Black asterisk, UES relaxation; double red arrow, LES relaxation.)
 1. Esophageal Anatomy and Physiology
11

Figure 1–13). The LEHPZ must relax to
accept the advancing bolus. Relaxation of
the LEHPZ occurs with the initiation of
the pharyngeal swallow and continues until
the peristaltic wave and the advancing bolus
have passed (Figure 1–14). At this time, the
LESM contracts and restores basal tone.
gitated or left behind debris. Reduced sec-
ondary peristalsis may result in prolonged
contact of retained food or regurgitated gas-
tric contents with the esophageal mucosa
and resultant tissue injury (esophagitis).
Tertiary Peristalsis

Secondary Esophageal Peristalsis Tertiary peristalsis is the result of simul-

Secondary esophageal peristalsis occurs
independently of the pharyngeal swallow. It
is reflexively initiated by luminal distention
caused by retained boluses in the esophagus
that may remain after incomplete primary
peristalsis or as a result from regurgitated
gastric contents (GER). It is an essential
mechanism to clear the esophagus of regur-
taneous nonperistaltic contractions of the
esophageal body. They are of no known
physiologic benefit. Tertiary contractions
may occur spontaneously or may be initi-
ated by swallow. They may affect the entire
esophagus or just a segment, are seen more
frequently in the aged esophagus, and are
frequently considered a sign of ineffective
esophageal body motility (Figure 1–15).

Figure 1–13. High-resolution manometry color topography plot displaying degluti-

tive inhibition. The primary peristaltic wave stops (black arrow ) with the initiation of a
second swallow (white arrow ).
Figure 1–14. High-resolution manometry color topography plot displaying relaxation
of the lower esophageal high-pressure zone (red double arrow ) with the onset of the
pharyngeal swallow (red asterisk ). (Black asterisk, contraction of the lower esophageal
sphincter muscle after the conclusion of esophageal peristalsis and passage of the
advancing bolus.)

Figure 1–15. Barium esophagram depicting

tertiary esophageal contractions (red arrows).
(Blue arrow, gastroesophageal junction at the
level of the diaphragm.)

12
 1. Esophageal Anatomy and Physiology
References
1. Merriam-Webster.com website. http://www.
merriam-webster.com. Retrieved May 8,
2011.
2. Sivarao DV, Goyal RK. Functional anat-
omy and physiology of the upper esopha-
geal sphincter. Am J Med. 2000;108(suppl
4a):27S–37S.
3. Jacob P, Kahrilas PJ, Logemann JA, Shah V,
Ha T. Upper esophageal sphincter opening
and modulation during swallowing. Gastro-
enterology. 1989;97(6):1469–1478.
4. Belafsky PC. Manual control of the upper
esophageal sphincter. Laryngoscope. 2010;​
120(suppl 1):S1–S16.
13
5. Richter JE, Wu WC, Johns DN et al. Esoph-
ageal manometry in 95 healthy adult vol-
unteers. Variability of pressures with age
and frequency of “abnormal” contractions.
Dig Dis Sci. 1987;32(6):583–592.
6. Liu J, Parashar VK, Mittal RK. Asymmetry
of the lower esophageal sphincter pressure:
is it related to the muscle thickness or shape
of the lower esophageal sphincter? Am J
Physiol. 1997;272:G1509–G1517.
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ageal junction pressure. Gut. 1999;44(4):​
476–482.
 2
Transnasal Esophagoscopy (TNE)

Introduction Indications for TNE

The ability to perform a comprehensive
evaluation of the esophagus in the office
without sedation has transformed the
care of persons with dysphagia and reflux.
Transnasal esophagoscopy (TNE) is safer,
universally preferred by patients, and as
accurate as sedated per-oral esophagos-
copy. This chapter discusses the indications,
technique, and expected findings of office-
based unsedated TNE.
The precise indications for TNE are still
being defined. The American Society for
Gastrointestinal Endoscopy (ASGE) and
the American College of Gastroenterology
have classified the indications for esopha-
goscopy into diagnostic and therapeutic
subcategories (Table 2–1).1,2 Danger symp-
toms and signs that necessitate expedited
endoscopy include dysphagia, odynopha-
gia, chronic cough, hemoptysis, suspected

Table 2–1. Relative Diagnostic and Therapeutic Indications for Esophagoscopy

Diagnostic Therapeutic

Dysphagia Placement of feeding tubes

Odynophagia
Globus
Weight loss/anorexia
Caustic ingestion
Gastroesophageal reflux
Foreign body evaluation
Evaluation of varices
Anorexia
Esophageal injection of steroids
Esophageal injection of botulinum toxin
Dilation of esophageal strictures
Endoscopic ablation of intestinal metaplasia
Endoluminal reflux procedures
Tracheoesophageal puncture and replacement
Endoscopic ultrasound
Placement of wireless pH telemetry capsule

15
 Clinical Esophagology and Transnasal Esophagoscopy
16
foreign body, anemia, and unexplained
weight loss (Table 2–2). The most frequent
indication for TNE at our institution is the
evaluation of solid food dysphagia (Figure
2–1). We utilize the 10-item Eating Assess-
ment Tool (EAT-10®) to document the ini-
tial severity of dysphagia and to monitor
treatment efficacy (Table 2–3). Esophagos-
copy is indicated for any person with an
EAT-10® greater than 2.3
Indications for TNE in persons with
gastroesophageal reflux disease (GERD) are
less well defined. Esophagoscopy is gener-
ally indicated to screen the esophagus in
persons with prolonged GERD symptoms
Table 2–2. Danger Signs and Symptoms
Necessitating Expeditious Endoscopy
Dysphagia
Odynophagia
Unexplained weight loss
Suspected foreign body
Chronic cough
Hemoptysis
Anemia of uncertain etiology
Figure 2–1. The most common indications for esophagoscopy.
(heartburn/regurgitation >5 years) to rule
out the presence of intestinal metaplasia,
dysplasia, and neoplasm. The majority of
patients with esophageal cancer are not
identified on screening endoscopy, how-
ever, but present with obstructing tumors.
The esophagus loses sensitivity when in-
testinal metaplasia progresses, and the symp-
tom of heartburn ceases to become a re-
liable predictor of esophageal neoplasia. The
most concerning history for esophageal cancer
is that of an individual who used to get heart-
burn but is now presenting with solid food
dysphagia and weight loss. TNE is also in-
dicated in patients with symptoms that
persist despite reflux medication to rule
out alternative causes of their symptom
such as infectious or allergic esophagitis
(Figure 2–2).
We employ early TNE to develop an
individualized treatment plan. Endoscopy
assesses the necessity for medical therapy.
Persons with reflux symptoms and a nor-
mal esophagoscopy can be treated conser-
vatively with a combination of nutritional
counseling, behavioral modifications, ant-
acids, alginates, H2-receptor antagonists,
and on-demand therapy with proton-pump
inhibitors as needed. Persons with signifi-
 2. Transnasal Esophagoscopy (TNE)
17

Table 2–3. The 10-Item Eating Assessment Tool (EAT10®)

To what extent are the following scenarios

problematic for you? Please circle the 0 = No 4 = Severe
appropriate response: problem problem

1. My swallowing problem has caused me to 0 1 2 3 4

lose weight.
2. My swallowing problem interferes with my 0 1 2 3 4
ability to go out for meals.
3. Swallowing liquids takes extra effort. 0 1 2 3 4
4. Swallowing solids takes extra effort. 0 1 2 3 4
5. Swallowing pills takes extra effort. 0 1 2 3 4
6. Swallowing is painful. 0 1 2 3 4
7. The pleasure of eating is affected by my 0 1 2 3 4
swallowing.
8. When I swallow food sticks in my throat. 0 1 2 3 4
9. I cough when I eat. 0 1 2 3 4
10. Swallowing is stressful. 0 1 2 3 4

pump inhibitor therapy, hiatal hernia re-

pair, and reflux surgery when indicated.
Extraesophageal (laryngopharyngeal)
reflux indications for TNE are controver-
sial. Chronic cough has been identified as
an independent risk factor for the presence
of esophageal cancer, and we routinely
screen the esophagus in persons with cough
>8 weeks.4 In patients with globus pharyn-
geus, TNE is recommended at the initial
patient visit. The entire aerodigestive tract
is evaluated from the nasal vestibule to the
pyloric sphincter. If pathology is identified,
it is treated appropriately. If the endoscopy
is normal, the patient is reassured, and the
Figure 2–2. Esophagoscopy revealing
globus is treated conservatively with an
extensive candidal esophagitis in an indi-
vidual with symptoms mistaken for GERD. appropriate combination of simple reas-
surance, hydration, humidification, weight
loss and exercise, and behavioral modifica-
cant esophageal injury such as high-grade tions for reflux disease. Over 80% of patients
erosive esophagitis, intestinal metaplasia, with globus and a negative endoscopy can be
esophageal stricture, or dysplasia are treated managed conservatively without the need for
more aggressively with prolonged proton- medication trials or further diagnostic testing.
 Clinical Esophagology and Transnasal Esophagoscopy
18

Twenty percent of persons with globus,
however, are profoundly disabled by the
symptom, and the workup proceeds with
manometry, fluoroscopy, ambulatory pH
testing, and cervical ultrasound as indi-
cated. The prevalence of intestinal metapla-
sia in persons with throat symptoms may
be as high as 18%.5 In addition, up to one-
third of persons with intestinal metaplasia
may have isolated symptoms of laryngo-
pharyngeal reflux (LPR). Nonetheless, we
do not routinely screen the esophagus for
throat symptoms such as dysphonia, throat
clearing, and postnasal drip in the absence
of cough, globus, heartburn, odynophagia,
and dysphagia.
The stomach is routinely evaluated in
all persons undergoing TNE (Figure 2–3).
Endoscopic evidence of gastric inflam-
mation is biopsied to rule out atrophic
gastritis and Helicobacter pylori infection
(Figure 2–4). Gastric polyps are prevalent
and frequently identified during TNE (Fig-
ures 2–5 and 2–6). Types of gastric polyps
include inflammatory polyps, adenomas,
and fundic gland polyps. Although the

Figure 2–3. Diagram of gastric anatomy. (D, duodenum;

PA, pyloric antrum.)

Figure 2–4. Helicobacter pylori acute Figure 2–5. Benign fundic gland polyp.
gastritis.

Figure 2–6. Dysplastic gastric polyp.
malignant potential for gastric polyps is
minimal, biopsy is indicated. The risk of
malignancy increases with increasing size
and in persons with familial polyposis syn-
dromes. Polyps >1 cm are typically removed
with an electrocautery snare. H pylori and
other forms of gastritis are the most com-
mon causes of inflammatory polyps and
adenomas, and proton pump inhibitor use
is the most common etiologic factor respon-
sible for the development of fundic gland
polyps. Although gastroscopy is performed
as part of routine TNE, the pylorus and
duodenum are not. Data are available to
suggest that esophagoscopy (with gastros-
copy) is sufficient for patients with reflux
and dysphagia. Persons with abdominal
pain, nausea, and a history of peptic ulcer
disease, however, have an increased preva-
lence of small bowel pathology and require
duodenoscopy.6
Technique of TNE
Prior to performing TNE, the patient is
screened with transnasal flexible laryn-
goscopy (TFL) and a tongue blade placed
2. Transnasal Esophagoscopy (TNE)
19
in the oropharynx to visualize the tonsils
and larynx, rule out a tight nasal vault, and
assess tolerance for a flexible unsedated
procedure. Ninety-eight percent of persons
who can tolerate a TFL can undergo a suc-
cessful TNE. Overly sensitive patients and
persons with an excessive gag reflex identi-
fied with the tongue blade may be better
evaluated with a sedated endoscopy. The
procedure is best performed on an empty
stomach, and patients are requested to
fast for 4 hours prior to TNE. An empty
stomach ensures an unhindered view of the
stomach and reduces nausea and gagging.
Recent food or drink, however, is only a
relative contraindication, and TNE can be
safely performed in persons without fasting.
The normal esophagus is well visualized in
a person after a recent meal. Normal gastric
emptying, however, may take up to 5 hours,
and a stomach full of food is often difficult
to examine. Food visualized in the stomach
after a 5-hour fast should raise the suspicion
for gastroparesis.
The procedure is performed with the
patient upright in an examination chair
(Figure 2–7). Keeping the nose comfort-
able is the key to successful TNE. The nasal
Figure 2–7. Positioning for office-based
unseated TNE.
 Clinical Esophagology and Transnasal Esophagoscopy
20
cavity is topically anesthetized and decon-
gested with a combination nasal spray (1%
tetracaine and 0.05% oxymetazoline). If the
nasal cavity is narrow, it may be dilated with
6″ cotton tipped applicators (Medline Indus-
tries, Mundelein, Illinois) bathed in 2% vis-
cous lidocaine (West-Ward Pharmaceutical
Corp, Eatontown, New Jersey). Three appli-
cators are sequentially inserted through the
nasal valve and advanced into the nasophar-
ynx. All three applicators are then removed
at once, and the endoscope is immediately
placed into the dilated nasal cavity. Three
percent of patients will not be able to toler-
ate TNE due to an excessively narrow nasal
vault. If three cotton tipped applicators can
be placed, the failure rate will be <1%.
We previously anesthetized the pharynx
with the liberal administration of benzo-
caine topical anesthetic spray (Cetylite
Inc, Pensauken, New Jersey) in all patients
undergoing TNE. Pharyngeal anesthesia
frequently causes difficulties with secretion
management and saliva aspiration, and we
have discontinued this practice. If a patient
has an excessive gag reflex, he or she is asked
to gargle and then swallow 10 mL of 2%
viscous lidocaine diluted 1:1 with tap water.
Viscous lidocaine in the esophagus obscures
visualization, clogs the suction port on the
esophagoscope, and is a nuisance. Diluting
the anesthetic achieves the anesthetic goal
and limits the hindrance of the more vis-
cous medication.
Table 2–4. Commercially Available Transnasal Esophagoscopes
Manufacturer Model
Pentax Medical EE-1580K
Olympus America PEF-V
Vision Sciences TNE 5000
*With TV-2.1 sheath.
There are three currently available trans-
nasal endoscopes (Table 2–4). The diameter
of these scopes varies slightly but is approxi-
mately 5 mm. The patient is positioned in
the sniffing position (see Figure 2–7), and
the endoscope is lubricated with 2% vis-
cous lidocaine and inserted into the most
patent nares. Viscous lidocaine is continu-
ously applied throughout the procedure to
improve the ease of passage and maximize
anesthesia. The endoscope is then advanced
either along the floor of the nose inferior
and medial to the inferior turbinate or
between the middle and inferior turbinates
in the middle nasal vault. The endoscope
is advanced past the nasopharynx and
positioned at the “home” position in the
oropharynx above the tip of the epiglot-
tis (Figure 2–8). The home position limits
patient discomfort and gagging so that the
base of the tongue, pyriform sinuses, and
larynx can be thoroughly evaluated.
After a thorough laryngoscopy and pha-
ryngoscopy have been performed, the clini-
cian’s hand is placed on the patient’s shoul-
der, and eye contact is made (Figure 2–9).
The patient is then asked if he or she is
comfortable and able to proceed. Placing
a hand on the shoulder, good communica-
tion, and eye contact will greatly improve
the tolerance and perceived comfort of the
procedure. The patient is then instructed to
put his or her chin to the chest and swallow
as the endoscope is advanced through the
Working
Diameter Channel Length
5.1 mm 2.0 mm 60 cm
5.2 mm 2.0 mm 65 cm
5.6 mm 2.1 mm 65 cm

upper esophageal sphincter (UES). Saying
“place your chin to your chest and imagine
you are swallowing a large strand of spa-
Figured 2–8. Home position for transna-
sal endoscopy.
Figure 2–9. Assistant touch and clinician eye contact will greatly improve TNE comfort
and tolerability.
2. Transnasal Esophagoscopy (TNE)
21
ghetti” provides a visible cue that relaxes the
patient and reduces anxiety. Passage of the
endoscope through the UES is performed
“blindly.” The clinician gently places the
endoscope into the pyriform sinus until
light resistance is encountered. The resis-
tance is maintained, and the endoscope is
advanced when the UES relaxes and the lar-
ynx elevates with swallow. The endoscope
is advanced 10 cm into the esophagus so
that a cough or retch does not inadver-
tently extubate the esophagoscope from the
esophagus. The proximal esophagus will be
visualized at the end of the procedure as
the endoscope is withdrawn. Withdrawal
centers the tip of the endoscope and affords
an optimal view.
If difficulty is encountered traversing
the UES, the patient is given a teaspoon of
2% viscous lidocaine mixed with 1:1 tap
water. He or she is instructed to hold the
 Clinical Esophagology and Transnasal Esophagoscopy
22
solution in the oral cavity, tuck the chin
to their chest, and swallow hard. Passage
of the esophagoscope through the UES is
assisted by the advancing lubricious bolus.
If difficulty intubating the esophagus is
still encountered, the procedure is termi-
nated, and a fluoroscopic swallow study
is obtained to evaluate for UES stricture,
cricopharyngeus muscle dysfunction, and
Zenker diverticulum.
After the esophagus has been intubated,
the suction on the endoscope is engaged,
and a 30-second pause is commenced. This
accommodation period allows the patient
to get acclimated to the endoscope in the
esophagus, reduces anxiety, and enhances
patient comfort. Before the examination
continues, a hand is again placed on the
patient’s shoulder, and eye contact is made.
The patient is then instructed, “This is as
bad as it is going to get” and is asked if he
or she is comfortable enough to proceed. If
the patient desires to continue, he or she is
informed that air will be introduced into
the esophagus and is encouraged to belch
if the urge is experienced. The endoscope
is then advanced into the distal esophagus,
Figure 2–10. Normal retroflexed view of the fundus
and gastric cardia.
and the squamocolumnar junction and gas-
troesophageal junction are visualized with
a combination of air insufflation, suction,
and irrigation. Having the patient swallow
will open up the gastroesophageal junction
(GEJ) and enhance visualization. If pathol-
ogy in the distal esophagus is noted, biopsy
is deferred until after the gastroscopy. The
endoscope is gently advanced into the
stomach. Air is insufflated to distend the
stomach, and the gastric body and pyloric
antrum are visualized. A retroflexed view of
the fundus and cardia is then achieved (Fig-
ure 2–10). Biopsies are obtained if necessary.
The air is then suctioned from the stomach,
and the endoscope is withdrawn back into
the distal esophagus. Distal esophageal biop-
sies are performed as required in a distal
to proximal direction to avoid blood from
obscuring the field of view. Four quadrant
biopsies are performed throughout every
centimeter of abnormal appearing mucosa.
The mid- and proximal esophagus is then
thoroughly examined as the endoscope is
withdrawn. Withdrawal centers the distal
tip of the endoscope and provides an opti-
mal view to evaluate the proximal esopha-
 2. Transnasal Esophagoscopy (TNE)
23

gus. Biopsies of normal appearing mid- and
proximal esophageal mucosa are routinely
performed in persons with dysphagia to
rule out eosinophilic esophagitis, which is
based on the presence of >15 eosinophils
per high-power field (HPF). The esophagus
is then suctioned free of air and water, the
endoscope is withdrawn, and the procedure
is completed.
Functional Esophagoscopy
Patients cannot be trusted to identify the
precise location of their dysphagia symp-
tom. One-third of patients who localize the
site of their swallowing difficulty to the cervi-
cal region will have an esophageal etiology to
their swallowing problem (Figure 2–11). The
success of the flexible endoscopic evalua-
tion of swallowing (FEES) in the evaluation
of oropharyngeal swallowing biomechanics
provided the framework for our use of func-
tional esophagoscopy in the evaluation of
esophageal phase dysphagia.7,8 The advent
of unsedated TNE affords the opportunity
to feed the patient during the examination
and combine the endoscopic evaluation of
the esophagus with the ability to evaluate
esophageal bolus transit in real time. We
have described the Guided Observation of
Swallowing in the Esophagus (GOOSE),
wherein a patient is administered various
foods and liquids during TNE to evaluate
sites of stasis, obstruction, and diminished
esophageal motility.9
The transnasal esophagoscope is placed
through the more patent nares and posi-
tioned in the oropharynx in the home
position just above the tip of the epiglottis.
The use of nasal anesthetic spray and pha-
ryngeal anesthesia is limited to ensure no
diminution of laryngopharyngeal sensation
and altered swallowing mechanics. FEES is
then performed with the TNE endoscope
according to an established protocol. The

Figure 2–11. Anterior-posterior fluoroscopic image display-

ing a 13-mm barium tablet stuck in the distal esophagus
(green arrow ) and the patients’ right index finger (red arrows)
localizing the site of dysphagia to the cricoid region.
 Clinical Esophagology and Transnasal Esophagoscopy
24

anatomy of the tongue base, hypophar- gus. The patient is given a 15-mL bolus of
ynx, larynx, and vocal folds are assessed. puree. Bolus transit and esophageal motility
Velopharyngeal closure and vocal fold are evaluated. With the endoscope in this
mobility are evaluated. Pharyngeal motor position, the patient is then administered
function is gauged using the pharyngeal 50 mL of water and then a bolus of cracker
squeeze maneuver. Pooling of secretions is consistency (Figure 2–13). The endoscope
noted and laryngopharyngeal sensation is
assessed with the tip of the endoscope. The
patient is first administered 10 mL of puree
(applesauce with green food coloring). If
the patient is able to safely tolerate this ini-
tial bolus, 50 and then 150 mL of puree
are administered. The patient is then given
10 mL of a thin bolus (water mixed with
green food coloring). If the patient is able
to safely tolerate this thin liquid bolus, 50
mL of water is administered. If the 50-mL
bolus is safely consumed, the patient is
asked to take sequential, unmetered swal-
Figure 2–12.  Endoscopic image of a
lows through a straw. If deemed safe, the dilated mid-esophagus during functional
patient is then given food the consistency of esophagoscopy (GOOSE) that does not re-
a dry cracker, and swallowing mechanics are quire air insufflation. Pooled water impreg-
observed. If deep penetration to the level of nated with green food coloring can be
the vocal folds, profound pooling, or aspi- visualized in the distal esophagus indicat-
ing a motility disorder or distal esophageal
ration is visualized during FEES, esopha-
pathology.
goscopy alone will be performed, without
GOOSE.
Assuming the absence of deep penetra-
tion and aspiration, the esophagoscope is
then passed through the UES into the cer-
vical esophagus. Any pooled food or liq-
uid from the recently completed FEES is
noted. The esophagus should be collapsed
at rest. An esophageal lumen that does
not require air insufflation to visualize is
abnormally dilated (Figure 2–12). Normal
esophageal transit time is approximately 13
seconds; thus, any bolus in the esophagus
that is present 13 seconds after comple- Figure 2–13. Endoscopic image dur-
tion of FEES is considered abnormal. The ing functional esophagoscopy (GOOSE)
entire length of the esophagus is evaluated, above the esophagogastric junction. The
proximal cracker bolus (C) is hindered by
and the presence of esophagitis, web, ring,
a mucosal stricture at the esophagogas-
stricture, or neoplasm is noted. The endo- tric junction (yellow arrows). Also seen is
scope is then positioned 2 cm above the erosive peptic esophagitis (green arrows)
aortic compression in the cervical esopha- above the squamocolumnar junction.

is then advanced to the distal esophagus
6 cm above the gastroesophageal junction.
Furthermore, 50-mL boluses of puree, thin
liquid, and cracker are then administered.
Distal esophageal motility and bolus pas-
sage through the lower esophageal sphincter
into the stomach are noted. The endoscope
is then passed into the stomach, and a retro-
flex view of the fundus and gastric cardia is
obtained. The patient is again administered
50 mL of puree, thin liquid, and cracker.
Bolus passage into the stomach is visualized
during retroflexion (Figure 2–14). The time
required from the initiation of the swallow
to transit into the stomach is noted. At the
conclusion of the examination, abnormal
appearing mucosa is biopsied, and random
sampling of the mid-esophagus is consid-
ered to rule out eosinophilic esophagitis.
The stomach is then suctioned free of air,
the endoscope is withdrawn, and the study
is complete.
Current diagnostics for esophageal func-
tion include videofluorography, impedance
manometry, and endoscopy. None of these
studies in isolation can provide complete
information about the esophagus. Guided
Figure 2–14. Retroflex endoscopic view
from within the stomach during functional
esophagoscopy (GOOSE) displaying
green impregnated applesauce travers-
ing the esophagogastric junction on its
way through the cardia.
2. Transnasal Esophagoscopy (TNE)
25
observation of esophageal swallowing
(GOOSE) is a safe and efficacious diagnos-
tic tool with which to evaluate the esopha-
geal phase of deglutition during TNE. The
procedure can assess bolus transit, regurgi-
tation, and swallowing safety and identify
mucosal pathology not detected by fluoros-
copy or manometry.9
Expected Findings on TNE
The most common findings on TNE in
a tertiary outpatient dysphagia center are
esophagitis, hiatal hernia, intestinal meta-
plasia, infectious esophagitis, esophageal
web, stenosis, allergic (eosinophilic) esoph-
agitis, and esophageal carcinoma (Figure
2–15). Approximately 40% of studies are
completely normal. If the clinician does not
identify an abnormality at least 50% of the
time, pathology is likely being missed. The
reader is referred to subsequent chapters for
a comprehensive discussion regarding these
pathologic entities.
Diagnostic Accuracy
Numerous studies have demonstrated that
TNE has equal diagnostic accuracy as con-
ventional sedated per-oral esophagogastro-
duodenoscopy (EGD).10–14 Randomized
crossover trials with sound scientific meth-
odology have concluded that the ability of
unsedated TNE to diagnosis esophagitis,
intestinal metaplasia, dysplasia, and carci-
noma is equivalent to sedated EGD.10,12,15
The key to improving diagnostic accuracy
of esophagoscopy is to ensure accurate
biopsy location and to obtain multiple
biopsies (>8) to reduce sampling error. The
diameter of the device and route of endo-
scope placement (oral/nasal) appear to have
little significance.
 Clinical Esophagology and Transnasal Esophagoscopy
26

3%
3%2%
6%

5%
36%

6%

16%

23%
Normal Reflux Esophagitis Hiatal Hernia
Intestinal Metaplasia Candida Stricture/Web
Eosinophilic Esophagitis Carcinoma Diverticulum

Figure 2–15. Expected findings on unsedated TNE.

Patient Tolerance and Safety The majority of patients prefer TNE.10

Ninety-five percent of unsedated TNE is
completed successfully. The 5-mm endo-
scope cannot traverse the nasal cavity com-
fortably in approximately 3% of patients,
and another 2% will have excessive gagging,
coughing, or anxiety necessitating early
termination. In general, as the nose goes so
does the TNE. If the nose is kept comfort-
able, the procedure will go smoothly. In the
small percentage of persons with excessive
gagging, a 2% viscous lidocaine gargle and
swallow may allow the procedure to con-
tinue comfortably. Less than 1% of patients
will experience mild anterior epistaxis or
self-limited laryngospasm.
The reasons for this preference include
enhanced comfort, reduced work absen-
teeism for patient and caregiver, timeliness,
cost, and safety. Most complications from
sedated EGD are cardiac and respiratory
compromise caused by IV medications.
Unsedated TNE entirely eliminates these
dangers.
Unsedated TNE represents the safest,
most efficient, and most cost-effective
means to evaluate the esophageal phase of
deglutition. It is diagnostically equivalent
to sedated per-oral esophagoscopy, is pre-
ferred to a sedated examination, and is the
procedure of choice to screen the esophagus
in patients with dysphagia and reflux.
 2. Transnasal Esophagoscopy (TNE)
27

References 9. Belafsky PC, Rees CJ. Functional oesoph-

agoscopy: endoscopic evaluation of the
1. Appropriate use of gastrointestinal endos- oesophageal phase of deglutition. J Laryn-
copy. American Society for Gastrointesti- gol Otol. 2009;123(9):1031–1034.
nal Endoscopy. Gastrointest Endosc. 2000;​ 10. Stroppa I, Grasso E, Paoluzi OA et al.
52(6):831–837. Unsedated transnasal versus transoral
2. DeVault KR, Castell DO; American Col- sedated upper gastrointestinal endoscopy:
lege of Gastroenterology. Updated guide- a one-series prospective study on safety
lines for the diagnosis and treatment of and patient acceptability. Dig Liver Dis.
gastroesophageal reflux disease. Am J Gas- 2008;40(9):767–775.
troenterol. 2005;100(1):190–200. 11. Murata A, Akahoshi K, Sumida Y, Yama-
3. Belafsky PC, Mouadeb DA, Rees CJ et al. moto H, Nakamura K, Nawata H. Prospec-
Validity and reliability of the Eating Assess- tive randomized trial of transnasal versus
ment Tool (EAT-10). Ann Otol Rhinol Lar- peroral endoscopy using an ultrathin vid-
yngol. 2008;117(12):919–924. eoendoscope in unsedated patients. J Gas-
4. Reavis KM, Morris CD, Gopal DV, Hunter troenterol Hepatol. 2007;22(4):482–485.
JG, Jobe BA. Laryngopharyngeal reflux 12. Thota PN, Zuccaro G Jr., Vargo JJ 2nd,
symptoms better predict the presence of Conwell DL, Dumot JA, Xu M. A random-
esophageal adenocarcinoma than typical ized prospective trial comparing unsedated
gastroesophageal reflux symptoms. Ann Surg. esophagoscopy via transnasal and transoral
2004;239(6):849–856; discussion 856–858. routes using a 4-mm video endoscope with
5. Nason KS, Murphy T, Schindler J et al. A conventional endoscopy with sedation.
cross-sectional analysis of the prevalence Endoscopy. 2005;37(6):559–565.
of Barrett esophagus in otolaryngology 13. Zaman A, Hahn M, Hapke R, Knigge K,
patients with laryngeal symptoms. J Clin Fennerty MB, Katon RM. A randomized
Gastroenterol. 2013;47(9):762–768. trial of peroral versus transnasal unsedated
6. Wildi SM, Glenn TF, Woolson RF, Wang endoscopy using an ultrathin videoendo-
W, Hawes RH, Wallace MB. Is esopha- scope. Gastrointest Endosc. 1999;49(3 pt 1):​
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2004;​59(3):349–354. Prospective evaluation of transnasal esoph-
7. Aviv JE, Murry T, Zschommier A, Cohen M, agogastroduodenoscopy: feasibility and
Gartner C. Flexible endoscopic evaluation study on performance and tolerance. Gas-
of swallowing with sensory testing: patient trointest Endosc. 1999;49(3 Pt 1):285–291.
characteristics and analysis of safety in 15. Jobe BA, Hunter JG, Chang EY, et al.
1,340 consecutive examinations. Ann Otol Office-based unsedated small-caliber endos-
Rhinol Laryngol. 2005;114(3):173–176. copy is equivalent to conventional sedated
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phagia. 1994;9(4):256–261.
 3
The Videofluoroscopic Esophagram
Introduction
Esophageal fluorography is an essential tool
in the evaluation of the patient with dys-
phagia. The videofluoroscopic esophagram
(VFE) evaluates deglutition from lips to
stomach and is the procedure of choice to
identify disorders of the cricopharyngeus
muscle and upper esophageal sphincter
(UES), the presence of esophageal webs
and rings, hiatal hernia, and esophageal
body motility. It is also used as an adjunct
to evaluate for esophagopharyngeal and
gastroesophageal reflux. A comprehensive
understanding of the indications, tech-
nique, and interpretation of the VFE is
essential for all swallowing clinicians.
Indications for VFE
The indications for VFE are presented in
Figure 3–1. The most common indication
for VFE is the evaluation of solid food dys-
phagia. Persons reporting the sensation of
food sticking in the neck or chest will have
an obstructive etiology of their symptom
approximately 45% of the time. In persons
29
with a normal esophagoscopy, persons with
solid food dysphagia will have an obstruc-
tive etiology over 90% of the time. The
cause of this obstruction may be secondary
to cricopharyngeal and upper esophageal
webs, cricopharyngeus muscle dysfunction,
peptic stricture, neoplasm, and esophageal
rings (Schatzki B). Although esophagos-
copy is the gold standard diagnostic tool
to evaluate esophageal mucosal pathology,
endoscopy is insufficient to effectively iden-
tify sites of obstruction. Endoscopy will
identify less than 60% of esophageal rings
identified on fluoroscopy.1 Although most
patients with solid food dysphagia require
esophagoscopy, we prefer to obtain a pre-
endoscopic VFE whenever possible. The
identification of an obstruction source can
provide the clinician with a road map to
target intervention with endoscopic dila-
tion or an alternative intervention such as
diverticulotomy or myotomy in the case of
Zenker’s diverticulum or cricopharyngeus
muscle dysfunction.
The second most common indication
for VFE is the comprehensive evaluation
of gastroesophageal reflux disease (GERD).
Complications of GERD include peptic
 Clinical Esophagology and Transnasal Esophagoscopy
30
Figure 3–1. Indications for VFE.
stricture, neoplasm, and ineffective esopha-
geal motility. In addition, hiatal hernia is
a primary factor in the etiology of severe
GERD. The VFE is an invaluable tool to
identify these entities and is performed on
all persons for whom surgical intervention
for GERD is contemplated.
Chronic cough (cough >8 weeks) is the
most common symptom responsible for
bringing a patient to visit a doctor in the
Western world. Causes of chronic cough
include reactive airway disease (asthma),
rhinitis (postnasal drip syndrome), postviral
vagal neuropathy (PVVN), and GERD. In
our experience, persons with hiatal hernia
represent a significant cohort of patients
with chronic cough that is particularly diffi-
cult to manage medically. Thus, we employ
the VFE to identify hiatal hernia and lower
esophageal sphincter incompetence as a
potential causative factor in patients with
chronic cough. The examination can also
screen for the presence of laryngeal penetra-
tion and pulmonary aspiration, which may
also cause coughing with meals or recur-
rent cough due to bronchitis and pneumo-
nia. Abnormal findings on VFE have been
reported in up to 12% of persons with
chronic cough.2
Patients with known oropharyngeal
dysphagia (OPD) have comorbid esopha-
geal dysfunction more than 35% of the
time. GERD is the suspected perpetrator
in Zenker‘s diverticulum, cricopharyngeus
muscle dysfunction, and ineffective esopha-
geal motility. The primary purpose of the
cricopharyngeus muscle is to protect the
upper airway from regurgitated gastric and
esophageal contents. Thus, we identify a
significant percentage of GERD, hiatal her-
nia, and esophageal dysmotility in persons
with cricopharyngeus muscle dysfunction
and recommend that an esophageal screen
or comprehensive VFE be performed in
all persons with OPD. In addition, the
VFE is utilized to identify the protective
function of the cricopharyngeus muscle
before considering UES modification (Fig-
ure 3–2). Surgically altering the protective
function of the UES in persons with sig-
nificant esophageal pathology can have dire
consequences.
 3. The Videofluoroscopic Esophagram
31

Figure 3–2. Right anterior oblique view of VFE displaying

profound cricopharyngeus muscle dysfunction (red aster-
isk) and a dilated esophagus (yellow arrows). Also visible are
tertiary contractions (green arrows). The VFE revealed severe
esophageal dysmotility not appreciated on this still image.
A protrusion on the back of the cricoid cartilage (red arrow)
suggests the presence of a cricopharyngeal web. Cricopha-
ryngeus muscle myotomy could have devastating conse-
quences, and a more conservative treatment approach with
dilation of the pharyngoesophageal segment is indicated.

Technique of VFE The risk of aspiration in an individual with

A systematic protocol is essential to ensure
the reproducibility and validity of the
VFE investigation. The protocol we use
for esophagography has been refined over
30 years of clinical practice at our cen-
ter. Adhering to protocol ensures repro-
ducibility between institutions, between
patients, and within patients pre- and
postintervention.
A comprehensive VFE is not feasible or
necessary for all patients. A desire to limit
radiation exposure, limitations in personnel
availability, and physical limitations partic-
ular to an individual patient may limit the
implementation of a comprehensive VFE.
profound oropharyngeal dysphagia may
also preclude the completion of a thorough
examination. These factors have led to the
development of the esophageal screen (ES)
as an alternative to the VFE when patient
limitations preclude the completion of a
full evaluation, and/or the clinical suspicion
for esophageal pathology is low.
The sensitivity of the ES is 63%, and the
specificity of the esophageal screen is 100%
when compared to the comprehensive
VFE.3 Therefore, an abnormal esophageal
screen may dictate further management,
but a normal ES cannot definitively rule
out esophageal pathology. A healthy ambu-
latory patient with the chief complaint of
 Clinical Esophagology and Transnasal Esophagoscopy
32

solid food dysphagia will have an esopha- properties of a nectar liquid. This con-
geal contribution to his or her swallowing centration provides a balance between the
complaint in over 60% of cases. We there- desired rheology, mucosal adherence, and
fore advocate at least an ES in all persons radiopacity to provide optimal anatomic
who undergo a videofluoroscopic swallow detail. Diluting the barium may be desired
study (VFSS) and a comprehensive VFE in in certain circumstances. If a patient has
most individuals. problems specifically with thin liquids,
The choice of contrast agent is para- the 60% w/v barium is diluted 50:50 with
mount in esophagography. Contrast that water. This provides a formulation that
is too viscous will not serve as a reliable models a thin-liquid swallow, but at the
surrogate to investigate safety with real-life
expense of anatomic detail and mucosal
liquids. Contrast that is not viscous enough adherence.
will not adhere to obstructive pathology The suspicion of a pharyngeal or esopha-
and may miss esophageal neoplasia, webs, geal perforation precludes the use of barium
and rings. Contrast with poor radiopacity in most cases. In this instance, the use of a
may miss significant pathology. Our stan- water-soluble contrast agent such as Gas-
dard protocols utilize a 60% weight/volume trograffin (Bracco Diagnostic Inc, Monroe
(w/v) ratio of barium sulfate (Ezpaque, Township, New Jersey) or Omnipaque (GE
Westbury, New Jersey; Figure 3–3). This Healthcare Inc, Buckinghamshire, United
barium formulation has the rheological Kingdom) is utilized. If barium extrava-
sates through a perforation, it can remain
in the mediastinum for months. This will
confound the interpretation of future
imaging studies, predispose to granuloma
formation, and increase the risk of devel-
oping mediastinitis. In addition, barium
will adhere to the mucosal surface of the
esophagus and obscure visualization dur-
ing endoscopy. The water-soluble contrast
agents are rapidly resorbed and do not bear
these risks. The benefits of the water-solu-
ble contrast agents must be weighed against
their potential to cause a chemical pneu-
monitis if aspirated and the risk of miss-
ing pathology secondary to the reduced
radiopacity. Esophagography with water-
soluble contrast agent alone, however, may
miss an esophageal perforation in over
20% of cases.4,5 Our protocol in persons
with a suspected pharyngeal or esophageal
perforation is to begin the study with a
water-soluble contrast agent (Gastrograf-
Figure 3–3. 60% weight/volume (w/v)
barium sulfate utilized for the videofluoro- fin). If the initial swallow fails to detect a
scopic esophagram (Ezpaque, Westbury, leak, barium sulfate is used to complete the
New Jersey). investigation. If the patient is scheduled for
 3. The Videofluoroscopic Esophagram
33

upcoming endoscopy in the next 4 hours,
however, barium is not utilized. Barium
is inert if aspirated in small quantities. If
the patient has oropharyngeal dysphagia
and is at risk for significant aspiration, the
benefits of using the water-soluble agents
must be weighed against the risk of chemi-
cal pneumonitis.
All fluoroscopic swallow studies are
recorded at 30 frames per second (fps) for
later playback and analysis. The ability to
review the studies in a stop-motion 30-fps
frame-by-frame manner is essential to
identify subtle and/or transient pathology.
Several commercially available recording
devices are available. We currently employ
nStream (Image Stream Medical, Inc, Lit-
tleton, Massachusetts), which is fully inte-
grated into our electronic medical record.
ing position in the anterior-posterior (AP)
projection with the knees slightly flexed
(Figure 3–4). When the patient is asked to
swallow, he or she is instructed to straighten
the knees and stand up tall. This allows the
fluoroscopist to follow the bolus from the
mouth to the gastric body. A protective
lead shield is used to shelter the reproduc-
tive organs. Clothing, clips, and jewelry
are removed so as not to obstruct the fluo-
roscopic view. A towel is draped over the
shoulders to protect from barium remnants
that may drip onto the patient. The esopha-
geal screen begins with the administration
of a single 20-mL bolus of 60% w/v barium
sulfate. The patient is instructed to, “swal-
low the entire bolus in one hard swallow.”
Instructing the patient to avoid a second

Esophageal Screen Technique

The ES is performed after the oropharyn-

geal phase of the VFSS (modified barium
swallow [MBS]). The reader is referred to
other publications that describe our com-
prehensive VFSS protocol.6 We utilize
an OEC Medical Systems mobile 9800
Radiographic/Fluoroscopic unit (OEC
Medical Systems, Salt Lake City, Utah) for
all fluoroscopic swallow studies. We prefer
the C-arm to fixed fluoroscopic units. The
flexibility of the C-arm affords the ability
to study patients of various sizes at diverse
angles and image projections. All studies
are performed in a lead-lined room by a
licensed radiology technician and speech
and language pathologist and later reviewed
by a physician licensed in fluoroscopy from
the Radiologic Health Branch (RHB) of Figure 3–4. Positioning for the esopha-
geal screen procedure. The knees are
the California Food, Drug, and Radia-
slightly flexed. The patient is instructed
tion Safety Division of the Department of to stand up slowly as the barium is swal-
Public Health. To facilitate tracking of the lowed so that the technician can follow
bolus, the patient is positioned in a stand- the bolus from the mouth to the stomach.
 Clinical Esophagology and Transnasal Esophagoscopy
34
swallow preserves the initial peristaltic
wave and avoids a false-positive assessment
of ineffective esophageal motility due to
deglutitive inhibition. The fluoroscopy
technician follows the bolus from the oral
cavity to its entry into the stomach. Passage
of the bolus is timed from its entry into
the esophagus until its exit into the stom-
ach. Normal esophageal transit time is less
than 15 seconds (approximately 2 cm/sec).
A bolus that takes more than 15 seconds to
clear the esophagus suggests the presence
of pathology such as ineffective motil-
ity, web, stricture, or neoplasm. After the
patient consumes the 20-cc AP bolus, he or
she is administered a 13-mm barium tablet
(Merry X-Ray Corp, San Diego, California).
The diameter of the tablet is manufactured
at 13 mm because historical wisdom sug-
gested that esophageal rings and strictures
became symptomatic when the normal
20-mm esophageal lumen was narrowed to
less than 13 mm. The 13-mm doctrine has
fallen out of favor, as the symptom of dys-
phagia is now understood as complex and
dependent on patient eating and chewing
habits, the presence of esophageal inflam-
mation, and other medical comorbidities,
access to health care, anatomic and mucosal
pathology, and visceral sensitivity. None-
theless, the 13-mm barium tablet increases
the sensitivity of the screening examination
to nearly 75% and serves as an essential tool
to gauge the degree of esophageal obstruc-
tion. The tablet is observed until it enters
the stomach. If there is significant delay in
transit, the fluoroscopic unit is turned off to
limit radiation exposure and intermittently
re-engaged every 60 seconds until it enters
the stomach or until a total of 5 minutes
has elapsed. The study is now complete.
Fluoroscopy time is limited to 30 seconds,
and the patient is instructed to drink two
16-oz glasses of water to prevent barium
constipation.
If the ES is normal and a high index of
suspicion for esophageal pathology remains,
the patient is referred for endoscopy or a com-
prehensive VFE as indicated.
Comprehensive VFE Technique
The patient is protected and positioned
in a standing knees-flexed upright posi-
tion in the AP projection similar to the ES
(see Figure 3–4). The comprehensive VFE
begins with the administration of a single
20-mL bolus of 60% w/v barium sulfate by
cup sip. The patient is again instructed to
“swallow the entire bolus in one hard swal-
low” to avoid dysmotility associated with
deglutitive inhibition. The bolus is followed
from the oral cavity until its entry into the
stomach as the patient slowly stands up.
Once the barium has exited the esophagus,
the patient is administered a 10-mL cup of
effervescent crystals (EZ-Gas II; E-Z-EM,
Lake Success, New York) and 10 mL of
water in rapid succession. A second 20-mL
bolus is then administered with identical
instructions. This allows the acquisition of
collapsed and partially collapsed mucosal
relief views, which helps identify esopha-
geal mucosal pathology. Once the barium
has cleared into the stomach, the patient
is administered a 13-mm barium tablet
(Merry X-Ray Corp, San Diego, California)
with a 2-oz cup of water. The tablet helps
identify sites of esophageal obstruction <13
mm. The tablet is observed until it enters
the stomach. If there is significant delay, the
fluoroscopic unit is turned off and inter-
mittently re-engaged every 60 seconds until
it enters the stomach or until a total of 5
minutes has elapsed.
The patient is then positioned prone in
the right anterior oblique (RAO) projection.
The patient is asked to lay chest down with
a folded pillow under his or her head and

rotated 40° to the left so that the right ear
is against the pillow and the right anterior
thorax is against the fluoroscopic table. The
left knee is flexed, and the right leg is kept
straight. The left arm is flexed at the elbow
and placed on the table above the head,
and the right arm is placed down at the
side. A cup of 60% w/v barium sulfate with
an elongated straw is placed in the reach-
ing left hand (Figure 3–5). This position
affords evaluation of esophageal motility
without the benefit of gravity and improves
visualization of the esophagus by separating
the organ from the distortion caused by the
thoracic spine. The patient is instructed to
take the largest sip possible and to, “swal-
low the entire bolus in one hard swallow.”
The barium is again followed from the oral
cavity until its entrance into the stomach.
After the barium has cleared the esophagus,
the patient is then instructed to consume
sequential barium swallows.
The patient is asked to gulp the barium
as fast as possible to completely consume
60 mL of barium from the bottle. This
Figure 3–5. RAO positioning for the videofluoroscopic esopha-
gram.
3. The Videofluoroscopic Esophagram
35
sequential swallow task maximally distends
the esophagus and is essential in identifying
subtle webs, strictures, hernias, and neopla-
sia. Esophageal body peristalsis should not
be evaluated during the sequential swallow
task secondary to the dysmotility caused
by deglutitive inhibition. The barium is
observed until it enters the stomach. If
there is significant delay, the fluoroscopic
unit is turned off and intermittently re-
engaged every 60 seconds with flash single
pedal-tap fluoroscopic views until it com-
pletely enters the stomach or until a total of
5 minutes has elapsed. The patient is then
evaluated for GERD.
The patient is placed on his or her back in
the supine position with the head on a pil-
low to simulate the sleeping position. Pro-
vocative maneuvers are then performed to
evaluate for GERD. The fluoroscopic unit
is turned on, and the patient is instructed
to raise the legs 15 cm off of the examina-
tion table to evaluate the effect of elevated
intraabdominal pressure on GERD (Figure
3–6). While in this position, the patient is
 Clinical Esophagology and Transnasal Esophagoscopy
36

Figure 3–6. Supine position for the videofluoroscopic esopha-

gram with legs elevated to increase the sensitivity of detecting
gastroesophageal reflux.

asked to bear down and perform a Valsalva Normal Videofluoroscopic

maneuver while drinking 80 mL of water.
The water siphon test (WST) relaxes the
lower esophageal sphincter and enhances
the identification of barium regurgitation
into the esophagus. Some investigators sug-
gest that the sensitivity of the WST may be
as high as 89% in identifying persons with
GERD.7 It is important to note that the
visualization of barium regurgitation from
the stomach into the esophagus on VFE
does not define the presence of GERD.
In addition, its absence does not rule out
the presence of GERD. The evaluation of
barium regurgitation on VFE purely serves
as an adjunct to other clinical indicators
and objective diagnostics to establish the
presence and severity of reflux disease and
associated disorders. The study is now com-
plete. Fluoroscopy time is limited to 2 min-
utes, and the patient is instructed to drink
three 400-mL glasses of water to prevent
barium constipation.
Esophagram
Esophageal Compressions
on VFE
There are four compressions that are visual-
ized on a normal VFE. The first compression
is that of the pharyngoesophageal segment or
PES. The PES refers to the anatomic compo-
nents that make up the UES. The UES refers
to the 3-cm region of high pressure appreci-
ated on pharyngoesophageal manometry.
The terms PES and UES may be used inter-
changeably. This region connects the hypo-
pharynx to the cervical esophagus and is iden-
tified at approximately 17 to 18 cm from the
oral commissure or nasal vestibule. The RAO
projection on the VFE provides an excellent
unimpeded view of the PES. This allows for
the reliable detection of cricopharyngeal webs,
cricopharyngeus muscle dysfunction, and
UES stenosis (Figures 3–7 and 3–8).
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The Project Gutenberg eBook of Loom and
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Title: Loom and spindle

or life among the early mill girls with a sketch of "the
Lowell offering" and some of its contributors

Author: Harriet Jane Hanson Robinson

Author of introduction, etc.: Carroll D. Wright

Contributor: Lucy Larcom

Release date: January 19, 2024 [eBook #72757]

Language: English

Original publication: New York: Thomas Y. Crowell & Company,

1898

Credits: Susan E., Fay Dunn and the Online Distributed

Proofreading Team at https://www.pgdp.net (This file
was produced from images generously made available
by The Internet Archive/American Libraries.)

*** START OF THE PROJECT GUTENBERG EBOOK LOOM AND

SPINDLE ***
Loom and Spindle
Harriet Jane Hanson at 18.
 LOOM AND SPINDLE
OR

Life Among the Early Mill Girls

WITH A SKETCH OF

“THE LOWELL OFFERING” AND SOME

OF ITS CONTRIBUTORS

BY

HARRIET H. ROBINSON
AUTHOR OF “WARRINGTON PEN PORTRAITS,” “MASSACHUSETTS IN THE
WOMAN SUFFRAGE MOVEMENT,” “THE NEW PANDORA,” ETC.

INTRODUCTION
BY THE
HONORABLE CARROLL D. WRIGHT

“Work is a shame to none; the shame is not to be working.”—Hesiod

 NEW YORK: 46 East 14th Street
THOMAS Y. CROWELL & COMPANY
BOSTON: 100 Purchase Street
 Copyright, 1898,
By Thomas Y. Crowell & Company.

Typography by C. J. Peters & Son, Boston.

Presswork by S. J. Parkhill & Co.

 INTRODUCTION.

Whenever the history of economic conditions in this country shall

be written, the author will express his gratitude for all works giving
the details of especial epochs and phases of industrial life. Among
them he will find no more interesting experience than that attending
the entrance of women to the industrial field. The author of “Loom
and Spindle” contributes something more than her personal
experiences at Lowell during the early years of the textile factories,—
she contributes an inside view of the workings of a new system of
labor, which had been transplanted from England, and which
originated with the application of power to spinning and weaving.
The attractions of good wages and comfortable environment were
the inducements held out by American manufacturers at Lowell to
secure a class of operatives which should bring success to their
experiment. The prejudice against mill operatives, as shown by
investigations in England, would otherwise have delayed the
establishment of the factory in America; that is, the factory as
controlled by a central power. With the attractions offered, it was
natural that the women of New England should accept situations as
weavers, spinners, etc., in the great textile works; but they brought
with them their educational and religious training; and, as they were
grouped together, it was natural also that they should continue the
cultivation of their minds, especially under the broadening influences
of mental contact. It is this aspect of the factory system to which Mrs.
Robinson has addressed herself. It was an experience in which she
took part; she saw it all, and was a part of it. She, with her
associates, chief among whom were Harriot F. Curtis, a writer who
attained an enviable position, the Currier sisters, Mrs. Chamberlain,
Eliza Jane Cate, Harriet Farley, the sculptress Margaret Foley, Lydia
S. Hall, Lucy and Emmeline Larcom, Sarah Shedd my first teacher,
and others, who became well known in literary, benevolent, and
other walks in public life, gave character to the early factory days in
New England, which are usually referred to not only as unique in
their features, but for the purpose of supporting the idea that modern
conditions are not as attractive, and that there has been a thorough
deterioration not only in the people employed in factories, but in their
home-life. Something of this note is sounded in the last chapter of
this book; yet it must be recognized that the factory system has been
and is a power in civilization,—a factor in developing it, in truth.
The factory girl of the early period was not degraded through her
employment or her surroundings. She stepped out of factory life into
professional or semi-professional occupations. She was succeeded
by a class originally beneath her, the members of which have in their
turn graduated from the factory, and stepped into higher callings.
This process has been repeated, the destiny of the factory being
ever to reach down and lift people up out of lowly into higher
conditions. This gives the surface appearance of deterioration, when
the real fact is that through the factory the lower orders, so far as
mental capacity is concerned, are being constantly elevated. The
author sees this, yet naturally cannot help regretting that the
heterogeneity of the factory population—natives coming from many
lands, with differing social ideas, with little or no training, with few
opportunities for advancement, with low earning capacity, and with
varied languages—has changed the atmosphere of the factory
community. The human lives involved are worth more in this
atmosphere than they were in the cloddish labor out of which they
have risen.
“Loom and Spindle,” valuable as it is for its details of economic
history, for the inspiration which comes from studying the lives and
characters of noble women, teaches the lesson which the author and
her associates taught,—that whatever is honest in employment is in
the service of God. Their lives emphasize the fact that the modern
system of industry has exercised a wonderful influence in securing
intellectual stimulation, and in dignifying every honest calling.
CARROLL D. WRIGHT.
Washington, May, 1898.
 CONTENTS.

CHAPTER PAGE

Introduction iii
I. Lowell Sixty Years Ago 1
II. Child-Life in the Lowell Cotton Mills 25
III. The Little Mill-Girl’s Alma Mater 40
IV. The Characteristics of the Early Factory Girls 60
V. Characteristics (Continued) 83
VI. The Lowell Offering and its Writers 97
VII. The Lowell Offering (Continued) 109
VIII. Brief Biographies of some of the Writers for 132
The Lowell Offering
IX. The Cotton Factory of To-day 202
LOOM AND SPINDLE.
 CHAPTER I.

LOWELL SIXTY YEARS AGO.

“That wonderful city of spindles and looms,

And thousands of factory folk.”

The life of a people or of a class is best illustrated by its domestic

scenes, or by character sketches of the men and women who form a
part of it. The historian is a species of mental photographer of the life
and times he attempts to portray; he can no more give the whole
history of events than the artist can, in detail, bring a whole city into
his picture. And so, in this record of a life that is past, I can give but
incomplete views of that long-ago faded landscape, views taken on
the spot.
It is hardly possible to do this truthfully without bringing myself
into the picture,—a solitary traveller revisiting the scenes of youth,
and seeing with young eyes a city and a people living in almost
Arcadian simplicity, at a time which, in view of the greatly changed
conditions of factory labor, may well be called a lost Eden for that
portion of our working-men and working-women.
Before 1836 the era of mechanical industry in New England had
hardly begun, the industrial life of its people was yet in its infancy,
and nearly every article in domestic use that is now made by the
help of machinery was then “done by hand.” It was, with few
exceptions, a rural population, and the material for clothing was
grown on the home-farm, and spun and woven by the women. Even
in comparatively wealthy families, the sons were sent to college in
suits of homespun, cut and made by the village seamstress, and
every household was a self-producing and self-sustaining
community. “Homespun was their only wear,” homespun their lives.
There was neither railway, steamboat, telegraph, nor telephone,
and direct communication was kept up by the lumbering stage-
coach, or the slow-toiling canal, which tracked its sinuous way from
town to city, and from State to State. The daily newspaper was
almost unknown, and the “news of the day” was usually a week or so
behind the times. Money was scarce, and most of the retail business
was done by “barter”—so many eggs for a certain quantity of sugar,
or so much butter or farm produce for tea, coffee, and other luxuries.
The people had plenty to eat, for the land, though sterile, was well
cultivated; but if the children wanted books, or a better education
than the village school could give them, the farmer seldom had the
means to gratify their wishes.
These early New Englanders lived in pastoral simplicity. They
were moral, religious, and perhaps content. They could say with
truth,—

“We are the same things that our fathers have been,
We see the same sights that our fathers have seen,
We drink the same stream, we feel the same sun,
And run the same course that our fathers have run.”

Their lives had kept pace for so many years with the stage-coach
and the canal that they thought, no doubt, if they thought about it at
all, that they should crawl along in this way forever. But into this life
there came an element that was to open a new era in the activities of
the country.
This was the genius of mechanical industry, which would build the
cotton-factory, set in motion the loom and the spinning-frame, call
together an army of useful people, open wider fields of industry for
men and (which was quite as important at that time) for women also.
For hitherto woman had always been a money-saving, rather than a
money-earning, member of the community, and her labor could
command but small return. If she worked out as servant, or “help,”
her wages were from fifty cents to one dollar a week; if she went
from house to house by the day to spin and weave, or as tailoress,
she could get but seventy-five cents a week and her meals. As
teacher her services were not in demand, and nearly all the arts, the
professions, and even the trades and industries, were closed to her,
there being, as late as 1840, only seven vocations, outside the
home, into which the women of New England had entered.[1]

[1] These were teaching, needlework, keeping boarders, factory

labor, type-setting, folding and stitching in book-binderies.
According to the census of 1885 (that of 1895 is not yet tabulated),
wherein the subject of “Woman in Industry” was first specialized,
by Hon. Carroll D. Wright, there are 113 industries, which,
subdivided, make 17,357 separate occupations. Women have
found employment in 4,467 of these, while of the 113 general
branches, they are found in all but seven.

The Middlesex Canal was one of the earliest factors in New

England enterprise. It began its course at Charlestown Mill-pond,
and ended it at Lowell. It was completed in 1804, at the cost of
$700,000, and was the first canal in the United States to transport
both passengers and merchandise. Its charter was extinguished in
1859, in spite of all opposition, by a decision of the Supreme Court.
And thus, in less than sixty years, this marvel of engineering skill, as
it was then considered, which was projected to last for all time, was
“switched off the track” by its successful rival, the Boston and Lowell
Railroad, and, with the stage-coach and the turnpike road became a
thing of the past.
The course of the old Middlesex Canal can still be traced, as a
cow-path or a woodland lane, and in one place, which I have always
kept in remembrance, very near the Somerville Station on the
Western Division of the Boston and Maine Railroad, can still be seen
a few decayed willows, nodding sleepily over its grass-grown
channel and ridgy paths,—a reminder of those slow times when it
took a long summer’s day to travel the twenty-eight miles from
Boston to Lowell.
 The Boston and Lowell Railroad, probably the first in the United
States, went into operation in 1835. I saw the first train that went out
of Lowell, and there was great excitement over the event. People
were gathered along the street near the “deepot,” discussing the
great wonder; and we children stayed at home from school, or ran
barefooted from our play, at the first “toot” of the whistle. As I stood
on the sidewalk, I remember hearing those who stood near me
disputing as to the probable result of this new attempt at locomotion.
“The ingine never can start all them cars!” “She can, too.” “She
can’t.” “I don’t believe a word of it.” “She’ll break down and kill
everybody,” was the cry.
But the engine did start, and the train came back, and the Boston
and Lowell Railroad continued an independent line of travel for about
the same number of years as its early rival; when, by the “irony of
fate,” its individuality was merged in that of a larger and more
powerful organization,—the Boston and Maine Railroad, of which, in
1895, it became only a section or division. But let us not regret too
much this accident of time, for who knows what will become of this
enormous plant during the next fifty years, when our railways,
perhaps, may be laid in the “unfeatured air.”
The first factory for the manufacture of cotton cloth in the United
States was erected in Beverly, Mass., in 1787, and in 1790 Samuel
Slater established the cotton industry in Pawtucket, R.I.; but the first
real effort to establish the enterprise was in Lowell, where a large
wooden building was erected at the Wamesit Falls, on the Concord
River, in 1813.
The history of Lowell, Mass., is not identical with that of other
manufacturing places in New England, and for two reasons: first,
because here were gathered together a larger number of factory
people, and among them were the first who showed any visible sign
of mental cultivation; and, second, because it was here that the
practice of what was called “The Lowell factory system” went into
operation, a practice which included the then new idea, that
corporations should have souls, and should exercise a paternal
influence over the lives of their operatives. As Dr. John O. Green of
Lowell, in a letter to Lucy Larcom, said: “The design of the control of
the boarding-houses and their inmates was one of the characteristics
of the Lowell factory system, early incorporated therein by Mr.
Francis Cabot Lowell and his brother-in-law, Patrick T. Jackson, who
are entitled to all the credit of the acknowledged superiority of our
early operatives.”
Cotton-mills had also been started in Waltham, Mass., where the
first power-loom went into operation in 1814; but, for lack of water-
power, these could be carried on to a limited extent only. It was
therefore resolved, by gentlemen interested, that the “plant” should
be moved elsewhere, and water privileges were sought in Maine,
New Hampshire, and in Massachusetts. Finally, Pawtucket Falls, on
the Merrimack River, was selected, as a possible site where a large
manufacturing town could be built up. Here land was bought, and the
place, formerly a part of Chelmsford, set off in 1826, was named
Lowell, after Francis Cabot Lowell, who, through his improvements,
was practically the inventor of the power-loom, and the originator of
the cotton-cloth manufacture as now carried on in America.
Kirk Boott, the agent of the first corporation, (as the mills,
boarding-houses,—the whole plant was called), was a great
potentate in the early history of Lowell, and exercised almost
absolute power over the mill-people. Though not an Englishman, he
had been educated in England, had imbibed the autocratic ideas of
the mill-owners of the mother country, and many stories were told of
his tyranny, or his “peculiarities,” long after he ceased to be a
resident.
Of his connection with the early history of Lowell, it is stated that,
before the water-power was discovered there, he went as agent of
the purchasers, to Gardiner, Me., and tried to buy of R. H. Gardiner,
Esq., the great water privilege belonging to his estate. Mr. Gardiner
would not sell, but was willing to lease it. Kirk Boott would not agree
to this, or Lowell might now have been on the Kennebec in Maine.
Then he came to Chelmsford, and saw the great Merrimack River
and its possibilities, and set himself shrewdly to work to buy land on
its banks, including the water-power. He represented to the simple
farmers that he was going to raise fruit and wool, and they, knowing
nothing of “mill privileges,” believed him, and sold the greatest water-