Atlas of Diagnostic Endoscopy

Third Edition
Atlas of Diagnostic Endoscopy
Third Edition

Dr Mohammad Ibrarullah, FACS, MS, MCh

Senior Consultant, Department of Surgical Gastroenterology,
Apollo Hospitals, Bhubaneswar, India
Formerly, Professor and Head of Surgical Gastroenterology
SV Institute of Medical Sciences, Tirupati, India
Sri Ramachandra Medical College & Research Institute, Chennai &
Hitech Medical College and Hospital, Bhubaneswar, India
CRC Press
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Library of Congress Cataloging-in-Publication Data

Names: Ibrarullah, Mohammad, author.

Title: Atlas of diagnostic endoscopy / by Dr. Mohammad Ibrarullah.
Description: 3 e. | Boca Raton : CRC Press, [2020] | Includes bibliographical references and index. |
Summary: “This book is a compilation of endoscopic images of the upper gastrointestinal tract.
The 3rd edition is enriched with high-resolution digital images highlighting the classification and
staging of endoscopically relevant diseases. It outlines the technique and interpretation of such images
proving to be a helpful guide to endoscopy practitioners”-- Provided by publisher.
Identifiers: LCCN 2019030549 (print) | LCCN 2019030550 (ebook) | ISBN 9780367345006
(hardback : alk. paper) | ISBN 9780429326240 (ebook)
Subjects: MESH: Gastrointestinal Diseases--diagnosis | Endoscopy, Gastrointestinal--methods |
Upper Gastrointestinal Tract--surgery | Atlas
Classification: LCC RC816 (print) | LCC RC816 (ebook) | NLM WI 17 | DDC 616.3/3--dc23
LC record available at https://lccn.loc.gov/2019030549
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Contents

List of abbreviations vii

Preface ix
Acknowledgments xi
Author xiii

1 Techniques of UGI endoscopy and normal anatomy 1

2 Esophageal webs, rings and strictures 9
3 Hiatal hernia and gastroesophageal reflux disease (GERD) 19
4 Motility disorders of the esophagus 37
5 Benign gastric ulcer 39
6 Chronic duodenal ulcer 55
7 Gastrojejunostomy 71
8 Benign tumors 83
9 Malignant tumors 93
10 Portal hypertension 109
11 Corrosive injury 125
12 Uncommon inflammatory lesions and tropical diseases of the UGI tract 135
13 Mallory–Weiss syndrome 147
14 Dieulafoy’s lesion 151
15 Gastric antral vascular ectasia (GAVE) 155
16 Foreign body 157
17 Tracheoesophageal fistula 163
18 Miscellaneous 167

Index 177

v
List of abbreviations

ACG American College of Gastroenterology

AGA American Gastroenterological Association
ASGE American Society for Gastrointestinal Endoscopy
CMV Cytomegalovirus
CT Computed tomography
D1 1st part of duodenum
D2 2nd part of duodenum
EVL Endoscopic variceal band ligation
FB Foreign body
GAVE Gastric antral vascular ectasia
GI Gastrointestinal
GE Gastroesophageal
GERD Gastroesophageal reflux disease
GIST Gastrointestinal stromal tumor
GJ Gastrojejunostomy
GOV Gastroesophageal varix
HIV Human immunodeficiency virus
HPF High-power field
HSV Herpes simplex virus
IGV Isolated gastric varix
LES Lower esophageal sphincter
LPF Left pyriform fossa
NET Neuroendocrine tumor
NSAID Nonsteroidal anti-inflammatory drug
PEG Percutaneous endoscopic gastrostomy
PHG Portal hypertensive gastropathy
RPF Right pyriform fossa
TEF Tracheoesophageal fistula
UGI Upper gastrointestinal

vii
Preface

Each passing year has seen tremendous advances in the field of both diagnostic and therapeutic endos-
copy. While preparing the current edition of the atlas, I also felt tempted to add a few chapters on recent
advances such as fluorescent endoscopy, magnification endoscopy, etc. However, on second thought I
decided to restrict myself to basic endoscopy since my target readers, as I mentioned in the first edition of
the atlas, are the “young doctors who wish to get initiated and practice endoscopy.” The aim of this atlas
is to provide them a strong foundation by familiarizing them with the basic concepts of endoscopy and
aiding in correct interpretation of the pathology. Notwithstanding the number of similar atlases available
online, it is always quick and easy to refer to a printed copy that is lying in the endoscopist’s consultation
chamber. Needless to say, printed images provide a longer-lasting impression as compared with those
seen on the computer screen. Effort has been made to replace some poor quality and repetitive images of
the previous edition with new ones, giving a fresh look to the current edition of the atlas. I sincerely hope
that the atlas, in its current form, will find wide acceptance amongst endoscopy practitioners.

ix
Acknowledgments

Those who provided professional, academic and technical support in compiling the atlas are

Prof. B Krishna Rau, Chennai

Prof. SR Naik, Lucknow
Dr D Srinivasa, Bangalore
Dr Gajanan Wagholikar, Pune
Dr Anuj Sarkari, Gorakhpur
Dr Amaresh Mishra, Bhubaneswar
Dr Anwar Basha, Tirupati
Dr T Shyamsundar, Nellore
Dr B Visweswara Rao, Srikakulum
Dr D Vijay Nagaraj, Cudappa
Dr D Gopikrishna Reddy, Tirupati
Dr M Srinivas, Rajmundry
TL Varalakshmi, Tirupati
V Dhanalakshmi, Tirupati
Dr Sidhant Kar, Bhubaneswar
Dr JM Rao, Bhubaneswar
Dr Neeraj K Mishra, Bhubaneswar
Dr Ambica P Das, Bhubaneswar
Dr Tapas Mishra, Bhubaneswar
Dr Sarat C Panigrahi, Bhubaneswar
Dr Devanand Mohapatra, Bhubaneswar
Dr Asutosh Mohapatra, Bhubaneswar
Dr Susant Sethi, Bhubaneswar
Dr S Shanmughanathan, Chennai
Gopala Bisoi, Bhubaneswar
Malaya Mukhi, Bhubaneswar

xi
Author

Dr Mohammad Ibrarullah is Senior Consultant in the Department of

Surgical Gastroenterology, Apollo Hospitals, Bhubaneswar. Born in the
state of Odisha, he obtained his graduate degree from SCB Medical College,
Cuttack, Odisha, in 1985 and postgraduate degree in general surgery
from JN Medical College, Aligarh, in 1988. He was associated with the
Department of Surgical Gastroenterology, Sanjay Gandhi Postgraduate
Institute of Medical Sciences, Lucknow, since its inception, and awarded
a postdoctoral (MCh) degree in the super-specialty in 1995. The same
year, he was selected as the “Travel Scholar of the International Society of
Surgery Foundation” by the International Society of Surgery, USA. He
has been a national faculty member in various academic forums and has
contributed articles and research papers in several national and interna-
tional journals and books.

xiii
 1
Techniques of UGI endoscopy and
normal anatomy

Preparation for endoscopy

Informed consent and counseling: The patient should be clearly informed about the proce-
dure and the likely discomfort he may experience. It should be explained that his coopera-
tion will make the procedure easier and quicker.

Overnight fasting: Routine endoscopy is usually performed in the morning hours after
overnight fasting. Coating agents like antacids or colored medications should be clearly
withheld. In case of obstructed stomach, prior nasogastric intubation and lavage should be
performed to clear the gastric residue.

Sedation and anesthesia: For routine UGI endoscopy, we use only topical pharyngeal anes-
thetics such as lignocaine viscous or spray. Sedation, in the form of intravenous Midazolam,
is occasionally used in children. For therapeutic endoscopy, such as foreign body removal,
stent placement etc., it is our practice to use intravenous propofol anesthesia with or with-
out endotracheal intubation.

Endotracheal intubation and monitoring: Endoscopy in a comatose or irritable patient is

fraught with the risk of aspiration, hypoxia and “bite” damage to the endoscope. It is our
practice to use prior endotracheal intubation and also monitor the vital parameters during
the procedure.

Instrument check: Prior to endoscopy, it is good practice to check the instrument, including
the light source, suction channel, airflow and display panel for any malfunction.

Position of the patient: Diagnostic endoscopy is always performed in the left lateral posi-
tion. Occasionally, in a patient with upper GI bleeding, it may be necessary to examine
the patient in the right lateral position. This is to displace the fundal blood pool that may
obscure the bleeding lesion.

Antibiotic prophylaxis: Antibiotic prophylaxis is not indicated for diagnostic endoscopy.

Current recommendations by the American Society for Gastrointestinal Endoscopy (ASGE)
exclude even conditions such as valvular heart disease, prosthetic valves, synthetic vascular
graft and prosthetic joints from the ambit of antibiotic prophylaxis. The few indications for
antibiotic prophylaxis are therapeutic endoscopy for cirrhosis with acute variceal bleeding,
cyst drainage and in patients with established GI tract infection who have the above listed
cardiovascular status.

1
2 Atlas of diagnostic endoscopy

The mouth guard is held between the teeth.

It is further supported by the index and
middle finger of the endoscopy assistant.
Alternatively, an elastic band attached to the
mouth guard can be used to keep it steady.

Figure 1.1 The mouth guard.

(a) (b)

Figure 1.2 View as the endoscope enters the oral cavity. (a, b) Dorsum of the tongue (T) and
hard palate (P).

The tip of the endoscope is slightly bent to fit the contour of the tongue. It is gently advanced over
the base of the tongue towards the pharynx.

(a) (b)

Figure 1.3 (a, b) Uvula (U) and the base of the tongue (T).
 Techniques of UGI endoscopy and normal anatomy 3

(a) (b)

Figure 1.4 (a, b) Epiglottis (E).

The epiglottis (E) is seen as the pharynx is entered.

(a) (b) (c)

Figure 1.5 (a–c) The laryngo-pharynx. Larynx (L) and both pyriform fossae (RPF, LPF). The arrow
points to the esophageal inlet.

As the scope passes below the epiglottis, the lar-

ynx and both pyriform fossae come into view.
The scope is kept in the midline at the esopha-
geal inlet (arrow in Figures 1.5 & 1.6) and the
patient is asked to take swallows. No undue
force should be applied at this stage. Entry into
the esophagus should be a voluntary effort sup-
plemented by a gentle push by the endoscopist.

Figure 1.6 Larynx, right and left pyriform

fossae (RPF & LPF, respectively) and the
esophageal inlet (arrow).
4 Atlas of diagnostic endoscopy

(a) (b)

Figure 1.7 (a) Concentric rings of trachea. (b) Tracheal bifurcation.

While negotiating the esophageal inlet, such an appearance indicates passage of the endoscope into
the trachea. The patient becomes restless and starts coughing violently. Withdraw the endoscope at
once. Reassure the patient and retry entering the esophagus after a while.

Figure 1.8 Tracheal impression (arrows) in the

proximal esophagus.

Esophageal mucosa is essentially featureless. The

tracheal impression can be seen in the proximal
esophagus. Aortic impression and pulsation can be
observed in the mid-esophagus.

Figure 1.9 Mid-esophagus.

 Techniques of UGI endoscopy and normal anatomy 5

(a) (b) (c)

(d) (e) (f )

Figure 1.10 (a–f) Z line: The squamocolumnar (gastroesophageal) junction.

Z line represents the junction of pale squamous epithelium of the esophagus with the pink colum-
nar epithelium of the stomach. This also marks the most proximal extent of the gastric folds. The
junction may not be quite apparent when it lies at the level of diaphragmatic indentation (arrow in
Figure 1.10a). In most cases, however, the junction can be made out clearly.

Figure 1.11 Gastric body. Figure 1.12 Junction of gastric body and antrum.

After crossing the GE junction, the tip of the endoscope is slightly angled up and to the right. As
the stomach is inflated, a tunnel (Figure 1.11) becomes apparent. The roof and the base of the tunnel
represent the lesser and greater curvatures, respectively. The endoscope is maintained close to the
lesser curvature and gradually pushed forward. The mucosal rugosity in the gastric body turns flat
marking the beginning of the antrum.
6 Atlas of diagnostic endoscopy

(a) (b) (c)

Figure 1.13 Pylorus. (a) Mucosal folds converging on the pylorus. (b) Mucosal folds around the
pylorus partially flattened out. (c) Antral mucosa completely flattened out revealing the circular
pylorus.

After inspecting the antrum, the endoscope is directed towards the pylorus. It is a common practice
to cross the pylorus, examine D1, D2 and then come back to the antrum and complete examination
of the remaining stomach. Crossing the pylorus is usually a frustrating experience for the beginner.
In our practice, we advise the trainee endoscopist to use intravenous hyoscine bromide (Buscopan)
to knock down gastric peristalsis, keep the pylorus in the center of vision, wait for the ring to open
and then attempt to negotiate it. However, after a few endoscopies (usually 8–10), it ceases to be an
issue and the endoscopist can cross the pylorus without much difficulty.

All the four walls of D1 are better visualized

when the tip of the endoscope is placed at the
pyloric ring (transpyloric view). Normally, the
D1 mucosa is featureless.

Figure 1.14 Transpyloric view of the duodenal

bulb (D1). The anterior wall (A), posterior wall
(P), superior wall (S) and inferior wall (I).

(a) (b) (c)

Figure 1.15 (a–c) Duodenal bulb.

 Techniques of UGI endoscopy and normal anatomy 7

(a) (b)

Figure 1.16 (a, b) The second part of the duodenum (D2) is marked by the circular mucosal folds.

The tip of the endoscope is impacted at the apex of D1 and rotated up and right. This maneuver
facilitates entry into D2. As the endoscope is withdrawn slightly, its tip slips further down into D3.
The ampulla of Vater can be seen on the medial wall of D2. This is the distal extent of examination
for routine UGI endoscopy.

(a) (b) (c)

Figure 1.17 (a–c) Ampulla of Vater (arrow) seen on the medial wall of D2.

The endoscope is now gradually withdrawn,

carefully examining all four walls of D2. The
junction of D1-D2 is better inspected at this
stage as the tip of the endoscope has a tendency
to slip down during forward examination.

Figure 1.18 Junction of D1 and D2.

8 Atlas of diagnostic endoscopy

(a) (b) (c)

Figure 1.19 (a, b) Antrum and pylorus. (c) Incisura angularis.

The endoscope is withdrawn into the antrum for examination of the remaining part of stomach. The
tip of the endoscope is flexed up, bringing into view the incisura angularis. In this position, the endo-
scope is gradually withdrawn maintaining constant insufflation and slight rotation to the left. By this
retroflexion, or “J” maneuver, the entire lesser curvature can be inspected as the fundus is approached.

(a) (b) (c)

Figure 1.20 (a–c) The gastric fundus, as it appears during retroflexion (“J” maneuver).

(a) (b)

Figure 1.21 (a, b) The gastric fundus and the GE junction.

Fluid tends to accumulate in the fundus as this is the most dependent part of the stomach dur-
ing endoscopy. This “fundic pool” needs to be sucked out to have a clear view of the mucosa. The
GE junction can be inspected from a close proximity by withdrawing and rotating the endoscope
further. Normally, the GE junction should appear snug around the shaft of the endoscope. This
completes the examination of the upper GI tract. The tip of the endoscope is rotated to the normal
position, air in the stomach is sucked out and the instrument is withdrawn.
 2
Esophageal webs, rings and
strictures

Webs and rings commonly present with dysphagia. Their appearance ranges from a thin, fibrous
membrane partially occluding the lumen, to well-formed, concentric, fleshy rings having all three
layers (i.e., mucosa, submucosa and muscles).

ETIOLOGY
●● Congenital
●● Iron-deficiency anemia (Plummer–Vinson syndrome, Paterson–Kelly syndrome)
●● Eosinophilic gastroenteritis
●● GERD
●● Tropical sprue
●● Autoimmune disorders
●● Idiopathic

Diagnosis of postcricoid webs/strictures may be technically difficult as these are obscured by the
cricopharyngeus. In such a situation, failure to intubate beyond the cricopharyngeus is often attrib-
uted by an inexperienced endoscopist to his own inefficiency or an uncooperative patient. When
suspected, the tip of the endoscope should be placed at the esophageal inlet and the patient is asked
to take swallows. The obstruction will be apparent when the cricopharyngeus opens transiently
during deglutition.

(a) (b) (c)

Figure 2.1 (a, b) Postcricoid web. The membrane occluding nearly two-thirds of the lumen
was evident just below the cricopharyngeal sphincter. The patient presented with anemia and
worsening of long-standing dysphagia. This could be explained as the endoscope was advanced
further. (c) Squamous cell carcinoma in the distal esophagus in the same patient.

9
10 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 2.2 (a–d) Postcricoid web. A thin, semitransparent membrane below the cricopharyngeal
sphincter. The membrane could be ruptured by gentle pushing with the tip of the endoscope.

(a) (b)

Figure 2.3 (a, b) Postcricoid web. A fleshy, concentric ring just below the cricopharyngeal
sphincter in an elderly woman who presented with anemia and mild dysphagia.
 Esophageal webs, rings and strictures 11

(a) (b)

(c) (d)

Figure 2.4 (a–c) Postcricoid rings. Multiple semicircular rings just below the cricopharyngeal
sphincter in a middle-aged man who presented with dysphagia. (d) Mucosal tear following
dilatation of the segment.

(a) (b)

(c) (d)

Figure 2.5 (a, b) Postcricoid ring. A fleshy, concentric ring just below the cricopharyngeal
sphincter in a middle-aged woman who presented with mild dysphagia. (c, d) The ring was
dilated with an endoscopic balloon.
12 Atlas of diagnostic endoscopy

(a) (b)

Figure 2.6 (a) Postcricoid membranous stricture in a middle-aged woman who presented with
long-standing dysphagia. (b) The affected segment after dilatation.

(a) (b)

(c) (d)

Figure 2.7 (a) Benign stricture in a young woman. Note the proximal one (black arrows) in the
mid-esophagus is wider and passable; the distal one (white arrow) is tighter. (b) A guidewire
across the distal stricture. (c) The distal stricture is being dilated with a balloon. (d) The same
after dilatation.
 Esophageal webs, rings and strictures 13

(a) (b)

Figure 2.8 (a, b) Schatzki’s ring. (c) Same as

seen on retroflexion of endoscope. Note the
(c)
associated hiatal hernia.

(a) (b) (c)

Figure 2.9 (a–c) Schatzki’s ring (arrows) with sliding hiatal hernia.

Schatzki’s ring is a well-demarcated circumferential stricture located at the squamocolumnar

­junction comprising mucosa and submucosa. This ring is more often an incidental finding, and
hiatal hernia is a universal accompaniment. Dysphagia, if present (when the ring is critically nar-
rowed), responds well to dilatation.
14 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

(e) (f )

Figure 2.10 (a–d) Schatzki’s ring at various stages of its appearance during endoscopy. (e, f)
The ring (arrow) inside the hiatal sac as seen on retroflexion.
 Esophageal webs, rings and strictures 15

(a)

(b)

(c) (d) (e)

Figure 2.11 Postcricoid ring and Schatzki’s ring. (a) Postcricoid ring in an elderly woman
presenting with mild dysphagia. (b) Close-up view of the same. (c) Schatzki’s ring (arrow)
with hiatal hernia in the same patient. (d) The ring (arrow) as seen through the hiatal sac on
retroflexion of the endoscope. (e) Close-up view of the same.
16 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 2.12 (a–c) Post-radiotherapy esophageal stricture in a patient with mid 1/3 squamous cell
carcinoma. (d) Same after dilatation.

(a) (b)

Figure 2.13 (a, b) Post-radiotherapy stricture in the mid-esophagus.

 Esophageal webs, rings and strictures 17

Figure 2.14 Post-sclerotherapy stricture at the lower end of esophagus. Esophageal varices
were treated with intra- and paravariceal alcohol injection. Obliterated varix appear as
mucosal tag.

Alcohol, in comparison with other sclerosants, has been associated with a higher incidence of stric-
ture formation.

Figure 2.15 Post-sclerotherapy stricture at the lower end of esophagus.

Esophageal strictures following corrosive injury and peptic esophagitis have been presented elsewhere.
 3
Hiatal hernia and gastroesophageal
reflux disease (GERD)

CLASSIFICATION OF HIATAL HERNIA

Type I: Sliding hiatal hernia – cardia in chest
Type II: Paraesophageal hernia – GE junction in normal
position, fundus in chest
Type III: Paraesophageal hernia – GE junction and fun-
dus of stomach in chest
Type IV: Intrathoracic stomach ± volvulus

Type I and type III are the commonest and second com-
monest variants, respectively.

Figure 3.1 Classification of hiatal

hernia.

(a) (b)

Figure 3.2 Sliding hiatal hernia.

SLIDING HIATAL HERNIA – ENDOSCOPIC DIAGNOSIS

●● Distance between the squamocolumnar junction and the diaphragmatic indentation (A & B
respectively in Figure 3.2) is >2 cm. Normally, it is <0.5 cm.
●● On retroflexion, the diaphragmatic indentation (black arrows in Figure 3.3) is not snug around
the endoscope. The “bell”-like appearance represents the hiatal sac. Gastric mucosa appears
drawn into the hiatal sac.

19
20 Atlas of diagnostic endoscopy

Figure 3.3 Sliding hiatal hernia; view on Figure 3.4 Lax lower esophageal sphincter (LES);
retroflexion. Note the diaphragmatic view on retroflexion. Note the squamocolumnar
indentation (black arrows) and the junction (arrows) is at the level of diaphragmatic
squamocolumnar junction (white arrows). indentation. This feature differentiates it from
sliding hiatal hernia despite the similarity in
appearance between the two.

(a) (b)

(c) (d)

Figure 3.5 Sliding hiatal hernia; view on retroflexion. (a) The diaphragmatic indentation (black
arrows) is not snug around the endoscope. The gastric mucosa has been pulled into the hiatal
sac. (b, c) The squamocolumnar junction (white arrows) is above the diaphragmatic indentation.
(d) Linear erosions in the esophageal mucosa stopping at the squamocolumnar junction.
 Hiatal hernia and gastroesophageal reflux disease (GERD) 21

(a) (b)

Figure 3.6 (a, b) Lax LES; View on retroflexion. Note the squamocolumnar junction (arrows) is
almost coinciding with diaphragmatic indentation.

(a) (b)

(c) (d)

Figure 3.7 Lax LES with sliding hiatal hernia and associated dysmotility. (a) Food debris at the
distal esophagus. The LES is open. (b–d) View on retroflexion.
22 Atlas of diagnostic endoscopy

Figure 3.8 Gastric mucosal prolapse through lax LES.

Figure 3.9 Sliding hiatal hernia and gastric mucosal prolapse.

(a) (b)

Figure 3.10 (a, b) Sliding hiatal hernia and gastric mucosal prolapse.
 Hiatal hernia and gastroesophageal reflux disease (GERD) 23

(a) (b)

(c) (d)

(e) (f )

Figure 3.11 Paraesophageal hernia (type II variant) with sliding hiatal hernia. (a) Sliding
component of hiatal hernia seen on forward view. (b–d) View on retroflexion. Note the
diaphragmatic margin (arrows). Note the diaphragmatic bridge (D) between two hiatal sacs.
(e) Close-up view of the sliding hernia sac (S) on retroflexion. Note the visible Z line and the lax
LES through which the esophageal body could be seen. (f) Close-up view of the paraesophageal
herniated fundus (P) on retroflexion.
24 Atlas of diagnostic endoscopy

ENDOSCOPIC GRADING OF
GERD
Savary Miller grading

Grade I
Oval or linear red patch situated above “Z”
line, often along a dorsal fold, may be cov-
ered with whitish exudate. Occasionally
many such lesions are present, but they are
not confluent.

Grade II
The erosive and exudative mucosal lesions
Figure 3.12 Oval erosions just above the Z line. are confluent but not involving the entire
circumference.

Grade III
Involvement of entire circumference but
stricturing is absent.

Grade IV
Presence of stricture or longitudinal short-
ening and/or the development of columnar
metaplasia.

Handbook & Atlas of Endoscopy,

Solothurn, Schweiz: Gasman 1978

Los Angeles grading

Figure 3.13 Reflux induced linear erosion. Grade A

One or more mucosal break(s) no longer
than 5 mm, that does not extend between the
top of two mucosal folds.

Grade B
One or more mucosal break(s) >5 mm long,
not extending between the tops of two muco-
sal folds.

Grade C
One or more mucosal breaks between the
top of two or more mucosal folds involving
<75% of the circumference.

Grade D
One or more mucosal break(s) involving at
Figure 3.14 Linear erosion. least 75% of the esophageal circumference.
Gut 1999; 45:172
 Hiatal hernia and gastroesophageal reflux disease (GERD) 25

(a) (b)

Figure 3.15 (a, b) Erosions in the distal esophagus.

(a) (b)

Figure 3.16 (a, b) Erosions and exudates at the GE junction.

(a) (b)

Figure 3.17 (a, b) Linear erosions at the GE junction.

26 Atlas of diagnostic endoscopy

Figure 3.18 Erosions extending up to the Figure 3.19 Erosion extending proximally.
mid-esophagus.

(a) (b)

Figure 3.20 (a, b) Linear ulcer extending from the GE junction to the proximal esophagus.

(a) (b) (c)

Figure 3.21 (a, b) Linear erosions. (c) Sliding hiatal hernia in the same patient.
 Hiatal hernia and gastroesophageal reflux disease (GERD) 27

(a) (b)

(c) (d)

Figure 3.22 (a–d) Erosions extending up to the squamocolumnar junction.

(a) (b)

Figure 3.23 (a, b) Sliding hiatal hernia. An ulcer at the six-o’clock position proximal to the
squamocolumnar junction.

(a) (b)

Figure 3.24 (a) Extensive ulceration involving the distal esophageal mucosa.
(b) Gastrojejunostomy stoma in the same patient showing small erosion (arrow).
28 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 3.25 (a, b) Esophagitis with sliding hiatal hernia. (c, d) View of the hernial sac on
retroflexion.

(a) (b) (c)

Figure 3.26 (a–c) Extensive esophageal involvement in GERD.

 Hiatal hernia and gastroesophageal reflux disease (GERD) 29

(a) (b)

(c) (d)

Figure 3.27 (a–c) Erosive esophagitis with sliding hiatal hernia. (d) View on retroflexion.

(a) (b) (c)

Figure 3.28 (a, b) Esophagitis with overlying exudates extending up to the mid-esophagus.
(c) A giant duodenal ulcer in the same patient.

(a) (b) (c)

Figure 3.29 (a, b) Erosive esophagitis. (c) Prepyloric ulcer with pseudo diverticulum in the same
patient.

Concomitant peptic ulcer is not unusual in patients suffering from severe esophagitis.
Hyperacidity is found in 28% of patients suffering from GERD.
Archives of Surgery 1989:124; 937.
30 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e) (f )

Figure 3.30 (a, b) Bile reflux esophagitis. Mucosal changes at the lower end of esophagus
in a patient who had undergone gastrojejunostomy about 10 years back. (c) Hiatal hernia
in the same patient. He was treated with Roux-en-Y conversion and partial fundoplication.
(d, e) Normal appearing esophageal mucosa, six months after the surgery. (f) Consequent upon
fundoplication, on retroflexion the gastric mucosa is seen tightly gripping the endoscope at the
cardia.

(a) (b) (c)

(d) (e) (f )

Figure 3.31 (a–c) Extensive ulceration involving distal esophagus. The patient underwent
Nissen’s fundoplication. (d, e) Endoscopy three months after surgery showing healed
esophageal ulcers. (f) Retroflexed view of the cardia subsequent to fundoplication.
 Hiatal hernia and gastroesophageal reflux disease (GERD) 31

(a)

(b)

(f )

(c) (d)

Figure 3.32 Peptic stricture (a) Fibrotic stricture at the squamocolumnar junction.
(b, c) Sliding hiatal hernia visible through the stricture. (d) Barium contrast study, in the same
patient, showing stricture (arrow) at the distal esophagus and proximal dilatation. Note the
diaphragmatic indentation (broken arrow) and the intervening hiatal sac.

Figure 3.33 Peptic stricture in distal esophagus.

32 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 3.34 (a, b) Peptic stricture (arrow) and sliding hiatal hernia. (c, d) Close-up view of the
stricture (arrow) on retroflexion showing fibrosis and nodularity.

(a) (b) (c)

Figure 3.35 (a) Peptic stricture involving distal esophagus. Note the diverticulum (arrow)
proximal to the stricture. (b, c) Sliding hiatal hernia in the same patient.

(a) (b)

Figure 3.36 (a, b) Peptic stricture and esophageal ulcers.

 Hiatal hernia and gastroesophageal reflux disease (GERD) 33

(a) (b)

Figure 3.37 (a, b) Barrett’s esophagus; flame-shaped extension of columnar epithelium into the
esophagus.

Barrett’s esophagus is a known complication of GERD. It

is characterized by a flame-shaped or finger-like exten-
sion of gastric columnar epithelium into the esophagus
that typically displays intestinal metaplasia. Depending
on the extent of involvement from the GE junction
(defined as the upper limit of visible gastric fold), it is clas-
sified as short-segment (<3 cm) or long-segment (>3 cm)
Barrett’s. However, endoscopic maximal (M) and circum-
ferential (C) extent of involvement in centimeters (Prague
C & M criteria) is the current recommendation to docu-
ment Barrett’s esophagus. Because of its premalignant
potential, four-quadrant biopsy, every 1–2 cm, and biopsy
of any suspicious lesion have been recommended to detect
dysplasia (Seattle protocol). Any visible lesion is char-
Figure 3.38 Short-segment Barrett’s acterized by the Paris classification. Mild and moderate
esophagus.
dysplasia are treated with conventional anti-reflux treat-
ment and kept under surveillance. High-grade dysplasia
is treated by endoscopic ablation or surgical excision.
Gastroenterology 2011; 140 e 18
Gastrointest Endosc 2003; 58 (suppl): 3

(a) (b)

Figure 3.39 (a, b) Barrett’s esophagus with sliding hiatal hernia.

34 Atlas of diagnostic endoscopy

Figure 3.40 Barrett’s esophagus. Figure 3.41 Barrett’s esophagus with

sliding hiatal hernia.

(a) (b)

(c) (d)

Figure 3.42 (a–c) Barrett’s esophagus with dysplastic nodule (arrow). (d) Associated sliding
hiatal hernia.
 Hiatal hernia and gastroesophageal reflux disease (GERD) 35

Figure 3.43 Barrett’s mucosal island just Figure 3.44 Barrett’s esophagus. Note the
above the Z line. finger-like projections as well as the island of
columnar epithelium.

Table 3.1 Surveillance protocol for Barrett’s esophagus

ASGE ACG AGA

Screening No Barrett’s in suspected Chronic GERD in age White male >50 y with
patients; no further >50 y GERD
screening required
No dysplasia Repeat endoscopy at 1 y Repeat endoscopy and Repeat endoscopy and
and every 3rd year every 3rd year every 5 y thereafter
thereafter. thereafter.
Low-grade Endoscopy every year Endoscopy every year Confirmed by two
dysplasia pathologists;
endoscopy every year,
otherwise every 2 y
High-grade Confirm biopsy; repeat Confirm biopsy; repeat Confirm biopsy; repeat
dysplasia endoscopy to exclude endoscopy to endoscopy to exclude
malignancy; exclude malignancy; malignancy; intensive
endoscopic ablation/ endoscopic ablation/ surveillance/
surgical excision surgical excision endoscopic ablation/
surgical excision
Abbreviations: ACG, American College of Gastroenterology; AGA, American Gastroenterological Association;
ASGE, American Society for Gastrointestinal Endoscopy.
 4
Motility disorders of the esophagus

(a) (b)

Figure 4.1 Achalasia cardia. (a) Dilated esophagus with food residue. (b) Non-relaxing lower
esophageal sphincter (LES).

Endoscopic features of achalasia cardia include dilated and tortuous esophagus containing food
residue. The LES initially offers resistance to the passage of the endoscope but “gives in” with mild
force. The most important aspect of endoscopy, however, is detection of esophageal malignancy
consequent upon long standing achalasia. It is also important to exclude secondary achalasia that
arises from submucosal infiltration of the GE junction by adjacent malignancy. In the latter situa-
tion, considerable force is required to negotiate the endoscope across the LES. Once in the stomach,
it is mandatory to retroflex and have an optimal view of the GE junction.

(b) (c)

(a) (d) (e)

Figure 4.2 Achalasia cardia. (a) Barium-contrast study showing dilated and tortuous esophagus
with “bird-beak” tapering. (b, c) Absent peristalsis resulting in food bolus impaction in the
mid-esophagus. (d) Appearance of the distal esophagus after removal of the food bolus.
(e) Non-relaxing LES.

37
38 Atlas of diagnostic endoscopy

(b)

(a)
(c)

Figure 4.3 (a) Barium-contrast study

showing dilated esophagus and epiphrenic
diverticulum (arrow) in a young woman
with achalasia cardia. (b) Dilated distal
esophagus. (c) Diverticulum (arrow).
(d) (d) Non-relaxing LES.
 5
Benign gastric ulcer

Figure 5.1 Ulcer just below the GE junction (arrow) seen on retroflexion.

Figure 5.2 A giant ulcer below the GE junction seen on retroflexion.

Based on the location, gastric ulcers are categorized into four types. I: ulcer located on the lesser
curve, II: associated with duodenal ulcer, III: prepyloric ulcer, IV: ulcer just below GE junction.
Types II and III ulcers are associated with hyperacidity and behave as a duodenal ulcer with respect
to symptomatology and treatment. Multiple ulcers are seen in association with NSAID use, chronic
liver disease, heavy smokers or acute viral infection. Ulcers located high on lesser curvature are
likely to be missed during forward passage of the endoscope and are best viewed on retroflexion.

39
40 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

(e) (f )

Figure 5.3 (a) Ulcer on the lesser curve (arrow) seen while entering the stomach. (b–d) Close-up
view. (e, f) View on retroflexion. The patient presented with hematemesis and melena. Note the
ulcer base showing stigmata of recent hemorrhage.
 Benign gastric ulcer 41

(a) (b)

(c) (d)

Figure 5.4 (a–d) Ulcer (arrow) high on the lesser curve as seen on retroflexion.

(a) (b)

(c) (d)

Figure 5.5 (a–d) Extensive ulceration involving proximal stomach. The patient, a known case of
hepatitis, presented with hematemesis.
42 Atlas of diagnostic endoscopy

(a) (b)

Figure 5.6 (a, b) Ulcer (arrow) in the body of the stomach. Such ulcer is likely to get hidden
between the gastric folds. Adequate distention is required for its visualization.

(a) (b)

(c) (d)

Figure 5.7 (a–d) Ulcer in the gastric body at various stages of its appearance during endoscopy.
Note the flat red spot, suggesting a recent episode of bleeding.
 Benign gastric ulcer 43

(a) (b) (c)

(d) (e) (f )

Figure 5.8 Endoscopy in an elderly man presenting with pain in the abdomen and retention
vomiting. (a) Retention esophagitis. (b–e) A giant ulcer on the incisura. (f) Another superficial
ulcer in the prepyloric region. The pylorus is deformed and narrowed. Note the gastric retention
in (c).

(a) (b)

Figure 5.9 (a, b) Ulcer on the incisura. Note another small ulcer (arrow) below it.
44 Atlas of diagnostic endoscopy

Figure 5.10 Ulcer on the incisura having flat Figure 5.11 Ulcer on the incisura having flat
red spots suggestive of recent hemorrhage. red spot.

Figure 5.12 Ulcer (arrow) in the antrum Figure 5.13 Ulcer on the incisura covered with
hidden by the blood pool. Note the distorted acid hematin.
pylorus (broken arrow).

(a) (b)

Figure 5.14 (a) Giant ulcer on the incisura with adherent clot. (b) Same ulcer one week later.
Though partial healing was evident, the patient presented with bleeding recurrence.
 Benign gastric ulcer 45

Figure 5.15 Oozing ulcer in the prepyloric Figure 5.16 Ulcer in the prepyloric antrum
antrum. having a visible vessel.

Figure 5.17 Multiple ulcers on the incisura Figure 5.18 Ulcer in the antrum with a clean
covered with acid hematin. base.

(a) (b)

Figure 5.19 (a, b) Giant prepyloric ulcer.

46 Atlas of diagnostic endoscopy

(a) (b)

Figure 5.20 (a, b) Prepyloric ulcers, erosions and pseudodiverticulum.

(a) (b)

Figure 5.21 (a, b) Prepyloric ulcer (arrows) hidden in the mucosal folds. Unless the endoscopist
is careful, such an ulcer may elude detection.

(a) (b)

Figure 5.22 (a, b) Multiple prepyloric ulcers (arrows).

 Benign gastric ulcer 47

(a) (b)

(c) (d)

Figure 5.23 (a, b) Ulcers on either side of the pylorus. (c, d) Close-up view of the ulcers.

(a) (b)

Figure 5.24 (a, b) Giant prepyloric ulcer showing recent evidence of bleeding.
48 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e) (f )

Figure 5.25 Multiple prepyloric ulcers in a patient with chronic liver disease. (a) Esophageal
varices. (b, c) Giant ulcers around pylorus (arrow). (d) Close-up view of the ulcer at the nine-o’clock
position. (e) Ulcer at the 12-o’clock position. (f) Superficial ulcer (arrow) in the duodenal bulb.

Figure 5.26 Multiple superficial ulcers in the Figure 5.27 Prepyloric ulcer.
antrum.

(a) (b)

Figure 5.28 (a, b) Prepyloric ulcer.

 Benign gastric ulcer 49

(a) (b)

(c) (d)

Figure 5.29 (a) Multiple prepyloric ulcers (1, 2, 3). (b–d) Close-up view of ulcer 3. Note the
adherent clot suggestive of recent bleeding.

(a) (b) (c)

Figure 5.30 (a, b) Giant ulcer on incisura with adherent clot. (c) Concomitant duodenal ulcer
(arrows).
50 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e) (f )

Figure 5.31 (a–f) Multiple ulcers (arrows) involving the antrum.

(a) (b) (c)

(d) (e) (f )

Figure 5.32 Multiple gastric and duodenal ulcers.

(a, b) Ulcers in the antrum. (c) Close-up view of the ulcer at the
two-o’clock position. (d) Ulcers in the prepyloric antrum. Note
the deformed pylorus and the duodenal ulcer seen through
it. (e) The duodenal ulcer appearing black due to presence of
(g)
acid hematin. (f, g) Close-up view of the duodenal ulcer.
 Benign gastric ulcer 51

Figure 5.33 Prepyloric ulcer.

Figure 5.34 Pyloric channel ulcer (arrow).

(a) (b)

Figure 5.35 (a, b) Pyloric channel ulcer with evidence of recent bleeding.
52 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

(e) (f )

(g) (h)

Figure 5.36 (a) Deformed pylorus (black arrow) and a giant prepyloric ulcer covered with altered
blood (white arrow). (b–d) Close-up view of the same ulcer (white arrow) after the blood was
cleaned. (e–g) Severe reflux esophagitis in the same patient. Entire esophagus covered with
thick exudates. (h) The exudates forming a membrane in the upper esophagus.
 Benign gastric ulcer 53

(a) (b) (c)

(d) (e) (f )

Figure 5.37 Hour-glass contracture of the stomach. (a) Multiple ulcers with cicatrization
(arrows) causing circumferential narrowing in the gastric body. (b) Ulcers (arrows) are better
seen on retroflexion. (c) Antrum, relatively healthy. (d–f) Ulcer healing and scarring (broken
arrow) evident after treatment with proton pump inhibitors for eight weeks. Note the mucosal
hypertrophy that could have resulted from obstruction as well as hyperacidity. The patient was a
chronic smoker.

(a) (b)

Figure 5.38 (a, b) Benign gastric outlet obstruction. Scarred and stenotic pylorus consequent
upon ulcer healing.
54 Atlas of diagnostic endoscopy

(a)

(b)

Figure 5.39 (a, b) Deformed pylorus with prepyloric pseudodiverticulum (arrow). Deformed
duodenal bulb can be seen through the pyloric ring.

(a) (b)

Figure 5.40 (a, b) Deformed and narrowed pylorus following ulcer healing.
 6
Chronic duodenal ulcer

Figure 6.1 Duodenitis. Erythematous patches involving duodenal bulb (D1).

(a) (b)

Figure 6.2 (a, b) Duodenitis with superficial ulcer (arrow) in D1.

55
56 Atlas of diagnostic endoscopy

Figure 6.3 An active ulcer on the anterior wall of D1.

(a) (b)

Figure 6.4 (a, b) Deformed duodenal bulb, multiple superficial ulcers and pseudodiverticula.

(a) (b)

Figure 6.5 (a, b) Chronic duodenal ulcer. Ulcer with a clean base present on the anterior wall.
Note the deformed bulb and the pseudodiverticula.

Endoscopic features of chronic duodenal ulcer

●● Deformity
●● Scarring
●● Pseudodiverticulum (outpouching of the mucosa)
●● Luminal narrowing

Giant duodenal ulcer is defined as an ulcer with a diameter of more than 2 cm.
 Chronic duodenal ulcer 57

(a) (b)

Figure 6.6 (a, b) Deformed duodenal bulb, ulcers (arrows) on the anterior wall and
pseudodiverticula.

Figure 6.7 Ulcer (arrows) extending Figure 6.8 A healing ulcer on the anterior
across the pylorus into the posterior wall wall of D1.
of duodenum.

(a) (b)

Figure 6.9 (a, b) Ulcer on the posterior wall extending from the pylorus.
58 Atlas of diagnostic endoscopy

(a) (b)

Figure 6.10 (a, b) A deep ulcer on the anterior wall of D1.

(a) (b)

Figure 6.11 (a, b) Deformed duodenal bulb and an active ulcer on the anterior wall.

(a) (b)

Figure 6.12 (a, b) A giant ulcer on the anterior wall of D1.

 Chronic duodenal ulcer 59

(a) (b)

Figure 6.13 (a, b) “Kissing ulcers” on the superior (white arrow) and inferior wall (black arrow) in D1.

(a) (b)

Figure 6.14 (a, b) Giant “kissing ulcers” in D1. Note the ulcer on the inferior wall (arrow).

(a) (b)

Figure 6.15 (a, b) Multiple ulcers (arrows) in D1.

60 Atlas of diagnostic endoscopy

(a) (b)

Figure 6.16 (a, b) Duodenal bulb showing extensive ulceration and Brunner’s gland hyperplasia.

Figure 6.17 Ulcer with surrounding edema in D1. Figure 6.18 Multiple superficial ulcers in D2.

(a) (b)

Figure 6.19 (a, b) Multiple erosions involving D2.

 Chronic duodenal ulcer 61

Complications of duodenal ulcer Endoscopic stigmata of ulcer bleeding

●● Acute ●● High risk

●● Bleeding ●● Spurting pulsatile bleeding

●● Perforation ●● Oozing ulcer base
●● Chronic ●● Visible vessel
●● Gastric outlet obstruction ●● Adherent clot
●● Bilioduodenal fistula/bile duct ●● Low risk

stricture ●● Flat pigmented/red spot

●● Clean ulcer base

(a) (b) (c)

Figure 6.20 (a) Spurting bleeding from the ulcer base (arrow) in D1. (b) Bleeding was controlled
by injecting adrenaline and saline into the ulcer base. (c) Visible vessel (arrow) in the ulcer base
as seen 48 h later.

(a) (b)

(c) (d)

Figure 6.21 (a) Actively oozing ulcer in D1. (b) The ulcer base was injected with adrenaline:saline
1: 10,000. (c, d) Ulcer base as seen after endoscopic control of bleeding.
62 Atlas of diagnostic endoscopy

Figure 6.22 “Visible vessel” in the ulcer base. Figure 6.23 Ulcer and the “visible vessel”
(arrow).

(a) (b)

Figure 6.24 (a, b) “Visible vessel” (arrow) in an otherwise clean ulcer base.

(a) (b)

Figure 6.25 (a, b) “Visible vessel” covered with fresh clot.

 Chronic duodenal ulcer 63

Figure 6.26 “Visible vessel” accentuated Figure 6.27 Ulcer on the anterior wall covered
by adherent clot. with clot.

(a) (b)

Figure 6.28 (a, b) Ulcer on the anterior wall completely covered with a fresh clot.

(a) (b)

Figure 6.29 (a) A deep ulcer partially covered with clot. (b) Same ulcer eight days later. The clot
has been replaced by a “flat red spot.”
64 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 6.30 (a, b) Giant duodenal ulcer with “flat red spot” (arrow) in the center.
(c, d) Appearance 24 h later.

(a) (b)

Figure 6.31 (a–b) Ulcer on the antero-superior wall of D1 showing a perforation (arrow)
in the center.(Continued)
 Chronic duodenal ulcer 65

(c) (d)

Figure 6.31 (Continued) (c–d) Ulcer on the antero-superior wall of D1 showing a perforation
(arrow) in the center.

(a) (b)

(c) (d)

Figure 6.32 (a) Deformed duodenal bulb showing accumulation of bilio-purulent fluid.
(b–d) A perforated ulcer (arrow) was seen lying below the fluid.

Suspected perforation is an absolute contraindication for endoscopy. In both of the above cases, clini-
cal signs and symptoms were misleading, suggesting acute exacerbation of duodenal ulcer only.
66 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 6.33 Duodenal stenosis: (a) Food residue in the antrum and (b) fundus. (c) Deformed
duodenal bulb and the pinhole opening (arrow) seen through pylorus. (d) Duodenal bulb. Note
the pseudodiverticulum (broken arrow) and the pinhole opening (arrow) at its center.

(a) (b) (c)

(d) (e) (f )

Figure 6.34 (a–c) Deformed duodenum with bilioduodenal fistula (arrow). (d–f) Multiple
superficial ulcers (arrow) in the gastric antrum in the same patient. Possibly, the fistula was
secondary to duodenal ulcer penetration. Though no active ulcer was noted in D1, the
deformed duodenum indicated its earlier existence.
 Chronic duodenal ulcer 67

(a) (b) (c)

Figure 6.35 (a) Choledochoduodenal fistula. Bile was seen pooling in D1 through a tiny opening
at the (arrow) apex. (b) Cannulation and injection of contrast opacified the common bile duct.
(c) Opacification of proximal biliary tree confirms presence of bilioduodenal fistula. Distal biliary
tree did not opacify because of stricture at the fistula site.

(a) (b) (c)

(d) (e) (f )

Figure 6.36 Choledochoduodenal fistula. (a) Deformed D1. An ulcer (arrow) was seen on the
superior wall. (b) Close-up view of the ulcer (arrow) revealed a tiny opening (broken arrow) in its
base exuding bile. (c–f) Further inspection of the opening (broken arrow) confirmed it to be the
bile duct.
68 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e) (f )

(i)
(g) (h)

(j) (k) (l)

Figure 6.37 Giant choledochoduodenal fistula. (a) Deformed D1. Note the pseudodiverticulum
(white arrow), an ulcer (broken arrow) and the passage (arrow) to D2. (b) Normal looking D2.
(c–e) Pseudodiverticulum (arrow) and closer view of the ulcer (broken arrow). (f) Probing
the medial wall of the ulcer led to an oblong opening. (g–i) Close-up view of the opening
suggested it to be a part of the bile duct wall having superior and inferior ends (broken white
arrows). (j) The bile duct mucosa was quite distinct in its appearance. (k) The superior opening
of the bile duct was cannulated and contrast injected. (l) This opacified the proximal biliary tree,
confirming the presence of a large choledochoduodenal fistula.
 Chronic duodenal ulcer 69

(a) (b)

Figure 6.38 (a, b) Deformed D1 with pseudodiverticula following healed duodenal ulcer.

(a) (b)

Figure 6.39 (a, b) Deformed D1 with pseudodiverticula and superficial ulcers.

(a) (b) (c)

Figure 6.40 (a) Deformed D1 and pseudodiverticuli seen through the pylorus. (b) Closer view of
the D1. (c) Close-up view of one of the diverticuli.
 7
Gastrojejunostomy

Peptic ulcer surgery accounted for the majority of the cases of gastrojejunostomy (GJ) in the past.
With the sharp decline in the incidence of elective surgery for peptic ulcer, the major indication for
GJ in the present time is gastric outlet obstruction and partial gastrectomy for various causes. Both
early as well late complications of GJ are best evaluated by endoscopy. It is imperative to enter and
inspect both the afferent as well as the efferent loop for any pathology.

Figure 7.1 Normal gastrojejunostomy (GJ) stoma. The efferent loop opening is clearly seen
(straight arrow). The afferent loop opening is hidden below the gastric mucosa (curved arrow).

Figure 7.2 GJ stoma. Figure 7.3 GJ stoma along the greater

curvature.

71
72 Atlas of diagnostic endoscopy

(a) (b)

Figure 7.4 (a, b) GJ stomal edema. Note the silk suture and the ulceration along the suture line.

(a) (b)

(c) (d)

Figure 7.5 Stomal edema. (a, b) The GJ stoma is obscured by the two lips of the edematous
jejunal mucosa. (c) The afferent loop (arrow head) and the efferent loop (arrow) openings were
identified by gentle manipulation. (d) Close-up view of the efferent loop opening.

Endoscopy in the early postoperative period is fraught with the risk of suture line dehiscence.
This is can be minimized by adhering to the following principles:

●● Should be performed by an experienced endoscopist only.

●● Use minimal distention and force.
●● Proceed only if lumen is visible.
●● Avoid entering too much into afferent or efferent loops.
 Gastrojejunostomy 73

(a) (b)

Figure 7.6 (a, b) Stomal ulcer around a silk suture.

(a) (b)

Figure 7.7 (a, b) Stomal ulcer close to efferent loop opening (black arrow). Multiple erosions
involving jejunal mucosa (white arrows).

(a) (b)

Figure 7.8 (a, b) Giant stomal ulcer (arrow).

74 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 7.9 (a) Small GJ stoma in the body of

the stomach. (b) A closer look shows presence
of an ulcer (arrow). (c, d) Close-up view of the
same ulcer on the gastric mucosal aspect of
the stoma. (e) The hypertrophic scar on the
abdominal wall of the patient. The unusually
small scar suggested it to be possibly a case
of GJ “without” vagotomy. The patient indeed
had both vagi intact for which he underwent
(e) laparoscopic truncal vagotomy.
 Gastrojejunostomy 75

Figure 7.10 GJ stomal ulcer bleeding. A fresh Figure 7.11 Stomal ulcer bleeding. “Flat red
clot covering the ulcer. spot” on the ulcer surface suggested recent
hemorrhage.

(a) (b) (c)

(d) (e) (f )

Figure 7.12 (a–f) Gastrojejunocolic fistula. Note the grossly ulcerated stoma and the feculent
contents of the efferent loop.
76 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 7.13 Gastrojejunocolic fistula. (a–c) Fistulous opening by the side of the GJ stoma
containing fecal matter. (d) Colonoscopy in the same patient showing two openings in the
transverse colon. The lower one was communicating with the stomach. Note staining of the
fistulous tract with methylene blue that the patient was made to drink during colonoscopy to
confirm the communication.

(a) (b)

(c) (d)

Figure 7.14 Gastrojejunocolic fistula. (a) Feculent contents in the stomach. Note the efferent
loop opening (arrow). (b) A close-up view of the efferent loop opening shows two passages.
(c) Entry through one of them (white arrows) led to the jejunal lumen. (d) Entry through the
other one (black arrow) revealed triangular mucosal folds and fecal matter, suggesting colonic
lumen, thus confirming presence of gastrojejunocolic fistula.
 Gastrojejunostomy 77

Endoscopic diagnosis of gastrojejunocolic fistula is

made on the following findings:
●● Feculent contents in the gastric lumen.
●● Grossly ulcerated stoma.
●● Visualization of colon while manipulating the
endoscope through the openings in the stoma.
●● Manipulation of the colonoscope in the transverse
colon may bring into view jejunal or gastric lumen.
●● Chromocolonoscopy: With the colonoscope in
(a) the transverse colon, the patient is asked to drink
methylene blue dye. Prompt appearance of the dye
in the colon confirms presence of a fistula between
the stomach and the colon.
Tropical Gastroenterology 2001: 22; 221

(b) (c) (d)

Figure 7.15 Gastrojejunocolic fistula.

(a) Unhealthy GJ stoma with feculent contents.
Colonoscopy was performed in the same
patient. (b) Jejunal mucosa was visualized as the
colonoscope was manipulated in the transverse
colon. (c) Gastric mucosa was seen next. This
was confirmed by asking the patient to drink
methylene blue, which was seen pooling in
the stomach. (d) Pylorus was also visualized
during the same study. (e) Specimen after en
block resection, showing stomach (S), jejunal
(J), colonic (C) segments and the fistulous
(e) communication, marked by the artery forceps.
78 Atlas of diagnostic endoscopy

(a) (b)

Figure 7.16 (a, b) Retrograde jejunogastric intussusception. This was an incidental finding in a
patient who underwent endoscopy for dyspeptic symptoms.

(a) (b)

(c) (d)

Figure 7.17 (a–d) Retrograde jejunogastric intussusception.

Retrograde jejunogastric intussusception is a relatively uncommon complication of gastrojejunos-

tomy. Efferent loop intussusception is more frequent than afferent loop. The usual presenting fea-
tures are pain, coffee-ground vomiting and an ill-defined lump in the epigastrium. Diagnosis is
confirmed on endoscopy. Early surgery is indicated to prevent strangulation of the jejunal segment.
 Gastrojejunostomy 79

(a) (c)

(b) (d)

Figure 7.18 (a–b) Retrograde jejunogastric intussusception. (c) Abdominal ultrasonography

showing a circular hyperechoic mass (arrow) inside stomach – the “‘target sign.” (d) Operative
photograph showing transmesocolic afferent loop (arrow) and the intussuscepted efferent loop
(broken arrow).

(a) (b)

Figure 7.19 (a, b) Retrograde jejunogastric intussusception. Jejunal loop congested and
pregangrenous.

(a) (b)

Figure 7.20 (a, b) Retrograde jejunogastric intussusception. Note the gangrenous jejunal loop.
80 Atlas of diagnostic endoscopy

(a) (b)

Figure 7.21 (a, b) Bile reflux gastritis. Note the sharply demarcated gastric mucosa because of
the inflammation.

(a) (b)

(c) (d)

Figure 7.22 (a, b) Inflammatory polyp close to the efferent loop opening in a patient with
severe bile reflux gastritis. (c, d) Another polyp close to the afferent loop opening. The patient
presented with recurrent anemia.
 Gastrojejunostomy 81

(a) (b)

Figure 7.23 (a, b) Inflammatory polyps at the GJ stomal margin.

(a) (b)

(c) (d)

Figure 7.24 (a–d) Recurrence of malignancy at the GJ stomal site in a patient who had
undergone subtotal gastrectomy for carcinoma two years back.
 8
Benign tumors

Gastrointestinal stromal tumor (GIST) is the commonest non-epithelial tumor of the GI tract. It arises
from the interstitial cells of Cajal, a part of the autonomic nervous system located in the muscular
propria. The stomach is the commonest site of its occurrence, followed by the small bowel, the esopha-
gus and the colorectum. It commonly presents with bleeding. Mucosal biopsy is usually non-yielding;
deeper biopsy may be required for diagnosis. The presence of spindle cells points to the diagnosis of
GIST that is further confirmed on positive immunohistology for CD 117 (c-kit). Surgical excision is
the preferred treatment. Tumor size <2 cm and a mitotic index <5/50 HPF suggest a low risk tumor.

(a)

(b)

Figure 8.1 (a, b) GIST at the lower end of the esophagus. This was an incidental finding on
endoscopy for dyspepsia.

83
84 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 8.2 (a–d) Sentinel polyp. Inflammatory polyp at the GE junction. This is more often an
incidental finding on endoscopy.

Figure 8.3 Inflammatory polyp at the GE junction.

 Benign tumors 85

(a) (b)

Figure 8.4 (a, b) Bleeding inflammatory polyp at the GE junction.

(a) (b)

(c) (d)

Figure 8.5 (a–c) Sliding hiatal hernia with inflammatory mucosal polyp, at various stages of its
appearance during endoscopy. (d) The same polyp, prolapsing below the GE junction, was seen
on retroflexion. Note the central ulceration.
86 Atlas of diagnostic endoscopy

(a) (b)

Figure 8.6 (a, b) GIST in the gastric fundus.

(a) (b)

(c) (d)

Figure 8.7 (a, b) GIST in the gastric body. (c) Tumor as seen on gastrotomy. Note the ulcerated
center, the site of bleeding in this patient. (d) Bisected tumor after excision.
 Benign tumors 87

(a) (b)

(c) (d)

Figure 8.8 (a–c) GIST with ulcerated surface in the gastric body. (d) Tumor after excision.

(a) (b)

Figure 8.9 (a) GIST in the gastric fundus. (b) Tumor after excision.
88 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 8.10 Multiple adenomatous polyps in (a) the gastric antrum, (b) the prepyloric region
and (c, d) D2

Figure 8.11 Multiple inflammatory polyps in Figure 8.12 Inflammatory polyps in the
the fundus. antrum.
 Benign tumors 89

Figure 8.13 Prepyloric submucosal polyp. Figure 8.14 Prepyloric inflammatory polyp.

(a) (b)

Figure 8.15 (a, b) Inflammatory polyp obstructing pylorus.

(a) (b)

Figure 8.16 (a, b) An inflammatory polyp arising from the pyloric ring. The patient presented
with recurrent hematemesis and melena.
90 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e)

(f )

Figure 8.17 (a–d) Hamartomatous polyp arising from the pyloric ring. The polyp had multiple
finger-like projections converging on a single stalk. (e) The polyp during surgical excision.
(f) The stalk (arrow) after excision. The polyp was an incidental detection in an elderly man who
underwent endoscopy for dyspepsia.

(a) (b)

Figure 8.18 (a, b) GIST at the junction of D1 and D2.The patient presented with recurrent
melena.
 Benign tumors 91

(a) (b)

Figure 8.19 (a) GIST in the second part of the duodenum. (b) Pancreaticoduodenectomy
specimen showing the ulcerated tumor (broken arrow). Note the position of ampulla of Vater
(arrow). The patient, a middle-aged man, presented with recurrent episodes of melena.

Figure 8.20 Submucosal lipoma at the apex Figure 8.21 Villous adenoma in D2.
of D1.
92 Atlas of diagnostic endoscopy

(a) (b)

Figure 8.22 (a, b) Villous adenoma completely filling the D2 lumen. The patient, a middle-aged
woman, presented with anemia and retention vomiting.

Figure 8.23 Lymphoid hyperplasia in D2. Figure 8.24 Ulcerated stalk in D2.The patient
presented with bleeding 10 days after snare
polypectomy.
 9
Malignant tumors

(a) (b)

Figure 9.1 (a, b) Ulcero-proliferative squamous cell carcinoma in the mid-esophagus.

(a) (b)

Figure 9.2 (a, b) Squamous cell carcinoma in the mid-esophagus. Note the impacted food
debris (whitish material).

(a) (b)

Figure 9.3 (a, b) Squamous cell carcinoma, ulcerated tumor.

93
94 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 9.4 (a–d) Squamous cell carcinoma in the mid-esophagus.

(a) (b) (c)

(d) (e) (f )

Figure 9.5 (a–c) Squamous cell carcinoma involving the mid-esophagus. (d) Distal tumor-free
lumen with guidewire in place. (e, f) Self-expandable metal prosthesis across the tumor.
 Malignant tumors 95

(a) (b) (c)

Figure 9.6 (a–c) Self-expendable metal stent across an inoperable tumor in the mid-esophagus.

(a) (b)

(c) (d)

Figure 9.7 (a, b) Self-expandable metal stent

across a malignant tumor. (c–e) The stent
(e) coated with food particles, as seen 48 h later.
96 Atlas of diagnostic endoscopy

Figure 9.8 Early carcinoma in the distal esophagus.

(a) (b)

Figure 9.9 (a, b) Small polyp at the Z line. Clinically, the polyp was thought to be inflammatory
(sentinel polyp); biopsy revealed in situ carcinoma.
 Malignant tumors 97

(a) (b)

(c) (d)

Figure 9.10 (a–c) Adenocarcinoma at the lower end of the esophagus. (d) View on retroflexion
showing extension of the tumor into the stomach.

(a) (b) (c)

(d) (e) (f )

Figure 9.11 (a–c) Adenocarcinoma at the GE junction with accumulated food debris. (d–f) View
after removal of the food debris. Increased circumferential involvement distally.
98 Atlas of diagnostic endoscopy

(a) (b) (c) (d)

Figure 9.12 (a, b) Adenocarcinoma at the GE junction. (c, d) View on retroflexion.

(a) (b) (c)

Figure 9.13 (a–c) Ulcerated tumor at the GE junction; view on retroflexion.

(a) (b) (c)

Figure 9.14 (a–c) Adenocarcinoma at the GE junction. The tumor extension into the stomach as
seen on retroflexion.
 Malignant tumors 99

Figure 9.15 Ulcerated tumor involving the gastric Figure 9.16 Polypoidal tumor filling the
fundus. entire fundus.

(a) (b)

Figure 9.17 (a, b) Polypoidal adenocarcinoma below the GE junction.

(a) (b)

Figure 9.18 (a, b) Bleeding polypoidal tumor in the fundus.

100 Atlas of diagnostic endoscopy

(a) (b)

Figure 9.19 (a) Giant ulcer with necrotic base involving lesser curve. Endoscopic biopsy was
negative for malignancy; hence the patient was treated with proton pump inhibitors alone.
(b) Partial healing was apparent on repeat endoscopy about six weeks later. But the biopsy from
the ulcer margin this time revealed evidence of carcinoma.

Malignant ulcers may also show signs of healing on conservative management. Strict follow-up to
demonstrate complete healing and repeated biopsies are mandatory to exclude malignancy.

(a) (b)

Figure 9.20 (a, b) Malignant ulcer involving the lesser curve and incisura.
 Malignant tumors 101

(a) (b)

(c) (d)

Figure 9.21 (a–d) Tumor (arrow) involving the distal body and antrum.

(a) (b) (c)

Figure 9.22 (a–c) Ulcero-

proliferative growth
involving the gastric body.
(d, e) Circumferential
(d) (e) involvement distally.
102 Atlas of diagnostic endoscopy

(a) (b) (c)

Figure 9.23 (a–c) Ulcerated tumor starting from the incisura to the pylorus (arrow).

(a) (b) (c)

Figure 9.24 (a–c) Ulcerated tumor involving the incisura and the lesser curvature. View on
retroflexion.

(a) (b)

(c) (d)

Figure 9.25 (a–d) Tumor involving the antrum and the pylorus.
 Malignant tumors 103

(a) (b)

(c) (d)

Figure 9.26 (a–d) Circumferential tumor around the pylorus.

(a) (b)

Figure 9.27 (a, b) Ulcerated tumor around the pylorus

104 Atlas of diagnostic endoscopy

Figure 9.28 Polypoidal tumor in the Figure 9.29 Ulcerated tumor around the
antrum. pylorus.

Figure 9.30 Polypoidal tumor around the Figure 9.31 Ulcerated tumor with elevated
pylorus. margin around the pylorus.

(a) (b)

Figure 9.32 (a, b) Superficial spreading carcinoma involving the body and antrum.
 Malignant tumors 105

(a) (b)

(c) (d)

Figure 9.33 (a–d) Linitis plastica; pangastric involvement.

(a) (b)

(c) (d)

Figure 9.34 (a) Tumor in the gastric antrum extending into (b) the duodenal bulb.
(c, d) Synchronous tumor in the second part of duodenum in the same patient.
106 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 9.35 Metachronous secondary from a malignant pituitary tumor involving (a, b) the
gastric body, (c) the duodenal bulb, (d) D2. The patient, a young man, had undergone excision
of prolactinoma four years back.

(a) (b)

(c) (d) (e)

Figure 9.36 Duodenal carcinoma. (a) Normal-appearing pyloric mucosa with evidence of
submucosal infiltration. (b) Infiltrated pylorus. (c, d) Tumor involving D1. (e) Tumor abruptly
stopping at the junction of D1 and D2.
 Malignant tumors 107

(a) (b)

Figure 9.37 (a, b) Polypoidal tumor (adenocarcinoma) in D1. The patient, a 21-year-old man,
presented with hematemesis.

(a) (b)

Figure 9.38 (a, b) Multiple submucosal polyps in D1. A deep mucosal biopsy was suggestive
of neuroendocrine tumor (NET). The patient, a 52-year-old woman, presented with upper
abdominal pain.

Figure 9.39 Ampullary carcinoma.

108 Atlas of diagnostic endoscopy

Figure 9.40 Circumferential involvement of D2 Figure 9.41 Duodenal infiltration by renal cell
secondary to pancreatic head carcinoma. carcinoma.
 10
Portal hypertension

CONN’S GRADING
Grade I: Small varices detectable only on performance of
Valsalva maneuver.
Grade II: Small varices (diameter of 1–3 mm) visible
­w ithout Valsalva maneuver.
Grade III: Varices with diameter of 3–6 mm.
Grade IV: Varices > 6 mm in diameter.

MODIFIED DAGRADI GRADING

Figure 10.1 Early varices Grade 1: Blue or red varices <2 mm in diameter.
Grade 2: Blue varices 2–3 mm in diameter.
Grade 3: Elevated blue veins 3–4 mm in diameter.
Grade 4: Tortuous blue varices >4 mm in diameter, almost
meeting in the midline.
Grade 5: Grape-like varices occluding the lumen and
showing the presence of small cherry-red varices overly-
ing blue-grey varices.

PAQUET’S GRADING
Grade I: Small varices without luminal prolapse.
Grade II: Moderately sized varices showing luminal
Figure 10.2 Single column early ­prolapse with minimal obscuring of the GE junction.
varix (arrow). Grade III: Large varices showing luminal prolapse with
substantial obscuring of the GE junction.
Grade IV: Very large varices completely obscuring the GE
junction.

MODIFIED PAQUET’S GRADING

Grade I: Varices extending just above the mucosal level.
Grade II: Varices projecting by one-third of the luminal
diameter that cannot be compressed with air insufflation.
Grade III: Varices projecting up to 50% of the luminal diam-
eter and in contact with each other.
Figure 10.3 Early varices.

109
110 Atlas of diagnostic endoscopy

WESTABY’S GRADING
Grade 1: Varices appearing as slight protrusions above
mucosa, which can be depressed with insufflations.
Grade 2: Varices occupying <50% of the lumen.
Grade 3: Varices occupying >50% of the lumen and which
are very close to each other with confluent appearance.

SOEHENDRA CLASSIFICATION

Figure 10.4 Blue varices. Grade I: Mild dilatation; diameter <2 mm; barely rising
above the relaxed esophagus; more marked in head-
down position.
Grade II: Moderate dilatation; tortuous; diameter 3–4 mm;
limited to the lower part of the esophagus.
Grade III: Total dilatation; taut; diameter >4 mm; thin-
walled; varices upon varices; in the gastric fundus.
Grade IV: Total dilatation; taut; occupy the entire esopha-
gus; frequent presence of gastric or duodenal varices.

ENDOSCOPIC RECORDING OF
ESOPHAGEAL VARICES (JAPANESE
RESEARCH SOCIETY FOR PORTAL
HYPERTENSION)

1. Fundamental color
Figure 10.5 Three columns of blue a. White (Cw)
varices.
b. Blue (Cb)

2. Red color signs (RCS): (small dilated vessels or micro-

telangiectasia on varix surface)
a. Red wale marking (RWM)
b. Cherry-red spot (CRS)
c. Hematocystic spot (HCS)
d. Diffuse redness (DR)

3. Form
a. Small, straight varices (F1)
b. Enlarged tortuous varices occupying <one-third of
lumen (F2)
c. Large coil-shaped varices occupying >one-third of
lumen (F3)
Figure 10.6 “Red wale” mark (arrow)
on the varix. 4. Location (longitudinal extent)
a. Lower one-third (Li)
b. Mid one-third; below tracheal bifurcation (Lm)
c. Upper one-third; above tracheal bifurcation (Ls)

5. Adjunctive findings
a. Erosion (E)
 Portal hypertension 111

Figure 10.7 “Red wale” mark (arrow) on Figure 10.8 Hematocystic spot, i.e.,
the varix. discrete elevated red spot (arrow) on varix.

Figure 10.9 Diffuse redness on the varices. Figure 10.10 Secondary varices, i.e., small
tortuous collaterals between main variceal
columns.

(a) (b)

Figure 10.11 (a, b) Fibrin plug (arrow) on a varix just below GE junction indicating the site of rupture.
(b) During examination, the plug got dislodged and the varix started bleeding actively (arrow).
112 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e) (f )

(g) (h) (i)

Figure 10.12 Pseudo varix. (a) Single column of vein showing focal ectasias. (b–h) Further
examination revealed multiple ectatic veins in the esophageal wall. (i) A normal GE junction
ruled out varices due to portal hypertension.

Figure 10.13 Pseudo varix; focal ectasias in Figure 10.14 Pseudo varix; single column
a single column of vein in the esophageal of tortuous vein in mid-esophagus. The GE
wall. junction was normal.
 Portal hypertension 113

Figure 10.15 Intravariceal sclerotherapy. Figure 10.16 Thrombosed varix following

Sclerosant being injected directly into the sclerotherapy.
varix.

Figure 10.17 Thrombosed varix. Figure 10.18 Thrombosed varix and ulcerated
esophageal mucosa.

Figure 10.19 Remnants of thrombosed and Figure 10.20 Esophageal ulcer following
obliterated varix. sclerotherapy.
114 Atlas of diagnostic endoscopy

COMPLICATIONS FOLLOWING
SCLEROTHERAPY

●● General
●● Fever
●● Anaphylaxis
●● Septicemia

●● Esophageal
●● Torn varix
●● Retrosternal pain
●● Dysmotility
●● Dysphagia
Figure 10.21 Bleeding from post-sclerotherapy ●● Ulcers
esophageal ulcer. ●● Perforation
●● Stricture
●● Squamous cell carcinoma

●● Pleuro-pulmonary
●● Atelectasis
●● Pleural effusion
●● Empyema

●● Distant
●● Gastric variceal bleeding
●● Bleeding from gastropathy
●● Portal vein periphlebitis
●● Portal vein thrombosis
●● Mesenteric vein thrombosis

Figure 10.22 Healed post-sclerotherapy ulcer

leaving behind irregular mucosa and mucosal
tags.

Figure 10.23 Mucosal tag Figure 10.24 Esophageal Figure 10.25 Esophageal
following variceal obliteration. ulcer and stricture formation stricture following
following sclerotherapy. sclerotherapy. Varices have
been completely eradicated.
 Portal hypertension 115

(a) (b)

Figure 10.26 (a, b) Endoscopic variceal band ligation (EVL). Ligated varix soon after release of
the band.

(a) (b)

Figure 10.27 (a, b) Ligated varix.

(a) (b)

Figure 10.28 (a, b) Bleeding from ulcerated varix following EVL.

116 Atlas of diagnostic endoscopy

(a) (b)

Figure 10.29 Thrombosed and ulcerated varix following EVL. (a) The band is still in place.
(b) The band has fallen off.

(a) (b)

(c) (d)

Figure 10.30 (a–d) Post-EVL ulcers. Punched-out ulcers (arrows) in the esophageal mucosa after
sloughing of the thrombosed varices.
 Portal hypertension 117

Classification of gastric varices

Type Appearance
1 Varices in the lesser curvature continuous with the esophageal
varix.
2 Fundal varices.
3 Both lesser curve and fundal varices.
British Journal Surgery 1990; 77:195.

Type Appearance
1 Varices appearing as inferior extension of esophageal varices
across the squamocolumnar junction.
2 (Nearly always accompanied by esophageal varices) located in
the fundus, which appear to converge towards the cardia.
3 Varices located in the fundus or body in the absence of
esophageal varices and appear unconnected to the cardia.
British Journal Surgery 1990; 75:195.

Figure 10.31 GOV: Gastroesophageal Varix; IGV: Isolated gastric varix. Hepatology 1992;
16:1343.
118 Atlas of diagnostic endoscopy

Figure 10.32 Junctional varix. Varices Figure 10.33 Varices just below the
extending from esophagus across the GE GE junction.
junction.

Figure 10.34 Junctional varix.

Figure 10.35 Junctional varix.

Figure 10.36 Varix extending along the lesser Figure 10.37 Single column of tortuous varix
curve. extending along the lesser curve.
 Portal hypertension 119

Figure 10.38 Varix below the GE junction. Figure 10.39 Diffuse varix along the lesser
curve.

Figure 10.40 Varix below the GE junction. Figure 10.41 Fundal varix.

Large gastric varices appear like “a bunch of grapes.” Small varices should be differentiated
from mucosal folds and prominent submucosal veins. Mucosal folds flatten out on distension.
Submucosal veins, unlike varices, do not show dilatation or tortuosity.

Figure 10.42 “White nipple” sign (arrow) on Figure 10.43 Isolated fundal varix.
fundal varix suggesting recent bleeding.
120 Atlas of diagnostic endoscopy

Figure 10.44 Fundal varix. Figure 10.45 Fundal varix.

Figure 10.46 Fundal varix appearing like a

bunch of grapes.

(a) (b)

Figure 10.47 (a) Fundal varix being injected with Cyanoacrylate glue. (b) The varix appears
rounded due to hardening of the glue inside. Some spilled out glue can be seen on the surface
of the varix.
 Portal hypertension 121

(a) (b) (c)

Figure 10.48 (a) Large fundal varix. (b) cynoacrylate glue injection. (c) Solidified varix.

(a) (b)

Figure 10.49 (a) Ulceration and oozing

from the surface of a solidified fundal varix.
Cyanoacrylate glue was injected a week
earlier. (b) About two months later, the
ulceration appearing more extensive and the
glue extruding out. (c) Continued oozing and
(c) further extrusion of the glue 12 days later.

Figure 10.50 Eradicated gastric varix.

Scarring and neovascularization in the varix
bearing area.
122 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

Figure 10.51 (a–d) Appearance of gastric mucosa in portal hypertensive gastropathy.

Portal hypertensive gastropathy (PHG) is most

often an incidental finding in patients of portal
hypertension. In <2% of patients, it may present
with significant upper GI bleeding. The endo-
scopic appearance of the gastric mucosa in PHG is
characterized by a beefy red appearance, petechial
hemorrhages, red spots and a mucosal pattern of
a white reticular network outlining erythematous
central areas (snake-skin appearance). Endoscopic
biopsies reveal submucosal edema, dilated sub-
mucosal veins, mucosal capillaries and venules.
Submucosal arterioles have thickened walls with
proliferation of endothelial and adventitial ele-
Figure 10.52 Portal hypertensive ments. The submucosal venules show morphologic
gastropathy. “Snake-skin” appearance of features of arterialization. The overall blood flow to
gastric mucosa. the stomach is increased. There are increased sub-
mucosal arteriovenous communications resulting
in reduction of effective mucosal blood flow.
 Portal hypertension 123

(a) (b)

Figure 10.53 (a, b) Mucosal appearance in portal hypertensive gastropathy.

(a) (b)

Figure 10.54 (a, b) Bleeding portal hypertensive gastropathy.

Figure 10.55 Duodenal varix.

(a) Esophageal varix in a patient
presenting with melena. (b, c) Varix
with “white nipple sign” was present
(a) in D2 signifying the site of bleeding.

(b) (c)
124 Atlas of diagnostic endoscopy

Duodenal varix is found in 0.5%–2.5% of

patients with portal hypertension. A higher inci-
dence of 43% has been reported in radiological
studies (splenoportogram).
American Journal of Gastroenterology 1993;
88:1942. Endoscopy 1996; 28:239. Radiology
1968; 8:90.

(a)

(b) (c)

Figure 10.56 (a–c) Ruptured duodenal varix. Solitary varix in D2 showing “white nipple sign.”
 11
Corrosive injury

In suspected cases of corrosive injury, endoscopy should be performed with utmost care and
gentleness following three basic principles: minimal insufflation, avoidance of blind and forceful
intubation.

(a) (b)

(c) (d)

(e) (f )

Figure 11.1 Early appearance following acid ingestion. (a) Inflamed pharyngeal mucosa.
(b, c) Thin, whitish membrane covering esophageal mucosa. (d) Inflamed mucosa beneath the
membrane. (e, f) Charred gastric mucosa. (Continued)

125
126 Atlas of diagnostic endoscopy

(g) (h)

(i) (j)

(k) (l)

Figure 11.1 (Continued) Appearance after four weeks when the patient presented with gastric
outlet obstruction. (g) Healed esophageal mucosa. (h) Inflamed gastric mucosa. (i) Prepyloric
antrum showing slough and displaced pylorus (arrow). (j) Removal of slough showing inflamed
mucosa. (k) Pyloric channel obscured by slough. (l) Barium study showing contracted antro-
pyloric region. The patient was treated with gastrojejunostomy.
 Corrosive injury 127

(a) (b)

(c) (d)

Figure 11.2 Acid injury. Early appearance.

(a, b) Minimal involvement of esophageal
mucosa. (c–e) Necrotic mucosa showing
thrombosed vessels in the stomach.
(e) (Continued)

ENDOSCOPIC GRADING OF CAUSTIC INJURY

Grade 1: Erythema/edema.
Grade 2a: Friability, hemorrhagic blisters, white exudate, superficial ulcers and erythema.
Grade 2b: 2a + deep or circumferential ulcers.
Grade 3a: Small areas of necrosis, brown-black, grayish discoloration, deep ulcers.
Grade 3b: Extensive necrosis.

Gastrointestinal Endoscopy 1991; 37:165

128 Atlas of diagnostic endoscopy

(f ) (g)

(h) (i)

Figure 11.2 (Continued) Three weeks after injury.

(f) Healed esophageal mucosa. (g) Obliterated
fundus of stomach. (h) Inflamed and narrowed body
of stomach. (i) Tubular antro-pyloric region. (j) Barium
(j) contrast study of the same patient corroborating the
endoscopic findings.
 Corrosive injury 129

(a) (b)

(c) (d)

Figure 11.3 Acid injury affecting various parts

of the esophagus, appearance in the first 72 h.
(a) Esophagus just distal to cricopharyngeal
opening. (b–e) Esophageal mucosa from
proximal to distal segment. (Continued)
(e) (f )
130 Atlas of diagnostic endoscopy

(f ) (g)

(h) (i)

(j) (k)

Figure 11.3 (Continued) Six weeks after the injury. (f) Tight stricture in the mid-esophagus.
(g–j) Stricture opened up by balloon dilatation. (k) Distal end, relatively healthy.
 Corrosive injury 131

(a) (b)

(c) (d)

Figure 11.4 Acid injury. (a) Proximal esophageal mucosa. (b) Distal esophageal mucosa. (c) Thick
eschar covering gastric body. (d) Inflamed antral mucosa.

(a) (b)

(c) (d)

Figure 11.5 (a, b) Acid injury to esophageal mucosa. (c) Note the hiatal hernia and the relatively
healthy gastric mucosa in the hernial sac. (d) Same as seen on retroflexion.
132 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e) (f )

Figure 11.6 Chemical burn in a patient who consumed spurious alcohol 24 h earlier. (a) Superficial
burn involving pharynx and (b) esophagus. (c) Hiatal hernia in the same patient. (d) Retroflex view
showing the hiatal sac and the junction of the affected esophageal mucosa and normal gastric
mucosa. (e) Close-up view of the same. (f) Multiple superficial ulcers in the gastric body.

(a) (b) (c)

(d) (e)

Figure 11.7 (a) Corrosive stricture in the mid-esophagus. (b) Guidewire across the stricture.
(c, d) Stricture bearing segment after dilatation. (e) Gastrojejunostomy in the same patient
performed earlier for antral stricture.
 Corrosive injury 133

(a) (b)

Figure 11.8 (a) Corrosive stricture involving mid-esophagus. (b) Same after balloon dilatation.

(a) (b)

Figure 11.9 Corrosive stricture (a) before and (b) after dilatation.

Figure 11.10 Corrosive stricture. Figure 11.11 Corrosive stricture after dilatation.
134 Atlas of diagnostic endoscopy

Figure 11.12 Corrosive stricture after dilatation.

 12
Uncommon inflammatory lesions and
tropical diseases of the UGI tract

(a) (b)

Figure 12.1 (a, b) Pharyngeal ulcers in an immunocompromised patient.

(a) (b)

Figure 12.2 (a, b) Human immunodeficiency virus (HIV)–associated idiopathic ulcer in the
mid-esophagus.

Esophageal involvement in HIV-infected patients can be

●● Fungal: Candida
●● Viral: Cytomegalovirus (CMV), herpes simplex virus (HSV)
●● Idiopathic
135
136 Atlas of diagnostic endoscopy

(a) (b)

Figure 12.3 (a, b) Herpes simplex virus (HSV) ulcers in the mid-esophagus showing minimal
involvement.

(a) (b)

(c) (d)

Figure 12.4 (a, b) HSV esophagitis. (c, d) Ulcers coalesce in the distal esophagus causing
mucosal necrosis
 Uncommon inflammatory lesions and tropical diseases of the UGI tract 137

(a) (b) (c)

(d) (e) (f )

Figure 12.5 HSV esophagitis. (a) Discrete ulcers in the proximal esophagus. (b–f) Ulcers
coalesce distally to cause circumferential involvement.

HSV esophagitis commonly presents with acute onset dysphagia, odynophagia and chest pain.
On endoscopy, the ulcers appear sharply demarcated, having raised margins. Typically known as
“volcano ulcers,” they may coalesce to cause confluent ulcers.

(a) (b) (c)

(d) (e) (f )

Figure 12.6 (a–e) CMV esophageal ulcers. These ulcers are deep, having irregular borders and
finger-like projections. (f) The distal esophagus appears normal.
138 Atlas of diagnostic endoscopy

Figure 12.7 Candida esophagitis. Figure 12.8 Candida esophagitis.

Figure 12.9 Candida esophagitis. Figure 12.10 Candida esophagitis.

Figure 12.11 Candida esophagitis. Figure 12.12 Candida esophagitis.

PREDISPOSING FACTORS FOR CANDIDA ESOPHAGITIS

Immunosuppression, diabetes mellitus, corticosteroid therapy, prolonged antibiotics, esophageal
obstruction and malignancy.
 Uncommon inflammatory lesions and tropical diseases of the UGI tract 139

(a) (b) (c)

(d) (e) (f )

Figure 12.13 (a–f) Esophageal ulcer in Behcet’s disease.

Gastrointestinal involvement occurs in 3%–16% of patients with Behcet’s disease. The esophagus
and the ileocecal region are the two most common sites of involvement.

(a) (b)

(c) (d)

Figure 12.14 Granulomatous sarcoma of the esophagus. Myeloid cell infiltration of the
esophageal mucosa in a patient with acute myeloid leukemia. (a) Ulcer in the epiglottis. (b–e)
Nodular and ulcerated mucosa with slough involving the entire esophagus. (f) No involvement
beyond the Z line. (Continued)
140 Atlas of diagnostic endoscopy

(e) (f )

Figure 12.14 (Continued) Granulomatous sarcoma of the esophagus. Myeloid cell infiltration
of the esophageal mucosa in a patient with acute myeloid leukemia. (a) Ulcer in the epiglottis.
(b–e) Nodular and ulcerated mucosa with slough involving the entire esophagus. (f) No
involvement beyond the Z line.

(a) (b) (c)

(d) (e) (f )

Figure 12.15 (a–f) Drug-induced esophagitis. Esophageal ulcers and erosions following
doxycycline ingestion the previous day.

DRUGS COMMONLY CAUSING ESOPHAGEAL INJURY

NSAIDs Vitamin C Tetracyclines Doxycycline

Potassium Chloride Ferrous Sulfate Quinine Sulfate Quinidine
Zidovudine
 Uncommon inflammatory lesions and tropical diseases of the UGI tract 141

(a) (b) (c)

(d) (e) (f )

Figure 12.16 Acute infectious gastroduodenitis. (a, b) Multiple ulcers in the gastric antrum
(c, d) in D1 and (e, f) in the descending duodenum. The patient presented with acute abdominal
pain, vomiting and fever. Mucosal biopsy was nonspecific. Such ulcers were possibly infective in
origin. The symptoms resolved on conservative treatment spanning over two weeks.

(a) (b) (c)

(d) (e) (f )

Figure 12.17 Acute infectious gastroduodenitis. (a) Normal-appearing esophagus and (b) fundus.
(c, d) Multiple ulcers in the antrum and around the pylorus. (e) Ulcers in D1 and (f) D2. Patient, a
13-year-old boy presented with acute abdominal pain, fever, loose motion and melena. He was
empirically treated with oral omeprazole and ciprofloxacin. (Continued)
142 Atlas of diagnostic endoscopy

(g) (h) (i)

(j) (k) (l)

Figure 12.17 (Continued) Endoscopy 12 days later for persistent symptoms showed (a) normal
esophagus, (h, i) mucosal edema and ulceration involving the fundus and body. Ulcers in
(j) antrum, (k) D1 and (l) D2 showing signs of healing. (Continued)

(m) (n) (o)

(p) (q) (r)

Figure 12.17 (Continued) Endoscopy a week later, for worsening of symptoms and
hematemesis, showed diffuse mucosal ulcerations involving (m) fundus, (n, o) body, (p) antrum,
(q) D1 and (r) D2. Mucosal biopsy from the lesions showed nonspecific inflammation. Serum
gastrin level was normal. The patient was treated with an anti–H. pylori regimen (pantoprazole,
clarithromycin and metronidazole). (Continued)
 Uncommon inflammatory lesions and tropical diseases of the UGI tract 143

(s) (t) (u)

CLINICAL
POSSIBILITIES IN
THE PRESENT CASE
●● H. Pylori infection
●● Viral infection
●● Food allergy
●● Crohn’s disease
(v) (w) ●● HIV infection

Figure 12.17 (Continued) Endoscopy two months later showed slight mucosal irregularity
suggestive of healed ulcers in (s) fundus, (t) body and (u) antrum. Complete mucosal healing was
observed in (v) D1 and (w) D2.

(a) (b)

(c) (d)

Figure 12.18 (a–d) Extensive ulceration of duodenum. Mucosal biopsy was nonspecific. The
patient presented with acute abdominal pain, fever and bloody diarrhea. The symptoms
resolved nearly three weeks after conservative management with antibiotics and proton pump
inhibitors. The disease possibly represented idiopathic segmental enteritis.
144 Atlas of diagnostic endoscopy

(a) (b)

Figure 12.19 (a, b) Duodenal tuberculosis. Ulcer on the anterior wall at the junction of D1
and D2. The patient presented with low-grade fever and weight loss. Biopsy of the ulcer margin
showed caseating granuloma.

(a) (b)

(c) (d)

(e) (f )

Figure 12.20 Duodenal tuberculosis. (a, b) Ulcer (arrow) at the D1–D2 junction. The patient
was started on proton pump inhibitors. (c, d) Repeat endoscopy about three weeks later
showed no signs of healing; instead the ulcer seemed to have worsened. Ulcer biopsy at this
stage suggested tuberculosis. (e, f) Endoscopy about one month after starting antituberculosis
treatment. The ulcer (arrow) showed marked reduction in size. The patient received the full
course of antituberculosis treatment.
 Uncommon inflammatory lesions and tropical diseases of the UGI tract 145

Figure 12.21 Pinworms in D1. Figure 12.22 Hookworm in D1.

(a) (b)

Figure 12.23 Biliary ascariasis. (a) T-tube cholangiogram showing an Ascaris lumbricoides
(roundworm) in the bile duct. (b) The worm was delivered out by a snare after endoscopic
sphincterotomy.

(a) (b)

Figure 12.24 Endoscopic retrograde cholangiogram showing a roundworm in the proximal

biliary tree. (b) The worm was extracted after grasping it with endoscopic “rat tooth” forceps.
146 Atlas of diagnostic endoscopy

Figure 12.25 Roundworm across a Figure 12.26 Roundworm in D3.

choledochoduodenostomy stoma. Note the
bile duct lumen (B) and the duodenum (D).
 13
Mallory–Weiss syndrome

Mallory–Weiss syndrome accounts for 5%–10% of all cases of upper gastrointestinal bleeding. The
typical presentation is frank hematemesis or blood streaking of vomitus that follows normal bouts
of vomiting occurring in the setting of alcoholism, food poisoning or hyperemesis gravidarum. On
endoscopy, it is characterized by one or more linear mucosal tear involving the GE junction. The
tear may extend for variable distance onto the GE junction. Bleeding from such a lesion is usually
mild and self-limiting and responds to conservative management. Endoscopic intervention, in the
form of local adrenaline saline injection, thermal coagulation, hemoclip application or banding
may be required in the rare event of continued bleeding.

Figure 13.1 Linear tear at the 10-o’clock position.

Figure 13.2 Linear tears at the two- and five-o’clock positions.

147
148 Atlas of diagnostic endoscopy

(a) (b)

(c) (d)

(e) (f )

Figure 13.3 (a, b) Linear lacerations (arrows) across the GE junction. The patient presented
with massive hematemesis following an alcoholic binge. (c, d) Repeat endoscopy 24 h later; the
altered blood in the lesion has been replaced by whitish slough. Note the sliding hiatal hernia.
(e, f) Lacerations extending on to gastric mucosa beyond the hiatal sac as seen on retroflexion.
 Mallory–Weiss syndrome 149

(a) (b)

Figure 13.4 (a, b) Lacerated esophageal mucosa and submucosal hematoma (arrow) at the Z line.

Figure 13.5 A linear tear at the GE junction.

 14
Dieulafoy’s lesion

Dieulafoy’s lesion (exulceratio simplex, cali-

ber-persistent artery) is characterized by the
presence of a thick-caliber submucosal arte-
riole that can cause torrential bleeding. This
lesion most commonly occurs in the proxi-
mal 6 cm of the stomach. Less commonly,
it may occur in the duodenum and the rest
of the GI tract. Endoscopic appearance of
duodenal Dieulafoy’s lesion ranges from a
pinpoint dot, clot or tortuous vessel to blood
oozing or spurting from normal mucosa.
Management includes injection sclerother-
apy, monopolar or bipolar heater probe appli-
cation, laser photocoagulation, band ligation,
Figure 14.1 Dieulafoy’s lesion just below GE application of hemoclip or surgical excision.
junction seen on retroflexion. Digestive Diseases and Sciences 1988; 33:801

(a) (b)

Figure 14.2 (a, b) Actively bleeding Dieulafoy’s lesion in the body of the stomach. The bleeding
point appeared exaggerated because of the adherent fibrin plug and clot.

151
152 Atlas of diagnostic endoscopy

(a) (b)

Figure 14.3 (a, b) Dieulafoy’s lesion in the proximal stomach appearing as a tiny protuberance.
The patient had massive hematemesis 48 h earlier.

(a) (b)

(c) (d)

Figure 14.4 (a–d) Dieulafoy’s lesion in D1, characterized by punctate oozing (arrow) from an
otherwise normal mucosa. Patient, a young woman, presented with recurrent melena.
 Dieulafoy’s lesion 153

(a) (b)

(c) (d)

Figure 14.5 (a) Dieulafoy’s lesion, quiescent at the time of examination, is covered with a small
clot and blood pool (arrow). Note the surrounding normal mucosa that differentiates it from
chronic duodenal ulcer. (b) Repeat examination the following day showed an actively bleeding
lesion. (c, d) Bleeding was controlled with adrenaline injection.
 15
Gastric antral vascular ectasia (GAVE)

(a) (b) (c)

(d) (e) (f )

Figure 15.1 Gastric antral vascular ectasia (GAVE). (a) Normal esophagus. (b, c) Punctate
telangiectasias confined to the antrum (d, e) Close-up view of the same. (f) Normal duodenum.

Gastric antral vascular ectasia (GAVE) accounts for nearly 4% of non-variceal UGI bleeding. The
entity commonly occurs in association with chronic liver disease, chronic renal failure, autoim-
mune connective tissue disorder, bone marrow transplantation, ischemic or valvular heart dis-
ease, hypertension, familial Mediterranean anemia and acute myeloid anemia. The pathogenesis
of the entity is not clearly understood. The presentation ranges from occult to frank GI bleed-
ing. Two types of lesions have been identified on endoscopy: punctuate or striped. Because of
similarity in appearance, the striped variety is also known as “watermelon” stomach. Though the
antral region shows predominant involvement, occasionally it may extend to the gastric fundus
as well. In chronic liver disease, it must be differentiated from portal hypertensive gastropathy
as the treatment modalities for both are quite different. Unlike PHG, reduction in portal pres-
sure has no effect on GAVE. Argon plasma coagulation, laser photocoagulation and heater probe
application are the accepted modalities of treatment. Rarely, antrectomy may be required for
uncontrolled hemorrhage.
Digestion 2008; 77: 131

155
156 Atlas of diagnostic endoscopy

(a) (b) (c)

Figure 15.2 (a, b) Punctate variety of GAVE. (c) Close-up view of the same.

(a) (b) (c)

Figure 15.3 Gastric antral vascular ectasia (watermelon stomach). (a, b) Linear disposition of
vascular ectasias, confined to the antrum, resemble the stripes of a watermelon. (c) Close-up
view of the same.

(a) (b)

Figure 15.4 Gastric antral vascular ectasia. (a, b) Linear telangiectasias confined to the antrum.
The patient, a 45-year-old woman, presented with recurrent episodes of melena.
 16
Foreign body

(a) (b)

(c) (d)

Figure 16.1 Coin impacted at the

esophageal inlet. (a) Localized to
esophageal inlet on chest X-ray.
(b–d) Endoscopic appearance and
extraction by using “rat-tooth”
(e) forceps. (e) Extracted coin.
157
158 Atlas of diagnostic endoscopy

Figure 16.2 Betel nut, swallowed Figure 16.3 A metal ring impacted at the
accidentally, lodged at the distal esophagus esophageal inlet.
in a child.
Esophageal inlet is the commonest site of foreign
body (FB) impaction. Dysphagia, odynopha-
gia, chest pain and excessive salivation are the
usual symptoms. Contrary to the common prac-
tice, FB extraction should always be performed
under general anesthesia. It is our practice to use
intravenous propofol anesthesia in adults and
intubation anesthesia in the pediatric age group.
A quiet patient, relaxed cricopharyngeus, secure
airway and proper instrument are paramount in
successful removal of a FB from the UGI tract.

MANAGEMENT GUIDELINES
Food bolus in esophagus: Remove urgently if the
patient is in distress. Remove electively if the
(a) patient is comfortable, but do not delay beyond
24 h.
FB in esophagus: Endoscopy and removal as
early as possible.
Smooth, rounded FB in stomach: Normal pas-
sage is expected in four to six days, but may take
up to four weeks. Endoscopic removal is recom-
mended for objects more than 2.5 cm in diam-
eter or longer than 6–10 cm or remaining in the
stomach for more than four weeks.
Sharp/pointed objects in stomach: Remove
urgently. If it has gone beyond the duodenum,
expectant but watchful management is advo-
(b)
cated for any signs of obstruction, perforation or
bleeding. Remove if it does not pass out in 72 h.
Figure 16.4 (a) A coin impacted at
the esophageal inlet (cricopharyngeal Button battery: Follow if it has gone beyond
sphincter). (b) Deep mucosal ulcer at the esophagus. Active removal is indicated for bat-
site of impaction, as seen after the coin tery more than 2 cm in diameter, age <5 y or if it
was extracted. remains in stomach for more than 48 h.
 Foreign body 159

(a) (b)

Figure 16.5 (a) Denture impacted at cricopharyngeal sphincter held by a snare. (b) After its
extraction.

(a) (b)

Figure 16.6 (a) A fish bone across the mid-esophagus (b) mucosal injury at the sites of
impaction (arrows) seen after its endoscopic removal.

(a) (b)

Figure 16.7 (a) A piece of salad (vegetable slice) impacted at the esophageal inlet and
(b) dislodged and pushed to the distal esophagus by endoscopic manipulation.
160 Atlas of diagnostic endoscopy

(b)

(a)
(c)

(d) (e) (f )

Figure 16.8 A coin swallowed two years back. (a) Localized to the upper abdomen (arrow)
on X-ray. (b) On endoscopy, the coin was found to be in the stomach. Such a rounded object
should have, in normal circumstances, passed out in a 24–48 h period. The persistence of the
object in the stomach was due to chronic duodenal ulcer leading to narrowed outlet. (c) Note
the deformed duodenal bulb, an active ulcer (arrow) and pseudodiverticulum (broken arrow).
(d, e) The coin was extracted with the help of a Dormia basket. (f) The extracted coin appeared
completely blackened due to the prolonged contact with the gastric secretions.
 Foreign body 161

Figure 16.9 A needle at the junction of the Figure 16.10 A coin in the fundus of the
body and the antrum. stomach.

Figure 16.11 Accidentally swallowed denture in

the stomach. Its quadrangular shape and the two
spikes (arrows) make its endoscopic extraction
extremely difficult and risky. Gastrotomy and
removal is our preferred approach for such an
object.

Figure 16.12 A needle in the second part of

duodenum. It was held at its proximal end and
delivered out along with the endoscope. Holding
the needle in such manner is essential to avoid
mucosal trauma.
162 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e)

Figure 16.13 (a) Plain X-ray showing multiple needles (arrows) in the GI tract. The patient, an
adult with a mental illness, was habitually swallowing sewing needles. (b) Two needles (arrows),
the upper one possibly in the descending duodenum. The patient was fortunate to pass out the
needles without any complications. (c) Needle persisting in the duodenum. (d) Endoscopic view
of the same. (e) The needle after its extraction.

(a) (b)

Figure 16.14 (a, b) A bile-stained tongue cleaner in descending duodenum. This was
accidentally swallowed by the patient about two months back. Endoscopy was done for
dyspeptic symptoms.
 17
Tracheoesophageal fistula

Tracheoesophageal fistula (TEF) can be congenital or acquired.

ETIOLOGY OF ACQUIRED FISTULA

●● Benign
●● Pressure necrosis by the cuff of endotracheal/tracheostomy tube
●● Penetrating injury
●● Erosion by impacted foreign body
●● Erosion by caseating mediastinal lymph node
●● Malignant
●● Locally advanced carcinoma
●● Mediastinal lymphoma after irradiation

(a) (b) (c)

(d) (e)

Figure 17.1 Benign TEF arising from pressure necrosis by the inflated tracheostomy cuff.
(a) Bubbling of tracheal secretion through the fistula. (b, c) A rent (arrow) was seen in the cervical
esophagus at 12-o’clock position. The transparent tracheostomy cuff is visible through the rent.
(d, e) The same rent (arrow) after removal of the tracheostomy tube.
163
164 Atlas of diagnostic endoscopy

(a) (b)

Figure 17.2 (a, b) Benign TEF consequent upon pressure necrosis by the inflated cuff of
tracheostomy tube. The tracheal opening (arrow) was visible upon entering the cervical
esophagus. Note the concentric tracheal rings.

(a) (b)

(c) (d)

Figure 17.3 Malignant

TEF. (a, b) Friable
tumor involving cervical
esophagus. (c, d) Tracheal
opening (arrow) was
visible while maneuvering
the endoscope in the
esophagus. (e, f) Closer
(e) (f )
view revealed the tracheal
rings (white arrow).
 Tracheoesophageal fistula 165

(a) (b)

(c) (d)

Figure 17.4 (a–d) TEF following necrosis of the intervening wall between the trachea and the
esophagus. The patient, a young man, had received radiotherapy for mediastinal lymphoma.
Note the esophageal lumen (black arrow), the necrotic wall (W) and the trachea (white arrow).
 18
Miscellaneous

(a) (b)

Figure 18.1 (a) Pigmentation involving the pharynx, the larynx and (b) the esophagus. Incidental
finding in an otherwise normal individual.

(a) (b)

(c) (d)

Figure 18.2 “Inlet Patch.” (a) Islands of heterotropic gastric mucosa (arrows) in the proximal
esophagus. (b) Patch on the right side. (c, d) Close-up view of the patch on the left side. This is
usually an incidental finding and has no clinical significance.

167
168 Atlas of diagnostic endoscopy

(a) (b)

Figure 18.3 (a, b) “Inlet patch” (arrow) in the proximal esophagus.

Figure 18.4 Spontaneous esophageal Figure 18.5 Glycogen acanthoma in the

hematoma. esophageal body.

Figure 18.6 Tertiary contraction waves in the Figure 18.7 Tertiary contraction waves and
esophagus – “feline esophagus.” gastric mucosal prolapse at the distal end of
the esophagus.
 Miscellaneous 169

(a) (b) (c)

Figure 18.8 Mucosal petechiae in a patient of idiopathic thrombocytopenic purpura (ITP) at

(a) the laryngo-pharynx and (b, c) the esophagus.

(a) (b)

Figure 18.9 (a, b) Esophago-gastric anastomosis. Note the residual suture (arrow).

(a) (b)

(c) (d)

Figure 18.10 Esophago-gastrostomy. (a) Bile reflux esophagitis. (b–d) Tumor recurrence at
esophago-gastrostomy site. The patient had undergone proximal gastrectomy for a GE junction
tumor. Note the residual sutures at the anastomotic site.
170 Atlas of diagnostic endoscopy

(a) (b)

Figure 18.11 Retching gastropathy. (a, b) Congested and ecchymosed gastric mucosa just
below the GE junction. This has resulted from repeated prolapse through the LES during the act
of retching and vomiting.

(a) (b)

Figure 18.12 Retching gastropathy. (a, b) Focal ecchymosed gastric mucosa just below GE
junction.

Figure 18.13 Retching gastropathy. Figure 18.14 Retching gastropathy.

 Miscellaneous 171

Figure 18.15 Angiodysplasia in the proximal Figure 18.16 Ecchymosis produced by

gastric mucosa. nasogastric tube.

(a) (b) (c)

Figure 18.17 (a, b) Pancreatic pseudocyst producing bulge in the proximal stomach. (c) CT scan
image of the same patient showing the thick-walled pseudocyst.

(a) (b)

Figure 18.18 (a) CT scan showing gastric intramural pseudocyst. (b) The edematous antral
mucosa. Patient, a known case of recurrent pancreatitis presented with gastric outlet
obstruction. Previously, he had undergone percutaneous catheter drainage for retrogastric
pseudocyst.
American Journal of Gastroenterology 2003; 98: 229
172 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e) (f )

(g) (h) (i)

Figure 18.19 (a) Gastric diverticulum in the fundus of the stomach (arrow). (b, c) Close-up view
of the same. (d) Dilated blood vessels in the wall of the diverticulum. (e) Giant juxtapapillary
diverticulum in the same patient. Note the papillary orifice (arrow) in the wall of the
diverticulum. (f) Multiple jejunal diverticuli (arrows) were also noted on enteroscopy. Barium
contrast study showing the (g) gastric diverticulum (arrow), (h) juxtapapillary diverticulum
(arrow) and (i) jejunal diverticuli. The patient presented with massive lower GI bleeding.
 Miscellaneous 173

(a) (b)

Figure 18.20 (a) Percutaneous endoscopic gastrostomy (PEG) tube in the stomach. (b) PEG
tube, indigenously prepared from Foley’s catheter.

(a) (b) (c)

(d) (e)

Figure 18.21 (a–c) True diverticulum (arrow) in the superior wall of D1. (d, e) Close-up view of
the same. Note the healthy and normal appearing mucosa inside the diverticulum.

Figure 18.22 Ectopic pancreas in D1. The umbilicated

appearance is quite typical.
174 Atlas of diagnostic endoscopy

(a) (b)

Figure 18.23 (a, b) Brunner’s gland hyperplasia imparting a velvety appearance to the duodenal
mucosa.

(a) (b)

Figure 18.24 Hemobilia. (a, b) Blood emanating from papilla (arrow) in a patient having
cholangiocarcinoma.
 Miscellaneous 175

(a) (b) (c)

(d) (e)

(f ) (g) (h)

Figure 18.25 Gallstone ileus. (a–c) Endoscopic view of D1 showing cholecystoduodenal

fistula (arrow). The excavated base of the ulcer is the gallbladder lumen. (d) Barium contrast
study showing dilated loop of the jejunum. (e) Fistula (arrow) delineated on contrast study.
(f) Impacted stone in the proximal jejunum, (g) being delivered by enterotomy. (h) The
offending stone. The patient, an elderly woman, presented with features of upper small bowel
obstruction.

(c)
(a) (b)

Figure 18.26 (a) Cholecystoduodenal fistula. Active pus discharge was noted in D1. (b) CT scan
showing air inside the distended gallbladder and (c) in the intrahepatic biliary radicles. The
patient, a known case of gallstone disease, was admitted with acute cholecystitis. Resolution
of his symptom coincided with the formation of such fistula, a fact not-so-well described in the
literature.
176 Atlas of diagnostic endoscopy

(a) (b) (c)

(d) (e) (f )

Figure 18.27 Bouvret’s syndrome. (a, b) An external bulge was noted in the antropyloric region.
(c) A large size gallstone was found impacted in D1. (d) Endoscopy performed 48 h later showed
pus discharge from the bulge. (e) The gallstone had passed down, the site of impaction showing
mucosal irregularity. (f) Postbulbar duodenum. The patient presented with gastric outlet
obstruction that resolved spontaneously with the passage of the offending stone.
Index

A cicatrisation, ulcers with, 53

concomitant ulcer, 49
Achalasia cardia, 37–38
deformed duodenal bulb, 54
Acid injury, 127–128, 131; see also Corrosive injury
deformed pylorus, 52, 54
to esophageal mucosa, 131
gastric and duodenal ulcers, 50
to esophagus, 129–130
gastric body ulcer, 42
Acute infectious gastroduodenitis, 141–143
hidden ulcer, 44, 46
Adenocarcinoma; see also Malignant tumors
incisura ulcer, 43, 44, 45, 49
at GE junction, 98
lesser curve ulcer, 40, 41
at GE junction with accumulated food debris, 97
outlet obstruction, 53
at lower end of esophagus, 97
prepyloric antrum ulcer, 45, 50
polypoidal adenocarcinoma below GE
prepyloric pseudodiverticulum, 54
junction, 99
prepyloric ulcer, 43, 45, 46, 47, 48, 49, 51, 52
Adenomatous polyps, multiple, 88
proximal stomach ulceration, 41
American Society for Gastrointestinal Endoscopy
pyloric channel ulcer, 51
(ASGE), 1
reflux esophagitis, 52
Ampulla of Vater, 7
retention esophagitis, 43
Ampullary carcinoma, 107; see also Malignant
stomach contracture, 53
tumors
stomach ulcer, 42
Angiodysplasia in proximal gastric mucosa, 171
superficial ulcers in antrum, 48
Antral mucosa, 131
ulcer below GE junction, 39
Antrum, 8
Benign tumors, 83; see also Gastrointestinal
ASGE, see American Society for Gastrointestinal
stromal tumor
Endoscopy
Bile reflux; see also Gastroesophageal reflux disease
esophagitis, 30
B gastritis, 80
Biliary ascariasis, 145
Barrett’s esophagus, 33; see also Gastroesophageal Bouvret’s syndrome, 176
reflux disease; Hiatal hernia Brunner’s gland hyperplasia, 60, 174
Barrett’s mucosal island above Z line, 35
with dysplastic nodule, 34
C
short-segment, 33
with sliding hiatal hernia, 33, 34 Candida esophagitis, 138
surveillance protocol for, 35 Carcinoma, ampullary, 107; see also Malignant
Benign gastric outlet obstruction, 53; see also tumors
Benign gastric ulcer Caustic injury, grading of, 127
deformed duodenal bulb, 54 Charred gastric mucosa, 125; see also Corrosive
Benign gastric ulcer, 39 injury
antrum ulcers, 45, 50 Chemical burn, 132; see also Corrosive injury

177
178 Index

Cherry-red spot (CRS), 110 esophageal mucosa, 127, 129, 131

Choledochoduodenal fistula, 67, 175 esophagus distal to cricopharyngeal
giant, 68 opening, 129
Chronic duodenal ulcer, 55 gastrojejunostomy, 132
actively oozing ulcer, 61 guidewire across stricture, 132
active ulcer, 56 healed esophageal mucosa, 126, 128
Brunner’s gland hyperplasia, 60 inflamed and narrowed stomach, 128
cannulation and injection of contrast opacified inflamed antral mucosa, 131
common bile duct, 67 inflamed gastric mucosa, 126
choledochoduodenal fistula, 67, 68 inflamed mucosa beneath membrane, 125
clot covered ulcer, 63 inflamed pharyngeal mucosa, 125
deep ulcer on D1, 58 necrotic mucosa and thrombosed vessels in
deformed D1 and pseudodiverticuli, 69 stomach, 127
deformed duodenal bulb and ulcers, 56, 57, 58, obliterated fundus of stomach, 128
60, 65 prepyloric antrum, 126
deformed duodenum with bilioduodenal pyloric channel obscured by slough, 126
fistula, 66 removal of slough showing inflamed
duodenal stenosis, 66 mucosa, 126
duodenal ulcer, 56, 61, 64 stricture bearing segment after dilatation, 132
duodenitis, 55 stricture in mid-esophagus, 130
endoscopic features of, 56 thick eschar covering gastric body, 131
endoscopic stigmata of ulcer bleeding, 61 tubular antro-pyloric region, 128
healing ulcer D1, 57 whitish membrane covering esophageal
kissing ulcers, 59 mucosa, 125
multiple erosions, 60 Corrosive stricture, 133; see also Corrosive injury
multiple ulcers, 56, 59, 60, 66 after dilatation, 133, 134
opacification of proximal biliary tree, 67 before dilatation, 133
pseudodiverticula, 56 in mid-esophagus, 132, 133
spurting bleeding from ulcer base, 61 CRS, see Cherry-red spot
ulcer extending into duodenum, 57 Cytomegalovirus (CMV), 135
ulcer on D1, 58, 64–65 esophageal ulcers, 137
ulcer with edema, 60
visible vessel accentuated by adherent clot, 63
D
visible vessel covered with clot, 62
Chronic duodenal ulcer, 56 Deformed pylorus, 52, 54; see also Benign
Circumferential tumor, 103; see also Malignant gastric ulcer
tumors Dieulafoy’s lesion, 151
CMV, see Cytomegalovirus actively bleeding, 151
Coating agents, 1 in D1, 152
Concentric rings of trachea, 4 examination, 153
Conn’s grading, 109; see also Portal hypertension below GE junction, 151
Corrosive injury, 125 in proximal stomach, 152
acid injury, 127–128, 129–130, 131 Diffuse redness (DR), 110
caustic injury grading, 127 Distal esophagus; see also Gastroesophageal reflux
charred gastric mucosa, 125 disease
chemical burn, 132 betel nut lodged at, 158
contracted antropyloric region, 126 dislodging and pushing to, 159
corrosive stricture, 132, 133, 134 early carcinoma in, 96
distal esophageal mucosa, 131 erosions in, 25
early appearance following acid ingestion, extensive ulceration, 30
125–126 mucosa, 131
 Index 179

Diverticulum from proximal to distal segment, 129

dilated blood vessels in wall of, 172 thin, whitish membrane covering, 125
giant juxtapapillary, 172 Esophageal rings, 9
true, 173 etiology, 9
DR, see Diffuse redness postcricoid rings, 11, 15
Drug-induced esophagitis, 140 Schatzki’s ring, 13–14, 15
Duodenal Esophageal strictures, 9
bulb ulceration, 6 benign, 12
carcinoma, 106 dilating distal, 12
stenosis, 66 etiology, 9
tuberculosis, 144 guidewire across distal stricture, 12
Duodenal bulb, deformed, 56, 57, 58 postcricoid membranous stricture, 12
with bilio-purulent fluid, 65 post-radiotherapy esophageal stricture, 16
Duodenal ulcer, 50; see also Benign gastric ulcer; post-sclerotherapy stricture, 17
Chronic duodenal ulcer Esophageal webs, 9
complications of, 61 etiology, 9
concomitant, 49 mucosal tear, 11
with flat red spot, 64 postcricoid webs/strictures, 9–10
multiple, 50 squamous cell carcinoma in distal
Duodenal varix, 123 esophagus, 9
ruptured, 124 Esophagitis; see also Gastroesophageal reflux
Duodenitis, 55 disease; UGI tract lesions and diseases
Duodenum bile reflux esophagitis, 30
bile-stained tongue cleaner in descending, 162 Candida, 138
with bilioduodenal fistula, 66 drug-induced, 140
extensive ulceration of, 143 erosive esophagitis, 29
needle in second part of, 161 erosive esophagitis with sliding hiatal
hernia, 29
with overlying exudates extending up to mid-
E
esophagus, 29
Ecchymosis, 171 reflux esophagitis, 52
Ectopic pancreas in D1, 173 retention esophagitis, 43
Edematous antral mucosa, 171 with sliding hiatal hernia, 28
Endoscopic retrograde cholangiogram, 145 Esophago-gastric anastomosis, 169
Endoscopic variceal band ligation (EVL), 115; Esophago-gastrostomy, 169
see also Portal hypertension Esophagus; see also Barrett’s esophagus; UGI tract
bleeding from ulcerated varix following, 115 lesions and diseases
post-EVL ulcers, 116 CMV esophageal ulcers, 137
thrombosed and ulcerated varix coin impacted at esophageal inlet, 157, 158
following, 116 discrete ulcers in proximal, 137
Epiglottis, 3 distal esophagus, 137
Esophageal esophageal ulcer in Behcet’s disease, 139
drug induced injury, 140 fish bone across mid-esophagus, 159
spontaneous hematoma, 168 glycogen acanthoma in, 168
varices, 110 granulomatous sarcoma of, 139–140
Esophageal mucosa; see also Corrosive injury; inlet patch in proximal, 168
Mallory–Weiss syndrome metal ring impacted at esophageal inlet, 158
healed, 126, 128 piece of salad impacted at esophageal
lacerated, 149 inlet, 159
minimal involvement of, 127 pigmentation involving, 167
proximal esophageal mucosa, 131 tertiary contraction waves in, 168
180 Index

Esophagus motility disorder, 37 linear telangiectasias confined to antrum, 156

achalasia cardia, 37 punctate variety of, 156
dilated esophagus, 38 Gastric mucosal prolapse, 168
diverticulum, 38 through lax LES, 22
non-relaxing LES, 38 sliding hiatal hernia and, 22
EVL, see Endoscopic variceal band ligation and tertiary contraction waves, 168
Gastric varices; see also Portal hypertension
classification, 117
F
eradicated, 121
FB, see Foreign body isolated, 117
Feline esophagus, 168 Gastroduodenitis, acute infectious, 141–143
Foreign body (FB), 157 Gastroesophageal junction (GE junction), 8,
betel nut lodged at distal esophagus, 158 33; see also Gastroesophageal reflux
bile-stained tongue cleaner in descending disease
duodenum, 162 adenocarcinoma at, 97, 98
coin extraction with dormia basket, 160 Dieulafoy’s lesion, 151
coin impacted at esophageal inlet, 157, 158 ecchymosed gastric mucosa, 170
coin in stomach fundus, 161 erosions and exudates at, 25
coin localized to upper abdomen, 160 fibrin plug on varix, 111
deep mucosal ulcer, 158 gastric fundus and, 8
denture impacted at cricopharyngeal inflammatory polyp at, 84, 85
sphincter, 159 junctional varix, 118, 119
denture in stomach, 161 linear erosions at, 25
dislodging and pushing to distal esophagus, 159 linear lacerations across, 148
fish bone across mid-esophagus, 159 linear tear at, 149
management guidelines, 158 linear ulcer at proximal esophagus, 26
metal ring impacted at esophageal inlet, 158 luminal prolapse, 109
mucosal injury at sites of impaction, 159 mucosal tear, 147, 149
multiple needles in GI tract, 162 normal, 112
needle at junction of body and antrum, 161 polypoidal adenocarcinoma, 99
needle in second part of duodenum, 161 ulcerated tumor at, 98
piece of salad impacted at esophageal inlet, 159 ulcer below, 39
Fundal varix, 119; see also Portal hypertension varices below, 118
being injected with cyanoacrylate glue, 120 Gastroesophageal reflux disease (GERD), 19;
as bunch of grapes, 120 see also Hiatal hernia
isolated fundal varix, 119 Barrett’s esophagus, 33–35
ulceration and oozing, 121 bile reflux esophagitis, 30
white nipple sign on, 119 distal esophageal mucosa ulceration, 27
distal esophagus ulceration, 30
endoscopic grading of, 24
G
and erosions, 24, 25, 26, 27
Gallstone ileus, 175 erosive esophagitis, 29
Gastric esophageal involvement in, 28
antrum tumor, 105 gastrojejunostomy stoma, 27
body, 5 giant duodenal ulcer, 29
diverticulum, 172 linear ulcer, 26
fundus, 8 Los Angeles grading, 24
intramural pseudocyst, 171 oval erosions above Z line, 24
mucosa, 126 peptic stricture, 31–32
Gastric antral vascular ectasia (GAVE), 155 prepyloric ulcer with pseudo diverticulum, 29
linear disposition of, 156 Savary Miller grading, 24
 Index 181

Gastroesophageal varix, 117; see also Portal GERD, see Gastroesophageal reflux disease
hypertension Giant
large fundal varix, 121 duodenal ulcer, 29
Gastrointestinal stromal tumor (GIST), 83; see also juxtapapillary diverticulum, 172
Benign tumors kissing ulcers, 59
in gastric body, 86 prepyloric ulcer, 52
in gastric fundus, 86, 87 GIST, see Gastrointestinal stromal tumor
inflammatory polyp at GE junction, 85 GJ, see Gastrojejunostomy
at junction of D1 and D2, 90 Glycogen acanthoma in esophageal body, 168
lipoma at apex of D1, 91 Granulomatous sarcoma of esophagus, 139–140
at lower end of esophagus, 83
lymphoid hyperplasia in D2, 92 H
multiple adenomatous polyps, 88
Hamartomatous polyp, 90
pancreaticoduodenectomy, 91
Hard palate, 2
polyp at GE junction, 84
HCS, see Hematocystic spot
polyp during surgical excision, 90
Hematocystic spot (HCS), 110, 111
polyp from pyloric ring, 89, 90
Hematoma, submucosal, 149; see also
polyp obstructing pylorus, 89
Mallory–Weiss syndrome
polyps in antrum, 88
Hemobilia, 174
prepyloric polyp, 89
Hernial sac on retroflexion, 28
in second part of duodenum, 91
Herpes simplex virus (HSV), 135
sentinel polyp, 84
esophagitis, 136, 137
sliding hiatal hernia with inflammatory mucosal
ulcers in mid-esophagus, 136
polyp, 85
Hiatal hernia, 19, 30; see also Gastroesophageal
stalk after excision, 90
reflux disease
ulcerated stalk in D2, 92
Barrett’s esophagus with sliding, 33, 34
with ulcerated surface in gastric body, 87
classification of, 19
villous adenoma completely filling D2 lumen, 92
erosive esophagitis with sliding, 29
villous adenoma in D2, 91
esophagitis with sliding, 28
Gastrointestinal tract, multiple needles in, 162
gastric mucosal prolapse through lax LES, 22
Gastrojejunocolic fistula, 75, 76; see also
hernial sac on retroflexion, 28
Gastrojejunostomy
Lax LES, 20, 21
endoscopic diagnosis of, 77
paraesophageal hernia with sliding, 23
Gastrojejunostomy (GJ), 71
peptic stricture and sliding, 32
bile reflux gastritis, 80
sliding, 19, 26, 27, 31
giant stomal ulcer, 73
Hookworm, 145
inflammatory polyp, 80, 81
HSV, see Herpes simplex virus
malignancy at stomal site, 81
HSV esophagitis, 136, 137; see also UGI tract lesions
retrograde jejunogastric intussusception, 78, 79
and diseases
small stoma in body of stomach, 74
discrete ulcers in proximal esophagus, 137
Gastrojejunostomy stoma, 27, 71
HSV ulcers, 136
in body of stomach, 74
Human immunodeficiency virus associated
edema, 72
idiopathic ulcer in mid-esophagus, 135
giant stomal ulcer, 73
along greater curvature, 71
I
malignancy at, 81
ulcer around silk suture, 73 Idiopathic thrombocytopenic purpura (ITP), 169
ulcer bleeding, 75 Incisura
ulcer close to loop opening, 73 angularis, 8
GAVE, see Gastric antral vascular ectasia giant ulcer on, 49
GE junction, see Gastroesophageal junction multiple ulcers on, 45
182 Index

Inflamed mucosa, 125, 126 M

Inflammatory polyp; see also Gastrojejunostomy;
Malignant tumors, 93
Gastrointestinal stromal tumor
adenocarcinoma, 97, 98
in antrum, 88
ampullary carcinoma, 107
arising from pyloric ring, 89
circumferential involvement of D2, 108
close to afferent loop opening, 80
circumferential tumor around pylorus, 103
close to efferent loop opening, 80
duodenal carcinoma, 106
at GE junction, 84, 85
duodenal infiltration by renal cell
at GJ stomal margin, 81
carcinoma, 108
multiple, 88
early carcinoma in distal esophagus, 96
obstructing pylorus, 89
in gastric antrum, 105
prepyloric inflammatory polyp, 89
involving antrum and pylorus, 102
sliding hiatal hernia with, 85
involving distal body and antrum, 101
Inlet patch, 167
involving lesser curve and incisura, 100
in proximal esophagus, 168
linitis plastic, 105
Interstitial cells of Cajal, 83
metachronous secondary, 106
Iron-deficiency anemia, 9
multiple submucosal polyps in D1, 107
ITP, see Idiopathic thrombocytopenic
polyp at Z line, 96
purpura
polypoidal tumor, 99, 104, 107
self-expandable metal stent, 95
J squamous cell carcinoma, 93, 94
superficial spreading carcinoma, 104
Jejunal diverticuli, 172
ulcerated tumor, 93, 98, 99, 103, 102, 104
Junctional varix, 118; see also Portal
ulcero-proliferative growth, 101
hypertension
ulcero-proliferative squamous cell carcinoma, 93
Juxtapapillary diverticulum, 172
Mallory–Weiss syndrome, 147
lacerated esophageal mucosa and hematoma, 149
K linear lacerations across GE junction, 148
linear tears, 147, 149
Kissing ulcers, 59
Mid-esophagus, 4
Modified Dagradi grading, 109; see also Portal
L hypertension
Modified Paquet’s grading, 109; see also Portal
Lacerated esophageal mucosa, 149; see also
hypertension
Mallory–Weiss syndrome
Mouth guard, 2
Laryngo-pharynx, 3
Mucosal
Larynx, 3
inflammation, 125, 126
pigmentation involving, 167
necrosis, 127, 136
Lax LES, 20, 21; see also Hiatal hernia
petechiae, 169
gastric mucosal prolapse through, 22
pharyngeal mucosa, 125
with sliding hiatal hernia, 21
ulcer at site of FB impaction, 158, 159
Left pyriform fossae (LPF), 3
Multiple
LES, see Lower esophageal sphincter
adenomatous polyps, 88
Ligated varix, 115; see also Portal hypertension
inflammatory polyps, 88
Linitis plastic, 105
jejunal diverticuli, 172
Lipoma, submucosal, 91
submucosal polyps, 107
Los Angeles grading, 24; see also Gastroesophageal
superficial ulcers, 56
reflux disease
Lower esophageal sphincter (LES), 20
LPF, see Left pyriform fossae
N
Lymphoid hyperplasia, 92 Necrotic mucosa, 127
 Index 183

P ligated varix, 115

mucosal appearance in gastropathy, 123
Pancreaticoduodenectomy, 91
mucosal tag following variceal obliteration, 114
Pancreatic pseudocyst, 171
Paquet’s grading, 109
Paquet’s grading, 109; see also Portal hypertension
post-EVL ulcers, 116
Paraesophageal hernia, 23
pseudo varix, 112
Peptic stricture, 31; see also Gastroesophageal reflux red wale mark on varix, 110, 111
disease; Hiatal hernia remnants of thrombosed and obliterated
in distal esophagus, 31, 32 varix, 113
and esophageal ulcers, 32 ruptured duodenal varix, 124
and sliding hiatal hernia, 32 sclerotherapy complications, 114
Pharyngeal; see also UGI tract lesions and diseases secondary varices, 111
anesthetics, 1 single column early varix, 109
mucosa, 125 single column of tortuous varix, 118
ulcers, 135 Soehendra classification, 110
Pharynx pigmentation, 167 solidified varix, 121
PHG, see Portal hypertensive gastropathy thrombosed and ulcerated varix following
Pinworms, 145 EVL, 116
Polypoidal tumor; see also Malignant tumors thrombosed varix, 113
in antrum, 104 ulceration and oozing from fundal varix, 121
in D1, 107 varices below GE junction, 118, 119
in fundus, 99 Westaby’s grading, 110
below GE junction, 99 white nipple sign on fundal varix, 119
around pylorus, 104 Portal hypertensive gastropathy (PHG), 122, 123;
Portal hypertension, 109 see also Portal hypertension
bleeding from post-sclerotherapy esophageal Postcricoid
ulcer, 114 membranous stricture, 10, 12; see also
bleeding from ulcerated varix following Esophageal strictures
EVL, 115 rings, 11
bleeding portal hypertensive gastropathy, 123 Post-radiotherapy esophageal stricture in mid-
blue varices, 110 esophagus, 16; see also Esophageal
Conn’s grading, 109 strictures
Dagradi grading, modified, 109 Post-sclerotherapy; see also Esophageal strictures;
diffuse redness on varices, 111 Portal hypertension
diffuse varix along lesser curve, 119 esophageal ulcer bleeding, 114
duodenal varix, 123 stricture, 17
early varices, 109 Prepyloric antrum, 45, 126; see also Benign gastric
endoscopic variceal band ligation, 115 ulcer
eradicated gastric varix, 121 Prepyloric polyp, 89
esophageal stricture, 114 Prepyloric ulcer, 48, 51; see also Benign gastric ulcer;
esophageal ulcer, 113 Gastroesophageal reflux disease
esophageal varices, 110 erosions and pseudodiverticulum, 46
fibrin plug on varix below GE junction, 111 giant, 45, 47
fundal varix, 119, 120 hidden in mucosal folds, 46
gastric mucosa in gastropathy, 122 multiple, 46, 48, 49
gastric varice classification, 117 with pseudo diverticulum, 29
healed post-sclerotherapy ulcer, 114 ulcers on either side of pylorus, 47
hematocystic spot, 111 Proximal biliary tree opacification, 67
intravariceal sclerotherapy, 113 Pseudodiverticula, 56
isolated gastric varix, 117 deformed D1 with, 69
junctional varix, 118 Pseudo varix, 112; see also Portal hypertension
184 Index

Pyloric channel ulcer, 51; see also Benign gastric in distal esophagus, 9
ulcer in mid-esophagus, 94
with evidence of recent bleeding, 51 ulcero-proliferative, 93
Pyloric ring Submucosal; see also Mallory–Weiss syndrome
hamartomatous polyp arising from, 90 hematoma, 149
inflammatory polyp arising from, 89 lipoma, 91
Pylorus, 6, 8 polyps, 107
Superficial ulcers, multiple, 56

R
T
RCS, see Red color signs
Red color signs (RCS), 110 TEF, see Tracheoesophageal fistula
Red wale marking (RWM), 110 Tertiary contraction waves in esophagus, 168
Reflux esophagitis, 52 Thrombosed varix, 113, 116; see also Portal
Renal cell carcinoma, duodenal infiltration by, 108; hypertension
see also Malignant tumors Tongue, 2
Retching gastropathy, 170 Topical pharyngeal anesthetics, 1
Retention esophagitis, 43 Tracheal bifurcation, 4
Retrograde jejunogastric intussusception, 78, 79 Tracheal impression in proximal esophagus, 4
Right pyriform fossae (RPF), 3 Tracheoesophageal fistula (TEF), 163
Roundworm, 146 etiology of acquired fistula, 163
RPF, see Right pyriform fossae following wall necrosis, 165
RWM, see Red wale marking malignant, 164
from pressure necrosis, 163, 164
Tumors, malignant, see Malignant tumors
S
Savary Miller grading, 24; see also Gastroesophageal
U
reflux disease
Schatzki’s ring, 13–14 UGI anatomy, 1
Sclerotherapy; see also Portal hypertension ampulla of Vater, 7
complications, 114 antrum, 8
esophageal stricture, 114 base of tongue, 2
esophageal ulcer, 113 concentric rings of trachea, 4
healed post-sclerotherapy ulcer, 114 dorsum of tongue, 2
intravariceal, 113 duodenal bulb, 6
Self-expandable metal stent, 95 endoscopic view, 2
Sentinel polyp, 84 epiglottis, 3
Sliding hiatal hernia, 19, 26, 27; see also Hiatal gastric body, 5
hernia gastric fundus, 8
Barrett’s esophagus with, 33, 34 GE junction, 8
erosive esophagitis with, 29 hard palate, 2
esophagitis with, 28 incisura angularis, 8
with inflammatory mucosal polyp, 85 junction of gastric body and antrum, 5
paraesophageal hernia with, 23 laryngo-pharynx, 3
peptic stricture and, 32 larynx, 3
visible through peptic stricture, 31 mid-esophagus, 4
Soehendra classification, 110 mouth guard, 2
Spontaneous esophageal hematoma, 168 preparation for endoscopy, 1
Squamocolumnar junction, 5 pylorus, 6, 8
Squamous cell carcinoma, 93; see also Malignant squamocolumnar junction, 5
tumors tracheal bifurcation, 4
 Index 185

tracheal impression in proximal esophagus, 4 with elevated margin around pylorus, 104
uvula, 2 at GE junction, 98
UGI tract lesions and diseases, 135 involving gastric fundus, 99
acute infectious gastroduodenitis, 141–143 involving incisura and lesser curvature, 102
biliary ascariasis, 145 around pylorus, 103, 104
Candida esophagitis, 138 starting from incisura to pylorus, 102
CMV esophageal ulcers, 137 Ulcero-proliferative
distal esophagus, 137 growth involving gastric body, 101
distally coalescing ulcers, 137 squamous cell carcinoma, 93
drug-induced esophagitis, 140 Uvula, 2
duodenal tuberculosis, 144
endoscopic retrograde cholangiogram, 145
V
esophageal involvement in HIV-infected
patients, 135 Varix, thrombosed, 113, 116; see also Portal
esophageal ulcer in Behcet’s disease, 139 hypertension
extensive ulceration of duodenum, 143 Villous adenoma in D2, 91, 92
granulomatous sarcoma of esophagus, 139–140 Visible vessel
hookworm in D1, 145 accentuated by adherent clot, 63
HSV esophagitis, 136, 137 in clean ulcer base, 62
mucosal necrosis, 136 covered with fresh clot, 62
pharyngeal ulcers, 135
pinworms in D1, 145
W
roundworm across choledochoduodenostomy
stoma, 146 Watermelon stomach, 155, see Gastric antral
roundworm in D3, 146 vascular ectasia
ulcers in proximal esophagus, 137 Westaby’s grading, 110; see also Portal
Ulcerated tumor, 93; see also Malignant tumors hypertension