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Tropical Hepatogastroenterology
“This page intentionally left blank"

xx
Tropical Hepatogastroenterology

BN Tandon MD, FNA, FAMS

Chairman, Digestive Diseases Foundation
Formerly Dean and Head, Department of Gastroenterology,
All India Institute of Medical Sciences, New Delhi

ELSEVIER
A division of
Reed Elsevier India Private Limited
Tropical Hepatogastroenterology
Tandon

ELSEVIER
A division of
Reed Elsevier India Private Limited

Mosby, Saunders, Churchill Livingstone, Butterworth Heinemann and

Hanley & Belfus are the Health Science imprints of Elsevier.

© 2008 Elsevier

All rights are reserved. No part of this publication may be

reproduced, stored in a retrieval system, or transmitted in any form
or by any means, electronic, mechanical, photocopying, recording or
otherwise, without the prior permission of the publisher.

ISBN: 978-81-312-0313-2

Medical knowledge is constantly changing. As new information

becomes available, changes in treatment, procedures, equipment and
the use of drugs become necessary. The authors, editors, contributors
and the publisher have, as far as it is possible, taken care to ensure
that the information given in this text is accurate and up-to-date.
However, readers are strongly advised to confirm that the
information, especially with regard to drug dose/usage, complies
with current legislation and standards of practice.

Published by Elsevier, a division of Reed Elsevier India Private Limited,

Sri Pratap Udyog, 274, Captain Gaur Marg, Sriniwaspuri,
New Delhi-110 065, India.

Commissioning Editor: Sonali Dasgupta

Managing Editor (Development): Shabina Nasim
Manager (Editorial Projects): Radhika Menon
Production Manager: Sunil Kumar
Production Executive: Ambrish Choudhary

Typeset by Krishtel eMaging Solutions Pvt. Ltd., Chennai-600 017.

Printed and bound at Replica Press, Kundli, India.

xx
Chapter

0
Preface

Why did I start this book?

In an era where libraries are accessible, and good textbooks published in the west are available, is there
the need for another book?
I believe that the answer is “Yes”. Medicine, in terms of both disease pattern and therapeutic practices,
shows tremendous geographical variations. Data and recommendations from different socioeconomic
settings may not correctly reflect the picture at home. Is diverticulitis the commonest cause of lower gastroin-
testinal bleeding? Should we always ask for ambulatory pH monitoring in patients with gastroesophageal
reflux? Does the diagnosis of gastrointestinal tuberculosis always require histological confirmation before
the initiation of antitubercular therapy? Does variceal bleeding in pregnancy mean mortality in a country
where prehepatic portal hypertension is common? Is interferon therapy appropriate for all settings of chronic
hepatitis? The answers to these and several other questions would depend largely on the country in which
the questions are asked. Medicine must be socially relevant for the community which it serves, and this
principle applies as much to primary health care as to the practice of secondary and tertiary-level medicine.
It is important for doctors to be able to refer to sources from their own medical environment, but they
are often handicapped from the lack of available literature. (To say nothing of the fact that books published
in the west are often prohibitively expensive!)
Yet, there is no scarcity of gastroenterologists who are very highly qualified. I was convinced that it
would be a shame not to tap their skills. I was fortunate that my colleagues offered enthusiastic support,
and this project was very quickly under way.
I took the decision to make this a book not about gastroenterology, which is a purely medical discipline,
but about gastrointestinal diseases, which is a medical-cum-surgical subject. Many chapters are written by
surgeons, who were able to write well about the indications and results of surgery. I did, however, ask them
to avoid intricate surgical details, since this book is not about teaching the reader how to actually operate
on a patient. The result has been a book that provides a gratifying balance between a medical and a surgical
perspective.
The other decision that I made at the start of the project was to ensure that the chapters did, indeed,
fulfill their objective of enabling the readers to treat patients according to current practices in the tropics.
This meant meticulous, even ruthless editing, and, while this has contributed generously to the time taken
to bring out the book (over four years), the approach has been uncompromising. I believe that the wait has
been worth the effort.
A word about the selection of chapters. From the start, this was not to be a textbook of gastroenterology.
This is primarily a selection of subjects of importance to the tropics, subjects that receive lesser emphasis

v
 vi Preface

in books published from other regions. In most cases the authors are those who have worked extensively
with the conditions that they have written about. At the end, this book has been able to include almost all
the chapters planned at the start of the project.

BN Tandon

xx
Chapter

0
Acknowledgments

There is no way that I could have completed an undertaking of this magnitude without substantial help.
I have several persons to thank for this.
I have always felt that my knowledge and skills derive from my association with my patients. It is
because of them that I am competent to write a book like this, and I am in their debt.
I have been particularly fortunate that the contributors, all senior professionals, have so willingly given
of their time and have written such excellent chapters.
Dr Siddharth Dutta Gupta and Dr Anil Agarwal have kindly provided illustrations for several chapters
in the book.
Mr Rajeev Banerji, Mr Sumeet Rohatgi, and Ms Shabina Nasim from Elsevier were the real force
behind this enterprise. I must say that they showed a rare combination of pressure and patience, and I have
developed a great respect for Elsevier because of their wonderful staff.
Mr Sajeev has provided extensive secretarial support. He has been the one constant throughout this
enterprise, and has organized my papers, maintained the records, arranged my meetings and telephone
calls, and more.
Mr Shankar has also provided considerable secretarial support, in association with Mr Sajeev.
All books during their preparation take on a life of their own, and this one was no exception, eating into my
personal time like a newborn baby. My work would have remained incomplete without the encouragement,
and sometimes tolerance, from my family and colleagues. Inevitably there were times when I wondered if
I would complete this project, and at such moments they were the ones who gave me the most hope, and
I am truly grateful.

BN Tandon

vii
“This page intentionally left blank"

xx
Chapter

0
Contributors

AC Anand vsm, md, dm, ficp, facg Anoop Saraya md, dm

Consultant and Professor (Hepatogastroenterol- Professor, Department of Gastroenterology and
ogy), Army Hospital R & R, New Delhi-110010 Human Nutrition, All India Institute of Medical
Sciences, Ansari Nagar, New Delhi-110029
Adarsh Chaudhary ms
Senior Consultant, Department of Gastrointestinal Anu Behari ms
Surgery, Sir Ganga Ram Hospital, New Delhi Assistant Professor, Department of Surgical Gas-
troenterology, Sanjay Gandhi Postgraduate Insti-
Ajay Duseja md, dm
tute of Medical Sciences, Lucknow-226014
Assistant Professor, Department of Hepatology,
Postgraduate Institute of Medical Education and
Research, Chandigarh Anurag Krishna ms, mch, fams
Senior Consultant, Department of Pediatric
AK Jain md, dm Surgery, Sir Ganga Ram Hospital, New Delhi
Professor, Department of Gastroenterology,
Banaras Hindu University, Varanasi Anurag Tandon md, dm
Senior Consultant, Metro Center for Liver and
AK Kakar ms Digestive Diseases, Noida
Professor and Head, Department of Surgery,
Maulana Azad Medical College, New Delhi Arun Kumar Sharma md
Assistant Professor, Department of Gastroenterol-
Anil Arora md, dm
ogy, Postgraduate Institute of Medical Education
Consultant Gastroenterologist and Hepatologist,
and Research, Chandigarh
In-charge Liver Clinic and Chief of Hepatologist
Services, Sir Ganga Ram Hospital, Rajinder Nagar,
New Delhi-110060 Atul K Sharma ms, dnb
Senior Adviser Surgery and GI Surgery, Command
Anil K Agarwal ms, mch Hospital (CC), Lucknow-226002
Professor and Head, Department of Gastrointesti-
nal Surgery, GB Pant Hospital and Maulana Azad BN Tandon md, fna, fams
Medical College, New Delhi Chairman, Digestive Diseases Foundation

ix
 x Contributors

Chandrasekhar md, dm MP Sharma md, dm, fams, ficp, facg

Senior Consultant, Department of Gastroenterol- Head, Department of Gastroenterology, Rockland
ogy, Yashoda Hospitals, Hyderabad Hospital, New Delhi

Deepak Govil md, phd N Ananthakrishnan ms, mnams, frcs (ed), frcs
Senior Consultant, Department of Surgical Gas- (glasgow), fams
troenterology, Apollo Hospital, New Delhi Director, Professor and Head, Department of
Surgery, Jawaharlal Institute of Postgraduate Med-
Ganesh Bhat md, dm ical Education and Research, Pondicherry-605006
Assistant Professor, Department of Gastroenterol-
ogy, Kasturba Medical College, Manipal Pankaj Vohra md
Diplomate American Board of Pediatrics;
Girish SP ms, mch Diplomate American Board of Pediatric Gastroen-
Resident, GB Pant Hospital, New Delhi terology; Senior Consultant, Pediatric Gastroen-
terology, Hepatology and Nutrition, Max Super
Gourdas Choudhuri md, dm, fams, ficp, facg Speciality Hospital, Saket, New Delhi-110017
Professor and Head, Department of Gastroen-
terology, Sanjay Gandhi Postgraduate Institute of PK Mishra ms, phd (aiims)
Medical Sciences, Lucknow-226014 Associate Professor, Department of Gastrointesti-
nal Surgery, GB Pant Hospital, New Delhi
Govind K Makharia md, dm, dnb, mnams
Premashis Kar md, dm
Assistant Professor, Department of Gastroenterol-
Professor of Medicine, Gastroenterology Division,
ogy and Human Nutrition, All India Institute
Department of Medicine, Maulana Azad Medical
of Medical Sciences, Ansari Nagar, New Delhi-
College and Dean, Faculty of Medical Sciences,
110029
University of Delhi, Delhi-110007
Kartar Singh md, dm Radha K Dhiman md, dm, mnams, facg
Professor, Department of Gastroenterology, Post- Assistant Professor, Department of Hepatology,
graduate Institute of Medical Education and Postgraduate Institute of Medical Education and
Research, Chandigarh Research, Chandigarh
Kaushal Madan md, dm Radha Krishnan md, dm
Assistant Professor, Department of Gastroenterol- Senior Resident, Department of Gastroenterology,
ogy, All India Institute of Medical Sciences, Ansari Sanjay Gandhi Postgraduate Institute of Medical
Nagar, New Delhi-110029 Sciences, Lucknow-226014

Manisha Dwivedi md, dm, ficp, facg K Rajkumar ms

Professor and Head, Department of Gastroen- Senior Resident, Department of Gastrointestinal
terology and Hepatology, MLN Medical College, Surgery, GB Pant Hospital and Maulana Azad
University of Allahabad, Allahabad Medical College, New Delhi

xx
 Contributors xi

Rajneesh Kumar ms nal Surgery, GB Pant Hospital and Maulana Azad

Senior Resident, Department of Gastrointestinal Medical College, New Delhi
Surgery, All India Institute of Medical Sciences,
Ansari Nagar, New Delhi-110029 SP Misra md, dm, frcp (london), frcp
(edinburg), fnasc, facg, ficp
Rakesh Aggarwal md, dm Professor of Hepatology, MLN Medical College,
Professor, Department of Gastroenterology, All University of Allahabad, Allahabad
India Institute of Medical Sciences, Ansari Nagar,
New Delhi-110029 SS Negi ms, mch
Consultant, Department of Gastrointestinal
Ramesh Roop Rai md, dm Surgery, Sir Ganga Ram Hospital, New Delhi
Professor and Head, Department of Gastroenterol-
ogy, SN Medical College, Jaipur Subrat Kumar Acharya md, dm
Professor and Head, Department of Gastroenterol-
S Nijhawan md, dm ogy, All India Institute of Medical Sciences, Ansari
Professor, Department of Gastroenterology, SMS Nagar, New Delhi-110029
Medical College, Jaipur
Sudhir Kumar ms
SS Gandhe Senior Resident, Department of Surgical Gastroen-
Research Assistant, Hepatitis Division, National terology, Apollo Hospital, New Delhi
Institute of Virology, Pune Sujoy Pal ms, mch
Assistant Professor, Department of Gastrointesti-
Saket Goel ms
nal Surgery, All India Institute of Medical Sci-
Associate Consultant, Department of Surgical
ences, Ansari Nagar, New Delhi-110029
Gastroenterology, Apollo Hospital, New Delhi
Suneet Sood ms, mams
Sanjay Jain md, dnb (fellow, gastroenterology) Professor, Department of Surgery, Universiti
Department of Gastroenterology, Sir Ganga Ram Teknologi Mara, Shah Alam, Malaysia
Hospital, New Delhi
Surinder S Rana md
Sanjoy Mandal ms, mch Assistant Professor, Department of Gastroenterol-
Senior Resident, Department of Gastrointestinal ogy, Postgraduate Institute of Medical Education
Surgery, GB Pant Hospital and Maulana Azad and Research, Chandigarh
Medical College, New Delhi
Sushma md (pathology)
Sethu Babu md, dm Senior Consultant, Global Hospital, Hyderabad
Senior Consultant in Gastroenterology, Sai Vani
Hospital, Hyderabad TK Chattopadhyay ms
Professor and Head, Department of Gastroin-
Shivendra Singh ms, mch testinal Surgery, All India Institute of Medical
Assistant Professor, Department of Gastrointesti- Sciences, Ansari Nagar, New Delhi-110029

Part / xx
 xii Contributors

Usha Dutta md, dm Vishal Gupta ms

Associate Professor, Department of Gastroenterol- Senior Resident, Department of Surgical Gastroen-
ogy, Postgraduate Institute of Medical Education terology, GB Pant Hospital, New Delhi
and Research, Chandigarh

Vidya A Arankalle phd, msc Vivek Tandon ms, mch

Deputy Director and Head, Hepatitis Division, Senior Consultant, Metro Center for Liver and
National Institute of Virology, 20-A, Dr Ambedkar Digestive Diseases, Noida
Road, Pune
VK Kapoor ms, facs, frcs, facg
Vikram Bhatia Professor and Head, Department of Surgical Gas-
Senior Research Officer, Department of Gastroen- troenterology, Sanjay Gandhi Postgraduate Insti-
terology, All India Institute of Medical Sciences, tute of Medical Sciences, Lucknow-226014
Ansari Nagar, New Delhi-110029

Vineet Ahuja, md, dm YK Chawla md, dm, mnams, facg

Associate Professor, Department of Gastroenterol- Professor and Head, Department of Hepatology,
ogy, All India Institute of Medical Sciences, Ansari Postgraduate Institute of Medical Education and
Nagar, New Delhi-110029 Research, Chandigarh

xx
Chapter

0
Contents

Preface v

Acknowledgments vii

Part I Esophagus 1

1 Cancer of the Esophagus 3

2 Corrosive Injuries of the Esophagus and Stomach 39
3 Gastroesophageal Reflux Disease 57
4 Achalasia Cardia 82

Part II Stomach 95

5 Peptic Ulcer Disease and Nonulcer Dyspepsia 97

6 Benign Tumors of the Stomach 116
7 Carcinoma of the Stomach 126

Part III Small Bowel 153

8 Tropical Malabsorption 155

9 Infections of the Small Bowel 167

Part IV Large Bowel 195

10 Management of Ulcerative Colitis 197

11 Benign Colorectal Tumors 213
12 Malignant Colorectal Tumors 221

xiii
 xiv Contents

Part V Liver 241

13 Jaundice in the Infant 243

14 Hepatitis Viruses: Virology and Epidemiology 261
15 Virological Diagnosis of Hepatitis 269
16 Hepatitis A Infection 277
17 Hepatitis B and D Virus 286
18 Hepatitis C: An Indian Perspective 311
19 Hepatitis E 321
20 Hepatic Drug Toxicity 330
21 Toxic Liver Injury 344
22 Hepatic Granulomas 354
23 Autoimmune Hepatitis 363
24 Cirrhosis of the Liver 375
25 Noncirrhotic Portal Fibrosis 388
26 Extrahepatic Portal Venous Obstruction 404
27 Budd-Chiari Syndrome 413

Part VI Liver Failure 423

28 Acute Liver Failure 425

29 Subacute Hepatic Failure 445
30 Benign Liver Tumors 450

Part VII Gallbladder and Biliary Tract 467

31 Gallstone Disease 469

32 Gallbladder Cancer and Cholangiocarcinoma 485
33 Choledochal Cysts 514
34 Benign Bile Duct Strictures 528

Part VIII Pancreas 537

35 Acute Pancreatitis 539

36 Chronic Pancreatitis 566
37 Cancer of the Pancreas 597

xx
 Contents xv

Part IX Parasitic Diseases 613

38 Intestinal and Extraintestinal Amebiasis 615

39 Hydatid Cyst of the Liver 629
40 Schistosomiasis 641

Part X Special Topics 651

41 Abdominal Tuberculosis 653

42 Diarrhea in Children 678
43 Nonvariceal Upper Gastrointestinal Tract Bleeding 703
44 Lower Gastrointestinal Bleeding 722
45 Hepatorenal Syndrome 738
46 Hepatic Encephalopathy 746
47 Ascites in Cirrhosis 755
48 Malignant Liver Tumors 761

Index 780
“This page intentionally left blank"

xx
Part
I

Esophagus

1 Cancer of the Esophagus 3

2 Corrosive Injuries of the Esophagus and Stomach 39
3 Gastroesophageal Reflux Disease 57
4 Achalasia Cardia 82
“This page intentionally left blank"

xx
Chapter

1
CANCER OF THE ESOPHAGUS
Rajneesh Kumar, Sujoy Pal, and TK Chattopadhyay

1.1 INTRODUCTION of adenocarcinoma has been increasing steadily

Esophageal cancer is an important cause of can- in the West.[2, 3] In USA, adenocarcinoma is the
cer related death in old age. Dysphagia, which is most common subtype of esophageal carcinoma
the predominant symptom, significantly affects the at present.[4]
quality of life of the patients. Therefore, palliation Certain geographic regions have a high inci-
of the disease is as important as the treatment for dence of esophageal carcinoma (Table 1.1). The
cure. so-called ‘Asian esophageal cancer belt’ stretches
More than two decades ago, in a classic review, from Turkey, east of the Caspian Sea through
Earlam and Cunha–Melo[1] noted that of every northern Iran, northern Afghanistan, southern
100 patients with esophageal carcinoma, 58 will regions of the former USSR such as Turk-
be explored, 39 will have the tumor resected, and menistan, Uzbekistan, Tajikistan; to India, China,
13 will die in hospital. Of the 26 patients leaving and Mongolia.[5] Other regions with high incidence
hospital with the tumor excised, 18 will survive for are certain parts of Africa (e.g., Transkei region of
1 year, 9 for 2 years, and 4 for 5 years. While this South Africa) and South America. The incidence
dismal prognosis may not be true any longer, no of esophageal cancer relative to other cancers in
single modality of treatment has been proven as the India is shown in Table 1.2. Men are more affected
gold standard even today. Hence the current focus than women, probably due to the high prevalence
is on early detection and multimodality treatment of risk factors like smoking and alcohol intake in
for achieving better results. males.

1.2 EPIDEMIOLOGY 1.2.2 Dysplasia/Carcinoma Sequence

1.2.1 Incidence and Prevalence
Various lesions of the esophageal epithelium
Both squamous cell and adenocarcinoma com- are precursors to cancer. They include chronic
monly affect the esophagus. Worldwide, squamous esophagitis, atrophy, dysplasia, papilloma, and
cell carcinoma (SCC) has been the most common carcinoma in situ.[6, 7] Esophageal carcinoma may
subtype. However, cancer incidence trends show develop at the site of these precursors. These
an overall decrease in SCC, whereas the incidence lesions are prevalent in high risk populations, and

3
 4 Chapter 1 / CANCER OF THE ESOPHAGUS

TABLE
fy 1.1 IARC (International Agency for 1.2.3 Risk Factors and Associations
Research on Cancer) (WHO):
Incidence of esophageal cancer 1.2.3.1 Alcohol and tobacco
world over (year 2000)
Alcohol and tobacco are well established etiologic
Country ASR (per 100,000 population) factors for esophageal carcinoma, and, in fact, are
Kenya 21.8 associated with most cancers of the upper aerodi-
Malawi 38.6 gestive tract.[8] Several carcinogens are present in
Botswana 37.2 cigarette smoke. These include nitrosamines and
Lesotho 37.2
polynuclear aromatic hydrocarbons such as ben-
South Africa 16.3
zpyrene. Pipe and cigar smoking is found to be
China 24.5
Mongolia 24.4
worse as a risk association. Black tobacco and hand
Iran 24.0 rolled cigarette smoking has a higher relative risk.
Turkmenistan 26.4 The risk increases with the number of cigarettes
India 7.5 and the duration of smoking.
World (overall) 10.7 For alcoholic drinks, the risk varies with the
ASR = age-standardized rate type of drink consumed. It is least with beer
and intermediate with wine. Alcohol and tobacco
exert a synergistic effect. They potentiate each
TABLE
fy 1.2 IARC (International Agency for other, leading to a field within the upper aero-
Research on Cancer) (WHO): digestive tract where the epithelium is exposed to
Incidence of esophageal and other carcinogens, and is thus prone to develop multiple
cancers in India (year 2000) tumors. This explains the high risk of synchronous
Site of cancer ASR (per 100,000 and metachronous carcinoma in the upper
population) aerodigestive tract in patients with esophageal
Males Females cancer.[9]
Oral 12.8 7.4 1.2.3.2 Dietary carcinogens
Pharynx 9.5 1.8
N-nitroso compounds like nitrosamines are known
Esophagus 7.5 5.1
dietary carcinogens, and are found in high levels
Lung 9.0 1.9
Larynx 6.2 0.7
in the diet in high incidence regions like the
Prostate 4.5 – Linxian Province of China.[10] Cured, smoked,
Stomach 5.6 2.8 or sun-dried salted meat, fish, or vegetables are
Colorectum 4.7 3.2 rich in such carcinogens. In Kashmir, Khuroo
Breast – 19.1 and colleagues[11] found that the high risk diet
Cervix – 30.6 contained substantial amounts of N-nitroso com-
Ovary – 4.8 pounds in foods such as salt, tea, dried fish, certain
ASR = age-standardized rate vegetables, and red chilies.
1.2.3.3 Nutritional deficiencies
may be present alongside invasive carcinoma in Certain micronutrient and vitamin deficiencies are
esophagectomy specimens. associated with esophageal cancer. Diets deficient

Tropical Hepatogastroenterology
 EPIDEMIOLOGY 5

in vitamins A, C, E, niacin, riboflavin, mag- fungi such as Fusarium, Alternaria, Aspergillus,

nesium, selenium, and zinc, diets rich in pro- and Cladosporium have been found contaminating
cessed and starchy foods, and diets poor in fresh the grains.[18] These can reduce nitrates to nitrites,
fruits and vegetables are associated with increased and can also decompose proteins and promote the
risks of esophageal carcinoma.[12] In the Transkei formation of nitrosamines.
region, pellagra used to be very prevalent. Patients
with pellagra had intensely inflamed esophageal 1.2.3.6 Chronic esophageal irritation
mucosa, which placed these patients at a very high
risk for developing esophageal carcinoma.[13] Chronic thermal and mechanical irritation due to
dietary factors is frequently associated with the
1.2.3.4 Environmental factors and pollutants risk of esophageal cancer. Hot tea is consumed in
large amounts in high incidence regions of Iran.[19]
The soil theory gained credence from studies Drinking of the plant extract ‘mate’ has a frequent
done in Transkei, South Africa.[14] There appears association in high incidence regions of South
to be an inverse correlation between mortality America.[20] Hot rice intake has been implicated
from esophageal cancer and the soil content of in China.[21]
molybdenum, manganese, zinc, magnesium, sili- In Iran and the Middle East, food grains contain
con, nickel, iron, bromine, iodine, chlorine, potas- fibrous material from contaminating seeds of com-
sium, sodium, phosphorus, and bicarbonate. How mon Mediterranean grass. This fibrous material
these substances affect the esophageal epithelium has carcinogenic properties.
is not known. Molybdenum is a cofactor of the Spicy and improperly chewed foods have
enzyme nitrate reductase which affects nitrite and been implicated in the risk of esophageal
nitrate content in plants. Petroleum contamina- carcinoma.
tion of water and occupational exposure of metal
dust such as chromium, chromates, beryllium may 1.2.3.7 Achalasia cardia
increase the risks of esophageal cancer.[15] Vul-
canization workers, plumbers, and pipe fitters Patients with long-standing achalasia are at high
have been identified in some studies as high risk risk of esophageal carcinoma, most likely from
groups.[16] chronic stasis and inflammation. The preva-
lence of esophageal carcinoma in various stud-
1.2.3.5 Infections ies of long-standing achalasia varies from 0% to
8.6%.[22–24] Recently, histological mapping of the
Human papilloma virus (HPV), especially types resected esophageal specimens has demonstrated
16 and 18, are implicated in the pathogenesis of marked hyperplastic changes of stratified squa-
cancers developing in several squamous epithe- mous epithelium and multiple foci of dysplastic
lia including cervix, vulva, larynx, and skin. HPV changes.[25] In recent studies, the changes in p53,
DNA sequence has been found in both benign and p16, p21, epidermal growth factor immunoreactiv-
malignant esophageal conditions.[17] Fungi have ity, marked squamous hyperplasia, and increased
been implicated as agents especially from studies numbers of CD3+ cells have been found in the at
in China. Of the various fungal infections of the risk epithelium.[26] The tumor usually occurs in the
esophagus, candida is the most common. Common dilated middle third part of the esophagus. Most

Part I / Esophagus
 6 Chapter 1 / CANCER OF THE ESOPHAGUS

of these are squamous cell carcinoma. However, 1.2.3.10 Others

reflux following myotomy may cause Barrett’s
esophagus and adenocarcinoma. The diagnosis Irradiation and chemotherapy have been impli-
is usually made late, and the prognosis is poor. cated as causing esophageal carcinoma in anec-
Patients with achalasia for over 15–20 years should dotal reports. Endoscopic sclerotherapy has been
undergo surveillance with 6-monthly endoscopy associated as an etiologic agent. However, it is
and biopsy.[27] believed that this relationship is only due to coex-
Some cases of carcinoma may clinically mimic isting factors.
achalasia; this presentation is termed pseudoacha- A previous history of gastrectomy for benign
lasia. Liu and colleagues[28] recently studied pseu- diseases is found in 0.7%–10.4% of patients with
doachalasia. They found that most cases were squamous cell carcinoma of the esophagus.[34] It
due to neoplastic infiltration of the myenteric is difficult to separate this risk from confounding
plexus, and a few represent a paraneoplastic syn- factors and formulate any definite guidelines for
drome due to a distant neoplasm (e.g., lung surveillance.
carcinoma). Plummer–Vinson syndrome (Paterson–Kelly
syndrome) is characterized by iron deficiency ane-
mia, atrophy of oral, pharyngeal and esophageal
1.2.3.8 Corrosive strictures
mucosa, and esophageal webs. These patients
Between 1% and 7% of patients with esophageal are predisposed to developing carcinoma in the
carcinoma have a history of corrosive intake. Car- upper digestive tract.[35] The risk of developing
cinoma develops after about 40 years.[29] Men are carcinoma is about 10%.
more frequently affected than females, and the Tylosis is a rare autosomal dominant disease
carcinoma usually develops at the region of the cor- characterized by hyperkeratosis of the palms and
rosive stricture. The mechanism is chronic inflam- soles. Up to 95% of these patients develop squa-
mation associated with the stricture. Appelqvist mous cell carcinoma by the age of 65 years.[36]
and Salmo[30] noted a better prognosis for these Celiac disease and scleroderma have been asso-
‘scar’ carcinomas and proposed that this was ciated with the development of squamous cell and
because of younger age, early obstructive symp- adenocarcinoma respectively, but the relationship
toms, and scar tissue which prevents early dissemi- is thought to be secondary.
nation of the tumor.[31] This risk of late malignancy Genetic predisposition has a relatively minor
has led some surgeons to perform esophagectomy role in esophageal carcinoma. In China a few fam-
in patients with severe corrosive injury of the ilies have been identified with a strong genetic
esophagus.[32] susceptibility of developing esophageal carci-
noma.[37]
1.2.3.9 Esophageal diverticula
1.2.3.11 Barrett’s metaplasia
Malignant transformation in chronic Zenker’s
diverticulum is rare, and a very small number of Barrett’s intestinal metaplasia is protective
cases have been reported. A large Mayo clinic response to acid reflux in the esophagus.
series of 961 Zenker’s diverticulum had a 0.3% Endoscopically it can be divided into three types:
prevalence of carcinoma.[33] (a) long segment Barrett’s where the metaplastic

Tropical Hepatogastroenterology
 PATHOLOGY 7

epithelium extends for more than 3 cm proximal It binds to EGFr to stimulate growth. The overex-
to the gastroesophageal junction; (b) short seg- pression of the ErbB2 and cyclin D1 genes has
ment Barrett’s where it is limited to within 3 cm been observed in 30%–50% and 40%–60% of
of the cardia; and (c) gastric cardia metaplasia, cases of esophageal carcinoma respectively. Ras
which is restricted to the region of the cardia mutations are uncommonly found with esophageal
only. The prevalence of Barrett’s is 5%–15% in carcinoma[42]
patients undergoing endoscopy for symptoms of Fragile histidine triad (FHIT) gene mutations
reflux.[38] The risk of adenocarcinoma in long have been found in 60%–100% of esophageal can-
segment Barrett’s metaplasia is 0.5% annually.[39] cer as well as in Barrett’s metaplasia. This appears
The magnitude of risk in short segment Barrett’s to be a relatively early event in carcinogenesis in
is less.[40] The risk is even lower in patients with Barrett’s epithelium.[43] Retinoblastoma (Rb) gene
gastric cardia metaplasia. Though no high risk product is a critical mediator of cell cycle arrest
group can be clearly identified in the patients with after DNA damage, and its mutations have been
Barrett’s metaplasia, some characteristics may found in 20%–40% of the tumors. The p53 gene
help in selecting patients at higher risk for devel- product regulates cell cycle, DNA repair, apop-
oping carcinoma. These include obesity, white tosis, and controls the cell cycle. P53 mutations
males, young age, ulceration, and long-standing are associated with poorly differentiated tumors
disease.[41] The presence of H. pylori has an inverse and poor survival in patients with esophageal ade-
relationship with the development of esophageal nocarcinoma.[44] P16 gene mutations have been
adenocarcinoma. identified in about 20% of esophageal squamous
cell carcinoma.
1.2.3.12 Genetics of esophageal carcinoma Esophageal carcinoma is not a vascular tumor,
but we have found VEGF (vascular endothelial
Several genetic mutations have been identified growth factor) expression to correlate with lymph
which are associated with esophageal carcinoma node metastasis and patient survival.[45]
(Table 1.3). Epidermal growth factor receptor In a recent review, the principal genes impli-
(EGFr) gene is overexpressed in approximately cated in the progression from Barrett’s metaplasia
30%–80% of cases. TGF-alpha (transforming to dysplasia and adenocarcinoma are the loss of
growth factor alpha) is expressed in 40% of tumors. p16 and p53 gene expression, increase in cyclin
D1 expression, induction of aneuploidy, and loss
of Rb, DCC (deleted in colon cancer), and APC
TABLE
fy 1.3 Expression of genetic mutations in
(adenomatous polyposis coli) gene chromosomal
esophageal carcinoma
loci.[46]
Tumor suppressor genes Oncogenes Others
FHIT EGFr Survivin
1.3 PATHOLOGY
Rb erbB2 VEGF
p53 Cyclin D1 E-cadherin
1.3.1 Squamous Cell Carcinoma
p16 Catenins
P14 Ki-67 Worldwide, this is the most common form of
Telomerase Interleukin-1
esophageal carcinoma. Most tumors (55%) are
Note: For details of abbreviations see text located in the middle third of the esophagus.[47]

Part I / Esophagus
 8 Chapter 1 / CANCER OF THE ESOPHAGUS

Thirty percent are located in the lower third, and spread correlates with lymphatic dissemination
15% in the upper third of the esophagus. (Table 1.4).[51–53]
As previously mentioned, there is some The esophagus is rich in submucosal lymphat-
evidence for a dysplasia—carcinoma-in-situ— ics, and longitudinal spread along the esophagus
invasive carcinoma sequence in esophageal carci- may give rise to tumor deposits in the submucosa
noma. Screening methods are designed to identify as far away as 15 cm from the main tumor.[54, 55]
these preinvasive lesions. It has been estimated that This fact itself is sufficient justification for a
carcinoma-in-situ takes 3–4 years to develop into total esophagectomy as opposed to a subtotal
invasive carcinoma.[48] esophagectomy.
Grossly, the lesion may vary from a subtle Blood borne metastasis may involve the lung,
mucosal abnormality to a macroscopically obvi- liver, bone, and kidney.
ous lesion that may be exophytic or endophytic. Lymph node micrometastases do not signifi-
Exophytic variants include fungating, polypoidal, cantly affect survival in patients with esophageal
or plaque-like tumors. Endophytic tumors are infil- carcinoma,[56] but bone micrometastases do. In one
trative. Microscopically, the tumor may vary from study, up to 90% of resected ribs were positive for
a well differentiated squamous type to poorly marrow micrometastases, and this factor correlated
differentiated pleomorphic cells. with prognosis on multivariate analysis.[57]
The tumor spreads by transmural invasion
through various layers of the esophageal wall.
Since there is no serosa, mediastinal structures 1.3.2 Adenocarcinoma
like the recurrent laryngeal nerve, aorta, trachea,
and others are involved early. Invasion of the Most adenocarcinomas arise in the background of
tracheobronchial tree is the most common, and Barrett’s metaplasia. However, this may not be
may lead to the formation of a tracheoesophageal identifiable in a large tumor. Often, it is difficult to
fistula. separate gastric carcinoma from an esophageal car-
Lymphatic spread occurs to the nodes of cinoma at the gastroesophageal junction. In a bid to
the mediastinum, neck, and upper abdomen. separate these tumors, Siewert proposed a classifi-
Twenty percent to thirty percent of lower third cation that is now commonly accepted.[58, 59] Ade-
tumors spread to the superior mediastinal nodes, nocarcinomas of the gastroesophageal junction are
and the same numbers of upper third tumors defined as tumors whose centers lie within 5 cm
involve abdominal nodes.[49, 50] Transmural tumor of the anatomic cardia. They can be subclassified
as:

TABLE
fy 1.4 Transmural extension of Type I – Adenocarcinoma of the distal esoph-
tumor: Correlation with nodal agus, located at least 1 cm above the
metastases[51–53] cardia and usually arising from an area
Tumor extent Nodal spread of Barrett’s metaplasia.
Mucosal 3% Type II – Tumors arising from cardiac epithe-
Submucosal 30% lium or from intestinal metaplasia at the
Muscularis propria 60% gastric cardia.
Transmural Nearly 100%
Type III – Subcardial gastric carcinoma.

Tropical Hepatogastroenterology
 SYMPTOMS AND SIGNS 9

The anatomic location of the tumor cen- outcome. While length of the tumor has a lesser
ter determines the assignment of subcategory. bearing on prognosis than the TNM stage, a recent
Ichikura and colleagues[60] have defined type II series found that the increasing length of the tumor
tumors (cardia carcinoma) as adenocarcinomas beyond 5 cm worsens the prognosis.[65]
with their epicenter between 1 cm proximal and It was previously thought that adenocarcinoma
2 cm distal to the esophagogastric junction. has a worse prognosis. However, this appears to
Lower esophageal adenocarcinoma spreads be a function of a more advanced stage at pre-
both to mediastinal as well as abdominal nodes. sentation. The long-term prognosis is otherwise
Adenocarcinoma of the cardia and subcardial similar to squamous cell carcinoma.[66] Osugi and
stomach spreads predominantly to the celiac, colleagues[67] showed that vascular and lymphatic
splenic hilar, and periaortic nodes.[61] invasion worsen the prognosis. Advanced age is no
longer considered a poor prognostic factor. Elderly
1.3.3 Uncommon Subtypes patients, if properly selected, have results as good
as younger patients.[68] Perioperative blood trans-
Verrucous carcinoma is a superficial, slow grow- fusion may worsen the prognosis.[69]
ing tumor. Spindle cell carcinoma is a poly- Lately, improved molecular techniques have
poidal tumor which tends not to infiltrate deeply. identified newer prognostic markers. Although
Mucoepidermoid and adenoid cystic carcinoma DNA aneuploidy (flow cytometry), p53 mutation,
are aggressive tumors, and nodal metastases are elevated EGF, EGFr, and TGF-alpha have corre-
common. lated with worse outcome, more evidence is needed
Small cell carcinomas are usually large exo- for the clinical relevance of these factors.
phytic masses. These are often associated with
squamous differentiation. Secretion of ACTH, 1.4 SYMPTOMS AND SIGNS
hypercalcemia, and SIADH may occur as associ-
ated paraneoplastic syndromes. Overall these are Although esophageal carcinoma is typically a dis-
aggressive tumors with poor survival. ease of old age (sixth to seventh decade), in our
country one frequently encounters much younger
1.3.4 Prognostic Factors patients. In fact the youngest patient in our expe-
rience was a 23 year old lady. The duration of
The most important prognostic factor is the TNM symptoms is typically short, as opposed to benign
stage. The depth of tumor infiltration, and the pres- esophageal disorders. Symptom duration longer
ence or absence of nodal and distant metastasis are than 6 months indicates an advanced tumor.[70]
primary determinants of prognosis. Recently, the Dysphagia is the cardinal symptom which, if
number of involved nodes has been identified as an present in an old individual, should be consid-
important factor. Involvement of more than four ered suspicious of an esophageal cancer. Dys-
nodes is associated with a poorer survival.[62, 63] phagia, initially to solids and later to liquids, is
A lymph node positivity ratio of more than 0.1 present in 90% of cases, and occurs once the
is a poor prognostic factor.[64] Gross morphology luminal compromise is at least two-thirds. The
and tumor type are not independent prognostic absence of serosa in most of the esophagus enables
factors. Some tumors such as verrucous carci- tumors to expand into surrounding tissues before
noma and spindle cell carcinoma carry a better luminal stenosis becomes symptomatic. Hence it

Part I / Esophagus
 10 Chapter 1 / CANCER OF THE ESOPHAGUS

follows that most patients with esophageal carci- obstructive airway disease and pulmonary infec-
noma present with an advanced malignancy. Only tions. Breath holding time is a useful bedside test
in regions of the world where screening has been to assess the pulmonary reserve. Details of car-
successfully employed (e.g., China), early lesions diopulmonary disease, diabetes, and tuberculosis
are detected in substantial numbers. should be carefully sought.
Anorexia and weight loss are frequently asso- Assessment for tobacco and alcohol abuse is
ciated symptoms, and are present in up to 75% important. In the Indian subcontinent, chewable
of the patients. Other symptoms like odynopha- forms of tobacco are quite commonly used. Careful
gia, regurgitation, and cough may be present. oral and pharyngeal examination may occasionally
A preceding history of heartburn may be the reveal synchronous tumors.
only indicator of reflux in Barrett’s esophagus
with malignant change. Sinister symptoms are
1.5 DIAGNOSTIC INVESTIGATIONS
weight loss (> 10%), hoarseness (from recur-
rent laryngeal nerve palsy), cough on swallowing Laboratory investigations usually show anemia
(from an esophagorespiratory fistula), and back and hypoalbuminemia. Serum alkaline phos-
or chest pain (indicating invasion of mediastinal phatase may be elevated in patients with liver or
structures).[71] Cough may be due to esophago- bone metastasis. Hypercalcemia may occur as a
respiratory fistula or aspiration due to an obstructed paraneoplastic syndrome in squamous cell car-
esophagus. Esophagorespiratory fistulae occur in cinoma. It is due to a parathyroid hormone-like
about 5% of the cases, and are essentially incur- peptide produced by the tumor. Hypercalcemia
able, with a short survival of 1.5 to 4 months.[72] may also be due to extensive bone metastasis. The
Significant cough in the absence of either of the rare small cell carcinoma is associated with other
above may occur in chronic smokers, and tuber- paraneoplastic syndromes.
culosis should be kept in mind in these poorly
nourished individuals. 1.5.1 Barium Swallow
Hematemesis is an uncommon symptom.
Although it is usually due to tumor erosion and Contrast radiography using barium sulfate gives
ulceration, massive exsanguinating hemorrhage valuable information. It shows the level of
can occur due to an esophagoaortic fistula from esophageal obstruction, its nature, proximal
tumor infiltration of the aorta. esophageal dilatation (usually not marked due to
Clinical features due to metastasis may be bone the short duration of illness), and the distal extent
pains, lump in the upper abdomen due to a lymph of the lesion particularly with regard to the involve-
nodal mass or hepatic metastasis, or a lump in the ment of the gastroesophageal junction and the
neck due to cervical nodal metastasis. stomach (Fig. 1.1). Barium swallow is particularly
Clinical examination may not reveal disease- useful in defining the presence of an esophagores-
specific findings in most patients. However, it is piratory fistula. Water soluble contrast agents like
important to assess the nutritional status of the ‘gastrografin’ should not be used because of the
patient by recording the body weight, triceps skin- potential of causing lung damage due to its hyper-
fold thickness, pedal edema, and pallor. Since these osmolarity. Esophageal axis deviation on barium
patients are frequently chronic smokers, clinical swallow predicts an advanced, unresectable tumor
examination should look for features of chronic (Table 1.5).[73, 74]

Tropical Hepatogastroenterology
 SCREENING 11

deviation is an important feature which predicts

unresectability.[75, 76]

1.5.2 Endoscopy
Fiberoptic endoscopy has now become the gold
standard for the diagnosis of esophageal carci-
noma. At least six biopsy samples from non-
necrotic tumor areas are required to get the best
possible yield nearing 100%. Occasionally, dilata-
tion of the tumor may be required before access
becomes adequate for biopsies. Nondiagnostic
biopsies may sometimes be an indication to take
a biopsy with a large angled cup forceps through a
rigid esophagoscope.
While brush cytology should complement the
FIGURE 1.1 yield of biopsy, it has not been used extensively in
Barium swallow showing irregular narrowing with the diagnosis of carcinoma esophagus.
shouldering in the distal esophagus, typical of esophageal In addition to biopsy, endoscopy can be used
carcinoma. to assess the degree of obstruction caused by the
tumor, the proximal and distal extent (in passable
lesions), the presence of a second synchronous
TABLE
fy 1.5 Constituents of axis deviation fy tumor, and to place a nasogastric tube for feed-
• Tortuosity of the esophageal axis proximal to the ing. The location of the tumor is measured in
tumor centimeters from the incisors. The distal extent of
• Angulation of the esophageal axis the tumor is particularly important in adenocarci-
• Deviation of the esophageal axis noma at the gastroesophageal junction, where the
– Above and below the tumor
extent of stomach involvement will influence its
– Of the tumor itself
use as the conduit of choice after esophagectomy.
– Abnormality of the distance of the tumor from
the spine When this cannot be assessed by endoscopy, this
should be seen by barium swallow.

1.6 SCREENING
Barium swallow was the cornerstone of diag-
nosis before the advent of endoscopy. Today, we Most cases of esophageal carcinoma are detected
continue to advocate this simple and cheap inves- in advanced stages, hence the long-term results
tigation before endoscopy because (i) it serves of therapy are poor. Detecting esophageal car-
as a roadmap to the endoscopist, and often for cinoma early is an effective way of improving
the surgeon who does not see the tumor himself survival. In these early cancers the long-term sur-
before surgery; (ii) its use in defining an esophago- vival sometimes exceeds 90%. Screening may
respiratory fistula is unquestionable; (iii) axis be useful in high risk populations with diseases

Part I / Esophagus
 12 Chapter 1 / CANCER OF THE ESOPHAGUS

like upper aerodigestive cancers, gluten enteropa- 1.6.1.2 Nonendoscopic methods

thy, Plummer-Vinson disease, achalasia, and males
over the age of 50 years with a history of heavy Two popular methods for screening have been
abuse of cigarettes or alcohol. developed and used extensively. The mesh cov-
ered balloon has been used in China and the
gelatin encapsulated sponge has been evaluated in
1.6.1 Screening for Squamous Cell Japan.
Carcinoma The balloon is swallowed and inflated in the
stomach with 20–30 ml of air. It is gradually with-
Screening for squamous cell carcinoma has been
drawn through the esophagus, and after removal is
effective only in high-incidence regions of the
smeared on a slide. The sponge sampler is swal-
world. One such region is the Linxian province
lowed and left in the stomach for 5 minutes where
of China, where nonendoscopic screening using
the gelatin dissolves and the sponge expands.
abrasive balloon cytology has been successfully
This is then withdrawn through the esophagus.
used to detect early carcinoma.[77] Various modal-
After removal it is shaken in fluid and cytologi-
ities which have been used for screening are as
cal examination is carried out after centrifugation
follows:
of the fluid. The largest experience of the use
of cytological screening has been in China.[79, 80]
1.6.1.1 Endoscopy The accuracy in symptomatic individuals is higher
Early lesions may appear as mild irregularity, than in asymptomatic individuals. Another form of
erythema, or ulceration, or they may be missed blind cytology is with a standard cytology brush
altogether on routine screening endoscopy. inserted through a nasoesophageal tube.
Chromoendoscopy increases the probability of
identifying dysplasia. Chromoendoscopy refers to 1.6.2 Screening in Barrett’s Esophagus
the vital staining of tissues with topical dyes to
1.6.2.1 Endoscopy
improve localization during endoscopy. The dyes
used are Lugol’s iodine, toluidine blue, indigo The annual risk for developing adenocarcinoma
carmine, and methylene blue. Lugol’s iodine stains in Barrett’s metaplasia is 0.5% to 1.5%.[81, 82]
the glycogen of the normal squamous epithelium Endoscopy with biopsy is, therefore, required for
black, and the biopsy should be taken from the surveillance in patients with Barrett’s metaplasia.
unstained areas.[78] The other dyes are taken up by Biopsies should be taken from each quadrant every
abnormal epithelium. Toluidine blue has an affinity 2 cm within the Barrett’s epithelium. Jumbo biopsy
for staining the cellular nuclei. Unfortunately these forceps and brush cytology increase the yield of
may be taken up in areas of inflammation, ero- positive diagnosis of dysplasia or cancer.
sions, and ulcerations also. Methylene blue stains In the absence of dysplasia, screening should be
absorptive epithelium like small intestine, colonic done once in 2–3 years.[81]
epithelium, and Barrett’s epithelium, but does not The presence of low-grade dysplasia war-
stain nonabsorptive epithelium such as squamous rants treatment with a high dose course of anti-
or gastric epithelium. Compared to nondirected secretory drugs and repeat biopsy. Endoscopy
biopsy, methylene blue increases the yield for should be done half-yearly for one year, and then
Barrett’s epithelium. yearly.

Tropical Hepatogastroenterology
 STAGING: IMAGING AND OTHER METHODS 13

TABLE
fy 1.6 Techniques used to increase the esophagus. Findings may include lung metasta-
efficacy of surveillance sis, changes of chronic obstructive airway dis-
• Magnification endoscopy
ease, pneumonitis, mediastinal widening, and
• Chromoendoscopy (e.g., by methylene blue) esophageal air-fluid level. The presence of pul-
• Brush cytology monary metastasis precludes long-term survival,
• Optical coherence tomography hence unnecessary expensive staging investiga-
• Laser induced fluorescence spectroscopy tions are avoided.
• Flow cytometry (to measure the DNA content)
• P53 immunohistochemistry TABLE
fy 1.7 AJCC (1997) TNM staging for
• Proton magnetic resonance spectroscopy (of esophageal esophageal carcinoma
biopsies)
T (Primary tumor)
• Tx : Tumor cannot be assessed
• T0 : No evidence of primary tumor
In high-grade dysplasia the risk of adenocar-
• Tis : High-grade dysplasia
cinoma is 27% over 3 years.[83] Current rec-
• T1 : Tumor invades lamina propria, muscularis mucosa, or
ommended treatment for high-grade dysplasia is submucosa. Does not breach submucosa
esophagectomy. Less often, authors recommend • T2 : Tumor invades into but beyond muscularis propria
intensive endoscopic surveillance.[84] • T3 : Tumor invades periesophageal adventia but does not
invade the adjacent organs
1.6.2.2 Other modalities • T4 : Tumor invades adjacent structures
N (Regional nodal metastasis)
Several techniques have been used to increase the
• Nx : Nodal status not assessable
efficacy of surveillance (Table 1.6).
• N0 : No nodes involved
Methylene blue is particularly used in screening
• N1 : Regional nodes involved
for Barrett’s epithelium.
M (Nonregional nodes and distant metastasis)
• Mx : Distant metastasis not assessable
1.7 STAGING: IMAGING AND OTHER • M1a *: Upper thoracic tumors metastatic to cervical
METHODS nodes. Lower thoracic tumors metastatic to celiac nodes
• M1b : Upper and lower thoracic tumors metastatic to
The American Joint Committee on cancer stag- other nonregional nodes or distant sites. Middle thoracic
ing system is based on the primary tumor, nodal tumors metastatic to any nonregional nodes or distant
involvement, and distant metastasis (Table 1.7).[85] metastasis
The tumor size and spread cannot be evaluated Stage grouping
clinically, and staging depends entirely upon imag- Stage 0 Tis N0 M0
ing. This staging system has been most applicable Stage I T1 N0 M0
to upper and middle third squamous cell carcinoma Stage IIa T2 N0 M0 , T3 N0 M0
as opposed to the lower third adenocarcinoma. Stage IIb T1 N1 M0 , T2 N1 M0
Stage III T3 N1 M0 , T4 N0 M0 , T4 N1 M0
Stage IV Any T, any N, M1a or M1b
1.7.1 Chest X-Ray
∗ No M category exists for middle thoracic tumors. Any non-
1a
Conventional posteroanterior chest radiographs regional nodal metastasis has the same prognosis as distant
should be done in all patients of carcinoma metastasis

Part I / Esophagus
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