Clinical Examination and Applied Medicine, Volume I-Gastroenterology Series (Mar 7, 2018) - (1946646938) - (CRC Press)

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xamination
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Clinical Examination and Applied Medicine, Volume I

and Applied Medicine
gastrointestinal diseases. Medical students or postgraduates will learn history
discount!
taking, clinical examination and find relevant applied medical knowledge
needed for bedside assessment of the patient.
THE CONTENT
Gastroenterology Series
The hope is that the book will guide towards a correct diagnosis by
• Nutrition and history and examination, but also provide relevant differential diagnosis,
Dietetics Practice localize the disease and identify the cause. This book intends to fill this gap
Volume I
• Psychology and inspire the reader to gain confidence not only in the performance of
• Health, Wellness, the examination but also to answer most bedside queries and problems.
and Exercise It will serve as an indispensable resource for preparation of undergraduate
Science and postgraduate viva and short and long case examination. This text is
• Health Education not a replacement for standard textbooks on the subject, but should serve
as collection of facts and relevant details in the clinical assessment of the
patient. This book is complemented by a second volume, in which numerous
THE TERMS diagrams and figures have been included to stimulate understanding and
• Perpetual access for learning along with a picture test and MCQ.
a one time fee
• No subscriptions or Dr Mushtaq Haroon, born in Pakistan, is an academician, educationist, and
access fees consultant in medicine for over 25 years with over 10 years experience as
• Unlimited professor of medicine at various medical colleges in Pakistan. To his credit,
concurrent usage he has 25 publications in peer-reviewed medical journals and published five
• Downloadable PDFs medical books as first author. He completed his early training in m
edical
• Free MARC records unit 1 of Services Hospital attached to Allama Iqbal Medical College,
Lahore and went to UK for higher training. He passed MRCP in 1988 and
was a
warded FRCP from London in 2000. Dr Haroon has been a pioneer in
For further information,
a free trial, or to order, computer-based medical education, having developed a vast collection of
contact: software for teaching. He was awarded the Life Time Achievement Award
sales@momentumpress.net for the most distinguished Iqbalian for professional excellence by the Chief
Minister of Punjab in Dec 2008. He is presently consultant in Pakistan Kidney
Mushtaq Haroon
and Liver Institute and Research Centre, Lahore Pakistan.
ISBN: 978-1-94664-693-4
Clinical Examination and
Applied Medicine
Clinical Examination and
Applied Medicine
Volume I
Mushtaq Haroon
MOMENTUM PRESS, LLC, NEW YORK

Clinical Examination and Applied Medicine: Gastroenterology Series,
Volume I
Copyright © Momentum Press, LLC, 2018.
All rights reserved. No part of this publication may be reproduced,

stored in a retrieval system, or transmitted in any form or by any
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First published in 2018 by

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www.momentumpress.net
ISBN-13: 978-1-94664-693-4 (paperback)

ISBN-13: 978-1-94664-694-1 (e-book)
Momentum Press Health Education C

ollection
Cover and interior design by Exeter Premedia Services Private Ltd.,

Chennai, India
First edition: 2018
10 9 8 7 6 5 4 3 2 1
Printed in the United States of America.

This book is dedicated to my loving wife, Romana.
My mother Asafa Ashfaq and father Engr. Ashfaq Hasan.
Abstract
This is the first in the series of books dealing simultaneously with exam-
ination technique with detail pathophysiological principles, differential
diagnosis and clinical interpretation, along with correlated and applied
medicine about the common diseases. A medical student or a postgraduate
doctor studying for higher exam will learn to take a good history, examine
the patient, and find relevant applied medical knowledge, which is needed
for assessment of the patient. It should also serve as an invaluable collec-
tion of facts to get through undergraduate or postgraduate examination.
This book attempts to answer pertinent questions such as how? and
why? about clinical examination while providing relevant information
needed for a thorough bedside assessment. It is hoped that the book will
not only serve to make a correct diagnosis by examination, but also give
relevant differential diagnosis, and localize the disease and determine its
cause. The book intends to fill this gap and inspire the reader to gain
confidence not only in the performance of the examination but also to
answer most bedside queries and problems. It will hopefully serve as an
indispensable resource for preparation of undergraduate and postgradu-
ate viva and bedside short and long case examination.
The Volume II of this book includes a section on radiology and endos-
copy. A wealth of diagrams and figures along with brief clinical note has
been included to stimulate understanding and learning. As a stimulus for
learning, picture test with MCQ and a short applied medical note has
been added. The book is not a replacement for standard textbook on the
subject, but it is hoped that it would be mastering relevant knowledge and
clinical skills to diagnose and assess the patient’s problem at the bedside
and also prepare for undergraduate and postgraduate examination.
Keywords
bedside assessment, esophageal diseases, gall bladder diseases, gastroenter-
ology images, GI clinical examination, GI diseases, GI examination skills,
GI investigations, history taking, intestinal diseases, intestinal pathology,
kidney diseases, liver diseases, pancreatic diseases, physical examination,
radiology, signs and symptoms, stomach diseases
Contents
Part I
Introduction and History Taking
Introduction 1
History taking 1
Physical findings 2
Diagnosis 2
Objective of history taking 2
Introductory remarks 2
History taking 3
Presenting complaints 3
History of presenting illness 3
Epigastric pain 4
Direct questions 5
Past history 5
Family history 6
Personal history 7
Socioeconomic status 8
Occupational history 8
History of Allergy and immunization 8
Travel history 8
Treatment history 9
Concluding remarks 9
Objective of examination 10
Common GI symptoms 10
Abdominal pain 11
Nausea and vomiting 14
Hematemesis 15
Hematochezia 15
Occult blood loss 16
Anorexia 16
Heartburn 16
x Contents
Dysphagia 16
Globus pharyngus 17
Flatulence 18
Dyspepsia 18
Halitosis 18
Diarrhea 19
Malabsorption 19
Constipation 19
Early satiety 20
Pruritus 20
Fever 20
Weight loss 20
Part II
General Physical Examination
Nutritional status and obesity 21
Body mass index 21
Co-morbidities 22
Secondary causes of obesity 22
Minimum screening 23
Vitamins 23
Anemia 24
Definition 24
Examination 24
History 25
Etiology 25
Blood loss 26
Dyserythropoietic anemia 26
Hemolytic anemia 26
Other causes of anemia 26
Causes of folic acid deficiency 27
Causes of B12 deficiency anemia 27
Other causes of macrocytic anemia 27
Clinical Features 27
Laboratory features of iron deficiency 28
Laboratory features of macrocytic anemia 29
Contents xi
Jaundice 30
Definition 30
Pathophysiology 30
Hepatic jaundice 31
Obstructive jaundice 31
Hemolytic vs. obstructive jaundice 32
Causes of hemolytic jaundice 32
Clubbing 33
Definition 33
Clinical presentation 33
Demonstration 34
Clinical stages 34
Pathogenesis 34
Causes of clubbing 35
Other types of clubbing 35
Etiology of clubbing 35
Peripheral edema 36
Definition 36
Examination 36
Causes of edema 37
Disease-focused examination 37
Signs of liver cell failure 37
Primary biliary cirrhosis 38
Chronic malabsorption 39
Peutz Jegher’s syndrome 39
Celiac disease 39
Inflammatory bowel disease 39
Acute hemorrhagic pancreatitis 40
Skin examination 40
Hands examination 40
Eyes examination 41
Neck examination 41
Oral examination 42
Examination of the lips 42
Examination of the mouth 42
Examination of the teeth and gums 43
xii Contents
Examination of the tongue 43

Examination of the Throat 45
Inspection 46
Prerequisites of examination 46
Regions of abdomen 46
Parameters of inspection 47
Diagrammatic representation of findings 47
1. Shape of Abdomen 48
2. Abdominal Movements 48
3. Epigastric Pulsations 48
4. Pigmentation and Rashes 49
5. Striae 50
6. Prominent Veins 50
7. Visible Peristalsis 51
8. Pubic Hair 51
9. Umbilicus 52
10. Hernial Orifices 52
11. Scars and Tap Marks 52
12. Surgical incisions 53
Palpation 53
Initial Requirements 53
Scheme of Palpation 54
Types of Palpation 54
Description of a mass 55
Localization of disease 56
Diagrammatic representation of findings 56
Rebound tenderness rigidity and guarding 57
Acute abdomen 57
Liver 58
Surface Anatomy 58
Palpation 58
Applied medicine 60
Causes of enlarged and tender liver 61
Causes of hepatomegaly 61
Cirrhosis 61
Causes of cirrhosis 62
Contents xiii
Types of cirrhosis 62
Finding on examination in cirrhosis 63
Parameters of decompansated cirrhosis 63
Complications of cirrhosis 64
Child Trucotte classification 64
MELD score 64
Cirrhosis and mortality 65
Investigations in cirrhosis 65
Portal hypertension 66
Classification of portal hypertension 66
Hepatic encephalopathy 68
Hepatic encephalopathy stages 68
Precipitating causes of encephalopathy 69
Differential diagnosis of altered metal state 69
Ascites in cirrhosis 70
Sudden worsening of ascites 70
Spontaneous bacterial peritonitis 70
Acute hepatitis 70
Causes of acute hepatitis 71
Diagnosis of acute hepatitis 71
Viral hepatitis A 71
Viral hepatitis B 72
Viral hepatitis C 72
Viral hepatitis D 74
Viral hepatitis E 74
Acute fulminant hepatitis 74
Acute fatty liver of pregnancy 75
Liver abscess 75
Liver mass 76
Investigation of liver mass 76
Liver hemangioma 78
Focal nodular hyperplasia 78
Hepatic adenoma 78
Hepatocellular carcinoma 78
Primary biliary cirrhosis 79
Primary sclerosing cholangitis 79
xiv Contents
Metastasis 80
Autoimmune hepatitis 80
NAFLD 81
Alcoholic liver disease 81
Hepato-renal syndrome 81
Wilson’s disease 82
Alpha-1 antitrypsin deficiency 82
Congestive hepatomegaly 82
Hereditary hemochromatosis 82
Spleen 83
Surface Anatomy 83
Palpation 83
Applied medicine 84
Splenomegaly 84
Hypersplenism 85
Splenectomy 85
Splenic infarction 85
Kidneys 85
Palpation 85
Differential diagnosis of right kidney 86
Differential diagnosis from spleen 87
Applied medicine 87
Renal tenderness 87
Chronic kidney disease 88
Causes of renal mass 89
Hematuria 89
Gallbladder 91
Palpation 91
Murphy’s sign 92
Enlarged bladder with jaundice 92
Enlarged bladder without jaundice 92
Applied medicine 92
Acute cholecystitis 92
Gallbladder tumors 92
Stomach and Esophagus 93
Applied medicine 94
Contents xv
Succussion splash 94
Virchow’s lymph node 94
Peptic ulcer disease 94
Zollinger Ellison syndrome 96
Functional dyspepsia 97
Carcinoma stomach 97
Upper GI bleeding 97
Gastroesophageal reflux 98
Diffuse esophageal spasm 99
Achalasia 99
Mallory-Weiss tear 100
Borehaave syndrome 100
Eosinophilic esophagitis 101
Cancer esophagus 101
Plummer Vinson syndrome 102
Zenker diverticulum 102
Barrett esophagus 103
Pancreas 103
Applied medicine 103
Acute pancreatitis 103
Chronic pancreatitis 105
Pancreatic pseudocyst 105
Carcinoma of pancreas 106
Intestines 106
Small intestinal and colonic pain 106
Melena and hematochezia 107
Irritable bowel syndrome 107
Inflammatory bowel disease 108
Differential diagnosis 108
Severity 109
Liver involvement 110
Extra intestinal involvement 110
Risk of cancer 110
Diarrhea 110
History 112
xvi Contents
Causes of chronic diarrhea 113

Acute diarrhea 114
Traveler’s diarrhea 114
Examination in diarrhea 115
Stool examination 115
Investigations/procedures/trials of therapy 116
Antibiotics in diarrhea 117
Secretory diarrhea 118
Celiac disease 118
Tropical sprue 119
Mesenteric ischemia 120
Carcinoid tumor 121
Familial adenomatous polyposis 121
Colorectal cancer 121
Intestinal obstruction 122
Pseudo-obstruction 123
Lymphoma of GI tract 124
Volvulus 125
Intussusception 125
Toxic megacolon 125
Appendicitis 126
Diverticulosis 127
Percussion 128
Indications of percussion 128
Shifting Dullness 129
Fluid Thrill 130
Puddle Sign 130
Encysted fluid 130
Percussion of urinary bladder and ovaries 131
Ascites 131
Causes of ascites 132
SAAG 133
Investigation of ascitic fluid 133
Workup of suspected TB 134
Contents xvii
Auscultation 135
Bowel sounds 135
Auscultatory of areas of abdomen 135
Rectal examination 135
Superficial examination 135
Per-rectal examination 136
Prostate 136
Genitourinary examination 137
Male 137
Female 138
Summary of examination 138
Investigations and Procedures 139
Specific biochemical tests 141
Paracentesis or ascitic tap 142
Scheme of Gastrointestinal Examination 145
About the Author 147
List of Contributors 149
Index 151
Foreword
Medicine is expanding at such rapid pace in our times that it is difficult to
keep up with the latest developments. The author has made every effort to
update the contents. Clinical examination may vary according to individ-
ual liking and bias, but as long as general technique is correct and a right
diagnosis is reached, minor variations do not matter.
Preface
The clinical examination and applied medicine, gastroenterology series is
produced in two volumes. This, Volume I deals with examination tech-
niques, pathophysiological principles, and clinical interpretation, besides
providing ample details of applied medicine about the common diseases.
A medical student or a postgraduate doctor studying for higher exam will
find relevant applied medical knowledge, which is needed for assessment
of the patient. It should also serve as an invaluable collection of facts to
get through undergraduate or postgraduate examination.
History taking and clinical examination form the foundation of diag-
nosis and pave the way for the correct management. Clinical examination
is an essential prerequisite for a medical student entering the clinical side
of his or her undergraduate career. It can haunt him or her at all stages of
the undergraduate and postgraduate life. It forms the basis of his or her
clinical practice during the professional career.
Pathophysiological principles of examination, where relevant, are
explained for a sound understanding. Once the pathophysiological basis
of signs and symptoms is understood, it can be applied to a variety of
clinical situations in different patients. The process then becomes one
of deduction, application of principle, and logical outcome, which is
the foundation and corner stone of knowledge. This book attempts to
answer pertinent questions such as how and why about clinical examina-
tion and bedside medicine. Further, interpretation of the physical finding
is important. It is not enough to know that there is a lesion, but it is
important to localize it and find a possible cause. The investigations and
treatment plan then depend upon proper differential diagnosis. The book
intends to fill this gap and provide some food for thought and inspire the
reader to gain confidence not only in the performance of the examina-
tion, but to answer most bedside queries and problems. It will hopefully
serve as an indispensable resource for preparation of undergraduate and
postgraduate viva and bedside short and long case examination.
xxii Preface
This new edition has been thoroughly revised and updated. It is

supplemented by Volume II of the book, which contains a section on
radiology, gastrointestinal related pictures with quiz and MCQ with a
section containing endoscopic images. Brief applied medical information
is provided with each figure to stimulate interest and improve memory.
The book is not a replacement for a standard textbook on the subject,
but it is hoped that it would help the objective of transferring relevant
clinical knowledge and provide the arsenal to solve bedside problems
of patients efficiently and appear in undergraduate and postgraduate
examination with confidence.
—Dr. M. Haroon
MBBS (Pb); MCPS (Pak); MRCP (UK)
FRCP (London)
Acknowledgments
I am ever grateful to the Almighty, Allah Subhana wa Taala for granting
me the knowledge and strength to reproduce what I have learned through
my teachers, colleagues, and students of Allama Iqbal Medical College,
Lahore, King Edward Medical University, Lahore, and Quaid-i-Azam
Medical College, Bahawalpur. I owe a lot to my appointment in King
Fahad Armed Forces Hospital, Jeddah, and Pakistan kidney and liver
institute, Lahore, where I have learned a lot, and I have been blessed to
find a learning and friendly environment. The task would never have been
possible without the blessings from the Lord Almighty.
PART I
Introduction and
History Taking
Introduction
Patient care begins with the development of a personal relationship
between the patient and the physician. In the absence of trust and confi-
dence between the two, the effectiveness of a therapeutic measure may not
be optimal. In many cases, confidence and reassurance to the patient maybe
all that is required. When no treatment is available or possible, the patient
should be given a feeling that the doctor is trying his or her best. A subjec-
tive assessment of the quality of life or assessment of what each patient values
most has to be made. This requires a detailed and intimate knowledge of
the patient, through unhurried conversation, in a comfortable atmosphere.
Improvement of the quality of life is the main goal in all incurable diseases.
As the cost of medical care continues to rise, it is becoming neces-
sary to apply stringent priorities in the expenditure on health care. In
most cases, prevention may be better than cure. Such measures as vacci-
nation, immunization, reduction in accidents and occupational hazards,
improved environmental control, and screening of newborns for common
diseases may be found to be economical. As investigations are becoming
increasingly expensive, it is mandatory to tailor the investigations accord-
ing to the need of the patient. The equation of cost versus benefit and
necessity should always be kept in mind. Confirmatory tests instead of
screening seem logical where the clinical diagnosis is almost certain.
History taking is an art as well as science that requires a thorough
knowledge of medicine along with patience and good command on the
language of the patient. The history is the written record of all the facts
about the patient’s present and past illnesses. It is best to use the patients’
words and not to suggest answers. Quite often, the main problem of the
patient may not be clinically significant, but some other problem on
2 CLINICAL EXAMINATION AND APPLIED MEDICINE
which the patient may be paying very little attention, may be more sig-
nificant for the doctor to reach a correct diagnosis. In order to write a
good history, patience, attention, concentration, and encouragement of
the patient is required.
Physical findings are subject to change. Just because the examination
is normal on one occasion does not guarantee that this will be the case
on subsequent examinations. Likewise, abnormal findings may disappear
in the course of illness. Therefore, repeat the physical examination as
frequently as the clinical situation warrants.
Diagnosis requires a logical approach, an analytic mind that is able to
interpret and synthesize ideas. It is most important to keep the objective
of history taking in mind.
Objective of History Taking

• To make a clinical diagnosis and then formulate a management plan with relevant
investigations and start management plan.
• To determine the etiology.
• To rule out relevant differential diagnosis.
• To pick any complications in relation to the disease.
• To look for other illnesses that the patient may not be aware of or which may be
silent for the time being.
• To know your patient’s socio-psychological and economic condition.
A good history should be able to fulfill these objectives. History is not

writing of an elegant essay of the patient’s complaints. Each question that
is asked should be directed toward a diagnosis or help to exclude relevant
differential diagnosis. It is best to use the patient’s words in history taking,
rather than using medical terms. Asking the most appropriate questions
in relation to patient’s complaint will save time and be most fruitful. This
art is best learned at the bedside after interviewing a large number of
patients.
A general introduction should include:
Introductory Remarks
Name Date of birth
Sex Occupation
Religion Date of admission
Address Mode of admission
Introduction and History Taking 3
History Taking
After introductory remarks, the presenting complaints are listed in
chronological order, that is, the most prolonged complaint first and most
recent last, which forced the patient to seek medical advice. It is also
possible to write the presenting complaints in order of importance, with
the most significant complaint first and least significant last. Mention any
known disease like hypertension, diabetes, and so on, if they are thought
to contribute to presenting complaints.
Presenting Complaints
• Diarrhea since 4 days
• Vomiting since 3 days
• Blood in stool since 1 day
Presenting Complaints
• Known case of rheumatoid arthritis since 10 years
• Severe pain epigastrium since 2 weeks
• Vomiting since 5 days
• Blood in the vomitus since 1 day
In the preceding example, rheumatoid arthritis, although did not

primarily bring the patient to the hospital, is considered the likely cause
of the underlying presenting problem. Therefore, they are mentioned in
the presenting complaints or can even be mentioned as opening remarks
in the history of presenting illness.
After the presenting complaint, the details of these complaints are
given. This is termed the history of presenting illness. It is described in
the same order as the presenting complaints, and one at a time. The open-
ing remark usually begins by mentioning when the patient was perfectly
healthy. At the end of the description of each complaint, a reasonable
conclusion about the underlying cause of the complaint should be possi-
ble. If not, there are deficiencies in the history taking or background med-
ical knowledge. The detailed description of the complaint should include:
Details of History of Presenting Illness

1. When and how it started?
2. How did it progress?
(Continued)
Details of History of Presenting Illness

3. What are its special characteristics?
4. Are there any associated features?
5. How has it affected the patient?
6. What medications have been used?
7. What investigations have been performed?
8. What was the presumed diagnosis, if any?
9. What was the effect or side effect of treatment?
10. Ask related questions to confirm the diagnosis.
11. Ask questions to exclude differential diagnosis.
Each presenting complaint is pursued with relevant questions until all

the details have been gathered. It is important to note how the complaint
started, progressed, and evolved. What are the precipitating and reliev-
ing factors, and whether there is any relation to any particular event like
meals or breathing? Also, ask how the complaint has altered the patient’s
lifestyle. At times, a lot of cross-questioning may be required until a fair
conclusion about the diagnosis is reached. A patient with abdominal pain
may be interviewed as follows:
Patient with Epigastric Pain

1. When did you first have the pain?
2. How did it start or what were you doing at the time?
3. Where exactly did it start and does it radiate?
4. How would to grade it in severity from 1 to 10?
5. What was its character (heaviness, stabbing, sharp, dull, colicky, and so on)?
6. How did it progress?
7. How long did it last?
8. Were there any associated symptoms (nausea, vomiting, sweating, fainting, fever,
palpitations, cough and phlegm, skin rash, and so on)?
9. What makes it worse?
10. What makes it better?
11. Is it related to anything like meals, exertion, body position, coughing, and so on?
12. Is there any local tenderness?
13. Did you take any treatment, and what was its effect?
14. Have you ever had any heart, lung, or ulcer problem?
15. History of similar problem in the past?
16. History of blood in stool or vomitus or passing black-colored stools?
17. Did you have any investigations?
During history taking, the doctor is thinking about peptic ulcer

disease, heart disease, pericardial disease, esophageal disease, pancreatic
disease, pleuritic problems, colonic problems, and skin, soft tissue, and
musculoskeletal problems.
The intention of these questions is to reach a fair diagnosis, exclude
relevant differential diagnosis, and determine any associated complication
or the cause of the underlying disorder, if applicable.
It is up to the doctor to decide which part of the patient’s history is
relevant, and which is not. A good doctor will prevent the patient form
side tracking and wasting time in irrelevant details. At the same time,
a vigilant physician will pick up minute detail in the history, which,
although not important to the patient, may clinch the diagnosis. In some
patients, however, the diagnosis is only possible after proper examination
or even after investigations. At the end of the history of presenting illness,
it is necessary to inquire about any other complaints the patient may have
in any of the major systems.
Direct Questioning in History

CNS History of headache, seizures, imbalance, dizziness, sensory or motor
problems, loss of consciousness, and so on.
CVS Chest pain, palpitations, dyspnea, syncope, orthopnea and paroxysmal
nocturnal dyspnea, and so on.
RT Cough, sputum, dyspnea, hemoptysis, and so on.
GIT Abdominal pain, dyspepsia, nausea, heartburn, diarrhea, and constipation.
MKL Joint pains, morning stiffness, limitation of movement and restricted
activities, and so on.
ENDO Changes in growth, weight, and metabolism. Ask about problems related to
thyroid, parathyroid, pancreas, and adrenal glands.
GUT Polyuria, dysuria, frequency, oliguria, and change in color and smell of urine.
History of passage of blood, stones, gravel, or any kidney problems should be
inquired.
CNS = central nervous system, CVS = cardiovascular system, RT = respiratory system,
GIT = gastrointestinal tract, MSKL = musculoskeletal system, ENDO = endocrine system,
GUT = genitourinary tract
Past History
This includes a detail of the patient’s past medical and surgical record. It
is not sufficient to say that nothing abnormal is detected. List import-
ant positive and negative findings in chronological order. Ask about past
illnesses and hospitalizations for any reason. Ask about past operations, if
any. A past illness may be the source of the present problem.
Details of Past Illness

How long have you had the illness? How well is your disease controlled?
What treatment are you taking for it? Is it associated with any complications?
Do you take your treatment regularly?
Direct questions about common diseases like diabetes, hypertension,

jaundice, peptic ulcer, asthma, joint disease, bowel problems, and so on
may be mentioned here or at the end of the presenting complaint.
Family History
Ask about the family members and any significant history of disease in
the immediate (first-degree relatives) or distant family. Has any relative,
an identical or similar illness? Does any relative suffer from an unusual
disease, or died from a rare condition?
Common GI Disease with Familial Incidence

• Peptic ulcer may run in families or more common in blood group O.
• Irritable bowel syndrome.
• Inflammatory bowel disease.
• Familial adenomatous polyposis (Gardner’s syndrome autosomal dominant).
• Peutz–Jegher’s syndrome (autosomal dominant).
• Familial gastric cancer.
• Colorectal cancer
• Hereditary hemorrhagic telangiectasia.
• GIST (gastrointestinal stromal tumors).
• Zollinger–Ellison syndrome.
If a disease happens to run in the family, it does not mean that all
the sufferers may have the same manifestations. In others, it may involve
a different system, for example, In Marfan syndrome, there may be pre-
dominant cardiac, musculoskeletal, or eye involvement. Ask about mar-
riages within the family, as consanguineous marriage may be the source
of rare autosomal recessive syndromes. What is the ethnic origin of the
family? Various ethnic groups have higher incidence of certain inherited
disorders.
Various diseases tend to run in families and have different modes of

inheritance. There are three basic kinds of inherited disorders. (1) Chromo-
somal abnormalities, (2) Mendelian disorders may be autosomal dominant,
autosomal recessive, or X-linked types, and (3) multifactorial disorders.
Some Chromosomal Disorders

Turner’s syndrome 45 X.
Klinefelter’s syndrome 47 XXY.
Down’s syndrome +21 (Trisomy 21).
Mendelian Disorders
Autosomal dominant
Familial hypercholesterolemia. Peutz–Jegher’s syndrome.
Gardner syndrome. Adult polycystic kidney.
MEN 1A Neurofibromatosis.
Autosomal recessive
Muconium ileus Sickle cell anemia.
Wilson’s disease. Hemochromatosis.
Cystic fibrosis.
X-linked
Hemophilia-A. G6PD deficiency.
Color blindness. Hypophosphatemic rickets.
Ask about the health of parents, if alive, and if dead, the cause of
death. Always ask about the probable cause of death and circumstances
leading to death. Ask about health of wife and children, if applicable.
Personal History
Ask about personal habits like tobacco use or smoking, addictions (espe-
cially alcohol and others) and hobbies. Ask about recent travel (especially
to areas where AIDS is common or endemic) and sex life, if thought
necessary for the diagnosis. It is necessary at this stage to take the patient
into confidence and tell him or her that their personal life will always
remain a secret. It may be necessary to inquire about beliefs and faith
and about psychological problems, as psychotherapy may be required as
a form of treatment. Ask about living conditions, as some diseases are
prone to occur in poor hygienic and overcrowded conditions.
Socioeconomic Status
Ask about the means of earning and whether the patient is well to do or
can hardly make both ends meet. The patient may have more than one
source of income. Also, ask about support from the family, as the patient
may have or is likely to develop a disabling illness. It may be important to
avoid choosing expensive medications, whenever possible, as the patient
may not be able to afford them.
Occupational History
Ask about the present and past occupations that the patient may have
had, as it may be related to the disease. Many a times, the disease may be
related to the patient’s work or workplace.
Occupational Lung Disease

Anthrax can affect the GI tract by eating undercooked and contaminated food.
The patient may have abdominal pain, nausea, loss of appetite, and bloody diarrhea.
Exposure to vinyl-chloride (plastic workers) may cause liver cancer.
Exposure to epoxy resins (rubber factory) may cause acute hepatitis.
Carbon tetrachloride exposure (dry cleaners) may cause acute liver toxicity.
Other exposures like cement, iron, graphite, cadmium, chromium, cotton worker,
chemical worker, and so on can have lung disease with increased mucous secretion and
variable obstruction.
Halides like chloride and fluoride in workers of textile and paper may cause dental
fluorosis, pulmonary edema, epistaxis, and dryness.
History of Allergy and Immunization
Ask the patient if there is any history to any material including drugs. If
yes, what kind of reaction was noted with the offending agent. Also, ask
about pervious or any regular course of immunization that the patient
has received.
Travel History
Ask about any history of travel in the recent past. This may be useful
especially in diarrheal illnesses and infectious diseases.
Treatment History
It is mandatory to take a detailed history of the past medical and surgical

treatment. This includes not only the treatment of the present problem,
but any significant and especially related problems in the past.
Some Related Questions

What diseases have you suffered in the past? What medication were you prescribed?
In what doses and for how long? What was the effect in terms of benefit?
What were the complications, if any? Are you still taking any treatment?
In a patient with IBD for example, it is important to note:
1. What form of treatment is the patient taking (or has taken in the past)?
2. What doses?
3. For how long?
4. What were the side effects?
5. Have there been any complications or any operations?
Without this information, adjustment of therapy may not be ideally

possible. Similarly, in a patient of GI cancer, the same questions are abso-
lutely essential.
Concluding Remarks
A good history should give a reasonable diagnosis of the patient’s problem

in most cases. Not only that, it should pick up complications associated
with that disease, assess the severity, chronicity, and determine how it has
affected the individual in terms of functional loss, if any. It should also
probe into other related or unrelated problems in different systems so
that a total picture of the patient’s problems may be viewed. The aim is
to offer the best possible treatment or cure if possible. This can only be
achieved through honest work, deliberation, patience, and knowledge of
the subject with a willingness and attitude to learn from experience, and
specially form mistakes.
In most cases, the diagnosis is reachable through a good history alone.
One is able to determine, to a reasonable extent, the type of illness, for exam-
ple, in neurology, whether it is a degenerative, inflammatory, neoplastic,
traumatic, genetic or congenital, toxic or metabolic disorder. Examination

helps to confirm the diagnosis, but at times, may give the only clues to
diagnosis. Still, in other cases, a diagnosis may not be reachable with a
good history and thorough examination, where a battery of investigations
is required. A typical example is PUO (pyrexia of unknown origin). Rarely,
the diagnosis is not made even after thorough investigations and becomes
obvious only after some time has passed and is then made retrospectively.
After the history, the patient is thoroughly examined with the d
iseased
system being examined first. Throughout the examination, a systematic
approach is adopted so that small details are not left out. One should
learn to examine with the intention to pick up physical signs, to deter-
mine the site of lesion, type of disease, and try to determine the cause. It
is not enough to determine that the patient has cirrhosis of the liver, but
it is imperative to determine the cause like hepatitis B or C virus, a lcohol
related, biliary cirrhosis, cardiac cirrhosis, Wilson’s disease, or alpha 1
antitrypsin deficiency etc. It is obvious that the management in some cases
is completely different. This book should help you achieve these goals.
Objective of Examination
• To confirm the diagnosis made during history taking.
• To demonstrate signs of disease and exclude differential diagnosis.
• To look for other signs that may be related or unrelated to the disease.
• To determine the site, type, and cause of illness.
• To determine the effects or complications of disease on different systems.
• To formulate a logical investigation plan in order to confirm or refute the diagnosis.
The art of history taking is best learned at the bedside of the patient.
There are no shortcuts, and practice makes one perfect. It is best to take
history and then read up the different diseases, which make up the differ-
ential diagnosis form a textbook of medicine. One can then learn from
the mistakes made in history taking and omissions made in the examina-
tion and plan of investigations.
Common GI Symptoms
In GIT, esophageal problems commonly manifest via problems in swal-
lowing and retrosternal pain, while gastric disorders are generally associ-
ated with acidity, appetite, and a bloated feeling. Disease of the intestine
manifests by nutritive problems with changes in stool quantity and qual-

ity. Pancreatic disease may be associated with diabetes, malabsorption,
or characteristic pain, while hepatobiliary disease may be associated with
jaundice, colicky right hypochondrial pain, and problems of digestion,
storage, and absorption. The gut may also be involved in various systemic
disorders (like vascular, infectious, inflammatory, and neoplastic).
Abdominal pain is the most important GI symptom that is, at times,
unbearable. When severe, it may be associated with nausea and vomiting
(common example being renal colic). Pain fibers are present in the muscle
layer of the hollow viscera and capsule of the solid organs. Pain is carried
by sympathetic, phrenic, coeliac, splanchnic, mesenteric, and pelvic nerves,
and not via the vagus. Visceral pain is usually felt in the center of the abdo-
men, while parietal pain is sharp and localized to the site of involvement.
Causes of Abdominal Pain

1. Visceral: stomach, intestine, pancreas, and so on. The pain is usually midline, dull,
and poorly localized. There may be colicky pain, especially with motility disorders,
for example, intestinal biliary or ureteric obstruction, irritable colon, and uterine
contraction.
2. Parietal: peritoneal inflammation causes sharp and localized pain and tenderness, or
it may be generalized in widespread process.
3. Referred: pancreatic to back, diaphragm to tip of left shoulder, ureteric to groin,
gallbladder to epigastrium.
4. Ischemic: mesenteric or splenic infarction. Testicular and fallopian tube torsion are
some examples.
5. Extra-intestinal: The origin of pain may be from thorax (lung, heart, and esophagus),
spine, or due to metabolic derangements (porphyria, Addisonian crisis, diabetic
ketoacidosis, and lead poisoning).
Although separated into different varieties of pain, most situations

may be a combination of more than one type.
Abdominal Pain According to Anatomy

1. Peptic ulcer pain is in the epigastrium, which may get worse with meals (gastric
ulcer) or be relieved (duodenal ulcer). It is burning in nature and demonstrates a
chronic and periodic character. It may awaken the patient at night form sleep.
2. In cholecystitis, there may be colicky pain, but more likely constant lasting for hours.
It may be in the epigastrium and right hypochondrium or with some localized perito-
nitis producing local guarding and referred to the tip of left shoulder if the diaphragm
is irritated.
(Continued)
Abdominal Pain According to Anatomy

3. Esophageal pain is usually retrosternal, but may radiate like the cardiac pain. It
may get worse after a heavy and fatty meal and may be relieved by smooth muscle
relaxants (nitrates).
4. Small intestinal pain is usually colicky and central, but may radiate to the back.
5. Large bowel pain may be central, along the colonic line or more often hypogastric
and poorly localized. The pain gets worse every 10 to 15 min. Small bowel obstruc-
tion, on the other hand, is associated with periumbilical colicky pain worsening
every 2 to 3 min.
6. Pancreatic pain may be very severe, periumbilical, and radiates to the back. It gets
worse on lying, and somewhat relieved on bending forward.
7. Renal pain is usually very severe colic on top of a constant pain, making the patient
toss and roll in bed. It may radiate to the groin.
When taking the history with the objective to determine the cause, it
is important to consider all anatomical structures in the area.
Epigastric pain: stomach, pancreatic, esophageal, and
cardiac problems.
Right hypochondrium: gallbladder, liver, and biliary tract
diseases. Sometimes, stomach and lower
lung pathologies.
Left hypochondrium: splenic diseases, and sometimes, stomach
and pancreas.
Right iliac fossa: appendix, ovary, pelvis, uterus, and
ureteric diseases.
Left iliac fossa: colon, ureteric, ovarian and pelvic diseases.
Central abdominal pain: pancreas, small bowel involvement.
Questions in Relation to Pain

1. Site?
2. Duration, timing and frequency. Also, continuous or intermittent?
3. Character (colic or continuous)?
4. Intensity?
5. Radiation?
6. Relieving factors?
7. Precipitating factors?
8. Associated features (vomiting, diarrhea, fever, dysuria, jaundice, or gynecological
symptoms, abdominal distension, or significant weight loss)?
9. History of recent drug intake?
Severe pain in the abdomen may be due to many surgical emergen-

cies, which need to be excluded. However, there are many non-surgical
causes of acute abdominal pain where conservative therapy is required in
most cases, as given next:
Acute Abdominal Pain—Non-surgical

1. Pepticulcer disease, hepatitis, and liver abscess.
2. Pancreatitis.
3. Irritable bowel syndrome.
4. Pyelonephritis and nephrolithiasis.
5. Diabetic ketoacidosis.
6. Acute MI (pain may be epigastric) and aortic dissection.
7. Electrolyte disturbance (severe hypokalemia, severe hypercalcemia).
8. Pulmonary embolism and pleuritis.
9. Dengue fever.
10. Sickle cell crisis.
11. Acute intermittent porphyria.
12. Acute Addisonian crisis.
13. Vasculitides.
14. Chronic bowel ischemia.
15. Pelvic inflammatory disease.
16. Familial Mediterranean fever.
17. Drugs.
18. Spinal pathologies.
19. Henoch–Schonlein purpura.
20. Herpes zoster.
Figure 1 Abdominal pain may be obvious as in this case of herpes

zoster and large tumor with herniation in the abdomen on the right
In order to reach a diagnosis, it is important to consider the anatom-

ical structures that are present at the site of pain while also considering
the possibility of radiation of pain and association with systemic disease.
A history typical of each disease will have to be elicited.
Causes of Acute Abdomen Pain (Surgical Intervention

May be Required)
1. Acute cholecystitis. 7. Volvulus.
2. Acute appendicitis. 8. Intussusception.

3. Acute liver abscess. 9. Ectopic pregnancy.
4. Acute pancreatitis. 10. Ruptured ovarian cyst.
5. Acute ischemic colitis. 11. Trauma and ruptured viscera.
6. Acute complicated peptic ulcer (per- 12. Hematoma.
foration).
Nausea and vomiting is a feature of a broad range of GI and extra-in-

testinal problems (functional, inflammatory, or obstructive). It is usually
associated with anorexia, lightheadedness, and sweating. The three stages
include nausea, retching, and rise in intra-abdominal pressure (contrac-
tion of abdominal muscles and descent of diaphragm). There is enhanced
vagal stimulation during vomiting. Prolonged vomiting can cause a met-
abolic alkalosis and hypokalemia.
Causes of Nausea and Vomiting

1. Gastritis and peptic ulcer disease.
2. Gastroenteritis.
3. Gallbladder disease, especially acute cholecystitis.
4. Liver disease (especially acute hepatitis).
5. Diabetic ketoacidosis.
6. Pancreatitis.
7. Intestinal obstruction.
8. Acute appendicitis.
9. Meningitis.
10. Kidney disease (infection and renal failure).
11. Pregnancy.
12. Alcohol.
13. Other causes (drugs, migraine, travel, raised intracranial pressure, acute MI, gastric
surgery, anorexia nervosa, Addisonian crisis, and so on).
It is important to ask relevant questions to determine the severity and

underlying cause.
Questions in Relation Vomiting

1. Duration, timing, and frequency?
2. Contents (blood, bile, food)?
3. Associated features (pregnancy, headache, jaundice, diarrhea, anorexia, and so on)?
4. Relieving factors?
5. Precipitating factors?
6. History of recent drug intake?
Hematemesis is due to leakage of blood from esophagus to the sec-

ond part of duodenum. All such patients should be admitted, an IV line
taken, blood sent for grouping and cross-matching, and watched closely
for hypovolemic shock. Blood in the vomitus may be bright red, with a
large bleed, especially, when there is a tear in the lower esophagus due
to forceful vomiting (Mallory–Weiss syndrome, p. 100). A spontaneous
transmural tear in the esophagus is called Borehaave syndrome. Coffee
ground v omitus indicates the presence of altered blood, which is due to
action of the acid in the stomach.
Causes of Hematemesis
1. Esophageal (varices, carcinoma, Mallory–Weiss tear, reflux esophagitis).
2. Stomach (gastritis, peptic ulcer, cancer, portal hypertensive gastropathy, and gastric
erosions).
3. Duodenum (ulcer).
4. Others (bleeding diathesis, thrombocytopenia, hereditary hemorrhagic
telangiectasia).
Clinical evidence of continued bleeding includes a rapid pulse

(>100bpm), falling BP, postural hypotension, even syncope, unexplained
anxiety and apprehension, recent hematemesis, and hematochezia.
Hematemesis when associated with melena (black and tarry stools) is
indicative of upper GI bleeding or rarely right-sided colonic bleeding. It
is due to the action of enzymes and bacteria on the blood or hemoglobin.
These stools are often very foul smelling.
Hematochezia (fresh bleeding per rectum) may be due to bleeding
from the small bowel, colon, or rectum. It may also represent a brisk
esophageal bleeding.
Causes of Hematochezia
1. Cancer of the colon or rectum. 6. Bowel infarction.
2. Piles or fissure. 7. Angiodysplasia.
3. Inflammatory bowel disease. 8. Intestinal polyps.
4. Bacillary dysentery and amoebic colitis. 9. Pseudomembraneous colitis.
5. Acute diverticulitis. 10. Coagulopathy and anticoagulation.
Occult blood loss is GI bleeding that cannot be seen by the naked eye
and is only detected by testing for occult blood by laboratory testing. It
can sometimes be as much as 200ml per day. It is a common cause of iron
deficiency anemia. Underlying malignancy must be excluded, especially
in the elderly patients. Any of the causes of hematemesis may be respon-
sible with minor blood loss. These patients may require, besides routine
workup, upper and lower endoscopy, barium studies, capsule endoscopy
CT or MR angiography, or Tc-99m-labeled RBC scan (blood pool imag-
ing study) to determine the site of bleeding if it is significant.
Anorexia is a nonspecific symptom of GI diseases and systemic dis-
eases. An example is acute hepatitis, where the patient does not want
to look at food. Another important cause of anorexia is drug-induced.
Severe anorexia, especially for proteins, is associated with carcinoma of
the stomach. Although called anorexia nervosa, young females rarely
complain of poor appetite.
Heartburn or retrosternal burning is a common symptom due to
reflux disease or hiatal hernia. It is worsened by a fatty or spicy meal,
alcohol, and smoking. The patient may experience acid coming up to the
mouth called water brash. The pain, due to esophageal spasm, at times
may mimic cardiac pain, occurring after a heavy meal and sometimes
being relieved by nitrates (smooth muscle relaxants) and antacids. Motil-
ity disorders of esophagus or loss of tone of the lower sphincter may also
produce heartburn.
Dysphagia or difficulty in swallowing can result from diseases of throat
down to the lower esophagus. It is a serious symptom that requires rapid
evaluation. Dysphagia can be caused by acid reflux, infection, or change
in motility. Painful swallowing is called odynophagia. If it is localized to
the throat (oropharyngeal dysphagia) and not associated with neuromus-
cular findings, it is likely mechanical and needs ENT evaluation. If there
are neuromuscular findings, it may require a videofluoroscopic swallow-

ing study. Esophageal dysphagia is localized to the chest and may be for
solids or liquid or both. If for solids only, it is likely to be a mechanical
problem where endoscopy or barium swallow is required. A progressive
nature is more suggestive of a carcinoma, while episodic nature is com-
mon in lower esophageal rings. Esophageal dysphagia for both solids
and liquids is likely to be motor where barium swallow or endoscopy or
esophageal motility study may be required. With reflux symptoms, it is
likely scleroderma and without it may be achalasia.
Causes of Dysphagia
• Esophagitis.
• Strictures.
• Carcinoma.
• Motility disorder (scleroderma).
• Achalasia.
• Diffuse esophageal spasm.
• Severe candidiasis.
• Esophageal compression (bronchogenic carcinoma, aortic aneurysm).
• Neuromuscular (motor neuron disease).
Questions for Dysphagia

1. Site? (the patient may pinpoint the site).
2. Duration?
3. To what type of food (solid or liquid)?
4. Associated symptoms (reflux, weight loss)?
5. Relieving and precipitating factors?
6. History of peptic ulcer, hematemesis, caustic ingestion, vomiting contents of previous
meal, anemia, hemoptysis, and so on.
Globus pharyngeus occurs in an anxious patient, usually a female, who

complains of dysphagia and a feeling of something sticking in the throat
(like a ball placed in the throat, which the patient tries to get rid by
repeated swallowing). It is associated with difficulty in taking a full breath.
This has to be differentiated from true dysphagia and is characteristically
relieved by anxiolytics with or without antidepressants. Endoscopy and
motility studies are normal.
Flatulence is excessive gas in the abdomen, which ultimately is passed

per rectum. Eructation is the excessive wind that is belched up from the
mouth. Most patients with flatulence or eructation swallow air (aeropha-
gia), which is a symptom of anxiety. Excess gas in the intestine may be due
to food intolerance, irritable bowel syndrome, and bacterial overgrowth.
Patients with acidity and ulcer disease also complain of gas and dyspepsia.
Dyspepsia or indigestion defined as epigastric pain for greater than
one month with any other upper abdominal symptom, including reflux
symptoms. Functional dyspepsia is said to be present if endoscopy is nor-
mal. It is a common (may be present in up to 80 percent of a population),
but non-specific symptom, which may be related to stomach, gallbladder,
liver, pancreas, or intestinal problems, may be similar. Dyspepsia is also a
common side effect of drugs, like antibiotics and NSAIDS and so on. It is
important to remember that ischemic heart disease and chronic ischemia
of the bowel may also present with dyspepsia-like symptoms. In some
cases, it may be related to underlying malignancy. Lastly, it may be a func-
tional and due to a psychological cause. Therefore, a good history and
examination are necessary to exclude important causes aforementioned.
Dyspepsia in any patient above the age of 60 years, or any of the red flags
mentioned as follows, necessitates looking for another cause and doing an
endoscopic examination. Also, give a trial of proton pump inhibitor and
check for H pylori, if there is no response.
Red Flags in Dyspepsia

1. Significant weight loss. 5. Fever.
2. Evidence of blood loss. 6. Jaundice.
3. Associated abdominal mass. 7. Severe acute abdominal pain.
4. Features of obstruction. 8. New onset of dyspepsia in elderly.
Halitosis or malodorous breath is most commonly due to local causes

in the mouth (biofilm produced over the tongue and gums and break-
down of proteins). However, the nose, sinuses, upper or lower airways,
esophagus, and stomach may occasionally be the source. Ketoacidosis
may be associated with a smell like acetone, and advanced liver failure
may be associated with fetor hepaticus (musty odor). Zenker’s divertic-
ulum may also be associated with bad smell due to putrid food in it.
Certain food may also give a bad smell from the mouth like garlic, onion,
fish, and so on. It must be emphasized that some anxious people may
complain of halitosis, which is not detected by others. Treatment involves
identifying the underlying cause and its removal associated with mouth
and tongue washes.
Diarrhea is the passage of frequent (usually more than five stools per
day) and soft stools (usually watery). Technically, it is the passage of more
than 200 g of stool per day. It must be differentiated form fecal inconti-
nence, especially in the elderly subjects. Urgency is the urge to defecate
and may be a feature of rectal carcinoma, loss of rectal tone, or dysentery.
Drugs, irritable bowel syndrome, and infectious causes are common. If
the diarrhea is more than two weeks, acute infectious causes are unlikely.
On the other hand, chronic diarrhea is said to be present if loose and fre-
quent stools (at least more than three per day) persist for greater than four
weeks or one month. The commonest cause is irritable bowel syndrome
and food allergies and sensitivity. It is important to consider inflamma-
tory bowel disease and gastrointestinal malignancy or TB in endemic
areas as a cause. See more detail of diarrhea in the previous section.
Malabsorption is due to failure to absorb from the intestine due to
digestive problems or absorptive problems. The stools are usually large,
bulky, foul smelling, difficult to flush, and slivery, especially when fat
malabsorption is associated (passage of more than 6 g of fat per day for
three consecutive days or total fat of more than 18 g within three days).
This is called as steatorrhea. Chronic pancreatitis is the most common
cause.
Constipation is the term applied to passage of infrequent and hard
stools with straining. It may be associated with incomplete evacuation
and abdominal pain (colic). It is important to note the severity, onset,
duration, and special characteristics to make a diagnosis and exclude rel-
evant differential diagnosis. Review medications that may alter motility
such as narcotics.
Causes of Constipation
1. Inadequate fiber, immobility, and habit. 10. Intestinal neoplasia (with obstruction).
2. Laxative abuse. 11. Depression.
3. Irritable bowel syndrome. 12. Parkinsonism.
4. Hypothyroidism. 13. Hirschprung’s disease.
(Continued)
Causes of Constipation
5. Diabetic neuropathy (may have 14. Spinal cord injury or disease.
diarrhea).
6. Hypercalcemia and hypokalemia. 15. Perianal pain, for example, fissure.
7. Anorexia nervosa. 16. Crohn’s disease.
8. Diverticular disease. 17. Multiple sclerosis.
9. Systemic sclerosis. 18. Drugs (iron, opiates, iron, calcium
antagonists, anticholinergics).
It is important to rule out organic causes such as those aforemen-

tioned, and in the elderly, with a recent change in bowel habit, to consider
carcinoma of the colon. Obstipation is the term applied to complete con-
stipation (without even passage of flatus). Most patients who complain
of constipation only require reassurance, dietary modification (increased
fiber and fluid), and regular exercise. Laxatives and stool softeners are also
available for conservative management refractory constipation.
Early satiety means the patient feels fullness and cannot eat further
even after a small meal. It is usually a feature of gastric disease like carci-
noma stomach or infiltration disease of the stomach or sometimes peptic
ulcer disease. Patients with motility disorders such as gastroparesis will
also have early satiety. Patients having bariatric procedures like sleeve
gastrectomy, gastric banding, gastric bypass, and so on, are prone to
develop this symptom as well.
Pruritus, in relation to gastroenterology disease, is related to liver
disease and obstructive jaundice. The rash associated with celiac disease
(dermatitis herpatiformis) is severely itchy. In primary biliary cirrhosis,
the pruritus may antedate all symptoms by months to years. In severe
chronic kidney disease (uremia), pruritus may also be a prominent feature.
Fever, in relation to gastroenterology disease, is indicated an underly-
ing infective process. Rarely, it may be associated with underlying malig-
nancy or connective tissue disorder.
Weight loss is an important symptom and signifies severe disease like
malabsorption, malignancy, or tuberculosis. Other causes like HIV infec-
tion, thyrotoxicosis and so on are considered if the history and examina-
tion are suggestive. Always document the weight and ask the amount of
weight loss and its duration. Also, whether it is associated with severe
anorexia or whether it is intentional or associated with depression.
PART II
General Physical
Examination
A general look at the patient may be extremely useful in defining the
cause, associated complications, or assist in the differential diagnosis.
In the following section, relevant physical signs are discussed in general
and especially in relation to the gastrointestinal system.
Nutritional Status and Obesity
Obesity is being considered as a disorder of energy homeostasis. About

2 billion people worldwide may be obese or over weight. Excess body
weight is one of the most important challenging public health problems,
which almost affects everyone in three individuals.
Look at the patient as a whole and assess the nutritional status.
A BMI gives a good idea about obesity, although it is not a direct measure
of adiposity. BMI is the weight in Kg divided by the height in meters
squared. In Asians, even a lower BMI is associated with higher risk; in
elderly, it is reverse.
Body Mass Index (BMI)
1. BMI 18.5 to <25Kg/m2 is considered normal.
2. BMI 25 to <30Kg/m2 is considered over weight.
3. BMI 30 to <35Kg/m2 is considered obesity I.
4. BMI 35 to <40Kg/m2 is considered obesity II.
5. BMI >40Kg/m2 is considered obesity III.
• Grade 1 overweight = BMI of 25–29.9 (23–25 for Asian

population).
• Grade 2 called obesity = BMI 30–39.9 (>25 for Asian p
opulation).
• Grade 3 morbid obesity = BMI >40kg/m . 2
BMI should be interpreted with caution as it is not a direct measure

of adiposity. A waist circumference is done in addition to BMI in people
with a BMI <35. The waist hip ratio (WHR) can also be used to predict
the risk of the patient, especially in terms of heart disease. It is calculated
by measuring the waist circumference midway between the costal mar-
gin and iliac crest divided by the maximum circumference around the
buttock. A value >1 for males and >0.85 for females is associated with
higher-risk insulin resistance, hypertension, diabetes, and dyslipidemia.
Look for Co-Morbidities in Obesity
1. Diabetes.
2. Hypertension (weight loss of 1Kg is associated with a decrease of BP 3–6mmHg in
systolic and 1–3mmHg diastolic pressure).
3. Heart disease.
4. Chronic lung disease.
5. Obstructive sleep apnea (sleep restriction associated with low leptin high ghrelin).
6. Chronic kidney disease.
7. Osteoarthritis, especially knees and back pain.
8. Cancer (increased risk of postmenopausal breast cancer).
9. Gallbladder disease is more common in obese.
10. GERD also increases with obesity.
An ideal goal is to lose no more than 0.5–1.0kg (1–2lb.) a week on a

balanced healthy diet with regular physical activity and behavior change
program. People should usually aim to lose a realistic 5 to 10 percent of
their original weight.
Who should lose weight?
1. Overweight and obese individuals BMI >25.

2. Severely obese (BMI 35–39.9) can gain significant health benefits
by losing excess weight, especially the patients with central obesity.
This is especially true if:
1. Positive family history of coronary heart disease.

2. Hypertension.
3. Dyslipidemia.
4. Diabetes mellitus.
Secondary Causes of Obesity

1. Hypothyroidism (slow metabolism) Rx subclinical does not reduce weight.
2. Cushing syndrome (central obesity).
General Physical Examination 23
3. Polycystic ovarian syndrome (50 percent are obese).

4. Medication-related (steroids, adrenergic antagonists, cyproheptadine sodium
valproate, carbamazepine, lithium, tricyclic antidepressants, phenothiazines,
thiazolidinediones, sulphonylureas, insulin).
5. Oral contraceptive use (uncommon).
6. Hypogonadism and GH deficiency (abdominal and visceral fat).
7. Eating disorders (bulimia nervosa, night-eating disorder).
8. Insulinoma.
9. Pseudohypoparathyroidism.
10. Hypothalamic (ventromedial hypothalamus) obesity.
11. Genetic syndromes (e.g., Prader–Willi syndrome, Fröhlich syndrome, Laurence
Moon–Biedl syndrome.
Obese people have a 60 percent chance of developing hypertension.

Congestive cardiac failure increases twofold with a BMI greater than 30.
IHD, stroke, diabetes, chronic kidney disease, and liver diseases are more
common in obese individuals. Osteoarthritis, gout, gallbladder disease,
dyslipidemia, and obstructive sleep apnea are more common in obese
individuals. In any patient, it is important to do a base line screening,
especially when weight is a problem.
Minimum Screening
1. Height.
2. Weight.
3. BMI.
4. Waist circumference.
5. Blood pressure.
6. Blood sugar fasting.
7. Fasting triglycerides.
8. Serum lipids.
9. Look for obstructive sleep apnea.
10. Look for medications that may increase weight.
11. Estimate the physical activity or inactivity.
12. Look for secondary causes of obesity.
13. Look for co-morbidities.
14. Family history.
Vitamins are organic compounds that humans cannot synthesize and

need an external supply in limited small quantities. Vitamin C and all the
groups of Vitamin B are all water soluble, while Vitamins A, D, E, and
K are fat soluble.
Vitamins Name Result of Deficiency

1. Vitamin A Retinol Night blindness.
2. Vitamin B1 Thiamine Beriberi, Wernicke’s encephalopathy.
3. Vitamin B2 Riboflavin Ariboflavosis (chilosis, glossitis).
4. Vitamin B3 Niacin Pellegra (dementia, diarrhea, dermatitis).
5. Vitamin B5 Pentothenic acid Uncommon (paresthesia, acne).
6. Vitamin B6 Pyridoxine Anemia.
7. Vitamin B7 Biotin Dermatitis or impaired growth.
8. Vitamin B9 Folic acid Megaloblastic anemia, birth defects.
9. Vitamin B12 Cyanocobalamin Megaloblastic anemia neuropathy.
10. Vitamin C Ascorbic acid Scurvy and bleeding gums.
11. Vitamin D Cholecalciferol Rickets and osteomalacia.
12. Vitamin E Tocopherol Fertility.
13. Vitamin K Phylloquinone Bruising and bleeding.
Anemia
It is a decrease in hemoglobin with or without a corresponding decrease

in the total red blood cell count below a normal range given for the age,
sex and race. Normal hemoglobin in adult males is 14–18g% while in
females is 12.5–16.5g%.
Figure 2 Gross anemia (pale complexion is best seen under the lower
eyelid)
Examination
The conjunctiva under the lower eyelids, tongue, hands, nails, and general
complexion of the patient indicate the amount of pallor (Figure 2), which
is usually proportional to the extent of anemia. Pale complexion without
anemia is seen with severe vasoconstriction seen in advanced heart failure.
History
A good history can only be taken while keeping the etiological causes in
mind. One can ask direct questions pertaining to each cause. A detailed
history of dietary habits, episodes of any blood loss (especially melena
or hematochezia), drug intake (especially aspirin and non-steroidal anti-
inflammatory drugs), passage of worms in stools, gut operations and
history of chronic diarrhea is essential to assess iron deficiency a nemia.
The commonest cause of anemia is blood loss, and in females, it is due
to excessive menstrual loss. Ask details regarding the sites, amount,
frequency, and duration of blood loss.
Recent studies indicate that IDA is associated with decreased work
performance, behavioral changes, and intellectual deterioration via
decreased monoamine oxidase activity and increased catecholamine
activity, especially in children. Incidence of infection is increased due
to reduced lymphocytes transformation, suppressed lymphokines pro-
duction, and impaired bactericidal activity of polymorphonuclear cells.
An increase in hemoglobin achieved with optimal replacement therapy
with intravenous iron is 0.27g% per day, while that with oral iron is
about 0.25g% per day.
Etiology
Anemia may be classified according to etiological and pathological classi-

fications. Morphological classification is based on size and chromatin con-
tent of red cells. Hypochromic and microcytic anemia is classically seen
in iron deficiency and thalassemia (rarely with sideroblastic anemia and
chronic disorders). Macrocytic anemia is seen with megaloblastic marrow
in B12 and folic acid deficiency, with normoblastic marrow in alcohol-
ics and polychromatophillic macrocytic in hemolysis. A normochromic
and normocytic anemia is associated with chronic disorders, infections,
malignancy, CRF, endocrine disorders, and connective tissue disorders. A
leukoerythroblastic anemia is associated with leukemia, myelosclerosis,
and metastatic carcinoma.
An etiological classification helps to formulate a plan of investigations
and workup.
Blood Loss
Menstrual loss.
Gut: worms, peptic ulcer, varices, piles, and angiodysplasia.
Lung: hemoptysis for example, TB or tumor.
Kidney: hematuria for example, stones or tumors.
Dyserythropoietic Anemia
A. QUANTITATIVE
Aplastic: Autoimmune or idiopathic, drugs and chemicals, radiation, infections, and
congenital.
Renal: Chronic renal failure.
Endocrine: Addison’s disease, thyroid, pituitary and parathyroid disease.
Marrow: Lymphomas, leukemia, and myelofibrosis.
B. QUALITATIVE
Primary dyserythropoietic anemia is rare.
Secondary: Vitamin B12 and folic acid deficiency, Iron deficiency anemia, thalas-
semia, hemoglobinopathies, aplastic anemia, myelofibrosis, and leukemia.
Hemolytic Anemia
a. INTRACELLULAR DEFECT:
Sickle cell anemia, thalassemia, and other types of hemoglobinopathies.
b. EXTRACELLULAR DEFECT:
Autoimmune hemolytic anemia, acquired hemolytic anemia, and microangiopathic
hemolytic anemia.
c. MIXED:
Burns, G6PD deficiency, lead poisoning.
Other Causes of Anemia

Malaria, incompatible transfusion, infections (bacterial endocarditis, clostridia,
hemophilus, salmonella, and meningococcus), and hypersplenism. Malignant hyperten-
sion, uremia, and tumors also rarely cause hemolysis.
The term megaloblastic change is used to describe marrow changes of

Vitamin B12 or folic acid deficiency anemia. In macrocytic anemia, there
are larger-sized RBCs (MCV >100fl) in the blood commonly seen in
B12 or folic acid deficiency. Folic acid deficiency can occur acutely, while
Vitamin B12 reserves may take several years to exhaust.
Causes of Folic Acid Deficiency

1. Decreased intake of green vegetables or increased use of alcohol.
2. Decreased absorption as in tropical sprue, coeliac disease, alcoholics, patient on
hemodialysis, and with drugs (tetracyclines, oral contraceptives, anti-convulsants).
3. Increased requirement pregnancy, infancy, tumors, and exfoliative skin diseases.
4. Decreased utilization with folic acid antagonists like methotrexate, trimethoprim,
and triamterene.
Causes of B12 Deficiency Anemia

1. Strict vegetarians.
2. Pernicious anemia and gastrectomy.
3. Malabsorption syndrome like ileal resection, tropical sprue, coeliac disease, chronic
pancreatitis, intestinal lymphoma, and drugs like neomycin, alcohol, and colchicine,
and so on.
4. Increased requirement as in pregnancy, tumors, and thyrotoxicosis.
5. Abnormal utilization (fish tape worm).
Other Causes of Macrocytic Anemia

Alcohol, chronic liver disease, myxedema, cytotoxic drugs, aplastic anemia, newborns,
pregnancy, COPD, preleukemia, and reticulocytosis may be associated with macrocytosis.
Clinical Features
These are best divided into general features that are shared by all types of
anemia, and specific features that are particular to the specific etiology of
the anemia. It is important to suspect aplastic anemia when there is evi-
dence of reduction of all the cell lines in the blood. The patient is pale with
evidence of bruising, indicating thrombocytopenia, and there may also
be evidence of infection indication leucopenia (Figure 3). Iron deficiency
Figure 3 Features of aplastic anemia showing pallor, bruising, and

skin infection. Koilonychia in IDA shown on the right as flattening
and early spooning of the nails
Figure 4 Features of iron deficiency anemia showing koilonychias and

bald tongue
anemia is the commonest form of anemia and may be suspected when

koilonychia, glossitis (Figures 3 and 4) or angular stomatitis is present.
The specific features helpful in diagnosing iron deficiency, mega-
loblastic, and hemolytic types of anemia are given in Figure 5.
CLINICAL FEATURES OF ANEMIA

Specific features General features
Jaundice (HA) Headache
Dizziness
Angular stomatitis
Fatigue
Glossitis (IDA) Poor memory
Dysphagia (IDA)
Hepatomegaly (HA) Dyspnoea
Gall stones (HA)

Palpitation
Splenomegaly (HA) Tachycardia
Murmur
Cocacola colored Heart failure
urine (HA) Angina
Koilonychia
(IDA)
Leg ulcers (HA)
Peripheral neuropathy
(B12 Deficiency)
Figure 5 Clinical features of anemia are separated according to the

etiology
IDA=Iron deficiency anemia, HA=hemolytic anemia
Laboratory Feature of Anemia
Iron Deficiency Anemia
1. The peripheral smear in Figure 6 shows hypochromia (pale red cells)

and microcytosis (smaller size of red cells).
2. The serum iron levels are low and the TIBC is increased.
3. The red cell indices demonstrate a low MCV and MCH.
Figure 6 Peripheral smear of IDA and macrocytic anemia. On the

left, hypochromic and microcytic smear; on the right, hyperchromic
macrocitic picture with hypersegmented polymorph
4. Serum ferritin levels and bone marrow iron staining on biopsy give
an indication of the total iron stores. Each microgram of ferritin in
the serum is equivalent to 8mg of stored iron provided there is no
liver injury as ferritin is an acute phase reactant.
5. Check for blood loss in stool, urine, and sputum. Also, check stool
for ova and cyst.
6. Endoscopy, barium studies, rarely technetium-labeled RBC for
Meckel’s diverticulum or chromium-labeled RBC studies for site of
blood loss are required.
Macrocytic Anemia
1. Peripheral smear shows variability in size and shape of red blood

cells. There is macrocytosis (Figure 6), increased MCV (>100fl),
decreased reticulocytes, RBC inclusions (basophilic stippling and
Howell–Jolly bodies), and hypersegmented polymorphs.
2. Marrow is hypercellular, megaloblastic with M/E (myeloid/
erythroid) ratio becoming 1:1.
3. Indirect bilirubin and serum LDH are raised due to hemolysis.
Beta leucine is increased in B12 deficiency only.
4. Serum B12 levels are less than 120pg./ml in B12 deficiency, while
serum folate is <0.5 ng/ml in folic acid deficiency.
5. Cytokinetics: ineffective erythropoiesis and thrombopoiesis
with intramedullary destruction of RBCs. There is a decreased
production or delivery of WBCs.
6. Schilling test is done to check the amount of labeled B12
absorption in pernicious anemia.
7. Methylmalonic aciduria is an index of B12 deficiency and uri-
nary formiminoglutamic acid is high in Vitamin B12 deficiency.
Figure 7 Patients with deep jaundice is likely to have obstruction or

cholestasis
Jaundice
It is the yellowish discoloration of the skin and mucous membrane, clin-

ically visible when bilirubin in the blood is usually greater than 3.0mg%.
It is best seen in the sclera because of the affinity of bilirubin for the elastic
tissue (Figure 7).
Pathophysiology
A rise in the serum bilirubin may be due to increased production of

bilirubin (hemolytic jaundice), decreased conjugation in the liver (hepatic
jaundice), or obstruction in biliary passages (obstructive jaundice). It
should be differentiated form caroteinemia, which also produces a faint
yellow discoloration while sparing the sclera.
A large portion of bilirubin is produced by breakdown of red
blood cells. It combines with albumin in a ratio of 2:1 and is trans-
ported to the liver. This indirect or unconjugated bilirubin is insolu-
ble in water and is not excreted in urine. After reaching the liver, it
is taken up and conjugated with two molecules of glucuronide and
excreted in bile as bilirubin diglucuronide. This conjugated bilirubin
or direct bilirubin is water soluble, and it will be excreted in the urine
if it diffuses back into the blood due to obstruction. Normally, it is
excreted in the bile, and upon reaching the intestine, it is acted upon
by intestinal bacteria and converted to urobilinogen (which undergoes
enterohepatic circulation) or excreted in the feces as stercobilinogen.
Urobilinogen, when present in the urine indicates patent biliary pas-
sages, or in other words, excludes obstructive jaundice. In hepatitis, at
times, severe inflammation of the hepatocytes presses the small biliary
passages, causing temporary obstruction. This results in itching, passage of
whitish-gray stools, and absence of urobilinogen in the urine. This is called the
cholestatic stage of viral hepatitis and only lasts a few weeks.
Hepatic jaundice is due to some liver insult commonly due to viral
hepatitis or at times drugs (like INH, PAS, ethanol, carbon-tetrachlo-
ride, imipramine, phenytoin can cause liver injury), and rarely may be
congenital (deficiency of specific enzymes). At times, severe inflammation
in viral hepatitis may mechanically obstruct the small biliary passages,
resulting in very high levels of bilirubin called cholestatic viral hepatitis.
Obstructive jaundice is a surgical problem because the cause of the
obstruction has to be removed in order to achieve a cure. Whenever there
is obstruction, it is associated with colicky pain in the right hypochon-
drium, fever with rigors, and chills due to infection and a rising jaundice.
This triad of Charcot is characteristic of ascending cholangitis. The stool
becomes pale due to absence of stercobilinogen, and there may be itching
due to deposition of bile salts in the skin.
Causes of Obstructive Jaundice

1. Drugs like chlorpropamide, oral contraceptives, chlorpromazine, and anabolic
steroids.
2. Primary biliary cirrhosis.
3. Carcinoma of liver or metastatic liver disease can cause biliary obstruction.
4. Post-hepatic causes, for example, gallstones, post-operative strictures of bile duct, and
cancer bile duct (cholangiocarcinoma), cancer of gallbladder or head of pancreas,
and periampullary tumors.
5. Choledochal cyst.
6. Parasites in the CBD or pressure from outside, for example, lymph nodes.
7. Congenital bile duct defects (bleary atresia).
8. Pancreatitis.
9. Sclerosing cholangitis.
Note
• Rarely, jaundice in a hemiplegic patient may be predomi-

nantly seen on the non-hemiplegic or normal side.
• Carotenemia appears as a yellow tinge of the skin in hypothy-
roidism or patients consuming excessive carrots.
• Patients with severe uremia may are quite pale, and the sallow
complexion may have superficial resemblance to jaundice.
HEMOLYTIC VS. OBSTRUCTIVE

JAUNDICE
Features of Features of
hemolytic jaundice obstructive jaundice
Jaundice is mild Jaundice is deep with
and has a greenish an orangish tinge
Fever with rigors
Anemia Bradycardia
Gall stone Colicky pain in
right hypo-
chondrium
Splenomegaly
Hyperlipidemia
in chronic cases
Dark coca-cola
colored urine
Itching and
bruising
Steatorrhea and
Leg ulcers features of
in congenital hemolytic malabsorption
anemias
Figure 8 Clinical features of hemolytic and obstructive jaundice
Causes of Hemolytic Jaundice

1. Congenital hemolytic anemia like hereditary spherocytosis, thalassemia, and sickle
cell anemia.
2. Autoimmune hemolytic anemia (warm and cold antibody-induced) and microangio-
pathic anemia.
3. Acquired infective causes like malaria, infectious mononucleosis, and mycoplasma
pneumonia.
4. Drugs like methyldopa, quinine, quinidine, pencillamine, hydralazine, and so on.
5. Mismatched transfusion, connective tissue disorders, uremia, malignancies, and
G6PD deficiency.
6. Rarely, hypersplenism or paroxysmal nocturnal hemoglobinuria.
Figure 9 Thalassemic patient with jaundice, typical facies

(prominent cheeks) also had hepatosplenomegaly
Clubbing
It is characterized by bulbous enlargement of the distal phalanx of one

or more fingers and toes (Figures 10 and 11) due to an increase in soft
tissue. There is loss of angle between the base of the nail and the adjacent
skin (Figure 11), fluctuation at the nail bed, and increased curvature of
the nail (Figure 11). It is usually painless, bilateral, and often reversible.
Figure 10 Clubbing in a patient with inflammatory bowel disease and

cirrhosis of the liver
Clinical Presentation
Clubbing usually first develops in the thumb and index finger and later
involves the other fingers. Early clubbing may be detected by measur-
ing the transverse diameter of index finger at the base of nail divided by
diameter at distal interphalyngeal joint. Normally, it is one or less; more
than one signifies clubbing. The normal angle between the nail plate and
the skin overlying the proximal end of the nail is 160° or less. Prolifer-
ation under the nail plate causes the angle to increase above 160° and
often exceeds 180°. This is appreciated with the finger at the level of the
eyes (profile sign, Figure 11). The edge of a paper placed parallel to the
long axis of the nail normally reveals a triangular area toward the base of
the nail. A diamond-shaped area is also revealed when two nails are held
back to back, as shown in Figure 11. These triangular or diamond-shaped
areas are lost in early clubbing. The normal root of the nail lies against
bone (DIPJ), but with clubbing, the root of the nail is separated from the
underlying bone by connective tissue and edema. This spongy material
makes the base of the nail to float when rocked from side to side or in the
longitudinal direction (floating sign). In advanced cases, there is a warm
club-like swelling of the distal phalanx.
CLUBBING DEMONSTRATED
Absent nail Nail root appears to float free
fold
Floating sign
Parrot beak nail
rocked with the fingers
Loss of angle best seen
at the level of the eye.
Profile sign
Loss of the normal diamond

shaped space between the two
finger nails when held
together back to back
1600 1800
Normal nail Clubbed nail

Note the loss of angle in the clubbed nail.
Figure 11 Different methods for the demonstration of clubbing
In relation to gastrointestinal disease, it is seen in about one-third of

the patients with cirrhosis. Rarely, with development of hepatopulmo-
nary syndrome, there may be associated cyanosis. Clubbing is also seen
in inflammatory bowel diseases and celiac disease. Clubbing is divided
into various stages, with different signs appearing as severity of clubbing
increases.
Clinical Stages of Clubbing

EARLY STAGE
1. Loss of normal angle (160∞ to 170∞) between the nail and the soft tissue around its
bed. It actually becomes 180∞ or greater and is the initial sign.
2. Shiny appearance of adjacent skin.
3. Fluctuation and softening of the nail bed causes rocking of the nail on palpation.
4. Increased convexity of the nail in both longitudinal and vertical direction.
ADVANCED STAGE
5. Clubbed or bulbous appearance of the finger tips.

6. Local warmth and signs of inflammation appear with involvement of the proximal bone.
7. Longitudinal striations and friable nails are nonspecific late signs.
Pathogenesis
It is not well understood, but the prerequisite seems to be peripheral

vasodilatation and A-V anastomosis due to proposed substances like
prostaglandins, ferritin, adenosine triphosphate, 5-hydroxytryptamine,

and bradykinin. Proliferation and edema of connective tissue between
the skin and the nail bed results in loss of normal angle and increased
sponginess of the nail base causing clubbing.
Causes of Clubbing
Insidious onset of clubbing over months may be due to inflammatory

causes, but rapidly progressive clubbing may be seen in malignant diseases.
In children, congenital heart disease, cystic fibrosis, and lung infection are
often considered. In adults, the two most common causes are infections
and intrathoracic neoplasm. Clubbing only in the toes may be seen in PDA
with reversal of shunt. Unilateral clubbing may be seen with aneurysm of
the aorta and large vessels, apical lung tumors, in hemiplegia and axillary
tumors. Clubbing may also be idiopathic or associated with trauma.
Other Types of Clubbing
When clubbing is associated with subperiosteal new bone formation

(resembling elm bark) in the distal diaphysis of the long bones of extrem-
ities, it is called hypertrophic osteoarthopathy. Lung and pleural tumors
account for one-third of the cases. The affected area appears inflamed,
painful, and edematous. Acropachy is an alternate name for clubbing and
ETIOLOGY OF CLUBBING
RT (75–80%) CVS (10–15%)

Bronchogenic carcinoma Bacterial endocarditis
Bronchiectasis Tetrology of Fallot
Lung abscess Atrial myxoma
Empyema Eissenmenger’s
Fibrosing alveolitis complex
Asbestosis
Local A-V
Pneumoconiosis
malformations
A-V fistula
Miscellaneous
GIT (5–10%)
(5–10%)
Cirrhosis of liver
Idiopathic
Ulcerative colitis
Hodgkin’s disease
Crohn’s disease
Malabsorbtion syndrome Grave's disease
Thyroid carcinoma
Gut carcinoma
Carcinoma thymus
Achlasia
Figure 12 Causes of clubbing are given in various systems in

descending order of importance
in Graves’ disease; it is called thyroid acropachy. In this condition, there

may be associated onycholysis. Pseudoclubbing is the term applied when
the nail appears to be clubbed, but in reality, there is only increased nail
curvature usually with chronic paronychia or abscess of the pulp space.
This can be confirmed by placing the thumbs of the patient back to back
as aforementioned. In true clubbing, a diamond-shaped empty space is
lost, while it is present normally and in pseudoclubbing.
Peripheral Edema
It is the collection of fluid in the interstitial space due to either altered

Starling’s forces or blockage of venous outflow. In relation to GIT, edema
may be seen in cirrhosis of liver, malabsorption syndromes, and protein
losing enteropathies.
Examination: Look for edema at dependent parts of the body, that
is, around the ankle (sacrum in bed bound patients). A constant pres-
sure when applied against a bony prominence for about 10 s leaves a pit,
which gradually fills up. This is seen when about 4 kg of fluid has already
collected. If the pit remains for a shorter period (less than 30 to 40s), the
cause is likely due to hypoalbuminemia (fast edema). A cardiac cause is
essentially ruled out when the venous pressure is normal and the pit stays
for longer period (more than 40 s) unless diuretics have been used (called
slow edema). Similarly, edema limited to the face or hands is not seen
with cardiac cause. In general, edema may be generalized with cardiac
disease, liver disease, kidney disease, and other causes of hypoalbumin-
emia. Local causes are due to venous or lymphatic obstruction or vascular
leakage or increased permeability.
Figure 13 Pitting edema shown in fluid overload conditions

Causes of Edema
1. CVS: congestive cardiac failure, right heart failure, and constrictive pericarditis.
2. Liver: chronic liver disease and cirrhosis.
3. GIT: malabsorption and protein losing enteropathies.
4. Kidney: chronic renal disease and nephrotic syndrome.
5. Lung: cor-pulmonale.
6. Drugs: calcium antagonists.
7. Others: allergy and angioedema, premenstrual edema, tight undergarments, wet
beriberi, severe obesity, cyclic edema.
8. Hypoalbuminemia: malnutrition.
9. Unilateral edema: DVT, tumor, or lymph node causing obstruction.
10. Lymphatic obstruction: When gross, it may also pit (filariasis, Milroy’s disease,
congenital lymphedema, malignant lymphatic invasion.
Disease-Focused Examination
In cirrhosis, signs of liver cell failure may appear, but quite often, one may
not find any sign, even with advanced liver disease. General examination
may reveal, spider angioma, jaundice, palmer erythema, and bruising.
There may be clubbing, leuconychia, Dupuytren’s contracture, gyneco-
mastia, and testicular atrophy.
Rarely, a sweet, fecal smell (fetor hepaticus) is noticed in the breath of
those with end-stage liver disease (due to dimethyl sulfide). Asterixis or
hepatic flap is demonstrable in early to late hepatic encephalopathy. The
patient is asked to fan out the fingers of the outstretched hands, with wrist
extended for 10 to 15s. There is coarse, irregular flexion and extension
Figure 14 Spider angioma in cirrhosis with raised central area and
branching capillaries
Figure 15 Leuconychia (white ban across the nail in

hypoalbuminemia) on the left, and clubbing associated with white
nails is seen in a case of cirrhosis on the right
of the fingers with lateral movements. It is due to false neurotransmis-

sion and inability to maintain posture and tone. It may also be seen in
advanced cardiac, renal, and respiratory failure and severe electrolyte dis-
turbance and overdoses.
Dupuytren’s contracture (Figure 16) is the cord like thickening of the
palmer fascia, resulting in fixed flexion of the lateral fingers, especially
the ring finger. It is usually bilateral and associated with consumption of
alcohol. It is not a sign of cirrhosis from other causes.
Figure 16 Dupuytren’s contracture in a patient with alcoholic

cirrhosis (left) and palmer erythema (redness predominant over the
thenar and hypothenar eminences) in chronic liver disease. The soles
of the feet may be similarly involved. Palmer erythema may also be
seen in pregnancy, thyrotoxicosis, rheumatoid, and polycythemia
In primary biliary cirrhosis, itching (from deposition of bile pig-

ments in the skin) is an early feature; therefore, scratch marks may be
visible along with hyperpigmentation and jaundice (also see page 79).
Hyperlipidemia may be associated with deposition, especially around the
eyes called xanthelasma (Figure 17).
Figure 17 Xanthelasma along the margin of the eye due to

hyperlipidemia and bruising in Vitamin K deficiency
Features of chronic malabsorption include generalized weight loss

and asthenia. Various deficiencies are associated with suggestive clinical
features, like calcium and Vitamin D (bone pain and deformity); pro-
tein (poor wound healing, failure to grow, and leukonychia); Vitamin
K (bruising); Vitamin A (night blindness); Vitamin B12 (paresthesia and
numbness); Vitamin B1 (weakness and lassitude; Vitamin B6 (dermatitis,
diarrhea, and dementia and iron deficiency (koilonychia)).
In Peutz–Jegher’s syndrome, brownish-black pigmented spots around
the mouth occur. The patient presents with chronic diarrhea due to intes-
tinal polyposis (in the stomach, small bowel, and large bowel).
In celiac disease, chronic diarrhea may be associated with an extremely
itchy bullous rash on the extensor surfaces called, dermatitis herpati-
formis (Figure 18).
Inflammatory bowel disease may be associated with large joint arthritis,
especially of the knees, liver involvement with sometimes signs of chronic
liver disease, clubbing, eye involvement with scleritis and uveitis, and
skin involvement with erythema nodosum and pyoderma gangrenosum
Figure 18 Dermatitis herpatiformis in a patient with coeliac disease

Figure 19 Pyoderma gangrenosum in a patient with ulcerative colitis
(Figure 19). This is an angry-looking ulcerating lesion of the skin, with

blackish areas representing gangrene seen in inflammatory bowel disease.
It may involve any part of the body. It is seen especially in ulcerative
colitis, but occasionally in Crohn’s disease (CD).
In acute hemorrhagic pancreatitis, bruising around the umbilicus is
called Cullen’s sign (Figure 30) and in the flank is called Gay Turner’s sign.
In the skin, in relation to gastrointestinal diseases, one may find pig-
mentation associated with chronic liver disease in hemachromatosis,
Peutz–Jegher’s syndrome, malabsorption syndrome, Cronkhite–Canada
syndrome. Acanthosis may be associated with carcinoma of the stom-
ach. Flushing along with diarrhea and wheezing is seen in carcinoid
syndrome. Glucagonoma may be associated with migratory necrolytic
rash. In hereditary hemorrhagic telangiectasia, skin telangiectasis may
be associated with GI bleeding. Porphyria in association with alcoholic
liver disease may be associated with vesicles on exposed skin surface.
Tight skin with loss of wrinkles and calcification in systemic sclerosis
maybe associated with dysphagia and bacterial over growth syndrome.
Bruising is seen in chronic liver disease and is due to a defective Vitamin
K-dependent coagulation factors. Hypersplenism may be associated with
thrombocytopenia and a petechial rash. Pruritus in obstructive jaundice
and chronic kidney disease is associated with scratch marks on the skin.
Cyanosis in relation to GI disease may rarely be associated with hepa-
topulmonary syndrome.
On the hands, one may find some signs of chronic liver disease like
clubbing, leukonychia, spider angioma, palmer erythema, bruising,
Dupuytren’s contracture, or asterixis. Clubbing may also be seen in
inflammatory bowel disease and malabsorption syndromes in relation to

gastroenterology. The hands may be pale like the complexion with anemia
related to gastrointestinal blood loss in a host of diseases.
In the eyes, one may find jaundice, uveitis (ulcerative colitis and CD),
and Biot’s spots (Figure 20) with night blindness, in Vitamin A deficiency.
Anemia is seen in a variety of GI causes. Kayser–Fleischer ring may be seen
in Wilson’s disease (Figure 20) associated with signs of chronic liver disease.
Figure 20 Kayser–Fleischer ring on the left seen as an outer rim of

golden brown color around the outer cornea. The patient also had
jaundice from chronic liver disease. Biot spot in Vitamin A deficiency
is seen at 9 o’clock on the sclera on the right
Examination of the neck involves looking for lymph nodes, thyroid

enlargement, thyroglossal cyst, large blood vessels, trachea and esopha-
geal abnormalities, and any other swellings. Left supraclavicular lymph
node enlargement is associated with carcinoma of the stomach or lung
and gastrointestinal malignancies and is called Virchow’s lymph node.
Figure 21 A young male with bull neck in lymphoma on the left (it
may also be seen in children with diphtheria). Goiter in a female on
the right
Lymphadenopathy, especially in the neck, may be the first feature of

lymphoma. Goiter may be associated with thyrotoxicosis or myxedema.
In relation to GIT, the former is associated with hypermotility and the
latter with hypomotility and at times, ascites. Medullary carcinoma of the
thyroid may be associated with diarrhea; thyroid abnormalities may occur
in chronic active hepatitis.
Oral Examination
This includes a detailed look at the lips, teeth, tongue, tonsils, and throat.
A torch, tongue depressor, and disposable gloves are all that may be
required during the examination. A careful look may provide valuable
clues to the diagnosis or presence of complications.
Examination of Lips
Appear blue in cyanosis and pale in anemia.
Aphthous ulcers on the inner surface of lips.
Angular stomatitis (fissure at the angle of mouth) seen in iron riboflavin deficiency.
Cleft lip or its repair may be obvious.
Herpes labialis (reddish crusted vesicles).
Cheilosis (seen in iron deficiency anemia).
Ulcer (may be due to cancer).
Pigmentation (in Peutz–Jegher’s syndrome).
Chancre (small firm indurated lesion in syphilis).
Examine the inside of the mouth with a torch and a tongue depressor.
Inspect the buccal mucosa, gums, teeth, and tongue. Also, carefully look
at the pillars of fauces, uvula, and the tonsils. Look for changes in color,
abnormal growths or masses, ulcers, and abnormal odor. Bad orodental
hygiene may be the source of many problems. Bleeding gums are com-
monly due to gingivitis. Whitish spots on the buccal mucosa (Koplik
spots) opposite the second molar may be seen in measles. Leukoplakia
is a premalignant disorder, where the buccal mucosa may appear like a
homogenous or nodular white patch that cannot be rubbed off. Biopsy
confirms the diagnosis. Red velvety lesion (erythroplasia) of the mouth,
even when asymptomatic, is more likely to be carcinoma in situ or invasive
carcinoma, than the white lesion. Any chronic ulcerative lesions that fail
to heal in one to two weeks should be considered potentially malignant.
Examination of Teeth and Gums

Look for caries of the teeth.
Tar deposition in heavy smokers.
Tetracycline staining (yellow-gray bands).
Pigmentation of gums in Addison’s disease.
Blue line on the gums indicates lead toxicity.
Hyperplasia of the gums is seen in chronic gingivitis and chronic phenytoin use.
Peg-shaped and notched upper incisor teeth (Hutchinson’s teeth).
Examine the tongue inside the mouth and then after protruding.
Look for the shape, size, wasting, and involuntary movements. Inspect
the tongue more closely on protrusion and look for deviation.
Examination of Tongue
Geographical tongue is a normal variant.
Fissured tongue may be a normal variant.
Anemia can be accessed from the pallor.
Central cyanosis is seen on the under surface of tongue.
White curd-like deposits occur in fungal infection or candida, but blackish deposits are
seen with other fungi.
Excessive coating (fur) occurs in smokers.
Strawberry tongue is seen in scarlet fever.
Dry tongue may indicate dehydration or seen in Sjogren’s or sicca syndrome.
Generalized papillary atrophy occurs in pernicious anemia and IDA.
Wasted flaccid and ipsilaterally deviated tongue is seen in lower motor neuron hypoglos-
sal palsy, for example, bulbar palsy. A weak and spastic tongue is seen in pseudobulbar
palsy and upper motor neuron lesion of the hypoglossal nerve.
Fasciculation may be seen in bulbar palsy.
Tremor may be seen in thyrotoxicosis.
Carcinoma of the tongue especially occurs on the side and under surface as growth or ulcer.
Red beefy tongue is seen in Vitamin B6, B12 deficiency and nicotinic acid poisoning.
Bald and pale tongue may be seen in pernicious anemia.
Aphthous ulcers are seen in bad orodental hygiene and CD.
Macroglossia is seen in acromegaly and amyloidosis.
Ulcers of the tongue may be seen in celiac disease, Reiter’s disease, Behcet’s disease, CD,
and in syphilis. Carcinoma of the tongue may also present as an ulcer.
Figure 22 Magenta tongue is seen especially in riboflavin (Vitamin

B2) deficiency (left). A geographical tongue is a normal variant and
should be differentiated from oral candidiasis or thrush, which usually
has a layer or coating like pseudo-membrane. This curdled milk-like
membrane can be whipped away, which leaves an erythematous mucosa
Figure 23 Coated tongue seen on the left may be normal or associated
with many fevers, especially typhoid. On the right, the tongue is
deviated to the right and that half is showing some wasting. This is
seen in lower motor neuron hypoglossal nerve palsy
Figure 24 Patient on the left has hereditary hemorrhagic

telangiectasia. They may bleed especially from gastrointestinal tract
due to presence of similar lesions. On the right, leukoplakia close to
the left tip of the tongue is seen as a whitish patch
Examination of the throat is mandatory, as it is one of the commonest

sites of infection. It includes a look at the orodental hygiene, tongue,
pharynx, and tonsils. Throat is a known source of sinus, chest, and ear
problems. A simple group-A beta hemolyticus streptococcal infection
may lead on to rheumatic fever and permanent cardiac disability.
Examination of the Throat

1. Aphthous ulcers are well-demarcated ulcers with red margins seen anywhere on the
mucous membrane.
2. Deviation of the uvula to the healthy side on saying “ah” occurs in vagal palsy.
3. Herpes zoster infection of the trigeminal or glossopharyngeal nerve is associated with

vesicles in the area of distribution.
4. Malignancy is recognized by an irregular hard growth, infiltration, and or ulceration.

There is lymph node enlargement in the area of drainage.
A white patch in the throat may be due to multiple causes depending

on the history. It may be simply follicular tonsillitis or may be a serious
infection like diphtheria. The differential diagnosis of this appearance is
given as follows:
Figure 25 Petechae are seen on the palate in a case of infectious

mononucleosis
White Patch in the Throat

1. In acute follicular tonsillitis, the enlarged tonsil has areas of visible pus.
2. In infectious mononucleosis, the enlarged tonsil is covered by a whitish membrane.
3. In candidiasis, there is patchy white curd-like membrane or whitish spots.
4. In diphtheria, the grayish membrane readily bleeds on attempted removal.
Clinical Examination: Inspection

Prerequisites of Examination
1. Introduce yourself, take permission, and explain briefly to the patient

what you are about to do, and that you will not hurt him or her.
2. The patient should be lying down supine in a comfortable position
and in good light.
3. The head may be supported with a small pillow.
4. Hands are kept by the side, while the face is turned to the opposite side.
5. Legs are kept straight. The knees may be flexed, but this does not
relax the abdominal muscles.
6. The patient breathes quietly with his mouth open.
7. The urinary bladder should be recently emptied.
8. Exposure of the abdomen should be adequate according to the age,
sex, and culture, from mid-thorax to pubis.
9. Start to look at the abdomen from the foot end moving toward the
right side, getting ready to palpate the abdomen. Also, examine the
sides of the abdomen and the back with the patient sitting.
The abdomen is artificially divided into four or nine quadrants for

reference purpose to localize the disease anatomically (Figure 26). This is
ARTIFICIAL REGIONS OF ABDOMEN

Mid-sternal line
Right upper Left upper

quadrant quadrant
Transumblical line
Right lower Left lower quadrant

quadrant
Mid clavicular lines
Epigastrium
Right hypo -
Left hypochondrium
chondrium
At 9th costal cartilage

L1 or trans pyloric
Right lumber Left lumber
L5 Trans - tubercular plane
Right iliac Left iliac fossa
fossa
Umblilical Hypogastric
region region
Figure 26 The artificial regions of the abdomen

useful for differential diagnosis, as any localizing features may pint to a

cause in the underlying anatomical structures.
After having met the prerequisites, one should comment on the
following features on inspection.
Parameters of Inspection
1. Shape of abdomen. 2. Abdominal movements.
3. Epigastric pulsations. 4. Pigmentation and rashes.
5. Striae. 6. Prominent veins.
7. Visible peristalsis. 8. Pubic hair.
9. Umbilicus. 10. Hernial orifices.
11. Scars and tap marks. 12. Surgical incisions.
Figure 27 The patient has general abdominal swelling with localized
fullness, especially in the epigastrium (on the left). Gross abdominal
distension due to ascites with striae due to stretching seen on the right
A diagrammatic representation of the findings on inspection is advis-

able. An example is given as follows.
DIAGRAMMATIC REPRESENTATION OF
FINDINGS
Shape of abdomen
Abdominal movement
Rashes and pigmentation
Scars
Epigastric pulsations
Visable peristalysis
Umbilicus
Striae
Tapmarks
Pubic hair
Hernial orifices
Figure 28 The scheme of general physical examination of GIT

1. Shape of Abdomen
A normal abdomen is scaphoid or flat in shape. Bulging or disten-
tion may be symmetrical or localized to one area (Figure 29).
Causes of Abdominal Distention

1. Abnormal masses or enlarged viscera. 4. Flatus or gas.
2. Free or encysted fluid in the abdomen. 5. Fat, that is, obesity.
3. Fetus in the hypogastrium. 6. Feces.
Figure 29 Swelling in the right hypochondrium was a tumor in

the liver. On the right, there is fullness in the left hypochondrium.
This was due to massive splenomegaly
2. Abdominal Movements
Normal movement during quiet breathing in females is thoraco-
abdominal (abdomen forms a concavity during inspiration), but
is abdomino-thoracic (abdomen bulges out during inspiration) in
males and infants of either sex. The patient uses the diaphragm
for breathing when there is chest pain (pleurisy), intercostal nerve
paralysis, or ankylosing spondylitis. Conversely, the patient uses
more chest muscles when there is large ascites, peritonitis, abdom-
inal tumors, liver abscess, or any because that restricts or limits the
diaphragmatic movement. The indrawing of the anterior abdom-
inal wall during inspiration (paradoxical movement) may be seen
when the patient is voluntarily doing it, or rarely, in paralysis of the
diaphragm.
3. Epigastric Pulsations
They are either due to transmission form the aorta, the heart, or
rarely from aneurysmal dilatation of an artery.
Causes of Epigastric Pulsations

1. Thin built (transmission from 4. Mass in front of aorta (carcinoma
aorta). stomach).
2. Aneurysm of abdominal aorta. 5. Pulsatile liver in tricuspid
regurgitation.
3. Hyperkinetic right ventricle.
4. Pigmentation and Rashes

Localized pigmentation (erythema abigne) may be seen with repeated
heat applications or infrared radiation to relieve the pain. Primary
biliary cirrhosis, hemochromatosis, and malabsorption syndromes
may be associated with generalized pigmentation.
(a) Bruising in the flanks may be seen in acute hemorrhagic pancre-
atitis (Gray Turner’s sign). If similar bruising is present around the
umbilicus, it is termed Cullen’s sign (Figure30). Bruising may also
be seen in chronic liver disease.
Figure 30 Bruising around the umbilicus in acute hemorrhagic

pancreatitis is called Cullen’s sign (similar bruising in the flanks is
called Gray Turner’s sign)
(b) Rose spots are small (pin head size), red blanchable spots
(Figure 31), found sparsely on the abdomen or back, in typhoid
fever. In paratyphoid fever, they are larger in size and greater in
number.
(c) Linea nigra is a brown-black-pigmented streak between umbili-
cus and symphysis pubis, seen in pregnancy, especially in multip-
arous women.
Figure 31 Typical rose spots are seen as pink-red spots on the
abdomen as shown
5. Striae
They are whitish-pink or brown marks due to rupture of elastic fibers
in the skin and are seen when there has been excessive stretching
of the skin (Figure 32). In Cushing’s syndrome, striae are typically
red-purple and predominantly on the abdomen and thighs.
Figure 32 Striae due to stretching in a patient history of gross ascites
Causes of Striae
1. Pregnancy. 3. Cushing’s syndrome.
2. Gross ascites. 4. Gross obesity.
6. Prominent Veins
Prominent veins on the abdomen are most commonly seen in portal
hypertension (Figure 33). Standing makes the veins more prominent
due to the effect of gravity. Emptying the vein with the fingers and
releasing one side at a time may determine the direction of flow, by
Figure 33 Dilated veins on the abdomen
noting the time taken to refill. The flow is in the direction that takes
less time to refill. Normal venous drainage is from the umbilicus
toward each quadrant, that is, centrifugally.
Causes of Prominent Veins

1. Portal obstruction in cirrhosis of the liver is associated with normal blood flow.
Rarely, a periumblical swelling with dilated veins (caput medusa) is seen.
2. In inferior vena-caval obstruction, the blood flow of the dilated veins is
upward toward the thorax.
3. In superior vena-caval obstruction, blood flow of dilated veins is toward the
groin.
7. Visible Peristalsis
A wave of contraction moving along the long axis of the gut may be
seen in obstruction, in an attempt to overcome it.
Visible Peristalses
1. Thin abdominal musculature, for example, elderly.
2. Pyloric obstruction.
3. Intestinal obstruction (for example, carcinoma).
1. Waves across the upper abdomen from left to right are seen in
pyloric stenosis.
2. Visible peristalsis in the central abdomen may be seen with
ileocaecal obstruction.
3. Visible colonic peristalsis travel form proximal colon to the site
of obstruction.
8. Pubic Hair
Normally, the upper border of the pubic hair is convex in males
and concave in females. A change in pattern in females may occur
Figure 34 Loss of pubic hair in hypopituitrism and hypogonadism
in ovarian and adrenal tumors. Similarly, sparse hair, or at times, a

change in pattern in a male may be seen with cirrhosis, hypopituita-
rism, and hypogonadism (Figure 34).
9. Umbilicus
Normal umbilicus is inverted and located centrally, somewhat nearer
to pubic symphysis, than the xiphi-sternum. An everted and trans-
verse slit “smiling” umbilicus is seen in abdominal distension from
any cause, but most commonly with a large ascites. An umbilicus
that has shifted upward, with a longitudinal slit, is seen in large
ovarian cyst or tumors.
10. Hernial Orifices
Inspect the inguino-femoral regions in privacy. While standing, ask
the patient to cough, to look for hernias. Examine the area along the
recti muscles and umbilicus for hernia, which develop due to weak-
ness of the abdominal wall (for radiology, see Figure 74).
11. Scars and Tap Marks
Previous abdominal surgical procedures are recognized by a typical
scar. Occasionally, they are associated with fibrotic bands that may
Figure 35 A patient with gross ascites and bandaged after taping on
the left, and edema involving the testis and penis on the right
Common abdominal incisions
Kocher or subcostal
(cholicystectomy)
Median incision
Paramedian (left)
Loin (kidney)
Transverse
McBurney
Transverse
Pubic
Vertical groin
Figure 36 Common abdominal incisions
be responsible for intestinal obstruction. A history of operations,

like nephrectomy, may necessitate adjustment of the doses of cer-
tain drugs or splenectomy, (patient is predisposed to pneumococcal
and salmonella septicemia) may help in patient management. Tiny
needle puncture marks on the abdomen are evidence of attempted
paracentesis. Larger marks may be due to laparoscopic procedures
or surgical incisions. Incision scars may be the site of herniation,
abdominal pain, infection, fistula, and discharge. It is also important
to remember that operations on the gut may result in indigestion,
diarrhea, or malnutrition, and deficiency of vitamins.
Clinical Examination: Palpation

Initial Requirements
1. After appropriate greeting and introduction, briefly explain your

intention and take permission from the patient to perform the exam-
ination.
2. Stand on the right side of the patient. Some doctors prefer to sit on
a stool besides the patient so that the elbow and the hand lie hori-
zontally in one plane during examination. This helps to avoid poking
fingers in the abdomen.
3. Properly expose the patient according to the age, sex, and circum-
stances ideally from the mid-thorax to pubis and to the mid-thigh,
when necessary.
4. The patient lies symmetrically, in a supine and relaxed posture with

flexed knees (the legs may be kept straight as flexing the knees does
not relax the abdominal muscles). The urinary bladder should have
recently been emptied.
5. Ask the patient if there is any tenderness so that this area may be
palpated last.
6. The patient should first breathe normally and then deeply with open
mouth turned to the opposite side.
Scheme of Palpation
1. Start by placing a warm hand flat on abdomen. Initially perform a

superficial palpation to get a gross idea about any area of tenderness
or mass and to gain the patient’s confidence. At times, superficial
palpation provides more information.
2. Palpate the abdomen with gentle movements at the metacarpopha-
langeal joints while keeping the forearm horizontally at the level of
the patient’s abdomen.
3. Watch the expressions of the patient for any discomfort or pain
while palpating.
Types of Palpation
1. Superficial: Gently palpate the whole of abdomen with the palm of

the hand.
2. Deep: To elicit tenderness, rigidity, and to detect visceral enlargement
(liver, spleen kidneys, and so on).
3. Dipping: To palpate the abdominal viscera when there is gross ascites,
which makes the conventional palpation less informative. Laying the
right hand flat on the abdomen, abruptly flex the metacarpophalan-
geal joint to displace the fluid. This allows the underlying viscera or
mass to hit the finger pulps.
4. Bimanual: It is used to palpate the kidneys and minor splenic
enlargement seen in Figure 37 (see palpation of spleen and kidneys).
5. Double-handed: It may be used in very obese patients where both
hands are laid flat on the abdominal wall on top of each other
Figure 37 Bimanual palpation of the spleen is shown
Figure 38 Double-handed palpation
(Figure 38). Dipping movements are made at the metacarpopha-

langeal joint of the upper hand, while the lower hand is used for
palpation.
Whenever a viscera is palpated or a mass discovered, it is imperative to

describe the findings comprehensively and comment on:
Description of a Mass
Site. Mobility.
Size. Borders.
Consistency. Surface.
Tenderness. Pulsation.
Number. Bruit.
Normal abdomen is non-tender with a soft or firm consistency. If

tenderness is noted, its site, severity, and point of maximum intensity
should be determined. Associated guarding and rigidity are also noted. At
the end, learn to draw all your findings as a diagrammatic representation.
Location: A mass present in the abdominal wall becomes prominent
when the patient attempts to rise from a lying position against resistance.
LOCALIZATION OF DISEASE
Epigastrium: Diseases of
pancreas, small bowel and
stomach transverse colon
Left hypochondrium: Diseases

of spleen and splenic flexure
Right hypochondrium:
Diseases of liver, gall
bladder and colon
Lumber: Disease of kidney
and descending colon
Iliac fossa: Diseases of sigmoid

and descending colon
gynaecological problems
appendicitis on the left
Hypogastrium: Urinary bladder
Figure 39 Pain or mass felt in a particular area indicates a disease of

the organs listed
This is because the contracted muscles push it forward. If it is freely

mobile on top of the muscle, it lies above it, but if it is relatively fixed and
moves in the long direction of the muscle, it lies within the muscle belly.
On the other hand, an intra-abdominal mass would disappear by this
maneuver, as the tight abdominal muscles conceal it.
DIAGRAMATIC REPRESENTATION
OF FINDINGS ON EXAMINATION
Liver is 6cm. in MCL

firm, modular and
mildly tender
Spleen is 5cm. in MCL
firm, smooth and non-
tender. Notch is palpable
Ascities in flanks
(shifting dullness +)
Caput medusae
Abdominal hernia
Dilated vein with
upward direction of flow
Figure 40 Imaginary findings of a patient with cirrhosis of the liver

are shown
Rebound tenderness: It is a severe pain felt on sudden release of pressure

during deep palpation. This is due to inflammation of the underlying vis-
cera. Rigidity is an involuntary or reflex increase in tone of the abdominal
muscles. It is due to underlying inflammation. Localized inflammation
produces local rigidity, whereas a generalized board-like rigidity is present
in peritonitis. Guarding is a voluntary contraction of the muscles in antic-
ipation of a painful stimulus.
Acute abdomen refers to acute sudden and severe pain usually due to
an acute surgical emergency (medical causes have to be ruled out). It may
be central abdominal or in either of the four quadrants. More likely, it
is diffuse and accompanied with a toxic-looking patient, with fever and
vomiting. On examination, there is not only tenderness, which is maxi-
mum over the pathology (depending on its cause), but signs of peritonitis
are demonstrable with guarding, rigidity, and rebound tenderness. The
bowel sounds may be absent (initially in intestinal obstruction they may
be hyperactive). Abdominal visceral perforation and obstruction are seen
in Figure 52.
Signs of Acute Abdomen

Murphy’s sign Seen in acute cholecystitis (palpation in the RHC at the level of
mid-clavicular line produces severe pain and the patient is unable
to take a full inspiration).
Cullen’s sign Seen in acute hemorrhagic pancreatitis (bruising around the
umbilicus).
Grey Turner’s sign Seen in acute hemorrhagic pancreatitis (bruising in the flank).
Obturator sign Seen in acute appendicitis (with the patient supine and passively
flexed knee and hip, the examiner externally rotates the hip. This
produces severe pain).
Psoas sign Seen in acute appendicitis.
Rovsing’s sign Seen in acute appendicitis (patient feels pain at McBurney’s point
when left lower quadrant is pressed).
Dance’s sign Seen in intussuption (sausage-shaped mass around umbilicus and
flat right iliac fossa).
McBurney’s sign Seen in acute appendicitis (with patient supine and relaxed, deep
palpation at 2 inches above the right anterior superior iliac spine,
at a line joining it and the umbilicus). Tenderness indicates a
positive sign.
Valentino’s sign Seen with perforated duodenal ulcer. (pain in the right lower
quadrant with perforation via the retroperitoneum with fluid
collection in the right paracolic gutter and peritonitis).
Medical Causes Mimicking Acute Abdomen

Metabolic Diabetic ketoacidosis, Addisonian crisis, uremia, acute
intermittent porphyria, Mediterranean fever.
Toxic Lead poisoning, narcotic withdrawal.
Hematological Sickle cell crisis, acute leukemia.
Renal Pyelonephritis, nephrolithiasis, perinephric abscess.
(Continued)
Medical Causes Mimicking Acute Abdomen

Connective tissue disease SLE, polyarteritis nodosa, Henoch–Schonlein purpura.
Cardiopulmonary causes Acute MI, pericarditis, pulmonary embolism, pneumonia.
Misc Herpes zoster, acute rheumatic fever, tabes dorsalis.
Surgical Causes of Acute Abdomen (Surgery May Be Required)

Hepatobiliary Acute cholecystitis, biliary colic, large liver abscess, trauma.
disease.
Stomach Perforated peptic ulcer.
Pancreas Acute pancreatitis.
Intestine Acute appendicitis, volvulus, intussuption, bowel rupture from
any cause, acute intestinal ischemia, diverticulitis, strangulated
hernia, bowel obstruction, Meckel’s diverticulum, splenic
rupture, toxic megacolon.
Genitourinary Testicular torsion, ectopic pregnancy, ruptured ovarian cyst.
Renal Renal colic, nephrolithiasis, ureteric colic.
Such patients require urgent clinical evaluation by an experienced sur-

geon and rapid workup, including plain X-ray abdomen, serum amylase,
abdominal ultrasound, and CT scan of the abdomen. Unnecessary delay
in investigation should not defer the decision to laparotomy if indications
are clear.
Measurement: The abdominal girth is measured in centimeters, usu-
ally at the level of the umbilicus. This helps to evaluate the progression or
regression of the disease, like ascites and abdominal masses.
Liver
Surface anatomy: The upper border of the liver is along the fourth-right
intercostal space or fifth rib in the mid-clavicular line, seventh rib in ante-
rior axillary line, and ninth rib in posterior axillary line. An oblique line
joining the ninth right and eighth left costal cartilage normally forms the
lower border.
Palpation
Start to palpate after the prerequisites have been met. Initially, assess the
gross enlargement of liver by superficial palpation. Then, palpate upward
from the right iliac fossa or below the suspected lower margin of liver,
lateral to the edge of right rectus muscle. The right palm is laid flat (to
avoid poking fingers) on abdomen so that the fingers lie parallel to the
edge of the liver, while the thumb is kept abducted (Figure 41). This may
best be achieved by keeping the forearm at the same level as the abdomen,
by bending over or sitting on a bedside stool. Coordinate the palpation
with the cycle of respiration (applying pressure during expiration and par-
tially releasing during inspiration).
The Correct Method of Palpation of the Liver
Figure 41 Palpation of liver is being demonstrated

1. Palpate with right hand from the RIF to the RHC.
2. Keep away from the lateral border of rectus.
3. Use the left hand to press on the lower ribs in the RHC if the liver lies close to the
costal margin.
4. Use the flat of the hand (do not poke your fingers).
5. Firmly press down and upward at the beginning of expiration when the abdomen is
maximally relaxed while looking at the patient’s facial expressions.
6. During each expiration, also advance the hand forward to meet the edge of the liver.
7. As the patient inspires, partially release the downward pressure, so that, as the liver is
pushed down, it slides past the palpating forefinger.
8. Kneading and uncoordinated movement is uncomfortable for the patient.
Note the following points
1. Span or size of the normal liver, as measured at the level of the

mid-clavicular line, is usually 8–15 cm. The upper border is marked
by dullness found on heavy percussion normally in the fourth inter-
costal space.
2. Tenderness: Note the site and severity (this is best seen in liver abscess,
viral hepatitis, and in congestive cardiac failure).
3. Consistency: The liver may be soft (normal), firm (most diseases), or
hard (in malignancy).
4. Edge and border may be sharp and smooth (normal) or ill-defined
and irregular (cirrhosis or malignancy).
5. Shape: It is best to draw the shape, to present your findings. Rediel’s
lobe, a tongue-shaped extension, may be palpable in the anterior
axillary line.
6. Surface may be smooth and soft with fatty liver or infections; hard
and irregular with metastasis, or nodular in post-necrotic cirrhosis.
7. Bruit may be heard in hepatoma or other vascular tumors.
8. Mobility: The liver is normally freely mobile, but may be fixed in
advanced malignancies.
9. Pulsations may be felt in the liver with each systole in tricuspid regur-
gitation.
10. Overlying skin may show a puncture mark of a pervious biopsy, swell-
ing in case of tumor, or erythema due to heat application for the
relieve of pain.
Palpate the rest of the liver in a similar fashion from below upward.
Mark the outline of the palpable liver and measure its enlargement in
centimeters vertically from the costal margin in the right mid-clavicular
line. Irregular enlargements should always be drawn and represented dia-
grammatically. The normal span in the mid-clavicular line is 12–15cm, in
anterior axillary line, 15–19cm, and in posterior axillary line, 19–24cm.
At the end, always try to identify the abnormality in relation to the
possible etiology and determine its complications. Therefore, in relation
to gastroenterology, look for and identify signs of liver cell failure, portal
hypertension, autoimmune manifestation, congestive cardiac failure,
biliary cirrhosis, and so on.
Applied Medicine
Tenderness of the liver is related to the stretch of the capsule which is the
most pain sensitive. Any sudden enlargement may cause the liver to be
tender. Most common causes are given as follows.
Causes of Enlarged and Tender Liver

1. Liver abscess (pyogenic or amoebic).
2. A congested liver in right heart failure, for example, due to cor pulmonale and
advanced mitral valve disease.
3. Acute viral hepatitis.
4. Any sudden enlargement of the liver produces pain due to stretching of its capsule.
Causes of Hepatomegaly
(IMPORTANT CAUSES ARE GIVEN IN ITALICS)
INFECTIONS:
Viral: Hepatitis, infectious mononucleosis, cytomegalovirus and Epstien Barr infection.
Bacterial: Typhoid, brucellosis, TB, and liver abscess.
Spirochetal: Weil’s disease, syphilis, and relapsing fever.
Parasitic: Schistosomiasis, hydatid cyst.
Protozoal: Malaria, amoebic liver abscess, and Kala-azar.
Fungal: Actinomycosis and histoplasmosis.
CONGESTIVE CAUSES:
Congestive cardiac failure, tricuspid valve disease, and constrictive pericarditis.
DEGENERATIVE CAUSES:
Fatty liver (Diabetes) and cirrhosis of liver (especially infiltrative disorders).
TOXIC CAUSES:
Testosterone tetracycline, sulphonamides, arsenic, phosphorus, chlorpromazine,
CCl4, and MAO inhibitors.
TUMORS:
Hepatoma, cholangioma, hemangioma, and sarcoma.
BILIARY OBSTRUCTION:
Gallstones, stricture common bile duct, and carcinoma head of pancreas.
BLOOD AND LYMPHORETICULAR DISEASES:
Leukemia, lymphomas, and Hodgkin’s disease.
STORAGE DISORDERS:
Hemochromatosis, amyloidosis, and glycogen storage disease.
CONGENITAL CAUSES:
Reidel’s lobe.
MISCELLANEOUS CAUSES:
Sarcoidosis, multiple myeloma, and hemolytic anemia.
Cirrhosis of the liver is a common disorder (usually post-necrotic from

viral hepatitis) in which the liver initially enlarges, but later may shrink
due to progressive fibrosis. Identify the cause by the history and associ-
ated signs that may be present. At times, special investigations may be
necessary.
Causes of Cirrhosis
1. Infections.
Viral hepatitis C.
Viral hepatitis B.
Schistosomiasis.
2. Metabolic and genetic.
Wilson’s disease.
Hemochromatosis.
Alpha 1 antitrypsin deficiency.
Cystic fibrosis.
3. Toxic and drugs.
NAFLD.
Alcoholic fatty liver disease.
Drug-induced like methotrexate, amiodrone, and alpha methyldopa.
4. Biliary disease.
Primary biliary cholangitis (formerly primary biliary cirrhosis).
Secondary biliary cirrhosis.
Primary sclerosing cholangitis.
5. Autoimmune.
Autoimmune hepatitis.
6. Unknown cause like cryptogenic cirrhosis.
7. Vascular.
Cardiac cirrhosis.
Budd–Chiari syndrome.
Veno-occlusive disease.
8. Granulomatous disease like sarcoidosis.
In cirrhosis of the liver, one should look for signs of liver cell failure and
signs of portal hypertension (Figure 42). There may rarely be some signs
to suggest the underlying cause of cirrhosis (Figure 42). It is important to
note that signs of liver cell failure may not be present in all cases of cirrhosis
and may even be absent in some advanced cases. Patients inevitably develop
portal hypertension, which is associated with ascites, splenomegaly, and
esophageal varices (also see pages 10, 22, 87, 110 and 129 in Volume II).
Absence of these signs should prompt one to look for alternate cause.
Types of Cirrhosis
1. Micronodular (<3mm). that is, alcoholic cirrhosis.
2. Macronodular (>3mm). that is, post-necrotic cirrhosis.
3. Mixed.
4. Compensated. Either no varices and ascites or only varices.
5. Decompensated. Ascites with or without varices or bleeding with or
without ascites.
FINDINGS ON EXAMINATION IN
CIRRHOSIS OF THE LIVER
Signs of liver Signs of portal
cell failure hypertension
Encephalopathy Esophagial varices
Jaundice Portal gastropathy
Fetor hepaticus Shrunken liver or
Gynaecomastia Hepatomegaly
Spider angioma Splenomegaly
Bruising Caput medusae
Astirixis
White nails Ascities
Clubbing
Transversly
Deputran slit umblicus
contracture
Palmer erythema Dilated veins
Testicular atrophy on abdomen
Decrease hair and rarely piles
Look for cause of cirrhosis
KF ring in Wilson disease
Pigmentation in hemochromatosis
Emphysema in alpha-1 AT deficiency
Signs of heart failure in cardiac cirrhosis
Parotid swellin and duputyren contracture in alcoholic cirrhosis
Diarrhea and xanthlesma in biliary cirrhosis
Figure 42 Signs of decompensated cirrhosis
Figure 43 Spider angioma (left) predominantly seen in the drainage

area of superior vena cava. Palmer erythema (right) in cirrhosis of
liver is most prominent over the hypothenar surface and may also be
present on the sole (planter erythema)
Clinically, it is important to determine whether the patient with

cirrhosis is decompensated or not. The criteria are given as follows.
Parameters of Decompensated Cirrhosis

1. Ascites (usually gross).
2. Hypoalbuminemia.
3. Prolonged prothrombin time.
4. Low platelet count.
5. Encephalopathy.
6. Varices or GI bleeding (portal gastropathy).
A patient with cirrhosis, during the course of illness, may be faced

with any of the complications given as follows.
Complications of Cirrhosis of the Liver

1. Hepatic encephalopathy. 7. Hepatopulmonary syndrome.
2. Esophageal varices. 8. Hyponatremia.
3. Ascites and spontaneous bacterial 9. Hypokalemia.
peritonitis.
4. Coagulopathy. 10. Hypoglycemia.
5. Hepatocellular carcinoma. 11. Malnutrition.
6. Hepatorenal syndrome.
Patients with cirrhosis may be classified according to the Child–

Turcotte–Pugh scoring into three classes according to severity of the dis-
ease. Class A is mild and well-compensated disease, class B is moderate
disease with a functional compromise, and class C is severe disease with
decompensation.
Child–Turcotte–Pugh Classification of Severity of Cirrhosis

Points 1 2 3
Encephalopathy None Mild to moderate severe (grade 3–4)
(grade 1–2)
Ascites None Mild-moderate severe (diuretic responsive)
(diuretic refractory)
Albumin g% >3.5 2.8 to 3.5 <2.8
Bilirubin mg% <2 2 to 3 >3
INR <1.7 1.7 to 2.3 <2.3
Class A = 5 to 6 points having least severe liver disease.
Class B = 7 to 9 points having moderately severe liver disease.
Class C = 10 to 15 points having severe liver disease.
Another scoring system is used in cirrhotic patients, which can give an

estimated three-month mortality in hospitalized and outpatient cirrhotic
patients. It is based on values of creatinine, bilirubin, and INR. Some
calculators also use serum sodium.
Model for End-Stage Liver Disease (Meld): Score

MELD = 10 ¥ {0.957 ¥ log e (creatinine) + log e (bilirubin) + 1.12 ¥ log e (INR)} + 6.43
3-month mortality according to MELD score
MELD score <9 10–19 20–29 30–39 >40
Hospitalized patients 4% 27% 76% 83% 100%

Outpatient cirrhotic 2% 6% 60%
If patient has been dialyzed in last one week, a creatinine of 4 is taken as standard
Any value <1 is taken as 1.
Cirrhosis and Mortality

1. No varices 1%
2. Varices 3%
3. Ascites 20%
4. GI bleeding 54%
5. Renal failure or infection 67%
Investigation in a case of cirrhosis includes complete blood count,

kidney functions and electrolytes, liver function tests, INR, urinalysis,
X-ray chest, ECG, ascitic fluid analysis, abdominal ultrasound, fibroscan,
CT abdomen (see Figure 76 in Volume II) with contrast, MRI with con-
trast (see Figure 78 in Volume II), alpha-fetoprotein, upper GI endoscopy.
Tests to look for the cause of cirrhosis may be required if the hepatitis
profile is negative. In endemic areas, schistosomiasis remains an import-
ant cause. Others causes like alcohol, drugs, biliary disease, heart fail-
ure, and hemochromotosis may occasionally be responsible. In younger
patients with cirrhosis, one should look for alpha 1 antitrypsin deficiency,
causes of congenital cirrhosis, Wilson’s disease, autoimmune hepatitis,
and so on.
Figure 44 Esophageal varices demonstrated in a barium swallow. On

the right, Caput Medusae (the periumblical swelling = head and the
surrounding dilated veins = snakes on the head of the Greek goddess)
Portal hypertension: The most common cause is cirrhosis of the liver

(90 percent of cirrhotics develop varices in their life time, (see Figures 44
and 87 in Volume II), but there are other causes of portal hypertension,
and a detailed history includes:
• History of jaundice (post-necrotic).

• History of blood transfusions, IV drug use (VHB and C).
• Pruritus (primary biliary cirrhosis).
• Family history of hereditary liver disease (hemochromatosis,
Wilson).
• History of alcohol abuse.
• History of portal pyemia or thrombotic tendency (Budd
Chiari).
• Travel abroad, for example, Middle East (schistosomiasis).
• History of lymphadenopathy, weight loss (lymphoreticular
diseases).
• History of fever, evening sweats, and contact with TB.
• History of drug and Vitamin A (may be associated with
CLD).
• History of right heart disease (cardiac cirrhosis).
Cirrhosis of the liver produces intrahepatic sinusoidal type of portal

hypertension. Portal hypertension may be classified as follows.
Classification of Portal Hypertension

1. Prehepatic Portal or splenic vein thrombosis
2. Intrahepatic Presinusoidal Schistosomiasis
Sinusoidal Cirrhosis
Postsinusoidal Veno-occlusive disease
3. Post-hepatic Hepatic vein thrombosis
Constrictive pericarditis
• Portal hypertension is said to be present when the hepatic

venous pressure gradient is more than 5mmHg. Patients with
gradient more than 12mmHg are likely to bleed.
• Portal hypertension is due to increased portal blood flow

due to dynamic splanchnic and systemic circulation. There is
mechanical obstruction to the outflow from the liver cirrhosis,
impaired production of nitric oxide causing increased vascular
resistance and sodium and water retention.
• The size of the varices correlated with the amount of portal
hypertension, and when the pressure hepatic venous pressure
gradient is >12mmHg, the risk of rupture increases. Once
present, they enlarge by 4 to 10 percent per year.
• About 30 percent of all patients with varices bleed per year.
The risk increases with advanced liver disease and rising wedge
hepatic venous pressure and hepatic venous pressure gradient.
• Risk of bleeding increases when red streaks (also called cherry
red sign or wale sign) are present on the variceal wall, with
larger size of the varices and with advanced cirrhosis, that
is, on Child classification C, presence of tense ascites, or
thrombocytopenia.
• The mortality with the first variceal bleed may reach 5
to 50 percent, and most of them die before reaching the
hospital.
• About 80 percent of patients rebleed within two years with
the maximum chance being early (within hours to days).
• About 20 percent of the cases with portal hypertension also
have gastric varices, which may reach almost 100 percent
when large esophageal varices are also present.
• Beta-blockers (nonselective) are used to reduce the portal
pressure and prevent bleeding.
• Variceal bleeding ceases spontaneously in as many as
40 percent of patients.
• Each episode of variceal bleeding is associated with a
30 percent mortality rate.
• Rebleeding occurs in 40 percent of patients within six weeks.
• Blood should be replaced in variceal bleed to a target of HCT
of 25 to 30 percent.
• The use of prophylactic antibiotics in variceal bleeding has

been demonstrated to decrease the rate of bacterial infections
and increase survival rates.
• Variceal hemorrhage has a two-year recurrence rate of approx-
imately 80 percent.
• Treatment includes stabilization, endoscopic ligation or
sclerotherapy, or endo-loop and splanchnic vasoconstrictors
like terlipressin or octreotide and TIPSS.
• Surgical options for varices include balloon tamponade while
one is waiting for emergency surgery. Decompressive shunts
include the distal splenorenal shunt (this is considered the
best option as encephalopathy occurs in only 10 to 15 percent
of patients), devascularization procedures like esophageal
stapling, and lastly, liver transplantation.
Hepatic encephalopathy is one of the most common complications of

advanced cirrhosis. It is clinically recognized by an alternation in the level
of alertness progressing to confusion, disorientation, restlessness, drows-
iness, and coma. In early stage, the patient may be unable to neatly draw
simple drawings on paper due to lack of concentration and false neuro-
transmission. This untidy drawing of a star or square is called construc-
tion apraxia. Its documentation helps help judge the progress of disease
as treatment is given.
Hepatic Encephalopathy: Stages

Neurological
Consciousness Behavior/intellect findings
Stage 0 Normal Normal Normal
Stage 1 Mild lack of Short attention span impaired Mild asterixis

awareness adding and subtraction
Stage 2 Lethargy Abnormal behavior disorientation Definite asterixis

and slurred speech
Stage 3 Somnolence Marked confusion gross Stupor, rigidity

disorientation Hyperreflexia
Stage 4 Coma Coma Decerebrate posture

The three most common causes of encephalopathy are infection, GI

bleeding, and renal involvement (that is, azotemia). In all cases, exclude
the precipitating causes.
Precipitating Causes of Hepatic Encephalopathy

1. Infections.
2. GI bleeding.
3. Azotemia and renal failure (dehydration and furosemide-induced).
4. Increase protein diet.
5. Drugs like sedatives, hypnotics, narcotics, and benzodiazepines.
6. Trauma, surgery, and stress.
7. Hypokalemia or hyponatremia.
8. Constipation.
9. Portosystemic shunting.
10. Development of hepatocellular carcinoma.
11. Acidosis.
12. Progressive liver disease.
13. Operative shunts and TIPS (transjujular intrahepatic portosystemic shunt).
The cause of encephalopathy is accumulation of toxic chemicals

(ammonia, short chain fatty acids, mercaptans, benzodiazepines, aromatic
amino acids, octopamines, and manganese), nitric oxide production with
false neurotransmission (inhibitory), GABA receptors up regulation, and
brain edema. It is treated by removal of the underlying cause, if possible,
and giving lactulose with rifaximin, or recently, broad spectrum antibiotic
for five days and single fecal transplant.
Differential Diagnosis of Altered Mental State

1. Hypoglycemia. 9. Delirium tremens.
2. Severe sepsis. 10. Liver failure.
3. Uremia and acidosis. 11. Respiratory failure.
4. Cerebrovascular accidents. 12. Epilepsy.
5. Drugs, overdose and poisoning. 13. Psychiatric problems.
6. Alcohol. 14. Wernicke psychosis.
7. Hyponatremia and Hypokalemia. 15. Severe dehydration.
8. Post-surgical procedure (TIPS or surgical shunts for cirrhosis).
Ascites in cirrhosis develops in cirrhosis as the liver decompensates

(Figure 44) and the pathophysiological causes are given as follows.
Causes of Ascites in Cirrhosis

1. High portal pressure (back pressure or increase resistance to flow).
2. Nitric oxide over produced in the GI tract causes splanchnic vasodilatation and
increase in portal blood flow, while local deficiency in the liver, especially due to
oxidative stress increases intrahepatic resistance.
3. Low oncotic pressure (hypoalbuminemia).
4. Under fill (protein-rich peritoneal fluid via leakage form liver surface, pulls in water
via osmosis).
5. Over fill (increase portal pressure via reflex, causes sodium and water retention via
the kidneys).
6. Associated heart or renal disease.
A sudden worsening of ascites and abdominal distension in a patient

with chronic liver disease needs to be assessed and cause determined and
treated. Common precipitating causes are given as follows.
Sudden Worsening of Ascites in Cirrhosis

1. SBP. 6. Associated heart failure.
2. Hepatocellular carcinoma. 7. Associated renal failure.
3. GI bleeding. 8. Vascular thrombosis.
4. Dietary indiscretion. 9. Acute liver injury.
5. Non-compliance to medication. 10. Progression of disease.
Development of infection in chronic ascites, and especially in chronic

liver disease, needs to be excluded when the patient develops sudden
worsening of ascites, fever, and tenderness over the abdomen, and devel-
opment of encephalopathy. The diagnosis is dependent on ascites fluid
analysis.
Diagnosis of SBP (Spontaneous Bacterial Peritonitis)

1. Positive ascetic fluid bacterial culture.
2. Neutrophil count in fluid >250.
3. No evidence of known intra-abdominal or surgical source of infection.
Acute hepatitis is most commonly due to viruses like HAV, HBV,

HCV, HDV superinfection on top of HBV, HEV, HGV, and transfu-
sion-transmitted agent or other viruses like Epstein Barr virus, cytomega-
lovirus, and herpes simplex.
Common Causes of Acute Hepatitis

1. Viral hepatitis.
2. Alcoholic hepatitis.
3. Drug-associated hepatitis.
4. Autoimmune hepatitis.
5. Ischemic hepatitis.
6. Metabolic causes of hepatitis, for example, Wilson’s disease.
7. Toxic hepatitis.
8. Pregnancy-associated hepatitis (acute fatty liver of pregnancy).
9. Other infections, for example, leptospirosis, brucellosis, yellow fever, toxoplasma.
The infection can range from asymptomatic to mild clinical to severe

and fulminant or chronic from (chronic form especially with HBV and
HCV).
Diagnosis of Acute Viral Hepatitis

1. HAV anti HA-IgM (IgG is indicative of past exposure or protection).
2. HBV HBsAg, anti-HBcAb IgM, PCR for HBV. HBcAg may be detected in
the liver. If serology is positive, do HBeAg and anti-HBe for progno-
sis and guide to therapy.
3. HCV anti-HCV and PCR for HCV (quantitative and qualitative).
4. HDV anti-HDV and PCR for HDV.
5. HEV anti HEV IgM and IgG.
6. Other viruses EB virus, CM virus, yellow fever, toxoplasmosis (IgM antibody).
Common Clinical Characteristics of Viral Hepatitis

Viral hepatitis A (single-stranded RNA picornavirus).
1. It is transmitted by feco-oral route (contaminated food and water).
2. It usually resolves within eight weeks, but rarely may continue for six months. It
does not lead to chronicity or carrier state, but may cause fulminant hepatitis in 0.4
percent cases.
3. It is more commonly associated in adults with anorexia, malaise vomiting, fever, and
jaundice, with sometimes upper respiratory or GI symptoms. In children, it may be
asymptomatic.
4. In acute infection, IgM is positive and remains for about six months. IgG becomes
positive after three to six months and remains for life.
5. May occur in epidemics.
6. Incubation is short (two to three weeks). Patient is most infectious one to two weeks
before the onset of jaundice. Once jaundiced, the patient may not be infective.
(Continued)

7. Immunization is available for prevention and for high-risk patients. Immunoglobulins
are protective if given within two weeks post-contact or exposure.
Viral hepatitis B (DNA retrovirus).
1. Typical symptoms are anorexia, nausea, vomiting and jaundice. There may
occasionally be autoimmune features like arthritis, glomerulonephritis, and
rash. Extra-hepatic manifestations include serum sickness, essential mixed
cryoglobulinemia and polyartritis nodosa, popular acrodermatitis, aplastic anemia,
polyarteritis nodosa.
2. Incubation is long (one to five months). Hepatitis lasting greater than six months is
termed chronic. Recovery is associated with positive anti-HBe.
3. The spectrum of disease varies for asymptomatic, carrier state, acute hepatitis, acute
fulminant hepatitis, chronic hepatitis depending on the age (it develops in 90
percent in infants, 25 to 50 percent in children 1 to 5 years, and 5 to 10 percent of
adults). The virus can occur in three states, that is, acute infection, chronic infec-
tion, and carrier. Mutant strains can occur.
4. Fulminant hepatitis carries a poor prognosis, requiring liver transplantation.
5. At birth, the infants have a 70 to 90 percent risk of acquiring hepatitis B during
delivery from the infected mother, unless the baby is given hepatitis B immune
globulin (HBIG) and are vaccinated immediately after delivery.
6. It is parentally transmitted (injection (needle sharing), transfusion (especially in
the past), tattooing, sexual, and organ transplantation). Risk of transmission after
needle stick injury is 30 percent in an unvaccinated individual. The virus is present
in the blood, saliva, breast milk, semen, and body fluids of infected patients. The
role of insect bite in transmission is unclear.
7. It can lead to chronicity (cirrhosis occurs in 10 to 30 percent without treatment)
and fulminant hepatitis occurs in 0.1 to 0.5 percent. The rate of chronicity is 2 to
6 percent of immune-competent adults, 30 percent in children 1 to 5 years, and 90
percent in infants.
8. In acute infection, HBsAg and anti-HBc IgM are positive. HBeAg, HBV DNA,
and DNA polymerase appear soon after HBsAg and signify active viral replication.
HBsAg appears before the onset of symptoms becomes undetectable in three to six
months.
9. Immunization is available and the vaccine is protective for up to five years in 80 to
90 percent cases and up to 10 years in 60 to 80 percent cases. Vaccination should be
done at birth and again at six years age.
10. Post-exposure prophylaxis includes giving HBV immunoglobulins and first dose of
vaccine (at different sites) within two weeks of exposure.
Viral hepatitis C (single-stranded RNA flavivirus).
1. It is transmitted by parenteral route. Needle stick injuries may result in about 3 per-
cent risk of HCV transmission. It can be as high as 10 percent. HCV can survive for
more than one week in blood in syringes. Casual contact and kissing is not considered
high risk for transmission. Sexual transmission occurs at approximately 0.2–2 percent
per year of relationship. Transmission from mother to infant (vertical) is rare.
2. Incubation period is around seven to eight weeks. Mothers with HCV can breast-
feed the child if there is no local injury.
3. Many patients may be asymptomatic or present with anorexia, nausea, vomiting,
fever, and jaundice. Only 20 percent present with jaundice, while majority remain
asymptomatic.
4. Up to 20 percent patients with alcoholic liver disease may also have HCV. The
liver enzymes may show a yoyo pattern.
5. About one-third of the patient’s progress to cirrhosis and fulminant hepatitis occurs
in <1 percent.
6. About 15 to 30 percent of patients exposed to HCV recover spontaneously, while
the remaining 70 to 85 percent develop chronic infection. Many cases are diag-
nosed when chronic liver disease is already established (usually over decades).
7. Anti-HCV is usually positive (90 percent) three months after exposure, but may
remain negative for up to nine months (it is indicative of exposure and is not
protective). HCV RNA appears within days to weeks of inoculation. ALT rises six
to eight weeks and anti-HCV ELISA takes eight weeks.
8. There are at least six different genotypes prevalent in different countries. In the
United States, genotype I is present in over two-third of the cases.
9. The RNA-dependent RNA polymerase, an enzyme for HCV replication, lacks
proofreading ability, and thus generates a large number of mutants (quasispecies).
10. Patients who have not cleared the HCV infection within 12 weeks of infection may
be considered for therapy. The course, duration, and success of treatment depends
on the genotype. It is important to do qualitative PCR (determine to genotype of
virus) and quantitative PCR (determine the viral load) before starting the treat-
ment.
11. The rate of spontaneous clearance is higher at younger age, female patients, and in
CC genotype (50 percent).
12. Progression to cirrhosis occurs in about 20 to 30 percent of patients with chronic
infection over a period of about 20 years. In patients with alcohol intake, the
incidence of cirrhosis increases 15-fold, while with HIV co-infection, it is increased
five-fold.
13. Hepatocellular carcinoma can develop in patients who have progressed to cirrhosis
(average time 28 years). This is unlike HBV, where hepatocellular carcinoma can
develop in patients who do not have cirrhosis.
14. Newborn to HCV positive mothers should be tested with PCR after one–two
months and anti-HCV after 18 months. They should be vaccinated against VHA
and VHB. Risk of perinatal transmission is about 5 to 6 percent, but becomes
almost 20 percent with coexisting HIV infection. Vertical (mother to infant) spread
also occurs at a low rate (5 percent or less). It is 40 percent if also HIV positive.
Breastfeeding is allowed, but should be avoided with cracked nipples and bleeding.
15. Progression from chronic hepatitis to cirrhosis can take almost 20 years and another
10 years to develop hepatocellular carcinoma, or hepatocellular carcinoma develops
in 1 to 4 percent of patients with cirrhosis each year.
(Continued)

16. Incubation is intermediate.
17. The commonest hematological complication of HCV infection is mixed cryoglob-
ulinemia (MC), seen in 40 to 50 percent of patients. It is diagnosed by finding high
level of rheumatoid factor and low complement in the serum. In some subjects,
non-Hodgkin B cell lymphoma (B-NHL) may evolve. Thrombocytopenia is also
common. Other associations include membrano-proliferative glomerulonephritis,
porphyria cutanea tarda, non-Hodgkin lymphoma, lichen planus, Sicca syndrome,
corneal ulcer, and peripheral neuropathy. HCV is an independent predictor of
diabetes mellitus.
18. No immunization or vaccine available.
19. Timely treatment can lead to a cure (non-detectable HCV RNA at 24 weeks after
completed treatment = SVR or sustained viral response). Many new treatments
have recently been available.
20. Patients who have an SVR have a > 99 percent chance of remaining HCV RNA
negative and are typically considered cured. Nearly 95 percent of patients with an
SVR have improved histologic findings, including fibrosis and histologic activity
index; in addition, these patients are less likely to develop cirrhosis and liver failure
and to die of liver disease.
Viral hepatitis D (defective RNA virus or delta agent).
1. It is transmitted by parenteral route (blood or body fluids).
2. Incubation is long.
3. It occurs as coinfection with acute HBV or superinfection in chronic HBV.
4. It presents either as unusually severe coinfection with HBV or acute exacerbation or
aggressive course of chronic HBV infection.
5. Antibody is detectable only weeks after the acute infection.
6. It can lead to chronicity.
7. No immunization available.
Viral hepatitis E (RNA virus has four genotypes).
1. It is enterically transmitted (feco-oral). Types 1 and 2 are associated with waterborne
outbreaks, while type 3 and 4 are food borne and sporadic.
2. Clinical features are like HAV infection.
3. In pregnancy, the infection can lead to fulminant hepatitis resulting in mortality.
4. Incubation is short.
5. It does not lead to chronicity (except possible with type 3 in immunocompromised
patients).
6. No immunization available.
7. It can rarely lead to fulminant hepatitis in any patient.
Acute fulminant hepatitis or acute liver failure is said to be present

when there is rapid synthetic liver dysfunction with acute liver injury
(encephalopathy and coagulopathy), which develops within eight weeks

of the onset of symptoms in a patient with a previously healthy patients or
two weeks of developing jaundice in patients with underlying liver disease.
Causes of Acute Liver Failure or Fulminant Hepatitis Failure (FHF)

1. Acute viral hepatitis (A, B, C, D, or E).
2. Drugs, especially paracetamol or INH, valporate, halothane, IV tetracycline.
3. Pregnancy associated (acute fatty liver of pregnancy).
4. Reye’s syndrome.
5. Wilson’s disease.
6. Autoimmune hepatitis.
7. Budd–Chiari syndrome.
8. Leptospirosis.
9. Liver metastasis.
10. Shock and CCF.
11. Poison (amanita phalliodes).
12. Cryptogenic.
Referral to Specialized Center in FHF

1. Hepatic encephalopathy especially < one-week interval form jaundice to
encephalopathy.
2. High INR >3 or PT >50.
3. Metabolic acidosis.
4. Persistent hypotension.
5. Rising creatinine >300μmol/L.
Acute fatty liver disease of pregnancy (AFLP) is a rare obstetrical emer-

gency classically occurring during the third trimester. It is more common
in multigravida with male child, especially if preeclampsia also is present.
Mortality for mother is <10 percent with good management and prompt
delivery. However, the mortality for the fetus is double. Patients present
with abnormal LFT with high INR, encephalopathy, and ascites. The
Swansea criteria are used for the diagnosis. A liver biopsy may be required.
Liver abscess (see Figure 82 in Volume II) is associated with intense
local tenderness (patient may not allow examination of the area) and at
times, a right-sided (sympathetic) pleural effusion may be associated.
Especially in pyogenic abscess, the patient has high-grade fever and looks
toxic. Other common abscess, especially in endemic areas, are amoebic.

A very large abscess may produce a local swelling or bulge in the right
hypochondrium.
A liver mass discovered on clinical examination, but more commonly
on imaging is a source of confusion, and one needs to exclude malignancy
and look for treatable causes.
Benign liver lesions include:
• Hemangioma of the liver

• Focal nodular hyperplasia
• Hepatic adenoma
• Regenerative nodules
• Rarely inflammatory or pseudotumor (look for associated
systemic chronic disease)
Malignant liver lesions include:
• Hepatocellular carcinoma (see Figure 70, 75, 77, 78 in Volume II)

• Cholangiocarcinoma (see Figure 81 in Volume II)
• Metastatic disease (Figure 84 in Volume II)
Investigating a liver mass is not an uncommon situation. Patients may

be asymptomatic or present with pain or swelling in the right hypochon-
drium. There may be features of underlying disease like cirrhosis, or there
may be compressive symptoms like jaundice. A history of the risk factors
for hepatic malignancy may be obtained. Features of the primary lesions
may also be present if the liver lesions are secondaries. Depending on the
history, the following investigations will help define a definite cause
Investigation of Hepatic Mass

1. Abdominal ultrasound.
2. Triphasic CT of the abdomen.
3. MRI of the abdomen with gadolinium.
4. Alpha-fetoprotein level.
5. Intra-operative ultrasound (most sensitive for liver metastasis).
6. Contrast-enhanced ultrasound (95 percent specificity and sensitivity for
malignancy).
7. Fine needle biopsy or surgical excision.

8. Other tests include CBC, ESR, coagulation profile, LFT, hepatitis screen, kidney
functions, X-ray chest, tumor markers, ascetic tap analysis, including malignant cells
and AFB-PCR, endoscopy, cholangiography or MRCP, and septic screen where and
as indicated.
• In a patient with CLD with chronic viral hepatitis infection,

and a solid nodule with high alpha-fetoprotein, do a triphasic
CT scan and MRI (typically the lesion is hypervascular with
washout in the portal or venous phase. See Figure 70, 75, 77,
and 78 in Volume II).
• Do percutaneous biopsies, if diagnosis is not established, or is
uncertain after imaging, and there is expected an impact on
the management.
• Nodules on ultrasound <1cm are followed three to six
monthly, and if there is no growth over two years, follow
routine surveillance.
• For nodules 1–2cm with cirrhosis, do CT scan, contrast
ultrasound, or MRI with contrast. If typical for hepatocellular
carcinoma, treatment is started.
• If after imaging, they are not typical, do a biopsy.
• If nodule is >2cm, with typical HCC on dynamic imaging,
biopsy is not necessary.
• If alpha-fetoprotein is >200ng/mL, biopsy is also not
required; otherwise, biopsy to confirm the diagnosis.
• If biopsies (by expert pathologists) are negative for HCC,
follow-up by ultrasound or CT scan at three to six months
until the nodule either disappears, enlarges, or displays
diagnostic characteristics of HCC.
• If the lesion enlarges but remains atypical for HCC, a repeat
biopsy is recommended.
• Imaging for HCC.
• Ultrasound shows solid, hypoechoic, isodense, rather than
hyperdense lesion (sensitivity 50 percent and specificity
97 percent). Presence of vascular invasion may be seen.
• Helical CT has a sensitivity of 70 percent and specificity of
93 percent). It can detect hyper vascular HCCs of 3mm size.
• MRI shows a high-intensity T2 and low-intensity T1. It is

better than a CT or ultrasound examination and can differen-
tiate dysplastic nodules and hemangiomas.
• Angiography is now done as a triphasic MRA with arterial,
portal or venous, and late venous phase.
• PET scan is best, especially to detect metastasis.
Liver hemangiomas are common benign lesions usually found

incidentally at any age and more common in females. Blood flow can
be demonstrated within the mass on Doppler, and CT scan shows a
hypodense well-demarcated mass, which are enhancing lesions with a
dynamic pattern (intense enhancement in arterial phase which is main-
tained in the portovenous phase) with contrast.
Focal nodular hyperplasia is usually an incidental finding on imag-
ing, especially in young women. It is a benign liver tumor arising from
hyperplastic response to anomalous arterial supply. Blood flow can be
demonstrated in the anomalous artery. Technetium-99 sulfur colloid scan
typically shows uptake in the mass similar to the rest of the liver. In a
triphasic CT scan, a feeding artery may be seen in the hyper-intense mass.
Delayed phase shows hypo-intense area.
Hepatic adenoma is a benign epithelial liver tumor usually seen in
premenopausal women taking oral contraceptives for some years. Patients
do not have underlying cirrhosis. There is a risk of bleeding in the tumor
or in the peritoneal cavity, which is accompanied by acute pain. On ultra-
sound, they are often large, hyperechoic with central hypoechoic area if
there is associated hemorrhage. Doppler may show venous flow. They are
found mostly in the right lobe of liver. Alpha-fetoprotein is normal. Lipid
content of the tumor is high, and this may be detected on the MRI.
Hepatocellular carcinoma (HCC See Figure 70, 75, 77, and 78 in
Volume II) may be primary, or secondary to cirrhosis (especially viral
hepatitis B or C or cirrhosis of any cause) or hepatotoxic drugs and tox-
ins. It is more common in patients with hemochromatosis. Incidence of
HCC exceeds 0.2 percent per year in patients with chronic HBV and 1.5
percent per year in patients with cirrhosis due to other causes. Alpha-fe-
toprotein is frequently very high.
Clinically, HCC may be asymptomatic, only having features of the

underlying disease or commonly presents with features of hepatic decom-
pensation in a patient with known cirrhosis (worsening ascites, encepha-
lopathy, jaundice, or bleeding). Weight loss, early satiety, pain in the right
hypochondrium, and mass in the right hypochondrium may be present.
With advanced disease obstructive jaundice, diarrhea, bone pain, or
dyspnea may develop. On examination, besides features of chronic liver
disease, there is usually hepatomegaly, splenomegaly, ascites, jaundice,
and occasionally, a hepatic bruit may be heard. Extrahepatic spread at the
time of diagnosis or disease recurrence is found in 10 and 20 percent. The
most common sites are lung, intra-abdominal lymph nodes, bone, and
adrenal gland. Brain metastases are extremely rare.
Intraperitoneal bleeding due to tumor rupture is associated with
sudden and severe abdominal pain and distension with an acute drop
in the hematocrit and hypotension. Fever may develop in association
with central tumor necrosis. A host of paraneoplastic syndromes, for
example, Precocious puberty, pseudo hypoparathyroidism, gynecomastia
and hypertrophic osteoarthropathy. Alpha-fetoproteins, aberrant alka-
line phosphatase, gamma-globulins, heptoglobulins, alpha-1 antitrypsin,
ceruloplasmin, gonadotrophins, and somatotrophins may be produced.
Primary biliary cirrhosis predominantly occurs in females, where itch-
ing and fatigue precedes all symptoms by many years. There is rising jaun-
dice in late stages (cholestatic picture with disproportionally increased
alkaline phosphatase) and features of malabsorption. There may be right
hypochondrial discomfort. Sometimes, features of Sicca syndrome are
associated. Lipid deposits (xanthelasmas and xanthomas) may be seen on
the skin with hyperpigmentation, and scratch marks from itching, and
hepatomegaly on examination. Anti-mitochondrial antibodies are fre-
quently positive (in 95 percent cases) with raised IgM levels.
Primary sclerosing cholangitis is a rare progressive sclerosing and
obstructive disease of extrahepatic or intrahepatic ducts or both. The alka-
line phosphatase is high. The patient may be asymptomatic at diagnosis,
and later develop chronic biliary obstruction, pruritus, right hypochon-
drial pain, and jaundice, with sometimes features of acute cholangitis.
Primary biliary cirrhosis remains a close differential diagnosis. There is an
association with inflammatory bowel disease. Diagnosis is established by

MRCP and ERCP, which show multifocal strictures of intrahepatic and
extrahepatic bile ducts. These patients are at increased risk of developing
cholangiocarcinoma.
Metastasis to the liver has to be differentiated from primary liver
tumors, and a search for the primary is necessary (see Figure 84). An
underlying primary malignancy may be suspected from a detailed his-
tory, examination, and laboratory tests (usually tumor markers and
imaging studies). A pan-CT scan with contrast is usually the first test
to localize the disease. MRI may give more detail in problem cases, and
indicate hepatic vascular invasion, but is more expensive, and nephro-
genic systemic fibrosis is an uncommon side effect. FDG positron emis-
sion tomography (PET) is the most sensitive test for the diagnosis of
liver metastases, but not readily available. Selective hepatic angiography
can demonstrate tumor blush and potential for treatment with tumor
embolization. Clinically, the patient may have features of the underly-
ing malignancy along with hepatomegaly, discomfort or pain in the right
hypochondrium, jaundice from obstruction of the biliary passages, and
abnormal liver function tests. Alpha-fetoprotein is normal with metastatic
disease of the liver, while 5’-nucleotidase may be elevated. An intraopera-
tive US (IOUS) of the liver has sensitivity of 96 percent for the detection
of focal liver lesions, while an ultrasound of the abdomen is 84 percent
sensitive. Contrast ultrasound improves the accuracy. At the end, a tissue
diagnosis is necessary; therefore, a biopsy becomes necessary especially
if the primary is not found. Exclude a hydatid cyst by an indirect hem-
agglutination test where necessary, especially in endemic areas. Atypical
hemangiomas and focal nodular hyperplasia may at times be difficult to
differentiate from metastatic disease.
Autoimmune hepatitis may present with non-specific features like
fatigue (present in more than two-third patients), hepatitis picture,
right hypochondrial pain or discomfort, and hepatomegaly with signs
of chronic liver disease or abnormal liver function tests in young adults.
Features of autoimmune disease may be present. There is an association
with primary biliary cirrhosis and sclerosing cholangitis. It may also be
associated with ANCA and hypergammaglobulinemia, especially IgG.
Diagnosis of Autoimmune Hepatitis (AIH)

1. ANA anti-nuclear antibody titer > 1:80 Type I AIH
2. ASMA anti-smooth muscle antibody (actin) Type I AIH
3. Anti SLA soluble liver antigen Type I AIH
4. Anti LKM liver, kidney, and microsomal antibody Type II AIH
These patients may respond to a course of steroids when other diagno-

sis have been excluded (viral hepatitis, drug toxicity, alcohol liver disease,
metabolic liver disease [Wilson’s, hemachromatosis, alpha-1 anti-trypsin
deficiency], primary sclerosing cholangitis, primary biliary cirrhosis, and
so on).
NAFLD (nonalcoholic fatty liver disease) is especially seen in dia-
betics and patients with metabolic syndrome. LFTs are abnormal (ALT
is > AST) and ultrasound and CT scan show fatty infiltration. Other
causes need to be excluded. It may be confirmed by biopsy. It can lead
to cirrhosis in about 1 percent of cases, and hepatocellular carcinoma in
<5 percent cases. All feature of the metabolic syndrome are risk factors
(DM, HTN, obesity, hyperlipidemia). Also see more information on
page 107, Volume II.
In alcoholic liver disease, there is a definite history of excessive alco-
hol intake or abuse with hepatitis causing AST/ALT ratio to be greater
than 2, with both being less than 500IU and MCV greater than 100.
Most patients remain asymptomatic until advanced liver disease has
developed. Most, if not all, heavy drinkers develop hepatic steatosis, of
which about 10 to 35 percent develop alcoholic hepatitis, and about 8
to 20 percent will develop cirrhosis. Patients with alcoholic liver dis-
ease (ALD), like patients with chronic viral hepatitis C infection, are at
higher risk of developing hepatocellular carcinoma. In ALD patients,
there is increased susceptibility to liver damage by acetaminophen
and iron over load. Also see NASH (nonalcoholic steatohepatitis) on
page 79, Volume II.
Hepatorenal syndrome is a consequence of a deranged hemodynamic
balance due to excessive vasodilation and hypotension (especially nitric
oxide-induced) causing kidney injury via compensatory vasoconstriction
in the kidney. It occurs in patients with advanced CLD and associated
with a low urine output and low urine sodium with maintained tubu-
lar function (i.e., ability to concentrate urine). Renal biopsy is normal.
Precipitating causes include overuse of diuretics, especially furosemide,
NSAIDS, infections, and volume loss.
Wilson’s disease may present in families and is suspected in younger
subjects with clinical features of cirrhosis and extrapyramidal symptoms.
Serum ceruloplasmin is reduced, liver biopsy shows increased copper, and
Kayser–Fleischer ring (Figure 20) may be seen on slit lamp examination.
Alpha-1 antitrypsin deficiency may also be associated with liver dis-
ease (cirrhosis) and lung disease (emphysema). It is a genetic disorder;
therefore, a family history may be available and patients have very low
levels of AAT and phenotyping. It is of variable severity, and smokers are
affected more with lung disease. It may be associated with a host of other
diseases. Many patients may be misdiagnosed as having COPD. There-
fore, do alpha-1 antitrypsin levels in those patients who have irreversible
airflow obstruction, abnormal LFTs or features of cirrhosis or necrotizing
panniculitis.
Congestive hepatomegaly and cardiac cirrhosis are suspected when
other causes are excluded and patient has advanced heart failure, espe-
cially right-sided. LFTs are abnormal, and in late cases, clinical features of
cirrhosis may be present with an enlarged and tender liver.
Hereditary hemochromatosis is an autosomal recessive disorder in
which the genetic defect leads to increased iron absorption, and even-
tual iron overload and target organ damage. The liver, pancreas, heart,
and pituitary may be involved. Most patients remain asymptomatic till
late in life, when features of target organ insufficiency begin to develop.
Arthopathy may be an early feature, with hands, wrist, shoulder, knees,
and ankles being involved. The involvement mimics pseudogout. The
skin may be pigmented brown as a late feature, and pancreatic involve-
ment may lead to diabetes (the name bronze diabetes is given to this
combination). Liver damage may lead to cirrhosis with an enlarged liver
(traditionally, in most cases, the liver is shrunken). The risk of hepa-
tocellular carcinoma, in patients who develop cirrhosis with hereditary
hemochromatosis, is 200 times that of the general population. Hypogo-
nadism and reduced libido is due to pituitary involvement. In women,
there may be amenorrhea. Osteoporosis and secondary hypothyroidism
may be present. Iron deposition in the cardiac muscles may lead to a

dilated cardiomyopathy. Iron study is done initially, with serum iron or
total iron-binding capacity if >45 percent in women, and >50 percent
in men, with serum ferritin if >200mcg/dL in women, >300mcg/dL in
men, is highly indicative of the disease, and in such cases, genetic testing
should be done.
Spleen
Surface Anatomy
The spleen weighs less than 1lb., is 3cm thick, 5cm. wide, and 7cm. long.
It lies between the 9th and 11th costal cartilage lateral to the vertebral
column.
Palpation
Superficial palpation gives an idea of the extent of enlargement, so that

one can begin deep palpation just below this level. The technique of exam-
ination (Figure 45) is the same, as described for palpation of the liver. The
right hand, in this case, is kept parallel to the line of the costal margin,
starting from the RIF toward the 9th left costal cartilage. If the spleen
is not palpable in the supine position, make the patient to roll over to
the right lateral position, with the left knee and hip flexed at right angle.
Figure 45 Palpation of spleen is shown

1. Palpate from the right iliac fossa.
2. Firmly press the lower ribs in the LHC if the spleen is not palpable,
to push it downward.
3. Use the right hand to palpate the spleen while coordinating with
respiration.
Palpate under the costal margin, while firm downward pressure is main-
tained on the lower lateral chest with the left hand, to bring the spleen out
to meet the palpating right hand.
The edge of the spleen is sharp and smooth with a notch palpable at
the lower outer edge. The organ enlarges toward the RIF, but occasionally,
it may only extend toward the LIF. As in the case of hepatomegaly, com-
pletely describe the enlargement and measure it in centimeters perpendic-
ular to the line of the costal cartilage in the mid-clavicular line.
Applied Medicine
Splenomegaly may be classified according to the size of the spleen.
CAUSES OF SPLENOMEGALY
Minor splenomegaly
Malaria, typhoid, SBE
and early cirrhosis
Moderate splenomegaly
Cirrhosis and any other cause
Very large spleen

Chronic myeloid leukemia
Myelofibrosis
Chronic malaria
Cirrhosis
Kala-azar
Figure 46 Causes of different degrees of splenomegaly are shown
Causes of Splenomegaly
Acute Infections
Malaria, typhoid and infectious mononucleosis.
Chronic Infections
Tuberculosis, bacterial endocarditis and brucellosis.
Parasitic Infections
Hydatid disease.
Congestive Causes
Cirrhosis and chronic mitral stenosis.
Hemolytic Causes
Hereditary spherocytosis, thalassemia, and auto-immune hemolytic anemia.
Blood Dyscrasias
Lymphomas and leukemias.
Connective Tissue Diseases

SLE and Felty’s syndrome.
Infiltrative Causes
Amyloidosis and Gaucher’s disease.
Miscellaneous Causes
Sarcoidosis, amyloidosis, splenic tumor, and myelofibrosis.
Hypersplenism is associated a very large spleen being responsible for

granulocytopenia, thrombocytopenia, and anemia.
Splenectomy is associated with predisposition to severe sepsis with
Str. pneumoniae, Salmonella, H-influenza, and E-coli. The risk is greatest
during the first three years after splenectomy due to the loss of splenic
macrophages that clear the opsonized bacteria and decreased IgM anti-
bodies formed in the spleen.
Splenic infarction is seen due to thromboembolic phenomenon, for
example, bacterial endocarditis or atrial fibrillation, vasculitis, DIC or
hypercoaguable states, and myeloproliferative disorders. It is quite usual
in patients with sickle cell anemia and vaso-occlusive crisis, which eventu-
ally causes auto-splenectomy. Local compression of the splenic artery may
also be a cause. With underlying infection, the chances are higher. The
patient usually presents with pain in the left hypochondrium, or it may
be discovered incidentally.
Kidneys
Palpation
The patient lies on his back, with the abdominal muscles relaxed, breath-
ing deeply with the mouth open, and turned to the other side. The kid-
neys are palpated bimanually from the right side (Figure 47). In general,
the kidneys may not be palpable, but any enlargement readily makes
them palpable. Rarely, one may even recognize the renal configuration
with a notch on the medial side toward the hilum.
Part of the right kidney may normally be palpable in thin individuals,
especially women. One or both kidneys may be freely mobile (floating
kidney) and may be found in any part of abdomen.
Figure 47 Palpation of the left kidney is demonstrated

1. Keep the right hand on top of the lumbar region.
2. The left hand is kept posteriorly in the lumbar area.
3. At the height of inspiration, the top hand is pressed down, while
the kidney is briskly pushed up with the bottom hand to bimanually
feel it.
4. Both kidneys are palpated in a similar manner.
Differential Diagnosis of the Right Kidney
1. A kidney is bimanually palpable in the loin, whereas the gallbladder

is best felt at the tip of the 9th costal cartilage.
2. Murphy’s sign is positive if there is an inflamed gallbladder (patient
winces and holds the breath on attempting to take a deep breath on
palpation at the 9th costal cartilage).
3. Gallbladder enlargement appears to come from under the costal
cartilages, while kidney is a deeper organ.
4. The percussion note above the kidney is resonant because of overly-
ing intestinal loops, while over the bladder is usually dull.
5. The kidney becomes palpable late during inspiration and disappears
on expiration, but can be pushed away temporarily under the loin
with pressure.
6. A perinephric abscess tends to bulge in the loin and may be associ-
ated with edema and redness of the overlying skin.
7. Renal diseases like pyelonephritis and nephrolithiasis usually pro-
duce heaviness in the renal area, while perinephric abscess results in
tenderness at the renal angle.
8. Remember that diseased organs produce their own set of symptoms,
for example, kidney disease with urinary problems and gallbladder
disease with jaundice.
Differentiating Left Kidney Enlargement from Splenic

Enlargement
While clinical examination should be enough to differentiate the two,

sometimes confirmation may be required by ultrasound examination of
the abdomen.
1. The enlargement of the spleen is usually in an oblique fashion from

the LHC toward the RIF, while the kidney enlarges in the downward
direction toward the LIF.
2. The shape of the two viscera is different with a notch over the outer
surface of the spleen with a sharp edge, while border of the kidney
is rounded.
3. Percussion over the kidney is resonant due to gas in the overlying
bowels. The spleen displaces the bowels, thus making the percussion
note over it dull. Of note is the dullness to percussion over the left
lower ribs in splenomegaly.
4. One can insert fingers under the costal margin with an enlarged kid-
ney, but this is difficult with an enlarged spleen unless the abdomen
is very lax.
5. Bimanual palpation is used for the kidney, while a small splenic
enlargement is appreciated by downward push of the spleen by the
left hand.
6. Movement of the kidney with respiration is slight, while that of
spleen is more.
Applied Medicine
Tenderness in the renal angle may indicate pyelonephritis or perinephric

abscess. Stones in the substance of the kidney may be silent or produce
vague heaviness in the loin. With renal pelvic stone, the pain may be
more dragging, while in case of the ureter, the pain is very severe, colicky,
and agonizing. Urinary bladder stones produce dysuria and frequency
with pain in the hypogastrium. Hematuria associated with infection is
not unusual. Dependent edema may be first apparent around the eyes
because of the loose tissue offering little resistance to fluid accumulation.
Generalized edema or anasarca is a common sequel of decompensated

nephrotic syndrome and CRF. In nephrotic syndrome, heavy proteinuria
may make the urine milky white in appearance.
Chronic kidney disease (CKD) is present when the glomerular
filtration rate (GFR) falls below 60mL/min per 1·73m2, or markers of
kidney d amage are present, or both, for at least three months. Diabetes
and hypertension are the most common causes of CKD, but incidence,
prevalence, and progression vary in different countries, by ethnicity and
by social status. Symptoms may start late and are initially nonspecific like
lethargy and loss of appetite.
In CKD, the patient has pallor (anemia), sallow complexion (uremic
look), band keratopathy, brown arc on nails (half and half nails), white
transverse lines on the nails usually paired (Muehrcke’s lines); there may
be bruising, pigmentation and scratch marks for itching. Examine the
BP while lying and standing (postural hypotension). Also, look at the
fundus for hypertensive and diabetic retinopathy (most patients will have
proliferative retinopathy in CKD). Look for vascular access or fistula in
a patient with end-stage renal disease. Metabolic acidosis is associated
with acidotic breathing, and in advanced disease, asterixis may be pres-
ent along with pericarditis associated with a pericardial rub. Fluid reten-
tion is common especially seen periorbitally in early disease; later, it may
be generalized with raised JVP and sometimes producing fluid overload
and pulmonary edema. Subcutaneous nodules may be palpated (calcium
CLINICAL FEATURES OF CRF

Uremic encephalopathy,
Anemia, hyperkalemia,
seizures, sleep disorder,
metabolic acidosis, hypo-
weakness and fatigue
calcemia, hyperphosphatemia, hypoglycemia,
Acidotic Band keratopathy
breathing hypertensive retinopathy
Uremic breath
Nausea, vomiting,
anorexia
Uremic gastritis Staging of kidney disease
Uremic colitis HTN, volume Stage 1: Normal or increased GFR
overload and CCF (>90 mL/min/1.73m2).
Itching, bruising,
Uremic pericarditis Stage 2: GFR (60–89 mL/min/1.73m2).
pigmentation
Stage 3a: GFR (45–59 mL/min/1.73m2).
Tetany, brown nails Renal osteodystrophy
Stage 3b: GFR (30–34 mL/min/1.73m2).
Sec hyperparathyroidism
Stage 4: GFR (15–29 mL/min/1.73m2).
Erectile dysfunction Hyperuricemia
Stage 5: GFR (less than 15 mL/min/1.73m2).
Polyuria, oliguria, Uremic neuropathy
proteinuria, hematuria, Restless leg syndrome
anuria
Edema
Peripheral vascular disease
Figure 48 Clinical features of chronic renal failure

phosphate deposits), while bone pain may occur in renal osteodystrophy

(osteoporosis, osteosclerosis, osteomalacia, or ostitis fibrosa cystica).
A vasculitis rash may indicate connective tissue disorder and the under-
lying cause. A scar of peritoneal dialysis maybe visible or indicative of
renal transplant. The kidney may be palpable if there is hydronephrosis or
tumor, and a renal bruit may be heard in renal artery stenosis. CKD may
be associated with a predominantly sensory peripheral neuropathy and
loss of reflexes. Finally, a urine examination for protein, sugar, 24-hour
protein, pH, specific gravity, blood, casts, leucocytes, nitrate, and urinary
sediment is performed. A serum dialysis profile is sent.
GFR is measured by DTPA or estimated using equations. Proteinuria
is associated with increased risk of progression of CKD and death.
Patients with CKD are 5 to 10 times more likely to die prematurely with
worsening renal function.
Causes of a Renal Mass

1. Hydronephrosis.
a. Hypernephroma in adults.
2. Tumors.
b. Wilm’s tumor in children.
3. Polycystic kidney.
4. Nephrotic syndrome (kidney is rarely enlarged).
Hematuria: The origin of blood in the urine may be from the kidney,
ureter, urinary bladder, prostate, or urethra. Hematuria may be painful or
painless. By far, the commonest cause is renal stones or trauma.
Causes of Hematuria
1. Renal. a. Kidney stones.
b. Glomerulonephritides.
c. Kidney tumors.
d. Kidney infections (pyelonephritis).
e. Polycystic kidney.
f. Renal vein thrombosis.
g. Renal TB.
h. Connective tissue diseases and vasculitis.
i. Hemolytic uremic syndrome.
j. HS purpura.
(Continued)
Causes of Hematuria
k. Good Pasture syndrome.
l. Sickle cell glomerulonephritis.
m. Trauma.
n. Severe exercise.
o. Lithotripsy.
2. Ureter a. Stone.
b. Stricture.
c. Malignancy.
d. Polyp.
e. Surgical instrumentation.
3. Bladder a. Transitional cell carcinoma.
b. Squamous cell carcinoma.
c. Cystitis.
d. Radiation.
e. Schistosomiasis.
4. Prostate a. Benign prostatic hyperplasia.
b. Prostatic cancer.
c. Prostatitis.
d. Transurethral resection of prostate.
5. Urethra a. Urethritis.
b. Trauma.
6. General causes a. Anticoagulation.
b. Antiplatelets.
7. Mimic hematuria a. Drugs like rifampicin, nitrofurantoin, and phenytoin.
b. Beetroot ingestion.
Patients with hematuria seek medical advice quickly due to the alarm-
ing symptom. Hematuria may be painful or painless. The most import-
ant cause of painless hematuria in an elderly male is transitional cell
carcinoma of the bladder.
Investigations of Hematuria
1. Urinalysis.
2. CBC and coagulation profile.
3. Renal function tests.
4. Urine culture and sensitivity.
5. Renal and urinary tract ultrasound.
6. IVP.
7. Cystoscopy.
8. Retropyelogram.
9. CT kidney or renal stone protocol or CT-A (angiogram) for renal vasculature.
10. CTD and vasculitis workup (initially ANA or ANCA if indicated).
11. Schistocytes for TTP.
12. Uric acid and calcium and parathyroid level (for associated kidney stones).
13. Urine cytology for bladder and urinary tract tumors.
14. Urine MBTB PCR for renal tuberculosis.
15. PSA.
16. Renal biopsy.
17. PNH (complement level).
18. Coagulation screen.
Gallbladder
The gallbladder is not normally palpable unless distended. An enlarged
gallbladder is felt as a pear shaped, smooth mass in the right hypochon-
drium, projecting beneath the 9th costal cartilage. It moves with respira-
tion and can be pushed to either side. An inflamed gallbladder is usually
quite tender.
Palpation
The gallbladder lies at the tip of the 9th costal cartilage (Figure 49). At
this site, press firmly with the flat of the fingers of the right hand pointing
PALPATION OF GALL BLADDER
9th costal cartilage
Umbilicus
A line joining the
anterior superior iliac
spine to the ubblilicus
when extended meets
the 9th costal cartilage
Anterior superior
iliac spine
Figure 49 Technique of palpation of gallbladder

toward the left shoulder. As the patient takes a deep inspiration, the
gallbladder moves down and may be palpable.
In acute cholecystitis, as the patient takes a deep breath, the impact
of the inflamed gallbladder with the examiner fingers makes him or her
wince with pain and hold the breath. This is called Murphy’s sign. This sign
may also be elicited with the right thumb at the site of the gallbladder
while the fingers curl around the side of the RHC.
Enlarged Gallbladder with Jaundice
Courvoisier’s law states that a palpable gallbladder in a jaundiced patient

cannot be due to a stone in the common bile duct. Causes like obstruc-
tion at a distal site in carcinoma of the head of pancreas, carcinoma of
ampulla of Vater, chronic pancreatitis, and compression of common
bile duct from outside are likely. A local pathology in the gallbladder
like stone or inflammation usually causes enough fibrosis to prevent any
enlargement.
Enlarged Gallbladder Without Jaundice
In this case, there is obstruction proximal to the junction of the cystic with
the common bile duct. It may be seen with acute cholecystitis due to stone
impacted in the cystic duct, mucocele and empyema of the gallbladder.
Applied Medicine
Acute cholecystitis: Presents with fever, pain in the right hypochondrium

(colicky), and nausea with vomiting. Anorexia and fatty intolerance may
be elicited. The pain may radiate to the left shoulder or the tip of the
scapular spine. Murphy’s sign is positive. Sometimes, there is increased
sensitivity and pain below the right scapula (between the 9th and 11 rib
posteriorly known as Boas sign). Sometimes, jaundice may be associated.
The cause in most cases are gallstones (Figure 83 in Volume II). See com-
plicated cholecystitis in Figure 73 in Volume II.
Gallbladder tumors may be benign or malignant. Many are discovered
when asymptomatic.
• Adenomatous polyps are associated with thickened

gallbladder wall having intramural diverticula. They may
be pedunculated, flat, complex, branched, or sessile. They
are generally benign, but their size determines the risk of
malignant potential.
• Half of the polyps are cholesterol polyps, which are multiple
and generally asymptomatic.
• Inflammatory polyps are associated with chronic inflamma-
tion. They have a narrow vascularized stalk.
• Other tumors may be fibromas, hemangioma, leiomyomas,
lipomas, granular cell tumors, and heterotropic tissue (gastric,
pancreatic, and intestinal epithelium).
• Gallbladder cancer are mostly adenocarcinomas seen in
the elderly, and most are associated with gallstones larger
than 3cm. Other risk factors include stippled calcification
of mucosa. Clinically, they are associated with weight loss,
anorexia, right upper quadrant pain or mass, jaundice and
sometimes, ascites. Many are asymptomatic and discovered
incidentally.
• Gallbladder growths are evaluated initially by abdomi-
nal ultrasound followed by CT scan (see Figure 81) or
MRI. P ercutaneous CT scan, guided biopsy is advised for
nonresectable tumors; otherwise, it may be associated with
seeding of the tumor. Therefore, surgical exploration is
necessary with a view to curative resection.
Stomach and Esophagus

Stomach and esophagus are not palpable, but fullness or mass in the
epigastrium may be seen in carcinoma of stomach. A left supraclavic-
ular lymph node may be palpable in this condition called Virchow’s
lymph node. Stomach diseases are associated with dyspepsia, early sati-
ety, nausea and vomiting, gastritis or burning epigastrium or retroster-
nally, changes in appetite. While esophageal diseases may be associated
with reflux symptoms, dysphagia or food sticking, nausea, vomiting, and
weight loss.
Applied Medicine
Succussion splash is heard by placing your ear close to the patient’s belly
while shaking it with both hands (Figure 50). If the patient has not eaten
in the last eight hours, it signifies delayed gastric emptying or outlet
obstruction caused by scarring or carcinoma.
Figure 50 The abdomen is suddenly shaken to hear the succussion

splash
Virchow’s lymph node may be palpable in the left supraclavicular region

in carcinoma of the stomach, pancreas, or lung.
Peptic ulcer disease in general includes gastric ulcer (Figure 61 in
Volume II) and duodenal ulcer (Figure 90 and 91 in Volume II). The
spectrum of peptic ulcer disease encompasses many similar diseases.
Spectrum of Peptic Ulcer Disease

1. Gastric ulcer. 10.
Combined gastric and duodenal
ulcer.
2. Duodenal ulcer. 11. Post-bulbar ulcer.
3. NSAID-induced ulcer. 12. Zollinger–Ellison syndrome.
4. Association with H pylori. 13. Post-gastrectomy or marginal ulcer.
5. Pyloric channel ulcer. 14. Meckel’s diverticular ulcer.
6. Giant gastric ulcer. 15. Malignant ulcer.
7. Childhood peptic ulcer disease. 16. Biliary gastritis and ulcer.
8. Curling’s ulcer (in trauma, burns, sepsis). 17. Portal gastropathy and ulcer.
9. Cushing’s ulcer (post-stroke or serious illness and surgery.
Gastric and duodenal ulcer diseases are common disorders responsible

for pain and discomfort in the epigastrium. There is little relationship
between the amount of pain and the severity of disease. The characteristic
features include:
a. Pointing sign: The patient localizes the tenderness to the epigastrium.

b. Periodicity: The history is chronic with relapses and remissions.
c. Relation to meals: The pain of duodenal ulcer is relieved by eating,
awakens the patient at night, and there is early morning pain. The
patient, therefore, may gain weight. In gastric ulcer, the pain gets
worse with meals, and the patient is afraid to eat and loses weight.
d. The pain may radiate to the back in penetrating ulcers that involve
the pancreas.
e. The site of pain and tenderness in gastric ulcer is slightly to the left of
the midline and a little higher in the epigastrium. While in duodenal
ulcers, it is lower and slightly to the right of the mid line.
f. There may be associated burning, dyspepsia, and retrosternal discom-
fort.
g. Nausea and vomiting especially occur in pyloric channel ulcers, with
the pain being relieved after vomiting.
H pylori testing is imperative in all cases of peptic ulcer disease and

active infection may be detected by stool antigen test (using monoclonal
antibody) or urea breath test (both have equal sensitivity and specificity).
Serology cannot distinguish between active and cured infections (sensitivity
and specificity is less than 90 percent). If a patient has recently used proton
pump inhibitors, antibiotics, or bismuth compound, the stool antigen test
and urea breath test may become falsely negative. Histological examination
of the biopsy (antral and corpus) specimens can also detect H pylori along
with the presence of acute chronic inflammation. A rapid urease test (RUT)
can be done on the biopsy (presence of infection is detected by color change
of the medium due to urea being hydrolyzed to ammonium. It can also be
falsely negative use of PPI, antibiotics, or bismuth compound.
H pylori infection causes gastritis, and duodenitis and may be associ-
ated with the following complications or sequelae.
• Atrophic gastritis (associated with iron and Vitamin B12

anemia).
• Gastric ulcer.
• Gastric adenocarcinoma.
• Gastric mucosal-associated lymphoma (MALT).
• Duodenal ulcer.
• Gastrointestinal bleeding.
• Heart burn (but not GERD).
Eradication requires high dose PPI (esomeprazole or raberprazole)

with two or three antibiotics (choice includes clarithromycin, tetracycline,
amoxacillin, levofloxacin, or metronidazole/tinidazole) given for 14 days
in most cases. Bismuth compound can be added. Choice depends on the
local sensitivity patterns. Do a urea breath test four weeks after the course
of antibiotic and PPI or six to eight weeks for stool antigen test to check
for cure (discontinue the PPI before these tests). Sometimes, retreatment
with a different regimen maybe required for patients who have failed to
cure their infection.
Common Complications of Ulcer Disease

1. Bleeding. 4. Penetration and associated
pancreatitis.
2. Perforation and peritonitis. 5. Narrowing and obstruction.
3. Malignant transformation (controversial).
Zollinger–Ellison syndrome may present as typical, but resistant peptic

ulcer disease or ulcers at atypical sites. It is due to a gastrinoma causing
hypersecretion of gastrin, which, in turn, stimulates gastric acid. There
may be diarrhea, which is caused by the hyperacidity causing damage to
the enterocytes, with inactivation of the pancreatic enzyme, and making
the bile acids insoluble. On endoscopy, one can see prominent gastric
folds due to hyperplasia of the parietal cell mass. Complications include
bleeding, perforation, and reflux with stricture. ZE syndrome should
be suspected in unresponsive peptic ulcer cases or when ulcers are pres-
ent in second part of duodenum or jejunum. It may also be associated
with MEN 1 (multiple endocrine neoplasia type 1) where patient also
has hyperparathyroidism and pituitary tumor. In these cases, look for
hypercalcemia and its features. There may be a family history because
it is autosomal dominant. Diagnosis is made by documenting elevated
fasting gastrin levels (while off acid suppressive medications for one week)
with acid hypersecretion (pH <2.0). In doubtful cases, secretin stimula-

tion may be performed, which causes gastrin release from the gastrinoma,
while in other patients, the gastrin remains same or falls. Most gastrino-
mas maybe localized via somatostatin receptor scintigraphy (SRS) with
111-Indium pentetreotide (OctreoScan) and CT scan, which is superior
to conventional CT scan and MRI.
Functional dyspepsia is a common disorder accounting for about 10 to
15 percent prevalence. It may be due to visceral hypersensitivity, abnormal
fundal accommodation, altered eating habits, food intolerance, change in
flora, eosinophilic infiltration of duodenum, and psychological factors.
Differential Diagnosis of Functional Dyspepsia

1. Peptic ulcer disease. 7. Cancer of the stomach.
2. Drug-induced. 8. Chronic bowel ischemia.
3. GERD. 9. Endocrine disorders (thyroid, parathy-
roid, and adrenal).
4. H pylori infection. 10. Coeliac sprue.
5. Gallstones. 11. Chronic pancreatitis.
6. Diabetic gastropathy. 12. Idiopathic.
It is, therefore, a diagnosis of exclusion when symptoms of dyspep-

sia, fullness, pain, or burning epigastrium are present for more than six
months with no evidence of structural or systemic disease and normal
endoscopy.
Carcinoma of the stomach: Patients usually present with poor appetite
(especially to proteins), significant weight loss, and sometimes, epigas-
tric fullness or mass. There may be symptoms of peptic ulcer disease.
Vomiting may be present or even obstructive symptoms. In advanced
cases, left supraclavicular lymph node may be enlarged (Virchow’s lymph
node). Endoscopy and biopsy are required to confirm the diagnosis. Bar-
ium study may show linitus plastic (leather bottle stomach, Figure 61 in
Volume II) in infiltrative carcinoma of the stomach.
Upper GI bleeding may be trivial or massive. Therefore, the initial
assessment includes recognition of resuscitation and IV access. The site
of bleeding may be from the mouth to the stomach, and even sometimes
the duodenum (see Figure 87, 88, 90, 91, 93, 94, 99, 100, 101, 103,
104 and 105 in Volume II for causes of upper GI bleeding). Vomited out
blood (hematemesis) may be coffee ground, due to action of gastric acid.

It may be dark red when fresh bleed has occurred and bright red if arterial
leakage has occurred. It is clinically assessed by the history:
Amount May be small or large associated with hypotension.

Color May be coffee ground or bright red.
Number of times Indicates severity.
Associated features History of ulcer disease.
Use of NSAIDS.
Occurring after forceful vomiting in Mallory–
Weiss
Weight loss, loss of appetite, and early satiety in
cancer stomach.
History of chronic liver disease in variceal
bleeding.
With melena, indicates upper GI bleed.
Drugs for anticoagulation may be the cause.
Abdominal pain, rigidity, and guarding sug-
gests a surgical abdomen and perforation.
Orthostatic hypotension occurs with about 15 percent volume blood loss.
Supine hypotension occurs with about 40 percent volume blood loss.
Gastroesophageal reflux is a common problem and occurs due to inef-

fective anti-reflux barriers (most important is the constant pressure in the
lower esophageal sphincter which is about 15mmHg above the gastric).
Precipitating Causes of Reflux

Alcohol. Carbonated drinks.
Caffeine. Citrus fruit.
Fatty meal. Smoking.
Chocolate. Obesity.
Tomato. Vinegar.
Drugs act via mucosal damage (beta agonists, calcium channel blockers, benzodiazepine,
estrogens, theophyllines, NSAID, iron, KCl, tetracycline, alendronate).
Patients have heartburn or retrosternal burning, especially after meals

and when lying down. There may be regurgitation, water brash, and
dysphagia. Patients with typical symptoms at least twice per week and for
four to eight weeks are considered to have GERD. It is important to note

that GERD may also be associated with many extra intestinal features like
dental erosions, halitosis, aphthous ulcers, sinusitis, otitis media (espe-
cially in children), post-nasal drip, chronic cough, aspiration pneumonia,
bronchiectasis, and sleep apnea. About half the patients with asthma also
have GERD. It is due to micro-aspirations causing irritation.
Warning Features with GERD (Further Evaluation Required)

1. Significant weight loss. 4. Family of gastrointestinal cancer.
2. Dysphagia. 5. Elderly patient.
3. Anemia or GI bleeding. 6. Unresponsive to therapy.
Diagnosis requires a compatible history, response to PPI (non-

responders are unlikely to have GERD), and sometimes, investigations
like upper GI endoscopy, barium study, 24-hour esophageal pH study
or manometry. Complications of chronic GERD include bleeding from
esophagitis, stricture and dysphagia, and Barrett esophagus, which is
premalignant. Chronic nocturnal symptoms, in particular, may be associ-
ated with the development of esophageal cancer.
Diffuse esophageal spasm involves the thoracic esophagus and is caused
by impairment of inhibitory innervation and associated with non-
peristaltic contractions. There is sparing of the lower esophageal sphincter.
Clinically, the patient may have chest pain, regurgitation, and dysphagia.
The disorder may be episodic. The chest pain has to be differentiated from
cardiac pain. Barium swallow may show tertiary contractions, which give
a cork screw appearance on barium study. A definitive diagnosis is made
by manometry study.
Achalasia is a motility disorder with impaired relaxation of the lower
esophageal sphincter, resulting in proximal dilatation. It may be primary
(loss of ganglion cells) and secondary (associated with diabetes, pseudo-
achalasia of malignancy, or Chaga’s disease). Patients present between 25
to 60 years of age.
It may be discovered either incidentally or with complaint of food
sticking retrosternally, dysphagia, halitosis, and retrosternal burning
or pain. On X-ray of the chest mediastinal widening, air-fluid levels,
absence of a gastric air bubble, or complications like aspiration pneu-
monia and lung abscess may be seen. A barium esophagogram shows
Figure 51 Fluoroscopic barium esophagogram showing achalasia

cardia with narrowing dilation of the proximal esophagus
(megaesophagus) with distal angulation or tortuous shape, giving it
a sigmoid shape (“bird-beak” appearance) caused by the persistently
contracted lower esophageal sphincter, which shows loss of peristalsis.
There is delayed emptying of barium
distal narrowing “bird-beak sign or rat tail sign” in the distal esophagus
with proximal dilatation (Figure 51). Esophageal mannometry typically
shows failed peristalsis and incomplete relaxation of the lower esopha-
geal sphincter. Treatment responds best to lower esophageal sphincter
myotomy. Other modalities of treatment are pneumatic dilatation and
botulinum toxin injection.
Mallory–Weiss tear is a longitudinal tear in the mucosa, on the
gastric side of the gastroesophageal junction, classically after forceful
vomiting (any sudden rise in intra-gastric pressure). It presents with
abdominal pain and hematemesis and features of blood loss (dizziness,
weakness, fainting, melena). It may be associated with hiatus hernia and
alcoholism.
Boerhaave syndrome, or spontaneous esophageal rupture, is a rare
but serious condition characterized by a complete transmural rupture of
the esophagus usually resulting from forceful vomiting (may be alcohol
related). It has a high mortality (25 to 89 percent). The tear is most com-
monly along the left posterolateral wall of the lower third of the esoph-
agus. Clinically, there is nausea and vomiting, followed by severe lower
thoracic and epigastric pain, which may radiate to the back or left shoul-
der, and may be worsened by swallowing. Hematemesis is not typically
observed (may be a feature of Mallory–Weiss tear). Mackler triad is the
combination of vomiting, lower chest pain, and subcutaneous emphy-
sema (in 50 percent at , but more common in late cases). Other findings
include shortness of breath (from pain and pleural effusion), tachypnea,
and abdominal rigidity. Sometimes, peripheral cyanosis, hoarseness
(recurrent laryngeal nerve involvement), tracheal shift, and a raised JVP
may be seen. Tachycardia, diaphoresis, fever, and hypotension develop as
sepsis develops and lead to multi-organ failure. The Hamman or medi-
astinal crunch are crackles that are synchronous with the heart beat (not
respiratory cycle) and heard best with the patient is in the left lateral
decubitus position. On investigation, ECG is normal and X-ray chest
or CT scan may show a left pleural effusion with pneumothorax, hydro-
pneumothorax, pneumomediastinum, periesophageal air, subcutaneous
emphysema, or mediastinal widening. Diagnosis is made on esophageal
swallow or barium esophagram with a water-soluble contrast. Manage-
ment is conservative for contained perforation, or sometimes, surgical
drainage and repair may be required.
Eosinophilic esophagitis has recently been increasingly recognized.
Clinically, patients have recurrent dysphagia, GERD, dyspepsia, and ret-
rosternal discomfort. An average delay of a few years in the diagnosis is
not uncommon. A history of food impaction is usually present. There
may be a history of allergic disorders with high IgE levels and peripheral
blood eosinophilia. On biopsy, one can demonstrate eosinophilic infiltra-
tion with >20 eosinophils per high-power field. Patients do not respond
to PPI. See various types of esophagitis in Figure 88 in Volume II.
Cancer of the esophagus may be squamous cell and is often at an
advanced stage at presentation. Alcohol, tobacco, and exposure to
nitrosamines and nitrosyl compounds are important risk factors. Pre-
disposition also occurs with achalasia, strictures, head and neck tumors,
Plummer–Vinson syndrome, celiac disease tylosis, and history of expo-
sure to radiation. Adenocarcinoma classically occurs in the mid and distal
esophagus and associated with chronic gastroesophageal reflux-produc-
ing Barrett epithelium, which progresses from low-grade to high-grade
dysplasia to adenocarcinoma. About 10 percent patients with GERD

may develop Barrett’s esophagus, of which 1 percent develop esopha-
geal adenocarcinoma. Other risk factors include smoking, obesity, and
possible exposure to environmental dietary and nutrition and certain
drugs.
Patients with cancer of the esophagus present with significant weight
loss and progressive dysphagia when the lumen is constricted by half to
two-thirds. Risk of aspiration pneumonia is increased. There is early spread
to local tissues (tracheobronchial tree, lymph nodes, vocal cord paralysis,
paralysis of diaphragm, and pleural effusion, while distant spread occurs,
for example, to bone and liver or other sites. Only early surgical resection
has been shown to improve survival rates in such patients before meta-
static disease has occurred.
Diagnostic Tools and Staging

Endoscopy and biopsy. Endoscopic ultrasonography (EUS).
Barium esophagraphy. Magnetic resonance imaging (MRI).
Contrast-enhanced computed tomography Positron-emission tomography (PET).
(CT).
Plummer–Vinson syndrome is said to be present when dysphagia, iron

deficiency anemia, and esophageal webs (Figure 89 in Volume II) are pres-
ent. These patients have an increased incidence of postcricoid squamous
cell carcinoma. Clinicallym patients may have koilonychias due to iron
deficiency along with signs and symptoms of anemia and later developing
dysphagia and progressive weight loss.
Zenker’s diverticulum is a pharyngoesophageal diverticulum (out-
pouching) that develops over time through a weak area in the posterior
aspect of the pharyngoesophageal junction (level of C5 and C6) called
Killian dehiscence. It is especially seen in the elderly women and present
with proximal esophageal dysphagia with halitosis, regurgitation of undi-
gested food, and occasionally, hoarseness. Reduced intake is associated
with weight loss. Recurrent aspiration occurs in one-third of patients.
Diagnosis is best made by fluoroscopic barium swallow. Rarely, a squa-
mous cell carcinoma can develop in them. CT scan and MRI with con-
trast demonstrate hypopharyngeal outpouching filled with air, fluid, or
oral contrast material. Endoscopy may lead to perforate untrained hands.
Treatment remains surgery or endoscopic division of diverticular wall

with stapling in symptomatic patients.
Barrett esophagus is the change of normal squamous epithelium lin-
ing of the lower esophagus with intestinal metaplasia. This is commonly
due to chronic reflux, with esophagitis leading to metaplasia. Prolonged
length of exposure to gastric content or bile, rather than the number of
episodes is responsible. Diagnosis is based on endoscopic findings and
confirmed on biopsy (finding specialized intestinal metaplasia [SIM] at
3 cm or sometimes less from the distal esophagus or squamocolomnar
junction or gastroesophageal junction). It may transform into esophageal
cancer; therefore, aggressive treatment and close monitoring is strictly
advised. Patients with chronic GERD should undergo endoscopy screen-
ing, especially if at high risk. The frequency of surveillance depends on
the degree of metaplasia.
Pancreas
The pancreatic beta cells secrete insulin, alpha cells secrete glucagon,
and the delta cells secrete gastrin. The pancreas also produces digestive
enzymes like amylase, trypsin, chymotrypsin, lipase, phospholipase, and
cholesterol esterase. Normally, it is not palpable, but a mass may be pal-
pable in the epigastrium in pancreatic carcinoma or pseudocyst formation
after acute pancreatitis. Chronic or acute pancreatic insult may be associ-
ated with secondary diabetes mellitus.
Applied Medicine
Acute pancreatitis is mostly due to biliary tract disease or alcohol in about

80 percent of cases. The pain of acute pancreatitis is severe and localized
to the epigastrium or upper abdomen and may radiate to the back. The
patient is in severe agony and finds some relief by leaning forward. There
may be nausea, vomiting, anorexia, and shock. In hemorrhagic pancreati-
tis, there may be bruising in the flanks (Gray Turner’s sign) or around the
umbilicus (Cullen’s sign, Figure 30). Serum amylase is markedly elevated
in acute pancreatitis. Serum calcium is often low in acute pancreatitis)
due to deposition of calcium salts.
Causes of Pancreatitis
They can be remembered by the word GET-hyper-ATICD.
1. Gallstones and biliary tract disease. 7. Hyperparathyroidism.
2. Ethanol (heavy consumption of alcohol). 8. Autoimmune.
3. Trauma, including surgery and post-ERCP. 9. Tumor of the pancreas.
4. Hypercalcemia. 10. Infections (usually viral).
5. Hypertriglyceridemia (usually >1000mg%). 11. Cystic fibrosis.
6. Drugs like hydrochlorothiazide, azathioprine, tetracycline, valproate, INH, bezafibrate.
Assessment of Severity of Acute Pancreatitis

The severity of disease can be assessed by various scores. Important parameters include:
1. Organ failure for <48 hours and longer than 48 hours.
a. CVS: Systolic BP <90.
b. Lungs: PaO2 <60.
c. Kidney: Creatinine >2mg%.
d. GIT: bleeding (500ml in 24 hours).
2. Local complications (pseudocyst, necrosis, fluid collection, abscess).
3. CT severity index (depends on fluid collections and percentage of necrosis).
4. Extra-pancreatic complications (pleural effusion, ascites, vascular complications).
5. Ranson score >3 (depends on age, leukocytosis, LDH, AST, BSL).
6. APACHE II score >8.
7. Glasgow criteria (includes age, PaO2, ANC, calcium, urea, LDH, albumin, and
sugar).
Mild pancreatitis = no organ failure and no local complications.
Moderate pancreatitis = Transient organ failure <48 hours.
Severe pancreatitis = with local or systemic complications or persistent organ failure.
In pancreatitis, selected investigations to diagnose and recognize

complications.
Investigations of Pancreatitis
1. CBC, urea, creatinine and electrolytes, lipid profile, serum calcium, LFT, LDH,
amylase, lipase, blood gases.
2. Blood sugar and GTT.
3. Plain x-ray abdomen (may show colon cutoff sign at splenic flexure or widening of
the duodenal “C” loop due to edema of pancreatic head).
4. Abdominal ultrasound.
5. Serum amylase and lipase.
6. CT abdomen.
7. MRCP (magnetic resonance cholingio-pancreatography).

8. ERCP (endoscopic retrograde cholangio-pancreatography).
9. Pancreatic function tests (for chronic pancreatitis).
10. Endoscopic ultrasound, if other imaging tests do not reveal a cause.
11. Fecal elastase and chymotrypsin in chronic pancreatitis.
Chronic pancreatitis is a relapsing and remitting condition and is asso-

ciated with:
Clinical Features and Imaging of Chronic Pancreatitis

1. Episodes of abdominal pain (hours to days even months or years).
2. Site is epigastric and may radiate to the back (some relief by leaning forward).
3. Steatorrhea.
4. Diabetes in one-fifth, but impaired glucose intolerance in two-third.
5. Weight loss.
6. Deficiency of fat-soluble vitamins.
7. Features of underlying disease, for example, hepatobiliary disease.
8. A left-sided pleural effusion may be due to pancreatitis.
9. Palin x-ray abdomen may show pancreatic calcification (30 percent) or pseudocyst.
10. U/S is usually the initial test for suspected cases.
11. CT may show pancreatic enlargement, duct dilatation, calcification, and
parenchymal atrophy.
12. MRA with pancreatic parenchymal sequence and secretin enhanced MRCP may be
used.
Fat malabsorption or steatorrhea is a characteristic feature of chronic

pancreatic insufficiency. The stools are bulky, frothy, malodorous, float, dif-
ficult to flush, and silvery white in appearance. Jaundice may occur in pan-
creatic disease due to biliary tract stone or carcinoma of the head of pancreas.
Pancreatic Pseudocyst
1. It is a collection of amylase-rich fluid in or adjacent to pancreas and surrounded by a
fibrous wall.
2. Most cases are the consequence of chronic or acute pancreatitis, and therefore
related to alcohol or gallstones. They account for 75 percent of all pancreatic masses
and may be single or multiple.
3. CT scan and MRI are best for diagnosis.
4. Complications include infection with abscess formation, rupture, bleeding, and mass
effect.
5. Most collections with acute pancreatitis resolve spontaneously and are encapsulated.
Larger than 6 cm size should be drained surgically, percutaneously, or endoscopically.
Pancreatic cancer has been described as the disease with vagueness and
variability in symptoms perplexing to both the patient and the doctor.
It is rapidly progressive and often found metastatic at presentation. The
prognosis is poor. It may be genetically predisposed, and 10 percent give
a family history. In these patients, smoking increases the chances of devel-
oping cancer a decade earlier. Endoscopic ultrasound and MRCP screen-
ing test can detect most lesions and are performed about once a year after
the age of 45 years or younger in Peutz–Jeghers syndrome.
There is association with superficial thrombophlebitis. CA 19–9 is
usually high. A contrast CT scan (see Figure 80a and 80b) is the pre-
ferred test, but MRI with contrast may be helpful, if it is not detected and
suspicion remains high. Sometimes, it may might not be detected even
when metastasis has occurred. ERCP, MRCP, and angiography may be
required. Endoscopic ultrasound and guided fine needle aspiration may
be another option in difficult to diagnose cases.
Clinical Features of Pancreatic Cancer

Most patients present late, only 20 percent being resectable.
1. Jaundice due to biliary obstruction, especially seen with tumor of head of pancreas.
2. Epigastric mass is a late sign.
3. Weight loss, anorexia, and cachexia.
4. Palpable gallbladder (Courvoisier’s sign).
5. Pain epigastrium and back.
6. New onset diabetes
7. Lymphadenopathy, especially left supraclavicular (Virchow’s node) and periumbilical
(Sister Mary Joseph’s node).
8. Diarrhea due to pancreatic enzymatic deficiency.
Intestines
1. Small intestinal pain is central, usually colicky, but may radiate to
the back.
2. Colonic pain can be felt centrally, along the line of colon or in the
hypogastrium. It is often poorly localized and frequently radiates to
the back, or rarely, the thighs.
3. Swelling or mass in the abdomen requires knowledge of the anatomy
to enumerate the list of differential diagnosis.
Applied Medicine
Melena or black, tarry, and sticky stools with an offensive odor results
from mild-upper GI bleeding. Fresh red blood passed per rectum is called
hematochezia.
Causes of Hematochezia
1. Hemorrhoids. 6. Ulcerative colitis.
2. Anal fissure. 7. Bacillary dysentery.
3. Amoebic dysentery. 8. Diverticulitis.
4. Carcinoma colon. 9. Infarction of gut.
5. Colonic polyps. 10. Angiodysplasia.
Irritable bowel syndrome is a common functional bowel disorder, espe-

cially in young and middle-aged adults. They present clinically in either
of the three ways: with chronic abdominal pain and constipation (spastic
colitis), chronic intermittent often painless watery diarrhea, or a combi-
nation of both. The basic pathology is altered intestinal motility. A good
history, exclusion of the relevant causes, establishes a diagnosis.
Irritable Bowel Syndrome: Diagnosis

There should be at least a 12-week history of abdominal discomfort or pain, intermit-
tent or continuous in last one year with two of the following once per week (Rome II
criteria).
1. Pain relieved by defecation.
2. Change in bowel frequency.
3. Change in bowel consistency.
No evidence of inflammatory, neoplastic, metabolic, or anatomic pathology to explain
the features.
Supporting features
Stools >3 per day or less than 3 per week.
Stools are loose and watery or hard and lumpy.
Incomplete evacuation, straining, or urgency.
Mucous in stools.
Bloating or feeling of abdominal fullness.
Look for other cause especially if
Stool for occult blood is positive.
There is history of weight loss.
There is fever.
(Continued)
Irritable Bowel Syndrome: Diagnosis

Examination is remarkable.
Patient awakens at night with symptoms.
There are abnormal labs.
Inflammatory bowel disease IBD (also called Granulomatous colitis)

includes Ulcerative Colitis and Crohn’s Disease. Both are associated with
chronic diarrhea (bloody more common in ulcerative colitis) with bloat-
ing, cramping abdominal pain, occasional nausea, vomiting with weight
loss and fatigue. They primarily affect the bowel, but have many extra-in-
testinal manifestations like arthritis (especially affecting the knees), liver
disease, uveitis, and pyoderma gangrenosum (ulcerated and gangrenous
skin lesions). In Volume II also see X-ray of ulcerative colitis in Figure
63, and Crohn’s disease in Figure 64, also see endoscopic appearance of
Crohn’s disease in Figure 98 and ulcerative colitis in Figure 99. MRI of
Crohn’s disease is shown in Figure 79.
Differences Between Ulcerative Colitis and Crohn’s Disease

Ulcerative colitis Crohn’s disease
Presentation Bloody diarrhea chronic diarrhea and crampy pain
Common site of pain Pain left lower abdomen pain right lower abdomen
Classic site Rectum always involved terminal ileum often involved
Pain Occasional frequent
Mucous Frequent occasional
Perianal disease No frequent (perianal skin tags)
Small intestinal obs. No May occur
Response to antibiotic No Yes
Coble stoning No Yes
Granuloma on biopsy No common
Skip lesions Absent common
Fistula and fissures Absent common
Strictures No common
Pseudopolyps Common absent
Abdominal mass Rare more common
Barium study lead pipe appearance string sign
Typical distribution Colon (back-wash ileitis) mouth to anus
Lesions Continuous inflammation skip lesion (patchy involvement)
Gross feature Extensive ulcers aphthous ulcers, cobble stone

Inflammation Mucosa and submucosal transmural involvement
Major complication Toxic megacolon strictures, abscesses, sinus and
and bleeding fistula formation
Cancer risk <5% 5–25%
With smoking Lower risk higher risk
Systemic symptoms Occasional frequent
Antibody in serum p-ANCA (perinuclear ASCA (anti-saccharomyces
anti-neutrophilic anti- cerevisiae antibody) +ve in half
body) +ve in two-third of the patients
In ulcerative colitis the treatment depends on the severity of disease.

High-grade fever, tachycardia, anemia, orthostatic hypotension, and
weight loss are systemic features suggestive of moderate to severe disease.
A sudden change in stool pattern (constipation) may be an indication for
development of toxic megacolon. Criteria of mild, moderate, and severe
disease are subsequently given.
Severity of Ulcerative Colitis and Crohn’s Disease

Mild Mod-Severe Fulminant
Stools /day <4 >6 >10
Blood in stool +ve or -ve +ve continuous
Anemia No mild transfusion
required
Tachycardia No yes yes
Fever No yes yes
Weight loss No some 10% of body weight
Abdominal tenderness No yes yes
Abdominal distension No yes yes
X-ray No No dilatation
Toxic patient No No yes
Prevalence 25% 45% <10%
Platelet count Normal Raised Raised
(Moderate is in between mild and severe disease)
Patients with inflammatory bowel disease commonly have liver

involvement which may take any form as shown in the following. The
commonest being pericholangitis.
Liver Involvement in Crohn’s Disease and Ulcerative Colitisd

Occur in about 15% over course of disease.
Pericholangitis. Focal and post-necrotic necrosis.
Hepatitis. Chronic active hepatitis.
Fatty change. Primary sclerosing cholangitis.
Amyloidosis and Hemosiderosis. Hyalne degeneration.
Extra-intestinal involvement in inflammatory bowel disease occurs in

about 15% over course of disease.
Extra-Intestinal Involvement in IBD

1. Arthritis of large joints especially knees.
2. Pyoderma gangrenosum.
3. Uveitis and episcleritis.
4. Clubbing.
5. Erythema nodosum.
6. Ankylosing spondylitis (may be associated).
7. Osteoporosis.
8. Iron, B12, folic acid, zinc, calcium, magnesium, Vitamin K deficiency.
9. Thrombo-embolic events and DVT.
10. Gallstones and kidney stones.
11. Fissures and fistula in Crohn’s.
12. Nephrolithiasis (mostly uric acid in UC and calcium oxalate in CD).
13. Aphthous stomatitis in Crohn’s.
14. Bronchiectasis.
15. Autoimmune hemolytic anemia.
Risk Factors for Colorectal Cancer in Ulcerative Colitis

1. Extent of disease (highest with pancolitis).
2. Duration of disease and younger age of onset.
3. Family history of gut cancer or primary sclerosing cholangitis.
Surveillance colonoscopy should be done once every three years and earlier when other
risk factors are present.
Diarrhea comes from the Greek word “dia,” meaning through and
“rhein,” meaning to flow. It is increase in frequency, loose in consistency, and
weight more than 200g per day or passage of loose or watery stools, three
or more times per day. Pathophysiologically, it may be classified as follows.
• Osmotic diarrhea: It is due to unusual amounts of poorly

absorbable, osmotically active solutes in the gut (lactose
intolerance, sorbitol, laxatives, and antacids).
• Secretory diarrhea: It is due to increased intestinal ion secre-
tion or inhibition of normal active ion absorption. (Cholera,
E. coli, VIPoma, medullary carcinoma of thyroid, carcinoid
syndrome, Zollinger–Ellison syndrome, bile salts, villous
adenoma). It does not respond to fasting.
• Inflammatory diarrhea: It is also called invasive diarrhea or
dysentery and is associated with fever, abdominal pain, and
blood with leukocytes in stool. Volume is usually <1L/24h.
It is secondary to colonic damage and exudation of mucus,
blood, and protein (ulcerative colitis, CD, microscopic colitis,
radiation enteritis, malignancy). Infecting agents include
shigella, salmonella, amebiasis, C. difficile, E. coli 0157:H7
toxin, ischemia, and CMV. Stool leukocytes is an inexpensive
test to differentiate inflammatory versus non-inflammatory
types.
• Non-Inflammatory diarrhea: It is watery, with nausea and
vomiting, volume >1L/24h, secondary to small intestine
disease. Norwalk and Rota virus, entrotoxins as in Giardia,
Staph. aureus, cholera. E. coli, bile acid, laxatives, and
malabsorption.
• Often two or more mechanisms may be present simultaneously.
• Malabsorption: It is said to be present when the fecal fat is
>7–10g/24h (chronic pancreatitis, tropical sprue, Whipple’s
disease, bacterial overgrowth, vagotomy, diabetes mellitus).
• Infections diarrhea: It is due to infectious agents, which are
commonly giardia, entamoeba histolytica, salmonella typhi,
cyclospora, while AIDS-related infections include cytomega-
lovirus and cryptosporidium.
• Motility disorders: May be associated with diabetic autonomic
neuropathy, hyperthyroidism, irritable bowel syndrome.
Diarrhea can be acute (less than 14 days) or chronic (>two weeks but
usually >one month). Chronic diarrhea may be inflammatory, osmotic
(malabsorption), secretory, motility-related, or factitious. Take a detailed

history in chronic diarrhea, try to determine the site of disease (small
bowel, large bowel, liver, pancreas, and so on) and effect of diarrhea (dehy-
dration, vitamin deficiency, iron deficiency, calcium deficiency, and so
on) and the cause (endemic area in amoebiasis, weight loss with cancer,
contact history in TB, features of liver disease, heart disease, HIV predis-
position, lactose intolerance, gluten sensitivity, features of thyrotoxicosis,
history of GI operation, and so on).
History
To determine the severity, site, cause, effect, and complications of disease:
1. Assess onset (what seemed to have precipitated it), duration, and severity of
diarrhea.
2. Stool color, consistency, volume, and frequency. Bloody diarrhea suggests inflamma-
tion, infection, or tumor.
3. Ask about the presence of mucous, blood, and tenesmus (it suggests dysentery, that is,
amoebiasis or shigellosis).
4. Fever, blood, and abdominal pain may suggest dysentery.
5. Recent travel (traveler’s diarrhea).
6. Unusual food ingestion (food poisonings).
7. Exposure to sick contacts or other people with same disease (cholera occurs in
epidemics).
8. Drugs taken in the recent past (especially antibiotics causing C difficile infection).
9. Relation to fasting (osmotic diarrhea ceases with fasting and secretory does not).
10. Family history (CD or ulcerative colitis or GI cancer).
11. Fecal incontinence.
12. Sexual practices and social habits (HIV).
13. Ask about features of steatorrhea (stools which are loose, frothy, silvery, foul
smelling, and difficult to flush), best seen in chronic pancreatitis.
14. Take history of weight loss (malignancy and TB or HIV).
15. Mushy stools appear oily are related to malabsorption.
16. Excessive flatus with diarrhea in CHO malabsorption.
17. Lactose intolerance is evident form history.
18. Nocturnal diarrhea or fecal soiling in autonomic neuropathy or sphincter
dysfunction.
19. Incomplete evacuation in IBS.
20. Look for features of various deficiencies (especially in chronic diarrhea).
Night blindness and hyperkeratosis of skin, in Vitamin A deficiency.
Leuconychia due to hypoalbuminemia.
Bruising, in Vitamin K deficiency.

Paresthesia may be seen in vitamin deficiency, especially B12.
Muscle wasting, decreased growth, and delayed wound healing with hypoproteinemia.
Tetany, in hypocalcemia.
Rickets in children and osteomalacia in adults, with Vitamin D deficiency.
Koilonychia and angular stomatitis in iron deficiency.
21. Non-GI causes like thyrotoxicosis, diabetic autonomic neuropathy, and medullary
carcinoma of thyroid are considered as a cause of chronic diarrhea when appropriate
history is present.
22. Try to exclude infection by sending the stool for culture and demonstrating parasitic
infestation.
23. Chronic liver disease and pancreatic causes are diagnosed by the history of such disease
in the past with abnormal liver or pancreatic function tests.
24. Try to rule out inflammatory causes (e.g., UC and CD) and neoplastic causes by
barium studies and endoscopic examination.
In any case of chronic diarrhea, a good history and examination may

suggest the diagnosis or direct toward targeted investigations. It should
also determine the severity, localize the disease to the anatomical site, pick
up complications, and determine the associated deficiencies.
Causes of Chronic Diarrhea

(Common Causes are Given in Italic Text)
Disease and Clue to the Diagnosis.
Giardiasis: weight loss and stool examination.
Chronicamoebiasis: endemic area, stool showing amoeba with ingested RBC.
Intestinal TB: history of contact, ileoceacel disease on barium biopsy oncolonoscopy.
Liver insufficiency: H/O liver disease and abnormal LFTs.
CD: extraintestinal manifestations, barium examination, and colonoscopy with biopsy.
Ulcerative colitis: chronic diarrhea with blood and extraintestinal manifestations, CT
with contrast and colonoscopy and biopsy.
Drugs: history and clear relation.
Thyrotoxicosis: clinically hyperthyroid with low TSH and high free T4.
Celiac disease: sensitivity to gluten and biopsy with IgA anti-transglutamase.
Tropical sprue: endemic area and response to tetracycline and folic acid.
Carcinoma colon: recent altered bowel habit in an elderly proved on endoscopic biopsy.
Acute pancreatitis: severe abdominal pain and markedly raised serum amylase (chronic
pancreatitis is intermittent with calcification of the pancreas with CT abdomen).
Bacterial overgrowth: intermittent diarrhea with predisposition to stasis or history of
bowel operation.
(Continued)
Causes of Chronic Diarrhea

(Common Causes are Given in Italic Text)
Intestinal operations: gastric operation or bowel resection.
Intestinal lymphoma: weight loss and lymphadenopathy.
Addison’s disease: pigmentation, hypotension with low AM cortisol.
Zollinger-Ellison syndrome: refractory ulcers with raised gastrin.
Carcinoid syndrome: episodic wheezing and flushing with raised 5 HIAA in urine.
Peutz-Jegher syndrome: oral pigmentation and intestinal polyposis.
Familial polyposis: barium or endoscopy.
Immunodeficiency: immunological tests.
Constrictive pericarditis: Kaussmaul’s sign, pulsus paradoxus, and echocardiography.
Autonomic neuropathy: long-standing diabetes.
Acute diarrhea is less than 14-day duration and usually due to infec-
tions or drugs. Contaminated food and water source is the commonest
cause. If due to preformed toxins, vomiting may be more prominent or
the only symptom.
Acute Diarrhea
1. Viruses: Rotavirus, Norwalk virus, and CMV.
2. Bacteria: Shigella, salmonella typhi, campylobacter, vibrio cholerae, E. coli.
3. Food poisoning: Salmonella, staph aureus, bacillus cereus, clostridium perfringens.
4. Drugs: Antibiotics, laxatives, magnesium-containing antacids, colchicine, digoxin,
quinidine, alcohol, H2-receptor antagonists, lactose- or sorbitol-containing
products.
Traveler’s diarrhea is commonly due to bacteria (over 80 percent),

viruses (5 to 8 percent), and parasites (less than 10 percent). Prevention
is with keeping good hygiene, regular hand washing, using bottled water,
pasteurized milk, and well-cooked food with avoidance of raw fruits and
vegetables and salads, and so on, from market places.
Traveler’s diarrhea
It may occur after the travel (makes you sorry you went). Most commonly E. coli.
1. Enterotoxins: Staphylococcus aureus, bacillus cereus, clostridium perfringens.
2. Bacteria: Shigella, salmonella species, enteroinvasive E. coli, Yersinia enterocolitica,
and Aeromonas species.
3. Viruses: Rotavirus, Norwalk virus.
4. Protozoa: Giardia lamblia, Entamoeba histolytica.
Left-sided disease is associated with small volume mushy stools, urge to

defecate, seldom foul-smelling, and occasionally, mixed with mucus, pus,
or blood with gripping hypogastric or LIF/RIF pain, which subsides after
an enema, a bowel movement, or the passage of flatus.
Organic diarrhea is sudden with a definable onset with daily occur-
rence; nocturnal symptoms; duration <3 months; weight loss >5kg; and
average daily fecal weight exceeding 400g.
Examination in Diarrhea
Signs to identify cause, severity, or complications of the diarrhea.
1. Signs of dehydration (to judge the severity and need for resuscitation).
2. Look for rigidity, guarding, and tenderness (complication of perforation).
3. Joint involvement (inflammatory bowel disease and Whipples disease).
4. Look for signs of chronic liver disease.
5. Thyroid swelling in thyrotoxicosis and medullary carcinoma of thyroid).
6. Lymphadenopathy (lymphoma, AIDS).
7. Hyperpigmentation (Addison’s and Whipples disease).
8. Dermatitis (pellegra and dermatitis herpatiformis in celiac disease).
9. Operation (vagotomy, ileal resection with dumping syndrome).
10. Eyes (uveitis in inflammatory bowel disease, Reiter syndrome).
11. Anus (perianal skin tag in CD, patulous in advanced age, general weakness, or
peripheral or central nerve involvement).
12. Signs of deficiency. (Vitamin A, B1, B2, B6, B12, C, D, K, Calcium, and protein.
and so on).
13. Kaposi sarcoma in AIDS.
Stool Examination
• Formed and brown are healthy or may be due to

incontinence.
• Blood outside of a normal, formed stool is likely to be
hemorrhoids, anal fissure, rectal tumor, or proctitis.
• Blood mixed with watery stool may be acute infectious
diarrhea or IBD.
• A yellow pasty stool is characteristic of giardiasis.
• Fatty, greasy stool may be seen in malabsorption syndrome
like chronic pancreatitis.
• Large flatus with a fatty, greasy stool may be seen in

carbohydrate malabsorption.
• Clear water with a solid, formed brown stool is likely to be
mixed with urine or factitious diarrhea.
• Semi-formed or pasty brown stool with mucus suggests
irritable bowel syndrome.
Investigations, procedures, or trials of therapy where diagnosis is not

possible.
• Stool culture, stool analysis with occult blood, WBCs, and

ova cyst.
• Stool for fat with Sudan stain.
• Clostridium difficile toxin and PCR for antibiotic-associated
colitis.
• Ultrasound abdomen for liver, pancreas, and gallbladder
disease.
• Thyroid function tests (serum calcitonin for medullary
carcinoma thyroid).
• Fecal electrolytes, osmolality, osmotic gap (for osmotic or
secretory process).
• Fecal pH is <5.3 in carbohydrate malabsorption.
• Endoscopy helps confirm antibiotic-associated colitis
(pseudomembraneous colitis) or IBD and tumors. Upper GI
endoscopy with small bowel biopsy is most useful in coeliac
and lymphoma.
• Barium x-rays of the stomach, small intestine, and colon
with chronic diarrhea for example, diverticulosis, CD, and
ulcerative colitis and GI tumors, and so on.
• Lactoferrin latex agglutination is a rapid semi-quantitative test
for fecal leukocyte detection, suggestive of invasive infectious
diarrhea.
• Do stool C/S when fever >101∞F; severe diarrhea; bloody
stools; fecal leukocytes, or occult blood; or persistent diarrhea
not treated with antibiotics is present.
• The Giardia stool antigen test is a rapid ELISA test with

98 percent sensitivity and 90 percent specificity.
• Serum antiendomysial antibody IgA assays to rule out celiac
sprue.
• Tumor markers like CEA (carcinoembryonic antigen), CA
19–9 for carcinoma pancreas, and alpha-fetoprotein for
hepatocellular carcinoma. Gastrin for Zollinger–Ellison
syndrome. 24-hour urine for 5 GIAA for carcinoid.
• Trial of lactose-free diet.
• Trial of treatment for IBS.
• Trial of salazopyrine or asacol for IBD.
• Trial of wheat-free diet for celiac disease.
• Trial of anti-tuberculous treatment.
• PBG or ALA in urine for acute intermittent porphyria.
Antibiotics in diarrhea are seldom required and most are self-limiting.

They are an important cause of diarrhea, especially pseudomembranous
enterocolitis (see Figure 104). Antibiotic may be used in the following
conditions:
• Entamoeba: Metronidazole + luminal antiamebic like

diodoquin.
• Salmonella: No antibiotic for nontyphoid, uncomplicated
diarrhea.
• Shigella: Moderate to severe cases: give ampicillin or
fluoroquinolone.
• Vibrio cholera: Use tetracycline.
• Yersinia: Give Bactrim, fluoroquinolones, or aminoglycosides.
• Campylobacter: Erythromycin may be used.
• C difficile: Omit antibiotics use oral metronidazole or
vancomycin or both.
• C perfringens: Do not treat with antibiotics.
• E. coli: Antibiotic increases HUS. Use Bactrim or third-
generation cephalosporins.
• Aeromonas species: Use third-generation cephalosporins.
• Listeria: No antibiotics unless invasive (ampicillin and

Bactrim).
• Plesiomonas: Use Bactrim or cephalosporin.
Secretory diarrhea is usually >1.5 liter/d, does not respond to is com-

plete fasting, and is not associated with inflammation or irritation of the
gut mucosa. It may be of two types and is classified as follows:
Diarrhea with Increase in Adenyl Cyclase

Cholera. Bacillus cereus infection.
E. coli infection. Theophyllines and caffeine.
Dihydroxy bile acids.
Diarrhea without Increase in Adenyl Cyclase

Clostridium. Serotonin-induced.
Staphylococcal. Cholecystokinin-induced.
Occasionally shigella. Villous adenoma.
Phenolphthalein- and oxyphenisatin-induced.
Celiac disease is gluten sensitivity resulting in autoimmune damage

(T-cell mediated) to the upper intestinal villi, associated with diarrhea,
ballottement, and abdominal pain in relation to eating wheat and wheat
products (gluten an alcohol-soluble fraction of wheat protein).
• In 30 percent, symptoms begin in early childhood when

a child starts to take wheat products and may persist into
adulthood.
• Diarrhea is explosive initially, later pale, frothy, foul,
greasy with flatulence, abdominal cramps, weight loss, and
paresthesia. Most clinical features are related to the defi-
ciency of vitamins, proteins, and calories. There is failure to
grow.
• Relapse and remission may occur. Wheat, barley, rye, and oats
trigger the malabsorption.
• Corn, maize, rice sago, and soya are safe. Wheat, barley, barn,
noodles, pasta, rye are unsafe and avoided.
• There may be associated autoimmune hypoadrenalism and

hypopituitarism, diabetes mellitus, thyroiditis, and other
connective tissue disorders.
• Lactase deficiency may be associated, which complicates the
clinical picture.
• Glossitis, chelosis, stomatitis, cutaneous hyperpigmenta-
tion, abdominal distension, and mild tenderness are present.
Dwarfism, tetany, rickets, or osteomalacia, and signs of
vitamin deficiency may appear.
• An very itchy rash called dermatitis herpatiformis on the
extensor surfaces may be present in some cases (Figure 18).
• Diagnosis depends on compatible history with biopsy of
jejunum or duodenum showing classical villous atrophy and
positive serology. It responds to gluten-free diet.
• Jejunal biopsy shows absence of villi.
• Anti-gliadin, anti-transglutaminase, and anti endomysial anti-
body (95 percent) are present and aid in the diagnosis.
• Chance of malignancy of small bowel and non-Hodgkin
lymphoma is higher.
• Arthritis, hyposplenism, and metabolic bone disease may be
associated.
Serological Tests for Coeliac Disease

1. IgA endomysieal antibody (100 percent sensitive and 90 percent specific).
2. IgA tissue transglutaminase (very specific).
3. IgG tissue transglutaminase (for diagnosis of coeliac in IgA deficient patients).
4. IgA and IgG antigliadien antibodies rarely used for diagnosis.
5. HLA DQ2 and DQ8 positivity not required in most.
Tropical sprue is a form of environmental enteropathy found in the

tropics (in the area around a band north and south of the equator to 30º
latitude). Patients present with chronic diarrhea associated with flatten-
ing of the villi in the small intestine (less than in coeliac disease). The
age of onset is not typically six months to two years as in celiac disease,
and there is no relation to wheat products. Patients may have fever, mal-
aise and fatigue, indigestion, steatorrhea, and abdominal cramps. There
may be features of Vitamin A, D, K, and B12 deficiency along with

iron deficiency. Folic acid deficiency is present, and its replacement may
reverse the signs and symptoms (serves as a diagnostic test). Other diar-
rheal infections and diseases have to be excluded along with over growth
syndromes, lymphoma, and GI malignancy. Barium study reveals dilata-
tion, thickening, and edematous mucosal folds with flocculation in entire
small intestine. A prolonged course of an antibiotic like Co-trimoxazole
or tetracycline for three to six months is given along with folic acid and
replacement of other deficient vitamins or iron as required.
Mesenteric ischemia is mostly suspected in the elderly patients (in
younger patients with obvious cause) with abdominal pain, especially
after meals when increased blood supply is required (intestinal angina).
Arterial occlusions are acute, while venous occlusions may produce
chronic symptoms. Plain x-ray abdomen may show thumb printing, but
may be normal and serves more to exclude other causes of pain. Color
Doppler ultrasound of the abdomen may identify the occlusion, espe-
cially venous (absence of flow). CT angiography (CTA) is quick, non-
invasive, and diagnostic (acute cannot be differentiated from chronic).
MRA and MRV take longer, but are diagnostic (without contrast MRI
has lower sensitivity). Splanchnic angiography is not required now-a-
days. Endoscopy done for other reasons may identify the affected bowel
(see Figure 103 in Volume II). Acute arterial embolism is the most seri-
ous, whereas arterial thrombosis and venous occlusion is more insidious
or subacute. Precipitating factors include advanced atherosclerosis, atrial
fibrillation, valvular heart disease, severe heart failure, shock, or hyperco-
agulable state. Malignancy, polycythemia, sickle cell anemia, pancreati-
tis, cirrhosis, hypotension, cardiomyopathies, and drugs like estrogens,
vasopressin, and pseudoephedrine, cocaine, and digoxin may rarely also
be associated.
Clinical Features of Mesenteric Ischemia

1. Sudden, severe disproportionate abdominal pain (usually periumbilical) in arterial
occlusion.
2. Intestinal angina (subacute) with thrombosis or venous occlusion.
3. Nausea and vomiting and fear of eating (pain worse after meals), and at times,
diarrhea.
4. Hematochezia occurs with bowel infarction.

5. High serum lactate in a predisposed patient with compatible history and leukocytosis
and high hematocrit.
6. No peritoneal signs, unless there is bowel infarction.
7. CTA shows SMA or SMV thrombosis, bowel wall edema, pneumatomosis, portal
vein gas, lack of bowel enhancement, or ischemia of other organs.
Carcinoid tumors are most commonly located in the terminal ileum.

When they spread to the liver, they may produce the typical triad of
diarrhea, wheezing, and flushing. In the heart, there can be pulmo-
nary and tricuspid valve thickening (pulmonary stenosis and tricuspid
regurgitation); in the GI, there may be diarrhea, cramps, nausea and
vomiting, hepatomegaly, and rarely, retroperitoneal fibrosis. Diagno-
sis requires 24-hour urine for 5-OH indole acetic acid (5-HIAA) and
imaging studies to locate the tumor (ultrasound, CT, and MRI with
contrast). Gastric carcinoid is shown in Figure 92. Other tests include
somatostatin receptor scintigraphy, capsule enteroscopy, endoscopy,
and biopsy.
Familial adenomatous polyposis (FAP) is an autosomal dominant dis-
ease, with a family history in about 80 percent cases. Clinically presents
with chronic diarrhea, is autosomal dominant, but symptoms usually
develop in childhood or adolescence. There is a chance of developing a
gut cancer possibly after 40 years. Various types of colonic polyps are
shown in Figure 100 in Volume II.
Clinical Features of Familial Adenomatous Polyposis

1. Age usually between 15 to 20 years. 5. Associated with adenoma and GI
carcinomas.
2. Abdominal pain. 6. Association with brain tumors.
3. Loose stool with blood and mucous. 7. Osteomas.
4. Weight loss. 8. Desmoid tumors and epidermoid cyst.
Colorectal cancer is a common disease of the elderly, being the third

most common cause of cancer death in the United States. Under the
age of 50 years. More than two-third of the patients are symptomatic.
Bleeding or hematochezia (more with right-sided cancer than left) is the
most common symptom associated with iron deficiency anemia; bring
the patient to the doctor’s attention. Rectal tumors are associated with
tenesmus, pelvic pain, and passage mucous with blood. Others include
change in bowel habit (with left-sided lesions, see Figure 72 and 85),
weight loss, pain, abdominal mass, or present with intestinal obstruction,
peritonitis, or severe bleeding. Some patients have metastasis at presen-
tation. Most elderly patients may remain asymptomatic, therefore the
importance of screening with colonoscopy (see Figure 101 in Volume II)
every 10 years or fecal immunochemical test (FIT for occult blood) if
they refuse colonoscopy. Second option is CT colonongraphy every five
years, FIT fecal DNA every three years, and flexible sigmoidoscopy every
5 to 10 years. Third option is capsule colonoscopy every five years. See
radiological images of colonic cancer in Figures 58, 72, and 85 with endo-
scopic appearance in Figure 101 in Volume II.
Investigations Include
1. Stool for fecal immunochemical test FIT.
2. Tumor markers including carcinoembryonic antigen (more for follow-up).
3. Colonoscopy or capsule colonoscopy.
4. CT colography.
5. Barium enema (double contrast).
6. Routine labs as required.
7. Tests to look for metastasis and for staging (CT scan of neck, chest, abdomen, and
pelvis, liver MRI, PET scan, and so on).
Intestinal obstruction is clinically recognized by increasing abdominal

pain (colicky), obstipation (complete constipation without even passage
of gas), and depending on the site of obstruction, vomiting (bilious) and
abdominal distension, which may be progressive. An urgent plain x-ray
of the abdomen (lying and erect) to look for multiple air and fluid levels
(Figure 52), abdominal ultrasound, and CT abdomen are required to
evaluate and diagnose the case. Free air under the diaphragm (Figure 52)
may be seen if there is rupture of viscera. In such cases, the abdomen is
rigid with guarding, and serum amylase is very high. Bowel sounds in the
initial stages of obstruction are increased (trying to overcome the obstruc-
tion, these being called borborygmi), but later the abdomen may be silent
with absent bowel sounds. Lower GI endoscopy may also be required for
diagnosis or for decompression.
Figure 52 Plain abdomen x-ray showing multiple air fluid levels
(arrows) with small bowels loop dilatation, highly suggestive of small
bowels obstruction. On the right gas under the diaphragm is seen
with hollow visceral perforation
Intestinal Obstruction
1. Adhesions and bands (usually 9. Mesenteric ischemia.
postoperative).
2. Malignancy (colorectal and gastric). 10. Gallstone ileus.
3. Acute appendicitis. 11. Tuberculous stricture.
4. Volvulus. 12. CD.
5. Hernia. 13. Parasites.
6. Intussusception. 14. Foreign body.
7. Fecal impaction. 15. Diverticular disease.
8. Near birth (imperforate anus, meconium ileus, volvulus, Hirschprung’s disease,

atresia).
An obstruction may be complete or incomplete, it may be mechanical

or adynamic, it may be small intestinal (high or low) or large intestinal,
and lastly, it may be simple or complicated, for example, strangulated
hernia. The cause may be in the lumen, in the wall or from outside in
mechanical obstructions.
Pseudo-obstruction can occur in a number of situations where the clin-
ical features may mimic obstruction, but in reality, there is none, and
there is no intra-abdominal disease. Causes can be divided into metabolic,
shock, retroperitoneal irritation, and drugs. Colonic pseudo-obstruction
may be associated with dilated cecum even up to 10 cm and dilated right-

sided colon on plain x-ray of abdomen (see Figure 69). Surgery is not
required and may increase mortality. Underlying causes need to identified
and treated while colonoscopic decompression may be offered.
Pseudo-Intestinal Obstruction
1. Hypokalemia. 7. Myxedema.
2. Pregnancy. 8. Intermittent porphyria.
3. Postoperative (especially GI 9. Drugs.
operations).
4. Diabetes (autonomic neuropathy). 10. Shock.
5. Uremia. 11. Stroke.
6. Myocardial infarction.
Lymphoma of the gastrointestinal tract may be Hodgkin lymphoma

(often localized to an axial group of lymph nodes, which spreads to nearby
nodes, or non-Hodgkin lymphoma (B cell or T cell type), which has
variable patterns, involves many peripheral lymph nodes with extranodal
involvement, and dissemination (see gastric lymphoma in Figure 94).
Particular types are more common at certain places like Burkitt’s lym-
phoma in Africa and heavy chain disease (alpha) in the Middle East.
Lymphadenopathy is the commonest presentation usually associated with
constitutional symptoms like fever, weight loss, night sweats, and at times,
pruritus in 30 percent of patients (these are associated with poorer progno-
sis). GI symptoms include abdominal pain, abdominal mass (ileium being
most common), features of obstruction, or even jaundice when bile duct
is involved. Chest, neurological, and bone involvement may be present.
Basic workup for lymphoma may be required.
• Complete blood count with differential.

• Peripheral smear to assess bone marrow function look for
abnormal cells.
• Renal and hepatic functions.
• Chemistry with blood glucose, calcium, albumin, and LDH
(increased in more than half of the cases).
• Beta-2 microglobulin elevation is associated with a poor
prognosis.
• Serum protein electrophoresis.

• HIV serology.
• Ultrasound abdomen.
• Pan CT scan with contrast or MRI.
• Lymph node biopsy.
• Bone marrow examination.
• Lumber puncture.
• Flow cytometry.
Volvulus is a complete twisting of a loop of intestine around its attach-

ment to the mesentery (see Figure 67 in Volume II). It can occur at any
site from the stomach to the sigmoid colon. In small children, it can pres-
ent with sudden onset of abdominal pain, bilious vomiting, and feeding
intolerance. In older children, vague features may be present, including
chronic intermittent vomiting and abdominal colicky pain, failure to
thrive, constipation, and bloody diarrhea. Examination may initially be
normal with later distension, tenderness, and obstructive features, and
untreated cases may develop ischemic bowel and sepsis. They have been
treated for irritable bowel syndrome and peptic ulcer disease.
Intussusception is a prolapse of a part of intestine, which along with
its mesentery, invaginates into an adjacent intestine like a telescope. It
presents with intermittent and colicky abdominal pain, vomiting, and
currant-jelly stools, most commonly in children. It commonly results in
intestinal obstruction if not transient. If untreated, it may result in isch-
emia of the bowel and sepsis. It can be enteroenteric, ileocolic, ileocecal,
or colocolic. Lipomas and polyps and malignant lesions of the gut may
serve as lead point, initiating the intussusception. Plain x-ray abdomen
may be initially normal or show small intestinal obstruction without a
localizing mass. One may also find lack of definition of the inferior part of
liver (absent liver edge sign), absence of gas in the right iliac fossa, a mass
in the right hypochondrium, and a crescent sign (due to intussuscepting
lead point bulging into the pocket of air. The right hypochondrial mass
and an “empty” right iliac fossa together constitute the classic “Dance’s
sign.” A barium enema, CT, or MRI is required to make a diagnosis.
Toxic megacolon is most commonly seen with inflammatory bowel
disease (early rather than late), infectious colitis, or ischemic colitis. The
patient is toxic, and colon is distended with a maximal colonic diameter

greater than 6cm on spine plain x-ray of the abdomen (see F igure 68 in
Volume II). It mostly involves the right or transverse colon. There may
be fluid levels with loss of haustrations with deep ulcers appearing as cav-
ities between projections. Ultrasound and CT scan are further useful in
diagnosis, whereas colonoscopy may be dangerous. Diarrhea, commonly
with blood, abdominal pain, and distension, are the usual presenting fea-
tures. On examination, the patient is febrile, toxic, tachycardiac, and at
times, having an altered level of consciousness. There is abdominal dis-
tension with tenderness with, at times, signs of peritonitis. It carries a
mortality of about 30 percent. Treatment varies depending on the cause
of toxic megacolon. The differential diagnosis includes Hirschprung’s
disease, megacolon occurring with chronic constipation, and intestinal
pseudo-obstruction. A dilated colon in a toxic patient may be seen in
volvulus and obstructing tumors.
Diagnostic Criteria of Toxic Megacolon

Colonic dilatation >6cm on x-ray + any three of the following:
1. Fever more than 38∞C.
2. Pulse rate more than 120 per min.
3. Leukocytosis more than 10,500/cumm with polymorpholeukocytosis.
4. Anemia.
Plus at least one of the following:
Dehydration. Electrolyte abnormality. Hypotension. Altered sensorium.
Appendicitis is the result of acute inflammation and infection of

the appendix. Clinically, the patient presents with pain classically in
the right iliac fossa associated with fever, nausea, and vomiting. Pain
may initially start in the periumbilical region (T10 innervation of the
appendix) and later settling in the right iliac fossa. Complication of
perforation (see Figure 71 in Volume II) is associated with generalized
abdominal pain, guarding, and rigidity indicative of peritonitis. Irrita-
tion of malpositioned appendix over the duodenum results in nausea
and vomiting, while irritation of the rectum results in dysentery-like
symptoms, and the ureter may result in dysuria. On examination, the
maximum area of tenderness is at the McBurney’s point. There may be
rigidity, guarding, and rebound tenderness. Pain in the right iliac fossa
due to palpation, or percussion in the left iliac fossa is indicative of

peritoneal irritation and called Rovsing’s sign. With retroceacal appen-
dix, hyper-extension of the leg at the hip while the patient is lying on
the left lateral side results in pain; this is called psoas sign. Internal rota-
tion of the flexed right thigh causing pain due to a pelvic appendicitis
is called obturator sign.
Differential Diagnosis of Appendicitis in Adults

1. Pelvic inflammatory disease. 10. Inflammatory bowel disease.
2. Renal calculi and pyelonephritis. 11. Colonic cancer.
3. Mesenteric lymphadenitis. 12. Gallstone ileus.
4. Typhilitis. 13. Ileo-ceacal tuberculosis.
5. Diverticulitis. 14. Healminthic infection.
6. Meckel diverticulum. 15. Ischemic bowel.
7. Henoch Schonlein purpura. 16. Diabetic ketoacidosis.
8. Volvulus, intussusception of intestine. 17. Hemolytic uremic syndrome.
9. Ovarian cyst, torsion, ectopic pregnancy, endometriosis.
Diverticulosis of the colon is most common on the left side (see

Figure 102 in Volume II). A low-fiber diet predisposes to mucosal her-
niation. In the west, about one-third of the population has diverticulosis
by age 50 years, and about two-thirds have it by age 85 years. It is com-
plicated by infection (diverticulitis) in about 10 to 25 percent of cases.
Patients present with a constant but vague deep abdominal pain,
which later localizes in the left lower quadrant. When diverticulitis devel-
ops, there is bloating, flatulence with either diarrhea, or constipation. The
patient may have fever and have features of acute abdomen. If there is
irritation of the urinary tract, it may cause urinary frequency and dysuria.
On examination, there is fever, tenderness in the left iliac fossa, disten-
sion, and sometimes, a mass (inflamed loops of bowel or an abscess).
Rectal examination may demonstrate left-sided tenderness and occult
blood in the stool.
Complications of Diverticulitis
1. Pericolic abscess. 4. Sepsis.
2. Colonic perforation. 5. Bowel obstruction.
3. Fecal peritonitis. 6. Fistula formation.
The initial investigations include complete blood cell count, urinal-

ysis, plain x-rays abdomen, ultrasound abdomen, urea, creatinine and
electrolytes, LFTs, LDH and blood sugar level. The most important test for
diagnosis is a CT scan to determine the extent of the disease and identify
complications. It may show wall thickening, inflammatory stranding, out
pouching, free gas in perforation, and abscess formation. Barium contrast
studies and colonoscopy or sigmoidoscopy is best avoided in the acute
setting. One has to differentiate acute diverticulitis form inflammatory
bowel disease, ischemic colitis, appendicitis, colon malignancies, irritable
bowel syndrome, urolithiasis, urinary tract infection, and various gyneco-
logic or obstetric problems in females.
Clinical Examination: Percussion

Percussion of the abdomen is done for the following reasons:
a. To determine enlargement of abdominal viscera (liver, spleen, and

urinary bladder).
b. To differentiate an enlarged kidney from a spleen in the left hypo-
chondrium.
c. To determine the presence of ascites by shifting dullness and fluid
thrill.
d. To determine a cystic fluid thrill in a localized effusion like a hydatid
cyst.
e. To demonstrate a tympanic note due to excessive gaseous distension.
f. To look for gas under the diaphragm in ruptures of abdominal
viscera.
The rules and technique of percussion have been mentioned in the

respiratory system. The same rules and techniques apply to the gastroin-
testinal system.
1. For the liver, start to percuss lightly from the RIF, working your
way up to the right hypochondrium. Before commenting on liver
enlargement, always percuss heavily the upper border of the liver to
determine its span.
2. For the spleen, start to percuss from the RIF toward the LHC at an
angle parallel to the margin of left of the lower ribs. Also, percuss in
the last intercostal space in the MCL in deep expiration and then in
deep inspiration. A minor splenic enlargement will produce a dull
note on inspiration, which becomes resonant on expiration. One can
also percuss from the back to the front between the 9th and 11th ribs,
as this is the normal anatomical position of the spleen.
3. Demonstrate the shifting dullness and fluid thrill first, and if neces-
sary, puddle sign.
a. Shifting dullness is demonstrable when ascites fills at least two-
third of the abdominal cavity. The dullness is not shifted if the
abdominal cavity is full of fluid.
With the patient lying supine, the maximum resonance
above and below the umbilicus is determined. (Make sure that
the dullness over the urinary bladder is marked beforehand or
the patient has emptied his bladder.) Then proceed to percuss
in either flank (preferably toward the side without any visceral
enlargement), until a stony dull area is reached. At this point,
DEMONSTRATION OF
SHIFTING DULLNESS
Resonant
Dull at Dull at
in centre
the sides the sides
When the patient lies supine the gas filled bowels

float to the top and fluid settels in dependent area
Fluid
When the patient turns to either side the fluid shifts

down due to effect of gravity thus converting the
upper area resonant and dependent area dull.
Figure 53 Demonstration of shifting dullness when there is free fluid

in the peritoneal cavity
Figure 54 Method of demonstrating fluid thrill is shown. The

examiner percusses heavily with the forefinger and feels the thrill with
the palm of the other hand as shown
turn the patient toward the opposite side while keeping your
hand in same place. Percussing this area after a few moments
reveals a tympanic resonant note due to shift of the free fluid
toward the dependent side and air filled bowels float to the top
(Figure 53). One may reconfirm by again percussing toward the
center to find dullness that again becomes resonant when the
patient is lying flat.
b. Fluid thrill: Fluid thrill may be demonstrated when large quan-
tity of fluid is present (usually more than 1–2 liters) so that it
occupies most of the abdominal cavity. With the patient lying
supine, feel the thrill on the palm of the left hand placed over the
lumbar region, as the opposite flank is heavily tapped with the
index finger (Figure 54). The hand of the patient is kept in the
middle to stop the transmitted impulse from abdominal wall.
c. Puddle sign is a sign to demonstrate small amounts of free fluid in
the peritoneal cavity, but it is not very useful.
d. Encysted fluid may be checked by firmly encircling the cyst with
the left ring and index fingers. The middle finger is kept away
from the abdomen, in the extended position. When it is sud-
denly tapped on the abdomen, as in percussion, the other two
fingers feel a thrill (Figure 55).
It is, however, an unreliable test and rarely used these days.
Such encysted fluids (hydatid cyst in the liver or spleen or other
Figure 55 For encysted fluid, a cystic thrill is being demonstrated
fluid filled cysts like pseudo-pancreatic cyst) are best diagnosed

by an ultrasound examination.
4. Percussion of the urinary bladder is done from the epigastrium
toward the pubic area. Normally, this area is resonant, but if the
bladder is full, as in urinary retention, it will be dull, depending on
the amount of distention. In females, make sure that it is not an
enlarged uterus by asking the patient about pregnancy and hearing
fetal heart sounds.
5. Percussion is helpful to delineate an enlarged ovarian cyst or tumors.
It arises from either iliac fossa and extends toward the umbilicus. It is
dull on percussion with a tympanic note at the surroundings.
6. Percussion may be used to delineate the boundaries of enlarged
abdominal viscera or other abdominal mass. It may help to deter-
mine solidity, spread, or extension. This may, however, be better
achieved by careful palpation of the area as well.
Applied Medicine
Ascites or collection of free fluid in the abdomen is most commonly due to

cirrhosis and portal hypertension (see Figure 44 and detail on page 66 and
67, and spontaneous bacterial peritonitis on page 70), heart failure, renal
disease, or malignancy (these three constitute about 80 to 90 percent of
the causes). In endemic areas, tuberculosis should be considered high in
the differential diagnosis.
Common Causes of Ascites

1. Cirrhosis 80 percent
2. Malignancy 10 percent
3. Heart failure 4 percent
4. TB 2 percent (higher in Asia)
5. Dialysis 1 percent
6. Pancreatic 1 percent
7. Others 2 percent
It is frequently noted that multiple causes are responsible.
Ascites may be due to a local process (these are mostly exudates like
malignancy and infections) or part of a generalized process which are
mostly transudative (CCF, CKD, CLD, hypoproteinemia, and so on).
Other causes include severe hypoproteinemia from any cause, especially
nephrotic syndrome, malnutrition, and protein losing enteropathy.
Constrictive pericarditis produces disproportionate ascites compared
to edema. Still other causes include alcoholic hepatitis, veno-occlusive
disease, associated with hemodialysis, chylous ascites, pancreatic disease,
myxedema, Whipple’s disease, and so on. More than 5 percent patients
may have more than one cause of the ascites, especially in patients with
multiple co-morbidities. To determine the cause of ascites, look for pre-
disposition factors, features of underlying disease, if any, and investiga-
tions already performed.
Categories of the Causes of Ascites

1. Portal hypertension: Cirrhosis of the liver, Budd–Chiari syndrome, portal vein
thrombosis, NASH and NAFLD, alcoholic steatohepatitis.
2. Cardiac: Right heart failure, constrictive pericarditis, CCF.
3. Malignant: GI malignancies, peritoneal carcinomatosis, liver metastasis, lymphoma.
4. Renal: Nephrotic syndrome, chronic renal failure, peritoneal dialysis.
5. Gastrointestinal: Protein losing entropathies, pancreatitis.
6. Infections: Tuberculosis, bacterial peritonitis, pancreatitis, connective tissue diseases,
familial Mediterranean fever.
7. Pulmonary: Cor pulmonale.
8. Gynecological: Ovarian tumors (Meig’s syndrome).
9. Chylous: Obstruction of thoracic duct.
10. Miscellaneous: Myxedema, endometriosis, Whipple’s disease, eosinophilic
gastroenteritis, and polyserositis.
Also, see more information of ascites in cirrhosis of liver and portal

hypertension in Volume II of the book (CT scan Figure 76), portal vein
thrombosis (Figure 109 and text), Budd–Chiari syndrome (Figure 114
and text), and tuberculous ascites (figure 126 and text).
SAAG (Serum to Ascitic Albumin Gradient

Serum albumin–ascetic albumin. If >1.1g%, consider portal hypertension
with 97 percent accuracy.
High SAAG >1.1. Low SAAG <1.1
Portal HTN drives fluid into abdomen. Protein leakage is followed by fluid
collection.
Cirrhosis. TB peritonitis.
Alcoholic hepatitis. Malignant ascites.
Cardiac failure and ascites. Bowel obstruction or infarction.
Budd–Chiari syndrome. Peritoneal carcinamatosis.
Portal vein thrombosis. Serositis.
Myxedema. SLE.
Fatty liver of pregnancy. Whipple’s disease.
Ovarian tumors.
Pancreatic ascites.
Protein loosing enteropathy.
Malnutrition.
Liver metastasis.
Investigations are dictated by the history and examination. However,

an ultrasound examination, with Doppler if required, diagnostic ascitic
tap, and CT abdomen and pelvis are essential in most cases. LFT, kidney
function tests, amylase, echocardiography, x-ray chest, and pulmonary
function tests, TFT, endoscopy, and connective tissue disease workup
may be required.
Investigations of Ascitic Fluid

1. Ascites may be clear, turbid (usually infection), bloody (usually malignant), or
milky (likely chylous).
2. Total cell count and differential (high polys in acute infections and predominant
lymphocytes in TB and any chronic ascites). Total cell count is high in infections or
exudates and low in transudates.
3. An ascites neutrophil count >500 and pH <7.35 is diagnostic of spontaneous bacterial
peritonitis. If the count is <250, a positive culture is required to make the diagnosis.
(Continued)
Investigations of Ascitic Fluid

4. Total protein content is >2.5g% in exudates and <2.5g% in transudates. Ascitic to
serum protein ration is <0.5 in transudate and >0.5 in exudates.
5. Ascitic to serum LDH is <0.6 in transudate and >0.6 in exudates.
6. A total serum albumin ascitic gradient (SAAG ratio) is high in portal hypertension
(>1.1gm/dl gives a 97 percent accuracy) and suggests a nonperitoneal cause of
ascites.
7. LDH (when high, suggests infection or malignancy or perforations).
8. Gram stain of the ascitic fluid. Gram stain and culture may be positive for bacteria
in spontaneous bacterial peritonitis and perforations.
9. Stain for acid-fast bacilli (mycobacterium tuberculosis).
10. Cultures (aerobic, anaerobic, and for TB). MBTB via PCR may be positive in tuber-
culosis. The adenosine deaminase activity is high and mesothelial cells are absent
from the ascitic fluid in tuberculous ascites.
11. Glucose.
12. Amylase is high in bowel perforation and pancreatitis.
13. Triglycerides is high in chylous ascites. Appears milky if >200mg% TG.
14. Cytology for malignancy (ascetic alpha-fetoprotein can also be done)
15. Ascetic lactate and pH have unclear utility.
16. Cholesterol level of >48mg% has a sensitivity and specificity >95 percent for
malignant ascites.
17. Serum pro brain natriuretic peptide (pro-BNP) is high in heart failure.
18. Bilirubin with brown fluid and suspected biliary perforation.
Intestinal tuberculosis may present with ileo-ceacal mass, tuberculous

lymphadenitis, tuberculous ascites, or military tuberculosis. Tuberculosis
is suspected especially in endemic areas in patients with associated low-
grade fever, night sweats, weight loss, vague ill health, history of contact,
or HIV positivity.
Workup for Suspected TB Ascites

1. Ascitic fluid MBTB PCR.
2. Smear positivity is <2%.
3. Culture form one liter fluid has about 70 percent sensitivity.
4. Laparoscopic biopsy has the highest yield approaching 100 percent.
5. Adenosine deaminase in the fluid may be useful in endemic areas.
6. PPD skin hypersensitivity test is not useful.
Clinical Examination: Auscultation

Bowel sounds are normally audible at a rate of about 6 times per m inute.
Increased bowel sounds are called borborygmi and may be heard in
diarrhea, early intestinal obstruction, and with gastrointestinal bleeding
(blood being an irritant, stimulates peristalsis).
AUSCULTATORY AREAS OF
THE ABDOMEN
Hepatic bruit in hepatoma Splenic rub
in infarction
Renal artery bruit

just lateral and
above umbilicus
in renal artery
Bowel stenosis
sounds
Abdominal aorta
bruit in aneurysm
Venous hum
in portal hypertension Inguinal ligament
Fetal heart sounds
Figure 56 Areas on the abdomen where auscultation may be done
Bowel sounds may be absent in late intestinal obstruction, perito-

nitis, or in severe hypokalemia. On auscultation, also comment on any
bruit over the liver, spleen, or kidneys. Rarely, a venous hum may be
heard between the umbilicus and xiphi sternum in cirrhosis. In pregnant
females, the fetal heart sounds may be heard with the fetoscope. The site
of auscultation in this case varies with the position and lie of the fetus.
Rectal and Genito-Urinary Examination

It is an essential part of GI examination and should be done after taking
proper permission and in privacy. Females should be examined in the
presence of a nurse. Always wear gloves during these examinations. Anat-
omy is shown in Figure 57.
Superficial examination includes looking for skin changes, ulcers,
rashes, nodules, swellings, infections, discharge, congenital anomalies,
and so on. Genital ulceration can be present in infections (Herpes sim-
plex and syphilis) and connective tissue disorders like Reiter’s syndrome
and Behçet’s syndrome or associated with squamous cell carcinoma.
Urinary bladder Rectum
Spine
Anal sphincter
Prostate
Testis Palpating finger in the anus
Figure 57 The prostate is felt like a chestnut by the pulp of the finger
Local Rectal Examination

1. Skin tags. 5. Ulcer and abscess.
2. Anal fissure. 6. Hematoma.
3. Fistula and sinus. 7. Warts.
4. External piles or hemorrhoids. 8. Rash.
For per-rectal examination, the patient is made to lie in the left lat-
eral position at the edge of the bed with the hip and knees well flexed.
Stand on the right side of the patient, facing his feet, and perform a local
examination with the buttocks separated with the left hand. After wearing
gloves and having richly lubricated the index finger of the right hand with
lubricating gel (usually lignocaine gel), gently insert the pulp of the finger
facing down, into the rectum as the patient is asked to bear down. Abort
the examination if it is very painful.
Per Rectal Examination

1. Feel the tone of the sphincter.
2. Feel the rectal canal irregularity and lumps.
3. Note any mass.
4. Feel the prostate in males.
5. Feel rectovasicular pouch in males.
6. Feel rectouterine pouch in females.
7. Look for stain on the finger upon withdrawal (blood, mucous, pus).
The prostate is felt with the pulp of the finger (after turning the hand
180°) like a firm smooth and rubbery swelling 2–3cm diameter. The
median sulcus is felt vertically between the lateral lobes. The overlying
mucosa should be smooth and mobile. In carcinoma of the gland, it
becomes hard (as if calcified) with irregular and nodular lateral surface. In
acute prostatitis, the gland is very tender.
In females, the cervix is felt like the tip of the nose, anteriorly. Press
the suprapubic area for a bimanual examination of uterus and ovarian
swelling. Remember that about 90 percent of rectal cancers are reach-
able by the finger and are felt as nodular, ulcerating, or cauliflower like
mass.
Genitourinary examination is a part of the urological and surgical
examination and is mentioned briefly here to complete the gastroentero-
logical examination.
Examination of the Male Genitalia

The scrotum is examined while the patient stands
1. Size (the left testis hangs slightly lower). Non-palpable testis may be due to unde-
scended testis, previous surgery, or retracted testis. In this case, look for it in the
inguinal canal (it can develop malignant change with time). Small size may be due
to hypogonadism or atrophy from chronic liver disease, alcohol, or drugs.
2. Swelling may be due to presence of fluid (Scrotal edema is common in any general-
ized cause of edema). Varicose veins feel like a bag of worms. The left varicocele may
be associated with left renal tumors or left renal vein thrombosis.
3. Look for any skin diseases, lesions, ulcers, and rashes, for example, scabies.
4. Consistency and fluctuation. Normal is firm, non-fluctuant, and mildly tender. Hard-
ness may be a sign of malignant change.
5. Tenderness. (Palpate gently with index finger and thumb). Orchitis is associated with
severe tenderness. Consider mumps if there is history of parotid gland swelling with
fever. Torsion is associated with pain and higher position of the testis.
6. Surface and shape.
7. Feel the epididymis and above it, the vas deferens and spermatic cord. They can be
involved in infection, for example, epididymo-orchitis.
8. Presence of bowel in the scrotum is indicative of indirect inguinal herniation (the
upper border is not palpable, with swelling descending from the abdomen).
9. Transluminancy is done to confirm the presence of fluid in the scrotum (hydrocele).
A solid mass will not transluminate (likely a tumor).
The pelvic examination is not a part of the GI examination unless

especially indicated. It is done with the gynecological examination and by
a trained gynecologist.
Examination of the Female Pelvis

With a nurse being present, and the patient lying in lithotomy the position
and urinary bladder emptied, take permission and begin examination
while wearing gloves
1. External genitalia examined for rashes, inflammations, swelling, ulcers, and so on.
Look for thrush, trichomonas, herpes, warts, abscess, Bartholin’s cyst. A discharge
may be bloody (menses, cancer, erosion, polypor mischarge), pus (is indicative of
inflammation or infection), clear of frothy and pale-yellow and itchy (in tricho-
monas) or whitish curdy or cheesy (in candidiasis).
2. Look for cystocele and rectocele while the patient is made to bear down.
3. Do a per vaginal examination with a lubricated index and middle fingers. Feel the
cervix and note its size, shape, tenderness, mobility, and consistency. Also feel the
fornices. Note any inconsistency and masses.
4. Note urinary incontinence by asking the patient to cough.
5. Do a bimanual palpation of the uterus with per vaginal and suprapubic palpation
simultaneously. Note the position of the uterus, size, consistency, tenderness, and
mobility. Fibroids are the commonest cause of uterine enlargement.
6. Do a visual examination of vagina and cervix with a well-lubricated speculum
inserted with blade closed and opened when fully inserted. Take a cervical smear for
cytology and vaginal smear for trichomonas, thrush, and hormonal assessment.
Summary of Examination
1. Approach the patient from the right, after a quick introduction and
permission, properly position and expose the patient as necessary
according to need and customs.
2. A quick visual survey during the initial approach to look for:
Jaundice, pallor, pigmentation, rash, and xanthelasma.
Signs of liver cell failure.
Signs of portal hypertension.
Signs of malabsorption.
Clubbing, leuconychia, palmer erythema, Dupuytren’s contracture,
and flapping tremor.
3. Quick look at the mouth, tongue, throat, and neck.
4. Look for abdominal distention, dilated veins, tap marks, striae,
bruising, pulsations, and peristalsis. Look at the umbilicus, hernial
orifices, and pubic hair for any abnormality.
5. Superficially palpate the abdomen and then do deep palpation tak-
ing extra care not to hurt the patient and ask him or her a couple
of times if there is any tenderness. Look for rigidity and guarding.
Palpate the various viscera with the correct method and note all the
details if any abnormality is detected. Lastly, feel for an aortic aneu-
rysm and the inguinal lymph nodes.
6. Heavy percussion is done to determine the upper border of the liver
on the right and the edge of the spleen on the left. Examine for fluid
thrill and shifting dullness.
7. Auscultate the abdomen for bruits and bowel sounds. Rarely, a
venous hum or a rub over the liver or spleen may be heard.
8. Take permission to examine the external genitalia and rectal exam-
ination.
Investigations and Procedures

Some important diagnostic tests, both general and specific, in relation to
gastroenterology are given as follows. The choice of tests depends on the
clinical suspicion.
1. Complete blood analysis and ESR.

2. Urinalysis.
3. Liver function tests.
4. Kidney function tests.
5. Thyroid functions.
6. Hepatitis profile.
7. Coagulation profile.
8. Lipid profile.
9. Septic screen.
10. Stool analysis (occult blood and ova and cysts).
11. Fecal immunochemical tests (FIT) or fecal occult blood test (FOBT).
12. Stool for C difficile (PCR).
13. Stool culture.
14. Total fat in stool.
15. Qualitative and quantitative PCR tests for hepatitis B and C.
16. Iron study, Vitamin B12, and folic acid levels.
17. Plain x-ray of the abdomen.
18. Abdominal ultrasonography with Doppler examination, if required.
19. Serum enzymes, for example, amylase, lipase, and so on.
20. CT scan of the abdomen with oral and IV contrast.

21. Triphasic CT abdomen.
22. Fibroscan (Transient elastography or fibroSure). It may be better
than biopsy at predicting HCV-related complications and five-year
mortality.
23. CT cholangiography.
24. Liver and spleen radionuclide scan.
25. MRI of the abdomen and pelvis.
26. Tumor markers.
27. Autoimmune markers, for example, for autoimmune hepatitis, anti-
LKM, and other autoimmune diseases that may affect the GI system.
28. Anti-mitochondrial antibody (chronic active hepatitis).
29. Anti-smooth muscle antibody (primary biliary cirrhosis).
30. Anti-saccharomyces cerevisiae antibody and p-ANCA (in Crohn’s
disease and ulcerative colitis, respectively).
31. IgA endomyseal antibody and IgA tissue transglutaminase (celiac
disease).
32. HIDA scan.
33. Upper GI endoscopy and biopsy.
34. Sigmoidoscopy or colonoscopy and biopsy.
35. Endoscopic retrograde cholangio-pancreatography (ERCP).
36. Barium swallow.
37. Barium meal and follow through.
38. Barium enema or double contrast.
39. Crosby peroral small bowel biopsy.
40. Capsule endoscopy and balloon and spiral enteroscopy.
41. Liver biopsy.
42. Gut hormones, including gastrin levels.
43. 5-OH indole acetic acid in 24-hour urine (carcinoid syndrome).
44. 24-hour urine for vanillylmandelic acid (VMA) in pheochromocy-
toma.
45. Pancreatic function tests.
46. D-xylose absorption test.
47. Mantoux and MBTB PCR for tuberculosis.
48. Lactose tolerance test.
49. Serum lactate level.
50. Schilling’s test (Vitamin B12 deficiency).
51. Breath test (for bacterial overgrowth).

52. Serum ammonia levels (for hepatic encephalopathy).
53. Angiogram (CT angiography).
54. Oral or i/v cholecystography.
55. Lymph node biopsy.
56. Porto-cavography.
57. Echocardiography.
58. Bernstein acid perfusion test.
59. Gastric analysis.
60. Toxicology screen.
61. HIV.
62. Laparoscopy.
63. Manometric bowel studies.
Specific Biochemical Tests

Tumor markers are not generally used for screening purpose, rather to
see the response to treatment or follow post-operatively to look for recur-
rence. They may be raised in other non-cancerous conditions and must
be interpreted in conjugation with the history, examination, imaging, and
biopsy. Some markers may indicate prognosis and treatment.
1. Carcinoembryonic antigen is a marker of gastrointestinal malignancy,

but also seen in breast, lung, gastric, pancreatic, bladder, kidney,
thyroid, head and neck, cervical, ovarian, liver malignancies. Slight
elevation may be seen in cigarette smokers, pancreatitis, hepatitis,
IBD, peptic ulcer disease, hypothyroidism, cirrhosis, and COPD.
2. High alpha-fetoprotein indicates hepatocellular carcinoma. It is also
raised in germ cell cancers of ovaries and testes. Slight high levels
may be present in liver cell regeneration, pregnancy, and IBD.
3. Anti-mitochondrial antibody is a marker of primary biliary cirrhosis.
4. Anti-smooth muscle antibody is found in most cases of chronic
active hepatitis or autoimmune hepatitis.
5. Amylase when very high is associated with pancreatitis, but may also
rise with acute surgical abdomen and parotitis.
6. Alkaline phosphatase, if very high, is seen in primary biliary
cholangitis, other causes of obstructive jaundice, or bone disease.
The isoenzyme of alkaline phosphatase may be required to determine

if it is coming from the bone or liver.
7. PSA (prostate-specific antigen) is raised in prostate cancer, but
inflammation of the gland may also raise it slightly.
8. Gamma-glutamyltransferase (GGT) is quite specific in detecting
early liver damage.
9. High levels of acid phosphatase are found in cancer of the prostate.
10. Very high gastrin levels are seen in Zollinger–Ellison syndrome.
11. Acid phosphatase and more commonly done PSA levels are high in
carcinoma of the prostate.
12. High levels of CA-19-9 are seen in pancreatic, colorectal, liver,
and stomach cancers. Slight elevations may be seen in pancreatitis,
inflammatory bowel disease, and thyroid disease.
13. BTA (bladder tumor antigen) may be seen in urinary bladder,
kidney, and ureter cancers. Infections of the urinary tract may raise
it slightly.
14. High CA-125 is typically found in ovarian cancer, but may be seen
in colorectal, breast, liver, and lung cancers also. Some elevation may
be seen in pregnancy, endometriosis, ovarian cysts, pelvic inflamma-
tory disease, pancreatitis, and chronic liver disease.
15. Fecal calprotectin is high in intestinal inflammatory conditions like
inflammatory bowel disease where it may be used as a diagnostic
and prognostic marker, coeliac disease, infectious colitis and colonic
cancer. It is normal in irritable bowel syndrome.
Paracentesis or ascitic tap is indicated for the diagnosis of various

causes of ascites and to rule out infection or suspected spontaneous bac-
terial peritonitis. Most of these collections are exudative, and turn out
to be malignant or tuberculous. On the other hand, a transudate is a
generalized process usually due to heart failure, cirrhosis of liver, kidney
disease, or hypoproteinemia, with collection of fluid in most other sites as
well. Large volume paracentesis is done to rescue the patient from acute
distress, discomfort, or threat of compression from tense ascites and respi-
ratory embarrassment.
It is best done under ultrasound guidance. It is usually avoided in an
uncooperative patient, pregnancy, severe bowel distension, extensive skin
disease, and uncontrolled coagulopathy.
Before the procedure, always do a CBC, urea, creatinine and electro-

lytes, LFT, coagulation profile, LDH, serum albumin, and abdominal
ultrasound.
Send the ascetic fluid for the following:
• TLC and differential count.

• RBC count.
• Ascitic albumin and protein.
• Ascitic LDH.
• Ascitic sugar.
• Gram stain.
• Cytology for malignancy.
• MBTB PCR is suspected.
• Ascitic fluid culture.
• Amylase, if required for pancreatitis.
• Triglyceride level, if chylous ascites suspected.
Complication and risk of tap or paracentesis include:
• Significant bleeding.
• Infection.
• Renal failure.
• Hyponatremia.
• Hepatic encephalopathy.
• Complicated bowel perforation.
• Paracentesis leak.
Paracentesis is performed under aseptic conditions wearing surgical

gloves. Pigtail drainage is best done under ultrasound guidance by the
radiologist. Bedside diagnostic ascetic tap is explained next:
• You need 2.5ml syringe for lignocaine, if required. 10ml

syringe for obtaining fluid with 20ml and 50ml syringes, and
a three-way tap available for more fluid. Aseptic skin prepara-
tion tray should be available with drapes, pyodine and alcohol
swabs, sterilized gauze pieces, opsite, and tape.
• Explain the procedure to the patient, mention the risks, and

obtain written consent.
• The patient is positioned in the supine position with head
somewhat elevated to drain the fluid to the dependent lower
abdomen.
• The best area may be 5cm above and medial to the anterior
superior spine (lateral to the rectus abdominus). Palpate and
percuss the area beforehand to avoid solid viscera or masses
and making sure there is fluid in the area and not gas. Note
that the inferior epigastric vessels run up the lateral border of
rectus abdominus to meet the superior epigastric vessels.
• Insert the needle of the syringe vertically with a single push
while applying slight negative pressure. This will instantly
suck the fluid and avoid over penetration, especially into the
bowel wall. For small fluid collections, or large volume para-
centesis, ultrasound guidance is required.
• Take out about 20–50ml fluid, and send to the lab in differ-
ent samples for hematology, biochemistry, histopathology, and
molecular biology.
• If large drainage is required, an IV cannula is used via a
Z-shaped oblique tract, so that the entrance hole and exit
hole in the abdomen are not superimposed to avoid leakage
after the procedure. The needle is removed and the cannula is
attached to the drip set and the other end to the urine bag for
collection of 1–2 liters at a time.
• For large volume paracentesis (more than five liters), replace-
ment with IV albumin at the rate of 8g per liter of ascites
may be required after the procedure. During the removal of
larger volume, the patient needs to be constantly monitored,
as there may be drop in BP. This requires IV fluid replenish-
ment and transiently stopping or reducing the rate of removal
of fluid. Complications of large volume paracentesis include
acute kidney injury, hypotension, and hyponatremia.
• After the procedure monitor the patient carefully for any signs
of shock and peritoneal irritation.
• For recurrent ascites in terminal patients, for example, under-

lying malignancy, a permanent drain may be left in place,
which does carry a higher risk of infection.
Scheme of Gastrointestinal Examination

Helpful Points in General Physical Examination
Anemia_______ Jaundice_______ Pigmentation___________

Tongue___________ Lymph nodes_________________________
Signs of liver cell failure_____________________________________
Features of portal hypertension _______________________________
Features of malabsorption____________________________________
Inspection
Shape of abdomen: Normal _______
Distended _______ Local _______ Generalized _______
Movement: Normal _______ Abnormal _______
Striae _______ Scar_______ Tap marks______________
Epigastric Pulsation _______________ Bruising _______________
Veins _______ Direction of flow_______
Peristalsis: _______ Direction_______
Umbilicus: Normal ______ Everted _______ Shifted _________
Hernial orifices: Normal______
Diagnosis___________________________________________
Palpation
Tenderness: Absent _______ Present _______ Site_______
Rebound _______ Rigidity _______ Guarding _______
Abdominal girth _______ cm.
Liver: Upper border ________ Span _______

Size in MCL _______ Consistency _______ Tender_______
Pulsation _______ Shape _______ Surface _______
Mobility _______ Bruit _______
Spleen: Normal _____ Enlarged __________________________
Notch _______ Tender _______ Bruit _______
Size in mid-clavicular line _______
Kidneys: Normal _______ Palpable_______ Tenderness _______
Gall Bladder: Normal _______ Murphy’s sign _______
Epigastrium: Normal _______ Mass _______ Splash _______
Hypogastrium: Normal _______ Mass _______
Iliac Fossa: Right _________________ Left _________________
Auscultation
Bowel sounds: Normal _______ Increased _______
Absent _______
Bruits: Not present _______ Kidney _______
Liver _______ Spleen _______
Diagnosis:
About the Author
Dr Mushtaq Haroon, born on 27-03-1956 in Pakistan, is an academi-
cian, educationist, and consultant in Medicine for over 25 years with over
10 year’s experience as Professor of Medicine at various Medical Colleges
in Pakistan. To his credit, he has 25 publications in peer-reviewed medical
journals and published five medical books as first author. He completed his
early training in Medical Unit 1 of Services Hospital attached to Allama
Iqbal Medical College, Lahore and went to UK for higher training. He
passed MRCP in 1988 and was awarded FRCP from London in 2000.
Dr Haroon has been a pioneer in computer-based medical educa-
tion, having developed a vast collection of software for teaching. He was
awarded the Life Time Achievement Award for “The Most Distinguished
Iqbalian for professional excellence” by the Chief Minister of Punjab
in Dec 2008. He is presently consultant in King Fahad Armed Forces
Hospital Jeddah, KSA.
List of Contributors
Mushtaq Haroon
MBBS (Pb); MCPS (Pak); MRCP (UK); FRCP (London)
Consultant Internal Medicine
King Fahad Armed Forces Hospital, Jeddah, KSA
Ex Professor and Head of Department
King Edward Medical University, Lahore, Pakistan
Chief Editor
Contributions
Sundus Mariyum Husnain
MBBS (Pb), FCPS (Pak).
Physician/Senior Registrar,
Allama Iqbal Medical College, Lahore, Pakistan.
Coeditor
Samir Ashfaq
MD
Fellow, Gastroenterology
Texas A&M Health Science Center,
Baylor Scott & White Health Center, Gastroenterology
Coeditor
Dr. Bahaa Elden Kailani

MBBS FRCP.
Consultant Gastroenterologist and Hepatologist,
King Fahad Armed Forces Hospital, PO BOX
9862, Jeddah 21159, Saudi Arabia.
bkailani@hotmail.com
Contributed the images in the endoscopy section
150 LIST OF CONTRIBUTORS
Dr. Ahmad Mohammad Ghanim

MD, JMCB
Consultant Diagnostic Radiology
Radio-diagnostic & Medical Imaging Department,
King Fahad Armed Forces Hospital/POBOX 9862, Jeddah 21159,
Saudi Arabia.
amhg3@yahoo.com
Contributed the images in the radiology section
Index
AAT. See Alpha-1 antitrypsin Chronic diarrhea, 113
deficiency Chronic kidney disease (CKD),
Abdominal movements, 48 88–89
Abdominal pain, 11–14 Chronic malabsorption, 39
Achalasia, 99–100 Chronic pancreatitis, 105
Acute abdomen, 57–58 Cirrhosis, 61–65
Acute cholecystitis, 92 CKD. See Chronic kidney disease
Acute diarrhea, 114 Clubbing
Acute fatty liver disease of pregnancy causes of, 35
(AFLP), 75 clinical presentation, 33–34
Acute hemorrhagic pancreatitis, 40 methods for demonstration, 33
Acute hepatitis, 70–71 other types of, 35–36
Acute pancreatitis, 103 pathogenesis, 34–35
AFLP. See Acute fatty liver disease of Colonic pain, 106
pregnancy Colorectal cancer, 121–122
Alcoholic liver disease (ALD), 81 Congestive hepatomegaly, 82
ALD. See Alcoholic liver disease Constipation, 19–20
Allergy and immunization history, 8
Alpha-1 antitrypsin deficiency (AAT), Diagnosis, 2
82 Diagnostic tests, 139–141
Anemia Diarrhea, 19, 110–112
clinical features of, 27–28 Diffuse esophageal spasm, 99
etiology of, 25–26 Diverticulosis, 127–128
examination, 24 Dupuytren’s contracture, 38
history of, 25 Dyserythropoietic anemia, 26
laboratory features of, 28–29 Dyspepsia, 18
Anorexia, 16 Dysphagia, 16–17
Antibiotics in diarrhea, 117–118
Appendicitis, 126–127 Early satiety, 20
Ascites, 131–134 Edema, peripheral, 36
in cirrhosis, 70 Encysted fluid, 130
Auscultation, 135 Eosinophilic esophagitis, 101
Autoimmune hepatitis, 80–81 Epigastric pulsations, 48–49
Esophageal dysphagia, 17
Barrett esophagus, 103
BMI. See Body mass index Familial adenomatous polyposis, 121
Body mass index (BMI), 21–22 Family history, 6–7
Boerhaave syndrome, 15, 100–101 Fever, 20
Bowel sounds, 135 Flatulence, 18
Fluid thrill, 130
Carcinoid tumors, 121 Focal nodular hyperplasia, 78
Celiac disease, 39, 118–119 Functional dyspepsia, 97
152 Index
Gallbladder Inspection, clinical examination

acute cholecystitis, 92 abdominal movements, 48
enlarged with jaundice, 92 epigastric pulsations, 48–49
enlarged without jaundice, 92 hernial orifices, 52
palpation, 91–92 pigmentation and rashes, 49–50
tumors, 92–93 prerequisites of, 46
Gastroesophageal reflux, 98–99 prominent veins, 50–51
Gastrointestinal examination scheme, pubic hair, 51–52
145 scars and tap marks, 52–53
Genito-urinary examination, 135–137 shape of abdomen, 48
Globus pharyngeus, 17 striae, 50
Guarding, 56 umbilicus, 52
Gums, oral examination, 43 visible peristalsis, 51
Intestinal obstruction, 122–123
Halitosis, 18–19 Intestinal tuberculosis, 134
Heartburn, 16 Intestines
Hematemesis, 15 acute diarrhea, 114
Hematochezia, 15–16 antibiotics in diarrhea, 117–118
Hematuria, 89–91 appendicitis, 126–127
Hemolytic anemia, 26 carcinoid tumors, 121
Hepatic adenoma, 78 celiac disease, 118–119
Hepatic encephalopathy, 68–69 chronic diarrhea, 113
Hepatic jaundice, 31 colorectal cancer, 121–122
Hepatocellular carcinoma, 78–79 diarrhea, 110–112
Hepatorenal syndrome, 81–82 diverticulosis, 127–128
Hereditary hemochromatosis, 82–83 familial adenomatous polyposis,
Hernial orifices, 52 121
History of presenting illness, 3–4 inflammatory bowel disease,
History taking 108–110
allergy and immunization history, 8 intestinal obstruction, 122–123
description of, 1–2 intussusception, 125
direct questioning, 5 irritable bowel syndrome, 107
family history, 6–7 left-sided disease, 115
objective of, 2 lymphoma of gastrointestinal tract,
occupational history, 8 124–125
past history, 5–6 melena, 107
personal history, 7 mesenteric ischemia, 120
presenting complaints, 3 organic diarrhea, 115
socioeconomic status, 8 pseudo-obstruction, 123–124
travel history, 8 secretory diarrhea, 118
treatment history, 9 stool examination, 115–117
H pylori testing, 95 toxic megacolon, 125–126
Hypersplenism, 85 Traveler’s diarrhea, 114
Hypochromic anemia, 25 tropical sprue, 119–120
volvulus, 125
Inflammatory bowel disease, 39–40, Intussusception, 125
108–110 Iron deficiency anemia, 28–29
Inherited disorders, 7 Irritable bowel syndrome, 107
Index 153
Jaundice surface anatomy, 58

eyes in, 41 viral hepatitis, 71–75
hepatic, 31 Wilson’s disease, 82
obstructive, 31 Lymphoma of gastrointestinal tract,
pathophysiology, 30–31 124–125
Kayser-Fleischer ring, 41 Macrocytic anemia, 25, 29

Kidneys Malabsorption, 19
chronic kidney disease, 88–89 Mallory-Weiss syndrome, 15
differential diagnosis, 86 Mallory-Weiss tear, 100
hematuria, 89–91 Marfan syndrome, 6
left kidney enlargement vs. splenic Melena, 107
enlargement, 87 Mesenteric ischemia, 120
palpation, 85–86 Metastasis, 80
Microcytic anemia, 25
Left-sided disease, 115
Leuconychia, 38 NAFLD. See Nonalcoholic fatty liver
Leukoerythroblastic anemia, 25 disease
Leukoplakia, 42 Nausea and vomiting, 14–15
Lips, oral examination, 42 Nonalcoholic fatty liver disease
Liver (NAFLD), 81
abscess, 75–76 Normochromic anemia, 25
acute fatty liver disease of Normocytic anemia, 25
pregnancy, 75
acute hepatitis, 70–71 Obesity
alcoholic liver disease, 81 co-morbidities, 22
alpha-1 antitrypsin deficiency, 82 nutritional status, 21–22
ascites in cirrhosis, 70 secondary causes of, 22–23
autoimmune hepatitis, 80–81 Obstructive jaundice, 31
causes of, 60–61 Occult blood loss, 16
characteristics, 59–60 Occupational history, 8
cirrhosis, 61–65 Occupational lung disease, 8
congestive hepatomegaly, 82 Oral examination
focal nodular hyperplasia, 78 lips, 42
hemangiomas, 78 teeth and gums, 43
hepatic adenoma, 78 throat, 45
hepatic encephalopathy, 68–69 tongue, 43–44
hepatocellular carcinoma, 78–79 Organic diarrhea, 115
hepatorenal syndrome, 81–82
hereditary hemochromatosis, Palpation, clinical examination
82–83 initial requirements, 53–54
mass, 76–78 scheme of, 54
metastasis, 80 types of, 54–55
nonalcoholic fatty liver disease, 81 Pancreas
palpation, 58–59 acute pancreatitis, 103
portal hypertension, 66–68 chronic pancreatitis, 105
primary biliary cirrhosis, 79 pancreatic cancer, 106
primary sclerosing cholangitis, Paracentesis, 142–145
79–80 Past history, 5–6
154 Index
Peptic ulcer disease, 94–95 carcinoma of stomach, 97

Percussion, clinical examination diffuse esophageal spasm, 99
ascites, 131–134 eosinophilic esophagitis, 101
intestinal tuberculosis, 134 functional dyspepsia, 97
rules and techniques, 128–131 gastroesophageal reflux, 98–99
Peripheral edema, 36 H pylori testing, 95
Personal history, 7 Mallory-Weiss tear, 100
Peutz-Jegher’s syndrome, 39 peptic ulcer disease, 94–95
Physical findings, 2 Plummer-Vinson syndrome, 102
Pigmentation, 49–50 succussion splash, 94
Plummer-Vinson syndrome, 102 upper GI bleeding, 97–98
Portal hypertension, 66–68 Virchow’s lymph node, 94
Pre-rectal examination, 137 Zenker’s diverticulum, 102–103
Presenting complaints, 3 Zollinger-Ellison syndrome, 96–97
Primary biliary cirrhosis, 38, 79 Stool examination, 115–117
Primary sclerosing cholangitis, 79–80 Striae, 50
Prominent veins, 50–51 Succussion splash, 94
Pruritus, 20 Superficial examination, 135
Pseudo-obstruction, 123–124
Pubic hair, 51–52 Tap marks, 52–53
Puddle sign, 130 Teeth, oral examination, 43
Throat, oral examination, 45
Rashes, 49–50 Tongue, oral examination, 43–44
Rebound tenderness, 56 Toxic megacolon, 125–126
Rectal examination, 135–137 Traveler’s diarrhea, 114
Retrosternal burning, 16 Travel history, 8
Rigidity, 56 Treatment history, 9
Tropical sprue, 119–120
Scars, 52–53
Secretory diarrhea, 118 Umbilicus, 52
Shape of abdomen, 48 Upper GI bleeding, 97–98
Shifting dullness, 129–130
Small intestinal pain, 106 Viral hepatitis, 71–75
Socioeconomic status, 8 Virchow’s lymph node, 41, 94
Specific biochemical tests, 141–145 Visceral pain, 11
Spleen Visible peristalsis, 51
applied medicine, 84–85 Vitamins, 23–24
palpation, 83–84 Volvulus, 125
surface anatomy, 83 Vomiting, 14–15
Splenectomy, 85
Splenic infarction, 85
Weight loss, 20
Splenomegaly, 84
Wilson’s disease, 82
Steatorrhea, 19
Stomach and esophagus
achalasia, 99–100 Xanthelasma, 39
Barrett esophagus, 103
Boerhaave syndrome, 100–101 Zenker’s diverticulum, 102–103
cancer of esophagus, 101–102 Zollinger-Ellison syndrome, 96–97
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EBOOKS Clinical Examination and Applied

Clinical Examination and Applied Medicine, Volume I

MOMENTUM PRESS, LLC, NEW YORK

Copyright © Momentum Press, LLC, 2018.

All rights reserved. No part of this publication may be reproduced,

First published in 2018 by

ISBN-13: 978-1-94664-693-4 (paperback)

Momentum Press Health Education C

Cover and interior design by Exeter Premedia Services Private Ltd.,

First edition: 2018

Printed in the United States of America.

Examination of the tongue 43

Causes of chronic diarrhea 113

This new edition has been thoroughly revised and updated. It is

Objective of History Taking

A good history should be able to fulfill these objectives. History is not

In the preceding example, rheumatoid arthritis, although did not

Details of History of Presenting Illness

Details of History of Presenting Illness

Each presenting complaint is pursued with relevant questions until all

Patient with Epigastric Pain

During history taking, the doctor is thinking about peptic ulcer

Direct Questioning in History

Details of Past Illness

Direct questions about common diseases like diabetes, hypertension,

Common GI Disease with Familial Incidence

Various diseases tend to run in families and have different modes of

Some Chromosomal Disorders

Occupational Lung Disease

History of Allergy and Immunization

It is mandatory to take a detailed history of the past medical and surgical

Some Related Questions

In a patient with IBD for example, it is important to note:

Without this information, adjustment of therapy may not be ideally

A good history should give a reasonable diagnosis of the patient’s problem

traumatic, genetic or congenital, toxic or metabolic disorder. Examination

manifests by nutritive problems with changes in stool quantity and qual-

Causes of Abdominal Pain

Although separated into different varieties of pain, most situations

Abdominal Pain According to Anatomy

Abdominal Pain According to Anatomy

Questions in Relation to Pain

Severe pain in the abdomen may be due to many surgical emergen-

Acute Abdominal Pain—Non-surgical

Figure 1 Abdominal pain may be obvious as in this case of herpes

In order to reach a diagnosis, it is important to consider the anatom-

Causes of Acute Abdomen Pain (Surgical Intervention

2. Acute appendicitis. 8. Intussusception.

Nausea and vomiting is a feature of a broad range of GI and extra-in-

Causes of Nausea and Vomiting

It is important to ask relevant questions to determine the severity and

Questions in Relation Vomiting

Hematemesis is due to leakage of blood from esophagus to the sec-

Clinical evidence of continued bleeding includes a rapid pulse

are neuromuscular findings, it may require a videofluoroscopic swallow-

Questions for Dysphagia

Globus pharyngeus occurs in an anxious patient, usually a female, who

Flatulence is excessive gas in the abdomen, which ultimately is passed

Red Flags in Dyspepsia

Halitosis or malodorous breath is most commonly due to local causes

It is important to rule out organic causes such as those aforemen-

Nutritional Status and Obesity

Obesity is being considered as a disorder of energy homeostasis. About

5. Clubbed or bulbous appearance of the finger tips.