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Jarrah Ali Al-Tubaikh

Internal Medicine
An Illustrated Radiological Guide

Second Edition
Jarrah Ali Al-Tubaikh
Department of Clinical Radiology
Amiri Hospital – Kuwait City
Kuwait City, Kuwait

All illustrations marked with were drawn by the author.

ISBN 978-3-319-39746-7 ISBN 978-3-319-39747-4 (eBook)

DOI 10.1007/978-3-319-39747-4

Library of Congress Control Number: 2016954639

© Springer International Publishing Switzerland 2017

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically
the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way,
and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology
now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the
absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for
general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and
accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to
the material contained herein or for any errors or omissions that may have been made.

Printed on acid-free paper

This Springer imprint is published by Springer Nature

The registered company is Springer International Publishing AG Switzerland

Preface
It is a privilege to write another introduction to
this book. When I wrote this book in Munich in
2010, I knew I was writing a book with an uncom-
mon combination, linking internal medicine to
radiology. I can still remember the comment of my
mentor Prof. Maximillian Reiser after he saw the
manuscript’s content. He told me: “Why did you
choose this layout and these disorders in particu-
lar?” I replied: “They are the most commonly
encountered diseases daily in any busy medical
department.”
Over the years, I have noticed how the chapter’s
download numbers are increasing in Springer’s
official website. This reflects, to me at least, the con-
tinuous demand for such topics worldwide, espe-
cially among newly coming radiologists. They are
the ones facing the fire daily in duties and emer-
gency calls from physicians and surgeons around
the clock. Moreover, radiology board teachings
concentrate more and more over emergency cases,
trauma cases, postoperative complications, and
cancer screening and monitoring. I can assure you
that almost 90 % of any radiologist’s daily routine
lies within one or more of the past four areas in
radiology. Internal medicine disorders and com-
plications are considered extracurriculum, and
maybe special interest radiology.
Within the past 5 years since the publication of
this book, I have noticed a skyrocketing increase in
the radiological referrals through my work in two
different hospitals. Sometimes, we get radiological
referral for simple disorders that do not need
radiological investigation, for example, more and
more demands for ultrasound to exclude inguinal
hernias, ultrasound for lipoma, CT for acute
appendicitis suspicion, polytrauma PAN-CT, etc.
As a radiologist, it is always nice to be needed;
however, technology can be a double-edged sword,
reducing the clinical experience of both the refer-
ring clinician and the radiologist. Many physicians,
unfortunately, started to use radiology as a substi-
tute for clinical examination and judgment.
Although such a phenomenon is not necessarily
widely found, it is there, no doubt about it.
I am pleased that the first edition of my book has
helped many physicians I know to change their
perspective toward radiological investigations. I
have been contacted by many physicians here in
Kuwait and outside of Kuwait who thank me for
detailing what they should order and how to
V
investigate certain diseases. In the same fashion,
many radiologists are pleased with the variety of
images that detail the medical disorders and facili-
tate their detection.
Based on the past positive feedbacks, I aimed to
expand the range of the book by including three
more medical fields, which are not directly linked
to internal medicine but however are important to
know. The second edition of this book exposes the
reader to occupational medicine and toxicology,
which are uncommonly seen as cases of attempt-
ing suicide and accidental intoxications. The
radiological literature is filled with different radio-
logical signs reported by many researches detailing
intoxications, which have become of great interest
since the data are accumulating over the years.
Chiropractic and osteopathic medicine are two
important fields that emerged more than a hun-
dred years ago, and they are rarely, if ever, men-
tioned or taught in medical schools or
board-certification programs, especially in spe-
cialties related to the orthopedics or the spine.
Although they are not considered part of conven-
tional medicine, both specialties have very solid
neuroanatomical and neuropathophysiological
basis. Chiropractic medicine in particular, founded
by D. D. Palmar and perfected by B. J. Palmar, uses
radiology as an essential part of its diagnostic tech-
niques. Their radiographic imaging techniques are
known as “spinography.” Personally, I have been
using their radiographic techniques in an exten-
sive fashion to diagnose lower back pain and kine-
siological disorders. Their radiological imaging
techniques proved to be very valid and very accu-
rate in diagnosing lower back pain, especially lum-
bar spine MRI with almost normal findings.
Unfortunately, such radiological knowledge is very
rarely encountered in commonly known radiolog-
ical journals. I sincerely hope that the reader will
find the chapter of chiropractic medicine imaging
interesting and informative.
Lastly, a very new medical specialty is arising
within the past 5 years: energy and quantum med-
icine. Although it started with the book What Is
Life? (1944) by the Nobel Prize winner Austrian
physicist Erwin Schrödinger, many new medical
and biological researchers are now using quantum
physics to define life, including Robert O. Becker,
Jerry Tennant, Hans-Peter Dürr, Fritz-Albert
Popp, Mae-Wan Ho, and so many others. Their
VI Preface
works have now evolved to so many applications,
emerging as unconventional therapies that use
waves and frequencies to heal, such as pulsed elec-
tromagnetic field (PEMF) therapy, microcurrent
therapy, phototherapy, and ultrasonic therapy. I
have been personally using these devices for myself
and my relatives and for special cases in the hospi-
tal, with a high success rate of controlling diseases
and complications. I documented my findings on
radiological images, imaging patients before and
after such unconventional, energetic therapy to
find out what has been changed in the disease sta-
tus radiographically. I took the opportunity of
publishing the second edition of this book to
introduce the reader to a whole new world that
uses therapies based on biophysics rather than bio-
chemistry for conventional, pharmacological
medicine uses.
In conclusion, I hope for the reader an interesting
journey through the book, and I hope that this
book can help someone somewhere in the world
save a life.
Jarrah Ali Al-Tubaikh, MD
Kuwait City, Kuwait
 VII

Contents

1 Gastroenterology ............................................................................................................................................................ 1
1.1 Liver Cirrhosis......................................................................................................................................................................... 2
Types of Liver Cirrhosis ......................................................................................................................................................... 2
1.2 Fatty Liver Disease (Liver Steatosis) ............................................................................................................................. 15
Types of Liver Steatosis ......................................................................................................................................................... 15
1.3 Recurrent Epigastric Pain .................................................................................................................................................. 17
Gastroesophageal Reflux Disease ..................................................................................................................................... 17
Differential Diagnoses and Related Diseases ................................................................................................................. 18
Peptic Ulcer Disease ............................................................................................................................................................... 24
Superior Mesenteric Artery Syndrome (Wilkie’s Syndrome) ..................................................................................... 27
Median Arcuate Ligament Syndrome (Celiac Trunk Compression Syndrome/Dunbar’s Syndrome) ........... 29
Recurrent Abdominal Pain of Childhood ........................................................................................................................ 29
1.4 Inflammatory Bowel Diseases ......................................................................................................................................... 30
Crohn’s Disease ........................................................................................................................................................................ 31
Extraintestinal Manifestations of CD ................................................................................................................................ 31
Ulcerative Colitis ..................................................................................................................................................................... 36
Extraintestinal Manifestations of UC ................................................................................................................................ 36
Differences Between Ulcerative Colitis and Crohn’s Disease .................................................................................... 39
Differential Diagnoses and Related Diseases ................................................................................................................. 39
1.5 Gastrointestinal Hemorrhage ......................................................................................................................................... 40
1.6 Pancreatitis.............................................................................................................................................................................. 41
Acute Pancreatitis ................................................................................................................................................................... 41
Differential Diagnoses and Related Diseases ................................................................................................................. 41
Chronic Pancreatitis ............................................................................................................................................................... 45
1.7 Jaundice.................................................................................................................................................................................... 48
Kernicterus ................................................................................................................................................................................ 50
Obstructive Jaundice ............................................................................................................................................................. 50
Bile Plug Syndrome ................................................................................................................................................................ 52
Infectious Ascending Cholangitis ...................................................................................................................................... 52
Choledochal Web .................................................................................................................................................................... 53
1.8 Diarrhea and Malabsorption ........................................................................................................................................... 54
Normal Anatomy ..................................................................................................................................................................... 54
Pathophysiology ..................................................................................................................................................................... 54
Common Causes of Diarrhea and Their Mechanism of Action................................................................................. 54
Sprue ........................................................................................................................................................................................... 55
Whipple’s Disease (Intestinal Lipodystrophy) ................................................................................................................ 56
VIPoma (Werner–Morris Syndrome/Pancreatic Cholera) ........................................................................................... 57

2 Neurology ............................................................................................................................................................................ 59
2.1 Stroke (Brain Infarction) .................................................................................................................................................... 62
Differential Diagnoses and Related Diseases ................................................................................................................. 62
2.2 Stroke Diseases and Syndromes .................................................................................................................................... 66
Moyamoya Disease (Progressive Occlusive Arteritis) .................................................................................................. 66
Cerebral Amyloid Angiopathy ............................................................................................................................................ 68
CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts
and Leukodystrophy)............................................................................................................................................................. 69
MELAS (Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-Like Episodes) ................. 70
Cortical Laminar Necrosis..................................................................................................................................................... 71
Man-in-the-Barrel Syndrome .............................................................................................................................................. 72
Locked-In Syndrome .............................................................................................................................................................. 73
Brain Stem Infarction Syndromes ...................................................................................................................................... 73
Subclavian Steal Syndrome ................................................................................................................................................. 75
VIII Contents

2.3 Intracranial Hemorrhage ................................................................................................................................................... 76

Epidural Hematoma ............................................................................................................................................................... 77
Subdural Hematoma.............................................................................................................................................................. 78
Subarachnoid Hemorrhage ................................................................................................................................................. 79
Intracerebral/Intraparenchymal Hemorrhage ............................................................................................................... 80
Intraventricular Hemorrhage .............................................................................................................................................. 81
Hemorrhage into Malignancy ............................................................................................................................................. 82
2.4 Meningitis ................................................................................................................................................................................ 82
Differential Diagnoses and Related Diseases ................................................................................................................. 84
2.5 Encephalitis ............................................................................................................................................................................. 85
Limbic Encephalitis ................................................................................................................................................................ 85
Acute Demyelinating Encephalomyelitis (ADEM) ........................................................................................................ 87
Hashimoto’s Encephalitis...................................................................................................................................................... 88
Rasmussen Encephalitis (Rasmussen Syndrome) ......................................................................................................... 89
Measles Encephalitis .............................................................................................................................................................. 89
Subacute Sclerosing Panencephalitis (SSPE) ................................................................................................................. 90
Japanese Encephalitis ........................................................................................................................................................... 90
West Nile Encephalitis ........................................................................................................................................................... 90
Tick-Borne Encephalitis (Spring–Summer Encephalitis) ............................................................................................ 90
Murray Valley Encephalitis ................................................................................................................................................... 91
St. Louis Encephalitis ............................................................................................................................................................. 91
Encephalitis Lethargica ......................................................................................................................................................... 91
2.6 Epilepsy..................................................................................................................................................................................... 92
Differential Diagnoses and Related Diseases ................................................................................................................. 93
2.7 Headache ................................................................................................................................................................................. 96
Migraine ..................................................................................................................................................................................... 96
Spontaneous Intracranial Hypotension (Schaltenbrand Syndrome) ..................................................................... 97
Idiopathic Intracranial Hypertension (Pseudotumor Cerebri) .................................................................................. 97
Temporal (Giant) Cell Arteritis ............................................................................................................................................ 98
2.8 Multiple Sclerosis and Other Demyelinating Diseases ........................................................................................ 99
Multiple Sclerosis .................................................................................................................................................................... 99
Neuromyelitis Optica (Devic’s Syndrome) ...................................................................................................................... 101
Marburg’s Type MS ................................................................................................................................................................. 102
Baló Concentric Sclerosis ..................................................................................................................................................... 103
Schilder’s Disease (Diffuse Myelinoclastic Sclerosis) ................................................................................................... 103
Susac’s Syndrome ................................................................................................................................................................... 103
Guillain–Barré Syndrome ..................................................................................................................................................... 104
2.9 Parkinsonism .......................................................................................................................................................................... 106
Differential Diagnoses and Related Diseases ................................................................................................................. 107
2.10 Dementia .................................................................................................................................................................................. 108
Alzheimer’s Disease................................................................................................................................................................ 108
Vascular Dementia.................................................................................................................................................................. 109
Frontotemporal Lobar Degeneration (Pick’s Disease) ................................................................................................. 109
Dementia with Lewy Bodies ................................................................................................................................................ 111
Progressive Supranuclear Palsy (Steele–Richardson–Olszewski Syndrome) ....................................................... 111
Multiple System Atrophy (Shy–Drager Syndrome) ...................................................................................................... 112
Subcortical Arteriosclerotic Encephalopathy (Binswanger’s Disease) ................................................................... 113
Prion Disease ............................................................................................................................................................................ 114
2.11 Huntington’s Disease .......................................................................................................................................................... 116
Differential Diagnoses and Related Diseases ................................................................................................................. 117
2.12 Heat Stroke (Pancerebellar Syndrome)....................................................................................................................... 117
2.13 Aphasia ..................................................................................................................................................................................... 117
Neural Control of Speech ..................................................................................................................................................... 118
Aphasia Pathophysiology and Subtypes ......................................................................................................................... 118
2.14 Squint (Strabismus) ............................................................................................................................................................. 122
Neural Control of Ocular Muscles ...................................................................................................................................... 122
Pathophysiology ..................................................................................................................................................................... 122
Related Disorders .................................................................................................................................................................... 122
 IX
Contents

2.15 Nystagmus ............................................................................................................................................................................... 124

Neural Control of Eye Movement ...................................................................................................................................... 124
Nystagmus Subtypes ............................................................................................................................................................. 125
2.16 Erectile Dysfunction ............................................................................................................................................................ 126
Neural Control Human Sexual Behavior .......................................................................................................................... 126
Pathophysiology ..................................................................................................................................................................... 127
Erectile Dysfunction Differential Diagnoses................................................................................................................... 127

3 Endocrinology and Metabolism ............................................................................................................................ 131

3.1 Graves’ Disease (Hyperthyroidism) ............................................................................................................................... 132
3.2 Hyperparathyroidism ......................................................................................................................................................... 133
Differential Diagnoses and Related Diseases ................................................................................................................. 134
3.3 Growth Hormone Diseases............................................................................................................................................... 138
Growth Hormone Insufficiency (Hypopituitarism)....................................................................................................... 139
Acromegaly and Gigantism ................................................................................................................................................. 140
Growth Hormone Insensitivity (Laron Syndrome) ....................................................................................................... 143
Carney’s Complex ................................................................................................................................................................... 143
3.4 Osteoporosis........................................................................................................................................................................... 145
Primary Osteoporosis ............................................................................................................................................................ 145
Secondary Osteoporosis....................................................................................................................................................... 148
Regional Migratory Osteoporosis of the Hip (Bone Marrow Edema Syndrome) ................................................ 148
3.5 Rickets and Osteomalacia ................................................................................................................................................. 149
Differential Diagnoses and Related Diseases ................................................................................................................. 150
3.6 Scurvy ........................................................................................................................................................................................ 152
3.7 Fluorosis ................................................................................................................................................................................... 154
3.8 Lead Poisoning (Plumbism) ............................................................................................................................................. 156
3.9 Adrenal Glands Abnormalities ....................................................................................................................................... 157
Cushing’s Syndrome............................................................................................................................................................... 157
Conn’s Syndrome (Hyperaldosteronism) ......................................................................................................................... 158
Addison’s Disease.................................................................................................................................................................... 159
Pheochromocytoma .............................................................................................................................................................. 160
Neuroblastoma ........................................................................................................................................................................ 161
X-Linked Adrenoleukodystrophy ....................................................................................................................................... 161
Testicular Adrenal Rest Tumors .......................................................................................................................................... 162
3.10 Sex Hormone Abnormalities ........................................................................................................................................... 162
Polycystic Ovary Disease (Stein–Leventhal Syndrome) .............................................................................................. 163
Precocious Puberty ................................................................................................................................................................ 163
Van Wyk and Grumbach Syndrome .................................................................................................................................. 164
Gynecomastia .......................................................................................................................................................................... 165
Intersex Disorders ................................................................................................................................................................... 166
Differential Diagnoses and Related Diseases ................................................................................................................. 168
3.11 Sheehan Syndrome (Postpartum Hypopituitarism) ............................................................................................. 170

4 Nephrology ......................................................................................................................................................................... 173

4.1 Hypertension.......................................................................................................................................................................... 174
Renal Artery Stenosis ............................................................................................................................................................. 174
Coarctation of the Aorta ....................................................................................................................................................... 178
Polyarteritis Nodosa ............................................................................................................................................................... 179
Takayasu Arteritis .................................................................................................................................................................... 180
Midaortic Syndrome .............................................................................................................................................................. 181
Preeclampsia ............................................................................................................................................................................ 181
Reversible Posterior Leukoencephalopathy Syndrome (Hypertensive
Encephalopathy) ..................................................................................................................................................................... 182
Nephroptosis (Floating Kidney) ......................................................................................................................................... 183
Riley–Day Syndrome (Familial Dysautonomia) ............................................................................................................. 183
Stafne’s Bone Defect of the Mandible .............................................................................................................................. 183
Hypertensive Heart Disease ................................................................................................................................................ 183
X Contents

4.2 Polycystic Kidney Disease ................................................................................................................................................. 185

Autosomal Dominant Polycystic Kidney Disease ......................................................................................................... 185
Autosomal Recessive Polycystic Kidney Disease .......................................................................................................... 186
Acquired Polycystic Kidney Disease.................................................................................................................................. 187
Differential Diagnoses and Related Diseases ................................................................................................................. 188
4.3 Renal Failure ........................................................................................................................................................................... 188
Examples of Renal Parenchymal Disorders According to Their Anatomical Involvement............................... 188

5 Cardiology ........................................................................................................................................................................... 193

5.1 Acute Chest Pain ................................................................................................................................................................... 194
Acute Coronary Syndrome................................................................................................................................................... 194
Acute Pulmonary Embolism ................................................................................................................................................ 197
Aortic Dissection ..................................................................................................................................................................... 199
Aortic Intramural Hematoma .............................................................................................................................................. 201
Penetrating Atherosclerotic Ulcer ..................................................................................................................................... 202
5.2 Diseases of the Great Vessels .......................................................................................................................................... 202
Thoracic Aortic Aneurysm.................................................................................................................................................... 202
Pulmonary Hypertension ..................................................................................................................................................... 203
Coral Reef Aorta ...................................................................................................................................................................... 205
Superior Vena Cava Syndrome ........................................................................................................................................... 205
5.3 Myocardial Diseases (Cardiomyopathies) .................................................................................................................. 206
Hypertrophic Cardiomyopathy .......................................................................................................................................... 206
Dilated Cardiomyopathy ...................................................................................................................................................... 208
Restrictive Cardiomyopathy ................................................................................................................................................ 208
Arrhythmogenic Right Ventricular Dysplasia ................................................................................................................. 208
Noncompaction Cardiomyopathy (Spongy Myocardium) ........................................................................................ 209
Peripartum Cardiomyopathy (Cardiomyopathy of Pregnancy) ............................................................................... 210
5.4 Endocarditis ............................................................................................................................................................................ 210
Infective Endocarditis ............................................................................................................................................................ 211
Löffler’s Endocarditis (Eosinophilic Endomyocardial Disease) ................................................................................. 213
Marantic Endocarditis (Nonbacterial Thrombotic Endocarditis) ............................................................................. 214
5.5 Pericardial Diseases ............................................................................................................................................................. 215
Differential Diagnoses and Related Diseases ................................................................................................................. 215

6 Rheumatology ................................................................................................................................................................... 219

6.1 Rheumatoid Arthritis .......................................................................................................................................................... 220
Differential Diagnoses and Related Diseases ................................................................................................................. 220
6.2 Ankylosing Spondylitis (Marie–Strümpell Disease) .............................................................................................. 228
Differential Diagnoses and Related Diseases ................................................................................................................. 231
6.3 Gout Arthritis ......................................................................................................................................................................... 232
Differential Diagnoses and Related Diseases ................................................................................................................. 233
6.4 CPPD and HADD .................................................................................................................................................................... 234
Calcium Pyrophosphate Dihydrate Crystal Deposition Disease .............................................................................. 234
Hydroxyapatite Crystal Deposition Disease ................................................................................................................... 235
6.5 Osteoarthritis ......................................................................................................................................................................... 237
6.6 Psoriasis and Psoriatic Arthritis ...................................................................................................................................... 241
Differential Diagnoses and Related Diseases ................................................................................................................. 241
6.7 Baastrup’s Disease (Spinout Process Impingement Syndrome) ...................................................................... 244
6.8 Scheuermann’s Disease (Juvenile Kyphosis Dorsalis)........................................................................................... 246
Criteria for Scheuermann’s Disease Diagnosis............................................................................................................... 247
6.9 Sjögren Syndrome (Myoepithelial Sialadenitis) ..................................................................................................... 249
Criteria to Diagnose SS Include .......................................................................................................................................... 249
6.10 Behçet Disease ....................................................................................................................................................................... 252
Clinical Criteria to Diagnose BD Require a Combination of Three or More
of the Following Findings..................................................................................................................................................... 252
 XI
Contents

6.11 Sharp Syndrome (Mixed Connective Tissue Disease) ........................................................................................... 253

6.12 Relapsing Polychondritis .................................................................................................................................................. 254
Diagnostic Criteria for Relapsing Polychondritis .......................................................................................................... 255
Differential Diagnoses and Related Diseases ................................................................................................................. 255
6.13 Reflex Sympathetic Dystrophy ....................................................................................................................................... 260
6.14 Polymyalgia Rheumatica ................................................................................................................................................... 264
6.15 Systemic Lupus Erythematosus...................................................................................................................................... 266
Differential Diagnoses and Related Diseases ................................................................................................................. 267

7 Pulmonology ...................................................................................................................................................................... 273

7.1 Pleural Diseases .................................................................................................................................................................... 275
Pleural Effusion ........................................................................................................................................................................ 275
Pneumothorax ......................................................................................................................................................................... 278
Pleural Calcification ................................................................................................................................................................ 280
7.2 Alveolar Lung Diseases ...................................................................................................................................................... 282
Types of Alveolar Lung Diseases ........................................................................................................................................ 282
How to Differentiate Between Cardiogenic Edema from ARDS on Plain Chest Radiographs? ...................... 284
Types of Pneumonias............................................................................................................................................................. 284
7.3 Atelectasis (Lung Collapse) .............................................................................................................................................. 287
Types of Pulmonary Atelectases ........................................................................................................................................ 287
7.4 Sarcoidosis............................................................................................................................................................................... 290
Pulmonary Sarcoidosis .......................................................................................................................................................... 291
Hepatic, Splenic, and Gastric Sarcoidosis ........................................................................................................................ 292
Dermatological Sarcoidosis ................................................................................................................................................. 292
Cardiac Sarcoidosis................................................................................................................................................................. 293
Neurosarcoid ............................................................................................................................................................................ 293
Musculoskeletal Sarcoidosis ................................................................................................................................................ 295
Head and Neck Sarcoidosis.................................................................................................................................................. 295
Genitourinary Sarcoidosis .................................................................................................................................................... 296
7.5 Emphysema ............................................................................................................................................................................. 297
7.6 Idiopathic Interstitial Pneumonias ............................................................................................................................... 300
Idiopathic Pulmonary Fibrosis ............................................................................................................................................ 300
Nonspecific Interstitial Pneumonia ................................................................................................................................... 302
Cryptogenic Organizing Pneumonia ................................................................................................................................ 302
Respiratory Bronchiolitis-Associated Interstitial Lung Disease ................................................................................ 303
Desquamative Interstitial Pneumonia.............................................................................................................................. 303
Lymphoid Interstitial Pneumonia ...................................................................................................................................... 303
Acute Interstitial Pneumonia (Hamman–Rich Syndrome) ......................................................................................... 304
7.7 Histiocytoses .......................................................................................................................................................................... 304
Langerhans Cell Histiocytosis ............................................................................................................................................. 305
Infection-Associated Hemophagocytic Syndrome ...................................................................................................... 307
Omenn Syndrome .................................................................................................................................................................. 307
Chédiak–Higashi Disease ..................................................................................................................................................... 307
Differential Diagnoses and Related Diseases ................................................................................................................. 307
Rosai–Dorfman’s Disease (Sinus Histiocytosis).............................................................................................................. 308
Xanthoma Disseminatum (Montgomery Syndrome) .................................................................................................. 308
Erdheim–Chester Disease (Lipogranulomatosis).......................................................................................................... 309
7.8 Hemoptysis ............................................................................................................................................................................. 310
Bronchopulmonary Sequestration .................................................................................................................................... 311
Anomalous Systemic Artery Supplying Normal Lung Parenchyma ....................................................................... 312
Pulmonary Vasculitis .............................................................................................................................................................. 312
Cardiac Bronchus .................................................................................................................................................................... 314
Dieulafoy Disease.................................................................................................................................................................... 314
7.9 Cystic Fibrosis (Mucoviscidosis) ..................................................................................................................................... 315
Pulmonary Manifestations of Cystic Fibrosis ................................................................................................................. 315
Nasal and Sinus Manifestations of Cystic Fibrosis ........................................................................................................ 316
XII Contents

Gastrointestinal (GI) Manifestations of Cystic Fibrosis ................................................................................................ 317

Genitourinary Manifestations of Cystic Fibrosis............................................................................................................ 319
Musculoskeletal Manifestations of Cystic Fibrosis ....................................................................................................... 319
7.10 Sleep Apnea Syndromes.................................................................................................................................................... 321
Obstructive Sleep Apnea Syndrome................................................................................................................................. 321
Upper Airway Resistance Syndrome................................................................................................................................. 324
Central Alveolar Apnea Syndrome (Ondine’s Curse) ................................................................................................... 324
Cheyne–Stokes Respiration ................................................................................................................................................. 325
Uncommon and Rare Causes of Sleep Apnea ............................................................................................................... 325

8 Dermatology ...................................................................................................................................................................... 327

8.1 Scleroderma (Systemic Sclerosis) .................................................................................................................................. 328
Differential Diagnoses and Related Diseases ................................................................................................................. 328
8.2 Lipoid Proteinosis (Urbach–Wiethe Disease) ........................................................................................................... 332
8.3 Dermatomyositis .................................................................................................................................................................. 335
8.4 Ochronosis (Alkaptonuria) ............................................................................................................................................... 337
8.5 Lymphedema.......................................................................................................................................................................... 338
Causes of Primary Lymphedemas ..................................................................................................................................... 339
Causes of Secondary Lymphedemas ................................................................................................................................ 339
Differential Diagnoses of Lymphedema .......................................................................................................................... 339
8.6 Neuropathic Itch (Pruritus)............................................................................................................................................... 343
Neural Control Pruritus ......................................................................................................................................................... 344
Differential Diagnoses of Neuropathic Itch .................................................................................................................... 344

9 Hematology ........................................................................................................................................................................ 347

9.1 Hemosiderosis and Hemochromatosis ....................................................................................................................... 348
Differential Diagnoses and Related Diseases ................................................................................................................. 349
9.2 β-Thalassemia Major (Cooley’s Anemia) ..................................................................................................................... 350
9.3 Sickle Cell Disease ................................................................................................................................................................ 353
The Lungs in SCD .................................................................................................................................................................... 354
The Skeletal System in SCD ................................................................................................................................................. 354
The Brain in SCD ...................................................................................................................................................................... 354
The Spleen in SCD................................................................................................................................................................... 354
9.4 Pernicious Anemia ............................................................................................................................................................... 357
9.5 Hemophilia .............................................................................................................................................................................. 358
Differential Diagnoses and Related Diseases ................................................................................................................. 359
9.6 Lymphomas............................................................................................................................................................................. 362
Cotswold Staging of Lymphoma ....................................................................................................................................... 363
Criteria for Therapy Response Assessment ..................................................................................................................... 363
Differential Diagnoses and Related Diseases ................................................................................................................. 363
9.7 Leukemia .................................................................................................................................................................................. 368
Acute Lymphoblastic Leukemia ......................................................................................................................................... 368
Acute Myeloblastic Leukemia ............................................................................................................................................. 368
Chronic Lymphocytic Leukemia ......................................................................................................................................... 369
Chronic Myelogenous Leukemia ....................................................................................................................................... 369
9.8 Multiple Myeloma (Kahler’s Disease) ........................................................................................................................... 374
9.9 Amyloidosis ............................................................................................................................................................................. 378
Classification of Amyloidosis (Clinical-Based Classification) ..................................................................................... 378
9.10 Evans’ Syndrome ................................................................................................................................................................... 382
9.11 Other Lymphatic Disorders .............................................................................................................................................. 383
Castleman’s Disease (Angiofollicular Lymph Node Hyperplasia) ............................................................................ 383
Kikuchi–Fujimoto Disease (Histiocytic Necrotizing Lymphadenitis) ...................................................................... 384
Kimura’s Disease ...................................................................................................................................................................... 384
9.12 Mastocytosis ........................................................................................................................................................................... 385
9.13 Myelofibrosis and Myeloid Metaplasia ....................................................................................................................... 387
 XIII
Contents

10 Diabetology ........................................................................................................................................................................ 391

10.1 Diabetic Hand and Diabetic Foot .................................................................................................................................. 393
Diabetic Angiopathy .............................................................................................................................................................. 393
Diabetic Peripheral Neuropathy, Osteopathy, and Infections .................................................................................. 394
Diabetic Myonecrosis ............................................................................................................................................................ 397
Diabetic Skin Changes and Infections ............................................................................................................................. 397
The Role of Doppler Sonography in DM.......................................................................................................................... 400
The Role of MRI in DM ........................................................................................................................................................... 401
Differential Diagnoses and Related Diseases ................................................................................................................. 406
10.2 Diabetic Brain and Nervous System ............................................................................................................................. 407
10.3 Diabetic Syndromes ............................................................................................................................................................ 408
Alström Syndrome .................................................................................................................................................................. 408
Bardet–Biedl Syndrome ........................................................................................................................................................ 409
Leprechaunism (Donohue Syndrome) ............................................................................................................................. 409
Prader–Willi Syndrome .......................................................................................................................................................... 410
Wolcott–Rallison Syndrome ................................................................................................................................................ 410
Wolfram Syndrome (DIDMOAD)......................................................................................................................................... 411
Rabson–Mendenhall Syndrome ......................................................................................................................................... 411
10.4 Diabetes Insipidus................................................................................................................................................................ 412
10.5 Obesity, Gastric Banding, and Liposuction ............................................................................................................... 415
Hormonal Obesity .................................................................................................................................................................. 415
Syndromic/Pathologic Obesity........................................................................................................................................... 416
Drug-Induced Obesity........................................................................................................................................................... 419
Gastric Banding ....................................................................................................................................................................... 419
Liposuction ............................................................................................................................................................................... 422
10.6 Lipoatrophic–Lipodystrophic Syndromes ................................................................................................................. 423
Congenital Generalized Lipodystrophy (Seip–Berardinelli Syndrome) ................................................................. 424
Familial Partial Lipodystrophy (Dunnigan–Kobberling Syndrome) ........................................................................ 425
Mandibuloacral Dysplasia .................................................................................................................................................... 425
Acquired Generalized Lipoatrophy (Lawrence–Seip Syndrome) ............................................................................ 425
Acquired Partial Lipoatrophy (Barraquer–Simons Syndrome) ................................................................................. 426
Parry–Romberg Syndrome (Progressive Facial Hemiatrophy).................................................................................. 426
10.7 Diabetic Nephropathy ........................................................................................................................................................ 427
Diabetic Nephropathy ........................................................................................................................................................... 427
Renal Papillary Necrosis ........................................................................................................................................................ 428
Diabetic Cystopathy (Neurogenic Bladder) .................................................................................................................... 430
Calcification of the Vas Deferens........................................................................................................................................ 430
Emphysematous Cystitis ....................................................................................................................................................... 430
Emphysematous Pyelonephritis ........................................................................................................................................ 431
Xanthogranulomatous Pyelonephritis ............................................................................................................................. 432
10.8 Lipomatosis ............................................................................................................................................................................. 432
Intestinal Lipomatosis ........................................................................................................................................................... 432
Pelvic Lipomatosis .................................................................................................................................................................. 434
Epidural Lipomatosis ............................................................................................................................................................. 434
Encephalocraniocutaneous Lipomatosis Syndrome
(Haberland Syndrome) .......................................................................................................................................................... 434
Lipomatous Hypertrophy of the Interatrial Septum.................................................................................................... 435
10.9 Hypoglycemia ........................................................................................................................................................................ 436
Differential Diagnoses and Related Diseases ................................................................................................................. 437

11 Infectious Diseases and Tropical Medicine .................................................................................................... 441

11.1 Fever ........................................................................................................................................................................................... 443
11.2 Giardiasis .................................................................................................................................................................................. 444
Differential Diagnoses and Related Diseases ................................................................................................................. 444
11.3 Amebiasis ................................................................................................................................................................................. 444
Intestinal Amebiasis ............................................................................................................................................................... 445
Hepatic Amebiasis .................................................................................................................................................................. 446
XIV Contents

Thoracic Amebiasis ................................................................................................................................................................ 447

Brain Amebiasis ....................................................................................................................................................................... 447
11.4 Leprosy (Hansen Disease) ................................................................................................................................................. 448
Skin Involvement .................................................................................................................................................................... 448
Nerve Involvement ................................................................................................................................................................. 448
Eye Involvement ...................................................................................................................................................................... 448
Mucosal Involvement ............................................................................................................................................................ 449
Bone Involvement .................................................................................................................................................................. 449
Post-therapy Leprosy ............................................................................................................................................................. 449
11.5 Toxoplasmosis ........................................................................................................................................................................ 451
11.6 Brucellosis (Malta Fever) ................................................................................................................................................... 454
11.7 Neurocysticercosis ............................................................................................................................................................... 455
11.8 Ascariasis .................................................................................................................................................................................. 458
Differential Diagnoses and Related Diseases ................................................................................................................. 458
11.9 Guinea Worm Disease (Dracunculiasis) ...................................................................................................................... 459
11.10 Hydatid Cyst (Echinococcosis) ........................................................................................................................................ 461
Echinococcus granulosus Disease ....................................................................................................................................... 461
Grading of the Liver Lesions by E. granulosus ................................................................................................................ 461
Differential Diagnoses and Related Diseases ................................................................................................................. 465
Echinococcus alveolaris Disease .......................................................................................................................................... 465
11.11 Chagas’ Disease (American Trypanosoma) ................................................................................................................ 466
Acute Chagas’ Disease ........................................................................................................................................................... 467
Subacute Chagas’ Disease .................................................................................................................................................... 467
Latent Chagas’ Disease .......................................................................................................................................................... 467
Chronic Chagas’ Disease ....................................................................................................................................................... 468
11.12 Schistosomiasis (Bilharziasis) .......................................................................................................................................... 468
Schistosoma Life Cycle ........................................................................................................................................................... 468
Schistosomiasis by S. japonicum ........................................................................................................................................ 469
Schistosomiasis by S. mansoni ............................................................................................................................................ 469
Schistosomiasis by S. haematobium ................................................................................................................................. 471
Differential Diagnoses and Related Diseases ................................................................................................................. 472
11.13 Tuberculosis ............................................................................................................................................................................ 473
Pulmonary TB ........................................................................................................................................................................... 473
Pleural TB ................................................................................................................................................................................... 475
Miliary TB ................................................................................................................................................................................... 476
Abdominal TB ........................................................................................................................................................................... 477
Hepatic TB ................................................................................................................................................................................. 477
Genitourinary TB ..................................................................................................................................................................... 478
Musculoskeletal TB ................................................................................................................................................................. 479
Tuberculous Lymphadenitis ................................................................................................................................................ 481
Dermatological TB .................................................................................................................................................................. 482
11.14 Typhoid Fever (Salmonellosis) ........................................................................................................................................ 483
11.15 Malaria....................................................................................................................................................................................... 485
Differential Diagnoses and Related Diseases ................................................................................................................. 485
11.16 Animal Bites and Stings ..................................................................................................................................................... 486
Rabies ......................................................................................................................................................................................... 487
Viper Bite ................................................................................................................................................................................... 488
Differential Diagnoses and Related Diseases ................................................................................................................. 488
Hymenoptera Stings .............................................................................................................................................................. 488
11.17 Filariasis .................................................................................................................................................................................... 490
11.18 Most Common Infections Causing Human Filariasis ............................................................................................ 490
11.19 Fever of Unknown Origin ................................................................................................................................................................... 492

12 Occupational Medicine and Toxicology ........................................................................................................... 495

12.1 Medications Toxicity............................................................................................................................................................ 496
Antibiotics ................................................................................................................................................................................. 496
Metformin (Glucophage, Oral Hypoglycemics) ............................................................................................................. 497
Methotrexate............................................................................................................................................................................ 497
 XV
Contents

Hypervitaminosis A ................................................................................................................................................................ 498

Anticonvulsants ....................................................................................................................................................................... 499
Amiodarone Toxicity .............................................................................................................................................................. 500
Cyclosporine A ......................................................................................................................................................................... 501
Glucocorticoids ....................................................................................................................................................................... 501
Gadolinium-Based Contrast Media ................................................................................................................................... 502
12.2 Drugs of Abuse ...................................................................................................................................................................... 503
Cocaine and Heroin (Opioids) ............................................................................................................................................. 503
Alcohol ....................................................................................................................................................................................... 504
Toluene Toxicity ....................................................................................................................................................................... 505
Methanol Toxicity.................................................................................................................................................................... 505
Amphetamines Abuse ........................................................................................................................................................... 506
Marijuana................................................................................................................................................................................... 506
Butane Poisoning .................................................................................................................................................................... 506
12.3 Gases, Inorganic, and Chemical Poisoning ............................................................................................................... 507
Arsenic Poisoning ................................................................................................................................................................... 507
Mercury Poisoning ................................................................................................................................................................. 508
Chronic Beryllium Disease (Berylliosis) ............................................................................................................................ 509
Pneumoconiosis ...................................................................................................................................................................... 509
Insecticides and Rodenticides Poisoning........................................................................................................................ 509
Carbon Monoxide Poisoning............................................................................................................................................... 510
Manganese Poisoning ........................................................................................................................................................... 511
Thallium Poisoning (Thallotoxicosis) ................................................................................................................................ 511
Methyl Bromide Poisoning .................................................................................................................................................. 511
Tattoos ........................................................................................................................................................................................ 512
12.4 Botanical, Environmental, and Organic Poisoning ................................................................................................ 512
Hypersensitivity Lung Diseases (Hypersensitivity Pneumonitis)............................................................................. 512
Cyanide Poisoning .................................................................................................................................................................. 513
Botulism ..................................................................................................................................................................................... 513
12.5 Drug-Induced Radiological Changes ........................................................................................................................... 514

13 Chiropractic Medicine .................................................................................................................................................. 517

13.1 The Human Fascia ................................................................................................................................................................ 519
13.2 Vertebral Malalignment (Subluxation) Syndromes............................................................................................... 520
Anatomy .................................................................................................................................................................................... 522
Somatovisceral Malalignment Symptoms ...................................................................................................................... 522
13.3 Imaging Signs ........................................................................................................................................................................ 523
13.4 Facet Joint Syndrome ......................................................................................................................................................... 523
Basic Anatomy ......................................................................................................................................................................... 523
Pathophysiology ..................................................................................................................................................................... 525
13.5 Imaging Signs ........................................................................................................................................................................ 525
13.6 Myofascial Pain Syndrome ............................................................................................................................................... 526
Anatomy .................................................................................................................................................................................... 526
Pathophysiology ..................................................................................................................................................................... 527
Some Known Symptomatology of Myofascial Trigger Points Origin ..................................................................... 527
13.7 Imaging of a Case Study .................................................................................................................................................... 528
13.8 Spinal Transitional Zone Syndromes ........................................................................................................................... 528
Basic Anatomy ......................................................................................................................................................................... 529
Pathophysiology ..................................................................................................................................................................... 529
13.9 Imaging Signs ........................................................................................................................................................................ 531
Lumbosacral Transitional Zone Syndrome ..................................................................................................................... 531
13.10 Imaging Signs ........................................................................................................................................................................ 532
13.11 The Dentate Ligament–Cord Distortion Phenomenon........................................................................................ 533
13.12 Imaging Signs ........................................................................................................................................................................ 536
13.13 Cervicogenic Headache ..................................................................................................................................................... 538
Anatomy .................................................................................................................................................................................... 538
Pathophysiology ..................................................................................................................................................................... 538
XVI Contents

13.14 Imaging Signs ........................................................................................................................................................................ 541

13.15 Cervicogenic Vertigo and Tinnitus ................................................................................................................................ 542
Anatomy .................................................................................................................................................................................... 542
Pathophysiology ..................................................................................................................................................................... 543
13.16 Imaging Signs ........................................................................................................................................................................ 543
13.17 Whiplash-Associated Disorder ....................................................................................................................................... 546
Basic Anatomy ......................................................................................................................................................................... 546
Pathophysiology ..................................................................................................................................................................... 546
13.18 Imaging Signs ........................................................................................................................................................................ 547
13.19 Thoracic Outlet Syndrome................................................................................................................................................ 549
Basic Anatomy ......................................................................................................................................................................... 549
Pathophysiology ..................................................................................................................................................................... 549
13.20 Imaging Signs ........................................................................................................................................................................ 550
13.21 Upper and Lower Crossed Syndromes ........................................................................................................................ 551
13.22 Imaging Signs ........................................................................................................................................................................ 552
13.23 Lumbago .................................................................................................................................................................................. 553
13.24 Imaging Signs ........................................................................................................................................................................ 554
13.25 Shin Splint Syndrome ......................................................................................................................................................... 554
13.26 Imaging Signs ........................................................................................................................................................................ 556
13.27 Cuboid Syndrome................................................................................................................................................................. 558
13.28 Imaging Signs ........................................................................................................................................................................ 558
13.29 Scoliosis, Kyphosis, and Lordosis................................................................................................................................... 559
13.30 Imaging Signs ........................................................................................................................................................................ 560
13.31 Sacroiliac Joint Dysfunction ............................................................................................................................................ 561
Basic Anatomy ......................................................................................................................................................................... 561
Pathophysiology ..................................................................................................................................................................... 562
13.32 Imaging Signs ........................................................................................................................................................................ 562
13.33 Psoas Syndrome .................................................................................................................................................................... 565
Basic Anatomy ......................................................................................................................................................................... 565
Pathophysiology ..................................................................................................................................................................... 565
13.34 Imaging Signs ........................................................................................................................................................................ 566
13.35 Piriformis Muscle Syndrome ............................................................................................................................................ 566
Basic Anatomy ......................................................................................................................................................................... 567
Pathophysiology ..................................................................................................................................................................... 567
13.36 Imaging Signs ........................................................................................................................................................................ 567
13.37 Coccydynia .............................................................................................................................................................................. 567
Anatomy .................................................................................................................................................................................... 567
Pathophysiology ..................................................................................................................................................................... 568
13.38 Differential Diagnoses and Related Diseases........................................................................................................... 569
13.39 Imaging Signs ........................................................................................................................................................................ 569

14 Energy Medicine .............................................................................................................................................................. 573

14.1 Microcurrent Therapy ......................................................................................................................................................... 574
Basic Electrical Healing Physiology ................................................................................................................................... 574
Microcurrent Therapy Benefits ........................................................................................................................................... 575
Microcurrent Therapy Healing Mechanisms .................................................................................................................. 575
Microcurrent Healing Cases................................................................................................................................................. 577
14.2 Pulsed Electromagnetic Field Therapy ........................................................................................................................ 577
Pulsed Electromagnetic Fields (PEMFs) ........................................................................................................................... 578
Pulsed Electromagnetic Fields (PEMFs) and Body Metabolism ............................................................................... 578
PEMF Therapy Healing Cases .............................................................................................................................................. 583
Further Reading .................................................................................................................................................................... 588

Index .......................................................................................................................................................................................... 591

 1 1

Gastroenterology

1.1 Liver Cirrhosis – 2

Types of Liver Cirrhosis – 2
1.2 Fatty Liver Disease (Liver Steatosis) – 15
Types of Liver Steatosis – 15
1.3 Recurrent Epigastric Pain – 17
Gastroesophageal Reflux Disease – 17
Differential Diagnoses and Related Diseases – 18
Peptic Ulcer Disease – 24
Superior Mesenteric Artery Syndrome (Wilkie’s Syndrome) – 27
Median Arcuate Ligament Syndrome (Celiac Trunk Compression
Syndrome/Dunbar’s Syndrome) – 29
Recurrent Abdominal Pain of Childhood – 29
1.4 Inflammatory Bowel Diseases – 30
Crohn’s Disease – 31
Extraintestinal Manifestations of CD – 31
Ulcerative Colitis – 36
Extraintestinal Manifestations of UC – 36
Differences Between Ulcerative Colitis and Crohn’s Disease – 39
Differential Diagnoses and Related Diseases – 39
1.5 Gastrointestinal Hemorrhage – 40
1.6 Pancreatitis – 41
Acute Pancreatitis – 41
Differential Diagnoses and Related Diseases – 41
Chronic Pancreatitis – 45
1.7 Jaundice – 48
Kernicterus – 50
Obstructive Jaundice – 50
Bile Plug Syndrome – 52
Infectious Ascending Cholangitis – 52
Choledochal Web – 53
1.8 Diarrhea and Malabsorption – 54
Normal Anatomy – 54
Pathophysiology – 54
Common Causes of Diarrhea and Their Mechanism of Action – 54
Sprue – 55
Whipple’s Disease (Intestinal Lipodystrophy) – 56
VIPoma (Werner–Morris Syndrome/Pancreatic Cholera) – 57
© Springer International Publishing Switzerland 2017
J.A. Al-Tubaikh, Internal Medicine, DOI 10.1007/978-3-319-39747-4_1
 2 Chapter 1 · Gastroenterology
1.1 Liver Cirrhosis
1 obstruction of the biliary tree, causing bile stagnation
Liver cirrhosis is a term used to describe the histological
development of regenerative hepatic nodules surrounded by
fibrous bands in response to chronic liver injury.
Cirrhosis is an advanced, diffuse stage of liver injury,
which is characterized by replacement of the normal liver
parenchyma by collagenous scar (fibrosis). Cirrhosis is
accompanied by diffuse distortion of the hepatic vasculature
and architecture, resulting in vascular disturbance between
the portal veins and the hepatic veins, plus porta hepatic
fibrosis. The major cirrhosis consequences are hepatic func-
tion impairment, increased intrahepatic resistance (portal
hypertension), and the development of hepatocellular carci-
noma (HCC).
Types of Liver Cirrhosis
5 Laennec’s cirrhosis is a type of micronodular liver
cirrhosis that is seen in patients with malnutrition,
alcoholism, or chronic liver steatosis.
5 Posthepatitic cirrhosis is a micro- and/or macronodular
liver cirrhosis commonly seen in patients with hepatitis
C virus or uncommonly B virus.
5 Postnecrotic cirrhosis is macronodular liver cirrhosis that
can arise due to fulminating hepatitis infection or due to
toxic liver injury.
5 Primary biliary cirrhosis (PBC) (vanishing bile duct
syndrome) is an autoimmune disease of unknown origin
characterized by progressive intrahepatic bile duct,
nonsuppurative inflammation, and destruction by T-cell
lymphocytes, which leads later on to micronodular liver
cirrhosis, hepatomegaly, with greenish-stain liver on gross
examination due to bile retention. PBC occurs in
middle-aged women in up to 90 % of cases. In symptomatic
PBC, patients may complain of jaundice in the first 2–3
years, which develops later into portal hypertension and
hepatosplenomegaly. In the asymptomatic PBC, the only
symptom is abnormal serum hepatobiliary enzyme levels.
PBC is classified pathologically into four main stages.
Florid duct stage (stage I PBC) is characterized by vanishing
intrahepatic duct and ductopenia due to destruction of the
intrahepatic bile duct basement membrane and cellular
bodies by lymphocytes. Ductular proliferation stage (stage
II) is characterized by small bile ducts proliferation in an
attempt to compensate the obstruction of the large bile
ducts. The liver characteristically contains few large ducts
and many small bile ducts. Scarring (stage III) is
characterized by fibrosis and intrahepatic collagen
deposition. Hepatic cirrhosis (stage IV) is characterized by
architectural hepatic disruption and accumulation of the
bile within the hepatocytes. The disease is diagnosed by
liver biopsy, plus detecting antimitochondrial antibodies
(AMA) in the serum.
5 Secondary biliary cirrhosis arises due to extrahepatic
within the liver. This type can be seen in cases of
congenital bile duct atresia, chronic biliary stone
obstruction, or pancreatic head carcinoma. The
inflammation in the secondary biliary cirrhosis arises
due to secondary infection of the bile, leading to
neutrophilic acute inflammatory reaction. In contrast,
PBC is a chronic, autoimmune disease with lymphatic
and plasma cell inflammatory reaction.
5 Cirrhosis due to metabolic disease is seen in glycogen
storage diseases, α1-antitrypsin deficiency disease,
hemochromatosis, and Wilson’s disease. All the metabolic
cirrhoses are micronodular except Wilson’s disease
(macronodular).
5 Cirrhosis due to circulatory disorders is observed in
patients with venous congestion due to right-sided heart
failure, veno-occlusive disease due to herbal medicine,
and Budd–Chiari syndrome. In congestive heart failure,
chronic hepatic venous congestion may lead to
intrahepatic hypertension, which results in sinusoidal
congestion, pressure atrophy, and necrosis of pericentral
parenchymal cells. Later, there is a collapse of the
necrotic cells with perisinusoidal and periportal collagen
deposition (fibrosis) extending to the central veins. These
changes are known as “nutmeg liver” on postmortem
liver examination.
Cirrhotic nodules are parenchymal nodules found in cir-
rhotic liver (seen in 25 % of imaging scans only), and they are
divided into three main types:
5 Regenerative nodules represent normal proliferation of
liver parenchyma. The development of regenerative
nodules can be explained pathologically by cellular repair
mechanism known as “cell-to-cell and cell-to-matrix
interaction.” Cell-to-cell interaction describes the process
of cellular inhibition when two cells touch each other
(e.g., skin wound healing). Cell-to-matrix interaction
describes the process of cellular proliferation inhibition
when the regenerated cells touch the tissue matrix
(connective tissue frame). In acute hepatitis, if the
connective tissue matrix is preserved, then damage to the
liver can be completely repaired without architectural
distortion or residuals. In contrast, in chronic hepatitis,
both the liver parenchyma and the connective tissue
frame are damaged. This matrix damage results in
random liver cell regeneration without cell-to-matrix
cellular inhibition, which will result in regenerative liver
nodule formation with fibrosis in between (liver
cirrhosis). These nodules do not function normally
because the relationship with the portal vein, hepatic
artery, and bile ducts (porta hepatis) is lost.
5 Dysplastic nodules are regenerative premalignant nodules.
5 HCC nodules are nodules composed of neoplastic cells
and are seen commonly in patients with cirrhosis due to
hepatitis C virus.
1.1 · Liver Cirrhosis
a b
. Fig. 1.1.1 An illustration shows the clinical pathological picture of Dupuytren’s contracture with illustrated thickening of the palmar
aponeurosis (a) and bilateral plantar nodules representing the clinical manifestation of Ledderhose disease (b)
Patients with cirrhosis are asymptomatic, unless they
develop signs of liver failure. Signs of liver failure include
yellowish discoloration of the skin (jaundice), develop-
ment of central arteriole dilatation with radiating vessels
on the face (spider nevi), white nail bed due to hypoalbu-
minemia, painful proliferative arthropathy of long bones,
gynecomastia and palmar erythema due to reduced
estradiol degeneration by the liver, hypogonadism
(mainly in cirrhosis due to alcoholism and hemochroma-
tosis), anorexia and wasting (>50 % of patients), and dia-
betes mellitus type 2 (up to 30 % of patients). Some
patients with liver cirrhosis may develop palmar fibro-
matosis.
Fibromatosis is a pathological condition characterized by
local proliferation of fibroblasts which manifests clinically as
soft-tissue thickening. Fibromatosis can affect the palmar
aponeurosis (Dupuytren’s contracture), causing limited hand
extension and possibly bony erosions (. Fig. 1.1.1). Palmar
fibromatosis that occurs in a bilateral fashion and is associ-
ated with bilateral plantar fibromatosis is called Ledderhose
disease (. Fig. 1.1.1). Other forms of fibromatosis in the body
include the male genital fibromatosis (Peyronie’s disease) and
fibromatosis of the dorsum of the interphalangeal joint
(Garrod’s nodes).
3 1
The development of portal hypertension can result in
splenomegaly, ascites, and prominent paraumbilical veins
(caput medusae). Multiple intra- and extrahepatic porto-
systemic collaterals develop to compensate the loss of the
large portal venous flow that cannot be maintained longer
due to increased intrahepatic venous pressure in portal
hypertension. Intrahepatic portosystemic shunts occur
when the portal vein communicates with the hepatic vein in
or on the surface of the liver through a dilated venous sys-
tem. In contrast, extrahepatic portosystemic shunts occur
when the intrahepatic portal vein runs toward the outside
of the liver communicating with the systemic veins.
Cruveilhier–Baumgarten syndrome is a condition character-
ized by patent paraumbilical vein as a consequence of portal
hypertension, which occurs as a part of portosystemic
shunts. Paraesophageal and paragastric varices develop in
patients with advanced liver cirrhosis and can cause life-
threatening upper gastrointestinal (GI) bleeding.
Hepatic encephalopathy is a potentially reversible com-
plication seen in advanced liver failure and cirrhosis charac-
terized by motor, cognitive, and psychiatric central nervous
system (CNS) dysfunction. Manifestations of hepatic
encephalopathy include daytime deterioration (grade 1),
disorientation in space (grade 2), or coma (grade 3).
 4 Chapter 1 · Gastroenterology
Flapping tremor (asterixis) may be seen in patients with
1 hepatic encephalopathy. The neurological manifestations of
hepatic encephalopathy are due to inability of the liver to
detoxify neurotoxins such as ammonia, phenols, short-
chained fatty acids, and other toxic metabolites within the
blood. These toxic metabolites cross the blood–brain barrier
and deposits within the basal ganglia causing encephalopathy.
Hepatic encephalopathy can be induced or exaggerated by
sedation, high-protein diet, GI hemorrhage, and the use of
diuretics.
Hepatopulmonary syndrome is an end-stage liver disease
characterized by pulmonary failure, and it is seen in 15–20 %
of cirrhosis patients. The diagnosis of hepatopulmonary syn-
drome requires the following three criteria: chronic liver dis-
ease, increased alveolar–arterial gradient on room air, and
evidence of intrapulmonary vascular dilatation. Patients with
hepatopulmonary syndrome present with liver cirrhosis with
hypoxia (30 % of decompensated liver patients). This hypox-
emia occurs due to pulmonary vascular dilatation and subse-
quent ventilation–perfusion mismatch due to decreased
hepatic clearance or increased hepatic productions of circu-
lating cytokines and chemical mediators (e.g., nitric oxide).
Hypoxic respiratory failure can occur with cases of massive
liver necrosis or fulminant hepatic failure.
Hepatitis C virus-related arthritis (HCVrA) may be seen
in patients with liver cirrhosis due to hepatitis C virus.
HCVrA affects 4 % of patients with HCV liver cirrhosis, and
it has two forms: a frequent symmetrical polyarthritis affect-
ing small joints similar to rheumatoid arthritis in a lesser
form and an intermittent mono-/oligoarthritis that involves
medium- and large-sized joints.
Signs on Plain Radiographs
5 Hepatic hydrothorax is defined as large pleural
effusion in a cirrhotic liver disease patient in the
absence of cardiac or pulmonary disease. Hepatic
hydrothorax is seen in 10 % of patients. The pleural
effusion can be right sided (67 %), left sided (17 %),
or bilateral (17 %).
5 Hepatopulmonary syndrome is visualized on plain
chest radiographs as reticulonodular interstitial
pattern located mainly at the lung bases (46–100 %
of cases).
5 Noncardiogenic pulmonary edema can be seen in
37 % in patients with fulminant hepatic failure.
5 Esophageal varices may manifest on chest
radiographs as focal lateral displacement of the
mediastinum.
5 On abdominal radiographs, ascites is detected as
loss of the abdominal gases and the normal psoas
shadows visualization. The abdomen structures are
blurry due to the overlying fluid shadow
(. Fig. 1.1.2).
. Fig. 1.1.2 Plain abdominal radiograph in a patient with
massive ascites shows complete blurry abdomen
1.1 · Liver Cirrhosis
Signs on US
5 Cirrhosis is detected as irregular nodular liver
contour with inhomogeneous echo-texture. Liver
right lobe atrophy with enlarged caudate lobe is a
typical finding (caudate lobe/right lobe ratio
>0.65) (. Figs. 1.1.3 and 1.1.4).
5 Mixed hypoechoic and hyperechoic texture of the
liver parenchyma is detected when regenerative
nodules are found.
5 Signs of portal hypertension include splenomegaly
(>12 cm), ascites, and dilated venous collaterals.
. Fig. 1.1.3 Transverse ultrasound image of a patient with
liver cirrhosis shows atrophied left lobe (white arrowhead), with
hypertrophied caudate lobe (black arrowhead)
. Fig. 1.1.4 Transverse ultrasound image of a patient with
liver cirrhosis due to hepatitis C virus shows irregular liver
contour (arrowheads), with two intrahepatic liver hypoechoic
masses, which were diagnosed on liver triphasic CT scan later as
hepatocellular carcinoma (HCC) masses (arrows)
5 1
Signs on Doppler Sonography
5 Hepatic veins: hepatic veins join immediately the
inferior vena cava, which is in direct
communication with the left atrium. Due to the
previous anatomical fact, the normal hepatic veins
waveform is “triphasic,” because it is affected by
left atrial cardiac motion and Valsalva maneuver
(. Fig. 1.1.5). In patients with cirrhosis, the
triphasic flow pattern is converted into biphasic
and monophasic depending on the severity of
cirrhosis.
5 Portal vein: it supplies 70–80 % of the incoming
blood to the liver, and the hepatic artery supplies
only 20–30 %. The normal portal venous flow is
always toward the liver (hepatopetal). The fasting
mean velocity of normal portal vein is
approximately 18 cm/s (range, 13–23 cm/s3), and
the flow pattern is normally flat or monophasic
(. Fig. 1.1.6). Mildly pulsatile portal venous flow
pattern can be seen normally in tall, thin patients
(. Fig. 1.1.7). Portal hypertension is detected as
hepatic blood flow away from the liver
(hepatofugal) due to increased intrahepatic venous
flow resistance. Portal vein diameter (>13 mm) and
splenic vein diameter (>10 mm) are other signs of
portal hypertension. Hepatic vein thrombosis can
be seen in patients with HCC, and it is visualized as
partial or complete loss of flow signal within the
portal vein.
5 Hepatic artery : the normal hepatic artery in a
fasting patient has a systolic velocity of
approximately 30–40 cm/s and a diastolic
velocity of 10–15 cm/s. The flow pattern
normally is monophasic and has low resistance,
with high diastolic flow (. Fig. 1.1.8 ). The
resistance index (RI), which is defined as the
maximal systolic velocity minus the
end-diastolic velocity divided by the maximal
velocity, varies normally in a fasting patient from
0.55 to 0.81. There is increase in hepatic artery RI
after mean or with age in a healthy person. The
hepatic artery diastolic velocity is less than the
peak portal vein velocity, and if the hepatic
diastolic velocity is greater than the portal vein,
one should suspect hepatic parenchymal
disease. Also, the RI increases in patients with
cirrhosis, and the after meal variation is absent
(. Fig. 1.1.9 ).
5 Cruveilhier–Baumgarten syndrome is detected as
a patent vein located at the umbilicus with
typical monophasic venous flow (. Fig. 1.1.10 ).
The vein can be followed by the probe until
identifying its relation to the intrahepatic portal
veins passing through the ligamentum teres
(. Fig. 1.1.11 ).
 6 Chapter 1 · Gastroenterology

. Fig. 1.1.5 Color Doppler waveform spectrum of the hepatic

. Fig. 1.1.8 Color Doppler waveform spectrum of the hepatic
veins shows the normal venous triphasic pattern
artery shows the normal monophasic, low-resistance with high
diastolic flow arterial pattern

. Fig. 1.1.6 Color Doppler waveform spectrum of the portal . Fig. 1.1.9 Hepatic artery color Doppler waveform spectrum
vein shows the normal monophasic pattern in a patient with alcoholic liver cirrhosis shows high RI
(arrowhead)

. Fig. 1.1.7 Color Doppler waveform spectrum of the portal

vein shows the physiologic portal vein pulsation in athletic tall
patient who came for a routine abdominal ultrasound checkup
1.1 · Liver Cirrhosis
7 1

a b

. Fig. 1.1.10 Color Doppler sonography image shows patent umbilical vein at the level of the umbilicus (arrowheads) in a patient with
chronic liver cirrhosis and Cruveilhier–Baumgarten syndrome
 8 Chapter 1 · Gastroenterology

1 a b

. Fig. 1.1.11 The same patient shows the connection of the patent umbilical vein to the dilated portal vein through the ligamentum
teres (arrowhead)
1.1 · Liver Cirrhosis
Signs on Barium Swallow
5 Esophageal varices are visualized as serpiginous
filling defects in the esophagus, usually located in the
lower third (. Fig. 1.1.12).
a b
. Fig. 1.1.12 Barium swallow (a) and axial thoracic-enhanced CT (b) images in two patients with esophageal varices. In (a), the varices
are visualized as serpiginous filling defects in the lower esophagus (arrowheads). In (b), esophageal varices are visualized as multiple
paraesophageal enhanced tubular densities adjacent to the esophageal wall (arrows)
Signs on CT
5 Cirrhotic liver appears small (<15 cm), with
atrophied right lobe and enlarged caudate and left
lobes. The liver contour is nodular and irregular
due to parenchymal atrophy and nodular
regeneration (. Fig. 1.1.13).
5 Regenerative nodules are divided into
micronodules (<3 mm in diameter) and
macronodules (>3 mm in diameter). They do not
enhance in arterial phase because they are
supplied mainly by portal vein and enhance like a
normal liver parenchyma. Occasionally, they may
accumulate iron within them, which will make
them seen in noncontrast scans as hyperdense
nodules (siderotic nodules), which are typically
seen in alcoholic liver cirrhosis.
5 Dysplastic nodules are siderotic nodules larger than
1 cm. They enhance homogeneously in both
arterial and portal phases and are usually not seen
in scans. Few nodules may show enhancement in
9 1
the arterial phase and only differentiated from
HCC by biopsy.
5 Hepatocellular nodule is seen as a hypodense area
in nonenhanced CT scan and shows enhancement
in the arterial phase, which is the key to HCC
diagnosis. Up to 50 % of nodules are not detected
in the arterial phase because they behave as a
normal liver parenchyma in the triphasic hepatic
scan. The nodules become hypodense again in the
portal venous phase of the scan (. Fig. 1.1.13).
5 Portal hypertension can be detected if the portal
vein diameter increases (>13 mm). Also,
splenomegaly, dilated perisplenic collateral
venous channels, and ascites may be found as
signs of portal hypertension (. Fig. 1.1.14).
5 Esophageal varices are seen as multiple, enhanced
nodular or tubular densities inside the esophageal
lumen (intraluminal varices) or adjacent to the
esophageal wall (paraesophageal varices)
(. Fig. 1.1.12).
 10 Chapter 1 · Gastroenterology

1 5 Enlarged porta hepatic lymph nodes might be

seen in end-stage cirrhotic liver.
5 Cruveilhier–Baumgarten syndrome is visualized as
an abnormal vein that arises from the right or left
intrahepatic portal vein and leaves the liver via
ligamentum teres to attach itself to the umbilicus
on the portal phase of contrast-enhanced liver CT
(. Fig. 1.1.15).
5 On chest HRCT, hepatopulmonary syndrome is
visualized as peripheral pulmonary arteriole
dilatation with increased numbers of terminal
branches extending to the pleura
(. Fig. 1.1.16).
5 Liver venous hypertension due to congestive heart
failure (nutmeg liver) may show characteristic
reticulo-mosaic pattern of enhancement on
. Fig. 1.1.14 Axial CT scan in a patient with liver cirrhosis
postcontrast examinations (. Fig. 1.1.17). shows massive ascites that nicely demonstrates ligamentum
teres (arrowhead)

. Fig. 1.1.13 Coronal nonenhanced CT image shows mildly

shrunken liver due to cirrhosis with mild irregular contour and
hypodense nodule in segment IVb (arrowhead), which was
proven later to be HCC
1.1 · Liver Cirrhosis
11 1

a b

c d

. Fig. 1.1.15 Sequential axial abdominal enhanced CT of a patient with liver cirrhosis shows patent umbilical vein arises from the left
portal vein (a), runs through ligamentum teres (b), and joins the umbilicus (c). The course of the patent vein can be seen in the coronal
image in (d)

. Fig. 1.1.16 Axial chest HRCT illustration shows multiple

dilated peripheral pulmonary arterioles demonstrating
hepatopulmonary syndrome in patients with liver cirrhosis
 12 Chapter 1 · Gastroenterology
1 a
. Fig. 1.1.17 Axial (a) and coronal (b) contrast-enhanced CT in a patient with right-sided heart failure due to tricuspid regurgitation
shows the characteristic reticulo-mosaic pattern of enhancement of hepatic venous congestion
Signs on MRI
5 Hepatic encephalopathy has bilateral and
symmetrical high-intensity signal on T1W images
in the basal ganglia, especially in the globus
pallidus (. Fig. 1.1.18). The extent of the basal
ganglia disease is related to the plasma level of
ammonia. Cerebellar atrophy may be seen in
advanced stages.
5 Regenerated nodules with or without hemosiderin
have low T2 signal intensity. In contrast, a hepatic
carcinoma nodule appears hyperintense on T2W
images and shows early arterial-phase contrast
enhancement.
5 In PBC, periportal hyperintensity signal on T2W
images is observed in the initial stages of the
disease (stages I and II), reflecting active periportal
inflammation (. Fig. 1.1.19). A periorbital halo sign
may be seen as low-intensity signal centered
around the portal venous branches on T2W images
b
(. Fig. 1.1.19). This sign is specific for the diagnosis
of PBC. Lastly, a peripheral small wedge-shaped
area may be seen in the early phases of liver
contrast study, which represents arterial–portal
shunting.
5 Up to 50 % of uncompensated cirrhotic patients
show dilated cisterna chyli, which is seen as high
T2 signal intensity structure adjacent to the aorta,
with delayed enhancement several minutes after
gadolinium injection. This sign is detected on CT in
1.7 % of uncompensated cirrhotic patients.
5 Plantar fibromatosis is visualized as bilateral
infiltrative masses located at the deep aponeurosis
adjacent to the plantar muscles in the medial
aspect of the foot (. Fig. 1.1.20). The masses
typically show low T1 and T2 signal intensities due
to the fibrous nature of the lesion. After contrast
injection, enhancement of the masses can be seen
in approximately 50 % of cases.
1.1 · Liver Cirrhosis
13 1

. Fig. 1.1.19 Axial T2W MR illustration of the liver

demonstrates the periportal hyperintensity (arrows) and the
periorbital halo sign (arrowheads)

. Fig. 1.1.18 Axial T1W MR illustration shows bilateral

symmetrical high density in the globus pallidus representing
sign of hepatic encephalopathy
 14 Chapter 1 · Gastroenterology

1 a

. Fig. 1.1.20 Axial-oblique T2W (a) and T1W postcontrast MRI of the feet shows bilateral hypointense plantal masses (arrowheads) on
image (a) diagnostic of Ledderhose disease (plantar fibromatosis). The masses show marked contrast enhancement after gadolinium
injection (b)

Further Reading Colli A, et al. Severe liver fibrosis or cirrhosis: accuracy of US

Ba-Ssalamah A, et al. Dedicated multi-detector CT of the
esophagus: spectrum of diseases. Abdom Imaging. 2009;
34:3–18.
Bonekamp S, et al. Can imaging modalities diagnose and
stage hepatic fibrosis and cirrhosis accurately? J Hepatol.
2009;50:17–35.
Chavhan GB, et al. Normal Doppler spectral-waves of major
pediatric vessels: specific patterns. Radiographics. 2008;
28:691–706.
for detection – analysis of 300 cases. Radiology.
2003;227:89–94.
Ito K, et al. Imaging findings of unusual intra- and extrahe-
patic portosystemic collaterals. Clin Radiol. 2009;64:200–7.
Kobayashi S, et al. MRI findings of primary biliary cirrhosis:
correlation with Scheuer histologic staging. Abdom
Imaging. 2005;30:71–6.
Lim JH, et al. Regenerative nodules in liver cirrhosis: findings
at CT during arterial portography and CT arteriography
1.2 · Fatty Liver Disease (Liver Steatosis)
with histopathologic correlation. Radiology. 1999;210:
451–8.
Martinez-Noguera A, et al. Doppler in hepatic cirrhosis and
chronic hepatitis. Semin Ultrasound CT MR. 2002;23:19–36.
Mauro MA, et al. Computed tomography of hepatic venous
hypertension: the reticulated – mosaic pattern. Gastrointest
Radiol. 1990;15:35–8.
Meyer CA, et al. Diseases of the hepatopulmonary axis.
Radiographics. 2000;20:687–98.
Palazzi C, et al. Hepatitis C virus-related arthritis. Autoimmun
Rev. 2008;8:48–51.
Schuppan D, et al. Liver cirrhosis. Lancet. 2008;371:838–51.
Sharma S, et al. MRI diagnosis of plantar fibromatosis – a
rare anatomic location. Foot. 2003;13:219–22.
Verma SK, et al. Dilated cisternae chyli: a sign of uncompen-
sated cirrhosis at MR imaging. Abdom Imaging. 2009;34:
211–6.
15 1
Signs on US
5 Fatty liver is visualized as highly echogenic liver.
The high liver echogenicity can be compared to
the echogenicity of the right renal cortex, which
will show marked difference in echogenicity
(. Fig. 1.2.1).
5 Focal fatty infiltration is seen as a focal, highly
echogenic area within a relatively isoechoic (normal)
liver parenchyma (. Fig. 1.2.2).
5 Focal sparring is seen as a focal area which is
relatively hypoechoic (normal) within a highly
echogenic liver.

1.2 Fatty Liver Disease (Liver Steatosis)

Accumulation of lipid within cells is a pathologic process.

Any type of lipid can accumulate within cells, such as choles-
terol, triglycerides, and phospholipids. Fatty liver disease
(steatosis) is characterized by accumulation of triglycerides
within hepatocytes.
Normally, free fatty acids are taken up by the hepatocytes
and then converted into cholesterol esters, triglycerides, ketone
bodies, or phospholipids. Some of the lipids combine with
apoproteins to form a specific type of lipoprotein called very-
low-density lipoprotein (VLDL), which is then secreted into
the blood. Liver steatosis can result from either excess delivery
of free fatty acids into the liver (e.g., diabetes mellitus), . Fig. 1.2.1 Transverse ultrasound image of the liver shows
increased formation of lipids within the liver (e.g., alcohol diffuse increase in liver echogenicity compared to the right renal
ingestion), hepatocytes disease (e.g., hepatitis), or decreased cortex (liver steatosis)
formation of VLDL by the liver (e.g., protein malnutrition).

Types of Liver Steatosis

5 Diffuse fatty infiltration: the liver is usually enlarged with

uniform decrease in density in the liver scan.
5 Focal fatty infiltration: there is an area of the liver that
shows fatty infiltration while the rest of the liver is
normal. It usually occurs in the same areas that are
supplied by the third inflow systemic veins (porta
hepatic, around ligamentum teres, and adjacent to
gallbladder). It is seen most commonly in the left lobe of
the liver.
5 Multiple fatty infiltrations: there are scattered low-density
areas within a normal density liver. This type can be
easily mistaken with metastases on
noncontrast-enhanced liver CT scan.
5 Focal sparring: there are areas of normal liver . Fig. 1.2.2 Transverse ultrasound image of the liver
parenchyma surrounded by large areas of low-density shows focal fatty infiltration involving segment VI and
diffuse fatty infiltration. This type also may simulate segment VII
neoplasms on noncontrast-enhanced liver CT scan.
 16 Chapter 1 · Gastroenterology

1 Signs on CT not show mass effect over the parenchyma around it

5 Hepatic steatosis is detected as diffuse or focal
reduction of the liver normal density on
noncontrast-enhanced scan (. Fig. 1.2.3). The normal
liver density is 8 HU (Hounsfield unit) above that of
the spleen (60 HU). Fatty liver density is 10 HU below
spleen density on noncontrast-enhanced scan (if the
normal spleen is 52 HU, then the fatty liver is <42 HU).
5 Focal fatty infiltration is seen as a hypodense area
with nonspherical margins (metastases usually have
round edge). The hypodense area or the mass does
and shows change over time (seen in films before the
current scan or after few months’ scan). The same
criteria are applied to the focal sparring, but the mass
will be isodense within a hypodense liver on
noncontrast-enhanced scan.
5 In both focal sparring and focal fatty infiltration,
hepatic vessels course within the fatty infiltration or
focal sparring undisturbed. In contrast, metastases or
other hepatic lesions will be cutting off the hepatic
vessels when they reach them.

a b

. Fig. 1.2.3 Axial precontrast (a) and postcontrast (b) abdominal CT images show diffuse hepatic steatosis. Notice the density of the liver
compared to the spleen in pre- and postcontrast images

Signs on MRI
5 Liver steatosis is diagnosed on MRI when the liver
intensity drops to >30 % difference on both T1W
in-phase and T1W out-of-phase images (. Fig. 1.2.4).

a b

. Fig. 1.2.4 Axial T1W in-phase (a) and T1W out-of-phase (b) MRI in a patient with liver steatosis shows drop in the liver signal intensity
>44 % in the T1W out-of-phase image (b), diagnostic of hepatic steatosis
1.3 · Recurrent Epigastric Pain
Further Reading
Alpern MB, et al. Focal hepatic masses and fatty infiltration
detected by enhanced dynamic CT. Radiology. 1986;158:
45–9.
Cassidy FH, et al. Fatty liver disease: MR imaging techniques
for the detection and quantification of liver steatosis.
Radiographics. 2009;29:231–60.
Karcaaltincaba M, et al. Imaging of hepatic steatosis and fatty
sparing. Eur J Radiol. 2007;61:33–43.
Sabir N, et al. Correlation of abdominal fat accumulation and
liver steatosis: Importance of ultrasonographic and
anthropometric measurements. Eur J Ultrasound. 2001;
14:121–8.
Salmonson EC, et al. Focal periportal liver steatosis. Abdom
Imaging. 1993;18:39–41.
Yates CH, et al. Focal fatty infiltration of the liver simulating
metastastic disease. Radiology. 1986;159:83–4.
1.3 Recurrent Epigastric Pain
Epigastric pain is a term used to describe dull achy pain
located at the area of the epigastrium beneath the xyphoid
process. Epigastric pain is a very common complaint
encountered in both medical and surgical casualty depart-
ments. Diagnosis often is established by proper history,
examination, and laboratory investigations. This topic dis-
cusses some causes of recurrent epigastric pain, in which
radiology can play an important role in establishing the
underlying diagnosis.
Gastroesophageal Reflux Disease
Gastroesophageal reflux disease (GERD) is a disease charac-
terized by reduction of the lower esophageal sphincter pres-
sure resulting in leaking of the stomach acidity into the lower
third of the esophagus, causing esophagitis and epigastric
pain.
The most common cause of GERD is hiatus hernia. Four
types of hiatus hernias are known: sliding, paraesophageal,
sliding and paraesophageal, and complete stomach hernia-
tion into the thorax.
Patients with GERD typically present with long-standing
mild to moderate epigastric pain with burning sensation,
usually postprandial. Severe cases of GERD may manifest
due to propagation of gastric acidity to the upper esophagus.
Symptoms like aspiration pneumonia, laryngitis, and teeth
decay may be seen uncommonly due to advanced
GERD. Medical treatments include antacids, histamine (H2)
blockers, and proton pump inhibitors. Surgical management
with gastric fundoplication is usually advised in cases where
the medical therapy fails to control the symptoms.
Barium swallow is the most sensitive method to detect
GERD and esophagitis. Esophagitis is defined as defects in
the esophageal mucosa due to exposure to the gastric reflux
acid and pepsin. Barrett’s esophagus (BS) is a condition
17 1
characterized by esophageal mucosal healing in a persistent
acid environment. This healing process is characterized by
metaplasia of the normal esophageal stratified squamous epi-
thelium into columnar, gastric-like epithelium. Metaplasia is
transformation of one cell type to another (e.g., cuboidal cell
to columnar cell). BS has the potential for neoplastic trans-
formation. Up to 50 % of patients with GERD show esopha-
geal dysmotility disorders (EDM).
On barium swallow, sliding hiatus hernia is detected by
identifying Schatzki ring. An esophageal ring is a short
annular narrowing of the esophagus <1 cm in diameter.
Esophageal A ring is a ring made up of smooth muscles that is
seen at the tubulovestibular junction (muscular ring).
Esophageal B ring (Schatzki ring) is an esophageal ring that is
only visible radiologically when there is sliding hiatus hernia
and is caused by propagation of the gastroesophageal junc-
tion above the diaphragm. Esophageal C ring is the normal
abdominal retroperitoneal esophageal part (3 cm long)
which makes a groove on the liver. In contrast to esophageal
ring, esophageal stricture is defined as an esophageal segment
with fixed narrowing. Esophageal web is an abnormal thick
1–2 mm diaphragm-like membrane that extends partially or
completely around the esophageal lumen and always indents
the esophagus anteriorly. The lower esophageal sphincter line
where mucosal change is observed between the esophagus
and the stomach on barium examination is sometimes
referred to as the Z-line.
Esophageal dysmotility disorders are a group of diseases
characterized by abnormal esophageal peristalsis seen on
barium swallow. Types of EDM are tertiary contractions,
corkscrew esophagus, esophageal achalasia, esophageal cha-
lasia, and presbyesophagus.
Tertiary esophageal contraction is a nonpulsatile, uncoor-
dinating contraction of the esophageal circular smooth mus-
cles. The normal primary and secondary contractions of the
esophagus help to push the food and fluids through the
esophagus. This type of dysmotility is often seen with old age
or GERD. Corkscrew esophagus is a term used to describe the
same dysmotility as in tertiary contractions but arises poste-
rior to the heart, causing pain in the retrocardiac region dur-
ing swallowing. Esophageal achalasia is a disease characterized
by contraction and narrowing of the esophagus due to a
defect in the normal neuronal plexuses within the esophageal
muscles, which results in failure of the smooth muscles to
relax when the food arrives. Achalasia is commonly seen in
the lower third of the esophagus. Achalasia can occur with-
out prior cause (primary) or due to underlying pathology like
Chagas’ disease or malignancy (secondary). Esophageal cha-
lasia is characterized by dilatation and widening of the gas-
troesophageal junction. Presbyesophagus is an asymptomatic
condition characterized by failure of the primary peristaltic
wave to pass completely through the esophagus, resulting in
a combination of tertiary contractions, aperistalsis, and fail-
ure of the lower esophageal sphincter to contract (curling
phenomenon).
Hiatus hernia can be congenitally seen in neonates and
children. The most common congenital hiatal hernias are
 18 Chapter 1 · Gastroenterology

Morgagni and Bochdalek’s hernias. Morgagni hernia is

1 stomach or bowel herniation into the thorax due to diaphrag- Signs on Chest Radiographs
matic defects that occurs in the anterior/inferior mediasti- 5 Hiatal hernia is diagnosed by finding the stomach
num. Bochdalek’s hernia is stomach or bowel hernia into the bubble within the thorax, rather than under the
thorax due to diaphragmatic defects that occurs in the infe- left hemidiaphragm (. Fig. 1.3.1).
rior/posterior mediastinum. 5 Morgagni hernia is demonstrated as a mass, bowel
loop, or stomach bubble lying in the inferior/
anterior mediastinum on lateral radiographs
Differential Diagnoses and Related Diseases (. Fig. 1.3.2). In contrast, Bochdalek’s hernia is
demonstrated as mass, bowel loop, or stomach
5 Steakhouse syndrome is a term used to describe acute bubble lying in the inferior/posterior mediastinum
food impaction of the esophagus, usually at its distal on lateral radiographs (. Fig. 1.3.3).
third. The most common cause of food impaction is 5 In esophageal achalasia, there is paramediastinal
esophageal webs. Patients often present to the emergency shadow (widening of the mediastinum), with air–
ward with acute esophageal food impaction, especially fluid level seen in the retrocardiac shadow
after meat ingestion, where the name came from. Patients (. Fig. 1.3.4).
present with intense retrosternal pain, which may be
cardiac in origin, especially if the impacted food presses
over the posterior cardiac border. Plain chest radiographs
should be performed to exclude bony material impaction
or signs of pulmonary aspiration.
5 Plummer–Vinson syndrome (Paterson–Kelly syndrome) is
a disease characterized by dysphagia, iron-deficiency
anemia, and esophageal webs. Patients are commonly
women (85 %), between 30 and 70 years of age. Upper
aerodigestive tract carcinoma is seen in 4–16 % of cases,
with almost all cases occurring at the postcricoid
location.

. Fig. 1.3.1 Posteroanterior plain chest radiograph shows

herniated stomach into the thorax with the gastric bubble
observed in the thorax (arrowhead)
1.3 · Recurrent Epigastric Pain
19 1

a b

. Fig. 1.3.2 Posteroanterior (a) and lateral (b) plain chest radiographs show right mediastinal mass on (a), which is seen located within
the anterior/inferior mediastinum on lateral radiographs (arrows). The patient is a child, and the mass was omental and bowel herniation
due to an anterior congenital diaphragmatic defect (Morgagni hernia)

a b

. Fig. 1.3.3 Posteroanterior (a) and lateral (b) barium enema radiographs in a baby with Bochdalek’s hernia show herniation of part of
the transverse colon through a posterior/inferior diaphragmatic defect (b)
 20 Chapter 1 · Gastroenterology
1 a
. Fig. 1.3.4 Posteroanterior (a) and lateral (b) plain chest radiographs in a patient with achalasia show mild widening of the
mediastinum and air–fluid level behind the cardiac silhouette (arrowheads), representing fluid content within the dilated esophagus
Signs on Barium Swallow
5 In esophagitis, there is mucosal granularity, thickened
mucosal folds due to edema, and linear ulcers seen as
linear barium defects. Stricture formation is a sign of
chronic ulceration (. Fig. 1.3.5).
5 Diagnosis of hiatal hernia depends upon
identification of the gastroesophageal junction,
which is typically located at the termination point of
the converging gastric mucosa. Schatzki’s ring is seen
as a uniform round esophageal narrowing with a
distended small pouch representing the herniated
stomach above the diaphragm (. Fig. 1.3.6).
Herniation of the gastric fundus or body into the
thorax is a definite sign of hiatus hernia. Esophageal
webs are identified as incomplete esophageal
narrowing located anteriorly.
5 Barrett’s esophagus is divided into two types:
short-segment and long-segment BS. Short-segment
BS is characterized by mucosal metaplasia <3 cm
above the gastroesophageal junction, whereas
long-segment BS is mucosal metaplasia >3 cm above
b
the gastroesophageal junction. BS is classically
suspected when multiple lower esophageal mucosal
ulcerations, mid-esophageal stricture, and hiatal
hernia are found. The explanation of such suspicion
lies in the fact that the new gastric epithelium
secretes acid, which causes regional ulcers and
esophageal stricture later on. A reticular ringlike
pattern of ulceration above the gastroesophageal
junction, which mimics areae gastricae, is a relatively
specific sign of BS (. Fig. 1.3.7).
5 In tertiary contractures, the esophagus wall is irregular
with fine, multiple contractions that run in a wavy
appearance (. Fig. 1.3.8).
5 In achalasia, there is narrowing of the distal
esophagus with dilation of the esophagus proximal
to the narrowing, giving the so-called mouse-tail
appearance (. Fig. 1.3.9).
5 In Plummer–Vinson syndrome, anterior transverse
linear esophageal filling defects (webs) with focal
esophageal stenosis and poststenotic dilatation are
typically found (. Fig. 1.3.10).
1.3 · Recurrent Epigastric Pain
21 1

a b

. Fig. 1.3.5 Barium swallow examinations show patients with esophagitis. In patient (a), there is mucosal granularity with thickened
mucosal folds (arrowheads). In patient (b), there is stricture seen at the distal end of the esophagus (arrow)
 22 Chapter 1 · Gastroenterology

. Fig. 1.3.6 Barium swallow image at the distal third of the

esophagus in a patient with hiatus hernia shows Schatzki’s ring
(arrowheads), with the herniated part of the stomach beneath it
(black arrow)

. Fig. 1.3.8 Barium swallow image shows the classical

appearance of esophageal tertiary contractures as irregular,
multiple contractions that run in a wavy appearance

. Fig. 1.3.7 Barium swallow image at the gastroesophageal

junction shows the specific pattern multiple ringlike ulcers and
stricture of the esophagus >3 cm above the gastroesophageal
junction (long-segment Barrett’s esophagus (BS))
1.3 · Recurrent Epigastric Pain
23 1

a b

. Fig. 1.3.9 Barium swallow (a) and enhanced CT image (b) of two patients with achalasia shows the classical “mouse-tail” appearance in
patient (a) (arrowhead) and prestenotic dilatation with fluid residual in patient (b) (arrow)

Signs on CT
5 Hiatus hernia is demonstrated by the stomach
fundus or body lying within the posterior
mediastinum (. Fig. 1.3.11).
5 Morgagni hernia is seen as the stomach or bowel
within the anterior/inferior mediastinum, whereas
Bochdalek’s hernia is seen as the stomach or bowel
within the posterior/inferior mediastinum.
5 Esophagitis is visualized as uniform,
circumferential wall thickening of the esophagus
with a target sign formation.

. Fig. 1.3.10 Lateral barium swallow image in a patient with

Plummer–Vinson syndrome shows multiple anterior esophageal
webs (arrowheads) with esophageal poststenotic dilatation
 24 Chapter 1 · Gastroenterology
. Fig. 1.3.11 Axial (a) and coronal (b) enhanced CT images show herniation of the stomach into the posterior mediastinum (behind the
heart and anterior to the vertebral column) through the esophageal hiatus (hiatus hernia)
Peptic Ulcer Disease
Peptic ulcer is a disease characterized by mucosal ulceration
of the esophagus, stomach, or duodenum. Erosion is defined
as an area of mucosal destruction that does not extend
beyond the muscularis mucosae into the submucosa, whereas
ulcer is defined as an area of mucosal destruction that extends
beyond the muscularis mucosae into the submucosa or
serosa (in perforation).
The gastric mucosa is divided into three types: cardiac
mucosa, body-type (oxyntic) mucosa, and antral (pyloric)
mucosa. The body-type mucosa contains parietal (oxyntic)
cells that secrete hydrochloric acid and intrinsic factor and
chief cells that produce lipase and the proteolytic enzymes
pepsinogens I and II. The antral mucosa contains endocrinal
cells that produce gastrin (G cells), somatostatin (D cells),
histamine (ECL cells), and serotonin (enterochromaffin
cells).
The main defensive mechanism against the harmful
effects of the acid is the production of the mucus layer.
Defects in the mucus layer result in gastritis and peptic
ulceration.
Peptic ulcer initially starts as inflammation of the gastric
mucosa (gastritis), which, when not properly treated, can
progress into gastric ulcer. Causes of gastric ulcers include
severe stress situations like burns (Curling ulcer), increased
intracranial pressure (Cushing ulcer), alcoholism, cocaine
abuse, nonsteroidal anti-inflammatory drug (NSAID)
abuse, and bile salt reflux into the stomach in patients with
gastroduodenostomy (Billroth I) and gastrojejunostomy
(Billroth II).
Peptic ulcer disease and gastritis are linked to infection of
the gastric or duodenal wall with Helicobacter pylori, a spiral-
shaped gram-negative bacterium which is normally found in
the gastric antrum. H. pylori gastritis is found in up to 80 % of
patients with peptic ulcers.
Zollinger–Ellison syndrome (ZES) is a disease charac-
terized by severe gastric ulcers due to parietal cell hyper-
plasia in the body and the fundus of the stomach, mostly
due to gastrinomas (>80 %). Gastrinomas are gastrin-pro-
ducing, non-B islet cell tumors that are commonly found
within the gastrinoma triangle. The gastrinoma triangle is
formed by a line joining the confluence of the cystic and
common bile ducts superiorly, the junction of the second
and third portion of the duodenum inferiorly, and the
junction of the neck and body of the pancreas medially. Up
to 25 % of gastrinoma cases are part of multiple endocrine
neoplasia (MEN) syndrome type I, an autosomal domi-
nant disorder with tumors of the parathyroid glands
(87 %), pancreas (81 %), and pituitary gland (65 %). Ulcers
are detected in the first part of the duodenum in 75 % of
patients with ZES.
Radiological manifestations of gastric ulcer disease are
defined according to the stage of the ulcer. There are signs
of acute and chronic ulcers. The usual techniques to detect
mucosal abnormalities are the double contrast barium
meal and modern virtual gastroscopy. Virtual gastroscopy
is a three-dimensional (3D) reconstruction rendering
technique that uses multiplanar CT sections to recon-
struct 3D images of the stomach interior that mimics the
images seen in upper gastrointestinal endoscopy of the
stomach.
1.3 · Recurrent Epigastric Pain
Signs on Plain Radiograph
5 The sign of gastrointestinal or peptic ulcer
perforation is usually diagnosed by the presence
of free air under the diaphragm on erect
abdominal or chest films (pneumoperitoneum)
(. Fig. 1.3.12).
. Fig. 1.3.12 Anteroposterior plain abdominal radiograph
shows collection of air under the right diaphragm due to
duodenal ulcer perforation (arrowheads)
25 1
Signs on US
5 In up to 30 % of cases, perforation of a peptic ulcer
does not show free pneumoperitoneum but
instead penetrate adjacent structures (confined
perforation). In suspected cases of perforation, a
sonogram of the epigastric region may show an
extra-luminal inhomogeneous fluid collection
seen within the subhepatic space. This fluid
collection represents gastric contents leakage.
5 The stomach wall is usually thickened, and the
stomach is atonic, dilated, and maybe fluid filled
due to gastric outlet obstruction.
5 The presence of high echoic areas within the
inhomogeneous fluid collection representing air is
a pathognomonic finding of perforation.
Signs of Acute Ulcer on Barium Meal
5 Ring sign: the mucosal edge of the ulcer is covered
with barium while the center is not.
5 Arc sign: it occurs when the barium covers part of
the ulcer’s edge (. Fig. 1.3.13).
5 Smudge sign: shallow smudge barium spot represents
the area of mucosal ulceration (. Fig. 1.3.13).
5 Prominent area gastrica: it is an area of columnar
epithelium located in the stomach antrum, which
is normally seen as 2–3 mm, sharply edged,
polygonal radiolucencies on double barium meal.
Prominent area gastrica suggests the possibility of
H. pylori gastritis.
5 In ZES, there are markedly thickened mucosal folds
(Rugae), mainly found in the body and the fundus
of the stomach.
 26 Chapter 1 · Gastroenterology

. Fig. 1.3.13 Barium meal images of the duodenum in two different patients show duodenal acute ulcer arc sign in patient (a)
(arrowhead) and smudge sign in patient (b) (arrow)

Signs of Chronic Ulcer on Barium Meal

5 Ulcer crater sign: it is seen as a round area filled
with barium, with gastric folds radiating from the
crater due to fibrosis. This sign arises due to deep
chronic ulcer’s edge that mimics a volcano crater.
5 Incisura: it is a fold in the greater curvature due to
stricture of the mucosal folds around an ulcer.
Incisura may be found as a normal finding in
double contrast barium enema as an area of
angulation of the lesser curvature (. Fig. 1.3.14).
5 Meniscus sign: the mucosa around the ulcer’s crater
makes a halo due to edema of the mucosa
(. Fig. 1.3.15).

. Fig. 1.3.14 Barium meal image in a patient with normal

examination shows the incisura (arrowhead)
1.3 · Recurrent Epigastric Pain
27 1

contrast injection, gastrinoma shows intense

contrast enhancement in the arterial phase
(. Fig. 1.3.17). Liver metastasis may be seen. On
MRI, gastrinoma shows low T1 and high T2 signal
intensities with marked contrast enhancement on
the early arterial phase of the scan.

. Fig. 1.3.15 Barium meal image of the duodenum in a

patient with chronic duodenal ulcer shows the meniscus sign
(arrowheads)

. Fig. 1.3.16 Axial CT illustration demonstrates thickening of

the stomach wall with nodularity as a sign of chronic gastritis
Signs on Virtual CT Gastroscopy (arrowheads)
5 The images can be viewed on multiplanar
reformation (MPR) images or on 3D reconstructed
images.
5 In benign ulcers, there is thickening of the
stomach wall with preservation of the wall
stratification. Mild enhancement may be seen after
contrast injection.
5 In malignant ulcers, there is marked wall
thickening, with strong enhancement more than
the adjacent normal gastric wall after contrast
injection.

. Fig. 1.3.17 Coronal postcontrast CT image of a patient with

Signs on Conventional CT and MRI
5 Gastritis and H. pylori infection is detected as a
marked thickening and nodularity of the stomach
wall, especially in chronic gastritis (. Fig. 1.3.16).
Biopsy of the nodules by endoscopy is important
to exclude malignancy transformation. Up to 80 %
of patients with stomach cancers that arise outside
the cardia have positive antibodies against H.
pylori.
5 In ZES, there is a hypodense nodule with or
without calcification often seen in the duodenum
or the pancreas on nonenhanced images. After
Zollinger–Ellison syndrome (ZES) shows highly enhanced nodule
located between the second part of the duodenum and the
pancreatic head within the boundaries of the gastrinoma
triangle representing gastrinoma (arrowhead)
Superior Mesenteric Artery Syndrome
(Wilkie’s Syndrome)
Superior mesenteric artery syndrome (SMAS) is a disease
characterized by compression of the third part of the duode-
num by the superior mesenteric artery axis, causing recur-
rent, intermittent, or chronic duodenal obstruction.
The left renal vein, the uncinate process of the pancreas,
and the third part of the duodenum pass in the space between
 28 Chapter 1 · Gastroenterology

1 Signs on Barium Meal

5 Typically, the third part of the duodenum shows
sudden, longitudinal filling defect in the middle, at
the area where the duodenum passes below the
SMA (pathognomonic) (. Fig. 1.3.19).
5 Dilatation of the first and second part of the
duodenum with or without gastric dilatation is
commonly seen.

. Fig. 1.3.18 Sagittal ultrasound image shows the normal

aorto-mesenteric angle

the retroperitoneal aorta and its branch, the superior mesen-

teric artery (SMA). The SMA can compress the left renal vein
or the third part of the duodenum, a phenomenon known as
“nutcracker phenomenon.”
Compression of the third part of the duodenum by SMA
is an uncommon clinical situation and has been attributed
to loss of the retroperitoneal and mesenteric fat, exaggerated
lumbar lordosis, abnormal high fixation of the ligament of . Fig. 1.3.19 Barium meal image in a patient with superior
Treitz, or an unusually low origin of the SMA. The theory of mesenteric artery syndrome (SMAS) shows the classical barium
signs. Notice the sudden barium filling cutoff of the third part of
loss of the peritoneal fat as a predisposing factor for SMAS is
the duodenum (arrowhead) by the superior mesenteric artery
strengthened by the fact that this syndrome is almost never (SMA) impression over the duodenum (arrow)
observed in obese patients. SMAS has an incidence of
0.013–0.3 %.
The normal aorto-mesenteric angle is about 45° with the
SMA-aorta distance of 10–28 mm (. Fig. 1.3.18), where the
third part of the duodenum passes across the aorta. Any con- Signs on CT
dition that narrows the SMA-aorta distance or the aorto- 5 The CT shows duodenal stenosis at the area where
mesenteric angle can produce SMAS. the duodenum passes beneath the SMA, with
Patients with SMAS typically present with postprandial duodenal poststenotic dilatation (. Fig. 1.3.20).
epigastric pain, nausea, bilious vomiting, and abdominal dis-
tension. The pain is often relieved when the patient lies in the
left lateral decubitus, prone, or knee–chest position. Acute
presentation of the disease can be seen in patients who suf-
fered a recent rapid weight loss (e.g., aesthetic regime).

Signs on Doppler US
5 The SMA shows high resistant waveform with low
diastolic flow in a fasting patient because the
intestine is not in vascular demand.
5 In a fasting patient, SMA stenosis (>70 %) shows
peak systolic velocity (PSV) >275 cm/s and
end-diastolic velocity (EDV) >45 cm/s. Also, there
is focal increase in velocity, with signs of
turbulence. Turbulence within the SMA is observed . Fig. 1.3.20 Axial CT illustration shows the typical appearance
as aliasing artifact with mosaic color flow. of superior mesenteric artery syndrome. The third part of the
5 Reduced aorto-mesenteric angle (<45o). duodenum is compressed as it passes beneath the SMA (arrow)
1.3 · Recurrent Epigastric Pain
29 1
Median Arcuate Ligament Syndrome
(Celiac Trunk Compression Syndrome/ Signs on CT Angiography
Dunbar’s Syndrome) 5 The median arcuate ligament shows extrinsic
compression of the celiac axis by a MAL
Median arcuate ligament syndrome (MALS) is a rare disease (. Fig. 1.3.21).
characterized by compression of the celiac trunk by the 5 Pancreaticoduodenal artery aneurysm may occur
median arcuate ligament of the diaphragm at the level of the in 3–18 % of cases of MALS.
aortic hiatus. In most patients, the celiac artery is displaced
cranially or the diaphragm is displaced caudally. The disease
has an incidence of 2:100,000 patients and has high female
incidence between 30 and 50 years of age.
Patients with MALS are classically young females (20–40
years) who are very thin presenting with recurrent, nonspe-
cific epigastric pain due to intestinal ischemia and sympa-
thetic–autonomic nerve plexi compression. The pain is often
postprandial and may be accompanied by vomiting, nausea,
and weight loss, making the clinical picture more like peptic
ulcer disease or gastritis. Postprandial pain typically starts
30 min after eating and may last 1–4 h. The pain can be initi-
ated by exercise and aggravated by deep expiration. Recurrent
diarrhea is frequently seen and explained by the irritation of
the celiac plexus. The symptoms appear most frequently in
adults.
Clinically, in patients with MALS, an epigastric bruit or . Fig. 1.3.21 Axial CT illustration shows the typical
thrill may be heard by auscultation, due to the high blood appearance of median arcuate ligament syndrome (MALS). The
velocity within the compressed celiac trunk. diaphragm compresses over the celiac trunk with arterial
stenosis (arrowhead)
Because of the rarity of this disease, assumption of MALS
must be carried out after excluding all the common causes of
epigastric pain like esophagitis, gastritis, and peptic ulcer dis-
ease by endoscopy.
MALS sometimes can be associated with cases of Recurrent Abdominal Pain of Childhood
Takayasu arteritis due to inflammation of the celiac trunk.
Recurrent abdominal pain of childhood is a common com-
plain of school children (8–15 %). It is defined as abdominal
or epigastric pain that occurs on at least three occasions
within a period of at least 3 months. The pain may be severe
Signs on Doppler US and associated with pallor. It is mostly psychogenic in origin
5 The normal celiac artery waveform is low with no need for radiological diagnosis. Any other pain that
resistant with high diastolic flow and no does not match this definition should be investigated.
turbulence. In a fasting patient, celiac artery
stenosis (>70 %) shows PSV >200 cm/s and EDV Further Reading
>55 cm/s. Anderson SR, et al. Plummer-Vinson syndrome herald by
5 MALS is characterized by celiac artery blood postcricoid carcinoma. Am J Otolaryngol. 2007;28:22–4.
velocity change during inspiration and Ba-Ssalamah A, et al. Dedicated multi-detector CT of the
expiration (Doppler sign of MALS). To confirm this esophagus: spectrum of diseases. Abdom Imaging. 2009;
sign, the celiac artery velocity during inspiration 34:3–18.
and expiration must be measured by comparing Bhattacharjee PK. Wilkie’s syndrome: an uncommon cause
the velocity difference. The stenosis in MALS of intestinal obstruction. Indian J Surg. 2008;70:83–5.
typically decreases when the patient stands in Bhattacharya D, et al. Superior mesenteric artery syndrome
upright position or when he takes deep (Wilkie’s syndrome) complicating recovery from poste-
inspiration because the celiac has a more caudal rior fossa surgery in a child – a rare phenomenon. Childs
orientation. In a real celiac trunk stenosis or Nerv Syst. 2008;24:365–7.
obstruction, the stenotic velocity does not change Canon CL, et al. Surgical approach to gastroesophageal reflux
with respiration. disease: what the radiologist needs to know. Radiographics.
2005;25:1485–99.
 30 Chapter 1 · Gastroenterology
Chen CY, et al. Differentiation of gastric ulcers with
1 MDCT. Abdom Imaging. 2007;32:688–93.
Coulier B, et al. Gastric ulcer penetrating the anterior
abdominal wall: ultrasound diagnosis. Abdom Imaging.
2003;28:248–51.
Ellison EC, et al. The Zollinger-Ellison syndrome: a compre-
hensive review of historical, scientific, and clinical consid-
erations. Curr Probl Surg. 2009;46:13–106.
Fishman EK, et al. CT of the stomach: spectrum of disease.
Radiographics. 1996;16:1035–54.
Foertsch T, et al. Celiac trunk compression syndrome requir-
ing surgery in 3 adolescent patients. J Pediatr Surg.
2007;42:709–13.
Frangos SG, et al. Recurrent celiac trunk compression syn-
drome. Int J Angiol. 1999;8:150–3.
Hayes R. Abdominal pain: general imaging strategies. Eur
Radiol. 2004;14:L123–37.
Iwazawa J, et al. Successful embolization of a ruptured pan-
creaticoduodenal artery aneurysm associated with the
median arcuate ligament syndrome. Indian J Radiol
Imaging. 2008;18:171–4.
Kim JH, et al. Imaging of various gastric lesions with 2D
MPR and CT gastrography performed with multidetector
CT. Radiographics. 2006;26:1101–18.
Kohler TR, et al. Pancreaticoduodenectomy and the celiac
trunk compression syndrome. Ann Vasc Surg. 1990;4:
77–80.
Levine MS. Barrett esophagus: update for radiologists.
Abdom Imaging. 2005;30:133–41.
Lippl F, et al. Superior mesenteric artery syndrome: diagnosis
and treatment from the gastroenterologist’s view. J
Gastroenterol. 2002;37:640–3.
Makam R, et al. Laparoscopic management of superior mes-
enteric artery syndrome: a case report and review of the
literature. J Minim Access Surg. 2008;3:80–2.
Okada M, et al. Radiographic findings of intractable gastric
ulcers with H2-receptor antagonists. Abdom Imaging.
1996;21:133–41.
Ortiz C, et al. Familial superior mesenteric artery syndrome.
Pediatr Radiol. 1990;20:588–9.
Payawal JH, et al. Superior mesenteric artery syndrome
involving the duodenum and jejunum. Emerg Radiol.
2004;10:273–5.
Ranschaert E, et al. Confined gastric perforation: ultrasound
and computed tomographic diagnosis. Abdom Imaging.
1993;18:318–9.
Reddy RR, et al. Superior mesenteric artery syndrome after
correction of scoliosis – a case report. Indian J Orthop.
2005;39:59–61.
Rubesin SE, et al. Gastritis from NSAIDS to Helictobacter
pylori. Abdom Imaging. 2005;30:142–59.
Santer R, et al. Computed tomography in superior mesen-
teric artery syndrome. Pediatr Radiol. 1991;21:154–5.
Stadler J, et al. The ‘steakhouse syndrome.’ Primary and
definitive diagnosis and therapy. Surg Endosc. 1989;3:
195–8.
Sugiyama K, et al. Analysis of five cases of splanchnic artery
aneurysm associated with celiac artery stenosis due to
compression by the median arcuate ligament. Clin Radiol.
2007;62:688–93.
Thompson WM, et al. Unusual manifestations of peptic ulcer
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pression syndrome: case series and review of current
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doi:10.1007/s11605-088-0702-9.
1.4 Inflammatory Bowel Diseases
Inflammatory bowel diseases (IBDs) are a group of diseases
characterized by idiopathic chronic inflammation of the gas-
trointestinal (GI) tract, extraintestinal manifestations, and
relapsing course. IBDs are divided into Crohn’s disease,
ulcerative colitis (UC), and indeterminate colitis (6 %).
Diagnosis of IBDs depends mainly on clinical presentation
and biopsy-proved inflammatory changes in a sample taken
by colonoscopy. Radiology offers multiple noninvasive meth-
ods to monitor the progression of the diseases and their com-
plications through barium studies, CT of the bowel, and MR
enteroclysis. Multiple radiographic signs are described in the
literature describing different stages of IBDs. An understand-
ing of the basic composition of the bowel wall is mandatory
for the radiologist to understand the radiographic signs
encountered while investigating IBDs in any radiological
modality.
Bowels are hollow organs composed of circumferential
wall and circular mucosal folds (plica circularis in intes-
tines and haustrations in the colon). The basic layers of the
entire GI tract are composed of the innermost layer
(mucosa), inner layer (submucosa), middle layer (muscu-
laris), and outer layer (adventitia and serosa). The mucosal
layer of the intestine is composed of columnar epithelium
with secretory activity and a thin layer of connective tissue,
containing capillaries and lymphatics (Peyer’s patches),
and usually called “lamina propria.” The lamina propria is
separated from the submucosa by a thin layer of smooth
muscles called the “muscularis mucosa.” Beneath the mus-
cularis mucosa lies the submucosa, which is a layer com-
posed of loose areolar connective tissue containing the
major lymphatic and vascular channels of the bowel wall.
Also, glandular (crypts of Lieberkuhn) and neural struc-
tures (Meissner’s plexus) lie within the submucosa. Below
the submucosa lies the muscular wall or “muscularis pro-
pria,” which is divided into an inner circumferential and an
outer longitudinal layer. Between layers is the myenteric
neural plexus of Auerbach. The outermost layer consists of
loose connective tissue called the “adventitia,” which is
covered by a thin line of peritoneal layer called the “serosa.”
The normal bowel wall is 3 mm in thickness on radio-
graphic examinations, and the mucosal folds are <3 mm in
thickness.
Another random document with
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“The principal defects may be presented under the following
headings:

1. Insufficiency in the amount of food allotted.

2. Wrong relative amounts of different classes of food, making it
difficult to serve balanced rations.
3. Unsatisfactory method of distribution of food among the
prisoners.
4. Inadequate system of food allotment and estimates at the
central office.”

Their observations at Sing Sing confirm the report of Warden

Kirchwey.
“With a view to varying the daily menu as much as possible a new
dietary was established early in the year by Dr. Emily C. Seaman, of
Columbia University. A new kitchen was provided in what was
formerly known as the old boiler room, with concrete floor, and walls
and ceiling enameled white. New equipment was installed, including
potato steamers, aluminum kettles, steam kettles, an electric meat
chopper, electric potato paring machine, large gas range for roasting
meats, and large coffee urns. Those employed in the kitchen and
mess hall are dressed in white duck suits. Tables with white
enameled tops and chairs with backs are being installed in place of
the old tables and stools. The new arrangement is reported to have
improved the quality and cleanliness of the food served.”

A Scientific Ration.

In order to make our contention clear, it seems necessary to impart

some technical information.
The value of food is estimated in calories. A calorie may be
expressed in terms of heat or in terms of work. In the laboratory and
by experimentation with human subjects the value of all foods has
been very scientifically demonstrated. Foods largely consist of
proteins, fats and carbohydrates, which have the function of
supplying the body with energy or the power to work. The proper
proportion of these constituents of food makes up a balanced ration
which satisfies our physical needs in the way of nourishment. We get
our carbohydrates from bread, fruits, vegetables, sugar and all grain
products. Fats are derived from meats, eggs, butter, milk, nuts, etc.
The proteins are derived from meats, eggs and some vegetables,
especially beans.
A calorie in terms of heat is defined as the amount required to raise
one pound of water four degrees Fahrenheit. In terms of work or
physical energy a calorie represents the amount of food required to
lift 100 pounds about 30 feet.
It has been ascertained that the average amount of calories required
daily is about 3000 calories for a man who takes exercise. 2500
calories are regarded sufficient for a man who does not take
exercise.
Now a good balanced ration for the average man who is working
moderately may be estimated in the following proportion:
Carbohydrates 2000 calories
Fats 800 calories
Proteins 300 calories
——
3100 calories

Dietary for a Prison.

At the request of the Prison Association of New York a dietary, with

cost values, was prepared by Mr. William Golden, General Inspector
and Dietitian of the Department of Correction, New York City, and Dr.
Emily C. Seaman, Instructor in physiology and chemistry in
Teachers’ College, Columbia University. They suggested a dietary for
fourteen consecutive days and made an estimate of the cost. The
average daily cost for each prisoner was 18.4c, based on prices
February, 1917.
As a sample we present their proposed bill of fare for three alternate
days:
 Wednesday.
Breakfast—Oatmeal with milk and sugar, fruit, bread, coffee with milk
and sugar.
Dinner—Roast beef, cornstarch pudding, rice, carrots, raisin sauce,
bread, coffee with milk and sugar.
Supper—Vermicelli soup, graham bread, tea with sugar.
Friday.
Breakfast—Puffed wheat with milk and sugar, bread, coffee with milk
and sugar.
Dinner—Bread, coffee with milk and sugar, salmon, scalloped rice
and tomatoes.
Supper—Bread pudding with raisins, bread, tea with sugar.
Sunday.
Breakfast—Rice with syrup, graham bread, coffee with milk and
sugar.
Dinner—Roast beef, baked potatoes, peas, graham bread, gelatine,
coffee with milk and sugar.
Supper—Cornstarch pudding, gingerbread, tea with sugar.
Now the dietary given above was prepared with special reference to
the physical requirements of the human system. The ingredients are
in the correct proportion to insure health and happiness. Let no one
think this menu is extravagant. The following table presents the
exact amounts given to each person with the cost value. It will
surprise many a warden to note that the total cost is little in excess of
the usual monotonous and haphazard dietary.

Daily Amount and Cost for Each Inmate.

Wednesday.
Oatmeal, 1 oz. $ .00234
Milk, ½ pint .01743
Beef, 9 oz. .06283
Coffee, ⅔ oz. .00530
Fruit, 1 piece .01
Cornstarch, ½ oz. .00138
Raisins, 2 oz. .01016
Bread, 24 oz. .03375
Rice, 1 oz. .00219
Cheese, ½ oz. .00735
Vermicelli, 2 oz. .0084 $ .16113
Estimated value in calories, 3000.

Friday.
Puffed wheat, 1 oz. $ .00235
Milk, ½ pint .01743
Salmon, canned, 4 oz. .05313
Rice, 1 oz. .00219
Tomatoes, 2 oz. .00644
Bread, 24 oz. .03375
Raisins, 2 oz. .01016
Coffee, ⅔ oz. .00530
Tea, .11 oz. .00115
Sugar, 2 oz. .00741 $ .13931
Estimated value in calories, 2600.

Sunday.
Rice, 1 oz. $ .00219
Syrup, 1 oz. .00226
Milk, ½ pint .01743
Sugar, 2 oz. .00741
Bread, 24 oz. .03375
Roast Beef, 9 oz. .06283
Potatoes, 10 oz. .025
Peas, 2 oz. .01087
Gelatine, 2 oz. .00375
 Cornstarch, ½ oz. .00276
Gingerbread, 8 oz. .02
Tea, .11 oz. .00115
Coffee, ⅔ oz. .00530 $ .19470
Estimated value in calories, 3800.
The average cost for these three days for each inmate, 16½ cents.
Now this is an imaginary bill of fare, not supposed to be served in
any institution in the world. It is a suggestion of possibilities. The new
service at Sing Sing may approximate to this list of eatables.

Eats in a Michigan Prison.

In the report of the Michigan State Prison for two years ending June
30, 1916, we find the daily menu for every meal in a whole year.
Twenty-six pages of the report are taken up with this schedule of
eatables.
An extract from this report explains the unusual pains to publish the
bill of fare.
“An old adage states that one of the avenues to a man’s heart is
through his stomach. The now existing system of intensive farming,
and of canning the surplus fruits and vegetables not consumed by
the prison commissary has furnished the Michigan State Prison with
unusual opportunity to supply food products. The opportunity is
reflected in the following menu, showing the food actually served
during the last fiscal year.”
We present the menu for a few days selected from different times of
the year:
Saturday, July 3, 1915.
Breakfast—Oatmeal, milk, sugar, bread, butter, coffee.
Dinner—Fried pork steak, mashed potatoes, cream gravy, stewed
tomatoes, bread, iced tea, cookies, strawberry shortcake.
Supper—Lunch from dinner, bread, coffee.
 Sunday, August 1, 1915.
Breakfast—Hot biscuits, syrup, fried potatoes, bread, butter, coffee.
Dinner—Roast beef, browned potatoes, beans, lettuce, radishes,
bread, mince pie, iced tea.
Supper—Lunch from dinner, bread, coffee.
Wednesday, December 15, 1915.
Breakfast—Liver and bacon, steamed potatoes, bread, gravy, coffee.
Dinner—Boiled beef, fried parsnips, steamed potatoes, onions,
mashed turnips, tomato pickle, bread.
Supper—Bean soup, corn bread, crackers, bread, coffee.
Thursday, February 24, 1916.
Breakfast—Baked hash, gravy, bread, coffee.
Dinner—Baked beans, pork, syrup, steamed potatoes, bread,
buttermilk.
Supper—Rice soup, corn bread, crackers, bread, coffee.
Tuesday, May 23, 1916.
Breakfast—Creamed potatoes, apple jelly, bread, coffee.
Dinner—Boiled pork, stewed beans, horseradish, mashed
rutabagas, green onions, bread, buttermilk.
Supper—Rice soup, rhubarb pie, bread, coffee.
Complete menus are given for 364 days, or for 1092 meals. No, we
were not quoting from the Ritz-Carlton cuisine, but from the culinary
department of a western penal establishment.

Elmira Reformatory.

The daily bill of fare at the Elmira Reformatory shows that the
question of the serving and the variety of food has had careful
thought. We quote from a recent report of the State Commission of
Prisons, N. Y.
“This institution has one of the best equipped kitchens in the State. It
is kept scrupulously clean and the waste has been reduced to a
minimum. A physician makes frequent inspections which include an
examination of the inmates employed in the kitchen and mess halls.
Special white suits are provided.”
Sunday.
Breakfast—Rolled oats, bread, coffee, syrup.
Dinner—Beef soup, corned beef, boiled potatoes, bread, coffee,
pudding.
Supper—Stewed raisins, spice cake, bread, butter, syrup, tea.
Monday.
Breakfast—Creamed rice, bread, coffee.
Dinner—Roast beef, brown gravy, potatoes, bread, coffee, rice
pudding.
Supper—Roast beef hash, bread, butter, syrup, tea.
Friday.
Breakfast—Rolled oats with milk and sugar, bread, coffee.
Dinner—Macaroni with tomato sauce, creamed potatoes, rice
pudding with raisins, bread, coffee.
Supper—Creamed rice, bread, butter, syrup, tea.

Albany, N. Y.

From the same report we learn of a more modest menu at the

Albany County Prison. Besides the conventional bread and coffee
served every morning, there was always an additional article of food.
Beginning with Monday in one week, these articles in consecutive
order were oatmeal, hash, rice and syrup, cornbeef hash, oatmeal,
hash, rice and jelly.
For supper the invariable ration was bread, beef stew and tea. For
dinner, always bread and coffee, meat four times weekly, pea soup
one day, bean soup one day, and on Sunday beans and eggs.
This menu is above the average for variety and quantity.
There are many institutions still serving bread and coffee night and
morning, and a dinner of weak soup, with more or less meat and
vegetables.

Buying for Institutions.

In the last report of the Board of State Charities, Ohio, Mr. Henry C.
Eyman, of Massillon, makes some wise suggestions in regard to
some economical variation of the dietary.
“By a little care in arranging the diet list a great saving may result. It
is easy to reduce the total cost of your food supply 25%. Does that
look unreasonable? Well, let us analyze some prices. We must use
present-day prices because we know not what tomorrow may bring.
Suppose you have potatoes on the bill of fare twice daily, or fourteen
times a week, the cost for 1000 persons would be at present prices,
$32.00 per meal, or $448.00 per week. Now substitute for potatoes,
rice three times, hominy twice and corn meal mush three times, your
total cost of potatoes will be six times $192.00; rice three times
$6.00; hominy twice $4.00; corn meal mush three times $5.00, or a
total of $207.00, as against $448.00, or a saving of $241.00 per
week, or $12,532 per year. Now let us substitute evaporated
peaches, evaporated apples and evaporated apricots for these same
goods canned. Fruits should be used once daily. The canned fruits
will cost an average of $14.00 a meal for 1000 persons, while the
evaporated fruit will cost an average of $4.00 for same number, a
saving of $10.00 per day, or $3,650.00 a year. Now you will admit
that fish is a desirable article of diet for at least 32 weeks a year.
Suppose fish be placed on your bill of fare twice a week for 32
weeks, or in all for 64 meals. Beef, pork or mutton will all cost about
the same, or for 1000 persons $45.00. Fish for same number, $18.00
to $20.00, or a saving per meal of $25.00 to $27.00, or for the year,
$1670.00. Now, in these three items just mentioned we have
effected a saving of $16,000.00, or more than 25% of your entire
food cost. The entire food cost for 1000 persons will run between
$40,000.00 and $45,000.00 per annum.
“It is an easy matter to take every article of food which makes your
dietary, calculate food values and prices and make your bill of fare in
accordance therewith. Entirely too much meat is used by all of us.
Beans, peas, asparagus, milk, cheese and spinach make an
excellent direct substitute. This is conservation, without loss in heat
units or even in the tastiness of the food.”

Dietary in Illinois.

In the Institution Quarterly, published by the Public Charity Service of

Illinois, Mr. Thomas Carroll, Traveling Steward for the Board, writes
in regard to the waste which has been so prevalent in public
institutions.
“The lack of proper distribution, indifference as to preparation, lack of
proper knowledge of the amounts of food required, have been chief
impediments encountered in some of the institutions. Non-utilization
of food up to its fullest possibilities has also been a serious drawback
in the past.”
Among the defects found in the institutions were:

1. Too much food of one kind. Entire lack of variety.

2. Poorly balanced menus.
3. An overamount of meat, occasionally an under supply.
4. Making of bones into soap instead of stock for soup.
5. Waste of fats.
6. Poor supervision in serving the food.
7. Inadequate chinaware or dishes in general.
8. Unsanitary conditions in the kitchen and in service.

“With the co-operation of managers, storekeepers, cooks and

servers, nearly all these defects have been remedied to a large
degree.”
One illustration will indicate the nature of the service of Mr. Carroll.
“One institution which usually purchased 11,000 to 13,000 pounds of
cooking oils and lard annually has not purchased a single pound
since the first visit of the Steward. Excessive fats are trimmed from
the meats, and are rendered in a large caldron expressly made for
that purpose, and there is at present a surplus of nearly 5,000
pounds on hand, notwithstanding the fact that every requisition for
fats and oils have been filled.
“By saving all bones the same institution has an excellent supply of
soup two or three times each week for the entire institution. It is of
excellent quality, superior to that served in most restaurants.”

Dietary for 1000 Persons.

At the special request of the Secretary of the Society,

Superintendent Eyman has prepared for our readers the following
table, to which we call the attention of all superintendents, wardens
and managers of public institutions. The estimates are based on the
food requirements for an institution having 1000 inmates, and
include the complete menu for every day in a week, with amounts,
prices and food values. This table was prepared before the President
had issued his request with reference to our abstinence from meats
and white bread on certain days of the week. It can readily be
modified to meet the present food conditions of the country.
His estimate of the daily cost for each inmate is only 16 cents and
thus indicates that a considerable variety may be served without
undue expense. It is not intended that any purveyor may follow the
exact program, but his suggestions are highly interesting.

BILL OF FARE FOR ONE WEEK FOR AN

INSTITUTION OF 1,000 INMATES
By Henry C. Eyman, Superintendent Ohio State Hospital, Massillon,
Ohio.

SUNDAY.

BREAKFAST.
Items Amount Cost
Baked beans 150lbs. (raw) $11.75
With pork 50lbs. 11.00
Evaporated fruit 90lbs. 9.45
Bread 80loaves 4.40
Butter 25lbs. 12.50
Milk 480lbs. 14.40
Coffee 8lbs. .96
Sugar 9lbs. .75

DINNER.
Roast pork 300lbs. 66.00
Gravy 10lbs. .50
Potatoes 5bushels 6.25
Bread 80loaves 4.40
Pie 29.50
Coffee 6lbs. .72
Tea 2lbs. .48
Sugar 9lbs. .75

SUPPER.
Tapioca pudding 5.85
Hot biscuit 6.00
Syrup 4.00
Butter 25lbs. 12.50
Tea 2lbs. .48
Sugar 9lbs. .75
Milk 480lbs. 14.40
———
Total cost Sunday for 1,000 inmates $217.79
Approximate cost for each inmate 21⅘ cents
Food value for each inmate, 2,700 calories.

MONDAY.
 BREAKFAST.
Items Amount Cost
Evaporated fruit 90lbs. $ 9.45
Oatmeal 71lbs. 3.20
Bread 80loaves 4.40
Butter 25lbs. 12.50
Milk 480lbs. 14.40
Coffee 8lbs. .96
Sugar 9lbs. .75

DINNER.
Beef Stew 26.84
Macaroni 85lbs. 5.95
Bread 80loaves 4.40
Tea 2lbs. .48
Coffee 6lbs. .72
Sugar 9lbs. .75

SUPPER.
lbs.
Cornmeal mush 70 5.85
(meal)
Evaporated fruit 90lbs. 9.45
Bread 80loaves 4.40
Butter 25lbs. 12.50
Tea 2½lbs. .60
Milk 480lbs. 14.40
Sugar 9lbs. .75
————
Total cost Monday for 1,000 inmates $132.75
Approximate cost each inmate 13¼ cents
Food value for each inmate, 2,631
calories.

TUESDAY.
 BREAKFAST.
Items Quantity Cost
Prunes 54lbs. $ 4.72
Boiled potatoes 5bushels 6.25
Rye bread 70loaves 3.50
Butter 25lbs. 12.50
Coffee 8lbs. .96
Milk 480lbs. 14.40
Sugar 9lbs. .75
DINNER.
Boiled pork 65lbs. } 12.50
Boiled cabbage 400lbs. }
Red beets 8bushels 8.00
Rye bread 70loaves 3.50
Sugar 9lbs. .75
Coffee 6lbs. .72
Tea 2lbs. .48

SUPPER.
Stewed corn 100lbs. 4.00
Rye bread 70loaves 3.50
Butter 25lbs. 12.50
Tea 2¼lbs. .52
Milk 480lbs. 14.40
Sour pickles 25gal. 3.00
Sugar 9lbs. .75
———
Total cost Tuesday for 1,000 inmates $107.70
Approximate cost each inmate 10⅘ cents
Food value for each inmate, 2,658 calories.

WEDNESDAY.

BREAKFAST.
Items Quantity Cost
Sausage 200lbs. $32.00
Oatmeal 71lbs. 3.20
Bread 80loaves 4.40
Butter 25lbs. 12.50
Coffee 8lbs. .96
Milk 480lbs. 14.40
Sugar 9lbs. .75

DINNER.
Boiled pork 300lbs. 66.00
Navy beans 165lbs. 18.00
Kraut 4.56
Bread 80loaves 4.40
Coffee 6lbs. .72
Tea 2lbs. .52
Sugar 9lbs. .75
SUPPER.
Gingerbread 4.80
Cornmeal mush 70lbs. 5.85
Evaporated fruit 90lbs. 9.45
Bread 80loaves 4.40
Butter 25lbs. 12.50
Tea 2lbs. .52
Milk 480lbs. 14.40
Sugar 9lbs. .75
———
Total cost Wednesday for 1,000 inmates $215.83
Approximate cost each inmate 21⅗ cents
Food value for each inmate, 2,631 calories.

THURSDAY.

BREAKFAST.
Items Quantity Cost
Evaporated fruit 90lbs. $ 9.45
Rice 50lbs. 5.00
Bread 80loaves 4.40
Butter 25lbs. 12.50
Coffee 8lbs. .96
Milk 480lbs. 14.40
Sugar 9lbs. .75

DINNER.
Beef Stew 26.84
Macaroni 85lbs. 5.95
Bread 80loaves 4.40
Coffee 6lbs. .72
Tea 2lbs. .48
Sugar 9lbs. .75

SUPPER.
Stewed tomatoes 50gal. 12.50
Cinnamon rolls 4.80
Evaporated fruit 90lbs. 9.45
Bread 80loaves 4.40
Butter 25lbs. 12.50
Tea 2lbs. .48
Milk 480lbs. 14.40
Sugar 9lbs. .75
————
Total cost Thursday for 1,000 inmates $145.88
Approximate cost each inmate 14⅗ cents
Food value for each inmate, 2,900 calories.

FRIDAY.

BREAKFAST.
Items Quantity Cost
Evaporated fruit 90lbs. $ 9.45
Farina 45lbs. 2.70
Bread 80loaves 4.40
Butter 25lbs. 12.50
Coffee 8lbs. .96
Milk 480lbs. 14.40
Sugar 9lbs. .75

DINNER.
Fish 300lbs. 27.00
Potatoes 5bushels 6.25
Navy beans 150lbs. 17.25
Bread 80loaves 4.40
Coffee 6lbs. .72
Tea 2lbs. .48
Sugar 9lbs. .75

SUPPER.
Oatmeal 71lbs. 3.20
Red beets 8bushels 8.00
Bread 80loaves 4.40
Butter 25lbs. 12.50
Tea 2lbs. .48
Milk 480lbs. 14.40
Sugar 9lbs. .75
————
Total cost Friday for 1,000 inmates $145.74
Approximate cost each inmate 14⅘ cents
Food value for each inmate, 2,627 calories.

SATURDAY.

BREAKFAST.
 Items Quantity Cost
Liver 225lbs. $29.25
Bacon 16lbs. 9.60
Oatmeal 71lbs. 3.20
Bread 80loaves 4.40
Butter 25lbs. 12.50
Coffee 8lbs. .96
Milk 480lbs. 14.40
Sugar 9lbs. .75

DINNER.
Pork 65lbs. } 12.50
Cabbage 400lbs. }
Red beets 8bushels 8.00
Bread 80loaves 4.40
Sugar 9lbs. .75
Coffee 6lbs. .72
Tea 2lbs. .48

SUPPER.
Hot rolls 6.00
Kraut 40gal. 4.80
Evaporated fruit 90lbs. 9.45
Butter 25lbs. 12.50
Tea 2lbs. .48
Milk 480lbs. 14.40
Sugar 9lbs. .75
———
Total cost Saturday for 1,000 inmates $150.29
Approximate cost each inmate 15 cents
Food value for each inmate, 2,730 calories.
It must be understood that in the preparation of this dietary for a
week Mr. Eyman had in mind the food necessities for the general
institution, not specializing for an establishment where men and
women are sent to repent. However, it is now recognized that a
wholesome and appetizing bill of fare should be prepared for
inmates of any home or institution in order for both health and
economy. Most wardens would cut out the Sunday pie. Something
more nutritious and wholesome could readily be substituted. The
loaves of bread are reported to weigh 2 lbs. each.

Expert Opinion.

In this connection we are glad to call attention to a portion of an

editorial from the Journal of the American Medical Association for
November, 1916:
“So long as it was held that a prison is merely an institution for the
safe detention of criminals, it was not to be expected that the
hygienic conditions prevailing in such a place would be in harmony
with the best experience or the newest schemes of sanitary science.
Food in such an institution was intended solely to keep the prisoner
alive and enable him to perform his allotted daily tasks. Penal
institutions are beginning, however, to be the seats of active reform.
With the acceptance of such a program as part of the function of our
prisons, the problem of nutrition can no longer be neglected entirely.
It may reasonably be contended that good housing conditions and
suitable diet do not of themselves secure reformation of the
misguided or the habitual criminal; but without some consideration of
the necessity of proper food, the best ends of the imprisonment for
crime cannot be attained. Malnutrition may or may not contribute to
the production of criminals; in any event, the physiologic and psychic
conditions attending the lack of palatable food and a well-balanced
ration are not such as are conducive to those mental attitudes that
lead to improved conduct and more wholesome life. It has been
remarked that while a prisoner is not incarcerated for the purpose of
being fed an ideal diet, nevertheless he should be fed so as to insure
good health and a stable nervous system. * * *
“It seems extraordinary that so little judgment is shown by prison
officials in varying and improving the dietary. The same unappetizing
stuff is served day after day and year after year, with no variety in
food or manner of preparation. A large number of the prisoners have
stomach troubles from this cause alone. Canned food is served
when fresh vegetables would be just as cheap. The meat is cooked
to death and is covered by a so-called sauce. The kitchen keepers
are not to blame; it is the fault of the system.
“The remedy for this fault is to be found in the appointment of trained
dietitians. So long as hospitals and other establishments which
incidentally cater to mankind have been slow to appreciate the need
of expert services in the planning and preparation of meals as well
as in the purchasing of rations, we can understand the inertia of the
prison management in this respect. But the time has apparently
come for the introduction of such efficiency and supervision as will
lead not only to economy of service but also to physiologic well-
being. If the dietary is as important as the coal supply or the
construction accounts, it deserves a dietitian rather than a stoker or
a skilled mechanic to be placed in charge of the food problems.”
 MICHIGAN STATE PRISON.
We have received the Report of the Board of Control of the Michigan
State Prison at Jackson. It is a pamphlet of 140 pages, including 40
full page cuts. There are also four folders of the farm plots. It is a
report which reports. We have already spoken of the 26 pages
reporting the menu for every meal for a year. We may learn the
names and duties of the 90 officers, and their salaries. One table
gives the age, nativity, crime, sentence, residence and previous
record of each inmate. The names are wisely withheld. The average
population was 986. Twenty-five men had escaped in the last two
years. We are informed of the date of the escape and the part of the
farm and premises from which they absconded. The date of their
return is specified. Ten were at large when the pamphlet was made
up. They are confident of apprehending these ten. They have no
barred windows, no locked doors, no armed guards. The men work
over a plantation of more than three thousand acres, of which 2,137
belong to the institution. They rent 900 acres. They had 507 cattle
when the report was made, having just sold 146 steers for $14,600.
The dairy of 200 cows supplies the institution with abundant milk and
butter. Horses, hogs, bees and poultry are also in evidence. “The
banner record in poultry this year was made by an inmate * * * who
without an incubator was responsible for hatching and raising more
than two thousand chickens.”
By no means do they confine their attention to farming. To put a
thousand men on a farm of three thousand acres and expect them to
support themselves and have a surplus is an absurdity. There are
various industries.
Twine plant, product 1916 $106,820.79
Canning factory, product 1916 62,949.58
Granite shop, product 1916 16,385.79
Brick and tile plant, product 1916 52,866.44
 Brooms, product 1916 5,696.25
The net earnings in two years were $206,206.18
They had paid to the efficient workmen 65,009.35
In the year 1917 they were anticipating a canned pack of
$100,000.00. Of the products of the farm “they eat what they can,
and can what they can’t.”

Canning Factory.

“The intensive production of fruits and vegetables on the farms

created a surplus which had to be cared for. * * * Hence the
necessity for the canning plant. This industry * * * has accomplished
more than any other one industry in the prison to insure the industrial
success of the institution.
“From the standpoint of a prison industry it ranks first, inasmuch as
the entire produce except the can is the direct result of prison labor.
While other industries require the purchase of material for
manufacturing, in the canning plant, the material, coming from the
prison farms, is also produced by prison labor.
“The refuse from the factory in the lines of fodder, husks, etc., from
the sweet corn; vines and pods from the peas; tops from the beets,
and pomace from the apples press, furnish largely the ensilage
ration for the large herds of cattle.
“The management is adding each year some new item to the pack of
canned goods, until now it includes all varieties of fruits and
vegetables, apple jelly, sorghum molasses, baked pork and beans,
spaghetti, and the generation of pure cider vinegar. (They may soon
rival the 57 varieties of Mr. Heinz.)
“The sanitary conditions in the factory are perfect. Any man, in order
to be eligible to work in this factory, must have a clean bill of health
from the prison physician. To further the sanitary conditions, the
equipment and entire interior of the plant is painted white.”

Consumers and any one interested may inspect this plant at any
time. Here they see the men, preparing the vegetables for canning,
in a white room, dressed in white caps, white coats, white shirts, and
white aprons.
They have copyrighted the label “Home Grown,” and adopted as
their slogan: “We grow, pack, sell and guarantee our own product.”
Their goods are sold in the open market, being very popular
throughout the State and in adjoining States.
They have long ago abolished the contract system which was really
a system of slavery. They have gone beyond the policy of raising
produce or manufacturing articles for State-use, but transact
business on the State-Account plan, disposing of the product
wherever they can find a market. They claim that under their system
of employing convicts, outside labor has nothing to fear from
competition. Contract labor may have been somewhat of a menace
to labor on the outside, but these men earning wages are engaged in
honest production and the product is distributed just as the fruits of
any other industry. Let me illustrate. A man working on a farm, in a
canning factory, in a cotton mill, commits a fault and is secluded from
the community but continues his work on another farm, in another
canning factory, in another cotton mill. He receives wages which
maintains his family. Competition is neither increased nor
diminished. When the man is released, he may return to his old job.
High authority in the labor unions has stated that there is no
objection to a system which affords fair play to the prisoner and also
to the working man. Laborers have justly opposed the exploitation of
prisoners under the lease and contract systems. They have not been
opposed to the development of prison industries on a fair basis.
They present no objection to a “State-Use” method, and we trust
they will not oppose the development of a few industries organized
under the State-Account plan which appears to have been so
successful in the Michigan State Prison.

Fair Exhibits.

The products of the prison industries and of the farm have been
shown at a number of County Fairs and also at the State Fair, and
the public has thus been informed of their activities and greatly
pleased therewith. Nought has been heard but favorable comment.

Kitchen and Dining Room.

The culinary department is managed on the most approved sanitary

scheme. None but healthy men are employed. They use every
vegetable which will grow in Michigan, as long as the season lasts,
and the canned product when the season is over. Every sanitary
precaution is taken in the preparation of the meat from the pasturage
and feeding of the stock, the slaughtering and handling of the
carcass, in the cooking and serving the various viands on the dining
table.

Objects.

It is not the object of the officers to exploit the men to the advantage
of the State. In the last two years they may have returned to the
State about $9,000, but in the same time they paid out to the men
the sum of $65,000 in wages. They are spending their surplus in
betterments. They have built dormitories, with rooms, not cells,
avoiding particularly the menagerie appearance. They aim to supply
the men with a wholesome and natural environment, believing that
thus they may accomplish the main object of a penal institution
which is the reformation and restoration of the offender.
A. H. V.
 THE PRISON AND THE PRISONER.
A Symposium, edited by Julia K. Jaffray, Secretary, National
Committee on Prisons and Prison Labor. Boston. Little, Brown and
Company. 1917. $2.50.
A volume of 216 pages, containing eleven chapters contributed by
fourteen men of high repute. Judge Wadhams, of New York City,
comments on the Indeterminate Sentence, favoring a liberal
application of the principle. Doctor Glueck and Doctor Salmon
describe the necessity for psychiatrical studies of the convict in order
to determine the best treatment for his welfare and also for the
interest of the community.
Thomas Mott Osborne briefly delineates the self-government plan as
instituted by him at Auburn and Sing Sing, and E. Kent Hubbard
describes a similar system adopted in the Connecticut State
Reformatory. “The Honor System” is condemned and there is no
word in its defense.
We commend the book to all those who wish in brief compass to
know what progress has been made in humanitarian ideals for the
reformation of prisoners and what the scientific analysis of modern
conditions indicates as the best measures to attain the cure and
prevention of crime. Like other compilations, however, the various
themes are not treated with equally judicial tone or
comprehensiveness.
 THE OFFENDER.
By Burdette G. Lewis, Commissioner of Correction, New York City.
Harper and Brothers. 382 pp. $2.00.
In this volume of 382 pages, Commissioner Lewis speaks from
careful observation and from conscientious study. The reader will
soon perceive that a judicial treatment is applied to the various
questions involved in dealing with penological problems. Various
systems of government are considered, the differences between the
Honor System and the Self-Government clearly indicated, and
valuable suggestions made as to the classes of prisoners to which
the various systems of government may be adapted. The subjects of
Probation and The Indeterminate Sentence are fairly presented and
discussed, the author coming to the conclusion that the
Indeterminate Sentence is far preferable to the determinate system
of the older penology.
The tendency today is to treat the offender in much the same way as
the insane are now treated. Originally these unfortunates were dealt
with as though possessed of demons. Gradually a reform was
introduced. Special institutions were established, and these have
been gradually improved to the extent that such afflicted persons are
given such occupation and such freedom as compatible with safety.
The result is that from 20 to 30 per cent. of them are either released
as cured or may be released under the custodial care of their friends
or relatives.
Mr. Lewis holds that the tendency to accord similar treatment after a
careful diagnosis of each case to the delinquent is likely to produce a
similar result. Each offender should be dealt with according to his
special peculiarity, the treatment aiming at the substitution of good
for bad habits, commitment to prison being used when it is not in the
interest of the individual or of society to release the convicted
criminal. Mr. Lewis advocates the retaining of old-established
methods as long as they are of service. These should not be
discarded merely because they are old. He claims that the leaders in
the movement agree that the new methods should be wisely tested
before they are introduced generally. It is clear that there must have
been good reasons for the adoption of any new method, but at the
same time he is strongly in favor of studying the human equation,
and of differentiating the treatment to suit each case.
In order to administer intelligently the large department under his
charge he has “found it necessary to proceed carefully and to
experiment widely before effecting a departure from the well-known
methods of treatment.” The processes as well as the result of Mr.
Lewis’s labors are given in the present volume. In Part I he
rehearses the fundamental social forces upon which one must
depend in order to check the development of the criminal. Among
these are the home, the church, the school, health and sanitation,
and the police.
In Part II are outlined the manner of utilizing the forces likely to
improve the offender; in short, all the forces of law, order and social
development in harmonious co-operation. The book is of serious
concern to all interested in social science and in the best means of
encouraging normal growth and development through a study of
existing conditions.
 PRISON ASSOCIATION OF NEW
YORK.
We acknowledge the receipt of the Seventy-second Annual Report
of our sister association in New York. It is a ponderous pamphlet of
648 pages full of information concerning Prison Progress in 1916.
This Association was incorporated in 1846.
Our members will be interested in knowing that their Executive
Committee, like our Acting Committee, has power to examine, and
inspect all prisons of the State. Not only do they have the power but
it is also enjoined upon them as a duty to make such visits and to
report annually to the State Legislature the condition of the prisons
and any circumstances “in regard to them as may enable the
Legislature to perfect their government and discipline.” The charter
also provides that the State shall print 500 copies of this annual
report. Many additional copies are purchased by the Association for
general distribution.
Their working staff contains twenty officers who are engaged in
parole and probation duties, in the work of inspection and research,
in securing employment and in affording relief.
The last 300 pages of this document are devoted to reports of the
inspection of the various prisons of the State. The officers do not
shrink from sharp criticism of undesirable features, and yet their
criticism is of a constructive type. Recommendations are made, and
the progress made since the last inspection is duly credited.
We have also received the Report of the New York State
Commission of Prisons, a bound volume of 592 pages. 328 pages
are devoted to description, recommendations and criticisms
connected with the prisons of the State from the large State Prisons
to the small village lock-ups. This appears to us a duplication of the
work of the Prison Association. Why should there be two
organizations doing the same work?
The report of the Prison Association contains much valuable
information with regard to legislation both recent and proposed, and
to the success of the reformatory measures recently introduced into
their penal system. Those who desire copies of the report may write
to this Association at 135 E. 15th St., New York City.
 NEW JERSEY PRISON INQUIRY
COMMISSION.
This Commission was appointed according to the provisions of a bill
of the legislature of the State passed in January, 1917. By January 1,
1918, the Commission had prepared an elaborate report of 822
pages giving a history and description of the prisons and penal
methods of the State, and also presenting their recommendations.
The historical record in general indicates a series of failures rather
than of successes in penal administration. The so-called
“Pennsylvania system,” the “Auburn Plan,” the method of contract
labor, the State-Use plan, the Parole work, the efforts at
Reformation, the partisan Boards, all have their share of more or
less condemnation.
The student of penology, however, will discover in this record
encouraging tendencies which may ultimately bring about a higher
type of treatment of those who go astray.
The Commission believes in giving the largest opportunities for work
in the open air and regards with detestation the “vicious rule of
silence.”
Their discussion with regard to the merits and demerits of a Central
Board of Control of all correctional institutions is deeply interesting
and illuminating. They have come to the conclusion that a “system
may be devised which will give to the State of New Jersey the
benefits of a centralized control of its correctional system as a whole,
but which will still leave to the separate institutions the advantages of
the personal interest and devotion which have been such important
factors in their development.” To accomplish this purpose, they
recommend the appointment of a Central Board by the Governor,
who without compensation, shall have a general power of
supervision and visitation of all correctional institutions. The local
boards are to be continued with authority to manage the several
institutions to which they are attached.
The principal recommendation of this Commission is to advise the
appointment of this Central Board with whom should be vested the
power to readjust, harmonize and improve the entire penal system of
the State.