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thefacts
the
Ankylosing
Spondylitis
and Axial
Spondyloarthritis
ii

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SECOND EDITION Breast Cancer: the facts
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thefacts
the

Ankylosing
Spondylitis
and Axial
Spondyloarthritis
SECOND EDITION

MUHAMMAD ASIM KHAN,

MD, FRCP, MACP, MACR
Professor Emeritus of Medicine,
Case Western Reserve University,
Cleveland, Ohio, USA
iv

Great Clarendon Street, Oxford, OX2 6DP,

United Kingdom
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It furthers the University’s objective of excellence in research, scholarship,
and education by publishing worldwide. Oxford is a registered trade mark of
Oxford University Press in the UK and in certain other countries
© Oxford University Press 2023
The moral rights of the author have been asserted
First Edition published in 2002
Second Edition published in 2023
Impression: 1
All rights reserved. No part of this publication may be reproduced, stored in
a retrieval system, or transmitted, in any form or by any means, without the
prior permission in writing of Oxford University Press, or as expressly permitted
by law, by licence or under terms agreed with the appropriate reprographics
rights organization. Enquiries concerning reproduction outside the scope of the
above should be sent to the Rights Department, Oxford University Press, at the
address above
You must not circulate this work in any other form
and you must impose this same condition on any acquirer
Published in the United States of America by Oxford University Press
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British Library Cataloguing in Publication Data
Data available
Library of Congress Control Number: 2022938866
ISBN 978–0–19–886415–8
DOI: 10.1093/​oso/​9780198864158.001.0001
Printed and bound by
CPI Group (UK) Ltd, Croydon, CR0 4YY
Oxford University Press makes no representation, express or implied, that the
drug dosages in this book are correct. Readers must therefore always check
the product information and clinical procedures with the most up-​to-​date
published product information and data sheets provided by the manufacturers
and the most recent codes of conduct and safety regulations. The authors and
the publishers do not accept responsibility or legal liability for any errors in the
text or for the misuse or misapplication of material in this work. Except where
otherwise stated, drug dosages and recommendations are for the non-​pregnant
adult who is not breast-​feeding
Links to third party websites are provided by Oxford in good faith and
for information only. Oxford disclaims any responsibility for the materials
contained in any third party website referenced in this work.
 Dedication

I dedicate this book to my father, Umar Khan, my mother, Hameeda Khanam,

and to her father, Sadr-​ud-​Din Khan (a high school principal who retired as
inspector of schools) for having inculcated in me the passion to pursue know-
ledge and impart it to others. They all worked tirelessly to re-​establish when
we became refugees, uprooted from our ancestral lands when I was a little
over three years old. Therefore, I also dedicate this book to all the refugees like
me in this world who may still be longing for a home, and most of them also
happen to share my faith.
vi

Advance praise

‘Written for patients by a patient who is also a leading authority on spondyloarthritis, this
book is an essential reference and reading for people living with axial spondyloarthritis—
with ankylosing spondylitis as its prototype—and their caregivers who want to learn
about the disease and how to manage it well.’
Michael Mallinson,
Patient Advocate and Volunteer,
Axial Spondyloarthritis International Federation (ASIF)
 Preface

There have been tremendous advances in clinical understanding, early disease

recognition, and more effective management of ankylosing spondylitis (AS)
and related diseases. The advent of newer imaging methods, such as magnetic
resonance imaging (MRI) and very low-​dose computerized tomography (CT),
have also facilitated early diagnosis and initiation of increasingly more effective
(but costly) drugs called “biologics” (administered by injection under the skin
or by intravenous infusion), and most recently JAK-​inhibitors that are taken
orally as tablets. These drugs target inflammatory proteins (cytokines), such as
tumor necrosis factor (TNF) and interleukin-​17 (IL-​17).
All these new development and progress in diagnosis and management of AS
and related diseases has necessitated this second edition of the book. I have
updated its title by adding the term “Axial Spondyloarthritis” that requires
some explanation.
The term “spondyloarthritis” (or SpA) refers to a family of chronic inflam-
matory non-​contagious (non-​infectious) forms of arthritis involving the spine
and the limbs that share many of their clinical features and genetic predis-
posing factors. Those patients with SpA who primarily have inflammation of
the joints and ligaments of the back and neck (i.e., the axial skeleton) are now
sub-​classified as having “axial spondyloarthritis” (axSpA); whereas those with
involvement predominantly of the peripheral (distal) limb joints (other than
hip and shoulder joints that are part of the axial skeleton), are labeled as having
“peripheral SpA.” The typical example of axSpA is AS, while that of peripheral
SpA is psoriatic arthritis (PsA).
X-​ray evidence of damage to the sacroiliac joints (sacroiliitis) is required for
the diagnosis of AS. We first reported in 1985 that one can clinically recog-
nize the disease even when there is no X-​ray evidence of sacroiliitis. We called
it “spondylitic disease without radiological evidence of sacroiliitis.” It is now
called “non-​radiographic axSpA” (nr-​axSpA). The name axSpA encompasses
both nr-​axSpA and AS.
Most of the current knowledge about axSpA was gained when the disease was
called AS, and this is my reason for the use of both AS and axSpA in the title of
vi

Preface

this second edition. It is my hope that the third edition of this book will simply
be titled Axial Spondyloarthritis: The Facts. The term “radiographic axSpA” (r-​
axSpA) has sometimes been equated with AS but I have preferred to use the
term AS in this book as it is the most widely accepted name.
This book is written in a clear and accessible style with American English
spellings for patients and their families and friends. But it is also ideal for
students and healthcare professionals of all levels who are looking for concise
and practical information on all aspects of AS/​axSpA. Discussions about the
associated forms of SpA, including PsA, reactive arthritis, inflammatory bowel
disease associated SpA, juvenile SpA, and some other diseases that may be
confused with SpA (the so-​called disease mimickers or look-​alikes) are also
discussed. A glossary of medical terms, a list of abbreviations, links to patient
support groups and other helpful organizations, a list of medical references for
further reading, and an index are also included.
People who are knowledgeable about their disease show more self-​responsibility,
comply better with recommended treatment, and are more likely to make posi-
tive behavioral changes that will help them achieve an improved health status
in the long run. I hope this book will serve people living with AS/​axSpA and
their families and friends in their need for self-​education.
Lastly, I would add that this book provides a general information that cannot
replace the care and knowledge provided by your professional healthcare pro-
viders. You need to consult them if you have questions as you read this book.
Muhammad Asim Khan
Professor Emeritus of Medicine
Case Western Reserve University, Cleveland, Ohio, USA

viii
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 Acknowledgments

I am most grateful to my wife Mastoora and my sons Ali and Raza for their
help; and also very thankful to the many patients, colleagues, and students who
have, over the years, enhanced my knowledge of ankylosing spondylitis, an
illness I have myself lived with for more than sixty-​six years.
x
 Contents

Abbreviations xiii

1 What is ankylosing spondylitis? 1

2 Axial spondyloarthritis 16
3 What is the underlying cause? HLA-​B27 and other
disease-​predisposing genes 22
4 Disease prevalence 31
5 Early symptoms and pointers to early diagnosis 36
6 Eye inflammation (acute anterior uveitis) 41
7 Other manifestations 45
8 Physical examination and laboratory tests 49
9 Radiology, MRI, and CT 57
10 Diagnosis and management of other forms of SpA
and “look-​alikes” 60
11 Other causes of chronic back pain 73
12 Assessment of disease activity and functional impairment 79
13 Patient education 85
14 Exercise and physical therapy 88
15 Management: An overview 101
16 Management: Patient’s role 105
17 Management: Rheumatologist’s role 108
18 NSAIDs and conventional DMARDs 111
19 Tumor Necrosis Factor inhibitors 117
xi

Contents

20 IL-​17 and IL-​23 inhibitors and targeted synthetic DMARDs 124

21 Living with the disease and its socio-​economic impact 128
22 Fused (ankylosed) spine and risk of fractures 137
23 Surgical treatment 141
24 Non-​traditional (complementary or alternative) therapy 145
25 Disease course and effect on life span 154
26 Brief illustrative case histories 157

Appendix 1. Patient support groups and other helpful

organizations 161
Appendix 2. Glossary 165
Appendix 3. Further reading 189
Index 199

xii
 Abbreviations

3D three-​dimensional
AAU acute anterior uveitis
ACE angiotensin-​converting-​enzyme
ACR American College of Rheumatology
ADL activities of daily living
AI artificial intelligence
AS ankylosing spondylitis
ASAS Assessment of SpondyloArthritis international
Society
ASAS H I ASAS Health Index
ASDA S Ankylosing Spondylitis Disease Activity Score
ASDA S _​C R P Ankylosing Spondylitis Disease Activity Score
based on CRP
ASIF Axial Spondyloarthritis International Federation
ASQoL ankylosing spondylitis quality of life measure
AP anteroposterior
axSpA axial spondyloarthritis
BASDA I Bath Ankylosing Spondylitis Disease Activity Index
BASF I Bath Ankylosing Spondylitis Functional Index
BAS- ​G Bath Ankylosing Spondylitis Patient Global score
BASM I Bath Ankylosing Spondylitis Metrology Index
BASRI Bath Ankylosing Spondylitis Radiology Index
b- ​D M A R D biologic DMARD
BiPAP bilevel positive airways pressure
BMC bone mineral content
BMD bone mineral density
BMI body mass index
CASPA R Classification Criteria for Psoriatic Arthritis
CBD cannabidiol
CD Crohn’s disease
vxi

Abbreviations

CDC Centers for Disease Control and Prevention in the

United States.
c- ​D MA R D conventional DMARD
CD- ​S p A CD-​associated spondyloarthritis
CES- ​D Center for Epidemiological Studies Depression
CLBP chronic low back pain
CNO chronic non-​infectious osteitis
COA Certificate of Analysis
COX cyclooxygenase
CPAP continuous positive airway pressure
CRP C-​reactive protein
cs- ​D M A R D conventional synthetic DMARD
CT computed tomography
DAS disease activity score
DEXA (o r D X A ) dual energy x-​ray absorptiometry
DISH diffuse idiopathic skeletal hyperostosis
DKK abbreviation for protein named Dickkopf
DMAR D disease modifying anti-​rheumatic drug
DXA dual-​energy X-​ray absorptiometry
EAM extra articular manifestation
EMA Europeans Medicines Agency
EMAS European Mapping of Axial Spondyloarthritis
EMR electronic medical record
ERAP endoplasmic reticulum aminopeptidase
ESR erythrocyte sedimentation rate
ESSG European Spondyloarthropathy Study Group criteria
EULAR European Alliance of Associations for Rheumatology
FACIT Functional Assessment of Chronic Illness Therapy
FDA Food and Drug Administration of USA
GI gastrointestinal
GP general practitioner
GWAS gnome-​wide association study
HAQ Health Assessments Questionnaire
HAQ- ​D I HAQ Disability Index
HAQ- ​S HAQ spondylitis
HCP healthcare providers
HLA human leucocyte antigen
HR- ​Q o L health-​related quality of life
IASP International Association for the Study of Pain

xiv
 Abbreviations

IBD inflammatory bowel disease

IBP inflammatory back pain
Ig immunoglobulin
IL Interleukin, such as IL-​17 and IL-​23
IBS irritable bowel syndrome
JAK Janus kinase
JAKi Janus kinase inhibitor
JAKin JAK inhibitors
JAS juvenile AS
JIA juvenile idiopathic arthritis
MCS Mental Component Score
MFI Multidimensional Fatigue Inventory
MHC major histocompatibility complex
mNY modified New York (criteria for ankylosing
spondylitis)
MRI magnetic resonance imaging
mSAS S S modified Stoke Ankylosing Spondylitis Spine Score
NASS National Axial Spondyloarthritis Society
NHAN ES National Health and Nutritional Examination Survey
NHS National Health Service of UK
NIH National Institute of Health of USA
nr-​a xS p A non-​radiographic axial spondyloarthritis
NSAID nonsteroidal anti-​inflammatory drugs
OA osteoarthritis
OCT optical coherence tomography
OTC over-​the-​counter
PAMP pathogen-​associated molecular pattern
PASS Patient-​Acceptable Symptom State
PCP primary healthcare provider
PCS Physical Component Score
PD phosphodiesterase
PET positron emission tomography
PGA Patient Global Assessment
PGE2 prostaglandin E2
PhD Doctor of Philosophy
PPD purified protein derivative
PPR pattern recognition receptor
PRO Patient Reported Outcome
PROM Patient Reported Outcome Measure

xv
xvi

Abbreviations

PsA psoriatic arthritis

QoL quality of life
RA rheumatoid arthritis
RAPID 3 Routine Assessment of Patient Index Data 3
r-​a xSpA radiographic axSpA
RCT randomized controlled trial
SAARD slow-​acting anti-​rheumatic drug
SAPHO synovitis, acne, palmoplantar pustulosis, hyperostosis,
and aseptic osteomyelitis
SASSS Stoke Ankylosing Spondylitis Spine Score
SEA seronegative enthesitis and arthritis
SF- ​3 6 Short-​Study Form-​36
SI sacroiliac (or sacroiliitis)
SI join t o r S I J sacroiliac joint
SpA spondyloarthritis or spondyloarthropathy
THA total hip arthroplasty
THC tetrahydrocannabinol
THR total hip joint replacement
TMJ temporo-​mandibular joint
TNF tumor necrosis factor
TNFi tumor necrosis factor inhibitor
ts-DMA R Ds targeted synthetic-DMARDs
UC ulcerative colitis
VAS visual analog scale
WBC white blood-​cell count
WHO World Health Organization
WLQ- ​2 5 Work Limitations Questionnaire-25
WPAI Work Productivity and Activity Impairment

xvi
 1
What is ankylosing
spondylitis?

% K ey points
◆ Ankylosing spondylitis (AS) is a chronic (long-​term), slowly progres-
sive, and painful inflammatory arthritis of the sacroiliac (SI) joints and
the spine that can lead to gradually progressive impairment of spinal
mobility.
◆ It affects both males and females, and the symptoms typically start
during adolescence and early adulthood, and it is very uncommon for
the symptoms to begin after age 45.
◆ The inflammation can also involve the hip and shoulder joints, and less
often other limb joints, such as knees, ankles, and heels.
◆ One or more episodes of acute eye inflammation (acute anterior uveitis)
can occur in >30% of patients, and 6 to 10% suffer from psoriasis and/or
inflammatory bowel disease.
◆ The disease is observed worldwide with very variable prevalence, e.g., it
affects one in 200 (0.5% prevalence) adults of European ancestry, but is
very uncommon in most of the sub-​Saharan African populations.
◆ Its cause is not fully understood but is largely genetically determined,
and there is a strong association with a gene called HLA-​B27.
◆ There is no cure as yet but most patients can be very well managed if
diagnosed and treated early with increasingly effective, though costly,
drugs that markedly reduce the risk of irreversible structural damage
and help patients pursue a very active and productive lifestyle.
  

Ankylosing Spondylitis and Axial Spondyloarthritis, Second Edition. Muhammad Asim Khan, Oxford University Press.
© Oxford University Press 2023. DOI: 10.1093/​oso/​9780198864158.003.0001
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2

What is ankylosing spondylitis? · the

thefacts

Introduction
Ankylosing spondylitis (AS) is a chronic (progressive) painful inflammatory
rheumatic non-contagious (non-infectious) disease that involves the back, i.e.
the sacroiliac (SI) joints and the spine, that often results in some degree of
stiffness (decreased flexibility) of the spine (Figure 1.1). The word ankylosing
comes from the Greek root ankylos, meaning bent, although it has now come to
imply something that restricts motion (stiffening) and may ultimately result in
fusion. When the joint loses its mobility and becomes stiff it is said to be anky-
losed. The word spondylitis means inflammation in the joints of the spine, and
is derived from spondylos, which is the Greek word for vertebra, and -​itis, which
implies presence of inflammation. The name therefore suggests that AS is an
inflammatory disease of the spine that can lead to stiffening of the back. It is
important to point out that the words spondylitis and spondyloarthritis should
not be confused with spondylosis, which relates to wear and tear in the spinal
column (degenerative disc disease) as we get older.

Ankylosing spondylitis in history

Skeletal specimens in several museum collections testify to the existence of
AS from the earliest times. But its first definite anatomical description can be
credited to Bernard Conner (1666–​1698). He was an Irish physician studying
medicine in France when some farmers brought him a skeleton they had found
in a cemetery. He wrote in his report, accompanied by the drawing of the
skeleton (see Figure 1.2), that the bones were “so straightly and intimately
joined, their ligaments perfectly bony, and their articulations so effaced, that
they really made but one uniform continuous bone.”
The clinical descriptions of the disease date from the late nineteenth cen-
tury, with a series of publications in the 1890s by Vladimir von Bechterew
(1857–​1927) in St Petersburg, Russia, Pierre Marie (1853–​1940) in France,
and Adolf Strümpell (1853–​1926) in Germany. Report of the earliest X-​ray
examination of a patient with AS was published in 1899, and the characteristic
X-​ray finding of obliteration of the SI joints was described in 1934.
The name ankylosing spondylitis is widely in use in English speaking countries,
with its translation spondylarthrite ankylosante in French, spondylitis ankylopoëtica
in Dutch, and espondilartritis ankylosante in Spanish. Older names include
Morbus Bechterew (Bekhterew’s or Bekhterev’s disease), Bekhterev-​Strümpell-​
Marie disease and Marie-​Strümpell spondylitis. Although the use of eponyms
is now discouraged for naming a disease, the term: “Morbus Bechterew” is
still being widely used in German-​speaking countries. Other names that have
been used include spondyloarthritis ankylopoëtica, pelvospondylitis ossificans, and

2
 Ankylosing spondylitis in history

Figure 1.1 Sites that may be involved in AS. The most involved sites are the sacroiliac
joints and the spine. They are marked by rectangles. Other, relatively less commonly
involved sites are hip and shoulder joints, and less often the knee joints. These sites are
marked by circles.
Reproduced with permission from Khan MA. “Spondyloarthropathies” in Hunder G (ed), Atlas of Rheumatology.
Philadelphia, PA: Current Medicine Philadelphia, 2005, 151–​80.

3
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 Colic persists with great intensity for ten to twelve hours,
interrupted only by rare periods of calm. At the end of this time,
however, it may suddenly disappear, and the animal may fall into a
semi-comatose state. This indicates the onset of necrosis in the
invaginated section, the painful reflexes no longer being transmitted
to the sympathetic system. The disappearance of colic is sometimes
regarded as a sign of improvement, but this improvement is illusory.
From this time onwards the animals stand stolidly, obstinately
refusing both food and drink. If they lie down, it is with great care.
Palpation of the right side of the abdomen is painful, and the animal
actively resents it. One of the most important and constant signs at
this stage is the absence of defæcation, due to obstruction of the
intestine, which is occluded. The animals may survive for ten, twelve,
or even fifteen days (see also Möller and Dollar’s “Regional Surgery,”
loc. cit.). The invaginated, necrosed portion may even be passed with
the fæces, and recovery may occur, the continuity of the intestinal
tube being secured by the adhesion of the serous surfaces; but such
spontaneous recoveries are exceptional. Usually after a few days
death results from peritonitis.
Occasionally, trifling invaginations may become reduced
spontaneously, Diarrhœa, with the passage of blood-stained material
is then seen for a time, a sign which alone at this stage would justify
the diagnosis of invagination.
Diagnosis. The intensity of the colic and the absence of
defæcation for several days afterwards, justifies the diagnosis of
invagination. Purgatives then remain without effect. In addition,
rectal exploration offers a valuable means of diagnosis. The last
portions of the intestine are found absolutely empty, and the arm
when withdrawn is found to be covered with viscous blood-stained
mucus, resulting from the sero-sanguinolent exudate, due to
compression of the blood-vessels.
In cases of this kind accompanied by the above-mentioned
symptoms abdominal exploration by the rectum should always be
practised, but it rarely gives exact information. The hand, when
passed towards the right flank, may sometimes reach the invaginated
part, which conveys the impression of a cylindrical swelling. The
invagination, however, can rarely be reached. If the operator is
successful, he will find that as he displaces this cylindrical mass or
attempts to grasp it, the animal shows signs of exaggerated
sensitiveness.
The prognosis is of exceptional gravity. Apart from the rare
cases where the invaginated portion becomes necrotic and is
eliminated, death is inevitable. Unless an operation is performed,
septic peritonitis may develop about the fifth or sixth day.
Treatment. The only treatment consists in surgical intervention.
Some practitioners have recommended giving large doses of
purgatives with the idea of causing changes in the neighbourhood of
the invaginated part; but such treatment presents little chance of
success. The same is true of the administration of large doses of olive
oil, either in the form of draught or of enema.
Siebert attempted reduction by generating CO2 from soda
bicarbonate dissolved in water and diluted HCl, injected successively
per rectum. In time fæces and CO2 escaped, and the patient
recovered. Siebert claims to have cured by this method a cow with
invagination of five days’ duration; but the effect of his treatment
may be doubted, as afterwards a portion of bowel was found in the
cow’s dung.
When diagnosis is certain, the only treatment that can be
recommended consists in performing laparotomy followed by
enterotomy. One cannot, however, operate in all cases, nor do all
cases offer the same chances of success. If the invagination is
situated in the first portion of the small intestine, and is hidden
beneath the circle of the hypochondrium, intervention is out of the
question, but if it has been detected by rectal exploration in the last
portion of the intestine, operation may prove successful. Only in
cases of the latter description should it be attempted.
Laparotomy is performed in the right flank according to the usual
method (see Möller and Dollar’s “Regional Surgery,” p. 313). After
opening the peritoneal cavity, the invaginated loop of intestine must
be sought. It is not always easy to discover amongst the mass of
intestines present, but can be recognised by its hardness and by the
congestion of neighbouring parts. After withdrawing it through the
abdominal opening, the operator may then proceed by one of several
methods.
 (1.) Some authors recommend grasping the two ends, drawing
them apart, and thus reducing the invagination. The actual
manœuvre is not difficult, but even when unattended by accident or
tearing of the intestine it is by no means always followed by recovery.
Although the intestine may not appear gangrenous externally,
necrosis often occurs eventually.
This method should only be practised during the first twenty-four
hours after the appearance of colic, and even then one must always
bear in mind the possible consequences just mentioned, and the
chances of rapidly fatal septic peritonitis.
(2.) The second method consists in removing the invaginated
portion of intestine. It is best to apply bichromatised catgut or silk
ligatures to all the arteries which pass from the mesentery into the
loop to be removed; after which the loop itself may be simply divided
an inch or two above and below the invagination, in order to be quite
certain that one is operating on healthy tissue, the divided ends
being held meanwhile by an assistant. The intestine is afterwards
sutured with a fine needle and bichromatised catgut or boiled silk.
The form of suture will be found described in Dollar’s “Operative
Technique.” It may be valuable to test the efficacy of decalcified bone
tubes for uniting the ends of the intestine.
The operation is long, delicate and difficult, and it is imperative
not to infect the abdominal cavity during its performance. To prevent
this the liquid and solid materials present in the bowel may be thrust
upwards and downwards away from the diseased part before the
section is made; and in this way the wound and the operator’s hands
are preserved from infection. The intestine should be kept closed
during the application of sutures by means of flat clamps cautiously
applied. In their absence the ends may be held by an assistant, whose
hands should previously have been carefully disinfected.
(3.) In cases where the serous coats of the two portions of bowel
constituting the invagination are to some extent adherent, another
operation of a less perilous character may be performed. This
consists in liberating the invaginated part by means of longitudinal
incision, without previously disengaging the parts, and without
resection. The invaginated (external) portion of intestine is divided
longitudinally; the gangrenous part immediately becomes visible,
and may be removed. The operator has then only to suture the
longitudinal wound, an operation which is much easier and demands
much less time than any circular intestinal suture whatever. These
operations must not be attempted except in response to the express
wish of the owner, who should be fully informed of the dangers to
which they expose the animal; for after the second day of
invagination local peritonitis has often developed and one is then
operating on injured or infected tissues, in itself a very unfavourable
modifying condition. The current formula that “the operation was
very successful” is not accepted in veterinary practice when the
patient dies three or four days afterwards. From the economic
standpoint it is better to slaughter animals of any value, for unless
secondary peritonitis has occurred, and the animal is not feverish,
the meat is fit for consumption. “Volvulus,” or twist of the intestine,
is said to be almost unknown in cattle, though Reichert records a
case of volvulus of the ileum.

COLIC AS A RESULT OF STRANGULATION.

The symptoms of this colic differ very little from those of the
preceding with which they are often confused. But in regard to its
causation the condition is essentially different.
Causation. Strangulation of the intestine in the ox may be
produced in several different ways: by the passage of a loop of
intestine through a tear in the epiploon, through the diaphragm,
mesentery, broad ligament of the uterus, the serous layer
surrounding the spermatic cord, etc., or by strangulation of an
intestinal loop by fibrous bands resulting from chronic peritonitis,
etc. Of these various causes, the three principal may here be
described:—
(1.) Tearing of the mesentery. As a result of mechanical violence
the epiploon or mesentery becomes fissured, and the peristaltic
movements cause a loop of intestine to pass through and become
fixed in the fissure. If the opening is narrow, as is usually the case,
the base of the intestinal loop, riding on the lower lip of the slit,
becomes constricted by the margins of the opening through which it
has passed.
 Fig. 69.—Schema of hernial strangulation.

(2.) In pelvic hernia a loop of intestine passes between the

spermatic cord and the walls of the pelvis. The fissure in this case is
in the serous fold which supports the large testicular arteries and the
vas deferens. The fold is often ruptured during castration, especially
during the practice of “bistournage,” in consequence of traction
exercised on the cord.
(3.) Pseudo-ligaments and fibrous bands due to chronic
peritonitis.—In local, subacute or chronic peritonitis false
membranes may become organised, forming fibrous cords or folds
connecting the parieto-visceral or inter-visceral surfaces. If by
accident a loop of intestine insinuates itself beneath one of these
fibrous bands, the passage of digestive material is first impeded and
then stopped. The intestine becomes engorged, and symptoms of
strangulation soon follow.
 The symptoms appear suddenly, and are similar to those of
invagination. They consist of very acute colic, which disappears after
ten to twelve hours.
The peristaltic movements drive the semi-digested food, whether
liquid or gaseous, towards the lower (strangulated) end, from which
it cannot escape. It therefore distends the herniated loop and sets up
intestinal engorgement. This constitutes the first stage of
strangulation, and is accompanied by severe disturbance in the local
circulation. The mucous membrane of the intestine becomes swollen
and infiltrated, so that it alone soon fills the entire neck of the hernia.
Necrosis of the loop of intestine is then only a matter of time.
The diagnosis of colic by strangulation is difficult. The condition
cannot often be recognised at an early stage, and may easily and
excusably be confused with invagination. Only in rare cases will
rectal and abdominal examination enable one to detect a pelvic or
mesenteric hernia.
The prognosis is even graver than in cases of invagination.
Intestinal hernia progresses very rapidly, necrosis soon sets in, and is
followed by fatal consequences if the condition be not relieved.
The treatment is exclusively surgical. As a general rule,
whenever colic is recognised as resulting from strangulated hernia, it
is immediately necessary to perform laparotomy in the right flank,
and after having discovered the cause of strangulation, to divide the
mesentery, epiploon, serous fold supporting the testicular cord, or
accidental fibrous bands, so as to free the herniated loop and avoid
necrosis. If necrosis already exist, the intestine may be resected,
exactly as in invagination.

DISEASES OF THE STOMACH.

In ruminants diseases of the gastric compartments are numerous,

and, although they have been recognised since the earliest times,
much remains to be discovered concerning at least some of them.
This fact results from the imperfect state of our knowledge
concerning the essential phenomena of gastric digestion in
ruminants. Digestion really consists of a number of different acts—
some mechanical or neuro-motor, some chemical; in addition to
which must be reckoned the phenomena of sensation, concerning
which patients cannot give any information.
The mechanical phenomena, consisting in the constant movement
of ingested material through the different compartments,
rumination, eructation, evacuation towards the intestine, etc., are
well known to us; and a careful examination of diseased animals
enables us to estimate the importance of changes in them.
On the other hand, the chemical phenomena are little understood.
It has hitherto been considered that the rumen, reticulum, and
omasum are only simple diverticula, with mechanical functions, and
that the abomasum is the reservoir in which the chemical changes
take place. Another view, which is perhaps not altogether justified,
presupposes that the chemical transformation of the food in the
abomasum takes place as in other animals, and in particular as in
man, in whom the chemistry of gastric digestion has been the object
of extremely careful research by certain French and other
pathologists. We do not believe (for reasons too long to be explained
here) that the gastric digestion of ruminants, or even of herbivora in
general, can be identified with that of omnivora.
The nature of the food being totally different, the chemical
reactions in the stomach and intestines are also different; in proof of
which we need only cite the single fact that ptyalin is absent from the
saliva. Straw and oats are not digested in the same way as a mutton
cutlet.
But even supposing that the broad outlines of physiological action
are the same, nothing has hitherto been discovered in veterinary
surgery respecting possible variations in the chemical processes
taking place in the stomach during different gastric diseases; and it
appears not improbable that in this direction causes might be
discovered which veterinary practitioners have hitherto sought
elsewhere. Excess or insufficiency of hydrochloric acid, and
variations in the quantity of the organic acids, play so important a
part in the theory of gastric pathology in man, that it is scarcely
surprising to find similar ideas recurring in the pathology of
domestic animals. The correctness of these views remains to be
proved; and without wishing actually to classify dyspeptic conditions
as in man, we may assert that diseases described under other names
stand in direct relation to variations in the gastric secretion or to
disturbance of gastric movements—e.g., simple chronic tympanites,
which, without a doubt, is often a neuro-motor dyspepsia.
The classification we shall adopt in studying the diseases of the
gastric compartments is, therefore, extremely simple. In the first
series we shall consider sudden, accidental, and temporary forms of
indigestion, and in the second series, acute or chronic forms of
gastric inflammation.

INDIGESTION.

GASEOUS INDIGESTION.

Gaseous indigestion, also described as indigestion of the rumen, is

characterised by the rapid accumulation of gases (chiefly carbon
dioxide, carbon monoxide, and marsh gas), due to fermentation in
the upper part of the rumen. It is common in oxen and sheep, and
has received the names of mephitic indigestion, acute tympanites,
meteorism, etc. It occurs during or immediately after feeding.
Causation. Numerous causes have been invoked to explain the
sudden occurrence of gaseous indigestion.
The most important is the particular condition of the animal at the
moment when it has been attacked. For if external influences alone
were responsible, there is no reason why all the animals of a given
herd or flock, or of a particular stable, which are under similar
conditions as regards feeding, etc., should not be affected in the same
way.
That the external causes cited (cold, excessive heat, stormy
weather, etc.) may affect different animals differently and
unfavourably is beyond doubt. But the temporary morbid condition
of the animal itself is the essential condition to the development of
indigestion.
In all probability the animal has in every case been more or less
unwell, except in those attacks of indigestion resulting from
progressive poisoning during the course of a meal, such as occur
when toxic plants like belladonna, veratrine, colchicum, poppies,
tobacco, hemlock, etc., have been eaten. In such temporary abnormal
states movement of the rumen is partly abolished, or at least is
markedly retarded, and, as a consequence of vaso-motor
disturbance, the mucous membrane is probably not so abundantly
covered with mucus nor so freely irrigated with secretion, as usual.
Under these conditions, if the animal, which may appear perfectly
well, is allowed to partake of soft, wet, fermentescible food, gaseous
indigestion is very likely to develop.
Cultivated grasses, like lucern, sainfoin, clover, and especially
grasses grown on artificially manured fields, are regarded as
particularly liable to cause gaseous indigestion. This conclusion
seems justified by experience, particularly by the fact that young
shoots or young, tender after-growths are very liable to fermentation.
This exaggerated tendency to fermentation of tender grasses has
even been held exclusively responsible for indigestion, and the
cessation of peristalsis in the rumen has been considered a secondary
phenomenon, due to distension.
Whether atony of the rumen be the primary condition and
abnormal fermentation secondary or inversely, whether
fermentation be primary and atony secondary, is not of importance;
for either view may be adopted without altering the results, and
without the theory being invalidated by the objection that other
animals subjected to similar influences had not contracted the
condition.
We have already drawn attention to the importance of the
condition of the animal’s health for the time being. Digestive
peristalsis being diminished, eructation, admixture of food in the
rumen, and its onward movement being impeded, fermentation
proceeds rapidly. As a consequence the rumen becomes distended,
and, cause and effect changing places, the distension in its turn
arrests peristalsis, which had previously only been checked.
Local chills, produced by ingestion of food covered with rime,
hoarfrost, or simply with dew, may favour gaseous indigestion; such
conditions retard or suspend the peristaltic movements by direct
local action, and probably by producing vaso-motor disturbance of
the mucous membrane. In very rare cases chill has an undeniable
influence, either by provoking general vaso-motor disturbance,
which reacts on the secretions, or neuro-motor trouble. Gaseous
indigestion is not uncommon in animals living on dry winter food,
which have been moved from their ordinary quarters and sent on
railway journeys or to fairs, etc. As a general rule this form of
indigestion is commonest in spring, when the transition from dry
winter food to grass, etc., has not been carefully effected. It is also
frequent during stormy weather in full summer. Marked barometric
changes seem to have an influence on the general health, and
particularly on the nervous system, thus favouring organic
fermentations.
Symptoms. The earlier symptoms of indigestion escape
observation, but they soon begin to develop rapidly, and are then
very easy to follow. They always exhibit the same characters,
developing, however, with more or less rapidity in different cases.
Soon after they commence feeding animals appear to experience
special discomfort, which causes those at grass to stop grazing; even
when stabled they stop feeding. From this time they show eructation,
repeated yawning, restlessness, and some anxiety.
In a quarter of an hour, or less, the left flank begins to project,
both laterally and vertically, so that eventually the walls of that part
of the abdomen may project above the transverse processes of the
lumbar vertebræ. The right flank also becomes swollen, as a
consequence of the intestine being thrust out of position. The animal
very rapidly shows general disturbance; the nostrils are dilated, the
mucous membranes congested, respiration becomes rapid, and
asphyxia threatens. The respiration soon becomes panting, for the
distended rumen paralyses the diaphragm and compresses the lungs.
To ease respiration the animals open the mouth, extend the neck,
and stand with the front limbs spread apart; but this fails to prevent
dyspnœa becoming more intense and asphyxia imminent.
The heart beats more rapidly, the superficial veins appear swollen,
and the mucous membranes cyanotic. The rhythmic contractions of
the rumen can no longer be detected by manual examination of the
left flank; and on auscultation one neither hears the liquid nor the
rolling sound, but only exaggerated crepitation. Finally, there is
marked tympanitic resonance on percussion.
In cases of very grave tympanites the gaseous pressure in the
interior of the rumen appears to stop the crepitation sound. The
animals soon become unable to walk or even to move, suddenly fall
to the ground, and die rapidly from asphyxia.
 The rapidity with which gaseous indigestion develops varies
greatly. Sheep and oxen may die from tympanites, within an hour or
even half an hour of their arrival in the field; but more frequently the
symptoms develop slowly, only becoming alarming after some hours
and continuing for twelve or even twenty-four hours without causing
death.
As a rule, the gas is voided by a series of eructations which empty
the rumen, and recovery follows; but when distension is extreme
eructation cannot occur, and gaseous indigestion then ends in
asphyxia and death.
Lesions. It might be imagined that this form of indigestion would
only appear when the rumen contains a large quantity of food; but, in
point of fact, the rumen often contains very little.
On post-mortem examination the rumen is found to contain an
enormous quantity of gas, which, when collected and submitted to
analysis, reveals approximately the following composition:—
Carbonic acid, 74 per cent.; carburetted hydrogen, 24 per cent.;
sulphuretted hydrogen, 2 per cent.; nitrogen, traces. The
composition of this mixture varies within certain limits, according to
its origin; but carbonic acid always predominates.
Lungwitz, after elaborate experiments with different foods kept in
closed vessels at the body temperature and with similar agents fed
for days as an exclusive aliment to oxen provided with a fistula of the
rumen for purposes of collection, found carbonic dioxide the
predominating gas in all cases, though the proportion varied with the
nature of the food.
Marsh gas varied from 16 to 39 per cent., being especially
abundant in cases of abstinence. Hydrogen sulphide was found only
in traces. Oxygen and nitrogen were present in small amount, and
were attributed to air swallowed with the food. In fermentation the
oxygen may be completely consumed.
The abdominal organs, particularly the intestine, are congested, as
a result of impediment to the venous circulation. The thoracic organs
exhibit the lesions of asphyxia.
Pathogeny. Death is due to carbonic acid poisoning, brought
about in two different ways—viz., progressive asphyxia, caused by
inability to inflate the lungs, and absorption of carbonic acid gas
from the rumen; by virtue of the laws of diffusion, part of the gas
contained in the rumen passes into the blood.
The diagnosis is always very easy, and even farm servants may
recognise the condition.
The prognosis varies, according to the rapidity with which the
disease develops. In rapid cases, where the condition is fully
established in thirty minutes to one hour, asphyxia may be
threatened from the beginning; but in others, e.g., when the attack
follows consumption of dry food, tympanites may develop slowly,
only attaining its maximum intensity after a considerable lapse of
time. In general one may say that tympanites is grave in proportion
to the rapidity with which the gas is generated.
Treatment. From the prophylactic point of view, it is necessary
to avoid suddenly changing animals from dry to green food; the
transition should be effected by giving mixtures of dry and green
food.
Curative treatment comprises a large number of methods.
The latest, and one of the most practical, consists in massage of the
left flank. The open hand is applied to the left flank and sharply
pressed directly downwards, care being taken not to injure the parts.
This manipulation excites reflex action, awakens the dormant
contractility of the rumen, and leads to restoration of peristaltic
movement. The gases pass into the omasum and abomasum, or in
many cases make their way into the œsophagus. The sudden
impulses sometimes cause food to be returned into the mouth,
eructation recommences, and the gas accumulated in the rumen is
partially and progressively evacuated. This manipulation is often
practised in breeding districts, particularly in the case of sheep, in
which the disease occurs with the same characters. The shepherd
fixes the animal between his legs, and, thrusting the extended fingers
of either hand into the flanks, makes sudden, sharp movements,
which again set up eructation and get rid of the excess of gas.
In Germany cold douches are often applied to the flanks. These
excite vaso-motor action and reflex peristaltic movements, which
result in eructations and in the evacuation of the rumen. But this is
not a very practical method, and necessitates arrangements which
seldom exist on sheep farms.
 The action of massage may be completed by administering
stimulants like wine, alcohol, or infusions of such aromatic plants as
cummin, fennel, peppermint, camomile, etc. These act first of all
mechanically, by clearing the terminal portion of the œsophagus.
Furthermore, they stimulate the mucous membrane of the rumen,
causing reflex peristaltic contractions, and, as a consequence,
circulation of the partly digested food; finally, the majority of them
arrest fermentation.
With the latter object, ether and assafœtida are also given. The use
of these drugs, however, entails disadvantages, and if the animal has
finally to be slaughtered renders the flesh unfit for consumption.
The giving of absorbents is probably most widely practised. The
ammonia which many of them contain absorbs carbonic acid,
thereby diminishing the pressure of gas contained in the rumen, and
therefore the distension of the first gastric reservoirs. Unfortunately
this action is only temporary, and if the drug is given in too
concentrated a form, the mucous membrane of the mouth, of the
œsophagus, and sometimes even of the rumen and reticulum, may be
irritated and inflamed, producing lesions of stomatitis, pharyngitis,
œsophagitis, contraction of the œsophagus, etc., which after recovery
from the acute condition may gravely affect the animal’s general
health. A further drawback is that the flesh rapidly acquires an
ammoniacal odour.
Perhaps the best internal treatment consists in administering
purgatives such as hyposulphite or sulphate of soda or sulphate of
magnesia, in doses of 10 to 20 ounces, according to the animal’s size,
or, in the case of pregnant animals, in small frequently repeated
doses. These check fermentation, and so arrest the evolution of gas,
whilst by their purgative properties they excite contraction of the
gastric reservoirs and cause eructation.
None of these methods of treatment, therefore, should be used
exclusively, but all may be utilised as auxiliaries to mechanical or
surgical measures, and all should be preceded by the use of the
probang and puncture of the rumen.
The first of these operations, the technique of which scarcely
requires description, is often of little value; for the solids and liquid
contents of the rumen being permeated with gases, rise as a
fermenting mass into the upper portions of the rumen, and
continually obstruct the open end of the catheter, so that very little
gas escapes.
Puncture of the rumen is much more effective and easier to
perform. The owner himself often operates with an ordinary pocket
knife, sometimes introducing a couple of fingers or a short length of
elder-wood tube into the wound thus produced.
The incision should be made at one stroke, for any hesitation may
cause the wall of the abdomen to recede from the rumen, which lies
immediately below. Should gas escape under the skin, emphysema,
which often extends to the loins and along the quarters, may be
produced, and may be followed by diffuse subcutaneous
suppuration, resulting from pyogenic germs entering the
subcutaneous tissue.
Large quantities of gas escape from the puncture, sometimes with
such force as to drive out the canula. The flow of gas then ceases. In
other cases the tube becomes blocked; because, as the pressure
within the rumen diminishes, the gases dissolved or mixed with the
partially digested food are freed, and the whole contents of the
rumen become converted into an aerated, bubbling mass. Liquid or
semi-liquid materials may be ejected to some distance, or may pass
between the skin and the muscles, or between the walls of the rumen
and the abdomen, producing various complications, like necrosis,
abscess formation, etc. Such accidents can be avoided by exercising
firm pressure with the fingers on the tissues surrounding the canula.
Even when the rumen has resumed its normal size recovery is not
certain, and may not occur for several hours, or even several days,
afterwards. The patients should therefore be kept under observation
for some time, and it is usually best to leave the canula in place for
one or two days, and to put the animal on low diet.
Necrosis of aponeurotic tissues, fistula formation, and local
peritonitis only occur if the instrument is dirty or is introduced in a
wrong direction.

IMPACTION OF THE RUMEN. INDIGESTION AS A RESULT OF OVER-EATING.

In this condition the rumen is over-distended with food. The

symptoms are principally due to abnormal fermentation, the
peristaltic action of the rumen being in abeyance, and the food failing
to pass towards the omasum and abomasum. Rumination is
generally suppressed.
The disease usually follows change of diet. When the diet has long
been restricted, as occurs during years of bad harvests, and animals
are afterwards set at liberty in rich pastures, they eat greedily,
distend the rumen with large quantities of green fodder, and set up
all the necessary conditions for this form of indigestion. Similar
results follow when gluttonous animals are freely supplied with rich
food. Working oxen also suffer if withdrawn from work and fed with
roots, beetroot refuse, brewers’ grains, or other manufacturing
residue for the purpose of fattening. These materials can only be
absorbed in moderate quantity, and the large amount of water, etc.,
they contain is apt to disturb the animal’s digestive powers, while
owing to its fine state of division such food cannot be returned to the
mouth for secondary mastication, and rumination therefore remains
incomplete: the food accumulates in the rumen, distending and
eventually paralysing it. This is a common result of feeding on semi-
liquid pulp, which in order to be ruminated should be mixed with
rough forage.
Insufficiency of drinking water is another and more frequent
cause, especially during the winter, because the ox-herd or cowman
is often too lazy to give a regular and sufficient supply unless water is
laid on in the stable itself. The dry food becomes compacted into a
mass, which cannot be returned to the mouth for rumination.
Moreover, less saliva is then secreted, and Colin has shown that
rumination is impossible when the parotid ducts are ligatured.
Symptoms. As may readily be imagined, the symptoms vary,
according to the quantity and digestibility of the food swallowed. In
the first place the appetite falls off: animals suffering from
commencing indigestion only take part of their food; later on
appetite ceases, and with it rumination. Trifling colic sets in,
resembling that due to congestion, and is indicated by unrest,
switching of the tail, lifting of the hind legs, slight groaning, moving
from side to side, and lying down and rising at short intervals. The
animals seem oblivious of their surroundings, anxious, and at times
semi-comatose.
 When the case has been neglected for several days the animal may
masticate without having any food in the mouth, and may attempt to
eructate and to regurgitate food; but such attempts always fail. It
then absolutely refuses food, and animals which have eaten large
quantities of green forage may show tympanites. If called in at this
period of the disease the veterinary surgeon finds nothing positive
except signs referable to the digestive apparatus. By methodically
examining the digestive tract, and in particular the stomachs, one
discovers during palpation of the left flank that the rumen is
distended. This is characteristic. By deep palpation it is even possible
to detect marked resistance and a certain characteristic firmness
resulting from accumulation of food. The percussion sounds over
this region are dull, and pressure causes pain, as though the rumen
and peritoneum were inflamed. When the open hand is laid flat on
the rumen and thrust downwards, no peristaltic movement can be
discovered. Finally, on auscultation the normal sounds, including
crepitation, fermentation, and rolling sounds are all absent.
There are no well-marked general symptoms. Respiration and
circulation are hardly accelerated, nor is the artery particularly tense.
Course and Termination. The course of the disease varies, and
the condition may be divided into two forms, acute and chronic. The
first develops in a single day, and may cause death by the same
mechanism as acute tympanites—i.e., asphyxia or carbonic acid
poisoning; the other continues for five, ten, or even twenty or thirty
days, according to the promptitude with which treatment is
undertaken.
In protracted cases, however, the indigestion itself ceases to be as
important as the complications. Sometimes spontaneous recovery
occurs, the food passing away towards the intestine, or even being
vomited, though the latter conclusion is rare. Recovery may also
follow from treatment. If the disease is neglected it may become
complicated with gastro-enteritis.
The diagnosis is not very difficult. Indigestion resulting from
impaction is distinguished from acute tympanites by its less rapid
course and by the less marked distension of the rumen (in this case
due to solid food), and from acute gastro-enteritis by the varying
degree of fever which accompanies the latter condition.
 Prognosis. The prognosis is always grave, even in cases of acute
indigestion resulting from eating green food.
In this case gaseous indigestion occurs as a complication, and
necessitates immediate intervention. The other forms may rapidly
yield to proper treatment, or, in spite of every care, may give rise to
prolonged complications.
Lesions. On post-mortem examination of animals which have
died of complicated forms of the disease, we find certain lesions
peculiar to gaseous indigestion associated with impaction of the
rumen.
If death has followed the consumption of root pulps, we see signs
of poisoning. As a consequence of prolonged stagnation of food in
the rumen, there follows an exaggerated organic fermentation,
whose products are absorbed through the stomach or intestine and
pass into the circulation.
These various fermentations, which may be of the lactic, butyric,
and even putrid order, produce changes in the mucous membrane of
the rumen; wide tracts of the epithelium may be shed, exposing the
corium, and producing enormous ulcerations, which in certain cases
implicate the entire inner surface of the rumen.
The treatment must be varied, according to the cause,
symptoms, and immediate complications. When the disease is of an
acute type, such as that produced by over-gorging with lucern and
green food, it is best to proceed as in gaseous indigestion, i.e., to
puncture the rumen and give frequent large doses of purgatives until
the stomach and bowels have been freely unloaded. The animals
should then be kept for some days on small quantities of easily
digested food, and should be allowed lukewarm, mucilaginous
drinks.
When tympanites and impaction occur simultaneously, immediate
surgical intervention becomes necessary, and gastrotomy may then
be performed by a very simple method.
Two loops of cord are passed around the abdomen, one behind the
hypochondriac circle, the other in front of the angle of the haunch.
Assistants placed on the right side draw these loops tight, so as to
immobilise the left flank. A bistoury is then thrust directly through
the walls of the abdomen and rumen. As a consequence of the
pressure exercised by the ropes, if not of the pressure of gas itself,
the food material contained in the rumen is often expelled in a
powerful stream. As the superposed tissues cannot very readily
change their mutual relations, the author of this suggestion claims
that there is little danger either of infectious materials passing into
the subcutaneous connective tissue, or of peritonitis; but this rude
treatment can only be resorted to in cases of extreme urgency, and it
appears by no means without danger.
Injections of 10 to 15 centigrammes of pilocarpine and 5 to 10
centigrammes of eserine are also useful.
When impaction of the rumen assumes a less acute form,
moderate doses of purgatives may be given and repeated daily, or
twice a day, until the peristaltic action of the rumen is restored and
resumes its normal rhythm. In certain cases, however, recovery is
only apparent. The food in contact with the walls of the rumen
breaks down, and passes away into the abomasum and intestine,
while appetite returns. The animals then resume feeding, and some
days afterwards show all their former symptoms. Low diet should
therefore always be continued for some time.
In spite of treatment, or in consequence of treatment being too
long delayed, no improvement may follow. The ingested food is not
expelled. Putrid fermentation results, auto-intoxication sets in, and
the temperature rises to 40° or 41° C. Unless gastrotomy is
performed death is then certain.
This operation should be undertaken whenever the fever rises to
40° C., and two-thirds of the contents of the rumen removed. The
rumen should not be completely emptied, as there is danger of
collapse of its walls. Complications in the region of the wound can be
avoided by drainage.
If the operation succeeds, the patients must be placed on very low
diet or on milk for some days, and should be given lukewarm
farinaceous drinks, and a little hay of good quality to excite
rumination. In old milch cows this operation is seldom followed by a
satisfactory recovery. Apart from the loss of milk, the animal loses
condition, refuses to feed, and gradually succumbs to exhaustion.

IMPACTION OF THE OMASUM (THIRD STOMACH).

 Definition. “A form of indigestion, of which the prominent
feature is the drying and impaction of the ingesta between the folds
of the third stomach. It may seem to be a primary disease, but in very
many cases it occurs as a result of some acute febrile or
inflammatory affection.” (Law’s “Veterinary Medicine,” Vol. II. p.
123.)
Synonyms. Dry murrain, clew-bound, fardel-bound, stomach
staggers, grass staggers, vertigo, chronic dyspepsia, chronic
indigestion.
Causes. Torpidity of the omasum, suppression of salivary
secretion, with absence of “waves of liquid floating the finely divided
food from the mouth or rumen to third stomach, are prime
conditions of desiccation of the contents.” The third stomach, like the
first and second, has no provision for liquid secretion, and depends
for its supply on constant flushing by swallowed fluids. Therefore, if
feeding and rumination are arrested and salivary secretion is
suppressed, and if movements of the rumen and resulting overflow
into the third stomach are checked, the ingesta of the third stomach,
compressed between its folds, becomes drained of liquid and
converted into a powder or dry mass. All febrile and inflammatory
affections tend to this end, and more or less drying, with impaction
of the contents of the omasum, is a constant feature in such cases.
But in the majority of cases this condition is to be looked on as a
secondary or subsidiary affection, and the real disease must be
sought elsewhere.
The explanation of the susceptibility of the third stomach in
constitutional troubles has been sought in the source of its
innervation. Electric stimulation of the vagus rouses the movements
of the first and second stomachs, but not those of the third. Action of
the third stomach is excited by stimulation of the spinal cord, and of
the sympathetic nervous branches going to the ganglionic cells in the
walls of the omasum (Colin and Ellenberger). Its nerve supply
coming from a different source, derangement of its function may
occur independently of antecedent disorder of the first or second,
and its motor supply coming from a source so closely related to the
vaso-motor centres, perhaps affords some explanation of the
connection of disorders of the omasum with febrile and
inflammatory diseases.
 Food is an important cause. Impaction of the omasum is a winter
disease—the time of dry feeding. Dry, fibrous, innutritious fodder,
and scarcity of water contribute to its production. It attacks cattle in
spring or autumn on pastures in which fresh grass grows among the
dead, dried, or withered stems of a previous growth. It occurs when
stock are fed on corn or corn stalks (maize stalks) affected with smut
or ergot, or on cereals or grasses similarly damaged, and in both
cases especially when the water supply is deficient or restricted.
Sheep and goats, which habitually drink little, suffer less than do
cattle, which drink freely.
Other causes. Fermented foods, microbian ferments and their
products, which tend to induce torpidity of the omasum, fever, and
lessened secretion of saliva, with diminished supply of liquid from
mouth or rumen.
Pericarditis, by causing vascular stasis in the omasum, may induce
torpor and impaction.
Lead poisoning paralyses action and favours impaction. Finely
divided food stuffs—meal and bran—eaten greedily, may pass in
quantity directly into the omasum and induce impaction. “The most
acute and fatal forms occur in connection with a sudden change from
dry to rich, luscious, green food in spring, the unwonted stimulus
giving rise to general irritation of the whole gastric mucosa, with
disordered and impaired function of all four stomachs, but especially
of the third. Such cases are usually congestive and inflammatory, and
the suspension of the gastric movements is a grand cause of
impaction. In such cases, too, the brain or spinal cord, or both, are
seriously involved, and the early death is preceded by torpor,
paralysis, violent delirium or convulsions, following largely the type
of acute lead poisoning.” (Law, loc. cit.)
The symptoms depend on the degree of impaction, and vary
from simple, irregular, or suspended rumination to severe gastric
and nervous disorder. The less acute cases are marked by failure to
re-establish regular rumination or partial convalescence from fever
or inflammation. The fever subsides, but the appetite remains
capricious, the muzzle dry, eyes dull, spirits low, and breathing
accelerated; the condition is sometimes accompanied by moaning.
Slight tympanites may appear, and the contents of the rumen may
feel solid, the mouth hot, clammy, and fœtid. The bowels are
constipated, the fæces small in quantity, hard, covered with mucus or
blood-streaked, and containing particles of undigested food; in other
cases diarrhœa may set in, to be followed later by constipation.
Alternations of constipation and diarrhœa may be repeated again
and again. Exploration by pressure of the closed hand over the
omasum will give an impression of solid resistance. There may be
slight shivering, the ears and limbs are cold, the hair is erect in
patches, dry and lustreless.
In cases occurring independently of previous disease, diarrhœa
may be the first symptom observed, the malady being preceded by
local irritation and congestion; but this soon gives place to
constipation or diarrhœa and the symptoms above mentioned. The
animal is found lying apart on its left side, with its nose in its right
flank, the pulse and breathing quickened, the eyes congested;
expiration is accompanied by a grunt. The patient walks with its back
arched and dragging its limbs. The appetite may continue, but only
in an impaired and irregular form, and as rumination ceases
grinding of the teeth becomes common. The secretion of milk is
diminished or arrested, emaciation advances day by day. Fœtid
eructation may be a marked symptom. This form may last from ten
to fourteen days, and merge finally into paralysis of the hind limbs,
drowsiness and stupor, or delirium and convulsions.
“In more acute cases (from sudden access of green food, change of
water, or ingestion of irritant plants), the affection partakes more or
less of the nature of congestion or inflammation of the viscus
(omasitis), and may run a rapidly fatal course” (Law, loc. cit.). The
animal is seen apart from the herd in a characteristic recumbent
position, the eyes are red and glassy, the eyelids semi-closed, the
patient shows much drowsiness and stupor, but when raised may
still feed in a sleepy, listless manner. The bowels are loose or
confined, the pulse and breathing accelerated, the right
hypochondrium is firm and tender, and the sound of fermentation
absent or subdued over the omasum. Soon nervous disorder appears,
the eyes glare wildly, the animal seeks relief in motion—sometimes
in a straight line, sometimes to one side—and being blind and
unconscious of obstacles, may fall into pits or ditches, knock against
trees, fences, gates, or buildings, and continue pushing against
resisting objects, breaking its horns or teeth; and otherwise
sustaining injury through violent muscular contractions.
Course. Chronic cases may continue indefinitely, with symptoms
of poor health, impaired digestion, and gradual loss of condition.
After death the omasum may contain dried food which the animal
consumed several months before the attack.
In cases ending in early recovery there occurs abundant diarrhœa,
“the fæces are mixed with flattened, dark, solid, and polished masses,
the impacted ingesta from the omasum. Tympany subsides;
movement in rumen and omasum and rumbling in bowels can be
heard. Appetite returns.” (Law.)
Diagnosis. The condition of the pulse and respiration, and the
grunting with expiration may lead to confusion with pneumonia.
At first there is no fever, tenderness is confined to the right flank;
there is an absence of pulmonary crepitation, of pleural effusion, and
of movement in the rumen and omasum. Signs of gastric and
intestinal disorder can be detected.
Lesions. The omasum is gorged—it may be twice its normal size—
solid, resistant, almost stony. The spaces between the leaves are
packed with dried food, which, when removed, carries a layer of
epithelium from the mucous membrane. (This (layer on contents) is
not inconsistent with health.)
The rumen contains ingesta packed in masses, more or less
offensive from putrefaction.
The abomasum is empty of food, but contains much mucus. Its
mucous membrane is congested.
The small intestine is red in places, empty and collapsed.
The larger intestine contains a quantity of dry, glistening pellets,
and much mucus.
Treatment follows the lines of impaction of rumen, though the
response is usually less certain, and always slower. Flax-seed tea,
several bucketfuls per day, will often succeed.
Epsom and common salts, with sol. ammoniæ, excite thirst;
liquids should be supplied freely.
In obstinate cases, and in absence of gastric or cerebral congestion,
20 croton beans, or 20 drops of croton oil, may be added to the
purgative. Nux vomica stimulates the nervous supply. Enemata may
be given freely.
Other remedies, stimulating contractility and secretion, are:
Eserine, 1½ grains; veratrine, 1 grain; barium chloride, 10 to 15
grains; or pilocarpin, 3 grains, hypodermically.
The patient may be days or even a week without alvine discharge
and recover.
If fever and symptoms of gastric congestion appear, a blister may
be applied to the right side over the omasum.
Nervous symptoms, such as dilated pupils, blindness, congested
mucous membrane, hot horns and ears, drowsiness or excitement,
are combated by applying cold water or ice to poll, etc.
When free action of the bowels is restored, laxative diet, roots
(pulped), green food, plenty of common salt, and free access to
drinking water should be prescribed.
During convalescence a course of tonics, including nux vomica, is
advisable to help in restoring normal gastric functions.

ABOMASAL INDIGESTION.

Primary indigestion in the abomasum appears to be rare in adults,

for until the present time no one has given a sufficiently
characteristic description of this disease to enable it readily to be
recognised. On the other hand, it is to be presumed, although final
proof has certainly not been furnished, that in cases of gaseous
indigestion, or of impaction of the rumen, the abomasum, whose
physiological action is predominant, must simultaneously suffer.
Primary abomasal indigestion, on the contrary, is common in
young animals before weaning, so that the condition has been given
the name of “milk indigestion.” It could not very well be otherwise,
for the abomasum is the only one of the gastric divisions which in
ruminants is active during the first few weeks of life. At this period it
is larger than the other gastric reservoirs; and the rumen, the
reticulum, and the omasum do not undergo great development till
weaning begins.
 Causation. Milk indigestion attacks young animals, under
varying conditions.
In animals suckled by the mother the disease rarely occurs, but yet
when the mothers are good milkers, like the Flemish, Norman,
Jersey, and Holland breeds, and when there is too long an interval
between the feeds, calves, which are naturally greedy, and in addition
are hungry, are apt to take too large a quantity of milk—in fact, they
often gorge to the fullest possible extent. Owing to its over-distended
state the abomasum either fails to secrete sufficient of the rennet
ferment necessary for coagulating the milk or secretes an
insufficiently active ferment. The first stage of digestion remains
incomplete, giving rise to so-called “milk indigestion.”
When the cows are employed in ploughing, etc., or in drawing
carts, not only are the calves fed at long intervals, but the milk is not
always of proper chemical composition even in the udder. As a result
of work, fatigue, over-exertion and irregular feeding, the cow’s yield
of milk for the time is less digestible than the normal supply, or may
even prove irritant to the calf’s stomach. Milk indigestion is thus set
up.
When the cows are fed on factory waste, like beetroot-pulp or
brewers’ grains, toxic or irritant products may even find their way
into the milk, which then irritates the little creature’s abomasum and
produces gastric indigestion. Just as in the production of congenital
alcoholism in man, the young animal is then ingesting, unknown to
those responsible for its well-being, chemical substances which
produce various pathological changes.
But milk indigestion is commonest of all in calves fed by hand. The
food usually given is a mixture of milk from the previous night, and
skim milk or even butter milk. It contains lactic ferments and various
microbes, some capable of producing toxic principles.
When swallowed and brought directly in contact with the mucous
membrane these cause abomasal indigestion.
Symptoms. Soon after feeding, the little animal appears dull and
somnolent, and shows moderate abdominal pain, suggesting trifling
colic.
This stage is soon followed by nausea; the breathing and the
heart’s action become rapid, vomiting efforts are made, and finally
milk, in the form of firm or partially softened curds, depending on
the time which has elapsed since the last feed was taken, are
vomited. The quantity ejected varies. Pressure over the right side of
the abdomen produces pain, and tympanites of the abomasum may
sometimes be detected on percussion.
The sensitiveness and gaseous inflation are confined to the middle
and lower zone of the hypochondrium. Soon after vomiting the
animal begins to improve. The patient seems brighter, relief is very
marked, and in some cases proves permanent; but more frequently a
certain degree of depression persists, the mouth emits a sourish
odour, and for a time the appetite remains poor. This temporary
irritation of the abomasum has a tendency to become permanent; or
even to extend to the intestine, in which the conditions appear more
favourable to the development of microorganisms than do those in
the stomach. Indigestion then becomes complicated with diarrhœic
enteritis.
The diagnosis presents no difficulty.
The prognosis is not serious, provided that the young animals
are carefully attended to; but such complications as diarrhœic
enteritis may become very grave if neglected.
The treatment. To prevent recurrences:
(1) The periods of feeding should be regulated;
(2) The cows should not be worked, or should be worked as little as
possible;
(3) Mixed milk, or milk which has already undergone lactic or
other fermentation, should be avoided.
If the calves must be reared by hand, the mixed milk should at
least be boiled or relatively pasteurised by heating to 70° or 80° C.,
and the buckets used for feeding should be kept scrupulously clean.
These precautions become absolutely necessary when diarrhœa
exists amongst the calves. Curative treatment consists in placing the
animals on low diet for two or three days after the attack of
indigestion, or in giving them boiled milk diluted with from one-half
to two-thirds of boiled water.
The addition of a mild saline purgative like sulphate of soda, in
doses of one-half to three-quarters of an ounce, usually ensures a
cure. Infusions of lime-tree flowers, peppermint, camomile, etc., may
advantageously be used to replace boiled water in diluting the first
foods.

ACUTE GASTRIC INDIGESTION IN SWINE.

The causes comprise putrid food, swill, spoilt turnips, potatoes,

apples, succulent vegetables, frozen food, and the admixture of
caustic alkaline powders (used in washing table dishes) with the
swill. Indigestible matters—hoof, horn, hair, bristles, tree bark, etc.—
when not rejected by vomiting, cause gastritis and indigestion.
Lastly, medicinal substances and poisons, paint and lead, sometimes
produce the disease.
Among the symptoms may be mentioned dulness, arching of the
back, standing with the feet brought together, erection of the bristles,
hiding under the litter, grunting, uneasiness, shifting from place to
place, tenseness of the abdominal wall, borborygmus; these may be
followed by diarrhœa and recovery. Speedier relief is afforded by
copious vomiting of irritant matters.
The treatment should commence with the free administration of
emetics. To combat alkaline poisoning vinegar may be given,
followed by a laxative. Prophylaxis calls for greater care in feeding.
 CHAPTER V.
ACUTE INFLAMMATION OF THE GASTRIC COMPARTMENTS.

RUMENITIS—RETICULITIS—GASTRITIS.

Causation. Acute primary inflammation of the first gastric

reservoirs, viz., the rumen and reticulum, is not common. It
sometimes accompanies such infectious disorders as foot-and-mouth
disease, gangrenous coryza, etc., but then constitutes an added
phenomenon which should be studied along with the original disease
itself. Rumenitis or reticulitis may however follow the ingestion of
irritant foods or plants, of very hot liquids, and more frequently still
of unskilfully compounded medicines. In such cases the mucous
membrane is directly attacked, and pathological congestion,
infiltration, and desquamation may follow, or even vesicles and
ulcerations may rapidly be formed.
Symptoms. Inflammation of the rumen or reticulum is
announced by loss of appetite, suspension of rumination or of
regular peristalsis, slight tympanites, and particularly by excessive
sensitiveness to palpation. This sensitiveness is general, but is more
specially marked in the left lower third of the abdominal cavity, and
in the retro-ensiform region which corresponds to the position of the
reticulum. Moderate fever is present.
These symptoms, which indicate the gravity and intensity of the
inflammation, may persist, become aggravated, provoke vomiting
from the rumen, and leave as a legacy motor dyspepsia, or even more
serious consequences. On the other hand, they may progressively
diminish and disappear for good.
Lesions. The lesions comprise hyperæmia of the walls of the
rumen and of the mucous membrane, extensive local exfoliation of
epithelium, and sometimes true ulceration of the mucous membrane.
 Diagnosis. The diagnosis is based on the exceptional
sensitiveness of the gastric compartments on palpation, and also on
the history, provided reliable information can be obtained.
Prognosis. The prognosis should be reserved, because it is never
possible to foretell whether acute lesions may not give place to
chronic disease, which, though apparently unimportant, may
terminate in grave consequences.
Treatment. Owing to their local action demulcent drinks and
teas are indicated. Cooked food is useful, because it makes little
demand on the digestive powers; steamed hay and farinaceous
substances are given, both on account of their nutritious qualities
and of the slight local irritation they cause when swallowed.
Lukewarm drinks and saline laxatives, such as the sulphate of
soda, and carbonate of soda or Carlsbad salt in small doses of 1½ to
2 ounces, seem most useful in combatting the reflex atony of the
digestive compartments.
Inflammation of the omasum, like that of the rumen and
reticulum, occurs as a secondary phenomenon in conditions like
rinderpest, Texas fever, foot-and-mouth disease, anthrax, and
gangrenous coryza (malignant catarrh); but primary inflammation is
much rarer even than that of the rumen and of the reticulum.
This is accounted for by the deep position of the omasum, which is
thus sheltered from external violence, early contact with irritant
foods and from the effect of chills, etc. It can only become inflamed
by the prolonged action of irritant food and drink, which have
already produced lesions in the rumen and reticulum; or as a
consequence of the prolonged stagnation of dry food in cases where
animals have been deprived of water.
Under these conditions inflammation of the omasum develops
slowly, and from the clinical point of view is identical with what was
formerly known as obstruction of the omasum. Obstruction or
impaction is probably much rarer than has been stated, in so far at
least as it constitutes a primary condition, for in the great majority of
cases it is consecutive to impaction, inflammation of the rumen, or
inflammation of the abomasum. Obstruction of the omasum, which
was formerly invoked in all doubtful and ill-defined cases of digestive
disturbance, seldom occurs as an isolated disease.
 It has been suggested that the omasum, being supplied with nerves
solely by the sympathetic system, and provided with a relatively weak
muscular coat, was more susceptible than the other reservoirs to the
reaction of abdominal reflexes, and therefore more subject to
inflammation, indigestion and obstruction. We do not hold that view,
because, as a result of its general situation and the position of its
orifices of communication, this compartment is easily able to expel
its contents so long as they are liquid. Its function appears chiefly to
be to complete the trituration of food after rumination.
We do not consider that inflammation of the omasum never
occurs, for we are well aware of the contrary, and that the
inflammation assumes a subacute course and is accompanied by
stasis of the semi-digested food between the mucous leaves which
partly fill the cavity. We simply wish to emphasise the view that the
condition is not a primary and isolated inflammation.
Symptoms. The symptoms are always vague and very difficult
clearly to define.
Inflammation of the omasum is indicated by relative loss of
appetite, marked thirst, general atony, and diffuse and vague
sensitiveness in the inferior half of the right hypochondrium (zone of
the asternal ribs). There are no pathognomonic symptoms.
Obstruction has also been described as accompanied by loss of
appetite, constipation, the passage of black, coated, fœtid and
sometimes blood-streaked fæces, symptoms of chronic tympanites
with fœtid eructations and sometimes vomiting. These sometimes
accompany hydrochloric acid dyspepsia, a form of chronic gastritis,
and, from our standpoint, the stagnation of food in the omasum is
only secondary. We therefore interpret the facts in quite a different
manner, and believe that only by a rational and physiological
interpretation of the symptoms observed can one diagnose the
condition.
Diagnosis. The diagnosis of inflammation of the omasum can
only be made by a process of exclusion; and although we are
admittedly dealing with a condition secondary to disturbance of the
rumen and reticulum, or on the other hand consecutive to
inflammatory states or to modifications in the secretion of the
abomasum (dyspepsia), the diagnosis does not present insuperable
difficulties.
 The prognosis is only grave when the primary acute or chronic
conditions of the other gastric compartments are serious.
The lesions comprise abnormal vascularity of the mucous
membrane and desquamation, and even gangrene, of the leaves. The
partially digested food is not passed on, becomes dry and hard, and
in time aggravates the local condition.
The treatment does not essentially differ from that of other
gastric inflammations. The object to be attained is to evacuate as
completely as possible, not only the omasum, but all the gastric
reservoirs, for which purpose one may freely administer demulcent
drinks—linseed gruel, bran mashes and lukewarm liquids containing
laxatives. At first such alkaloids as arecolin and pilocarpine may be
subcutaneously injected to ensure energetic and speedy evacuation.
Later on slightly stimulant aromatic infusions, like infusions of
sage, peppermint, hyssop, thyme, etc., stimulate the functions of the
stomach and hasten the return of normal conditions.

ACUTE GASTRITIS.

The term “acute gastritis,” sometimes “gastro-enteritis,” is used in

bovine pathology to indicate inflammation of the abomasum. If this
inflammation is confined to the superficial epithelial layers it is
defined as superficial catarrh of the abomasum; if, on the contrary, it
extends to the deep epithelium of the gastric glands and to the
mucous corium, it is termed deep-seated gastritis.
Clinically it is impossible to make these distinctions. We simply
recognise degrees of gravity, and only in this way can one diagnose
acute gastritis, phlegmonous gastritis, ulcerative gastritis, etc.
Causation. The abomasum frequently becomes inflamed as a
consequence of irritant foods, apart altogether from lesions of the
rumen or reticulum, the mucous membrane lining the abomasum
being so much more delicate than that of either of the two first
compartments.
Irritant plants, parasites, acid drinks, very cold water, certain acid
or toxic industrial residues like mouldy brewers’ grains, fermented
vegetable pulp, decomposed beet, etc., and mouldy or spoilt forage of
any kind may all produce acute gastritis.