Gastroenterology

WB SAUNDERS
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Harcourt Publishers Limited 2002
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I

Contributors
Jennifer E Adolf
Internist Private Practitioner
Ledgewood Equine Medical Center
Ontario, New York, USA
Dorothy Ainsworth
Associate Professor of Medicine
Department of Clinical Sciences
College of Veterinary Medicine
Cornell University
Ithaca, New York, USA
Fairfield T Bain
Internal Medicine Practitioner
Haygard-Davidson-McGee Associates
Lexington, Kentucky, USA
Michael A Ball
Private Practitioner
Early Winter Equine Medicine and Surgery
Lansing, New York, USA
Jacqueline Bartol
Rochester Equine Veterinary Clinic
Rochester, New Hampshire, USA
William V Bernard
Rood & Riddle Equine Hospital
Mark Bowen
HBLB Resident in Equine Thoracic Medicine
Sefton Equine Referral Hospital
Royal Veterinary College
University of London
Hatfield, Herts, UK
T Douglas Byars
Director of Internal Medicine
Christina 5 Cable
Early Winter Equine Medicine and Surgery
Lansing, New York, USA
Gary Carlson
Professor of Equine Medicine
Department of Medicine
School of Veterinary Medicine
University of California, Davis
Davis, California, USA
Noah D Cohen
Associate Professor of Medicine
LA Medicine and Surgery, CVM
Texas A and M University
College Station, Texas, USA
Thomas J Divers
Professor of Medicine
Cornell University
Richard Drolet
Professor of Pathology
Universite de Montreal
Departement de Pathologie et Microbiologie
Saint Hyacinthe, Quebec, Canada
Normand G Ducharme
Professor of Surgery
Cornell University
G Barrie Edwards
Professor of Equine Studies
University of Liverpool
Leahurst
Neston, South Wirral, UK
xi
CONTRIBUTORS
Ryland B Edwards III
Clinical Assistant Professor of Large Animal Surgery
University of Wisconsin
Madison, Wisconsin, USA
Andrew T Fischer Jr
Chino Valley Equine Hospital
Chino, California, USA
Lisa A Fortier
Assistant Professor of Surgery and Molecular Medicine
Cornell University
David E Freeman
Associate Professor of Equine Surgery
Head of Equine Surgery and Medicine
University of Illinois
Urbana, Illinois, USA
Sarah L Freeman
Lecturer in Equine Surgery
Department of Farm Animal and Equine Medicine and
Surgery Studies
Hatfield, Herts, UK
John Freestone
Resident Veterinarian
Coolmore Australia
Jerry's Plains
New South Wales, Australia
Susan L Fubini
Professor of Surgery
Cornell University
Earl Gaughan
Professor of Large Animal Surgery
Kansas State University
Veterinary Medical Teaching Hospital
Manhattan, Kansas, USA
Robin D Gleed
Associate Professor of Anesthesiology
Cornell University
xii
Laurie R Goodrich
PhD candidate for cellular and molecular biology
Cornell University
Richard Hackett
Professor of Large Animal Surgery
Cornell University
Reid Hanson Jr
Associate Professor of Surgery
Department of Large Anrmal Surgery and Medicine
Auburn University
Auburn, Alabama, USA
Philip D Van Harreveld
Associate
Vermont Large Animal Clinic
Milton
Vermont, USA
Mark H Hillyer
Lecturer in Equine Soft Tissue Surgery
Department of Veterinary Medicine
University of Bristol
Langford House, Bristol, UK
J Geoff Lane
Senior Lecturer in Veterinary Surgery
School of Veterinary Science
Langford House, Bristol, UK
Jean-Pierre Lavoie
Professor of Equine Medicine
Departement de Science Cliniques
Universite de Montreal
Saint Hyacinth, Quebec, Canada
Sandy Love
Head of Division of Equine Clinical Studies
Department of Veterinary Medicine
University of Glasgow
Bearsden, Glasgow, UK
J Lyons
Veterinary Student
Faculty of Veterinary Medicine
University College Dublin
Dublin, Republic of Ireland
Tim S Mair
Bell Equine Veterinary Clinic
Mereworth, Maidstone
Kent, UK
Celia Marr
Head of Equine Division
Department of Farm Animal and Equine Medicine and
Surgery
Hatfield, Herts, UK
PO Eric Mueller
Department of Large Animal Medicine
University of Georgia
Georgia, USA
Michael J Murray
Professor in Equine Medicine
Marion Dupont Scott Equine Medical Centre
Leesburg, Virginia, USA
James A Orsini
University of Pennsylvania School of Veterinary
Medicine
Philadelphia, Pennsylvania, USA
Simon F Peek
Clinical Assistant Professor of Medicine
Department of Medical Sciences
The University of Wisconsin-Madison
Madison, Wisconsin, USA
Gillian Perkins
Instructor in Large Animal Medicine
Cornell University
Scott Pirie
Lecturer in Veterinary Medicine
Easterbush Veterinary Centre
University of Edinburgh
Rosylin, Midlothian, UK
Chris J Proudman
Lecturer in Equine Surgery
University of Liverpool
Leahurst, Neston
South Wirral, UK
CONTRIBUTORS
Claude A Ragle
Associate Professor of Equine Surgery
College of Veterinary Medicine,
Washington State University
Pullman, Washington, USA
Peter Rakestraw
Assistant Professor of Large Animal Surgery
Large Animal Medicine and Surgery
Sarah Ralston
Associate Professor of Animal Sciences
Department of Animal Science
Rutgers University
New Brunswick, New Jersey, USA
Johanna M Reimer
Rood and Riddle Equine Hospital
BA Rucker
SW Virginia Vet Services
Lebanon, Virginia, USA
Elizabeth Santschi
Clinical Associate Professor of Large Animal Surgery
University of Wisconsin-Madison
Madison Wisconsin, USA
Jim Schumacher
Professor of Equine Surgery
Auburn University
Auburn, Alabama, USA
Chris M Schweizer
Lecturer in Therogeniology
Cornell University
Stacey A Semevolos
Lecturer in Large Animal Surgery
LA Medicine and Surgery, CVM
Kim Sprayberry
Practitioner of Internal Medicine
xiii
CONTRIBUTORS
Frank GR Taylor
Senior Lecturer in Equine Medicine
Division of Companion Animals
Langford, Bristol, UK
Beth Valentine
Assistant Professor
Department of Biomedical Sciences
College of Veterinary Sciences
Oregon State University
Corvallis, Oregon, USA
Catherine Walsh
Resident in Anaesthesiology
Department of Clinical Veterinary Medicine
University of Cambridge
Cambridge, UK
R Weller
Student in Equine Surgery
Department of Farm Animal and Equine Medicine
and Surgery Studies
Hatfield, Herts, UK
Jamie Whiting
Internist
Dubai Equine Hospital
Dubai, UAE
Alison A Worster
Resident in Animal Surgery
Cornell University
-
Plate 2.1 Normal peritoneal fluid sample showing neu
trophils and large mononuclear cells (macrophages and
mesothelial cells). A small number of red blood cells are
present caused by iatrogenic bleeding during collection of
the sample
Plate 2.2 Peritoneal fluid from a horse with early bowel
rupture showing the presence of plant material in the
fluid in the absence of an increase in neutrophils
Plate 2.3 Peritoneal fluid from a horse with hemoperi
toneum showing free red blood cells and erythrocyto
phagia by a macrophage
Plate 2.4 Yellow-green discoloration of peritoneal fluid
caused by leakage of bile into the abdomen
Plate 2.5 Normal endoscopic view of the stomach of a 2-
week-old foal. The stomach is seen along the right side
and greater curvature. The squamous mucosa (top) is nor
mally pale, and because the stomach wall of foals is rela
tively thin, submucosal vessels can be seen. Often the
spleen can be observed through the relatively translucent
stomach wall of foals. The glandular mucosa (bottom) is
normally red
Plate 2.6 Normal endoscopic view of the stomach of an
adult horse. The stomach is seen along the greater curva
ture. The squamous mucosa (top) is normally pale and the
glandular mucosa (bottom) is normally red
Plate 2.7 Normal endoscopic view of the stomach of an
adult horse, seen along the lesser curvature of the stom
ach. Gastric secretions can be seen at the bottom of the
plate and the antrum and pylorus lie underneath the shelf
of squamous mucosa along the lesser curvature. The
cardia, through which the endoscope has entered the
stomach, is just out of view at the top of the photograph
(arrow)
Plate 4.1 Transillumination of large colon wall showing
mucosal stages of cyathostome larvae
Plate 4.2 Tapeworms (Anoplocephala perfoliata)
Plate 4.3 Strongylus vulgaris arteritis. Section through
mesenteric artery showing S. vulgaris larvae and
associated arteritis (courtesy JL Duncan)
Plate 4.4 Ascarid impaction. Post-mortem appearance
showing numerous ascarids causing obstruction of the
small intestine (courtesy MJ Martinelli)
Plate 11.1 In the early stage of distributive shock mucous
membranes become brick red and can form a dark red line
bordering the teeth
Plate 11.2 During the late stages of distributive shock
mucous. membranes become cyanotic
Plate 12.1 A large area of ulceration of the gastric squa
mous mucosa adjacent to the margo plicatus along the
right side of the stomach in a 3-year-old Standardbred
racehorse that had poor appetite, weight loss, and inter
mittent abdominal discomfort
Plate 12.2 Generalized erosion and ulceration of the
gastric squamous mucosa along the lesser curvature in a
4-year-old Thoroughbred race horse with a poor appetite
and low-grade intermittent abdominal discomfort. The
endoscope can be seen entering the cardia at the top left
of the photograph

Plate 12.3 The antrum of a 6-year-old Thoroughbred
steeplechase horse that presented because of poor perfor
mance and poor appetite. There is thickening with ulcera
tion of a ruga
Plate 12.4 Ulceration and inflammation with fibrosis of
the pylorus of the horse in Plate 12.1. There is pylori
.
c
stenosis because of chronic ulceration and fibrosis. This
resulted in delayed gastric emptying and the ulceration
seen In Piate 1 L.l (among other sites of ulceration). The
tissue surrounding the pylorus felt very stiff when
manipulated with a biopsy forceps
Plate 12.5 Squamous cell carcinoma in a 15-year-old
horse that presented because of tachypnea and recent
poor appetite. Multiple neoplastic masses can be seen in
the gastric squamous mucosa. The neoplasia had extended
into adjacent abdominal viscera
Plate 13.1 Adhesions of jejunum causing kinking of
intestine and partial obstruction
Plate 13.2 Pedunculated lipoma originating closed to the
mesenteric attachment to jejunum. This horse suffered
recurrent colic as a result of partial obstruction caused by
this lipoma
Plate 13.3 Short loop of ileum and distal jejunum
entrapped and strangulated through the epiploic foramen
Plate 13.4 Edema and sub-serosal hemorrhage of small
intestine. These changes are characteristic of anterior
enteritis
Plate 13.5 Mid-jejunal intussusception. Surgeon's finger
present at the point of invagination of intussusceptum
into intussuscipiens
Plate 16.1 Type 4 rectal prolapse
Plate 17.1 Post-mortem appearance of extensive fibrin
deposition in diffuse septic peritonitis
Plate 17.2 Thick, turbid, orange peritoneal fluid typical of
acute septic peritonitis (left) compared with peritoneal
fluid sample from a normal horse (right)
Plate 17.3 Large mesenteric abscess due to Streptococcus
equi subsp. equi ('bastard strangles'), post-mortem
appearance
Plate 17.4 Omental and mesenteric adhesions to a mesen
teric abscess caused by foreign body penetration of the
jejunum
Plate 17.5 Hemangiosarcoma of the spleen causing hemo
peritoneum in a pony
Plate 17.6 Focal annular lymphosarcoma lesion of the
small intestine causing partial bowel obstruction and
recurrent colic
Plate 17.7 Large mesenteric abscess which caused chronic
and recurrent colic (post-mortem appearance)
Plate 17.8 Gross post-mortem appearance of the large
colon of a case of sub-acute grass sickness, note the black
coating over the firm fecal impaction exposed following
reflection of the colonic wall
Plate 18.1 Post-mortem appearance of granulomatous
enteritis showing enlargement of the mesenteric lymph
nodes
Plate 18.2 Preputial edema in a gelding, caused by
hypoproteinemia secondary to small intestinal
malabsorption (alimentary lymphosarcoma)
Plate 18.3 Severe alopecic skin lesions secondary to
small intestinal malabsorption (chronic inflammatory
bowel disease)
Plate 18.4 Severe coronitis as part of the skin lesions
associated with multisystemic eosinophilic epitheliotropic
disease
Plate 19.1 Large calcium bilirubinate choledocholith
(arrow) obstructing the common bile duct at the junction
of left and right hepatic ducts
Plate 19.2 Gross lipemia in a plasma sample (left) com
pared with a normal plasma sample (right)
Plate 19.3 Fatty infiltration of the liver
Plate 21.1 Large colon of a horse with phenylbutazone
toxicosis. Note the line of demarcation between the
affected right dorsal colon and the remainder of the large
colon
Plate 23.1 Multifocal erosions and ulcer in the gastric
squamous mucosa in a 4-week-old foal with no clinical
signs of gastric ulcers. The ulcer at the top of the photo
graph has contracting margins and is healing
Plate 23.2 Bleeding ulcer in the gastric glandular mucosa
of a 4-month-old foal that had been treated for pneumo
nia but had a poor appetite that persisted afer a favor
able clinical response to the pneumonia
Plate 23.3 Linear erosions and ulcers in the antrum,
extending to the pylorus in a 5-month-old foal with inter
mittent, mild to moderate abdominal discomfort
Plate 23.4 Severe duodenitis in a 4-month-old foal that
presented with fever for 5 days, diarrhea, and acute
abdominal discomfort. There was severe, hemorrhagic
ulceration of the gastric squamous and glandular mucosal
surfaces. The duodenal mucosa was replaced by a fibrino
necrotic exudate. A large blood clot is at the lower right of
the photograph
Plate 23.5 Contracture of the stomach of a 3-month-old
foal, as a sequel to severe ulceration of the squamous
mucosa along the lesser curvature. The foal reportedly
had not had ulcer signs and was presented to the hospital
for fever of unknown origin.
Plate 25.1 Overo mare and lethal white foal
Plate 27.1 Post-mortem appearance of the small intestine
of a foal affected by Costridium perfringens type C show
ing hemorrhagic enteritis
Plate 27.2 Photomicrograph of cryptosporidial oocysts
(pink structures) in feces from a foal with cryptosporidial
diarrhea (100 x)
Plate 28.1 Tyzzer's disease. Filamentous bacterium,
Clostridium pi/iformis, from the liver section of an affected
foal
Preface
Gastrointestinal diseases constitute a large and diverse
group of diseases. Many of them are common and seri
ous, and they are encountered in horses of all ages,
breeds and types. The Manual of Equine Gastroenterolog
is a comprehensive guide to the diagnosis and treat
ment of gastrointestinal disorders in horses and foals.
The last 30 years have seen a dramatic advancement
in our knowledge about gastrointestinal diseases of the
horse, and this, coupled with advances in surgical
techniques and therapeutics, has led to considerable
improvements in the success rates for treatment of the
conditions. In some cases, successful treatment of an
individual horse involves the input of expertise in the
fields of surgery, internal medicine and critical care. A
these disciplines become more and more specialised, so
it becomes increasingly difcult for individual veterin
arians to keep abreast of developments in all of these
areas. One of the main objectives of this manual is to
condense information from these separate felds into
one, readily accessible source.
We feel this text is unique in at least 2 ways: frst and
foremost are the many wonderful contributions from
experts in the feld of equine gastroenterology; second,
there is an almost equal blend of contributions from
European and American clinicians in private practice
or from university hospital clinicians. We would like to
dedicate this manual to all of our contributing authors,
who have in this text, as in their many other publica
tions, contributed greatly to our understanding of the
diagnosis and treatment of equine gastrointestinal dis
orders. We would like to thank Anne Littlejohn and
Debbie Lent for their assistance in maintaining
communications with the many authors, forwarding
materials from North America to Europe and preparing
several chapters. We trust you will fnd the book a useful
source of information for the management of equine
gastrointestinal disorders.
Tim Mair
Tom Divers
Norm Ducharme
2001
xv
1
Physical examination
General physical examination
and auscultation
F Taylor
HISTORY AND GENERAL
OBSERVATIONS
When exploring the history of a patient with suspected
gastroenteric disease the following topics should be
included.
has there been an associated change in the dietary
management?
were there any medications or other treatments
prior to the onset?
is the grazing safe (e.g. check for sandy topsoil,
agrochemicals, poisonous plan ts)?
is the animal's food intake reduced; if so is this
associated with inappetance or evidence of
dysphagia?
is the animal's demeanor normal, depressed,
excitable?
in cases of abdominal pain, was the onset acute and
severe or insidious and low grade; is the pain
continuous or intermittent?
are feces being passed; if so in what volume and
consistency, and with what regularity?
is the worming history suited to the animal's
environment?
has this animal suffered previous episodes; are
other animals in the group affected?
In addition, the age and sex of the patient may help to
narrow the differential diagnoses. For example, neona
tal foals are prone to meconium retention (day 1) and
systemic infections which may involve the alimentary
tract (days 1-4). Older foals become susceptible to
gastrointestinal parasites and/or gastroduodenal ulcer
ation, and horses below 3 years of age are more likely to
succumb to intussusception than adults. In stallions, the
possibility of inguinal herniation of the small intestine
should be considered in all cases of colic. In the mare,
uterine torsion in late gestation can produce colic-like
signs, whereas postpartum colic may be associated with
hemorrhage into the broad ligament, or rupture of the
cecum or colon during fetal expulsion.
PHYSICAL EXAMINATION AND
AUSCULTATION
The initial physical examination of a patient with
suspected gastroenteric disease should pay particular
attention to the head and trunk. Additional aids to
physical examination will be required and are outlined
in the latter part of this section.
The head
The rate, regularity, and quality of the pulse are most
easily appreciated at the facial artery as it crosses the
horizontal ramus of the mandible. The rate and
regularity are dictated by the heart (see below), but the
quality will also be influenced by peripheral events. An
increasing pulse rate of deteriorating qualit suggests
circulatory compromise and impending shock.
The color of the mucous membranes and the capil
lary refll time (CRT) reflect the horse's circulatory
3
1 PHYSICAL EXAMINATION
status. The normal appearance is moist and pink and
the normal CRT is less than 2 seconds. The CRT indi
cates whether perfusion, hydration, and vascular tone
are impaired. Increasing refll times indicate progres
sively inadequate perfusion and are usually accompa
nied by dryness and discoloration of the membranes.
The mouth should be examined to detect abnormal
ities of tooth wear, sharp edges on the cheek teeth, or
other dental or mucosal diseases which may interfere
with feeding.
The thorax and abdomen
Abnormal swellings, particularly of the ventral
thorax and abdomen, may reflect edema associated
with venous and/or lymphatic congestion, or hypo
proteinemia. Abdominal distention in cases of colic is
frequently a result of tympany.
The heart is auscultated to assess rate and regularity.
Increases in the heart and pulse rate are influenced to
some extent by pain, but most particularly by dehydra
tion, decreased venous return, and toxemia.
Rapid, shallow respiration can be a feature of pain
and/or metabolic acidosis. Severe gastric distention or
hindgut tympany will exert pressure on the diaphragm
resulting in dyspnea. On rare occasions dyspnea
accompanies rupture of the diaphragm, especially if
the hindgut is prolapsed.
Slight increases in rectal temperature can be associ
ated with pain, but signifcant increases suggest infec
tion. In cases of colic, temperatures in excess of 38.6C
(101F) suggest a differential diagnosis of a systemic
disease for which colic is an early incidental sign, for
example salmonellosis or acute peritonitis. A decreasing
temperature, coupled with a rapid weak pulse, indicates
the development of shock and carries a grave prognosis.
Abdominal auscultation
Abdominal auscultation enables appreCIation of gut
activity and its greatest value is in the assessment of
colic. At least four sites should be auscultated: these are
both paralumbar fossae and both sides of the lower
abdomen behind the costal arch.
Two types of sound can be appreciated: weak sounds
associated with localized bowel contractions (mixing
the ingesta), and louder fluid sounds or borborygmi
associated with propulsion of ingesta. Sounds heard in
the right paralumbar fossa reflect ileocecal (and possi
bly cecocolic) valve activit and differ from sounds
heard at the other sites. Here, a period of silence is
broken once or twice a minute by a sudden rush of fluid
rumbling as secretions from one compartment pass
through the valve and hit the gas-fluid interface of the
next.
4
Increased movement (hyperperistalsis) can be pro
voked by a simple obstruction in an otherwise healthy
gut. The best example is spasmodic colic in which con
tinuous sounds, of greater than usual intensity, are
heard at all sites. In contrast, reflex movement is
reduced by inflammation and ischemia. A absence of
sound, or infrequent sounds of reduced intensit, may
therefore be associated with peritonitis or the develop
ment of gut hypoperfusion during colic. An absence of
sound is also associated with alimentary paralysis as in
postoperative ileus and grass sickness.
The presence of entrapped gas (tympany) is
denoted by low-pitched tinkling sounds which may be
superimposed on other alimentary sounds - as, for
example, in tympany associated with spasmodic colic.
The localization of entrapped gas in a segment of the
large bowel may be appreciated by simultaneous
percussion and auscultation over the abdominal wall. A
resonant 'hollow' sound is audible where a volume of
gas is trapped against the body wall.
Nasogastric intubation
F Taylor
Apart from therapeutic applications, a nasogastric tube
may be used to deliver sugar solutions for absorption
tests, to assess fluid reflux, and to permit decompres
sion in cases of gastrointestinal obstruction, or (with
care) to indicate the site of esophageal obstruction.
Nasogastric tubes are manufactured in foal, pony, or
horse sizes. Tubes with an additional hole set in the side
of the leading end are recommended and transparent
tubes are preferable since they allow the passage of
fluid to be seen. Because proprietary tubes are not grad
uated along their length, it is useful to make an indeli
ble mark around the circumference at a point that will
indicate that the leading end is approaching the
entrance to the larynx or esophagus. This distance is
approximately 30 cm for pony tubes and 35 cm for
horse tubes.
RESTRAINT
The horse is positioned diagonally in a corner with its
quarters against the wall to restrict backward and lateral
movements. The handler should stand to the left of the
horse's head with his/her back to the horse to minimize
injury if the horse rears. A secure headcollar is essential
but additional restraints will depend upon the horse's
temperament. A horse that struggles during intubation
is more likely to suffer a nosebleed and it is best to apply
a twitch to such patients. Sedation is possible where
clinical circumstances permit, but this will diminish the
swallow reflex as the tube is passed and could affect the
results of an absorption test if intubation is used for this
purpose.
PROCEDURE
The uncoiled tube is draped around the clinician's
neck to prevent it from trailing on the floor; this also
leaves the clinician's hands free to control the tube's
passage. In cold weather a rigid tube should be softened
by passing warm tap water through it. The frst 10-
12 em of the leading end is then coated liberally with a
water-soluble lubricant and the tube is grasped just
behind this point for controlled insertion.
The right-handed clinician will be most comfortable
standing to the right of the horse's head with his/her
back to the horse. The handler should attempt to keep
Figure 1.1 Insertion of a nasogastric tube. The thumb of
the left hand is used to elevate the alar cartilage of the
right nostril and the tube is inserted along the floor of the
open nostril
PHYSICAL EXAMINATION 1
the head in a flexed position and the clinician rests
his/her left hand on the bridge of the nose above the
muzzle. Care should be taken not to occlude the oppo
site nostril inadvertently. The thumb is then used to ele
vate the alar cartilage of the right nostril, opening wide
the entrance to the nasal cavit.
The lubricated end of the tube is then placed on the
floor of the open nostril, slightly inclined toward the
nasal septum with its curvature directed downward
(Figure l.1), and advanced gently so that it follows the
floor of the ventral meatus. The tube's advance is
stopped once its preset mark arrives at the nostril, indi
cating that the leading end is approaching the larynx or
esophagus. In most cases, onward passage will result in
entry into the larynx and trachea. To avoid this, the
tube should be turned through 90 degrees before being
advanced further. This has the effect of raising the level
of the leading end with respect to the larynx, thereby
bringing it closer to the opening of the esophagus lying
above the larynx.
Gentle pressure by the leading end against the
esophageal opening will then cause the tube to be
admitted by a swallow. If the tube is accidentally passed
into the larynx, it should be withdrawn to the nostril
mark, given an additional 90 degree turn to raise the
leading end higher, and advanced again. Aternatively,
if gentle pressure meets total resistance the tube is with
drawn 2-3 cm and gently readvanced in the hope of
provoking a swallow.
If this maneuver fails on 3-4 occasions, the operator
should suspect that the end is pushing against the
pharyngeal recess above both the larynx and the
esophagus. In this instance the leading end is lowered
by turning the tube back through approximately
90 degrees before being advanced again.
CHECKING THE POSITION OF THE TUBE
The commonest error is to pass the tube into the larynx.
In this instance air can be blown or sucked through the
tube without resistance and shaking the larynx will pro
duce a palpable 'rattle'. If the tube is clean, then unto
ward effects are unlikely - it is simply withdrawn and
repositioned. When entering the esophagus, there is
often an accompanying swallow which may be repeated
on the downward passage of the tube. Successful intu
bation is indicated by an increase in the resistance to
passage (esophageal tone) and the appearance of a
swelling in the upper third of the left jugular groove
which moves down the neck following the line of the
esophagus. In addition, there is resistance to air being
sucked through the tube due to esophageal collapse at
the leading end. Alternatively, a short, sharp blow of air
5
down the tube produces a momentary inflation of the
esophagus which is seen in the left jugular groove; this
is a useful test if a distinct swelling has not been seen to
travel down the jugular groove.
Once satisfed that the tube is correctly placed the
clinician can advance it to the stomach. There is usually
an audible release of gas as the tube enters the stomach
and gaseous 'bubbling' sounds can be heard when
listening at the open end of the tube.
TUBE WITHDRAWAL
Any fluid medication which has been given by tube and
which is occupying its dead space should be blown
through to the stomach before removal. Failure to do so
may result in inhalation of spilt fluid as the tube is with
drawn over the larynx. Thereafter, the tube should be
withdrawn slowly and carefully. Particular care should
be taken not to rush out the last 50 cm, otherwise
trauma to the highly vascular nasal mucosa may result
in a nosebleed.
Rectal examination
POE Mueller
INTRODUCTION
The rectal examination is one of the most important
and helpful diagnostic techniques for evaluating adult
horses with abdominal disease. It is frequently essential
in evaluating the need for surgery in horses with acute
abdominal pain (see Chapter 9). Rectal examination
may be used to identif
position of intestinal segments
distention of bowel
abnormalities of bowel wall thickness
mesenteric lymphadenopathy
mesenteric pain
abnormal masses such as tumors, abscesses,
intussusceptions, foreign bodies
excessive abdominal fluid
pneumoperitoneum
bowel rupture
cranial mesenteric arteritis/aneurysm
rectal perforation.
In addition, palpation of other intra-abdominal organs
is possible, including the urinary bladder, uterus and
ovaries, left kidney, and spleen.
6
TECHNIQUE
,,"" ,,, ,''1'' ,,' \""1' %Jlr'iMF'o ' ,
When performing a rectal examination, proper
restraint is of the utmost importance to insure the
safety of the horse and the examiner. Inadequate
restraint may result in iatrogenic rectal perforation, a
potentially fatal complication of rectal examination, or
serious injury to the examiner. Horses with signs of
unrelenting abdominal pain should be sedated with an
alpha2 agonist agent such as xylazine (0.3-0.5 mg/kg
i.v.) , detomidine (7-10 !lg/kg i.v.) or romifdine
(40-120 !lg/kg i.v.). For more profound sedation, and
to reduce the chance of the horse kicking, the alpha2
agonist may be combined with butorphanol (20 !lg/kg
i.v.). A nose twitch should always be used to control the
patient and promote relaxation of the rectum.
Adequate lubrication of the examiner's hand and arm
is necessary to minimize irritation to the rectal mucosa.
Hydrated methylcellulose and mineral oil are the most
commonly used lubricant. Initial introduction of the
examiner's hand through the anal sphincter is often met
with great resistance. This should therefore be per
formed with a slow and steady motion. The fingers and
thumb of the hand should be kept together, in an
extended position throughout the entire examination.
Once the hand is through the anal sphincter the feces
within the rectum are evacuated. The amount and con
sistency of fecal material in the rectum should be noted.
Absence of fecal material, or the presence of dry, fibrin
and mucus-covered feces is abnormal and is consistent
with delayed intestinal transit. Fetid, watery fecal mater
ial is often present in horses with colitis. Large amounts
of sand within the feces may be indicative of a sand
impaction or sand-induced colitis. After evacuation of
feces from the rectum, intrarectal administration of
50-60 ml of 2% lidocaine via a 60 cc catheter tip syringe
(alternatively a soft tube such as an intravenous exten
sion set connected to a regular syringe can be used) may
help promote further rectal relaxation and reduce strain
ing. The syringe may also be used to administer addi
tional lubrication into the rectum at this time.
The examiner's arm is then re-introduced into the
rectum and advanced slowly and steadily as far as com
fortably possible. The arm is left in this position without
excessive movement for 20-30 seconds. In most cases
this initial delay in internal palpation will allow the rec
tum to relax around the examiner's arm, facilitating a
more thorough palpation of the more cranial aspects of
the abdomen. Initial examination of the caudal aspects
of the abdomen with a half-inserted arm is not recom
mended because it usually results in straining and
excessive peristaltic contraction of the rectum. This pre
cludes a safe and thorough examination of the more
cranial abdominal contents.
The most severe complication associated with rectal
palpation is iatrogenic perforation of the rectum (see
Chapter 16). Although rare, tears usually occur dorsally
between the 10 o'clock and 12 o'clock positions. Most
rectal tears can be avoided by proper restraint, ade
quate lubrication, and a steady and careful palpation
technique. If a peristaltic contraction or increased resis
tance is felt during examination, the hand should
immediately be withdrawn from the rectum to avoid
potential rectal injury as the descending colon can tear
as it contracts on the examiner's hand.
The exact sequence of abdominal structures pal
pated during rectal examination may vary from practi
tioner to practitioner. Rega
r
dless of the sequence, the
examination should be performed in a consistent, sys
tematic manner to assure a complete and thorough
examination and minimize the chance of missing a
lesion. The author prefers a clockwise approach, start
ing with the spleen in the left dorsal abdominal quad
rant. This is followed by examination of the right dorsal,
right ventral, and left ventral quadrants. The pelvic
canal and more caudal structures are then examined
just before removal of the hand from the rectum.
In general, palpable characteristics of the abdominal
contents and viscera are often helpful in identifing the
particular segment of the intestine involved in horses
with colic. Severe gas or ingesta-distended intestine,
tight mesentery or tenia (bands), or thickened or turgid
intestine are indicative of intestinal obstruction or
strangulation. Free peritoneal gas or crepitus within the
intestinal wall is usually indicative of intestinal rupture.
A gritty or granular texture of the peritoneal cavity is
indicative of intestinal rupture with contamination of
the serosal and peritoneal surfaces with ingesta. It
should be emphasized that rectal examination fndings
should always be interpreted in conjunction with the
physical examination and laboratory fndings.
RECTAL PALPATION OF THE NORMAL
HORSE
In the normal horse, moist, soft fecal balls should be
present in the rectal ampulla. The descending colon is
easily identifable in the caudal abdomen. It contains
multiple, distinct fecal balls and is freely movable within
the abdomen. Other intra-abdominal structures palpa
ble in the normal horse starting in the left dorsal
abdominal quadrant, and progressing in a clockwise
direction include
caudal border of the spleen
nephrosplenic (renosplenic) ligament
caudal pole of the left kidney
PHYSICAL EXAMINATION 1
mesenteric stalk
ventral cecal tenia (no tension)
cecal base (empty)
pelvic flexure (Figure 1.2).
Normally, the duodenum and remaining small intes
tine are too soft and relaxed to be identifed unless an
underlying abnormality exists.
The spleen is located in the left dorsal abdomen.
The caudal edge of the spleen is palpable against the
body wall. The nephrosplenic ligament can be palpated
coursing from the head of the spleen, to the right, to
the caudal pole of the left kidney. Immediately dorsal to
the ligament is the renosplenic space. Three to four fn
gers may be placed in the renosplenic space. The cau
dal pole of the left kidney is palpable just to the right of
the spleen; it may not be possible to reach the kidney in
some large horses. Moving the arm to the right and cra
nially along the dorsal midline, the aorta, duodenum,
and mesenteric stalk may be palpated. The pulse in the
aorta is easily palpable; the duodenum is identifed as a
small intestinal structure perpendicular and attached to
Figure 1.2 Caudal view of a standing horse demonstrating
abdominal structures that are palpable in the normal
horse during rectal examination. Starting in the left dorsal
abdominal quadrant, and progressing in a clockwise
direction, palpable structures include: caudal border of
the spleen, renosplenic ligament, caudal pole of the left
kidney, ventral cecal tenia, cecal base, and the pelvic
flexure
7
the mesenteric stalk. The mesenteric stalk is usually pal
pable as a sheet of tissue, with a pulse that is only occa
sionally palpable. In large horses it may not be possible
to reach far enough to palpate the root of mesentery.
Continuing to move in a clockwise direction, the
base of the cecum is palpable in the right dorsal abdom
inal quadrant. Depending on the amount of ingesta in
the cecum, it may or may not be palpable. The ventral
and sometimes medial cecal tenia are usually palpable
by moving the hand laterally and caudally, hooking the
tenia with the tips of the examiner's forefngers. These
bands usually course in a dorsocaudal to ventrocranial
direction, just to the right of the midline. Because the
majority of the body and apex of the cecum are beyond
the examiner's reach, the tautness of the ventral and
medial cecal tenia is used as an indicator of the amount
of ingesta within the cecum. Normally the cecal tenia
should be loose and easily movable. With increased
amounts of ingesta in the cecum, the tenia become
more taut. Pain elicited upon palpation of the ventral
or medial cecal tenia may be associated with tension of
the ileum or its mesentery. This has been associated
with pain originating from the ileum and its vascula
ture, such as occurs with entrapment of the ileum in the
epiploic foramen. The duodenum is attached dorsal to
the base of the cecum, but is normally too soft and
relaxed to be palpable. It may, however, sometimes be
palpable as it distends during a peristaltic contraction.
A the hand is moved ventral and caudal to the
pelvic brim, fecal balls in the small colon are usually eas
ily identifed. Small intestine is not usually felt unless it
contracts, when it may be palpable as a tight tubular
structure.
Moving caudally and to the left side, the pelvic flex-
8
ure may or may not be palpable in the caudal left
abdomen, depending on the amount of ingesta within
the large colon. If the pelvic flexure and left dorsal
large colon are palpable, they may be identifed by soft
ingesta, and the absence of the tenia and haustra (sac
culations). The adjacent left ventral colon contains sim
ilar contents and has two free tenia and haustra. The
tenia should course in a cranial-to-caudal direction,
from the left caudal abdomen to the left cranial
abdomen (Figure 1.2). The left dorsal colon does not
have haustra and contains only one mesenteric tenia.
Additional structures in the caudal abdomen
included in a complete rectal examination include:
bladder, uterus and ovaries in the mare, the aortic
bifurcation, and the internal inguinal rings in the
stallion. The inguinal rings are identifed just cranial,
lateral, and slightly ventral to the iliopectineal emi
nence of the anterior brim of the pelvis. In stallions, the
inguinal rings are large enough for insertion of a fnger.
If the testis or epididymis has descended, the ductus
deferens is palpable in the caudomedial aspect of the
ring. In geldings, the inguinal ring is palpable as only a
slight depression and decreases in size with age.
BIBLIOGRAPHY
Rectal examination
KopfN (1997) Rectal examination of the colic patient. In
Curent Therap in Equine Medicine 4th edn, N E Robinson
(ed.). W B Saunders, Philadelphia, pp. 170-4.
White N A (1998) Rectal examination for the acute abdomen.
In Current Techniques in Equine Surger and Lameness 2nd
edn, N A White and] N Moore (eds). W B Saunders,
Philadelphia, pp. 262-70.
2
Additional diagnostic procedures
Rectal biopsy
|1yl O|
Diffuse lesions within the mucosa and submucosa of the
hindgut are often associated with chronic diarrhea and
can be characterized with surprising frequency in the
histopathology of a rectal mucosal biopsy. Rectal biopsy
is easily undertaken in the standing horse and therefore
offers a clear advantage over more proximal intestinal
biopsies which must be obtained either under general
anesthesia or via a standing flank laparotomy.
A variety of human rectal and cervical biopsy instru
ments are suitable for this purpose. The most suitable
have a folding upper jaw that cuts the specimen against
a rigid lower jaw (Figure 2.i).
|gure2. 1 Rectal bi opsy i nstrument with a fol di ng upper
jaw and ri gid lower jaw
PROCEDURE
The horse is restrained as for rectal palpation. The pro
cedure is usually without discomfort to the patient,
apart from the clinician's hand passing into the rectum,
and the necessary restraints are minimal.
A lightly lubricated gloved hand is introduced
through the anal sphincter to wrist depth and the
closed end of the sterilized instrument is passed into
the cupped palm using the other hand (Figure 2.2).A
mucosal fold in the roof of the rectum is palpated and
held between fnger and thumb and the instrument
advanced with the jaws open to 'snag' the fold in an
adjacent dorsolateral position. Taking biopsies from a
dorsolateral position (at 1 o'clock or 1 1 o'clock) avoids
damage to the dorsal vasculature.
|gure 2. 2 Rectal bi opsy i n the horse. A fol d of rectal
mucosa i s hel d between a fi nger and the thumb of one
hand and the i nstrument advanced to obtain a bi opsy
Z ADDITIONAL DIAGNOSTIC PROCEDURES

The jaws are closed and the sample is removed and
transferred fixative. If required, a second biopsy for
homogenization and culture may be attempted in the
opposite dorsolateral position. This specimen should
be transferred to sterile saline.
It should be noted that while rectal biopsies can
reflect pathology in the more cranial large bowel, nor
mal (negative) specimens do not rule out the presence
of colonic lesions.
Liver biopsy
| Tyl O|
Most of the equine hepatopathies are associated with
diffuse lesions so that biopsy usually provides a repre
sentative sample for histopathology. Contraindications
for biopsy are
clinical evidence of concurrent coagulopathy
suspicion of liver abscessation.
Several medical biopsy instruments are suitable for
the purpose. The 14-gauge disposable Tru-cut needle
(Baxter Healthcare Corporation, C) retrieves good
specimens with practice. A 1 53-mm (6-in) length is suit
able for most horses. A spring-loaded automatic biopsy
needle is also available.
BIOPSY SITE
The optimal site for biopsy on the right side can be
ascertained by ultrasonography. If the liver cannot be
visualized by ultrasound on the right, it can almost
always be seen in the left ventral rostral abdomen just
caudal to the diaphragm in front of the spleen. In the
absence of ultrasound the approach is the same for all
instruments. A site is selected in the 1 3th intercostal
space on the right hand side, just in front of the 14th
rib, midway between a 'wedge', the upper and lower
limits of which are delineated respectively by imaginary
lines drawn from the point of the hip to the point of the
shoulder, and from the point of the hip to the point of
the elbow. The 1 4th rib is located by counting back
from the 1 8th rib, ignoring 'floating ribs' ( Figure 2. 3) .
PROCEDURE
Depending upon temperament, the horse may need to
be sedated. An area 100 cm square is clipped and surgi
cally prepared at the chosen site. Using sterile precau-
1
||gure 2.3 The site for liver bi opsy in the horse. A site is
sel ected in the 1 3th intercostal space on the right si de
between an i magi nary l i ne from the point of hi p to the
point of shoul der, and another line from the poi nt of hip
to the point of el bow
tions the skin and intercostal muscle beneath are infl
trated down to the parietal pleura with 4-5 ml of 2%
lignocaine using a 39 ? 0. 8 mm needle.
A 5 mm skin incision is then created just in front of
the 1 4th rib, taking care to avoid the intercostal vessels
and nerves that run along the caudal border of the
acacent rib. The biopsy needle is introduced through
the incision, into intercostal muscle and then directed
some 1 0 degrees backwards to pass through the
diaphragm. If insertion is made at the point of fuJI expi
ration, the risk of damage to the lung is minimized.
When released from the operator's grip, the needle
should be seen to move with the respiratory excursions
of the diaphragm.
The needle is then advanced 5 cm or so into the
liver, which has a 'solid' feel, at this point the instru
ment is operated. On withdrawal the core of tissue
should be dark in color and sink in fxative. If the frst
attempt yields nothing (or a pale tissue that does not
readily sink) , two further attempts may be made
through the same incision, redirecting the needle
slightly and maintaining sterile precautions. If there is
prior clinical evidence of liver infection, a sample
should also be submitted for culture in a sterile con
tainer.
If the procedure is unsuccessful, it is possible to
repeat it at a different site, preferably after a lapse of 24
hours. Using a 'blind' procedure it is advisable to try
one intercostal space further back, but in older horses
atrophy may cause the liver to be drawn further
forward.
A single interrupted suture may be placed in the
wound. The horse is rested for at least 1 hour to permit
clotting within the biopsy tract.
Complications are rare. Tissues other than liver (e. g.
diaphragm, lung, colon) may be inadvertently sampled
without untoward effect. However, if the core of tissue
obtained does not have the 'feel', color, or texture of
liver it is advisable to give a short course of antibiotics in
case of bowel penetration. Serious hemorrhage is a rare
complication of liver biopsy in the horse, even in
advanced disease.
Cl inical pathology
| 1yl O|
Clinical pathology is complementary to a thorough clin
ical examination rather than a substitute. It should be
used to confirm a diagnosis or to assist in the systematic
deduction of a diagnosis. Routine clinical pathology
includes hematology, serum or plasma biochemistry,
fluid, electrolyte, and acid-base balance, and fecal
analysis.
HEMATOLOGY
Useful parameters of hematology in the evaluation of
gastroenteric disease are the packed cell volume (PCV) ,
indicators of anemia, and the white cell count (WBC) .
In sub-acute (>36 hours in duration) or chronic condi
tions, the plasma fibrinogen concentration should also
be requested; in some laboratories this assay is under
taken by the hematologist.
Erythrocyte parameters
The PCV is a useful monitor of dehydration and hypo
volemia if used on a sequential basis. In general terms,
a PCVgreater than 45 per cent indicates a reduction in
extracellular fluid volume and a loss of sodium. Patients
with a PCV greater than 60 per cent usually have a poor
prognosis, but this is not invariably so.
Anemia is indicated by a significant reduction in
PCV, red cell count (RBC) and hemoglobin concentra
tion (Hb) . However, acute hemorrhage is only reflected
in the hematology profile afer 1 2-24 hours, by which
time there is a compensatory influx of tissue fluid. This
reduces the PCV, RBC, and Hb, and dilutes plasma
protein concentrations. Chronic anemia in the horse is
often non-regenerative and is usually associated with
chronic inflammatory processes. However, a chronic
regenerative anemia could reflect chronic hemorrhage
into the gut or abdomen.
ADDITIONAL DIAGNOSTIC PROCEDURES Z
Leukocyte parameters
Leukopenia (WC 6.0 ? 1 0"/1 ) , predominantly due to
neutropenia, is a feature of peracute/acute diseases of
the gastrointestinal tract, for example gut ischemia (as
in surgical colics) , peritonitis, or salmonellosis. In these
situations the count may fall to 2-3 ? 1 0"/1, and
neutropenia is especially pronounced in the presence
of endotoxin.
Leukocytosis may accompany acute, progressive, or
more chronic inflammation of the gastrointestinal
tract. This 'reactive leukocytosis' usually features neu
trophilia and may be accompanied by immature band
forms (,left shift') in acute conditions and a monocyto
sis in chronic conditions.
Eosinophilia is popularly associated with parasitism,
but high burdens of mature worms do not seem to
affect the circulating eosinophil count. In many
instances eosinophilia probably reflects some form of
hypersensitivity response.
Plasma fibrinogen concentration
The fibrinogen concentration is raised by inflammation,
most particularly septic infammation, and its level indi
cates the severity of disease. Concentrations increase
within 1-2 days of an infection, but peaks are not
attained until 3-4 days. A modest increase may therefore
reflect early disease, or alternatively, a chronic low grade
inflammation. High concentrations indicate advanced
and serious disease with a guarded prognosis.
PLASMA OR SERUM BIOCHEMISTRY
Total plasma protein (TPP)
Sequential TPP estimations can be used to monitor dehy
dration in cases of colic or diarrhea. However, in the
severely compromised gut there may be a concurrent
and progressive loss of protein into the peritoneal cavity
or bowel lumen, thus rendering the technique inferior
to sequential determinations of PCV in whole blood.
Albumin
In horses, hypoalbuminemia is almost invariably associ
ated with a protein-losing enteropathy as a result of
some lesion within the intestinal mucosa. Much rarer
causes are glomerulonephropathy, liver failure, or
massive exudative effusion.
Globulins
Apart from dehydration, total globulin concentrations
may also be increased by
1 1
Z ADDITIONAL DI AGNOSTIC PROCEDURES
acute and chronic inflammatory processes -
increases in acute phase protein and
immunoglobulin concentrations respectively
strongyle parasitism - increases in IgG(T)
liver failure - decreased catabolism of globulins.
Albumin:globulin (A:G) ratios
In health, the A:G ratio approximates to 1 . 0. Shifts in
the ratio may occur in a number of pathological states.
However, the information is seldom useful since it lacks
specificity. It follows from the preceding paragraphs
that a fall in this ratio, because of a decrease in albumin
and/or an increase in globulin, may be a feature of
either inflammatory intestinal disease, strongyle para
sitism, liver failure, or any inflammatory process.
Serum alkaline phosphatase (SAP or ALP)
The brush border of the intestinal epithelium is richly
endowed with ALP and cellular damage increases its cir
culating concentration. However, ALP is not organ spe
cific and damage to bone or the biliary tract of the liver
will also increase the circulating ALP concentration.
Many laboratories will assay the isoenzyme intestinal
alkaline phosphatase (lP) which may help to identit
the origin of a raised ALP.
FLUID, ELECTROLYTE, AND ACID-BASE
BALANCE
Fluid, electrolyte, and acid-base disturbances are asso
ciated with severe diarrhea and those acute colics in
which fluid is sequestered in the gut lumen and/or
there is associated strangulation. In diarrhea, the extent
of fluid and electrolyte losses and the development of
acidosis depends upon the severity of the enteric lesion
and whether or not the patient continues to drink
during the illness.
Fluid balance
Simple blood parameters such as PCV and TPP can be
used to indicate the severity of dehydration (see
above) . However, where facilities exist they are best
used in a serial manner to follow the course of dehy
dration over a critical period. Most serum or plasma
biochemistry parameters, including urea, are also
raised by acute dehydration. However, increases in
both urea and creatinine beyond their normal ranges
indicate prerenal failure associated with deteriorating
perfusion.
1Z
Electrolyte balance
The interpretation of serum or plasma electrolytes in
gastroenteric disease should be undertaken with
caution. Increases in sodium, potassium, and chloride
concentrations are consistent with water deprivation
and dehydration, but there is usually a concurrent
loss of electrolytes to the gastrointestinal tract. High
obstructive colic is associated with a loss of water,
sodium, and chloride from the plasma, but in cases of
lower bowel pathology relatively more potassium and
bicarbonate ions are lost. A meaningful interpretation
of electrolyte shifts can only be undertaken with a
knowledge of the concurrent acid-base status.
Acid-base balance
Metabolic acidosis is the most common acid-base disor
der in horses and occurs most frequently in association
with obstructive gastrointestinal disease and diarrhea.
The underlying causes of acidosis in these situations are
either increased base loss and/or reduced peripheral
perfusion (most commonly) causing a switch to
predominantly anaerobic metabolism in tissues with a
consequent build up of lactate.
Although blood gas and pH measurements provide
the only accurate guide to acid-base status, plasma
bicarbonate estimations are acceptable for most clini
cal situations. However, this requires venous blood
samples to be collected anaerobically for immediate
processing using equipment that may not be readily
available. In practical terms however, the need to
correct a metabolic acidosis by specifc bicarbonate
therapy is rare if fluid and electrolyte requirements
are met.
FECAL ANALYSIS
Fecal worm egg count (FWEC) (see Chapter 4)
Strongyle eggs are readily identifed i n the laboratory
using a flotation technique, but it is difcult to distin
guish between large and small species. However, small
strongyle (cyathostome) eggs usually comprise the vast
m<ority of the count (>90%) .
Presence of fecal larvae ( see Chapter 4)
Unlike worm eggs, larvae are separated from a fecal
sample by sedimentation using the Baermann appara
tus. Alternatively, a wet fecal smear may be examined
under the microscope. Fresh samples should be
analyzed rapidly and not refrigerated.
Bacterial culture of feces
Fecal samples inevitably contain a great many organ
isms with differing requirements for culture in vitro.
When submitting samples it is therefore necessary to
defne the organism(s) of interest to enable selective
culture in the laboratory. In suspected salmonellosis the
num bers of Salmonella organisms shed may be very low,
even during the acute stage of disease. In consequence,
a minimum of three and preferably fve fecal samples
should be collected from the rectum at 24-hour inter
vals to increase the possibilit of detection. adequate
sample should occupy half a universal tube, approxi
mately 10 ml; swabs are usually unsatisfactory.
Clostridiosis (usually Clostrdia perfringens or diJcile) is
another differential diagnosis in cases of
peracute/ acute toxemic colitis. A half universal tube of
feces taken from the rectum is submitted for anaerobic
culture as soon after collection as possible, again swabs
are unsatisfactory. Specifc toxin analysis may also be
performed for f perfrngens and difficile.
Fecal leukocytes
The presence of leukocytes and occasionally epithelial
cells in a fecal sample suggests infammatory injury to
the distal intestinal mucosa; they are a feature of severe
diarrhea (fluid feces) , particularly in the acute stage.
High numbers suggest the presence of an intestinal
pathogen such as Salmonella spp.
Fecal blood
If blood is clearly visible in the feces a red discoloration
suggests a recent, distal source such as the small colon
or rectum, while a dark to black discoloration (melena)
suggests a source in the proximal gastrointestinal tract
or large colon. Chronic gastrointestinal loss is usually
occult and may be associated with a state of chronic
regenerative anemia. In the laboratory, fecal occult
blood may be detected qualitatively by demonstrating
the presence of hemoglobin. Fecal occult blood tests in
the horse are not as sensitive or specifc as they are in
most other species.
Fecal sand
Sand ingestion from topsoil or water courses may be
associated with colonic impaction and severe diarrhea.
If this is suspected then feces should be tested for the
presence of sand. One volume of feces is mixed vigor
ously with two volumes of water in a clear container and
allowed to settle. Sand sediments to the base of the mix
ture; the feces of a healthy individual from an adjacent
location should be tested for comparison.
ADDI TI ONAL DIAGNOSTIC PROCEDURES Z
Abdominocentesis
(abdominal paracentesis)
T M|
INTRODUCTION
Abdominocentesis can be one of the most useful diag
nostic techniques in horses affected by abdominal
disease. Analysis of the peritoneal fluid reflects the
changes that occur in the tissues and organs within the
abdomen and on the peritoneal surface. The technique
can be useful in the determination of the need to per
form surgery in acute abdominal pain, as well as in the
diagnosis of peritonitis, hemoperitoneum, and some
forms of abdominal neoplasia (see Chapter 1 7) .
ABDOMINOCENTESIS IN THE ADULT
HORSE
A rectal examination should always be performed
before abdominocentesis in order to recognize an
extremely gas-distended or ingesta-flled cecum or large
intestine. If these abnormalities are identifed, extreme
care must be taken when performing abdominocentesis
to avoid accidental enterocentesis.
Abdominocentesis can be performed using either a
needle or a blunt-ending cannula such as a teat cannula
or metal bitch urinary catheter. A blunt-ended cannula
is recommended in horses with intestinal distention or
when a heavy viscus is known to be lying on the ventral
abdominal floor. In other horses, the simplest method
is to use an 1 8- or 1 9-9auge, 3. 8 cm (l. 5 inch) hypoder
mic needle. Longer needles may be necessary in obese
horses because of the thickness of the layer of retroperi
toneal fat. The most dependent site of the ventral
abdomen is prepared and the needle is inserted directly
through the linea alba (Figure 2. 4) . Alternatively the
needle can be placed just to the right of the midline to
reduce the risk of splenic puncture. A 3.8 cm needle
may be too short in large and fat horses, since it may not
be long enough to penetrate through the layer of sub
peritoneal fat (Figure 2. 5) . Entry of the needle into the
peritoneal cavity is indicated by the flow of varying
amounts of fluid which is collected into a sterile tube
containing edetic acid (EDTA) for cytological analysis,
and a second plain sterile tube (not containing addi
tives) for culture and sensitivity if required. Normal
peritoneal fluid is pale yellow and clear. If the needle
penetrates bowel (usually cecum or colon) (Figure 2.6)
intestinal contents may drip from the needle; this fluid
1
I
`
0
||gure 2.4 Abdomi nocentesis showi ng the position of
needle placement at the most dependent part of the
abdomen. The needle is i nserted through the l i nea alba
and sub-peritoneal fat to enter the peritoneal cavity
||gure2.5 Abdomi nocentesis showi ng fai l ure to penetrate
the sub-peritoneal fat l ayer because the needl e is too
short
1
||gure2.6 Abdomi nocentesis showi ng accidental puncture
of the intesti ne
will appear dark brown or yellow and turbid and will
have a characteristic malodor. If this happens the
needle should be either completely withdrawn, or with
drawn until it exits the bowel and its tip lies in the
peritoneal cavity. As peritoneal fluid drains through
the needle, it will clear it of contaminated material, and
the sample will be suitable for cytology. An accidental
enterocentesis such as this is very unlikely to cause any
problems in adult horses. Although a mild inflamma
tory peritoneal reaction will result antibiotic therapy is
unlikely to be necessary.
Peritoneal fluid usually flows from the needle spon
taneously, although repeated relocation and reposition
ing of the needle tip may be required until it enters a
pocket of peritoneal fluid. Aspiration rarely helps, and
may simply suck omentum, peritoneum, or bowel wall
into the needle. If fluid is not obtained, insertion of a
second or third needle a few inches away will often be
successful. Air may be blown into one of these needles
using a sterile syringe to break the vacuum in the
abdomen and permit drainage of peritoneal fluid
through the most ventrally placed needle.
Accidental puncture of the spleen will result in
drainage of dark red blood. If this happens, the needle
should be withdrawn and a new needle inserted at
a different site. If hemoperitoneum is suspected,
comparison of the PC of the sample obtained by
abdominocentesis with the PC of peripheral blood
may help determine whether the blood was obtained
from a splenic puncture or a true hemoperitoneum.
Blood obtained from the spleen will have an elevated
PC compared to the PCV of peripheral blood; com
monly the PCVof splenic blood will be 65 per cent or
greater than the peripheral blood PCV. The PC of
true peritoneal fluid obtained from horses with hemo
peritoneum is likely to be lower than the peripheral
blood PCV. Blood contamination of the peritoneal
fluid sample may also arise from accidental puncturing
of a vessel in the body wall or the bowel . In such cases,
blood will often be seen to swirl in the peritoneal fluid
as it drains from the needle. This blood contamination
frequently stops spontaneously, but if it doesn't the
needle should be repositioned, or withdrawn and a
fresh needle inserted at a separate site.
In horses where no peritoneal fluid can be obtained
despite several attempts, insertion of a blunt cannula
may prove more successful. In this technique, a small
^
||gure 2.7 Abdomi nocentesis showi ng use of a teat can
nul a. A stab i nci si on i s first made using a no. 1 5 scalpel
bl ade. The teat cannul a is then forced through the li nea
alba and advanced i nto the peri toneal cavity
ADDITI ONAL DIAGNOSTIC PROCEDURES Z
||gure 2.8 Ultrasonogram of the ventral abdomen of a
normal horse showing a pocket of anechoic peritoneal
fl ui d. This scan was obtained usi ng a 1.5 MHz li near array
probe
stab incision is made through the skin and up to the
linea alba. The teat cannula is then forced through
the incision into the peritoneal cavity (Figure 2. 7) . This
procedure should be performed using aseptic tech
nique and sterile gloves should be worn because there is
a greater risk of contamination from handling the can
nula. Blood from the skin incision can drip down the
cannula and contaminate the sample. This can be pre
vented by placing sterile gauze around the teat cannula.
A teat cannula should also be used in horses with intesti
nal distention since it incurs a lower risk of puncturing
and damaging the bowel wall than a needle. However,
bowel distended by sand is easily penetrated using
either a needle or a cannula, and extreme care must be
taken when performing abdominocentesis in horses
with suspected sand impaction. Sand may be seen in the
peritoneal fluid sample in cases where inadvertent
enterocentesis has occurred.
If repeated attempts at paracentesis are unsuccess
ful, diagnostic ultrasonography using a 7. 5 MHz
transducer may be employed to identit pockets of peri
toneal fluid in the ventral abdomen (Figure 2. 8) . This
can be used to guide placement of a needle or cannula
to an appropriate area. It can be diffcult to obtain peri
toneal fluid samples from mares in late pregnancy
because of the position of the gravid uterus, and ultra
sonography should also be used in such cases to locate
peritoneal fluid.
ABDOMINOCENTESIS IN THE FOAL
Abdominocentesis is often not performed in the foal
because of fears of puncture or laceration of the bowel
1 b
wall. Abdominocentesis however, can yield significant
information in determining the cause of colic or
abdominal distention in foals (see Chapter 22) . If possi
ble, abdominocentesis in the foal should not be per
formed before a complete transabdominal ultrasound
examination is carried out. This examination can deter
mine the quantity and location of peritoneal fluid in
the abdomen. Foals with excessive abdominal fluid are
good candidates for abdominocentesis as they can be
heavily sedated, placed in lateral recumbency and
restrained well for the procedure. To prevent inadver
tent laceration of the bowel in a foal, a teat cannula can
be used rather than hypodermic needles. A small local
block can be performed with 2% mepivacaine on the
ventral abdomen to the right of midline, or where fluid
is located (being sure to avoid the spleen and the umbil
ical remnants) . A small stab incision is made with a no.
15 blade to penetrate skin and the abdominal muscula
ture. The sterile teat cannula is then gently introduced
into the abdomen and fluid is collected for evaluation.
Omental heriation may occasionally follow teat can
nula abdominocentesis in foals. This is generally not a
serious problem as the omentum can be cut off flush
with the skin and an abdominal wrap applied. If the
abdominocentesis is performed caudal to the umbilical
area, this problem is less likely to occur. In older foals
abdominocentesis can be performed safely in the same
way as in adult horses using an I S-gauge needle or teat
cannula, provided the foal is adequately sedated and
restrained.
Analysis of peritoneal fluid
1 M|
INTRODUCTION
Analysis of peritoneal fluid obtained by abdominocen
tesis can be an important component of the evaluation
of horses with abdominal diseases. It may aid in the
decision to undertake exploratory surgery in the
horse with acute colic (see Chapter 9) , and it may be
diagnostic in horses affected by peritonitis, abdominal
abscesses, and hemoperitoneum (see Chapter 1 7) , or
by some forms of abdominal neoplasia (see Chapter
1 7) . It is also helpful in the evaluation of adult horses
and foals with uroperitoneum (see Chapters 1 7 and
22) .
Samples of peritoneal fluid should be assessed by
gross visual examination, total protein determination,
and cytological examination.
1
CHARACTERISTICS OF NORMAL
PERITONEAL FLUID
The characteristics of normal peritoneal fluid from
adult horses are summarized in Table 2. 1 .
Normal peritoneal fluid i s odorless, non-turbid, and
clear to pale yellow in color. The total nucleated cell
count is normally less than 3-5 ? 1 0911 ( 3000-5000
cells/I) , with a total protein concentration of less than
25 gil (2.5 gl dl) .
Peritoneal fluid from foals has a lower total nucle
ated cell count (less than 1 .5 ? 1 09/1 or 1500 cells/l)
but similar total protein values to adult horses. Foal
peritoneal fluid urea nitrogen levels (mean 1 . 96
mmol/I) are similar to plasma urea nitrogen (mean
2.0S mmol/I); peritoneal urea levels are elevated in
Gross appearance
Specific gravity
Total protein
Total nucleated
cell count
Differential cell
count
Clear or slightly turbid
Straw colored or colorles
1.016
S Zbgi (usually 15 gil)
(mainly albumin)
S 5.0 ? 109/ 10000 cllsIl)
(usually S 2.0 7 10911)
2090% neutrophils
5-0% mononuclearl
mesothelial cells
035% lymphoctes
bW eosinophils
0-1% basophils
Total red cell count Negligible
Fibrinogen
Glucose
Creatinine
Urea nitrogen
lactate
Total bilirubin
Amylase
lipase
GGT
Negligible ( 0.1 gil) (does not
clot on standing)
5.0.4 mmOh (wJ15mgl)
161-237 jmoVI (J.82.7mg0
5.b.Z mol (!1-23ml)
0.41.Z mmol" (3.8-10.9 mgldl)
5J5jmolll (0.3-.8 mgl)
T4lUll
J1U
U
foals with uroperitoneum. The ratio of peritoneal to
plasma creatinine is the preferred method of confirm
ing uroperitoneum in foals (see Chapter 22) . The iden
tification of calcium carbonate crystals in peritoneal
fluid can also be helpful in the diagnosis of uroperi
toneum in adult horses.
Peritoneal fluid collected into tubes containing
dipotassium EDTA is suitable for performing both cell
counts and cytological examinations. Alternatively,
fluid may be collected into a plain tube and mixed with
an equal volume of 50% ethanol for cytological exami
nation. Smears can be made directly from the fluid or
by cytocentrifugation. Wright, Leishman, Giemsa, or
trichrome stains are suitable for cytological examina
tion. A gram stain should be performed in cases of sus
pected peritonitis. There is some variation in the total
nucleated cell count of peritoneal fluid in normal
horses, although counts greater than 5 ? 1 09/1 are gen
erally considered abnormal. Most horses have total
nucleated cell counts less than 2 ? 1 09/1. These cells
consist of mainly neutrophils and large mononuclear
cells (macrophages and mesothelial cells) in an approx
imate ratio of 2:1 (neutrophils:mononuclear cells)
(Plate 2. 1 ) . Small numbers of lymphocytes and
eosinophils are sometimes present. There are no red
blood cells in normal peritoneal fluid, although it is not
unusual to see small numbers of red cells as a conse
quence of iatrogenic bleeding from the sampling pro
cedure. Phagocytized material (cellular debris and
neutrophils) is commonly observed in macrophages as
a normal fnding. Bi- and tri-nucleate mononuclear
cells, and mitotic figures can sometimes be seen in
normal horses.
INTERPRETATION OF CONTAMINATED
PERITONEAL FLUID SAMPLES
The sample of peritoneal fluid obtained by abdomino
centesis may become contaminated by blood or intesti
nal contents. While in some cases it may be evident
during abdominocentesis that iatrogenic blood conta
mination of the sample has occurred (red streaking of
the yellow fluid) , in other cases it may be difficult to dis
tinguish this from internal hemorrhage. Blood contam
ination due to iatrogenic vessel or splenic damage is
likely to contain platelets that may be identifed on
microscopy, and splenic blood will contain large
numbers of small lymphocytes, whereas a true
serosanguinous peritoneal fluid due to red blood cell
diapedesis will probably contain very few platelets.
Heavily blood-contaminated samples due to inadver
tent splenic tap are likely to clot on standing, whereas
true hemoperitoneum samples should not.
ADDITI ONAL DI AGNOSTIC PROCEDURES Z
It should be remembered that some blood contami
nation of the peritoneal fluid sample does not necessar
ily negate the value of the tap. Blood contamination of
up to 1 7 per cent of the volume of the peritoneal tap
does not significantly alter the interpretation of the
nucleated cell count and protein concentration,
although the red cell countwill be increased significantly.
EFFECTS OF ENTEROCENTESIS
Inadvertent enterocentesis rarely causes signifcant
complications to adult horses, but it may result in peri
tonitis and abdominal wall cellulitis in foals or adult
horses with distended bowel.
Experimental enterocentesis in normal horses has
been shown to cause an increase in nucleated cells in
the peritoneal fluid within 4 hours. The peritoneal fluid
total nucleated cell counts peak at 2 days (mean 1 1 . 3 ?
1 09/1 or 1 1 333 cellS/il) and then decline rapidly to day
4. Toxic changes can be identifed in the neutrophils,
but bacteria are not generally evident. The specifc
gravit of peritoneal fluid is also increased following
enterocentesis, but red blood cell counts in the fluid do
not change.
EFFECTS OF PRIOR ABDOMINAL
SURGERY
Exploratory abdominal surgery without any bowel
resection or anastomosis causes an increase in total
nucleated cell counts, percentage of neutrophils, total
protein, and fibrinogen in peritoneal fluid. These
changes are evident within 1 day and remain elevated
for at least 6 days. The total nucleated cell count in the
fluid can exceed 13.7 ? 1 09/1 ( 1 3 700 cell/Ill) on the
first day after surgery, and can increase to levels as high
as 400 ? 1 09/1 (400 000 cells/ Ill) over the next few days.
Healthy horses that have had small colon resection have
been shown to have similar changes in nucleated cell
counts in peritoneal fluid, but they also show increases
in red blood cell counts.
Laparoscopy also alters the characteristics of the
peritoneal fluid. Insuflation of the abdominal cavity
increases the total nucleated cell count and total pro
tein concentration in the fluid. These changes have
been attributed to the formation of carbonic acid by the
insuflating gas ( carbon dioxide) .
Open castration has also been shown to induce a
non-septic peritoneal inflammatory reaction, with total
nucleated cell counts rising to approximately 30 ? 1 09/1
5 days after the surgery. The cell counts are expected to
return toward normal within 7 days of castration.
1J
Z ADDITI ONAL DIAGNOSTIC PROCEDURES
Peritoneal fluid can change after parturition, depend
ing on the nature of the delivery. Normal unassisted
parturition has no effects on peritoneal fluid color, clar
ity, specific gravity, fibrinogen concentration, or total
protein concentration. The total nucleated cell count
was shown to increase in one study, but it stayed within
the normal range. All peritoneal fluid parameters
remain normal over the week following parturition.
Uncomplicated dystocias cause an increase in
nucleated cell count and percentage of neutrophils, but
values usually remain within the normal range.
Complicated dystocias can result in elevated total pro
tein concentration and percentage neutrophils, but the
total nucleated cell count remains within the normal
range. If the total protein concentration, total nucle
ated cell count, and percentage of neutrophils are ele
vated following parturition, further medical or surgical
therapy may be indicated.
EFFECTS OF DISEASE
the peritoneal fluid changes with specific diseases,
the fluid can become more turbid because of increases
in protein, red blood cells, and/or white blood cells.
Increased turbidity may be caused by the presence of
low numbers of red blood cells (which may not cause
red discoloration of the fluid) . Changes in the color of
the peritoneal fluid ranging from golden to orange to
red indicate leakage of red cells (usually from capillar
ies in ischemic bowel wall) . With very early (within 1-2
hours) strangulating obstructions and most simple
obstructions of the small or large intestine, peritoneal
fluid is usually normal. With persistent simple obstruc
tions, the nucleated cell count and differential cell
count remain normal, but the total protein concentra
tion may rise. After a few hours of strangulating intesti
nal lesions, red cells appear in the fluid which becomes
serosanguinous. However, prior to the appearance of
gross sanguinous coloration of the fluid, the presence
of red cells may need to be confirmed by centrifugation
of a sample of the fluid and/ or cytological examination.
With longer-standing strangulating obstructions or
severe intestinal inflammation, the peritoneal fluid may
become grossly serosanguinous, with increases in
nucleated cell count and total protein concentration.
Neutrophils in the peritoneal fluid increase in number
as ischemic bowel undergoes degeneration and
mucosal sloughing. Stimulation of the neutrophils by
the bacteria and toxins leaking into the abdomen
causes toxic changes to the cells (vacuolation, karyoly
sis, and karyorrhexis) . The degree of this change as well
1d
as the numbers of neutrophils entering the fluid is a
reflection of the degree of intestinal degeneration and
the amount of intestine involved. In most strangulating
intestinal lesions, cytological examination of peritoneal
fluid reveals increased total nucleated cell counts (5-
30 ? 1 09/1) with 90 per cent to 95 per cent neutrophils.
Dark brown turbid fluid with the smell of ingesta.
increased nucleated cell count, and increased protein
concentration is suggestive of bowel necrosis and leak
age. In such cases, the total nucleated cell count may
exceed 1 00 ? 109/1. The identifcation of plant material,
intra- or extra-cellular bacteria, and protozoa is indica
tive of bowel rupture (Plate 2.2) .
Horses affected by non-strangulating intestinal
infarction usually show changes in the peritoneal fluid
that are similar to those seen in strangulating intestinal
infarction. This includes an increase in protein, red
blood cells, and white blood cells. Nucleated cell
counts may exceed 1 00 ? 1 09/1 and may be as high as
400 ? 1 09/1.
Although the identifcation of changes in peritoneal
fluid can be extremely helpful in evaluating horses with
intestinal ischemia, it must be remembered that
changes may not always be identified even in the pres
ence of severe bowel wall compromise. In some cases,
compartmentalization of fluid occurs, and samples of
peritoneal fluid can be normal because the diseased
segment of bowel is separated from the rest of the
abdomen by an anatomical barrier. Thus,
abdominocentesis of horses with small intestinal, ileo
cecal, or cecocolic intussusceptions, small intestinal
incarceration in the epiploic foramen, and strangula
tions in a diaphragmatic hernia can yield normal fluid.
Blood-tinged fluid is indicative of splenic puncture.
intra-abdominal or iatrogenic hemorrhage, or severe
intestinal necrosis. In the case of splenic puncture, the
PCV of the fluid is greater than the peripheral blood
PCV, and contains large numbers of small lymphocytes.
Fluid from horses with hemoperitoneum is expected to
have a lower PCV than peripheral blood, and has
erythrocytophagia (Plate 2. 3) and very few platelets.
Bacteria may be identifed in peritoneal fluid
b
ecause of leakage through ischemic bowel wall or
bowel rupture. They may also be seen in the peritoneal
fluid of horses with abdominal abscesses. Bacteria may
be present free in the fluid or phagocytized within
neutrophils. They are rarely present in large numbers
(other than in cases of bowel rupture) and careful
examination of a gram-stained smear is necessary to
identit them.
Fat may occasionally be observed in peritoneal fluid
samples. This is most likely to have come from the
retroperitoneal fat, but if the horse has been previously
treated with mineral oil, leakage of the oil from a
ruptured bowel into the peritoneal cavity should also be
considered as a possibilit. Ether placed in the sample
will dissolve fat but not mineral oil. Grossly lipemic peri
toneal fluid is occasionally observed in nursing foals.
Most of these foals have mild intestinal discomfort (e.g.
ilells) and recover with supportive medical treatments.
True and persistent chylous effusions have been rarely
identifed in young foals ( 1 2-36 hours of age) associ
ated with congenital segmental aplasia of the lymphatic
system of the small intestine. Affected foals present with
colic and chyloperitoneum, at surgery afected small
intestinal segments appear thickened, discolored, and
distended. If the affected segment of bowel is not too
long, resection and anastomosis can be successful.
Chyloperitoneum has also been described in a small
number of adult horses, usually as a secondary feature
to other intra-abdominal diseases (such as intra-abdom
inal abscess, large colon torsion, tearing of mesenteric
adhesions) .
Grey or black discoloration of peritoneal fluid has
been identifed in a small number of horses afected by
melanomas of the peritoneal cavity. Yellow-green discol
oration of peritoneal fluid may be seen when there has
been leakage of bile into the peritoneal cavity (Plate 2. 4) .

l
'
' ' `

`` I
Gro88apparance Total proteln (g/l} Nucleatedcell Cgtolpg
count (10/l)
Normal Odorless, clear to <2. 5 <5. 0 2: 1 ratio of non-
pale yel low degenerative neutrophils
to macrophages,
no RBCs.
lmple Odorless, clear to Normal to mi l d Normal to mi l d Predominantly non-
o8truOlon turbid, pale yellow i ncrease (2.S-3.0) i ncrease (3.0-8.0) degenerative neutrophils.
VeQearlg Odorless, clear to Normal to mi l d Normal to mi l d Predominantly non-
8trangulatlng turbid, pale yellow i ncrease (2.5-3.0) i ncrease (3.0-B.0) degenerate neutrophi ls,
o8truOlon few RBCs.
tragulatlng Serosangui nous, Moderate to Moderate to marked Degenerate neutrophi l s
o8truOlon turbid marked i ncrease increase |>10.0) intra- or extracel l ul ar
(3. 5-6.0) bacteria, RBCs.
lnte8tlnal Mal odorous, turbid, Moderate to marked Decreased (<2.0) Degenerative neutrophi l s,
rupture dark red to brown i ncrease (3. 5-6.0) i ntra- or extracel l ul ar
bacteria, plant material,
protozoa, RBCs.
Enterocente8l8 Mal odorous, turbid, <2.5 Few or no Plant material, protozoa.
green to brown nucleated cells
Hemoperltoneum Dark red Si mi l ar to peripheral Simi l ar to peripheral PCV less than PCV of
blood blood peripheral blood,
erythrocytophagia, few or
no pl atelets.
plenlc punOute Dark red Si mi l ar to peripheral Si mi l ar to peripheral PCV greater than PCV of
blood blood peripheral blood. High
numbers of small
lymphocytes.
Perltonltl8 Thick turbid, dark >2. 5 >10. 0 High numbers of
yel l ow to orange degenerate and non-
degenerate neutrophi ls,
intra- and extra-cel l ul ar
bacteria.
1
The absence of gross or cytological abnormalities in
the peritoneal fluid does not rule out compromised
intestine. Some strangulating lesions, such as intussus
ceptions, external hernias, and epiploic foramen
incarcerations may not demonstrate abnormalities in
the peritoneal fluid because of sequestration of the
fluid in the omentum, intussuscipiens, or hernial sac.
Ultrasound examination of the entire abdomen is of
great importance in these cases.
Late in the course of strangulation obstructions,
when distended loops of intestine can be palpated
per rectum, and when gastric reflux may be present,
abdominal paracentesis is unlikely to provide any useful
diagnostic information, and there is a higher risk of
intestinal damage from the procedure. In these cases,
therefore, referral for exploratory surgery is carried out
without performing abdominocentesis in the field,
because of the risk to the patient and the examiner.
However, if gastrointestinal rupture or very advanced
gut necrosis are suspected, their confrmation by
abdominal paracentesis indicates the need for immedi
ate euthanasia.
Characteristic changes to the peritoneal fluid in
horses with different categories of acute abdominal
disease are summarized in Table 2.2. Changes seen in
horses with peritonitis and abdominal neoplasia are
described in Chapters 1 1 and 17.
Carbohydrate absorption
tests
|Ty| O|
These tests assess the functional integrity of the small
intestine by measuring the efciency of sugar absorption
from the intestinal lumen. They are indicated where
weight loss is occurring in the absence of an obvious
cause, despite an adequate food intake. Pathological
changes that interfere with cellular transport mecha
nisms reduce sugar uptake into the bloodstream.
The most commonly used carbohydrate absorption
tests in the horse include the oral glucose absorption
test, the D( )-xylose absorption test, the starch toler
ance test, and the oral lactose tolerance test.
THE ORAL GLUCOSE ABSORPTION TEST
The most useful of the carbohydrate absorption tests in
horses is the oral glucose absorption test (OGAT) . This
test is inexpensive, simple to perform, and offers good
Z
empiric information on the efficiency of small intestinal
absorption.
Procedure
The horse's weight is estimated as accurately as possible
(e. g. using a girth weighband) and the animal is fasted
overnight on an inedible bedding. Access to water can
be allowed until 2 hours before the test begins.
One gram per kilogram bodyweight of anhydrous or
monohydrate D-glucose is weighed out and a fresh solu
tion is prepared as 20 per cent weight/volume in warm
water. A 'fasting' sample of blood is taken immediately
before the test (time zero) . All samples that cannot be
processed within 1 hour must be collected into potas
sium oxalate-sodium fluoride anticoagulant.
A nasogastric tube is passed and the entire solution is
delivered as a bolus into the stomach. Further blood
samples are taken at 30, 60, 90, 1 20, and 1 80 minutes
and submitted for glucose estimation. absorption
curve is then plotted arithmetically. A modifed test pro
cedure employing a reduced number of sampling times
(time zero and 1 20 minutes) can also be used and has
the advantage of being more practical and economic to
use in the feld.
Interpretation
Under normal conditions the absorption curve has two
phases. In the first 2 hours glucose is continuously
absorbed from the small intestine and the fasting
plasma glucose concentration doubles. The second
phase is insulin-dependent and shows a progressive fall
to a resting level which is achieved by 6 hours. The sam
pling times suggested above should demonstrate these
features when absorption is not compromised. A late,
but normal-sized glucose peak may occur in cases of
delayed stomach emptying.
A flat line indicates a state of total malabsorption
and usually constitutes a grave prognosis. The principal
causes are progressive inflammatory or neoplastic cellu
lar infltrations of the gut wall. The diagnosis is defined
by histopathology.
intermediate cure between normal absorption
and total malabsorption suggests a state of partial mal
absorption that is more difcult to interpret. The cause
may be reversible, for example inflammatory change
associated with parasitism. In addition, some clinically
normal horses produce a partial malabsorption result
that may reflect a rapid gut transit time. Without know
ing the precise nature of a lesion or functional distur
bance, it is not possible to be certain that such cases will
not revert to normal given time and supportive treat
ment. However, the test can be repeated at a later date
to monitor the patient's progress.
THE D(+)-XYLOSE ABSORPTION TEST
The D( +)-xylose absorption test is essentially the same
as the OGAT, but is considered to provide a more accu
rate assessment of absorption. However, the shape of
the xylose absorption curve is influenced by factors that
can also cause anomalies in the glucose absorption
curve, i. e. the rate of gastric emptying, intestinal transit
time, intralumenal bacterial overgrowth, and immedi
ate dietary history. In addition, the costs of xylose and
its assay are considerably more than those of glucose
and at present commercial laboratories do not process
the samples routinely. On balance, the practitioner is
advised to use the OGAT.
The peak plasma levels of xylose are reached 60-90
minutes after an oral dose of 0. 5 or 1 .0 g xylose/kg body
weight, administered as a 1 0% solution by nasogastric
tube.
THE STARCH TOLERANCE TEST
The test is performed by administering 2 g corn
starch/kg body weight as a 20% solution. This test
assesses both small intestinal absorptive and pancreatic
exocrine function.
THE ORAL LACTOSE TOLERANCE TEST
This test has been used to assess persistent non-systemic
diarrhea with malabsorption in the suckling foal, that is
associated with lactase defciency caused by prior
intestinal epithelial damage. This may follow on from
other causes of diarrhea such as rotavirus infection. A
reduced tolerance curve may suggest the need to
restrict or prevent milk access for a short period until
small intestinal epithelial repair has occurred. The test
is performed by administering 1 . 0 g lactose as a 20%
solution.
Endoscopy
M! Mu||y
INTRODUCTION
Endoscopy is indispensable for making diagnoses or
ruling out several possibilities of alimentary tract disor
ders. Endoscopy is used most commonly to examine the
esophagus, stomach, and proximal duodenum, but an
ADDITI ONAL DIAGNOSTIC PROCEDURES Z
endoscope can also be inserted through an enterotomy
to view the lining of the small or large intestine.
Proctoscopy is feasible, but the rectum must be carefully
and thoroughly evacuated to be able to see the mucosal
surface adequately.
There is a great variety of endoscopic equipment
available that can be used for alimentary endoscopy.
The decision as to which endoscopic equipment to pur
chase will be based on several factors, including
the tpe of practice and its caseload
whether the equipment will stay within a clinic or
be transported around
equipment costs
the interests of the practice owners.
ENDOSCOPIC EQUIPMENT
99(o'`\^llm^tm7 u\^'D1 %"''"1',=, "NW",""O''HII,""!" ""o'Y'',P,S",
This can be divided into two categories
fberoptic
electronic (video) .
Fiberoptic endoscopic equipment uses glass fber
bundles to transmit light to the area to be viewed and to
transmit the image to an eyepiece. Recently developed
technology uses a light-transmitting gel to deliver illu
mination from the light source. The viewed image is
magnifed by a lens system within the eyepiece. The
quality of an image viewed through a fberoptic endo
scope is determined by the number of fbers in the
endoscope and the intensity of the light source. The
more fbers the better the image resolution. High qual
ity gastroscopes have approximately 30 000 fbers while
endoscopes of lesser quality may have as few as 1 2 000
fbers. The 60 W halogen lamps used in most portable
endoscope light sources provide poor illumination of
an adult horse's stomach. More powerful light sources
are available (up to 300 W xenon lamps), but these are
large and heavy and therefore less portable.
A video-endoscope system uses glass fber bundles to
transmit light, with a charge-coupled-device (CCD)
chip on the end of the endoscope that transmits the
image. The light source (300 W xenon lamp) and pro
cessing of the electronic signal generated by the CCD
are in the endoscope processor. With most video-endo
scopic systems, a color image is obtained by transmit
ting white light through a red-green-blue color wheel
that rotates approximately 30 times per second. The
processor combines sequential red, green, and blue
images generated by the CCD chip into a composite
red-green-blue image. Olympus utilizes a 'color' CCD
in which white light is transmitted through the endo
scope, and red, green, and blue flters over the CCD
Z1
elements create post-illumination color. The number of
pixel elements per CCD varies from 32 000 to 500 000.
A CCD chip with more pixels provides a larger, but not
necessarily better, image. Enhancement of image
quality is achieved through processor electronics.
Because the image produced by a video-endoscope is
the result of processing electric signals from thousands
of pixel elements on the CCD chips, the appearance of
the image is, in many respects, artifactual. Color repre
sented by different processors can be of varied hues.
Color artifacts are not unique to electronic endoscopes,
fiberoptic endoscopes tend to render an image with
more of a yellow hue than the true color of the object
being viewed.
Other characteristics of endoscopes to be consid
ered include
how the object is illuminated
the field of view
deflection of the endoscope tip
ergonomics of the control section
ease of cleaning and maintenance.
The surface being viewed should be illuminated
evenly, but many endoscopes do not accomplish this.
With some the center of the area being viewed is exces
sively illuminated compared to the periphery, while
with other endoscopes one side of the area viewed is
excessively illuminated and the other side is under-illu
minated. This results from the point where the trans
mitting light bundles are configured on the tip of the
endoscope (along with the viewing lens or CCD, air
water channel, biopsy channel, etc. ) . The standard field
of view for a gastroscope is 1 00 degrees, larger fields of
view are accomplished using lenses of greater convexity.
This can create a ' fish-eye' effect that distorts the image
being viewed. Most endoscopes manufactured today
can be completely immersed in cleaning and disinfect
ing solution, facilitating cleaning and maintenance.
Other important considerations include the size or
availability of a biopsy channel, whether one needs an
extra biopsy channel, and the effectiveness of air-water
channels.
Fiberoptic and video-endoscope systems each have
characteristics that may be perceived as advantages or
disadvantages (Table 2. 3) . Video-endoscope systems are
more expensive, but the cost difference between elec
tronic and fberoptic systems is based on the processor
and monitor rather than the endoscope. Video-endo
scope systems are more cumbersome and are generally
poorly suited for transporting on a frequent basis.
Video-endoscope systems are advantageous, however, as
they include the client in the examination process, and
they facilitate documentation of endoscopic images.
Fiberoptic endoscopes can be used with a video
endoscope processor by using an adapter with a CCD
chip. The adapter fits over the eyepiece of the endo
scope and the image is returned to the processor and
displayed on a monitor. Analog cameras, such as those
used with arthroscopes, also can be used with a fber
optic endoscope for viewing on a monitor.
Finally, a paramount consideration in deciding which
endoscope system to purchase is its expected durability
and the company's ability and commitment to service
the endoscope. This also includes the availability of a

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'
.
Feature Fleroptlc Elctronlc
{Wlthout camera}
Cost (new) $8000-$1 5 000 $20 000-$45 000
5000-1 0 000 1 5 000-30 000
Portabi l ity Good Poor to fai r
I mage qual ity Fai r to very good Very good
Image capture Poor Good
Teaching/client Poor Good
communication
Di si nfecti on Good Good
Avai l abl e accessories Good Good
ZZ
loaned endoscope if one' s endoscope requires extensive
repair work. The gastroscopic examination places con
siderable strain on the endoscope, and a well-made
endoscope used extensively for that purpose will require
maintenance ever 1-2 years. Many of the relatively inex
pensive 2 to 3-meter endoscopes are not sufciently
durable to withstand repeated gastroscopic procedures
and will require frequent maintenance. These issues
must be clarifed in writing with the manufacturer prior
to any purchase. In most cases, it is advisable to purchase
an endoscope that is in the manufacturer's product line,
rather than one custom built. Finally, the likelihood of
endoscope damage, either from excessive wear and tear
or direct damage to the endoscope, is inversely propor
tional to the experience of the endoscopist. inexpe
rienced endoscopist should expect that endoscope
damage will occur, and thus the manufacturer's main
tenance agreement and availability of loaned endo
scopes are critically important.
Endoscope dimensions
An important decision to be made in acquiring endo
scopic equipment involves the dimensions of the endo
scope. Flexible endoscopes are available from several
manufacturers in many lengths and diameters (Table
2. 4) , and each length/diameter combination deter
mines how the endoscope may be used. A working
length of 1 1 0 cm with an outer diameter of 1 0 mm
(standard human gastroscope) is usually sufcient to
reach the stomach of foals up to 30-40 days of age. A
length of 1 60-1 80 cm with a maximum outer diameter
of 1 2.5 mm (human slim colonoscope) is required for
gastroscopy in weanling foals. For most equine gastric
endoscopy a minimum working length of 200 cm is
required. This length will usually permit adequate
observation of the squamous mucosa and much of the
glandular body, although examination of the antrum
and pylorus in standing adult horses will not be possi
ble. endoscope 200 cm long is usually sufcient to
examine the proximal duodenum in foals up to 6
months old. In older foals endoscopy of the proximal
duodenum may be possible using an endoscope 200 cm
long, with the foal placed in lateral recumbency under
general anesthesia. A 250-cm endoscope will permit
thorough examination of the stomach, including the
antrum and pylorus, of most adult horses, while a
length of 280-300 cm is required to perform duo
denoscopy in adult horses.
TECHNIQUES FOR ENDOSCOPIC
PROCEDURES
Endoscopy of the esophagus is often performed in
emergency situations, for example cases of choke,
when there is little time for patient preparation. Horses
need to be properly sedated or anesthetized to pass
an esophageal obstruction safely and effectively.
Endoscopy is useful in identifing the location and type
of obstructing material, but this material cannot usually
be removed by endoscopy. For elective esophagoscopy,
feed and water may be restricted for 2 hours. In many
Endo8copetgpe ]plcaldlmen8lon8 Comment8
{fM flbeHplc, VM Vldeo}
Gastroscope, human (f,v)
Colonoscope, human (f,v)
Smal l bowel endoscope (v) (Penta x)
Equine gastroscope (v) (Fujinon)
Equine gastroscope (v) (Pentax)
WoHlng Uuter
length dlametr {o.d.}
1 00-1 1 0 L 9-1 0. 5 mm
1 55-1 70 cm 1 1 . 5-1 6 mm
250 em 1 0 mm
280 cm 1 4. 5 mm
300 cm 1 0 mm
Gastroscopy i n neonates.
Not l ong enough for adult gastroscopy.
o. d. too great for passage through foal
nasal passages.
Suitable for all ages except adult
duodenoscopy.
Large o.d. inappropriate for foals.
Suitable for all ages, i ncl udi ng adul t
duodenoscopy.
Z
Z ADDITI ONAL DI AGNOSTI C PROCEDURES
cases, it is useful to perform gastroscopy at the time of
esophagoscopy, because there may be both gastric and
esophageal disorders. The procedures described below
apply to gastroscopy and duodenoscopy.
Foals
1 . Suckling foals not eating solid feed are allowed to
nurse until 2-4 hours before endoscopy.
2. Feed is withheld from foals eating solid feed for
8-12 hours, with nursing permitted until 2-4 hours
before endoscopy. Longer periods of fasting can be
used but the foal ' s hydration status should be
considered.
3. Sedation is not always required in neonatal foals,
although if the foal struggles excessively sedation
will facilitate the procedure for both the foal and
the endoscopist. Options for sedation include
xylazine 0.5 mg/kg i.v.
xylazine 0.5 mg/kg i.v. plus diazepam 0.1 mg/kg i.v.
xylazine 0.5 mg/kg i.v. plus butorphanol
0. 01-0.02 mg/kg i.v.
4. The procedure may be performed with the foal
standing or lying on a mat. To restrain a young foal
for standing endoscopy, a handler should hold the
foal around the chest and rump and the
endoscopist (if right handed) should bring the left
arm around the back of the foal ' s head so that the
poll rests in the crook of the left elbow. The right
hand advances the endoscope while the left hand is
used to guide the endoscope through the left nares.
Using this restraint, the typical response of foals to
jerk the head backwards can be controlled.
Adult horses
. Feed is withheld for 8-12 hours, water for 2-4 hours.
Longer periods of fasting can be used to ensure
complete empting of the stomach, but this is not
usually necessary. The person responsible for fasting
the horse should be instructed to remove hay and
bedding and to muzzle the horse. Horses will eat
straw, shavings, sawdust, their own manure (even
through a muzzle) if hungry enough. None of these is
conducive to a thorough examination of the stomach.
2. Sedation is required for a standing endoscopic
examination. Options for sedation include
Z4
xylazine 0.5-0.7 mg/kg i.v.
acepromazine 0.03 mg/kg i.v. then 20 minutes
later xylazine 0. 5-0.7 mg/kg i.v. , this facilitates a
relatively longer examination, for example
duodenoscopy
detomidine 0.02 mg/kg i.v., this facilitates a
relatively longer examination, for example
duodenoscopy.
3. General anesthesia may be elected to examine the
dependent portion of the stomach (glandular) or if
the antrum and pylorus must be observed using an
endoscope less than 240 cm long.
4. A nose twitch is useful in the restraint of many horses.
5. If delayed gastric emptying is suspected or known,
pre-treatment (45 minutes) with bethanechol,
0.025 mg/kg S. c. , will facilitate advancing the
endoscope throughout the stomach.
ENDOSCOPIC PROCEDURE
The animal usually fnds the passage of the endoscope
through the nares the most objectionable part of the
procedure. The endoscope is advanced to the rima glot
tis, and into the esophagus. In older foals and adult
horses, swallowing can be facilitated by squirting water
through the endoscope air-water channel or the biopsy
channel onto the rima glottis. It is better to have the
horse swallow and then pass the endoscope than try
to force the endoscope into the esophagus, because
the endoscope may inadvertently and unknowingly
retroflex and then be advanced into the mouth.
If the horse coughs excessively during or immediately
after passing the endoscope into the esophagus, the soft
palate has probably been displaced dorsally. Inducing a
swallow or flexing the head will resolve this. Some horses
will use their pharyngeal muscles to grab the endoscope
as it is being passed, making it diffcult to pass and to
withdraw. This requires patience by the endoscopist to
advance or withdraw the endoscope safely and effectively.
The esophagus should be carefully examined as the
endoscope is advanced. In an adult horse the lower
esophageal sphincter and entrance into the stomach is
typically 1 70-180 cm from the nares. Some resistance
may occur at the lower esophageal sphincter, but it
should be relatively easy to advance the endoscope into
the stomach.
The stomach is distended by insufflation of air
through the endoscope until the non-glandular and
glandular regions of the gastric surface can be
observed. Distention with air is tolerated by foals and
horses, and only rarely has been associated with signs of
abdominal discomfort in the patients examined by the
author. Gastric contents should be thoroughly rinsed
from the stomach surface using tap water flushed
through the biopsy channel. Excessive fluid within the
stomach may need to be aspirated; this may be accom
plished through the endoscope biopsy channel, or
often more effectively using a nasogastric tube. If there
is a large volume of fluid or feed in the stomach and the
horse has defnitely been fasted for an adequate period,
3g3SIIlC outlet obstruction should be suspected.
When the endoscope frst enters the stomach the
enrloscopist sees the right side and the greater curva
ture of the stomach (Plates 2. 5, 2. 6) . As the endoscope
is advanced it travels against the right side of the stom
ach and then dorsally. it is advanced further toward
the caudal portion of the stomach the lesser curvature
and cardia can be seen (Plate 2.7) . When observing the
cardia the endoscope is pointing cranially, so that the
left side of the animal appears on the left side of the
endoscopist 's field of view.
In order to view the antrum and pylorus, the endo
scope must be further advanced until it has passed
ventral to the ridge formed by the lesser curvature. The
endoscope will slide ventrally into the dependent por
tion of the stomach as it is advanced toward the pylorus.
It then will become submerged in gastric fluid and the
remains of ingesta, and the endoscopist's view will be
obscured. It will be helpful to insuflate with air and
perhaps aspirate fluid, and then carefully advance the
endoscope until the antrum and pylorus can be seen.
This may require several minutes and it is important to
be patient. The endoscope usually cannot be advanced
(a)
to the pylorus without adequate gastric contractions.
Forcing the endoscope to advance can bow the endo
scope inside the stomach. This can damage the endo
scope and can cause discomfort to the horse as the
endoscope stretches the stomach wall. Make use of the
animal's intrinsic gastroduodenal motility to assist
advancing the endoscope to the pylorus and into the
duodenum. If motility is poor or absent, pre-treatment
with bethanechol, 0.025 mg/kg S. c. , will often help.
With sufcient length the endoscope may be
advanced through the pylorus into the duodenum. It
will initially move into the duodenal ampulla and when
advanced further the lens will be pressed against
mucosa and the feld of view will be a blurred red.
the proximal duodenum extends past the pylorus it
makes a I SO-degree turn caudally; this is what the endo
scope must do to continue to be advanced (Figure 2.9) .
I n most cases the endoscopist will be able t o see t o the
major duodenal papilla, but not further, by advancing
the endoscope a few centimeters while rotating the
endoscope and maximally retroflexing the tip. In this
way the endoscopist is actually looking b<ck at the
(b)
N
N
||gure2.9 I ll ustrations of the stomach depicting the path taken by the endoscope as it is advanced around the stomach to
the antrum, through the pylorus, and into the duodenum. The hash l i nes represent the outl i ne of the proximal descend
i ng duodenum. a) I n this illustration the left hemi sphere of the stomach has been removed just to the l eft of mi dl i ne.
Notice that the endoscope must travel along the ci rcumference of the stomach i n order to reach the gastric antrum. As the
endoscope i s advanced around the ci rcumference of the stomach it becomes i mmersed i n gastric contents. When the
endoscope i s advanced i nto the duodenum the ti p must be retroflexed to observe duodenal papi llae. Rarel y the cl i ni ci an
mi ght be able to advance the endoscope aborally into the duodenum, but the configuration of the duodenum with
respect to the stomach makes this very di fficul t. b) I n this illustration the caudal hemi sphere of the stomach has been
removed. In thi s vi ew, the torque stresses placed upon the endoscope as it i s advanced toward the pylorus and the duo
denum can be appreciated. When the procedure i s performed properly, the majority of these stresses are applied to the
cables controlli ng the ti p deflection. Advanci ng the endoscope with excessive force or otherwise i mproperly will cause
more of these forces to be applied to the endoscope i nsertion tube causing expensive damage to the instrument
Zb
duodenal papilla, rather than forward. One will notice
that when the endoscope is frst pulled back to leave the
duodenum, it will appear as if the endoscope is advanc
ing into the duodenum.
In some cases it may be desirable to obtain a biopsy
through the endoscope. The biopsy channel diameter in
gastroscopes is usually restricted to 2.8 mm, however in
large diameter colonoscopes the biopsy channel diame
ter can be 3.6-4.0 mm. Consequently most biopsies will
be very small. Biopsies of gastric squamous mucosa are
usually unrewarding because very little mucosa can be
obtained. Gastric glandular and duodenal mucosal biop
sies are larger because mucosa can be torn away as the
biopsy forceps is withdrawn. These biopsies are often suf
ficient for diagnostic purposes. Biopsy sites will bleed,
often impressively, but this is not a concern unless the
patient has a severe bleeding disorder.
When the endoscopic procedure is completed it is
helpful to remove air from the stomach. Post-endoscopy
abdominal discomfort is unusual, but can be prevented
by keeping the duration of the examination as short as
possible and removing the air insuflated into the stom
ach. If discomfort does occur it will rapidly resolve after
treatment with flunixin meglumine, 0. 5 mg/kg i.v.
CARE OF ENDOSCOPIC EQUIPMENT
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The manufacturer should provide thorough written
instructions on the care and maintenance of the endo
scope, and the sales representative should demonstrate
its operation, cleaning, and proper storage. After use,
the endoscope should be cleaned in an enzymatic solu
tion (e. g. Endozime, Ruhof Corp. , Valley Stream, N
that removes adhered mucus, blood, etc. The endoscope
biopsy channel should also be cleaned. After rinsing the
endoscope in water it should be allowed to dry thor
oughly, preferably by hanging vertically. A 3-m-long
endoscope may need to be dried by hand. For disinfec
tion the endoscope should be immersed in a 2. 4% solu
tion of glutaraldehyde (e. g. Cidex,Johnson andJohnson
Medical Inc. , Arlington, TX) for 1 5-30 minutes.
Ultrasonographic
examination of the abdomen
LM M||, ! LyOD, DOb ||mD
Examination of the abdomen requires a range of imag
ing depths and thus, ideally, a selection of transducers
Zo
should be available to optimally image the entire
abdomen in horses of all ages and sizes. For evaluation
of the ventral body wall and peritoneal fluid, high fre
quency (6. 5-10 MHz) transducers provide excellent
resolution and adequate penetration in horses of all
types. In foals and small ponies, the deeper structures
within the abdomen can be visualized satisfactorily with
mid-frequency (4-6.5 MHz) transducers, while in the
mature horse, imaging depths in excess of 25-30 em
may be required, thus low (2. 25-3.5 MHz) transducers
are necessary. The ventral abdomen can be imaged
equally well with sector or linear transducers. For
deeper abdominal imaging, sector transducers are
required to provide flexibility to image between the ribs
and around gas. The key requirement for examination
of the caudal abdomen and pelvic contents per rectum,
is a transducer that is suffciently small to be easily
manipulated within the rectum, while still providing an
adequate imaging feld. Linear transducers are pre
ferred for most gynecological work because they are
||gure2.1 0 A transverse ultrasonogram of the right dorsal
abdomen from a normal horse: the duodenum can be seen
runni ng ventral to the kidney and dorsal to the cecum
||gure2. 11 A transverse ultrasonogram of the caudoventral
abdomen from a normal horse: smal l intesti nal loops (5|)are
visible and there i s a distinct layer of retroperitoneal fat
easy to manipulate over the reproductive tract. In con
trast, for examination of the caudal portions of the
intestine per rectum, the smaller microconvex trans
ducers have the advantage that they can be positioned
to image in any direction, increasing the range of the
imaging feld. For transcutaneous examination, sector
transducers are the most flexible and the area under
investigation may have to be clipped and the skin
cleaned. No specific preparation is necessary for rectal
examination. However, since the procedure may
involve prolonged examination periods and it is gener
ally necessary to reach fairly far proximally into the
rectum, the operator should ensure that the horse is
adequately restrained and consider the use of drugs
sllch as probantheline or hyoscine to reduce rectal
straining and decrease the risk of injury to the rectum.
NORMAL ULTRASONOGRAPHIC
ANATOMY OF THE INTESTINE AND
PERITONEAL CAVITY
The stomach can be identifed in the left cranial
abdomen. Typically it is recognized as an echogenic
curve caused by gas along the greater curvature. The
||gure 2. 12 A transverse abdomi nal ultrasonogram
obtained per rectum showing normal smal l i ntesti ne. The
wal l (between arrows) i s composed of five di screte layers
that are normal ly measured i n combi nati on
||gure 2. 13 A transverse ultrasonogram of the crani oven
tral abdomen. Peritoneal fl ui d is vi si bl e between the sec
tions of l arge intestine (LI) and coul d be sampl ed in thi s site
stomach lies beneath the uniformly echogenic spleen.
Fluid is rarely visible within the stomach in normal
adults but occasionally a small amount of fluid will be
visualized within the ventral portion of the stomach in
the foal. The duodenum is a consistently recognizable
landmark, visible in most horses (Figure 2. 1 0) . It can be
identifed in the right dorsal abdomen, running cau
dally, ventral to the liver and right kidney. The individ
ual sections of the remainder of the small intestine
cannot be consistently identifed in all animals. Motile
loops of small intestine, with small amounts of lumenal
contents, are visible in the caudoventral abdomen
(Figure 2. 1 1 ) in around 66 per cent of normal horses
and in the cranial abdomen in 25 per cent of horses.
The small intestine can also readily be assessed in the
mid-abdomen via rectal examination (Figure 2. 1 2) . The
small intestinal wall is composed of fve discrete layers,
however, the resolution of most ultrasonographic units
is such that the layers are usually measured in combina
tion to defne the total wall thickness (Table 2. 5) .
Large intestine i s visible i n all quadrants of the
abdomen. It is recognized ultrasonographi cally by its
location, size, and the sacculated appearance of its con
tour. The thickness of the large intestinal wall can be
documented (Table 2. 5) but the gas within the colon
obscures the lumen so that it is not possible to deter
mine the diameter of individual loops of large intestine
(Figures 2. 13, 2. 1 4) . Waves of peristalsis within the
||gure 2. 14 A transverse abdomi nal ultrasonogram
obtained with a 10 MHz l i near transducer i l l ustrati ng the
di screte layers of the abdomi nal wal l
ZJ
2.5tap t
8eglon 8ecommended truOure8
tran8ducer eXamlned
frequencg{MHz}
Cranioventral Foals: 1 0-5 Spleen
Adults: 6. 5-5 Large intestine
Smal l i ntestine
Ca udoventra I Foals: 1 0-5 Large intestine
Adults: 6. 5-5 Smal l i ntestine
Bladder
Right dorsal Foals: 1 0-6.5 Liver
Kidney
Adults: 5-2. 25 Duodenum
Cecum
Left dorsal Foals: 1 0-6.5 Spleen
Kidney
Adults: 5-2.25 Large colon
Mi d-abdomen Adults: 6. 5-5 Aoroi l iac
(transrectal quadrification
route) Bladder
Small intestine
Cecum
Large colon
Smal l colon
*FreemanandLyOnt, unub||theddata
cecum run in a dorsal to ventral direction, while the
motion of the remainder of the large intestine runs in
the sagittal plane, so that it is possible to distinguish the
cecum from the right ventral and dorsal colon. Large
intestine should not normally be present within the
nephrosplenic space, and in most horses the entire left
kidney is readily visualized in the left caudodorsal
abdomen. Occasionally gas within the small colon is vis
ible in the nephrosplenic area, but it is usually possible
to appreciate that this runs caudal, not cranial, from
the nephrosplenic space into the remainder of the
abdomen. Gas within the small colon can also
Zd
ujeOlVe uantlIatlVe
a8888ment8 mea8urement8
oflnte8tlne oflnt8Ilne"
Motility of col on and Col on:
smal l i ntesti ne
wall thickness 0. 1 8 0.04 cm
Presence/absence of
smal l i ntesti ne motility 2-6 contractions!
mi n
Volume and character
of peritoneal fl ui d
Motil ity of col on and Smal l i ntestine:
smal l i ntesti ne
wall thickness 0. 1 6 0. 05 cm
Presence/absence of
smal l intesti ne di ameter 1 .8 0.8 cm
Vol ume and character motil ity 6-1 5 contractions!
of peritoneal fl ui d mi n
Motility and nature Colonic and small intestinal
of i ntestinal contents wall thickness
(see data above)
Presence/absence of
i ntestine in the
nephrosplenic space
Motility of colon and Colonic and smal l intesti nal
smal l i ntesti ne wal l thickness
(see data above)
frequently b identifed as echogenic cures in the left

caudodorsal abdomen.
The ventral body wall is composed of subcutaneous,
muscle, and fat layers that can be distinguished ultra
sonographically (Figure 2. 14) . Peritoneal fluid can be
identifed in the cranioventral abdomen in most horses
(Figure 2. 1 3) , and ultrasonography is occasionally use
ful to identif a site for abdominal paracentesis when
unguided techniques have been unsuccessful. In smaller
horses and foals the bladder may be visible in the
caudoventral abdomen and in the mid- and late-term
mare the gravid uterus is identifed in this location.
CLINICAL INDICATIONS FOR
ABDOMINAL ULTRASOUND IN HORSES
PRESENTING WITH COLIC
Ultrasonographic examination can be used to evaluate
the anatomical location, contents, wall thickness, and
motility of various regions of the intestine. This is par
ticularly useful in foals, weanlings, or small ponies with
colic, when the size of the animal precludes rectal pal
pation of the gastrointestinal tract. It is also useful in
horses presenting with clinical signs consistent with a
surgical lesion in which rectal examination has
proved inconclusive. In a study comparing the ultra
sonographic and rectal detection of distended small
intestine as a criteria indicating that surgical inter
vention was necessary in seventeen horses presenting
with signs of colic, ultrasonography had a sensitivity of
100 per cent with a specificity of 83 per cent, comparing
favorably to rectal examination which had a sensitivit
of 1 00 per cent and specificit of 75 per cent. With
ultrasonography, it is possible to evaluate portions of
intestine in the cranial abdomen that are out of reach
from the rectum. Ultrasonography is also valuable in
evaluating intra-abdominal masses and peritoneal effu
sion and in horse with low-grade but persistent pain
where partial intestinal obstruction is suspected.
CLINICAL INDICATIONS FOR
ABDOMINAL ULTRASOUND IN HORSES
PRESENTING WITH WEIGHT LOSS
The clinical indications for abdominal ultrasonography
in horses with weight loss are less specific.
Ultrasonography should be considered in horses with
palpable intra-abdominal masses or abdominal disten
tion, and if there is laboratory evidence of hepatic,
renal, or intestinal disease, and in horses with abnormal
peritoneal fuid analysis. In horses with protein-losing
enteropathy and malabsorption, ultrasonography can
be a useful adjunctive aid to allow measurement of the
thickness of specifc portions of the intestine and this
may be valuable in determining the response to
therapy.
SMALL INTESTINAL LESIONS
Obstructed intestine is heavy and tends to fall to the
ventral abdomen. If the examination is performed on a
recumbent foal, it is important to evaluate the most
dependent areas of the abdomen carefully, since small
intestinal intussusceptions and other localized lesions
will tend to fall to the lowest point of the abdomen
depending on the body position (Figure 2. 1 5) . In the
adult horse distended loops of small intestine are
occasionally visible in the left dorsal quadrant of the
abdomen although more frequently with small intesti
nal obstruction, the abnormal small intestine is visible
in the right and ventral abdomen (Figures 2. 1 6, 2. 17) .
Incarcerated segments of bowel are amotile and fre
quently have extremely thickened walls reflecting intra
mural edema. If this is severe the intestinal wall has a
low echogenicity, and in areas where there is no con
current distention the intestine often has a corrugated
appearance ( Figure 2. 1 8) . In foals small intestinal intus
susception produces a characteristic bull's eye appear
ance, with concentric rings formed by the walls of the
intussusceptum and intussuscipiens and fluid within
the intussusceptum. Ileocecal intussusceptions are not
visible because the gas within the cecum obscures the
||gure2. 1 5 A transverse abdomi nal ultrasonogram from a
4-week-old foal with smal l intesti nal volvul us i l lustrating a
di stended. amotile segment of smal l intesti ne. The foal is
in lateral recumbency and thi s i mage has been obtained
from the ventral mi dl i ne and therefore. because of
gravity. stati onary i ngesta i n the obstructed segment has
settl ed i nto hori zontal layers
Z
Figure 2. 16 A l ongi tudi nal ultrasonogram of the left dorsal
abdomen from a 5-year-ol d stal l i on with a right i ngui nal
herni a. Multi ple distended loops of smal l intestine 5')are
visi bl e
Figure 2. 17 A l ongi tudi nal ultrasonogram of the crani o
ventral abdomen from an aged pony gel di ng with an
obstruction of the smal l i ntestine by a pedunculated
l i poma. Fl ui d-fi l l ed di stended smal l i ntesti nal loops with
thickened wal ls are vi si bl e
Figure 2.18 A l ongitudi nal ultrasonogram of the cranio
ventral abdomen from a 1 5-year-old pony gel di ng with
smal l i ntesti nal entrapment in the epi pl oi c foramen. A
segment of non-distended smal l intestine with hypo
echoic, edematous wal l s has a corrugated appearance
(arrows)
intussuscipiens. However, it is possible to visualize dis

tended small intestine in the right and mid-abdomen
proximal to the obstruction. Adhesions are recognized
as portions of intestine that are stationary and remain in
consistent relationship to each other, or to other
abdominal structures that the intestine is adherent to,
such as abscesses, hernias, or the body wall (Figure
2. 19) . The presence of both distended and collapsed
loops of intestine is strongly suggestive that there may
be an anatomical obstruction.
LARGE INTESTINAL LESIONS
Ultrasonography is the most sensitive tool available for
diagnosis of left dorsal displacement of the large colon
(nephrosplenic entrapment) . With this condition, large
colon is visualized in the nephrosplenic space obscur
ing part or all of the left kidney. However, it is possible
for the large intestine to attain a position dorsal to the
left kidney or for small colon to enter the space without
entrapment. Therefore, to confirm the diagnosis of left
dorsal displacement, it is necessary to ensure that large
intestine can be identifed running into the space from
a cranial location. Provided that the entrapped portion
is distended, gas shadowing creates a straight dorsal
border of the spleen and the most dorsal portions of the
spleen are obscured. In some horses fluid and ingesta
may be visible within the entrapped portion and this
can enable some of the more dorsal areas of the spleen
to be identifed (Figure 2. 20) . Cecocecal and cecocolic
intussusceptions can also be specifi cally identifed and
have a bull's eye appearance, similar to that described
for small intestinal intussusception. Specifc differentia
tion of other surgical forms of large colon disease from
generalized tympany or large colon impaction is dif
cult. However, transrectal ultrasonography can be use
ful in the identification of small colon obstruction
(Figure 2. 21 ) . Most of the small colon is easily palpable
per rectum, however measurement of bowel wall thick
ness can be useful to distinguish between simple
obstructions and those where the bowel wall is compro
mised and edematous. The presence of gas free within
the peritoneal cavity, accompanied by particulate fluid
is consistent with gastrointestinal rupture and conse
quently warrants a poor prognosis.
GENERALIZED INFLAMMATORY AND
INFILTRATIVE INTESTINAL DISEASES
Ultrasonography can be very valuable in distinguishing
between small intestinal distention due to enteritis, or
ileus from physical obstruction and strangulation. The
ADDITI ONAL DIAGNOSTI C PROCEDURES Z
(a) (b)
(c) (d)
|gure 2. 1 9 Abdomi nal ultrasonograms from a 1 5-year-old Shetl and pony with mural abscessati on and small i ntesti nal
adhesions. I n l ongi tudi nal (al and transverse (b) i mages of the affected intesti ne, the wal l s are hypoechoic and extremely
thickened. The arrows i ndi cate the area at whi ch the two adjacent segments do not move relative to each other,
i ndi cati ng that adhesi ons have formed. In other areas of the abdomen, in l ongi tudi nal (cl and transverse (d) i mages, both
di stended and col l apsed loops are vi si ble, suggesting that there i s intesti nal obstruction
|gure2.20 A transverse ultrasonogram of the l eft dorsal
abdomen from a 2-year-old gel di ng with left dorsal dis
placement of the large col on. In thi s area the entrapped
portion of intestine i s not tympani ti c and therefore sound
penetrates the intestine so that the spl een i s only parti al ly
obscured by acoustic shadows (arrows) caused by
intesti nal gas
1
|gure 2.21 A transverse ultrasonogram of the caudal
abdomen obtained per rectum from an aged gel di ng.
Thickened areas of smal l colon (SC) are due to obstruction
of the smal l colon by a pedunculated l i poma
wall thickness, diameter of the lumen, appearance of
the intestinal contents, and the intestinal motility
should be considered. Motility is assessed by observing
the intestinal walls and contents over a few seconds;
organized waves of motility should be apparent. Amotile
bowel may be completely motionless, or there may be
random bi-directional movement, particularly as the
abdomen moves in horses that are breathing heavily.
With physical obstruction the intestine is usually
amotile, whereas with enteritis some degree of motility
generally is retained, and in some cases, the motility is
increased. Small intestinal wall thickening is present
with strangulation and may also be seen with enteritis
and peritonitis, but the presence of intestinal motilit
should help to distinguish these from cases of small
intestinal obstruction. With colitis the large intestinal
wall is thickened and fluid ingesta may be visualized.
Infltrative bowel diseases produce focal or multi
focal wall thickening in various segments of intestine.
Information on the distribution and extent of infltra
tion can be obtained with ultrasonography in these
cases (Figure 2. 22) . In particular, differentiation of
small from large intestine is achieved and the wall
thickness documented. When combined with other
imaging modalities such as labeled granulocyte scintig
raphy, ultrasonography is used to characterize individ
ual areas of intestine in which there is scintigraphic
evidence of inflammation. However, intestinal wall
thickening may extend beyond the primary site since
protein-losing lesions may be associated with secondary
bowel edema leading to thickening and reduction in
the echogenicity of the bowel wall (Figure 2. 23) .
Regardless of its specific nature, infltrated areas of
Z
|gure 2.22 Transverse ultrasonograms of the (a) crani al ,
(b) mi d-, (c) ri ght ventral abdomen from an 1 1 -year-old
mare with chroni c eosi nophi l ic enteritis demonstrati ng
that the l arge colon vari es i n thi ckness. I n the most
severely affected area (C), the five-layered appearance of
the colon has been l ost
(a)
(b)
||gure2.23 Transverse abdomi nal ultrasonograms from a
6-year-old mare with pl asmacytic-Iymphocytic enteritis,
affecti ng pri marily the l arge col on. a) I n the caudal ventral
abdomen the large colon has irregul ar thi ckeni ng of the
wal l and loss of the five-layered appearance due to cel l u
l ar i nfi ltrate. b) In the crani al ventral abdomen, the smal l
intestine is markedl y thickened with hypoechoic wal l s due
to bowel edema secondary to i ntesti nal protein loss
intestine are generally echogenic with irregular walls
and there may be loss of the normal fve-layered appear
ance. However, at present it is not possible to specif
cally differentiate the various forms of infltrative
disease using ultrasonography (Figures 2. 22-2. 24) .
THE ABDOMINAL WALL IN THE
POSTOPERATIVE COLIC PATIENT
Ultrasonographic examination of celiotomy incisions is
an accurate means of identification of incisional infec
tion. The technique is ea
y to perform and ultrasono-

ADDITIONAL DIAGNOSTIC PROCEDURES Z
(a)
(b)
||gure2.24 Transverse ul trasonograms from a 1 6-year-old
gel di ng with i ntesti nal lymphosarcoma. a) The most
severely affected segment of smal l i ntestine has markedl y
thickened walls, l oss of the normal intesti nal wal l struc
ture, and a reduced l umen. b) I n a less severely affected
proxi mal segment there i s wal l thi ckeni ng and moderate
di stention
graphic signs of infection may precede the onset of clin
ical signs by up to 30 days. The presence of hyperechoic
foci with acoustic shadowing indicating gas, and accu
mulation of anechoic or echogenic fluid within the sub
cutis are indicative of incisional infection (Figure 2. 25) .
I n a study of 50 horses that had undergone exploratory
celiotomy, the accuracy of ultrasonography in the early
detection of incisional infection was assessed and the
sensitivity was 1 00 per cent with a specifcit of 88 per
cent using these subjective assessment criteria. Horses
with ultrasonographic evidence of infection should be
observed for clinical signs of infection for at least 1
month following the ultrasonographic examination. In
Z ADDITI ONAL DIAGNOSTIC PROCEDURES

addition the early introduction of antibiotic therapy or
removal of individual skin sutures may avert the devel
opment of more serious complications. Hernia forma
tion occurs occasionally following celiotomy. The
presence of distended loops of intestine suggests partial
||gure 2.25 A transverse ultrasonogram of the ventral
abdomi nal wal l from a horse that has purul ent drai nage
from a cel i otomy i nci si on performed 1 days previously. A
tract (arrows) extends from a coll ection of hypoechoic
material resul ti ng from i nci si onal infection
||gure 2.26 A l ongitudi nal ultrasonogram of the ventral
abdomi nal wal l from a horse that has developed dehis
cence of the abdomi nal muscl e 8 days after expl oratory
cel iotomy. I ntesti ne is located between the muscl e defect
(arrows) and had adhered to the subcutaneous tissue
5
or complete intestinal obstruction, while intestine
adhered to the incision or within a hernia is apparent
because adhered areas do not move relative to the
surrounding structures (Figure 2.26) .
Nuclear scintigraphy
0
KWl | |DO LM M||
INTRODUCTION
Gamma scintigraphy is a relatively new technique for
the diagnosis of abdominal disease in horses, whereas in
humans and small animals it is a well-established tool
for this purpose. Techniques used in humans and small
animals are described in Table 2. 6.
In the horse scintigraphic techniques in gastro
enterology involve the use of three types of agent.
1 . Radiopharmaceuticals, consisting of a radionuclide
and a carrier, whose biological activity causes it to
localize in specific tissues
99mTc-methylendiphosphonate (MDP) for dental
scintigraphy
99mTc-sulfur colloid for hepatic scintigraphy.
2. Radioactive agents which get entrapped in specifc
cell populations
99mTc-hexamethyl propylene amine oxine
(HMPAO) and
l
l
I
In oxine to label leukocytes for
scintigraphic imaging of inflammation
99mTc-tetrofosmin and 99mTc-methoxy-isobutyl
isonitrile (MIBI) for scintigraphic imaging of
neoplasia. These radiopharmaceuticals are
currently under investigation as unspecifc
tumor-labeling agents in thoracic and abdominal
neoplasia in the horse.
3. Inert, non-toxic radioactive agents to assess motility
of the gastrointestinal tract
99mTc-sulfur colloid and
Il
I In-diethylene
triaminepentaacetic acid (DTPA) to assess
gastric emptying. These techniques have been
used in experimental studies to investigate the
effect of prokinetics.
DENTAL SCINTIGRAPHY
In horses with suspected dental disease scintigraphy of
the head with 99mTc_MDP can provide substantial infor
mation on the exact localization and extent of the prob
lem. Skeletal scintigraphy with 99mTc_MDP is the most
commonly performed scintigraphic imaging procedure
ADDI TI ONAL DI AGNOSTIC PROCEDURES Z
U8edfor the dlagno8l8 of 8adlopharmaceutlcal
Dental disorders Technetium (99mTc) methyl endi phosphonate (MOP)
Esophageal motil ity 99mTc-sul fur col l oi d
Gastric emptying 99mTc-sulfur col l oi d
99mTc-diethyl enetri ami nepentaacetic aci d (OTPA)
Gastric secretory function 99mTc-pertechnetate
Gastrointesti nal bleedi ng 99mTc-l abel ed red bl ood cel l s
Gastrointesti nal neopl asi a 99mTc-methoxy-isobutyl-isonitrile (MI B!)
I nfl ammatory gastrointesti nal conditions Techneti um (99mTc), Gal l i um (67Ga), I ndi um (1I I I n) l abel ed l eukocytes
Hepatobi l i ary i magi ng 99mTc-sulfur col l oi d
99mTc-i mi nodi acetic aci d (I DA)
in veterinary medicine. Bony abnormalities can be
detected before there are radiographic or ultrasono
graphic changes. In cases of dental disease radiographs
are often inconclusive, especially in the early stages of
the disease. Bone scintigraphy has been proven to be a
sensitive and specific method to detect changes in the
alveolar bone surrounding the diseased tooth.
Principle
The uptake of 99mTc-MDP depends on blood flow and
bone metabolism. In the case of dental disease there is
an increased bone turnover in the alveolar bone
adjacent to the tooth.
Indications
1 . I lorses with suspected den tal disease, in which
radiographs are inconclusive.
2. Horses with recurrent sinusitis to rule out an
underlying tooth problem.
3. Horses in which multiple dental disease is suspected.
Technique
Horses are injected intravenously with 1 0 MBq/kg
99mTc_MDP. Three hours after injection left and right
lateral, and ventral and dorsal images of the teeth are
acquired, for 60 seconds, into a 256 ? 256 matrix.
Interpretation
In the normal horse the alveoli, the vertical ramus of
the mandible, the zygomatic arch, the temporo
mandibular joints, and th

ethmoids are seen as areas
of increased activity. The teeth can be identified as
regions of decreased activity within the alveolar bone.
These anatomical structures get less distinct with age
and in old horses blend completely into the back
ground activity. Horses with a tooth root abscess show a
focal increase of activity over the diseased tooth (Figure
2. 27) , whereas horses with periodontal disease show a
linear increase over the involved arcades (Figure 2. 28) .
H08
r|ght
veoum
re trm
Figure 2.27 Tooth root abscess. A l eft lateral and a dorsal
scintigraphic image of the head of a 1 5-year-old
Warmblood gel di ng. The horse had a 6-month hi story of
recurrent swel l i ng over the left maxi l l a. Radi ographs were
inconclusive. Scintigraphy with 99mTc-MDP reveal ed a focal
uptake over the root of the second maxi l l ary cheek tooth
on the l eft side, suggestive of a tooth root abscess
b
S00Sl
PH
VPu M
e lF8l
||gure 2.28 Periodontal di sease. A left lateral scintigram,
3 hours after injection of 99mTc-MDP, of the head of a 2S
year-old Connemara gel di ng that presented with progres
sive weight loss. No evidence of dental disease was seen
on intra-oral examination or radiographs. The i mage
shows a l i near increase of radi oactivity over the upper and
lower arcade, suggestive of severe periodontal disease
INFLAMMATION AND INFECTION
67Ga, I I I In, and 99mTc-labeled leukocytes have been vali
dated as a sensitive technique for the diagnosis of
abdominal abscesses in horses (Figure 2.29) . 99mTc_
labeled leukocytes have been used successfully for the
identification of focal or generalized intestinal inflam
mation (Figure 2. 30) . It appears to be most useful in
acute infammatory conditions and eosinophilic enteri
tis. Variable results have been obtained imaging
lymphocytic-plasmacytic enteritis. The procedure is
particularly helpful for characterization of the distribu
tion of lesions within the gastrointestinal tract.
Principle
99mTc-HMPAO is a lipophilic compound which gets
trapped within white blood cells. It labels a mixed
leukocyte population, of which granulocytes account
for around 75 per cent. The distribution of activity
reflects the distribution of granulocytes in the patient's
body.
Indications
1 . Identifi cation or localization of abdominal
abscesses.
o
L
||gure 2.29 Abdomi nal abscess. A scintigram of the right
mid-abdomen of a 6-year-old gel di ng with a 3-week hi s
tory of fever of unknown origi n. An hour after injection of
99mTc-l abel ed l eukocytes there was a circul ar i ncrease of
activity caudal to the l ung, suggestive of an abdomi nal
abscess
2. Identification or localization of inflammatory bowel
disease.
3. Evaluation of animals with fever of unknown origin.
4. Identification and localization of tooth root
abscesses.
5. Monitoring disease progression or response to
therapy.
Technique
The procedure can be divided into four steps.
1 . Isolation of leukocytes from peripheral blood
200 ml of venous blood is taken, using a 1 4
gauge needle, into 40 ml acid-citrate dextrose
anticoagulant
20 ml is centrifuged at 2000 G for 10 min to
obtain cell free plasma
the remaining blood is left at room temperature
for 60 min to allow the red blood cells to
sediment
the leukocyte and platelet-rich plasma is
removed and centrifuged at 1 50 Gfor 5 min, the
resulting pellet contains a mixed population of
leukocytes
the superatant is centrifuged at 2000 G for 10 min
to produce cell-free plasma for washing the cells.
Figure 2.30 Inflammation of the smal l i ntesti ne. A scinti
graphic image 1 hour after i njection of 99mTc-HMPAO
labeled leukocytes of the right caudodorsal abdomen of a
1 4-year-old Thoroughbred mare. The horse presented with
weight loss of 3 weeks duration. The scintigram shows two
linear regions of i ncreased activity in the right dorsal
abdomen, suggestive of i nfl ammation of the smal l intestine
2. In vitr labeling
to form 99mTc-HMPAO, 10 MBq/kg 99mTc_
pertechnetate is added to one vial, containing
0.5 mg HMPAO, 7. 6 1g stannous chloride
dehydrate, and 4.5 mg sodium chloride with
nitrogen and immediately mixed with the
isolated leukocytes
after an incubation time of 10 min at room
temperature the labeling is stopped with 10 ml
of cell-free plasma
the cells are centrifuged at 1 50 G for 5 min and
the resulting pellet resuspended in 5 ml cell-free
plasma.
3. Reinjection
the labeled leukocytes must be injected back
into the horse immediately through a 1 2-gauge
catheter.
4. Examination with Gamma-Camera
1 hour after injection static images are acquired
of the area of interest for a minimum of 1 00 000
counts in a 256 ? 256 matrix with a general all
purpose collimator and processed with
dedicated software.
Interpretation
In the normal horse there is activity in the liver, spleen,
salivary glands, and bone marrow reflecting the normal
distribution of granulocytes in the patient. In the horse
a high activity is seen in the lung, which may be caused
by the destruction of damaged labeled leukocytes by
pulmonary i ntravascular macrophages. Free 99mTc and
radiolabel byproducts are excreted via the urinary tract
accounting for a mild increase in uptake in the kidneys
and bladder. As leukocytes migrate into sites of inflam
mation or abscessation there is an increase in activity
(Figures 2. 29, 2. 30) .
HEPATIC SCINTIGRAPHY
Hepatic scintigraphy with 99mTc-labeled sulfur colloid is
the only technique for visualizing the functioning
reticuloendothelial system of the liver in the horse. It is
used to determine hepatic size, shape, and intra
abdominal location of the liver. Lesions greater than
2. 5 em in diameter can be identifed.
Principle
Colloid particles are readily phagocytized by stellate
cells of the liver (Kupffer cells) . Since these cells are
evenly distributed throughout the liver, the displayed
activity corresponds to the size and shape of the organ.
To avoid trapping of the 99tnTc-labeled sulfur colloid in
the reticuloendothelial system of the lungs, agents that
concentrate in the polygonal cells of the liver have to
be used (ethylenediamine-N-N-bis(a-2-hydroxy phenyl)
acetic acid derivatives EDBHA) .
Indications
1 . Assessmen t of the reticuloendothelial system of the
liver.
2. Determination of the size, form, and intra
abdominal location of the liver.
3. Investigation of diseases of the biliary tract.
Technique
The procedure can be divided into four steps.
1 . Synthesis of EDBHA and 99mTc labeling of EDBHA
as described by Theodorakis et ul. ( 1 982) .
2 . Preparation of 99mTc-labeled colloid using a
commercially available kit according to the
manufacturer' s instructions.
3. Examination with Gamma-Camera, 3-50 minutes
after intravenous injection of the
radiopharmaceutical, dorsal, left and right lateral,
and lateral oblique views of the ventral thoracic and
dorsal abdominal areas are acquired.
J
Interpretation
The scintigrams show extensive uptake by the liver, with
less uptake by the kidneys and bladder; and slight
uptake by the lungs. Biliary secretion of radioactivity
into the intestines is evident. The right kidney appears
to be in contact with the caudal margin of the liver. The
separate liver lobes are readily discernible.
Breath hydrogen tests
T M| |
Breath hydrogen measurements can be used to investi
gate gastrointestinal function in horses, although the
techniques and interpretation of results require further
refnement at the time of writing. These tests have
distinct advantages over other tests of gastrointestinal
function in being simple to perform, non-invasive, safe,
and well-accepted by patients. The technique is based
on the fact that, when carbohydrate comes in contact
with bacteria in the gastrointestinal tract, it is fermented
and hydrogen is produced as a by-product. A propor
tion of this hydrogen diffuses from the intestinal lumen
into the portal circulation and is subsequently exhaled
in breath. Since relatively few bacteria are present in the
stomach and small intestine of healthy animals, hydro
gen excreted in the breath originates almost entirely
from the large intestine. Using this knowledge, mea
surement of breath hydrogen can be used to investigate
small intestinal carbohydrate malabsorption, small
intestinal bacterial overgrowth, and to assess oro-cecal
transit time.
Breath hydrogen tests are usually performed by
monitoring exhaled hydrogen concentration following
a test meal containing either an absorbable carbo
hydrate (such as lactose or glucose) or a non
absorbable carbohydrate (such as lactulose) . Studies to
date in horses have shown variation between animals
following the ingestion of identical test meals. Further
research and modifcation of the technique are
required before it can be applied clinically.
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3
Laparoscopy
CA Ragle
Instrumentation
Laparoscopy can best be defined as abdominal explo
ration employing a type of endoscope called a laparo
scope. The word laparoscopy is derived from lapara,
meaning flank, and skopein, meaning to examine.
Laparoscopic procedures are desirable because they
allow improved viewing of the abdomen and are less
invasive than traditional operative techniques. The
number and variety of surgical procedures performed
in horses under laparoscopic guidance has steadily
increased during the last decade and many of these pro
cedures are applicable to equine gastroenterology.
LAPAROSCOPIC EQUIPMENT
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There is a paucity of laparoscopic equipment that is man
ufctured specifically for use in the horse. Luckily, many
of the instruments intended for use in humans can be
used successfully in the horse. Equipment designed for
use in humans is often being used at the far limits of its
capacity in horses because of their larger size. The wide
spread use of arthroscopy in equine hospitals paved the
way for the use of laparoscopy. Since many veterinary
hospitals already own a light source, light cable, video
camera, and a monitor for arthroscopy, laparoscopic
capability only requires the addition of a laparoscope,
insuflator, and operating instruments.
Laparoscope
Laparoscopes are available in various lengths, diame
ters, and angles of view. Scopes longer than 50 cm are
recommended for use in the equine abdomen. A scope
length of 35 cm is adequate for use in foals and can be
used in adults when the structures to be viewed are near
the scope portal. Larger diameter laparoscopes offer
greater light transmission and are less likely to be dam
aged; the most commonly used diameter for equine
applications is 10 mm. A 30 degree angled view scope is
preferred to a zero degree scope because an angled
view permits a more complete examination from a
single scope portal. Many surgeons also prefer the 30
degree scope because of its similarity to the 30 degree
arthroscope, which makes triangulation and instrument
manipulation more familiar. A 45 degree angle of view
laparoscope is also available. The laparoscope is
inserted into the abdomen via a previously placed
sheath and removable trocar. This sheath should be of
adequate length (10.5-15 cm) to extend through the
paralumbar fossa and be sturdy as to protect the laparo
scope against the necessary torque and stresses encoun
tered from manipulating the scope through this often
heavily muscled portal.
Insufflator
Insuflators are used to create and maintain pneumo
peritoneum, which is necessary for clear viewing and
maneuvering the instruments and laparoscope in the
abdomen. Commercial insuflators permit careful
regulation of gas flow and intra-abdominal pressure.
Because of the large size of the equine abdomen, a
high flow insuflator (> 10 l/min) is recommended.
Alternative methods of insuflation include adaptation
of a flow meter to a carbon dioxide tank or using room
air via exhaust from a suction unit. Both of these
methods require use of in-line micropore flters and
close manual monitoring of intra-abdominal pressure.
Carbon dioxide (C02), nitrous oxide (N20) and
41
3 LAPAROSCOPY
helium (He) are the gases most commonly used for
laparoscopic insufflation. Currently carbon dioxide is
the most widely accepted because it is least likely to
cause gas emboli and it is affordable. The primary dis
advantage is that it reportedly converts into carbonic
acid on moist peritoneal surfaces, and this can cause
postoperative discomfort to the patient.
Light source
Light sources provide illumination of the body cavit
during the laparoscopic procedure. For diagnostic and
operative techniques the 150 watt and 300 watt intensi
ties are most commonly used. Although a 150 watt light
source is suitable for some procedures, a 300 watt light
source is well worth the added expense, especially when
video recording or digital image capture is used. Light
sources with xenon or halogen bulbs produce higher
intensity light and more heat than the standard tung
sten light bulb. Photodocumentation (35 mm) is best
accomplished using a flash generator, but video record
ing. digital images, or color thermal prints can be
accomplished with a 300 watt tungsten or a 150 watt or
greater xenon light source.
Video camera and mon itor
A video camera is essential for adequate viewing
because most operative laparoscopic procedures
require both hands for simultaneous manipulation of
instruments. This makes performing surgery under
direct viewing through an eyepiece difcult, if not
impossible. Use of a video camera and monitor also
decreases the risk of contamination of the surgical site
and allows recording of the procedure for later review.
Characteristics of a video camera most important for
use in equine laparoscopy are that it is immersible for
chemical sterilization and that it is compact in size with
suficient resolution and color representation to pro
vide true images. A camera with at least 300 lines of res
olution is recommended. Newer 3-chip cameras have
over 800 lines of resolution. It is important to match the
light sensitivity of the camera with the intensity of the
light source to insure clear and bright images. Monitors
should provide a clear picture, have a minimum screen
size of 33 cm (13 in) (the larger the better and two mon
itors are often helpful), and ample plug-in jacks to allow
addition of a video recorder, film recorder, digital
image capture unit, or thermal printer. A mobile cart
that can accommodate all the various components is
the best way to organize the video system. This facili
tates easy setup and efcient connection of all cables
and tubing at surgery. A vertical stacking scheme allows
placement of the monitor on the top of the unit, pro
viding unobstructed viewing of the screen. When
42
possible the gas source used for insuflation should also
be attached to the cart.
Instrumentation
Instruments for intra-abdominal use should be at least
30 cm in length. Whenever available the longer 43 cm
instruments should be obtained, as the greater length is
rarely a hindrance and very helpful when needed. The
most commonly available diameters are 5 mm and
10 mm, but well-designed, sturdy instruments are more
important than the actual diameter. Use of a cannula is
often omitted in equine laparoscopy, allowing use of
custom-made instruments of varying shapes and diame
ters. A basic instrument set would consist of
two tissue forceps (one grasping and one claw)
scissors
ligature introducer/knot advancer
suction/irrigation cannula
laparoscope cannula and trocar
Knowles uterine forceps
Chambers catheter
30 cm uterine catheter (Figure 3.1)
biopsy instrument and injection needle.
Additional instruments for the complete kit include an
endoscopic clip applier and staplers.
Advanced laparoscopic techniques often include the
use of electrosurgery or laser. These require specialized
instrument depending on the specific technique.
Intracorporeal suturing requires the use of laparoscopic
needle holders and assistant needle holders. A auto
suture device (Figure 3.2) and specialized knots such as
the modifed roeder, jamming anchor knot, and
Aberdeen knot can simplit an otherise technically
challenging procedure. Tissue specimen retrieval bags are
helpful for intraoperative storage and subsequent removal
Figure 3.1 Endoscopy instruments (top to bottom): ligation
loop, suction/lavage tip, scissor, atraumatic grasping
forcep, Semm forcep
Figure 3.2 Disposable auto suturing device (Endostitch,
United States Surgical Corporation, Norwalk, CT)
of diseased tissues. Laparoscopy accessories are rapidly
being developed to minimize the infrequent but impor
tant risks of endoscopy; one example is modifed trocars
that are expanded radially after penetrating the abdomi
nal wall. This creates portals with less trauma and helps to
avoid damage to epigastric abdominal wall vessels.
Surgery table
Several laparoscopic procedures are best performed
with the horse in dorsal recumbancy under general
anesthesia. For these procedures, putting the horse in
the Trendelenberg position (head down and hindquar
ters raised) allows the viscera to displace cranially and
better expose the anatomy of the caudal abdomen.
Although it is possible to raise the end of a standard
surgical table and accomplish this, when the desired
degree of tilt is achieved, the table is usually too high for
the surgeon to operate comfortably without standing
on a stool. For these reasons we have constructed a
laparoscopy table that is low to the ground and when
tilted reaches an optimal height for performing surgery
Figure 3.3 A custom-designed tilt table allows the horse to
be positioned in the Trendelenberg position without
exceeding a comfortable operating height for the surgeon
LAPAROSCOPY 3
(Figure 3.3). The table is tilted using a tripod-style
hydraulic jack (Figure 3.4). The horse should be
secured with a chest brace and tail tie to allow the table
to tilt without the horse slipping forward (Figure 3.5).
Figure 3.4 Hydraulic lift used to tilt the surgery table for
endoscopy on a horse in dorsal recumbency
Figure 3.5 A horse in dorsal recumbency is prepared to be
tilted into the Trendelenberg position. A chest brace prevents
the horse from slipping forward when the table is tilted
43
3 LAPAROSCOPY
Indications for laparoscopy
Laparoscopy is a useful diagnostic tool to evaluate the
abdominal cavity. This evaluation is often aimed at
making a specifc diagnosis or determining prognosis of
intra-abdominal disease. Direct viewing of the abdomi
nal cavity using laparoscopy offers the clinician visual
access to areas which normally cannot be seen using
celiotomy techniques (e.g. epiploic foramen, nephros
plenic ligament, duodenum, etc.). This visual access
permits direct assessment of abdominal viscera, often
more informative and accurate than secondary imaging
or diagnostic techniques. In addition to increased diag
nostic and prognostic ability, laparoscopy also can be
used to provide therapeutic intervention of intra
abdominal disease. A balanced diagnostic approach
that uses laparoscopy in addition to clinical and labora
tory methods offers the greatest opportunity for accu
rate diagnosis, prognosis, and treatment.
The clinician needs to have a clear understanding of
the caveats of laparoscopy. For any meaningful exami
nation of the abdominal cavity to take place adequate
free space between the viscera and body wall must exist.
For this reason laparoscopy is rarely indicated in horses
with signifcant abdominal distension. Adequate view
ing cannot be achieved without adequate room inside
the abdominal cavity. When the intestines are full of
ingesta or gas adequate pneumoperitoneum cannot be
established. The more free space available in the
abdominal cavity the greater the viewing potential and
the lower the intra-abdominal pneumoperitoneum
infation pressure that is needed. Lower intra-abdomi
nal inflation pressures translates to less pain and better
cardiopulmonary function of the horse. Another con
sideration is that standing laparoscopy should be
approached very cautiously in any horse in which
diaphragmatic hernia may be a differential. The poten
tial for creating a pneumothorax must be appreciated
in such horses.
It is also important to note that complete examina
tion of all intra-abdominal viscera and surfaces cannot
be achieved. It is an axiom of laparoscopy that 'what you
see, you see but what you don't, you don't'. Added to
that is 'if you don't look you will never see'.
Laparoscopy of the standing horse offers the best view
ing of the dorsal aspect of the abdominal cavity while
the ventral aspects are best viewed using a ventral
abdominal approach with the horse in dorsal recum
bancy.
Finally it must be emphasized that performing
exploratory laparoscopy on horses will affect the peri
toneal fluid parameters. These have been reported as
an increase in mean leukocyte counts (mean leukocyte
44
count 31960/II) and protein concentrations (mean
2.5 g/ dl) of peritoneal fuid within 24 hours of
laparoscopy. A a comparison abdominal fluid collected
from ponies 24 hours after exploratory celiotomy had
mean leukocyte counts of 137 857/ll and mean protein
concentrations of 4.7 g/ dl 24 hours postoperatively.
Peritoneal fluid cell counts have been reported to reach
their peak about 5 days after celiotomy in normal
horses. It is unknown how long peritoneal values take to
return to preoperative values after celiotomy or
laparoscopy. Operative complications directly related
to diagnostic laparoscopy are rare. The most common
complications are minor punctures of the spleen and
cecum or injury to the epigastric vessels during trocar
placement. These complications are minimized by
proper presurgical preparation of the horse and exer
cising care during portal placement.
Diagnostic laparoscopy has been performed in
horses with chronic weight loss, chronic colic, intra
abdominal hemorrhage, and peritonitis, and for diag
nosing abdominal neoplasia, intestinal adhesions, and
evaluating the reproductive tract. The laparoscope has
been used to view and evaluate rectal tears, rectal pro
lapses, mesocolic ruptures, gastric ruptures, abdominal
abscesses, splenic hematomas, retroflexion of the large
colon, vaginal and uterine tears, and uterine artery rup
tures (Figures 3.6-3.12) An analysis of 105 diagnostic
laparoscopies in the horse revealed an overall sensitivity
of 75 per cent for diagnosis of disease with a specificity
of 18 per cent.
Biopsy of the liver, spleen, and kidney under laparo
scopic viewing is also possible and allows selective sam
pling of abnormal areas. It may also allow for a larger
and possibly more diagnostic specimen than is possible
with a true cut or biopsy gun. Laparoscopy can be used
Figure 3.6 Subcapsular splenic hematoma in a horse
viewed from a left paralumbar fossa portal during
standing endoscopy
following celiotomy to evaluate surgical results if they
are in question (e.g. integrit of an intestinal anastamo
sis or bowel viability) . If a diagnosis indicates a need for
surgical correction, laparoscopy may also be useful;
many surgeries traditionally done via laparotomy or
celiotomy can be performed laparoscopically, including
removal of infected umbilical remnants, repair of
ruptured bladders in neonatal foals, repair of inguinal
herniation in stallions, cryptorchidectomy, ovariec
tomy, granulosa cell tumor removal, hernia repair,
adhesiolysis, colopexy, and removal of cystic calculi.
Laparoscopy can also be used as an educational tool
in improving transrectal palpation skills. A systematic
and thorough approach to transrectal examination is
necessary to assess normal as well as abnormal condi
tions in the abdominal cavity; accurate mental images of
transrectally palpated structures are vital when evaluat
ing conditions of the equine abdomen. Clinicians
cannot expand their palpation skills without a method
to develop accurate mental images and the ability to
Figure 3.7a Retroflexion of the large colon viewed left
paralumbar fossa portal
Figure 3.7b Ventral colon in a dorsal pOSition. Diaphragm
(D), spleen (Sp), and stomach (St) are visible in the
periphery
LAPAROSCOPY 3
Figure 3.8 Laparoscopic cystotomy for removal of a S cm
diameter urolith in a gelding
Figure 3.9 Exploratory laparoscopy for chronic colic
revealed a large melanoma tumor on the left dorsal body
wall of a mare. Smaller melanomas were visible
multifocally throughout the abdomen
Figure 3.10 Laparoscopic-guided aspiration of a hepatic
abscess
45
3 LAPAROSCOPY
Figure 3.11 Incarceration and adhesion of jejunal
mesentery in the inguinal ring. This occurred as a
complication of eventration subsequent to a cryptorchid
castration via an inguinal approach
Figure 3.12 Aspiration of a hematoma in the mesentery of
the small colon. A post-parturient mare was referred for
evaluation of colic and a mass in the caudal abdomen
link that visualization to a spatial orientation and tactile
sense. Videolaparoscopy performed during transrectal
palpation provides the opportunity to link visual, tac
tile, and mental images of important structures in the
normal equine abdomen. Structures that can normally
be palpated transrectally and viewed with videoendo
scopic imaging are: uterine body, uterine horn, ovaries,
bladder, left and right inguinal rings, spleen, nephro
splenic ligament, left kidney, root of the mesentery,
aorta, duodenum, small colon, base and ventral band of
the cecum, and peritoneum. The left dorsal and left
ventral colon and the pelvic flexure may or may not be
palpahle.
46
Surgical procedures
PRESURGICAL PREPARATION FOR
LAPAROSCOPY
Reducing the quantity of ingesta in the gastrointestinal
tract is important prior to elective laparoscopic proce
dures. This requires a minimum of 48-72 hours and is
accomplished by feding reduced quantities of feed or
using a low bulk/residue diet such as a pelleted ration.
The degree to which the gastrointestinal tract needs to
be debulked depends on the procedure and the
amount of intra-abdominal body fat. Predicting the
amount of internal body fat can be difcult, as it does
not always correlate with the outward appearance of the
horse. Transrectal palpation can help determine the
amount of fat present in the mesorectum and caudal
abdomen. In the standing patient, adequate viewing of
the right cranioventral abdomen requires the greatest
amount of ingesta reduction. Reduced bulk is also more
important when the patient is operated on in dorsal
recumbancy with the rear quarters elevated
(Trendelenberg position) . In addition, the longer the
procedure is anticipated to last, the more important the
preoperative preparation. The horse should have a con
cave shape to the paralumbar fossa when properly pre
pared prior to laparoscopy. Laparoscopy is preceded by
12-24 hours of withholding feed to reduce stomach
contents; water intake is not restricted.
It is important to assess the tractability of the patient
when considering standing procedures. Immature and
untrained patients are better candidates for operation
under general anesthesia. A tilt table (end to end) and
ventilatory support should be available when
laparoscopy is performed with the horse under general
anesthesia. Restraining stocks for standing procedures
should have adjustable sides to allow unimpeded
manipulation of the scope and the instruments.
Preparation of the abdomen for aseptic surgery is a
necessary routine step prior to laparoscopy. The left
and right flanks from dorsal mid-line to the fold of the
flank ventrally, and from caudal to the tuber coxae to
the 15th rib cranially should be prepped for surgery.
When exploratory laparoscopy is performed with the
horse under general anesthesia and in dorsal recum
bancy, the entire ventral abdomen is prepared for
surgery. It is important to shave and prepare 5-10 cm to
either side of the ventral midline for instrument portals.
Laparoscopy, whether performed standing or under
general anesthesia, requires the abdomen to be inflated
with gas. It is recommended that intra-abdominal
pressures he the minimum that allows adequate
viewing. This minimizes patient discomfort in standing
horses and the negative effects of increased pressure on
cardiopulmonary function in anesthetized horses.
Cardiopulmonary function is least affected when intra
abdominal pressure is below 20 mmHg.
TECHNIQUE FOR DIAGNOSTIC
STANDING LAPAROSCOPY
The horse is sedated with either a combination of
xylazine (0.3-0.9 mg/kg i.v.) and butorphanol
(0.01-0.033 mg/kg i.v.) , or detomidine (0.025 mg/
kg i.v.) . Pre-operative placement of an intravenous
catheter facilitates further drug administration. The
patient's tail is raised and tied to the stocks or ceiling.
This adds to stability of the patient and improves safety
for equipment and personnel. Tying the tail up can pre
vent the laparoscope or instruments from being
wedged between the patient and sidebar of the stocks if
the patient were to fall. Rectal palpation should
precede laparoscopy to confrm clearance in both
paralumbar areas for trocar placement. A sterile drape
is placed on the patient from head to tail. The drape is
placed over the dorsum covering the sides of the horse
and stocks. The drapes are attached to the patient
around the neck and tail using non-penetrating towel
clamps. It is important not to attach the drapes to the
stocks as they can easily be dislodged or torn when the
patient moves. Fenestrations are made bilaterally at the
flanks and sealed to the patient using adhesive strips or
flm. Local anesthesia is obtained by injecting 20-30 ml
of mepivacaine (or an equivalent local anesthetic
agent) in the center of the paralumbar fossa through a
2.5 em, 20-gauge needle. Pneumoperitoneum is estab
lished through a 30 cm x 5 mm metal uterine catheter
placed into the right paralumbar fossa through a 1.5 cm
incision in the skin. Use of a long metal uterine catheter
or Verse needle ensures that the gas is insuflating the
abdominal cavity and not being placed into the
retroperitoneal space. The catheter is subsequently
removed and the laparoscopic cannula with sharp tro
car is placed through the same site.
Cannulas can be placed without pneumoperi
toneum or after the abdominal cavity has been inflated.
The author prefers to inflate the abdomen frst.
Abdominal distension should be adequate to prevent
collapse of the abdominal wall during trocar insertion.
The catheter used for insufflation is removed and the
same site is re-used as the scope portal. The cannula
with the sharp trocar should be inserted with a frm
twisting motion, being careful to prevent excessive pen
etration of the abdominal wall. Directing the trocar in a
slightly ventral direction prevents iury to the
LAPAROSCOPY 3
sublumbar muscles and kidney. The trocar should not
be directed excessively cranially or caudally as damage
to the cecum or broad ligament of the uterus could
result. Gas will escape from the trocar/cannula when
the abdominal cavity is entered; the trocar is replaced
by the laparoscope and abdominal exploration begins.
Detailed descriptions of the laparoscopic abdominal
anatomy of the standing horse, the dorsally recumbent
horse, and the dorsally recumbent foal are available.
When performing laparoscopy in the standing horse it
is helpful to think of the abdominal cavity in terms of
regions and spaces (Figure 3.13) . Each of these regions
and spaces can be viewed by manipulation of the laparo
scope from a single portal in the left and right flank.
The abdomen is divided at the level of the cecum into a
cranial and caudal region. The caudal region consists of
two spaces, right caudal and left caudal, that are on the
respective sides of the mesocolon of the descending
colon. The cranial region is divided into four spaces.
From the right side the right lateral and right medial
spaces can be accessed. The right lateral is viewed
between the cecum and the body wall. The right medial
is viewed between the root of the mesentery and the
cecum. The left cranial region is divided into left lateral
and left medial spaces. The left lateral space is between
the spleen and body wall. The left medial space is
between the mesocolon of the descending colon and
the spleen.
Laparoscopic examination from the right flank is
performed in a clockwise direction around the
abdomen. It is important to develop a consistent and
thorough sequence of examination. The following
structures can be seen and evaluated from the right
side: the base of the cecum, root of the mesentery,
descending duodenum, right lobe of the liver,
Figure 3.13 Standing laparoscopy allows a thorough
examination of the dorsal aspect of the abdominal cavity
47
3 LAPAROSCOPY
diaphragm, perirenal fat around the right kidney, parts
of the small intestine and large colon, small colon and
rectum, right ovary and horn of the uterus in mares,
and the right internal inguinal ring in males.
The left side of the abdomen is explored in an anti
clockwise direction. Upon insertion of the scope, the
nephrosplenic ligament, perirenal fat, and the caudal
proximal border of the spleen can be seen. The scope
can be passed cranially past the spleen where the dorsal
surface of the stomach, the diaphragm, and the left lat
eral lobe of the liver are seen. A the scope is angled
ventrally, parts of the small intestine, the large colon,
the mesentery of the small intestine and the small colon
can be seen. Usually peritoneal fluid can also be
obselVed. A the scope is angled caudally toward the
pelvic cavity, the left ovary and uterus can be evaluated;
in males, the left inguinal ring is seen. The bladder and
rectum may also be examined.
Depending on the horse's problem, entering both
sides of the abdomen with the laparoscope may not be
indicated. However, to completely evaluate the
abdomen in a horse with an unknown problem, enter
ing both sides is necessary. Additional portals can be
established for instruments. These may be located in
the paralumbar fossa or in the 17th and 16th intercostal
spaces whichever offers the best access. A Chambers
catheter works well to atraumatically manipulate viscera
to allow more complete laparoscopic exploration.
Common procedures utilizing the standing laparo
scopic approach include splenic, renal, hepatic, lymph
node, and abscess biopsies. When performing a splenic
biopsy the laparoscope is inserted into the left paralum
bar fossa and the spleen is directly visualized and a
biopsy site selected. Biopsy of either the left or right
kidney is performed via a left or right flank approach
respectively. The caudal border of the kidney is the best
laparoscopic biopsy site. The hepatic biopsy is
approached from the right flank area and requires
longer instruments (uterine biopsy forceps) to obtain a
sample. Abdominal abscesses and lymph node
aspiration can also be performed under laparoscopic
guidance.
LAPAROSCOPIC TECHNIQUE FOR THE
VENTRAL ABDOMINAL APPROACH
Preoperative procedures include a thorough history,
physical examination, and a complete blood count.
Transrectal palpation should be performed in all horses
large enough to permit the examination. Horses are
withheld from feed or placed on a low residue diet (e.g.
complete pelleted feed) for 24-72 hours prior to the
operation. The aim is to reduce the amount of ingesta
48
in the large colon to provide adequate free space in the
abdominal cavit for viewing and manipulation of the
genital tract. This is especially important in obese
horses. Intraoperative anesthesia monitoring should
include arterial blood pressure, arterial blood gases,
end-tidal CO2 tension, and electrocardiography.
Ventilatory function should be supported by positive
pressure ventilation. Perioperative antibiotics (pro
caine penicillin G, 22 000 IU /kg i.m. q. 12 h) are insti
tuted prior to surgery and continued for 24 hours.
Horses are anesthetized, placed in dorsal recum
bancy, and aseptically prepared and draped for abdom
inal surgery. The patient's tail is secured to the
operating table and a padded rope is placed across the
front of the chest to prevent patient displacement dur
ing tilting of the table. A urinary catheter is passed to
facilitate decompression of the bladder. A 1.5 cm inci
sion is made with a number 11 blade, on the midline at
the level of the umbilicus and a teat cannula is placed
for abdominal insufflation. Insuflation is achieved by
use of a high-flow electronic laparoflator or by a CO2
cylinder equipped with a regulator, flow meter, and
pressure gauge. When insufflation reaches intra
abdominal pressures of 20 mmHg, the teat cannula is
removed and the laparoscopic sleeve with sharp trocar
is placed through the abdominal wall. The abdomen
should be insuflated sufciently to allow placement of
the sharp trocar without excessive collapse of the
abdominal wall. The sharp trocar is removed from the
sleeve and replaced by the laparoscope (10 mm x
57 cm, 30 degree angle). Videolaparoscopic viewing of
the abdominal cavity begins and the area of the pelvic
inlet is identifed. At this point the table is tilted elevat
ing the rear quarters of the patient and displacing the
abdominal viscera cranially. When the ventral surface of
the uterus is seen tilting of the table is stopped. The
angle of incline is approximately 30 degrees from the
horizontal.
Instrument portals can be established as needed dur
ing the exploration. Portals are established by making a
1.5-cm skin incision followed by a 1-cm incision in the
external sheath of the rectus abdominis muscle. The
portals are completed by blunt penetration of the
remaining abdominal wall, using a 5-mm or 10-mm con
ical tip trocar. Instruments are placed through these
portals without a cannula. A Chambers mare catheter
functions well to manipulate viscera to aid viewing and
provide tactile feedback. The surgeon can operate from
either side of the horse. If there are assistant surgeons
one is opposite the primary surgeon and the second is
with the primary surgeon. The video monitor is placed
opposite the primary surgeon (Figure 3.14). It can be
advantageous to have two video monitors, one on either
side of the horse. The surgical table can be tilted to
Figure 3.14 Horse undergoing laparoscopy in the
Trendelenberg position. This approach allows better
access for operative procedures of the caudal abdominal
cavity
elevate either the head or the rear quarters to improve
viewing of the cranial and caudal aspects of the
abdomen respectively. When the exploration is com
plete the operating table is returned to a horizontal
position. The abdomen is decompressed by allowing
the CO2 to escape through the laparoscopic sleeve.
After removal of the sleeve, the portal is closed with a
single simple interrupted suture of 3 polyglactin 910,
and skin is apposed using a subcuticular simple contin
uous pattern of 0 polyglyconate. Instrument portals are
closed with a simple continuous subcuticular pattern of
o polyglyconate and the skin edges are secured by appli
cation of cyanoacrylate. The portals are covered with
elastic tape for added protection in the early postopera
tive period.
Phenylbutazone (4.4 mg/kg p.o. q. 12 h) is adminis
tered for 1-3 days after surgery to reduce postoperative
inflammation. Discharge instructions suggest the horse
be confined in a stall or small paddock and walked in
hand for 2 weeks. Exercise or free turn out is permitted
thereafter. Feeding instructions are for a gradual return
to the horse's normal diet over the course of 1 week.
Intraoperative complications are minimal with
proper preoperative preparation of the horse.
Inadequate visualization of the genital tract can occur
LAPAROSCOPY 3
because of too much ingesta in the gastrointestinal tract
and/ or marked distension of the urinary bladder if not
catheterized. These problems can be eliminated by
increasing the duration of feed withdrawal or using a
low residue diet (complete pelleted feed) preopera
tively and maintaining a urinary catheter during the
operation. Damage to vessels of the ventral abdominal
wall (primarily the deep epigastrics) can occur during
portal placement. This is best avoided by using sharp
dissection only through the level of the external rectus
sheath. A conical obturator is adequate and safe for
completion of the portal. Commercial portal access
devices are available to minimize abdominal wall vessel
injury (InnerDyne, Inc., Sunnyvale, C).
BIBLIOGRAPHY
Blackfordj T, Schneiter H L, VanSteenhouse Lj, et at. (19R6)
Equine peritoneal fluid analysis following celiotomy.
Equine colic research. Proceedings of the Second Symposium at
the Univesity of Georgia, pp. 130-2.
Boure L, Marcoux M, Laverty S (1997) Laparoscopic
abdominal anatomy of foals positioned in dorsal
recumbency. Vet. Surg. 26:1.
Boure L, Marcoux M, Lavoie j P (1997) Laparoscopic
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Boure L, Marcoux M, Lavoiej P (1998) Use of laparoscopic
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Edwards R B, Ducharme N G, Hackett R P (1995)
Laparoscopic repair of a bladder rupture in a foal. Vet.
Surg. 24:60.
Embertson R M, Bramlage L R (1992) Clinical uses of the
laparoscope in general equine practice. Proc. Am. Assoc.
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Fischer A T (1991) Standing laparoscopic surgery, Vet. Ctin.
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Fischer A T (1999) Laparoscopically assisted resection of
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214:1813.
Fischer A T,jr (1997) Diagnostic and surgical laparoscopy. In
Equine Endosco
p
2
nd
edn,j L Traub-Datgatz, C M Brown
(eds). C V Mosby, St Louis, pp. 217-31.
Fischer A T jr, Vachon A M (1992) Laparoscopic
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inguinal repair in two stallions.] Am. Vet. Med. Assoc.
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Galuppo L D, Snyder j R, Pascoe j R (1995) Laparoscopic
anatomy of the equine abdomen. Am.] Vet. Res. 56:518.
Galuppo L D, Snyder j R, Pascoe j R et at. (1996)
Laparoscopic anatomy of the abdomen in dorsally
recumbent horses. Am.] Vet. Res. 57:923.
Gross M E,jones B D, Bergstresser D R et at. (1993) Effects of
abdominal insufflation with nitrous oxide on
cardiorespiratory measurements in spontaneously
breathing isoflurane-anesthetized dogs. Am.] Vet. Res.
54:1352.
49
3 LAPAROSCOPY
Hendrickson D A, Wilson D G (1997) Laparoscopic
cryptorchid castration in standing horses. Vet. Surg. 26:335.
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Saunders, Philadelphia, p. 47.
Hurd W W, Pearl M L, DeLancey J 0, et al. (1993)
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673-676.
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Palmer S E (1993) Standing laparoscopic laser technique for
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50
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.J. Am. Vet. Med. Assoc. 210:1121.
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4
Pa rasite-associated gastroi ntesti na I
disease
S Love
This chapter focuses on clinical aspects of the principal
parasite infections of the horse, i.e. large strongyles,
small strongyles (cyathostomes), tapeworms, and
ascarids. Brief notes are included on some minor infec
tions including bots, Coccidia spp., Crptosporidium spp.,
Oxyuris pqui, and Strongyloides westeri.
INTRODUCTION
Parasite-associated gastrointestinal diseases are almost
certainly under-diagnosed. This may reflect a compla
cent attitude on the part of veterinary surgeons and/or
owners based upon their over confdence in the effcacy
of modern anthelmintic products. However the princi
pal reason for poor clinical recognition of parasitic
intestinal disease is the lack of availability of diagnostic
methods of suffcient sensitivity and specifcity. Much of
what is known about the clinical aspects of parasitic
infections of the horse is derived either from general
observations undertaken during artifcial infections
(large strongyles, cyathostomes, ascarids) or more
recently fom quantitative epidemiological studies on
colic risk factors (cyathostomes, tapeworms). Although
the cumulative body of evidence supports a role for
various parasites in many types of colic, weight-loss
syndromes, and diarrhea, defnitive information will
require detailed longitudinal, clinicopathological stud
ies, ideally on both experimentally infected animals as
well as on cohorts of naturally infected animals. The
development of serodiagnosis of Anoplocehala perfoliata
has advanced the knowledge available on clinical
aspects of tapeworm infection by completion of
case-control studies on colic cases. Although it will be
technically complex to produce similar diagnostic
assays for cyathostome and large strongyle infections,
they are essen tial tools for objective studies on disease
prevalence, clinical effects, and therapy.
FEATURES OF EQUINE PARASITE
INFECTIONS
Occurrence of disease
The occurrence of parasite-associated disease depends
on three main factors
l. the abundance of parasite larvae and eggs in the
external environment
2. the numbers of parasites of one species within an
individual animal
3. the management of the horses.
The abundance of parasite larvae and eggs in
the exteral environment
This varies according to ambient temperature and
humidity so that there is variation with season and also
geographical region. In temperate climates, the highest
numbers of larvae on pasture usually occur in late sum
mer or early autumn. Pasture larvae and eggs survive
best in wet, mild conditions but the larvae die quickly
in dry, hot weather. Both eggs and larvae are fairly
resilient to frosty conditions. Ascarid eggs (the infective
stage) are particularly adapted to survive for prolonged
periods of many months (even years) in the external
environment. The numbers of pasture eggs and larvae
are affected by the levels of worm egg output by grazing
animals, and this is intrinsically related to the intensity
of the adult worm burden (see below).
53
4 GASTROINTESTINAL PARASITES AND THEIR CONTROL
The number of parasites of one species within
an individual animal
This varies with
the level of pasture contamination (see above)
host immunity: this occurs as an absolute feature in
ascarid infections in animals greater than 2 years of
age but is much more variable in large strongyle,
cyathostome, and tapeworm infections
individual propensit to infection: it is a fact that,
with any parasite infection, in all host species the
majority of worms are present within the minority
of animals, i.e. there is natural predisposition of
certain individuals to parasite infection.
Management of the horses
The likely exposure to parasite infection via contami
nated pasture will be affected by the grazing practices
and the parasite control program applied on the pas
ture, and also on any premises on which the animal(s)
were kept previously. It is always important to consider
this information as it pertains to the whole grazing
group, not just to the individual animal.
Summary of equine parasite biology
Understanding the timing of onset of clinical signs and
aspects of treatment! control requires a working knowl
edge of the essential features of the biology of the main
pathogenic parasites.
Strongyles
The strongyles, synonym 'red worms', exist in two sub
families.
1. Strongylinae (large strongyles), these are Strnglus
vulgars, S. edentatus, S. equinus, and Trodontohorus
spp. The essential features of the large strongyles
include
a direct, migratory (intestinal arteries) life cycle
(except for Triodontophorus spp.)
a pre-patent period of 6-10 months
the adult stages are large intestinal
all stages are susceptible to modern
anthelmintics.
2. Cyathostominae (small strongyles/ cyathostomes)
There are 8 genera and 40 species of cyathostomes. The
essential features include
a direct, non-migratory life cycle
a pre-patent period of 6-20 weeks
a propensity for arrested larval development within
the large intestinal mucosa (for as long as 2-3 years)
the adult stages are large intestinal
54
the luminal adults, luminal larvae, and developing
mucosal larvae (Plate 4.1) are susceptible to
modern anthelmintics
arrested larvae are poorly susceptible to modern
anthelmintics (this varies with different products)
resistance to benzimidazole compounds is common
resistance to pyrantel salts is apparently increasing.
Ascarids
There is one species of ascarid - Parscars equorum. Its
essential features include
a direct, migratory (gut-liver-lung-gut) life cycle
a pre-patent period of 3 months
the adult stages are small intestinal
prolifc egg producers
adult and luminal laral stages are susceptible to
modern anthelmintics
migrating larval stages have low susceptibility to
modern anthelmintics.
Tapeworms
The three species of tapeworm that afect horses are
Anoplocehala perfoliata (common) (Plate 4.2), A. magna,
and Paranolocehala mammillana. Their essential fea
tures include
an indirect life cycle with the oribatid mite as the
intermediate host
a pre-patent period of 6-10 weeks
the adult stages are either cecal (A. peroliata) or
small intestinal (A. magna and P. mammillana); the
latter can also occur in the stomach
A. peroliata and A. magna are susceptible to pyrantel
salts given at a high dose rate.
PATHOGENESIS OF PARASITIC
GASTROINTESTINAL DISEASE
Pathophysiological details of equine parasite infections
have only been studied at a superfcial level. A consider
ation of the existing facts and hypotheses is helpful in
understanding clinical parasitism.
Enteropathy is known to occur with large strongyle,
cyathostome, and tapeworm infections, but not with
ascarids. Particularly with cyathostomes, there is an
inflammatory reaction at the site of laral penetration
into and emergence from the large intestinal mucosa.
The severity of the typhlitis/colitis varies from a mini
mal reaction to marked, diffuse lesions with edema,
discoloration and local lymph node enlargement. The
inflammatory lesion causes transmucosal protein
leakage. Foci of fbrous reaction occur where migrating
large strongyle lalVae re-enter the large intestine, and
there can be local intramural abscesses at these sites.
Adult large strongyles also feed on the mucosal surface
causing superfcial damage. Tapeworms cause regions
of ulceration and edema at the ileocecal valve, the
severity depending on the numbers of tapeworms pre
sent. Ascarids do not cause intestinal lesions but it is
thought that their presence is indicated by their con
sumption of nutrients from the host's intestinal tract.
Intestinal motility changes have been documented
for both large strongyle and cyathostome infections.
Although the precise mechanisms of this effect are not
known, it has been hypothesized that these may result
from either pharmacological activity of substances
released from the parasites and/or a host response to
such substances. The proposed pharmacological sub
stances may either exert their effect directly on intesti
nal muscle or nelVes, or they may alter intestinal
motility via alteration to intestinal blood supply (see
below). It is possible that tapeworms produce similar
pharmacodynamic substance(s).
Altered mesenteric blood fow in animals with
Strnglus vulgars infestations is a long-recognized patho
genic event during lalVal migration, but the detailed
pathophysiology remains unclear. It may be a conse
quence of substances produced by the parasite (see
above), but it is no longer considered to be the result of
physical thromboembolism from arterial lesions (Plate
4.3). Reduction in mesenteric blood fow can result in
either single or multiple areas of ischemic bowel wall, i.e.
the entit known as non-strangulating intestinal infarction.
CLINICAL FEATURES OF PARASITIC
ASSOCIATED DISEASE 'ENTITIES'
Non-strangulating intestinal infarction
This is rare nowadays, reflecting the current low preva
lence of Strnglus vulgars infection. The preliminary
signs are the presence of either anorexia or fever, and
clinical signs include
severe colic (sometimes recurrent bouts)
cardiovascular compromise
endotoxemia
sanguinous peritoneal fluid
reduced borborygmi
nasogastric reflux
distended viscus palpable per rectum
occasional thickening or pain found on rectal
palpation of the mesenteric arter
ischemic areas of either small and/or large
intestine found at exploratory laparotomy
PARASITE-ASSOCIATED GASTROINTESTINAL DISEASE 4
mesenteric arterial thickening and/or thrombus at
post-mortem examination with possible grossly
visible S. vulgars lalVae.
Mild strongyle-associated colic
This is suspected if there is non-specifc mild colic and
often occurs if there is a sub-optimal parasite prophyl
axis program and/or frequen t intake of new animals of
unknown worming history on the premises. It has been
proven to occur when there is poor control of cyatho
stomes, i.e. it is not just a large strongyle disease.
Cecocolic intussusception
There is recent evidence of cecocolic intussusception
associated with heavy cyathostome infections, particu
larly in young (less than 4-year-old) horses. The clinical
features are detailed in Chapter 14. There may be con
current signs of other cyathostome entities (see below).
Larval cyathostomosis (see Chapter 21)
This is more common in Europe than in other regions.
Often an individual animal is affected but it can also be
a group condition. There is a seasonal prevalence with
the condition seen more during late winter and early
spring than at other times of the year, and there is also
an age prevalence, the condition being more common
in animals less than 6 years old. Clinical signs include
sudden, rapid weight loss, possibly reaching
emaciation within 10 days
diarrhea, sudden onset
mild to severe colic
variable demeanor, often fairly bright
not usually endotoxemic
peripheral edema
fever
cyathostome lalae are often grossly evident on
close inspection of feces
recent anthelmintic dosing may precipitate the
onset of disease by removing hypothesized
'feedback' of intestinal to mucosal cyathostomes,
and stimulating resumption of development of
lalVae arrested in development within the mucosa
mucosal edema with gross thickening and a
'peppered' appearance on close examination of
cecal and/ or colonic surface at post-mortem
examination.
Cyathostome-associated weight loss in young
horses
This occurs in animals up to 6 years of age. It can affect
individuals or a group of animals and is indicated by
55
rapid, marked weight loss
peripheral edema
fever.
Although large strongyles are now rare, mixed large
and small strongyle infections, i.e. 'strongylosis' will
produce similar clinical features.
Recurrent cyathostome-associated diarrhea
This occurs in aged ponies and is indicated by
repeated bouts of diarrhea
weight loss
anorexia.
Autumnal cyathostome-associated weight loss
in weanlings
This affects foals 69 months old, i.e. older foals eating
signifcant quantities of grass, and affects both indivi
duals and groups of animals. It is indicated by
sudden poor thrift, often in mild, damp conditions in
September and October.
Ascarid-associated ill thrift
This is a common condition indicated by non-specifc ill
thrift or weight loss in older foals, weanlings and year
lings, that can progress to emaciation unless treated.
Occasionally there are concurrent non-specifc respira
tory signs including a nasal discharge and cough.
Ascarid impaction (Plate 4.4) (see Chapter 13)
This rare condition occurs in older foals, weanlings,
and yearlings causing
colic
a distended small intestinal viscus that is detected
on radiography/ultrasonography or by palpation
per rectum if examination is feasible
minimal cardiovascular compromise
nasogastric reflux.
Tapeworm-associated colic
This is indicated by non-specifc mild (spasmodic) colic
and ileal impaction together with serological! epidemio
logical evidence of tapeworm infection. The clinical
features are detailed in Chapters 9 and 13.
INVESTIGATION OF SUSPECTED
PARASITE-ASSOCIATED DISEASE
There are no distinctive clinical features which enable a
definitive diagnosis of gastrointestinal parasitism, and
56
in only a few instances are there specifc ancillary tests
by which confrmation of an entity can be achieved.
Clinical history
When a horse is presented with signs of weight loss
and/ or diarrhea and/ or colic it is appropriate to inves
tigate the history relevant to parasitism. The key points
to consider are
grazing management: is it full time, part time, or
not at all?
anthelmintic dosing:
is it individual or shared?
if it is shared, how many are
in the cohort?
what is the frequency and
product(s) used for both
individual diseased animal
and grazing cohort?
if known, what was the dos
ing regimen in any previous
ownership(s)?
previous evidence of parasite-associated disease on
premises and/ or in grazing cohort?
It is easy to over-interpret and/or over-simplif this
information. Certainly parasite-associated diseases com
monly occur in animals which have been receiving
prophylactic anthelmintics. Common reasons for
failure of parasite control programs include
anthelmintic resistance
incorrect dosing intervals
lack of synchronization of dosing of anthelmintics
in grazing cohort
acquisition of horses infected with worm stages
unaffected by 'standard' anthelmintic dosing:
particularly cyathostomes arrested in development
in large intestinal mucosa and/or migrating ascarid
larvae. Cyathostome-associated illnesses can occur
years after the parasites were ingested (mucosal
arrested stages can survive multiple doses of
anthelmintics) so that evidence of good parasite
control applied to the current premises should not
be taken as conclusive evidence on which to
exclude parasitism.
Fecal tests
Large strongyle and cyathostome eggs
In clinical practice there is often too much diagnostic
emphasis given to the fecal worm egg count (FC). In
particular, negative counts are often inappropriately
used as the basis of excluding parasitism. It should be
borne in mind that the pathogenic stages of both large
strongyles and cyathostomes are larval, i.e. not egg-
laying stages. Also, it is notoriously difficult to correlate
the FC with the size of the parasite burden giving
further confusion to interpretation of test data. A a gen
eral guideline, in an individual clinical case, a strongyle
fecal egg count of 200 epg or less is low, whereas more
than 1000 is high. Probably it is more meaningful to
obtain FC from at least half the grazing cohort and
use the data as an overall (but rather insensitive) index
of parasite challenge to the individual clinical case.
Certainly FC results for animals suspected of either
large strongyle and/or cyathostome-associated illnesses
should only be used as possible support of a positive
diagnosis, and never to rule out a diagnosis.
Ascarid eggs
The pathogenic stages of ascarids are the egg-laying
luminal adults. Therefore ascarid infection should be
strongly suspected in an animal less than 2 years old
with non-specific signs of ill thrift and a high ascarid
fecal egg count. Ascarids are prolific egg producers and
counts of several (or even tens of) thousands can occur.
Note that although FCs have high sensitivity for
ascarid infection, they have low specificit, it is there
fore possible that an ill thriven youngster could have co
existing diseases.
Tapeworm eggs
Tapeworm infection is not readily detected by the
'routine' methods for FC utilized in most commer
cial laboratories, but special centrifugation/flotation
methods have been developed and should be utilized
when tapeworm infection is suspected.
Cyathostome larvae
A simple fecal examination can be very useful for evi
dence of cyathostome-associated illness: larvae are often
present in large numbers in the feces and can be
detected by careful visual inspection of samples and/ or
microscopy. The larvae are very thin, about 0.5-1.5 em
in length and white, pink, or red. If not evident on
visual inspection, then dilution of the sample with tap
water in a petri dish and screening with a light micro
scope is readily performed.
Hematology/blood biochemistry
There are no specific blood analysis results associated
with parasitic infections but both large strongyle and
cyathostome infections can result in
neutrophilia
hypoalbuminemia
hyperglobulinemia (especially betaglobulinemia
detected by serum protein electrophoresis)
low albumin:globulin ratio
increased serum alkaline phosphatase
anemia
Hypoalbuminemia may be only minor in ascarid infec
tions.
Serology
A quantitative serological assay has been validated for
tapeworm infection and successfully used to investigate
colic cases: it is commercially available in the UK.
TREATMENT
Symptomatic aspects
In parasite associated illnesses the likely principal clini
cal symptoms to be addressed in the treatment plan will
be
1. Colic, treat with
analgesics (and possibly surgery for either
ischemic intestine, Stronglus vulgars or
ileal! cecal disorders, Anoplocephala perfoliata)
(see Chapters 13 and 14).
2. Diarrhea, typically cyathostome-associated, treat
with
antidiarrheal agents; codeine phosphate elixir
given 'to effect', or guideline regimen is
3 mg/kg t.i.d. (days 1-9) then 2 mg/kg t.i.d.
(days 10-14) then 1 mg/kg t.i.d. (days 15-20)
fluid/electrolyte support (details in Chapters 9
and 20); oral or stomach tube routes may be an
option for cases with moderate to mild severity
anti-inflammatory treatment (of
typhlitis/ colitis); not NSAIDs (which could
exacerbate protein-losing enteropathy);
preferred protocol is oral prednisolone at
1 mg/kg s.i.d. (in the morning, days 1-20)
followed by 1 mg/kg every other day (in the
morning, days 21-40). It is hypothesized that in
addition to anti-inflammatory effects, the
corticosteroid renders mucosal cyathostomes
more susceptible to an anthelmintic via
reduction of the immune mechanisms which
contribute to mucosal arrested larval
development.
nutritional support to counteract any weight
loss.
Anthelmintic aspects
In cases where parasitism is either confirmed or where
the index of suspicion of parasitism is high, then it is
usually appropriate to include anthelmintics in the
57
treatment plan. However, clinicians should consider
the importance of potential side effects of anthel
min tics when given in clinical disease. Specifcally,
there are reports which suggest possible associations
beteen recent anthelmintic administration and onset
of either parasite-associated colic or cyathostomosis.
Therefore in a clinical situation, treatment with
anthelmintics might either exacerbate the disease
and/ or induce overt signs of disease in apparently
healthy grazing companions of the affected cases.
It should be emphasized that the recommended
anthelmintic usage for treatment of clinical disease
states has a different basis from that of parasite control
programs (see below). Specifc anthelmintic therapeu
tic regimens are preferred for the different parasite
associated diseases.
This condition can be treated with
oral ivermectin 0.2 mg/kg, or
oral moxidectin 0.4 mg/kg, or
oral oxfendazole 10-50 mg/kg, or
oral fenbendazole 7.5 mg-l0 mg/kg on
5 consecutive days.
Cyathostomosis and cyathostome-associated
conditions
Affected clinical cases are treated with the following
regimen
days 1-5 fenbendazole 7.5 mg/kg on 5
consecutive days
day 6 ivermectin 0.2 mg/kg or moxidectin*
0.4 mg/kg
consecutive days
day 21 ivermectin 0.2 mg/kg or nil (if
moxidectin" was given on day 6)
consecutive days
day 36 ivermectin 0.2 mg/kg or moxidectin
0.4 mg/kg
thereafter follow the protocol for grazing cohorts
(see below).
*moxidectin has the potential for toxicity in thin, debilitated
animals, and careful computation of dosage is required.
**moxidectin has persistent action such that it is inappropriate
to treat as ofen as the lO-day intervals suggested for ivermectin.
In-contact grazing cohorts are treated with the follow
ing regimen
days 1-5 fenbendazole 7.5 mg/kg
58
day 6
days 31-35
day 36
day 61-65
day 66
days 91-95
day 96
either ivermectin 0.2 mg/kg, or
moxidectin 0.4 mg/kg
fenbendazole 7.5 mg/kg
moxidectin 0.4 mg/kg.
Ascarid-associated disease
Ascarid-associated disease can be treated with either
oral ivermectin 0.2 mg/kg, or
oral moxidectin 0.4 mg/kg, or
oral fenbendazole 10 mg/kg on 5 consecutive days, or
oral levamisole 8.0 mg/kg (this drug is not licensed
in Europe).
Repeat treatment at 14-21 day intervals on three
targeted occasions.
Tapeworm-associated colic
This condition is treated with either
oral pyrantel pamoate 13.2 mg/kg (in the US), or
oral pyrantel embonate 38 mg/kg (in Europe).
PARASITE CONTROL PROGRAMS
Parasite-associated diseases are largely preventable by
sustained control programs, but it should be empha
sized that no single parasite control program is recom
mended for every management situation. The strategy
adopted should be custom designed with regard to age
and type of animals, the local environment and climate,
and the practicalities of available labor.
The objective of a parasite control program is to
minimize beteen-horse transmission of the infective
stages. This is achieved mainly by preventing infective
larvae (strongyles) and eggs (ascarids) from contami
nating the pasture. The details of the life cycle of tape
worms are not known but they are controlled by
keeping their total numbers down.
Knowledge about the parasites' life cycles and their
susceptibility to anthelmintics is used to design control
programs.
Large strongyles have a long migration period
within the host when the parasites are readily
susceptible to modern anthelmintics.
Hosts have a lifelong susceptibility to cyathostomes.
Hosts cannot be rendered 'worm free' by dosing
the larval stage of cyathostomes - every horse has
cyathostomes arrested in development within the
intestinal mucosa where they are protected from
anthelmintic action.
Cyathostome populations readily develop
anthelmintic resistance - benzimidazole resistance
is ubiquitous and pyrantel resistance is becoming
increasingly common in the United States.
Frequent dosing selects for anthelmintic resistant
parasite populations.
Strngl (large and small) eggs and larvae survive in
feces or on herbage for months in moist, temperate
climatic conditions.
Ascarid eggs are highly resilient and can survive for
years in the external environment.
Age immunity to ascarids occurs.
Anthelmintic compounds are not all equally
effective against all parasite species.
Parasite control programs should focus on
strongyles, especially cyathostomes.
Ascarids will be controlled incidentally by cyathostomc
interal dosing programs but not by either strategic or
selective dosing options (see below).
Twice yearly, double-dose pyrantel is considered
necessary for tapeworm control.
Although bots are a common cause of concern to
owners, their control is not essential. Only
ivermectin, moxidectin, and organophosphates are
.41.
1\,d,
Programs Guidelines
effective against bots. All bots exist within the host
during winter months.
In many countries most horses graze for part or all
of the year, so year-round dosing is often required.
Co-grazing horse pasture with sheep and/or cattle
can safely reduce the numbers of equine parasite
larvae on the grass.
The options for parasite control are listed in Table 4.1.
Piperazines, phenothiazines, and organophosphates
are drugs that are available but are used infrequently.
Additional guidelines for control programs include
dose all horses from 6 weeks of age
use the same product for an entire year, but with
incorporation of specifc doses to deal with
tapeworms (pyrantel in April and October) and
bots (ivermectin or moxidectin in early winter)
after one year's continuous use of one product,
change to an unrelated product the following year,
and change again in the third year, i.e. the
anthelmintic classes are used in a 3-year cycle
emphasize the correct dosing interval (see Table
4.1) for different anthelmintic classes to the horse
owner
screen for anthelmintic resistance using fecal egg
count reduction tests (FECRT) twice a year (the
FECRT establishes the efciency of the
anthelmintic in reducing fecal egg output using
Comments
1. Interval dosing Year round pro-/benzimadazoles, Synchronized dosing of all animals
4 weekly; ivermectin, 810 weekly;
pyrantel, 4 weekly; moxidectin 13 weekly.
2. Strategic dosing Spring/summer only using same Regional variations in pasture
anthelmintics as for interval dosing. cyathostome infectivity affect the
timing of dosing.
Synchronized dosing of all animals.
3. Targeted dosing Year round only dose animals that have Monthly worm egg counts on all
a positive FWEC using same anthelmintics animals.
as for interval dosing.
4. Continuous in-feed Year round pyrantel pamoate daily in Not available in Europe
feed.
5. Pasture hygiene Twice-weekly pasture fecal collection. Capital/labor expense high.
Effective if combined with 1, 2, or 3
above, especially 2.
6. Predacious fungi (fungi Year round daily in-feed administration. Not yet fully validated or licensed.
that are natural predators
for strongyle eggs)
59
FEC results from one fecal sample taken pre
treatment (day 0) and one sample taken on day
10-14 post-treatment); ideally the FEC should be
reduced by 90 per cent at day 10-14, and failure to
achieve this level of reduction suggests anthelmintic
resistance
anthelmintic resistance (only reported in
cyathostomes) is an irreversible feature - once it
has developed on a particular premises to a
particular class of drug, any product from that class
should not be included in the worm control
program again.
CLINICAL ASPECTS OF MINOR EQUINE
INTESTINAL PARASITES
Bots
The four main species of bots are Gasterophilus intesti
rudis, G. nasalis, G. haemorrhoidalis, and G. pecorum
the life cycle is direct - the Oy lays eggs on either
the legs or head of the host during the summer, the
host ingests the eggs and the larval stage is spent in
the host's stomach during the winter
they are essentially non-pathogenic
they can be controlled by early winter dosing with
either ivermectin 0.2 mg/kg, moxidectin
0.4 mg/kg, or organophosphates (not Europe).
Strongyloides westeri
This parasite occurs commonly in the foal, but it is not
found in adult horses
it is rarely pathogenic but can cause diarrhea
the life cycle is direct - the foal ingests the parasite
in the dam's milk or acquires it through
transcutaneous infection
S. westen is treated with oral anthelmintics, but often
an increased dosage than that recommended for
strongyles is required (check package insert)
Oxyuris equi
This is the common large intestinal pinworm
it is non-pathogenic other than causing pruritus
during egg laying, when adult stages protrude from
anus, resulting in tailhead excoriation
treatment is oral anthelmintics with most classes
being effective (check package insert).
60
Habronema spp.
There are three species - Habronema muscae, H. majus,
and H megastoma (synonym Draschia megastoma)
they are common in the US but rare in Europe
intermediate hosts are muscoid flies which deposit
infective larae either around the mouth and
muzzle, or on wounds and skin leading to 'summer
sores'; the larvae are then swallowed by the host
adult stages occur in the stomach where they may
result in increased mucus production and/ or
formation of fibrous nodules but, although the
pathogenic importance of these parasites is unknown,
they are probably not associated with clinical disease
treatment is by either oral ivermectin 0.2 mg/kg, or
oral moxidectin 0.4 mg/kg.
Crptosporidium spp. (see Chapter 27)
These parasites
can cause diarrhea in immunocompromised foals
infection can be detected using serum antibody or
fecal tests (specifc techniques are required for fecal
detection) in apparently healthy individuals
there are no known effective therapeutic agents.
Cocidia spp.
A few case reports describe Eimea leukarti to be present
in diarrheic horses and several surveys report 40-60 per
cent prevalence of E. leukarti oocysts in the feces of
healthy foals
fecal detection requires specific methods
no disease occurred after experimental E leukarti
infection studies
overall coccidiosis does not appear to be a common
clinical entity in the horse.
BIBLIOGRAPHY
Austin S M, Oi Pietro] A, Foreman] H (1990) Parswris
equarm infections in horses. Camp. Cant. Educ. Pact. Vet.
12:110-18.
Little S E, Moore] N, Oi Pietro] A (eds) (1999) Proceedings
of the conference on equine cyathostomes. Vet. Parasitol.
85:2,3.
Proudman C.J (1999) The role of parasites in equine colic.
Equine Vet. Educ. 11:219-24.
Southwood W, Baxter G M, Bennet 0 G, Ragle CA (1998)
Ascarid impactions in young horses. Camp. Cant. Educ.
Part. Vet. 20: 100-6.
Herd, R P (1986) Parasitolog, Veterinary Clinics of North
America: Equine Practice 2. W B Saunders, Philadelphia.
5
Differential diagnosis and evaluation of
dysphagia
JG Lane
INTRODUCTION
Dysphagia literally means diffculty in eating and
although horses may be afflicted with a range of clinical
conditions that limit their ability to gain access to food,
ranging from blindness to disorders of the cervical
spine, for the purposes of these notes the discussion will
be limited to diseases which compromise the ability to
prehend, masticate, and swallow ingesta.
NORMAL DEGLUTITION
It is conventional to subdivide deglutition into oral,
pharyngeal, and esophageal phases.
Oral phase of deglutition
This phase of deglutition is under voluntary control.
The prehension of ingesta depends upon a normal
incisor dentition for grasping herbage, and lip mobility
with which to contain the ingesta in the mouth and to
help manipulate it toward the cheek teeth. For mastica
tion. a healthy molar and premolar dentition and full
function of the temporomandibular joints are required.
The masticatory muscles which close the temporo
mandibular joints are innervated by the mandibular
branch of the trigeminal nerve (V), with the caudal
belly of the digastricus muscle which opens the mouth
innervated by the facial nerve (VII). The function of the
tongue in deglutition is to assist in the movement of
food boluses around the mouth and to gather them up
onto the base of the tongue prior to the onset of the
pharyngeal phase. The tongue is suspended on the
hyoid apparatus and the lingual musculature is inner
vated by the hypoglossal nere (XII).
Pharyngeal phase of deglutition
The presence of a food bolus on the base of the tongue
triggers a series of highly coordinated, split-second,
involuntary reflexes that collectively make up the
process of swallowing, and which include both pharyn
geal and esophageal phases of deglutition. During
deglutition, respiration is suspended after inspiration,
and expiration follows immediately after swallowing is
completed. Contraction of the base of the tongue drives
the bolus caudally into the oropharynx. At the same time
the larynx dislocates from the intrapharyngeal ostium,
the soft palate is elevated, the apex of the epiglottis retro
verts, and the arytenoid cartilages and vocal cords
adduct. The combined effect is to protect the nasal and
lower airways. The contraction of the levator palatini
muscles causes the ostia of the auditory tube diverticula
to shorten and dilate thereby allowing the exchange of
air for pressure equilibration across the ear drum.
The caudal movement of the bolus of ingesta is
accelerated by a wave of contraction of the constrictor
muscles of the pharynx, the pharyngeal stripping wave.
Liquid boluses tend to be squirted through the lateral
food channels on either side of the retroverted epiglot
tis, whereas solid boluses pass directly over the closed
larynx. The upper esophageal sphincter formed by the
cricopharyngeus muscle is normally closed, but it must
relax to allow the passage of the bolus into the esopha
gus. Following deglutition the larynx returns into the
intrapharyngeal ostium before respiration is resumed.
Esophageal phase of deglutition
After each bolus has passed into the proximal esopha
gus primary peristaltic waves are initiated by closure of
the cricopharynx. Primary esophageal peristalsis carries
63
5 UPPER ALIMENTARY TRACT DISEASES
individual boluses to the cardia, but the process is not
completely eficient and small quantities of ingesta are
left at variable levels in both the cervical and thoracic
esophagus even in normal horses. This ingesta is either
picked up in the bolus of a subsequent primary wave, or
by locally generated secondary peristalsis which is trig
gered by segmental stretch responses.
DIAGNOSIS OF DYSPHAGIA
Clinical signs
The signs of dysphagia include
an unwillingness to eat
slow eating
messy feeding
rejection of semi-masticated food onto the ground
(quidding)
productive coughing
nasal reflux of saliva, ingesta, and fluids.
Horses that are unable to eat and swallow food lose
weigh t rapidly, and this process is accelerated if the
horse develops secondary inhalation pneumonia which
is not an uncommon sequel to dysphagia.
In addition to a clear case history recording the
circumstances and rate of onset of dysphagia, careful
observation of the patient's attempts to eat and drink
can be invaluable to deduce which phase of deglutition
is awry. Whenever a horse shows return of ingesta from
its mouth, the site of the lesion causing the dysfunction
must lie in the oral cavity or oropharynx, certainly no
further caudal than the epiglottis. Nasal reflux of
ingesta points to an abnormalit of the pharyngeal or
esophageal phase of deglutition.
During the external assessment of the patient evidence
of systemic and/or toxic disease, including strangles,
botulism, grass sickness, rabies, upper motor neuron
disease, lead poisoning, and tick paralysis should be
noted. Thoracic auscultation (using a rebreathing bag)
should check for signs of inhalation pneumonia. Local
lymphadenopathies and firm distension of the esopha
gus to the left side of the trachea are abnormalities that
might be found during palpation of the throat area.
Useful information can be obtained by attemptng to
pass a nasogastric tube. This procedure should deter
mine whether pharyngeal swallow reflexes are still pre
sent, or whether the upper alimentary tract is physically
obstructed.
64
Oral examination
Under sedation and with a Hausmann gag or similar
mouth speculum in place, a detailed inspection of the
oral cavit should be carried out. In particular, one
should look for evidence of
absence of teeth or dental malalignment
enamel pointing of the cheek teeth
fractures of the dental crowns
periodontitis
soft tissue lesions of the buccal cleft and palate
oral foreign bodies
lesions of the tongue.
The structures involved may require hands-on manipu
lation to complete the examination, and a tell-tale foul
smell points to the presence of stale entrapped ingesta.
Most defects of the palate cannot be appreciated
from an examination of the mouth in a conscious
animal, because they are generally restricted to the sof
palate and the restricted opening of the equine jaws
prevents direct inspection of the more caudal oral
cavity. General anesthesia is necessary to complete
the inspection of the oral cavity, and the tendency of
the soft tissues to obscure the view, particularly toward
the base of the tongue, can be overcome by the use of
an endoscope passed through a polyethylene mare
speculum. Again, general anesthesia is required for a
more detailed manual examination of the caudal oral
cavity, especially in the region of the epiglottis and
aryepiglottic folds.
Endoscopy
Endoscopy per nasum is necessary to confirm whether
pharyngeal paralysis is present. The usual fndings of
pharyngeal paralysis include
a mixture of saliva and ingesta on the walls of the
nasopharynx
persistent dorsal displacement of the palatal arch
poor nasopharyngeal constrictor activity during
deglutition
failure of dilation of one or both auditory tube
diverticulum ostia after swallowing.
Many horses where functional pharyngeal paralysis is
diagnosed are in fact aflicted with pharyngeal hemi
plegia, i.e. unilateral glossopharyngeal neuropathy, for
example in cases of guttural pouch mycosis. However,
true pharyngeal paralysis may be seen in cases of botu
lism. Whenever a neurological cause of dysphagia is sus
pected, it is always correct to inspect the auditory tube
diverticula for evidence of mycosis or diverticulitis.
Inspection of the floor of the nasopharynx per
nasum for diagnosis of a palatal defect presents no
DIFFERENTIAL DIAGNOSIS AND EVALUATION OF DYSPHAGIA 5
dificulties even in quite young foals if an endoscope
with a diameter of 8.0 mm or less is available. Not all
palatal clefts occur as simple midline linear defects,
although these are the most common form in younger
patients with nasal reflux. The various permutations of
unilateral hypoplasia of the soft palate and pseudo
uvula formation can escape confrmation until the
patient is considerably older.
Other abnormalities which may cause dysphagia and
which can be confrmed by endoscopy of the pharynx
and larynx include
epiglottal entrapment, with or without a sub
epiglottic cyst
epiglottal hypoplasia
iatrogenic palatal defects after 'over-enthusiastic'
palate resection for dorsal displacement of the soft
palate
fourth branchial arch defects
evidence of sub-epiglottic foreign bodies, usually in
the form of unilateral edema in the region of the
aryepiglottic folds
intrapalatal cysts
nasopharyngeal cicatrix
laryngeal chondropathy
pharyngeal neoplasia
pharyngeal distortion by external compressive
lesions such as neoplasia or abscesses.
Clearly it is helpful to obtain some impression of the
extent of tracheal aspiration of ingesta accompanying
the dysphagia, and tracheoscopy is useful in this context.
Esophagoscopy is often a less rewarding technique
than might be imagined in the investigation of dyspha
gia, simply because physical or functional obstructions
of the esophagus invariably lead to a build-up of ingesta
and saliva in the lumen that, in turn, prevents a detailed
inspection of the area under suspicion. Prior to the
examination the patient should be starved for 3-4
hours. Examination of the esophagus is made easier by
passing the endoscope distal to the area of interest, and
by inflating the esophagus using the air channel of the
endoscope. Examination can then be performed dur
ing retraction of the endoscope. Evidence of conditions
such as esophagitis, megaesophagus, stricture, rupture,
tracheoesophageal fstula, diverticulum, intramural cyst
dysautonomia, and neoplasia may be found.
Radiography
Radiography, particularly with fluoroscopic studies
using contrast media, provides a means for the dynamic
investigation of deglutition. Clearly it is preferable for
the patient to take up the contrast medium voluntarily
and, in the author's clinic, bran mash impregnated with
barium sulfate is offered to the horses. A variety of fla
vorings are included to make the meal more palatable.
The shortcomings of the technique are that it is depen
dent on the enthusiasm of the patient to eat and also it
takes no account of dysphagias that vary between differ
ent food materials. Although it has been found that
sedation does not signifcantly distort the process of
deglutition, most horses will take part in the investiga
tion without resentment, once they are familiar with the
ambient noises of the radiographic equipment. The
sequence of events that make up deglutition is very
rapid and facilities for video-recording of the fluoro
scopic images for subsequent analysis, including slow
motion replay, are invaluable. The forced introduction
of barium sulfate suspension into the mouth through a
syringe is far from satisfactory, but it can be helpful to
outline intra-oral, pharyngeal, and esophageal lesions.
CONDITIONS COMPROMISING THE
ORAL PHASE OF DEGLUTITION
Lip and tonge lesions
Facial paralysis inhibits the ability of the horse to pre
hend and retain ingesta. Hypoglossal nerve injuries
with lingual paralysis are rare in the horse and trauma,
either in the form of lacerated wounds or tongue-strap
strictures, accounts for the majority of tongue lesions in
this species. Horses with a severely injured tongue may
be unable to maneuver ingesta around the mouth, and
are inclined to drop food or to collect it in the buccal
cleft. Foreign bodies may become buried in the lingual
tissues and the painful suppurative response can reduce
a horse's inclination to eat.
Dental disorders (see Chapter 6)
Those conditions that are associated with periodontitis,
which causes extreme discomfort, are most likely to
provoke quidding.
Temporomandibular joint disorders
These are rare in the horse but when they do occur they
cause marked pain and a rapid loss of bodily condition.
Disuse leads to obvious atrophy of the masticatory mus
cles. Clinical examination shows resentment of attempts
to open the mouth, and even under general anesthesia
the range of opening may be severely reduced. The
diagnosis is confrmed by radiography of the area in two
planes. Ultrasonography may be more helpful.
Hyoid apparatus disease
Hyoid apparatus involvement usually accompanies
otitis media in the horse, and ankylosis of the temporo
hyoid articulation is a likely result. Pathological fracture
65
of the stylohyoid bone follows and one of the effects of
this is a limited ability to move the tongue. Radiography
of the area and endoscopy of the guttural pouches con
tributes to the diagnosis.
Oropharyngeal and tongue-hase foreign bodies
The most common foreign bodies at this site are bram
bles which become lodged in the sub-epiglottal area,
causing acute-onset dysphagia. Endoscopy per nasum
will show edema in the aryepiglottic folds, even if the
j()]'(ign body itself cannot be seen. Such an endoscopic
finding is an indication for an oral examination under
general anesthesia.
Oropharyngeal tumors
These are unusual in horses and they tend to cause
dysphagia simply by virtue of the space they occupy.
PHARYNGEAL PHASE OF DEGLUTITION
Oropharyngeal and tongue-base foreign bodies (see
above)
These are discussed above in Conditions compromising
the oral phase of deglutition.
Congenital palatal defects (see above) (see also
Chapter 6)
These are discussed in Chapter 6.
Iatrogenic palatal defects (see Chapter 6)
Excessive palatal resection in the treatment of DDSP is
a disastrous complication because it is irreparable.
Iatrogenic defects can usually be differentiated from
congenital palatal deformities because the end points
of the resection are generally visible and the margin of
the free border has a tighter, rounded appearance.
Epiglottal entrapment and sub-epiglottic cysts
These conditions cause dysphagia because of space
occupation and restriction of movement of the epiglot
tis. However, horses with this condition are more likely
to be presented for the investigation of abnormal respi
ratory noises and/ or exercise intolerance.
Pharyngeal and intrapalatal cysts
These again cause dysphagia because of the space-occu
pying lesion. However, horses with these conditions are
more likely to be presented for the investigation of abnor
Illal respiratory noises and/ or exercise intolerance.
Nasopharngeal cicatrization
Nasopharyngeal cicatrization limits the effciency of
pharyngeal constrictor function, but horses with this
66
disorder are more likely to present for the investigation
of respiratory noises and/ or exercise intolerance.
Compromised glottic protection
Compromised glottic protection leading to the aspira
tion of ingesta into the lower airways may arise sponta
neously in cases of arytenoid chondropathy, or through
iatrogenic causes, such as complications of prosthetic
laryngoplasty or partial arytenoidectomy. The precise
cause of post-laryngoplast dysphagia is not known, but
over-abduction of the arytenoid cartilage, cicatrization
associated with reactive implants, and nerve injuries are
among the possible causes.
Pharyngeal paralysis (see above)
The most common causes of pharyngeal paralysis are
guttural pouch mycosis, ATD diverticulitis, botulism,
and lead poisoning.
Fourth branchial arch defects
Congenital fourth branchial arch defects generally
include aplasia, or at least hypoplasia, of the cricopha
ryngeal muscles, with the effect that the proximal
esophageal sphincter remains permanently open.
Horses with fourth branchial arch defects may cough
when eating and drinking, and show a nasal discharge.
Afflicted horses may swallow air involuntarily and may
be confused with stereotypic 'wind-suckers'.
Intralumenal pharyngeal neoplasia
Pharyngeal neoplasia is rare in horses, and most of
these proliferations turn out to be lymphosarcoma.
Retopharyngeal abscessation and neoplasia
Retropharyngeal space occupying masses, such as
enlarged lymph nodes occurring in horses with stran
gles, cause dysphagia because of external compression
of the pharynx, and also because of the pain associated
with the movement of food boluses over the lesions.
ESOPHAGEAL PHASE OF DEGLUTITION
Fourth branchial arch defects
See above Conditions compromising the pharyngeal
phase of degluttion.
Abscessation and neoplasia causing exteral compres
sion (see above)
It is not uncommon for cases of intrathoracic lympho
sarcoma to present with a degree of dysphagia caused
by esophageal compression by a mediastinal mass. In
some cases a mass of neoplastic tissue may protrude
DIFFERENTIAL DIAGNOSIS AND EVALUATION OF DYSPHAGIA 5
through the thoracic inlet and be palpable at the base
of one or both jugular grooves.
Megaesophagus (see Chapter 7)
Megaesophagus has been reported sporadically in the
horse, sometimes as a primary congenital disorder and
sometimes secondary to other conditions causing
restriction of esophageal function, such as vascular ring
strictures. Coughing, nasal reflux of ingesta, and disten
tion of the cervical esophagus may all be features.
Confirmation is by contrast radiography.
Esophageal impaction (choke) (see Chapter 7)
Obstruction by impacted, dry ingesta (,choke') is typi
cally associated with the ingestion of inadequately
soaked sugar beet pulp in the UK. Horses with 'choke'
present in an acutely distressed state with copious reflux
of saliva to the nostrils. The cervical esophagus may be
palpably distended with frm ingesta and passage of a
stomach tube beyond the pharynx is generally not
possible.
Stictures of the esophagus (see Chapter 7)
Strictures are thought to be the sequel of episodes of
acute obstruction, and horses with this condition are
presented with recurring 'choke'. Confrmation of the
diagnosis is best achieved by contrast radiography.
Dysautonomia (grass sickness) (see Chapter 17)
Grass sickness produces dysphagia in its acute form but
colic in the sub-acute and chronic forms. The condition
is sten in horses of all ages throughout the UK and
northern Europe, but has been reported only once
in Australia. Afflicted horses are generally severely
dtpressed, with patchy sweating, elevated pulse rate,
and ileus. The dysphagia arises as a part of total gas
trointestinal stasis, and nasal reflux of ingesta adds
to the pitiful appearance of the patients. There is
currently no reliable in vitr diagnostic test, but the radi
ographic demonstration of esophageal stasis and the
endoscopic identifcation of ulceration of the
esophageal mucosa are helpful pointers to the likely
diagnosis.
Rupture of the esophagus (see Chapter 7)
Esophageal rupture carries a poor prognosis unless the
patient is presented for treatment soon after the injur
has occurred, because of the rapid advance of contami
nation and cellulitis into the surrounding tissues. Most
ruptures are caused by obvious external trauma, but a
number of horses have been referred to the author's
clinic where rupture of the pharyngeal or esophageal
wall has occurred through excessively forceful attempts
to pass a stomach tube or, in one case, an endotracheal
tube.
Intramural inclusion cysts (see Chapter 7)
These may be encountered in young horses and cause
dysphagia through space occupation restricting the
passage of esophageal boluses. The lesions may be seen
as bulges in the esophageal wall at endoscopy, or be
demonstrated by ultrasonography or contrast radio
graphy.
Intramural neoplasia of the esophagus (see Chapter 7)
Esophageal neoplasia is rare in the horse, but squamous
cell carcinoma at this site has been reported.
Many of the conditions outlined above are described in
greater detail elsewhere in this book, together with
explanations of their etiology, defnitive diagnosis and,
when applicable, methods of treatment.
BIBLIOGRAPHY
Baker G] (1982) Fluoroscopic investigations of swallowing in
the horse. Vet. Radiol. 23:84.
Baum K H, Modransky P D, Halpern N E, Banish L D (1988)
Dysphagia in horses: the differential diagnosis. Parts 1 and
2. Compo Cont. Educ. Pct. Vet. 10:1301-7 and 1405-10.
Brown C M (1992) Dysphagia. In Curent Therap in Equine
Medicine3rd edn, N E Robinson (ed.). W B Saunders,
Freeman D E (1980) Diagnosis and treatment of diseases of
the guttural pouch. Parts 1 and 2. Compo Cont. nauc. Pact.
Vet. 2:S3-S11 and S25-S32.
Lane] G (1983) Fourth branchial arch defects. In
Proceedings of the 15th Bain-Fallon Memorial Lectures,
Australian Equine Veterinary Association, 209-212.
67
6
Diseases of the oral cavity and soft
palate
Dental disease
bA Kucker
Equine dental disorders are quite common, a preva
lence of 10-S0 per cent has been reported in the gen
eral equine population. The author's review of 325
dental records revealed 30 per cent with normal denti
tion. The remaining 70 per cent showed the following
distribution
3.4 per cent had mild-to-severe periodontal disease
6.4 per cent had worn out, broken, or missing teeth
8.9 per cent had exaggerated transverse molar
ridging
15.4 per cent had incisor malocclusion
IS. l per cen t had oral ulceration secondary to
sharp molar points
:7.S per cent had other molar malocclusions.
The total exceeds 100 per cent because 30 per cent of
the horses had more than one problem. Eighty per cent
were presented without any history of dental difculty.
MTPL PMPTNY
The horse has evolved into an almost continuous
grazer. Forage is selected by the prehensile lips, cut off
with the incisors, and moved caudally with the tongue
for grinding by the molars. The rows of mandibular
cheek teeth are set 30 per cent closer together than the
maxillar cheek teeth (anisognathism) , and grinding
of forage is done with a side-to-side motion of the
mandible. Consequently, the mandibular teeth wear
more on the buccal side and the maxillary teeth wear
more on the palatial aspect, producing a slope to the
occlusal surface of 10-15 degrees.
The visible crown is comprised of layers of dentine,
cementum, and enamel, these layers wear at different
rates. The two prominences on the erupting cheek
teeth are worn down with occlusion to form an irregular
chewing surface. Except for the frst cheek tooth, either
a slight undulation or transverse ridges ( two per tooth)
form on the occlusal surface. The six cheek teeth func
tion as one long tooth and malocclusion or disease
involving individual teeth effects the function of the
entire arcade.
Pulp is soft, gelatinous material that flls the central
part of the tooth, the pulp cavity. Masticatory forces
cause the pulp to be replaced with secondary dentine
from the occlusal surface to the root. Dentine eventu
ally flls the pulp cavity in old horses. The root elongates
with age by deposition of cementum. This extra root
helps to anchor the tooth in the alveolus in aged horses.
MNMLLPTUH
Traditionally teeth have been identifed according to
their anatomic function. Each tooth is given a letter
designation: I = incisor, C = canine, P = premolar, M =
molar. A lower case letter indicates a deciduous tooth;
an upper case letter indicates a permanent tooth. The
location of the tooth is indicated by the position of the
tooth number around the letter. The head is divided
into four quadrants represented by the four corners of
the letter. For example, the right second upper incisor
is connoted as 21. The anatomic system is more com
monly used but is sometimes confusing as there is more
69
than one name for the same tooth, i. e. the right upper
third premolar is also the right upper second cheek
tooth.
The Modifed Triadan System identifes teeth
numerically according to their location. Each tooth has
a three digit number describing its position. The frst
digit of the number represents the quadrant of the
head. The frst quadrant is the upper right, continuing
clockwise around the head, i.e. the upper left is quad
rant 2, the lower left is quadrant 3, and the lower right
is quadrant 4. The next two digit identit the location
within the quadrant, with a maximum of 1 1 teeth in
each arcade. The central incisors are numbered 1 while
the last molars are numbered 1 1. The lower left second
premolar is 306. The Modifed Triadan system allows
for the presence of a lower wolf tooth.
Deciduous teeth are indicated by substituting the
numbers 5 to 8 for the frst digit beginning again with
the upper right side of the head, thus 807 designates
the deciduous right lower third premolar. This system
simplifes written and computer records.
MTPL HUPTM
Knowing the normal time when teeth erupt is essential
for practitioners to properly age and anticipate prob
lems associated with eruption. Table 6.1 lists expected
eruption times for most horses, however times may vary
as much as 6 months.
Eruption
6-8 days
4 weeks
5-9 months
P THNMPTM
Age determination up to 8 years is based on tooth erup
tion and incisor wear. From 8 years to the late teens or
early twenties age is determined on incisor wear, shape
of the incisor occlusal surface, and the incisor angle of
occlusion in profle. Mter 20 years molar wear may aid
in aging because the upper frst molars (l09 and 209)
are beginning to wear to the root, which has no enamel,
causing these teeth to hollow out on the occlusal
. surface.
Age determination is accurate until all the per
manent teeth are in wear, after this aging becomes
more an art than a science. Many factors affect wear
including
management
forage tpes
breed
dental care
vices
trauma
malocclusion.
Soils with high silica content may cause the teeth to
wear more quickly. Horses kept stalled, getting minimal
grazing time, and consuming a diet of fne hay, will
chew with limited lateral excursion. Lack of lateral
excursion promotes molar malocclusion and affects
wear on both incisors and molars.
Teeth
Temporary
First incisor
Second incisor
Third incisor
Premolar Present at birth or first 2 weeks
Permanent
First incisor
Second incisor
Third incisor
Canine
First premolar (wolf tooth)
Second premolar
Third premolar
Fourth premolar
First molar
Second molar
Third molar
70
Eruption
2.5 years
3.5 years
4.5 years
3.5-5 years
5-6 months
2 years 6 months
2 years 8 months
3 years 8 months
9-14 months
2 years
3-3.5 years
In Wear
3 years
4 years
5 years
3- months later
3- months later
3- months later
2 years
3 years
4 years
Cups and stars
Incisors have an invagination of the enamel layer on
the occlusal surface that is partially flled with cemen
tum. This invagination, called a cup or infundibulum,
is oval shaped and eventually wears off the tooth. The
cup is lost from the lower frst incisors (301 and 401)
at 5-7 years, lower intermediate incisors (302 and 402)
69 years, and for the lower corner incisors (303 and
4(3) 7-10 years. Cup loss on 101 and 201 is at 9 years,
102 and 202 is at 10 years and 103 and 203 is at 11
years.
A the incisor wears, the cup becomes smaller, moves
distally and the dental star appears rostral to the cup.
The dental star is formed from secondary dentin that
has been deposited in the pulp (dental) cavit as the
tooth ages. Initially the dental star is wide but with wear
hecomes oval then round. The age range for the
appearance of the star is 6-7 years for the lower 01 s, 7-9
years for the lower 02s, and 8-10 years for the lower 03s.
Star appearance for upper 01s, 02s, and 03s is 11, 12,
and 13 years, respectively.
Shape
The shape of the occlusal surface of the incisors
changes with age. When the permanent incisors erupt,
the occlusal surface is wider medial-to-lateral than ros
tral-to-caudal. The shape changes to oval at 6-7 years,
then becomes rounded at age 9-12 years, and triangu
lar at 14-17 years. After 20 years the incisors are wider
rostral-to-caudal than medial-to-lateral. Remember that
lack of incisor wear, seen in stabled horses, may inter
fere with age determination.
Hooks
Hooks may form on one or both the upper corner
incisors from changes in occlusion. Sometimes called 7
and 11 year hooks, they may occur any time after 6 years
and are not very dependable for age determination.
Incisor hooks seldom remain after age 12-13 unless a
malocclusion is present.
Galvayne's groove
Galvayne's groove is a slight indentation of the tooth
material on the lateral aspect of the upper corner
incisors (03s). The groove is bilateral but the grooves
on either side may not appear at the same time. The
groove appears at around 10-11 years, is halfay down
the tooth at 15 years, and all the way down at 20 years.
The groove is seen only on the lower one half of the
teeth at 25 years and is completely gone at age 30
years.
DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6
Incisor profi l e
In young horses the incisors meet at an obtuse angle,
almost vertically. The angle gets more acute with age.
The incisor profle is not an exact age determiner but it
helps in age approximation.
b1Mb MTPL bPb
Signs of dental disease are diverse and may present in
many ways from subtle to obvious. A complete history,
coupled with presenting signs, and a thorough oral
examination with a full mouth speculum is needed to
reach a diagnosis. The oral cavit should be inspected
visually, and each tooth palpated during the examination.
Latex gloves should always be worn when performing
dental manipulations.
Signs of dental problems include:
abnormal eating behavior (head tilt, quidding,
dropping grain)
excessive salivation
discharge or fetid odor from mouth
refuses to eat, eats slowly, or eats hay but not grain
long (greater than 0.6 cm) hay particles in fces
poor body condition
dorsal displacement of the soft palate
swelling or bumps on the maxilla or mandible
purulent drainage from fstulae over the maxilla or
mandible
purulent nasal discharge
resists bridling or rears when bridled
head tilts while ridden or lunged
sticks tongue out of the mouth or over the hit
slightly opens the mouth when head is in a vertical
position
refuses to maintain frame or vertical head carriage
resists turns to one or both sides (may be very
subtle)
head tossing or shaking
unexplained or subtle lameness (oral examination
should he included in lameness examination)
mouthing or chewing the hit
slow in transitions
Nervous or fractious horses should be lightly sedated to
facilitate the examination. Most horses do not object to
the full-mouth speculum, but it can become a weapon
on an excitable horse. Horses 4 years old and under
object to a speculum because the incisor plate lip
pinches the gingiva behind the incisors. Grinding down
the lip will prevent pinching. To avoid pressing injured
cheek tissue into sharp molar points, lightly float the
maxillary arcade prior to using the speculum.
71
The author prefers not to pull the tongue out of the
mouth unless necessary. A 'tongue depressor' made
from PVC pipe is handy for pushing the tongue to the
side. Stainless steel wire inserts are available for
improved arcade visualization.
VLPNMTPL bHHb
Mandibular and maxil lary brachygnathia
The most common developmental oral abnormality is
a mandible shorter than the maxilla or 'parrot
mouth'. If the mandible is longer than the premaxilla
(shortened premaxilla), the condition is called 'sow
mouth'. Both abnormalities are thought to be inher
ited. Sow mouth is less common than parrot mouth
and is usually seen in small breeds, particularly minia
ture horses. Foals may be normal at birth, but develop
these disorders by the time they are 2-6 months old.
The conditions may be partial with between 10-90 per
cent of the incisor occlusal surface in contact, or com
plete, with no incisor contact. Assessment of severity
should be done with the nose pointed toward the
ground. Raising the head to a horizontal position lets
the mandible slide caudally and will exacerbate the
appearance of parrot mouth.
Parrot mouth has also been classified as an 'overbite'
or 'overjet' deformity. An 'overjet' is where the maxilla
protrudes further than the mandible, but the incisor
arcades are maintaining their usual anatomic positions.
An 'overbite' is an extreme protrusion of the upper
incisors, and the incisors are deviated ventrally in front

of the lower incisors. Ove,jet is seen more often in
Quarter Horses, and limited evidence suggests brachy
gnathia may be an aspect of developmental ortho
pedic disease. Overbite is more commonly seen in
Thoroughbreds and may have a familial predilection in
this and possibly other breeds. Overbite therapy in a
mature horse is palliative, however, horses are capable
of performing and maintaining themselves without dif
ficulty. Routine correction for molar malocclusion and
occasional shortening of the incisors is required. With
overbite the lower incisors are in 'occlusion' with the
hard palate just caudal to the upper incisors. The
incisors should be examined annually and maintained
with a smooth, level surface.
Treatment
Treatment for parrot or sow mouth is more successful if
started while the horse is less than 6 months of age.
Conservative treatment for parrot or sow mouth in foals
utilizes one or more of the following.
72
1. For partial brachygnathia, eliminate any lip
formation on the rostral or caudal edge of the
incisors that arises from lack of wear.
2. Remove hooks or ramps occurring from molar
malocclusion and shorten exaggerated transverse
ridges on both upper and lower molar arcades.
3. Ensure there is no contact between the molar
arcades when the mouth is at rest. It is the author's
opinion that hooks, ramps, or transverse ridges tall
enough to make contact with the opposite molar
arcade (when at rest) may retard mandibular
growth.
4. The mandible in parrot mouths may be narrower
than normal, leading to a lip forming on the buccal
side of the upper premolars. This lip should be
floated off preserving the normal occlusal angle. If
the occlusal angle of the arcades is too steep,
restore it to 10-15 degrees.
A bite plate may be needed for horses with no incisor
contact. The plate attaches to a halter and projects
between the incisors beyond the lips. The plate provides
incisor contact preventing ventral deviation of the pre
maxilla and upper incisors. The bite plate also separates
the molar arcades. This separation eliminates possible
opposing molar contact at rest.
Surgical therapy for overjet involves the application
of a premaxillary tension band restricting rostral devel
opment of the maxilla. Under general anesthesia, a
hole is drilled through the alveolar bone between
deciduous upper 06s and 07s, with a 3.2 mm bit. Half of
a 30 cm length of stainless steel (18-20 gauge) wire is
passed through the hole. The wires are brought forward
and twisted together as they pass across the diastema.
One strand of the wire goes on the labial side of the
incisors, the other strand to the palatal side. A large
gauge needle inserted in the gingiva between the
contralateral first and second incisor is used to pass the
labial wire caudally. This wire is then passed between
the ipsilateral first and second incisors, re-emerging
on the labial side. The palatal wire is passed rostrally
between the central incisors and is then twisted with the
other wire on the labial surface of the ipsilateral first
incisor. The wires are cut off and covered with a small
amount of acrylic to minimize irritation to the lips. This
procedure is repeated on the opposite side of the
mouth.
Small notches may be cut into the teeth, as needed,
with a Dremel tool and a small-diameter burr to anchor
the wire at the gingival margin. Tension wires are left in
place for 2-6 months, and need to be checked daily by
the owner for failure, to flush out impacted food mate
rial, and to observe improvement. Mandibular tension
bands can be used to treat sow mouth.
Application of tension wires for overbite correction
wilL instead, exaggerate this condition by further ven
tral deviation of the premaxilla. A bite plate will need to
be applied until the ventral premaxilla deviation is cor
rected. Simultaneous or alternating tension wiring and
bite plate application may be needed to correct foals
with severe overbite (2-3 cm shortening of the
mandible). Complete correction may not be obtained.
A bite plate applied after 6 months of age may have
limited correction on an overbite.
Surgical correction of a possible heritable disease is
open to ethical debate. Correction will improve grazing
ability and mastication, and will minimize complica
tions from molar malocclusion. Owners should be
informed of the possible inheritable tendencies and
encouraged to not breed these animals.
Dental tumors
Odontomas, tumors with histologic presence of both
dentine and enamel, are rare in horses. Odontomas
originate from dental epithelium and four types have
been identifed in the horse. These are ameloblastomas
(adamantinomas) and three types of odontomas:
ameloblastic, complex, and compound. Mesodermal
tumors, cementomas, and odontogenic myxomas, have
not been reported in the horse. Diagnosis is based
on radiographic and histologic examination. Amelo
blastomas are usually seen in mature horses and
odontomas are commonly found in younger animals.
Ameloblastic odontomas usually present as a con
genital, frm, non-painful, 2-3 cm nodule. Foals are
otherwise normal. The mass slowly enlarges during the
next weeks or year to reach a size of 15 cm, involving
vital structures. Treatment is surgical eXCISIOn.
Odontogenic tumors generally do not metastasize, but
they are invasive and successful removal depends on
location and extent of bony, sinus, and soft tissue
involvement. If extensive tumor involvement prohibits
removal, affected animals may live for months or years
before euthanasia is required.
Dentigerous cysts
Dentigerous cysts (heterotopic polyodontia), also
known as ear teeth or aural fstulae, are odontogenic
cysts frequently containing stratifed squamous or gob
let cell epithelium. They are commonly found at the
base of the ear, other locations include the mandible,
maxilla, and maxillary sinus. These cysts may have a
seromucous or purulent discharge. Careful excision
usually results in complete resolution. Radiographs are
needed to differentiate between tumors, dentigerous
cysts, and fluid cysts.
Cysts
Fluid flled cysts occasionally occur in the mandible,
maxilla, and paranasal sinuses. They produce a variable
degree of facial deformity and present as a smooth,
frm, non-painful, gradually enlarging swelling.
Aspiration of a pale yellow clear to turbid fuid coupled
with a radiolucent center is indicative of a cyst. Surgical
removal is the treatment of choice.
Polyodontia
Supernumerary teeth are considered congenital
because they arise from abnormal differentiation of
tooth germinal tissue. The condition is only recognized
after tooth eruption. Incisors are the teeth most often
affected. One extra tooth or an entire incisor arcade
may be present. Extra molars may appear within the
molar arcades, from the hard palate or as an extra last
molar. Customary treatment is to maintain the length of
any extra teeth that do not wear. Removal is seldom
indicated.
Oligodontia
Too few teeth are more frequently encountered than
too many teeth. Congenital oligodontia may involve
deciduous or permanent incisor or molars. Acquired
oligodontia is usually from trauma and subsequent
damage to existing teeth or to developing tooth buds.
Treatment is directed at maintaining the proper height
of teeth that are unopposed and not wearing properly.
Retai ned deciduous teeth
Retained 'caps' may occur in either the incisor or molar
arcades. The erupting permanent tooth normally dis
rupt the circulation to the root of the deciduous tooth.
The deciduous tooth loosens and separates as the per
manent tooth reaches the gingiva.
Incisor caps
Incisor caps frequently are retained because the perma
nent tooth erupts caudally to the deciduous root. In
most cases the root is vestigial and the cap slips off eas
ily. Loose caps should be extracted prior to using a full
mouth speculum as the incisor plate can pinch soft
tissue between the cap and permanent tooth beneath.
Occasionally caps are frmly held in place by 1-2 cm of
root. Removal requires sedation and local anesthesia.
The gingiva is incised over the root and the root ele
vated with a curved bone chisel. The mucosa may be left
to granulate in with daily flushing with a mild disinfec
tant by the owner. Incisor caps should be removed if the
opposing cap is gone and the permanent tooth is in
73
wear. Sometimes 702 and/or 802 overlap the erupting
302/402, impacting these permanent teeth. Removal or
trimming off the impacting part of the deciduous tooth
is indicated.
Premolar caps
Removal of the cap is indicated if the cap is loose, trap
ping food, or causing maleruption of the permanent
tooth. If the permanent tooth can be palpated above
the gingiva, the caps should be removed. A deciduous
premolar, still securely attached, should be extracted if
a putrid odor is detected on the operator's gloved
hand. This indicates that forage is fermenting around
the cap or between the cap and the permanent tooth.
The associated gingivitis may lead to early periodontal
disease. Starch fermentation between the cap and per
manent tooth may lead to early infundibular necrosis.
The fourth premolar is the last permanent tooth to
erupt and is most often impacted or deviated.
Infectious dental disease
Infectious disease involving the cheek teeth may be
divided into three categories
infundibular necrosis
periodontal disease
periradicular disease.
These terms do not identif the cause and one classif
cation may progress to another.
Infundibular di sease or necrosis
Dental caries or decay is the destruction of the cemen
tum, enamel, and dentin secondary to fermentation of
carbohydrates. Baker observed infundibular necrosis at
an incidence of 80 per cent in horses over 15 years. The
frst upper molar is the most common site.
Hypoplasia of cementum in the enamel invagination
(infundibulum) of the upper cheek teeth allows food to
pack into these pockets. Carbohydrate fermentation
and resulting acid production dissolves and weakens
the tooth material. Cementum hypoplasia may not be
visible until some crown wear exposes the defect
grade I disease is restricted to cement erosion
grade II involves both cement and surrounding
enamel
grade III includes the dentin.
Although the mandibular cheek teeth do not have
infundibula, fracture of the exposed crown may lead to
decay.
Lesions may be innocuous in some horses. Apical
and lateral extension may not produce pulpitis because
74
secondary dentine production preseres the pulp cav
ity. Progression of the necrosis leads to coalescence of
the rostral and caudal infundibula into a single large
pocket. Sequelae include pulpitis, with or without fac
ture, apical migration and infection (periradicular dis
ease or apical periostitis), sinusitis and nasal discharge.
Endodontic treatment for pulpitis has been
described. Sinusitis is treated with lavage and drainage.
Extraction may be done intra-orally, via sinus trephina
tion and repulsion, or through lateral buccostomy and
elevation of the tooth intact or in sections.
If a coalesced pocket is present but there is no pulpi
tis or alveolar infection, the occlusal surface of the
opposing tooth should be maintained level with the
other teeth in that arcade. The opposing tooth may
develop a hump corresponding to the defect in the
damaged tooth. This malocclusion predisposes the
arcade for wave or step formation, fracture of the dis
eased tooth, periodontal disease, and loss of additional
teeth.
Periodontal di sease
Periodontitis is
inflammation of the gingiva with progression to
formation of gingival pockets in the interproximal
spaces
resorption of alveolar bone
loss of gingival attachment
destruction of the periodontal ligament
tooth loosening.
Periodontal disease has been described as the most
common dental disease of horses. The normal shearing
forces of mastication are essential for sustaining healthy
periodontium. Molar malocclusion interferes with nor
mal lateral excursion and proper grinding of forage.
Periodontal disease is often secondary to malocclu
sions. The initial stages of periodontal disease (regres
sion of inflamed gingiva, small pockets of trapped
forage) may locate acacent to a minor malocclusion. A
minor malocclusion may be a single tooth with a flat
tened table angle or exaggerated transverse ridges.
Animals exhibiting dysmasesis: quidding, dropping
grain, head tilt, and excessive salivation should be
examined closely for early periodontal disease. The frst
lesions are caused by trapped forage in the gingival sul
cus at molar junctures, this may be unilateral. Retained
premolar caps trap food, leading to periodontitis, but
this usually resolves after normal grinding resumes. The
only clue may be a subtle putrid odor requiring a
thorough digital and visual examination to identify the
location of the lesion. Gingival hyperemia and swelling
are usually present. The pocket enlarges via a cycle of
irritation, inflammation, and erosion of the periodontal
ligament, gingiva, and alveolar bone. The erosion of the
periodontal ligament creates a gap in the interproximal
space and the tooth loosens. Severe alveolar sepsis even
tually causes tooth loss.
Treatment for early periodontitis includes correc
tion of any malocclusion, and routine (every 6 months)
dental maintenance. This may prevent or slow the dis
ease progression. Flushing out the trapped food and
packing the pockets with metronidazole tablets may
restore the gingiva when minimal pocketing is present.
This can be repeated every other day until resolution
or until it is decided that therapy is unsuccessful.
Additionally, the owner should flush out the mouth
twice daily with an appropriate disinfectant. Grinding
the opposing tooth out of occlusion, using a rotary
burr, will aid in minimizing food packing into the sul
cus. The opposing tooth is shortened 2-3 mm.
Treatment of advanced periodontitis consists of cor
recting any malocclusions and evaluation of the dis
eased tooth for extraction. If the tooth wiggles easily
and is painful, extraction is indicated. Affected animals
with advanced periodontitis are usually over 15 years
old. Extraction is generally easy because of the shorter
resere crown and minimal periodontal ligament
attachment. Grasp the tooth with a cap extractor, move
the handles side to side and then rotate the occlusal
surface lingually (palatally).
When several teeth are involved, usually the second,
third, and fourth cheek teeth, only one tooth may
appear loose enough to extract. Extraction of this tooth
will frequently reveal advanced periodontitis of the
other two, requiring their extraction. Probe the alveo
lus for tooth fragments and flush with antibiotics or dis
infectants after extraction. Packing the alveolus with
gauze is generally not necessary. The alveolus grau
lates in and covers with gingiva in 2-3 weeks. GlVe
systemic antibiotics effective against anae
.
roi
.
and
gram-negative bacteria when widespread gmglVItlS or
regional lymph nodes are enlarged.
Slightly unstable teeth should be left insituas long as
possible. Removing occlusion by grinding down th
opposing tooth will enable the diseased tooth to stabI
lize in some cases.
Peri radicular disease
Peri radicular disease is infection or inflammation of the
pulp and surrounding tissue. Synonymous tens ar
alveolar periostitis, periapical osteitis, and chrOnIC OSSI
ting periostitis. One text defnes periodontal disease as
alveolar periostitis. Signs include
painful bony swelling
external or intra-oral fstula formation
maxillary sinusitis
sinus empyema
signs associated with painful chewing.
Painful bony swellings (pseudocysts) appear secondary
to eruption of permanent premolars. Retained decidu
ous premolars impede normal permanent tooth erup
tion. The fourth premolar is most commonly afected
because it is erupting between two permanent teeth. A
radiographic change seen with pseudocysts is lysis of
surrounding bone. The alveolar periostitis seen with
pseudocysts typically resolves after the permanent tooth
is in wear.
Hematogenous bacteria may infect the hyperemic
tooth root, leading to periapical abscess formation. This
is called anachoretic pulpitis and results in periradicu
lar disease. Treatment is the removal any retained caps,
malocclusion, or abnormal wear. Radiographs are indi
cated to assess tooth placement and root involvement.
Rostral upper second premolar hooks put caudal
pressure on the lower premolars, crowding the perma
nent teeth. Permanent teeth may be impacted or
displace medially during eruption. The teeth that are
impeding the eruption may need their mesial surfaces
ground off. This can be done with a diamond cut off
wheel or end cut rotating burr with appropriate guard.
Antibiotic and anti-inflammatory therapy should be
initiated and continued for 2-4 weeks.
Apical abscess formation may produce a drainig
tract. This more severe form has been termed chronIC
ossiting periostitis. Contrast radiology will help deter
mine tooth involvement and extent of the fstula.
Typical treatment is extraction of the diseased tooth.
Complications from removal of a tooth with an intact
periodontal ligament are frequent. Medical treatment
in the form of 48 weeks of appropriate antibiotics,
immune stimulants, and weekly intravenous sodium
iodide (2-3 treatments of 25 0 ml, 20% solution) has
been successful in saving abscessed teeth.
Endodontic treatment with exposure of the affected
alveolus, removal of the apices and pulp, and flling the
pulp cavit has had limited success. Mandibular teeth
are better candidates than maxillary teeth because of
their simpler root structure.
Antibiotic therapy
Mixed bacteria are most commonly cultured from
periodontal pockets and dental abscesses. Antibiotics
should be broad spectrum. Trimethoprim-sulfa,
30 mg/kg p.o.q. 12 h, may be used singly or in combi
nation with procaine penicillin G, 22 000-44 000 IU/kg
Lm. q. 12 h. Potassium penicillin, 22 000
-
44 000 ll.kg
Lv. q. 6 h can be substituted for procame penICIllin.
If ac/cri1cs Jraglis is suspected, penicillin may be
75
combined with metronidazole, 15-20 mg/kg p.o. q.
6-8 h. Ceftiofur, 2-4 mg/kg i.v. or i.m. q. 8-12 h, is also
effective. Sodium iodide 20%, 250 ml/500 kg i.v. weekly
for 2-3 weeks can resolve apical infections that do not
appear to be responding to antibiotics.
Malocclusions
The incidence of incisor and particularly cheek teeth
malocclusions is quite high. Detection and correction
of malocclusions is often done after periodontitis or
severe abnormalities of wear have developed. Many
malocclusions are easily recognized, for example ros
tral upper and caudal lower hooks. Thorough exami
nation can reveal small, but signifcant, abnormalities.
It is sometimes necessary to carefully evaluate the
height of the exposed crown on all teeth in order to
determine abnormal dentition. Proper correction of a
molar malocclusion includes restoring the normal
table angle.
Correction of hooks, ramps, and wave or step mouth
has traditionally been done with cutters and hand tools.
Cable grinders and reciprocating electric or air floats
have eliminated the need for these tools. Power tools
are safer and quicker than cutters.
Molar malocclusions can be indicated by pain
response with lateral excursion, or by incisor malocclu
sions, f()r example
offset mandible
rostral lip on the upper 01 and 02 incisors
unilateral hook on upper or lower 03 incisors.
Normal incisors will be level and parallel to the ground
when viewed at eye level. Deviations from this require
incisor reduction or alignment. Incisors should be
repaired after molar corrections unless a full mouth
speculum cannot be applied to the incisors.
Incisor malocclusions can be treated with hand tools
for minor problems. Treatment of abnormalities need
ing more than 2 mm removed from the surface of the
tables should be done with power tools. After 1 or 2 mm
has been removed excursion to molar contact is deter
mined. When lateral excursion to molar contact is
shortened to 5-6 mm, stop removing incisor height.
Even if the table surface is not level, stop at this point
and recheck the animal in 6 months time when further
correction can be made.
Hooks and ramps
Upper 06 hooks may be secondary to overjet of the
upper premolars, erupting into wear ahead of the lower
06s, or shaping of the lower 06s without corresponding
upper 06 shaping (iatrogenic hooks). After hook
removal, the affected teeth should be viewed from both
76
sides of the mouth, assuring removal of excess tooth
material from the occlusal surface. Lower 06 ramps may
be secondary to eruption into wear ahead of the upper
06 or oveIjet of the lower premolars.
Rear hooks are usually found on the last lower
molars (1 1s) and secondary to upper 06 hooks. As
upper front hooks get longer, they also get thicker, forc
ing the mandible caudally. Caudal mandibular dis
placement pushes the lIs out of occlusion causing a
hook to form.
Hooks and ramps are best removed with guardeu
rotary grinders.
Tall teeth
Tall teeth consist of dominant cheek teeth that are
taller than the other teeth in the arcade. One to three
teeth may be involved and determination of which
teeth have excess crown requires experience.
Observation of the contralateral arcades is beneficial
because the condition frequently is unilateral. The
occlusal angle on the affected tooth is often too flat.
Dominant teeth are often lower 06s with or without
07s and 08s, lower 08s, 09s, and lIs. Upper teeth
involved are 06s, 09s, and lOs. It is common to have a
tall upper 10 on one side and tall lower 07 or 08 on
the other side of the mouth. Correction is achieved by
shortening the affected tooth to the level and angle of
the rest of the arcade.
Step mouth
Step mouth is an abrupt difference in tooth height and
results from untreated dominant teeth. Tall teeth grad
ually increase in height, while the opposing tooth is
worn too short. If treated before the short tooth is wor
to the root, the mouth can be restored to normal. Step
mouth can be secondary to permanent tooth extraction
when the unopposed tooth is not maintained properly.
Correction is achieved by grinding down the taller teeth
or cutting through these teeth, thereby restoring them
to the arcade height.
Wave mouth
Wave mouth is the gradual excessive increase in tooth
height on both arcades causing an'S' shape on the
occlusal surfce. Correction is initially done with a
grinder and then fnished by shaping by hand. There
will be minimal or no occlusion at the spot where a wave
is corrected. The teeth that were too tall, prior to cor
rection, will again be too tall in 6 months, but the exces
sive height will be only 1-2 mm. The correction should
be repeated ever 6 months until both arcades are nor
mal in exposed crown height and angle.
Table angles
The normal tilt to the cheek teeth occlusal surfaces is
from 10-15 degrees. Animals under 3 years of age may
normally have steeper angles. The angle decreases
when all permanent cheek teeth are in wear.
Shear mouth is an extreme type of excess angle,
caused by mandibular arcades that are too narrow or by
severe chronic incisor tilt. Animals with shear mouth
can chew on one side of the mouth until the sheared
mandibular teeth reach the hard palate.
Flattened table angles occur secondary to lack of
lateral excursion. Horses chewing more up and down,
rather than side to side, wear the taller side of the teeth
(buccal upper and lingual lower) more than the lower
side. The primary cause of lack of lateral excursion, or
side-to-side chewing motion, is oral pain. The oral pain
can be caused by malocclusions, periodontitis, peri
radicular disease, or trauma. The table angles may be
flatter than normal or the upper cheek teeth may have
a slight hollowed out appearance or depression in the
center of the tooth, running the length of the upper
arcade. Decreased angles are also found on teeth worn
down to the root.
Correction is made by restoring the angle, but this
may be difcult in old horses because there may be very
little exposed crown left. When the decreased table
angle is unilateral, the incisors will not separate as much
on the affected side during lateral excursion.
Exaggerated transverse ridges
Cheek teeth have a slight buccal-to-lingual (palatal)
undulation to the occlusal surface. Each tooth, except
for the frst, has two of these transverse ridges. The posi
tion of the maxillary ridges is equidistant between the
cingula. The crests have a smooth rounded top and
match the rounded depression on the opposing tooth.
The height difference of the low and high spots is
normally 1-2 mm.
Exaggerated transverse ridges are present when the
ridge height exceeds the distance between the molar
arcades in the resting mouth (see Figure 6.1).
Exaggerated transverse ridges may affect the entire
pair of arcades or just one pair of teeth. Exaggerated
transverse ridges accentuate the buccal points on the
cingula. The crests of the ridges become less rounded
and more angular, like a row of saw teeth. The caudal
ridge on maxillary teeth wears an exaggerated groove in
the juncture between the mandibular teeth.
Exaggerated transverse ridges interfere with lateral
excursion and the normal rostral-caudal movement of
the mandible. The shearing force of chewing is directed
to the sides of the ridges i nstead of parallel to the long
Figure 6.1 Ridges block rostral-caudal motion. Occlusal
forces are directed along the lines indicated
c) open arrows = abnormal occlusial forces
- thin arrows = normal forces
axis of the reserve crown. Periodontal pocketing
appears when a groove is worn down to the gingiva.
Unilateral exaggerated transverse ridges can hold the
mandible to one side, while one exaggerated transverse
ridge can wedge apart teeth in the opposing arcade.
Correction is achieved by shortening the ridge
height to a point where there is no contact between the
arcades when the mouth is at rest. Usually one-half of
the excessive height is shortened on both arcades.
Listening to occlusion while pushing the mandible lat
erally will produce a more uniform, even sound after
the ridges have been shortened. Also the rostral move
ment of the mandible, when the nose is pointed toward
the ground, will increase.
Deviated teeth
Buccal or lingual deviation is secondary to impaction or
trauma. Common sites of tooth deviations are
lingual deviations - lower 07s, 08s and 09s
buccal deviations - upper 07s and 09s, lower lOs.
Deviations of 1-2 mm do not usually cause problems.
Deviations of more than 3 mm allow food to pack
between the teeth leading to periodontitis and eventual
tooth loss. Treatment is removal of the deviated portion
of tooth preventing soft tissue irritation.
Geriatric malocclusions
Treating malocclusions in horses over 20 years old is
usually palliative. Teeth worn to the roots can no longer
grind. Loose teeth are extracted and tall teeth are
shortened enough to prevent soft tissue damage.
77
Disorders of the mouth
NP bII
MTHULTM
Disorders of the mouth most frequently result in saliva
tion and/or failure to prehend, masticate, or swallow
food properly. Acute salivation (ptyalism) may be
caused by the inabilit to swallow normal saliva or from
excessive production of saliva. To determine the cause
of ptyalism a thorough physical examination and history
are necessary to differentiate between local causes and a
more generalized disease. In adults, the most common
causes of excessive salivation are choke and red clover
poisoning. In foals the commonest cause is esophagitis
secondary to gastroduodenal ulcer syndrome.
PHYbLPLAPNMPTM
Disorders of the mouth and palate may be diagnosed by
oral examination in some cases. The entire oral cavity
should be evaluated looking in particular for
lacerations
ulcerations
vesicular disease
foreign bodies
abscesses of tooth roots or soft tissue
fractured teeth
injury to the palate
evidence of chemical injury.
Sedation (e.g. detomidine with butorphanol) and the
careful use of an equine mouth speculum may be
needed to examine the mouth. Without proper seda
tion, the mouth speculum becomes dangerous both to
the examiner if the patient 'throws' its head, and to the
patient as excessive biting on it may cause a fractured
tooth or even a fractured mandible.
TPPTHMbb HPL LPVTY
bPb PM PTYPLbN
Factors causing oral cavity disease and ptalism are
listed below.
1. The most common foreign body found in the
mouth of a horse is a wooden stick large enough
to become lodged between the upper arcade of
teeth, or a smaller stick penetrating the soft tissue
of the pharyngeal cavity or soft palate.
78
2. Blisters, ulceration, or cellulitis may affect the
tongue.
3. Burrs or grass awns may be stuck in the mouth and
cause salivation. This may occur as an outbreak or
a farm problem.
4. Patients that have licked mercury blister
compounds are prone to severe oral erosions.
5. Most vesicles are idiopathic, but consider vesicular
stomatitis, which appears most commonly in the
US in New Mexico and Colorado, occurring every
3-7 years.
6. Immune-mediated pemphigus can result in vesicle
formation in the oral cavity but is rare.
7. Actin|aci//us/ignicrcsiican cause wooden tongue
in the horse (see Figure 6. 2).
8. Sialadenitis, fractured teeth, or fractured bones of
the mouth may cause excessive salivation.
9. Primary pharyngitis or epiglottiditis,
retropharyngeal lymphadenopathy, guttural
pouch empyema, pharyngeal edema, improper
mastication and swallowing, and choke are other
frequent causes of ptyalism.
10. Fracture or inflammation of the hyoid apparatus.
Figure 6.2 Wooden tongue (Actinobacillus lignieresii
n!ection)
PMbb
Ancillary diagnostic tests include radiography, ultra
sonography, and endoscopy of the mouth, guttural
pouch, and/or pharyngeal area. If the temporohyoid
articulation is being evaluated, both lateral and
dorsoventral radiographic views may be required.
Ultrasonography may elucidate an area that can be
aspirated for cytology and culture. The horse should be
observed carefully from a distance to ascertain whether
the abilit to prehend, masticate, and swallow is
retained. In some cases, a complete oral examination
under general anesthesia may be necessary before a
cause can be determined.
THPTNMT
Treatments may include
removal of foreign bodies
tooth extraction
antibiotic therapy for infectious causes
intravenous fluids to replace and maintain fuids
and electrolytes
non-steroidal anti-inflammatory drugs (NSAIDs)
other symptomatic treatment, e.g. 0.2% potassium
permanganate as a mouth disinfectant or
furacin/prednisolone spray for pharyngeal edema
and inflammation.
Penicillin is often the initial choice for an antibiotic
since many commensal oral organisms are sensitive to
it. Some cases may require a tracheotomy if laryngeal!
pharyngeal swelling is compromising the airway.
Regarding equine fluid therapy, it is important to
remember that the anion of highest concentration in
saliva is chloride, with a relatively low concentration of
bicarbonate. When an equine develops an acid-base
disturbance as a result of salivary loss, it is typically
hypochloremic metabolic alkalosis although with pro
gressive dehydration metabolic acidosis may occur.
Oral tumors in horses are rare (see Chapter 5).
Odontopathic tumors such as odontomas are most
common in the maxillae of young horses while
ameloblastomas primarily affect the mandible of older
horses. The most common soft tissue tumor of the
horse's oral cavity is squamous cell carcinoma (Figure
6. 3) . These tumors can involve any region of the
mouth, occur in older horses, and produce a character
istic fetid smell.
Figure 6.3 Weight loss and dysphagia due to squamous cell
carcinoma of the oral cavity
Cleft palate
5P5emevOIO8nU NU DuchIme
MTHULTM
Congenital cleft palate in horses is an uncommon
deformity affecting approximately 0.05-0.2% of the
equine referral population. Most defects affect the cau
dal aspect of the soft palate, and more rarely extend to
the hard palate. In addition midline clefts are more
common than lateral defects. This disease leads to nasal
regurgitation of milk and, later on, feed material, pre
disposing a horse to tracheal aspiration and aspiration
pneumonia. Mfected animals therefore often have
recurrent lower airway infection and stunted growth.
Treatment is achieved through surgical repair, but the
anesthetic episode is complicated by the status of the
lower airway. Success, defned as sufcient closure to
prevent nasal regurgitation and aspiration, is obtained
in 50-70 per cent of animals, but multiple revisions are
often needed. Aquired cleft palates are usually caused
iatrogenically following surgery to the soft palate.
PMPTNY, NHYLY, PM
PHYbLY
The hard and soft palate function to
prevent feed contamination of the nasal cavity and
nasopharynx while eating
maintain an appropriate size and stability to the
79
nasal cavity and nasopharynx so that upper airway
impedance is minimized during exercise.
The hard palate separates the nasal cavity from the oral
cavity. Anatomically, the hard palate is formed by the
fusion of the palatine processes of the incisive and max
illae bones and the horizontal plates of the palatine
bone. These palatine processes normally fuse during
embryological life in a rostral-to-caudal plane around
day 47 of gestation. These bones are covered by pseudo
stratifed columnar ciliated epithelium on the nasal
aspect and keratinized stratifed squamous epithelium
with a lamina propria submucosa continuous with the
fibrous periosteum on the buccal aspect.
The soft palate separates the nasopharynx from the
oropharynx. Anatomically, the soft palate consists of an
oral mucous membrane continuous with the hard
palate, the palatine glands, the palatine aponeurosis,
the palatinus and palatopharngeus muscles, and a
nasopharyngeal mucous membrane resembling the
nasal mucosa. The caudal free margin of the soft palate
continues dorsally on either side of the larynx to form
the palatopharyngeal arch. The coordinated function
of four muscles determines the soft palate position
the tensor veli palatini muscle tenses the rostral
aspect of the soft palate during exercise
the levator veli palatini muscle elevates the soft
palate during swallowing to close the choanae
the palatinus muscle shortens the soft palate and
depresses it toward the tongue
the palatopharyngeus muscle also shortens the soft
palate.
The innervation of the soft palate is through the
pharyngeal branch of the vagus nerve, mandibular
branch of the trigeminal nerve, and the glossopharyn
geal nere.
TLY
There are two forms of cleft palate: congenital and
acquired. Hard palate cleft results from a failure of the
lateral palatine processes of these bones to fuse during
embryonic development. Since palate fusion occurs in a
rostral-to-caudal plane, one can assume that the cleft
extends caudally from the cleft origin where it is identi
fed in the hard palate. The etiology of soft palate con
genital cleft is unknown, but the condition is heritable
in other species such as Charolais cattle and Abyssinian
cats. Other factors implicated include exposure to
toxic, nutritional, and metabolic abnormalities inu/a.
Acquired cleft palates are a complication of dental
or upper airay surgery. Hard palate clefts, perhaps
80
better defned as oronasal fstulae, result from inadver
tent fracture of the palate by a tooth punch during
repulsion of upper cheek teeth. Soft palate clefts can
result from using a hook knife through a nasal
approach during axial division of the aryepiglottic
folds. A nasal approach with this instrument is no
longer recommended for that specifc reason. Excessive
resection of the caudal free edge of the soft palate for
treatment of dorsal displacement of the soft palate can
also result in a soft palate cleft.
PPTHPHYbLY
Regarding the digestive function, the hard palate has a
static role while the soft palate dynamically closes the
choanae during swallowing, predominately through the
action of the levator veli palatini. Failure of this strict
separation between airway and digestive tract leads to
contamination of the nasal cavity and tracheal aspira
tion of feed material. The degree of nasal and airway
contamination is dependent on the size and location of
the cleft. Any cleft rostral to the levator veli palatini
muscle on the soft palate results in nasal or naso
pharyngeal contamination. Clefts caudal to levator veli
palatini muscles cause less consistent and signifcant air
way contamination and therefore result in less or no
lower airway disease.
The respirator role of the palate is mainly a func
tion of the soft palate. A cleft soft palate (in addition to
the resulting tracheal contamination) leads to dorsal
displacement of the soft palate during exercise and,
therefore, an increase in expiratory impedance. This
expiratory resistive load appears to be caused by the soft
palate'S inability to form a proper laryngo-palatal seal
around the epiglottis and arytenoid cartilages. During
exhalation, this results in airflow being directed to the
oropharynx, thus lifting the soft palate into the
nasopharynx and partially occluding its lumen, causing
an expiratory obstruction.
bMPLNMT PM HbTHY
There is no breed or gender predisposition for congen
ital cleft palate, and the condition is discovered in most
cases in the frst few weeks of life because of the obvious
clinical signs. The appearance of milk at the nostrils
(Figure 6.4) and coughing after nursing are distressful
for both the foal and for its carers. Some horses with
more caudal and shorter clefts go unnoticed for many
months and present with a history of recurrent lower air
way infection, stunted growth, and an occasional obser
vation of feed material at the nostrils. The authors have
also obsered cleft palate in association with wr nose.
Figure 6.4 The most common clinical sign of congenital
cleft palate in the horse is milk or feed material exuding
from both nostrils (note: milk appears at the left nostril)
Acquired cleft palate usually presents with a history
of observation of clinical signs shortly after a surgical
procedure for treatment of upper airway disease or,
more rarely, after treatment of dental disease.
LLMLPL bMb
The clinical signs observed with cleft palate vary depend
ing on the location and length of the cleft and include
milk, water, or food exuding from both nostrils
coughing while nursing or eating
un thriftiness
stunted growth
purulent nasal discharge
fever
depression
chronic pneumonia.
It is unclear whether the stunted growth is a result of
loss of caloric intake associated with nasal regurgitation,
ill effects of chronic lower airway disease, or both these
conditions. The severit of the most common complica
tion of this disease, chronic infection of the lower air
ways, will signifcantly influence the survival rate.
MVbJPJM PM PMbb
A presumptive diagnosis of congenital cleft palate can
be made based on clinical signs alone. A defnitive
diagnosis is made by a combination of oral examination
and endoscopic evaluation of the nasal cavity and
nasopharynx. In young foals an oral examination with
digital palpation can assess the integrity of the hard
palate and, with adequate illumination, the most rostral
aspect of the sof palate. Therefore, endoscopic exami
nation of either the oral or nasal cavity is essential to
diagnose the presence and extent of cleft palate. Given
the risk of damage to the endoscope during an oral
endoscopic examination, and accepting the fact that
most equine veterinarians have a greater familiarity
with examining the nasal cavity and nasopharynx, a
nasal endoscopic examination is recommended. Oral
endoscopic examinations should only be undertaken
under general anesthesia. It is surprising how often a
diagnosis of cleft palate is missed, but reasons for the
difculty in making this diagnosis are related to the
quality of equipment used, the endoscopic feld-of-view
size (i.e. small pediatric endoscope) , and, of course, the
rarity of this condition. It is imperative that an endo
scope with adequate illumination and a large feld of
view be used. Pediatric endoscopes have a small feld of
view and are a reason for failing to identi{ a cleft
palate. Whenever possible, a regular endoscope (8-
10 mm) should be used to examine the nasal cavity and
nasopharynx. The endoscopic diagnosis of cleft palate
is made if a lack of palate continuity is observed, or by
observation of other oral structures that are not
normally visible from the nasopharynx (Figure 6.5).
Figure 6.5 The caudal midline of the soft palate is the most
commonly affected area in horses with congenital cleft
palate (note: the oropharynx mucosa can be seen during
nasal video endoscopy)
81
Congenital hard palate cleft is always on the midline,
while soft palate cleft may be on the midline ( axial) or
to one side (abaxial) . The presence of a cleft will allow
obseration of the structures on the floor of the
nasopharynx. The most obvious is the 'white' oro
pharynx mucosa with its numerous folds and rounded
elevations containing the tonsils and the glossoe
piglottic fold at the base of the epiglottis (Figure 6.5).
Because saliva often obscures the floor of the orophar
ynx, one can mistakenly assume the soft palate is intact
if it is covered with mucus or other secretions. These
secretions must be removed to determine if the palate is
intact underneath.
THPTNMT
The treatment of choice for cleft palate is one-stage
surgical correction of the defect, but the high compli
cation rates ( dehiscence of the repair site, chronic
nasal discharge, and high mortality rates) and frequent
need for revisions have limited the number of horses
receiving surgical treatment. The status of the lower
airay influences the anesthetic risk to the patient.
Delay in repair greatly increases the chance of lower
airway infection and poor growth, but the size of the
oral cavit and nasopharynx in young foals limits the
surgical manipulation that can be performed.
Therefore, the ideal age for repair is unknown. The
authors prefer operating on an animal beteen 2-4
weeks after birth.
82
5urgIIepprmm
Transhyoid
pharngotomy
Mandibular
symphysiotomy
Amant ag r
Allows surgical access to caudal
two-thirds of the sof palate.
Animal Is more comforble
postoperatively.
Allows surgical access to the hard
palate and rostral thirdmthe
sof palate.
Surgical approaches
Mandibular symphysiotomy and/ or transhyoid pharyng
otomy are the most widely described surgical
approaches, and their respective values and disadvan
tages are indicated in Table 6.2. Although neither
approach gives exceptional access for unhindered
manipulations, they allow acceptable access with long
instruments so that primary repair of the cleft palate is
possible. Good exposure can be attained via the trans
hyoid pharyngotomy for defects affecting the caudal
two-thirds of the soft palate. In fact, the exposure is bet
ter than that attained by a mandibular symphysiotomy
for this region of the soft palate. However, a transhyoid
pharyngotomy is insufcient when the entire soft palate
or both the hard and soft palates are affected.
For both procedures the animal is anesthetized and
placed in dorsal recumbency with nasotracheal intuba
tion or intubation via tracheostomy. Whenever possible,
nasotracheal intubation is preferable to prevent com
plications associated with tracheostomy and to mini
mize postoperative pain caused by multiple incisions.
Appropriate broad-spectrum antibiotics and non
steroidal anti-inflammatory drugs are given preopera
tively.
Mandibular symphysiotomy ( Figure 6.6)
Mter aseptic preparation of the ventral mandibular
area, a ventral midline incision is made from the basi
hyoid bone extending rostrally to the lower lip. The
skin incision in the ventral mandible area is extended
DI dvantag r
I l lumination must come from
. surgeon's headlight or placement of a
flexible oral light.
Posible damage to hyoepiglotticus
muscle leading to exercise intolerance
because of epiglotic retroversion.
Invasive procedure.
More disomfort to animal.
Requires orhopedic instrumenttion
for fixation of the mandible.
Higher morbidity associated with
fixation (e.g. pin migration, draining
tracs)
through the mylohyoid muscle. The lower lip is not
incised, but a horizontal incision is placed at its base to
allow the lip (Figure 6.7) to be placed orally (Figure
6.8) so the ventral aspect of the symphysis is exterior
ized. A 3. 2 mm drill hole is placed in the symphysis at
Basihyoid
bone
Thyroid
cartilage
Incision
site
Figure 6.6 Mandibular symphysiotomy - note the incision
site extends from the basihyoid bone rostrally to the
mandi bular symphysis
the intended site for screw fixation after the symphys
iotomy. The symphysis is separated longitudinally using
an osteotome. A more abaxial dissection is made on
approximately 1.5 cm of the medial wall of one of the
mandibles. The geniohyoid (Figure 6.9) and genioglos
sus tendon insertions on the mandible are transected
and tagged. The incision is bluntly extended on the
lateral edge of these muscles toward the oral mucosa
avoiding the sublingual salivary gland and the duct of
the mandibular salivary gland (Figure 6.10) . Care must
be taken to avoid damaging the hypoglossal and lingual
nerves at the caudal and medial aspect of the incision.
The oral mucosa is incised to allow separation of the
mandible and access to the palate.
The incision is closed a follows: the oral mucosa is
sutured from caudal to rostral with an absorbable
monofilament suture (no. 0) in a simple continuous
pattern. The geniohyoid and genioglossus tendons are
reattached using an absorbable suture material (no. 1 )
in a simple interrupted or cruciate pattern. The
mandible is fixed with an appropriate length 4. 5 mm
screw placed in lag fashion. Alternatively cross pinning
can be used instead of screw fixation. The lip is replaced
in its proper anatomical position and the oral mucosa
closed as described earlier. The stromal tissue of the lip
is closed with absorbable suture (no. 0) in a simple
Figure 6.7 At the base of the
lower lip a transverse incision
is made in the subcutaneous
tissue and extended to the oral
mucosa
83
interrupted pattern. The mylohyoid muscle and sub
cutaneous tissues are re-apposed separately with an
absorbable suture (no. 0) in a simple continuous
pattern. The skin is closed in a routine manner.
Transhyoid pharyngotomy
An approximately 8-10 em ventral midline incision is
made extending from the caudal extent of the thyroid
84
Figure 6.8 The lip can be placed
orally to expose the mandibular
symphysis so the lip is spared a
vertical incision
Figure 6.9 After the symphys
iotomy has been performed.
the tendon of insertion of the
geniohyoid muscle is transected
in its mid-body
cartilage to the rostral extent of the basihyoid bone.
The incision is extended by bluntly separating the
sternohyoid muscle on the midline. The basihyoid bone
is separated longitudinally using an osteotome. The
incision is extended deeper by blunt dissection of the
loose fascia between the pharynx and basihyoid bone. It
is crucial that the fascia encircling the hyoepiglotticus
muscle be identifed and retracted laterally so it does
not damage this muscle or its innervation. The pharyn-
Incision line
)
Cleft
Palatine artery
Ridge in hard
palate
Figure 6.10 A mucosa-periostea I-sliding flap is made by
incising the mucosa and periosteum lateral to the defect
and sliding the flaps axially (note: position of the palatine
artery in order to avoid it)
geal mucosa is tented and incised with curved scissors
on the midline. Four stay sutures are placed at each cor
ner of the pharyngeal mucosal incision and retracted
out of the incision. A Gelpi retractor is placed in the
pharyngeal mucosa to obtain exposure to the soft
palate. Additionally, an army-navy retractor or a 2. 5 cm
malleable retractor is needed to retract the base of the
tongue rostrally.
Closure is obtained by re-apposing the oral mucosa
using an absorbable monoflament suture (no. 0) in a
simple continuous pattern. The basihyoid suture is re
apposed with a wire suture, and the soft tissues over the
basihyoid bone are re-apposed using a few absorbable
sutures (no. 0) in a simple interrupted pattern. The
sterohyoid muscle is partially re-apposed using three
or four absorbable sutures (no. 0) in a simple inter
rupted pattern, leaving the rest of the incision to heal
by second intention.
Clef palate repair
The use of long instruments and an intra-oral light
source greatly improve the visibility and accessibility of
the palate and are a necessary part of cleft palate repair.
Hard palate repair
A mucosa-periosteal sliding flap is used to close the
hard palate. Using a no. 12 curved Parker-Kerr blade,
the nasal and oral mucosa at the axial edge of the cleft
are incised to the hard palate, thus separatng the nasal
mucosa-periosteal flap from the oral mucosa
periosteal fap. An incision parallel to the long axis of
the cleft is performed through the mucosa and perios
teum of the hard palate as abaxial as possible but still
axial to the palatine artery (Figure 6.10). Using a curved
blunt periosteal elevator, a mucosa-periosteal flap is
freed from the underlying hard palate on both sides of
the cleft. The flaps are slid axially toward each other
and sutured together in one layer through both the
periosteum and mucosa using monoflament absorb
able suture (no. 0 or no. 1) . The defect at the donor site
is left to heal by second intention.
Sof palate repair
Transection of the insertion of the tensor veli palatini
tendon or fracture of the hamulus of the pterygoid
bone are no longer recommended. These procedures
were originally performed to reduce tension on the ros
tral aspect of the soft palate. However, they result in
instability of the rostral aspect of the soft palate during
exercise and increase upper airay impedance.
Therefore, these procedures should not be performed
in horses intended for athletic performance.
If a1equatesat a/atetissueis available for repair with
minimal tension on the incision site, the standard
method for closure of the soft palate in horses involves
a three-layer closure of the defect using a combination
of vertical and horizontal mattress patterns. Using a
long-handled cured Metzenbaum scissor, a 2 mm sec
tion of palate is removed at the periphery of the cleft
palate. The nasal and oral mucosa are separated using a
no. 12 curved Parker-Kerr blade, exposing (when pre
sent) the palatinus muscle (Figure 6.11a). The nasal
mucosa is then apposed using a monoflament
absorbable suture material (no. 00) in a simple contin
uous pattern (Figure 6.11 b) . Interrupted vertical mat
tress sutures penetrating the oral mucosa and stromal
tissue (palatinus muscle, levator veli palatini muscle, or
aponeurosis of tensor veli palatini) are then placed
1. 25 cm lateral to the cleft using monoflament
absorbable suture material (no. 0) creating the strength
layer of the closure (Figure 6. 11 c) . Finally, the everted
oral mucosal layer is apposed using a monoflament
absorbable suture material (no. 00) in a simple contin
uous pattern (Figure 6.11 d) . Another technique, the
double opposing Z-plasty, frst developed in humans to
improve speech and allow adequate maxillary growth
following surgery, has been used by the authors with
some success in horses but appears to have no advan
tage over the standard method.
If sign;[cant sat a/ate tissue is missing and palate
repair without tension is impossible, then buccal
mucosal flaps are used (Figure 6.12) . This technique
can only be done via a mandibular symphysiotomy. The
object of this technique is to create two buccal mucosal
85
a) b) Cleft palate
Nasal mucosa

Stromal tissue
c)
Soft palate
Hard palate
Figure 6.11 Closure of the soft palate. a) The nasal and oral mucosa are separated using a no. 1 2 curved Parker-Kerr blade.
b) The nasal mucosa is apposed using a monofilament absorbable suture material (no. 00)in a simple continuous pattern.
c) Interrupted verical mattress sutures penetrating the oral mucosa and stromal tissue are placed 1.25 cm lateral to the
cleft creating the strength layer of the closure. d) The everted oral mucosal layer is apposed using a monofilament
absorbable suture material (no. 00)in a simple continuous pattern
flaps with their base on the palatoglossal arch. Starting
at the palatoglossal arch, an incision is made sharply
extending rostrally. The incision length must match the
width of the soft palate defect. The width of the flap
must match the length of the soft palate ( Figure 6. 12a) .
Using submucosal dissection and appropriate hemo
stasis, the flap is dissected free up to the palatoglossal
arch. Care is taken to avoid the deep fascial vein. The
mucosal flap is rotated so its mucosal side is facing the
nasopharynx and sutured to the nasal mucosa free edge
of the cleft palate. The same procedure is repeated on
the contralateral side. The second flap is placed over
the sutured flap so its mucosa is facing the oropharynx.
The edge of this second flap is sutured to the oral
mucosa of the free edge of the cleft palate. The donor
sites are left to heal by second intention.
Postoperative care
Postoperatively, the animal is treated with appropriate
antibiotics, with the duration depending on the
presence and severity of lower respiratory infection.
Appropriate analgesics are needed if a symphysiotomy
has been performed. A non-steroidal anti-inflammatory
drug should be used for 5-7 days to minimize swelling
and, therefore, increase the likelihood of healing.
86
Because of the pre-existing airway infection, monitor
ing the patient after surgery is critical.
It is not known what the best postoperative feeding
technique is to allow the palate to heal. Ideally, par
enteral nutrition for 7-10 days would give the greatest
protection to the surgery site. However, this treatment
is expensive and alternative feeding regimes can be
used with acceptable results. The authors recommend
feeding young foals through a nasogastric tube and
feeding a soft gruel to adult horses.
PHMbb
The overall morbidity rate for complications after clef
palate repair approaches 1 00 per cent. However, the
rate of successful healing of a repaired cleft palate may
be as high as 70 per cent after one or more surgeries. It
is not uncommon for one or two revisions to be needed
to obtain sufcient healing to resolve clinical signs.
Short-term morbidity is higher for the mandibular
symphysiotomy approach than the trans hyoid pharyn
gotomy, probably because of the technique required to
repair the symphysiotomy as well as its associated soft
tissue trauma. Reported complications associated with
mandibular symphysiotomy include dehiscence of the
a) b)
Figure 6.12 Schematic of how buccal mucosal flaps are used. a) Starting at the palatoglossal arch, an incision is made
sharply extending rostrally. The incision length must match the width of the soft palate defect. The width of the flap must
match the length of the soft palate. b) The mucosal flap is rotated so that its mucosal side is facing the nasopharynx and
sutured to the nasal mucosa free edge of the cleft palate. The procedure is repeated on the other side.
lip, osteomyelitis of the mandibular pin tracts, and sub
mandibular abscesses. In addition, tongue paralysis can
result from damage to the hypoglossal or lingual nerves
during surgery.
One potential long-term complication following
transhyoid pharyngotomy is epiglottic retroversion at
exercise, because this approach has the potential to
cause trauma to the hyoepiglotticus muscle and/or its
innervation. Previous studies have identifed pharyn
geal surgery and intermandibular abscesses as predis
posing factors for developing epiglottic retroversion.
Local anesthesia of the glossopharyngeal and hypoglos
sal nerves has also reproduced epiglottic retroversion.
There are no reports concerning respiratory func
tion of the soft palate during exercise following cleft
palate repair. Dorsal displacement of the soft palate was
not found in one cleft palate repair case where the
authors were able to perform video endoscopic exami
nation 1 year after surgery, in this case the nasopharynx
appeared stable.
PHVM1M
Because the etiology is not well understood prevention
may be difcult. However, because of heritability con
cerns, it is recommended that owners should neither re-
breed the same dam and sire who have produced off
spring with congenital cleft palate, nor breed from
horses afected with congenital cleft palate.
LHPHY
Signs of dental disease
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Baker G] ( 1970) Some aspects of equine dental disease.
Equine Vet. ] 2: 105-10.
Baker G] ( 1971 ) Some aspects of equine dental radiolog.
Equine Vet. ] 3:46-51 .
Baker G] ( 1974) Some aspects of equine dental decay. Equine
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Baker G] ( 1985) Oral disease of the horse. In Veternar
Dentistr, C E Harey (ed. ) . W B Saunders, Philadelphia,
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Baker G] ( 1991 ) Dental morphology, function and
pathology. In Poceedings o/the 37th Annual Convention o/the
Amercan Association 0/Equine Pactitioners, San Francisco,
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Dixon P M ( 1997) Dental extraction and endodontic
techniques in horses. Comp. Cont. Educ. Pact. Vet.
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and preoperative evaluation. Comp. Cont. Educ. Pact. Vet.
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Easley K] ( 1 991 ) Recognition and Management of the
Diseased Equine Tooth. In Proceedings oJthe 37 Annual
Convention ojthe American Association ojEquine Practitioners,
San Francisco CA. pp. 1 29-139.
Easley] E ( 1 996) Dentistry and Oral Disease. In Smith, B.P.
(ed. ) Large Animal Inteal Medicine. Mosby, St Louis,
pp. 688-97.
Gaughan E M and Debowles R M (eds) ( 1 998) Vet. Clin. N
Am. Equine Pract. Dentistr. W B Saunders, Philadelphia,
August, 1 4( 2) .
Gaughan E M and Debowles R M ( 1 993) Congenital diseases
of the equine head. In Vet. Clin. N Am. Equine Pact. The
Equine Head. W B Saunders, Philadelphia, April,
9( 1 ) :93-1 10.
Gift LJ, DeBowles R M, Clem M F, Rashmir-Raven A, Nyrop
KA ( 1 992) Brachygnathia in horses: 20 cases ( 1979-1989)
[Am. Vet. Med. Assoc. 200( 5) : 715-71 9 .
Hance R S and Bertone A L ( 1 993) Neoplasia. In Vet. Clin. N
Am. Equine Pract. The Equine Head. W B Saunders,
Philadephia, April, 9( 1 ) :21 3-34.
Hawkins] F, Dallap D L ( 1 997) Lateral buccostomy for
removal of a supernumerary tooth . .f. Am. Vet. Med. Assoc.
21 1 ( 3) : 339-340
Kilic S, Dixon P M, Kempson S A ( 1 997) A light microscopic
and ultrastructural examination of calcified dental
structure of horses. The occlusal surface and enamel
thickness. Equine Vet. .f., 29(3) : 1 90-197
Kilic S, Dixon P M, Kempson S A ( 1997) Ultrastructural
enamel fndings. Equine Vet. ]. , 29(3) : 1 98-205
Kilic S, Dixon P M, Kempson S A ( 1 997) Dentine. Equine Vet.
. f, 29(3) : 206-21 2
Kilic S, Dixon P M, Kempson SA ( 1 997) Cement and the
amelocemental junction. Equine Vet . .f. , 29(3) : 21 3-219.
Lane] G ( 1 994) A review of dental disorders of the horse,
their treatment and possible fresh approaches to
management. Equine Vet. Educ. , 6( 1 ) : 1 3-21 .
Mueller P O E ( 1991 ) Equine dental disorders: cause,
diagnosis, and treatment. Compo Cant. Educ. Pract. Vet. 1 3,
pp. 1451-1 460.
Rucker B A ( 1 996) Incisor procedures for field use. In
Poceedings oJthe 42nd Annual Convention oJthe Amercan
Association ojEquine Pactitioners, Denver CO, pp. 22-5.
Scrutchfield W L and Schumacher] ( 1 993) Examination of
the oral cavity and routine dental care. In Vet. Clin. N Am.
i'quine Pact. The Equine Head. W B Saunders, Philadelphia,
April, 9( 1 ) : 123-32.
88
Scrutchfield W L, Schumacher], Martin M T ( 1 996)
Correction of abnormalities of the cheek teeth. In
Proceedings oJthe 42nd Annual Convention oJthe American
Association oj Equine Pactitioners, Denver CO, pp. 1 1-21 .
Uhlinger C ( 1991 ) Common abnormalities of premolar and
molars In Proceedings oJthe 37th Annual Convention oJthe
Amercan Association ojEquine Practitioners, San Francisco,
pp. 1 23-7 .
Cleft palate
Bowman K F, Tate L P, Evans L G, et al. ( 1 982) Complications
of cleft palate repair in large animals. ]. Am. Vet. Med.
Assoc. 1 80: 652-7.
Bowman K F, Tate ]r L P, Robertson] T ( 1 990) Cleft
palate. In Current Practice ojEquine Surger, N A White
and] N Moore (eds) . ] B Lippincott, Philadelphia,
pp. 277-80 .
Furlow L T ( 1 986) Cleft palate repair by double opposing Z
plast. Plastic &constr. Surg. 78:724-33.
Gaughan E M, DeBowes R M ( 1 993) Congenital diseases of
the equine head. Vet. Clin. N Am. Equine Pact. 9:93-1 1 0.
Grossman B S, Brinkman] F, Grant B: A new approach for
intra-oral surgery in the horse: a lip-sparing
modification of mandibular symphysiotomy.]. Equine
Vet. Sci. 1 : 107-9.
Holcombe S], Derksen F], Stick] A, Robinson N E ( 1 997)
Effects of bilateral hypoglossal and glossopharyngeal nerve
blocks on epiglottic and soft palate position in exercising
horses. Am . .f. Vet. &s. 58(9) : 1 022-1026.
Holcombe S], Derksen F], Stick] A, Robinson N E ( 1 997)
Effect of bilateral tenectomy of the tensor veli palatini
muscle on soft palate function in horses. A 58
(3) : 31 7-321 .
Mason T A, Speirs V C, Maclean A A, Smyth G B ( 1997)
Surgical repair of cleft soft palate in the horse. Vet. Rec.
100:6-8.
Nelson A W, Curley B M, Kainer R A ( 1 971 ) Mandibular
symphysiotomy to provide adequate exposure for intraoral
surgery in the horse . .f. Am. Vet. Med. Assoc. 1 59: 1 025-31 .
Sager M, Nefen S ( 1 998) Use of buccal mucosal flaps for the
correction of congenital soft palate in three dogs. Vet.
Surg. 27:358-63.
Semevolos S A, Ducharme N G ( 1 998) Surgical repair of
congenital cleft palate in horses: 8 cases ( 1979-1997) .
Proceedings of the 44th annual conference of the
American Association of Equine Practitioners, Baltimore,
pp. 267-8.
7
Esophageal diseases
SL Fubini
ANATOMY AND PHYSIOLOGY
The cranial cervical esophagus is on the median plane
just above the trachea. At the level of the proximal one
third of the neck, the esophagus passes to the left, rarely
to the right, of the trachea and becomes more super
ficial. Dorsolaterally the esophagus is in proximity to
the common carotid artery, vagosympathetic trunk and
recurrent laryngeal nerves. At the mid-cervical region,
the esophagus inclines steeply to the thoracic inlet.
From there, it passes to the right of the aortic arch and
enters the diaphragm to the left of the midline. In the
abdominal cavity, the esophagus enters the cardia of
the stomach at the level of the 14th rib.
The cranial two-thirds of the esophagus consists of
two helical layers of striated muscle. The distal third is
composed of smooth muscle. The esophageal mucosa is
made up of moderately keratinized stratified squamous
epithelium arranged in longitudinal folds. The esopha
gus is unique to other hollow viscera of the gastro
intestinal tract in that only the abdominal portion of
the esophagus has a serosal covering. The remainder is
covered by the tunic adventitia which is rich in blood
supply, nerves, and elastic fbers. The blood supply of
the cervical esophagus originates from the carotid arter
ies and the thoracic part is supplied by the esophageal
artery and a branch of the gastric artery. A combination
of the central nervous system, intrinsic and extrinsic
nerves, and myogenic factors act to integrate
esophageal peristalsis and lower esophageal sphincter
relaxation. Horses are prone to gastric rupture, and it is
unknown exactly why this is so. One theory has been
that there is a powerful caudal esophageal sphincter
that prevents vomiting in response to intragastric pres
sure. However, this has not been shown to be the case
experimentally. It is more likely that the vomiting reflex
is poorly developed in horses.
ESOPHAGEAL DISORDERS
Clinical signs
Obstruction of the esophagus (,choke') in the horse is
typically manifested by feed and water appearing at the
nostrils and mouth, and is associated with salivation,
dysphagia, and flapping of the lower lip. Early in the
condition, when feed is offered affected horses will
show interest but do not eat. Coughing may occur, and
affected horses appear anxious and may show some
retching as they attempt to swallow. A time progresses,
affected animals will become dehydrated and inappe
tent.
Diagnosis
The horse's hydration status is evaluated by assessing
skin turgidity, mucous membrane color, and capillary
refll time. The neck and laryngeal area should be
palpated for any subcutaneous emphysema or mass
lesions. A detailed oral examination should be per
formed to look for abrasions and to rule out cleft palate,
dental disease, or other foreign bodies in the mouth.
The lower ailWay should be examined by auscultation
with a rebreathing bag to detect any evidence of adven
titious lung sounds compatible with aspiration pneu
monia. Thoracic radiographs should be taken if there is
any suspicion of lower ailWay pathology. Nasogastric
intubation is essential in most instances to determine
89
the location of the esophageal obstruction. Minimal
laboratory tests include packed cell volume (PCV) , total
plasma protein (TPP), and plasma electrolyte concen
trations to determine the horse's metabolic and hydra
tion status. It should always be remembered that rabies
and other causes of dysphagia must be on a differential
diagnosis list when dealing with a suspected esophageal
obstruction (see Chapter 5).
Esophagoscopy
When examining the esophagus by esophagoscopy, it is
ideal to have the animal sedated and if possible pass the
endoscope distal to the area of interest and examine
the site as the endoscope is moved in an oral direction.
The esophagus is continuously insuflated with air to
dilate it and allow better observation of lesions. The
normal esophagus has off-white colored longitudinal
mucosal folds. To view the entire esophagus, a 3 m
endoscope is necessary in an adult horse, and if an area
of suspicion is seen, it should be examined repeatedly
to rule out an artifact. If the esophageal lumen is
obstructed, esophagoscopy may be useful to help
evaluate the nature of the obstruction.
Radiographic examination
Most esophageal obstructions occur in the cervical area.
Diagnostic radiographs of this area can be obtained
with portable radiographic equipment. Examination of
lesions in the thoracic esophagus requires high power
equipment with a good abilit to penetrate (increased
kVp and r capacit.) Plain or survey radiographs
demonstrate lesions such as radio-opaque foreign
bodies or peri-esophageal gas (Figure 7.1). For a com
plete esophageal study, positive contrast esophagogra
phy is necessary. A radiograph taken after
administration of barium paste (e.g. Novopo-que,
Alcon Laboratories, Lafayette, IN) will allow evaluation
of mucosal folds. An aqueous-based contrast agent (e.g.
Gastrografn, ER Squibb and Sons, Inc., Princeton, r)
should be used if there is suspected esophageal perfo
ration. An esophagogram is especially useful when
esophageal strictures and fistulae are suspected. The
study is performed by administering positive-contrast
material under pressure through a cuffed nasogastric
tube. Double-contrast radiography, simultaneous
administration of air, and a positive contrast agent,
allows examination of the mucosa in a distended esoph
agus. This technique is useful to evaluate the extent of
mucosal injury following foreign body obstruction.
Esophageal radiography is a useful technique but
artifacts are common. To avoid the appearance of arti
facts during swallowing, xylazine should be adminis
tered 5 minutes before the radiographs are taken. The
90
Figure 7.1 Survey radiograph showing an esophageal
obstruction due to a feed impaction
entire area of interest should be fully distended when
contrast radiography is performed.
GENERAL SURGICAL CONSIDERATIONS
Restraint and anesthesia
Some esophageal procedures can be performed in the
standing sedated animal. These include esophagotomy
of the cervical esophagus or exposure of the esophagus
and manipulation. If extensive surgical procedures are
necessary general anesthesia is recommended. For
surgical procedures involving the thoracic esophagus,
general anesthesia and positive pressure ventilation is
required.
When operating on the esophagus it is imperative to
use gentle tissue handling, strict aseptic technique, and
the prevention of any undue tension on the sutures.
Perioperative antibiotic therapy is appropriate as are
non-steroidal anti-inflammatory drugs. It is absolutely
essential that a nasogastric tube be placed before induc
tion of anesthesia because passage is very difcult once
a horse is anesthetized. The tube should extend past the
level of obstruction.
Surgical approaches
Cranial cervical esophagus
The cranial one-third of the cervical esophagus can be
approached from either side of the neck. The skin inci
sion is made dorsal to the jugular vein. The cutaneous
coli muscle is reflected caudally, the sternocephalicus
muscle and jugular vein are retracted ventrally, and
the brachiocephalicus muscle is retracted dorsally. The
incision is then extended through the omohyoideus
muscle.
Mid-cervical esophagus
In the middle one-third of the cervical esophagus, the
ventral midline approach is preferred. The sternothyro
hyoideus muscles are separated, and the trachea is
retracted to the right of midline.
Caudal cervical esophagus
In the caudal cervical region, the esophagus is located
dorsal to the trachea. A ventrolateral approach is used.
A skin incision is made ventral to the left jugular vein.
The sternocephalicus and brachiocephalicus muscles
are retracted, and the deep cervical fascia is incised to
expose the esophagus. The vagosympathetic trunk and
recurrent laryngeal nerve must be avoided. Retractors
should be adequately padded.
Thoracic esophagus
For lesions in the thoracic esophagus, a rib resection is
generally performed from the left side. A skin incision is
made directly over the rib. Subcutaneous tissues, cuta
neous trunci, latissimus dorsi, and external abdominal
oblique muscles are incised. Subperiosteal dissection is
continued to isolate the rib. The rib is transected
dorsally with Gigli wire or a saw and disarticulated at
the costochondral junction. The pleura is incised and a
thoracic retractor is placed to spread the adjacent ribs.
The carotid sheath and vagosympathetic trunks should
be identifed and retracted.
Esophageal layers
When the esophagus is incised it separates easily into
to distinct layers. The frst layer is the outer, relatively
ESOPHAGEAL DISEASES 7
inelastic muscle layer and adventitia. The elastic inner
layer composed of mucosa and submucosa contains the
greatest amount of fascia and greatest tensile strength
during esophageal closure. Traditionally, when operat
ing on the esophagus these two distinct layers are closed
separately. When mucosa and submucosa are being
closed together it has been recommended that the
knots be tied within the esophageal lumen to prevent
contamination of the wound with ingesta migrating
along the suture tract. The muscle and adventitia are
then closed separately. A wide variet of suture patterns
are appropriate. Typically, a non-absorbable, non
reactive monoflament suture such as polypropylene or
nylon is recommended, or a long-lasting absorbable
monoflament such as polyglyconate. There has been
debate in the last few years whether the mucosa or the
submucosa are the true functional holding layers of the
esophagus. In 1988 Dallman reported that the submu
cosa had the greatest strength, and that including the
mucosa in the closure did not enhance the repair.
Some advocate a one-layer closure of the esophagus
with an absorbable monoflament suture using the sul
mucosa as the strength layer and not penetrating the
mucosa.
Incisional closure
In the cervical area the incision is closed by re-apposing
each layer incised with absorbable suture material,
given the potential contamination of the surgery site.
Drains are generally placed to
minimize dead space
allow evacuation of contaminated fluids.
The lack of a serosal covering may contribute to com
plications following surgery, including leakage and
dehiscence.
Closure of the left hemithorax following a thoraco
tomy for exposure of the thoracic esophagus is carried
out as follows
using long acting local anesthesia the intercostal
nerves of the resected rib as well as the two adjacent
ribs cranial and caudal are desensitized
a 28th French chest drain is then placed in the
chest at the 8th intercostal space and secured to the
skin with a non-absorbable suture
the intercostal muscles are closed in a simple
continuous pattern using no. 3 polyglactin 910
suture material
at this time continuous low pressure suction is
applied to the chest drain to reduce the
pneumothorax
the latissimus dorsi is then closed in a simple
continuous pattern using the same material
91
the subcutaneous tissue and cutaneous trunci are
closed together with no. 1 polyglactin 910 suture
material
the skin is closed with staples and an impervious
impregnated drape is applied over the incision and
drain site
the drain is closed with a syringe case glued into
place
on recovery a Heimlich valve is applied to the drain.
SPECIFIC DISORDERS
Esophageal obstruction
A lumen obstruction is ver common following inges
tion of feed or foreign material. Foreign bodies such as
carrots, apples, and wood chips may obstruct the esoph
agus, as well as feed impactions. Impactions can be
secondary to a narrowing of the esophagus from some
other pathology. Feed impaction has been associated
with greed and poor dentition, and is known to be com
mon in Shetland ponies. The most common sites of
obstruction have been reported to be the cranial cervi
cal esophagus, the esophagus at the thoracic inlet, and
the caudal esophagus sphincter in the hiatal area.
However, in this author's experience, obstructions are
also common in the cranial and mid-cervical region.
Rarely, extralumenal compression of the esophagus can
occur secondary to neck trauma and subsequent fbro
sis, mediastinal abscessation and neoplasia, or vascular
anomalies.
Treatment
Medical management
Because of the risk of aspiration pneumonia, a horse
with suspected esophageal obstruction should be kept
in a stall and not allowed to eat or drink until treatment
is initiated. All bedding should be taken away or a
muzzle applied to prevent any oral intake. Spontaneous
resolution of esophageal obstruction may happen with
sedation only. If resolution is not apparent in several
hours, the horse should be sedated and a nasogastric
tube should be passed to the level of the obstruction.
Esophagoscopy can be performed as well, although
sometimes it is difcult to be precise about a diagnosis
if the proximal esophagus is distended with gas and
fluid.
If spontaneous resolution does not occur, tissue han
dling and manipulation should be gentle to help pre
vent any further damage to the esophagus. The horse's
head is lowered with the use of sedation, and repeated
lavage at the site of the obstruction is performed
92
Figure 7.2 Lavage of an esophageal obstruction using a
stomach tube placed through a larger cuffed tube in an
effort to prevent aspiration of feed material
(Figure 7.2). Some clinicians like to pass a large diame
ter malleable endotracheal tube through the nose into
the esophagus, and then pass a small lavage tube
through the lumen of the endotracheal tube. This tech
nique allows the lavage fluid and food to drain through
the larger diameter tube, thereby minimizing the risk of
aspiration. Patience is required as it may take several
attempts to -dislodge the impaction with lavage. If
repeated attempts are unsuccessful to dislodge the
impaction or foreign body, the horse can be anaes
thetized and these procedures repeated with the horse
relaxed under general anesthesia and with a endo
tracheal tube with inflated cuff in place.
Surgcal therap (esophagotomy)
If it is impossible to relieve an obstruction with medical
management, an esophagotomy is indicated. Ideally,
the incision is made in a healthy area of esophagus adja
cent to the foreign body. If the esophageal wall appears
to be without compromise, a primary closure can be
attempted which should allow for rapid healing.
Following surgery, food and water are withheld initially
for 48 hours, and the horse is kept hydrated with
intravenous fluid therapy. Following this time, small
amounts of feed are introduced, usually in the form of
a pelleted slurry. In 1982, Stick recommended a pel
leted diet (7 g/kg in 5 liters of water t.d.s.). Studies have
shown that hay may predispose wound dehiscence.
Different recipes exist for feeding horses via stomach
tube, and these are noted in the reference list (Orsini
and Divers, 1998). If the esophageal wall is not normal
and the surgeon elects to leave the wound open to heal
by secondary intention, placement of an esophageal
feeding tube until the wound contracts is advocated. If
an esophagostomy tube is elected, the current recom
mendation is to position the caudal end of the tube in
the stomach. If left to heal by secondary intention, a
traction diverticulum is likely to result, however usually
these are asymptomatic.
Once the obstruction is relieved, the integrity of the
mucosa of the esophagus should be checked via
esophagoscopy. Circumferential mucosal defects are
prone to stricture.
Esophageal rupture
Esophageal rupture can be a catastrophic lesion.
Ruptures of the cranial esophageal sphincter can be
very difcult to visualize with esophagoscopy. The most
likely cause for such a perforation is repeated naso
gastric intubation. The more distal esophageal ruptures
are easier to see using esophagoscopy. Diagnosis can be
aided by radiography and ultrasound examination.
Horses with closed cerical esophageal perforation
quickly develop subcutaneous emphysema and cellulitis
around the area. Unfortunately the cellulitis can extend
down fascial planes toward the mediastinum and
thoracic cavit. The horse may be so dyspneic that a
tracheotomy is required.
Treatment
Most esophageal perforations will have to heal by sec
ondary intention. Adequate ventral drainage is essential
to prevent migration of the infection to the thoracic
inlet, and the wound is allowed to heal by contraction
and epithelialization. The horse can be fed by placing
an esophagotomy tube through the rupture site and
allowing tissues to contract down around the tube.
Alternatively it can be fed through a tube placed distally
to the esophageal perforation in a normal area of the
esophagus. Typically, although these horses have a
long-drawn-out hospital course, they do well with
aggressive wound care. However, some horses take a
long time to granulate the wound and allow migration
of esophageal mucosa over the granulating bed.
Intermittent fluid therapy may be necessary.
Mucosal disease
Mucosal disease is most commonly caused by ulceration
secondary to an obstruction. For this reason all horses
that have had resolution of an obstruction should be
checked with esophagoscopy. If a mucosal defect is pre
sent, current recommendations are to feed a pelleted
ration, and administer broad-spectrum antibiotic and
anti-inflammatory drugs. Surgical management should
be delayed for 60 days until the lumen of the stricture
site is of maximal diameter and mucosal healing is com
plete. It is possible that in the future 'bougienage' or
inflation of a cuffed tube or balloon at the site of a stric
ture might be feasible. However at this point, there are
no published reports of using these techniques in
horses, although there are anecdotal reports of success
expressed on a popular equine server (ECN - equine
clinicians' network).
Esophageal stricture
Esophageal strictures can be congenital or acquired.
Acquired strictures can result from either external
trauma such as a kick or from internal trauma, i.e.
foreign body or feed impaction. Strictures can also
result following mucosal disease or esophageal surgery.
Prognosis varies with the nature of the stricture. There
are three types of annular lesions which are categorized
depending on which layers of the esophagus are
involved
1. mural lesions that involve only the adventitia and
muscularis
2. esophageal rings or webs that involve only the
mucosa or submucosa
3. annular stenosis that involves all layers of the
esophageal wall.
Treatment
Clinical and experimental studies indicate that stricture
formation can occur as soon as 15 days after circumfer
ential mucosal loss, but there is little change in lumen
diameter for the next 15 days. Between 30-60 days post
injury, the lumen diameter increases with the largest
change occurring between days 30-45. Therefore, as
mentioned earlier, surgical incision of a stricture
should be delayed until 60 days after the traumatic
incident. Pelleted mash has been found to be the most
palatable feed. Other alternatives include intravenous
total parenteral, or partial parenteral nutrition, or
extra-oral alimentation using an esophagostomy tube.
93
Surgical management
The surgical management of an esophageal stricture
will depend on the layer of the esophagus that is
involved, although this may not be known prior to the
start of surgery. Surgery should be performed under
general anesthesia, and once again a stomach tube
should be passed to the level of the obstruction prior to
induction of the anesthesia.
Esophagomyotomy
A esophagomyotomy is indicated for an esophageal
stricture confned to the muscularis and adventitia. The
esophagus is exposed and gently freed from surround
ing tissue. Once the esophagus is isolated a longitudinal
incision is made through the adventitia and muscle
allowing mucosa and submucosa to bulge through the
incision. The stomach tube is gently advanced to deter
mine if the lumen will allow passage easily across the
strictured site. The muscle should be separated from
the mucosa around the entire circumference of the
esophagus. In most instances, the myotomy is left open
and the rest of the surgical incision is drained and
sutured in a routine manner.
Partial esophageal resection
This procedure is most appropriate for lesions confned
to the mucosa and submucosa. Once again the esopha
gus is approached and freed from surrounding tissues.
The muscularis and adventitia are incised in a longitu
dinal manner, and the strictured area of mucosa and
submucosa dissected free and resected (Figure 7.3).
The mucosa is closed only if possible to do so without
excessive tension. It is ideal to close the muscularis
because it seres as a muscular tube upon which the
mucosal defect can regenerate. It may be necessary to
feed the horse through a separate esophagotomy site or
via extra-oral alimentation.
Complete esohageal resection
A resection and anastomosis of all layers of the esopha
gus is an option if all layers are involved or the muscu
lature is damaged and is not useful as a scaffold for
mucosal regeneration. Minimizing tension and good
apposition of tissue layers are necessary. It is suggested
that prior to surgery the horse is trained to tolerate an
elastic martingale that prevents elevation of the head.
The esophagus is approached and isolated. Rubber
tubing rather than clamps may be less traumatic when
manipulating the esophagus. Transection is performed
in healthy tissue cranial and caudal to the lesion, and a
two-layer anastomosis is performed. Past recommenda
tions are to close the mucosa and submucosa in simple
continuous or interrupted pattern followed by closure
94
Figure 7.3 Esophagomyotomy and resection of a
mucosal stricture via a ventral incision
of the muscular layer in a simple interrupted pattern
(see General surgical considerations). If necessary, ten
sion relieving incisions adjacent to the anastomosis can
be performed. Extra-oral alimentation or feeding by
esophagostomy after surgery may be advantageous.
Esohaglasty
Esophagoplasty is a longitudinal incision in the esopha
gus closed in a transverse manner. This has had limited
applicability in the horse and is only recommended for
lesions less than 2 cm in length.
Esohageal relacement
In small animals and humans, other tissues have been
used to create a feeding tube to replace a diseased
esophagus. These include jejunum, colon, stomach,
and skin. These pedicle grafts have limited applicabilit
in the horse.
Muscular patch grafing
There is one successful report in the literature using a
muscular patch graft of the sternocephalicus tendon. In
this case, the esophagus was exposed and the lesion was
identifed and resected. Both sides of the mucosal
defect were apposed to the muscle body of the tendon
using pre-placed mattress sutures. Again, this proce
dure requires appropriate drainage and the same feed
ing instructions mentioned above.
Fenestrtion thrugh a cicatrix
The fnal procedure reported for esophageal stricture is
the one currently employed in our hospital. The esoph
agus is isolated and an esophagotomy is performed
through the strictured area followed by fenestration of
the mucosal and submucosal cicatrix. This may need to
be done in several places until one is able to pass a stom
ach tube past the strictured segment easily. Following
this, an esophagostomy tube is placed through the
defect and the horse is fed through the tube until the
site constricts down enough for the tube to be removed
and the horse can eat again normally. A this incision
heals a traction diverticulum is formed. The hope is
that a large enough lumen diameter will be created to
make a second procedure unnecessary.
Esophageal diverticulum
There are two types of diverticulum.
I. Traction or true diverticulum, resulting from
contraction of periesophageal fbrous scar tissue
often secondary to wound or previous surgery. This
condition is usually asymptomatic and appears as a
wide neck on a barium swallow esophagogram.
2. A pulsion or false diverticulum, resulting from
protrusion of mucosa and submucosa through a
defect in the esophageal musculature (Figure 7.4).
These diverticulae may be caused by external
trauma or by some fluctuation in esophageal
intralumenal pressure and overstretch damage to
esophageal muscle fbers by impacted feed stuff. A
pulsion diverticulum appears spherical and flask
like on an esophagogram. They may enlarge over
time and become evident as a large swelling in the
neck resulting in dysphagia.
Figure 7.4 Pulsion diverticulum viewed via
esophagoscopy
Treatment
Treatment of traction diverticulum is rarely necessary.
Treatment of a pulsion diverticulum involves isolation
of the esophagus and either inversion of the redundant
mucosal sac into the lumen of the esophagus or resec
tion of the sac.
Esophageal fistula
Esophageal fstulae can result from healing of
esophagotomy incisions or after esophageal perfora
tion. They can be diagnosed clinically or by contrast
radiography when barium is administered under pres
sure. Most fstulae will heal once ventral drainage is
established (Figure 7.5). If healing does not occur, it
may be necessary to perform a resection of the sinus
tract and closure of the stoma.
Figure 7.5 Secondary healing of an esophagotomy site.
This horse had previous esophageal surgery and the tube
was placed to permit extra-oral feeding
95
Figure 7.6a Positive contrast esophagogram showing a
filling defect typical of an intramural esophageal cyst
Intramural esophageal cysts
Cysts have been found within the wall of the esophagus,
that are consistent histologically with a keratinizing
squamous epithelial inclusion cyst. These cysts can be
diagnosed on the basis of clinical examination and
radiography (Figure 7.6a). Clinical signs include
dysphagia
regurgitation
a palpable soft tissue mass in the neck (in some cases).
Filling defect are present on contrast radiography.
Surgical treatment recommendations include removal
of the cyst 'in toto' by gently dissecting it free following
esophagomyotomy, or marsupialization (Figure 7.6b).
The advantage of the latter is that there is less risk of
entering the esophageal lumen.
Other anomalies
Congenital abnormalities
Congenital abnormalities of the esophagus are rare.
There have been occasional reports of tubular duplica
tion in young animals; the signs include dysphagia and
regurgitation. Congenital esophageal dilatation (ecta
sia) was reported in a 4-month-old foal with a history of
intermittent milk regurgitation.
Esophageal neoplasia
Reports of esophageal neoplasia are also very rare. There
have been two horses mentioned in the literature with
squamous cell carcinoma. Resection and anastomosis is
96
Figure 7.6b Intramural esophageal cyst removed at
surgery (top). Incision of the cyst shows the creamy cyst
contents (bottom)
possible early in the disease process but the prognosis is
poor.
Megaesophagus
Primary megaesophagus is also very rare in the horse. It
is most likely caused by a generalized motor dysfunction
similar to that reported in dogs. However mega
esophagus secondary to gastric ulceration in foals is
more common. Presumably repeated gastroesophageal
reflux, impaired peristalsis, and partial obstruction of
the cardia contribute to the development of mega
esophagus. Therapy involves treatment of the primary
problem, i.e. the gastric ulcerations, and if necessary
surgical correction of gastric outflow obstructions.
COMPLICATIONS OF ESOPHAGEAL
SURGERY
Unfortunately, complications including dehiscence are
common following esophageal surgery for a number of
reasons.
I. It is difficult to work on the esophagus without
having resulting tension on the tissues.
2. The esophagus is in constant motion due to
swallowing and diaphragmatic movement, and
there is constant irritation by food and saliva.
3. The lack of a serosal covering may contribute to a
delay in healing. The serosa is believed to contribute
to a fibrin seal following incision and to provide
alignment of apposed tissue layers after suturing.
4. The horse with an esophageal obstruction suffers
electrolyte abnormalities because of the loss of
large amounts of saliva and subsequent
dehydration, hyponatremia, and hypochloremia,
and initial transient metabolic acidosis due to the
loss of bicarbonate. Later, progressive metabolic
alkalosis results because of progressive
hypochloremia.
5. Because of the proximity of the recurrent laryngeal
nerves to the esophagus it is possible to damage
these structures during surgical manipulation.
Careful attention to atraumatic tissue handling is
necessary.
Other complications include
extension of infection down fascial planes to the
thoracic cavity and mediastinum resulting in
pleuritis and mediastinitis
aspiration pneumonia is the most common lower
airway complication
Horner's syndrome has been reported secondary to
esophageal surgery
laminitis can develop from some of the dietary
management processes that are necessary.
Prognosis
Many complications can be dealt with by careful tissue
handling, perseverance, and sophisticated medical
management. In surgery, efforts to minimize tension
and use of strict aseptic technique lessen the likelihood
of incisional problems. Adequate ventral drainage and
careful apposition of tissues to prevent dead space
following surgery is also ideal. Feed impactions and
foreign body obstructions have been reported to have a
short-term survival rate of 78 per cent, although 37 per
cent are reported to have some problems with recurring
obstruction. Mural strictures involving only the muscle
and adventitia of the esophagus have a good prognosis.
If the mucosa and submucosa are involved, penetration
of the esophageal lumen is necessary, making the prog
nosis more guarded. In most instances, esophageal per
f'rations can be managed successfully with adequate
ventral drainage and long-term wound care. In our
experience, cranial esophageal perforations are
exceedingly difcult to manage.
ESOPHAGEAL DISEASES
BIBLIOGRAPHY
Aanes W A (1975) The diagnosis and surgical repair of
diverticulum of the esophagus. Poc. Am. Assoc. Equine
Pact. 21 :211.
Bowman KF, Vaughan] R, Quick C B, et al. (1978)
Megaesophagus in a colt.] Am. Vet. Med. Assoc. 172:334.
7
Craig D R, Shivy D R, Pankowski R L, et al. (1989) Esophageal
disorders in 61 horses - results of nonsurgical and surgical
management. Vet. Surg. 18:432.
Craig D R, Todhunter R] (1987) Surgical repair of an
esophageal stricture in a horse. Vet. Surg. 16:251.
Dallman M] (1988) Functional suture-holding layers of the
esophagus in the dog.] Am. Vet. Med. Assoc. 192:638.
Freeman D E, Naylor] N (1978) Cervical esophagotomy to
permit extra oral feeding in the horse.] Am. Vet. Med.
Assoc. 172:314.
Fubini S L, Starrak G S, Freeman D E (1999) Esophagus. In
Equine Surgey 2nd edn,] A Auer and] A Stick (eds.). W B
Saunders, Philadelphia, pp. 199-209.
Hackett R P, Dyer R M, Hofer R E (1978) Surgical correction
of esophageal diverticulum in a horse.] Am. Vet. Med.
Assoc. 173:998.
Hoffer R E, Barber S H, Kallfelz FA, et al. (1977) Esophageal
patch grafing as a treatment for esophageal stricture in a
horse.] Am. Vet. Med. Assoc. 171:350.
Moore] N, Kintner L D (1976) Recurrent esophageal
obstruction due to squamous cell carcinoma in a horse.
Corell Vet. 66:589.
Murray M], Ball M M, Parker G A (1988) Megaesophagus
and aspiration pneumonia secondary to gastric ulceration
in a foal.] Am. Vet. Med. Assoc. 192:381.
Oakes M G, Hosgood G, Snider III T G, Hedlund C S,
Crawford M P (1993) Esophagotomy closure in the dog.
Vet. Surg. 22:451-6.
Orsini] A, Divers T] (1998) Manual of Equine Emergencies 1st
edn. W B Saunders, Philadelphia, pp. 658-63.
Orsini] A, Donawick W] (1986) Surgical treatment of
gastroduodenal obstructions in foals. Vet. Surg. 15:205.
Peacock E E, Van Winkle L (1984) Healing and Reair of
Viscera Wound Reair 3rd edn. W B Saunders, Philadelphia,
p. 451.
Roberts M C, Kelly W R (1979) Squamous cell carcinoma of the
lower cervical esophagus in a pony. Equine Vet.] 11: 199.
Sams A E, Weldon A D, Rakestraw P (1993) Surgical
treatment of intramural esophageal inclusion cysts in
three horses. Vet. Surg. 22:135-9.
Scott E A (1982) Surger of the equine oral cavity. Vet. Ctin.
N Am. Large Anim. Pact. 4:3.
Scott E R, Snoy P, Prasse K W, et at. (1977) Intramural
esophageal cyst in a horse.] Am. Vet. Med. Assoc. 171:652.
Shamir M H, Shahar R,]ohnston D E, Mongil C M (1999)
Approaches to esophageal sutures. Camp. Cant. Ed.
21:414-20.
Sisson S (1975) Equine digestive system. In Sisson and
Gossman's Anatomy of the Domestic Animals 5th edn, R Getty
(ed.). W B Saunders, Philadelphia, p. 454.
Stick] A, Derksen F], McNitt D L, et al. (1983) Equine
esophageal pressure profile. Am.] Vet. Res. 44:272.
Stick] A, Derksen F ], Scott G A (1981) Equine cervical
esophagostomy: Complications associated with duration
and location of feeding tubes. Am.] Vet. Res. 42:727.
Stick] A, Krehbiel] D, Kunze D], et at. (1981) Esophageal
healing in the pony. Comparison of sutured vs.
nonsutured esophagotomy. Am.] Vet. Res. 42:1506.
97
Stick] A, Robinson N E, Krehbiel] D (1981) Acid-base and
electrolyte alterations associated with salivary loss in the
pony. Am.]. Vet. Rs. 42:733.
Stick] A, Siocombe R F, Derksen R], Scott E A (1983)
Esophagotomy in the pony: Comparison of surgical
techniques and form of feed. Am.]. Vet. Rs. 44:2123.
Stick J H (1982) Surgery of the equine esophagus. Vet. Cin. N
Am. Larg
e Anim. Pact. 4:33.
98
Todhunter RJ, Stick] A, Siocombe R F (1986) Comparison of
three feeding techniques after esophageal mucosal
resection and anastomosis in the horse. Corell Vet. 75:16.
Todhunter RJ, Stick] A, Trotter G W, et al. (1984) Medical
management of esophageal stricture in seven horses.
]. Am. Vet. Med. Assoc. 185:784.
8
Etiolog
y
, risk factors, and
pathoph
y
siolog
y
of colic
Factors associated with
increased risk of colic
NO Cohen
Colic is considered by horse owners and equine veteri
narians to be one of the most important (if not the most
important) medical problems of horses. The term colic
comprises nearly 100 conditions recognized to result in
abdominal pain. Because a comprehensive review of the
determinants of the many disorders that cause colic is
beyond the scope of this chapter, factors known to con
tribute to the development of colic will be described
here. Despite the magnitude of the problem of equine
colic, relatively little is known about factors that cause it,
particularly those forms of colic examined in the feld
by veterinarians.
SIGNALMENT
Age, sex, and breed have been associated with increased
risk of colic. Some forms of colic appear to be more
prevalent in younger animals (e.g. intussusception in
younger horses, laral cyathostomosis in horses less
than 6 years old) while strangulating lipomas, for exam
ple, are more common in older horses. Colic can affect
horses of any age. Risk of colic, risk of requiring surgical
treatment for colic, and prognosis for survival appear to
be higher in older horses than in younger horses.
Some forms of colic are gender-specifc (e.g. uterine
torsion or scrotal herniation). Although not substanti
ated by an epidemiologic study, colonic torsion appears
to be more prevalent among mares. Sex has not been
consistently associated with the general complaint of
colic.
The Arabian breed has been identifed in multiple
epidemiological studies to be associated with increased
risk of colic. The meaning of this obseration remains
unknown. The association may be related to difering
management practices for Arabians, increased concern
for management of colic among owners and caretakers
of Arabians, or a genetic predisposition to gastrointesti
nal disorders among Arabians. Alternatively, Arabians
may have been less likely to be selected for the control
populations for these epidemiological studies. Feca
liths and impactions of the small colon appear to be
more prevalent in younger miniature horses while
Standardbreds appear to be at increased risk of scrotal
hernias.
Discrepancies in observations made between studies
with regard to age, sex, and breed can be confusing to
veterinarians wanting to apply the results of epidemio
logical studies of colic. These discrepancies may result
from differences between studies such as the outcome
used for analysis (e.g. colic in general form versus a spe
cifc form), or the population studied, also the relation
ship for a given factor may be more complex than a
simple bivariate comparison allows (e.g. effects of
management may vary with age). Those observations
that are repeatable should be considered to have
greater credibility.
MEDICAL HISTORY
History of previous colic has been repeatedly identifed
as a risk factor for colic. In one study the effect was mod
ifed by the caretaker - the risk of colic for horses with
101
8 COLIC
previous colic nearly doubled if the horse was cared for
by a non-owner. Horses with history of previous surgery
for colic are at increased risk of colic. The association of
previous colic or previous surger for colic with future
colic is important information for horse owners and
farm managers.
FARM MANAGEMENT FACTORS
Management practices are of particular importance
because they can be changed and, consequently, can
reduce the incidence of colic. Dietary factors can pre
dispose to colic, however, epidemiological studies have
yielded conflicting result. Some studies have impli
cated the type (e.g. corn) or amount (i.e. increased risk
with increased amount) of concentrate fed, whereas
others have implicated change in diet, particularly a
change in the type, quality, or batch of hay/forage fed.
It is reasonable to believe that many types of concen
trate can be fed safely to horses - although excessive
amounts may predispose to colic, laminitis, and endo
toxemia -and that changes in diet, particularly changes
in forage/hay predispose to colic. Because diet is widely
regarded as an important risk factor for colic, dietary
practices may be modifed to decrease the risk.
However, little reliable information is available and it is
apparent that further epidemiologic studies of diet and
colic are much needed.
Management practices have been associated with
increased risk of colic but few studies have been con
ducted. It is likely that management factors vary
between regions and countries. Factors associated with
colic in one area may not be relevant in other areas.
Despite this limitation, some management factors are
consistently associated with colic or are sufciently
plausible to merit discussion.
Constant access to water is important to prevent
colic, and it is likely that the quality and palatability of
the water is also important. Horse owners and farm
managers should be advised about the importance of
continuous access to fresh water.
Housing practices contribute to colic. The greater
the density of horses per unit area, the greater the risk
of colic. Changes in stabling, particularly a change from
being kept on pasture to being kept in a stall, predis
pose to colic. A greater proportion of time grazing at
'pasture is associated with lower risk of colic; however,
access to lush pasture predisposes to colic. Although as
yet ill-defined, activity level seems likely to play a role in
colic. Changes in activity level have been sh
o
wn to pre
dispose to colic, although specifc types of changes in
activity or types of activity have not been demonstrated.
There is a lack of consistent evidence to show that any
102
particular activit or level of activity predisposes to colic;
however, it has been suggested that brood mares may be
at increased risk of colic, and strenuous exercise may
predispose to ileus and dehydration resulting in colic.
PREVENTATIVE MEDICINE FACTORS
Surprisingly, there is little epidemiologic evid
e
nce of an
association between preventative medical practices and
colic. Although no association between colic and fre
quency of dental care has been documented, dental dis
orders are thought to predispose to certain forms of
colic (e.g. choke, large colon impaction). It would be
advisable to conclude that routine dentistry is impor
tant for equine health.
With regard to parasite control, limited and conflict
ing evidence has been reported. In general, good
parasite control programs will decrease the risk of colic.
One example would be a program designed to mini
mize herd average fecal egg counts. Because tapeworms
are associated with spasmodic colic and ileal impactions
in the UK specifc targeting of tapeworms may be nec
essary for some farms. Administration of anthelmintics
effective against larae of cyathostomes should decrease
the incidence of colic. Consistent epidemiologic
evidence is lacking to show that any particular
anthelmintic either predisposes or prevents colic rela
tive to other anthelmintics. Recent deworming, how
ever, may predispose to colic, particularly laral
cyathostomosis and ascarid impaction in foals and
weanlings. Parasite-associated colic probably varies
between geographic regions and between farms, and it
is worth emphasizing the importance of parasite con
trol to horse owners and farm managers.
WEATHER
There are conflicting reports of an association of colic
with weather-related factors. Some investigators report
an increased incidence of colic during warmer months
of the year (possibly associated with increased dehydra
tion from sweating) and some report an increased
incidence during cooler months (possibly because of
decreased water intake in cold weather). Investigators
have failed to fnd an association beteen incidence of
colic and ambient temperature, change in ambient
temperature, change in barometric pressure during the
24 hours prior to colic, mean monthly temperature,
mean monthly rainfall, or mean monthly rainfall
weighted for temperature. Recently, a signifcant
change in weather during the 3-day period prior to
examination was significantly associated with colic.
ETIOLOGY, RISK FACTORS, AND PATHOPHYSIOLOGY OF COLIC 8
Although clinical experience would suggest an associa
tion of colic with weather-related factors, these factors
have not been confrmed.
Clearly much work remains to determine the many
causes of colic. It is likely that colic results from a com
bination of multiple predisposing factors. Although no
single cause is likely to be sufcient or necessary to
result in colic, efforts to alter factors that predispose to
colic and to characterize horses at increased risk for
colic should be made by veterinarians and those respon
sible for the care of horses. Confrmation of the beneft
of interventions to decrease colic are rare, but vitally
important. Because risk factors are likely to vary by type
of colic, studies of risk factors for specifc types of colic
are needed.
Pathophysiology of
intestinal obstruction
DE Freeman
PATHOPHYSIOLOGY OF INTESTINAL
DISTENTION
Intestine proximal to an obstruction becomes dis
tended with secretions, gas, fluid, and digesta, and the
bowel wall and mesentery become stretched resulting in
abdominal pain. Veins in the small intestinal wall are
compressed as lumenal pressure increases, and capil
lary hydrostatic pressure and capillary fltration rate
increase. If capillary fltration into the interstitium over
whelms fluid removal through lymph flow, then tissue
edema and a net secretion of fluid into the intestine
develops.
Four hours of experimentally induced intralumenal
pressure of up to 18 cmH20 (13.2 mmHg) induced
mild edema in the lamina propria of equine jejunal
villi. Experimentally induced intralumenal pressure in
pony jejunum to 14 cmHp (10 mmHg) increased
vascular resistance but without an effect on oxygen
consumption or viability. Experimentally induced
intralumenal pressures of 25 cmH20 (18.4 mmHg) for
120 minutes in equine small intestine caused shorten
ing of villi, loss of mesothelial cells, neutrophil infltra
tion, seromuscular edema, and a decreased number of
vessels in the seromuscular layer and, to a lesser extent,
in the mucosa. Decompression of distended small intes
tine caused progression of morphologic lesions in the
seromuscular layers and mucosa, perivascular hemor
rhage in the seromuscular layer, and an increased
vascular density, but to less than control values. These
changes could contribute to formation of serosal adhe
sions.
PATHOPHYSIOLOGY OF INTESTINAL
ISCHEMIA
Ischemic changes in the metabolically active mucosa can
be graded in severity from Grade I (development of a
subepithelial space, called Gruenhagen's space, and
slight epithelial lifting at the villus tip), through pro
gressive loss of the epithelial layer in sheets, starting at
the villus tip, to Grade V (complete loss of the villus archi
tecture, with severe mucosal hemorrhage and loss of the
lamina propria). Sensitivity of villus tip cells to anoxia is
not caused by the countercurrent mechanism in small
intestinal capillaries because anoxic injury to equine
jejunum in vitr causes the same progression of epithe
lial damage. In the equine colon, unlike the small intes
tine, complete ischemia causes cellular necrosis and
detachment of small clusters of surface epithelial cells.
In experimental models of colonic ischemia and in clin
ical cases of colonic volvulus in the horse, ischemic vas
cular injury causes capillary plugging and thrombosis.
Intestinal smooth muscle is more resistant to
hypoxia than is mucosa, and crypt cells are more resis
tant than are villus cells, factors that can play a part in
recovery from an ischemic insult. The early stages of
mucosal repair involve restitution, whereby the villus
contract to reduce the size of the defect and adjacent
viable cells cover the exposed villus stroma. This repair
process can cover pony jejunum with stunted villi lined
with cuboidal epithelium within 12 hours after a Grade
I ischemic iury.
ENDOTOXEMIA
When ischemia or inflammation destroys the integrity
of the intestinal epithelial barrier, the lipopolysaccha
ride component of the outer wall of enteric gram
negative microorganisms gains access to the circulation
(Figure 8.1). Clinical and laboratory signs of endotox
emia are more pronounced in horses with colitis than
in horses with strangulating lesions (see Chapter 11).
Circulating and tissue-fxed mononuclear phagocytes
release the cytokines, lipid-derived mediators, and coag
ulation/fbrinolytic factors that are critical to genera
tion of responses to endotoxin. The cytokine, tumor
necrosis factor (TNF a)' induces synthesis of other
cytokines (such as the interleukins), prostaglandins,
and tissue factor, and initiates an acute-phase response
and fever. The most important lipid-derived mediators
103
8 COLIC
are cyclooxygenase-derived metabolites of arachidonic
acid, and these are responsible for the early hemo
dynamic responses to endotoxin. Thromboxane and
prostaglandin F2a cause vasoconstnctlOn and
prostaglandin 12 and prostaglandin E2 cause vasodila
tion. Another important lipid-derived mediator is
platelet-activating factor (PA) , which aggregates
equine platelets and increases thromboxane B2 produc
tion from equine peritoneal macrophages. Horses with
endotoxemia also develop a hypercoagulable state and
consumptive coagulopathy, presumably secondary to
synthesis of tissue factor by mononuclear cells. The
response to endotoxin influences survival in horses with
gastrointestinal tract diseases.
Cytokines, lipid-derived mediators,
coagulation/fibrinolytic factors

Changes in cardiovascular and
respiratory systems, motility,
and coagulation
Endothelial cell
iCyosolic .
calcium
Calpaln
MEDIATORS
OF CELL
DAMAGE
A
T
P
Xanthine
o _

dehydrogenase
Xan hine
oxidase
ypoxanthine Uric acid
Fe3+

MOTILITY DISTURBANCES IN
INTESTINAL OBSTRUCTION
Non-strangulating occlusion of pony jejunum causes
loss of gastric contractile activit in the distended stom
ach and immediate continuous spiking activity in intes
tine proximal to the obstruction. Jejunal distention in
ponies increases the amplitude of rhythmi contrac
tions in the distended segment. Occlusion of blood sup
ply to the pony ileum decreases motility in the ischemic
bowel, increases motilit in the more proximal seg
ment, and has no effect on the distal segment. Ileus
is a common postoperative complication of intestinal
surgery in horses, and adrenergic and dopaminergic
Ischemia === Reperfusion
===========
Figure 8.1 Pathways and mechanisms in the pathophysiology of ischemia and reperfusion injury in the intestine.
Increased shading in the mucosal epithelium represents increased cell damage. ATP = adenosine triphosphate;
SOD = superoxide dismutase; O2 = superoxide radical; OH = hydroxyl radical; HP2 = hydrogen peroxide; Fe3+ = ferric iron;
O2 = oxygen; HOCI = hypochlorous acid; PAF = platelet activating factor; LTB4 = leukotriene B4; TXA2 = thromboxane A2;
PGI2 = prostaglandin 12; PGE2 = prostaglandin E2; PGF2a = prostaglandin F2u; PGD2 = prostaglandin O2; fMLP = formyl
methionyl-Ieukyl-phenylalanine
104
ETIOLOGY, RISK FACTORS, AND PATHOPHYSIOLOGY OF COLIC 8
stimulation appears to occupy a central role in its
pathogenesis (see Chapter I I).
Continuous infusions of prostaglandin E
I
(PGE
I
)
decreased motility in pony stomach, left large colon,
small colon, left dorsal colon, and jejunum (more
than in the ileum). Also, intravenous infusion of
prostaglandin E2 (PGE2), but not prostaglandin F2"
(PGF2,) mimicked the disrupted motilit patterns
induced by endotoxin in the stomach, small intestine,
and large intestine of ponies. Nitric oxide from
myenteric neurons also appears to act as an inhibitory
neurotransmitter to circular smooth muscle of equine
jejunum and could be released from macrophages in
inflamed small intestine.
REPERFUSION INJURY
Reperfusion iury is the exacerbation of tissue damage
that occurs when ischemic tissue is reoxygenated
(Figure 8.1). The most widely accepted explanation for
reperfusion injury is initiation of tissue damage by reac
tive oxygen metabolites (ROMs) and exacerbation by
neutrophils (Figure 8.1). Initiation of reperfusion
injury depends on conversion of xanthine dehydrogen
ase to xanthine oxidase (Figure 8.1), and activity of
these enzymes is high in equine small intestine but not
in equine colon. Neutrophil accumulation in equine
colonic mucosa peaks during the first 10 minutes of
reperfusion after low flow ischemia, and this coincides
temporally with mucosal necrosis.
Attempts to demonstrate reperfusion injury in
equine intestine have met with varied success. The
intestinal model that allows more complete display of
the expected paradigms of reperfusion injury is the seg
mental hypo perfusion or low flow model, which causes
mild tissue damage during the ischemic period. The
clinical equivalent to this is intestine subjected to
decompression or to hypoperfusion. In contrast with
laboratory animals, pharmacologic manipulation of
reperfusion injury is unrewarding in equine intestine.
PATHOGENESIS OF ADHESION
FORMATION
Peritoneal ischemia and inflammation (trauma, disten
tion, bacteria, and foreign material) are thought to pre
dispose to adhesions by causing an imbalance between
fbrin deposition and fbrinolysis in the peritoneal
cavity. If fbrin is not removed, the ingrowth of fbro
blasts and subsequent deposition of collagen converts
fbrinous adhesions to fbrous adhesions.
Plasmin, antithrombin III, and protein C are
responsible for fbrinolysis. Plasminogen is converted to
plasmin by tissue plasminogen activator (tPA) , which is
a key regulator of fbrinolysis. Inhibitors of fbrinolysis
include plasminogen activator inhibitor-l (P AI-I) and
alpha- 2 anti plasmin which inhibit tPA and plasmin,
respectively. PAI-l increases in inflammation and
ischemia possibly explaining the decreased activity of
tPA in these disease conditions. Concentration of tPA
decreases in peritoneal fluid following peritoneal
trauma.
BIBLIOGRAPHY
Factors associated with increased risk of colic
Cohen N D (1997) Epidemiology of equine colic. Vet. Clin. N
Am. Equine Pract. 13:191-201.
Proudman C] (1991) A two year, prospective survey of equine
colic in general practice. Equine Vet.] 24:90.
Reeves M (1992) Risk and prognostic factors in colic. In
Current Therapy in Equine Medicine, 3rd edn, N E Robinson
(ed.). W B Saunders, Philadelphia, pp. 206-10.
White N A (1990) Epidemiology and etiology of colic. In The
Equine Acute Abdomen, N A White (ed.). Lea and Febiger,
Pathophysiology of intestinal obstruction
Allen D, White N A and Tyler D E (1988) Morphologic effects
of experimental distension of equine small intestine. Vet.
Surg. 17:10-14.
Dabareiner R M, Sullins K E, Snyder] R, et al. (1994)
Evaluation of the microcirculation of the equine small
intestine after intraluminal distension and subsequent
decompression. Am.] Vet. Res. 54:1673-82.
Davies] V and Gerring E L (1985) Effects of experimental
vascular occlusion on small intestinal motility in ponies.
Equine Vet.] 17:219.
Freeman D E, Cimprich R E, Richardson D W, et aL (1988)
Early mucosal healing and chronic changes in pony
jejunum after various types of strangulation obstruction.
Am.] Vet. Res. 49:810.
Gerring EL and Hunt] M (1986) Pathophysiology of equine
postoperative ileus: effect of adrenergic blockade,
parasympathetic stimulation and metoclopramide in an
experimental model. Equine Vet.] 18:249.
Granger D N, Kvietys P R, Mortillaro N A, et al. (1980) Effect
of luminal distension on intestinal transcapillary fluid
exchange. Am.] Physiol. 239:G516G523.
Hunt] M and Gerring E L (1985) The effect of prostaglandin
E] on motility of the equine gut.] Vet. Pharacol. Therap.
8:165.
Johnston] K, Freeman D E, Gillette D, et al. (1991) Effects of
superoxide dismutase on injury induced by anoxia and
reoxygenation in equine small intestine in vitro. Am.] Vet.
Res. 52:2050.
King] Nand Gerring E L (1989) Obserations on the colic
motor complex in a pony with a small intestinal
obstruction. Equine Vet.] Supplement 7:43-5.
King] Nand Gerring E L (1991) The action of low dose
endotoxin on equine bowel motility. Equine Vet.] 23:11.
Moore] N and Barton M H (1998) A update on
105
8 COLIC
endotoxemia Part 1: mechanisms and pathways. Equine.
Vet. Educ. 10:300-6.
Moore R M, Muir W W and Granger D N (1995) Mechanisms
of gastrointestinal ischemia-reperfusion injury and
potential therapeutic intelVentions: a review and its
implications in the horse.] Vet. Int. Med. 9: 115-32.
Parks A H, Stick] A, Arden W A, et ai. (1989) Effects of
distension and neostigmine on jejunal vascular resisitance,
oxygen uptake, and intraluminal pressure changes in
ponies. Am.] Vet. Rs. 50:54-8.
106
Rakestraw PC, Snyder] R, Woliner M], et ai. (1996)
Involvement of nitric oxide in inhibitory neuromuscular
transmission in equine jejunum. Am.] Vet. Rs. 57:1206.
Snyder] R (1989) The pathophysiology of intestinal damage:
effects of luminal distension and ischemia. Vet. Clin. Noh
Am. Equine. Pac. 5:247-70.
Southwood L L and Baxter G M (1997) Current concepts in
management of abdominal adhesions. Vet. Clin. N Am.
Equine Pac. 13:415.
9
Clinical evaluation of the colic case
Clinical signs of colic
<
T Mair
MECHANISMS OF ABDOMINAL PAIN
Abdominal pain can be differentiated into visceral pain,
parietal (somatic) pain, and referred pain. Visceral pain
is most commonly observed in colic, and refers to the
dull, non-specifi c, poorly localized pain resulting from
visceral disease. The horse's response to this pain is to
move about excessively in an attempt to remove the dis
comfort. In contrast, parietal pain is more localized and
may occur in response to diseases affecting the parietal
peritoneum. Referred pain is rarely recognized in the
horse.
Painful stimuli activate free nerve endings of small
A-delta and C afferent nerve fbers. Tissue hormones
such as bradykinins, histamine, leukotrienes and
prostaglandins can either activate pain receptors or
lower the threshold for other stimuli. A-delta fibers
mediate sharp, sudden, well-localized pain that follows
some forms of injury. C fbers mediate dull, poorly
localized painful sensations; these fibers are found in
muscle, periosteum, parietal peritoneum, and viscera.
Since A-delta fibers are not present in the viscera, cut
ting, crushing, or tearing pain sensation is not per
ceived at this site. However, visceral nociceptors are
sensitive to stretching or tension caused by distention,
traction (e. g. from a neoplasm) , or forceful muscular
contraction (e. g. oral to a bowel obstruction) . The pari
etal peritoneum and mesentery are sensitive to pain,
but the visceral peritoneum and omentum are insensi
tive. Tension must develop rapidly to be perceived as
painful; slowly developing tension may be painless.
Inflammation can also cause visceral pain by direct
mechanisms or indirectly by lowering nerve-ending
thresholds. Ischemia causes pain by increasing the
tissue concentrations of metabolites around sensory
nerves, and by lowering the threshold of noxious
stimuli.
CLINICAL SIGNS OF COLIC
The horse affected by colic due to gastrointestinal pain
may behave in a variety of ways. To a large extent the
signs will be determined by the severity of the pain, but
it must be recognized that there is a wide variation
dependent on the personality of the individual horse.
Some horses appear to be more stoical and tolerant of
pain than others.
Despite this variation in signs, it should be possible
to classif the degree of pain exhibited by the horse into
one of several groups
no pain
mild pain
moderate pain
severe pain
depression.
The horse with mild pain may demonstrate one or
more of the following signs
occasional pawing
turning the head to the flank
stretching out
lying down for longer than usual ( Figure 9. 1 )
quivering of the upper lip
1J
9 COLIC
inappetence
backing up to the wall
'playing with' or 'nosing' water.
With moderate pain the following may be seen
restlessness
pawing
cramping with attempt to lie down
crouching
kicking at the abdomen
lying down
rolling ( Figure 9. 2)
turning the head to the flank
dog-sitting position
groaning.
The horse in severe pain will show one or more of
the following
sweating
violent rolling
Igufe9.J Mi l d colic characterized by restlessness and lying
down more often than usual
Igufe 9.Z Moderate colic in a foal that is rol l i ng repeat
edly
!d
dropping to the ground
extreme restlessness
other signs of pain listed above.
The stage of depression may be seen after a severe bout
of colic as advanced intestinal necrosis and endo
toxemia produce a state of indolence. Alternatively,
depression may be seen as an early sign of other
diseases that produce colic, especially inflammatory
diseases such as colitis and peritonitis. Depression is
also common in horses affected by anterior (proximal)
enteritis after nasogastric decompression of the
stomach.
In general terms, the more severe the disease, the
greater the severity of pain. Strangulating obstructive
diseases usually cause more severe pain than simple
obstructions. However, early in the course of strangulat
ing diseases the pain may not be as severe, and late in
the course of these conditions depression takes over as
the predominant sign. Severe pain that is continuous
may be more likely in cases of severe tmpany or in
strangulating diseases where there is bowel wall stretch
ing or tension on the mesentery. When pain changes
rapidly from severe and uncontrollable to total relief
or depression, gastric or bowel rupture should be
considered.
The horse that present with signs of depression
(especially animals that are found like this frst thing in
the morning) should be evaluated for 'tell-tale' signs of
previous pain. In particular, skin abrasions and swelling
around the eyes, abrasions over the tuber coxae, and
marks on the walls of the stable indicate violent rolling
by the horse.
Igufe 9.5 Stretched out ('trestle table') appearance in a
horse with a jejunojejunal intussusception
In some diseases the clinician may notice character
istic clinical signs suggesting the presence of a particu
lar disease, for example
a dog-sitting position is seen in horses with gastric
distention
a stretched-out (,trestle table' ) position is seen in
horses with small intestinal intussusceptions (Figure
9. 3) and sand impactions
foals that roll onto their backs and lie in dorsal
recumbency for long periods may be affected by
gastric ulceration.
It should be noted that these signs are not specific for
these diseases and not all animals with these conditions
will demonstrate these signs. However, their observa
tion can help raise the index of suspicion for a particu
lar disease.
Physical examination of a
horse with col ic
PD Van Harreveld and EM Gaughan
A physical examination of a horse with colic should be
performed in a quick, thorough, and systematic fash
ion, so that a working diagnosis can be established and
proper treatment initiated. Information gathered dur
ing the physical examination will allow the attending
veterinarian to make the appropriate decisions about
disease severity, prognosis, and course of therapy.
Because of the possible need for surgical interention it
is important to consider diagnosis of obstructive disease
as early as possible.
HISTORY
An accurate history will provide valuable information
regarding current and past health and colic concerns.
This can be very benefcial in determining the specific
cause of abdominal pain. The initial history should
include
signalment
duration of clinical signs
severity and frequency of pain
the time when the horse was last obsered to be
normal.
An accurate history can also help determine if a horse's
colic is acute, chronic, or recurrent. Nutritional history
can help determine if feed materials or feeding practices
CLINICAL EVALUATI ON OF THE COLIC CASE 9
could predispose to colic (e. g. poor quality hay may pre
dispose to impaction; grain overload predisposes to colic
and laminitis). Certain geographic locations or previous
housing locations can also be important, for example
in horses predisposed to sand accumulations and
enterolith formation. Availabilit of water and drinking
habits should be reviewed. Acute changes in water intake
from defects in automatic watering systems or freezing
temperatures can lead to obstructive colic (impaction
can occur secondary to decreased water intake) . An
understanding of the parasite control program, date of
last deworming, and agent used can be especially impor
tant for younger horses. In mares, breeding history and
pregnancy status should be documented. A complete
description of treatments administered prior to and
after the onset of colic, including medications, is impor
tant for assessment. Manure production, volume, and
character should be determined.
CLINICAL EXAMINATION
For the physical examination of a horse with colic, a con
sistent, effective, and systematic examination of the var
ious body systems should be routinely completed. It is
important to use a similar system of examination for each
horse to ensure complete evaluation and comparison
between one horse and others. Routine equipment to
perform a complete examination includes thermome
ter, stethoscope, nasogastric tube, pump, rectal sleeve,
and lubricant. Instrumentation for abdominocentesis
and diagnostic ultrasound can also be very helpful.
Initially, an affected horse should be evaluated
quickly from a distance. This can provide information
regarding
the type and severity of pain
the animal's general condition
signs of colic
mentation
the presence of wounds or lacerations
the degree of abdominal distention
any other external signs.
Assessments of fecal output can also be made.
Rectal temperature
The body temperature should be determined prior to
performing a rectal examination because a pneumo
rectum can lead to a reduced temperature. The normal
temperature range for horses is 37. 5-38.5C. Increases
in body temperature can occur after anxiety, excite
ment, or exertion. Temperatures greater than 39.5C
may suggest an inflammatory or primary infectious
!
9 COLIC
process, such as colitis, proximal enteritis, peritonitis,
or pleuritis. Body temperature elevation can also occur
early after stomach or intestinal rupture, leading to sep
tic peritonitis. Decreased temperature (hypothermia) ,
in addition to tachycardia, is indicative of the develop
ment of circulatory compromise and potential shock.
Respiratory rate
The respiratory rate of a horse with colic will usually be
elevated because of pain or metabolic acidosis. Dyspnea
or shallow breathing can result from pressure applied
to the diaphragm by severe gastric or intestinal disten
tion. The rate and character of respiration should be
noted, but these do not usually provide any direct
insight into the causes of colic.
Heart rate
A horse's heart rate can usually be obtained by auscul
tation of the heart at the thorax, it can also be obtained
by palpation of the facial artery or other peripheral arter
ies. Palpation of a peripheral pulse can offer a reflection
of cardiovascular function and tissue perfusion. The
absence of a palpable pulse may indicate cardiovascular
compromise. In relation to gastrointestinal origins, it
may be wise to palpate the digital arteries in order to
detect the potential early development of laminitis.
The normal equine heart rate is 24-40 bpm.
Elevations of heart rate in horses with colic are usually
the result of anxiety, pain, and hypovolemia. Heart rate
elevation is a good indicator of the severity of pain and
indirectly, the original intestinal disorder. Pulse assess
ment should always be used in addition to other physi
cal examination data to determine the potential presence
of a surgical condition. Horses with a functional or mild
intestinal obstruction can have intermittent heart rate
spikes, whereas horses with strangulating lesions usually
have sustained heart rate elevations up to 80-90 bpm. A
sustained elevation in heart rate is critical to a more com
plete understanding of the diagnosis and prognosis.
Mucous membranes and jugular vein filling
The character and color of mucous membranes can
reflect the circulatory status of the patient. Normal
mucous membranes are moist and pink. Physiological
capillary refll time is usually 1 .5 seconds or less. When
peripheral vascular circulation is impaired capillary
refll time is prolonged, this is considered severe when
increased to 4 seconds or more. The moisture of the
mucous membranes can reflect the overall hydration
status of the patient. Dry mucous membranes can indi
cate systemic dehydration. Pale mucous membranes
can occur with shock from hypovolemia or pain. Dark
1 !
mucous membranes or a toxic line are usually
associated with septic or endotoxic shock, following
resorption of bacterial endotoxins from intestinal com
promise or enteritis. Skin elasticity is maintained
through water content in the tissues. A fold of skin can
be pinched over the cervical region or eyelid to evaluate
hydration. The skin fold should flatten within 1-2 sec
onds in normally hydrated skin, however, this should
only be assumed to be a crude assessment. Manual
occlusion of the jugular vein can be useful in determin
ing the state of venous blood pressure and circulating
fluid volume. With substantial hypovolemia, jugular fll
ing is either prolonged or absent.
Abdominal auscultation (see Chapter 1 , General
physical examination and auscultation)
Intestinal motility can be evaluated subjectively by
auscultation of the abdomen using a stethoscope. The
frequency, duration, intensity, and location of intestinal
sounds should be noted. Normally, organized inter
mittent peristaltic sounds can be heard. Auscultation
should be performed on both the right and left flanks
as well as the ventral abdominal wall, or over all four
quadrants, dorsal/ventral and left/right. Colonic and
small intestinal sounds can best be heard at the left
flank, whereas cecal sounds can be heard at the right
flank. The presence of sounds associated with sand in
the large colon are best detected on auscultation of the
ventral abdominal wall. Excessive frequency of sounds
or intestinal hyperactivit is associated with conditions
such as enteritis or spasmodic colic. The absence of
intestinal sounds over a prolonged period of time may
indicate ileus or obstructive disease. Abdominal per
cussion during auscultation can reveal gas-distended
bowel when a high-pitched resonant sound (ping) is
present.
NASOGASTRIC INTUBATION (see Chapter 1 ,
Passage of a nasogastric tube should be performed for
all horses presenting with colic. The inability of a horse
to regurgitate means that the stomach may rupture if it
becomes overloaded or distended. It is important to
detect and alleviate fluid or gas distention from the
stomach U early as possible. Reflux into the stomach
usually occurs with small intestinal obstruction or
enteritis, it can also occur secondary to colonic
displacement leading to compression of the duode
num. The stomach should be decompressed with a
nasogastric tube and a siphon established allowing fluid
contents to drain. Removal of gastric contents can be
challenging, and repeated efforts to create a siphon by
moving the stomach tube back and forward may be
necessary. In cases where increased pressure of the
stomach causes complete closure of the cardia, blowing
air into the tube while moving it into the stomach may
allow the tube to move forward. Introducing a local
anesthetic agent (lidocaine hydrochloride 2%, 60 ml)
into the esophagus through the tube can also be
attempted. In healthy horses, only small amounts of
fluid 500 ml) can be retrieved from the stomach. The
pH of normal stomach contents is 5 or less. In cases of
small intestinal obstruction or enteritis, many liters of
fluid can be removed from the stomach. In these cases
the fluid pH is increased as a result of bicarbonate-rich
pancreatic and intestinal secretions.
RECTAL EXAMINATION (see Chapter 1 ,
Rectal examination and Chapter 9, Rectal examination
for the acute
Rectal examination may be the most revealing compo
nent of the physical examination of a horse with colic
and should be performed in all cases when possible.
This is especially important if surgical therapy is being
considered. Only 40 per cent of the abdomen can rou
tinely be explored by examination per rectum. Prior to
performing a rectal examination the patient should be
properly restrained. It may also be necessary to use anal
gesics or sedatives such as xylazine (0. 2-l . 1 mg/kg Lv.
or Lm. ) to relieve anxiety. A twitch can also be applied
for restraint, and this may help to reduce straining. The
use of a local anesthetic (lidocaine hydrochloride
2%, 120 ml) enema can help reduce rectal straining.
Voluminous use of a lubricant such as K-Y jelly or
methyicellulose is usually required. The rectum should
be entered slowly and feces carefully evacuated. The
arm should then be carefully advanced as the tension in
the rectal wall diminishes. Relaxation can take up to 30
seconds in many horses. It is important to keep the
examination hand and fingers cone shaped and not
force entry against rectal peristaltic waves. Feces recov
ered during rectal examination should be examined for
the presence of sand or blood. The presence of sand
can be detected by placing feces in a container of water
and looking for sand separating away from the ingesta.
If fresh blood is present at the end of the examination,
a rectal abrasion or tear should be suspected and
further evaluated. Normal structures palpable during
examination per rectum include the spleen, left kidney,
nephrosplenic ligament, root of mesentery, cecum,
medial cecal band, pelvic flexure, the small colon, and
the bladder when distended. The inguinal canals can be
felt in stallions, and the uterus and ovaries in mares.
CLI NICAL EVALUATI ON OF THE COLIC CASE
ABDOMINOCENTESIS (see Chapter 2,
Abdominocentesis and Analysis of peritoneal fluid)
W!_W1
9
Abdominocentesis can provide useful information
when other examination techniques fail to reveal a
clear diagnosis, or when further determination is
required of the severity of the lesion. It is also indicated
in cases where rectal examination does not yield defni
tive fndings and the signs of colic persist. This proce
dure can be performed using a hypodermic (I8-gauge)
needle or a blunt cannula (bitch catheter or teat can
nula) . The most dependent site of the abdomen, to the
right of midline, should be selected to avoid the spleen
and stomach. Abdominocentesis should probably be
avoided in any foal with abdominal distention or small
intestinal distention. The cannula technique is pre
ferred in foals as trauma to the thin intestinal walls can
be minimized, however, ultrasonographic evaluation is
preferred in foals. Peritoneal fluid should be evaluated
grossly for volume, color, turbidity, and food particles.
The fluid can be examined microscopically for leuko
cyte and erythrocyte counts as well as total protein
determination. Normal peritoneal fluid is clear or straw
colored, with a protein concentration up to 2.5 g/dl
(25 gil) and total white blood cell count (WBC) of less
than 5000 cellS/il (5.0 ? 1 0 9/1), consisting mostly of
macrophages and neutrophils. The presence of food
particles or bacteria in the peritoneal fluid can indicate
loss of bowel integrity and a poor prognosis. Prior to
euthanasia, abdominocentesis findings should be con
frmed by repeating the technique in at least one differ
ent site to rule out enterocentesis. Blood-tinged fluid is
consistent with advanced intestinal disease such as
intestinal strangulation. Neutrophil counts can increase
in inflammatory conditions such as long-standing
impaction or strangulation and can exceed 1 00 000/111
(l00 ? 1 09/1) . Neutrophil counts greater than 50 000
cellS/il (50 ? 1 09/1) can be suggestive of an intra
abdominal abscess or of primar bacterial peritonitis.
ULTRASOUND EXAMINATION (see Chapter
Ultrasound examination of the
Ultrasonography can provide additional information in
the examination of a horse with colic, especially in foals
and small horses where rectal examination cannot be
performed. Abdominal ultrasound can be performed
transcutaneously or per rectum. Abnormalities com
monly detected with ultrasonography include peri
toneal effusion, adhesions, masses, small intestinal
distention, ileus, intussusception, and left dorsal dis
placements of the large colon.
1 ! !
9 COLIC
CLINICAL PATHOLOGY
For many horses, laboratory assessment of blood is not
essential for treatment success. However, with severe or
changing cases WBC, packed cell volume ( PCV) and
total plasma proteins (TPP) are often helpful. The PCV
and TPP are useful for assessment of the degree of
dehydration, and are necessary to monitor the efcacy
of volume replacement. Normal PCV values range
between 32-46 per cent, but may vary slightly according
to the horse' s age, breed, and athletic condition.
Splenic contraction following transport and anxiety
may raise the PCV values above normal. Packed cell vol
ume can be of use in determining the prognosis of a
colic case. The higher the PCV, the greater the rate of
mortality, with values greater than 65 per cent associ
ated with a poor prognosis. Normal total protein levels
range between 5. 5 and 7. 5 gldl (55-75 gil) . Plasma
protein in a colic patient is usually increased as a result
of dehydration. Plasma proteins can be decreased by
sequestration of protein into the abdominal cavity as a
result of peritonitis or into the intestinal lumen as a
result of enteritis. Neither the PCV nor the TPP can be
used as specifc indicators of a surgical lesion, but can
help determine the severity of the lesion, the degree of
shock, and the response to treatment.
The total WBC is useful in determining conditions in
which surgery is contraindicated. White blood cell count
elevations are often obsered in horses with proximal
enteritis or intra-abdominal abscesses. Severe leukope
nia 3000 celli Ill, 3.0 ? 109/1) can indicate gram-neg
ative sepsis or endotoxemia as a result of salmonellosis
or severe acute peritonitis from intestinal rupture.
Blood gases and electrolytes can show changes in a
horse's metabolic state and can be of limited value in
determining the prognosis or diagnosis for a horse with
colic. They are valuable in preparation for anesthesia
and in monitoring a horse's postoperative recuperation.
Rectal examination for the
acute abdomen
POE Mueller
INTRODUCTION
A complete and thorough rectal examination is an
essential component of a diagnostic evaluation when
examining horses with abdominal pain. Rectal exami
nation fndings should always be considered in con-
! 12
junction with the results of the physical examination,
nasogastric intubation, abdominocentesis, and labora
tory evaluation. A rectal examination should always be
performed before abdominocentesis in order to recog
nize an extremely gas-distended or ingesta-flled cecum
or large intestine. If these abnormalities are identifed,
extreme care must be taken when performing an
abdominocentesis to avoid accidental enterocentesis.
Occasionally, rectal examination fndings clearly
indicate the specifc disease, such as a renosplenic
entrapment, early ileal impaction, or herniation of
small intestine through the inguinal ring in a stallion.
More often, however, rectal examination does not yield
a specifc diagnosis, but gives information regarding the
severity of the problem and the need for surgical inter
vention. Abnormal rectal examination fndings include
abnormal positioning of the intestine
distention of the intestine with gas or ingesta
excessive mural thickness
the presence of intra- or extralumenal masses.
The size and depth of the peritoneal cavit in the
horse limit palpation to the caudal 30-40 per cent.
Because of the inabilit to examine the entire peri
toneal cavity, subtle abnormalities identifed on exami
nation are ofen used to make inferences concerning
the more cranial regions of the peritoneal cavity.
Consequently, the lack of abnormal rectal examination
fndings does not completely rule out an intestinal
abnormality.
The technique for rectal examination is described in
Chapter 1 . When performing a rectal examination in
horses with colic, proper restraint is even more impor
tant than normal to ensure the safet of the horse and
the examiner. Horses with signs of unrelenting abdom
inal pain should be sedated with xylazine (0. 3-0.5 mgl
kg i.v. ) , detomidine (7-10 Ilglkg i.v. ) , or romifdine
(40-120 Ig/kg i.v. ) ; these drugs can be administered
with butorphanol (20 Ilg/kg i. v. ) to provide stronger
analgesia and more profound sedation.
Absence of fecal material on initial insertion of the
hand into the rectum, or the presence of dry, fbrin
and mucus-covered feces is abnormal and is consistent
with delayed intestinal transit. Fetid, watery fecal mater
ial is often present in horses with colitis. Large amounts
of sand within the feces may indicate a sand impaction
or sand-induced colitis.
In general, palpable characteristics of the abdominal
contents and viscera are often helpful in identifing the
particular segment of the intestine involved and the
severit of the condition. Severe gas-filled or ingesta-dis
tended intestine, tight mesenter or tenia (bands) , or
thickened or turgid intestine are indicative of intestinal
obstruction or strangulation. Free peritoneal gas or
crepitus within the intestinal wall is usually indicative of
intestinal rupture. A gritty or granular texture to the
peritoneal cavity is indicative of intestinal rupture with
contamination of the serosal and peritoneal surfaces
with ingesta.
Because the majority of the body and apex of the
cecum are beyond the examiner's reach the tautness
of the ventral and medial cecal tenia is used as an
indicator of the amount of ingesta within the cecum.
Normally the cecal tenia should be loose and easily
movable (Figure 9. 4) . With increased amounts of
ingesta in the cecum the tenia become more taut. Pain
elicited on palpation of the ventral or medial cecal tenia
may be associated with tension of the ileum or its
mesentery. This has been associated with pain originat
ing from the ileum and its vasculature, such as that
occurring with entrapment of the ileum in the epiploic
foramen.
fgufe9.4Caudal view of a standi ng horse demonstrati ng
abdomi nal structures that are pal pabl e i n the normal
horse duri ng rectal exami nation. Starting i n the left dorsal
abdomi nal quadrant, and progressi ng in a clockwise di rec
tion, pal pabl e structures i nclude: caudal border of the
spl een, renospl eni c l igament, caudal pole of the left ki d
ney, ventral cecal teni a, cecal base, and the pel vi c flexure.
Thel Melton, CAD special ists, Department of Educational
Resources and Dr IN Moore, Department of Large Ani mal
Medicine, University of Georgi a, Athens, GA JUbU, with
permission
CLI NI CAL EVALUATI ON OF THE COLIC CASE 9
RECOGNITION OF INTESTINAL
ABNORMALITIES
Small intestine
Palpable small intestinal distention is always an indica
tion of small intestinal obstruction. The obstruction
may be a physical obstruction such as an ileal impaction
or small intestinal strangulation, or it may be a func
tional obstruction such as ileus secondary to enteritis or
non-strangulating intestinal infarction. The small intes
tine is of a similar diameter to the descending colon.
The small intestine is distinguished from the descend
ing colon by the absence of both an anti-mesenteric
band and fecal balls. During early obstruction, one to
to loops of easily compressible small intestine may be
identified (Figure 9. 5) . P the disease progresses the
distention increases and multiple loops of tightly dis
tended, fluid-flled intestine are palpable side by side
(Figure 9. 6) .
Non-specifc small intestinal distention is the most
common fnding in horses with small intestinal lesions.
However, specifc fndings identified on rectal examina
tion will occasionally lead to a diagnosis. ileal
fgufe 9.b Caudal view of a standi ng horse demonstrating
an ileal i mpacti on with earl y smal l intesti nal di stention.
The il eum may be pal pabl e as a firm, tubul ar structure in
the center of the abdomen coursing toward the cecum.
Thel Melton, CAD speci al i sts, Department of Educati onal
Resources and Dr IN Moore, Department of Large Ani mal
Medi ci ne, University of Georgi a, Athens, GA JUbU, with
permission
! !
9 COLIC
Igufe 9.bCaudal view of a standi ng horse demonstrati ng
severe smal l i ntesti nal distention. Multiple l oops of gas
and fl ui d-di stended smal l intestine are pal pable. Thel
Melton, CAD speci al i sts, Department of Educati onal
Resources and Dr JN Moore, Department of Large Ani mal
Medi ci ne, University of Georgia, Athens, GA JUbU, with
permission
impaction, detected early in the disease process, may be
palpable as a frm, tubular structure in the center of the
abdomen coursing toward the cecum (Figure 9.5) .
Herniation of small intestine through the inguinal ring
in a stallion is palpable as small intestinal distention
with a segment of small intestine or mesentery coursing
into one of the inguinal rings. If the herniated loop of
small intestine is not distended, the specifc diagnosis of
inguinal herniation may not be evident. In these cases
the inguinal rings often feel asymmetric, and gentle
traction on the mesentery associated with the affected
ring elicits a painful response. Jejunojejunal intussus
ception causes generalized small intestinal distention,
but the intussusceptum is occasionally palpable as an
extremely thickened, edematous, tubular structure in
the caudal aspect of the abdomen. Ileocecal intussus
ception is difcult to identif per rectum, but early in
the disease process is occasionally identifed as a turgid
mass in the right dorsal abdomen and sometimes it can
be appreciated that it is within the cecum.
Rectal examination fndings in horses with proximal
enteritis may mimic those of a physical obstruction.
With enteritis, however, the small intestinal distention is
often less severe and easily compressible. With naso-
! 14
gastric decompression and intravenous fluid therapy
the intestinal distention often decreases.
Obstruction of the small intestine causes absorption
of fluid from the ascending colon and rapid dehydra
tion of the ingesta in the ascending colon. The colon
becomes hard and indurated and feels as if it were vac
uum sealed. In a horse with an early small intestinal
obstruction, and little or no palpable small intestinal
distention, the inexperienced examiner may interpret
this fnding as a primary large colon impaction. The
tenia and haustra of an ascending colon that is secon
darily dehydrated contour to the ingesta within the
intestinal lumen and are easily palpable. This is in con
trast to a primary large colon impaction, where the
tenia and haustra become less distinct with increasing
colonic distention (see below, Large colon) .
Cecum
Cecal distention may be a primary problem, such as
impaction of the cecum with ingesta or fluid, or more
commonly secondary to obstruction of the large or
small colon. Early in the development of a cecal
impaction, the apex of the cecum becomes distended
with ingesta, but is beyond the reach of the examiner.
Therefore, palpation of the ventral cecal tenia is used as
an indirect indicator of cecal flling. Normally the
cecal tenia should be loose and easily movable. With
increased flling of the cecum with ingesta, the tenia
become more taut and the cecum displaces toward the
midline. P the cecum becomes further distended, the
weight of ingesta in the apex pulls the cecal base cra
nially within the abdomen, and the ventral tenia, which
normally courses from the right dorsal to right ventral
quadrant, crosses diagonally across the caudal
abdomen, from the right dorsal to left cranioventral
quadrant. P the cecum flls above the cecocolic orifce,
complete obstruction occurs and the cecal base flls
with fluid and gas (Figure 9. 7) . The distended cecum
flls the right dorsal and ventral abdominal quadrant.
In cases of severe cecal tympany, either primary or sec
ondary to a large colon obstruction, the cecal base feels
like a tightly distended balloon in the right dorsal quad
rant. With marked cecal mural edema, the haustra
between the tenia become more prominent. The pres
ence of severe cecal mural edema or emphysema is an
indicator of intestinal compromise and possible cecal
rupture, and is associated with a poor prognosis for
survival.
Cecal impaction and right dorsal displacement of
the large colon may be difcult to distinguish during
rectal examination. In cases of right dorsal displace
ment of the large colon, the cecal base and tenia are dif
fcult to feel, and the examiner's hand can palpate the
Igufe9.J Caudal view of a standi ng horse demonstrating
a pri mary cecal i mpaction. With i ncreased fi l l i ng of the
cecum with i ngesta, the teni a become more taut and the
cecum displ aces toward the mi dl i ne. As the cecum fi l l s
above the cecocolic orifice compl ete obstruction occurs
and the cecal base fi l l s with fl ui d and gas. Thel Melton,
CAD special ists, Department of Educational Resources and
Dr IN Moore, Department of Large Ani mal Medi ci ne,
University of Georgia, Athens, GA JUbU, wi th permission
dorsal aspect of the distended colon cranially and
another structure (cecum and its attachment) can be
felt medial to the colon. While in cecal impaction, cra
nial palpation qf the dorsal aspect of the distended
cecum is limited by the dorsal attachment of the cecum.
Large colon
Abnormalities of the large colon have a variety of intesti
nal positions and degrees of intestinal distention, and
include large colon impaction, left and right dorsal colon
displacement, and colon volvulus. Impaction of the large
colon usually occurs at the pelvic flexure and may be felt
in the left or right caudal abdominal quadrants. The
colon is enlarged and easily identifable on palpation
(Figure 9. 8) . The two free tenia of the ventral colon
course in a cranial-to-caudal direction, from the left
cranial abdomen to the left caudal abdomen. P the
impaction enlarges, the tenia may continue to the right
caudal abdomen, with the pelvic flexure lying in the right
caudal abdomen, just cranial to the pelvic rim. The con
sistency of the ingesta forming the impaction may vary
CLI NICAL EVALUATI ON OF THE COLIC CASE 9
Igufe 9.8Caudal view of a standing horse demonstrating
i mpaction of the ventral colon and pelvic flexure. The
colon i s enl arged and easi l y i dentifi abl e on palpation. The
two free teni a of the ventral colon course i n a crani al
to-caudal di recti on, from the left crani al abdomen to the
left caudal abdomen. Thel Melton, CAD special ists,
Department of Educational Resources and Dr IN Moore,
Department of Large Ani mal Medi ci ne, Uni versity of
Georgia, Athens, GA JUbU, with permission
from soft and indentable to frm and indurated. With
severe impaction, the colon may fll the entire caudal
abdomen, and the haustra of the ventral colon become
indistinct. It is imperative that the examiner ensures
that the colon is not displaced. Primary large colon
impactions are usually treated medically, whereas horses
with colon displacements and secondary impaction
require surgery for resolution of the impaction.
Horses with impactions or obstructions (enteroliths)
of the right dorsal colon and transverse colon most
often present with generalized cecal and large colon
tmpany. Occasionally, however, the lesion may be
identifed on rectal examination. In these cases, the
impaction or enterolith may be ballotted with the exam
iner's fngertips, but cannot be palpated in its entirety.
Abdominal surgery is generally necessary to confrm the
diagnosis.
Left dorsal displacement of the large colon (reno
splenic entrapment) can be diagnosed by rectal exami
nation if the colon is not markedly distended. The left
dorsal and ventral colon become entrapped within the
renosplenic space, between the spleen and left kidney
! ! b
9 COLIC
(Figure 9. 9) . The majority of the colon is palpable on
the left side of the abdomen with the tenia coursing
from the left craniodorsal abdomen to the left caudo
ventral abdomen and if suffciently enlarged to the
right caudoventral abdomen. Following the tenia cra
nially and dorsally, the examiner can feel them enter
the renosplenic space. When moving the hand from left
dorsal abdomen to the dorsal midline, the examiner
should feel the head of the spleen, large colon and asso
ciated tenia, renosplenic ligament, and left kidney to
confrm the diagnosis ofleft dorsal colon displacement.
With increased duration, the cecum often becomes sec
ondarily distended with gas. If the colon is severely dis
tended, the colon may fll the left caudal abdomen and
preclude examination of the renosplenic region. In this
case, left dorsal displacement may be suspected but
should be confrmed with percutaneous ultrasonogra
phy. Displacement of the spleen medially and ventrally
may be associated with left dorsal displacement, but this
fnding alone does not confrm the diagnosis of left
dorsal displacement.
Igufe9.9Caudal view of a standi ng horse demonstrati ng
a left dorsal di splacement of the l arge col on. The left ven
tral and dorsal col on are entrapped within the renospl eni c
space. The colon is pal pabl e on the left si de of the
abdomen with the tenia coursing from the left craniodor
sal abdomen to the l eft caudoventral abdomen. Fol l owing
the tenia crani al ly and dorsally, the exami ner can feel the
tenia enter the renospl eni c space. Thel Melton, CAD spe
ci al i sts, Department of Educational Resources and Dr JN
Moore, Department of Large Animal Medi ci ne, University
of Georgi a, Athens, GA JUbU, with permission
! ! b
Right dorsal displacement of the large colon may
assume a variety of anatomic confgurations, but the
common fnding for all right dorsal displacements is
displacement of the left ventral and dorsal colon lateral
to the cecum (Figure 9. 10) . The colon retroflexes on
itself and passes between the cecum and right body wall.
The colon and associated tenia are felt immediately cra
nial to the pelvic canal, coursing from the right caudal
abdomen, transversely across the abdomen, and then
continuing toward the left cranial abdomen. The pelvic
flexure usually comes to lie in the left cranial abdomen
beyond the reach of the examiner. The colon displaces
the cecum medially, and cranially, making it difcult to
palpate. With increased duration, the cecum often
becomes secondarily distended with gas. The degree of
intestinal distention is variable and severe gas disten
tion of the colon will preclude complete examination of
the abdomen.
Torsion or volvulus of the large colon i s easy to diag
nose in the later stages of the disease. The horse' s
abdomen is visibly distended and the large colon flls
Igufe 9.J Caudal view of a standi ng horse demonstrat
ing a right dorsal di splacement of the large col on. The left
ventral and dorsal colons are displaced lateral to the
cecum. The colon and associated teni a are felt i mmedi
ately crani al to the pelvic canal , coursi ng from the right
caudal abdomen, transversely across the abdomen, and
then conti nui ng toward the left crani al abdomen. Thel
Melton, CAD special ists, Department of Educational
Resources and Dr JN Moore, Department of Large Ani mal
Medi ci ne, University of Georgi a, Athens, GA JUbU, with
permission
the entire abdomen (Figure 9.11) . In extremely
advanced cases, the examiner cannot introduce the
hand beyond the pelvic rim. The marked colonic dis
tention causes the colon to fan-fold (pretzel ) within the
limited space of the abdominal cavit. This is often evi
dent as colonic tenia coursing transversely across the
caudal abdomen. With intestinal compromise, colonic
mural edema develops and is characterized by a thick
ened colon wall and mesentery, and haustra between
the tenia becoming more prominent.
In the early stages of colon volvulus colonic disten
tion may not be severe. Often the pelvic flexure and left
colons will be evident in the left abdominal quadrant.
The pelvic flexure may be moderately distended with
gas, displaced cranially, and appear to be suspended
within the middle left abdomen. The haustra and tenia
of the ventral colon may be palpated dorsal to the dor
sal colon, indicating malpositioning of the colon. The
rest of the colon and the entire cecum are displaced cra
nially and beyond the reach of the examiner. In these
cases, persistent abdominal pain and progressive colonic
distention are often evident on sequential examinations.
Igufe 9.JJ Caudal view of a standing horse demonstrat
ing a volvul us of the l arge colon. The large colon fi l l s the
entire abdomen. The marked colonic distension causes the
colon to fan-fold withi n the l i mited space of the abdomi
nal cavity. Thi s is often evi dent as colonic tenia coursing
transversely across the caudal abdomen. Thel Melton, CAD
special ists, Department of Educational Resources and
Dr IN Moore, Department of Large Animal Medicine,
University of Georgia, Athens, GA JUbU, with permission
Descending colon and rectum
Rectal examination of the horse with obstruction of the
proximal descending colon (fecalith or enterolith) is
usually characterized by generalized cecal and colonic
tympany, and marked rectal mucosal edema. Impaction
of the middle to distal descending colon has additional
fndings of continuous, solid, ingesta within the
descending colon. This forms a uniform, smooth tube
of variable length in the central caudal abdomen
(Figure 9. 12) . Individual fecal balls and haustra of the
descending colon are not usually evident in horses with
descending colon impaction. The ingesta is most often
soft and easily indentable, in contrast to large colon
impactions. In severe cases the entire descending colon
becomes impacted with ingesta. When this occurs, the
rectal ampulla may be pulled ventrally and to the left of
midline, because of the weight of the ingesta in the
descending colon and tension on the mesentery. This
makes complete examination of the rest of the
abdomen diffcult if not impossible.
Igufe 9.JZ Caudal view of a standi ng horse demonstrat
ing an impaction of the descendi ng colon with secondary
cecal and col onic tympany. I ndi vi dual fecal bal l s and
haustra of the descendi ng colon are not usual ly evident i n
horses wi th descending colon impaction. The rectal
ampul l a is pul l ed ventral l y and to the left of mi dline,
because of the weight of the ingesta in the descending
colon and tension on the mesentery. Thel Melton, CAD
specialists, Department of Educational Resources and
Dr IN Moore, Department of Large Ani mal Medicine,
University of Georgia, Athens, GA JUbU, with permission
! !J
9 COLIC
Defects in the rectal mucosa, abnormal rectal
mucosal thickening, or frank blood on the sleeve after
rectal examination are indications of possible rectal
perforation. If a rectal perforation is suspected, a thor
ough digital evaluation of the distal descending colon
and rectum should be performed with adequate
restraint and a bare hand. The distal descending colon
and rectum are circumferentially examined, moving
from a cranial-to-caudal direction. If a tear is identifed,
the horse owner should immediately be informed of the
situation, and emergency frst aid procedures should be
initiated (see Chapter 16) .
SUMMARY
Rectal examination is an essential component of the
diagnostic evaluation of horses with abdominal pain.
Proper restraint of the horse during rectal examination
is of the utmost importance to insure the safety of the
horse and the examiner. The examination should be
performed in a consistent, systematic manner to ensure
a complete and thorough examination and to minimize
the chance of missing a lesion.
Most often rectal examination does not yield a spe
cifc diagnosis, but yields information regarding the seg
ment of intestine affected, the severity of the problem,
and the need for surgical interention. In general, dis
tention of any segment of intestine, large intestinal
tenia coursing horizontally across the abdomen, or
intra- or extra-lumenal masses are abnormal fndings
and indicate intestinal obstruction and/or malposition
ing. Rectal examination fndings should always be con
sidered in conjunction with the results of the physical
examination, nasogastric intubation, abdominocente
sis, and laboratory evaluation. Serial rectal examina
tions are often necessary to determine resolution or
progression of the disease and the need for surgical
interention (see Decision for surgery) .
False (non-gastrointestinal)
colics
T Mair
Colic is not a specifc disease or diagnosis, but simply
represents a clinical syndrome related to abdominal
pain. Although colic is generally associated with dis
eases of the gastrointestinal tract, conditions of other
body systems can sometimes cause abdominal pain, and
other painful diseases may produce clinical signs that
are difcult to differentiate from pain due to gastro-
! ! d
intestinal disease. These conditions are commonly
known as 'false' colics.
A differential diagnosis list of the more common
causes of 'false' colic are listed in Table 9. 1 .
Differentiation between ' true' and 'false' colics
depends upon obtaining an accurate history and per
forming a careful physical examination coupled, where
appropriate, with further diagnostic procedures such
as clinical pathology.
'
Although not always true, horses
Female reproduttive tract Uterine torsion
Dystoclas
Uterine hematoma
Uteri ne perforation
Retained placenta
Granulosa cell tumor
Ovulation
Male epro0uCtW tract Orchitis
Seminal vesicultis
Urinar tract Cystic calculi
Renal calculi
Ureteral calculi
Urethral calculi
Pelonephritis
Cytitis
Ruptured bladder
LWl Acute hepatitis
Cholangiohepatitis
Choledocholithi asis
Spleen Splenic abscess
Splenomegaly
Respitor tract Pleuritis
Pleuropneumonia
Cardiovascular QN0 Aortoiliac thrombosis
Aortic rupture
Acute hemorrhage
Myocardial infarcion
Pericarditis
Musculoskeletal sytem Laminitis
Acute exerlonal
rhabdomyolyis
Nervus stem Tetanus
Boulism
Seizures
Hypocalcemic tetany
Equine motor neuron
disease
exhibiting colic caused by disorders of systems other
than the gastrointestinal tract generally paw and lie
down for prolonged periods, but rarely roll violently.
Medical therapies for colic
T Mai r
INTRODUCTION
The majorit of colic cases encountered in practice are
associated with mild and non-specific signs. In one sur
vey, carried out over a 2-year period in general practice
in the UK, colics were categorized as
spasmodic and undiagnosed colics - 72 per cent
pelvic flexure and other impactions - 14. 5 per cent
surgical lesions (including strangulating
obstructions) - 7 per cent
fatulent colic - 5.5 per cent
colitis - 1 per cent.
The majority of colics encountered in first opinion prac
tice will, therefore, be amenable to medical therapy. In
many cases the response (or lack of response) to simple
medical treatments will also be helpful diagnostically.
AIMS OF MEDICAL TREATMENT
The aims of medical therapy in equine colic are to
relieve pain
restore normal propulsive motility of the gut
correct and maintain hydration and electrolyte or
acid-base balance
treat endotoxemia
treat bacterial or parasitic infections (if present) .
The first two aims given above need to be accomplished
without masking the clinical signs that must be moni
tored for proper assessment of the horse's condition
and progress.
A wide variet of therapeutic agents are used to treat
colic. These include
analgesics to control visceral pain
agents to soften and facilitate the passage of ingesta
(laxatives)
fluids and electrolytes to improve cardiovascular
function during endotoxic and hypovolemic shock
anti-endotoxin therapy
anti-inflammatory drugs to reduce the adverse
efects of endotoxin
agents to normalize intestinal contractions during
adynamic ileus
therapy for ischemia-reperfusion injury
antimicrobial drugs
anthelmintics.
Analgesic therapy
Relief of visceral pain in horses with colic is essential
both on humane grounds and to minimize injury to the
horse and attending personnel during evaluation and
therapy. Even in mild cases owner distress over animal
pain is an important consideration.
The most satisfactory method of pain relief is to cor
rect the cause of increased intramural tension resulting
from distention or spasm. This may take time however,
and it is often necessary to provide temporary pain relief
chemotherapeutically to allow a thorough clinical exam
ination without risk of injury to the horse and personnel.
It is important to select a drug that will accomplish the
desired effect without creating complications such U
depressing gut activity, predisposing to hypovolemia and
shock, or, most important, masking the signs of develop
ing endotoxemia. The commonly used analgesic drugs,
their dosages, and relative effcacy for the control of
abdominal pain are summarized in Table 9. 2.
Drug Doge Fh|tcj
Dipyrone 10 mg/g poor to
moderate
Phenylbutazone 2.2-4.4 mg/g poor to
moderate
Flunixin meglumine 0.251.1 mg/kg good to
excellent
Ketoprofen 1.1-2.2 mglkg good
Xylazine hydrochloride 0.2-1.1 mg/g excellent
Detomidine hydrochloride 10-401g/9 excellent
Romifidine hydrochloride 40-
8
0
1
g/9 excellent
Acepromazine 0.034.1 mg/g poor
Morphine sulfate 0.3-0.66 mg/kg* good
Pethidine 2.0 mglkg poor
Butorphanol tartrate 0.05-0.075 mg/kg** good
Pentazocine 0.3-0.6 mg/kg poor to
moderate
'Use only with xylazine or another alpha2 adrenoceptor agonist
to avid CN$excitement
"Doses in the upper range may cause ataxia
! !
9 COLIC
Walking
Walking the horse with mild colic frequently appears to
be beneficial, and in some cases may be the only treat
ment necessary. Walking appears to have an analgesic
efect in addition to stimulating intestinal motility. It
also helps to prevent injury to the horse caused by
falling to the ground and rolling.
Gastric decompression
Gastric distention frequently occurs secondarily to
small intestinal obstruction or small intestinal ileus.
Since horses do not vomit, nasogastric intubation is nec
essary to determine if gastric distention is present and
to provide relief. Decompression of the stomach is nec
essar to relieve pain, and to prevent gastric rupture
and death. Large volumes of reflux ( 1 0-20 liters) may
be obtained in some cases and if necessary an
indwelling nasogastric tube may left in place to allow
frequent (approximately every 2 hours) decompres
sion.
Non-steroidal anti-inflammatory drugs
(NSAIDs)
Among the most useful analgesics for both surgical and
non-surgical disease are the non-steroidal anti-inflam
matory drugs. The therapeutic and adverse effects of
these drugs result from inhibition of cyclooxygenase
(COX) enzyme-mediated biosynthesis of prosta
glandins. The NSAlDs non-selectively block both COX-
1 and COX-2 enzymes. Prostaglandins directly and
indirectly stimulate nerve endings. These drugs are
most effective as analgesics when some degree of
inflammation is present. The NSAlDs commonly
employed (dipyrone, phenylbutazone, flunixin meglu
mine, and ketoprofen) differ greatly in efcacy in the
treatment of visceral pain in horses.
Dipyrone
Dipyrone is a very weak analgesic drug that can provide
only short term relief in cases of mild abdominal pain.
Combined with hyoscine N-butylbromide it is effective
in relieving intestinal spasm. It failure to help reduce
or stop pain in individual cases should signal that a con
dition exists that is more serious than a simple intestinal
spasm or tympanitic colic.
Phenylbutazone
Phenylbutazone provides no greater relief from visceral
pain than does dipyrone. However, the toxic side effects
of phenylbutazone are numerous and include gastro
intestinal ulceration and nephrotoxicity. For this reason
the dosage should not exceed 4. 4 mg/kg ever 1 2
!2
hours. Phenylbutazone has been shown to be superior
to flunixin meglumine in maintaining gastric motility
during endotoxemia, but this is likely to be of only
minor importance in horses being treated for abdomi
nal pain.
Flunixin meglumine
Flunixin meglumine is the most effective of the NSAIDs
used to control visceral pain in horses. It has been
shown to block the production of prostaglandins,
specifically thromboxane and prostacyclin, for 8-12
hours after a single dose ( 1 . 1 mg/kg) . The duration of
analgesia produced varies from 1 hour to more than 24
hours depending on the cause and severity of the pain.
Although this drug has basic side effects similar to
phenylbutazone, there is a greater risk associated with
its use in its ability to mask clinical signs of intestinal
strangulation or obstruction by reducing heart rate,
relieving pain, and improving mucous membrane
color. If administered to horses in which the precise
cause of colic has not been ascertained, it is essential to
monitor closely rectal examination findings, nasogas
tric reflux, peritoneal fluid, and heart and respiratory
rates over the following few hours. It should be admin
istered to control severe pain and to diminish the
efects of endotoxins in horses needing transport to a
referral center for surgery.
Ketoprofen
Ketoprofen blocks both the cyclooxygenase and lipo
oxygenase pathways. It is not as effective as flunixin in
alleviating abdominal pain.
RamiJenazone
This is another non-steroidal anti-inflammatory drug
sometimes used in combination with phenylbutazone.
Eltenac
Eltenac is a potent non-steroidal anti-inflammatory
drug with anti-pyretic and anti-edematous properties. It
is a relatively weak analgesic, but the anti-edema prop
erties may make it useful in the postoperative colic
patient.
Sedatives
Alpha
2
agonist sedative drugs include xylazine, detomi
dine, and romifdine. These agents are effective anal
gesics in horses affected by abdominal pain, but they
have the disadvantage of decreasing gastrointestinal
motility for the duration of the period of sedation.
Xylazine
Xylazine produces both sedation and visceral analgesia
by stimulating alpha
2
adrenoceptors in the CNS,
thereby decreasing neurotransmission. At a dose rate of
l . l mg kg-I i.v., the visceral analgesia provided by
xylazine appears to be similar to that of flunixin and the
narcotics. The duration of effect of xylazine is much
shorter (usually 1 0-30 minutes) than that of flunixin
making xylazine more useful for controlling pain
during evaluation of the cause of colic and its specifc
therapy.
Potentially detrimental side effects of xylazine
include bradycardia, decreased cardiac output, tran
sient hypertension followed by hypotension, ileus and
decreased intestinal blood flow; these may affect its
use in horses in shock. In contrast to the bradycardia,
hypertension, and intestinal hypotension which last
only a few minutes, the ileus and hypotension can be
prolonged. A reduced dosage of 0.2-0.4 mg/kg i.v.
can be administered in an attempt to reduce the sever
ity and duration of the side effects. Alternatively it can
be used at the lower dosage in combination with a
narcotic agonist such as butorphanol.
Detomidine
Detomidine, another alpha
2
adrenoceptor agonist, is a
more potent sedative and analgesic than xylazine. The
same complicating effects are likely to be present for
detomidine as for xylazine. Detomidine will reduce
intestinal motility similarly to xylazine and can mask
many of the signs that assist the clinician in diagnosing
the cause of the colic. Since it is such a potent drug, any
signs of colic obsered within an hour of administration
are an indication that a severe disease that requires
surgery is present. Therefore it is a useful drug when
used with caution and preferably at the low dose rate of
10 rg/kg i.v. Potentiated sulfonamides should not be
given to horses sedated with detomidine.
Rmifdine
Romifdine has a similar action to xylazine and detomi
dine. At a dose rate of 40-80 Ilg/kg i.v. it provides
potent analgesia lasting 1-3 hours.
Aceromazine
Phenothiazine tranquilizers have a peripheral vasodila
tory effect which is contraindicated in horses with
reduced circulatory volume because they block the life
saving vasoconstriction that maintains arterial blood
pressure and insures, within limits, perfusion of vital
organs.
Narcotic analgesics
The analgesic and sedative effects of these drugs result
from interaction with central and/ or peripheral opioid
receptors.
CLINICAL EVALUATI ON OF THE COLIC CASE 9
Morphine
Morphine and pethidine are opioid receptor agonists.
They are potent analgesics, but morphine in particular
can cause excitement in horses unless used in combina
tion with drugs like xylazine. Morphine is known to
reduce progressive motility of the small intestine and
colon while potentially increasing mixing movements
and increasing sphincter tone. The disadvantages of
morphine are sufcient to discourage its use in most
horses with abdominal disease.
Pethidine
Pethidine is a narcotic agonist with few side effects and
provides slight to moderate analgesia of relatively short
duration in horses with abdominal pain. Used repeat
edly it can potentiate obstructions caused by impactions
by reducing colon activity.
Butorhanol
Butorphanol is a partial agonist and antagonist which
gives the best pain relief of the drugs in this group, with
the fewest side effects. It can be used in combination
with xylazine or the other alpha
2
adrenoceptor agonists
in horses with moderate to severe abdominal pain to
increase the level of analgesia. The dose can vary from
0.05-0.075 mg/kg. Doses exceeding 0. 2 mg/kg can
cause excitement. Butorphanol reduces small intestinal
motility but has minimal efect on pelvic flexure activity.
It is potent enough to stop colic for short periods of
time when it is caused by severe intestinal disease but
the pain from large colon torsion or small intestinal
strangulation may not be altered. When administered
without xylazine or another alpha
2
adrenoceptor ago
nist, even small doses of butorphanol may occasionally
cause head jerking.
Pentazocine
Pentazocine is a partial agonist which is slightly more
effective than dipyrone but less effective than xylazine
and flunixin in relieving visceral pain.
Spasmolytics
Increased frequency of intestinal contractions, for
example in spasmodic colic or spasms occurring oral to
intralumenal obstructions, cause pain which can be
relieved by spasmolytics. Spasmolytic drugs include
cholinergic blockers such as atropine and hyoscine N
butyl bromide.
Atropine
Atropine is not recommended for use in horses with
colic because its effect in relaxing the intestinal wall and
preventing contractions can last for several hours or
! 2!
9 COLI C
even days creating tympany and complicating the initial
problem with ileus.
Hyoscine
Hyoscine has a shorter muscarinic cholinergic blocking
effect compared to atropine and is effective in relaxing
the bowel wall. It is available in Europe combined with
dipyrone and is administered intravenously in doses of
20-30 m!.
Laxatives
Laxatives are commonly used in horses with colic to
increase the water content and softness of ingesta
thereby facilitating intestinal transit. The most common
indication for their use is in the treatment of large
colon impactions. In severe impactions, the effective
ness of laxatives is increased by administering oral and
intravenous fluids concurrently. These medications
should never be administered orally in horses with naso
gastric reflux.
Mineral oil (liquid parafn)
Mineral oil (liquid paraffn) is the most frequently used
laxative in equine practice. It is a surface lubricant and
is administered at a dosage of 5-10 ml/kg once or twice
a day by nasogastric tube. Its effects are considered mild
and it is safe for prolonged use. It is commonly admin
istered with water or saline and is considered by many
clinicians as the lubricant of choice for mild colonic
impactions.
Psyllium hydrophilic mucilloid
Psyllium hydrophilic mucilloid is a bulk-forming laxa
tive which causes the fluid and ion content of feces to
increase by absorbing water. It has been considered to
be particularly useful for treating sand impactions. A
dose of 1 g/kg can be administered per os up to four
times a day. P a long-term treatment, it may be admin
istered daily for several weeks to help eliminate sand
from the large colon. Recently the efcacy of psyllium
hydrophilic mucilloid in treating sand impactions has
been questioned.
Osmotic laxatives
Magnesium sulfate (Epsom salt) and sodium chloride
(table salt) can be used as osmotic laxatives in horses.
Research has shown that magnesium sulfate also stimu
lates water secretion in the colon by a reflex action
immediately on administration. Undiluted osmotic lax
atives will cause enteritis by osmotic damage to the
mucosal cells, so each dose of 0. 5-1.0 gm/kg should be
diluted in 4 liters of warm water and administered by
nasogastric tube once or twice a day. Epsom salt should
!22
not be administered longer than 3 days because of
severe enteritis and possible magnesium intoxication.
Dioctyl sodium succinate (DSS)
DSS is a surface-active agent with wetting and emulsifing
properties. It reduces surface tension and allows water
and fat to penetrate the ingesta. A dose of 1 0-20 mg/kg
can be administered as a 5% solution by nasogastric tube
every 48 hours. DSS can cause damage to the mucosa and
increases fluid permeability of colon cells, this can result
in mild abdominal pain and diarrhea.
Fluid therapy and cardiovascular support
Fluid, electrolyte, and acid-base imbalances commonly
occur in equine gastrointestinal diseases. While univer
sally employed to support horses with severe intestinal
obstructions requiring surgery, the value of fluid ther
apy for colic in a feld situation has not been widely
appreciated. Fluid therapy is rarely, if ever, contraindi
cated in adult horses with colic. The type of fluid and
rate of administration will change from the initial ther
apy, which is designed to replace the deficits, to mainte
nance therapy, which is designed to keep pace with
ongoing requirements. Detailed descriptions of fluid
therapy in the horse are provided elsewhere (see
Chapter 9) .
Intravenous administration of polyionic-balanced
electrolyte solutions (e.g. Hartmann' s solution) will
help to maintain the intravascular fluid volume and aid
tissue perfusion. Normal saline (0. 9% sodium chloride)
may also be used initially for rehydration, but should
not be used long term without evaluation of serum elec
trolytes and acid-base balance because it tends to pro
mote acidosis, hypokalemia, and hypernatremia. The
hydration status of the horse should be assessed by clin
ical observations and measurement of packed cell vol
ume and total serum/plasma protein. The percentage
dehydration of the patient can be estimated, and this is
used to calculate the volume of fluid necessary to cor
rect the horse's fluid defcit. Horses with severe colonic
impactions may beneft from overhydration in an
attempt to hydrate and break up the impaction; a bal
anced electrolyte solution can be administered continu
ously at a rate of approximately 4-5 l/h for a 500 kg
horse. Horses with continued fluid loss by gastric evacu
ation and sequestration of fluid into the bowel have
increased maintenance fluid requirements. The packed
cell volume and plasma protein levels of such cases
should be regularly monitored to assess the degree of
dehydration. If available, measurements of serum elec
trolytes and blood gases are also helpful in determining
the type and quantity of fluids to be given, and to mon
itor the effects of treatment.
In severe hypovolemic and hypotensive shock,
hypertonic saline (7% sodium chloride, 4 ml/kg) can
be administered initially to provide a rapid improve
ment in cardiovascular function. However, this treat
ment must be followed within 2 hours by isotonic fluid
therapy to replace the volume defcit.
The bicarbonate defcit and replacement require
ments are based on the volume of the extracellular fluid
compartment, body weight, and base defcit as deter
mined by arterial or venous blood gas analysis. The
following formula is used to calculate this defcit
bicarbonate defcit (mEq) = 0.3 ? body weight (kg)
? base defcit (mEq/l)
One half of the defcit should be replaced over the frst
several hours, and then the blood gas analysis repeated.
If the plasma protein concentration is low (less than
45 gil) and the horse is dehydrated, administration of
plasma (minimum of 2 liters given slowly intravenously)
will help to maintain plasma oncotic pressure and avoid
inducing pulmonary edema during rehydration with i.v.
fluids. Plasma is also helpful in treating horses with
en do toxemia (see below) .
Anti-endotoxin therapy
Endotoxin is the toxic lipopolysaccharide component
of the outer cell envelope of gram-negative bacteria.
Entry of endotoxin into the circulation occurs when the
intestinal mucosal barrier is damaged, for example in
strangulating and ischemic bowel disorders, and this
initiates a series of deleterious events involving the syn
thesis and release of numerous inflammatory media
tors. Severe endotoxemia frequently results in death.
The treatment of endotoxemia is discussed in greater
detail in Chapter 1 1 .
Purifed endotoxin-specifc IgG containing antibod
ies against lipopolysaccharide extracts of a variety of
gram-negative bacteria is available in the UK This treat
ment aims to promote the clearance of endotoxins
from the circulation prior to its interaction with inflam
matory cells and the subsequent production of pro
inflammatory mediators. Treatment early in the course
of the disease is therefore necessary.
Active immunization of horses with mutant core
polysaccharide vaccines is available in the US, although
the duration and degree of protection aforded by these
vaccines is uncertain. Hyperimmune plasma directed
against gram-negative core antigens provides antibodies
with cross-reactivity against a wide range of bacteria.
Normal equine plasma (2-10 liters) administered
slowly intravenously may also be benefcial, supplying
protein, fbronectin, complement, antithrombin III,
and other inhibitors of hypercoagulability.
Anti-inflammatory treatment of endotoxemia
Flunixin meglumine has been shown to suppress
prostaglandin and thromboxane production, and to
improve the clinical signs in equine endotoxemia.
Flunixin appears to be more effective than phenylbuta
zone and other NSAIDs in this respect. A low dose of
funixin (0. 25 mg/kg i.v. q. 8 h) effectively suppresses
endotoxin-induced Cclooxygenase-derived products
without masking the clinical manifestations of endotox
emia. This treatment is valuable in the postoperative
management of many colic cases.
Drugs that alter intestinal motility
Postoperative ileus is the most common indication for
pharmacological manipulation of intestinal contractile
activity. Ileus may also occur in association with proxi
mal duodenitis-jejunitis (anterior enteritis) and peri
tonitis. There are two general methods by which drugs
may correct ileus caused by any disease. First, drugs may
directly stimulate contraction of intestinal smooth mus
cle. Second, certain agents block the mechanisms by
which the disease inhibit motility, thereby restoring
normal contractions. Continuous or repeated gastric
decompression must be provided in addition to drug
therapy. The management of postoperative ileus is dis
cussed in greater detail in Chapter 1 1 .
Neostigmine methyl sulate
Neostigmine is an acetyl-cholinesterase inhibitor that
directly stimulates intestinal contractions. Doses of
0.0044 mg/kg (2 mg for an average sized adult horse)
can be administered subcutaneously or intravenously.
The duration of effect is very short ( 1 5-30 minutes) and
up to fve doses may be given at 20-60 minute intervals.
If there is no response to this dose rate, and assuming
that the horse is not showing any evidence of side
effects, the dose of neostigmine can be increased by 2-
mg increments up to a total of 10 mg per treatment.
Neostigmine induces disorganized segmental contrac
tions, and can actually decrease propulsive motility of
the jejunum and delay gastric emptying. It can also
cause abdominal pain by stimulating spasmodic
regional contractions. For these reasons many clini
cians do not favor its use in clinical cases. However,
studies have shown that neostigmine can improve cecal
and colonic motility.
Metoctoamide
Metoclopramide is a non-specifc dopaminergic antago
nist that also augments the release of acetylcholine
from intrinsic cholinergic neurons and has adrenergic
blocking activity. It is a potent gastrointestinal stimulant
when given at a dosage of 0. 25 mg/kg i.v. ( diluted in
! Z
9 COLIC
500 ml of saline and administered over a period of
30-60 minutes) , but in some cases has proved unsuit
able because it can produce severe CNS side effects
(excitement, sweating, and restlessness) . However, it
may be safely administered to most horses as a continu
ous infusion at 0.04 mg kg-1 h-1
Domperidone
Domperidone, a newer dopaminergic antagonist does
not cross the blood-brain barrier and at a dose rate of
0.2 mg/kg i.v. has been shown to block dopaminergic
receptors and prevent postoperative ileus induced
experimentally. It has potential for use in clinical cases.
Cisapride
Cisapride is a substituted benzamide with gastrointesti
nal prokinetic properties. The mode of action is
believed to be enhancement of release of acetylcholine
from postganglionic intramural interneurons leading
to increased calcium flux. Cisapride does not have any
dopamine-blocking activity. In normal horses cisapride
has been shown to augment the amplitude of gastric
contractions, stimulate jejunal activity coordinated with
gastric contractions, enhance contractile activity of the
large and small colons, and stimulate coordinated activ
ity at the ileocecocolonic junction. An injectable prepa
ration of cisapride is no longer available but 1 0 mg
tablets, available for the treatment of motility disorders
in humans, can be administered orally in horses.
Although there is anecdotal evidence that cisapride is
also effective when administered rectally (0. 2 mg/kg) ,
offering advantages in horses with gastric reflux, recent
studies have demonstrated that it cannot be detected in
the blood of horses after administration by this route.
Lidocaine (lignocaine)
Lidocaine has been used in horses with colic primarily
to treat ileus, but recently it has been found to be an
effective analgesic as well. Lidocaine exerts it analgesic
properties by decreasing afferent trafc through small
C fbers. In addition, it has anti-inflammatory proper
ties and decreases the influx of inflammatory cells. The
plasma levels necessary for analgesia are much lower
than those required to block normal peripheral nerve
conduction. Lidocaine has also been shown to decrease
reperfusion injury by inhibiting the release of free radi
cals and decreasing the migration of neutrophils at the
site of iury. Preliminary studies suggest that the proki
netic effect of lidocaine may be useful in postoperative
ileus. initial intravenous bolus at a dose rate of
1 . 3 mg/kg (administered slowly over 5 minutes) can be
followed by a continuous intravenous infusion at a rate
of 0.05 mg kg-1 min-1 (diluted in saline or lactated
Ringer's solution) . Signs of toxicity include muscle
! Z4
fasciculations, ataxia, and possible seizures. These signs
are more likely to happen if the initial bolus is adminis
tered too rapidly.
Erthrmycin lactobionate
Erythromycin is a macrolide antibiotic that appears to
have a prokinetic action on the intestine that is inde
pendent of its antimicrobial action. It acts on enteric
cholinergic neurons through motilin and/or 5-HT3
receptors to stimulate the release of acetlcholine. A
dose of 2. 2 mg/kg diluted in 1 liter of saline and
infused over 60 minutes may be administered every 6
hours. Alternatively it may be administered as a contin
uous intravenous infusion at a rate of 0. 1 mg kg-l h-1 A
recent study in normal horses determined that a lower
dose of 1 .0 mg/kg is effective in stimulating both cecal
and small intestinal propulsive activity. Doses higher
than 10 mg/kg can potentially disrupt propulsive activ
ity. There has been some concern that the prokinetic
response may diminish with repeated treatments
because of down-regulation of motilin receptors. An
association between erythromycin therapy and the
occurrence of colitis induced by Clostridium dicile in a
small number of horses has led some clinicians to ques
tion the safety of this therapy.
Acetylpromazine (acermazine) and yohimbine
These drugs are a-adrenergic antagonists. Their use is
based on the assumption that sympathetic hyperactivity
contributes to postoperative ileus. Norepinephrine
inhibits the release of the excitatory neurotransmitter
acetlcholine by stimulating alpha-2 receptors located
presynaptically on cholinergic neurons. Acepromazine
facilitates small intestinal transit in normal ponies. The
drug can also produce hypotension via antagonism of
alpha-l adrenergic receptors, so it is essential that the
horse should be well hydrated prior to administration.
Yohimbine hydrochloride is a competitive antago
nist that is selective for alpha-2 adrenergic receptors.
When administered at a dose rate of 0. 1 5 mg/kg intra
venously it can reduce the severity of postoperative
ileus especially when used in combination with
bethanecol.
Bethanecol
Bethanecol is a muscarinic cholinergic agonist, which
stimulates gastrointestinal smooth muscle cells causing
them to contract. At a dose rate of 2.5 mg/kg, subcuta
neously, bethanecol was shown to improve gastrointesti
nal motility in an experimental model of postoperative
ileus when administered in combination with yohim
bine. Bethanecol has also been shown to increase the
rate of gastric and cecal emptying in normal horses. A
common use of be thane col in horses is in the treatment
of gastric atony following correction of an outflow
obstruction in foals with duodenal ulcers. Side effects,
including abdominal cramps, diarrhea, salivation, and
gastric secretion, arise from enhanced parasympathetic
tone.
Spasmodic colic
W8
T Mair
Spasmodic colic is the most common type of colic
encountered in adult horses. It probably accounts for
some 40 per cent of colic cases seen in general practice.
ETIOLOGY AND PATHOGENESIS
Spasmodic colic is believed to arise from spasms, or
abnormal and uncontrolled contractions, of the small
intestine. These dysfunctional contractions do not con
tribute to aboral movement of ingesta through the
intestinal tract but result in pain to the horse due to
stimulation of mural stretch receptors. It is a func
tional disorder that is rarely associated with any
morphological changes of the intestinal wall. It is
attributed to an increase in peristalsis and a propensit
to spasm.
Numerous causes of spasmodic colic have been pro
posed, for example
excitement
physical exertion and fatigue
parasitic migration through the bowel wall or
vessels
moldy feed
excessive grain or insufcient fber
weather changes
but none of these has been proven. individual pre
disposition to spasmodic colic occurs in some horses
resulting in recurrent bouts of colic.
The intestinal spasms are invariably transient and do
not persist long enough to cause signifcant bowel
obstruction. It is possible, however, that these abnormal
movements may predispose to a malposition of the
intestine that could then lead to a strangulation
obstruction.
CLINICAL SIGNS AND DIAGNOSIS
Uncomplicated spasmodic colic is characterized by
intermittent mild to moderate abdominal pain,
increased small intestinal and colonic sounds, and
increased heart rate (see below) . The paroxysmal
attacks of colic usually last from 5-10 minutes and are
separated by pain-free intervals during which the
horse's appearance and behavior are normal. There are
usually no metabolic derangements or changes in the
peritoneal fluid. The respiratory rate and heart rate
increase mildly during bouts of pain, but quickly return
to normal when the horse is quiet. The heart rate is
rarely elevated to more than 60 bpm.
The clinical signs of spasmodic colic include
intermittent pain
mild to moderate abdominal pain indicated by
pawing, flank watching, recumbency, and rolling
increased borborygmi
semi-liquid feces.
The hyperperistaltic activity is often audible at some
distance from the horse, and frequently has a 'metal
lic' sound. Feces may be passed frequently and in small
amounts, and may have a soft to semi-liquid consis
tency.
Rectal fndings are often unremarkable, however
one or more spastically constricted loops of small intes
tine may be palpable; these loops may subsequently be
felt to relax. In other cases mild gaseous distention of
the duodenum or cecum may be palpable.
Nasogastric intubation does not reveal any gastric
reflux and results of abdominal paracentesis are
routinely normal.
The diagnosis of spasmodic colic is usually made on
the basis of the characteristic clinical signs, the absence
of other signifcant fndings on rectal examination, and
the response to treatment with analgesic and spas
molytic drugs.
TREATMENT
Many horses with mild spasmodic colic improve sponta
neously and require no treatment. However, if the
animal is in pain at the time of examination, some form
of analgesia should be provided. The administration of
a spasmolytic and analgesic drug combination such as
hyoscine and dipyrone will quickly abolish the spasms
and thereby relieve the pain. Xylazine, detomidine,
romifdine, and non-steroidal anti-inflammatory drugs
are also effective treatments. The treatment may be
repeated after several hours if necessary, but most cases
show no recurrence of colic when the effects of the
initial medication wears off.
The prognosis for recovery is excellent provided
there is no subsequent or associated malpositioning of
the bowel.
!2b
9 COLIC
Acute colic - the decision to
refer
T Mai r
The primary aim of the initial evaluation of the horse
affected with acute colic is to attempt to distinguish
horses with mild or uncomplicated disease processes
from those with potentially life-threatening diseases.
Referral of the colic case to an equine hospital may be
required to permit further evaluation and monitoring,
surgery and/or intensive care.
The initial assessment of the horse with acute colic
on the farm is fraught with difculties, even for the
most experienced equine clinician. Distraught owners,
absence of competent lay assistance, and inadequate
facilities for handling and restraint are just a few of the
problems that the veterinarian may encounter.
accurate diagnosis of the cause of acute colic may be dif
ficult or impossible to achieve in such circumstances.
However, the clinician should not be too concerned
about the inabilit to reach a specifc diagnosis in all
cases. Careful assessment and appropriate management
of acute colic cases are of much greater importance
than reaching a specifc diagnosis. Indeed, in many
cases of acute colic, a specifc diagnosis of the cause will
never be reached.
The past few decades have seen dramatic improve
ments in survival rates of horses undergoing surgical
treatment for a variety of diseases causing colic. These
improvements have been associated with better under
standing of the diseases, their pathophysiology and
methods of treatment, and greater availability of surgi
cal facilities. However, despite improvements in survival
rates, many horses with intestinal ischemia and other
surgical diseases of the abdomen still die in spite of sur
gical intervention. A delay in making the decision to
refer the case can represent one of the most critical fac
tors that impacts upon the chances of survival. Early
referral is therefore of vital importance, and the pri
mary veterinarian needs to address the question of
whether or not the case should be referred to a surgical
center (whether this be part of his or her own practice,
another private practice, or an academic institution) as
a matter of priority.
The decision to refer a horse with acute colic should
be regarded separately to the decision to perform
surgery. In some cases, the diagnosis of a surgical lesion
may be made at the initial assessment of the patient,
and immediate referral must, therefore, take place.
However, in many other cases, the decision to perform
surgery (see Colic - decisions for surgery) is only made
after re-assessment of the case over time and after eval-
!2b
uating the response to medical treatments. By the time
that the decision to perform surgery is reached in such
cases, the horse should already be located at the surgi
cal facility so that surgery can be undertaken immedi
ately. It is imperative, therefore, that referral of such
cases should have taken place before the fnal decision
to undertake surgery is reached.
Referral of a horse with acute colic should never be
regarded as unnecessary, even if the horse recovers
without surgery. Early transport of horses in abdominal
pain to a surgical facility does not constitute a decision
to perform surgery; it seres only to transfer the horse to
a location where it can be re-assessed (using further
diagnostic procedures that might not be available in the
feld) and where immediate surgery can be undertaken
as and when deemed necessary. The surgeon is the
most qualifed person to decide whether or not surgery
should be performed. The referring veterinarian need
not feel embarrassed or inadequate if the surgeon
decides that surgery is unnecessary - most owners will
be only too pleased to learn that their horse does not
require major (and expensive) surgery.
EVALUATION OF THE PATIENT
The evaluation of the horse with acute colic is under
taken as described in other sections in this chapter. The
veterinarian should then be in a position to make a
qualifed judgment about the necessit to refer the
horse to a surgical clinic. This judgment may need to be
constantly re-evaluated if initial referral is not deemed
necessary but the abdominal pain persists or recurs. It is
important that the results of examinations are carefully
documented so that accurate comparisons at different
times can be made. In this way important trends in the
course of the illness can be identifed. This is particu
larly important if a subsequent examination is carried
out by a different veterinarian in the practice. A printed
colic sheet listing the various procedures and providing
spaces for recording the fndings at each examination is
of considerable value. In some cases the need for imme
diate referral will be obvious without the necessity of
undertaking all components of the evaluation.
Factors which are helpful in determining the need
for referral include
signalment
geographical location
medical history (especially relating to previous
episodes of colic)
management and deworming history
severit of pain and progression of colic since its
onset
fecal production
response to medical therapy (see Medical therapies
for colic)
results of physical examination (see Physical
examination of a horse with colic)
hematocrit (PCV) and total plasma protein (TPP)
estimations
results of nasogastric intubation
results of rectal examination
appearance of peritoneal fluid.
Signalment
Age, sex, and breed may be important clues indicating
the possibility of certain diseases (e. g. meconium
impaction in foals less than 48 hours of age, inguinal
herniation in stallions and Standardbreds, strangulat
ing lipomas in horses over 1 5 years of age, colonic tor
sion in recently foaled mares, etc. ) . Miniature horses
with marked abdominal pain are likely to have a small
colon impaction, and it may be wise to assume that this
is the cause of colic in such animals unless proven
otherwise. Although the signalment will not necessarily
indicate the presence of a certain disease, it can be use
ful information that should be kept in mind during the
rest of the evaluation.
Geographical location
Geographical location can be important, since some
diseases have a much higher incidence in certain loca
tions, for example enterolithiasis in California.
Medical history
A history of previous illness may be helpful in making a
decision about the case or in guiding the veterinarian
toward specifc diagnostic procedures. For example, a
history of strangles ( Stretococcus equi subsp. equi infec
tion) in a horse with chronic or recurrent colic may sug
gest the possibility of an abdominal abscess; a history of
infrequent, recurrent bouts of mild spasmodic colic
may suggest the likelihood of a further bout of spas
modic colic.
Management and deworming history
Factors relating to the general management and
deworming history that can be helpful include
1. general history
housed or at grass
type of feed
use of the animal
daily routine
parasite control
2. recent history
when the last feed was given
consumption of feed and water
recent changes in feeding, bedding, housing, or
routine
recent deworming
pregnancy
recent exercise.
Some diseases, such as tympanitic (distention) colic, are
more likely to affect pastured horses than stabled
horses. Horses subjected to changes in diet or exercise
regime, or decreased water consumption because of
cold weather, may be more prone to develop colonic
impactions. Appearance of colic following administra
tion of an anthelmintic drug may suggest the possibility
of larval cyathostomosis or intestinal obstruction by
ascarids (in young horses) .
Severity of pain and progression of colic since
onset
The most important factors of the recent history are the
time that has elapsed since the onset of clinical signs
and the severity of pain. The duration of colic may be
known precisely if the horse was observed at the onset
of clinical signs, but is often unknown, especially in
horses that are found with colic frst thing in the morn
ing. Skin abrasions around the eyes and over the tuber
coxae are indicative of recent rolling and other violent
behavior caused by severe pain. Marks on the stable
walls caused by the horse' s kicking and excessive distur
bance of the bedding, or flattening of an area of grass at
pasture, are further evidence that the horse is in severe
pain.
In general terms, horses showing signs of having
been in severe abdominal pain are more likely to have a
surgical lesion than horses showing signs of mild
abdominal pain. However, horses with a strangulating
intestinal lesion that has been in existence for more
than 46 hours may not currently show signs of pain
because of advanced necrosis of the affected bowel wall.
Such cases usually show signs of severe depression
(standing quietly with the head low and showing no
interest in the surroundings) , and there is likely to be
evidence of previous periods of severe pain as outlined
above. This stage of indolence is associated with severe
endotoxemia and may be mistaken by the owner as an
indication that the horse' s condition is improving.
Although the degree of behavioral pain that the horse is
demonstrating is important, it must be remembered
that some horses are more stoical than others. Also, old
horses and ponies affected by strangulating lipomas
may sometimes not demonstrate the severe signs of
pain that might be expected.
!2J
9 COLIC
Fecal production
The nature and quantit of feces passed by the horse
since the onset of colic can be useful information.
Decreased or absent fecal production is likely in horses
affected by intestinal obstruction. Soft, 'cow-pat' or diar
rheic feces might indicate colitis.
Response to medical therapy
Failure to eliminate abdominal pain or the recurrence
of abdominal pain following administration of appro
priate analgesic and other drugs (see Medical therapies
for colic) may raise the index of suspicion of a surgical
lesion. However, certain factors must be taken into con
sideration when interpreting the response to therapy.
Wherever the cause of colic is uncertain, and especially
in horses where referral at some point in the future is
considered possible, administration of potent non
steroidal anti-inflammatory drugs, such as flunixin meg
lumine, should be avoided. Such agents may mask the
early clinical signs of endotoxemia, thereby delaying the
decision to refer the horse or to undertake surgery until
extensive irreversible tissue damage has taken place. The
use of other, short-acting analgesic agents is therefore
recommended in cases of uncertain etiology. Good
clinical response to a weak analgesic, such as dipyrone,
suggests that the horse is very unlikely to be affected by
a lesion that requires surgical intervention.
Following the initial evaluation of the horse, it
should be possible to classit the problem into one of
three categories
! . a relatively benign problem requiring medical
therapy
2. a problem requiring surgical correction
3. a problem which might require surgery, but for
which there is at present no conclusive evidence.
Horses affected by conditions falling into the frst cate
gory should receive appropriate medical therapy. This
will usually involve the administration of an analgesic
agent, possibly with other drugs such as laxatives. In
many cases such treatment can be adequately per
formed in the feld and referral to a hospital is unnec
essary. However, in horses with medical problems that
may require intensive therapy (such as colitis, peritoni
tis, etc. ) , then referral to an equine hospital should be
considered early in the course of the condition.
Horses with diseases in the second category require
prompt referral to a surgical facility after appropriate
preparation before transport (see Horse preparation
for referral transport) .
Horses with problems ftting the third category may
be treated on the farm with an appropriate analgesic and
re-examined after a period of approximately 2 hours. At
!2d
the time of the re-evaluation, the horse may be found to
have either improved, to have developed conclusive signs
indicating the need for referral, or to have remained
unchanged. A decision as to whether or not referral is
necessary can be made at the time of re-examination.
Alternatively, referral may be considered at the time of
the frst examination, especially if the horse is showing
any signs of dehydration or poor peripheral perfusion.
Additional factors to evaluate
For a detailed discussion of
results of the physical examination
hematocrit ( PCV) and total plasma protein (TPP)
estimations
results of nasogastric intubation
results of rectal examination
appearance of peritoneal fluid
see Physical examination of a horse with colic, and
Colic - decisions for surgery.
A systematic clinical examination should be per
formed to include the cardiovascular system, abdomen
and state of peripheral circulation (Table 9. 3) .
Cardiovascular sytem
Hear rate
Pulse qual ity
Appearance of mucous membranes
Examination of the abdomen
Abdomi nal distention
Auscultation
External palpation
Rectal examination
Abdominal paracentesis
State of peripheral perfsion and hydration
Capillary refill time
PCV
TPP
FACTORS WHICH MIGHT INDICATE A
NEED FOR REFERRAL
The decision to refer the horse affected by acute colic is
frequently made as a result of a combination of factors
rather than one single observation. Some of these
factors are listed in Table 9.4.
Severe unrelenting pai n
Absence of response to anal gesics
Rapid recurrence of pai n following admi nistration
of analgesics
Persistently elevated hear rate (especially over
b bpm)
Progressively rising heart rate
Positive rectal findings
Large quantities or persistence of gastric reflux
Persistently reduced or absent borborygmi
Serosangui nous peritoneal fl ui d with i ncreased total
protei n and nucleated cel l count
Exudative peritoneal fl ui d i ndicating peritonitis
Progressive cardiovascul ar deterioration with ri si ng
PCV (> 55%), TPP, i njected or cyanotic mucous
membranes, and prolonged capi llary refill ti me
(> sec)
Progressive abdomi nal distention
Profuse watery di arrhea
Recurrent bouts of colic over a period of days or
weeks, especi al ly if the frequency of bouts or
severity are i ncreasing
Chronic colic persisti ng > 4 hours where no
di agnosiS has been reached
Colic - decisions for surgery
EM Gaughan and PD Van Harreveld
INTRODUCTION
Although the decision for general anesthesia and surgi
cal treatment of horses with colic should not be made
lightly, early surgical intervention often results in the
best outcome. Although the vast majorit of horses with
signs of colic do not require surgical therapy, when
signs do suggest the need for surger, performing it
early in the course of the disease leads to greater suc
cess. This may also imply that some horses may have sur
gical exploration performed when more conservative
care may have allowed survival. However, surgery may
reduce the morbidity of some colic cases and return
horses to normal in a more satisfactory fashion.
Therefore, straightforard, timely decisions, based
most often on physical examination fndings generally
provide the greatest success rate for horses with colic.
In deciding the need for surgery in an individual
horse there is no single criterion that can be relied on.
Many horses with acute abdominal pain will require
repeated reassessments over a period of time before a
decision to perform surgery is reached. A change in one
or more clinical parameters may determine the need
for surgical or medical therapy. In other cases a deci
sion can be made at a single examination. Careful con
sideration of the horse's pain, response to analgesic
therapy, cardiovascular status, rectal examination find
ings, amount of gastric reflux, and abdominocentesis
are necessary in determining the need for exploratory
surgery. Some of the more important indications for
performing exploratory laparotomy (celiotomy) in
horses with acute abdominal pain are
severe, unrelenting abdominal pain
pain that is refractory to analgesics or that shows
only temporary improvement with analgesics
persistently elevated heart rate
large quantities of gastric reflux
absence of borborygmi
abnormalities on rectal examination
serosanguinous abdominal fluid with increased
total protein and total nucleated cell count
progressive abdominal distention that is becoming
life threatening.
See also Table 9. 5.
PHYSICAL EXAMINATION
Many horses with colic have physical examination fnd
ings which directly indicate that surgical treatment is
required for survival. A thorough physical examination
may be the most important aspect of the management
of horses with colic, and it can certainly lead to appro
priate and timely decisions for medical care and
surgery. Components of the physical examination that
are useful in assessing the need for surgery are
heart rate
respiratory rate
rectal temperature
degree of pain
rectal examination
nasogastric intubation.
Hear rate, respiratory rate, and rectal
temperature
Determination of vital signs should be completed for
every horse with colic. Respiratory rate may be the least
useful vital sign in assessing colic but the character of
breathing may be supportive in the final assessment.
Body temperature determination can be very important
in the cascade of decision making. Fever should be just
cause to re-examine a decision for surgery. A fever can
!2
9 COLIC
Diagnostic examination Signs that suggest surgical
exloration
Signs tat sugges furher
monitoring and medical
management
Temperatur Normal El evated
Hear rate Elevated Normal
Abdominal pain Severe unrelenting Mi ld
Recal examination Multiple disended loops of small intestine
Tight tenia and haustra of the large colon
Thickened edematous i ntestinal wall
Nasogastric Intubation Reflux greater than T liter and pH >
Appearance of abominal fluid Opaque and dark to orange or brown/green Clear yellow color
be an indication that inflammation or sepsis may be the
cause of the colic pain, and that surgical manipulation
may not appropriately address the primary lesion.
However, some febrile horses can have abdominal pain
severe enough to warrant surgical intervention.
A horse' s heart rate is the vital parameter that can
provide the most insight into current systemic status
and prognosis for surival. A sustained, elevated heart
rate can indicate deterioration in the cardiovascular sta
tus related to progression of the gastrointestinal tract
disease, and the requirement for emergency surgical
treatment. In general, a heart rate which has risen to
60-70 bpm within 6 hours of the onset of colic gives rise
for concern, particularly if it remains high during quiet
interludes and in the face of adequate analgesia.
Degree and nature of pain
Pain is likely to be the most consistent indication for
surgical treatment of horses with colic. Horses with
severe, unrelenting colic that is unresponsive to anal
gesics usually require emergency surgical management.
If pain is readily modifed and managed with analgesic
medications or physical manipulation, surgery may not
be imminently necessary. Episodic, moderate to severe
abdominal pain usually indicates the need for aggres
sive treatment and often surgery. Recurrent or chronic
pain, in the face of appropriate conservative manage
ment and additional diagnostic findings quite often
indicates that surgery will be required to reach a suc
cessful outcome.
Rectal examination
Abnormalities in intestinal location, texture, and con
tent that are palpable per rectum can also provide
!
distinct indications for surgery. Small intestinal disten
tion which is palpable on rectal examination and is pre
sent without fever usually requires emergency surgery.
The magnitude of distention and tympany should be
assessed, for multiple loops of small intestine and very
tight tenia and haustra of the large colon usually indi
cate that surgical treatment will be necessary. Intestine
which has a thickened or edematous texture on rectal
examination may justif surgical exploration of the
abdomen. Heavy, non-indentable intestine, believed to
be filled with impacted ingesta may also be an indica
tion for surgery when conservative treatment fails. If the
impacted ingesta is in the cecum, early surgical inter
vention should be strongly considered.
Passage of a nasogastric tube can be a diagnostic aid as
well as therapeutic in the evaluation and treatment of
horses with colic. Because of the normal function of the
cardiac sphincter, horses do not vomit and spontaneous
reflux of small amounts of gastrointestinal contents has
been associated with a grave prognosis. A nasogastric
tube should be passed very early in the course of the
evaluation of any horse with severe unrelenting colic
pain. This procedure should probably be a part of the
total baseline examination of any horse with colic.
Placing a nasogastric tube into the gastric lumen can
reveal the magnitude and nature of fluid and ingesta
sequestered or refluxed into the stomach. The pres
ence of a substantial volume (> I liter) of easily obtain
able gastric reflux and fluid with an increased pH (> 5)
have been associated with the potential need for surgi
cal treatment. Reflux as a single abnormal finding does
not necessarily indicate a need for surgery. The results
of passing a nasogastric tube should be interpreted in
combination with the systemic physical examination,
including body temperature and rectal examination.
Horses with proximal enteritis can have ver large vol
umes of basic fluid reflux from the stomach via a naso
gastric tube. Horses with proximal enteritis, however,
are frequently febrile and the colic pain associated with
the disease is often palliated with decompression of the
stomach through a nasogastric tube. With this response,
surgery may not be essential. Pain again becomes the
determining factor, in combination with nasogastric
reflux, whether or not surgery is required to treat
affected horses.
EVALUATION OF PERITONEAL FLUID
Results of peritoneal fluid evaluation can lend evidence
that surgery may be indicated for horses with colic. The
results of abdominocentesis may not be as essential in
decision making when a horse is located at the surgical
venue, as it may be when decisions are being made for
referral to the surgical site. Most physical examination
fndings override a requirement for abdominocentesis.
However, peritoneal fluid can be readily and safely har
vested, and some quick information can be determined
without extensive laboratory evaluation (see Chapter
2) . When the normally clear yellow color of peritoneal
fluid changes to opaque and dark, to orange or
brown/green, then substantial compromise of bowel
integrity is likely and the decision for referral for
surgery is well grounded or arguably too late. The total
protein content of peritoneal fluid can be readily
obtained from a refractometer and elevations in pro
tein can also support decisions for surgery. However, a
total protein content of less than 2.5 g/ dl (25 gil) does
not always mean that vascular compromise is absent.
Brown/green fluid with particulate matter present can
indicate that the intestine has ruptured. It must also be
recalled that an inadvertent tap of the bowel lumen
can confuse the diagnostic picture and, therefore,
abdominocentesis results should continue to be inter
preted in close conjunction with the physical examina
tion fndings.
ULTRASONOGRAPHY
Ultrasonographic examination of the abdomen per rec
tum and from a ventral, percutaneous approach can
provide additional information that may lead to a deci
sion for surgery (see Chapter 2) . The percutaneous
examination is especially helpful for foals with colic,
and can be helpful in the assessment of adults as well.
Volumes of peritoneal fluid and some indication of its
nature can be determined with ultrasonography. Small
intestine, when distended, can be examined in cases
that are not suitable for rectal palpation, and therefore,
earlier decisions for surgery may be appropriately
made. Motility patterns and texture of bowel may also
be assessed with careful ultrasound examination.
Thickened intestinal wall, occasionally with gas patterns
in the submucosa, and protracted ileus can also support
decisions for surgery. Specifc diagnoses are not
commonly determined with ultrasound, but some are
possible. Left dorsal displacement of the large colon
(nephrosplenic entrapment) can be diagnosed by ultra
sonographic examination from a percutaneous site at
the dorsal aspect of the left side of the abdomen and
surgery may be necessary if other management tech
niques fail. Occasionally, intra-abdominal masses can
be detected by ultrasound examination from an exter
nal or rectal approach, and when associated with colic
signs, surgery may be indicated. Intussusceptions in
foals can often be diagnosed by ultrasound examina
tion.
RESPONSE TO MEDICAL THERAPY
Another indication that a horse may require surgical
treatment is when appropriate medical or conservative
therapy has failed to resolve colic signs. Surgery may be
necessary with recurrent pain, especially if it is severe.
Low grade pain can also become an indicator of surgi
cal need when typical management with analgesic med
ication and physical manipulation do not succeed in an
acceptable time course. Repetitive and frequent admin
istration of non-steroidal anti-inflammatory drugs can
be problematic, in that a confused and inappropriate
assessment of colic signs can be made and time lost
when surgery may be required. The high dose of flu
nixin meglumine ( 1 .0 mg/kg) is best administered at
1 2 hour intervals. More frequent administration is not
indicated and can only serve to delay more appropriate,
aggressive treatment. At times, failure of conservative
management to improve the conditions found on rectal
examination can also be an indication for surgery. This
is most common when managing large intestinal
impactions. Some large colon impactions and many
cecal impactions require surgical decompression
because of continued mild colic signs and a lack of
improvement in the original status of the affected intes
tine.
The concept of recurrent signs and possible failure
to respond as expected to conservative management
techniques is also historically important. Surger may
be an earlier consideration in case management if a
! 1
9 COLIC
chronic course is already known at the frst examina
tion. This is also an important time to review previous
medication with clients. All physical examination and
ancillary diagnostic findings must be interpreted in
light of current and previous medications.
CLINICAL PATHOLOGY
Occasionally, laboratory tests can lead decision making
toward surgery. Laboratory results alone are rarely the
sole indications for surgery. Complete blood count
(CBC) , electrolyte, and blood gas determinations are
solid support for physical examination indications for
surgery. elevated white blood cell count may support
a diagnosis of an intra-abdominal abscess and a need
for surgery. Elevation in hematocrit, anion gap, and
deterioration from normal electrolyte and blood gas
profles are consistent with cardiovascular compromise
resulting from the progression of an intestinal lesion
that requires surgical treatment. Laboratory data may
also be a helpful diagnostic tool in the rare case of colic
not caused by intestinal disease, for example liver
disease.
CONCLUSIONS
Many factors must be considered when making the
decision to perform surgery. Sometimes surgical explo
ration of the abdomen is necessary before a diagnosis
can be made. Most pre-surgical diagnoses are not defin
itive of a precise lesion but suggest which anatomic
aspect of the intestines is involved. At times the source
of colic pain is not apparent and surgical exploration is
indicated for diagnostic and potentially therapeutic
purposes. This approach should not be undertaken
lightly but should be considered in a timely manner as
case management progresses. Timely, as early initiation
of surgical treatment is a major factor in the successful
outcome for horses that need surgery.
Preparation of the horse for
referral transport
M 6 W MWGWW ? `
A Worster
INTRODUCTION
The objective of preparing a referral patient is to
improve or stabilize the hemodynamic status of the
12
patient and reduce morbidity during transport. Early
aggressive treatment aims to
stabilize hypovolemia
provide adequate analgesia
counteract endotoxemia
provide gastric decompression.
Because of sweating, decreased water intake, increased
intestinal secretions, and decreased intestinal absorp
tion, hypovolemia can be signifcant in both large colon
and small intestinal disorders. A large colon can pool
up to 40 liters of fluid with additional loss of sodium
and protein through the compromised mucosal wall.
Small intestinal ileus, obstruction, and anterior enteritis
create pooling of fluids in the intestinal tract and reflux
in the stomach. Hypovolemia from third-space fluid loss
is exacerbated with intestinal strangulation or volvulus.
Endotoxemia from compromised bowel causes further
hypovolemia by maldistribution of blood and an
increase in endothelial permeability.
MANAGEMENT OF HYPOVOLEMIA
A large gauge catheter should be placed for intravenous
administration of fluids and medications. A 10- to 1 4-
gauge catheter should be used in an adult horse, while
smaller foals may require a 1 6- or I S-gauge catheter.
The catheter length used should be greater than S.5 cm
(3.5 in) for a foal and 14 cm (5.5 in) for an adult. The
jugular vein is the most common site for aseptic
catheter placement. The catheters should be as non
thrombogenic as possible. Catheter materials ranked
according to their decreasing reactivity are polypropy
lene, Teflon, silicon, rubber, nylon, polyvinykhloride,
and polyurethane. The more commonly used 14 cm
(5. 5 in) , 14-gauge catheters are made of Teflon or
polyurethane and tend to cycle at the insertion site.
Teflon is a short-term catheter material and should be
replaced after 2-3 days of use. The polyurethane
catheter is less reactive and may maintain functionality
without morbidity for 1 0-21 days. Therefore, a
polyurethane, central venous catheter (20 cm/S.O in,
16-gauge, e.g. Mila International, Inc, Erlanger, K is
often used as a long-term catheter. This over-the-wire
catheter is more flexible and less prone to cycling at the
insertion site. The central venous catheter also has a
one-way intralumenal valve, that prevents blood loss or
air embolism if the fluid administration set becomes dis
connected during transport. Wrapping the catheter site
prior to transportation helps prevent inadvertent
removal.
Isotonic fluids such as lactated Ringer's solution or
plasmalyte are appropriate to replace a defcit within
CLI NI CAL EVALUATION OF THE COLIC CASE 9
oweight Litr dficit Clinical signs
defcit (%) (SO .kg hor)
N|l0 >1
Moderate -1
Severe >T
the interstitial spaces. To estimate replacement volume
of fluids needed, use
per cent dehydration ? body weight (kg) = liters of fluid
(see Fluid and electrolyte therapy and acid-base bal
ance in horses with abdominal pain) . Therefore, a
500 kg horse that is 5% dehydrated would require
25 liters of fluid to become normovolemic (see Table
9.6) . Isotonic fluids expand the interstitial space but do
not maintain the vascular volume; so with ongoing
endotoxemia and hypovolemic shock, hypertonic solu
tions or colloids may be more appropriate for pro
longed transport. These solutions may be followed with
isotonic fluids during transport, provided the horse's
degree of pain and movement is adequately controlled.
Hypertonic saline 7. 5% ( 1 -4 ml/kg) may be admin
istered to maintain vascular volume for up to 60 min
utes. Hypertonic saline will draw fluid from the
interstitial and intracellular space and should be fol
lowed by isotonic fluids within 1-2 hours. Hypertonic
saline may be combined with dextrans to prolong the
effect. Synthetic colloids also help maintain the intravas
cular volume (dextrans for 2-6 hours or hetastarch for
up to 24 hours) . Plasma administration should be con
sidered in cases of hypoproteinemia 4.0 g/dl) or sep
sis. Plasma is the most physiologic fluid and may help
maintain intravascular oncotic pressure for 2-3 days.
Plasma has anti-endotoxin effects as well as macro
globulins, antithrombin III, and fibronectin.
MANAGEMENT OF PAIN
Adequate analgesics are critical to control the patient
during transport. This is especially important if a horse
is transported while receiving intravenous fluids; it is
important to have it confned and adequately con
trolled. Adequate analgesics, such as alpha2 adrenergic
agonists and anti-inflammatory drugs, are important for
mediation of pain. Alpha
2
adrenergic agonists have been
shown to have the most immediate and potent effect on
gastrointestinal pain. Xylazine (0. 2-l . 0 mg/kg) has a
3J Decreased skin turgor
~ Sunken eyes, depression
>b Cold extremities, recumbency
profound analgesic efect for 1 5-30 minutes and deto
midine (0. 006-0.02 mg/kg) for 30-60 minutes. When
there is mild visceral pain, a prolonged analgesic effect
may be apparent for up to 4 hours. Xylazine and deto
midine worsen hypotension and decrease gastrointesti
nal motility. Although xylazine has a shorter duration of
action, its use is preferable since it has less pronounced
hypotensive effects and decreased gastrointestinal
motility compared to detomidine. Butorphanol
(0. 01-0.02 mg/kg) may potentiate the analgesic effects
of the alpha
2
agonists for up to 4 hours. Therefore,
xylazine in combination with butorphanol is commonly
administered intramuscularly for a prolonged effect.
Flunixin meglumine ( 1 . 1 mg/kg) is commonly used
for visceral pain and is a potent anti-inflammatory drug
which acts by inhibiting the cyclooxygenase pathway.
Flunixin has a 2-hour delayed onset and duration of
action of 1 2-24 hours. Gastrointestinal ulceration and
masking of surgical colic are potential risks when multi
ple flunixin doses are given.
MANAGEMENT OF ENDOTOXEMIA
AND HEMODYNAMIC DISTURBANCES
A low dose of flunixin (0.25-0.5 mg/kg) is benefcial in
endotoxemic shock because it inhibits prostaglandin-I
mediated vasodilation and minimizes hypotension.
Ketoprofen ( 1 . 1 mg/kg) inhibits both the cyclooxygenase
and lipooxygenase pathways. It is less ulcerogenic but also
has decreased analgesic properties compared to flunixin.
Other drugs frequently used to decrease endotoxin
include polymyxin B (6000 IU/kg i.v.) , antiserum
( Salmonella typhimurum) 1 . 5 ml/kg i.v., dimethylsulf
oxide (DMSO) 0. 5-1. 0 g/kg i.v. b. i. d. , and pentoxi
flline (8. 5 mg/kg p. o. b. i.d. ) . Both polymyxin B and
hyperimmune antiserum bind lipid A, the core
lipopolysaccharide of circulating endotoxin. Polymyxin
B has been shown to decrease the effects of endotoxin
in foals. Conversely, the use ofhyperimmune antiserum
in one study increased endotoxic effects in foals. DMSO
is an oxygen-free radical scavenger and may be useful in
preventing damage from cell membrane peroxidation
!
9 COLIC
that can accompany en do toxemia. Interestingly,
numerous studies have shown no benefit in intestinal
reperfusion injury with DMSO administration.
Pentoxiflline decreases tumor necrosis factor and
interleukin-5 release by macrophages, decreases throm
boxane _ release by platelets, increases red blood cell
deformability, and causes vasodilation. The decreased
thrombin formation and vasodilation may be beneficial
for treatment of laminitis as well as endotoxemia. The
hemodynamic effects may make pentoxiflline use
more appropriate in postoperative colic or after stabi
lizing hypotension in medical cases.
GASTROINTESTINAL PREPARATION
Nasogastric intubation with a large diameter ( 1 . 5 cm or
5/8 in) tube is essential in horses with small intestine
Igufe 9. T5 Nasogastric i ntubation. The nasogastric tube
should be secured to the hal ter pri or to transportation
! 4
disease. Nasogastric intubation is recommended for
horses being transported for over 3 hours, a heart rate
more than 50 bpm, or signs of progressive small intes
tine disease. Although nasogastric intubation has not
been proven to prevent gastric rupture, the high
esophageal sphincter tone in horses can cause signif
cant gastric distention from small intestinal disease.
The nasogastric tube should be secured to the halter
(Figure 9. 13) and the distal limbs should be wrapped
prior to transport.
CONCLUSION
Early referral and aggressive treatment are particularly
important for any condition involving strangulated
bowel that can become irreversibly compromised
within 5 hours. A good preoperative physical status is
directly correlated to an improved prognosis following
surgery. The recent increase in long-term survival rates
in small intestine disease from 50-80 per cent may be
attributed to earlier referral and better patient stabiliza
tion techniques. Early, aggressive medical therapy with
referral has helped decrease the morbidity and mortal
ity of colicky horses.
I ntravenous catheterization
and complications
T Divers
INTRODUCTION
Intravenous catheter placement is performed in virtu
ally all horses and foals that are hospitalized for any
gastrointestinal disorder. Intravenous catheterization is
performed in a smaller percentage of horses treated on
the farm. There are many things to consider when plac
ing or evaluating an intravenous catheter in the horse
how long the catheter will be needed
cost
ease of placement
type of medication to be administered
volume and rate of administration
venous access.
Once the catheter is placed, questions that arise include
when to replace it
whether or not to bandage
the frequency of heparinization
signs of complications.
Signs of complications and management of the
catheter is particularly relevant since the horse with gas
trointestinal problems has the greatest complication
rate of any critical care equine.
CATHETER TYPES
There are three basic types of catheters in general use
1 . over-the-needle
2. through-the-needle
3. over-the-wire ( Seldinger) .
Most intravenous catheters that are commercially avail
able are made of either Teflon or polyurethane. Silastic
or silicone catheters are infrequently used by equine
practitioners and are not readily available. With the
widespread availability of long polyurethane over-the
wire catheters, there is currently very little indication
for silastic catheters.
Teflon over-the-needl catheters
These are less expensive and easier to place than
polyurethane over-the-needle or over-the-wire catheters
and through-the-needle catheters. Therefore, Teflon
catheters are frequently used when
intravenous catheterization time is expected to be 2
days or less
speed of catheter placement is critical ( e. g. in cases
of severe abdominal pain, septic shock, etc.)
placement of the catheter is expected to be difcult
because of either restraint problems or difculty in
visualizing the vein
help is minimal.
Teflon catheters are generally stiffer and more throm
bogenic than polyurethane catheters. Because of their
stiffness they are also at greater risk of kinking at the
skin-vein junction than softer catheters. Their stifness
may also cause increased movement at the skin-vein
junction resulting in a seemingly greater incidence of
cellulitis at this site in comparison to over-the-wire
polyurethane catheters. On very rare occasions, a
Teflon catheter may break off at the kink site. Another
disadvantage of Teflon over-the-needle catheters is that
if there is repeated manipulation of the needle within
the catheter during a difcult placement, fraying of the
catheter tip may occur enhancing thrombogenecity.
Polyurethane catheters
Polyurethane catheters can be purchased as over-the
needle or over-the-wire types. Polyurethane over-the
needle catheters are more expensive than Tefon
over-the-needle catheters but are less thrombogenic
and can be left in place for longer. Polyurethane over
the-needle catheters are indicated when
the time of catheterization is expected to be more
than 2 days
the medical condition, for example sepsis and/or
protein-losing enteropathy, make the horse more
prone to thrombosis
adequate help is not present to place an over-the
wire catheter.
Polyurethane over-the-wire catheters
These are the most commonly used catheters for
horses and foals in intensive care. The over-the-wire
polyurethane catheters are longer and more flexible
than over-the-needle polyurethane or Teflon catheters
and are, therefore, more likely to float in the middle of
the vein, have less contact with the vessel wall and are,
therefore, less thrombogenic. In neonatal foals, the
catheter tip is generally in the anterior vena cava or the
right heart which further decreases any chance of
thrombosis. If the catheter is found by X-ray (all com
mercial catheters are radio-opaque) to be in the right
ventricle, it should be backed out to prevent damage to
the ventricular wall. The catheter tip may reside in the
anterior vena cava in some adult horses if placed low in
the neck and may, therefore, be used to measure cen
tral venous pressure. The over-the-wire polyurethane
catheters have the following disadvantages
more than one person may be needed to place the
catheter
flow rate is generally a maximum of 3-4 liters/hour
increased expense.
Additionally these catheters are available as single,
double, or multi-lumen catheters. The multi-lumen
catheters are especially useful for critical care foals
receiving parenteral nutrition, antibiotics, crystal
loids/ colloids, and other medications. Some
polyurethane catheters have silver sulfadiazine and/or
chlorhexidine impregnated into the catheter material
which reduces catheter-related infections. Although the
initial investment is an added expense, these catheters
are often left in place for several days to several weeks.
Like all catheters, they may occasionally become
occluded or displaced by horses rolling in the stall or
the recovery room, excessive rubbing at the catheter, or
by the mare chewing on the foal' s catheter.
Polyurethane through-the-needle catheters
These catheters are also available in different lengths.
These are excellent catheters but some veterinarians
find the peel-of-needle more awkward than the over
the-wire method.
! b
9 COLIC
In the great majority of horses and foals catheters are
placed down the jugular vein. The upper middle cervi
cal area is most often selected and the area clipped and
scrubbed. A local anesthetic is used in many foals and
also in a few 'needle shy' horses prior to needle place
ment. If an over-the-needle catheter is used, the
catheter should be flled with heparinized saline prior
to jugular puncture. The over-the-wire method is
demonstrated in Figures 9. 14, 9. 15, and 9. 16. After
Figure 9. T4The l-wire is pushed through the adaptor and
needl e i nto the l umen of the jugul ar vein
Figure 9.T5The polyurethane catheter i s fed over the wire
into the jugul ar vein
! b
placement of the catheter, a short extension set is
attached to the catheter and a cap placed at the end.
The catheter and extension set are then sutured (occa
sionally glued) to the skin. The catheters are generally
left unwrapped for most adult horses, but foals may
require wrapping as they are more prone to scratch the
catheter with their hind feet or the mare may chew at
the catheter. On rare occasions it may be necessary to
place the catheter in a vein other than the jugular vein.
Cellulitis of the neck, unilateral or bilateral j ugular vein
thrombosis ( partial or complete) , and severe head
edema, are some of the reasons for choosing another
site. The cephalic and lateral thoracic veins are alterna
tive sites. Over-the-wire catheters have remained func
tional in these sites for at least 3 weeks. If a venous site
cannot be located in a foal, i ntra-osseous fluids should
be considered.
CATHETER REPLACEMENT
There is no set time that a catheter must be replaced.
Teflon catheters are generally replaced every 2-3 days.
Polyurethane over-the-needle catheters may be left in
for several more days if there is no local swelling or pain
and there is no evidence of developing occlusion as
determined by resistance to medication flow. Using the
same criteria, over-the-wire catheters are commonly left
in place for 1-2 months if needed.
Figure 9. TbThe catheter placement is complete and the
wire i s withdrawn. The catheter hub and the attached
extension can now be sutured to the ski n
COMPLICATIONS
Complications are common in horses with gastrointesti
nal disorders for a number of reasons
colicky signs such as rolling increase the chance of
the catheter kinking and contamination at the
skin-vein junction
rapid placement in an emergency situation
increases the chance of contamination
rapid intravenous fluid flow rates as required for
many horses with abdominal pain or diarrhea
increase turbulence at the tip of the catheter and
further damage the endothelial wall increasing the
chance of thrombosis.
Additionally, horses with sepsis resulting from ischemic
or inflammatory bowel disease have excessive stimula
tion of procoagulants, and horses with protein-losing
enteropathy have loss of anticoagulant.
The to most common complications are thrombo
sis and phlebitis/cellulitis. Thrombosis may be either
septic or aseptic. If the thrombi form initially at the
catheter tip, it is most commonly aseptic thrombosis,
although if the patient has been bacteremic, septic
thrombi may form at this site. If the thrombus begins at
the catheter-skin junction, cellulitis is often present
and the thrombosis is most commonly septic. Fever and
moderate to severe pain on palpation are generally pre
sent with septic thrombi. Ultrasound examination
(7 MHz linear probe) will allow visualization of the
thrombus and help determine that an abscess is pre
sent. Severe head edema may occur from jugular
thrombosis if the opposite vein is abnormal and/or the
patient keeps its head abnormally low for a prolonged
time. Nasal edema may be so severe that a tracheostomy
must be performed.
Another complication is physical kinking of the
catheter preventing flow. If this occurs the catheter
should be replaced and not simply repositioned. On a
rare occasion the catheter may break into the vein. If
the broken catheter can be trapped in the jugular vein
it should be surgically removed. If the broken catheter
passes into the lung, as determined by radiographs, it
should be left alone where, based upon a limited num
ber of cases, it does not appear to cause a problem. If
the catheter is lodged in the heart it must be removed.
TREATMENT OF THROMBOPHLEBITIS
If a thrombus forms at the tip of the catheter the
catheter should be removed, a sonogram performed on
the vein, and the horse monitored for signs of sepsis. If
there is evidence that the thrombus might be infected,
fever, extreme pain on palpation, or thrombus forming
in a septic patient, the catheter tip should be cultured
and the patient treated with antibiotics. Initial anti
microbial therapy might be a combination of intra
venously administered penicillin and aminoglycoside,
or a third generation cephalosporin if a catheter can be
placed in another vein. If oral antimicrobials are
needed, enrofloxacin would provide good coverage
against gram-negative organisms which are most com
mon with catheter-tip septic thrombosis. Antimicrobials
should be continued until the vein is not painful on pal
pation, the sonogram shows a solid thrombus, and the
neutrophil count 'has returned to normal. In a rare
refractory case, the vein might need to be surgically
removed.
If cellulitis is noted at the skin-vein junction the
catheter should be removed immediately and any
serum or exudate present at the opening should be
carefully aspirated and cultured ( aerobically and anaer
obically) . The most common organisms at this site are
Staphylococcus spp. Antimicrobial therapy, trimetho
prim-sulfonamides, enrofloxacin, cefazolin or ceftiofur,
or a combination of penicillin and aminoglycoside
should begin immediately. The skin opening might
need to be nicked slightly to help guarantee outward
drainage. The area should be hot-packed frequently
and ichthammol may be applied to the area. If the cel
lulitis has caused only a partial occlusion of the vein,
aggressive therapy might allow the vein to return to
normal. If the vein is not entirely thrombosed and the
gatrointestinal tract is functional, anti-platelet therapy
(aspirin 0. 25 g/kg p.o. every other day) should be
administered.
CATHETER MANAGEMENT
The site of catheter placement should be kept as clean
and dr as possible. The area is better visualized if it is
not bandaged, but in foals and adult horses that are fre
quently recumbent, bandaging is preferred. Immediate
flushing of any irritating medication, for example
phenylbutazone, should be performed with either
isotonic crystalloids or heparinized saline. If no fluids
are being administered, heparinized saline should be
administered after each intravenous medication and at
least tice daily. Ideally, the catheter should not be used
for blood collection, although this is often not practical
in some foals. If the catheter has become occluded for
whatever reason, or accidentally disconnected from the
fluids such that blood backs up into the line, replace
ment of the catheter should be considered based upon
economics, potential degree of contamination, and
availability of other veins.
1J
9 COLIC
Fluid and electrolyte
therapy and acid-base
balance in horses with
abdominal pain (Figure 9. 1 7)
N M
T Di vers
EXPECTED ABNORMALITIES
Horses with abdominal pain may have a variety of fluid,
electrolyte, and acid-base disturbances. In milder cases
of abdominal pain there are usually minimal fluid and
electrolyte abnormalities, including an occasional
mildly diminished serum calcium concentration. In
more severe disorders, interstitial and intravascular vol
ume is depleted as fluid accumulates in an obstructed
bowel. Serum sodium and chloride usually remain nor
mal since the accumulating intralumenal fluid is nearly
isotonic. Serum chloride may be abnormally low if there
has been profuse sweating and/or gastric reflux. If
endotoxemia develops, additional fluids are lost from
the intravascular compartment because neutrophil and
platelet margination on capillary membranes causes
' leaky membranes' . Endotoxin also stimulates cytokine
production and arachidonic acid metabolism which can
decrease cardiac output and vascular tone, and cause
'maldistribution' of blood, further diminishing blood
pressure and perfusion to organs. Either localized
bowel ischemia and/or a more general perfusion
abnormality result in enhanced anaerobic metabolism
and generation of lactic acid causing a decrease in
plasma bicarbonate and a corresponding increase in
the anion gap. Dehydration and/or diminished perfu
sion of the kidneys results in azotemia. If there is
enhanced portal absorption of endotoxin, sorbitol
dehydrogenase is frequently elevated.
Fluid losses are further aggravated by lack of oral
intake which should be between 30-60 ml kg-I day-I .
Although the initial loss in body fluid is extracellular
fluid, considerable intracellular fluid may be lost with
more prolonged abdominal pain and lack of fluid
intake. This may be particularly true for impaction colic
of several days' duration. Because of the movement in
intracellular fluid, the packed cell volume and protein
may be relatively normal in spite of severe dehydration,
and hypertonic saline would be a poor choice of fluid
therapy. Sweating causes loss of chloride, potassium,
and calcium, and may result in the loss of considerable
amounts of body fluids and electrolytes. Alkalosis with
an increased anion gap (mixed alkalosis, acidosis) may
be present if severe sweating has caused hypochloremia.
! d
Although serum sodium and chloride are generally nor
mal and calcium low in the great majority of horses with
abdominal pain, potassium is more variable. It may be
low if there is prolonged anorexia or high if there
is pronounced azotemia. Total body potassium can
become severely depleted because of anorexia and con
tinuing urinary losses. Intravenously administered
fluids are likely to cause further urinary loss of potas
sium, even when potassium is added to the fluids.
Magnesium may be abnormally high and clinically
important if a dehydrated horse has been given
magnesium sulfate per os.
estimate of the liters of fluid to be given in order
to correct dehydration can be made by estimating per
cent dehydration and multiplying this by the body
weight in kilograms. The percentage of dehydration is
best determined by the change in body weight but this
is often not possible. Clinical and laboratory fndings
that help estimate per cent dehydration include
dryness of mucus membranes
speed of distention of the occluded jugular veins
skin turgor
elevations in blood urea nitrogen and creatinine
packed cell volume
plasma protein concentration
urine specifc gravity.
A 1 gil increase in plasma protein suggests a 7-8 per
cent loss in extracellular fluid.
THERAPY - INTRAVENOUSLY
ADMINISTERED LUIDS
======= = .. -.
The basic goals of fluid therapy in horses with abdomi
nal pain are to
restore intravascular volume
promote tissue perfusion
initiate urination
help correct electrolyte and acid-base disturbances
without promoting tissue edema.
The most important aspect of fluid therapy in horses
with strangulating lesions of the intestine is to quickly
increase intravascular volume such that cardiac output
and perfusion pressures are normalized. In many cases
a 2- ml/kg bolus of hypertonic saline is the initial
treatment of choice. This is the safest and most rapid
method of increasing perfusion pressure without pro
moting tissue edema. Hypertonic saline also promotes
diuresis and lowers pulmonary hypertension caused by
prostanoid or neutrophil-released mediators. It must be
followed by appropriate amounts of isotonic fluids
(generally a commercial polyionic crystalloid contain-
U
U
MOagammbydra1m
andbasppmaim+
MOagammbyma1mO
mviouspmsionamIi1ies
2~mllg Hyperonic saline followed
by polyionic crystalloid B1 mllglhr
/ I
Estimate dehydration and replace
deficitover -12hours; provide for
maintenance and additional losses
No urine produced within 1 hr Adequate urine produced
I
/ Horse
deteriorates
Check CVP , F, Protein and PCV remain
protein, jugular within normal range, blood /
distention and recal pressure returns to normal, Protein drops belownormal,
exam, ultrasound or peripheral pulses normalize, PCV remains high which
catheterize bladder to heart rate decreases, color suggests leaky membranes,
determine (urine and CRT of membranes protein-losing enteropathy
production) improved
I
CVP high CVP normal or
andor
evidence of
overhydration
and ittle or
no urine
Stop IVfluids
Treat for
oliguric renal
failure
lowand no
signs of
overhydration
Continue with
polyionic
crystalloids 1
mllkglhr and
add colloids
Continue with
polyionic crystalloids
A1 mllglhr
depending upon
losses and physical
parameters, blood
pressure and lab
findings

Urine produced
or peritonitis; perfusion
pressure low, increased
anion gap, persistently high
heart rate
Add colloids (plasma
and/or Hetastarch),
continue crystalloids,
reassess need for surgery
PCV, protein,
hearrate,
perfusion normal
Continues at T.b x
maintenance (0-:20
mllkglday) and
additional losses
Figure 9.T JGui de for intravenous fl ui d therapy i n horses with abdomi nal pai n
tmpCOC
Administer 8-12
mllghr of polyionic
crystalloid until plasma
protein is maintained
between ..b g1dl.
Continue fluids to
maintain protein in that
range until impaction is
relieved
Magammbyma1m
emion @W H
/
Reflux present No reflux
Give bx bV(kg) = L
of polyionic crstalloid
plus losses equal to
reflux over -: 2hrs
Reassess
I
Give b A bV(kg) = L
of polyionic crystalloid
over -12hours if
desirable -oral fluids
may be used here
* decreased skin turgor, dry mucous
membranes
+slowCRT, cold extremities, discolored mucous
membranes, high hear rate
m
C
2

l
O

t
L

o
2
C
^
O
m
C
l

O
U
9 COLIC
ing sodium, chloride, potassium, and calcium with
acetate) . Hypertonic saline should not be used in
horses with more chronic dehydration.
Crystalloids should be administered at 410 ml kg-I
h-I until the patient is stabilized and estimated dehydra
tion is one and one-half times corrected. Maintenance
fluids should be 40-100 ml kg-I day-I plus additional
fluids to compensate for excessive loss from gastric
reflux. Calcium borogluconate (22 mg/kg) can be
added as needed to the crystalloid fluid in order to
maintain ionized calcium within the normal range
(> 1 . 4 mmol/l) . Maintaining ionized calcium within the
normal range may help promote normal intestinal
motility and cardiac function. It should be used cau
tiously or not at all if cardiac arrhythmias are present
and if reperfusion injury of ischemic bowel is a possibil
ity. Additional potassium ( 20-40 mEq KCI/l) may be
required in horses that have normal renal function and
are experiencing a pronounced diuresis from the
crystalloid therapy. Potassium should not be used in
Quarter horses believed to be positive for the HYPP
gene. Sodium bicarbonate is rarely indicated in horses
experiencing abdominal pain. The acidosis that is pre
sent is virtually always a high anion gap/lactic acidosis
which should be corrected by improving perfusion and
oxygenation and by surgical repair of devitalized bowel.
Colloid therapy is synergistic with crystalloid therapy
in promoting the goals of fluid therapy. Without ade
quate oncotic pressure, crystalloids quickly move from
the intravascular space and may cause tissue edema
and/ or unnecessary loss of fluids in the urine. This loss
of intravascular fluid may be particularly pronounced
if the horse is experiencing systemic inflammatory
response and has ' leaky membranes' . In horses with
strangulating intestinal lesions, plasma protein should
be maintained at 50 gil (5. 0 g/dl) or greater to have
maximal effect of the intravenously administered fluids
without promoting tissue edema. Equine plasma is the
ideal fluid for those horses since it has crystalloid prop
erties, colloid properties, and contains many additional
proteins that can have anti-inflammatory and anti
thrombotic properties. Hydroxyethyl starch is an excel
lent synthetic colloid that can be administered to horses
in addition to isotonic or hypertonic crystalloids.
Colloid oncotic pressure changes with either plasma,
hydroxyethyl starch, or concentrated albumin can be
measured with a colloid osmometer (Wescor Co.,
Logan, UT) .
exception for maintaining oncotic pressure
would be in the use of intravenous fluids for treating
impactions of the large intestine. In this case, crystal
loids should be given at a fast rate, 8 ml kg-I h ` without
colloids such that plasma protein decreases to
4.5 g/ dl. The increase in hydrostatic pressure and
14
drop in oncotic pressure should cause movement of the
fluids into transcellular fluid sites, i. e. intestinal lumen,
such that the impaction is softened. This can generally
be done without harm to other body organs assuming
there is no generalized capillary disorder, and cardiac,
renal, and respiratory function are normal. When large
amounts of fluids are given to horses, the fluids should
ideally be warmed to near body temperature prior to
administration.
Some horses with abdominal pain may need only
oral fluids, or oral fluids in addition to intravenously
administered fluids. Horses with large bowel impac
tions often beneft from orally administered fluids. If
there is no abnormal gastric reflux 1 g/kg magnesium
sulfate mixed in 8 ml/kg of warm water should be given
via nasogastric tube. The magnesium sulfate may cause
an almost immediate reflex secretion of fluid into the
large intestine. The magnesium sulfate should not be
administered more than twice daily in order to avoid
hypermagnesemia. If the horse tolerates the initial oral
fluids, up to 8 1/450 kg of either isotonic or slightly
hypertonic fluids may be given every 4 hours to an adult
horse. Granular sodium chloride, potassium chloride,
or sodium bicarbonate may be added to water if elec
trolytes are desirable. Tonicity can be determined by
remembering that
1 g of sodium chloride equals 1 7 mEq or 34 mmol
1 g of potassium chloride equals 1 4 mEq or
28 mmol
1 g of sodium bicarbonate equals 1 2 mEq or
24 mmol.
Oral fluids are ideally administered via gravity flow
rather than by pump. On rare occasions, gravit admin
istration of isotonic fluids may be given per rectum.
This would only be indicated for horses with colonic
impactions when oral fluids can not be given and eco
nomic considerations prevent administration of intra
venous fluids.
Preoperative preparation
P Rakestraw
INTRODUCTION
One of the most important components of preoperative
patient preparation is correction of fluid, acid-base,
and electrolyte abnormalities to improve the patient's
cardiovascular status prior to induction of general
anesthesia (see Fluid and electrolyte therapy and
acid-base balance in horses with abdominal pain) .
Another important area to attend to is pain manage
ment. Most horses referred for colic have already been
treated with varying amounts of analgesics such as
xylazine, detomidine, romifdine, and butorphanol.
Depending on how severe the pain is at the time of
admission, these drugs are likely to be given in the
immediate preoperative period. Most of these drugs
have certain undesirable side effects such as brady
cardia seen with xylazine, detomidine, or romifidine
administration, and respiratory depression seen with
butorphanol administration. Consequently it is impor
tant that these drugs be used only when necessary, and
that their use in the preoperative period is recorded for
the information of the anesthesia personnel. Flunixin
meglumine, in addition to its analgesic properties,
should be given prior to surgery to abate the adverse
effects of endotoxemia.
PRE-OPERATIVE THERAPIES
Thirty minutes prior to induction of anesthesia, the
author routinely initiates broad spectrum antibiotic
therapy such as aqueous penicillin G (22 000 IV/kg Lv.
q. i. d. ) and gentamicin (6.6 mg/kg i.v. s.i. d. ) . We have
not seen any detrimental effects using the once daily
dose of gentamicin as long as the horse is well hydrated.
Antibiotics are discontinued 24 hours after surgery in
most cases that do not require intestinal resection.
Horses with severe large colon distention may have
compromised venous return and excessive respiratory
excursions. In these cases, when rectal examination
indicates a gas-distended large colon adjacent to the
body wall, percutaneous decompression can be per
formed by placing a 1 4gauge catheter through the
flank (after sterile preparation and local anesthesia)
and into the colon.
Prognosis for acute
abdominal pain
P Rakestraw
Because of the significant economic and emotional
strains placed on the owner when their horse is treated
for acute abdominal pain, it is important that the vet
erinarian supplies them with as accurate a prognosis as
possible for the animal's survival. In certain instances
this is difcult to do without surgical exploration.
However, numerous studies have attempted to identif
specifc preoperative prognostic indicators to deter
mine the probability of short term survival in horses
with acute abdominal crisis. Some of the factors that
can be helpful in predicting the prognosis are
heart rate
capillary refill time
packed cell volume
total plasma protein
blood lactate.
Many of these factors are indirectly related to the
degree of intestinal ischemia which leads to cardio
vascular compromise. In several studies heart rate has
been found to be a valuable prognostic indicator. In
one study horses with heart rates of 40, 80, 1 00, and
1 20 bpm had survival probabilities of 0.90, 0.50, 0.25,
and 0.10 respectively. Capillary refill time above 4 sec
onds has been associated with a poor prognosis in sev
eral studies. Packed cell volumes (pe) of 56 per cent,
60 per cent, 64 per cent, and 68 per cent were associ
ated with survival rates of 0.46, 0.44, 0.44, and 0.23
respectively. Horses with both an elevated pe and
hypoproteinemia (Total protein 50 gil or 5 g/dl)
have a poorer prognosis than those with a similarly ele
vated pe and normal serum protein. Blood lactate
levels, a measure of peripheral tissue hypoperfusion, in
the range of 0-75, 761 00, and greater than 1 01 mg/dl
were associated with 0.93, 0.33, and 0.25 survival proba
bilities respectively.
Other laboratory parameters that have been used as
prognostic indicators include
systolic blood pressure
blood urea nitrogen
white blood cell and protein concentration in
peritoneal fluid
activity of antithrombin III in blood and peritoneal
fluid
fibrinolytic activity in blood and peritoneal fluid
procoagulant activit in blood.
In most cases use of these single variables, or multi
variate predictive models based on several of these
variables have limited value in improving the clinician' s
abilit to predict the outcome over clinical experience,
which takes into account both the above variables as
well as variables unique to the individual case.
Another strategy to predict outcome is to base the
prognosis on the outcome of horses with similar lesions.
Retrospective studies have been performed to evaluate
outcome for the majority of different types of acute
abdominal crises. In reviewing these, the clinician
should realize that cases in retrospective studies have
been collected over a series of years, and consequently
changes in surgical and medical treatment, and/or
141
L00lio ellsslftlo of f08W suv1 ( ) ...
STOMACH Ulcers and associated obstrucions I nsuficient data
SMALL INTESTINE (non-ileal) Strangulating and non-strangulating i nfrction
SMALL INESTINE (non-ileal) Simple obstrucion
SMALL INTESTINE (ileum) Strangulating and non-strangulatlng i nfarction bJ
SMALL INTESTINE (ileum) Simple obstrucion ~
CECUM Strangulating and non-strangLlating i nfarcion b
CECUM Simple obstruction ~
LARGE COLON Strangulating or non-strangulating i nfarcion ~
LRGE COLON Simple obstruction
LARGE COLON Agenesis or atresia poor
SMALL COLON Non-strangulating or non-i nfarcting b
SMALL COLON Simple obstrucion 1
SMALL COLON Agenesisatresia poor
PERITONEUM Septic Inflammation b
"The information in this tble is given as a guideline only, many other risk factors such as status of cardiovascular disease, exent of
lesion, degree of peritoneal contamination, and experience of the surgeon and anesthetist, mus also be considered
"" Long term survival rate can mestimated at 5\%less than shor term survival
changes in the timing of referral and surgical decisions
may have improved the prognosis of similar cases at the
current time. For example, one frequently quoted study
determined that only 49 per cent of horses with
strangulating small intestinal lesions were discharged.
However, in a more recent study, 87 per cent of horses
with strangulating small intestinal lesions were dis
charged. The prognosis for horses with strangulating
lesions of the large colon varies dramatically depending
on the degree of intestinal compromise as well as how
much of the large intestine is involved, i.e. can the large
colon be resected back to healthy bowel? Most horses
with non-strangulating lesions such as impaction colic
that has failed to respond to medical treatment, or large
colon displacement, have a ver good prognosis with
surgical interention. The expected short term survival
rates for horses with surgical lesions affecting different
parts of the intestinal tract are shown in Table 9. 7.
In general, the prognosis for horses with acute
abdominal pain has improved signifcantly over the last
20 years. In a recent surey of equine veterinary special
ists, delays in initiating surgery are believed to be the
! 42
most common cause of surgical failure. Increases in the
survival rates of horses undergoing colic surgery are
thought to result from early recognition and referral of
these cases by the primary care veterinarians. The
timely identifcation of these cases occurs through judi
cious use of analgesics and increased awareness of signs
indicating that the horse needs to be referred for more
intensive care. It is also critical that the referral center
makes the appropriate decision whether to treat a horse
medically or to intervene surgically.
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abdomen. In The Equine Acute Abdomen. Lea and Febiger,
Philadelphia pp 102-142
Colic - decisions for surgery
Mueller P fand Moore] N ( 1998) . Gastrointestinal
emergencies and other causes of colic. In Manual ofEquine
Emergencies Eds. ] A Orsini and T] Divers. W B Saunders,
Philadelphia pp 156164
preoperative management, and surgical approaches. In
Equine Surgery. 2nd Edition. Eds. ] A Auer and] A Stick.
W B Saunders, Philadelphia, pp 224-232
White N A ( 1990) . Examination and diagnosis of the acute
abdomen. In: The Equine Acute Abdomen Ed. N A White.
Lea and Febiger, Philadelphia pp 102-142
Preparation of the horse for referral
transpor
Arden W A, Siocombe R F, Stick] A, et al. ( 1990)
Morphologic and ultrastructural evaluation of effect of
ischemia and dimethyl sulfoxide on equine jejunum. Am.
]. Vet. Rs. 51 : 1 784.
Durando M M, MacKay R], Linda S, et al. ( 1994) Effects of
polymyxin B and Salmonella tphimurium antiserum on
horses given endotoxin intravenously. Am.]. Vet. Res.
55:921.
Freeman D E ( 1 997) Surgery of the small intestine. Surgical
management of colic. Vet. Clin. ^ Am. 299.
Geor R], Weiss D], Burris S M ( 1 992) Effects of furosemide
and pentoxiflline on blood flow properties in horses. Am.
]. Vet. Res. 53:2043,.
Hardy], Rakestraw P ( 1999) Postoperative care and
complications associated with abdominal surgery: In, Auer
]A, Stick]A: Equine Surgery, 2nd edition. W B Saunders,
Philadelphia, 294-305.
MacAllister C G, Morgan S], Borne A T, et al. ( 1993)
Comparison of adverse effects of phenylbutazone, flunixin
meglumine, and ketoprofen in horses. ]. Am. Vet. Med.
Assoc. 202: 71 .
Mathews KA ( 1 998) The various types of parental fluids and
their indications. Advances in fluid and electrolyte
therapy. Vet. Clin. Âm. 28:483-513.
Moon P F, Snyder] R, Haskins S C, et al. ( 1991 ) Effects of
! 4d
9 COLIC
highly concentrated hypertonic saline-dextran volume
expander on cardiopulmonary function in anesthetized
normovolemic horses. Am. J Vet. Res. 52: 161 1-18.
Moore R, Muir W, Bertone A, et al. ( 1995) Effect of dimethyl
sulfoxide, allopurinol, 21-aminosteroid U74006F, and
manganese chloride on large colon ischemia-reperfusion
injury in horses. Am. J Vet. Res. 56:671.
Orsinij A, Kreuder K. ( 1998) Intravenous catheter
placement: In Orsini j A, Divers T J: Manual ofEquine
Emergencies. Philadelphia, W B Saunders, 1 2-15.
Orsinij A, Kreuder K ( 1 998) Nasogastric tube placement: In,
Orsini jA, Divers TJ: Manual ofEquine Emergencies.
Philadelphia, W B Saunders, 53-5.
Reeves Mj, Vansteenhousej, Stashak T S, et aL ( 1990) Failure
to demonstrate reperfusion injury following ischemia of
the equine large colon using dimethyl sulfoxide. Equine
Vet.J 22: 126.
Semrad SD, Hardee GE, Hardee MM, et aL Low dose flunixin
meglumine: Effects on eicosanoid production and clinical
signs induced by experimental en do toxemia in horses.
Equine Vet. J 19: 201, 1987.
Spier Sj, Snyder j R, Murray MJ. ( 1996) Fluid and electrolyte
therapy for gastrointestinal disorders. In Lare Animal
Inteal Medicine. 2nd edition, B P Smith (ed. ) . Mosby, St
Louis, MO, pp. 775-83.
Van Hoogmoed L V, Snyder j R ( 1997) Acunctive methods
in equine gastrointestinal surger. Surgical management
of colic. Vet. Clin. NAm. 231-234.
Intravenous catheterization and
complications
Bregenzer T, Conen D, Sakmann P, Widmer A F ( 1998) Is
routine replacement of peripheral intravenous catheters
necessary? Arch. Inte. Med. 158: 1 51-4.
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Gardner S Y, Reef V B, Spencer P A ( 1991 ) Ultrasonographic
evaluation of horses with thrombophlebitis of the jugular
vein: +cases ( 1985-1988) . J Am. Vet. Med. Assoc. 199:370-3.
Prognosis for acute abdominal pain
Freeman D E ( 1 997) Surgery of the small intestine. In Vet.
Clin. A. Am. Equine Pact. Surgical Management ofColic. W B
Saunders, Philadelphia, 1 3:299.
Furr M f, Lessard P, White N A ( 1 995) Development of a
colic severity score for predicting the outcome of equine
colic. Vet. Surg. 24:97-101 .
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after small intestinal resection and anastomosis in horses.
Vet. Surg. 18: 415-423.
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of blood lactate levels in equine colic. Equine Vet. J
8:49-54.
Orsini j A, Elser A H, Galligan D T, et al. ( 1 988) Prognostic
index for acute abdominal crisis (colic) in horses. Am. J
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Parry B W, Anderson G A, Gay C C ( 1 983) Prognosis in
equine colic: A study of individual variables used in case
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Pascoe P j, Ducharme N G, Ducharme G R, et al. ( 1 990) A
computer-derived protocol using recursive partitioning to
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Pelosoj G, Cohen N D, Taylor T S, et al. ( 1 996) When to send
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Proc. Am. Assoc. Equine Pac. 42:250-3.
10
Surgery for colic (including anesthesia)
Anesthesia for colic surgery
K LCCU
Many gastrointestinal lesions in horses cause colic that
requires laparotomy for defnitive diagnosis and treat
ment. The ventral midline approach is favored for most
laparotomies because it permits direct observation and
exteriorization of the majority of the intestine; this
approach necessitates general anesthesia in dorsal
recumbency. Flank laparotomy, because it allows much
more limited access to the abdomen, is rarely indicated
but may be carried out either in lateral recumbency
under general anesthesia or standing with local anes
thesia. Because standing flank laparotomy is rarely per
formed, local anesthesia will not be discussed in this
chapter.
Some patients with signs of colic have surgical
lesions that cause minimal interference with other body
systems, for example horses with chronic intermittent
colic. Most horses with lesions requiring emergency
laparotomy have a range of ongoing, serious pathologi
cal processes that interfere with anesthesia and substan
tially increase the risks associated with anesthesia. Safe
anesthesia of horses with colic is one of the greatest
challenges in veterinary anesthetic practice.
Convention suggests that patients be stabilized prior
to induction of anesthesia. Many horses with colic have
pathology that is proceeding so rapidly that permanent
injury is imminent and it is difcult, or impossible, for
stabilizing measures to keep up with the rate of deterio
ration in the cardiovascular, pulmonary, and metabolic
systems. Occasionally, intractable pain may necessitate
induction of general anesthesia on an emergency basis
before the horse's behavioral response to abdominal
pain endangers both horse and handlers. Rapidly pro
ceeding pathology and intractable pain often conspire
to reduce the time available for stabilizing the patient
and preparing facilities for anesthesia. This inevitably
increases the risks associated with anesthesia of patients
with colic. Centers that perform colic surgery should be
organized so that patients can be processed and anes
thetized as efciently as possible.
THE PULMONARY SYSTEM IN HORSES
WITH COLIC
Distention of abdominal contents is a common conse
quence of colic. This distention impedes movement of
the diaphragm and decreases chest wall compliance. It
also pushes the resting (end-expiratory) position of the
diaphragm cranially, this may stretch the muscle fibers
of the diaphragm so that they are operating beyond the
optimal length for myofbril contraction. The end
result is that the work of breathing is increased and the
diaphragm becomes more susceptible to fatigue.
The cranial displacement of the diaphragm also
tends to reduce the functional residual capacity (FRC)
of the lung, i. e. the volume of gas left in the lung at the
end of tidal expiration is reduced. The latter process
increases the number of airways that are collapsed and
encourages alveolar collapse. In turn, alveolar collapse
increases venous admixture, the passage of blood
through the lungs without oxygenation, and, hence
reduces arterial oxygen content.
Endotoxins absorbed from the intestine during colic
damage pulmonary vascular endothelium. This, in
turn, may initiate loss of integrity of the pulmonary
145
10 COLIC
vascular endothelium, accumulation of water in the
pulmonary interstitium, and thus inhibit diffusive gas
exchange.
The conscious horse compensates for these prob
lems by increasing ventilatory drive and redistributing
pulmonary perfusion away from collapsed lung tissue.
Unfortunately adoption of dorsal recumbency exacer
bates most of the pathophysiological processes men
tioned above and most anesthetic drugs reduce, or
obtund completely, the efcacy of the compensatory
mechanisms. The net effect is that hypercapnea and
hypoxia are common in horses anesthetized for colic
surgery. Equipment for augmenting inspired oxygen
and controlling ventilation is necessary for safe anesthe
sia of most patients undergoing colic surgery. Centers
undertaking surgery on patients for the relief of colic
should have an anesthetic machine designed for horses
and equipped with a circle rebreathing system and a
mechanical ventilator. Such a machine should have
5 cm diameter hoses
a large carbon dioxide absorber
the ability to deliver a tidal volume of 20 liters ten
times per minute
the ability to generate a peak inspiratory pressure of
40 cmH
2
0.
THE CARDIOVASCULAR SYSTEM IN
HORSES WITH COLIC
Distention of the abdomen in horses with colic may be
sufcient to reduce venous return and hence reduce
cardiac output. Even simple intestinal obstruction,
unaccompanied by strangulation or thromboembolism,
induces secretion of a large volume of fluid into the
lumen of the gut. If ischemia is present in the intestine
then disruption of the intestinal mucous membrane
exacerbates this accumulation of intralumenal fluid
and also permit release of endotoxins into the peri
toneum. These endotoxins attach to macrophages
that are responsible for release of proinflammatory
cytokines, mobilizing arachidonic acid and, hence, the
production of vasoactive substances such as throm
boxane and prostacyclin. Thromboxane causes vaso
constrIctIOn that occurs early in endotoxemia.
Vasoconstriction is soon superseded by persistent
vasodilation mediated by prostacyclin. The net result of
these processes is reduced total blood volume, pooling
of blood, and reduced perfusion pressure. The con
scious horse may compensate for these processes by
increasing heart rate and vasoconstriction of non-essen
tial vascular beds. Nevertheless, if the pathological
processes persist, reduced perfusion leads to an
146
increase in anaerobic metabolism, lactic acidosis, and
the classic signs of shock.
The cardiovascular compensatory mechanisms men
tioned above tend to be attenuated by most of the drugs
used in anesthetic practice, hence animals with cardio
vascular impairment before anesthesia are likely to
need intensive cardiovascular support during anesthe
sia. Intraoperative events such as
change in posture of the patient during hoisting to
and from the operating table or
release of incarcerated ischemic bowel ( e.g.
internal hernia)
often produce hypotension and hypoperfusion because
the cardiovascular system is unable to compensate for
these sudden challenges.
PREPARATION OF THE PATIENT
Ideally, preparation of the patient for anesthesia should
involve a thorough physical examination. This may
involve all organ systems but should focus on assessing
the degree of pulmonary and cardiovascular impair
ment. Cardiac rhythm should be ascertained prior to
induction of anesthesia; the presence of atrial fbrilla
tion increases the likelihood of intraoperative hypo
perfusion. Laboratory tests on venous blood should
include
hematocrit
total plasma protein
base defcit of the extracellular fluid
anion gap
serum concentrations of sodium, potassium, and
ionized calcium.
A large bore catheter 14 gauge) should be placed in
a jugular vein so that intravenous fluids may be given
rapidly either by gravity or with a pump. In animals with
known fluid defcits, it is appropriate to place more
than one catheter to speed volume replacement.
Correcting pre-anesthetic volume and metabolic
and electrolyte abnormalities takes time. The extent to
which this is practical, or worthwhile, in the face of
ongoing disease processes and/or intractable pain,
requires the exercise of clinical judgment. Horses with
colic often need to be anesthetized with cardio
pulmonary and metabolic disruptions that are only
partially corrected or sometimes not corrected at all.
A distended stomach may rupture when the patient
goes to ground during induction of anesthesia.
Therefore, in all horses with colic, a nasogastric tube
should be placed prior to induction of anesthesia and
left in place until the end of anesthesia. This permits
decompression of the stomach and allows removal of
gastric fluid during surgery.
A mentioned above, damage to intestinal mucous
membrane releases endotoxins that initiate the produc
tion of vasoactive arachidonic acid metabolites such as
thromboxane and prostacyclin. These can be inhibited
by non-steroidal anti-inflammatory drugs ( NSAIDs) . A
appropriate NSAID (e.g. flunixin meglumine 1 .0 mg/
kg Lv.) should be given as soon as damage to the intesti
nal mucous membrane is suspected.
Both sodium or potassium penicillin and potenti
ated sulfonamides cause cardiovascular depression that
may become important during anesthesia. Whenever
possible they should be given well in advance (> 30
min) of anesthesia. Drugs less likely to produce
hypotension should be chosen if practical.
Analgesia and chemical restraint of the horse with
colic is usually accomplished with drugs that act at
alpha
2
adrenoceptors, Le. xylazine, detomidine, or
romifidine. Occasionally, these drugs are augmented by
opioid agonists such as butorphanol or meperidine.
The adverse side effects of these drugs are considerable
(see below) , nevertheless they are usually outweighed
by the necessit for pain relief and chemical restraint.
Immediately before induction of anesthesia the
mouth should be washed out with water from a 0. 5 liter
dose syringe. This prevents food material being carried
into the trachea during orotracheal intubation.
INDUCTION OF ANESTHESIA
Induction of anesthesia should be accomplished with a
technique that puts the horse into recumbency gently
to minimize the possibility of rupture of distended
bowel. The walls and floor of the induction area should
be padded with a durable, washable surface, that is also
non-skid. It is usual to restrain both head and tail with
ropes or to use an induction gate/false wall or purpose
built induction table with belly-bands. Immediately
after induction, an oro tracheal tube should be inserted
through a gag held between the incisors. Mechanically
controlled ventilation should be started promptly with
an oxygen-enriched mixture. The ventilator should be
set initially to deliver a tidal volume of 10-15 ml/kg at a
rate of 6-10 breaths per minute. The volume in the
accessory cuff of the oro tracheal tube should be
acusted to just prevent escape of tidal gas during inspi
ration.
The horse should then be placed on the operating
table where a system for supporting the horse, with even
distribution of its weight, is crucial to avoid compressive
muscle ischemia. Foam pads or mattresses flled with
air or water are used for this purpose. In dorsal recum-
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 1 0
bency the head should be supported in a slightly flexed
position to optimize nasal venous drainage.
BRIEF REVIEW OF THE DRUGS USED IN
ANESTHESIA
The impaired pulmonary, cardiovascular, and meta
bolic status of many patients with colic influences the
pharmacokinetics and pharmacodynamics of anesthetic
drugs. In general the conditions that cause surgical colic
also decrease the volume of distribution of injectable
drugs and increase the fraction of those drugs that are
in 'active' form. A a result most injectable anesthetic
drugs can be expected to have increased potency and
duration in these patients, although high sympathetic
tone may transiently counteract these processes early in
the course of an anesthetic. Decreased cardiac output
will also cause the depth of anesthesia to increase more
rapidly when inspired anesthetic concentration is
increased, hence changes in the depth of anesthesia of
a hypovolemic patient should be monitored carefully
during inhaled anesthesia.
Alpha2 adrenoceptor agonists
The dose-dependent sedation and analgesia that alpha
2
adrenoceptor agonists produce has made them an
important part of the management of horses with colic.
Most horses that are presented for surgery at a sec
ondary or tertiary care facility have already received one
or more doses of an alpha
2
adrenoceptor agonist. The
ubiquitous use of these drugs in horses with colic
should not be allowed to distract from their adverse
side effects. Intravenous administration of alpha
2
-
adrenoreceptor agonists causes transient vasoconstric
tion and an increase in blood pressure, but bradycardia,
often accompanied by second degree heart block,
ensues; cardiac output may be reduced to half its
normal value when conventional doses are used. This
hypoperfusion is usually characterized by prolonged
hypotension. Through muscle relaxation of upper air
way musculature, the resistance of the upper airways is
increased and this increases the work of breathing.
Arterial oxygen tension decreases a little in response to
these drugs. Intestinal motility is reduced for several
hours after these drugs are given. Inadvertent overdose
with an alpha
2
adrenoceptor agonist can be reversed
with an antagonist such as yohimbine (0. 05 mg/kg i.v.)
or tolazoline ( 2-4 mg/kg i.v. ) .
When used as an adjunct to ketamine, the cardio
vascular side effects of xylazine are attenuated to some
extent by the sympathetic effects of ketamine. The dose
of xylazine used as an adjunct to ketamine is minimized
147
10 COLIC
by the addition of diazepam and/ or butorphanol to the
technique (Table 10. 1 ) . Dosing with alpha
2
adrenocep
tor agonists to control pain before surgery can substan
tially reduce the dose necessary during induction of
anesthesia.
Protocol 1
Premedication
xyl azi ne 0.4 mg/kg Lv.
butorphanol 0.02 mg/kg Lv.
I nduction
diazepam 0.1 mg/kg Lv.
ketami ne 2.2 mg/kg
Protocol 2
Premedication
xylazine 0.4 mg/kg Lv.
butorphanol 0.02 mg/kg Lv.
Induction
1 l iter 5% guaifenesin 2000 mg ketami ne gi ven
to effect
Acepromazine
Acepromazine is an unreliable tranquilizer in horses
experiencing colic pain. It antagonizes alpha) adreno
ceptors and tends to produce systemic vasodilation and
hypotension. In animals with high sympathetic tone, for
example animals in pain, the inhibition of alpha) recep
tors tends to prevent the vasoconstriction that ordinar
ily occurs in the skin and splanchnic vascular beds with
endogenous catecholamines; it has little effect, how
ever, on the beta receptor mediated vasodilation seen
in the muscle with endogenous catecholamines. The
net result is amplifcation of acepromazine's hypoten
sive effects in patients that are excited or in pain.
Acepromazine can also produce permanent para
phimosis or priapism that may disable a stallion. All of
these effects severely limit the use of acepromazine in
patients with colic.
Benzodiazepines
Diazepam and midazolam are classifed as sedatives,
however when they are given as sole agents to horses
they tend to produce ataxia but little obvious sedation.
They are often used as adjuncts to ketamine when their
muscle relaxing properties aid induction of anesthesia
and orotracheal intubation. Although they have mini
mal sedative properties, they reduce the dose require-
148
ment for other drugs that may have serious adverse side
effects, for example xylazine.
Opioids
Although some opioids tend to produce excitement in
horses when given alone, butorphanol, pentazocine,
meperidine, and morphine can all be given without
causing excitement. Butorphanol is probably the most
widely used opioid in horses and seems to act primarily
on kappa receptors. It provides good visceral analgesia
after 0.02 mg/kg i.v.
Ketamine
Ketamine is a dissociative anesthetic agent that is often
used to induce anesthesia in horses with colic. Although
its direct effect on the cardiovascular system is depres
sant, this property is counteracted by a general increase
in sympathetic tone, so that its net effect is fairly neu
tral. When used alone, it produces a poor quality of
induction of anesthesia, characterized by a short period
of ataxia and hypersensitivity. When given after an
alpha
2
adrenoceptor agonist it produces a much
smoother induction. The quality ofinduction with keta
mine is also improved by using other adjunct drugs
such as guaifenesin or diazepam (Table 1 0. 1 ) .
Guaifenesin (glyceryl guaiacolate ether, GG)
Guaifenesin (GG) is neither analgesic nor anesthetic, it
acts on interneurons in the spinal cord to produce mus
cle relaxation. GG facilitates a smooth induction with
ketamine or thiopental and allows the dose of these
drugs to be reduced. It is usually administered as a 5%
solution in water or 5% dextrose. Concentrations of
1 0% or greater have been associated with phlebitis and
cause necrosis if inadvertently injected perivascularly.
The principal disadvantage of using 5% GG is that a
large volume must be infused over a short period
(0. 5-1. 0 liters in 2-4 minutes for most horses) . This is
difcult to accomplish if the drug is being given by
gravity through a 1 0 drop/ml infusion set and 1 4-gauge
catheter, however a pressure infusor may be used to
squeeze the bag of GG and expedite the process.
Thiopental or ketamine can be mixed with the GG or
may be given as a bolus when the GG starts to make the
horse sway (Table 1 0. 1 ) . Guaifenesin alone has minimal
effects on the cardiovascular or respiratory systems and
those effects that are seen are probably caused by the
effects of recumbency rather than the drug itself.
Thiopental
Thiopental is an ultrashort-acting barbiturate that
induces recumbency very soon after intravenous
administration. It causes profound cardiovascular
depression and transient apnea even when GG or other
adjunct medications reduce the dose. The cardio
depressant properties of thiopental make it much less
popular than ketamine for induction of anesthesia in
patient with colic.
Propofol
Propofol is used for induction of anesthesia in humans,
dogs, and cats. The dose required for induction of anes
thesia in horses is very large and expensive even when it
is given with GG to reduce the dose. The quality of
induction of anesthesia is quite variable. Since it
appears to confer no important advantages over con
ventional methods of inducing anesthesia, it is unlikely
that propofol will fnd favor for anesthetizing horses
with colic.
Telazol
Telazol is a proprietary combination of tiletamine,
a dissociative anesthetic, and zolazepam, a benzodi
azepine. It has been used to induce anesthesia in horses
premedicated with xylazine or detomidine. Its effects
last longer than those of conventional xylazine-keta
mine combinations and, hence, may give more time
aft er induction of anesthesia for inhaled anesthetics to
reach therapeutic levels. Use of tiletamine-zolazepam
(1. 0 mg kg-I of the combination, IV) in horses with colic
is yet to be evaluated objectively, however this combina
tion may fnd a place in anesthetic practice.
Inhaled anesthetics
Modern inhaled anesthetics are potent and usually
administered with oxygen as the carrier gas. Breathing
an oxygen-enriched gas mixture probably confers a
significant safet margin for patients with impaired gas
exchange and perfusion that are undergoing pro
longed anesthesia. Because inhaled anesthetics do not
depend on metabolism for their elimination, it is rela
tively easy to titrate the dose (inhaled concentration) to
accommodate changing surgical needs and physiologi
cal status.
Halothane and isoflurane are the most commonly
used inhaled anesthetics in horses. Although isoflurane
is somewhat less potent than halothane (Table 10. 2) , its
low solubility in blood makes it easier to acjust depth of
anesthesia with isoflurane than with halothane. In the
ory, this should also lead to faster recovery from anes
thesia with isoflurane; in practice the time taken to
stand is quite similar, however the quality of recovery is
usually better after isoflurane. Isoflurane may cause
more depression of ventilation than halothane,
SURGERY FOR COLIC (I NCLUDI NG ANESTHESI A) 10
although this is a mute disadvantage in patients that are
mechanically ventilated. Both anesthetics reduce
cardiac output and systemic arterial blood pressure,
however, at equivalent doses cardiac output is likely to
be greater with isoflurane than with halothane suggest
ing better tissue perfusion with isoflurane. The latter
attribute, along with easier control of anesthetic depth,
suggests that isoflurane is a better choice of anesthetic
for horses where the cardiovascular system is challenged
and unstable, as is often the case in horses with colic.
Infusion of 40 g kg-I min-I of ketamine can be used
to reduce the inspired concentration of halothane or
isoflurane by approximately 25 per cent, this amelio
rates the cardiovascular depression caused by anes
thetic doses of these drugs. The latter technique,
although useful, is not without risk in patients with
altered pharmacokinetics and pharmacodynamics. It is
recommended that anesthetic depth is monitored care
fully and that the infusion be stopped as soon as the
most intense surgical stimulation is over so that the dis
sociative effects of ketamine have dissipated before the
horse starts to recover from anesthesia.
Sevoflurane is a relatively new addition to the veteri
nary armamentarium; its blood solubility is even lower
that that of isoflurane, and hence depth of anesthesia
can be increased or decreased rapidly with sevoflurane.
The cardiodepressant effects of sevoflurane are
probably quite similar to those of isoflurane, however
horses recover more quickly and usually more smoothly
from anesthesia after sevoflurane. Although experience
with sevoflurane in horses is still accumulating, it
appears that the better quality of recovery after sevoflu
rane is more noticeable after prolonged (> 2 h) anes
thetics, often the case with colic surgery. Sevoflurane is,
as yet, substantially more expensive than the other
inhaled agents in the US. Whether or not the extra cost
is worthwhile is a matter of debate.
Desflurane is an even newer inhaled anesthetic. It is
less potent than the aforementioned inhaled agent,
requires a vaporizer that is heated, and has the potential
to permit even more rapid changes in depth of anes
thesia and recovery. At present, its cost will probably pre
clude its general use in veterinary medicine. Desflurane
has yet to be widely evaluated in horses with colic.
Hal othane
Isoflurane
Sevoflurane
Desfl urane

0.9
1. 3
2.3
8.0
149
10 COLIC
Nitrous oxide is much less potent than any of the
inhaled drugs mentioned above. It is used in many non
human species to enable the dose of other agents to be
reduced. Unfortunately, the volume of nitrous oxide
required in inspired gas (50%) reduces the inspired
oxygen fraction below that considered prudent in anes
thetized horses. Nitrous oxide also tends to accumulate
in gas spaces, including the intestine where it may
exacerbate the ileus already present in many horses
with colic. Nitrous oxide has no place in anesthetizing
horses with colic.
Neuromuscular blockade
Neuromuscular blockade may be used to reduce the dose
of inhaled agents that is necessary to produce muscle
relaxation. In horses, the most commonly used of
these agents is atracurium. The usual initial dose is
0.1 mg kg-I Lv., subsequent doses are half of the initial
dose and are given when neuromuscular transmission
stars to reappear. Assessment of the extent of neuromus
cular blockade is best accomplished with a peripheral
nerve stimulator, applied so that it causes contraction of
muscles served by the peroneal nerve or facial nerve. The
latter is more accessible in horses undergoing colic
surgery. Non-depolarizing muscle relaxants such
atracurium should always be reversed (0. 5 mg kg-I
edrophonium i.v. slowly) before recovery from anesthesia
in case persistent neuromuscular block causes weakness
that delays recovery. Because neuromuscular-blocking
agents have no effects in the central nerous system, ade
quate depth of anesthesia should always be ensured while
they are being used. The depolarizing neuromuscular
blocker, succinyl choline, has been used in horses to expe
dite induction of anesthesia, but it has no place in the
anesthesia of horses for colic surgery because it may cause
hyperkalemia and decrease blood pressure.
Parasympatholytics
Drugs such as atropine and glycopyrrolate decrease gas
trointestinal motility for several hours and may exacer
bate the postoperative ileus that is a component of
many colics. When used in conjunction with dopamine
or dobutamine, atropine and glycopyrrolate can cause
dangerous tachydysrhythmias. These drugs should be
used with great caution in patients with surgical colic.
MONITORING PATIENTS DURING
ANESTHESIA
Depth of anesthesia
Anesthetic requirement varies with changing levels of
surgical stimulation, duration of anesthesia, and
150
changing physiological status of the patient, among
other things. In order to avoid relative overdose of anes
thetic drugs in horses with colic, it is essential to moni
tor depth of anesthesia carefully because anesthetic
requirement may be much less than that extrapolated
from healthy animals and may vary considerably during
anesthesia.
A sluggish palpebral reflex is a sign of a light plane
of anesthesia that is usually just suitable for exploratory
laparotomy. Rotation of the eyeball, causing a small
amount of sclera to be visible, is likewise associated with
a surgical plane of anesthesia with inhaled anesthetics.
In very deep anesthesia the eyeball is central.
Occasional, slow nystagmus may also be seen in a light
surgical anesthetic plane, however this is sometimes
confused with variable small oscillations of the eye that
are seen in very deep anesthesia.
The precise dose of an inhaled anesthetic can be
measured using an anesthetic vapor analyzer that sam
ples gas from the endotracheal tube. At the end of expi
ration, the concentration in this location is known as
the end-tidal concentration and approximates the con
centration in the alveolar gas and hence the 'dose' of
the inhaled agent being given. In healthy animals
undergoing surgery, the end-tidal concentration of
most potent anesthetics should be 1 . 2-1 . 6 MC, where
MC is the minimum alveolar concentration of the
anesthetic drug (see Table 1 0. 2) that produces a lack of
response to surgical stimulation in 50 per cent of
patients. Unfortunately, the anesthetic requirement of
patients undergoing surgery for colic may be quite dif
ferent ( usually less) than that of healthy patients and
may change during the course of anesthesia, hence the
use of a monitor of end-tidal anesthetic concentration
does not relieve the clinician of responsibility for con
tinuously monitoring the depth of anesthesia.
Cardiovascular function
Palpation of the pulse and obseration of the color of
the mucous membranes are important but insensitive
monitoring tools. The electrocardiogram is probably
the most commonly applied monitor because it is easy
to apply and allows detection of cardiac dysrhythmias,
however it gives little quantitative information about
pump function of the heart.
The mean systemic blood pressure is a sensitive indi
cator of cardiovascular function. Under inhaled anes
thesia, systemic hypotension is generally a characteristic
of low perfusion. Systemic blood pressure can be mea
sured indirectly by a cuff device, encircling the tail or a
limb, that is inflated with air to a pressure exceeding the
systolic pressure, and hence sufcient to prevent flow
past the cuff. The cuf is then slowly deflated; the cuff
pressure at which intermittent flow is first detected
approximates systolic pressure and the cuff pressure at
which flow becomes continuous approximates diastolic
pressure. The method of detecting flow distal to the
cufI'may be based on phase shift of ultrasound (the
Doppler method) or on pressure oscillations in the air
cuff ( the oscillometric method) . Although reasonably
reliable for measuring blood pressure in healthy horses,
these indirect methods often fail when blood pressure is
low or during peripheral vasoconstriction, therefore
they are of limited value in anesthetizing patients that
are undergoing surgery for relief of colic.
Systemic blood pressure is best measured directly
with a calibrated pressure transducer attached to
catheter in a peripheral artery, via a saline-flled, low
volume, low compliance tube. In horses in dorsal
recumbency, the transducer is usually zeroed at the
level of the shoulder joint, this approximates the right
atrial level. After sterile skin preparation, a 20-gauge
catheter is inserted into the facial arter, transverse
facial artery, or the great metatarsal artery; this catheter
should be flushed frequently with heparinized saline.
Many modern electrocardiographs come with a pres
sure amplifier and channel for displaying both the pres
sure waveform and numeric values for systolic, mean,
and diastolic pressures. An inexpensive alternative for
measuring mean blood pressure is to use an aneroid
manometer as the transducer. This must be separated
from the saline in the connecting tube by a column of
air; prior to connecting to the catheter the manometer
must be zeroed by locating the meniscus of the saline at
the level of the shoulder joint while the air space is open
to atmospheric pressure.
Mean arterial pressure should be maintained
around 80 mmHg and corrective action taken if pres
sure drops below 70 mmHg.
Cardiac output is an important measure of cardio
vascular function and has been measured in horses
using the thermodilution technique. This method is
technically difcult because it necessitates placing a
thermistor catheter into the pulmonary artery and gives
variable results because of oscillations in the baseline
temperature of blood in the pulmonary artery. It is
hoped that new technology, using indicators that can be
easily measured in the systemic circulation (e.g. lithium
or ultrasound velocity) , will be validated and fnd a
place in equine anesthetic practice.
Central venous pressure (C) can be measured
with a transducer or water manometer applied to a
catheter in, or near, the right atrium. For this purpose
in adult horses, a 70 cm ( 28 in) 1 . 1 mm internal diame
ter catheter is often introduced via the jugular vein. In
dorsal recumbency CVP is usually 5-10 cmH
2
0, but
because the central venous pressure is low, small incon-
SURGERY FOR COLIC (INCLUDI NG ANESTHESI A) 10
sistencies in determining the level for zero cause con
siderable variability in this normal value. Nevertheless,
CVP is a valuable tool for measuring changing cardio
vascular status. If the venous return to the heart is low,
as is the case in relative or absolute hypovolemia, then
Cwill be low. It will increase as the hypovolemia is
corrected.
Pulmonar function
Movement of the chest wall and the rebreathing bag or
bellows provides a rough indication of ventilatory func
tion but gives little information about the efciency of
gas exchange in the lungs. Modern capnographs con
tinuously measure partial pressure of carbon dioxide in
the endotracheal tube; a capnograph is often incorpo
rated in anesthetic agent monitors (see above) . End
tidal carbon dioxide is usually 48 mmHg greater than
arterial carbon dioxide partial pressure but increases
and decreases with it. In horses with extensively col
lapsed lung or severe spatial mismatch of pulmonary
perfusion and ventilation, the difference between end
tidal and arterial carbon dioxide tensions may exceed
15 mmHg. In any case, when end-tidal carbon dioxide
exceeds 60 mmHg, an increase in alveolar ventilation
should be instituted. End-tidal carbon dioxide usually
forms a plateau that lasts until the next inspiration; tail
ing off of this plateau is often caused by small leaks
around the accessory cuff or at a connector. Complete
disappearance of the carbon dioxide plateau is associ
ated with disconnection from the breathing system or
indicates cessation of pulmonary perfusion (Le. cardiac
arrest) . If the capnograph does not approach zero dur
ing inspiration, the most likely cause is increased
machine dead space either from exhausted carbon
dioxide absorber or a malfunctioning one-way valve.
Pulse oximeters use the relative light-absorbing
properties of hemoglobin and oxyhemoglobin to
measure arterial saturation with oxygen (S
p
02) ' A light
emitting diode and sensor are incorporated into a
spring-loaded clip that is usually applied to the tongue
margin so that light passes through the tongue. Because
the ability to detect a signal from the equine tongue
depends upon the design of the clip, it is advisable to
test a pulse oximeter before purchase. When S
p
0
2
is less
than 90 per cent, tissue oxygenation is seriously com
promised and corrective measures should be instigated.
Although pulse oximetry is primarily designed to detect
inadequate oxygen exchange in the lung, it is also a very
useful indicator of perfusion. The audible or visual
signal that accompanies each pulse, is very reassuring
because it continuously confirms the presence of
peripheral blood flow. Diffcult in obtaining a signal
with a probe that ordinarily functions well on the horse
151
10 COLIC
tongue, may be associated with poor tissue perfusion
due to decreased overall perfusion (e.g. shock) or
vasoconstriction (e. g. after an alpha
2
adrenoceptor
agonist) .
The partial pressures of oxygen (Pa0
2
) and carbon
dioxide (PaC0
2
) in arterial blood are probably the best
objective measure of pulmonary function (see below) .
Blood tests
The introduction of small, inexpensive, accurate equip
ment for ' bedside' use has greatly increased the ability
of clinicians to detect and treat abnormalities during
anesthesia. These bedside monitors can be used to
intermittently measure such things as arterial pH,
PaC0
2
, Pa0
2
, bicarbonate, base excess of the extracellu
lar fluid, plasma sodium, potassium, ionized calcium,
creatinine, and glucose. To date, values for hematocrit
derived from these bedside monitors have been unreli
able, probably because the machines are calibrated for
humans and the characteristics of equine red blood
cells are different from those of humans. From a practi
cal point of view, hematocrit and plasma protein
concentration are probably best measured using
microhematocrit tubes, a centrifuge, and a refracto
meter.
COMMON COMPLICATIONS OF
ANESTHESIA
Hypoxia and hypoventilation
Horses under inhaled anesthesia for colic surgery usu
ally breath a mixture of gas that is more than 90 per
cent oxygen. Given a perfectly functioning lung, this
should produce a Pa0
2
of more than 500 mmHg. In
practice Pa02 values between 70 mmHg and 200 mmHg
are often encountered. Values in this range are usually
associated with more than 90 per cent hemoglobin sat
uration with oxygen, hence they do not present an
immediate threat to oxygen delivery. They do, however,
suggest considerable pulmonary venous admixture that
warrants remedial action because oxygen delivery may
be threatened if inspired oxygen decreases (as is likely
during recovery from anesthesia) . When Pa0
2
is less
than 70 mmHg, there is significant hemoglobin desatu
ration and remediation should be pursued urgently.
Normal PaC0
2
is 40 4 mmHg. Collapsed lung,
restricted chest movement, and anesthetic drug
induced inhibition of ventilatory drive conspire to
cause hypercapnea in anesthetized horses. A PaC0
2
of
less than 55 mmHg is generally considered acceptable,
however PaC0
2
in excess of this is likely to be associated
with an unacceptable respiratory acidemia.
152
Both hypoxia and hypercapnea occur in horses anes
thetized for colic surgery despite the early initiation of
mechanically controlled ventilation with an oxygen
enriched mixture. Treatment of both usually revolves
around manipulation of the ventilatory pattern. A tidal
volume of 1 0-15 ml/kg and a respiratory rate of 6-1 0
breaths per minute are usually sufcient t o maintain
Pa0
2
and PaC0
2
within acceptable limits in anes
thetized horses. In horses with distended abdomens it
may be necessary to increase tidal volume and/or
breathing rate to decrease PaC0
2
In order to reduce
the amount of the lung that is collapsed, peak inspira
tory pressure should be increased. Application of more
than 40 cmH
2
0 pressure on the alveoli may cause them
to rupture, hence peak inspiratory pressure should not
be permitted to exceed this value. Collapse of lung tis
sue between breaths can be minimized by application of
5-10 cmH
2
0 positive end-expiratory pressure (PEEP) .
Unfortunately all of these maneuvers increase mean
intrathoracic pressure which increases pulmonary
vascular resistance, reduces venous return, and, in turn,
decreases cardiac output. These side effects often
predicate support for the cardiovascular system and
ultimately limit the extent to which ventilation can be
manipulated.
Many ventilators permit change in the ratio of inspi
ratory time to expiratory time (I:E) . Assuming constant
breathing rate, increasing I:E prolongs the time avail
able for ventilation of slowly filling parts of the lung.
Unfortunately, prolonging the inspiratory period
proportionately reduces the period available for lung
emptying and return of intrathoracic pressure to
atmospheric pressure. In any individual, the process of
determining the best I: E is necessarily empiric, however
optimal values are usually between 1 :2 and 1 :3.
Hypotension and hypovolemia
Hypovolemia in horses with colic is usually inferred
clinically from increased hematocrit, increased plasma
protein concentration, skin turgor, etc. Under anesthe
sia, hypovolemia causes systemic hypotension, defined
as mean arterial blood pressure less than 70 mmHg.
During anesthesia hypotension is usually treated in
several ways. The inhaled dose of anesthetic should
be minimized immediately hypotension is detected.
Switching from halothane anesthesia to isoflurane or
sevoflurane will usually increase blood pressure.
Intravenous infusion of a balanced electrolyte solution
should commence. Large volumes of balanced ele
crolyte solutions ( 20-30 liters) need to be given to
counteract hypovolemia because such fluids are not
confned to the blood but distribute throughout the
extracellular space. This may be an advantage because
in patients for colic surgery the hypotension/hypo
volemia may be related to depletion of the entire
extracellular space. Quite often in the preoperative
period, and occasionally during anesthesia (e. g. after
an acute hemorrhagic episode) , hypotension/hypov
olemia may be so severe that there is insuffcient time
for rehydration with a balanced electrolyte solution.
Under such circumstances infusion of 4 ml/kg hyper
tonic (approximately 7. 2% w/v) saline solution may be
used. This operates by drawing water into the blood
down an osmotic gradient from the interstitial fluid,
thus increasing blood volume. The benefi cial effect of
this is short lived (approximately 30 min) . Because it
tends to cause dehydration of the interstitial fluid
compartment, hypertonic saline should be followed
immediately by 30-40 ml/kg of an isotonic, balanced
electrolyte solution.
Large volumes of balanced electrolyte solutions,
coupled with ongoing protein loss from incontinent
bowel, may lead to a signifi cant decrease in plasma pro
tein and osmotic pressure. Because this may potentiate
hypovolemia and lead to edema, hypoproteinemia
should be addressed by infusing a fluid with high col
loidal osmotic pressure, for example equine plasma,
hydroxyethyl starch, or dextran. Intraoperative hemor
rhage and dilution by infused fluid may lead to
decreased hematocrit. Although a degree of hemodilu
tion may be acceptable on the grounds that it reduces
peripheral vascular resistance, the hematocrit should
not be allowed to fall below 30 per cent as this may
threaten oxygen delivery during the increased oxygen
requirement seen in recovery from anesthesia. Whole
blood, packed cells, or polymerized bovine hemoglobin
(Oxyglobin) may be used to replace red cells.
Sympathomimetics are commonly used to counter
act the cardiovascular depression ordinarily seen
during inhaled anesthesia of equids. Cardiovascular
depression is likely to be even more pronounced in
horses with abdominal crisis, hence the use of sympath
omimetics is almost universal. Dobutamine is a beta
adrenoceptor agonist that is infused intravenously at
1-5 flg kg-I min-I. Very shortly after starting infusion of
dobutamine, cardiac output and systemic arterial blood
pressure increase and there is splenic vasoconstriction
causing the hematocrit to increase. At higher doses
peripheral vascular resistance increases, heart rate
increases, and tachydysrhythmias may be seen. The
short plasma half-life of dobutamine makes it ideal for
infusion because overdose can be treated easily by
reducing the infusion rate. A alternative to dobuta
mine is dopamine. At infusion rates of 1-5 flg kg-I min-I
the predominant effects are mediated through
dopamine receptors (increasing the splanchnic and
renal blood flow) and mixed betal- and beta
2
adreno-
SURGERY FOR COLIC (I NCLUDING ANESTHESIA) 10
ceptors (increasing cardiac contractility and rate) ; in
horses undergoing acute abdominal surgery these are
probably benefcial effects. At infusion rates over 5 fg
kg-I min-I, dopamine predominantly stimulates alpha
adrenoceptors and, hence, causes vasoconstriction; this
may lead to an unwanted increase in peripheral vascu
lar resistance. Norepinephrine is an active metabolite
of dopamine that may accumulate after prolonged
dopamine administration, requiring reduction of the
infusion rate of dopamine. Tachydysrhythmias are very
common with overdose of dopamine. Ephedrine is a
mixed alpha and beta adrenoceptor agonist that can
increase cardiac output and systemic blood pressure. It
is usually given as a bolus of 0. 03 mg/kg that is repeated
once, after an interval of 5 minutes, if insufcient effect
is seen. The effects of ephedrine last for approximately
20-30 minutes, thus making it less suitable for infusion
than dobutamine or dopamine. Metabolic acidosis and
endotoxemia may cause down regulation of adreno
ceptors while hypovolemia may decrease the volume of
distribution of sympathomimetics, hence the dose of
any sympathomimetic must be titrated carefully in
patients undergoing surgery for relief of an abdominal
crisis.
Perfusion of the myocardium is largely dependent
on diastolic systemic blood pressure. When diastolic
blood pressure is less than 35 mmHg myocardial perfu
sion is compromised and cardiotonics such as dobuta
mine and dopamine are unlikely to be effective. A
specific alpha\ agonist such as phenylephrine (0. 01
mg/kg i. v. ) may be warranted under these circum
stances, despite the fact that it will redistribute perfu
sion away from the splanchnic circulation and increase
systemic vascular resistance. Phenylephrine is also used
as a treatment for renosplenic entrapment where its
constrictive effect on the splenic capsule decreases
splenic volume and discharges red cells into the
intravascular space.
Reperfusion of strangulated bowel may cause local
injury by releasing free radicals that contribute to the
death of the intestine hours to days after the end of
surgery. The decision on whether to excise potentially
viable bowel that has experienced ischemia is based on
clinical judgment and therefore prone to error. In such
circumstances the early infusion of a free radical
scavenger, for example dimethylsulfoxide (DMSO)
1 mg/kg i.v. in 5 liters 5% dextrose, may be warranted.
Clinical experience suggests that DMSO has no delete
rious effect on the course of anesthesia.
Metabolic acidosis
Metabolic acidosis is a common complication of
acute abdominal crisis in horses, it is largely caused by
153
10 COLIC
anaerobic metabolism in poorly perfused tissues.
Moderate metabolic acidemia (pH 7. 40-7. 25, base
excess O.O-S.O mEq/l) usually resolves after rehydration
with balanced electrolyte solution. Severe acidemia has
multiple adverse effects including desensitization of
adrenoceptors that are important in treating hypoper
fusion in anesthesia. Conventional therapy involves
sodium bicarbonate (S.4% w/v, 1 mEq/ml) given intra
venously over 1 5-30 minutes at a dose sufcient to cor
rect the base excess to -6 mEq/l, i.e.
sodium bicarbonate dose (mEq) *
base defcit difference from -6 (mEq/l) ^
[0.3 ? body weight]
where the volume of distribution of the sodium bicar
bonate is represented by 0. 3 of the body weight. Sodium
bicarbonate has fallen into disfavor because it causes an
increase in blood tonicity, hypernatremia and paradox
ical respiratory acidosis of spaces that are accessible to
the carbon dioxide that is generated by buffering, for
example the intracellular space and CSF. Nevertheless,
judicious use of sodium bicarbonate is justifable in
horses with colic; indeed, because sodium bicarbonate
(S.4%) is hypertonic, it has similar effects to infusion of
hypertonic saline (see above) on blood volume (a bene
fcial effect in most horses with colic) , plasma sodium,
and plasma tonicity. A with hypertonic saline, these
effects are transient and should be mitigated by infu
sion of a balanced electrolyte solution. Paradoxical
acidosis is a problem with bicarbonate infusion but its
effects may be minimized if ventilation is adjusted to
maintain normocapnea.
Tromethamine (TRIS, THAM, 0.3 molar) is an alter
native treatment for acidosis that distributes through
out the extracellular and intracellular spaces. The dose
of tromethamine is usually calculated thus
tromethamine dose (ml of 0. 3 molar solution)
base defcit difference from -6 ^ body weight (kg)
The solution of tromethamine does not contain sodium
nor is it substantially hypertonic, therefore it does not
cause a large increase in blood volume or dehydrate the
extracellular or intracellular spaces. Because it buffers
acid without generating carbon dioxide, it does not
cause paradoxical acidosis. It is used principally in those
patients where a period of hypernatremia and hyper
tonicity are contraindicated.
Other abnormalities that are often encountered
include hypokalemia and hypocalcemia; both com
pound the hypotension that is usual in these patients,
decrease gastrointestinal motility, contribute to delayed
recovery from anesthesia by causing muscle weakness,
154
and therefore warrant treatment. Potassium may be
given by augmenting balanced electrolyte solution
with 20 mEq/1 potassium chloride. Calcium gluconate
( 23%, 0. 2-0.5 ml/kg) may be infused over 20 minutes
and then ionized calcium re-evaluated.
Movement
Because it is incumbent on the anesthetist to maintain a
minimal plane of anesthesia, occasionally horses move
during surgery. Increasing the inspired concentration
of anesthetic may take several minutes to take effect and
may lead to signifcant cardiovascular depression. Small
increments of ketamine (0. 1-0.2 mg/kg) or instituting
an infusion of ketamine (approximately 40 Ilg kg-I
min-I) may be sufcient to stop movement, however
when ketamine is given toward the end of anesthesia it
may cause disorientation and excitation during recov
ery. Xylazine (0. 1 mg/kg) may be used but it has the
risk of substantial cardiovascular depression. Toward
the end of anesthesia butorphanol (0.02 mg/kg, i.v. )
may be the best choice.
RECOVERY FROM ANESTHESIA
Mter anesthesia, horses should be moved to a stall with
padded floor and walls. Ideally there should be no
right-angled corners in the recovery area. The stall
should be quiet and have lights with a dimmer so that
stimulation can be minimized if necessary. Pulse quality
and mucous membrane color should be observed care
fully after change in posture to lateral recumbency as
this may initiate an hypotensive crisis that requires
interention. A demand valve may be used to continue
controlled ventilation with oxygen until the horse has
partially recovered from anesthesia.
Post-anesthetic airway obstruction is recognized as a
cause of anesthetic morbidity and mortalit, hence
maintenance of the airway is especially important dur
ing the prolonged recovery that often accompanies
colic surgery. There is little objective evidence to favor
any particular strategy for maintaining a patent airway.
The author prefers to instill 6 ml of 0. 1 5% phenyl
ephrine into each nostril 30 minutes prior to the end of
surgery, this reduces, but does not eliminate, the need
for mechanical airay dilation after extubation. Once
the horse reaches a light plane of anesthesia, the author
removes the oro tracheal tube and subjectively assesses
the airway by feeling for air movement at the external
nares and listening for upper airay noise. Upper air
way obstruction detected at this time can usually be
treated by inserting a tube into the nasopharynx and
taping it to the outside of the head to prevent aspira-
tion. (An old orotracheal tube is suitable for this pur
pose. For adult horses it should be approximately
20 mm internal diameter and cut to about 45 cm long.)
An alternative method is to leave an orotracheal tube in
place until after the horse stands. This tube should be
taped securely to the outside of the head and obsered
carefully for kinking when the horse starts to move.
Endotoxemia, hypoproteinemia, systemic vasocon
striction, and inspiration against an occluded upper air
way have all been implicated in causing pulmonary edema
in the recovery room. This potentially fatal condition
occurs infrequently, but any patient that starts to produce
stable white or pink tinged froth from the nares should
promptly be given the diuretic frusemide ( 1 mg/kg i.v. ) .
This should be repeated if no improvement has been seen
after 5-10 minutes. Although the diuresis may have
adverse efects on a dehydrated/hypovolemic patient, the
exigencies of pulmonary edema override the other con
cers. Additional therapy consisting of oral application
15 g of nitroglycerine 2% cream has been used empiri
cally to reduce pulmonary hypertension.
Horses that have eidence of venous admixture dur
ing anesthesia (Pa0
2
200 mmHg while breathing
>90% oxygen) should receive oxygen supplementation
during recovery by insufiating 1 5 l/min oxygen into
the trachea. A stallion urinary catheter inserted via the
nose or oro tracheal tube and secured to prevent aspira
tion, is suitable for this. In many horses this can be left
in place until after standing. If recovery is slow, assisting
the patient into sternal recumbency improves pul
monary function.
Horses that are slow to stand may be physically
assisted by supporting the head and tail by pulling on
ropes threaded through appropriately placed rings in
the wall of the recovery stall. Very weak horses may
require hoisting using a purpose-built webbing harness
(like the Anderson Equine Sling) and a mechanical or
electric pulley (2000 kg capacity) secured to the ceiling
of the recovery space. The support for the pulley must
be engineered for the large forces that can be gener
ated by a struggling horse.
Surgical approaches to the
abdomen
NL UCfmP
INTRODUCTION
A number of different surgical approaches to the
abdominal cavity of the horse are available to the
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
surgeon. The site of the lesion(s) and anesthetic con
siderations (e. g. possible impairment of venous return
for mares late in gestation) dictate the position of the
animal and the abdominal approach required. If there
is no financial constraint the decision on where to
make the abdominal incision must be based on which
approach gives the best access to the anticipated lesion,
and gives the least morbidity to the patient. Other fac
tors, for example the facilities and equipment that are
available, must also be considered. Invasive surgical
approaches are described in this chapter, but in some
horses laparoscopy (although it allows only partial
abdominal exploration) can be useful, albeit mainly as
a diagnostic procedure. This section describes the stan
dard surgical approaches for horses with gastrointesti
nal disease (see Chapter 3 for details on laparoscopic
approaches) .
PREOPERATIVE PREPARATION
There are two main approaches to the equine abdomen
(Figure 10.la, b)
1. ventral incisions such as midline or paramedian
2. left or right flank incisions made either through the
paralumbar fossa or by a 1 7th or 1 8th rib resection.
Surgical entry into the abdomen is made with the horse
under general anesthesia in dorsal or lateral recum
bency, except for paralumbar fossa celiotomies that can
be done with the animal standing. The surgical area is
clipped, and a 5 cm linear band is shaved at the
intended incision site to allow better adhesion of the
adhesive impervious dressings applied as part of the
incisional draping in the operating room. In addition,
ventral abdominal approaches require, in males, sutur
ing of the prepuce using a continuous pattern to pre
vent intraoperative urine contmination of the surgical
incision. Following aseptic preparation of the surgical
site, impervious iodine-impregnated dressing is applied
to prolong suppression of microbial growth. After
proper draping, the incisions are made as described
below.
STANDARD SURGICAL APPROACHES
Ventral midline celiotomy (laparotomy)
A ventral midline celiotomy is performed with the horse
in dorsal recumbency. This is the preferred approach
for the vast majority of horses with abdominal surgical
disease. Its limitation is poor exposure of the structures
in the pelvic cavity and dorsal abdomen.
155
10
a
b
COLIC
1 7th ri b
Resection
V
1
Fl ank
,

Figure 1 0. 1 Schematic representati on of
the location of a) ventral i nci si ons (mi d
l i ne or paramedi an), b) fl ank i nci si ons
made ei ther through the paral umbar
fossa or by a 1 7th or 1 8th ri b resection
The incision is made with a no. 22 Parker-Kerr
blade, starting at the umbilicus and extending proxi
mally for 1 5-30 em (Figure 1 0. l a) . The length of the
incision is based on the size of the animal and whether
manipulation of the large intestine, requiring a larger
incision, is anticipated. Following cauterization of
cutaneous and subcutaneous arteries the incision is
extended through the subcutaneous tissue. A 2. 5 em
incision is made into the linea alba with a no. 1 0
Parker-Kerr blade taking meticulous care since the
linea alba cannot be tented. It is useful to start the inci
sion in the linea alba near the umbilicus as the linea
alba is wider at that location, minimizing the chance of
an unplanned paramedian incision. Once the linea alba
has been incised over 2-4 em, a long-handled Russian
forceps is placed into the abdomen (still outside the
peritoneum) and directed cranially while lifting the
linea alba. This serves as a guide and protects viscera
from inadvertent injury during the approach. The inci
sion is then extended cranially taking care to stay on the
linea alba. If the rectus abdominus muscle is inadver
tently incised, the midline ridge on the dorsal aspect of
the linea alba can be palpated, or a hemostat placed in
the rectus abdominus muscle on each side of the inci-
156
sion to identif the direction of the correction needed
to return to the linea alba. The lateral movement of the
hemostat will be arrested by the linea alba on one side
of the incision while it is unimpeded through the rectus
abdominis muscle on the other side (Figure 10.2) . The
peritoneum is bluntly penetrated and separated along
the incision plane with the surgeon's fngers.
If an incision must be extended caudally to increase
access to structures near or in the pelvic cavity of males,
the midline skin and subcutaneous incision must be
extended laterally to the prepuce (left or right side
depending on the surgeon's preference) . By blunt dis
section, the prepuce is reflected to the opposite side to
expose the linea alba. The linea alba incision can then
be extended toward the pubis bone as required.
Ventral paramedian celiotomy (laparotomy)
A ventral paramedian celiotomy is also performed with
the horse in dorsal recumbency. In horses without prior
ventral midline incisions, this approach has no real
advantage for structures accessed over the ventral mid
line incision. Perhaps, when an incision needs to be
extended toward the pelvic inlet, the ventral parame-
.
Abdominal
inCISion
Abdomen
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 1 0
External obloque
muscle
Figure 1 0.2 If the rectus abdomi nus
muscle i s i nadvertently incised, a
hemostat can be placed i n the latter
muscle on each side of the incision

Inernal obloque
muscle
Transverse
musle
to identify the di recti on of the
correcti on needed to return to the
l i nea al ba. Note that the lateral
movement of the hemostat wi l l be
arrested by the l i nea al ba on one
side of the incision whi l e it i s uni m
peded through the rectus abdomi nis
on the other side
dian incision has a slight advantage. In these cases, the
prepuce does not need to be reflected much prior to
entry into the abdomen. In the author's opinion, the
main use of the ventral paramedian incision is for
horses with excessive fbrosis from previous ventral mid
line incisions or if prior use of mesh has minimized the
attractiveness of a ventral midline incision.
The skin incision is located 5-7 cm on either side of
the ventral midline, again starting at the level of the
umbilicus and extending cranially 1 5-30 cm (Figure
1 O. la) . After extension of the incision through the sub
cutaneous tissue, the paramedian incision is sharply,
using a no. 10 Parker-Kerr blade, extended through
the external sheath of the rectus abdominis muscles.
Following this incision, the rectus abdominis muscle is
bluntly separated and the internal sheath sharply
opened using the same technique as described for the
linea alba in a ventral midline incision in order to pro
tect abdominal viscera from iatrogenic injury. If the
incision needs to be extended beyond the prepuce, the
skin and subcutaneous incision is deviated laterally at
the level of the prepuce on the desired side. After inci
sion of the skin and subcutaneous tissue, the prepuce is
reflected toward the midline and the incision through
the body wall is made in the same plane as the incision
proximal to the prepuce. In general, a paramedian
approach gives exposure similar to the ventral midline
incision but has a more complicated and longer abdom
inal closure.
Paralumbar flank celiotomy {laparotomy}
A paralumbar flank celiotomy is made with the horse
either standing or anesthetized in lateral recumbency.
A lf paralumbar celiotomy allows limited abdominal
exposure for correction of nephrosplenic entrapment,
closure of the nephrosplenic space, and exteriorization
of a section of the small intestine or small colon. A rght
paralumbar celiotomy allows limited access to the base
of the cecum and the descending duodenum.
The skin incision is centered in the left or right
paralumbar fossa starting 5-7 cm below the transverse
process of the lumbar vertebrae and extending toward
(without invading it) the fold of the flank (Figure
1 0. lb) . After incision of the subcutaneous tissue, the
external abdominal muscle is sharply extended along
the plane of the skin incision. If only one arm is
needed for abdominal manipulation or for exterioriza
tion of the small intestine or small colon, a modifed
grid approach is preferable. In this case, the internal
oblique muscle is separated bluntly along its fber ori
entation, and the transverse abdominal muscle is
sharply incised along the plane of its muscle fbers
together with the peritoneum using curved Mayo
scissors. This combined incision of the transverse
abdominal muscle and peritoneum facilitates secure
closure of the peritoneum. A good closure of the peri
toneum prevents air introduced into the abdomen
during standing surgery from escaping from the
abdomen into the subcutaneous tissue postoperatively.
If further exposure is required (e. g. for closure of the
renosplenic space) , instead of a modifed grid
approach, the incision is opened as described above
except that the internal oblique muscle is sharply
incised in the same plane as the skin incision.
Flank celiotomy {laparotomy} through the
1 7th or 1 8th rib
Flank celiotomies through the 1 7th or 1 8th rib resec
tion are done in horses anesthetized in lateral recum
bency where access to the left or right dorsal quadrant
157
10 COLIC
is desired. This approach allows significantly greater
abdominal exposure of the left or right abdominal
viscera compared to the paralumbar fossa/flank
celiotomy. It is generally done on the right side for
procedures such as typhlectomy, resection of the right
dorsal colon, or improved access to the ileocecal valve
(Figure 10. 3) . It is done on the left side for procedures
such as closure of the nephrosplenic space and correc
tion of nephrosplenic entrapment. Either the 1 7th or
18th rib resection gives similar exposure. However, the
1 7th rib resection allows a more secure closure if a
stormy recovery is anticipated, since incorporating the
1 6th and 1 8th ribs on either side can bolster the
strength layer of this incision.
The skin incision is curvilinear along the lateral sur
face of the selected rib. The most dorsal aspect of the
incision is extended sharply to the ribs, incising the
attachment of the external oblique muscle and the
insertion of the internal oblique muscle. The incision is
made on the rib, and the periosteum covering the rib is
reflected exposing the rib. Following elevation of the
periosteum at the dorsal aspect of the incision, a right
angle forceps is used to encircle the exposed rib with a
Gigli wire. After transection of the rib with the Gigli
wire, the rib is elevated away from its periosteum until
its distal end is reached. At the distal end of the rib, the
periosteum cannot be easily elevated as it adheres to the
fbrocartilaginous aspect of the rib. The rib is freed from
the intercostal muscles by sharp dissection at its distal
end. A moist towel is placed on the remaining proximal
portion of the rib to prevent inadvertent damage to
viscera during exteriorization. The periosteum on the
medial aspect of the rib is incised and the peritoneum is
bluntly separated along the line of the incision.
Figure 10.3 Right 1 7th rib resection gi ves reasonabl e
access for typhlectomy, resection of right dorsal col on, and
transection at the i l eocecal valve. I n thi s horse the large
i ntestine, including the right dorsal colon, i s exteriorized
158
Other approaches
A thorough knowledge of equine abdominal anatomy
allows the surgeon to perform many other incisions to
suit the particular gastrointestinal disease. For instance,
the author has used a transverse incision centered over
the umbilicus to allow better exposure of the pelvic cav
ity. Likewise, specifc access to a dorsal diaphragmatic
tear may be made through a thoracotomy; or to access
the dorsal and cranial aspect of the stomach the sur
geon may need to perform a thoracotomy followed by
an incision into the diaphragm. In conclusion, the sur
geon faced with an unusual lesion should feel free to
use an unusual approach that is directed to the sus
pected lesion, and not be limited by a time-enforced
paradigm of a few selected incisions.
Surgical exploration of the
abdomen
NL UCf0P
INTRODUCTION
Abdominal surgery in horses is now a routine proce
dure conducted at many equine hospitals around the
world, primarily for the diagnosis and treatment of
acute colic. This procedure requires delicate and
thorough surgical manipulation to localize, identif,
and correct the particular abnormality. The surgical
approach into the abdomen and the site of the lesion
will determine which structures are seen frst on entry
into the abdomen. This section describes the principles
one follows for complete exploration of the abdomen
and manipulation of the viscera.
ABDOMINAL EXPLORATION
Initial exploration
Proximal to any obstructive lesion, bacterial fermenta
tion associated with intestinal stasis and continued
production of secretions lead to intestinal distension.
Such distension will often be immediately apparent on
opening the abdomen.
1 . In a small intestinal obstruction, the distended
small intestine often bulges out of the incision. The
surgeon proceeds to explore the abdomen while an
assistant keeps the intestine wall moist with sterile
isotonic solution.
2. In obstructive lesions affecting the small or large
colon, the distended large colon may bulge out of
the incision on entry into the abdomen. Gas
accumulated in the large intestine must be
evacuated before the abdomen is explored to
ensure minimal serosal irritation of the viscera. This
can be done by placing a 1 4- or 1 6-gauge needle
(attached to a suction tube) into a tenial band, and
after tunneling the needle through the intestinal
wall the tip is inserted into the lumen. The author
prefers oversewing the puncture site with a pre
placed simple interrupted absorbable
monoflament suture (size 00 or 000) in a cruciate
pattern. Suturing the decompression tract is
optional in the adult horse, but should be
considered in foals as they have thinner and more
likely to leak bowel walls. The author has observed
signifcant adhesions developing in young animals
at decompression sites that were not sutured.
3. To minimize serosal irritation during abdominal
exploration, one liter of lactated Ringer' s solution or
1 % carboxymethylcellulose* can be instilled into the
peritoneal cavity. The surgeon dons an impervious
sleeve and proceeds with abdominal exploration.
*1 % carboxymethylcellulose is prepared by adding 10 g of
carboxymethylcellulose powder to 200 ml of boiling sterile
water and adding sufcient sterile water to form a 1 liter
solution. The preparation is then autoclaved at 121C for a
total of 20 minutes.
SURGERY FOR COLIC (INCLUDI NG ANESTHESIA) 1 0
Detailed exploration
The abdominal cavity (divided into four quadrants)
and the pelvic cavity are explored briefly with the vis
cera in situ. The objective is to identif the lesion(s) so
that appropriate equipment (i.e. surgical instruments
for anastomosis, colon table, etc.) can be requested. It is
neither crucial nor benefcial to spend a lot of time
looking for a precise diagnosis by palpation alone as
exteriorization will enable the surgeon to identif the
majority of intestinal problems. Therefore, abdominal
exploration is often completed after the distended
intestinal segment has been exteriorized and the lesion
identifed and corrected.
The surgeon assesses each abdominal quadrant and
the pelvic cavity for
1 . normal abdominal viscera, including the urogenital
tract and ligamentous and vascular structures (i. e.
cranial mesenteric artery) , that should be present
2. abnormal fndings, such as the presence and nature
(gas, frm ingesta, etc.) of intestinal distention,
intestinal wall thickness, tight bands, or abnormal
location of an intestinal segment.
Table 10. 3 shows the structures that the surgeon should
evaluate in the four abdominal quadrants and the
pelvic cavit.
Figures 1 0.4-10.6 outline abdominal palpation of
selected structures that cannot be exteriorized.
Depending on the size of the animal and the target

Lef crani al quadrant
Right crani al quadrant
Right caudal quadrant
Left caudal quadrant
Pelvic cavity
Structures to pal pate
Body and cranial edge of the spleen; gastrospl eni c l i gament; fundus of the stomach;
omentum; lef hemi-diaphragm; l eft lobe of l iver; small i ntestine; small colon as it joi ns
the transverse col on and duodenal-colic l igament between the di stal aspect of the
duodenum and the most proximal aspect of the smal l colon; the l ef ventral and dorsal
colon medial to the spleen; the di aphragmatic and sternal flexures near the stomach.
Ri ght ventral and dorsal colon; right and quadrate l obe of the l iver; to or three ducts
of the bi l iary tree; proxi mal duodenum; epiploic foramen; pylorus and antrum of
stomach; right hemi-diaphragm; diaphragmatic and sternal flexures; right dorsal and
ventral colon; omentum; crani al mesenteric artery; ri ght ki dney; and, i f enlarged, right
adrenal gl and.
Cecum; i leocecal valve; smal l i ntesti ne; ri ght ureter if disended; and, when appropriate,
right i ngui nal ri ng or right ovary, uterine horn, and broad l igament.
Left dorsal and ventral colon; pelvic flexure; body of spleen; nephrosplenic l igament; lef
ki dney; and, i f enl arged, left adrenal gl and and ureters; smal l i ntestine; smal l colon; and,
when appropriate, lef i ngui nal ring or lef ovary, uterine horn, and broad l i gament.
Bl adder; descendi ng colon and rectum; and, when appropriate, uterus and vas deferens
159
10 COLIC
Mesenter Duodenum
organ, some of these structures can be seen by a combi
nation of
retraction of the abdominal incision
placement of an intra-abdominal moist towel to
retract local abdominal viscera
use of suction
tilting of the operating table.
However, the surgical view is restricted and manipu
lation is diffcult at best.
Right cranial abdominal quadrant
Using the stomach as the reference point, the pylorus is
identified as a fi rm muscular structure from which the
160
Figure 1 0.4 Schema i l l ustrati ng
identification of the epi pl oi c
foramen. Lateral vi ew of the right
crani al abdomi nal quadrant as
exami ned through a ventral mi d
l i ne i ncision. The duodenum i s
identified fi rst, by applyi ng trac
tion on the duodenum with the
thumb and forefi nger the surgeon
can use a finger to probe the duo
denum's now tense mesentery in
a cranial -to-caudal di rection unti l
the epipl oi c foramen i s identified
Figure 1 0. 5 Schema i l l ustrating pal
pati on of the right dorsal col on and
transverse colon. Crani al vi ew of the
right crani al abdomi nal quadrant as
exami ned through a ventral mi dl i ne
incision
duodenum is found. By tensing the descending duode
num, its mesentery becomes palpable, and the epiploic
foramen and medial surface of the liver can be identi
fied (Figure 10.4) . The right dorsal colon can be pal
pated axial to the duodenum as it joins the transverse
colon (Figure 10. 5) .
Right caudal abdominal quadrnt
By following the base of the cecum, the surgeon can pal
pate the ascending duodenum as it traverses the
abdomen from right-to-Ieft around the cranial mesen
teric arter (Figure 1 0.6) . The latter can be palpated as
an irregular frm structure with fremitus in cases of
thromboembolic colic associated with Strnglus vulgaris
5t0mch umenum Ltnt&l

mewnttK aOeQ
laral migration. When present, the right ovary and
uterine horn can be palpated along the dorsal body wall
caudal to the right kidney.
Let caudal abdominal quadrant
By following the medial surface of the spleen dorsally,
one can identif the nephrosplenic ligament (the
ventral component of the suspensory ligament of the
spleen) between the dorsal-ventral surface of the spleen
and the left kidney (Figure 1 0. 7) . When present, the
left ovary and uterine horn can be palpated along the
dorsal body wall caudal to the left kidney.
Let cranial abdominal quadrnt
By following the medial surface of the spleen cranially,
one can identif the gastrosplenic ligament between the
Figure 10.6 Schema i l l ustrati ng
palpation of the ascendi ng duo
denum and crani al mesenteric
artery. Lateral view of the right
crani al abdomi nal quadrant as
examined through a ventral mid
l i ne i nci si on
cranial-ventral surface of the spleen near the hilus and
left part of the greater curvature of the stomach (Figure
1 0. 8) .
EXTERIORIZATION OF VISCERA
If not already present, the surgeon places an impervious
drape around the incision to receive the exteriorized
bowel. Prior to the manipulation of small intestine, 1
liter of a 1 % solution of carboxymethylcellulose can be
placed into the abdomen to prevent serosal irritation
during manipulation; this is recommended in foals but
optional for adults.
If the small intestine is distended, it is best to identif
the ileum and exteriorize the small intestines starting
Figure 10.7 Schema i l l ustrating pal pation of
the nephrospl enic ligament. View: left
caudal abdomi nal quadrant as exami ned
through a ventral mi dl i ne i nci si on. The sur
geon can identify this l igament by following
the spleen dorsal l y and caudally
161
10 COLIC
Pelvic
flexure
distally until the lesion is found. The apex of the cecum
is exteriorized and pulled caudally exposing the dorsal
and lateral bands of cecum. Tracing the dorsal band
rostrally, the ileocecal fold is identifed and followed
toward the base of the cecum until the ileum is found
and identifed by its thicker wall and the antimesenteric
attachment of the ileocecal folds. While manipulating
the small intestine, the intestinal wall itself is grasped
while taking care not to pull on the mesentery, which is
especially friable in foals ( Figure 10. 9) . The small intes
tine is exteriorized until the obstruction is localized, or
the duodenum is reached. The goal is to exteriorize the
obstruction site to determine the best means of correct
ing the problem. The following algorithm gives the sug
gested steps to locate and exteriorize an intestinal
obstruction (Figure 10. 1 0) . If the obstructed site cannot
be exteriorized, one should attempt to reduce the
obstruction abdominally and then exteriorize the
involved intestinal segments.
If the large intestine is distended and is the site of
intestinal lesions, the incision is lengthened appropri
ately to allow its safe exteriorization. Rupture of the
large intestine is a real possibility during manipulation
and exteriorization if it is distended. If the viability of
the large intestine wall is also compromised, the risk of
rupture increases substantially. After a lengthened inci
sion has been made and gas decompressed from the
cecum and large intestine, the surgeon places an arm
underneath the left colon while an assistant lifts and
retracts the left side of the incision (Figure 10. 1 1 ) . The
goal is to exteriorize the pelvic flexure frst. If the colon
is markedly distended by fluid and solid materials, a
162
Figure 10.8 Schema i l l ustrating
palpation of the gastrospl eni c
l i gament. Vi ew: l eft crani al
abdomi nal quadrant as exam
ined through a ventral mi dl i ne
i nci si on. The gastrospl eni c l i ga
ment i s found between the
medi al surface of the spleen
and the left greater curvature
of the stomach, the left colon
i s medi al to the surgeon's hand
Figure 10.9 For exteriorization of the small intestine, the
surgeon handl es the intesti nal wal l and avoids the fragi l e
mesentery
decision must be made as to whether an enterotomy
needs to be performed to empty the colon prior to
further manipulation.
The small colon is exteriorized by fnding its charac
teristic contents in the caudal abdomen and retracting
it out of the abdomen. Alternatively, the small colon
may be identifed by palpation of the duodenocolic
ligament or the descending colon in the pelvic cavit.
y
Is the smal l
intestine
distended?
E
Yes
Determine i f an obstruction is present by intra-abdomi nal
exploration usi ng an i mpervious steri l e sl eeve
I
Expl oratory steps
Divide abdomen into four quadrants and pelvic cavity
Perform in situ assessment based on Table 1 0. 3
Assess for normal abdomi nal viscera
Assess for abnormal fi ndi ngs
Distention
Intesti nal wal l thickness
Abnormal location of intesti nal segment
I
9
I s obstructi on site
found?
I Can obstructi on be exteriorized?
I
If the smal l intesti ne i s i nvol ved
If the large intestine i s invol ved it i s usual l y gas
grasp and l i ft the site taki ng care
di stended:
not to pul l on the lesions or the
Relieve distention with gas suction.
mesentery of the bowel i nvolved i n
Make sure the incision is l ong enough.
the l esi on
Pl ace forearm under the left ventral and dorsal col on
and l ift the col on i n a sl ightl y rostral di recti on to
exteriorize the pelvic flexure.
Then lift and pull the colon in a caudal di recti on unti l
Fi nd the i l eocecal junction and
the sternal/di aphragmatic flexures are exteriorized.
begin exteri ori zi ng the smal l
intestine from distal to proxi mal
unti l the lesion i s found or the

I lf lesion i s not found r
duodenum is reached
Starti ng in proximal jejunum, ' mi l k' smal l intestine content distally
I
Replace empty smal l intestine into abdomen si multaneously unti l i l eocecal valve is reached
I
Place forearm under the left ventral and dorsal colon and lift the colon in a sl i ghtl y rostral
di recti on to exteriorize the pelvic flexure, then lift and pul l the colon i n a caudal di rection
until the sternal/di aphragmatic flexures are exteriorized.
I
Reach into the pelvic cavity and grasp the smal l col on. Exteriorize the smal l colon from
distal to proxi mal unti l the lesion i s found or the transverse colon i s reached. If the smal l
intesti ne has not been exteriorized, fi nd the i l eocecal j unction and begi n exteriorizing the
r
smal l i ntestine from di stal to proxi mal .
Figure 10. 10 Algorithm summarizing the steps needed to identify and exteriorize various intesti nal lesions
1 63
10 COLIC
Pelvic
flexure
CONCLUSION
The surgeon must remember that the goal is to correct
the cause of the intestinal obstruction or disease and
that multiple abnormalities can be present in the same
animal. For exam
p
le. it is not uncommon to have a
large colon displacement. presumably because of
rolling. together with another disease process.
Therefore, complete but efcient intestinal examina
tion is a sine qua non condition of proper abdominal
surgery.
Evaluation of gut viability
c ||PPmO
In many cases the appelranee of strangulated bowel
leaves little doubt about th
e 0rr0 for resection. but no
method can provide consistnt
g
llidance since the via
bility of bowel that has incurred subtle changes is dif
cult to determine. The
difference between the viability
of the small intestine and large colon of horses is clini
cally important. but frequently overlooked. Criteria of
viability and the consequences of an incorrect decision
are different for the two segments (Figure 10. 12) . In the
equine large colon. the term viable refers to the
affected segment's ability to recover fully without
undergoing further mucosal necrosis resulting in death
from endotoxemia and peritonitis. Although progres-
16
Figure 1 0. 1 1 Exteriorization
of the large intestine with a
ventral mi dl i ne i ncision. The
surgeon is on the right side
of the horse while an assis
tant retracts the left side of
the i nci si on. By placi ng the
l eft colon over the surgeon's
arm l i ke a towel, the surgeon
can l ift the left colon whi l e
attempting to exteriorize the
pelvic flexure first
sive necrosis is a concern in the small intestine, a seg
ment judged viable because it clearly can survive and
repair the ischemic injury could be at great risk for
developing adhesions (Figure 10. 12) . Adhesions are
less likely in the large colon. A important issue for
both segments is the expense of intestinal resection
(Figure 1 0. 1 2) . The added cost of a longer anesthesia
time, surgical expenses, and intensive aftercare could
be reasons for intraoperative euthanasia when there are
fnancial constraints. Increased duration of surgery for
resection could extend anesthesia time beyond safe
limits for draft breed horses.
SMALL INTESTINE
Only one study has compared different methods of
assessing viability in equine (pony) jejunum and it
found that all intestinal segments recovered from dif
ferent tpes of ischemia without developing adhesions,
despite pessimistic predictions based on clinical judg
ment (Figure 1 0. 1 3) and fluorescein fluorescence.
However in another study, jejunal segments subjected
to identical tpes and duration of ischemia were at
considerable risk of adhesion formation, even when the
bowel yielded a viable fluorescent pattern with fluores
cein. Differences between the studies that could have
predisposed the animals to adhesions in the latter study
were
strangulation of four segments versus one segment
per animal
SMALL INTESTINE
Questi onabl e vi abi l ity
I
Incorrect decision
Resection
I
Lon.g surgery
Expensive treatment
Anastomotic problems
Risk of adhesions
Good prognosis
I
If vi abl e
I
I
Correct decision
No resection
I
Short surgery
I nexpensive treatment
No anastomotic problems
Less risk of adhesions
Excellent prognosis
I
I
If non-viable
I
I
I ncorrect decision Correct decision
Resecti on No resection
I
I
Long surgery Short surgery
Expensive treatment I nexpensive treatment
Anastomotic problems No anastomotic probl ems
Risk of adhesions Great risk of adhesions

Good prognosis Poor prognosis
I
LARGE I NTESTI NE
Questi onabl e vi abi l ity
I
I
I
I ncorrect decision*
Resection
I
Long surgery
Expensive treatment
Good prognosis
No risk of recurrence
If vi abl e
I
I
Correct decision*
No resecti on
I
Short surgery
I nexpensive treatment
Excellent prognosis
Risk of recurrence
I
I f non-viabl e
I
I
I ncorrect decision Correct decision
Resecti on
I
Long surgery
Expensive treatment
Endotoxemia
I
Fai r-good prognosis
No risk of recurrence
No resecti on
I
Short surgery
Expensive treatment
Severe endotoxemi a
Poor prognosis
Risk of recurrence
Figure 10. 12 Consequences of errors in assessi ng the viabi l ity of smal l and large intestine in random order. *The decision
to resect or not resect large col on after volvulus must consider the possi bi l ity of recurrence of the volvulus, a factor that
can j ustify resection of questi onabl e colon in some cases
more traumatic methods for inducing ischemia
omission of antibiotics and flunixin meglumine in
the postoperative management.
Clinical criteria of viability are
serosal color
bowel wall thickness
presence or absence of mesenteric arterial pulses
spontaneous motility or motility evoked by
snapping a fnger against the intestinal wall
improvement in color after correction of the
strangulation.
Spontaneous or evoked motilit will appear sluggish in
viable strangulated bowel because of 'splinting' of the
muscle wall by edema and hemorrhage. Edema and
hemorrhage in the intestinal wall is not unusual afer
strangulation because occlusion of thin-walled veins
causes rapid mural congestion (Figure 10. 1 3) . Such
changes lead to high false-positive results (unnecessar
intestinal resections) because short intestinal segments
with these changes can survive without forming adhe
sions (Figure 10. 14) . Enterotomies are not recom
mended for viability assessment in the small intestine
because of the risk of adhesions and because mucosal
165
10 COLIC
Figure 10. 13 Appearance of a segment of 4 meters of smal l
i ntesti ne that was strangul ated i n the epi pl oic foramen
and was not resected. The horse recovered and did not
develop a known problem over a 2-year follow-up period
appearance is usually severe enough to lead to an
unnecessary resection. With long segments of question
able viability, the risk of adhesions to bowel left in situ
must be balanced against the risk of adhesions with
resection and anastomosis (Figure 10. 12) .
The advantages of fluorescein fluorescence (visual
or qualitative fluorescence) in equine small intestine
are that it allows rapid assessment of large areas of
bowel and is simple to use, safe, and inexpensive.
Fluorescein is given through the jugular catheter as a
10% solution at a dosage of 15 mg/kg of body weight,
and a portable ultraviolet lamp is used to demonstrate
fluorescence in the darkened room approximately 5
minutes after injection. Unfortunately interpretation of
equivocal fluorescein patterns is subjective and prone
to error, and patterns that have been regarded as non
viable in the intestine of other species are viable in the
horse. Fortunately, non-viable bowel does not stain
from surface contact with the dye, and the hyperfluo
rescent pattern caused by perivascular leakage in non
viable bowel seems to be rare. In viable intestine
rendered hemorrhagic and edematous by venous occlu
sion, intramural hemorrhage shields fluorescein in the
tissues from ultraviolet light, and a hypofluorescent or
' non-fluorescent pattern is produced. This accounted
for the high false-positive results, low overall accuracy,
and low overall specificity for fluorescein in one study
on pony jejunum.
The Doppler pencil probe (9 mHz) , calibrated to a
Doppler flowmeter, can be used to detect blood flow at
several points in the mesenteric vessels and in the
1 66
Figure 10. 14 Segment of smal l intestine 1 5 mi nutes after
release from 3 hours of venous strangul ati on obstructi on.
This segment di d not cause postoperative compl i cations,
and adhesions and other obstructive lesions were not
found at necropsy 45 days later. From Freeman et a/.
(1 988) Am. J. Vet Res. 49:895-900, with permi ssion
intestinal wall. The tip of the gas-sterilized probe is
coated with sterile, water-soluble gel to enhance con
tact. It is held at a 45 degree angle to the tissue surface
and is pointed upstream in the direction of blood flow.
Doppler arterial signals are then judged as present
(viable) or absent (non-viable) . The Doppler technique
is most suitable for identifing small areas of ischemia
and for selecting well-perfused margins for intestinal
anastomosis. However, it is impossible to scan large seg
ments of ischemic bowel adequately, and as a result the
Doppler can miss foci of infarction.
In a study on pony jejunum, Doppler ultrasound was
found to be superior to fluorescein fluorescence and
clinical judgment in predicting an intestinal segment's
viability after it had been subjected to venous occlusion.
This is consistent with the results of similar studies in
dogs and cats. After combined arterial and venous
occlusion, fluorescein fluorescence is superior to clini
cal judgment and Doppler ultrasound in viable loops.
However, the Doppler technique is inferior to fluores
cein and clinical judgment in detecting non-viable seg
ments, regardless of the method of inducing ischemia.
The superiority of fluorescein has been attributed to its
ability to assess microvascular perfusion which corre
lates closely with tissue viability, whereas the Doppler
device mainly detects blood flow in large vessels.
Other methods that could be applied to viability
assessment in equine small intestine are surface
oximetry and measurement of surface temperature.
The perfusion fluorometer (quantitative fluorescence) ,
laser-Doppler flow meter, and tetrazolium analysis of
the mucosa, have some potential but are cumbersome
and require special equipment. In clinical cases, a mean
intralumenal hydrostatic pressure of 15 cmH
2
0 in intes
tine proximal to an obstruction was significantly associ
ated with low survival; however, this may be more useful
as an indicator of prognosis than intestinal viability.
The author has modified clinical criteria, based on
the findings of one report, and tends to leave intestine
in place that has scattered ecchymoses, dark pink to
light red discoloration, and mural edema as the pre
dominant changes (Figures 10. 13 and 10. 14) . In a
recent clinical study where this approach was used, long
and short-term outcomes were better when such
segments were left in place rather than resecting the
intestine. Although intestinal damage was considerably
more severe in the resected groups, the results would
suggest that a more optimistic approach can be applied
to leaving questionable small intestine in place. The risk
of adhesions exists, especially in the more severely com
promised segments, but might not be worse than after
anastomosis. In addition, it is not unusual for distended
intestine to develop edema and serosal hemorrhages,
and yet be sufciently viable to heal an anastomosis
(Figure 1 0. 1 5) .
In conclusion, fluorescein fluorescence offers little
improvement over clinical judgment, although it is
accurate when it produces a viable fluorescent pattern.
A viable fluorescent pattern in a questionable segment
therefore means that the segment could be left in place,
but a non-viable pattern is an indeterminate fnding. In
the author's experience, the most unpredictable out-
Figure 10. 15 End-to-end anastomosis made in hemor
rhagic and edematous smal l intestine to avoid resection of
too much bowel. At a repeat celiotomy 5 days later, a
smal l adhesion was broken down proxi mal to the anasto
mosis and the horse did not develop any compl ications
over a 3-year fol l ow-up period
SURGERY FOR COLIC (I NCLUDI NG ANESTHESIA) 10
come arises with the rare small intestinal segment that
appears normal at surgery after release of strangulation,
but deteriorates subsequently because of undetected
vascular thrombosis or possibly reperfusion injury.
Another important issue is the amount of bowel that
can be removed, and recent evidence suggest that
removal of 60-70 per cent is close to the limit.
LARGE INTESTINE
The large intestinal disease that is most likely to cause
difcult with viability assessment is large colon volvu
lus, and the decision to resect is further complicated by
poor access to viable margins, the risk of recurrence
(Figure 1 0. 1 2) , and selection of a method for prevent
ing recurrence. A segment that appears viable based
on serosal appearance can have irreversible mucosal
changes and microvascular thromboses. A pelvic flex
ure colotomy can be very useful in such cases, as it
allows evacuation of the bowel and assessment of bleed
ing from the cut edges. If the mucosa is dark red, the
prognosis is better than if it is black, but dark discol
oration of the mucosa can be associated with viability.
Visual assessment of motility in the large intestine is not
as reliable as in the small intestine, because large intesti
nal motility normally appears sluggish.
Evaluation of histologic changes from frozen biop
sies has been used to assess the degree of epithelial
injury to the equine large colon. A full thickness intesti
nal biopsy is cooled to -150C to -160C in 2-methyl
butane immersed in liquid nitrogen until the solution
almost reaches its freezing point (approximately 5-10
minutes) and is processed for immediate evaluation.
The prediction of viability is based on assessment of
hemorrhage and edema in the mucosa and submucosa,
the extent of epithelial cell damage, and the intersti
tium to crypt ratio (normal I: C 1 ) . Intestine is less
likely to survive with a greater than 50 per cent loss of
the crypt epithelium, and an I: C ratio greater than 3.
Formalin-fixed sections can be used for delayed viability
assessment and to help decide beteen the need for
further treatment, surgery, or euthanasia, if the clinical
course deteriorates after surgery.
Combined evaluation of tissue blood flow (surface
oximetry or laser Doppler) and histologic injury
(frozen tissue sections) has been recommended to
assess large colon ischemia. Surface oximetry is a mea
sure of the partial pressure of oxygen on the tissue sur
face (PsO) and is determined by oxygen content in
blood beneath the probe, the diffusion distance from
the vessels to the surface, the local tissue oxygen
consumption, and blood flow. A good outcome is asso
ciated with a Ps0
2
> 20 mmHg. The disadvantages are
167
10 COLIC
that the equipment is expensive, only small areas of tis
sue can be evaluated, and contact between probe and
tissue should be constant. Pulse oximetry can be used to
assess oxygen saturation, but it has not been evaluated
in the horse and it may not be as sensitive to decreases
in local tissue blood flow as surface oximetry.
Fluorescein fluorescence might be more suitable for
assessing large intestine than for small intestine because
the large intestine has a lower risk of adhesions in seg
ment that produce a viable pattern. The fberoptic per
fusion fluorometer has the advantage over qualitative
fluorescence of providing quantitative information and,
therefore, is an objective measure of perfusion. Results
were inconclusive in one study on experimental
ischemia in equine small and large intestine, although
it did identif the ventral colon as more susceptible to
ischemia than the dorsal colon. In horses with large
colon obstruction, an intralumenal hydrostatic pressure
greater than 38 cmH
2
0 had a high sensitivity, speci
ficity, and positive and negative predictive values for
predicting low survival.
Viability assessment of the small colon has not been
studied to the same extent as it has for the large colon
and small intestine, but this segment has some unique
ischemic lesions that can be difcult to evaluate. The
small colon seems very sensitive to pressure necrosis at
the site of a focal impaction, and resection is indicated
for segments with black and green discoloration. Also,
the entire small colon proximal to an obstruction
should be examined because it is not unusual for an
impaction to move distally and reimpact at several sites,
causing scattered areas of mural necrosis.
Enterotomy, resection, and
anastomosis techniques
NL UCfm6
INTRODUCTION
Enterotomy, resection, and anastomosis are basic pro
cedures used to surgically treat horses with a variety of
gastrointestinal diseases. The indications for the use of
these procedures will be covered in the following chap
" ters where specifc disease entities are discussed.
In the last 20 years many studies have provided
equine surgeons with signifcant information, thereby
increasing the success of abdomin
a
l surgery.
Information is now available on the preferred location
of intestinal incisions, some factors associated with the
occurrence of obstructive intra-abdominal adhesions,
1 68
and measurable effects of various suture patterns and
materials. The introduction of new synthetic suture
materials, development of stapling instruments, and
institution of early surgical intervention have paralleled
these studies. All these factors have contributed to the
reduced morbidity and mortality of horses with 'surgi
cal colic' . Yet, in many of the decisions to be made at
surgery, there remain considerable preferen.ces of the
surgeon, both in the interpretation of the available data
and in the techniques to use. Whenever possible, this
chapter will focus on the techniques that are supported
by facts, and it will limit itself to a few of the more com
mon alternatives. The introduction of laparoscopic
techniques has forced some changes in surgical proce
dures, and will likely transform these procedures in
years to come.
SUTURE MATERIALS
A variety of suture materials can be used and to some
extent the choice of which material to use is based on
the surgeon' s preference. Intuitively monoflament
suture materials are superior to multiflament materials
because they have less likelihood of capillary action that
might wick intestinal contents to the serosal surface. In
addition some suture materials such as chromic catgut
have been shown to be more inflammatory and increase
the risk of adhesion formation.
Non-absorbable suture materials are only used in
animals where delayed healing is expected because of
the nutritional status of the patient. A continuous pat
tern of these non-absorbable sutures is avoided in
young animals for fear the anastomosis site will not
enlarge as the animal grows and, therefore, will result in
a delayed stricture.
Exposure of suture materials at the serosal surface
increases the risk of adhesions at the anastomosis/
enterotomy site, and therefore small suture materials
are preferred (no. 00 or no. 000; 3 or 2 metric) .
The ideal suture material has not been conclusively
studied, but synthetic absorbable materials such as
polyglycolide, polyglactin 91 0, poly-p-dioxanone, poly
glyconate, and polyglecaprone 25 are recommended at
this time in procedures where staples are not used.
SUTURE PATERNS
The various suture patterns used for an intestinal anas
tomosis and enterotomy are shown in Figure 1O. 16a-h.
The effects of the suture pattern on an intestinal
enterotomy/anastomosis should be considered in the
light of several parameters, all of which have been
reviewed in many studies
the diameter of the intestinal segment at the site
its bursting strength
alignment of intestinal layers
the likelihood of inducing adhesions.
For optimal bursting strength two-layered anastomoses
are used.
In horses, exposed mucosa and seromuscular raw
edges have been associated with an increased risk of
b
I
SURGERY FOR COLIC (INCLUDI NG ANESTHESIA) 10
U
Figure 10. 16 Suture patterns used in equi ne i ntesti nal
procedures, a) si mpl e interrupted, b) si mpl e continuous,
c) Gambee - continued
1 69
10 COLIC
d
e
J
3 r
`

Figure 10. 16 Suture patterns used in equi ne i ntesti nal procedures continued the inverting patterns of d) Lember
(interrupted or continuous), e) Cushi ng continued
adhesion at the enterotomy/anastomosis site (Figure
1 0. 1 7) . Simple interrupted patterns, even the Gambee
technique, can result in such exposure. Therefore,
when apposing patterns are used, they are often over
sewn with an inverting pattern.
Exposed suture material also increases the risk of
adhesion at the enterotomy/anastomosis site. There
fore, inverting suture patterns in the seromuscular layer
result in less adhesions than interrupted patterns.
Small-sized suture material (no. 000 or 00; 2 or 3
metric) and less reactive material (avoid chromic
catgut) should be targeted.
Many surgeons feel that a simple continuous pat
tern results in more reduction of an anastomosis
diameter than a simple interrupted pattern. One
equine study found this to be untrue. However, if the
surgeon over-tightens the suture material in an effort
to obtain a leak-proof anastomosis, there is the poten-
170
tial for a purse-string anastomosis. Therefore, if a
simple continuous pattern is used it should cover only
one half of the anastomosis before being tied, and a
second continuous pattern should be used on the
remaining half.
Because maintenance of proper lumen diameter at
the enterotomy or anastomosis site is critical (especially
in the small intestine, pelvic flexure, and small colon) , a
double-inverting pattern or three-layered anastomosis
should be avoided.
In conclusion, to decrease the morbidity of entero
tomy/anastomosis procedures, the standard procedure
for hand-sewn anastomosis is a two-layer closure with
the frst layer closed with a simple continuous pattern.
Some surgeons prefer this layer to be in the mucosa
submucosal layer while others also include the sero
muscular layer in the intestinal layer. A second
inverting pattern is placed in the seromuscular layer.
h
SURGERY FOR COLIC (I NCLUDI NG ANESTHESIA) 1 0
9
-- .
Figure 10. 16 Suture patterns used in equi ne intesti nal pro
cedures - continued: the inverting patterns of f) Connell,
g) Schmeiden, h) Marshal l U
1 7 1
10 COLIC
Figure 10. 17 Adhesions at the site of an end-to-end
anastomosis performed with a suture pattern resulting in
exposed mucosa. Dr Rick Hackett, with permission
STAPLES AND STAPLING EQUIPMENT
^'>^1~<)`;^^:''!+`~'\I`'`-\''1l*))l) \&`^\&^`
`
`'~.P!` (FW:)y;};;:W\l' 8';y(`.`.`?'
When using staples, at least in adults, 4.8 mm staples are
preferable to 3. 8 mm staples because the closing height
in the former staples (2 mm versus 1 .5 mm) is preferable
given the thickness of a normal equine intestinal wall.
INTESTINAL PREPARATION FOR
ENTEROTOMIES AND ANASTOMOSIS
Following exteriorization, the intended enterotomy/
anastomosis site must be properly prepared to prevent
abdominal contamination by intestinal contents.
Barrier drapes are placed surrounding the abdominal
incision as part of the normal surgical incision draping
in order to prevent the fluids that are being used to
keep the exteriorized intestine moist, from soaking
through the drapes into non-sterile areas. Therefore,
after the intestinal segment that requires incision or
resection has been exteriorized, the remaining bowel is
replaced in the abdomen. The surgeon should leave
sufcient bowel exteriorized away from the incision to
prevent abdominal contamination from spillage of
intestinal content. A moist towel is placed under the
intended enterotomy/resection site and used to isolate
it from the normal exteriorized bowel and the sterile
surgical feld.
If signifcant splatter of intestinal content is
expected during the enterotomy/resection procedure,
an impervious drape should be used to prevent abdom
inal contamination; and the exposed bowel should be
irrigated frequently to prevent adherence of intestinal
contents to te serosa.
172
If the enterotomy must be made near or into the
abdomen (i. e. right ventral colon enterotomy) , an
impervious drape is sutured to the bowel around the
intended intestinal incision site using a simple continu
ous pattern.
ENTEROTOMIES
The enterotomy site is determined by the site and type
of lesion. The purpose of the enterotomy is to evacuate
the contents of a section of bowel or to allow entry of an
instrument, lavage device, or the surgeon's fngers or
hand into the intestinal lumen to remove an obstructive
lesion such as an enterolith, foreign body, or impaction.
More rarely, an enterotomy is made to help assess the
viability of an intestinal segment by inspection of the
mucosa or to allow biopsy of a mural anomaly.
Many investigators have studied the ideal location
within each intestinal segment for an enterotomy. In
the large intestine, antimesenteric band enterotomies
are quicker to heal, have less inflammation, and result
in more accurately apposed intestinal layers with a
higher bursting strength than enterotomies through
the sacculations. Equally important, enterotomies adja
cent to tenia bands result in a narrower lumen and a
predisposition to postoperative obstruction at the anas
tomosis site. Because of the thickness and line of ten
sion of the longitudinal muscle fbers forming the tenia
bands, transverse closure of an enterotomy made on the
tenia is likely to result in an unwanted increased tension
at the suture line. Table 10. 4 summarizes the current
recommendations regarding enterotomies in horses.
ANASTOMOSIS
General considerations
The length of intestine that can be resected without
special dietary modifcation is still a matter of conjec
ture. The concern is that extensive intestinal resection
can result in 'short bowel syndrome' where a decrease
in absorptive surface leads to carbohydrate, lipid, and
mineral malabsorption. resulting in weight loss and
poor performance. It has been shown that resection of
60 per cent of the small i ntestine in a normal pony can
result in malabsorption syndrome. However, the length
of a strangulated small intestine can increase up to 25
per cent, making the true length of small intestine
resected less clear. Clinical experience has revealed that
resection of up to 50 per cent of the small intestine
does not interfere with normal intestinal function.
Furthermore, there are anecdotal reports suggesting
SURGERY FOR COLIC (I NCLUDI NG ANESTHESIA) 10
Intestinal
segment
Location of enterotomy Diredion of cloure
Small intestine Al ong the l ong axis opposite the
mesenteric attachment
Transverse closure to
mi ni mize stricture
Cecum At the apex on either side of the
dorsal bands to prevent postoperative
contact between enterotomy and
incision site
Longitudi nal closure
Large colon Along the l ong axis opposite the
mesenteric attachment and on the
anti-mesenteric band when possible,
avoid pelvic flexure to mi ni mize
l umenal stricure
Longitudi nal closure
Smal colon On the anti mesenteric band Longitudinal closure
that possibly up to 70 per cent of the small intestine
length can be resected with enough residual small intes
tine to adapt sufciently to maintain appropriate diges
tive function. The ventral and dorsal colon can be
resected up to the level of the cranial aspect of the
cecocolic ligament, the colon adapts by increasing the
absorptive (inter-crypt) area of its remaining length,
allowing normal colonic function. It is unclear how
much small colon can be resected, but clinical experi
ence suggests that the small colon resection limit has
not been identified yet.
If signifi cant fluid and gas is present in the intestines
proximal to the intended anastomosis site, the intesti
nal content should be evacuated through an entero
tomy in the section of intestine to be resected. To avoid
tearing the mesentery during the milking of intestinal
content, the mesentery of the affected bowel is not
transected until the evacuation is complete. This is not
always possible since the mesentery of the affected
bowel may need to be transected so the intestine can be
moved away from the incision. Evacuation of intestinal
content has three objectives
I . to help identit the margin of resection needed
2. to minimize contamination of the surgical site and
abdomen during transection and anastomosis of
the intestine.
3. mimimize postoperative ileus
The section of intestine to be resected must have clear
viable margins and be near an intact blood supply. The
section to resect is chosen based on
1 . viable margin in the small intestine or small colon
2. proximity of the next vascular arcade.
The surgeon should target 30-50 cm of normal intes
tine on either side of the non-viable intestinal segment.
The mesentery segment is transected by starting the
intended line slightly distal to the first vascular pedicle
(Figure I D. 18) . One should be careful to leave 1-2 cm
of normal mesentery beyond the remaining vessels to
prevent their inadvertent puncture during closure of
the mesentery (Figure ID. 18) . This is especially impor
tant in the small colon mesentery where fatty tissue
interferes with identifcation of mesenteric vessels. The
goal is to resect as much compromised mesentery as
possible while allowing complete closure of the mesen
teric defect. Each mesenteric vessel is either double
Figure 10. 18 Mesenteric resecti on in preparation for
intesti nal anastomosis. Note that 1 -2 em of normal mesen
tery i s left beyond the remai ni ng vessels to prevent their
i nadvertent puncture duri ng closure of the mesentery
1 73
10 COLIC
ligated with no. 00 (3 metric) synthetic absorbable
suture material or stapled with an appropriate stapling
device. If the vessel ligation must be placed in thick
ened, edematous mesentery, larger suture materials
should be used and the stapling device avoided. When a
long section of mesentery must be resected, it is possi
ble to lose proper alignment of the intestinal segment.
This can lead to an inadvertent 180 degree rotation of
the anastomosis. To prevent such an occurrence either
of the following two techniques can be used.
1 . During ligation of the frst mesenteric vessel, one
suture end is left long, clamped by a hemostat, and
placed in an Allis tissue forceps (Figure 10. 19) . The
following mesenteric vessel ligation sutures are
treated similarly until all are incorporated
successfully into the Allis tissue forceps.
2. The defect in the mesentery is closed frst. The
mesentery is closed leaving approximately 15 cm of
unsutured mesentery to allow appropriate access
during the anastomosis procedure. Two methods
174
Long suture
grasped by
hemostats
Ligature
can be used to close the mesentery using no. 00 or
no. 000 (3 or 2 metric) synthetic absorbable suture
material
In most cases, the surgeon can start in the middle
of the mesenteric defect and close the defect
toward the intestine using a simple continuous
pattern (Figure 1 0. 20)
In extensive small intestinal resection where large
mesenteric defects are created, the surgeon can
start at one end of the mesenteric defect and
gather the mesentery in an 'accordion-like'
fashion toward the other side of the mesenteric
defect (Figure 10. 21 ) .
After the anastomosis is completed, the remammg
mesenteric defect is closed with a simple continuous
pattern using an absorbable suture material.
Following evacuation of the intestine or the move
ment of fluid and gas content, the flow of ingesta, oral
and aboral ( 20-25 cm) from the intended line of
intestine transection, is blocked by the placement of
Figure 10. 19 One end of the suture
used for mesenteric vessel ligation is
clamped with a hemostat and i ncor
porated i nto an Al l is tissue forceps.
Subsequent sutures are i ncorpo
rated i n order, preservi ng the order
of mesenteric vessel l i gati on
Cut end of
small intestine
Figure 10.20 The mesenteric defect is closed toward the
i ntesti ne usi ng a si mpl e continuous pattern. A 101 5 cm
section of i ntesti ne i s left unsutured to facil itate the
anastomosis
NE5EDIEQ
intestinal clamps (e. g. Doyen or Glassman) or encir
cling Penrose drains (Figure 1 0. 22) . All instruments
capable of serosal damage can induce adhesions and
the author prefers Penrose drains because they are the
least traumatic. The intestinal clamp or the Penrose
drains should be removed as soon as the anastomosis
appears leak-proof, this is usually after the first layer of
anastomosis is completed.
The surgeon must decide which anastomotic proce
dure to perform. Although much information has been
published on equine intestinal anastomosis, the ideal
technique has not been identifed, probably because
many techniques are successful and the type of anasto
mosis has no efect on survival rate according to at least
one study.
Hand-sewn anastomoses
One advantage of hand-sewn techniques is the ability to
perform an end-to-end anastomosis that physiologically
approximates normal intestinal transit most closely. In
addition, a hand-sewn anastomosis is readily adaptable
to various thicknesses of intestinal wall, leading to a
secure anastomosis in most conditions. The disadvan
tages are associated with an inherent increase in conta
mination associated with open bowel procedures that
require more manipulation of the intestines and result
in more foreign bodies at the anastomosis.
Figure 10.21 The mesentery is sutured in an
accordion-l ike pattern to prevent formation of
a mesenteric defect
Figure 10.22 The flow of i ngesta in the proxi mal and di stal
intestine is arrested usi ng Penrose drains 2025 cm away
from the intended l i ne of transection to prevent i nadver
tent contami nation duri ng enterotomy or anastomosis
procedures
175
10 COLIC
_ -------
--- /
Figure 10.23 The intestine i s transected at a sl ight angl e to
ensure that the anti-mesenteric intesti nal wal l retai ns ade
quate perfusion since it i s the intesti nal section furthest
from its blood supply
Once it has been decided to use a hand-sewn anasto
mosis, the intestine is transected at a slight angle so the
antimesenteric side is shorter than the mesenteric side
(Figure 1 0. 23) . This ensures adequate blood flow to the
area of intestinal wall most distant from the blood sup
ply. The open end of the intestine is covered by moist
gauze until the next transection is done.
Stapled anastomosis
The major advantage of the stapling technique is asso
ciated with the closed nature of the anastomosis that
limits potential contamination. In addition, the B
shaped configuration of the staple closure yields better
tissue blood flow. Speed of technique and decreased tis
sue handling have often been mentioned as advantages
of the stapling technique, but these advantages are
negated if the stapled line is oversewn. The main disad
vantages of the stapling technique are the cost and the
need for familiarity with the use and pitfalls of the
equipment, and the inability to create end-to-end
anastomosis.
Standard types of anastomosis
Anastomosis at specifc sites, such as jejunocecal or
jejunocolic anastomoses, is discussed in the respective
chapters covering diseases of these sites. The following
section focuses on the general principles used in equine
intestinal anastomosis.
There are three main types of anastomosis
end-to-end
end-to-side
side-to-side.
1 76
In all small intestine and small colon procedures,
end-to-end or functional end-to-end anastomoses are
preferred. End-to-side procedures are sometimes used
for jejunocecal anastomosis. Side-to-side anastomosis
are more commonly used for jejunocecal, colocolonic
anastomosis and for jejunocolic anastomosis (in cecal
bypass procedures) .
cO0-ID-0O08O85IDmD5/5
This procedure can only be done at the time of writing
using a hand-sewn technique unless the end-to-end
anastomosis stapling instrument is used. Staple anasto
mosis is not recommended because of the resulting
small-diameter anastomosis with the current stapling
instrument (EEA) .
The anastomosis is started at the mesenteric side.
The site is critical because bleeding and swelling asso
ciated with the transected mesentery can make it diffi
cult to identif the intestinal layers at this site. After
the knot is tied at the mesenteric site, one end of the
suture is left long and clamped with a hemostat. A stay
suture is placed at the antimesenteric side joining
both ends of the transected intestinal segments. This
divides the intestine into two equal halves. Using the
needle end of the suture placed at the mesenteric
attachment, the near side is closed using the surgeon's
preferred apposing pattern, usually a simple continu
ous pattern through all layers. The suture is tied when
the antimesenteric stay suture is reached. The intes
tine is rotated and a second strand of suture material
is used to finish the frst layer using the same pattern
(Figure 1 0.24) .
Figure 10.24 After the fi rst half of the anastomosis is com
pleted, the intestine i s rotated and a second strand of
suture material i s used to fi ni sh the fi rst layer using the
same pattern
cO0ID-5/00 8O85IDmD5/5
This procedure is done using a hand-sewn technique.
Occlusion of the flow of ingesta can be done with a
Penrose drain for the small intestinal segment but must
be made with an intestinal clamp for the large intestinal
segment (Figure 1 0.25) . If the proximal intestinal seg
ment needs to have its lumen enlarged. a longitudinal
Figure 10.25 End-to-side anastomosis, occl usi on of the
flow of i ngesta may require the use of an intesti nal cl amp
if it i s performed between the smal l and large intestine
Cecum
Incision i n cecum for
anastomosis
Small
intestine
Figure 10.26 End-to-side anastomosis - a l ongi tudi nal i nci
sion i s made at the anti mesenteric side of the proximal
i ntesti nal segment to enl arge its l umen for a sufficient
length anastomosis
incision is made midway between the mesenteric and
antimesenteric side (Figure 1 0. 26) . These anastomoses
are started at the mesenteric side of the proximal
intestinal segment; again. after the frst knot is tied, one
end of the suture is left long and clamped with a hemo
stat. A stay suture is placed at the antimesenteric side
joining both ends of the transected intestinal segments
to divide the anastomosis into two equal halves. Closure
is performed as described above. To minimize distrac
tion force on the anastomosis, an additional Marshall
'u' suture is placed I cm caudal to the anastomosis site
where the anticipated line of tension is expected
(Figure 1 0.30) .
>/00-ID-5/00 8O85IDmD5/5
Hand-sen anastomosis
After transection of the intestine the open ends are
sutured as described in enterotomies. The bowel ends
are laid alongside each other (in the proper direction
to create, wherever possible. an isoperistaltic anastomo
sis. Figure 1 0. 28) . and a stay suture is placed at one end
of the intended incisional line. Another suture is placed
at the other end of the intended incision line, and a
simple continuous pattern is used to appose the sero
muscular layer of each intestinal segment. Once this
layer is completed, both intestinal segments are incised
parallel to this suture line, and the far layer of the anas
tomosis is closed with a simple continuous pattern
taking care not to over-tighten the suture creating a
Cecum
Marshall U sutures
Anastomisis
I l eocecal
fol d
Cecocol i c
fold
Figure 10.27 Si de-to-side hand-sewn jejunocecal anasto
mosis - 1 cm caudal to the anastomosis side where the
antici pated l i ne of tension i s expected, an addi tional cruci
ate suture is pl aced
177
10 COLIC
Figure 10.28 Si de-to-side hand-sewn intesti nal anastomo
si s -the intesti nal segments are overlapped and when pos
si bl e are pl aced i n such a way as to create an isoperistaltic
anastomosis
purse-string effect (Figure 10. 29) . At each end of the
frst layer, a Marshal ' u' suture is placed to reinforce the
corner of the anastomosis, and the near side of the
anastomosis is closed using a simple continuous pattern
oversewn by an inverting seromuscular pattern (Figure
10.30) .
Stapled anastomosis
Since the bowel has been previously transected with sta
ples using the gastrointestinal anastomosis or tissue
anastomosis instruments, the bowel end does not need
to be closed, and the potential for contamination is
avoided. The stapled intestinal end has exposed
mucosa and seromuscular layers and should be over
sewn with an inverting pattern. A stay suture is placed in
the middle of the intended anastomosis site to lift that
section of intestine. Using a no. 10 Parker-Kerr blade, a
stab incision is made at the antimesenteric side into
each intestinal segment to be anastomosed (Figure
1 0. 31 ) . Each arm of the GI is inserted into the lumen
and directed toward one end of the intended anasto
mosis site (Figure 10. 32) . After the instrument is fred,
it is withdrawn, loaded with another cartridge, and rein
serted in the opposite direction. It is critical that the
instrument be fred across the previous staple line on
the far side of the anastomosis (Figure 1 0. 33) . If this lat
ter procedure is not done, a leakage will occur at the
intersection of the two staple lines. The instrument is
withdrawn and the anastomosis line is inspected for
1 78
Figure 10.29 Si de-to-side hand-sewn i ntesti nal anastomo
si s - after seromuscular apposition of the far side of the
anastomosis i s completed, both intesti nal segments are
incised paral l el to thi s suture line and the far layer of the
anastomosis i s closed with a si mple continuous pattern
Figure 10.30 Si de-to-side hand-sewn smal l intesti nal anas
tomosis - the near side of the anastomosis i s cl osed using
a simple interrupted pattern oversewn by an invering
seromuscular pattern
integrity. The defect where the instrument was inserted
is usually sutured closed as for an enterotomy, but a line
of TA staples can be used to close this defect as well.
The staple lines are inspected for integrity and are over
sewn if deemed necessary. A in a hand-sewn anastomo
sis, to minimize distraction force on the anastomosis, a
Marshal ' u' suture is placed 1 em caudal to the anasto
mosis side where the anticipated line of tension is
expected.
Mesentery
Figure 10.31 Si de-to-side stapl ed anastomosis - using a no. 1 0 Parker-Kerr blade, a stab i nci si on i s made into each i ntesti
nal segment to be anastomosed
Figure 10.32 Si de-to-side stapl ed anastomosis - each arm
of the GIA stapl i ng instrument i s i nserted into the l umen
and di rected toward one end of the intended anastomosis
site
Figure 10.33 Si de-to-side stapl ed anastomosis - the
stapl i ng instrument (GIA multifi re) i s appl ied in the oppo
site di rection maki ng sure that the i nstrument i s fired
across the previous stapl e l i ne on the far side of the
anastomosis
179
10 COLIC
uOCI/DO8l0O0-ID-0O08O85IDmD5/5
This procedure is done with stapling techniques only. It
has been termed a functional end-to-end because of its
gross appearance as the anastomosis matures (Figure
1 0.34) . However, motility following functional end-to
end anastomosis is akin to that of a side-to-side anasto
mosis and the motility pattern is inferior to an
end-to-end anastomosis. The author prefers this type of
anastomosis because it is closed and the result is a larger
lumen, which is associated with less postoperative ileus
than sutured end-to-end anastomosis.
Figure 10.34 Functional end-to-end anastomosis in the
smal l colon 3 weeks postoperatively. Note the end-to-end
appearance of the smal l colon at this early ti me postoper
atively. The horse was euthanized for unrel ated reasons
180
A 1 cm section of the antimesenteric corner is cut
with straight Mayo scissors and each arm of the CI sta
ple introduced into each intestinal segment, being care
ful to direct the anastomosis toward the mesentery
(Figure 10. 35) . After the instrument is fred, another
cartridge is loaded and the instrument is fired again to
create a stoma approximately 1 . 5-2 times the diameter
of the intestinal segment (Figure 10.36) . The introduc
tion site of the stapling instrument is closed with a line
of staples or hand sewn. In earlier descriptions of this
technique, veterinary surgeons would oversew this seg
ment, but it was found that this inversion can lead to an
intussusception. Instead, the author recommends
covering the exposed mucosal edge with a fold of
mesentery (Figure 10. 37) .
CONCLUSION
Because of the time period required for enterotomies
and anastomoses of the large colon, the speed associ
ated with a stapling instrument is a signifcant factor.
However, edema present in many disease processes
affecting the large colon may prevent the use of staples
where time may be most important. When an intestinal
procedure is performed in horses, a two-layer closure is
standard with the second layer sutured in an inverting
pattern. Most incisions are made on the antimesenteric
side, and when applicable, centered on the tenia bands.
Since the performance of an enterotomy or anastomo
sis increases the risk of intra-abdominal adhesions, the
surgeon should consider coating the anastomosis site
Figure 1 0.35 Functi onal end-to-end anastomo
sis - the arm of the GIA stapl i ng i nstrument is
i ntroduced into the anti mesenteric openi ng
created i n each i ntesti nal segment. Care must
be taken to di rect the anastomosis toward the
mesentery
Line of
mesenteric apposision
with carboxymethylcellulose or an absorbable adhesian
barrier (Interceed, Ethicon, Inc, USA) (see Surgical
exploration of the abdomen) .
Cl osure of the abdomen
NL UC|mP
INTRODUCTION
The goals of abdominal closure are to obtain a secure
apposition of the strength layer of the incision, and to
Figure 1 0.36 Functional end-to-end anastomosi s
the arm of the GI A stapl i ng instrument i s re-intro
duced into the intesti ne to i ncrease the length of
the anastomosis
Figure 10.37 Functional end-to-end anastomosis - after
the anastomosis i s completed. the mesentery i s closed
with a si mpl e continuous pattern using an absorbable
suture material (no. 000; 2 metric). Care is taken to cover
the exposed i ntesti nal edges with a fold of mesentery
duri ng mesenteric closure.
prevent incisional seromas/hematomas and contamina
tion, so that primary closure occurs unimpeded. Factors
that influence healing of such incisions can be divided
into
physiological status of the patient
(hypoproteinemia, old age, etc.)
status of the wound (degree of contamination,
repeat incisions, suture considerations (i. e. tpe,
pattern) ) .
Although the surgeon has little influence on patient
factors, he/she can influence wound factors that
affect the prevalence of some incisional complications.
Complications of incisional closures include
181
10 COLIC
dehiscence
infection
drainage
hernia.
For example, incisional dehiscence can occur because
the sutures break or cut through tissue, knots slip, or
there is premature degradation of the suture material.
The surgeon can influence the prevalence of incisional
dehiscence, as well as other incisional complications, by
selecting an appropriate suture material and pattern for
abdominal closure, based on the incision status, and the
size and physiological status of the animal. Since an
incisional infection increases the risk of hernia from
6-1 7 times, it is worth making every effort to prevent
incisional contamination. Incisional infection rates
increase with open bowel procedures, probably because
of inadequate prevention of incisional contamination.
Prior to closing the abdomen, contaminated instru
ments must be discarded and the surgeon must don a
new gown and/or gloves if they are contaminated. All
overlaid small, contaminated drapes around the inci
sion should be removed. If contaminated drapes are
well secured, their removal could result in incisional
and abdominal contamination. Therefore, well-secured
contaminated drapes should be covered by new sterile
imperious drapes. Any incisional contamination
should be lavaged with sterile physiologic solution con
taining appropriate broad-spectrum antibiotics.
Aside from the obvious consequences of incisional
dehiscence and hernia, i ncisional drainage and infec
tion increase hospitalization time and are associated
with increased costs. The purpose of this chapter is to
review the surgical factors for incision closure that influ
ence the prevalence of incision complication rates.
SUTURE MATERIALS
The goal is to re-appose the strength layer of each inci
sion with suture material at least as strong as the linea
alba (Table 1 0. 5) .
However, currently there is no known suture mater
ial as strong as the linea alba. The suture materials'
strengths are shown in descending order in Table 1 0. 6.
Chromic catgut should be avoided in incision closures
because the material' s rapid loss of strength leads to an
unacceptable complication rate.
Given the strength of polyester suture material and
the signifcant tension on equine incisions, these non
absorbable sutures were commonly used in the past.
However, many equine abdominal surgeries are clean
contaminated or contaminated procedures where the
risk of incisional contamination or infection is
182
Incisions
Ventral midline
Ventral paramedi an
Paralumbarllank
17th or 1 8th rib
resection
Strength layr
Linea al ba
External sheath of recus
abdominis muscle
External oblique abdomi nis
muscle and its aponeurosis
Externi and i nterni
i ntercostales muscles and
external oblique muscle.
The adjacent ribs can be
i ncorporated in the closure.
increased. Since infected non-absorbable suture materi
als create permanent suture sinuses, non-absorbable
suture material should be avoided. Although suture
sinuses have a low morbidity, their removal is generally
required to resolve a draining tract. Furthermore, a sur
gical revision may require mesh placement to manage
an incisional hernia, and a suture sinus can force a
delay or an additional surgical/anesthetic procedure to
resolve the infection process. Absorbable sutures are
therefore preferred, and no. 2 polyglycolic acid and no.
3 polyglactin 910 are the next strongest sutures to use.
Suture material Breaking strength
mean 'SE'
(ewons)
5 Polyester multifilament braided 270.5 7.3
2 Polyglycolic acid multifilament 213. 5 2.8
braided
3 Polyglacin 910 multifilament
braided
2 Polydioxanone monofilament
2 Polypropylene monofilament
1 Polyglycolate monofilament
2 Nylon monofilament
209.1 7.8
1 57.8 6.1
1 37.2 3.2
14. 1 3.7
1 13.0 7.0
Means with diferent supercripts are significantly different
from one anoher (P 0.05)
A well as the in-vitr data reported in Table 1 0.6, there
is ample clinical experience to indicate that the
strength of these synthetic suture materials (no. 2 poly
glycolic acid and no. 3 polyglactin 910) are suffcient for
secure abdominal closure. Their multiflament nature
increases the risk of suture sinus formation, but when
the suture material degrades the infection resolves. The
monoflament sutures are weaker and have a higher
rate of knot slippage because of their lower coefcient
of friction, but the absorbable monoflament sutures
may be acceptable in situations such as infected or con
taminated wounds in lighter weight animals. The non
absorbable monoflament suture material in horses, as
in humans, is less than ideal. Nylon is weaker and
polypropylene has been associated with suture sinuses,
although its strength is similar to polyglyconate and
polydioxan suture materials.
Absorbable mono- or multiflament sutures are also
generally used to close the other layers (no. 2 for mus
cular and no. 0 for subcutaneous tissues) . Skin incisions
are usually closed with staples for increased speed. Two
exceptions to the use of skin staples occur when
the incision is compromised to a degree that
evisceration during recovery is possible
a flank incision through the 1 8th rib resection has
been done.
These incisions are intrinsically weaker and are associ
ated with a higher complication rate than others. In
these situations the author recommends closure of the
skin incision with monoflament sutures (no. 1 or no. 2)
in a continuous pattern protected with an oversewn
stent bandage.
SUTURE PATERN
The peritoneum is only closed in standing laparotomy
to minimize the possibilit of air escaping the abdomen
postoperatively and reaching the subcutaneous tissue.
The incision strength layer (Table 1 0. 5) can be closed
by selecting one of many suture patterns: simple
interrupted, cruciate, and simple continuous. Bio
mechanically, the continuous suture patterns are
stronger than simple interrupted patterns, but the
cruciate and near-far-far-near patterns have not been
critically evaluated in horses. Although biomechanical
studies identifing the strongest abdominal closure in
horses are incomplete, clinical studies i ndicate that
near-far-far-near suture patterns should be avoided,
because they are associated with an increased risk of
incisional drainage and infection. The author prefers to
close an incision in two or three sections of simple con
tinuous pattern. The other layers (fascial, muscular,
and subcutaneous) are also generally closed with a
simple continuous pattern.
Perhaps more important than the suture pattern is
the bite size. The optimal bite size for closure of the
strength layer of an adult equine incision is 1 5 mm from
the incisional edge.
INCISIONAl PROTECTION DURING
RECOVERY
A critical postoperative time for the surgical incision is
immediate recovery, since the incision is not yet pro
tected by a fbrin seal and is, therefore, exposed to con
tamination because of its proximity to the floor and the
likelihood of urine and other recovery stall contami
nants. For this reason, the author suggests placing a
sterile stent bandage, secured with non-absorbable
sutures placed in a simple continuous pattern, over the
incision. The stent and skin are then covered by an
adhesive, impervious drape extending at least 10 em on
all sides of the incision (Figure 1 0. 38) .
Since the stent increases the risk of incisional infec
tion by harboring blood and incisional drainage mater
ial in a milieu adjacent to the incision, it should be
removed immediately if it becomes wet or contami
nated, and within 24 hours in almost all other cases.
The flank/rib resection incisions are the exception
Figure 10.38 Ventral abdomi nal incision i mmedi ately post
operative. Note the stent bandage suture over the incision
for tension rel ief and i mpervious i odi ne-i mpregnated
drape appl ied over the i nci si on site
1 83
1 0 COLIC
where a stent can be kept for 5-7 days if changed daily,
because the incision tension increases the risk of
incisional seroma/hematomas.
CONCLUSION
Adherence to aseptic techniques and incisional closure
based on the biology of healing will influence the
suture material and pattern used. This should signif
cantly impact and lower the prevalence of incisional
complications, which can be as high as 37 per cent of all
abdominal incisions.
Repeat laparotomy
NL UCfmP
INTRODUCTION
Repeat laparotomy is required in up to 10 per cent of
horses undergoing surgery for acute abdominal pain.
An acute need for a repeat laparotomy is generally
based on
the persistence of ileus
a return of abdominal pain
a deterioration in cardiovascular status.
Indications for a delayed repeat laparotomy are usually
related to recurrence of the initial problem or associ
ated with the formation of obstructive intra-abdominal
adhesions. Evaluation similar to that made prior to the
initial emergency laparotomy, such as a thorough phys
ical examination and the assistance of judicious ancil
lary testing, are useful for the decision to re-operate.
Confounding variables associated with the previous
surgery and intensive supportive care complicate the
interpretation of the clinical and clinicopathological
data. For example
the acid-base status is usually more controlled
postoperatively because of intravenous fluid and
electrolyte therapy
pain may be attenuated by analgesics
cardiovascular status is better stabilized by various
medications that combat endotoxic shock.
However, rectal palpation of mild to moderately dis
tended loops of small intestine can be tolerable because
of the ileus, and cytological examination of the peri
toneal fluid is always abnormal perioperatively. Aside
from the financial implications that the attending vet
erinarian must balance in deciding whether or not to
184
re-operate, the knowledge that the incidence of many
complications, such as incisional infections, increases
while the long-term prognosis for survival declines in
horses subjected to repeat laparotomy must also be
taken into consideration.
HOW TO MAKE THE DECISION
Deviation from a normal postoperative recovery is an
important sign indicating the need to assess whether or
not a problem is present; appropriate measures may
then be undertaken in a timely fashion. Of course,
there is a significant range for 'normal' postoperative
recovery. Horses with necrotic bowel at the initial
surgery may take 2-3 days for their cardiovascular
system to return to normal, and older horses (> 15 years
of age) have a more prolonged persistence of elevated
heart rate (>60 bpm) postoperatively (>3 days) .
Abnormalities that are causes for concern are summa
rized in Table 1 0. 7.
The main indications for a repeat laparotomy are to
remove necrotic intestine or revise an unacceptable
anastomosis. Since the goal of perioperative intra
venous fuid therapy is to restore extracellular fuid
volume and normal acid-base balance, persistence of
anomalies may indicate a serious intra-abdominal prob
lem. For example, the packed cell volume should be
normal within 24 hours. Persistence of a signifcant
elevation in packed cell volume (> 50%) may be an indi
cation of signifcant endotoxemia, and the clinician
must be concerned that bowel necrosis and peritonitis
may be the source. Mural necrosis, associated with post-
Persistence of elevated hematocrit > 50% after 24 h
Hear rate el evation greater than 80 bpm for > 48 h
Clinical signs of persisent or deteriorating
endotoxemla for > 48 h
Divergence in the changes i n hematocrit (increasing)
and total plasma protei n concentration
(decreasing)
Elevation i n recal temperature
DepreSSion for more than 48 h
Abdominal distention
Severe abdominal pain
Persistent ileus (nasogastric reflux) afer 72 h
Hematological changes consistent with degenerative
left shif
Appearance of mixed bacterial contamination i n
previously 'aseptic' peritoneal fluid
ischemic degeneration or reperfusion injury, and anas
tomosis leakage both lead to intra-peritoneal migration
of intestinal contents and gram-negative organisms.
This leads to overwhelming absorption of bacteria and
endotoxins resulting in persistent endotoxemic shock.
In addition, the septic peritonitis resulting from the
abdominal contamination leads to a tremendous
amount of intravascular fuid and fibrin shift into the
abdominal cavit so dehydration and hypoproteinemia
occur. Therefore, any clinical or clinicopathological
evidence of persistent endotoxic shock warrants further
investigation. Ileus is a feature of abdominal surgery in
any species. However, persistent signs of ileus, such as
nasogastric regurgitation and abdominal distention, are
abnormal if the primary problem was minor or treated
early. and should always be evaluated if they persist
more than 72 hours. This is because ileus and abdomi
nal distention can be signs of intestinal necrosis, anas
tomosis complications, and improper electrolyte
balance. Therefore, any one or more of the abnormali
ties described in Table 10. 7 warrant further investiga
tion. The clinician must look for a reasonable
explanation for the abnormal postoperative course.
The clinician has an advantage in knowing the risk
factors in the postoperative period requiring revision
surgery (Table 10. 8) .
Any prior abdominal surgery may lead to obstructive
adhesions.
Judging intestinal viability is still very much an
imperfect science. Given the morbidity of intestinal
anastomosis, each surgeon must make a decision based
on apparent viability at a point in time, with the goal of
resecting only bowel that has vascular damage that will
proceed to necrosis or enough serosal inflammation to
result in abdominal adhesions. Sometimes the decision
f
a rpa
:
Compromised bowel not resected
I l eal stump not resected in horses with i leocecal
intussuception
Enterotomy and anastomosis i n compromised bowel
I l eocecal anastomosis
Smal l colon i mpaction treated without evacuation
of the large i ntesti ne
Incomplete abdomi nal exploration
Dead:
Primary conditions: nephrosplenic entrapment
large colon volvulus
cecal i mpaction/dysfuncion
is so difficult at the initial surgery that a 'second-look
laparotomy' is planned. Usually the decision is made
early in the postoperative period based on one or more
of the abnormal signs listed in Table 1 0. 7. Laparoscopy
can sometimes be used for these purposes, but it is not
commonly done because of
incomplete abdominal exploration with
laparoscopy
frequent abdominal distention in postoperative
colic which interferes with laparoscopic observation
concerns with the effect of abdominal insuflation
on a ventral abdominal incision.
SURGICAL PROCEDURE AND
REVISIONS
Acute repeat laparotomy
Preparations for a repeat laparotomy are the same as
for emergency laparotomy except
there is a more frequent need for a plasma
transfusion to combat hypoproteinemia
there is an increased rate of incisional
complications requiring special consideration
there is more frequent consideration for parenteral
nutrition because of the inherently longer feed
deprivation in these horses.
Usually the same incision is used. After appropriate
aseptic preparation, the skin sutures/staples are
removed using a separate instrument package. The
incision is cleaned with sterile physiological saline solu
tion and the surgeon dons a new glove. The subcuta
neous and fascia lata sutures are removed.
Exploration of the abdomen is targeted toward the
suspected area. The surgeon must be very careful not to
pull on any anastomoses as they may have been weak
ened by postoperative swelling. Instead, the bowel on
either side of the anastomosis is grasped and exterior
ized taking care not to apply any tension on the anasto
mosis. If an anastomosis is leaking, it is isolated
immediately by placing a sterile moist towel around the
site, and placing the area over an impervious drape.
The surgeon must then identit the cause of the anasto
motic failure. If it is associated with necrotic bowel, fur
ther resection is required. When no intestinal necrosis
is present, it is possible that only one or more sutures
are required to correct the leakage. However, primary
anastomosis failure is rare. Therefore, if necrotic bowel
did not cause the failure, it is important to carefully ver
it that there is no kink or abnormal tension on the
anastomosis because of its placement or orientation.
This is more often the case in ileocecal and jejunocecal
1 85
10 COLIC
anastomoses. Alternatively, there may be a more distal
obstruction present.
Another type of anastomosis complication is
impaction at the site. This is seen when
the lumen of the anastomosis is small and is further
reduced by postoperative swelling
a small colon enterotomy or anastomosis was
performed yet the large intestine was not evacuated.
In the former case the surgeon must decide if the
anastomosis should be enlarged or if removal of the
impaction by digital manipulation is sufcient.
Enlargement of the anastomosis can only be done by
incising between two simple interrupted sutures or
between the end and start of two continuous patterns,
as an incision between two points on a continuous anas
tomotic suture would be catastrophic (Figure 10. 39) .
One area prone to complication is the distal stump
of the ileum where viability may deteriorate because of
an associated transection of the ileal artery as part of a
distal jejunal resection (Figure 10. 40) . This is especially
true during treatment of ileocecal intussusception,
because the distal blood flow is often compromised in
these cases - mural blood flow from the ileocecal area
and the blood supply from the ileal artery branch of the
ileocecocolic artery.
Other obstruction sites encountered include an
internal rent as with incomplete closure of the ileocecal
fold or when a mesenteric rent extends dorsally near
Cecum
InciSion to enlarge
anastomosIs
Anastomosis
Figure 10.39 Enl argement of the jejunocecal end-to-side
anastomosis can only be done by i nci si ng between two
si mpl e interrupted sutures or between the end and the
start of two continuous patterns
1 86
Cecum
Medial
cecal artery
artery
JeJuno Ileum
Right
colle artery
Figure 10.40 Schematic drawing showing vascul ar supply to
di stal jejunum and i leum. A technical error that may result in
postoperative devitalization of the i leal stump i s transection
of the i l eal artery during the jejunal resection. This is espe
cially true during treatment of i l eocecal i ntussusception
the root of the mesentery. Although a dorsally extend
ing rent can be repaired, the procedure is difcult. One
needs to identif the two segments of bowel and apply
sufcient traction to tense the mesentery. Moist towels
must be placed into the abdomen to prevent acacent
bowel from obstructing the view of the surgeon. The
surgeon must place one hand on the backside of the
mesenteric defect to prevent inadvertent suturing of
adjacent structures. Using the aid of assistants and long
instruments, after retraction of the body wall, the sur
geon suctions peritoneal fluid, and sutures the defect
from dorsal to ventral. A assistant with a long-handled
needle holder is often needed to grasp the tip of the
needle, because the surgeon's one hand is unavailable
for any manipulation other than protecting the far side
of the mesentery. The size of the vessels near the cranial
mesenteric artery is signifcant, and extreme care is
needed to avoid them while closing the defect.
Delayed repeat laparotomy
Horses that are re-operated months after their emer
gency procedure usually have a different type of abnor
mality. The surgeon can use the surgical approach
of preference; the author prefers re-entering the
abdomen at the previous site unless a mesh is present,
when a mesh is present a parallel incision lateral to the
mesh is used.
Entry into the abdomen is more problematic
because adhesions to the previous incision may be
present. With a ventral incision, it is not uncommon to
find the apex of the cecum adhered to the incision.
Care must be taken to avoid entering the adhered viscus
during dissection to allow uncontaminated abdominal
exploration.
Problems encountered are usually related to the
presence of adhesions or a mesenteric rent defect and
are treated as described in Chapter 13. If recurrence of
the initial condition is seen (e. g. nephrosplenic entrap
ment, large colon volvulus, cecal impaction) , strong
consideration should be given to undertaking a more
permanent treatment, such as obliteration of nephro
splenic space, colopexy, and complete cecal bypass.
ABDOMINAL CLOSURE AND
POSTOPERATIVE CARE
Abdominal closure is similar to that for an emergency
laparotomy but requires care to avoid the frayed inci
sional edge. Sutures may need to be placed at a greater
distance from the incision edge for that reason. It is
unclear what is the ideal pattern and suture material
required for a repeat laparotomy closure. The author
prefers a simple continuous pattern (with absorbable
material) . Multiflament sutures should be avoided
because the condition of the body wall weakens the inci
sion, not because the suture materials fail. In addition,
given that the incidence of incisional infection may
be as high as 88 per cent in a repeat laparotomy, the
use of non-absorbable multiflament suture materials
becomes almost contraindicated.
Postoperatively, the author prefers to apply an
abdominal support bandage for these horses because of
the suture incision weakness.
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pressure in horses with strangulating and
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Purohit R C, Hammond L S, Rossi A, et al. ( 1 982) Use of
thermography to determine intestinal viability. Pmc.
Equine Colic Rs. Symp. 1 7-18.
Sullins K E, Stashak T S, Mero K N ( 1 985) Evaluation of
fluorescein dye as an indicator of small intestinal viability
in the horse. ]. Am. Vet. Med. Assoc. 186:257-61 .
Sullins K E, Stashak T S, Mero K N, McChesney A E ( 1986)
Intravenous fluorescein dye as an indicator of small and
large intestinal viability in the horse. Proc. Equine Colic Res.
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Van Hoogmoed L, Snyder] R ( 1 998) Intestinal viabilit. In
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Enterotomy, resection, and anastomosis
techniques
Archer R M, Parsons] C, Lindsay W A, Wilson] W, Smith D F
( 1 988) A comparison of enterotomies through the
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1 0 COLIC
Baxter G M, Hunt R], Tyler D E, Parks A H, ]ackman B R
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Beard W L, Robertson] T, Getzy D M ( 1 989) Enterotomy
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location and suture pattern Vet. Surg. 18: 1 35-40
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( 1 995) Jejunal intussusception: Complications of
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( 1 989) Vet. Surg. 18: 415-23
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1 88
Young R L, Snyder] R, Pascoe] R, Olander H], Hinds D M.
( 1 991 ) A comparison of three techniques of pelvic flexure
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Closure of the abdomen
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hernias in the horse: incidences and predisposing factors.
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Assoc. 210:78-81.
Ingle-Fehr] E, Baxter G M, Howard R D, Trotter G Wand
Stashak T S ( 1 997) Bacterial culturing of ventral median
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Factors affecting incisional complication rates associated
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Vet. Med. Assoc. 195:639-42.
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three horses. ]. Am. Vet. Med. Assoc. 207; 742-4.
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study of biomechanical properties of the adult equine
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Repeat laparotomy
H uskamp B, Bonfg H ( 1986) Relaparotomy as a single
therapeutic principle in postoperative complications of
horses with colic. Poceedings ojthe 2nd Symposium on Equine
Colic Research 2: 317-21 .
Ingle-Fehr] E, Baxter G M, Howard R D, Trotter G W,
Stashak T S ( 1 997) Bacterial culturing of ventral median
celiotomies for prediction of postoperative incisional
complications in horses. Vet. Surg. 26:7-13.
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evaluation of repeat celiotomy in 53 horses with acute
gastrointestinal disease. Vet. Surg. 1 8:424-31 .
1 1
Postoperative treatment and
complications
Postoperative monitoring
NG Ducharme
INTRODUCTION
Correct postoperative care after intestinal surge!' is
crucial to ensure the comfort of the equine patient.
Early recognition of clinical signs is essential for suc
cessful management of postoperative complications.
Th" intensive Circ discussed in this section is also rele
vant to horses under observation as possible surgical
candidates or under intensive medical care.
The important goals of postoperative care are
to return or maintain the cardiovascular status
to identif and manage ileus
to recognize promptly various postoperative
complications.
Th< various abdominal postoperative complications are
pam
ileus
peritonitis
anastomosis and enterOlOmy obstructions or failure
anterior enteritis
incisional problems
diarrhea.
Non-abdominal complications include
shock
hypoproteinemia
dehydration
laminitis
thrombophlebitis
lal)'ngospasm
laryngeal paralysis
h}poxic cerebral injul)'
wounds sustained during a colic episode
myopathy.
Immediatey upon recovery, the cardiovascular status
must be maintained with appropriate intravenous fluid
and plasma therapy. Csing acid-base and electrolyte
status combined \ith packed cell volume and total pro
tein concentration, the tye of intravenous fluid and its
administration rate is chosen (see Chapter 9)
Another signifcant consideration is postoperative
ileus. In horses this primarily small intestinal disease is
characteri_ed by reflux of intestinal secretions into the
stomach causing abdominal pain, this may result in
gastric rupture if left untreated. Ileus is commonly
seen after treatment of small intestinal diseases associ
ated with intestinal ischemia or severe inflammation
(Le. 'high risk' patients). It may also be seen after sur
gical treatment of large bowel disease. Postoperatively,
for prevention of ileus, the electrolyte status (including
calcium, potassium, and chloride) must be maintained
in phYSiological balance. The author does not rou
tindy feed horses (at 'high risk' for ileus), recovering
from imestinal surgery until the third day postopera
tively. It is important, on recovel)', to place a naso
gastric tube in these 'high risk' patients to evaluate the
presence of gastrointestinal reflux every 2 hours for
the first 24-hour postoperative period. Fluid is not
offered until naogastric reflux ha c,eased. A mall
amount of water (1-2 liters) is then offered every 2
hours for the next 12-24 hours. If the horse can cope
with oral water for that period, solid food is slowly
189
1 1 COLIC
reintroduced. It is reasonable to return to water and
feed intake as carly as possible within the first 24hour
postoperative period in patients at 'low risk' for ileus.
For early return to feed, water is olrered frs! as
described above, followed by a mouthful of grass or
handful of soft hay after a fw hours. Patients must be
monitored for ileus - elevation of heart rate and/of
return of abdominal pain are good indicators of the
need for nasogastrk intubation. Note that ileus may
not be obvious for up to 48 hours in the postoperAtive
period.
PROTOCOLS FOR MONITORING
PATIENTS
For appropriate intensive care, a rational plan must be
made to ensure an appropriate nature and frequency of
checks. The two monitoring protocols described in the
following paragraphs are used at the author's hospital.
Both protocols should be kept at the patient's side
1. Colic evaluations made every ___ hours
2. Medications
(attached to the stall door) for frequent consultation,
The use of protocols such as these allows the care givers
to provide the best quality intensive care for the patient.
The primar protocol rekcL the postoperative
treatment plan. This is outlined in Table 11.1, it
includes 'red flag' indicators that should trigger an
immediate veterinar evaluation and decision.
The actual lime of each evaluation, treatment, or
check ordered in the primary protocol (Table 11.1) is
recorded on the secondary colic protocol (Table 11.2).
The purpose of this protocol is to characterize the spe
cifc orders in the primary protocol (for example, time
medication i ;iminitererl, lime of na.ogaslric reflux
checks, etc.). Furthermore, it allows a rapid evaluation
of the progression of the patient's condition. A com
mon error in any protocol is to record a decimal alone
(for example . 9 mg/kginstead of O. 9 mg/kg). The former
should never be tolerated as it can be misinterpreted as
9 mg/kg if the decimal point is not seen. Finally, for
increased safety, it is best to indicate both the dose and
volume of medications to be administered.
.
) intravenous fluids type _ rate
b) non-steroidal anti-inflammatory agents dose time route
<)
antIbiotics
gram positive dose time route
gram negative dose time route
anaerobes dose time route
d) others (I.e. vasodilators) dose time route
e) motillty modifiers
3. Packed cel! volumeltotal protein concentration every hours
4. laboratory tests {other than PCV every __ hours
5. Suction nasogastric tube or check tor reflux every hours
6. Other instructions __
7. Contact the attending veterinarian if any of the following occurs
a) severe pain
b) heart rate greater than _
c) respiratory rate greater than_
d) packed cell volume greater than _or len than
e) total protein concentration greater than _or less than
f temperature greater than_
g) intravenous fluids cannot be administered at prescribed rate
h) nasogastrk tube is removed by horse or tube becomes obstructed
i) other
-Antibiotks with activity igalnst the following organisms hould be considered
190
Tae 1 1.2 Stdr colic ealuat
POSTOPERATIVE TREATMENT AND COMPLICATIONS 1 1
case number: Name: I Owner: I Clinician:
Date
Time
Rectal temperature
Respiration rate
Heart rate and character
Color of mucous membrane
Capillary refill time
Packed cell volume and total protein
Attitude/degree of pain
Gut motility (all four quadrants)
Feces and urine (charactertvolume)
Digital pulse (quality)
Medication
Fluid therapy
Flush catheter
Feed and water consumption
Gastric reflu)
Other comments
Treatment of endotoxemia
DM Ainsworh
PATHOPHYSIOLOGY
Endotoxin is a complex molecule comprised of
a lipid moiety (lipid A)
a core polysaccharide
repetitive units of O-specific polysaccharide.
As an integral component of the cell wall of gram-nega
tive bacteria, concentrations of endotoxin increase in
the surrounding milieu whenever bacteria undergo
periods of rapid growth or death. Systemic manifesta
tiOllS of endotoxemia occur when the intestinal
mucosal harrier is compromised, allowing endotoxin to
access the peritoneal ca,ity or systemic circulation. In
addition to enteric diea3e, horse with hepatic discae,
retained placcntas or metritis, hemorrhagic or hypo
volemic shock, pneumonia, severe trauma, and sep
tiu'mia are at risk for the development of endotoxemia.
Systemically, endotoxin activates numerous host
defense mechanisms, leading to the formation or
release of free radicals, lipid mediators (eicosanoids,
leukotrienes, platelet-activating factor), '-"tokines
(tumor necrosis factor alpha (TF.) , interleukin-l and
6 (IL-I, IL-6, and fac.tors involved in coagulation (tis
sue thromboplastin, plasminogen activator inhibitor
(PAl), tissue plasminogen activator (tPA), factor XII).
This endotoxin response, calied the systemic inflamma
tory response syndrome (SIRS), is a sellperpetuating
response which primarily targets the structural and
functional integrity of the endothelial ce!Is.
Manifestations of the SIRS include
fever
tachypnea
tachycardia
pulmonar hyertension
systemic hypotension
cardioV.scular collapse.
Imbalances in coagulation path\\'ays may cause
microvascular thrombi formation, tissue hypoxia, and
muhi-organ dysfunction or failure. Horses wth endo-
191
1 1 COLIC
lm.,cmia and SIRS are H increlVd risk for the dc\"C\op
Im:m of laminitis. g,mroimcnina[ ilels and diarrhea,
jugular I'eln thromlx)Sis. disseminated intular
cogubuiou (DIC, <nd rena failure.
TREATMENT PRINCIPLES
Tlu: trc7Hment optio05 fllr c:ndoloxcmia <I'
intrHvenous fluids
llon-teroidal anti-inflammilory drugs (NSAIDs)
biological prdtlcl and drugs which ncutrali7c
endntxin
KlunKorti(:()id
agent dircctt:d a!int central inflammatolT
mediators
free radi)al s(:av\:nKcr.
aillnctj\': therapies.
Intravenous fluids
The primar Irc;uneOI goal is l idelllifr and alleviate
(ifplKSihld the primlry inching eveol. Thereafter, sup
punil'l nlC'ltlIrcs designe to ('nmbat or prevent the
dC'dopmtnI of shock and 3|bOftissue perfsion arc
impiclllcllwd_ Ag't.\ivC in!nous f1uid-lherapy
T(-SlOre pla,ma volume and COntt cid-- imb
3nC( is imti{utt11 immcdiatd)-_ Depending on the
degree of cndotoxemia, imrwllOlIs c
l
't<l1oill thlrapy
at rd 01 !)- mllkg for the fir flO hours may initiall y
be IlccS$ary. III shocked hor_ hypertonic saline wlll
tinns (i.5%) given intran:nousl) (4 ml/kgJ over a
1:-20 minute peiod, are hcndidal but should be fol
lowed by intr,,'enous isotonic cItalloid solutions sup
plemented with puta.'illm chloride (20 mEq/I). If
!H:m(ldynamic renal failure dcvclops, intraveIlous
furosemide (0.5 mg/kg i.v., one or twice) and/or
dopamine infuiollS (2-5 pg/kg/min) are started. A
cndotoxcmic ho1e are often hypoproteinemic, over
aggressive fluid therapy may decrease plasma ollcotic
pressure, promoting Ihe development of wInni1 and
peripheral (cema. WI)('I) tOtal serum protein levels are
le!\ than 4f) gil (4.0g/dl: albumin 199/l or 1.9 g/dl),
fn.h or liol.en plasma or serum (sec below) should be
adcninistert'd \\11h the rali1.tion that the amount of
plama required 10 incrC3SC p$olein k-wIs hy I gldl may
exceed 10 litrs. Howt .. -r. 1-3 liufl of fresh or froM-II
plasma lIlay be beneficial in >upphing hOlh antitrom ..
hin III and fihronectin and in IIurrllg the deop
nWn! Hf C"o:tgulopalhies (sec belo",). Dxtrn 40
(10-15 ml/kj i.,. mer 30 min) or lIetast a.ch JO ml/kg
arc also beneicial in increasing plasma 11I1cotic pres
.mre in (ndoloxtmic horses.
192
Non . steroldal antlinfJammator drugs (NSAlDs)
Ouring cllciowxcmia. nllmhr.ne-bound phospholipltS
> acti\'Id, rdt4.inK arachidonic acid which 1
me t abolized by either
cyd,x)xYcnase (COX) to form prostaglandins
(PE, p(;F,, I>Gly) and thrombxane (), nc
lip!xcnasC (LOX), t Jorm Icukotrienes (I:r.,
ITt:" LTD,. and LTE,).
The lipid mcdiatnrs !xen potenl dkci on ,"a<(:ul'll"
and hronchial smooth muscle, on micro\"aS(:ul.lr I)('r
meahility, and on platelet and granulocyte function and
integrity. DurinK endotoxemia. increases in plasma
TXJ\ and PGI corrdate with the developmcnt of pul
monar hypertenon and systemic hyotension, respec
tively. Increasc in plasma PGF1 are also associated with
decreat: in lung function. the development of pul
monary hypetension and hypoxemia. ; on-steroidal
anti-infiammatol)' drugs (NSAIDs) are uscd to inhibit
or attlnuatc COX pathways lIld thus ameliorate the
eITects of endoLOxemia. Bas upon experimcntal
trials, !lunixin mcg!umine (0.2::0.5 mg/kg i.\'. two
three times daily) is more efectivc in antgonizing tht
drecl. of endotoxin-induced eicosanoid production
than OIher NSAlDs such as phen)lbulolle, dip)'ruue,
and ibuprolen. (In conu ... s t. phenylbutaHe, Uillike
fiunixin meglumine) does nut mask the Crciouiar
alterations that might otherwise p1l1ng a disioll for
surgk"al intervention.) Eltel1ac (0.5 IIIg/kg) is anllther
SAID which will all'iate s!me of Ih clinical allolab
oratory filldin of c(
l
uinc encioloxemia. Limited
experimental and dinica! data on kVloprJfn, touted <
both a COX and LOX inhibitor 5uggcst thal it i as clll
ca!:inliS as fiunixin meglumine in inhibiting increases in
prostagI3ndiu. mmor necrosis factor, and leukotrienes
when ketoprofen is giv!n al a dosage of 0.25-0.5 mg/kg
i.v. b.i.d. nr t.i.d. While ketoprofen has the touted
added beneft of inhihit.ing LOX, the relative impor
tance of the leuko!riencs in the pathophysiology of
enciotoxelllia has not heen determined in the eq;line
species. Bast-d on poJcine studies, these ararhidonir
acid metabolites playa minor role. Toxicit} studies sug
gest that kctnpmkn i less ukcJgni than phenylbu
tazonc or flunixin megtuminc. When I\SAIDs arc
administered In Cnd\lxmic foals, anti-ukel medica
tiuns sucll <famutidine (1 mg/kg p.o. s.i.d.) sucr lf,uc
(1-2 g p.o. t.i.d.) or ()mepral.Olc (Illig/kg p.o_ s.i.d_)
should he given ("(lIlcucrently.
Biological products and drugs that neutralize
endotoxin
It might be exptcted lhat administl<ttioll of
immunoglohulins l!irec.tcd against endo\xin would
either confer protection against the development of, or
Illitigate the existing signs of endotoxemia. Antibodies
formed against the conserved regions of endotoxin
(core of lipopolysaccharide) are produced llsing bacte
ria with mutations in the outer 0 polysaccharide region
which exposes the core region. Thus(;ommercial prepa
rations of hyperimmune serum or plasma containing
antibodies against mutant Erheirhia I:oli 05) or
Salmondfa typhimuriwn (Re mutant) haw been utilized.
Cnfortunatdy, data from equine trials have both sup
ported and refuted the therapeutic benefit of anti-ndo
toxin antibodies. In one double blind clinical study,
administration of 1-2 liters of plasma containing.J5 anti
hodies 10 horses \"ilh clinical signs of endotoxemia \,'as
associated with an increased sUD.ival rate (87% versus
!(Y. in controls), an improvement in clinical appear
ance, and a shorter duration of hospitalization when
compared with horses treated with pre-immun( plasma.
Yet, in experimental studies of sub-lethal endotoxemia,
treatment of foals with antij5 .m either
failed to improve clinical !dinicopathologic
parameters, or
was <ss(){:iated with a deterioration in the clinical
signs and rytokine response.
While it is difficult to compare these SlIIdies one for
one, differences in outcome may be at!ributcd to
differences in the volume and/or anti-endotoxin
titer
the nature of antibody developed and its <lvidity for
the inner core regions of native endotoxin
the IgG isorype produced (e.g. I gGa, IgGb, IgGc, or
Iget).
In addition, tbe presence of other products included in
lhe plasma - fbron(ctin, coagulation factors, and
antithrombin III - not present in the serum, may also
have contributed to the differtnces between the clinical
and experimental trials.
Another therapeutic approach to endotoxin inacti
\ar.ion, utilized in experimental trials and on a limited
clinical basis, entails the use of polymyxin B sulfate.
This cationic polypeptide antibiotic is purported to
bind to and neutralize lipid A. When polymyin B is
given at a dosage of 6 000 It] /kg of body weight prio to
{ndotoxin challenge, there is < reduction in the severity
of clinical signs of endOloxemia and in the magnitude
of the TNF" and 11.-6 response. Interestingly, in an
experimental endotoxin trial, foals pre-treated with
]xllymyin B fared better than those pre-treated with
Salmonela typhimurium hyperimmune sera. However the
use of Polymyxin B can be associated with the develop
ment of adverse eflects. Its binding aidiry to anioni{:
phospholipids of cell membranes makes it nephro-, oto,
and neurotoxic. Caution should be exercised with iL'i
use in endotoxemic horses at risk for the development
of hemodynamic renal failure. In an effort to minimize
drug toxicities (this require extravasation of the drug),
polymyxin B has been conjugated 1 dextran 70. When
this combination is given intravenously (4 g polymyin
Bextran conjugate/kg body wt) por to endotoxin
challenge, clinical alterations and elevations in
eicosanoids and cytokines are prevented. The poten
tially promising results of this study remain t be exam
ined in clinical cases with fulminant endotoxemia.
Glucocoricoids
Known for their membrane-stabilizing properties, the
administration of (orti(osteroids should reduce the
clinical signs of cndotoxemia given that these agents
prevent aggregation, adhesion, and degranulation
of neutrophils
stimulate liptXortin synthesis, an inhibitor of
phospholipase (and thus arachidonic acid
metabolism)
block complement acthJtion
attenuate cytokine secretion
inhibit inducible nitric oxide synthase
exhibit antioxidant efects.
Such eff ects should decrease capillary leakage and
prevent hypovolemia and t. he formation of interstitial
edema. However, in an experimental model of endo
toxic shock in anesthetized ponies, dexamethasone
(2 mg/kg) or prednisolone (IO mg/kg) administered
afe intravenous endotoxin were inferior to flunixin
meglumine in preventing eicosanoid synthesis and the
accompanying hemodyn<mic changes that occur dur
ing the frst 2 hours of endotoxin challenge. In
addition, their immunosuppressive effects and their
potential for precipitating laminitis makes glucocorti
coid usc less routine during endotoxin therapy.
Agents directed against central inflammatory
mediators
Several lines of evidence support the role of TN Fa as a
central mediator of endotoxin.
These include the fnd
ings that
1. TF is detected early in the circulation of horses
or foals following administration of
lipopolysaccharide
2. infusion ofT:IFa causes physiologic and pathologic
changes indisl.inguishable from those observed in
animals with endotoxemia
3. in mice and baboons, passive immunil.ation with
antibodies UTKFa confers protection <gainst the
193
1 1 COLIC
lelhal dftCl of endotoxin and intravascular
F,srh"rrla coi administr-uion
4. ill hUn];!n p<ljtnL Wilh mcningocuccal septicemia,
8tIU0TNF" icli\11), a useful prcdictoroffilaI
olltcome.
11ms, drus Ol biOlOg|l pJO0uc \D3l ClDCl rCOuce
the formation ofTNF" or 'nculr
.
lli drculaLing levls
of this cytokillC, have b'en SLUdicd.
"cnwxifyin<' is a melhylxamhinc dcrivaliw that, in
addition lO QOSQOUCSlCt inhibition, reduces ill
lJilm production I)f TF" by macrophage; exposed to
('nciotoxin. It 88O reduces neutrophil adhesion and
dcgr;llul;tion. decrt:asc superoxide rddical formation,
mp
J
lresse philR(:ytusiM, and inhibits lDcproduction of
illltrfrn amma, 1lJ, HAl, and tissue thrombo
phlstin. Pl:ntoxifllinc also impro\'cs dcformability of
nythmcytcs (rhcO!OgiC properties). In clinical cases of
cndntoxcmia, pcmoxifIIinc is administered (7.5 mg/
k p.o. b,i.d.) not only for il ami-TNF" effects, but aim
in an efort 1 improve the perfusion of the hoof
bminae (rheologic propenies). In experimental endn
IOl('mia models, pentoxifylline admininercd W min
ures arwr endotoxin ch .. l!en_c aU.enuatec endotoxin
iuducc. ."\ tempcr.ture and 1piIalOry rate cletiols
hut 11;11 IW dTect M ht'mawlogicaI parmeters or on
cicO'lloid and c}'t1ki0e (including TNFQ) production.
Clinic;1 tilL, examning lDC cflicacy of QcDOm @ll0C
in pJ<0linK laminitis have nOi DCCDconducted at the
lime f)f'riting.
t',xpcrimcntal trials have also examined the efk<lc),
of UdiniSte1ing antihodies directed against TNFa in
equine endotuxemil: mndd. In Miniature Horw., if
anti-TNFg antih()(lie (2 mg/kg of murine monoclonal
antibodies ditelcd :K"inst recombinant equine TNFg)
are given prior enommdn Challenge. an appreciable
amelioration of th: clinical and hcmatologic repomc
i found. Ho 1 if amiTNFg antibodics (O.l mg/kg
of rahhit. PQIyc10naI antibodies directed against recom
binant human TF ) ar aoministercd 15 minutes after
the start of endotoxin challenge, a beneficial effect >
lIot ollserveo. With additional experimental and dini
(:<11 trials anti-TNF lIlay prove useful during certain
siages or cndoloxemia in clinical c<e.
Free radical scavengers
J)urinl (ndOlOxemia. tC3LI oxygen spQci (ROS)
arc _ctIcIHIcO Dy(CliVdted phagoc)'lcs and b the imra
cellular xaDthine oxiO3s !ylr % hich is activated
(Urin_ ichcmic reperfuron injUr. ROS 1 atk
\inlt<1l1y all biTh<miLwl cell COmpnent hill polyunsat
urated rallY acids. located within lDc phospholipid
mcmhr<IlC stnl(ture of the cell and cellular organell,
< mOM susCptiblC to their effckts. ROS also LH1b
194
enl
.
yme inactivation, dp()lymerization of nucleic acids
and polrâcchatiOCs, and increases in capillary penne
ability and prostaglanUin pt1duction~
The laroids are 21ainosleroid CO0QUDU8 with
stctral si0ilatiliC t cortieoslCroids. They lack glu
COCOt0COtO Ot minClOrlicod eet It blied
thallhe lalaroids 1D$CtllDC0vCSpreferentially within
the mcmbnllc of the \".sc'Ular endOthelium and inhibit
lipid pernxidation, allenuate cylVkine production, sup
pre! the exprelSion of adhelion molecules, and inhibit
trdnSClldothelial neutrophil migration and activation.
Although cin$al lI3\$in CDOOlOXcm!Chorses arc lack
ing, trcatmCllt Oneonatal calves with tirilazad mesylate
(1.5 mg/kg i.v.), either priOr to or following endotoxin
challenge attenuated IDC dinical signs of endotoxemia
and suppressed tbe generation of TN Fa'
DimethyI$ulfoxidc (DMSO) is also classified as a free
radical scavenger and its use ha. been advocated in
numerous equine infl3mmatory conditions. Dosage
recommendations 3tdV3t3DC ranging from 20 mg/kg
i.v. b.Ld. to 1 g/kg Lv. .i.d. administered as a 10% solu
tion. Rigorous D1C3 or experimental trials reg-Jrding
its eficacy in equine endotoxcmia arc lacking. In an
expcrimcntal studr of neonatal calves challenged with
endotoxin, DMSO faile lO suppress eicosanoid pr
dtio0 or exert any QtOIcLlNC effeeLS against endo
f w. I0deed L3D'tS eWDibitCd p1lOngtn of
clinical fmp1omse, hyotension, and D@c03
cOmpard to lOC cOntls. In <II experimental tlldy of
reperfusion injury, DMSC (1 g/kg i.v. as a 10% slu
tion) was ineffective in providing a mucosal protective
df{.ct tl) the equine jejunum.
Two other agents that arc tDought til protec.t againsl
free n\dical ijl!ry include
1. allopurinol. an inhibitor of xanthine oxidase that
catl)'es the formation of super oxide anion from
uric acid
2. :\acetylcysteine, an &gent that replenishcs
glutathione, a 03_Otintracellular antioxidant.
Although allopurinol administration (50 rng/kg i.v.)
failed t prevent HUCOS3 !D_U(in anesthetized horses
with expcrimemally.indu(ed i'Chemic bowe! injury, in a
different study, the pre-treatment O!horses (50 mg/kg
i.v.) significantly reduced endotoxin-induced increases
in xamnine oxidase aClhiry. Clinical trials documenting
i.\ 4f4acy in endolm:(mia 3tC currently lacking.
:0 inforton is avilablC tc_'aIU0@ thC ef c of
Ncel}lcylDc (:AC) in the horse. In sUIne 8gLR
wt endmoxemia. NAC decreases neutph1l
plateletaggregating actiily, markedly 1cUUcCs pu.
monar hypertension, and aUenuUS vascular pre
ability CD8D@cS. In dogs, QICItCHlHCD\ with AC
(150 mg/kg i.v. followt!d by a 20 mg kg
-I
h-
I
infnsion)
increases glutathione peroxidase adivit, improve
myocardial function and tissue oxygen extraction, and
decreases T;Fa production.
Adjunctive therapies
Antibiotics
In many endotoxemic horses, a compromised intestinal
murosa enhances systemic absorption of endotoxin and
baCleria. This situation, as well as intravenous catheter
placement and fluid administration, provides portals
of entry for infectious organisms suggesting that
rndotoxic horses should receive antimicrobials.
Nevertheless, arguments both for ,lld against anti
microbial use can be made. The advantages of using a
broad spectrum antibiotic include prevention of
secondary complications snch as scpticemia, septic
phlt'bitis, and septic pulmonary, rcnal and hepatic
emboli. The major disadvantages to their usc include
exacerbation of dinical signs by increasing circu!at.ing
endotoxins, nephrotoxicosis, and alterations in gastro
intestinal flora producing diarrhea or secondary Ii. mgal
infections.
Depending on microbial sensitivity patterns for spe
cillL hospital or practice settinb' S, third generation
cephalosporins like ceftiofur (2.2-3.3 mg/kg i.v. b.i.d.)
alolle or in combination with sodium or potassium
penicillin (22 DOO Ill/kg i.v. q.i.d.) can be used initiaHy.
The aminoglycosides in combination with penicillin
can he used if renal function is not compromised (gen
tamicin 6.6 mg/kg i.v. s.i.d., amikacin 12-15 mg/kg i.v.
s.i.d.). Oxytetracycline (6.6 mg/kg in I liter of saline
administered slowly i.v. s.i.d.) is the treatment of choice
in endotoxemic horses with Ehrlichia rislici infections
(Potomac horse fever), but it has also heen associated
with toxic nephropathies. Metronidazole (15-25 mg/kg
p.o. h.i.d. to t.i.d.) is included in the therapeutic
n-gimen if anaerobic org-,misms are involved.
Therapies targeting gastrointestinal tract
function
Nasogastric intubation in horses with obstructive,
inflammatory, or strangulating bowel disorders
removes ingesta and prevents !<stric rupture. In adult
horses (450-!OO kg) with colitis, activated charcoal
(\-2 kg in several liters of water) . ;Ih or without the
addition of bismuth subsalicylate 0-2 liters) \;a na.o
gaslri( tube is used to decrease endotoxin absorption
and to inhibit inflammatory mediator production
within the intestinal tract.
In endotoxemia, ileus develops from electrolyte
alterations and from the generation of inflammatory
mediators. Thus, intravenous fluids should be supple-
mented with potassium chloride (15-20 mEq/l)
and/or calcium borogluconate (200 milS liters of
fuids) to correct potential electrolyte imbalances
contributing to gastrointestinal stasis. Intravenous
lidocaine bolus (1.3 mg/kg) toHowed by a 24 hour lido
caine drip (0.05 mg kg-I min-I) signifcantly decreases
reflux volume in horses with ileus. However, side effecs
of lidocaine administration include muscle fascicula
tions, ataxia, and delayed detection of laminitic pain.
Therapies preventing laminitis secondary to
endotoxemia
Although experimental studies fail to demonstrate a
defnitivc association between endotoxemia and the
development of laminitis, it is well recognized clinically
that such horses are at risk. A it has been shown exper
imentally that endotoxin chalknge alters nitric oxide
(vasodilatory) pathways in equine digital vessels, it is
likely that lipopolysaccharide contributes 1 the vascu
lar alterations observed in laminitis. I lorses with endo
toxemia are treated prophylactically against laminitis by
housing them in well-bedded stalls
providing frog support by taping lily pads to the
soles
applying a half-inch (I.3cm) band (IO-20 mg) of
2% glyceryl trinitrate paste over the digital arteries
daily
limiting carbohydrate intake.
Additional therapies include the administration of pen
toxifylline (7.5 mg/kg p.o. b.i.d., see above) and flu
nixin meglumine (0.25 mg/kg i.v. t.i.d.). Horses with
acute-onset laminitis benefit from the addition of anal
gesics (2.2-4.4 mg/kg phenylbutawne i.v. or p.o. s.i.d.)
and possibly by the addition of a ROS scavenger
(DMSO 0.1-1 g/kg, diluted as a 10% solution i.v. s.i.d
or b.i.d.) to their therapeutic regimen. Corrective trim
ming to shorten the toe is advocated in acute cases.
Therapies for horses with disseminated
intravascular coagulation (D|C)
in healt.h, the cndothelial cell surface provides a
thrombo-resistant surface because of its synthesis and
secretion of prostacyclin, {PA, protein S and the expres
sion of thrombomodulin. In elldotoxemia, this
tbrombo-resistance is impaired by
the expression of procoagulant substances such as
tissue thromboplastin and phospholipids
direct activation of the intrinsic ,md extrinsic
coagulation pathways
act. ivation and aggregation of platelet (platelet
activating factor)
195
1 1 COLIC
increases in factors that inhibit fbrinolysis (PAl)
decreases in factors that either potentiate
fbrinolysis (tPA and protein C) or that inhibit
thrombin formation (anti-thrombin Ill).
The net efect is that during endotoxemia, a hyper
coagulable and hypofbrnolytic state develops causing
mkrothrombi formation, perusion abnormalities and
multi-organ failure. Hemorrhagic diathesis, a less com
mon clinical manifestation afOle, mayaIso be observed.
To date, no controlled studies of the prevention or
treatment of DIC in the horse have been reponed.
Intuitively, intravenous fluid therapy, a mainstay in any
horse with endotoxemia, is initiated to deter multi
organ failure. Although controversial, the administra
tion of subcutaneous heparin has been recommended
[0 reduce thrombin formation. Its efcacy, however, is
dependent on complexing with antithrombin III, which
may become defcient in coagulopathies. In general,
when antithrombin III activity is less than 60 per cent,
or when life-threatening hemorrhage is occurring,
fresh heparinized plasma (I5-30 mg/kg) should be
provided intravenously. The dosage for heparin admin
istration mnges from 12."-150 IU/kg b.i.d. s.c., for 2-3
days, but secondary complications such as thrombocyto
penia, anemia, and hemorrhage may occur. Heparin
use has not been recommended in laminitic horses
since heparin induces red cell aggregates which may
make lamina! perfusion worse.
CONCLUSIONS
In summar endotoxemia is a complex multi-systemic
inflammator response involving numerous mediators.
At the time of writing, there remains no single best
therapeutic agent to treat endotoxemia. A number of
different drugs and approaches show promise in exper
imental trials, but appear most useful if given prior to
endotoxin challenge. In general, intravenous fluids
coupled with flunixin meglumine administration has
proved to be the mainstay of therapy.
Nutritional support after
alimentary tract surgery
Sl Ralston
INTRODUCTION
While many horses recover from abdominal surger
without special nutritional management, careful atten-
196
tion to feeding horses following abdominal surgery (".an
dramatically affect the outcome of a case. Immediate
postoperative care is critical to ensure proper wound
healing and reduce the risk of adhesions and infection.
Prolonged fasting (> 3 days in adults, less in foals and
neonates) will result in atrophy of the intestinal
mucosa, reduced wound healing, increased susceptibil
ity to infection, and increased risk of adhesions and
diarrhea. Enteral alimentation is critical to the mainte
nance of gastrointestinal mucosa. The primary energy
source utilized by enterocytes is glutamine obtained
from the lumen, not the blood. Lack of enteral alimen
tation for as little as 3 days causes mucosal atrophy in
dogs. Clinically normal horses fasted for only 5 days
have reduced immune competence. In other species it
has been demonstrated that malnutrition adversely
affects wound healing. Even the anticipation of eating
will stimulate gastrointestinal motility, this may help
reduce adhesions, and will also enhance metabolic
responses to the nutrents ingested. Failure to provide
adequate nutrtional support in the immediate postop
erative phase will potentially jeopardize the chances of
survival, especially in complicated cases where dehis
cence of suture lines, ileus, and gasuic reflux are prob
lems. Long term management becomes crtical in cases
where large portions of either large or small intestine
are resected.
IMMEDIATE POSTOPERATIVE CARE
Non-complicated cases
Reintroduce feed as soon after surgery as possible. The
need for energy, protein, B vitamins, and perhaps
vtamin C are increased in the immediate postoperative
phase. If dehiscence or gastric reflux is not a concern,
the horse should be offered small amounts
(0.25-0.5 g/kg) of good quality alfalfa or alfalfa/grass
mix hay every 1-2 hours after recovery from anesthesia.
If the horse has a history of allergy or intolerance to
alfalfa, grass hay can be used. If this regimen is toler
ated, hay can be offered freely and concentrats can be
re-introduced within 24 hours. A 14-16% protein con
centrate should be used for the frst 1-2 weeks after
surgery with B vitamins (10-20 m! of B-omplex solu
tion/day) and perhaps vitamin C (0.02 gm/kg bj.d.)
added to the feed durng the frst 4-5 days. Bnm mashes
are commonly used, but are not necessary. Bran is not
laxative but is a good source of fber and contains 16%
protein and over 1% phosphorus. Prolonged (> 1-2
weeks) daily administration of bran or bran mahes is
contraindicated, especially if the horse is not fed a
legume-based forage with suffcient calcium to counter
the high phosphorus content. The horse's body condi
tion and previous ration will dictate the amount of con
centrate offered.
Inappetance
Inappetant horses should be allowed to grdle as soon
and as frequently as possible or have freshly cut grass
(not law clippings) brought to them if available. Any
horse that refuses to try to graze when given access to
fresh grass is a good candidate for extra-Dral alimenta
tion. Carrots, apples, and sweet feed (grain mixes with
molas.es) also can be used to stimulate intake.
Dehiscence concerns
In cases where dehiscence of suture lines after an
intestinal resection is of concern, hay runes or complete
pclkted feed (balanced feeds designed to be fed with
out hay, 0.25-0.5 gm kg-I feeding-I ) (:an be soaked UJ
make a slurry. The slurry can be offered orally ever 2-3
hours or delivered via nasogastric tube. Liquid diets,
such as Ensure HN (it wi!! need to be diluted wth water
to prevent hyerosmolar problems), Osmolile or
EquiCare (0.1-0.25 ml kt
l
feeding- I) ran also be used
if the larger particle diets arc not wlerated.
Ileus
Voluntary oral intake of even small amounts of nutrient
slurries should be encouraged if at all possible. Horses
with ileus may beneft from having very small amounts
(10
-
-20 ml) of nutrient solutions such as the liquid diets
or slurries flushed into their mouths. If the ileus persists
for more than a day or to, consider parenteral nutri
tion (see below).
Gastric reflux
11 gastric reflux or other concers prtvent feed intake
for more than 48 hours, parenteral nutrition should be
considered. Intravenous administration of only 5% dex
trost is not recommended, however. It will not provide
signifcant amounts of calories and will stimulate
insulin release which will inhibit lipolvsis, thereby pro
moting catabolism. Fifty per cent dextrose, amino acid
and lipid solutions are available for intravenous admin
istration and should he employed when oral or intra
gastric alimentation is impossible. If the clinicians
and/or their technicians arc unfamiliar ".,th com
pounding such solutions, human hospitals will fre
quelltly be willing to assist in the fonnulation and
preparation of the bags. B-complex vitamin solutions
(10-20 mI!day) should be added to the nutrient solu
tions. The solutions should only be delivered tbrough a
venous catheter (preferahly a centml venous catheter)
placed using proper sterile technique and dedicated
only to the delivery of nutrients. Drugs should never be
added to the parenteral nutrient solutions, nor should
blood samples be drawn from the catheters.
Intravenous administration of as little as 0.20 per cent
of the hore's estimated caloric and protein needs is
better than total starvation.
LONG TERM CRE
Celiotomy, cecal resection, and minor
resection
There are no special requirements once the horse has
recovered from surger if only the cecum or less than 50
per cent of the duodenum orjejunum were removed or
if resection was not necessary. The horse can be
returned to a normal, well-balanced ration appropriate
for its age and activity within 2-3 weeks of surgery.
Major large colon resection
If both the left and right colons are removed, the horse
wll require higher than maintenance protein and phos
phorus, decreased fber, and possibly inrreased B vita
mins. Alfalfa, excellent quality legume/grass mix hay
and/or pasture are the forages of choice. Concentrates
may be needed to maintain weight hut no more than
0.4 g/kg should be offered per meal. Pclleted,
extruded, or textured grains can be used. Fats or edible
oils (S 1.0 ml/kg) may be added to further increase
caloric intake, but they fIlust be introdured slowly. If
only grass hay is fed, protein supplementation will be
necessar.
Major small intestinal resection
If more than 60 per cent of the small intestine is
removed it is best to avoid large amount of grain or
concentrates. No more than 0.2 g/kg should be offered
per feeding U avoid overwhelming the residual small
intestinal digestive and absorptive capacity. Beet pulp
based 'complete' freds arc recommended. Ideally 50
per cent or more of the ration should be high quality
legume hay or pasture. If the ileum is intact, edible veg
etable oils may be llsed to incrca.c calO
l
ic intake (up to
1.0 ml ktfl day-I).
Ileal bypass or resection
Removal of the ilcum will increase the necd for fat
soluble vitmins A and E. Ddkiency signs however may
appear only 1-2 years after surger. It is not known if
oral supplementation of increased amount of these
two vitamins (60000 IV retinyl palmitate, 1000 IU alpha
197
1 1 COLIC
tocopherol/cay) will be prcventative. Parenteral
adminiSlr31ion may be neccs$lry if dinical signs of ddi
ciCEK' appear. Ther also may < increased need for
Cd kium and a reduced tolcrdncc for fl. Te rdron
should contain at let 0.8 p cent clcium and edible
oit shnuld not he ll .>upplemen.
Postoperative shock and
organ failure
LR Goodrich
INTRODUCION
In 1895
,
James Collins Warrell referred L shock as 'a
momentary paue in the act of death'. More recent def
initi()n have defnrd it d a 'gcncra!il.cd inadequacy of
blood fl(lw tn tissues rdative to their metabolic
demand !t'ading t wdespread cdlular hypoxia and
vi[<1 organ dyfunclion'. Depending on the context of
pr'senl'Hion, shoIk varies in its description between its
phsiol(giC<' and iL dinical pUetcu, For clinicians
a more approprilue definition my h 'the stte in
which profound and widespread reduclion in efTecth-
tisue perfu>ion leads to re\Cl"ibk, and then, i pro
longed, irr\trible cellular injury'.
Despite recent ad Y < mCe5 in diagnostics and cardio
\'ascular treatment, shock remains an important came
ofcomplinttion and dcath in b()(h humans and domc
lie animals. A survey of 259 surgical colic cases revealed
that over 50 per ccm of falalities occurred in the post
operative period, and 70 per cellt of these were due to
shock as weI! as pOSlopcrauve ileus. In the light of these
findings it becomes apparent that a fundamental
understanding of the procem:s leading to circulatory
inadequacy is an essential element in successful man
agement of Ihis morhid yndromc.
CLASSIFICATION
Se\e!' 1 da.ifcalion s"Slems exi" that describe the dif
ferent types of shock. TIle most common s)s1m us
insults of YI1M5 tioloies according to the character
of the pre .. . iling drculalOr}
,
disruption. The four
primary C.Hegori<' are
(anii(gnk shMk
obstructhe shock
hypo\olemic shock
distributive shock.
19B
Cnrdiotir and ooslrriw ShfXk
These condition. ndate I() an inability of the heart to
pump blood, and M a restriction of ca ejection.
respti\dy. Since these Slates of shock are nOl gener
alyassocilued "th JlOpert
i
ve complications follow
ing gastrointestinal surger they will not b discu
funner. The other two classifctions It are more
commonly seen following gasuointestinal surgery arc
hypovolemic and distribllli\c shock.
HyJn ic (JI(r gk) lhodt
This refers to the It)$S of whole hllx)i, uually because of
ll:morrhage, resulting in !os of intTavascular \olume.
Othr causes include loss of plasma (exudation into
lumem of hol1o .. . organs or body cavities), or loss of Im'
protein fluid (as in diarrhea). Tht: !ac.k of intravascular
volume results in pcwr \;s!ular flJling volume, leading
to decreased cardiac return and hence, decreased
cardiac output, arterial flow, and pressure.
Di.liri!mtiV .11iock (.(ir and tndolo.ni)
This occurs as a fesuh of expansion or the imlv'scu
Jar space by localiled or gener.tized loss of vascular
resistance. This is the 1Il0t common form of shock
that gastrointestinal surgeons deal ";th, it i often
initiated hy serticmia and/or e.ndoLOlemia. Other
causes can h neurogenic in orign such a anesthetic
mUihap, spinal cord injury, or anaphylaxis. The result
uf Ihc cau> i similar to hypo\'oiemic shok in tht
..
.
,$Cular flling volum. and cardiac retur and output
arc all reduced. In addition there a lo of loc.l con
[TIll mechlni.\m rhlH HC rf_ponsible for matching
capillary blonc! flow with tissue needs. This point
become important in that, although cardiac output
may be increased in the early stages of Stpticl ender
toxic hod., Ihe bJ()od flow to local parenchymal tissue
may be decreased resulting in tis,ue hypoxia and
dysfunction.
The classification s)'Sters indicate that shock is
neatly separated into specifc catcgories, however vari
ous clinical events may initiate two 1I more forms of
shock. For instance, horses with strangulated intet.in(
may have hypovolemic components due to losses of
intralumcnal fluid welt as losses of fluid due to 5Cvere
dehydration from sweating. In addition to lhi ongoing
hypo\olemic shock, los of control mechanisms (dis
trihutive shock) because of conCUfTent scps i ra} add
to the stale of prograsivc shock. Conlly. horses in
.. hich sepsis is the initialing f<ctor may not only have
por regulation of\"scular wnc but aloabnonnal cap
i ry and vnou peml abilil) lh lea f1 fluid 10
and hypovolemia. Terefore cale
g
Olizations ;lre lI!Cfll
in understanding th<.' pathophysiologic origins of each
inilb!l insult. Nevertheless, if effecthe tht"Tdpy i5 not
instituted early in any category of shock, the end result
is olien similar for all c_ategories.
PATHOPHYSIOLOGY
Hypovolemic shock
Hypovolemic shock in the postoper<ttive period most
commonly occurs because of mesenteric vessel bleeds
from the small intestine, small colon, or occasionally
from the {:olonic vessels in cases of large colon resec
tion. Circulating blaac! \'nhnne constitutes <tpproxi
mately 8 per cent. of IXJdy weight. Adult animals can lose
up to one-third of this volume and survive with a rea
sonably good prognosis. How(ver when the volume loss
is greater than this there exists an obligatory need for
resuscitation.
Fo horses in hypovolemic shock due hemor
rhage, it is helpful to understand events occuring at
the vessel wall. Discontinuity of the vessel wall occurs
and platelets become activated because of changes in
laminar blood flow. This exposes receptors on the
platelet surface and allows exposure of the platelet to
collagen on the damaged vessel wall. Platelel then
extrude their contents, including thromboxane, sero
tonin, and bradykinin which causes vasoconstriction,
and platelet factor 4. Additional plate\el then adhere
to the vessel wall, adding to the growing clump at the
site of vascular disruption.
Fibrin formation occur within minutes as protein
dOlling factors in the plasma undergo a cascade of
activation. The fbrin strand stabilizes the platelet
dump as it forms. If the defect in the vessel wall is
small and pressure is low the platelet-fhrin aggregate
will fll the detect and blood wi\! cease to exit th(
vessel. Often the hlood that has leaked out of the
vessel into thc surrounding tissue will also form a
platelet-fbrin clot and contribute to the cessation 01
bleeding. Adequate hemostasis does not always occur
especially when the injured vessel is large and the pres
sure is low. The platelet-fibrin clot may not be large
enough to occlude the defects and bridge the cut sur
jl.es. In this case, the surrounding dot joins with the
clot inside the vessel to bridge the defects. Each pulse
forces more blood through the hole into the surround
ing clot. in arteries that are large and under high pres
sure, but the pressure from the surrounding clot may
never reach a point where it is equal the pressure
inside the artery. Tn arteries, muscle spasm reduces the
diamCln of the vessel defect which the dot must span
ill order to seal the hole, but constant pulsatile pres
sure may reduce effective occlusion of the defect in the
vascular wall. If pressure in the clot surrounding the
injured artery does not reach the pressure present
",ithin the artery bleeding into the interstitium o
abdominal cavity, then hemorrhage will continue until
adequate surgical intervention has taken place or sys
temic hypotension develops. At that point, pressure in
the arter drops to the level of the surrounding tissue
clot. If systemic arterial pressure reaches 50 mmHg or
lower, the platelet-fbrin plug may seal the defects.
Often, before this time, it is likely that over 30 per cent
of circulating blood volume wi\! have been lost. It is
important to consider that dilution and reduction of
blood viscoity resulting from volume expansion with
large volumes of crita\!oid fluids, may further chal
lenge the clot-hypotension relationship.
The compensatory mechanisms activated during
this described attempt to control hemorrhage include
baroreceptor reOexes and the sympathoadrenal
systems. Receptors are present in the walls of the great
vessels and arc sensitive to reduced hydrostatic pres
Sllres. Most important are the receptors in the carotid
sinuses and aortic arch, that detect decreased pressures
within the hrain and general circulation. These recep
tors are responsible for initiating elevation in heart r.te,
vasoconstriction, and increases in arterial blood pres
sure, via sympathetic nelVe activity. Sympathetic activa
tions induce an increase in venous tone and the blood
is not allo\\'ed to pool in veins. This in tur increases the
pre-load on the heart.
Arterial constriction during hemorrhagic shock is
not, over<lll, unibrm. Peripheral vasoconstriction is
most severe at the splanchnic, cutaneous, and skeletal
tissue areas. Areas such as the brain and heart are
spared however, so that when a systemic drop in blood
pressure occurs blood is preferentially shunted to these
organs that are . ital in the most immediate sense. The
skeletal muscle vascular beds maintain fairly adequate
perfusion because of reflex vasodilation in response to
the autocoidal efrects of cellular metabolic products.
The reflex sympathetic activty initiates pacemaker cells
through beta, receptors, increasing heart rate. Other
sympathetic nelVe fibers innelVate the adrenal medulla
and cause catecholamine release.
A renal contribution homeostasis is of major
importance in animals sUlviving this acute phasr of
hemorrhage. In response to decreased renal perfusion,
specialized cells next to each glomerulus produce ren
nin and secrete it into dferent arterioles. This induces
angiotensin I formation from angiotensinogen. The
renin-angiotensin system is responsible for the release
of aldosterone which increases sodium and water
resorption and antidiuretic horrom (ADH), whid,
increases permeability of pores in the collecting ducts
of the kidney so that water can pass back into the renal
interstitium and thrn into the vascular space instead of
199
1 1 COLIC
being excreted as urine. This reflex is <n important fac
lor ill maintaining adequate bloori pressure 612 hours
following blood loss.
The reflexes described above are the body's altempt
U1 maintain blood pressure. These events occur at the
same time that activation of the clotting cascad" is fUlle
lionillg i1 stop profuse hemorrhage. In horses suffering
from hypovolemic shock due to diarrhea or inadequate
oral fluid the same reflexes (increased cardiac output,
vasocooslTiction, ;md Wdler retention to maintain blood
pressure) occur.
Distributive shock
Although hypovolemic shock is occasionally seen in the
perioperativc period of gastrointestinal surgery, by far
the most common type of shock seen in the horse is
distributive shock caused by sepsis, endotoxemia, or
splanchnic ischemia associated \\th acute strangulating
and non"strangulating intestinal infarction. Often alt
three conditions can cuntribute to shock. Several inves
tigawrs have determined that up to 40 per cent of
horses with colic presented to a veterina!)' college are
endolOxemic, and most endotoxemic horses have
intestinal strangulation obstruction or severe inllamma
lory intstinal diseases. Furthermore, the prognosis for
sUlvival is inversely correlated with the presence of
lipopolysaccharide in the circulation. In some cases all
three causes may be contributing to distributive shock.
Early and late phase pathologic events usually char
acterizc distributive shock caused by sepsis or endotox
cmia. In the early phase, increased cardiac output occurs
along with reduced peripher.l! vascular resistance, nor
mal to slightly decreased mean arterial pressure and
fever with warm extremities. It is in this phase that the
lipopolYS<lccharide components of the outer membranc
of enteric hacteria initiate the host's mononuclear
phagocytes n:sulting in symhesis of proinflammatory
mediators. The most widely recognized mediators
include the C)'tokines, lipid-derived mediators, and coag
ulation/fibrinolytic factors. Cytokims most commonly
involved include tumor necrosis factor, interleukins,
and interferons. Lipid-derived mediators include throm
boxane (TX and prostaglandins (PGS, PGF2a, and
PGJ"). Release offibrinolytic factors in this stage of shock
resul in decreases in plasma antithrombin III activity,
protein C, and plasminogen anivity. This also results in
coagulation times indicative of the presence of a hyper
coagulable state in endotoxemic horses with colic. It
should be mentioned that during the early stage of sep
tic/ endotoxcmic shock in which the above mentioned
mediators arc bcing relcased, a syndrome named the sys
telTJic inflammatory response syndrome (SIRS) has been
used to describe the sequence of evenL, and the (on-
200
current clinical events. This term refers to an exagger
ated systemic response to an inju!)'. V'bile not only used
to describe the events of shock, it is commonly used ill
humans to describe various states of shock. Briefly, SIR\)
develops when the local response to iIUry or to an
initiating stimulus becomes amplifed. If homeostasis is
not re-established, the multipk inflammatory cascades
result in loss of microcirculatory function and subse
quent damage to other organs. This leads into the
second stage of distributive shock caused by
sepsis/ endotoxemia.
The late phase of septic and cndotoxic shock is char
acterized by decreased myocardial and peripheral vas
cular tone, incnased microvascular permeability,
increased intravascular coagUlation, and leukocyte
adherence. Progression of the inflammator cascades
initiated in SIRS ensues and vascular hyoreactivity pre
vails as the one distinct and important <bnormality. The
prevailing opinion is that lipopolysaccharides and select
cytokines induce the calcium-insenitive form of the
nitric oxide ynthasc molecule within the VAscular wall.
Over-production of nitric oxide leads indirectly to sup
pression of calcium mobilizatioJl and a decreascd
contractile function. In many cases the progression of
SIRS results in multiple organ dysfunction syndrome
(MODS). In human medicine there exist various scor
ing systems eval u<ting v.ious serologic parameters such
as creatinine, bilirubin, and platelet count. A the scores
incre;e, the incidence of mortality also increases. For
example four body systems suffering from dysfullction
resuits in 80 per cent mortalit.ics. In the horse MODS is
most commonly asociated with the gastrointestinal
tract. The gut h; been termed the 'motor of failure' in
its capability of generating the demise of ot.her organ
systems. Reperfusion of the gut can be responsible for
activation of calcium influx with oxygen radicals
adding to mucosal ifjuy
bacterial translocation with heightened
endotoxemia
the release of cytokines resulting in wsodilation
and vascular leakage.
The combination of these three factors increases the
predisposition to MODS. Other organs that can com
monly be secondarily affected are the kidney, liver, and
lungs.
CLINICAL FINDINGS
Hypovolemic shock
Horses experiencing hypovolemic shock due to helllOr
rhage commonly have elevated heart rates, pale mUCOllS
membranes, a thready rapid pulse, prolonged capillary
refll time, and cool extremities. Often they are sweat
ing and agitated. If hemorrhage continues unmiti!<.ted,
eventual collapse ensues. Rectal temperature may be
normal or decre-d-. If shock is protracted the horse
may he oIiguric. A circulatory and respiratory function
deterior.te, the gums may take on a gray-blue color.
If bleeding is not controlled acute death occurs.
Laboratory eVMuation is frequently not helpful in the
acute phases but may reveal metabolic acidosis,
increases in lactic acid, and increases in blood urea
nitrogen. Hematocrit often stays unchanged in the
acute phase of hemorrhagic shock but evcntually
decreases during the later phases especially if large
doses of crystalioid fluid therapy are instituted. Plasma
protein usually parallels this. It i important to remem
ber that the various components of blood are being lost
equa!Iy, and the relative proportions of red cell mass
and plama will remain unchanged. Ultrasonography
is the diagnostic modality of choice in cases where
hemorrhage into the abdominal cavity is suspected.
Hemoperitoneum is easily evaluated with ultrasound
using a 5.0 MHz probe transabdominally. Blood
appears hypoechoic with swirling of the cellular ele
ments. Questionable aooominal bleeding can be more
accurately confrmed by paracentesis. Although analysis
of peritoneal fluid is not always straightforward in mak
ing Ihis determination, a helpful rule of thumb is that a
packed cell volume of 5 per cent or greater, and a total
protein of 3.5 gldl or greater support the presence of
frank hemorrhage.
The clinical fndings among horses experiencing
hypovolemic shock resulting from vascular fluid loss
dm' to acute diarrhea or inflammatory bowel condi
tions, can look similar to those horses with acute hem
orrhage. Labor, ltory evaluation however may reveal
relatively early declines in plasma protein concentra
tion and electrolyte abnormalities as well as a marked
metabolic acidosis. However, because infection may
also be occurring in these horses the findings can often
be similar to those in horses with distributive shock due
to sepsis.
Distributive shock
Horses in the initial stages of distributive shock due to
sepsis or endotoxemia have clinical signs consistent
with the 'early' phase. These signs include fever with
warm extremities, depression, tachycardia, increased
respiratory rate, injected mucous membranes (Plate
11.1), hypocapnea and leukopenia or leukocytosis.
Hemodynamically, horses have decreased arteria! pres
sure, elevated cardiac output, and low peripheral vascu
lar resistance. As distributive shock progresses, cardiac
output begins to fall along with arterial pressure.
Horses in acute abdominal crisis, and in particular with
splanchnic ischemia, exhibit sweating, tachycardia,
weak pulses, and cyanotic mucous membranes (Plate
11. 2). laboratory evaluation may reveal hemoconcen
tration, leukopenia, coagulation abnormalities, meta
bolic acidosis, and elevation of blood urea and
creatinine levels. This stage is often referred to as the
'late', 'cold', or 'hypodynamic' stage of shock. Gross
hypoperfusion is occurring resulting in multiple organ
dysfunction syndrome.
TREATMENT
"MW*P
Hypovolemic shock
Initial goals in the treatment of hypovolemic shock
include partial restoration of circulating blood volume,
maintenance of oxygen delivery to tissues, and support
of coagulation and thrombus formation when hypo
volemic shock is due to hemorrhage. It is important to
remember that supportive therapy in hypovolemic
shock due to hemorrhage does not end when the bleed
ing is controlled. Many pathologic processes continue
following control of hemorrhage and, if allowed to
progress, these processes result in damage to other
organ systems such as the gastrointestinal tract and the
pulmonary system. Failure of these systems can be rec
ognized as ischemia-reperfusion injury and pulmonary
edema, respectively,
To restore partial circulating blood volume rapidly,
a large bore catheter should be placed and crstalloid
fluids given in appropriate dosages. Options forcrystal
loid fluids include saline, lactated Ringer's solution,
plasmalyte, and hypertonic saline. Replacement volume
should be calculated according to total loss as well as
maintenance volume required. Crystalloid fluids move
freely from the intravascular to the interstitial space and
approximately 20 per cent remain in the intravascular
space. Lactated Ringer's solution consists of sodium
and chlorde with added calcium, potassium, and lac
tate (buffer solution). Plasmalyte and normasol include
other buffers as well as magnesium. Lactated Ringer's is
inferior to normasol and plasmalyte when blood is
being transfused since the calcium added to these solu
tions can interact with citrate antic()agulant in col
lected blood. Hypertonic saline is advantageous in
hypovolemic shock for many reasons. Initially this solu
tion can rapidly expand intravascular fluid volume.
Additionally, there is evidence that other beneficial
cffect include modulation of neutrophil activity
thereby potentially decreasing the incidence of
ischemia-reperfusion injury and bacterial translocation.
201
1 1 COLIC
It is important to rememocr however that unless bleed
ing in the patient with hypovolemic shock is controlled,
hypertonic saline should not be used because of the
rapid volume expansion and the resulting effects of dis
lodging a tenuous clot formation. Alternatively, colloid
fluids may be considered for volume expansion. These
include hetastarch, plasma, dextrans, and 5% albumin.
Colloids contain large molecules, which prevent egress
of fluid out of the intrav<lscular space allowing both an
expansion of plasma volume and an associated increase
in cardiac output. The volume of crystalloid fluids
infused would have to be three times that of colloids for
an cfJllivalt>n! improvement in cardiac peIfonnance.
Hetastarch should be administered at 6 ml/kg in place
of hypertonic saline. Similar to hypertonic saline,
concerns regarding initiation of bleeding exist for
hetastarch as well.
To increase the oxygen-arrying capabilities for the
horse in hypovolemic shock due to hemorrhage, whole
blood should be administered. The blood volume
needed should be estimated according to the horse's
weight, suspected volume of blood lost, and present
packed cell volume and total protein. Packed cell vol
umes of less than 20 per cent and total protein values of
less than 3.5 gldl should be treated with the adminis
tnion of whole blood. For an adult horse, blood vol
ume is approximately 8 per cent of body weight or 40
liters. If the packed cell volume drops from 36 to 12 per
cent a loss of erythrocytes is at least 27 liters of blood.
Generally, replacing 20-0 per cent of the defcit is ade
quate therefore 7-10 liters of blood should maintain
the oxygen-carrying capacity of blood. Up to 25 per
cent of the donor's blood volume can be removed at
one collection (10 liters in a 500 kg horse). This may be
repeated ever 30 days. Cross matching should be per
formed prior to administration, or transfusion should
be performed from a universal donor. Alternatively,
blood substitutes such as Oxyglobin (Biopure,
Cambridge, MA) can be administered, however cur
rently, for an adult hore, these prOdUCL are prohibi
tivelyexpensive.
If cessation of bleeding relies on a tenuous clot for
mation, antifbrinolytic drugs should be considered.
Options include aminocaproic acid, transexamic acid,
and conjugated estrogens. Of these choices amino
caproic acid has been used most often in horses, given
intravenously in doses of 20 g in 500 ml saline per
450 kg horse (loading dose), and then 1 0 g twice t
three times daily. There have been no proven efficacy
trials in horses at the time of wrting.
The 'low' doses offlunixin meglumine (0.25 mg/kg
i.v. t.i.d.) should be administered as an adjunct in an
attempt to minimize the inflammatOI) cascades initi
ated by ischemia resulting from compromised
202
blood-bowel layer, hypoxic cellular injur, and any
potential foreign leukocytes from blood transfusions.
Broad spectrum antimicrobial therapy should also
be used in cases where translocation of bacteria due to
splanchnic ischemia is suspected. It should be consid
ered, however, that the toxic potential of these druw is
enhanced by dehydration or volume contraction.
Distributive shock
Distributive shock postoperatively is commonly associ
ated with acute and extensive disruption of the gastro
intestinal mucosa. This is one of the most commonly
treated syndromes in the horse postoperatively as well
as the second most common reason for postoperative
mortality. If not treated in its early stages, progression
to the late stages results in a decreased prognosis and
complications such as multiple organ failure. Horses
with septic and splanchnic ischemia should recdve ade
quate replacement of intravascular volume with the iso
tonic crystalloid fluids mentioned above. Much like the
treatment of hypovolemic shock, the most important
goal of distributive shock treatment is volume replace
ment. Monitoring of clinical signs during treatment wi!!
be an adequate representation of therapeutic suf
ciency. When replacing volume in the treatment of dis
tributive shock however, the clinician should be less
hesitant in the usc of hypertonic saline since the com
mencement of hemorrhage is not an issue. Hypertonic
saline along with hyperoncotic fluids allow the tempo
rary shift of interstitial and extravascular fluid the
intravascular space causing increased myocardial con
tractility because of temporary increased sodium and
potassium ions "-lthin the V'dscu!ar space. This rapid
method of volume expansion, though, should be fol
lowed immediately with isotonic crystalloid solution.
Additional benefts of administrdtion of hypertonic
saline in the septic/endotoxemic horse relate to its
effects on neutrophils. Hypertonicity has been associ
ated with eliminating the receptors on leukocytes that
respond to lipopolysaccharides thereby attenuating
endothelial damage. Furthermore, resuscitation with
hyertonic saline and lactated Ringer's solution appar
ently resulted in a reduced rate of early bacterial
translocation to mesenteric lymph nodes in one study.
Acid-base normalization is also very important in
the treatment regimen of distributive shock. In the
early stages of sepsis, a respiratory alkalosis may be evi
dent. However, as shock progresses a metabolic acidosis
is the primary acid-bae abnormallty caused by an
anaerobic metabolism in the tissues as well as renal
hyoperfusion. Often mild cases of metabolic acidosis
will resolve without administration of bicarbonate when
a sufcient amount of volume replacement is adminis-
teredo This of course is the most physiologic route in the
treatment of acid-base abnormalities. When metabolic
acidosis is severe (pH 7. 1 ) or fluid replacement does
not correct the abnormality then administration of
bicarbonate is necessary. The following formula may be
followed as a guide to estimate the dose of bicarbonate
U1 he administered.
:aHCO replacement (mEg) 0.3 7 body weight (kg)
? base defcit
Periodic monitoring of blood gas will allow proper
adjustment in dosing.
Antibiotic therapy is indicalfo in riislrihwivf h()rk
caued by sepsis. Often in cases of eXlensive bowel com
promise and resection many different bacterial isolates
are possible, however, isolation of these organisms is
rare. Therefore combinations of high doses of peni
cillin G and an aminoglycoside are commonly used
because of their broad spectrum of bactericidal activity.
This combination of antibiotics should be continued
paMthe arute phase of distributive shock because of lhe
possibility of sepsis and/or splanchnic-ischemia.
Anti-inflammatory therapy is extremely important in
horses with distributive shock due to sepsis/endotox
emia. The use of flunixin meglumine has become stan
dard in the treatment of distributive shock. This drug
acts by inhibiting cydooxygenase and will prevent or
attenuate the early hemodynamic responses to endo
toxin. Various studies have found that flunixin meglu
mine signifcantly reduces endotoxin-induced increases
in plasma concentrations of thromboxane and
prostaglandins. The 'low dose' commonly used in clini
cal situations is 0.25 mg/kg i.v. Li.d. This dose will
rewin the ability to prevent generation of cyclooxyge
na.{'-derived products and has minimal toxic side
effecs. Following surgery however, it is important to
keep in mind that postoperative pain resulting from
intestinal manipulation may require initial higher doses
(0.5 mg/kg) and slow decreasing of the dose over a
period of 3- 4 days. It should be mentioned that
although some debate still exists regarding the use of
steroid therapy in distributive shock, extensive clinical
trials in the human population reveal no beneficial
effects and occasional adverse effects when used.
Therefore, although exact extrapolations cannot be
made to the equine population, steroids are not recom
mended.
Polymyin B is a recent addition to the treatment
armamentarium for distributive shock due to
sepsis/ endotoxcmia. This antibiotic is reported to bind
and remove endotoxin from the circulation by binding
the lipid A region of endotoxin. Studies in foals pre
lTeated with polymyxin B that underent induced
experimental endoloxemia had reduced signs of
endotoxemia, absence of leukopenia and lower than
expected tumor necrosis factor levels in serum.
Recommended doses are 1000-3000 Ie/kg given intr
venously twice daily. While these doses are sub
therapeutic antibiotc doses, polymyxin B can be
nephrotoxic and dose monitoring of creatinine and
blood urea nitrogen should be performed.
Plasma products are available with antibodies
directed against the core oligosaccharide and lipid A
regions of endotoxins from mutant gram-negatve
bacleria. V'hile many referral centers administer these
product, their effcacy still remains in question.
Hyerimmune plasma products may however provide
the septic/ endotoxemic horse with levels of antithrom
bin III that appear to be defcient in horses with colic.
Heparin injected into the plasma before transfusion
may improve the efcacy by activating antithrombin III
prior to administration.
PentoxifyIIine (6.6-8.0 mg/kg p.o. hj.d.) is another
drug used to treat horses for endoloxemia. In both
in vitu and 7 vivo studies in horses, pentoxiflIine
reduced endotoxin-induced production of cytokines,
thromboxane, and tissue factrs. Clinical trials have
revealed that when used alone its benefcial cllecs may
be minimal but when combined with flunixin meglu
mine, hemodynamic responses to endotoxin may be
reduced more efectively than with either drug alone.
Supplemental oxygen therapy is not usually neces
sary for horses in which arterial oxygenation tensions
are normal (PaO 100 mmHg) or dose to normaL In
these cases hemoglobin is fully saturated and further
supplementl oxygen therapy will he of little beneft.
However, when arterial oxygen tensions fall below
85 mmHg hemoglobin desaturation IIlay occur and
supplemental oxygen can be delivered in the standing
horse through nasal or transtracheal catheter place
ment. F10ws of 15 l/min should be administered with
adjustmenL made according to blood gas measure
mlnts.
PERIOPERA TlVE MONITORING
. ire this chapter is dedicated to postoperative assess
ment and treatment of shock, treatment will be more
effective if instituted to patients preoperatively.
Treatment should begin prior to induction for generAl
anesthesia in patients when large amounts of intestinal
compromise are suspected. Although there are situa
tiOIlS in which patient can not be volume expanded
adequately preoperatively, every effort should he made
to promote proper treatment as soon as possible. Care
may be expedited by placement of two large-bore
catheters and fluids administered under pressure.
203
1 1 COLIC
Adequat supplies of necessary treaunem modalities
should be available along 'Hilh the equipment to ade
quately monitor treatment. Prior planning for critical
care for patients in shock is important in situations
where there are small time frames. Proper anesthetic
monitoring is also crcial (see Chapter 10). Often dfec
tive treatment and monitoring during anesthesia of the
colic patient has a direct outcome in the postoperative
period.
THE FUTURE
The feld of shock has become an intensely studied area
with new advances being made frequently. A new
developments occur in both the monitoring and treat
ment of shock clinicians will become more efective in
its early diagnosis, monitoring, and treannent. This
chapter has covered most current monitoring and treat
ment techniques that have been clinically evaluated in
the equine patient. A sound clinical trials reveal new
techniques it is the responsibility of clinicians to judi
ciously use the new methods to benefit the equine
patients.
Postoperative pain
W
LR Goodrich
INTRODUION
.#.y_ @@
Postoperative pain is a complication that gastrointesti
nal surgeons deal with frequent.Iy. Abdominal pain,
otherwise called colic, is defned as 'an unpleaant
experience that is commonly associated with tissue
injury'. Various physiologic sources of pain include
the type of stimuli
the various receptors that are stimulated
the neuroanatomic pathways transporting the pain
stimulus from the site of injury to the central
nervous system
the various reactions in response to pain.
Thus postopemtive pain, induced by gastrointestinal
surgical procedures, induces a series of behaviorl,
neurophysiological, endocrine, metabolic, and cellular
responses (the stress response) that initiate, maintain,
and intensif the release of pain and inflammatory
mediators. Itshould be stated that pain is a complex sen
sation that can manifest diferently in horses affected by
similar abdominal problems. It is the surgeon's respon-
204
sibility to interpret clinical signs exhibited by their
patients and judiciously manage pain based on a com
plee understanding of the facton involved.
NEUROANATOMY AND
PATHOPHYSIOLOGY
Sensory neuroreceptors arc located in the mu(:{)a and
muscularis of hollow vscer, within serosal structures
such as the peritoneum, and within the mesentery. i
addition to nociception (the perception of noxious
stimuli), [hf ensory nellror(ce
p
!or. arf' rfspnnsiblc for
regulation of motility, secretion, and blood flow to the
gastrointestinal tract.
Neuroreceptors responsible for the p<Tcepton of
pain are separated into two distinct types of afferent
nerve fbers
L myelinated A-delta fibers
2. unmyelinated C fibers.
A-deita fbers are responsible for mediating sharp,
well-localized pain associated with an acute injury.
These fbers transmit soma to parietal pain i a spinal
nerves. C fbers are found in viscera, peritoneum, and
mesentery, as well as in muscle and periosteum. C fbers
convey nociception from abdominal viscera and this
pain tends to be dull, burning, diffuse, and of a more
gradual nature in onset. C fibers utilize substance P and
calcitonin gene-related peptide as neurotransmitters.
Local regulatory reflexes within the gut are activated
when C fbers are stimulated.
Three pathways mediate abdominal pain
I . frst-order neurons, that innervate the viscera, carry
information to the thoracolumbar sympathetic
nervous system, and then synapse in the dorsal
horn of the spinal cord
2. second-rder neurons, which ascend from the
dorsal horn via the spinothalamic and
spinoreticular tracts to synapse with the thalamus
and reticular formation
3. third-order neurons, which progress from the
spinothalamic system to the somatosensor cortex
and from the spinoreticular system to the limbic
system and frontal lobe of the cortex.
These multiple inputs of nociception in the eNS clabo
rate the variability of pain.
Abdominal visceral nociceptors respond to mechan
ical and chemical stimuli. The primary mechanical sig
nal to which visceI'.t nociceptors arc sensitive i. stretch.
This difers to somatoparietal nociceptors in that cut
ting, tearing, or crushing of viscera does not elicit pain.
The visceral stretch receptors are located in the muscu-
lar layers of the ho!low viscem, between the muscularis
lllucosa and submucosa, also in the serosa of solid
or!ans as well as in the mesentery. Mechanoreceptor
stimulat.ion can result from rapid distention of a viscus
(small intestinal strangulating obstruction), torsion of
thtO mesentery (large colon volvulus), or tension on the
mesente!l' (small intestinal adhesions).
Chemical nociceptors are located primarily within
the lIlucosa and submucosa of the hollow viscer<. These
rtOceptors are directly stimulated by mediators of pain
and inflammation. Such chemicals include histamine,
serotonin, bmdykinin, leukotrienes, prostaglandin E,
illtnleukins (IL-l, IL-), neutrophil-chemotactic pep
tides, nen'e growth factor (:GF) and neuropeptides
including substance P and calcitonin gene-related pep
tide. Collectively, these mediators have been referred to
as the 'sensitizing soup' because their accumulation is
thought to result in visceral sensitization.
This visceral sensitization has been describtOd as
resulting from the recruitment of certain (silent) affer
ent receptors. With prolonged or recurrent peripheral
stimulation because of distention or stretching of the
mesentery, the excitability of the second-order neurons
is enhanced and outlasts the duration of increased
periphtT<1 stimulation. This has betOn referred to as
central nervous system 'wind-up' and results in hyper
algt"sia. After the peripheral stimulation subsides, sensi
tilt"d second-order neurons continue to fre and
sub-threshold stimull that are othlWise non-painful are
still perceived as painful.
The biochemical resuit of hyeralgesia can be
cxplaincd by the accumulation of Lhemical mediators
which enhance neural sensitivity and intensif the pain
nsponse. Once transduced the electrical impulses are
transmitted to (:fiber terminals in the dorsal horn (sec
olld-order neurons) where the excitator neuropep
tides such as tachykinins, neurokinins, and amino acid
glutamate arc released and cause an increase in mem
brane excitability and activate postsynaptic recepLrs,
primarily :-methyl-D-aspartate (NMDA).
Te phenomenon of vjscral sensitization has not yet
heen demonstrated in horses. However in humans it has
been supported by experiments in which repeated series
of balloon inflations in the colon led to an increase in
pain intensity and a 228 per (ent increase in the size of
the area where pain is experienced. It is highly probable
that the equine patient has similar decreases in pain
t.hreshold with ongoing pain. Furthermore, it has been
demonstrated in the equine patient aswell as the human
patient that preoperative treatment with local or
regional anesthesia or non-steroidal anti-inflammatory
drugs (NSAlDs) results in reduced severit of postoper
ative pain. This implies that CNS response to peripheral
injur can be mediated by prior reduction of afferent
input to the spinal cord and eNS. Conversely, recurrent
gastrointestinal pain (e.g. with re-laparotomy) may sen
sitize intestinal receptors making perception of baseline
afferent activt more painful.
CLINICAL SIGNS
Postoperative pain is usually less intense than the pain
exprinced preoperatively unless
postoperative ileus results in similar distention
there is ongoing tissue ischemia
there is recurrence of the original lesion or the
original lesion was not corrected surgically
a new lesion has developed.
Abdominal pain can be sepamted into three distinct
calegories
vsceral
somatoparietal
referred.
Visceral pain is caused by noxious stimuli triggering vis
ceral nociceptors. Somatoparietal pain is initiated by
stimulation of the parietal peritoneum, and referred
pain is pain perceived in areas remote to the diseased
organ. In the equine patient it is difficult to differenti
ate these various types of pain.
In asessing pain the general attitude of the patient
should frst be noted. It is helpful to assess the horse's
attitude from outside the stall since the tendency to lie
down can be inhibited when a person is in the stall with
the patient. Signs are varied and include pawing, turn
ing the head toward the flank, kicking with the hind
feet at the abdomen, crouching in attempt to lie down,
stretching and appearing to attempt to urinate, grind
ing the teeth, dropping to and rolling on the ground,
sweating, and quivering of the upper lip.
The severity of pain can vary from mild (occasional
pawing) to severe (dropping to the ground and rolling
volently). Postoperatively most horses are administered
analgesic doses of NSAlDs, the severity of pain must
therefore be considered in this light, i.e. the pain exhib
ited would most likely be worse without the analgesics.
a rule, the more severe the aooominal lesion, the
greater the pain. However, difterent horses manifest
pain in a variety of ways and some horses have a greater
tolerance to pain than others.
The exteral appearance of the animal can be help
ful in assessing the disease
bloating indicates distention of the cecum and/or
large colon
splinting of the abdomen usually indicates
somatoparietal pain from the peritoneum or pleur
205
1 1 coue
sweating also indicates severe pain and potential
response to endotoxic shock.
DIAGNOSIS
Together with the clinical signs, temperature, pulse,
and respiratory rates should be monitored postopera
tively, these are commonly elevated in horses exhibiting
pain. Auscultation should be performed over the left
and right paralumbar regions and propulsive sounds
should be quantified. Progressive sounds il! be heard
only once every 2-4 minutes when the colon has en
emptied or the horse has not eaten, with normal motil
ity these sounds are heard every 6-10 seconds. In almost
all horses with abdominal pain propulsive sounds v'
be reduced. While auscultating the abdomen percus
sion should he performed to detect pockets of gas in
intestine up against body walL Right paralumbar 'pings'
can indicate cecal tmpany, left paralumber 'pings' can
indicate gas within the large colon.
Rectal examination can be a helpful diagnostic prn
cedure in horses with postoperative pain. Rectal exami
nation postopen'tiveiy, as preoperatively, should be
done carefully and gently. Postoperatively, special atten
tion should be paid to minimizing straining in response
to the examination to avoid any increased stresses on
the incision line. Chemical sedation, the use of a twitch,
and rectally administered Ildocaine (lignocaine) may
al! contribute UJ a reduction in straining.
t:ltr<sound examination is an extremely useful diag
nostic [001 forsmal1 iIltestinal problems (see Chapter 2).
V-!hen small intestinal distention is suspected a5 the
cause of pain transabdominal ultrasound is very helpful.
Other diagnostics that should be considered in
assessing postoperative pain are gastroscopy, radiology
(especially in foals), and abdominocentesis. White
blood cell count. and total proteins should be inter
preted on the basis of the tpe of lesion identifed in
surgery, the degree of contamination, and the length of
time since surgery. In general, in the author's exper
ence, white blood cell count and total protein measure
ment in the abdomen postoperatively have not been
higher than 40 000-50 000 cells/l and 3.5-4.0 gldl,
respectively at approximately 4--5 day; following
abdominal surger in cases that were progressing well.
TREATMENT
Goals
The goal in treating postoperative pain is to provide
quick efective analgesia, and to eliminate the reflexes
206
(ileus, intestinal spasm) causing the pain. Although
elimination of the problem is not always possible,
reduction of pain with effective analgesics will decrease
the reflex inhibition of motility. This in tur often
resolves the common causes of postoper<tivc pain such
as distention due to ileus, and inflammation due to
intestinal manipulation. Effective analgesia will also
eliminate or minimize the vsceral sensitization or 'wind
up' that ultimately requires higher and more frequent
doses of analgesics resulting in toxic side effects.
Decompression
Decompression is the best way to relieve pain due to a
distended vscus. Nasogastric intubation can reduce gas
tric tympany or remove gastrointestinal reflux due to
ileus. One of the most common reasons for postopera
tive pain in the horse is ileus of the small intestine
especially following extensive small intestinal resection.
Nasog-<stric tubes can be left in place for chronic
decompression, however some clinicians feel that tubes
left in place may also initiate gastrc reflux. Regardles
of this, ifhorses are sufering postoperative pain, a naso
gastric tube should be passed and the presence of
reflux determined.
Walking or acupuncture
Walking may also have an analgesic efect on abdominal
pain especially mild pain. This is a common therapy
that appears to increase motility and reduce anxiety.
Some surgeons have also used acupuncture. "I'hile clin
ical data are lacking, some clinicians teel that the posi
tive effects can be appreciated and the risk of hann or
toxic effects is minimal.
Systemic analgesia is the most common method used to
control colic. Various classes of drugs exist that have
been used for abdominal pain. Clinical trials reporting
anecdotal evdence of efcacy have influenced clini
cians' choice of drugs. Drug trials also exist that have
used distention models to mimic abdominal pain.
According to these trials drugs exhibiting the best effi
cacy were flunixin meglumine, xylazine, detomidine,
and butorphanol, see Table 1 1.3.
The most useful and commonly used perioperative
analgesics are the non-steroidal anti-inflammatory
drugs. These drugs reduce the production of throm
boxane, prostaglandins, and prostacyclin through the
inhibition of cydooxygenase (COX) enzymes. It is now
known that there are to isoforms of COX, designated
as COX-l and COX-2. The constitutive enzyme COX-l
perorms 'housekeeeping' activities in platelets, gastro-
POSTOPERATIVE TREATMENT AND COMPLICA nONS 1 1
1Wl1A"""."dtr.;--
".i Un-
.
An.lgulc DOS.,. Efelv-n ..
Aspirin 20-40 mg/kg p.o. poor
BWtorphanol 0.02-.075 mglkg Lv. good
Chloral hydrate 30-0 mg/kg Lv. titrated fair
Deomidine 1(40 mglkg i.v. excellent
Dipyrone 10 mglkg Lv. or tm. fair
Eltenac 0.51 mg/kg undetermined
Flunixin meglumine 0.25-1.1 mg/kg Lv. or Lm. exceUent
Ketoprofen
Udocaine2%
Phenylbutazone
Xylazine
intestinal mucosa, and the kidneys. COX-2 is upregu
lated in inflamed tissues but is found only in small
amounts in normal cells. It is understood that inhibi
tion of COX-! is the cause of adverse eflecs of NSAIDs
and that anti-inflammator and analgesic effects result
from COX-2 inhibition. Prostaglandins (PGE and
PGI) sensitize nen:e endings t pain and are poten
tially responsible for amplification (visceral sensitiza
tion) of pain during bowel distention, ischemia, and
inflammation. Furthermore. prostaglandins facilitate
transmission of nociceptive impulses peripherally and
affect pain perception in the brain. Flunixin has been
shown to specifcally block thromboxane and prostacy
din for 8--12 hours after a single dose. Its advantages are
the maintenance of normal blood flow to the bowd
during obstruction and a return of intestinal motility.
Flunixin can also be helpful in diminishing the
response to endotoxin release. For these reasons flu
nixin is the most effcacious and commonly used drug
to control postoperative pain in the horse. Inability to
control postoperative pain with flunixin should alert
the dinician to investigate the source of pain further.
Generic dosages commonly used by this author are
immediately postoperatively 0.5 mg/kg Ll.d. for 2-3
da.,., and then
0.25 mg/kg Li.d. for a further 2-3 days.
The dosage and frequency of administration should be
based on the intra-operative fndings. the demeanor of
1.1-2.2 mgikg Lv. good (variable)
slow Lv. bolus 1. 3 mg/kg over good
5 min. then i.v. drip at
0.05 mg kg-' min-1
2.2-.4 mglkg Lv. fair
0.2-1. l mg/kg Lv. or i.m. goocH)ceUent
the horse (horses with a low threshold to pain may need
more frequent dosing immediately), and any ongoing
reason for pain (ileus).
Phenylbutazone does not appear to provide visceral
analgesia as effectively as flunixin and does not inhibit
prostaglandin formation as weB nor for as long as flu
nixin. Furthermore its potential for toxic side effect is
greater. Its use appears to be more effective for muscu
loskeletal problems than for vsceral pain, although the
mechanism for this difference has not been elucidated.
Kt:toprofen has also been clinically tested in horses
with colic, the results indicate it provides signifcant
pain relief similar to flunixin. It also has similar effects
to flunixin in suppressing the effects of endotoxemia
and it reportedly has the least toxic side effects when
compared to phenylbutazone and flunixin.
Dipyrone is another lSAID reported to have anti
spasmodic effecL on the bowel due U inhibition of
bradykinin. Some inhibition of prostaglandin forma
tion does also appear to occur with its use.
Other NSAIDs have not been useful in treating colic.
Aspirin has a shon half life and has little to no effect on
abdominal pain.
Alpha2 agonists and sedatives
Alpha2 agonists are potent analgesics that bind to and
transduce biological effects of the endogenous
catecholamines epinephrine and norepinephrine.
207
1 1 COLIC
Recently, alpha.adrenergic receptors have been phar
macologically characterized into four subtypes
alpha.a
alphb
alpha2c
a!pha. d.
The alpha and alpha2c receptors are abundant
throughout the eNS and are coexpressed in some sites,
where alphatbs are absent in the brain.
The sedative and analgesic properties of adrenergic
receptor agonists are the result of inhibition of the nOf
adrenergic input to the hippocampus, thalamus, the
cerebral cortex, which results in behavioral depression
and reduced sensory processing. The central alpha
adrenoreceptor stimulation thereby modulates the
release of norepinephrine and causes direct inhibition
of neuronal fring. In many cases of postoperative colic
one dose can result in permanent relief of abdominal
pain. Visceral analgesia produced by xylazine at
l . l lllg/kggiven intravenously issimilar to that produced
by opioids and flunixin. however the duration is shorter
( 1 04 min). Bradycardia, decreased cardiac output,
hypotension. ileus, and reduced blood flow are all poten
tial side effects. Prolonged effects of xylazine can often
b accomplished with 0.4-2.0 mg/kg intramuscularly.
Detomidine is an alpha2 adrenergic agonist like
xylazine and has profound analgesic and sedative prop
erties. Similar to xylazine, its actions are centrally medi
ated. It can completely alleviate signs of colic for up to 3
hours. When compared to flunixin. or butorphanol.
detomidine had 5uperior analgesia. In fact. analgesic
effects can be sufciently strong to mask an ongoing or
new lesion. The comfort of the clinician in administer
ing detomidine is often much higher postoperatively
fo!Iowing explordtion of the abdomen than when
attempting to decide if a patient is a surgical case. Along
with the intense analgesia provided with detomidine.
reduced intestinal motility occurs along with reduced
cardiac output and reduced blood pressure. Other side
effects include sweating. salivation, and snoring.
Opioids
Opioid refers to all drugs. natural or synthetic, that
bind to opioid receptors and exert morphine-like
effects. Classifcation of opioids is based on a functional
breakdown of activity at opioid receptors. Therefore,
they are classifed as agonists, agonist.-antagonists
(mixed opioids), and antagonists. Opioids exen their
efects on the central nervous system in both the spinal
cord and brain. Antinociceptive pathways are present in
the eNS that descend the spinal cord and prevent
ascending pain-arrying tracts from completing their
208
route. First order neurons are prevented from releasing
excitatory neurotransmitters because of the pre- and
post-synaptic effects on the dorsal horn. Opioid ago
nists or agonis!S-antagonisl are helpful in controlling
colic. Pure agonisl such < morphine are potent
analgesics but they can also cause eNS excitation.
Furthermore, morphine is known to reduce progressive
motility of the small intestine and colon, while poten
tially increasing mixing movements and sphincter tone.
These concerns often discourage its use in the post
operative gastrointestinal patient.
Butorphanol is a partial agonist and antagonist
which prmides the most analgesia with the least side
effects. It has been reported to be superior for visceral
analgesia compared to f1unixin but not as efcacious as
the alpha2 agonists. When used in combination with
xylazine or detomidine excellent analgesic efect. can
be maintained. The dosage postoperatively is usually
0.05 mg/kg to 0.1 mg/kg intravenously. Butorphanol
does reduce small intestinal motility but has no effect
on the cardiovascular system except at higher doses.
Lidocaine (lignocaine)
It has been hypothesized that lidocaine alters sympa
thetic tone to the bowel by suppresing trdnsmission
through afferent sensory pathways. Experimentally
serosal damage. intestinal distention, endotoxemia,
peritonitis. and surgical manipulation have al! been
associated with enhanced sypathetic stimulation.
Lidocaine may prevent reflexive inhibition caused by
one or several of these factors by blocking lransmission
through afferent nerves. These factors have been docu
mented to increase the release of non-adrenergic and
non-cbolinergic neurotransmitters with alteration in
motility in rats and dogs. Lidocaine may inhibit the
release of neurotransmitters rather than alter sympa
thetic neurotransmission. None the less, clinical efects
in reducing postoperative ileus and pain have been
reponed in the horse. The dose rate reported is an
intravenous bolus of 1.3 mg/kg given slowly followed by
0.05 mg kg-I min-I. Side effects that may be produced
include muscle fasciculations, ataxia, delayed detection
of laminitis pain and potentially increased incisional
infection rates.
CONCLUSION
Proper postoperative pain management and successful
alleviation of pain is critical in minimizing patient mor
bidity. Pain increases patient risk during anesthesia
because of the larger amounts of drugs required to
maintain a stable plain of anesthesia. Pain enhances the
inflalnmawry response, this in turn increases the pro
dunion of pain neurotransmitters which further raise
Ihe inflammalor response resulting in an elevation in
the excitahility of sensory neurons. Pain produces a
depressed state, increases inflammation, reduces wound
ilt'alillg, and depresses the immune response.
Pharmacotherapy should be directed at peripheral noci
ceptofs, primary and secondary spinal neurons, and
pain-proclssing areas in the eNS. These areas include
"pioid receptors, drugs that bind to alphat reLeptors,
and drugs that reduce d HOU prostaglandin synthesis.
Based on the intraoperative procedures done in
.. ach horse, appropriatl analgtsia should hI provided
in Ihe perioperative stages. Preventative pain manage
mellt should be instituted before progression ofdinical
sigm occurs postoperatively in these horses. Often
early, subtle signs of pain lIlay be overlooked. Early
diagnosis and tnatment of abdominal pain decreases
overall patient morbidit), and the cost of patient care,
thereby allowing tbe clinicians' tilile to be better spent
on illore productilie endeavors.
Abdominal adh esions
SL Fubini
INTRODUCTION
'Adhesions are both the salvation and the bane of the
abdominal sUIgnm' (editorial, Th I.anal,July 5, 1980).
Formation of a fbrous union beh,'een serosal surfaces is
esselltial for a successful completion of abdominal
surge!' sucb as an intestinal resection. Howelier,
unwanted adesions are responsible for RO-90 per cent
of intestinal obstruction in humans. Adhesions are also
a grave prohlem in urogenital surgery and are responsi
ble for the frequent failure of infertilit surgery' in
WOllle11. Pathological adhesions arc the most common
reason for deatb and repeated episodes of abdominal
pain after small intestinal surgery in horses, There is
speculation in the veterinar literature that the percent
age of 'symptomatic adhesions' is higher in the horse
than other species. With sucb a high prevalence of
adhesions in humans and horss, it is possihle that
studies focusing on adhesion prevention in bumans
could be applied to the horse a'pd vice lersa.
INCIDENCE OF ADHESIONS
It is virtually impossible to aecurately determine the
incidence of postoperatile adhesions in horses because
so many animals are managed medically, remain
asymptomatic, or die or are euthanized without an
examination, Estimates of the incidence of adhesions
are taken fromreports following repeat celiotomy and
necropsy, or from experimental studies. Adhesions
were the second-most common (18.9%) reason for
repeat laparotomy in one study, All the horses that had
obstructing adhesions at the second surge!' had a
small intestinal lesion at the first surgery. Other
reports documenting the incidence of adhesions in
horses following small intestinal surgery range from
6 22 per cent. and 5 per cent follov"oing all equine
intestinal surgc!'_
It may be that the smali intestinal serosa is more
prone to damage from distention, ischemia, and manip
ulation. Furthermore, the multiple loops of the small
bowel with its long mesentery' and relatively small
lumen make it more likely to become compromised
from adherence to acUacent loops and subsequent
mechanieal obstfULtion. Other risk factors include
borses that require repeat celiotomy, deyeiop peritoni
tis, or have prolonged ileus.
There is speculation that adhesions are more com
mon in foals and Miniature Horses than in adults.
However, without specific, controlled studies concrele
conclusions cannot be made.
PATHOPHYSIOLOGY
Adhesions result when there is an imbalance between
fbrin deposition and fibrinolysis. Trauma to the vis
ceral or parietal peritoneum results in an inflammatory
response and rdeae of mediators including histamine,
serotonin, prostaglandin E, and cytokines causing an
increase in capilla!' permeability and extravasation of
protein into the abdominal fluid. The tissue inju!' also
resulL in release of tissue thromboplastin which acti
Y<ltes the intrinsic coagulation ca.cade. This set the
stage for fibrin deposition bet\veen adjacent surfaces,
Concurrently the fibrinolytic system is activated by tis
Slle plasminogen activators released fom inflammato!'
cells. Plasminogen is converted to plasmin which, in
turn, lyses fbrin,
This delicate balance is maintained by plamin (con
verted from plasminogen), antithrombin III, and pro
tein C. In altered disease states such as the preselln of
ischemic bowel or peritonitis, there may be alterations
in these regulators. Antit.hrombin III and protein C
both halie activit)' against coagulation factors. Protein C
also inactivates plasminogen activator inhibitor-l
thereby promoting fibrinolysis. The prima!' inhibitors
of fbrinolysis are plasminogen activator inhibitor-I.
which prevents the formation of plamin by inactivating
209
1 1 COLIC
tisslle plasminogen aclivlI[Of, and a[ph-antjplasmin
I,"hkh inaClhdU plasmin.
If Ill( 5l1d re.\ult is 311 imrainncllt in fbrinolysi.,
(hen fbrin()l1 bnds become infhrated "llh fbmblasts
whi.-h produn collagen a a potcntially p'ommelll
arlhtion. This proccs is usualy complete by 7-14 cla
Imt lhcn: may I rcnwdding II limV.
EXPERIMENTAL MODELS OF
ADHESION FORMATION
Unfortunately. thQre is IL one completely repro
dudhlc mudd for adhcion production. Over the years,
(Jp{:rim(!ntal sludic haW! used either lllodels where
scr(ls<ll trauma i cn:al,d or an ischemic insult is
simulated. Typicll1) hthnratory animals arc used and
hrcausc of the diffcrt:nr pathways involved extrapola
tion !xtwccn speciLs is questionable.
Traul1nuic models include abr.Li()n oflbe serosal sur
facCli or p<:ritoT1cum, serosal drying in the presence of
frh undolted blood, intcninal ditcnli{)n, and sutur
ing of peritoneal or sersal defecL, Ischemic models
include combination of arterial and venOllS occlusion,
or a cI;unping of the intestinal or uteline wall.
SURGICAL PROTOCOL
Adherellce to the surgical pr
i
lll:ipies of minimizing
'time, tmuma. ltnd nash' is the best way to decrease the
J\k of p')topcratlvc adhe.ions. Short, efficient surgical
times, "ith gentk tissue handling, strict adherenre to
,1\{ptir t{'(:hniqllc, and minima! foreign material left in
the abdomen i ideal. Expo.cd mucosa, drying of the
N!\^d, and ischemic tissue all increase the risk of adhe
sions. SnUe urgcons adl'ocate omentectomy for adhe
sion prevention. Horses should be on broad-spectrum
antibintics and non-stcmidal anti-inflammatory drugs
perioperativc1y if abdominal contamination is antici
pated. Thcrap!:lltic regimens can he aqjusted afer
surg(:I1'
ADHESION PREVENTION
I" a I"el'it:l" 4nick in 1991, Pijlman 1 aI. dcrib 'fve
fund:un('nlal attacks' lor idhcsiun rrlntion frst
describcd by Bo}' in 1912, te <r Mill thc bis for
t:urrt'llt ildhcsion s!Udies. nlc categorie arc 10
limit or prc'l'nt rxriwneal injury
rren'l c'!I<tgulation ofs(rous exudate
JCmov(' 1dissolve the deposited tibrin
210
keep the fhrin-coattd peritollea! surfaces apart
inhibit the tihroblauic proliferation once
csuhlished.
T calcgmics call be regrouped into fourdi\i!;iolls.
Hurln o the injiammntmy 'u
D:casing peritol1CUl infammation is best done b
adhering W atptic and atrdumatic surgical pinciples.
I t also hclp. avoid dCurc of the peritonea! defect z1>
thi has been hown !V increase: adhC'.ions. One recent
study adl'ocates ptl!wpcratil'c pcritonc<1 lamge <^ a
mechanism to remol'e fbrin that tmps b<cteria, thereby
preventing peritonitis and subsequent adhesion forma
tion.
TherdpeU!ic: agents that have been tudjed as anti
inflammatory agentq indudc
I. Corticosteroids -studies in laboratory animals arc
poorly controlled and are cOntroversial. Repeated
corticosteroid use is nOI rommcndcd in the horse
became of the risk 01" laminitis and the possibility of
a ncgati\'( impar.t on wnund healing.
2. NOIH[(roicla\ antiinflammatorydrugs . these are
mulincly used perioperauvely in horses undergoing
abdominal surger. Again, sludies in Iilboratory
animals ha\( nOI been ctmcillsiv.
Inhibit;,,,o wn
g
flivn
Heparin, a cofactor of antithrOmbin Ill. h n ud
dinically and in one e7perimental tlldy for ahesioll
prevculon. In theory hcparin decrcas thrombin pro
duction and timulaw5 plasminogen :Clivdtor activity
which promote5 fbrinolysiS. There is not a consensus
on dosage or route of administrdtion of heparin
(reporLS I'l I from 10-120 [u/kg q. 6-21 h), but it
needs to be administered at the time of urgery.
Heparin therapy may cause agglutination of red blood
cells :nd a drop in packed cell volume.
Enhanunvml ojjbri7/o!)l"\
Studies using plasminogen aCtiv:tors including fihrino
Iin, $trep[okif)ae, ann urokinase were varied and
inconclusive. More recently, time-type plasminogen
activator appears to be effective and safe in rat and rab
bits. FUr/her .Iudies are needed and the cost of [he
product is high.
;:e+o{+oqac-s
High molecular "eight substanccs and ph}"ca barriers
hl been used in the peritoneal cvity kcep fbrn
covered surface, apart long enough to allow ror
mesolhelial repir and to pn:vent adhesions. Sodium
c;uboxymelhyl cellulOSe (SCMC) h been used most
fommonly in the ho @ a 1 % solUion at a doSt of
7 ;ljkg. It is used to coat serosal surfaces and to help
protect the bowel during intestinal manipulation.
Polyvinylpyrrolidone, dextrans, and hyaluronan are
othn polymer solutions thal have shown some promise
t'xp(rimentally. For more details on these and physical
barrkrs, see Southwood and Baxter ( 1 997) and
Chapter JO.
ADHESION TREATMENT
Horses with evidence of partial obstftlction (Iow-grade
abdominal pain) may r(spond to medical management
induding demal work and a laxative diet such as
pasture or low-residue feeds.
In some cases of adhesions, euthanasia may b indi
caled. In other instances, repeat celiotomy with
adhesiolysis and/or bypass of the affected segment may
be successful. Unfortunately, broken-down adhesions
ar{ highly vascular and may re-form unless the involved
tissues are resected.
The long term sunival rate following repeat
celiotomy is poor. Hopefully, as our peri- and intra
openttive anesthetic and surgical knowledge advanc('s,
so will our understanding and ability to prevent cala
strophic adhesions.
I leus
P Rakestraw
DEFINITION AND INCIDENCE
lIeus is the impairment of aboral transit of gatrointeti
llal contenL'i. The term has been uscd in dillerent ways
in the equine literature, sometimes vel;' broadly to
include both functional and mechanical obstructions,
and sometimes its use is limited to functional impair
ment of gastrointestinal transit. In this chapter the
author defnes the term ileus as a functional obstruc
tion (adynamic ileus) of aboral gastrointestinal transit.
Ileus is one of the mOSl commonly encountered
complications of equine gastrointestinal surgery. In
ho!"s, postoperative ileus (POI) occurs predominantly
after correction of lesions involving the small intestine.
POI may also be seen after correction of ascending
colon lesions, primarily large colon vohulus. Traumatic
handling of the intestine, intetinal dilention, resec
tion and anastomosis, and intestinal ischemia may con
tribute to ileus in these cases. Other conditions that
havc been associated with ileus are anterior enteritis,
peritonitis, electrolyte imbalances, endotoxemia, and
anesthesia. In a recent report, POI developed in 21 per
cent of horses undergoing surgical lreatment of colic,
and 1 3 per cent of these cases dicd. Although current
management of these cases has improved, postopera
tive ileus is still associated with 40 per cent of all post
operative deaths in horses "'th colic.
PHYSIOLOGY OF NORMAL MOTILITY
Inteslinal smooth muscle cells demonstrate cyclic
changes in membrane eIf'ctrical poto"lllial that are
called 'slow waves' or 'pacesetter potentials'. The
smooth muscle cells arc connected to each other by gap
junnions which enable the electrical activity of one cell
to affect the activity of an adjacent cell (electrical
coupling) through the movement of ions. Since the
frequency of the membrane oscillations is highest in
proximally located cells. thesc slow waves are initiated
orally and propagated aborally. They are sub-threshold
in that they do not depolariLc the ceIl suffciently to
reach the threshold to generate an action potential.
111ese sub-threshold fluctuations afe controlled primar
ily by inlrinsic properties of the smooth muscle cdls.
Additional depolari7ing (excitator) input from the
enteric (intrinsic) or autonomic (extrinsic) !lelVOUS
system allows the memhrane to reach the threshold
potential necessary to generale an action potentiaL
'Spike potentials' or spiking activity refer to membrane
fluctuations which exceed the depolariLation threshold
for an anion potential o are associated with muscle
contraction. Spiking potentials are usually super
imposed on slow waves since at the peak of slov,' \\a\'e
depolari/.ation the cell is closest 1 its threshold for
generating an action potentiaL This is why slow waves
are also called pacesetter potentials.
The activity level of the intestinc is not constant bw
goes through periods of quiescence alterating with
periods of spiking activity. The patter of these difkr
em activity periods in the stomach and small imestine is
called the migrating myoelectric complex (MMe).
There are four phases of the \fMC
phase 1 describes a period with no spike potentials,
so no contractions occur
phase 2 is a perod of intermittent spike potentials
phase 3 is associated with regular spiking activity
phase 4 is associated with rapidly diminishing
contracliie activity.
Each phase migrates down thc stomach and small intes
tine. Phase 3 is generally associated with propulsion of
ingesta, and in the horse phase 2 has also been associ
ated with propagation of ingesta. In the cecum and
211
1 1 COLIC
large int("tjnc. ()W \\"
.
vcs and spiking aCliviry aIm
occur. H,\\,'c\'CI' M1C:' arc no. evident. Instead. short
spikt" bursts (SSB) o7cur during mixing, and long spike
hurm (L5B) rluring pl'Opulsioli ofingsla.
PATHOPHYSIOLOGY AND
THERAPEUTIC MODIFICATION
It should he e\;nclll from the above description of the
ph)si{)k1 of norma] m()tility [hal mallY different rae
LOrs must he pr('ci dy coordinated in order to produce
!)I'OdUClive mOlility pa\terns. The intestine must 11A~
tract in a CO(lNlinaled manner, while the aboral s.cction
is simuhalHolLsly inhibited and relaxed U allow pro
gressive Iranit t V\\14 An imbalance in Ihe E:tors
conlmUing eXcitaTion and inhihition of gastrointestinal
Iran .smnmh muscle may pn:disposc a horse to ikus.
Cons('qucmly. an attempt ha. .. heen made to identify
prokintlic agcn
t
.. that wnnld restore the halance
1>('t\'l'n cxduuo!'' and inhihitol)' control of (lmtractil
ity. Ph,U'ltlaco[ogical modulation aimed at int:rcasing
I')c.llatr) <lc.lt\lty has principally inmlvcd Ih adminis
tr
.
Uillll HI par.t'ympathomimti(: agnl, such ...,
hClh<lm:cnl or Ilco:tiglnjnt. whic:h inne<SC cholincrgic
Iransmis.ion. Similarly, clipride urh :n indiT.'Ct
p<uas)1Ipa[homim('tic h timuhlting serotonin rccep
41 . Iand so cnhandng acetcholine rd. Aucmpls
hind, inhihitm) components or contractilily ha\'e
r(lctlSI \ the ..ympathctk !rtem. S)111pathelic hyper
act"'i1r shoulc repond alpha adrenergic blockers
such 5 ))himhlne lnd acepromaJine. while adminis
tration of alpha adrenergic druhT such as "ylal.ne and
dctomidinc sh(Jultl dt:creasc motility. Metodopramide,
\hirh is <n1idopaminergir. among other propcrtie,
and mJllstr:r()itlal allli.illflammat(H), drugs have also
h('en used 10 intryr:m: ill ilem cases.
DIAGNOSIS
Disruption of propulsil'e motility rcsull in Ihe seques
[rati(111 of fluid. gas, and ingesta in the _egment of the
gasLrointsliL1al {('C! which is drfullt:tional and in the
iIHCstinc proximal m the ahnormal arca. Thi disten
lion 1L1.MI primaril)' in Ihe stomach and small intC5-
lillt', but tan ()<.ur in the larJc inltline. especially with
(olilis, enrlotu)emia, or iKhemia following a large
n,jon tJh11111S. The Imljor dinical signs and fndin
secn ill ht)J's alTerted by ptoperative ileus a
riepr$iotl
anorexia
aMominal pain
212
decn:a.'d or ah.ent borblllJ'gmi
abdominal (Iitention
elcvilVd heart nie
con
g
eslerl mul,)us mmbranes
prolonged capillalJ r(fJl time
natric rellux.
1e frst signs ... OKiatcd wllh ilelL' are repf un anri
anor()(ia. A the inltstillt! distends the horse demon
strates inaeasinp .i
g
lb or abdominal distnss such QN
pawing, flank watlhing, lying down, and rolling:.
Borbor'gmi arc u.uaHy dC:rt:a.t:d or ahsent. The hear!
ratc is initiall> Cle\'a!ed becal\e of the pain associated
with t.he distnlion.
'
1'11(: mucous memhranes hccollll'
discolored and capillary refill [ime is prolonged.
Heroc(JI\cemratio!l is rdIcClcd hy iJl(:rf<ls(:s ill the
packed cdl volume and total protein. Decreases in
plasllla (:hloride and potas. illm are the most comlllon
electrolyte ahnormalities seen, although sodium and
calcium may also b low. A the everity of the intesti
nal distention illcl'easts, abdominal distention may
become gro[r visihle. Rectal examination will help
determine if the small or large imestine is illvolw'd. In
foals, hmh <lbdominal radiograph)' and ultrasO!ln
grnphy can be quite hdprul in asMing distention. In
adnlts naastric decompresion orten relrit\ 310
litt1 of IIl1iC\. Tht.' response to nasl> tric del'om
p
rc
sion provides all important due that Ihe
p
roblt:m is
functional prohlem. Arter decompresiull the horse
should show some improvement such M (kcrcad
pain and htarl "Ue. Ir no alle\-latioll of signs are
observed, cartful lhllught should he gh'en to {he likeli
hood that the problem may he a mechanical It'Sion
and not a functional ileus.
SUPPORTIVE THERAPY
Although a varll:IY of prokinctir agent have hl'en
administered {() hones with ileu in an attempt
improve gastrointestinal motility, th(: lack of consenslls
as to which OIlC, if any, are effcctive attests to thir
therapemk limitatiolls (Table 1 1 .4) Consequelltly, th
hallmark ofLreatmclIt remains supportive therapy, with
fluid, add-o<lsc, and electrolyte therapy being L
important trCattnenl In ally hor:c with .. olie
Antihiotics are also indicated ir there is compromised
intne or the pihility or harlr (onlination&
CautilJll should be exerci sed whcn lreating le hor
with the common analgesics (snch Wthe alpha <lonistJ
")!<., .ne. dClOmidine and romifidinc, and the narcotic
agonist-antagonist butorphanol) < these medications
have the potential 10 depress gall'(inlestinal motilit}'
with n:pcatcd usc.
111.41mmuand Inlent o
prativeUeus
Fluid, acid-base, and electrolyte therapy
Antibiotics
flunixin meglumine
phenylbutazone
ketoprofen
Polymyxin B
Dimethylsulfoxide
Hyperimmune serum/plasma
Prokinetic agents
bethanecol
neostigmine
acepromazine
yohimbine
erythromycin
metodopramide
cisapride
lidocaine
NASOGASTRIC DECOMPRESSION
Rt'pl'ated attempts to relieve gastric distention are
imperative in trcating a suspectcd ilcus case. In certain
(a.,e reflux may not he obtaincd during thc first
allemp!. In horses \"hcre nasogastric reflux is obtained
the tube can he left in place or reliloved and intermit
t"lltly replaced to check for reflux. Tlw frequency of
attempting to decompress a horse with reflux depends
both on the dinical signs and the amount of reflux
Idrit-ved at each session. An increaing heart rate is
prohably one of the most sensitive clinical indications to
allempt to retrieve reflux. Increasing abdominal pain is
another indication. A the volume of reflux begins to
decline and reaches less than 1-2 l/h, the interval
h(,tw(en reflux attempts can he increased. It is not
l!llusual to ohw.in a liter or more per hour of rdlux frolll
horses, especially those who have:l nasogastric tube left
in place. This should not be mistaken as a condition that
lll"Ccssarily requires continued tratment. II" there is any
doubt, the tube should be withdrawn and the horse's
hean rate and level of pain monitored closely.
ANTIINFLAMMATORY
'ANTI'ENDOTOXIN DRUGS
Int('stinal distention, ischemia, and trauma occurring
dllrillg decompression and/or resection and anastomo
sis all induce inflammation of the bowel wall with an
increase in the production of inflammatory mediators
such as prostaglandin 12and Et
.
and tumor necrosis fac
tor. Endotoxin can also stimulate production of these
mediators. Each of thee inflammatory lIlediators has
heen shown to depress motillty when infused experi
mentally into horses. Consequently non-steroidal anti
inflammatory drugs are recommended for horses with
gastrointestinal inflammatioll that have ileus or arc at
risk of developing ileus. The most commonly used
NSAID is flunixin meglumine (0.25 mg/kg t.i.d. i.v. or
l . l mg/kg h.i.rl. i.v.). It alleviates some of the systemic
effecL of endotoxin and also provides some analgesic
relief. The other comlllonly used KSAID is phenylhuta
zone (2.0-1.1 rug/kg h.i.d. p.o. or i.v.). Although this
drug is not as potent as flunixin in blocking the cardio
vascular efICcts of endotoxin, it does appear effective in
reducing the motility disturbances associated with
experimental endotoxin infusion. Ketoprofen (2.2 mg/
kg h.i.d. i.v.) has not been evaluated in ileus models,
however because of its anti-prostaglandin and anti
IcukO!ri{ne actions, it lIlay also be effective in promot
ing motility. In addition to blocking cndotoxin effccts,
thc analgesic propertics of these drugs may attenuatc
potential inhibitory sympathetic reflexes. High dosages
and prolonged use of NSAID may inhibit large bowel
motility.
Another drug that is used at the author's hospital to
treat horses with ileus is polylllyxin B (6000 IV/kg s.i.d.
i.v.) a cationic antibiotic that binds lipid A ,md neutral
izes endotoxin. Dimethylsulfoxide (DMSO) is a
hydroxyl radical scavenger commonly used to treat
endotoxemia and other inllammatol}' processes in
horses at a dosage of 0.5-1. 0 g/kg (10% solution i n 5%
dextrose). Although it has not been evaluated relativc
to promoting gastrointcstinal motility, its anti-inflam
matory actions may be bendkial in preventing or
decreasing the scverity of ileus. Commercially available
hyperillllllune serum contains anti-I.PS antibodies to
Elrlilil'hia loli or Salmonella Iyphimurium. These anti-LPS
antibodies theoretically cross react \\ith endo[Oxins
from all gram-negative bacteria. The evidence for their
efficacy has not been conclusivc.
PROKINETIC AGENTS
Bethanecol
Bethanccol chloride is a muscarinic chdlincrgic agonist
which stimulates acetylcholine receptors on gastro
intestinal smooth muscle. causing them to contract.
Support for the use of bethanecol in the treatnlt'nt of
motility disorders in tht horse is predicated on ohserva
tions in normal horses that it increases the rate of
213
1 1 COLIC
gastric and ceciI emptying as measured by radiolahded
isotopes, and it induces premature MMC phase 3-likc
activity in the ileum. Although its eflicacy in the treat
ment of experimentally induced mO(.ililY dysfunction
has betn questioned in the horse and other species, its
prokinetic effcts in norml! horses and the clinical
impres.ion of its benefit in treating horses with ileus
.llppons it usc in the treatment of certain gaslro
illlcstinal motility dysfunctions such as POI and ceca!
impactions. The recommended dose is 0.025 mg/kg i.v.
or N`, (wr 4 hours. The most common side effect of
!he drug is salivation, with abdominal cramping and
diarrhea occurring les frequently.
Neostigmine
Neostigmine methylsulfate is a cholinesterase inhibitor
which increases the level of acetylcholine at the synaptic
junction. In studies on normal horses the efects of
neostigmine (0.022 mg/kgi.v.) varieddepmdingon the
location of the gatrointestinal tract examined. It was
shown to delay !f astric emptying and decrease propulsive
motility in the jejunum, to increase propulsive motility
at the pelvic flexure. In another study, neostigmine
increased the amplitude of rhythmic contractions in
both resting and distended jejunum in anesthetized
ponies. More recently, neostigmine (0.025 mg/kg s.c.)
wa. shown to induce premature phase 3-like activity in
the ileum ,Uld increase the rate of cecal emptying. There
has heen no consensus as to the recommended use of
this drug. It appears to be an effective drug for large
colon motilit problems, but these OCCUI" infrequently.
Some evidence suggeSL'i it Illay also be useful for POI with
small intestinal motility dysfunction. I Iowever, its usc for
impactions or in cases with excess gastrointestinal dis
tention has not been recommended because of the
apparent force of drug-induced contractions. The most
COillmon side effect is ahdominal pain.
Acepromazine and yohimbine
Both of these drugs arc alpha adrenergic antagonists.
Elevated serum catecholamines have been associated
with increased synthesis of norepinephrine in the bowel
wall in humans after laparotomy. :\orepinephrine is an
inhihitory neurotransmitter released by post-synaptic
sympathetic Ileurons at the enteric ganglia. It inhibits
the relea.e of the excitatory neurotr.lllsminer acetyl
choline by stimulating alpha-2 receptors located on
cholinergic neurons. Acetylpromazine maleate (ace
promalinc) facilitates small intestinal transit in normal
ponies. Rased on clinical impression. acepromazine
(0.01 mg/kg i.m. q. 4 h) is thought to reduce the sevn
ity of POI in horses with small intestinal lesiom. Care
. h()u!d be taken 10 make Sllre the horse is well hydrated
214
as the drug can produce hypotension. Yohimbine
administered at 75 Ilg/kg was demonstrated to attenu
ate some of the negative effects that endotoxin has on
propulsive motility. Since this dntg is a seJectiw alpha
antagonist it docs not produce the hypotensive
response seen with acepromazine.
Erythromycin
Erythromycin is a macrolide antibiotic that enhances
gastrointestinal motility by acting on motilin receptors
on smooth muscle, and by acting on enteric neurons
through motilin and/or 5-HT receptors to stimulate
the releae of acetylcholine. It is a commonly used drug
to treat gastroparesis in humans. At 0.5-1.0 mg/kg in I
liter of saline infused over 60 minutes four times daily.
the drug induces small int.estinal phase 3-like activity
and increases the rate of gastric and cecal emptying in
normal horses. Side eflcts are infrequent but some
clinicians have reponed obse!\ling abdominal pain and,
in a fCw cases, diarrhea.
Metodopramide
Metodopramide is thought to exert its prokinetic
actions primarily though dopamine receptor antago
nism. It mily also indirectly stimulate acetylcholine
release and block adrenergic activity. In a POI model,
metodopramide was more efl"nive in restoring gastro
intestinal coordination, a measurement of motility
strongly correlated to return of normal transit, than
adrenergic antagonists or cholinergic agonists. In
horses the drug is commonly administered al a dosage
of 0.25 mg/kg, diluted in 500 ml of saline, infused over
30-60 minutes. Some evidence suggests that a continu
ous infusion (0.04 mg kg-I h-I) may be more effective.
Metodopramide (especially at the 0.25 rng/kg dose)
may cause extrapyramidal side cffecb such as excite
ment, restlessness, and sweating. It may also produce
abdominal cramping.
Cisapride
Cisapride is probably the most commonly used pro
kinetic in human medicine. It appears to function a an
indirect cholinergic stimulant by .electively enhancing
the releae of acetylcholine from postganglionic oen
rons in the myenteric plexus. In numerous trials in
other species cisapride appeared more effective than
metoc\opramide in stimulating progressive smaIl and
large intestinal motility in experimental ileus models. It
has also been shown to be effective in prcvcnting POI in
horses. Unfortunately it is only available as an ofal
preparation which is ullsuiLable for horses \'1th reflux .
Recently it was found that the drug is not absorbed in a
consistent manner rectally ill horses and so this route of
Mlministration should not be rdied on. Lse of the oral
preparation in horses with large colon motility dysfunc
tion may be efcacious. The bioav:iIahility of the oral
preparation in the horse is not as good as in humans
and so the recommended dose is 0.3-0.4 mg/kg.
lidocaine (lignocaine)
Lidocaine hydrochloride has four proposed mecha
nisms 01 action. It may
reduce the concentration of circulating
fatecholamines by supprcssinl tht
svmpathoadrcnal response
. suppress activty of the primary afferent neurons
imol\'ed in reflex inhibition of gut motility
3. stimulate smooth muscle directly
4. decrease the infammator response.
Tlw dose used to treat horses is an initial holus of
1. 3 mg/kg i.v. administered over 5 minutes followed by
(J.U} mg kg mire' in saline over 24 hours. Side effects
include muscle fascicul:tions, trembling, and ataxia.
PROGNOSIS
It is the author's impression that the incidence of POI is
decreasing. This may be because of more timely refer
r<lls and improved anesthetic, surgical, and medical
management of the high risk cases. \Vhen ileus docs
O("(.Ul". the horse is ohen treated with different pro
kinetic agents depending on \'hich clinician happem to
tah care of the horse. This author prefers to use lido
caine in caes with significant small intestinal inflamma
tion as the frst prokinetic followed by erythromycin.
Ilowe\'Cr, the author ha seen other clinicians usc all of
the prokinetic :gents discussed above. It is likely that
each of them will promote motility toa limited cxtent in
certain cascs, but nonc of them will dramatically increae
progressive motility in tht' horse with ilcus. However, it
is also the author's impression that with appropriate sup
portive therapy the ileus will most likely be transitory and
r{'so]ve in 2- days. In cases where it docs not respond,
a serond laparotomy may be indicated.
I mpaction at the anastomosis
P Rakestraw
Impaction at the anastomosis is an uncommon surgical
complication. In one repoft, 53 of 648 cases treat.ed
surgically for acute gastrointestinal obstruction were
suqjected to a repeat celiotomy. Only 3 (5.5%) of these
53 repeat celiotomy cases had impaction at an anasto
mosis. When they occur, they are often associated with
too rapid an increase in the amoum of food ofkred to
the patient in the postoperative period. Although some
cases of 'ileus' may actually involve impactions at the
anastomosis and resolve vlth fluid therapy and time, it
is often necessary to perform a second laparotomy to
correct this condition.
Impaction at the site of anastomosis of the small
intestines occurs early in the postoperative pcriod, i.e.
day 3-7 postoperatively. For small intt>stinal lesions
without nasog:stric reflux, the author often ofIcrs a
small amount of feed (a handf\ll of alfalfa) within the
frst 24 hours <nd slowly increases the amount fed at 3-4
hour intervals over the next 72 hours. It has been sug
gested that this early return to feed facilitates the return
of normal gatrointestinal motility, since withholding
feed can decrease gastrointestinal motility. With small
feed increases and careful monitoring of the patient it is
unusual for impactions to develop. If feding is
increased too rapidly and an impaction occurs, a sec
ond surgery may be necessary to massage the impaction
pat the anastomosis. In most instances it is not neces
sary to redo the anastomosis, except if there is a stric
ture or an apparent surgical errOf with the existing
anastomosis. The author has seen the leat number of
problems with single layer interrupted end-to-end
jejunqjunostomies. Two layer closures of endow-end
jejUltojunostomies may potentially restrict relaxation
and dilation of the anaswmosis site as a peristaltic wave
aUempL to propel ingesta across the anastomosis. Some
surgeons feel that jejunoileostomies arc more predis
posed to functional problems and therefore are more
likely to lead to an impaction. This is why
.
ijunocecos
tomies arc preferred. A large stoma in a side-tn-side
jejunocecostomy minimizes the risk of impaction at the
site btl! has the potential to allow reflux of ingesta back
into the jejunum trom the cecum during cecal contrac
tions. An endow-side jejunocecostomy may decrease
this reflux problem but because of thc smaller stoma it
may increase the occurrence of impaction early postop
natively. A compromise would be a '/ish mouth' end-to
side jejunocecostomy anastomosis.
Impaction at an an:stomosis in the large colon usu
ally occurs because the stoma which was made when the
colon was very inflamed and edematous has decreased
in size over time. Therefore impaction at the site of
anastomosis of the large intestines occurs late in the
postoperative period, i.e. month 1-3 postoperatively.
Surgical correction is necessay to enlarge the stoma.
The sm:ll colon is potentially more susceptible to
impaction at the anastomosis (Of enterotomy) because
215
1 1 COLIC
of the firm consistency of the ingesta in this region.
These impanions at the site of anaswmosis of the small
colon occur early in the postoperative period, i.e. day
3-7 posloptfatively. Vlith careful management, for
example emptying the large (olon at surgery, fluid ther
ap)" and slow placement hack on feed (small handfuls
of allall"l ), these also occur infrequently. A with the
small intestine, it is usually not necessar to redo the
anastomosis unless a stricture or surgical error is
apparent.
It should be remembered that appropriate timing 01
a re1aparotomy may make the diference between a suc
cessful ourcorne or a f;lilure and should IH! he delayed
if the horse is not responding as expected medically.
I ncisional compl ications
NG Ducharme
INTRODUCTION
Approprhnc lluimp<.'dcd wound healing reSU!L in sum
clem slnngth in the tissue layers to allow a return to
excn:is( for the various athletic activities that horses are
expected to perform. The prevalence of incisional (Olll
plirariolls alter gastrointestinal surgery in horses ranges
trom fi-37 per cenl. The I"arious incisional complica
tions indudc
d<hicnC{
drainage
heria.
Ally incisiollal drainage at an incision is suggestive of
abnormal wound healing. Drainage delays wound heal
ing and weakClls abdominal fascia.
PREDISPOSING FACTORS
The veterinarian and animal a!tendallt responsible for
postoperative care of palient should 1) a\vare of the
i]J{H;\scd risks 10 animals experiencing incisional com
piic<ltions. Factors that influence th occurrence of inci
sional complications are either
under the cOlllrol of the surgeon, or
outwith the control of the surgeon.
Farlors in the former group that surgeon can control
,!re
ue 01 optimal surgical tchniques and materials
(sec Chapter 1)
216
duration of surger, this should be less than 2 hours
usc ofgood perioperative pain control
length of convalescent period, the horse should be
kept out of training until at least 2 months
postoperatively.
Factors that incretse the risk ofincisional complications
but are beyond the control of the surgeon are
open bowel procedures involving the large intestine
repeat incisions in the same animals
debilitating conditions such as hypoproteinemia
stormy recover
agf of (he animal, animals less than I year of al{(
have a lower incisiona! complication rate than older
horses, perhap because of the lower weight of tlw
animal or the ability to assist the recovery of tJltse
patienl.
CLINICAL SIGNS
Acute incisional disruption (dehiscence)
Acute incisional dismption generally occurs withill H
days of surgery tnd, fortunately, is extremely rare. \:arly
clinical signs arc brown serosanguinous discharge with
a progressive increase in drainage from the incision.
Palpation of the incision with a sterik, gloved hand
will reveal gaps in the incisional wall apposition.
Ohse!\atioll of omentum at the incision site is a grave
sign of impending dehisccnce. In most cases, physical
examination identifies the diagnosis and extent of the
problem. In some cases ultrasound examination will
assist in defining the extent of the lesion.
Incisional hemorrhage
Clinical signs are obvious in so far as blood is draining
from the incision within a few hours after surge!)'.
using physical examination, the clinician can deter
mine if the hemorrhage is due to tn arterial bleeder
from the incision, one or more venous bleeders
from the incision, or intra-abdominal hemorrhage.
Incisiona! arterial hleeders have a small stream of hem
orrhage spurting from the incision while venous hleed
ers 001( out of the incision at one or more sites.
Intra-abdominal hemorrhagc is manifested by moder
ate to large amounts of blood oozing from one ur more
incisional sites. If there is a high rate and volume of
abdominal hemorrhage, allY of tire following systemic
signs of hemorrhage may be seen
incional bleeding
decreased pulse quality
blanching of mucous membranes
increased respirato!)' rate
itKre;lsed heart rate
illtfa-abdominal pain
decreasing hematocrit after 24 hours.
III addition. the accumulatjon of intra-alxiominal fluid
{ail he fo!Iowed by abdominal ultrasound.
If excess serosanguinous fluid was left in the
abdomen, or one or more linea alba sutures failed, peri
tOlwal fluid will leak out of the abdomen. Because of
tht' dye effect of blood on peritonea! fluid, it may be dif
ficult to diffrentiate this condition from intra-abdomi
nal hemorrhage. However. measuring the packed cell
\'()Iume of the fluid draining out of the abdonwn or col
len(d by abdomiuocentesis will differemiate the two
conditions. I n additioll, ultrasound examination of the
inci.i{)n will identil' i!l{:isional defects and increasing
pnitoneal lluid volume, The latter would not be
,'x
l
wcted to on:ur within a few hours of surgez.
Incisional drainage and infection
Any incisional drainage, except perhaps Jill' mild bletd
ing ;] few hours postoperatiwly. should be considered
abnormal and may represent an incisional infection.
The presellce of serosanguinous fluid or purulent
drainage should be evaluated carefully, and Olle should
dosdy monitor the degree of peri-incisional sweHing
and tenderness. If a large quantity of fluid drips from
the inci,ion. the possibility of peritonitis and partial
dehiscence of the incision should be considered. ASter
sterile preparation at the drainage site. a sample should
Ilt, obtained for cytological and/or bacteriological
cvaillation.
IncisionaI hernias
Incisional herias may be .ec[)!ldaz:' to
>utun' or abdomina! wall failure in the
pot[)perathe period
incisional infection
carly return 1 exercise.
Tlw last cauS of incisional heria is ,,'en in horses
tumed out too early after surger . , The strength of tbe
abdominal wall does not return to normal until many
months after surgery. Therefore, horses should be
restricted 1 a box stall for 6 weeks postoperativdv,
although daily hand walking should be allowed. The
abdominal incision should be evaluated prior to turn
ing the animal out to pasture br an additional 6 weeks.
III the author's experience, alter 3 months tbe risk of
incisional heria is negligible. A rennt report suggests
that a 2-month postoperative incision has suHkielll
strength to withstand normal activity.
Two types of incisional h(rias can be seen post
operatively.
1 . A Traditional hernia within t.he incision with a
reducible herial sac, tbese should he surgicalIv
revised.
2. IIerniation tbat is actually a thinning of selected
areas of the inclsioll. In jumpers and br{)[xi mares,
t.hinning of inc isiona 1 areas should be repaired
6ther by applying a mesh over tbe arca or by a
complete revision of the incision. Other horses,
even racehorses, wirh unrep,\ired thinning of
incisional areas can be regularly oh<>erved. since it
does not necessarily become a true hernia despite
strenuous athletic activity.
TREATMENT
IncisionaI dehiscence
The treatment for incisional dehiscence is smgical
revision. A belly bandage \',i[h a sterile moist dressing
placed immediately on the incision is applied prior
induction of anesthesia. Tbe belly bandage alone \\i!l
not prevent evisnration and should not sen'e as sole
Treatment. The principles of tn'atment at surgery are
debridement of the incision
bacterial sampling of the tissues.
If the reason for dehiscence is Etilure of a sutnre mater
ial, tben revision with a larger-sized (greater strength)
suturc call he done. Copious lavage of the im;ision site
with sterile physiological solution containing broad
spectrm antibiotics should be performed, If significanr
contamination of the incision is present or the body
wall is the reason for dehiscence of the incision, tben
through-and-through sutures should he used (Figllre
1 1 . 1 ) . St(el sutures with rubber ste!lls are required in
an interrupted vertical mattress of the incision.
If the horse is too weak and sick for general anesthe
sia, a plastic mesh (e.g. Proxplast, Goshen Laboratories,
Goshen, N can be sutured superfcial to the skin over
tbe incision (after local anesthesia). This leads to open
peritoneal drainage and requires all abdominal ban
dage (Figure 11. 2) for support to prevent dehiscence.
The mesb is removed once a bed of granulation tissue is
present underneath the mesh, but continuous abdomi
nal support is needed fI)r lIlonths.
Incisional hemorrhage
Whell indsional bleeding is noted the source of the
bleeding must be identificd, A preswre bandage should
treat incisional bleeding associated with incisional
21 7
1 1 COLIC
Figure 11.1 Placement of through-and-through steel
sutures in the repai r of incisionai dehiscence
" esse! leakage. The ojc<: ri\ is to arrest. bleeding by
applying counter pressure. It i.' i mportant thil. enough
pressHre be applied not only to prc\t'.nt hlood from
(scaping the incision, but (qually important) to pre
\'t'l)t subcutaneous hClnorrhage since it predisposc
im: isional illfection (Figure 1 1 .3).
I f imra-ahdominal hemorrhuge OCCllrs, i t is
t'xtn."l1lt:iy r"n that the clinician Il(eds to (or :houic)
fe-anesrhetize the animal to searc:h for [he hleeder. The
goa[ i' (() 'prly sufcen pn:ssuTc to sC<i the abdomen
and pre\'ent the horiy's loss of red blood (elis. ''cn
serious hemon"hagt' is prest.n1 , hlood vl.ll soak Ihrough
rhe belly handages. Rather than r(moving the bandage,
a seculid layer can he applied with mOTe press un:. If this
stops the hemorrhage or reduces it to a slow drip, the
hlndages can be left in place for G8 hours. If this dDe
not stop rhe hemorrhage, the inner handll:ges must he
tuo loose and should be rese!.. On recognition of
abdominl1 hemorrhage, any heparin therapy alrt'ady
initiattd should be cisrominued and preparation (0
Figure " .3 Postoperative indsional bleeding, not subcuta
neous hemorrhage
21 8
Figure 11.2 Equine reusable abdominal bandages being
applied
identify : m appropriate blood donur (crossmatch)
should be initiawd. Intr.\,CClOlIS fl uid adminislralion
rats should be a{ljusl.cc appropriatc!r (S(, Chaptn 9
Fluid and e1ectrolyle therapy and acid-hase balann;' ill
horses with abdominal pain). If syswmk signs of illlra
ahdominal bleeding appear t increase in severity, th{'
intravenous administration of 4lIlinocapmic acid ( to g
in ! liter of physiological saline solution, up t thrt'('
tlInts rlaily per 450 kg horse) should be considered.
Incisional drainage and infecion
IndsionaI infections arc treated with approprialt:
drainage, removal of selected skin slIttlfcs/stapl<:5. and
topical cleaning and lavage of {he: i ncision. Sysl('mic
antibiotic.s wmally have already been administered at
the time infenions uccur hu may need L be changed
according t hacHrial rulturc results. It is importam to
remember that incisional infeclions increase tbe risk of
incisional herniation from f()ur- to ninelcenfolrl.
Incisional hernia
Surgical repair of a hernia is made either by primary
rtpair or placement of a mesh. Prior to repai r ,til sigll:
of inflammation and i nfec.ion mml be resolved. This
generally entitles the surgeon [() l.'<it 1-2 months
before attempting repair SQ that a finn and defi ned
hernia ring is present. If a suture sinlls is present, (h{
surgeon mllsi. wait for the suture [0 he absorhed and tht
infection l rcsolV(". If a non-absorbable suture was
used, the suture should be removed prior to attempting
any surgical repair. This can be done with the h()rsc
standing or under genNai anesthesia. SlIrgical repair
should nOl be attempted for itt leas[ I month afer
cessation of drlinage.
BCCatlSe of the elfect of l(!nsion (In a hcriorrhapll)',
4 24-hourfasting (feed only) is recommended. The horse
is <Hlelhelized, and the skin overlying the heria sac i"
grasped with 2 or 3 Lahey thyroid forceps. After apply
ing slight ul1sion on the 11(mia sac, a fusiform incision
ovt'r lhe htrnia ring is made. The incision is exrcn<icrl
t I he heria ring t",king cart! to ligate or camcfize any
1igniflt:anlblccders. Asmall 2-3 cm incision iS lh(n made
through the hernia sac: at the hernia ring. allowing imro
dU<"liOIl of one of the surgeon's fngers. The surgeon
a. . sesSCs the prescnc( or absence of adhesions and pr ..
n:t'ds with the resectiun of lhe heria !ac afler proper
Iransenion/dissenion of the adhesions. The heria sac.
and O\'erlyng skin is then resected. Primary repair is used
i f t he ('dge of [hc hernia ring (:an tx re-appoed with
minimal tension. All appositional paner (simple
i nterrupted or cfuciale) is us(d (sec Chapter 10 for con
sickrarion of ttturc maLerials). The subcuLaneous laver
and slin arc clo!ed in an aCC('plable manner.
'
\k!h is used when the lension on the incision edge
is signific3m or when it is needed to rt"pair 'spot' thin
lling of an inc:isiollal are .. Two types of mesh have been
used: Marlex (Dowd lnc., Provi<knce, RI) alld
Pn)xplast (Gosht'n l.ahontUlries, Goshen. N. Marlex
ha" a tend(:nc:y to sag and should rhcrcfore be placed
wid1 appropriate (ellsioJl. Absorbable mesh made of
polyglactin 91 0 or polyglycolic acid IS available, blH to
Lilt' amhor's knowledge iL has not been used in horses.
For humans, Lhse absorbahle meshes have been
n:port<'d to ser as tcmporary suppOrt until indsional
inkction is resolved. followed b' plaeemenr ora penna
m:1It mesh. Meshes arc cut. 8 em largcr than the (ldecl
tn allm,' their edges Ie> be folded and to ()V('r!:IP the her
Ilia r
K
e by 2-3 em. The mesh call be used as an ovnl '
ulltier twO conditions
1 . t support <1\ incision that has bc(:11 dosed
primarily but where signitkam tension is present
2. O\'l'r an incision sitc that has thinning area') whcn:
no primal)' repair is needed.
:sh contacting Ih<; abdominal cavil}' can resull in
intt.til1e! adhering to the mcsh. It is Lllrcfore recom
Ilu:ndcd the me.. h be placed snbfascially, blll this is
r<lrdy
,
if C'er, possihle in the horse. Snmetimes the
p(:riwneum (
.
an be disscc.lt:d free from tht heria sac,
allowing it t form a barrir between the mesh and the
inl(:stines, LJsually the mesh is lIsed as :n tnl sutured
L tIlt: t:dgc of the defect. Two m<:.hes an: used with their
t'dges folded o\tr with the folds opposite lht abdominal
cavity (Figure 1 1 . 4). 111 allca . (s, mcshts are sccuf(d with
absurhable suture material, preferably monofilamenl,
S()nH sutures 1USt he pr-c-piaccrl in the mesh.
Pos(operdtivcly, it is imporlam t minimire im.:ision<tl
s\lIing. Therefore, mm-stl'roidal anti-inflammatory
dlg are aomini.'il.ered for 35 da
y
s, By applying pres-
Figure 1 1.4 Mesh placement for equine hernia repair.
Note that the edges are folded over with the folded edge
opposite to the abdominal cavity
slire abdominal bandages do redu<:e s . ..elling and mini
mize the likelihood of sermas. They should be llstd
,
,
,ith caution and tilored t the individual, as lhc) are
associated with preputjal swelling. In addition, alxiomi
nal bandages c: increase rhe likelihood of infection
when a male manag(.' to urinate in th bandage, or ill
hot weather as sweating (><:CUfS, leading t a moist warm
environment nCir the incision.
CONCLUSIONS
The incisional complication r<lC appcars to be deuea
ing becaw;e ofimprovenlents in surgical le(:hniqlle nd,
prohably. earlier surical interention. COrdui atten
tion to prevention and carly
recognition ami trealment
are the key in managi ng thc!e frequent complications.
Postoperative compl ications
- myopathy/neuropathy
. : . . .
.
BA Valentine
INTRODUCTION
Post-ancsthclic myopathy/neuropathy rerers 1.0 a range
or clinical scenarios in which dysfunction of skeletal
muscle and/ or peripheral nerves occurs in horses fol
lowing genral anesthcsia. This dysfuncioll may be
local ized or generalized, painful or non-painful, and
clinical signs may be evident during the immediate
reco\ery period or appear da}'s later, ." suc:h. post
anesLhetic myopathy/neuropathy is not a single ciinic()
pathologk entity, but rather is a maniftation or a
!pectrum of induced or inherem neuromuscular dys
function evident following anesthesia. It is estimated
21 9
1 1 COlK
that from !f per (ent of horses undergoing general
anesthesia lIlay devdop clinical signs of post-anesthetic
myopathy/neuropathy, and that development of these
disorders is the cause of 8-0 per cent of anesthesia
related deaths in horses. It is also likely that subclinical
myopathy occurs, particularly in horses with inherent
defects of muscle function.
PATHOGENESIS
;Cllromllscular dysfunction may be due to one or more
"I' thl' following
muscle fiber necrosis
o\'cra!l musc1e weakness
peripher,t1 nerve dysfunction.
Muscle fiber necrosis
Iusck fibt']" necrosis is accompanied by variably
increased serum activities of creatine kinase (CK),
aspart<lIC aminotransferase (AST), and lactic dehydro
genase (LDH). Lorah/.cd or generalized fiber necrosis
!11I5 following ischemia caused by compres.ion of the
muscle groups during recumbency or by systemic
h'p<Jtension, and may involve reperfusion injury as well
as ischemic injury. Generation of lipid pcroxidation
prod'lCts following musde membrane damage allow.
li)r th likelihood that oxidative injury plays a role in
the duration and extent of muscle il-Uury. Mllscle Hber
necrosis may also occur due , or be exacerbated by,
lllld<,rlying inherent myopathic conditions such as sele
nium/vitamin E deficiency, ex('nional rhabdomyolysis,
and polysan'baride storage myopathy.
Overall muscle weakness
Owrall muscle weakness may occur because of severe
ckctrolyte imbalances, h)perkakmic periodic paralysis,
or polysaccharide storage myopathy. In these cases,
muscle fiber necrosis may be minimal or inapparent,
imd serum anivities of CK, AST, and LDH may be
normal or only slightly increased.
Peripheral nerve injuries
l'eripheral ller'e i!-uuries may he due U1 nerve compres
sion or swelling of associated soft tissue. Serum activities
of CK, AST, and LDH will be relatively normal.
RISK FACTORS
Risk faClo[s cited for horses include large si7_e, heav
muscling, high level of fimess, and breed, \vth Quarter
220
horses, draft breeds, Thoroughbreds, and Stanrlardhrcds
thought be at higher risk. Data support these
hypotheses, however, are scanty and sometimes contra
dictory. Other, better substantiated, risk factors include
prolonged duration of general anesthesia
type of padding
positioning during surgery
systemic hypotension.
The tye of anesthetic agent employed, as well as other
medications administered, may also play a role,
Halothane anesthesia has most often been associated
. ith post-anesthetic myopathy in the hnrs{_
Administration of aminoglycoside antibiotics has I)(en
discouraged because of possible neuromuscular block
ade, however a recent study concluded that a single
high dose of gentamicin sulfate administered perioper
ativcly did not affect neuromuscular fimctioll in horses
anesthetized with halothane. Delay of elective surgery
in horses with increased serum activities ofCK, AST, or
LDH may decrease the incidence of post-anesthetir
myopathy, but this hypothesis ha not been carcfillly
investigated.
TYPES OF NEUROMUSCULAR
DYSFUNCTION
Malignant hyperthermia
Los of thermoregulator function, with subsequent
r.pid increase in body temperatllre and associated mus
cle rigidity, myonecrosis, and respiratory dysfunction, is
an uncommon but frequently fatal complication occur
ring during general anesthesia. Susceptible individuals
are those with underlying myopathy resulting in abnor
mal intramuscular calcium regulation, in \,'hich certain
anesthetic agents, in particular halothane, can trigger a
cycle of unregulated calcium release from the muscle
s;\rcoplamic reticulum to result in continuous muscle
fibcr contraction and associated heat production. A
such, this unique disorder is more appropriately classi
fied under he heading of 'anesthetic-related myopa
th(, and should be distinguished fi'om hyperthermia
occurring during the recovel)' period {see below). True
malignant hyperthermia in humans alld swine has beell
fmmd to he due to genetic alterations of the skeletal
lIJuscle ryanodille receptor, a vital link in muscle
excitation-contraction coupling. Other underlying
myopathic disorders, however, have also been found to
predispose individuals to anesthetic-related malignan!
hyperthermia. An anesthetic-related malignant hyper
thermia-type reaction has b('en reported ill sever.!l
breeds of horses. Quarter horses with hyperkalemic
periodic paralysis (HYPP) lIlay be more susceptible to
anesthetic-induced malignant hyperthermia. Sporadic
in l.ito testing of muscle samples from affected horses
has revealed an exaggerated contracture response to
halothane and caflCine, however a specific defect in
skeletal muscle of aflected horses has not yet been iden
tified. It is interesting to note that several studies have
found evidence for abnormal skeletill muscle calciulIl
regulation in Thoroughbreds prone to recurrent exer,
lional rhabdomyolysis, and it is possible thaI this t}e of
defect may predispose aflected horses to inesthetic
rc1;tted malignant hyperthermia.
Post-anesthetic hyperthermia (post
anesthetic hypermetabolic syndrome)
Development of hyperthermia in horses during the
recovery phase of anesthesia should be diflerent.iated
from 'true' inesthetic-induced malignant hyperther
mia. The term 'post-anesthetic hypermetabo\ic syn
drome
'
is perhaps more appropriate. Post-anest.hetic
hypermetabolic syndrome may he accompanied by vary
ing degrees of myonecrosis. Yyopathies resulting in
uncoupling of mitochondria, ill which mitochondrial
oxidative phosphorylation is not properly 'linked' to
the electron transport system, may result in excessive
muscle heat production and hyperthermia. Uncoupled
mitochondria are a relatively non-specitk consequence
of milny different myopathic conditions, and have been
reported in the skeletal muscle of horses prone to exer"
tional rhabdomyolysis. Draft breeds may be more prone
1 development of post-anesthetic hypcrmetabolic
syndrome, possibly because of the high incidence of
polysaccharide storage myopathy in these breeds.
localized myonecrosis
Development of swelling and pain in isolated muscle
groups is perhaps the most common form of post-anes
thetic myopathy in the horse. Muscle groups under COIl!
pression from the weight of the hore during surgery arc
most susceptible. A muscle fber necrosis, in itself, is
neither painful nor results in swelling, i t is clear that
\'asntlir factors must play a role in this disorder. The
concept that this disorder is a manifestation of a
compartment syndrome, in which increased muscle
pressnre against a tight fascia results in vascular com
promise, is weI! accepted. Proper padding and position
ing 01 limbs during anesthesia and recognition and
treatment of hypotension will reduce the incidence of
this phenomenon, but its continued sporadic occur
rence indicates that other factors are likely to playa roIc.
The possible role of marginal to low levels of antioxi
dants, in particular selenium and vitamin E, must b
emphasi7ed, as it is entirely possible that < lack of these
compounds may allow a cycle of increasing membrane
ijuy that causes magnifcation of the low-level muscle
injuy that is likely to occur in ally horse undergoing
general anesthesia. I t is suspected thai selenium status
may be more important than vitamin E status in protec
Lion of equine skeletal muscle from injury. In particular,
masseter myopathy as a post-anesthetic complication
could reflect an underlying selenium deficiency.
Generalized myonecrosis
Horses with generalized myonecrosis and weakness
following anesthesia resemble horses with exertional
myopathy, and these entities miy be related in .ome
cases. Systemic hypotension, however, has been shown
to induce generalized post-anesthetic myop:Hhy in
apparently normal horses. In addition to weiknl'ss,
affected horses often have hard, painful muscles, which
igain suggests that vascular damage must be involved.
Serum icivities of CK, AST, and LDH are generally
extremely high, and affected horses may develop overt
myoglobinuria. As with localized myollecrosis, the
antioxidant status of the horse could play a role in pro
tection or predisposition to development of general
ized myonecrosis following generAl illesthesia.
Localized weakness
Localized weakness, most often involving a forelimb, is
considered to be more often a manifestation of peri ph
eral neuropathy than of myopathy. Affected horses will
exhibit evidence of partial to complete limb paralysis
with motor and, in some cases, sensory deficits. Muscle
swelling or pilin is generally absent. Proper padding
and positioning of the limb during surwr to avoid
compression of peripheral nerve trunks, or pressure
damage to the surrounding muscles, will reduce the
incidence of this disorder. Damige to nerves may be
structuml or non-structural (conduction block).
Generalized weakness
GeneraIi7(d weakness, in the absence of massive muscle
necrosis, can result in recumbency with inability to rise.
Causes ciled include severe electrolyte imbalance and
altered skeletal muscle energy metabolism. The liltter
is an interesting concept, especially given the altered
energy mcmbo1ism that is thought to Ix the cause of
skeletal muscle dysfunction in horses "'ith polysaccha
ride storage myopathy. Draft horses with polysacchiride
storage myopathy may have prolonged weakness and
prolonged recumbent following ane.thesia, with mini
mal to no increase in serum activities of musde enzymes
during the recovel
'
phae. Continued monitoring of
serum CK and AST, however, may be indicated in these
221
1 1 COLIC
breeds and in other horses suspected of having polysar
charidc storage myopathy, as thefe is evidence that Oll
going muscle irtlry can occur up t 5 days Of more
ro!lo\\'ing apparent recover. This phenomenon may
explain cases of sudden onset of recumbency or rhab
dOlTlyoiysis occurring hours or days after apparent full
ncovcly.
PREVENTION
Clearly, proper padding and positioning, maintenance
of systemic blood pressure, and minimizing total dura
tion of anesthesia arc the best preventative measures. A
reeeill study suggests that use of dobutamine may
improve intramuscular blood flow during halothane
anesthesia. In selenium defcient areas, administration
of selenium and vitamin E prior U surgery may be of
benefit. The lise of dantrolene prior to surgely, to
reduce calcium release during excitation-ontractiOll
coupling, is of uncertain benefit. and may, in fad, result
ill prolonged postoperative weakness. Given the lack of
data to support the hyothesis that abnormal ealdum
fluxes art' involved in every case of post-anesthetk
myopathy, ils usefulness in prevention of this disorder
must Iw considered questionable at besi. Preliminary
studies of draft breeds with underlying poly<accharide
storage myopathY suggest that a low carbohydrate, high
fat diet may reduce the degree and duration of mnscle
iljury following anesthesia.
THERAPY
Horses with ohvious signs of muscle necrosis, either
localiwd or generaliled, should be treated immediately
with intral'enous dimethylsulfoxide (DMSO 1 g/kg
1% solution in 5% dextrose). This free-radical-seav
enging agent can dmmatically reduce on-going muscle
injury associated \i th oxidative i!ur.
Administration of selenium and vitamin l: may also
aid in reducing fiber necrosis.
Correction of any electrolyte or acid-base alter
ations, as wdl as supportive therapy such as analgesics,
tranquilizers, Of sedatives arc indicated to reduce pain
and anxiety.
The decision to hoist a recumbent ho{e by use of a
tail rope or sling is made depending on the duration of
recumbency and the nature of the horse. A calm horse
that is maintaining sternal recumbel!cy should be
dose!y monitored, and may regain the strength to rise
within a few hours. For an anxious horse that is
struggling !.rise, or one that cannot maintain sternal
recllmlwl!q', use of a hoist and sling may be critical.
222
The placement of the slung horse illlo a pool or foot
t 'lk would be ideal.
Administration of lipids, either intravenomly or
through a nasogastric tube, may benefit horses with
weakness or rhabdomyolysis due to polysaccharide
storage myopathy.
Fasciotomy may relieve pressure in localized myo
pathy due to compartment syndrome.
Splinting or hobbling of limbs that are weak due to
myopathy or neuropathy may be indicated.
In cases with severe myonecrosis, aggressive fluid
therapy U maintain renal function is critic,t!.
PROGNOSIS
Under most circumstances, myonecrosis will be fol
lowed by myofber regeneration with minimal to no
scarring. Persistent weakness during the regeneration
phase, and the potential for myoglobinuric lIephrosi.
may, however, necessitate aggressive supportive care
for several days fol\ov".jng the onset of myopathy.
Repeat determination of serum CK and AST activities
is useful for evaluation of recover. The serum half-life
of CK is extremely short, and serum activities follow
ing a single bout of muscle iliUly should be reduced
by at least 50 per cent evelT 24 hours. If serum CK
activity is found 1 be persistently high or inneasing,
particularly in a horse that is no longer rnllnbem,
underlying myopathy leading to on-going muscle
injuy should be suspected. The prognosi for recovery
fiom peripheral neuropathy will depend on whether
there is axonal damage or simple conduction hlock.
Resolution of conduction block may be rapid, whereas
repair of axonal damage, if it OCCllrs at all, may rake
weeks to lIIonth..
- thrombophlebitis
( Walsh
INTRODUCTION
Thrombophlehiti< is defined < thrombosis of a I'ein
associated with inflammation of the vessel wall.
Thromhosis rarely occurs witho\lf the presence of
inflammation. Septic thrombophlebitis is the terlll lIsed
when the thrombus becomes infected.
1ne pathogenesis is multifllctmial. The use of
indwelling intravenous catheters, coupled with the fi-e
quem administration ofirnlant drub'S ill patients that may
have a coagllopathy as a result of their primar disease,
comhine to put horses with severe gastrointestinal disease
at rdatively high risk of developing thrombophlebitis.
The jugular vein is the most frequently affected site
because it is commonly used for venipuncture.
PATHOGENESIS
In the normal animal there is a balance het\\'een prou}
agulam and anticoagulant activiTy. Thromhosis occurs
when the balance tips in favor of coagulation. Factors
That promote coagulation include
\ascular intimal damage
a hypen:oaglliable state
stasis of blood flow.
Th('e factors result in inappropriate activation of
!]ormal hemostatic mcchanisms.
Hemostasis
Damage to a blood vessel initiates the process of hemo
\tasis. This comprises a series of complex events involv
ing pl,udel plug formation and activation of the
do((in, cascade t"wlllually resulting in formation of a
fibrin dol.
(lfldfl flug/omlfllirm
Endothdial ce!Is normally resist adherence to platelets
I)\' a variety of mechanisms. Damage to endothelial (:ells
results in platelet adherence to subendothelial coHagen
and la(tor VI!! (von Willebrand 's factor). This result in
pla1<"kt activation whidl involves contractioll and secre
tin!} of granular contents including adenosine diphos
phal(' (ADP), which in turn attrads and anivates more
platdets. Platelet aggregation is enhanced by throm
boxan (1)which is generated from membrane
d("l'ivcd arachidonic acid. The result is formation of a
plalelet plug.
Bood(i)!'l/alion
Activation of the coagulation cascade results in the for
Illation of the fbrin clot. The extrinsic pathway is initi
awd by tissue factor or tissue thromboplastin which is
d('rived from damaged tissues. The intrinsic pathway is
initiated when blood comes illlo contact with subendo
thelial collagen or platelels, which are highly negaTively
charged. Apart from tissne factor. all the necessary clot
ting factors are present in normal plasma, many of
lhem are serine proteases.
The r'O classically described pathways converge to
activate factor X to Xa. Factor Xa forms prothrombi
!lase by forming a complex with factor V, platekt phos
pholipid and ionized cakiulll, Prothrombin<sc deaw
prothrombin to form thrombin. Thrombin cleaves
fbrinogen to form fibrin, which undergoes covalent
linkage to form the insoluble clot.
Limitatioll 0/dot/onwlioll
Clot formation is normally limited to the site of blood
\esse\ iljury by mechanisms that inhibit clotting factors,
the most important being antithrombin III, and by fb
rinolytic processes that destroy the clot. Antithrombin
In neutralizes serine protease dotting factors, includ
ing thrombin, its dlects are potentiated by heparin.
Fibrinolysis is activated al the same lime as coagulation,
the main fibrinolytic elll_yme bing plasmin, whose pre
cursor, plasminogen is incorporated within the dOL as it
forms. Plasminogen is activated by lissue plasminogen
activator derived from endothelial cells and probably
enters the clot bv diffusion.
Thrombus/ormation
&.'veral faclOrs conspire to increase the risk of occllr
rence of thrombophlebitis in postoperative colic
patients
patients are frequently in a hypercoagulable state
mechanical irritatioll of the vessel intima is caused
by venipuncture or by the presence of an
inlravenous catheter
several of the drugs uscd in colic patients can cause
chemical damage to the endothelium, for example,
thiopentone, phenylbUiazone, and guaifenesin
(GGE).
Hypercoagulability in horses with colic: the
role of antithrombin III
Antithrombin III is a natural inhibilOr of coagulation,
normally accounting for over 70 per cent of the antico
agulatingeffect of plasma. Antithrombin III forms com
plexes with activated serine proteases, these are then
removed hy the reticuloendothelial system. On its own
antithrombin III is a weak inhibitor of the activated
serine proteases of the coagulation cascade, especially
thrombin and factor Xa, its activity is markedly
increased by heparin. Antithrombin 1II is thus con
sumed during the coagulation process.
In equine patients with gastrointestinal disease, [he
most likely cause of coagulopathy is endotoxemia.
Endotoxin has lllallY effects including
direct damage to endothelium
platelet aggregation
223
1 1 COLIC
activa.Lion of coagulation G1.<cacc and decrease in
i.l1l tilhromhin III acthity.
A numhcr of swdies ha\'t! shown thar horses with sc\'cn
syslt'mic disease haV( lower than normal a<:ti\'ity of
antirhrOlnbin HI. In one study, amilhrnmbin III a<:ti\'ity
was found lO hC rcdl1ced in horses [hat had undergone
stll'gi<ltl correction of largl colon torsion, for 1-3 days
pnsropcnlli\,tiy. Antithromhin III activit), thell
i l lceased lo normal in horses that survived, hu
rt:maincd 1()t' in horses that died.
III anolher study it was '()lllld that horses that had
lOdt'rgont" colic surgel}' shO\t'd a dCCTcasc in
i\lHilhrombin il l Ccriviry. this fcreased to ahout 50 pt'r
('l'nl ofiLS normal \allJ( after 4 days rhen increased to
normal O\tr abou[ a week. This (:hang<: w<'i coupled
with a rlccfa$<: in anivir of coagulation ra<:tors L
approximaltly 25 per (:Cn! of normal ' days postopera
li"dy, fiJUowed hy an in<r(!as( 10 normal .Kti . . ity over
lhl: t)ext week. Th( rcsuital1l rende-ncr to coagulation
was cxplained hy the fan thaI <:oagu\atioll factors are
still dfectiv(' at 20 per (('Ill of norma] activity It.'\'d
wber(a antilhromhill I II requin:s ilt kaS! 75 per ullI.of
l1<mnal activity t he cfecr.in: .
In humans, it is well rc(:ognized Ihilt postoperative.'
patillIls with antithromhin If I dcfu:it'llcy are at
in(T('as{'cl risk or thromhocmholism: the risk is said t
be modcratt: if antithromhin III activit), i!i betweclI
;>0-7:) per cenl ann severe if antithromhin III ;u.ti\ity is
less than !1J per cent. The same may well apply t
horsc 's.
CLINICAL SIGNS OF
THROMBOPHLEBITIS
Thrombophlebitis is usuaHy rt!.u1ilr diagll(}cd 011 the
basis of the following dini<:al signs.
I . The affened vei n is hard and cord-lik( on
palpatioll.
2. Sc.'ptic thrombophlebitis houlc be nspccl(;d if th('
antned vein is hot, swollen. or painful on
palpation (Figure 1 1 .5). If the jugular \'I.in is
alTected the horse m;:\y <ppear to ha\'e a stiff n: d.
Sllppuralion or exudation from sites of skin
P1l11CttIn.' suggests septic thromhopllk:hitis. though
u'liuii lis without v<:in invol . tllwnl' is Iso a
possibility. Septic rhrmnhophlehitls should also he
suspected in any hor.e with unexplained pyrexia
p<lsfoperativelr
:,t Ril;ucraljllglllar !hromhophlt:hiris may result in
t"dt:lIla or the soft tissues of the Iwad cansing
dysphagia and dyspllei often severt" cnough to
l1t!ct!.sitale lradleosloll1Y.
224
Fi9ur 11.5 A 12-year-oJd gelding with 'welling of the left
jugular vein. Septic thrombophlebitis was diagnosed ultra
sonographi<ally. The horse had a history of endotoxemia
and the vein had previously been catheterized
4 Rare cOlllplications or thrombophlebitis incl lld(
lhnHnbocmholism :ncl endocarditis.
Ultrasonographic findings
Thrombophlebitis i' charaClCr1/cd 1IIlra()n{)grctphi(:all)'
by the pre'cnce of a mass in the \,{!scl lllmcn r<lging in
appearance from hypocchoic w cchogenic (Figurc.$
1 1 .6, 1 1 .7}. Thickening of the vessel wall is often pfl'
sene A fibrin sleeve may also be dNecu>d around the
catheter if present, and may ais() be recognized whtn
the cathetcr has becn removcd.
The thrombu can usually he seen [0 be "((itched to
the endothelium and may partially or complt:tt:l'
occlude the lumen. VtTlOUS <:ongeslioTl may h(: disti ll
guishahit proximal to the thromhus,
A sptic thromhus appears ultrasollographi(:ally as a
het<:rng('I1<:olls ra.'s in "rhien ancrhoic or hypocrhoi<:
art:as represent areas of fluid o necrosis. AITa of pus
within t.he thrombus appear hypocchoi<: and f1occulclH.
Cltrasonography is useful t confirm the presence of
septic: thromhophlebitis ann r select an arta of throrn
bus w aspirale ror culture.
Cltrasonography may be usdul in moniLoring the
n!!pollse to therapy.
(a)
(b)
Figure 1 1.6 Transverse (al and longitudinal (b) ultrasonographi< images of the lef jugular vein of a mare with a history of
endotoxemia following surgical (orrection of a 360 degree torsion of the large (olon. The vessel wall is slightly thickened.
The lumen of the vein is of normal appearance. The surrounding tissues are unusually hypoechoic and in the transverse
image have a honeycomb (ppearance typical of edema. Dr Cel ia M.rr, with permission
(a) (b)
Figure 11.7 Septic thrombophlebitis. Transverse (a) and longitudinal (b) ultrasonographic images of the right jugular vein
of the mare in Figure 1 1 .6. The vein had previously been catheterized. The lumen of the vein is completely filled with a
hete(ogeneou5 thrombu containing multiple anechoic foci, indicating the presence of fluid pockets (arrows). In the Ion
gitudinal image. the thrombu has a laminar appearance caused by the accumulation of layers of blood cells proximally.
Dr Celia Marr, with permission
225
1 1 COLIC
PREVENTION
Prevention oj' thrombophlebitis is centered around
treatmellt of the underlying cause - in horses with
gastrointestinal disease this is usually endotoxcmia
and disst'minaled intravascular coagulation
measures to minimize venous trauma and scrupulous
management of indwelling catheters - it is advisable
to avoid repeated venipuncture in horst'S at increa,ed
risk of thrombophlebitis due tocoagu]opathy
anticoagulaill therapy is recommended by some
authors hut remains a controversial topic
Catheter management
indwt'lling catheters are commonly used ill horses
undergoing intensive care. Most cases of thrombo
phlebitis OCfur in veins that are or have been
c<llhetcrilcd. There is little information regarding the
J
'
reqtwncv of catheter-related thrombophlebitis, One
tudy reported an incidence of 29 per cent in associa
tion with !lllid therapy. risk factors including presence
o!
'
pw('xia and usc' ofhollH>pndun:d fluids.
Pathophysiology of catheter-induced
thrombophlebitis
Endothelia! damage occurs in the area of entr of the
cathNer and at sites of contact of the catheter with the
vessd intima. Platelet aggregation and the coagulation
cascade are initiated by the presence of foreign material
in the bloodstream. Studies suggest that a fibrin sleeve
starts to form on tlw (Catheter within abon 30 minuws,
beginnillg at its point of enu)
'
and at the tip where it
cOlltacts the endothelium. There is a marked difference
in lJw thrombogenicity of different catheters resulting
from their surface properties length, gauge, and stifl
ness. (;ener,IUy, longer and higher gauge catheters are
more thrombogenic because they contact the vessel wall
over a greater area and thus cause more extensive
cndothelial triuma. However, catheters made of softer
materials are less thrombogenic, whatever their size,
because they tend to float fredy within the bloodstream
withont contacting the vt:ssd wall. Readily available
catheters include
the shorter, stiffer catheters made from
polytetr'fllloroNhylene (PTFE), these should not
he Ieli ill for more than 72 hours
the sofwr catheters available in various lengths, and
incre'lsillgly in higher gauges allowing rapid
iuhlSioll rates, made from polyurethane. lhat can be
maintained fi)r seyeral weeks if carefully managed.
Infectioll mal' ()(
'
cur especially if catheter man;lgement
' pOOL The incidence of positive bacterial cultUrtS
226
froIll catheters has ben estimated at around 70-75 per
cent, with most isolates found to be skin commellSals.
However the relevance of positive culture is unclear as
there appears to be little correlation in these studie
between positive culture and thrombophlebitis.
Guidelines for catheter use
Good catheter management will reduce the incidem:e
of thrombophlebitis by reducing contamination of the
catheter and trauma to the site.
I. Insertion, surgical preparation of the site, and
placement of the catheter using aseptic technique
minimizes the risk of contamination at tht: tillle of
insertion. There is also a lower incidence of
complications if the catheter is placed by an
experiencd person, probably because tr,l\lma to
periva.cular tissues is reduced and there is greater
accuracy in puncturing the vein.
2. The cat.heter should be firmly sutured to the skin to
minimize movement at the site of skin pelletration.
reducing the risk of infection and the degree of
tissue trauma.
3. The use of extension sets is advisable, to avoid the
need to maniplllate the catheter directly, so
reducing its movement and the risk of
contamination from the skin of the horse.
4. Flushing the c_atheter ever 4 hours with heparinized
saline soliuiol helps to prevent dot formation within
t.h(: catheter. Blocked (or othetwise damaged)
catheters sbould b removed and replaced.
5. The catheter should be removed as soon as it is no
longer required.
5. There are many potential sites of contamination and
infection of catheters, induding thre"way taps,joins
in fluid administration sets, fluid bags and any
additions to them. Careful aseptic handling of all
equipment usd is important. It has been suggested
that all fluid lines should be replaced ever 24 hour,.
It is vel)' important to check veins regularly for signs of
thrombophlebitis.
Some authors recommend the use of antiseptic skin
ointl\lent and dressings while others consider that the
use of antiseptics encourages the development of resis
tant strains of micro rganisms, or that their use has no
dkct on th incidenre of thromhophlehitis or positivc
cultures from the catheter.
Anticoagulant therapy
Aspirin
Aspirin given at a dose of 5-15 mg/kg per os (:\ry
other day reduces platelet aggregation and may he
givell concomitantly with other :-SAlD therapy.
Heparin
The anlicoagubwl dTcct of heparin dqlend 1J the
patiLlIt hain ade
q
mH. autithromhin III ani\ilr.
hq)arin hind to antithrombin III alltl grcatl' cuhal1es
iL powney a (:rin( prOlc: Sl inhihilUr. Heprin is nO
!lsd
1I1 for the r('solution of existing Ihrumbi ami has a

limilrd elTect in pn:\clllinR thcir e"l(nsion. If used,
ahe .
.
. fore. it mut h i"en prophylanir.ally. prdiTdhly
pre"uperativeiy, hefore the conumplion of antitlHom .
bin III and librin formation occur, it may then haH
sonw dfcct in preventing thrombophlebitis in patients
'It risk. The tlgg(:stc::d dlag(: rc:gimcn is
initial d{)se DO IV/kg s.c.
12:, lL
'
/kg .$. q. 12 h for six doses
100 IL'/kg s.c. q. 12 h subsequently.
Tht rct\lcin dose i recommended hecause if U uni
hmn doS(: is ued, serum heparin gradually incrcas.cs.
Thi d()sinK regimen, when administered to he,llrhy
hors.:s, resulted in a plalna heparin concentration
bt'IWet!l O.O-O.2 IU/m1. this is the lhcmpcmic range
o[ 101, dose heparin prophylaxis used in humans.
SuhnllalltUS adminisu",uion a\'()id peak. of plasma
Iwp,lIin thai ma' he more likel) to result in ad\er$(.
tff
Tht' nl(l comnwlI compliation orhqin Ihertp)
is anemia (ren cell lIlaA may b reduced b 3. per
unl). (nd r'd cell agglUlination ill the micrm'a.-:lia-
1 has been suggt:sted M the mllSl likdy L!C- The
rcd cdl count rl'O\'CI ',ithin 96 hours of l:e!lion of
ht'p;nin the,-"p)'. The signili:allce of Ihi oi)s(:n'ation is
unKllown.
Ol.lwr complit:aLioos of heparin adminislr<tion that
h'l\ ht'en dC(:fibed in horses inLlude fawl Iwmor
rhag-e (at higher dl)se.), thrombo<ytopcnia, and
painful \'ening at injection sites.
TREATMENT
Ont:e thrombophlebitis has been recogni7.cd, sympto
mal,it- treatmcnt is Tl'commcnded as follows
!`1 the L&llheler, if prt'$Cnl, and (:ulture th(, tip.
dO l111t use the \'ein for \'eniptmClurc::
hmpacking 111<)' help by increaîng blood lIow to
fhe arca
fnon"teroical :uui-inllimmaloy dnlgs t rduce
inflammatiou
lIe antibimirs {broad spcclnlll or as dinatd by
(.uhurc and scnsiti\
ity) in Sptic thromhophll'bitis

L(cp th( head ek'\'ted, for example by cros.o-rying
irbildterl thromhophl
bitis is prcscnt
trad1coswmy lIlay be nccc::sr in bilateral
dlrombophlebitis ir dyspnea is $'\ere
surgical drainagE mar be ncccs-'f' ifsuppurdtion i
prllI
\Tin rctilm ra} he indicTed in S\'trc 1& Ibat
do not respond to medicl mallagemenl.
In IHllomplic,ued bL or thrmbophlebitis,
rccanali7ation of T.hc I'ein commonly occurs, Ihis may
IC1\lrll ! normal Of there may b a degree of stricture.
In mOfe severe cases the thrombus may undergo
organil,atjO!l ithout n:canalilation.
Postoperative complications
- peritonitis
T Mair
INTRODUCION
l'erilOnili is defined as inflammation of the peritoneal
lining of lht (bdominal cavi
)
. The condition is dis
w' 1 in greater detail in Chapter 17. Peritonitis ocurs
M .ome nr.grce in all hOfSC. following abdominal
s
UTrry ause of the Imtllna assoiatd "ith tht
surgery, handling of the intestinal tran, etc. In mot
ces this is self-limiting <nd of little clinicl signii
(alice. Ilowevcr, septic PCI'itOliitis is U serious and
pottntially lifc . d\f("ltelling ctJmp!iLtion of abdominal
SHrg':" thil rlluire prompt and aggresiy(' therapy.
CAUSES OF POSTOPERATIVE
PERITONITIS
The mllst C:(llHlllOn cause of postoperative septic peri
tonitis is leakage of ndll!uxins and/or bacteria from
the bowel lulTIcn ill to the pc::ritolleal cavity. This may he
Jue to nCClIis of Ihe entirc howe! wall or a mucosal
injul1' only.
Contamination c)f the rxrioneal cavit} may also
oc(:ur at, the tim of surgery espccjal!y when entero
tom) or oov;cI r(
'
section and anasLOmosi procedures
arc pcrfomled, Some degree of local collt,,-lIlinalion of
the ahdomen at the siles of cntcrolOmr is almost
inC\i l ahle, but pmided that the sUll!cl1' is l:rfonned
cleanly U possible. this loclli7cd contalllimlion i
unlikely t1J I:ause scrious dilrusc septic p rilonili s.
11(> c\c, if W1T widespread contamination 1C1
thcn 'l more S'\t'rediffuc septic peritonitis mr result.
The causes of peritonitis in the poslop<.dti,'c period
arc listed iu Table II .. '.
227
1 1 COLIC
Contamination of the abdomen
at time of surgery from -gut contents
- break in asepsis
-swabs, etc.
leakage of enterotomy or anastomosis
Progressive bowel necrosis following strangulation
Secondary bowel necrosis due to -prior distention
- ileus
- persistent shock
Chronic small intestinal distention and necrosis
Chronic large bowel impaction and necrosis
Enteritis/colitis
Perforated ulcer
Incisional infection and dehiscence
Sever'll studies of postoperative complications in
colic cases have been published, and these have shown
(on !lining results with respect to the rates of postoper
ative pcritouilis. In the study by Phillips and \VahnsIcy
( I993) generalized septic peritonitis was recorded in 9
of 149 horses (6%) undergoing exploratory laparo
tomies for colic. The most frequent fatal postoperative
complications that occurred in this study were general
izt'd septic peritonitis and bm''el obstruction caused by
adhesions. However, eight of the nine horses with peri
[())litis had pre-operative ahscessation, rectal tear, or
advanced bowd ischemia.
All horses will develop low grade non-septic peritonitis
following colic surgery, and peritoneal fluid total nucle
aled cell counts and total protein concentnltions are
likd)' to h( elevated (see Chapter 2 Analysis of peri
toneal fluid). In IIIOSI cases this will be lIIild and self
limiting. Howevtcr, diffuse septic peritonitis rC<
l
uires
specific therapy and is potentia!!y life-threatening
unless treatment is instituted early. The early recog
nition of postoperative peritonitis is therefore impor
tant. Some or all of the following signs and findings
should alert the clinician to the possibility of septic
peritonitis
depression
alxlominal pain
ileus
gastric reflux
intestinal distention
fever
228
anorexia
tachycardia
leukopenia
hyoproteinemia
diarrhea.
None of these findings is specific to peritonitis and al!
of them can be seen in varying degrees in association
with other postoperative complications. However, the
prsence of one or more of these signs should be LT1
sidered as suspicious of septic peritonitis.
Confirmation of the presence of postoperative septic
peritonitis can be dificult because of the non-specific
nature of the clinical signs and the fact that peritonitis
is always present in the postoperative patient. However,
analysis of peritoneal fluid should be performed in
cases suspected of being affected by septic peritonitis.
Exploratory laparotomy (celiotomy) without entero
tomy will result in an elevated peritoneal nucleated cdl
count for up to 14 days after surgery. The total nucle
ated cell count of peritoneal fluid can increase up to
400 x 109/1 (400 000 cells/t) with more than 90 per
cent neutrophils in healthy horses followng surgery
without enterotomy. Likewise, the total protein concen
tralion may exceed 3.5 gil in such normal horses recov
ering from surgery. Meamrement of total nucleated cell
coums and total protein levels are therdore unreliable
for the diagnosis of septic peritonitis. However cytology
of peritoneal fluid and examination of a gram-stained
preparation can be more helpful. In particular the iden
tifkation of one or more of the following abnormalities
should be considered signif(_ant
numerous toxic and degenerate neutrophils
free bacteria in the fluid
phagocytized bacteria within neutrophils or
macrophages
food particles and plant materia!
fbrin particles.
:icrobial culture of peritoneal fluid is indicated not
only to identity the pathogens present, but also to help
tailor the antimicrobial therapy more spedfcally.
Peritoneal fluid pH and lactate dehydrogenase
{LDH} concentration, and comparison of plasma and
peritoneal glucose concentrations can also be helpful
in determining whether L not sepsis is present. The
most consistently useful indicators of sepsis includr
a plasma to peritoneal glucose concentration
difference of more than 2.8 mmol/l (50 mg/dl)
peritoneal fluid pH less than 7.3
peritoneal glucose concentration less than
l . 7 mmol/l (30 mg/dl)
peritoneal fbrinogen concentration more than
2 g/I (200 mg/dl).
LDH activity in peritoneal fluid is a less reliable indi
cator of sepsis than these parameters.
Occasionaliy localized areas of periLOnitis may
become 'walled oW by fibrin, this may result in rela
tively normal-looking peritoneal fluid in samples
obtained from the ventral abdomen. Thtc absence of
specific abnormalities in peritoneal fluid should !lot,
therefore, rule out the presence of peritonitis and clini
cal judgment becomes more impof1ant than depcn
dence on laboratory test resulL.
Ultrasonographic examination can be helpful in
(,valuating th patient for septic peritonitis. Excessive
ptritoneal lIuid may be present and this often sbows
hetcrogeneous echogenicity. Hyperechoic particles in
the fluid an consisnt with the presence of gas bub
bIes. Fibrin tab'S on the intestinal stTosa and peri
toncum cause a roughening of these surfaces. Small
intestinal distention with ,aing degrees of mural
edema and some evidence of motility is commonly
()bser\'d in these cases (this contrasts with horses with
small intestinal strangulation that usually have dis
tenrkd loops with mural edema but no motility). Viscus
rupture is often accompanied by the presence of abun
d,l!lt fluid that appears hypoechoic and contains hyper
echoic panicles of ingesta. Pneumoperitoneum may
occur with bowel rupture but can also he seen following
rtce!H laparotomy. Free abdominal gas lIlay I seen in
a hyperechoic area underlying the body wall in the
dorsal ahdomen. Reverberation artifacts may also he
present.
TREATMENT
In lhe postoperative patient, the diagnosis of septic
peritonitis is likely to be an indication for repeat laparo
lOmv, unless a specific cause of the peritonitis (such as
known contaminatioll at the time of the initial surge!)')
is recognized. Repeat laparotomy permits identification
of the source of spsis and this lIlay dictate the appro
priate treatmelll (e.g. resection of leaking bowd, etc.).
Opt'n peritoneal lavage and use of intra-peritoneal
antibiotics will he helpful, and placement of abdominal
drains to permit postoperative lavage may also be con
sidered.
Peritoneal lavage and drainage an helpful in the
treatment of postoperative peritonitis, and may help to
reduce the incidence of intraabdominal adhesions.
The lavage is continued every 412 hours until there is
a decrease in the peritOll(al lluid cell count and protein
concentration, an increase in pH and glucos{ concen
tration, and an improvement in the cytological appear
ann" of the fluid. These and other treatments for septic
peritonitis are described in Chapter 17.
Postoperative complications
- l aminitis
CS Cable
INTRODUCTION
Laminitis that occurs in thc postopcratil'e equine
patient can be ont' of the most frustrating and deadly
complications of gastrointestinal disease. Bv defnition,
laminitis is an inflammation of the lalllil1at within the
hoof. The interdigitating laminae create a bond
hctween the hoof wall and third phalanx. Inflammation
and/or necrosis of the laminae can result in a break
down of this hond, resulting in rotation or ventral dis
placement of the third phalanx away from the hoof
wall. This rotation is also thought to resuit from [he pull
of t.htc deep digital flexor tendon, which broadly
attaches to th{ palmar surface of the bone, once the
laminae arc no longer holding the third phalanx tightly
against the hoof wall. Laminitis results in pain ranging
widely from mild to severe and unrelenting.
PATHOPHYSIOLOGY
Horses recovering from any gastrointestinal disease that
camed endotoxemi<l afe at risk of developing laminitis.
There are several theories to the etiology of laminitis
in hors{s with endotoxemia, although experimenml
administration of endotoxin in h()rs has not reulted
in laminitis.
One theory is that laminitis occurs bec.ause of alter
atiollS in digital circulation. VenoCOllstriction and high
hydrostatic interstitial fluid pressures are thought to
interfere with microcirculation in the foot, resulting in
ischemic necrosis of the epidermal lamcllae and subse
quent rotation, or ventral displacement (sinking), of
the distal phalanx.
A recent theo!)' (introduced bv Dr Christopher
Pollitt) suggests that certain enzymes are responsible
for the destruction of the normal lamellar structure.
The matrix lIlctalloproteinase 2 and 9 (MMP) {n7yllles
haw been found in normal hoof tissue in low concen
trations, but the levels become elevated in laminitic
feet. It is believed that \.,hen these enzym{s arc activated
they destroy the lamellar attachments resulting in
laminitis. What triggers the release of these enzymes is
not completely understood, but i t may be substances
released from organisms that normally inhabit the
equine gastrointestinal tract. For example Stuptl:((us
bUlIil has experimentally aC!hatd equine MMP-2 and
resulted in lamellar separatioll.
229
1 1 COLIC
CLINICAL SIGNS
Horses affected with laminitis ;fe frst observed to be
reluctant to move. The front limbs are generally
affected although 1I1 occasion all four limbs will he
involwd. 11l{ll forced to walk, affected horses will shift
their weight to their hind limbs and tend to keep their
front fcc ahead of their shoulders. They arc especially
reluctant to tur. The diagnosis can eaily be made by
the palpation ofa hounding pulse in the digital arteries,
increased heat i n both hooves, and the bilateral dinical
signs. Horses arc reluctant to bear weight L either
front foot when tlK contralateral limb is picked up. If
digital pressure is applied either manually or with hoof
testers, pain is elicited diffusely in the toe area.
There are tWO main syndromes that result from pro
gression of t.he clinical signs.
I. Horses experiencing primary rotation of the pedal
bone may develop a ventral dcpression to the sole
(outlining the tip oft.he pedal bone). Fluid and
blood accumulate under the sol. This fluid
accumulation can undermine the entire sole and
drainage Hlav be observed at the corOllary bands in
the heel area.
2. Horses experienci ng primal)' ventral displacement
can be recognized by the hair at the corona!)' bands
being directed horiwmal and parallel to the
ground as their follicles migrate distally to the kvel
of the COrOlla!)' bands. In addition, one can palpate
a depression at the cranial asp<CI of the paster just
above the coronary bands as the coffin joint mOl'es
away from the area.
Radiographic evaluation (lateral view) with a linear
radiodense material taped to the outside of the hoof at
the toe area can help identif}' the manifestation of this
disease and its severity, and demonstrate any fluid and
gas accumulation in the laminar tissue.
PREVENTION AND TREATMENT
Prevention of laminitis in the postoperative patient is of
paramount importance, since lamellar damage will
have already occurred by the time the horse shows din
ic;t1 signs of lameness. Horses with endotoxemia should
he considered as likely laminitis candidates, and should
receive anti-endotoxin seHUIl or plasma, and an anti
cndotoxic dose of fIunixin meglumine (0.25 mg/kg
t.i.d.). Othcr supporti\' tr4atments include the applica
tion of frog pads to aid circulation in the foot and to
apply counterpressure against the pull of the deep digi"
tal flexor tUndon. In tht pat horses with laminitis werc
Iwaled wilh acepromazine or nitroglycl'ine to bdp
230
increase blood flow to the feet in accordance with the
vasoconstriction theo!)'. However, i t has been reportcd
that vasodilation occurs in the developmental phase of
laminitis and is a possible triggering factor for activating
enzymes responsible for laIinitis. Therefore, it is llO
longer dear if vasodilators are indicated because they
could accentuate the laminitic crisis. \\,ith the currellt
state ofkllowledge the author recommends again.t the
use of vasodilators in horses at risk of developing
laminitis. However once the laminitis has developed,
she advocates the use of such vasodilators as acepro
maline, nitroglycerine or other vasodilator drugs.
Phenylbutazone should be implemented in aCUle cases
of laminitis in addition to low doses of fIunixin meglu
mine for pai n relief. When :SAID toxidty is a risk
dilllte intrav(noUS DSO ( 1 00 mg/kg b.i.d.) can be
administered in intravenous fluids for its anti-inflam
mator dfects.
Horses with acute and progressive laminitis can ben
efit from a deep digital flexor tenotumy performed in
the standing animal as surgical treatment. The ratio
nale for this treatment is that in horses '.vith severe lam
inar de.truction the unopposed pull of the deep digital
tlexor tendon can lead to severe rotation of the distal
phalanx.
Return to performance is likely for horses that do
not have significant rotation 5 degrees) or sinking of
the distal phalanx.
- colitis
TJ Divers
INTRODUCTION
Horses undergoing abdomina! surge!) arc known to he
at increased risk of developing colitis/diarrhea com
pared to other surgical/anesthetic procedures. This is
not of great surprise since these horses have often
undergone period of ileus and, in some cases,
ischemic/inflammatory bowel dise<se. The ileus is fur
ther aggravated by the i ntended anorexia both prior 1
lhe surgery and for one or more days after the surger.
The lack of normal fermentable fber r(,aching the
colon diminishes volatile fatty add productioll which
may permit overgrowth of pathogenic organisms sllch
as SrlmOlwllu -'pp. L1 CUI.Ilridium difdll. Approxim<ltdy
10 per cent of normal horses arc positive for SlIlmrlnpllfl
spp. when tested by polymerase chain reaction (peR)
yet mure than 40 per cent of horses with ahdominal
disorders are positive indicating that changes in motility
and/or normal fora are important to the proliferation
and/or shedding of the organisms. Additionally most
horses undergoing abdominal surgery afe treated with
ant.ibiotics which may further disrupt intestinal flora
and normal volatile fatty acid production. Finally post
operative colic patienL are kept in intensive cafe
environments that might be more likdy to harbor
pathogenic orgimisms such U Salmone/In spp. or
Clo.l/rrium difirik which arc dillic_ult to eradica1e from
the environment. Other factors that may predispose
postoperative colic patients to infectious diarrhea
include weight loss and deCeaSt,d cell"mediated immu
nity which are likely t occur in many, if not all, POST
operative colic cases. Small intestinal reflux might also
predispose the gastrointestinal entrance of infectious
organisms hecause of a persistently high gastric pH.
CAUSES
Causes can generally be divided into olle of two groups
infectious/inflammator causes
motility/dysfunction causes.
The two predominant infeCl.ious causes afe
Salmonella 'pp. and Clostridium diUifilf. Both can be
('ndemic or epidemic in critical care hospitals. Both an
{overed in more detail in Chapter 20.
(;auses of mot.ility dysfunction such as peritonitis or
illlestinal hemorrhage and bowd shortening, especiallv
colonic resection, may result in diarrhea. Iiorses with
colonic res{'ctioll generally have watery k{:es, some
times hemorrhagic, for several days up tn 2 weeks
f(}lIowing colonic resection. Laxatives and ver large vol
umes of intravenously administered fluids may cause
diarrhea, but this should resolve within l2-24 hours
after discontinuing t.he laxatives, and even more quickly
after discontinuing or slowing the rat.e of intravenous
fluids. Diarrhea may follow resolution oflarge intestinal
impactions. but this is genpr;l\y the resllit of laxatives
giV('!l per os and should resoh'e promptly If thl"
diarrhea persists an infectious agent should bc strongly
considered.
DIAGNOSIS
The pre_seller of watery feces aft(r abdominal surge
ry
should immediately indicate diagnostic tests 1 deter
mille the cause and severit' of the prohlem. These
should inclnde
abdominal ultrasound to determine the volume
and echodensity of the peritoneal fluid
fecal cultures, gram stain and Clostridium toxin
testing
complete blood count and serum chemistries
complete clinical examination.
In most cases of infectious diarrhea the patient will
he febrile and the complete blood count v.uld releal
hemoconcentration, a neutropenia with toxic changes,
and a decreased serum sodium and chloride.
Ahdominal sounds may he absent or more 'nuidy' than
normal. ! peritonitis is a (:(Hlcer based on the prior
surgical procedure, clinical and laborator evidence of
acute inflammatory disease, and ultrasound fIndings,
abdominocentesis should be pen()Hned (see Post
operath'e complications - peritonitis). There shmtld be
a good indication for this since
unwarranted abdominocentesis will increase yentral
abdominal s,\'e!ling and negatively affect wound
healing
interpretation might he difTIcult depending Oil
prior intestinal pr<Keelures that are routinely
expected to cause some degree of peritonitis.
Fresh fecal samples should he submitted to the labo
rator for aerobic and anaerobi<: bacterial C_!llture, gram
stain, and C/usilirium rif firil! toxin assay (ELISA or
peR). If a Salmunella spp. is grown, bacterial sensitivity
should be pent>nned. Clm/ridiwH pnfrnglll toxin
(cnterotoxin) assay might also be requt>sted, but results
are difficult to interpret. C{o.l/ridiUIl jllljingls toxin
testing would be desirable, but is nO!. readily available.
peR might also be requested it}r deTection of SflllIIOlid/fI
spp., but it is so sensitive that a positive finding docs nO!
always mean that Sflllllon,lIa spp. is the cause of the diar
rhea. Likewise, a positive culture of Sa/mlnf/la spp. does
not prove that it is the cause of the diarrhea, hilt this it
makes it more likely than a positive peR.
TREATMENT
Treatmnts for each disorder are covered in Chapter :().
PREVENTION
The prevention of postoperath'e coliti is not always pos
sible but its incidence might be f(duced by
routine culturing of intensive care patients and
their stalls
judicious use ofantibiotic_s
provision of roughage as soon as possible after
surgery.
231
1 1 COLIC
TIl t<: \)l" 01"",1 llIi(;robial iJl()(:i\hml, although
tmlikcir L1J he hannful, are nnt of pm\cn value. Routine
nthtlrill of 1)l)slOp
"
'r;;tie. crilkal !are palient\ and
thcr Slalls allows delce.lion of inftr(iou'l org,mi | #,
N(' P:UiCIlIS IWHld H(X be 1xpr tn infcdt, em'i
I"nnlOtots uruil propcr dcanillK pmccdurcs ha\'c been
applkd ;uld the cllvironm('nl i cul!un--nqc for
known p;;thogcns. Ilypochiorilc lOa)' he used on stal
s\llfac(. and ghHar,do(:hydc IIscd to disinfect equip
m('1 th.u can ))('1 otherwise Irri!ild. Fuot haths
('(>lll<!jllin appmpria\c r
l
l;al<:rnary anullonia disinfcc-
1;1Il1 should he usee Oil Illlt,h entering and leaving the
1
)()slnrx'l1uivt Irilir U
1
("art an:, and [ht walking sur
(;In's rlisinkclcd hut kepI dry and lighted (sunshine or
uhr+\\'iolt:t li!hl if
'
possibk) All persollllel should
wash their hands with c:hlorhexidinc or anothcr soap
l)('twt'l"U <asc"s. use iudhidnally pr1pared equipmem,
for ('xanlpll' slIlmach tuhcs. and takc net:essary precau
tions U prc:ve-nt tJw spre<ld of <In illknious ageIlt on
flotlling-. Any horse dl.:\"doping diarrhea should he
mo'd U all i!o!;ltio(l tildlity.
Alllihimic. sh()uld tUlly be U.';td if necessary, as cvcn
Jhln'llwr.llly administered ,mtihiotil." lllight increase
til(' intjdellfC of wI:H:rial (()Iitis. 1()Sl onll antimicro
hi;lls hul1ld 11111 he lSlt until lht hor1\(' has O'1 on a
norlal rHllghage (fitt lilrS "= 1 dO};. 1etronidawle is
uli:1l ;'ppmpri;m'l)' used rollowing colonic enter.
(t)lIil.: s, hIli [itl loulille adminilrati()n or melronida
.011' in the hopI' of pre\'llting Clstridium dif cl#
di<llTlw:\ should nnt he encourged and i nOl h
.p.
sun.t:ssll,l.
- cardiac arrhyth mias
M Bowen
INTRODUCTION
em!i;!f arrhphmias durin! lhe
I
xriopcrati\"c ptriod
art' common and :I!'C usually a rd]('Clion of IIlctabo!il:
dilIIrh,\lI:('s mther Ih;m lUll' primar) cardiac di Sa.'.
. Many of Ihest: Qnhytiullia> art of lillie or nn COI
l1n:uCt ami nuly lew cast' rec
l
uirc spcific interen
tioll, Tlwrapy is imlic:ucd i there is M compromise to
c;nti:,( outpul or pcriplu;r.,1 pcrr"sinn. I ir the
rh,thnt i. of < tn)t' that ma)' dcsuhililC into a more
IIwlilmtrll lifethreatening <trrhylluuia SIKh s \'ClHric
ul;;r fihrilbtiltl.
232
RECORDING AN ELECTROCARDIOGRAM
TIle use of radiotelemetric 01" COlltinuom ambul<ll}
(Holter) dectrocardi(graphy during the pcriopcnu\
period facilit;ues the prompt detection of :lThythmias.
! luwr intermit1ent u (lr paper (nce c!celro
GHdiogntph), will be sufcient ror the diagnOlis nr
persistent rhYlhm disturbance. Electrocardiognph' is
indicated in the ponoper"ti\'t prriod if either
a fopid pU!k rate is detecH
'(! that cannot be

explained hr lhe le\el of pain Of cndotoxcmia, or
the pulse rate is greatCr than 80 bpm.
Electrocardiography h(ltL!d also be considered during
the e-v<lluation of horses with reported abdominal pain
but no clinical evidence of gastrointestinal disease, as
horses with priml!)' cardiac disease may presenl with
clinical higls of ditres. that can he mistakcn for abdom
ina! pain.
A .itandard modifed h<se apcx le<d stem is re("()JIl
mended for the dUI:umentatioll of arrhythmia.. Thi.
comprises placing lhe right arm (R or positive) cIcc
trode over the hean bsc 1M th( right h'nd ide, tht' lel
anT (IA nel;tti\"l) e1c<:twde along the jugular gronv('
on the left hand side flf the lltCk. The earth (\el lcg)
mlll m:utl'al (right leg) c be pla$Id O'r the >Lpula.
Recordingsshauld be made in lead I, which wll prouce
a Ji(ivc P Y1 and a nqativc QR cumple. For
details of interprCtation artn! EKr; readers arc ocferred
to Ihe reommcnced lelIS <II Ihl: end or this chapt(r.
PREVALENCE AND CLINICAL
SIGNIFICANCE OF ARRHYTHMIAS IN
THE PERI OPERATIVE PERIOD
Ventricular arrhythmias
Vcntrkular <lrrhythmi<ls represent tht, most common
significant arrhYlhmia in !hl: postoperative period in
the horse. Their ECG ch<raC:l('ristic; arc oj" a wide
ahnormal QR morphology. that is unrelated to a
prcl:eding P wave .h\wn in Figure I I .S. Vent.ricular
arrh),thmias can he defined as ventricular premature
dcpo]lTization with a single LHopie COlllpleX, C()up!cL,
Of triplKts, reprL'lIIing t and three consecutive com
plexes. 11 'entl'icular t.achycardia as a sus t ained velllriL
Illar arrh)hmia wilh an increased n. Ventricular
t;chrcardia may he further ddlncd as parox, per-
1\iMing for up 10 Iwrnty complexes or slIstained. A
accccr.tLd idiO\cntricular rh)'lhm i s a sustaiul A~
tricular <ll"rh)"lhmia wilh a I < tc similar J sinus rhythm
and such its diagnosis ma) r:a.i1y be mi'l d ' cardiac
allscultatioll alone.
"
V RT VF
Figure 11.8 A sample from an ambulatory ECG of a horse 24 hours post-celiotomy, showing sinus tachycardia with isolated
VPDs (P,), a couplet of VPDs (P,), ventricular tachycardia (V progressing to R on T phenomenon (RT) and ventricular fib
rillation (VF) leading to death. Movement artifact is indicated by A. The horse had multiple electrolyte disturbances
(hypocalcemia, hypokalemia, and hypomagnesemia), was acidotic and endotoxemic and had disseminated intravascular
coagulation
Vrnlrirulur prnnf/uU' toimiUltim,\
Sin!(le infrequent isolated ventricular premature depo
Iariltions (VPDs) may be detected in normal horses
during ambulatory monitoring and are not considered
abnormal if they occur infrequently.
Fntlrirular tachycardia
Ventricular tachyc_ardia (V) at rapid rates may signifi
cantly reduce cardiac output thus reducing tissue per
fusion. The increase in heart rate increases myocardial
oxygen demand, but this demand is not met because of
5
decreased output. The myocardium may become
hypoxemic and predispose to further destabili7_ation of
this rhythm into ventricular fibrillation (Y) (Figure
1 L9). V is usually non-responsive to therapeutic
agents and carries a hopeless prognosis in the adult
horse.
VPDs do not in themselves constitute a significant com
promise to cardiac output, however they may be a
predictor of a destabilizing arrhythmia. In one clinical
study comparing the incidence of ventricular arrhyth-
_J
, _"
' "
, ,
Y I V "
, " '"
, I
-
I I V
I V "
Y - - Y
, 1
A
V
,
`
E
,
,
,
,
I I
- , , ,
- J J _ I
J
F
, v
, v\
lvv JVV VV
Figure 11.9 Ambulatory ECG of a horse 36 hours post-celiotomy that had developed enterocolitis and septicemia. The ECG
shows sinus tachycardia (S) until after the administration of xylazine (100 mg Lv.) as an analgesic. The horse developed
asystole (A) and subsequently electrical-mechanical dissociation (E) and ventricular fibrillation {F}. Each line represents 30
seconds of recording
233
1 1 COLIC
mias in the postoperative period of both celiotomies
and elective orthopedic surger, there was an increased
incidence ofvcntricular arrhythmias in the horses with
gastrointestinal disease. In the frst 3 days postopera
tively, H of the 35 horses having undergone a celiotomy
had ventricular premature dcpolarizations, of which
four had paroxysmal ventricular tachycardia, whereas
none of the control group had ventricular arrhythmias.
Despite this incidence, only one of the horses with
paroxysmal ventricular tachycardia warranted specific
anti-arrhythmic therapy. In the remaining horses, the
V1 resolved without therapy and ventricular arrhyth
mias did not influence sumv,,! mIts. In another _ludy
of 21 cases of ventricular arrhythmias in the horse, 7
horses had gastrointestinal tract disease. Four cases
(19%) had ventricular arrhythmias in the 4hour
period folloVing celiotomy for strangulating or non
strangulating lesions. Three of these cases died, one
because of gastrointestinal tract disease, one during
treatment for multiform ventricular tachycardia, and
the remaining horse died .3 months after discharge with
c\idence of myocardial fbrosis found on postmortcm
examination. These studies indicate an increased inci
dence of ventricular arrhythmias in the postoperative
period after gastrointcstinal disease. However their inci
dence rarely poses a signifcant problem and specifc
anti-arrhythmic agcnt are rarely required. The man
agement of the underlying problem usually results in a
conversion to normal sinus rhythm.
Atrial fibrillation
Atrial fbrillation (AF) is characterized by an irregularly
irregular heart rate. The ECG characteristics are a lack
ofP waves and the baseline fluctuations around the iso
e!ectic axis in flOe fbrillation waves (Fwaves). The Q;
complex has a normal confguration represcnting a
supraventricular rhythm. A is occasionally encoun
tered in the posloperath'c colic patient, but in isolatjon
it is unlikely to have any clinical significance. Therapy
should be delayed as spontaneous conversion may
occur. If A persists then therapy with quinidine sulfate
should only be considered once the horse is othelWise
healthy. Side effects of quinidine sulfate include
hyotension, supraventricular and ventricular tachy
cardia, colitis, and tympanic colic.
Bradydysrhythmias
ClinicaHy significant bradydysrhythmias are uncommon
hut can be seen in association with the use of alpha
agonist in horses with underlyng cardiovascular dis
ease or severe cardiovascular compromise (Figure
1 1 .9). Treatment of bradydysrhymias caused by alpha.,
agonisl should include the use of parasympatholytic
234
agent. and/or alpha antagonists. Atipamazole is the
only alpha.antagonist available in the UK although it
does not have a veterinary product license for use in the
horse. Following sedation wth detomidine (lO-20 Il
g/
kg i.v.), atipamawle should be used at a dose rate of
JOG-I60 Ilg/kg intravenously. Atipamawle causes an
increase in heart rate after 2-4 minutes, although atrio
ventricular block may still persist. Excessive arousal and
hyperesthesia may be obsered. Intramuscular use of
alpha2 agonists causes less profound effects on heart
fate than when given intravenously and should he
considered in 'high-risk' patients where sedation is
reCuind.
PATHOGENESIS OF CARDIAC
ARRHYTHMIAS IN THE
POSTOPERATIVE PERIOD
Horses that develop cardiac arrhythmias in the post
operative period following celiotomy rarely have any
underlying cardiac pathology. The factors considered
to be important in the pathogenesis of these arrhyth
mias include
acid-base or electrolyte disturbances
hypoxia
poor myocardial perfusion
endotoxemia and drug administration.
In humans and dogs it is recognized that autonomic
dysfunction produced by intestinal distention or pain
arising from the gastrointestinal tract may kad to
cardiac arrhythmias but, currently, there is no spccific
cvidence that this occurs in horses. In horses wth poly
morphic ventricular arrhythmias, primary myocardia!
palholob'Y should be considered.
ELECTROLYTE BASIS OF CARDIAC
AUTOMATICITY
In the normal myocardia! cell the resting potential,
maintaincd by ion-selective membrane channels,
increases because of a slow influx of sodium ions until
the threshold potential is reached. Once the threshold
potential is exceeded there is a large and rapid influx of
sodium ions into the cdl, cauing depolarization.
Calcium influx maintains depolarization and causes
muscle contraction. Movement of potassium ions from
the intercellular space leads to repolarization. An
aerobic-encrgy dependent ion pump reSlor'es nOlI!!al
intracellular e!ectronegativty with sodium in the extra
cellular space and potassium within the cell. Changes to
any ofthes(, ion gradients across the cell membrane will
affect the automaticity of different parts of the
myocardium and thus enable the production and prop
agation of an arrhythmia.
Potassium
Hypokalemia can occur due to loss ofsenlm potassium
through the gastrointestinal tract 1 kidney, or by
dilution of existing serum potassium. Dilutional
hypokalemia can ocnlr due to the prolonged use of
polyonic intravenous fluid therapy solutions, such as
lactated Ringer's solution, that do not provide mainte
nance requirements for the normal horse. Serum potas
sium concentrations arc aflccted by the patient's
acid-base status. Potassium is a largely intracellular
{:ation, which is exchanged for extracellular hydrogen
ions during acidosis resulting in an increase in extracel
lular potassium concentration despite total body losses.
Therefore potassium abnomlalities may go unnoticed
in t.he face of a co-existing acidosis. During prolonged
postoperative ileus, both gastrointestinal losses of potas
sium and prolonged fluid therapy occur, thus placing
these patients at an increased risk of developing
hypokalemia. Because of gastrointestinal loss of hicar
bonate there may be co-cxisting metabolic acidosis
which can result in under diagnosis of this electrolyte
disturhance.
Arrhythmia. associated with hyokalemia are due to a
reduction in the anion gradients of the cell. The reduced
ion gradient of potassium changes the resting potential
so that there is a reduced difference bet 'een the resting
potential and the thre5hold potential. Because there is a
reduced requirement for spontaneous influx of sodium
to reach the threshold potential, the cell becomes more
susceptible to spontaneous excitability which can lead to
ventricular arrhythmias (Figure 11.8).
Rapid intra\'enous administration of potassium chlo
ride is contraindicated as bradycardias, induding atrial
standstilI, can occur. Potassium should be given by a
slow intravenous infusion at no more than 0.3 mmol
kg h
-
I. For maintenance 20 mmo! of potassium chlo
ride can be added 1 each liter of lactated Ringer's
solution.
Hyperkalemia can occur in patients with hyper
kaIemic periodic par.\ysis, anuric renal failure, or
uropertoneum. These indivduals are at particular risk
of developing atrial standstill and third degree atrio
ventricular hlock, but fatal ventricular arrhythmias may
also occur. Lfe-threatening hyperkakmia is treated
I'.-i th insulin (0.1 IV/kg) with dextrose (0.5-1 g/kg).
The extracellular concentration of potassium can also
be reduced following the intravenous administration of
sodium bicarbonate (1 mrol/kg) and the slow admin
istration of cakium (0.2-0.4 mlJkg of a 23% solution of
calcium borogluconate) may have a cardioprotective
effect in hyperkalemia.
Calcium
Hypocalcemia occurs due to rapid losses into the
gastrointestinal tract. Calcium is important for cardiac
muscle contractions and for maintaining depolariza
tiOll after rapid sodium influx into the cell. Profound
hyocalcemia can result in ventricular tachycardia
(Figure 1 1 .8). The detection of hypocalcemia can be
complicated by abnormalities in serum albumen.
Calcium is largely protein bound in plasma, and alter
ations in serum albumin wn be reflected by similar
changes in total serum calcium. Although algorithms
havc been produced to equate ionized calcium to total
serum calcium and serum albumen, their results are
unreliahle in the horse. Determination of ionized
calcium (the metabolically active component) is more
useful (normal ionized calcium 1 .31.6 mmol/I).
Calcium can be administered as calcium boroglu
conate, given by slow intravenous infusion in saline
(0.2-0.4 ml/kg of a 23% solution of calcium horoglu
conate, then re-assess calcium status). Excessive admin
istration can cause atrioventricular hlock at moderate
hyercalcemia, profound hyercalcemia can result in
ventricular fbrillation and death. For maintenance, up
to 4 ml of 23 % calcium horogluconate can be added
to each 5 liters of lac.tatcd Ringer's solution to be given
intravenously over 2-3 hours.
Magnesium
Magnesium is an intracellular cation and therefore
plasma concentrations do not reflect total body con
centrations. Magnesium has many intracellular func
tions but its cardiac effects are mediated via its actions
on proton pumps, affecting intracellular calcium and
potassium transport across the cell membr,es.
Hyomagnesemia the important electrolyte abnor
mality detected in horses with ventricular arrhythmias
after colic surgery, particularly when ac.companied
by hypokalemia and hypocalcemia (Figure 1 1 .8).
Magnesium is used in other species as an anti-arrhyth
mic agent even when no underlying hypomagnesemia is
documented. The exact mechanism of action of mag
nesium therapy is still to be elucidated but may repre
sent a calcium channel-blocking ellect. Magnesium
sulfate can be administered by slow intravenous infu
sion or repeat bolus injections (Table 11.6).
Other factors
Acidosis, myocardial hypoxemia and endOloxemia will
affect the serni-pcrmcable selective ion channels of the
235
1 1 COLIC
ceIl membrane and can increase cellular automaticit
and therefore predisp(le U ectopic foci of depolariza
tion. Because acidosis is usually a manifestation of
peripheral under-perfusion, intravenous fluid therapy
with polyionic solutions is suitable for correction of
add-base disturbances if there is normal renal func
tion. Hyoxemia is also likely to reflect hypotension
and should be corrected by administration of crystal
loids or colloid therapy.
ANTI-ARRHYTHMIC TREATMENT
Specific ami-arrhythmic agents are only indicated In
severe life-threatening arrhythmias. In al cases, allY
underlying cause must be determined and !Teated.
Rapid Of multifocal (more than one contiguration of
ventricular complex) arrhythmias and the presence of
the R on T phenomenon are indications for specific
therapy. Th R on T phenomenon is a ventricular
rhythm where the QRS complex is associated with the
preceding T wave (Figure 1 1.9). This rhythm is unstable
because it represents depolarization and repolarization
occurring simultaneously and thus is likely to progress
to fibrillation. Therapy should also be considered if
there is a signifcant compromise to cardiac output, this
may manifest as weakness, collapse, or increases in
serum creatinine due to poor renal perfusion.
ANTI-A IC THERAPY IS WARRANTED
IF THERE IS
RAPID VENTRICULAR TACHYCARDIA GREATER
THAN IOOhpm
MULTIFORM VENTRICULAR ECTOPY
Ron T PHENOMENON
SIGNIFlCA HEMODYNAMIC EFFECTS
Specific agents
Doses of drugs for tbe control of ventricular arrhyth
mias arc listed in Table 1 1 .6. Ventricular alThyt.hmias
can be treated with class I anti-arrhythmic agent. These
drugs block sodium channels and therefore stabilize
the membranes of excitable cells The use of c1as.
IB agents, such as lidocaine (lignocaine), has blTn
1eHe 11.8wmfr" trto ala lymi
D ... Indftlonl DOe end .dministr.tion Side efec
Lignocaine hydrochloride Ventricular arrhythmias 0.5 mg/kg Lv. q. 5 min eNS excitability
Quinidine gluconate Ventricular and supraventricular 2.2 mglkg bolus q. 10 min hypotension,
arfhyhmis up to 10 mg/kg total, colitis,
or 0.7-3.0 mg kg-' h-1 arrhythmias
diluted in saline
Quinidine sulfate Supraventricular 10 gf450 kg p.o. q. 2- h hypotension,
arrhythmias colitis,
arrhythmias
Propanoloi Ventricular tachycardia 0.05-0.16 mglkg Lv. b.Ld. hypotension
Procainamide Ventricular and supraventricular 1 mg kg-' min-' Lv. hypotension
arrhythmias up to 20 mglkg
MagnMium sulfate Ventricular tachycardia 4 mglkg Lv. q. 5 min
Hypomagnesemia up to 5 mg/kg total
Atropine sulfate Bradydysrhythmias up to 0.1 mg/kg Lv. s.c. may induce initial
bradycardia if given
i.v., ileus
Glyoopyrro!ate Bradydysrhythmias 0.01 mglkg Lv. ileus
Atipamazole Alpha, agonist-induced arrhythmias 100-160 Iglkg Lv. excitability
xamethasone Immune-mediated myocarditis 0.02-.2 mglkg use reduclng dose
or profound AV block regime
236
rt,omme](led for vent.ricular arrhythmias because of
tht short duration of action on sodium channels, which
is Ies. likely J affect the underlying sinus rate.
Lid(llaille (lignocaine) can lead to focal or generalized
sdnlres, thus horses receiving lidocaine (lignocaine)
should be monitored carefully and the infusion discon"
tinued if muscle fasciculalions arc obsered. The class
I B drugs, such +15 quinidine and procainamide, which
an classically resered for the treatment of supraven
triclilar arrhythmias, lack the neurological side effects
of lidocaine (lignocai ne) and are therefore considered
the drugs of choice for the treatment of ventricular
arrhythmias in the consdous horse.
In!wenous magnesium snlfate has been used suc
n'ssfull' as an anlidysrhythmic agent which is effective
1 patients evrn with normal serum magnesium
cOllcemrations. Its use in the horse has not heen fully
c\al uated.
I'mpanolol , a beta-blocker, may he henefcial in
Ire,Uing ventricular tachycardias together with other
ag("nL, but should be used with care if there is compro
mised myocardial function as its usc will further reduce
cardiac output.
AFERCARE AND PROGNOSIS
Onre drug therapy has commenced, the patient should
1) ohser,ed carefully for sign> of cardiac and non
cardiac complications. The underlying calise of the
cardiac arrhythmia must be addressed. Measurement of
the cardiac i()enzymes of lactate dehydrogenase and
cre<line kinase can he useful U document myocardial
!It'CH)sis which may ha\"C occurred, and if increased,
<nti-inflammatory agents are indicated. The prognosis
lill" most arrhythmias occurring in the postoperative
period will depend on the ability to identify and treat
the underlving cause(s). The prognosis \111 also depend
on the type of arrhythmia, for example if there is a
lTlultifocal sustained ventricular tachycardia or R on T
phcTlomenon then the prognosis is guarded. In the
mjority of cases with monomorphic ventricular arrhyth
mias that resolve "'lthout spcdfic therapy, the prognosis
is good and the arrhythmia is unlikely U recur once the
primary g- astrointestinal lesion has resolved.
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Poslal1lteS.hell<: reTumhenq in a Belgan flly with
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(;1=<1 R D ([9) Ju,tl"ht'l; my"palhy. In r:n' Oth
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! I. (1 978) Serum LhemistI) change in ho,,, es during
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c.rdi<Jpulmonal'' . . rt 4 blt:: in ha!ulh d T ' anl"thcti7ed
pO"le. ;,,,.). 1'''' J, f9: 146.'-72.
Postoperative complications -
thrombophlebitis
BYW M and Vale 8 H (19) Intr.Wnoucta lion
. 'nd associaud problems ill the hore_ C. OmlI.
l'l, \t, 4 Sm-27.
fl;IOll I. R (19J) JUlIlar Ihr(lmbophlebili (,wlting fmRl an
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1:'10248-:49.
Gerhards II (1987) (AntithIlnbin 11\ determination in the
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dclkienq'.) TlnrlLI. Pmx. Ei 47_:5.
Cuhards 11 (1 9f!7) (1IYIH"""gLllahiliLY an eLiologica! faclor
ill the deyclupmtllt ofjllj:ulu "ein lhrombmis in horSt'S.)
D/,oi. l;m",.I. WIC/lr, 94 173_174,
Gerhards H and :brhardt C ( 19R8) PI<sma heparin values
and hemostl!is in e{luid after subclIIaneous
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4913-18.
Holland M. Kcll) A B tl "I. (1986) AllIithrombin III a((h'ity in
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phamlnlog' and ther . [Xlllic \in hOls.J \. ln.
M 8( 1) 2:.
Morris D 0 (1989) Thrombophlebiti s in horsn: the
conuibutioo, ofh"moslalK d)",fu""I., Up1"> n
C Cni. F4uf. P. I'l. II 1313.
;tor J J (I!I) F.nrllloxemi a in hones

) Yd. I M :
167-181.
un\< R (199tH F.ndnl.mia ill hu,. IIP",'i2() {21
.
239
1 1 COLIC
Reef, V B (1998) Cardiovd.,wlar ultra.onography. In Equine
D;"R"OMic Ultrasound, V Reef (Id.). I B Saundtr,
Spurlock S L and Spurlock G H (1990) Risk factors of
catheter related complications. Comp. ConI. Edu(, l'rod.
\..1. 12(2);241-24H.
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425.43().
Traub-Darga!] J Land Dargatz D A (1994) A rctr<Jspcctivc
study of vein thrombosis in hor.o. treated with
intrawnous fluids in a veTerinary teaching hospitaL J Ve.
Inl. Mfd. 8(4):264- 256.
Postoperative complications - peritonitis
Blackford] T, Schneiler H L, van StcenhouseJ L and Sanders
W L (1986). Equine peritonea! fluid analysis following
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(1999). Ultrasound evaluation of cquine gastrointestinal
disorders. Conlp_ Gmt_ Edw. Pme/. VI. 21,253-262
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postoperati.'e management and complications. ret, Clin.
N. Am. l.argeAnim. Praet. 4:167-184
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the ,-esults of 151 exploratory laparotomie. in hores wilh
g:utrointcstinal disea.es. lui1Vel.J. 25:427-431
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surg{'ry. Vtl. Surg. J 7:f-9
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'
concentration, and la<tate
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in horse..J Am. Vrt. Mtd. Aof. 214:1032-1036
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ThlF"l,ineArlll"Abd, N A Whit(
'
(cd_) Lca and
Febiger, Philadelphia, pp. 323 5.
240
Postoperative complications - laminitis
Eastman TG, Honnas C M, Hague B, tl aL (1999) Ikep
digital flexor tenotomy a a treatment for {'hron;c
laminitis in hores: 3 caes ( 1 98B-1997}.
J
. Am. Vet. M,'d.
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.
'
hite :\ A {l990} Intensive care, monitoling, and
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Aru/Abdomr, : A \'hite (cd.). Lea and Febiger,
Philadelphia, pp. 32f-30.
Postoperative complications - colitis
l'arraga M E, Spier S j, Thurmond M, Hir<h 0 ( 1 997) A
dinkal t.rial of probiotic administnttion for prevention of
Salmonella shedding in the postoperative period in hon('_
with colic. I Vtt. In/. Md, I I (I) 36-41.
RUlala W A, Cole E C, Thomann C A, Weber D J (1998)
Stability and bactericidal actiitj' of chlorine WitttiOT.
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Postoperative complications -cardiac
arrhythmias
BonaguraJ D. Diagnosis of cardia< arrhythmias. In Cum'nl
Thuahin Equine l"mdiu, : E Robinson (I'd.). W B
Man C M. Treatment of cardiac arrhythmias and cardiac
failure. In Cun-rot Theapy in EquinePractice, N E Robinson
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Man C M, Reef V B (1991) ECG of the month.i- Am \"1. Mtd.
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ReimerJ .\, Reef V B, Sweeney R W (1992) Ve!llricular
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Marr (d.) W B Saunders, London, pp. 179-209.
12
Diseases of the stomach
MJ Murray
Gastric ulceration in the
adult
INTRODUCTION
Gastric ulceration is the most common disorder of the
equine stomach and in recent years the widespread
nature of this disorder has gained increased recogni
lion. Gastric ulceration can manifest itself in many ways
in horses, and varies in severity from mild and inconse
quential to severe and debilitating.
ETIOPATHOGENESIS
The equine stomach is lined dorsally by a stratifed
squamous epithelium and ventrally by a glandular
epithelium; these epithelia have different functions and
different susceptibilities to peptic injury. The squamous
portion of the stomach has no secretory or absorptive
function, and appears to serve as a reservoir for ingesta.
Because the equine gastric squamous mucosa has no
surface barrier to hydrochloric acid, and the epithelium
has limited properties to prevent peptic injury, its pro
tection from peptic injury depends on limited exposure
to acidic gastric secretions.
The equine gastric glandular epithelium is histologi
cally and physiologically similar to the lining of the
stomach of other animals and humans. It secretes
hydrochloric acid and pepsin as well as some water and
electrolytes, and a variety of endocrine mediators are
produced within this mucosa. The gastric glandular
mucosa has evolved elaborate mechanisms to protect
itself from peptic injury, including a mucus/bicarbon
ate barrier that prevents back difusion of hydrochloric
acid, mucosal blood flow, cellular restitution, and
growth factors that promote mucosal healing. Blood
flow is dependent on mucosal prostaglandins and nitric
oxide synthesis.
Hydrochloric acid is secreted by parietal cells via an
H+-K+-ATPase pump, of which there are more than one
million per cell. Hydrochloric acid is secreted by the
stomach under the influence of vagus nerve stimula
tion, gastrin, and histamine, with histamine appearing
to be the most potent stimulus of gastric acid secretion
in horses. In addition to stimulating hydrochloric acid
secretion by the stomach, gastrin appears to stimulate
secretion of water, sodium, chloride, and bicarbonate
from the pancreas into the duodenum; some of these
secretions normally reflux into the stomach.
The equine stomach secretes hydrochloric acid con
tinuously, even when the horse is not eating. Gastric
acid secretion is pronounced even in neonatal foals.
Gastric acidit is least when the horse eats, because eat
ing stimulates secretion of bicarbonate-rich saliva that
can neutralize some gastric acid, and roughage absorbs
the gastric secretions so that they do not contact the
mucosal surface. Once a horse stops eating, gastric acid
ity can rapidly increase, with pH falling below 2.0, and
acidity remaining high while the horse does not eat.
The gastric mucosa is damaged by excessive expo
sure to hydrochloric acid and the proteolytic enzyme
pepsin. Lesions in the gastric squamous mucosa form
within 24-48 hours if horses are prevented from eating,
because the gastric hydrochloric acid comes into con
tact with the mucosal surface and there is no inherent
protection from hydrochloric acid-induced injury. Feed
deprivation per se does not induce lesions in the
241
12 COLIC
glandular mucosa, because it is protected from
hydrochloric acid.
Lesions in the gastric glandular portion of the
stomach occur when there is impairment of mucosal
resistance, permitting exposure of the mucosa to
hydrochloric acid and pepsin. This can occur with ill
ness or from administration of excessive NSAIDs, and
possibly intensive exercise. In one study, during intense
treadmill exercise blood flow in the gastric antrum was
reduced by a greater proportion than in any other
abdominal organ. Factors that impair mucosal resis
tance in the glandular mucosa of adult horses are
poorly understood, but studies in laboratory animals
have implicated reperfusion injury as a cause of
impaired mucosal resistance and ulceration. The rela
tively high prevalence (25%) with which lesions in the
antral mucosa of adult horses have been obsered by
the author is suggestive of underlying factors that are
affecting mucosal blood flow in that part of the
stomach.
In humans Helicobacter pylor bacteria have been
determined to be the predominant cause of gastric and
duodenal ulceration. Helicobacter spp. bacteria have
been found in several domestic animal species, but not
in equine species.
EPIDEMIOLOGY
Horses of all breeds and uses can have gastric ulcers.
The prevalence of gastric lesions is influenced by the
management and use of the horse. Horses turned out
onto pasture and used lightly typically have normal
stomachs or only very mild erosions. In contrast, horses
kept in box stalls and trained intensively have a high
prevalence, up to 90 per cent, of gastric lesions. Most
lesions are seen in the gastric squamous mucosa, but
the prevalence of lesions in the gastric glandular
mucosa has ranged from 10-40 per cent in diferent
endoscopic studies. Endoscopic studies have found that
the prevalence and severity of lesions in the gastric
squamous mucosa, but not the glandular mucosa,
increases as the intensity of training (exercise)
increases. Recent studies have demonstrated that
intense exercise, for example American Thoroughbred
race training, can induce and maintain gastric
squamous mucosal ulcers.
Whereas the prevalence of gastric lesions is greatest
in horses used intensively, clinical problems associated
with gastric ulcers occur in horses used for many activi
ties, including breeding. Management is probably a
factor, because type of food eaten and eating behavior
can influence gastric ulceration. Restricting access to
roughage or feeding a large amount of concentrate,
242
thus reducing the amount of time a horse consumes
roughage, promotes increased gastric acidity and dam
age to the gastric squamous mucosa. Feeding concen
trates stimulates a greater post-prandial serum gastrin
response than feeding roughage, and gastrin is a potent
stimulus to hydrochloric acid secretion. In one study,
feeding alfalfa hay was associated with less gastric injury
than feeding brome grass hay, and it was speculated
that the protein content of the alfalfa might act as a
buffer. In another study, horses moved from pasture
turnout to stall confnement with free access to timothy
grass hay suffered from gastric lesions within 7 days.
CLINICAL SIGNS
The signs of gastric ulcers in horses can be vague and
non-specifc, they include
abdominal discomfort, indicated by mild-to
moderate colic and frequent lying down
poor appetite, Le. not eating well, picking at feed,
or not fnishing feed
poor body condition, rough hair coat
attitude changes (dull, 'sour', or agitated)
belching, this is a sign of impaired gastric emptying
and involvement of the pylorus.
There is often poor correlation between ulcer sever
ity and clinical signs. Horses with deep, bleeding ulcers
may have relatively mild signs, whereas horses with
superfcial erosions may have greater discomfort.
DIAGNOSIS
Endoscopy is the most reliable method for diagnosis. A
3 m-long, 10-11 mm diameter endoscope is preferred
as an all purpose gastroscope. Most gastric lesions
develop in the squamous mucosa, usually adjacent to
the margo plicatus (Plate 12.1) along the right side or
the lesser curvature (Plate 12.2) of the stomach. Lesions
also develop in the glandular mucosa, and in adult
horses most of these are found in the antrum (Plate
12.3). Lesions affecting the pylorus are typically
thought of as a problem unique to foals, but with
increased use of 3 m endoscopes, pyloric ulceration and
fbrosis has been found in adult horses (Plate 12.4).
Duodenal ulcers appear to be very uncommon in adult
horses.
In lieu of an endoscopic examination, the veterinar
ian will need to rely on clinical signs and response to
treatment that suppresses gastric acidit to make a
diagnosis of gastric ulceration. With simple gastric ulcer
disease, clinical signs should subside within 1-2 days.
For example, if a horse's appetite is poor because of
ulcers, treatment to suppress acid will result in improved
appetite within 24-48 hours. If abdominal discomfort is
caused by ulcers, this should resolve within 24 hours of
beginning treatment. With gastric emptying disorders
or duodenal ulceration, response to treatment may be
less satisfactory. Also, because the signs of gastric ulcers
are vague, one may incorrectly perceive a response to
treatment and neglect the true diagnosis.
When a horse is evaluated for a condition for which
gastric ulceration is a possible cause, the veterinarian
should obtain a minimum database consisting of a com
plete blood count (CBC) , serum chemistry profile, and
preferably a urine analysis. Gastric ulceration in itself
will not cause changes in any blood parameter in adult
horses, with the exception of severe pyloric ulceration
with fibrosis and restricted gastric outflow in which
there may be anemia and mild hypoproteinemia. If
abdominal discomfort is a clinical problem, a rectal
examination should be done. Peritoneal fluid analysis
and abdominal ultrasonography should be considered
in cases of colic in which gastric ulceration is a possible
diagnosis. Fecal occult blood will not be an indicator of
gastric bleeding in horses because the large intestinal
microflora will have excessively digested heme pigment
rendering the fecal occult blood test ineffective.
TREATMENT
The primary principle of treating gastroduodenal
ulcers in horses is to reduce gastric acidity; this provides
symptomatic relief and creates an environment that is
conducive to ulcer healing. Natural processes that pro
mote ulcer healing are initiated within hours of peptic
injury, and individual ulcers can heal without treat
ment. However, in an acidic environment, new ulcers
can form, and in trials examining the effect of the
proton pump inhibitor omeprazole, acid suppression
always resulted in markedly superior ulcer healing com
pared to vehicle or sham treatment. Therefore, in a
horse that has clinical signs referable to gastric ulcera
tion, treatment is recommended.
Treatments that reduce gastric acidity include
antacids, histamine type-2 receptor antagonists (H2
antagonists), and the proton pump inhibitors.
Antacids, such as magnesium oxide and aluminum
hydroxide, neutralize existing gastric acid but only for a
brief time (30-120 min). Antacids can provide sympto
matic relief, but must be given in large volumes every
2-4 hours to facilitate ulcer healing. The H2 antagonists
block hydrochloric acid secretion by gastric parietal
cells by competitively inhibiting the histamine tpe-2
receptor on parietal cells. The effect of the H2 antago-
DISEASES OF THE STOMACH 12
nists is dependent on plasma levels and at recom
mended doses gastric acidity is reduced for 1-8 hours.
There is considerable variability between horses in the
magnitude and duration of effect of H2 antagonists.
The drugs cimetidine and ranitidine have been used
most extensively in foals and horses, and both drugs
have poor bioavailability 20%) after oral administra
tion. Reducing the dose of an H2 antagonist, even by
one-third, from its recommended dosage can render
the drug completely ineffective in suppressing gastric
acidity in many horses.
The proton pump inhibitors omeprazole and lanso
prazole irreversibly bind to the parietal cell H+-K+
ATPase (proton pump) that secretes hydrochloric
acid. At recommended doses omeprazole can block
hydrochloric acid secretion for 24 hours in horses.
Omeprazole, both in the enteric-coated granule for
mulation available for human use and in a new paste
formulation for horses, has been shown to be highly
effective in promoting gastric ulcer healing in horses.
In several trials, ulcer healing in omeprazole-treated
horses was substantially superior to healing in con
trols. Importantly, in one set of trials, ulcer healing
occurred in more than 77 per cent of omeprazole
treated horses that remained in race training, and
this has not been noted in horses treated with H2
antagonists.
Sucralfate, the major components of which are
sucrose octasulfate (SOS) and aluminum hydroxide,
can facilitate healing of gastric and duodenal ulcers in
humans. Clinical experience suggests sucralfate can
promote healing of lesions in the gastric glandular
mucosa of horses. Sucralfate binds to gastric glandular
mucosa and enhances mucus production, mucosal
prostaglandin synthesis, and mucosal blood flow.
Sucralfate can be administered concurrently with an H2
antagonist. Concurrent administration may reduce H2
antagonist absorption by 10 per cent, but this has not
appeared to affect efcacy in horses. Importantly,
sucralfate can substantially interfere with the absorp
tion of other drugs, particularly fluoroquinolones, and
thus its use with other medications should be deter
mined on a case-by-case basis.
Aluminum hydroxide has been shown to enhance
gastric mucosal nitric oxide, and this should promote
mucosal blood flow. Misoprostol is a prostaglandin El
analog that may promote healing of gastric glandular
mucosal lesions by increasing mucosal blood flow.
Misoprostol can cause inappetance, diarrhea, and
abdominal discomfort, and for these reasons it is not
used routinely to treat gastric ulcers. However miso
prostol has been used together with other medications
to treat severe gastric glandular mucosal ulcers in a
small number of foals and horses with apparent success.
243
12 COLIC
The treatments that enhance mucosal resistance to
peptic injury and appear to facilitate healing are only
appropriate for the gastric glandular mucosa. Squamous
mucosal lesions can occur while a horse is being treated
with sucralfate. If an endoscopic examination has not
been performed, treatments such as sucralfate should
always be accompanied by acid-suppressive therapy.
In some horses, ulceration will affect the pylorus and
gastric emptying will be impaired. Often, severe squa
mous mucosal ulceration will accompany impaired gas
tric emptying. Treatment with an acid-suppressive drug
may result in improved clinical signs, but gastric ulcera
tion will persist or worsen. Treatment to improve gastric
emptying will usually result in improved clinical signs
and facilitate ulcer healing. Bethanecol has been shown
experimentally and clinically to enhance gastric empty
ing and facilitate ulcer healing. Chronic administration
of bethanecol may be required and appears to be safe.
Cholinergic signs (salivation, diarrhea, abdominal dis
comfort) are rare at the recommended dosages.
The duration of treatment required for ulcers will
vary depending on the severity of lesions and the man
agement of the horse. Gastric erosions are more super
fcial than ulcers (erosions can cause signifcant clinical
signs!) and thus will heal more quickly. Deep ulcers may
require weeks to heal because granulation of the ulcer
bed followed by epithelial contracture is necessary for
complete healing. Time required for healing also will
be dependent on the magnitude and duration of acid
suppression. Because of its unique mode of action,
omeprazole can suppress gastric acidity for 24 hours,
and in a study examining the enteric-coated granule
formulation of omeprazole considerable healing of the
gastric squamous epithelium was apparent within 47
days of starting treatment. If there is delayed gastric
emptying (pyloric or duodenal stricture, etc.) a longer
duration of treatment may be required.
PREVENTION
Prevention of gastric ulcers can be very challenging.
Some horses appear to develop ulcers more readily
than others, and these horses are likely to have recur
rence after successful treatment. The medically ideal
preventive measure is to take a horse out of work and
turn it out onto pasture. In many cases this is neither
desirable nor possible. Feeding management can be
modifed to promote more continuous roughage
consumption and less concentrate consumption. In
one study, alfalfa hay appeared to ofer some gastric
protection compared to brome grass hay. Nutritional
management to prevent gastric ulcers is incompletely
understood at this time.
244
Drug (size)
Antacid
MaaloxTC
Mylanta double strength
Ha antagonist
Cimetidine (800 mg tablets)
(150 mg/ml)
Ranitidine (1 SO, 300 mg
tablets)
(25 mg/ml)
Proton pump inhibitor
Omeprazole (20 mg capsules
of enteric coated granules)
Omeprazole (paste
formulation)
Mucosal protectant
Sucralfate (1 9 tablets)
Misoprostol (200 Ig tablets)
Motility modifier
Bethanecol (5.15 mg/ml)
Bethanecol (50 mg tablets)
Recommended
dosage
240 ml (8 oz),
q
. 4 h
24 ml (8 oz),
q
. 2 h
25 mg/kg p.o.,
q
. 6 h
7 mg/kg Lv.,
q. 6- h
7 mg/kg p.o.,
q
. 8 h
1.5 mg/kg i.v.,
q
. 8 h
1 mgkg p.o.,
once daily
4 mg/kg p.o.,
once daily
10-20 mg/kg p.o.,
q. 8 h
1.5 Ig/kg p.o.,
q
. 812 h up to
2.5 lg/kg p.o.,
q
.8h
0.02 mg/kg s.c.,
q. 6- h
0.35 mg/kg p.o.,
q.8h
Antacids are not effective in preventing gastric
ulcers, particularly in race horses. In a feed deprivation
model, ranitidine prevented ulcer formation, but clini
cal experience with race horses suggests that ranitidine
is not effective in treating or preventing gastric ulcers in
race horses that remain in training. Omeprazole, in a
new paste formulation, was found to prevent formation
of gastric ulcers in horses in intensive race training at a
dosage of 2 mg/kg, once daily. This is an impressive
accomplishment for the compound, but may not be
practical on a widespread basis.
DISEASES OF THE STOMACH 1 2
Endoscopic
examination
Squamous
lesions
Glandular
lesions Treatment recommendation
No ? ? omeprazole paste, 4 glkg p.o., once daily for weeks, or
ranitidine, 7 mg/kg p.o., q. 8 h for 4 weeks, or
cimetidine, 25 mgfkg p.o., q. 6 h for 4 weeks
Yes Yes No omeprazole paste, 4 mg/kg p.o., once daily for 2-3 weeks, or
ranitidine, 7 mg/kg p.o., q. 8 h for 3- weeks, or
cimetidine, 25 mg/kg p.o., q. 6 h for 3- weeks
Repeat endoscopy afer treatment
Yes No Yes sucralfate, 10-20 mglkg p.o., q. 8 h for 2- weeks
Repeat endoscopy after treatment
Yes Yes Yes omeprazole paste, 4 mg/g, once daily for 2-3 weeks, or
ranitidine, 7 mglkg p.o., q. 8 h for 3 weeks, or
cimetidine, 25 mg/g p.o., q. 6 h for 3 weeks, and
sucralfate, 10-20 mglkg p.o., q. 8 h for 2- weeks
Repeat endoscopy after treatment
Gastric impaction
Gastric impaction can occur as a primary condition, but
often it is diagnosed at surgery as a fnding secondary to
other disturbances in the intestinal tract. In some cases
there may be predisposing causes, such as ulceration or
fibrosis at the pylorus, whereas in other cases gastric
impaction may occur spontaneously. Gastric impaction
can proceed to rupture.
ETIOPATHOGENESIS
Factors that predispose to gastric impaction include
ingestion of certain feed stuffs, including beet pulp,
bran, straw, wheat, and barley - beet pulp and bran
can become desiccated within the stomach and may
not become rehydrated by water or gastric
secretions
dental disorders - roughage may be incompletely
masticated
keding a horse that has signs of colic - there may
be poor gastric empting associated with
generalized decreased gastrointestinal motility.
The clinical signs of gastric impaction are those associ
ated with abdominal discomfort. If the signs are mild
and resolve spontaneously or with analgesics, owners
are often inclined to feed the horse, worsening the
impaction. Most stomach impactions are diagnosed
at surgery, presumably because they become so large
that the degree of pain warrants surgery. A stomach
impaction may be suspected during an examination for
colic if it is diffcult to pass a nasogastric tube into the
stomach. With gastric distention, the gastroesophageal
junction can become distorted, making it difcult to
pass a nasogastric tube. If poorly macerated or digested
feed material is recovered from the nasogastric tube
when the horse has not eaten for several hours, a gastric
impaction may be suspected. On rectal examination,
the spleen may be displaced caudally and medially,
although this fnding is not specifc for gastric
impaction or dilation.
Endoscopy may be helpful in the diagnosis,
although simply identifing a stomach full of ingesta is
not diagnostic for an impaction, and it is diffcult to
assess distention by endoscopy. Radiography may be
useful in some cases, when the impacted stomach will
be noted to displace the diaphragm cranially (Figure
12.l).
245
1 2 COLIC
Figure 12.1 Radiograph of the caudal thorax and cranial
abdomen of a horse that presented with colic. The stom
ach is full of a radio-opaque material and there is accumu
lation of gas. Gastric lavage recovered desiccated bran,
which had been fed to the horse as a putative laxative
after the horse had been mildly injured after falling from
a jump on a cross-country course. The horse had fallen on
its sternum, note that the diaphragm appears irregular
cranially
TREATMENT
If gastric impaction is suspected, the horse should be
transferred, with a nasogastric tube in place, to a facility
at which surgery can be performed if necessary.
Medical treatment can include gastric lavage to remove
as much ingested material as possible. This may need to
be done repeatedly. Instillation of 100-200 ml of 8%
dioctyl sodium sulfosuccinate (DSS) may facilitate
hydration of desiccated ingesta. Treatment with anal
gesics and intravenous fluids should also be done, as
needed, although it is doubtful that intravenous fluid
administration will substantially increase the hydration
of desiccated gastric contents. Gastric motility stimu
lants should be avoided if the extent of the impaction is
not known, because of a possibilit of inducing gastric
rupture. We have treated gastric impactions that were
diagnosed at surgery with bethanecol, 0.02 mg/kg, S.c.,
q. 8 h, with no adverse effects.
Surgical treatment can include direct infusion of
balanced polyionic fluids into the impaction through
the stomach wall. The stomach is massaged to break
down the impaction and facilitate movement of fluid
into the ingesta. Alternatively, fluid may be infused via a
246
nasogastric tube, followed by massage of the stomach.
Postoperatively, the horse should be held off feed for
48-72 hours. A gastroscopic examination is indicated,
both to document resolution of the impaction and to
determine whether there is an underlying disorder in
the stomach.
Gastric dilation
ETIOPATHOGENESIS
Dilation of the stomach with fluid or gas usually
results from another intestinal disturbance. Normally,
a small amount of duodenal contents, consisting of
gastric efluent, bile, and pancreatic secretions,
refluxes back into the stomach. If there is excessive
intestinal secretion or intestinal obstruction, a large
volume of fluid can move from the duodenum into
the stomach. It is possible for fluid to spontaneously
reflux from the stomach into the esophagus, but with
distention, the gastroesophageal junction is distorted
such that it is tightly closed. This promotes progressive
gastric distention as fluid continues to move into the
stomach from the duodenum.
Primary gastric dilation may occur if a horse eats
highly fermentable material, generating a large volume
of gas. This is dissimilar to frothy bloat in ruminants, in
which a stable gas/fluid froth develops in the rumen as
a result of plant/rumen microbial interactions. Gas also
may accumulate secondary to generalized impaired
gastrointestinal motility from a variety of disorders.
Normally, excessive gas in the stomach exits either via
the small intestine or it can be belched. If gastric dis
tention is excessive, the normal release mechanisms
may be impaired and the gas will continue to accumu
late.
The clinical signs are the same as those for gastric
impaction, although the onset may be more acute and
the signs more severe. Affected horses are often tachy
pneic because of compression of the thorax by the dis
tended stomach. Diagnosis of primary gastric dilation
can be presumed if passage of a nasogastric tube
releases a large volume of gas, relieving the colic
episode. If a large volume of fluid is retrieved, gastric
dilation may have been resolved, but the underlying
cause of enterogastric reflux will need to be deter
mined.
TREATMENT
Treatment is removal of excessive fluid or gas via a
nasogastric tube, or at surgery via needle aspiration. A
underlying reason for the gastric dilation should be
determined and treated appropriately. Because the
cause of gastric dilation in horses is dissimilar to frothy
bloat in ruminants, treatments designed for frothy bloat
are not indicated for gastric dilation in horses. Also,
products designed to treat 'stomach gas' in humans,
such as simethecone, are not indicated for horses with
gastric distention.
Gastric rupture
Gastric rupture occurs as a sequel to gastric distention
from ingesta, fluid, or gas. The adult equine stomach can
hold up to 20-25 liters when maximally distended. With
distention, gastric rupture can occur from simple
excessive distention, but also the integrity of the wall of
the stomach may become compromised because of
decreased blood flow. Distention of the small intestine
has been demonstrated to signifcantly reduce mural
hlood flow, and it is likely this occurs in the stomach with
distention. In some cases, it has appeared that rupture
occurred as a result of an infarction of a portion of the
stomach wall, without apparent substantial distention.
Gastric perforation from ulceration happens rarely in
adult horses. Because of extensive contamination of the
peritoneal cavity with stomach contents, treatment is not
possible and humane destruction of the horse is required.
Gastric squamous cell
carcinoma
INTRODUCTION
Squamous cell carcinoma affects the esophageal and
gastric squamous mucosa. The neoplasm is uncommon
and by the time clinical disease associated with squa
mous cell carcinoma is recognized treatment is rarely
possible.
ETIOPATHOGENESIS
Neoplastic cells originate in the squamous epithelial
mucosa of the esophagus or stomach. In humans there
DISEASES OF THE STOMACH 1 2
are dietary, genetic, and environmental factors that
may contribute to esophageal cancer, but because
esophageal and gastric neoplasias are so uncommon in
horses contributing factors are not known. The rate of
growth and aggressiveness of alimentary squamous cell
carcinoma in horses is variable. In some horses tumors
remain localized within the stomach, whereas in other
horses tumors may extend through the stomach wall
and spread to other abdominal viscera or metastasize to
other locations in the body.
CLINICAL SIGNS
Typical signs associated with, but not diagnostic for,
squamous cell carcinoma include
chronic weight loss
poor appetite
abdominal discomfort
lethargy.
Ascites or edema may occur in some cases. If the
esophagus is involved, dysphagia or ptyalism will be the
predominant signs. Involvement of the stomach with
squamous cell carcinoma at the cardia may also result in
dysphagia, while involvement at other sites in the stom
ach may result in signs of obstruction to outflow (colic)
and/ or weight loss. In some cases tachypnea will be a
prominent sign, either because of metastasis to the
thorax or pressure on the diaphragm from an enlarged
tumor.
DIAGNOSIS
Neoplasia is one of a number of potential conditions to
consider when presented with a horse with chronic
weight loss (see Chapter 18), recurrent colic (see
Chapter 17), and/or chronic diarrhea (see Chapter
21). The diagnostic evaluation should consist of a com
plete physical examination including rectal examina
tion, routine blood work (CBC, serum chemistry
panel), urinalysis, and peritoneal fluid analysis.
Endoscopy (Plate 12.5), ultrasonography, laparoscopy,
and laparotomy can be used to further evaluate the
patient.
Many horses with squamous cell carcinoma will have
anemia, leukocytosis, and hyperfbrinogenemia. Some
will have hypoproteinemia due to bowel inflammation
and protein exudation, whereas other cases will have
hyperglobulinemia.
Peritoneal fluid will vary from normal, if the tumor is
confned within the stomach, to an exudate if the tumor
has spread. Neoplastic cells from a primary gastric
247
1 2 COLIC
squamous cell carcinoma occasionally will be observed
in a sample of peritoneal fluid, and will be large, poorly
differentiated epithelial cells with a bluish, ground
glass-appearing cytoplasm (Wright's stain).
If gastric squamous cell carcinoma is suspected,
cytology of aspirated stomach contents may reveal
large, poorly differentiated squamous carcinoma cells.
Endoscopy can be useful, particularly in diagnosing
esophageal or gastric squamous cell carcinoma. A
biopsy will usually be diagnostic, even on the small
tissue specimen that can be obtained through an
endoscope. Ultrasonography can be used to determine
whether there is excessive abdominal fluid, to possibly
identif a mass, and to detect any abnormalities within
the parenchyma of the liver or spleen (occasionally,
gastric squamous cell carcinoma will metastasize to the
spleen).
Successful treatment of esophageal or gastric squa
mous cell carcinoma has not been reported in horses.
If small, localized tumors are found, surgical excision
or endoscopic laser ablation may be attempted.
Intralesional injection of cisplatin can be successful
for cutaneous squamous cell carcinoma and,
although not reported for the treatment of gastric
squamous cell carcinoma, could be done through an
endoscope.
248
BIBLIOGRAPHY
Gastric ulceration in the adult
Andrews F M,Jenkins C, Frazier D, BlackfordJ (1992) The
effect of oral omeprazole on basal and pentagastrin
stimulated gastric secretion in young female horses. Equine
Vet.]. supp!. 13:80-3.
Hojgaard L, Mertz N A, Rune SJ (1996) Peptic ulcer
pathophysiology: acid, bicarbonate, and mucosal function.
Scand.]. Gastroenterol. supp!. 21:10-15.
McCarthy D M (1990) Sucralfate. N Engl.]. Med.
325:1017-25.
Murray MJ (1992) A comparative review of the
aetiopathogenesis and treatment of peptic ulcer. Equine
Vet.] supp!. 13:63-74.
Murray M J (1997) Suppression of gastric acidity in horses.
] Am. Vet. Med. Assoc. 211:37-41.
Murray M J, Haven M L, Eichorn E S, et al. (1997) The effects
of omeprazole on healing of naturally-occurring gastric
ulcers in Thoroughbred race horses. Equine Vet.]
29:425-9.
Squamous cell carcinoma
Campbell-Beggs C L, Kiper M L, MacAllister C, Henry G,
RoszelJ F (1993) Use of esophagoscopy in the diagnosis of
esophageal squamous cell carcinoma in a horse.]. Am. Vet.
Med. Assoc. 202:617-18.
McKenzie E C, MillsJ N, BoltonJ R (1997) Gastric squamous
cell carcinoma in three horses. Aust. Vet.] 75:480-3.
Olsen S N (1992) Squamous cell carcinoma of the equine
stomach: a report of fve cases. VetRec. 131:170-3.
Tenant B, Keirn D R, White K K et al. (1982) Six cases of
squamous cell carcinoma of the stomach of the horse.
Equine Vet. J 14:238.
15
Diseases of the large colon that can
result in colic
Impactions
RR Hanson
INTRODUCTION
The large colon, with distinct motility patterns coordi-
nated by a myoelectrical pacemaker at the pelvic flex-
ure has distinct non-rhythmic haustral movements and
stronger well-defined rhythmic retropulsive and propul-
sive contractions to move ingesta along the gastro-
intestinal tract. These complex functions require the
coordination of motility patterns to facilitate digestion
as the large colon serves as the primary site for water
resorption and microbial fermentation of carbohy-
drates to produce volatile fatty acids. Abnormal rhyth-
mic contractions of the large colon result in partial or
complete simple intestinal obstruction and often
develop at sites of narrowed lumenal diameters just
orad to the pelvic flexure or the transverse colon.
The pathogenesis of colonic impaction likely
involves dysfunctions of the myoelectrical pacemaker at
the pelvic flexure. Dissociation of the normal sequences
and dysfunctions of motility patterns are theorized to
result in abnormal transit and fluid resorption, predis-
posing the horse to functional abnormalities such as
colonic impaction. In horses with colonic impaction,
the digesta appears to be retainedjust orad to the pelvic
flexure, involving a long segment of the ventral colon
and does not simply involve the pelvic flexure alone.
The digesta is usually firm and contains fibrous feed
material, although sand and gravel can cause a similar
obstructive lesion.
EPIDEMIOLOGY
In one hospital study of large colon impactions in
horses, the median age of the horses was 7.1 years
(range 1-29 years), with most of the affected horses
being female (63%). No breed predisposition was iden-
tified. In another study impaction of the large colon
accounted for 13.4 per cent of 1100 colic cases referred
to a university hospital and for 9 per cent of cases in a
normal farm population.
ETIOLOGY
Large colon impactions may be promoted by
reduced water intake
poor quality feed
limited exercise
participation in show activities
foreign material in the hay
poor dentition
foaling
colonic motility alterations.
Cold weather may reduce water consumption or freeze
the water source entirely. Horses provided with water
from tanks, buckets, and automatic waterers are signifi-
cantly associated with an increased risk of colonic
impaction, compared to horses that drink from natural
water sources. Winter pasture may force consumption
of poor quality roughage. Changes in management con-
ditions, such as sudden restriction of exercise because
of musculoskeletal injury, stable change, a move from
pasture to barn housing, shipping, and systemic disease,
may also predispose to colonic impaction. In one study,
279
15 COLIC
more than 50 per cent of the horses examined for
colonic impaction had an increase in the duration of
stall confinement in the 2 weeks preceding the colic
episode.
Amitraz, a formamidine acaricide that interrupts
colon motility, has been used to experimentally induce
colonic impactions in horses. Its mechanism of action
may involve the mediation of intrinsic enteric neuro-
modulators that affect the coordination of myoelectri-
cal activity from the pacemaker regions in the large
intestine and, possibly, fluid and ion transport.
Cockspur hawthorn fruit ingestion and naturally occur-
ring impaction colic could have similar pathogenesis.
The incidence of colonic impaction is influenced by
soil composition and geographic region. Foreign mate-
rials, such as nylon cord stripped from rubber feeders,
fence pieces, or bailing twine left in hay, combine with
fecal material to form impactions that usually require
surgical correction. Impactions may accompany other
conditions such as non-strangulating displacement of
the colon.
CLINICAL SIGNS
Horses with colonic impaction usually have intermittent
clinical signs of abdominal pain with a gradual onset,
and are often partially or completely anorexic. Some
horses show acute signs of abdominal pain while others
have mild or no signs of abdominal pain. Mild signs,
such as rolling the lip, playing with water, looking at the
abdomen, stamping the feet, or backing up, may occur
while the obstruction is incomplete. Abdominal pain
becomes more severe as the mass becomes larger,
heavier, the colon muscles spasm, or obstruction causes
gas distension.
The heart and respiratory rates are initially normal,
but increase with progressive signs of abdominal pain
and endotoxemia. The mucous membranes are pink or
blanched, while the capillary refill time is usually nor-
mal. These indicators of perfusion remain normal until
the bowel deteriorates releasing endotoxin. Most
horses with a large colon impaction have decreased or
absent intestinal borborygmi on auscultation, but
normal or increased intestinal sounds can occur.
Transrectal palpation is useful for diagnosing
colonic impactions. In most cases, a large doughy-to-
firm mass is palpable in the area of the pelvic flexure or
the left ventral colon while transverse colon impactions
or more isolated sand impactions are not usually palpa-
ble. Gas distention of the ascending colon or cecum is
common. Nasogastric reflux may be obtained if the
impaction is located in the right dorsal colon and is
impinging on the duodenum.
280
CLINICAL PATHOLOGY
Clinical laboratory values are initially normal but
abnormalities may develop over time. An increase in
the systemic packed cell volume and total protein con-
centration may be evidence of mild dehydration in
some horses. If the dehydration goes undetected or is
untreated, the impaction may progress or become
refractory to medical treatment. An increase in the
peritoneal fluid total protein concentration and low
systemic white blood cell counts can occur if the
impaction causes devitalization of the colonic mucosa.
Therefore peritoneal fluid total protein concentration,
as an indicator of colonic wall degeneration, should be
followed closely in horses that are treated medically for
long periods.
DIAGNOSIS
The diagnosis is usually made on transrectal examina-
tion where an ingesta-filled pelvic flexure is palpated in
most cases. Alternatively either the impaction is out of
reach or gas distention of the colon and cecum prevents
transrectal palpation of the impaction. Horses with a
history of recent increase in stall confinement and mild
intermittent signs of abdominal pain should be
examined closely for large colon impaction.
TREATMENT
Colonic impaction is a common cause of colic and often
responds to medical management directed at
restricting diet
controlling pain
maintaining hydration
reducing muscular intestinal spasms in the area
around the impaction
hydrating the colon ingesta to allow passage offeces
and establish normal colon function.
Feed should be withheld until transrectal palpation
findings are normal and there is evidence of intestinal
transit. Very small amounts of hay or grazing may stim-
ulate bowel motility, but further addition of ingesta to
the impaction should be avoided. Most horses respond
to sedation, analgesia, and intragastric administration
of laxatives. Aggressive medical treatment for 3-5 days
may be necessary, although softening and movement of
the impacted mass should be felt sooner than this dur-
ing transrectal palpation.
Intravenous fluid therapy may be necessary in horses
that do not respond to initial treatment with analgesics
DISEASES OF THE LARGE COLONTHAT CAN RESULT IN COLIC 15
and laxatives. Most horses with colon impactions are
slightly dehydrated. Aggressive oral administration of
fluids (4-8 liters per nasogastric tube every 6 h) is help-
ful but labor is intensive. Intravenous fluid administra-
tion may increase the water content of the impacted
ingesta in horses by altering the passive forces that gov-
ern transmucosal fluid transport, raising the capillary
hydrostatic pressure, and decreasing plasma protein
concentration. Intravenous fluids should be adminis-
tered at 2-5 l/h or three to five times the recommended
maintenance rate through a large bore (l4-gauge x 12.5
cm) jugular catheter. Over-hydration can be monitored
by assessment of the horse's packed cell volume and
total protein concentration which should be main-
tained at 5.0-5.5 g/dl. In a study of 147 horses hospital-
ized with colon impactions that did not respond to
initial farm treatment, the mean duration of medical
treatment with xylazine, flunixin meglumine, and intra-
venous fluids was 2 days (range 1-8 days). Eighty per
cent of these hospitalized horses responded to medical
treatment.
While the ingesta is being hydrated to soften the
impaction, it is often necessary to relieve visceral pain.
Relief of visceral pain helps moderate the effects of
adrenergic inhibition of intestinal motility. Xylazine
hydrochloride, an alpha, adrenoceptor agonist, modu-
lates the release of norepinephrine and directly inhibits
neuronal firing, causing sedation, analgesia, bradycar-
dia, and visceral pain relief. Xylazine may cause a cessa-
tion of intralumenal pressure changes and reduce
jejunal and colonic motility for up to 2 hours. This
effect may be beneficial in relieving intestinal spasms
around the impaction mass. The latter may, in turn,
allow fluid absorption and passage of gas. Treatment
with xylazine (0.2-0.4 mg/kg i.v, or i.m.) can be
repeated. Butorphanol (0.01-0.02 mg/kg i.v. or i.m.) or
detomidine (0.01-0.02 mg/kg i.v, or i.m.) is also bene-
ficial for similar reasons, but close monitoring of the
horse is essential to ensure that the analgesics are not
masking signs indicative of the need for abdominal
surgery.
Flunixin meglumine reduces prostaglandin-medi-
ated visceral pain during intestinal obstruction or dis-
tention and reduces the systemically evident effects of
endotoxin without inhibiting intestinal motility.
Because flunixin meglumine can mask clinical signs of
endotoxemia and intestinal strangulation obstruction,
careful monitoring of the horse after the drug is admin-
istered is essential. The recommended low dose
(0.25-0.5 mg i.v. q. 6 h), however, enables treatment of
horses with colonic impactions without masking impor-
tant clinical signs that are indicative of a failing cardio-
vascular system. Treatment with flunixin meglumine
should be continued after correction of the colonic
impaction until horses are eating regularly and intesti-
nal transit has returned to normal.
Laxatives, cathartics, and emollients are given to
alter fecal consistency and to promote transit of ingesta
in horses with colonic impactions. The stomach should
first be siphoned and if more than 2 liters of fluid is
obtained, small-intestinal ileus or delayed gastric emp-
tying is likely. Instillation of additional fluid should be
done cautiously, if at all, in these patients.
Mineral oil (2-4 liters p.o.) is a common, non-toxic
emollient that acts to lubricate the ingesta and coat the
intestine to facilitate the passage of ingesta through the
intestine. Mineral oil can be used as a fluid marker to
determine the speed ofintestinal transit. The oil usually
appears in the feces 12-24 hours after nasogastric
administration. However, since the oil may pass around
a firm mass of ingesta, the presence of oil in the feces
does not always signify resolution of the impaction.
Mineral oil should not be given to horses with nasogas-
tric reflux or if strangulation obstruction is suspected.
Bulk cathartics (bran, psyllium mucilloid, methyl-
cellulose) cause hydrophilic retention of colonic water;
this retention stimulates intestinal transit. Psyllium
mucilloid is non-toxic and may be used for 1-3 weeks if
necessary. Bulk laxatives, however, can take days to
begin working and should not be relied on for all
colonic impactions. Magnesium sulfate (l g/kg p.o. q.
24 h for 2-3 days) is a saline cathartic that acts largely
via an osmotic effect to increase fecal water content.
Magnesium sulfate may cause more gastrointestinal
distention and thus stimulate a greater gastrocolic
response than other laxatives. It can affect systemic
hydration and should be administered only to well-
hydrated horses, or preferably in combination with
intravenous or intragastric fluid administration.
Magnesium sulfate is associated with the risk of devel-
opment of diarrhea, and effective safe dosing of this
product is debated.
Dioctyl sodium sulfosuccinate (DSS) is an anionic
surfactant that stimulates fluid secretion from the
intestinal mucosa and reduces surface tension allowing
water to penetrate impacted material. The usual dose is
10-20 mg/kg of a 5% solution mixed with 2-8 liters of
water given via a nasogastric tube. Toxicity occurs at
doses ranging from 0.5-1.0 g/kg. Repeated dosing of
DSS may cause mucosal irritation, dehydration, and
toxicity. For these reasons, DSS should be used no more
than twice during a 48 hour interval. DSS can be used
alone but is frequently mixed with mineral oil. It is not
known whether mixing the two compounds is advanta-
geous or detrimental to the treatment of impactions.
The use of prokinetic drugs to treat horses with
colonic impactions is controversial. Intestinal contrac-
tions induced by neostigmine, which acts on the large
281
DISEASES OFTHELARGE COLON THAT CAN RESULT IN COLIC 15
Ingested sand may cause foreign body enteritis or it may
accumulate in the ventral colon, pelvic flexure, and/or
transverse colon causing impaction. The inflammatory
response, associated with accumulation of a sufficient
volume of sand, can result in colonic rupture.
EPIDEMIOLOGY
Sandy environments such as those found in Florida,
California, and Arizona, are common locations for
horses with this disorder. Young horses and horses with
indiscriminate eating habits occasionally consume sand
voluntarily, making them more prone to developing the
condition.
ETIOLOGY
Horses stabled in a sandy environment and fed from
the ground appear to be at risk. Offending sand is gen-
erally fine beach sand or clay, but gravel or bluestone
shale can occasionally be found. Sand is also found in
the feces of clinically normal horses.
CLINICAL SIGNS
Clinical signs range from mild to severe pain and nor-
mal to deteriorating cardiovascular status. Most horses
with clinical signs of sand colic are older than I year of
age. Sand impactions of the ventral colon may be
substantial (25 kg); however, they are often difficult to
palpate transrectally because of their location in the
cranial portion of the gastrointestinal tract and hence
may be out of reach. Cecal and large colon gas disten-
tion is inevitably present. Horses with this condition
may have small amounts of diarrhea and clinical signs
of endotoxemia.
Abdominal paracentesis should be conducted cau-
tiously since the sand-impacted colon can be inadver-
tently lacerated. An abdominal paracentesis should not
be performed in horses that clearly require surgical
intervention or in horses in which the procedure may
be of low diagnostic value. Sand present within an
enterocentesis is pathognomonic for the disease.
Auscultation of the ventral abdomen of horses with
sand impaction may reveal 'friction-like' rub sounds
compatible with sand borborygmi.
DIAGNOSIS
Sand impaction can be difficult to differentiate from
feed impaction, and tests for fecal sand do not correlate
well with the presence of sand in the colon. History or
observation of sand in the feces only indicates exposure
to sand. Sand may be detected during transrectal palpa-
tion or it may be found on the rectal sleeve. Dissolving
feces in water and observing for sand in the bottom of a
bucket or on a rectal sleeve may provide evidence of the
possibility of sand impaction. Although small amounts
of sand are frequently found in feces and do not neces-
sarily reflect sand impaction, large amounts of sand are
more indicative of sand accumulation. Comparison of
the normal discharge of sand in normal horses from
that of the diseased horse may assist in the diagnosis of
sand impaction.
Ultrasonographic examination of the ventral
abdomen along the midline caudal to the xiphoid
process with a 5-MHz ultrasound probe may reveal the
presence of sand in the ventral colon, appearing as
floating starburst spicules as the sand is suspended in
the ingesta. Abdominal radiographs, if available, can
aid in the diagnosis of sand impaction.
TREATMENT
Psyllium mucilloid (0.5-1.0 g/kg p.o. q. 6-24 h) has
been implemented to lubricate the gastrointestinal
tract and assist in the movement of sand out of the
body. A solution of psyllium mucilloid and 4-8 liters of
water must be pumped rapidly into the stomach via a
nasogastric tube before the psyllium mucilloid forms a
gel. The treatment is maintained for several days to a
week depending on the severity of the case. The feces
should be monitored for the rate of expulsion of the
sand. Psyllium, however, had no effect in hastening
sand evacuation from the large intestine in a controlled
experimental study in six normal ponies. Further
studies on the effect of psyllium in the diseased colon
are needed.
Intravenous fluid therapy may be necessary in horses
that do not respond to initial treatment with analgesics
and laxatives. Intravenous fluid administration may
increase the water content of the impacted ingesta in
horses by raising the capillary hydrostatic pressure and
decreasing plasma protein concentration. The recom-
mended administration rate for intravenous fluids is
2-5 l/h or 2.5 times the maintenance rate.
Horses with sand impactions often do not respond
to medical treatment alone and require surgical inter-
vention. In many horses surgical exploration must be
undertaken without an accurate pre-operative diagno-
sis; because of abdominal pain, large colon distention,
and deteriorating cardiovascular signs. Sand impactions
most commonly involve the pelvic flexure and/or the
right dorsal colon. A colotomy along the pelvic flexure
283
15 COLIC
allows for tap water lavage and drainage of colonic
ingesta and sand. To prevent abdominal contamination
it is important to deliver most of the large colons from
the abdomen before beginning the colotomy. It can be
difficult to remove excessive sand present in the right
dorsal colon through a pelvic flexure colotomy.
However, the use of a large bore nasogastric tube
inserted into the colon lumen from the pelvic flexure
colotomy to the right dorsal colon can aid in the
removal of the sand. Copious lavage of the right dorsal
colon, with manipulation of the colon to suspend the
sand in the lavage, is needed to adequately dissipate the
sand. Judicious technique eliminates the need for mul-
tiple colotomies which prolong the surgery and compli-
cate the recovery period. Septic peritonitis can be
minimized by using aseptic technique, atraumatic han-
dling of the intestines, and appropriate supportive care.
Sand impaction of the pelvic flexure may act as a
pendulum, predisposing the horse to volvulus of the
colon. Cranial displacement of the pelvic flexure and
non-strangulating and strangulating colonic displace-
ments are associated with this condition. Postoperative
complications include the recurrence of the disease,
septic peritonitis, diarrhea, and incisional dehiscence.
OUTCOME
The mortality rate is higher with sand impactions than
ingesta impactions of the large colon. In recent studies,
44 of 48, and 30 of 40 horses with sand impaction were
discharged from the hospital, and at 12 months follow-
ing discharge 38 of 48 horses and 24 of 40 horses were
alive. If the sand can be completely removed from the
colon without unnecessary contamination, the progno-
sis for horses with sand impaction is no worse than for
those horses with ingesta impaction.
PREVENTION
Minimizing exposure to sand is important in preventing
recurrence. This requires that horses eat their feed
raised off the ground (in a manger or in buckets) or
separated from sand (on rubber mats or in feeding
troughs). Hay containing sand should not be a part of
the horses' diet. Feeding hay free of sand prior to pas-
ture turnout lessens the horse's desire for aggressive
grazing and their exposure to sand.
Intermittent administration of psyllium mucilloid
for several weeks may be indicated to remove accumu-
lated sand. Longer term administration often results in
an increased rate of degradation of the mucilloid by
colonic microbes and a decrease in the laxative effect.
284
Administration of a moist bran mash containing 450 g
of psyllium mucilloid, once a week, is a useful prophy-
lactic measure to prevent the occurrence of sand
impaction colic in horses exposed to sand.
Displacement of the large
colon
RP Hackett
INTRODUCTION
The large colon in an adult horse is approximately
3.4 meters in length (11% of the total gastrointestinal
tract) and has a capacity of approximately 81 liters
(38% of the total). The large size and mobility due to
sparse mesenteric attachments of the ascending colon
predispose it to a variety of displacements. The colon is
looped back upon itself at the pelvic flexure and then
folded at the sternal and diaphragmatic flexures to fit
within the abdomen (Figure 15.1). Colonic mobility is
restricted only by attachments to the cecum and trans-
verse colon. Colon diameter varies from approximately
Figure 15.1 Normal equine cecum and colon viewed with
the horse in dorsal recumbency. The dorsal colon isshaded
dark gray
Figure 15.4 Entrapment of the colon over the renosplenic
ligament isrelieved by using the arm and back of the hand
to displace the spleen axially and ventrally while the palm
and grouped fingers are used to sweep the colon dorsally
then laterally
sweep the colon dorsally then laterally (Figure 15.4).
Once entrapment is relieved, the left colon is exterior-
ized for direct inspection. Vascular injury to the
entrapped segment is rare. Pelvic flexure enterotomy
for relief of secondary impaction is rarely necessary.
The survival rate following surgical treatment of LDDC
is extremely favorable (92% in one study).
Relief of LDDC via standing flank celiotomy may be
attempted under certain circumstances. Left flank
celiotomy should be employed only in those cases in
which a diagnosis of LDDC is absolutely certain as diag-
nosis or treatment of other forms of displacement or
other causes of obstruction can rarely be accomplished
by this approach. The standing approach is ordinarily
used in patients who are poor candidates for general
anesthesia either because of advanced pregnancy or
physical size (large draft horses), or because of eco-
nomic constraints. Following phenylephrine infusion as
described above, a left flank celiotomy (gridding the
internal oblique and transversus abdominus muscles) is
performed. The left colon is needle decompressed of
gas as much as possible, lifted over the splenic base and
manipulated ventrally to a position axial to the splenic
apex. This procedure is markedly facilitated by phenyle-
phrine-induced splenic contraction. Normally, the apex
of the spleen is near or even across the ventral midline,
well beyond the reach of most surgeons.
Horses successfully treated for LDDC are at
increased risk of one or more recurrences. The actual
prevalence of recurrence is unknown, rates from 2-22
per cent are reported. These recurrence rates do not
justify additional surgical procedures to prevent recur-
Kidney
Edge of
L- incision
Figure 15.5 Schema representing obliteration of the reno-
splenic space. Five or six sutures are placed in a cruciate
pattern between the capsule of the dorsal aspect of the
spleen and the renosplenic ligament
renee following a single episode of LDDC however such
procedures should be considered in horses experienc-
ing a second bout of LDDC. Obliteration of the reno-
splenic space via a left flank celiotomy or an 18th or
17th rib resection approach has been successfully used
to prevent recurrences of LDDC. This procedure does
not prevent other types of colonic displacement, as
compared to colopexy or elective colonic resection, but
may be more satisfactory in horses used for athletic pur-
poses. For this procedure, the horse is anesthetized in
right lateral recumbency. The authors prefer an 18th
rib resection (see Chapter 10). Once the abdomen is
entered, the renosplenic entrapment is relieved without
the use of phenylephrine. An assistant's hand is then used
to lift the body of the spleen so that the tension between
the dorsal aspect of the spleen and the renosplenic liga-
ment is reduced. Five or six sutures of #2 polypropylene
material are placed in a cruciate pattern between the
capsule of the dorsal aspect of the spleen and the reno-
splenic ligament (Figure 15.5). The space is closed from
ventral to dorsal with the aim of eliminating the space at
its most dorsal and caudal aspect such that the colon
cannot be entrapped in this location.
Right dorsal displacement of the colon (RODe)
Displacement of the large colon between the cecum
and right body wall (Figure 15.6) results in signs of
colic due to obstruction. The cause of this problem is
unknown. Most commonly the pelvic flexure and left
colon pass in a craniocaudad direction between
cecum and right body wall. These structures then turn
287
15 COLIC
Figure 15.6 Right dorsal displacement of the colon viewed
with the horse in dorsal recumbency
craniad placing the pelvic flexure in the cranial
abdomen. Less commonly, the pelvic flexure and left
colon pass caudocraniad between the cecum and body
wall, also with the pelvic flexure in the cranial
abdomen. Either type may be accompanied by
180-360 volvulus of the large colon. As with LDDC,
the clinical signs of right dorsal displacement of the
colon are extremely variable ranging from a pro-
longed course of very mild colic to an acute episode of
severe pain and tympany. Rectal examination reveals
large colon segments with variable tympany passing
from between the cecum and right body wall, behind
the cecum and then forward. The pelvic flexure ordi-
narily is not palpable. In cases accompanied by 270
or greater volvulus, edema in the wall of the colon
may be evident by rectal palpation. This finding may
be confirmed ultrasonographically.
The treatment of RDDC is surgical. Exploratory
celiotomy under general anesthesia confirms the diag-
nosis. In most cases, the colon can be repositioned
after gas decompression of the colon and cecum. In
cases accompanied by severe impaction, evacuation of
the colon by pelvic flexure enterotomy and lavage may
be necessary to safely manipulate and reposition the
colon. Resection of the colon will be necessary in the
rare case in which colonic viability has been compro-
mised by an accompanying volvulus. The prognosis for
RDDC unaccompanied by colonic ischemia is very
good.
288
Large colon volvulus

RP Hackett
INTRODUCTION
Volvulus of the large colon can occur anywhere along
the length of the colon. In a report of 109 cases of volvu-
lus,47 (43%) occurred at the level of the cecocolic fold
and ampulla coli, 33 (30%) in the left colon or sternal
and diaphragmatic flexures, 26 (24%) across the cecal
base and transverse colon and 3 (3%) affected the right
colons cranial to the cecocolic fold (Figures 15.7, 15.8,
15.9). The twist is typically clockwise as viewed from
behind the horse. Clinical signs associated with volvulus
of the colon are largely attributed to the degree of
volvulus as outlined in Table 15.1.
Based on the clinical signs, the degree of volvulus
appears to remain relatively static over time in many
horses. In some horses however, the twist appears to
progress with time (hours or even days) resulting in
intensification of clinical signs. Depending on the
degree of vascular obstruction, large colon volvulus is
defined as either non-strangulated colon volvulus or
strangulated colon volvulus.
Figure 15.7 Schematic representation of the equine large
colon viewed with the horse in dorsal recumbency, show-
ing the regions most commonly involved by torsions. 1 =
area at the base of the colon where torsions may origi-
nate; the cecumisoften involved in these cases. 2 = area of
right colon where torsion may originate and does not
involve the cecum
DISEASES OFTHE LARGE COLON THAT CAN RESULT IN COLIC 15
NON-STRANGULATED COLON
VOLVULUS
Degree of
colon rotation
90-270
>360
Effect
None
Obstruction of lumen to
passageof ingesta (partial
obstruction)
Obstruction of lumen to
passageof ingesta and gas
(complete obstruction). Mild to
moderate venous compromise
resulting in colonic edema
Strangulation obstruction of
colon
Figure 15.8 Volvulus of the large colon involving the ster-
nal and diaphragmatic flexures, viewed with the horse in
dorsal recumbency
Figure 15.9Volvulus of the large colon and cecum, viewed
with the horse in dorsal recumbency
The clinical presentation of horses with colon volvulus
varies widely as might be predicted from the above dis-
cussion. Horses with a twist of 90-270 resemble those
with impaction colic. Abdominal pain is usually mild
and readily controlled with analgesic medications. Vital
signs, hydration, and peripheral perfusion remain
within normal limits. There is no evidence of abdomi-
nal tympany and borborygmi are normal. Signs may
remain static for days or progress over 12-24 hours.
Rectal examination in many horses is normal early in
the course of disease. Mild tympany of the left colon or
cecum may be evident in some horses. Feed impaction
of the left colon may be evident in some cases of longer
duration. This can be distinguished from pelvic flexure
impaction because the left dorsal colon is empty in a
pelvic flexure impaction and filled with ingesta in a left
colon torsion.
Clinical signs in horses with a 270-360 colonic
volvulus are more intense, largely because of progres-
sive gaseous distention of intestinal segments proximal
to the twist. Signs of pain are more profound and are
more refractory to analgesic drugs. Moderate tachy-
cardia (60-90 bpm) is common. Indicators of hydration
and peripheral perfusion are relatively normal.
Abdominal distention is evident. The occasional horse
will have nasogastric reflux. Rectal examination typi-
cally reveals moderate to marked tympany of the left
ventral and dorsal colon. Colonic bands may be ori-
ented transversely if the pelvic flexure has shifted to the
right of midline as the left colon distends. Tympany of
289
15 COLIC
the cecal base is typical. Mild edema of the colonic wall
may be evident on rectal palpation or ultrasonographic
evaluation.
Treatment
The treatment for non-strangulated colon volvulus is
surgical. Progressive colon tympany and signs of severe
abdominal pain clearly indicate the need for surgery in
horses with 270-360 colonic volvulus. In horses with a
90-270 volvulus, clinical signs are relatively mild and
resemble those of colonic impaction. Such horses are
often treated conservatively for many days. However,
unless the presence of a treatable impaction is con-
firmed by rectal examination, mild colonic volvulus
should be strongly considered in horses with signs of
mild to moderate abdominal pain that persists for
longer than 24-48 hours. Surgical exploration is
warranted in such horses.
The surgical approach for management of non-
strangulated colon volvulus is ventral midline
celiotomy. Following needle decompression of the
cecum and large colon, the colon is exteriorized for
inspection. Volvulus affecting the left colons or of the
right colons between the cecocolic fold and sternal and
diaphragmatic flexures are apparent by direct inspec-
tion. Volvulus across the cecal base and right dorsal
colon-transverse colon junction is evident only by pal-
pation. The right dorsal colon is followed distally to
determine a twisting where its ampulla funnels down at
Figure 15.10 Evacuation of the colon via pelvic flexure
enterotomy in a horse with large colon volvulus
290
its junction with the transverse colon. Horses with long-
standing non-strangulated colon volvulus will often
have secondary impaction of colonic segments with
firm ingesta. Manipulation of the heavy, distended
colon in these horses is difficult and bears a substantial
risk of colonic rupture. Evacuation of the colon via
pelvic flexure enterotomy and lavage is prudent before
correction of the volvulus is attempted (Figure 15.10).
Correction of volvulus involving the left colons and of
the right colons between the cecocolic fold and sternal
and diaphragmatic flexures is readily accomplished
under direct visualization. Relief of volvulus across the
cecal base and right dorsal colon-transverse colonjunc-
tion is accomplished blindly. While an assistant holds
the right dorsal colon as vertically as possible, the sur-
geon places a hand on both sides of the ampulla of the
right dorsal colon just dorsal to the twist. The colon is
rotated in an anticlockwise direction to correct the
typical clockwise volvulus (Figure 15.11) Correction of
volvulus is confirmed by ability to trace the cecocolic
fold from the cecum onto the right ventral colon and by
palpation of a normal junction between the right dorsal
colon and transverse colon. If the latter procedure is
not performed, a 360 volvulus across the cecal base
and transverse colon may be left in place.
Figure 15.11 Schematic drawing showing manipulation
required to correct the typical large colon volvulus. While
an assistant holds the right dorsal colon as vertically as
possible, the surgeon places a hand on both sides of the
ampulla of the right dorsal colon just dorsal to the twist.
The colon is rotated in an anticlockwise direction to
correct the typical clockwise volvulus
OTHER NON-STRANGULATING COLON
DISPLACEMENTS
In addition to those described above, other non-stran-
gulating abnormalities of colon placement have been
described. The most common of these is retroflexion
(cranial displacement) of the left colon such that the
pelvic flexure is located in the cranial abdomen. Also,
herniation of the colon through large internal defects
(diaphragm, gastrosplenic ligament, mesocolon) may
be considered a form of non-strangulating displace-
ment. Clinical signs associated with such problems
mimic those of the more common forms of non-
strangulated colonic displacement.
STRANGULATION OF THE LARGE COLON
Strangulation of the large colon is typically due to volvu-
lus, although strangulation due to internal hernia may
occur rarely. Volvulus of the large colon exceeding 360
0
results in peracute abdominal crisis that is rapidly life
threatening. This degree of volvulus leads not only to
complete colonic obstruction but also to endotoxemia
and sequestration of blood in the strangulated segment.
Strangulated colonic volvulus constituted 6.5 per cent
of surgical colics at university referral centers. The fatal-
ity rate for these cases was 72 per cent. Periparturient
mares are particularly at risk. Volvulus of the colon is
typically hemorrhagic rather than ischemic - venous
drainage of the colon is compromised but arterial
inflow is relatively intact. This results in engorgement of
the colonic wall with fluid and blood. Mild signs of
colic, perhaps due to non-strangulated displacement,
occasionally precede signs of severe colic by hours or
even a couple of days. In most cases however, there is an
acute onset of severe abdominal pain and rapidly pro-
gressive abdominal distention. Signs of cardiovascular
compromise including tachycardia, dehydration, pro-
longed capillary refill time, and deterioration of
mucous membrane color rapidly ensue. Rectal exami-
nation commonly reveals marked colonic tympany,
thickening of the colonic wall and, often, orientation of
colonic tenia transversely across the abdomen.
Strangulated large colon volvulus is a surgical emer-
gency and the prognosis is substantially enhanced by
early surgical intervention. The approach to surgical
treatment generally parallels that for non-strangulated
colonic volvulus as described above. The colon is
decompressed, evacuated through pelvic flexure
enterotomy and the volvulus is corrected. In addition,
the surgeon's assessment of colonic viability will influ-
ence case management. Although a number of tech-
niques for objective s s ~ s m n t of equine intestinal
viability have been described (fluorescein perfusion,
surface oximetry, intralumenal pressure, frozen sec-
tions histopathology, Doppler blood flow), these proce-
dures are not in common practice, however, because of
either lack of availability or concern about their relia-
bility. Subjective parameters (color, thickness, motility,
mesenteric pulse) are ordinarily employed but are of
limited accuracy. Often colonic damage is overesti-
mated because of the color changes and edema typical
of hemorrhagic strangulation. Gross appearance of the
colonic mucosa at the enterotomy site is a more reliable
subjective criterion, as postoperative outcome is largely
dependent on mucosal survival. Intact reddish mucosa
suggests a favorable prognosis. A black mucosa, particu-
larly when coupled with blood staining of colonic con-
tent, indicates loss of mucosal integrity and a poor
prognosis. Cases with a clearly viable colon are man-
aged as for non-strangulated volvulus (described
above). Resection of colon that is non-viable or of ques-
tionable viability is indicated in cases with volvulus of
the right colon at the level of the cecocolic fold or in
the left colon or sternal and diaphragmatic flexures.
Resection is not possible in cases with non-viable colon
due to volvulus across the cecal base and transverse
colon, and euthanasia is indicated. Cases with unre-
sectable colon of marginal viability should be given a
chance through recovery from anesthesia and intensive
therapy for endotoxic shock. In these cases, pharmaco-
logical intervention is often used to combat postopera-
tive hypoperfusion of the large colon - medications
such as heparin are used to decrease vascular resistance
by minimizing intravascular coagulation in low flow
states and dimethylsulfoxide (DMSO) to reduce
endothelial swelling. In addition these animals become
progressively hypoproteinemic associated with the
mucosal necrosis and plasma therapy is needed. These
cases may respond over several days as surviving cells
in the mucosal crypts regenerate to restore mucosal
integrity and prevent endotoxin absorption and colonic
water loss. Such cases are candidates for a 'second look'
surgery if not responding positively after 2-3 days.
PREVENTION OF COLON VOLVULUS
The recurrence rate for colonic volvulus in non-brood
mares is approximately 5 per cent, brood mares are at a
higher risk. Mares that have had one volvulus have a 15
per cent chance of a second one. Mares that have expe-
rienced a volvulus two or more times have an 80 per cent
chance of another recurrence. Such mares are candi-
dates for colopexy by fixation of the lateral band of the
left ventral colon to the cranial ventral abdominal wall
about 15 ern to the left of the ventral midline. A contin-
291
15 COLIC
Ventral
midlineincision
I
Figure 15.12 Colopexy. The lateral taenia of the ventral
colon (line of x's) is sutured to the ventral abdominal wall
about 15cmto the left of the ventral midline (dotted line).
Inset: relationship of fixation to ventral midline incision.
uous or simple cruciate pattern of no. 2 non-absorbable
monofilament suture is ordinarily used. This procedure
has been described through a ventral midline celiotomy
or via laparoscopy and prevents recurrence of volvulus
(and other types of colonic displacement) (Figure
15.12). Complications of this procedure are not uncom-
mon and include colic, incisional hernia, catastrophic
rupture of the left colon, and enterocutaneous fistula.
The safety of this procedure in horses used for athletic
endeavors has not been established. Some surgeons pre-
fer elective resection of the large colon near the termi-
nation of the cecocolic fold to prevent recurrence of
volvulus and other displacements in athletes. Weight
loss and soft stools are early complications of this pro-
cedure but normal nutritional performance can be
expected to return within 5-6 months.
292
Primary colonic tympany
II
RP Hackett
Primary colonic tympany is a functional colic - there is
no mechanical bowel obstruction yet there is distention
of the large colon, or the large colon and cecum, with
gas. Tympany is often idiopathic but may arise from
either overproduction of gas or, more commonly, from
delayed evacuation of normal gas. Gas overproduction
has been associated with a rapid dietary change to
highly fermentable concentrates or forages. Delayed
evacuation of gas may be associated with a number of
factors leading to diminution of colonic motility
parasitism
lack of exercise
colitis
peritonitis
stressors such as transport or surgery
parasympatholytic agents including drugs, toxins,
or plants.
The severity of clinical signs is proportional to the
degree of colonic distention. Cases with mild to moder-
ate colonic distention exhibit signs of mild to moderate
abdominal pain and corresponding tachycardia. Such
cases may spontaneously resolve or be successfully man-
aged medically through treatment with analgesics and
with mineral oil to promote colonic evacuation and
reduce gas production.
In severe cases of colonic tympany, signs include
marked colic pain, abdominal distention, tachycardia,
tachypnea, and cardiovascular deterioration. Marked
distention of the colon is evident on rectal and ultra-
sonographic examination but colonic mural thickness
is normal and there is no evidence of displacement or
lumenal obstruction. Peritoneal fluid is typically unre-
markable. The veterinarian must be aware that such
horses cannot be readily distinguished from those
affected with colonic tympanyt0.05 263472n
preparation and local anesthesia, the catheter is placed
into the distended viscus. Suction accelerates the
decompression but is not essential. After decompres-
sion, as the catheter is withdrawn, a broad spectrum
antibiotic solution such as neomycin or gentamicin
should be injected through the catheter to reduce like-
lihood of local peritonitis or cellulitis along the needle
track in the body wall. If clinical signs of tympany
return, it is likely that tympany is secondary rather than
primary and surgical exploration is indicated.
Non-strangulating infarction
of the large colon
RP Hackett
Infarction of the large colon in the absence of
mechanical strangulation has most commonly been
associated with arteritis of the cranial mesenteric artery
due to Strongylus vulgaris infection. The failure of post-
mortem examinations to demonstrate emboli has led
to the speculation that vasoactive mediators released
from the arteritis at the mesenteric root lead to spasm
of colonic vessels and, in some cases, to colonic infarc-
tion. The higher prevalence of non-strangulating
infarction in younger horses as well as the observation
that it appears to be less common with modern
anthelmintic therapy, support the role of Strongylus vul-
garis in its etiology. Clinical signs associated with
verminous arteries vary markedly. Intestinal ischemia
results in signs of abdominal pain and motility dis-
ruption (increased or decreased) and may account
for many self-limiting, undiagnosed cases of colic.
Infarction leads to bowel necrosis and accompanying
clinical signs due to ileus and endotoxemia. Horses
with acute colonic infarction demonstrate moderate to
severe signs of pain, progressive abdominal distention,
tachycardia, and reduced peripheral perfusion. The
colon is often fluid or gas distended on rectal examina-
tion. Peritoneal fluid early in the course of the disease
may be normal or slightly hypoproteinemic. In
advanced cases, the fluid may be serosanguinous with
high white blood cell counts. A serious or deteriorat-
ing clinical status, particularly when accompanied by
abnormal peritoneal fluid findings, should lead to
exploratory celiotomy. Surgical resection of infarcted
bowel, if possible, is warranted.
Ischemia and infarction of bowel has also been
associated with disseminated intravascular coagulation
and other systemic coagulation disorders, shock, and
embolization of thrombi from remote sites.
Enterolithiasis
AT Fischer, Jr
INTRODUCTION
Enterolithiasis in horses has been reported over the last
several hundred years. Recent articles have suggested
that the frequency of enterolithiasis is increasing in
California. In the same article, the authors reported
that horses with enteroliths represented 15 per cent of
the horses presenting with colic, and 27 per cent of
the horses that underwent exploratory laparotomy.
Enteroliths are composed of ammonium magnesium
phosphate which is supplied both by the digestive
processes of intestinal bacteria and by feeds. The
enteroliths typically form around a central nidus.
DIAGNOSIS
Enterolithiasis is most common in Arabian horses,
Arabian crosses, and Quarter horses but it has been
documented in all breeds. In the author's population of
horses with enteroliths between 40-50 per cent are
Arabian or Arabian crosses. If Quarter horses are added
to this group, 63 per cent of the cases are included.
There does not appear to be any sex bias but stallions
are reportedly underrepresented. Enteroliths are rare
in horses less than 3 years of age but have been reported
as early as I year old. Enteroliths are most commonly
diagnosed in middle-aged horses. In our hospital popu-
lation, any horse presenting with colic over 4 years of
age undergoes abdominal radiography unless other
factors dictate that this is unnecessary.
Horses presenting with enterolithiasis may have
recurrent colic
an attitude change
scant, mucus-covered feces, no feces, or soft pasty
feces.
In some horses with enteroliths, the first change noted
by the owner is that the horse goes offits feed and stops
eating. Some of the horses with enterolithiasis will have
passed enteroliths or the owners will have found
enteroliths on the pasture. Most horses with enteroliths
will present with a moderate amount of discomfort but
some will be severely uncomfortable because of either
total obstruction of the bowel and gas accumulation
oral to the obstruction, or deterioration of the bowel
wall due to pressure necrosis.
Physical examination of horses with enteroliths is
rarely diagnostic. Most of the clinical signs shown by
293
DISEASES OFTHE LARGE COLONTHAT CAN RESULT IN COLIC 15
The small colon should be examined to make sure that
there are no enteroliths present. If enteroliths are pre-
sent in the small colon, they are most commonly
removed without moving them inside the bowel as they
are usually firmly lodged. If the part of the small colon
where the enterolith is lodged is easily exteriorized, the
procedure for removal is the same as for removal from
the right dorsal colon. If the enterolith is lodged in the
proximal small colon and cannot be exteriorized, an
antimesenteric teniotomy may be performed to mobi-
lize the enterolith and bring it to an area more
amenable to removal. Alternatively, the enterolith may
be removed from where it is lodged after appropriate
isolation of the bowel with laparotomy sponges and
drapes. The bowel should be stabilized with stay sutures
and an assistant's hand placed underneath the
enterolith. An antimesenteric enterotomy is performed
and the enterolith is removed. The bowel is closed in
two layers and lavaged. It is helpful to remove the horse
from the ventilator and allow spontaneous non-assisted
respiration when removing enteroliths from the proxi-
mal small colon as the diaphragmatic excursions can
contribute to tearing of the bowel and contamination of
the abdomen. The closure of the abdomen is routine.
POSTOPERATIVE CARE
The care for a horse following surgical removal of an
enterolith is identical to any other abdominal surgery.
Acid-base and electrolyte status should be assessed reg-
ularly until the horse is back on full feed and supple-
mented appropriately with intravenous fluids. Early
return to feeding is believed to be beneficial. As soon as
the horse shows an interest in food, a limited amount of
grazing is allowed. Gradual return to full feed occurs
over the first few days after surgery. Mineral oil is
administered by nasogastric intubation if there are
large amounts of ingesta left in place at surgery. Dietary
restriction usually only occurs when there is compro-
mise to the intestinal wall that is unable to be removed
at surgery. Horses with compromised intestinal wall are
fed small amounts of feed for the first 5-7 days after
surgery while allowing the bowel wall to heal. Repeated
doses of mineral oil are administered during this time.
The horses are exercised by walking in hand for the first
30 days after surgery. Turnout into a small pen occurs
for 30-60 days after surgery.
COMPLICATIONS
Intra-operative complications include rupture of the
intestinal tract while trying to manipulate the enterolith.
Ifthis occurs deep in the abdominal incision, gross con-
tamination of the abdominal cavity occurs and the horse
is euthanized. Serosal tearing occurring during manip-
ulation of the intestine may be repaired by direct sutur-
ing or placing omental grafts over the area. Frequently
when serosal tearing occurs, the bowel is friable and
attempts to suture the tear only result in more tears. The
serosal tears may be left unsutured if necessary. Some
horses may have extensive pressure necrosis where
enteroliths have been lodged in the proximal small
colon. The affected bowel is usually discolored black and
green. If the section of bowel can be removed by either
a wedge resection or full-thickness section, then this is
done. More commonly, the damaged bowel is within the
abdominal cavity and cannot be exteriorized. In these
cases, as long as the bowel is thickened and has not
started to thin with total necrosis, the bowel may be left
in place and the horse fed small quantities for the first
week after surgery. Most of these horses will have an
uncomplicated recovery with no future complications.
The most frequent postoperative complications
include colitis and incisional drainage. Colitis is man-
aged by returning to early feeding, attention to fluid
and electrolyte abnormalities, and administration of
plasma (see Chapter 11). If the horse is not eating,
force feeding of a complete ration is helpful to ensure
that enough nutrients are available to the horse and
subjectively this seems to decrease the duration of the
colitis. Incisional drainage is best managed by daily
cleaning of the discharge from the incision with dilute
betadine or chlorhexidine in saline. Peritonitis is
another reported complication but is decreasing in
frequency because of earlier surgical intervention and
earlier recognition of the presence of enteroliths by
abdominal radiography.
PREVENTION AND RECURRENCE
Abdominal surgery for the removal of enteroliths is very
rewarding with high success rates. Future research
should examine the role of diet and genetic predisposi-
tion toward the development of enteroliths. Recurrence
has been reported in 7.7 per cent of horses operated on
for enterolithiasis and these horses were less likely to
have undergone dietary modification. A genetic predis-
position is possible because breed predilections have
been reported. In a recent study 9.6 per cent of horses
with enteroliths had siblings that were also affected. The
effect ofenvironment must be examined in these horses.
Dietary management should include feeding a minimal
amount of alfalfa hay or pellets, and increasing the per-
centage of grass-type hay in the diet. Alfalfa has been
considered a contributing factor because ofits high mag-
295
15 COLIC
nesium content and protein content contributing to the
liberation of ammonium during digestion by the intesti-
nal microflora. Wheat bran has been similarly impli-
cated because of its high phosphorus and' magnesium
content. Alkaline pH in the colon of horses undergoing
surgery for enteroliths has been demonstrated and this
was felt to be a factor in the formation of enteroliths.
Studies involving the implanting of enteroliths into
fistulated ponies with acidic pH in their colons demon-
strated that the enteroliths would dissolve. This obser-
vation led to administration of apple cider vinegar (one
cup given orally twice daily over hay or grain) in an
attempt to lower colonic pH. Personal observation has
not validated this therapy as most of the horses that are
operated on at the author's hospital have been given
apple cider vinegar for several years prior to surgery. The
magnesium content of water might be contributory, but
Lloyd et at. (1987) calculated that water with a very high
magnesium content would supply only 10 per cent of the
magnesium in an alfalfa hay diet, making it a less impor-
tant concern in prevention of enteroliths.
Increased vigilance by veterinary surgeons for the
presence of enteroliths by routine abdominal radiogra-
phy of horses admitting with colic allows for earlier
surgical intervention with more successful outcomes.
Segmental eosinophilic
colitis
GB Edwards
INTRODUCTION
Segmental eosinophilic colitis is an uncommon disease
that results in a local obstructive lesion of the colon
wall. Affected segments of bowel show variable mucosal
necrosis, submucosal oedema, and eosinophil infiltra-
tion of the lamina propria and deeper layers of the
colon wall. No cause has been established although a
parasite-associated etiology is suspected.
CLINICAL SIGNS
Affected horses usually present with mild to moderate
intermittent colic. The pain is responsive temporarily to
analgesics, but recurs as the action of the analgesic
wears off. There may also be varying degrees of abdom-
inal distention for a few hours to several days. The heart
rate varies depending on the duration of disease, but is
usually in the range 36-75 (mean 52) bpm. Capillary
296
refill time and mucous membrane colour are normal
unless the horse has become dehydrated or is affected
by toxemia secondary to peritonitis.
RECTALEXAMINATION
Rectal examination typically reveals varying degrees of
large colon and cecal distention, and a relatively soft
impaction of the pelvic flexure and left ventral colon.
Mural edema may be evident in the pelvic flexure and
left dorsal colon, and in some cases the corresponding
mesocolon may also be edematous. This is sometimes
accompanied by a segmental, firm enlargement
(approximately 10 em diameter) of the left dorsal
colon.
ABDOMINOCENTESIS
Peritoneal fluid shows evidence of non-septic peritoni-
tis. It is usually turbid and yellowI orange colored. In a
few cases sanguinous peritoneal fluid is obtained. The
total nucleated cell count is elevated (10-250 x 10
9
/ 1)
and consists predominantly of neutrophils. The total
protein concentration is also elevated (> 30 gil).
SURGICAL FINDINGS AND TREATMENT
At surgery, cecal and small intestinal distention may be
present, this should be relieved prior to lifting the left
colon and part of the right colon from the abdominal
cavity. Serosal lesions are usually present in the left
dorsal colon just aboral to the pelvic flexure. These
changes vary from slight petechiation, to erythema, to a
discrete well-defined area of serosal necrosis. The
lesions are usually well demarcated. Occasionally
lesions may be found oral to the pelvic flexure, or there
may be multifocal lesions involving the left dorsal, left
ventral, and right ventral colons. The colonic contents
are usually relatively soft and can be removed via an
enterotomy in the left ventral colon without recourse to
lavage (which reduces the risk of peritoneal contamina-
tion). On the mucosal surface, the lesions are charac-
terized by edema and dark discoloration. In some cases
there may be areas of necrosis evident on the surface.
Treatment consists of removal of the impaction, and
surgical resection of the affected segment of colon. In
very mild cases where the lumenal occlusion is minimal,
resection of bowel may not be necessary, although there
is a risk of subsequent worsening of the disease postop-
eratively. In cases where the segment of abnormal colon
is short, a wedge resection may be performed with liga-
tion of segmental vessels but leaving the colic artery and
vein intact. When resection of longer lengths of left
dorsal colon is required, the colic vessels should be
double ligated and the compromised segment of bowel
transected at an oblique angle. Following resection, the
colon is repaired by end-to-end anastomosis. The defect
in the colonic mesentery should be closed with a simple
continuous suture pattern.
In horses in which the segment of compromised left
dorsal colon is too long to allow resection and end-to-
end anastomosis, and in horses with lesions affecting
both the left dorsal and left ventral colons, a partial
resection of both the ventral and dorsal colons should
be performed. Following double ligation of the colonic
vessels, a side-to-side anastomosis 15-18 em long is
created between the left dorsal and left ventral colons,
prior to resection of the affected bowel segment and
closure of the proximal ends with a double layer of
inverting sutures.
PROGNOSIS
In one review of 22 cases of segmental eosinophilic col-
itis, long-term follow-up information was available for
18 cases. Of these horses, 16 were alive and well, with no
history of colic, 3 months to 7 years following discharge
from the clinic. One horse in which resection of the
colon was not performed had recurrence of colic
symptoms.
BIBLIOGRAPHY
Impaction
Dabareiner R M (1998) Impaction of the ascending colon
and cecum. In Current Techniques in Equine Surgeryand
Lameness, N AWhite,J N Moore (eds). W B Saunders,
Dabareiner R M, White N A (1995) Large colon impaction in
horses: 147 cases (1985-1991).J Am. Vet. Med. Assoc.
206(5):679-85.
Freeman D E, Granger D N, Taylor A E (1992) Comparison
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water, dioctyl sodium sulfosuccinate, and magnesium
sulfate on fecal composition and output in clinically
normal horses. Am.J Vet. Res. 53(8):1347-53.
KaneeneJ B, Miller R, Ross W A, Gallagher K, MarteniukJ,
RookJ (1997) Risk factors with colic in the Michigan
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Roberts M C, Seawright A A (1983) Experimental studies of
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Ross M, Hanson R R (1992) Impaction of the Ventral Large
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Sellers A F, LoweJ E (1986) Review of large intestinal motility
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Sullins K E (1999) Diseases of the Large Colon. In Calahan
P T, Mayhew I G, Merritt A M, MooreJ N (eds): Equine
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Young R L, SnyderJ R, PascoeJ R, Olander HJ, Hinds D M
(1991) A comparison of three techniques for closure of
the pelvic flexure enterotomies in normal equine colon.
Vet. Surg. 20(3):185-9.
Sand impaction
Hammock P D, Freeman D E, Baker GJ (1998) Failure of
psyllium mucilloid to hasten evacuation of sand from the
equine large intestine. Vet. Surg. 27(6):547-54.
Ragle C A, Meagher D M, Lacroix C A, Honnas C M (1989)
Surgical treatment of sand colic. Results in 40 horses. Vet.
Surg.18(1):48-51
Ross M, Hanson R R (1992) Sand impaction of the large
colon. In Auer JA (ed.): Equine Surgery, W.B. Saunders,
Specht T E, Colahan P T (1988) Surgical treatment of sand
colic in equids: 48 cases (1978-1985).J Am. Vet. Med.
Assoc. 193(12):1560-4.
Young R L, SnyderJ R, PascoeJ R, Olander HJ, Hinds D M
(1991) A comparison of three techniques for closure of
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Surg.20(3):185-9.
Displacement of the large colon
Left dorsal displacement of the colon
Baird A N, Cohen N D, Taylor T S, WatkinsJ P, SchumacherJ
(1991) Renosplenic entrapment of the large colon in
horses: 57 cases (1983-1988).J Am. Vet. Med. Assoc.
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White N A, Lessard P (1986) Risk factors and clinical signs
associated with cases of equine colic. Proc. Am. Assoc.
Equine Pract. 32:637-44.
Santschi E M, Slone D EJr, Frank W M II (1993) Use of
ultrasound in horses for diagnosis of left dorsal
displacement of the large colon and monitoring its
nonsurgical correction. Vet. Surg. 22:281-4.
Sivula NJ (1991) Renosplenic entrapment of the large colon
in horses: 33 cases (1984-1989) J Am. Vet. Med. Assoc.
199:244-6.
Right dorsal displacement of the colon (RODe)
Hackett R P (1983) Nonstrangulated colonic displacement in
horses.J Am. Vet. Med. Assoc. 182:235-40.
Large colon volvulus
Barclay W P, FoernerJ J, Phillips T N (1980) Volvulus of the
large colon in the horse. J Am. Vet. Med. Assoc. 177:629-30
White N A, Lessard P (1986) Risk factors and clinical signs
associated with cases of equine colic. Proc. Am. Assoc.
Equine Pract. 32:637-44.
Fischer A T, Meagher D M (1986) Strangulating torsions of
the equine large colon. Compo Cont. Educ. Pract. Vet.
8S:25-30
Harrison I W (1988) Equine large intestinal volvulus. A review
of 124 cases. Vet. Surg. 17:77-81
297
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Hance S R, Embertson R M (1992) Colopexy in broodmares:
44 cases (1986-1990).J Am. Vet. Med. Assoc. 201:782-7
Enterolithiasis
Blue M G, Wittkopp R W (1981) Clinical and structural
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179(1) :79-82.
Blue M G (1979) Enteroliths in horses - a retrospective study
of 30 cases. Equine Vet.]. II (2) :76--84.
Fischer A T (1990) Enterolithiasis. In Current Practice of Equine
Surgery, N AWhite,] N Moore (eds).] P Lippincott,
Hassel D M, Langer D L, Snyder] R, Drake C M, Goodell
M L, Wyle A (1999) Evaluation of enterolithiasis in equids:
900 cases (1973-1996).]. Am. Vet. Med. Assoc.
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Hassel D M, Yarbrough T B (1998) A modified teniotomy
technique for facilitated removal of descending colon
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298
Hintz H F, Lowe] E, Livesay-Wilkenset al; (1988) Studies on
equine enterolithiasis. Proc. Am. Assoc. EquinePract. 34:53-9.
Lloyd K, Hintz H F, Wheat] D, Schryver H F (1987)
Enteroliths in horses. Cornell Vet. 77(2): 172-86.
Peloso] G, Coatney R W, Caron] P, Steficek B A (1992)
Obstructive enterolith in an l l-month-old miniature
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Yarbrough T B, Langer D L, Snyder] R, Gardner I A, O'Brien
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Vet.]. 32:86--93.
16
Diseases of the small colon and rectum
JSchumacher
Diseases of the small colon
ENTEROLITHS
Enteroliths, or intestinal calculi, are mineralized con-
cretions that develop in the large colon by concentric
deposition of salts around a central nucleus, usually a
small silicon stone or metal object. Enteroliths can
remain within the large intestine for long periods unas-
sociated with signs of clinical disease, and it is only when
they obstruct the lumen of the large or small colon that
the horse shows signs of abdominal pain.
Enteroliths are primarily composed of ammonium
magnesium phosphate crystals (struvite). Because
ammonia is constantly produced from microbial activity
within the large intestine, and phosphates are abundant
in common horse feeds, the concentration of magne-
sium, rather than ammonia or phosphate, in the feed
may influence the formation of enteroliths. Diets of
alfalfa hay containing a high concentration of magne-
sium have been incriminated in the formation of
enteroliths.
Epidemiology
The prevalence of enterolithiasis is high in the south-
western US, and university teaching hospitals in
California, Florida, and Indiana have twice the preva-
lence of enterolithiasis as other schools in the US. The
Arabian seems to be the breed most commonly affected
by enterolithiasis, and females of all breeds are more
likely than males to develop enteroliths. The reason for
the predisposition of females to the development of
enterolithiasis is unknown, but fluctuations in the con-
centration of prostaglandins in the serum associated
with the reproductive cycle may affect gastrointestinal
motility, thereby predisposing females to the formation
of enteroliths.
The time required for an enterolith to form is
unknown, but reports of enterolithiasis occurring in
horses younger than 4 years old are rare. Enterolithiasis
in an II-month-old miniature horse has been reported.
The mean reported age of horses requiring abdominal
surgery because of an obstructive enterolith is 10 years.
Clinical signs and diagnosis
Diagnosis of obstructing enterolithiasis is based on clin-
ical signs and physical examination. An obstructing
enterolith blocks the passage of feces but may allow pas-
sage of gas and intestinal lubricants, such as mineral oil.
An enterolith within the small colon typically causes
complete obstruction, and affected horses tend to show
signs of more severe abdominal pain than horses with
partial or intermittent obstruction of the transverse or
right dorsal colon. Palpation of an enterolith in the
small colon is usually possible only when it is lodged in
the rectum or distal portion of the small colon. An
enterolith in the proximal aspect of the small colon is
usually beyond the reach of the examiner, and small
colon distal to the enterolith is usually flaccid and diffi-
cult to identity. If the enterolith has lodged in the mid-
dle or distal portion of the small colon, loops of
gas-filled small colon may be recognized.
Diagnosis of enterolithiasis in horses showing clini-
cal signs of the disease can sometimes be confirmed by
radiography. Radiography is less helpful in the diagno-
sis of enterolithiasis of the small colon than it is for
diagnosis of enterolithiasis of the large colon (i.e.
299
16 COLIC
transverse colon), however, and the absence of radi-
ographic findings does not preclude the presence of
an enterolith.
Treatment
Treatment of horses suffering from obstruction of the
small colon by an enterolith is by removal of the
enterolith through a laparotomy (celiotomy). If possi-
ble, the enterolith should be manipulated a few cen-
timeters distally or proximally so that the enterotomy
can be made in a normal portion of intestine. Studies
show that longitudinal enterotomies made through the
antimesenteric tenia of the small colon are superior to
those made adjacent to the tenia, as determined by
maintenance of the diameter of the lumen, ease of clo-
sure, and minimal interruption of the blood supply.
Enterotomy performed through the antimesenteric
tenia results in less hemorrhage and less inflammation.
and sutured incisions through the tenia are stronger
than sutured incisions adjacent to the tenia at 96 hours.
Closure of the mucosa as a separate layer offers no
advantage or disadvantage in healing in normal horses.
Complications associated with enterotomies of the
small colon include leakage, visceral adhesions, and
stricture formation. Factors that may adversely affect
the outcome of surgery of the small colon in the horse
include the small colon's relatively poor blood supply,
its high concentration of collagenase, its high intralu-
menal concentration of bacteria (including large con-
centrations of anaerobic organisms), its muscular
activity; and the presence of particulate feces. The
mesocolon of the small colon is relatively short, making
exteriorization of the proximal and distal ends of the
small colon difficult or impossible. The risk of peri-
toneal contamination is high if enterotomy or resection
and anastomosis are necessary for those parts of the
small colon that are difficult to exteriorize.
An enterolith in the proximal end of the small colon
must often be repelled into the right dorsal colon and
then into the left dorsal colon for removal through an
enterotomy. An enterolith can be most easily and safely
dislodged and repelled proximally by retrograde infu-
sion of water into the small colon. To repel an
enterolith proximally, a stomach tube is inserted into
the rectum and passed into the small colon. The tube is
guided to the obstruction by the surgeon and. while the
small colon is occluded by holding it tightly to the tube,
water is infused into the intestine until the lumen
expands to a size large enough to allow the enterolith to
be dislodged proximally. The enterolith is then
repelled into the left dorsal colon where it can be
removed safely via enterotomy remote from the abdom-
inal cavity.
300
Prognosis
Prognosis for survival of horses undergoing surgery for
enterolithiasis is determined by the cardiovascular
health of the horse and the in tegrity of the affected area
of intestine. In one study, 58 per cent of 24 horses oper-
ated on for enterolithiasis survived, and in another
study of 34 horses treated surgically for enterolithiasis,
survival following surgery was 70.6 per cent. In another
report, over 85 per cent of horses operated on for
enterolithiasis survived.
Prevention of recurrence
To prevent enterolithiasis from reforming following
surgery, the feeding area should be elevated or free of
gravel, and the amount of alfalfa fed to the horse (and
the rest of the herd) should be decreased and replaced
by another type of hay. Colonic pH below 6.6 tends to
prevent the formation of enterolithiasis, and decreasing
the amount of hay and increasing the amount of grain
in the diet tends to decrease the pH of colonic contents.
Adding vinegar to the diet is another method of
decreasing colonic pH.
FOREIGN BODY OBSTRUCTION
Foreign materials involved in obstruction of the small
colon include nylon fibers from halters, hay nets, or
twine, cords from rubber material, synthetic fencing
material, disposable plastic sleeves, and tops of feed
sacks (Figure 16.1). The foreign material becomes
coated with mineral precipitate increasing its bulk. The
resulting masses are irregular. often containing projec-
tions that cause necrosis of the obstructed intestine.
The ingested foreign material may remain within the
Figure 16.1 Ingested plastic trash can liner occluding the
rectum and small colon
large colon for a considerable period of time before
passing into and obstructing the small colon.
Obstruction of the small colon caused by ingestion of
foreign material occurs generally in horses 3 years old
or less, probably because young horses are less discrim-
inate in their eating habits.
Obstruction of the small colon by a foreign body usually
results in a gradual onset of vague signs of anorexia,
dullness, and abdominal pain. If the obstruction is
located in the most distal part of the small colon, tenes-
mus may be observed. Systemic effects of the obstruc-
tion are minor initially, even in horses showing signs of
marked pain, and the hematocrit may remain
unchanged for many days. Affected horses remain unre-
sponsive to medical therapy. The obstruction may be
difficult to locate by palpation per rectum, owing to its
small size and tendency to lodge in the proximal por-
tion of the small colon. The obstruction is usually asso-
ciated with an impaction that extends into the large
colon.
Treatment
The obstruction must be removed before the small
colon surrounding it becomes necrotic. At surgery, the
obstruction should be manipulated a few centimeters
distally or proximally so that the enterotomy can be
made in normal intestine, but if the involved segment
cannot be exteriorized, the obstruction should be
repelled proximally by retrograde infusion of water into
the small colon and removed through an enterotomy at
the pelvic flexure of the large colon.
FECAL IMPACTION
Fecal impaction is the most common disorder of the
small colon. Ponies, American Miniature Horses, and
Arabians, especially female Arabians, appear to be
affected by fecal impaction of the small colon more fre-
quently than are other breeds, whereas the condition is
less common in Quarter horses. Impactions of the small
colon appear to be most common in aged horses and
yearling ponies.
Fecal impaction of the small colon may be related to
ingestion of bedding or poor-quality hay, poor denti-
tion, inadequate hydration, parasitic damage, or disor-
ders of intestinal motility. The small colon becomes
impacted most frequently during the fall and winter,
and this seasonal predilection may be related to inade-
quate water consumption or dietary changes. Old
horses may be predisposed to impaction of the small
DISEASES OFTHE SMALLCOLON AND RECTUM 16
colon because of deterioration in dentition and gas-
trointestinal function. Because of the narrowing of the
lumen of the large colon through the transverse colon
into the small colon, this area of the intestine may be
predisposed to impaction. Predilection for obstruction
by ingesta of the small colon may also result from
decreased moisture content of the ingesta in this loca-
tion.
Horses with fecal obstruction of the small colon initially
exhibit mild signs of colic. Deterioration in physical
condition progresses slowly and results from distension
of viscera with gas and fluid proximal to the impaction.
Deterioration progresses slowly because the location of
the small colon at the distal end of the intestinal tract
provides a large space for ingesta, gas, and fluid to accu-
mulate proximal to the obstruction.
Diagnosis of impaction of the small colon on the
basis of clinical signs and clinicopathologic data is fre-
quently difficult. Consistently observed clinical features
of affected horses are reduced production or absence of
feces and absent or reduced borborygmi. Abdominal
distension is often present, and nasogastric reflux can
be obtained occasionally. Although the heart rate is
usually high, clinicopathologic data are normal, this is
consistent with experimentally induced obstruction of
the small colon in horses. White blood cell count, con-
centration of electrolytes, hematocrit, and concentra-
tion of plasma total protein show little deviation from
normal.
Examination per rectum is often helpful in the diag-
nosis of fecal impaction of the small colon. One or
more loops of tubular, firm, digesta-filled intestine can
be identified during examination per rectum, and the
single, free tenia can often be identified on the colon,
confirming the segment of intestine involved.
Treatment
Objectives of medical treatment of horses with fecal
impaction of the small colon are to maintain hydration,
stimulate gastrointestinal motility, to soften the
impaction by the administration of osmotic laxatives or
lubricants, and to control pain. Intravenous administra-
tion of a balanced electrolyte solution is used to overhy-
drate the horse and to initiate fluid secretion into the
intestine to directly hydrate and soften the mass of
ingesta. Intestinal motility is stimulated by exercise,
fluid therapy, and replacement of potassium and cal-
cium. Frequent urination can be used to clinically assess
the response to overhydration.
Treatment of horses with fecal impaction of the
small colon by administration of an enema has been
301
DISEASES OF THE SMALL COLON AND RECTUM 16
Figure 16.4 Trichobezoar removed from the small colon
have an uneven, furrowed, velvet-textured surface. The
smooth surface of phytoconglobates and bezoars may
allow them to obstruct the lumen for relatively long
periods without causing severe damage to the mucosa.
Obstruction caused by ingestion of fibrous, non-
digestible material is seen most commonly in horses less
than 3 years old and in horses with poor dentition.
Treatment
Treatment of horses affected by fecaliths, phytoconglo-
bates, or bezoars is by surgical removal of the obstruct-
ing mass. If the obstructed segment of small colon
cannot be exteriorized, the mass should be repelled
into the large colon by retrograde infusion of water and
removed through an enterotomy at the pelvic flexure.
INTRAMURAL HEMATOMA
An intramural or submucosal hematoma is an uncom-
mon lesion of the small colon or rectum caused by hem-
orrhage between the mucosa and muscularis.
Hemorrhage occludes the intestinal lumen and dissects
along the intestine producing intestinal necrosis. The
condition occurs most commonly in old horses.
Histological examination of lesions reveals no evidence
ofthe cause, and the source of hemorrhage contributing
to the formation of mural hematoma is not evident dur-
ing gross or microscopic examination of resected colon.
The condition causes signs of abdominal pain, and
because the hematoma obstructs the lumen, examina-
tion per rectum of affected horses may reveal tympany
of the large colon. The rectum is usually devoid offeces,
but various amounts of clotted blood may be found.
Treatment of horses with the condition is by resec-
tion of the affected intestinal segment followed by an as-
tomosis of the proximal and distal segments of colon. At
surgery, the lesion is recognized as a dense, circum-
scribed mass attached to the wall of the small colon or
rectum. If the affected segment cannot be exteriorized
a colostomy may be necessary.
MESOCOLIC RUPTURE
Mesocolic rupture and subsequent segmental ischemic
necrosis of the small colon occur as a complication of
foaling and are the result of direct trauma caused by the
foal as it positions itself for delivery. During late preg-
nancy, the fetus is positioned ventrally, but during the
first stage of labor, the foal rotates into dorsal position
for delivery using vigorous reflex movements of its neck
and forelimbs. During these movements, the small
colon of the mare may become trapped between uterus
and dorsal body wall, causing the mesocolon to tense
and tear.
Mesocolic rupture can also result from type IV rectal
prolapse, a condition sometimes associated with partu-
rition. The vascular arcade of the mesocolon may
stretch and tear when more than 30 ern of the rectum
and small colon prolapses through the anus (see
Diseases of the rectum, Rectal prolapse).
Regardless of the cause of mesocolic rupture, infarc-
tion results, causing functional obstruction and pro-
gressive signs of colic. Segmental ischemic necrosis of
the small colon caused by disruption of the meso-
colonic vasculature should be considered when exam-
ining post-parturient mares that show signs of
abdominal pain, particularly when the cardiovascular
health of the horse deteriorates slowly and concentra-
tion of protein and the nucleated cell count in the peri-
toneal fluid increase. A consistent finding in affected
horses is failure to pass feces.
STRANGULATING LESIONS OF THE
SMALL COLON
Segments of the small colon may strangulate when they
become involved in a volvulus or intussusception, or
more commonly when entwined with a pedunculated
lipoma or the pedicle of an ovary. Volvulus occurs when
a segment of intestine twists around its mesentery. The
condition has been associated with adhesions and
abscesses. Volvulus of the small colon is unusual, pre-
sumably because it has a short mesentery.
Strangulating pedunculated lipomas are rarely seen
in horses younger than 9 years, and they most com-
monly affect horses greater than 15 years. In the US,
Quarter horses and Morgans appear to be the breeds
303
16 COLIC
most at risk of strangulation of the small colon by a
pedunculated lipoma, and females are more commonly
affected than males. Compared to other segments of
the mesentery, the mesocolon and mesorectum may be
predisposed to formation of lipomas because of the
large amount of fat in these areas, but even so, the small
colon is much less likely than the small intestine to
become strangulated by a pedunculated lipoma.
Clinical signs anddiagnosis
Signs ofcolic initiated bystrangulation of the small colon
are sudden in onset, but the general clinical course of
physiological deterioration may occur more slowly than
when more proximal segments of the gastrointestinal
tract become strangulated. Serosanguinous fluid con-
taining increased concentration of nucleated cells and
total protein is obtained during abdominal paracentesis
of affected horses, and tympany of the large colon and
absence offeces are evident on examination per rectum.
Treatment
Treatment of horses with a strangulating lesion is by
reduction of the volvulus or entrapment followed by
resection of the infarcted segment of small colon and
anastomosis of the proximal and distal segments.
Horses seem able to compensate for the considerable
loss of absorptive capacity that occurs when a long seg-
ment of small colon is removed.
NON-STRANGULATING INFARCTION OF
THE SMALL COLON
Primary vascular lesions with segmental infarction
caused by mesenteric thromboembolism are uncom-
mon because the small colon receives most of its blood
supply from the caudal mesenteric artery, this is rarely
affected by occlusive verminous arteritis. Often, during
abdominal exploration or at post-mortem examination
of horses affected by non-strangulating infarction of the
small colon, no evidence of arteritis of the caudal
mesenteric artery can be found. Treatment of affected
horses is by resection of the infarcted segment and anas-
tomosis of the proximal and distal segments. If the
affected segment of small colon cannot be exteriorized,
colostomy or transrectal exteriorization followed by col-
orectostomy must be performed.
INTESTINAL ATRESIA
Intestinal atresia of foals results in complete occlusion
of the intestinal lumen. The condition is rare, except in
304
crosses between predominantly white Overo Paint sires
and dams.
The etiology of intestinal atresia is unknown, but the
condition may be the result of a simple recessive gene,
developmental arrest, or vascular compromise to the
fetal gut resulting in ischemic necrosis of the affected
portion of intestine. The condition has been associated
with other congenital abnormalities, such as renal age-
nesis or hypoplasia, cerebral gliomata, hydrocephalus,
schistosomas reflexus, and infection with equine her-
pesvirus Type I. The distal portion of the large colon
and proximal end of the small colon are the segments
most commonly missing.
The types of intestinal atresia are classified accord-
ing to the tissue involved. In type I atresia, or mem-
brane atresia, a diaphragm or membrane occludes the
intestinal lumen. In type 2, or cord atresia, the proximal
and distal blind ends are joined by a small cord of con-
nective tissue, with or without mesentery. In type 3, or
blind-end atresia, the proximal and distal blind seg-
ments of colon are completely separated, and the cor-
responding mesentery is absent.
Clinical signs of intestinal atresia are recognized within
a few hours after birth and may include depression, pro-
gressive abdominal distension and discomfort, tenes-
mus, absence of feces, no response to administration of
enemas, and an empty, blind-ending rectum as deter-
mined by digital palpation or endoscopic examination.
The anus is usually normal. Intestinal atresia can usually
be diagnosed by observation of clinical signs, proc-
toscopy, and contrast radiography using barium ene-
mas. Definitive diagnosis is made during exploratory
laparotomy (celiotomy).
Treatment
Foals suffering from intestinal atresia have a poor prog-
nosis for survival, and for white Overo Paint foals with
aganglionosis, the prognosis is grave. Surgical correc-
tion following early diagnosis offers the only chance of
survival for the affected foal. Untreated foals die within
the first days of life after developing endotoxemia,
severe metabolic disturbances, and occasionally fibri-
nous peritonitis. The blind ends can be resected, and
the proximal and distal segments of colon anastomosed
if the atretic segment is located in an exteriorizable part
of the intestine and is not extensive. Alternatives to
resection and anastomosis include colostomy or pulling
the blind-ended small colon through an incision in the
rectum and suturing it to the anus. The foal should be
examined for other congenital abnormalities before
intestinal atresia is corrected.
Diseases of the rectum
RECTAL TEARS
Causes
Rectal tears occur most commonly during palpation per
rectum of reproductive structures to assess fertility or
diagnose pregnancy, and during palpation per rectum
of the abdomen to determine the cause of intestinal or
urogenital disease. Palpation per rectum is not without
risk of injury to the wall of the rectum or small colon,
and experience in examining the contents of the
abdomen per rectum does not preclude the possibility
of causing a rectal tear. Iatrogenic rectal tears and their
complications are a leading cause of malpractice suits
against veterinarians.
Rectal tears can also occur during administration of
an enema, especially in foals, as a result of either exces-
sive hydrostatic pressure or puncture of the rectum by
the enema tubing. Rectal tears have also been associ-
ated with dystocia, rupture of a mural hematoma of the
small colon, and accidental entry of the stallion's penis
into the rectum of the mare during copulation.
Perforation of the mare's rectum by the penis of a stal-
lion is most likely to occur when breeding is forced or
when angulation or tipping of the labia makes vaginal
entry difficult.
Spontaneous rupture of the rectum is rare and diffi-
cult to substantiate, but it has been reported to result
from ischemic necrosis due to thrombosis of the caudal
mesenteric artery and its branches, caused by migration
of Strongylus vulgaris. Neurogenic fecal retention and
extensive perineal and rectal melanomas can predis-
pose to spontaneous rupture of the rectum. In a few
cases, histological examination of tissue surrounding an
iatrogenic rectal tear has demonstrated a lesion that
weakened the wall of the rectum.
Progression
Complications associated with tears that occur caudal to
the peritoneal reflection include perianal fistulae, dis-
secting cellulitis, and formation of rectal diverticulae
and strictures. Tears of the intraperitoneal portion of
the rectum or small colon frequently cause fecal-
induced septic peritonitis resulting in death, even with
the best medical therapy.
Epidemiology
Rectal tears occur in horses of all ages, but the injury
occurs most frequently in young horses. Young horses
may be at risk of incurring a rectal tear because of their
DISEASES OFTHESMALL COLONAND RECTUM 16
small size, nervousness, resentment to palpation, and
excessive straining. Stallions and geldings are at greater
risk of receiving a rectal tear during examination per
rectum than are mares. Repeated examination of mares
may make them more accustomed to the procedure
and less likely to resist, also the diameter of the rectum
of males is smaller than that of mares. Arabian horses
are at increased risk of rectal injury, perhaps because
they have a relatively small anus and rectum and seem
to resist palpation more than horses of other breeds.
Anatomy
The rectum extends from the pelvic inlet to the anus, a
distance of approximately 30 cm in a 450-kg horse. The
cranial portion of the rectum is approximately 15-20
ern long, is attached to the mesorectum, and is covered
by peritoneum. The caudal portion, which includes a
flask-shaped dilatation, the ampulla recti, is approxi-
mately 10-15 ern long and is not covered by peritoneum
but is attached to the surrounding structures by con-
nective tissue and muscular bands. Because the peri-
toneal reflection extends caudally to within 15-20 cm of
the anus, rectal tears most often occur within the peri-
toneal segment of the rectum or small colon, with sub-
sequent development of septic peritonitis. The distance
from the anus to the caudal end of the peritoneal space
is longer in old and fat horses than in young and thin
horses, however, and thus a rectal tear of an old, fat
horse has a greater chance of involving the retroperi-
toneal, rather than the peritoneal, portion of the rec-
tum than does a tear in a similar location in a young,
thin horse.
In a study of 42 horses affected by a rectal tear, the
distance from the anus to the tear varied from 7.5-60
cm, and most tears occurred at the pelvic inlet, a dis-
tance of 25-30 em from the anus. The tears occurred
most often in the dorsal aspect of the rectum, between
10-12 o'clock, and the direction of the tear was usually
longitudinal.
The pelvic inlet, besides being the most common site
of the rectum at which the reproductive organs are pal-
pated, is where the rectum narrows and is deflected
downward. The rectal wall is often stretched forward at
this point, reducing its pliability. Tears in this location
are at the junction of the rectum and terminal part of
the small colon, and many tears are, in fact, located in
the caudal portion of the small colon.
Tears often occur along the edges of the dorsal
mesocolic band, because in this area, as the longitudi-
nal muscle thickens to form the mesenteric tenia, the
thickness of the circular muscle decreases. In addition,
microvascular studies of the small colon of horses indi-
cate that the area adjacent to each side of the band may
305
16 COLIC
be inherently weak because at this area, the short termi-
nal arteries penetrate the wall.
Classification
Rectal tears are classified according to the layers of the
rectal wall disrupted. Tears restricted to just the mucosa
or the mucosa and the submucosa are classified as
grade I (Figure 16.5). In grade 2 tears, only the muscu-
laris is torn, causing a mucosal-submucosal hernia to
develop (Figure 16.6). The mucosa and submucosa,
because of their elasticity and numerous folds, can
stretch without perforation, while the overlying con-
tracted muscles rupture. Although grade 2 rectal tears
result in no contamination of the peritoneal cavity, they
could contribute to development of an iatrogenic grade
3 or 4 rectal tear.
Grade 3 tears involve the mucosa, the submucosa,
and muscularis and include tears that extend into the
mesentery. Tears that cause formation of a serosal diver-
ticulum are classified as grade 3a (Figure 16.7), and
tears that enter the mesentery are classified as grade 3b
(Figure 16.8). The intact serosa or mesorectum of a
grade 3 rectal tear prevents particulate fecal matter
from contaminating the peritoneal cavity, but bacteria
are not excluded and septic peritonitis results. Grade 3
rectal tears are often accompanied by dissecting cellu-
Figure 16.5 Grade 1 tear: only the mucosa or mucosa and
submucosa are torn
306
litis and separation of tissue. Tears that perforate all lay-
ers and extend into the peritoneal cavity are classified as
grade 4 (Figure 16.9). Grade 3 rectal tears commonly
progress to grade 4.
Figure 16.6 Grade 2 tear: the muscularis is torn, but the
other layers of the rectal wall remain intact
Figure 16.7 Grade 3a tear: all layers except the serosa are
torn, forming a serosal diverticulum
Figure 16.8 Grade 3b tear: the tear enters the mesentery
Prevention
Failure of the rectal wall to relax during palpation is a
major factor in the development of a tear. Producing a
rectal tear in the relaxed rectum is difficult, and so the
best way to prevent a rectal tear is to ensure that the rec-
tum is relaxed before proceeding with palpation.
Horses should be adequately restrained to perform pal-
pation per rectum, and if the horse is fractious, it
should be sedated, or a twitch or lip chain should be
applied. The hand and arm should be lubricated liber-
ally. The fingers should be introduced in coned fashion
and feces evacuated from rectum. The hand should be
inserted to slightly beyond the desired site of palpation
so that by dragging the rectal wall caudally, tension on
the rectal wall is reduced, allowing structures to be pal-
pated through a relaxed rectum. If the horse strains
excessively or if a strong contraction occurs, the hand
should be withdrawn. If the horse continues to strain or
if deep palpation is required, epidural anesthesia or a
parasympatholytic drug should be administered.
Extreme caution should be exercised when examin-
ing young horses and small ponies per rectum, because
their fractious nature and small size put them at high
risk for rectal damage. To avoid perforating the fragile
rectal mucosa of the newborn foal during treatment for
impaction of meconium, enema tubes should be
Figure 16.9 Grade 4 tear: the tear perforates ali layers and
extends into the peritoneal cavity
smooth, well-lubricated, and never forced into place,
and solutions should be administered by gravity flow.
Clinical signs, diagnosis and immediate
treatment
Tachycardia, intestinal ileus, pyrexia, sweating, reluc-
tance to move, and signs of abdominal discomfort after
palpation per rectum, administration of an enema, or
breeding indicate that the horse may have received a
serious rectal injury. A small amount of blood-tinged
material on the examiner's sleeve usually indicates that
only minor trauma has occurred, but the presence of
whole fresh blood on the sleeve or sudden relaxation of
the rectum, especially when the horse is straining, indi-
cates that the rectum has been seriously injured.
If a tear is suspected, the horse should be sedated,
peristalsis slowed, and the rectum evaluated carefully by
digital examination. Administration of parasympa-
tholytic drugs or caudal epidural anesthesia may be
effective in stopping peristalsis of the rectum and relax-
ing the rectum and anal sphincter. Propantheline bro-
mide, 30-35 mg per 450 kg body weight, given
intravenously, produces rapid, effective reduction of
peristalsis for up to 2 hours and prevents straining to
allow digital and endoscopic evaluation of the tear.
Precise evaluation of the layers of the rectum involved
307
16 COLIC
in the injury is best gained by digital palpation, using a
well-lubricated surgical glove or bare hand. Feces
should be removed carefully from the tear and acljacent
portion of the rectum. Palpation of a thin, flap-like
membrane indicates that the tear probably extends only
through the mucosa, but the presence of a thick-walled,
cavity-like depression bounded by a thin, tough mem-
brane that prevents extension of the hand into the
abdominal cavity is characteristic of a grade 3 tear.
Failure to recognize that a grade 3 or 4 tear has
occurred can delay treatment and increase legalliabil-
ity. Immediate and intensive treatment not only
increases the chances of the horse's survival but also
aids defense against a malpractice action. Negligence is
difficult to disprove when a serious tear is not recog-
nized immediately. Circumstances in which the horse is
managed initially may make the difference in winning
or losing a case in court. The client should be informed
immediately that the rectum has been torn and the
gravity of the condition should be described.
Survival of the horse depends largely on the course
of action instituted at the time of injury. Unless mea-
sures are taken immediately to prevent peritoneal cont-
amination and progression of a grade 3 tear, endotoxic
shock and death usually result. The tear should be care-
fully packed with medicated gauze sponges, and the rec-
tum should be carefully packed from the anus to cranial
to the tear with 3-inch (7.5 ern) stockinette filled with
0.25 kg of rolled cotton. A purse-string suture or towel
clamp should be placed in the anus to keep the packing
material within the rectal lumen. A parasympatholytic
drug or caudal epidural anesthesia should be adminis-
tered to stop peristalsis and prevent straining.
Before being transported to a surgical facility, a
horse that has suffered a grade 3 or 4 rectal tear should
receive a fecal softener, such as mineral oil, tetanus pro-
phylaxis, and broad-spectrum antimicrobial therapy,
using such drugs as penicillin, gentamicin, and metron-
idazole. The horse should also receive flunixine meglu-
mine for its analgesic, anti-endotoxic, and
anti-inflammatory effects, and fluid therapy should be
administered. Peritoneal fluid should be obtained by
abdominal centesis to assess the degree of peritoneal
contamination, and for bacterial culture and sensitivity
testing. Comparison of this fluid with fluid obtained
later at the surgical facility may help determine the seri-
ousness of the tear and the extent of peritoneal conta-
mination.
In a study of 35 horses that had received a grade 3
rectal tear, first-aid measures taken at the time the tear
occurred had a marked influence on outcome. First-aid
measures were considered adequate in 14 horses, of
which 11 (79%) survived, whereas only 50 per cent of
those horses that did not receive adequate first-aid sur-
308
vived. Horses given adequate first-aid were admitted
with less severe peritoneal inflammation, as demon-
strated by lower mean and median concentrations of
white blood cells in the peritoneal fluid.
Definitive treatment
Grade 1 tears usually heal without serious complica-
tions, and horses suffering from a grade 1 tear are usu-
ally treated conservatively by administration of
broad-spectrum antibiotics and a stool softener. Horses
with a grade 1 tear should not be palpated per rectum
unless absolutely necessary for 3 to 4 weeks. Horses with
a grade 2 tear are treated similarly to horses with a
grade 1 tear, but antimicrobial therapy is unnecessary.
Horses with a full-thickness tear into the retroperi-
toneal portion of the rectum have a better prognosis for
survival than do horses with similar tears in the peri-
toneal region. They tend to heal with the main compli-
cations being the formation of perirectal abscesses.
Dorsally positioned perirectal abscesses can be drained
rectally or perianally, and ventrally positioned abscesses
can be drained through the dorsal wall of the vagina.
Treatment options for horses with a grade 3 tear into
the peritoneal region of the rectum include conserva-
tive (medical) management, primary closure with
access either through the rectal lumen or via celiotomy,
or diversion of feces to prevent fecal contamination of
the tear so that healing can proceed by second inten-
tion. Feces can be diverted by colostomy (end or loop
colostomy) or with a temporary indwelling rectal liner.
If second intention healing has begun in horses with a
grade 3 tear, then continued medical management,
including packing the tear with medicated gauze
sponges or repeated manual evacuation of the tear
(under epidural anesthesia), and intensive antibiotic
therapy can be successful.
Grade 4 tears usually result in contamination of peri-
toneal surfaces with particulate fecal material, making
euthanasia of horses with a grade 4 tear justified. If the
peritoneal surfaces have not been contaminated with
particulate fecal material, then the same techniques
used to repair grade 3 tears can be used. If the horse
incurred a grade 3 or 4 tear during evaluation of colic,
an exploratory celiotomy should be performed to deter-
mine if intestinal obstruction requiring surgical correc-
tion is present.
Primary repair
Primary closure of grade 3 rectal tears is considered
contra-indicated by some surgeons because of the likeli-
hood of creating a dead space which may predispose to
formation of an abscess, and because attempts to close
tears primarily per rectum with the horse standing may
cause the tear to enlarge or perforate and may increase
contamination of damaged tissue. In one study, how-
ever, primary closure of the rectal tear, used as the sole
means of repair or used in conjunction with other tech-
niques, was shown to improve chances of survival, and
formation of an abscess during convalescence was not
evident. Primary suture closure was successful in six of
seven horses for which it was the principal method of
treatment. In this study, the tear was repaired primarily
only if it was minimally contaminated with feces. The
tear was not sutured if the ability of the tissue to hold
sutures was in doubt, either because of extensive sepa-
ration of tissue layers or marked edema.
If the tear is close to the anus, it can be sutured per
rectum with the horse standing or recumbent. Repair
can be performed using a blind, one-handed suturing
technique, but the disadvantage of this technique is the
difficulty with which it is performed by those inexperi-
enced in this method. Ineffective attempts to suture the
tear in this manner may cause the tear to enlarge or per-
forate. An alternative method of suturing the tear per
rectum involves the use of an expandable and
adjustable speculum that allows visual and surgical
access to the tear, however this speculum is not widely
available.
A grade 3 tear was sutured successfully on an anes-
thetized experimental horse by prolapsing the rectum.
The distal end of the small colon was intussuscepted
into itself, and the rectal mucosa exteriorized through
the anus, allowing the tear to be seen from the mucosal
side. Intussusception was accomplished by introducing
a hand into the rectal lumen and advancing it 4-5 cm
proximal to the tear. An assistant, working through a
laparotomy (celiotomy), initiated the intussusception
by pushing a saline-soaked gauze sponge into the finger
tips of the hand inside the rectal lumen. This allowed
the palpator to grasp the rectal wall and retract the rec-
tum through the anal orifice. The tear was then lavaged
and sutured directly. A rectal tear, located approxi-
mately 40 cm proximal to the anus, of another horse
was successfully repaired with the horse standing, by sta-
pling the tear after intussuscepting the affected portion
of the rectum toward the anus with stay sutures placed
on either side of the tear.
When exposing the damaged segment of rectum by
intussusception, the rectum should not be exteriorized
under tension for a prolonged time to avoid tearing or
thrombosis of the mesenteric vessels. The short meso-
colon and large amounts of mesenteric and retroperi-
toneal fat may prevent intussusception and
exteriorization of the damaged segment of rectum in
most horses, but the technique may be useful if the
horse is young and thin. The technique should be
attempted only if the tear is recent, because the manip-
ulations may worsen the tear if the surrounding tissue is
edematous.
Grade 3 or 4 tears can be sutured through a laparo-
tomy (celiotomy), but the ability to see and repair the
tear by direct suturing from the abdomen depends
largely on the distance of the tear from the anus. In
mares, a midline prepubic incision between the mam-
mary glands may provide good exposure of tears more
than 25 ern from the anus. Exposure may be improved
by elevating the hindquarters. A paramedian incision is
used to expose rectal tears of geldings and stallions.
The incision is extended caudally as far as possible, but
exposure of the distal end of the small colon and rec-
tum is less than exposure achieved in the mare. Few
tears can be sutured from a flank approach, but certain
conditions, such as advanced pregnancy or excessive
edema of the udder may make a flank approach neces-
sary. If the tear extends into the dorsal mesentery, as
many do, suturing the tear through a ventral midline
celiotomy is difficult. The dorsal position of the tear
limits the exposure of the tissue, and fat in the mesorec-
tum makes the edges of the tear difficult to identity.
Creating an enterotomy in the antimesenteric tenia of
the small colon or the rectum opposite a dorsal tear
permits surgical access to the tear.
If a tear cannot be adequately closed primarily using
any of these suturing techniques, the horse should be
considered a candidate for a colostomy or installation
of a temporary, indwelling, rectal liner.
Temporary, indwelling, rectal liner
A temporary, indwelling, rectal liner can be implanted
to divert fecal material from a grade 3 or 4 tear until the
tear is healed sufficiently by secondary intention to pre-
vent bacterial contamination of the peritoneal cavity.
To construct the rectal liner, each end of a 5 x IO-cm
plastic rectal ring is trimmed to form a 5 x 7.5-cm ring.
Holes are drilled 1.5 cm apart around the circumfer-
ence of the ring at one edge of the central groove, and
a no. 5 polyester suture is laced through these holes.
The hand is removed from a plastic palpation sleeve,
and the rectal ring is inserted into the small end of the
sleeve. A rubber band is placed around the sleeve and
over the central groove in the ring at the end opposite
the polyester suture. The sleeve is glued to the end of
the ring with cyanoacrylate, and the sleeve is inverted
over the ring.
To implant the prosthesis, a laparotomy (celiotomy)
is performed, and the rectal ring is passed through the
rectal lumen by a non-scrubbed assistant and posi-
tioned proximal to the rectal tear by the surgeon per-
forming the celiotomy. The portion of small colon
containing the ring is exteriorized through the
309
16 COLIC
celiotomy. Care is taken to position the rectal ring in
the most distal portion of the small colon that can be
exteriorized at the celiotomy to ensure that the end of
the liner extends beyond the anus when the horse
recovers from anesthesia. A strand of heavy chromic
catgut is passed circumferentially around the intestine
over the groove in the ring close to the polyester suture,
through a small perforation in the mesocolon, and tied
sufficiently tight to initiate pressure necrosis of colon
beneath it. Four interrupted absorbable sutures are
placed equidistantly around the circumference of the
colon to include the circumferential suture, the intesti-
nal wall, and polyester suture in the rectal ring. These
four retention sutures and the circumferential ligature
are oversewn with 2-0synthetic absorbable suture, using
an interrupted Lembert pattern. This inverting suture
line maintains continuity of the intestine when the ring
and encircling ligature slough 9-12 days after surgery.
The small colon is lavaged with water through a
stomach tube passed retrograde up the sleeve, and 4
liters of mineral oil is infused into the right dorsal por-
tion of the large colon. The contents of the large colon
should be removed through an enterotomy at the pelvic
flexure to decrease the amount of ingesta passing
through the rectal ring. Either before or after the pros-
thesis is implanted, the rectal tear is sutured, if possible,
to prevent a grade 3 tear from progressing to a grade 4
tear or to prevent a grade 4 tear from forming a
mucosal-to-serosal fistula.
A reduced volume ofsoft feces is maintained by feed-
ing a pelleted ration and by administering mineral oil
via stomach tube until the ring and liner detach.
Because the end of the liner tends to disappear into the
rectum when the horse assumes recumbency, horses
can be kept standing until the rectal tear heals, or an
embroidery hoop can be attached to the end of the
liner to prevent the liner from retracting into the rec-
tum.
The primary advantage of a temporary, indwelling,
rectal liner over a diverting colostomy is that use of a
rectal liner requires one surgical procedure, whereas a
colostomy requires a second surgical procedure to re-
establish continuity of the small colon after the tear has
healed. The temporary, indwelling, rectal liner should
not be used if more than 25 per cent of the circumfer-
ence of the rectum is torn, if the rectum is too small to
accommodate the rectal ring, or if the tear is too far
proximal to accommodate the rectal liner. The tempo-
rary indwelling liner requires continuous postoperative
maintenance to prevent impaction of the ring with
feces and retraction of the distal end of the liner into
the rectum. Complications of this technique include
separation of the prosthesis from the rectal wall before
the rectal tear is sufficiently healed, insufficient length
310
of the rectal liner, and conversion of a grade 3 to a
grade 4 tear.
Colostomy
Colostomy can be used to treat horses with a grade 3 or
grade 4 rectal tear by temporarily or permanently
diverting feces to allow the rectal tear to heal by second
intention. The colostomy is termed a loop colostomy or
an end colostomy, depending on whether an intact
loop or a transected segment of small colon is used to
create the stoma. Both techniques of colostomy require
two surgical procedures - one to form the stoma and
the other to restore continuity of the small colon after
the tear has healed. Both techniques allow complete
diversion of feces, but loop colostomy may be more eas-
ily and quickly performed and revised, and atrophy of
the distal segment of the small colon is more easily pre-
vented with this technique of colostomy.
Loop colostomy is performed in the left flank, cra-
nial to and level with the fold of the flank, using either
a single or double-incision technique. Horses are anes-
thetized and positioned in lateral recumbency, or
surgery is performed with the horse standing. Marking
the proposed site for the stoma on the skin with sutures
before the horse is anesthetized ensures that the stoma
is created in the proper location.
To perform a single-incision colostomy as described
by Freeman et at. (1992), an incision is made at the pro-
posed site of the stoma and extended 12-15 em dorsally
through the skin, subcutaneous tissue, and fascia of the
external abdominal oblique muscle, parallel with the
costal arch. The internal abdominal oblique muscle
and aponeurosis, the transversus abdominis aponeuro-
sis, and peritoneum are perforated bluntly, and a loop
of small colon, located at least 1 meter from the peri-
toneal reflection, is exteriorized. Both arms of the loop
are apposed with absorbable suture, using a continuous
pattern, for 8 em, at a third to half the distance from the
mesentery to the antimesenteric tenia. The suture line
is angled toward the mesentery at the end of the loop so
that the antimesenteric tenia can be exposed through
the cutaneous incision. The loop of small colon is then
positioned in the ventral aspect of the abdominal inci-
sion so that the loop protrudes 2-3 em above the skin.
The proximal part of the loop is positioned ventral to
the distal part.
The seromuscular layer of the colon is apposed to
edges of the abdominal musculature and fascia by sev-
eral interrupted sutures. The abdominal wall is closed
dorsal to the loop, forming a snug fit around the loop
but without impinging on the lumens. The antimesen-
teric tenia of the exteriorized segment of small colon is
incised longitudinally to expose the lumen of the small
DISEASES OFTHE SMALL COLONAND RECTUM 16
colon, and the incised edge of the small colon is
sutured to the skin with simple interrupted, non-
absorbable sutures.
The double-incision technique may reduce the risk
of peristomal herniation and stomal prolapse. To create
a double-incision colostomy as described by Freeman et
at. (1992), a 12-15 em incision is made approximately
10 cm below the left tuber coxae. A loop of small colon
is exteriorized, and the arms of the loop are apposed
with absorbable suture as described for the single-inci-
sion technique. A second incision, 6-8 em long, is made
in the lower region of the flank, and the sutured loop of
colon is manipulated from the upper incision through
the lower incision until the loop protrudes above the
skin for 2-3 cm. The loop is incised and sutured to the
body wall as described for the single-incision technique.
The stoma should be no larger than the diameter of the
small colon to avoid prolapse. To decrease contamina-
tion of the rectal tear following colostomy, feces in the
distal segment of small colon should be removed by
lavage through the stoma.
Following colostomy, the horse should be fed a laxa-
tive diet, and ointment should be applied to the skin
around the stoma. A cradle should be applied if the
horse has a tendency to mutilate n o t - 2 T c 1 4 6 4 4 7 7 . 7 2 T [ ( c 0 . 0 - 7 4 6 - 3 2 2 0 4 a 1 T c 8 . 9 4 6 3 8 1 n d ) T j 8 . 9 2 9 1 7 0 7 3 . 4 2 5 . 2 g
16 COLIC
obstruction and dehiscence can develop because of
shifting of muscle layers when the horse stands.
Postoperative treatment
Regardless of the manner by which a horse with a grade
3 or 4 rectal tear is treated, the horse should receive
broad-spectrum, bactericidal, antimicrobial drugs and
flunixin meglumine. The peritoneal cavity should be
lavaged daily with copious amounts of a balanced
polyionic electrolyte solution or physiologic saline solu-
tion (Figure 16.10), and horses should receive a bal-
anced polyionic electrolyte solution at sufficient rate to
correct dehydration. The horse should be fed a com-
plete pelleted ration and no hay to reduce bulk, and
mineral oil should be administered, as needed, to pre-
vent production of formed feces. Table salt can be
added to each feeding to encourage water consump-
tion.
Prognosis for survival of horses with rectal
tears
donut at the anus. Type 2 prolapse, sometimes referred
to as a complete prolapse, is an eversion of all or a por-
tion of the ampulla recti (Figure 16.12). A type 2 pro-
lapse is generally larger and more cylindric than a type
1 prolapse.
Type 3 prolapse is also an eversion of all or a portion
of the ampulla recti, but it is accompanied by intussus-
ception of the peritoneal portion of the rectum or
colon (Figure 16.13). Type 4 rectal prolapse is an exten-
sive intussusception of the peritoneal portion of the
rectum or colon through the anus (Figure 16.14 and
Plate 16.1). With type 4 prolapse, the exposed intestine
is frequently ischemic because of vascular compromise
caused by stretching and tearing of mesenteric blood
vessels as the mesocolon is forced into the pelvic canal
by the intussusception. In the first 3 types, the prolapse
is continuous with the mucocutaneous junction of the
anus, but if a finger can be introduced for several
In a report of 42 horses with a grade 3 or 4 tear of the
rectum or small colon, mortality was 64 per cent. This
study found that horses with a tear into the mesentery
(grade 3b) had a better prognosis for survival than did
horses with a lateral or ventral tear (grade 3a). In
another study, however, horses with grade 3b tears had
a worse prognosis for survival than did horses with a
grade 3a tear. Of the horses with a grade 3b tear, 44 per
cent were discharged compared to 74 per cent of the
horses with a grade 3a tear. In both studies, horses with
a grade 4 tear had a grave prognosis for survival.
iii i
c
RECTAL PROLAPSE
Cause
Figure 16.11 Type 1 prolapse: the rectal mucosa alone is
prolapsed
'''''' ",,,l,, "
Rectal prolapse in the horse is sometimes associated
with conditions that cause tenesmus, such as constipa-
tion, diarrhea, neoplasia, dystocia, urethral obstruction,
or colic. Factors that may predispose to rectal prolapse
include loss of tone in the anal sphincter, loose attach-
ments of the mucous membrane to the muscular coat of
the rectum, or loose attachments of the rectum to
perirectal tissues. Females are more likely than males to
develop rectal prolapse.
Classification
i II j i j
"<:" "
! I ! CI
I I C
Rectal prolapses are classified according to the tissue
involved. Prolapse of the rectal mucosa alone is classi-
fied as a type 1 prolapse (Figure 16.11). Type 1 prolapse
is usually seen as a circular swelling, resembling a large
312
Figure 16.12 Type 2 prolapse: all or a portion of the
ampulla recti is everted
16 COLIC
ANORECTAL LYMPHADENOPATHY
Enlargement of the anorectal lymph nodes, which are
situated dorsally along the rectum in the retroperi-
toneal space, can cause extralumenal obstruction of the
rectum resulting in signs of abdominal pain. Other clin-
ical signs associated with the condition include
anorexia, lack of production of feces, tenesmus, and
pyrexia. Anorectal lymphadenopathy occurs primarily
in young horses, and although the cause is usually
unknown, it may develop secondary to rectal or vaginal
trauma or from gravitation of an abscess in the gluteal
muscles into the perirectal tissues. Sepsis of an anorec-
tal lymph node can extend into the peritoneal cavity
causing septic peritonitis. Bacteria cultured most com-
monly from perirectal abscesses are Streptococcus zooepi-
demicus and EScherichia coli.
Diagnosis of anorectal lymphadenopathy is con-
firmed by digital palpation per rectum, transrectal
ultrasonography, and cytologic examination of an aspi-
rate or biopsy from an affected lymph node. Peritoneal
fluid, obtained by abdominocentesis, should be exam-
ined cytologically to determine if sepsis extends into the
abdominal cavity.
Treatment of affected horses is aimed at relieving,
and then preventing, fecal obstruction of the rectum.
Laxatives, such as mineral oil, should be administered
orally to keep feces soft, a complete pelleted ration
should be fed to reduce intestinal bulk, and broad-spec-
trum antimicrobial drugs should be administered.
Celiotomy is warranted when signs of pain cannot be
controlled by relieving constipation, or when secondary
complications necessitate abdominal exploration.
When a mature abscess is detected ultrasonographi-
cally, it should be lanced using a perianal incision.
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315
17
Other conditions
Abdominal distention in the
adult horse
T Mair
INTRODUCTION
Abdominal distention is classically regarded as being
caused by one of the 'seven f's'
fat feces
fetus flatus
food foreign body
fluid
Gaseous distention
Fluid distention
Gastrointestinal tympany
(distentionttympanitic cOlic)
Intestinal obstruction!
impaction
Ileus
Pneumoperitoneum
Ascites
Peritonitis
Uroperitoneum
Hemoperitoneum
Fetal hydrops
Although pregnancy (Figure 17.1) or obesity can be
regarded as 'normal' or 'physiological' causes of
Figure 17.1 Abdominal distention and ventral edema in
late gestation
Weakened body wall Ventral body wall hernias
Ruptured. prepubic tendon
Cushing's disease
abdominal distention in adult horses, other conditions
that result in an enlarged abdomen are pathological,
and may be associated with serious and possibly life-
threatening disease. The most common and most
important diseases associated with abdominal disten-
tion in the adult horse are listed in Table 17.1.
GASTROINTESTINAL TYMPANY
(DISTENTIONITYMPANITlClFLATULENT
COLIC)
__
Gastric, cecal, or colonic tympany occur as a result of
accumulation of excessive gastrointestinal gas due to
317
17 COLIC
Feeding highly fermentable substrate (especially
soluble carbohydrates), e.g. grain, lush grassand
clover, wilted grass/grass clippings
Abrupt change in feeding (especially forage)
Feeding horse when it is exhausted or overheated
Electrolyte abnormalities, e.g- hypocalcemia,
hypokalemia
Cold water engorgement
Therapeutic administration of atropine
Aerophagia
Inadequate mastication
Rapidfeed engorgement
Interruption of GI motility from stress, excitement,
or pain
Impactions
Displacements
Late pregnancy
Ileus secondary to anE1sthesia, surgical manipula-
tion of the intestines (seeChapter 11), vascular
compromisE1 (thromboembolic colic) and liver
disease. Adult horses rarely exhibit abdominal
distension after small intestinal obstruction,
unlike foals.
increased fermentation and/or ineffectual gastroin-
testinal motility (see Chapters 12,14, and 15). Overcon-
sumption of readily fermentable food stuffs such as
fresh grass, grain, or beet pulp results in the production
of large amounts of lactic acid and volatile fatty acids.
Volatile fatty acids inhibit gastrointestinal motility and
thereby promote further fermentation and production
of gas. If the rate of gas production exceeds the ability
of the gastrointestinal tract to move the gas through, or
if progressive motility of the intestinal tract is impaired,
then gas will accumulate in the stomach, cecum,
and/or large colon. Distention inhibits vagal motility,
while fermentation continues. Moderate to severe dis-
tention may increase the contractility of other segments
of the gastrointestinal tract, resulting in spasms that
may cause pain.
Factors associated with distention colic are summa-
rized in Table 17.2.
The clinical signs and degree of pain with distention
colic vary depending on the rate of gas accumulation
and the part of the gastrointestinal tract involved. In
mild cases there may be only vague signs of dullness and
inappetence. In more severe cases there is often inter-
mittent colic that is most severe with intestinal spasm. In
318
the most severe cases, especially where there is gastric
tympany, there is acute distress and signs of severe
uncontrollable pain.
Heart and respiratory rates are often elevated if the
pain is severe, or if the distention compromises respira-
tory function (due to pressure on the diaphragm) or
venous return. The heart rate may reach 100 bpm or
more. The mucous membranes are usually pale but may
become cyanotic.
Abdominal distention is most likely in cases of large
intestinal tympany. Large colon tympany tends to result
in bilateral abdominal distention, whereas cecal tym-
pany results in distention of the right flank and right
paralumbar fossa. Abdominal borborygmi may be
increased in frequency if the distention is mild or mod-
erate, but with severe distention, borborygmi may be
absent. Tympanitic, 'tinkling' sounds may be heard as
the horse breathes or moves. Percussion of the
abdomen may be helpful in identifying the region of
the gastrointestinal tract that is distended. In cases of
cecal tympany, percussion with a stethoscope over the
right flank reveals high-pitched pinging sounds.
Rectal examination reveals gas-filled sections of the
gastrointestinal tract. In primary gastric tympany, the
spleen may be displaced caudally by the enlarged stom-
ach. Primary gastric tympany needs to be differentiated
from cases of gastric distention secondary to small
intestinal obstruction; in the latter cases, several loops
of distended small intestine may be palpable. In cases of
cecal tympany, the distended cecum is palpated in the
upper right caudal quadrant of the abdomen. The ven-
tral band of the cecum stretches across the pelvic inlet
from cranial in the right dorsal quadrant to ventral in
the left ventral quadrant. Distention of the large colon
is readily identified by the location of the distended vis-
cus, its size, and the presence of longitudinal bands
except at the pelvic flexure.
Uncontrolled, progressive distention of the stomach
may result in rupture. The rupture is usually located
along the greater curvature. Signs of impending rup-
ture include severe pain, tachycardia (usually> 100
bpm), abdominal distention and retching. Cyanotic
and pale mucous membranes are usually present.
Commonly, once the stomach ruptures, the signs of
severe pain disappear, but signs of shock, sweating, and
collapse rapidly follow. Ingesta is evident in the
peritoneal fluid, and the serosa of the intestines feel
roughened on rectal examination; euthanasia is recom-
mended in such cases.
Treatment
The primary objective of treatment is to evacuate the
gases from the region of distention and to prevent
17 COLIC
foreign body obstruction (see Chapter 16)
sand impaction (see Chapter 15)
non-strangulating intestinal infarction (see Chapter
15).
ILEUS
Intestinal ileus is characterized by a decrease in propul-
sive motility, an increase in fluid and particulate transit
time, and distention of the intestine. Horses with small
intestinal ileus have ongoing nasogastric reflux and the
presence of distended loops of small intestine that are
palpable per rectum; such cases may have mild to mod-
erate abdominal distention if the intestinal distention is
severe and affects the majority of the small intestine.
Horses with ileus of the large intestine are more likely
to have significant abdominal distention due to tym-
pany. Conditions that may predispose to intestinal ileus
and abdominal distention include
primary large intestinal tympany (see above)
postoperative ileus (see Chapter 11)
non-strangulating intestinal infarction (see Chapter
15)
grass sickness (see Grass sickness)
peritonitis (see Peritonitis)
therapeutic administration of atropine
electrolyte abnormalities (hypocalcemia,
hypokalemia)
colitis (see Chapter 20)
stress.
PNEUMOPERITONEUM
Pneumoperitoneum, the presence of free gas in the
peritoneal cavity, is usually caused by gastrointestinal
rupture and per-acute peritonitis (see Peritonitis).
Affected horses present with signs of severe shock,
tachycardia, sweating, reluctance to move, and rapid
death.
ASCITES
Ascites associated with the accumulation of a transuda-
tive effusion in the peritoneal cavity is uncommon in
horses. The causes of ascites in the adult horse include
neoplasia (Figure 17.2)
hypoproteinemia
right-sided heart failure
uroperitoneum.
320
Figure 17.2 Ascites and ventral edema due to multicentric
lymphosarcoma in a horse
The diagnosis of ascites is achieved by identification
of abdominal distention, fluid ballottement, diagnostic
ultrasonography, and abdominal paracentesis. Fluid
ballottement of the adult equine abdomen is not easily
performed but it is relatively easier in ponies and minia-
ture horses than in larger horses. Diagnostic ultrasound
is useful to confirm the presence of large quantities of
anechoic free peritoneal fluid. Abdominal paracentesis
yields clear, watery fluid with a total nucleated cell
count less than 10.0 x 10
9/1
(usually < 2.0 x 10
9/1)
and
total protein concentration less than 25 g/I (usually <
15 g/I). In some cases the fluid may have the appear-
ance of a modified transudate (i.e. fluid has the charac-
teristics of a transudate but has a modest increase in cell
count or total protein concentration).
Ascites has been reported to occur in association with
lymphosarcoma, squamous cell carcinoma, mesothe-
lioma, and various other carcinomas and adenocarcino-
mas. Mesothelioma is extremely rare, but may cause the
greatest amount of abdominal fluid accumulation since
it is a tumor of the fluid-producing cells of the peritoneal
lining. Abdominal neoplasia commonly produces other
clinical signs such as weight loss and abdominal pain (see
Gastrointestinal neoplasia).
Hypoproteinemia and hypoalbuminemia due to
protein-losing enteropathy (see Chapter 21), hepatic
disease (see Chapter 19) and renal disease are more
commonly associated with peripheral edema, but may
occasionally present with ascites. Likewise, horses in
right-sided heart failure usually present with signs of
exercise intolerance,jugular pulse, and ventral abdom-
inal and limb edema, but ascites may sometimes be
evident.
PERITONITIS FETAL HYDROPS
OTHER CONDITIONS 17
Peritonitis rarely causes severe abdominal distention
due to fluid accumulation, but intestinal ileus associ-
ated with per-acute or acute peritonitis may result in
abdominal distention (see Peritonitis). In cases of
per-acute peritonitis due to bowel rupture, gas accu-
mulation in the peritoneal cavity (pneumoperi-
toneum) (see above) may also produce abdominal
distention. Other clinical signs associated with acute
peritonitis include colic, tachycardia, tachypnea,
pyrexia, guarding of the abdomen, reluctance to
move, scanty diarrhea, and reduced gut sounds (see
Peritonitis) .
UROPERITONEUM
Uroperitoneum is rare in adult horses (see Chapter 22
for discussion of uroperitoneum in foals), but urinary
bladder rupture occasionally occurs following trauma,
in peri-parturient mares, and in male horses following
urethral obstruction by a calculus. Diagnosis ofuroperi-
toneum is based on identification of a high peritoneal
fluid creatinine:serum creatinine ratio, possibly with
the presence of calcium carbonate crystals in the peri-
toneal fluid. Hyponatremia, hypochloremia, and hyper-
kalemia are often present. Identification of the site of
urinary tract disruption is usually achieved by
endoscopy. Ultrasonography can also be helpful in the
evaluation of uroperitoneum. Free urine in the
abdomen usually presents as anechoic fluid, but
because of the large amount of calcium carbonate crys-
tals and mucus, it may also appear as hypoechoic fluid.
The site of bladder rupture may sometimes be visual-
ized by transabdominal ultrasound in foals, or transrec-
tal examination in adults.
HEMOPERITONEUM
Hemoperitoneum due to rupture of the middle uter-
ine artery in mares, splenic rupture following trauma,
rupture of a verminous aneurysm of the cranial mesen-
teric artery, etc., may cause abdominal distention and
pain due to fluid (blood) accumulation in the
abdomen. However, other clinical signs related to
hypovolemic shock (tachycardia, tachypnea, cold
extremities, pale mucous membranes, weakness) will
predominate. The causes, diagnosis, and management
of hemoperitoneum are discussed elsewhere in this
chapter.
Fetal hydrops results from the accumulation of exces-
sive amounts of fluid within the amnion (hydrops
amnion or hydramnios) or chorioallantois (hydrops
allantois or hydrallantois). These are rare conditions
that occur in the last trimester of pregnancy of multi-
parous mares. Hydrallantois is the more common of
these two dropsical conditions. Typically there is a sud-
den onset of abdominal distention and ventral edema
with affected mares showing variable degrees of colic
and difficulty in defecation. Dyspnea and cyanosis may
also be present. Rectal examination should be per-
formed with care since passage of the forearm will be
impeded by pressure from the large fluid-filled uterus.
The fetus is usually not palpable due to the massive
quantities of fluid. Transabdominal ultrasonography
can be used to verify the presence of excessive fluid, and
an examination from both sides of the abdomen can be
helpful to eliminate the possibility of twins. Feces tend
to be covered with mucus because of prolonged passage
through the lower gastrointestinal tract. Ventral
abdominal rupture may result from the presence of an
excessive weight of fetal fluid, and there is a further risk
of uterine rupture. Affected mares usually abort, and
recommended treatment involves induction of parturi-
tion with administration of intravenous fluids and grad-
ual removal of excess allantoic fluid. The foals are often
abnormal and affected by a variety of congenital abnor-
malities.
VENTRAL BODY WALL HERNIAS AND
PREPUBIC TENDON RUPTURE
Defects of the abdominal wall in pregnant mares may
involve stretching and/ or rupture of the transverse
abdominus and oblique abdominal muscles, the rectus
abdominus muscles and the prepubic tendon. Apart
from those associated with hydropic conditions (see
above) or twin pregnancies, most cases occur in mares
close to term. Draft breeds and older mares appear to
be at greater risk. In extreme cases rupture may lead to
hemorrhage, shock, and death. Typical clinical signs
include a sudden change in the contour of the ventral
abdomen, ventral edema, reluctance to move, and
intermittent colic. If the prepubic tendon is ruptured,
the pelvis will appear tilted and a lordosis will be pre-
sent. The mammary gland may be displaced craniad
and ventrad because of loss of its caudal attachment to
the pelvis. Confirmation of the tentative diagnosis can
be difficult. Palpation of the defect per rectum is usually
not possible because of the advanced stage of preg-
nancy. External palpation is often unrewarding due to
321
OTHER CONDITIONS 17
CLASSIFICATION AND ETIOLOGY OF
PERITONITIS
Classifications of peritonitis are
primary or secondary - indicating the origin of the
disease
peracute, acute, or chronic - depending on the
onset and duration
diffuse or localized - indicating the region affected
Peritoneal fluid from normal foals is significantly dif-
ferent to adult horses with respect to total nucleated
cell count. In the foal, a nucleated cell count greater
than 1.5 x 10
9/1
(1500/1.11) should be considered as ele-
vated.
Dispersal of fluid within the peritoneal cavity is
rapid, aided by peristalsis and movement of the horse. It
is absorbed from the abdominal cavity mainly by lym-
phatic vessels beneath the mesothelial basement mem-
brane on the surface of the diaphragm. Small stoma in
the mesothelial lining provide access to the lymphatics.
The constant production and clearance of peritoneal
fluid ensures an effective clearance mechanism for bac-
teria, cells, and foreign material entering the peritoneal
cavity.
septic or non-septic - whether or not bacteria are
present.
Primary peritonitis (bacterial infection without an
obvious intraperitoneal source) is rare in adult horses
but may be associated with immunodeficiency or
immunosuppression.
Secondary peritonitis may be caused by numerous
diseases including external trauma, diseases of the gas-
trointestinal tract, breeding and foaling injuries, intra-
and postoperative infection, etc. (Table 17.4).
Peritonitis in the horse is most frequently secondary,
acute, diffuse, and septic. The severity of the disease is
related to a number of factors including the underlying
cause, the nature of the infectious agent(s), the resis-
tance of the host, speed of recognition and interven-
tion, and the response to initial therapy.
A variety of different bacterial species have been iso-
lated from the peritoneal fluid of horses with septic
peritonitis. Mixed bacterial infections are common.
Common isolates include
Escherichia coli
Streptococcus zooepidemicus
Staphylococcus spp.
Actinobacillusequuli
Rhodococccus equi
Bacteroides spp. (especially B. fragilis)
Peptostreptococcus spp.
Clostridiumspp.
Fusobacterium spp.
Peritonitis is an inflammatory disease. The inciting
cause, be it septic or non-septic, results in the activation
of macrophages and other cells, with the subsequent
release of eicosanoids, histamine, serotonin, and other
mediators. These lead to vasodilation and increased vas-
cular permeability followed by the migration of inflam-
matory cells and transudation of fluid containing fibrin
and clotting factors, complement and immunoglobu-
lins, into the peritoneal cavity. The inflamed peri-
toneum becomes a freely diffusible membrane,
allowing a massive outpouring of fluid and plasma pro-
teins from the circulation. This is a defensive reaction
that may result in the neutralization and phagocytosis
of bacteria, and rapid lymphatic clearance from the
abdomen. The fibrinolytic activity of mesothelial cells is
reduced and fibrin is deposited to seal off perforations
and to localize areas of infection. Intestinal ileus may
also occur as a result of sympathetic stimulation, and
this further helps to reduce dissemination of contami-
nated peritoneal fluid.
PATHOPHYSIOLOGY
Clear or slightly turbid
Straw colored or colorless
< 1.016
<25 gil (usually <15 gil)
(mainly albumin)
< 10.0 x 10
9
/1 (usually
< 2.0 x 109fl)
20-90% neutrophils
5-60% mononuclear/mesothe-
lial cells
0-35% lymphocytes
0-5% eosinophils
0-1 % basophils
Negligible
Negligible 0.1 gil) (does not
clot on standing)
5.0-6.4 mmol/l (90-115 mg/dl)
161-237 ~ m o (1.8-2.7 mg/dl)
3.9--8.2mmolll (11-23 mg/dl)
0.4--1.2mmolll (3.8-10.9 mg/dl)
5-13 ~ m o (0.3-0.8 mg/dl)
0-14 lUll
0-36 lUll
Grossappearance
Specific gravity
Total protein
Total red cell count
Fibrinogen
Total nucleated
cell count
Differential cell
count
Glucose
Creatinine
Urea nitrogen
Lactate
Total bilirubin
Amylase
Lipase
323
17 COlle
. .
.
.
.
'.> .
hi.
. .
Infectious or Septic Non-septic Parasitic Traumatic Iatrogenic
Surgical complications; Ruptured bladder,
ureter or kidney
Verminous Breeding or Recta! tear
arteritis foaling
-anastomosis failure injur Uterine
-non-viable tissue Parasitic laral perforation:
-poor asepsis migration Penetrating -Infusion
- wound infection and larval abdominal -biopsy
cathostomosis wound -AI
Intestinal accidents with
transmural movement of
bacteria
Chemical agents:
-bile
Perforating lesions
(ascarids, Blunt Enterocentesis
-gastric juice tapeworms) abdomina!
Abdominal, renal, or
retroperitoneal abscess
Uterine rupture
or perforation
Metritis
Urachal
infection
Postcastration
Enteritis
Septicemia
Cholangitis
- pancreatic juice
Foreign body
Neoplasia:
-ovarian
-abdominal
infection
If the peritoneal defenses are successful at contain
ing the inflammatory process, the disease may be con
trolled and a period of cellular repair begins with a
return of mesothelial cell fibrinolytic activity and
removal of fbrin deposits. However, if the defense
mechanisms arc ovenheImed or contamination of the
peritoneum continues, the inflammatol)' process per
sists and becomes generalized throughout the peri
toneum. Blockage of the lymphatic drainage channels
with fibrin and inflammatory debris leads to the accu
mulation of fluid and bacterial toxins within the peri
toneal cavity. Plasma sequestration within the abdomen
may result in the development of hypovolemic shock,
and absorption of bacterial endotoxins may result in
sew'n' metabolic derangements associated with endo
toxemia. Prolonged inflammation and fbrin deposi
tion may be followed by fbrous scarring and adhesion
foration (Plate 17.1).
324
trauma Cecal
trocharization
Ruptured
diaphragm Liver
biopsy
SIGNALMENT AND HISTORY
Peritonitis may occur in horses of either sex. and all
ages and breeds. A predisposing cause may be noted in
some cases, for example abdominal surgery, trauma,
breeding, or foaling injuries. Peritonitis secondar to
internal abscessation is most commonly seen in young
horses, less than 5 years of age. A prior respiratory infec
tion, such as Siuptococcus equi subsp. equi (strangles) may
have preceded the onset of peritonitis in some cases.
CLINICAL SIGNS
The presenting clinical signs in individual cases of peri
tonitis vary depending on the nature and extent of the
peritonitis, and t.he severity of systemic signs associated
OTHER CONDITIONS 17
with hypovolemia and endotoxemia. From a clinical
standpoint, cases may be classified as peracute, acute, or
chronic, although there can be considerable overlap
between these categories. Localized peritonitis may be
present with few or no overt clinical signs, whereas dif-
fuse septic peritonitis usually causes severe clinical dis-
ease.
Peracute peritonitis
In peracute peritonitis (e.g. following gastric rupture),
the horse may be found dead or present with profound
toxemia rapidly leading to circulatory failure and death
within a few hours. The clinical signs of peracute peri-
tonitis are
profound depression
cold extremities
congested to cyanotic mucous membranes
tachycardia
weak, thready pulse
tachypnea
sweating
colic
ileus
collapse
death within several hours
and are overshadowed by signs of endotoxemic and
hypovolemic shock.
Acute peritonitis
In acute peritonitis with diffuse bacterial contamination
of the abdomen, for example following perforation of
the gastrointestinal or female reproductive tracts, the
clinical signs may include
depression
colic
inappetence
pyrexia
congested mucous membranes
weak peripheral pulses
tachycardia
tachypnea
ileus or decreased gut sounds
reduced fecal output
excessive nasogastric reflux
abdominal distention
sweating
diarrhea
abnormal rectal findings
guarding of the abdomen
reluctance to move, defecate, or urinate
muscle fasciculations.
Acute peritonitis is, therefore, an important differ-
ential for horses presenting with colic, especially if
there is concurrent pyrexia. In the absence of thera-
peutic intervention, signs of endotoxemia and circula-
tory collapse become more pronounced and death may
ensue after a period of several hours to several days.
Chronic peritonitis
The clinical signs of chronic peritonitis may be low
grade and non specific, and include
depression
inappetence
progressive weight loss
reduced fecal output
low grade chronic or intermittent abdominal pain
persistent or intermittent pyrexia
decreased gut sounds
chronic diarrhea
ventral edema.
The presence and severity of these signs are very vari-
able from case to case.
INVESTIGATION AND DIAGNOSIS
The diagnostic procedures used in peritonitis are
abdominal paracentesis
hematology
serum/plasma electrolytes and biochemistry
rectal palpation
ultrasonography
urogenital examination
laparoscopy
exploratory laparotomy.
Abdominal paracentesis
A definitive diagnosis is usually made by examination of
peritoneal fluid (Plate 17.2). Abdominal paracentesis is
generally a safe and simple technique (see Chapter 2).
The peritoneal fluid should be collected into EDTA
and plain containers for cytology, gram stain and pro-
tein estimation, and into aerobic and anaerobic blood
culture bottles for bacterial culture. Use of an antimi-
crobial removal device may be helpful for culture of
fluid from horses that have already been treated with
antibiotics.
A diagnosis of peritonitis can frequently be made by
direct visual examination of the fluid. The fluid may be
yellow to white and turbid, indicating a high nucleated
cell count. If left to stand, the cells will settle at the bot-
tom of the container and fibrin clots may develop. If the
325
17 COLIC
fluid is shaken, the high protein concentration causes it
to froth. Alternatively, the fluid may be homogeneously
blood stained suggesting hemoperitoneum or intestinal
infarction, or turbid and brown-green in color suggest-
ing contamination with intestinal contents.
Normal peritoneal fluid usually has a total nucleated
cell count ofless than 2.0 x 10
9/1
with a predominance
of neutrophils (Table 17.3). Peritonitis is characterized
by an elevation of the total nucleated cell count (fre-
quently > 100 x 10
9
11) with a high proportion of neu-
trophils (frequently> 90%). In chronic peritonitis, in
addition to a neutrophil reaction, an increase in
macrophages or mononuclear cells, and the presence
of reactive mesothelial cells may be seen. Reactive
mesothelial cells may be mistaken for neoplastic cells,
and consultation with an experienced clinical patholo-
gist may be prudent in such cases.
Microscopic evaluation of the fluid is important in
addition to performing total and differential cell
counts. Toxic or degenerative changes to neutrophils
are common in cases of sepsis. Free or phagocytized
bacteria may be observed in a proportion of cases, and
gram staining can be helpful to guide the initial antimi-
crobial therapy. Bacteria will be cultured or identified
cytologically in only about 70 per cent of cases, and fail-
ure to identify or culture bacteria from peritoneal fluid
does not, therefore, rule out septic peritonitis. The
presence of multiple bacterial species during micro-
scopic examination or following culture usually indi-
cates intestinal leakage or rupture. The presence of
food material or intestinal protozoa indicates either
inadvertent enterocentesis or bowel rupture.
The normal total protein concentration of peri-
toneal fluid is less than 25 gil, and this rises rapidly in
acute peritonitis (frequently> 50 gil). Peritoneal fib-
rinogen concentration may be increased, especially in
chronic peritonitis; concentrations greater than 0.1 gil
(10 mg/dl) are significant. It should be noted that fib-
rinogen concentration will also be increased by blood
contamination of the sample.
Peritoneal pH and comparison of plasma and peri-
toneal glucose concentrations can also be useful to eval-
uate if the peritonitis is bacterial in origin. A
plasma-peritoneal glucose difference of greater than
2.8 mmol/I (50 mg/dl), or a peritoneal pH less than 7.3
with a peritoneal glucose of less than 1.7mmol/l
(30 mgld1) are both highly suggestive of septic peri-
tonitis.
Serial analyses of peritoneal fluid samples obtained
during the course of treatment are helpful in monitor-
ing the success of therapy. Serial cultures may be neces-
sary to identify emerging or resistant strains of bacterial
species. Bacterial cultures are frequently negative
despite the presence of bacteria in the peritoneal fluid.
326
In order to improve the culture rate, peritoneal fluid
should be collected into blood culture medium - if the
horse has already been given antibiotics, fluid should
first be passed through an antimicrobial-removal
device.
Hematology, serum/plasma electrolytes and
biochemistry
The hematological and biochemical changes that may
be seen in peritonitis are listed below, these changes
vary depending on the stage, severity, and type of peri-
tonitis.
Peracute peritonitis
1. Elevation of hematocrit and red cell figures occur as
a result of hemoconcentration.
2. Endotoxemia causes leukopenia, neutropenia, and a
degenerative left shift.
3. Plasma fibrinogen values are likely to be normal or
low.
4. Protein sequestration into the peritoneal cavity may
result in hypoproteinemia, but this is often offset by
the concomitant dehydration; serum protein levels
may, therefore be normal or elevated.
5. Electrolyte imbalances are often present, including
hypocalcemia, hyponatremia, hypokalemia, and
hypochloremia.
6. Metabolic acidosis.
7. Raised creatinine concentration as a result of pre-
renal or renal azotemia.
Acute peritonitis
1. There is often an initial leukopenia and neutrope-
nia, which is followed by leukocytosis, neutrophilia
and left shift.
2. Plasma fibrinogen will be normal in the early stages
of acute peritonitis, after which it is likely to be ele-
vated (up to 10 gil); it can take 48 hours for peak
concentrations to be reached.
3. Hypoproteinemia, often with a decrease in the albu-
min:globulin ratio, reflects protein sequestration
into the abdomen; if dehydration is present, hyper-
proteinemia may be observed.
4. Electrolyte imbalances may be present as for pera-
cute peritonitis.
Chronic peritonitis
Laboratory values are extremely variable.
1. Hematology may show normal white cell figures, or
there may be a leukocytosis and neutrophilia (with
or without a left shift). Occasionally a monocytosis
will be present.
OTHER CONDITIONS 17
2. There may be anemia due to chronic inflammation
and bone marrow suppression.
3. Plasma fibrinogen is likely to be elevated 5 gil).
4. Hyperproteinemia due to hypergammaglobuline-
mia may be present in some cases. The
albumin:globulin ratio may be decreased. Serum
protein electrophoresis may demonstrate elevation
of alpha, beta and gamma globulin ratios indicative
of chronic inflammation.
Rectal palpation
In peracute cases where there has been contamination
of the abdominal cavity with gastrointestinal contents, a
gritty feeling to the serosal surface of the bowel may be
felt, and in some cases crepitus may be present due to
free gas within the cavity. Distended large and small
intestine may occur secondary to ileus.
In acute and chronic peritonitis, rectal findings may
be non-specific. In many cases the examination will
elicit pain. An impression of bowel floating in abdomi-
nal fluid may be detected in some cases. Distended
bowel or secondary impaction of the pelvic flexure may
be palpable. In mares with uterine rupture, a fibrinous
adhesion may be identified over the affected area.
Occasionally abdominal masses or abscesses may be pal-
pated, and mesenteric lymph nodes may be enlarged.
Ultrasonography
Abdominal ultrasonography frequently reveals an exces-
sivequantityofhypoechoic to echogenic peritoneal fluid.
The echogenicity of the fluid increases with the cellular
content. In the presence oflarge amounts of fluid, loops
ofintestine and intra-abdominal organs appear separated
from one another and lifted from the ventral aspect of
the abdomen. Particles observed floating freely in the
peritoneal fluid may be caused by fibrin or ingesta. Fibrin
tags or adhesions between bowel and the parietal peri-
toneumor between the abdominal organs may be evident
in some cases. The presence of free gas in the abdominal
cavity is suggestive of either bowel rupture or the pres-
ence of gas-producing bacteria.
Urogenital examination
A urogenital examination should be performed in
mares with a history of recent covering or foaling to
identify vaginal, cervical, or uterine tears. Recently cas-
trated males should also be evaluated for an infected
castration wound.
Laparoscopy and exploratory laparotomy
Diagnostic laparoscopy is most helpful in cases of sus-
pected abdominal abscessation or neoplasia, where a
mass is palpable per rectum. Only the dorsal part of the
abdominal cavity can be explored in the standing horse,
allowing visualization of the serosal surfaces of the
colon, small intestine, and stomach, and parts of the
urogenital tract, spleen, and liver. The technique is con-
traindicated in cases where gross bowel distention or
adhesions are present in the area where the laparo-
scope is to be introduced.
Exploratory laparotomy (celiotomy) should be con-
sidered for diagnostic, therapeutic, and prognostic rea-
sons. The procedure should not be undertaken until
stabilization of the patient and treatment of hypov-
olemia and endotoxemia have been accomplished.
TREATMENT
Prompt and aggressive treatment is required. The treat-
ment objectives in peritonitis are to
reverse endotoxic and hypovolemic shock
eliminate infection
correct the primary cause of peritonitis
relieve pain
correct metabolic and electrolyte abnormalities
correct dehydration
correct hypoproteinemia
provide nutritional support.
The first treatment priority is to stabilize the patient.
Hypovolemia and endotoxemia need to be addressed
early and aggressively. Restoration of cardiovascular
function is essential before further treatment priorities
such as antibiotic therapy, peritoneal lavage and
drainage, and surgical treatments.
Fluid therapy
Intravenous fluid therapy is necessary to correct hypov-
olemia, metabolic acidosis, and electrolyte imbalances.
The principles of fluid therapy are described elsewhere
(see Chapter 9). Regular monitoring (every 4-6 hours)
of the packed cell volume (PCV), total plasma protein
(TPP) , blood gas analysis, and electrolyte concentra-
tions is necessary to assess the response to this therapy.
Plasma therapy
If the total plasma protein concentration falls to less
than 45 gil, slow intravenous plasma therapy (2-10
liters) is indicated to maintain plasma oncotic pressure
and to minimize the risk of pulmonary edema during
rehydration with intravenous fluids. Fresh equine
plasma is also beneficial in the treatment of endotox-
emia by supplying fibronectin, complement, antithrom-
bin III, and other inhibitors of hypercoagulability.
327
17 COLIC
Antibiotic therapy
Antimicrobial therapy should be initiated immediately
after peritoneal fluid samples have been obtained for
culture. Antibiotic therapy, therefore, needs to be
started before the results of culture and susceptibility
are available. In most cases of septic peritonitis a mix-
ture of gram-positive and gram-negative aerobes and
anaerobes will be present, and the antibiotic therapy
must have sufficient spectrum to control the antici-
pated flora.
Antimicrobial combinations commonly used in ini-
tial therapy include
I. Na.' or K+ penicillin 22000-44000 IV/kg i.v., q. 6 h
or
ceftiofur 2-4 mg/kg i.v., q. 8-12 h
plus
2. gentamicin 2.2 mg/kg i.v., q. 8 h, or
6.6 mg/kg i.v., q. 24 h
or
amikacin 6.6 mg/kg i.v., q. 8 h, or
15 mg/kg i.v., q. 12 h
plus
3. metronidazole 15-25 mg/kg p.o., q. 6 h.
This regime may be modified once the results of cul-
ture and sensitivity are available. These antibiotics will
achieve adequate levels within the peritoneal fluid,
intraperitoneal administration of antibiotics is there-
fore unnecessary.
Toxic side effects of aminoglycosides, especially
renal tubular necrosis, are important considerations in
the hypovolemic septic horse. Routine pharmacological.
monitoring should be undertaken in such cases to min-
imize the risk of toxicity.
Other antimicrobials that can be useful in the treat-
ment of some cases of peritonitis (dependent on the
culture and sensitivity results) include
Antibiotic therapy should be continued until the
clinical signs have resolved and clinicopathological
parameters (peripheral white blood cell count, plasma
fibrinogen, and characteristics of the peritoneal fluid)
are normal. Generalized septic peritonitis may require
antimicrobial therapy of 1-6 months.
Gastric decompression
Nasogastric intubation to allow gastric decompression
should be performed in all cases with evidence of gas-
trointestinal ileus. Repeated nasogastric intubation
every 3-4 hours, or placement of an indwelling naso-
gastric tube may be necessary in some cases.
Anthelmintics
Anthelmintic treatment is indicated in all cases with a
suspected parasitic etiology (verminous arteritis due to
migration of Strongylus vulgaris larvae or larval cyathos-
tomosis). Fenbendazole (10 mg/kg p.o. daily for 5 days)
or ivermectin (0.2 mg/kg p.o.) are recommended.
Analgesic and anti-inflammatorytherapy
Analgesics may be required to control the pain associ-
ated with peritonitis. Commonly used analgesics
include flunixin meglumine (0.5-1.0 mg/kg i.v.) and
xylazine (0.2-1.1 mg/kg i.v). Flunixin meglumine
should also be used for its anti-inflammatory and anti-
endotoxin effects; a dose rate of 0.25 mg/kg, q. 6 h is
effective for this purpose.
Heparin therapy
Heparin therapy has been recommended to prevent
adhesion formation and to render bacteria more sus-
ceptible to cellular and non-cellular clearing mecha-
nisms. A dosage of 40-80 IV/kg, q. 8 h is suggested.
Enrofloxacin should be used in adult horses only,
because of its adverse effects on cartilage in young
horses.
The duration of antibiotic therapy depends on sev-
eral factors including
the severity of the peritonitis
the underlying cause of the peritonitis
the degree of loculation of infection by fibrin
the etiological agents
the response to treatments.
I. sodium ampicillin
2. trimethoprim-sulfadiazine
3. enrofloxacin
25-100 mg/kg i.v.,
q. 6-8 h
15 mg/kg p.o., q. 12 h
1.5-2.5 mg/kg p.o.,
q. 12 h.
Abdo'minal drainageand lavage
The aims of abdominal drainage and lavage include
removal of bacteria, enzymes, and toxins from the
peritoneal cavity
removal of degenerative neutrophils and cellular
debris
removal of blood
removal of ingesta and foreign material
dilution of adhesion-forming substrates such as
fibrinogen and fibrin.
Although drainage and lavage can be performed rel-
atively easily, some doubts exist about how effectively
the large peritoneal surface area can be treated in this
way because of the size and limited access to many parts
328
of LIH: abdominal c.wity. In <dditioTl then. arc (OI}ccms
thal lavage may disseminatc a localized infection
throughout tht: (:avity. Oesl}ile these concerns peri.
tonciillavagc and drainage arc considered by man}' din
icians to be beneficial ill acute CaSCs of pcrilOllilis where
there is a purulell t effusion and poor response to initial
Tlt'<iicallhcrapy.
The process is usually performed 2-3 tinu:s a day fot'
2-3 days uTllil the pel;toneal fluid whitt cell count and
I()tal pn)tein concentration show an improvement.
Both peritoneallav.ge and rh"ainage em he perf<mned
c . fct\c1y using a single ingress! egress catheter placed
on (he ventral midline at the most dependent aspect of
I.he abdomen (Figure 17.4). Acmativdy, two catheters
(an he used - one egress calhettr on the .. entral mid
IiIH' and one ingress cathtI.(r in one of the paralurhar
fos 'a(. A variet of fcnc!trated drains can he used stich
a. a nmshroom crdin, thoracic ('annula (e.g. 32 French
gauge), Foley catheter, or sHrilized scgmfnI. of naso
gastric lube. After sedating the horse., the site for draill
ill,<rlion is prepared aseptically, and the . .kin and suh
CLH.aneous tissue is infiltrated with local anesthetic. A I
ern stab incision is made through the skin, subcma
)lelllIS {issue, and linea alba to allow insertion of the
drain. If a mushroom drain or Foley catheter is being
used, it can be stretched over a metal probe {sm:h a' a
felliale canine or Chambers marc catheter) l aid its
insertion. If the howel is inadvertently punnured dur
Illg insertion, the drain should not he removed until rht
iljlll) can be repaired surgically under general ane!
tbesia. The risk of penetrating rhf> bowel (or lIlcrwj in
the.' pregnant ran) can Iw rduced by uitrasono
graphic scanning of the area prior to placing the drain.
When rhe drain is being used as an ingnss cannula,
1 O-:O iilen of warmed Javag< solution (balanced
polyionic fluid) is infused, anrl the drain is flushed WiIh
heparinized saline and closed. If the horse stans to show
signs of abdominal discomfort when the fluid is being
infllsed, the infusion should be stoppd at a smaUer vol
lime Lhan intended. Heparin may he added t rhe lavagt'
fluid (5000 IU/l) in an allcrnpt to decrease peritoneal
flbrin formation and so to allow beltel' an:ess of amibi
otics lO the bacleria. The horse is then walked fur 15 to
30 minutes prior to opening th< catheter to allow the
fluid to drai n otLL The volume of fluid rC(lYered should
he measured; approximately the SaTJl( v(}lum should be
recovered as was infused. Following drainage, the
c.tfheter should be filled with heparin, closed and pr
a'ned with a sterile bandage Unit the neXllreatment. If
ahdominal pain occur when the lavage fluid is being
infused, the rate of infusion should be slowed, or tlll.
hors(' may be {f('awd \'lth an analgesic such as xylazinc.
Complications of peritoneal drainagc indude vis
rnal puncture during insertion, local subcutaneous tis-
OTHER CONDITIONS 17
Figur 17,4 Foley catheter inserted in the ventral midline
to permit abdominal lavage and drainage
sue irriracion and cellulitis. 2scending infection,
obstruction of the: drain hy fihrin, and hcrni<tion of
omentum OJ' illlcStine !hTO\lgh the drain or drditI .ite.
All horss treated by peritoneal lavage and dr.inagc arc
Sus(cplible to hemoconcentration, plasma protein loss
and electrolyte disturbances. FrequeIlt moniLOring of
these param(:ters, and. replat:cmcnt therapy as neces
sar, arc required.
The addition of povidone-iodine or antibiotics to the
lavage fluid is unnecesr and lIlay cause a chemical
peritonitis and increasen morbidity. Their usc is there
fore not recomm(:nded.
Surgical treatment
The aims of surgical therapy of peritonitis are to ideo
,.if' and rtJ'nove the source of abdominal (.oo1mination
and to remove seplic material. Many cases of peritonitis
will recover wlthout resorting to surgical invasion of lhe
abdominal cavity. although the source or peritoneal
contamination may remain undiagnosed. 1n those ca.es
where no underlying cause of the peritonitis (.an be
established, surgical explora{ion may help to identif
the <31lSe; however, in many other cases, no ohvious
source of contamination will be found. The decision to
perform or not to perform an exploratory laparotomy
can, therefore, he .. er difficult. Some surgeons may opt
to penorm surgery in ever C:' ie in the hope of identfy
ing and treating the underlying (ause. Alternatively,
surgical exploration of the abdOIIltn may be limited to
the following si tuations
I. cases where an abdominal mass of unknown etiolog
has been identifed
2. cases where an ahdominal abscess has been identi
fied and where surgical removal, drainage. or marsu
pialil. a(ion is considered possible
329
17 COLIC
3. mares with a ruptured uterus
4. cases with abdominal wall trauma
5. postoperative horses where anastomosis failure is
considered possible
6. cases where intestinal perforation is considered
likely (e.g. where food material or intestinal proto-
zoa are identified in the peritoneal fluid)
7. cases with severe and intractable or worsening
abdominal pain
8. cases where medical therapyand abdominal drainage
fail to result in improvement within 24-48 hours
9. cases which demonstrate a deterioration in the clini-
cal features, despite aggressive medical therapy,
within 12 hours.
Surgical exploration of the abdomen permits effec-
tive open abdominal lavage via the laparotomy wound.
Open peritoneal drainage via a small abdominal wound
loosely sutured with monofilament stainless steel reten-
tion sutures has also been described, but the risk of
ascending infection is considerable with this technique.
PROGNOSIS
The prognosis depends on many factors including the
etiology, severity, duration, and treatment. The mortal-
ity rates in published series of peritonitis range from 25
to 70 per cent.
No single clinical or laboratory parameter can be
used reliably in an individual case to assess the progno-
sis. However, horses with peracute peritonitis, and those
cases which show a poor response to initial therapy tend
to have the highest mortality rate. Horses with postop-
erative peritonitis are also reported to have a high mor-
tality rate. Other factors that may have a detrimental
effect on survival include severe endotoxemia, severe
dehydration, severe colic, laminitis, diarrhea, paralytic
ileus, and coagulopathies. Horses with peritoneal fluid
that has a very low glucose concentration also tend to
have a poorer prognosis. Abdominal adhesions or
abscess formation can also have a negative effect on
long-term prognosis.
Abdominal abscesses
T Mair
INTRODUCTION
Internal abscessation of the mesentery or of parenchy-
mous abdominal organs is recognized most commonly
330
as a complication of Streptococcus equi subsp, equi infec-
tion (strangles) (Plate 17.3). However, mesenteric
abscessation can also arise spontaneously in horses that
have no previous history of overt respiratory infection,
or as a consequence of intestinal leakage (e.g. following
penetration by a foreign body, or adjacent to an anasto-
mosis leakage) or surgical contamination. These
abscesses are most commonly located in the small
intestinal mesentery. Other bacteria that are commonly
isolated from mesenteric abscesses include Streptococcus
equi subsp. zooepidemicus, Escherichia coli, Salmonellaspp.,
Rhodococcus equi (in foals), and anaerobes.
Abscess formation following strangles is believed by
some to be more likely if the horse received inadequate
antibiotic therapy during the acute respiratory disease
(compared to horses that received no antibiotics at all),
but it may also occur in horses that received no treat-
ment during the acute stage of infection.
SIGNALMENT AND HISTORY
Horses of any age and either sex can develop abdomi-
nal abscesses, but they are most common in young
adults (less than 5 years of age). A history of recent
strangles infection (within the preceding few months)
may be present. In foals less than 6 months of age,
Rhodococcus equi infection may result in abdominal
abscessation, and these foals may demonstrate other
signs of pulmonary infection. A history of recent
abdominal surgery or castration may be significant.
Heavily parasitized horses may also be at increased risk
of developing abdominal abscesses, since migrating par-
asite larvae (large strongyles) can carry bacteria with
them as they migrate through the mesenteric tissues.
CLINICAL SIGNS
The clinical signs associated with abdominal abscesses
are very variable, and are dependent on the size and
position of the abscess, the degree of bowel involve-
ment, and the degree of associated peritonitis.
The common clinical signs include
chronic weight loss
inappetence or anorexia
persistent or intermittent pyrexia
pyrexia of undetermined origin
acute colic
chronic or recurrent colic
depression
diarrhea (especially foals infected by Rhodococcus
equi).
Colic may be caused by external cmnpnssiol ohhe
itllestinal lumen, tmction on th( mesenter. or adhe
sions l the intesLint or omentum (Plate 17.4).
Abscesses are an uncommon cause of acute colic, and
were recorded in 0.4 per cent of one large !ieries of sur
gicaJ colics compiled in the lSA.
DIAGNOSIS
Horses with abdominal abscesses can be diff iculllO dif
fen1l1iate from animals with otht!f <:auses of chronic
weight loss or chronic/imermittent colic (see The
difT{rentiaI diagnosis and evaluation of chronic and
recurrent colic), The following techniques ra)' he
help/iIi in making a rliagnosis
reClai examination
hematology :nd serum biochemistry
ahdominal paracenlesis
ultrasonography
laparoscopy
t"xpioralory laparotmy (celiotomy)
nuclear scintigraphy.
Rectal examination may reveal an abnormal mas"
that may be painful to palpation. These mases arC uSu
all) palpated in the midline or in the ventral qu:dranrs.
l.oups of adherent and distended small intestine may be
palpated acHacenr to the abscess. However. many
abs(:esses will not be palpabl<: per rectum.
Hematological changes are frequently non-specifc., hut
may include leukocytosis, neutro
p
hilia, monocytosis,
and hyerfbrinogenemia. J lyperproteinemia, hyper
globulinemia, hypoalbumincri:. and hypocalcemia
may be derccted by serum bim:hcmistl)'. Peritoneal fluid
changes are not consistenr in all cases, but there is lISll
ally evidence of low -rade peritonitis with elevated total
nucleated cell count, neutrophil count, and prolein con
centration. Bacteria are not reliably present in the fluid.
Allor th<se abnoralities may be _"cen ,,jlh other dis
east's, including some cases or abdominal neoplasia, and
differentiation ber'een absn:ssation and neoplasia can
be a significant challenge. Both neoplasia and abscessel
ra)' sometimes be present in the same horse.
Enlargement of the anorectal lymph nodes and sub
sequent abscess formacion can calIse excralumenal
obstruction of the rectum resulting in signs of abdomi
nal pain (see Chapter 16). Other clinical signs associ
<ted with the cOlldition include anorexia, lack of
production of feces, tenesmus. and pyn:xia. Anorectal
abscesses arc most (:ommonly identified -n foals, but
thf)' can sometimes anecl "dull horses. Sepsis can
extend inlO the peritoneal cavity causing septic peri
lonitis. Diagnosis of anorectal abscess at ion is confrmcd
OTHER CONDITIONS 17
Figure 17.5 Ultrasonogram obtained tramrectally showing
a large multilowlated post-castration absce55
by digital palpation per rcc[m, I.ransrectal ultrasonog
Tiphy. and ctologic examination of an aspirate or
biops)' from an affected lymph node. Peritoneal Auid,
obtained by abdominocemesis, should be examined
cytologically to determine if sepsis extends into the
abdomina! c:avit)
,
.
Lltrasound examination (transrcclal and/or trans
ahdominal) may he helpful. espc(:ially if a ma is palpa
ble per rec:rum. Post-c<!lration (including
cl)'prorchidt:cr
,
omy) abscesses are usually located adja
cent to one inguinal canal (Figure 17.5). Mesenteric
abscesses may he difficuh to image. depending on their
location. Confirmation of an ahdominal abscess may
require surgical exploration, eithcr by ... ay of diagnostic
laparoscopyor exploratory laparotomy (celiotomy).
udcar scintigraphy using tcchnctium-99m labeled
white blood cells can sometimes be used to identif an
abscess lhat cannot be localized by other tt:chniqm::s
(see Chapter 2).
TREATMENT
SuccessrUI treatment may be achieved in some (ases by
prolonged antibiotic therapy. AtteIC1pts to culture the
offending organism should always be made to help
select the appropriate anlibiolic(s). Peritoneal fuid
should be collccted for bOlh aerobic and anaerobic cul
ture. If feasible. a needle aspirace of the absccss should
be made percultlncously, utili1ing ultrasound guidance.
Aternativdy. samples llIay be obtained by centesis via
exploratory laparotomy (cdiotomy) or laparoscop)'.
Antibioric therapy will be re
<
uiced fOT C minimum of 30
days, and not infrequently for 2- months. Procaine
penicillin (22000 Ie/kg b.i.d. Lm.) is the antibiotic of
choice [or cases involving St-ttor.oCCU. equi. However,
331
17 COLIC
prolonged courses of intramuscular penicillin are likely
to result in muscle soreness and resentment by the
patient. Switching to an oral antimicrobial medication
is preferable in horses that require prolonged courses
of antibiotics. Potentiated sulfonamides (30 mg/kg
s.i.d. or b.i.d.), enrofloxacin (7.5 mg/kg s.i.d. or 4.0
mg/kg b.i.d.), metronidazole (15 mg/kg q.i.d. or 20-25
mg/kg b.i.d.) and rifampicin (5.0-7.5 mg/kg b.i.d.)
can be useful in this regard. Treatment should be con-
tinued until such time as the clinical and laboratory
changes (including fibrinogen) have returned to nor-
mal. If the abscess is palpable per rectum or can be
imaged by ultrasound, treatment should be continued
until such time as the abscess is no longer appreciable.
In foals with suspected or confirmed Rhodococcus equi
infection, oral treatment with erythromycin ( 25 mg/kg
t.i.d.) and rifampin (5-10 mg/kg b.i.d.) is indicated.
Other treatments for peritonitis (see Peritonitis)
may be indicated depending on the degree of peri-
toneal inflammation and sepsis.
Surgical therapy is frequently not possible owing to
the location of the abscess, but may be indicated in
some circumstances. In particular, surgery may permit
intestinal by-pass in cases of small intestinal
obstruction
abscess resection
abscess drainage by needle aspiration
marsupialization of abscess to the body wall.
PROGNOSIS
The prognosis for horses with abscesses uncomplicated
by intestinal obstruction is guarded to good. Many such
horses will recover with prolonged medical therapy. In
one report of 25 cases of abdominal abscesses, 17 of the
horses recovered following prolonged antibiotic treat-
ment. A clinical or laboratory improvement after 2
weeks of treatment is a positive and encouraging sign.
The prognosis is much poorer in cases where intra-
abdominal adhesions form. The prognosis for foals
affected by Rhodococcus equi mesenteric abscessation is
generally very poor.
Hemoperitoneum
'UP
FT Bain
CAUSES
Hemoperitoneum (hemorrhage into the peritoneal
cavity) can be caused by a variety of conditions in horses
332
Neonate
Rupture of umbilical vessels
Rupture of spleen
Fractured ribs
Older foal and adults
Idiopathic
Splenic rupture
Hepatic rupture
Kidney rupture
Uterine or ovarian artery rupture
Coagulopathy
Idiopathic -associated with liver orkidney biopsy
post-surgery
Splenic and other neoplasia
Lacerated iliac artery (pelvic fracture)
of all ages. Some of the common causes of hemoperi-
toneum are listed in Table 17.5.
In neonates, rupture of the internal umbilical struc-
tures is the most common cause of hemoperitoneum.
Hemoperitoneum can also occur secondarily to rup-
ture of the spleen or liver, or it can be caused by frac-
tured ribs and diaphragmatic tearing during dystocia.
In older foals and adult horses, idiopathic hemo-
peritoneum is occasionally seen as a clinical entity; this
appears to be most common in older horses, rupture
of a mesenteric vessel being suspected in these cases.
External trauma can also result in hemorrhage into
the peritoneal space of foals and adults as a result of
rupture of the spleen, liver or kidney, or due to frac-
ture of one or more ribs. Hepatic rupture may also
occur in association with hyperlipemia and fatty infil-
tration of the liver (see Chapter 19). A common cause
of hemoperitoneum is hemorrhage from the uterine
or ovarian artery in aged brood mares during the peri-
partum period. In the male horse, severe abdominal
hemorrhage following castration may occur occasion-
ally, although the more common hemorrhagic compli-
cation following castration is external hemorrhage.
Almost all horses have some blood in the abdomen fol-
lowing castration. Intra-abdominal hemorrhage due to
severe coagulopathy may also be considered (although
this is not as common as arterial rupture), and it can
occur iatrogenically after biopsy procedures on the
liver or kidney. Abdominal neoplasia may cause intra-
abdominal hemorrhage because of invasion and rup-
ture of local vessels or hemorrhage from the tumor
itself; the latter occurs commonly in cases of heman-
giosarcoma (Plate 17.5).
OTHER CONDITIONS 17
CLINICAL SIGNS
The most common clinical signs of hemoperitoneum
are those related to hemorrhagic shock due to acute
loss of blood volume
profound sweating
tachycardia
tachypnea
weak peripheral pulses
pale mucous membranes
trembling
distress.
In some situations, there are signs of abdominal
pain, and some horses with intra-abdominal hemor-
rhage may resemble a horse affected by severe colic.
Abdominal distention may also be seen.
DIAGNOSIS
The most useful and rapid diagnostic aid for hemoperi-
toneum is the abdominal ultrasound examination
(Figure 17.6). A routine, comprehensive evaluation of
the abdomen should be performed including imaging
both sides of the abdomen to include a scan of all major
anatomic structures of the patient. In peripartum
brood mares, this includes examination of the caudal
flank and inguinal areas for evidence of a hematoma in
either uterine broad ligament. In all patients, the
spleen should be examined closely for any evidence
that it is the origin of the hemorrhage. Tears of the cap-
sule of the liver or spleen can sometimes be appreciated
Figure 17.6 Ultrasonogram of the abdomen in a horse with
hemoperitoneum showing a large quantity of echogenic
peritoneal fluid
by ultrasonography. The ultrasound appearance of
hemorrhage is that of a cloudy, homogenous echogenic
swirling fluid (swirling in a manner similar to smoke
which is very characteristic of active bleeding). The ori-
gin mayor may not be evident, but the swirling may be
most active adjacent to the ruptured vessel. Clotted
blood may gravitate ventrally and be seen as variably
dense, laminated, echogenic material beneath a more
echolucent fluid (Figure 17.6). In neonates, the umbil-
ical structures should be closely examined.
Abdominocentesis may be useful for diagnosis and
characterization of hemorrhage. The presence of
platelets may reflect recent or active hemorrhage,
whereas the presence of erythrophagocytosis suggests
that the blood has been present for at least several
hours. Cytologic identification of inflammatory cells
may suggest rupture of an organ such as the uterus or
bowel in a postpartum mare. More often abdominocen-
tesis with cytologic evaluation is helpful in identifying
the complicated hemorrhagic abdominal effusions
other than simple vascular rupture.
TREATMENT
The treatment options for hemoperitoneum are
keep patient quiet
intravenous fluid therapy with
whole blood
polyionic fluids
polymerized bovine hemoglobin
fresh plasma
autotransfusion
corticosteroids
naloxone
epsilon-aminocaproic acid
analgesics
intra-nasal oxygen
surgery.
Treatment of the hemoperitoneum depends on the
origin of the hemorrhage as well as the severity of blood
loss. In patients with acute hemorrhagic shock, replace-
ment oflost blood volume and oxygen-carrying capacity
is critical. In certain situations, medical treatment alone
is deemed best. This includes most mares with sus-
pected uterine artery hemorrhage where surgical explo-
ration may be ineffective and result in additional and
possibly fatal hemorrhage. In some foals, medical man-
agement alone is useful. Application of a belly wrap or
abdominal support bandage may be helpful in increas-
ing intra-abdominal pressure and reducing hemor-
rhage. Transfusion with compatible, fresh, whole blood
is the most common approach. This provides oxygen-
333
17 COLIC
INTRODUCTION
M Hillyer
Gastrointestinal neoplasia
Reported sites of
occurrence
Mesentery
Wall of small and large
intestine
Stomach
Small and largeIntestine
Small and large Intestine
Duodenum
Jejunum
Small colon
Stomach
Duodenum
Jejunum
Rectum
Large Intestine
Cecum
Not specified
Neurofibroma
Myxosarcoma
Adenosarcoma
Lymphosarcoma
Adenocarcinoma
Leiomyoma
Leiomyosarcoma
Lipoma
Primary gastrointestinal
neoplasms
Neoplasia ofthe gastrointestinal tract of the horse is not
common. While neoplasms have been reported in
almost all of the tissues of the equine gastrointestinal
tract, some locations and types of neoplasia are more
common than others, the common types tending to
produce characteristic syndromes with typical clinical
signs. The recognition of such signs in a horse helps to
raise the index of suspicion of a gastrointestinal neo-
plasm, in turn allowing a more targeted approach to the
investigation and an earlier diagnosis. For example, the
presence of chronic weight loss, recurrent colic and/or
choke after feeding, and fecal occult blood would raise
the suspicion of a gastric carcinoma, while an acute
strangulating obstruction of the small intestine in an
aged pony would be suggestive of a strangulation by a
pedunculated lipoma. These 'typical' scenarios are
described later in this section.
these patients. Abdominal ultrasound remains a critical
diagnostic tool for this problem.
carrying capacity as well as fresh coagulation factors
from the plasma. Time is often a factor in the acquisi-
tion of whole equine blood since storage of equine
blood is not practiced. In some instances, the adminis-
tration of polymerized bovine hemoglobin (Oxyglobin,
Biopure Corporation, Cambridge, MA, USA) may be
effective in providing sufficient oxygen-carrying capac-
ity until whole blood transfusion can be arranged. The
author has used doses of 7.5-15 ml/kg in foals with
hemoperitoneum with beneficial effects as evidenced
by decreased heart and respiratory rates and improved
attitude and alertness.
The question of fluid resuscitation in hemorrhagic
shock is a controversial one. The phrase 'hypotensive
resuscitation' has been discussed in the literature. This
is based on the concept that rapid normalization of
blood pressure may lead to dislodgment of the develop-
ing clot and further bleeding. An extensive discussion
of the therapy of hemorrhagic shock is beyond the
scope of this section, however it is worth noting that this
concept may be critical to the outcome of the patient in
some situations. Another modality for transfusion ther-
apy in these cases is autotranfusion. This can be accom-
plished with the use of a variety of vacuum blood
collection systems with an anticoagulant (approxi-
matelyone fifth of the quantity normally used for whole
blood transfusions) and filtered administration set.
Concern for infection is critical and evaluation of the
collected blood for leukocytes and evidence of sepsis is
mandatory prior to readministration.
Medications that are considered supportive of hem-
orrhagic shock include corticosteroids (prednisolone
sodium succinate 2 mg/kg) and naloxone (0.03 mg/kg
i.v.). Aminocaproic acid has been used as an inhibitor
of fibrinolysis in hemoperitoneum due to uterine artery
rupture in the mare at an initial dose of 20 g/450 kg (in
fluids) followed by 10 g/450 kg q. 6 h (in fluids). The
use of hypertonic saline and colloid fluids is considered
controversial because of the rapid rise in arterial blood
pressure caused by these fluids. Fresh plasma may be
beneficial in replacing clotting factors lost into the peri-
toneal space during massive hemorrhage.
In some patients, the decision for surgical explo-
ration might be necessary. This will depend on the clin-
ical determination as well as ancillary diagnostic aids
that indicate a reasonable ability to identify the source
and control the hemorrhage. Drainage of the blood
may be required in order to lessen abdominal pain, but
this should not be performed routinely as the fluid pres-
sure in the abdomen may slow the bleeding and some
of the red cells may be resorbed.
The most critical factor of all is the early recognition
of hemoperitoneum as the cause of the clinical signs.
Delayed recognition is a common cause of death in
334
OTHER CONDITIONS 17
Secondary gastrointestinal neoplasms
Melanoma
Mesothelioma
Testicular seminoma
Teratoma
Transitional cell carcinoma
Gastrointestinal neoplasms are usually classified
according to their cell type and site of origin (Table
17.6). This section will concentrate on the primary neo-
plasms, although metastasis to the gastrointestinal tract
of other tumors may also occur (Table 17.7).
PREVALENCE
Previous reports of equine pathology studies suggest an
estimated incidence of gastrointestinal neoplasia of less
than 0.1 per cent of routine post-mortem examinations
and about 5 per cent of horses with clinical signs of
abdominal disease.
The most common neoplasm of the gastrointestinal
tract is the mesenteric lipoma. However, it is often clin-
ically insignificant and therefore not included and
hence under-represented in many surveys of abdominal
neoplasia. When significant the lipoma may produce
signs only related to its physical properties, namely as a
space-occupying mass causing a simple intestinal
obstruction, or more commonly as a pedunculated
mass causing a strangulating intestinal obstruction.
The two most frequently reported neoplasms of the
equine gastrointestinal tract are the gastric squamous
cell carcinoma and the alimentary lymphosarcoma
(although most surveys of gastrointestinal neoplasia
have failed to record lipomas). It is probable that there
is an approximately equal prevalence of both of these
tumors, but it is interesting to note an apparent higher
incidence of gastric squamous cell carcinomas in North
America, while the alimentary lymphosarcoma may be
relatively more common in Europe.
ETIOLOGY
Aswith many neoplasms in other species, the etiology of
gastrointestinal neoplasia in the horse is still poorly
understood. Gastric squamous cell carcinomas have
been associated with geographical areas and linked to
conditions causing chronic gastric mucosal irritation
such as parasites and physical irritants, but the true
etiology is likely to be multifactorial. The etiology of
lymphosarcoma and the other gastrointestinal neo-
plasms is presently unknown.
PRESENTATION AND CLINICAL SIGNS
Horses with a gastrointestinal neoplasm will usually pre-
sent with a chronic and insidious history of weight loss.
Weight loss will usually be seen as a result of one or
more of the following events
reduced feed intake
altered digestion and/or absorption from the
intestinal tract
increased protein loss into the intestinal tract or
peritoneal cavity
increased nutrient requirements of the neoplasm
altered energy requirements as a result of effects of
the neoplasm.
Recurrent colic, diarrhea, and poor performance or
exercise intolerance may also be features of gastroin-
testinal neoplasia, together with an intermittent
pyrexia. Typically the neoplasms occur in mature or
aged animals.
The exception to this is the pedunculated mesen-
teric lipoma causing an intestinal strangulation and
signs of acute colic, described in more detail elsewhere
(see Chapter 13).
INVESTIGATION
Clinical signs and history
As previously stated, horses with a gastrointestinal neo-
plasm will usually present in poor body condition with a
history of progressive weight loss. Careful questioning
of the owner may be needed to elucidate other signs
such as reluctance to feed, low grade abdominal dis-
comfort, or altered fecal consistency. An intermittent
pyrexia may also be present. Physical examination of
the horse is often unrewarding but is essential, together
with a thorough history, in order to eliminate other
more common causes of weight loss (see also Chapter
18) such as
inadequate or unsuitable feeding
dental or swallowing disorders
excessive exercise/energy demands
parasitism.
In addition the clinical examination may reveal the
involvement of other tissues/organs as well as the gas-
trointestinal tract.
335
17 COLIC
Clinical pathology (see Chapter 2)
Non-specific changes are often seen in the clinical
pathology results from blood samples of horses with gas-
trointestinal neoplasia.
Anemia may be present as a result of non-specific
chronic inflammatorydisease orin association with blood
loss. The blood loss may be marked as in cases of gastric
squamous cell carcinoma where red cells may be lost into
both the bowel lumen and the peritoneal cavity.
White blood cell parameters are usually normal or
may reflect the chronic inflammation which may
accompany a gastrointestinal neoplasm. Intestinal lym-
phosarcoma will rarely be associated with abnormal
lymphocytes circulating in the blood.
Reduced plasma protein concentrations may be seen
in conjunction with the weight loss and altered nutrient
metabolism. Low albumin concentrations are often
seen with malabsorption syndromes/protein losing
enteropathies such as the diffuse intestinal lymphosar-
coma. However, in many cases the total protein concen-
tration remains in the normal range as a result of
increased globulin concentrations associated with the
chronic inflammatory response.
Increased concentrations of the intestinal fraction of
the alkaline phosphatase enzyme (lAP) may also indi-
cate the presence of intestinal disease.
Hypercalcemia has been reported in association with
both lymphosarcoma and gastric carcinoma.
Rectal findings (see Chapter I)
Rectal examination is essential in the investigation of any
case with suspected gastrointestinal neoplasia. Although
normal findings may be present in many animals, an
increased volume of peritoneal fluid, distention of the
intestine, or an abnormal tissue mass or masses will
increase the index ofsuspicion of gastrointestinal disease
and allow further directed investigations to be selected.
Abdominal paracentesis (see Chapter 2)
Collection of a sample of peritoneal fluid is another
important part of the investigation of a case of sus-
pected gastrointestinal neoplasia. Many cases, such as
intestinal lymphosarcoma or adenocarcinoma, may
have normal or non-specific inflammatory peritoneal
fluid. But other cases, typically the gastric squamous cell
carcinoma, may have exfoliated neoplastic cells in the
peritoneal or pleural fluid from which a diagnosis of
abdominal neoplasia may be made.
Ultrasonography (see Chapter 2)
Percutaneous or per rectum ultrasonography can pro-
vide additional information on the volume and charac-
336
ter of the peritoneal fluid. Intestinal distention may be
recognized together with abnormal bowel wall thicken-
ing and abnormal tissue masses. Ultrasonography also
allows guided collection of fluid or tissue samples for
further evaluation.
Laparoscopy (see Chapter 3)
Laparoscopic examination of the equine abdomen is a
useful minimally invasive technique for visualization of
the abdominal organs and for collection of tissue sam-
ples for histological examination. The primary site of
the neoplasm may be seen or secondary effects such as
bowel obstruction or abdominal metastasis recognized.
OTHER INVESTIGATIONS
Sugar absorption tests (see Chapter 2)
Glucose or xylose absorption tests are useful to demon-
strate a state of malabsorption from the small intestine
that may occur with a diffuse intestinal lymphosarcoma.
Although not diagnostic, a reduced uptake curve of the
sugar is highly suggestive of an infiltrative condition of
the small intestine.
Nuclear imaging (see Chapter 2)
Despite not being widely available the use of radio-
labeled markers may provide a novel method of identi-
fying a gastrointestinal neoplasm.
Exploratory laparotomy/celiotomy
Although expensive and highly invasive, exploratory
laparotomy provides the ultimate method for explo-
ration of the abdomen and collection of tissue samples
for histological examination. In clinical practice it is
often used as the last stage of the investigation, when
other, less invasive, techniques have failed to give a
definitive diagnosis. It also may provide the opportunity
for surgical removal and hence treatment of a discrete
neoplasm. Laparoscopy may allow direct visualization of
a neoplasm/mass and biopsy in some cases without
needing to resort to a laparotomy.
CASE SCENARIOS
Mesenteric lipoma (Figure 17.7)
Mesenteric lipomas
are often clinically insignificant in older horses
occasionally cause a simple intestinal obstruction
usually cause a strangulating intestinal obstruction
OTHER CONDITIONS 17
affect middle-aged and older animals, especially
ponies
have an acute onset colic related to intestinal
obstruction
are successfully removed by early surgery.
Figure 17.7 Post-mortem photograph of a pedunculated
lipoma causing a small intestinal strangulation in an aged
pony
Gastric squamous cell carcinoma (Figure 17.8)
Features of gastric squamous cell carcinomas include
the following:
they affect middle-aged and older horses
there is a proposed increased incidence in males
weight loss and inappetance are major features
pyrexia and colic are also common
esophageal involvement may cause recurrent choke
anemia is often a marked feature
they are usually exfoliative therefore abdominal or
thoracic paracentesis is often diagnostic
Figure 17.8 Post-mortem photograph of a gastric squa-
mous cell carcinoma in the stomach of a horse
local metastasis is common and abnormal tissue
masses may be palpable per rectum
gastroscopy allows identification and biopsy of the
neoplasm
a primary mass on the greater curvature of the
stomach may be identified by ultrasound or
visualized laparoscopically.
Lymphosarcoma (Figure 17.9)
Features of lymphosarcomas include the following:
any age of horse can be affected, often young adults
progressive weight loss is the major sign and may be
the only sign
diarrhea may be present if the large intestine is
involved
hypoalbum0 0909 Td26d(i4a5e)Tm(v418.64 Tmr9(the)Tj8sual48.8Tmd4c5.8 407.9728 578.64 Tm(8.8oma)TjTd(0 8.m(Lym26[(may)-3r 0 8.8 448.431gu.0419(any)-3293(is5248 Tc -20.373 -1.255 Td()Tm(v418.329293(is5248 Tc67 Tmny)51.255 Td8sual48.8Tm8 4618.3565782 606.48 T2 T8.8Tj0 Tc -18.25 -y)-(on66.96 5.2677 589.T8.85898 57(be)].08 668.8 30.25 -y)-(o373 -1.2558be)]T05 005 Tc 9.um(ol05 Tc 9.5571 0 1436Tj8sual48. 4849430.25 -y)-(o Td()Tj0.05 Tc 8.9809 29.167Tc 5 0 2(the)Tj8.9087 0.1388 666.4597 0 0 822 55508 5 0 2(the)suga8 0 0 896535 Tc 10.02.7306jor) 0 2(the)absorpTJ0.05 T3 606.48 Tm(the)T.16 8 30 0 2(the)373 -1.2558be)]T05 085 Tc 9.um(ol05 Tc 9.4998 309.35m[(39 kedl 0 0 8.8 377.4118 34oma)TjTdTc 38 30 0 2(the)decTc sm(Lymphosarcoma)Tj/T1_90 T08 30 0 2(the)3f0 0 8.8 377.41124597 0 0 822 8.8 -18.2547 556.56 Tm(ifTj0.05 Tc 9.1071 0 0 6308.7.2547 556sm(ol.9087 0.1388 66(8.8oma)TjT340 8.82.7.2547 556)-3r 0 8.8 448.431gu.0419(any)8 66728 30.2547 556)73 -1.25e)Te)]T05 Td((is5248 Tc67 Tmny)51.250i98sual48.8Tm8 4618.3565782 6066.9728 578.622 556jor)016 606.48abdo.26al.9087 0458.8 0 0 8.8 348.93Tc5 -18016 606.48414ace-3r i 8.8 466.65.6is)]TJ0iTj9.0044 0 0 81v41809 Td26d2.6711 -016 606.480 0 8.8 4Tm( 8.8 397.834316 f)T -016 606.48normal.90870.05 Tc 8.9809 29.17358.490048(the)Tj8.9087 0.56ss)-326(85 Tc 9.r Tcal.9087 0.1388 694(involved)Tj3Tc 2 8.490048(the)exa.26aTJ0.05 T3 606.48 Tm(the)80 Tc Td490048(the)iTj9.0044 0 0(th145.206 0 Td(Tc 389d490048(the)0 0 8.8 4Tm( 8.8 397.83416 48)T 490048(the)normal.90870.05 Tc 8.9809 29.17358.41.50 8.8 37 0 0 8994524Tj/T1_1 1 Tf-95e)Tj8sual43m(8708.41.50 8.8 tine)Tjic 589.68 T0.05 Tc 9.1071 0510.56.41.50 8.8 tpaTJe-3Tj9.004j-8 309.7885 Tc 9.r Tcal.9087 031 1 Tf2556j5 Tc 9.biops6 Tm(the)Tc (is)]TJj0.0248 Tc -20.373 -)Tj0.03.40m[(inegno 0 c Tmny)51.25969433 556.56 Tm(large)Tj8338ss)-326e
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OTHER CONDITIONS 17
persists for 48 hours or longer. Recurrent colic refers to
bouts of abdominal pain which recur at variable inter-
vals from hours to days to weeks. As with other types of
colic, the abdominal pain usually emanates from the
gastrointestinal tract, but may also arise from other
body systems.
The diagnosis of the cause of chronic and recurrent
colic can be difficult to achieve, even after exhaustive
investigations including, in some cases, surgical explo-
ration of the abdomen. Chronic and recurrent colic
cases are often frustrating to deal with, but the under-
standable concern of owners place the veterinarian
under some pressure to find an explanation for the
clinical signs. Pregnant mares affected by recurrent
colic seem to be at increased risk of abortion and
owners of such animals should be made aware of this
possibility.
CAUSES OF CHRONIC AND RECURRENT
COLIC
Abdominal pain is usually caused by one of the follow-
ing mechanisms
bowel wall (mural) stretching
mesenteric traction
mucosal, parenchymal, or peritoneal inflammation.
Stretchingof the bowel wall
The majority of conditions causing stretching of the
bowel wall and chronic pain are forms of simple
obstructions. Strangulating obstructions and infarctive
conditions usually have a much more rapid course and
are unlikely to lead to chronic or recurrent pain. These
simple obstructions can be physical (e.g. gastric and
colonic impactions or ileal muscular hypertrophy) or
functional (e.g. spasmodic colic).
Mesenteric traction
Conditions that result in pain due to traction on the
mesentery include chronic impactions, neoplasia,
abscessation, and splenomegaly.
Inflammatory lesions
Mucosal inflammatory diseases include sand irrita-
tion, colitis, and cyathostomosis. Parenchymal inflam-
matory disorders include hepatitis and cholangitis.
Peritoneal inflammation can be caused by septic peri-
tonitis, abdominal abscessation, and intra-peritoneal
neoplasia.
The common causes of chronic and recurrent colic
are listed in Tables 17.8 and 17.9.
Gastric Condjtjons
gastric ulceration
squamous cell carcinoma
chronic gastric impaction
Partial gbstructjonsQf the bowel lumen
Small intestine
pyloric/duodenal stenosis
ileal hypertrophy
hypertrophy of cecal mucosa
intestinal neoplasia (Plate 17.6)
ileocecal intussusception
other ileocecal obstructions
adhesions
mesenteric abscess
Meckel's diverticulum
Large Intestine
cecocecal intussusception
cecocolic intussusception
recurrent large bowel displacements, e.g.
nephrosplenic entrapment
colonic torsion (180or less)
enteroliths
adhesions
diaphragmatic hernia
sand impaction
Inflammalgrydjseases
cyathostomosis
colitis
NSAIDtoxicity/right dorsal colitis
MotUtty
spasmodic colic
cranial mesenteric arteritis
thromboembolic disease
chronic grass sickness
cecal dysfunction
color'lic impaction
small colon impaction
INVESTIGATION OF CHRONIC AND
RECURRENT COLIC
The clinical examination of the horse with chronic or
recurrent colic is similar to that carried out in horses
with acute colic (see Chapter 9). Following a routine
clinical examination it will often be determined that
immediate surgery is not required and that time is avail-
able to undertake further diagnostic tests and labora-
tory investigations. Clinical examination of horses
demonstrating recurrent bouts of transient colic
339
17 COLIC
Liver conditiqos
hepatitis
cholangitis
cholelithiasis
Pancreas
chronic pancreatitis
pancreaticneoplasi.a
Urogenjtjl tract
cystitis
urolithiasis
bladder neoplasia
ovulation
granulosa cell tumor
testicular teratoma
SW.un
splenic neoplasia (lymphosarcoma,
hemangiosarcoma)
splenic hematoma
splenomegaly
Perjtqoeal cAvity
peritonitis
intraperitoneal abscess (Plate 17.7)
intraperitoneal neoplaSia
ThorAcicdjsejse
pericardial effusion
pleuritis
should, wherever possible, be undertaken during an
episode of abdominal pain.
The evaluation of horses with chronic and recurrent
colic may include some or all of the procedures listed in
Table 17.10. A careful assessment of the history and a
thorough clinical examination are essential compo-
nents in every case.
History
Pain
The onset of pain associated with lesions such as intus-
susceptions is frequently sudden; there may be an initial
episode of severe pain, followed by milder and inter-
mittent bouts of colic. With other slowly developing
lesions, such as neoplasms, the onset of clinical signs is
usually more insidious. An increasing frequency of
recurrent bouts of colic with a shorter time interval
between bouts may indicate a progressively worsening
obstruction of the bowel lumen (e.g. external compres-
sion from a space-occupying mass or an intramural infil-
340
History
pain -duration
onset
frequency
time interval between bouts
is it related to feeding?
previous medical - previous abdominal
history surgery
previous colic history
respiratory infections
drug therapies (e.g.
NSAID)
weight loss
in-contact horses
management - exercise
grazing
anthelmintic treatments
dental prophylaxis
nutrition
access to water
Signalment
age
color
Clinical examination
gastrointestinal tract
other body systems
Laboratory investigations
hematology
biochemistry
monosaccharide absorption tests
fecal analysis
Abdominocentesis
Endoscopy
Radiography
Ultrasonography
Biopsy
Response to treatment
Diagnostic laparoscopy
Exploratory surgery
trate). Bouts of pain that show an association with feed-
ing may indicate gastric ulceration, neoplasia, or a par-
tial obstruction of the bowel lumen. Recurrent bouts of
pain in mares at regular intervals of about 3 weeks
would suggest ovulation-related pain.
In recurrent colics it is useful to know the duration
of bouts of pain and whether or not the pain resolves
OTHER CONDITIONS 17
spontaneously, and also whether or not the pain
responds to simple spasmodic drugs.
Previous medical history
Previous abdominal surgery or injury can predispose to
intra-abdominal adhesions, which can result in recur-
rent bouts of pain. Likewise, a history of previous peri-
tonitis or abdominal abscessation might indicate the
possibility of adhesions or recurrence of the original
disease. A history of a respiratory infection (especially
strangles) in the recent past could suggest the develop-
ment of an abdominal abscess.
The recent or current administration of drugs
should be recorded. Non-steroidal anti-inflammatory
drug (NSAID) therapy can predispose to gastrointesti-
nal ulceration. Recent administration of an
anthelmintic might suggest a parasite-associated prob-
lem (such as cyathostomosis).
A history of chronic or recent weight loss may be pre-
sent in cases of abdominal neoplasia, abscessation, and
chronic peritonitis.
In-contact horses
Similar disease problems in in-contact horses is suspi-
cious of infectious, parasitic, nutritional, toxic, or man-
agement problems.
Management, nutrition, and access to water
Access to and quality of water should be evaluated.
Inadequate access to water can predispose to intestinal
impactions. Rations excessively high in carbohydrate
can result from overfeeding grain and concentrates,
and underfeeding roughage, likewise access to lush
grass can result in high carbohydrate ingestion. These
diets may result in excessive gas production within the
bowel and may cause diarrhea. Group feeding may
allow aggressive horses to overeat in preference to less
dominant individuals. Sudden changes in feeding prac-
tices and irregular time interval between feeds may also
result in intestinal complications.
Poor quality roughage, eating coarse bedding mate-
rials, and inadequate mastication of roughage resulting
from dental disease can result in colonic impactions.
Sandy pastures or feeding horses in sand schools can
result in excessive ingestion of sand.
Inadequate parasite control can result in a signifi-
cant parasite burden, which can predispose to several
types of colic.
Signalment
Young foals and yearlings are particularly prone to
gastric ulceration, as are young adult horses in race
training. Intussusceptions, foreign body ingestion, and
cyathostomosis are also more common in young horses.
Older horses are more likely to suffer from motility dis-
orders and neoplasia. Pedunculated lipomas are most
common in old ponies. Grey horses may be more at risk
of developing melanomas.
Clinical examination
A thorough physical examination should be carried
out, paying particular attention to the gastrointestinal
tract (see Chapter 9), but also including evaluation of
other body systems. Repeated examinations are likely to
be required, and examination while the horse is show-
ing signs of pain is preferable. Hospitalization of
affected horses can be extremely helpful to allow
repeated examinations over several days or weeks.
Rectal examination is likely to be the most useful
diagnostic technique. Some significant findings that
may be identified by rectal examination in horses pre-
senting with chronic or recurrent colic include
pelvic flexure impaction
abnormal masses such as neoplasms and abscesses,
enteroliths, intussusceptions, cystic calculi, and
broad ligament hematomas can also be detected in
some cases
muscular hypertrophy of the small intestine can
occur within a period of 2-3 weeks in the segment
of intestine proximal to a partial obstruction, this
may be palpable as several loops of thickened,
rubbery-feeling bowel
distended small intestine proximal to a (partial)
bowel obstruction
segments of small intestinal hyperperistalsis are
occasionally palpable in horses with spasmodic
colic.
Abdominal auscultation may be helpful in the diag-
nosis of some conditions. A characteristic 'sand and
water' sound may be heard in the ventral rostral
abdomen in cases of sand impaction. A loud 'fluid
through a pipe' sound can be heard with spasmodic
colic or chronic distention of a portion of the small
intestine proximal to a partial obstruction such as ileal
hypertrophy.
Laboratory investigations
Unlike the horse with acute abdominal disease, in
animals with chronic or recurrent colic there is often
time to perform routine clinicopathological evalua-
tions. In many cases laboratory results will be unre-
markable or reveal non-specific changes, but in some
cases laboratory results may be diagnostically helpful
341
OTHER CONDITIONS 17
undiagnosed. Exploratory surgery via a ventral laparo-
tomy/ celiotomy or diagnostic laparoscopy are often
performed as a final attempt to diagnose the cause of
the problem. However, even these procedures may fail
to yield a diagnosis in some cases and owners of affected
horses should be warned of this possibility prior to
surgery being undertaken.
Grass sickness
RS Pirie
INTRODUCTION
Grass sickness is a dysautonomia of Equus spp. charac-
terized by damage to neurons of the autonomic,
enteric, and somatic nervous systems. The disease was
first reported in the east of Scotland in 1907. Although
the northeast region of Scotland still has the highest
incidence of grass sickness, the disease has been recog-
nized throughout the United Kingdom as well as in
many other northern European countries including
Norway, Sweden, Denmark, France, Switzerland, and
Germany. No histologically confirmed cases have
occurred in Australasia, Asia, Africa, North America, or
Ireland. All members of the Equus spp. appear to be
susceptible to grass sickness, with the disease having
been reported in horses, ponies, donkeys, and captive
exotic equids. A clinically and pathologically indistin-
guishable disease known as mal seco (dry sickness) has
also been reported in the Patagonia region of
Argentina and in Chile and the Falkland Islands. Many
clinical similarities exist between grass sickness and
other dysautonomias in man (familial dysautonomia)
and other domestic species (feline dysautonomia,
canine dysautonomia). Although equids were previ-
ously thought to be the only herbivores susceptible to
dysautonomia, recently a clinically and pathologically
similar disease has been identified in the brown hare in
the UK (leporine dysautonomia) and the constipated
form of mucoid enteropathy of caged rabbits has also
been classified as a dysautonomia.
Grass sickness can be divided into three subdivisions
(acute, subacute, and chronic) which are characterized
clinically by varying degrees of gastrointestinal immotil-
ity and dysphagia, although it should be emphasized
that there is a continuum between these divisions. The
acute and subacute forms of the disease are invariably
fatal, however a proportion of mildly affected horses
with the chronic form may survive. Despite extensive
research the cause of grass sickness still remains
unknown.
EPIDEMIOLOGY
Age
Grass sickness has been confirmed in horses from 4
months of age onwards, however the peak incidence
occurs in 2-7-year-olds and is therefore considered pre-
dominantly a disease of the young adult horse.
Gender
Traditionally, no gender predisposition was thought to
occur, however results from a recent epidemiological
study suggested that mares were at a slightly reduced
risk.
Body condition
At the onset of disease, grass sickness cases are usually in
significantly better body condition than would be
expected from a reference population. Very rarely will
an animal in poor body condition contract grass sick-
ness.
Season
In the northern hemisphere, the highest incidence
occurs in the spring and summer months, with the peak
number of cases in the UK occurring between April and
July. Despite this obvious peak in incidence, cases will
occur in every month of the year. In the southern hemi-
sphere (e.g. Argentina), the highest incidence occurs
from October to February.
Grazing
As the name implies, grass sickness is almost exclusively
a disease of grazing equids with reported cases being
extremely rare in housed animals. Occasionally a strong
association will exist with certain premises.
Movement to new premises
Animals on a property for less than 2 months are at
greater risk and many cases will occur within weeks fol-
lowing movement to a new pasture or premises.
Climate
Cool (7-10C), dry weather tends to occur in the 10-14
days preceding outbreaks.
Anthelmintic history
Recent evidence suggests that grass sickness is encoun-
tered more commonly in horses receiving frequent
anthelmintic treatments compared to those animals
which do not. This finding is independent of the effect
343
17 COLIC
Geographical location
Age
Gender
Body condition
Season
Grazing
Movement to new premises
Climate
Anthelmintic history
of increased frequency of changing pastures. The rea-
son for this apparent association is unclear, however it is
not considered likely that anthelmintic drugs them-
selves are directly responsible and decreasing the use of
anthelmintics is clearly not advisable.
ETIOLOGY
The etiology of grass sickness is unknown. Numerous
epidemiological studies have found no evidence for a
conventional infectious agent. Considerable evidence
exists to suggest that a natural neurotoxin may be
implicated and the presence of a neurotoxic compo-
nent in the plasma of acute cases has been demon-
strated experimentally. Investigations into the possible
role of toxic plants, viruses, and fungal, chemical, and
bacterial toxins has failed to identify the cause. Current
investigations include
the potential involvement of an ingested mycotoxin
the possible role of toxin release from Clostridium
botulinum
an oxidative stress-mediated neural damage.
To date none of these investigations have yielded
conclusive results.
CLINICAL SIGNS
Acute form
The onset and progression of clinical signs in the acute
form is rapid with death occurring in less than 48 hours.
Animals will usually present with depression/somno-
lence, inappetance, and rapid progression to varying
degrees of abdominal pain in many cases. The degree
of colic may however be relatively mild and inconsistent
with the profound elevation in pulse rate. The pulse is
usually weak and may exceed 100 bpm in many cases.
Pyrexia (up to 40C) and bilateral ptosis mayor may not
be present. Muscle fasciculations of the triceps and
quadriceps muscle groups may be observed and sweat-
ing may be generalized or localized to the flanks, neck,
and shoulder regions. Dysphagia is almost invariably
present but can be difficult to appreciate due to co-
existing inappetance. It may be apparent however,
when observing the animal attempting to drink when
many cases will flick their muzzle through the water or
'paw' at the water bucket, presumably through frustra-
tion. Excessive dribbling of saliva is often present and
probably results from a combination of excessive saliva
production and the reduced ability to swallow.
Dehydration is usually present which can be demon-
strated by prolonged tenting of the skin. Some horses
Acute Subacute Chronic
depression/somnolence
distended abdomen
ileus
tachycardia
salivation
gastric reflux
muscle tremors
ptosis
patchy/generalized sweating
dysphagia
small intestinal
distension
colic (occasionally)
colon impactions (occasionally)
344
'tucked up' abdomen
weight loss
dysphagia
tachycardia
colic (asdisease progresses)
gastric reflux (asdisease progresses)
patchy sweating
ptosis
muscle tremors
colon Impaction
reduced gut motility
severe weight loss
markedly 'tucked up' abdomen
base-narrow stance
rhinitis sicca
bilateral ptosis
slightly elevated heart rate
60 bpm usually)
muscle tremors
patchy sweating
mild colic
reduced gut motility
OTHER CONDITIONS 17
will show spontaneous gastric reflux with foul smelling
green or brown fluid exiting from both nostrils, and in
those that do not, passage of a nasogastric tube will
invariably result in the retrieval of many liters of mal-
odorous reflux. A generalized, marked reduction in
intestinal motility is evident during abdominal ausculta-
tion. As the disease progresses, abdominal distention
becomes apparent in most cases. Rectal examination in
acute cases will reveal a dry rectal mucosa and some
cases will strain excessively during the rectal examina-
tion. Frequently, distention of the small intestine can be
appreciated and consequently the rectal findings in
many acute cases can appear similar to those encoun-
tered in some surgical colic cases with associated small
intestinal obstruction. In some cases, a hard secondary
impaction of the large colon can be palpated in the cau-
dal abdomen. The distinct corrugated nature of this
structure will often distinguish it from the relatively
smooth outline of a primary colonic or cecal impaction.
The prognosis in acute cases is hopeless, therefore
euthanasia is required after this diagnosis is made.
Subacute form
Generally the clinical signs in subacute cases are similar
but less severe than those of acute cases. The duration
of clinical signs is longer and the outline of the
abdomen quickly develops a marked 'tucked up'
appearance. This finding does not appear to be entirely
due to loss of body condition, although significant
weight loss does become apparent. Affected animals are
almost invariably dysphagic. Persistent tachycardia is
present with or without any evidence of abdominal
pain. Patchy sweating, usually around the flanks, neck
and shoulder, and muscle tremors of the triceps and
quadriceps muscle groups are often present.
Nasogastric reflux and small intestinal distention are
usually absent early on in the course of the disease, how-
ever these may develop in a small number of cases as the
disease progresses. Also as the disease progresses many
subacute cases will exhibit worsening episodes of colic.
Colonic and cecal impaction is common and readily
appreciated during rectal examination. Although a
small number of cases that present initially as subacute
cases will gradually progress to the chronic stage, the
vast majority will die or require euthanasia within 7 days
of the onset of signs.
Chronic form
The clinical signs in the chronic form are more insidi-
ous in onset. The most obvious signs include severe
weight loss with the development of a distinct 'tucked
up' abdomen (Figure 17.10). Affected horses will often
have a very base-narrow stance, thus adopting the char-
Figure 17.10 Chronic grass sickness case showing a typical
'tucked up' abdomen, this sign may occur early in the
course of the disease before profound lossof body condi-
tion becomes apparent
acterisuc 'elephant on a tub' posture (Figure 17.11).
Some cases will show apparent weakness and a reduced
anterior phase to the stride will result in occasional toe
dragging. Bilateral ptosis is often present resulting in a
sleepy, depressed expression. Persistent tachycardia is
present, however the heart rate is lower than in acute
and subacute cases, rarely exceeding 60 bpm. Varying
degrees of muscle tremor, patchy sweating, and abdom-
inal pain are present. Signs of colic are usually mild and
transient. Varying degrees of dysphagia are common
but the associated reduction in appetite can make this
difficult to appreciate. Frequently, affected horses will
accumulate chewed food between the cheeks and molar
teeth, often resulting in a fetid odor to the breath.
Abdominal auscultation usually reveals a reduction in
intestinal motility. Small intestinal distention and
Figure 17.11 Chronic grass sickness case adopting a base-
narrow ('elephant on a tub') stance
345
17 COLIC
colonic impaction are rare, therefore rectal examina-
tion usually reveals a lack of contents within the palpa-
ble regions of the colon and cecum. Many chronic cases
will have severe rhinitis with the accumulation of dry
hemorrhagic mucoid material on the nasal septum and
nasal turbinates. Although this can be appreciated by
close inspection of the rostral nasal septum using a pen
torch, often the animal will have a distinctive 'snuffling'
sound during breathing that originates from the nasal
cavity. Until relatively recently, the mortality in chronic
cases was reported to be 100 per cent, however strict
selection of treatment candidates and adherance to
good management protocols has considerably
improved the prognosis in some chronic cases (see
below). The suggested criteria for selection of cases for
treatment are summarized in Table 17.14.
CLINICAL PATHOLOGY
No alterations in blood clinical chemistry or hemato-
logic parameters are pathognomonic for grass sickness.
As one of the major differential diagnoses of grass sick-
ness is colic, most of the comparisons of clinical chem-
istry parameters have been made between grass sickness
cases, normal controls, and colic cases. Plasma cortisol,
catecholamine, and histamine concentrations are sig-
nificantly higher in acute and subacute grass sickness
cases than in colic cases and normal animals. This find-
ing has been attributed to increased sympathoadrenal
activity. The acute phase proteins, haptoglobin and oro-
somucoid, are increased in all three forms of grass sick-
ness but not in the majority of colic cases. Also the
protein content of peritoneal fluid is higher in grass
sickness cases compared with medical colics. The
author, however, considers that none of these analyses
is of value as a clinical diagnostic tool.
PATHOLOGY
Grosspathology
Acute grass sickness cases have a stomach distended
with green/brown fluid. The small intestine is usually
normal in color but distended with fluid throughout its
entire length. In some acute cases and the majority of
subacute cases the colon is impacted with hard, dry
digesta. When the colon wall is peeled away from the
firm impaction, a black coating is usually left on the sur-
face of the impacted ingesta (Plate 17.8). Examination
of the mucosal surface of the distal esophagus will often
reveal longitudinal linear ulceration as a consequence
of gastric reflux. In chronic grass sickness cases, the
346
main feature is profound emaciation with the gastroin-
testinal tract lacking in contents. Interestingly, some
chronic cases of mal seco have colonic impactions at
post-mortem examination.
Histopathology
Characteristic neuronal lesions occur in multiple auto-
nomic ganglia such as the cranial, cervical, stellate, and
coeliacomesenteric, in dorsal root ganglia, in specific
brain stem nuclei, and ventral horn and intermedialat-
eral gray matter of the spinal cord. In the acute lesion
affected neurons show a chromatolytic change, staining
homogenously with dyes such as hematoxylin and eosin
(H&E) and cresyl violet. There is loss of Nissl granules,
neuronal swelling, and vacuolation, and sometimes
pyknotic nuclei are evident. Degeneration and loss of
enteric neurons also occur in the submucous and
myenteric plexuses. In acute and subacute cases, this
damage is widespread throughout the jejunum, ileum,
and small colon (and possibly the large colon) with the
ileum being the most severely affected. In chronic cases
however, the distal small intestine, particularly the
ileum, may be the only severely affected area of the gas-
trointestinal tract.
DIAGNOSIS
Confirmation of a diagnosis of grass sickness can only
be made by demonstrating the characteristic
histopathologic lesions in the autonomic or enteric
ganglia at post-mortem examination, or by ileal biopsy
at laparotomy. This latter technique can be useful in the
ante-mortem diagnosis of acute and subacute cases
where surgical colic is a major differential diagnosis. In
chronic cases however where subsequent treatment is
being considered, anesthesia and surgery are likely to
adversely affect the outcome. Rectal biopsy is not yet a
reliable technique in grass sickness as the enteric neu-
rons in the rectum are only mildly affected and only a
small sample can be obtained.
In most cases therefore, an ante-mortem diagnosis is
made on clinical signs and history. Although no single
clinical sign is truly pathognomonic for the disease and
many clinical signs may overlap with other diseases,
repeated clinical examinations and thorough rectal
examinations can be extremely accurate when consid-
ered in conjunction with the animal's recent history.
Dysphagia in a horse with continuous or intermittent
colic, nasogastric reflux, a firm corrugated colon
impaction, and small intestinal distention is strongly
suggestive of acute or subacute grass sickness. Rapid
weight loss with the development of a marked 'tucked
OTHER CONDITIONS 17
up' appearance in a horse with dysphagia and rhinitis is
highly suggestive of the chronic form. Other signs that
will aid in the diagnosis include patchy sweating, muscle
tremors, salivation, and ptosis.
Because surgical colics are the major differential
diagnoses with respect to acute and subacute grass sick-
ness, careful consideration of the entire clinical presen-
tation is extremely important. Table 17.13 highlights
some of the most significant findings which may aid in
the differentiation between surgical colics and acute or
subacute grass sickness cases. It should be noted how-
ever that these differences do not necessarily apply to
all colic cases requiring surgical intervention.
Other ancillary diagnostic techniques which may aid
in the diagnosis of grass sickness include esophageal
endoscopy and contrast radiography. Endoscopic
examination of the distal esophagus of acute and occa-
sionally subacute cases may reveal longitudinal linear
ulceration of the mucosa and intermittent retrograde
flow of gastric fluid. Abnormal esophageal motility has
also been demonstrated by the use of radiographs and
image intensification following barium swallow. In
these cases a large reservoir of contrast material is seen
to pool in the distal esophagus.
Depression/somnolence more apparent than signs of
abdominal pain
Presence of gastric and small intestinal distension in
the absenceof pain or in the presenceof!11iJJJ.
/intermittent pain
High pulse rate in the absence of pain or in the
presenceof mildliatermittent pain
Grosslynormal peritoneal fluid
TREATMENT
Any attempts to treat acute and subacute cases have
failed and these cases should be euthanased following
diagnosis. Consequently only chronic cases should be
considered for treatment. In some apparently mild, sub-
acute cases it may be necessary to observe the animal for
up to 7 days in order to establish whether it will develop
into a chronic form. If the animal is completely dys-
phagic, refluxing gastric fluid, and/or showing signs of
severe colic, euthanasia is required before this observa-
tion period is complete. Table 17.14 summarizes the
S2.t:lle. ability to swallow
A of intestinal motility
None or only mild/intermittent colic
S2.t:lle. appetite present
Pulserate <60 bpm
suggested criteria for the selection of treatment candi-
dates with the chronic form of grass sickness. It is the
opinion of the author that by far the most significant
criteria necessitating euthanasia in chronic cases are
severe dysphagia and total inappetance.
General management
Nursing provides the mainstay of the treatment, and
the recovery rate for chronic cases has improved dra-
matically with the instigation of a good management
regimen as detailed below. Housing is advisable in the
early stages of the disease. The use of palatable high
energy, high protein feed is indicated, however the
animal's individual preference will often dictate the
food consumed. This preference will often change
from day to day and even from feed to feed. The fre-
quent provision of feed is indicated with a recommen-
dation of 4-5 feeds per day. Preferred feeds include
molasses-containing feeds, crushed oats, and high
energy cubes. Soaking these feeds may facilitate swal-
lowing in some cases, however whether to dampen
the feed or not is again dependent on the individual
animal's preference. The energy content of the feed
may be improved by the addition of up to 500 ml of
corn oil, however this should be done gradually.
Palatability can be improved by adding dilute
molasses or succulents such as cut grass, carrots, or
apples. It should be noted that these items are to
improve palatability only and contain insufficient
energy to form the whole diet. The consumption of
concentrate feed in order to minimize excess weight
loss is vital to the survival of the individual case.
Nasogastric feeding has been attempted in some cases
with extremely limited success and therefore the indi-
cation for such treatment remains questionable. The
importance of nursing, frequent human contact, fre-
quent grooming, and regular walking out and hand
grazing cannot be overemphasized. Occasionally it
may be necessary to hand feed some cases when
appetite is especially poor. In many cases despite a
moderate degree of food intake, the body weight will
continue to decrease quite dramatically during the
347
17 COLIC
frSI 2-4 wtcks. The prognosis however is con.ider.bl)'
poofer if this decrease in body Wight continw:s
beyond 6 .e durton.
Therapeutic agents
Intestinal motility enhancers
Cisapride is an indirect cholinergic agent which fdli
Illes acetylcholine release from the myenteric plexus of
the gut. Unlike the related compound metoclo
pramide. cisapride lacks central antidopaminergic
propenies. The use of cisapride (0 . .-.8 mg/kg p.o.
toLd. for 7 days) has been shown t increase gut motilit
in chronic cases of grass sickness. Because cisaprirc may
increase colic signs approximately : hours afer admin
istration, it may indirectly interfere with the overall
demeanor and appetile of the animal. Any decision
therefore to adminislcr cisapride should take into
account the pOIcntial beneficial versus detrimental
effects on the individual clinical signs; i.e. increased
inl('stinal motility versus colic and inappetance. The
apparent contribution of the severity of each clinical
sign to the over-ill seventy of lhe diase will therefore
delermine whether cisapride lherapy is required. In
ariltn, chaprde i expensive and i not currenlly
licensed for \'etrinar usc.
Analgesics
Nunsteroidal antl-inflammatory drugs are suitble for
analgesia in .ronic c as they do nO[ adversely affect
intetinal motility. Chronic casts may have mild, tran
sienl episodes of colic fonoving feeding and fiuni"in
meglumine (0.5-1.1 mg/kg Lv.) or phenylbutazone
(2.2-4.4 mg/kg) may he administered under such cir
cumSlance5.
Appetite stimulants
Inappetance is a mOjor ddermining factor in the sur
\';\,al of many cases of chrunic grASS sickness. It is impor
tant however. t dttcrmine if the lack of food intake is
mainly because of inappctance or dysphagia. Diazepam
has prov .. n to be mildly benefcial as an appetite stimu
lant in a very limited number of chronic cases. The
effective dose varies \ilh the individual hut 0.05 mg/kg
;'\'. q. 2 h, or as nccewry, is . suggelcd ltng point.
A limilarcompound, brnlilolam (2IlR/kg slo i.\.) has
recently heen used a lIn appttite stimulant in chrnic
grass sickness casC$ with slightly more succe than
diaupam. BrotilOlam iii not however licensed for u in
horses and no control trials hae been conducted 1
assess its full wurth in the treaunenl of chronic grass
sickness (ases.
348
OUTCOME
OSI swviving chronic gran sid:C cae are capable
of rC$uming normal work. Residual abnormalities may
howeer PCTill in some survivors, including mild d
phagia. excessive s'ealing, long silky coat g, and
multiple small areas of pilrection. Although most of
the residual problems lend to improve with time, they
may fail to rewlve completely.
PREVENTION
Although no guaranteed mClhod uf prevention 3re
known, consideration of the associated rik factors
allows certain precaUlions t be taken. This is panictl
larly relevant in high risk areas during March to July.
These precautions include
h[using new arrival$ for a 2-month perod before
turn out
avoiding any change in pasture during the high risk
5eason
avoiding the use of plslure where lhe disea.. ha
occurred before
hnusing hones may alliO be adviable in highrisk
areas, if the
p
receding 7-10 comccutiv days h
been cool and dlj'.
Allhese praution$ are especially relent ror 2-8
year-lds.
Pancreatic diseases
T Mair
INTRODUCION
The pancreas i a triangular shaped organ that lies
transversely on the d()ral wall of the abdomen, the
greater part being to the right of the midline. It has an
averdge weight of ahout 3SO g. It is attached dorsally by
conne<tive tissue \0 the kidneys and adrenals. the IdS
trophrenic ligament, the suspensory ligament of the
spleen, Ihe poslerior vena cava. the portal fissure, and.
Inc gastropancreatic fold. The ventral 5urbce i a
cent 10 the base of Ihe ce..um and the large colon.
There are tWO ducts
Ihe larger p&(jc dI' opens inlo the duodenal
cti\'eniculum alongside the bile duct
Ihe (Jn. w' panc(ali due ends on a papilla in Ihe
duodenum opposile the main pancreatic duct.
OTHER CONDITIONS 17
The pancreas is a compound gland that has impor-
tant exocrine and endocrine functions. Digestion in the
small intestine is partly dependent on pancreatic secre-
tions, but also on biliarysecretions and mucosal enzymes.
The volume ofpancreatic fluid secreted bya 100kg pony
is approximately 10-12 IIday. Secretion is under both
neural and hormonal control. Pancreaticjuice contains
bicarbonate ions, amylase, lipase, and peptidases.
The islets of Langerhans account for only about 2
per cent of the total weight of the pancreas. Two major
cell types are present in the islet tissue
a cells secrete gastrin and glucagon
cells are the source of insulin.
The rate of insulin secretion is highly dependent on
blood glucose concentration. The major effect of
insulin is to increase the utilization of glucose by most
body tissues. This is achieved by increasing the trans-
portation of glucose across the cell membrane.
DIABETES MELLITUS
Five separate forms of diabetes mellitus are recognized
I. insulin-dependent diabetes mellitus
2. non-insulin-dependent diabetes mellitus
3. secondary diabetes mellitus
4. gestational diabetes mellitus
5. impaired glucose tolerance.
Diabetes mellitus is rare in horses; it is most com-
monly associated with insulin resistance induced by
pituitary adenomas. Only insulin-dependent diabetes
mellitus will be considered further here.
chronic weight loss despite good or increased
appetite
depression
inappetence
intermittent colic
persistent or recurrent pyrexia
jaundice.
If there is concurrent insulin-dependent diabetes
mellitus, polyuria and polydipsia may also be observed.
Clinical pathological abnormalities are inconsistent,
but may include
raised serum amylase
raised serum lipase
raised peritoneal fluid amylase
increased fractional excretion of amylase
hypocalcemia
hyperglycemia
glucosuria
hypertriglyceridemia
raised serum gamma glutamyl transferase
hyperbilirubinemia.
Reference values for amylase and lipase acnvines
should be established by each laboratory. Serum amy-
lase activity for normal horses usually ranges from
14-35 IU/1, and values less than 50 IU/1 are generally
considered to be normal. Peritoneal fluid amylase activ-
ity is usually slightly lower than serum activity. Serum
lipase activity is normally less than 87 IU/I (Table
17.15). The fractional secretion of amylase (FEarn) is
calculated by the following formula
urine amylase serum creatinine
X X 100 = FEarn
serum amylase urine creatinine
FEarn in normal horses is less than 1 per cent.
Interpretation of pancreatic enzyme activity in
horses can be difficult because the enzymes are not
exclusively of pancreatic origin, and may be released
from other tissues such as the gastrointestinal tract. In
addition, renal disease may result in decreased excre-
CHRONIC PANCREATIC DISEASE AND
INSULIN-DEPENDENT DIABETES
MELLITUS
Pancreatic exocrine insufficiencies are common causes
of maldigestion in other species but they appear to be
rarely diagnosed in the horse. Insulin-dependent dia-
betes mellitus is very rare. However, adult horses and
ponies may develop signs of exocrine pancreatic insuffi-
ciency, with or without associated insulin-dependent
diabetes mellitus, following destruction of the pancreas
by diseases such as neoplasia (pancreatic adenocarci-
noma) and chronic pancreatic necrosis. Chronic
eosinophilic pancreatitis has been reported and is
assumed to be caused by parasite (Strongylus equinus and
S. edentatus) migration through the gland. The clinical
signs associated with chronic pancreatic disease may
include
Amylase (lUll)
Lipase (lUll)
Glucose (mmolll)
Serum
14-35
23-87
4.0-5.6
Peritoneal flUid
0-14
0-36
4.9-6.4
349
17 COLIC
tion of amylase thus leading to elevated serum levels. In
the diagnosis of acute pancreatitis (see below) sec-
ondary damage to the pancreas from hypovolemia or
reflux of duodenal contents up the pancreatic duct can
result in release of pancreatic enzymes into the circula-
tion.
The diagnosis of insulin-dependent diabetes melli-
tus can be confirmed by performing either an oral glu-
cose tolerance test (see Chapter 2) or intravenous
glucose tolerance test. The intravenous glucose toler-
ance test is performed by administering intravenous
glucose (0.5 g/kg) as a bolus (e.g. 40 or 50%), and col-
lecting samples at times 0, 15, 30, 45, 60, 120, 180 and
240 minutes for glucose and insulin estimations.
Insulin-dependent diabetics will have high plasma glu-
cose concentrations, which fail to decrease as fast as
normal, with little increase in insulin levels.
Confirmation of chronic pancreatitis or pancreatic car-
cinoma is generally made either at exploratory laparo-
tomy or at post-mortem examination.
Owing to the difficulties in diagnosing chronic pan-
creatic disease in the horse, treatments have rarely
been attempted. Once the horse has developed
insulin-dependent diabetes mellitus due to destruction
of the islets of Langerhans, the only effective treatment
is the exogenous administration of insulin. The insulin
dosage should be assessed by monitoring the response
to small doses administered initially, and then gradu-
ally adjusting the dosage. In one report of diabetes
mellitus associated with pancreatitis in a pony, prota-
mine zinc insulin (0.5-1.0 IV/kg) was found to be
more effective in decreasing the hyperglycemia than
regular insulin.
HYPERINSULINEMIA
Hyperinsulinemia secondary to increased release of
insulin by a pancreatic tumor has been reported in a 12-
year-old pony. Hyperinsulinemia induces hypoglycemia,
which can also be seen following fraudulent or thera-
peutic injections ofinsulin. Clinical signs depend on the
degree of hypoglycemia, but may include
trembling
ataxia
tachycardia
tachypnea
mydriasis
nystagmus
sweating
unawareness of surroundings
recumbency
seizures
350
coma
death.
Signs may wax and wane depending on the animal's
diet.
ACUTE PANCREATITIS
Acute pancreatitis is a rare cause of severe abdominal
pain in horses. The cause is uncertain and ante-mortem
diagnosis is rarely made because the clinical signs
mimic other gastrointestinal diseases producing acute
colic (especially small intestinal strangulating obstruc-
tions and anterior enteritis). The pancreas is not easily
visualized during routine surgical exploration of the
abdomen, and may be overlooked at necropsy, espe-
cially if gastric rupture has occurred.
Acute pancreatitis can occur in association with ade-
novirus infection in Arabian foals affected by combined
immunodeficiency syndrome (CID). Infection of the
pancreatic duct by Cryptosporidium spp. may also occur
in foals affected by cm (see Chapter 26). Pancreatitis is
also sometimes found in association with hyperlipemia
(see Chapter 19). It has been speculated that excess
lipid is deposited in and around the pancreas in hyper-
lipemia. This lipid is subsequently hydrolyzed by pan-
creatic lipase and released as free fatty acids. Free
(unbound to albumin) fatty acids are cytotoxic and
when the albumin-binding capacity is exceeded then
pancreatic vascular injury occurs resulting in necrotiz-
ing pancreatitis.
The clinical signs of acute pancreatitis in adult
horses include
severe abdominal pain
hypovolemic shock
tachycardia
tachypnea
pronged capillary refill time
sweating
cold extremities
gastric distention and voluminous nasogastric
reflux.
Specific diagnostic features are not evident from the
clinical signs or clinical pathology findings. Abdominal
sounds are variable but are often reduced or absent. No
specific abnormalities are detected by rectal examina-
tion. Peritoneal fluid may be serosanguinous or frankly
hemorrhagic.
Most affected horses die within 24 hours. No spe-
cific therapy apart from symptomatic treatment for
abdominal pain and hypovolemic shock has been
described.
OTHER CONDITIONS 17
Causes of colic associated
with reproduction and the
reproductive tract in the
brood mare
eM Schweizer
GENERAL CONSIDERATIONS FOR
MARES DEMONSTRATING SIGNS OF
COLIC
Colic in the brood mare, as in any other equine patient,
represents both diagnostic and treatment challenges.
In addition to the more commonly encountered gas-
trointestinal compromises that result in abdominal
pain, the female equine is also susceptible to abdominal
pain that is either the direct result of a reproductive
abnormality or is secondary to a reproductive event that
has resulted in a compromise to the normal function of
another body system. Likewise certain conditions are
more likely, or they may only occur, in certain repro-
ductive classes of mares (i.e. open, pregnant, foaling,
and early postpartum). It is the responsibility of the
practitioner to accurately differentiate and identify the
source of the problem(s) and to take steps to correct
the situation.
In the event that the mare is pregnant, the practi-
tioner is faced with not one, but potentially two patients
simultaneously. The best course of treatment for one
may be in direct conflict with what is optimal for the
other. The potential value to the owner of the mare rel-
ative to the foal, and the chances of survival for each in
the given situation demands careful consideration by
the practitioner and a prioritization of treatment
options. In ideal circumstances both the mare and the
unborn foal can be saved. The goals of treating a colicky
pregnant mare therefore are
to identify and correct whatever abnormality is
present as soon as possible
to support placental function as needed to maintain
fetal viability throughout the insult to the mare and
throughout the remaining length of gestation.
The aim for the foal is to maintain an optimal envi-
ronment within the mare's womb for as long as possi-
ble, allowing the foal to mature and to be born with a
reasonable chance of survival outside the womb.
In general, where surgery is needed in the pregnant
mare, anesthesia of the dam presents little danger to
the unborn foal provided the anesthetic experience is
uncomplicated. Late gestation mares, however, repre-
sent more of a challenge. It has been reported that
approximately 18 per cent of all pregnant mares requir-
ing colic surgery abort their pregnancies postopera-
tively. Care must be taken therefore to quickly identify
the need for surgery and to proceed without delay
before the dam's condition can deteriorate further.
Throughout the surgery it is vital to make sure that arte-
rial oxygenation (> 80-100 mmHg) and blood pressure
are kept optimal for the duration of the anesthetic so
that adequate placental perfusion and exchange is
maintained. Beyond surgery a rapid full recovery by the
dam is optimal for both patients. Continued or
repeated stress to the mare may be detrimental to the
pregnancy. A great potential danger to the mainte-
nance of the unborn foal is the development of endo-
toxemia in the mare.
It is believed that endotoxemia in the pregnant mare
results in the release of prostaglandins, and may also
alter uteroplacental blood flow. Prostaglandins have
the potential effect of inducing abortion in pregnant
mares of less than 150 days gestation by causing luteoly-
sis of both the primary (ovulatory) corpus luteum and
secondary corpora lutea and therefore termination of
ovarian progesterone production when the pregnancy
is still dependent on an ovarian source of progesterone
for maintenance. In mares of more than 150 days gesta-
tion pregnancy maintenance is dependent on progesto-
gen production by the placenta and so is unaffected by
a loss of ovarian progesterone, however clinical evi-
dence suggests that chronic exposure of the gravid
uterus, at this point, to high levels of prostaglandins (as
is the case during endotoxemia) may perhaps be
responsible for inducing uterine contractions resulting
in abortion. Administration of intravenous fluid sup-
port and flunixin meglumine are beneficial in treating
the effects of endotoxemia, and in both instances (i.e.
gestation < 150 days and gestation >150 days) the timely
administration of supplemental progesterone has been
shown to prevent pregnancy loss in endotoxic mares.
At present there are only two available types of prog-
esterone supplementation proven to be effective in
achieving adequate blood levels of progesterone to
maintain pregnancy. They are
injectable progesterone in oil (150-300 mg i.m,
s.i.d, in an average 450 kg (1000 Ib) mare)
altrenogest (22-44 mg p.o. s.i.d. in an average
450 kg (1000 Ib) mare).
It is the author's preference to initiate supplemental
progesterone therapy to a pregnant mare as soon as
possible after the onset of severe colic or repeated colic
episodes that are occurring over a short span of time in
the event that endotoxemia is just around the corner.
The thought is also to give the pregnancy some addi-
351
17 COLIC
tional support during a time of severe or chronic stress
in general. Again, it is the author's preference to initi-
ate progesterone therapy in a time of crisis using the
injectable progesterone (loading dose of 300 mg i.m.).
Follow-up daily oral supplementation may be used in
those cases where there has not been severe intestinal
damage that may interfere with absorption and/or
where the mare is not refluxing. Otherwise daily injec-
tions continue until either the mare can begin to take
oral supplementation or the need for supplementation
has ended.
Once begun, therapy should be continued at least
until the mare has fully recovered and has returned to a
stress-free environment, and physiologically the mare is
able to maintain the pregnancy on her own. In mares
where the insult has occurred during the first 120 days
of gestation the release of prostaglandins has likely
resulted in the termination of ovarian progesterone
production, and therefore exogenous progesterone
supplementation must be provided until the placenta is
capable of maintaining the pregnancy on its own (i.e. at
> 150 days). If there is pressure to discontinue proges-
terone supplementation sooner in these early gesta-
tional mares, it is important to ascertain whether there
is enough remaining ovarian progesterone production
to support the pregnancy (i.e. blood progesterone lev-
e1s> 2 ng/ml and preferably> 5ng/ml) before therapy
is discontinued. If the mare is being supplemented with
injectable progesterone this will not be possible as the
progesterone assays will register an amount reflective of
both the exogenous and endogenous levels. If the mare
is being supplemented with the oral altrenogest then
measurement of blood levels of progesterone will only
reflect endogenous production. In mares where the
insult has occurred after the pregnancy is no longer
dependent on an ovarian source of progesterone (i.e.
>150 days) it should be safe to begin to discontinue the
progesterone supplementation as soon as the insult and
stress during recovery have ended. In both instances it
is the author's preference to 'wean' the mares off sup-
plementation gradually over 10-14 days, rather then
terminating progesterone supplementation abruptly.
REPRODUCTIVE-ASSOCIATED COLIC IN
THE NON-PREGNANT MARE
Colic during estrus
Occasionally the clinician will be presented with a mare
that demonstrates abdominal pain in association with
ovulation during estrus. This is probably similar to the
sensitivity and lower abdominal or back pain that some
women experience coinciding with ovulation, com-
352
monly known as mittelschmerz. In the author's experi-
ence sensitive mares of this type will demonstrate inap-
petance and acute mild to moderate colic signs similar
to those demonstrated by horses with acute, short-lived
'gas colic'. These mares typically respond well to a 250
mg i.v, dose of flunixin meglumine to control their dis-
comfort and laxatives (e.g. mineral oil) to lessen the
possible discomfort associated with passage of feces
through the pelvic area and defecation at this time.
Usually the signs resolve immediately with medication
or within a few hours ifleft unmedicated. It is important
before this diagnosis is made to rule out any other pos-
sible cause of the abdominal pain, to ascertain that the
mare is indeed in estrus with a large follicle or recent
ovulation present on one or both ovaries at the time,
and that the affected ovary is demonstrably painful to
palpation. Further credibilityFu tootherandor
ot58 2.738 0[()-992.8 3294(low616 Tm(or)Tj9.92 0 85 611.729666ot58 2.738 0(bloo -1.255 00 Tc 5.816 39 5)Tj3t58 2.738 0(prog111er15.0935 Tc 9.738 0 0 8.8 3.68 Tm(8 2.738 0(5 Tc 8.9097 0 0 Td(follicle420.753m(8 2.738 0(bly)Tj0.048 Tc 8.8 0 0 8ted59416 8 2.738 0(b(p 578.64 Tm(pain, 8.8 476155 1.84 Td8 2.738 0((mare)9.10-8.8 457.374ed5925s18 2.738 0(bly)Tj0.048 Tc 8.8 0 0 8800 095s18 2.738 0(col.8 344-20.8 T 1.848 0 T[()-992.8 1 0 0 8.8 .)T Tm8 Tm(thatn.)T26202495271 556chr15ic,42 556.56 Tm(time,)Tj50...982495271 556cycl.8 344.9097 0 0 8.8796.795iTj0 8.8 4495271 556.56urrence0.05 Tc 9.11 0 0 84cen42 Td495271 556(mare)Tj0 Tc 8.8 0 9.0.8 319495271 556bly)Tj0.048 Tc 8.8 0 0 855. 095s495271 556col.8 344.9045 0 8.8349 0 Td[episod[(ovary)-39-1768 2T 1.848 0 Tdeverj97 0 8.14 0 8.8 9 351.81318-216.56 Tm(on86.8 369.5days,Tc 8.9097 0 0 883.05 Tc 9.2770 8.819484545.28 Tcoinciding)Tj0.048 Tc 8.8 0 0 4235961.2484545.28 TTc 9.c 8.9097 0 0 8.8 416.7913 5 29853.0484545.28 T0 8.8 47513 8.8 476155 1.700484545.28 T 8.8')Tj0 Tc53 8.8 4761558454459 484545.28 The5 Tc 8.90)Tj6.56 Tm(time,)Tj00 8897.819 0 8.8 eriodsto)Tj5947)-39-05 00T 1.8 2T69.5Long-1ermo)Tj59420 0 85(ma8 369.5soluTm( Tm(pos-)12ther)Tj0.0.0434ther)T16 Tm(or)Tj9.80.9623 0 0 82556.53 Tc 88 Tm(oproat)m-1.255 0098.8 476155 6in20.Tc 88 Tm(oinclud Tc 8.8 58 8.8 296.795iTj8.8 4445.Tc 88 Tm(otre5 0 8.8 496.7795 545.7.05 Tc 9.25.7Tj63 5 5d(cause).9342 556.56 Tm(time,)Tj2555 585 5d(causeTc 9.c 8.9097 0 0 024(palpation46n4273 5 5d(causesuppt)m.93m(ind9.99 Tc 8.8 0 98 23.53 T 5d(causeprog111er15.09358 029.9623 0 0 84ed9714 T 5d(cause(altrenog111)Tj0.048 Tc 8.8 0 0 o)Tj7892 83.2.738 0(5944m(or)Tj9.262670 8.8 457.332550157 83.2.738 0(mg/kg)Tj0.048 Tc 8.8 0 0 3 1.449 83.2.738 0[(p.o.)-821(s.i.d.))-8719.0616 Tm(or)TjTj8038 0 0 8.8 3 5)Tj2 83.2.738 0( 49v Tm(ovari4258 8.8 296.795iTj8 8.0 81 83.2.738 0(1071 0 0 8.8 4765 6os-7701.4188 5romTc 8.9097 0 0 9531 8.8 0 0 o)Tj789 T825571 556(c6urring)Tj...44555 534.24 T9j8(l825571 556during)Tj..39.555 534.24 72.213.0425571 55662 Tc 8.8 29.9048 Tc 8.8 0 0 3905 0(l825571 556physiologicm(ind.9097 0 0 896 416.7913 5 5)T68l825571 556brTc ing)Tj0 Tc 5.048 Tc 8.8 0 0 886.8381 825571 556seas 8.8 296.7795 8 0291 8.8 0 0 o)Tj62 58512545.28 TThenare)Tj0 Tc 8.8 0 320.098512545.28 T0 8.8 4751892 0 85 611.75(1.55512545.28 T 8.8)Tj0.048 Tc 8.8 0 0 3 7in28 4412545.28 T8 Tm(pri423.0480 4731.4188 normalTj97 0 8224os-19.8 369.5cycl.ng)Tj0.0487(is.8 369.5(i.eto)Tj5967 0 ..075 8.8 4761554.286.55512545.28 Tspring)Tj....569 0 Td(t470 019 T812545.28 T41 -1.20.048 Tc 8.8 0 0 8.4d)Tj55512545.28 Tsum 0 8.8 496.7795 540583 8.8 0 0 o)Tj85d()Tj52cause).r),42 556.56 Tm(time,)Tj235)Tj)Tj52caus8.0r,)-9.1oinT16 Tm(or)Tj9.61555 534.24 455779j)Tj52caus(extrem8)Tj0.048 Tc 8.8 0 0 37.24 95s4Tj52caus(casesTc 8.9097 0 0 920 8.8 476155Tj023.4Tj52caus(Ther8.8 475011555 534.2442724 76s4Tj52caus(chr15icare)Tj46 416.7913 54045.77()Tj52cause).dicm0 0 8.8 4.048 Tc 8.8 0 0 18 28.8 44Tj52causeis.8 496.7795 542c 9.11 0 0 85.7T1(ma83905...8 0nom(ovari243.048 Tc 8.8 0 0 313.449 3905...8 0possiat).8 496.7795 54556(palpation47.6578 3905...8 041 -1.2Tj0 Tc 8.8 0 366.2138 3905...8 00 8.8 4750821Tc 8.8 0 3826.70 T3905...8 0 8.8)TjTj0698.8 47615505..43T3905...8 0has-1.20.048 Tc 8.8 0 0 82359.92 3905...8 0noTc 8.9097 0 0 9521Tc 8.8 0 8ted3Tj2 3905...8 0pot.93im(ind.8 0 i6Tc 05 T97.83.781 3905...8 [(value.0426(a T(94(a616 Tm(or)Tj9.259.11 0 0 85. 28860 37.221 556broo -1.2pri46.9048 Tc 8.8 0 0 324d)181 37.221 556 8.8,42 556.562 4738 369.5sh).8 496.7795 540944Tc 8.8 0 366.6277(37.221 556ca 8.8 4.048 Tc 8.8 0 0 383.766(37.221 556b).8 496.44550481.4898 369.5ovariectomize -1.20.0487T188 369.5toTc 8.9025250481.2738 369.5facilitat8)Tj0.0484d)001.4188 a.8 496.7795 543249.11 0 0 85. 28892 3685)T0 8.8 erman Tm(ov 0 (1.(palpation42.0 81 3685)T0 8.8soluTm()Tj0.048 Tc 8.8 0 0 37Tj794163685)T0 8.8toTc 8.9097 0 0 90 Tc 8.8 0 387Tj0983685)T0 8.8th8)TjTj36 Tc 8.8 0 9825 0(163685)T0 8.8proat)mto)Tj/T1_0 550f8.9023795 543Tc 8.543T5. 291.(3 29321 556Post-1071 0 0 8.8 4767795 543143Tc 8.543T360 8608(3 29321 556hematomao)Tj/T1_2 550f8..048 Tc 8.8 0 0 o)Tj37.4332557T0 8.8ATc 8.9097 0 0 960 8.8 47615305..887932557T0 8.8seco1 -1.2Tj8796.795iTjted3900132557T0 8.8scenario(ind9.921Tc 8.8 0 371.4935132557T0 8.8th5 Tc 8.90)87.048 Tc 8.8 0 0 38....10132557T0 8.8sometimesTc 8.9020 0 85(588 369.5results-1.20.048556.5 her)TjinT-9216col.8 -452(sign)T16 T-18.70(l 1.848 0 Tdi 8.8 47631950481.1701.4188 associm0 0 8.8 4.0485T1(98 369.5Tc 9.c 8.90.886.562 1748 369.5ov71 0 0 8.8 4.0484d44a8 369.5is.8 496.7795 548.8 416.7913 518.77738)1288 Tm(oth8)TjTj74555 534.24435557s.8)1288 Tm(oforma0 0 8.8 9.78Tc 05 T97.85 02)T0)1288 Tm(oof(ind.8 0 i6Tc 05 T97.86.15 6o)1288 Tm(oa.8 496.366.0480 7938 369.5larg).8 496.7795 541609.11 0 0 85. 2862T0)Tj(causehematomao)Tj5455.555 534.24 5d783.0)Tj(cause0 8.8 9.39.555 534.24 63.813.0)Tj(cause62 Tc 8..048 Tc 8.8 0 0 383.6Tj55)Tj(cause0varj97 0 8491.048556868 369.5seco1 arj97 0.0485T3038 369.5toTc 8.90 T950481.78Tc 69.5ov71 0 0 .8.8 476313795 -20.1l 1.848 0 TdOccas 0 alTj97 0 897 0 0 90 Tc 8.8 0 3 8.509829056..8 00 8.8 475048796.795iTj6...445529056..8 0normal8.8 4763288 0 i6Tc 05 T97.03d)095529056..8 0post-1071 0 0 8.8 4767795 541986Tc 05 T97.63.9025529056..8 0hemorrhag813T57.25.28 T8nto8.8 9.39.555 534.24 15.813.057.25.28 T62 Tc 8.8 39.9048 Tc 8.8 0 0 33j(9057.25.28 T 49vious.8 496.306os-1068 369.5foll.871 r97 0 897 0 0 9926Tc 05 T97.06.188.057.25.28 Tstructu.8)Tj0.048 Tc 8.8 0 0 4 5d1941657.25.28 T6oTc 8.9097 0 0 9764Tc 8.8 0 455.656 457.25.28 Tform(ind.8 0 i6Tc 05 T97.88.7059057.25.28 TaTc 8.9097 0 0 953 Tc 8.8 0 986.1581657.25.28 Tcorpus.8 4750839.11 0 0 85. 28627 268545.28 Themorrhag.87m(ind.8 0 i6Tc 05 T9736 d)027 268545.28 Tis.8 496.1550481.178 369.5excessiv).8 496.7795 54..569 0 Td(t415.3c 5.268545.28 T41 -1.20.048 Tc 8.8 0 0 835578590568545.28 T497 0 843450481.08Tc 69.5larg).8 496.7795 540884Tc 8.8 0 46852227 268545.28 Thematoma,-1.2Tj8674.11 0 0 85. 27657 2 7in2.28 T60-3008.8 9.3426 8.8 0 0 326.618 T2 7in2.28 Tmm(ind.8 0 i6Tc 05 T97343.8427 2 7in2.28 TinTc 8.9097 0 0 8244Tc 8.8 0 353.9121 2 7in2.28 Tdiameter,42 556.56 Tm(time,)Tj93T1(m3 2 7in2.28 Twill8.8 4764Tj50481.768 369.5form.8.8 4764T86.562 7028 369.5This-1.20.0482 1828 369.5is.8 496.236.0480 8801.4188 usualTj97 0.04855262 her)Tja 8(94(iso848616 Tm(or)Tje,)104.11 0 0 85. 2 (13T5465...8 01 0e -1.2Tj808355 534.24 18..82T5465...8 0ev Tm(ov54556(palpation41.4178 5465...8 041 -1.29.39.555 534.24 5750133T5465...8 00 8.8 4750821Tc 8.8 0 383.874T5465...8 0 8.8)Tj56.56 Tm(time,)Tj96.4542T5465...8 [(typicmlTj-319Twill816 Tm(or)Tj91672 8.8 0 0 4 5d826 5465...8 0co1tinu8)Tj0.048 Tc 8.8 0 0 48555742T5465...8 [(to-360(cyct).16 Tm(423795 -21.8178 1.848 0 TdnormalTj97 0.048551901.4188 as.8 496.7795 542893Tc 05 T97343.6526T2ted2.8 00 8.8 475214255 534.24 58.782552ted2.8 0hematomao)Tj0.048 Tc 8.8 0 0 482583j552ted2.8 0slowTj97 0 82986.562 9048 369.5regressesTc 8.9097 0 0 816555 534.2446 d51(982ted2.8 0over)TjTj2 Tc 8.8 0 98ed2539T2ted2.8 00 8.8 40.048 Tc 8.8 0 0 499 8182T5ted2.8 0fol848697 0 826795 -235088 1.848 0 Tdlowing-1.20.04855698Tc 69.5weeks.8 496.7795 54243255 534.24 51.0212T524d15.28 T41 -1.20.048 Tc 8.8 0 0 6..73178524d15.28 TTinTc 8.9097 0 0 8103Tc 05 T97385539098524d15.28 Tsomeo)Tj0.048 Tc 8.8 0 0 48 29498T524d15.28 Tcases)Tc 8.9097 0 0 874796.795iTj435541798524d15.28 Tmo1thsto)Tj/T1_1 550f810j26 8.8 0 44460 83438524d15.28 TIto)Tj/T1_2 550f8..048 Tc 8.8 0 0 477..432T524d15.28 Thas.8 496.7795 542381 8.8 0 0 493d)068T524d15.28 Tbeen)TjTj2 Tc 8.8 0 297Tj09821556..8 00 8.8 4751536 8.8 0 0 31558222821556..8 0author'sind.(467.048 Tc 8.8 0 0 49252142521556..8 00 8s Tc 8.8 359795 -2252088 1.882T69.5ovaria 8.8 4767795 54027555 534.24 28..026T2Tj84.8 0hematomas-1.20.048 Tc 8.8 0 0 76455.4T2Tj84.8 0usualTj97 0 8498.048553178 369.5occursTc 8.9097 0 0 8874.11 0 0 843556631T2Tj84.8 0Tc 9out97 0 8492.048 Tc 8.8 0 0 466.4696T2Tj84.8 0causing-1.20.048557(98 369.5anj97 0 8485795 -225998 1.827 69.5outwar -1.20.048440868 369.5signsTc 8.9097 0 0 8848 c 05 T9735645521 190 84.28 Tdetectableo)Tj0.048 Tc 8.8 0 0 481d)027 190 84.28 Ti 8.8 4767795 5419.555 534.2441559733T190 84.28 T0 8.8 4Tj8468.11 0 0 8430 818T190 84.28 T 8.8,8.8 9.4779.11 0 0 84 7i927 190 84.28 Tbu Tc 8Tj2 Tc 8.8 0 975d8098190 84.28 T0 8.8 40.048 Tc 8.8 0 0 492.63j55190 84.28 Tocca848697 0 8 51795 -2252868 1.848 0 Tds 0 al8.8 4767795 540821Tc 8.8 0 32559774.180.8 0 8.8t470.5c 5.180.8 0a1 -1.20.048 Tc 8.8 0 0 89050027 180.8 [(it)-542Thas.16 Tm(or)Tj92381 8.8 0 0 5. 26468.168572.28 Tbeenov0.048 Tc 8.8 0 0 891 9098.168572.28 Tcolic.Tc 8.9097 0 0 .562 8.8 0 0 5. 283n2.1 7i68.28 TManagem Tm(ov0.048 Tc 8.8 0 0 3n257217T1 7i68.28 Tis8.8 4767795 54037c 8.8 0 0 625783451 7i68.28 Taime -1.256.56 Tm(time,)Tj91 3449 1 7i68.28 Tat97 0 829750481.3098 369.5allevia0 ng-1.209097 0 0 .2 Tc 8.8 0 947in739 1 7i68.28 T0 8.8 47513796.795iTj464.6183 1 7i68.28 T 8.8's)TjTj898 Tc 8.8 0 99556.9551 7i68.28 Tpain.8 4750915 8.8 0 0 5. 278 5.14 264.28 Tdur ng-1.20 .2 Tc 8.8 0 326.1339.14 264.28 T0 8.8 4Tj889555 534.24n41.4249.14 264.28 Tacute97 0 8378.048 Tc 8.8 0 0 65.4417T14 264.28 Tiso1 0e -1.2.90454.048557348 369.5episode.-1.20.04844013 her
OTHER CONDITIONS 17
disposition by keeping the mare out of ovulatory estrus
with the use of altrenogest as described above.
Ovarian tumors
Occasionally the presence of a large ovarian tumor
(most commonly a granulosa-theca cell tumor) may
result in the presentation of a mare with the primary
complaint of intermittent colic especially associated
with exercise, with or without the more common com-
plaint of behavioral abnormalities. In the author's expe-
rience, this history has accompanied the presentation
of young race fillies or mares who have been referred
for intermittent colic, reluctance to train, and/or poor
performance who upon examination have been discov-
ered to have an abnormally enlarged ovary. It is likely
that the pain associated with the enlarged ovary is the
result of the stretch on the broad ligaments as the
tumor bounces up and down with the mare's move-
ments. Treatment is surgical removal of the affected
ovary.
Vaginal injuries during service
Colic signs may also occur secondary to natural service
of an open, estrus mare. In situations where a stallion's
penis is long relative to the mare's vagina, the stallion is
forceful and vigorous during intromission and thrust-
ing, and/or the mare is restrained so she is unable to
move forward to protect herself from internal abuse,
during copulation the mare's vagina may be bruised
and even torn to the degree where the stallion's penis
penetrates into the peritoneal cavity through the cra-
nial vaginal wall. Such injuries may be suspected any
time there is fresh blood on the stallion's penis or com-
ing through the vulva of the mare immediately follow-
ing dismount, and these findings warrant an immediate
manual vaginal examination of the mare to ascertain
the degree of injury. Immediate sexual rest of the mare
is indicated to prevent further damage, as many times a
full vaginal rupture during copulation is preceded by a
vaginal contusion that occurred during a previous cover
during the same cycle. This kind of injury may be pre-
vented via AI breeding or by the judicious use of a
breeding roll where live cover breeding is mandated by
a breed registry and is unavoidable. Colic signs may be
mild to severe immediately following the cover and are
sometimes accompanied by tenesmus, or the signs may
develop gradually over the next few days following the
traumatic cover. A potentially severe peritonitis may
form after gross contamination of the peritoneal cavity
via direct contact with the stallion's penis, his ejaculate,
or vaginal flora. Acute and severe colic signs may also
develop if a portion of the mare's viscera becomes
entrapped through the vaginal rent. Treatment for this
injury in general includes sexual rest (30-60 days),
broad spectrum antibiotics, and a Caslick procedure to
prevent further peritoneal contamination via possible
pneumovagina. The rent in the vagina is usually small
and dorsal to the cervix and is left to heal on its own
much as a colpotomy site would be. The mare should be
prevented from lying down for the first several days fol-
lowing the injury so as to further lessen the likelihood
of secondary herniation of viscera. If the rent is in the
vaginal floor or if it is excessively large however, an
attempt to suture and close the deficit should be made.
It is important to remember that the mare may have
conceived as a result of the breeding so routine follow
up rectal ultrasound examinations of the reproductive
tract in order to check for pregnancy should be per-
formed 14-18 days post-ovulation.
COLIC IN THE PREGNANT MARE
Many pregnant mares show signs of abdominal pain at
one point or another during the course of their gesta-
tion. These episodes are typically very brief and mild. A
mare may suddenly flank watch or kick at her belly for a
few moments and become agitated, or perhaps she may
become quiet, inappetent, and even lay down for a little
while. No doubt some of these signs of discomfort may
be attributed to uncomfortable, vigorous movements of
the foal, mild stretching of the broad ligaments upon
the movement of the mare or the foal, or mild digestive
upsets. In most instances these signs resolve sponta-
neously on their own with little or no need for treat-
ment. It is also worth mentioning that many
inexperienced owners may become alarmed upon find-
ing a late gestation mare who is lying down and groan-
ing and mistake it for a colic episode when in fact all she
is doing is trying to rest. The ever increasing size of the
gravid uterus in these late-term mares presses the
abdominal viscera up hard against the mare's
diaphragm when she lies down making breathing diffi-
cult and causing her to groan. Upon rising these mares,
however, are comfortable and go about their business
which usually entails looking for something to eat.
Fortunately the sort of episodes described above form
the majority of colic cases reported in pregnant mares,
however more serious conditions can and do occur.
Feed impactions
Individual mares seem to be prone to developing feed
impactions within their large colon and/or cecum as
pregnancy advances. The exact mechanism behind how
this occurs is unknown, but in all likelihood the increas-
ing size of the gravid uterus adversely effects bowel
353
17 COLIC
motility in these mares leading to an increase in the
transit time of the ingesta through the large colon. This
in turn leads to increased water resorption from the
slow-moving feed materials resulting in an impaction.
These mares usually present initially as low grade colic
with decreased manure production and mildly elevated
heart rates, but the longer standing the impaction the
more her clinical signs may deteriorate as gas builds up
behind the impaction. Direct palpation of the
impaction per rectum is often difficult due to the pres-
ence of the enlarged uterus and fetus which fill the cau-
dal abdomen obscuring the viscera. Treatment includes
aggressive overhydration with intravenous and or oral
fluids, and oral laxatives or mild cathartics such as (min-
eral oil, dioctyl sodium sulfosuccinate (DSS), and low
dose magnesium sulfate) to try to soften, lubricate, and
shift the mass of impacted ingesta. It is also important to
judiciously control the mare's pain with an analgesic
such as flunixin meglumine as needed to prevent her
from rolling, during the course of which she may inad-
vertently cause a torsion of her colon or gravid uterus.
Hand walking may also help to take her mind off her
discomfort, and help stimulate her gastrointestinal
tract, but be careful that an overzealous owner does not
exhaust the mare in their attempt to do something
helpful. Feed should be limited as much as possible
throughout the episode so as not to compound the sit-
uation, but in long-standing impactions the mare
should be supported parenterally as complete anorexia
may compromise the pregnancy. As in all things pre-
vention is the best route and care should be taken to
ensure that all pregnant mares have access to and are
consuming plenty of fresh, clean water and have plenty
of opportunity to move about freely. Laxative feeds
(grass and mashes) should be incorporated into the
mares' diets whenever possible. Individuals who have
demonstrated a tendency toward impactions in the past
may be preemptively administered mineral oil: either in
their feed on a regular basis if they will eat it or via naso-
gastric tube at the first sign of decreased or dry manure
production if they are not too stressed by the proce-
dure.
Dorsoretroflexion of the uterus
Cases of colic caused by dorsoretroflexion of the uterus
in gravid mares are extremely rare in the author's clini-
cal experience, but have been reported to occur.
Affected mares typically present sometime between 7.5
and 11 months of gestation with acute, moderate to
severe colic signs accompanied by abdominal straining,
constipation, and swelling of the vulva and perineal
region. Administration of analgesics is typically ineffec-
tive in controlling the mare's pain. Diagnosis of this
354
condition is made upon finding a tense uterus within
the pelvis with the fetal head and limbs in a normal
birth presentation overlying and obscuring palpation of
the mare's cervix. (It is important to differentiate the
presence of a tense uterine wall in this painful condi-
tion from the occasional incidental rectal finding in
late-gestation mares of a foal that is overlying the mare's
cervix dorsally but which is encased in a relaxed uterus
and causing no discomfort to the mare.) Vaginal exam-
ination is performed following the rectal examination
to differentiate between a mare with a dorsoretroflexed
uterus and a mare who is actively aborting. In the for-
mer case the cervix will be found to be closed in the cra-
nial extent of the vaginal canal and ventral to the fetus
which is palpable dorsal to the vagina through the vagi-
nal wall. This is in direct comparison to the aborting
mare whose cervix will be dilated and the fetus and its
membranes will be readily palpable within the vaginal
canal through the dilated cervix. Treatment of dor-
soretroflexion includes the administration of uterine
relaxants - 200 mg isoxsuprine i.m.: or 200 Ilg clen-
buterol slow i.v, or i.m, once, or repeatedly over 3-6
hour intervals for 1-2 days (van de Plassche 1987) - and
repelling the now relaxed uterus containing the fetus
back into the abdomen via careful rectal manipulation.
Resolution of colic signs usually occurs within 15 min-
utes of administration of the uterine relaxants, and it
has been reported that restricting the mare's food
intake and regular hand walking helps to return the
mare to normal within a few days. The cause of this
condition is unknown, but once the condition has been
corrected reported relapses are uncommon. Aborting
mares will occasionally exhibit colic signs preceding the
abortion.
Uterine torsion
Included in the differential for any third trimester mare
with signs of colic is uterine torsion. Uterine torsion in
mares has been reported to occur from 180-540
degrees in either direction, and unlike the cow, the site
of the twist is frequently cranial to the cervix within the
uterine body. This condition is rarer in mares than it is
in the bovine. The reason for this seems to be that the
dorsal attachments of the broad ligaments make the
equine uterus less prone to 'flipping over' along its long
axis. As in the bovine, however, the cause of uterine tor-
sion in the mare still seems likely to be the result of
inopportune fetal activity possibly combined with get-
ting up and down or rolling over by the dam. Affected
third trimester mares typically present pre-term with
signs of persistent/recurrent mild to moderate colic.
Except in cases where a segment of bowel has become
compromised as a result of the uterine twist, these
mares will typically continue to pass feces. The severity
of the pain sometimes .etms to be related to the degree
of torsion, and mares who also have bowel entrapped
along with the twisted uterus may demonstrate severe
pain. (kcasionally affected term mares will present at
parturition wth a dystocia that is a result of the t\lsted
uterine body ocduding normal delivery of the foaL
Diagnosis of uterine torsion is made typically by rec
tal {xaminaljon as the tvist is usually cranial to the
cervix and therefore is not readily palpable per vagina
in the pre-term mare. Rectal identifcation of the taut
hands of the stretched broad ligaments is the hallmark
of this condition. The broad ligament from one side of
the uterus is pulled over the top of the uterus past mid
line toward the side of the direction of the uterine twist.
The other broad ligament is pulled ventrally under
neath the uterus away Ii-om the side of the twist.
Therefore when viewed from the back of the marc a
countercloek\vise ist to the marc's left wll fnd the
right broad ligament pulled horiwntally over the top of
the uterus to the left and the left broad ligament will be
pulled ventrally underneath the marc's uterus t the
mare's right. Conversely a clockwise twist of the uterus
t th(" mare's right will find the left broad ligament
pnl!t'd horizonta!Iy over the top of the uterus to the
marc's right and the right broad ligament pulled ven
trallv under the uterus to the mare's left. The practi
ti(mer can often make an educated guess as to the
degree of the torsion based on the palpable tightness of
the broad ligament bands and the twist in the uterus
itself. Likewise an impression of the dtgree of possible
uterine compromise may h made based upon the feel
of the uterine wall (Le. either thick and taut or sti!!
somewhat pliable) and/or its appearance on rectal
ultrasound. Occasionally the small colon becomes con
stricted as a result of the uterine twist and may obstruct
the examiner's ability to perform a filll rectal examina
tion to determine the extent of the insult.
The fNllS will typically be displaced cranially in the
alomen by the twist. in th Illerine body and may be
out of reach of the practitioner per rectum. In this
instance, fetal viability may not be determinable via rec
tal examination and instead may be determined by
detection of fetal cardiac motion or spontaneous fetal
movement via transabdominal ultrasound of the mare.
Depending on the degree of the twist and the duration
of the insult, the blood supply to the uterus may
become suffciently compromised to (;ame fetal death.
The uterus likewise may become edematous and friable
and in some extreme cases even necrotic, and the risk
of uterine rupture and peritonitis becomes a real possi
hilit\', It is therefore important to hoth the foal's and
the mare
'
g continued well being that the presence of a
llttrin(" torsion he r<pidly identified after it occurs and
OTHER CONDITIONS 17
immediate steps taken to correct the torsion and return
the uterus to its normal position <nd confguration.
Options for correcting the uterine torsion include
rolling the mare
standing flank surgery
ventral midline celiotomy, and
in the case of foaling mares who have an open
cen1x and a less than 270 degree t\vist (so that the
clinician, per vagina, can get an arm through the
t"1St and alongsidt the foal) manual rotation of the
foal (and uterus) through th(" c("n1x to a normal
position may be possible.
Vl11en the marc is tractable and there are no indica
tiollS that the twisted uterus has alrtady ruptured, it is
the preference of this author and many others to correCt
the uterine torsion in a pre-term mare via a standing
flank laparotomy. A incision is made through the
mare's flank using a grid approach, and the incision is
preferably made on the side that the marc's uterus is
twisted to. The direction of the twist is (:onfirmed via
intra-abdominal palpation of the uterus and the broad
ligaments, and then the uterus is dctorsed by carefully
reaching underneath the uterus and gently rocking the
uterus to gd up enough momentum to lift the twisted
uterus up and pushing it over in the opposite direction
of the twist to return it to its normal position. I needed
the foal's limbs may somttimes be grasped through the
uterine wall to help the surgeon facilitate this maneuver,
but at all times care should be taken not to cause any
tears in the uterine wall. This may be especially chal
lenging if the uterus has become friable. If the preg
nancy is advanced enough it may require that a second
incision be made in the opposite flank and two surgeons
work simultaneously (one pushing and the other
pulling) to untv.ist the uterus and return it to its normal
position. Afkr the torsion has been corrected the sur
geon then carefully palpates the dorsal smface of the
uterus and broad ligaments to confrm that the uterus is
no longer twisted. The surface of the uterus is also care
htlly palpated for the presence of any tears (especially
where it was twisted) and an assessment of fetal viability
is made by trng to detect spontaneous fetal movement
or the presence of a heart beat in the foal's chest pal
pated careh!!ly through the uterine wall. If the foal is
dead, once the torsion has been corrected the mare
should go on to abort naturally postoperatively, or deliv
ery can he induced. The delivery of the dead fetus
should be supersed so any malpositiol1s may be quickly
corrected, and to assist the mare and minimize her
abdominal effort to rt'duce stuss on the surgical inci
sion. If the foal is alive and has not heen compromised
too severely the pregnancy usually progresses unevent
fully and successfully to term after surgical correction.
355
17 COLIC
Rather than surgery some pracuuoners prefer to
correct the less severely twisted and compromised uter-
ine torsions by administering general anesthesia to the
mare and rolling her to untwist the uterus. Two meth-
ods have been described. In both methods the mare is
placed in lateral recumbency on the same side that the
uterus is twisted to (i.e, if the mare's uterus is twisted to
her left side she is placed with her left side down). The
mare is then rolled from one side, up into a dorsal posi-
tion, and then over onto her opposite side and then up
into a sternal position. In the first method this maneu-
ver is done quickly so that the weight and inertia of the
heavily gravid uterus will hold the uterus still while the
mare is quickly rolled around it. In the second method,
a plank is positioned on the mare's flank and weighted
down by a person sitting or standing on it, the mare is
then slowly rolled over as described above. The
weighted plank is used to hold the gravid uterus still as
the mare is rolled carefully around it, effectively untwist-
ing the uterus. Care must be taken to identity the direc-
tion of the uterine twist correctly in the first place so
that the mare is positioned on the proper side, other-
wise these maneuvers may tighten the twist further if
the mare is rolled in the wrong direction. Once the
maneuver has been completed the mare is re-examined
rectally to ascertain whether the uterus has been
untwisted. If the uterus is still torsed additional rolling
attempts may be made. If the torsion is judged to have
been corrected then the mare is permitted to wake up
and care is taken to ensure she gets to her feet without
rolling around during recovery and possibly retorsing
her uterus. The 'plank in the flank' technique in the
author's experience is particularly successful in correct-
ing uncomplicated bovine uterine torsions, but the
same degree of success is not typical in the mare. This
may be a result of the fact that the mare's flank is much
shorter and more tightly muscled than a cow's thereby
making it more difficult to effectively place the plank to
hold the mare's gravid uterus in place while she is
rolled. It has also been the reported experience of some
practitioners that use of these rolling techniques results
in a higher risk of complications after successful correc-
tion of the twist. For these reasons therefore it is not the
author's first choice for attempting to correct uterine
torsion in a mare.
In the foaling mare, it may be possible to correct a
uterine torsion per vagina provided the twist is less than
270 degrees and the cervix is dilated enough to permit
the clinician to reach the foal and place his or her arm
ventrolaterally along the foal's body. The foal is then
grasped and manipulated so as to rock it side to side
progressively in the opposite direction of the twist until
enough momentum is achieved to flip the foal up and
over taking the uterus with it to resolve the twist. Once
356
the twist has been fully corrected and the foal posi-
tioned as needed to achieve a normal presentation then
the foal may be delivered. This maneuver requires some
finesse and upper body strength to accomplish, but can
be quite successful. The use of an epidural to control
straining, and positioning the mare in a standing posi-
tion with the hind end slightly elevated to provide the
maximum room to maneuver within her will also maxi-
mize the chances for success. (The abdominal viscera as
well as the foal will be pushed backwards into the pelvis
when the mare is recumbent, effectively decreasing the
available space in which to work.) The use of a detor-
sion rod in an awake mare is not recommended. It
should also be remembered that it is contraindicated to
anesthetize a dystocia mare to facilitate correction with-
out being able to elevate or hoist her hind end up at the
same time to provide room to work inside her.
A ventral midline celiotomy is indicated to correct
uterine torsion in the mare in those cases where the
uterus is already believed to be severely compromised,
or where the gastrointestinal tract has become entan-
gled in and compromised by the torsed uterus. This
approach permits better access to the abdominal viscera
and uterus which can then be more fully examined and
repaired than could be accomplished with a flank
surgery. In the case of very late pre-term mares it may
also permit easier manipulation to effect the untwisting
of the large, gravid uterus. This approach is also indi-
cated when other correction techniques have failed,
and there is the advantage that a c-section can also be
performed during the course of the procedure to facili-
tate delivery of the foal if needed. The risk of incisional
complications following this procedure in a heavily
gravid and subsequently foaling mare must be recog-
nized, and therefore this technique should be reserved
for those situations where it is absolutely indicated.
Potential complications that may follow resolution
of the uterine torsion using any of these described tech-
niques include
tearing of the uterus and resultant peritonitis in the
mare
premature placental separation and subsequent
death and abortion of the foal.
Prognosis for the mare in general is good provided
there has been no severe uterine damage or peritonitis.
Prognosis for the live foal is also good provided the
degree or duration of the torsion has not been severe
and is expediently corrected.
Other conditions duringpregnancy
Other pregnancy related conditions that may cause
signs of abdominal pain in a pregnant mare include
OTHER CONDITIONS 17
pending prepubic tendon or other abdominal wall rup-
tures and imminent uterine rupture. Rupture of the
prepubic tendon or other abdominal wall musculature
is most commonly seen secondary to trauma or to the
stress of the weight of excessive ventral edema or an
abnormal pregnancy (hydrops or twins). The pain
demonstrated by the affected mare is a direct result of
the tearing of the abdominal support structures and/or
the possible herniation and strangulation of bowel
through the rents. Uterine rupture may also occur sec-
ondary to trauma or to a uterine torsion, placental
hydrops, or twin pregnancy. In the event of uterine rup-
ture the mare typically shows signs of colic just prior to
the rupture itself. Once the uterus ruptures there is typ-
ically an immediate respite in the colic signs because
the tension is relieved. The mare's signs however will go
on to deteriorate as secondary hemorrhage occurs
and/or peritonitis develops. In both scenarios, signs of
colic may not be the classic sign of the disorder but may
well be what the owner recognizes and reports. In each
presented case of colic the clinician is therefore
reminded to be as thorough as possible during the
examination and work up of a pregnant mare in order
to correctly identify the source of the pain.
COLIC IN THE PARTURIENT MARE
In the normal course of foaling, stage III labor (passage
of the placenta) normally causes some degree of dis-
comfort and pain to the mare. The signs associated with
the uterine contractions that are normally occurring at
this time range from mild discomfort (occasional kick-
ing at belly, stretching out and posturing as if to urinate,
laying down quietly in a sternal position, and flank
watching) to semi-dramatic bouts of pain (agitation, fre-
quently getting up and down, rolling, etc.). The major-
ity of mares seem to pass their placentas within 30-60
minutes of the foal's delivery (> 3 hours = retained). It
is not unusual for signs of discomfort to persist (usually
for no more than an additional hour) after passage of
the placenta, since uterine contractions continue as the
mare begins to involute and oxytocin release is stimu-
lated by the foal's initial nursing. More extreme demon-
strations of discomfort associated with these 'after
cramps' seems to occur more frequently in maiden
mares than in experienced multiparous mares. If the
mare is distracted enough by this pain that she is negli-
gent of her foal she may be successfully managed with a
single administration of low dose flunixin meglumine
(0.5 mg/kg i.v. is usually adequate) and hand walking
(if needed) to provide her with relief and distraction
from her discomfort. Typically throughout these
episodes a mare's vital signs are stable ( mild elevation
in heart and respiratory rates), and the mare recovers
quickly with little or no recurrence past the initial
episode. She remains bright and comfortable, with a
good appetite and interest in her foal and maternal
duties. This is in stark contrast to the parturient mare
whose pain is caused by serious parturition-related
pathologies.
Arterial rupture
Rupture of the middle uterine artery (most commonly),
utero-ovarian artery, or the external ileac artery at or
around the time of foaling is a significant cause of colic
and death in older (> 11 years) foaling mares. Rupture
of the middle uterine artery or utero-ovarian artery may
result in the formation of a large, painful hematoma in
the ipsilateral broad ligament that may dissect below
the serosal uterine surface if the hemorrhage is con-
tained within these structures. Pain results from the
stretching of, and pulling on, these structures as the
hematoma forms. Formation of this clot and the associ-
ated drop in arterial blood pressure due to blood loss
stops active hemorrhage. If the broad ligament or
serosa subsequently rupture and hemorrhage is no
longer contained then the mare will rapidly bleed out
into her abdominal cavity. Rupture of the external ileac
artery, because of its anatomic location, results in the
mare directly and fatally bleeding into her abdomen.
Fatal bleeds are most common in aged mares (> 18
years), and unfortunately the first occurrence of this
disorder is often a fatal one.
Age-related degeneration of the arterial structures
themselves has been theorized as a predisposing cause.
One study (Stowe 1968) has looked at copper levels in
older and affected mares and found that at the time of
foaling copper levels are significantly lower in older
mares than in younger mares, and that levels in affected
mares were lower than those in age-matched unaffected
mares. Copper has been associated with helping to
maintain vessel elasticity, so it is plausible that
decreased levels may predispose a mare to arterial rup-
ture at the time of foaling or during pregnancy when
arterial structures are under increased stress.
During pregnancy the uterine arteries increase in
diameter and tortuosity, and there is increased stress
within these structures due to concurrent increases in
blood flow, stretching of the broad ligaments, and fetal
movements. Parturition places additional stress on
these structures because of increased mean arterial
pressure during the foaling process and direct pressure
on these vessels as the foal is pressed through the pelvic
canal. The right middle uterine artery has been
reported to be the most frequently affected of these sus-
ceptible vessels. One theory as to why this occurs is that
357
OTHER CONDITIONS 17
fact that volume re-expansion will lead to an increase in
the mare's blood pressure which may renew or worsen
blood loss with disastrous results. The use of crystalloid
fluids to effect volume re-expansion may also dilute
blood coagulation factors and decrease blood viscosity
at a time when both are needed to promote hemostasis.
As a direct result of this therapeutic challenge, there are
two approaches to managing affected mares that survive
the initial stages of the hemorrhage - one conservative,
the other more aggressive. Regardless of the therapeu-
tic course chosen the single most important measure
that must be taken is to keep the mare as quiet as possi-
ble so as to cause no increases in her mean arterial pres-
sure (MAP).
The conservative approach to treatment primarily
involves minimizing stress or excitement of the affected
mare. The mare is kept in a quiet, darkened stall with or
without her foal (depending on which is least stressful
to the mare, and which is safest for a valuable foal).
Transportation of the mare is contraindicated, and
must be balanced against what can be accomplished
therapeutically on the mare's home farm. Tranquilizers
are usedjudiciously to help keep the mare calm, and, in
the case of acepromazine, to help reduce MAP directly.
Naloxone (8-32 mg/500 kg i.v., Le Blanc 1997) has
been anecdotally reported to be helpful in some mares.
Naloxone treatment promoted death in rabbits with
experimental hemorrhagic shock (Sherman 1998).
Analgesics (butorphanol 0.01-0.04 mg/kg i.m., Vivrette
1997) are also used as needed to control the mare's
pain. Attempts at volume re-expansion with fluids or
whole blood transfusions are indicated to preserve car-
diac output and perfusion but may increase MAP and
disturb any present hemostasis.
The more aggressive therapeutic approach involves
utilizing all of the above treatments as well as the care-
ful application of subtotal volume re-expansion with
crystalloid fluids to support tissue perfusion and whole
blood transfusions or synthetic oxygen-earrying fluids
(oxyglobin) as indicated to support tissue oxygenation.
Extreme care must be taken to keep MAP below normal
levels. It is also important to remember that anemia in
general is well tolerated provided blood volume is main-
tained, and that autotransfusion of about two-thirds of
the red blood cells lost into the abdominal cavity will
occur over time. For this reason whole blood transfu-
sion of affected mares is not advocated by many until
the mare's pevis less than 20 per cent. A further sig-
nificant consideration is that all mares must be carefully
cross matched with donor blood to avoid sensitization to
incompatible blood types and possibly causing neonatal
isoerythrolysis in future foals. In this regard the use of
synthetic oxygen-carrying fluids (oxyglobin 7.5-10
ml/kg, Sprayberry 1999) may have a distinct advantage
over whole blood transfusion as they are non-reactive in
terms of blood compatibility, and high volume expan-
sion is not required so support with minimal increases
to MAP is possible. When evaluating each mare for the
possibility of using more aggressive attempts at support
it is important to consider carefully what will be most
beneficial to the eventual outcome - a low hypotensive
state or the utilization of a low level of support for per-
fusion and oxygenation. At the time of this writing,
there are presently no survival comparisons for the two
approaches and the clinician can only use his or her
best judgment.
Additional agents and therapeutic measures have
been used or suggested for treatment of mares with
uterine artery rupture and may be beneficial. These
include simple supportive measures such as nasal oxy-
gen (if tolerated well by the mare) and applying exter-
nal pressure to the mare's abdomen via a belly wrap.
Hemostatic promoting agents such as aminocaproic
acid (10-20 mg/kg slow i.v.), intravenous 10% formalin
(anecdotal), and conjugated estrogens have also been
used. Anti-inflammatory agents (flunixin meglumine
and glucocorticoids) as well as antioxidant drugs (vita-
min E) may give support. Pentoxifylline (7.5 mg/kg
p.o., Britt and Byars 1997) is purported to increase red
blood cell deformability and may increase oxygen deliv-
ery to ischemic tissues, and therefore may be of benefit.
Finally, careful use of broad spectrum antibiotics ('care-
ful use' because affected mares have volume depletion
so some potential toxic effects of antibiotics may be
amplified) may also be indicated to protect against
infections that may occur secondary to ischemic dam-
age to the mare's bowel.
As discussed the prognosis for mares with uterine
artery ruptures is guarded. For those that survive the
acute episode, it is imperative that they be kept quiet for
several weeks as the clot resolves and the vessels slowly
repair as increases again in MAP during this period can
cause renewed bleeding. Final resolution of the
hematoma may take months depending on its initial
size. Mares that have survived their first episode ofuter-
ine artery rupture have a high likelihood of recurrence
with subsequent pregnancies and foalings. It is there-
fore recommended that affected mares are not re-bred.
If the mare has no other value than as a producer, and
must be re-bred it is recommended that the hematoma
be fully resolved prior to re-breeding and that the
mare's managers have a nurse mare lined up in case the
dam is lost on the next foaling. Prevention includes
keeping the pregnancy as stress free as possible (avoid
heavy exercise, stressful procedures, long transporta-
tion, etc.), and limiting roughage intake toward the end
of gestation so as to minimize cecal distention at the
time of foaling.
359
17 COLIC
Gastrointestinal complications of parturition
Gastrointestinal complications occur in parturient
mares as both a direct and an indirect result of the foal-
ing process. Portions of bowel may become entrapped
between the mare's pelvis and the gravid uterus during
the course of labor and become damaged. The small
colon is the structure most commonly traumatized in
this manner, resulting in bruising, ischemic compro-
mise from mesenteric tears, and even rupture and
extravasation of fecal material into the peritoneum.
Where small colon bruising has occurred mares experi-
ence compromised function and may present as consti-
pated immediately post-foaling, and by 48 hours
post-foaling they may begin to demonstrate signs of
colic with or without an elevation in temperature. By 72
hours if damage has been severe enough, the compro-
mised bowel may become leaky and peritonitis may
result. Diagnosis is made via rectal examination with the
identification of impacted small colon or a sausage-
shaped mass (the damaged segment) somewhere along
the length of small colon. Abdominocentesis will also
confirm the presence ofleaky, compromised bowel and
peritonitis in extreme cases. Surgical resection of the
damaged bowel may be indicated.
The tremendous increase in abdominal pressure
that occurs during the course of active expulsion of the
foal (stage II labor) may result in the rupture of a full or
gas-dilated viscus. The cecum in particular seems prone
to this kind of trauma with many ruptures occurring
near its base. The immediate effect is a disastrous peri-
tonitis due to contamination of the abdominal cavity
with the cecal contents that ultimately is fatal. Mares
rapidly demonstrate signs of severe shock immediately
post-foaling if there is a ruptured bowel, and diagnosis
can be confirmed via direct palpation of 'gritty' conta-
minated visceral surfaces or abdominocentesis reflect-
ing the gross fecal contamination. Mares experiencing
this kind of injury are doomed, and immediate
euthanasia once the diagnosis has been verified is the
kindest course. Limiting consumption oflarge amounts
of hay in late pregnancy immediately preceding foaling
may help prevent this sort of rupture by decreasing dis-
tention of the bowel with ingesta.
Perineal injuries
Mares who experience perineal damage (Ist, 2nd, and
"3rd degree perineal lacerations, vestibular bruising,
hematomas, excessive vulvar stretching, etc.) at foaling,
or who are especially sensitive to the pain of the nor-
mally postpartum swollen and inflamed perineal tissues
may experience a reluctance to defecate and secondary
constipation. Anti-inflammatory drugs (phenylbuta-
zone or flunixin meglumine) as well as local treatment
360
with topical anti-inflammatory ointments are indicated
to relieve pain and swelling of tissues. Administration of
oral laxatives (mineral oil) and laxative feeds (bran
mashes, grass, etc.) may help to soften the feces and
make their passage less painful to the mare so that she
is more willing to defecate.
Large colon displacements and tcrslon
For some as yet unknown reason, brood mares are
especially susceptible to large colon displacements and
torsions especially during the first 100 days post-foal-
ing. The combination of the sudden increase in avail-
able abdominal space post-foaling and changes in
exercise and metabolism in the postpartum mare has
been theorized as predisposing the brood mare's
colon, on its long mesentery to wandering from its
normal position. Vital signs and the degree of colic in
an affected mare are reflective of the severity of the
colonic disorder, i.e. a large colon volvulus will pre-
sent as a violently painful colic with a very high heart
rate (60-100 bpm) whereas a simple colonic displace-
ment may present with mild to moderate signs of colic
with a relatively normal heart rate. Diagnosis is once
again made by identification on rectal examination of
an abnormally positioned, gas-distended colon, and in
cases of torsion with bowel compromise analysis of
abdominal fluid will be reflective. Surgical correction
is required.
Uterine rupture
Rupture of the uterus at or near foaling can cause peri-
tonitis and/or abdominal pain. Diagnosis is made by
rectal and ultrasound examination in addition to
abdominocentesis and ventral midline celiotomy when
needed for both diagnosis and repair. If the tear is small
and dorsal postpartum, conservative treatment with
antimicrobials, crystalloids, colloids, peritoneal
drainage, and NSAIDs may be successful. There should
be no infusions made into a torn uterus. If there is gross
peritoneal contamination the prognosis is poor.
Inversion of the uterine horn
Lastly, though rare in horses, inversion of a uterine
horn post-foaling frequently results in acute pain within
the first few hours of foaling that is unresponsive to low-
dose analgesics. Pain is the result of the ovary and tip of
one horn becoming inverted and entrapped within the
uterine lumen. The myometrium proceeds to spasm
resulting in an intussuscepted ring. In response many
mares will begin to strain and the condition may
progress to a complete prolapse of the uterus through
the vulvar lips if left uncorrected. In the author's expe-
OTHER CONDITIONS 17
rience, invagination of a uterine horn has most com-
monly occurred in conjunction with a retained pla-
cen tao It may be caused by
the weight of the placenta pulling on the horn in
which it is retained
sudden pulling during attempts at manual removal
of the placenta
sudden pulling if the mare steps on portions of
expelled placenta left to drag behind her.
Dystocia has also been reported as having a predis-
posing association with uterine prolapse.
Diagnosis of an inverted uterine horn is made
based on the finding per rectum of a blunted uterine
horn with a tense mesovarium disappearing into the
center of the blunted tip. In minor intussusceptions,
the ovary may not yet be entrapped (this is not as
painful to the mare) and is still palpable at the very tip
of the blunted horn. Palpation of this area is often
painful to the mare and sedation is recommended.
The inverted horn may also be felt per vagina, within
the lumen of the uterus.
In cases where there is a retained placenta it is best
to gently remove the portion of attached placenta if it
will come away readily so as to decrease the tension on
the horn. In cases where the placenta cannot be
detached the author prefers to cut off the majority of
the exteriorized hanging placenta at a level just below
the vulva to decrease the strain on the invaginating
horn and hopefully prevent progression to a full uter-
ine prolapse. Direct treatment and correction of the
invaginated uterine horn includes controlling the
mare's straining and pain (sedation, epidural), manual
reduction of the inverted horn per vagina (may
require the use of uterine relaxants (aceprornazine,
clenbuterol), or even general anesthesia (halothane)
to relieve the encircling spasm in the myometrium),
and full replacement of the previously invaginated
horn and ovary to their normal position (manually if
they can be reached, or use intrauterine sterile saline
to fully dilate the uterine horns thus ensuring that the
previously entrapped horn is fully expanded).
Supportive therapy in the form of intravenous fluids,
NSAIDs, antibiotics, tetanus prophylaxis, etc., may also
be indicated (especially in cases complicated by
retained placenta). Careful use of low dose oxytocin
(10-20 IV i.m.), once the horn has been returned fully
to its normal position, may also aid in rapid normal
involution and prevention of a recurrence. The author
has also seen two mares with inverted uterine horns
secondary to retained placentas who also had low ion-
ized calcium levels at presentation. Correction of low
calcium levels to normal may also help restore normal
uterine tone.
BIBLIOGRAPHY
Abdominal distention in the adult horse
Distention colic
Ducharme N G, Fubini S S (1983) Gastrointestinal
complications associated with the use of atropine in
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Messer N T (1987) Distention colic. In Current Therapy in
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RobertsonJ T (1990) Diseases of the stomach. In The Equine
Acute Abdomen, N A White (ed.). Lea and Febiger,
Whi te N A (1990) Diseases of the caecum. In The Equine Acute
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Uroperitoneum
Beck C, DartAJ, McClintock S A and Hodgson D R (1996)
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Gibson KT, Trotter G Wand Gustafson S B (1992)
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] Am. Vet. Med. Assoc. 200:1692-94.
Jones P A, Sertich P S andJohnstonJ K (1996)
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Fetal hydrops
Frazer G S, Embertson R and Perkins N R (1997)
Complications of late gestation in the mare. Equine Vet.
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Van de Plassche M (1987) Prepartum complications and
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N.E. Robinson (ed.). W.B. Saunders, Philadelphia,
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Van de Plassche M, Bouters R, SpincemailleJ and Bonte P
(1976) Dropsy of the foetal sacs in mares. Vet. Rec. 99:67-9.
Ventral body wall hernias and prepubic
tendon rupture
Frazer G S, Embertson R and Perkins N R (1997)
Complications oflate gestation in the mare. Equine Vet.
Educ. 9:306--11.
Hanson R and Todhunter R (1986) Herniation of the
abdominal wall in pregnant mares.] Am. Vet. Med. Assoc.
189:790-3.
Perkins N and Frazer G (1994) Reproductive emergencies in
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Cushing'sdisease
Hillyer M H, Taylor F G R, Mair T S, Murphy D, Watson
T D G and Love S (1992) Diagnosis of
hyperadrenocorticism in the horse. Equine Vet. Educ.
4:131-4.
KolkJ H van der (1998) Diseases of the pituitary gland,
including hyperadrenocorticism. In Metabolic and
Endocrine Problemsof the Horse,. T D G Watson (ed.).
W.B. Saunders, London, pp. 41-59.
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17 COLIC
Kolk] H van der, Kalsbeek H C, Garderen Evan, Wensing T
and Breukink H] (1993) Equine pituitary neoplasia: a
clinical report of21 cases (1990-1992). Vet. Rec.
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Love S (1993) Equine Cushing's disease. Br. Vet.].
OTHER CONDITIONS 17
Pancreatic diseases
Argenzio RA (1990) Physiology of digestive, secretory and
absorptive processes. In: TheEquineAcuteAbdomen.
N AWhite (ed.). Lea and Febiger, Philadelphia, pp. 25-35.
Bulgin M S and Anderson B C (1983) Verminous arteritis and
pancreatic necrosis with diabetes mellitus in a pony. Compo
Cont. Educ. Pract. Vet. 5:S482-S485.
Byars T D (1990) Pancreatitis. In: TheEquine Acute Abdomen.
N A White (ed.). Lea and Febiger, Philadelphia, p. 408.
Hamir A N (1987) Verminous pancreatitis in a horse. Vet. Rec.
121:301-2.
Lilley C Wand Beeman G M (1981) Gastric dilatation
associated with acute necrotizing pancreatitis. EquinePract.
3:8-15.
Mair T S, Freestone], Hillyer M H, Love S and Watson E D
(1995) The pancreas. In TheEquineManual, A] Higgins
and I M Wright (eds). W.B. Saunders, London,
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McClureJJ (1987) Acute pancreatitis. In: Current Therapy in
EquineMedicine2
nd
edn, N E Robinson (ed.). W.B.
Parry BWand Crisman M V (1991) Serum and peritoneal
fluid amylase and lipase reference values in horses. Equine
va.]. 23:390-1.
Ross MW, Lowe] E, Cooper B], Reimers T] and Froscher
BA (1983) Hypoglycemic seizures in a Shetland pony.
Cornell Vet. 73:151-69.
Reproductive-associated causes of colic in the
broodmare
Asbury A C (1993) Care of the mare after foaling. In: Equine
Reproduction, A 0 McKinnon and] L Voss (eds). Lea and
Ball BA and Daels P F (1997) Early pregnancy loss in mares:
applications for progestin therapy. In: Current Therapy in
EquineMedicine 4th edn, N E Robinson (ed.). W.B.
Blanchard T L, Varner D D and Schumacher] (1998) Manual
of EquineReproduction. Mosby, St Louis.
Bosu W T Kand Smith C A. Ovarian abnormalities. In: Equine
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Britt B and Byars T D (1997) Hagyard-Davidson-McGee
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AmericanAssociation of Equine Practitioners. AAEP,
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Frazer G S (1998) Periparturient problems and dystocia. In:
Proceedings from theBluegrass EquineReproductive Symposium,
October 18-21, Hagyard-Davidson-McGee Associates, PSG
Immegart H M (1997) Abnormalities of pregnancy. In: Current
Therapy in LargeAnimal Theriogenology, R.S. Youngquist
(ed.). W.B. Saunders, Philadelphia pp. II 3-29.
Immegart H M and Threlfal W R (1998) Accidents of
breeding. In: EquineInternal Medicine, S.M. Reed and W.M.
Bayly (eds). W.B. Saunders, Philadelphia, p. 800.
Le Blanc M M (1997) Immediate care of the postpartum
mare and foal. In: Current Therapy in LargeAnimal
Theriogenology, R SYoungquist (ed.). W.B. Saunders,
Lofstedt R M (1993) Miscellaneous diseases of pregnancy and
parturition. In: Equine Reproduction, A 0 McKinnon and
] L Voss (eds). Lea and Febiger, Philadelphia, pp.
596-603.
Maxson A D, Giger U, Sweeney C R et al. (1993) Use of bovine
hemoglobin preparation in the treatment of cyclic ovarian
hemorrhage in a miniature horse.] Am. Vet. Med. Assoc.
203:1308-11.
Parente E] (1999) Colic in the peripartum mare. In:
Proceedings from the Comprehensive Preventative Medicinefor the
Mare and FoalHighlightingNutritional Management and
Developmental Orthopedic Disease Seminar, March 13-14,
Hilltop Farm.
Plumb D C (1995) Veterinary Drug Handbook2nd edn. Iowa
State University Press, Ames, IA.
Santschi E (1997) Prepartum conditions. In: Current Therapy
in Equine Medicine4th edn, N E Robinson (ed.). W.B.
Sherman D M and Lafarenko VA (1998) The mechanism of
the action of opiate receptor antagonists in acute shock-
induced blood loss. Eksp. Klin. Farnakol. 61(1):25-9.
Sprayberry K A (1999) Hemorrhage and hemorrhagic shock.
In: Proceedings from theBluegrass Equine Medicineand Critical
Care Symposium, October 24-27. Hagyard-Davidson-McGee
Associates, PSG
Stowe H D (1968) Effects of age and impending parturition
upon serum copper of Thoroughbred mares.] Nutrition
95:179.
Trotter G W (1992) Surgical diseases of the caudal
reproductive tract. In: Equine Surgery,]A Auer (ed.). W.B.
Vaala W E (1999) Periparturient problems in mares. In:
Proceedings from theComprehensive Preventative Medicinefor the
Mare and FoalHighlightingNutritional Management and
Developmental Orthopedic Disease Seminar, March 13-14,
Hilltop Farm.
van de Plassche M (1987) Prepartum complications and
dystocia. In: Current Therapy in Equine Medicine2nd edn,
N E Robinson (ed). W.B. Saunders, Philadelphia, pp.
537-42.
Vasey] R (1993) Uterine torsion. In: Equine Reproduction, A 0
McKinnon and] L Voss (eds). Lea and Febiger,
Vivrette S (1997) Parturition and postpartum complications.
In: Current Therapy in Equine Medicine4th edn, N E
Robinson (ed.). W.B. Saunders, Philadelphia pp. 547-51.
Zent W W (1987). Postpartum complications. In: Current
Therapy in Equine Medicine2nd edn. N E Robinson (ed.).
W.B. Saunders, Philadelphia, pp. 544-7.
363
18
Chronic weight loss
NBll
Differential diagnosis and
evaluation of chronic
weight loss
MULM
The maintenance of a normal and constant body weight
is a balance beteen input and output (Figure 18.1).
/ Nutrients OU Feces,
Nutrients IN HORE urine, sweat
Metabolic consumption
Figure 18.1 Balance between input and output necessary
to maintain body weight
Nutrients in the diet are the input. The output is the
sum of nutrients used in metabolism and exercise, and
nutrients lost or excreted in feces, urine, and sweat.
Weight loss occurs when the output of nutrients
exceeds the input of nutrients.
btMM t LHML WbH Lbb
Weight loss is a common problem that can affect horses
of all ages; there are numerous potential causes.
However, there is no precise defnition of weight loss,
and individual owners and veterinarians often vary
enormously in their opinions about 'normal' body
condition and in their concern about weight loss.
It is sometimes easy to determine whether a horse is
losing weight from the physical findings and an accu
rate history. However, in many cases, establishing
whether a problem exists or not, and its severity, can be
very difcult. In general, chronic weight loss should be
investigated if a horse has noticeably lost weight, and
fails to regain it, for no obvious reason.
Chronic weight loss (or wasting) is not a disease, nor
is it a diagnosis, but simply a state of afairs. Discerning
the cause of weight loss can vary from a straightforward
to a highly complex evaluation of the patient since
numerous management, environmental, and animal
factors can impact on a horse's ability to maintain
adequate body condition.
A horse that is losing weight for no obvious reason
usually falls into one of three categories
1. the horse is healthy, but affected by some form of
imposed environmental stress or deprivation
2. the horse is affected by a disease that is causing the
weight loss with no other overt clinical signs
3. the horse is geriatric.
The fi rst decision the veterinarian must make is
whether the case is a thin well horse or a thin ill horse?
Although this sounds very basic, it is very important,
and every effort should be made at the outset to deter
mine which category a particular horse fts into.
bbbbbNbM t YLM1M
The body condition of an individual horse can be
assessed by documenting the fat:lean ratio or body con
dition score. Estimating and recording the body condi
tion score may be important for legal reasons. If a horse
367
18 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
is being examined over a period of time, then regular
recording of body weight is helpful in monitoring the
course of weight loss or a disease, and for assessing the
response to therapy. A number of different systems for
assessing body condition have been described. One
such system is shown in Table lS.I.
Usual goals for body condition scores are about 4-5
for performance and sport, and 5-6for reproduction.
Body condition
score
2
3
4
5
6
7
8
9
368
Definition
Extreme emaciation. No fatty
tissue. Wasted muscles especially
noticeable over bones. Flat shelf
over transverse processes
Emaciation. Slight fat cover.
Prominent bones. Wasted
muscles
Thin. Fat covers transverse
processes and half-way up
spinous processes. Tailhead
prominent but individual
vertebrae not seen. Ribs seen
sharply
Moderately thin. Slight back
ridge. Ribs barely discernable
Moderate. Back is flat (no crease
or ridge). Ribs easily felt but not
seen
Moderately feshy. Fat feels
spongy over ribs and around
tailhead. Back crease slight or
absent
Fleshy. Back crease definite. Ribs
covered but individual ribs can
be palpated. Fat is palpable in
neck and rump
Fat. Back creased. Neck thick.
Fat along withers, behind
shoulders and inside thighs
Too fat. Back crease is deep. Fat
bulging on neck, along withers,
behind shoulders, around
tail head and inside thighs
FbML LUbbb t LHML
WbH Lbb
Chronic weight loss may occur in the following situa
tions
lack of food, water, or both
poor quality of food or water
failure to eat or swallow food
failure to digest or absorb food
increased or abnormal loss of nutrients once
absorbed
increased utilization of nutrients once absorbed
neuromuscular disease.
bbbbbNbM t bMVMNbML
M NMbNbML tLb
Managemental and environmental factors leading to
weight loss may be multifactorial and other horses on
the premises should be examined for assessment of
body condition. If other animals are also demonstrating
evidence of weight loss, then a management problem
becomes more likely. The most likely environmental
causes include
insufcient food
insufcient grass
the wrong sort of food
insuffcien t water
excessive work
irregular severe work in an unft horse.
If environmental or managemental factors are
thought to be important in causing chronic weight loss,
then the attending veterinarian must examine these fac
tors carefully him/herself. Information and history sup
plied by the owner or manager cannot be relied upon
to be truthful. Owners often give misleading or inaccu
rate replies to questions about a horse's management or
feeding because they are embarrassed and concerned
that they may appear negligent. Likewise, managers or
trainers may try to mislead or to conceal information.
Wherever possible, the attending veterinarian should
spend some time at the owner's premises assessing the
general management and feeding, and observing the
horse in its own environment.
Assessment of nutrition
A careful assessment of the nutritional status is essential
in the evaluation of chronic weight loss, it is worth
remembering also that documentation of body condi
tion can be important in humane and legal actions. The
following questions should be addressed
1. Is enough food being offered?
2. Is the food of adequate quality?
3. Is the horse allowed to eat?
4. Is the food palatable?
If possible the veterinarian should make a direct
assessment of what the horse is being fed by asking the
owner to show him or her exactly what is fed and in
exactly what quantities. If the horse is pastured, a direct
assessment of the quality of the pasture and the stock
ing density should be made. An average 450 kg horse at
rest will obtain adequate intake of energy from 8- 10 kg
of hay and 2-4 kg of grain per day. Some individual
horses will require more than this to maintain a con
stant body weight, and some will require less. Increased
energy requirements occur if the horse is in work, or is
pregnant or lactating.
Many inexperienced horse owners are unaware of
the dietary needs of their horses, especially in relation
to increased work levels. Although they may provide
adequate quantities of food to meet the requirements
for maintenance and light work in the winter months,
they often fail to adjust the ration in the summer
when the horse is exercised more vigorously. Other
owners fail to feed adequate amounts of food during
cold winter weather. Another common cause of weight
loss is the reliance of inexperienced horse owners on
supplements and products advertised to improve
digestion and metabolism. This often leads to under
feeding especially in the winter when pasture quality
has declined.
Some horses always lose weight when kept in full
work especially during the winter time. Many breeding
stallions lose weight during the breeding season. Such
horses are not considered abnormal if they regain
weight when rested or, in the case of breeding stal
lions, when the breeding season ends. Late pregnancy
and lactation impose increased demands for energy
and nutrients. A mare in late pregnancy may require
20 per cent more nutrients than for normal mainte
nance, and at peak lactation may require up to 50 per
cent more.
Competition for available food may be important in
groups of horses. This may be particularly important
with respect to new introductions to a group of horses,
or 'slow eaters'. A horse that is low in the pecking order
in a group may be unable to eat because it cannot
approach the food without other horses bullying it and
chasing it away.
Poor palatability of the food may become a problem,
especially when it has become spoiled or contaminated
by some substance. This is likely to affect the whole
batch of feed, and several or all horses exposed to that
batch are likely to be affected.
CHRONIC WEIGHT LOSS 18
Availability of water
Horses require free access to clean water. If water is
restricted then weight loss will result, partly due to an
associated decrease in voluntary food intake. An average
horse requires 20-30 liters of fresh water per day when
doing light work in a temperate climate. Increased
demands for water occur with increased work load,
lactation, and increased environmental temperature.
Assessment of general management
An assessment of the general management and preven
tive medicine practices is helpful at this stage. Careful
questioning of the owner is carried out to assess in
particular:
internal parasite control (see Chapter 4)
routine dental care (see Chapter 6).
bbbbbNbMtWbH Lbb
bbLb WH bbbb
If environmental and managemental factors have been
ruled out as the cause of chronic weight loss, or if
disease is suspected but the associated clinical signs are
obscure, then the horse requires careful observation
and examination, often over a protracted period of
time. It may be preferable to hospitalize the horse for
several days so that its behavior, locomotion, eating,
and drinking can be monitored constantly. Thorough
and systematic clinical examinations should be per
formed and repeated regularly until, hopefully, some
indication of a specifc disease or a diseased body system
is identifed. Routine hematological, serum biochemi
cal, and parasitological profles should be undertaken
at this time. Further clinicopathological examinations
may be performed as deemed necessary (e.g. abdomi
nal paracentesis, rectal biopsy, oral glucose tolerance
test, urinalysis, etc.). Further clinical procedures, such
as diagnostic ultrasonography, radiography, laparo
scopy, etc., may also be performed if appropriate.
LLMLL FHLY
Over reliance on laboratory tests to diagnose the cause
of chronic weight loss must be avoided. However,
clinicopathological investigations can be an important
aid in the diagnosis of certain diseases.
Hematology
Hematology tests may reveal
leukocytosis and neutrophilia - these are indicative
of chronic inflammation, and may be observed in
369
infectious diseases (e.g. peritonitis, internal
abscesses) or neoplasia
anemia -this occurs in chronic inflammatory
diseases or neoplasia
dyserythropoiesis - this can be confirmed by bone
marrow aspirate or biopsy
immune-mediated hemolytic anemia and/or
thrombocytopenia - these conditions are
sometimes associated with neoplasia
hyperfibrinogenemia - this is another sensitive
indicator of inflammation and may be seen in both
infectious and neoplastic conditions.
Serum biochemistry
Decreased serum or plasma total protein or albumin
concentration is evidence of hypoproteinemia, which is
suggestive of one of the following conditions
severe malnutrition
protein-losing enteropathy (e.g. parasitism, colitis,
inflammatory and neoplastic bowel diseases)
glomerular disease
chronic liver disease
peritonitis or pleuritis.
In chronic liver conditions, the total protein con
centration is often normal, but albumin concentration
may be sub-normal and globulin concentration raised
(decreased albumin:globulin ratio).
Increased serum or plasma total protein (hyperpro
teinemia) and total globulin (hyperglobulinemia) may
occur in inflammatory processes, infections, parasitism,
liver disease, and neoplasia. Raised gamma globulins
are suggestive of infection, whereas raised beta globu
lins are suggestive of parasitism.
Urea concentration may be raised for a number of
different reasons
increased tissue catabolism and protein turnover
associated with disease
high protein diet
dehydration
renal failure.
In practice, increased urea concentration is rarely
identified as a direct result of increased tissue catabo
lism or high protein diet. If renal failure is suspected,
further laboratory analyses should be performed
including serum creatinine, electrolytes, urinalysis, and
acid-base estimations.
Increases in the concentrations of acute and chronic
liver enzymes suggest an active liver problem. Serum
enzymes can be helpful in assessing liver disease (see
Chapter 19), these include
370
gamma glutamyl transferase (GGT)
aspartate aminotransferase (AST)
alkaline phosphatase (A)
glutamate dehydrogenase (GLDH)
iditol dehydrogenase ( IDH)
arginase (ARG).
Further laboratory tests of liver disease and liver
function include
bilirubin
serum bile acids
serum proteins
blood ammonia.
Fecal examinations
A fecal egg count reflects the presence of adult egg
laying strongyles (or other nematode parasites) in the
intestine. The fecal egg count gives no indication of the
burden of immature larval stages of parasites, and is
therefore of little use in the diagnosis of larval cyatho
stomosis (see Chapter 2 1). Direct microscopy of a wet
preparation of feces may be helpful in identifing the
presence of cyathostome larvae.
Fecal occult blood may be positive with gastrointesti
nal ulceration or neoplasia, but the presence of para
sites or a recent rectal examination may also cause a
positive test result. This test is more likely to be positive
in cases where bleeding has occurred in the distal
intestinal tract than in cases where bleeding has
occurred in the proximal gastrointestinal tract.
Peritoneal fluid analysis
Total nucleated cell count and total protein should be
measured to differentiate between transudates and
exudates (see Chapter 17). Cytology may occasionally
document the presence of neoplastic cells due to intra
abdominal neoplasia.
Both aerobic and anaerobic cultures of peritoneal
fluid should be performed if intra-abdominal infection
is suspected (see Chapter 17).
LUbbb t LHML WbH Lbb
The common diseases associated with obscure chronic
weight loss include
1. conditions interfering with prehension of food,
and/ or swallowing
2. persistent low-grade pain
3. conditions interfering with digestion and intestinal
absorption
4. protein-losing enteropathies
5. chronic liver disease
6. chronic kidney disease
7. chronic low-grade infection
8. neoplasia
9. chronic heart disease
l0. chronic pulmonary disease.
Conditions interfering with prehension of
food and/or swallowing
Prehension, mastication, and swallowing are integrated
functions and abnormalities in one or more phases of
eating and swallowing can lead to reduced food (and
water) intake and, as a result, weight loss. Secondary
inhalation pneumonia is a common sequel to severe
dysphagia, in which case weight loss will become accel
erated (with the development of additional clinical
signs). The causes and investigation of dysphagia are
described in detail in Chapter 5.
It is helpful to observe the horse eat and drink, and
to examine the stall for evidence of partially chewed
food. Signs indicative of dysphagia may be subtle or
obvious (depending on the severity of the disease), and
include
an unwillingness to eat or a protracted time taken
to eat food
dropping semi-masticated food from the mouth
while eating ('quidding')
the accumulation and 'balling-up' of food in the
mouth
halitosis
nasal return of saliva, food, and water
gulping, but not swallowing, water
dipping and splashing the muzzle in water
productive coughing.
Particular attention should be paid to the oral cavity
and teeth if there appears to be quid ding of food or
painful mastication (see Chapters 5and 6). The ability
of the horse to flex its neck and to eat and drink from
the ground should also be assessed.
Important causes of dysphagia include
facial paralysis (see Chapter 5)
lip lesions (see Chapter 5)
temporomandibular joint and hyoid lesions (see
Chapter 5)
dental disorders (see Chapter 6)
lingual trauma and abnormalities (see Chapter 5)
congenital and acquired palatal defects (see
Chapters 5 and 6)
pharyngeal paralysis (see Chapter 5)
pharyngeal compression (see Chapter 5)
pharngeal and palatal cysts (see Chapter 5)
epiglottal lesions (see Chapter 5)
4th branchial arch defects (see Chapter 5)
megaesophagus (see Chapters 5 and 7)
esophageal obstruction (see Chapters 5and 7)
esophageal strictures/stenosis (see Chapters 5 and
7)
grass sickness (especially in the UK) (see Chapters 5
and 17).
Persistent low-grade pain
Persistent low-grade pain affects the animal's well
being, reduces its appetite, and may affect its willing
ness to move about and graze. Common causes of
low-grade pain and weight loss include chronic colic,
chronic lameness, and neoplasia.
Chronic colic is discussed fully in Chapter 17.
Common causes of chronic low-grade colic include
diffuse or localized peritonitis (see Chapter 17)
chronic grass sickness (especially in the UK) (see
Chapter 17)
chronic inflammatory bowel disease (see
Malabsorption syndromes)
Right dorsal colitis (see Chapter 21)
neoplastic bowel infltrates (see below and Chapter
17)
abdominal neoplasia (see Chapter 17)
gastric ulceration (see Chapter 12)
ileal hypertrophy (see Chapter 13)
chronic intussusceptions (see Chapter 13)
sand irritation (see Chapter 15)
enteroliths (see Chapter 15)
cholelithiasis (see Chapter 19)
cystic calculi.
Chronic lameness includes conditions such as
laminitis, navicular syndrome, and degenerative joint
disease. These conditions may be associated with
chronic weight loss, but signs directly referable to the
underlying disease are usually also present.
Conditions interfering with digestion and
intestinal absorption
If a horse with weight loss has been obsered to eat
adequate quantities of an appropriate diet, then
decreased feed digestion or absorption should be
considered as a possible cause of the weight loss. In sim
plistic terms, dietary proteins, fats, and non-cellulose
carbohydrates are digested and absorbed in the equine
small intestine. Undigested and unabsorbed nutrients
pass into the large intestine where they are broken
down by cecal and colonic microorganisms, and the
breakdown products are absorbed predominantly as
volatile fatty acids. Undigested material, chiefly fber, is
lost via the feces.
371
Conditions causing maldigestion in the adult horse
are very poorly understood. Pancreatic disease and
dysfunction appear to be very rare (see Chapter 17).
Specific brush-border enzyme defciencies have not
been described in adult horses. However, mal digestion
probably occurs in conjunction with diseases that afect
intestinal absorption such as inflammatory bowel dis
ease (see Malabsorption syndromes).
In general, enteropathies of the adult horse that
affect the hind-gut, or both the fore- and hind-gut, are
associated with diarrhea (see Chapters 20and 2 1). If
fore-gut dysfunction is the only problem, then diarrhea
commonly does not occur, and the clinical presentation
will be characterized by progressive weight loss due to
malabsorption (and maldigestion). However, if small
intestinal function is very severe, then diarrhea may also
occur in the absence of any apparent large intestinal
lesions.
5m |nt85t|nmd|g85t|onnd
mb5orpt|on
A malabsorption syndrome can be produced by several
diseases of the small intestine, including
diffuse alimentary lymphosarcoma
granulomatous enteritis
eosinophilic enteritis
lymphocytic-plasmacytic enteritis
mycobacterial enteritis
parasitism.
These diseases are discussed in greater detail in
Malabsorption syndromes.
Typically, horses with malabsorption syndromes
present with progressive weight loss despite a normal
or even increased appetite. Affected animals are ofen
bright and alert in the early stages of the disease.
However, in the later and advanced stages of malab
sorption syndromes, there may be debility, depression,
and inappetence.
The cause of small intestinal malabsorption cannot
be determined by clinical examination or routine
laboratory evaluations. Rectal examination sometimes
reveals evidence of bowel-wall thickening, and this may
be further evaluated by diagnostic ultrasonography.
Enlargement of mesenteric lymph nodes may also be
appreciable on rectal examination.
Hypoalbuminemia in a wasting horse is strongly
suggestive of malabsorption and/or protein-losing
enteropathy; other important causes include renal and
liver disease (see below). Occasionally serum globulin
levels may be elevated in chronic inflammator bowel
disease, resulting in a normal total protein level and
decreased albumin:globulin ratio. Serum protein elec-
372
trophoresis can be helpful in determining the nature of
any hyperglobulinemia. Elevations in both alpha and
beta globulin fractions are frequently found in chronic
inflammatory bowel disease. A elevation of predomi
nantly the beta-globulin fraction may be suggestive of
signifcant parasitic laral migration. Lymphosarcoma
is occasionally accompanied by low or undetectable
serum IgM levels. Lymphocytic-plasmacytic enteritis is
often associated with an increased serum IgA concen
tration.
Chronic enteropathies may sometimes, but not
always, be associated with raised serum concentrations
of alkaline phosphatase, in particular the intestinal
isoenzyme of alkaline phosphatase.
Peritoneal fluid is frequently normal in horses with
chronic infltrative bowel disease. The fluid is usually
normal even in horses with intestinal lymphosarcoma.
Occasionally, increased eosinophil numbers will be
found in the peritoneal fluid of horses with eosinophilic
bowel infltrates.
Assessment of small intestinal absorptive capacity
should be performed by a monosaccharide absorption
test (such as the oral glucose tolerance test or the xylose
absorption test) (see Chapter 2)in all horses where mal
absorption is suspected. Although the results of these
tests may be suggestive of a malabsorption syndrome,
they cannot provide defnitive proof or diagnose the
underlying cause. Rectal biopsy may be helpful if the
inflammatory or neoplastic infltrate extends to that part
of the intestinal tract. However, in most cases of small
intestinal malabsorption, the results of histological
examinations of rectal biopsies will be unremarkable.
Exploratory laparotomy and multiple full-thickness
bowel wall biopsies may be the only way to obtain a defn
itive diagnosis in the living horse. However malabsorb
ing horses are usually thin or debilitated, and are not
good surgical candidates and some will suffer wound
complications following surgery. Standing laparoscopy
is associated with much lower morbidity and may permit
biopsy of mesenteric lymph nodes which could provide
useful diagnostic information.
Lrg8 |nt85t|n md|g85t|on nd
mb5orpt|on
Inflammatory and neoplastic infltrates may affect the
large intestine as well as the small intestine. Severe infl
trative and inflammatory large bowel diseases com
monly result in progressive weight loss with diarrhea
(see Malabsorption syndrome and Chapter 2 1).
Parasitism affecting the large intestine can also result in
chronic weight loss. Laral cyathostomosis is typically
associated with a severe protein-losing enteropathy and
sudden onset diarrhea in young adult horses during the
winter time (see Chapter 21). However, in a small num
ber of cases laral cyathostomosis may cause progressive
and rapid weight loss and subcutaneous edema (associ
ated with hypoproteinemia) in the absence of diarrhea.
Cyathostome larvae may be found in the feces of such
cases (although fecal egg count is frequently negative),
and laboratory abnormalities typical of laral cyathosto
mosis will also be present (leukocytosis, neutrophilia,
hypoalbuminemia, hyper-betaglobulinemia, elevated
intestinal alkaline phosphatase). Cyathostome infec
tions have also been reported to cause a seasonal
malaise syndrome in adult horses during the autumn
and winter, characterized by vague signs of inappetence
and ill-thrift.
Protein-losing enteropathies
Protein-losing enteropathies comprise a group of dis
eases where there is lumenal loss of fluid, electrolytes,
plasma proteins, and nutrients. Protein-losing
enteropathies can affect both the small and large
intestines. Common causes include
inflammatory bowel disease (see Malabsorption
syndromes)
right dorsal colitis (see Chapter 21)
intestinal neoplasia (see Malabsorption
syndromes)
gastrointestinal ulceration (such as NSAD toxicity)
(see Chapters 12, 20, and 2
1)
larval cyathostomosis (see Chapter 21)
severe parasitism (see Chapter 4).
These diseases result in continual loss of plasma pro
teins into the gut lumen. Many of the diseases result in
maldigestion and malabsorption as well. Clinico
pathological abnormalities are non-specifc but include
anemia, leukocytosis, and hypoalbuminemia.
Hypoalbuminemia may result in ventral and limb
edema in these cases.
Chronic liver disease
Chronic liver diseases such as pyrrolizidine tOXICIty,
chronic active hepatitis, cholelithiasis, cholangio
hepatitis, and cirrhosis can be associated with chronic
weight loss in the absence of overt clinical signs of
hepatic failure. These diseases result in weight loss
due to inappetence, maldigestion (due to inadequate
bile acid production), and inadequate or improper
processing of amino acids into nomlal plasma pro
teins in the liver. The diagnosis is usually achieved by
estimation of serum proteins, liver enzynle and bile
acid concentrations, and biopsy. Liver disease is dis
cussed in detail in Chapter 19.
Chronic kidney disease
Chronic renal failure is an uncommon but important
cause of chronic weight loss. The potential causes
include
chronic glomerulonephritis
tubulointerstitial disease
chronic septic pyelonephritis
bilateral renal hypoplasia or dysplasia
chronic oxalate nephrosis
polycystic renal disease.
Congenital renal diseases such as renal hypoplasia,
dysplasia, or polycystic renal disease should be sus
pected in young horses (less than 5 years of age) that
present with evidence of chronic renal failure.
Acquired renal diseases are usually insidious in onset,
and the initial renal injury may have occurred months
or years prior to the onset of clinical signs. Identifing
the precise cause of chronic renal failure may be very
difcult because many horses have evidence of
advanced glomerular and tubular disease, or 'end-stage
kidney disease' by the time clinical signs of chronic
renal failure become apparent.
Chronic weight loss is the most common presenting
clinical sign in horses with chronic renal failure. Other
signs that may be noted include
inappetence
ventral edema
polyuria/polydipsia
rough hair coat
lethargy
exercise intolerance
uremic odor and halitosis
excessive dental tartar.
Weight loss occurs for several different reasons in
horses with chronic renal failure. A increase in the
concentrations of nitrogenous wastes in the blood has a
central appetite-suppressant efect. Also azotemia can
cause oral ulceration and gingivitis, reducing appetite,
and in the gastrointestinal tract excess urea and
ammonia can lead to ulceration and protein-losing
enteropathy.
The diagnosis of chronic renal failure is made by
identifing persistent isosthenuria (urine specifc
gravity 1.008-
1
.0
1
4) in combination with azotemia
(increased serum urea and creatinine concentrations)
and typical clinical signs. Additional clinicopathological
abnormalities may include
anemia
hypoalbuminemia
hyponatremia
hyperkalemia
373
hypochloremia
hypercalcemia
hypophosphatemia
metabolic acidosis or alkalosis.
Diagnostic ultrasonography and renal biopsy can
provide additional information.
Chronic low-grade infection
Chronic low-grade infection, either localized or sys
temic, may result in chronic weight loss with few other
overt clinical signs. Vague signs such as depression
and inappetance may be present. Diseases which may
present in this way include
chronic internal abscesses (see Chapter 17)
chronic pneumonia or lung abscesses
endocarditis
localized peritonitis (see Chapter 17)
cholangiohepatitis (see Chapter 19)
equine infectious anemia ( EIA)
leptospirosis
brucellosis
mycobacterial infections.
Persistent or intermittent pyrexia may be present,
and this may give an important clue as to the possibility
of a chronic infectious (or inflammatory) process.
Hematology and plasma fbrinogen estimation may
indicate a chronic septic process (leukocytosis, neutro
philia, hyperfibrinogenemia). Increased serum globu
lin levels (primarily gamma globulins) may be present
due to chronic antigenic stimulation. Abdominal para
centesis may be helpful in the diagnosis of localized
peritonitis or intra-abdominal abscesses (see Chapter
17). Nuclear scintigraphy using radio-labeled white
blood cells might be useful to localize focal septic
lesions such as internal abscesses. Specifc serological
tests are necessary to diagnose EIA, leptospirosis, and
brucellosis. Biopsy and/ or culture are necessary to
diagnose mycobacterial infections. Horses with chronic
immune mediated disorders may also have intermittent
or persistent fever and weight loss.
Neoplasia
Cancer cachexia is an important paraneoplastic syn
drome that is recognized in all species, including the
horse. It is characterized by a state of malnutrition and
wasting despite adequate nutritional intake, and is
believed to be caused by complex alterations in carbo
hydrate, lipid, and protein metabolism. In addition to
weight loss, cancer cachexia may result in an increase in
infections due to an impairment of the immune system,
and decreased wound healing.
374
Weight loss may also occur in association with neo
plastic disease as a result of
low-grade pain (see above)
physical obstruction (causing dysphagia or chronic
colic)
small intestinal malabsorption (see above)
reduced appetite.
Apart from weight loss, the clinical features of inter
nal neoplasia are variable, and depend on the nature of
the neoplasm, its size, the presence or absence of other
paraneoplastic syndromes, and the mass effects of the
neoplasm on organs and tissues.
The major types of abdominal and thoracic neo
plasia are listed in Table 18.2. Abdominal neoplasia is
considered further in Chapter 17.
Lymphosarcoma (lymphoma) is the most frequently
encountered malignant neoplasm in the horse. It
accounts for 1-3 per cent of all equine tumors. This
neoplasm is most common in mature horses, but may
occur at any age (it has been recognized in an equine
fetus). Four clinical categories of lymphosarcoma are
recognized
1. generalized/multicentric lymphosarcoma
2. alimentary/intestinal lymphosarcoma
3. mediastinal/thoracic lymphosarcoma
4. cutaneous lymphosarcoma.
Considerable overlap between these categories can
occur.
The clinical manifestations of lymphosarcoma vary
depending on the degree of organ involvement and the
specific organs involved in an individual patient. The
typical clinical signs associated with the different forms
of lymphosarcoma are summarized below.
1. Generalized/multicentric form
depression
weight loss
lymphadenopathy
intermittent fever
ventral and limb edema
chronic, intermittent colic
thickened eyelids.
2. Alimentary/intestinal form
depression
weight loss
ventral edema
chronic, intermittent colic
intermittent fever
diarrhea
ascites.
3. Mediastinal/thoracic form
depression
inappetence
weight loss
exercise intolerance
ventral thoracic and pectoral edema
tachypnea
respiratory distress
bilateral fi rm masses at the base of the jugular
grooves
intermittent fever.
4. Cutaneous form
solitary or multiple dermal or subcutaneous
masses
later development of visceral neoplasia (this may
take months to years).
Thoracic neoplasia
Primar lung tumor
Pulmonary granular cell tumor
Pulmonary adenocarcinoma
Anaplastic bronchogenic carcinoma
Pulmonary carcinoma
Bronchogenic squamous cell carcinoma
Pulmonary chondrosarcoma
Bronchial myxoma
Pleural neoplasia
Mesothelioma
Mediastinal and thymic tumor
Thymoma
Lymphosarcoma
Metastatic and secondar thoracic neoplasia
Hemangiosarcoma
Adenocarcinoma
Renal carcinoma
Rhabdomyosarcoma
Malignant melanoma
Fibrosarcoma
Hepatoblastoma
Chond rosarcoma
Neuroendocrine tumor
Lymphosarcoma
Undifferentiated sarcoma and carcinoma
Abdominal neoplasia
Pancreas
Pancreatic adenoma and adenocarcinoma
Spleen
Lymphosarcoma
Melanoma
Hemangiosarcoma
Liver
Lymphosarcoma
Hepatocellular carcinoma
Biliary carcinomal cholangiocellular
carcinoma
Hemangiosarcoma
Adnal gland
Pheochromocytoma
Stomach
Gastric polyp
Leiomyoma and leiomyosarcoma
Gastric adenocarcinoma
Small intestine
Lymphosarcoma
Leiomyoma and leiomyosarcoma
Adenocarcinoma
Lipoma
Cecum, large and small colons
Lymphosarcoma
Adenocarcinoma
Intestinal myxosarcoma
Lipoma and lipomatosis
Recm
Lipoma
Lymphosarcoma
Polyps
Leiomyosarcoma
Melanoma
Pritoneum
Disseminated leiomyosarcomatosis
Omental fibrosarcoma
Mesothelioma
Kidey
Renal cell carcinoma
Adenoma
Transitional cell carcinoma
Embryoma
Ovar
Cystadenoma
Teratoma
Dysgerminoma
Granulosa cell tumor
Chronic heart disease
Heart failure may result in weight loss due to inef
ciency of the circulation of nutrients and oxygen to
peripheral tissues. Other clinical features of congestive
heart failure include exercise intolerance, depression,
venous distention, edema, tachypnea and coughing.
Diagnosis is made by auscultation, ECG, and cardiac
ultrasound examinations.
375
Chronic pulmonary disease
Horses affected by chronic obstructive pulmonary
disease (COPD) commonly maintain normal body
condition, but severe and long-standing disease may be
associated with weight loss. Other signs indicative of this
condition will be present (chronic cough, tachypnea
and dyspnea, nasal discharge, exercise intolerance,
wheezing and crepitant lung sounds).
Thoracic neoplasia (see above) may produce weight
loss before other signs indicative of the primary condi
tion become evident. Likewise, chronic interstitial pul
monary inflammatory disease and fbrosis may present
with weight loss as one of the earliest clinical signs.
Diagnosis of these conditions is aided by careful
thoracic auscultation, radiography, tracheal aspiration
or bronchoalveolar lavage, diagnostic ultrasonography,
and biopsy.
Figure 18.2 Marked asymmetric gluteal atrophy in a
horse affected by polyneuritis equi
376
MbULLL M
MbUNUbLUL bbbb
_ i;. a _"
Muscle atrophy and weight loss may occur as a result of
local or generalized neurological or neuromuscular
disease. Pronounced symmetrical muscle atrophy (most
severe in the triceps, scapula, quadriceps, lumbar,
sacral, and neck muscles) is seen in equine motor
neuron disease. Other signs are expected in this disease
including trembling, lying down more often than nor
mal, shifting weight on the rear legs, and holding all
four legs closer together than normal. Asymmetric
muscle atrophy affecting the gluteal musculature is
common in other neurological conditions such as
polyneuritis equi (Figure 18.2) and equine protozoal
myeloencephalitis. Chronic weight loss is also a com
mon presenting sign in horses affected by chronic grass
sickness (see Chapter 17).
Malabsorption syndromes
_ Wl 1 I I [
MULM
Malabsorption syndrome refers to the group of diseases
that results in the impairment of digestive and/or
absorptive processes arising from structural or func
tional disorders of the small intestinal tract and its asso
ciated organs (including the pancreas and liver). In the
adult horse, such diseases that are confned to the small
intestine usually result in chronic weight loss, whereas
chronic diseases of the large intestine result in diarrhea
and protein-losing enteropathy (see Chapter 21).
However, small intestinal diseases may result in sec
ondar large intestinal dysfunction due to abnormal
amounts of carbohydrates, fats, and amino acids enter
ing the large bowel from the ileum. In addition, many
of the chronic infltrative diseases that result in small
intestinal malabsorption can affect the large bowel con
currently. Thus, in clinical cases there is often a combi
nation of both small intestinal and large intestinal
malfunction.
The primary clinical sign associated with malabsorp
tion syndromes in adult horses is chronic weight loss. If
the disease process is limited to the small intestine, then
weight loss may be the only clinical sign, and it becomes
important to rule out other causes of weight loss (see
Differential diagnosis and evaluation of chronic weight
loss). Although malabsorption syndromes will affect the
digestion and absorption of carbohydrates, protein,
and fat, diagnostic tests in the horse usually concentrate
on dysfunction of carbohydrate digestion/absorption.
Inadequate fat absorption is of limited importance in
the horse, although malabsorption of fat soluble vita
mins may result in clinical conditions, such as dermati
tis, neurological diseases, and retinal dysfunction.
Increased protein loss from the intestine (protein-los
ing enteropathy) is more commonly associated with
large intestinal disease due to the larger surface area of
the equine large intestine. However, concurrent small
intestinal malabsorption and signifcant protein-losing
enteropathy is likely to cause severe and rapid weight
loss.
LUbbb t NLbFM
bYMNb
The common causes of malabsorption syndrome in the
adult horse are listed in Table 18.3.
o

Extensive small intestinal resection
Chronic inflammatory bowel diseases
granulomatous enteritis
eosinophilic gastroenteritis
multisystemic eosinophilic epitheliotrophic
disease
Iymphocytic-plasmacytic enterocolitis
Alimentary lymphosarcoma
Enteric infections
mycobacterial infection
enteric fungal infections
Idiopathic villous atrophy
Congestive heart failure
Intestinal ischemia
Parasitism
Extensive small intestinal resection
Insufcient absorptive area is a common cause of
small intestinal malabsorption. This can be caused by
extensive! excessive small intestinal resection following
surgery for small intestinal strangulations. The greater
the amount of small intestine resected, the greater the
risk of malabsorption. Small sections of resected bowel
have no untoward long-term effects, but extensive
resections may result in the horse becoming a 'digestive
cripple'. The precise amount of small intestine that can
safely be resected appears to vary from horse to horse,
and the residual bowel is probably capable of compen
sation for the loss of the resected portion over time.
One study suggested that no more than 60 per cent of
the small intestine could be safely resected, but other
studies suggest that up to 70per cent can be removed
without causing subsequent malabsorption. Other
problems that are sometimes observed following
extensive small intestine resection in horses and ponies
include anorexia and liver disease.
Chronic inflammatory bowel disease
Chronic inflammatory bowel disease ( CI BD) is the col
lective term for the group of infltrative bowel diseases
that produce similar clinical signs to one another (pri
marily chronic weight loss). These diseases are not as
well defned in the horse as they are in other species,
and their etiology is generally unknown. Both the small
and large intestines, the regional lymph nodes, and
sometimes other abdominal organs, may be involved
( Plate 18.1). The cellular infltrate may consist of a
mixed cellular population or there may be a predomi
nance of specifc cell types such that CIBD may be
classifed into a number of different disease types.
Differentiation between these diseases usually relies
upon histopathological examination.
Granulomatous enteritis is characterized by diffuse
granulomatous lesions, predominantly in the small
intestine, with lymphoid and macrophage infltration of
the lamina propria, and variable numbers of plasma
cells and giant cells. There is marked villous atrophy
and an absence of lesions attributable to other forms of
granulomatous change (such as mycobacterial and fun
gal infections). No etiological agent has been identifed
in granulomatous enteritis, although it has been pro
posed that the disease may result from an abnormal
host inflammatory reaction to intestinal bacteria, or
dietary components. The pathology of the condition
has similarities to that of Johne's disease in cattle and
Crohn's disease in man. Chronic mycobacterial infec
tion of the intestine has similar histopathological
lesions, however, acid-fast organisms can be identifed
in Ziehl-Neelson stained sections.
Granulomatous enteritis can occur in any age or
breed, or either sex, although it appears to be most com
mon in young adult horses ( 1-5 years of age). It has also
been most commonly reported in the Standardbred. A
familial predisposition to the disease has been sug
gested, and one report documented the occurrence of
the condition in three sibling Standardbred horses.
Chronic eosinophilic infltrates may take the form of
377
diffuse inflammatory cell infltration of the small intesti
nal mucosa with eosinophils and lymphocytes, or an
eosinophilic granulomatous infltrate. Mucosal ulcera
tion, enlargement of ileal Peyer's patches, and mesen
teric lymphadenopathy are frequently present. The
etiology of the condition is unknown, but the nature of
the inflammatory infltrate has led to the suggestion
that it represents an immune-mediated response to
parasites. The condition of multisystemic eosinophilic
epitheliotrophic disease has gastrointestinal as well as
cutaneous, hepatic, and pancreatic lesions.
Lymphocytic-plasmacytic enteritis is characterized
by mucosal infltration by lymphocytes and plasma cells
in the absence of granulomatous change.
Alimentary lymphosarcoma may be a primary neoplas
tic disease, or it may represent part of a multicentric
disease or a metastatic spread from a primary focus
somewhere else in the body. The disease may take the
form of discrete focal tumor masses in the bowel wall
(usually associated with chronic or recurrent colics; see
Chapter 17) or a diffuse intestinal infiltrate of neo
plastic cells that may cause malabsorption. Both small
and/ or large intestines may be affected, and mesenteric
lymph nodes are also commonly infltrated by malig
nant cells. Villous atrophy is commonly present in asso
ciation with small intestinal infltrates. Mucosal ulcers
are also commonly present, and these can contribute to
serum protein leakage and hypoproteinemia. Lumenal
bleeding can result in a blood-loss anemia in addition
to the typical anemia of chronic inflammation/
neoplasia. Lesions may also be present in other organs
throughout the body, and these may give rise to addi
tional clinical signs and abnormalities of clinical pathol
ogy. Although lymphosarcoma can affect horses of any
age, the disease is more commonly seen in horses over
5years old.
Enteric infections
Mycobacterial granulomatous enterocolitis is rare, and
is usually associated with avian strains of Mycc|act-num
tu|-rcu/csis or M. intruc-//u/ar-. There are also rare
report of enteric fungal infections due to As-rgi//us
]umigatus or Histq/asma casu/atum. It has been sug
gested that fungal infections may be most likely in
horses undergoing chronic antibiotic or corticosteroid
treatments.
LLMLL bMb
The clinical signs associated with chronic infltrative
small intestinal diseases are generally similar regardless
378
of the pathological lesion (apart from horses affected
by alimentary lymphosarcoma and multisystemic
eosinophilic epitheliotropic disease which may have
signs related to involvement of other body systems).
The clinical presentation is characterized by chronic
weight loss. Other signs are variable and may include
diarrhea
intermittent or chronic colic
variable appetite - increased appetite, normal
appetite, inappetence, or anorexia
depression
lethargy
peripheral and dependent edema ( Plate 18.2)
pyrexia
skin lesions.
Skin lesions occurring in horses with malabsorption
include thin hair coat, patchy alopecia, and focal areas
of scaling and crusting ( Plate 18.3). Severe, and often
highly pruritic, skin lesions may be present in horses
affected by multisystemic eosinophilic epitheliotrophic
disease ( Plate 18.4).
Mbb
The general approach to evaluation of horses present
ing with signs of chronic weight loss is described in
detail above (see Differential diagnosis and evaluation
of chronic weight loss). Clinicopathological fndings
are non-specifc, but may include
hypoalbuminemia
hyperglobulinemia or hypoglobulinemia
neutrophilia (occasionally neutropenia)
anemia
hyperfbrinogenemia
raised serum alkaline phosphatase
reduced glucose absorption during oral glucose
absorption test
reduced xylose absorption during D(+)-xylose
absorption test
elevated serum IgA concentration
depressed serum IgM concentration
(lymphosarcoma) .
Enlarged mesenteric lymph nodes may be palpable
per rectum in some cases (especially in cases of alimen
tary lymphosarcoma). Abnormally thickened bowel wall
may occasionally be palpated per rectum, and this
can sometimes be confrmed using ultrasonography.
Abdominal paracentesis frequently yields normal peri
toneal fluid. Neoplastic cells are rarely present in the
peritoneal fluid of horses with alimentary lymphosar
coma. Elevated numbers of eosinophils may sometimes
be observed in horses with eosinophilic infiltrative
disease,
Rectal biopsy may yield a histopathological diag
nosis in a small proportion of cases, but only if the
inftrative lesion extends back to this level of the
intestinal tract.
A diagnosis of small intestinal malabsorption is
made using a carbohydrate absorption test such as the
oral glucose absorption test or the D( + )-xylose absorp
tion !est (see Chapter 2). The oral glucose absorption
test is more commonly employed because of the ease of
analyzing plasma glucose levels. Horses can be divided
into three groups on the basis of the results of the oral
glucose absorption test
onnal absorption - the glucose levels at 50 and
120 minutes are within the normal range as defined
by the mean 2 SD of the result_ of Roberts and
Hill (1973), and the glucose level at 120 minutes
shu\\' a greater than 85 per cent increase over the
rCHing level.
2, Partial malabsorption - the glucose levels at 60 and
120 minutes arc below the normal range as defned
hy the mean : 2 SD of the results of Roberts and
HilI ( 1 973), and the glucose level at 120 minutes
shows a less than 85 per cent but greater than
15 per cent increase over the resting level.
:. Total malabsorption - the glucose levels at 50 and
120 minutes are below the normal range as defned
by the mean 2 SD of the results of Roberts and
Hill (1973), and the glucose level at 120 minutes
shows a less than 15 per cent increase over the
resting level.
I Iorses with ' total malahsorption' are likely to have a
diffuse infltrative small intestinal disease. Horses with
'normal absorption' are likely to have a histologicalIy
normal small intestine. Horses with a 'partial malab
sorption' re.ult may have evidence of an inflammatory
infiltrate or villous atrophy, hut they may also have
histologically normal intestine, and further diagnostic
tesl should be carried out.
Confirmation of rhe diagnosis of infltrative small
intestinal diseases and vllous atroph} is made by histo
logical examination of sections of slllall intestin(\ Full
thickness bowel \,;al1 hiopsies may be obtained at
exploratory laparotomy for thi. purpose, although
horses with malabsorption state. are often not good
(andidates for m'jor exploratory surgery, and vmund
complicatiolls arc common in the postoperative period
because of hypoproteinemia and the (atabolic state. If
suge!' is to be performed, biopsies should be tken
from any grossly abnormal section of bowel, but if the
bowel appears grossly normal then at least three small
intestinal biopsies should be taken from the proximal,
CHRONIC WEIGHT LOSS 1 8
mid- and distal small intestine, Biopsies should also be
obtained from the ceCUlIl and large colon at the same
time. Biopsies of mesemeric lymph nodes often reveal
similar pathological change to small illlcstinal infl
trates, and at least one lymph node should be biopsied
at the same time as the bowel wal! biopsies are taken,
Bowel wall and lymph node biopsies can also be suc
cessfully obtained via a flank laparotomy that can be
perormed in the standing horse utilizing local anesthe
sia. This approach greatly reduces the complications
associated with ventral midline wound healing.
Alternatively, mesenteric lymph node biopsies may he
taken ia laparoscopic techniques in the standing
patient, thereby eliminating the necessity for general
anesthesia and signifcantly reducing the risk of wound
complications. However, the sensitivity of this approach
for the diagnosis of small intestinal infltrative disease
has not yet been assessed.
TREATMENT
The prognosis for horses afected by malabsorption syn
dromes is generally guarded to very poor. By the time
that the precise diagnosis is reached, the disease is fre
quently well-advanced. Horses affected by difuse ali
mentary lymphosarcoma have a hopeless prognosis and
should be humanely destroyed, although chemother
apy may prolong survival for 6-12 months. Treatment
of fimg'<l1 enterocolitis with systemic antifungals is
usually unrewarding.
Some horses with CIBD !nay henefit frm heing fed
highly digestible feeds. Provision of a palatable, easily
assimilated high energy and protein source is indicated.
Supplementing the diet with electrolytes, minerals, and
vitamins is also useful. Feeds with high quality fber con
tent may also contribute to body weight g'<in in that they
may be more extensively converted from cellulose to
volatile free fatty acids in the cecum; this type of diet is
especially beneficial t horses affected by CIBD without
diarrhea. Feeding more fhquent meals in smaller
amounts may also aid in better digestion and absorp
tion. l<:nteral feeding through an indwelling nasogastric
tube is rarely indicated in view of the poor long-term
prognosis. There i. no justifcation in tf)ing to sustain a
severely debilitated horse when the progllosis is so poor.
Corticosteroid therapy is often ineffective in treating
CIBD, although some cases of eosinophilic infltrates
and lymphocytic-plasmacytic enterocolitis appear to be
responsive to corticosteroids. Parenterally administered
dexamethasone is likely to he more effective than oral
corticoMeroids, and prolonged courses are required.
Surgical resection of limited areas of afected bowel
may produce some short term benefL, but the diffuse
379
nature of the lesions usually precludes this therapeutic
option.
LFHY
chronic weight loss
Brown C M ( 1 989) Chronic weight loss. In Problems in Equine
Medicine, C M Brown (ed. ) . Lea and Febiger, Philadelphia,
pp. 6-22.
Divers TJ, Mohammed H 0, CummingsJ F ( 1998) Equine
motor neuron disease. In Curent Therapy in Equine
Medicine, 4th edn, N E Robinson (ed. ) . W B Saunders,
East L M, Savage CJ ( 1998) Abdominal neoplasia (excluding
urogenital tract) . Vet. Clin. N Am. Equine Pract. 14: 475-93.
ForemanJ H ( 1998) Changes in body weight. In Equine
Inteal Medicine, S M Read and W M Bayly (eds) . W B
Saunders, Philadelphia, pp 1 35-9.
Kronfeld D S ( 1993) Staration and malnutrition of horses:
recognition and treatment. ]. Equine Sci. 1 3: 298-304.
Kronfeld D S ( 1998) Clinical assessment of nutritional status
of the horse. In Metabolic and Endocrne Problems ofthe Horse,
T D G Waton (ed. ) . W.B. Saunders, London,
1 84-217.
Mair T S, Hillyer M H ( 1991 ) Clinical features of
lymphosarcoma in the horse: 77 cases. Equine Vet. Educ.
4: 108-13.
Rebhun W C, Bertone A ( 1984) Equine lymphosarcoma.
]. Am. Vet. Med. Assoc. 1 84:720-1.
Savage CJ ( 1 998) Lymphoproliferative and
380
myeloproliferative disorders. Vet. Clin. N Am. Equine Pract.
1 4:563-78.
Scarratt W K Crisman M V ( 1998) Neoplasia of the
respiratory tract. Vet. Clin. N Am. Equine Pract. 1 4:451-73.
Taylor F G R ( 1 997) Chronic wasting. In Diagostic Techniques
in Equine Medicine, F G R Taylor and M H Hilyer (eds) .
W B Saunders., London, 65-70.
Malabsorption syndromes
Cohen N D, Loy j K Lay j C, Craig T M, McMullan W C
( 1992) Eosinophilic gastroenteritis with encapsulated
nematodes in a horse. ]. Am. Vet. Med. Assoc.
200: 1518-20.
Duryea j H, Ainsworth D M, Maudlin E A, Cooper B j,
Edwards R B ( 1997) Clinical remission of
granulomatous enteritis in a Standardbred gelding
following long term dexamethasone administration.
Equine Vet.]. 29: 1 64-7
Kemper D L, Perkins G A, Schumacher j, EdwardsJ F,
Valentine B A, Divers T j, Cohen N D ( 1 999) Equine
Iyphocytic-plasmacytic enterocolitis: a retrospective
study of 14 cases. Equine Vet. ]
MacAllister C G, Mosier D, Qualls C W, Cowell R L ( 1990)
Lymphocytic/plasmacytic enteritis in two horses. ]. Am.
Vet. Med. Assoc. 196: 1995-8.
Mair T S, Hillyer M H, Taylor F G R, Pearson GR ( 1991 )
Small intestinal malabsorption i n the horse: an assessment
of the specifcity of the oral glucose tolerance test. Equine
Vet.]. 23: 344-6.
Roberts M C ( 1 985) Malabsorption syndromes in the horse.
Compo Cont. Educ. Pract. Vet. 7:S637-S646.
Roberts M C, Hill F W G ( 1973) The oral glucose tolerance
test in the horse. Equine Vet.]. 5: 1 71-3.
19
Hepatic and biliary tract diseases
Acute hepatic disease with
failure
TJ Divers
There are a large number of equine disorders that may
cause hepatic disease but few ever result in hepatic fail
ure. For example, horses with strangulating or inflam
matory intestinal diseases frequently have evidence of
liver disease (elevated hepatic enzymes in the serum)
caused by portal hypoxia and/or increased concentra
tion of endotoxin in the portal circulation, but these
conditions rarely progress to liver failure.
Many disorders that cause chronic liver disease, e.g.
pyrrolizidine alkaloid toxicosis, may present with acute
signs of hepatic failure. Those disorders that cause
chronic liver disease are covered elsewhere in this text
(see Pyrrolizidine alkaloid intoxication and Chronic
liver disease) .
In ponies and miniature horses, the most common
cause of acute hepatic disease and failure is hepatic lipi
dosis (see Hyperlipemia) . In adult horses, the most
common syndrome causing acute hepatic disease with
failure is Theiler's disease.
Theiler's disease is a subacute hepatic necrosis often
resulting in hepatic failure and acute encephalopathy
in horses. It has been termed 'serum hepatitis' because
often there is a history of the affected horses receiving
tetanus antitoxin 410 weeks prior to the onset of
clinical signs. In some cases, the affected horses may not
have received tetanus antitoxin, but may have been in
contact with another horse that had received tetanus
antitoxin. In other cases, there is no history of equine
origin biological products being administered. The
disease appears to be more common in late summer or
early fall. This apparent seasonal pattern could suggest
a vector spread of the disease, or could simply reflect
the fact that many foaling mares may receive tetanus
antitoxin in the spring of the year along with their new
born foal. Most commonly, only one horse on a farm is
affected, although outbreaks are reported and other
horses on the farm may have evidence of liver disease,
e.g. elevated enzymes, without clinical signs of hepatic
failure. A specifc tetanus antitoxin product and/or
the same batch and lot number, may be found to be
responsible for a high number of cases. A nearly
identical clinical and pathological syndrome has been
described in pastured horses in France.
Clinical signs
The clinical signs of Theiler's disease, or any severe
hepatic necrosis, are attributable to the rapid loss of
hepatocyte function and collapse of the liver
parenchyma. The most common clinical signs seen with
Theiler's disease are
signs of central nerous system (CNS) disorder
jaundice
discolored urine.
The CNS signs are variable and may range from
acute depression to maniacal behavior. Blindness may
be present and the affected horses may be ataxic. Icteric
381
19 CHRONIC WEI GHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DI SEASE
membranes can be noted in most cases, although in
peracute cases this may not be pronounced. The urine
may be abnormally dark indicating bilirubinuria and,
in a few cases, red if there is a concurrent microangio
pathic hemolytic process.
Neurologic signs are frequently observed with acute
hepatic failure and are referred to as heatoencehalo
pathy. Hepatoencephalopathy is a metabolically induced,
potentially reversible, functional disorder of the brain.
Neurologic signs are the most pronounced and clini
cally troublesome signs in most cases of equine hepatic
failure. Signs of hepatoencephalopathy may vary from
depression to bizarre maniacal behavior. Common
signs include
apparent blindness
ataxia
head pressing
propulsive circling
frequent yawning.
The pathophysiologic mechanism of hepatoencephalo
pathy is undoubtedly complex but is mostly due to
abnormal hepatic protein metabolism. The failing liver
may be unable to sufciently convert colonic-derived
ammonia to urea via urea cycle enzymes located in the
hepatocyte. The effect of excessive ammonia on the
central nervous system (CNS) may include one or more
of the following
enhancement of neurotransmitters
interference with normal neurotransmission
structural changes in the blood-brain barrier
changes in cerebral blood flow
interference with biochemical or
electrophysiological pathways in the brain.
Cerebral edema with development of Alzheimer tpe
II cells are characteristic of high CNS ammonia.
Alzheimer type II cells may result from hepatic failure,
primary hyperammonemia or severe uremia. In rare
cases, the cerebral edema may be so severe that hernia
tion occurs. Additionally, there may be decreased
hepatic extraction of gut synthesized y-aminobutyric
acid (GABA) which may additionally serve as a potent
inhibitory neurotransmitter. The GABA-ergic neuro
transmission is also closely linked to an increase
in natural benzodiazepines. Furthermore, abnormal
accumulation of glutamate may serve as excitatory
neurotoxins. Complex interactions of these neurotoxins
may determine if the horse with hepatoencephalopathy
is depressed or maniacal. The movement of GABA into
the CNS may be aided by an increased aromatic to
branched chain amino acids ratio in the plasma, and by
increased concentrations of plasma bile acids. Increased
amounts of aromatic amino acids, which are normally
382
metabolized by the liver, may also sere as false neuro
transmitters. In adult horses with hepatic failure, the
CNS signs of severe depression are rarely caused by
inadequate hepatic gluconeogenesis and hypoglycemia.
Horses with acute hepatic failure and/or Theiler's
disease generally have increases in both conjugated and
unconjugated bilirubin, with the increase in unconju
gated being the most pronounced in all acute diseases
except biliary obstruction. The unconjugated portion
becomes elevated because of lost hepatocellular
function with reduced uptake and conjugation of the
bilirubin.
Intravascular hemolysis and red discoloration of the
urine may be seen occasionally with equine hepatic
failure. This occurs most frequently with acute hepatic
necrosis, e.g. Theiler's disease, and is often, but not
always, a terminal event. The cause of the hemolysis
may be a microangiopathic hemolytic anemia caused
by the physical damage to the red cells as they pass
through the necrotic liver.
Severe bleeding problems are not commonly
obsered in horses with acute liver failure. Wen bleed
ing occurs, it is generally prolonged bleeding associated
with hepatoencephalopathy and self-inflicted physical
trauma. Hemorrhage in horses with liver failure is gen
erally a result of failure in both the extrinsic and intrin
sic pathways of coagulation causing prolongation of
both prothrombin and partial thromboplastin times.
These occur because of decreased hepatic production
of clotting factors. Factor VII has the shortest half-life,
so prothrombin time (PT) should be prolonged prior
to prolongation of partial thromboplastin time (PTT)
with liver failure. In some horses with liver failure, the
PTT may sometimes be prolonged beyond the normal
range prior to the PT being prolonged. The reason for
this is unknown. Disseminated intravascular coagula
tion (DIC) may be present in some horses with acute
severe liver failure. The cause of this is often multifacto
rial and may include decreased hepatic production of
antithrombin III, plasminogen, and high molecular
weight proteins that inhibit excessive coagulation.
Additionally, overwhelming hepatic tissue damage
and/or increased circulating endotoxin may stimulate
release of soluble proteins that afect coagulation.
Fibrin degradation products (FDPs) are often abnor
mally high in horses with liver failure since the liver is
the organ responsible for clearance of circulating FDPs.
An increase in FDPs, PT and PIT would be expected in
horses with liver failure and these fndings should not
be overinterpreted as being diagnostic for DIC. If a liver
biopsy is required, this can generally be performed
safely in spite of the prolongation in PT and PTT, since
platelet counts generally remain normal in horses with
liver failure.
Diagnosis
The diagnosis is based on
history
clinical fndings
laboratory confrmation of hepatic disease and
hepatic failure.
Hepatic disease can be detected most easily by measur
ing serum or plasma activity of liver-derived enzymes
including
gamma glutamyl transferase (GGT)
aspartate aminotransferase (AST)
sorbitol dehydrogenase (SDH)
glutamic dehydrogenase (GD)
lactate dehydrogenase (LDH-5) .
Gamma glutamyl transaminopeptidase will be elevated
in all cases of Theiler's disease and is most often in the
range of 1 00-300 IV/I. Aspartate aminotransferase
should be measured because it may provide an indica
tion of prognosis, i.e. those horses having values
greater than 4000 IV /1 have a poor prognosis. The
repeated measurement of AST may also be used to
measure recovery as the AST would be expected to
decrease within 3-5 days if the horse is going to
recover. Gamma glutamyl transaminopeptidase, on the
other hand, will frequently elevate further during the
first 3 days of the illness in spite of clinical improve
ment and eventual recovery in an affected horse. A
decrease in SDH in the serum would be expected to
occur more rapidly in improving horses than a
decrease in AST, because of its shorter half-life, and
measuring SDH can provide prognostic information
more quickly than measuring AST.
Total serum bile acids may also be used to detect
liver disease. In horses with Theiler's disease, the
measurement of serum or plasma bile acids rarely adds
further information than that provided by the measure
ment of hepatic enzymes. Virtually all horses clinically
affected with Theiler's disease will have total serum
bilirubin values greater than those commonly observed
with anorexia. Total bilirubin in horses showing clinical
signs caused by Theiler's disease is generally in the
range of 12-20 mg/dl (205-340 fmol/I ) . The percent
age of bilirubin in the unconjugated form is almost
always greater than 70 per cent, although there is some
increase in conjugated bilirubin in affected horses. The
conjugated bilirubin values are generally 1.5-5.0 mg/dl
(25.5-85.5 Jmol/I ). The PT and PTT times are gener
ally abnormally high in comparison to a control sample,
but rarely offer information not already gathered from
the measurement of direct and indirect bilirubin, bile
acids, and hepatic enzyme activity in the serum or
HEPATIC AND BI LIARY TRACT DISEASES 19
plasma. Other laboratory fndings that are frequently
abnormal in Theiler's disease include
moderate to severe acidosis
hypokalemia
polycythemia
increased plasma aromatic amino acids
hyperammonemia
A more defnitive diagnosis of Theiler's disease can
only be made by liver biopsy. If the history, clinical
fndings, and laboratory fndings are characteristic of
Theiler's disease, a biopsy is not imperative, and in
many cases, may not be easy to perform since the liver is
often shrunken and may be difcult to visualize with
ultrasound examination. Microscopic examination gen
erally reveals marked hepatocellular necrosis involving
the entire lobule, most severe in the central and mid
zonal hepatocytes. There is some fatty change and a
very mild-to-moderate accumulation of lymphocytes
and a few neutrophils. The degree of bile duct prolifer
ation is ofen positively correlated with the duration of
the disease. On necropsy examination, the liver is
usually smaller than normal, tan in color, and may
have markedly congestive centrilobular patterns. The
borders of the liver are sharp.
Therapy
There is no specifc therapy for Theiler's disease
although supportive therapy is often successful. The
affected horse should not be stressed if at all possible.
Stressful situations such as moving the animal to
another facility or weaning the mare's foal often exac
erbate the clinical signs of the hepatoencephalopathy.
Sedation should be used only when necessar to control
fulminant hepatic encephalopathy causing propulsive
behavior. Xylazine (0.2-0.4 mg/kg) can be used to
control bizarre behavior in order to prevent injury of
the animal and to allow catheter placement. Doses of
xylazine that cause lowering of the head should be
avoided if possible as low-head position and hypoventi
lation may worsen cerebral edema. Phenobarbital can
be used but diazepam should be avoided since it may
worsen hepatoencephalopathy. The benzodiazepine
receptor antagonist, flumazinil (0.2 mg/kg given slowly
intravenously) may be administered for uncontrolled
hepatic encephalopathy, but its efcacy in both horses
and humans is unproven.
Intravenous fluids are probably the most important
component of treatment for hepatic encephalopathy in
horses! The intravenous fluids should consist of a
balanced electrolyte solution, preferably without lac
tate, and should be supplemented with potassium
20-40 mEq/l, and 5-10 g dextrose per 100 ml. Sodium
383
19 CHRONI C WEI GHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
bicarbonate should be given only if blood pH is less
than 7.1 and/or bicarbonate is less than 1 4 mEq/1.
Additional potassium may be given as potassium
chloride mixed in molasses and administered per os via
a dose syringe. Fresh frozen plasma may be used but
hetastarch or stored whole blood should be avoided.
Supplemental vitamins can be administered but are not
necessary in the treatment.
An effort should be made to decrease ammonia pro
duction in the bowel and this can be done by adminis
tering neomycin 5.0 mg/kg p.o. q. 8 h by dose syringe
for 2 days. With fulminant hepatic encephalopathy in
the horse, I prefer not to pass a nasogastric tube since
nasal bleeding could occur. Nasal bleeding could exac
erbate the hepatic encephalopathy if the blood is swal
lowed and because of insufcient clotting proteins the
bleeding may be prolonged. Lactulose 0.2-0.5 ml/kg q.
8-12 h may also decrease ammonia production in the
bowel and can be used concurrently with neomycin.
Both lactulose and neomycin may cause diarrhea if
given in excessive dosages or for prolonged periods.
Vinegar (acetic acid) may also be effective in decreasing
blood ammonia when it is administered per os at 8 oz
(240 ml)/450 kg horse. Affected animals should be fed
high carbohydrate, high branch chain amino acid
(BCAA) feeds, with moderate to low total protein
content. Sorghum and/or cracked corn mixed with
molasses or commercially prepared BCAA paste are
ideal. Carbohydrates should be fed in frequent small
amounts. A moderate protein grass hay should be fed
rather than alfalfa hay or spring-cut grass hay. Affected
animals should be protected from sunlight in order to
prevent photosensitization.
Anti-oxidant, anti-inflammatory and anti-edema
therapy is indicated in acute hepatic failure. The anti
oxidant, anti-edema treatment include dimethylsulfox
ide, acetyicysteine and mannitol given intravenously
and vitamin E given intramuscularly. Ati-inflammatory
therapy should include flunixin meglumine and
pen toxiflline.
Cases of fulminant hepatic necrosis that do not
respond quickly to medical therapy are generally hope
less. In the future extracorporeal liver support might be
helpful in managing some horses.
Prognosis
Horses with Theiler's disease that can be maintained
for 3-5 days without deterioration and that continue to
eat often recover. A decline in the SDH and PT, along
with improvement in appetite, are the best positive pre
dictive laboratory and clinical indicators of recovery.
Horses that have fulminant encephalopathy that cannot
be easily controlled with sedatives have a very poor
384
prognosis, although some will recover. The degree of
hyperbilirubinemia is a less powerful prognosticator
than encephalopathy. Those animals that continue to
eat during the frst 3 days of the illness generally have a
good prognosis. If the affected horse recovers, which
many do within 5-10 days, its long-term prognosis is
excellent. There is no evidence that severe hepatic
fbrosis and/or neoplasia occur following Theiler's
disease in the horse.
MISCELLANEOUS CAUSES OF ACUTE
HEPATIC DISEASE AND FAILURE
There are only scattered reports of other causes of
acute hepatic disease and failure in adult horses.
Mycotoxicosis or other hepatotoxins make up the bulk
of these reports. Fusarium moniliorme toxins, especially
fumonisin B, may cause hepatic disease and rarely
hepatic failure in horses eating the fungi-contaminated
corn. Leukoencephalomalacia is the most common
disease and clinical syndrome caused by this toxin.
Aspergllus flavus and aflatoxins B" B2 and Mj contami
nation of grain may cause hepatic necrosis and fulmi
nate hepatic failure in horses. Fortunately aflatoxicosis
is rare in horses in most parts of the world. Pyrrolizidine
alkaloid-containing plants may also cause acute hepatic
disease and failure, although chronic disease with acute
failure is most common (see Pyrrolizidine alkaloid
intoxication). Septic portal vein thrombosis is rare in
horses but should be considered in adult horses with
acute hepatic encephalopathy.
Primary hyperammonemia
SF Peek
INTRODUCTION
Primary hyperammonemia in the absence of signifcant
hepatic disease is an uncommon cause of encephalopa
thy in horses. The reports of primary hyperammonemia
in adult horses are limited to a single case report from
the United Kingdom and a series of cases from the
north eastern United States. In addition, a potentially
inherited condition of Morgan horses causing primary
hyperammonemia and clinical disease in weanlings has
also been reported in the United States. Experimentally
hyperammonemia can be induced by the ingestion of
urea but there are no clinical reports of spontaneous
urea poisoning in horses. By comparison with rumi-
nants horses are considered to be fairly resistant to the
toxic effects of urea.
ETIOLOGY
The etiology of primary hyperammonemia in adult
horses is unknown. The association between primar
hyperammonemia and antecedent or concurrent signs
of gastrointestinal disease, without biochemical evi
dence of liver disease, raises suspicion that excessive
ammonia production within the large intestine is a
possible etiology.
CLINICAL SIGNS
The clinical signs associated with primary hyper
ammonemia in adult horses include acute encephalo
pathy, blindness, and gastrointestinal signs that can vary
from colic to acute diarrhea. The clinical signs relating
to gastrointestinal dysfunction typically precede the
development of encephalopathy.
CLINICAL PATHOLOGY
Consistent abnormal laboratory fndings identifed in
adult horses with primary hyperammonemia include
evidence of dehydration, severe hyperglycemia (> 275
mg/dl or IS mmol/I), and metabolic acidosis (venous
pH < 7. 15) . A blood ammonia concentration of greater
than 150 mg/ml in the absence of clinical and bio
chemical evidence of liver disease is considered diag
nostic, but clinical cases of primary hyperammonemia
frequently have blood ammonia concentrations in
excess of 250 mg/ml prior to treatment. Accurate mea
surement of blood ammonia concentration requires
rapid and careful sample handling. Ideally a control
sample should be obtained from a normal, healthy
horse and quantitated simultaneously for comparative
purposes. Individuals with primary hyperammonemia
that present with acute diarrhea may also develop
severe electrolyte abnormalities and life-threatening
hypoproteinemia.
TREATMENT
Treatment of primary hyperammonemia is predomi
nantly supportive but should include administration of
products per os to decrease the production and intesti
nal absorption of ammonia. Recovery is possible if
horses can be supported during the acute encephalo-
pathic stage and any concurrent intestinal disease does
not become a life-threatening problem. Intravenous
fluid therapy is important to maintain tissue perfusion
and to correct specifc electrolyte and acid-base abnor
malities. Dextrose-containing fluids should be avoided
due to the severe hyperglycemia that accompanies this
condition. Individual horses with primary hyperam
monemia may survive following intensive intravenous
fluid therapy with balanced polyionic fluids. In cases
where hypoproteinemia becomes a complicating factor,
fresh blood, plasma, or plasma expanders should be
considered. The addition of bicarbonate to intravenous
fluids should be considered when systemic pH falls
below 7. 10. The acidifing agent lactulose (90-120 ml
p.o. q.i.d. ) can be used to decrease ammonia absorp
tion from the large intestine by increasing the conver
sion of ammonia to ammonium ions, which are not
absorbed from the lumen. In addition oral antibiotics
such as neomycin (20-30 mg/kg q.i.d. ), or metronida
zole ( l 0-15 mg/kg q.i.d.) may be administered to
decrease ammonia-producing bacteria within the large
intestine.
POSTMORTEM FINDINGS
Histologic abnormalities in the brain of horses that
have died or been euthanized due to primary hyperam
monemia include edema and frequent Alzheimer type
II cells. Alzheimer type II cells are diagnostic for hyper
ammonemia and will therefore also be seen in horses
that exhibit hepatic encephalopathy ante mortem due
to either acute or chronic liver failure. Cases of primary
hyperammonemia that demonstrate diarrhea ante
mortem may also have moderate to severe inflamma
tory changes in the large colon and cecum, although no
specifc infectious etiologic agent has so far been
associated with the condition.
HYPERAMMONEMIA IN MORGANS
Etiology
Persistent hyperammonemia has been documented in
two related Morgan weanlings. The same stallion sired
the affected horses and their dams were sisters. Based
upon the familial relationship and the demonstration
of abnormal serum and urine amino acid con
centrations it is suggested that this condition may be an
inherited disorder that is analogous to the hyperor
nithinemia, hyperammonemia, and homocitmllinemia
(HHH) syndrome in man. HHH syndrome is a rare
autosomal recessive disorder that results from
385
19 CHRONI C WEI GHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DI SEASE
abnormal ornithine transport into mitochondria with
subsequent ornithine accumulation and a reduced
ability to clear ammonia through the urea cycle.
Clinical signs
The affected foals were clinically normal until approxi
mately 2 weeks post-weaning when they began exhibit
ing generalized unthriftiness and abnormal behavior.
The neurologic status of both individuals deteriorated
and they were euthanized at approximately 7 months of
age. Seizure activity was reported in one foal, but both
demonstrated other signs of encephalopathy including
severe depression, propulsive circling, teeth grinding,
and dementia.
Clinical pathology
Unlike primary hyperammonemia of adults, where no
biochemical evidence of hepatic dysfunction has been
documented, one of the weanlings did have enzymatic
evidence of hepatocellular disease while the other had
a prolonged bromosulfthalein (BSP) retention time.
Severe hyperammonemia (200-500 mg/ml ) was docu
mented on several separate occasions in both indivi
duals. Serum ornithine and glutamate concentrations
were elevated in both weanlings compared to controls.
Urinary orotic acid concentration was measured in one
of the two foals and was found to be signifcantly
elevated.
Treatment
Although supportive therapy including intravenous
fluids, oral lactulose, and the provision of a low protein
diet was instituted, both horses were euthanized due to
a progressive deterioration in neurologic status.
Post-mortem findings
Necropsy fndings were not specifc but included
plasmacytic/lymphocytic hepatitis as well as histologic
changes in the central nervous system consistent with
hyperammonemia.
Biliary tract disease
SF Peek
INTRODUCTION
Cholangiohepatitis is the most commonly encountered,
clinically signifcant form of biliary tract disease in
386
horses. Other forms of true biliary disease appear to be
very uncommon in horses, but biochemical evidence of
hepatobiliary injur and dysfunction, including eleva
tions in serum bilirubin, gamma glutamyl transferase
(GGT) , alkaline phosphatase (A), bile acids, and
prolonged exogenous dye excretion tests frequently
accompany both acute and chronic hepatic diseases
such as Theiler's disease, Tyzzer's disease, hepatic
lipidosis, and pyrrolizidine alkaloid toxicity. Rarely, bio
chemical and clinical evidence of biliary tract disease
may occur in association with the so-called 'chronic
active hepatitis', abscesses, granulomas, or infltrative or
obstructive neoplastic conditions, such as primary
cholangiocarcinoma, hepatic adenocarcinoma, or
metastatic hepatic tumors.
CHOLANGIOHEPATITIS
Although this condition probably begins as a cholangi
tis, the term cholangiohepatitis is appropriate because
clinically signifcant inflammatory biliary disease in
horses is extremely rare without extension into the peri
portal region of the liver. It is probable that many mild
cases of cholangitis/ cholangiohepatitis are undiag
nosed because horses are asymptomatic, but the condi
tion predisposes horses to chronic, active, inflammatory
hepatobiliary disease and the formation of biliary
calculi. Chronic cholangiohepatitis may frequently be
associated with signifcant intrahepatic or extrahepatic
calculus formation. Discrete calculi can often be visual
ized ultrasonographically or at post mortem examina
tion, but some horses with cholangiohepatitis develop a
more sonolucent 'sludge-like' material within the bil
iary tract. With severe suppurative cholangiohepatitis,
particularly if the condition is long standing, signifcant
periportal and bridging fbrosis can occur. Clinically
signifcant hepatobiliary disease appears to be more
common in middle-aged to older horses. Due to the
absence of a gall bladder, the nomenclature surround
ing biliary calculi in the horse has been confusing. The
term cholelithiasis broadly refers to calculi anywhere
within the biliary tract, but in man it has come to be syn
onymous with calculi within the gall bladder. It is per
haps more appropriate in horses to refer to intrahepatic
calculi as hepatoliths and extrahepatic calculi, usually
located within the common bile duct, as choledocho
liths (Plate 19. 1 ) .
Etiopathogenesis
The etiopathogenesis of cholangiohepatitis in adult
horses is presumed to be ascending bacterial infection
from the proximal small intestine. Evidence for this
comes from retrospective studies documenting the iso
laticm of predominantly gram-negative, enteric bacteria
such as Eschechia coli, Enteobacte spp. and Citrobacte
spp. from clinical cases. The ascending infection is
believed to predispose to calculus formation by creating
a nidus around which the calculus forms. The composi
tion of calculi in horses is predominantly calcium bili
rubinate and calcium phosphate, analogous to brown
pigment stones in man.
Cases of cholangiohepatitis commonly present with the
non-specific clinical signs of fever, icterus, colic, weight
loss, and encephalopathy.
Careful history taking will often reveal recurrent
bouts of mild-to-moderate colic coincident with fever
in the preceding days to weeks. Significant weight
loss will commonly accompany more chronic cases.
Occasionally signs of hyperammonemic hepatic
encephalopathy can be seen when complete calculus
obstruction to biliary outflow occurs or the disease
process has progressed to fulminant hepatic failure.
Serum biochemical abnormalities include large
increases in the hepatobiliary enzymes GGT and A,
alongside moderate increases in the hepatocellular
enzymes aspartate transaminase (AST) and sorbitol
dehydrogenase (SDH). Total serum bilirubin is ele
vated, frequently well above the levels typically seen with
anorexia alone, with the direct reacting or conjugated
fraction representing more than 25 per cent of the
total. The ratio of direct to indirect bilirubin is a very
helpful parameter in the diagnosis of cholangiohepati
tis because the proportionate increase in the direct
reacting fraction is fairly specific to this condition in
horses. Bilirubinuria may also be observed. Serum bile
acids will be elevated in many cases of cholangiohepati
tis, and can reach very high levels (> 1 00 mmol/l ) in
cases with significant biliary obstruction. Horses with
either maniacal or depressive hepatic encephalopathy
in association with complete calculous obstruction or
severe, chronic cholangiohepatitis will have elevated
blood ammonia levels. Typically hematologic changes
are consistent with chronic, active inflammation and
include neutrophilia and hyperfibrinogenemia. If the
condition is more than 2-3 weeks in duration hyper
globulinemia may also be documented.
Although clinical and laboratory findings can be
highly suggestive of the condition, a definitive diagnosis
of cholangiohepatitis requires liver biopsy. It is recom
mended that in vitro measurements of clotting function,
specifcally the prothrombin time and activated partial
thromboplastin time, be made prior to hepatic biopsy.
Frequently these indices are normal but they may be
prolonged if the biosynthetic capacity of the liver
has diminished in association with advanced post
inflammatory fibrosis. The biopsy procedure is best
performed under light sedation and ultrasonographic
guidance using a 14-gauge biopsy needle. Sufcient
biopsy material should be obtained for aerobic and
anaerobic culture as well as for routine histopathology.
Visualization of the liver via ultrasound lessens the risk
of inadvertent colonic, diaphragmatic, or pulmonary
iury, that can occur when the procedure is per
formed blind using traditional anatomic landmarks.
Histologically the liver tissue should be evaluated for
both the severity of inflammation and the presence
and extent of any periportal and bridging fbrosis.
Advanced bridging fibrosis should carry a more
guarded prognosis, particularly when it is accompanied
by biochemical evidence of liver failure such as hypo
albuminemia, hypoglycemia, and altered clotting times.
Bile duct hyperplasia is invariably reported but repre
sents a non-specific response to liver injury.
In normal horses the liver can best be visualized
between the 1 1th and 16th intercostal spaces on the
right side, and the 9th and 1 1 th spaces on the left side.
In cases of cholangiohepatitis the liver image can fre
quently be visualized over a much greater area due to
hepatomegaly. The degree of hepatomegaly, bile duct
dilation, and the presence of signifcant hepatoliths
should be evaluated ultrasonographically. It is not
Figure 19. 1 Sonogram from a 14-year-ol d Thoroughbred
mare with chol angiohepatitis and hepatolithiasis. Ultra
sonographical ly there is an obvious di l ated bile duct with
an intral umi nal hepatolith (white arrow). Note the vari
ably hyperechoic appearance of the hepatic parenchyma
(dark arrows). The image was obtained with a 3.5 MHz
sector scanner
387
19 CHRONIC WEI GHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
possible to visualize bile ducts via ultrasound in the nor
mal horse. However, signifcant bile duct dilation and
discrete calculi may be detected in many clinical cases
(Figure 19.1). The echogenicity of calculi and degree of
acoustic shadowing will vary with the extent of mineral
ization. With experience it may be possible to charac
terize the hepatic parenchyma as being diffusely more
echogenic than normal, particularly in cases where
signifcant hepatic fibrosis has occurred.
Medical management
Long term antimicrobial therapy is essential in the suc
cessful treatment of cholangiohepatitis and choledo
cholithiasis/hepatolithiasis in adult horses. In certain
situations where biliary obstruction is complete, or the
horse is in uncontrollable abdominal pain, surgery
may be considered (see below) . The choice of specifc
antibiotics should be ideally based upon both aerobic
and anaerobic cultures of liver biopsy material. If biopsy
culture results are either unavailable or negative, then
broad spectrum antibiotics such as potentiated sulfon
amides, cephalosporins, or fluoroquinolones would be
appropriate choices. Although the spectrum of activity
of the aminoglycosides is limited to aerobic, gram-nega
tive bacteria, a good clinical response to this family of
antibiotics is often observed. The duration of anti
microbial therapy will vary on a case by case basis but
experience suggest that weeks to months of therapy are
necessary. Treatment failure can commonly be associ
ated with premature antibiotic withdrawal, and it is
worth considering that both clinical and biochemical
resolution should be confrmed before treatment is
stopped. Many horses will show substantial clinical
improvement in terms of appetite, absence of fever, and
weight gain while still demonstrating signifcant bio
chemical evidence of hepatobiliary disease. It is recom
mended that antibiotic treatment be continued until
serum GGT and A levels have been normal for 2-4
weeks. Repeated ultrasonographic evaluation of the
liver during the course of therapy can be useful in
assessing improvements in hepatomegaly, bile duct
dilatation, and the resolution of any identifable calculi.
Intravenous polyionic fluid therapy can be a very useful
adjunct to antimicrobial therapy both in cases of acute
cholangiohepatitis and during long-term therapy when
an individual horse clinically deteriorates.
Individuals that present with hyperammonemic
hepatic encephalopathy may be treated with products
to reduce both the production and absorption of
ammonia in the large intestine. The oral administration
of either neomycin (20-30 mg/kg q.i.d.) or metronida
zole ( 10-1 5 mg/kg q.i.d.) has been recommended to
alter cecal and colonic bacterial flora and thereby
388
reduce ammonia production. Lactulose (90-120 ml
p.o. q.i.d. ) can be given as an acidifing agent to alter
lumenal pH and increase the conversion of ammonia to
non-absorbable ammonium ions. Adult horses with
hepatic encephalopathy can vary from somnolent to
violent and maniacal and will often require chemical
restraint for both their own protection and that of
people around them. If the hepatic encephalopathy
accompanies fulminant liver failure the prognosis
should be extremely guarded. Intensive intravenous
fluid therapy to correct and maintain hydration, elec
trolyte and acid-base status are essential parts of the
therapy of cases of cholangiohepatitis that present with
concurrent fulminant liver failure.
Specifc bile salt therapy with compounds such as
ursodeoxycholic and chenodeoxycholic acid is contra
indicated in horses, not only because cholesterol rich
calculi are extremely rare but also because these com
pounds have been shown to be metabolized to pro
inflammatory hepatotoxic compounds in other hind
gut fermenters such as rabbits. There is however,
specifc evidence to support the use of intravenous
dimethylsulfoxide (DMSO) in the medical manage
ment of brown pigment stones in man, and by analogy
its use is justifable in cases of equine choledocholithia
sis and hepatolithiasis. DMSO can be given intra
venously at a dose of 1 g/kg s.i.d. for 5-7 days, diluted to
a 5% solution in fluids.
Surgical management
Surgical management of cholangiohepatitis and biliary
calculi should probably be resered for cases of com
plete biliary obstruction with severe, unrelenting
abdominal pain that is unresponsive to conventional
analgesics. Cases of complete obstruction often present
with hyperammonemic encephalopathy and will there
fore beneft from intensive supportive medical manage
ment as well as surgical relief of the obstruction.
Anecdotal and published reports of successful surgical
management by either manual lithotripsy or choledo
cholithomy do exist but bile peritonitis carries such a
grave prognosis that great care should be taken when
attempting to either remove, or 'milk' calculi into the
proximal small intestine at laparotomy. Recurrent
obstruction is likely because most cases will have addi
tional intrahepatic calculi that are inaccessible to the
surgeon, and these may continue to partially or com
pletely obstruct biliary outflow post-surgically.
OTHER CONDITIONS
Hepatic abscesses, neoplasia, and parasitic granulomas
are documented, but rare causes of obstructive hepato-
biliary disease in horses. Cholangiocarcinoma is the
commonest form of primary hepatic neoplam bnt liver
metastases may be seen in association with primary
tumors such as !ymphosarcoma, squamous cell carci
noma, and melanoma, However, clinical and biochemi
cal evdence of biliar tract disease is often absent, even
with significant parenchymal infiltration, unless there is
obstruction to biliary drainage. This is most commonly
associated with space occupying lnasses that impede
extrahepatic biliary flow through the right and left
hepatic ducts and the common bile duel.
Occasiona!!y elevations in GGT, AP, and bilirubin
arc .een in association with colonic (espedaUy 180"
rotations of the large colon) and proximal small intesti
nal disease in adult horses and foals. Foals with severe
gastroduodenal ulcnation that progresses to signifICant
stricture fOrmation close 10 the duodenal papilla may
haw elevations in [hese enzymes due to compromised
hiliar outflow. Furthermore, horses with colonic dis
placement or torsion may have elevations in the
hepatobiliary enzymes probably because of abnormal
extrahepatic biliary drainage rather than true hepat(}
biliary disease. It is worth remembering that donkeys,
mules. and asses have a higher (up to 3 times) normal
lerel of GGT compared to horses.
Pyrrolizidine alkaloid
intoxication
GP Carlson
INTRODUCTION
PyrroliLidine alkaloid intoxication is the most common
came of chronic liver failure in horses in the wester
C nited States and toxicity has been recogni7ed in many
("()untries around the world. Pyrolb:irline alkaloid-:on
taining toxic plants (Table 19.1) tend 10 be unpalatable
and are generally ",'oided by horses. Poor pasture con
ditions or over grazing may contribute to consumptioll
of these plants, however intoxication is more likely to
occur folIo"ing the feeding of contaminated hay.
Pelleted or (:ubed hay may pose a particular risk since
the presence of poison()LL planL can not be seen. For
some plants, such as Amsinckia interedia, toxic alkaloids
are concentrated in the seeds that may be found in
srret'nings of grain harested from contaminated felds.
Such screenings are highly toxic and feeding relatively
modest amounts can lead to massive liver damage and
functional failure within days.
HEPATIC AND BILIARY TRACT DISEASES 19
T.b.11 . li 1k1"p'lnt
Botanical name Common name
Amsinckia intermedia Fiddleneck, fireweed,
or tareed
Senecio vulgaris Common groundsel
Senecio fideJli Woolly groundsel or
Ridell's groundsel
Senecio jacobaea Tansy or common
ragwort. ragwort, or
stinking Willie
Crota/aria spp. Rattle box
Heliotropium europaeum Common heliotrope or
potato weed
Cynog/ossum officinale Hounds tongue
Horses generally present with depression, anorexia,
and weight loss for variable periods of time. Horses with
areas of unpigmented skin may develop photosensitiv
ity. Thc clinical course may vary from several days to
several months but when sufcient livcr damage has
occurred to produce functional failure, there may be an
abrupt onset of profound clinical signs and in many
cases death. The appart'lll aC!l11' onset of clinical i11nt'.s
generally represents the end stage of a chronic, pn)
gressive disease process. Clinical signs and death may
occur up to a year after the contaminated feed was
eaten. Since all horses with access to a contaminated
feed sourn are at risk, a histor of other animals with
progressive depression, weight loss, icterus, anrl death
should alert the clinician to a possible common cause.
ETIOLOGY
Pyrrolilidinc alkaloid toxicity is largely determined by
the total dose of the pyrrolizidine alkaloid ingested.
Toxi{: cffecL are cumulative and tend to be progressive;
thus, ingestion of relatively small quantities over a long
periorl of time may produce similar effects to those
ohsel\led folIov'ing ingestion of larger quantities for a
shorter time period. Pyrrolizidine alkaloids are proxi
mate toxins which are metabolized in the liver to highly
reactive, unstable metabolites (the dehydroalhloids)
which are potent alkylating agents. These compounds
arc responsible for much of the direct hepatocellular
389
damage. Hydrolysis of the dehydroalkaloid yields the
dehydroaminolcohol, which can be both antimitotic
and carcinogenic. These toxic metabolites are thought
to be responsible for the production of the megalo
cytes, which are a characteristic, histopathologic feature
of this disease.
Experimental feeding studies indicate several stages in
the development of pyrrolizidine alkaloid toxicity.
Initially modest characteristic liver lesions may develop
along with associated biochemical evidence of liver
damage without producing overt clinical signs. In a
report of racing horses fed Senecio-contaminated
alfalfa hay, poor performance was one of the earlier
indicators of disease. Later, progressive liver damage
results in compromised hepatic function, and at this
stage clinical signs become evident with progressive
development of
depression
anorexia
weight loss
variable icterus.
The final phase of the disease process occurs with the
onset of filure of function and terminal hepatic
decompensation. The onset of severe clinical signs may
occur quite suddenly and represent the end stage of a
disease process that may have been developing for an
extended period of time. Vital signs (temperature,
pulse, and respiratory rate) are often within normal
limits unless the horse has become agitated or convul
sive. Clinically detectable icterus can be quite variable
until the final stages of the disease process when
icterus may be moderate to severe. Central neurologic
signs range from moderate depression to compulsive
walking, excessive yawning, ataxia, apparent blindness,
and head pressing, to maniacal behavior, convulsions,
coma, and death. Self-inflicted trauma may occur in
horses that become oblivious to their surroundings.
Intravascular hemolysis may occur in the terminal
stages of the disease with resultant hemoglobinuria.
Photosensitivity may be noted in non-pigmented areas
of the skin. Although laryngeal paresis, edema, ascites,
and diarrhea have been reported they are not com
mon features in horses with pyrrolizidine alkaloid
intoxication.
A history of exposure to pyrrolizidine alkaloid-con
taining plants and clinical signs compatible with pro
gressive liver failure would allow a tentative diagnosis of
pyrrolizidine alkaloid intoxication. This is particularly
true if there had been previously confrmed cases from
390
the same property or from other animals on the same
feed.
CLINICAL PATHOLOGY
Elevation of liver-derived serum enzyme activities (SDH
and AST) is associated with active liver damage, but
activities may decrease toward normal until the later
stages of the disease process when marked elevation
may again be noted. Elevation of GGT and A activities
reflects the focus of the pathologic process in the peri
portal regions and the biliary system. Sustained moder
ate to marked elevation in these enzymes provides an
early and persistent indication of liver involvement. The
bromosulfthalein (BSP) clearance half time and the
serum bile acid concentration are generally increased.
Serum bilirubin concentrations may remain within nor
mal limits until the horse reaches a state of functional
failure. Total serum bilirubin generally remains less
than 10 mg/ dl (170 mmol/l) and the direct-reacting
bilirubin rarely accounts for more than 25 per cent of
the total. The blood urea nitrogen (BUN) is generally
below normal in horses with functional failure.
Foodstuffs can be tested for the presence of
pyrrolizidine alkaloids.
PATHOLOGY
Demonstration of typical liver lesions on biopsy or at
necropsy is necessary for confrmation of the diagnosis.
The liver is often small and frm and nodules of regen
erating liver tissue may be noted in some long-standing
cases. Typical lesions of pyrrolizidine alkaloid intoxica
tion are megalocytosis, periportal fibrosis, biliary hyper
plasia, and occlusion of the central veins. Liver lesions
tend to be progressive and as normal hepatic architec
ture is damaged and replaced by fbrous tissue, the
prognosis becomes less favorable. Well-developed
lesions of veno-occlusion are also considered an
unfavorable indication. Exposure to massive doses of
pyrrolizidine alkaloids may produce acute centrilobular
necrosis, as has been documented experimentally in a
number of species.
TREATMENT AND PROGNOSIS
There are no specifc recommendations for treatment
of the damage produced by these toxic plants other
than removal of the contaminated feed source.
Complications associated with photosensitivity can be
reduced if the horses are housed out of direct sunlight,
and retention of appetite and maintenance of body
weight are the most useful prognostic indicators. Even
horses with moderate histologic evidence of liver dam
age may survive if they maintain a normal appetite. It is
often recommended that horses with liver disease be
put on a low protein diet. This recommendation may
not always be appropriate, it may be better to feed
something that the horses will eat, alfalfa hay for exam
ple, than to offer a lower protein feed source that the
horses refuse to eat. It is critical to provide adequate
caloric intake of a nutritionally balanced diet of grain
and forage or hay. Some horses with extensive liver
damage survive, but remain unthrifty and may not be
able to handle the stress of active athletic training.
Vigorous supportive care may be unrewarding in a
horse with clinical signs of advanced liver failure and
histologic evidence of generalized fibrosis with loss of
normal hepatic architecture.
Chronic active hepatitis
GP Carlson
INTRODUCTION
Chronic active hepatitis is not a specific disease entity,
but is a descriptive term for a group of conditions
characterized by active, progressive, inflammatory liver
disease of some duration. The history is often one of
depression, weight loss, and variable icterus. Signs are
often intermittent and may be associated with fever.
Some horses have a history of previous or active intra
abdominal disease. There has, thus far, been no clear
evidence of association with advancing age, viral dis
ease, or drug administration. The disease can progress
to the point of liver failure with major central nervous
system involvement and death. Unusual cutaneous
manifestations such as moist lesions at the coronary
bands may be present. Liver lesions lend to be located
in the periportal region and the histopathologic
diagnosis is often cholangiohepatitis.
Clinical signs vary with the degree of liver damage and
the presence any underlying disease process. Horses
often present with anorexia, weight loss, variable
icterus, and moderate to marked depression.
Neurologic signs may progress to convulsions, coma,
and death. Some horses have elevated rectal tempera-
ture, pulse, and respiratory rates. The moderate to high
fever noted in some horses with chronic active hepatitis
is not a common feature of many of the other causes of
liver failure, unless there have been complications.
Petechial or ecchymotic hemorrhages may be noted in
the visible mucous membranes. Intra-abdominal prob
lems such as an enlarged anterior mesenteric artery,
thickened bowel, or mass lesion may be noted. Some
horses develop a moist exfoliative dermatitis at the
coronary bands and in some cases this may be the
presenting complaint.
CLINICAL PATHOLOGY
Laboratory evaluation provides evidence of liver
damage and allows an assessment of the degree of
functional failure. Initially liver-derived serum enzyme
activities may be slightly to moderately elevated. Later
in the disease process substantial elevation of liver
derived serum enzyme activities and marked elevation
of the enzymes that reflect biliary damage, GGT and
A, will be noted. Serum bilirubin may be markedly ele
vated with direct-reacting bilirubin comprising up to 40
per cent of the total. The urine is strongly positive for
bilirubin and serum bile acids are greatly elevated. The
BUN is often low and hypoglycemia will be noted in
some horses. The hemogram may show evidence of an
inflammatory response with a leukocytosis, left shift,
and monocytosis. Total plasma protein concentration is
generally elevated, largely because of an increase in
globulins. Culture of liver biopsy specimens may be
rewarding since bacterial agents may contribute to
hepatitis or cholangitis.
PATHOLOGY
Histopathologic lesions are most prominent in the peri
portal region with hepatocyte damage and loss, variable
fbrosis and an inflammatory infiltrate. The cellular
component of this infiltrate tends to be mononuclear
cells, except those cases with suppurative hepatitis that
may have a marked neutrophilic response. There is
often evidence of cholangitis with biliary hyperplasia
and bile stasis. Bacteria may colonize the liver during
bacteremia, via the portal drainage from damaged
bowel, or as an ascending process from the common
bile duct. Viral agents or idiosyncratic reactions to
drugs are thought to be major factors in the develop
ment of chronic active hepatitis in other species. The
pathogenesis of the skin lesions is unclear, but these
lesions appear to represent an immune-mediated
vasculitis associated with liver disease.
391
TREATMENT
intensive supportive care is indicated until horses
regain their appetite. A fairly consistent favorable
response to corticosteroids can he anticipated. Initial
!Tfatlllcnt should consist. of 20-40 mg of dexametha
sone given hy injection. This dose rate is maintained for
) 5 days {depending upon the response), and is then
gradually decreased o\"cr the next 7-1O days. At this
lime the horse may be placed on onll prednisone at
40/l-6QO mg/day. Treatment may be necessary for 46
weeks or longer with careful monitoring of clinical signs
and biochemical parameters. R;I:lI'rial infection may
play a role. especially in horses with fever and a
neutrophilic intlamlllatory infiltrate on liver biopsy,
and systemic antibiotics arc indicated, Improvement in
attilllde and appetite are among the earliest and most
consiMelll indicators of response to therapy,
Chronic liver disease
GP Carlson
Horses with chronic: liver disease may present with a his
tory of clnonic progressively developing clinical signs or
they may pnst'nt with recently recognized and f!lmi
\lant clinical signs at the end stage of function<l failure,
Several of the more .pecific and common causes for
chronic liver failure have been discussed in other sec
tions {pyrro!izidine alkaloid !oxicosi, chrnnic active
hepatitis, biliary (ract disease, and hyperlipemia). This
St'rliOll will address chronic liver failure of undeter
mined cause as well as some of the less common causes
of liver disease such as hepatic neoplasia.
CHRONIC LIVER FAILURE OF
UNDETERMINED CAUSE
The history, clinical signs, and dinical patholob' data
fOr these cases may essentially be the same a described
for horses with pyrrolizidine allwloid intoxication
except perhaps for the absence of a history of exposure
to toxic plants. Most horses I-I-ith chronic liver failure
prese!H with chronic. weight loss, depression, variable
icterus, and progressive neurologic signs terminally.
Clinical signs arc generally non-specific and laboratory
indications of liver damage such as serum enzyme
auivities (SDH, AST, <lnd I.OH) may be only mod{'tIy
elevated if the process of hepatocyte destruction is no
longer \'(1
) active, while GGT and A tend to be elevated
in disease processes that involve the biliary system.
392
Indicators of compromised livtr function such as bile
acids, total and direct bilirubin, BU:, blood ammonia.
blood glucose, and the ratio of plasma branched
chain to aromatic amino acids may only be abnomJ<lI
during the termimll stage of the disease process.
Hypoproteinemia and hypoalbuminemia are not COIll
mon features of chronic liver failure in the horse, bUlan
increase in globulins is a frequent finding. Po\ycythemiil
Illay be noted in some horses with chronic liver failure.
\1casures of liver function such a BSP or indocyanine
green clearance would probably indicate altered liver
funnion. However, the routine application of these
diagnostic procedures is limited by the lact that sterile
pnparations of BSP are no longer commercially avail
able in the United States and indocyanine green is
expensive. Imaging of the liver using ultrasound pro
vides a non-invasive means to evaluate liver location,
size, and texture. This information can be most helpful
in determining the most appropriate site for liver
biopsy. It is possihle in some instances to identify masses,
abscesses, enlarged bile ducts, and bile stones using
these techniques. The most useful diagnostic tool in the
animal manifesting clinical and biochemical evidence
ofliver failure is the liver biopsy. It is possible with ultra
sound-guided liver biopsy to obtain tissue samples from
areas with focal liver lesions. However, most horses with
chronic liver failurt have ilwolvement of over 80 per
cent of the liver and liver biopies generally provide
representative samples for histological evaluation.
The liver has a great capacity for regeneration and
repair following injur. Chronic liver failure generally
result from processes in which there has been damage
to hepatocytes, hepatocyte loss, inflammation, and pro
gressive replacement of hepatic parenchyma by fibrosis.
Potential causes or factors that may contribute to the
development of chronic liver failure include
recurrent bacterial or viral infections
immunological reactions
parasitism
exposure to toxic chemicals or pharmaceutical
agenL
poisonous plants
mycotoxins
chronic hypoxia
dietary imbalances
iron overload
trauma
amyloidosis.
In many instances at the end stage of liver failure it is
not po.sible t determine the specific cause or causes of
the liver injur and subsequent fbrosis, a over time
many factors may have contributed to progressive
damage and loss of function.
KLEIN GRASS (PAN/CUM COLOR TUM
i
Chronic liver disease has been reported from Texas in
horses grazing pasture planted to Klein grass as well as
horses fed Klein-grass hay. Icterus, anorexia, and pro
gressive weight loss were the principal signs with some
horses developing colic signs. Elevated GGT activity,
total and direct bilirubin, blood ammonia, and BSP
clearance times were noted. Typical liver lesions
included bridging hepatic fbrosis, cholangitis, and
hepatocellular regeneration. The toxic principal is
thought to be a saponin. Although death losses were
reported in horses with advanced liver lesions, most
horses recovered after Klein grass was removed from
the diet. The sporadic nature of the disease suggests
individual susceptibility, variability in the amount of
feed ingested and perhaps seasonal or maturational
variation in the content of the toxic principal.
ALSIKE CLOVER
Horses grazing alsike clover may develop signs of liver
failure, especially photosensitization, anorexia, and
icterus. Several horses on a farm may be affected at one
time. Generally these horses are on a clay soil pasture
containing large amounts of alsike clover. The disease
appears to have yearly fluctuations in areas where alsike
clover is common (eastern USA and Canada) suggest
ing that environmental factors contribute to either the
toxicity of the plant or growth of a hepatotoxin on the
plant. Removal of afected horses from the pasture and
supportive care treatments result in complete recovery
of most caes. If the horses are not removed from
the alsike clover, the disease may progress to hepatic
fibrosis, fulminant hepatic failure, and death.
HEPATIC NEOPLASIA
Primary liver tumors are relatively rare in horses.
Cholangiocarcinoma occurs mainly in older horses,
which may present with anorexia, weight loss, icterus,
edema, and abdominal distention. This tumor tends to
produce multiple masses within the liver. Extrahepatic
metastasis may occur with involvement of the peritoneal
and pleural cavities, intestine, spleen, and lung.
Cholangiocarcinoma has been reported in combination
with hepatocellular carcinoma in one horse and in
another horse with concurrent septic cholangiohepatitis.
Hepatocellular carcinoma has been reported pri
marily in young horses less than 3 years of age. These
tumors are often solitary and may be multilobulated.
Clinical signs include depression, anorexia, weight loss,
abdominal distention, intermittent diarrhea, and
hyperemic mucous membranes. Modest elevation of
liver enzyme activity may be observed. Polycythemia or
erythrocytosis as indicated by marked elevation in the
hematocrit has been noted in these patients, this may
be due to secretion of an erythropoietin-like substance
by the tumor. In one patient hepatocellular carcinoma
was associated with an increase in serum alpha feta
protein, a globulin normally produced by fetal liver
cells. However, it is not proven that this protein is a con
sistent indicator of hepatocellular carcinoma in horses.
The liver is frequently involved with metastatic
lesions from primary tumors arising from other sites.
These tumors include lymphosarcoma, mammary carci
noma, bronchogenic carcinoma, squamous cell carci
noma, granulosa cell tumor, and Sertoli cell tumor. In
most instances these lesions do not result in massive or
generalized liver damage and the only biochemical
indication in some horses may be modest elevation of
liver-derived serum enzyme activities. Most horses do
not manifest clinical or biochemical evidence of liver
failure although depression, anorexia, weight loss, and
edema may be features of an invasive and generalized
neoplastic process. Ultrasonic evaluation of the liver
may provide evidence of focal neoplastic lesions within
the liver parenchyma.
IRON OVERLOAD,
HEMOCHROMATOSIS
Iron is a highly reactive element that plays an essential
role in oxidation-reduction reactions. Iron balance is
largely regulated by intestinal absorption as there is no
mechanism for excretion of excessive iron stores.
Newborn foals given an oral intestinal inoculum con
taining ferrous fumarate during the first day or to of
life developed acute liver failure due to iron overload.
This was probably associated with an inability of the
newborn animal to effectively regulate intestinal
absorption of iron. Additionally, newborn foals nor
mally have high serum iron and high per cent transfer
rin saturation at birth, rendering them less able to
deal with a sudden massive iron intake. Clinical signs
developed within a few days with rapid progression of
anorexia, depression, icterus, collapse, and death.
Liver lesions included massive necrosis, bile ductule
proliferation, inflammatory infi ltrate, and bile stasis.
Deficiencies of vitamin E and selenium may play a
permissive role in the tissue damage of iron toxicity.
Vitamin E and selenium are thought to exert protective
effects due to their anti-oxidant properties. Acute iron
overload with liver damage has also been reported in a
few adult horses given iron supplements orally.
393
1 9 CHRONI C WEI GHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DI SEASE
Iron overload or hemochromatosis associated with
chronic hepatic cirrhosis has been reported in adult
horses. Clinical signs in these horses included depres
sion, anorexia, weight loss, icterus, ventral edema,
and terminal hepatic encephalopathy. Liver-derived
enzyme activities and serum bilirubin were increased.
Histologic lesions included disruption of hepatic archi
tecture, bridging fbrosis, and bile duct hyperplasia.
Iron accumulation was noted within hepatocytes,
macrophages, and Kupffer's cells as indicated by
Prussian blue staining. Liver iron concentrations, mea
sured in two horses, were very high (6700 and 18 437
ppm wet weight ), some 20-1 00 times that found in the
liver of control horses. Iron accumulation was not
noted in other tissues in these horses. Serum iron was
high in one of these horses and within the normal
range in the other. Interestingly, none of the reported
horses with confrmed hemochromatosis had a dietary
history suggestive of excessive iron intake, and only one
horse had been fed a vitamin and mineral supplement
that contained iron.
This condition in horses has some similarities with
familial idiopathic hemochromatosis, an inherited dis
order of humans, in which excessive intestinal absorp
tion of iron leads to hepatic cirrhosis associated with
iron accumulation in the liver and other tissues. This
disorder of humans is associated with high serum iron
and nearly complete saturation of transferrin. The few
published reports in horses suggest a sporadic occur
rence although multiple cases of liver failure in horses
with high serum iron may occur on given properties.
There is at present no evidence that the disorder in
horses is inherited. Since excessive dietary iron has not
been a consistent feature in these horses, it has been
suggested that for unknown reasons excessive intestinal
iron absorption occurs with resultant accumulation of
iron in the liver. We have noted high serum iron in
some horses with chronic liver failure, although a causal
relationship to liver damage could not be established. It
is possible that the accumulation of iron in the liver is
the result of liver failure, and may not be the cause of
liver failure. Secondary iron overload occurs in humans
with alcoholic cirrhosis.
RIGHT HEPATIC LOBE ATROPHY
Atrophy of the right hepatic lobe is a rare and often
unnoticed condition of horses. The condition has been
reported in adult horses with colic due to major
gastrointestinal abnormalities, and is also an incidental
fnding at necropsy. Although the pathophysiology of
this condition is unresolved it has been suggested that
this condition may result from compression of the liver
394
associated with chronic distention of the right dorsal
colon. High grain, low fber diets may contribute to this
condition.
Hyperl i pem ia
T Mai r
INTRODUCTION
Hyperlipemia is a disorder of lipid metabolism charac
terized by hypertriglyceridemia and fatty infltration of
body organs. The disease is most common in ponies,
miniature horses, and donkeys, although it occasionally
affects larger horses. The condition is usually precipi
tated by periods of anorexia, malnutrition, stress, and
other diseases, and occurs most commonly in the winter
months. The clinical signs are often vague initially, but
the condition progresses rapidly and is frequently fatal
unless early and aggressive therapy is instituted.
EPIDEMIOLOGY
Hyperlipemia is most commonly seen in small pony
breeds, such as Shetland ponies and Welsh Mountain
ponies, and in donkeys. Two retrospective studies from
equine referral hospitals in the USA reported an
incidence of hyperlipemia of 1 1 per cent in miniature
ponies and 1 8 per cent in donkeys presented to these
hospitals. The condition is relatively rare in larger horse
breeds, but is occasionally identifed in horses affected
by other diseases including renal disease, lympho
sarcoma and pituitary adenoma (Cushing's disease or
hyperadrenocorticism) .
The incidence of hyperlipemia is higher in mares
than in stallions and geldings. This predisposition is
partly explained by the fact that hyperlipemia is com
mon in pregnant and lactating mares. However, there
also appears to be an inherently higher risk in females
that is independent of the reproductive status.
Hyperlipemia can be seen in horses and donkeys of
all ages, although it is uncommon in animals less than
18 months of age, with older animals being at greater
risk (possibly due to an age-related decrease in insulin
sensitivity). It is occasionally diagnosed in ill foals and
has been seen as a congenital condition in foals born to
hyperlipemic dams.
Hyperlipemia is often seen as a complication of
other diseases, especially gastrointestinal diseases.
Some of the more common diseases identifed in asso-
Intesti nal parasitism
Colitis
Colonic i mpaction
Gastric i mpaction
Dysphagia and dental disorders
Esophageal obstruction
Esophageal ulceration
Lymphosarcoma.
Hyperadrenocorticism (Cushing's disease)
Peritonitis
Metritis
Laminitis
Renal fai l ure
Liver di sease
Septicemia
Hypocalcemic tetany
Post-injection abscess
Sub-solar abscess
C1atlon with hyperlipemia are summarized in Table
1 9.2. Many of these diseases are thought to predispose
to hyperlipemia by causing inappetence or anorexia. In
addition to disease, hyperlipemia may be induced by
periods of enforced malnutrition, such as inadequate
availability of pasture or competition for food. Pregnant
mares, especially in the last trimester, and lactating
mares have increased nutritional requirements and are,
therefore, at greater risk of developing hyperlipemia.
Obesity and stress are other important risk factors for
the development of the disease. Stress factors that have
been implicated include transportation, change of
environment or diet, inclement weather, and the
stress of pregnancy, lactation, and disease.
PATHOGENESIS
Hyperlipemia represents an excessively rapid mobiliza
tion of the body's fat reserves (Figure 19. 2) in response
to stress or failure to maintain energy homeostasis. In
response to negative energy balance and after depletion
of glycogen reserves, non-esterifed fatty acid (NEFAs)
Figure 1 9.2 Schematic representation of the metabolic
fate of non-esterified fatty acids mobi l i zed from adi pose
tissue (NEFA = non-esterified fatty acids; TG = triglycerides;
VLDL = very low density l i poproteins; LPL = l i poprotein
l i pase) (adapted from Watson 1 998)
are mobilized from fat stores and released into the cir
culation (Figure 19. 2). The majority of NEFAs are taken
up by the liver where they may overhelm the oxidative,
gluconeogenic, and ketogenic pathways and are esteri
fed to form triglycerides. Triglycerides then accumu
late in the liver and are exported in the circulation in
the form of very low density lipoproteins (VLDLs)
(Figure 19.3). This process occurs at such a fast rate that
the VLDLs cannot be utilized by peripheral tissues, and
plasma levels become excessive. VLDLs are also taken
up by cells of the reticuloendothelial system resulting in
fatty infltration of many organs.
Adipose tissues represent energy stores that form as
a result of esterifcation of free fatty acids to produce
triglyceride. This esterifcation is promoted by the
action of insulin and glucose. In the presence of nega
tive energy balance, lipolysis takes place in adipose tis
sues, mediated by glucagon which activates the enzyme
hormone sensitive lipase (HSL) . HSL is normally inhib
ited by insulin and glucose, but with reduced insulin
and glucose levels (which occur in negative energy bal
ance), and enhanced glucagon activity HSL is activated.
HSL can also be activated by hormones released in
response to stress (such as adrenocorticotrophic hor
mone - ACTH, glucocorticoids, and catecholamines)
and by hormones released in pregnancy and lactation
(progesterone and growth hormone) .
The lipolysis induced by HSL results in the release of
NEFAs into the circulation. NEFAs may be used by
tissues for oxidation as a source of energy. However,
most NEF As are taken up by the liver where they can be
used for ketogenesis or gluconeogenesis, or they are
395
1 9 CHRONIC WEI GHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
Adi pose tissue
Plasma NE FA transport to the liver
Normal ponies 8.2 S.2 mmol/h
Hyperl i pemic ponies 148.2 8.4 mmollh
Normal ponies
Figure 1 9.3 Schematic representation
of non-esterified fatty acid (NEFA) and
very l ow density l i poprotein (VLDL)
metabol ism i n ponies with hyper
lipemia. Ki netic data are shown for
NEFA transport to the liver, hepatic
VLDL-triglyceride (TG) synthesis, and
VLDL-triglyceride fractional catabolic
rate i n normal and hyperlipemic ponies
(adapted from Watson 1 998)
6.6 4.4 mmol/h
Hyperl i pemi c ponies
1 90. 6 3.9 mmollh
esterifed to form triglycerides. The horse has a poor
capacit for ketogenesis, and most NEFAs are used to
produce triglycerides. These triglycerides are exported
from the liver in the form of VLDLs that can be utilized
as a source of energy in peripheral tissues or re-stored
in adipose tissue. In the presence of food deprivation,
plasma VLDL levels rise excessively and triglycerides
accumulate in the liver.
The clearance of VLDL triglycerides from the circu
lation is promoted by lipoprotein lipase (LPL), and it
has been suggested that raised plasma triglyceride levels
in hyperlipemia may be caused by reduced clearance of
VLDLs due to inhibition of the action of LPL. LPL
activity may be inhibited by azotemia and endotoxemia.
However, studies of ponies with hyperlipemia suggest
that the activit of LPL is increased rather than
reduced.
Insulin resistance probably plays an important role
in the pathogenesis of hyperlipemia. Tissue resistance
to insulin results in a diminished ability to regulate
HSL. Thus, when the enzyme is activated in response to
a negative energy balance, or as a result of stress or
concurrent disease, lipolysis progresses in an excessive,
uncontrolled way. NEFAs are released in excessive
amounts that overwhelm the liver's oxidative, gluco
neogenic, and ketogenic capacity, such that triglyc
erides are produced resulting in hypertriglyceridemia
and hyperlipemia. Insulin resistance is common in
ponies and donkeys, and is exacerbated by obesit and
pregnancy/lactation.
396
CLINICAL SIGNS
Clinical signs of hyperlipemia will be compounded by
the signs relating to the underlying disease or cause,
such as diarrhea or dysphagia. In addition, fatt infltra
tion of the liver and kidneys may produce signs of
hepatic and renal failure. The initial signs of hyper
lipemia are often vague and include anorexia, lethargy,
and weakness (Table 19. 3) . Rapid progression of the
disease is common, with the development of ataxia,
muscle fasciculations, head pressing, profound depres
sion, recumbency, convulsions, coma, and death.
Sudden death occasionally occurs as a result of hepatic
rupture. Dysphagia is obsered in some cases, and may
result from encephalopathy or myopathy involving the
muscles of mastication; alternatively dysphagia may be
caused by an underlying primary esophageal disease
such as choke. Pregnant mares may abort sponta
neously or undergo premature labor.
Some animals demonstrate a period of rapid weight
loss and development of ventral edema at the onset of
the disease. This may reflect the primary underlying dis
ease or may develop as a consequence of subcutaneous
thrombosis caused by the hyperlipemia. Edema might
also develop as a result of rapid fatty infltration of the
liver, partial obstruction of the portal circulation, and
increased hydrostatic pressure in subcutaneous abdom
inal veins. Likewise, mild intermittent abdominal pain
(restlessness, flank watching, and rolling) may be caused
by a primary gastrointestinal disease, or may occur as a
Anorexia
Lethargy
Weakness
Ataxia
Muscle fasciculations
Dysphagia
Sham drinking
Profound depression
Head pressing
Circling
Reumbency
Seizures
Nysagmus
Weight IOS5
Ventral edema
Ascites
Abdomi nal pain
Reduced intesti nal motil ity and fecal output
Pyrexi a
Tachycardia
Tachypnea
Congested mucous membranes
Icterus
Halitosis
Aborion
Sudden death
result of hepatomegaly and stretching of the liver
capsule. Intestinal motility and fecal output are often
reduced, and this may predispose to colonic impaction.
The clinical course of hyperlipemia is rapid in most
cases. The average interal between the onset of clinical
signs and death or euthanasia is 6- 10 days. In a few
cases a more protracted clinical course may occur.
DIAGNOSIS
Plasma triglycerides
Gross lipemia in blood samples centrifuged or left to
stand is the simplest way to diagnose hyperlipemia in
practice (Plate 19. 2) . However, this is a relatively insen-
HEPATIC AND BILIARY TRACT DISEASES 19
sitive method of diagnosis, especially in animals
with mild degrees of hyperlipemia and animals with
hyperlipidemia (see below) . Accurate measurements of
plasma triglyceride levels are recommended to assess
the degree of hyperlipemia and to monitor the course
of the disease during treatment.
Plasma triglyceride levels of greater than 5 mmol/l
(500 mg/ml) in ponies with clinical signs of hyper
lipemia are diagnostic. Triglyceride concentrations of
1-5 mmol/l ( l 00-500 mg/ml) can be present in ponies
without clinical or pathological evidence of hyper
lipemia; this has been classifed as hyperlipidemia, and
may sometimes progress to hyperlipemia if adequate
nutritional support is not provided. However, triglyc
eride levels in this range can sometimes be present in
clinically normal pony mares during pregnancy.
Normal plasma triglyceride levels in donkeys are
higher than in ponies. Healthy, non-pregnant donkeys
may have levels as high as 3. 5 mmol/l (350 mg/ml).
Triglyceride levels in suckling foals are also higher than
in adults because of the relatively high daily fat intake.
Plasma concentrations of other lipids, such as chol
esterol, phospholipids, and NEFAs, are also raised in
hyperlipemia. However, increases in concentrations of
these lipids are not as great as triglycerides, and they are
not routinely assessed for diagnosis. Identifcation of
fatty infltration of liver biopsies is diagnostic but has
no advantage over simple measurement of plasma
triglycerides.
Clinical chemistry
Monitoring of serum or plasma biochemistry panels can
help to
detect the presence and severity of organ failure in
hyperlipemia
determine appropriate supportive therapies
monitor the course of treatment, and
detect underlying primary conditions.
Table 19. 4 lists an appropriate chemistry panel for
this purpose.
Biochemical measurements of some substances may
be complicated due to interference by high triglyceride
levels. This can be overcome by clearing the plasma or
serum of lipids prior to analysis by ultracentrifugation
or chemical precipitation.
Blood glucose concentrations may be normal, low,
or elevated, depending on the duration of anorexia,
previous glucose therapy, and the presence or absence
of Cushing's disease. Metabolic acidosis is often
present, as shown by decreased arterial pH, decreased
PC02, decreased bicarbonate levels, and a base defcit
of 0-24 mEq/1.
397
1 9 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
T _ ". IIs In' f Invttnv
anmn hylpli In lUi (
Wtn 1_
Metabolic status

triglycerides

glucose

hydration status- albumin
PC
electrolytes - No
K
".
Ca2
add-base status - pH
HCO)-
peol
Livr damage and function
gamma glutamyl transferase (GGn

alkaline phosphatase (AP)

bile acids

ammonia
Rena! function
ammonia
urea nitrogen
creatinine
Fan)' inlHtration of the liver result. in elevations of
liverderived emymes, including GGT, AP, LDH, and
SDH. Liver funelion may be impaired, as asscs.ed by
elevations of bilirubin, hile acids, and ammonia. Fatty
infltration of the kidneys can result in impaired renal
li.mction, and elevation of plasma concentrations of
urea and creatinine. These metabolites may also he
increased as a result of dehydration, and reassessment
following rehydration is required to a'sess the degree of
renal failure.
P!a.ma albumin concentrations may be normal, or
e1evated (associated with dehydration), or reduced
(associated with chronic hepatopathy, a primary
gastrointestinal lesion, or parasitism). Serum protein
electrophoresis can he helpful in as.'iessing underlyng
conditions such as intestinal parasitism.
PATHOLOGY
T}ica! pathological findings in ponies and donkeys
am'eled hy hyperlipemia include faty infiltration of the
tissues, espedaJIy the liver and kidneys (Plate 19.3). The
liver and kidneys are enlarged, yellow, friable, and
greasy. In severe cases, the surface of the liver may be
398
fissured, or there may be capsular rupture and associ
ated hemorrhage. Fatt infltration of other organs
including adrenals, skeletal muscle, and myocardium
may be evident. Necrotizing pancreatitis is present in
some cases (see Chapter 17). Vascular thrombosis can
occur secondary to hyperlipemia and fat embolism, and
can result in focal hemorrhages, myocardial infarction,
and renal infarction.
TREATMENT
The treatment of hyperlipemia has nve different objec
tives
1. treatment of underlying or concurrent disease
2. correction of dehydration, electrolyte and
acid/bae imbalances
3. symptomatic therapies
4. nutritional support
5. normalization of lipid metabolism
Treatment of underlying or concurrent
disease
Intestinal parasitism is a common cause of hyperlip
emia in ponies and donkeys, therefore appropriate
anthelmintic therapy is required in all cases "'th con
firmed parasitic burdens, and should be administered
to all other cases where no obvious cause of the hyper
lipemia is identified. Other treatments for underlying
diseases should he administered as appropriate, such as
pergolide therapy for Cushing's disease.
Correction of dehydration, electrolyte, and
acid-base disturbances
Correction of dehydration, electrolyte and acid-base
abnormalities is essential. Intravenous fluid and c1ectf(}
lyte therapy is generally required, the principles of
which are discussed in Chapter 9. Correction of severe
acidosis in the presence of liver failure may require the
administration of intravenous bicarbonate. Blood gas
analysis should be used when available to monitor the
response to bicarhonate therapy, since too rapid an
increase in blood pH may exacerbate signs of hepatic
encephalopathy, and overdosing of bicarbonate can
lead to persistent metabolic alkalosis and respiratory
depression.
Dextrose should be added to the intravenous
polyionic fluids or <ldministered as 5% dextrose solu
tions in animals with hypoglycemia. "hen 5% dextrose
solutions are being administered, monitoring of serum
electrolytes should be undertaken, and potassium chlo
ride or calcium g!uconate administered as necessa!).
Care must be taken to avoid overdosing with dextrose,
since this can result in transient or prolonged periods
of hyperglycemia with associated diuresis, dehydration,
and hyponatremia.
Symptomatic therapies
Symptomatic therapies include the use of analgesia,
non-steroidal anti-inflammatory drugs, and anti-ulcer
treatments. These are used as necessary on an individ
ual basis. Therapies for hepatic encephalopathy (see
above) may also be beneficial. Plasma transfusions have
been used in hyperlipemic patients with hypoprotein
emia, en do toxemia, and in foals with failure of passive
transfer of immunity.
Nutritional support
Nutritional support is an essential component of
therapy of hyperlipemia in all cases. Mfected animals
should be maintained in positive energy balance in
order to limit the mobilization of NEFAs from adipose
tissues.
In animals that are still eating, fresh and highly palat
able foods, such as grass, leaf hay, rolled grains, and
high energy feeds with added molasses, should be fed.
In animals that are inappetent or anorexic, enteral
feeding via a nasogastric tube should be undertaken.
Even in animals that are still eating voluntarily, supple
mentation by enteral feeding should be considered
if the plasma triglyceride levels exceed 5 mmol/l
(500 mg/ml). Glucose and electrolyte solutions, com
mercial enteral formulations, and slurries made from
hay or pelleted feeds can all be administered by naso
gastric tube.
Glucose in the form of dextrose can be administered
Parameter Day
1 2
Water (I) 8 8
Dextrose (g) 1 20 1 60
Casein or dehydrated cottage
cheese (g) 1 20 120
Dehydrated lucerne meal (g) 600 600
Electrolyte and vitamin
mixture (9) 80 80
orally at a dose of approximately 1 00 g once or twice a
day for miniature horses and small ponies. Plasma glu
cose levels should be monitored on a daily basis during
the period of treatment. Excessive glucose administra
tion might exacerbate lactic acidosis: to reduce this risk
it has been suggested that 1 00 g of galactose is substi
tuted for the glucose on alternate days, galactose is
slowly converted to glucose thus minimizing the pro
duction of lactic acid.
Nutritionally complete formulations are preferred
to simple glucose solutions for enteral administration.
Commercially available formulations for use in horses
can be used, or recipes of formulations incorporating
water, dextrose, casein or dehydrated cottage cheese,
dehydrated grass meal, and electrolyte/mineral mix
tures can be used (Table 19.5) . Commercial enteral for
mulations for use in humans have also been successfully
used in ponies and donkeys with hyperlipemia.
The daily ration of enteral feeding should be calcu
lated and divided into 4-1 2 small feeds so that the total
volume of each feed should not exceed 3 liters for
miniature horses, 5 liters for small ponies and 7 liters
for larger ponies and horses. The daily basal require
ment for digestible energy (DE) input can be calculated
from the following formula
DE (Mcal/day) = 0.975 + 0.021 x body weight in kg
The daily DE requirement may be multiplied by a
'stress factor' of 1 . 2-2.0 to compensate for the
increased metabolic rate associated with stress and hos
pitalization. One suggested protocol for enteral feeding
of hyperlipemic ponies based on calculation of basal
and 'stress-adjusted' DE requirements is as follows
day 1
day 2
3 4
8 8
200 240
1 80 240
600 700
80 80
75% of basal DE requirement
1 00% of basal DE requirement
5 6 7
8 8 8
320 320 360
240 300 360
700 800 800
80 80 80
399
day 3
day 4 and
subsequent days
75% of 'stress-adjusted' DE
requirement
1 00% of 'stress-acusted' DE
requirement.
This procedure of increasing the plane of nutrition
allows the gastrointestinal tract to become tolerant to
the regime.
In afected animals with compromised gastrointesti
nal function, such as ileus and diarrhea, intravenous
nutrition is required. In most cases, the constant intra
venous administration of 5% dextrose at 1-2 ml kg-I hrl
is used. Although this will not fully meet the animal's
total nutritional requirements, it has proved effective in
clinical caes. Overdosing with glucose must be avoided
since it can result in diuresis, dehydration, hypona
tremia, and enhancement of hepatic lipidosis. Amino
acid solutions can also be administered intravenously,
but this significantly increases the cost of treatment.
Plasma glucose levels should be monitored regularly,
and electrolytes added as necessary. Human parenteral
nutrition formulations can also be used, but these
preparations are expensive and careful monitoring is
required.
Anabolic steroids and multivitamin preparations are
commonly administered to hyperlipemic patients to
assist hepatic function. Corticosteroids should be
avoided since they stimulate HSL and may induce
laminitis.
The induction of abortion or premature foaling in
pregnant mares has been recommended, since this
significantly reduces the demands for energy. However,
prematurely delivered foals have a high mortality rate
because of the immaturity of body systems and suscepti
bility to infectious disease. There is also a risk of
retained placenta and laminitis in the mare. Lactating
mares that develop hyperlipemia should have their
foals weaned if possible.
Normalization of lipid metabolism
Two approaches to modifing lipid metabolism in
hyperlipemic patients are possible
1. reducing the net release of NEFAs from adipose
tissues
2. accelerating the removal of triglycerides from
plasma VLDLs to adipose tissues and skeletal
muscle.
The release of NEFAs from adipose tissue is promoted
by the action of HSL. Reducing the stimulus for lipoly
sis may be achieved by
providing a positive energy balance
removing stress factors
400
removing the hormonal influences of pregnancy
and lactation.
The activit of HSL is inhibited by the action of insulin,
and thus exogenous insulin therapy has been recom
mended in the treatment of hyperlipemia. Protamine
zinc insulin has been used most frequently, at dosages
of 30-80 IU ( 0. 1-0.3 IU/kg) by intramuscular injection
once or twice a day. Insulin in combination with glucose
and galactose administration also promote the re-ster
ifcation of NEFAs. The efcacy of insulin therapy has
been questioned in view of the fact that most hyper
lipemic ponies and donkeys are insulin resistant: how
ever, this treatment is unlikely to be harmful so long as
the patient are normoglycemic and are receiving oral
or intravenous glucose. The following regimen has
been suggested for treatment of a 200 kg pony
day 1
day 2
day 3
day 4
30 IU protamine zinc insulin i.m. and
1 00 g glucose p.o., both b.i.d.
1 5 IU protamine zinc insulin i.m. b.i.d.
and 1 00 g galactose p.o. s.i.d.
as for day 1
as for day 2.
Stimulation of LPL in order to increase the clearance
of triglycerides from the plasma has been attempted
by means of heparin therapy; 100-200 IU /kg of
heparin may be administered intravenously twice a
day. However, the rationale for this therapy has been
questioned because the activity of LPL in affected
ponies has been shown to be at it physiological maxi
mum. There is also a risk of hemorrhage with heparin
therapy.
PROGNOSIS
The prognosis for animals with hyperlipemia is poor.
The reported mortality rate for the disease (including
animals that are euthanased) ranges from 57-85 per
cent. In individual patient, the nature and severity of
the underlying disease has an important impact on the
prognosis. The degree of measured lipemia does not
appear to influence the prognosis, although animals
with hyperlipidemia (triglycerides < 5 mmol/l) have a
much better prognosis than those with hyperlipemia
(triglycerides > 5 mmol/l).
Plasma triglycerides and blood biochemistry (see
above) should be monitored during treatment, and
these results can be helpful in assessing the prognosis.
In animals that recover, plasma triglycerides usually
return to normal values within 310 days. Early diagno
sis and prompt initiation of therapy result in the best
chances for survival.
PREVENTON
:: =:. :. _--" ..__ .. _. - ,.
Risk factors for hyerlipemia in susceptible classes of
equids include
obesity
stress
malnutrition
pregnancy and lactation
parasitism
Avoiding these factors will therefore help in prevent
ing this diseae. Particular emphasis should be placed
on providing adequate nutrition to susceptible
animals without allowing them to become obese, and
providing good routine parasite control measures.
Food intake and general demeanor should be care
fully monitored following periods of enforced stress
such as disease, transportation, inclement weather,
change of environment, etc. Exercise regimes may be
helpful in reducing insulin insensitivity. Plasma triglyc
eride levels may abo be measured at times of stress
and during pregnancy and lactation. The early identi
fcation and treatment of hyperiipt'mia is far more
likely to result in recovery than identification laler in
the course of the disease.
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JohnstonJ K, Divers T.l, Reef V B, Acland H (1919)
Cholelithiasis in horses: Ten cases (1982-1986) J. Am. Vl.
AId. A.I.mr. 194:40;-9.
Ram .,,,,,, t W (1990) J)i'ea. '''.' of the li\"" .
.
. FI. in. N. Am.
f:uinFPrdo 2:105-1 14.
R"dV B,Johnston] K Divers T.l, Acland H (1990)
Cltrasonographic filldings in horses with cholelithiasis:
Eight (as("s (1985-191l7)
.
f Am. ltl. Med. Assoc.
196: IH36-1I.
Schneider [) A (l!N7) Choiestasis and biliary calculi in
horse<. (;omj" Coni. Fdllf P,.,ul. Vt. 19(f):744-il3.
Pyrrolizidine alkaloid intoxication, Chronic
active hepatitis, Chronic liver disease
Barton M H, :\orris, D D (199il) Diseases ofth" l.iver. In
F.quinliIntl'7{1[A1dirinf, S M R"ed and W M gayly (cds).
W B Saund"rs, l'hila(klphia, PI" 707-3H.
Carlson (; P (1992) Icterus in the Horse. In lelmllal)
G(lrlato,y (2nd "dn), : V Anderson, (cd.). Lea &
Febigcr: Philadelphia, pp. fiHH-702.
Corick] L, Carln G K, Bridges C H ( 1 9RR) Kkin gra,",.
a"ociated hepatotoxicosis in horst'S
.
j /"m. \'I. Md. A'.loc.
193:932-5.
]akov.-;ki R M (1994) Right l
"
'pati(" lobe mrophy ill hores: 17
cases (1 9R:-1993) J Am. 1',1. l\1ni. A.Wf. 204,]()?7-61 .
Lavoie] 1', T""ser",, E (1993) ),1;,,,i,,e iron overload and liver
fibrosis n'",,"biing haerno<hrolllatosis in a racing POllY.
!quiw lel.j. 2:552-4.
I.cS<ard P, Wilson W D, Olander H.l, Rogers Q R, 1endel V E
(19Hf) ClinicopaThologic study of horses slIn'iving
pyrrolizidilW alkaloid (Smri( vulgaris) toxicosi<. Am. j. Iftl.
Rn 17:1776-80.
Mendel V E, Wilt l R, Gilchdl B S, I (II. ( 19HIl) Pvrroliljdinl'
alkaloid-induced liver disasc in hors,'s: an "arly diagnosis.
Am.I \,1. Re'. 49:572-.
Mullaney T P, Bwwn C M (19H!I) Iron toxicity in "eonatal
foals. Equin' V,I.
.
f 20:1 1 9-21.
Pearson E G, Hed
.
"nlm 0 R. l'op[wngd R H (1991) llel'''';'
cirrhosis and h"mochromatosis ill three horses. J . Am. VI.
Med. AmY., 201,1053-.
Hyperlipemia
BurkholderWj, Thatcher. c: D (1992) Emera! nutritiollal
support of sick horses. In Curr e! 7'tjl' in fquint
Mfdici7lt (3rd edn), l E Rohinson (cd.) \-\' B Saunders,
Philadelphia, PI" 727-31
Golenz 1 R. Knight D A, Ymrdlk St] (1992) l'se of a
human en[('ral r"eding preparatioll for treatment "r
hyperlipemia and nutriti"nal support during h"aling of an
oesophageal lacera!.ion in a miniature hor'l" j. Am. ltl.
Md. A",, 200:951-3.
Harris P A, Frape D L,Jdlcolt l B. l.lIe,"s D M, Meyer H,
Savage C] (199.) ;utritional aspt'cL of metabolic
diseases. Hyp"rlipaemia. In T"Equillt Manual. AJ
Higgins and 1 M \'right ("ds) \ B Saunder<. l.ondon,
pp. 181-3.
Jefcott L B. Field] R (1985) Epidemiologkal apcct" of
hyperlipaemia in poni"s ill southeaster Amtralia. Amlr.
llel. J. 62:110-1.
Mogg T D, Palmer,,) E (1995) Ilyperlipidemia, hyplTlipemia.
and hepatic lipidosi, in American miniature hors"" 23
cast'. (Hl90-1991).j. Am. le. J\fd. AlSll{. 207:(i01-7.
401
Moore B R, Abood S K, HinchcliffK W ( 1 994) Hyperlipaemia
in 9 miniature horses and miniature donkeys. ) Vet. Inte.
Med. 8: 376-81 .
Naylor j M, Kronfeld D S, Acland H ( 1980) Hyperlipemia in
horses: effects of undernutrition and disease. Am. ). Vet.
Res. 41 :899-905.
Reid S W j, Mohammed H 0 ( 1996) Survival analysis
approach to risk factors associated with hyperlipaemia in
donkeys. ] Am. Vet. Med. Assoc. 209:1449-52.
Watson T D G ( 1998) Equine hyperlipaemia. In Metabolic and
402
Endocrne Poblems ofthe Hose, T Watson (ed. ) . W B
Saunders, London pp 23-40.
Watson T D G, Love S ( 1994) Equine hyperlipaemia. Compo
Cont. Educ. Pact. Vet. 1 6: 89-97.
Watson T D G, Murphy D, Love S ( 1992) Equine
hyperlipaemia in the United Kingdom. Clinical features
and blood biochemistry of 1 8 cases. Vet. Rec. 1 31 : 48-51 .
Wensing T H, Schotman Aj, Kronemanj ( 1974) Effect of
treatment with glucose, galactose, and insulin in
hyperlipemia in ponies. Tijdschr. Dierfeneesk 99:919.
20
PCUI0 0BffD0B
General principles of
treatment of acute diarrhea
in adult horses
WWWWWWWWWWW
TJ Divcrs
The most important treatment for horses with severe
diarrhea is to give intravenous fluids to correct extracel
lular fluid deficits (especially intravascular volume
defcits) , and any electrolyte and acid-base abnormali
ties. A balanced polyionic crystalloid, with or without
hypertonic saline, is the preferred intravenous fluid.
Hypertonic saline may be used if there is extremely
poor perfusion and shock is apparent, but this must be
followed by appropriate and generally large volumes of
polyionic crystalloids. The long-term use of sodium
chloride will result in acidosis. Once the patient is seen
to urinate, potassium should be added (20-40 mEq/l)
to the crystalloids. Potassium should be used in all cases
unless there is oliguric renal failure, the horse has the
hyperkalemic periodic paralysis (HYPP) gene, or the
serum potassium is abnormally high. Athough the
amount of potassium lost in diarrhea is not as great as
sodium, anorexia and continual loss of potassium in
urine generally cause a severe total body potassium
deficit.
The rate of fluid administration depends upon the
severity of dehydration. Clinically this can be crudely
determined by examining
dryness of mucous membranes
skin turgor
speed of distension of the jugular vein when
compressed.
Packed cell volume (PCV) and degree of azotemia
provide laboratory evidence of the degree of dehydra
tion, although PCV is quite variable, and blood urea
nitrogen (BUN) and creatinine can be affected by
intrinsic renal factors in addition to pre-renal infu
ences (dehydration) . Fluid replacement should include
volume replacement (per cent dehydration ? body
weight in kg = liters needed)
maintenance needs (60-100 ml kg-I day-I
)
ongoing losses, these are variable depending upon
the degree of dehydration.
The initial volume deficit should ideally be replaced
within 6-12 hours or less, depending on cardiopul
monary status, evidence of edema formation, plasma
protein concentration remaining greater than 4. 5 gl dl
(45 gil) , and urine output. If urination is oliguric and
there is minimal or no decline in the degree of
azotemia in spite of rapid fluid therapy for several
hours, intrinsic renal failure should be considered.
If colloids are also being administered, fluid deficits
can be replaced much faster. Because of the loss ofalbu
min and decreased oncotic pressure in most horses with
acute colitis, it becomes increasingly difcult to main
tain the crystalloid fluids in the intravenous space, thus
promoting organ dysfunction (e.g. kidney, lung,
.
nd
heart) and edema in all interstitial spaces, both vlSlble
and occult, including the colon and feet. Therefore,
treatment with a colloid fluid such as plasma or het
astarch is generally indicated if economics permit. The
amount administered is generally controlled by eco
nomics, but 2-1 0 liters of plasma or 1 0 ml/kg het
astarch are generally used as the initial treatment.
Supplemental calcium should be added ( 1 1 g cal
cium borogluconate per 500 kg horse) to 5 liters fluids
4b
20 ACUTE AND CHRONIC DIARRHEA
if there are obvious signs of hypocalcemia, e. g.
diaphragmatic flutter. If the ionized calcium is low
( l.2 mmol/I) but there are no clinical signs, the same
amount of calcium borogluconate can be added to 20
liters of crystalloid fluids. Repeated calcium treatment
should be performed only when the ionized calcium
remains low.
In cold weather, fluids should be given at nearly
body temperature. They are ideally administered
through an over-the-wire polyurethane catheter since
horses with colitis have the highest rate of jugular
thrombosis of any equine patient.
Oral fluids should be provided free choice unless the
patient is colicky and has gastric reflux after passage of
a nasogastric tube. These fluids should include both
clean freely available water, and water with electrolytes.
Electrolyte supplements containing sodium chloride
(30 g), sodium bicarbonate ( 1 2 g) , dextrose (20 g) , and
potassium chloride (5 g) per gallon of water is a fre
quently used mixture that is only slightly hypertonic.
Glutamine could be added to the fluid mixture since it
is thought to support enterocyte function, and decrease
endotoxin absorption and bacterial translocation. This
would considerably affect cost, and the benefts are
unproven in equine colitis. If the patient has a meta
bolic acidosis and normal anion gap, the amount of
chloride in the solution should be decreased by substi
tuting potassium bicarbonate (5-10 g) for 5-10 g of the
sodium chloride.
ML bMYMMWMU
MMVbMUb fLUb
Some horses with mild diarrhea can be adequately rehy
drated using oral fluids. If there is no gastric reflux, flu
ids can be given via an indwelling 'capped' nasogastric
tube. A 500 kg horse may be given 4 liters of a solution
(l5g sodium chloride, 5 g sodium bicarbonate, 4 g dex
trose, 10 g potassium bicarbonate, and 1 0 g potassium
chloride) every 30 minutes so long as signs of abdomi
nal pain are absent. Larger volumes may result in
abdominal pain and too rapid transit time. Higher
concentrations of sodium chloride may cause metabolic
acidosis.
Treatment to help negate the effects of
endotoxin/ cytokine/systemic inflammatory response
should be routinely provided for all colitis cases. This
would include flunixin meglumine (0. 3 mg/kg q. 8 h) ,
and plasma with antibody against core lipopolysaccha
ride. Polymyxin B in combination with dextran 70 is
sometimes used in the hope of binding endotoxin.
4b
Over the years, a variety of drugs have been used to
try to 'slow
'
the intestines or promote development of a
more formed stool. Loperamide (0.04l.6 mg/kg p. o. )
may be used in non-infectious diarrheal conditions. Its
primary beneft could be an antisecretory effect.
Phenoxybenzamine has an antisecretory effect but
should not be used because of its hypotensive effect.
Bismuth subsalicylate (up to 4 1/500 kg q. 12 h) may
have antidiarrheal, antibacterial, and anti-inflammatory
properties but historically has had little effect on severe
infectious diarrhea in the adult horse, other than mak
ing the feces block. It is often effective in treating non
infectious diarrhea in adult horses and some infectious
diarrheal conditions in foals. Kaolin and pectin should
not be used in severe diarrhea as they may worsen mal
absorption and increase ion loss during diarrhea.
Activated charcoal has been used (0. 5 kg/500 kg) in
acute equine colitis. Early treatment may decrease
intestinal endotoxin absorption while other therapies
are being employed. Recently, a compound containing
naturally occurring macro-and micro-minerals was
reported to prevent many ofthe clinical fndings of tox
emia in a lincomycin model of equine colitis. Further
research on this product as a treatment for equine coli
tis is needed before any recommendations can be
made.
The use of products that contain Lactobacillus spp.
are frequently recommended in the treatment of
equine colitis. Although they probably cause no harm
they are also of no proven beneft.
Additional treatment in the hope of preventing
laminitis, an all-too-frequent occurrence in acute diar
rhea, includes nitroglycerin patches applied over the
digital arteries for 1 2 hours each day, for up to 3 days
during the greatest risk period. Support wraps on the
limbs can help prevent leg edema. The tail should be
protected by covering it with a plastic obstetric sleeve
loosely taped with elastic bandage at its base. The per
ineum should be cleaned as needed to prevent contact
dermatitis and/or scalding. Silver sulfadiazine oint
ment should be applied topically if dermatitis develops.
Prevention and/ or early treatment of irritant dermatitis
is especially important in stallions.
Salmonellosis
TJ Divcrs
bFMMLY
Salmonella spp. are gram-negative bacteria that belong
to the Enterobacteriaceae family. Salmonella spp. are
divided into serogroups (A through I) based upon their
common l antigens. All Salmonella spp. are considered
pathogenic, although a few serotypes are responsible
for the majority of serious infections in horses;
Salmonella typhimurum (a serotype in serogroup B)
being the most serious. Other Salmonella spp. reported
to cause mild to serious diarrhea in horses are S. agona
and S. anatum (both group B) , S. newort (group C) and
S. kreeld (group E) . Virulence genes on plasm ids and in
chromosomes are important in the establishment of
infection and disease. Salmonella abortosuis, a cause of
equine abortion often without diarrhea, is found in
Europe but not North America.
A low ( 1 %) percentage of normal horses shed
enough Salmonella spp. in the stool to permit a positive
fecal culture. The percentage of positive cultures is
higher (approximately 5%) if polymerase chain reac
tion (PCR) methods are used. Horses with abdominal
pain have increased shedding (5% via culture and up to
40% via PCR) suggesting Salmonella spp. are common
inhabitants of the gastrointestinal tract, but are gener
ally shed in low numbers in the stool unless there is an
abdominal disorder. Changes in intestinal motility and
volatile fatt acids production by normal flora may
increase the ability of Salmonella spp. to attach to the
intestinal mucosa and to proliferate. The increased
shedding of Salmonella spp. in horses with abdominal
pain does not signifcantly affect mortality, but is un
desirable because of the potential for colitis and
increased environmental shedding.
Salmonella spp. have numerous virulence factors that
enhance their toxicity
adhesion fmbriae that permit attachment to
intestinal epithelial cells
gene products which activate macropinocytosis
cytotoxins that either directly, or indirectly via
cytokines, cause epithelial cell damage
enterotoxins that cause increased secretion of
extracellular fluid and electrolytes into the
intestinal lumen.
Intestinal epithelial cell damage is a result of
cytokine activation, leukocytic enzymes and reactive
oxygen species production. The loss of intestinal bar
rier permits endotoxin absorption which, along with
inflammatory mediators, is responsible for systemic
effect. Intestinal attachment and invasion is thought to
be most common in the distal small intestine, cecum,
and colon, initially via specialized enterocytes called M
cells. Highly virulent Salmonella spp. contain genes
(type III secretory) that promote secretion of virulent
proteins. Salmonella organisms are invasive facultative
anaerobes that survive and multiply within
macrophages in the intestinal lamina propria and
ACUTE DIARRHEA 20
mesenteric lymph nodes. Virulence proteins of
Salmonella spp. may interfere with macrophage activity
allowing the organism to proliferate within
macrophages. Proliferation within the epithelial cells
and/ or intestinal macrophages is necessary for progres
sion to enterocolitis. Bacteremia is believed to be rare
in adult horses but is common in foals. In adult horses,
bacteremia must occasionally occur because hepatic,
renal, and mesenteric lymph node abscesses have been
reported caused by Salmonella spp.
bK fMLb f bMLNMbLLbb
MM bFbNLY
There are at least three major risk factors that deter
mine whether exposed horses have clinical disease.
These include
virulence of the salmonella strain
inoculation dose
host defenses.
Host defenses include both humoral and cell-medi
ated immunit, along with enteric protection facilitated
by normal enteric flora and low gastric pH.
Horses may become infected by several means
including environmental salmonella or Salmonella spp.
shed by birds, rodents, ind other animals, including
contact with other horses. Birds may pose a special risk
since they often congregate around horse feeds where
infected dropping may contaminate the feed.
Risk factors for infection include
any change in intestinal motility
abdominal pain
change in intestinal flora that may occur with
antibiotic administration and anorexia
innate stress factors that may affect the horse's
immune response.
Horses with impaction colic are particularly at risk.
Outbreaks tend to be more common in tertiary-care
hospitals where these factors are common, on brood
mare farms with a high-densit population of mares and
foals, or on farms where horses have been fed feed con
taminated with Salmonella spp. Hot weather, increasing
numbers of horses and foals on a farm, and wet flooring
in barns or hospitals all seem to increase infection rates.
LLMLML bMb MM LMMY
MMbb
The clinical signs are variable (Table 20. 1 ) and include
fever, mild abdominal pain, anorexia, and depression
41
8MeVT |!
8olIo
Adult horses
Foals
Fever
Inappetence or anorexia
Depression
Abdominal pain
Diarrhea - varying from nil to
severe and watery
Small colon impaction
Fever
Depression
Anorexia
Hemorrhagic diarrhea
Pneumonia
Meningitis
Septic arthritisiphysitis
without diarrhea in some horses, but most horses that
are clinically affected have moderate to severe, watery
diarrhea. Foals may develop hemorrhagic diarrhea
(rarely seen in adult horses) , pneumonia, meningitis,
and lameness due to either septic arthritis or physitis.
Small colon impactions in adult horses frequently have
associated salmonellosis.
Most clinically affected horses have neutropenia,
vacuolated neutrophils (toxic changes ) , hypo
chloremia, hyponatremia, elevated PCV, and azotemia.
Acidosis will be present if the anion gap (lactate) is
increased. Hypoproteinemia generally occurs within a
couple of days even in those horses without diarrhea. A
rebound neutrophilia may occur after the initial neu
tropenia. Importantly, coagulation abnormalities such
as thrombocytopenia and low antithrombin III may
occur in more severe cases resulting in colonic, pul
monary, and limb thrombosis. Elevations in sorbitol
dehydrogenase are expected, but liver disease is rarely
of clinical signifcance.
The organism can be cultured from feces, mesen
teric lymph nodes, and cecum or colonic mucosa of
infected horses. If the feces are very watery, negative
culture results are often reported; as the fecal consis
tency becomes more formed, repeat cultures should be
positive if the horse has salmonellosis. Feces can be
plated directly onto brilliant green agar and/or can be
placed in selenite broth (40C) overnight for enrich
ment. PCR testing is more sensitive than fecal culture
and may be performed on watery fecal samples. A posi
tive PCR does not confrm that a Salmonella sp. is the
cause of the diarrhea and occasionally false negatives
occur. Appropriate history (see above) , clinical fnd
ings, eliminating other causes of diarrhea, and a heavy
4
growth of Salmonella spp. from feces is the most appro
priate route to reach an ante-mortem defnitive diagno
sis. PCR may be too sensitive for practical use since 45
per cent of horses with abdominal pain are positive.
In foals complete blood count (CBC) , electrolyte,
clinical chemistry, and coagulation markers are similar
to those in the adult horses, although the number of
bands are often greater, and electrolyte abnormalities
are generally more severe. Blood cultures, joint fluid,
cerebrospinal fluid, or tracheal aspirates may be salmo
nella positive in infected foals.
bMNbM
Antibiotic therapy is imperative in nursing foals but
probably has little or no positive effect in adult horses.
The antibiotic(s) of choice for foals should be ones that
have historically been effective in vitro and in vivo
against Salmonella spp. (e. g. amikacin or a group-3
cephalospori n) and are likely to be effective against
translocation of other enteric bacteria. Once the sensi
tivity is known, a less toxic antibiotic with better intra
cellular penetration may be added or substituted. In
adult horses, bacteriocidal antibiotic usage might be
justifed based upon severe leukopenia, compromised
immune system, skin wounds, invasive procedures (e. g.
abdominocentesis) or in the hope of preventing bacter
ial translocation. Enrofloxacin (5 mg/kg i.v. s. i. d. ) can
be used in adult horses if antibiotics are deemed neces
sary. Prolonged use of broad-spectrum antibiotics
should be avoided or fungal colitis and pneumonia may
develop.
Fluid therapy is the most important treatment in
adult horses, this should consist of crystalloids and
plasma. The initial crystalloid could be hypertonic
saline if perfusion appears abnormal. Early treatment
with plasma is important in both adults and foals.
Plasma provides oncotic properties that improve the
crystalloid treatments by helping to maintain the crys
talloid fluid in the intravascular compartment for a
longer time. Plasma also has anti-thrombotic properties
such as anti-thrombin III and protein C, which may
help prevent colonic vessel thrombosis. Thrombosis of
colonic vessels is a frequent post-mortem fnding in
Salmonellosis cases that die. Commercial plasma con
tains an antibody against endotoxin but this propert is
probably not as important as albumin, anti-thrombin
III, fbronectin, and other proteins. The preferred iso
tonic fluids are those that have a slightly alkalinizing
effect. Isotonic sodium chloride given in large volumes
over several days causes an acidosis. The crystalloids
should be provided at a sufcient volume to maintain
urine output, return the blood urea and creatinine to
normal, and normalize PCV and electrolytes.
Additional potassium chloride (20-40 mEq/l) is usually
required to maintain normal potassium concentrations.
Isotonic bicarbonate (l.25%) is sometimes needed if
the horse or foal has plasma bicarbonate of less than 16
mEq/1 and a normal anion gap. If isotonic bicarbonate
is administered, it should contain 40 mEq/1 potassium
chloride.
Additional treatments should be provided to combat
the effects of endotoxemia or endotoxin-induced
cytokines or prostanoids. Of these, flunixin meglumine
(0. 3 mg/kg q. 8 h) appears to be the most valuable,
although its use should be limited in a sick foal (only
one or a few treatments) . Foals should be treated with
appropriate gastric protectan ts and/or prostaglandin
E
I
(misoprostol, 2-4 Ig/kg p. o. q. 12-24 h) if non
steroidal anti-inflammatory drug therapy is needed for
more than 2 days. Additional therapies in the early
stages of the disease intended to combat the effects of
endotoxin and pro-inflammatory cytokines include
polymyxin B (6000 IU/kg i.v.) and dimethylsulfoxide
(DMSO) . DMSO (0.05-0.1 g/kg i.v. q. 12-24 h) may be
administered in the intravenous fluids during the initial
48 hours of treatment in the hope of diminishing oxida
tive injury to the colon. Nitroglycerine cream (2%) is
often applied over the digital arteries every 12 hours
during the first 3 days in the hope of maintaining more
normal perfusion to the feet.
Most orally administered intestinal protectants seem
to have minimal beneft. Activated charcoal (l g/kg)
given early in the course of the disease may help bind
lumenal endotoxin. The horse should be fed palatable
grass hay ad lib. during the early stages of the disease if
there is no abdominal pain. As the toxemia resolves the
affected horse should also be fed small amounts of
grain. Both free water and electrolyte-enriched water
(30g sodium chloride, 1 09 sodium bicarbonate, 5g
potassium chloride, 109 of dextrose/gallon of water)
should be provided.
FMbb
If early and aggressive therapy is provided the survival
rate is high. Laminitis, severe thrombocytopenia with
infarction of the bowel, and oliguric renal failure are
poor prognostic fndings in the adult horse. Meningitis,
pneumonia, septic physitis, or septic arthritis worsen
the prognosis in foals. Other complcations include
venous thrombosis, uveitis, cellulitis (often associated
with severe limb or scrotal edema) , fungal pneumonia
(caused by severe ulceration of the bowel, antibiotic
administration, and fungal overgrowth) , rectal pro
lapse, and iatrogenic necrosis of the tail caused by a
ACUTE DIARRHEA 20
tight tail wrap. Although considerable body weight is
lost during the disease process, the weight will generally
return to normal upon resolution of the diarrhea when
the plasma protein concentration returns to normal.
The majority of adult horses that survive salmonellosis
have formed manure within 2 weeks after the initial
episode of diarrhea. A low percentage (probably 5%)
of cases may have more chronic diarrhea, persistent
hyporoteinemia and failure to gain weight.
Horses with salmonellosis can be expected to shed
the organism in signifcant numbers (easy to culture)
for 1-2 months. After that time, the shedding numbers
generally decrease so that most samples are culture-neg
ative by standard methods. When the horse is shedding
heavily, it should be isolated from other horses or put in
a large pasture with non-stressed, healthy adult horses.
Although macrophages and neutrophils are involved in
the pathogenesis of Salmonellosis, they are also inti
mately responsible for prevention of disease in other
wise healthy but exposed horses.
LML MM FbVbMM
All infected horses in a hospital environment should be
isolated, and all attendants should wear examination
gloves when handling the horse and disposable boots
when in the stall. Any rodent or bird movement from
that stall should be prevented. The contaminated stall
should be cleaned of organic debris by scrubbing the
stall with a suitable disinfectant-detergent (I-stroke env
iron, Calgon Vestal Laboratories Inc., St Louis, MO)
and then treated with 10% hypochlorite for at least 1 5
minutes prior to rinsing with tap water. Complete dry
ing should then be permitted and environmental sam
pling should indicate the absence of Salmonella spp.
before another horse is allowed to enter the stall. Stalls
that have wooden walls are more difcult to disinfect
than stalls constructed from other materials, but water
sealants applied to the wood might be helpful.
Horses and foals at increased risk of contracting
Salmonella spp. should be given special protection. Gas
sterilized stomach tubes should be used for all such
horses, especially those being evaluated for abdominal
pain. Foals should be housed apart from horses with
abdominal pain. Prophylactic administration of probi
otics to postoperative horses had no effect on the shed
ding of Salmonella spp. or on the prevalence of diarrhea
in one large study. Stalls should be kept as dry as possi
ble. Cultures and sensitivity should be performed on all
sick horses admitted to a hospital to keep track of the
source of infection and drug resistance patterns. Sick
horses should not be housed in the same wards as sick
cattle since cattle may shed the organisms in greater
4
numbers. Molecular techniques may be required to
determine the origin of the initial infection during an
outbreak. All people, especially children, the elderly,
and immunosuppressed individuals should be pre
vented from having contact with infected horses, their
housing, or bedding. Salmonella typhimurum DT 1 04
(resistant to ampicillin, chloramphenicol, sulfon
amides, and tetracycline) has been isolated from horses
and appears to be particularly virulent in people.
Clostridial diarrhea in adult
horses
TJ Divcrs
Clostridial diarrhea in adult horses may result from
infections with toxigenic strains of Clostrdium difcile or
C. perJrngens. C perJrngens type A with enterotoxin has
been frequently incriminated as a cause of adult horse
diarrhea, but has been diffcult to document. An unclas
sified type of C perJrngens that produces a beta2 toxin
has been recently reported as a cause of diarrhea in
adult horses. Toxigenic C diffcile has been well docu
mented in adult horses and much is known about the
etiopathogenesis of this disease. In many intensive care
veterinary hospitals, C. difcile is a more common cause
of diarrhea in adult horses than are Salmonella spp.
bFMMLY
Clostridium perJrngens is thought to cause diarrhea by
elaboration of either an enterotoxin or a newly
described beta2 toxin. C perngens is considered to be
normal flora of the equine intestinal contents, and it is
often cultured in low numbers ( 1 0 CFU/g) from the
feces of normal horses. The numbers of C. peringens in
the stool may increase in horses with diarrhea, even
when another organism is thought to be responsible for
the diarrhea. A low percentage of C. perfrngens strains
(type A) produce an enterotoxin which has the poten
tial to cause intense fluid secretion into the lumen of
the bowel. Production of the enterotoxin and gastroin
testinal attachment and absorption are necessary to
develop diarrhea. The diarrhea is likely to be a result of
a combination of hypersecretion effects and tissue dam
age. Enterotoxins stimulate guanylyl cyclase and cause
accumulation of intracellular cyclic guanosine
monophosphate (GMP) , which opens the chloride
channels triggering intestinal secretion. C perngens
enterotoxin may also induce a pro-inflammatory
cytokine response with production of interferon
4
gamma, interleukin-l and 6. In humans, enterotoxi
genic C perfrngens is usually associated with food poi
soning, and much less commonly with antibiotic
administration or other factors that disrupt intestinal
flora or motility. Enterotoxin can rarely be found in the
feces of healthy horses, but may be found in normal
feces of horses with colic.
The incidence and etiopathogenesis of a recently
described C peringens producing a beta2 toxin is
unknown. The type of C peJrngens producing this
toxin is not described. Afected horses were all adults
and most had a hemorrhagic diarrhea, suggesting that
if this toxin was the cause of the diarrhea, then it has the
ability to cause severe intestinal necrosis. The toxin can
also be found in the feces of horses with intestinal dis
orders other than colitis, similar to the fndings for C.
perngens type A and enterotoxin.
The etiopathology of C. di cile is well described i n
both horses and other species. Pathogenic strains of C.
difcile produce either toxin A or B or both in the
intestinal track. Toxin A is an enterotoxin which causes
both hypersecretion and cytotoxicity similar to that pre
viously described for C peringens enterotoxin. Tumor
necrosis factor (TNF) and other cytokines are undoubt
edly involved in the cytotoxicity of toxin A. Toxin B (a
cytotoxin) causes severe intestinal inflammation and
necrosis. C. difcilinduced inflammatory changes to
the intestinal mucosa and disturbances of the intestinal
microflora may permit translocation of other intestinal
bacteria into the blood and other organs.
There are several circumstances that either predis
pose to or are necessary for the development of C. dif
cile. Exposure to a toxigenic strain of the bacteria is a

prerequisite. Clostridium difcile is rarely found in nor
mal equine feces. A great source of hospital and occa
sionally farm environmental contamination may be
antibiotic-treated foals which may shed the toxigenic C
difcile in normal feces. Foals with diarrhea, regardless
of its etiology, may be another source of environmental
contamination as toxigenic C difcil can frequently be
found in the feces of diarrheic foals, although cause
and efect in the foals is more difcult to prove.
In the majority of adult horses with C difcile diar
rhea, prior and recent antimicrobial therapy is almost
always in the history, suggesting that some disruption of
normal flora is required in order for the L difcile to
proliferate in the colon. Antimicrobials that most com
monly predispose to C. diffcil colitis include
erythromycin
trimethoprim/ sulfonamides
beta-lac tam antibiotics.
Although antimicrobials given per os and reaching a
high concentration in the colon are most likely to pre-
dispose to diarrhea, antimicrobials given by the par
enteral route may also predispose to C difcile colitis.
Foals treated with erythromycin per os actually increase
the risk of C diffcile colitis in their dams. This is espe
cially true if the mare and foal have been to a veterinary
hospital or farm where the C. diffcile is more likely to be
in the environment. Presumably the erythromycin
treated foals have enough erythromycin in their feces to
contaminate the mare's feed and/or water predispos
ing the mare to the C difcile colitis.
Foals less than 4 months of age treated with ery
thromycin rarely develop severe diarrhea. The risk of C
dilfcil diarrhea in horses treated with
trimethoprim/sulfonamide is much less than with ery
thromycin. Other antibiotics, even injectable ones such
as ceftiofur, may occasionally predispose to C diffcile
diarrhea.
Another predisposing risk factor is withholding
roughage, a common occurrence both for most surgical
procedures requiring general anesthesia and in ill
anorexic horses. Volatile fatty acids produced by nor
mal fiber fermentation in the colon are protective
against the overgrowth of C. diffcile. Intestinal stasis
associated with many cases of abdominal pain also pre
disposes to overgrowth of the organism.
LLMLML bMbMM LLMLML
FMMLLML fMMb
The clinical signs and clinical pathological fndings of
Clostridium spp. diarrhea in adult horses are not very dif
ferent from salmonellosis and monocytic ehrlichiosis.
Colic and signs of severe toxemia accompany a large
number of cases, although the severily of C diffcile diar
rhea can vary similarly to Salmonella spp. or Ehrlichia rs
ticii. The most severe cases of C. diffcile diarrhea show
the following signs
tympanitic abdominal distension
passage of scant liquid feces
bowel necrosis and death.
The tympanitic gas distension may be more common
with C. difcile colitis than with other infectious diar
rheal diseases in adult horses. Other cases have only
slightly liquid feces and few signs of toxemia. Fever is
present early in the course of the disease in most cases.
In more advanced cases, the temperature may be sub
normal but the heart rate remains high, extremities are
cold and membranes are discolored. A hyponatremia
and hypochloremia are present in most infectious
equine diarrheal diseases. Azotemia may be pro
nounced with toxemia. The neutrophil count is often
low early in the course of the disease and immature
ACUTE DIARRHEA 20
neutrophils and toxic changes may be noted, but these
fndings are not different from other infectious causes
of diarrhea in adult horses.
MMbb
The diagnosis of Clostridium perrngens as a cause of diar
rhea in horses is diffcult. There is usually no common
predisposing event as in humans, i. e. outbreak of food
poisoning or prior antibiotic administration as with C
difcile. Furthermore, the organism is frequently pre
sent in the manure of normal horses, and both the
organism and enterotoxin can be found in horses with
abdominal disorders, i. e. colic without diarrhea. If C
perringens is to be blamed as the cause of colitis, there
should be
large numbers of organisms > lOs/ml feces) in the
stool
some evidence of sporulation
presence of enterotoxin in the feces
and other causes of the diarrhea should be ruled out.
The presumptive diagnosis of beta2 toxigenic C pe
frngens would be based upon clinical signs (most often
hemorrhagic diarrhea) and detection of the beta2 gene
by PCR. All other causes of diarrhea should be ruled out
until more information becomes available on the inci
dence and pathogenesis of this organism.
The diagnosis of C difcile is the most straightfor
ward of the three clostridial organisms associated with
diarrhea.
In adult horses, there is almost always a history of
antibiotic administration that precedes the diarrhea
for 1-6 days.
It should be considered more strongly in horses
that have been or are housed in veterinary hospitals
or farms with foals that are being treated with
antibiotics, and/or foals with diarrhea.
A gram stain of the feces may reveal large numbers
of C. difcileIike organisms.
Toxin A or B, or both, should be found in a fecal
sample. The toxin assay ( ELISA) can be performed
within 1 hour. The fecal sample should be taken
immediately to the laboratory or frozen for the
fecal toxin assay. Detection of the toxin in the feces
is faster and more practical than isolation of the
organism and cytotoxicity assay.
PCR assays are now available that can, within a few
hours, detect the C difcile toxin gene in the
feces.
Feces with C. di cile are generally colored green to
brown and are less commonly hemorrhagic.
4
Hemorrhagic diarrhea was reported to be common in
horses that had the novel beta2 toxin in the feces.
bMNbM
Treatment of clostridial diarrhea in horses can be
divided into two categories
1 . general supportive treatment (see General
principles of treatment of acute diarrhea in adult
horses) including
fuids (crystalloids and colloids)
anti-inflammatory drugs
intestinal protectants
2. antimicrobial therapy.
The antimicrobials of choice are metronidazole or
chloramphenicol. Metronidazole would be the frst
choice since most (but not all) C. difcile organisms are
very sensitive to the drug, and it has been used success
fully for a decade in treating this condition. However
there have been several horses at one facilit in the US
that had metronidazole-resistant strains of C. diffcile.
One advantage of chloramphenicol, although not as
sensitive against most C diffcile organisms, is it is less
readily absorbed by the intestine than metronidazole,
and would therefore be expected to have a higher con
centration in the colonic ingesta. Oral antimicrobial
treatment should be continued for at least 7 days.
Relapses may occur when the treatment is discontin
ued, but subsequent clinical episodes are usually
milder. Most horses with C difcile diarrhea have a clin
ical response to the above treatment within 2-3 days if
the diagnosis is correct. All other oral antimicrobial
treatments should be discontinued. If there is fear of
bacterial translocation of other enteric bacteria, sys
temic aminoglycosides may be used if renal function is
normal and monitored. Synthetic bismuth and diocta
hedral smectite have a favorable in vitro effect against C.
difcile and these should be evaluated further in the
horse.
If Clostrdium pefngens is believed to be the cause of
the diarrhea, oral metronidazole and/or intravenously
administered penicillin may be used.
FbVbMM
Prevention of Clostridium difcile infection may be dif
cult in intensive care hospitals with large numbers of
foals and adult horses receiving broad-spectrum antibi
otics. C diffcil forms heat-resistant spores but surface
disinfection with hypochlorite may be successful in
destroying most cells. Routine hand washing by all per-
47
sonne I and isolation of infectious horses and foals
should be performed. Housing high risk adult horses in
stalls not previously occupied by antibiotic-treated foals
might be ideal, but is often not practical. Feeding a fer
mentable fber as soon feasible after abdominal
surgery might be helpful by increasing the normal bac
terial metabolic products in the colon that are known to
inhibit C difcile growth. The use of narrow spectrum
antibiotics (as narrow spectrum as possible) and cau
tion in using orally administered antibiotics other than
metronidazole and chloramphenicol in high risk horses
could be helpful in decreasing the incidence of C diff
cil colitis. Mares with foals being treated with ery

thromycin should be fed from a container raised off the
ground to decrease exposure to the foal's feces con
taining erythromycin and possibly toxigenic C. diffcile.
Foals should not be allowed to drink water from a
shared water bucket immediately after being dosed with
erythromycin.
Potomac horse fever
JM artoI
Potomac Horse Fever (PHF) is the common name
given to the equine infectious enterocolitis caused by
Ehrlichia risticii. It is also known as equine monocytic
ehrlichiosis (EME) because of 1 risticii's predilection
for peripheral monocytes and macrophages. The dis
ease was frst reported along the Potomac River in
Maryland in 1979, but presently has been confrmed
throughout the United States, Canada, and in Europe.
Several surveys have identifed 16-33 per cent of
clinically normal horses to be seropositive, many of
which have had no history of illness. Previous studies
have indicated that the majority of disease caused by
PHF is subclinical. There is also evidence that many
horses with relatively low immunofluorescence assay
(IFA) titers ( 1:320) may have not been infected but
have false positive titers influenced by administration of
other equine vaccines. It predominantly causes diar
rhea in adu
i
t horses and yearlings, but not in foals.
Currently there is evidence for the involvement of 1 ris
ticii in brood mare reproductive problems and abor

tions.
The clinical syndrome may be characterized by one
or more of the following clinical signs
fever
depression
anorexia
dehydration
diarrhea
colic
laminitis.
Many cases manifest signs of colitis in varying
degrees. The onset of clinical signs usually occurs 7-14
days after infection, and following a transient fever 2-4
days post-infection with 1 risticii. Diarrhea develops in
less than 60 per cent of cases of PHF even though it is
thought to be a primary clinical sign. More often
affected horses are depressed, anorexic, febrile, and
toxemic, and have complete blood count (CBC) and
chemistry fndings suggestive of colitis. Laminitis is a
serious sequela to PHF and is seen in 5-30 per cent of
cases. The apparent increased incidence of laminitis
associated with PHF compared to other enteric disor
ders might be explained by the presence of 1 rsticii in
circulating mononuclear cells and the resulting release
of proinflammatory cytokines.
bFbNLY
PHF has a seasonal occurrence and is frequently
reported to be associated with close geographical prox
imity to a river although this is not a prerequisite. It is
infectious and minimally contagious. Epidemiological
studies have supported the infectious nature of the dis
ease supporting a helminth vector. Until recently no
arthropod vectors had been identified. Studies investi
gating the role of several species of ticks, flies, and non
equine mammals in the transmission of Ehrlichia risticii
have been unsuccessful in implicating any of them as
the vector. Currently, investigators are examining the
role of aquatic insects as intermediate hosts.
Experimental oral infection of horses via nasogastric
administration of feces from infected horses has been
successful in transmitting the disease. Large numbers of
rsticii are shed into the lumen of the colon in exfoli
ated colonic epithelial cells at the time of the diarrhea
and for 4-8 days after it has begun. However, casual
contact with infected horses and contaminated feces
does not generally provide a high enough level of expo
sure to result in natural infection. Polymerase chain
reaction (PCR) testing has determined that large num
bers of E. risticii are present in the blood on day 1 after
experimental intravascular infection, and for nearly 2
weeks after if untreated. At the time of the diarrhea and
for 4-8 days after it has begun, casual contact with
infected horses and contaminated feces does not gener
ally provide a high enough level of exposure to result in
natural infection.
Indirect oral transmission through concentration of
1 rsticii in a helminth or coprophagus arthropod, and
inadvertent ingestion by a horse is likely. Neorickettsia
ACUTE DIARRHEA 20
spp., also in the family Ehrlichieae, are transmitted
through ingestion of infected helminths. Similarities in
DNA structure between 1 risticii and Neorckettsia
helminthoeca, the etiologic agent of salmon poisoning in
dogs transmitted by a fluke, raised the question of
helminth transmission in the horse. A rickettsial
pathogen parasitizing fsh in japan, also transmitted by
flukes, was isolated and found to share 99 per cent DNA
homology with 1 risticii. Thus, more evidence is pro
vided for the potential of helminth transmission in the
horse. Similarly, 1 rsticii may be concentrated in
coprophagous insects which are unknowingly ingested
by the horse. Tenebrio beetle species have been identi
fied in large numbers on PHF endemic farms. They are
known to be intermediate hosts of nematodes, as well as
Ehrlichia sennetsu, an ehrlichial pathogen of humans
closely related to other ehrlichial organisms. The
involvement of an arthropod or helminth would be con
sistent with the seasonalit of the disease. More recently
1 rsticii, or a nearly identical organism, has been found
in freshwater stream operculate snails (Pleuroceridae:
quga spp.) and in cercariae released in their secretions.
Water environments make up the natural habitat of
these snail species. The possibility of snails being a
potential vector is supported by evidence that PHF is
associated with close proximity to water (rivers, ponds,
streams) and that horses on dry pastures in endemic
areas usually do not develop the clinical disease.
Environmental stress factors are not associated with risk
of the disease.
The paricular virgulate cercariae of fresh water snails
in which E. rsticiiwas isolated are associated with trema
todes of the family Lecithodendriiae, common parasites
of bats in North America which use freshwater snails
and aquatic insects as intermediate hosts. Using PCR
testing, E. rsticii positive metacerariae were identifed
in immature and adult caddisflies, mayflies, damselflies,
dragonflies, and stoneflies. In additon E. risticii PCR
posItIve adult trematodes in the family
Lecithodendriiae were found in the intestines of bats.
The gene sequences of the metacercariae and adult
trematodes were found to be essentially identical to the
1 6S rRNA gene sequences of E. risticii from horses and
snails in northeren California. This new information
indicates that there is a broad range of intermediate
hosts for trematodes that act as vectors for 1 risticii.
Therefore, aquatic insects are likely to play an impor
tant role in the epidemiology of PHF. Horses may acci
dentally ingest aquatic flies in addition to snails carrying
the 1 risitcii infected metacercariea. Aquatic insects as a
potential vector is also supported by evidence that PHF
is associated with close proximity to water.
Different strains of 1 risticii, as compared to the
1984 isolate, were isolated from clinically sick horses in
4 1
the early 1990s. It is known that PHF is caused by diver
gent strains. Multiple strains may account for incom
plete vaccine efcacy since commercial vaccines are
made of the single 1984 isolate. Divergent strains may
also account for difculties in interpretation of diag
nostic tests in horses with clinical signs consistent
with PHF. False negative results or lower titers may
occur if diagnostic tests identif only a single tpe strain
of 1 risticii.
E. risticii may also cause abortion. Abortions in the
seventh month of gestation have been seen with both
experimental 1 risticii infection and natural infection.
Abortion was accompanied by placentitis and retained
placenta in mares that had fully recovered from the
enterocolitis while 3-6 months pregnant. risticii was
cultured from the fetal tissues. Gross and histologic evi
dence of enterocolitis, hepatitis, and lymphoid hyper
plasia were present. The frequency of PHF-associated
abortion is unknown but it seems more likely that it
would occur in endemic areas. E. risticii, as an agent of
abortion, must be taken into consideration in cases of
late-term abortions on endemic farms with confrmed
cases of PHF. Since a large proportion of disease due to
E. risticii is subclinical, and therefore undetected, it
should be considered in cases of late-term abortions in
herds without histor of illness.
LLMLML bMb
The disease is characterized by one or more clinical
signs including
fever
depression
anorexia
dehydration
diarrhea
colic
laminitis.
Physical examination and laboratory test results are
consistent with enterocolitis and endotoxemia. The
onset of clinical signs occurs 7-1 4 days post-infection
following a transient, often subclinical fever 2-4 days
post-infection. The initial fever spike may be accompa
nied by partial anorexia. Diarrhea only occurs in a
small percentage of infected horses ( 60%) but when
it does occur it can be severe and accompanied by
abdominal pain and/or laminitis. Fever is generally
present at the time of the diarrhea which occurs 7-1 0
days after infection. Fever and laminitis may occur
without diarrhea. The complete blood count and
chemistry panel are characterized by hemoconcentra
tion (often severe), leukopenia, occasional monocyto-
44
sis, pre-renal and/or renal azotemia, hypoproteinemia
(often severe), hyponatremia, hypochloremia, and
hypokalemia. It is common to see a marked leukocyto
sis after leukopenia in clinical PHF. Because these fnd
ings are similar to those found in acute endotoxemia,
diarrhea caused by Salmonella spp. is the primary differ
ential diagnoses.
MMbb
At the time of writing, accurate practical diagnosis of
PHF is complicated. Cell culture from infected blood
would be the most sensitive and accurate means of
diagnosis, but is not rapid enough to be of practical
use. The PCR uses genomic amplifcation to identif a
unique genomic sequence of Ehrlichia risticii, the par
tial 1 6S rRNA sequence. A combination of PCR and
indirect immunofluoresence assay (lFA) is employed
to increase diagnostic accuracy and decrease time for
test results. A whole blood, EDTA sample is submitted
for PCR and E. rsticii organisms are identifed in the
buf coat component of the sample. The PCR is a sen
sitive and specifc test that does not seem to be influ
enced by vaccination. It also aids in interpretation of
low IFA titers in clinically sick horses. Even a titer as
low as 1:80 with a positive PCR test is indicative of
probable infection given clinical signs and time of
year. One disadvantage of PCR is possible sample cont
amination. Positive and negative controls are included
during testing to limit false negative and false positive
results. The genes that PCR detects may exhibit minor
sequence divergence among strains of individual
species, and so may be useful for detection of variant
strains of a single species as occur in E. risticii or may
make defnitive diagnosis complicated if the PCR does
not detect all possible divergent strains.
The diagnosis of PHF can also be made by detecting
seroconversion of consecutive serum samples. Five to
seven days after the frst titer is sufcient time to collect
the second sample. A four-fold or greater change in IFA
titer is diagnostically signifcant in rickettsial disease as
stated by the Center for Disease Control. However fail
ure to seroconvert does not rule out infection because
the onset of clinical signs can be delayed as long as 1 4
days, and the horse may have already seroconverted by
the time the frst sample was obtained. Another compli
cating factor is the ability of horses in endemic areas to
maintain very high titers for prolonged periods of time
without clinical disease. The bottom line in accurate
diagnosis of PHF is best made by considering the over
all picture, including clinical signs, geographic loca
tion, and season of year, and using this information to
interpret test results.
bMNbM MM FbVbMM
Treatment considerations for PHF are similar to those
for any acute colitis in the horse
1. addressing hydration status, acid-base defcits, and
electrolyte abnormalities with intravascular fluids is
the basis of supportive therapy in acute colitis
2. signs of endotoxemia warrant the use of low anti
endotoxic doses of NSAIDs like flunixin meglumine
3. H plasma transfusion of at least 3-6 liters is
benefcial in severe hypoproteinemia by providing
albumin to increase plasma oncotic pressure as well
as in endotoxemia by providing anti-thrombin III,
coagulation inhibitors, and plasma proteins.
Specifc treatment of PHF includes administration
of oxytetracycline at 6.6 mg/kg Lv. q. 12-24 h for 3-5
days. If the diagnosis is correct, a favorable response to
therapy is usually seen within 1 2-24 hours, manifested
by resolution of fever, depression, and anorexia.
Diarrhea typically resolves within 3-4 days or fails to
develop if treatment is instituted prior to onset.
Although it has been discussed extensively among prac
titioners, it is unlikely that oxytetracycline will exacer
bate or cause disease by organisms such as Salmonella
spp. or Clostridium spp. The high risk of laminitis, a
sometimes f atal sequela, often outweighs the risks of
oxytetracycline when there is a high index of suspicion
of PHF and diagnosis is still pending.
Laminitis is a frequent complication of PHF with a
5-30 per cent rate of occurrence. Because of the high
risk involved, it is prudent to take preventative measures
against laminitis in patients with suspected PHF.
Unfortunately, efcacy of any one prophylactic treat
ment for laminitis is difcult to assess , therefore there
are many options and combinations
1. Lily pads, NSAIDs (phenylbutazone, flunixin
meglumine, aspirin) , and DMSO are frequently used.
2. More recently topical application of nitroglycerine
ointment to the digital arteries has been
recommended for vasodilatory effects and clinical
obserations seem to be consistent with some success.
3. The use of pentoxifylline, a methylxanthine
derivative has become a popular therapy as well. It
may increase blood flow to hypoxic tissues by
improving the flexibility of red blood cells,
reducing blood viscosity, and inhibiting thrombus
formation. Experimentally it has been shown to
inhibit tissue-damaging inflammatory mechanisms
including inhibition of tumor necrosis factor. These
effects may deem it effcacious in laminitis
prevention but it has not been proven. Currently
studies are being performed to evaluate the efcacy
ACUTE DIARRHEA 20
of pentoxiflline in the treatment of endotoxemia
in horses.
Presently vaccination effcacy is questionable. There
are numerous cases of clinical PHF in vaccinated
horses. A possible explanation is the identifcation of
new disease-causing strains of Ehrlichia rsticii. Studies
on vaccine efcacy have shown that annual immuniza
tion is inadequate, with only 50 per cent of vaccinates
being fully protected 6 months after vaccination. Based
on this evidence, recommendations for vaccination are
that horses in endemic areas be vaccinated every 3-4
months from July to November (peak incidence) after
an initial vaccination protocol of 2 doses, 3 weeks apart,
initiated in April. This protocol increases the likelihood
of more complete protection. Even if complete protec
tion is not achieved, vaccination may lessen the severit
of disease and is therefore strongly recommended.
Possible explanations for the marginal nature of the
vaccines include defciencies in the antibody response
of the horse from the inactivated vaccine and the anti
genic variation of divergent strains of the organism. No
serious adverse vaccine reactions have been reported
and the vaccine has not been proven unsafe for preg
nant mares. Vaccination is probably unnecessary for 2
years after natural disease because of the long-lived
immunity evidenced by clinical resistance to re-infec
tion for 20 months.
Non-steroidal anti
inflammatory drug toxicity
D Lohcn
MULM
Non-steroidal anti-inflammatory drugs (NSADs) are
frequently administered to horses with colic, endotox
emia, musculoskeletal disorders, and other medical
problems because of the antipyretic, analgesic, and anti
inflammatory properties of the drugs. In addition to
these therapeutic properties , NSAIDs also exhibit toxic
properties. The mechanisms, clinical signs, clinical
pathology, diagnosis, treatment, and prevention of
NSAID toxicity are reviewed in this section.
NbLMMMbNb f ALY
The major toxicities related to NSAIDs include
gastrointestinal tract damage
renal damage.
4 1 b
Gastrointestinal tract abnormalities are the most
common manifestations of NSAlD toxicity. Gastric
ulceration is the condition most commonly detected,
and it can develop anywhere in the gastrointestinal tract
(from the mouth to the rectum) . Renal toxicosis also
may develop. The primary mechanism of both thera
peutic and toxic effects of NSADs is related to inhibi
tion of the cyclooxygenase enzymes. Two isoforms of
the cyclooxygenase enzyme have been identifed
cyclooxygenase-l (COX- I)
cyclooxygenase-2 (COX-2) .
COX-l i s produced constitutively and thought to
play an important role in maintaining physiologic
homeostasis; it is found in such tissues as the stomach
and kidney, and in the endothelium and platelets. In
contrast, COX-2 is an inducible enzyme thought to be
associated with inflammation, and is produced by a vari
ety of cells including monocytes, fbroblasts, synovio
cytes, and chondrocytes. It has been postulated that
drugs which inhibit COX-l more than COX-2 will have
greater toxic potential because they inhibit physiologic
functions to a greater extent. Evidence exists that the
ulcerogenicity of the following drugs decreases in
sequential order:
phenylbutazone
flunixin meglumine
ketoprofen.
The differing toxicity may relate to varying afnities
of these agents for the COX-l and COX-2 isoforms.
Inhibition of cyclooxygenase results in inhibition of
prostanoid synthesis. In the stomach, inhibition of
cyclooxygenase can increase acid secretion, decrease
output of mucus and bicarbonate, impair vasodilation,
and diminish epithelial restitution, cell division, and
angiogenesis. Inhibition of cyclooxygenase also
increases the severit and impairs the healing of existing
ulcers. In the kidney, prostaglandin E2 (PGE) and
prostacyclin (PGI) produce vasodilation in the autoreg
ulatory response of renal blood flow to hypoperfusion;
consequently, hypovolemia, hemorrhage, or renal dis
ease will increase the risk of renal NSAlD toxicosis.
Damage is greatest at the renal crest (papilla) and pap
illary crest necrosis may be associated with subsequent
nephro- or ureterolithiasis and chronic renal failure.
Not all of the adverse effects of NSAIDs are attribut
able to cyclooxygenase inhibition. The NSAIDs also
cause injury from a variety of mechanisms, including
microvascular damage, increased intracellular concen
tration of reactive oxygen and other free radicals, direct
local injury (particularly with ion trapping in the stom
ach) , inhibition of cell division, and reduced hydropho
bicity of the gastric mucus coat.
4b
Although the toxicity of NSAIDs is dose-related, pre
disposing factors such as dehydration or sepsis con
tribute to the development of NSAlD toxicity. Some
horses may have an idiosyncratic predisposition and,
experimentally, arthritic animals may be more suscepti
ble to NSAlD-induced gastropathy than healthy animals.
The latter fnding is important because NSAlDs are
often administered to chronically lame horses. In some
areas, concurrent use of to or more NSAlDs is com
mon. Combination of two NSAlDs will prolong their
pharmacologic effect and increase the risk of toxicity.
LLMLML bMb
Clinical signs of NSAlD toxicosis are usually referable to
the gastrointestinal tract and include inappetance or
anorexia, lethargy, and occasionally fever. Oral or lin
gual ulceration may also lead to difculty in prehension
and mastication. Esophageal ulceration may result in
signs of apparent pain (stretching of the neck, groan
ing) during swallowing, and ptyalism. Gastric ulceration
may result in inappetance, particularly for grain by some
horses. Horses that have gastric outflow obstruction
associated with gastroduodenal ulceration may exhibit
ptyalism, reflux esophagitis, and, in severe cases, spon
taneous nasogastric reflux. Horses with ulceration any
where in their gastrointestinal tract may exhibit signs of
colic which may be intermittent and varying in severity.
Horses with colonic ulceration may have unformed
stools or diarrhea, and edema of the ventrum. Intestinal
damage caused by NSAIDs can disrupt the mucosal bar
rier of the intestinal tract, resulting in endotoxemia.
Clinical signs of endotoxemia (e.g. altered appearance
of mucous membranes, fever, and dehydration) may be
seen in some horses with NSAlD enteropathy.
LLMLML FMMLY
The most consistent clinicopathologic abnormality in
horses with NSAlD toxicosis is hypoproteinemia and
hypoalbuminemia, presumably from loss and microbial
digestion in the intestinal tract. These fndings are
more commonly observed with involvement of the dis
tal portions of the intestinal tract, and are unreliable as
a diagnostic tool for horses with NSAlD gastropathy.
Some horses will have decreased concentration of cal
cium, attributable in part to intestinal loss of protein
bound calcium.
In chronic cases, horses may be anemic from inflam
mation or intestinal blood loss. Occult blood may be
found in the feces of horses with more distal enteric
involvement, but these tests often lack sensitivity and
false positive results may be expected for up to 24 hours
after rectal palpation.
The concentration of leukocytes is usually within the
reference range, although leukocytosis and hyperfb
rinogenemia, associated with inflammation, and
leukopenia and neutropenia, presumably caused by
endotoxemia, can be seen in some horses with NSAID
toxicosis. Results of peritoneal fluid analysis are often
within reference ranges, but increased concentration of
nucleated white blood cells, total protein, and fbrino
gen may be seen. When abnormal, cytologic examina
tion of peritoneal fluid is more consistent with
non-septic than septic inflammation.
Pre-renal or renal azotemia may be observed in some
horses with NSAID toxicosis. Pre-renal azotemia may be
associated with dehydration. Renal azotemia is not
often found clinically and is generally observed late in
the course of disease. Other urinary indices of renal
damage are generally insensitive; urinalysis may reveal
hematuria. Serum concentration of phosphorous may
be increased but this also is an insensitive indicator of
renal NSAID toxicosis.
MMbb
Diagnosis is usually made on the basis of history of
NSAID use, clinicopathologic fndings, and clinical
signs. Endoscopy can be useful to visualize the location
and extent of esophageal, gastric, and, when possible,
duodenal lesions. Gastric lesions are more common in
the glandular epithelium, although non-glandular
lesions can be observed. In some cases, contrast radiog
raphy or scintigraphy may be useful to document
delayed gastric emptying. Lesions of the jejunum,
ileum, cecum, and colon can be difcult to identif
without celiotomy and enterotomy. It has been sug
gested that isotope-labeled white blood cell scinti
graphic scans may identif colonic ulceration; the
sensitivit and availability of the procedure is probably
quite limited. Ultrasonographically horses with renal
crest necrosis may have increased echogenicity of the
renal crest and echogenic debris in the renal pelvis.
bMNbM
In all cases treatment should include discontinuation of
NSAIDs. In horses with acute overdose (e. g. inadvertent
administration of a full 12-g tube of phenylbutazone
paste), gastric lavage and administration of 4.5 liters ( 1
gallon) per 450 kg of mineral oil via a nasogastric tube
may be of beneft to reduce the absorption of the
ingested NSAID. Treatment for gastri ulceration with a
proton-pump inhibitor (e.g. omeprazole) , an Hz-blocker
ACUTE DIARRHEA 20
(e.g. ranitidine) , or sucralfate should be implemented
for horses with gastric ulceration. Regardless of the site
of NSAID toxicity, administration of misoprostol, a syn
thetic analog of prostaglandin E
I
'
may be of beneft
because it has been demonstrated to prevent phenylbu
tazone-induced gastrointestinal lesions in horses. The
drug can be administered orally (5 Ilg/kg q. 12 h or 2
Ilg/kg q. 6 h) . Some clinicians avoid use of this drug
because gastrointestinal side effects have been described
in people and anecdotally among horses. For manage
ment of colonic lesions, the reader is referred to Chapter
21 , Right dorsal colitis. Horses with strictures of the
pylorus, duodenum, jejunum, or colon may require
surgical management.
FbVbMM
Prevention of NSAID toxicosis can be achieved in many
horses by avoiding the use of NSAIDs or by limiting the
dose and duration of treatment to the minimum that is
required to control the problem, however some horses
may experience NSAID enteropathy. Use and develop
ment of less ulcerogenic agents (e.g. ketoprofen or
agents that are more COX-2 selective) could prevent
NSAID toxicosis in some horses. Limiting the extent of
predisposing factors such as dehydration should
decrease the risk of NSAID toxicosis. Some clinicians
administer anti-ulcer medications to prevent gastric
ulceration in horses treated with NSAIDs. described
above, administration of misoprostol can prevent or
limit the severity of NSAID-induced enteropathy.
Toxic colitides
DLohcn
MULM
Various toxic causes of enteritis and colitis have been
reported. In this section a discussion of cantharidin tox
icosis is presented, along with a brief review of other
toxic causes of colitis. Non-steroidal anti-inflammatory
drug toxicity and right dorsal colitis are discussed else
where in this book (see Chapters 20 and 21) .
Cause
Cantharidin is a toxic principle found in many of the
'blister' beetles (Epicauta spp. ) (Figure 20.1) that cause
4 1 1
Figure 0.1 Beetle, cu! sp., associated with bl ister
beetle toxicosis (photograph courtesy of Dr DG Schmitz)
blistering of mucosal surfaces. Cantharidin toxicosis
results from ingestion of dead blister beetles in alfalfa
hay l; very rarely, other alfalfa products. Male beetles
produce the toxin and pass it to females during mating;
concentration of cantharidin is highest in the
hemolymph and genitalia of the beetles.
Some species of blister beetles feed and mate in
large groups. The modern forage harvesting technique
of simultaneously cutting and crimping forage can
result in entrapping these swarms of beetles, resulting
in a large number of insects in a small number of bales
or flakes of forage. Ingestion of as little as 46 grams of
dried beetles (about 100 beetles) can be lethal to a
horse, although lethal doses have a wide range, proba
bly because of such factors as predominate gender
ingested and inter- and intra-species variation among
beetles in the production of toxin.
The toxin rapidly causes hypovolemic shock and
pain because of the extensive necrosis and sloughing of
the mucosal lining of the proximal gastrointestinal
tract. In the urinary tract, cantharidin causes ulceration
and hemorrhage of the bladder mucosa, ureters, and
renal pelvis; variable amounts of renal tubular damage
may occur. Cardiac toxicity is less common, abnormali
ties include ventricular myocardial necrosis and peri
cardial effusion.
Cl i nical Si gns (Table 20. 2)
Onset and duration of clinical signs of cantharidin toxi
cosis vary from hours to days. Horses often sweat pro
fusely and have elevation in rectal temperature, heart
rate, and respiratory rate. Mucous membranes are gen
erally congested and may have a bright, brick red color;
the capillary refill time will be prolonged. Signs of colic
4
Inappetance
Depression
Playing with water
Salivation
Pollakidipsia
Pollakiuria
Sweating
Pyrexia
Tachycardia
Tachypnea
Colic
Diarrhea
Hematuria or hemoglobinuria
Synchronous diaphragmatic flutter
Muscle fasciculations
Stiff gait
Sudden death
of variable severity are commonly observed. Affected
horses are usually inappetant or anorectic and
depressed. Often they will submerge their muzzles in
water and appear to be playing in it. Pollakidipsia and
pollakiuria are frequently observed, the latter being
particularly common if the horses survive longer than
68 hours. Hematuria can be seen, usually later in the
course of the disease. Because hypocalcemia often
develops in horses with cantharidin toxicosis, some
horses may demonstrate synchronous diaphragmatic
flutter, muscle fasciculations, a stiff gait, or other less
common signs of hypocalcemia (including abnormal
facial expressions - the so-called sardonic grin, cardiac
arrhythmias, hindlimb ataxia, laryngospasm, and dys
phagia) . The course of disease can be very acute and
sudden death may occur.
Diagnosis
Although the clinical signs described are non-specifc,
together they may be strongly suggestive of cantharidin
toxicosis. A history of eating alfalfa hay (or possibly
other alfalfa products) and finding blister beetles in the
hay supports the diagnosis - however beetles may not be
found because they often appear only in a small portion
of a bale that has already been consumed. Occasionally,
blister beetle body parts can be identifed macro- or
microscopically in the gastrointestinal contents or feces
of affected horses. Clinicopathologic fndings often
include hypocalcemia, hypomagnesemia, hypopro
teinemia, and elevated creatine phosphokinase.
The toxin can be identifed in urine or gastric con
tents using high pressure liquid chromatography or gas
chromatography and mass spectrometry. The earlier in
the disease that a sample is collected, the higher the
probability of fnding the toxin; cantharidin in urine is
essentially non-detectable by 3-4 days after intoxica
tion. For analysis at least 500 ml (a little more than 1
pint) of fresh urine should be submitted; or at least 200
g (about 7 ounces) of solid stomach contents. Serum
samples (at least 24 ml) can also be submitted, although
the test is much less sensitive using serum.
Treatment (Table 20.3)
Appropriate treatment is symptomatic and should be
administered promptly. Activated charcoal ( 1 -3 g/kg
p. o. ) may adsorb cantharidin. Administration of min
eral oil will help to evacuate intestinal contents, includ
ing toxins, from the gastrointestinal tract, and may bind
some of the lipid-soluble cantharidin. Because the oil
can interfere with the adsorptive activity of charcoal,
these to substances probably should not be adminis
tered concurrently. Fluids should be administered
intravascularly to combat dehydration and, once rehy
drated, to promote diuresis, unless contraindicated for
physiologic reasons (e. g. marked hypoproteinemia or
myocardial disease) . Diuresis with furosemide should
be avoided because it may exacerbate hypocalcemia.
Calcium borogluconate (24 mg calcium/kg body
weight) and/or magnesium sulfate (6 mg/kg body
weight) often need to be supplied in intravascular flu
ids. Diluted calcium solutions should be given slowly
intravascularly and should not be administered through
the same line as bicarbonate solutions.
Intestinal protectants, particularly sucralfate (20
mg/kg p. o. q. 6 to 8 h) , should be of beneft in treating
the gastritis. Analgesics are often required to manage
pain. Adequate pain relief may not be possible with
Mineral oil
Activated charcoal
Intravenous fluid therapy
Calcium borogluconate
Magnesium sulfate
Analgesics
xylazine
detomidine
romifidine
butorphanol tartrate
flunixin meglumine
Antibiotics
'
.
ACUTE DI ARRHEA 20
flunixin meglumine, so xylazine, detomidine, or romif
dine, alone or in combination with butorphanol tar
trate should be considered, although these drugs
markedly suppress colonic motility. Furthermore,
affected horses may be more susceptible to the ulcero
genic effects of NSAlDs because of dehydration and
concurrent intestinal damage. Broad - spectrum antimi
crobials are usually administered because of damage to
the intestinal mucosal barrier. If used, the potential for
nephrotoxicity must be considered.
Currently there is no antidote for cantharidin toxi
cosis. Prognosis is often poor but varies based upon the
amount of toxin ingested, the stage of disease when
treatment is implemented, and the quality of intensive
care provided. Prognosis can likely be reflected by the
severity of clinical signs and time from exposure to ini
tiating treatment.
Prevention
Many species of blister beetles prefer the perimeter of
felds. Because they do not migrate far, avoiding simul
taneous cutting and crimping of forage from the
perimeter of felds may help prevent cases. Cutting hay
when adult beetles are less active (early and late cuttings)
should decrease the risk of intoxication. Pesticides are
available that facilitate control of blister beetles. If a case
is diagnosed, it is advisable to either discontinue feeding
the implicated batch of alfalfa hay or to inspect each
flake for evidence of blister beetles. The beetles can be
recognized by a prothorax that is narrower than the
head and abdomen (Figure 20. 1 ) , and it should be
remembered that not all toxic beetles are striped.
Mb AMb
A variet of plants (Table 20. 4) and other chemical
compounds (Table 20. 5) can be toxic to horses. Acorns
and the blossoms, buds, leaves, and stems of oak
( Quecus spp.) may be toxic to horses. Clinical signs in
horses may be peracute or acute, including colic, hem
orrhagic diarrhea, and sudden death. Renal toxicit can
also occur. Rarely, ingestion of acorns can cause gastric
impaction. Diagnosis is based on history of exposure,
fnding acorns in the intestinal tract, detecting high uri
nary phenolic content, and necropsy.
Some species of blue-green algae found in stagnant
pond water can cause hemorrhagic diarrhea and signs
of liver disease (including photosensitization) when
ingested. Diagnosis is generally presumptive on the
basis of clinical signs and apparent exposure. Avocado
toxicity may cause diarrhea, colic, and edema of the
lips, tongue, head, and neck.
41

Acorn/oak
Algae
Avocado
Castor bean
Oleander
Selenium-accumulating plants (e.g. P5!Ilguu5
spp.)
Heath (Erica spp.)
Japanese yew
Potato
St John's wort (Klamath weed)

;
, "
Amitraz
Arsenic
Linseed oil
Mercury
Mycotoxins
Organophosphates
Propylene glycol
Salt
Reserpine
Selenium
Siaframine
Seeds of the castor bean plant ( Ricinus communis)
can cause severe colitis and diarrhea in horses. The
plan t is found predominately in southern regions of the
United States. Diagnosis is based on finding seeds in the
feed, history of ingestion, or necropsy. Castor oil (oil
derived from this plant) has been used experimentally
to produce colitis in horses.
Oleander is often grown as an ornamental hedge in
the southern and western United States. Although the
toxic element is a cardiac glycoside, horses that ingest
oleander may develop profuse watery or hemorrhagic
diarrhea.
Selenium may accumulate in some plants grown in
areas where there is a high selenium content in the soil,
for example Astrgulus spp. Acute toxicosis may result in
diarrhea, respiratory distress, and abnormal posture or
gait, the serum concentration of selenium may be useful
diagnostically. Chronic forms of intoxication (e.g. alkali
disease) appear to be more common than acute forms.
Amitraz is an acaricide for cattle that is not approved
for use in horses because these animals are more sensi
tive to its effects. Although colonic impaction is the
more common side effect, some affected horses will
develop diarrhea.
47
Products containing arsenic are used as herbicides,
insecticides, moluskicides, rodenticides, and defoliants.
Horses may become intoxicated from ingesting shrubs
or grass contaminated by arsenicals, or when their for
age is contaminated. Arsenicals vary in their potency
(e.g. sodium arsenite and arsenic trioxide are both her
bicides used to kill weeds and bush but trioxide is about
1 0 times less toxic on a weight basis) . Peracute or acute
toxicosis can result in diarrhea which may be hemor
rhagic. Specifc treatment for arsenic intoxication
includes sodium thiosulfate ( 20-30 g diluted in 300 ml
water p. o. ) or dimercaprol (BA) . The latter com
pound is administered intramuscularly as an antidote
for trivalent arsenical intoxication (3 mg/kg) , and its
efcacy is questionable. Concentrations of arsenic in
the liver or kidneys that are greater than 1 0 ppm are
considered diagnostic.
Raw linseed oil is occasionally used as a laxative in
horses, it is i ncreasingly being recommended as a feed
additive as a source of linolenic acid. Linseed oil is par
tially saponified by gastrointestinal secretions to form
soap and glycerine, both of which act as irritants to the
intestinal mucosa. Administration of linseed oil (2. 5
ml/kg twice at an interval of 12 hours) can cause diar
rhea, inappetance, lethargy, and colic in healthy horses.
Conceivably, a lower dose could cause similar signs in a
horse with pre-existing mucosal irritation.
Ingestion of mercur-treated seed grains or applica
tion of mercuric blisters can result in toxicity to the ali
mentary tract and kidneys. Because treatment of grains
with mercuric fungicides is no longer practiced, inges
tion (licking) of mercuric blisters is the most common
route of exposure. Diagnosis can be made by history of
exposure, clinical signs, and increased tissue concentra
tions of mercury.
Various mycotoxins (toxins produced by fungi) can
result in diarrhea in horses, including aflatoxins, tri
chothecenes, and slaframine. The latter mycotoxin is
produced by Rhizoctonia leguminicola on red clover grass
and hay, it also causes excessive salivation. However
diarrhea is rare with mycotoxins. Diagnosis can be
made on the basis of clinical signs, identifing the toxin
in grains or hay, or increased concentrations of toxins
or their metabolites in tissues.
Organophosphates used as pesticides can cause diar
rhea in horses. Signs of urination, lacrimation, and sali
vation also may be observed. Diagnosis can be made on
the basis of clinical signs and determination of
cholinesterase activity in the blood or brain. Treatment
for organophosphate toxicosis should include adminis
tration of activated charcoal (0. 5-1 kg/500 kg) by naso
gastric tube and atropine (0. 25-0. 5 mg/kg; 1 /4 of the
dose given Lv. and the remainder given i. m. ) . If
detected within 24 hours of intoxication, the oxime
2]AM can be used (20 mg/kg i.v. q. 1 2 h or 1 0-15
mg/kg s.c. as needed) .
Propylene glycol is used by large animal veterinarians
to treat cattle with ketosis and is present in so-called 'safe'
motor vehicle antifreezes. Because propylene glycol
physically resembles mineral oil, it can be inadvertently
administered to horses. Clinical signs usually develop
within 30 minutes of administration, can include diar
rhea, and may be fatal. If the error is detected promptly,
efforts to evacuate the stomach by siphoning and admin
istration of sodium bicarbonate intravenously to combat
probable acidemia may be of beneft.
Intoxication with salt can result in diarrhea. History
of access or ingestion of salt without access to water and
serum (or CSF) concentration of sodium can support a
diagnosis. Administration or ingestion of hypotonic flu
ids or 5% dextrose to such horses is contraindicated
and may exacerbate neurological signs.
Grain overload
N aII
MULM
Despite widespread awareness among horse owners
about the seriousness of the condition, grain overload is
still recognized as a relatively common disease. To some
degree it is more related to a sudden change in the
amount of concentrate, as many performance horses
are fed a considerable volume of concentrates as part of
their daily ration, but they have become accustomed to
it. That particular horse may require a greater amount
of inadvertent ingestion of concentrate than the horse
that has never been fed concentrates before. In addi
tion, it is the amount of soluble carbohydrate in the
concentrate that is the predator, so the corn/maize
containing products are generally a greater danger
than a grain product such as oats. Although horses are
rarely fed barley, this grain can be extremely high in sol
uble carbohydrates. Many cases of grain overload are
related to the excessive feeding of cor during the win
ter months under the false pretense that this practice
will increase heat production and aid the horse in keep
ing warm. Actually, the fermentation of fber in the
cecum and large intestine generates a greater amount
of heat than the digestion of concentrates.
There are several sequelae to the sudden ingestion of
soluble carbohydrates ranging from mild colic and the
ACUTE DIARRHEA 20
development of diarrhea to death resulting from a rup
tured stomach. Laminitis developing as a result of the
overingestion of soluble carbohydrates is a well-docu
mented occurrence. Indeed, the ability of soluble car
bohydrates to induce laminitis has been used as a
standard method for the scientifc study of that disease.
The signs of symptomatic grain overload may
include
colic
abdominal distension
lameness caused by laminitis
trembling
sweating
diarrhea.
Clinical examination fndings relate to endotoxic
and hypovolemic shock, gastritis, and ileus, and may
include
hyperemic to purple mucous membranes
tachycardia
tachypnea, (endotoxic and/or hypovolemic shock)
gastric reflux
colonic distension
gas 'pings' and decreased motility on abdominal
auscultation.
Clinical fndings are variable depending on the indi
vidual case.
NMMMbNbM
Treatment options for grain overload are summarized
in Table 20.6.
The most immediate concern following the
overingestion of soluble carbohydrates is gastritis and
Activated charcoal
Mineral oil
Magnesium sulfate
Flunixin meglumine
Aspirin
Antihistamines - doxylamine or diphenhydramine
Intravenous polyionic fluids - lactated Ringer's
Plasma
Pentoxifylline
Frog supports
Glyceryl trinitrate
solution
hypertonic saline
sodium bicarbonate
471
subsequent overdistension of the stomach. In such
cases, the horse tpically shows signs of colic, and the
passage of a nasogastric tube is essential to prevent
stomach rupture. There is the possibility of continued
fluid production and accumulation in the stomach, so
the nasogastric tube may be left in place or the horse
carefully monitored for the recurrence of stomach dis
tension.
If the horse is not (or has stopped) refluxing, the
administration of activated charcoal (0.5 kg or l ib) or
mineral oil (4 liters or 1 gal) is thought to be helpful in
reducing toxin absorption from the gastrointestinal
system. The administration of 0.5 kg ( l Ib) of magne
sium sulfate (Epsom salts) per os with 4 liters ( 1 gal) of
water is indicated if evaluating a horse suspected to
have grain overload, before clinical signs develop, in
order to speed the evacuation of the gastrointestinal
system.
Systemic therapy may include flunixin meglumine at
the 0.25 mg/kg dose for its ' anti-endotoxic' properties
or at a higher dose for the anti-inflammatory effects
should laminitis be developing. In addition, the admin
istration of aspirin ( 10 mg/kg p. o. or i.v. s. i. d. ) may be
of benefit in maintaining digital perfusion; if the horse
is still refluxing, aspirin can be administered per rec
tum. Although aspirin has not been proven to inhibit
equine platelets after endotoxin stimulation, it will
increase bleeding time in normal horses. Other sys
temic therapy may include an antihistamine (doxy
lamine 0. 5 mg/kg S. c. q.i. d. or diphenhydramine 1
mg/kg i. m. b. i. d. ) for the frst 24 hours.
Many of these horses are also moderately to severely
dehydrated, this can be determined by physical exami
nation and further characterized by measurement of
plasma total protein and packed cell volume. There can
also be a variable degree of acidosis present (both lactic
acidosis from decreased perfusion and an increase in
organic acids from the grain digestion) , so lactated
Ringers is a good choice of fluids. In severe cases, the
administration of bicarbonate may be necessary to cor
rect the acid-base disturbance. If the horse is experi
encing severe hypovolemic shock, the administration of
hypertonic saline (7% sodium chloride) can be of sig
nifcant benefit as the initial fluid, but must be followed
within several hours by a volume replacement quantit
of normotonic polyionic fluids. Many of these horses
may require the additional supplementation of calcium
. and potassium. Also, if the signs of endotoxemia are
severe, the administration of plasma (especially hyper
immune endotoxin plasma) can be of beneft as well as
the administration of pentoxirlline (8. 4 tng/kg p. o.
t.i. d. ) .
a potential prophylaxis against laminitis treat
ment should focus on maintaining laminar circulation.
477
First and foremost is the volume replacement fluid ther
apy. Frog supports (rubber pads or other suitable mate
rial) should be placed on the feet, and the stall bedding
made deep and soft. The application of glyceryl trini
trate cream ( nitroglycerine) to the coronary area has
been shown to increase digital blood flow in both nor
mal and laminitic feet; a thin coating of a 2% cream of
nitroglycerine in a band 2. 5 cm wide around the limb
can be applied once or twice daily to an area of skin
starting at the coronary band. In recent studies, the use
of isoxsuprine has not been shown to have a clinical
effect because of low bioavailability and therefore is no
longer recommended. If laminitis has developed, the
treatment must be aggressive and instituted without
delay (see Chapter 1 1 ) .
Acute diarrhea i n adult
horses - other causes
TJ Divcrs
There are many causes of acute diarrhea in adult horses
other than salmonellosis, clostridiosis, ehrlichiosis, can
tharidin toxicosis, cyathostomosis (see Chapter 21 ) ,
and non-steroidal anti-inflammatory toxicity. A review
of a computer generated (Consultant*) list of all
reported causes of diarrhea in adult horses revealed
more than 30 causes. The great majority of these are
rare and will not be discussed here but can be found on
Consultant.
ALbb
Toxic causes of acute diarrhea include excessive salt
ingestion, accidental administration of propylene gly
col, excessive administration of linseed oil > 1 ml/kg)
or even mineral oil, nicotine ingestion and organophos
phate toxicity. Toxins that more commonly cause other
organ system failure and/ or acute death, but which may
cause diarrhea, include monensin, foxglove, heavy
metal, or castor bean toxicosis. Toxins that may cause
diarrhea in grazing horses are found in tall fescue grass
(Festuca arundinacea) contaminated with endophytic
fungus (Acremonium coenophialum) and slaframine toxin
(Rhizoctonia legminicola) , most commonly found as
*Consultant on-line database, White, M E, College of
Veterinary Medicine, Cornell University, Ithaca, ^.
www,_J,LOmc.0upH8uIHI
black mold on clover. Both of these toxins are more
commonly associated with clinical signs other than diar
rhea - fescue fungus is associated with agalactia and
clover fungus with excessive salivation.
Hoar alyssum (Berteroa incana) , a member of the
mustard family, may cause diarrhea, fever, and limb
edema in horses either grazing the plant or consuming
alfalfa hay contaminated with large amounts of the mus
tard plant. Berteroa incana is most commonly found in
the northern United States and southern Canada.
Horses will rarely ingest acorns, oak leaves, or oak buds
but if ingested, diarrhea and subcutaneous edema may
occur. Acute renal failure is uncommon in horses after
acorn ingestion. Other dietary causes of acute diarrhea
include sand, rapid changes in forage, especially lush
grass or green hay, and ingestion of large amounts of
highly fermentable carbohydrates. Diarrhea and oral
ulcers have also been reported in horses ingesting
Quassia amar (Simarubaceae) wood chips.
Ub
Drug administration may be another cause of acute
diarrhea in adult horses. Antibiotics may occasionally
calise diarrhea without causing c1ostridiosis, although
this is rare in the adult horse. This may occur from the
disruption of normal flora which may cause abnormal
colonic fermentation and changes in volatile fatty acid
concentrations and/or osmolality of the colonic
ingesta. Neomycin may cause intestinal mucosal dam
age when given in suffcient quantities or for prolonged
periods. Misoprostol and chenodeoxycholic acid are
secretagogues causing active secretion of chlorine and
bicarbonate ions and passive eflux of sodium, potas
sitlm, and water into the intestinal lumen, and which
may cause diarrhea. Any hypertonic drug given per os
has the potential to cause diarrhea via either osmotic
laxative effect or activation of the gastric/colic reflux.
Dioctyl sodium sulfosuccinate (DSS) may produce diar
rhea via several mechanisms, including intestinal
mucosal damage.
bMMb MbbMML NLY
Acute diarrhea may also occur in association with
deranged motility. This may be the result of peritonitis
(see Chapter 1 7) , gastric ulcers, colonic displacement,
drug administration, or organophosphate toxicit.
Gastric ulcers are infrequently associated with diar
rhea in adult horses. In these cases the mechanism to
explain the diarrhea is unknown, but it may involve a
gastrocolic or gastroenteric reflex causing increased
ACUTE DIARRHEA 20
fluid secretion into the large colon. This reflux is medi
ated by afferent neural receptors in the gastroduodenal
mucosa. Proximal duodenitis/jejunitis and gastric
administration of hypertonic fluids (e. g. magnesium
sulfate) are other conditions or treatments that may
cause diarrhea by stimulating this reflex.
Colonic displacements generally cause abdominal
pain and abdominal distension, but in a rare case, may
present with acute or subacute diarrhea. Some horses
develop acute diarrhea almost immediately after receiv
ing intravenous antibiotics. These include ery
thromycin, which is thought to stimulate motilin
receptors and intravenous penicillin (idiosyncratic) .
Tapeworm infections, Anoplocephala spp. are known to
affect ileocecal motilit and may cause colic and/ or pas
sage of loose stool. Massive exposure of the immuno
logically naive horse to large strongles may cause colic
and diarrhea, although this is more common in foals
(acute strongyle syndrome) .
MLbML MfbLMb
Additional bacterial, fungal, and viral agents that may
cause diarrhea include Aeromonas spp. , Mycobacteum
avium, Aspergllus spp., and rarely Histoplasma spp.
Aeromonas spp. have recently been incriminated as a
cause of acute diarrhea in horses. In a relatively large
study, the organism was found in the feces of 55 per
cent (22 of 40) horses with diarrhea and was not iso
lated from any of the 34 control horses. Salmonella spp.
were found in some of the aeromonas-positive horses,
and c1ostridiosis was not evaluated, making it only spec
ulation that the Aeromonaswas the cause of the diarrhea.
Aeromonas spp. , a gram-negative rod, commonly found
in the water and soil, may be a primary cause of acute
diarrhea in horses or it may just be more frequently iso
lated in equine diarrheic feces. Aeromonas spp. have
been incriminated as a cause of diarrhea in humans.
Strains producing virulence-associated adhesions, cyto
toxin, enterotoxin, or with invasive properties are
believed to be potential pathogens. Gastroenteritis asso
ciated with Aeromonas spp. is reported to be most com
mon in humans and horses in the summer months, and
it has been suggested that the infection may occur from
contaminated drinking water. Aeromonas spp. are gener
ally susceptible to enrofloxacin, gentamicin, and
amikacin.
Mycobacterum avium has been infrequently docu
mented as a cause of diarrhea in horses. Chronic weight
loss and chronic diarrhea are the most common pre
senting signs with M. avium. Granulomatous enterocol
itis and hepatitis with mesenteric lymphadenopathy are
the characteristic lesions.
47
MbFbLLbb
Aspergillus colitis is well documented in horses. In vir
tually all cases, the Aspegllus sp. is a secondary invader,
following a toxic or infectious colitis and broad-spec
trum antibiotic administration. When fungal colitis
occurs, it will often disseminate to the lungs or other
organs and the prognosis is extremely grave.
LMFMY
General princi ples of treatment of acute
diarrhea in adult horses
Brooks H W, Hall G A, Wagstafs A], Mitchell A R ( 1 998)
Detrimental effect on villus form during conventional
oral rehydration therapy for diarrhea in calves; alleviation
by a nutrient oral rehydration solution containing
glutamine. Vet.J 155( 3) : 263-74.
Ecke P, Hodgson D R, Rose R] ( 1998) Induced diarrhea in
horses Part 2: Response to administration of oral
rehydration solution. VetJ 1 55: 161-70.
Salmonellosis
Cohen N D, Martin L], Simpson R B ( 1996) Comparison of
polymerase chain reaction and microbial culture for
detection of salmonella in equine feces and
environmental samples. Am. J Vet. Res. 57(6) : 780-786.
Hartmann F A, Callan R], McGuirk S M, West S E H ( 1 996)
Control of an outbreak of Salmonellosis caused by drug
resistant Salmonella anatum in horses at a veterinary
hospital and measures to prevent future infections.J Am.
Vet. Med. Assoc. 209(3): 629-31 .
Parraga M E, Spier S], Thurmond M, Hirsh D ( 1997) A
clinical trial of pro biotic administration for prevention of
Salmonella shedding in the postoperative period in horses
with colic. J Vet. Inte. Med. 1 1 ( 1 ) :36-41.
Spier S
.
I ( 1993) Salmonellosis. Vet. Clin. ^ Am. J'quine Pract.
9( 2) : 385-94.
Clostridial diarrhea in adult horses
Baverud V, Franklin A, Gunnarsson A, et al. ( 1 998) Clostrdial
difcil associated with acute colitis in mares when foals are
treated with erythromycin and rifampicin for Rhodococcus
equi pneumonia. Equine Vet. J 30(6) :482-8.
Donaldson M T, Palmer.I E ( 1 999) Prevalence of Clostridium
perfringens enterotoxin and Clostridium difcile toxin A in
feces of horses with diarrhea and colic. J Am. Vet. Med.
Assoc. 215(3) :358-61 .
Herholz C, Miserez R, Nicolet], et al. ( 1 999) Prevalence of
beta-2 toxigenic Clostridium perfringens in horses with
intestinal disorders. J Clin. Micrbiol. 37(2): 358-61.
.lang S S, Hansen L M, Breher.I E, et al. ( 1997) Antimicrobial
susceptibilities of equine isolates of Clostridium dicil and
molecular characterization of metronidazole-resistant
strains. CZin. Infect. Dis. Sep. 25 supp!. 2:S266-7.
Potomac horse fever
Barlough.l E, Reubel G H, Madigan] E, et al. ( 1998)
Detection of Ehrlichia risticii, the agent of Potomac horse
474
fever, in freshwater stream snails ( Pleuroceridae: Juga
spp.) from northern California. Appl. Environ. Microbial.
64:8.
Biswas B, Mukherjee D, Mattingly-Napier B L, et al. ( 1991 )
Diagnostic application of polymerase chain reaction for
detection of Ehrlichia risticii in equine monocytic
ehrlichiosis ( Potomac horse fever) . J Clin. Microbial. 29: 10.
Dutta S l,Vemulapalli R, Biswas B ( 1 998) Association of
defciency in antibody response to vaccine and
heterogeneity of Ehrlichia risticii strains with Potomac
horse fever vaccine failure in horses. J Clin. Microbial. 36:2.
Long M T, Goetz T E, Whiteley H E, et al. ( 1 995)
Identifcation of Ehrlichia risticii as the causative agent of
to equine abortions following natural maternal infection.
J Vet. Diagn. Invest. 7:201-5.
Palmer
.
l E ( 1993) Potomac horse fever. Vet. Clin. N Am.
Equine Pract. 9: 2.
Pusterla N, Chase
.
l S, ]ohnson E, et al (2000) Potomac horse
fever: discovery of the ontermediate and defnitive host of
the helminithic vector of Ehrlichia risticii. Proc 1Annual
ACVMForum
Pusterla N, Leutenegger C M, Sigrist B, et al (2000) Detection
and quatifcation of Ehrlichia risticii genomic DNA in infected
horses and snails by real-time PCR. Vet. Parasitol. 90:1-2
Pusterla N, Madigan] E, Chae] S, et al (2000) Helminthic
transmission and isolation of Ehrlichia risticii, the causative
agent of Potomac horse fever, by using trematode stages
from freshwater stream snails .
.
f. Clin. Micrbiol. 38:3.
Reubel G H, Bariough] E, Madigan] E ( 1 998) Production
and characterization of Ehrlichia risticii, the agent of
Potomac horse fever, from snails ( Pleuroceridae: Juga
spp.) in aquarium culture and genetic comparison to
equine strains. J Clin. Microbiol. 36:6.
Wen B, Rikihisa Y, Yamamoto S, et al. ( 1 996) Characterization
of the SF agent, an Ehrlichia sp. isolated from the fluke
Stellantchasmusfalcatus, by 1 6S rRNA base sequence,
serological, and morphological analyses. Int. J Syst.
Bacterol. 46: 1 .
Non-steroidal anti-inflammatory drug toxicity
Griswold D E, Adams] L ( 1 996) Constitutive cyclooxygenase
(COX-I) and inducible cyclooxygenase (COX-2) : rational
for selective inhibition and progress to date. Medicinal Res.
H. 16 (2) : 1 81-206.
Johnston S A, Fox S M ( 1997) Mechanisms of action ofanu
inflammatory medications used for treatment of
osteoarthritis.J Am. Vet. Med. Assoc. 210(10) : 14861492.
MacKay R.I, French T W, Nguyen H T, Mayhew I G ( 1983)
Effects of large doses of phenylbutazone administration to
horses. Am .
.
f. Vet. Rs. 44 (5) : 774-780.
McCarthy D M ( 1995) Mechanisms of mucosal injury and
healing: the role of non-steroidal anti-inflammatory drugs.
Scand. J Gastroenterol. 30 supp!. 208: 24-29.
Snow D H, Douglas T A, Thompson H, Parkins.l], Holmes P
H ( 1981 ) Phenylbutazone toxicosis in equidae: a
biochemical and pathophysiological study. Am . .f. Vet. Res.
42 ( 10) : 1 754-1759 .
Toxic colitides
Helman R G, Edwards W C ( 1 997) Clinical features of blister
beetle poisoning in equids: 70 cases ( 1983-1996) . J Am.
Vet. Med. Assoc. 2 1 1 : 1018-21 .
Schmitz D G ( 1989) Cantharidin toxicosis in horses . [ Vet. Int.
Med. 3:208-15.
Smith B P (ed) ( 1990 and 1996) Large Animal Intemal Medicine
( 1st and 2nd edns) . C V Mosby, St Louis.
Acute diarrhea in adult horses - other causes
Dave B, Rubin W ( 1999) Inhibition of gastric secretion
relieves diarrhea and postprandial urgency associated with
irritable bowel syndrome or functional diarrhea. Dig. Dis.
Sci. 44(9) : 1 893-8.
LUc |KKHL 20
Freeman D L, Ferrante P L, Palmer] L ( 1 992)
Comparisons of the effects of intragastric infusions of
equal volume of water, dioctyl sodium sulfosuccinate,
and magnesium sulfate on fecal composition and
output in clinically normal horses. Am. ]. Vet. Res.
53(8) : 1 347-53.
Hathcock T L, Schumacher], Wright], Stringfellow] ( 1999)
The prevalence of Aeomonas species in feces of horses
with diarrhea. ]. Vet. Int. Med. 1 3: 357-60.
47b
21
Chronic diarrhea
Differential diagnosis and
evaluation of chronic
diarrhea in the adult horse
T Mair
INTRODUCTION
Chronic diarrhea occurs sporadically in horses and is a
relatively uncommon clinical syndrome. In the adult
horse, chronic diarrhea is almost invariably associated
with large intestinal (cecal and colonic) disease, caused
either by physical damage to the colonic wall or physio
logical disturbances of colonic function. Unfortunately,
from a diagnostic viewpoint, most of the different
diseases that can result in chronic diarrhea can present
with very similar clinical and clinicopathological fnd
ings. In addition, many of the causes and mechanisms
of chronic diarrhea are poorly understood. For these
reasons, horses affected by chronic diarrhea are often
diagnostic and therapeutic challenges. A defnitive
diagnosis of the cause of chronic diarrhea will be
achieved in only 60-70 per cent of cases, and in many of
these the diagnosis will only become apparent following
The clinical signs associated with diseases causing
chronic diarrhea are summarized in Table 21.1.
diarrhea - variable consistency
- persistent or recurrent
pyrexia
inappetence
depression
weight loss
subcutaneous edema
colic (chronic or recurrent)
To be considered 'chronic' diarrhea will have been
present for at least 7-14 days. In many cases the diarrhea
will persist for weeks or months. The nature of diarrhea
varies from case to case and may vary over time in indi
vidual cases. Some diseases causing chronic diarrhea will
present with recurrent bouts of diarrhea separated by
periods of relatively normal fecal consistency. Feces may
vary from soft ' cowflop' or 'cowpat' consistency to watery
diarrhea. Fiber content of feces is variable.
Rectal temperature, heart rate, and respiratory rate
are frequently normal. However, pyrexia (persistent or
intermittent) may be present in some inflammatory
diseases such as larval cyathostomosis, peritonitis, sand
enteropathy, and some cases of gastrointestinal neopla
sia. Other signs of systemic illness such as depression and
427
inappetence may also accompany these diseases. Weight
loss may occur in many of the diseases, but may be absent
in some, especially those caused by motility abnormali
ties or other physiological disturbances of colonic func
tion. Peripheral subcutaneous edema (especially ventral
abdominal) is commonly present due to hypoprotein
emia caused by protein-losing enteropathy.
DIFFERENTIAL DIAGNOSIS
The more common causes of chronic diarrhea are
listed in Table 2l.2.
Cyathostomosis
Mixed strongyle infections
Peritonitis
Inflammatory bowel
diseases
NSAID toxicity
Salmonellosis
Chronic liver disease*
Sand enteropathy
- granulomatous enteritis
colitis
- Iymphocytic-plasmacytic
enteritis/colitis
- eosinophilic enteritiscolitis
Chroni non-specific colitis
Idiopathic colonic dysfunction
Giardiasis**
*chronic diarrhea Is a rare manifestation of chronic liver
disease
**giardiasis is of questionable significance as a cause of
diarrhea
EVALUATION OF CHRONIC DIARRHEA
Thorough and repeated clinical and laboratory evalua
tions are often required to diagnose the cause of
428
Clinical history
Management, nutriion, parasite control
Signalment
Phyical examination
Hematology and plasma fibrinogen
Serum biochemistry
Serum protein electrophoresis
Abdominocentesis
Fecal examinations - worm egg count
examination for larvae
other parasitological
examinations
white blood cells
baceriology
Sugar absorption tests
Rectal biopsy
Ultrasonography
Exploratory surger and bowel wall/olonic lymph
node biopsies
chronic diarrhea, but even after exhaustive tests the
clinician and owner of an afected horse should be
aware that a defnitive diagnosis may not be attainable.
Some of the important components of the examination
of affected horses are summarized in Table 2l.3. A a
general rule, horses with chronic diarrhea but with no
weight loss, normal plasma albumin levels, and no other
overt clinical signs, are likely to have no pathological
lesions identifiable (even at post-mortem examination).
Clinical history, management, nutrition, and
parasite control
A full clinical history and evaluation of management
and nutrition are important. These aspect are dis
cussed more fully in Chapter 18, Diferential diagnosis
and evaluation of chronic weight loss. The history relat
ing to routine parasite control measures applied to the
horse (and other in-contact horses) should also be
assessed (see Chapter 4), bearing in mind the tendency
of many owners to answer questions about parasite con
trol in terms of what they believe should be done rather
than what is actually done!
Signalment
Age can be useful in assessing the likelihood of a partic
ular disease being present. For example, larval cyatho
stomosis is most common in horses less than 5 years of
age, whereas chronic inflammatory bowel diseases and
intestinal neoplasia are most common in older horses
(over 10 years of age) .
Although there are virtually no characteristic physical
findings of individual diseases causing chronic diar
rhea, a full and detailed physical examination should
always be undertaken. Physical examination of the large
intestine is restricted to abdominal auscultation and
percussion, transabdominal ballottement, and trans
rectal palpation. Borborygmi may be heard more fre
quently than normal as a result of increased motility of
the large bowel caused by irritation or inflammation.
Sand in the large intestine can sometimes be detected
by auscultation behind the xiphoid.
The rectal examination is the most useful physical
examination technique for assessing the large intestine
(see Chapter 1). The primary objective of the rectal
examination is to assess the size, consistency, and posi
tion of segments of the large intestine. Evaluation of the
wall thickness and texture, the mesenteric structures
(blood and lymphatic vessels, and lymph nodes), and
other organs (such as the spleen) may also be helpful in
diagnosing the cause of chronic diarrhea.
Hematology and plasma fibrinogen
Hematological changes occurring in diseases of the large
intestine are frequently non-specific, but are helpful
all the same in evaluating cases of chronic diarrhea.
Neutrophilic leukocytosis, with or without hyperfbrino
genemia, is commonly seen in chronic inflammatory and
neoplastic conditions of the large intestine. Neutrophilia
is also frequently seen in cases of larval cyathostomosis.
Anemia may be present in chronic inflammatory and
neoplastic conditions. Hemoconcentration, with an
increase in packed cell volume (PCV) may occur if the
horse is dehydrated, but this is less likely in chronic as
compared with acute diarrhea.
Serum biochemistry and serum protein
electrophoresis
Electrolyte losses (especially sodium, potassium, cal
cium, and bicarbonate) may occur as a result of severe
CHRONIC DIARRHEA 21
diarrhea, but are less likely in chronic diarrhea than in
acute colitis. Plasma protein levels vary depending on
the degree of gastrointestinal loss of albumin and
globulin. Hypoproteinemia and hypoalbuminemia are
common in chronic enteropathies, and may be accom
panied by reduced, normal, or elevated globulin levels.
Serum protein electrophoresis is sometimes useful for
differentiation of parasitic colitides from other
enteropathies. Serum alkaline phosphatase (in particu
lar the intestinal isoenzyme of alkaline phosphatase)
may become elevated in chronic enteropathies. The
degree of abnormality in the levels of total protein,
albumin, and alkaline phosphatase relate to the severit
of the chronic enteropathy, and can be helpful, to a
limited extent, in predicting prognosis. Elevated liver
enzymes are indicative of liver damage which can some
times cause chronic diarrhea; further assessment of
liver function (e.g. bile acids) and liver biopsy should be
considered to more fully evaluate the nature of the
disease in such cases (see Chapter 19).
Abdominocentesis
Examination of peritoneal fluid is most useful in diag
nosing peritonitis and some cases of intestinal neoplasia
(see Chapters 2 and 17).
Fecal examination
Gross examination of the feces can provide informa
tion about digestion and transit time in the large
intestine. Increased fecal particle size, especially the
presence of large fber particles, with loose or watery
stool is suggestive of poor mastication, poor colonic
digestion or decreased colonic transit time. Feces con
taining sand or gravel are not necessarily abnormal,
but a large amount of sand implies that significant
quantities of sand may be present in the colon. The
presence of blood in the feces implies hemorrhage
into the distal colon, this may occur with some inflam
matory conditions involving the small colon or rectum;
frank hemorrhage observed following rectal examina
tion should alert the clinician to the possibility of a
rectal tear (see Chapter 16). Cyathostome larvae may
be identified by the naked eye in the feces of horses
affected by laral cyathostomosis, especially if the lar
vae are alive and moving. In other cases, microscopical
examination of a wet smear of feces may be required
to identif larae.
Cytological examinations are used mainly for para
sitological evaluation (see Chapter 4). Examination
for cyathostome larvae, and eggs of small and large
strongyles, tapeworms, and roundworms is helpful if a
parasite-associated disease is suspected. Coccidia and
429
Cryptosporidia spp. are occasionally observed, but in
most cases are not considered to be pathogenic.
Tests for occult blood are used to detect mucosal
inflammation. These tests detect not only occult blood
but also degraded blood. A positive test indicates sig
nifcant hemorrhage into the gastrointestinal tract, but
the source and amount of hemorrhage within the tract
cannot be determined. However, the test can prove
negative even in the presence of signifcant hemor
rhage into the proximal gastrointestinal tract because
of extensive degradation of the blood in the lower
intestinal tract.
Examination for fecal inflammatory cells (white
blood cells) has been used to assess the presence of
inflammatory lesions in the bowel. This test is more
likely to be positive in horses with acute enterocolitis
than in chronic enteropathies. However, the presence
of large numbers of fecal white blood cells is indicative
of an inflammatory lesion, and suggests that the lesion
is located in the distal gastrointestinal tract.
Fecal cultures are important in the evaluation of
horses with acute colitis but are less important in
chronic diarrhea. Salmonella spp. may be cultured from
horses affected by chronic diarrhea, but there is likely
to be another underlying cause of the diarrhea.
Ultrasonography
Ultrasonography is complementary to rectal examina
tion and can be helpful in the evaluation of chronic
diarrhea. Abnormalities that may be identifed in
horses affected by chronic diarrhea using transcuta
neous and/or transrectal ultrasonographic examina
tions, include peritoneal effusion, masses and abscesses,
and increased bowel wall thickness (see Chapter 2).
Biopsy and exploratory surgery
Rectal mucosal biopsies are easily and safely obtained
(see Chapter 2) and are sometimes diagnostic in cases
of chronic enteropathy. However, for a diagnostic yield
from this procedure, the pathological lesions must
extend to the rectum, and in most cases of chronic
enteropathy the rectum is not affected; diagnostically
useful information can be expected in only about one
third of cases of chronic enteropathy. Full-thickness
bowel wall biopsies of the cecum and large colon, and
associated lymph nodes, are more likely to be diagnosti
cally useful, but attaining such biopsies is only possible
via a surgical approach (flank or ventral midline
approach). Laparoscopy offers a safer and easier tech
nique for observing the dorsal surfaces of the cecum
and large colon in a standing patient, and direct biopsy
of abnormal masses and colonic lymph nodes can be
achieved by this method.
430
General principles of
treatment of chronic
T Mair
INTRODUCTION
A in acute colitis and diarrhea, chronic diarrhea can
result in signifcant lumenal loss of fluid, electrolytes, and
protein. Since the precise causes of chronic diarrhea are
frequently difcult to establish, specifc treatments are
often not possible. Horses with chronic diarrhea often lose
weight as a result of chronic protein loss, and euthanasia
may become necessary on humanitarian grounds.
FLUID AND ELECTROLYTE THERAPY
The rate of fluid administration depends upon the
severity of dehydration. This can be determined by
examining the
dryness of mucous membranes
skin turgor
speed of distention of the jugular vein when
compressed
PC
blood urea nitrogen (BUN).
Fluid replacement should include
volume replacement (percent dehydration x body
weight in kg = liters needed)
maintenance needs (60-100 ml kg-I dayl)
ongoing losses that are variable, depending upon
the degree of dehydration.
The principles of fluid and electrolyte therapy are
discussed in greater detail in Chapter 20.
Dehydration is often not a major problem in animals
affected by chronic diarrhea, and these horses may
compensate for persistent increased fecal fluid loss by
increased water consumption. Nevertheless, free access
to water and electrolyte solutions should be available.
Intravenous or oral fluid therapy, and treatment of
acid-base disturbances should be administered as
necessary (see Chapter 20).
PLASMA THERAPY
Intestinal diseases that cause chronic diarrhea com
monly involve loss of plasma proteins into the intesti-
nal lumen with resulting hypoproteinemia and hypo
albuminemia. These horses may beneft from plasma
transfusions. Plasma or colloid infusions are particu
larly important in horses that are dehydrated and are
receiving intravenous fluid therapy (see Chapter 20),
since the low oncotic pressure caused by hypoprotein
emia may result in sequestration of administered fluid
into tissue spaces, thereby worsening tissue edema and
predisposing to multi-organ failure. Plasma transfu
sions are indicated when the total plasma protein con
centration falls to 50 gil (5.0 g/dl) or less, or the
plasma albumin concentration is 15 gil (1.5 g/dl) or
less. Initially 5-10 liters of either commercially avail
able plasma or cross-matched plasma from a donor
should be administered intravenously. The effect of a
single intravenous dose of plasma is short-lived and
multiple transfusions (in combination with other treat
ments) are likely to be necessary to result in a sus
tained increase in the measured total plasma protein
and albumin concentrations.
ANTHELMINTICS
Anthelmintics are indicated in all cases where a para
sitic etiology is suspected. Even in horses with chronic
diarrhea where no specifc diagnosis is reached,
anthelmintic therapy should be considered. Larvicidal
doses of anthelmintics suitable for the treatment of
confirmed or suspected cases of strongyle-associated
disease include
ivermectin
moxidectin
fenbendazole
oxfendazole
ANTIBIOTICS
0.2 mglkg p.o.
0.4 mg/kg p.o.
7.5 mglkg p.o. for 5 consecutive
days
10-50 mg/kg p.o.
Oral antibiotics are generally contraindicated in cases
of chronic diarrhea since they may either cause or
worsen a colonic microflora imbalance, thereby wors
ening the diarrhea. Salmonella spp. are not considered a
m,or cause of chronic diarrhea and, even in cases
where they are isolated, another underlying cause of
diarrhea may be present. However, a small percentage
of horses with chronic diarrhea do appear to improve
with antibacterial therapy using potentiated sulfon
ami des or metronidazole (the reason for this is uncer
tain). Antibiotics are indicated in horses with chronic
diarrhea due to peritonitis (see Chapter 17).
CHRONIC DIARRHEA 21
TRANSFAUNATION
Transfaunation using cecal contents or fresh feces from
a normal horse has been used as a treatment of horses
with chronic diarrhea in an attempt to replace some of
the normal bacterial flora in the colon. Unfortunately
there are no controlled studies of the technique and
reports of its successful use are anecdotal only.
Transfaunation can be achieved by introducing the
material via stomach tube or directly into the cecum via
laparotomy. Fecal slurry should be obtained from a nor
mal horse that is negative for Salmonella spp. on culture.
Fresh cecal contents obtained at euthanasia provide
higher numbers of bacteria. The suggested dose is 5-6
liters of fluid repeated for 2 or 3 treatments.
PROBIOTICS
The use of products that contain Lactobacillus spp. is
frequently recommended in the treatment of chronic
diarrhea in adult horses. Although they probably cause
no harm they are also of no proven beneft.
MOTILITY MODIFYING AGENTS AND
ANTISECRETORY DRUGS
A variety of drugs have been suggested to try to 'slow'
the intestines or promote development of a more
formed stool
codeine phosphate (1-3 mg/kg p.o. once or twice a
day to effect) has proven useful as a non-specifc
treatment of chronic diarrhea in adult horses
loperamide (0.04-1.6 mg/kg p.o.) may be used in
non-infectious diarrheal conditions, its primary
beneft could be an antisecretory efect
phenoxybenzamine has an anti-secretory effect but
should not be used because of its hypotensive
effect.
INTESTINAL PROTECTANTS AND
ADSORBENTS
Bismuth subsalicylate (up to 4 1/500 kg q. 12 h) may
have antidiarrheal, antibacterial and anti-inflammator
properties but is relatively inefective in diarrhea in the
adult horse. Kaolin and pectin should not be used in
severe diarrhea as they may worsen malabsorption and
increase ion loss during diarrhea. Activated charcoal
has been used (0.5 kg/500 kg) in acute equine colitis,
but is relatively ineffective in chronic diarrhea.
431
OTHER TREATMENTS
Iodochlorohydroxyquin (5-10 g p.o. s.i.d.) is helpful in
a small number of horses with chronic diarrhea. The
mechanism of action of the drug is unknown, but it may
involve a change in the colonic microflora. The drug
may also have antiprotozoal activit but there is very lit
tle evidence to suggest that this is important in relation
to the treatment of chronic diarrhea in the adult horse.
NUTRITIONAL SUPPORT
Horses with chronic diarrhea and protein-losing
enteropathy benefit from additional protein in the diet.
Often these horses are also in a state of energy, mineral,
and vitamin malnutrition. They should be fed alfalfa
hay ad lib., as well as a high protein-energy concentrate,
a mineral supplement providing calcium, magnesium,
zinc, copper, and iron, and fat and water-soluble vita
mins. Some horses with chronic diarrhea beneft from
being turned out to grass; this may promote normaliza
tion of gastrointestinal flora. Any change of diet should
be gradual. Gradual change from high roughage to low
roughage, or occasionally vice versa, may cause the stool
to normalize in a few horses with idiopathic chronic
diarrhea.
Larval cyathostomosis
0111
TMair
INTRODUCTION
In recent years larval cyathostomosis has become an
increasingly common problem in many areas of the
world. The increasing prevalence of the disease is asso
ciated with an increased prevalence of cyathostomes in
grazing horses. The cyathostomes are now ubiquitous
parasites, and virtually all grazing horses in temperate
areas are assumed to be infected by them. This
increased prevalence of cyathostomes has occurred
over the last 30 years since the introduction and wide
spread use of interval treatment with broad-spectrum
anthelmintics such as benzimidazoles, pyrantel, and
ivermectin. Interal treatment using these drugs has
been highly effective at reducing the prevalence of
large strongyles such as Stronglus vulgaris, but it is rela
tively ineffective at controlling the cyathostomes. Even
in well-managed horses, cyathostome infection is likely
432
and is probably responsible for subclinical production
losses that are difcult to quantif. When the parasite
burden becomes high, overt clinical disease is more
likely to be manifested, particularly in young horses.
The most clearly defned disease syndrome associ
ated with cyathostome infection is the acute diarrheal
syndrome called larval cyathostomosis (previously
known as laral cyathostomiasis or acute laral cyatho
stomiasis), that occurs most typically in young adult
horses in the winter. However, a number of other
clinical syndromes associated with these parasites have
been recognized, including the following
recurrent diarrhea in older and aged horses and
ponies
rapid weight loss and peripheral edema without
diarrhea
chronic weight loss and ill-thrift
seasonal (late autumn to spring) 'malaise
syndrome'
non-specifc colic
cecocecal and cecocolic intussusceptions
non-strangulating intestinal infarction
weight loss with or without diarrhea in weanlings
during the autumn.
There may be some overlap between these diferent
clinical presentations in individual cases.
ETIOLOGY AND PATHOGENESIS
The cyathostomes (or small strongyles) comprise a
large group of eight genera and over 40 species of
nematode parasites (see Chapter 4). The potential role
of different species in causing different clinical mani
festations is at present unclear. The parasites have a
direct life cycle, with adults laying eggs that pass out in
the feces and contaminate the pasture. In temperate cli
mates (including the UK, most of continental Europe,
and the northern half of the US) the eggs hatch within
about I week during the summer, but hatching and
development are delayed during colder times of year.
In southern temperate zones (the southern half of the
US), hatching of larvae occurs rapidly all year round,
although the larae do not survive long during hot dry
weather. Moisture and oxygen are essential for hatch
ing and development, but levels of these are usually
adequate in the fecal pile. Infective third-stage larae
cannot ingest nutrients so they survive on the pasture by
consuming limited, intracellular energy reseres. The
duration of their survival is inversely proportional to the
environmental temperature because they utilize their
energy reseres faster in hot weather. The environmen
tal constraints on the cyathostome life cycle result in
Spring
Summer
Autumn
Winter
+++ excellent
++ good
+ fair
Northern temperate areas
Development Persistence
+++ +++
++ +
+++ +++
+++
patterns of transmiSSIOn that are seasonal and pre
dictable. These patterns of cyathostome development
and persistence on the pasture in different geographi
cal locations are summarized in Table 21.4.
The pre-infective frst stage larvae (Ll) develop in
the presence of warmth and moisture via second stage
larvae (L2) to infective third stage larae (L3) that are
eaten by grazing horses. In the gut, the infective larvae
exsheath in the small intestine and invade the wall of
the cecum and large colon. Within the mucosa and sub
mucosa the L3 become surrounded by a fbroblastic
cyst, and either develop into fourth stage larvae (L4) or
enter a state of arrested larval development (also called
hypobiosis or inhibited larval development). At some
stage, the encysted L4 break out of the cyst and migrate
back to the lumen of the cecum and colon where they
develop into ffth stage larvae (L5) and eventually egg
laying adults. Early L3 undergoing arrested larval devel
opment may remain in this state for a few months to
several years. The signal or stimulus for these larvae to
resume their development is unclear, although climatic
conditions seem to be important. In addition there is
evidence that anthelmintic therapy which removes the
population of adult cyathostomes from the lumen, and
stressful conditions (such a travelling or change of
premises, parturition, etc.) can also stimulate resump
tion of development of these larvae and precipitate
clinical disease.
Cyathostome-associated diseases have traditionally
been attributed to the synchronous emergence of large
numbers of previously inhibited L3 and L4 stages from
the cecal and colonic walls, thereby leading to physical
disruption of the mucosa and resultant tphlitis and
CHRONIC DIARRHEA
Southern temperate areas
Development Persistence
++ ++
++ ++
+ +
21
colitis. Gross lesions in the wall of the cecum and large
colon are characterized by generalized inflammation,
mucosal edema, and ulceration. The inflammation
probably results in diarrhea as a result of increased
active and passive secretion of fluid, electrolytes, and
protein. Protein loss can be severe, resulting in pro
found hypoproteinemia and hypoalbuminemia. Altera
tions in intestinal motility may occur as a result of larval
migration, and this may also be important in the patho
genesis of diarrhea and colic that can occur in cyathos
tome infections. In addition, there is the possibility that
the larvae themselves may release substances or stimu
late local host cells to release mediators that cause vaso
constriction and mucosal edema, thereby adding to the
pathological effects.
The intensity of cyathostome infection may be an
important factor in determining the nature and severity
of the clinical disease. Thus, mild infections might be
more likely to produce clinical signs of 'malaise
syndrome', recurrent diarrhea, or non-specifc colic,
whereas heavy infections may cause acute, severe diar
rhea and rapid weight loss, or colic caused by cecal intus
susceptions or non-strangulating intestinal infarction.
In addition to the pathological damage caused by
emerging larvae, mucosal larval penetration by infective
L3 may be important as a cause of disease. Reduced
weight gain, altered protein metabolism, and transient
neutrophilia have been recognized within the frst 46
weeks of experimental 'trickle' cyathostome infections.
This disease process may be particularly important in
weanlings grazing contaminated pasture during the late
summer to autumn, when pasture larval counts may be
very high.
433
EPIDEMIOLOGY
Diseases associated with acute larval cyathostomosis
typically occur in young adult horses (1-6 years of age)
during the winter to early spring (November to April in
northern temperate climates). The disease tends to be
sporadic, although multiple cases may occur in similarly
aged horses managed together. Factors that increase
the risk of high cyathostome burdens in horses include
overstocking and use of permanent horse pastures
poor parasite control methods applied to young
grazing horses
failure to use routine larvicidal anthelmintics with
activity against arrested cyathostome larae
resistance by cyathostomes to anthelmintics.
Factors that have been associated with the onset of
clinical disease in individual cases include
season, late winter to early spring
recent administration of anthelmintics
stressful situations such as travel, new environment,
parturition, etc.
other diseases, e.g. alimentary lymphosarcoma.
The incidence of larval cyathostomosis is unknown, but
there are many anecdotal reports that suggest an
increasing prevalence in northern temperate zones. In
the UK surveys have shown that cyathostomosis is the
most common cause of chronic diarrhea in adult
horses.
CLINICAL SIGNS
The typical clinical signs of acute larval cyathostomosis
include
sudden onset of profuse diarrhea that becomes
chronic
diarrhea of variable nature ('cowpat' to watery)
diarrhea that may be continuous or intermittent
weight loss - this is often severe and rapid, and may
precede the onset of diarrhea by up to 48 hours
weakness
depression
subcutaneous edema of the limbs, ventral
abdomen, and prepuce
variable signs of colic
abdominal distention due to cecal/colonic tympany
pyrexia.
The disease can affect horses of all ages, but is com
monest in horses less than 6 years of age. The disease
tends to be most severe in the very young and the very
old. In many cases, signs of systemic illness (dehydra-
434
tion, signs of endotoxemia, anorexia, etc.) are not as
marked as in other acute coli tides in the adult horse.
However, in severe cases there may be evidence of
dehydration and acid-base imbalance, and in some
cases the disease may cause apparent 'sudden death'.
DIAGNOSIS
Diagnosis is usually achieved by a combination of some
or all of the following.
Histor and eidemiolog
The history and epidemiology include a combination of
season, age, recent administration of anthelmintics
and the history of parasite control, recent stress, and
concurrent disease.
Fecal examination
Numerous cyathostome larvae may be observed by the
naked eye either in the feces or on the rectal glove fol
lowing a rectal examination. Gently scraping the wall of
the rectum with the fngers during a rectal examination
may yield higher numbers of larvae. Larvae are variable
in their size and appearance depending on which species
are present, some appear white while others are red.
Microscopical examination of a wet preparation of
feces may be necessary to confrm the presence of L4
and L5. Larvae may be difcult to detect in the feces of
some cases, especially if the horse has recently been
treated with an anthelmintic.
Fecal worm egg counts are of little help diagnosti
cally because the disease is caused by the larval stages
of the parasites. However, a high strongyle worm egg
count in either the affected animal or in-contact horses
suggests poor routine parasite control.
Fecal cultures sometimes yield Salmonella spp.
and/ or Camplobacter spp.
Hematological examination
Routine hematological examination usually reveals
leukocytosis and neutrophilia. Some cases may also
show anemia and/ or mild eosinophilia.
Serum biochemistr
Serum biochemistry usually reveals a profound hypo
albuminemia. The total protein concentration may be
low, normal, or even elevated because of variable hyper
globulinemia. Some cases show elevated serum alkaline
phosphatase levels.
Serum protein elctrophoresis
This may show elevated beta-globulin levels and some
times elevated alpha-globulin levels.
Histologcal examination
Histological examination of rectal biopsies is rarely
diagnostic. However, biopsies of the cecum and/or
large colon are likely to show characteristic pathological
changes including edema and eosinophilic inflamma
tion, and possibly the presence of mucosal larvae.
Unfortunately cecal and colonic biopsies can only effec
tively be obtained surgically via a laparotomy.
TREATMENT
Despite the fact that in many cases an accurate diagno
sis of larval cyathostomosis is readily achieved (by
identification of numerous larvae in feces) the disease
carries a high death rate. Successful treatment can be
expected in little more than 40 per cent of severe cases.
Many affected horses appear to survive for several days
or weeks, but then show a rapid deterioration followed
by death. Mild cases treated early in the course of the
disease have a better prognosis.
Treatment consists of
anthelmintics
corticosteroids
fluids and electrolytes
plasma therapy
antidiarrheal agents
nutritional support.
In mild cases, especially if treatment is instituted early,
anthelmintics alone may be successful. However, in
severe cases intensive treatment with other agents will
be required. Even with intensive therapy many cases
die.
Anthelmintics
Fenbendazole, ivermectin, and moxidectin are active
against the mucosal stages of cyathostome larvae. These
agents are more effective against the maturing (as
opposed to inhibited) larvae. For this reason, repeated
doses of anthelmintics are recommended in order to
kill parasites as they develop from an arrested state.
Frequent anthelmintic dosing at 10-14 day intervals on
two to fi ve occasions is advocated. The following larvici
dal doses of these drugs are suggested
fenbendazole 7.5-10.0 mg/kg p.o. s.i.d. for 5 days
ivermectin 0.2 mg/kg p.o.
moxidectin 0.4 mg/kg p.o.
The use of fenbendazole and either ivermectin or
moxidectin in individual cases (alternating treatments)
is used by many clinicians. However, increasing preva
lence of benzimidazole resistance among populations
CHRONIC DIARRHEA 21
of cyathostomes may limit the effectiveness of fen ben
dazole in certain locations. Particular care should be
taken when calculating the dose of moxidectin because
of the increased risk of toxicity with this drug, especially
since many affected horses are in a catabolic state.
Corticosteroids
Corticosteroid therapy has proven beneficial in the
treatment of clinical cases. Dexamethasone (50 Ilg/kg)
administered by intravenous or intramuscular injection
can be given for 1-5 days, followed by oral prednisolone
(l mg/kg p.o.) until the diarrhea has resolved. The
prednisolone is then 'tailed off over the next 7-10 days.
Two potential mechanisms have been attributed to the
beneficial effects of steroids in this disease
1. their anti-inflammatory activit
2. the steroid-induced immunosuppression may
encourage resumption of laral development and
render the parasite more susceptible to the effects
of anthelmintics.
It is important that the potential side effects of corticos
teroid (especially dexamethasone) therapy are recog
nized.
Non-steroidal anti-inflammatory drugs are generally
ineffective in this disease. Their use should be under
taken with extreme caution because of the increased
risk of toxic side effects due to concurrent hypo
proteinemia and dehydration.
Fluid, electrolytes, and plasma therapy
Therapy with intravenous or oral fluids and electrolytes
are often beneficial, and are essential in cases with
clinical dehydration. Guidelines for these therapies are
given elsewhere (see General principles of treatment of
chronic diarrhea in adult horses and Chapter 20,
General principles of treatment of acute diarrhea in
adult horses). Plasma therapy is also benefcial even
though measured plasma albumin will remain elevated
for only a short time.
Antidiarrheal agents
Various antidiarrheal agents have been employed in the
treatment of larval cyathostomosis. Codeine phosphate
(3 mg/kg p.o. t.i.d., adjusted depending on fecal con
sistency) is commonly used. This drug reduces gastro
intestinal secretions and delays intestinal transit, and
has proved to be effective in the control of diarrhea in
adult horses Typically, an improvement in fecal consis
tency is apparent within 48 hours of instituting codeine
therapy, and the dosage can be acusted on an empiri
cal basis thereafter. Side effects can be seen with higher
435
doses of codeine phosphate, including sedation and
predisposition to colonic impaction.
OTHER CLINICAL PRESENTATIONS
Recurrent diarrhea
Bouts of recurrent diarrhea associated with larval
cyathostomosis were frst reported in aged ponies,
although the problem can also occur in other age
groups. Bouts of diarrhea may occur several times a
year, but are most common in the winter and spring.
They are associated with the presence of low numbers
of cyathostome larvae in the feces. In most cases, the
periods of diarrhea respond to anthelmintic therapy.
Weight loss and edema
Rapid and severe weight loss with the development of
subcutaneous edema associated with hypoalbuminemia
may sometimes occur in larval cyathostomosis in the
absence of diarrhea. In some of these cases, diarrhea
will develop at a later stage (days to weeks after the
initial clinical signs). Cyathostome larvae are present in
the feces.
Seasonal malaise syndrome
A seasonal (late autumn to spring) malaise syndrome
has been identifed in adult horses in the UK, and is
believed to be caused by cyathostome infection. This
syndrome is characterized by reduced appetite,
lethargy, and weight loss with variable fecal consistency
(from normal to mild diarrhea). Affected horses
respond to treatment with larvicidal doses of
anthelmintics.
Non-specific colic
Cyathostome infection is being increasingly recognized
as a cause of colic. In one epidemiological study the
effect of different anthelmintic programs on the inci
dence of colic was compared. This study demonstrated
a marked decrease in the incidence of colic on farms on
which effective cyathostome control was achieved com
pared with the incidence recorded on farms where
cyathostome control failed.
Cecocecal and cecocolic intussusceptions
A recent report has described four horses affected by
cecal intussusceptions with clinical and/ or pathological
evidence of concurrent laral cyathostomosis. All four
horses demonstrated a variable number of other signs
of larval cyathostomosis, such as diarrhea, pyrexia,
436
weight loss, and subcutaneous edema, and cyathostome
larae were identifed in the feces.
PREVENTION
Prevention of laral cyathostomosis is dependent on
effective parasite control measures, especially in the
foal and young adult horse. The reader is referred to
Chapter 4 for more information concerning parasite
control.
Strongylosis
T Mair
Equine strongylosis involves mixed infections of large
strongyles (subfamily Strongylinae) and small strongyles
(subfamily Cyathostominae). The large strongyles have
a direct life cycle, with parasitic and free-living stages.
They have been recognized for many years as an impor
tant cause of colic. The small strongyles have increased
in prevalence in recent years and are a major cause of
diarrhea as well as being implicated in the cause of colic
(see Larval cyathostomosis).
The pathogenicity of large and small strongyles is
greatest in young horses. Nearly all grazing horses will
harbor mixed strongyle burdens. Clinical signs that can
be associated with these infections include
colic
ill thrift
weight loss
anorexia
poor hair coat quality
diarrhea
episodes of pyrexia.
However, most infected horses show no overt clinical
signs.
Stronglus vulgaris is the most common of the large
strongyles and is considered to be the most pathogenic.
The pathogenesis of S. vulgaris is the result of thrombo
embolic arteritis of the cranial mesenteric arter and its
major branches. Within 2 weeks of infection infective
larvae penetrate the intestinal mucosa and cause arteri
tis of submucosal and serosal arteries, and a marked
inflammatory reaction. The larvae then migrate up the
intestinal arteries to the cranial mesenteric artery. The
larvae continue to develop in these arteries and pene
trate the intima, causing arteritis of the ileocolic and
associated arteries. Agamous adults develop within 3-4
months and are carried by the blood stream to the
cecum and large colon. Here they form cysts containing
the worms surrounded by necrotic debris and neutro
phils adjacent to thrombosed terminal intestinal arter
ies. The cysts eventually erode through the intestinal
wall to release the adult parasites into the lumen.
The importance of Strnglus vulgars as a cause of
diarrhea in the horse is uncertain. Diarrhea could be
caused by thromboembolic damage to the bowel or dif
fuse vasoconstriction in the intestinal wall, resulting in
inflammatory damage and motility changes.
Diagnosis of strongylosis may be diffcult. Since clin
ical disease is usually caused by the immature, migratory
laral stages of the parasites, the fecal worm egg count is
unreliable. However, a high strongyle fecal worm egg
count does suggest inadequate routine parasite control,
increasing the index of suspicion of strongylosis.
Hematological changes, such as anemia, leukocytosis,
neutrophilia, and eosinophilia, are non-specifc and
unreliable indicators of strongyle larval migration.
Likewise, hypoalbuminemia and hyperbetaglobulin
emia are inconsistent changes that may occur in horses
affected by diarrhea for other reasons.
Although clinical disease is most commonly associ
ated with larval migration, heavy burdens of adult
strongyles can also cause disease characterized by
ill thrift and weight loss
poor performance
anemia
diarrhea
colic.
In these cases the fecal strongyle worm egg count is
expected to be high.
Treatment of suspected strongylosis includes symp
tomatic treatments (see General principles of treatment
of chronic diarrhea in adult horses) and larvicidal doses
of anthelmintics. Return to normal intestinal function
may be protracted and in some patients repeated
anthelmintic dosing may be required.
Chronic inflammatory bowel
disease and intestinal
neoplasia
T Mair
Chronic inflammatory and neoplastic diseases, such as
lymphosarcoma, granulomatous en teri tis/ colitis, lym
phocytic-plasmacytic enteritis/colitis, and eosinophilic
enteritis/ colitis, primarily afect the small intestine and
CHRONIC DIARRHEA 21
are associated with malabsorption and chronic weight
loss (see Chapter 18). However, if the large intestine is
afected as well then diarrhea is likely. Chronic inflam
mation of the large intestine results in hypersecretion
of fluid and electrolytes, reduced absorption of water,
and motility abnormalities.
Rectal examination fndings in these cases may
include enlarged mesenteric lymph nodes and palpable
thickening of the bowel wall. The rectum itself may be
thickened and friable. Ultrasonography can be helpful
to confrm bowel wall thickening. Moderate to severe
hypoalbuminemia and mild to moderate hyperglobu
linemia are often present. Elevated serum alkaline
phosphatase may be present. Non-specifc hematologi
cal abnormalities (anemia, leukocytosis, neutrophilia,
hyperfbrinogenemia) may also be identifed. Diagnosis
of inflammatory or neoplastic bowel infltrates usually
depends on histopathology of bowel wall biopsies.
Rectal biopsy may be diagnostic in some cases. The
diagnosis and treatment of these diseases are described
in more detail in Chapters 17 and 18.
Chronic idiopathic colitis was diagnosed as a com
mon cause of diarrhea in one clinical review of horses
with chronic diarrhea. This disease was diagnosed only
by histopathological examinations (obtained at post
mortem examination). The disease was characterized
by diffuse, non-specifc inflammatory changes in the
lamina propria and/or submucosa, and some also
had mucosal ulceration. The cause of this syndrome
remains uncertain.
Sand enteropathy
T Mair
INTRODUCTION
Accumulation of large quantities of sand in the gastro
intestinal tract is an uncommon cause of chronic diar
rhea. Sand accumulation is more commonly associated
with impaction of the colon and colic (see Chapter
15). Light sandy soils, overstocking, poor pasture
management, inadequate nutritional supplementation,
drought conditions, and feeding horses in sand
schools can all result in horses consuming signifcant
quantities of sand. Sand accumulates within the cecum
and large colon where it probably irritates the mucosa
and disrupts normal motility patterns leading to diar
rhea. Fine sand tends to accumulate in the ventral
colon, whereas coarse sand may accumulate in the
dorsal colon.
437
CLINICAL SIGNS
Diarrhea associated with sand enteropathy is usually rel
atively mild and is not associated with severe dehydra
tion. The diarrhea may be persistent or intermittent.
There may be associated fever, decreased appetite,
weight loss, and episodes of colic. Complete obstruction
of the colon results in persistent colic (see Chapter 15).
Severe irritation and mucosal inflammation may result
in secondary peritonitis that may become septic if bowel
perforation occurs. In such cases, the horse will develop
signs of endotoxemia with tachycardia, congested
mucous membranes, prolonged capillary refll time,
and a toxic rim at the gum/incisor margin.
DIAGNOSIS
Sand may be identifed in the feces in large quantities.
If a fecal solution is made by mixing feces and water
together, sand will sediment to the bottom of the con
tainer when the solution is allowed to stand for a few
minutes. Frank or occult blood may be present in the
feces. Transrectal palpation may reveal an impacted
segment of colon (unless the transverse or right dorsal
colon is involved in which case they are not normally
palpable per rectum). Auscultation of the abdomen
may reveal decreased frequency of borborygmi, and a
characteristic sound of 'pouring sand' over the ventral
abdomen. This sound is only heard in association with
progressive contractions of the colons. Radiography
can also be used to identif radiodense sand in the
intestinal tract in the cranioventral abdomen, especially
in small horses and ponies.
Hematology is often normal, but in some cases there
may be evidence of hemoconcentration (pe 45-55%
and total protein 72-80 gil (7.2-8.0 g/dl. Plasma
fbrinogen may be normal or elevated.
Peritoneal fluid is usually normal, although there
may be an increased total protein concentration.
Increased nucleated cell counts and protein levels will
be found if peritonitis is present. Abdominocentesis
should be undertaken with caution in horses suspected
of sand impaction because of the increased risk of
enterocentesis. However, identifcation of sand particles
in the sample of peritoneal fluid is diagnostic when seen.
TREATMENT
Intravenous and/ or oral fluid therapy should be admin
istered as necessary. Psyllium hydrophilic mucilloid is a
bulk laxative that hydrates intestinal contents and stim
ulates intestinal motility. By mixing with sand in the
438
colon, it promotes evacuation of the sand-psyllium
mucilloid mixture from the intestinal tract. A dose of
0.25-0.5 kg/500 kg body weight is mixed with 4-8 liters
of water and administered rapidly through a nasogastric
tube. In order to reduce the risk of the gel blocking the
nasogastric tube, some authors recommend administra
tion by nasogastric tube of the powder mixed with 2
liters of mineral oil; this is followed by the administra
tion of 4 liters of water through the tube. Magnesium
sulfate (Epsom salt) can be administered at the same
time. Once the clinical signs are relieved, prolonged
therapy is frequently necessary to remove the accumu
lated sand. Dry psyllium (1 g/kg) can be added to the
feed daily for several weeks. This may be repeated after
3-4 months; continuous daily feeding of psyllium
mucilloid should not be continued more than a few
weeks at a time. The efcacy of this form of treatment
has recently been questioned and in one experimental
study psyllium mucilloid was found to be ineffective in
removing sand from the intestinal tract. High fber
ingredients in the diet, such as wheat bran, may also be
helpful in removing accumulated sand from the colon.
Alternative bulk-forming laxatives can be used.
Ispaghula husk at 300-400 g/450 kg mixed with 4 liters
of water and administered immediately by nasogastric
tube has proved useful in some cases. The treatment
can be repeated at daily interals for 4-5 days.
Surgical therapy is occasionally needed if there is com
plete colonic obstruction (see Chapter 15). In horses
developing peritonitis secondary to sand enteropathy,
antibiotics and other therapies for peritonitis are
required (see Chapter 17, Peritonitis).
PREVENTION
Prevention of the disease is important and recurrence
of clinical signs in individual horses is common.
Feeding horses from elevated bins (with rubber mats
underneath) and allowing grazing only in felds with
adequate growth to prevent ingestion of sand are vital
to avoid this condition.
Equine right dorsal colitis
NO Cohen
INTRODUCTION
Right dorsal colitis has been clinically and experimen
tally associated with administration of phenylbutazone
to horses. Clinical signs in horses with this condition
include inappetance, anorexia, weight loss, intermit
tent or sporadic episodes of acute abdominal pain, and
diarrhea. Some horses with right dorsal colitis can be
managed medically. Early recognition of this condition
is likely to be important for successful medical manage
ment. The purpose of this section is to describe
methods for the diagnosis and management of right
dorsal colitis.
CAUSE
Right dorsal colitis (RDC) has been associated with
administration of phenylbutazone. Although the condi
tion may develop in horses given excessive amounts of
the drug, RDC may develop in horses that receive
recommended doses of phenylbutazone (4.4 mg/kg
p.o. b.i.d.) for periods as brief as 1 week. Other non
steroidal anti-inflammatory drugs (e.g. flunixin meglu
mine) can also cause RDC but they are less frequently
associated with the condition. Dehydration and physio
logic stress associated with performance may increase
the risk of RDC. Idiosyncratic or genetic predisposition,
protein composition of the diet, or concurrently admin
istered drugs may also contribute to development of
right dorsal colitis. Concurrent administration of
phenylbutazone and flunixin meglumine prolongs the
pharmacologic effects of these drugs. Young perfor
mance horses, horses with chronic lameness, and
ponies may be more likely to develop RDC. It is
unknown why the right dorsal colon is affected in
particular.
Salmonella spp. have been isolated from the feces of
horses with right dorsal colitis. The clinical importance
of isolating Salmonella spp. is unclear because appar
ently healthy horses may shed Salmonella spp. and
gastrointestinal disease predisposes to enteric
salmonellosis. Salmonellosis can cause diarrhea,
abdominal pain, and protein-losing enteropathy in
horses. Although these clinical signs are observed in
horses with RDC, Salmonella spp. are not likely to be
causally associated with RDC.
CLINICAL SIGNS
The clinical signs of right dorsal colitis are
colic
weight loss
diarrhea
inappetence
icterus
ventral edema.
CHRONIC DIARRHEA 21
Physical examination of horses with RDC may reveal
few abnormalities and clinical signs are non-specifc.
Horses may have signs of acute abdominal pain (colic).
Ofen episodes of colic are recurrent and some horses
may be presented when they are apparently healthy
for evaluation of intermittent colic (see Chapter 17).
Although weight loss is seen in horses with RDC, some
horses may be in good body condition. Weight loss is
probably related to duration of the condition. Some
horses with RDC may have diarrhea but the feces usu
ally have a normal consistency. When present diarrhea
is rarely profuse. Though rarely reached, the right dor
sal colon may feel edematous and thickened when pal
pated per rectum. Because of inappetance or anorexia,
some horses may have icteric mucous membranes.
Occasionally, horses with RDC will have edema of the
ventrum or limbs attributable to hypoproteinemia.
CLINICAL PATHOLOGY
Common hematologic abnormalities of horses with
RDC include anemia, hypoproteinemia, and hypoalbu
minemia. Decreased PC probably results from colonic
loss of blood and/or chronic inflammatory disease.
Occult blood can be found in the feces of affected
horses but the tests that are currently available are not
highly sensitive. False positive results can occur when
the test is performed on feces collected from a horse
within 24 hours following a rectal examination.
Hypoproteinemia is very common in horses with
RDC. Based on the results of the clinical history, physi
cal fndings, urinalysis, peritoneal fluid analysis, and
serum biochemistry, hypoproteinemia can be attrib
uted to gastrointestinal loss in affected horses. Because
it is the most abundant protein in equine plasma and
has a lower molecular weight than globulins, albumin is
often decreased in horses with gastrointestinal inflam
matory disease. Because of decreased intravascular
oncotic pressure, hypoproteinemia and hypoalbumin
emia may exacerbate hypovolemia, further predisposing
to NSAID-induced intestinal damage. The hypoprotein
emia is rarely severe enough to cause dependent
edema. The concentration of leukocytes is usually
within the reference range, although leukocytosis and
hyperfbrinogenemia, associated with inflammation,
and leukopenia and neutropenia, possibly caused by
endotoxemia, can be seen in some horses with RDC.
Hypocalcemia is frequently obsered in horses with
RDC. Hypocalcemia may result from inadequate dietary
intake associated with abdominal pain, loss of protein
bound calcium into the gastrointestinal tract, and
decreased protein-bound calcium associated with
hypoalbuminemia and hypoproteinemia. Because the
439
ionized fraction of calcium is rarely decreased severely,
signs of tetany are not generally observed in horses with
RDC. Other serum biochemical abnormalities are not
consistently observed. Some horses may have prerenal
azotemia and hyperbilirubinemia associated with
decreased ingestion of water and feed. In dehydrated
horses that become hemoconcentrated, the decreased
PCV and hypoproteinemia may not be apparent until
they are rehydrated. Cytologic and biochemical analysis
of peritoneal fluid rarely reveals abnormalities. In some
horses an increased concentration in peritoneal fuid of
total protein, fibrinogen, and nucleated cells may be
observed. Grossly, the affected colon will appear thick
ened, edematous, and reduced in cross-sectional diam
eter. Varying degrees of nlceration may be observed if
the mucosal surface is inspected.
DIAGNOSIS
None of the clinical or clinicopathologic fndings
observed is specifc for RDC. Consequently diagnosis is
difcult. Localizing a problem to the right dorsal colon
exclusively can only be made anatomically by examin
ing the gastrointestinal tract by celiotomy or necropsy
(Plate 21). Because celiotomy is invasive, it is often
desirable to recognize the condition and establish a
presumptive diagnosis accurately. This can be accom
plished on the basis of interpreting fndings of signal
ment and history, clinical signs, and clinicopathologic
fndings, particularly hypoalbuminemia.
The chief complaint is often non-specifc and history
of recurrent episodes of anorexia, lethargy, and colic is
frequently described. History of administration of non
steroidal anti-infammatory drugs (NSAID) is of partic
ular importance. The condition is frequently seen in
horses that have a history of use for competitive perfor
mance. Such horses often receive NSAIDs, including
phenylbutazone, for management of musculoskeletal
pain. Moreover, such horses may be predisposed to
adverse effects of NSAIDs because of dehydration and
physiologic stress associated with strenuous exercise
and travelling. Ascertaining an accurate history of
NSAID administration can be difcult, particularly in
cases where blame may be an issue.
The amount and duration of NSAID administered
may be important. It is, however, importnt to recog
nize that colonic inflammation or ulceration may develop in
horses receiving doses of phenylbutazone tolerated by many
other horses.
Findings of history and the aforementioned physi
cal, clinical, and clinicopathologic attributes should
make a diagnosis of RDC likely. Similar fndings, how
ever, can be seen in horses with gastric and small intesti-
440
nal ulceration caused by administration of NSAIDs and
with other causes of chronic colic. If possible, gas
troscopy (see Chapter 2) should be performed in all
horses with clinical signs suggestive of RDC. Clinical
signs of RDC are similar to those associated with gastric
ulceration. Because colonic inflammation and ulcera
tion can occur independently of, or concurrently with,
gastric ulceration, it may be necessary to treat some
horses with colonic ulceration for gastric ulceration.
Defnitive localization requires visualization of the right
dorsal colon, this is best achieved via celiotomy.
Ultrasonographic examination of the right dorsal colon
can provide a non-invasive method of identifing
colonic mural thickening that might be associated with
right dorsal colitis. The sensitivity of this technique,
however, appears limited. It has been suggested that
isotope-labeled white blood cell scintigraphic scans may
identif colonic ulceration; the sensitivit and availabil
ity of the procedure is likely to be quite limited.
TREATMENT
Initially RDC was described as a condition requmng
surgical management and carring a poor prognosis.
Surgical management entails bougienage, or either
bypassing or resecting the affected portion of the colon.
Many cases of RDC, however, can be managed medically.
The principal aims of medical management are to
avoid treatment with NSAIDs
minimize stress for the horse
implement dietary management.
Certain drugs may also be of beneft in managing this
condition (see below).
Avoidance of NSAIDs
Because RDC has been induced in horses by adminis
tration of phenylbutazone, NSAIDs should not be
administered to horses with this condition. Compliance
with this recommendation can be difcult because
some horses continue to have episodes of colic during
medical management and caretakers may be tempted
to treat these episodes with flunixin or other NSAIDs.
Also some horses may have a problem (e.g. chronic
lameness) that the owners want to continue to treat
with an NSAID because of availability, cost, and clinical
effectiveness for the problem. Nevertheless, these drugs
should be avoided because some horses may have an
idiosyncratic or other predisposition to RDC; the mag
nitude of doses and the duration of administration of
phenylbutazone in horses with RDC are not necessarily
unusually high relative to recommended doses.
Minimizing stress for the horse
Physiologic stress and dehydration appear to increase
the risk of gastrointestinal ulceration induced by
NSADs. Minimizing physiologic stress and avoiding
dehydration may help decrease the risk of recurrence
and promote healing in horses with RDC. Examples
of management practices designed to decrease stress
include discontinuing or decreasing the frequency of
performance, strenuous exercise, and travelling. Horses
with RDC should be provided access to adequate
amounts of water. Efforts should be made to ensure or
enhance consumption of water
provide salt in a block or as granules on the feed, or
sweeten the water with flavored preparations (this
may be of particular benefit in horses that are being
transported for long periods or to environments
with water that is less palatable to the horse).
Implementing dietary management
Dietary management is directed toward providing a low
hulk diet in the form of a pelle ted concentrate, and
restricting or eliminating ingestion of roughage. These
changes aim to decrease the mechanical and physio
logic load of the colon. A complete pelle ted diet (i.e.
pellets containing both concentrate and adequate
dietary roughage) will decrease intestinal fll in the
colon, therehy decreasing the mechanical load of the
colon. A diet lower in fber should decrease the physio
logic load of the colon because the cecum and large
colon are the primary sites in horses of fber digestion
and exchange of fluid and electrolytes. Concentrate
should be fed in smaller amounts and more frequently
(4-6 feedings per day), rather than twice daily. Some
horses will not eat complete pellets and some will eat
bedding or wood if roughage is withheld. Such horses
should be allowed to eat fresh grass in small amounts
(approximately 5-10 minutes of grazing 4-6 times
daily). Roughage should be eliminated or restricted to
small amount of fresh grass for a period of 3-6 months.
The importance of and optimal duration for restriction
of roughage is unknown.
Drug therapy
Drugs used to treat right dorsal colitis are
psyllium mucilloid
misoprostol
sucralfate
metronidazole
sulfasalazine
linoleic acid
intestinal protectants and adsorbents.
CHRONIC DIARRHEA 21
Psyllium mucilloid
Feeding psyllium mucilloid may promote colonic heal
ing in horses with RDC. In other animal species, psyl
lium mucilloid has been demonstrated to increase the
concentration of short-chain fatty acids of the large
bowel, and short-chain fatty acids can positively influ
ence colonic mucosal repair. The amount and duration
of psyllium mucilloid administered orally that is
required to alter the colonic concentration of short
chain fatty acids and the role of short-chain fatty acids in
repair of RDC in horses is unknown. Continuous feed
ing according to manufacturers' recommendations for
3-6 months is suggested, or feeding 30-60 g (1-2 oz) of
psyllium mucilloid once or twice daily for the same dura
tion may be considered. Horses should be returned to
their usual diet over a period of several days to decrease
the risk of inducing other digestive disorders.
Misoprostol
Specific chemotherapy for RDC remains speculative
because the pathophysiology is unknown. Because
misoprostol has been demonstrated to prevent
phenylbutazone-induced gastrointestinal ulceration in
horses, administration of this synthetic analog of
prostaglandin E) may be of beneft in horses with RDC.
The drug can be administered orally (2.5-5 Jg/kg
q. 12 h or 2 Jg/kg q. 6 h). The latter regimen may
better mimic constitutive production of prostanoids by
cyclooxygenase-l (COX-I), whose inhibition may be
associated with the toxic effects of NSAIDs. It is
unknown if misoprostol will improve colonic healing or
be cytoprotective for the colon; side-effects may include
colic. The author has not observed colic in horses
receiving misoprostol at a dose of 2 Jg/kg q. 6 h.
Sucra/fate
Because sucralfate has been demonstrated to diminish
intestinal discomfort and reduce intestinal disturbances
following radiotherapy for pelvic cancer in humans, it
has been suggested that sucralfate may promote healing
of colonic ulcers in horses. The extent to which sucral
fate influences NSAID-induced colonic disease in
horses has not been determined. Because the drug is
relatively inexpensive and has few side effects, adminis
tration of sucralfate (22 mg/kg p.o. q. 8-12 h) does not
appear to be contraindicated for treating RDC. Other
medications used routinely to treat gastric ulceration in
horses (antacids, proton-ion pump blockers such as
omeprazole, and H2-receptor antagonists such as raniti
dine) would not be expected to be effective because
their principal mechanism of action is to decrease
gastric acidity.
441
Metronidazole and sulfasalazine
In humans, NSAID-induced enteropathy has been
treated with sulfasalazine and metronidazole with vary
ing success. These agent have not been evaluated for
the management of colonic lesions induced by NSAIDs
in horses. Metronidazole has anti-inflammatory effects
in the intestinal tract of other species, including models
of NSAID-enteropathy. Metronidazole can decrease the
neutrophilic adherence to intestinal mucosa in experi
mental NSAID-induced enteropathy. Adherence of
neutrophils to vascular endothelium contributes to
NSAID-induced gastric mucosal injury, suggesting that
metronidazole may be of benefit in RDC. The author
has used metronidazole in the management of RDC in
horses at a dose of 1 0-15 mg/kg p.o. b.i.d.
Linoleic acid
Oral administration of dietary linoleic acid may be
effective for managing NSAID-induced gastric ulcera
tion because linoleic acid may result in modulation of
the profile of pro-inflammatory eicosanoids produced
during inflammation. Administration of corn oil has
been suggested, presumably because it has been
demonstrated to increase gastric prostaglandin E2 in an
experimental model of gastric ulceration in rats. In
addition corn oil can provide additional dietary calories
that will be absorbed principally by the distal small
intestine. The benefts of feeding omega-3+/omega to
fatty acid diets to prevent or help repair intestinal
mucosal injury are unknown in the horse.
Intestinal protectants and adsorbants
The benefit of intestinal protectants and adsorbants,
such as bismuth subsalicylate, mineral oil, and activated
charcoal, for treating RDC is unknown and cannot be
recommended. Although these agents generally do not
cause harm, it is unclear whether the salicylate liberated
from bismuth subsalicylate in the colon could potenti
ate NSAID-induced colitis.
PROGRESSION AND PROGNOSIS
Owners should be advised that horses with RDC may
experience episodes of colic during medical manage
ment, these episodes should follow a trend of decreas
ing frequency and severity. If a colonic stricture
develops, the severity, duration, or frequency of
episodes may progress. Owners should be advised that
successful medical management is dependent upon
compliance to recommendations by the veterinarian.
Continued physiologic stress, administration of
NSAIDs, and feeding roughage may promote recur-
442
rence or exacerbate the condition and ultimately lead
to stricture of the right dorsal colon. Colonic stenosis
has been described in horses with chronic, severe RDC,
and stenosis or stricture of the colon generally requires
surgical management and entails a guarded to poor
prognosis. Early recognition of the problem prior to the
development of irreversible lesions and dietary man
agement with elimination or restriction of roughage
may enable recovery in some horses, thereby obviating
the need for surgical intervention.
Several methods are available for monitoring the
progress of horses with this condition. Some horses will
have occasional episodes of mild abdominal pain prior
to resolution of signs. Such horses may require surgical
evaluation and management. Monitoring the PCV and
concentration of total protein is of benefit. These values
should increase with resolution of colonic inflamma
tion, usually over a period of 2-8 weeks. If the right
dorsal colonic wall appears thickened sonographically,
repeated ultrasonographic examination may facilitate
assessment of relative changes.
Chronic diarrhea in adult
horses - other causes
T Mair
INTRODUCTION
A wide variety of diseases have been reported to result
in chronic diarrhea in horses. In some of these diseases,
diarrhea is a minor or unusual presenting sign of the
disease, for example, diarrhea is sometimes seen in
horses affected by the following conditions
abdominal abscess (see Chapter 1 7)
abdominal neoplasia (see Chapter 1 7)
cecal impaction (see Chapter 1 4)
chronic intussusceptions
chronic renal failure
congestive heart failure
Cushing's disease
enteroliths (see Chapter 1 5)
grass sickness (see Chapter 17)
hyperlipemia (see Chapter 19)
intestinal diverticulae (see Chapter 13)
malnutrition/starvation
myeloproliferative leukemia
non-strangulating intestinal infarction (see
Chapters 13 and 15)
pancreatic diseases (see Chapter 17)
peritonitis (see Chapter 17).
Toxic causes of diarrhea are described in Chapter 20.
IDIOPATHIC CHRONIC DIARRHEA
Some horses with chronic diarrhea remain undiag
nosed after exhaustive diagnostic testing, and even after
post-mortem examination. These horses are described
as being affected by idiopathic chronic diarrhea. In
many cases, the horses are well in other respects, have
normal serum chemistries, and maintain normal body
condition. The diarrhea is a nuisance and management
problem, rather than a signifcant veterinary or welfare
problem. It is assumed that many of these cases are
caused by physiological osmolality disturbances or
motility abnormalities affecting the cecum and large
colon.
Some horses with idiopathic chronic diarrhea will
respond to dietary modifcation. If the affected horse is
stabled, then turning it out to pasture and maintaining
it on a grass only diet may be helpful. Alternatively, a
horse affected by idiopathic chronic diarrhea at pasture
may beneft from being stabled and maintained on a
dry hay diet. Fresh water as well as water spiked with
electrolytes should be available to these horses at all
times.
Other treatments that can be benefcial in the man
agement of idiopathic diarrhea include the following
(see also General principles of treatment of chronic
diarrhea in adult horses)
iodochlorhydroxyquin
metronidazole or potentiated sulfonamides
anthelmintics ( larvicidal doses)
transfaunation
probiotics
codeine phosphate and other motility-modifing
drugs
acetic acid (vinegar) .
CHRONIC SALMONELLOSIS
Chronic salmonellosis appears to be a rare cause of
chronic diarrhea in adult horses. Although Salmonella
spp. can frequently be cultured from the feces of horses
with chronic diarrhea, other underlying causes of the
diarrhea (such as cyathostomosis, lymphosarcoma,
infammatory bowel disease, etc.) may be present. Some
horses recovering from acute salmonellosis will be
affected by chronic or intermittent diarrhea and
remain persistent shedders of Salmonella spp. ; this situa-
CHRONIC DIARRHEA 21
tion may persist for several months. Systemic antibiotics
are of questionable value in these cases even when
sensitivity test results are followed. Affected animals are
a potential health hazard to other animals and to
humans, and they should be isolated and treated symp
tomatically until such time as shedding in the feces can
no longer be detected.
INTESTINAL TUBERCULOSIS
Mycobacterium tuberculosis (usually avium) and
Mycobacterium paratuberculosis can rarely cause chronic
granulomatous enteritis and colitis, presenting clini
cally with chronic weight loss, inappetance, and chronic
diarrhea. Other signs relating to involvement of other
body systems (including the skin, lungs, and skeleton)
may also be present. The diarrhea may be intermittent
or persistent. Ulceration of the mucosal surface of
the colon can occur in some affected horses.
Histopathologically, acid-fast bacteria can be found in
the gut wall and mesenteric or colonic lymph nodes. In
some cases, acid-fast bacteria may be identifed in rectal
biopsies. Culture of the organisms from feces takes
several weeks and is frequently unsuccessful, although
acid-fast organisms can sometimes be found in fecal
smears. The intradermal skin test is unreliable in horses
because of the presence of many false positive reactions.
There are no reports of attempts to treat affected
horses, although isoniazid (5-20 mg kg-l dayl ) and/or
rifampin (10 mg/kg b. i. d. ) might be considered.
NEOSPORA CNINUM
Neospora caninum has been diagnosed as a possible cause
of colitis in a middle aged horse that demonstrated
signs of chronic diarrhea and anemia. At necropsy,
tachyzoites of N caninum were identifed in sections of
the colon and mesenteric lymph nodes.
HISTOPLASMOSIS
Histoplasmosis has been identifed in a small number of
horses affected by chronic diarrhea and weight loss.
Although there are enzootic areas of histoplasmosis in
the USA, cases are rarely reported. Histolasma capsula
tum has been diagnosed as a cause of granulomatous
colitis, resulting in chronic diarrhea and protein-losing
enteropathy. The organism can also cause peritonitis,
pulmonary infection, and abortion. Diagnosis is
achieved by bowel wall biopsy. Skin tests are unreliable.
No attempts at treatment have been reported.
443
2 1 ACUTE AND CHRONIC DIARRHEA
GIARDIASIS
Giardia equi infection has been described as a rare cause
of chronic diarrhea, decreased appetite, and abdominal
pain in adult horses, but the signifcance of the proto
zoal organism is uncertain; it can be detected in the
feces of some normal foals and adult horses. Diagnosis
of giardiasis should be based on the exclusion of other
causes of chronic diarrhea (this is diffcult to achieve in
many cases), the repeated detection of giardial cysts in
the feces (by zinc sulfate centrifugal flotation or
immunofluorescence), and response to treatment with
metronidazole.
TRICHOMONAS EQUI
" W-'' ,,i'',h".',,'","','"*"m" "",I"C,,,oi! "'J,'"''''' ,",,"""'".,,"""
Trichomonas equi is a common flagellate parasite of the
equine large intestine. Although the organism is com
monly present in the feces of horses with chronic diar
rhea, it is unlikely to play any role in the pathogenesis of
diarrhea. Experimental infections with the organism
have failed to cause clinical disease. Chronic fluidit
of the colonic contents in horses with diarrhea may
encourage secondary proliferation of the organism.
However, empirical treatment of horses affected by
diarrhea where the organism is present might be con
sidered if another cause cannot be identifed. Diagnosis
is achieved by identifing the organism microscopically
in wet fecal smears.
EIMERIA LEUKARTI
Eimeria leukarti is a protozoan parasite that is adapted to
the small intestine of horses, and has been associated
with mild, self-limiting diarrhea in juvenile horses.
Oocysts are commonly found in the feces of normal
foals. Experimental infections with the organism have
failed to cause clinical disease and it is unlikely that this
organism is a signifcant cause of diarrhea in adult
horses.
HEPATIC DISEASE
Chronic hepatic disease is a rare cause of diarrhea.
Alterations in intestinal microflora, portal hyperten
sion, and defciency of bile acids may be involved in the
pathogenesis. The diagnosis and treatment of chronic
hepatic diseases are discussed in Chapter I g.
444
PERITONITIS
Diarrhea is an unusual presenting clinical sign associ
ated with peritonitis. The disease is described in detail
in Chapter 17.
INTESTINAL LYMPHANGECTASIA
Lymphangectasia involves a disturbance of lymphatic
drainage of the intestine, resulting in loss of protein
rich lymph into the intestinal lumen. This disease was
diagnosed at post-mortem examination in one horse
that had a history of intermittent diarrhea and weight
loss. The affected horse had hypoproteinemia and an
abnormal oral glucose absorption curve. No specifc
cause was identifed, and no treatment was described.
INTESTINAL FIBROSIS
Diarrhea has been recorded in horses and ponies
affected by intestinal fbrosis. Affected animals usually
have a history of chronic weight loss and recurrent
colic. Thickening of the intestine may be palpable per
rectum. Diagnosis is achieved by surgical examination
and biopsies that show submucosal fbrosis of the small
intestine. The only reported treatment has been resec
tion of affected segments of bowel.
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22
Clinical evaluation of the foal
bvlutl0n 0 the 0l wlth
c0llc
CSCabIc
INTRODUCTION
Colic in the foal is commonly encountered in equine
practice and has numerous etiologies. Evaluation of the
foal with colic is a diagnostic challenge since the rectal
examination - one of the primary tools used in the eval
uation of colic in the adult horse -cannot be used in foals.
Furthermore, foals tend to be less tolerant of abdominal
pain than adults, making it diffi cult to distinguish
between conditions requiring medical or surgical
therapy. A significant number of foals with enteritis will
be initially examined for abdominal pain. Evaluation of
the foal with colic should include a thorough history, sig
nalment, physical examination, clinicopathologic data,
and other diagnostic aids such as ultrasound examina
tion of the abdomen and/or radiographic study of the
abdomen (with or without contrast medium) . The infor
mation obtained from these procedures can narrow the
list of differential diagnoses and help make the decision
as to whether medical or surgery therapy is warranted.
HISTORY
The historical events surrounding colic in the foal can
provide clues as to the true etiology of the colic episode.
Especially in the neonate, the peripartum events should
be discussed. Normal parameters for neonates are
gestational age - mean 341 days (range 31 5-365)
time to suckling reflex - normally suckles within 20
minutes
time to standing - mean 57 minutes (range 15-1 65)
time to nursing from mare - mean III minutes
(range 35-420) .
In general, a foal that is not able to stand and nurse
by 2 hours of age should be considered potentially
abnormal.
Adequate intake and/or absorption of colostrum
should be evaluated by immunoglobulin (IgG) testing.
Inadequate immunoglobulin l evels can result from
maternal disorders (premature lactation or agalactia) ,
or from illness in the foal. A foal with partial or com
plete failure of passive transfer will be much more sus
ceptible to infectious causes of colic (enteritis) , than
the foal with adequate passive transfer.
Other information that should be obtained includes
age of the foal at the onset of colic
specific signs, e.g. bruxism, milk or food
regurgitation (reflux), nursing behavior, passage of
meconium and/ or character of feces, straining to
urinate or defecate, rolling and/ or lying on the
back
drugs administered and their effect
previous or current disease on the farm and its
treatment, e.g. diarrhea, respiratory infection (e.g.
Kodococcusequi).
Furthermore, previous or concurrent disease in the
afected foal such as septicemia or musculoskeletal
disorders may predispose to gastrointestinal ileus,
ulceration, and/or peritonitis. Neonates undergoing
intensive care, especially those with premature body
449
ZZ GASTROINTESTINAL DISEASE IN THE FOAL
systems are predisposed to functional obstruction of
the gastrointestinal tract resulting from ileus. Older
foals with a history of diarrhea and/or chronic colic
and failure to thrive are more likely to have intermit
tent or chronic ileocecal intussusception or gastric
ulceration.
SIGNALMENT
Age at the onset of signs of colic can help form the dif
ferential diagnosis in a foal with colic, especially for the
neonate. For example, foals with atresia coli, lethal
white syndrome ( ileocolonic aganglionosis) , or meco
nium impactions usually present within 12-36 hours of
birth with a distended abdomen and failure to pass
meconium. Neonates with uroperitoneum usually pre
sent at 3 days of age with depression, distended
abdomen, and/or abnormalities with urination.
The breed of the horse can also help indicate disease
processes, for example, miniature horse foals are quite
predisposed to small colon impaction due to fecaliths.
EVALUATION AND PHYSICAL
EXAMINATION
A complete physical examination is paramount in the
evaluation of the foal with colic, especially in the new
bor, as overlooking other congenital disorders not
associated with the cause of the abdominal pain can
lead to a disastrous end result, as well as needless waste
of money by the owners.
Observation from a distance
Examination of the foal should begin by observing the
foal in its environment uithoutrestraint. Valuable infor
mation can be obtained by simply standing quietly at
the side of the stall. By observing the foal with the mare
in a stall or in a small paddock, the clinician can get a
better idea of the true severity of pain, as foals that are
being restrained often can not or will not display mild
to moderate signs of pain. The foal's nursing behavior
can also be observed, for example the foal that nurses
then detaches from the teat early and retreats to grind
it teeth and salivate, might indicate possible gastric
ulceration.
Foals should also be observed for abnormalities of
the musculoskeletal system such as lameness and angu
lar o flexural deformities; these are problems that the
owner may or may not be aware of. Lameness especially
warrants closer investigation as septic arthritis requires
immediate treatment and may decrease the prognosis
450
Figure 22.1 Foal with a ruptured bladder straining to
urinate frequently, the posture is characterized by spread
hind legs, a sunken back (concave shape), and elevated tail
significantly, the owner must be made aware of the
problem and appraised as to the potential for treatment
at this time or in the near future.
Foals that are straining can be observed in the
stall, to ascertain if they are straining to defecate or
urinate. Foals that are straining to defecate arch their
backs (convex shape) and elevate their tails, while
foals straining to urinate will usually spread their legs,
sink their backs (concave shape) and elevate their
tails (Figure 22. 1 ) . This distinction is important and
can help guide further diagnostics. Methods to pre
vent excessive straining should be used such as
epidural anesthesia or l idocaine enemas. At the
author' s hospital foals have been seen to develop sec
ondary uroperitoneum, because of excessive straining
to urinate or defecate.
After the distant examination is complete the foal
should be restrained for a thorough physical examina
tion. During the physical examination it is again very
important to evaluate all body systems, not just the
gastrointestinal system. The age of the foal will dictate
normal parameters for the heart rate and respiratory
rate. A neonate will have an elevated heart rate and
respiratory rate compared to an older foal. Neonates
less than 1 week of age will have heart rates in the
range of 70-100 bpm and respiratory rates in the
range of 20-40 breaths per min, whereas older foals
will have heart rates in the range of 30-60 bpm and
respiratory rates in the range of 1 2-20 breaths per
min (Table 22. 1 ).
CLI NICAL EVALUATION OF THE FOAL ZZ
TU.1rl :t IIlI
Capihaq
Age Heartrate(bpm} kerpiratoryrate Iemperature refihtime
(breathrperm/n} (C} (rec}
newborn 40-80 (at birth) 60-80 (first hour) 37.2-38.9 <2
130-150 (during atempts 20-40 (first day)
to stand)
70-100 (first day)
7 days 70-100 20-40
3 months 30-60 12-20
Ldl0Dvd5Cudl5y5I0
The cardiovascular system should be evaluated care
fully. Mucous membranes should be moist and pink,
with a capillary refll time of 1-2 seconds. Tachycardia
can represent pain, hypovol emia, endotoxemia, and/ or
septi cemia. However, bradycardia may represent hypo
glycemia which may warrant immediate treatment with
intravenous dextrose. Bradycardia can also be present
with severe hyperkalemia as can be seen with uroperi
toneum. Murmurs are only common during the neo
natal period, usually caused by the incomplete closing
of the ductus arteriosus. This often results in a loud,
grade I-IV systolic left-sided murmur at the third inter
costal space.
K05ldIDly5y5I0
The respiratory system should also be evaluated care
fully. Breath sounds are easily auscultated in the new
born, unlike the adult. Foals should be evaluated as to
the pattern of breathing and for any lack of breath
sounds indicating severe respiratory disease, greatly
increasing complications while under anesthesia.
Neonates should also be evaluated for the possibilit of
fractured ribs - displaced rib fractures can lead to
laceration of the lung tissue and pneumothorax.
d5IlD/OI05I/Od5y5I0
The gastrointestinal system should, of course, be evalu
ated carefully for evidence of the cause of colic.
Abdominal distension can be detected on visual exami
nation. Abdominal distension can be caused by fluid
inside or outside the gastrointestinal tract as well as gas
distension of the small or large intestine (see
Differential diagnosis and evaluation of the foal with
abdominal distension) . Unlike the adult, gas or fluid
distension of the small intestine can cause visible
38.0-39.0 <2
37.5-38.5 <2
abdominal distension in the foal, whereas colonic
distension is more likely to cause visible abdominal
distension in the adult horse (see Chapter 1 7) .
Excessive fluid within the abdomen can be caused by
ascites
peritonitis
uroperitoneum
hemoperitoneum.
Fluid and/ or gas distension of the intestinal tract can be
caused by either enteritis or bowel obstruction (stran
gulating or non-strangulating) and can not be defni
tively diagnosed without radiographs or an ultrasound
examination of the abdomen. Abdominal distension can
be measured by shaving some hair on the dorsal aspect
of the foal's back as a marker and using white tape to
measure the circumference of the abdomen. This can be
effective at sequential examinations to determine if the
foal's abdomen is increasing or decreasing in size.
K0CId0kdOdIDO
A digital rectal examination can be performed, espe
cially in the neonate to check for the presence of
retained meconium. The meconium is hard and
pelleted and usually felt at the brim of the pelvis. A
digital rectal examination should also be performed in
neonates without a history of meconium passage to
check for any fecal straining. The lack of fecal straining
and only the presence of mucus are indicative of a con
genital disorder such as atresia coli or ileocolonic agan
glionosis. If a digital examination is to be performed
the rectal temperature should be tken frst. If the foal
is febrile and' colicky' , enteritis should be suspected.
~u5CuIdIDO dO0 ddIDO
Auscultation of the abdomen can be performed to
determine if there is gastrointestinal motility.
451
Simultaneous percussion and auscultation and a char
acteristic ' ping' can determine the presence of a gas
distended viscus. Abdominal ballottement can be used
to detect fluid present within the abdominal cavity.
Abdominal palpation can be rewarding in some foals,
however it is not useful if the abdomen is tense or in
older foals. Palpation of the external umbilicus should
be performed in all young foals to evaluate for
drainage, heat, or enlargement. Umbilical hernias
should also be evaluated and determined if reducible.
Non-reducible hernias usually indicate entrapped
bowel. A transabdominal ultrasound examination is
needed to fully evaluate the umbilical remnants. Intact
male foals should also be palpated externally in the
scrotal area to determine if an inguinal ( scrotal) hernia
is present. If present, it must be determined if the her
nia is reducible. Congenital inguinal hernias can be
manually reduced multiple times a day and after a few
weeks the vaginal ring will often decrease in size with
resolution of the hernia.
ckd/OdIDO DID0 0y05
An examination of the anterior chamber of the eye
should also be part of the physical examination of a
neonate. Uveitis characterized by fibrin within the ante
rior chamber may indicate sepsis or blunt trauma to the
eye. The yellow fbrin in the anterior chamber may
make the normally brown iris appear green.
OTHER DIAGNOSTIC PROCEDURES
Another diagnostic procedure that can be performed
on foals of all ages is the passage of a nasogastric tube.
Obtaining gastric refux in the neonate can be dificult,
even with a distended stomach. However, if gastric
reflux is obtained the presence of a functional or
mechanical obstruction of the stomach or small intes
tine is indicated. For neonates, a stallion catheter can
often be used to check for reflux, in older foals a small
sized nasogastric tube can be used. Older foals may
need to be sedated to prevent injury to the foal, han
dlers, or veterinarian.
Sedation during examination
Foals that are in severe pain can be hard to restrain, and
are dangerous and dificult to examine. Sedation of
these foals is warranted to prevent injury to handlers,
technicians, clients, and veterinarians. During the
examination, small doses of xylazine (0. 5 mg/kg i.v.)
can be administered to allow both the physical
452
examination to proceed and the placement of ajugular
catheter to administer further medications and intra
venous fluids. Xylazine, an alpha agonist, is a good
choice for short-acting sedation, also providing analge
sia. The effects of xylazine usually last from 1 0-20 min
utes with an intravenous dosage. This drug dosage can
also be administered with butorphanol, a mixed opioid
agonist/antagonist, to provide additional analgesia and
prolong the sedative effects. Other alpha agonists such
as detomidine, are not used in the author's hospital for
sedation of foals because of the profound sedation they
impart, as well as the duration of action which may
delay the decision for surgery. An overdose of the alpha
agonists can be reversed with yohimbine.
Radiography ( see section on Diagnostic imaging)
Although, because of their size, a rectal examination
can not be performed in foals, abdominal radiographs
can be taken easily. Lateral views are the standard views
taken, with the foal standing or in lateral recumbency
after sedation. Dorsoventral views are usually not neces
sary, and can be quite stressful for a foal with moderate
to severe abdominal distension. From these radi
ographs the nature of the distension - small versus large
intestine - can be determined. Large loops of distended
small intestine with hairpin turns, for instance, repre
sent an obstruction of the small intestine. Fluid outside
the gastrointestinal tract can also be identifi ed.
Contrast radiography can be used to identify
obstruction of the gastrointestinal tract and/or disrup
tion of the urinary tract. Barium can be used to identify
obstruction of the distal or proximal gastrointestinal
tract. Barium can be administered through a nasogas
tric tube at 5 ml/kg (30% w/v) to identify delayed gas
tric emptying and/or duodenal stricture. It has also
been reported that barium administered via a Foley
catheter as an enema at a dosage of 20 ml/kg has been
used to identif obstructions of the small and large
colon. According to one report, meconium impactions
and atresia coli have been identified using this
technique.
Ultrasonography (see section on Diagnostic imaging)
Ultrasonography has also been used to identify lesions
of the gastrointestinal tract in foals and adults, and can
provide valuable information for the foal with colic
and/ or distended abdomen. A 5-MHz probe can be
used to evaluate the abdomen and determine the
quantity and character of peritoneal fluid.
Abdominocentesis can be performed after fuid is iden
tifed to decrease the risk of enterocentesis.
Ultrasonography can also be used to identif abscesses
or enlarged lymph nodes within the gastrointestinal
tract and abnormalities or abscesses of the umbilical
remnants. Both small and large intestine can be imaged
to determine wall thickness and motility. The small
intestine can be imaged also to determine lumenal size
(diameter) . In a recent report, adult horses with acute
abdominal pain were evaluated via transabdominal
ultrasound prior to abdominal surgery. Horses within
this study with abnormal small intestine and lack of
motility detected on ultrasound prior to surgery, were
found to have 100 per cent sensitivity, specifcity, and
posi tive and negative predictive values for having a
strangulating small intestinal lesion at surgery.
Although a similar study needs to be performed in foals,
from this study, it is highly predictive that foals with
abdominal pain and similar ultrasonographic fndings
(dilated, non-motile small bowel) would likely require
surgery.
Endoscopy
Endoscopy is used in foals with abdominal pain to assess
the esophagus, stomach, and proximal duodenum (see
Chapters 2 and 23) . It can also be used to assess the rec
tum and small colon if other procedures fail to provide
a diagnosis. Most commonly endoscopy is used to assess
the stomach for gastric ulceration. The stomach is often
assessed to confrm a diagnosis of gastric ulceration and
to monitor response to treatment. Foals should be
sedated or even anesthetized if necessary, to facilitate a
complete endoscopic examination. To assess the
stomach, foals will often need to be withheld from food
and water and/or milk for 2-6 hours (depending on
age and amount of intake) before he examination to
allow the stomach to empty.
Gastroscopy in foals under 1 month of age can be
performed using a scope that is 1 meter in length and
10 mm or smaller in diameter. Older foals (46 months
of age) will require an endoscope 2 meters in length to
evaluate the stomach and duodenum. The endoscope
should be passed through the nostril and then into the
esophagus. Passage is continued until the stomach is
entered. At this time, the stomach should be distended
with air to facilitate a complete examination. If the
stomach contains fluid and/or feed material, it may be
possible to suction off the fluid, alternatively the proce
dure can be postponed for several hours. Retention of
fluid or feed material within the stomach may indicate
pyloric or duodenal stricture. The surfaces of the
stomach should be evaluated for areas of ulceration or
erosions. After complete evaluation of the stomach
(squamous portion, glandular portion, and margo
plicatus and pyloric antrum) then the scope can be
advanced through the pylorus into the duodenum.
Again, the duodenum will need to be distended with air
CLINICAL EVALUATION OF THE FOAL ZZ
for best viewing. The mucosal surface of the duodenum
should be evaluated for erosions, ulceration, or stric
tures.
Abdominocentesis
Abdominocentesis, a mainstay for evaluation of colic in
the adult, is often not performed in the foal due to fears
of puncture or laceration of the bowel wall (see Chapter
2) . Abdominocentesis however, can yield signifcant
information in determining the cause of the acute
abdomen or to determine surgical versus medical
therapy. At the author's hospital abdominocentesis in
the foal is not performed before a complete transab
dominal ultrasound examination of the foal has been
made. This examination can determine the quantity
and location of peritoneal fluid in the abdomen. Foals
with excessive abdominal fluid are good candidates for
abdominocentesis as they can be heavil y sedated,
placed in lateral recumbency, and restrained well for
the procedure. To prevent inadvertent laceration of the
bowel in a foal, a teat cannula is used rather than hypo
dermic needles. A disadvantage of using a teat cannula
for abdominocentesis is that an omental hernia may
subsequently occur in a small percentage of foals.
Although this is a rather benign complication it can be
alarming to the owner. A small local block can be per
formed with 2% mepivacaine on the ventral abdomen
to the right of midline, or where fluid is located,
although avoiding the spleen and the umbilical rem
nants. A small stab incision is made with a no. 1 5 blade
to penetrate skin and the abdominal musculature. The
sterile teat cannula is then gently introduced into the
abdomen and fluid is collected for evaluation.
Furthermore, from this position foals with uroperi
toneum can have a drain placed to help evacuate the
excessive fluid. In older foals abdominocentesis can be
performed from a standing position with an 1 8-gauge
needle or teat cannula. Abdominocentesis can be per
formed safely in these foals if the foal is adequately
sedated and restrained.
CLINICOPATHOLOGIC DATA
Information obtained from clinicopathologic tests can
shed valuable information about the condition and
prognosis of the foal. In all foals presented for evalua
tion of colic, a complete blood count, chemistry panel,
and venous blood gas analysis should be performed. An
abdominocentesis should be performed when applica
ble. Immunoglobulin levels should also be evaluated in
neonates.
The complete blood count can detect and/or
453
ZZ GASTROI NTESTINAL DISEASE IN THE FOAL
confrm sepsis, hypoproteinemia, or anemia. The pres
ence of band neutrophils (left shift) with or without
toxic changes on the hemogram can also help deter
mine the severity of infection.
Electrolyte analysis is also very important not only in
the diagnosis of abdominal disorders in foals, but can
direct initial treatment as foals with colic can have sig
nifcant fluid loss or sequestration. Portable electrolyte
units such as the I-Stat, can make electrolyte and blood
gas analysis in the feld feasible, quick, and very afford
able, thus reducing the time between recognition of the
problem and its treatment. Electrolyte values for foals
can be different to those for adults, as foals often have
higher phosphorus and lower sodium values than
adults. Electrolyte values for certain diseases are very
characteristic, such as uroperitoneum and enteritis.
Foals with uroperitoneum usually have
hyponatremia
hypochloremia
azotemia
hyperkalemia.
Whereas foals with enteritis often have
hyponatremia
hypochloremia
acidemia.
Glucose should also be evaluated in neonates because
foals that are unable to nurse can develop profound
hypoglycemia. Glucose is usually part of a routine
chemistry panel but can also be evaluated with a gluco
meter or reagent strip in the feld for quick analysis.
Venous or arterial blood gas should be a routine part
of the complete clinicopathologic data set on a foal with
abdominal pain. Severe abdominal distention can
lead to respiratory compromise in the young foal.
Furthermore, if neonates are allowed to remain in lat
eral or dorsal recumbency, they may also have difculty
maintaining normal oxygenation.
Evaluation of the peritoneal fluid in foals includes
total protein, total nucleated cell count, red blood cell
count, and a cytologic examination. The normal range
of total protein in abdominal fluid is the same in foals
and adults, less than 2.5 g/dl. The total nucleated cell
count however, has been reported to be lower in foals
than adults and as such nucleated cell counts greater
than 1 .5 x 1 09/1 ( 1 500 cellS/il) are considered abnor
mal. Cytologic examination of the fluid is also impor
tant in the foal, as in the adult, to screen for bacteria,
plant material, or degenerative changes in the cells.
Foals with suspected uroperitoneum should have a sam
ple of abdominal fluid evaluated for creatinine levels.
This level should be compared to the creatinine level in
serum, and if the ratio of peritoneal creatinine to serum
454
creatinine is greater than or equal to 2: 1 , the diagnosis
of uroperitoneum can be confrmed.
Thorough evaluation of the foal with abdominal
pain including a complete physical examination, and
using additional modalities such as radiography, ultra
sound, endoscopy, and clinicopathologic data, enables
the veterinarian to compile a l ist of differential diag
noses, initiate treatment, and decide between medical
and surgical therapy in the foal. Although these cases
can be challenging, the outcome can be quite success
ful .
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pr0cedureS ln te 0l
[MRcimcr
Ultrasonography of the gastrointestinal tract of the foal
is particularly rewarding because of the high incidence
of small intestinal disorders and the reduced digestive
development of the colon in the foal. In contrast to the
value of ultrasonography in identifing small intestinal
problems, the content of the colon often contains a
large amount of gaseous material which impedes ultra
sonographic evaluation. Plain radiography may be use
ful in the evaluation of disorders in the foal in which a
large amount of gas is present within the small intestine
or colon. Diaphragmatic hernias and pneumoperi
toneum can also be diagnosed with radiography.
Contrast radiography is primarily useful in the diagno
sis of meconium impactions, colonic atresia, and duo
denal stricture in the foal.
ULTRASONOGRAPHY
The abdomen should be clipped as for exploratory
celiotomy. In l ieu of clipping, liberal amounts of alco
hol may be applied to the region to be examined in
some cases. If possible, the examination should be per
formed with the foal in a standing position because
fluid-flled, edematous, or intussuscepted segments of
intestine, or any excessive peritoneal effusion, will tend
to gravitate to the dependent portion of the abdomen.
Such abnormalities may be difcult to visualize with the
foal in lateral recumbency. Otherwise an attempt
should be made to place the transducer as far beneath
the foal as possible, or to elevate the foal' s abdomen in
order that the transducer may be positioned ventrally.
Ultrasonography performed with the foal in dorsal
recumbency will rarely be rewarding as gas-flled seg
ments of intestine will often obscure visualization of
underlying structures. Transducer frequencies in the
range of 7. 5-5.0 MHz are recommended for evaluation
of the gastrointestinal tract of the foal. Depth display
depends in part on limitations of the transducer fre
quency used; generally using a depth display of 10 cm
initially, and altering it during the examination is
appropriate. If there is a large amount of fluid ingesta
or peritoneal effusion present, then a greater depth dis
play will enable visualization of deeper structures and a
lower frequency transducer may be necessary. A shorter
depth display and possibly a higher frequency trans
ducer will provide optimal diagnostic images if detailed
imaging of a structure adjacent to the body wall is
desired. The presence of gas at any depth obviates an
increase in depth display as the ultrasound beam will
not penetrate beyond that point.
Ultrasonography enables visualization of portions of
the stomach, duodenum, jejunum, and some segments
of the large intestine and small colon (if flled with fluid
contents or meconium).
The stomach
The stomach can be visualized from the left cranial
abdomen in the young foal. Occasionally the stomach
will be in contact with the ventral body wall, or at least
be visible immediately dorsal to the ventral aspect of the
liver when viewed from the ventral abdomen (Figure
22.2) . Mild curds surrounded by anechoic fluid, uni
form echogenic fluid, or gas-bubble-Iaden fuid is nor
mally seen in suckling foals within the stomach lumen
(Figure 22.3) . Otherwise only the stomach wall will be
seen as the high gas content of the ingest will result in
a bright linear echo at the lumen, and the character of
the gastric contents will not be appreciable. In cases in
Figure 22.2 Normal stomach in a neonatal foal as viewed
from the left cranioventral abdomen. Cranial is to the left.
In this case the stomach is visible immediately dorsal to the
spleen
which there is gastric distension due to increase in gas
tric fluid content, the lumen of the stomach and the
borders of the stomach may be visible (Figure 22. 4) . A
gas-fluid interface may also be noted in some cases.
Small intestine
The small intestine normally has few contents within its
lumen (Figure 22.5) , and grossly visible motilit may be
difcult to discern. In disease states, the small intestine
can be evaluated for wall thickness, lumen content,
degree of distension, and motility. Amotile loops of
intestine that appear taut are typical of complete
mechanical obstruction such as small intestinal volvulus
(Figure 22.6), while a less taut appearance may be seen
with incomplete mechanical obstruction, or functional
ileus as seen in some cases of enteritis (Figure 22. 7) . In
Figure 22.3 Normal stomach in a neonatal foal as viewed
from the left cranial abdomen. Notice the echogenic
material (presumed to be mild curds) surrounded by fluid
Figure 22.4 Markedly fluid-filled stomach in a neonatal
foal with anterior enteritis. Cranial is to the right. Notice
the splenic vein (arrows) which can be used as a landmark
455
Figure 22.5 Normal small intestine dorsal to the spleen, as
visualized from the ventral abdomen in a neonatal foal
Figure 22.7 Distended fluid-filled loop of small intestine
(amotile in real time) in a foal with ileus due to enteritis
Figure 22.9 Gas-bubble-Iaden fluid in the colon (long axis
view) of a young foal with colitis
456
Figure 22.6 Distended fluid-filled small intestine (short axis
view) with sedimentation of contents in one segment
(arrows) in a foal with complete mechanical obstruction
and ileus found to be due to small intestinal volvulus. It
should be noted that differentiation between mechanical
ileus and severe functional ileus may be difficult
Figure 22.8 Thickened or edematous small intestinal wall
(short axis view) with increased lumenal fluid content,
amotile in real time, in a neonatal foal with abdominal
pain and diarrhea. The foal died at 48 hours of age
because of clostridial enteritis
Figure 22.10 Small intestinal intussusception, short axis view
cases in which strangulation has resulted in devitaliza
tion of the affected segment, differentiation of me chan
ical ileus from enteritis with functional ileus may be
difcult. Devitalized segments of strangulated small
intestine may appear less taut because of loss of intesti
nal tone, and thicker as edema of the wall develops.
Typically small intestine enteritis is manifest a hyper
motile fluid-flled segments of small intestine with nor
mal wall thickness. Infrequently, the wall may be
thickened or edematous (Figure 22.8) . In cases of
necrotizing enteritis gas may be seen within the wall of
the intestine (it should be noted that gas may also be
seen within the wall of devitalized strangulated small
intestine) or the wall may appear very thin. Increased
fluid content in the large intestine (Figure 22.9) may be
observed in some cases of enteritis, and its presence
may be of help in the differentiation of functional from
mechanical small intestinal ileus. The diagnosis may be
unclear in some instances and repeat ultrasound exam
inations may be of beneft.
Small intestinal intussusceptions have a typical
'bull's eye' appearance when viewed in short axis
(Figure 22. 1 0) . Variable amounts of small intestinal dis
tension proximal to the lesion may accompany intussus
ception. It is particularly important to position the foal
standing if possible in order that the most dependent
portion of the abdomen can be examined with ultra
sound. Affected loops of fluid-flled or edematous intes
tine, or intussuscepted intestine; will tend to gravitate to
the most dependent area of the abdomen.
Colon
The colon often contains gaseous ingesta and its lumen
is generally not easily evaluated in the equine. In foals
with colitis, the contents of the colon may appear as
bubble-laden fluid (Figure 22.9) . Meconium appears as
hypoechoic structures within the large and/or small
colon (Figure 22. 11) . Because meconium can be visual
ized in the normal equine neonate a diagnosis of meco
nium impaction by ultrasound alone can be erroneous.
Peritoneum
Peritoneal effusions can be identifed in foals with peri
tonitis, uroperitoneum, hemoperitoneum, and transu
dates. Effusions due to accumulation of transudate may
be identifed in foals with mechanical gastrointestinal
obstructions. The fluid may appear anechoic in cases of
uroperitoneum, transudative effusions, and ruptured
viscus. In cases of ruptured viscus, the effusion may
range in appearance from anechoic to echogenic, and
may or may not contain a large amount of gas bubbles
or other echoes within the fluid (Figure 22.1 2) . Gas
echoes within the fluid are not always identifed in cases
Figure 22. 11 Meconium (arrows) in a foal with a
meconium impaction. Because meconium m
a
y be seen in
the intestine normally, the diagnosis of meconium
impaction should not be based on the results of ultra
sonography alone
Figure 22.12 Marked peritoneal effusion with particulate
matter in a foal with a ruptured viscus. The spleen is
indicated by arrows
of ruptured viscus, however a gas-fluid or gas-spleen
interface may be seen from the left paralumbar fossa
(with the foal in a standing position) in cases with
signifcant pneumoperitoneum. Abdominocentesis
should be performed to confrm the type of fluid
present as the ultrasound appearance of effusions is not
specifc. Visual inspection of the fluid, as well as exami
nation of the fluid microscopically (particularly if the
cell count is normal) is very important to rule out a rup
tured viscus.
Ultrasonography has obviated radiography for most
gastrointestinal disorders in the foal because of the
457
Figure 22. 13 Distended barium-filled stomach, 30 minutes
after administration of barium sulfate via nasogastric
tube, in an unthrifty weanling foal with bruxism,
inappetance, and gastric reflux. Notice the absence of
barium in the small intestine. Duodenal stricture was
confirmed at surgery
portbility of the ultrasound units and because of its
ability to both visualize intestinal motility in real time
and detect peritoneal effusions. It is often not possible
to distinguish mechanical from functional obstructions
with radiography, and ultrasonography may provide
more diagnostic information in such cases.
Diaphragmatic hernias may be identifed radiographi
cally, as with ultrasonography. Radiography, in combi
nation with contrast studies, is most useful for the
diagnosis of atresia coli, meconium impactions, and
evaluation of gastrointestinal transit time. Standing
lateral radiographs are exposed at 1 0-15 r and
80-120 kVp, with an 8:1 grid, flm focal distance of
1 meter, and rare earth film screen combination. Gas
caps are normally seen over the stomach, small intes
tine, cecum, and colon. For contrast studies, barium sul
fate is administered at 5-1 0 ml/kg as a 30 per cent w/v
solution by nasogastric tube. The stomach should begin
to empty by 15 to 30 minutes and be nearly empty by 2
hours, at which time contrast material may be seen in
the cecum and colon. Duodenal stricture will result in
gastric distension and retention of barium (Figure
22.13) . Retrograde contrast radiography is highly sensi
tive and specific for evaluating obstructions of the small
colon or transverse colon, such as those due to meco
nium impaction. Approximately 500-1000 ml of barium
sulfate solution (30% w/v) for a 50 kg foal is adminis
tered via enema into the rectum by gravity flow using a
soft flexible catheter. The author has found that a Foley
catheter has been unnecessary for such studies.
Sedation of the foal may be required in some cases.
Administration of barium should be discontinued when
the barium flows back around the catheter or the
foal becomes uncomfortable. Radiographs are taken
458
Figure 22. 1 4 Lateral radiographic view following a barium
sulfate enema of a 30-hour-old foal with colic due to
meconium impaction. Notice the silhouetting of
meconium balls in the rectum and terminal small colon,
and the marked gas distension of the colon
Figure 22. 15 Lateral radiographic view of the abdomen
following a barium sulfate enema of an 8-hour-old foal
with abdominal distension and colic. Notice the barium
through the small colon, it has entered the large colon and
ended in a blind pouch. Exploratory celiotomy revealed a
wall or diaphragm closure between the left and right ven
tral colons at the level of the sternal flexure, with intact
mesentery. An anastomosis was performed and the foal
recovered uneventfully. In the vast majority of cases of
atresia coli, a large segment of the large, transverse, or small
colon is absent, and surgical correction is rarely feasible
immediately. Meconium impaction will appear as filling
defects within the small colon or rectum, with silhouet
ting of the fecal balls by the barium (Figure 22.14) . If
the obstruction is just proximal to the pelvic inlet, a
widening of the small colon at this location because of
meconium may be observed. Atresia coli may also be
diagnosed by retrograde contrast radiography in most
cases. The contrast material will stop abruptly in a blind
pouch (Figure 22. 1 5) . Tapering ofthe contrast material
Figure 22.16 Lateral radiographic view following barium
enema of the terminal small colon and rectum of a 1-day
old foal with abdominal pain and distension. An inadequate
amount of barium sulfate has been administered to reach
the small colon, however notice the empty corrugated
appearance of the small colon. Because of intractable
abdominal pain, the foal was taken to surgery rather than
continue with the diagnostic procedure. Atresia coli was dis
covered at exploratory surgery and the foal was euthanized
within the small colon indicates that an inadequate
amount of contrast material has been administered to
reach the transverse colon (Figure 22.1 6) and more
barium may be required. In general, standing radi
ographic views have been sufcient in the author' s
experience, however ventrodorsal views may be neces
sary in some cases. Occasionally the atretic segment is
too proximal to be diagnosed with a retrograde contrast
study. Incidentally, a collapsed corrugated appearance
to the small colon has been observed by the author in
some cases of atresia coli ( Figure 22. 1 6) .
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INTRODUCTION
Abdominal distension can occur in foals of any age and
is most often accompanied by signs of abdominal pain.
Abdominal distension can occur in the foal however,
without signs of colic. Abdominal distention occurs
most commonly in adult horses with large colon disten
sion (see Chapter 1 7) . However, in foals, small and
large intestinal distention, as well as excessive abdomi
nal fluid accumulation, will lead to abdominal disten
tion. Abdominal distention in the foal is most
commonly caused by gastrointestinal disorders, usually
some tpe of intestinal obstruction (functional or
mechanical, congenital or acquired) . However, other
disorders such as rupture or leakage of the urinary tract
can lead to uroperitoneum and subsequent abdominal
distention. This section considers the differential diag
nosis of abdominal distention in the foal and the evalu
ation of foals with this condition.
History
Evaluation of the foal with abdominal distention begins
with a thorough history, including peripartum events.
Neonates should be evaluated as to their immunoglob
ulin status and treated if partial or complete failure of
passive transfer is suspected.
PHYSICAL EXAMINATION
A initial step in the physical examination is to take
the rectal temperature as a fever may indicate infectious
causes of the distention. Foals with abdominal
distension often have elevated heart rates. When large
quantities of peritoneal effusion are present, the foal
often develops hypovolemic shock. When gram-nega
tive bacterial infection is the culprit, endotoxemia may
also be a potential source of the tachycardia. Therefore,
thorough evaluation is necessary to treat the foal appro
priately. Foals with abdominal distention may also have
elevated respiratory rates as excessive fluid can press
upon the diaphragm causing difculty in breathing,
especially when the foal is recumbent. Furthermore,
the chest should be auscultated carefully to determine
if pleural fluid is present (possibly extending from the
abdomen) , also leading to difculty in breathing.
Examination of the distended abdomen should include
external palpation, radiography, and/or an ultrasound
examination to determine the cause of the distention.
RADIOGRAPHY AND
ULTRASONOGRAPHY
To determine the exact location of the gastrointestinal
obstruction or site of urine leakage, contrast studies will
need to be performed. For the location of gastrointesti
nal obstructions in the rectum and small colon, barium
enemas can be performed. The authors prefer to infuse
barium through a Foley catheter via gravity flow. The
Foley catheter after it is inflated, keeps the barium
459
within the rectum and small colon. For identifing the
site of leakage in cases of uroperitoneum. contrast cys
tography or excretory cystography can be performed.
Retrograde injection of dye into the bladder followed
by simple abdominocentesis will allow the clinician to
determine whether or not uroperitoneum is present.
but the site of leakage will remain unknown. Further
more. collection of abdominal fluid for cytology. creati
nine measurement and culture and sensitivity should be
performed prior to retrograde injection of dye.
ABDOMINOCENTESIS
Abdominocentesis is best performed in cases of abdom
inal distension after radiographs and/or ultrasound
examination has been performed. The risk of bowel
perforation is low if there is a large amount of peri
toneal fluid within the abdomen. However. if large gas
distended or fluid distended loops of bowel are present
on radiography or ultrasound examination. then
abdominocentesis is often not performed to avoid the
risk of laceration of the bowel wall. To decrease the
risk of inadvertent bowel wall perforation when
abdominocentesis is performed. the foal should be well
restrained with adequate levels of sedation and sub
cutaneous local anesthetic infltration. Furthermore.
abdominocentesis with the use of a teat cannula is often
preferred over an 1 8-gauge needle to prevent bowel
laceration.
Cytologic evaluation of the abdominal fluid will help
narrow the list of differential diagnoses for foals with
abdominal distension. High nucleated cell counts with
bacteria present can represent bacterial peritonitis due
to sepsis. ruptured abscess. or ruptured viscera. A
mentioned in Evaluation of the foal with colic.
Clinicopathologic data the normal nucleated cell count
of abdominal fluid in foals is lower than that in adults.
NASOGASTRIC INTUBATION
Because small intestinal distension can lead to abdomi
nal distension in the foal. then all foals that present with
abdominal distension should be evaluated for gastric
reflux. via a small bore nasogastric tube or stallion
catheter. Lack of reflux does not mean there is no accu
mulation of fluid within the stomach. however obtain
ing reflux indicates some form of bowel obstruction
(functional or mechanical) . Evaluation of the pH of the
sample can help determine if the reflux is from the
stomach or the small intestine. Intestinal fluid from the
small intestine will have a higher pH (68) than that
refluxed from the stomach which is more acidic.
460
EXPLORATORY SURGERY
There are many differential diagnoses for foals with
abdominal distension. and often the exact reason can
not be elucidated until an exploratory celiotomy is per
formed. However. careful and thorough diagnostics can
help guide the veterinarian toward the true nature of
the problem and help decide what treatment is
warranted. The following sections describe differential
diagnosis for foals with abdominal distension.
NEONATES
Neonatal foals are those within the frst 2 weeks of age.
In these foals congenital as well as acquired disorders of
the gastrointestinal and urinary tract must be consid
ered as differential diagnoses for foals with abdominal
distension. these include
meconium retention
intestinal atresia - atresia coli. atresia recti. atresia
ani
ileocolonic aganglionosis
uroperitoneum
fecaliths
peritonitis
enteritis/colitis.
Meconium retention (see Chapter 25)
Meconium retention is one of the most common causes
of abdominal pain and abdominal distension in the
neonatal foal. Meconium is comprised of swallowed
amniotic fluid and intestinal secretions that accumulate
within the gastrointestinal tract in foals during gesta
tion. Meconium is usually a dark color and pelle ted in
shape. These meconium pellets can be quite frm and
dry and often lead to difculty in passage through the
newborn foal's narrow pelvis and rectum. Colts are
thought to be more commonly affected than fllies.
because of their relatively smaller pelvic size. Meconium
may be retained within the rectum. small colon. and even
within the large colon. Foals should begin to pass their
meconium within a few hours of birth. Foals may pass
small amounts of meconium then begin to show signs of
discomfort. Typical signs of meconium retention include
straining to defecate. colic, and gradual abdominal
distension as fluid and ingesta accumulate within the
gastrointestinal tract proximal to the obstruction.
Evaluation of these foals includes a thorough physi
cal examination including evaluating the character of
straining if present. Foals that are straining to defecate
will have their backs arched with their tails in the air.
Digital palpation of their rectum will often reveal
retained meconium. Plain radiographs can reveal the
retained meconium within the rectum and/or small
colon with gas/fluid-distended colon proximal to the
obstruction. Contrast radiography with barium enemas
( administered through a Foley catheter) can also be
performed to help determine the location and nature
of the obstruction.
Intestinal atresia (see Chapter 1 6)
Intestinal atresia in the horse is a rare occurrence. It has
been reported to occur in the colon ( atresia coli) , and
in the rectum or anus ( atresia recti or ani) of the horse.
Atresia coli is approximately twice as common as other
types of atresia in the horse.
The most popular theory regarding the pathogene
sis of intestinal atresia is that of a vascular accident. The
vascular accident is theorized to arrest growth and
result in atrophy of a bowel segment which becomes the
atretic segment. Louw's theory has been tested and
shown that every type of atresia can be duplicated by
selective ligation of mesenteric vessels.
Foals with intestinal atresia are born 'normal'.
However, they usually present within the frst 24-48
hours of life for signs of colic, failure to pass their
meconium, and abdominal distension. Administration
of an enema will only produce clear water and mucous
- no fecal coloration. Foals with abdominal distension
and/or colic with no history of meconium passage
should be strongly suspected of intestinal atresia.
Evaluation of these foals should include a thorough
history, physical examination, and immunoglobulin
testing. Results of a complete blood count and chem
istry panel are non-specifc for this condition. Plain
radiographs of the abdomen and contrast studies may
help determine the site of obstruction.
Ileocolonic aganglionosis (lethal white
syndrome) (see Chapter 25)
This gastrointestinal disorder has been reported to
occur in white foals out of Overo-Overo Paint crosses.
Both male and female foals can be atfected. Recently it
was reported that a recessive gene is responsible for this
disease. The affected foals suffer from a lack of myen
teric ganglia within the ileum, cecum, and/or the
entire large colon. The lack of myenteric ganglia results
in lack of propulsive motility within the gastrointestinal
tract.
These foals, although normal at birth, will begin to
show signs of colic within 1 2-24 hours of birth, they will
not pass any meconium, and digital palpation or admin
istration of enemas will not produce any fecal material.
There is no treatment for these foals at the time of writ
ing and euthanasia is recommended. However, horses
can now be tested prior to breeding to determine if they
carr the gene responsible for the disease, using a DNA
test on the animal's blood or hair. The veterinary genet
ics laboratory at the University of California, Davis can
perform the test.
Uroperitoneum
Uroperitoneum is a common cause of abdominal dis
tension in foals and is the result of urine l eaking from
the urinary tract into the abdomen. Possible sites of
urine leakage include the urachus, ureter, urethra, or
most commonly, the bladder. Colts and fllies can be
affected, however colts are more commonly affected.
The pathogenesis of uroperitoneum includes increased
abdominal pressure during delivery, external trauma,
infection within the urachus, or necrotic cystitis. Tears
or defects within the bladder occur most commonly on
the dorsal aspect of the bladder.
Foals that develop uroperitoneum may not show
clinical signs for 2-3 days following the formation of the
defect within the urinary tract. Clinical signs include
progressive abdominal distension, tachycardia, tachyp
nea, depression, and decreased interest in nursing.
Although many foals will have stranguria or oliguria,
foals with defects within the urinar tract have been
known to urinate normally.
The evaluation of foals with suspected uroperi
toneum involves a thorough physical examination. The
external umbilicus, prepuce, and vulva of foals should
be examined closely. Urine leakage into the subcuta
neous tissues or retroperitoneally from tears of the ura
chus, ureters, or urethras can lead to subcutaneous
swelling and edema. Complete blood counts may only
reveal hypovolemia, unless concurrent sepsis or infec
tion is present. Electrolyte abnormalities resulting from
uroperitoneum classically include hyponatremia,
hypochloremia, hyperkalemia, and azotemia. An ultra
sound examination of the abdomen should reveal
excessive amounts of peritoneal fluid (Figure 22. 1 7) .
Imaging a fluid-distended bladder should not lead to
discounting uroperitoneum as the diagnosis, as the
urine accumulation can, of course, originate from a dif
ferent site. The diagnosis can be confrmed through the
collection of abdominal fluid. Abdominocentesis
should yield voluminous clear, pale yellow fluid. The
fluid should be evaluated via cytology and comparison
of the creatinine values from serum versus abdominal
fluid. The diagnosis can be confrmed when the creati
nine concentration of the abdominal fluid is twice that
of the serum concentration.
Treatment of foals with uroperitoneum almost
always requires surgical repair of the defect. How
ever, stabilization of the electrolyte and acid-base
461
Figure 22.17 Abdominal ultrasonogram of a foal with a rup
tured bladder. There is a large excess of anechoic peritoneal
fluid in which the collapsed bladder is seen 'floating'
abnormalities must be performed prior to surgery to
prevent anesthetic complications or even death.
Medical stabilization should include drainage of the
excessive abdominal fluid, either through a teat can
nula or small chest trocar (for more continuous
drainage over several hours ) . Removal of the urine will
not only reduce pressure on the diaphragm allowing
the foal to breathe more easily, but will decrease both
serum creatinine and more importanty potassium con
centrations.
Intravenous fluids should be administered to correct
hypovolemia and electrolyte abnormalities. Normal
saline can be administered intravenously along with
dextrose to combat hypoglycemia and promote move
ment of potassium intracellularly. Severe or non
responsive hyperkalemia can also be treated with
intravenous calcium (4 mg/kg slowly LV. over 1 0 min
utes) or subcutaneous insulin (0. 1 IV/kg) regular
insulin LV. Furthermore, for foals with severe or non
responsive hyperkalemia, attempts at complete
drainage of abdominal fluid should be made along with
catheterization of the bladder to prevent further accu
mulation of urine within the abdomen. At the author's
hospital, foals with uroperitoneum are not anesthetized
until the serum potassium is below 5. 5 mEq/dl. We
believe that at this level, the risk of cardiac arrhythmias
is much less under general anesthesia.
Fecaliths (see Chapter 16)
Fecaliths occur more commonly i n pony or miniature
horse foals than in the larger breeds. These concretions
of fecal material and other ingested material (such as
shavings) can occur in neonates, but also cause obstruc-
462
tions in older foals. Fecaliths cause abdominal disten
sion and mild to moderate colic, similar to that seen
with meconium impactions, as gas and ingesta accumu
late proximal to the obstruction. The obstruction is
commonly within the small colon. Although the
obstruction is usually quite distal within the intestinal
tract, enemas are usually not effective and surgical
removal of the object is often necessary.
Peritonitis
Peritonitis can occu in any age foal and often results in
abdominal distension and low-grade colic with profound
depression. Peritonitis in foals can have many different
etiologies, including bacterial, chemical, or traumatic.
Neonates can develop bacterial peritonitis from
systemic bacterial infection (sepsis)
severe bacterial enteritis
leakage of bacteria from a gastroduodenal ulcer
that has perforated
leakage of bacteria from an umbilical remnant
abscess
a mesenteric abscess
damage of the gastrointestinal tract from parasite
migration.
Chemical peritonitis can occur from uroperitoneum or
hemoperitoneum. Trauma to the abdomen of foals can
result in hemoperitoneum from several diferent sources,
including the spleen, liver, or umbilical remnants.
OLDER FOALS
The more common causes of abdominal distention in
older foals are
small intestinal obstructions - intussusceptions,
volvulus
fecaliths
peritonitis
enteritis/ colitis.
Small intestinal obstructions such as intussusception
can lead to abdominal distention; these tpically occur
in foals that are 3-5 weeks of age, however, older foals
and horses can be affected as well. Intussusceptions can
occur in two forms, acute and subacute. The acute form
is indicated by a sudden onset of severe unrelenting
pain. The subacute form includes chronic colic,
anorexia, and an unthrifty appearance.
Small intestinal volvulus can also result in abdominal
distension, but again the acute nature of the pain often
precedes the development of distention. Small intesti
nal volvulus commonly occurs in foals that are 2-4
months of age.
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INTRODUCTION
This section provides a general guide to the medical
management of a foal with colic. The goals of medical
therapy are to
correct the primary cause of colic
correct electrolyte and metabolic imbalances
provide pain relief
provide continued nutritional support
provide decompression of the bowel
provide intestinal rest if distension persist.
Treatment for gastic ulceraton is covered elsewhere
(see Chapter 23) .
Foals are more likely to show signs of colic with
enteritis than adults, therefore ' colicky' foals are often
treated medically. If aggressive medical management
does not relieve the pain or distension, or if ancillary
tests such as ultrasound and radiography suggest
obstruction, surgical exploration should be considered
(see Evaluation of the foal with colic) .
FLUID THERAPY
Supportive care of the equine neonate begins with fluid
therapy to restore and maintain fluid homeostasis. The
total body water of a foal accounts for 70-75% of its
body weight. Gastrointestinal disease can result in
severe fluid shifts because of loss of sodium, protein,
and fluid into the gastrointestinal lumen or peri
t(meum. Endotoxemia and the resultant activation of
the inflammatory cascade results in pooling within the
gastrointestinal capillary beds and increased permeabil
ity to macromolecules, exacerbating the fluid shifts.
The resultant hypovolemia, if progressive, can lead to
decreased perfusion of the tissues, anaerobic metabo
lism, and metabolic acidosis.
Indicators of dehydration that can be used to calcu
late the percentage dehydration include
decreased skin turgor
dry mucous membranes
decreased urinary output
sunken eyes
muscle weakness.
Hypovolemic shock is suspected when the following are
observed
decreased distensibility of the jugular vein
prolonged capillary refll time
cold extremities
increased heart rate
decreased pulse pressure
decreased skin turgor.
Increases in the packed cell volume and total protein
are indicators of dehydration but are not specifc.
Aotemia, elevated blood urea nitrogen and creatinine,
can occur secondarily to dehydration but renal failure
should be ruled out by urinalysis and response to fluid
therapy. Interestingly, even without clinically detectable
dehydration, fluid therapy can be very benefcial in the
management of colic in foals and adult horses.
Calculations for fluid volume are
volume defcit = (% dehydration) x (body weight (kg
maintenance fluids = (60 - 1 20 ml x
(body weight (kg per day plus
ongoing losses = (estimated volume) =
(liters) to be given over 1 day
The electrolyte abnormalities most commonly
encountered with gastrointestinal disease in the foal
include
hyponatremia
hypochloremia
hypokalemia
hypoglycemia
metabolic acidosis.
Mild colic with a hypermotile intestine and no obstruc
tion can occasionally be managed with small amounts of
fluid given via a nasogastric tube. The total volume to
be placed directly into the stomach should be small
(8-1 2 ml/kg) . In most instances intravenous adminis
tration of a balanced polyionic electrolyte solution such
as plasmalyte or lactated Ringer' s solution is preferred.
Bicarbonate is required for the treatment of severe
metabolic acidosis (HC03 < 1 6 mEq/dl) with a normal
anion gap. The following calculation should be used to
determine the bicarbonate defcit
(base defcit) x (0. 4) x (body weight (kg = HC03
defcit (mEq)
or
(normal HC03 - measured HC03) x (0. 4) x
(body weight (kg = HC03 defcit (mEq)
One half of the defcit should be replaced over
1-4 hours and the remainder over the following
463
1 2-24 hours. Isotonic bicarbonate is nearly 1 . 25% and
intravenous bicarbonate solution comes commercially
prepared as 8. 4% ( 1 mEq/ml) and 5% (0. 6 mEq/ml)
solutions. Successful management of metabolic acidosis
in the foal with diarrhea can sometimes be achieved by
administering oral bicarbonate. This should be
attempted only when the foal is well hydrated and the
anion gap is normal. The base defcit can be calculated
by converting I gram bicarbonate into 1 2 mEq and dos
ing orally.
Hypokalemia occurs as a result of decreased intake
and loss through the gastrointestinal tract and urine.
Potassium may be added to the intravenous fluids at
approximately 20-40 mEq/liter. The potassium supple
mentation should not exceed 3-5 mEq kg/d and 0.5 mEq
kg/h. Hyperkalemia in the foal with gastrointestinal dis
ease is usually secondary to metabolic acidosis and
translocation of the potassium to the extracellular space.
In a rare case it may be a result of acute renal failure.
Treating the metabolic acidosis with bicarbonate-rich
fluids generally corrects the hyperkalemia. Dextrose
solutions (2.5-5. 0%) promote the movement of potas
sium back into the cells. Insulin 0. I IU /kg regular
insulin i.v.) can also be used but is generall y not recom
mended. If severe cardiac arrhythmias or atrial standstill
are detected, calcium gluconate can be administered at
4 mg/kg i.v. slowly over 10 minutes to protect the heart.
NUTRITION
Enteral nutrition I foals with abdominal distension
and colic can be contraindicated. A muzzle can be
placed on a foal that is reasonably bright and active to
prevent nursing until the colic subsides. Foals with colic
that are being fed with a nasogastric tube should be fed
only very small amounts of milk. If the foal tolerates the
small quantities, the amount can be increased slowly
over a few days to maintenance levels of 1 5-20% body
weight per day. Parenteral nutrition should be consid
ered in foals that may be unable to receive enteral nutri
tion for more than 24-36 hours. Since neonates have
minimal reserves of glycogen and fat, food deprivation
for 1 day may have profound effects. Parenteral nutri
tion is also indicated in prematurity, septicemia, and
diarrhea where the gastrointestinal tract is unable to
transport and digest milk. The decision to do partial or
total parenteral nutrition is based on the gastrointesti
nal tract function. It is important to continue stimulat
ing the enterocytes by feeding small amounts of milk
(50 ml q. 1-2 hr) if possible. Any electrolyte abnormali
ties should be corrected with fluids prior to initiating
TPN. A foal should receive approximately 1 00-150 kcal
kg-I day-I . Parenteral nutrition derives its energy from
464
Foal's weight (50 kg)
Level of nutritional support
Total daily calories
Non-nitrogen O|000dmbuW
100 kcal/kg/d
100 kcal x 50 kg
= 5000 kcal
40% dextrose = 2000 kcal dextrose
60% l i pi d = 3000 kcal lipid
O
A. Ratio of 300 non-nitrogen calg of nitogen
5000 total daily kcal / 300 (ratio) = 1 6. 5 9
nitrogen
B. 16.5 9 nitrogenl16% nitrogen i n protein = 1 00 9
protein
C. Example to determi ne volume of an ami no 8.4%
acid solution:
100g nitrogen/0.084 ami no acid solution =
1 176.5 ml
three sources; amino acid solutions, dextrose, and
lipids. The non-protein nitrogen sources; dextrose and
lipids should be distributed at 40% and 60%, respec
tively. The ratio of non-nitrogen calories to grams of
nitrogen has been extrapolated from humans to be
approximately 1 50-300. Protein contains 16% nitrogen,
therefore an amino acid solution can be approximated
by dividing the protein by 6.25. The kcal derived from
protein is 4 kcal/g, glucose i s approximately 4 kcal/g,
and fat is 9 kcal/ g. This value should lie within the ratio
of non-nitrogen calories to grams of nitrogen.
Strict attention to aseptic techniques should be paid
when managing the TPN solutions since they can sup
port the growth of bacteria and fungi. The amino acids
should be mixed with the dextrose before adding the
lipids. A freshly made bag can be kept refrigerated for
24 hours prior to use. The solution should be delivered
through a TPN dedicated intravenous line and very
careful handling of the catheter ports and intravenous
lines should be undertaken with daily replacement of
the lines. When beginning the TPN, start at approxi
mately one-third of the desired rate. Monitor the blood
frequently for lipemia, and the urine and blood for
hyperglycemia (blood glucose > 1 80 mg/dl ) . Increase
the flow rate slowly if normoglycemia is maintained.
ANALGESICS
Controlling pain in a colicky foal that is rolling is
important in reducing self inflicted trauma, as well as
decreasing inflammation that is causing ileus. Non
steroidal anti-inflammatory drugs (NSAIDs) can be of
beneft but should be used judiciously because of the
ulcerogenic efects on the glandular portion of the
stomach and renal papillary necrosis. Drugs with a low
cyclooxygenase-l :cyclooxygenase-2 ratio are thought to
be safest. Unfortunately, pharmacokinetics and toxicity
trials of NSAIDs in the foal are not well documented.
Flunixin meglumine (0.5-1 .0 mg/kg i. v.) has been
reported to be the most effective drug for gastrointesti
nal pain. Ketoprofen has been documented as the least
ulcerogenic NSAID compared with phenylbutazone
and flunixin meglumine in the horse, but anecdotal
reports indicate that its pain relief in colic is not as pro
nounced as flunixin meglumine. Butorphanol, an opi
oid analgesic, (0.01-0.04 mg/kg i. m. or i.v. ) can be used
in addition to, or to limit the amount of, NSAIDs given
when gastroduodenal ulceration is a concern. Xylazine
(0. 1-0.5 mg/kg i.v.) provides sedation and analgesia,
but can cause profound decreases in gastrointestinal
motility. If repeated doses of analgesics are required
surgical exploration should be considered.
DECOMPRESSION
A nasogastric tube can be passed to relieve gastric dis
tension. Unfortunately, the diameter of a foal's nasal
passages limits the size of the nasogastric tube to either
a stallion catheter or a 1 em diameter nasogastric tube.
A stylet can be used for ease of swallowing and passage
of the tube from the nasopharynx into the esophagus.
The stomach can be lavaged gently with small amounts
of water (60 ml at a time) . Frequently, even if reflux is
present in the stomach, it is difcult to manually extract
the fluid. The tube should be left in place and capped
to prevent air aspiration.
Percutaneous bowel trocarization is indicated if
severe abdominal distension coupled with respiratory
compromise persists. The owner should be warned of
the inherent risks of peritonitis and that the foal may
require surgical exploration if the condition persists.
The foal should be sedated and/or placed in lateral
recumbency. The abdomen should be percussed for a
prominent gas ping. The area where the ping is heard
best should be clipped and prepared aseptically. A small
lidocaine bleb should be infused at the puncture site. A
1 6-1 8-gauge 1 .5-inch needle or 3.5-inch catheter over
stylet can be advanced through the skin and body wall
into the distended viscus and air should be drained. A
small volume of antibiotic (i. e. amikacin or gentamicin)
should be infused as the needle/catheter is withdrawn.
The foal should be maintained on systemic antibiotic
therapy for 3-5 days following trocarization.
CLI NICAL EVALUATI ON OF THE FOAL ZZ
PROKINETICS
Motility enhancing drugs are considered controversial
in the foal with colic. Surgical and/or obstructive dis
eases should be ruled out before administering proki
netic agents. The most common indication for
prokinetic agents in a foal is ileus secondary to sep
ticemia, enteritis or neonatal maladjustment. The
dosages and side effects have been extrapolated for the
most part from human and small animal studies, and
little data exists in the literature on foals. Cisapride
(0.2-0.4 mg/kg p.o. q. 4-8 h) is a third generation ben
zamide that acts as a serotonin agonist within the myen
teric plexus. Cisapride has effects on the colon,
esophagus, stomach, and small intestine and, therefore,
can impact the entire gastrointestinal tract. Cisapride
has been well tolerated in adult horses. Metoclo
pramide (0. 25-0.50 mg/kg i.v. as a I-h infusion q. 4-8 h
or 0. 6 mg/kg p.o. or per rectum q. 4-6 h) , a dopamine
antagonist, has been well documented to increase gas
tric emptying with coordinated increase in tone of the
lower esophageal sphincter and contraction of the
stomach. Caution and constant monitoring for neuro
logic signs should be used when giving this medication
because of the permeability of the blood-brain barrier
and extra-pyramidal signs. Erythromycin, ( 1 .0-2.0 mg/
kg i.v. administered as a I-h infusion q. 6 h or p. o. q.
6 h) at sub-antibiotic levels stimulates motilin receptors.
Ranitidine ( 1-2 mg/kg p. o. or i. m. q. 8-12 h) , an H2-
blocker, has also been shown to have effects on gas
trointestinal motility and positive effects on gastric
emptying disorders. Ranitidine would be a wise choice
since it is also useful in treating gastric ulceration. A
acetylcholine esterase inhibitor, neostigmine (0.02 mg/
kg s. c. ) , is a potent prokinetic agent and can sometimes
cause severe cramping and colic in the horse. It has
been used successfully along with sedation in foals with
non-obstructing large colon gas distension.
bu|glcl declSl0n 0| the0l
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CSCabIc
INTRODUCTION
Foals with colic are challenging cases to manage.
Often the most difcult aspect of their management is
determining when and if the foal requires surgery.
Delaying surgery may unnecessarily compromise the
foal's physical condition and increase the risks of
465
ZZ GASTROINTESTINAL DISEASE I N THE FOAL
general anesthesia. Furthermore, delaying surgery
when devitalized bowel is involved can change a
closed bowel operation into a resection and anastomo
sis, thereby greatly reducing the overall prognosis. On
the other hand, placing a neonatal foal under general
anesthesia to perform an exploratory celiotomy can
greatly increase the risk of pneumonia and/or peri
tonitis. Furthermore, there is still a great deal of con
troversy regarding the risk of foals developing
postoperative intra-abdominal adhesions, despite
recent publications suggesting that foals are not at
greater risk than adult horses of these complications.
These conflicting factors make the surgical decision
for abdominal surgery in foals difcult.
The decision to perform surgery in a foal should be
made only after a complete and thorough physical
examination has been performed with careful atten
tion being paid to the historical events preceding the
colic. In addition, laboratory values (along with radio
graphs, ultrasound, and possibly an endoscopic exami
nation) can be very helpful in making the surgical
decision.
HISTORY AND PHYSICAL
EXAMINATION
A mentioned in previous chapters, a complete history
can be very beneficial in providing clues to the origin of
the colic episode. The following can provide valuable
information
peripartum events
age of the foal at the onset of clinical signs
farm history of disease
previous illness or surger
feeding program
anthelmintic history
For example, a poor-doing weanling with a history of
chronic intermittent colic is highly suggestive of a
chronic ileocecal intussusception.
The physical examination should be performed
keeping in mind the differences in the normal values of
heart rate and respiratory rate between neonates and
older foals (see Evaluation of the foal with colic) . Those
foals with an elevated temperature should be closely
evaluated for sepsis and/or enteritis as the cause of
colic. Enteritis in foals can be especially difcult to dis
tinguish from surgical lesions, as the foal often becomes
quite painful from intestinal distension before diarrhea
is present. In the author' s experience, Clostridial
enteritis in particular causes moderate to severe pain in
the foal requiring frequent analgesia.
Foals with colic often have distended abdomens.
466
The severit of distension can be monitored by repeat
edly measuring around the foal' s abdomen at specifc
points with a tape to detect changes. Foals with severe
abdominal distension can have great difculty breath
ing properly. These foals will require decompression
(percutaneous or surgical) of the gas-distended bowel
even if the lesion is usually amenable to medical ther
apy. Percutaneous methods of bowel decompression
carry risks in the neonatal foal, mostly from peritonitis
after the bowel puncture because of the thinness of the
intestinal wall.
Palpation of the foal externally can aid in identifying
large obstructions within the abdomen, but is often
impossible on a larger foal or one in severe pain. The
foal with colic should always be evaluated for hernias
(umbilical or inguinal/scrotal) and other congenital
defects. Reducible hernias are not a surgical emer
gency, but entrapped (non-reducible) hernias require
immediate surgery. Ruptured indirect inguinal hernias,
(inguinal hernias that have broken through the vaginal
tunic) , although not strangulating in nature, often
require immediate surgery as they can dissect through
the subcutaneous tissues becoming very large and much
more difcult to manage.
A nasogastric tube (small size) should also be passed
in foals with colic, however, the presence of reflux does
not always indicate a mechanical obstruction.
Furthermore the lack of reflux does not rule out a small
intestinal surgical lesion. The presence of reflux alone
therefore is not conclusive for a surgical lesion. The pH
of the reflux can help identif its source - acidic reflux
originating in the stomach and basic reflux usually orig
inating in the small intestine. Furthermore, a gram
stain of a reflux sample may help identif bacterial
enteritis, especially if an overhelming population of
one tpe of bacteria is found.
Foals tend to be more sensitive to gastrointestinal
pain than adults, and this makes it difcult to decide to
perform surgery on a foal, on the basis of signs of pain.
However, the foal displaying persistent, severe pain that
is not responsive to analgesia is a candidate for an
xploratory celiotomy. Even if ileus alone is the culprit,
decompression of the bowel can relieve the pain and
speed recovery.
LABORATORY EXAMINATION
A in the adult, a foal should be evaluated using a com
plete blood count, chemistry panel, and abdominocen
tesis if possible. The presence of leukopenia, left shift,
or evidence of toxic neutrophils suggests sepsis; infec
tious causes of colic, such as enteritis, should then be
considered. Neonatal foals should be evaluated further
by gamma globulin levels (IgG) to assess passive transfer
of immunoglobulins and the likelihood of sepsis. Foals
that have less than 800 mg/dl (80 g/I) of IgG are
treated for failure of passive transfer in the author's
hospital.
Chemistry panels are performed to evaluate the
foal ' s electrolyte status. Marked hyponatremia and
hypochloremia suggest enteritis. Hyperkalemia with
hyponatremia and hypochloremia suggests uroperi
toneum.
Abdominocentesis can be very helpful in identifing
surgical lesions in foals. Care must be taken to avoid
inadvertent bowel puncture when acquiring the sam
ple, so in the author's hospital an ultrasound examina
tion of the abdomen is performed to locate the area
where fluid is most likely to be obtained. Foals with
moderate to marked abdominal distension from bowel
distension are usually not evaluated via abdominocen
tesis because of the higher risk of bowel perforation.
The fluid is analyzed for white blood cell count, total
protein, and cytology. White blood cell counts greater
than 1500-3000/111 ( 1 .5-3.0 x 1 09/1) are considered
abnormal in foals. If uroperitoneum is suspected, the
fluid should be evaluated for creatinine concentration
and its level compared with serum creatinine concen
trations. If the ratio is greater than 2: 1 urinary tract
rupture/perforation is likely.
ADDITIONAL DIAGNOSTIC
PROCEDURES
The use of radiographs and/or ultrasound has greatly
enhanced the veterinarian's ability to determine the
location of the gastrointestinal obstruction in the foal
and decide if surgery is necessary. Although plain radi
ography can help determine the nature of the foal ' s
abdominal distension if present (i. e. small versus large
bowel distension) , contrast radiography is often much
more specifc in giving the location of the lesion.
Contrast radiographs taken after barium has been
administered can enhance the view of the gastroin
testinal tract and locate specific sites of obstructions.
Barium can be administered to the foal through a
nasogastric tube, dose syringe, or through a Foley
catheter (barium enema) . Barium administered
through a dose syringe can help identif problems
with the oral cavit, soft palate, esophagus, or cardia.
Barium administered through a nasogastric tube
should be made into a solution (30% w/v) and dosed
at 5 ml/kg. This can help identif lesions of the car
dia, stomach (e.g. gastric ulcers) , or duodenal stric
tures. Barium administered via an enema can help
identif lesions of the rectum, small colon, and even
the distal large colon at a dose of 1 8-20 ml/kg. Foals
are best sedated for this procedure
Evaluation of the foal' s abdomen via ultrasound can
also greatly help in the decision for medical versus sur
gical treatment. Although a rectal examination (a stan
dard and often vital part of the examination of an adult
horse with colic) cannot be used in the foal, an ultra
sound examination can help provide the information
needed to make the decision for surgery. Identification
of thickened and non-motile small intestine is highly
suggestive of a strangulating small intestinal lesion.
Other lesions that can be identifed include intussus
ceptions which appear as a 'bull's-eye' lesion (rings with
a circular echogenic core) , and copious amounts of
abdominal fluid suggesting either uroperitoneum or
peritonitis if the fluid is echogenic.
CONCLUSION
Differentiating surgical versus medical therapy in a foal
with colic can be a formidable task. Severe pain often
dictates our decision, but this degree of pain can some
times be caused by relatively minor obstructions.
Initially medical therapy is often chosen for the less
obvious surgical patients. However, progressive abdom
inal distension, persistent pain, and/or changing
abdominocentesis values all warrant an exploratory
celiotomy. Improved surgical techniques and medica
tion used to minimize adhesion formation (see
Chapters 10 and 1 1 ) appear to have kept the rate of
adhesion formation following exploratory celiotomy
low. In this author's opinion, it is better to perform a
careful, early exploratory celiotomy on a relatively sta
ble foal than frantic, desperate surgery on a dying one.
BIBLIOGRAPHY
Evaluation of the foal with colic
Chaffin M K, Cohen N D ( 1995) Assessing the histor,
signalment, and examination findings in foals with colic.
Vet. Med. 8: 765-9.
Chaffin M K Cohen N D ( 1995) Diagnostic tests and
procedures in foals with colic. Vet. Med. 8:770-6.
Cohen N D, Chaffin M K ( 1995) Assessment and initial
management of colic in foals. Compo Cont. Educ. Pact. Vet.
1 7( 1 ) :93-102.
Cudd T A ( 1990) Evaluation of acute abdominal pain. In
Equine Clinical Neonatolog, A M Koterba, W H Drummond,
P C Kosch (eds. ) . Lea and Febiger, Philadelphia, pp.
367-78.
Cudd T A, Wilson] H ( 1990) Diagnostic techniques for
abdominal problems. In A M Koterba, W H Drummond,
P C Kosch (eds.) Equine Clinical Neonatology, Lea and
Febiger, Philadelphia, pp 379-412.
467
ZZ GASTROINTESTINAL DISEASE I N THE FOAL
Klohnen A, Vachon A M, Fisher A T ( 1996) Use of diagnostic
pain. ] Am. Vet. Med. Assoc. 209(9): 1597-1601 .
Koterba AM ( 1990) Physical examination. I n A M Koterba,
W H Drummond, P C Kosch (eds.) Equine Clinical
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Murray M] ( 1997) Foal stomach and duodenum. In Equine
Endoscoy] L Traub-Dargatz, C M Brown (eds. ) 2nd edn.
Mosby, Baltimore, pp 159-71 .
Orsini,] A ( 1997) Abdominal surgery i n foals. Vet. Clin. North
Am. Equine Pact. 13(2) :393-413.
Diagnostic imaging procedures in the foal
Fisher A T, Yarbrough TY ( 1995) Retrograde contrast
radiography of the distal portions of the intestinal tract in
foals. ] Am. Vet. Med. Assoc. , 207:734-7.
Reef V B ( 1 992) Pediatric abdominal ultrasonography. In
Equine Diagnostic Ultrsound, W Saunders, Philadelphia,
pp. 364-403.
Reimer] M and Bernard W V ( 1998) Abdominal sonography
of the foal. In Equine Diagnostic Ultrasonography, N W
Rantanen and AO McKinnon (eds): Williams and Wilkins,
Baltimore, 627-36.
Reimer] M ( 1998) The Gastrointestinal Tract: The Foal. Atlas 0/
Equine Ultrsonography. Mosby, St Louis, pp. 200-1 1 .
Differential diagnosis and evaluation of the
foal with abdominal distension
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atresia in foals. Compo Cont. Educ. Pract. Vet.
17( 12) : 1510-16.
Chafn M K Cohen N D ( 1995) Assessing the history,
signalment and examination fndings in foals with colic.
Vet. Med. 8: 765-776.
Cohen N D, Chaffn M K ( 1994) Intestinal obstruction and
other causes of abdominal pain in foals. Compo Cont. Educ.
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Cohen N D, Chafn M K ( 1 995) Assessment and initial
management of colic in foals. Compo Cont. Educ. Pract. Vet.
17 ( 1 ) :93-9.
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Fisher A T ]r, Yarbrough T B ( 1995) Retrograde contrast
radiography of the distal portions of the intestinal tract in
foals. ] Am. Vet. Med. Assoc. 207:734.
Medical therapy in the foal with abdominal
pain
Cohen N D, Chaffn M K ( 1995) Assessment and initial
management of colic in foals. Compo Cont. Educ. Pact. Vet.
1 7( 1 ) :93-103.
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Vaala W E ( 1998) Neonatology. In Manual o/Equine
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that require surgery in foals. Compo Cont. Educ. Pract. Vet.
14: 535-7.
Cable C S, Fubini S L, Erb H N et aL ( 1996) Abdominal
surgery in foals: a review of 1 19 cases ( 1977-1994) . Equine
Vet. ] 29(4) : 257-61.
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pain. ] Am. Vet. Med. Assoc. 209(9) : 1 597-601.
Orsini, ] A ( 1997) Abdominal surger i n foals. Vet. Clin. N
Am. Equine Pract. 13(2) :393-413.
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Equine Vet. ] 28( 2) : 1 39-45.
23
Stomach diseases of the foal
NJ NUff
StI00u00eDl ulLeItl0D
MTHULTM
There are many similarities between gastric ulceration
in foals and adult horses, but there are also important
differences
the clinical signs are frequently more severe in foals
involvement of the duodenum is common in foals
but rare in adult horses
there is greater potential for debilitating or fatal
sequelae to gastroduodenal ulceration in foals.
Peptic disorders afecting the esophagus, stomach,
and duodenum have been recognized as important
conditions in foals for many years. In a 1964 report of
post-mortem fndings of severely ulcerated stomachs
from foals, the author suggested that lesions might have
resulted from Gasteophilus intestinalis larvae, foreign
body trauma (stones), or corticosteroid administration.
In the 1970s and early 1980s the veterinary literature
saw clinical reports that described fatal consequences of
severe, perforating gastroduodenal ulcers in foals. For
several years thereafter the typical 'ulcer' cases were
considered to be either foals which died suddenly as a
result of gastroduodenal perforation or foals showing
bruxism, ptyalism, or dorsal recumbency. In subse
quent years, the number of foals examined for gastro
duodenal lesions greatly increased and an expanded
spectrum of gastroduodenal lesions and clinical syn
dromes was described. Recently, more has been learned
about gastric development and physiology from endo
scopic and clinical fndings, and methods of treatment
and prevention of gastroduodenal ulcers in foals have
changed.
bTPTMbMbbb
The anatomy and physiology of the stomach of foals is
inherently the same as that in adult horses (see Chapter
12), but there are developmental issues that are perti
nent to gastroduodenal ulceration in foals. The gastric
stratifed squamous and glandular epithelia undergo
substantial development during late gestation and the
neonatal period. During mid-gestation the gastric squa
mous epithelium is eight to ten cells thick, with a single
layer of basal cells. Cells are polyhedral in shape and are
not stratifed. In the last month of gestation the basal
layers of the squamous mucosa become more numer
ous, epithelial cells become flattened and stratifed,
and a superfcial layer of keratinized cells develops.
Differentiation of the glandular mucosa can be appreci
ated by mid-gestation, and there is some staining for
mucosubstances in superfcial cells. By the last month of
gestation the glandular mucosa appears more differen
tiated and surface epithelial cells stain strongly for
mucosubstances, but there is no mucus layer over the
epithelium.
Mter birth, the gastric squamous epithelium under
goes vigorous epithelial hyperplasia, including
increased epithelial cell layers, thickening of the kera
tinized layers, and pronounced epithelial projections
extending into the lamina propria. The squamous
mucosal hyperplasia probably results from increasing
exposure to an acidic environment, in conjunction with
responses to local and possibly milk-derived growth
factor effects. The glandular mucosa appears fully
469
Z GASTROINTESTINAL DISEASE IN THE FOAL
differentiated, and there is a substantial mucous layer
covering the mucosal surface.
Recent studies have demonstrated that foals are
capable of substantial gastric acidifcation by 2 days of
age. In one report, I-day-old foals tended to have a rela
tively high gastric pH and had few pH recordings less
than 4.0, but by 2 days of age, highly acidic pH values
were recorded more frequently. By 1 week of age,
gastric pH recordings were frequently less than 2.0. In
another report a similar temporal association with age
was found, and nursing was associated with an abrupt
increase in gastric pH, and conversely, gastric pH
became highly acidic when foals remained recumbent
and did not nurse for more than 20 minutes.
Gastric ulceration is classically considered to result
from an imbalance of aggressive factors (hydrochloric
acid and pepsin) and protective factors (mucus/bicar
bonate barrier, mucosal blood flow, etc.), and in the
young foal this balance can easily be shifted toward pep
tic injury. The gastric squamous epithelial mucosa has
minimal resistance to peptic iury, whereas the gastric
glandular mucosa has an array of protective mecha
nisms. Thus, lesions in the gastric squamous mucosa are
primarily due to excessive exposure to hydrochloric
acid and lesions in the gastric glandular mucosa are
primarily due to impaired mucosal defenses.
Gastric acid secretion is regulated by several endo
crine and paracrine mediators, and the balance between
stimulation and inhibition of acid secretion may be more
easily perturbed in the young animal than in an adult.
Mucosal protection also may be more easily perturbed
in foals compared to adult horses. Lesions in the gastric
glandular mucosa have been obsered with greater
prevalence in young foals compared to adult horses.
In normal foals, glandular mucosal lesions are typi
cally erosions, and these usually heal spontaneously. In
foals with a clinical disorder, this can range from a
painful musculoskeletal problem to septicemia, there
is an increased prevalence and severity of gastric
glandular mucosal lesions, presumably resulting from
impaired gastric mucosal blood flow, which reduces
gastric mucosal resistance to peptic injury.
Young foals also have a high prevalence (up to 50%)
of squamous mucosal lesions, which are primarily ero
sions (Plate 23. 1). The gastric mucosa in the young foal
(up to 30 days old) is relatively thin and is characterized
by desquamation of superfcial epithelial layers. These
traits may render this mucosa more susceptible to
peptic injury. Fortunately, in most cases the squamous
mucosal erosions heal without consequence.
We have not observed gastric lesions on post
mortem examinations of aborted fetuses or in term
foals that died as a result of dystocia. However, we have
observed gastric lesions in foals as young as 2 days old,
470
regardless of the length of gestation. It appears that the
neonatal foal stomach secretes hydrochloric acid soon
after birth, even if the foal is born prematurely.
The pathophysiology of duodenal ulcer disease in
foals is assumed to involve peptic injury to the duodenum;
this may result from insufciencies in duodenal mucosal
defenses or pancreatic secretions that can neutralize
acidic gastric effluent. Conversely, in some foals duode
nal disease appears to reflect more widely distributed
enteritis and may not result directly from peptic injury.
In humans, duodenal ulcer disease is considered to
be a peptic disorder, but recently Helicobacter pylori has
been considered to be the primary direct cause of duo
denal ulceration. The bacteria only colonize gastric
glandular mucosa, so infection of the duodenum must
be preceded by metaplasia of areas of duodenal mucosa
to gastric mucosa, which probably results from peptic
injury. Helicobacter spp. have been identifed in many
animal species. Several investigators have examined
equine gastric mucosa for Helicobacter spp. by light
microscopy, mucosal urease activity, and by using poly
merase chain reaction, but to date no evidence of
Helicobacter infection in equids has been reported.
Whereas glandular and squamous mucosal lesions
typically heal spontaneously, the inherent susceptibilit
of the foal gastric mucosa to peptic injury enhances
the possibility for severe and catastrophic ulceration to
occur. Any condition that shifts the balance from heal
ing to further peptic injury will promote the type of
gastroduodenal ulcer disease that is classically associ
ated with foals.
ULLbH bYMHNbb
There are several manifestations and complications of
gastroduodenal ulcers in foals
mild gastric erosions with no apparent clinical signs
('silent ulcers')
stress-induced gastric lesions in foals with another
disorder
sudden onset severe gastric ulceration
duodenal ulcer and duodenitis
gastric outlet obstruction
gastric or duodenal perforation with peritonitis
pyloric ulceration
duodenal ulceration
gastroesophageal reflux
pyloric or duodenal stricture.
'Silent ulcers'
This term refers to the absence of clinical signs in a foal
with gastric lesions. It is unlikely that foals with duo de-
nal lesions will be free of clinical signs. The large major
ity of foals with 'silent ulcers' have mild erosive lesions
that heal spontaneously. A small subset of foals with
gastric lesions but no clinical signs will develop more
severe gastric lesions and may present with a sudden
onset of severe or catastrophic signs reflecting gastric
outlet obstruction or pseudo-obstruction, or perfora
tion.
Stress-induced gastric lesions
Foals with any clinical disorder have a greater preva
lence of lesions in the gastric glandular mucosa (Plate
23.2) than normal foals. Also, there may be greater risk
for ulceration of the gastric squamous mucosa if the
foal's appetite and milk or feed intake is diminished
because of illness. In a prospective study, the prevalence
for gastric glandular lesions in foals in a neonatal inten
sive care unit that did not receive ulcer prophylaxis was
40 per cent. This included foals born prematurely,
demonstrating that sufcient gastric acid can be
secreted to cause peptic injury in a premature foal.
Gastric ulceration is highly prevalent in human
intensive care units, and the incidence approaches 100
per cent in patients with severe burns. Gastric ulcera
tion secondary to physiologic stress probably results
from disturbances in mucosal blood flow. In several
animal models of stress, exposure to a physiologic stres
sor has been shown to reduce mucosal blood flow and
cause gastric lesions. Recently, investigators have shown
that reducing gastric mucosal constitutive nitric oxide
synthesis causes mucosal lesions whereas enhancing
nitric oxide synthesis protects against stress-induced
gastric mucosal lesions.
Stress is commonly considered to be a factor in
gastric ulcer development in people, and the term is
typically used to refer to psychological stress. In fact,
this type of stress has not been associated with an
increased prevalence of gastric lesions in most human
studies. Situations that we might perceive as being
stressful, such as long-distance transportation, herd
pressures, etc., have not been documented to affect the
incidence or prevalence of gastric lesions in foals. In
individual animals, however, many clinicians believe
that these situations may be stressful and contribute to
ulcer development.
Sudden onset severe gastric ulcers
Occasionally, foals will present because of acute abdom
inal discomfort or depression, and will have no history
of a current problem or other disorder found on exam
ination. Gastroscopy will reveal substantial ulceration,
tpically in the gastric antrum and at the pylorus (Plate
23.3), but also in the gastric squamous mucosa. It is
STOMACH DISEASES OF THE FOAL Z
usually not possible to determine a cause for the severe
ulceration, which can be worse than lesions found in
foals that have an underlying disorder. The appearance
of the glandular mucosal ulcers often implies some dis
turbance to gastric mucosal blood flow, and treatment
that should improve mucosal blood flow (sucralfate,
misoprostol) has appeared to beneft these foals.
Duodenal ulceration and duodenitis
Duodenal ulceration occurs with much less frequency
than gastric ulceration and in one retrospective study
duodenal ulcers were found in 28 of 511 (5%) foals
necropsied at a veterinary teaching hospital. Duodenal
ulcer disease is found almost exclusively in foals, and
foals of any age can be affected. Predisposing causes of
duodenal ulceration in foals are not known. Duodenitis
often accompanies enteritis, regardless of the cause.
Lesions occur primarily in the proximal duodenum,
and range from diffuse inflammation to focal, bleeding
ulcers. Lesions are seldom confned to the duodenum.
Gastric ulceration, and often esophagitis, accompanies
duodenal ulceration, because of impaired gastric
empting. In fact, presenting signs often appear to
relate more to complications of duodenal ulceration
rather than the duodenal disease itself.
Duodenal ulceration can be difcult to confrm ante
mortem. Most cases present with acute abdominal dis
comfort or with depression. Foals that have the 'classic'
gastroduodenal ulcer signs of bruxism and ptyalism
often have duodenal ulcer disease. Fever is often pre
sent, due to either a concurrent enteritis or peritonitis
secondary to ulcer perforation. Duodenoscopy is the
most specifc means of diagnosis (Plate 23.4).
Alternatively, if one can only examine the esophagus
and stomach, the presence of esophageal erosion or
ulceration and severe gastric ulceration is consistent
with duodenal ulceration and impaired gastric empty
ing.
The prognosis for duodenal ulceration is worse than
for simple gastric ulceration, because of associated com
plications (see below). Duodenal ulceration does not
seem to recur, as gastric ulceration often does, and
there can be complete resolution if there are no com
plications.
Gastric outlet obstruction or pseudo
obstruction
Gastric empting results from coordinated myoelectric
activit that originates in the gastric antrum and is
propagated toward the pylorus and into the proximal
duodenum. Inflammation, erosion, and ulceration
afecting the pylorus or duodenum can impair gastric
emptying and cause pseudo-obstruction. Fibrosis may
471
result from severe ulceration and can cause stricture of
the pylorus or duodenum.
There are several potential sequelae to impaired gas
tric emptying. Retention of acidic gastric contents can
cause severe gastric ulceration. Reflux of acidic gastric
contents into the esophagus often occurs with impaired
gastric emptying, leading to esophagitis, esophageal
ulceration, and megaesophagus. Gastric pseudo
obstruction implies a reversible condition, and if an
affected foal is treated aggressively, normal gastric
emptying can usually be restored. If ulceration has
progressed to fbrosis and stricture (Plate 23.5), the
long-term prognosis is less favorable.
Signs associated with impaired gastric emptying
include
poor appetite
belching
poor body condition
spontaneous nasal reflux of gastric contents
ptyalism (secondary to esophagitis).
If impaired gastric empting is suspected, endoscopy is
crucial to determine the nature and location of the
obstruction (stricture or pseudo-obstruction), and
whether medical or surgical treatment is indicated. In
lieu of endoscopy, barium contrast radiography may be
useful to document delayed gastric emptying. Scinti
graphy has also been used.
Treatment of gastric pseudo-obstruction with a pro
kinetic drug is usually effective. The author prefers
bethanecol, 0.02 mg/kg s.c., q. 68 h initially, then
0.35 mg/kg p.o., q. 8 h. If impaired empting is due to
a partial stricture of the pylorus, medical management,
which includes bethanecol and treatment for ulcer
healing, can be effective, but must be maintained con
tinuously. With severe stricture of the pylorus or duode
num, surgical bypass (see below) will be required.
Perforation of the stomach or duodenum
Perforation is a dramatic, although infrequent, sequel
to gastroduodenal ulceration. In many cases, perfora
tion is not preceded by typical gastric ulcer signs and
foals are found acutely depressed, in pain, or dead.
Most foals presented with perforation have widespread
peritonitis, which can have a tremendous fbrinous
component. In such cases it is possible for peritoneal
fluid cell count and protein to be normal because of
sequestration of cells and protein in fbrin clots within
the omentum. Careful inspection of a Wright's or gram
stained slide for bacteria may confrm a perforated vis
cus. Occasionally, a perforation in the stomach or in the
duodenal ampulla will be sealed by the greater omen-
472
tum. In these cases there will be evidence of peritonitis
(fever, shock, peripheral blood leukocytosis or leuko
penia, hyperfbrinogenemia, increased peritoneal white
blood cell count, and protein concentration) but the
foal's condition will stabilize with intensive treatment.
Clinical signs vary depending on the location and sever
ity of gastroduodenal lesions. Foals with gastric squa
mous or glandular mucosal erosions often will have no
apparent clinical signs. Conversely, it is probable that
clinical signs will be expressed in a large majority of
foals with duodenal lesions.
The clinical signs most often associated with gastro
duodenal lesions include
poor nursing
bruxism
dorsal recumbency
depression
ptalism
diarrhea without fever or abnormalities in the
leukogram
chronic poor condition.
Whereas these clinical signs are considered to be evi
dence of gastroduodenal ulcers, they are not specifc
for this condition. Poor nursing, diarrhea, and abdomi
nal discomfort are associated with a number of gastro
intestinal disorders in foals. Bruxism is a non-specifc
sign of abdominal pain. Ptyalism is a sign of esophagitis,
and while most cases of esophagitis in foals are
secondary to gastroesophageal reflux, other causes
(foreign body, candidiasis) should be considered. Fever
often accompanies gastroduodenal ulcer conditions,
particularly if there is duodenitis or perforation of a
gastric or duodenal ulcer.
Importantly, if a foal is showing signs characteristic
for gastroduodenal ulcer disease, then the veterinarian
should presume that the foal has severe gastroduodenal
disease. One should perform or refer the animal for
further evaluation and treat very aggressively to reduce
the likelihood of catastrophic consequences.
Mbb
Although the clinical signs described for gastroduode
nal ulceration in foals may be non-specifc they should
alert the veterinarian to the strong possibility that
gastroduodenal ulceration is a problem in the foal. If
gastroduodenal ulceration is suspected, an endoscopic
examination should be performed. It is vital to deter
mine the extent and severity of ulceration so that appro
priate treatment and management of the foal can
commence in order to avoid or minimize catastrophic
consequences. In cases with severe ulceration with
hleeding, aspiration of gastric contents will recover
brown-black fluid or material similar in appearance to
coffee grounds.
Because gastroduodenal ulceration may be sec
ondary to other disorders or can cause significant com
plications, a thorough evaluation of the foal is required.
A minimum database (CBC, serum chemistry profile,
uine analysis) should be collected. Other useful diag
nostic procedures may include abdominal radiography,
abdominal ultrasonography, and peritoneal fluid analy
sis. In neonatal foals with hleeding gastroduodenal
ulcers, fecal occult blood tests may be positive. In older
foals, the test is usually negative because of colonic
bacterial digestion of hemoglobin.
Radiography can be used to detect intestinal atony
or, using a barium contrast agent, to detect delaye
gastric emptying. With severe duodenal or pyloric ulcer
ation, survey radiographs of the cranial abdomen may
reveal accumulation of fluid within the stomach.
Contrast radiography has not been reported to be a reli
able method for detecting gastric lesions in foals, with
the possible exception of very severe lesions. In many
foals with ulceration at the pylorus or in the duodenum
complete emptying of barium contrast is usually
delayed > 2 hours), and an irregular mucosal border
may be noted in the descending duodenum. If stricture
has occurred, this may be noted. If the descending duo
denum is to be imaged, the volume of contrast material
(20-40% aqueous suspensions of barium sulfate)
placed into the stomach should not exceed 0.5-1 liter
in a foal, and 1-2 liters in a weanling/yearling, or the
proximal descending duodenum will be obscured by
contrast within the stomach.
Abdominal ultrasonography and paracentesis can be
useful when gastric .r duodenal perforation is sus
pected. Ultrasonography may reveal gastric or small
bowel distension with fluid, free fluid in the peritoneal
cavity, or fluid with gas (anaerobic growth) in the peri
toneal cavity. Paracentesis may reveal an inflammatory
reaction with gastric or duodenal perforation, but in
some cases peritoneal fluid analysis can be misleading
because inflammatory cells may be sequestered in
fbrinous exudate.
In lieu of an endoscopic examination, the veterinar
ian will need to rely on clinical signs and treatment
response, as well as the results of a thorough evaluation.
Treatment must include aggressive suppression of
gastric acidity and may include mucosal protectants
and drugs that enhance gastric emptying. With simple
gastric ulcer disease, clinical signs should subside within
1-2 days. For example, if a foal's appetite is poor
because of ulcers, treatment with effective acid suppres
sion will result in improved appetite within 24-48
hours. If abdominal discomfort is caused by ulcers, this
should resolve within 24 hours of the start of treatment.
With gastric emptying disorders or duodenal ulcera
tion, response to treatment may be less satisfactory.
Conversely, clinical improvement may be noted in the
absence of improvement in lesions, because suppres
sion of gastric acidity may be sufcient to alleviate pain,
but insufcient to facilitate healing. In such cases, there
can be a false belief in treatment success, only to have
catastrophic complications develop later.
THbTNbMT (TablesZ3.J, Z3.Z)
The treatment objectives for gastroduoden;! ulcers in
foals are similar to those in adult horses (see Chapter
12), the main aim being the suppression of gastric acid
ity, but there should be a heightened sense of urgency if
the foal is exhibiting clinical signs characteristic of
gastroduodenal ulceration. Because glandular mucosal
lesions form in a relatively large percentage of foals,
treatment with a mucosal protectant is often indicated.
Also, treatment with a drug that stimulates gastric
emptying is indicated whenever ptyalism is noted.
If the foal has abdominal discomfort or if gastric
obstruction or pseudo-obstruction are suspected, the
foal should be given an H2 antagonist intravenously or
intramuscularly. Use of a prokinetic drug should be
restricted until diagnostic evaluation is completed,
although in the author's experience administration of
bethanecol to foals with known pyloric or duodenal
strictures did not induce discomfort or worsen their
condition.
Oral treatment can be given when the foal is permit
ted to nurse or ingest feed. Use of an H2 antagonist or
omeprazole (proton pump inhibitor) is indicated,
rather than an acid neutralizing product. Sucralfate,
and in selected cases misoprostol, can be added to the
treatment when oral intake is permissible. A with adult
horses, misoprostol can cause abdominal discomfort
and diarrhea in foals,
a
nd if given it should be adminis
tered at the lower end of the dosage range (1.5 j1g/kg
p.o., b.i.d.) to test for tolerance, then gradually
increased.
473
|!NtIth||
o II0|It
e
Scenario 3: Foal is not nursing well, it has frequent mild
Drug (size) Recommended abdominal discomfor, and is lethargic. Physical
dosage
examination and results of minimum database are within
normal limits. Endoscopy reveals extensive erosion and
Antacid
ulceration of the gastric squamous mucosa, ulceration in
MaaloxTC 240 ml (8 oz.), q. 4 h
Mylanta double strength 240 ml (8 oz.), q. 2 h
the glandular mucosa of the antrum, and hyperemia of the
mucosa at the pylorus.
H2antagonist
Cimetidine (800 mg tablets) 25 mg/kg p.o., q. 8 h
Treatment recommendation Treatment
duration
(150 mg/ml) 7 mg/kg Lv., q. 6 h
Ranitidine (300 mg tablets) 7 mg/kg p.o., q. 8 h
(25 mg/ml) 1.5 mg/kg Lv., q. 8 h
Initial treatment
cimetidine, 7 mg/kg Lv., q. 6 h, or 2-4 days, until
ranitidine, 1.5 mg/kg Lv., q. 8 h, and foal nurses or
Proton pump inhibitor
bethanecol, 0.02 mg/kg s.c., q. 8 h ingests feed
Omeprazole (20 mg capsules 1 mg/kg p.o., s.Ld.
of enteric coated granules)
Omeprazole (paste 4 mg/kg, p.o., s.Ld.
formulation)
Subsequent treatment
omeprazole paste, 4 mg/kg s.i.d. or 3 weeks
ranitidine, 7 mglkg p.o., q. 8 h, and
sucralfate, 10-20 mg/kg p.o., q. 8 h, and 3 weeks
bethanecol, 0.35 mglkg p.o., q. 8 h 10-21 days
Mucosal protectant Repeat endoscopy
Sucralfate (1 9 tablets) 10-20 mgkg p.o., q. 8 h after treatment
Misoprostol (200 Ig tablets) 1.519/kg p.o., q. 8-12 h
up to 2.5 Ig/kg p.o., Scenario 4: Foal is presented because of depression and mild
q. 8 h
abdominal discomfort. Physical examination reveals signs of
cardiovascular shock and fever. CBC reveals leukopenia and
Motility modifier
Bethanecol (5.15 mg/ml) 0.02 mg/kg s.c., q. 6- h
Bethanecol (50 mg tablets) 0.35 mg/kg p.o., q. 8 h
mild anemia. Peritoneal centesis yields a small volume of
fluid with the appearance of increased neutrophils and a
few intracellular bacteria. Gastroscopy reveals severe
ulceration of the gastric squamous mucosa and ulceration
of the glandular mucosa of the antrum and pylorus.
Because of poor gastric contractilit the endoscope cannot
letmI
me t gl0 4It
|m| . .
be advanced into the duodenum.
duration
Scenario 1: Foal has mild signs of diminished nursing,
Initial treatment
occasional mild abdominal discomfort, mild lethargy.
cimetidine, 7 mg/kg Lv., q. 6 h. or 4-7 days, until
Physical examination and results of minimum database are
ranltidine, 1.5 mg/kg Lv., q. 8 h, and foal nurses or
within normal limits. Endoscopy not done.
bethanecol, 0.02 mg/kg s.c., q. 8 h ingests feed
Subsequent treatment
duration
omeprazole paste, 4 mg/kg s.Ld. or 3-12 weeks
ranltldlne, 7 mg/kg p.o., q. 8 h, and
omeprazole paste, 4 mg/kg, s.Ld., or 2-3 weeks sucralfate, 10-20 mg/kg p.o., q. 8 h, and 3-4 weeks
ranitidine, 7 mg/kg p.o., q. 8 h, or 2-3 weeks bethaneco.l, 0.35 mg/kg p.o., q. 8 h 3-12 weeks
cimetidine, 25 mglkg p.o., q. 6 h 2-3 weeks Repeat endoscopy
after 4-7 days,
Scenario 2: Foal is not nursing well, it has frequent mild then every
abdominal discomfort, and is lethargic. Physical 7-14 days
examination and results of minimum database are within
normal limits. Endoscopy not done. Associated treatment
broad spectrum antimicrobial treatment 2-4 weeks
Treatment recommendation Treatment anti-Inflammatory therapy as needed
duration intravenous fluid support as needed
intravenous nutritional support while foal is nil
omeprazole paste, 4 mg/kg s.i.d., or 3-4 weeks
per os
ranitidine, 7 mg/kg p.o., q. 8 h, and
sucralfate, 10-20 mg/kg p.o., q. 8 h 3-4 weeks
474
The duration of treatment depends on the severity
of the gastroduodenal lesions as determined by
endoscopy. Some lesions can heal remarkably quickly
(within 10 days); this is probably an age-related phe
nomenon. In other cases treatment will be required for
several weeks. If treating empirically, the duration of
treatment should be based on the severity of presenting
signs and evidence for complications rather than the
clinical response to treatment, which can occur within a
few days and thus be misleading as to the progress of
healing. A minimum duration of 2 weeks' treatment is
necessary, but 3 weeks is more prudent. If clinical signs
are severe, a treatment duration of 46 weeks is reason
able to ensure complete healing.
Surgery has been performed to bypass a strictured
pylorus or duodenum with mixed results. The bypass
procedure itself is relatively straightforward for experi
enced surgeons, but several weeks are usually required
for coordinated motility patterns to be established with
the stomach and the anastomosis site. In the interven
ing period, treatment to suppress gastric acidity and
enhance motility should be maintained. Many foals that
require gastroduodenal bypass surgery are severely ill at
the time of surgery and the surgery is attempted as a
salvage procedure. In most cases this either fails or the
foal fails to thrive. However, some foals have gone on to
thrive and perform well. For the procedure to be suc
cessful, the owner must accept a substantial long-term
commitment, both financially and in the care of the
foal.
PHbVbMTM
Prevention of gastric ulceration in foals at high risk of
developing ulcers is best accomplished using acid sup
pressive treatment. Foals of all ages admitted to our hos
pital are routinely treated with an acid suppressive drug,
and of these foals examined at post mortem, virtually
none had gastric ulcers. This contrasts sharply with the
stomachs of foals not treated prophylactically. The prac
tice of ulcer prevention has become commonplace in
equine neonatal ICUs in the United States. There has
not been a study to determine the optimal prophylactic
dose of acid suppressive drug for foals, and in our hospi
tal we typically use either cimetidine at 7 mg/kg Lv., q.
68 h, or ranitidine 7 mg/kg p.o., q. 8 h. Use of a mucosal
protectant such a sucralfate is reasonable, but should be
given in conjunction with an acid suppressive drug.
Other situations that may warrant ulcer prophylaxis
in f()als include transportation, weaning, showing, or
housing the foal in overcrowded conditions. None of
these situations has been shown to increase the risk for
gastric ulceration, but they may afect the foal's milk or
feed intake, and thus contribute to ulcer formation in
individual animals.
StIlL eD00ISltlSm
NJ Nu||y
Endoparasitism of the stomach of foals is relatively
uncommon because modern anthelmintics and para
site control programs are highly efective against para
sitic species that may infect the stomach. Gasterohilus
spp. ( G. intestinalis, G. nasalis, and G. haemorhoidalis) are
the most common gastric endoparasites, but occasion
ally infection with spirurid nematodes (Drschia mega
stoma, Habronema muscae, H. majus) and the minute
worm (Trchostronglus axei) occur.
MbbPHlLUbbPP.
Etiopathogenesis
The most common infestation of the stomach is with
larvae of the common bot fly Gasterophilus intestinalis.
Infestation is seasonal, primarily in the fall and winter
months, and the larvae are readily killed by the iver
mectin anthelmintics. Occasionally a foal may present
with a severe infestation of G. intestinalis or G. nasalis
larvae and have clinical signs referable to the gastro
intestinal tract. The eggs (nits) of the common bot fly
are laid on the horse's legs from where they are
ingested. The larvae of G intestinalis develop within the
stomach and attach to the squamous or glandular
mucosa, usually adjacent to the margo plicatus or in the
dorsal fundus. The larvae will move within the stomach
periodically. Usually the larvae are solitary, but occa
sionally they will congregate into large clusters. The
larvae of G. nasalis tend to develop and accumulate
within the proximal duodenum.
The larae make a small defect in the mucosa, but
even with a large number of larae there usually is only
minimal damage to the mucosa. There are reports,
though, of gastric rupture associated with Gastero
philus larvae infestation.
Clinical signs
Usually there are no associated clinical signs. Clinical
signs do occur however when there is a large number of
Gasterophilus larvae within the stomach or duodenum,
particularly if they are in a large cluster. The signs of
Gasterophilus infestation can mimic those of gastro
duodenal ulceration or there may be vague signs of
475
abdominal discomfort. If lmvae are congegrated at the
cardia the foal may have signs of bruxism and ptyalism.
If many larvae are attached to the mucosa of the proxi
mal duodenum there may be signs of gastric pseudo
obstruction.
Diagnosis
Endoscopy is required for a defnitive diagnosis.
Gastroscopy is performed because the foal presents with
either signs of abdominal discomfort or signs more sug
gestive of gastroduodenal ulceration. Some foals will
have concurrent gastric ulceration, but because most
foals with Gasterophilus larvae do not have gastric
ulcers the association between the ulceration and the
Gasterophilus infestation is unclear.
Treatment
Larvae of Gasterophilusspp. are highly susceptible to treat
ment with ivermectin, 200 llg/kg. There can be complete
elimination of the larvae within 2448 hours of treat
ment. The benzimadazole and pyrimidine anthelmintics
are ineffective in eliminating Gasterophilus larvae.
bPHUH MbNTbb
The spirurid nematodes that can infect the equine
stomach are Daschia megastoma, Habronema muscae, and
H majus. Once relatively common, gastric infection
with these parasites is now rarely encountered. Clinical
problems resulting from spirurid infection are uncom
mon, but those that do occur result from infection with
D. megastoma which produces large, tumor-like lesions
in the gastric glandular mucosa. These lesions contain a
large number of larvae, and clinical problems result
only if the lesion obstructs the pylorus or if stomach
perforation occurs.
NMUTb bTNLM WHN
Typically, infection with Trichostronglus axei is light and
causes no clinical problem. The larae invade the gastric
glandular mucosa and may cause hypertrophic thicken
ing and inflammation ifthe infestation is acute and heavy.
Infection with this parasite can cause sudden weight loss
in horses. The larvae are efectively eliminated by the
benzimadazole anthelmintics and ivermectin.
476
StIlLbSLeSS
NJ Nu||y
Abscessation in the wall of the stomach is an infrequent
fnding. Abscesses can form secondary to severe gastric
ulceration, Rhodococcus equi bacteremia, foreign body
penetration, or septic peritonitis. Signs of gastric absces
sation are variable and similar to abscessation in other
organs
fever
neutrophilia
hyperfbrinogenemia
anemia
weight loss
and possibly colic.
Diagnosis may be made endoscopically, radiographi
cally, or ultrasonographically. Treatment should
include drainage, but since this is usually not possible,
outcomes are usually poor. There is often extensive
involvement of abdominal viscera.
LHPMY
Gastroduodenal ulceration
Furr M 0, Murray M] and Ferguson D C (1992) The effects
of stress on gastric ulceration, T" T4, rT" and cortisol in
neonatal foals. Equine Vet.J 24:37-40.
Murray M, Hart], Parker G A (1987) Equine gastric ulcer
syndrome: Prevalence of gastric lesions in asymptomatic
foals. Poc. Am. Assoc. Equine Pact. 33:769.
Murray M] (1989) Gastroendoscopic appearance of gastric
lesions in foals: 94 cases (1987-1988}.J Am. Vet. Med.
Assoc. 195:1135-42.
Murray M], Mahaffey E A (1993) Age-related characteristics
of the equine gastric squamous epithdial mucosa. Equine
Vet.J 25:514-17.
Sanchez L C, Merritt A M, Lester G D (1998) Effect of
ranitidine on intragastric pH in clinically normal neonatal
foals.J Am. Vet. MedAssoc. 212:1407-12.
Wilson] H (1986) Gastric and duodenal ulcers in foals: A
retrospective study. Poc. Second Equine Colic Rs. Symp.
pp.126-8.
Gastric endoparasitism
Drudge] H, Lyons E T (1986) Inteal parsites of horses.
Hoechst-Rousse1 Vet. Company [place].
24
Small intestinal diseases associated
with colic in the foal
J Orsini
INTRODUCTION
There are a number of congenital defects and anom
alies that may cause colic and/or small intestinal
obstruction or strangulation in foals. These include
scrotal or inguinal hernia, umbilical hernia, and the
congenital anomalies called Meckel's diverticulum
and mesodiverticular band. Diaphragmatic hernia can
occur in foals but it is usually the result of trauma
and is a very rare congenital defect. Other very rare
congenital defects that may cause colic in foals
include segmental lymphatic aplasia with chyloab
domen (chyloperitoneum) , and jejunal diverticulum.
Congenital mesenteric defects, especially in the
mesentery of the small intestine, may lead to incar
ceration of a loop of small intestine ending in stran
gulation or volvulus. A persistent mesodiverticular
band may predispose the adjacent mesentery to
rupture.
The major challenge, in fact, is diagnostic. Rectal
palpation yields helpful, sometimes defnitive, diagnos
tic information in the adult horse but is not generally
feasible in the foal because of its small size. It therefore
can be diffcult to distinguish medical from surgical
cases of colic. Frequently a 'watch and wait' or 'medical
treatment frst' approach can carry as much risk as
exploratory surgery.
Other acquired small intestinal diseases in foals
causing colic and which may require surgical correction
include
volvulus
impaction by ascarids or meconium
intussusception
abdominal abscess.
CONGENITAL DEFECTS ASSOCIATED
WITH COLIC
Scrotal and inguinal hernia
Scrotal hernia may be noticed within a few days of birth
as a soft, fluctuant swelling in the inguinal region and
scrotum. The hernia can be reduced easily when the
foal is rolled onto its back. Scrotal hernias in adult
horses are not easily reduced and the difference
between adults and foals is probably because of the rel
atively shorter, wider, and more direct confguration of
the foal's inguinal canal. Scrotal hernias in foals often
resolve spontaneously, and strangulation of small intes
tine is rare. The size of the external inguinal ring does
not seem to play a role in the problem, usually the
external rings are 5 cm in length on both sides. Scrotal
hernias usually occur on one side only, but bilateral her
nias may occur (Figure 24.1) .
A fgure-of-eight bandage may be applied over the
scrotum and prepuce to encourage resolution of the
hernia. The bandage should be made of adhesive elastic
material and care must be taken not to cover the anus
or end of the prepuce with the bandage. Surgical cor
rection is recommended for an uncomplicated hernia if
it does not resolve spontaneously by 3-6 months, or if
the owner is concerned because of an apparent increase
in the size of the hernia. Correction with castration is
recommended. Surgical correction may be done by
an inguinal approach with castration
laparoscopic repair with castration
an inguinal approach without castration
a midline celiotomy with closure of the vaginal ring.
The last two methods may cause atrophy of the
477
24 GASTROINTESTINAL DISEASE IN THE FOAL
Figure 24.1 Sonogram obtained from a 1-week-old
Standardbred colt with a bilateral inguinal hernia. Notice
the excess fluid contained within the scrotum, the normal
testicle (three arrowheads), and the adjacent jejunum
with normal peristalsis (five arrowheads). From Reef V B
(ed.) (199B) Equine Ultrasonography, W B Saunders,
Philadelphia, with permission
testicle, and the last method may cause intra-abdominal
adhesions. The intestines need not be exposed or eval
uated if strangulation has not occurred and there is no
clinical evidence of intestinal abnormality.
Although most inguinal hernias are indirect in
horses (Le. the intestine passes through the vaginal ring
into the vaginal tunic) , foals can present 4-48 hours
after birth with a direct inguinal hernia. This occurs
when there is rupture of the common vaginal tunic and
jejunum and occasionally a testicle escapes through this
rupture into the subcutaneous space of the scrotum
and prepuce. Direct or ruptured inguinal hernia in
foals causes intermittent colic, severe scrotal and
preputial swelling and edema, with skin excoriation and
splitting caused by abrasion against the inside of the
thigh. These hernias are usually not reducible and
surgery is required. The torn edges of the common
vaginal tunic should be repaired as much as possible to
the level of the vaginal ring. The superfcial or external
inguinal ring should also be sutured, preferably with a
continuous pattern to obtain a more complete seal.
Usually the intestine is viable, but progressive necrosis
has been reported.
Umbilical hernia
Umbilical hernia occurs in 0.5-2 per cent of young
horses. It is considered the second most common con
genital defect in horses (the most common being cryp
torchidism, accounting for 1 per cent of hospitalizations
478
of young horses in one study) . Females are at greater
risk for the defect, with an odds ratio of about 2: 1.
Digital palpation and ultrasonography (Figure 24.2)
are used to determine the size and shape of the hernial
ring, contents of the herial sac, its reducibilit, and the
nature of the tissue surrounding the ring. A thickened
fbrotic ring holds sutures more reliably if the hernia is
repaired surgically. Hernial contents may include
omentum,jejunum, ileum, cecum, and ventral colon, as
well as an antimesenteric portion of small intestinal wall
called a Richter's or parietal hernia.
Smaller hernias may resolve spontaneously and
incarceration of intestine in the hernial ring is rare. In
one report, 13 of 147 horses with umbilical hernias
admitted to a university hospital had developed compli
cations, including intestinal strangulation, abscessation,
and enterocutaneous fstula. Surgical repair is usually
undertaken for cosmetic reasons. Frequent monitoring
of hernias and early repair of large hernias (> 10 cm) is
recommended, because strangulation may develop at
any time. Strangulation should be suspected in a non
reducible umbilical hernia that increases in size and
warmth, and is painful, frm, or edematous. Severity of
pain is not a reliable indicator of strangulation or other
complications. When a loop of small intestine is
involved, it usually dissects back to the inguinal region
where most of the swelling occurs.
Surgical reduction is necessary for umbilical hernias
that contain incarcerated intestine. With the foal in a
dorsal recumbent position, a 10-15 cm incision is made
cranial to the hernia ring to avoid accidental puncture
of incarcerated bowel. Once the abdomen has been
opened and the involved intestine identifed, the inci
sion is extended to and around the hernial ring. The
incarcerated bowel and its attachments to the hernial
ring may be resected. If an enterocutaneous fstula is
involved, special care should be taken to clean the fs
tula and isolate it from the surgical feld by packing it
and suturing skin over it.
Meckel's diverticulum and mesodiverticular
band
Meckel' s diverticulum and the mesodiverticular bands
are congenital anomalies that arise from remnants of
the vitelline duct and arteries. In the embryo, the
vitelline duct connects the lumen of the gut to the yolk
sac. The vitelline arteries run on either side of the
mesentery from the aorta to the yolk sac. A the yolk sac
regresses and involutes at 5-10 weeks of gestation, the
right vitelline artery becomes the cranial mesenteric
artery, the left vitelline artery regresses, and the vitelline
duct also involutes. Anomalies result if the vitelline duct
persists as a tubular projection from the distal jejunum
SMALLINTESTINAL DISEASES ASSOCIATED WITH COLIC IN THE FOAL 24
Figure 24.2 Sonograms of the umbilicas and ventral abdomen obtained from a 9-month-old Quarter horse colt with an
umbilical hernia. The right side of these sonograms is cranial, and the top is ventral, a) sonogram of the umbilical swelling
demonstrating the large umbilical abscess (arrows) associated with the umbilical hernia, b) sonogram of the thickened
ileum trapped within the hernia. From Reef V B (ed.) (1998) Equine Ultrasonography, W B Saunders, Philadelphia, with
permission
or ileum or if the left or right vitelline arteries persist as
bands of tissue (Figure 24.3) . Any of these anomalies
may cause incarceration, strangulation, or volvlus of
the small intestine, and the diverticulum may become
infected and necrotic. Most of the reported cases have
been in adult horses, although there are reports of a 3-
month-old foal and a 6-month-old foal that were
affected. It was initially thought that these anomalies
were quite common in horses, but recent studies sug
gest that they are quite rare. However when they are
Figure 24.3 A large Meckel's diverticulum with a diameter
equal to that of the small intestine
present, they are often if not always implicated in mor
bidity and mortality.
Mesenteric defects
Congenital mesenteric defects, especially in the mesen
tery of the small intestine, may lead to incarceration of
a loop of small intestine, and may end in strangulation
or volvulus. These defects are rare. A persistent mesodi
verticular band may predispose the acacent mesentery
to rupture.
Chyloabdomen
Chyloabdomen is a rare condition that may cause colic
in foals 12-36 hours after birth. Affected foals seem
healthy initially and then develop signs of colic but usu
ally without reflux or abdominal distension.
Abdominocentesis yields a copious flow of milky,
opaque fluid with a triglyceride concentration 100
times the reference value. The cell count may be nor
mal and the nature of the fluid precludes protein deter
minations with a refractometer.
Surgical findings include an abdomen full of white,
opaque fluid and a variable length of jejunum that is
thick-walled, turgid, and discolored white to yellow.
Associated mesenteric lymphatics are white and
markedly distended. Subserosal lymphatic vessels are
distended with lymph, and some rupture to form coa
lescing yellow-white plaques. The condition seems to be
caused by congenital absence of a communication
between afferent and efferent lymph vessels from the
involved lymph nodes, with subsequent mesenteric lym
phangitis and lymphangiectasis. Intestine proximal to
479
Figure 24.4 Sonogram of the left side of the thorax
obtained in the tenth intercostal space from a 1-month
old Standardbred filly with a diaphragmatic hernia. The
fluid-distended small intestine (SI) is immediately adjacent
to the ventral lung with no diaphragm separating them
the affected segment is usually distended, and this, pos
sibly associated with the irritation of chyle in the
abdomen, could explain the signs of colic.
Resection of the affected intestine can produce a sat
isfactory outcome. Conservative treatment with anal
gesics, antibiotics, and intravenous fluids led to a full
recovery in one foal with chyloabdomen.
Diaphragmatic hernia
Diaphragmatic hernias can occur in foals, either as a
rare congenital defect in which there is incomplete
fusion of the pleuroperitoneal folds in the dorsal tendi
nous portion of the diaphragm, or more commonly as a
result of trauma. They can be treated successfully by
direct closure or by insertion of a mesh implant.
Presenting signs are usually non-specifc, but ultra
sound (Figure 24.4) and radiographic examinations
may reveal loops of bowel in the thoracic cavity. Most
cases are diagnosed at surgery without a preoperative
diagnosis.
ACQUIRED SMALL INTESTINAL
DISEASES ASSOCIATED WITH COLIC
Gastroduodenal ulcers and obstructions (see
Chapter 23)
Gastric ulcers are common in foals of all ages, particu
larly those treated with non-steroidal anti-inflammatory
drugs or subjected to various forms of stress. Diarrhea is
the most common clinical sign of gastroduodenal
480
ulcers, but teeth grinding, salivation, and signs of colic
are also suggestive of ulcers. Gastric reflux and fever
may also be observed. Ulcers may not always be mani
fested by signs of acute colic. Laboratory studies may
show high total white blood cell counts or elevated
plasma fbrinogen levels. The medication history is
helpful in evaluating the possibility of ulcers. In foals, a
regimen of phenylbutazone at 10 mg kg-I d-I may pro
duce severe gastrointestinal ulcers and diarrhea as early
as day 3 of treatment. Flunixin meglumine is also poten
tially ulcerogenic, but low doses (0.5-1.1 mg kg-I d-I)
have been used safely in neonates. Ulceration may be
suspected in a foal with colic if there is a history of non
steroidal anti-inflammatory drug treatment or of signif
icant stress such as surgery, transportation, or other
illness; however these factors can be difcult to docu
ment. There can sometimes be an outbreak of duo
denal ulcers in a herd.
Ulcers with outflow obstruction can be diffcult to
confrm by contrast radiography. Diagnostic signs on
plain radiographic flms include aspiration pneumonia,
dilated fluid-flled esophagus, and gastric distension;
gas may be present in the hepatic duct. Endoscopy is
more sensitive and specifc than radiography in diag
nosing esophageal and gastric lesions, and it also allows
biopsy. Endoscopic studies have shown erosions and
ulcers in a substantial proportion of foals that do not
have signs of colic.
Ulcers can be managed medically, although duode
nal and gastric ulcers can perforate. Severity of pain is
not always a reliable guide. Perforation has occurred in
moribund foals showing no or only mild signs of gas
trointestinal disease and in which ulcers were not sus
pected. Surgery is indicated if barium contrast
radiographs suggest gastroduodenal obstruction, illus
trated by reflux of fluid from the stomach to esophagus,
an enlarged gastric silhouette, and delayed gastric emp
tying (> 2 hours) . Surgery is undertaken to prevent
complications - primarily ulcer perforation and gastric
outflow obstruction - as well as to relieve colic and pro
mote mucosal healing. Surgery has been used success
fully to repair a perforated gastric ulcer in a foal.
Foals younger than 4 months of age are at a greater
risk of developing gastroduodenal obstruction sec
ondary to ulcers. Potential sites of obstruction are the
cardia, gastric antrum, pylorus, and duodenum. Many
affected foals have been depressed, weak, and anorectic
in the days or weeks preceding examination, and radi
ographic views show gastric and esophageal distension.
Volvulus of the small intestine
Volvulus of the small intestine is the most common indi
cation for intestinal surgery in the foal. It most often
Figure 24.5 Sonogram of the abdomen obtained from a
3-week-old Thoroughbred colt with a small intestinal
volvulus. Turgid distended loops of jejunum are filled
with anechoic fluid with only a small amount of ingesta
distended (white arrow). From Reef V B (ed.) (1998)
Equine Ultrasonography, W B Saunders, Philadelphia,
with permission
involves the distal jejunum and ileum. Any length of
small intestine ranging from a few centimeters to sev
eral meters may be twisted or knotted. Volvulus is seen
most often in foals younger than 3 months and may be
a result of changing feeding habits as the foal adapts to
digesting bulkier adult food. Other reported risk factors
include peritonitis, previous abdominal surgery, and
parasite burden.
Pain may seem to fluctuate but quickly becomes
severe, and affected foals often lie on their sides or
assume a position of dorsal recumbency. A the foal's
condition deteriorates, the small intestine begins to dis
tend with gas; at this point, the abdomen becomes dis
tended and peristalsis is not evident on abdominal
auscultation. Rapid and labored respiration, high fever,
a weak and rapid pulse, and injected mucous mem
branes indicate a deteriorating condition, and differen
tiate volvulus (sometimes too late for successful
intervention) from ileus. Ultrasonography has proven
to be a useful ancillary diagnostic modality (Figure
24.5) .
At surgery, the twisted loop is often located close to
the ileocecal valve and is generally recognized easily by
its purple congested appearance. In some cases the twist
is very loose and easily freed, whereas in others it is dif
ficult to reduce. Ater correcting the volvulus, resection
and anastomosis can be p
t
rformed.
Small intestinal impaction
Ascarid impaction (see Chapter 13)
Intestinal stages of Parscars equorum may cause intesti
nal obstruction, intussusception, abscessation, and even
rupture in older foals (2-4 months) , but this is more
common in weanlings (median age 5 months; range
4-24 months) . Affected foals usually appear parasitized
and unthrifty, and impaction usually follows
anthelmintic treatment by 1-5 days. A history of recent
anthelmintic administration should always raise the
question of a possible ascarid impaction in a foal with
acute colic. Impactions may occur without anthelmintic
treatment however. Because foals develop a natural
immunity to this parasite, infection rates decline after 6
months of age. Ultrasonography has been used to con
frm an ascarid impaction in those cases where the
cause for the acute abdominal crisis is unclear (Figure
24.6) .
Surgical removal of impacted ascarids is indicated in
foals with clinical signs of obstruction. Impactions may
occur at more than one site, but distal jejunum and
ileum are the most common sites, followed by the
cecum and other parts of the jejunum, and the pelvic
flexure. Enterotomy is required to relieve the
impaction and resection may be indicated if the bowel
Figure 24.6 Sonogram of the abdomen obtained from a 5-
month-old Paint colt with an ascarid impaction. The thick
echogenic ascarid worm (arrow) is surrounded by fluid in
the small intestine. From Reef V B (ed.) (1998) Equine
Ultrasonography, W B Saunders, Philadelphia, with
permission
481
is devitalized. Damage to the intestinal wall at the site of
the impaction often causes peritonitis and adhesions,
and the mortality rate may be as high as 92 per cent.
To prevent ascarid impaction, heavily parasitized
f()als should be wormed with a slow-acting drug such as
a benzimidazole (e.g. thiabendazole - the least effective
and therefore the safest, and fenbendazole) .
Ivermectin, also slow acting but highly effective against
this parasite, can be given 3 weeks later. The goal of
treatment is to reduce the numbers gradually, rather
than kill all the ascarids simultaneously leaving a mass
of dead worms in the lumen of the bowel.
Meconium impaction (see Chapter 25)
Retention of meconium is a frequent cause of intestinal
obstruction in neonates, most commonly involving the
rectum and small colon. Most cases respond to medical
treatment with enemas, intravenous fluids, and laxa
tives. Meconium impaction may be diffcult to differen
tiate from ruptured bladder and from atresia ani, a
relatively rare congenital defect. Foals with ruptured
bladder are usually older (usually at least 3-4 days of
age) . If medical treatment does not result in the passage
of meconium, or if colic signs persist, surgery may be
indicated.
In a recent study, 8 of 24 foals with meconium
impaction required surgery, and 2 of these 8 required
an enterotomy. Of these 8 foals, there were 7 with fol
low-up information after surgery; 2 were euthanized
because of serosal adhesions after enterotomies to evac
uate the impaction, and 4 matured and raced without
complications.
Intussusception
Small intestinal intussusception has been regarded as
being a common condition in foals, but recent clinical
experience and the results of two retrospective studies
which did not identif a single case in a series of 87 foals
with colic, suggest that it is very rare. The small intestine
can invaginate into the cecum or into itself, conditions
that may begin as simple obstructions and progress to
strangulation as the tissue becomes edematous and the
vascular supply is compromised (Figures 24.7 and 24.8) .
The cause of intussusceptions is not known, but they
have been associated with bacterial and protozoal
(Eimeria leukarti) infection in one case, and treatment
with an organophosphate anthelmintic in another.
Intussusception can present as acute colic that is dif
ficult to distinguish from volvulus. In other cases signs
may be subacute or chronic. The subacute form may fol
Iowa bout of diarrhea in young foals, they may also grind
their teeth and show moderate signs of colic. Those with
the chronic form become anorectic and unthrift and
482
Figure 24.7 Sonogram of the ventral abdomen obtained
from a 3-day-old Thoroughbred colt with an intussuscep
tion. Notice the characteristic target or 'bull's-eye' sign of
the intussusception. The 'bull's-eye' sign is created by the
edematous outer intussuscipiens (solid arrow), a fluid layer
between the outer intussuscipiens and the inner intussus
ceptium, and the more echogenic inner intussusceptum
(open arrow). From Reef V B (ed.) (1998) Equine
permission
Figure 24.8 Sonogram of the ventral abdomen obtained
from a 5-day-old Thoroughbred colt with an intussuscep
tion. Notice the fibrin between the thick outer intussuscip
iens (outer arrows) and the inner intussusceptum (inner
arrow). From Reef V B (ed.) (1998) Equine
permission
they are often only diagnosed at necropsy, underscoring
the importance of exploratory celiotomy in diagnosing
unexplained and persistent colic. Gentle traction and
manipulation can relieve an intussusception, although a
jejunocecostomy is sometimes necessary.
Necrotizing enterocolitis
This is a rare but highly fatal disease of newborn foals,
particularly those stressed at birth by dystocia, placental
disease, and other causes of immaturity. The cause is
probably multifactorial, although intestinal ischemia or
hypoxia is a predisposing factor for this disease in
human infants. In foals, the intestinal mucosa is usually
intact but gas-forming bacteria seem to colonize the
bowel wall and cause gas accumulation. Bowel perfora
tion can follow. Gross appearance of the affected bowel
includes submucosal emphysema, hemorrhage, edema,
and inflammation in the intestinal wall.
Radiographs are often diagnostic. Segments of intes
tine viewed in cross section have a double-ring appear
ance caused by a radiolucent layer of gas separating
layers of the bowel wall. Many linear strips or 'bubbles'
of gas can be seen in the intestinal wall (pneumatosis
intestinalis, Figure 24.5) and gas distension of the
affected segment should be evident. Gas in the peri
toneal cavity is evidence of rupture.
Surgery to resect affected intestine; nutritional, fluid,
and electrolyte support; and antibiotics are required.
The prognosis is poor especially if surgery is delayed, the
lesions are too extensive for intestinal resection, or the
foal is too debilitated for other reasons.
Abscess
Mesenteric and intestinal abscesses can cause intestinal
obstruction and colic in foals. Foals with abscesses in
the umbilical remnants are usually younger than
Figure 24.9 Sonogram obtained from a 2-month-old
Thoroughbred filly with an abdominal abscess. The
abscess (arrows), which is lying against the floor of the
ventral abdomen, has a multi loculated appearance. From
Reef V B (ed.) (1998) Equine Ultrasonography, W B
Saunders, Philadelphia, with permission
6 weeks of age. Foals with mesenteric abscesses
(Stretococcus spp. and Rodococcus equi) are usually 2-6
months old, and may have no pulmonary involvement.
Clinical signs of abscesses in foals include recurrent,
mild colic in some but not all cases, fever unresponsive
to antibiotics, neutrophilic leukocytosis, and hyperfb
rinogenemia. Mesenteric abscesses are heavy and tend
to migrate to the ventral abdomen where they can be
detected by ultrasound examination (Figure 24.9) .
Surgical treatment by bypass or marsupialization is pos
sible in some cases.
POSTOPERATIVE MANAGEMENT AND
COMPLICATIONS
Close postoperative monitoring is needed to avoid
potentially fatal complications of abdominal surgery in
foals. The main concerns in the immediate postopera
tive period are ileus and hypovolemic or endotoxic
shock. Sepsis accounts for signifcant morbidity and
mortality in foals following abdominal surgery, and
antibiotic therapy must be tailored to the different
metabolism of very young foals, with adequate coverage
for gram-negative bacteria in any septicemic foal.
Peritonitis may occur following leakage of bacteria from
the bowel into the peritoneal cavity. Foals seem to be
especially prone to intestinal adhesions after abdominal
surgery, and may require a second procedure when
signs of colic and obstruction recur. Small intestinal
lesions are associated with a higher incidence of abdom
inal adhesions than colonic lesions. Experimentally,
adhesions have been shown to result from ischemia or
distension of the small intestine.
OUTCOME AND PROGNOSIS
In certain respects foals are good candidates for
surgery. Their size mitigates some of the problems of
abdominal surgery in adult horses, and survival rates of
foals do not seem to be signifcantly worse than survival
rates of adult. This is not true for very young foals, how
ever. Foals younger than 1 week of age had the worst
odds of survival, and the odds improved for the 1-
month-old group, and improved even further for the
1-3-month-old foals. In a recent report of 67 foals with
surgical colic, only 10 per cent of foals under 14 days of
age survived to maturity compared to 46 per cent of
foals between 15-150 days of age. Short-term survival
for foals of this age with colic surgery has been reported
as 63-65 per cent, and long-term surival is about 40 per
cent, similar to the reported long-term survival of older
horses undergoing colic surgery (45 per cent) . A
483
expected, colic surgery surival rates vary widely accord
ing to the diagnosis, the compromised condition of
many surgical colic patients is also a signifcant con
founding factor in survival. One of the major challenges
in foals is diagnostic. Because rectal examination is not
possible, it may be even more dificult to distinguish
medical from surgical cases of colic. Frequently a 'watch
and wait' or 'medical treatment frst' approach can
carry as much risk as exploratory surgery.
BIBLIOGRAPHY
Crowe M W, Swerczek T W (1985) Equine congenital defects.
Am.] Vet. Res. 46(2): 353-8.
Edwards G B, Scholes S R, Edwards S E R, et al. (1994) Colic in
four neonatal foals associated with chyloperitoneum and
congenital segmental lymphatic aplasia. In: Proceedings of
the Fifth Equine Colic Research Symposium, Athens, GA, p. 35.
Freeman D E, Koch D B, Boles C L (1979) Mesodiverticular
hands as a cause of small intestinal strangulation and
volvulus in the horse.]. Am. Vet. Med. Assoc.
175(10):1089-94.
Freeman D E, OrsiniJ A, Harrison I W, et al. (1988)
Complications of ur hili cal herias in horses: 13 cases
(1972-1986).]. Am. Vet. Med. Assoc. 192:804-7.
Freeman D E, Spencer P A (1991) Evaluation of age, breed,
and gender as risk factors for umbilical hernia in horses of
a hospital population. Am.]. Vet. Res. 52:637-9.
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Hooper R N (1989) Small intestinal strangulation caused by
Meckel's diverticulum in a horse.]. Am. Vet. Med. Assoc.
194(7):943-4.
Klohnen A, Wilson D G (1996) Laparoscopic repair of scrotal
hernias in two foals. Vet. Surg. 25:414-16.
Lundin C S, Sullins K E, White N A, et al (1989) The
pathogenesis of peritoneal adhesions in the foal
(abstract). Vet. Surg. 18:65.
Markel M D, PascoeJ R, Sams A E (1987) Strangulated
umbilical hernias in horses: 13 cases (1974-1985).]. Am.
Vet. Med. Assoc. 190:692-4.
OrsiniJ A (1997) Abdominal surgery in foals. Vet. Clin. N Am.
Equine Pract. 13(2) :393-413.
Priester W A, Glass M D, Waggoner, N S (1970) Congenital
defects in domesticated animals: general considerations.
Am.] Vet. Rs. 31:1871-9.
Robertson J T (1982) Obstructive diseases - congenital
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Mansmann, E S McAllister, P W Pratt (eds). American
Veterinary Publications, Santa Barbara, C, 1982, pp.
559-71.
Sprinkle F P, Swerczek T W, Crowe M W (1984) Meckel's
diverticulum in the horse. Equine Vet. Sci. 4(4):175-6.
Spurlock G H, RobertsonJ T (1988) Congenital inguinal
hernias associated with a rent in the common vaginal
tunic in five foals.]. Am. Vet. Med. Assoc. 193:1087-8.
van der Velden M A (1988) Ruptured inguinal hernia in new
born colt-foals: A review of 14 cases. Equine Vet.].
20:178-81.
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diverticulum in a foal.]. Am. Vet. Med. Assoc. 183:1092.
25
Large and small colon diseases
associated with colic in the foal
Retained meconium
W Bernard
INTRODUCTION
Meconium is a product of glandular secretions, swal
lowed amnionic fluid, epithelial cells, mucus, and bile.
Throughout gestation this material is moved along the
fetal gastrointestinal tract by peristalsis and is stored in
the colon and rectum. Meconium varies in color from a
glossy black to a dark brown. The consistency and form
of this frst stool can be hard, grape-size pellets or a
sticky, tarry toothpaste-like material. The change to a
less tenacious material generally indicates that the
meconium has been passed.
The initial passage of meconium usually begins in
the frst few hours after birth. Meconium passage is gen
erally complete within 24 hours, however it can take up
to 48 hours. The time spent evacuating meconium is
not the critical factor when considering meconium
retention. The degree of pain, discomfort, and strain
ing, and alterations in the routine foal behavior are the
critical factors to be considered when evaluating the
possibility of meconium retention. It is not atypical for
newborn foals, standing or in lateral recumbency, to
strain considerably when passing meconium. These
attempts should be productive. Male foals (possibly as a
result of narrowed pelvic inlet) and foals resulting from
prolonged gestation appear to be predisposed to meco
nium retention. Meconium retention has been classi
fed as either high or low impaction. A low impaction is
an obstruction of the small colon/rectum at the pelvic
inlet. The incidence of low impactions far outnumbers
that of high impactions. High impaction is a more prox
imal obstruction of the gastrointestinal tract, in the
author's experience this generally occurs in the trans
verse or right dorsal colon.
Clinical signs
Clinical signs of meconium retention may include any
combination of the following
repetitive unproductive tenesmus
tail flagging/ swishing
stretching
posturing as if to defecate (kyphotic posture -
humped back)
abdominal pain
abdominal distension
lack of interest in suckling.
Figure 25.1 Meconium retention in a 24-hour-old foal.
Dorsal recumbency
485
Frequent efforts at defecation may be confused with
attempts to urinate. Advanced signs of abdominal pain
include dorsal recumbency (Figure 25.1), rolling from
side to side, or violent collapse. Meconium retention is
the most common cause of abdominal pain in the new
born foal (see Chapter 22). It should be noted that the
clinical signs seen with meconium retention are non
specifc, and other diferentials of abdominal pain
should be considered.
DIAGNOSIS
Diagnosis of the condition is based upon clinical signs,
physical examination fndings, and other diagnostic
testing. Digital examination can identif fecal material
at the pelvic inlet, however, absence of a positive digital
finding should not rule out meconium retention. If
retention is suspected, response to a mild enema can be
diagnostic. If clinical signs of abdominal pain persist,
then abdominal radiology and ultrasonography should
be pursued. Passage of a nasogastric tube may identif
gastric reflux, and peritoneal fluid analysis may be use
ful in ruling out other causes of abdominal pain.
Abdominal ultrasound can be used to identif the pres
ence of meconium in the gastrointestinal tract (this is
not necessarily indicative of impaction) and to rule out
other disease processes. Radiographs of the abdomen
can identif meconium and/or gas distension of the
small or large intestine. Contrast radiography (barium
enema), can be very useful if other diagnostics are not
defnitive. A barium enema is performed using a soft
rubber catheter, and gravity flow of 500-1000 ml of liq
uid barium contrast material.
Differential diagnoses for foals showing clinical signs
of meconium retention include
bladder rupture
rectal irritation
congenital atresias
ileocolonic aganglionosis.
TREATMENT
Treatment of meconium retention varies with severity
and duration. Simple, cautious manual removal of fecal
. material can occasionally be all that is necessary. Mild
enemas usually provide adequate softening and lubrica
tion for passage of retained material. Enema solutions
vary in quantity and contents. Commercial products are
available and can be effective. A safe, non-irritating
enema solution consists of 500-1000 ml of warm water
with 5-10 ml of sof, non-irritating soap. Repetitive
486
enemas can be irritating to the sensitive rectal mucosa,
it is preferable to use fewer large volume enemas rather
than frequent small volume procedures. Foals that
develop rectal irritation from enemas can demonstrate
the same clinical signs as meconium impaction, this may
lead to further enema administration and further irrita
tion. Eventually the foal may develop toxemia unless the
irritating enemas are discontinued. Sot flexible
catheters are much preferred over the rigid counterparts.
Gravity flow, retention enemas containing 4% acetylcys
teine have been recommended and can be effective.
The use of laxatives or cathartics given via nasogas
tric tube may be benefcial particularly if the impaction
is suspected to be proximal. Mineral oil (200-400 ml),
castor oil (30 ml) and milk of magnesia (120 ml) have
been recommended. The effectiveness of these prod
ucts is more likely via stimulation of gastrointestinal
motility rather than a direct effect on the meconium.
Cathartics should be used cautiously as they can be very
irritating to the mucosal lining of the gastrointestinal
tract. It is unlikely that fluid therapy is useful in soften
ing meconium impactions. A straining foal with a pelvic
obstruction and full bladder (as a result of fluid ther
apy) may be more prone to bladder rupture.
Pain control is an important aspect of therapy. A col
icky foal can not effectively pass meconium. Analgesics
are benefcial when used judiciously. Passage of a naso
gastric tube to assess the presence of gastric distension
should be a routine procedure in the diagnostics and
therapy of a colicky foal. If abdominal distension
becomes excessive despite therapy, then cecal trocariza
tion and/or surgical exploration may become neces
sary. It is rare that abdominal surgery is required to
resolve low impactions. Surgery may be necessary if
there is unrelenting, non-responsive pain and/or
severe gas distension. In these circumstances an alter
native cause of abdominal pain or a proximal meco
nium obstruction (right ventral or transverse colon) is
generally identified.
Atresia coli
EM Santschi
INTRODUCTION
Atresia coli is an uncommon, apparently sporadic con
dition of neonatal foals. Foals affected with atresia coli
initially nurse well, but can not pass meconium. The
ingestion of food causes fluid and gas to accumulate,
and the intestine becomes distended causing colic.
LARGE AND SMALL COLON DISEASES ASSOCIATED WITH COLIC IN THE FOAL 25
EPIDEMIOLOGY
Age
Atresia coli is a congenital condition, therefore clinical
signs of colic and bloating are seen only in foals within
48 hours of birth.
Gender
There is no gender predisposition.
Genetics
Atresia coli has been reported in American Paint
horses, Arabians, Appaloosas, Morgans, Quarter horses,
Standardbreds, and Thoroughbreds. No genetic predis
position has been noted.
ETIOLOGY
The cause of atresia coli is unknown. The condition is
thought to be caused by a congenital loss of blood sup
ply to a portion of the colon leading to ischemic local
necrosis of the gut. Because of the rare occurrence of
atresia coli, such vascular accidents are presumed to be
random events.
CLINICAL SIGNS
Foals affected with atresia coli will usually show signs of
abdominal pain and progressive abdominal distension
within 24 hours of birth. No meconium is passed and
none can be detected by palpation or enemas.
Occasionally, a blind-ended rectum can be palpated
digitally. Abdominal radiographs and ultrasound
demonstrate gas and fluid-flled intestinal segments.
CLINICAL PATHOLOGY
There are no pathognomonic pre-mortem tests for atre
sia coli. A the foal becomes moribund, alterations in
blood clinical chemistry and hematological parameters
can be seen due to dehydration and endotoxemia.
PATHOLOGY
Gross pathology
Segments of the colon are not present. Most foals with
atresia coli are type 1, a blind-end atresia - the oral dis
connected segment is dilated with meconium, fuid,
and gas, and the rectal segment is usually atretic (Figure
25.2). Other congenital abnormalities of the cardiac
Figure 25.2 Surgical photo of a foal with atresia coli. The
blind end of the right ventral colon is closest to the cam
era. The pelvic flexure and all large colon aboral were not
present in this foal.
and central nervous system have been reported in foals
affected with atresia coli, and may be discovered on
DIAGNOSIS
The major differential diagnoses of atresia coli are
Overo lethal white syndrome and meconium
impaction. Overo lethal white syndrome can be elimi
nated in the majorit of foals by examination of pedi
gree and physical appearance of the foal. One useful
clinical sign that will discriminate between atresia coli
and an impaction is that most foals with meconium
impaction will produce some feces or fecal staining.
Abdominal radiographs using barium enemas can also
be used to discriminate between a foal with atresia coli
and one with a meconium impaction.
Proctoscopy may be helpful in some foals with
atresia coli. Confrmation of colonic atresia can only
be made at exploratory laparotomy. However, a pre
sumptive diagnosis of colonic atresia can be made in
non-Overo lineage horses by the appearance of colic
signs within 24 hours of birth and the lack of fecal
staining.
TREATMENT
Treatment of atresia coli requires either surgical anas
tomosis of the discontinuous segments or a colostomy
of the blind end of the oral segment. Several attempts
have been made at surgical correction, but to the
487
author's knowledge, none of the treated foals have
survived to adulthood. One foal was followed for 18
months after surgery and reported as healthy but was
then lost to follow up, and another foal survived 16
months after the surgery, but succumbed to colic
caused by intestinal adhesions (Ducharme, personal
communication, 1999). Ileus, adhesions, and peritoni
tis are the most common reasons for failure. Because of
the guarded prognosis and the high cost of treatment,
most foals with atresia coli are euthanized after
exploratory surgery. An additional concern is the
reported concurrent occurrence of other congenital
abnormalities. Foals should receive a thorough physical
examination before surgery to try and detect other con
ditions. If correction is attempted, owners should be
advised that other conditions could become apparent at
a later date.
Surgical correction is not possible in all foals
affected with atresia coli because of an inability to phys
ically reappose the blind-ended segments. Permanent
colostomy is unlikely to be successful. If anastomosis is
attempted, it should focus on removing as much ingesta
as possible from the proximal segment, removing any
compromised bowel in the proximal blind-ended sec
tion, and suturing the sections together. Because of the
disparate sizes of the lumens of the segments, hand
suturing is recommended using 3-0 monoflament
absorbable suture material, and an end-to-side anasto
mosis is usually performed to maximize the lumen size
of the distal segment. Two suture lines are recom
mended, the frst appositional and the second invert
ing. Feeding after surgery should begin slowly as
initiation of motility in the previously distended seg
ments may be delayed.
Ileocolonic aganglionosis
EM Santschi
INTRODUCTION
Ileocolonic aganglionosis is a congenital absence of
myenteric ganglia in the terminal portion of the ileum,
'cecum, large colon, and small colon. The disease was
first reported in the US in 1977 and primarily occurs in
all-white offspring born to parents of the Overo spotting
pattern. The condition is always fatal. Fmils affected
with ileocolonic aganglionosis are referred to as 'Lethal
whites', so the condition is referred to as Overo lethal
white syndrome (OLWS).
488
EPIDEMIOLOGY
Age
Overo lethal white syndrome is a congenital agan
glionosis, therefore clinical signs are seen only in foals
within 48 hours of birth.
Gender
There is no gender predisposition.
Genetics
Overo lethal white syndrome is seen in foals born to
parents of Overo lineage. The parents are not always of
Overo coloration, but often are because the gene
responsible for OLWS also causes a prominent Overo
color pattern.
ETIOLOGY
The cause ofOLWS is the inheritance of to alleles of a
specifc mutation in the gene that codes for endothelin
receptor B. Allele-specifc testing reveals that the muta
tion is most common in American Paint horses, but is
also found in Quarter horses, American Miniature
horses, Pintos, Thoroughbreds, Saddlebreds, and
Standardbreds. The lethal mutation in the endothelin
receptor B gene results in a single amino acid substitu
tion in the frst transmembrane domain of the seven
transmembrane domain g-protein coupled receptor.
This alteration in the protein composition is thought to
be sufcient to substantially alter the function of the
endothelin B receptor. The mechanism by which the
receptor causes aganglionosis is not known. However,
multiple investigations in multiple species indicate the
importance of the endothelin signaling pathway in the
normal development of the neural crest cells that
become epidermal melanocytes and enteric neurons.
CLINICAL SIGNS
Foals born affected with OLWS are born white or
almost entirely white (Plate 25. 1). Small areas of pig
ment can occur on the body, especially the forelock and
tail. They have pigmented retinas but their irises are
white, giving an appearance of 'glass eyes'. OLWS foals
are apparently normal at birth, and will stand and nurse
well. However, they eventually show signs of colic from
intestinal distension caused by a functional obstruction.
The appearance of signs of colic are variable, but most
often occur within 24 hours of birth. Lethal white foals
most commonly do not pass feces, but occasionally
some fecal staining can be obtained after enemas.
LARGE AND SMALL COLON DISEASES ASSOCIATED WITH COLIC IN THE FOAL 25
Abdominal ultrasound and radiographs will demon
strate variable amounts of intestinal distension, and
foals will generally bloat and die within 48 hours of
birth.
CLINICAL PATHOLOGY
There are no pathognomonic pre-mortem tests for
OLWS. A the foal becomes moribund, alterations in
blood clinical chemistry and hematological parameters
can be seen, presumably because of dehydration and
endotoxemia.
PATHOLOGY
Gross pathology
Milk is found in the stomach and duodenum.
Meconium is found in the ileum, cecum, and colon but
is not impacted and is typically not found in the small
colon, which contains only mucus. Gas and fluid disten
sion of the intestine varies, but always involves the small
intestine over much of its length. The small colon is
atretic and appears tortuous and tightly contracted
(Figure 25.3).
HISTOPATHOLOGY
Myenteric ganglia are absent in the ileum, cecum, and
colon of affected foals.
Figure 25.3 Gross necropsy photo of the small colon of a
foal affected with Overo lethal white syndrome. The small
colon is atretic and contracted, and contains no meco
nium.
DIAGNOSIS
Confrmation of OLWS can be made by demonstrating
the lack of myenteric ganglia in the small colon of foals
at necropsy and by demonstration of homozygosity for
the OLWS mutation in the gene encoding endothelin
receptor B. The major differential diagnoses of OLWS
are atresia coli and meconium impaction. Meconium
impaction can be diagnosed by digital examination,
abdominal radiographs with contrast material, and by
ultrasound. Atresia coli can sometimes be diagnosed by
abdominal radiographs with contrast material, but is
definitely found by exploratory laparotomy. A presump
tive diagnosis ofOLWS can be made in all-white foals of
Overo parentage that bloat and colic within 48 hours of
birth, and that do not pass feces.
TREATMENT
Attempts to treat OLWS either medically or surgically
are doomed to fail because of the extensive nature of
the lesion. The intractable nature of the condition
means that foals should be euthanized once a presump
tive diagnosis is made.
PREVENTION
Allele-specific testing is available to test breeding stock
for the presence of the genetic mutation that causes
OLWS. By testing breeding stock and not breeding
heterozygotes the occurrence of OLWS can be elimi
nated.
BIBLIOGRAPHY
Retained meconium
Shires G M (1991) Diseases of the small colon. In: Equine
Medicine and Surg, P T Colahan, I G Mayhew, A M
Merritt,] N Moore (eds). American Veterinary
Publications, Goleta, CA, pp. 659-60.
Atresia coli
Estes R, Lyall W (1979) Congenital atresia of the colon: a
review and report of four cases in the horse.] Equine Med.
Surg. 3:495-8.
Fischer A T, Yarborough T Y (1995) Retrograde contrast
radiography of the distal portions of the intestinal tract of
foals.] Am. Vet. Med. Assoc. 207:734-7.
Nappert G, Laverty S, Drolet R, Naylor] (1992) Atresia coli in
7 foals (1964-1990). Equine Vet.] supp!. 13:57-60.
Young R L, Linford R L, Olander H] (1992) Atresia coli in
the foal: a review of six cases. Equine Vet.] 24:60-2.
489
Ileocolonic aganglionosis
Gariepy C E, Cass D T, Yanagisawa M (1996) Null mutation of
endothelin receptor B gene in spotting lethal rats causes
aganglionic megacolon and white coat color. Poc. Nat.
Acad. Sci. 93:867-72.
Hultgren B D (1982) Ileocolonic aganglionosis in white
490
progeny of overo spotted horses. J. Am. Vet. Med. Assoc.
180:289-92.
Santschi E M, Purdy A K Valberg SJ, Vrotsos P D, Kaese H,
MickeisonJ R (1998) Endothelin receptor B mutation
associated with lethal white syndrome in horses. Mamm.
G. 9:306-9.
27
Diarrhea in the foal
Foal heat diarrhea

J Freestone
INTRODUCTION
Foal heat diarrhea is experienced by 75-80 per cent of
normal foals. Foal heat diarrhea, as the term implies,
occurs in foals from 6-1 4 days of age and coincides with
the first estrus cycle in the post-partum mare. This
appears to be coincidental as foals separated from their
dams and fed a controlled diet will still develop diar
rhea at the same age. The cause of foal heat diarrhea
has been widely debated with strongyloidosis and
changes in milk composition largely eliminated as pos
sible causes. From the work of Masri et at. ( 1 986) it
appears that the diarrhea results from a physiological
change within the gastrointestinal tract as the foal
develops a normal bacterial flora.
CLINICAL SIGNS
Foal heat diarrhea is most commonly a mild diarrhea
that is malodorous and self limiting over a 7-day period.
In a small number of foals the diarrhea may be profuse
and may be prolonged, or it may initially resolve and
then reoccur for an additional 2-3 days. The odor of
diarrhea caused by rotavirus can often be distinguished
from that of foal heat diarrhea. Foals show no adverse
clinical signs with foal heat diarrhea, and remain bright,
alert and responsive, afebrile, and they continue to
suckle. The diarrhea 'scalds' the perineal area resulting
in hair loss.
DIAGNOSIS
The diagnosis of foal heat diarrhea relies on the clinical
signs presented by the foal. Routine hematology and
biochemistry is normal. Foal heat diarrhea needs to be
differentiated from other infectious causes of diarrhea
including nutritional causes, viral diseases, and salmo
nellosis. On a large Thoroughbred stud the most likely
differential diagnosis is rotavirus diarrhea. A good rule
of thumb is to monitor the foal's nursing behavior and
the size of the mare's mammary glands - foals with foal
heat diarrhea will rarely go 'off suck' in contrast to foals
with infectious causes of diarrhea.
TREATMENT
There is no treatment necessary for foal heat diarrhea
as the condition is self limiting. The foal's perineal area
can be cleaned and protected from scalding with the
application of petroleum jelly or zinc oxide. If the foal
deteriorates or the diarrhea is prolonged another cause
for the diarrhea should be considered and the use of
anti-ulcer medications, intestinal protectants, antibi
otics, and fluid therapy considered.
Viral diarrhea in foals
TD Byars
INTRODUCTION
Foals are most susceptible to viral diarrheas during the
neonatal, perinatal, and suckling periods by virtue of
493
being immunologically naive. The causative or associ
ated viruses include
equine herpesvirus Type-l (EHV-l)
adenovirus
coronavirus
equine viral arteritis (EVA)
rotavirus
parvovi rus
viral infections that have not been completely
identifed but noted on fecal electron microscopy.
Most viral diarrheas are considered to be highly
infectious and are rarely diagnosed at the time the
symptoms are present. The exception is rotavirus, the
most commonly recognized viral gastroenteritis in foals
that is readily diagnosed by ELISA testing. Viral diar
rheas should be suspected whenever an outbreak of foal
diarrhea is present and routine microbiology is non
diagnostic. Viral diarrhea can be diagnosed by
ELISA (rotavirus A)
electron microscopy of tissues and feces
polymerase chain reaction testing and
immunoperoxidase (EHV-l)
virus isolation from fecal or tissue samples obtained
at post-mortem examination.
Unlike food animals where sacrifce to confrm a
diagnosis may be elected, foals represent a population
of companion animals where viral infections may be sus
pected but not confrmed, since the time involved in
treatment can compromise ante-mortem diagnosis and
post-mortem viral isolation. Koch's postulates are rarely
documented in identifing viral causes of enteritis in
the equine species.
CLINICAL SIGNS
Often viral diarrheas can not be differentiated from
bacterial diarrheas since incubation periods may be
similar and the clinical presentation can vary from
acute to moderate severity, dependent upon the degree
of insult and age of the foal. Clinical signs can vary from
slight - a febrile foal that is not nursing, to profound -
profuse watery to lightly hemorrhagic diarrhea accom
panied by colic. The diarrhea can be fetid, and vary in
color and consistency. In some cases atypical enteritis
may be present in that the clinical assessment and blood
values are consistent with enteritis but diarrhea is not
present at the time of examination. Colic caused by
enteritis may be difcult to differentiate from a surgical
colic if blood values are reasonably normal and fever is
not present (see Chapter 22) . Abdominal pain associ
ated with the early stages of viral enteritis can be severe,
494
with tympany and occasionally gastric reflux. Further
clinical diagnostic procedures are indicated in these
cases with ultrasound examination being the diagnostic
method most useful to rule out intussusception, volvu
lus, torsion, or peritonitis. A percentage of enteritic
foals are unresponsive to analgesics and cannot be dif
ferentiated from surgical cases until tympany has been
relieved by the use of pro kinetics or, more rarely, per
cutaneous trocarization. Trocarization is usually con
traindicated wherever surgical options are available
since foals should be considered more susceptible to
secondary peritonitis than adults.
TREATMENT
Treatments for viral diarrheas are generally empirical
and symptomatic
fluid and electrolyte therapy
plasma
antibiotics
anti-ulcer therapy
anti-diarrheal medications
analgesics
antipyretics
Precautionary antibiotics and anti-ulcer medications
(see Chapter 23) should be prescribed. Fluid therapy,
oral or parenteral, for maintenance of normal hydra
tion is the main objective of treatment. Fluid therapy is
necessary to correct dehydration, shock, and electrolyte
imbalances. In some cases colloids (plasma, albumin, or
hetastarch) may assist in the intravascular retention of
crystalloid (fluid) therapy. Other treatments include
the use of antidiarrheal medications, analgesics, and
antipyretics. The fluids and colloids selected are based
on laboratory fndings, electrolyte and acid-base imbal
ances, and clinical signs. Oral supplementation should
include access to fresh and electrolyte water, and a salt
block. Potassium defcits can be corrected in intra
venous fluids at a rate of 0.5 mEq kg-1 h-1 or orally as
potassium chloride in the form of 'lite' salt mixed with
yogurt. Patients with reflux, ileus, or extreme cachexia
may beneft from the initiation of total parenteral nutri
tion (with or without lipids) . Antidiarrheal medications
are rarely effective in altering the course of the diarrhea
but medications such as bismuth subsalicylate and
kaolin may help reduce bowel inflammation and pro
vide for secondary toxin absorption and resorption
when combined with activated charcoal. Oral plasma
from adult donors has been used in cases of viral diar
rhea in foals with questionable efcacy. Analgesic use in
viral diarrheas should emphasize the discriminating use
of ulcerogenic non-steroidal anti-inflammatory drugs
(NSAlDs) . Dipyrone is not currently available commer
cially but has provided excellent analgesia in mild colic,
along with its anti-pyretic activity, in foals with diarrhea
of various causes. Intravenous and intramuscular butor
phanol (in small animal dilutions) is useful in the con
trol of colic without cardiovascular or ulcerogenic side
effects. Xylazine may also be used to control colic but
temporarily affects cardiovascular function and potenti
ates ileus.
ROTAVIRUS AND SIMILAR VIRAL
INFECTIONS
Rotavirus diarrhea is considered to be species specifc
but may involve variant strains in foals. Exposure is from
carrier adults, infected foals, and mechanical transmis
sion by humans and fomites. The incubation period is
1-2 days and it is highly infectious to suckling foals of
any age. The pathogenesis of infection primarily
involves the intestinal epithelial cells. Villi become
shortened or denuded, crypts become hyperplastic, and
the ensuing diarrhea is combined secretory and malab
sorptive enteritis. Additionally carbohydrate enzymes
and lactose become defcient. The diarrhea, if present,
is usually watery and distinctly fetid. Diagnosis is by
ELISA testing or electron microscopy of feces for viral
particle identification. Treatment is non-specific and
the virus can be shed for approximately 5-7 days after
the diarrhea has resolved. Medications containing lac
tase have been used to improve digestion of milk lac
tose, but the efcacy of this treatment remains
unproven. A commercial modifed live virus vaccine is
currently available for use in mares prior to foaling to
accentuate colostral antibodies. Foals from vaccinated
mares can still become infected with rotavirus although
the clinical signs may be attenuated.
In Ireland and central Kentucky a unique cyclic epi
zootic of a suspected form of rotavirus diarrhea was
noted in 1987 and 1995, nicknamed the 'pink-rosewater
diarrhea' or '36-hour scours'. The disease was highly
infectious with virtually every foal at respective farms
heing clinically affected within 36 hours of birth. The
clinical signs include a pinkish watery diarrhea, rela
tively non-fetid, usually complicated by dehydration
and colic associated with abdominal tympany. Colics
were often severe and unresponsive to analgesics.
Neostigmine used to relieve tympany was most effective
in the resolution of colic. Often treatments were empir
ical or symptomatic. Routine sanitation procedures,
including pressure washings and disinfection, were inef
fective. Washings and disinfection of the mares' udders
were also ineffective. Foaling in paddocks or pens out
side the barn environment resulted in a dramatic cessa-
DIARRHEA IN THE FOAL 27
tion of new clinical cases. Viral particles were noted on
fecal electron microscopy without a definitive identif
cation of the causative viral etiology.
PROGNOSIS
The prognosis for foals with viral diarrhea is usually
favorable with fluid therapy and supportive care.
Secondary complications with bacterial infections or
the gastric ulcer syndrome can reduce the number of
favorable outcomes. Foals having survived viral diarrhea
are usually immune to subsequent infections, although
rotavirus is known to recur occasionally, albeit with
reduced clinical severit.
Salmonellosis in the foal
J L Whiting and TD Byars
Salmonella spp. are the most commonly diagnosed
causative agents of bacterial enterocolitis in the adult
equine, and has been reported as the most common
cause of bacterial diarrhea in the foal. In foals less than
14 days of age, Salmonella infections can lead to bac
teremia, septicemia, septic shock, and death, with diar
rhea occurring secondarily. Other bacteria, including
Actinobacillus equuli, Escherchia coli, Stretococcus spp. and
Klebsiella spp. may also cause diarrhea secondarily to
septicemia.
Young and immunocompromised animals are more
susceptible to Salmonella infections, in that exposure to
a lower dose of the organism can result in infection. This
increased susceptibility of the young may in part be
because of a less sophisticated or less well established
microflora within the gastrointestinal tract. Experimental
data have shown the signifcance of normal gastroin
testinal flora in restricting the ability of the Salmonella
organism to establish and proliferate within the intestine.
The most common source of exposure and infection
in the foal is another horse. Often the mare herself is an
asymptomatic carrier, shedding the organism during
the stress of parturition and exposing the foal to the
pathogen in utero or in the post-foaling environment.
PATHOGENESIS
Salmonella spp. are gram-negative, facultative, anaerobic
bacteria, which usually gain access to the gastrointesti-
495
nal tract via the fecal-oral route. The bacteria must
combat a number of non-specifc host defense mecha
nisms - gastric acidity, normal intestinal flora, peristal
sis, intestinal mucus, lactoferrin and lysozyme
secretions within the gastrointestinal tract - in order to
establish infection. Salmonella organisms have many
virulent properties enabling them to establish infection
within the host. Among these are flagellar and chemo
tactically directed motility, capsular and surface anti
gens, macrophage-induced proteins, endotoxin,
enterotoxin, cytotoxin, plasmids, and iron-chelating
enzymes. Once Salmonella organisms come in close
proximity to, or possibly in contact with, the brush bor
der of enterocytes, the microvilli and tight junctions
undergo degeneration. Flagellar motility may enable
the organism to approach enterocytes close enough for
adhesion to occur. Surface 0 antigens and fmbriae
may then facilitate adherence of the bacteria to the host
receptor cells.
The bacteria migrate through the enterocyte and
access the lamina propria where their presence stimu
lates an inflammatory response. The macro phages and
neutrophils recruited will phagocytize the bacteria, and
it is within these phagocytic cells that Salmonella organ
isms survive and multiply, while remaining protected
from antibiotics, antibodies, and complement. Flagella
are thought to protect the organism from intracellular
killing, while macrophage-induced proteins produced
by Salmonella spp. have been shown to block fusion of
the phagosome and lysosome, allowing intracellular
survival and multiplication.
Both phagocytized and free Salmonella organisms
travel via the lymphatics to regional lymph nodes where
they persist in stimulating an inflammatory response.
From here the bacteria continue via efferent lymphatics
to drain into the blood circulation. Once in the circula
tion, the bacteria are generally cleared via the reticu
loendothelial system, primarily through the liver and
the spleen. Septicemia and its sequelae (more common
in the neonate than the adult) can occur if the infection
is not contained by the mononuclear phagocytic system.
Immunity against Salmonella spp. requires both cell
mediated and humoral immunity as the bacteria are
intracellular pathogens. The neonate's predisposition
toward bacteremia and septicemia may be because of
factors such as delayed gut closure at birth, immature
cellular immune response, and decreased complement
activity.
Inflammation within the bowel wall results in villus
blunting and degeneration and abnormal extrusion of
enterocytes. Cytotoxins may in part be responsible for
cellular destruction by inhibiting protein synthesis. The
diarrhea in the disease process of Salmonella infections
is a result of malabsorption because of this destruction
496
of epithelial cells. Additionally, enterotoxins may
induce secretion of fluid from intact intestinal epithe
lial cells.
Lipopolysaccharide (LPS), or endotoxin, is a com
ponent of the outer membrane of gram-negative bacte
ria, and contributes greatly to the pathogenesis of
salmonellosis. Endotoxin activates a variet of host cells
(platelets, macrophages, endothelial cells, leukocytes)
and host tissues to release inflammatory mediators such
as arachidonic acid metabolites, prostaglandins,
leukotrienes, tumor necrosis factor, interleukins, gran
ulocyte and macrophage stimulating factor, and reac
tive oxygen radicals. LPS can also stimulate both the
intrinsic and extrinsic clotting cascades and activate
complement by the classical and alternative pathways.
Endotoxemia leads to alterations in hemodynamics,
homeostasis, metabolism, and endothelial integrity,
resulting in tissue injury, vascular collapse, and multi
ple-organ system failure (see Chapter 1 1 ) .
CLINICAL SIGNS
Clinical signs of salmonellosis are variable and can
range from mild enteritis to fulminating septicemia
(Table 27. 1 ) .
Manifestations are attributed to enterocolitis, sep
ticemia, and endotoxemia. Early in the course of the
disease, fever, decreased nursing, and depression are
commonly found. Neonates can present with hypother
mia. Foals frequently show signs of moderate to marked
abdominal pain and can have associated abdominal dis
tension. Other differential diagnoses must be consid
ered in the neonate as colic symptoms may accompany
mechanical gastrointestinal obstruction, for example
meconium impaction, intussusception, volvulus, and
colon torsion (see Chapter 22) . Ileus often occurs, con
tributing not only to colic and distension, but also to
decreased or absent normal progressive motility
Pyrexia
Depression
Decreased nursing
Abdominal pain
Abdominal distension
Ileus
Dehydration
Prolonged capillary refill time
Diarrhea
sounds. Fluid and gas sounds are frequently appreci
ated when auscultating the abdomen. Dehydration, as
evidenced by decreased skin elasticity, dry mucous
membranes, and sunken eyes, can become severe with
ongoing fluid losses that may lead to poor tissue perfu
sion. Endotoxemia contributes to decreased perfusion
by stimulation of various inflammatory mediators
(thromboxanes, prostaglandins, leukotrienes, and cate
cholamines) which can cause both vasoconstriction and
hypotension. Clinically, vasoconstriction is seen early in
the course of endotoxemia and is represented by pale
mucous membranes, whereas decreased vascular tone
appears as muddy, dark-red, congested mucous mem
branes with a toxic line along the gingiva. Additional
findings associated with poor perfusion include tachy
cardia, elevated pulse rate and intensity, prolonged cap
illary refill time, cold extremities, and depressed
mentation.
Clinical signs of bacteremia may manifest as infec
tions evident in other organ systems such as
pneumonia
septic arthritis
uveitis
osteomyelitis
skin abscesses
meningitis
nephritis.
Severe septicemia can lead to septic shock, multiple
organ system failure, and circulatory collapse.
Diarrhea may not be present initially and neonates
may die rapidly from severe septic shock before diar
rhea develops. Diarrhea associated with acute
Salmonella enterocolitis is most often profuse and liq
uid with little solid material present. Flecks of blood
may rarely be present. Foals will defecate in increased
frequency and volume. Colic and straining during defe
cation are common features associated with the high
volume of diarrhea produced, while rectal prolapse can
occur.
CLINICAL PATHOLOGY
Although not diagnostic for the disease, the most con
sistent hematological abnormalities found with severe
Salmonella diarrhea infections are
leukopenia
neutropenia with a degenerative left shift
toxic changes (cytoplasmic vacuolation and toxic
granules) seen in granulocytes.
A inversion of the neutrophil:lymphocyte ratio can
indicate sepsis. A rebound neutrophilic leukocytosis
may occur later in the course of disease, sometimes
indicating recovery. Thrombocytopenia can be found
in some cases. Fibrinogen can be variable, with low
1 00 mg/dl) values being attributed to coagulopathy
and elevated (> 1 000 mg/dl) values being attributed to
inflammation. Hematocrit is generally markedly
increased because of hemoconcentration and splenic
contraction. Total plasma protein is initially quite ele
vated because of hemoconcentration, but will decrease,
along with serum albumin levels, with ongoing enteric
losses secondary to mucosal damage or generalized
endothelial damage. Many neonates will have
decreased serum immunoglobulin G (IgG) levels
because of protein catabolism commonly associated
with septicemia. Foals that experience a failure of pas
sive transfer (FPT) are predisposed to septicemia, and it
can be hard to differentiate if the low IgG led to sep
ticemia or if it was a result of septicemia.
Electrolyte and acid-base imbalances can be pro
found with Salmonella enterocolitis and commonly
include
hyponatremia
hypokalemia
hypochloremia
hypocalcemia
metabolic acidosis.
Hypoglycemia in foals may be marked as a conse
quence of decreased glycogen stores in the liver and
bacterial depletion due to sepsis. Azotemia is usually
prerenal in origin, but can be caused by acute renal fail
ure or bacterial nephritis in profoundly dehydrated,
endotoxemic, or septicemic animals. Hepatic enzymes
may be mild to moderately increased as a consequence
of absorption of bacterial toxins (endotoxins) .
Endotoxin-mediated lactic acidosis can result from
poor perfusion. Mediators of inflammation stimulated
by endotoxemia can lead to a hypercoagulable state fol
lowed rarely by disseminated intravascular coagulation
(DIC), as evidenced by prolonged prothrombin time,
partial thromboplastin time, depletion of antithrombin
III and increased fibrin degradation products.
DIAGNOSIS
Diagnosis of Salmonella spp. as the causative agent of
diarrhea is demonstrated by a positive fecal culture,
while a positive blood culture is needed to diagnosis
Salmonella septicemia. Isolation of the organism from
fecal material is variable as Salmonella spp. may be inter
mittently shed in the feces. With acute enteritis, the
feces can have little solid material and the chance of
culturing the bacteria is diminished (although better
497
than in adult horses) . A minimum of three to fve con
secutive 1 gram fecal cultures taken 24 hours apart are
recommended to increase the chance of isolating the
organism. Fecal cultures from the mare should also be
submitted to assist in determining the source of infec
tion.
TREATMENT
Therapy for salmonellosis is aimed at maintaining
hydration and electrolyte balance in the face of ongo
ing losses, reducing the effects of endotoxemia, pre
venting or treating bacteremia, and gastroprotectant
therapy (Table 27. 2) .
Aggressive intravenous fluid therapy may be
required as dehydration can rapidly become severe in
the foal with enterocolitis, and effects of decreased
intravascular volume can be profound. Electrolyte and
acid-base abnormalities can be marked and serum
parameters should be monitored frequently to main
tain balance. Isotonic fluids are routinely used to
restore and maintain hydration status, with additional
electrolytes, for example potassium and bicarbonate,
added as indicated by deficits found in serum chemistry
analysis. Potassium chloride should not be adminis
tered at a rate greater than 0. 5 mEq kg-I h-I in the foal.
In the severely affected foal with poor perfusion, signs
of septic shock or reduced plasma oncotic pressure
(hypoproteinemic: <4.0 mg/dl or 40 gil; hypoalbu
minemic: 1 . 8 mg/dl or 18 gil; and hemoconcen
trated with ventral or distal limb edema) , colloids such
as hydroxyethyl starch, at a dose of 10 ml/kg, can be
Intravenous fluid therapy
Isotonic fluids
Bicarbonate
Potassium chloride
Colloids
Plasma
Hyperimmune plasma
Dexrose
Partial or total parenteral nutrition
Antibiotics
Polymyxin B
Flunixin meglumine
Pentoxifylline
Bismuth subsalicylate
Activated charcoal
Live yogurt
Anti-uler therapies
498
beneficial. Intravascular volume can be expanded, and
vascular perfusion and oncotic pressure improved with
a decrease in interstitial fluid accumulation. Colloids
are generally followed by continued crystalloid fluid
therapy. When used in conjunction with colloids, a
decreased amount of crystalloid fluids are required.
Plasma is recommended in the hypoproteinemic foal
with hypoalbuminemia and/or low IgG levels. In addi
tion, plasma contains coagulation factors and
antithrombin III, which could benefit the endotoxemic
patient. Hyperimmune plasma containing
immunoglobulin-recognizing LPS core antigen has
been recommended in horses with Salmonella infec
tions at a dose of 0. 4 ml/kg. Fluids containing dextrose
(5% solution) or oral supplementation via a nasogastric
tube may be required in the foal that has stopped nurs
ing. Alternatively, the catabolic patient may benefit
from oral supplementation with high-nitrogen oral
solutions (osmolite) , partial parental nutrition (PPN)
or total parental nutrition (TPN) .
Although antibiotic therapy will not alter the course
of the diarrhea or reduce the incidence of shedding of
the Salmonella organism, it is recommended that foals
with Salmonella infections be treated with antibiotics in
the hope of preventing bacteremia and to treat any sites
of secondary infection. Appropriate antibiotic therapy
should be established based on sensitivity results of fecal
or blood cultures. Ideally lipid-soluble antibiotics such
as trimethoprim-sulfonamides and chloramphenicol,
should be used as the Salmonella organism survives
intracellularly. Often the Salmonella spp. isolated, espe
cially in nosocomial infections, will be resistant to the
aforementioned antibiotics, and other broad-spectrum
choices such as third generation cephalosporins or
penicillin and aminoglycoside combinations are found
to be more effective. Antibiotics may contribute to the
release of endotoxins in cases of rapid bacterial death.
For this reason patients can be treated with medications
that decrease the effects of circulating endotoxin prior
to initiation of antimicrobial therapy. Polymyxin B, at a
low dose of 6000 IU /kg, binds and removes endotoxin
from circulation. Cyclooxygenase inhibitors such as flu
nixin meglumine (0.25 mg/kg Lv. t. Ld. ) will both ame
liorate the effects of endotoxemia by decreasing
synthesis of prostaglandins and thromboxanes, and
decrease the secretory component of diarrhea by block
ing prostaglandin-mediated hypersecretion of entero
cytes. Non-steroidal anti-inflammatory drugs should be
used cautiously in foals because of the greater risk of
gastroduodenal ulcers. Pentoxiflline (7.5 mg/kg p. o.
bj.d.) has been shown to reduce endotoxin-induced
synthesis of tumor necrosis factor, a contributor to
endotoxemia associated with sepsis. In addition, pen
toxiflline increases red blood cell deformability,
decreases blood viscosit, decreases platelet aggrega
tion, and decreases thrombus formation, thereby com
bating conditions contributing to impairment of
regional blood flow.
Bismuth subsalicylate is commonly used as an intesti
nal protectant. The bismuth is thought to have anti
endotoxic and weak antibacterial properties while the
salicylate has anti prostaglandin activity which may
decrease enterocyte hypersecretion. Activated charcoal
and/ or mineral oil can be used to decrease absorption
of endotoxin. Yogurt or other lactobacillus-containing
products can be used to help reintroduce benefcial
flora to the gastrointestinal tract.
Anti-ulcer medication is routinely recommended
and administered prophylactically and therapeutically
to ill foals because of their predisposition to gastric
ulcer syndrome. Omeprazole (a gastric acid (proton)
pump inhibitor), or famotidine, ranitidine, cimetidine
(H2 antagonists) , and sucralfate (a cytoprotective
agent) are commonly used medications. It is interesting
L recall that one important host barrier to Salmonella
infections is the ability of acidic pH in the stomach to
prevent live bacteria from gaining access to the intes
tine. Changing gastric pH with anti-ulcer medication
may in fact enhance infection.
PREVENTION AND CONTROL
The Salmonella organism is relatively prevalent within
the environment and can be shed in the feces of clini
cally normal horses. The most common route of infec
tion is fecal-oral. The mare is often found to be
shedding the organism and the foal has probably con
tracted it from her. Neonates are at greater risk during
the frst 24 hours of life as the organism may gain access
via the gastrointestinal tract prior to gut closure.
Overcrowding, improper sanitation, and inadequate
umbilical care all put the neonate at risk for Salmonella
bacteremia and consequent septicemia.
Adequate colostral antibody absorption is important
to develop the foal's immune defense system. A serum
IgG concentration of more than 800 mg/ dl at 24 hours
of age is recognized as optimal passive conference of
immunity in the neonatal foal. This immunit is espe
cially important in the neonate at risk for sepsis. Plasma
transfusions with hyperimmune plasma from donors
vaccinated against mutant strains of]-5 Escherichia coli or
Salmonella typhimurium have been reported to provide
IgG protection against gram-negative core antigens, but
clinical response to this therapy is variable. In addition,
plasma provides opsonins which improve the foal's
immune function. Sick neonates can experience
increased immunoglobulin consumption, possibly
because of sequestering of IgG within the intravascular
space or at sites of inflammation, and can beneft from
plasma transfusions even if initial colostral absorption is
adequate. Autogenous vaccines have been used to stim
ulate immunity against Salmonella spp., but approved
and proper preparation is difcult.
Animals identifed as infected with Salmonella spp.
should be kept isolated from the general population
until they culture negative. Both mares and foals should
be cultured. Infected animals can continue to shed
organisms in their feces intermittently for several days
to weeks. Daily fecal cultures should be taken beginning
at 4 weeks after the cessation of clinical signs, and three
to fve negative cultures are needed before putting the
animal in contact with other foals can be considered.
Clostridial enterocolitis in
foals
TJ Divers
Clostridial diarrhea has been diagnosed in foals at an
increasing rate over the past 5 years. It is unclear if this
is a result of increased prevalence of the disease or
increased use of more sensitive diagnostic tests for
intestinal clostridial toxins.
ETIOPATHOGENESIS
Clostrdium perringens type C is a well-proven cause of
colic and diarrhea (often hemorrhagic) in young foals.
The disease almost always occurs in foals less than 5 days
of age ,that have received sufcient colostrum.
Pancreatic trypsin is inhibited by a trypsin inhibitor in
colostrum, which undoubtedly plays a role in the poten
tial for C perfringens colonization and increased toxin
concentration in the foal's small intestine during the
frst week of life. C perfringens tpe C produces a beta
toxin which causes severe intestinal necrosis and hem
orrhagic diarrhea. A the intestinal wall becomes dam
aged the organism can be found in the blood of many
affected cases. In later stages of the disease the organ
ism can be found in the peritoneal fluid. C perfringens
type C diarrhea can be either a farm problem or it can
present as an isolated case. Foals, such as orphan foals,
that may be given both colostrum and milk in unusually
large amounts via a nasogastric tube may be at
increased risk. Although unconfrmed, exposure to the
organism may be via the mare rather than environmen
tal contamination.
499
Clostrdium peirngens tpe A has been incriminated
as a cause of diarrhea in foals of all ages. Proof of the
relationship between C. perngens type A in the foal's
stool, and diarrhea in foals has been difcult. A in
adult horses, C peiringens type A organisms are more
common in foals with diarrhea than in healthy foals,
but no toxin marker has been found in the foal that dis
tinguishes a pathogenic strain of C perfingens type A
from non-pathogenic strains. C perfngens type A
enterotoxin and/or its enterotoxin gene can be found
in both normal and diseased foals. C perfngens type A
may cause diarrhea in foals, but more research is
needed to prove cause and effect. A similar situation
exist with C. dij cil and its relationship to foal diar
rhea. C dijcile has been reported, and has frequently
been incriminated as causing outbreaks of diarrhea in
young foals (generally 3 weeks of age) . In these out
breaks there has been no history of prior antibiotic
treatment to predispose the animals to the proposed C.
dijcil diarrhea. Proving cause and effect has been dif
fcult since normal foals may have both C dijcile and its
toxin in their stool. This situation is also well-known in
children. It may be that C dijcile is a primary pathogen
in some cases of foal diarrhea, or it may be present in
the stool in greater numbers because of the diarrhea, or
it may be acting with another pathogen to cause diar
rhea. Other pathogens that may be present simultane
ously include Crptosporidium spp., Bacteroides frgilis,
rotavirus type A, or a virus similar to rotavirus but
smaller than type A.
CLINICAL SIGNS
Colic often precedes the diarrhea by a few hours and
can be severe. Mild to moderate abdominal distension
generally precede the diarrhea. There may be some
reflux after passage of a soft nasogastric tube, but more
commonly reflux is absent or minimal. Fever is often
present. Clostrdium peringens type C generally causes a
hemorrhagic enteritis with blood-stained diarrhea
(Plate 27. 1 ) . Diarrhea associated with C dij cile or C
perfngens type A is more commonly brown and fetid.
DIAGNOSIS
The diagnosis of clostridial enteritis, or any enteritis in
foals, should be based on signalment and historical
information, for example age of the foal, clinical find
ings, fever, leukopenia, low serum sodium and chloride,
liquid gut sounds on auscultation, in addition to fecal
cultures and toxin assays. Radiographic examination,
performed using 85 kVp and 20 r with rare earth
500
screen cassettes, is useful in distinguishing ententls
from surgical conditions, for example intussusception,
in the colicky foal. Small intestinal obstructive lesions
have a few distinct inverted U-shaped loops of bowel and
there is less intestinal gas distension than with enteritis.
Ultrasound examination of the abdomen using a 5-mHz
probe is most helpful in differentiating between surgical
disorders and enteritis as causes of abdominal pain. The
small intestine of foals with enteritis is generally more
hypoechoic than normal (Figure 27. 1) and the motility
may be increased. With strangulating diseases of the
small intestine, motility of the distended intestine is usu
ally absent. The ultrasound examination should be per
formed with the foal standing if possible.
Fecal cultures should be submitted for Clostrdium
spp. culture (anaerobic media) and toxin assay
(c diff
cile toxin A and B, and C peiringens alpha and entero

toxin) . For toxin assays, the sample should ideally be
delivered immediately to the laboratory or the feces
frozen and sent by overnight mail. An estimate of the
number of C. peiringens organisms in the feces may be
helpful in determining signifcance, but quantitative
cultures require that a fresh sample (ideally taken from
the rectum) be kept under anaerobic conditions and
delivered immediately to the laboratory. Large num
bers of C peringens (> 1 03 colony-forming units/ml of
feces) would be supportive of the diagnosis. A gram
stain of the feces is helpful in the diagnosis if there are
Figure 27.1 Ultrasonogram of the abdomen of a foal
affected by dostridiosis showing multiple distended loops
of small intestine with grossly thickened intestinal walls. In
real time hypermotile movement of intestinal contents is
evident, helping to differentiate enteritis from mechanical
obstructions of the small intestine
a large number of gram-positive rods. Spores are more
commonly seen with C difcile and the organism can
often be more curved in appearance and have a darker
gram-positive stain than C perfrngens. Genotyping
would be needed U determine C. perfringens type (A-E) .
Blood cultures should be performed on young foals
I week of age) with diarrhea as C perfngens type C
can often be found in the blood or peritoneal fluid in
the later stages of the disease.
TREATMENT
Treatments that can be helpful for clostridial diar
rhea are shown in Table 27. 3.
Signs of abdominal pain should be controlled to
minimize injury to the foal. Dipyrone (22-33 mg/kg
i.v.) or butorphanol (4-6 mg/kg i.m.) can be used ini
tially. Low doses of flunixin meglumine can be used
sparingly. Foals with colic, ileus, and severe or progres
sive 'gaseous' abdominal distension that have been
unresponsive to appropriate medical treatment and are
believed not to have an obstructive disorder, can be
given neostigmine (0.2-0.4 mg/foal s. c.) after sedation
with xylazine in an attempt to evacuate the gas.
Lactated Ringer's solution should be given to reduce
fluid deficits. Potassium chloride (20 mEq/l) should be
added if the foal is hypokalemic, or if sodium bicarbon
ate and dextrose have been administered, and if the
foal has been seen to urinate. Additional potassium is
generally needed in foals having diarrhea for more than
2 days or in foals receiving large volumes of intravenous
fuids. If the foal appears weak add 10 g dextrose/I
unless the blood glucose concentration is normal. If the
Analgesics - dipyrone
- butorphanol
- flunixin meglumine
Neostigmine
Lactated Ringer's solution
Potassium chloride
Dextrose
Sodium bicarbonate
Plasma
Dobutamine
Antibiotics - penicillin
- amikacin
- metronidazole
H2-blockers - ranitidine
- famotidine
Pepto bismol/yogurt
blood glucose is normal add 5 gil. Bicarbonate should
only be used if the acidosis is severe and/or persistent.
Two liters of plasma should be given intravenously
(preferably the plasma should have antibodies against
endotoxin, although the LPS antibodies may not be as
important as some naturally occurring factors in
plasma, e.g. anti-thrombin III). Clostrdium perfingens
type C and D antiserum can be given orally to affected
foals. If the foal is in hypotensive shock and the plasma
and polyionic fluids do not improve the condition (as
determined by monitoring the blood pressure or by
clinical impressions, e. g. poor capillary refill, severe and
persistent tachycardia, and cold extremities) , dobuta
mine (5-10 I-g kg-J min-I) should be administered via a
slow intravenous drip.
Antimicrobial therapy should include intravenous
penicillin, 44 000 IV/kg i. v. q. 6 h, and amikacin,
18 mg/kg q. 24 h, (carefully monitor urine production,
serum creatmme, and amikacin trough levels) .
Metronidazole, 1 0 mg/kg p.o. q. 1 2 h, may also be
administered. Broad spectrum antibiotics are indicated
as bacterial translocation to other organs can occur.
Ranitidine 1 . 5-2.2 mg/kg i. v. q. 8 h or famotidine
0.7-1. 4 mg/kg i.v. once daily should be used in the
hope of preventing gastric ulcers. Once the colic sub
sides, these or other H2-blockers or proton pump block
ers can be given per os.
Pepto bismol (56-1 1 2 g ( 2-4 oz) p. o. q. 4-6 h) with
28-56 g ( 1-20z) yogurt may be of some benefit in
reducing toxin absorption and re-establishing normal
intestinal flora. The foal can be allowed to nurse but
should not be force-fed milk.
PROGNOSIS
The prognosis with Clostrdium perfrngens type C is vari
able, intestinal necrosis rapidly occurs in a few cases
with large numbers of the organism being identified in
both blood and peritoneal fuid. Less severely affected
cases respond dramatically to treatment and may
appear normal within 2-3 days. C di cil and C perrin
gens type A-associated disease seems to produce a more

protracted diarrhea. The prognosis for either infection
is generally good if the foal is nursing at recognition of
the disease, or if nursing is strong after 24 hours of
treatment. Gastric ulceration, electrolyte imbalances,
and cachexia may be signifcant problems in a few foals.
CONTROL
Clostrdium perfingens type C diarrhea is often an iso
lated event on a farm requiring few control measures.
501
Cleaning the mare's udder prior to the foal nursing
may be the most appropriate control measure and
should be routinely recommended. C. perfringens tpe C
toxoids are available but would not routinely be recom
mended for the pregnant mare unless the farm has a
proven problem with C perfringens type C. A more sig
nificant problem exists with farm outbreaks of foal diar
rhea presumed to be associated with either C. diffcile or
C. perfringens type A. It may help to ensure cleanliness of
the mare at parturition, disinfect the foaling area, and
avoid using a common foaling stall. Prophylactic use of
metronidazole, 10 mg/kg q. 1 2 or 24 h, from day 1 (do
not administer prior to colostrum) to day 5 appears to
be helpful in stopping outbreaks on some farms.
Lactobacillus acidophilus probiotics may be administered
for either prophylaxis or treatment but their eficacy is
not proven. Hospitalized foals, either with or without
diarrhea may be shedding C. diffcile in the greatest
numbers. Their stalls should be disinfected with an
appropriate disinfectant (hypochlorite, glutaraldehyde,
or phenolics) , and all personnel entering and leaving
the stall should wash hands and wear protective cloth
ing and boots.
Rhodococcus equi as an
agent of intestinal disease
KA Sprayberry
INTRODUCTION
Rhodococcus equi is a gram-positive, facultative intracellu
lar aerobe, it is known primarily as a pathogen of the
respiratory tract of the juvenile horse. The organism is a
saprophytic inhabitant of the soil, favoring soils in warm
climates where the manure of herbivores is present.
Such soils promote survival and amplifcation of R. equi
populations because molecules produced by fermenta
tive digestion in the equine hindgut are growth factors
for the organism. The typical manifestation of disease
caused by this bacterium is an abscessing, pyogenic,
granulomatous bronchopneumonia in foals aged 1-6
months, but many extrapulmonary manifestations of
infection, including colitis and abdominallymphadeni
tis, have been described.
Originally classed taxonomically in the genus
Cornebacterum, the organism was reclassifed as
Rhodococcus spp. on the basis of genetics, chemistry, and
ecology. Members of this genus are soil inhabitants,
having in common the production of red pigment, but
only R. equi has been reported as a pathogen in animals
502
or humans. The organism 1b M the same taxonomic
order (Actinomycetales) as mycobacteria. Myco
bacteria, like R. equi, are primarily pathogens of the res
piratory and intestinal tracts, causing pulmonary and
intestinal tuberculosis in humans (M. avium, M. bovis,
and M. tubeculosis) andJohne's disease, a chronic, gran
ulomatous inflammation of the intestinal tract of ungu
lates (M. paratuberculosis). The tuberculous, pyogenic
granulomas of mycobacteria infections are histologi
cally similar to rhodococcal abscesses in their composi
tion of infected macrophages and multinucleate giant
cells with neutrophilic infltration.
EPIDEMIOLOGY AND PATHOGENESIS
Because the bacterium resides endemically in tpes of
soils which support populations of horses, it is an agent
to which most, if not all, horses are exposed. The inci
dence of disease associated with Rhodococcus equi, how
ever, varies. On some farms R. equi pneumonia is rare,
while on others clinical disease occurs enzootically,
even though the organism can be cultured from the soil
of both. This incongruity is likely to be a result of dif
ferences in the type of soil, climate, prevalence of dusty
conditions, stocking rate, and intensity of management
that exist between farms, as well as differences in viru
lence among resident strains of the organism. Virulent
strains of R. equi are characterized by the presence of a
15 or 17.5 kDa virulence-associated protein (VapA) on
the cell membrane. Farms which have clinical disease
due to R. equi are usually endemic premises for VapA
strains of the organism, while farms having little inci
dence of disease are infected less heavily with the viru
lent organism. This protein is encoded for by an 85 or
90-kilobase plasmid. Though long recognized as an
identifing marker for virulent strains, it has recently
been shown conclusively that this plasmid is in fact a vir
ulence factor for the organism. The presence of the
plasmid is essential for intracellular replication within
macrophages and subsequent development of disease.
The organism dwells and replicates within phagosomes
after being phagocytized by macrophages, preventing
(by an unknown mechanism) the usual fusion of the
phagosome with a lysosome. Macrophages thus infected
do not undergo the respiratory burst associated with the
lysosomal enzymatic activation which mediates intracel
lular killing. Infection of macrophage cells by R. equi
eventually causes the degeneration and death of the
immune cell, possibly by inappropriate lysosomal rup
ture and degranulation into the cytoplasm. Neutrophil
cells of both foals and adult horses function as effective
phagocytes, and can effectively process and destroy R.
equi.
Inoculation of foals occurs via either the respiratory
route, following inhalation of aerosolized particles, or
the oral route, via ingestion. In dusty conditions, bacte
ria present in the soil and feces become aerosolized, serv
ing as the direct source of exposure and pulmonary
infection for foals. Colonization of the bowel by
Rwdococcus. equi occurs when foals ingest infected soil
or forage, are coprophagous, or swallow expectorated,
bacteria-laden sputum. R. equi pneumonia is also preva
lent in areas with grass pasture and little or no dust or
exposed soil. In these circumstances, feces from adult
horses serving as passive carriers may be an important
source of exposure for foals. In adult horses, ingestion
results in passive passage of the organism through the
intestinal tract, with resultant deposition of the bac
terium back into the environment. In immunologically
naive foals, however, the organism thrives and replicates,
resulting in signifcant amplifcation of bacterial num
bers in the environment and enhanced risk to other
young stock if manure produced by infected foals is not
promptly removed. During the optimal environmental
conditions that prevail during summer months, R. equi
numbers in contaminated soil can multiply by ten-thou
sand-fold in 2 weeks, such that 1 gram of soil could
theoretically contain millions of virulent organisms.
CLINICAL SIGNS
The clinical picture of pulmonary disease mediated by
Rodowccus equi has been well described. Young foals
aged 1-6 months are typically affected. Foals in this age
category are particularly susceptible to infection
because they are in an immunologic stage of waning
maternal antibody. Most foals reach this age with its
characteristic antibody 'trough' when warmer tempera
tures and dusty conditions are beginning to prevail,
increasing the aerosolization of bacteria. Foals often
present with an apparently acute onset of clinical dis
ease characterized by
fever
tachypnea
depression.
However the actual onset and early development of
lesions in lung tissue is insidious and clinically silent.
The disease process and degree of pulmonary involve
ment are typically well advanced by the time clinical
signs are evident and a diagnosis is made. The incuba
tion period may vary. In one study virulent organisms
sprayed into the trachea of healthy foals resulted in the
development of fever in 11-16 days. Evaluation of the
thorax with radiography or ultrasound usually demon
strates the presence of cavitary lesions representing a
multifocal, abscessing pattern of bronchopneumonia.
The perihilar regions, and the cranial and cranioventral
areas of the lungs tend to be most severely affected, and
the hilar lymph nodes are often involved. In some cases
a more atpical interstitial pneumonia may occur.
In addition to pulmonary disease, extrapulmonary
manifestations of infection may be observed, including
mesenteric lymphadenitis
ulcerative colitis
immune-mediated polysynovitis
uveitis and keratoconjunctivitis
osteomyelitis
septic synovitis
cutaneous pyogranulomas.
Of these extrapulmonary lesions, enteric disease
(ulcerative colitis and mesenteric lymphadenitis) is the
most common. Ulcerative colitis and/or mesenteric
lymphadenitis were present concurrently with pneumo
nia in 50 per cent of foals with Rodococcus equi infection
in one survey. Any of the extrapulmonary manifesta
tions of disease may precede signs of pneumonia, but
once such clinical signs are observed, further evaluation
will usually document the presence of underlying and
concurrent pulmonary disease.
Intestinal colonization by Rodococcus equi may
include several manifestations. Enterocolitis in the
form of diffuse infltration of the lamina propria and
submucosa by infected macrophages and multinucleate
giant cells occurs. Affected segments have grossly thick
ened, corrugated mucosa with multiple, irregularly
shaped, well-demarcated foci of necrosis and crateri
form ulcers, from 0. 5-4 cm in diameter. Histologically,
the granulomatous infltrate can be seen to fll the lam
ina propria, distort villi, and displace intestinal glands
and crypts. These areas of granulomatous infltrate are
associated with those areas of the lamina propria and
submucosa that are associated with lymphoid follicles.
Cecal, colonic, and mesenteric lymph nodes may also
become enlarged and frm. Foals with enteric infections
commonly demonstrate the following clinical signs
diarrhea
fever
variable weight loss.
In some cases cellular obstruction of the lymph
nodes and lymphatic vessels leads to ascites; affected
foals will show chronic weight loss and appear unthrifty
and potbellied in addition to producing diarrhea.
Although R. equi can be cultured from the stool of many
foals or horses, documentation of increasing R equi
numbers in the feces, over the normal background
numbers present, may be helpful in identifing
clinically affected foals.
503
In the intestinal form of infection, it is likely that
Rodococcus equi utilizes the specialized microfold cells
in the intestinal wall as a route of entry to
macrophages in Peyer's patches and discrete lymphoid
follicles diffusely distributed along the intestinal tract.
These microfold cells, or M-cells, are interspersed
among the villous enterocytes, and function as anti
gen-presenting cells, delivering lumenal antigen to
immune cells in the submucosa and lamina propria
for processing. Once the bacteria are ensconced
within the phagosomes, they travel with the
macrophage and may subsequently access lymph
nodes in the mesentery of the small intestine, cecum,
and large colon, causing enlargement and abscessa
tion of these nodes. They may also enter the lacteal
and lymph vessels, eventually gaining access to the cir
culation via the thoracic duct. The bacteria can then
become hematogenously distributed, resulting in
abscessation at random sites. Such abscesses often
develop in the peritoneal cavity, but in horses and in
other species, including humans, R. equi abscesses
have been reported in a variet of locations. In
humans, the organism has caused disease in both
immunocompetent and immunocompromised individ
uals, though it occurs more commonly in patients with
dysfunctional cell-mediated immunity such as HIV
patients and transplant recipients. Respiratory tract
disease, including chronic, granulomatous pneumonia
and extrapulmonary infections such as mediastinitis, is
the most common disease manifestation in humans,
but thyroid abscesses, post-injection gluteal abscesses,
renal abscesses, and a variety of other affected body
sites have all been reported. Only about 30 per cent of
humans with R. equi infections report any contact with
herbivores or soil where herbivores have been.
TREATMENT AND PREVENTION
Diarrhea is the primary presenting sign in foals with
abdominal lymphadenitis or colitis. Diarrhea may also
develop as a complication of antimicrobial treatment
with erythromycin and rifampin. The erythromycin/
rifampin combination is the anti-rhodococcal treat
ment regimen of choice, because of
the drugs' lipophilic properties, permitting good
penetration across abscess walls and into the
intracellular space of macrophages
the synergistic action of the to agents combined.
Disruption of colon microflora is thought to cause
the diarrhea in affected foals, necessitating (in some
cases) adjustment of erythromycin doses to a lower
rate in the recommended dose range or temporary dis-
504
continuation of the drugs for 24-48 hours. In some
cases the diarrhea will be self-limiting and will not
necessitate any alteration in dosing. Occasionally treat
ment with different antimicrobial drugs is necessary.
Hyperthermia is another complication occasionally
encountered in foals being administered ery
thromycin. The problem occurs most frequently in
very hot weather when the thermoregulatory mecha
nisms are already challenged to a maximum in a pneu
monic foal.
Successful management of farms with an enzootic
Rodococcus equi presence must address the issues of pro
phylactic measures for the disease, early identification
of affected foals, and effective therapy of ill foals.
Immune prophylaxis is an active area of research, and
much remains to be elucidated and understood. For
instance, administration of hyperimmune serum to
young foals has been shown to reduce the incidence
and mortality of Rodococcus equi pneumonia on
enzootic premises but is not effective at treating estab
lished disease. Vaccination of mares and their foals with
a preparation of VapA protein extract was not protec
tive for clinical disease and may have enhanced the like
lihood of R. equi pneumonia in the foals. Preventative
measures that are known to be effective, however,
include
prompt removal and composting of manure from
infected foals
rotating pastures to decrease erosion of pasture into
dusty paddocks
segregation of ill foals from the general population.
These measures effectively reduce the numbers of
the infective organism in the environment, reducing
the immune challenge to the at-risk population of foals
in their immunologically vulnerable phase.
Equine cryptosporidial
diarrhea
NO Cohen
INTRODUCTION
Diarrhea is a common and often serious disease of foals.
Protozoal diarrhea in foals caused by the coccidian par
asite Crptospordium parum is being increasingly recog
nized. The purpose of this chapter is to review the
epidemiology, clinical signs, diagnosis, treatment, and
prevention of C parum infection in horses.
LIFE CYCLE AND TRANSMISSION
Infection of foals occurs by ingestion of the infective,
sporulated oocysts. These excyst in the small intestine
and attach to the epithelium in a location described as
intracellular but extracytoplasmic. Amplification
occurs both through asexual and sexual multiplica
tion. Oocysts are formed that are capable of autoinfec
tion prior to excretion (thin-walled oocysts) or that
are immediately infectious when shed in feces (thick
walled oocysts) . Transmission occurs either via the
fecal-oral route or by ingestion of contaminated food
or water. Sources of infection for horses are unknown
but, as for people, contaminated municipal water may
be important. Conflicting evidence exists as to
whether mares are the source of infection for foals,
however, in the author's experience mares are not the
source of infection for foals. In Texas cattle do not
appear to be an important source of infection for
horses.
EPIDEMIOLOGY
Prevalence
Prevalence varies with the method of detection used
and the population studied. Infection among clinically
normal, mature horses is rare (approximately 0-5%) .
Prevalence at breeding farms may be higher, particu
larly among foals. Prevalence is higher among foals with
diarrhea than among clinically normal foals, and preva
lence may approach 1 00 per cent among diarrheic foals
at farms during an outbreak.
Signalment
Foals are at increased risk of infection, particularly
those from 1-4 weeks of age, however diarrhea associ
ated with Cryptosporidium parvum may be seen in foals
younger or older than this.
The time from infection to shedding oocysts for
cryptosporidial diarrhea in foals is unknown. Most foals
shedding cryptosporidial oocysts have been older than
5 days of age. Although cryptosporidial diarrhea has
been described in foals with diarrhea observed at 2 days
of age, cryptosporidial infection should be ranked
lower in the differential diagnosis for diarrhea of a 2-
day-old foal than in that of a foal aged 5-10 days.
Cryptosporidial infection and diarrhea are rare in
mature horses. Evidence of predisposition by sex or
breed does not exist, although most epidemiological
studies of equine cryptosporidiosis have been con
ducted in groups of mares and foals.
I mmune status
Immunocompromised foals, such as those with severe
combined immunodefciency disease, are at increased
risk. However, immunocompetent foals can also
develop cryptosporidial diarrhea. Although the disease
will generally be more severe among immunocompro
mised foals, severe or fatal diarrhea can occur in
immunocompetent foals.
Farm epidemics
Some farms experience epidemics of cryptosporidial
diarrhea. Recurrence during ensuing years is rare. A
high density of foals, a municipal water source, foaling
in stalls (versus pasture) , and poor hygiene may be risk
factors for infection and disease.
CLINICAL SIGNS
Clinical signs in foals var with age and immune status
and are usually limited to the gastrointestinal tract and
related organs. Diarrhea associated with cryptosporidial
infection is more prevalent during the first 3-4 weeks of
life, but older foals, weanlings, and yearlings can be
afected. Among immunocompromised foals with com
bined immunodeficiency, signs are often severe and
can progress rapidly. In these foals sites other than the
small intestine may be infected including the stomach,
common bile duct, colon, and major pancreatic ducts.
Among immunocompetent foals, clinical signs associ
ated with cryptosporidial infection will vary from absent
to fatal diarrhea. Inapparently infected foals may repre
sent a source of infection for other foals. The severity of
signs may be related to agent factors (inoculum size, vir
ulence) , host factors (age, immunocompetence) , and
environmental factors (water source, housing prac
tices) . In older foals (i. e. 3-6 months) the diarrhea may
be more chronic and can persist until foals are 9-12
months of age. In all infected foals concurrent infection
with other putative enteropathogens ( Salmonella spp.,
rotavirus, coronavirus, adenovirus) may be observed.
DIAGNOSIS
Ante-mortem diagnosis of cryptosporidial infection is
generally based on detection of oocysts in the feces.
Fecal samples should be submitted as fresh material or
in recommended preservative ( 1 0% formalin or
sodium acetate-acetic acid-formalin) . Oocysts can be
detected using either concentration or staining tech
niques. Concentration of oocysts may be accomplished
by flotation or sedimentation. Regardless of technique,
505
distinguishing oocysts from yeast is an important diag
nostic issue.
In veterinary diagnostic laboratories, three tech
niques are commonly used
flotation of oocyst
acid-fast staining of oocysts
detection of oocysts using an immunofluorescence
assay (IFA) .
Sedimentation techniques are rarely used in veteri
nary diagnostic laboratories. Of the flotation tech
niques used, flotation in Sheather's sugar solution is
most common. Prompt processing is important because
oocysts collapse and lose their spherical shape when left
in Sheather's sugar solution.
Acid-fast staining of fecal specimens is widely used
for detection of Cryptosporidium parvum. The technique
is simple and staining kits are commercially available.
The organisms appear as red spheres (46 mm in diam
eter) against a dark, counter-stained background, while
yeast generally do not appear red (Plate 27. 2) . The
technique has relatively poor specifcity making it a
poor choice for a screening test. However, it is useful
clinically as a diagnostic test because of its good sensi
tivity, availabilit, and low cost.
The IFA test has relatively low sensitivity but excel
lent specificity. A commercial immunofluorescence
assay is available (Meridian Diagnostics Inc., Cincinnati,
OH) that simultaneously detects cryptosporidial and
giardial organisms. The high cost relative to staining
techniques and specialized microscopic equipment
needed are limitations of the IFA. To date, reliable
enzyme-linked immunosorbent assays have not been
developed and validated for detecting Cryptosporidium
parvum in samples from horses. Flow cytometric meth
ods are more sensitive than IFA or acid-fast staining, but
are not widely available.
The pattern of oocyst shedding by foals is variable in
duration (from days to many weeks) and can be inter
mittent. Shedding may be antecedent, concurrent, or
subsequent to the onset of diarrhea. Because of the vari
able duration and the intermittent pattern of shedding,
multiple samples (at least three) should be submitted
for detecting Cryptosporidium parvum in feces from foals.
It may be easier to detect oocysts in unformed feces
than in formed feces.
TREATMENT
Although over 1 20 different treatments have been
tested in a variety of animals, to date no specifc
chemotherapy or immunotherapy has been proven to
be convincingly effective for treating Cryptosporidium
506
parvum in people and other mammals, and none has
been evaluated in a controlled clinical trial among
foals. Those treatments that may have greatest potential
for use in foals include paromomycin and bovine
colostrum.
Paromomycin is an expensive aminoglycoside antibi
otic that is poorly absorbed from the gastrointestinal
tract. Paromomycin reduced the duration and severity
of diarrhea and eliminated oocyst shedding in neonatal
calves experimentally infected with Cryptospordium
parvum. Paromomycin was efective in treating a cat
with cryptosporidiosis. Doses used in calves have ranged
from 50-100 mg/kg administered orally once or tice
daily. No data exist for the use of this drug in foals.
Adverse effects of paromomycin in humans include
diarrhea, nausea, and abdominal cramps. A for all
other agent used to treat cryptosporidial infection,
experimental and clinical evidence also exists indicat
ing a lack of efectiveness of paromomycin. No antibi
otic approved for use in horses has been demonstrated
to be effective in the treatment of cryptosporidial
diarrhea.
Hyperimmune bovine colostrum has been used with
varying success as a means of prophylaxis and therapy of
cryptosporidiosis in animals and patients with AIDS. A
factor limiting the use of hyperimmune bovine
colostrum is its availability. Pooled bovine colostrum,
however, is more readily available. Pooled bovine
colostrum from non-immunized animals also may be
protective in controlling cryptosporidiosis; non
immunoglobulin factors in the colostrum may provide
protection. Use of hyperimmune or pooled bovine
colostrum has not been uniformly successful. The ben
efts of administration of colostrum or hyperimmune
colostrum to foals, regardless of their age, with cryp
tosporidiosis is unknown.
Treatment of foals with severe combined immuno
defciency is likely to be unsuccessful. In immunocom
petent foals, infection is often subclinical or mild and
self-limiting; in these foals no treatment or supportive
care is needed. In more severely affected foals further
treatment may be necessary.
CONTROL AND PREVENTION
The prevention and control of cryptosporidiosis can be
difcult. Currently, immunization effective at prevent
ing cryptosporidiosis in horses and foals is lacking.
Although some chemotherapeutic agents have shown
preventive potential, the cost-effectiveness of such pro
phylaxis is often a limiting factor. Oocysts shed in feces
are infective, extremely resistant to environmental fac
tors, and can survive for months if not exposed to
extremes of temperature or desiccation. Oocysts can be
killed by steam, 10% formalin, 5% ammonia, and undi
luted commercial bleach, although prolonged expo
sure is necessary which can be difcult to achieve. Good
sanitation may help by decreasing the oocyst burden in
the foals' environment. Specifc sanitation strategies
would include providing uncontaminated water, rigor
ous cleaning (preferably with steam) and disinfecting
foaling stalls, removing all the bedding, and isolating
diarrheic foals.
ZOONOTIC CONSIDERATIONS
Ingestion of oocysts in people can cause gastrointestinal
disease in immunocompetent and immunosuppressed
people. People working with animals, including farmers
and veterinarians, are considered to be at increased
risk. Cryptosporidiosis has occurred in veterinary stu
dents exposed to infected calves and foals. Efforts to
minimize transmission in persons handling infected
foals should include instruction regarding, and rigor
ous attention to, hygiene, protective clothing (possibly
to include face mask, gloves, gown or coveralls, and
boots) , and efforts to disinfect contaminated areas.
Persons with primary or acquired immunodefciency
should not be exposed to foals with diarrhea in which a
diagnosis of cryptosporidiosis is possible. Because of the
low prevalence of infection, mature horses do not
appear to be an important source of environmental
contamination.
Diarrhea - other causes
JF Freestone
ANTIBIOTIC-INDUCED DIARRHEA
Antibiotic-induced diarrhea occurs because of the inhi
bition of the normal anaerobic bacterial flora and the
secondary proliferation of pathological bacteria. In
adult horses antibiotic-induced colitis is generally
severe and can rapidly be fatal. In foals antibiotic
induced diarrhea is generally mild and will often
resolve quickly once the antibiotics are discontinued.
Diarrhea can be induced by a number of antibiotics.
Some antibiotics will cause a problem only in certain
regions and this is probably a reflection of differences
in the normal intestinal bacterial flora. In foals the
antibiotic most commonly associated with diarrhea is
erythromycin. Erthromycin is widely used in combina-
tion with rifampin for the treatment of Rhodococcus equi
infections. Diarrhea that develops in a foal on ery
thromycin will generally resolve 48 hours after the
antibiotic is discontinued. Often the foal needs to con
tinue receiving antibiotics for the R equi infection.
Trimethoprim sulfamethoxazole and rifampin can be
used when problems of either hyperthermia or diar
rhea have developed secondary to the use of ery
thromycin. R equi infections have resolved in response
to this antibiotic combination.
SEPTICEMIA
Diarrhea is a common clinical sign in the septicemic
foal. Septicemia usually develops in the frst 7 days of
life. Foals may be normal at birth, become infected and
then deteriorate, or be born septicemic with weakness
and inability to stand and nurse. The common clinical
signs in the septicemic foal initially are lethargy, depres
sion, and failure to nurse, followed by diarrhea. The
common bacteria implicated in neonatal septicemia are
Escherchia coli, Actinobacillus spp., Klebsiella pneumoniae,
and Stretococcus spp. The basis for treatment of these
foals is antibiotics to kill the infectious agent with sup
porting medical therapy and nursing care for the
neonate.
Another foal diarrhea syndrome which has not been
widely reported has been termed 'fetal diarrhea'. The
newborn foal with fetal diarrhea will be born covered in
liquid yellow-brown feces. These foals are infected in
utero, and there may be an accompanying placentitis.
The amniotic fluid is contaminated with feces and the
foal is subject to aspiration pneumonia. These foals are
generally septicemic and may appear healthy and
robust at birth but will often be unable to stand and will
then rapidly deteriorate. Other foals born with fetal
diarrhea will progress normally and it is assumed these
foals develop diarrhea shortly prior to birth and have
limited exposure to the severely contaminated environ
ment. All foals born with evidence of fetal diarrhea
should be treated with broad spectrum antibiotics and
closely monitored for signs of deterioration.
NUTRITIONAL CAUSES OF DIARRHEA
Nutritional causes of diarrhea in foals have been associ
ated with overfeeding, use of milk replacers, and a rapid
change in diet from mare's milk to milk replacers (e. g.
orphaned foals) . In foals deprived of mares colostrum
and milk for 48 hours because of the possibility of
neonatal isoerythrolysis, and supplemented with milk
replacer, it is common for a self-limiting diarrhea to
507
develop. Foals with these forms of diarrhea remain clin
ically normal.
Lactase deficiency and lactose intolerance have both
been reported in foals. These are both are unusual
causes of diarrhea. Lactase deficiency can be evaluated
by use of an oral lactose tolerance test.
Ingestion of sand and dirt by foals can also cause
diarrhea secondary to local irritation of the lining of the
gastrointestinal tract. Diagnosis can be made by exam
ining the feces for sand or in severe cases using abdom
inal radiography. Treatment with orally administered
methyl cellulose may be efective in removing the sand
and dirt.
EQUINE HERPESVIRUS
____WiI#I* WA"'Iif"_;{'"'t"_'
Foals infected in utero with equine herpesvirus may
develop diarrhea although it is not the predominant
clinical sign in these foals. Often the infected foal will
appear normal at birth but will fail to stand and nurse
and then progressively deteriorate, developing severe
respiratory distress terminally. These foals are treated
and supported as septicemic foals, although treatment
is generally unsuccessful. A definitive diagnosis is made
on histopathological changes in the lung, liver, and the
Iymphoreticular tissues at necropsy.
CANDIDIASIS
Candida albicans is a commensal organism of the
mucous membranes and gastrointestinal tract.
Superficial infections have been reported in foals.
Systemic candidiasis is rare and generally occurs in foals
treated with prolonged broad spectrum antibiotics for
septicemia. Immunocompromised foals are also predis
posed to candidiasis.
Diarrhea has been reported in foals with systemic
candidiasis, but this is considered an unusual cause. A
these foals are often immunocompromised or have
been treated long term with antibiotics, the diarrhea
may not be directly due to the Candida infection.
PARASITES
Strongyloides westeri
Strongloides westeri is a questionable cause of diarrhea in
young foals. Transmission occurs by ingestion of infec
tive larvae from the mare's milk or via skin penetration.
The pre-patent period is 8-14 days. Attempts to estab-
508
lish a clear association between infective larvae and the
induction of diarrhea have been unsuccessful.
Treatment of mares on the day of parturition with iver
mectin was unsuccessful in blocking vertical transmis
sion. Treating foals with ivermectin or oxibendazole is
effective.
Strongyle i nfections
Equine strongylosis occurs secondary to mixed infec
tions with large strongyles and cyathostomes (small
strongyles) . These mixed infections cause gastrointesti
nal tract irritation and clinical signs of intermittent soft
feces, but can also cause persistent diarrhea in foals.
The severit of the clinical signs is related to the parasite
load. Foals grazing pasture containing high levels of
strongyle eggs, or immunologically naive foals with a
good worming history that are subsequently exposed to
strongyle infections are at risk of developing clinical
signs of strongyle parasitism. These clinical signs
include lethargy, depression, decreased weight gain, a
rough hair coat, and diarrhea. Treatment with iver
mectin is effective in controlling these mixed infec
tions.
Proliferative enteropathy in
foals
J-P Lavoi e and R Drol et
Proliferative enteropathy is a transmissible enteric dis
ease affecting a number of mammalian species, notably
pigs. It has a worldwide distribution and its causal agent
has been recently identified and classifed as Lawsonia
intracellulars, an obligate intracellular bacterium.
CLINICAL PRESENTATION
The disease has been described sporadically in horses,
either as isolated cases or as outbreaks in breeding
farms. Foals 47 months of age appear most suscepti
ble to the disease. Common clinical signs include
depression, rapid and severe weight loss, subcutaneous
edema, diarrhea, and colic. Extremely poor body con
dition with a rough hair-coat and a pot-bellied appear
ance are common findings in affected foals. The
disease may lead to death within a few days or cause
chronic growth retardation. Concomitant respiratory
tract infection and intestinal parasitism are also found
in some foals.
CLINICAL PATHOLOGY
Hypoproteinemia is the most consistent laboratory find
ing. Other commonly observed abnormalities include
transient leukocytosis, anemia, increased creatine
kinase, hypocalcemia, hypochloremia, and hypona
tremia.
DIFFERENTIAL DIAGNOSIS
The clinical signs presented by foals with proliferative
enteropathy resemble those associated with common
gastrointestinal diseases caused by parasites, infections
caused by Salmonella spp., Clostridium spp., and
Rodococcus equi, or sand impactions. However, these
conditions are unlikely to cause outbreaks of disease
characterized by weight loss, diarrhea, colic, and severe
hypoproteinemia in foals of this age group.
DIAGNOSIS
Post-mortem diagnosis of proliferative enteropathy is
based on identifing the characteristic intracellular bac
teria within the apical cytoplasm of proliferating crypt
epithelial cells of the intestinal mucosa, using a silver
stain (Figure 27.2) . The severe hyperplasia of the
intestinal crypts often causes a grossly detectable thick
ening of the mucosa of the distal small intestine.
Polymerase chain reaction analysis and immunohisto
chemistry confirm the presence of Lawsonia intrcellu
lars in intestinal tissue. Isolation of the organism is not
a practical means of diagnosis as it cannot yet be culti
vated in conventional cell-free media and the technique
is available in only a few research institutions.
Ante-mortem diagnosis of proliferative enteropathy
is based on clinical signs, hypoproteinemia, and the
exclusion of common enteric infections. The presence
of the organisms can be detected using polymerase
chain reaction analysis of fecal samples. Although spe
cific, to date this technique has revealed a low sensitivit
in horses. The use of serology for the diagnosis of
Lawsonia intrcellularis infection in a small number of
foals suggests that this technique may be promising.
THERAPY
Erythromycin estolate (25 mg/kg p.o. q. 6-8 h) alone
or combined with rifampin (7 mg/kg p.o. q. 12 h) for a
minimum of 21 days is effective in controlling the dis
ease. Additional symptomatic treatment such as antimi
crobial, anti-ulcer therapy and parenteral feeding may
Figure 27.2 Intestinal crypts from a foal with proliferative
enteropathy. Numerous bacteria are agglomerated withi n
the apical cytoplasm of the crypt enterocytes (arrow
heads). Warthi n Starry silver stain.
be required in some foals. Foals with severe hypopro
teinemia may benefit from administration of plasma
intravenously.
OUTCOME
Without appropriate antimicrobial therapy the disease
may lead to death. However a rapid improvement
24-48 h) in attitude, appetite, weight gain, and colic
signs or diarrhea may be observed in foals following
administration of erythromycin and/or rifampin. The
increase in plasma protein concentration lags com
pared to the improvement noted on other parameters
during therapy.
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N Am. Equine Pract. 2: 329-36.
Martens RJ, Malone P S, Brust D M ( 1985) Oral lactose
tolerance test in foals: techniques and normal values. Am.
J Vet. Res. 46: 2163-6.
McClureJJ, AddisonJ D, Miller R 1 ( 1 985)
Immunodefciency manifested by oral candidiasis and
bacterial septicemia in foals. J Am. Vet. Med. Assoc.
186: 1 1 95-7.
Reilly L K, Palmer J E ( 1994) Systemic candidiasis in four
foals. J Am. Vet. Med. Assoc. 205: 464-6.
Thamsborg S M, Leifsson P S, Grondahl C, Larsen M, Nansen
P ( 1 998) Impact of mixed strongyle infections in foals
after one month on pasture. Equine Vet. J 30: 240-5.
Prol iferative enteropathy in foals
Duhamel G E, Wheeldon E B ( 1 982) Intestinal adenomatosis
in a foal. Vet. Patho!. ; 19: 447-9.
Frank N, Fishman C E, Gebhart C] et al. ( 1 998) Lawsonia
intmcellularis proliferative enteropathy in a weanling foal.
Equine Vet. ]; 30:549-52.
Lavoie
.
J P, Parsons D, Drolet R ( 1998) Proliferative
enteropathy in foals: a cause of colic, diarrhea and
protein-losing enteropathy. Poc. Am. Assoc. Equine Pact.
44: 1 34-5.
McOrist S, Gebhart C], Boid R et al. ( 1 995) Characterization
of Lawsonia intmcellularis gen. nov., sp. nov., the obligately
intracellular bacterium of porcine proliferative
enteropathy. Int. ] Syst. Bacterol; 45:820-5.
Williams N M, Harrison L R, Gebhart C] ( 1996) Proliferative
enteropathy in a foal caused by Lawsonia intmcellularislike
bacterium. ] Vet. Diag. Invest; 8: 254-6.
5 1 1
26
Diseases of the rectum and anus in the
foal
EM Santschi
Atresia recti and ani
INTRODUCTION
Atresia recti and ani are rare conditions of neonatal
foals. Foals affected with atresia recti and ani initially
nllrse well but cannot pass meconium normally. The
ingestion of food causes fluid and gas to accumulate
and the intestine becomes distended causing colic.
EPIDEMIOLOGY
A
g
e
Atresia recti and ani are congenital conditions, there
fore clinical signs of colic and bloating in foals with this
condition are only seen within 48 hours of birth.
Gender and
g
enetics
Atresia recti and ani are rare conditions and no genetic
predisposition has been noted.
ETIOLOGY
Atresia recti and ani probably have different, and as yet
unknown, causes. Atresia ani occurs when the anal
membrane persists - during normal embryologic devel
opment the anal membrane breaks down resulting in a
caudal opening in the terminal portion of the fetal gut.
The most commonly accepted cause of intestinal atre
sias, including atresia recti, is a congenital loss of blood
supply to a portion of the gut, leading to ischemic local
necrosis. However the cause of the vascular insult is
unknown.
CLINICAL SIGNS
Atresia ani is easily diagnosed as there is no visible anus.
Foals affected with atresia ani usually show signs of
abdominal pain and progressive abdominal distention
within 48 hours of birth. Some foals with atresia ani
have either a rectovaginal fstula or rectourethral fstu
lae, so small amounts of feces may be passed through
the vulvae or penis. Foals with atresia recti may have an
anus, but digital palpation will reveal a blind pouch and
no feces. Caudal abdominal radiographs may help
delineate the extent of atresias. Elevating the foal's
hindquarters will cause gas to fll the terminal patent
gut and the caudal blind pouch can be determined.
PATHOLOGY
Gross patholo
g
y
For atresia ani there is no anus and there is haired skin
where the anus should be. There may be a communica
tion between the urethra and rectum. For atresia recti
there is a discontinuity between the anus and terminal
small colon.
DIAGNOSIS
These conditions are diagnosed by clinical signs.
491
TREATMENT
Treatment of atresia ani requires surgical anastomosis
of the terminal rectum and the skin, and closure of any
urethral or vaginal fstulae. Surgery can be performed
under general anesthesia or under sedation and
epidural anesthesia. A 2.0 x 1.0 cm elliptical incision
(long axis oriented vertically) is made where the anus
should be, and the terminal rectum is retracted cau
dally. The terminal rectum is opened and sutured to
the skin. It is helpful to frst suture the rectum using
four equally spaced interrupted sutures and then flling
in between them with interrupted sutures.
Closure of urethral or vaginal fistulae with the rec
tum requires dissection of the border of the fstulae and
492
a to-layer closure. The mucosa of the fstula is
removed and the submucosal tissues sutured together.
The rectal mucosa is then closed separately.
There is little information about correction of atresia
recti. Surgical correction (via rectal pull through) is dif
fcult because of the inaccessibility of the blind-ended
segments in the pelvic cavity. Permanent colostomy
might be an option for salvage.
BIBLIOGRAPHY
Benamou A E, Blikslager A T, Sellon D C (1995) Intestinal
atresia in foals. Compo Cont. Educ. Pact. Vet. 17:1510-16.
28
Hepatic diseases in foals
Portosystemic shunts
LA Fortier
INTRODUCTION
Portosystemic shunts (PSS) are anomalies of the porto
systemic circulation that allow direct communication
between the portal circulation and a systemic vein such
as the vena cava. The shunting vessel(s) circumvents
portal blood from entering the hepatic circulation and
being cleared of toxic metabolites by the liver.
Portosystemic shunts are classified as
congenital or acquired
intrahepatic or extrahepatic
single or multiple.
This chapter primarily addresses congenital PSS,
although the fundamental pathophysiology and med
ical management described applies to acquired shunts
as well.
Intrahepatic shunts represent a failure of the
ductus venosus to close normally 2-3 days following
birth. Embryologically the ductus venosus provides a
direct communication between the left umbilical vein
and the caudal vena cava. In the neonate, when the
ductus venosus fails to close, portal blood drains into
the left hepatic vein just prior to entering the caudal
vena cava. Congenital extrahepatic shunts most com
monly originate from the portal vein but may also
originate from the left gastric vein, splenic vein,
cranial or caudal mesenteric vein, or gastroduodenal
vein, and typically empty in the caudal vena cava or
azygous vein.
Only five cases of congenital portosystemic vascular
anomalies have been reported in horses, of these five
cases
two were classified as single extrahepatic
one as multiple extrahepatic
one as single intrahepatic
one was designated as an arteriovenous anomaly.
A presumptive diagnosis of PSS is based on history, clin
ical signs, and blood tests, while a definitive diagnosis
requires hepatic scintigraphy or positive-contrast por
tography. Medical management may provide temporary
relief from the signs of hepatic encephalopathy.
However, without surgical ligation of the shunt vessel(s)
progressive deterioration occurs.
PATHOPHYSIOLOGY
Portosystemic shunts divert portal blood away from the
liver thereby allowing noxious substances such as
ammonia, mercaptans, short-chain fatt acids, and false
neurotransmitters that are normally cleared by the liver
to remain in the systemic circulation, resulting in
hepatic encephalopathy. Ammonia has been widely
suggested as the major neurotoxin of hepatic disease.
Hyperammonemia emerges from decreased hepatic
conversion of ammonia to urea and is a characteristic
sign of PSS in horses. Ammonia exert its toxic effects
on neuronal cell membranes and impairs neurotrans
mission through competing with potassium and subse
quently inhibiting the sodium-potassium-dependent
adenosine triphosphatase. Portal blood comprises
75-80 per cent of total hepatic blood flow and 50 per
cent of hepatic oxygen supply. Portal blood therefore
51 3
determines the environment of the hepatocyte through
its hormone, nutrient, and oxygen content. Shunting of
portal blood from the liver results in liver atrophy due
to the lack of hepatic blood flow and concurrent
decreased supply of hepatotrophic factors such as
insulin and glucagon.
Poikilocytosis (erythrocyte malformation) and
microcytosis with normochromic erythrocytes are com
mon fndings on blood laboratory results in foals with
PSS. The cause of poikilocytosis in PSS remains unde
fned and the microcytosis is believed to result from
metabolic toxins interfering with iron uptake and
metabolism or disrupting erythrocyte membrane
integrit. Neither poikilocytosis nor microcytosis are
specifc for PSS, however, they are considered indicative
of serious hepatobiliary disease
CLINICAL SIGNS
The signalment for foals with PSS is inconsistent.
Belgian, Thoroughbred, Quarter horse, and Arabian
foals presented for a wide variety of clinical signs
beteen the ages of 2 weeks and 11 months. The pre
senting history and clinical signs may include
1. small body size for age
2. episodic signs of hepatic encephalopathy including
disorientation
seizures
stupor
head pressing
circling
undirected aggression
apparent cortical blindness
non-responsiveness to auditory stimuli
coma.
Neurologically, all reported cases had normal proprio
ceptive responses and in the cases with apparent corti
cal blindness, pupillary light reflexes were assessed as
normal. Differential diagnoses based on clinical signs
tpically include PSS, bacterial or viral meningitis, and
idiopathic cerebral edema. A defnitive diagnosis is
based on clinical laboratory data and positive-contrast
portography or hepatic scintigraphy.
DIAGNOSIS
In addition to a thorough physical and neurological
examination, blood should be submitted for routine
hematologic and serum biochemistry tests, and deter
mination of serum concentrations of blood ammonium
and bile acids. Foals with PSS are typically microcytic
514
and normochromic with normal hematocrit and total
protein values (Table 28.1). There may be a mild
mature neutrophilia present, consistent with a stress
leukogram. Poikilocytosis is typically noted on red
blood cell morphology as mild to moderate.
Serum biochemistry values are typically within nor
mal limits, including serum gamma glutamyl trans
ferase and blood urea nitrogen concentrations, with the
possible exceptions of increased total bilirubin concen
trations and hypoglycemia. In all reported cases of PSS
in foals, blood ammonia and total serum bile acid con
centrations have been increased over normal values.
Increased concentrations of total serum bile acids and
blood ammonia, with normal hepatic enzyme concen
trations in foals, should be considered indicative of con
genital portosystemic vascular anomalies (Table 28.1).
Blood ammonia concentrations are typically at least sev
enfold greater than age-matched controls and are con
sidered a more defnitive indicator of congenital PSS in
foals than increased total serum bile acid concentra
tions. Correct handling of blood samples for blood
ammonia concentration determination is critical to
obtain reliable, diagnostic results. Blood samples from
the patient and an age and species-matched control
should be collected and transported on ice for immedi
ate evaluation. Freezing or storage of plasma is discour
aged as it may result in spuriously high or low values.
Pre- and postprandial determination of serum bile acid
values, while valuable in dogs and cats in the diagnosis
of PSS, are of little value in foals due to the physiology
and anatomy of the alimentary canal, particularly the
absence of a gallbladder.
Diagnostic test
hemogram
serum biochemistry
panel
blood ammonia
serum bile acids
Abnormalities noted with
P55
microcytosis, poikilocytosis
: hyperbilirubinemia,
hypoglycemia
usually increased more than
7 x normal
increased
cerebrospinal fluid* : increased nucleated cell
count, red blood cell count,
and total protein
: indicates all these conditions are present
* following seizures
Positive-contrast portography remains the diagnostic
technique of choice for shunt confirmation and loca
tion. The surgical approach for access to the portal cir
culation may be made through either a ventral midline
celiotomy or through a right flank incision. If shunt lig
ation is to be performed during the same anesthetic
procedure as the contrast portogram, then a right flank
approach is recommended since this is the preferred
approach for shunt ligation (see Treatment, Operative
techniques) . Foals have a relative straight-branching
mesenteric venous pattern, allowing catheters to be
readily advanced within the cranial mesenteric vein and
potentially into the portal vein or shunt. A iodinated
contrast agent such as Renografin-76 is injected as
needed (typically 50-80 ml) to opacif the portal
venous system and abdominal radiographs are obtained
during the last few seconds of positive-contrast injec
tion. If a shunt cannot be identified by positive-contrast
portography, a liver biopsy should be obtained to look
for hepatic dysplasia or microvascular shunting, this has
been reported in dogs but has not been recognized in
foals. The hepatic histologic abnormalities observed in
hepatic dysplasia are similar, and possibly indistinguish
able from those observed in animals with PSS.
Fluoroscopically assisted portography is typically unre
warding in foals due to the depth of their abdomens.
Hepatic scintigraphy is useful for shunt confirmation
but provides no information on shunt location and is
therefore also a less rewarding technique than positive
contrast portography.
Additional diagnostic tests that may be beneficial
include abdominal ultrasound and cerebrospinal fluid
evaluation. Abdominal ultrasonography may identif
the PSS, however, a positive-contrast porto gram should
still be performed preoperatively to confirm the ultra
sound findings and determine the pattern and direc
tion of portal blood flow. Cerebrospinal fluid analysis in
foals with PSS should be normal or reveal a slightly
increased total nucleated cell count, a mildly increased
total protein concentration, and an elevated red blood
cell count, consistent with trauma, but not indicative of
myelitis.
TREATMENT
Preoperative management
If anesthesia, portography, and surgical ligation of the
shunt are being considered, medical management of
the hepatic encephalopathy must be obtained before
anesthesia and surger are attempted. Gaining manage
ment of the hepatic encephalopathy may require sev
eral days of intense medical therapy. Extreme caution
HEPATIC DISEASES IN FOALS 28
should be exercised when handling foals exhibiting
signs of hepatic encephalopathy. The frequent stum
bling and undirected aggression may be harmful not
only to the people handling the foal, but to the foal as
well, necessitating a well-padded stall and possibly heavy
sedation. To control seizures and aggressive behavior,
tranquilizers, particularly benzodiazepines, and barbi
turates should be administered cautiously, starting at
half of the recommended dose, since animals with PSS
are very susceptible to their depressive effects. In the
preoperative period, medical management should
be directed toward reducing encephalopathic toxins.
Medications should be judiciously chosen to include
those that do not require or interfere with hepatic
metabolism. The drugs of choice for ulcer prophylaxis
medication should be ranitidine or famotidine, because
unlike cimetidine, they are excreted primarily by the
kidneys and do not interfere with hepatic metabolism
of drugs. Metronidazole is frequently used in small
animals to reduce the number of ammonia-producing
bacteria in the colon, and if administered should be
given at half the recommended dose as it is metabolized
primarily in the liver and peripheral neuropathies have
been reported after its administration in humans with
PSS. Intravenous administration of dimethyl sulfoxide
should be avoided as it is an effective carrier molecule
and could increase the transport of encephalopathic
toxins from the alimentary canal into the brain. Foals
should be maintained on a low protein diet to reduce
ammonia production, while maintaining their energy
and fluid requirements. Lactated Ringer's solution
should not be administered to severely affected animals
because it may induce alkalosis and worsen the
encephalopathy. Oral administration of lactulose
and/ or neomycin should be considered. Lactulose is a
synthetic disaccharide which bypasses small intestinal
digestion. In the colon it acts as a cathartic and lowers
the fecal pH thereby inhibiting ammonia generation by
fecal bacteria.
Operative techniques
In foals affected with PSS, anesthesia may be poorly
tolerated because of the severe metabolic effects of the
disease. The use of tranquilizers, especially benzodi
azepines, and barbiturates for anesthetic induction or
sedation should be avoided if possible because, as noted
above, animals with PSS are very susceptible to their
depressive effects. Mask or nasal intubation for induc
tion using oxygen and isoflurane offers a relatively safe
anesthetic protocol. During surgery, the foal should be
kept warm and supported with intravenous fluids con
taining glucose. All personnel involved in the anesthe
sia, contrast portogram, and surgical ligation should be
515
aware of the added risks and it should be stressed that
anesthetic and surgical times be kept to an absolute
minimum.
The preferred surgical approach for PSS ligation in
foals is a large right paracostal incision with an 18th rib
resection. This approach is superior to a ventral median
celiotomy to provide adequate exposure where the
depth of the abdomen and volume of small and large
intestines preclude adequate exposure to the portal cir
culation. A thorough understanding of portal vascular
anatomy is paramount for shunt identifcation. A patent
ductus venosus represents the most diffcult PSS to
identify and ligate. Most are located in the left or
central hepatic divisions and may be managed by left
hepatic vein attenuation which is technically easier than
intracaval techniques or intraparenchymal dissection,
particularly in the depth of an equine foal abdomen.
Mter the shunt is located, a catheter is placed in a
jejunal vessel to facilitate measuring portal pressures
during shunt ligation. If shunt ligation is performed
during the same anesthetic procedure as the positive
contrast portogram, the same jejunal catheter may be
used for contrast injection and portal pressure moni
toring. The catheter is connected to a water manometer
or pressure transducer and the shunt is ligated with
non-absorbable suture while the portal pressure is mon
itored and abdominal viscera are obsered for signs of
cyanosis and congestion. Cellophane banding instead
of suture ligation for shunt attenuation should be con
sidered so that progressive and partial attenuation of
the shunt vessel is possible while monitoring the portal
pressure and abdominal viscera for signs of portal
hypertension. In dogs there was no difference in clini
cal outcome between those cases where partial shunt
attenuation was performed to avoid portal hyperten
sion, versus complete occlusion of the shunt vessel.
There are no data on normal portal vascular pressures
in foals. Until more information is available regarding
PSS ligation in foals, it would seem reasonable to follow
the guidelines set out for small animals which caution
that portal hypertension develops when portal pres
sures increase more than 10 cmH20 over baseline
values or when visceral congestion is visible during or
after shunt ligation.
Postoperative management
Postsurgical care consists of intensive supportive care
similar to that described for preoperative management
in addition to monitoring wound healing and observing
for portal hypertension. Portal hypertension is charac
terized by
ileus
shock
51 6
bloody diarrhea
abdominal pain.
Foals may still require treatment for hepatic
encephalopathy and should be maintained on a low
protein diet until complete resolution of clinical signs.
Postoperative blood ammonia and serum bile acid con
centrations are usually monitored for signs of improve
ment. However, in small animals, there is no correlation
between declining blood ammonia or total serum bile
acids and resolution of clinical signs. Blood ammonia
and serum bile acid values may never return to normal,
this is most likely the result of permanent hepatic
parenchymal abnormalities.
OUTCOME AND PROGNOSIS
Surgical mortality in foals with congenital PSS is high
with only one successful case of PSS ligation reported in
the literature. Interestingly, two out of fve reported
cases of foals with PSS were full blooded Belgians, with
one case occurring in a Thoroughbred, one an Arabian,
and one a Quarter horse. The heritabilit of PSS in
horses is unknown but there is accumulating evidence
that these anomalies are inherited in certain purebred
dogs and cats. With so few cases of PSS reported in foals,
it is not possible to determine heritability, but this pos
sibilit should be kept in mind and discussed with the
foal's owners prior to surgical correction. The mortality
associated with surgical correction of PSS should
decrease with early diagnosis, surgical attenuation of
the shunt through a right fank approach instead of
a ventral midline celiotomy, and most importantly,
appropriate and aggressive preoperative and postopera
tive management.
Tyzzer's disease
W Bernard
Tyzzer's disease is an acute, fulminate bacterial hepati
tis, myocarditis and! or colitis. The disease has been
reported in foals from 7-92 days of age. The causative
organism, Clostridium piliformis, is a flamentous bac
terium (Plate 28.1). The disease occurs sporadically,
however has been reported in outbreaks and is
endemic in certain geographic locations. The route of
infection is thought to be via ingested feces. Soil is
contaminated by infected individuals or possibly
rodents .
CLINICAL SIGNS
Clinical signs of Tyzzer's disease include
sudden death
depression
anorexia
coma/stupor
seizures
hyper- or hypothermia
icterus
petechiation
abdominal pain
diarrhea.
Clinical signs can be variable, however the overwhelm
ing nature of the clinical presentation is the acute and
rapidly progressive course of the disease. Tyzzer's dis
ease should be a primary differential diagnosis for a foal
that, having had no history of illness, is suddenly found
dead. Clinical diagnosis of C. pilifaris can be challeng
ing as the signs are non-specifc and severe, often
including central nervous system signs and septic shock
with cardiovascular collapse. Foals may present in a
coma/stupor or exhibit seizures. Physical examination
identifes variable signs of sepsis and cardiovascular
shock. Icterus of mucous membranes is variable, as the
acute nature of the disease may not have resulted in a
signifcant hyperbilirubinemia. Petechiation and high
fevers may be present. Abdominal pain and/or hemor
rhagic enterocolitis can be associated. The abdominal
pain is likely to be secondary to colitis or acute swelling
of the liver capsule. Myocarditis is an occasional fnding
on necropsy associated with this disease.
DIAGNOSIS
Ante-mortem diagnosis is diffcult as there is no rapid
defnitive diagnostic test. Signalments with appropriate
age classifcation, acute onset, and associated clinical
signs should suggest Tyzzer's as a possibility. Liver
biopsy with appropriate histopathology can be diagnos
tic but the long time course involved makes biopsy of
little use in therapy unless immediate impression
smears can be evaluated. Serum or plasma liver
enzymes (AST, SDH, and GGT) are moderately to
markedly elevated, with increases dependent upon the
time course of the disease. Affected foals are often
severely acidotic and hypoglycemic. Although these lab
oratory parameters are not specifc, severe acidosis and
hypoglycemia alone should suggest pursuit of a diagno
sis of hepatic disease. Blood cultures should be per
formed but are rarely diagnostic. Polymerase chain
reaction (PCR) testing is currently being evaluated.
Gross necropsy identifes typical white spots in the
hepatic parenchyma. Histopathology confrms a diag
nosis of Tyzzer's disease. Warthin Starry stains identif
flamentous bacteria in affected tissue (Plate 28.1).
Routine bacterial culture techniques are unrewarding.
TREATMENT
Successful treatment of a defnitively diagnosed case of
Tyzzer's disease has not been reported in the literature.
Emergency therapy with appropriate fluid volume, dex
trose, and bicarbonate replacement therapy will vary
depending on cardiovascular status and interference
with intermediary metabolism. Routine therapy for sep
tic shock should be provided. The lack of antibiotic sen
sitivity testing necessitates a choice of broad spectrum
antimicrobial therapy. High doses of intravenous peni
cillin in combination with an aminoglycoside or other
broad spectrum intravenous therapy are appropriate
choices.
Congenital disorders
JE Adolf
BILIARY ATRESIA
There have been two reported cases of biliary atresia in
foals; one foal with extrahepatic atresia and one foal
with histopathologic evidence of both extrahepatic and
intrahepatic atresia. Both foals were presented to the
veterinary hospitals at approximately one month of age
for clinical signs including
lethargy
anorexia
failure to thrive
recurring high fever
colic
polydipsia
polyuria
icterus.
Serum biochemistry of one of the foals suggested bil
iary obstruction, as evidenced by extremely increased
values of bilirubin (conjugated and imconjugated),
alkaline phosphatase, and gamma glutamyl transferase
(GGT). Hepatocellular disease was also suspected based
on an increased sorbitol dehydrogenase (SDH). Ante
mortem diagnoses were not made in either foal, and
both underent a post-mortem examination. The livers
517
were enlarged and firm on gross examination. The
entrance of the bile duct into the duodenum was absent
in one foal, and although the extrahepatic bile duct
appeared grossly normal in the other foal, its patency
was not assessed. Histologic abnormalities noted in
both livers included extensive bile duct proliferation,
cholestasis characterized by bile-distended canaliculi,
severe fibrosis, hepatocyte degeneration, and a com
plete lack of bile ducts within the remaining portal
triads.
Although the exact pathogenesis is not known, sev
eral theories have stemmed from the human literature.
These include
congenital absence (either from lumen destruction
or duct underdevelopment)
a deficit in bile flow in uteo
excretion of a biliary toxin
postnatal destruction secondary to a chronic
cholangiohepatitis.
In both foal reports, the authors hypothesized that
the biliary atresia was a congenital anomaly. In the
future, when biliary atresia is suspected, hepatobiliary
scintigraphy, as well as a liver biopsy, could be
attempted as ante-mortem diagnostic tools, as this was
successful in diagnosing a 21-day-old lamb with biliary
atresia.
SEROUS CYSTS
Serous cysts are occasionally encountered on the
diaphragmatic surface of the liver in foals. They are usu
ally small and multiple, although they can be large and
solitary. Their origin is unknown but they could be
serosal inclusion cysts, part of a congenital biliary
abnormality or they could be of endodermal origin. On
most occasions these cysts are encountered incidentally
on necropsy.
Neoplastic conditions
JE Adolf
There have only been two reports regarding hepatic
neoplasia in foals. The frst report was a mixed hamar
toma in a late-term aborted fetus. Histological findings
included
atypical hepatocytes (large hepatocyte-like cells with
eccentric nuclei and voluminous cytoplasm)
abnormal biliary ducts
51 8
fbroblastic-fbrocytic interstitial tissue
a lack of structural organization.
The second report was of a hepatoblastoma of a full
term, stillborn foal. On gross pathologic examination,
the liver contained numerous, light tan masses, that
were lobulated with necrotic centers on cross section.
The tumor had metastasized to the thoracic cavity, as
evidenced by enlarged tracheobronchial lymph nodes.
Histopathologically there were two distinct epithelial
cell types within the liver nodules: fetal and embryonal
cell types, with the latter cell type predominating. The
architecture of the tracheobronchial lymph nodes was
obliterated by infiltration of embryonal-type cells. This
is the only reported case of hepatoblastoma in a foal.
Hepatoblastomas have been reported in a fetus, a wean
ling, yearlings and young adults. Erythrocytosis is a fea
ture of many cases.
Infectious processes
__i
JE Adolf and TJ Divers
BACTERIAL ORIGIN
Septicemia and/or endotoxemia
Bacterial septicemia is a common condition in foals
during the neonatal period. Manifestations of sep
ticemia range from pneumonia, enteritis, and poly
arthritis, to death from septic shock and multiple
system organ failure. The liver can be affected in sep
ticemia by a variety of pathophysiologic mechanisms. A
relatively common fnding in septic foals is the presence
of icterus, characterized by hyperbilirubinemia (pri
marily unconjugated) without elevations in other liver
parameters or evidence of intravascular hemolysis. The
underlying etiology for the hyperbilirubinemia is
unknown, but possible etiologies include intestinal sta
sis (secondary to septicemia) and increased resorption
of bilirubin, liver immaturity, damage to erythrocytes,
lack of nutritional intake, intrahepatic cholestasis, or an
isolated defect in bilirubin excretion. This hyperbiliru
binemia is generally mild to moderate and resolves if
the septicemia is successfully treated. Mild hyperbiliru
binemia can also be found in healthy equine neonates.
In addition, increased liver enzyme values other than
bilirubin (alkaline phosphatase, GGT, and SDH) can be
elevated in normal neonatal foals.
Septicemia can lead to bacterial hepatitis via
hematogenous inoculation. Common bacterial isolates
from foals with sepsis include the gram-negative
bacteria EScheichia coli, Actinobacillus equuli, Klbsiella
pneumoniae, Enterobacter spp., and Salmonella spp., as
well as the gram-positive bacteria Streptococcus spp. and
Staphylococcus spp. A. equuli in particular has been
known to cause hepatitis and nephritis, characterized
by multifocal abscessation. Clinical signs associated with
bacterial hepatitis are similar to those signs commonly
seen in septic foals and include
weakness
depression
decreased to absent suckle reflex
icterus.
If the hepatitis is severe enough to cause extensive
hepatic necrosis and subsequent hepatic failure, then
other signs associated with hepatic encephalopathy may
be present (i.e. seizures) . The bilirubin and hepatocellu
lar enzymes will be increased in these cases and
histopathologic fndings would include leukocytic infl
trate (primarily neutrophils) in the periportal tissue and
sinusoids, Kupfer cell hypertrophy and hyperplasia,
degeneration of hepatocytes, and focal areas of hepatic
necrosis. Treatment should encompass general support
ive care, as in any intensive care neonate, and antibiotic
therapy (either broad spectrum or preferably those indi
cated via culture and sensitivity). If hepatic encephalopa
thy is present, then other treatments are indicated (see
Chapter 19). The prognosis depends on a variet of
factors such as the bacterial agent involved, evidence of
multisystem involvement, and the severity of the hepatitis.
There have been a select number of cases of undiag
nosed severe, acute hepatitis seen in 3-week to 3-month
old foals, that have resembled Tyzzer's disease. Some
foals were outside the age range for Tyzzer's disease and
therefore were felt to have another type of hepatitis.
Clinical signs noted were
high fever
recumbency
shock
icterus.
Hematology and serum biochemistry were suggestive of
septicemia and/or endotoxemia (leukopenia, neutro
penia, degenerative left shift) , as well as hepatitis
(increased liver enzymes and bilirubin) . Liver biopsies
for histopathology and culture were not performed
because of the presence of thrombocytopenia or other
coagulation abnormalities. The foals were treated with
supportive care (fluids, oxygen therapy, anti-inflamma
tory therapy) and antibiotics. Because the foals subse
quently recovered defnitive diagnoses were not made.
Finally, the liver can be most severely affected by sep
tic and/or endotoxic shock conditions, that can then
lead to fulminant hepatic failure and death. The hepatic
system, as well as the cardiovascular, pulmonary, and
renal systems, are the target organs most commonly rec
ognized as being affected in shock conditions. The bio
chemical and immunological events that take place in
septic and/ or endotoxic shock are numerous and com
plex; only a brief overview related to the liver will be dis
cussed here (see also Chapter 11) . During severe septic
or endotoxic states, a large number of vasoactive medi
ators and hormones are involved in altering the hemo
dynamic system (i.e. interleukins, prostaglandins, tumor
necrosis factor, complement, oxygen free radicals, nitric
oxide, glucocorticoids, opioids) . This exaggerated res
ponse to sepsis and/ or endotoxemia is otherwise known
as the systemic inflammatory response syndrome (SIRS) .
The hemodynamic changes that occur in SIRS include
increased cardiac output (initially)
reduced peripheral vascular resistance (which leads
to hypotension)
narrowed arterial-venous oxygen diferences
lactic acidemia
increased vascular permeability.
SIRS and its profound systemic effects lead to defective
cellular mitochondrial function and specifc visceral
microcirculatory defects. The fnal outcome is
decreased hepatic oxygenation.
Decreased hepatic oxygenation leads to hepatocellu
lar damage, this is characterized microscopically by vac
uolation of hepatocytes with swelling of mitochondria
and endoplasmic reticulum, increased lipid accumula
tion, Kupffer cell vacuolation, and dilation of the bile
ducts. With widespread hepatic damage liver function is
impaired. If this impairment is accompanied by the dys
function of other organ systems, the condition is known
as multiple organ dysfunction syndrome (MODS).
Diffuse hepatic necrosis and hepatocellular apoptosis
with subsequent hepatic failure can occur secondary
to the aforementioned hepatocellular changes. When
hepatic failure is coupled with the failure of other
organ systems, then the term multiple organ failure
(MOF) is used. In human patients, the incidence of
MOF in association with septicemia is 30 per cent. In
foals, the incidence of MOF has not been reported. The
treatment for septic and/or endotoxic foals with sec
ondary hepatitis and hepatic necrosis could include
appropriate antibiotic therapy
fluids
oxygen therapy
dimethyl sulfoxide (DMSO), for its anti-oxidant and
anti-inflammatory properties
acetlcysteine, a glutathione donor, used for its anti
oxidant properties
non-steroidal anti-inflammatory drugs
51 9
The reader is referred elsewhere for a more compre
hensive description of the treatments of endotoxic
shock (see Chapter 11) and liver failure (see Chapter
19). The prognosis for foals affected with septic and/ or
endotoxic shock with secondary liver involvement is
guarded to grave, due to the fact that MODS or MOF is
likely to be present as well.
Ascending infection
Cholangiohepatitis can occur in foals secondary to an
ascending bacterial infection. There are two primary
locations for the origin of infection
1. the umbilical vein
2. the hepaticoduodenal junction, where the common
hepatic duct enters the duodenum.
The umbilicus can serve as a portal of entry for bacter
ial pathogens. Most foals with an umbilical infection are
less than 8 weeks old and there may be an association
between a patent urachus and infection. Not all
affected foals will have a palpable abnormality of the
umbilicus since the infection can reside internally.
Although the urachus is the most common structure of
the umbilicus to become infected, the umbilical vein
can be involved as well. If this occurs, then the infection
can ascend into the hepatic parenchyma. In one report,
four out of eight foals with an infected umbilical vein
developed an ascending hepatitis. Diagnosis is based
primarily on ultrasonographic fndings, but also
includes umbilical palpation, laboratory data (complete
blood count (CBC) and liver enzymes), and bacterial
cultures (umbilical, blood and/or another septic
focus). Treatment consists of antibiotic therapy and, in
some cases, surgical marsupialization of the infected
umbilical vein to the ventral abdominal wall. Surgical
removal of the entire umbilical vein has been attempted,
but is not preferred, because of the likelihood of hem
orrhage from the liver during the procedure.
Cholangiohepatitis, originating from the hepatico
duodenal region, can be a sequela of gastroduodenal
ulceration in foals. Duodenal strictures may occur sec
ondary to duodenal ulceration, these could then cause
cholangiohepatitis through two mechanisms. If the
stricture occurs at the hepaticoduodenal area, then bile
duct obstruction and ascending cholangiohepatitis can
follow. A stricture that occurs aborad to the bile duct
opening can cause bile stasis, reflux of ingesta into the
bile duct, and an ascending infection that extends to
the liver. The former condition, with complete bile duct
obstruction, warrants a very poor prognosis. Diagnosis
is based on clinical signs associated with gastroduodenal
ulcers and obstructive disease (lethargy, decreased
interest in nursing, diarrhea, bruxism, colic, nasogastric
520
reflux), endoscopic and radiographic evidence of out
flow obstruction, and laboratory evidence of liver
involvement (increased liver enzymes, icterus).
Treatment involves surgery, where the duodenal stric
ture can be bypassed, and anti-ulcer and antibiotic
therapies. Reported surgical options include gastro
jejunostomy and duodenojejunostomy, and if the bile
duct is completely obstructed, then a hepaticojejunos
tomy can be performed. If a needle aspirate or liver
biopsy is taken at the time of surgery, it could support a
diagnosis of cholangiohepatitis (portal hepatitis, biliary
hyperplasia). If surgery is successful, and normal bile
flow is restored, the liver enzymes will decline over time,
indicating a resolution of the cholangiohepatitis.
Except for one reported foal with peri-duodenal absces
sation and secondary biliary obstruction, reported post
operative complications were not related to continued
hepatic disease.
VIRAL DISEASES
Equine herpesvirus type-1 (EHV-1)
EH-l is a well-known cause of abortion and stillbirths
in the equine. In some cases, a live foal is produced,
which is either premature or full term. In the majority
of cases, neonatal EH-l infections are fatal, although
there are two reported cases of neonatal foals with con
frmed EH-l viremia that survived. Common clinical
presentations for foals born infected with EH-l
include
weakness
inability to stand unassisted
failure to nurse
depression.
Findings on physical examination may include
icterus
tachycardia
tachypnea
dyspnea.
A fundic examination may reveal dark red optic discs
and irregularly dilated vessels. Complete blood count
values can be profoundly abnormal, including leukope
nia, neutropenia, and lymphopenia. Biochemical analy
sis may reveal hyperbilirubinemia and elevated liver
enzymes, but these are uncommon fndings. If bone
marrow of an affected foal was collected, it might show
severe toxic changes in the myeloid scores, a depletion
of myeloid elements, and a left shift within the myeloid
line. The clinical course will usually deteriorate rapidly
and may be accompanied by signs of respiratory distress
and/ or failure (persistent hypoxemia, hypercapnia).
The foals usually die within 3-5 days. Typical post
mortem examination fndings include
moderate to severe multifocal necrotizing hepatitis
moderate to severe necrotizing bronchiolitis and
bronchopneumonia
focal or massive necrosis in the lymphoreticular
organs.
The demonstration of intranuclear inclusion bodies in
affected organs such as the liver and lung is pathogno
monic for EHV-I infection. Defnitive diagnosis is based
on virus isolation (blood, tissues), immunohistochemi
cal or fluorescent antibody staining (hemolymphatic
organs, liver, lung, etc.) and/or polymerase chain reac
tion (peR) testing (tissues, amniotic fluid). Treatment
for EHV-l has recently been attempted using acyclovir
at doses of 8-16 mg/kg p.o. t.i.d. In this report two out
of three treated foals survived, and survival may have
been influenced by the administration of acyclovir.
Cytomegalovirus
Equine herpesvirus type-2 is a cytomegalovirus that is of
questionable signifcance in its pathogenicity. There
has been one report of a foal that had diffuse hepatic
necrosis and cellular pigmentation without the pres
ence of inclusion bodies on post-mortem examination,
that was attributed to cytomegalovirus infection.
PARASITIC DISEASES
Large strongyles
Both Strnglus edentatus and S. equinus larvae can pene
trate the wall of the cecum and subsequently inoculate
the liver. S. equinus larvae migrate through the liver
capsule, causing hemorrhagic, fbrinous inflammation,
and then penetrate the bile duct, where fbrosis can
occur secondarily. S. edentatus larvae will reach the liver
through the portal circulation and then migrate
through the liver, leaving small white foci to be appreci
ated grossly. Diagnosis is based on clinical evidence of
parasitism (failure to thrive, rough hair coat, debility),
clinicopathologic evidence of hepatitis (increased liver
enzymes) and if performed, histopathologic evidence
of hepatitis (inflammatory infltrate, possible fbrosis,
possible larvae identifcation within a core of necrotic
eosinophils). Due to the long pre-patent period of S.
edentatus and S. equinus (8-11 months), a fecal worm
egg count will most likely be negative in affected foals.
Treatment should consist of larvicidal anthelmintic reg
imens, including ivermectin, moxidectin (not for use in
foals < 4 months of age), fenbendazole (10 mg/kg for
5 days or 50 mg/kg for 3 days) or thiabendazole
(440 mg/kg once).
Ascarids
Parascaris equorum larvae will penetrate the small intesti
nal wall and migrate to the liver as part of the migratory
life cycle. The migration of larvae through the liver can
cause focal hemorrhages and small, white, nodular
lesions. Microscopically, lesions are characterized by
inflammatory infltrate (predominately lymphocytes
and eosinophils) around the portal triads, and fbrosis.
The diagnostic fndings are similar to those mentioned
for strongylosis, except that with a shorter pre-patent
period (l 0-12 weeks), a fecal flotation is more likely to
be positive for ascarid eggs. Treatment consists of larvi
cidal anthelmintics, such as moxidectin (not for use in
foals < 4 months of age) or fenbendazole at 10 mg/kg
for 3 days. Ivermectin at a regular dose (0.2 mg/kg) is
not effective against the ascarid larvae.
Flukes
Although liver flukes (Fasciola heatica) are a rare occur
rence in the equine, there have been reports of natural
and experimental infections in adult horses and foals. F
hepatica infections may be clinically inapparent or may
be associated with clinical signs such as lethargy, poor
hair coat quality, and exercise intolerance. Diagnosis
is based on a fecal examination and/or necropsy,
although not all infections appear to be patent.
Treatment consists of fasciolicides, such as triclabenda
zole, carbon tetrachloride or oxyclozanide.
OTHER INFECTIOUS CONDITIONS
Leptospirosis
Leptospirosis is a spirochete infection that can lead to
equine abortions, stillbirths, or premature live births.
Necropsies performed on aborted fetuses or stillborn
foals ofen reveal an enlarged, pale liver and icterus.
Histopathologic fndings are quite characteristic,
including hepatocellular dissociation, mixed leukocytic
infltration of portal triads and giant cell hepatopathy.
Originally, the cause of giant cell hepatopathy was not
known, but was subsequently identifed in cases of lep
tospirosis. There have been no reports of hepatic dis
ease in live foals infected with leptospirosis. Diagnosis
following an abortion or stillbirth is made by bacterial
cultures and fluorescent antibody testing of representa
tive organs and characteristic histopathologic lesions,
with a possibility of identifing the spirochete on micro
scopic samples.
521
Ehrlichia ristic;
Ehrlichia rsticii, the causative agent of equine monocytic
ehrlichiosis or Potomac horse fever (see Chapter 20),
has recently been recognized as an abortifacient.
Experimentally and naturally infected mares tend to
abort at around 7 months gestation. Histopathologic
findings on the aborted fetuses have been consistent,
including
lymphohistiocytic enterocolitis
hepatitis
myocarditis
lymphoid hyperplasia.
Diagnosis is based on the characteristic microscopic
lesions, isolation of E rsticii from fetal tissues and
serum titers from infected mares suggestive of infec
tion. There have not been any reported cases of live
foals born from dams infected during gestation.
Toxic disorders
EX
IRON TOXICITY
In 1983, various reports from around the United States
indicated an emerging cause of toxic hepatopathy in
foals. The cases were subsequently linked to the
administration of an oral proprietary nutritional paste
containing viable primary cultures and fermentation
products as well as vitamins and iron (as ferrous
fumarate). Experimental reproductions of the disease
found that the iron in the oral supplement was the toxic
principal. Affected neonatal foals were all given the
paste shortly after birth and began to show clinical signs
within 2-5 days. Only those foals that received the paste
before ingesting colostrum appeared to be affected.
The predominant clinical signs were
depression
marked icterus
ataxia
aimless wandering
colic
convulsions.
Marked elevations in liver enzymes, primarily GGT,
alkaline phosphatase, and bilirubin, were noted on
serum biochemical analyses. Some foals also had
elevated SDH and aspartate aminotransferase (AST)
values. Other clinicopathologic abnormalities indica
tive of hepatic failure included hyperammonemia, high
522
aromatic to branch chain amino acid ratio, and pro
longed prothrombin time and partial thromboplastin
time. Except for two foals in one experimental report,
all foals died after exhibiting ante-mortem signs of
hepatic encephalopathy (seizures, head pressing, and
coma). Pathologic fndings were similar among affected
foals
gross liver atrophy
hepatocyte necrosis
prominent bile duct proliferation
occasional periportal fbrosis.
Many foals also demonstrated Alzheimer type II cells
within cerebral tissue (found in cases of hepatic
encephalopathy), multifocal, acute catarrhal to hemor
rhagic enteritis, lymphoid necrosis, and renal cortical
necrosis. The oral paste was taken off the market shortly
after these cases were reported.
NSAIO TOXICITY
Non-steroidal anti-inflammatory drugs (NSADs) are
known occasionally to cause hepatotoxicosis in
humans, and this has been infrequently reported in
horses. To date, no cases have been reported in foals,
although the author has seen two foals at the veterinary
hospital with rising liver enzymes (SDH, GGT, alkaline
phosphatase) while they were receiving oral carprofen.
Liver enzymes decreased after discontinuation of the
carprofen and no long-term adverse efects were noted.
Carprofen in particular has been associated with hepa
tocellular toxicosis in dogs. NSAD-related hepatotoxic
ity is believed to be an idiosyncratic reaction in people
and dogs, except for acetaminophen and aspirin, which
cause time and dose-dependent hepatic disease.
Despite the absence of reported NSAD-induced hepa
totoxicity in foals, the monitoring of liver enzymes
in foals receiving NSADs, especially carprofen, is
warranted.
OTHER HEATOTOXINS
----------
With the exception of iron toxicity, report of hepato
toxins in foals, especially plant and chemical toxins, are
rare. However, there are many substances that are
potential hepatotoxins in horses (see Chapter 19), an
abbreviated list is given here.
Common drugs include
carbon tetrachloride
tetracycline
erythromycin
rifampin
phenobarbital
copper
glucocorticoids
anabolic steroids
diazepam
Hz blockers.
Hepatotoxic plants include
pyrrolizidine alkaloid-containing plants
alsike clover
blue-green algae
lantana.
Chemical substances include
tannic acid
phenols
phosphorus
mycotoxins.
The tpe of liver damage induced by these substances
will dictate any observed liver enzyme abnormalities
(i.e. cholestatic versus hepatocellular enzyme derange
ments) . So, for any foal with unexplained liver enzyme
elevations, hepatotoxicosis secondary to drugs, plants,
or other chemical substances, should be considered
and investigated.
Other liver diseases
HYPERAMMONEMIA IN MORGANS
There have been two reports of persistent hyperam
monemia leading to signs of hepatic failure in Morgan
weanlings and yearlings. Clinical signs, such as weight
loss, depression, and other signs associated with hepatic
encephalopathy, wer
e
noted soon after weaning. Blood
tests demonstrated elevations in liver enzymes and
blood ammonia levels (typically >300 Jlg/ml) . In
addition, some cases experienced hemolytic crises.
Histopathologic fndings in the liver were variable and
included lymphocytic-plasmacytic periportal hepatitis,
portal fbrosis, bile duct hyperplasia, karyomegaly, and
cytomegaly. Although the exact etiology of this disease
is unknown it may be caused by an inherited defect in
ammonia metabolism. The disease has some similarities
to an inherited disorder in humans, known as hyper
ornithinemia, hyperammonemia and homocitrullinuria
(HHH) syndrome. In both equine reports there were
pedigree similarities suggesting a genetic component.
In the most recent report, amino acid profles revealed
increased serum ornithine and glutamate and
increased urine orotic acid concentrations, similar to
the HHH syndrome. All of the described cases are
deceased - they either died or were euthanized due to
treatment failure and clinical deterioration.
PORTAL VEIN THROMBOSIS
A portal vein thrombosis was seen in a 6-week-old thor
oughbred with Streptococcus zooepidemicus cellulitis and
pneumonia and Rodococcus equi polyarthritis and pneu
monia. Based on the hematology and serum biochem
istry, bacteriologic fndings, and the presence of an
umbilical abscess, the thrombosis was presumably sec
ondary to a septic process. The thrombus (see Figure
28.1) occupied 90 per cent of the portal vein, as well as
the primary intrahepatic portal vein branches. The liver
parenchyma appeared normal ultrasonographically,
but histopathologic examination revealed diffuse hepa
tocellular atrophy and poorly developed vascular pro
fles. Liver enzyme abnormalities were present - GGT,
SDH, and alkaline phosphatase were elevated.
Treatment was aimed at the septic process and included
antibiotics and anti-inflammatory drugs. Repeat ultra
sound examinations demonstrated a recannulization of
the portal vein and the development of hyper echo genic
foci in the liver parenchyma. A the thrombus resolved,
the liver enzymes declined. Despite the presence of
abnormal echogenic foci in the liver, no permanent
liver function abnormalities were detected. Portal vein
Figure 28.1 A hyper-echoic thrombus can be seen within
the lumen of the portal vein of a Thoroughbred foal. The
thrombus appears to have some mineralization and is cast
ing an acoustic shadow. The liver parenchyma appears
normal on the sonogram.
523
thrombosis has been well described in humans and
occasionally occurs in horses. Affected adult horses
tend to exhibit signs of hepatic encephalopathy, but the
aforementioned foal and one other foal that the author
(TJ Divers) treated with this condition did not. This dis
crepancy may be related to the fact that foals have much
smaller colons, and are therefore less likely to overpro
duce ammonia. Affected animals may also exhibit diar
rhea, because of portal hypertension secondary to the
thrombosis.
NEONATAL ISOERYTHROL YSIS
Rarely, a foal develops signifcant liver disease (continu
ally elevating GGT) and dysfunction (rising direct
bilirubin) while being treated for neonatal isoerythroly
sis (NI). This is more often a problem in foals requiring
multiple blood transfusions. The exact cause of the liver
disease/dysfunction is unknown, but may involve
hypoxic damage, hemochromatosis, and biliary hyper
plasia from excessive bilirubin secretion (bilirubin
secretion in bile is the rate-limiting step in bilirubin
metabolism/ excretion). Most of the foals do eventually
recover from both the NI and liver disease so relatively
few necropsies are available to collect further informa
tion regarding this condition.
PERINATAL ASPHYXIA
Perinatal asphyxia most commonly affects the neuro
logic system, but hepatic damage can also occur follow
ing a hypoxic insult. Although hepatic damage in this
context has not been specifically reported in foals, peri
natal asphyxia is not an uncommon occurrence in
equine neonates and therefore hypoxic-induced liver
damage is possible. A in humans, icterus and liver
enzyme elevations would be present if there was suf
cient liver damage. Treatment would include support
ive care (i.e. oxygen therapy) and addressing the needs
of any other affected organ system.
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525
Index
Abdomen
auscultation 4, 11 0
physical examination 4
Abdominal abscesses 330-332
Abdominal closure 181-184, 187
Abdominal distention 317-322
Cushing's disease 322
distention colic 317-319
fecaliths 462
fetl hydrops 321
foals 451
diferential diagnosis and evaluation
459-462
hemoperitoneum 321
ileocolonic aganglionosis 461
ileus 320
intestinal atresia 461
intestinal obstruction/impaction
319-320,462
meconium retention 460-461
peritonitis 321, 462
pneumoperitoneum 320
potential causes 317
uroperitoneum 321, 461-462
ventral body wall hernias and prepubic
tendon rupture 321-322
Abdominal drainage and lavage 328-329
Abdominal pain see Pain
Abdominal quadrants, palpation 159-161
Abdominocentesis 13-16
chronic and recurrent colic 342
in foals 15-16, 453
abdominal distention 460
bowel wall perforation 453, 460
decision for surger 467
hemoperitoneum 333
instrumen ts 13
in peritonitis 325-326
ultrasonography and 15, 16
Abortion 355, 412, 414, 520, 521, 522
colic and 351, 352, 354
Acepromazine (acetylpromazine) 24 119,
121, 124, 148,359
N-Acetylcysteine 194-195
Acid-base balance 12
abdominal pain and 138-140
expected abnormalities 138
in distributive shock 202-203
hyperlipemia and 398-399
Acors 419, 423
Acremonium coenohialum 422-423
Actinobacillus ligieesii 78
Acupuncture 206
Acute abdomen
prognosis 141-142
rectal examination 112-119
Adamantinomas 73
Adenocarcinoma 337
Adhesions 209-211
experimental modeling 210
in foals 466, 483
gut viability and 164, 165, 166-167
incidence 209
in intestinal obstruction 104, 105, 259,
264
pathophysiology 104, 105, 209-210,
259,264
prevention 210-211
surgical protocol 210
sutures and 168, 170, 172, 180-181
treatment 211
ultrasonography 30, 31
Adipose tissues 395
Aeromonas spp. 423
AfIatoxins 384, 420
Age determination 70-71
Airway, after anesthesia 154-155
Albumin:globulin (A:G) ratio 12
Albumin levels 11
Alfalfa 196, 295-296, 299, 300, 418, 419
Alkaline phosphatase 12, 386, 387, 388,
389,391,398
Alkaloid intoxication 389-391
Allopurinol 194
Alopecia 378
Alpha
2
agonists
in anesthesia 147
-induced arrhythmias 234, 236
postoperative pain relief 207-208
Alpha fetoprotein 393
Alsike clover 393
Altrenogest 351,352
Aluminium hydroxide 243
Alveolar periostitis 74, 75-76
Alzheimer tpe II cells 382, 385, 522
Ameloblastomas 73, 79
Aminocaproic acid 218, 334, 359
Amitraz 280, 420
Ammonia toxicity see Hyperammonemia
Amsinckia intermedia 389
Amylase activit 349
Analgesia
in colic 119-122, 124
dosages and effcacy 119
gastric decompression 120
narcotics 121
NSAIDs 120
sedatives 120-121
spasmolytics 121-122
walking 120
during transport 133
foals 464-465
in grass sickness 348
in peritonitis 328
postoperative pain 206-208, 209
Anastomosis 172-181, 255
atresia ani 492
atresia coli 488
cecal bypass 271
end-to-end 175, 176
functional 180, 181
end-to-side 176, 177
general considerations 172-175
hand-sewn 175-176, 177-178
impaction at 215-216
purse-string 170, 178
revisions/complications 185-187
enlargement 186
leaking 185
rotation 174
side-to-side 176, 177-179, 255-256
stapled 176, 178-179, 180, 181
see also Sutures
Anatomic system, dental nomenclature
69-70
Anatomy
in laparoscopic examination 47-48
rectal palpation of normal horse 7-8
ultrasonographic 26-28
in videolaparoscopy 45-46
Anemia 11
Anesthesia, general
colic surgery 145-155
blood tests and 152
cardiovascular system and 146,
150-151, 152, 153
complications 152-154, 219-222
depth of anesthesia 150
drugs used 147-150
induction 147
monitoring patients 150-152
preparation of patient 146-147
pulmonary system and 145-146,
151-152, 154-155
recover 154-155
pregnant mare and 351
Anesthesia, local
laparoscopy 46, 48-49
Anisognathism 69
Anoplocehal maga 54
Anolocehal peroliata 53, 54, 57, 259, 274
Anorectal abscesses 331
Anorectal lymphadenopathy 314
Antacids 243, 244, 473, 474
Anthelmintics
in chronic diarrhea 431
control programs 56, 58-60
cyathostomosis 435
precipitation of disease 433
grass sickness and 343-344
resistance 54, 56, 59, 60, 435
side efects 58
treatments 57-58
see also specifc agents
527
INDEX
Anti-arrhythmic therapy 236-237
Antibiotic-induced diarrhea 410,411,
412,423,507
Antibiotic tberapy
abdominal abscesses 331-332
biliary tract disease 388
chronic diarrbea 431
clostridial disease 410-411, 412, 501
distributive shock 203
endotoxemia 195
periradicular disease 75-76
peritonitis 328
post-anestbesia myopathy/neuropathy
and 220
postoperative colitis 232
preoperative 141
salmonellosis 408, 409, 499
thrombophlebitis 137
Anticoagulant therapy 226-227
Antidiarrbeal agents 435-436
Anti-endotoxin therapy 123,193,203,
213,230
Antifreezes 421
Antihistamines 422
Anti-inflammatory agents
adhesions and 210
in distributive shock 203
ileus and 213
in peritonitis 328
Antimesenteric enterotomy 295
Antimesenteric teniotomy 295
An tioxidant status 221
Antithrombin III activity 223-224, 227
Arabian borses 295, 350
Arachidonic acid metabolism 104, 147,
192
Arsenic intoxication 420
Arterial oxygen levels 145
Arterial rupture, at parturition 357-359
Arteritis, mesenteric 55, 262, 436-437
A.carids 521
biology and life cycle 54
control programs 59
egg survival 53
fecal tests 57, 521
ill thrift 56
impaction 56, 262, 481-482
pathogenesis 55, 521
treatment 58, 521
Asci tes 320, 503
Aspartate aminotransferase 220, 221-222,
383,387,390,392
Aspergillosis 424
A.lpegllus spp. 378, 384, 423, 424
Asphyxia, perinatal 524
Aspiration pneumonia 64, 79, 89, 92, 507
Aspirin 207, 226, 422
Astrgulus spp. 420
Atipamazole 234, 236
Atracurium 150
Atresia ani 461, 491-492
Atresia coli 461, 486-489
Atresia recti 461, 491-492
Atrial fbrillation 234
Atropine 121-122, 150,236,420
Aural fstulae 73
Auscultation 4, 110
colic 254
foals 451-452
Auto suturing device 42, 43
528
Autotransfusion 334, 359
AV block, profound 236
Avocado toxicity 419
Azotemia 138, 373
Bacteria
peritoneal fluid analysis 18
see also specifc diseases
Bacteroides fagilis 75-76
Barium enema 459-460
Bermuda grass 259
Berteroa incana 423
Bethanecol 124, 213-214, 244, 246
Bezoars 302-303
Bicarbonate estimation 12, 123,154,203,
463-464
Bile acids 383, 391
Bile duct hyperplasia 387
Bile fluid leakage 19
Bile salt therapy 388
Biliary atresia 517-518
Biliary calculi 386-389
Biliary tract disease 386-389
Bilirubin levels 382, 383, 384, 387
Biochemistry
hyperlipemia 397-398
parameters 11-12
parasite-associated diseases 57
Biopsy
chronic diarrhea and 430
endoscopic 26
laparoscopic 44, 48
in malabsorption syndromes 379
see also specifc sites
Bismuth subsalicylate 195,406,431
Bismuth, synthetic 412
Bite plate 72, 73
Blister beetles 417-418, 419
Blood flow, viability and 166, 167-168
Blood pressure
in anesthesia 150-151, 152-153, 153
arterial rupture, parturition 358, 359
in hypovolemic shock 199-200
Blood substitutes 202
Blood tests, anesthesia and 152
Blood transfusions 202, 218, 333-334, 359
Blood volume 199
Blue-green algae 419
Body condition score 367-368
Body weight balance 367
Bone scin tigraphy 34-36
Borborygmi 4
Bots 60
Botulism 64
Bougienage 93
Bowel sounds 4, 110, 206
Bowel wall biopsy 342,372,380
Bradydysrhythmias 232, 234, 236
Breath hydrogen tests 38
Brood mare
abdominal pain in pregnancy (non
colic) 356-357
colic 351-361
general considerations 351-352
non-pregnant mare 352-353
parturient mare 357-361
pregnant mare 351-352, 353-357
copulation injuries 305, 353
hemiperitoneum 332, 333
hyperlipemia and 394, 395
post-parturient, cecal perforation 274
recurrent volvulus 291-292
Brotizolam 348
Bruxism 471
Buccal mucosal flaps 85-86, 87
Bull's eye sign 29, 30, 456, 457, 482
Butorphanol 24,47, 119, 121, 148, 154
postoperative pain 206, 207, 208
Calcium 235
post-anesthetic myopathy and 222
see also Hypercalcemia, Hypocalcemia
Calcium borogluconate 140, 405-406, 419
Calcium gluconate 154
Cancer cachexia 374-375
Candidiasis 508
Cantharidin toxicosis 417-419
Capillary refll time (CRT) 3-4, 110
Capnograph 151
Carbohydrates
absorption tests 20-21, 379
fermentation and dental disease 74
soluble, in grain overload 421-422
Carbon tetrachloride 521
Carboxymethylcellulose 159, 161,
210-211,271
Cardiac arrhythmias
in foals 464
postoperative 232-237
aftercare and prognosis 237
anti-arrhythmic treatment 236-237
electrocardiography 232
electrolyte status and 234-236
pathogenesis 234
prevalence and signifcance 232-234
Cardiac output, in anesthesia 151
Cardiogenic shock 198
Cardiovascular function
in colic 146
anesthesia and 146, 150-151, 152,
153
foals 451
small intestinal obstruction 253
fluid therapy 123
Caslick procedure 353
Castor bean plant 420
Castration 17,327,331,332,477
Cathartics 281, 486
Catheters 134-137
complications 135, 137, 226
considerations 134-135
guidelines for use 226
management 137, 226
during transport 132-133
materials 132
replacement 136
treatment of thrombophlebitis 137, 226
types 135-136
Cecal acidosis 275-276
Cecal bypass 271
Cecal content transfer 431
Cecal distention 268-269
Cecal impaction 269-272
clinical signs and diagnosis 269-270
epidemiology and etiology 269
prognosis and prevention 271-272
treatment 270-271
Cecal infarction 276
Cecal intussusceptions 272-274
Cecal perforation 271, 274-275
Cecal trocarization 268-269
Cecal tympany 268-269,319
Cecocecal intussusceptions 30, 272-274,
436
Cecocolic intussusceptions 30, 55,
272-274,436
Cecum
anatomy and function 267-268
rectal examination 8, 114-115
Celiotomy
in colic, indications for 129-132
postoperative colic, ultrasonography
33-34
repeat 184-187
acute 185-186
decision-making 184-185
delayed 186-187
surgical procedure and revisions
185-187
techniques
flank, through 17th or 18th rib
157-158
other approaches 158
paralumbar flank 157-158
ventral midline 155-156, 356
ventral paramedian 156-157
Cellophane banding 516
Cellulitis, catheter-related 135, 136, 137
Cellulose digestion 267-268
Central nervous system 'wind-up' 205
Central venous catheter 132
Cen tral venous pressure 151
Cerebral edema 382
Charcoal, activated 195,406,409,419,
420,431
Chemotherapy 338
Chenodeoxycholic acid 423
Chloral hydrate 207
Chlorambucil 338
Chloramphenicol 412
Chlorhexidine-impregnated catheters 135
Choke 67, 89
Cholangiocarcinoma 389, 393
Cholangiohepatitis 386-388, 520
Choledocholithomy 388
Choledocholiths 386
Cholelithiasis 386
Chronic obstructive pulmonary disease
(COPD) 376
Chyloabdomen 479-480
Chyloperitoneum 19
Chylous effusions 19
Cimetidine 243, 244, 245
Cirrhosis, chronic hepatic 394
Cisapride 124,214-215,348,465
Cisplatin 248
Citrobacter spp. 387
Cleft palate 79-87
acquired 65, 66, 80, 81
clinical signs 81
etiology and pathophysiology 80
investiga tion and diagnosis 81-82
prevention 87
prognosis 86
treatment 82-86
complications 86-87
Clenbuterol354
Clinical pathology 11
chronic and recurrent colic 341-342
neoplasia 336
weight loss 369-370
see also Acid-base balance,
Biochemistry, Electrolyte balance,
Fluid balance, Hematology
Clostridial diarrhea 13, 410-412
clinical signs and clinical pathology
411,500
diagnosis 411-412, 500-501
etiopathology 410-411, 499-500
in foals 456, 499-502
prognosis 501
treatment and prevention 412, 501-502
Clostridium diffcile 230-231,410-412,500,
501
antibiotic-associated infection 124
Clostrdium peringens 258, 261, 410, 411,
412, 499-502
Clostridium piliforis 516-517
CNS signs, in Theiler's disease 381-384
Coagulation status
adhesions and 209-210
endotoxin and 104, 191-192
liver disease and 382
normal 223
salmonellosis 408
see also Thrombophlebitis
Coccidiosis 60
Cockspur hawthor fruit 280
Codeine phosphate 57, 431, 435-436
Colic
acute, decision to refer 126-129
cecal diseases 267-278, see also specifc
disorders
chronic and recurrent
causes 339, 340
defned 338-339
differential diagnosis 338-343
investigation 339-343
congenital defects 477-480
distention 317-319
clinical signs and diagnosis 318
treatment 318-319
foals 477-484
large colon diseases 279-298, 485-490,
see also
specifc conditions
medical therapies 119-125
aims 119
analgesia 119-122, 124
anti-ndotoxin therapy 123
anti-inflammator 123
cardiovascular support 123
fluid therapy 122-123
intestinal motility alterations 123-125
laxatives 122
walking 120
parasitic infection
cyathostome 436
mild strongyle-associated 55
tapeworm-associated 56, 58
treatment 57, 58
preoperative preparation 140-141
preparation for referral transport
132-134
risk factors 101-103
farm management factors 102
medical history 101-102
preventative medicine factors 102
signalment 101
weather 102-103
INDEX
small intestinal 249-266
epidemiology 250-251
outcome and prognosis 483-484
postoperative management and
complications 483
see alo specifc disorders
spasmodic 125
surgery for 145-188
anesthesia 145-155
closure of abdomen 181-184
evaluation of gut viability 164-168
exploration of abdomen 158-164
repeat laparotomy 184-187
surgical approaches 155-158
techniques 168-181
ultrasonography
indications for 29
postoperative 33-34
Colic, clinical evaluation 107-144
clinical pathology 132, 466-467
clinical signs 107-109
decision for surgery 129-132, 465-467
decision to refer 126-129
false (non-gastrointestinal) colics
118-119
fecal production 128
geographical location 127
management and deworming history
127
medical history 127
pain severity 127, 130
peritoneal fluid analysis 131
physical examination 109-112,
129-131,466
abdominocentesis III
clinical examination 109-110
heart rate 110, 129-130
history 109, 466
jugular vein flling 110
mucous membranes 110
nasogastric intubation 110-111,
130-131
rectal examination I l l , 112-119,
130
rectal temperature 109-110, 129-130
respiratory rate 110, 129-130
ultrasonography I l l, 131
progression of colic 127
response to medical therapy 128,
131-132
signalment 127
Colitis
chronic idiopathic 437
granulomatous 443
parasite-associated 54-55, 57
prevention 231-232
segmental eosinophilic 296-297
ultrasonography 32, 456, 457
see alw Equine right dorsal colitis
Colloid therapy 139, 140,201,405
Colon
exteriorization 162-164
rectal palpation 8
resection length and viability 173
ultrasonography, foals 456, 457
see also Large colon, Small colon
Colonic biopsy 167
Colonic ulceration. NSAlD toxicosis 416
529
INDEX
Colopexy 291-292
Colostomy 310-312
Colostrum 449, 499, 507
bovine 506
Combined immunodefciency syndrome
(eID) 350
Compartment syndrome 221,222
Conduction block 221, 222
Copper levels 357
Coronary bands, dermatitis 391
Corticosteroids 57, 193,210,334,338,
379,392,435
Creatine kinase activity 220, 221-222
Crypt enterocytes, proliferating 509
Cryptosporidial diarrhea 504-507
zoonotic considerations 507
CrjJtospordium spp. 60, 350, 504-507
Crystalloid therapy 138-140, 192,
201-202,359,405
Cushing's disease 322
Cyathostomes
anthelmintic resistance 54, 59, 60
biology and lifecycle 54
clinical features 55-56
control programs 58-60
diarrhea 56, 57
intussusceptiollS 55, 272, 274
investigation 56 57
clinical history 56
fecal test 56- 57
hematology/biochemistry 57
pathogenesis 54-55
treatment 57,58
weight loss 55-56
Cyalhostomosis 432-436
clinical signs 55, 434
diagnosis 434-435
epidemiology 434
etiology and pathogenesis 432-433
malabsorption and 372-373
treatment 58, 435-436
weight loss and 372-373
Cyclooxygenase inhibition 192, 206-207
Cyclophosphamide 338
Cyproheptadine 322
Cystotomy, laparoscopic 45
Cytokine response 103-104, 191, 193-194
Cytology, peritoneal fluid 16, 17, 18, 19,20
Cytomegalovirus 521
Cytosine arabinoside 338
Cytotoxins 407, 410, 411, 496
Dantrolene 222
Database, on-line 422
Decompression
cecal 268-269
foals 465
gastric 120, 206, 246, 247
ileus and 213
Decompression tract 159
Deglutition 63-64
compromised 65-67
Dehiscence 182,197,216,217,311
Dehydration
acute diarrhea 405-406
in anesthesia 152-153
clinical parameters 12
estimation of 138
fluid therapy see Fluid therapy
530
Dental abscess 35
Dental anatomy 69
Dental caries 74
Dental cysts 73
Dental disease 69-77
developmental disorders 72-77
infectious 74-76
signs 71-72
Dental eruption time 70
Dental nomenclature 69-70
Dentl scintigraphy 34-36
Dental tumors 73
Dentigerous cysts 73
Depression 108, 382, 387
Dermatitis 391, 406
Desflurane 149
Dessicated feed 245, 246
Detomidine 24, 47,119, 121,206,207,
208,234
Dexamethasone 193, 236, 379, 392
Dextrans 192, 211
Diabetes mellitus 349-350
Diaphragmatic hernia 261, 480
Diaphragm, displaced 245, 246
Diarrhea
hemorrhagic, clostridial 412
infectious, postoperative colitis
230-232
recurrent 56, 436
Diarrhea, acute 405-425
aspergillosis 424
bacterial infections 423
clostridial, in adult horses 410-412
deranged intestinal motility 423
drug-induced 415-417, 423
grain overload 421-422
NSAID toxicity 415-417
principles of treatment 405-406
oral rehydration 406
toxic coli tides 417-421
cantharidin toxicosis 417-419
toxicities 422-423
see also Potomac horse fever,
Salmonellosis
Diarrhea, chronic 427-446
chronic inflammatory bowel disease
437
defned 427
differential diagnosis 428
Eimera leukarti 444
equine right dorsal colitis 438-442
evaluation 428-430
general principles of treatment
430-432
giardiasis 444
hepatic disease 444
histoplasmosis 443
idiopathic 443
intestinal fbrosis 444
intestinal lymphangiectasia 444
intestinal neoplasia 437
intestinal tuberculosis 443
larval cyathostomosis see
Cyathostomosis
Neospor caninum 443
other causes 442-444
peritonitis 444
salmonellosis (chronic) 443
sand enteropathy 437-438
strongylosis 436-437
Trichomonas equi 444
Diarrhea in foals 493-511
antibiotic-induced 507
candidiasis 508
clostridial enterocolitis 499-502
crptosporidial 504-507
equine herpesvirus 508
fetal 507
foal heat 493
nutritional causes 507-508
proliferative enteropathy 508-509
Rhodococcus equi 502-504
salmonellosis 495-499
septicemia 507
strongyle infection 508
Strngloides weste 508
viral 493-495
Diazepam 24, 148, 348
Digestible energy (DE) input 399-400
Dimercaprol 420
Dioctahedral smectite 412
Dioctyl sodium succinate 122,246,281,
423
Dipyrone 119, 120,207
Disinfection procedures 232
Disseminated intravascular coagulation
(DIC) 195-196,382
Distention see Abdominal distention,
specifc sites
Distributive shock 198
clinical fndings 201
pathophysiology 200
treatment 202-203
Disuse atrophy 311
DMSO (dimethylsulfoxide) 133-134, 153,
194,195,222,388
Dobutamine 153
Dog-sitting position 109
Domperidone 124
Donkeys, hepatic disease 389, 396, 397,
398,399,400
Dopamine 153, 192
Doppler techniques 166- 167
Draft breeds 221-222
Drainage, peritoneal 229
Draining tract 182
Daschia megastoma 476
Dry sickness (mal seco) 251,343
Duodenal perforation 472
Duodenal stricture 458
Duodenal ulceration 470, 471, 472
Duodenitis 471
Duodenoscopy 24, 25-26
Duodenum
anatomy 249
in endoscopy 25-26
Dysautonomia 67, 343
Dyserythropoiesis 370
Dysmasesis 74
Dysphagia 63-67
compromised deglutition 65-67
defned 63
diagnosis 64-65
normal deglutition 63-64
post-laryngoplasty 66
weight loss and 371
Ear teeth 73
ECN, equine-clinicians' network 93
Edrophonium 150
Ehrlichia nsticii 412-414,415,522
FimPa leukarti 60, 273, 444, 482
Elt'ctrocardiography 150-151, 232-234
Electrolyte balance 12
acutt diarrhea 405-406
cardiac automaticity and 234-236
chronic diarrhea 429
/,)als 454
peritonitis 326-327
Electrolyte therapy
ill anesthesia 152-13, 154
in colic 122-123
")als 463-464
Elephant on a tub posture 345
ELISA 231, 494, 495
Eltmac 120, 192,207
Emaciation 368
If alw Weight loss
Emollit'nts 281
Encephalopathy
primary hyperammonemia 384-386
Theiler's disease 381-384
Endoscopy 21-26
cleft palate 81-82
duodenal ulceration 471
dysphagia 64-65
equipment 21-23, 26
filals 453
gastric squamous cell carcinoma 247, 248
gastric ulceration 242-243, 245
gastroduodenal ulceration 472-473
procedures 23-26
adult horses 24
biopsy 26
duodenum 25-26
esophagus 24
foals 23, 24
stomach 24-25
see also Laparoscopy
Endotoxemia
coagulopathy and 223-224, 22.
hepatic infection in foals 518-520
intestinal obstruction 103-104
laminitis and 229, 230
management during transport 133-134
pathophysiology 103-104, 191-192
peritoneal fluid analysis and 18
in pregnant mare 351-352
salmonellosis 407, 408, 409, 496- 497,
498-499
treatment principles 192-196
antibiotics 195
anti-inflammatory therapy 123
biological products 192-193
disseminated intravascular
coagulation and 195-196
endotoxin nentralization 123, 193
fluid/ electrolytes 192
free radical scavengers 194-195
ga.trointestinal tract fimction and 195
glucocorticoids 193
NSAIDs 192
prevention of laminitis 195
TNF
,
and 193-194
Endotoxemic shock see Distributive shock
Endotoxin 191
Endotoxin response 191-192,200,519
End-tidal carbon dioxide 151
End-tidal concentration of anesthetic 150
Enema 305, 459-460, 486
Enrofloxacin 408
Enteral formulations 399-400
Enteritis
anterior 257-258, 261
atypical 494
eosinophilic 32, 36
in foals 455, 456, 457, 499-502
granulomatous 377, 443
hemorrhagic 500
lymphocytic-plasmacytic 33, 36, 372,
378,379
rectal examination 114
scintigraphy 36
Enterobacter spp. 387
Enterocentesis 13-14, 17, 19
Enterocolitis
granulomatous 378
Rhodococcus equi infection 503
Enterocutaneous fistula 478
Enterolithiasis 293-296
clinical signs and diagnosis 293-294,
299-300
complications 295
large colon 293-296
postoperative care 295
prevention and recurrence 295-296,
300
small colon 299-300
surgery 294-295, 300
Enteroliths 295, 299
Enterotomy
gut viability and 165-166
intestinal preparation 172
site 172, 173
see also Sutures
Enterotoxins 410, 411,496,500
Eosinophilia 11
Eosinophilic infltrates, chronic 377-378,
379
Ephedrine 153
Epicauta spp. 417-418, 419
Epidural anesthesia 307, 308, 313
Epiglottal entrapment 66
Epiglottic retroversion 87
Epiploic foramen entrapment 260
Epsom salts 122
Equine infectious enterocolitis see
Potomac horse fever
Equine monocytic ehrlichiosis see
Potomac horse fever
Equine right dorsal colitis 438-442
cause 439
clinical pathology 439-440
progression and prognosis 442
treattnent 440-442
Erythroctye parameters 11
Erythrocytophagia 18, 19
Erythrocytosis 518
Erythromycin
clostridial diarrhea 124,410-411,412,
507
as prokinetic 124, 214, 465
Escherichia coli 314, 387
Esophageal cysts, intramural 67, 96
Esophageal disorders 89-98
clinical signs 89
diagnosis 89-90
INDEX
general surgical considerations 90-92
complications/ prognosis 9697
incisional closure 91-92
surgical approaches 91
see also specifc disorders
Esophageal diverticulum 93, 95
Esophageal fstula 95
Esophageal impaction 67, 89
Esophageal neoplasia 67, 96, 247-248
Esophageal obstruction 89, 92-93
Esophageal peristalsis 63-64
Esophageal phase of glutition 63-64,
6667
Esophageal replacement 94
Esophageal resection 94
Esophageal rupture 67, 93
Esophageal stricture 67, 93-95
Esophageal tone 5
Esophageal ulceration 416
Esophagitis 471, 472
Esophagomyotomy 94
Esophagoplasty 94
Esophagoscopy 23-24, 24, 65, 90
Esophagotomy 92-93, 94-95
Esophagus
anatomy and physiology 89, 91
congenital abnormalities 96
fenestration of cicatrix 94-95
muscular patch grafting 94
physical examination 89-90
radiography 90
Estrogens, conjugated 359
Estrus 352, 493
Evacuation, large colon 290
Exercise-related colic 242, 3.3
Exercise therapy 120, 206, 260, 286, 319,
329, 357
Exteriorization of viscera 161-164
Eyeball, in anesthesia 150
Eyes, examination 452
Facial paralysis 65
Famotidine 192
Fasciola hepatica 521
Fasting, effects 196
Fecal analysis 12-13, 56 57, 370, 411-412,
429-430
in rectal examination 6
Fecal blood 13
Fecal cultures 13, 497-498, 499, 500-501
Fecal egg reduction count tests (FERCT)
59-60
Fecal impaction 301-302
see also Grass sickness
Fecaliths 302, 303, 462
Fecal worm egg count (FWEC) 12,5657,
60,437
Feed see Nutrition, Nutritional support
Feed impactions, in pregnancy 353-354
Fenbendazole 58, 435
Fescue grasses 422-423
Festuca spp. 422-423
Fetal diarrhea 507
Fetal hydrops 321
Fever 129-130,374,391,411,414
531
INDEX
Fiberoptic endoscopy 21, 22
Fibrin activity
adhesions and 105, 209-210
in hypovolemic shock 199
in liver disease 382
normal 223
in peritonitis 323, 324
Fibrosis, intestinal 444, 471-472
Flatulent colic see Colic, distention
Flexor tenotomy, deep digital 230
Flotation techniques 506
Fluid balance 12
Fluid therapy
abdominal pain and 138-140,
463-464
cecal impaction 270
colic 122-123
diarrhea
acute 405-406
chronic 430
viral 494-495
distributive shock 202-203
during transport 132-133
en do toxemia 192
foals 463-464
hepatoencephalopathy 383-384
hypovolemic shock 201-202,334,
:58-359
intestinal impaction 139, 140,280-281
peritonitis 327
salmonellosis 408-409, 499
Flunixin meglumine
in endotoxemia 123, 192, 195
pain relief 119, 120
Fluoroscence studies 65,166-167, 168
Foaling see Parturition
Foals
abdominocentesis 15-16
antibiotic-induced diarrhea 410, 411,
412
an ti-ulcer medication 192
cecal perforation 274
colicky pregnant mare and 351-352
diarrhea see Diarrhea in foals
endoscopy 23, 24, 26
gastric ulceration see Gastric ulceration
in foals
hepatic diseases see Hepatic diseases in
foals
iron overload 393, 522
large and small colon disease and colic
485-490
medical therapy of pain 463-465
analgesics 464-465
decompression 465
nutrition 464
prokinetics 465
pancreatitis, acute 350
parasite infections, ill thrift 56
peritoneal fluid 16-17, 19,323,454
salmonellosis 408, 409, 495-499
small intestinal disease and colic
477-484
532
stomach diseases
abscesses 476
endoparasitism 475-476
ulcer syndromes 470-472
Foals, clinical evaluation 449-468
abdominal distention, diferential
diagnosis 459-462
abdominocentesis 453, 460
clinicopathological data 453-454,
466-467
endoscopy 453
histor 449-450, 459, 466
nasogastric intubation 452, 460
physical examination 450-453, 459,
466
radiography 452, 457-458, 459-460,
467
sedation 24, 452
signalment 450
surgical decision re colic 465-467
ultrasonography 28, 29, 452-453,
454-457,459-460,467
Foreign bodies
impaction 280
oral cavity 65, 66, 78
small colon obstruction 300-301
Formalin 359
Fourth branchial arch defects 66
Free fatty acids 395
Free radicals 194, 195
Frog supports 422
Frusemide 155
Functional residual capacity 145
Fungal enterocolitis 378, 379
Fungal toxins 251, 384, 420
Fungi, predacious 59
Furosemide 192
Galvayne's groove 71
Gamma glutamyl transferase (GGT) 383,
386,387,389,390,391,398
Gasterophilus spp. 60, 475-476
Gastric abscess 476
Gas tric acid secretion 470
Gastric decompression 120, 206, 246,
247
Gastric dilation 246-247
Gastric emptying 480
impaired 244, 471-472
Gastric erosions 244, 470
Gastric impaction 245-246
Gastric lavage 417, 465
Gastric lesions, stress-induced 471
Gastric mucosal biopsies 26
Gastric outlet obstruction/pseudo-
obstruction 471-472, 480
Gastric perforation see Gastric rupture
Gastric reflux, nutritional support and
197
Gastric rupture 247, 318, 472
Gastric squamous cell carcinoma
247-248,337
Gastric ulceration 241-245
clinical signs 242
diagnosis 242-243
epidemiology 242
etiopathogenesis 241-242, 416
NSAD toxicosis 416
prevention 244
treatment 243-244, 245, 417
Gastric ulceration, foals 389, 469-475,
480
clinical signs 472
diagnosis 472-473
etiopathogenesis 469-470
prevention 475
treatment 473-475
ulcer syndromes 470-472
gastric outlet obstruction/pseudo-
obstruction 471-472
perforation 472
silent 470-471
stress-induced gastric lesions 471
sudden onset severe 471
Gastrin 241
Gastroduodenal bypass surgery 475
Gastrointestinal neoplasia 334-338, 437
investigation 335-336
presentation and clinical signs 33.,
374-375
prevalence and etiology 335
treatment and prognosis 338
types and sites 334-335
Gastrointestinal tympany 317-319
Gastroscopy 21, 22, 23, 24-25, 26
foals 453
Gastrosplenic ligament 260
Giant cell hepatopathy 521
Giardiasis 444
Gingivitis 74, 75
Globulins 11-12
Glottic protection, compromised 66
Glucocorticoids 193
Glucose absorption tests 20-21, 336, 350,
372,379
Glucose therapy, in hyperlipemia 399,
400
Glycopyrrolate 150, 236
Grain overload 421-422
Granulosa-theca cell tumor 353
Grass sickness 67, 251, 343-348
clinical pathology and pathology 346
clinical signs 344-346, 347
diagnosis 256-257, 346-347
epidemiology and etiology 343-344
risk factors 251
treatment 347-348
Guaifenesin 148
Habronema spp. 60, 476
Halothane 149, 152
Hamartoma, mixed 518
Head
edema 136, 137
physical examination 3-4
Healing, incisions 181, 196
Heart auscultation 4
Heart disease, chronic 375
Heart failure 375
Heart rate 4, 110, 130,450-451
Helicobacter spp. 470
Hemangiosarcoma 332
Hematology
parameters 11
parasite-associated diseases 57
peritonitis 326-327
weight loss 369-370
Hematoma
at parturition 357, 358, 359
intramural 303
laparoscopic aspiration 46
post-ovulation 352-353
rupture 358
subscapular splenic 44
Hemiperitoneum 321
Hemochromatosis 393-394
Hemodynamic disturbances,and
transport 133-134
Hemoglobin concentration II
Hemoperitoneum 18, 19,201,332-334
Hemorrhage
at parturition 357-359
fecal examination 429, 430
hematology profle 11
hypovolemic shock and 199,200-201,
202
incisional 216-217, 218
intra-abdominal 216-217, 218
liver failure and 382
treatment 217-218
Hemorrhagic diathesis 196
Hemorrhagic shock see Hypovolemic
shock
Hemostasis 223
Heparin therapy 196, 203, 210, 227, 328,
329,400
complications 227
Hepatic abscess 44, 45
Hepatic diseases 381-386, 389-401
acute, with failure 381-384
chronic active hepatitis 391-392
chronic liver failure 392-394
chronic, weight loss and 373
primary hyperammonemia 384-386
pyrrolizidine alkaloid intoxication
389-391
right hepatic lobe atrophy 394
Sfe also specifc conditions
Hepatic diseases in foals 513-525
ascending infection 520
biliary atresia 517-518
hyperammonemia in Morgans 523
leptospirosis 521
neonatal isoerythrolysis 524
neoplasia 518
parasitic 521
perinatal asphyxia 524
portal vein thrombosis 523-524
portosystemic shunts 513-516
septicemia/ endotoxemia 518-520
serous cysts 518
toxic disorders 522-523
Tyzzer's disease 516-517
Hepatic enzyme activity 383, 384, 386,
387,389,390,391,392
neoplasia and 393
Hepatic enzymes
in hyperlipemia 398
Hepatic fbrosis 386, 387, 521
Hepatic neoplasia 388-389, 393
in foals 518
metastatic 393, 518
Hepatic scintigraphy 37-38
Hepatitis
chronic active 391-392
serum see Theiler's disease
Hepatoblastoma 518
Hepatocellular carcinoma 393
Hepatoencephalopathy
bacterial infection and 519
cholangiohepatitis 387, 388
iron toxicity 522
in portosystemic shunts 513, 514, 515,
516
therapy and prognosis 383-384
Hepatoliths 386
Hepatotoxins 384, 389-391, 522-523
Herniation
internal 260-261
post-<eliotomy 34
Herniorrhaphy 218-219
Herpesvirus, equine 508, 520-521
Hetastarch 192
HHH syndrome 385-386, 523
Histolasma spp. 378, 423, 443
Histoplasmosis 443
Hooks, of teeth 71, 76
Hormone sensitive lipase (HSL) 395-396,
400
Hyaluronan 211
Hydrochloric acid secretion 241-242
Hydroxyethyl starch 139, 140
Hyoid apparatus disease 65-66
Hyoscine 122
Hyperalgesia 205
Hyperammonemia 382, 384-386, 387, 388
in Morgans 385-386, 523
portosystemic shunts 513-514
Hyperbilirubinemia 384
Hypercalcemia 235
Hypercapnia 146, 152
Hypercoagulability 223-224
Hyperfibrinogenemia 370
Hyperglobulinemia 370, 372
Hyperimmune products 123, 133, 193,
203
Hyperinsulinemia 350
Hyperkalemia 235, 462, 464
Hyperkalemic periodic paralysis (HPP)
220-221,405
Hyperlipemia 350, 394-401
associated diseases 395
pathogenesis and pathology 395-396,
398
prognosis and prevention 400-401
treatment 398-400
Hyperlipidemia 397, 400
Hypermetabolic syndrome, post
anesthetic 221
Hyperproteinemia 370
Hyperthermia 504, 507
malignant 220
post-anesthetic 221
Hypoalbuminemia 11, 372, 373, 431, 433
Hypobiosis 433
Hypocalcemia 154, 235, 406, 418,
439-440
Hypoglossal nerve injuries 65
Hypoglycemia 350
Hypokalemia 154, 235, 464
Hypomagnesemia 235
Hypoproteinemia 370, 430-431, 433, 439,
440
INDEX
Hypotension 152-153, 221
Hypotensive shock 123
Hypoventilation 152
Hypovolemia
in anesthesia 152-153
management during transport 132-133
Hypovolemic shock 198
arterial rupture at parturition 358-359
clinical fndings 200-201
fluid therapy 123, 334
pathophysiology 199-200
treatment 201-202, 463
Hypoxia
in anesthesia 146, 152
Ileac arteries, external, rupture 357, 358
Ileal biopsy 256-257, 342
Ileal bypass 197-198
Ileal impaction 113-114,257,258-259
Ileocecal intussusception 29-30, 114, 186
Ileocecal ligament 250, 267
Ileocecostomy 255
Ileocolonic aganglionosis 304, 461, 487,
488-489
Ileocolostomy 273, 274
Ileum
anatomy 250
muscular hypertrophy 259
obstructive conditions 254, 255
rectal palpation 8, 113-114
vascular supply 186
Ileus 211-215, 262, 320
anti-inflammatory anti-endotoxin drugs
213
clinical signs 212
defnition and incidence 211
diagnosis 212
in foals 455, 456, 457, 465
medical therapy 123-125
nasogastric decompression 213
nutritional support and 197
pathophysiology 212
prognosis 215
prokinetic agents 213-215, 465
supportive therapy 212-213
treatment 195
III thrift, parasite-associated 56
Immunofluorescence assays 414, 506
Immunoglobulin therapy 123, 192-193
Impaction see specifc sites and
conditions
Inappetance 197, 348
Incision
protection during recovery 183-184
strength layer 182, 183
Incisional closure 181-182
Incisional complications 181-182,
216-219
predisposing factors 216
treatment 217-219
Incisional drainage 182, 217, 218
Incisional hemorrhage 216-217, 218
Incisional hernias 182, 217, 218-219,
322
Incisional infections 33-34, 182, 217, 218
Incisor caps 73-74
Incisor profle 71
Infltrative bowel disease 30, 32-33, 372
malabsorption and 377-378
533
INDEX
Inflammatory bowel disease
chronic (CIBD) 372, 377-378, 379, 437
Inflammator diseases
parasite-associated 54-55, 57
scintigraphy 36-37
ultrasonography 30, 32-33
Inflammatory response
hematology profle 11
peritoneal fluid analysis and 18
in salmonellosis 496
Infundibular disease/necrosis 74
Ingesta
prehension 63
reduction pre-laparoscopy 46
Inguinal hernias 261, 477-478
reduction 452, 477
ruptured 478
Inguinal rings, palpation 8
Inspiratory time:expiratory time (I:E) 152
Insuflation 17, 24-25, 26, 41-42, 44,
46-47,48
Insulin
resistance 396, 400
secretion 349, 350
therapy 235, 350, 464
Insulin-dependent diabetes mellitus
349-350
Intensive care plan 190-191
see also Postoperative treatment and
complications
Interstitium:crypt (I:C) ratio 167
Intestinal abscesses 483
Intestinal absorption, normal 379
Intestinal alkaline phosphatase 12
Intestinal atresia 304, 461
Intestinal clamps 175, 177
Intestinal content, evacuation 173
Intestinal diverticulae 262
Intestinal flora
antibiotic disruption 231
modification 406, 431, 432, 502
Intestinal obstruction
exteriorization, algorithm 162, 163
adhesion formation 105
en do toxemia 103-104
intestinal distention ID3
intestinal ischemia 103
motility disturbances 104-105
reperfusion injury 104, 105
Intestinal protectants and absorbants 431,
442
Intestinal wall thickening 32, 456, 457
Intra-abdominal foraminae 260
Intralumenal pressure, viability and 167,
168
. Intrapalatal cysts 66
Intussusceptions
foals 462, 482
rectal prolapse repair 313-314
repair of rectal tear 309
small intestinal 261-262
ultrasonography 29-30, 456, 457
see also specifc sites
534
Intussusceptum 262
Intussuscipiens 261
Iodochlorohydroxyquin 432
Iron toxicit 393-394, 522
Ischemia 18, 103
Isoflurane 149, 152
Isoniazid 443
Isosthenuria 373
Isoxsuprine 354, 422
Ispaghula husk 438
Ivermectin
in control programs 59
therapeutic regimens 58, 60, 435
Jejunocecostomy 255
Jejunojejunal intussusception 114
Jejunum, anatomy 249-250
Jugular vein flling 110
Jugular vein thrombosis 406
Kaolin and pectin 406, 431
Ketamine, in anesthesia 147-148,149,
154
Ketoprofen 119, 120, 192,207
Kidney biopsy 48
Kidney disease, chronic 373-374
Klein grass 393
Lactase defciency 508
Lactate dehydrogenase 220, 221, 228,
229, 383,392,398
Lactated Ringer's solution 201-202
Lactation 395, 400
Lactic acidosis 275, 399
Lactobacillus spp. 406, 431, 502
Lactose intolerance 508
Lactose tolerance test 21
Lactulose 388
Lameness, chronic 371
Laminitis 229-230
clinical signs 230
defined 229
diagnosis 230
endotoxemia and 195
pathophysiology 229, 421
Potomac horse fever and 413, 414, 415
prevention and treatment 194, 195,
230, 406,422
Lausoprazole 243
Laparoscopy 41-50
biopsy 44, 48
colic, chronic and recurrent 342-343
complications 44, 49
defned 41
effects on peritoneal fluid 17
equipment 41-43
indications for 44-46
in peritonitis 327
surgical procedures 46-49
presurgical preparation 46-47
standing approach 46, 47-48
ventral abdominal approach 48-49
Laparotomy see Celiotomy
Large colon
anatomy 284-285
colic-associated diseases in foals
485-490
decompression 292-293
impaction at anastomosis 215-216
laparoscopic evaluation 44, 45
non-strangulating infarction 293
primary tympany 292-293
resection, nutritional support and
197-198
retroflexion, at laparoscopy 45
strangulating lesion 291
trocarization 292-293
viability 164, 165, 167-168
Large colon displacement 284-288, 360
left dorsal (LDDC) 285-289
treatment 286-287
non-strangulated 285-288
right dorsal (RDDC) 287-288
rectal examination 114-115, 117
Large colon impactions 279-282
clinical signs and diagnosis 280, 283
epidemiology and etiology 279-280,
283
outcome and prevention 282, 284
sand impaction 282-284
treatment 280-282, 283-284
Large intestinal obstruction
radiography 458-459
ultrasonography 30, 31,32, 33
Large intestine
malabsorption syndromes 372-373, 376
Larval cyathostomosis see Cyathostomosis
Lavage
esophageal 92
gastric 417, 465
peritoneal 229
retrograde 300, 301, 302, 303
Lawsonia intracellularis 508, 509
Laxatives 122, 231, 281, 438, 486
Lazaroids 194
Leaky membranes 138, 139, 140
Leiomyoma 338
Leiomyosarcoma 338
Leptospirosis 521
Lethal white syndrome 304, 461, 487,
488-489
Leukocytes
parameters 11
radiolabelled 36-37, 417, 440
Leukocytosis II, 369-370
Leukoencephalomalacia 384
Leukopenia 11
Levamisole 58
Lidocaine (lignocaine) 124,207,208,
215, 236-237
Linea alba incision 156
Lingual paralysis 65
Linoleic acid 442
Linseed oil 420
Lipase activit 349
Lipemia, gross 397
Lipid-derived mediators 103-104, 191,
192
Lipid metabolism 395-396
normalization of 400
see also Hyperlipemia
Lip lesions 65
Lipoma, pedunculated 29, 30, 32,
259-260,303-304,336-337
Lipoprotein lipase (LPL) 395, 396, 400
Lipoproteins, very low density (VLDL)
395, 396, 400
Liquid diets 197
Lithotripsy 388
Liver biopsy 382, 383, 387, 390, 391, 392,
515
procedure 10-11, 48
Liver failure 387
plant toxins 389
potential causes 392-394
undetermined cause 392
Liver flukes 521
Loperamide 406, 431
Louw's theory 461
Lung tumors 375
Lymphangiectasia, intestinal 444
Lymphosarcoma 33, 66-67, 320, 337, 338
weight loss and 372, 374-375, 378, 379
Magnesium 235
Magnesium oxide 243
Magnesium sulfate 122, 140, 235, 236,
237, 419
Malabsorption
carbohydrate absorption tests 20-21
large intestinal 372-373
small intestinal 372
total/partial 379
Malabsorption syndromes 376-380
causes 377-378
alimentary lymphosarcoma 378
chronic inflammator bowel disease
377-378
enteric infections 378
small intestinal resection 377
treatment 379-380
Maldigestion, weight loss and 371-373
Malignant hyperthermia 220
Malocclusions 76-77
Malpractice action 308
Mal seco 251, 343
Management
cleaning procedures 232
clostridial diarrhea 412
factors in weight loss 368-369
gastric ulceration and 242, 244
parasite-associated disease 54, 56,
58-60
practices predisposing to colic 102
right dorsal colitis 441
salmonellosis 409-410, 499
Mandibular brachygnathia 72-73
Mandibular symphysiotomy 82-84, 86-87
Maniacal behavior 382, 383, 387, 388
Mares see Brood mare
Martingale, elastic 94
Masseter myopathy 221
Mastication 63
Matrix metalloproteinases 229
Maxillary brachygnathia 72-73
Mean arterial pressure (M) 359
Meckel's diverticulum 478-479
impacted 260-261
Meconium 460
Meconium impaction 482, 485, 486
diagnosis 457, 458, 487, 489
Meconium passage, normal 485
Meconium retention 460-461, 485-486
Megaesophagus 67, 96
Melanomas 19, 44, 45
Melena 13
Mercur toxicity 78, 420
Mesenteric abscesses 331, 332, 483
Mesenteric arteritis 55, 262, 436-437
Mesenteric defects, congenital 479
Mesenteric lipoma 336-337
Mesenteric lymphadenopathy 378
Mesenteric lymph node biopsy 342, 372,
380
Mesenteric resection 173-174, 175
Mesenteric stalk, palpation 7-8
Mesh placement 219
Mesocolic rupture 303
Mesodiverticular bands 260, 478-479
Mesothelioma 320
Mesperidine 148
Metabolic acidosis 12
in colic 153-154, 154
in distributive shock 202-203
Metoclopramide 123-124, 214, 465
Metronidazole 232, 412, 442
Microangiopathic hemolytic anemia 382
Microcytosis 514
Microfold cells (M-ells) 504
Midazolam 148
Migrating myoelectric complex (MMC)
211-212
Milk replacements 507-508
Mineral oil
in colic 122
in peritoneal fluid analysis 18-19
Minimal alveolar concentration (MAC)
149, 150
Misoprostol 243, 244, 417, 423, 441
Mittelschmerz 352
Modifed Triadan System 70
Monocytosis 11
Morgans 303, 381, 385-386, 523
Morphine 119, 121, 148, 208
Motility
abnormal, medical therapy 123-125
bowel sounds 4
disturbances
acute diarrhea 423
cecal impaction and 269
intestinal obstruction 104-105
modifcation in chronic diarrhea 431
normal physiology 211-212
ultrasonography 32
Motility enhancers see Prokinetic agen t
Motor neuron disease 376
Mouth
disorders of 78-79
physical examination 4, 78
Moxidectin
control programs 59
therapeutic regimens 58, 60, 435
toxicity 58, 435
Mucosal disease, esophageal 93
Mucosal protectant 473, 474
Mucosal ulcers 378
Mucosa-periosteal sliding flap 85
Mucous membranes 3-4, 201
colic and 110
toxic line 11 0
Multiple organ dysfunction syndrome
(MODS) 200, 201, 519
Multiple organ failure (MOF) 519
INDEX
Multisystemic eosinophilic
epitheliotrophic disease 378
Muscle atrophy 376
Muscle fber necrosis 220
Muscle weakness, overall 220
Mustard plant toxicity 423
Mycobacterial infection, intestinal 377,
378, 423, 443
Mycobacterum spp. 423, 443
Mycosis 64
Mycotoxicosis 384
Mycotoxins 251, 384, 420
Myeloencephalitis 376
Myocarditis, immune-mediated 236
Myonecrosis 221
Myopathy, post-anesthetic 219-222
pathogenesis 220
prevention and prognosis 222
therapy 222
Naloxone 334, 359
Narcotic analgesics 121
Nasal edema 137
Nasogastric intubation 4-6
in colic 110-111, 130-131, 253
in endotoxemia 195
foals 452, 460
management during transport 134
procedure 4-6
Nasopharyngeal cicatrization 66
Necrotizing enterocolitis 483
Necrotizing hepatitis 521
Neomycin 423
Neonatal isoerthrolysis 524
Neonates
abdominal distention 460-462
normal parameters 449, 450-451
Neoplasia see Gastrointestinal neoplasia
and specifc tumors
Neospora caninum 443
Neostigmine 123, 214, 281-282, 465, 495
Nephrosplenic entrapment see Large
colon displacement, left dorsal
Nephrosplenic ligament, palpation 7
Neurofbroma 338
Neurological disease 376
Neurological signs, alkaloid intoxication
390
Neurolomuscular disease 376
Neuromuscular blockade 150
Neuropathy, post-anesthetic 219-222
pathogenesis 220
prognosis and prevention 222
therapy 222
Neurotoxins 382
Neutropenia 11
Neutrophilia 369-370
Neutrophils
in peritoneal fluid 16, 17, 18, 19
in reperfusion injury 104, 105
Nitric oxide 105, 195, 200, 471
Nitroglycerine cream 195, 409, 422
Nitrous oxide 150
Nociceptors 204-205, 208
Non-esterifed fatty acid (NEFA) 395-396,
397,399, 400
Non-strangulating infarction
large colon 55, 58, 293
small colon 304
small intestine 55, 58, 262
535
INDEX
Norepinephrine 153
NSAJDs (non-steroidal anti-inflammatory
drugs)
adhesions and 210
cecal perforation and 274
colic 120
endotoxemia 192
hepatic toxicity 522
postoperative pain 206-207
toxicity 415-417
acute overdose 417
mechanisms 415-416
right dorsal colitis 438-442
treatment 417
Nuclear scintigraphy see Scintigraphy
Nutrition
assessment of 368-369
needs 369
Nutritional support
alier surgery 196198
long-term care 197-198
in chronic diarrhea 432
foals with abdominal pain 464
in grass sickness 347-348
right dorsal colitis 441
Nutrition-induced diarrhea 507-508
Oat stones 302-303
Obstruction see Intestinal obstruction,
specifc sites
Obstructive shock 198
Odontomas 73, 79
Oleander, toxicity 420
Oligodontia 73
Omental hernia 16, 453
Omeprazole 192, 243, 244, 245
Oocyst" cryptosporidial 505-506, 507
Opioids 148, 208
Oral cavity
disorders of mouth 78-79
see also Cleft palate, Dental disease, Soft
palate
Oral examination 64, 81-82
Oral glucose absorption tests 20-21, 336,
350, 372, 379
Oral lactose tolerance test 21
Oral tumors 79
Organophosphates 59, 60, 420-421
Oropharyngeal lesions/tumors 66
Orotracheal tube 154-155
Ossifying periostitis, chron
i
c 74,
75-76
Ovarian tumors 353
Overbite 72, 73
Ovetjet deformity 72, 76
Overo lethal white syndrome 304, 461,
487, 488-489
Oxfendazole 58
Oxyclozanide 521
Oxygen saturation, viabilit and 166, 167,
168
Oxygen therapy 154, 155, 203, 359
Oxytetracycline 415
Oxytocin 361
Oxuris equi 60
Pacemaker activity 249, 250, 268
Packed cell volume (PCV) 11
in colic 112
536
Pain
acute abdominal, prognosis 141-142
classifcation of severit 107-108,
205-206
colic
chronic and recurrent 339, 340-341
decision for surgery 130
decision to refer 127
management during transport 133
mechanisms of 107, 204-205
meconium retention 486
medical therapy in foals 463-465
analgesics 464-465
decompression 465
nutrition 464
prokinetics 465
ovulation-related 340, 352
parietal 107, 205
parturition 357
persistent low-grade 371
diagnosis 206
neuroanatomy and pathophysiology
204-205
treatment 206-209
referred 107, 205
visceral 107, 119-122, 124, 205
weight loss and 371
Palate
anatomy, embryology and physiology
79-80
see also Cleft palate, Soft palate
Palpation
abdominal quadrants and pelvic cavity
159-161
foals 451-452
rectal. normal horse 7-8
rectal tears and 305, 307
transrectal, and videolaparoscopy
45-46
Palpebral reflex 150
Pancreas, anatomy and function 348-349
Pancreatic diseases 348-350
chronic 349-350
Pancreatic fluid 349
Pancreatitis
acute 350
chronic eosinophilic 349
Panicum coloratum 393
Paracentesis see Abdominocentesis
Paradoxical acidosis 154
Paralytic ileus 258
Paranoplocehala mammillana 54
Parascaris equorum see Ascarids
Parasite infections 53-60
clinical features of disease entities
55-56, 60, 273, 276, 475-476
control programs 58-60
features 53-54
abundance of larvae/ eggs in
environment 53
occurrence of disease 53-54
parasite biology 54
parasite burden 54
investigations 56-57
minor 60
pathogenesis 54-55
treatment
anthelmintic aspects 57-58
symptomatic aspects 57
see also specifc parasites and diseases
Parasympatholytic drugs 150, 307, 308
Parenteral nutrition 197
foals 464
Parietal hernia 261
Parrot mouth 72
Partial pressure of carbon diolide
(paCO,) 152
Partial pressure of oxygen (PaO,) 152
Partial thromboplastin time (PT) 382,
383, 387
Parturition
colic and 357-361
effects on peritoneal fuid 18
gastrointestinal complications 360
PCR 230, 231, 408, 411, 413, 414, 509
Pelvic cavity, palpation 159-161
Pelvic flexure
colotomy 167
enterotomy 287, 294-295
exteriorization 162, 163, 164
rectal examination 8, 115, 116, 117
Penrose drains 175, 177
Pentazocine 119, 121, 148
Pentoxirlline
endotoxemia 133, 134, 194, 195, 203,
415
hypovolemia 359
Pepsin 241, 242
Pergolide 322
Periapical abscess 75
Periapical osteitis 74, 75-76
Perineal injuries 360
Periodontal disease 35, 36, 74-75
Peripheral nerve injuries 220
Periradicular disease 74, 75-76
Perirectal abscesses 308, 314
Peritoneal effusion, ultrasonography
457
Peritoneal fluid
analysis 16-20
abdominal surgery, efcts 17
ascites 320
bowel rupture 18, 19
chyloabdomen 479
in colic 111, 131
contaminated samples 15, 17
disease effects 18-20
enterocentesis efects 17
fat in 18-19
hypovolemic shock 201
laparoscopy efects 44
in malabsorption 372
neoplasia 336
parturition effects 18
postoperative peritonitis 228-229
in weight loss 370, 372
normal characteristics 16-17, 322-323,
349
foals 16-17, 19, 323, 454
see also Abdominocentesis
Peritoneum
anatomy and physiology 322-323
ultrasonography, foals 457
Peritonitis 321. 322-330
acute 325. 326
bile 3RR
chemical 462
chronic 325. 326-327
classifcation and etiology 323. 324
copulation-induced 353
in foals 462
gastric rupture 472
investigation and diagnosis 325-327
medical treatment 327-330
peracute 325. 326
peritoneal fluid analysis 18. 1 9
causes 227-228
treatment 229
prognosis 330
signalment and history 324
surgical treatment 329-330
ultrasonography 32. 457
Pethidine 1 19. 121
Pharyngeal cysts 66
Pharyngeal hemiplegia 64
Pharyngeal neoplasia 66
Pharyngeal paralysis 64. 66
Pharyngeal phase of deglutition 63. 66
Pharyngeal stripping wave 63
Pharngeal swallow reflexes 63
Phenothiazines 59. 121
Phenoxybenzamine 406. 431
Phenylbutazone 1 19. 120. 192. 195. 207.
230
toxicit 120. 207. 274. 417
see also Equine right dorsal colitis
Phenylephrine 153. 154-155. 286. 287
Photodocumentation 42
Photosensitivity 389. 390
pH. stomach contents 1 1 1
Physical examination 1-8
auscultation 4
general observations 3
head 3-4
history 3
thorax and abdomen 4
see also Nasogastric intubation. Rectal
examination; specifc conditions
Phytoconglobates 302-303
Pink-rosewater diarrhea 495
Pinworm 60
Piperazines 59
Placenta. retained 361. 414
Placentitis 507
Plank in the flank technique 356
Plant toxins 389. 393. 419-420
Plasma fbrinogen concentration 1 1
Plasmalyte 20 I
Plasma therapy 123. 140. 192. 1 93. 203.
327. 430
Platelet plug formation 223
Pneumatosis intestinalis 483
Pneumoperitoneum 41. 44. 47. 48. 320
Poikilocytosis 514
Polymyxin B 133. 193. 203. 406
Polyneuritis equi 376
Polyodontia 73
Polysaccharide storage myopathy 221-222
Polyvinylpyrrolidone 211
Portal vein thrombosis 384. 523-524
Portography. positive-ontrol 515
Portosystemic shunts 513-516
Positive end-expirator pressure (PEEP)
152
Post-anesthetic airway obstruction 154
Postoperative treatment and
complications
abdominal adhesions 209-21 1
cardiac arrhythmias 232-237
colitis 230-232
foals 483
ileus 21 1-215
incisional complications 216-219
myopathy/neuropathy 219-222
nutritional support 196-198
immediate 196-197
long-term care 1 97-198
peritonitis 227-229
postoperative monitoring 189-191
protocols 190-191
postoperative pain 204-209
postoperative shock and organ failure
198-204
thrombophlebitis 222-227
treatment of endotoxemia 191-196
Potassium supplements 1 40. 154. 235.
405. 464
Potomac horse fever 412-415
clinical signs and diagnosis 412-413.
414
treatment and prevention 415
Prednisolone 57. 193. 334
Prednisone 338. 392
Pregnancy
abdominal distention in 317. 321-322
abdominal pain (non-colic) 356-357
colic in 351-352. 353-357
endotoxemia in 351-352
hyperlipemia 396. 397. 400
see also Brood mare. Parturition
Prehension 371
Premolar caps 74
Prepubic tendon rupture 321-322. 357
Preputial edema 378
Pressure bandages 217-218. 359
Pressure. intralumenal. and obstruction
103
Probiotics 406. 431. 502
Procainamide 236. 237
Progesterone 351-353
Prokinetic agents 213-215. 281-282. 348.
465. 473. 474
Proliferative enteropathy 508-509
Propanol 236. 237
Propantheline bromide 307
Propofol 149
Propulsion. normal physiology 21 1-212
Propylene glycol 421
Protamine zinc insulin 350
Protein-losing enteropathies
cyathostomosis 433
Protein metabolism. abnormal hepatic
382
Prothrombin time (PT) 382. 383. 387
Proton pump 241
inhibitors 243. 244. 473, 474
INDEX
Pseudocysts 75
Psyllium. dr 438
Psyllium mucilloid 122, 283, 284. 438. 441
Ptosis. bilateral 345
Ptyalism 78. 471 . 472
Pulmonar disease. chronic 376
Pulmonary edema 155. 201
Pulmonar function
anesthesia and 146. 151-152. 154-155
in colic 145-146
Rodococcu equi infection 503
Pulmonary hypertension 155
Pulmonary neoplasia 375
Pulpitis 74. 75
Pulse 3, 7. 8
Pulse oximetry 151-152, 168
Pulse rate 3
Pulsion (false) diverticulum 95, 262
Purse-string effect 170, 178
Pyrantel salts 54. 58. 59
Pyrrolizidine alkaloid intoxication
389-391
Quarter horses 1 40. 220-221 . 295. 303
Quassia amara 423
Qucu spp. (oak) 419. 423
Quidding 64. 371
Quinidine salts 234. 236. 237
Radiography
contrast studies 65. 90. 452. 457-458,
459-460. 467
dysphagia 65
enterolithiasis 294
esophagus 90
foals 452. 457-458. 459-460, 467
gastric impaction 245-246
Radiopharmaceuticals 34. 35
Ramifenazone 120
Ranitidine 243. 244, 245. 465
Reactive oxygen metabolites (ROM) 104.
105
Reactive oxygen species (ROS) 194
Rectal biopsy 9-10. 342. 372
Rectal examination 6-8
abdominocentesis and 1 3
applications 6
colic 1 1 1 . 1 12-1 19. 130. 253
chronic and recurrent 341
foals 451
in peritonitis 327
recognition of abnormalities
cecum 1 14-1 1 5
descending colon and rectum
1 17-1 18
large colon 1 15-1 17
small intestine 1 13-1 14
rectal tears and 305. 307
technique 6-8. 1 12-1 1 3
complications 7
lubrication 6
palpation of normal horse 7-8
videolaparoscopy and 45-46
Rectal liner 309-310
Rectal prolapse 312-313
Rectal prosthesis 309-310
Rectal tears 305-31 2
causes 305
classifcation 306-307
537
INDEX
Rectal tears - continued
prevention 307
prognosis 312
treatment
colostomy 310-312
defnitive 308
immediate 307-308
primary repair 308-309
rectal liner, temporar 309-310
Rectal temperature 109-110
in colic 129-130
Rectum, anatomy 305-306
Rectus abdominus muscle, celiotomy
incisions 156, 157
Red cell count (RBC) I I
Red clover grass 420
Red worms see Cyathostomes, Strongyles,
large
Rehydration see Fluid therapy
Renal failure, weight loss and 373-374
Renal function, in hypovolemic shock
199-200
Renosplenic entrapment see Large colon
displacement, left dorsal
Renosplenic space, palpation 7
Reperfusion injury 104, 105, 201
Resection
length, and viability 167, 172-173, 377
nutritional support and 197-198
small intestine 255-256, 377
see also Sutures
Respiration, evaluation 4, 451
Respiratory rate J lO, 129-130, 152
foals 450-451
Restraint
anesthesia and 147
endoscopy 24
foals 450, 452
nasogastric intubation 4-5
Reticuloendothelial system of liver,
scintigraphy 37-38
Retropharyngeal abscess/ neoplasia 66
Rhabdomyolysis, recurrent exertional 221
Rhinitis 346
Rhizoctonia leguminicola 420, 422-423
Rhodococcus equi 330, 332, 502-504
epidemiology and pathogenesis 502-503
treatment and prevention 504
Richter's hernia 261
Richter-type hernia 260
Ricinus communis 420
Rickettsiae see Potomac horse fever
Rolling 108, 109
therapeutic 286, 356
Romifdine 119, 121
Rotavirus diarrhea 493, 494, 495
R on T phenomenon 236, 237
Saline therapy 192, 201-202
in abdominal pain 138-140
acute diarrhea 405, 406
in colic 122, 123
Salmonella spp. 495-496
postoperative colitis 230-231
in right dorsal colitis 439
serogroups 407
virulence factors 407, 496
538
Salmonella typhimurium DTl04 410
Salmonellosis 406-410
chronic 443
clinical signs and diagnosis 407-408,
496498
control and prevention 409-410, 499
etiopathology 406-407, 495-496
fecal culture 13, 498, 499
in foals 408, 409, 495-499
prognosis 409
risk factors and epidemiolog 407
treatment 408-409, 498-499
Salt intoxication 421
Sand enteropathy 437-438
Sand impaction 282-284
clinical signs and diagnosis 15, 283
treatment 283-284
Scalding, perineal 493
Scin tigraphy 34-38
dental 34-36
hepatic 37-38
inflammation and infection 3637
labeled white blood cells 36 37, 417, 440
techniques and agents 34, 35
Scours, 36hour 495
Scrotal hernias 477
Seasonal malaise syndrome 373, 436
Sedation
endoscopy 24
foals 24, 452
hepatoencephalopathy 383
in pain relief 120-121
rectal examination I l l, 112
rectal examination and 6
standing laparoscopy 47
Segmental eosinophilic colitis 296 297
Selenium 221, 222, 393
toxicity 420
Senecio spp. 389, 390
Septicemia 496, 497, 507, 518-520
Septic shock see Distributive shock
Seroconversion 414
Serology, tapeworm infection 53, 57
Serosal diverticulum 306
Serosal irritation 159
Serous cysts 518
Serum alkaline phosphatase (SA) 12
Serum hepatitis see Theiler's disease
Serum protein electrophoresis 57, 372,
429
Severe combined immunodefciency
(SCID) 505, 506
Sevoflurane 149, 152
Shear mouth 77
Shock, postoperative 198-204
classifcation 198-199
clinical fndings 200-201
defned 198
perioperative monitoring 203-204
treatment 201-203
Short bowel syndrome 172
Shunt ligation 515, 516
Sialadenitis 78
Silent ulcers 470-471
Silver sulfadiazine 135, 406
Sin usi tis 74
Skin lesions 378
Siaframine 420, 422-423
Slurry feeds 197
Small colon
enteroliths 299-300
fecal impaction 301-302
fecaliths, phytoconglobates and bezoars
302-303
foreign body obstruction 300-301
intramural hematoma 303
mesocolic rupture 303
non-strangulating infarction 304
obstruction, ultrasonography 30, 32
strangulating lesions 303-304
trauma at parturition 360
viability assessment 168
Small intestinal diverticulum 262
Small intestinal entrapment,
ultrasonography 29-30
Small intestinal impaction, in foals
481-482
Small intestinal intussusception; in foals
482
Small intestinal lesions, ultrasonography
29-30
Small intestinal obstruction
causes 258-262
foals, radiography 458
medical treatment 257-258
prognosis 263-264
simple 251-252
strangulating 252-253, 261
surgical correction 254-257
ultrasonography 29-30, 32
Small intestine
causes of disease 258-262
colic
foals 477-484
medical, prognosis 263-264
outcome and prognosis 262-263,
483-484
postoperative management and
complications 483
surgical, prognosis 262-263
see also specifc diseases
edematous 456, 457
impaction at anastomosis 215
malabsorption syndromes 372, 376380
maldigestion 372
resection
anastomosis 255-257
malabsorption and 377
nutritional support and 197-198
viability 164-167, 172-173, 255
ultrasonography, foals 4!5-457
Sodium chloride, as laxative 122
Sodium thiosulfate 420
Soft palate
dorsal displacement (DDSP) 65, 66
repair 85-86
see also Cleft palate
Sorbitol dehydrogenase 383, 384, 387,
390,398
Sow mouth 72
Spasmolytics 121-122
Spirurid nematodes 476
Spleen, palpation 7
Splenic biopsy 48
Splenic puncture 14-15, 17, 18, 19
esophageal 67, 96, 247-248
gastric 247-248
oral cavity 79
Stallions 148, 305, 353 see also
Castration
Standardbreds 261, 273, 377
Standing flank celiotomy 46,47-48,355
Staphylococcus spp. 137
Staples/stapling 172, 176, 178-179, 180,
181, 183
Starch tolerance test 21
Stt'nt bandage 183-184
Step mouth 76
Stomach
anatomy and physiology 241-242,
469-470
contracture 472
diseases see specifc conditions
endoscopy 24-25, 26
radiography 458
ultrasonography 455
Stomach worms 476
Stomatitis 78
Strangulating lesions
large colon 291
peritoneal fluid analysis 18, 19,20
small colon 303-304
small intestine 252-253, 260, 261
Stretococcus bovis 229
Stretococcus equi 331
Stretococcus zooeidemicus 314
Slress
gastric lesions in foals 471
right dorsal colitis and 440, 441
Strongyles, large
clinical features of infection 55, 56
control programs 58, 59
hepatic disease 521
investigations 5657
mixed infections see Strongylosis
pathogenesis 54-55
treatment 57
Strongyles, small see Cyathostomes
Strongloides wester 60, 508
Strongylosis 436437
clinical signs 56, 436
diagnosis 437
diarrhea and 508
Stronglus edendatus 54, 349, 521
Stronglus equinus 54, 349, 521
Stronglus vulgars 54, 55, 57, 262, 273,
436-437
Sub-epiglottic cysts 66
Succinyl choline 150
Sucralfate 192, 243, 244, 245, 419, 441
Sugar beet feeds 67, 197
Sulfasalazine 442
Summer sores 60
Supraventricular arrhythmias 236, 237
Surface oximetry 166, 167
Surgery
colonic impactions 282
left dorsal displacement of large colon
286 287
pregnant mare and 351, 355, 356
Surgery, for colic 145-188, 254-255,
263-264
anesthesia see Anesthesia, general
approaches to abdomen 155-158,254
flank celiotomy through 17th or
18th rib 157-158, 287
other approaches 158
paralumbar flank celiotomy 157-158
preoperative preparation 155
ventral midline celiotomy 155-156,
356
ventral paramedian celiotomy
156157
incisional protection 183-184
sutures 182-183
duration 263
evaluation of gut viability 164-168, 255
large intestine 164, 165, 167-168
small intestine 164-167
exploration of abdomen 158-164, 254
detailed 159-161
exteriorization of viscera 161-164
initial 158-159
postoperative care see Postoperative
treatment and
complications
prognosis 263-264
repeat laparotomy 184-187
abdominal closure 187
decision 184-185
delayed 186 187
procedure and revisions 185-187
survival rates 263
techniques 168-181
anastomosis see Anastomosis
enterotomies 172
intestinal preparation 172
staples 172
sutures see Sutures
Sutures
auto suturing device 42, 43
bite size 183
materials 168
strength 182-183
patterns 168-172, 172, 183
sinuses 182, 183, 218
Swallowing 63-64
diffculties see Dysphagia
Sweating, effects of 138
Sympathomimetics 153
Systemic inflammator response
syndrome (SIR) 191-192,200,519
Table, laparoscopy 43, 48-49
Tachydysrhythmias 153
Tapeworms
colic 56, 57, 58
control programs 59
in ileal impaction 259
in intussusceptions 273
pathogenesis 54, 55
INDEX
serodiagnosis 53, 57
treatment 57, 58
Technetium isotopes 34-37
Teeth
age determination 70-71
deviated 77
eruption time 70
exaggerated transverse ridges 77
retained deciduous 73
table angles 77
tall 76
see also Dental entries
Teflon catheters 135, 136
Telazol, 149
Temperature
colic 129-130
indications 4
normal values 109-110
Temporomandibular joint disorders 65
Tension bands, dental 72-73
Tetanus antitoxin 381
Tetrazolium analysis 166167
Theiler's disease 381-384
therapy 383-384
Thermodilution technique 151
Thiopental 148-149
Thoracic neoplasia 374, 375, 376
Thoracotomy 158
Thorax, physical examination 4
Thoroughbreds 221
Thrombophlebitis 137, 222-227
defned 222
pathogenesis 223-224, 226
prevention 226227
septic 222, 224, 225, 227
treatment 227
Thrombosis, catheter-related 135, 136,
137
Thrombus formation 223
Thromoboembolic arteritis 262, 436437
Tiletamine-zolazepam 149
Tirilazad mesylate 194
TNF. 193-194
Tolazoline 147
Tongue lesions 65, 66, 78, 87
Tonicity, determination 140
Tooth root abscess 35
Total nucleated cell count, peritoneal
fluid 16, 17, 18, 19
Total plasma protein (TPP) 11
Total protein
in colic 112
peritoneal fluid 16, 17, 18, 19
Toxic coli tides, and acute diarrhea
417-421
cantharidin toxicosis 417-419
see also Colitis, right dorsal, NSAlDs,
toxicity
Tracheoscopy 65
Traction (true) diverticulum 93, 95
Training, videolaparoscopy 45-46
Tranquillizers 359
Transfaunation 431
Transhyoid pharyngotomy 82, 84-85, 86,
87
Transport, preparation for 132-134
Trendelenberg position 43, 46, 49
Trestle table appearance 108, 109
539
INDEX
Trchomonas equi 444
Trchostronglus axei 476
Trichothecenes 420
Triclabendazole 521
Triglycerides 395, 396, 397-398, 399, 400,
479
Triodontohorus spp. 54
Tromethamine 154
Tuberculosis, intestinal 377, 378, 423, 443
Tympanitic colic see Colic, distention
Tympany, bowel sounds 4
Typhlectomy 158
Typhlotomy 270-271
Tyzzer's disease 51 6-51 7
Ultrasonography 26-34
abdominocentesis and 15, 16
biliary tract disease 387, 388
cecal intussusceptions 274
clinical indications for 29
colic 29, 131
chronic and recurrent 342
postoperative 33-34
foals 453-454, 454-457, 458, 459-460,
467
colon 457
peritoneum 457
small intestine 457
stomach 455
gastroduodenal ulceration, in foals
472-473
gut viability and 166-167
hemoperitoneum 333
hypovolemic shock 201
inflammatory and infltrative diseases
30, 32-33
large intestinal lesions 30
in liver failure 392
normal anatomy in 26-28
in peritonitis 327
postoperative peritonitis 229
sand impaction 283
small intestinal lesions 29-30, 456, 457
technique and equipment 26
thrombophlebitis 224-225
transducers 26, 455
weight loss and 29
Umbilical hernias 261 , 452, 478, 479
strangulation 478
Umbilical infection 520
Urea levels 370, 373
Urea nitrogen, peritoneal fluid 16-17
Urine, red discoloration 382
Urogenital examination 327
Uroliths 45
Uroperitoneum 1 7, 321, 461-462
in foals 450, 454
540
Uterine artery rupture 357-359
Uterine contractions, normal 357
Uterine horn, inversion 360-361
Uterine prolapse 360-361
Uterine rupture 357, 360
Uterine torsion 354-356
Utero-ovarian artery rupture 357, 358
Uterus, dorsoretroflexion 354
Vaccines
Ehrlichia risticii 414, 415
mutant core polysaccharide 123
R. equi 504
rotavirus 495
Salmonella spp. 499
Vaginal injuries 353
Vascular hyporeactivity 200
Vasculits, immune-mediated 391
Vasodilators, and laminitis 230
Venous admixture 145, 152, 155
Ventral body wall hernias 321-322
Ventral edema 317, 320, 321
Ventricular arrhythmias 232-234, 236,
237
Ventricular premature depolarizations
233
Ventricular tachycardia 232, 233-234,
236, 237
Vesicular stomatitis 78
Viability of gut 164-168, 172-173, 185,
255, 377
Video-ndoscopy 21-22, 23
Video-fluoroscopy 65
Videolaparoscopy 42, 45-46, 48-49
Vincristine 338
Vinegar 296, 300, 384
Viral diarrhea 493-495
Viral diseases, hepatic 391 , 520-521
Virulence-associated protein A (VapA)
502
Vitamin A 197-198
Vitamin B 196, 197-198
Vitamin E 197-198, 221 , 222, 393
Vitelline duct and arteries 478-479
Volatile fatty acid (VFA) production
267-268
Volvulus
gut viability and 165, 167
large colon 288-290
at parturition 360
non-strangulated 289-290
prevention 291-292
rectal examination 1 16-1 1 7
strangulation 291
treatment 290, 291
small colon 303
small intestinal 29, 260, 261
foals 455, 456, 462, 480-481
Volvulus nodosus 261
Walking 120, 206, 329, 357
Water intake 102, 109, 279, 369
Wave mouth 76
Weakness
generalized 220-221
localized 220
overall muscle 220
Weather 102-103, 279
Weight loss 367-380
assessment of body condition 367-368
causes 368, 370-376
chronic inflammatory bowel diseases
372, 379
digestion and absorption problems
371-372, 376
heart disease, chronic 375
infection, low-grade chronic 374
kidney disease, chronic 373
liver disease, chronic 373
neoplasia 374-375
neurological! neuromuscular disease
376
persistent low-grade pain 371
prehension/swallowing difculties 371
protein-losing enteropathies 373
pulmonary disease, chronic 376
clinical pathology 369-370
cyathostome-associated 55-56, 436
defnition 367
differential diagnosis and evaluation
367-376
environmental factors 368-369
gastrointestinal neoplasia 335
nutrition, assessment of 368-369
in right dorsal colitis 439
ultrasonography, indications for 29
White cell count (WBC) 1 1 , 1 12
Wooden tongue 78
Wound healing 1 81 , 196
Wry nose 80
Xanthine metabolism 104, 105
Xylazine
abdominal pain relief 1 19, 120-121
in anesthesia 147-148, 154
in endoscopy 24
sedation 47, 452
side effects 121
Xylose absorption test 21, 372
Yohimbine 1 24, 147, 214
Zolazepam 1 49
Zoonotic considerations 410, 507
Z-plasty, double opposing 85

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