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BRITISH LIBRARY CATALOGUING IN PUBLICATION DATA A catalogue record for this book is available from the British Library LIBRARY OF CONGRESS CATALOGING IN PUBLICATION DATA A catalog record for this book is available from the Library of Congress NOTE Medical knowledge is constantly changing. As new information becomes available, changes in treatment, proce dures, equipment and the use of drugs become necessary. The editors/authors/contributors and the publishers have taken care to ensure that the information given in this text is accurate and up to date. However, readers are strongly advised to confirm that the information, especially with regard to drug usage, complies with the latest legis lation and standards of practice. Existing UK nomenclature is changing to the system of Recommended International Nonproprietary Names (rINNs). Until the UK names are no longer in use, these more familiar names are used in this book in preference to rINNs, details of which may be obtained from the British National Formulary.
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I
Contributors Jennifer E Adolf
Christina 5 Cable
Internist Private Practitioner
Private Practitioner
Ledgewood Equine Medical Center
Early Winter Equine Medicine and Surgery
Ontario, New York, USA
Lansing, New York, USA
Dorothy Ainsworth
Gary Carlson
Associate Professor of Medicine
Professor of Equine Medicine
Department of Clinical Sciences
Department of Medicine
College of Veterinary Medicine
School of Veterinary Medicine
Cornell University
University of California, Davis
Ithaca, New York, USA
Davis, California, USA
Fairfield T Bain
Noah D Cohen
Internal Medicine Practitioner
Associate Professor of Medicine
Haygard-Davidson-McGee Associates
LA Medicine and Surgery, CVM
Lexington, Kentucky, USA
Texas A and M University College Station, Texas, USA
Michael A Ball Private Practitioner
Thomas J Divers
Early Winter Equine Medicine and Surgery
Professor of Medicine
Lansing, New York, USA
Department of Clinical Sciences College of Veterinary Medicine
Jacqueline Bartol Private Practitioner
Cornell University Ithaca, New York, USA
Rochester Equine Veterinary Clinic Rochester, New Hampshire, USA
Richard Drolet Professor of Pathology
William V Bernard
Universite de Montreal
Private Practitioner
Departement de Pathologie et Microbiologie
Rood & Riddle Equine Hospital
Saint Hyacinthe, Quebec, Canada
Lexington, Kentucky, USA Normand G Ducharme Mark Bowen
Professor of Surgery
HBLB Resident in Equine Thoracic Medicine
Department of Clinical Sciences
Sefton Equine Referral Hospital
College of Veterinary Medicine
Royal Veterinary College
Cornell University
University of London
Ithaca, New York, USA
Hatfield, Herts, UK G Barrie Edwards T Douglas Byars
Professor of Equine Studies
Director of Internal Medicine
University of Liverpool
Haygard-Davidson-McGee Associates
Leahurst
Lexington, Kentucky, USA
Neston, South Wirral, UK
xi
CONTRIBUTORS
Ryland B Edwards III
Laurie R Goodrich
Clinical Assistant Professor of Large Animal Surgery
PhD candidate for cellular and molecular biology
University of Wisconsin
Department of Clinical Sciences
Madison, Wisconsin, USA
Cornell University Ithaca, New York, USA
Andrew T Fischer Jr Private Practitioner Chino Valley Equine Hospital Chino, California, USA Lisa A Fortier Assistant Professor of Surgery and Molecular Medicine Department of Clinical Sciences College of Veterinary Medicine Cornell University Ithaca, New York, USA David E Freeman
Richard Hackett Professor of Large Animal Surgery Department of Clinical Sciences Cornell University Ithaca, New York, USA Reid Hanson Jr Associate Professor of Surgery Department of Large Anrmal Surgery and Medicine Auburn University Auburn, Alabama, USA
Associate Professor of Equine Surgery Head of Equine Surgery and Medicine
Philip D Van Harreveld
University of Illinois
Associate
College of Veterinary Medicine
Vermont Large Animal Clinic
Urbana, Illinois, USA
Milton Vermont, USA
Sarah L Freeman Lecturer in Equine Surgery Department of Farm Animal and Equine Medicine and Surgery Studies Royal Veterinary College University of London Hatfield, Herts, UK
Mark H Hillyer Lecturer in Equine Soft Tissue Surgery Department of Veterinary Medicine University of Bristol Langford House, Bristol, UK
John Freestone
J Geoff Lane
Resident Veterinarian
Senior Lecturer in Veterinary Surgery
Coolmore Australia
School of Veterinary Science
Jerry's Plains
University of Bristol
New South Wales, Australia
Langford House, Bristol, UK
Susan L Fubini
Jean-Pierre Lavoie
Professor of Surgery
Professor of Equine Medicine
College of Veterinary Medicine
Departement de Science Cliniques
Cornell University
Universite de Montreal
Ithaca, New York, USA
Saint Hyacinth, Quebec, Canada
Earl Gaughan Professor of Large Animal Surgery Department of Clinical Sciences Kansas State University Veterinary Medical Teaching Hospital Manhattan, Kansas, USA
Sandy Love Head of Division of Equine Clinical Studies Department of Veterinary Medicine University of Glasgow Bearsden, Glasgow, UK
Robin D Gleed
J Lyons
Associate Professor of Anesthesiology
Veterinary Student
Department of Clinical Sciences
Faculty of Veterinary Medicine
Cornell University
University College Dublin
Ithaca, New York, USA
Dublin, Republic of Ireland
xii
CONTRIBUTORS
Tim S Mair
Claude A Ragle
Private Practitioner
Associate Professor of Equine Surgery
Bell Equine Veterinary Clinic
College of Veterinary Medicine,
Mereworth, Maidstone
Washington State University
Kent, UK
Pullman, Washington, USA
Celia Marr
Peter Rakestraw
Head of Equine Division
Assistant Professor of Large Animal Surgery
Department of Farm Animal and Equine Medicine and
Texas A and M University
Surgery Royal Veterinary College
Large Animal Medicine and Surgery College Station, Texas, USA
University of London Hatfield, Herts, UK
Sarah Ralston Associate Professor of Animal Sciences
PO Eric Mueller
Department of Animal Science
Associate Professor of Surgery
Rutgers University
Department of Large Animal Medicine
New Brunswick, New Jersey, USA
College of Veterinary Medicine University of Georgia
Johanna M Reimer
Georgia, USA
Private Practitioner
Michael J Murray
Lexington, Kentucky, USA
Rood and Riddle Equine Hospital Professor in Equine Medicine Marion Dupont Scott Equine Medical Centre
BA Rucker
Leesburg, Virginia, USA
Private Practitioner
James A Orsini Associate Professor of Surgery 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 Department of Clinical Sciences Cornell University Ithaca, New York, USA
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 Department of Clinical Sciences Auburn University Auburn, Alabama, USA Chris M Schweizer Lecturer in Therogeniology Cornell University Ithaca, New York, USA
Scott Pirie Lecturer in Veterinary Medicine
Stacey A Semevolos
Easterbush Veterinary Centre
Lecturer in Large Animal Surgery
University of Edinburgh
LA Medicine and Surgery, CVM
Rosylin, Midlothian, UK
Texas A and M University College Station, Texas, USA
Chris J Proudman Lecturer in Equine Surgery
Kim Sprayberry
University of Liverpool
Practitioner of Internal Medicine
Leahurst, Neston
Haygard-Davidson-McGee Associates
South Wirral, UK
Lexington, Kentucky, USA
xiii
CONTRIBUTORS
Frank GR Taylor
R Weller
Senior Lecturer in Equine Medicine
Student in Equine Surgery
Division of Companion Animals
Department of Farm Animal and Equine Medicine
University of Bristol Langford, Bristol, UK
and Surgery Studies Royal Veterinary College University of London
Beth Valentine
Hatfield, Herts, UK
Assistant Professor Department of Biomedical Sciences
Jamie Whiting
College of Veterinary Sciences
Internist
Oregon State University
Dubai Equine Hospital
Corvallis, Oregon, USA
Dubai, UAE
Catherine Walsh
Alison A Worster
Resident in Anaesthesiology
Resident in Animal Surgery
Department of Clinical Veterinary Medicine
Department of Clinical Sciences
University of Cambridge
Cornell University
Cambridge, UK
Ithaca, New York, USA
-
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 2.4 Yellow-green discoloration of peritoneal fluid caused by leakage of bile into the abdomen
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 2.5 Normal endoscopic view of the stomach of a 2week-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 2.3 Peritoneal fluid from a horse with hemoperi toneum showing free red blood cells and erythrocyto phagia by a macrophage
Plate 4.1 Transillumination of large colon wall showing mucosal stages of cyathostome larvae
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 4.2
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)
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 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 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 12.2 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 12.5 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 12.4 Ulceration and inflammation with fibrosis of the pylorus of the horse in Plate 12.1. There is pyloric . 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 13.1 Adhesions of jejunum causing kinking of intestine and partial obstruction
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 13.2
Mid-jejunal intussusception. Surgeon's finger Plate 13.5 present at the point of invagination of intussusceptum into intussuscipiens
Plate 13.3 Short loop of ileum and distal jejunum entrapped and strangulated through the epiploic foramen
Plate 16.1 Type 4 rectal prolapse
Edema and sub-serosal hemorrhage of small intestine. These changes are characteristic of anterior enteritis Plate 13.4
Plate 17.1 Post-mortem appearance of extensive fibrin deposition in diffuse septic peritonitis
Plate 17.4 Omental and mesenteric adhesions to a mesen teric abscess caused by foreign body penetration of the jejunum
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 17.5 Hemangiosarcoma of the spleen causing hemo peritoneum in a pony
Plate 17.3 Large mesenteric abscess due to Streptococcus
Plate 17.6 Focal annular lymphosarcoma lesion of the small intestine causing partial bowel obstruction and recurrent colic
equi subsp. appearance
equi
('bastard
strangles'),
post-mortem
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)
Gross lipemia in a plasma sample (left) com Plate 19.2 pared with a normal plasma sample (right)
Plate 18.4 Severe coronitis as part of the skin lesions associated with multisystemic eosinophilic epitheliotropic disease
19.1 Large calcium bilirubinate choledocholith (arrow) obstructing the common bile duct at the junction of left and right hepatic ducts Plate
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 after 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 27.1 Post-mortem appearance of the small intestine of a foal affected by Clostridium perfringens type C show ing hemorrhagic enteritis
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 27.2 Photomicrograph of cryptosporidial oocysts
(pink structures) in feces from a foal with cryptosporidial diarrhea (100 x)
Plate 25.1 Overo mare and lethal white foal
28.1 Tyzzer's disease. Filamentous bacterium, Clostridium pi/iformis, from the liver section of an affected foal Plate
Preface Gastrointestinal diseases constitute a large and diverse
foremost are the many wonderful contributions from
group of diseases. Many of them are common and seri
experts in the field of equine gastroenterology; second,
ous, and they are encountered in horses of all ages,
there is an almost equal blend of contributions from
breeds and types. The Manual of Equine Gastroenterology
European and American clinicians in private practice
is a comprehensive guide to the diagnosis and treat
or from university hospital clinicians. We would like to
ment of gastrointestinal disorders in horses and foals.
dedicate this manual to all of our contributing authors,
The last 30 years have seen a dramatic advancement
who have in this text, as in their many other publica
in our knowledge about gastrointestinal diseases of the
tions, contributed greatly to our understanding of the
horse, and this, coupled with advances in surgical
diagnosis and treatment of equine gastrointestinal dis
techniques and therapeutics, has led to considerable
orders. We would like to thank Anne Littlejohn and
improvements in the success rates for treatment of the
Debbie
conditions. In some cases, successful treatment of an
communications with the many authors, forwarding
Lent
for
their
assistance
in
maintaining
individual horse involves the input of expertise in the
materials from North America to Europe and preparing
fields of surgery, internal medicine and critical care. As
several chapters. We trust you will find the book a useful
these disciplines become more and more specialised, so
source of information for the management of equine
it becomes increasingly difficult for individual veterin
gastrointestinal disorders.
arians to keep abreast of developments in all of these areas. One of the main objectives of this manual is to
Tim Mair
condense information from these separate fields into
Tom Divers
one, readily accessible source. We feel this text is unique in at least 2 ways: first and
Norm Ducharme 2001
xv
1 Physical examination
General physical examination and auscultation F Taylor
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
HISTORY AND GENERAL OBSERVATIONS
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
When exploring the history of a patient with suspected
signs, whereas postpartum colic may be associated with
gastroenteric disease the following topics should be
hemorrhage into the broad ligament, or rupture of the
included.
cecum or colon during fetal expulsion.
•
has there been an associated change in the dietary management?
•
were there any medications or other treatments prior to the onset?
•
•
•
PHYSICAL EXAMINATION AND AUSCULTATION
is the grazing safe (e.g. check for sandy topsoil, agrochemicals, poisonous plan ts)?
The initial physical examination of a patient with
is the animal's food intake reduced; if so is this
suspected gastroenteric disease should pay particular
associated with inappetance or evidence of
attention to the head and trunk. Additional aids to
dysphagia?
physical examination will be required and are outlined
is the animal's demeanor normal, depressed,
in the latter part of this section.
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
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 quality suggests circulatory compromise and impending shock. The color of the mucous membranes and the capil lary refill time (CRT) reflect the horse's circulatory 3
1
PHYSICAL EXAMINATION
status. The normal appearance is moist and pink and
Increased movement (hyperperistalsis) can be pro
the normal CRT is less than 2 seconds. The CRT indi
voked by a simple obstruction in an otherwise healthy
cates whether perfusion, hydration, and vascular tone
gut. The best example is spasmodic colic in which con
are impaired. Increasing refill times indicate progres
tinuous sounds, of greater than usual intensity, are
sively inadequate perfusion and are usually accompa
heard at all sites. In contrast, reflex movement is
nied by dryness and discoloration of the membranes.
reduced by inflammation and ischemia. An absence of
The mouth should be examined to detect abnormal
sound, or infrequent sounds of reduced intensity, may
ities of tooth wear, sharp edges on the cheek teeth, or
therefore be associated with peritonitis or the develop
other dental or mucosal diseases which may interfere
ment of gut hypoperfusion during colic. An absence of sound is also associated with alimentary paralysis as in
with feeding.
postoperative ileus and grass sickness.
The thorax and abdomen Abnormal
swellings,
particularly
The 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
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.
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 significant increases suggest infec tion. In cases of colic, temperatures in excess of 38.6°C
(101°F) 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
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
Abdominal auscultation enables appreCIation of gut
ble mark around the circumference at a point that will
activity and its greatest value is in the assessment of
indicate that the leading end is approaching the
colic. At least four sites should be auscultated: these are
entrance to the larynx or esophagus. This distance is
both paralumbar fossae and both sides of the lower
approximately 30 cm for pony tubes and 35 cm for
abdomen behind the costal arch.
horse tubes.
Two types of sound can be appreciated: weak sounds associated with localized bowel contractions (mixing the ingesta), and louder fluid sounds or borborygmi
RESTRAINT
associated with propulsion of ingesta. Sounds heard in the right paralumbar fossa reflect ileocecal (and possi
The horse is positioned diagonally in a corner with its
bly cecocolic) valve activity and differ from sounds
quarters against the wall to restrict backward and lateral
heard at the other sites. Here, a period of silence is
movements. The handler should stand to the left of the
broken once or twice a minute by a sudden rush of fluid
horse's head with his/her back to the horse to minimize
rumbling as secretions from one compartment pass
injury if the horse rears. A secure headcollar is essential
through the valve and hit the gas-fluid interface of the
but additional restraints will depend upon the horse's
next.
temperament. A horse that struggles during intubation
4
PHYSICAL EXAMINATION
1
is more likely to suffer a nosebleed and it is best to apply
the head in a flexed position and the clinician rests
a twitch to such patients. Sedation is possible where
his/her left hand on the bridge of the nose above the
clinical circumstances permit, but this will diminish the
muzzle. Care should be taken not to occlude the oppo
swallow reflex as the tube is passed and could affect the
site nostril inadvertently. The thumb is then used to ele
results of an absorption test if intubation is used for this
vate the alar cartilage of the right nostril, opening wide
purpose.
the entrance to the nasal cavity. The lubricated end of the tube is then placed on the floor of the open nostril, slightly inclined toward the
PROCEDURE
nasal septum with its curvature directed downward
The uncoiled tube is draped around the clinician's
floor of the ventral meatus. The tube's advance is
(Figure l.1), and advanced gently so that it follows the neck to prevent it from trailing on the floor; this also
stopped once its preset mark arrives at the nostril, indi
leaves the clinician's hands free to control the tube's
cating that the leading end is approaching the larynx or
passage. In cold weather a rigid tube should be softened
esophagus. In most cases, onward passage will result in
by passing warm tap water through it. The first 1012 em of the leading end is then coated liberally with a
entry into the larynx and trachea. To avoid this, the tube should be turned through 90 degrees before being
water-soluble lubricant and the tube is grasped just
advanced further. This has the effect of raising the level
behind this point for controlled insertion.
of the leading end with respect to the larynx, thereby
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
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. Alternatively, 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 Figure 1.1 Insertion of a nasogastric tube. The thumb of the left hand is used to elevate the alar cartilage of the
which moves down the neck following the line of the esophagus. In addition, there is resistance to air being
right nostril and the tube is inserted along the floor of the
sucked through the tube due to esophageal collapse at
open nostril
the leading end. Alternatively, a short, sharp blow of air 5
1
PHYSICAL EXAMINATION
down the tube produces a momentary inflation of the esophagus which is seen in the left jugular groove; this
TECHNIQUE ,,"" ,,, ,''11'' ,,�' \"1"""10' %Jlr'iMF'ot�' ,
is a useful test if a distinct swelling has not been seen to
When
travel down the jugular groove.
restraint is of the utmost importance to insure the
Once satisfied that the tube is correctly placed the
performing
a
rectal
examination,
proper
safety of the horse and the examiner. Inadequate
clinician can advance it to the stomach. There is usually
restraint may result in iatrogenic rectal perforation, a
an audible release of gas as the tube enters the stomach
potentially fatal complication of rectal examination, or
and gaseous 'bubbling' sounds can be heard when
serious injury to the examiner. Horses with signs of
listening at the open end of the tube.
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 romifidine
TUBE WITHDRAWAL
(40-120 !lg/kg i.v.). For more profound sedation, and
Any fluid medication which has been given by tube and
agonist may be combined with butorphanol (20 !lg/kg
to reduce the chance of the horse kicking, the alpha2 which is occupying its dead space should be blown
i.v.). A nose twitch should always be used to control the
through to the stomach before removal. Failure to do so
patient and promote relaxation of the rectum.
may result in inhalation of spilt fluid as the tube is with
Adequate lubrication of the examiner's hand and arm
drawn over the larynx. Thereafter, the tube should be
is necessary to minimize irritation to the rectal mucosa.
withdrawn slowly and carefully. Particular care should
Hydrated methylcellulose and mineral oil are the most
be taken not to rush out the last 50 cm, otherwise
commonly used lubricants. Initial introduction of the
trauma to the highly vascular nasal mucosa may result
examiner's hand through the anal sphincter is often met
in a nosebleed.
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
Rectal examination POE Mueller
INTRODUCTION
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
The rectal examination is one of the most important
of sand within the feces may be indicative of a sand
and helpful diagnostic techniques for evaluating adult
impaction or sand-induced colitis. After evacuation of
horses with abdominal disease. It is frequently essential
feces from the rectum, intrarectal administration of
in evaluating the need for surgery in horses with acute
50-60 ml of 2% lidocaine via a 60 cc catheter tip syringe
abdominal pain (see Chapter 9). Rectal examination may be used to identifY •
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.
(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
In addition, palpation of other intra-abdominal organs
excessive peristaltic contraction of the rectum. This pre
is possible, including the urinary bladder, uterus and
cludes a safe and thorough examination of the more
ovaries, left kidney, and spleen.
cranial abdominal contents.
6
PHYSICAL EXAMINATION
The most severe complication associated with rectal
•
mesenteric stalk
palpation is iatrogenic perforation of the rectum (see
•
ventral cecal tenia (no tension)
Chapter 16). Although rare, tears usually occur dorsally
•
cecal base (empty)
between the 10 o'clock and 12 o'clock positions. Most
•
pelvic flexure (Figure 1.2).
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. Regardless 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
1
Normally, the duodenum and remaining small intes tine are too soft and relaxed to be identified 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 fin 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 identified as a small intestinal structure perpendicular and attached to
just before removal of the hand from the rectum. In general, palpable characteristics of the abdominal contents and viscera are often helpful in identifYing 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 findings should always be interpreted in conjunction with the physical examination and laboratory findings.
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 identifiable in the caudal abdomen. It contains multiple, distinct fecal balls and is freely movable within the abdomen. Other intra-abdominal structures palpa
Figure 1.2 Caudal view of a standing horse demonstrating
ble in the normal horse starting in the left dorsal
abdominal structures that are palpable in the normal
abdominal quadrant, and progressing in a clockwise
horse during rectal examination. Starting in the left dorsal
direction include
abdominal quadrant, and progressing in a clockwise direction, palpable structures include: caudal border of
•
caudal border of the spleen
•
nephrosplenic (renosplenic) ligament
kidney, ventral cecal tenia, cecal base, and the pelvic
•
caudal pole of the left kidney
flexure
the spleen, renosplenic ligament, caudal pole of the left
7
1
PHYSICAL EXAMINATION
the mesenteric stalk. The mesenteric stalk is usually pal
ure may or may not be palpable in the caudal left
pable as a sheet of tissue, with a pulse that is only occa
abdomen, depending on the amount of ingesta within
sionally palpable. In large horses it may not be possible
the large colon. If the pelvic flexure and left dorsal
to reach far enough to palpate the root of mesentery.
large colon are palpable, they may be identified by soft
Continuing to move in a clockwise direction, the
ingesta, and the absence of the tenia and haustra (sac
base of the cecum is palpable in the right dorsal abdom
culations). The adjacent left ventral colon contains sim
inal quadrant. Depending on the amount of ingesta in
ilar contents and has two free tenia and haustra. The
the cecum, it may or may not be palpable. The ventral
tenia should course in a cranial-to-caudal direction,
and sometimes medial cecal tenia are usually palpable
from the left caudal abdomen to the left cranial
by moving the hand laterally and caudally, hooking the
abdomen (Figure 1.2). The left dorsal colon does not
tenia with the tips of the examiner's forefingers. These
have haustra and contains only one mesenteric tenia.
bands usually course in a dorsocaudal to ventrocranial direction, just to the right of the midline. Because the
Additional
structures
in
the
caudal
abdomen
included in a complete rectal examination include:
majority of the body and apex of the cecum are beyond
bladder, uterus and ovaries in the mare, the aortic
the examiner's reach, the tautness of the ventral and
bifurcation, and the internal inguinal rings in the
medial cecal tenia is used as an indicator of the amount
stallion. The inguinal rings are identified just cranial,
of ingesta within the cecum. Normally the cecal tenia
lateral, and slightly ventral to the iliopectineal emi
should be loose and easily movable. With increased
nence of the anterior brim of the pelvis. In stallions, the
amounts of ingesta in the cecum, the tenia become
inguinal rings are large enough for insertion of a finger.
more taut. Pain elicited upon palpation of the ventral
If the testis or epididymis has descended, the ductus
or medial cecal tenia may be associated with tension of
deferens is palpable in the caudomedial aspect of the
the ileum or its mesentery. This has been associated
ring. In geldings, the inguinal ring is palpable as only a
with pain originating from the ileum and its vascula
slight depression and decreases in size with age.
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. As the hand is moved ventral and caudal to the
pelvic brim, fecal balls in the small colon are usually eas ily identified. 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
BIBLIOGRAPHY Rectal examination KopfN (1997) Rectal examination of the colic patient. In
Current Therapy 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 Surgery and Lameness 2nd edn, N A White and] N Moore (eds). W B Saunders, Philadelphia, pp. 262-70.
2 Additional diagnostic procedures
Rectal biopsy
PROCEDURE
F Taylor
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 finger 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.
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 2.1).
Figure
2.1 Rectal biopsy instrument with a folding upper jaw and rigid lower jaw
Figure
2.2 Rectal biopsy i n the horse. A f o l d of rectal mucosa is held between a finger and the thumb of one hand and the i nstrument advanced to obtain a biopsy 9
2
ADDITIONAL DIAGNOSTIC PROCEDURES
The jaws are closed and the sample is removed and transferred to 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 F Taylor 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, CA) 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 precau10
Figure 2.3 The site for liver biopsy in the horse. A site is sel ected in the 1 3th intercostal space on the right side between a n imaginary line from the point of h i p to the point of shoulder, and another line from the point of hip to the point of el bow
tions the skin and intercostal muscle beneath are infil trated down to the parietal pleura with 4-5 ml of 2% lignocaine using a 39 x 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 acljacent 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 fixative. If the first 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.
ADDITIONAL D IAGNOSTIC PROCEDU RES
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.
Clinical pathology F Taylor 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.
2
Leukocyte parameters Leukopenia (WBe < 6.0 x 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 x 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 inflammation, 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)
Erythrocyte parameters The PCV is a useful monitor of dehydration and hypo volemia if used on a sequential basis. In general terms, a pev greater 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 after 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.
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 11
2 •
• •
ADDITIONAL DIAGNOSTIC 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 (lAP) which may help to identity 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. 12
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 specific 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 identified i n the laboratory using a flotation technique, but it is difficult to distin guish between large and small species. However, small strongyle (cyathostome) eggs usually comprise the vast m
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.
ADDITIONAL DIAG N OSTIC PROCE D U RES
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 define 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 five fecal samples should be collected from the rectum at 24-hour inter vals to increase the possibility of detection. An adequate sample should occupy half a universal tube, approxi mately 10 ml; swabs are usually unsatisfactory. Clostridiosis (usually Clostridia perfringens or diJficile) 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. Specific toxin analysis may also be performed for C. perfringens and difficile.
2
Abdominocentesis (abdominal paracentesis) T Mair
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
Fecal leukocytes The presence of leukocytes and occasionally epithelial cells in a fecal sample suggests inflammatory 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 specific 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.
A rectal examination should always be performed before abdominocentesis in order to recognize an extremely gas-distended or ingesta-filled cecum or large intestine. If these abnormalities are identified, 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 13
2
ADDITIONAL DIAGNOSTIC PROCEDURES
I'"
----------------�
Figure 2.6 Abd o m inocentesis showing accidental pu ncture of the intestine
6 6
Figure 2.4 Abdominocentesis showing 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
Figure 2.5 Abdominocentesis showing fa i l ure to penetrate the sub-peritoneal fat l ayer because the needle is too short 14
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 PCV of the sample obtained by abdominocentesis with the PCV 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
ADDITIONAL DIAG NOSTIC PROCEDU RES
PCV compared to the pev of peripheral blood; com monly the pev of splenic blood will be 65 per cent or greater than the peripheral blood pev. The PCV of true peritoneal fluid obtained from horses with hemo peritoneum is likely to be lower than the peripheral blood pev. 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
2
Figure 2.8 Ultrasonogram of the ventral abdomen of a normal horse showing a pocket of anechoic peritoneal fluid. This scan was obtained usi ng a 7.5 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 identity 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 difficult 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.
6 Figure
2.7 Abdominocentesis showing use of a teat can nula. A stab i ncision is first made using a no. 1 5 scalpel blade. The teat can nula is then forced through the linea alba and advanced into the peritoneal cavity
ABDOMINOCENTESIS IN THE FOAL Abdominocentesis is often not performed in the foal because of fears of puncture or laceration of the bowel 15
2
ADDITIONAL DIAGNOSTIC PROCEDURES
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 herniation 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.
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 x 1 0911 ( 3000-5000 cells/�I) , with a total protein concentration of less than 25 gi l (2.5 gl dl) . Peritoneal fluid from foals has a lower total nucle ated cell count (less than 1 .5 x 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
Clear or slightly turbid Straw colored or colorless
Specific gravity
<
Total protein
<
Total nucleated cell count
<
Differential cell count
20-90% neutrophils 5-60% mononuclearl
T Mair
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. 16
25 gil (usually < 15 gil) (mainly albumin) 5.0 x 109/1 « 10000 cells/Ill) (usually < 2.0 x 10911)
mesothelial cells 0-35% lymphocytes 0-5% eosinophils 0-1% basophils
Analysis of peritoneal fluid INTRODUCTION
1.016
Total red cell count
Negligible
Fibrinogen
Negligible « 0.1 gil) (does not clot on standing)
Glucose
5.0-6.4 mmo"l
Creatinine
161-237 j.l.moVI (1.8-2.7
Urea nitrogen
3.9-8.2
lactate
0.4-1.2 mmol" (3.8-10.9 mgldl)
Total bilirubin
5 1 3 j.l.molll (0.3-0.8 mgldl)
Amylase
0-14 lUll
lipase
0-361UIJ
GGT
0-6 lUll
m mo l/!
-
(90-115 mgldl)
mgldl)
(11-23 mgldl)
ADDITIONAL DIAGNOSTIC PROCEDURES
foals with uroperitoneum. The ratio of peritoneal to plasma creatinine is the preferred method of confirm ing uroperitoneum in foals (see Chapter 2 2 ) . 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 x 1 09/1 are gen erally considered abnormal. Most horses have total nucleated cell counts less than 2 x 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 finding. 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 diffic ult 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 identified 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.
2
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 significant 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 x 1 09/1 or 1 1 333 cellS/ill) and then decline rapidly to day 4. Toxic changes can be identified in the neutrophils, but bacteria are not generally evident. The specific gravity 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 x 1 09/1 ( 1 3 700 cell/Ill) on the first day after surgery, and can increase to levels as high as 400 x 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. Insufflation 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 insufflating 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 x 1 09/1 5 days after the surgery. The cell counts are expected to return toward normal within 7 days of castration. 17
2
ADDITIONAL 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 As 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 18
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 (530 X 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 x 109/1. The identification of plant material, intra- or extra-cellular bacteria, and protozoa is indica tive of bowel rupture (Plate 2.2 ) . Horses affected b y 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 x 1 09/1 and may be as high as 400 x 1 09/1. Although the identification 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 identified in peritoneal fluid because 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 identity 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
2
ADDITIONAL DIAGNOSTIC PROCEDURES
ruptured bowel into the peritoneal cavity should also be considered as a possibility. 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 identified 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 affected 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 identified in a small number of horses affected 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) .
T..- t.���.Qf.i:J�fl��;iJ,�t"lhoi's.. ."dJn ...u,�.�_. a.......lft.ldi.. ,
'
"
,
,
"
,
i
,
"
"
,
"
"
c
""
,
Gross appearance
Total protein (gil)
Nucleated cell count (x 10911)
Cytology
Normal
Odorless, clear to pale yellow
< 2.5
< 5.0
2: 1 ratio of nondegenerative neutrophils to macrophages, no RBCs.
Simple obstrudlon
Odorless, clear to turbid, pale yellow
Normal to mild increase (2.S-3.0)
Normal to mild i ncrease (3.0-8.0)
Predominantly nondegenerative neutrophils.
Very early strangulating obstrudlon
Odorless, clear to turbid, pale yellow
Normal to mild increase (2.5-3.0)
Normal to mild i ncrease (3.0-B.0)
Predominantly nondegenerate neutrophils, few RBCs.
Strangulating obstrudion
Serosanguinous, turbid
Moderate to marked i ncrease (3. 5-6.0)
Moderate to marked increase (> 10.0)
Degenerate neutroph ils ± intra- or extracel lular bacteria, RBCs.
Intestinal rupture
Malodorous, turbid, dark red to brown
Moderate to marked increase (3. 5-6.0)
Decreased
Enterocentesis
Malodorous, turbid, green to brown
< 2.5
Few or no nucleated cells
Plant material, protozoa.
Hemoperitoneum
Dark red
Similar to peripheral blood
Similar to peripheral blood
PCV less than PCV of peripheral blood, erythrocytophagia, few or n o platelets.
Splenic pundure
Dark red
Similar to peripheral blood
Similar to peripheral blood
PCV greater than PCV of peripheral blood. High n umbers of small lymphocytes.
Peritonitis
Thick turbid, dark yellow to orange
> 2.5
> 10.0
High numbers of degenerate and nondegenerate neutrophi ls, intra- and extra-cellular bacteria.
(< 2 .0)
Degenerative neutrophil s, i ntra- or extracel l ular bacteria, plant material, protozoa, RBCs.
19
2
ADDITIONAL DIAG N OSTIC PROCEDURES
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 confirmation 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 F Taylor These tests assess the functional integrity of the small intestine by measuring the efficiency 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 20
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. An absorption curve is then plotted arithmetically. A modified 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 field. 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 infiltrations of the gut wall. The diagnosis is defined by histopathology. An intermediate curve between normal absorption and total malabsorption suggests a state of partial mal absorption that is more difficult 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.
ADDITIONAL DIAG NOSTIC PROCEDURES
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.
2
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 type 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 1*"�,ffi,yfMA' \W,'''"",",8lr"WWI'c>'''ii'«M", %"'';'"1',,,=, """NW""',"""O>'�'H�I�I,"'","!&" """oMB'Y'''',P,S",
This can be divided into two categories
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 deficiency 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 MJ Murray
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
• •
fiberoptic electronic (video) .
Fiberoptic endoscopic equipment uses glass fiber 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 magnified by a lens system within the eyepiece. The quality of an image viewed through a fiberoptic endo scope is determined by the number of fibers in the endoscope and the intensity of the light source. The more fibers the better the image resolution. High qual ity gastroscopes have approximately 30 000 fibers while endoscopes of lesser quality may have as few as 1 2 000 fibers. 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 fiber 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 filters over the CCD 21
2
ADDITIONAL DIAGNOSTIC PROCEDURES
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
Tabl. U A co",parlson ��Ptlclittl incllldlnl Jilht sO\:Ircf' a�:....r"or .· •
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 fiberoptic 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 fiber 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
; �. �. ���spttms . . " . ..' . . " <.; .
.. .
.
ii
.
,
" .
Feature
Fiberoptic (without camera)
Electronic
Cost (new)
$8000-$ 1 5 000 £5000-£ 1 0 000
$20 000-$45 000 £ 1 5 000-£30 000
Portabil ity
Good
Poor to fair
Image qual ity
Fai r to very good
Very good
Image capture
Poor
Good
Teaching/client communication
Poor
Good
Disinfection
Good
Good
Available accessories
Good
Good
22
.
ADDITIONAL DIAG N OSTIC PROCEDURES
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 every 1-2 years. Many of the relatively inex pensive 2 to 3-meter endoscopes are not sufficiently durable to withstand repeated gastroscopic procedures and will require frequent maintenance. These issues must be clarified 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. An 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.
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 sufficient 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
=
video)
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. An endoscope 200 cm long is usually sufficient 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
Endoscope dimensions
Endoscope type (f = flberoptic, v
2
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 identifYing 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
Typical dimensions Outer Working length diameter (o.d.)
Gastroscope, human (f,v)
1 00-1 1 0
Colonoscope, human (f,v)
Comments
9-1 0. 5 mm
Gastroscopy in neonates.
1 55-1 70 cm
1 1 .5-1 6 mm
Not long enough for adult gastroscopy. o.d. too great for passage through foal nasal passages.
Small bowel endoscope (v) (Penta x)
250 em
1 0 mm
Suitable for all ages except adult duodenoscopy.
Equine gastroscope (v) (Fujinon)
280 cm
1 4. 5 mm
Large o.d. inappropriate for foals.
Equine gastroscope (v) (Pentax)
300 cm
1 0 mm
Suitable for all ages, including adult duodenoscopy.
em
23
2
ADDITIONAL DIAGNOSTIC 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 I . 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 l . Feed is withheld for 8-12 hours, water for 2-4 hours.
Longer periods of fasting can be used to ensure complete emptying 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 • 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. 24
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 finds 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 difficult 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 definitely been fasted for an adequate period, a gastric outlet obstruction should be suspected.
ADDITIONAL DIAG N OSTIC PROCEDURES
When the endoscope first 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. As 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 insufflate 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
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 sufficient 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 field of view will be a blurred red. As 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 b e 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
\
(a)
2
\
(b)
Figure 2.9 Illustrations 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 ines represent the outline of the proximal descend ing duoden u m . a) In this illustration the left hemisphere of the stomach has been removed just to the l eft of midl ine. Notice that the endoscope must travel along the c i rcumference of the stomach i n order to reach the gastric antrum. As the endoscope is advanced around the circumference of the stomach it becomes i m mersed i n gastric contents. When the endoscope is advanced into the duodenum the tip must be retroflexed to observe duodenal papi llae. Rarely the cli nician might be able to advance the endoscope a borally into the duodenum, but the configuration of the duodenum with respect to the stomach makes this very difficult. b) In this illustration the caudal hem isphere of the stomach has been removed . In this view, the torque stresses placed upon the endoscope as it is advanced toward the pylorus and the duo denum can be appreciated. When the procedure is performed properly, the majority of these stresses are applied to the cables controlling the tip deflection. Adva ncing the endoscope with excessive force or otherwise i m properly will cause more of these forces to be applied to the endoscope insertion tube causing expensive damage to the instrument 25
2
ADDITIONAL DIAGNOSTIC PROCE D U R ES
duodenal papilla, rather than forward. One will notice that when the endoscope is first 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 insufflated into the stom ach. If discomfort does occur it will rapidly resolve after treatment with flunixin meglumine, 0.5 mg/kg i.v.
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 sufficiently small to be easily manipulated within the rectum, while still providing an adequate imaging field. Linear transducers are pre ferred for most gynecological work because they are
CARE OF ENDOSCOPIC EQUIPMENT ill'·.·:("''''U':"":'':"''"'"';I,"'::i:;i:'':i@;:'''i':>¢�I''M'':''"*''''='''lI©_I.""mli"'V!i ' kP_"':'''("*"''il:::U';'''''''M:8l£i�'''d''''Affi:"i:e;:"",:�,,<,:,'''""
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, NY) 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 ofglutaraldehyde (e.g. Cidex,Johnson andJohnson Medical Inc. , Arlington, TX) for 1 5-30 minutes.
Figure 2.1 0 A transverse ultrasonogram of the right dorsal abdomen from a normal horse: the d uodenum can be seen running ventral to the kidney a nd dorsal to the cecum
Ultrasonographic examination of the abdomen eM M arr, J Lyons, a n d 5 Freeman
Examination of the abdomen requires a range of imag ing depths and thus, ideally, a selection of transducers 26
Figure 2.1 1 A tra nsverse ultrasonogram of the caudoventral abdomen from a normal horse: sma l l intestinal loops (51) are visible and there is a d istinct layer of retroperitoneal fat
ADDITIONAL DIAG N OSTIC PROCE D U R ES
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 field. 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 inj ury to the rectum.
NORMAL ULTRASONOGRAPHIC ANATOMY OF THE INTESTINE AND PERITONEAL CAVITY The stomach can be identified in the left cranial abdomen. Typically it is recognized as an echogenic curve caused by gas along the greater curvature. The
2
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 identified 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 identified 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 five discrete layers, however, the resolution of most ultrasonographic units is such that the layers are usually measured in combina tion to define the total wall thickness (Table 2.5 ) . Large intestine i s visible i n all quadrants of the abdomen. It is recognized ultrasonographically 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 . 1 3 , 2 . 1 4 ) . Waves of peristalsis within the
Figure 2 . 1 2 A transverse abdominal u ltrasonogram obtained per rectum showing normal small i ntesti ne. The wa l l (between arrows) is com posed of five discrete layers that are normally measured in combination
Figure 2.13 A transverse ultrasonogram of the cranioven tral abdomen. Peritoneal fluid is visible between the sec tions of large intestine (LI) and could be sam pled in this site
Figure 2.14 A transverse abdominal ultrasonogram obtained with a 10 MHz l i near transducer i l l ustrating the discrete layers of the abdo m i n a l wall 27
2
ADDITIONAL DIAGNOSTIC PROCEDURES
"
Table 2.5 Normal ultrasonographlc features of the in_tine Region
Recommended transducer frequency (MHz)
Strudures examined
Subjedlve assessments of Intestine
Quantitative measurements of Intestine·
Cranioventral
Foals: 1 0-5
Spleen
Motility of colon and sma l l i ntestine
Colon:
Adu lts: 6.5-5
Large intestine Small i ntestine
wall thickness 0. 1 8 ± 0.04 cm Presence/absence of sma l l i ntestine
motility 2-6 contractions! min
Volume and character of peritoneal fluid Ca udoventra I
Foals: 1 0-5
Large intestine
Adults: 6.5-5
Small intestine
Foals: 1 0-6.5 Adults: 5-2.25
Left dorsal
Foals: 1 0-6.5 Adults: 5-2 .25
Mid-abdomen (transrectal route)
Adults: 6.5-5
wall thickness 0 . 1 6 ± 0.05 cm diameter 1 .8 ± 0.8 cm
Volume and character of peritoneal fl uid
motility 6-1 5 contractions! min
Liver Kid ney Duodenum Cecum
Motility and nature of i ntestinal contents
Colonic and small intestinal wall thickness (see data above)
Spleen Kidney Large colon
Presence/absence of intestine in the nephrosplenic space
Aortoiliac quadrification Bladder Small intestine Cecum Large colon Small colon
Motility of colon and smal l i ntestine
*Freeman and Lyons, unpublished data
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 28
Small i ntestine:
Presence/absence of sma l l intestine
Bladder
Right dorsal
Motility of colon and sma l l intestine
Colonic and sma l l intestinal wa l l th ickness (see d ata above)
�
frequently b� identified as echogenic curves 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 . 1 4 ) . Peritoneal fluid can be identified in the cranioventral abdomen in most horses (Figure 2 . 1 3) , and ultrasonography is occasionally use ful to identifY 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 identified in this location.
ADDITIONAL D IAGNOSTIC PROCE D U RES
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 sensitivity of 1 00 per cent and specificity 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.
2
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 . 1 7) . 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
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 fluid analysis. In horses with protein-losing enteropathy and malabsorption, ultrasonography can be a useful adjunctive aid to allow measurement of the thickness of specific 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
Figure 2. 1 5 A transverse abdominal ultrasonogram from a 4-week-old foal with sma l l intestina l volvulus i l lustrating a distended. a motile segment of small intestine. The foal is in lateral recumbency and this i m age has been obtained from the ventral midline a nd therefore. because of gravity. stationary ingesta i n the obstructed segment has settled into horizontal layers 29
2
ADDITIONAL DIAGNOSTIC PROCE DURES
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 . 1 9 ) . The presence of both distended and collapsed loops of intestine is strongly suggestive that there may be an anatomical obstruction .
LARGE INTESTINAL LESIONS Figure 2 . 1 6 A longitudinal ultrasonogram of the left dorsal abdomen from a 5-year-ol d sta l l ion with a right i nguinal hernia. Multi ple distended loops of small intestine (51) are visi ble
Figure 2.17 A longitudinal u ltrasonogram of the cranio ventral abdomen from an aged pony gelding with a n obstruction of t h e sma l l i ntestine b y a pedunculated lipoma. Flu id-filled distended small intesti n a l loops with thickened walls are visible
Figure 2.18 A longitud inal ultrasonogram of the cranio ventral abdomen from a 1 5-year-old pony gelding with smal l i ntestinal entrapment in the epiploic foramen. A segment of non-d istended small intestine with hypo echoic, edematous wa l ls has a corrugated appearance (arrows) 30
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 identified 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 identified (Figure 2.20) . Cecocecal and cecocolic intussusceptions can also be specifically identified and have a bull's eye appearance, similar to that described for small intestinal intussusception. Specific differentia tion of other surgical forms of large colon disease from generalized tympany or large colon impaction is diffi cult. However, transrectal ultrasonography can be use ful in the identification of small colon obstruction (Figure 2.2 1 ) . 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
ADDITIONAL DIAGNOSTIC PROCE D U RES
(a)
(c)
2
(b)
(d)
Figure 2. 1 9 Abdominal u ltrasonograms from a 1 5-year-old Shetland pony with m u ra l a bscessation and small i ntestinal adhesions. I n longitud inal (al and transverse (b) i mages of the affected intest i ne, the walls are hypoechoic and extremely thickened. The arrows indicate the area at which the two adjacent segments do not move relative to each other, indicating that adhesions have formed. In other areas of the a bdomen, in longitudinal (cl and transverse (d) i m ages, both distended and collapsed loops are visible, suggesting that there is intestinal obstruction
Figure 2.20 A tra nsverse ultrasonogram of the l eft dorsal a bdomen from a 2-year-old g elding with left dorsal d is placement of the large colon. In this area the entrapped portion of intestine is not tympanitic and therefore sound penetrates the intestine so that the spleen is o n ly partially obscured by acoustic shadows (arrows) caused by intestinal gas 31
2
ADDITIONAL DIAGNOSTIC PROCEDURES
Figure
2.21 A transverse ultrasonogram of the caudal abdomen obtained per rectum from a n aged gelding. Thickened a reas of sma l l colon (SC) are due to obstruction of the sma l l colon by a peduncu lated 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 motility 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. Infiltrative bowel diseases produce focal or multi focal wall thickening in various segments of intestine. Information on the distribution and extent of infiltra 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, infiltrated areas of 32
Figure 2.22 Tra nsverse ultrasonograms of the (a) cra nial, (b) mid-, (c) right ventral abdomen from a n 1 1 -yea r-old mare with chronic eosinop h i l ic enteritis demonstrati ng that the l a rg e colon varies i n thickness. In the most severely affected area (C), the five-layered a p pearance of the colon has been lost
ADDITIONAL DIAGNOSTIC PROCEDURES
(a)
(a)
(b)
(b)
2
Figure 2.23 Transverse abdominal ultrasonograms from a 6-year-old mare with plasmacytic-Iymphocytic enteritis, affecting primarily the l a rge colon. a) In the caudal ventral abdomen the large colon has irregular thickening of the wa l l and loss of the five-layered appearance due to cel l u lar infi ltrate. b) In the cra n i a l ventral abdomen, the small intestine is markedly thickened with hypoechoic wa lls due to bowel edema secondary to i ntestinal protein loss
Figure 2.24 Transverse ultrasonograms from a 1 6-year-old gelding with i ntesti nal lymphosarcoma. a) The most severely affected segment of small i ntestine has markedly thickened walls, loss of the normal intestinal wall struc ture, and a reduced l u me n . b) In a less severely affected proximal segment there is wall thickening and moderate distention
intestine are generally echogenic with irregular walls and there may be loss of the normal five-layered appear ance. However, at present it is not possible to specifi cally differentiate the various forms of infiltrative disease using ultrasonography (Figures 2.22-2.24) .
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 o f 5 0 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 specificity 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
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-
33
2
ADDITIONAL 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
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 -
R Wel ler a n d eM M a rr
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.
Figure 2.25 A transverse ultrasonogram of the ventral abdominal wall from a horse that has purulent drainage from a cel iotomy incision performed 7 days previously. A tract (a rrows) extends from a collection of hypoechoic material resu lting from incisional infection
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 specific 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 unspecific 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 Figure
2.26 A longitud inal u ltrasonogram of the ventral abdom inal wall from a horse that has developed deh is cence of the abdominal muscle 8 days after exploratory cel iotomy. I ntestine is located between the muscle defect (arrows) and had adhered to the subcutaneous tissue 34
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
ADDITIONAL DIAG N OSTIC PROC E D U RES
Used for the diagnosis of
Radiopharmaceutical
Dental disorders
Technetium (99mTc) methylendiphosphonate (MOP)
Esophageal motil ity
99mTc-sulfur colloid
Gastric e m ptying
99mTc-sulfur colloid 99mTc-d iethylenetriaminepentaacetic acid (OTPA)
Gastric secretory function
99mTc-pertechnetate
Gastrointestinal bleeding
99mTc-labeled red blood cells
Gastrointestinal neoplasia
99mTc-methoxy-isobutyl-isonitrile (MIB!)
Inflammatory gastrointestinal conditions
Technetium (99mTc), G a l l i u m (67Ga), Indium (1I I In) l a beled leukocytes
Hepatobiliary imaging
99mTc-sulfur colloid 99mTc-im inodiacetic acid (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.
2
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) .
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.
u dal
right
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 x 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
ventral
ro tral
Figure 2.27 Tooth root abscess. A l eft lateral a n d a dorsal scintigraphic image of the head of a 1 5-year-old Warmblood gelding. The horse had a 6-month history of recurrent swe l l i n g over the left maxi l l a . Radiog raphs were inconclusive. Scintigraphy with 99mTc-M D P revealed a focal uptake over the root of the second maxi l lary cheek tooth on the l eft side, suggestive of a tooth root a bscess 35
2
ADDITIONAL DIAGNOSTIC PROCEDURES
audal
L
G
l en. yen
aJ
fo
tral
Figure 2.28 Periodontal disease. A left lateral scintigram, 3 hours after injection of 99mTc-MDP, of the head of a 2S year-old Connemara gelding that presented with progres sive weight loss. No evidence of dental disease was seen on intra-oral examination or radiographs. The image shows a linear increase of radioactivity over the upper and lower arcade, suggestive of severe periodontal disease Figure
2.29 Abdom inal abscess. A scintigram of the right mid-abdomen of a 6-year-old gelding with a 3-week his tory of fever of unknown orig i n . An hour after injection of 99mTc-labeled leukocytes there was a circu lar increase of activity caudal to the l u ng, suggestive of an abdom inal a bscess
INFLAMMATION AND INFECTION 67Ga, I I IIn, 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 inflammatory 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 . Identification or localization of abdominal abscesses. 36
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 4gauge needle, into 40 m l 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 G for 5 min, the resulting pellet contains a mixed population of leukocytes • the supernatant is centrifuged at 2000 G for 10 min to produce cell-free plasma for washing the cells.
ADDITIONAL DIAGNOSTIC PROCE D U R ES
2
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
Figure 2.30 Inflammation of the small intestine. A scinti graphic image 1 hour after injection 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 reg ions of i ncreased activity in the right dorsal abdomen, suggestive of inflammation of the small intestine
2. In vitro labeling • to form 99mTc-HMPAO, 10 MBq/kg 99mTc_ pertechnetate is added to one vial, containing 0.5 mg HMPAO, 7.6 1lg 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 x 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
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 identified. 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 at. ( 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. 37
2
ADDITIONAL DIAGNOSTIC PROCEDURES
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.
Traver D S, Thacker H L ( 1 979) Malabsorption syndromes in the horse: use of rectal biopsy in differential diagnosis.
Proc. Am. Assoc. Equine Pract. 24:487-98.
Fecal analysis Morris D D, Whitlock R H, Palmer J E ( 1 983) Fecal leukocytes and epithelial cells in horses with diarrhea. Cornell Vet.
73:265-74.
Abdominocentesis Adams, S B, Fessler,j R, Rebar A H ( 1 980) Cytologic
Breath hydrogen tests T Mair
interpretation of peritoneal fluid in the evaluation of equine abdominal crisis. Cornell Vet. 70:232-46 Bach L G and Ricketts S W ( 1974) Paracentesis as an aid to the diagnosis of abdominal disease in the horse. Equine
Vet. ). 6: 1 1 6-2 1 Coffman J R ( 1 980) Peritoneal fluid. Vet. Med. Small Anim.
Breath hydrogen measurements can be used to investi gate gastrointestinal function in horses, although the techniques and interpretation of results require further refinement 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 modification of the technique are required before it can be applied clinically.
Clin. 75: 1 285-8
Crowell R L, Tyler R D, Clinkenbeard K 0 and MacAllister C 0 ( 1 987) Collection and evaluation of equine
peritoneal and pleural effusions. Vet. Clin. N. Am. Equine
Pract. 3:543-561 Tulleners E P ( 1 983) Complications o f abdominocentesis in the horse. ]. Am. Vet. Med. Assoc. 1 82:232 White N A ( 1 990) Abdominal paracentesis. In The Equine Acute Abdomen, N A White (ed. ) . Lea and Febiger, Philadelphia. pp. 1 24-3 1 .
Analysis o f peritoneal fluid Fischer A T ( 1997) Advances in diagnostic techniques for
horses with colic. Vet. Clin. N. Am. Equine Pract. 1 3:203- 1 9
Fischer A T , Lloyd K C K , Carlson G P ( 1 986) Diagnostic laparoscopy in the horse . ). Am. Vet. Med. Assoc.
1 89:289-292 Frazer G S, Burba D, Paccamonti D ( 1 996) Diagnostic value of peritoneal fluid changes in the postpartum mare. In.
Proc. Am. Assoc. Equine Pract. 42:266-7. Grindem C B. Fairley N M. Uhlinger C A and Crane S A
( 1 990) Peritoneal fluid values from healthy foals. Equine Vet. ). 22:359-61 Hanson R R. Nixon A J. Gronwall R ( 1 992) Evaluation of peritoneal fluid following intestinal resection and anastomosis in horses. Am. ). Vet. Res. 53:216-221 MalarkJ A. Peyton L C and Galvin MJ ( 1 992) Effects of blood contamination in equine peritoneal fluid analysis. ). Am.
Vet. Med. Assoc. 201 : 1 545-8. May K A. Cheramie H S and Prater D A ( 1 999) Chyloperitoneum and abdominal adhesions in a miniature horse . ). Am. Vet. Med. Assoc. 2 1 5:676-678 Santschi E M. Grindem C B. Tate L P and Corbett W T ( 1 988) Peritoneal fluid analysis in ponies after abdominal surgery. Vet Surg. 1 7:6-9 Schumacher J , Spano J S. McGuire J. Scrutchfield W L and
'BIBLIOGRAPHY Rectal biopsy Lindberg R, Nygren A, Persson S G B ( 1 996) Rectal biopsy diagnosis in horses with clinical signs of intestinal disorders: a retrospective study of 1 1 6 cases. Equine Vet. )'
28:275-84. 38
Feldman R G ( 1 988) Effects of castration on peritoneal fluid constituents in the horse. ). Vet. Intern. Med. 2:22-25 Schumacher J , Spano J S and Moll H D ( 1 985) Effects of enterocentesis on peritoneal fluid constituents in the horse. ). Am. Vet. Med. Assoc. 1 86: 1 30 1 -1 303 Tulleners E P ( 1 983) Complications of abdominocentesis in the horse. ). Am. Vet. Med. Assoc. 1 82:232-4. Van Hoogmoed L. Snyder J R. Christopher M ( 1 996) Peritoneal fluid analysis in peripartum mares.). Am. Vet.
Med. Assoc. 209 : 1 280-2.
ADDITIONAL DIAGNOSTIC PROCE D URES
Carbohydrate absorption tests Dietz H H ( 1 98 1 ) D (+)-xylose absorption test in the horse. A clinical study. Nord. Vet. Med. 33: 1 1 4-20. Jacobs K A, Bolton] R ( 1 982) Effect of diet on the oral glucose tolerance test in the horse. ]. Am. Vet. Med. Assoc. 1 80:884-6. Loeb, W F, McKenzie, L D, Hoffsis, G F ( 1 972) The carbohydrate digestion-absorption test in the horse. Technique and normal values. Cornell Vet. 62:524-3 1 . Murphy D , Reid S W], Love S ( 1 997) Modified oral glucose tolerance test as an indicator of small intestinal pathology in horses. Vet. Rec. 1 40:342-3. Roberts M C, Hill F W G ( 1973) The oral glucose tolerance test in the horse. Equine Vet.]. 5 : 1 7 1-3. Roberts M C, Norman P ( 1 979) A re-evaluation of the d (+)xylose absorption test in the horse. Equine Vet.]. 1 1 239-43.
2
ultrasound in horses for diagnosis of left dorsal displacement of the large colon and monitoring its nonsurgical correction. Vet. Surgery, 22, 281-284. Wilson D A, Badertscher R R, Boreo M], Baker G], Foreman ] H ( 1 989) Ultrasonographic evaluation of the healing of ventral midline abdominal incisions in the horse. Equine
Vet. ]. (suppl. 7 ) , 1 07-1 1 0.
Nuclear scintigraphy Butson R], Webbon P M, Fairbairn S M ( 1 995) Tc-99m HMPAO labeled leucocytes and their biodistribution in the horse: a preliminary investigation. Equine Vet. ]. 27(4) 3 1 3-315 Hoskinson ] ], Tucker R L ( 1 996) Scintigraphic imaging of inflammation and infection. In Handbook of Veterinary Nuclear Medicine, R B Berry, G B Daniel (eds) . North Carolina State University, Raleigh, NC, pp. 1 62-78.
Endoscopy
Koblik P D , Lofstedt], ]akowski R M, ]ohnson K L ( 1 985) Use of I I I In-labeled autologous leukocytes to image an
Adamson P, Murray M J . ( 1 990) Gastric endoscopy. In Equine Endoscopy, ] L Traub-Dargatz, C M Brown (eds) .
abdominal abscess in a horse . ]. Am. Vet. Med. Assoc. 186: 1 3 1 9-22. Theodorakis M C, Bermudez A], Manning] P, Koritz G D,
C V Mosby, St Louis, pp. 1 1 9-37. Knyrim K ( 1 989) Optical performance of electronic imaging systems for the colon. Gastroenterology 96:776. Lamar A M ( 1 997) Standard fiberoptic and video endoscopic equipment. In Equine Endoscopy 2nd edn,] L Traub Dargatz, C M Brown (eds) . C V Mosby, St Louis, p. 13.
Ultrasonographic examination of the abdomen in the gastrointestinal patient
Hillidge C ] ( 1 982) Liver scintigraphy in ponies. Am. ]. Vet. Res. 43: 1 5 6 1 - 1565. Weller R, Livesey L, Bowen I M, et al. (200 1 ) Comparison of radiography and scintigraphy in the diagnosis of dental disorders in the horse. Equine Vet. ]. , 33: 49-58. Weller R, Weaver M, Livesey L, Bowen I M and Marr C M (2000) Nuclear scintigraphy with 99mTc-HMPAO labeled leucocytes in the assessment of horses with malabsorption.
Vet. Radiol. Ultrasound, 4 1 : 563.
Bernard W V, Reef V B, Reimer] M, Humber K A, Orsini] A ( 1 989) Ultrasonographic diagnosis of small-intestinal intussusception in three foals.]. Am. Vet. Med. Assoc., 1 94:395-397. Klohnen A, Vachon A, Fischer A ( 1 996) Use of diagnostic ultrasonography in horses with signs of acute abdominal pain.]. Am. Vet. Med. Assoc., 209 : 1 597-1606. Santschi E M, Slone D E, Frank W M ( 1 993) Use of
Breath hydrogen tests Bracher V and Baker S] ( 1 994 ) . Breath tests for investigation of gastrointestinal disease. nquine Vet. Educ. 6: 1 73-6 Murphy D, Reid S W] and Love S ( 1 998 ) . Breath hydrogen measurement in ponies: a preliminary study. Res. Vet. Sci. 65:47-51
39
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 't"1"' W,H, '*' "",",�X�"', "A,,) wh", fcc " ee'),''''''
There is a paucity of laparoscopic equipment that is man ufactured 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, insufflator, 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 Insufflators are used to create and maintain pneumo peritoneum, which is necessary for clear viewing and maneuvering the instruments and laparoscope in the abdomen. Commercial insufflators permit careful regulation of gas flow and intra-abdominal pressure. Because of the large size of the equine abdomen, a high flow insufflator (> 10 l/min) is recommended. Alternative methods of insufflation 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 filters 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 cavity 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 difficult, 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 sufficient 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 efficient 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 insufflation 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. An auto suture device (Figure 3.2) and specialized knots such as the modified roeder, jamming anchor knot, and Aberdeen knot can simplity an otherwise technically challenging procedure. Tissue specimen retrieval bags are helpful for intraoperative storage and subsequent removal
Figure 3.1 loop,
Endoscopy instruments (top to bottom): ligation
suction/lavage
forcep, Semm forcep
tip,
scissor,
atraumatic
grasping
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 3.2
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 modified 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
Figure 3.4
Hydraulic lift used to tilt the surgery table for
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
endoscopy on a horse in dorsal recumbency
Figure 3.3 A
Figure 3.5
custom-designed tilt table allows the horse to
A horse in dorsal recumbency is prepared to be
be positioned in the Trendelenberg position without
tilted into the Trendelenberg position. A chest brace prevents
exceeding a comfortable operating height for the surgeon
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 specific 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 significant 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 inflation 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 31 960/IlI) and protein concentrations (mean 2.5 g/dl) of peritoneal fluid within 24 hours of laparoscopy. As a comparison abdominal fluid collected from ponies 24 hours after exploratory celiotomy had mean leukocyte counts of 137 857/lll 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
standing endoscopy
paralumbar
fossa portal
during
3
LAPAROSCOPY
following celiotomy to evaluate surgical results if they are in question (e.g. integrity 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 3.8
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 3.7b
Ventral colon in a dorsal pOSition. Diaphragm
(D), spleen (Sp), and stomach (St) are visible in the
Figure 3.10
periphery
abscess
Laparoscopic-guided aspiration of a hepatic
45
3
LAPAROSCOPY
Surgical procedures PRESURGICAL PREPARATION FOR LAPAROSCOPY
Figure
3.11
mesentery
Incarceration
in the
inguinal
and ring.
adhesion This
of
jejunal
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
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 feeding 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 difficult, 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
LAPAROSCOPY
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 confirm 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 film. 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 insufflating 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 first. 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 firm twisting motion, being careful to prevent excessive pen etration of the abdominal wall. Directing the trocar in a slightly ventral direction prevents i�ury to the
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. As 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. As 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 cavity 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. Insufflation 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 insufflated sufficiently 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 identified. 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
3
LAPAROSCOPY
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, CA).
BIBLIOGRAPHY
Figure
3.14
Trendelenberg
Horse
undergoing
position.
This
laparoscopy
approach
allows
in
the
better
access for operative procedures of the caudal abdominal cavity
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 University 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 adhesiolysis in a standardbred filly. Vet. Surg. 26:258. Boure L, Marcoux M, Lavoiej P (1998) Use of laparoscopic equipment to divide abdominal adhesions in a filly.] Am.
Vet. Med. Assoc. 212:845.
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
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.
Equine Pract. 38:165. Fischer A T (1991) Standing laparoscopic surgery, Vet. Ctin.
N. Am. Equine Pract. 7:641. Fischer A T (1999) Laparoscopically assisted resection of umbilical structures of foals.] Am. Vel. Med. Assoc.
214:1813. Fischer A T,jr (1997) Diagnostic and surgical laparoscopy. In Equine Endoscopy 2nd edn,j L Traub-Datgatz, C M Brown (eds). C V Mosby, St Louis, pp. 217-31. Fischer A Tjr, Vachon A M (1992) Laparoscopic cryptorchidectomy in horses.] Am. Vet. Med. Assoc.
201:1705. Fisher A T, Lloyd K C K, Carlson G P el al. (1986) Diagnostic laparoscopy in the horse.] Am. Vet. Med. Assoc. lR9:289. Fischer A T, Vachon A M, Klein S R (1995) Laparoscopic inguinal repair in two stallions.] Am. Vet. Med. Assoc.
207:1599. Galuppo L D, Snyderj R, Pascoe j R (1995) Laparoscopic anatomy of the equine abdomen. Am. ] Vet. Res. 56:518. Galuppo L D, Snyderj 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
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LAPAROSCOPY
Hendrickson D A, Wilson D G (1997) Laparoscopic cryptorchid castration in standing horses. Vet. Surg. 26:335. HulkaJ F , Reich H (1994) Textbook of Laparoscopy. W B Saunders, Philadelphia, p. 47. Hurd W W, Pearl M L, DeLanceyJ 0, et al. (1993) Laparoscopic injury of abdominal wall blood vessels: a report of three cases. Obstet. Gynecol. 82 (4 pt 2, supp!.):
673-676. Mehl M, RagleC, Mealey R (1998) Laparoscopic diagnosis of subcapsular splenic hematoma in a horse. .J. Am. Vet. Med.
Assoc. 213:1171. Palmer S E (1993) Standing laparoscopic laser technique for ovariectomy in five mares . .J. Am. Vet. Med. Assoc. 203:279. RagleC A (1999) Urinary tract surgery in the adult horse. Proceedings of the 9th annual ACVS symposium, pp. 164-7. RagleC A, Schneider R K (1995) Ventral abdominal approach for laparoscopic ovariectomy in horses. Vet. Surg.
24:492. RagleC A, Schneider R K, Southwood L L (1996) Abdominal laparoscopy in horses. Compo Cont. Educ. Pract. Vet.
IS:1231.
RagleC A, Southwood L L, Galuppo L D (1997) Laparoscopic diagnosis of small colon ischemic necrosis following rectal
50
prolapse and mesocolic rupture in two postpartum mares. .J. Am. Vet. Med. Assoc. 210:1121. RagleC A, Southwood L L, Hopper S A, Buote P L (1996) Laparoscopic assisted granulosa cell tumor ovariectomy in two mares. .J. Am. Vet. Med. Assoc. 209:1646. RagleC A, Southwood L L, Howlett M R (1998) Ventral abdominal approach for laparoscopic cryptorchidectomy in horses. Vet. Surg. 27:138. RagleC A, Southwood L L, Schneider R K (1998) Injury to abdominal wall vessels during laparoscopy in three horses. .J. Am. Vet. Med. Assoc. 212:87. Santschi E M, GrindemC B, Tate L P, et al. (1988) Peritoneal fluid analysis in ponies after abdominal surgery. Vet. Surg.
17:6. Trostle S S, White N A, Donaldson L, et al. (1998) Laparoscopic colopexy in horses. Vet. Surg. 27:56. WalmsleyJ P (1999) Review of equine laparoscopy and an analysis of 158 laparoscopies in the horse. Equine Vet. .J.
31:456. Witherspoon D M, Kraemer DC, Seager S W J (1980) Laparoscopy in the horse. In Animal Laparoscopy, L M Harrison and D E Wildt (eds). Williams and Wilkins, Baltimore, p. 157.
4 Parasite-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., Cryptosporidium 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 confidence in the efficacy 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 sufficient sensitivity and specificity. Much of what is known about the clinical aspects of parasitic infections of the horse is derived either from general observations undertaken during artificial infections (large strongyles, cyathostomes, ascarids) or more recently from 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, definitive 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 Anoplocephala 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 external 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 propensity 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.
•
•
• •
Ascarids There is one species of ascarid - Parascaris equorum. Its essential features include • • •
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 Strongylus vulgaris, S. edentatus, S. equinus, and Triodontophorus spp. The essential features of the large strongyles include • a direct, migratory (intestinal arteries) lifecycle (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 • • •
•
54
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
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.
• •
•
a direct, migratory (gut-liver-lung-gut) life cycle a pre-patent period of 3 months the adult stages are small intestinal prolific egg producers adult and luminal larval stages are susceptible to modern anthelmintics migrating larval stages have low susceptibility to modern anthelmintics.
Tapeworms The three species of tapeworm that affect horses are Anoplocephala perfoliata (common) (Plate 4.2), A. magna, and Paranoplocephala 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. perfoliata) or small intestinal (A. magna and P. mammillana); the latter can also occur in the stomach
A. perfoliata 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 superficial 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 larval 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
PARASITE-ASSOCIATED GASTROINTESTINAL DISEASE
leakage. Foci of fibrous 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 superficial 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 flow in animals with Strongylus vulgaris 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 flow can result in either single or multiple areas of ischemic bowel wall, i.e. the entity known as non-strangulating intestinal infarction.
•
Non-strangulating intestinal infarction This is rare nowadays, reflecting the current low preva lence of Strongylus vulgaris 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 artery ischemic areas of either small and/or large intestine found at exploratory laparotomy
mesenteric arterial thickening and/or thrombus at post-mortem examination with possible grossly visible S. vulgaris lalVae.
Mild strongyle-associated colic This is suspected if there is non-specific 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 •
• •
CLINICAL FEATURES OF PARASITIC ASSOCIATED DISEASE 'ENTITIES'
4
• • • • •
•
•
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 lalVae 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
4 • • •
GASTROINTESTINAL PARASITES AND THEIR CONTROL
in only a few instances are there specific ancillary tests by which confirmation of an entity can be achieved.
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
• •
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 •
This occurs in aged ponies and is indicated by •
Clinical history
repeated bouts of diarrhea weight loss anorexia. •
Autumnal cyathostome-associated weight loss in weanlings This affects foals 6-9 months old, i.e. older foals eating significant 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-specific ill thrift or weight loss in older foals, weanlings and year lings, that can progress to emaciation unless treated. Occasionally there are concurrent non-specific respira tory signs including a nasal discharge and cough.
•
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-specific 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
is it full time, part time, or not at all? is it individual or shared? if it is shared, how many are in the cohort? what is the frequency and anthelmintic dosing: 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-simplifY 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 • •
Ascarid impaction (Plate
grazing management:
•
•
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 (FWEC). 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-
PARASITE-ASSOCIATED GASTROINTESTINAL DISEASE
laying stages. Also, it is notoriously difficult to correlate the FWEC with the size of the parasite burden giving further confusion to interpretation of test data. As 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 FWEC 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 FWEC 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 FWECs have high sensitivity for ascarid infection, they have low specificity, 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 FWEC 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)
• • •
4
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, Strongylus vulgaris 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
4
GASTROINTESTINAL PARASITES AND THEIR CONTROL
treatment plan. However, clinicians should consider the importance of potential side effects of anthel mintics when given in clinical disease. Specifically, there are reports which suggest possible associations between 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). Specific anthelmintic therapeu tic regimens are preferred for the different parasite associated diseases.
•
• •
• •
• •
•
• •
• • •
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 •
•
•
•
•
•
•
fenbendazole 7.5 mg/kg on 5 consecutive days day 6 ivermectin 0.2 mg/kg or moxidectin* 0.4 mg/kg days 16-20 fenbendazole 7.5 mg/kg on 5 consecutive days day 21 ivermectin 0.2 mg/kg or nil (if moxidectin" was given on day 6) days 31-35 fenbendazole 7.5 mg/kg on 5 consecutive days day 36 ivermectin 0.2 mg/kg or moxidectin 0.4 mg/kg thereafter follow the protocol for grazing cohorts (see below). days 1-5
*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
58
days 1-5
fenbendazole 7.5 mg/kg
or
or
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).
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 between-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. •
•
days 91-95 day 96
or
Repeat treatment at 14-21 day intervals on three targeted occasions.
to treat as often as the lO-day intervals suggested for ivermectin.
In-contact grazing cohorts are treated with the follow ing regimen
day 61-65 day 66
or
Ascarid-associated disease can be treated with either
This condition can be treated with •
days 31-35 day 36
either ivermectin 0.2 mg/kg, moxidectin 0.4 mg/kg fenbendazole 7.5 mg/kg either ivermectin 0.2 mg/kg, moxidectin 0.4 mg/kg fenbendazole 7.5 mg/kg either ivermectin 0.2 mg/kg, moxidectin 0.4 mg/kg fenbendazole 7.5 mg/kg either ivermectin 0.2 mg/kg, moxidectin 0.4 mg/kg.
Ascarid-associated disease
•
Non-strangulating intestinal infarction
day 6
• •
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
PARASITE-ASSOCIATED GASTROINTESTINAL DISEASE
•
•
•
•
• •
•
•
•
•
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. Strongyle (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 interval 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
,.4;.1.
•
•
4
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 specific 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 efficiency of the anthelmintic in reducing fecal egg output using
"'1S\!�·,,"dIod,
Programs
1. Interval dosing
Guidelines
Comments
Year round pro-/benzimadazoles,
Synchronized dosing of all animals
4-6 weekly; ivermectin, 8-10 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
4
•
GASTROINTESTINAL PARASITES AND THEIR CONTROL
FWEC results from one fecal sample taken pre treatment (day 0) and one sample taken on day 10-14 post-treatment); ideally the FWEC 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)
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 larvae 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.
Cryptosporidium spp. (see Chapter
27)
These parasites • •
•
can cause diarrhea in immunocompromised foals infection can be detected using serum antibody or fecal tests (specific techniques are required for fecal detection) in apparently healthy individuals there are no known effective therapeutic agents.
Coccidia spp.
A few case reports describe Eimeria 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) Paraswris equarum infections in horses. Camp. Cant. Educ. Pract. Vet.
12:110-18.
Oxyuris equi
This is the common large intestinal pinworm •
•
60
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).
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. Prart. Vet. 20: 100-6. Herd, R P (1986) Parasitology, 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 difficulty 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 nerve (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 eflicient 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.
Oral examination Under sedation and with a Hausmann gag or similar mouth speculum in place, a detailed inspection of the oral cavity should be carried out. In particular, one should look for evidence of • •
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 abnormality of the pharyngeal or esophageal phase of deglutition.
Physical examination 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.
Nasogastric intubation Useful information can be obtained by attempting 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
•
• •
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 soft 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 findings 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 afflicted 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
difficulties 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 confirmation until the patient is considerably older. Other abnormalities which may cause dysphagia and which can be confirmed 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 fistula, 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
5
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 significantly 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 tongue 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 confirmed 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
5
UPPER ALIMENTARY TRACT DISEASES
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.
CONDITIONS COMPROMISING THE 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 Chapter
palatal
defects
(see
above)
(see
also
6)
These are discussed in Chapter 6. Iatrogenic palatal defects (see Chapter
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-laryngoplasty 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
6)
Excessive palatal resection in the treatment of DDSP is disastrous complication because it is irreparable. a 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. Nasopharyngeal cicatrization
Nasopharyngeal cicatrization limits the efficiency 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.
Pharyngeal neoplasia is rare in horses, and most of these proliferations turn out to be lymphosarcoma. Retropharyngeal 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.
CONDITIONS COMPROMISING THE ESOPHAGEAL PHASE OF DEGLUTITION Fourth branchial arch defects
See above Conditions compromising the pharyngeal phase of degluttion. Abscessation and neoplasia causing external 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
5
DIFFERENTIAL DIAGNOSIS AND EVALUATION OF DYSPHAGIA
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 firm ingesta and passage of a stomach tube beyond the pharynx is generally not possible. Strictures 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'. Confirmation of the diagnosis is best achieved by contrast radiography. Dysautonomia (grass sickness) (see Chapter
Rupture of the esophagus (see Chapter
7)
Esophageal rupture carries a poor prognosis unless the patient is presented for treatment soon after the injury 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, definitive diagnosis and, when applicable, methods of treatment.
17)
Grass sickness produces dysphagia in its acute form but colic in the sub-acute and chronic forms. The condition is st'en in horses of all ages throughout the UK and northern Europe, but has been reported only once in Australia. Afflicted horses are generally severely dt'pressed, 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 vitro diagnostic test, but the radi ographic demonstration of esophageal stasis and the endoscopic identification of ulceration of the esophageal mucosa are helpful pointers to the likely diagnosis.
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. Pract. Vet. 10:1301-7 and 1405-10. Brown C M (1992) Dysphagia. In Current Therapy in Equine Medicine3rd edn, N E Robinson (ed.). W B Saunders,
Philadelphia, pp. 171-5. Freeman D E (1980) Diagnosis and treatment of diseases of the guttural pouch. Parts 1 and 2. Compo Cont. nauc. Pract. 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 Rucker Equine dental disorders are quite common, a preva lence of 1 0-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 difficulty.
DENTAL ANATOMY
more on the buccal side and the maxillary teeth wear more on the palatial aspect, producing a slope to the occlusal surface of 1 0-15 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 first 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 fills 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 fills 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.
NOMENCLATURE Traditionally teeth have been identified 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 =
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 maxillary cheek teeth (anisognathism) , and grinding of forage is done with a side-to-side motion of the mandible. Consequently, the mandibular teeth wear
=
=
=
69
6
UPPER ALIMENTARY TRACT DISEASES
than one name for the same tooth, i.e. the right upper third premolar is also the right upper second cheek tooth. The Modified Triadan System identifies teeth numerically according to their location. Each tooth has a three digit number describing its position. The first digit of the number represents the quadrant of the head. The first 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 digits identity 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 Modified Triadan system allows for the presence of a lower wolf tooth. Deciduous teeth are indicated by substituting the numbers 5 to 8 for the first digit beginning again with the upper right side of the head, thus 807 designates the deciduous right lower third premolar. This system simplifies written and computer records.
AGE DETERMINATION 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 profile. Mter 20 years molar wear may aid in aging because the upper first 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 types breed dental care vices trauma malocclusion.
DENTAL ERUPTION 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.
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 fine 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
Eruption 6-8 days 4-8 weeks 5-9 months 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
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
70
In Wear 3 years 4 years 5 years
3-4 months later 3-4 months later 3-4 months later 2 years 3 years 4 years
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
6
Cups and stars
Incisor profile
Incisors have an invagination of the enamel layer on the occlusal surface that is partially filled 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 first incisors (301 and 401) at 5-7 years, lower intermediate incisors (302 and 402) 6-9 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. As 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) cavity 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 01s, 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.
In young horses the incisors meet at an obtuse angle, almost vertically. The angle gets more acute with age. The incisor profile is not an exact age determiner but it helps in age approximation.
SIGNS OF DENTAL DISEASE 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 cavity 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: •
•
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 14-1 7 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.
•
• •
• •
•
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 feces poor body condition dorsal displacement of the soft palate swelling or bumps on the maxilla or mandible purulent drainage from fistulae 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
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 halfway 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.
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
6
UPPER ALIMENTARY TRACT DISEASES
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.
DEVELOPMENTAL DISORDERS 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.
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
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 identified 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, firm, 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 fistulae, are odontogenic cysts frequently containing stratified 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.
6
Cysts
Fluid filled cysts occasionally occur in the mandible, maxilla, and paranasal sinuses. They produce a variable degree of facial deformity and present as a smooth, firm, non-painful, gradually enlarging swelling. Aspiration of a pale yellow clear to turbid fluid 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. Retained deciduous teeth
Retained 'caps' may occur in either the incisor or molar arcades. The erupting permanent tooth normally dis rupts 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 firmly 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
6
UPPER ALIMENTARY TRACT DISEASES
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.
secondary dentine production preserves 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 frac 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 disease
Periodontitis is •
•
These terms do not identifY the cause and one classifi cation may progress to another.
• • •
Infundibular disease 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 first 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
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 acljacent 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 first 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
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
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 reserve 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 gra �u lates in and covers with gingiva in 2-3 weeks. GlVe systemic an tibiotics effective against anaero i � and . . gram-negative bacteria when widespread gmglVItlS or regional lymph nodes are enlarged. Slightly unstable teeth should be left in situ as long as possible. Removing occlusion by grinding down th opposing tooth will enable the diseased tooth to stabI lize in some cases.
�
�
Periradicular disease is infection or inflammation of the pulp and surrounding tissue. Synonymous ten s ar alveolar periostitis, periapical osteitis, and chrOnIC OSSI tying periostitis. One text defines periodontal disease as alveolar periostitis. Signs include
�
•
painful bony swelling external or intra-oral fistula 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 affected 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 draini g tract. This more severe form has been termed chronIC ossitying periostitis. Contrast radiology will help deter mine tooth involvement and extent of the fistula. 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 4-8 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 filling the pulp cavity has had limited success. Mandibular teeth are better candidates than maxillary teeth because of their simpler root structure.
�
Antibiotic therapy
Peri radicular disease
•
•
6
�
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 l.kg Lv. q. 6 h can be substituted for procame penICIllin. If Bacteroides Jragilis is suspected, penicillin may be
�l!
75
6
UPPER ALIMENTARY TRACT DISEASES
combined with metronidazole, 1 5-20 mg/kg p.o. q. 6-8 h. Ceftiofur, 2-4 mg/kg i.v. or i.m. q. 8-1 2 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 significant, 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 worn 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 surface. Correction is initially done with a grinder and then finished 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 every 6 months until both arcades are nor mal in exposed crown height and angle.
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
6
Table ang les
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 difficult 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 first, 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 -t
thin arrows
=
=
abnormal occlusial forces
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
6
UPPER ALIMENTARY TRACT DISEASES
Disorders of the mouth MA Ball INTRODUCTION 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 inability 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.
PHYSICAL EXAMINATION 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
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. Actinobacillus lignieresii can 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.
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.
ETIOPATHOGENESIS OF ORAL CAVITY DISEASE AND PTYALISM Factors causing oral cavity disease and ptyalism 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
Figure 6.2
infection)
Wooden tongue (Actinobacillus Jignieresii
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
6
DIAGNOSIS 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 ability 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.
Figure 6.3 Weight loss and dysphagia due to squamous cell carcinoma of the oral cavity
TREATMENT Treatments may include • • • •
• •
removal of foreign bodies tooth extraction antibiotic therapy for infectious causes intravenous fluids to replace and maintain fluids 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.
Cleft palate SA Semevolos and NG Ducharme INTRODUCTION 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, defined as sufficient 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.
ANATOMY, EMBRYOLOGY, AND PHYSIOLOGY 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
6
UPPER ALIMENTARY TRACT DISEASES
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 stratified columnar ciliated epithelium on the nasal aspect and keratinized stratified 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 palatopharyngeus 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 nerve.
ETIOLOGY 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 fied 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 in utero. Acquired cleft palates are a complication of dental or upper airway surgery. Hard palate clefts, perhaps 80
better defined as oronasal fistulae, 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 specific 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.
PATHOPHYSIOLOGY 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 significant air way contamination and therefore result in less or no lower airway disease. The respiratory 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.
SIGNALMENT AND HISTORY There is no breed or gender predisposition for congen ital cleft palate, and the condition is discovered in most cases in the first 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 observed cleft palate in association with wry nose.
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
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.
6
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 soft 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 difficulty in making this diagnosis are related to the quality of equipment used, the endoscopic field-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 field of view be used. Pediatric endoscopes have a small field of view and are a reason for failing to identify a cleft palate. Whenever possible, a regular endoscope (810 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).
CLINICAL SIGNS 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 severity of the most common complica tion of this disease, chronic infection of the lower air ways, will significantly influence the survival rate.
INVESTIGATION AND DIAGNOSIS
Figure 6.5 The caudal midline of the soft palate is the most commonly affected area in horses with congenital cleft
A presumptive diagnosis of congenital cleft palate can be made based on clinical signs alone. A definitive
palate (note: the oropharynx mucosa can be seen during nasal video endoscopy)
81
6
UPPER ALIMENTARY TRACT DISEASES
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 observation 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.
TREATMENT 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 airway 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 cavity 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 between 2-4 weeks after birth.
Surgical .pproach
Adv.nt.....
Transhyoid pharyngotomy
Allows surgical access to caudal two-thirds of the soft palate. Animal Is more comfortable postoperatively.
Mandibular symphysiotomy
Allows surgical access to the hard palate and rostral third of the soft palate.
82
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 insufficient 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••dv.nt..... Illumination must come from . surgeon's headlight or placement of a flexible oral light. Possible damage to hyoepiglotticus muscle leading to exercise intolerance because of epiglottic retroversion. Invasive procedure. More discomfort to animal. Requires orthopedic instrumentation for fixation of the mandible. Higher morbidity associated with fixation (e.g. pin migration, draining tracts)
6
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
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
the intended site for screw fixation after the symphys iotomy. The symp hysis 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
Basihyoid bone
mandible and access to the palate. The incision is closed
as
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. in
a simple
interrupted or cruciate pattern.
mandible is fixed with an appropriate length
1)
The
4.5 mm
screw placed in lag fashion. Alternatively cross pinning Thyroid cartilage
Incision site
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
Figure 6.6 Mandibular symphysiotomy - note the incision
is closed with absorbable suture (no.
0) in a simple
site extends from the basihyoid bone rostrally to the mandi bular symphysis
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
6
UPPER ALIMENTARY TRACT DISEASES
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
interrupted pattern. The mylohyoid muscle and sub
cartilage to the rostral extent of the basihyoid bone.
cutaneous tissues are re-apposed separately with an
The incision is extended by bluntly separating the
0) in a simple continuous
sternohyoid muscle on the midline. The basihyoid bone
absorbable suture (no.
pattern. The skin is closed in a routine manner.
is separated longitudinally using an osteotome. The incision is extended deeper by blunt dissection of the
Transhyoid pharyngotomy
loose fascia between the pharynx and basihyoid bone. It is crucial that the fascia encircling the hyoepiglotticus
8-10 em ventral midline incision is
muscle be identified and retracted laterally so it does
made extending from the caudal extent of the thyroid
not damage this muscle or its innervation. The pharyn-
An approximately
84
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
Incision line
Palatine artery
/
) Cleft
Ridge in hard palate
Figure 6.10 A mucosa-periosteaI-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 monofilament 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 sternohyoid 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. Cleft 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. 1 2 curved Parker-Kerr blade, the nasal and oral mucosa at the axial edge of the cleft are incised to the hard palate, thus separating the nasal mucosa-periosteal flap from the oral mucosa periosteal flap. An incision parallel to the long axis of
6
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 monofilament absorb able suture (no. 0 or no. 1 ) . The defect at the donor site is left to heal by second intention. Soft 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 airway impedance. Therefore, these procedures should not be performed in horses intended for athletic performance. If adequate soft palate tissue is 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 curved 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 monofilament 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 monofilament absorbable suture material (no. 0) creating the strength layer of the closure (Figure 6.11c). Finally, the everted oral mucosal layer is apposed using a monofilament absorbable suture material (no. 00) in a simple contin uous pattern (Figure 6.11d) . Another technique, the double opposing Z-plasty, first 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 significant soft palate 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
6
UPPER ALIMENTARY TRACT DISEASES
b)
a) Nasal mucosa
Cleft palate
.=,.:". = .. ---,--".,--'T-rr-ri7'''(...
-
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 vertical 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 . 1 2a) . 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.
PROGNOSIS The overall morbidity rate for complications after cleft 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 sufficient healing to resolve clinical signs. Short-term morbidity is higher for the mandibular symphysiotomy approach than the transhyoid 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
DISEASES OF THE ORAL CAVITY AND SOFT PALATE
a)
6
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 identified 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.
PREVENTION Because the etiology is not well understood prevention may be difficult. 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 affected with congenital cleft palate.
BIBLIOGRAPHY Signs of dental disease Baker G] ( 1 99 1 ) Disease of the teeth. In Equine Medicine and Surgery 4th edn, vol 2, P T Colahan,] G Mayhew, A M Merritt,] N Moore (eds) . American Veterinary Publications, Santa Barbara CA, pp. 550-70.
Baker G] ( 1 970) Some aspects of equine dental disease. Equine Vet. ] 2 : 105-10. Baker G] ( 1 971 ) Some aspects of equine dental radiology. Equine Vet. ] 3:46-5 1 . Baker G ] ( 1 974) Some aspects o f equine dental decay. Equine Vet.] 3 : 1 27-30. Baker G] ( 1 985) Oral disease of the horse. In Veterinary Dentistry, C E Harvey (ed. ) . W B Saunders, Philadelphia, pp. 203-35 . Baker G] ( 1 99 1 ) Dental morphology, function and pathology. In Proceedings o/the 3 7th Annual Convention o/the American Association 0/Equine Practitioners, San Francisco, . pp. 83-93. Dixon P M ( 1 997) Dental extraction and endodontic techniques in horses. Comp. Cont. Educ. Pract. Vet. 19:628-38. Dixon P M ( 1 997) Dental extraction in the horse: indications and preoperative evaluation. Comp. Cont. Educ. Pract. Vet. 19:366-75.
87
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Easley K] ( 1 996) Equine Dental Development and Anatomy. In ProceedinKs oJ the 42nd Annual Convention oJ the American Association oj Equine Practitioners, Denver CO. pp. 1 - 1 0. Easley K] ( 1 99 1 ) Recognition and Management of the Diseased Equine Tooth . In Proceedings oJ the 37th Annual Convention oj the 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 Internal Medicine. Mosby, St Louis,
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 ojEquine Practitioners, Denver CO, pp. 1 1-2 1 .
Uhlinger C ( 19 9 1 ) Common abnormalities of premolar and molars I n Proceedings oJ the 3 7th Annual Convention oJ the
American Association ojEquine Practitioners, San Francisco,
pp. 1 23-7 .
pp. 688-97.
Gaughan E M and Debowles R M (eds) ( 1 998) Vet. Clin. N. Am. Equine Pract. Dentistry. 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 Pract. 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 K A ( 1 992) Brachygnathia in horses: 20 cases ( 1 9 79-1989) Vet. Med. Assoc. 200 ( 5 ) : 7 1 5-71 9 .
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 oj Equine Surgery, N A White and ] N Moore (eds) . ] B Lippincott, Philadelphia, pp. 277-80 .
.f. Am.
Furlow L T ( 1 986) Cleft palate repair by double opposing Z plasty. Plastic &constr. Surg. 78:724-33.
Am. Equine Pract. The Equine Head. W B Saunders,
Gaughan E M, DeBowes R M ( 1 993) Congenital diseases of
Hance R S and Bertone A L ( 1 993) Neoplasia. In Vet. Clin. N. Philadephia, April, 9 ( 1 ) :2 1 3-34. Hawkins] F, Dallap D L ( 1 997) Lateral buccostomy for removal of a supernumerary tooth . .f. Am. Vet. Med. Assoc. 2 1 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 findings. Equine Vet. ]. , 29 (3) : 1 98-205 Kilic S, Dixon P M, Kempson S A ( 1 997) Dentine. Equine Vet. .f., 29 (3) :206-2 1 2 Kilic S , Dixon P M , Kempson S A ( 1 997) Cement and the amelocemental junction. Equine Vet. .f. , 29(3) : 2 1 3-21 9 . Lane ] G ( 1 994) A review o f dental disorders o f the horse, their treatment and possible fresh approaches to management. Equine Vet. Educ. , 6 ( 1 ) : 1 3-21 . Mueller P O E ( 199 1 ) Equine dental disorders: cause, diagnosis, and treatment. Compo Cant. Educ. Pract. Vet. 1 3, pp. 14 5 1-1 460. Rucker B A ( 1 996) Incisor procedures for field use. In Proceedings oJ the 42nd Annual Convention oJ the American Association oj Equine Practitioners, 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. iI'quine Pract. The Equine Head. W B Saunders, Philadelphia,
April, 9 ( 1 ) : 1 2 3-32.
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Cleft palate
the equine head. Vet. Clin. N. Am. Equine Pract. 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 : 1 07-9.
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. AJVR 58 ( 3 ) : 3 1 7-32 1 . Mason T A, Speirs V C, Maclean A A, Smyth G B ( 1 997) Surgical repair of cleft soft palate in the horse. Vet. Rec. 100:6--8. Nelson A W, Curley B M, Kainer R A ( 1 97 1 ) Mandibular symphysiotomy to provide adequate exposure for intraoral surgery in the horse . .f. Am. Vet. Med. Assoc. 1 59 : 1 025-3 1 . 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 ( 1 979- 1 997) . 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 fibers. 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. As time progresses, affected animals will become dehydrated and inappe tent. Diagnosis Physical examination The horse's hydration status is evaluated by assessing skin turgidity, mucous membrane color, and capillary refill 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
7
UPPER ALIMENTARY TRACT DISEASES
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 insufflated 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 ability to penetrate (increased kVp and rnA capacity.) 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. Gastrografin, ER Squibb and Sons, Inc., Princeton, r-.u) 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
ESOPHAGEAL DISEASES
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 difficult 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 identified and retracted.
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 variety of suture patterns are appropriate. Typically, a non-absorbable, non reactive monofilament suture such as polypropylene or nylon is recommended, or a long-lasting absorbable monofilament 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 monofilament suture using the sul:r 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 •
•
•
•
Esophageal layers When the esophagus is incised it separates easily into two distinct layers. The first layer is the outer, relatively
7
•
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
7 •
•
•
•
UPPER ALIMENTARY TRACT DISEASES
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 very 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 fibro sis, mediastinal abscessation and neoplasia, or vascular anomalies.
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
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 difficult 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). 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. Surgical therapy (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
ESOPHAGEAL DISEASES
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, 1 998). 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 difficult 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 cervical esophageal perforation quickly develop subcutaneous emphysema and cellulitis around the area. Unfortunately the cellulitis can extend down fascial planes toward the mediastinum and thoracic cavity. The horse may be so dyspneic that a tracheotomy is required.
7
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
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
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
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UPPER ALIMENTARY TRACT DISEASES
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 An esophagomyotomy is indicated for an esophageal
stricture confined 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 confined 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 serves 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 esophageal 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. Esophagoplasty 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. Esophageal replacement 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 applicability in the horse. Muscular patch grafting 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 identified 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. Fenestration through a cicatrix The final procedure reported for esophageal stricture is the one currently employed in our hospital. The esoph agus is isolated and an esophagotomy is performed
ESOPHAGEAL DISEASES
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. As 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 fibrous 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 fibers 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.
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 fistulae 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 fistulae 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 Figure 7.4
Pulsion diverticulum viewed via
esophagoscopy
7
Secondary healing of an esophagotomy site.
This horse had previous esophageal surgery and the tube was placed to permit extra-oral feeding
95
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UPPER ALIMENTARY TRACT DISEASES
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 defects 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.
7
ESOPHAGEAL DISEASES
I. It is difficult to work on the esophagus without
2.
3.
4.
5.
having resulting tension on the tissues. The esophagus is in constant motion due to swallowing and diaphragmatic movement, and there is constant irritation by food and saliva. 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. 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. 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'orations can be managed successfully with adequate ventral drainage and long-term wound care. In our experience, cranial esophageal perforations are exceedingly difficult to manage.
BIBLIOGRAPHY Aanes WA (1975) The diagnosis and surgical repair of diverticulum of the esophagus.
Proc. Am. Assoc. Equine
Pract. 21:211. Bowman KF, Vaughan] R, Quick C B,
et al. (1978) Am. Vet. Med. Assoc. 172:334. Craig D R, Shivy D R, Pankowski R L, et al. (1989) Esophageal Megaesophagus in a colt.]
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 Surgery 2nd edn,]A Auer and]A Stick (eds.). W B Saunders, Philadelphia, pp. 199-209. Hackett R P, Dyer R M, Hoffer 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 grafting 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. Cornell Vet. 66:589. Murray M], Ball M M, Parker GA (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 ofEquine 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 Repair of Viscera Wound Repair 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.
SamsA E, WeldonA D, Rakestraw P (1993) Surgical treatment of intramural esophageal inclusion cysts in three horses. Vet. Surg. 22:135-9. Scott EA (1982) Surgery of the equine oral cavity.
Vet. Ctin.
N. Am. Large Anim. Pract. 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 Grossman's Anatomy of the Domestic Animals 5th edn, R Getty
(ed.). W B Saunders, Philadelphia, p. 454. Stick]A, DerksenF], McNitt D L,
et al. (1983) Equine
esophageal pressure profile. Am.] Vet. Res. 44:272. Stick]A, DerksenF ], Scott GA (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
7
UPPER ALIMENTARY TRACT DISEASES
Stick] A, Robinson N E, Krehbiel] D
(1981) Acid-base and
electrolyte alterations associated with salivary loss in the pony.
Am.]. Vet. R£s. 42:733.
Stick]A, Siocombe RF, Derksen R], Scott EA
Am.]. Vet. R£s. 44:2123. Stick J H (1982) Surgery of the equine esophagus. Vet. Clin. N. Am. Large Anim. Pract. 4:33.
98
(1986) Comparison of
three feeding techniques after esophageal mucosal resection and anastomosis in the horse.
(1983)
Esophagotomy in the pony: Comparison of surgical techniques and form of feed.
Todhunter RJ, Stick] A, Siocombe RF
Todhunter RJ, Stick]A, Trotter G
Cornell Vet. 75:16. W, et al. (1984) Medical
management of esophageal stricture in seven horses.
]. Am. Vet. Med. Assoc. 185:784.
8 Etiology, risk factors, and pathophy siology 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 field 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, larval 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-specific (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 identified in multiple epidemiological studies to be associated with increased risk of colic. The meaning of this observation remains unknown. The association may be related to differing 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 cific 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 identified as a risk factor for colic. In one study the effect was mod ified 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 surgery for colic with future colic is important information for horse owners and farm managers.
particular activity 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.
FARM MANAGEMENT FACTORS
Surprisingly, there is little epidemiologic evidence 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, specific targeting of tapeworms may be nec essary for some farms. Administration of anthelmintics effective against larvae 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 larval 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.
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 results. 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 modified 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 sufficiently 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 shown to pre dispose to colic, although specific 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
PREVENTATIVE MEDICINE FACTORS
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 find an association between 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 significant change in weather during the 3-day period prior to examination was significantly associated with colic.
E TIOLOGY, RISK FACTORS, AND PATHOPHYSIOLOGY OF COLIC
Although clinical experience would suggest an associa tion of colic with weather-related factors, these factors have not been confirmed. 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 sufficient 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. Confirmation of the benefit 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 specific types of colic are needed.
Pathophysiology of intestinal obstruction DE Freeman
PATHOP HYSIOLOGY 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 filtration rate increase. If capillary filtration 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 infiltra 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
8
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 vitro 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 contracts 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 IV ischemic i�ury.
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-fixed mononuclear phagocytes release the cytokines, lipid-derived mediators, and coag ulation/fibrinolytic 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
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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 (PAF), 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.
MOTILITY DISTURBANCES IN INTESTINAL OBSTRUCTION Non-strangulating occlusion of pony jejunum causes loss of gastric contractile activity 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 motility 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
Cytokines, lipid-derived mediators, coagulation/fibrinolytic factors
�
Changes in cardiovascular and respiratory systems, motility, and coagulation
�
MEDIATORS OF CELL DAMAGE
Endothelial cell ATP
iCytosolic . calcium � Calpaln
Xanthine dehydrogenase
[H�2 2J0 2 0 +H +02 0 �===02==
Xan hine oxidase ypoxanthine
o�
·
Uric acid
Fe3+
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. A T P SOD
=
O2
oxygen; HOCI
=
PGI2
=
superoxide dismutase; O2 =
superoxide radical; OH
hypochlorous acid; PAF
prostaglandin 12; PGE2
=
methionyl-Ieukyl-phenylalanine
104
=
=
=
hydroxyl radical; HP2
platelet activating factor; LTB4
prostaglandin E2; PGF2a
=
=
=
=
adenosine triphosphate;
hydrogen peroxide; Fe3+
leukotriene B4; TXA2
prostaglandin F2u; PGD2
=
=
=
ferric iron;
thromboxane A2;
prostaglandin O2; fMLP
=
formyl
ETIOLOGY, RISK FACTORS, AND PATHOPHYSIOLOGY OF COLIC
stimulation appears to occupy a central role in its pathogenesis (see Chapter I I). Continuous infusions of prostaglandin E I (PGEI) 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 motility 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 i�ury 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 hypoperfusion 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 fibrin deposition and fibrinolysis in the peritoneal cavity. If fibrin is not removed, the ingrowth of fibro blasts and subsequent deposition of collagen converts fibrinous adhesions to fibrous adhesions. Plasmin, antithrombin III, and protein C are
8
responsible for fibrinolysis. Plasminogen is converted to plasmin by tissue plasminogen activator (tPA) , which is a key regulator of fibrinolysis. Inhibitors of fibrinolysis 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 NA (1990) Epidemiology and etiology of colic. In The Equine Acute Abdomen, NA White (ed.).Lea and Febiger, Philadelphia, pp. 49-64.
Pathophysiology of intestinal obstruction Allen D, White NA 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 EL (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 NA, et al. (1980) Effect of luminal distension on intestinal transcapillary fluid exchange. Am.] Physiol. 239:G516--G523. Hunt] M and Gerring EL (1985) The effect of prostaglandin E] on motility of the equine gut.] Vet. Pharmacol. 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 EL (1989) Observations on the colic motor complex in a pony with a small intestinal obstruction. Equine Vet.] Supplement 7:43-5. King] Nand Gerring EL (1991) The action of low dose endotoxin on equine bowel motility. Equine Vet.] 23:11. Moore] N and Barton M H (1998) An update on 105
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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
Rakestraw PC, Snyder] R, Woliner M], et ai. (1996) Involvement of nitric oxide in inhibitory neuromuscular transmission in equine jejunum. Am.] Vet. Res. 57:1206.
Snyder] R (1989) The pathophysiology of intestinal damage: effects of luminal distension and ischemia. Vet. Clin. North Am. Equine. Prac. 5:247-70. SouthwoodLL and Baxter G M (1997)Current concepts in
distension and neostigmine on jejunal vascular resisitance,
management of abdominal adhesions. Vet. Clin. N. Am.
oxygen uptake, and intraluminal pressure changes in ponies. Am.] Vet. Res. 50:54-8.
Equine Prac.
106
13:415.
�9
Clinical evaluation of the colic case
Clinical signs of colic
____I1If_____
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-specific, 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 fibers. 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 fibers 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 classify 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 107
9 • • •
• • • • • • • • • •
COLIC
inappetence backing up to the wall 'playing with' or 'nosing' water.
•
With moderate pain the following may be seen
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 tympany 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 presents with signs of depression (especially animals that are found like this first 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.
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
• •
dropping to the ground extreme restlessness other signs of pain listed above.
Figure 9.1 Mild colic cha racterized by restlessness and lying down more often than usua l
Figure 9.2 Moderate colic in a foal that is rolling repeat edly 108
Figure 9.3 Stretched out ('trestle table') appearance in a horse with a jejunojejunal intussusception
CLINICAL EVALUATION OF THE COLIC CASE
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 colic PD Van H a rreveld and E M 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 intervention it is important to consider diagnosis of obstructive disease as early as possible.
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. Availability 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 • •
HISTORY
• •
An accurate history will provide valuable information regarding current and past health and colic concerns. This can be very beneficial 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 observed 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
9
• • •
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 37.5-38.5°C. Increases in body temperature can occur after anxiety, excite ment, or exertion. Temperatures greater than 39.5°C may suggest an inflammatory or primary infectious 109
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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 refill time is usually 1 .5 seconds or less. When peripheral vascular circulation is impaired capillary refill 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 10
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 fill 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 hyperactivity 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 as 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
9
CLIN ICAL EVALUATION OF THE COLIC CASE
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.
ABDOMINOCENTESIS (see Chapter 2, Abdominocentesis and Analysis of peritoneal fluid) WIl���!Il!W�_W'11f
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 defini tive findings 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/ill (5.0 x 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 firmed 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 x 1 09/1) . Neutrophil counts greater than 50 000 cellS/ill (50 x 1 09/1) can be suggestive of an intra abdominal abscess or of primary 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. 111
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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 efficacy 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 specific 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 observed in horses with proximal enteritis or intra-abdominal abscesses. Severe leukope nia « 3000 celliIll, < 3.0 x 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 findings should always be considered in con1 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-filled cecum or large intestine. If these abnormalities are identified, extreme care must be taken when performing an abdominocentesis to avoid accidental enterocentesis. Occasionally, rectal examination findings clearly indicate the specific 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 specific diagnosis, but gives information regarding the severity of the problem and the need for surgical inter vention. Abnormal rectal examination findings 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 cavity in the horse limit palpation to the caudal 30-40 per cent. Because of the inability to examine the entire peri toneal cavity, subtle abnormalities identified on exami nation are often used to make inferences concerning the more cranial regions of the peritoneal cavity. Consequently, the lack of abnormal rectal examination findings 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 safety 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 romifidine (40-120 Ilg/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, 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 indicate a sand impaction or sand-induced colitis. In general, palpable characteristics of the abdominal contents and viscera are often helpful in identifying the particular segment of the intestine involved and the
CLINICAL EVALUATION OF THE COLIC CASE
severity of the condition. Severe gas-filled or ingesta-dis tended 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 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.
Figure 9.4 Caudal view of a sta nding horse demonstrating abdom inal structures that are palpable in the normal horse during rectal exa m inatio n . Starting i n the left dorsal abdom inal quadrant, and progressing in a clockwise direc tion, palpable structures include: caudal border of the spleen, renosplenic l igament, ca udal pole of the left kid ney, ventral cecal tenia, cecal base, and the pelvic flexure. Thel Melton, CAD special ists, Department of Educational Resources and Dr IN Moore, Department of Large Animal Medicine, U n iversity of Georg ia, Athens, GA 30602, with permission
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 two loops of easily compressible small intestine may be identified (Figure 9.5). As the disease progresses the distention increases and multiple loops of tightly dis tended, fluid-filled intestine are palpable side by side (Figure 9.6) . Non-specific small intestinal distention is the most common finding in horses with small intestinal lesions. However, specific findings identified on rectal examina tion will occasionally lead to a diagnosis. An ileal
Figure 9.5 Caudal view of a sta n d i n g horse demonstrating a n ileal i m paction with early small intestinal distention. The ileum may be palpable as a firm, tubu lar structure in the center of the abdomen coursing toward the cecum. Thel Melton, CAD specialists, Department of Educational Resources and Dr IN Moore, Department of Large Animal Med icine, U n iversity of Georg i a , Athens, GA 30602, with permission 1 13
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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 finding 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
Figure 9.6 Caudal view of a standing horse demonstrating severe sma l l i ntesti nal distention. Multiple loops of gas and fluid-distended sma l l intestine are pal pable. Thel Melton, CAD specialists, Department of Educational Resources a nd Dr IN Moore, Department of Large An imal Med icine, U n iversity of Georgia, Athens, GA 30602, with permission
impaction, detected early in the disease process, may be palpable as a firm, 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 specific 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 difficult to identifY per rectum, but early in the disease process is occasionally identified as a turgid mass in the right dorsal abdomen and sometimes it can be appreciated that it is within the cecum. Rectal examination findings 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 naso1 14
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 filling. Normally the cecal tenia should be loose and easily movable. With increased filling of the cecum with ingesta, the tenia become more taut and the cecum displaces toward the midline. As 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. As the cecum fills above the cecocolic orifice, complete obstruction occurs and the cecal base fills with fluid and gas (Figure 9.7) . The distended cecum fills the right dorsal and ventral abdominal quadrants. 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 difficult to distinguish during rectal examination. In cases of right dorsal displace ment of the large colon, the cecal base and tenia are dif ficult to feel, and the examiner's hand can palpate the
CLIN ICAL EVALUATION OF THE COLIC CASE
9
Figure 9.7 Ca udal view of a standing h orse demonstrating a primary cecal impaction. With i ncreased fi l l i ng of the cecum with i ngesta , the ten i a become more taut and the cecum displa ces toward the midline. As the cecum fills above the cecocolic orifice complete obstruction occurs and the cecal base fills with fluid and gas. Thel Melton, CAD special ists, Department of Educational Resou rces and Dr IN Moore, Department of Large Animal Med icine, U niversity of Georgia, Athens, GA 30602, with permission
Figure 9.8 Ca udal view of a standing horse demonstrating impaction of the ventral colon and pelvic flexure. The colon is enlarged and easily identifiable on palpation. The two free tenia of the ventral colon course i n a cranial to-caudal d i rection, from the left cra nial abdomen to the left caudal a bdomen. Thel Melton, CAD special ists, Department of Educational Resources and Dr IN Moore, Department of Large Animal Med icine, University of Georgia, Athens, GA 30602, with 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.
from soft and indentable to firm and indurated. With severe impaction, the colon may fill 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 tympany. Occasionally, however, the lesion may be identified on rectal examination. In these cases, the impaction or enterolith may be ballotted with the exam iner's fingertips, but cannot be palpated in its entirety. Abdominal surgery is generally necessary to confirm 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
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 identifiable 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. As 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
1 15
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(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 sufficiently 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 confirm the diagnosis of left 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 fill the left caudal abdomen and preclude examination of the renosplenic region. In this case, left dorsal displacement may be suspected but should be confirmed with percutaneous ultrasonogra phy. Displacement of the spleen medially and ventrally may be associated with left dorsal displacement, but this finding alone does not confirm the diagnosis of left dorsal displacement.
Right dorsal displacement of the large colon may assume a variety of anatomic configurations, but the common finding for all right dorsal displacements is displacement of the left ventral and dorsal colon lateral to the cecum (Figure 9 . 1 0 ) . 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 difficult 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 o r 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 fills
Figure 9.9 Caudal view of a sta nding h orse demonstrating a left dorsal displacement of the large colon. The left ven tral and dorsal colon are entrapped within the renosplenic space. The colon is palpable on the left side of the abdomen with the tenia coursing from the left cran iodor sal abdomen to the l eft caudoventral abdomen. Following the tenia cranially and d orsa lly, the examiner can feel the tenia enter the renosplenic space. Thel Melton, CAD spe cialists, Department of Educational Resources and Dr IN Moore, Department of Large Animal Med icine, U n iversity of Georg ia, Athens, GA 30602, with permission
Figure 9.10 Caudal view of a standing h orse demonstrat ing a right dorsal displacement of the large colon. The left ventral and dorsal colons a re displaced lateral to the cecum. The colon and associated tenia are felt immedi ately cranial to the pelvic can a l , coursi ng from the right caudal abdomen, transversely across the abdomen, and then conti n u ing toward the left cranial a bdomen. Thel Melton, CAD special ists, Department of Educational Resources and Dr IN Moore, Department of Large Animal Med icine, U n iversity of Georg ia, Athens, GA 30602, with permission
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CLIN ICAL EVALUATION OF THE COLIC CASE
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 cavity. 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.
Figure 9.11 Caudal view of a standing h orse demonstrat ing a volvu lus of the l a rge colon. The large colon fills the entire abdomen. The marked colonic distension causes the colon to fan-fold with i n the l i m ited space of the abdomi nal cavity. This is often evident as colonic tenia coursing transversely across the ca udal abdomen. Thel Melton, CAD special ists, Department of Educational Resources and Dr IN Moore, Department of Large Animal Medicine, U n iversity of Georgia, Athens, GA 30602, with permission
9
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 findings 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 difficult if not impossible.
Figure 9.12 Caudal view of a standing h orse demonstrat ing an impaction of the descend ing colon with secondary cecal and colonic tympany. I ndividual fecal balls and ha ustra of the descending colon are not usua l ly evident in h orses with descending colon impaction. The rectal ampulla is pul led ventrally a n d to the left of mid line, because of the weig h t of the ingesta in the descending colon and tension on the mesentery. Thel Melton, CAD specialists, Department of E duca tiona l Resources and Dr IN Moore, Depa rtme n t of Large Animal Medicine, U n iversity of Georgia, Athens, GA 30602, with permission 1 17
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 identified, the horse owner should immediately be informed of the situation, and emergency first aid procedures should be initiated (see Chapter 1 6) .
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 cific diagnosis, but yields information regarding the seg ment of intestine affected, the severity of the problem, and the need for surgical intervention. 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 findings and indicate intestinal obstruction and/or malposition ing. Rectal examination findings 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 intervention (see Decision for surgery) .
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 reproductive tract
Uterine torsion Dystoclas Uterine hematoma Uterine perforation Retained placenta Granulosa cell tumor Ovulation
Male reproductive tract
Orchitis Seminal vesiculitis
Urinary tract
Cystic calculi Renal calculi U reteral calculi Urethral calculi Pyelonephritis Cystitis R uptured bladder
Liver
Acute hepatitis Cholangiohepatitis Choledocholithiasis
Spleen
Splenic abscess Splenomegaly
Respiratory tract
Pleuritis Pleuropneumonia
Cardiovascular system
Aortoiliac thrombosis Aortic rupture Acute hemorrhage Myocardial infarction Pericarditis
False (non-gastrointestinal) colics T Mair
Colic is not a specific 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 difficult to differentiate from pain due to gastro1 18
Musculoskeletal system
Laminitis Acute exertlonal rhabdomyolysis
Nervous system
Tetanus Botulism Seizures Hypocalcemic tetany Equine motor neuron disease
9
CLINICAL EVALUATION OF THE COLIC CASE
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 Ma i r
INTRODUCTION The majority 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 flatulent 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.
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 as 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 efficacy for the control of abdominal pain are summarized in Table 9.2.
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 variety 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 effects of endotoxin
Drug
Dosage
Dipyrone
10 mg/kg
Efficacy poor to moderate
Phenylbutazone
2.2-4.4 mg/kg
poor to
Flunixin meglumine
0.25-1.1 mg/kg
good to
Ketoprofen
1.1-2.2 mglkg 0.2-1.1 mg/kg 10-4011g/k9 40-80 1lg/k9 0.034J.1 mg/kg 0.3-0.66 mg/kg* 2.0 mglkg 0.05-0.075 mg/kg** 0.3-0.6 mg/kg
moderate excellent
Xylazine hydrochloride Detomidine hydrochloride Romifidine hydrochloride Acepromazine Morphine sulfate Pethidine Butorphanol tartrate Pentazocine
good excellent excellent excellent poor good poor good poor to moderate
'Use only with xylazine or another alpha2 adrenoceptor agonist to avoid eNS excitement "Doses in the upper range may cause ataxia
1 19
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 effect 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 essary 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 COX1 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 efficacy 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 every 1 2 120
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 effects 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 Alpha2 agonist sedative drugs include xylazine, detomi dine, and romifidine. 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 alpha2 adrenoceptors in the CNS,
CLINICAL EVALUATION OF THE COLIC CASE
thereby decreasing neurotransmission. At a dose rate of 1 . 1 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 specific 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.
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 sufficient 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.
Detomidine Detomidine, another alpha2 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 observed 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.
Butorphanol 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 alpha2 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 effect 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 alpha2 adrenoceptor ago nist, even small doses of butorphanol may occasionally cause head jerking.
Rnmifidine Romifidine 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.
Pentazocine Pentazocine is a partial agonist which is slightly more effective than dipyrone but less effective than xylazine and flunixin in relieving visceral pain.
Acepromazine 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.
Spasmolytics
Narcotic analgesics The analgesic and sedative effects of these drugs result from interaction with central and/ or peripheral opioid receptors.
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 121
9
COLIC
even days creating tympany and complicating the initial problem with ileus.
not be administered longer than 3 days because of severe enteritis and possible magnesium intoxication.
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!.
Dioctyl sodium succinate (DSS) DSS is a surface-active agent with wetting and emulsifying 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.
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 paraffin) Mineral oil (liquid paraffin) 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. As a long-term treatment, it may be admin istered daily for several weeks to help eliminate sand from the large colon. Recently the efficacy 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 122
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 field 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 deficit. Horses with severe colonic impactions may benefit 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.
CLINICAL EVALUATION OF THE COLIC CASE
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 deficit. The bicarbonate deficit and replacement require ments are based on the volume of the extracellular fluid compartment, body weight, and base deficit as deter mined by arterial or venous blood gas analysis. The following formula is used to calculate this deficit bicarbonate deficit (mEq)
=
0.3 x body weight (kg) base deficit (mEq/l)
x
One half of the deficit should be replaced over the first 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 . Purified endotoxin-specific 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 afforded 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 beneficial, supplying protein, fibronectin, complement, antithrombin III, and other inhibitors of hypercoagulability.
9
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 f1unixin (0.25 mg/kg i.v. q. 8 h) effectively suppresses endotoxin-induced CYclooxygenase-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 inhibits 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 sulfate 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 five 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 2mg 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. Metoctopramide Metoclopramide is a non-specific 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 1 23
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 its analgesic properties by decreasing afferent traffic through small C fibers. 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 i�ury. Preliminary studies suggest that the proki netic effect of lidocaine may be useful in postoperative ileus. An 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 1 24
fasciculations, ataxia, and possible seizures. These signs are more likely to happen if the initial bolus is adminis tered too rapidly. Erythromycin 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 acetylcholine. 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 difficile in a small number of horses has led some clinicians to ques tion the safety of this therapy. Acetylpromazine (acepromazine) 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 acetylcholine 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
9
CLIN ICAL EVALUATION OF THE COLIC CASE
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 illl !
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.
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 • •
• •
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 propensity 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 insufficient fiber weather changes
but none of these has been proven. An 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 significant 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,
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 findings 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 significant findings 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, romifidine, 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. 125
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 difficulties, 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. An 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 inability to reach a specific diagnosis in all cases. Careful assessment and appropriate management of acute colic cases are of much greater importance than reaching a specific diagnosis. Indeed, in many cases of acute colic, a specific 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 eval126
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 final 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 serves 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 field) and where immediate surgery can be undertaken as and when deemed necessary. The surgeon is the most qualified 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 qualified judgment about the necessity 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 identified. 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 findings 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 severity of pain and progression of colic since its onset
CLI NICAL EVALUATION OF THE COLIC CASE
• •
•
•
• • •
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 specific diagnostic procedures. For example, a history of strangles ( Streptococcus 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
9
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 first 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 4-6 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. 1 27
9
COLIC
Fecal production The nature and quantity 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 classity the problem into one of three categories I . 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 first 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 field 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 fitting the third category may be treated on the farm with an appropriate analgesic and re-examined after a period of approximately 2 hours. At 128
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 first 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 system
Heart rate Pulse qual ity Appearance of mucous membranes Examination of the abdomen Abdominal d istention
Auscultation External palpation Rectal examination Abdominal paracentesis Nasogastric intubation State of peripheral perfusion 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.
CLIN ICAL EVALUATION OF THE COLIC CASE
Severe unrelenting pain Absence of response to a n a l gesics Rapid recurrence of pain following administration of analgesics Persistently elevated heart rate (especially over 60 bpm) Progressively rising heart rate Positive rectal findings Large quantities or persistence of gastric reflux Persistently reduced or absent borborygmi Serosanguinous peritoneal fluid with i ncreased total protei n and nucleated cell count Exudative peritoneal fluid indicating peritonitis Progressive cardiovascular d eterioration with rising PCV (> 55%), TPP, i njected or cyanotic mucous membranes, and prolonged cap i llary refill time (> 2 sec) Progressive abdominal d istention Profuse watery d i a rrhea Recurrent bouts of colic over a period of days or weeks, especially if the frequency of bouts or severity are increasing Chronic colic persisting > 24 hours where no diagnosiS has been reached
9
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
Colic - decisions for surgery EM Gaughan and PD Van H a rreveld
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 majority of horses with signs of colic do not require surgical therapy, when signs do suggest the need for surgery, 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, straightforward, timely decisions, based most often on physical examination findings 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
Many horses with colic have physical examination find 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.
Heart 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 1 29
9
COLIC
Diagnostic examination
Signs that suggest surgical exploration
Signs that suggest further monitoring and medical management
Temperature
Normal
Elevated
Heart rate
Elevated
Normal
Abdominal pain
Severe unrelenting
Mild
Rectal examination
Multiple distended loops of small intestine Tight tenia and haustra of the large colon Thickened edematous i ntestinal wall
Nasogastric Intubation
Reflux greater than 1 liter and pH > 5
Appearance of abdominal fluid
Opaque and dark to orange or brown/green
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 survival. 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 modified 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 1 30
Clear yellow color
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 justify 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. Nasogastric intubation 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
CLINICAL EVALUATI ON OF THE COLIC CASE
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 very 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 findings 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 findings.
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.
9
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. Specific 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. Surgery may be an earlier consideration in case management if a 131
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COLIC
chronic course is already known at the first 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.
patient and reduce morbidity during transport. Early aggressive treatment aims to • • • •
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. An 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 profiles 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
_r I
_7
r ?FUJIi IMIIII 711 J r
A Worster INTRODUCTION The objective of preparing a referral patient is to improve or stabilize the hemodynamic status of the 132
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 significant 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 4gauge 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) , 1 4-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, KY) 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 deficit within
9
CLINICAL EVALUATION OF T H E COLIC CASE
Body weight deficit (%)
Liter deficit (SOO.kg horse)
Clinical signs
Mild
5-7
25-35
Decreased skin turgor
Moderate
8-10
40-50
Sunken eyes, depression
Severe
>10
>50
Cold extremities, recumbency
the interstitial spaces. To estimate replacement volume of fluids needed, use per cent dehydration x 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 confined and adequately con trolled. Adequate analgesics, such as alpha2 adrenergic agonists and anti-inflammatory drugs, are important for mediation of pain. Alpha2 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
profound analgesic effect 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 alpha2 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 beneficial 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 typhimurium) 1 .5 ml/kg i.v., dimethylsulf oxide (DMSO) 0.5-1.0 g/kg i.v. b.i.d., and pentoxi fylline (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 of hyperimmune 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 1 33
9
COLIC
that can accompany endotoxemia. Interestingly, numerous studies have shown no benefit in intestinal reperfusion injury with DMSO administration. PentoxifYlline decreases tumor necrosis factor and interleukin-5 release by macrophages, decreases throm boxane B2 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 pentoxifYlline use more appropriate in postoperative colic or after stabi lizing hypotension in medical cases.
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 signifi cant gastric distention from small intestinal disease. The nasogastric tube should be secured to the halter (Figure 9 . 1 3 ) and the distal limbs should be wrapped prior to transport.
GASTROINTESTINAL PREPARATION
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.
Nasogastric intubation with a large diameter ( 1 .5 cm or 5/8 in) tube is essential in horses with small intestine
CONCLUSION
Intravenous 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 • •
Figure 9.13 Nasogastric intubation . The nasogastric tube should be secured to the halter prior to transportation 1 34
• •
when to replace it whether or not to bandage the frequency of heparinization signs of complications.
CLIN ICAL EVALUATION OF THE COLIC CASE
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.
and can be left in place for longer. Polyurethane over the-needle catheters are indicated when •
•
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-needle 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 difficult because of either restraint problems or difficulty in visualizing the vein help is minimal.
9
•
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.
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 stiffness 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 difficult placement, fraying of the catheter tip may occur enhancing thrombogenecity.
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 catheters Polyurethane catheters can be purchased as over-the needle or over-the-wire types. Polyurethane over-the needle catheters are more expensive than Teflon over-the-needle catheters but are less thrombogenic
Polyurethane through-the-needle catheters These catheters are also available in different lengths. These are excellent catheters but some veterinarians find the peel-off-needle more awkward than the over the-wire method. 1 35
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 filled with heparinized saline prior to jugular puncture. The over-the-wire method is demonstrated in Figures 9.14, 9 . 1 5, and 9.16. After
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 j ugular 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 9.14 The l-wire is pushed through the adaptor and needle into the lumen of the jugular vein
Figure 9.15 The polyurethane catheter is fed over the wire into the jugular vein
1 36
Figure 9.16 The catheter placement is complete and the wire i s withdrawn. The catheter hub and the attached extension can now be sutured to the skin
CLINICAL EVALUATI O N OF THE COLIC CASE
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 anticoagulants. The two 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 j ugular 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,
9
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 gastrointestinal 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 dry 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 twice 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. 1 37
9
COLIC
Fluid and electrolyte therapy and acid-base balance in horses with abdominal pain (Figure 9.1 7) Jii&
T Divers
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. 1 38
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. An 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 findings 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 specific gravity.
A 1 gil increase in plasma protein suggests a 7-8 per cent loss in extracellular fluid.
THERAPY - INTRAVENOUSLY ADMINISTERED FLUIDS
-------.;;..;;.; .;;. .;;;.",. ;;. -, --...-.
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 2-4 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-
Horse appears dehydrated·
appears dehydrated but no obvious perfusion abnormalities
2-4 mllkg
Hypertonic saline followed
by polyionic crysta lloid 3-10 mllkglhr
/1
No urine produced within
I
hr
Impaction Colic
Horse
and has proof perfusion+
I
/�
Protein and PCV remain
Administer 3-12
deficit over
mllkglhr of polyionic
6-12 hours; provide for
maintenance and additional losses
between 4.0-4.5 g1dl.
Horse
PCV, protein,
deteriorates
/'
maintain protein in that
heart rate, perfusion normal
pressure returns to normal,
exam, ultrasound or
peripheral pulses normalize,
PCV remains high which
catheterize bladder to
heart rate decreases, color
suggests leaky membranes,
Continues at 1.5
determine (urine
and CRT of membranes
protein-losing enteropathy
maintenance
production)
improved
or peritonitis; perfusion
mllkglday) and
pressure low, increased
additional losses
Continue with
andlor
low and no
polyionic crystalloids
evidence of
signs of
4-10 mllkglhr
overhydration
overhydration
depending upon
and I ittle or
losses and physical
no urine
parameters, blood pressure and lab findings
Treat for oliguric renal failure
polyionic crystalloids 1 0 mllkglhr and
range until impaction is relieved
=
L
of polyionic crystalloid plus losses equal to reflux over
6-1 2 hrs
I Give 5% X BW (kg)
=
L
of polyionic crystalloid over 6-12 hours if
desirable - oral fluids may be used here
Protein drops below normal, Reassess
x
(60-120
anion gap, persistently high
CVP normal or
Stop IV fluids
Give 5% x BW (kg)
Continue fluids to
within normal range, blood
Continue with
No reflux
crystalloid until plasma
protein, jugular
I�
Reflux present
protein is maintained
distention and rectal
CVP high
/ �
Estimate % dehydration and replace
Adequate urine produced
Check CVP± , PCV,
appears dehydrated Perfusion pressures normal
Horse
�
�
heart rate
n C Z
� rm
Add colloids (plasma and/or Hetastarch),
�
continue crystalloids, reassess need for surgery
Urine produced
add colloids
Figure 9.1 7 Guide for intravenous fluid therapy i n horses with abdominal pain
*
decreased skin turgor, dry mucous
membranes + slow CRT, cold extremities, discolored mucous membranes, high heart rate
r C
�
o
z o
"T1 -I ::I: m
n o r-
R
�
m W ID
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 4-10 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) . An 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 -I without colloids such that plasma protein decreases to < 4.5 g/ dl. The increase in hydrostatic pressure and 140
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 benefit 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, gravity 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
CLI NICAL EVALUATIO N OF THE COLIC CASE
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, romifidine, 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 4-gauge catheter through the flank (after sterile preparation and local anesthesia) and into the colon.
specific 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 • • • • •
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 difficult to do without surgical exploration. However, numerous studies have attempted to identify
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 (pev) 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 pev and hypoproteinemia (Total protein < 50 gil or 5 g/dl) have a poorer prognosis than those with a similarly ele vated pev and normal serum protein. Blood lactate levels, a measure of peripheral tissue hypoperfusion, in the range of 0-75, 76-- 1 00, and greater than 1 0 1 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 • • •
•
• •
Prognosis for acute abdominal pain
9
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 activity 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 ability 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
Lo�tlon of lesion
elllsslflc.tlon of I.slon
Sltort term survlv.1 (,,) ...
STOMACH
U lcers and associated obstructions
Insufficient data
SMALL INTESTINE (non-ileal)
Strangulating and non-strangulating i nfarction
85
SMALL INTESTINE (non-ileal)
Simple obstruction
90
SMALL INTESTINE (ileum)
Strangulating and non-strangulatlng i nfarction
68-70
SMALL INTESTINE (ileum)
Simple obstruction
90-100
CECUM
Strangulating and non-strangLllating i nfarction
60
CECUM
Simple obstruction
80-90
LARGE COLON
Strangulating or non-strangulating i nfarction
40-50
LARGE COLON
Simple obstruction
80-90
LARGE COLON
Agenesis o r atresia
poor
SMALL COLON
Non-strangulating or non-infarctin g
65
SMALL COLON
Simple obstruction
75
SMALL COLON
Agenesis/atresia
poor
PERITONEUM
Septic Inflammation
50
"The information in this table is given as a guideline only, many other risk factors such as status of cardiovascular disease, extent of lesion, degree of peritoneal contamination, and experience of the surgeon and anesthetist, must also be considered "" Long term survival rate can be estimated at 5-10% less than short 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 very good prognosis with surgical intervention. 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 significantly over the last 20 years. In a recent survey of equine veterinary special ists, delays in initiating surgery are believed to be the 1 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 identification 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.
BIBLIOGRAPHY Clinical signs of colic Hardy J ( 1 999) Failure of body organ systems. Gastrointestinal system. Proceedings of Bluegrass Equine Medicine and Critical Care Symposium, October 24-27 1999, Lexington, Kentucky.
White N A ( 1 990) Examination and diagnosis of the acute
abdomen. In The Equine Acute Abdomen, N A White (ed. ) . Lea and Febiger, Philadelphia. pp. 1 02-42.
9
CLI NICAL EVALUATION OF THE COLIC CASE
Physical examination of a horse with colic
Proudman C] ( 1 992) . A two year, prospective survey of
Ragle C A ( 1 999) The acute abdomen: diagnosis,
Rooney] R ( 1 970) Autopsy of the Horse. Williams and Wilkins, Baltimore, pp. 69-96.
preoperative management, and surgical approaches. In
Equine Surgery 2nd edn,] A Auer,] A Stick (eds) . W B Saunders, pp. 224-32. White N A ( 1 990) Examination and diagnosis of the acute abdomen. In TheEquine Acute Abdomen, N A White (ed. ) . Lea and Febiger, Philadelphia, pp. 1 02-42.
equine colic in general practice. Equine Vet. ]. 24 90-3
Acute colic - the decision to refer Baxter G ( 1 992) . The steps in assessing a colicky horse. Vet.
Med. 87: 1 0 1 2-18. Coffman ] R ( 1987 ) . Deciding when to refer the horse with
Rectal examination for the acute abdomen Kopf N ( 1 997) Rectal examination of the colic patient. In Current Therapy in Equine Medicine 4th edn, N E Robinson (ed. ) . W B Saunders, Philadelphia, pp. 1 70-4. Mueller P O E ( 1 995) Diseases of the large intestine causing colic. In The Equine Manual, A] Higgens, I M Wright (eds) . W B Saunders, Philadelphia, pp. 482-95. Mueller POE, Moore ]N ( 1 998) Classification and pathophysiology of colic. In Manual ofEquine Emergencies,
Treatment and Procedures, ] A Orsini, T] Divers (eds) , W.B. Saunders, Philadelphia, pp. 1 5 6-64. White N A ( 1 990) Examination and diagnosis of the acute abdomen. In White N A (ed ) : The Equine Acute Abdomen, Lea and Febiger, Philadelphia, pp. 1 1 6-24. White N A ( 1 998) Rectal examination for the acute abdomen. In White NA, Moore]N (ed) : Current Techniques in Equine Surgery and Lameness, 2nd edn, W B Saunders, Philadelphia, pp. 262-70.
Medical therapies for colic Barton M H ( 1 995) . Treatment of equine endotoxemia.
Proceedings 41st Annual Convention of the American Association ofEquine Practitioners Lexington, Kentucky, 4 1 : 1 1 2-16. Clark E S ( 1 992). Pharmacologic management of colic. In Current Therapy in Equine Medicine 3rd edn, N E Robinson (ed. ) . W B Saunders, Philadelphia, pp. 201-6. Hardy] ( 1 999) . Failure of body organ systems. Gastrointestinal system. Proceedings ofBluegrass Equine Medicine and Critical Care Symposium, October 24-27,
colic. In Current Therapy in Equine Medicine 2nd edn, N E Robinson (ed. ) . W B Saunders, Philadelphia, pp. 30-2. Edwards G B ( 1 998) . Gastroenterology 1. Colic. In Equine
Medicine, Surgery and Reproduction. Eds. T Mair, S Love, ].Schumacher and E.Watson. W.B.Saunders, London, pp. 20-54. Mueller P O E and Moore ] N ( 1998) . Classification and pathophysiology of colic. In Manual ofEquine Emergencies. Eds. ] A Orsini and T] Divers. W B Saunders, Philadelphia. pp 1 5 6-164 White N A ( 1 990 ) . Examination and diagnosis of the acute abdomen. In The Equine Acute Abdomen. Lea and Febiger, Philadelphia pp 102-142
Colic - decisions for surgery Mueller P 0 and Moore] N ( 1 998 ) . Gastrointestinal emergencies and other causes of colic. In Manual ofEquine Emergencies Eds. ] A Orsini and T] Divers. W B Saunders, Philadelphia pp 156-164 Ragle C A ( 1 999) The acute abdomen: diagnosis, 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 ( 1 990) . 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 transport Arden W A, Siocombe R F, Stick] A, et al. ( 1 990)
Lexington, Kentucky. Murray R ( 1998). Endotoxemia in horses. Vet. Rec. Suppl. In
Morphologic and ultrastructural evaluation of effect of
Practice 20: 88-94. Proudman C] ( 1 991 ) . A two-year prospective survey of colic in general practice. Equine Vet. ]. 24:90-3. Seahorn T L and Cornick-Seahorn ] ( 1 994) Fluid Therapy. In Emergency Treatment in the Adult Horse, ] L Bertone (cd. ) . W B Saunders, Philadelphia, 1 0:517-25. Van Hoogmoed L and Snyder ] R ( 1 997). Adjunctive methods in equine gastrointestinal surgery. In Surgical Management of Colic, D E Freeman (ed. ) . W B Saunders, Philadelphia, 13:221-42.
]. Vet. Res. 5 1 : 1 784.
ischemia and dimethyl sulfoxide on equine jejunum. Am. Durando M M, MacKay R], Linda S, et al. ( 1 994) Effects of polymyxin B and Salmonella typhimurium antiserum on horses given endotoxin intravenously. Am.]. Vet. Res.
55:92 1 . Freeman D E ( 1 997) Surgery o f the small intestine. Surgical
management of colic. Vet. Clin. N. Am. 299. Geor R], Weiss D], Burris S M ( 1 992) Effects of furosemide and pentoxifYlline on blood flow properties in horses. Am.
]. Vet. Res. 53:2043,. Hardy], Rakestraw P ( 1 999) Postoperative care and
Spasmodic colic Edwards G B ( 1998 ) . Spasmodic colic. In Equine Medicine,
Surgery and Reproduction. T S Mair, S Love, ] Schumacher and E D Watson (cds). W B Saunders, London, p. 29. Foreman ] H ( 1 998) . Diseases of the small intestine. In Equine
Internal Medicine. S M Reed and W M Bayly (cds) . W B Saunders, Philadelphia, pp. 627-636 Hillyer M H and Mair T S ( 1 997 ) . Recurrent colic in the mature horse: a retrospective review of 58 cases. Equine
Vet. ]. 29:421-4
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. ( 1 993) Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses. ]. Am. Vet. Med.
Assoc. 202:7 1 . Mathews K A ( 1 998) The various types of parental fluids and their indications. Advances in fluid and electrolyte therapy. Vet. Clin. N. Am. 28:483-513. Moon P F, Snyder] R , Haskins S C, et al. ( 1991 ) Effects of
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highly concentrated hypertonic saline-dextran volume expander on cardiopulmonary function in anesthetized normovolemic horses. Am. J Vet. Res. 52:1 61 1-18. Moore R, Muir W, Bertone A, et al. ( 1995) Effect of dimethyl sulfoxide, allopurinol, 2 1-aminosteroid U74006F, and manganese chloride on large colon ischemia-reperfusion injury in horses. Am. J Vet. Res. 56:67 1 . Orsinij A , Kreuder K . ( 1 998) 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 M j, 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
Gardner S Y, Reef V B, Spencer P A ( 1991 ) Ultrasonographic evaluation of horses with thrombophlebitis of the jugular
vein: 46 cases ( 1 985-1988 ) . 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. N. Am. Equine Pract. Surgical Management of Colic. W B Saunders, Philadelphia, 1 3:299.
Furr M 0, 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 . MacDonald M H, Pascoe j R, Stover S M, et al. ( 1 989) Survival after small intestinal resection and anastomosis in horses.
Vet. Surg. 1 8 : 4 1 5-423. Moorej N, Owen R, Lumsdenj H ( 1976) Clinical evaluation of blood lactate levels in equine colic. Equine Vet. J 8:49-54.
meglumine: Effects on eicosanoid production and clinical signs induced by experimental en do toxemia in horses.
Orsini j A, Elser A H, Galligan D T , et al. ( 1 988) Prognostic
Equine Vet. J 19:20 1 , 1987.
Vet. Res. 49:1 969-1972. Parry B W ( 1994) Prognostic evaluation of equine colic cases.
Spier Sj, Snyder j R, Murray MJ. ( 1996) Fluid and electrolyte therapy for gastrointestinal disorders. In Large Animal Internal Medicine. 2nd edition, B P Smith (ed. ) . Mosby, St Louis, MO, pp. 775-83. Van Hoogmoed L V, Snyder j R ( 1997) Acljunctive methods in equine gastrointestinal surgery. Surgical management of colic. Vet. Clin. N. Am. 231-234.
Intravenous catheterization and complications Bregenzer T, Conen D, Sakmann P, Widmer A F ( 1998) Is
index for acute abdominal crisis (colic) in horses. Am. J
In Abdominal disease in equine practice, jN Moore ( ed . ) . Veterinary Learning Systems, Trenton, Nj, p p . 34-40. Parry B W, Anderson G A, Gay C C ( 1 983) Prognosis in equine colic: A study of individual variables used in case assessment. Equine Vet. J 15:337-344. Pascoe P j, Ducharme N G, Ducharme G R, et al. ( 1 990) A computer-derived protocol using recursive partitioning to aid in estimating prognosis of horses with abdominal pain in referral hospitals. Can.J Vet. Res. 54:373-378. Pelosoj G, Cohen N D , Taylor T S, et al. ( 1 996) When to send a horse with signs of colic: Is it surgical, or is it referable?
routine replacement of peripheral intravenous catheters
A survey of opinions of 1 1 7 equine veterinary specialists.
necessary? Arch. Intern. Med. 158: 1 51-4.
Proc. Am. Assoc. EquinePrac. 42:250-3.
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Surgery for colic (including anesthesia)
Anesthesia for colic surgery RD Gleed Many gastrointestinal lesions in horses cause colic that requires laparotomy for definitive 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 difficult, 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 efficiently 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 myofibril 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
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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 efficacy 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 cmH20.
THE CARDIOVASCULAR SYSTEM IN HORSES WITH COLIC Distention of the abdomen in horses with colic may be sufficient 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 permits 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 fibrilla tion increases the likelihood of intraoperative hypo perfusion. Laboratory tests on venous blood should include • • • • •
hematocrit total plasma protein base deficit 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 deficits, 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 j udgment. 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
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
decompression of the stomach and allows removal of gastric fluid during surgery. As 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) . An 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 alpha2 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 necessity 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 1 0- 1 5 ml/kg at a rate of 6-10 breaths per minute. The volume in the accessory cuff of the orotracheal tube should be acljusted 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 filled with air or water are used for this purpose. In dorsal recum-
10
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. As 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 alpha2 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 alpha2 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 alpha2adrenoreceptor 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 alpha2 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
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COLIC
by the addition of diazepam and/or butorphanol to the technique (Table 1 0 . 1 ) . Dosing with alpha2 adrenocep tor agonists to control pain before surgery can substan tially reduce the dose necessary during induction of anesthesia.
Protocol 1 Premedication xylazine 0.4 mg/kg Lv. butorphanol 0.02 mg/kg Lv. Induction diazepam 0.1 mg/kg Lv. ketam i 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 ketamine given to effect
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 alpha2 adrenoceptor agonist it produces a much smoother induction. The quality of induction with keta mine is also improved by using other adjunct drugs such as guaifenesin or diazepam (Table 1 0. 1 ) .
Acepromazine
Guaifenesin (glyceryl guaiacolate ether, GG)
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 amplification 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.
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 difficult 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.
Benzodiazepines Diazepam and midazolam are classified 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 adj uncts 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 require148
Thiopental Thiopental is an ultrashort-acting barbiturate that induces recumbency very soon after intravenous
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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 find 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 after 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 find 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 safety 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 acljust 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,
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 agents, 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.
. malwalar;COfW8I'ItfiClon,,'" "j1,,�lbhorsU> •. ;. Halothane Isoflurane Sevoflurane Desflurane
0.9
1.3 2.3
8.0
149
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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 as 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 nervous 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 MAC, where MAC 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 observation 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 sufficient to prevent flow past the cuff. The cuff is then slowly deflated; the cuff
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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-filled, 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 artery, 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 difficult 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 find a place in equine anesthetic practice. Central venous pressure (CVP) 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 cmH20, but because the central venous pressure is low, small incon-
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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 CVP will be low. It will increase as the hypovolemia is corrected.
Pulmonary 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 efficiency 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 4-8 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 (Sp02) ' 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 p02 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. Difficulty in obtaining a signal with a probe that ordinarily functions well on the horse 151
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tongue, may be associated with poor tissue perfusion due to decreased overall perfusion (e.g. shock) or vasoconstriction (e.g. after an alpha2 adrenoceptor agonist) . The partial pressures of oxygen (Pa0 2 ) and carbon dioxide (PaC02 ) 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 PaC02 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. Treatmen t 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 sufficient 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 20 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 cmH2 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 confined to the blood but distribute throughout the extracellular space. This may be an advantage because
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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 insufficient 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 beneficial 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 significant 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. An 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 beta2 adreno-
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ceptors (increasing cardiac contractility and rate) ; in horses undergoing acute abdominal surgery these are probably beneficial effects. At infusion rates over 5 flg 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 insufficient 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
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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 sufficient to cor rect the base excess to -6 mEq/l, i.e. sodium bicarbonate dose (mEq) base deficit difference from -6 (mEq/l) [0.3 x body weight] =
x
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 justifiable 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 ficial effect in most horses with colic) , plasma sodium, and plasma tonicity. As 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 deficit difference from -6 x 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 significant 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 sufficient 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 intervention. 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 mortality, 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 airway dilation after extubation. Once the horse reaches a light plane of anesthesia, the author removes the orotracheal tube and subjectively assesses the airway by feeling for air movement at the external nares and listening for upper airway 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-
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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 observed 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 ifn o improvement has been seen after 5-10 minutes. Although the diuresis may have adverse effects on a dehydrated/hypovolemic patient, the exigencies of pulmonary edema override the other con cerns. Additional therapy consisting of oral application 15 g of nitroglycerine 2% cream has been used empiri cally to reduce pulmonary hypertension. Horses that have evidence of venous admixture dur ing anesthesia (Pa02 < 200 mmHg while breathing >90% oxygen) should receive oxygen supplementation during recovery by insuffiating 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 NG Ducharme INTRODUCTION A number of different surgical approaches to the abdominal cavity of the horse are available to the
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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 contamination 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
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a
b
1 7th rib Resection
Flank
\
\ \ \
,:
(
�. � 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 inci156
Figure 1 0. 1 Schematic representation of the location of a) ventral incisions (mid line or paramedian), b) flank incisions made either through the paralumbar fossa or by a 1 7th or 1 8th rib resection
sion to identify 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 fingers. 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-
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
Abdominal
External obloque
inCISion
muscle
-= -
_ _
-
Abdomen Inernal obloque
Transverse
muscle
muscle
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Figure 1 0.2 If the rectus abdominus muscle is inadvertently incised, a hemostat can be placed i n the latter muscle on each side of the incision to identify the direction of the correction needed to return to the linea a l ba. Note that the lateral movement of the hemostat will be arrested by the linea alba on one side of the incision while it is unim peded through the rectus abdomi n is on the other side
dian incision has a slight advantage. In these cases, the prepuce does not need to be reflected as 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 fibrosis 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 . l a ) . 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.
closure of the nephrosplenic space, and exteriorization of a section of the small intestine or small colon. A right 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 modified grid approach is preferable. In this case, the internal oblique muscle is separated bluntly along its fiber ori entation, and the transverse abdominal muscle is sharply incised along the plane of its muscle fibers 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 modified 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 .
Paralumbar flank celiotomy {laparotomy}
Flank celiotomy {laparotomy} through the 1 7th or 1 8th rib
A paralumbar flank celiotomy is made with the horse either standing or anesthetized in lateral recumbency. A left paralumbar celiotomy allows limited abdominal exposure for correction of nephrosplenic entrapment,
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 1 57
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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 1 8th 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 fibrocartilaginous 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.
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, specific 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.
Surgica l exploration of the abdomen II
NG Ducharme 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, identify, and correct the particular abnormality. The surgical approach into the abdomen and the site of the lesion will determine which structures are seen first 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. Figure 10.3 Right 1 7th rib resection gives reasonable access for typhlectomy, resection of right dorsal colon, and transection at the i leocecal valve. In this horse the large intestine, including the right dorsal colon, is exteriorized 158
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.
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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 monofilament 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 significant 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 sufficient sterile water to form a 1 liter solution. The preparation is then autoclaved at 1 2 1 °C for a total of 20 minutes.
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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 identify the lesion(s) so that appropriate equipment (i.e. surgical instruments for anastomosis, colon table, etc.) can be requested. It is neither crucial nor beneficial to spend a lot of time looking for a precise diagnosis by palpation alone as exteriorization will enable the surgeon to identify the majority of intestinal problems. Therefore, abdominal exploration is often completed after the distended intestinal segment has been exteriorized and the lesion identified 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 findings, such as the presence and nature (gas, firm 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 cavity. 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
·�_:�i����.;�e��{t(�·:��.�"���j.�i;.·· Structures to palpate Left cranial quadrant
Body and cra n ia l edge of the spleen; gastrosplenic ligament; fundus of the stomach; omentum; left hemi-diaphragm; left lobe of l iver; small i ntestine; small colon as it joins the transverse colon and duodenal-colic l igament between the d i stal aspect of the duodenum and the most proximal aspect of the small colon; the left ventral and dorsal colon medial to the spleen; the diaphragmatic and sternal flexures near the stomach.
Right cranial quadrant
Right ventral and dorsal colon; right and quadrate lobe of the l iver; two or three d ucts of the b i liary tree; proximal duodenum; epiploic foramen; pylorus and antrum of stomach; right hemi-diaphragm; d iaphragmatic and sterna l flexures; right dorsal and ventral colon; omentum; cranial mesenteric artery; right kidney; and, if enlarged, right adrenal gland.
Right caudal quadrant
Cecum; i leocecal valve; small i ntestine; right ureter if d istended; and, when a p propriate, right inguinal ring or right ovary, uterine horn, and broad l igament.
Left caudal quadrant
Left dorsal and ventral colon; pelvic flexure; body of spleen; nephrosplenic l igament; left kidney; and, if enlarged, left adrenal gland and ureters; sma l l i ntestine; small colon; and, when appropriate, left inguina l ring or left ovary, uterine horn, and broad ligament.
Pelvic cavity
Bladder; descending colon and rectum; and, when appropriate, uterus and vas d eferens
159
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Mesentery
Duodenum
Figure 1 0.4 Schema illustrating identification of the epiploic foramen. Lateral view of the right cranial abdominal quadrant as examined through a ventral mid line i ncision. The duodenum is identified first, by applying trac tion on the duodenum with the thumb and forefinger the surgeon can use a finger to probe the duo denum's now tense mesentery in a cranial-to-caudal direction until the epiploic foramen is identified
Figure 1 0.5 Schema i l lustrating pal pation of the right dorsal colon and transverse colon. Cranial view of the right cranial abdominal quadrant as examined through a ventral midline incision
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 difficult at best. Right cranial abdominal quadrant
Using the stomach as the reference point, the pylorus is identified as a firm muscular structure from which the 160
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 1 0.4) . The right dorsal colon can be pal pated axial to the duodenum as it joins the transverse colon (Figure 10.5 ) . Right caudal abdominal quadrant
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 artery (Figure 1 0.6) . The latter can be palpated as an irregular firm structure with fremitus in cases of thromboembolic colic associated with Strongylus vulgaris
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
10
Figure 10.6 Schema illustrating
-----Sloma(h
Duodenum
Cr.noal mesent�nc Irtf!ty
larval migration. When present, the right ovary and uterine horn can be palpated along the dorsal body wall caudal to the right kidney.
palpation of the ascending duo denum and cranial mesenteric artery. Lateral view of the right cranial abdominal quadrant as examined through a ventral mid line incision
cranial-ventral surface of the spleen near the hilus and left part of the greater curvature of the stomach (Figure 1 0.8) .
Left caudal abdominal quadrant
By following the medial surface of the spleen dorsally, one can identify 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. Left cranial abdominal quadrant
By following the medial surface of the spleen cranially, one can identify the gastrosplenic ligament between the
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 identify the ileum and exteriorize the small intestines starting
Figure 10.7 Schema illustrating palpation of the nephrosplenic ligament. View: left caudal abdominal quadrant as examined through a ventral midline incision. The sur geon can identify this l igament by following the spleen dorsally and caudally 161
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Figure 10.8 Schema i l lustrating
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 identified and followed toward the base of the cecum until the ileum is found and identified 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 first. If the colon is markedly distended by fluid and solid materials, a 162
palpation of the gastrosplenic ligament. View: l eft cranial abdominal quadrant as exam ined through a ventral midline incision. The gastrosplenic l iga ment is found between the medial surface of the spleen and the left greater curvature of the stomach, the left colon is medial to the surgeon's hand
Figure 10.9 For exteriorization of the small intestine, the surgeon handles the intestinal wall and avoids the fragile 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 finding its charac teristic contents in the caudal abdomen and retracting it out of the abdomen. Alternatively, the small colon may be identified by palpation of the duodenocolic ligament or the descending colon in the pelvic cavity.
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SURGERY FOR COLIC (INCLUDING ANESTHESIA)
Determine if an obstruction is present by intra-abdominal exploration using an impervious sterile sleeve
I Exploratory steps Divide abdomen into four q uadrants and pelvic cavity Perform in situ assessment based on Table 1 0.3 Assess for normal abdominal viscera Assess for abnormal findings Distention Intestinal wall thickness Abnormal location of intestinal segment
I
y
Is obstruction site found?
I
Is the small intestine distended?
EJ
9
Can obstruction be exteriorized?
I
Yes
If the small intestine is involved grasp and lift the site taking care not to p u l l on the lesions or the mesentery of the bowel i nvolved in the lesion
Find the ileocecal junction and begin exteriorizing the small intestine from d istal to proximal until the lesion is found or the duodenum is reached
If the large intestine is involved it is usually gas distended: Relieve distention with gas suction. Make sure the incision is long enough. Place forearm under the left ventral and dorsal colon and l ift the colon in a sl ightly rostral direction to exteriorize the pelvic flexure. Then lift and pull the colon in a caudal direction until the sternal/diaphragmatic flexures are exteriorized.
I
�
lf lesion is not found
Starting in proximal jejunum, 'milk' small intestine content distally Replace empty small intestine into abdomen simultaneously until i leocecal valve is reached
I
r-
I
Place forearm under the left ventral and dorsal colon and lift the colon in a slightly rostral direction to exteriorize the pelvic flexure, then lift and p u l l the colon in a caudal direction until the sternal/diaphragmatic flexures are exteriorized.
I Reach into the pelvic cavity and grasp the sma l l colon. Exteriorize the small colon from distal to proximal unti l the lesion is found or the transverse colon is reached. If the sma l l intestine h a s not been exteriorized, find the ileocecal junction a n d beg i n exteriorizing the smal l intestine from distal to proximal.
-
Figure 10.10 Algorithm summarizing the steps needed to identify and exteriorize various intestinal lesions 1 63
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Figure 1 0. 1 1 Exteriorization of the large intestine with a ventral midline i ncision. The surgeon is on the right side of the horse while a n assis tant retracts the left side of the incision. By placing the left colon over the surgeon's arm like a towel, the surgeon can l ift the left colon while attempting to exteriorize the pelvic flexure first
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 example. it is not uncommon to have a large colon displacement. presumably because of rolling. toge th e r with another disease process. Therefore, complete but efficient intestinal examina tion is a sine qua non condition of proper abdominal surgery.
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 1 0 . 1 2 ) . Adhesions are less likely in the large colon. An 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 financial constraints. Increased duration of surgery for resection could extend anesthesia time beyond safe limits for draft breed horses.
Evaluation of gut viability
SMALL INTESTINE
D E Freeman
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 types 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, j ejunal segments subjected to identical types 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
In many cases the appell-ranee of strangulated bowel leaves little doubt about the need for resection. but no method can provide consist..e n t gllidance since the via bility of bowel that has incurred subtle changes is diffi 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 1 0 . 1 2) . 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 progres164
•
strangulation of four segments versus one segment per animal
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
10
SMALL INTESTINE Questionable viability I
I
I
If viable
If non-viable
I
I
I
I
Incorrect decision
Correct decision
Correct decision
Incorrect decision
Resection
No resection
Resection
No resection
Short surgery
Long surgery
Short surgery
I
I
Lon.g surgery
I
I
I
Expensive treatment
Inexpensive treatment
Expensive treatment
Inexpensive treatment
Anastomotic problems
No anastomotic problems
Anastomotic problems
N o anastomotic problems
Risk of adhesions
Less risk of adhesions
Risk of adhesions
Great risk of adhesions
I
I
I
I
Good prognosis
Excellent prognosis
Good prognosis
Poor prognosis
LARGE INTESTIN E Questionable viability I
I
I
If viable
If non-viable
I
I
I
I
Incorrect decision*
Correct decision*
Correct decision
Incorrect decision
Resection
No resection
Resection
No resection
Long surgery
Short surgery
Long surgery
Short surgery
I
I
I
I
I
I
Expensive treatment
Inexpensive treatment
Expensive treatment
Expensive treatment
Anastomotic problems
No anastomotic problems
Anastomotic problems
No a nastomotic problems
Endotoxemia
Severe endotoxemia
I
Good prognosis
Excellent prognosis
Fair-good prognosis
Poor prognosis
No risk of recurrence
Risk of recurrence
No risk of recurrence
Risk of recurrence
Figure 10.12 Consequences of errors in assessing the viabi l ity of small and large intestine in random order. *The decision to resect or not resect large colon after volvulus must consider the possibility of recurrence of the volvulus, a factor that can justify resection of questionable 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 finger against the intestinal wall improvement in color after correction of the strangulation.
Spontaneous or evoked motility 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 after strangulation because occlusion of thin-walled veins causes rapid mural congestion (Figure 10. 1 3 ) . Such changes lead to high false-positive results (unnecessary intestinal resections) because short intestinal segments with these changes can survive without forming adhe sions (Figure 1 0 . 1 4) . Enterotomies are not recom mended for viability assessment in the small intestine because of the risk of adhesions and because mucosal 165
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Figure 10.14 Segment of small intestine 1 5 m i n utes after
intestine that was strangulated in the epiploic foramen and was not resected. The horse recovered and did not develop a known problem over a 2-year follow-up period
release from 3 hours of venous strangulation obstruction. This segment did not cause postoperative complications, 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 permission
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 1 0 . 1 2) . 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 ponyjejunum. 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
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 identifYing 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 j udgment 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
Figure 10.13 Appearance of a segment of 4 meters of small
1 66
SURGERY FOR COLIC (INCLU DING ANESTHESIA)
the mucosa, have some potential but are cumbersome and require special equipment. In clinical cases, a mean intralumenal hydrostatic pressure of 15 cmH20 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 1 0 . 1 3 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 sufficiently 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 finding. In the author's experience, the most unpredictable out-
Figure 10.15 End-to-end anastomosis made in hemor rhagic and edematous small intestine to avoid resection of too much bowel. At a repeat celiotomy 5 days later, a small adhesion was broken down proximal to the anasto mosis and the horse did not develop any complications over a 3-year follow-up period
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 suggests that removal of 60-70 per cent is close to the limit.
LARGE INTESTINE The large intestinal disease that is most likely to cause difficulty 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 - 1 50°C to - 1 60°C 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 between 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 Ps02 > 20 mmHg. The disadvantages are 167
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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 fiberoptic 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 identify 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 cmH20 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 difficult 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 NG Ducharme 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 specific disease entities are discussed. In the last 20 years many studies have provided equine surgeons with significant information, thereby increasing the success of abdomin al 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 monofilament suture materials are superior to multifilament 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 9 1 0, poly-p-dioxanone, poly glyconate, and polyglecaprone 25 are recommended at this time in procedures where staples are not used.
SUTURE PATTERNS The various suture patterns used for an intestinal anas tomosis and enterotomy are shown in Figure 1 O . 16a-h. The effects of the suture pattern on an intestinal enterotomy/anastomosis should be considered in the
SURG E RY FOR COLIC (INCLUDING ANESTHESIA)
light of several parameters, all of which have been reviewed in many studies
10
a
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 Figure 10.16 Suture patterns used in equine i ntestinal procedures, a) simple interrupted, b) simple continuous, c) Gambee - continued
1 69
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d
e
J
\
-.
"' .;;,, �, ... "
,
Figure 10.16 Suture patterns used in equine intestinal procedures continued (interrupted or continuous), e) Cushing - 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 poten170
-
"
the inverting patterns of d) Lembert
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 first 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.
SURGERY FOR COLIC (INCLU DING ANESTHESIA)
10
9
------
-------
Figure 10.16 Suture patterns used in equ i ne intestinal pro cedures - continued: the inverting patterns of f) Connell, g) Schmeiden, h) Marshall U
h
171
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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
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 """"m;'"'"'_';V;"*"';"f\;V'';>''''_'''""'N''#.(;i'i:'''�"''©>''''':''=;'''''"'''''';1"11�1'>'@1"""""'''":''''''' ; JlNi\i'···''�N;:''1'>,,, ,�,,,,"'''"":I@�%;"",II�U"W<18''"''''''''"'1%,9·.·.'"'
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 sufficient 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 field. If significant 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 the serosa. 172
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 fingers 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 burstin g 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 fibers 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 modification 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 intestine 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
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Intestinal segment
Location of enterotomy
Diredion of closure
Small intestine
Along the long axis opposite the mesenteric attachment
Transverse closure to m i n imize stricture
Cecum
At the a pex on either side of the dorsal bands to prevent postoperative contact between enterotomy and incision site
Longitudinal closure
Large colon
Along the long axis opposite the mesenteric attachment and on the anti-mesenteric band when possible, avoid pelvic flexure to m i n i m ize lumenal stricture
Longitudinal closure
Small 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 sufficiently 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 significant 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
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. 1 8 ) . 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 I D . 1 8 ) . This is especially impor tant in the small colon mesentery where fatty tissue interferes with identification 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
I . to help identity 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.
Figure 10.18 Mesenteric resection in preparation for intestinal anastomosis. Note that 1 -2 em of normal mesen tery is left beyond the remaining vessels to prevent their i nadvertent puncture during closure of the mesentery 1 73
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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 1 80 degree rotation of the anastomosis. To prevent such an occurrence either of the following two techniques can be used. 1 . During ligation of the first mesenteric vessel, one suture end is left long, clamped by a hemostat, and placed in an Allis tissue forceps (Figure 1 0 . 1 9 ) . 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 first. The mesentery is closed leaving approximately 15 cm of unsutured mesentery to allow appropriate access during the anastomosis procedure. Two methods
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
Ligature
Long suture grasped by hemostats
174
Figure 10.19 One end of the suture used for mesenteric vessel ligation is clamped with a hemostat and incor porated i nto an Allis tissue forceps. Subsequent sutures are incorpo rated in order, preserving the order of mesenteric vessel ligation
SURG E RY FOR COLIC (INCLUDING ANESTHESIA)
Cut end of small intestine
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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 identified, probably because many techniques are successful and the type of anasto mosis has no effect on survival rate according to at least one study.
Hand-sewn anastomoses
Figure 10.20 The mesenteric defect is closed toward the intestine using a simple continuous pattern. A 10-1 5 cm section of i ntestine is left unsutured to facil itate the anastomosis
Mesentery
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 proximal and distal intestine is arrested using Penrose drains 20-25 cm away from the intended l ine of transection to prevent inadver tent contamination during e nterotomy or a nastomosis procedures 175
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____
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----------� 7----
---
/
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) .
End-to-end anastomosis
Figure 1 0.23 The intestine is transected at a s light angle to ensure that the anti-mesenteric intestinal wall retains ade quate perfusion since it is the intestinal 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.
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 identify 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 first layer using the same pattern (Figure 1 0.24) .
Standard types of anastomosis Anastomosis at specific 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
Figure 1 0.24 After the first half of the a nastomosis is com pleted, the intestine is rotated and a second strand of suture material is used to finish the first layer using the same pattern
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
End-to-side anastomosis 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
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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 first 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) .
Side-to-side anastomosis Hand-sewn anastomosis
Figure 10.25 End-to-side anastomosis, occlusion of the flow of ingesta may require the use of an intestinal clamp if it is performed between the small and large intestine
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
Cecum Incision in cecum for anastomosis
Marshall · U · sutures Anastomisis I leocecal fold
Cecocolic fold
Small intestine
Figure 10.26 End-to-side anastomosis - a longitudinal inci sion is made at the anti mesenteric side of the proximal i ntestinal segment to enlarge its lumen for a sufficient length anastomosis
Figure 10.27 Side-to-side hand-sewn jejunocecal a nasto mosis - 1 cm caudal to the anastomosis side where the anticipated line of tension is expected, an additional cruci ate suture is placed 177
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Figure 10.28 Side-to-side hand-sewn intestinal anastomo sis - the intestinal segments are overlapped and when pos sible are placed in such a way as to create an isoperistaltic anastomosis
Figure 1 0.29 Side-to-side hand-sewn intestinal a nastomo sis - after seromuscular apposition of the far side of the anastomosis is completed, both intestinal segments are incised parallel to this suture line and the far layer of the anastomosis is closed with a simple continuous pattern
purse-string effect (Figure 10.29 ) . At each end of the first 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 0.3 1 ) . Each arm of the GIA is inserted into the lumen and directed toward one end of the intended anasto mosis site (Figure 10.32 ) . After the instrument is fired, it is withdrawn, loaded with another cartridge, and rein serted in the opposite direction. It is critical that the instrument be fired 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 1 0.30 Side-to-side hand-sewn smal l intestinal anas tomosis - the near side of the anastomosis is c losed using a simple interrupted pattern oversewn by an inverting 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. As 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.
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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Mesentery
Figure 1 0.31 Side-to-side stapled anastomosis - using a no. 1 0 Parker-Kerr blade, a stab incision is made into each i ntesti nal segment to be anastomosed
Figure 10.32 Side-to-side stapled anastomosis - each arm of the GIA stapling instrument is inserted into the lumen and directed toward one end of the intended anastomosis site
Figure 10.33 Side-to-side stapled anastomosis - the stapling instrument (GIA multifi re) is appl ied in the oppo site direction making sure that the instrument is fired across the previous staple l i ne on the far side of the anastomosis 179
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Functional end-to-end anastomosis 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.
A 1 cm section of the antimesenteric corner is cut with straight Mayo scissors and each arm of the CIA sta ple introduced into each intestinal segment, being care ful to direct the anastomosis toward the mesentery (Figure 10.35) . After the instrument is fired, 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
Figure 10.34 Functional end-to-end anastomosis in the small colon 3 weeks postoperatively. Note the end-to-end appearance of the small colon at this early time postoper atively. The horse was euthanized for unrelated reasons
Because of the time period required for enterotomies and anastomoses of the large colon, the speed associ ated with a stapling instrument is a significant 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 Functional end-to-end a nastomo sis - the arm of the GIA stapling instrument is i ntroduced into the anti mesenteric opening created i n each i ntestinal segment. Care must be taken to direct the anastomosis toward the mesentery 180
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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Figure 1 0.36 Functional end-to-end anastomosis the arm of the GIA sta pling instrument is re-intro duced into the intestine to i ncrease the length of the anastomosis
Line of mesenteric apposision
Figure 10.37 Functional end-to-end anastomosis - after the anastomosis is completed. the mesentery is closed with a simple continuous pattern using an absorbable suture materia l (no. 000; 2 metric). Care is taken to cover the exposed i ntestinal edges with a fold of mesentery during mesenteric closure.
with carboxymethylcellulose or an absorbable adhesian barrier (Interceed, Ethicon, Inc, USA) (see Surgical exploration of the abdomen) .
Closure of the a bdomen NG Ducharme INTRODUCTION The goals of abdominal closure are to obtain a secure apposition of the strength layer of the incision, and to
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. type, 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
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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 impervious 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, incisional 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.
Incisions
Strength layer
Ventral midline
Linea alba
Ventral paramedian
External sheath of rectus abdominis muscle
Paralumbarlflank
External oblique abdominis m uscle and its aponeurosis
1 7th or 1 8th rib resection
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 9 1 0 are the next strongest sutures to use.
Suture material
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 significant 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
Breaking strength mean 'SEM'
(Newtons) 5 Polyester multifilament braided
270.5 ± 7.3
2 Polyglycolic acid multifilament
2 1 3. 5 ± 2.8
braided
3 Polyglactin 910 multifilament
209.1 ± 7.8
braided 2 Polydioxanone monofilament
1 57.8 ± 6.1
2 Polypropylene monofilament
1 37.2 ± 3.2
1 Polyglycolate monofilament
1 46 . 1 ± 3.7
2 Nylon monofilament
1 13.0 ± 7.0
Means with different superscripts are significantly different from one another (P < 0.05)
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
As well as the in-vitro 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 sufficient for secure abdominal closure. Their multifilament nature increases the risk of suture sinus formation, but when the suture material degrades the infection resolves. The monofilament sutures are weaker and have a higher rate of knot slippage because of their lower coefficient of friction, but the absorbable monofilament sutures may be acceptable in situations such as infected or con taminated wounds in lighter weight animals. The non absorbable monofilament 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 multifilament 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 monofilament sutures (no. 1 or no. 2) in a continuous pattern protected with an oversewn stent bandage.
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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 fibrin 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
SUTURE PATTERN The peritoneum is only closed in standing laparotomy to minimize the possibility 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 identifying 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,
Figure 10.38 Ventral abdominal incision immediately post operative. Note the stent bandage suture over the incision for tension rel ief and i m pervious iodine-impregnated drape applied over the incision site 1 83
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where a stent can be kept for 5-7 days if changed daily, because the incision tension increases the risk of incisional seroma/hematomas.
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.
CONCLUSION Adherence to aseptic techniques and incisional closure based on the biology of healing will influence the suture material and pattern used. This should signifi cantly impact and lower the prevalence of incisional complications, which can be as high as 37 per cent of all abdominal incisions.
Repeat laparotomy NG Ducharme 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
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 fluid therapy is to restore extracellular fluid 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 significant elevation in packed cell volume (> 50%) may be an indi cation of significant endotoxemia, and the clinician must be concerned that bowel necrosis and peritonitis may be the source. Mural necrosis, associated with post-
Persistence of e levated hematocrit > 50% after 24 h Heart rate elevation greater than 80 bpm for > 48 h Clinical signs of persistent or deteriorating endotoxemla for > 48 h Divergence in the changes i n hematocrit (increasing) and total plasma protei n concentration (decreasing) Elevation i n rectal temperature DepreSSion for more than 48 h Abdominal d istention Severe abdominal pain Persistent ileus (nasogastric reflux) after 72 h Hematological changes consistent with degenerative left shift Appearance of mixed bacterial contamination in previously 'aseptic' peritoneal fluid
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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 fluid and fibrin shift into the abdominal cavity 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
T" 10.. ." � from tlte primary celIotoMY kI'lOM te lncte.A:;tl!ie MH fOf a repeat celiotomy �:
Compromised bowel not resected Ileal stump not resected in h orses with i leocecal intussuception Enterotomy and anastomosis in compromised bowel Ileocecal anastomosis Small colon impaction treated without evacuation of the large intestine Incomplete abdominal exploration Delayed:
Primary conditions: nephrosplenic entrapment large colon volvulus cecal i mpaction/dysfunction
10
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 insufflation 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 identity 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 ity 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 •
•
Cecum Medial cecal artery
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 sufficient. 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
artery
J eJuno Ileum Right colle artery
Figure 10.40 Schematic drawing showing vascular supply to distal jejunum and ileum. A technical error that may result in postoperative devitalization of the ileal stump is transection of the ileal artery during the jejunal resection. This is espe cially true during treatment of ileocecal i ntussusception
the root of the mesentery. Although a dorsally extend ing rent can be repaired, the procedure is difficult. One needs to identify the two segments of bowel and apply sufficient traction to tense the mesentery. Moist towels must be placed into the abdomen to prevent acljacent 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. An 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 significant, and extreme care is needed to avoid them while closing the defect.
Delayed repeat laparotomy
Figure 10.39 Enlargement of the jejunocecal end-to-side anastomosis can only be done by incising between two simple interrupted sutures or between the end and the start of two continuous patterns 1 86
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
SURGERY FOR COLIC (INCLUDING ANESTHESIA)
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.
10
Pedrick T P, Moon P F, Ludders] W, Erb H N, Gleed R D ( 1998) The effects of equivalent doses of tromethamine or sodium bicarbonate in healthy horses. Vet. Surg. 27:284-9 1 .
Surgical exploration o f the abdomen Hay W ( 1 999) Abdominal adhesion prevention in horses. Proceedings of the 9th A merican College of Veterinary Surgery Symposium, San Francisco, pp. 1 1 6-- 1 7. Southwood L L, Baxter G M ( 1997) Current concepts in management of abdominal adhesions. Vet. Clin. N. Am. Equine Pract. 1 3:415-35.
Evaluation of gut viability 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) . Multifilament 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 multifilament suture materials becomes almost contraindicated. Postoperatively, the author prefers to apply an abdominal support bandage for these horses because of the suture incision weakness.
BIBLIOGRAPHY
Anesthesia for colic surgery Bottoms G D, Fessler] F, Roesel 0 F, Moore A B , Frauenfelder H C ( 1 98 1 ) Endotoxin-induced hemodynamic changes in ponies: effects of flunixin meglumine. Am.]. Vet. Res. 42: 1 5 1 4-18. Hardy], Bednarski R M, Biller D S ( 1 994) Effect of phenylephrine on hemodynamics and splenic dimensions in horses. Am. ]. Vet. Res. 55:1 570-8. Lukasik V, Gleed R D, Scarlett] M, et al. ( 1 997) Intranasal phenylephrine reduces post anesthetic upper airway obstruction in horses. Equine Vet. ]. 29:236--8 . Moore] N, Garner H E, Shapland] E, Hatfield D G ( 1981 ) Prevention of endotoxin-induced arterial hypoxemia and lactic acidosis with flunixin meglumine in the conscious pony. Equine Vet.]. 1 3:95-8. Muir W W, Sams R ( 1992) Effect� of ketamine infusion on halothane minimum alveolar concentration in horses. Am.
I
Vet. Res. 53: 1 802-6.
Allen D, White N A, Tyler D E ( 1 986) Factors for prognostic use in equine obstructive small intestinal disease. ]. Am. Vet. Med. Assoc. 189:777-80. Brusie R W, Sullins K E, Silverman D G, Rosenberger] L ( 1 989) Fluorometric evaluation of large and small intestinal ischemia in the horse. Equine Vet. ]. 2 1 :358-63. Bulkley G B, Zuidema G D, Hamilton S R, et al. ( 1 98 1 ) Intraoperative determination o f small intestinal viability following ischemic injury: a prospective controlled trial of two adjuvant methods (Doppler and fluorescein) compared with standard clinical judgement. Ann. Surg. 1 1 93:628-37. Freeman D E, Gentile D G, Richardson D W, et al. ( 1988) Comparison of clinical judgement, Doppler ultrasound, and fluorescein fluorescence as methods for predicting intestinal viability in the pony. Am. ]. Vet. Res. 49:895-900. Freeman D E, Hammock P, Baker G], et al. ( 1 999) Short-term and long-term survival and prevalence of postoperative ileus after small intestinal surgery in the horse. Submitted to Equine Vet. ]. Hughes F E, Slone D E ( 1 997) Large colon resection. Vet. Clin. N. Am. Equine Pract. 1 3:341-50. Moore R M, Hance S R, Hardy] , et al. ( 1 996) Colonic luminal pressure in horses with strangulating and nonstrangulating obstruction of the large colon. Vet. Surg. 25: 1 34-4 1 . Purohit R C, Hammond L S, Rossi A , et al. ( 1 982) Use of thermography to determine intestinal viability. Pmc. Equine Colic Res. 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. 186:257-6 1 . 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. Symp. pp 280-8. Van Hoogmoed L, Snyder] R ( 1 998) Intestinal viability. In Current Techniques in Equine Surgery and Lameness 2nd edn, N A White and] N Moore (eds) . W B Saunders, Philadelphia, pp. 273-9.
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 antimesenteric band and the sacculation of the small (descending) colon of ponies. Equine Vet. ]. 20:402-13.
1 87
10
COLIC
Baxter G M, Hunt R], Tyler D E, Parks A H, ]ackman B R ( 1 992) Stapled side to side versus end to end jejunal anastomosis in the horse. Vet. Surg. 1992;21 :47-55. Beard W L, Robertson] T, Getzy D M ( 1 989) Enterotomy technique in the descending colon of the horse. Effect of location and suture pattern Vet. Surg. 1 8 : 1 35-40 Dean P W, Robertson] T ( 1 985) Comparison of three suture techniques of the small intestine on the horses. Am. ]. Vet. Res. 46: 1 282-6. Dean P W, Robertson ] T, ]acobs R M ( 1 985) Comparison of suture materials and suture pattern for inverting intestinal anastomosis of the jejunum in the horse Am. ]. Vet. Res. 46:2027-77. Frankeny R L, Wilson D A, Messer N T 4th, Campbell-Beggs C ( 1 995) Jejunal intussusception: Complications of functional end-to-end stapled anastomosis in two ponies. Vet. Surg. 1995;24:515-17. Freeman D E ( 1997) Surgery of the small intestine. Vet. Clin. N Am. 1 3:261-30 1 . Hanson R R , Nixon A], Calderwood-Mays M, Gronwall R, Pendergast] F ( 1988) Comparison of staple and suture technique for end-to-end anastomosis of the small colon in the horse. Am. ]. Vet. Res. 49: 1 62 1-8. Hocking M P, Carlson R G, Courrington K R ( 1 990) Altered motility and bacterial flora after functional end-to-end anastomosis. Surgery 108:384-9 1 . Latimer F G, Blackford ] T , Walk N ( 1996) Closed one stage end-to-endjejunojenunostomy in horses utilizing linear stapling instrumentation. 25:25-432. MacDonald M H, Pascoe] R, Stover S M, Meagher D M ( 1 989) Vet. Surg. 18:415-23 Mackey V S, Pascoe] R, Peterson P R ( 1 987) A potential technique error in stapled side-to-side anastomosis of the small intestine in the horse. Vet. Surg. 16: 1 89-92. Phillips T], Wamsley] P ( 1 993) Retrospective analysis of the results of 1 5 1 exploratories in horses with gastrointestinal disease. Equine Vet. ]. 25:427-3 1 . Ross M W, Stephens P R, Reimer] M ( 1 988) Small colon intussusception in a broodmare. ]. Am. Vet. Med. Assoc. 192:372-4. Sullins K E, Stashak T S ( 1 989) Evaluation of two techniques for large intestinal resection and anastomosis in the horse J Invest. Surg. 2 : 1 1 5-24.
1 88
Young R L, Snyder] R, Pascoe] R, Olander H ], Hinds D M. ( 1 99 1 ) A comparison of three techniques of pelvic flexure enterotomies in normal equine colon. Vet. Surg. 20: 1 85-9.
Closure of the abdomen Gibson K T, Curtis C R, Tuner A S et al. ( 1 989) Incisional hernias in the horse: incidences and predisposing factors. Vet. Surg. 18:360-6. Honnas C M and Cohen N D ( 1 997) Risk factors for wound infection following celiotomy in horses. ]. Am. Vet. Med. Assoc. 2 10:78-8 1 . Ingle-Fehr] E, Baxter G M, Howard R D, Trotter G W and Stashak T S ( 1 997) Bacterial culturing of ventral median celiotomies for prediction of postoperative incisional complications in horses. Vet. Surg. 26:7-13. Kobluk C N, Ducharme N G, Lumsden] H et al. ( 1 989) Factors affecting incisional complication rates associated with colic surgery in horses: 78 cases ( 1 983-1985 ) . ]. Am. Vet. Med. Assoc. 195:639-42. Trostle S S and Hendrickson D A ( 1 995) Suture sinus formation following closure of ventral midline incisions in three horses.]. Am. Vet. Med. Assoc. 207;742-4. Trostle S S, Wilson D G, Stone W C and Markel M D ( 1 994) A study of biomechanical properties of the adult equine linea alba: Relationship of tissue bite size and suture material breaking strength. Vet. Surg. 23:435-441 . Wilson D A, Baker G ] & Boero M J . Complications of celiotomy incisions in horses. Vet. Surg. 24:506-14.
Repeat laparotomy H uskamp B, Bonfig H ( 1 986) Relaparotomy as a single therapeutic principle in postoperative complications of horses with colic. Proceedings oj the 2nd Symposium on Equine Colic Research 2 : 3 1 7-21 . 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. 26:7-1 3. Parker] E, Fubini S L, Todhunter R] ( 1 989) Retrospective evaluation of repeat celiotomy in 53 horses with acute gastrointestinal disease. Vet. Surg. 1 8:424-3 1 .
11 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 Cilrc 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
•
thrombophlebitis
•
lal)'ngospasm
•
laryngeal paralysis
•
h}poxic cerebral injul)'
•
wounds sustained during a colic episode
•
myopathy.
Immediately 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 type of intravenous fluid and its administration rate is chosen (see Chapter
9)
Another significant consideration is postoperative ileus. In horses this primarily small intestinal disease is characteri�_ed by reflux of intestinal secretions into the
•
to return or maintain the cardiovascular status
stomach causing abdominal pain, this may result in
•
to identify and manage ileus
gastric rupture if left untreated. Ileus is commonly
•
to recognize promptly various postoperative
seen after treatment of small intestinal diseases associ
complications.
ated with intestinal ischemia or severe inflammation
Th<� various abdominal postoperative complications are
(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
•
pam
•
ileus
calcium, potassium, and chloride) must be maintained
•
peritonitis
in phYSiological balance. The author does not rou tindy feed horses (at 'high risk' for ileus), recovering
•
anastomosis and enterOlOmy obstructions or failure
•
anterior enteritis
from imestinal surgery until the third day postopera
•
incisional problems
tively. It is important, on recovel)', to place a naso
•
diarrhea.
Non-abdominal complications include
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 na�ogastric reflux ha� c,eased. A �mall
•
shock
•
hypoproteinemia
amount of water (1-2 liters) is then offered every 2
•
dehydration
hours for the next 12-24 hours. If the horse can cope
•
laminitis
with oral water for that period, solid food is slowly 189
11
COLIC
reintroduced. It is reasonable to return to water and feed intake as carly as possible within the first 24-hour postoperative period in patients at 'low risk' for ileus. For early return to feed, water is olrered firs! as described above, followed by a mouthful of grass or handful of soft hay after a few 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
(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 primary protocol refkcL� the postoperative treatment plan. This is outlined in Table 11.1, it includes 'red flag' indicators that should trigger an immediate veterinary 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 cific orders in the primary protocol (for example, time medication i� ;uimini�terer:l, 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.
1. Colic evaluations made every ___ hours 2. Medications .) intravenous fluids b) non-steroidal anti-inflammatory agents <) antIbiotics· gram positive
type__ dose
rate time
dose dose
time
gram negative
time
route route
time time
route route
anaerobes
dose
d)
others (I.e. vasodilators)
dose
e)
motillty modifiers
route
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 c)
b)
heart rate greater than _ respiratory rate greater than_
d) e)
packed cell volume greater than _or len than _ total protein concentration greater than _or less than _
f)
temperature greater than_
g) h) i)
intravenous fluids cannot be administered at prescr ibed rate nasogastrk tube is removed by horse or tube becomes obstructed other
-Antibiotks with activity ilgalnst the following organisms �hould be considered
190
POSTOPERATIVE TREATMENT AND COMPLICATIONS
Table
11
11.2 Standard colic evaluatiOn
case number:
I
Name:
I
Owner:
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
Systemically, endotoxin activates numerous host defense mechanisms, leading to the formation or release of free radicals, lipid mediators (eicosanoids,
DM Ainsworth
leukotrienes,
platelet-activating
factor),
'-")'tokines
(tumor necrosis factor alpha (TNF.) , interleukin-l and
PATHOPHYSIOLOGY
6 (IL-I, IL-6», and fac.tors involved in coagulation (tis sue thromboplastin, plasminogen activator inhibitor
Endotoxin is a complex molecule comprised of •
a lipid moiety (lipid A)
•
a core polysaccharide
•
repetitive units of O-specific polysaccharide.
tory response syndrome (SIRS), is a sell�perpetuating
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
(PAl), tissue plasminogen activator (tPA), factor XII). This endotoxin response, calied the systemic inflamma
when
the
intestinal
mucosal harrier is compromised, allowing endotoxin to access the peritoneal ca,ity or systemic circulation. In addition to enteric di�ea3e, horse� with hepatic disca.se,
response which prim arily targets the structural and functional
integrity
of
the
endothelial
ce!Is.
Manifestations of the SIRS include •
fever
•
tachypnea
•
tachycardia
•
pulmonary hypertension
•
systemic hypotension
•
cardioV".!scular collapse.
retained placcntas or metritis, hemorrhagic or hypo
Imbalances
volemic shock, pneumonia, severe trauma, and sep
microvascular thrombi formation, tissue hypoxia, and
in
coagulation
path\\'ays
may
cause
tiu'mia are at risk for the development of endotoxemia.
muhi-organ dysfunction or failure. Horses with endo-
191
11
COLIC
lm.,:cmia and SIRS are
;\1
increlUc d risk for the dc\"C\op
Im:m of laminitis. g,mroimcnina[ ilells and diarrhea,
jugular I'eln thromlx)Sis. disseminated intr.wascular coagubuiou
(DIC),
Tlu: trc,Hment optio05 fllr c:ndoloxcmia
• • • •
I.�
by either
cyd,x)xYf:cnase (COX) to form prostaglandins
•
lip ox�cnase (LOX), to Jorm Icukotrienes (I:rn.,
(PCE�, p(;F2,., I>Gly)
and thromboxane
(TXA.,), nc
ITt:" LTD,. and LTE,).
The� lip id mcdiatnrs !;:xen potenl dkci.S on ,"a.<;(:ul'll"
and hronchial smooth muscle, on micro\"aS(:ul.lr I)('r
llon-steroidal anti-inflammillory drugs (NSAIDs)
endnt/)xin
acti\'lIICd, rdt:4.�inK arachidonic acid which
•
iln:
intravenous fluids biological
Ouring cllciowxcmia. nll'mhr.ne-bound phospholipltSC
1\ is
me a t bolized
TREATMENT PRINCIPLES
•
Non..steroldal antl·infJammatory drugs (NSAlDs)
meahility, and on platelet an d granulocyte function and
prodtlcl� and drugs which ncutrali7c
integrity. DurinK endotoxemia. increases in plasma
TXJ\ and PGI� corrdate with the developmcnt of pul
KlunKorti(:()id�
monary hypertension and systemic hypotension, respec
agent!; dircctt:d a!f.lin�t central inflammatolT
tively. Increasc� in plasma PGF1� are also associated with
mediators •
free radical s(:av\:nKcr.�
•
a�illnctj\'t: therapies.
decrea�t:� in lu ng function. the development of pul
monary hypertension and hypoxemia. ;o..!on-steroidal anti-infi ammatol)' drugs (NSAIDs) are uscd to inhibit
or attl�nuatc COX pathways lI.Ild thus ameliorate the
Intravenous fluids
eITects of
The prima ry Irc;tuneOI
goal
is
10
idelllifr and alleviate
(ifplKSihld the primllry inching eveol. Thereafter, sup
punil'l:! nlC'lt.�lIrcs designed to ('nmbat or prevent the
dC'idopmt:nI of shock and
cosun-
tissue perfusion arc
impiclllcllwd_ Agj.,'Tt-..s.\ivC in!r.t\1:nous f1uid-lherapy T(-SlOre pla.,ma volume and COntTt
acid---base
to
imbal-
3nC(1) is imti{utt:11 immcdiatd)-_ Depending on the
endoLOxemia.
Basc:rl upon experimcntal
trials, !lunixin mcg!umine (0.2::0-0.5 mg/kg i.\'. two
OJ"
three times daily) is more efl"ectivc in antagonizing tht:'"
drecl.� of endotoxin-induc.ed eicosanoid produ ction than OIher NSAlDs suc.h as phen),lbulal:olle, dip)'ruue,
and ibuprolen. (In conu ... .!s t. phenylbutaHme, Uillike
fiunixin megl umine, does nut mask the C'drciio\
prolong a dr;:cisioll
for
degree of cndotoxemia, imrnwllOlIs cl)o'8t<1l1oill thl�rapy
surgk"al intervention.) Eltel1ac (0.5 IIIg/kg) i.s anllther
be Ilcc�S$ary. III shocked hor��_ hypertonic saline wlll
oratory
at r.Hd 01 !")-8 mllkg for the fir» flOW hours may initiall y
�SAID whic.h will all�'iate some of Ih� clinical allolab·
given intran:nousl)· (4 ml/kgJ over a
filldin� of c(luinc encioloxemia. Limited experimental and dinica! data on kCloprofen , touted a�
lowed by intr,,j\'enous isotonic cIJ'l'talloid solutions sup
ca!:inliS as fiunixin meglumine in inhibiting increases in
!H:m(ldynamic:
intraveIlous
when ketoprofen is giv!;:n al a dosage of 0.25-0.5 mg/kg
dopamine infusiollS (2-5 p.g/kg/min) are started. A�
added benefit of inhihit.ing LOX, the relative impor
aggressive fluid the rapy may decrease plasma ollcotic
enciotoxelllia has not heen determined in the eq;line
tinns
(i.5%)
1:>--20 minute period_ are hcndidal but should be fol
plemented with puta.'i.�illm chloride (20 mEq/I). If renal
failure
dcvclop s,
furosemide (0.5 mg/kg i.v., one or twice) and/or
cndotoxcmic horses are often hypoproteinemic, over pressure,
promoting
Ihe development of wInnie and
peripheral ('clema. WI)('I) tOtal serum protein levels are
both a COX and LOX i nhibitor , 5uggcst thal it i� as clll prostagI3ndiu�. mmor necrosis fact.or, and leukotrienes
i.v. b.i.d. nr t.i.d. While ketoprofen has the touted
tance of the leuko!riencs in the pathophysiology of
species. Bast-d on
porcine
studies, these ararhidonir
acid metabolites playa minor role. Toxicit}' studies sug
le!i..\ than 4f) gil (4.0g/dl: albumin < 199/l or 1.9 g/dl),
gest that kctnpmkn i� less ukcrogcnic: than phenylbu
adcninistert':d \\11h the r�·ali1.ation that the amount of
administered In
fn·.�h or li·ol.en
plasma
or serum (sec below) should be
pla.�ma required 10 incrC:3SC p rolein k-wIs hy I gldl may
exceed 10 liters. Howt....-er. 1-3 liu�fli of fresh or froM-II plasma lIlay be beneficia l in supphing hOlh antithrom ..
hin III and fihronectin and in II�u:.rrillg the de\o"C!op nWn!
Hf C"o:tgulopalhies
( 10-15 ml/kj( i.,·. m·er
(sec belo",). Dextran 40
30 min)
or lIetasta.·ch JO ml/kg
arc also beneficial in increasing plasma 11I1cotic pres
.mre in (�ndoloxt':mic horses.
192
tazonc or flunixin megtuminc . When I\SAIDs arc endOlox�mic
foals, anti-ukel· medica
tiuns sucll a.� 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
expt�cted
lhat
administl
of
immunoglohulins l!irec.tcd against endo\Oxin would
POSTOPERATIVE TREATMENT AND COMPLICATIONS
either confer protection against the development of, or
11
and neurotoxic. Caution should be exercised with iL'i
Illitigate the existing signs of endotoxemia. Antibodies
use in endotoxemic horses at risk for the development
formed against the conserved regions of endotoxin
of hemodynamic renal failure. In an effort to minimize
(core of lipopolysaccharide) are produced llsing bacte
drug toxicities (this require extravasation of the drug),
ria with mutations in the outer 0 polysaccharide region
polymyxin
which exposes the core region.Thus(;ommercial prepa
this combination is given intravenously (4 g polymyxin
B has been conjugated (0 dextran 70. When
rations of hyperimmune serum or plasma containing
B-dextran conjugate/kg body wt) prior to endotoxin
antibodies
challenge,
against
mutant
Salmondfa typhimuriwn (Re
Elrherirhia
I:oli
05)
or
mutant) haw been utilized.
clinical
alterations
and
elevations
in
eicosanoids and cytokines are prevented. The poten to
Cnfortunatdy, data from equine trials have both sup
tially promising results of this study remain
ported and refuted the therapeutic benefit of anti-cndo
ined in clinical cases with fulminant endotoxemia.
be exam
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
Glucocorticoids Known for their membrane-stabilizing properties, the administration of (orti(osteroids should reduce the
ance, and a shorter duration of hospitalization when
clinical signs of cndotoxemia given that these agents
compared with horses treated with pre-immun(� plasma.
•
Yet, in experimental studies of sub-lethal endotoxemia, treatment of foals with antij5 .If'rum either •
•
•
was
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
•
the IgG isorype produced (e.g. I gGa, IgGb, IgGc, or Iget).
metabolism) •
block complement acth�J.tion
• •
inhibit inducible nitric oxide synthase
•
exhibit antioxidant effects.
attenuate cytokine secretion
Such effects 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
after
intravenous endotoxin were inferior to flunixin
meglumine in preventing eicosanoid synthesis and the
In addition, tbe presence of other products included in lhe plasma - fibron(�ctin, coagulation factors, and antithrombin III - not present in the serum, may also have contributed to the differt�nces 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 polymyxin B is given at a dosage of 6 000 It] /kg of body weight prior to {�ndotoxin challenge, there is
stimulate liptXortin synthesis, an inhibitor of phospholipase � (and thus arachidonic acid
failed to improve clinical or dinicopathologic parameters, or
prevent aggregation, adhesion, and degranulation of neutrophils
B fared better than those pre-treated with
Salmonella typhimurium hyperimmune sera. However the use of Polymyxin B can be associated with the develop ment of adverse eflects. Its binding a�idiry to anioni{: phospholipids of cell membranes makes it nephro-, oto,
accompanying hemodyn
Agents directed against central inflammatory mediators Several lines of evidence support the role of TNFa as a central mediator of endotoxin. These include the find ings that
1.
T�F� 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
to TKFa
confers protection
193
11
COLIC
lelhal dft:Cl� of endotoxin and intravascular
enl.yme inactivation, d�p()lymerization of nucleic acids and po lrsaccharides, and increases in capillary penne
F,srh"rirllia coli administr-uion
4. ill hUn];!n p
ilcli\11), i� a useful prcdictoroffillaI
The lazaroids are 21·aminosleroid
or b iological prod ucLS that either reduc e
the formation ofTNF" or 'nculr.lli�.c· drculaLing levels of this cytokillC, have bt.'en SLUdicd.
"cnwxifylli n<.' is a melhylxamhinc dcrivaliw that, in
addition to phosphodiester� inhibition, reduces
lJilm
ill
production I)f T�F" by macrophage;; exposed to
('nciotoxin. It
reduces neutrophil adhesion and
dcgr;lllul;ttion. decrt:asc� superoxide rddical format.ion,
mpJlresse� philR()(:ytusiM, and inhibits the production of
illlt:rft:rnn �amma, 1l�J, HAl, and tissue thrombo
phlstin. Pl: ntoxifyllinc also impro\'cs dcformability of
nythmcytcs (rhco!ogic properties). In clinical cases of cndntoxcmia, pcmoxifyIIinc is administered (7.5 mg/ k� p.o. b,i.d.) not only for il.� ami-TNF" effects, but aim
in an effort 10 improve the perfusion of the hoof bminae (rheologic propenies). In experimental endn IOl(('mia models, pentoxifylline admininercd W
min·
ures arwr endotoxin ch..l!enKc aU.enuateci endotoxin· iuducc.."(\ tempc'r.lture and
r"f:Spi ral ory
rate cle';tdtiolls
dTect (m ht'mawlogicaI parameters or on cicO'!;!lloid and c}'tokine (i ncl uding TNFQ) production. Clinic;!1 trillL, examining the cflicacy of penioxilYllinc in pre\i(�nlinK laminitis have nOi been conducted at the hut 11;1(1 IW
l im e f)f�'riting.
t',xpcrimcntal trials have also examined the eflk
f.<)
compounds with
structural s imila rities to cortieoslCroids. They lack glu
olltcome.
11ms, dru�s
ability and prostaglandin product ion.
enommdn Challenge. an appreciable
amelioration of th�: clinical and hcmatologic re�pomc i� found. Ho....·el·er, i f ami-TNFg antibodics (O.l mg/kg of rahhit. PQIyc10naI antibodies directed against recom· binant human T�Fg ) arc aoministercd 15 minutes after the start of endotoxin challenge, a beneficial effect is lIot ollserveo. With additional experimental and dini (:<11 trials anti-TNF� lIlay prove useful during certain siages or cndoloxemia in clinical case�.
cocorticoid or
mineralocorti c oid
enects. It is believed
thallhe lal';aroids insert them�lves preferentially within the mcmbnlllc of the \".lsc..'Ular endOthelium and inhibit lipid pernxidation, allenuate cy tok ine production, sup pre!l.� the exprel'Sion of adhellion molecules, and inhibit trdnSClldothelial neutrophil migration and activation. Although cl i n ica l trials in endotoxemic horses arc lack· ing, trcatmCllt of neonatal calves with tirilazad mesylate (1.5 mg/kg i.v.), either pri or to or following endotoxin
challenge attenuated tbe 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 in flammatory conditions. Dosage recommendations are variable ranging from 20 mg/kg i.v. b.Ld. to
1 g/kg Lv. �.i.d. administered as a 10% solu·
tion. Rigorous dinica! or experimental trials reg-J.rding its efficacy in equine endotoxcmia arc lacking. In an
experiment al stud r of neonatal calves challenged with endotoxin, DMSO failed to suppress eicosanoid pro
d uctio n or exert any prOlective effeeLS against endo toxema i .
I n deed , (;ah'cs exhibite d
a
prolongation of
clinical compromise, hypotension, and hypoglycemia as
compared to
the c ontrols. In
reperfusion injury, DMSC)
(1 g/kg i.v. as a 10% solu
tion) was ineffective in providing a mucosal protective df{'.ct tl) the equine jejunum.
Two other agents that arc t hought til protec.t againsl free n\dical i�jl!ry include
1. allopurinol. an inhibitor of xanthine oxidase that catal)'�es the formation of superoxide anion from uric acid 2. :\·acetylcysteine, an &gent that replenishcs glutathione, a major intracellular antioxidant. Although allopurinol administration (50 rng/kg i.v.) failed to prevent mucosal injury in anesthetized horses with expcrimemally.indu(;ed i.'iChemic bowe! injury, in a different study, the
pre-treatment
of horses (50 mg/kg
Free radical scavengers
i.v.) significantly reduced endotoxin-induced increases
J)urinll: (�ndOlOxemia. reacti�'(' oxygen speci� (ROS)
ic..\ efficac y in endolm:('mia are currently lacking.
arc Keller,lIed by (lCliVdted phagoc)'lcs and by the imra cellular xant hine
oxidase
!>yslcrn
hich is activated
.....
(lurinK i�chcmic reperfur.ion i njury. ROS can attack \inlt<1l1y all biochemical cell COmponents hill polyunsat urated rallY acids. located within the phospholipid mcmhr<1IlC stnl(·ture of the cell and cellular organell�, an·
194
mOM su scepti ble to their effects. ROS also
(""USC
in xamnine oxidase aClhiry. Clinical trials documenting
:-.10 information is avai l a ble rCb'ilrding the effir ....cy of N-acel}'lcyslt'inc (:>:AC) in the horse. In sUIne spt'cic..>s with
endmoxemia.
NAC
decreases
ne utrophil
or
platelet·aggregating acti�ily, markedly reduces p ul.
monary hypertension, and aUenu;l.tes vascular perme
ability changes. In dogs, pretreatment with �AC (150 mg/kg i.v. followt!d by a 20 mg kg -I h-I infnsion)
11
POSTOPERATIVE TREATMENT AND COMPLICATIONS
increases glutathione peroxidase
adivity,
improve�
mented
with
potassium
chloride
(15-20
mEq/l)
myocardial function and tissue oxygen extraction, and
and/or calcium borogluconate (200 milS liters of
decreases T;\Fa production.
fluids) to correct contributing
caine drip (0.05 mg kg-I min-I) significantly decreases
Antibiotics
reflux volume in horses with ileus. However, side effects
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 horses
should
receive
antimicrobials.
Nevertheless, arguments both for ,lIld 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
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 definitivc association between endotoxemia and the development of laminitis, it is well recognized clinically that such horses are at risk. As it has been shown exper imentally that endotoxin chalknge alters nitric oxide (vasodilatory) pathways in equine digital vessels, it is likely that lipopolysaccharide contributes
to the vascu lar alterations observed in laminitis. I lorses with endo
toxemia are treated prophylactically against laminitis by
• housing them in well-bedded stalls •
cephalosporins like ceftiofur (2.2-3.3 mg/kg i.v. b.i.d.)
•
daily
penicillin (22 DOO Ill/kg i.v. q.i.d.) can be used initiaHy. 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 rislicci 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.
or
horses with
strangulating
bowel
•
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 targeting gastrointestinal tract function Nasogastric intubation in
applying a half-inch (I.3cm) band (IO-20 mg) of 2% glyceryl trinitrate paste over the digital arteries
alolle or in combination with sodium or potassium The aminoglycosides in combination with penicillin
providing frog support by taping lily pads to the soles
cillL hospital or practice settinbS ' , third generation
inflammatory,
stasis. Intravenous
lidocaine bolus (1.3mg/kg) toHowed by a 24 hour lido
Adjunctive therapies
r-ndotoxic
potential electrolyte imbalances
to gastrointestinal
obstructive, disorders
removes ingesta and prevents !fOO 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
Therapies for horses with disseminated intravascular coagulation (DIC) 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
•
thrombomodulin.
In
elldotoxemia,
this
the expression of procoagulant substances such as tissue thromboplastin and phospholipids
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-
of
tbrombo-resistance is impaired by
direct activation of the intrinsic ,md extrinsic coagulation pathways act.ivation and aggregation of platelets (platelet activating factor) 195
11
COLIC
• increases in factors that inhibit fibrinolysis (PAl) • decreases in factors that either potentiate
tion to feeding horses following abdominal surgery (".an
fibrinolysis (tPA and protein C) or that inhibit
postoperative care is critical to ensure proper wound
thrombin formation (anti-thrombin Ill). The net effect is that during endotoxemia, a hyper coagulable and hypofibrinolytic state develops causing mkrothrombi formation, perfusion 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 efficacy, however, is dependent on complexing with antithrombin III, which may become deficient 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
dramatically affect the outcome of a case. Immediate 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 nutrients ingested. Failure to provide adequate nutritional 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 critical in cases where large portions of either large or small intestine are resected.
make lamina! perfusion worse.
CONCLUSIONS In summary endotoxemia is a complex multi-systemic inflammatory response involving numerous mediators.
IMMEDIATE POSTOPERATIVE CARE
Non-complicated cases Reintroduce feed as soon after surgery as possible. The
At the time of writing, there remains no single best
need for energy, protein, B vitamins, and perhaps
therapeutic agent to treat endotoxemia. A number of
vitamin C are increased in the immediate postoperative
different drugs and approaches show promise in exper
phase. If dehiscence or gastric reflux is not a concern,
imental trials, but appear most useful if given prior to
the
endotoxin challenge. In general, intravenous fluids
(0.25-0.5 g/kg) of good quality alfalfa or alfalfa/grass mix hay every 1-2 hours after recovery from anesthesia.
coupled with flunixin meglumine administration has proved to be the mainstay of therapy.
horse
should
be
offered
small
amounts
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 concentrates can be
Nutritional support after alimentary tract surgery Sl Ralston INTRODUCTION
re-introduced within 24 hours. A 14-16% protein con centrate should be used for the first 1-2 weeks after surgery with B vitamins (10-20 m! of B-complex solu tion/day) and perhaps vitamin C (0.02 gm/kg bj.d.) added to the feed during the first 4-5 days. Bnm mashes are commonly used, but are not necessary. Bran is not laxative but is a good source of fiber and contains 16% protein and over 1% phosphorus. Prolonged (> 1-2 weeks) daily administration of bran or bran ma�hes is
While many horses recover from abdominal surgery
contraindicated, especially if the horse is not fed a
without special nutritional management, careful atten-
legume-based forage with sufficient calcium to counter
196
POSTOPERATIVE TREATMENT AND COMPLICATIONS
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 lawn 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 ofconcern, 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 to make a slurry. The slurry can be offered orally every 2-3 hours or delivered via nasogastric tube. Liquid diets, such as Ensure HN (it wi!! need to be diluted with water to prevent hyperosmolar problems), Osmolile or EquiCare (0.1-0.25 ml ktf 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 benefit 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 two, consider parenteral nutri tion (see below).
Gastric reflux 11 gastric reflux or other concerns prt'"vent 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 significant 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)
11
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 horse's estimated caloric and protein needs is better than total starvation.
LONG TERM CARE
Celiotomy, cecal resection, and minor resection There are no special requirements once the horse has recovered from surgery 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 2-3weeks of surgery.
Major large colon resection Ifboth the left and right colons are removed, the horse will require higher than maintenance protein and phos phorus, decreased fiber, 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 necessary.
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 to avoid overwhelming the residual small intestinal digestive and absorptive capacity. Beet pulp based 'complete' fr-ceds 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.5c calOlic intake (up to 1.0 ml ktfl day-I).
Ileal bypass or resection Removal of the ilcum will increase the necd for fat soluble vitamins A and E. Ddkiency signs however may appear only 1-2 years after surgery. It is not known if oral supplementation of increased amount� of these two vitamins (60000 IV retinyl palmitate, 1000 IU alpha
197
11
COLIC
tocopherol/clay)
will
be
prcventative.
Parenteral
Cn.rdiogtnir and ooslrurliw ShfXk
ndate
adminiSlr31ion may be necc:s$lry if dinical signs of ddi
These condition.�
ciCEK}' appear. Ther� also may � an increased need for
pump blood, and
C' d kium and a reduced tolcrdncc for fals. The rdrion
resp«ti\dy. Since these Slates of shock
should contain at least 0.8 per cent calcium and edible oit.� shnuld not he ll� a.� liupplemenlS.
I()
I() an inability of the heart to
a restriction of cardiac ejection.
are nOl gener i J>OSlOperatve complications follow ing gastrointestinal surgery they will not be discu.� funner. The other two classifications Ihat are more ally associl ued ",;th
commonly seen following gasuointestinal surgery arc
P os toperativ e sh ock and organ failu re
hypovolemic and distribllli\"c shock.
HyJmwlnnic (JI(1Twrrlwgk) lhodt This refers to the It)$S of whole hllx)(i, u�ually because of llt:morrhage, resulting
LR Goodrich
in
!os� of intTavascular \·olume.
Oth�r causes include loss of plasma (exudation into lumem of hol1o..... organs or body cavities), or loss ofIm'-' protein fluid (as in diarrhea). Tht: !ac.k of int.ravascular
INTRODUCTION In 1895, James Collins Warrell referred
volume results in pcwr \';ls!;ular flJling volume, leading LO
shock as 'a
momentary pau�e in the act of death'. More recent def
definr-d it a.� a 'gcncra!il.cd inadequacy of blood fl(lw tn tissues rdative to their metabolic initi()n� have
demand� !t'ading to
widespread cdlular hypoxia and
vi[
ph�siol()giC
a more approp rilue definition may he 'the state in which profound and widespread reduclion in efTecth-e tissue perfu$ion leads to re\·Cl"5ibk, and then, if pro longed, irre\"t)r�ible cellular injury'. Despite recent ad.....mCe5 in diagnostics and cardio \'ascular treatment, shock remains an important came ofcomplinttion� and dc:ath in b()(h humans and domc�
lie animals. A survey of 259 surgical colic cases revealed that over 50 per cc:m 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 i t 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.
to decreased cardiac return and hence, decreased cardiac output, arterial flow, and pressure.
Di.liri!mtiVlr .11iock (.�(ir and tndolo.xnnic) This occurs as a fesuh of expansion or the iml'"dv'dscu Jar space by localiled or gener.t1ized loss of vascular
resistance. This is the 1Il000t common form of shock
that gastrointestinal surgeons deal ",;th, it is often
initi ated hy sertic�mia and/or e.ndoLOltemia. Other
causes can he neurogenic in origin
such as anesthetic
mUihaps, spinal cord injury, or anaphylaxis.The result
uf Ihc:$(' cauSC$ is similar to hypo\'oiemic shock in that . ....,,$Cular filling volum�. and cardiac return and output arc all
reduced.
In addition there a lo� of loc.ll con
[TIll mechl\ni.\m� rhlH
J+ft'
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 St:pticlender toxic �hod., Ihe bJ()od flow to local parenchymal tissue may be decreased
resulting in tis.,ue hypoxia and
dysfunction. The classification s)'Sterns indica.te that shock is
neatly separated into specific catcgories, however vari ous clinical events may initiate two
Of
more forms of
shock.. For instance, horses with strangulated inte�t.in('
CLASSIFICATION Se\"e!'"...1 da.��ificalion s�"Slems exi" that describe the dif
of shock.. TIle most common s),s[("m uses insults of variolls etiologi es according to the character ferent types
of the pre......ili ng drculalOr}, disrupt ion. The four
primary C".Hegori<.'S are •
("anii(lg�nk shMk
•
obstructh·e shock
•
hypo\"olemic shock
•
distributive shock.
19B
may have hypovolemic components due to los ses of intralumcnal fluid u welt as losses of fluid due to 5Cvere dehydration from sweating. In addition to lhi� ongoing
hypo\'olemic shock, loss of control mechanisms (dis trihutive shock) because of conCUfTent scps i� rna}' add to the stale of prograsivc shock. Con�-el"M!ly. horses in
....hich sepsis is the initialing factor may not only have poor regulation of\"3scular wnc but also abnonnal cap illary and venou� pemll_'abilil)· lhat leads
10
fluid 10M
and hypovolemia. Therefore calegOlizations ;lre lI!ioCflll in understanding th<.' pathophysiologic origins of each
inilb!.l insult. Nevertheless, if effecth·e tht"Tdpy i5 not
POSTOPERATIVE TREATMENT AND COMPLICATIONS
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
11
injured artery does not reach the pressure present ",ithin the artery bleeding into the interstitium or abdominal cavity, then hemorrhage will continue until adequate surgical intervention has taken place or sys temic hypotension develops. At that point, pressure in the artery drops to the level of the surrounding tissue clot. If systemic arterial pressure reaches 50 mmHg or lower, the platelet-fibrin 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 visco�ity resulting from volume expansion with large volumes of cry'ita\!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.lte, 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 turn increases the pre-load on the heart. Arterial constriction during hemorrhagic shock is not, over
199
11
COLIC
being excreted as urine. This reflex is
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
following blood loss. The reflexes described above are the body's altempt
humans to describe various states of shock. Briefly, SIR-\)
maintain blood pressure. These events occur at the
develops when the local response to iI�Ury or to an
same time that activation of the clotting cascad", is fUlle
initiating stimulus becomes amplified. If homeostasis is
lionillg to stop profuse hemorrhage. In horses suffering
not re-established, the multipk inflammatory cascades
to
from hypovolemic shock due to diarrhea or inadequate
result in loss of microcirculatory function and subse
oral fluid the same reflexes (increased cardiac output,
quent damage to other organs. This leads into the
vasocooslTiction, ;md W'dler retention to maintain blood
second
pressure) occur.
sepsis/endotoxemia.
stage
of
distributive
shock
caused
by
The late phase of septic and cndotoxic shock is char acterized by decreased myocardial and peripheral vas
Distributive shock
cular
tone,
incn�ased
microvascular
permeability,
Although hypovolemic shock is occasionally seen in the
increased
intravascular coagUlation, and
perioperativc period of gastrointestinal surgery, by far
adherence. Progression of the inflammatory cascades
leukocyte
the most common type of shock seen in the horse is
initiated in SIRS ensues and vascular hyporeactivity pre
distributive shock caused by sepsis, endotoxemia, or
vails as the one distinct and important
splanchnic ischemia associated \\�th acute strangulating
prevailing opinion is that lipopolysaccharides and select
and non"strangulating intestinal infarction. Often alt
cytokines induce the calcium-insen�itive form of the
three conditions can cuntribute to shock. Several inves
nitric oxide �ynthasc molecule within the VAscular wall.
tigawrs have determined that up to 40 per cent of
Over-production of nitric oxide leads indirectly to sup
horses with colic presented to a veterina!)' college are
pression of calcium mobilizatioJl and a decreascd
endolOxemic, and most
horses have
contractile function. In many cases the progression of
intestinal strangulation obstruction or severe inllamma
SIRS results in multiple organ dysfunction syndrome
endotoxemic
lory int�stinal diseases. Furthermore, the prognosis for
(MODS). In human medicine there exist various scor
sUlvival is inversely correlated with the presence of
ing systems eval u
lipopolysaccharide in the circulation. In some cases all
as creatinine, bilirubin, and platelet count. As the scores
three causes may be contributing to distributive shock.
incre;!.�e, the incidence of mortality also increases. For
Early and late phase pathologic events usually char
example four body systems suffering from dysfullction
acterizc distributive shock caused by sepsis or endotox
resuits in 80 per cent mortalit.ics. In the horse MODS is
cmia. In the early phase, increased cardiac output occurs
most commonly as.'!ociated with the gastrointestinal
along with reduced peripher.l! vascular resistance, nor
tract. The gut h;!.� been termed the 'motor of failure' in
mal to slightly decreased mean arterial pressure and
its capability of generating the demise of ot.her organ
fever with warm extremities. It is in this phase that the
systems. Reperfusion of the gut can be responsible for
lipopolYS
mediators
include the C)'tokines, lipid-derived mediators, and coag ulation/fibrinolytic factors. Cytokim�s most commonly involved include tumor necrosis factor, interleukins,
•
activation of calcium influx with oxygen radicals
•
bacterial translocation with heightened
adding to mucosal if!jury endotoxemia •
the release of cytokines resulting in wsodilation and vascular leakage.
and interferons. Lipid-derived mediators include throm
The combination of these three factors increases the
boxane (TXA..,) and prostaglandins (PGS, PGF2a, and
predisposition to MODS. Other organs that can com
PGJ"). Release offibrinolytic factors in this stage ofshock
monly be secondarily affected are the kidney, liver, and
resulL� in decreases in plasma antithrombin III activity,
lungs.
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 ofsep tic/endotoxcmic shock in which the above mentioned mediators arc bcing relcased, a syndrome named the sys
CLINICAL FINDINGS
Hypovolemic shock
telTJic inflammatory response syndrome (SIRS) has been
Horses experiencing hypovolemic shock due to helllOr
used to describe the sequence of evenL, and the (:on-
rhage commonly have elevated heart rates, pale mUCOllS
200
11
POSTOPERATIVE TREATMENT AND COMPLICATIONS
membranes, a thready rapid pulse, prolonged capillary
output begins to fall along with arterial pressure.
refill time, and cool extremities. Often they are sweat
Horses in acute abdominal crisis, and in particular with
ing and agitated. If hemorrhage continues unmiti!f
splanchnic ischemia, exhibit sweating,
eventual collapse ensues. Rectal temperature may be
weak pulses, and cyanotic mucous membranes (Plate
tachycardia,
normal or decre-d-�. If shock is protracted the horse
11.2). laboratory evaluation may reveal hemoconcen
may he oIiguric. As circulatory and respiratory function
tration, leukopenia, coagulation abnormalities, meta
deterior.tte, the gums may take on a gray-blue color.
bolic
If bleeding is not controlled acute death
occurs.
creatinine levels. This stage is often referred to as the
Laboratory eVMuation is frequently not helpful in the
'late', 'cold', or 'hypodynamic' stage of shock. Gross
acute
phases
but
may
reveal
metabolic
acidosis,
increases in lactic acid, and increases in blood urea
acidosis,
and
elevation
of blood
urea
and
hypoperfusion is occurring resulting in multiple organ dysfunction syndrome.
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 is important to remem ber that the various components of blood are being lost
TREATMENT
-. ---.--------
Hypovolemic shock
equa!Iy, and the relative proportions of red cell mass
Initial goals in the treatment of hypovolemic shock
and plasma will remain unchanged. Ultrasonography
include partial restoration of circulating blood volume,
is the diagnostic modality of choice in cases where
maintenance of oxygen delivery to tissues, and support
hemorrhage into the abdominal cavity is suspected.
of coagulation and thrombus formation when hypo
Hemoperitoneum is easily evaluated with ultrasound
volemic shock is due to hemorrhage. It is important to
using a
5.0
MHz probe
transabdominally.
Blood
remember that supportive therapy in hypovolemic
appears hypoechoic with swirling of the cellular ele
shock due to hemorrhage does not end when the bleed
ments. Questionable aooominal bleeding can be more
ing is controlled. Many pathologic processes continue
accurately confirmed by paracentesis. Although analysis
following control of hemorrhage and, if allowed to
of peritoneal fluid is not always straightforward in mak
progress, these processes result in damage to other
ing Ihis determination, a helpful rule of thumb is that a
organ systems such as the gastrointestinal tract and the
packed cell volume of 5 per cent or greater, and a total
pulmonary system. Failure of these systems can be rec
protein of 3.5 gldl or greater support the presence of
ognized as ischemia-reperfusion injury and pulmonary
frank hemorrhage.
edema, respectively,
The clinical findings among horses experiencing
To restore partial circulating blood volume rapidly,
hypovolemic shock resulting from vascular fluid loss
a large bore catheter should be placed and crystalloid
dm' to acute diarrhea or inflammatory bowel condi
fluids given in appropriate dosages. Options for crystal
tions, can look similar to those horses with acute hem
loid fluids include saline, lactated Ringer's solution,
orrhage. Labor,ltory evaluation however may reveal
plasmalyte, and hypertonic saline. Replacement volume
relatively early declines in plasma protein concentra
should be calculated according to total loss as well as
tion and electrolyte abnormalities as well as a marked
maintenance volume required. Crystalloid fluids move
metabolic acidosis. However, because infection may
freely from the intravascular to the interstitial space and
also be occurring in these horses the findings can often
approximately 20 per cent remain in the intravascular
be similar to those in horses with distributive shock due
space. Lactated Ringer's solution consists of sodium
to sepsis.
and chloride with added calcium, potassium, and lac tate (buffer solution). Plasmalyte and normasol include
Distributive shock Horses in the initial stages of distributive shock due to
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
sepsis or endotoxemia have clinical signs consistent
tions can interact with citrate antic()agulant� in col
with the 'early' phase. These signs include fever with
lected blood. Hypertonic saline is advantageous in
warm extremities, depression, tachycardia, increased
hypovolemic shock for many reasons. Initially this solu
respiratory rate, injected mucous membranes (Plate
tion can rapidly expand intravascular fluid volume.
hypocapnea and leukopenia or leukocytosis.
Additionally, there is evidence that other beneficial
11.1),
Hemodynamically, horses have decreased arteria! pres
cffect�
sure, elevated cardiac output, and low peripheral vascu
thereby
include
modulation
lar resistance. As distributive shock progresses, cardiac
ischemia-reperfusion injury and bacterial translocation.
potentially
of neutrophil
decreasing
the
activity
incidence
of
201
11
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 intravn! 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-carrying 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 tnuion 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 20-40 per cent of the deficit 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 every 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 hor�e, these prOdUCL� are prohibi tivelyexpensive. If cessation of bleeding relies on a tenuous clot for mation, antifibrinolytic 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 to three times daily. There have been no proven efficacy trials in horses at the time of writing. 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 injury, 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 import.ant goal of distributive shock treatment is volume replace ment. Monitoring of clinical signs during treatment wi!! be an adequate representation of therapeutic suffi 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 to 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 benefits 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 hypertonic 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-ba�e abnormallty caused by an anaerobic metabolism in the tissues as well as renal hypoperfusion. Often mild cases of metabolic acidosis will resolve without administration of bicarbonate when a sufficient amount of volume replacement is adminis-
POSTOPERATIVE TREATMENT AND COMPLICATIONS
11
teredo This of course is the most physiologic route in the
endotoxemia, absence of leukopenia and lower than
treatment of acid-base abnormalities. When metabolic
expected
acidosis is severe (pH
<
7 . 1 ) or fluid replacement does
tumor
necrosis factor levels
in
serum.
Recommended doses are 1000-3000 Ie/kg given intra
not correct the abnormality then administration of
venously twice daily. While
bicarbonate is necessary. The following formula may be
therapeutic antibiotic doses, polymyxin B can be
these doses are sub
followed as a guide to estimate the dose of bicarbonate
nephrotoxic and dose monitoring of creatinine and
to
blood urea nitrogen should be performed.
he administered.
:-';aHCO� replacement (mEg)
=
x
0.3 x
body weight (kg)
base deficit
Plasma
products
are
available
with
antibodies
directed against the core oligosaccharide and lipid A regions of endotoxins from mutant gram-negative
Periodic monitoring of blood gas will allow proper
bacleria. Vo.'hile many referral centers administer these
adjustment in dosing.
product�, their efficacy still remains in question. Hyperimmune plasma products may however provide
Antibiotic therapy is indicalf'o in riislrihwivf' �h()rk cau�ed by sepsis. Often in cases of eXlensive bowel com
the septic/endotoxemic horse with levels of antithrom
promise and resection many different bacterial isolates
bin III that appear to be deficient in horses with colic.
are possible, however, isolation of these organisms is
Heparin injected into the plasma before transfusion
rare. Therefore combinations of high doses of peni
may improve the efficacy by activating antithrombin III
cillin G and an aminoglycoside are commonly used
prior to administration.
because of their broad spectrum ofbactericidal activity.
PentoxifyIIine (6.6-8.0 mg/kg p.o. hj.d.) is another
This combination of antibiotics should be continued
drug used to treat horses for endoloxemia. In both
paM the arute phase of distributive shock because of lhe
in vitru and
possibility of sepsis and/or splanchnic-ischemia.
reduced endotoxin-induced production of cytokines,
ex
vivo studies in horses, pentoxifylIine
Anti-inflammatory therapy is extremely important in
thromboxane, and tissue factors. Clinical trials have
horses with distributive shock due to sepsis/endotox
revealed that when used alone its beneficial cllects may
emia. The use of flunixin meglumine has become stan
be minimal but when combined with flunixin meglu
dard in the treatment of distributive shock. This drug
mine, hemodynamic responses to endotoxin may be
acts by inhibiting cydooxygenase and will prevent or
reduced more effectively than with either drug alone.
attenuate the early hemodynamic responses to endo
Supplemental oxygen therapy is not usually neces
toxin. Various studies have found that flunixin meglu
sary for horses in which arterial oxygenation tensions
mine significantly reduces endotoxin-induced increases
are normal (PaO� 100 mmHg) or dose to normaL In
in
these cases hemoglobin is fully saturated and further
plasma
concentrations
of
thromboxane
and
prostaglandins. The 'low dose' commonly used in clini
supplemental oxygen therapy will he of little benefit.
cal situations is 0.25 mg/kg i.v. Li.d. This dose will
However, when arterial oxygen tensions fall below
rewin the ability to prevent generation of cyclooxyge
85 mmHg hemoglobin desaturation IIlay occur and
na.�{'-derived products and has minimal toxic side
supplemental oxygen can be delivered in the standing
effects. Following surgery however, it is important to
horse through nasal or transtracheal catheter place
keep in mind that postoperative pain resulting from
ment. F10ws of 15 l/min should be administered with
intestinal manipulation may require initial higher doses
adjustmenL� made according to blood gas measure-
(0.5 mg/kg) and slow decreasing of the dose over a
ml':nts.
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
PERIOPERATlVE MONITORING
trials in the human population reveal no beneficial effects and occasional adverse effects when used.
....i.'h re this chapter is dedicated to postoperative assess
Therefore, although exact extrapolations cannot be
ment and treatment of shock, treatment will be more
made to the equine population, steroids are not recom
effective
mended.
Treatment should begin prior to induction for generAl
Polymyxin B is a recent addition to the treatment armamentarium
for
distributive
shock
due
to
if
instituted
to
patients
preoperatively.
anesthesia in patients when large amounts of intestinal compromise are suspected. Although there are situa
sepsis/endotoxcmia. This antibiotic is reported to bind
tiOIlS in which patient� can not be volume expanded
and remove endotoxin from the circulation by binding
adequately preoperatively, every effort should he made
the lipid A region of endotoxin. Studies in foals pre
to promote proper treatment as soon as possible. Care
lTeated with polymyxin B that underwent induced
may be expedited by placement of two large-bore
experimental
catheters and fluids administered under pressure.
endoloxemia had
reduced signs of
203
11
COLIC
Adequat� supplies of necessary treaunem modalities
sibility to interpret clinical signs exhibited by their
should be available along 'Hilh the equipment to ade
patients and judiciously manage pain based on a com
quately monitor treatment. Prior planning for critical
plete understanding of the facton; involved.
care for patients in shock is important in situations where there are small time frames. Proper anesthetic monitoring is also crucial (see Chapter 10). Often dfec tive treatment and monitoring during anesthesia of the
NEUROANATOMY AND PATHOPHYSIOLOGY
colic patient has a direct outcome in the postoperative Sensory neuroreceptors arc located in the mu(:{).')a and
period.
muscularis of hollow viscera, within serosal structures such as the peritoneum, and within the mesentery. i:l
THE FUTURE
addition to nociception (the perception of noxious stimuli), [hf' �ensory nellror('cep!or.� arf' rf'spnnsiblc for
The field of shock has become an intensely studied area
regulation of motility, secretion, and blood flow to the
with new advances being made frequently. As new
gastrointestinal tract�.
developments occur in both the monitoring and treat
Neuroreceptors responsible for the p
ment of shock clinicians will become more effective in
pain are separated into two distinct types of afferent
its early diagnosis, monitoring, and treannent. This
nerve fibers
chapter has covered most current monitoring and treat ment techniques that have been clinically evaluated in the equine patient. As sound clinical trials reveal new
L myelinated A-delta fibers
2. unmyelinated C fibers.
techniques it is the responsibility of clinicians to judi
A-deita fibers are responsible for mediating sharp,
ciously use the new methods to benefit the equine
well-localized pain associated with an acute injury.
patients.
These fibers transmit somatoparietal pain �ia spinal nerves. C fibers are found in viscera, peritoneum, and mesentery, as well as in muscle and periosteum. C fibers
P os toperative pain
convey nociception from abdominal viscera and this pain tends to be dull, burning, diffuse, and of a more um
calcitonin gene-related peptide as neurotransmitters.
LR Goodrich INTRODUCTION
Local regulatory reflexes within the gut are activated when C fibers are stimulated.
= = = :.:.:....
.
_ _ . .._._.. _._. _ ..
Postoperative pain is a complication that gastrointesti nal surgeons deal with frequent.Iy. Abdominal pain, otherwise called colic, is defined as 'an unplea�ant 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
•
gradual nature in onset. C fibers utilize substance P and
Three pathways mediate abdominal pain I . first-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-order 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
stimulus from the site of injury to the central
spinothalamic system to the somatosensory cortex
nervous system
and from the spinoreticular system to the limbic
the various reactions in response to pain.
system and frontal lobe of the cortex.
Thus postopemtive pain, induced by gastrointestinal
These multiple inputs of nociception in the eNS clabo..
surgical procedures, induces a series of behavioral,
rate the variability of pain.
neurophysiological, endocrine, metabolic, and cellular
Abdominal visceral nociceptors respond to mechan
responses (the stress response) that initiate, maintain,
ical and chemical stimuli. The primary mechanical sig
and intensify the release of pain and inflammatory
nal to which visceI'".ti nociceptors arc sensitive i.� stretch.
mediators. I tshould be stated that pain is a complex sen
This differs to somatoparietal nociceptors in that cut
sation that can manifest differently in horses affected by
ting, tearing, or crushing of viscera does not elicit pain.
similar abdominal problems. It is the surgeon's respon-
The visceral stretch receptors are located in the muscu-
204
POSTOPERATIVE TREATMENT AND COMPLICATIONS
11
lar layers of the ho!low viscem, between the muscularis
input to the spinal cord and eNS. Conversely, recurrent
lllucosa and submucosa, also in the serosa of solid
gastrointestinal pain (e.g. with re-laparotomy) may sen
or!fans as well as in the mesentery. Mechanoreceptor
sitize intestinal receptors making perception of baseline
stimulat.ion can result from rapid distention of a viscus
afferent activity more painful.
(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
CLINICAL SIGNS Postoperative pain is usually less intense than the pain exp�ri�nced preoperatively unless
• •
postoperative ileus results in similar distention
serotonin, bmdykinin, leukotrienes, prostaglandin E�, illtnleukins (IL-l, IL-6), neutrophil-chemotactic pep
•
there is recurrence of the original lesion or the original lesion was not corrected surgically
tides, nen'e growth factor (:-.JGF) 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
there is ongoing tissue ischemia
•
a new lesion has developed .
Abdominal pain can be sepamted into three distinct calegories
• visceral
resulting from the recruitment of certain (silent) affer
•
somatoparietal
ent receptors. With prolonged or recurrent peripheral
•
referred.
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
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 as well as the human patient that preoperative treatment with local or regional anesthesia or non-steroidal anti-inflammatory drugs (NSAlDs) results in reduced severity of postoper ative pain. This implies that CNS response to peripheral injury can be mediated by prior reduction of afferent
Visceral pain is caused by nox:ious 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 t.hese various types of pain. In a�sessing pain the general attitude of the patient should first 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, sweat.ing, and quivering of the upper lip. The severity of pain can vary from mild (occasional pawing) to severe (dropping to the ground and rolling violently). 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 ofways and some horses have a greater tolerance to pain than others. The external 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 pleura
205
11
coue
• sweat.ing also indicates severe pain and potential
(ileus, intestinal spasm) causing the pain. Although elimination of the problem is not always possible,
response to endotoxic shock.
reduction of pain with effective analgesics will decrease the reflex inhibition of motility. This in turn often resolves the common causes of postoper
DIAGNOSIS
as distention due to ileus, and inflammation due to 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.'iIl 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 tympany, 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
intestinal manipulation. Effective analgesia will also eliminate or minimize the visceral 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 viscus. 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-
Walking or acupuncture
the incision line. Chemical sedation, the use of a twitch,
Walking may also have an analgesic effect on abdominal
and rectally administered Ildocaine (lignocaine) may
pain especially mild pain. This is a common therapy
al! contribute
that appears to increase motility and reduce anxiety.
to
a reduction in straining.
t:ltr
Some surgeons have also used acupuncture. "VI'hile clin
nostic [001 forsmal1 iIltestinal problems (see Chapter 2).
ical data are lacking, some clinicians teel that the posi
V-!hen small intestinal distention is suspected a5 the
tive effects can be appreciated and the risk of hann or
cause of pain transabdominal ultrasound is very helpful.
toxic effects is minimal.
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 type of lesion identified in surgery, the degree of contamination, and the length of time since surgery. In general, in the author's experi 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 surgery in cases that were progressing well.
Non-steroidal anti-inflammatory drugs 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 evidence of efficacy 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
TREATMENT
drugs. These drugs reduce the production of throm
Goals
inhibition of cydooxygenase (COX) enzymes. It is now
boxane, prostaglandins, and prostacyclin through the
The goal in treating postoperative pain is to provide
known that there are two isoforms of COX, designated as COX-l and COX-2. The constitutive enzyme COX-l
quick effective analgesia, and to eliminate the reflexes
performs 'housekeeeping' activities in platelets, gastro-
206
POSTOPERATIVE TREATMENT AND COMPLICAnONS
Table
11
l1�Ait"""""" ."dtblfrrNtlYi.��;"'--
",.... io� Udomtn.l-"'�
.
An.lgulc
DOS.,.
Effectlv-n...
Aspirin
20-40 mg/kg p.o.
poor
Butorphanol
0.02-0.075 mglkg Lv.
good
Chloral hydrate
30--60 mg/kg Lv. titrated
fair
Detomidine
1()-.40 mglkg i.v.
excellent
Dipyrone
10 mglkg Lv. or tm.
fair
Eltenac
0.5--1 mg/kg
undetermined
Flunixin meglumine
0.25-1.1 mg/kg Lv. or Lm.
exceUent
Ketoprofen
1 .1-2.2 mgikg Lv.
good (variable)
Udocaine2%
slow Lv. bolus 1.3 mg/kg over
good
5 min. then i.v. drip at 0.05 mg kg-' min-1 Phenylbutazone
2.2-4.4 mglk.g Lv.
fair
Xylazine
0.2-1. l mg/kg Lv. or i.m.
goocH!)(ceUent
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 eflects of NSAIDs and that anti-inflammatory and analgesic effects result from COX-2 inhibition. Prostaglandins (PGE� and PGI) sensitize nen:e endings to 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 specifically 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 efficacious 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
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 visceral 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 significant 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 l...;'SAID reported to have anti spasmodic effecL� on the bowel due to 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.
• 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.
Alpha2 agonists and sedatives
The dosage and frequency of administration should be based on the intra-operative findings. the demeanor of
Alpha2 agonists are potent analgesics that bind to and transduce biological effects of the endogenous catecholamines epinephrine and norepinephrine.
207
11
COLIC
Recently, alpha... adrenergic receptors have been phar macologically characterized into four subtypes • • • •
alpha.a alph�b alpha2c a!pha..,d.
The alph�a 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 firing. 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 0-40 min). Bradycardia, decreased cardiac output, hypotension. ileus, and reduced blood floware all poten tial side effects. Prolonged effects of xylazine can often be 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 sufficiently 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 ifa 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. Classification of opioids is based on a functional breakdown of activity at opioid receptors. Therefore, they are classified as agonists, agonist.�-antagonists (mixed opioids), and antagonists. Opioids exen their effects 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-carrying 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 as 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 efficacious as the alpha2 agonists. When used in combination with xylazine or detomidine excellent analgesic effect.� 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 suppres�ing trdnsmission through afferent sensory pathways. Experimentally serosal damage. intestinal distention, endotoxemia, peritonitis. and surgical manipulation have al! been associated with enhanced sympathetic 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 effects 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
POSTOPERATIVE TREATMENT AND COMPLICATIONS
11
inflalnmawry response, this in turn increases the pro
so many animals are managed medically, remain
dunion of pain neurotransmitters which further raise Ihe inflammalory response resulting in an elevation in
asymptomatic, or die or are euthanized without an examination, Estimates of the incidence of adhesions
the excitahility of sensory neurons. Pain produces a
are taken from reports following repeat celiotomy and
depressed state, increases inflammation, reduces wound
necropsy, or from experimental studies. Adhesions
ilt'alillg,
were the second-most common (18.9%) reason for
and
depresses
the
immune
response.
Pharmacotherapy should be directed at peripheral noci
repeat laparotomy in one study, All the horses that had
ceptofs, primary and secondary spinal neurons, and
obstructing adhesions at the second surge!)' had a
pain-proclC'ssing areas in the eNS. These areas include
small intestinal lesion at the first surgery. Other
"pioid receptors, drugs that bind to alphat reLeptors,
reports documenting the incidence of adhesions in
and drugs that reduce df! IIIlVD prostaglandin synthesis.
horses following small intestinal surgery range from
Based on the intraoperative procedures done in ..ach horse, appropriatlC' analgt·sia should hI:' provided
6--22 per cent. and 5 per cent follov"oing all equine intestinal surgc!)'_
in Ihe perioperative stages. Preventative pain manage
It may be that the smali intestinal serosa is more
mellt should be instituted before progression ofdinical
prone to damage from distention, ischemia, and manip
sigm occurs postoperatively in these horses. Often
ulation. Furthermore, the multiple loops of the small
early, subtle signs of pain lIlay be overlooked. Early
bowel with its long mesentery' and relatively small
diagnosis and tn�atment of abdominal pain decreases
lumen make it more likely to become compromised
overall patient morbidit), and the cost of patient care,
from adherence to acUacent loops and subsequent
thereby allowing tbe clinicians' tilile to be better spent
mechanieal obstfULtion. Other risk factors include
on illore productilie endeavors.
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.
Ab dominal a dh es ions
However, without specific, controlled studies concrele conclusions cannot be made.
SL Fubini INTRODUCTION
PATHOPHYSIOLOGY
'Adhesions are both the salvation and the bane of the abdominal sUIgnm' (editorial, Th� I.anal,July 5, 1980).
Adhesions result when there is an imbalance between
Formation of a fibrous union beh,'een serosal surfaces is esselltial for a successful completion of abdominal surge!)' sucb as an intestinal resection.
Howelier,
unwanted adJ:Iesions 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 infertility 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 veterinary 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 hors�s, it is possihle that studies focusing on adhesion prevention in bumans could be applied to the horse a'pd vice liersa.
fibrin deposition and fibrinolysis. Trauma to the vis ceral or parietal peritoneum results in an inflammatory response and rdea�e 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' cells. Plasminogen is converted to plasmin which, in turn, lyses fibrin, This delicate balance is maintained by pla�min (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
INCIDENCE OF ADHESIONS
also
inactivates
plasminogen
activator
inhibitor-l
thereby promoting fibrinolysis. The prima!)' inhibitors It is virtually impossible to aecurately determine the
of fibrinolysis are plasminogen activator inhibitor-I.
incidence of postoperatilie adhesions in horses because
which prevents the formation of pla�min by inactivating 209
11
COLIC
tisslle plasmi nogen ac.:livlI[Of, and a[ph�-antjplasmin I,"hkh inaClh�dU� plasmin. If Ill(" (!lId re.\ult is 311 imrainncllt in fibrinolysi.�, (hen fibrin()l1� bands become infihrated "llh fibmblasts whi.-h produn� collagen and a potcntially pt-'ommelll arlht"�ion. This proccs.� is usually complete by 7-14 clays Imt lhcn: may I)c rcnwdding 0\"1:( lime:.
EXPERIMENTAL MODELS OF ADHESION FORMATION Unfortunately. there is om one completely repro dudhlc mudd for adhc�ion production. Over the years, (�J(p{:rim(!ntal sludic� haW! used either lllodels where scr(ls
i
Adherellce to the surgical prlll:ipies of minimizing 'time, tmuma. ltnd nash' is the best way to decrease the Ji\k of p').�topcratlvc adhe.�ions. Short, efficient surgical times, "'Iith 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 seTOS", and ischemic tissue all increase the risk of adhe sions. SnUle �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 after surg(:I1'·
ADHESION PREVENTION I" a I"el'it:l" 4tnick in 1991, Pijlman 1'1 aI. dc:scribcd 'five fund:un('nlal attacks' lor ildhcsiun rr�l�ntion first describc.'d by Bo}'� in 1912, these
• •
limit or prc'l'Cnt rx-riwneal injury rren'lU c'!I
210
keep the fihrin-coatt:"d peritollea! surfaces apart
• inhibi t the tihrobla.uic proliferation once csuhlished.
Th� c:alcgmics call be regrouped into four di\i!;iolls.
Hetiur.liQn ofthe injiammntmy 'IJ"uu,n
Dt:c:rcasing peritollC"dl inflammation is best done by adhering W a.�t'ptic and atrdumatic surgical pr-inciple-s. I t also hclp.� In avoid dC»iurc of the peritonea! defect ;IS thi� has been �hown tn i ncrease:: adhC'..sions. One recent study adl'ocates ptl!'lwpcratil'c pcritonc
TherdpeU!ic: agents that have been �tudjed as anti inflammatory agentq indudc I . Corticoste roids - studies in laboratory animals arc
poorly controlled and are cOntroversial. Repeated corticosteroid use is nOI r�ommcndcd in the horse became of the risk 01" lamini tis and the possibility of a ncgati\'(' impar.t on wnund healing. 2. NOIH[('roicla\ anti·inflammatorydrugs ..... these are muli ncly used perioperauvely in horses undergoing abdominal surgery. Again, sludies in Iilboratory animals ha\"(� nOI been ctmcillsive. Inhibit;,,,, ojwnguffllivn Heparin, a cofactor of antithrOmbin Ill. has �n used
SURGICAL PROTOCOL
•
•
10
dinically and in one e7t.perimental �tlldy for arlhesioll
prevcu lion. In theory hcparin decrca.';-('s thrombin pro· duction and �timulaw5 plasminogen :.
Studies using plasminogen aCtiv:.ltors including fihrino I�in, $trep[okif)a�e, ann urokinase were varied and inconclusive. More recently, ti�me-type plasminogen activator appears to be effective and safe in rat� and rab bits. FUr/her .�Iud ies are needed and the cost of [he product is high.
SeparaJ;OIl oflur/al'.l High molecular "'Ieight substanccs and ph}"Sical barriers hal'� been used in the peritoneal cavity
kcep fibrin to allow ror mesolhelial repair and to pn:vent ad hesions. Sodium c;uboxymelhyl cellulOSe (SCMC) h� been used most fommonly in the horr.e a., a 1 % solUTion at a doSt' of c.overed surface., apart long
enough
to
POSTOPERATIVE TREATMENT AND COMPLICATIONS
11
7 ;ljkg. It is used to coat serosal surfaces and to help
peritonitis, electrolyte imbalances, endotoxemia, and
protect the
manipulation.
anesthesia. In a recent report, POI developed in 21 per
Polyvinylpyrrolidone, dextrans, and hyaluronan are
cent of horses undergoing surgical lreatment of colic,
othn polymer solutions thal have shown some promise
and 1 3 per cent of these cases dicd. Although current
bowel
during
intestinal
t'xp(�rimentally. For more details on these and physical
management of these cases has improved, postopera
barrkrs,
tive ileus is still associated with 40 per cent of all post
see
Southwood
and
Baxter
( 1 997)
and
Chapter JO.
operative deaths in horses "'�th colic.
ADHESION TREATMENT
PHYSIOLOGY OF NORMAL MOTILITY
Horses with evidence of partial obstftlction (Iow-grade
Inteslinal smooth muscle cells demonstrate cyclic
abdominal pain) may r('spond to medical management
changes in membrane eIf'ctrical poto:"lllial that are
induding demal work and a laxative diet such as
called
pasture or low-residue feeds.
smooth muscle cells arc connected to each other by gap
In some cases of adhesions, euthanasia may be indi
'slow waves' or 'pacesetter potentials'. The
junnions which enable the electrical activity of one cell
repeat celiotomy with
to affect the activity of an adjacent cell (electrical
adhesiolysis and/or bypass of the affected segment may
coupling) through the movement of ions. Since the
be successful. Unfortunately, broken-down adhesions
frequency of the membrane oscillations is highest in
caled.
In
other instances,
ar{� highly vascular and may re-form unless the involved
proximally located cells. thesc slow waves are initiated
tissues are resected.
orally and propagated aborally. They are sub-threshold
The
repeat
in that they do not depolariLc the ceIl sufficiently to
celiotomy is poor. Hopefully, as our peri- and intra
reach the threshold to generate an action potential.
openttive anesthetic and surgical knowledge advanc('s,
111ese sub-threshold fluctuations afe controlled primar
so will our understanding and ability to prevent cala
ily by inlrinsic properties of the smooth muscle cdls.
strophic adhesions.
Additional depolari7:ing (excitatory) input from the
long
term
sunival
rate
following
enteric (intrinsic) or autonomic (extrinsic) !lelVOUS system allows the memhrane to reach the threshold
I leus P Rakestraw
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
DEFINITION AND INCIDENCE
depolari/.ation the cell is closest
to
its threshold for
generating an action potentiaL This is why slow waves lIeus is the impairment of aboral transit ofga�trointe�t.i
are also called pacesetter potentials.
llal contenL'i. The term has been uscd in dillerent ways
The activity level of the intestinc is not constant bw
in the equine literature, sometimes vel;' broadly to
goes through periods of quiescence alternating with
include both functional and mechanical obstructions,
periods of spiking activity. The pattern of these difkr
and sometimes its use is limited to functional impair
em activity periods in the stomach and small imestine is
ment of gastrointestinal transit. In this chapter the
called the migrating myoelectric complex (MMe).
author defines the term ileus as a functional obstruc
There are four phases of the \-fMC
tion (adynamic ileus) of aboral gastrointestinal transit.
•
Ileus is one of the mOSl commonly encountered complications of equine gastrointestinal surgery. In ho!"SCs, 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
phase 1 describes a period with no spike potentials, so no contractions occur
•
phase 2 is a period of intermittent spike potentials
•
phase 3is associated with regular spiking activity
•
phase 4 is associated with rapidly diminishing contracliie activity.
handling of the intestine, inte�tinal di�lention, resec
Each phase migrates down thc stomach and small intes
tion and anastomosis, and intestinal ischemia may con
tine. Phase 3 is generally associated with propulsion of
tribute to ileus in these cases. Other conditions that
ingesta, and in the horse phase 2 has also been associ
havc been associated with ileus are anterior enteritis,
ated with propagation of ingesta. In the cecum and 211
11
COLIC
. vcs and spiking aCliviry aIm large: int("�tjnc. �()W \\"J
• decn:a.'lCd or ah.�ent borblllJ'gmi
occur. H,\\,'c\'CI' M�1C:' arc no. evident. Instead. short
•
abdominal (Ii�tention
spikt" bursts (SSB) occur during mixing, and long spike
•
elcvillCd heart nile
rluring pl'Opulsioli ofingcsla.
• •
congeslerl mul,,()us m�mbranes prolonged capillalJ' r(.'fiJl time
•
na�astric rellux.
hurm
(L5B)
PATHOPHYSIOLOGY AND THERAPEUTIC MODIFICATION
11le first signs .....O«Kiatcd . wllh ilelL'; are riepft's..'liun anri anor(:)(ia. A� the inlt'stillt! distends the horse demon
It should he e\;nclll from the above description of the ph)'si{)k�1 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 (011tract in a CO(lNlinaled manner, while the aboral s.cction is simuhalH�olLsly inhibited and relaxed gressive Iran�it to
OCCIir.
allow pro
to
An imbalance in Ihe Eu: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 prokint'lic agc-n.. t that wnnld restore the halance 1>('t\\'l'l'n cxduuo!')' and inhihitol)' control of (lmtractil ity. Ph,U'ltlaco[ogical modulation aimed at int:rcasing I');c.llator),
. trUillll
HI'
par.t'ympathomim�ti(:
ag�nl.�,
such
...,
hClh
Similarly,
cli'
....urh as
::In indiTl..'Ct
p
and so cnhandng acetylcholine
hind,
rc:l�dSC. Aucmpls
inhihitm), components or contractilily ha\'e
r(lctlSI� (.In the ...ympathctk !ir�tem. S)111pathelic hyper act"'i1r shoulct re�pond
such
iU
In alpha adrenergic block.ers )�)himhlne lind acepromaJ:ine. while adminis
tration of alpha adrenergic druhT); such as "ylal.ine and dctomidinc sh(Jultl dt:creasc motility. Metodopramide,
strates inaeasinp; .�igIlN or abdominal distn�ss such a.\ pawing, flank watl:hing, 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 distf"nlion. '1'11(: mucous memhranes hccollll' '
discolored and capillary refill
[ime is prolonged.
Hernoc(JI\cemratio!l is rdIcClcd hy iJl(:rf"
c:dl volume and tot.al protein. Decreases in
plasllla (:hloride and potas. �illm are the most comlllon
electrolyte ahnormalities seen, although sodium and calcium may also b�� low. As the �everity of the intesti nal distention illcl'east's, abdominal distention may become gro�[r visihle. Rectal examination will help determine if the small or large imestine is illvolw'd. In foals, hmh K'''t'� ric del'omprcs- sion provides all important due that Ihe problt:m is a functional prohlem. Arter decompressiull the horse
should show some improvement such ...� (kcrca.�ed pain and ht:arl "Ue. Ir no alle\-latioll of signs are observed, cart:ful lhllught should he gh'en to {he likeli· hood that the problem may he a mechanical It'Sion and not a functional ileus.
\\'hirh is
SUPPORTIVE THERAPY Although a varll:IY of prokinctir agent.� have hl'en
DIAGNOSIS Disruption of propulsil'e motility rcsull� in Ihe seques [rati(111 of fluid. gas, and ingesta in the _�egment of the gasLroint�sliL1al {(';iC! which is dr;fullt:tional and in the iIHC'stinc proximal m the ahnormal arca. Thi� disten lion OC(:UI"!\ primaril)' in Ihe stomach and small intC'5lillt', but tan ()<:C.ur in the larJ{c inlt"Sline. especially with (olilis, enrlotu)(emia, or iKhemia following a large
n,jon �·tJh11111S. The Imljor dinical signs and findin� secn ill ht)J�'s alTerted by p(lstoperative ileus arc
administered {() hones with ileu� in an attempt
to
improve gastrointestinal motility, th(: lack of consenslls as to which OIlC, if any, are effcctive attests to th�ir therapemk limitatiolls (Table 1 1 .4) Consequelltly, th� hallmark ofLreatmc-lIt remains supportive therapy, with fluid, add-o
trCattnenl�
In
ally
hor:t.c
with
rnm!
..olie
Antihiotics are also indicated ir there is compromised
inte.�tine or the pos.�ihility or har.ll'rial ('onlamination
,
CautilJll should be exercised whcn lreating lhesc horses with the common analgesics (snch as the alpha
•
rieprc$Sio tl
agonist-antagonist butorphanol)
•
anorexia
have the potential 10 depress ga�ll'()inlestinal motilit}'
•
aMominal pain
with n:pcatcd usc.
212
a�
these medications
POSTOPERATIVE TREATMENT AND COMPLICATIONS
TIIbtt 11." Trutments and InInltgelTlent of postoJMrativeUeus
Fluid, acid-base, and electrolyte therapy Antibiotics Nasogastric intubation Non-steroidal anti-inflammatory drugs flunixin meglumine phenylbutazone ketoprofen
11
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 the�e 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
Polymyxin B
l . l mg/kg h.i.rl. i.v.). It alleviates some of the systemic
Dimethylsulfoxide
effecL� of endotoxin and also provides some analgesic
Hyperimmune serum/plasma Prokinetic agents
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
bethanecol neostigmine
drug is not as potent as flunixin in blocking the cardio
acepromazine
vascular efICcts of endotoxin, it does appear effective in
yohimbine erythromycin
experimental endotoxin infusion. Ketoprofen (2.2 mg/
reducing
metodopramide cisapride
the
motility disturbances
associated with
kg h.i.d. i.v.) has not been evaluated in ileus models, however because of its anti-prostaglandin and anti
lidocaine
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
NASOGASTRIC DECOMPRESSION
potential inhibitory sympathetic reflexes. High dosages and prolonged use of NSAID may inhibit. large bowel motility.
Rt'pl'ated attempts to relieve gastric distention are
Another drug that is used at the author's hospital to
imperative in trcating a suspectcd ilcus case. In certain
treat horses with ileus is polylllyxin B (6000 IV/kg s.i.d.
(a.,e� reflux may not he obtaincd during thc first
i.v.) a cationic antibiotic that binds lipid A ,md neutral
allemp!. In horses \"hcre nasogastric reflux is obtained
izes
the tube can he left in place or reliloved and intermit
hydroxyl radical scavenger commonly used to treat
endotoxin.
Dimethylsulfoxide
(DMSO)
is
a
t"'lltly replaced to check for reflux. Tlw frequency of
endotoxemia and other inllammatol}' processes in
attempting to decompress a horse with reflux depends
horses at a dosage of 0.5- 1 . 0 g/kg (10% solution i n 5%
both on the dinical signs and the amount of reflux
dextrose). Although it has not been evaluated relativc
Idrit-ved at each session. An increa�ing heart rate is
to promoting gastrointcstinal motility, its anti-inflam
prohably one of the most sensitive clinical indications to
matory actions may be bendkial in preventing or
allempt to retrieve reflux. Increasing abdominal pain is
decreasing the scverity of ileus. Commercially available
another indication. As the volume of reflux begins to
hyperillllllune serum contains anti-I.PS antibodies to
1-2 l/h, the interval
Elrlil'ril'hia loli or Salmonella Iyphimurium. These anti-LPS
h(,tw('en reflux attempts can he increased. It is not
antibodies theoretically cross react \\ith endo[Oxins
decline and reaches less than
l!llusual to ohw.in a liter or more per hour of rdlux frolll
from all gram-negative bacteria. The evidence for their
horses, especially those who have:l nasogastric tube left
efficacy has not been conclusivc.
in place. This should not be mistaken as a condition that lll"Ccssarily requires continued tr�atment. II" there is any doubt, the tube should be withdrawn and the horse's hean rate and level of pain monitored closely.
PROKINETIC AGENTS
Bethanecol ANTI·INFLAMMATORY 'ANTI'·ENDOTOXIN DRUGS
which stimulates acetylcholine receptors on gastro
Int('stinal distention, ischemia, and trauma occurring
Support for the use of bethanecol in the treatnlt'Cnt of
dllrillg decompression and/or resection and anastomo
motility disorders in tht� horse is predicated on ohserva
sis all induce inflammation of the bowel wall with an
tions in normal horses that it increases the rate of
Bethanccol chloride is a muscarinic chdlincrgic agonist intestinal smooth muscle. causing them to contract.
213
11
COLIC
gastric and cecilI emptying as measured by radiolahded
as the drug can produce hypotension. Yohimbine
isotopes, and it induces premature MMC phase 3-likc
administered at 75 Ilg/kg was demonstrated to attenu
activity in the ileum. Although its eflicacy in the treat
ate some of the negative effects that endotoxin has on
ment of experimentally induced mO(.ililY dysfunction
propulsive motility. Since this dntg is a seJectiw alpha�
has bet�n questioned in the horse and other species, its
antagonist
prokinetic effects in normll! horses and the clinical
response seen with acepromazine.
it
docs
not
produce
the
hypotensive
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 u:" (wry 4-fi 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 effects of neostigmine (0.022 mg/kgi.v.) varied depmdingon the location of the ga�trointestinal tract examined. It was shown to delay !fastric emptying and decrease propulsive motility in the jejunum, to increase propulsive motility at the pelvic flexure. In another study, neostigmine
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 relea�e 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 efl"ccts are infrequent but some clinicians have reponed obse!\ling abdominal pain and, in a fCw cases, diarrhea.
Metodopramide
increased the amplitude of rhythmic contractions in
Metodopramide is thought to exert its prokinetic
both resting and distended jejunum in anesthetized
actions primarily though dopamine receptor antago
ponies. More recently, neostigmine (0.025 mg/kg s.c.)
nism. It mily also indirectly stimulate acetylcholine
wa.� shown to induce premature phase 3-like activity in
release and block adrenergic activity. In a POI model,
the ileum ,Uld increase the rate ofcecal emptying. There
metodopramide was more efl"enive in restoring gastro
has heen no consensus as to the recommended use of this drug. It appears to be an effective drug for large
intestinal coordination, a measurement of motility strongly correlated to return of normal transit, than
colon motility problems, but these OCCUI" infrequently.
adrenergic antagonists or cholinergic agonists.
Some evidence suggeSL'i it Illayalso be useful for POI with
horses the drug is commonly administered al a dosage
In
small intestinal motility dysfunction. I Iowever, its usc for
of 0.25 mg/kg, diluted in 500 ml of saline, infused over
impactions or in cases with excess gastrointestinal dis
30-60 minutes. Some evidence suggests that a continu
tention has not been recommended because of the
ous infusion (0.04 mg kg-I h-I) may be more effective.
apparent force of drug-induced contractions. The most
Metodopramide (especially at the 0.25 rng/kg dose)
COillmon side effect is ahdominal pain.
may cause extrapyramidal side cffecb such as excite
Acepromazine and yohimbine
abdominal cramping.
ment, restlessness, and sweating. It may also produce
Both of these drugs arc alpha adrenergic antagonists. Elevated serum catecholamines have been associated with increased synthesis of norepinephrine in the bowel
Cisapride Cisapride is probably the most commonly used pro
wall in humans after laparotomy. :\orepinephrine is an
kinetic in human medicine. It appears to function a� an
inhihitory neurotransmitter released by post-synaptic
indirect cholinergic stimulant by .�electively enhancing
sympathetic Ileurons at the enteric ganglia. It inhibits
the relea�e of acetylcholine from postganglionic oen
the relea.�e of the excitatory neurotr.lllsminer acetyl choline by stimulating alpha-2 receptors located on
other species cisapride appeared more effective than
cholinergic neurons. Acetylpromazine maleate (ace
metoc\opramide in stimulating progressive smaIl and
promalinc) facilitates small intestinal transit in normal
large intestinal motility in experimental ileus models. It
rons in the myenteric plexus. In numerous trials in
ponies. Rased on clinical impression. acepromazine
has also been shown to be effective in prcvcnting POI in
(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
horses. Unfortunately it is only available as an ofal preparation which is ullsuiLable for horses \'I1th reflux.
.�h()u!d be taken 10 make Sllre the horse is well hydrated
Recently it was found that the drug is not absorbed in a
214
POSTOPERATIVE TREATMENT AND COMPLICATIONS
11
consistent manner rectally ill horses and so this route of
surgically for acute gastrointestinal obstruction were
Mlministration should not be rdied on. Lse of the oral
suqjected to a repeat celiotomy. Only 3 (5.5%) of these
preparation in horses with large colon motility dysfunc
53 repeat celiotomy cases had impaction at an anasto
tion may be efficacious. The bioav:aiIahility of the oral
mosis. When they occur, they are often associated with
preparation in the horse is not as good as in humans
too rapid an increase in the amoum of food ofkred to
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
the patient in the postoperative period. Although some cases of 'ileus' may actually involve impactions at the anastomosis and resolve vlo'ith 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
reduce the concentration of circulating
intestines occurs early in the postoperative pcriod, i.e.
fatecholamines by supprcssinll; tht>
day 3-7 postoperatively. For small intt>stinal lesions
svmpathoadrcnal response �. suppress activity of the primary afferent neurons imol\'ed in reflex inhibition of gut motility
without nasog:astric reflux, the author often ofIcrs a small amount of feed (a handf\ll of alfalfa) within the first 24 hours
3. stimulate smooth muscle directly
hour intervals over the next 72 hours. It has been sug
4. decrease the inflammatory response.
gested that this early return to feed facilitates the return
Tlw dose used to treat horses is an initial holus of
1.3 mg/kg i.v. administered over 5 minutes followed by I mire' in saline over 24 hours. Side effects
(J.U} mg kg
include muscle fascicul:ations, trembling, and ataxia.
of normal ga�trointestinal 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 feeding
is
increased too rapidly and an impaction occurs, a sec ond surgery may be necessary to massage the impaction
PROGNOSIS It is the author's impression that the incidence of POI is decreasing. This may be because of more timely refer r
pa�t 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 lea�t 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 .i�junocecos 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 je:junocecostomy anastomosis. Impaction at an an:astomosis in the large colon usu ally occurs because the stoma which was made when the
I mp action at th e anastomos is P Rakestraw
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 necessary to enlarge the stoma.
Impaction at the anastomosis is an uncommon surgical
The sm:all colon is potentially more susceptible to
complication. In one repoft, 53 of 648 cases treat.ed
impaction at the anastomosis (Of enterotomy) because
215
11
COLIC
of the firm consistency of the ingesta in this region.
•
duration of surgery, this should be less than
These impanions at the site of anaswmosis of the small
•
usc of good perioperative pain control
colon occur early in the postoperative period, i.e. day
•
length of convalescent period, the horse should be
3-7 poslopt.'fatively. V·lith careful management, for
kept out of training until at least 2 months
example emptying the large (olon at surgery, fluid ther
postoperatively.
ap)" and slow placement hack on feed (small handfuls of allall"l ) , these also occur infrequently. As with the small intestine, it is usually not necessary 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 difference between a suc cessful ourcorne or a f;lilure and should IHl!. he delayed
2 hours
Factors that incretlse 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
• • •
if the horse is not responding as expected medically.
debilitating conditions such as hypoproteinemia stormy recovery 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 tJlt�se patienl.';.
I ncisional comp l ications NG
Ducharme
CLINICAL SIGNS
INTRODUCTION Approprhnc lluimp<.'dcd wound healing reSU!L� in sum clem sln�ngth 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
Acute incisional disruption (dehiscence) Acute incisional dismption generally occurs withill H days of surgery tlnd, 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!\latioll of omentum at the incision site is a grave sign of impending dehisccnce. In most cases, physical
•
d<'hi�cnC{�
examination identifies the diagnosis and extent of the
•
drainage
problem. In some cases ultrasound examination will
•
hernia.
assist in defining the extent of the lesion.
Ally incisiollal drainage at an incision is suggestive of abnormal wound healing. Drainage delays wound heal ing and weakClls abdominal fascia.
Incisional hemorrhage Clinical signs are obvious in so far as blood is draining from the incision within a few hours after surge!)'.
PREDISPOSING FACTORS
using physical examination, the clinician can deter mine if the hemorrhage is due to tin arterial bleeder from
The veterinarian and animal a!tendallt� responsible for
the
incision,
one
or
more
venous bleeders
from the incision, or intra-abdominal hemorrhage.
postoperative care of palient� should 1:)(' a\vare of the
10 animals experiencing incisional com
Incisiona! arterial hleeders have a small stream of hem
i]J{H�;\scd risks
orrhage spurting from the incision while venous hleed
piic
ers 001:(' out of the incision at one or more sites.
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
• use 01 optimal (sec Chapter
216
surgical t�chniques and materials
10)
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 •
inci.�ional bleeding
• •
decreased pulse quality blanching of mucous membranes
POSTOPERATIVE TREATMENT AND COMPLICATIONS
•
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 suturees failed, peeri tOlwal fluid will leak out of the abdomen. Because of tht' dye effect of blood on peritonea! fluid, it may be dif ficult to diffcreentiate 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 diffeeremiate thee 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 ,'xlwcted to on:ur within a few hours of surgez:·.
Incisional drainage and infection Any incisional drainage, except perhaps Jill' mild blet�d ing it few hours postoperatiwly. should be considered abnormal and may represent an incisional infection. The preeseellce 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 hernias may be .�ec[)!ldaz:' to •
>utun' or abdomina! wall failure in the po�t[)perath·e period • incisional infection • carly return 10 exercise. Tlw last cauS{' of incisional hernia 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 !O a box stall for 6 weeks postoperativdv, although daily hand walking should be allowed. The abdominal incision should be eevaluated 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 hernia is negligible. A ren�nt report suggests that a 2-month postoperative incision has suHkielll strength to withstand normal activity.
11
Two types of incisional h(�rnias can be seen post operatively. 1 . A Traditional hernia within t.he incision with a
reducible hernial 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 incisiona1 areas should be repaired 6ther by applying a mesh over tbe arca or by a complete revision of the incision. Other horses, eveen racehorses, wir.h 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 10 induction of anesthesia. Tbe belly bandage alone \\i!l not prevent evisn�ration 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 thee reason for dehiscence is Etilure of a sutnre mater ial, tbeen revision with a larger-sized (greater strength) suturc call he done. Copious lavage of the im;ision site with sterile physiological solution containing broad spectrnm 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 (Figllree 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, NY) can be sutured superficial to the skin over tbe incision (after local anesthesia). This leads to open peritoneal drainage and requirees 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 Wheell indsional bleeding is noted the source of the bleeding must be identificd, A preswre bandage should treat incisional bleeding associated with incisional
217
11
COLIC
Figure 11.1 Placement of through-and-through steel sutures in the repa i r of incisionai dehiscence
Figure 1 1 .2 Equine reusable abdominal bandages being applied
appropria te blood donur
(cross·match)
" esse! leakage. The o�jc<: ri\'� is to arrest. bleeding by
identify
app lyi n g counter pressure. It i.'i i mportant thil.t enough
should be initiawd. Intr.d\,CClOlIS fl uid adminislralion
m :.
pressHre be applied not only to prc\'t'.n t hlood from
rat.(�s should be a{ljusl.ccl appropriatc!r (S(,:(: Chaptn 9
(�scaping the incision, but (�qually importan t) to pre
Fluid and e1ectrolyle therapy and acid-hase balan n;' ill
\'t'l)t subcutaneous hClnorrhage since it predisposc� i m: isi onal If
illfection (Figure 1 1 .3).
imra-ahdominal
t'xtn."l1lt:iy
r"n�
hemorrhuge
OCCllrs,
it
is
tha t t.he clinician Il(�eds to (or ::;houici)
fe-anesrhetize the animal to searc:h for [he hleeder. The goa[ i'i
(()
�'prly sufficient pn:ssuTc to sC
and pre\'en t the horiy's loss of red bl ood (elis. 'A'hcn serious hemon"hagt' is prest.'n 1 , hlood vl.'ill soak Ihroug-h
rhe bell y handages. Rather than r(�moving the bandage, a
seculid layer can he applied with mOTe press un:. If this
s to ps the hemorrhage or reduces it to a slow d ri p, the hll:ndages can be left in place for G-8 hours. If th is dDe�
not stop rhe hemorrhage , the inner handll:ges must he tuo
loose
and should be rese!..
horses with abdominal pain). If syswmk s igns of illlra ahdominal bleeding appear
On
recognition of
abdominll:1 hemorrhage, any he parin therapy alrt'ady initiatt:d should be clisrominued and preparation
(0
to
in c rease in severity, th{'
intravenous administration of 4l lIlino capmi c acid
( to g
in !4 liter of physiological saline solution, up to th rt'(' tlInts rlaily per 450
kg horse) shou l d be considered.
Incisional drainage and infection IndsionaI
infections
arc
t reated
with
approprialt:
drainage, removal of selected skin slIttlfcs/stapl<::5i. and
topical
cl eaning
{he.:
and lavage of
antibio tic.s wmally have
alread y
i ncision . Sysl('mic
been administered a t
the time i n fenions uccur hut may need
LO
be changed
according to hacH'rial rulturc results. It is import.am to
remember that incisional infeclions i nc rease tbe risk of incisional he rniation from f()ur- to ninelcenfolrl.
Incisional hernia Surgical repai r of a hernia is made either by primary
rtpair or placement of a mesh. Prior to repai r ,til sigll:oi of infla mmatio n and i nfec.tio n
mml
generally entitles the surgeon before attempting repair
SQ
[()
be resolved. This
l.'I-<:l it 1-2
mo n t hs
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 an d tht: in fec tion lO rcsolV(". If a non-absorbable suture was used , the suture should be removed prior to attempting
any surgi ca l repair. This can be done with the h()rsc�
standing or
under genNai anesthesia. SlIrgical repair
should nOl be attem p ted Figure " .3 Postoperative indsional bleeding, not subcuta
neous hemorrhage
218
for
itt leas [ I month after
cessation of dr�linage.
BCCatlSe of the elfect of l(!nsion (In
a
hcrniorrhapll)',
POSTOPERATIVE TREATM ENT AND COMPLICATIONS
4i 24-hourfasting (feed only)
11
is recommended. The horse
is
sac,
a fusiform incision
ovt'r lhe ht�rnia ring is made. The incision is exrcn
I he hernia ring t",king cart!
to
ligate or camcfize any
1\igniflt:anl blccders. 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 fingers. The su rgeon a....sesSCs
the prescnc(� or
absence
.. of adhesions and pro
n:t'ds with the resectiun of lhe hernia !;ac afler proper Iransenion/dissenion of the adhesions. The hernia
sac.
and O\'erlying skin is then resected. Primary repair is used
Figure 1 1 .4 Mesh placement for equine hernia repair. Note that the edges are folded over with the folded edge opposite to the abdomi nal cavity
i f t h e.: ('dge of [hc hernia ring (:an tx� re-appo�ed with tension. All
minimal
appositional
panern
in terrupted or cfuciale) is us(�d (sec Chapter
(simple
10 for con
slire abdominal ba ndages do redu<:e s.....elling and mini
sickrari on of �ttturc maLerials). The subcuLaneous laver ' and slin arc clo!ied in an aCC('plable manner.
mize the likelihood of serumas. They should be llstd ,,,ith caution and tailored to the individual, as lhc)' are
\k!ih is used when the lension on the incision edge
associated with preputjal swelling. In addition, alxiomi
is signific3m or when it is needed to rt"pair 'spot' thin
nal bandages c:an increase rhe likelihood of infection
lling of an inc:isiollal are.. . Two types of mesh have been
when
used:
hot weather as sweating (><:CUfS, leadi ng to a moist warm
Marlex
(Dowd
lnc.,
Provi
Pn)xplast (Gosht'n l.ahontUlries, Goshen.
RI)
alld
NY) . Marle x
a
male
manag(.'S to urinate in t.h� bandage, or ill
environment nCiir the incision.
ha" a tend(:nc:y to sag and should rhcrcfore be placed wid1 appropriate (ellsioJl. Absorbable mesh made of
910
polyglactin
or polyglycolic acid IS available, blH to
CONCLUSIONS
Lilt' amhor's knowledge iL has not been used in horses. been
The incisional complication r<1lC appcars to be deuea.�
as tcmporary suppOrt unti l indsional
ing becaw;e of improvenlents in surgical le(:hniqlle �nd,
inkction is resolved. followed b�' plaeemen r ora penna
prohably. earlier surgical intervention. COlrdui atten
For
humans,
n:port<'d to m:1It
absorbahle
Lh�se
ser\'t�
mesh. Meshes arc cut. 8
tn allm,,' their edges
Ie>
em
meshes
have
larg-cr than the (ldecl
be folded. and to ()V('r!:IP the her
tion to preven tion and carly recognition ami trealment are
the key in managi ng thc!;.e frequent complications.
Ilia �rlKe by 2-3 em. The mesh call be used as an ovn-ll'l'
ulltier twO conditions 1.
to
support <\1\ incision that has bc(:11 dosed
primarily but where signitkam tension is present 2. O\'l'r an incision sitc that has th inning area') whcn: no
primal)' repair
is needed.
�1<:sh contacting Ih<; abdominal cavil}' can resull in intt.�.stil1e!i adhering to the mcsh. I t is Lllt�rcfore 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: hernia sac, allowing it
to
form a barri�r between the mesh and the
Postoperative com pl ications - myopathy/neu ropathy .
:
... .
BA Valentine INTRODUCTION Post-ancsthclic
myopathy/neuropathy rerers 1.0 a range.:
or clinical scenarios in which dysfunction of skeletal
inl(:stines, LJsually t.he mesh is lIsed as :an t·nlay suture d
muscle and/ or peripheral nerves occurs in horses fol
tIlt: t:dgc of the defect. Two m<:.�hes an: used with th ei r
lowing gen�ral anesthcsia. This dysfunct.ioll may be
LO
t'dges folded o\'t':r with the folds opposite lht: abdominal
local ized or generalized, painful
cavity (Figure 1 1 .4). 111 allca..(�s, mcsht�s are sccuf(�d with
clin ical signs may be evident during the immediate
or
non-painful, and
absurhable su ture material, preferably monofilamenl,
reco\'ery period or appear da}'s later, ."\.5 suc:h. post
S()nH� sutures 11IUSt he pr-c-piaccrl in the mesh.
anesLhetic myopathy/neuropathy is not
Pos(operdtivcly, it is imporlam to minim ire im.:ision<-tl s\\,'('lIing.
Therefore,
mm-stl'roidal
anti-inflammatory
d l'llg� are aomini.'il.ered for 3-5 days, By
a pplying
pres-
pathologk en tity, bu t rather is
a
a
single ciinic()
manif�tation or
a
!ipectrum of induc ed or inherem neuromuscular dys function evident following anesthesia. I t is estimated
219
11
COlK
that from !�fi 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--60 per cent of anesthesia related deat.hs in horses. It is also likely that subclinical myopathy occurs, particularly in horses with inherent defects of muscle function.
horses, draft breeds, Thoroughbreds, and Stanrlardhrcds thought to be at higher risk. Data to support t.hese hypotheses, however, are scanty and sometimes contra dictory. Other, better substantiated, risk factors include • • • •
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
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 to 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, heavy muscling, high level of fimess, and breed, \v:ith Quarter
220
prolonged duration ofgeneral anesthesia type of padding positioning during surgery systemic hypotension.
The type 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 thermoregulatory 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;\rcopla�mic 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
POSTOPERATIVE TREATMENT AND COMPLICATIONS
periodic paralysis (HYPP) lIlay be more susceptible to anesthetic-induced malignant hyperthermia. Sporadic in l.itro 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}pe of defect may predispose aflected horses to ilnesthetic 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' ilnesthetic-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. Ylyopathies 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 10 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 hor.;e during surgery arc most susceptible. As muscle fiber necrosis, in itself, is neither painful nor results in swelling, i t is clear that \'asntlilr 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 be emphasi7:ed, as it is entirely possible that il lack of these
11
compounds may allow a cycle of increasing membrane i�jury that causes magnification of the low-level muscle injury 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 ent.ities mily 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 weilknl'ss, affected horses often have hard, painful muscles, which ilgain suggests that vascular damage must be involved. Serum ilctivities 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 illlesthesia.
Localized weakness Localized weakness, most often involving a forelimb, is considered to be more often a manifestation of periph 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 surw�ry to avoid compression of peripheral nerve trunks, or pressure damage to the surrounding muscles, will reduce the incidence of this disorder. Damilge to nerves may be structuml or non-structural (conduction block).
Generalized weakness GeneraIi7(�d weakness, in the absence ofmassive 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 polysacchilride 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�,' pha�e. Continued monitoring of serum CK and AST, however, may be indicated in these
221
11
COLIC
breeds and in other horses suspected of having polysar
The placement of the slung horse illlo a pool or foot
charidc storage myopathy, as thefe is evidence that Oll
'l.Ilk t would be ideal.
going muscle ir�tlry can occur up to 5 days Of more
Administration of lipids, either intravenomly or
ro!lo\\'ing apparent recovery. This phenomenon may
through a nasogastric tube, may benefit horses with
explain cases of sudden onset of recumbency or rhab-
weakness or rhabdomyolysis due to polysaccharide
dOlTlyoiysis occurring hours or days after apparent full
storage myopathy.
n�covcly.
Fasciotomy may relieve pressure in localized myo pathy due to compartment syndrome. Splinting or hobbling of limbs that are weak due to
PREVENTION
myopathy or neuropathy may be indicated.
Clearly, proper padding and positioning, maintenance
therapy
In cases with severe myonecrosis, aggressive fluid to
maintain renal function is critic,t!.
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 deficient areas, administration of selenium and vitamin E prior
to
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 hypothesis 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 il�jury following anesthesia.
PROGNOSIS Under most circumstances, myonecrosis will be fol· lowed by myofiber 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 recovery. The serum half-life of CK is extremely short, and serum activities follow ing a single bout of muscle il�iUly should be reduced by at least 50 per cent evelT 24 hours. If serum CK activity is found
1.0
be persistently high or inneasing,
particularly in a horse that is no longer r�nllnbem, underlying
myopathy
leading
to
on-going
muscle
injury should be suspected. The prognosi� for recovery fi·om peripheral neuropathy will depend on whether
THERAPY
there is axonal damage or simple conduction hlock.
Horses with ohvious signs of muscle necrosis, either localiwd or generalil:ed, should be treated immediately (DMSO 1 g/kg 10% solution in 5% dextrose). This free-radical-seav
with intral'enous dimethylsulfoxide
Resolution of conduction block may be rapid, whereas repair of axonal damage, if it OCCllrs at all, may rake weeks to lIIont.h.�.
enging agent can dmmatically reduce on-going muscle injury associated \�i th oxidative i!�ury. 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.
Pos toperative com pl ications - th rombophleb itis ( Walsh
The decision to hoist a recumbent ho{';e by use of a tail rope or sling is made depending on the duration of
INTRODUCTION
recumbency and the nature of the horse. A calm horse that is maintaining sternal recumbel!cy should
be
Thrombophlehiti<; is defined
as
thrombosis of a I'ein
dose!y monitored, and may regain the strength to rise
associated
within a few hours. For an anxious horse that is
Thromhosis rarely occurs witho\lf the presence of
struggling !.o rise, or one that cannot maintain sternal
inflammation. Septic thrombophlebitis is the terlll lIsed
recllmlwl!q', use of a hoist and sling may be critical.
when the thrombus becomes infected.
222
with
inflammation
of
the
vessel
wall.
P-OSTOPERATIVE TREATMENT AND COMPLICATIONS
11
of
The rn'O classically described pathways converge to
indwelling intravenous catheters, coupled with the fi-e·
activate factor X to Xa. Factor Xa forms prothrombi
quem administration ofirnlant drub 'S ill patients that may
!lase by forming a complex with factor V, platekt phos
have a coagl.llopathy as a result of their primary disease,
pholipid and ionized cakiulll, Prothrombin
comhine to put horses with severe gastrointestinal disease
prothrombin to form thrombin. Thrombin cleaves
1ne
pathogenesis
is
multifllctmial.
The
use
at rdatively high risk of developing thrombophlebitis.
fibrinogen to form fibrin, which undergoes covalent
The jugular vein is the most frequently affected site
linkage to form the insoluble clot.
because it is commonly used for venipuncture. Limitatioll 0/dot/onrwlioll
Clot formation is normally limited to the site of blood
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
\esse\ il�jury by mechanisms that inhibit clotting factors, the most important being antithrombin III, and by fib 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 bt.�ing plasmin, whose pre cursor, plasminogen is incorporated within the dOL as it
•
a hypen:oaglliable state
forms. Plasminogen is activated by lissue plasminogen
•
stasis of blood flow.
activator derived from endothelial cells and probably
Th('�e factors result in inappropriate activation of !]ormal hemostatic mcchanisms.
enters the clot bv diffusion. Thrombus/ormation
&.'veral faclOrs conspire to increase the risk of occllr
Hemostasis
rence
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,il; cascade t"wlllually resulting in formation of a
thrombophlebitis
in
postoperative
colic
•
patients are frequently in a hypercoagulable state
•
mechanical irritatioll of the vessel intima is caused by venipuncture or by the presence of an
fibrin dol.
inlravenous catheter
(Jlf/ldfl f!lug/omlfllirm
•
thiopentone, phenylbUiazone, and guaifenesin
I)\' a variety of mechanisms. Damage to endothelial (:ells
(GGE).
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 which is generated from membrane
d("l'ivcd arachidonic acid. The result is formation of a plalelet plug. Blood (i)(/!,'1l/alion Activation of the coagulation cascade results in the for Illation of the fibrin 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.
several of the drugs uscd in colic patients can cause chemical damage to the endothelium, for example,
Endothdial ce!Is normally resist adherence to platelets
boxant� (TXA,)
of
patients
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
11 •
COLIC
activa.Lion of coagulation G1.<;cacl.c and decrease in
i.l1l tilh romhi n III acth·ity. A
nu
mh c r of swdi es ha\'t! shown
thar horses with
sc\'cn�
syslt'mic disease haV(� lower than normal a<:ti\'ity of antirhrOlnbin HI. I n 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 Antithromhin
pnsropcnlli\,t·iy.
illcreased
normal
lo
in
horses
III
thell
activit),
that
survived,
hut
rt:maincd 1()\It,' in horses that died.
III anolher study it was '()lllld that horses that had �lOdt'rg:ont"
colic
surgel}'
shO\\lt'd
a
dCCTcasc
in
i\lHilhrombin i l l C\criviry. this fkcreased to ahout 50 pt'r ('l'nl
ofiLS no r m al \'allJ(� after �4 days rhen increased to
normal O\·t�r abou[ a week. This (:hang<: w<.t.'i coupled with
a
rlccf�a$<: in an i vi ry of coagulation ra<:tors
LO
approximalt':ly 25 per (:Cn! of normal '2 days postopera li"dy, fiJUowed hy an in<:r(!as(� 10 normal .Kti.... ity over lhl:' t)e-xt week. Th(' rcsuital1l rende-ncr to coagulation was c.xplained hy the fan thaI <:oagu\atioll factors are still dfectiv(' at 20 per (('Ill of norma] activity It.'\'d wber('a� antilhromhill I I I requin:s ilt kaS! 75 per u�llI.of
l1<mnal activity to he cffecr.in: . In humans, it is well rc(:og-nized Ihilt postoperative..' patil'lIls
with
antithromhin
If I
dcfu:it'llcy
are
in(T('as{'cl risk or t hrom hocmholism: the risk is said
Fi9ur� 11.5 A 12-year-oJd gelding with 'Swelling of the left jugular vein. Septic thrombophlebitis was diagnosed ultra· sonograph i<:ally. The horse had a history of endotoxemia and the vein had previously been catheterized
at to
be modcratt: if antithromhin I I I activit), i!i betweclI
;>0-7:) per cenl ann severe if antithromhin III ;u.:ti\·ity is less than !l1J pe-r cent. The same may well apply to 4
horsc..'s.
Rare cOlllplications or thrombophlebitis incl lld(� lhnHnbocmholism :.incl endocarditis.
Ultrasonographic findings
CLINICAL SIGNS OF THROMBOPHLEBITIS
Thrombophlebitis i'i charaClCr1/cd 1IIlra�()n{)grctphi(:all)'
Thrombophlebitis is usuaHy rt!.u1ilr diagll(}�cd 011 the basis of the following dini<:al signs. I . The affened vei n is hard and cord-lik(�
by the pre'icnce of a mass in the \,{�!iscl lllmcn r
1 1 .6, 1 1 .7}.
on
w
cchogenic (Figurc..$
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 wht�n
palpatioll.
2. Sc..'ptic thrombophlebitis �houlct be �nspccl(;d if th(' ant-ned vein is hot, swollen. or pa infu l on palpation (Figure 1 1 .5). If the jugular \'I..! in is
the cathetcr has becn removcd. The thrombus
can
usually he seen [0 be "-((itched to
t.he endothelium and may parti ally or complt:tt:l�'
alTected the horse m;:\y
occlude the lumen. Vt:TlOUS <:ongesl.ioTl may h(: disti ll
Sllppuralion or exudation from sites of skin
guishahit· proximal to the thromhus,
P1l11CttIn.' suggests sep tic thromhopllk:hitis. though u'liui i lis without v<:in invol...t"llwnl' is �Iso
a
A s�ptic t.hromhus appears ultrasollographi(:ally het<:rng('I1<:olls rna.')s in "rhien ancrhoic
or
as
a
hypocrhoi<:
possibility. Septic rhrmnhophlehitls should also he
art:as represent areas of fluid
suspected in any hor.se with unexplained pyrexia
within t.he thrombus appear hypocchoi<: and f1occulclH.
p
:,t Ril;ucraljllglllar !hromhophlt:hiris may result in t"dt:lIla or th e soft tissues of the Iwad cansing dysphagia and dysplleit often severt" cnough to l1t!ct!.ssitale lradleosloll1Y. 224
or
necrosis. AITa.� of pus
Cltrasonography is useful to confirm the presence of septic: thromhophlebitis ann bus
w
r.o
select an art�a of throrn
aspirale ror culture.
Cltrasonography may be usdul in moniLoring: the n!!'pollse to therapy.
POSTOPERATIVE TREATMENT AND COMPLICATIONS
11
(b)
(a)
Figure 1 1 .6 Transverse (al and longitudinal (b) ultrasonographi< images of the left 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 (l;ppearance typical of edema. Dr Cel ia M.arr, with permission
(b)
(a)
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
11
COLIC
PREVENTION
froIll catheters has b�en estimated at around 70-75 per
Prevention oj' thrombophlebitis is centered around
However the relevance of positive culture is unclear as
cent, with most isolates found to be skin commellSals.
•
treatmellt of the underlying cause - in horses with gastrointestinal disease this is usually endotoxcmia and disst'minaled intravascular coagulation
•
appears to be little
correlation in
these studie�
between positive culture and thrombophlebitis.
Guidelines for catheter use
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 to coagu]opathy
•
there
anticoagulaill therapy is recommended by some authors hut remains a controversial topic
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
Catheter management
insertion. There is also a lower incidence of
indwt'lling catheters are commonly used ill horses
complications if the catheter is placed by an
undergoing intensive care. Most cases of thrombo phlebitis
OCfur
in
veins
that
are
or
have
been
c
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 entry 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 abont. 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
experienc�d 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 every 4 hours with heparinized saline soliuiol1 helps to prevent dot formation within t.h(: catheter. Blocked (or othetwise damaged) cathet.ers sbould be 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 us�d is important. It has been suggested that all fluid lines should be replaced every 24 hour,.
cndothelial triluma. However, catheters made of softer
It is vel)' important to check veins regularly for signs of
materials are less thrombogenic, whatever their size,
thrombophlebitis.
because they tend to float fredy within the bloodstream
Some authors recommend the use of antiseptic skin
withont contacting the vt:ssd wall. Readily available
ointl\lent� and dressings while others consider that the
catheters include
use of antiseptics encourages the development of resis
•
the shorter, stiffer catheters made from polytetr'-lfllloroNhylene (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.
tant strains of micro--organisms, 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
Infectioll mal' ()('cur especially if catheter man;lgement
other day reduces platelet aggregation and may he
IS
givell concomitantly with other :-.ISAlD therapy.
pOOL The incidence of positive bacterial cultUrt�S
226
POSTOPERATIVE TREATMENT AND COMPLICATIONS
Heparin
•
The anlicoagubwl dTcct of heparin dqlend�
UII
pati'·lIt
ani\·ilr.
ha'in� adeqmH.· autithromhin
III
the
hq)arin hind� to antithrombin III alltl grcatl�' cuhallces iL� powney as a �(:rin(' prOlc:ll.Sl· inhihilUr. Heparin isnO! !lsd·1I1 for the r('solution of existing Ihrumbi ami has a
11
tradlcoswmy lIlay be: nccc::s,'\arr in bilateral
dlrombophlebitis ir dyspnea is $(.'\·ere
•
•
surgical drainagE' mar be ncccs-'IiIf)' ifsuppurdtion is
prest'llI
\Tin rt'-scctilm rna}' he indicaTed in St.'\'t:rc case!> Ibat do not resp ond to medical mallagemenl. In
IHll·omplic',ued
C'dSl.'S
or
thrombophlebitis,
limilrd elTect in pn:\·clllinR thcir e"l(�nsion. If used, ahe...·fore. it must he.: �i"en prophylanir.ally. prdiTdhly
rccanali7.ation of T.hc I'ein commonly occurs, Ihis may
pre"uperativeiy, hefore the con.�umplion of antitlHom..
I·C1\lrll
bin III and librin formation occur, it may then haH· sonw dfcct in preventing thrombophlebitis in patients
10
normal Of there may be.: a degree of stricture.
In mOfe severe cases the thrombus may undergo organil,atjO!l ....ithout n:canalilation.
'It risk. The �tlgg(:stc::d dl�ag(: rc::gimcn is •
in itial d{)se DO IV/kg s.c.
q. 12 h for six doses 12 h subsequently.
•
12:, lL' /kg s.c.
•
100 IL'/kg s.c. q.
Tht· rct\l.Ic:in� dose i� recommended hecause if a uni hmn doS(: is u�ed, serum heparin gradually incrcas.cs.
Thi� d()sinK regimen, when administered
to he'llr.hy
hors.:s, resulted in a pla�lna heparin concentration
bt'IWet�!l O.O�-O.2 IU/m1. this is the o[ 101,· dose heparin prophylaxis
lhcmpcmic range used in humans.
Suhnllallt.'OUS adminisu",uion a\'()id� peak.� of plasma Iwp,lIin thai ma�' he more.: likel)' to result in ad\·er$(.' t·ffefl�.
Tht' nl(��l comnwlI complication or hqmrin Iher-tp), is anemia (ren cell lIlaAA may be reduced by 3..� per u·nl). (lnd rt'd cell agglUlination ill the micrm'a.-.c:lila1Uf('
has been suggt:sted
the mllSl likdy
callst.'.
The
rcd cdl count rl'l:O\'CI'li ',ithin 96 hou rs of l:e!lSalion of ht'p;nin the,-"p)'. The signilit:allce of Ihi� oi)s(:n'ation is unKllown.
P ostoperativ e complications - p eritonitis T Mair INTRODUCTION l'erilOnili.� is def'ined as inflammation of the peritoneal lining of lht"
cavir )'. The condition is dis
w.'.-s<.'"(1 in greater detail in Chapter 17. Peritonitis occurs 10 .<,ome nr.grce in all hOfSC.'I following abdominal sUTKr.ry �ause of the Imtllna associated "ith tht'
surgery, handling of the intestinal tran, etc. In most
cases this is self-limiting
(alice. Ilowevcr, septic PCI'itOliitis is
OJ
serious and
pott'ntially lifc..d\f("ltelling ctlmp!iC'dtion of abdominal SHrg':"), thil(
rl'Cluire� prompt and aggres.�iy(' therapy.
Ol.lwr complit:aLioos of heparin adminislr
(at
higher
dl)se.� ),
thrombo<:·ytopcnia,
and
CAUSES OF POSTOPERATIVE PERITONITIS
painful �\\'ening at injection sites. The mllst C:(llHlllOn cause of postoperative septic peri tonitis is leakage
TREATMENT
mal,it- treatmcnt is Tl'commcnded as follows 1"<'1110\'('
the
ler, if prt'$Cnl, and (:ulture th(, tip.
(";llhe
dO l111t use the \'ein for \'eniptmClurc:: •
•
hm packing 111<1)' help by increa$ing blood lIow to
•
injul1' only. Contamination c)f the rx.'riloneal cavit}' may also oc(:ur at, the tim� of surgery espcc:jal!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
fhe arca
inC\·iahle, l but pm\ided that the sUll!;cl1' is lK:rfonned as
II�
cleanly
non"5teroiclal :uui-inllilmmalory dnlgs to rrduce
inflammatiou •
and/or bacteria from
Jue to nCCl·I��is of Ihe entirc howe! wall or a mucosal
Ont:e thrombophlebitis has been recogni7.cd, sympto
•
of �ndll!uxins
the bowel lulTIcn ill to the pc::ritolleal cavity. This may he
lI�e antibimirs {broad spcclnllll or as dinated by
unlikely
as til
11(>\\c\·c,· if
possible. this locl'lli7.cd contalllimllion is I:ause scrious dilrusc septic pc::rilonilis. mnrc
widespread contamination
"(;C\I",,".
(.uhurc and scnsiti\·ity) i n SI.�ptic thromhophll'bitis
thcn 'l more S<.'\It.'re diffu�c septic peritonitis mar result.
irbilateral thromhophl�bitis is prcscnt
arc listed iu Table I I ..').
L:("cp th(' head ek'\'3.ted, for example by c:ros.o;-rying
The causes of peritonitis in the poslop<.'rdti,'c period
227
11
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 Non-strangulating intestinal infarction 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'l,'el obstruction caused by adhesions. However, eight of the nine horses with peri [())litis had pre-operative ahscessation, rectal tear, or advanced bowd ischemia.
• •
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 pr�sence of one or more of these signs should be COIl" sidered as suspicious of septic peritonitis. Confirmation of the presence of postoperative septic peritonitis can be difficult 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/�tl) with more than 90 per cent neutrophils in healthy horses following 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 signifi(_ant •
CLINICAL SIGNS AND DIAGNOSIS 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
depression alxlominal pain ileus gastric reflux intestinal distention fever
228
anorexia tachycardia leukopenia hypoproteinemia diarrhea.
• •
• •
numerous toxic and degenerate neutrophils free bacteria in the fluid phagocytized bacteria within neutrophils or macrophages food particles and plant materia! fibrin particles.
:v1icrobial culture of peritoneal fluid is indicated not only to identity the pathogens present, but also to help tailor the antimicrobial therapy more spedfically. Peritoneal fluid pH and lactate dehydrogenase {LDH} concentration, and comparison of plasma and peritoneal glucose concentrations can also be helpful in determining whether Of 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 fibrinogen concentration more than 2 g/I (200 mg/dl).
11
POSTOPERATIVE TREATMENT AND COMPLICATIONS
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 pt·ritoneal lIuid may be present and this often sbows hetcrogeneous echogenicity. Hyperechoic particles in t.he fluid an� consis«�nt 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 ,·a�·ing 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
P os toperative 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 definition, 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.
echoic panicles of ingesta. Pneumoperitoneum may occur with bowel rupture but can also he seen following
PATHOPHYSIOLOGY
rt·ce!H laparotomy. Free abdominal gas lIlay Ix seen in a hyperechoic area underlying the body wall in the
Horses recovering from any gastrointestinal disease that
dorsal ahdomen. Reverberation artifacts may also he
camed endotoxemi
present.
There are several theories a.� to the etiology of laminitis in hors{�s with endotoxemia, although experimenml administration of endotoxin in h()r�s has not re�ulted
TREATMENT
in laminitis.
In lhe postoperative patient, the diagnosis of septic
atiollS in digital circulation. VenoCOllstriction and high
One theory is that laminitis occurs bec.ause of alter peritonitis is likely to be an indication for repeat laparo
hydrostatic interstitial fluid pressures are thought to
lOmv, unless a specific cause of the peritonitis (such as
interfere with microcirculation in the foot, resulting in
known contaminatioll at the time of the initial surge!)')
ischemic necrosis of the epidermal lamcllae and subse
is recognized. Repeat laparotomy permits identification
quent rot.ation, or ventral displacement (sinking), of
of the source of s�psis and this lIlay dictate the appro
the distal phalanx.
priate treatmelll (e.g. resection of leaking bowd, etc.).
A recent theo!)' (introduced bv Dr Christopher
Opt'n peritoneal lavage and use of intra-peritoneal
Pollitt) suggests that certain enzymes are responsible
antibiotics will he helpful, and placement of abdominal
for the destruction of the normal lamellar structure.
drains to permit postoperative lavage may also be con
The matrix lIlctalloproteinase 2 and 9 (MMP) {�n7.yllles
sidered.
haw been found in normal hoof tissue in low concen
Peritoneal lavage and drainage an� helpful in the
trations, but the levels become elevated in laminitic
treatment of postoperative peritonitis, and may help to
feet. It is believed that \.,'hen these enzym{�s arc activated
reduce the incidence of intra-abdominal adhesions.
they destroy the lamellar attachments resulting in
The lavage is continued every 4- 1 2 hours until there is
laminitis. What triggers the release of these enzymes is
a decrease in the peritOll(�al lluid cell count and protein
not completely understood, but i t may be substances
concentration, an increase in pH and glucos{� concen
released from organisms that normally inhabit. the
tration, and an improvement in the cytological appear
equine gastrointestinal tract. For example StuptlJl:(}("'( us
ann" of the fluid. These and other treatments for septic
bUlIil
peritonitis are described in Chapter 17.
resulted in lamellar separatioll.
has experimentally aC!h·at�d equine MMP-2 and
229
11
COLIC
increase blood flow to the feet in accordance with the
CLINICAL SIGNS
vasoconstric tion theo!)'. However, i t has been reportcd Horses affected with laminitis ;lfe first observed to be reluctant
to move. The front limbs are generally
affected although
011
occasion all four limbs will he
involwd. 1A1l Cll 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
that vasodilation occurs in the developmen tal phase of laminitis and is a possible triggering factor for activating
enzymes responsible for laminitis. Therefore, it is llO longer dear if vasodilators are indicated because they
could accentuate the laminitic crisis. \-\,ith the currellt
state ofkll owledge the author recommends again.�t t he
reluctant to turn. The diagnosis can ea�ily be made by
use of vasodilators in horses at risk of developing
increased heat i n both hooves, and the bilateral dinical
she advocates the use of such vasodilators as acepro
the palpation ofa houndi ng pulse in the digital arteries, signs. Horses arc reluctant to bear weigh t
Oil
either
front foot when tlK contralateral limb is picked up. If
laminitis. However once the laminitis has developed, maline,
ni troglycerine, or other vasodilator drugs.
Phenylbutazone should be i mplemen ted in aCUle cases
digital pressure is applied either manually or wi th hoof
of laminitis in addition to low doses of fIunixin meglu
There are tWO main syndromes that result from pro
dilllte intrav(�noUS D�SO ( 1 00 mg/kg b.i.d.) can be
testers, pain is elicited diffusely in the toe area, gression of t.he clinical signs.
I. Horses experiencing primary rotation of the pedal bone may develop a ventral dcpression to th e sole
(outli ning the tip oft.he pedal bone). Fluid and
blood accumulate under the sole . This fluid
accumulation can undermine the entire sole and drai nage 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 bei ng directed horiwmal and parallel to the ground as their follicles migrate distally to the kvel
mine for pai n relief. When :\'SAID toxidty is a risk,
administered in intravenous fluids for its anti-inflam matory 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 t he deep digital tlexor tendon can lead to severe rotation of the distal phalanx.
Return to performance is likely for horses that do
not have si gnificant
rotation « 5 degrees) or sinking of
the distal phalanx.
of the COrOlla!)' bands. In addition, one can palpate
a depression at the cranial asp<�CI of the pastern just above the coronary bands as the coffin joint mOl'es away from the area.
P os topera tiv e compl ica tions - colitis
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 l aminar tissue.
PREVENTION AND TREATMENT
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
Prevention of laminitis in the postoperative patient is of
not of great surprise since these horses have often
paramount importance, since lamellar damage will
undergone
have already occurred by the time the horse shows din
a
period of ileus and, in some cases,
ischemic/inflammatory bowel disease. The ileus is fur
ic;t1 signs of lameness. Horses with endotoxemia should
ther aggravated by the i ntended anorexia both prior to
he considered as likely laminitis candidates, and should
lhe surgery and for one or more days after the surgery.
receive anti-endotoxin seHUIl or plasma, and an anti
The lack of normal fermentable fiber r(,aching the
cndotoxic dose of fIunixi n meglumine
(0.25 mg/kg t.i.d.). Othcr supporti\'(' trcatments include the applica
colon dimini shes volati le fatty add productioll which
tion of frog pads to aid circulation in the foot and to
as
may permit overgrowth of pathogenic organisms sllch
Sr.lmOlwllu -'pp.
Of
CUI.Ilridium diffidll!. Approxim
apply counterpressure against the pull of the deep digi tal flexor t("ndo n . In tht' pa�t horses with laminitis werc
10 per cen t of normal horses arc positive for SlIlmrlnpllfl
spp. when tested by polymerase chain
Iwaled wilh acepromazine or nitroglycl'l"ine to bdp
yet mure than
230
reaction (peR)
40 per cent of horses with ahdominal
POSTOPERATIVE TREATMENT AND COMPLICATIONS
11
•
fecal cultures, gram stain and Clostridium toxin
and/or shedding of the organisms. Additionally most
•
complete blood count and serum chemistries
horses undergoing abdominal surgery afe treated with
•
complete clinical examination.
disorders are positive indicating that changes in motility and/or normal flora are important to the proliferation
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
a�
Salmone/In
spp.
or
Clo.l/ririium d.ifJirik which arc dillic_ult to eradica1e from the environment. Other factors that may predispose postoperative
colic
patients
to
infectious diarrhea
include weight loss and deCl"eaSt,d cell"mediated immu nity which are likely to occur in many, if not all, POST operative colic cases. Small intestinal reflux might also predispose to the gastrointestinal entrance of infectious
In most cases of infectious diarrhea the patient will he febrile and the complete blood count v.,-auld relieal hemoconcentration, a neutropenia with toxic changes, and
a
decreased
serum
sodium
and
chloride.
Ahdominal sounds may he absent or more 'nuidy' than normal. !r peritonitis is a (:(Hlcern based on the prior surgical procedure, clinical and laboratory 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 •
organisms hecause of a persistently high gastric pH.
testing
unwarranted abdominocentesis will increase yentral abdominal s,\'e!ling and negatively affect wound healing
CAUSES
•
prior intestinal pr
Causes can generally be divided into olle of two groups
•
infectious/inflammatory causes
•
motility/dysfunction causes. The
two
predominant
Salmonella 'ipp. and
interpretation might he difTIcult depending Oil expected to cause some degree of peritonitis. Fresh fecal samples should he submitted to the labo
ratory for aerobic and anaerobi<: bacterial C_!llture, gram infeCl.ious
causes
afe
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 very large vol umes of intravenously administered fluids may cause diarrhea, but this should resolve within l2-24 hours
stain, and C/usiliriium riif firil!! toxin assay (ELISA or
peR).
should
If a Salmunella spp. is grown, bacterial sensitivity be
pent>nned.
Clm/ridiwH pnfringelll toxin
(cnterotoxin) assay might also be requt>sted, but results are difficult to interpret. C{o.l/ridiUIIl jll'ljringrtls �� 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/mllnf/la spp. does not prove that it is the cause of the diarrhea, hilt this it makes it more likely than a positive
peR.
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
TREATMENT
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
Treatm�nts for each disorder are covered in Chapter :i!().
considered.
PREVENTION DIAGNOSIS The prevention of postoperath'e coliti� is not always pos The pre_seller of watery feces aft(�r abdominal surgery should immediately indicate diagnostic tests 10 deter mille the cause and severit�' of the prohlem. These should inclnde •
abdominal ultrasound to determine the volume and echodensity of the peritoneal fluid
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
11
COLIC
TIlt' t�<;(: \)l" 01"",1 llIi(;robial iJl()(:i\hml�, although
RECORDING AN ELECTROCARDIOGRAM
tmlikcir 1(1 he hannful, are nnt of pm\'cn value. Routine nthtlrill� of 1)l)slOp"'�r;;ti�e. crilkal ("are palient\ and thc:ir Slalls allows delce.lion of inft'r(iou'l org,mi..ms.
TIle use of radiotelemetric 01" COlltinuom ambul
N('", P:UiCIlIS �IWHld H(X be 1,.·xposerl tn infcdt.,,(j em'i
period facilit;ues the prompt detection of :llThythmias.
I"nnlOt:ots uruil propcr dcanillK pmccdurcs ha\'c been applkd ;uld the cllvironm('nl i.� cul!un--nq;
can ))('1 � otherwise �Irri!il�d.
Fuot haths
('(>lll
1)()slnrx'l1uivt: I.rilir.. 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 iudh·idnally prcpared equipmem, for ('xanlpll' slIlmach tuhcs. and takc net:essary precau tions
to
prc:ve-nt tJw spre
flotlling-. Any horse dl.:\"doping diarrhea should he mon:d
In
all i!>o!;ltio(l tildlity.
Alllihimic.5 sh()uld tUlly be U.';t�d if necessary, as cvcn
Jhln'llwr.llly administered ,mtihiotil."S lllight increase til(' intjdellfC· of wI:H:rial (�()Iitis. �1()Sl onll antimicro hi;lls �hul1ld 11111 he lISl'ft until lht: hor1\(' has OC'"C1l on a nornlal rHllghage (fit·t lilr S(....'(·r..1 dOl}";. �1etronidawle is ulit:1l ;'ppmpri;m'l)' used rollowing colonic entert,. (t)]lIil.: s, hIli [itl: loulille admini�lrati()n or melronida .1"011' in the hopI' of pre\'Cllting Clostridium
difficil#1
di
Postoperativ e compl ications - cardiac arrh y th mias
(Holter) dectrocardi(lgraphy during the pcriopcnu\'e ! luw(.'Ver intermittent u�
(lr paper (nce c!celro
GHdiogntph), will be sufficient ror the diagnO!lis nr persistent rhYlhm disturbance�. Electrocardiogn.ph�' is indicated in the ponoper"ti\'t'" prriod if either
•
a flopid pU!k rate is detec H'(! that cannot be ..
explained hr lhe le\'el of pain Of cndotoxcmia, or
•
the pulse rate is greater than 80 bpm.
Electrocardiography �h(ltL!d also be considered during
the e-v
lhe rig-ht arm (RA or positive) cIcc
trode over the hean b
anTI (I.A or nel!:;tti\"l�) e1c<:twde along thejugular gronv(' on the left hand side flf the llt.'Ck. The earth (\el"! lcg)
mlll m:utl'al (righ t leg) can be placed O\'er the scapula. Recordings.shauld be made in lead I, which w ill produce
a JX).�i(ivc P
and a nq�ativc QRS cumplex:. For
wave
details of i nterpretation artln! EKr; readers arc ocferred to Ihe re<:ommcncied lell:IS
PREVALENCE AND CLINICAL SIGNIFICANCE OF ARRHYTHMIAS IN THE PERIOPERATIVE PERIOD
Ventricular arrhythmias Vcntrkular
M Bowen
the horse. Their ECG ch
INTRODUCTION
prcl:eding P wave
a.s .�hown
in Figure I I .S. Vent.ricular
arrh),thmias can he defined as ventricular premature em!i;!f arrhph mias durin!( lhe I x�riopcrati\"c pt�riod art' common and :I!'C usually a rd]('Clion of IIlctabo!il:
dcpo];lTization� with a single (,Hopie COlllpleX, C()up!cL�,
di�lIIrh,\llI:('s mther Ih;m lUll' primar)' cardi ac diSf'a.'ie.
plexes. 01' '·entl'icular t.achycardia as a susained t velllriL
. Many of Ihest:
art' of lillie or nn COIl.o;e
nuly lew cast'S recl uirc specific interven tioll, Tlwrapy is imlic:ucd if there is .1 compromise to
li1n:uCt· ami
c;!nti:,( outpul or pcriplu;r.,1 pcrr"sinn. rh�,thnt i.� of
a
00'
ir the
tn)t' that ma)' dcsuhilil.C into a more
Of trip le ts, reprL'SClIIing tVI() and three consecutive com
Illar arrh)'lhmia wilh an increased nilI.'. Ventricular t;tchrcardia may he further ddlncd as paroxs)"Inal, per1\iMing for up 10 Iwr.nty complexes or slIstained. An accc:!cr.ttL·d idiO\·cntricular rh)'lhm s i a sustaiul.'i.l
tricular
... ...tc
similar
10
''CIl
sinus rhythm
IIwlilotmtrll life·threatening
and a.� such its diagnosis ma)," r:a.�i1y be mi'lli('d �' cardiac
ul;;r fihrilbtiltl"l.
allscultatioll alone.
232
11
POSTOPERATIVE TREATMENT AND COMPLICATIONS
"
VT
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 (VT) 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
Vrnlrirulurprnnfl/uU' tiepoimiUltirm,\
decreased
Sin!(le infrequent isolated ventricular premature depo
hypoxemic and predispose to further destabili7_ation of
output.
The
myocardium
may become
(YF)
Iaril-ations (VPDs) may be detected in normal horses
this rhythm into ventricular fibrillation
during ambulatory monitoring and are not considered
1 L9). VF is usually non-responsive to therapeutic
abnormal if they occur infrequently.
agents and carries a hopeless prognosis in the adult
Fntlrirular tachycardia Ventricular tachyc_ardia
(Figure
horse.
(VT)
at rapid rates may signifi
VPDs do not in themselves constitute a significant com
cantly reduce cardiac output thus reducing tissue per
promise to cardiac output, however they may be a
fusion. The increase in heart rate increases myocardial
predictor of a destabilizing arrhythmia. In one clinical
oxygen demand, but this demand is not met because of
study comparing the incidence of ventricular arrhyth-
5 , _" I --'I
' "Oy
,
V
I
V
A
""i • ,
V
E
Y
,
I
_ J. V , 'j
Y -y -y Y
,
, " ' "'f ,
,
,
-1
--;
'-y
,
,
,
,
I
-J\
I
I
J,
J\
-,
�
,
_II F
,
v
, v\Jv\ftJ\ANv
,
,
II
J\
lv'N"-vJVVVV
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
11
COLIC
mias in the postoperative period of both celiotomies and elective orthopedic surgery, there was an increased incidence ofvcntricular arrhythmias in the horses with gastrointestinal disease. In the first 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,,! mIt's. 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 48·hour period folloVl.ing 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 fibrosis found on post·mortcm 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 significant problem and specific 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 fibrillation (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 fibrillation waves (Fwaves). The QR.';; complex has a normal configuration represcnting a supraventricular rhythm. AF 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 AF persists then therapy with quinidine sulfate should only be considered once the horse is othelWise healthy. Side effects of quinidine sulfate include hypotension, 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 underlying 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 with detomidine (lO-20 Ilg/ 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 observed. 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 reCjuin"d.
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 with 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, cau�ing 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!ectronegativity with sodium in the extra cellular space and potassium within the cell. Changes to any ofthes(, ion gradients across the cell membrane will
POSTOPERATIVE TREATMENT AND COMPLICATIONS
affect t.he automaticity of different parts of the myocardium and thus enable the production and prop agation of an arrhythmia.
11
calcium borogluconate) may have a cardioprotective effect in hyperkalemia.
Calcium Potassium Hypokalemia can occur due to loss ofsenlm potassium through the gastrointestinal tract or kidney, or by dilution of existing serum potassium. Dilutional hypokalemia can ocnlr due to the prolonged use of polyionic 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 hypokalemia 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 bety,,'een the resting potential and t.he 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 I h- I. For maintenance 20 mmo! of potassium chlo ride can be added \0 each liter of lactated Ringer's solution. Hyperkalemia can occur in patients with hyper kaIemic periodic par.l\ysis, anuric renal failure, or uroperitoneum. These individuals are at particular risk of developing atrial standstill and third degree atrio ventricular hlock, but fatal ventricular arrhythmias may also occur. Life-threatening hyperkakmia is treated I'.-ith 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 mrnol/kg) and the slow admin istration of cakium (0.2--0.4 mlJkg of a 23% solution of
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 hypocalcemia 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 win 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 .3--1 .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 hypercalcemia, profound hypercalcemia can result in ventricular fibrillation and death. For maintenance, up to 40 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,mes. Hypomagnesemia was 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 injec.tions (Table 11.6).
Other factors Acidosis, myocardial hypoxemia and endOloxemia will affect the serni-pcrmcable selec.tive ion channels of the
235
11
COLIC
ceIl membrane and can increase cellular automaticity and therefore predisp(l�e to 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. Hypoxemia is also likely to reflect hypotension and should be corrected by administration of crystal loids or colloid therapy.
occurring simultaneously and thus is likely to progress to fibrillation. Therapy should also be considered if there is a significant compromise to cardiac output, this may manifest as weakness, collapse, or increases in serum creatinine due to poor renal perfusion. ANTI-ARRHYTHMIC THERAPY IS WARRANTED IF THERE IS RAPID VENTRICULAR TACHYCARDIA GREATER THAN IOOhpm
ANTI-ARRHYTHMIC TREATMENT
MULTIFORM VENTRICULAR ECTOPY Ron T PHENOMENON
Specific ami-arrhythmic agents are only indicated In severe life-threatening arrhythmias. In all 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
SIGNIFlCANf 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 bl;Tn
Teble 11.i DNoJ-UIed for"" trtattnent of alt'dlac lti'i'hythmils D....
Indfcftlonlf
DOle end .dministr.tion Side effects
Lignocaine hydrochloride
Ventricular arrhythmias
0.5 mg/kg Lv. q. 5 min
eNS excitability
Quinidine gluconate
Ventricular and supraventricular arrhythmias
2.2 mglkg bolus q. 10 min up to 10 mg/kg total, or 0.7-3.0 mg kg-' h-1
hypotension, colitis, arrhythmias
diluted in saline Quinidine sulfate
Supraventricular
10 gf450 kg p.o. q. 2-6 h
arrhythmias
hypotension, colitis, arrhythmias
Propanoloi Procainamide
MagnMium sulfate
Atropine sulfate
Ventricular tachycardia
0.05-0.16 mglkg Lv. b.Ld.
hypotension hypotension
Ventricular and supraventricular
1 mg kg-' min-' Lv.
arrhythmias
up to 20 mglkg
Ventricular tachycardia Hypomagnesemia
4 mglkg Lv. q. 5 min up to 50 mg/kg total
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 IJ.glkg Lv.
excitability
Immune-mediated myocarditis
0.02-0.2 mglkg
use reduclng dose regime
�xamethasone
or profound AV block
236
POSTOPERATIVE TREATMENT AND COMPLICATIONS
rt�,omme]J(led for ven t.ricul ar arrhythmias because of tht short duration of action on sodium channels, which is
Ies.> likely
to
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 fasciculal.ions arc observed. The class
I B drugs, such
.IS
quinidine and procainamide, which
an� classically reserved for the treatment of supraven triclilar arrhythmias, lack the neurological side effects
of lidocaine (l ignocai ne ) and are therefore considered
the dr ugs of choice for the treatment of ventricular arrhythmias in the consdous horse. In!r;wenous magn esi um snlfate has been used suc n'ssfu ll�' as an an lidysrhythmic agent which is effective Hl 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 heneficial in
Ire,Uing ventricular tachycardias together with other
Barton :\1
H, :\1oure
11
H :-J, 1\orton N ( 1997) Effecl� of
pentoxi!yliine infusion
on response of horse� to in vivo
challenge exposure with endotoxin. Am. .f. Vtl. /Us. 58:1291-9.
(;argilc .1 1., MacKay R .l, Dankcrt.! R, Skclley L ( 199.'i) Effect of trealment of Miniature
Horses with a monoclonal
antihody again�t equine tumor necrmi� fact (T:\,F) on
clinical, hematologic and circulating T:">:F H,spnme� giwn endotoxin. Am.J. Vtl. JUl. 56:1151-9.
Durando M M, MacKay R.J. Linda 5, Skelley l.A (1994) HfecUi of polymyxin B and Salmonella Iyphimurium
,mlherurn on h()r�('� given ('ndO(oxin intra\·enous!y. Am. f. \'el. Hr.. 55,921-7.
Olson :\ C, l leIl),er P W and DodamJ R ( 1 995) Mediators and vascular drecl� in respome to endotoxin. 8r. \/el. .f.
151:489-.>;22.
Shuster R, Trauh·Dargatz.J, Baxler G (1997) Su"'''y of
diplomates .of the American College ofVrterinary Internal Medicine and the American College of Veterinary Surgeons regarding clinical aspects and treatment of endotoxemia in
Spapcn H, Zhang
hurses. .f. ,1m.
I'fl. Mfd. ,bsoc. 210:87-92.
Ii, Vincent J J. ( 1 997) Potential therapeutic
'-ah", of laz arnid� in endoroxemia and mh(,r f.orm• .of
sepsis. SIwek 8,321-327.
ag("nL�, but should be used with care if there is compro mised myocardial function as its usc will further reduce cardiac output.
Nutritional support after alimentary tract surgery l.<:,wis, I . D ( 1 995) F.quine Clinical Nutrilion. Williams and Wilki"" Philadelphia, pp. 389-417.
Ralston, S L (1991) Fe
AFTERCARE AND PROGNOSIS Onre drug therapy has commenced, the patient should
Cli"icallVu/rilion, .J M �aylor, S L Ralslon, (cds). Mosby Yearbook, St Loui�, MO, pp. 432-46.
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
to
document myocardial
!It'CH)sis which may ha\"C occurred, and if increased,
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 sustain ed ven tricul ar tachycardi a or R on T phcTlomeno n then the prognosis is guarded. In the m�jority ofcases with monomorphic ventricular arrhyth
mias that resolve "'lthout spcdfic therapy, the prognosis
is good and the arrhythmia is unlikely to recur once the
primary g-astrointestinal lesion has resolved.
Postoperative shock and organ failure Arden W A ( 1 999) Circulatolj' Shock. In Equint SUTgt1)' 2nd cdn,j A Aucr and.! A Stick (cd.). \II B Saunders,
Philadelphia, pp. 40-5.
Byars T D ( 1 999) :\fultiple organ dysfunction syndrome. In
l'rortl'dings oflilt Blv.rgms:; f;qui.w Mtdiriru and Crilical Dm
S),mposium. Octoher 24--27, Lexington, Kentucky. llumJ M, Ed"·.lrds G B and Clarke K W (1986) lncid
diagnosis and treatmem of postoperalivc complications in colic cascs. f;quint Vel. .J.
IS( 4) :264-270.
Moore.! A ( j 99()) Pathophysiology of Circulatory Shock. In Tilt EqllilU' Acul� Abdomen, l\ A \',-'hite (ed). Lea and
Febiger, Philadelphia, pp. 90-9. MooreJ A ( 1 999)
Fndotoxemia and Ihe _
inllammatory response syndrome. In Procftdi"gs oftht Blufgrass Fquin� M�didn' "",I en/iml e,m S)'mpo,ium,
October 24--27, Lexington,
Kenlucky.
Orsini J A ( 1 99(1) Shock. In I-AplilU' Surgtry, ht edn. J A AU
Postoperative pain
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238
BioI.
53:155-{j3.
Ragle C A, SnyderJ R, Meagher D M, fI al. ( 1 992) Surgical treatment. of colic in American ),finiature Horses: 1 fi cases
( 1 9BO-I9H7).). Am. IItl. Med. Assof. 201:329-31 .
Baxter G M (199J) intra-abdominal adhesions in horses. Compo Uml. Edur. Pmcl. I'd.
Ilcparin in preventing intra-abdominal adhesions secondary to �xperimentaHy induced peritonitis in the horse. Vf/, Surg. 16:459-62. I'arker./ E, Fubini S L, Todhunter R./ ( 1 989) R<,trmp"cti\'e evaluation of repeat celiotomy in 53 horses wilh acme gastrointestinal disease. \'.1. SuW, 18:424-3 1. Pbillips T./, WalmsleyJ P ( 1 993) Retrospective analysis of the results of 151 exploratory laparotomks ill horsl's witb gastrointestinal dis('ase. J-."qui'lf VH}. 2.�:427-3l. I'ijlman H M, Oil)")" P j , Brommer E.! P, Verner I I M ( 1 994) Prevention of adhesions, t�·um. .f. Olistrl. Gyntml, l&prod.
Sch�..mme M, Bul�on R ( 1 997) Abdominal adhesions - h..v" we made any progress? t Jjuint Vfl, J. 29:252-254. Southwood L I" Ba"ter G M ( 1 997) Current concepts in management of abdominal adhesions. \.,,/ r.lin .>,,'• •;m. Equine Prado
13:415-35.
Southwood L L, Bax!.er G :\1 , Hut
Sullins K E, White 1\ A, Lundin CS, tl al. (1991) Treatment of iSLhemia induced pnitoncal adhesions in fnab. Vet. Surg.
20:348. Swanwick R A, Milne F./ ( 1 973) The non-suturing of parietal peritoneum in abdominal surgery of the horse. V,I. /Vr.
93:328-35, Vachon A M, Fisdln A T ( 1 995) Small intestinal herniation through the epiploic foramen: ,,3 Ca5{" ( I 9R7-1993) t Jjuine Vtl,j.
27:373-80.
Yaacobi Y. Israel AA, Goldberg E I' ( 1 993) Preve"tion of postoperative abdominal adhesions by tissue precoating with polymer solutions. J. Surg. Rts. 55:422-6.
Ileus Adams S B, I.amarC H, Masty.! ( 1 984) Motility of the distill ponion of the j�junmn and pelvic t1exure in ponies: En..,c�� of six drugs. Am. J. Vft, He,I, 45:795-799. Hliks!ager A T, Bowman K F, Levin .! F, el a[ ( 1 994) Evaluation of factors associated "ith postoperative ileus in horses: 31 c�ses ( 1 990-1992). j. Am. Vtl. MFd. ..hsllC. 205:174B-1752. Dart AJ, l'eauroiJ R, Hodgson D R ( 1 996) Hficacy of metodopramide for the treatment of ileus in horses following small int...stinal surgery: 70 cases ( 1 981-1992).
AU,I'. V,t.}.
74:280-284.
Davies.! V, Gerriug E L ( 1 983) EITect of spasmolytic analgesic drug., on the motility patterns of the equine small intestine. {k,. V.t. Sci, 33:334-339. Eades S C, MooreJ :-.I ( 1993) Blockade of endotoxin-induced cecal hypoperfusion and ileus with an alpha"amagonist in horses. Am,). Vtl. lVJ. 54:586-590. Gcrring E L, HuntJ M ( 1 986) Pathophysiology of (,quint· ilells: elTI'ct of adrenergic blockade, parasympathetic stimulation and mctodopramidc in an eXpt'rimental model, l�quinf �ffl. J. I8:249-25.�. Gerring r: L, King.! 1\, Edwards G B (1991) A multicenter Inal of cisaprirle in the prophylaxis of equine postopt'ralive ibiS. Equ;". ""I. i';duc, 3:143-145,
POSTOPERATIVE TREATMENT AND COMPLICATIONS
KingJ �',
C.crrinM }: L (1<Ja9) A",Utgollism of endotoxin
i"dun:d di�rtl plion of cqui ne howd mUlilif)' by f1un;>:;n
.md phcn�·In..llaJ.on('. f"ijllm" l'H.). snppl. 7:81-5.
l.t�,·r (; U. ;\kniu A M, :-':c\,wirth L. tl nl. (1998) Effect of Alpha.-adrenc!l,';c. clloline!"). ';!". anri nOIl-steroKial anl.i ,nll,,,,,mamry dn'!;'''o myc>(:kClrical 3CI;"ily of ilcum, (ccu.n. and right "('nlTal colon and creal emMillg of
roldinlJbded markc'r,; in dinicillly normal ponies . .1m.J. lit. IV... 59::-IW-:-I:l7, 1.(.'\I",r (; D, Merrh ,\ M, �eu..�rth I� d nl.. (1998) Effect of " 1�1hr
ikum, cecum. and l'ij::;h t venLral col"n, lind n:ntl emptying ot ntdinJaix'led mark.cl"$ m clinically norm�1 ponies. .4"'-1-
I'". I�. ;19:�28-�34. :\\al",\., E D. TurnrrT ,\. Wibon J H (19911) !llIral'('nOm lior><:Ain.:: for Ill(! treatmen t of i!cu•. Sj.�lh Colic SY'''f''>,<;um /(',ll'lIrrit ,1/lllram; amtr,ICI 42. N.l\'afr.. C B, ROll.....I AJ ( 1 9�16) Ganroinlestinal moti lity and discasl' in \;II'gc ;uo!tllals,). V,t Inlml. Mtd. 10:51-,';9.
!>"rk� A II. StickJ A, Arden W A, ,1 al. ( 1 9119) Effects of distcillion �nd nCtlSlil!'minc on jejunal '-asn>iar rcsist.mec, H"ygl'!l uplaltl: and intraluminal pressure fhang'" in
p"llic�. Am.). 11ft. JVl, :'10:.'i4-!',1!. }kynold'J C. Putman ? E ( J �)2) Pmkinclie agcnt\. (;all,,,,,qll!l'(l/. r.lin. N. Alii. 2J :567_:'196,
Sama S K, (llt.emn
.l.iYC:lClectriC ;md collU-dctik In AIIII.I nt (;Il'/>Ilinl�.
Impaction at the anastomosis Frt't'mll:n D F. ( 1997) Suq;:cry
rar"�'I'J E , FlO!>ian S L Ttldhunlc,' R J ( (989) Retro('p<,<:(i,'"
" '"
),'>!lits dul'lng illtt:rdigestil" :, llonf" " ding, and dig,,,ti,,,, pcriod�. ,1m,.!, I'", }V,. 51:5t;].
Incisionai complications Ducharme :'" G, Freeman D E, Ste�!c.d R R, Dean P W, Young \) R ( I ('192) Principles of in(C$Lina! surge,)". In r:qui"F "",,,1,.'"1. lsI eeln) AAu"r (cod.), W B Saund"r�.
Philadelphia, p, :.125. l1"nl1;\� C M, Cohen N ( 1 997) Ris!c. f.telon for wound inf..ctinn foll".,ing .;elfntom)' in hOr.ln. 1 Am. V,I. M,d.
:'-'w·. 21O:7�t.
InKk-Feh rJ Eo 8;0>:,..,' (; M, I·!<,.,... .. n! R n. Trnuc:r C W.
Sla�hak T S (1m) B3cler,al eul tminp; of"cnlraJ m..-dian 'TliolOmics for prcdK:lioli ofpt�lop.,r.!lil'L' ;nci�Jonal t"CJlnplicatioJls in horses. �'". .""�. 26:7-13. Ko.Iw�" (: E, 5t�ha" T S (19��) Preclisposin.: factors. diagnosh. and mll:llilgc:mcnl of large ahdorninal dt:fc:clS in hflrstsalld call1e. ). ,t'''. Yd. ,\1,,1. A�......., 2()(":607�i11. I'hillips TJ, \\!am�k1'J I' (1995) RCUUSPCCli\"c ana!)'Sis ofthe r..�"h\ of 151 uplorn\omies in holYS ..itll gastroim�tina[ c\i.'<:'
11
Wilson D A, Baker GJ, Boel'<) MJ (1995) C..omplicalion, of celiotomy inci.<.ion$ in horK$. V". SU11l. 24:506-514.
Postoperative complications myopathy/neuropathy Bloom 8 A. Valentine BA, Glc(."(1 R D, Cable C S (1999) Poslal1lteSl.hell<: re(:umhenq in a Belgian filly with
p<>I) 'SiH:.-hari(k .'II!>r"ge mynpalh)'. VI'I'. IW.. 144:73--7�.
(;1=<1 R D ([996) J>u,;tal�"ht'l;" S"rn-A Nixon (ed,j.
my"palhy. In r:qwn' Orthofxdic
M�by. SI 1..
f faguc H A, ;\1artinc1. t: A, lbrtslidd S M ( !Y9H) HlecL� of high·dose gt:ntamkin wl fale on neuromuscular blockade in halothan_Il��hetiled hona. Prrx. Am, Anoc, t'quirtt
/1'ad. 44;240-241 . Harris I' A (willi COntnbUliollS hy :\la¥hew J G ) (199M) Ylu�culO!kelcllll dire;ase. In fquil11 fl1lrrnal Mfdiril1t, S M R"cd, W M n;ayl)' (erM. W B Saunders, Philadelphia, 1998, pp. 388-91 .
Johnson B 1) , H�alh R IJ , Bowman B , Phillips R W, Rich L D,
VO.IS.! I. ( 1 978) Serum chemistI)' chan ge� in ho,,,,,es during am,'1thcsia: A pilot study im'es{i galing
of postanesthetic m)'osi ti� i n
Ihc pos.�ibk c;1U�es hor�s. J. Equint MId. SlIrg, 2:
10')... 122. 1,,,,, Y-I l L, Clarke K W. Alihl,ai H I K, Song D ( 1 99H) EIl"cn_ "f dopamine, clohUl.1mine, dopexaminr., phenylephrine, and !ialine soIulion on intrnmwcu lar blood flow and olher c.ardi<Jpulmonal'}' ......rt..blt::s in ha!ulh..nc.....anl"!jthcti7ed pO" le�.
;,,,,.). 1'''' J&,� f>9:
146.'-72.
Postoperative complications thrombophlebitis BaYlyW M and Vale 8 H (198'1) Intr.l.W'nous cathclcrizalion . ';nd associau!d problems ill the horse_ Co",p. Oml. I-AI«. l'mrl, \tl, 4 Sm-2�7. fl;I
EttlingerJJ,
PiI!merJ 1:: ami BeuSt'" C (199'.1)
Ba<et.eria found
on !nlr.."enolls ealheleN removed from hOl'se�,
1:'10248-:249.
\on. RI!<.
II (1987) (Antithwlnbin 11\ determination in the hor�. Refenmct' "allit's and acqllir"rl ant.ithromhin III dclkienq'.) TlpnrlLI. Pmx. E'i 47_:;5. Cuhards 11 ( 1 9f!7) (1IYI'H"""gLllahiliLY _ an eLiologica! faclor ill the deyclupmt:llt ofjllj::;ulu "ein lhrombmis in horSt'S.) D/,o;cit. l;m",.I. WIC/lr, 94 173_174, Gerhards H and �:b�rhardt C ( 1 9R8) PI
and
hemostlt!is in e{luid� after subclIIaneous
admini....:rati<>tI nft',...·. d.»e calcium heparin. Am.J. \/tl. !Us.
4913-18.
Holland M. Kcll)' A B tl ",I. (1986) AllIithrombin III a((h'ity in hor�C:$with large colon tOl"$ilJO . ..l,rn.)' VtJ. &. 47(4) 897-900. Mum., B R and HinchcHf K W (lW'l) Heparin: a review of ilS phamlat:nlog)' and ther..[Xlllic 'IS(' in hOl�s.J \w. lnl. Mtd. 8( 1) 2�:V->. Morris D 0 (1989) Thrombophlebitis in horsn: the conuibutioo, ofh"moslalK: d)",fu""I>O., 10 p;< 11">g ..nes.is.
C4I>Ifp. Coni. F4uf. Pm" . I'lf. II 13S6-1394. ;\torri� J) J) (I!)!II) F.nrlllloxemia in hones .. ). Yd. Inf. Mm. :> 167-181. �un"t\< R ( 1 99tH F.ndnlO�.,mia ill hu,.,;c;.. III Pr",'icr2() {21
��.
239
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Reef, V B ( 1998) Cardiovd..,wlar ultra.onography. In Equine D;"R"OMic Ultrasound, VB Reef (I'd.). IN B Saundt'r�, Philadelphia, pp. 215-72. Spurlock S L and Spurlock G H (1990) Risk factors of catheter related complications. Comp. ConI. Edu(, l'rod.
Postoperative complications - laminitis
Spurlock S L, Spurlock G H �I ,,{. ( 1990) Long-term jugular vein catheterization in horses. J. Am. Vfl. Med. AlI"". 196
Pollitt C C ( 1 999) Equine laminitis: A revised pathophysiology. Proc. ."-m. As.IOC. Eqllim Pract. 45: I H8-192. ....'. hite :\ A { l 990} Intensive care, monitoling, and compIkatioTlS of acute abdominal di�ease_ In Tlu F.quillf Aru/t' Abdomrn, :\ A \\-'hite (cd.). Lea and Febiger, Philadelphia, pp. 32fi.-30.
\·..1. 12(2);241-24H.
425..-43().
Traub-Darga!]J L and Dargatz D A ( 1 994) A rctr<Jspcctivc study of vein thrombosis in hor.o;c. treated with intraw�nous fluids in a veTerinary teaching hospitaL J. Vet.
Eastman TG, Honnas C M, Hague B, tl aL ( 1999) Ikep digital flexor tenotomy a� a treatment for {'hron;c laminitis in hor�es: 3� ca�es ( 1 98B-1997}. J. Am. Vet. M,'d. Anac. 214(4), 517-9.
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 celiotomy. PrrK. Equin' Colic &s. Symp. 2:112-115 Fontaim, G L, Rodgerson, D H, Hanson, R R and Steiger, R ( 1 999). Ultrasound evaluation of cquine gastrointestinal disorders. Conlp_ Gmt_ Edw;. Pme/. V�I. 21,253-262 McIlwraith C W (l982). The acute abdominal patient, postoperati.'e management and complications. �ret, Clin.
N. Am. l.argeAnim. Praet. 4:167-184
Phillips TJ and Walm�leyJ P ( 1 993) Retrospective anal�is of the ,-esults of 151 exploratory laparotomie.� in hor�es wilh g:utrointcstinal disea.�es. £l[ui1U' Vel.J. 25:427-431 S;Hlt.\chi E M, Grindem C n, Tate L I' and Corbett W T (1988). Peritoneal fluid anal�'sis in ponies after abdominal surg{'ry. Vtl. Surg. J 7:fi.-9 Van Hoogmoed L, Rodger L D, Spier SJ, Gardner I A, Yarbrough T B and SnyderJ R (1999). Evaluation of peritoneal fluid pl!, gIUC08{' concentration, and la<:tate dehydmgenase activity for detection of septic peritonitis in horse.� .J. Am. Vrt. Mtd. Assoc. 214:1032-1036 White N A (1990}. lnten�ivc care, monitoring, and comp!ication� ofanilC abdominal disease. Peritonitis. In Thl F"l',ine Arlll" Abdm1um, N A Whit(' (cd_) Lca and Febiger, Philadelphia, pp. 323---5.
240
Postoperative complications - colitis l'arraga M E, Spier Sj, Thurmond M, Hir
Postoperative complications - cardiac arrhythmias BonaguraJ D. Diagnosis ofcardia<: arrhythmias. In Cum'nl Thuah in Equine l"mdiu, :\ E Robinson (I'd.). W B Saunders, Philadelphia, pp. 240-249. Man C M. Treatment of cardiac arrhythmias and cardiac failure. In Cun-rot Therapy in Equine Practice, N E Robinson (cd.). W B Saunders, Philadelphia, pp. 250-254. Man C M, Reef V B (1991) ECG of the month.i- Am \"1. Mtd. A",ae. 198(9}, 1533-1534
ReimerJ .\1, ReefV B, Sweeney R W ( 1 992) Ve!llricular arrhythmias in horses: 21 cases ( 1 984-1989) I Am. V�1. Mtd. Assoc., 201(8}:1237-1243
RedV B ( 1 999) Arrhythmias. In CrmiiDingy nftluHmw, C .\1 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 stratified 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 diffusion 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 acidity 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
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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 observed by the author is suggestive of underlying factors that are affecting mucosal blood flow in that part of the stomach. In humans Helicobacter pylori 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.
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 confinement 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-specific, they include •
•
• • •
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 different 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
abdominal discomfort, indicated by mild-to moderate colic and frequent lying down poor appetite, Le. not eating well, picking at feed, or not finishing 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 superficial 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 fibrosis 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 acidity to make a diagnosis of gastric ulceration. With simple gastric ulcer disease, clinical signs should subside within 1-2 days.
DISEASES OF THE STOMACH
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 type-2 receptor on parietal cells. The effect of the H2 antago-
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 efficacy 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
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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 ficial than ulcers (erosions can cause significant 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 4-7 days of starting treatment. If there is delayed gastric emptying (pyloric or duodenal stricture, etc.) a longer duration of treatment may be required.
Drug (size)
Recommended dosage
Antacid MaaloxTC Mylanta double strength
Ha antagonist Cimetidine (800 mg tablets)
(150 mg/ml) Ranitidine tablets)
240 ml (8 oz), q. 4 h 240 ml (8 oz), q. 2 h 25 mg/kg p.o., q. 6 h
(1 SO, 300 mg
7 mg/kg Lv., q. 6-8 h 7 mg/kg p.o.,
(25 mg/ml)
1.5 mg/kg i.v.,
q. 8 h
q. 8 h
Proton pump inhibitor Omeprazole
(20 mg capsules 1 mg/kg p.o.,
of enteric coated granules) Omeprazole (paste formulation)
once daily
4 mg/kg p.o., once daily
Mucosal protectant Sucralfate
(1 9 tablets)
Misoprostol
(200 IJg tablets)
10-20 mg/kg p.o., q. 8 h 1.5 IJg/kg p.o., q. 8-12 h up to 2.5 lJg/kg p.o., q.8h
Motility modifier Bethanecol
(5.15 mg/ml)
Bethanecol
(50 mg tablets)
0.02 mg/kg s.c., q. 6-8 h 0.35 mg/kg p.o.,
q.8h
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 modified to promote more continuous roughage consumption and less concentrate consumption. In one study, alfalfa hay appeared to offer some gastric protection compared to brome grass hay. Nutritional management to prevent gastric ulcers is incompletely understood at this time. 244
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
Endoscopic
Squamous
examination
lesions
Glandular lesions
No
?
?
Yes
Yes
No
Treatment recommendation •
omeprazole paste, 4 mglkg p.o., once daily for 3-4 weeks, or 7 mg/kg p.o., q. 8 h for 4 weeks, or
•
ranitidine,
•
cimetidine,
• •
25
mgfkg p.o., q. 6 h for
cimetidine, 25 mg/kg p.o., q. 6 h for Repeat endoscopy after treatment No
Yes
•
4 weeks
omeprazole paste, 4 mg/kg p.o., once daily for 2-3 weeks, or ranitidine, 7 mg/kg p.o., q. 8 h for 3-4 weeks, or
•
Yes
12
sucralfate,
10-20 mglkg p.o.,
q.
3-4 weeks
8 h for 2-4 weeks
Repeat endoscopy after treatment Yes
Yes
Yes
• • • •
4 mg/kg, once daily for 2-3 weeks, or 8 h for 3 weeks, or cimetidine, 25 mg/kg p.o., q. 6 h for 3 weeks, and sucralfate, 10-20 mglkg p.o., q. 8 h for 2-4 weeks omeprazole paste,
ranitidine, 7 mglkg p.o., q.
Repeat endoscopy after treatment
Gastric impaction Gastric impaction can occur as a primary condition, but often it is diagnosed at surgery as a finding 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 emptying associated with generalized decreased gastrointestinal motility.
CLINICAL SIGNS AND DIAGNOSIS 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 difficult to pass a nasogastric tube into the stomach. With gastric distention, the gastroesophageal junction can become distorted, making it difficult 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 finding is not specific for gastric impaction or dilation. Endoscopy may be helpful in the diagnosis, although simply identifying a stomach full of ingesta is not diagnostic for an impaction, and it is difficult 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
12
COLIC
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
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 possibility 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
Dilation of the stomach with fluid or gas usually results from another intestinal disturbance. Normally, a small amount of duodenal contents, consisting of gastric effluent, 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.
CLINICAL SIGNS AND DIAGNOSIS 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.
DISEASES OF THE STOMACH
TREATMENT Treatment is removal of excessive fluid or gas via a nasogastric tube, or at surgery via needle aspiration. An 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
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 •
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 significantly 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
12
• • •
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 hyperfibrinogenemia. 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 confined within the stomach, to an exudate if the tumor has spread. Neoplastic cells from a primary gastric 247
12
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 identifY 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).
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.
21:10-15. (1990) Sucralfate. N. Engl.]. Med. 325:1017-25. Murray MJ (1992) A comparative review of the Scand.]. Gastroenterol. supp!.
McCarthy D M
aetiopathogenesis and treatment of peptic ulcer. Equine Vet.]. supp!. 13:63-74.
Murray MJ (1997) Suppression of gastric acidity in horses. ]. Am. Vet. Med. Assoc. 211:37-41. Murray MJ, 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 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
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
131:170-3. (1982) Six cases of
stomach: a report of five cases. VetRec. Tenant B, Keirn D R, White K K, et al.
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
EPIDEMIOLOGY
RR Hanson
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 identified. 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.
INTRODUCTION The large colon, with distinct motility patterns coordinated by a myoelectrical pacemaker at the pelvic flexure has distinct non-rhythmic haustral movements and stronger well-defined rhythmic retropulsive and propulsive contractions to move ingesta along the gastrointestinal 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 carbohydrates to produce volatile fatty acids. Abnormal rhythmic 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, predisposing the horse to functional abnormalities such as colonic impaction. In horses with colonic impaction, the digesta appears to be retained just 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.
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 significantly 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 conditions, 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 neuromodulators that affect the coordination of myoelectrical activity from the pacemaker regions in the large intestine and, possibly, fluid and ion transport. Cockspur hawthorn fruit ingestion and naturally occurring impaction colic could have similar pathogenesis. The incidence of colonic impaction is influenced by soil composition and geographic region. Foreign materials, 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 normal. 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-tofirm 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 palpable. 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 concentration 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 examination 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 stimulate 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 during transrectal palpation. Intravenous fluid therapy may be necessary in horses that do not respond to initial treatment with analgesics
DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
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 helpful but labor is intensive. Intravenous fluid administration may increase the water content of the impacted ingesta in horses by altering the passive forces that govern transmucosal fluid transport, raising the capillary hydrostatic pressure, and decreasing plasma protein concentration. Intravenous fluids should be administered 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 maintained at 5.0-5.5 g/dl. In a study of 147 horses hospitalized with colon impactions that did not respond to initial farm treatment, the mean duration of medical treatment with xylazine, flunixin meglumine, and intravenous 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, modulates the release of norepinephrine and directly inhibits neuronal firing, causing sedation, analgesia, bradycardia, and visceral pain relief. Xylazine may cause a cessation 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 beneficial 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-mediated visceral pain during intestinal obstruction or distention 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 administered 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 important clinical signs that are indicative of a failing cardiovascular system. Treatment with flunixin meglumine should be continued after correction of the colonic
15
impaction until horses are eating regularly and intestinal 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 emptying 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 nasogastric reflux or if strangulation obstruction is suspected. Bulk cathartics (bran, psyllium mucilloid, methylcellulose) 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 wellhydrated horses, or preferably in combination with intravenous or intragastric fluid administration. Magnesium sulfate is associated with the risk of development 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 advantageous or detrimental to the treatment of impactions. The use of prokinetic drugs to treat horses with colonic impactions is controversial. Intestinal contractions induced by neostigmine, which acts on the large 281
DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
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 generally 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 normal 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 distention is inevitably present. Horses with this condition may have small amounts of diarrhea and clinical signs of endotoxemia. Abdominal paracentesis should be conducted cautiously since the sand-impacted colon can be inadvertently 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
15
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 palpation 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 necessarily 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 recommended 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 intervention. In many horses surgical exploration must be undertaken without an accurate pre-operative diagnosis; 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
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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 multiple colotomies which prolong the surgery and complicate the recovery period. Septic peritonitis can be minimized by using aseptic technique, atraumatic handling 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 displacements are associated with this condition. Postoperative complications include the recurrence of the disease, septic peritonitis, diarrhea, and incisional dehiscence.
OUTCOME
Administration of a moist bran mash containing 450 g of psyllium mucilloid, once a week, is a useful prophylactic 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 transverse colon. Colon diameter varies from approximately
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 following 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 prognosis 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 pasture 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 accumulated 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.
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Figure 15.1 Normal equine cecum and colon viewed with the horse in dorsal recumbency. The dorsal colon is shaded dark gray
DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
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Kidney
L-
Figure 15.4 Entrapment of the colon over the renosplenic ligament is relieved 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 exteriorized 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 diagnosis 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 economic 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 phenylephrine-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-
Edge of incision
Figure 15.5 Schema representing obliteration of the renosplenic 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 experiencing a second bout of LDDC. Obliteration of the renosplenic 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 purposes. 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 ligament 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 renosplenic 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
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Large colon volvulus ~Rm!!l~ilil$lI!iI~dlilM.n.·IT1ml]!WI.~~
RP Hackett
INTRODUCTION
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 prolonged 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 ordinarily 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 diagnosis. 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 compromised by an accompanying volvulus. The prognosis for RDDC unaccompanied by colonic ischemia is very good.
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Volvulus of the large colon can occur anywhere along the length of the colon. In a report of 109 cases of volvulus,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, showing the regions most commonly involved by torsions. 1 = area at the base of the colon where torsions may originate; the cecum is often involved in these cases. 2 = area of right colon where torsion may originate and does not involve the cecum
DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
Degree of colon rotation
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Effect None
90°-270°
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
>360°
Strangulation obstruction of colon
NON-STRANGULATED COLON VOLVULUS Figure 15.8 Volvulus of the large colon involving the sternal and diaphragmatic flexures, viewed with the horse in dorsal recumbency
Figure 15.9 Volvulus 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 discussion. 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 abdominal 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 progressive gaseous distention of intestinal segments proximal to the twist. Signs of pain are more profound and are more refractory to analgesic drugs. Moderate tachycardia (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 typically reveals moderate to marked tympany of the left ventral and dorsal colon. Colonic bands may be oriented transversely if the pelvic flexure has shifted to the right of midline as the left colon distends. Tympany of
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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 confirmed 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 nonstrangulated 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 inspection. Volvulus across the cecal base and right dorsal colon-transverse colon junction is evident only by palpation. 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
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its junction with the transverse colon. Horses with longstanding 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 colon junction is accomplished blindly. 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 (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
DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
OTHER NON-STRANGULATING COLON DISPLACEMENTS In addition to those described above, other non-strangulating 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 displacement. Clinical signs associated with such problems mimic those of the more common forms of nonstrangulated colonic displacement.
STRANGULATION OF THE LARGE COLON Strangulation of the large colon is typically due to volvulus, 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 fatality 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 progressive abdominal distention. Signs of cardiovascular compromise including tachycardia, dehydration, prolonged capillary refill time, and deterioration of mucous membrane color rapidly ensue. Rectal examination 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 emergency 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 influence case management. Although a number of techniques for objective asse~sment of equine intestinal
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viability have been described (fluorescein perfusion, surface oximetry, intralumenal pressure, frozen sections histopathology, Doppler blood flow), these procedures are not in common practice, however, because of either lack of availability or concern about their reliability. Subjective parameters (color, thickness, motility, mesenteric pulse) are ordinarily employed but are of limited accuracy. Often colonic damage is overestimated 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, particularly when coupled with blood staining of colonic content, indicates loss of mucosal integrity and a poor prognosis. Cases with a clearly viable colon are managed as for non-strangulated volvulus (described above). Resection of colon that is non-viable or of questionable 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 unresectable colon of marginal viability should be given a chance through recovery from anesthesia and intensive therapy for endotoxic shock. In these cases, pharmacological intervention is often used to combat postoperative 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 experienced a volvulus two or more times have an 80 per cent chance of another recurrence. Such mares are candidates 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 contin291
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Ventral midline incision
I
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 • • • • • •
Figure 15.12 Colopexy. The lateral taenia of the ventral colon (line of x's) is sutured to the ventral abdominal wall about 15 cm to 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 uncommon 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 prefer elective resection of the large colon near the termination of the cecocolic fold to prevent recurrence of volvulus and other displacements in athletes. Weight loss and soft stools are early complications of this procedure but normal nutritional performance can be expected to return within 5-6 months. 292
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 moderate colonic distention exhibit signs of mild to moderate abdominal pain and corresponding tachycardia. Such cases may spontaneously resolve or be successfully managed 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 ultrasonographic examination but colonic mural thickness is normal and there is no evidence of displacement or lumenal obstruction. Peritoneal fluid is typically unremarkable. The veterinarian must be aware that such horses cannot be readily distinguished from those affected with colonic tympanyt0.05 263472n
DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
preparation and local anesthesia, the catheter is placed into the distended viscus. Suction accelerates the decompression but is not essential. After decompression, as the catheter is withdrawn, a broad spectrum antibiotic solution such as neomycin or gentamicin should be injected through the catheter to reduce likelihood 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 postmortem 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 infarction. 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 vulgaris in its etiology. Clinical signs associated with verminous arteries vary markedly. Intestinal ischemia results in signs of abdominal pain and motility disruption (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 examination. 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 deteriorating 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.
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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 population, 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
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DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
The small colon should be examined to make sure that there are no enteroliths present. If enteroliths are present 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 mobilize 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 proximal 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 regularly until the horse is back on full feed and supplemented 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 compromise 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.
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Ifthis occurs deep in the abdominal incision, gross contamination of the abdominal cavity occurs and the horse is euthanized. Serosal tearing occurring during manipulation of the intestine may be repaired by direct suturing 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 managed 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 predisposition 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 predisposition 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 percentage of grass-type hay in the diet. Alfalfa has been considered a contributing factor because ofits high mag-
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nesium content and protein content contributing to the liberation of ammonium during digestion by the intestinal microflora. Wheat bran has been similarly implicated 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 demonstrated that the enteroliths would dissolve. This observation 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 important concern in prevention of enteroliths. Increased vigilance by veterinary surgeons for the presence of enteroliths by routine abdominal radiography 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 infiltration 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 abdominal 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
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refill time and mucous membrane colour are normal unless the horse has become dehydrated or is affected by toxemia secondary to peritonitis.
RECTAL EXAMINATION 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 peritonitis. It is usually turbid and yellow I orange colored. In a few cases sanguinous peritoneal fluid is obtained. The total nucleated cell count is elevated (10-250 x 109 / 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 contamination). On the mucosal surface, the lesions are characterized 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 postoperatively. In cases where the segment of abnormal colon is short, a wedge resection may be performed with liga-
DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
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-toend 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 colitis, 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 A White,J N Moore (eds). W B Saunders, Philadelphia, pp. 270-2. 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 of the effects of intragastric infusion of equal volumes of 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 (USA) equine population. Prevo Vet. Med. 30(1):23-6. Roberts M C, Seawright A A (1983) Experimental studies of drug induced impaction colic in the horse. Equine Vet.J 15(3):222-8. Ross M, Hanson R R (1992) Impaction of the Ventral Large Colon. In Auer J A (ed): Equine Surgery, W.B. Saunders, Philadelphia, pp 390-2. Sellers A F, LoweJ E (1986) Review of large intestinal motility
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and mechanisms of impaction in the horse. Equine Vet.J 18(4):261-3. Sullins K E (1999) Diseases of the Large Colon. In Calahan P T, Mayhew I G, Merritt A M, MooreJ N (eds): Equine Medicine and Surgery, Mosby, St Louis, MO, pp 741-2. 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, Philadelphia, pp 393-4. 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 the pelvic flexure colotomies in normal equine colon. Vet. 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. 198:1423-6. 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
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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 features of equine enteroliths.]. Am. Vet. Med. Assoc. 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 ofEquine Surgery, N A White,] N Moore (eds).] P Lippincott, Philadelphia, pp. 348-51. 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. 214(2):233-7. Hassel D M, Yarbrough T B (1998) A modified teniotomy technique for facilitated removal of descending colon enteroliths in horses. Vet. Surg. 27:1-4.
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Hintz H F, Lowe] E, Livesay-Wilkens et 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 horse.]. Am. Vet. Med. Assoc. 201 (1l):1745-6. Rose] A, Rose E M, Sande R D (1980) Radiography in the diagnosis of equine enterolithiasis. Proc. Am. Assoc. Equine Pract.26:211-9. Yarbrough T B, Langer D L, Snyder] R, Gardner I A, O'Brien T R (1994) Abdominal radiography for diagnosis of enterolithiasis in horses: 141 cases (1990-1992).]. Am. Vet. Med. Assoc. 205(4):592-5.
Eosinophilic colitis Edwards G B, Kelly D F, Proudman C] (2000) Segmental eosinophilic colitis in horses a review of 22 cases. Equine Vet.]. 32:86--93.
16 Diseases of the small colon and rectum J Schumacher
Diseases of the small colon ENTEROLITHS Enteroliths, or intestinal calculi, are mineralized concretions 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 unassociated 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 magnesium, rather than ammonia or phosphate, in the feed may influence the formation of enteroliths. Diets of alfalfa hay containing a high concentration of magnesium have been incriminated in the formation of enteroliths.
Epidemiology The prevalence of enterolithiasis is high in the southwestern US, and university teaching hospitals in California, Florida, and Indiana have twice the prevalence 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 clinical signs and physical examination. An obstructing enterolith blocks the passage of feces but may allow passage 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 difficult to identity. If the enterolith has lodged in the middle or distal portion of the small colon, loops of gas-filled small colon may be recognized. Diagnosis of enterolithiasis in horses showing clinical signs of the disease can sometimes be confirmed by radiography. Radiography is less helpful in the diagnosis of enterolithiasis of the small colon than it is for diagnosis of enterolithiasis of the large colon (i.e.
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transverse colon), however, and the absence of radiographic 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 possible, the enterolith should be manipulated a few centimeters 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 closure, 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 intralumenal concentration of bacteria (including large concentrations 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 peritoneal 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 infusion 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 abdominal cavity.
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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 operated 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 projections 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
DISEASES OF THE SMALL COLON AND RECTUM
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 discriminate in their eating habits.
Clinical signs and diagnosis 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, tenesmus may be observed. Systemic effects of the obstruction are minor initially, even in horses showing signs of marked pain, and the hematocrit may remain unchanged for many days. Affected horses remain unresponsive 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 portion of the small colon. The obstruction is usually associated 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 frequently 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 dentition, inadequate hydration, parasitic damage, or disorders of intestinal motility. The small colon becomes impacted most frequently during the fall and winter, and this seasonal predilection may be related to inadequate water consumption or dietary changes. Old horses may be predisposed to impaction of the small
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colon because of deterioration in dentition and gastrointestinal 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 location.
Clinical signs and diagnosis 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 accumulate proximal to the obstruction. Diagnosis of impaction of the small colon on the basis of clinical signs and clinicopathologic data is frequently 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, concentration of electrolytes, hematocrit, and concentration of plasma total protein show little deviation from normal. Examination per rectum is often helpful in the diagnosis 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 administration of a balanced electrolyte solution is used to overhydrate 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 calcium. 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
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tomosis of the proximal and distal segments of colon. At surgery, the lesion is recognized as a dense, circumscribed 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
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, nondigestible 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, phytoconglobates, or bezoars is by surgical removal of the obstructing 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 uncommon lesion of the small colon or rectum caused by hemorrhage 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 during gross or microscopic examination of resected colon. The condition causes signs of abdominal pain, and because the hematoma obstructs the lumen, examination 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 resection of the affected intestinal segment followed by an as-
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 pregnancy, 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 parturition. 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, infarction results, causing functional obstruction and progressive signs of colic. Segmental ischemic necrosis of the small colon caused by disruption of the mesocolonic vasculature should be considered when examining post-parturient mares that show signs of abdominal pain, particularly when the cardiovascular health of the horse deteriorates slowly and concentration of protein and the nucleated cell count in the peritoneal 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, presumably because it has a short mesentery. Strangulating pedunculated lipomas are rarely seen in horses younger than 9 years, and they most commonly affect horses greater than 15 years. In the US, Quarter horses and Morgans appear to be the breeds
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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 and diagnosis Signs ofcolic initiated by strangulation 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 containing 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 segment of small colon is removed.
NON-STRANGULATING INFARCTION OF THE SMALL COLON Primary vascular lesions with segmental infarction caused by mesenteric thromboembolism are uncommon 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 anastomosis of the proximal and distal segments. If the affected segment of small colon cannot be exteriorized, colostomy or transrectal exteriorization followed by colorectostomy must be performed.
INTESTINAL ATRESIA Intestinal atresia of foals results in complete occlusion of the intestinal lumen. The condition is rare, except in
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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 agenesis or hypoplasia, cerebral gliomata, hydrocephalus, schistosomas reflexus, and infection with equine herpesvirus 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 according to the tissue involved. In type I atresia, or membrane 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 connective tissue, with or without mesentery. In type 3, or blind-end atresia, the proximal and distal blind segments of colon are completely separated, and the corresponding mesentery is absent.
Clinical signs and diagnosis Clinical signs of intestinal atresia are recognized within a few hours after birth and may include depression, progressive abdominal distension and discomfort, tenesmus, absence of feces, no response to administration of enemas, and an empty, blind-ending rectum as determined by digital palpation or endoscopic examination. The anus is usually normal. Intestinal atresia can usually be diagnosed by observation of clinical signs, proctoscopy, and contrast radiography using barium enemas. Definitive diagnosis is made during exploratory laparotomy (celiotomy).
Treatment Foals suffering from intestinal atresia have a poor prognosis for survival, and for white Overo Paint foals with aganglionosis, the prognosis is grave. Surgical correction 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 fibrinous 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 SMALL COLON AND RECTUM
Diseases of the rectu m 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 excessive hydrostatic pressure or puncture of the rectum by the enema tubing. Rectal tears have also been associated 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 stallion 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 difficult 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 predispose 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, dissecting cellulitis, and formation of rectal diverticulae and strictures. Tears of the intraperitoneal portion of the rectum or small colon frequently cause fecalinduced 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
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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 approximately 10-15 ern long and is not covered by peritoneum but is attached to the surrounding structures by connective tissue and muscular bands. Because the peritoneal reflection extends caudally to within 15-20 cm of the anus, rectal tears most often occur within the peritoneal segment of the rectum or small colon, with subsequent 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 retroperitoneal, rather than the peritoneal, portion of the rectum 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 distance 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 palpated, 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 longitudinal muscle thickens to form the mesenteric tenia, the thickness of the circular muscle decreases. In addition, microvascular studies of the small colon of horses indicate that the area adjacent to each side of the band may
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be inherently weak because at this area, the short terminal arteries penetrate the wall.
Classification
litis and separation of tissue. Tears that perforate all layers and extend into the peritoneal cavity are classified as grade 4 (Figure 16.9). Grade 3 rectal tears commonly progress to grade 4.
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 muscularis 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 contracted 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 diverticulum 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 celluFigure 16.6 Grade 2 tear: the muscularis is torn, but the other layers of the rectal wall remain intact
Figure 16.5 Grade 1 tear: only the mucosa or mucosa and submucosa are torn
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Figure 16.7 Grade 3a tear: all layers except the serosa are torn, forming a serosal diverticulum
DISEASES OF THE SMALL COLON AND RECTUM
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Figure 16.8 Grade 3b tear: the tear enters the mesentery
Figure 16.9 Grade 4 tear: the tear perforates ali layers and extends into the peritoneal cavity
Prevention
smooth, well-lubricated, and never forced into place, and solutions should be administered by gravity flow.
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 rectum is relaxed before proceeding with palpation. Horses should be adequately restrained to perform palpation 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 liberally. 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 palpated 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 examining 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
Clinical signs, diagnosis and immediate treatment Tachycardia, intestinal ileus, pyrexia, sweating, reluctance 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, indicates 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 parasympatholytic drugs or caudal epidural anesthesia may be effective in stopping peristalsis of the rectum and relaxing the rectum and anal sphincter. Propantheline bromide, 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
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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 membrane 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 legalliability. 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 recognized 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 measures are taken immediately to prevent peritoneal contamination and progression of a grade 3 tear, endotoxic shock and death usually result. The tear should be carefully packed with medicated gauze sponges, and the rectum 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 administered 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 prophylaxis, and broad-spectrum antimicrobial therapy, using such drugs as penicillin, gentamicin, and metronidazole. The horse should also receive flunixine meglumine 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 seriousness of the tear and the extent of peritoneal contamination. 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 demonstrated by lower mean and median concentrations of white blood cells in the peritoneal fluid.
Definitive treatment Grade 1 tears usually heal without serious complications, and horses suffering from a grade 1 tear are usually 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 retroperitoneal portion of the rectum have a better prognosis for survival than do horses with similar tears in the peritoneal region. They tend to heal with the main complications 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 conservative (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 intention. 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 peritoneal 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 determine if intestinal obstruction requiring surgical correction is present.
Primary repair Primary closure of grade 3 rectal tears is considered contra-indicated by some surgeons because of the likelihood 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
DISEASES OF THE SMALL COLON AND RECTUM
cause the tear to enlarge or perforate and may increase contamination of damaged tissue. In one study, however, primary closure of the rectal tear, used as the sole means of repair or used in conjunction with other techniques, 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 separation 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 inexperienced in this method. Ineffective attempts to suture the tear in this manner may cause the tear to enlarge or perforate. 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 anesthetized 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 rectum through the anal orifice. The tear was then lavaged and sutured directly. A rectal tear, located approximately 40 cm proximal to the anus, of another horse was successfully repaired with the horse standing, by stapling 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 mesocolon and large amounts of mesenteric and retroperitoneal 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-
16
ulations may worsen the tear if the surrounding tissue is edematous. Grade 3 or 4 tears can be sutured through a laparotomy (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 mammary 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 rectum 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 necessary. 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 mesorectum 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 prevent 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 circumference 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 positioned proximal to the rectal tear by the surgeon performing the celiotomy. The portion of small colon containing the ring is exteriorized through the
309
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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 intestinal wall, and polyester suture in the rectal ring. These four retention sutures and the circumferential ligature are oversewn with 2-0 synthetic 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 portion 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 prosthesis 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 of soft feces is maintained by feeding 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 rectum. 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 reestablish 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 circumference 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 temporary 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 easily and quickly performed and revised, and atrophy of the distal segment of the small colon is more easily prevented with this technique of colostomy. Loop colostomy is performed in the left flank, cranial to and level with the fold of the flank, using either a single or double-incision technique. Horses are anesthetized 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 proposed 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 aponeurosis, and peritoneum are perforated bluntly, and a loop of small colon, located at least 1 meter from the peritoneal 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 incision 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 several 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 antimesenteric tenia of the exteriorized segment of small colon is incised longitudinally to expose the lumen of the small
DISEASES OF THE SMALL COLON AND RECTUM
colon, and the incised edge of the small colon is sutured to the skin with simple interrupted, nonabsorbable 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-incision 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 contamination 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 laxative 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
16
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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 solution (Figure 16.10), and horses should receive a balanced polyionic electrolyte solution at sufficient rate to correct dehydration. The horse should be fed a complete pelleted ration and no hay to reduce bulk, and mineral oil should be administered, as needed, to prevent production of formed feces. Table salt can be added to each feeding to encourage water consumption.
donut at the anus. Type 2 prolapse, sometimes referred to as a complete prolapse, is an eversion of all or a portion of the ampulla recti (Figure 16.12). A type 2 prolapse 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 intussusception of the peritoneal portion of the rectum or colon (Figure 16.13). Type 4 rectal prolapse is an extensive 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
Prognosis for survival of horses with rectal tears 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.
RECTAL PROLAPSE
iii i
c Figure 16.11 Type 1 prolapse: the rectal mucosa alone is prolapsed
Cause Rectal prolapse in the horse is sometimes associated with conditions that cause tenesmus, such as constipation, diarrhea, neoplasia, dystocia, urethral obstruction, or colic. Factors that may predispose to rectal prolapse include loss of tone in the anal sphincter, loose attachments 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 Rectal prolapses are classified according to the tissue involved. Prolapse of the rectal mucosa alone is classified as a type 1 prolapse (Figure 16.11). Type 1 prolapse is usually seen as a circular swelling, resembling a large 312
' ' ' ",,,l,, "
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i II
j
i
j
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CI
I I
C
Figure 16.12 Type 2 prolapse: all or a portion of the ampulla recti is everted
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COLIC
ANORECTAL LYMPHADENOPATHY Enlargement of the anorectal lymph nodes, which are situated dorsally along the rectum in the retroperitoneal space, can cause extralumenal obstruction of the rectum resulting in signs of abdominal pain. Other clinical 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 anorectal lymph node can extend into the peritoneal cavity causing septic peritonitis. Bacteria cultured most commonly from perirectal abscesses are Streptococcus zooepidemicus and EScherichia coli. Diagnosis of anorectal lymphadenopathy is confirmed by digital palpation per rectum, transrectal ultrasonography, and cytologic examination of an aspirate or biopsy from an affected lymph node. Peritoneal fluid, obtained by abdominocentesis, should be examined 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 pelle ted ration should be fed to reduce intestinal bulk, and broad-spectrum 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 ultrasonographically, it should be lanced using a perianal incision.
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(1995) Loop colostomy for treatment of grade-3 rectal tears in horses: seven cases (1983-1994).]. Am. Vet. Med. Assoc. 207:1201-1205. Blue M G (1979) Enteroliths in horses - a retrospective study of 30 cases. Equine Vet.]. 11: 76--84. Blue M G, Wittkopp R W (1981) Clinical and structural features of equine enteroliths.]. Am. Vet. Med. Assoc. 179: 79-82. Byars T 0 (1993) Management of impaction colics in the horse. Equine Pract. 15:30-34. Dart A], Pascoe] R, Snyder] R (1991) Mesenteric tears of the descending (small) colon as a postpartum complication in two mares.]. Am. Vet. Med. Assoc. 199:1612-1615. Dart A], Snyder] R, Pascoe] R, Farver T B, Galuppo L 0 (1992) Abnormal conditions of the equine descending (small) colon: 102 cases (1979-1989) 200:971-978. Edwards G B (1992) A review of 38 cases of small colon obstruction in the horse. Equine Vet.]. supp!. 13:42-50. Evard] H, Fischer A T, Greenwood L 0 (1988) Ovarian strangulation as a cause of small colon obstruction in a foa!. Equine Vet.]. 20:217-218. Fischer A T (1990) Enterolithiasis. In Current Practice of Equine Surgery, N A White,] N Moore (eds). Philadelphia.] B Lippincott, pp. 348-51. Freeman 0 E (1996) Comments on loop colostomy in horse. ]. Am. Vet. Med. Assoc. 208:336.
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Gay C C, Spiers V C, Christie B A, Smyth B, Parry B (1979) Foreign body obstruction of the small colon in six horses. Equine Vet.]. 11:60-63. Guglick M A, MacAllister C G, Ewing P], Confer A W (1996) Thrombosis resulting in rectal perforation in a horse . .f Am. Vet. Med. Assoc. 209:1125-1127.
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Hintz H F, Lowe] E, Livesay-WilkinsP et al. (1988) Studies on equine enterolithiasis. Proc. Am. Assoc. Equine. Pract. 24:53-59. Hjortkjaer R K (1979) Enema in the horse. Distribution and rehydrating effect. Nord. Vet. Med. 31:508-519. ]effcott L B, Rossdale P 0 (1979) A radiographic study of the foetus in late pregnancy and during foaling .[. Reprod. Fertil. supp!. 27:563-569. Johnson H W (1943) Submucous resection for surgical correction of prolapse of rectum.]. Am. Vet. Med. Assoc. 102:113-115. Keller S 0, Horney F 0 (1985) Diseases of the equine small colon. Camp. Cant. Educ. Pract. Vet. 7:S113-S120. Livesey M A, Keller S 0 (1986) Segmental ischemic necrosis following mescolic rupture in postparturient mares. Camp. Cont. Educ. Pract. Vet. 8:763-768. Lloyd K, Hintz H F, Wheat] 0, Schryver H F (1987) Enteroliths in horses. Cornell Vet. 77:172-186. Magee A A, Ragle C A, Hines M T, Madigan] E, Booth L C (1997) Anorectal lymphadenopathy causing colic, perirectal abscesses, or both in five young horses.]. Am. Vet. Med. Assoc. 210:804-807.
Mason T A (1978) Strangulation of the rectum of a horse by the pedicle of a mesenteric lipoma. Equine Vet.]. 10:269. Mazan M R (1997) Medical management ofa full-thickness tear of the retroperitoneal portion of the rectum in a horse with hyperadrenocorticism.]. Am. Vet. Med. Assoc. 210:665-667.
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McClure] T, Kobluk C, Voller K, Geor R], Ames T R, Sivula N (1992) Fecalith impaction in four miniature foals.J Am. Vet. Med. Assoc. 200:205-207. Meagher D M (1972) Obstructive disease in the large intestine of the horse: diagnosis and treatment. Proc. Am. Assoc. Equine Pract. 18:169-179. Murray R C, Green E M, Constantinescu G M (1992) Equine enterolithiasis. Compo Cont. Educ. Pract. Vet. 14:1104-1112. Nappert G, Laverty S, Drolet R, Naylor] (1992) Atresia coli in 7 foals (1964-1990). Equine Vet.]. supp!. 13:57-60. Pearson H, Waterman A E (1986) Submucosal haematoma as a cause of obstruction of the small colon in the horse: a review of four cases. Equine Vet.J 18:340-341. Peloso] G, Coatney R W, Caron] P, Steficek B A (1992) Obstructive enterolith in an l l-month-old miniature horse.J Am. Vet. Med. Assoc. 201:1745-1746. Rose] A, Rose E M, Sande R D (1980) Radiography in the diagnosis of equine enterolithiasis. Proc. Am. Assoc. Equine Pract.26:211-220. Ross M W, Stephens P R, Reimer] M (1988) Small colon intussusception in a brood mare.J Am. Vet. Med. Assoc. 192:372-374. Ruggles A], Ross M W (1991) Medical and surgical management of small-colon impaction in horses: 28 cases (1984-1989).JAm. Vet. Med. Assoc. 199:1762-1766. Sanders-Shamis M (1985) Perirectal abscesses in six horses.J Am. Vet. Med. Assoc. 187:499-500. Sayegh A I, Adams S B, Peter A T, Wilson D G (1996) Equine rectal tears: Causes and management. Compo Cont. Educ. Pract. Vet. 18:1131-1143. Slone D E, Humburg] M,]agar] E, Powers R D (1982) Noniatrogenic rectal tears in three horses.J Am. Vet. Med. Assoc. 180:750-751. Speirs V C, Christie B A, van Veenendaal] C (1980) The management of rectal tears in horses. Aust. Vet.J 56:313-317.
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Spensley M S, Meagher D M, Hughes] P (1985) Instrumentation to facilitate surgical repair of rectal tears in the horse: a preliminary report. Proc. Am. Assoc. Equine Pract.31:553-563. Spiers V C, van Veenendaal] C, Christie B A, Lavelle R B, Gay C C (1981) Obstruction of the small colon by intramural haematoma in three horses. Aust. Vet.]. 57:88-90. Stashak T S, Knight A P (1978) Temporary diverting colostomy for the management of small colon tears in the horse: A case report. J Equine Med. Surg. 2:192-200. Stauffer V D (1981) Equine rectal tears - a malpractice problem.J Am. Vet. Med. Assoc. 178:798-799. Stewart R H, Robertson] T (1990) Surgical stapling for repair ofa rectal tear.J Am. Vet. Med. Assoc. 197:746-748. Taylor T S, Valdez H, Norwood G W, Hanes G E (1979) Retrograde flushing for relief of obstruction of the transverse colon in the horse. Equine Pract. 1:22-28. Taylor T S, Watkins] P, Schumacher] (1987) Temporary indwelling rectal liner for use in horses with rectal tears. J Am. Vet. Med. Assoc. 191:677-680. Turner T A, Fessler] F (1980) Rectal prolapse in the horse. J Am. Vet. Med. Assoc. 177:1028-1032. Watkins] P, Taylor T S, Schumacher], Taylor] R, Gillis] P (1989) Rectal tears in the horse: an analysis of 35 cases. Equine Vet.J 21:186-188. Welker B, Modransky P (1992) Rectal prolapse in food animals. Part II. Surgical options. Compo Cont. Educ. Pract. Vet. 14:554-558. Wilson D G, Stone W C (1990) Antimesenteric enterotomy for repair of a dorsal rectal tear in a mare. Can. Vet.J 31:705-707. Yarbough T B, Langer D L, Snyder] R, Gardner 1 A, O'Brien T R (1994) Abdominal radiography for diagnosis of enterolithiasis in horses: 141 cases (1990-1992).J Am. Vet. Med. Assoc. 205: 592-595.
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17 Other conditions
Abdominal distention in the adult horse T Mair
Gaseous distention
Gastrointestinal tympany (distentionttympanitic cOlic) Intestinal obstruction! impaction Ileus Pneumoperitoneum
Fluid distention
Ascites Peritonitis Uroperitoneum Hemoperitoneum Fetal hydrops
Weakened body wall
Ventral body wall hernias Ruptured. prepubic tendon Cushing's disease
INTRODUCTION Abdominal distention is classically regarded as being caused by one of the 'seven f's' • • • •
fat fetus food fluid
• feces • flatus • foreign body
Although pregnancy (Figure 17.1) or obesity can be regarded as 'normal' or 'physiological' causes of
abdominal distention in adult horses, other conditions that result in an enlarged abdomen are pathological, and may be associated with serious and possibly lifethreatening disease. The most common and most important diseases associated with abdominal distention in the adult horse are listed in Table 17.1.
GASTROINTESTINAL TYMPANY (DISTENTIONITYMPANITlClFLATULENT COLIC) $W~%MillIfIW:%_~WW:S~f%IW~%i®fBIl(IiiIII!II@*""i~"j_ _ '",,='M@MJilM&'i@('MM!M.,"'lI!I,"*i>B)l'='~!W'i0iI'ii@MII",'ffi;;;i=£5j
Figure 17.1 Abdominal distention and ventral edema in late gestation
Gastric, cecal, or colonic tympany occur as a result of accumulation of excessive gastrointestinal gas due to
317
17
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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 Rapid feed engorgement Interruption of GI motility from stress, excitement, or pain Impactions Displacements Late pregnancy Ileus secondary to anE1sthesia, surgical manipulation of the intestines (see Chapter 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 gastrointestinal motility (see Chapters 12,14, and 15). Overconsumption 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 distention may increase the contractility of other segments of the gastrointestinal tract, resulting in spasms that may cause pain. Factors associated with distention colic are summarized in Table 17.2.
Clinical signs and diagnosis 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 intermittent 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 respiratory 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 tympany results in distention of the right flank and right paralumbar fossa. Abdominal borborygmi may be increased in frequency if the distention is mild or moderate, 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 stomach. 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 ventral 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 viscus, 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 rupture 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 recommended in such cases.
Treatment The primary objective of treatment is to evacuate the gases from the region of distention and to prevent
17
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• 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 propulsive 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 moderate 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 tympany. 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 transudative 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.
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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 miniature 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 109/1 (usually < 2.0 x 109/1) and total protein concentration less than 25 g/I (usually < 15 g/I). In some cases the fluid may have the appearance of a modified transudate (i.e. fluid has the characteristics 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, mesothelioma, and various other carcinomas and adenocarcinomas. 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 abdominal and limb edema, but ascites may sometimes be evident.
OTHER CONDITIONS
17
PERITONITIS
FETAL HYDROPS
Peritonitis rarely causes severe abdominal distention due to fluid accumulation, but intestinal ileus associated with per-acute or acute peritonitis may result in abdominal distention (see Peritonitis). In cases of per-acute peritonitis due to bowel rupture, gas accumulation in the peritoneal cavity (pneumoperitoneum) (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) .
Fetal hydrops results from the accumulation of excessive 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 multiparous mares. Hydrallantois is the more common of these two dropsical conditions. Typically there is a sudden 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 performed 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 parturition with administration of intravenous fluids and gradual removal of excess allantoic fluid. The foals are often abnormal and affected by a variety of congenital abnormalities.
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 ofuroperitoneum is based on identification of a high peritoneal fluid creatinine:serum creatinine ratio, possibly with the presence of calcium carbonate crystals in the peritoneal fluid. Hyponatremia, hypochloremia, and hyperkalemia 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 crystals and mucus, it may also appear as hypoechoic fluid. The site of bladder rupture may sometimes be visualized by transabdominal ultrasound in foals, or transrectal examination in adults.
HEMOPERITONEUM Hemoperitoneum due to rupture of the middle uterine artery in mares, splenic rupture following trauma, rupture of a verminous aneurysm of the cranial mesenteric 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.
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 present. 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 pregnancy. External palpation is often unrewarding due to 321
OTHER CONDITIONS
17
• septic or non-septic - whether or not bacteria are present.
Grossappearance Specific gravity Total protein Total nucleated cell count Differential cell count
Total red cell count Fibrinogen Glucose Creatinine Urea nitrogen Lactate Total bilirubin Amylase Lipase
Clear or slightly turbid Straw colored or colorless
< 1.016 <25 gil (usually <15 gil) (mainly albumin) < 10.0 x 109/1 (usually < 2.0 x 109fl) 20-90% neutrophils 5-60% mononuclear/mesothelial 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 ~mol/l (1.8-2.7 mg/dl) 3.9--8.2 mmolll (11-23 mg/dl) 0.4--1.2 mmolll (3.8-10.9 mg/dl) 5-13 ~mol/l (0.3-0.8 mg/dl) 0-14 lUll 0-36 lUll
Peritoneal fluid from normal foals is significantly different to adult horses with respect to total nucleated cell count. In the foal, a nucleated cell count greater than 1.5 x 109/1 (1500/1.11) should be considered as elevated. 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 lymphatic vessels beneath the mesothelial basement membrane 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 bacteria, cells, and foreign material entering the peritoneal cavity.
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
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 gastrointestinal tract, breeding and foaling injuries, intraand 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 resistance of the host, speed of recognition and intervention, and the response to initial therapy. A variety of different bacterial species have been isolated 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. • Clostridium spp. • Fusobacterium spp.
PATHOPHYSIOLOGY 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 vascular permeability followed by the migration of inflammatory cells and transudation of fluid containing fibrin and clotting factors, complement and immunoglobulins, into the peritoneal cavity. The inflamed peritoneum becomes a freely diffusible membrane, allowing a massive outpouring of fluid and plasma proteins 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 contaminated peritoneal fluid.
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. . ...
Infectious or Septic
Non-septic
Parasitic
Surgical complic ations;
Ruptured bladder, ureter or kidney
Verminous arteritis
-anastomosis failure
'.>.
hi.
Traumatic
Iatrogenic
Breeding or
Recta! tear
foaling injury
.«
Uterine perforation:
-non-viable tissue - poor asepsis
Parasitic larval
migration
Penetrating
-Infusion
- wound infection
and larval
abdominal
-biopsy
cyathostomosis
wound
-AI
Blunt abdomina! trauma
Enterocentesis
Intestinal accidents with transmural movement of bacteria
Abdominal, renal, or retroperitoneal abscess
Chemical agents: -bile
Perforating lesions
-gastric juice - pancreatic juice
tapeworms)
(ascarids,
Cecal trocharization
Foreign body
Ruptured diaphragm
Neoplasia:
Uterine rupture or perforation
.
Liver biopsy
-ovarian -abdominal
Metritis Urachal infection Post·castration Enteritis
infection
Septicemia Cholangitis
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 fibrin deposits. However, if the defense mechanisms arc ovenvheImed 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
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 secondary 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.
toneal cavity. Plasma sequestration within the abdomen may result in the development of hypovolemic shock, and absorption of bacterial endotoxins may result in
CLINICAL SIGNS
sew'n' metabolic derangements associated with endo toxemia. Prolonged inflammation and fibrin deposi tion may be followed by fibrous scarring and adhesion formation (Plate
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17.1).
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
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 diffuse septic peritonitis usually causes severe clinical disease.
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Acute peritonitis is, therefore, an important differential for horses presenting with colic, especially if there is concurrent pyrexia. In the absence of therapeutic intervention, signs of endotoxemia and circulatory collapse become more pronounced and death may ensue after a period of several hours to several days.
Chronic peritonitis 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 peritonitis 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.
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 variable 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 protein estimation, and into aerobic and anaerobic blood culture bottles for bacterial culture. Use of an antimicrobial 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 bottom of the container and fibrin clots may develop. If the
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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 suggesting contamination with intestinal contents. Normal peritoneal fluid usually has a total nucleated cell count ofless than 2.0 x 109/1 with a predominance of neutrophils (Table 17.3). Peritonitis is characterized by an elevation of the total nucleated cell count (frequently > 100 x 109 11) with a high proportion of neutrophils (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 pathologist 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 antimicrobial therapy. Bacteria will be cultured or identified cytologically in only about 70 per cent of cases, and failure to identify or culture bacteria from peritoneal fluid does not, therefore, rule out septic peritonitis. The presence of multiple bacterial species during microscopic examination or following culture usually indicates 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 peritoneal fluid is less than 25 gil, and this rises rapidly in acute peritonitis (frequently> 50 gil). Peritoneal fibrinogen concentration may be increased, especially in chronic peritonitis; concentrations greater than 0.1 gil (10 mg/dl) are significant. It should be noted that fibrinogen concentration will also be increased by blood contamination of the sample. Peritoneal pH and comparison of plasma and peritoneal glucose concentrations can also be useful to evaluate 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 mgl d1) are both highly suggestive of septic peritonitis. Serial analyses of peritoneal fluid samples obtained during the course of treatment are helpful in monitoring the success of therapy. Serial cultures may be necessary to identify emerging or resistant strains of bacterial species. Bacterial cultures are frequently negative despite the presence of bacteria in the peritoneal fluid.
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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 peritonitis.
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 prerenal or renal azotemia.
Acute peritonitis 1. There is often an initial leukopenia and neutropenia, 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 elevated (up to 10 gil); it can take 48 hours for peak concentrations to be reached. 3. Hypoproteinemia, often with a decrease in the albumin:globulin ratio, reflects protein sequestration into the abdomen; if dehydration is present, hyperproteinemia may be observed. 4. Electrolyte imbalances may be present as for peracute 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
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 hypergammaglobulinemia 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 abdominal 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 palpated, and mesenteric lymph nodes may be enlarged.
Ultrasonography Abdominal ultrasonography frequently reveals an excessive quantity ofhypoechoic 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 peritoneum or 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 presence 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 castrated males should also be evaluated for an infected castration wound.
Laparoscopy and exploratory laparotomy Diagnostic laparoscopy is most helpful in cases of suspected abdominal abscessation or neoplasia, where a
17
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 contraindicated in cases where gross bowel distention or adhesions are present in the area where the laparoscope is to be introduced. Exploratory laparotomy (celiotomy) should be considered for diagnostic, therapeutic, and prognostic reasons. The procedure should not be undertaken until stabilization of the patient and treatment of hypovolemia and endotoxemia have been accomplished.
TREATMENT Prompt and aggressive treatment is required. The treatment 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 hypovolemia, 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 concentrations 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 endotoxemia by supplying fibronectin, complement, antithrombin III, and other inhibitors of hypercoagulability.
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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 mixture of gram-positive and gram-negative aerobes and anaerobes will be present, and the antibiotic therapy must have sufficient spectrum to control the anticipated flora. Antimicrobial combinations commonly used in initial therapy include I. Na.' or K+ penicillin or ceftiofur plus 2. gentamicin
or amikacin plus 3. metronidazole
22000-44000 IV/kg i.v., q. 6 h 2-4 mg/kg i.v., q. 8-12 h 2.2 mg/kg i.v., q. 8 h, or 6.6 mg/kg i.v., q. 24 h 6.6 mg/kg i.v., q. 8 h, or 15 mg/kg i.v., q. 12 h
25-100 mg/kg i.v.,
q. 6-8 h 2. trimethoprim-sulfadiazine 15 mg/kg p.o., q. 12 h 3. enrofloxacin 1.5-2.5 mg/kg p.o., q. 12 h. 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 several factors including • • • • •
the the the the the
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Gastric decompression Nasogastric intubation to allow gastric decompression should be performed in all cases with evidence of gastrointestinal ileus. Repeated nasogastric intubation every 3-4 hours, or placement of an indwelling nasogastric 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 cyathostomosis). Fenbendazole (10 mg/kg p.o. daily for 5 days) or ivermectin (0.2 mg/kg p.o.) are recommended.
Analgesic and anti-inflammatory therapy 15-25 mg/kg p.o., q. 6 h.
This regime may be modified once the results of culture and sensitivity are available. These antibiotics will achieve adequate levels within the peritoneal fluid, intraperitoneal administration of antibiotics is therefore 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 minimize the risk of toxicity. Other antimicrobials that can be useful in the treatment of some cases of peritonitis (dependent on the culture and sensitivity results) include I. sodium ampicillin
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.
severity of the peritonitis underlying cause of the peritonitis degree of loculation of infection by fibrin etiological agents response to treatments.
Analgesics may be required to control the pain associated 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 antiendotoxin 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 susceptible to cellular and non-cellular clearing mechanisms. A dosage of 40-80 IV /kg, q. 8 h is suggested.
Abdo'minal drainage and 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 relatively 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
OTHER CONDITIONS
of LIH: abdominal c.wity. In
may disseminatc a
localized
17
(OI}ccms
infection
th roughout tht: (:avity. Oesl}ile t.hese concerns peri.
tonciillavagc and drainage arc conside red by man}' din icians. to be beneficial ill ac ute CaSCs of pc:-rilOllilis where there is a purulel l t effusion and poor response to initial Tllt'
2-3 days uTllil the pel;toneal fluid whitt: cell count and I()tal pn)tein concentration s how an improvement. Both peritoneallav.1ge and rh"ainage c..fft�cti\'c1y
em
he perf<mned
using a single ingress!egress catheter placed
on (he ve ntral midline at the most de pend ent aspect of I.he abdomen (Figure 17.4). A..ltcmativdy, two catheters ("an
he used - one egress calhett:"r on the ....entral mid
IiIH' and one ingress catht·I.(·r in one of the paralurnhar
Figure 17,4 Foley catheter inserted in the ventral midline to permit abdominal lavage and drainage
fos..'ia('. A variety of fcnc!ltrated d rains can he use d stich a.� a nmshroom cirdin, thoracic ('annula (e.g. 32 French gauge), Foley catheter, or sH.'rilized sc-gmf'nI. of
naso
sue
irriracion
and
cellulitis.
2scending
infection,
gastric lube. After sedati ng the horse.�, the site for draill
obstruction of the.: drain hy fihrin, and hcrni<,tion of
ill,><'rlion is prepa red aseptically, and the ..,kin and suh
omentum
OJ'
illlcStine !hTO\lgh the drain or drditI .�ite.
tissue is infiltrated with local anesthetic. A I
All hors�s treated by peritoneal lavag-e and dr.:linagc arc
ern stab incision is made through the skin, subcma
Sus(cplible to hemoconcentration, plasma protein loss
CLH.aneous
{issue, and linea alba to a llow insertion of the
and electrolyte disturbances. FrequeIlt mon i LOring of
drain. If a mushroom drain or Foley catheter is being
these param(:ters, and. repl at:cm cnt therapy as neces
used, it can be stretched over a metal probe { sm:h a'i a
sary, arc required.
)lelllIS
felliale can ine or Chambers marc catheter) lO aid its
The addition of povidone-iodine or antibiotics to the
insertion. If the howel is inadvertently punnured dur�
lavage fluid is unnecess,ary and lIlay cause a chemical
Illg insertion, the drain should not he removed until r.ht'"
peritoni tis and increasen morbidity. Their usc is there
il�jlll)' can be repaired surgically under general ane!t
fore not recomm(:nded.
tbesia. The risk of penetrating rhf> bowel (or lIlcrwj in the.' pregnant rnan�)
can Iw rt�duced by uitrasono
graphic sc anning of the area prior to placing the drain. When rhe drain is being used as an ingn�ss cannula,
1 O-:�O iilen; of warmed polyionic fluid) is infused,
Javag<.· anrl
solution
(balanced
th e 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 stopp��d at a smaUer vol lime
Lhan intended. Heparin may he added to 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 ho rse 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 pro
a'ned with a sterile bandage Unlit the neX llreatment. If ahdominal pain
occurs
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-
Surgical treatment The aims of surgical th erapy of peritonitis are to ideo ,.if)' and rt::J'nove the source of a bdominal (.oo13mination and
to
remove s.eplic material. Many cases of per itoni tis
will recover wlthout resorting to surgical invasion of lhe abdominal
cavity.
alth ough
the source or peritoneal
contamination may remain undiagnosed. 1n those ca.�es where no un derlying c.ause of the peritonitis (.an be
est.ablished, surgical explora{ion may help to identify 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 lap a rotomy can, therefore, he ....er)' difficult. Some surgeons may opt to penorm surgery in every C:i:1..i' e in the hope of ide ntify ing and treating the underlying (ause. Alternatively, su rgi cal explora ti on of the abdOIIlt:n may be lim ited to the following si tuations
I. cases where an abdominal mass of unknown e tiology has been identified
2. cases where an ahdo minal abscess has been identi fied and where surgical removal, drai nage. or
marsu
piali la . (ion is consi.dered 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 protozoa are identified in the peritoneal fluid) 7. cases with severe and intractable or worsening abdominal pain 8. cases where medical therapy and abdominal drainage fail to result in improvement within 24-48 hours 9. cases which demonstrate a deterioration in the clinical features, despite aggressive medical therapy, within 12 hours. Surgical exploration of the abdomen permits effective open abdominal lavage via the laparotomy wound. Open peritoneal drainage via a small abdominal wound loosely sutured with monofilament stainless steel retention 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 mortality 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 prognosis. 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 postoperative peritonitis are also reported to have a high mortality 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 parenchymous abdominal organs is recognized most commonly
330
as a complication of Streptococcus equi subsp, equi infection (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 anastomosis 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, Salmonella spp., 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 treatment during the acute stage of infection.
SIGNALMENT AND HISTORY Horses of any age and either sex can develop abdominal 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 parasite 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 involvement, 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).
OTHER CONDITIONS
17
Colic may be caused by external cmnpn:ssio ll ohhe itllestinal lumen, tmction on th(� mesentery. or adhe sions
lO
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 l'SA.
DIAGNOSIS Horses with abdominal abscesses can be difif culllO dif fen�1l1iate 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 rna)' he
h elp/iIi in making a rliagnosis •
reClai examination
•
hematology :dnd serum biochemistry
•
ahdominal
•
ultrasonography
Figure 17.5 Ultrasonogram obtained tramrectally showing a large multilowlated post-castration absce55
by digital p alpatio n per rcc[Um, I.ransrectal ultrasonog
paracenlesis
Ti:lphy. and cyto logic examination of an aspirate or biops)' from an affected lymph n o de. Peritoneal Auid,
•
laparoscopy
•
t"xpioralory laparotom y (celiotomy)
•
nuclear scintigraphy.
obtained by abdominocemesis, should be examined
cytologically to determine if sepsis extends int.o the abdomina! c:avit)- ,.
Rectal examination may reveal an abnormal mas.."i
Lltrasound examination (transrcclal and/or trans
that may be painful to palpation. These ma.�ses arC uSu
ahdominal) may he helpful. espc(:ially if a ma� is palpa
all)' palpated in the midline or in the ventral qu:.tdranrs.
ble
l.oups of adherent and distended small intestine may be
cl)'prorchidt:cr,omy) abscesses are usually located adja·
palpated abs(:esses
acHacenr will
to
not
the
abscess.
be
palpabl<:
However. many per
rectum.
per
rec:rum.
Post-c
(including
cent to one inguinal canal ( Fig ure 17.5). Mesenteric abscesses may he difficuh to image. depending on their
H e matologic al changes are frequently non-specific., hut
location. Confirmation of an ahdominal abscess may
may include leukocytosis, neutrophilia, monocytosis,
require surgical exploration, eithcr by .....ay of diagnostic
and hyperfibrinogenemia. J lyperproteinemia, hyper
laparoscopyor explora.tory laparotomy (celiotomy).
globulinemia, hypoalbumincrni:.t. and hypocalcemia
�udcar scintigraphy
u s in g
tcchnctium-99m labeled
may be derccted by serum bim:hcmistl)'. Peritoneal fluid
white blood cells can sometimes be
changes are not consistenr in all cases, but there is
abscess lhat cannot be localized by other tt:chniqm::s
lISll
ally evidence of low-grade peritonitis with elevated total
(see Chapter
used
to identify an
2).
nucleated cell count, neutrophil count, and prolein con centration. Bacteria are not reliably present in the fluid. Allor th
_"cen
,,,·jlh other dis
TREATMENT
east's, including some cases or abdom inal neoplasia, and
differentiation bern'een absn:ssation and neoplasia can
SuccessrUI treatment may be achieved in some (ase s by
be a significant challe nge . Both neoplasia and abscesselO
prolonged antibiotic therapy. AtteI'C1pts to culture the
rna)' sometimes be present in the same horse.
offendin g organism should always. be made to help
Enlargement of the anorectal lymph nodes and sub
select the appropriate anlibiolic(s). Peritoneal fluid
sequent abscess formacion can calIse excralumenal
should be coll cc ted for bOlh aerobic and anaerobic cul
obstruction of the rectum resulting in sig ns of abdomi
ture.
nal pain (see Chapter
If feasible. a needle aspirace of the absccss should
16). Other clinical signs associ
be made percultl.ncously, utili1.ing ultrasound guidance.
of
AJternativd y . samples llIay be obtained by centesis via
production of feces, tenesmus. and pyn:xia. Anorectal
exploratory laparotomy
abscesses arc
Antibioric therapy will be re<:]uiced
most
(:ommonly identified -in foals, but
thf")' can sometimes anecl "dull horses. Sepsis can
(cdiotomy) or laparoscop)'.
fOT Ci minimum of 30
days, and not infrequently for 2-6 months. Procaine
(22000 Ie/kg b.i.d. Lm.) is the antibiotic of St-rtptor.oCCU.f equi. However,
extend inlO the peritoneal cavity causing septic peri
penicillin
lonitis. Diagnosis of anorectal abscess ation is confirmcd
choice [or cases involving
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 continued until such time as the clinical and laboratory changes (including fibrinogen) have returned to normal. 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 peritoneal 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 treatment. A clinical or laboratory improvement after 2 weeks of treatment is a positive and encouraging sign. The prognosis is much poorer in cases where intraabdominal 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 hemoperitoneum are listed in Table 17.5. In neonates, rupture of the internal umbilical structures is the most common cause of hemoperitoneum. Hemoperitoneum can also occur secondarily to rupture of the spleen or liver, or it can be caused by fractured ribs and diaphragmatic tearing during dystocia. In older foals and adult horses, idiopathic hemoperitoneum 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 fracture of one or more ribs. Hepatic rupture may also occur in association with hyperlipemia and fatty infiltration 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 peripartum period. In the male horse, severe abdominal hemorrhage following castration may occur occasionally, although the more common hemorrhagic complication following castration is external hemorrhage. Almost all horses have some blood in the abdomen following 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 intraabdominal hemorrhage because of invasion and rupture of local vessels or hemorrhage from the tumor itself; the latter occurs commonly in cases of hemangiosarcoma (Plate 17.5).
OTHER CONDITIONS
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 hemorrhage may resemble a horse affected by severe colic. Abdominal distention may also be seen.
DIAGNOSIS The most useful and rapid diagnostic aid for hemoperitoneum 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 capsule 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
17
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 origin 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 umbilical 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 abdominocentesis 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, replacement oflost blood volume and oxygen-carrying capacity is critical. In certain situations, medical treatment alone is deemed best. This includes most mares with suspected uterine artery hemorrhage where surgical exploration may be ineffective and result in additional and possibly fatal hemorrhage. In some foals, medical management alone is useful. Application of a belly wrap or abdominal support bandage may be helpful in increasing intra-abdominal pressure and reducing hemorrhage. Transfusion with compatible, fresh, whole blood is the most common approach. This provides oxygen-
333
17
COLIC
carrying capacity as well as fresh coagulation factors from the plasma. Time is often a factor in the acquisition of whole equine blood since storage of equine blood is not practiced. In some instances, the administration of polymerized bovine hemoglobin (Oxyglobin, Biopure Corporation, Cambridge, MA, USA) may be effective in providing sufficient oxygen-carrying capacity 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 developing 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 therapy in these cases is autotranfusion. This can be accomplished with the use of a variety of vacuum blood collection systems with an anticoagulant (approximatelyone 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 hemorrhagic 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 peritoneal space during massive hemorrhage. In some patients, the decision for surgical exploration might be necessary. This will depend on the clinical 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 pressure 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
these patients. Abdominal ultrasound remains a critical diagnostic tool for this problem.
Gastrointestinal neoplasia M Hillyer
INTRODUCTION 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 neoplasm, 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.
Primary gastrointestinal neoplasms
Reported sites of occurrence
Lipoma
Mesentery Wall of small and large intestine
Squamous cell carcinoma
Stomach
Lymphosarcoma
Small and large Intestine
Adenocarcinoma
Small and large Intestine
Leiomyoma
Duodenum Jejunum Small colon
Leiomyosarcoma
Stomach Duodenum Jejunum Rectum
Neurofibroma
Large Intestine
Myxosarcoma
Cecum
Adenosarcoma
Not specified
OTHER CONDITIONS
17
etiology is likely to be multifactorial. The etiology of lymphosarcoma and the other gastrointestinal neoplasms is presently unknown. 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 neoplasms, 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 clinically 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 As with 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
PRESENTATION AND CLINICAL SIGNS Horses with a gastrointestinal neoplasm will usually present 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 gastrointestinal neoplasia, together with an intermittent pyrexia. Typically the neoplasms occur in mature or aged animals. The exception to this is the pedunculated mesenteric 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 neoplasm 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 discomfort, 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 gastrointestinal 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 gastrointestinal 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 lymphosarcoma 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 lymphosarcoma. However, in many cases the total protein concentration 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 indicate 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 suspected 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 provide additional information on the volume and charac-
336
ter of the peritoneal fluid. Intestinal distention may be recognized together with abnormal bowel wall thickening 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 samples 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 demonstrate 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 radiolabeled markers may provide a novel method of identifying a gastrointestinal neoplasm.
Exploratory laparotomy/celiotomy Although expensive and highly invasive, exploratory laparotomy provides the ultimate method for exploration 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
• affect middle-aged and older animals, especially ponies • have an acute onset colic related to intestinal obstruction • are successfully removed by early surgery.
17
• 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 Td 26d ( i4a5e)Tm (v418.64 Tm r9(the)Tj 8sual48.8
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 squamous cell carcinoma in the stomach of a horse
OTHER CONDITIONS
persists for 48 hours or longer. Recurrent colic refers to bouts of abdominal pain which recur at variable intervals 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 exploration of the abdomen. Chronic and recurrent colic cases are often frustrating to deal with, but the understandable 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 following 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 irritation, colitis, and cyathostomosis. Parenchymal inflammatory disorders include hepatitis and cholangitis. Peritoneal inflammation can be caused by septic peritonitis, abdominal abscessation, and intra-peritoneal neoplasia. The common causes of chronic and recurrent colic are listed in Tables 17.8 and 17.9.
17
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 (180° or less) • enteroliths • adhesions • diaphragmatic hernia • sand impaction Inflammalgrydjseases • cyathostomosis • colitis • NSAIDtoxicity/right dorsal colitis MotUtty dj~Qrgel] • 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 available to undertake further diagnostic tests and laboratory 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 components in every case.
History Pain
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
The onset of pain associated with lesions such as intussusceptions is frequently sudden; there may be an initial episode of severe pain, followed by milder and intermittent 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 compression from a space-occupying mass or an intramural infil-
340
trate). Bouts of pain that show an association with feeding may indicate gastric ulceration, neoplasia, or a partial 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
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 recurrent bouts of pain. Likewise, a history of previous peritonitis 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 development of an abdominal abscess. The recent or current administration of drugs should be recorded. Non-steroidal anti-inflammatory drug (NSAID) therapy can predispose to gastrointestinal ulceration. Recent administration of an anthelmintic might suggest a parasite-associated problem (such as cyathostomosis). A history of chronic or recent weight loss may be present in cases of abdominal neoplasia, abscessation, and chronic peritonitis.
In-contact horses Similar disease problems in in-contact horses is suspicious of infectious, parasitic, nutritional, toxic, or management 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 practices and irregular time interval between feeds may also result in intestinal complications. Poor quality roughage, eating coarse bedding materials, 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 significant 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
17
training. Intussusceptions, foreign body ingestion, and cyathostomosis are also more common in young horses. Older horses are more likely to suffer from motility disorders 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 showing 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 presenting 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 diagnosis 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 evaluations. In many cases laboratory results will be unremarkable or reveal non-specific changes, but in some cases laboratory results may be diagnostically helpful 341
OTHER CONDITIONS
undiagnosed. Exploratory surgery via a ventral laparotomy / 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
17
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 predominantly 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.
INTRODUCTION Body condition Grass sickness is a dysautonomia of Equus spp. characterized 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 recognized 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 indistinguishable 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 previously 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 immotility 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.
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 sickness.
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 hemisphere (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 following movement to a new pasture or premises.
Climate Cool (7-10°C), dry weather tends to occur in the 10-14 days preceding outbreaks.
Anthelmintic history Recent evidence suggests that grass sickness is encountered 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
• •
the potential involvement of an ingested mycotoxin the possible role of toxin release from Clostridium botulinum • an oxidative stress-mediated neural damage. Geographical location
To date none of these investigations have yielded conclusive results.
Age Gender Body condition
CLINICAL SIGNS
Season Grazing
Acute form
Movement to new premises Climate Anthelmintic history
of increased frequency of changing pastures. The reason for this apparent association is unclear, however it is not considered likely that anthelmintic drugs themselves 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 component in the plasma of acute cases has been demonstrated 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 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/somnolence, 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 40°C) and bilateral ptosis mayor may not be present. Muscle fasciculations of the triceps and quadriceps muscle groups may be observed and sweating 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 coexisting 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 frustration. 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 demonstrated 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 (as disease progresses) gastric reflux (as disease 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
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 malodorous reflux. A generalized, marked reduction in intestinal motility is evident during abdominal auscultation. 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 examination. Frequently, distention of the small intestine can be appreciated and consequently the rectal findings in many acute cases can appear similar to those encountered 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 caudal 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, however 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.
17
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 loss of body condition 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 abdominal 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
Chronic form The clinical signs in the chronic form are more insidious 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 17.11 Chronic grass sickness case adopting a base-
narrow ('elephant on a tub') stance
345
17
COLIC
colonic impaction are rare, therefore rectal examination usually reveals a lack of contents within the palpable 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 hematologic parameters are pathognomonic for grass sickness. As one of the major differential diagnoses of grass sickness is colic, most of the comparisons of clinical chemistry parameters have been made between grass sickness cases, normal controls, and colic cases. Plasma cortisol, catecholamine, and histamine concentrations are significantly higher in acute and subacute grass sickness cases than in colic cases and normal animals. This finding has been attributed to increased sympathoadrenal activity. The acute phase proteins, haptoglobin and orosomucoid, are increased in all three forms of grass sickness 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 Gross pathology 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 surface 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 gastrointestinal 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 autonomic ganglia such as the cranial, cervical, stellate, and coeliacomesenteric, in dorsal root ganglia, in specific brain stem nuclei, and ventral horn and intermedialateral 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 gastrointestinal 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 neurons 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 considered 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
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 sickness, careful consideration of the entire clinical presentation 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 however 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 occasionally 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 absence of pain or in the presence of!11iJJJ. /intermittent pain High pulse rate in the absence of pain or in the presence of mildliatermittent pain Grossly normal 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, subacute 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 dysphagic, refluxing gastric fluid, and/or showing signs of severe colic, euthanasia is required before this observation period is complete. Table 17.14 summarizes the
17
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 candidates 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 dramatically 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 frequent provision of feed is indicated with a recommendation of 4-5 feeds per day. Preferred feeds include molasses-containing feeds, crushed oats, and high energy cubes. Soaking these feeds may facilitate swallowing 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 indication for such treatment remains questionable. The importance of nursing, frequent human contact, frequent 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
firSI 2-4 wt:cks. The prognosis however is con.�ider.tbl)' poofer if this decrease in body W('ight continw:s beyond 6 .... · Cek.5 duration.
OUTCOME �OSI swviving chronic gran sid:.nC5S cases are capable of rC$uming normal work. Residual abnormalities may however PCT":'iilil in some survivors, including mild dys
Therapeutic agents
phagia. excessive s�'ealing, long silky coat growth, and
Intestinal motility enhancers
multiple small areas of pil�rection. Although most of
Cisapride is an indirect cholinergic agent which fadli
the residual proble ms lend to improve with time, they
Iltles acetylcholine release from the myenteric plexus of
may fail to rewlve completely.
the
gut.
Unlike
the
pramide. cisapride
related
lacks
compound
central
propenies. The use of cisapride toLd. for 7 days) has been shown
antidopaminergic
(0..5-0.8
to
metoclo
mg/kg p.o.
increase gut motility
in chronic case s of grass sickness. Because cisaprirlc may increase colic signs approximately :2 hours after admin istration, it may indirectly interfere with the overall demeanor and appetile of the animal. Any decision
PREVENTION Although no guaranteed mC'lhod� uf prevention 3re known, consideration of the associated ri�k factors allows certain precaUlions
therefore to adminislcr cisapride should take into
These precautions include
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 di�ase will therefore delermine whether cisapride lherapy is required. In adrlil.ton, chapride i� expensive and is not currenlly licensed for \ eterinary usc.
to
be taken. This is panictl
larly relevant in high risk areas during March to July.
h[)using new arrival$ for a 2-month period. before turn out
•
avoiding any change in pasture during the high risk 5eason
•
avoiding the use of plI.slure where lhe disea...e ha�
•
hnusing hon;es may alliO be advisable in high·risk
occurred before areas, if the preceding 7-10 comccutive days have been cool and dlj'.
'
Analgesics
A1llhese pr�aution$ are especially rele\'3nt ror 2-8-
Nun·steroidal antl-inflammatory drugs are suitable for
year-olds.
analgesia in �.h ronic cast'S as they do nO[ adversely affect inte�tinal motility. Chronic cast's may have mild, tran sienl episodes of colic fonov.ing 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
Pancreatic diseases
cumSlance5.
T Mair
Appetite stimulants
INTRODUCTION
Inappetance is a mOljor ddermining factor in the sur \';\,al of many cases of chrunic grASS sickness. It is impor tant however.
to dt':tcrmine if the
lack of food intake is
mainly because of inappctance or dysphagia. Diazepam has prov..n to be mildly beneficial 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 .. sugge'ilcd litarting
point.
A liimilarcompound, brnlil.olam (2IlR/kg slow i.\'.) has recently heen use d
as
lI.n appt'tite stimulant in chronic
grass sickness casC$ with sligh tly more suc cess than diaupam. BrotilOlam iii not however licensed for use in ho rses and no co ntrol trials have been conducted 10 assess its full wurth in the treaunenl of chronic grass sickness (ases.
348
The pancreas i§ a triangular shaped organ that lies transversely on the d()r�al 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 IfdS trophrenic ligament, the suspensory ligament of the spleen, Ihe poslerior vena cava. the portal fissure, and. Inc gastropancreatic fold. The ventral 5urbce i�
adja
cent 10 the base of Ihe ce..:um and the large colon. There are •
tWO
ducts
Ihe larger pan&T8C.(jc dIU' opens inlo the duodenal cti\'eniculum alongside the bile duct
•
Ihe
(J(cn.w')pancr(alic duet ends on
a papilla in Ihe
duodenum opposile the main pancreatic duct.
17
OTHER CONDITIONS
The pancreas is a compound gland that has important exocrine and endocrine functions. Digestion in the small intestine is partly dependent on pancreatic secretions, but also on biliary secretions and mucosal enzymes. The volume ofpancreatic fluid secreted by a 100 kg pony is approximately 10-12 IIday. Secretion is under both neural and hormonal control. Pancreatic juice 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 transportation of glucose across the cell membrane.
DIABETES MELLITUS Five separate forms of diabetes mellitus are recognized I. 2. 3. 4. 5.
insulin-dependent diabetes mellitus non-insulin-dependent diabetes mellitus secondary diabetes mellitus gestational diabetes mellitus impaired glucose tolerance.
Diabetes mellitus is rare in horses; it is most commonly associated with insulin resistance induced by pituitary adenomas. Only insulin-dependent diabetes mellitus will be considered further here.
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 diabetes mellitus is very rare. However, adult horses and ponies may develop signs of exocrine pancreatic insufficiency, with or without associated insulin-dependent diabetes mellitus, following destruction of the pancreas by diseases such as neoplasia (pancreatic adenocarcinoma) 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
• 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 amylase 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 activity 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 amylase
serum creatinine X
urine creatinine
X
100
=
FEarn
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-
Amylase (lUll) Lipase (lUll) Glucose (mmolll)
Serum
Peritoneal flUid
14-35 23-87 4.0-5.6
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) secondary damage to the pancreas from hypovolemia or reflux of duodenal contents up the pancreatic duct can result in release of pancreatic enzymes into the circulation. The diagnosis of insulin-dependent diabetes mellitus can be confirmed by performing either an oral glucose tolerance test (see Chapter 2) or intravenous glucose tolerance test. The intravenous glucose tolerance test is performed by administering intravenous glucose (0.5 g/kg) as a bolus (e.g. 40 or 50%), and collecting 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 glucose concentrations, which fail to decrease as fast as normal, with little increase in insulin levels. Confirmation of chronic pancreatitis or pancreatic carcinoma is generally made either at exploratory laparotomy or at post-mortem examination. Owing to the difficulties in diagnosing chronic pancreatic 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 gradually adjusting the dosage. In one report of diabetes mellitus associated with pancreatitis in a pony, protamine 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 12year-old pony. Hyperinsulinemia induces hypoglycemia, which can also be seen following fraudulent or therapeutic 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 obstructions and anterior enteritis). The pancreas is not easily visualized during routine surgical exploration of the abdomen, and may be overlooked at necropsy, especially if gastric rupture has occurred. Acute pancreatitis can occur in association with adenovirus 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 hyperlipemia. This lipid is subsequently hydrolyzed by pancreatic 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 necrotizing 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 examination. Peritoneal fluid may be serosanguinous or frankly hemorrhagic. Most affected horses die within 24 hours. No specific therapy apart from symptomatic treatment for abdominal pain and hypovolemic shock has been described.
OTHER CONDITIONS
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 gastrointestinal 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 reproductive 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 practitioner 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 relative 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 environment within the mare's womb for as long as possible, 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-
17
sent more of a challenge. It has been reported that approximately 18 per cent of all pregnant mares requiring colic surgery abort their pregnancies postoperatively. 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 arterial 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 maintenance of the unborn foal is the development of endotoxemia 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 luteolysis 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 gestation pregnancy maintenance is dependent on progestogen production by the placenta and so is unaffected by a loss of ovarian progesterone, however clinical evidence 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 support 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 progesterone 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 addi351
17
COLIC
tional support during a time of severe or chronic stress in general. Again, it is the author's preference to initiate 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 injections 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 progesterone supplementation sooner in these early gestational mares, it is important to ascertain whether there is enough remaining ovarian progesterone production to support the pregnancy (i.e. blood progesterone leve1s> 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 supplementation 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 experience sensitive mares of this type will demonstrate inappetance 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 discomfort 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 possible 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 credibility
OTHER CONDITIONS
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 complaint of behavioral abnormalities. In the author's experience, 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 discovered 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 movements. 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 thrusting, 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 cranial vaginal wall. Such injuries may be suspected any time there is fresh blood on the stallion's penis or coming through the vulva of the mare immediately following 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 prevented 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
17
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 following 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 performed 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 gestation. 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 spontaneously on their own with little or no need for treatment. It is also worth mentioning that many inexperienced owners may become alarmed upon finding a late gestation mare who is lying down and groaning 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 difficult 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 increasing 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 presence of the enlarged uterus and fetus which fill the caudal abdomen obscuring the viscera. Treatment includes aggressive overhydration with intravenous and or oral fluids, and oral laxatives or mild cathartics such as (mineral 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 inadvertently 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 situation, but in long-standing impactions the mare should be supported parenterally as complete anorexia may compromise the pregnancy. As in all things prevention 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 nasogastric tube at the first sign of decreased or dry manure production if they are not too stressed by the procedure.
Dorsoretroflexion of the uterus Cases of colic caused by dorsoretroflexion of the uterus in gravid mares are extremely rare in the author's clinical 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 ineffective 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 condition 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 examination is performed following the rectal examination to differentiate between a mare with a dorsoretroflexed uterus and a mare who is actively aborting. In the former case the cervix will be found to be closed in the cranial extent of the vaginal canal and ventral to the fetus which is palpable dorsal to the vagina through the vaginal 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 dorsoretroflexion includes the administration of uterine relaxants - 200 mg isoxsuprine i.m.: or 200 Ilg clenbuterol 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 minutes 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 torsion in the mare still seems likely to be the result of inopportune fetal activity possibly combined with getting 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
17
OTHER CONDITIONS
mares will typically continue to pass feces. The severity
immediate steps taken to correct the torsion and return
of the pain sometimes .�et'Cms to be related to the degree
the uterus to its normal position
of torsion, and mares who also have bowel entrapped
Options for correcting the uterine torsion include
along with the twisted uterus may demonstrate severe pain. (kcasionally affected term mares will present at parturition with 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 t\vist is usually cranial to the cervix and therefore is not readily palpable per vagina in the pre-term mare. Rect.al identification of the taut hands of the stretched broad ligaments is the hallmark of this condition. The broad ligament from one side of
•
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'C the foal) manual rotation of the foal (and uterus) through th(" c("n1x to a normal position may be possible.
the uterus is pulled over the top of the uterus past mid
Vl11en the marc is tractable and there are no indica
line toward the side of the direction of the uterine twist.
tiollS that the twisted uterus has alrt'Cady ruptured, it is
The other broad ligament is pulled ventrally under
the preference of this author and many others to correCt
neath the uterus away Ii-om the side of the twist.
the uterine torsion in a pre-term mare via a standing
Therefore when viewed from the back of the marc a
flank laparotomy. An incision is made through the
countercloek\vise �ist to the marc's left will find the
mare's flank using a grid approach, and the incision is
right broad ligament pulled horiwntally over the top of
preferably made on the side that the marc's uterus is
the uterus to the left and the left broad ligament will be
twisted to. The direction of the twist is (:onfirmed via
the
intra-abdominal palpation of the uterus and the broad
mare's right. Conversely a clockwise twist of the uterus
pulled ventrally underneath the marc's uterus
ligaments, and then the uterus is dctorsed by carefully
to
th(" mare's right will find the left broad ligament
reaching underneath the uterus and gently rocking the
pnl!t'Cd horizonta!Iy over the top of the uterus to the
uterus to gd up enough momentum to lift the twisted
marc's right and the right broad ligament pulled ven
uterus up and pushing it over in the opposite direction
to
trallv under the uterus to the mare's left. The practi
of the twist to return it to its normal position. If needed
ti(mer can often make an educated guess as to the
the foal's limbs may somt'Ctimes be grasped through the
degree of the torsion based on the palpable tightness of
uterine wall to help the surgeon facilitate this maneuver,
the broad ligament bands and the twist in the uterus
but at all times care should be taken not to cause any
itself. Likewise an impression of the dt'Cgree of possible
tears in the uterine wall.
uterine compromise may h� made based upon the feel
lenging if the uterus has become friable. If the preg
This may be especially chal
of the uterine wall (Le. either thick and taut or sti!!
nancy is advanced enough it may require that a second
somewhat pliable) and/or its appearance on rectal
incision be made in the opposite flank and two surgeons simultaneously
(one
pushing
and
the
other
ultrasound. Occasionally the small colon becomes con
work
stricted as a result of the uterine twist and may obstruct
pulling) to untv.,;ist the uterus and return it to its normal
the examiner's ability to perform a filll rectal examina
position. Afkr the torsion has been corrected the sur
tion to determine the extent of the insult.
geon then carefully palpates the dorsal smface of the
The fNllS will typically be displaced cranially in the
uterus and broad ligaments to confirm that the uterus is
alx:!omen by the twist. in th� Illerine body and may be
no longer twisted. The surface of the uterus is also care
out of reach of the practitioner per rectum. In this
htlly palpated for the presence of any tears (especially
instance, fetal viability may not be determinable via rec
where it was twisted) and an assessment of fetal viability
tal examination and instead may be determined by
is made by trying to detect spontaneous fetal movement
detection of fetal cardiac motion or spontaneous fetal
or the presence of a heart beat in the foal's chest pal
movement via transabdominal ultrasound of the mare.
pated careh!!ly through the uterine wall. If the foal is
Depending on the degree of the twist and the duration
dead, once the torsion has been corrected the mare
of the insult, the blood supply to the uterus may
should go on to abort naturally postoperatively, or deliv
become sufficiently compromised to (;ame fetal death.
ery can he induced. The delivery of the dead fetus
The uterus likewise may become edematous and friable
should be supervised so any malpositiol1s may be quickly
and in some extreme cases even necrotic, and the risk
corrected, and to assist the mare and minimize her
of uterine rupture and peritonitis becomes a real possi
abdominal effort to rt'duce stu�ss on the surgical inci
hilit\', It is therefore important to hoth the foal's and
sion. If the foal is alive and has not heen compromised
the mare
'
g
continued well being that the presence of a
lltt'Crin(" torsion he r<tpidly identified after it occurs and
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 uterine torsions by administering general anesthesia to the mare and rolling her to untwist the uterus. Two methods 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 position, and then over onto her opposite side and then up into a sternal position. In the first method this maneuver 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 untwisting the uterus. Care must be taken to identity the direction of the uterine twist correctly in the first place so that the mare is positioned on the proper side, otherwise 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 correcting 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 correction 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 positioned 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 position with the hind end slightly elevated to provide the maximum room to maneuver within her will also maximize 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 detorsion 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 without 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 entangled 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 indicated 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 facilitate delivery of the foal if needed. The risk of incisional complications following this procedure in a heavily gravid and subsequently foaling mare must be recognized, 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 techniques 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 during pregnancy Other pregnancy related conditions that may cause signs of abdominal pain in a pregnant mare include
OTHER CONDITIONS
pending prepubic tendon or other abdominal wall ruptures 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 secondary to trauma or to a uterine torsion, placental hydrops, or twin pregnancy. In the event of uterine rupture the mare typically shows signs of colic just prior to the rupture itself. Once the uterus ruptures there is typically 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 discomfort and pain to the mare. The signs associated with the uterine contractions that are normally occurring at this time range from mild discomfort (occasional kicking 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, frequently getting up and down, rolling, etc.). The majority 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 stimulated by the foal's initial nursing. More extreme demonstrations 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 negligent 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
17
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 contained within these structures. Pain results from the stretching of, and pulling on, these structures as the hematoma forms. Formation of this clot and the associated 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 rupture 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 susceptible vessels. One theory as to why this occurs is that
357
OTHER CONDITIONS
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 therapeutic course chosen the single most important measure that must be taken is to keep the mare as quiet as possible so as to cause no increases in her mean arterial pressure (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 used judiciously 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 cardiac 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 careful 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 maintained, 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 transfusion of affected mares is not advocated by many until the mare's pev is less than 20 per cent. A further significant 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
17
over whole blood transfusion as they are non-reactive in terms of blood compatibility, and high volume expansion 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 perfusion 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 oxygen (if tolerated well by the mare) and applying external 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 (vitamin 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 delivery to ischemic tissues, and therefore may be of benefit. Finally, careful use of broad spectrum antibiotics ('careful 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 damage 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 ofuterine artery rupture have a high likelihood of recurrence with subsequent pregnancies and foalings. It is therefore 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 transportation, 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 foaling 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 compromise from mesenteric tears, and even rupture and extravasation of fecal material into the peritoneum. Where small colon bruising has occurred mares experience compromised function and may present as constipated 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 compromised bowel may become leaky and peritonitis may result. Diagnosis is made via rectal examination with the identification of impacted small colon or a sausageshaped 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 peritonitis 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' contaminated visceral surfaces or abdominocentesis reflecting 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 distention 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 normally postpartum swollen and inflamed perineal tissues may experience a reluctance to defecate and secondary constipation. Anti-inflammatory drugs (phenylbutazone 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-foaling. The combination of the sudden increase in available 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 present as a violently painful colic with a very high heart rate (60-100 bpm) whereas a simple colonic displacement 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 peritonitis 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 peritoneal antimicrobials, crystalloids, colloids, 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 lowdose 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
rience, invagination of a uterine horn has most commonly occurred in conjunction with a retained placen 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 predisposing 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 uterine 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 ionized calcium levels at presentation. Correction of low calcium levels to normal may also help restore normal uterine tone.
17
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 horses.] Am. Vet. Med. Assoc. 182:229-31. Messer N T (1987) Distention colic. In Current Therapy in Equine Medicine 2nd edn, N E Robinson (ed.). W B Saunders, Philadelphia, pp. 68-70. RobertsonJ T (1990) Diseases of the stomach. In The Equine Acute Abdomen, N A White (ed.). Lea and Febiger, Philadelphia, pp. 338-46. Whi te N A (1990) Diseases of the caecum. In The Equine Acute Abdomen, N A White (ed.). Lea and Febiger, Philadelphia, pp.369-74.
Uroperitoneum Beck C, DartAJ, McClintock S A and Hodgson D R (1996) Traumatic rupture of the urinary bladder in a horse. Aust. Vet.] 73:154-5. Gibson K T, Trotter G Wand Gustafson S B (1992) Conservative management ofuroperitoneum in a gelding. ] Am. Vet. Med. Assoc. 200:1692-94. Jones P A, Sertich P S andJohnstonJ K (1996) Uroperitoneum associated with ruptured urinary bladder in a postpartum mare. Aust. Vet.] 74:354-8.
Fetal hydrops Frazer G S, Embertson R and Perkins N R (1997) Complications of late gestation in the mare. Equine Vet. Educ. 9:306--11. Van de Plassche M (1987) Prepartum complications and dystocia. In Current Therapy in Equine Medicine 2nd edn., N.E. Robinson (ed.). W.B. Saunders, Philadelphia, pp.537-40. Van de Plassche M, Bouters R, Spincemaille J 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 the mare. Vet. Clin. N. Am. Equine Pract. 10:643-70.
Cushing's disease 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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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. 133:594-7. Love S (1993) Equine Cushing's disease. Br. Vet.].
OTHER CONDITIONS
Pancreatic diseases Argenzio R A (1990) Physiology of digestive, secretory and absorptive processes. In: TheEquineAcuteAbdomen. N A White (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. Equine Pract. 3:8-15. Mair T S, Freestone], Hillyer M H, Love S and Watson E D (1995) The pancreas. In The Equine Manual, A] Higgins and I M Wright (eds). W.B. Saunders, London, pp.560-63. McClure JJ (1987) Acute pancreatitis. In: Current Therapy in EquineMedicine2nd edn, N E Robinson (ed.). W.B. Saunders, Philadelphia, pp. 46-7. Parry B Wand Crisman M V (1991) Serum and peritoneal fluid amylase and lipase reference values in horses. Equine va.]. 23:390-1. Ross M W, Lowe] E, Cooper B], Reimers T] and Froscher B A (1983) Hypoglycemic seizures in a Shetland pony. Cornell Vet. 73:151-69.
Reproductive-associated causes of colic in the brood mare Asbury A C (1993) Care of the mare after foaling. In: Equine Reproduction, A 0 McKinnon and] L Voss (eds). Lea and Febiger, Philadelphia, pp. 976-80. Ball B A 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. Saunders, Philadelphia, pp. 531-3. Blanchard T L, Varner D D and Schumacher] (1998) Manual ofEquine Reproduction. Mosby, St Louis. Bosu W T K and Smith C A. Ovarian abnormalities. In: Equine Reproduction. A 0 McKinnon and] L Voss (eds). Lea and Febiger, Philadelphia, pp. 397-403. Britt B and Byars T D (1997) Hagyard-Davidson-McGee Formulary. In: Proceedings from theAnnual Conventionof the AmericanAssociation ofEquine Practitioners. AAEP, Lexington, KY, pp. 170-7. Frazer G S (1998) Periparturient problems and dystocia. In: Proceedings from the Bluegrass Equine Reproductive 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
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breeding. In: Equine Internal 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: CurrentTherapy in LargeAnimal Theriogenology, R SYoungquist (ed.). W.B. Saunders, Philadelphia, pp. 157-60. 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 FoalHighlighting Nutritional Management and Developmental Orthopedic Disease Seminar, March 13-14, Hilltop Farm. Plumb D C (1995) Veterinary Drug Handbook 2nd 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. Saunders, Philadelphia, pp. 541-6. Sherman D M and Lafarenko V A (1998) The mechanism of the action of opiate receptor antagonists in acute shockinduced blood loss. Eksp. Klin. Farnakol. 61(1):25-9. Sprayberry K A (1999) Hemorrhage and hemorrhagic shock. In: Proceedings from the Bluegrass 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. Saunders, Philadelphia, pp. 730-50. Vaala W E (1999) Periparturient problems in mares. In: Proceedings from the Comprehensive Preventative Medicinefor the Mare and FoalHighlighting Nutritional Management and Developmental Orthopedic Disease Seminar, March 13-14, Hilltop Farm. van de Plassche M (1987) Prepartum complications and dystocia. In: CurrentTherapy 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, Philadelphia, pp. 456-60. Vivrette S (1997) Parturition and postpartum complications. In: CurrentTherapy 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 T Mair
Differential diagnosis and evaluation of chronic weight loss INTRODUCTION The maintenance of a normal and constant body weight is a balance between input and output (Figure 18.1). /I Nutrients IN
�
Nutrients OUT
�
Feces,
urine, sweat
HORSE �
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.
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 difficult. 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 affairs. 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 first 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 fits into.
DEFINITION OF CHRONIC WEIGHT LOSS Weight loss is a common problem that can affect horses of all ages; there are numerous potential causes. However, there is no precise definition 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.
ASSESSMENT OF BODY CONDITION 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 5-6 for reproduction.
POTENTIAL CAUSES OF CHRONIC WEIGHT LOSS Chronic weight loss may occur in the following situa tions • • • • •
•
Body condition score
Definition
Extreme emaciation. No fatty tissue. Wasted muscles especially noticeable over bones. Flat shelf over transverse processes
2
Emaciation. Slight fat cover. Prominent bones. Wasted muscles
3
Thin. Fat covers transverse processes and half-way up spinous processes. Tailhead prominent but individual vertebrae not seen. Ribs seen sharply
4
Moderate ly thin. Slight back ridge. Ribs barely discernable
5
Moderate. Back is flat (no crease or ridge). Ribs easily felt but not seen
6
Modera tely fleshy. Fat feels spongy over ribs and around tailhead. Back crease slight or absent
7
Fleshy. Back crease definite. Ribs covered but individual ribs can be palpated. Fat is palpable in neck and rump
8
Fat. Back creased. Neck thick. Fat along withers, behind shoulders and inside thighs
9
Too fat. Back crease is deep. Fat bulging on neck, along withers, behind shoulders, around tailhead and inside thighs
368
•
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.
ASSESSMENT OF ENVIRONMENTAL AND MANAGEMENTAL FACTORS 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 • • • • • •
insufficient food insufficient grass the wrong sort of food insufficient water excessive work irregular severe work in an unfit 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
CHRONIC WEIGHT LOSS
1. 2. 3. 4.
Is enough food being offered? Is the food of adequate quality? Is the horse allowed to eat? 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.
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).
ASSESSMENT OF WEIGHT LOSS ASSOCIATED WITH DISEASE 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 specific disease or a diseased body system is identified. Routine hematological, serum biochemi cal, and parasitological profiles 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.
CLINICAL PATHOLOGY 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
18
•
•
•
•
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
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.
• • • • • •
Further laboratory tests of liver disease and liver function include • • • •
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 (AP) glutamate dehydrogenase (GLDH) iditol dehydrogenase ( IDH) arginase (ARG).
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 identifying 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).
CAUSES OF CHRONIC WEIGHT LOSS 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
CHRONIC WEIGHT LOSS
5. chronic liver disease 6. chronic kidney disease 7. chronic low-grade infection 8. neoplasia 9. chronic heart disease 10. 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 quidding of food or painful mastication (see Chapters 5 and 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) pharyngeal and palatal cysts (see Chapter 5) epiglottal lesions (see Chapter 5)
• • • •
•
18
4th branchial arch defects (see Chapter 5) megaesophagus (see Chapters 5 and 7) esophageal obstruction (see Chapters 5 and 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 2 1) neoplastic bowel infiltrates (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 observed 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 fiber, is lost via the feces. 371
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CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
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 deficiencies have not been described in adult horses. However, maldigestion probably occurs in conjunction with diseases that affect 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 20 and 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.
Small intestinal maldigestion and malabsorption 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 often 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 inflammatory bowel disease, resulting in a normal total protein level and decreased albumin:globulin ratio. Serum protein elec372
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. An elevation of predomi nantly the beta-globulin fraction may be suggestive of significant parasitic larval 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 infiltrative 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 infiltrates. 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 definitive proof or diagnose the underlying cause. Rectal biopsy may be helpful if the inflammatory or neoplastic infiltrate 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 defin 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.
Large intestinal maldigestion and malabsorption Inflammatory and neoplastic infiltrates may affect the large intestine as well as the small intestine. Severe infil 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. Larval cyathostomosis is typically associated with a severe protein-losing enteropathy and sudden onset diarrhea in young adult horses during the
CHRONIC WEIGHT LOSS
winter time (see Chapter 21). However, in a small num ber of cases larval 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 larval 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 N SAID toxicity) (see Chapters 12, 20, and 21) 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-specific 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.
18
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. IdentifYing the precise cause of chronic renal failure may be very difficult 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. An increase in the concentrations of nitrogenous wastes in the blood has a central appetite-suppressant effect. 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 identifYing persistent isosthenuria (urine specific gravity 1.008-1.01 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
18 • • • •
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
hypochloremia hypercalcemia hypophosphatemia metabolic acidosis or alkalosis.
Diagnostic ultrasonography and renal biopsy can provide additional information.
Weight loss may also occur in association with neo plastic disease as a result of • •
• •
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 ( E IA) 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 fibrinogen 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. Specific 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
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. 2. 3. 4.
generalized/multicentric lymphosarcoma alimentary/intestinal lymphosarcoma mediastinal/thoracic lymphosarcoma 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
CHRONIC WEIGHT LOSS
weight loss exercise intolerance • ventral thoracic and pectoral edema • tachypnea • respiratory distress • bilateral firm 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).
18
• •
Liver Lymphosarcoma Hepatocellular carcinoma Biliary carcinomal cholangiocellular carcinoma Hemangiosarcoma Adrenal gland Pheochromocytoma Stomach Squamous cell carcinoma Gastric polyp Leiomyoma and leiomyosarcoma Gastric adenocarcinoma Small intestine Lymphosarcoma Leiomyoma and leiomyosarcoma Adenocarcinoma Lipoma Cecum, large and small colons Lymphosarcoma
Thoracic neoplasia Primary lung tumors 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 tumors Thymoma Lymphosarcoma Metastatic and secondary thoracic neoplasia Hemangiosarcoma Squamous cell carcinoma Adenocarcinoma Renal carcinoma Rhabdomyosarcoma Malignant melanoma Fibrosarcoma Hepatoblastoma Chond rosarcoma
Adenocarcinoma Intestinal myxosarcoma Lipoma and lipomatosis Rectum Lipoma Lymphosarcoma Polyps Leiomyosarcoma Melanoma Peritoneum Disseminated leiomyosarcomatosis Omental fibrosarcoma Mesothelioma Kidney Renal cell carcinoma Adenoma Transitional cell carcinoma Embryoma Squamous cell carcinoma Ovary Cystadenoma Teratoma Dysgerminoma Granulosa cell tumor
Neuroendocrine tumor Lymphosarcoma Undifferentiated sarcoma and carcinoma Abdominal neoplasia Pancreas Pancreatic adenoma and adenocarcinoma Spleen Lymphosarcoma Melanoma Hemangiosarcoma
Chronic heart disease Heart failure may result in weight loss due to ineffi 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
18
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
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 fibrosis 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.
NEUROLOGICAL AND NEUROMUSCULAR DISEASE a
�_���_lMiiWiI';'J!.
_""�
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 _I
WIiIUIlllliA
11._001IIS
[
INTRODUCTION
Figure 18.2 Marked asymmetric gluteal atrophy in a horse affected by polyneuritis equi 376
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 confined 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 ondary 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 infiltrative 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,
CHRONIC WEIGHT LOSS
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 significant protein-losing enteropathy is likely to cause severe and rapid weight loss.
18
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 70 per 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
CAUSES OF MALABSORPTION SYNDROME The common causes of malabsorption syndrome in the adult horse are listed in Table 18.3.
Table 18,3 �01N!'1OAQUSU of malablorpiton syndrome in tI'/f.•ultholM 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 Insufficient 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
Chronic inflammatory bowel disease ( C I BD) is the col lective term for the group of infiltrative bowel diseases that produce similar clinical signs to one another (pri marily chronic weight loss). These diseases are not as well defined 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 infiltrate may consist of a mixed cellular population or there may be a predomi nance of specific cell types such that CIBD may be classified 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 infiltration 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 identified 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 identified 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 infiltrates may take the form of 377
18
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
diffuse inflammatory cell infiltration of the small intesti nal mucosa with eosinophils and lymphocytes, or an eosinophilic granulomatous infiltrate. 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 infiltrate 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 infiltration by lymphocytes and plasma cells in the absence of granulomatous change.
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
Alimentary lymphosarcoma
•
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 infiltrated by malig nant cells. Villous atrophy is commonly present in asso ciation with small intestinal infiltrates. 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 5 years old. Enteric infections Mycobacterial granulomatous enterocolitis is rare, and is usually associated with avian strains of Mycobacterium tuberculosis or M. intracellulare. There are also rare reports of enteric fungal infections due to Aspergillus fumigatus or Histoplasma capsulatum. It has been sug gested that fungal infections may be most likely in horses undergoing chronic antibiotic or corticosteroid treatments.
CLINICAL SIGNS The clinical signs associated with chronic infiltrative small intestinal diseases are generally similar regardless 378
• • •
• • • •
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).
DIAGNOSIS 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 findings are non-specific, but may include • • • • • • •
•
• •
hypoalbuminemia hyperglobulinemia or hypoglobulinemia neutrophilia (occasionally neutropenia) anemia hyperfibrinogenemia 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 confirmed 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
CHRONIC WEIGHT LOSS
be observed in horses with eosinophilic infiltrative disease,
18
mid- and distal small intestine, Biopsies should also be obtained from the ceCUlIl and large colon at the same
Rectal biopsy may yield a histopathological diag
time. Biopsies of mesemeric lymph nodes often reveal
nosis in a small proportion of cases, but only if the
similar pathological change to small illlcstinal infil
inf-iltrative lesion extends back to this level of the
trates, and at least one lymph node should be biopsied
intestinal tract.
at the same time as the bowel wal! biopsies are taken,
A diagnosis of small intestinal malabsorption is
Bowel wall and lymph node: biopsies can also be suc
made using- a carbohydrate absorption test such as the
cessfully obtained via a flank laparotomy that can be
oral glucose absorption test or the D (+ )-xylose absorp
performed in the standing horse utilizing local anesthe
tion !est (see Chapter 2). The oral glucose absorption
sia. This approach greatly reduces the complications
test is more commonly employed because of the ease of
associated
analyzing plasma glucose levels. Horses can be divided
Alternatively, mesenteric lymph node biopsies may he
with
ventral
midline
wound
healing.
into three groups on the basis of the results of the oral
taken �ia laparoscopic techniques in
glucose absorption test
patient, thereby eliminating the necessity for general
�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
the standing
anesthesia and significantly reducing the risk of wound complications. However, the sensitivity of this approach for the diagnosis of small intestinal infiltrative disease has not yet been assessed.
shu\\'S 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 defined hy the mean
:t
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 1 5 per cent increase over the resting level.
:-I. Total malabsorption - the glucose levels at 50 and 120 minutes are below the normal range as defined 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.
TREATMENT The prognosis for horses affected 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 diffuse ali mentary lymphosarcoma have a hopeless prognosis and should be humanely destroyed, although chemother apy may prolong survival for 6-1 2 months. Treatment of fimg'
systemic antifungals is
usually unrewarding. Some horses with CIBD !nay henefit from heing fed highly digestible feeds. Provision of a palatable, easily
I Iorses with ' total malahsorption' are likely to have a
assimilated high energy and protein source is indicated.
diffuse infiltrative small intestinal disease. Horses with
Supplementing the diet with electrolytes, minerals, and
'normal absorption' are likely to have a histologicalIy
vitamins is also useful. Feeds with high quality fiber con
normal small intestine. Horses with a 'partial malab
tent may also contribute to body weight g'
sorption' re.�ult may have evidence of an inflammatory
may be more extensively converted from cellulose to
infiltrate or villous atrophy, hut they may also have
volatile free fatty acids in the cecum; this type of diet is
histologically normal intestine, and further diagnostic
especially beneficial tn horses affected by CIBD without
tesl.� should be carried out.
diarrhea. Feeding more fh�quent meals in smaller
Confirmation of r.he diagnosis of infiltrative small
amounts may also aid in better digestion and absorp
intestinal diseases and villous atroph} is made by histo
tion. l<:nteral feeding through an indwelling nasogastric
logical examination of sections of slllall intestin(\ Full
tube is rarely indicated in view of the poor long-term
thickness bowel \,;al1
hiopsies may be obtained at
prognosis. There i.� no justification in tf)ing to sustain a
laparotomy for thi.� purpose, although
severely debilitated horse when the progllosis is so poor.
exploratory
horses with malabsorption state.� are often not good
Corticosteroid therapy is often ineffective in treating
(·andidates for m'ljor exploratory surgery, and vmund
CIBD, although some cases of eosinophilic infiltrates
complicatiolls arc common in the postoperative period
and lymphocytic-plasmacytic enterocolitis appear to be
because of hypoproteinemia and the (�atabolic state. If
responsive to corticosteroids. Parenterally administered
surge!)' is to be performed, biopsies should be taken
dexamethasone is likely to he more effective than oral
from any grossly abnormal section of bowel, but. if the
corticoMeroids, and prolonged courses are required.
bowel appears grossly normal then at least three small
Surgical resection of limited areas of affected bowel
intestinal biopsies should be taken from the proximal,
may produce some short term benefiL�, but the diffuse
379
18
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
nature of the lesions usually precludes this therapeutic option.
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 4:45 1-73.
BIBLIOGRAPHY
Taylor F G R ( 1 997) Chronic wasting. In Diagnostic Techniques
in Equine Medicine, F G R Taylor and M H Hilyer (eds) . W B Saunders., London, 65-70.
Differential diagnosis and evaluation of chronic weight loss
Malabsorption syndromes
Brown C M ( 1 989) Chronic weight loss. In Problems in Equine
Cohen N D, Loy j K, Lay j C, Craig T M, McMullan W C
Medicine, C M Brown (ed. ) . Lea and Febiger, Philadelphia, pp. 6-22. Divers TJ, Mohammed H 0, CummingsJ F ( 1 998) Equine motor neuron disease. In Current Therapy in Equine Medicine, 4th edn, N E Robinson (ed. ) . W B Saunders, Philadelphia, pp. 321-2. East L M, Savage C J ( 1 998) Abdominal neoplasia (excluding urogenital tract) . Vet. Clin. N. Am. Equine Pract. 14: 475-93. ForemanJ H ( 1 998) Changes in body weight. In Equine Internal Medicine, S M Read and W M Bayly (eds ) . W B Saunders, Philadelphia, pp 1 35-9. Kronfeld D S ( 1993) Starvation and malnutrition of horses: recognition and treatment. ]. Equine Sci. 1 3: 298-304. Kronfeld D S ( 1 998) Clinical assessment of nutritional status of the horse. In Metabolic and Endocrine Problems of the Horse, T D G Wat�on (ed. ) . W.B. Saunders, London, 1 84-217. Mair T S, Hillyer M H ( 1 99 1 ) 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
( 1 992) Eosinophilic gastroenteritis with encapsulated nematodes in a horse. ]. Am. Vet. Med. Assoc. 200: 1 5 1 8-20. 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 Iyrnphocytic-plasmacytic enterocolitis: a retrospective study of 14 cases. Equine Vet. ]. MacAllister C G, Mosier D, Qualls C W, Cowell R L ( 1 990) Lymphocytic/plasmacytic enteritis in two horses. ]. Am.
Vet. Med. Assoc. 196: 1 995-8. Mair T S, Hillyer M H, Taylor F G R, Pearson GR ( 1 991 ) Small intestinal malabsorption i n the horse: an assessment of the specificity 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.
tetanus antitoxin 4-10 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 specific 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 • •
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
•
signs of central nervous 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 WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
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 hepatoencephalo 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 sufficiently 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 type 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 serve 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 observed in horses with acute liver failure. When 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 affect 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 findings 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.
HEPATIC AND B ILIARY TRACT DISEASES
Diagnosis The diagnosis is based on • • •
history clinical findings laboratory confirmation 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 flmol/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 J.lmol/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
19
plasma. Other laboratory findings that are frequently abnormal in Theiler's disease include • • • • •
moderate to severe acidosis hypokalemia polycythemia increased plasma aromatic amino acids hyperammonemia
A more definitive diagnosis of Theiler's disease can only be made by liver biopsy. If the history, clinical findings, and laboratory findings 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 difficult 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 often 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 specific 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 necessary 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 efficacy 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
CHRONIC WEIGHT 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 insufficient 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 treatments include dimethylsulfox ide, acetyicysteine and mannitol given intravenously and vitamin E given intramuscularly. Anti-inflammatory therapy should include flunixin meglumine and pentoxifylline. 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 first 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 fibrosis 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 moniliforme 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. Aspergillus 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 significant 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-
H E PATIC AND B ILIARY TRACT DISEASES
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 primary 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 findings identified 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-
19
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 specific 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 acidifying 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.
POST·MORTEM 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 specific 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
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
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.
horses. Other forms of true biliary disease appear to be very uncommon in horses, but biochemical evidence of hepatobiliary injury and dysfunction, including eleva tions in serum bilirubin, gamma glutamyl transferase (GGT) , alkaline phosphatase (AP), 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 infiltrative or obstructive neoplastic conditions, such as primary cholangiocarcinoma, hepatic adenocarcinoma, or metastatic hepatic tumors.
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 significantly 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 findings were not specific but included plasmacytic/lymphocytic hepatitis as well as histologic changes in the central nervous system consistent with hyperammonemia.
Biliary tract disease SF Peek
CHOLANGIOHEPATITIS Although this condition probably begins as a cholangi tis, the term cholangiohepatitis is appropriate because clinically significant 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 significant 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, significant periportal and bridging fibrosis can occur. Clinically significant 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 ) .
INTRODUCTION
Etiopathogenesis
Cholangiohepatitis is the most commonly encountered, clinically significant form of biliary tract disease in
The etiopathogenesis of cholangiohepatitis in adult horses is presumed to be ascending bacterial infection from the proximal small intestine. Evidence for this
386
HEPATIC AND BILIARY TRACT DISEASES
comes from retrospective studies documenting the iso laticm of predominantly gram-negative, enteric bacteria such as Escherichia coli, Enterobacter spp. and Citrobacter 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. Clinical signs and diagnosis 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 AP, 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 obs truction 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, specifically the prothrombin time and activated partial thromboplastin time, be made prior to hepatic biopsy. Frequently these indices are normal but they may be
19
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 1 4-gauge biopsy needle. Sufficient 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 i�ury, 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 fibrosis. 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 1 6th 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 significant hepatoliths should be evaluated ultrasonographically. It is not
Figure 19.1 Sonogram from a 14-year-old Thoroughbred mare with chola n giohepatitis and hepatolithiasis. Ultra sonographically there is an obvious dilated bile duct with an intraluminal 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 WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
possible to visualize bile ducts via ultrasound in the nor mal horse. However, significant 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 significant 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 specific 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 suggests 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 confirmed before treatment is stopped. Many horses will show substantial clinical improvement in terms of appetite, absence of fever, and weight gain while still demonstrating significant bio chemical evidence of hepatobiliary disease. It is recom mended that antibiotic treatment be continued until serum GGT and AP 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 identifiable 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 acidifying 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. Specific 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, specific 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 justifiable 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 reserved 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 benefit 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-
HEPATIC AND BILIARY TRACT DISEASES
biliary disease in horses. Cholangiocarcinoma is the commonest form of primary hepatic neopla�m 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 evidence of biliary tract disease is often absent, even
T.b1.1�1
. �ltidiM1I1k.1OickD''ita1nl",p'lnts
Botanical name Amsinckia intermedia
associated with space occupying lnasses that impede extrahepatic biliary flow through the right and left
Common groundsel
Senecio fideJli
Woolly groundsel or
180"
Senecio jacobaea
stinking Willie
nal disease in adult horses and foals. Foals with severe gastroduodenal ulcnation that progresses to signifICant the duodenal papilla may
haw elevations in [hese enzymes due to compromised hiliary outflow. Furthermore, horses with colonic dis
Tansy or common ragwort. ragwort, or
rotations of the large colon) and proximal small intesti
10
,
Ridell's groundsel
Occasiona!!y elevations in GGT, AP, and bilirubin
stricture fOrmation close
Fid dleneck fireweed,
Senecio vulga ris
hepatic ducts and the common bile duel. arc .�een in association with colonic (espedaUy
Common name
or t a rweed
with significant parenchymal infiltration, unless there is obstruction to biliary drainage. This is most commonly
19
Crota/aria spp.
Rattle box
Heliotropium europaeum
Common heliotrope or potato weed
placement or torsion may have elevations in the hepatobiliary enzymes probably because of abnormal
Cynog/ossum officinale
Hounds tongue
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.
Horses generally present with depression, anorexia, and weight loss for variable periods of time. Horses with areas of unpigmented skin may develop photosensitiv
Pyrrolizidine alkaloid intoxication
ity. Thc clinical course may vary from several days to several months but when sufficient 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
GP Carlson
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
INTRODUCTION
eaten. Since all horses with access to a contaminated feed sourn� are at risk, a history of other animals with
PyrroliLidine alkaloid intoxication is the most common
progressive depression, weight loss, icterus, anrl death
came of chronic liver failure in horses in the western
should alert the clinician to a possible common cause.
C nited States and toxicity has been recogni7.ed in many ("()untries around the world. Pyrrolb:irline alkaloid-<:on taining toxic plants (Table
19.1) tend 10 be unpalatable
ETIOLOGY
and are generally ",'oided by horses. Poor pasture con ditions or over grazing may contribute to consumptioll
Pyrrolilidinc alkaloid toxicity is largely determined by
of these plants, however intoxication is more likely to
the total dose of the pyrrolizidine alkaloid ingested.
occur
the feeding of contaminated hay.
Toxi{: cffecL� are cumulative and tend to be progressive;
Pelleted or (:ubed hay may pose a particular risk since
thus, ingestion of relatively small quantities over a long
folIo"l'oing
t.he presence of poison()LL� planL� can not be seen. For
periorl of time may produce similar effects to those
some plants, such as Amsinckia intermedia, toxic alkaloids
ohsel\led folIov.'ing ingestion of larger quantities for a
are concentrated in the seeds that may be found in
shorter time period. Pyrrolizidine alkaloids are proxi
srret'nings of grain harvested from contaminated fields.
mate toxins which are metabolized in the liver to highly
Such screenings are highly toxic and feeding relatively
reactive, unstable metabolites (the dehydroalhloids)
modest amounts can lead to massive liver damage and
which are potent alkylating agents. These compounds
functional failure within days.
arc responsible for much of the direct hepatocellular 389
19
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
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 failure 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 confirmed 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 AP 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 confirmation of the diagnosis. The liver is often small and firm 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 fibrous 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 specific 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,
H E PATIC AND B ILIARY TRACT DISEASES
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-
19
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 AP, 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 fibrosis 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
19
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
Indicators of compromised livt�r function such as bile
TREATMENT
acids, total and direct bilirubin, BU:-I, blood ammonia. intensive supportive care is indicated until horses regain their appetite. A fairly consistent favorable response to corticosteroids can he anticipated. Initial !Tf"atlllcnt 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 4-6 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,
blood glucose, and the ratio of plasma branched chain to aromatic amino acids may only be abnomJ
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
as
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 pn�parations 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
Chronic liver disease
these techniques. The most useful diagnostic tool in the animal manifesting clinical and biochemical evidence
GP Carlson
ofliver failure is the liver biopsy. It is possible with ultra sound-guided liver biopsy to obtain tissue samples from
Horses with chronic: liver disease may present with a his
areas with focal liver lesions. However, most horses with
tory of clnonic progressively developing clinical signs or
chronic liver failurt have ilwolvement of over 80 per
they may pn�st'nt with recently recognized and fi.!lmi
cent of the liver and liver biop�ies generally provide
\lant clinical signs at the end stage of function
representative samples for histological evaluation.
Several of the more .�pecific and common causes for
The liver has a great capacity for regeneration and
chronic liver failure have been discussed in other sec
repair following injury. Chronic liver failure generally
tions {pyrro!izidine alkaloid !oxicosi�, chrnnic active
result� from processes in which there has been damage
hepatitis, biliary (ract disease, and hyperlipemia). This
to hepatocytes, hepatocyte loss, inflammation, and pro
St'rliOll will address chronic liver failure of undeter
gressive replacement of hepatic parenchyma by fibrosis.
mined cause as well as some of the less common causes
Potential causes or factors that may contribute to the
of liver disease such as hepatic neoplasia.
development of chronic liver failure include
CHRONIC LIVER FAILURE OF UNDETERMINED CAUSE
fOr these cases may essentially be the same a� described pyrrolizidine
allwloid
recurrent bacterial or viral infections
•
immunological reactions
•
parasitism
•
The history, clinical signs, and dinical patholob'Y data for horses with
•
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
exposure to toxic chemicals or pharmaceutical agenL�
•
poisonous plants
•
mycotoxins
•
chronic hypoxia
•
dietary imbalances
•
iron overload
•
trauma
•
amyloidosis.
indications of liver damage such as serum enzyme
In many instances at the end stage of liver failure it is
auivities (SDH, AST,
not po.�sible to determine the specific cause or causes of
elevated if the process of hepatocyte destruction is no
the liver injury and subsequent fibrosis, a� over time
longer \'('1)' active, while GGT and AP tend to be elevated
many factors may have contributed to progressive
in disease processes that involve the biliary system.
damage and loss of function.
392
H E PATIC AND B ILIARY TRACT DISEASES
KLEIN GRASS
(PAN/CUM COLORA 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 fibrosis, 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 affected horses from the pasture and supportive care treatments result in complete recovery of most cases. 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,
19
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 two 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 infiltrate, 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
19
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
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 fibrosis, 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 confirmed 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 finding 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 fiber diets may contribute to this condition.
Hyperlipemia T Mair
INTRODUCTION Hyperlipemia is a disorder of lipid metabolism charac terized by hypertriglyceridemia and fatty infiltration 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 identified 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 identified in asso-
H E PATIC AND B ILIARY TRACT DISEASES
19
Intestinal parasitism Colitis Colonic impaction Gastric i mpaction Dysphagia and dental disorders Esophageal obstruction Esophageal ulceration Lymphosarcoma. Hyperadrenocorticism (Cushing's disease) Peritonitis Metritis Laminitis
Figure 1 9.2 Schematic representation of the metabolic fate of non-esterified fatty acids mobilized from adipose tissue (NEFA non-esterified fatty acids; TG triglycerides; VLDL very low density l i poproteins; LPL lipoprotein lipase) (adapted from Watson 1 998) =
=
=
=
Renal failure Liver disease 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 1 9 . 2 ) in response to stress or failure to maintain energy homeostasis. In response to negative energy balance and after depletion of glycogen reserves, non-esterified fatty acid (NEFAs )
are mobilized from fat stores and released into the cir culation (Figure 1 9.2). The majority of NEFAs are taken up by the liver where they may overwhelm the oxidative, gluconeogenic, and ketogenic pathways and are esteri fied 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 infiltration of many organs . Adipose tissues represent energy stores that form as a result of esterification of free fatty acids to produce triglyceride. This esterification 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 NEFAs are taken up by the liver where they can be used for ketogenesis or gluconeogenesis, or they are 395
19
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER D ISEASE
Adipose tissue
Plasma N E FA transport to the liver Normal ponies 8.2 ± S.2 mmol/h Hyperlipemic ponies 148.2 8.4 mmollh
Normal ponies 6.6 ± 4.4 mmol/h Hyperlipemic ponies 1 90.6 3.9 mmollh
esterified to form triglycerides. The horse has a poor capacity 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 activity 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 obesity and pregnancy/lactation. 396
Figure 1 9.3 Schematic representation of non-esterified fatty acid (N EFA) and very low density lipoprotein (VLDL) metabolism in ponies with hyper lipemia. Kinetic data are shown for NEFA transport to the liver, hepatic VLDL-triglyceride (TG) synthesis, and VLDL-triglyceride fractional catabolic rate in normal and hyperlipemic ponies (adapted from Watson 1 998)
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, fatty infiltra 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 observed 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 infiltration 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
H E PATIC AND BILIARY TRACT DISEASES
Anorexia Lethargy Weakness Ataxia Muscle fasciculations Dysphagia Sham drinking Profound depression Head pressing Circling Recumbency Seizures Nystagmus Weight IOS5 Ventral edema Ascites Abdominal pain Reduced intestinal motility and fecal output Pyrexia Tachycardia Tachypnea Congested mucous membranes Icterus Halitosis Abortion Sudden death
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 classified 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. Identification of fatty infiltration of liver biopsies is diagnostic but has no advantage over simple measurements of plasma triglycerides. Clinical chemistry Monitoring of serum or plasma biochemistry panels can help to •
• •
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 interval 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-
19
•
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 deficit of 0-24 mEq/1. 397
19
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
IIocIWtlNstry IMnt' for Invtltigltinv
T__ ".4
and monltDrlng hyptrilpemli In liqUids (from
fissured, or there may be capsular rupture and associ ated hemorrhage. Fatty infiltration of other organs including adrenals, skeletal muscle, and myocardium
WttiQn 1_
may be evident. Necrotizing pancreatitis is present in some cases (see Chapter
Metabolic status
17).
Vascular thrombosis can
occur secondary to hyperlipemia and fat embolism, and
•
triglycerides
•
glucose
•
hydration status - albumin
•
electrolytes -
can result in focal hemorrhages, myocardial infarction, and renal infarction.
PCV No· K·
TREATMENT
". Ca2• •
The treatment of hyperlipemia has nve different objec
add-base status - pH
tives
HCO)-
peol
1 . treatment of underlying or concurrent disease 2. correction of dehydration, electrolyte and
Liver damage and function •
gamma glutamyl transferase
•
alkaline phosphatase
•
bile acids
•
ammonia
acid/ba�e imbalances
(GGn
3. symptomatic therapies
(AP)
4. nutritional support 5. normalization of lipid metabolism
Treatment of underlying or concurrent disease
Rena! function •
ammonia
•
urea nitrogen
•
creatinine
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
Fan)' inlHtration of the liver result..'; in elevations of liver·derived emymes, including GGT, AP, LDH, and SDH. Liver funelion may be impaired, as asscs.�ed by elevations of bilirubin, hile acids, and ammonia. Fatty infiltration of the kidneys can result in impaired renal li.mction, and elevation of plasma concentrations of urea and creatinine. These metabolites may also he
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
increased as a result of dehydration, and reassessment
Correction of dehydration, electrolyte and acid-base
following rehydration is required to a')sess the degree of
abnormalities is essential. Intravenous fluid and c1ectf(}
renal failure.
lyte therapy is generally required, the principles of
P!a.�ma albumin concentrations may be normal, or
which are discussed in Chapter 9. Correction of severe
e1evat.ed (associated with dehydration), or reduced
acidosis in the presence of liver failure may require the
(associated
administration of intravenous bicarbonate. Blood gas
with
chronic
hepatopathy,
a
primary
gastrointestinal lesion, or parasitism). Serum protein
analysis should be used when available to monitor the
electrophoresis can he helpful in as.'iessing underlying
response to bicarhonate therapy, since too rapid an
conditions such as intestinal parasitism.
increase in blood pH may exacerbate signs of hepatic encephalopathy, and overdosing of bicarbonate can lead to persistent metabolic alkalosis and respiratory
PATHOLOGY
depression.
T}pica! pathological findings in ponies and donkeys
polyionic fluids or
Dextrose should be am'eled hy hyperlipemia include fatty infiltration of the
added
to
the
5%
intravenous
dextrose solu
tions in animals with hypoglycemia. ""hen
5% dextrose
19.3). The
solutions are being administered, monitoring of serum
liver and kidneys are enlarged, yellow, friable, and
electrolytes should be undertaken, and potassium chlo
greasy. In severe cases, the surface of the liver may be
ride or calcium g!uconate administered as necessa!)'.
tissues, espedaJIy the liver and kidneys (Plate
398
HEPATIC AND BILIARY TRACT DISEASES
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, endotoxemia, 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, leafy 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
Water (I)
Day 1
2
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 1 9 .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 • •
75% of basal DE requirement 1 00% of basal DE requirement
day 1 day 2
3
4
5
6
7
8
8
8
8
8
8
8
Dextrose (g)
1 20
1 60
200
240
320
320
360
Casein or dehydrated cottage cheese (g)
1 20
1 20
1 80
240
240
300
360
Dehydrated lucerne meal (g)
600
600
600
700
700
800
800
80
80
80
80
80
80
80
Electrolyte and vitamin mixture (9)
19
399
19
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
•
day 3
•
day 4 and subsequent days
75% of 'stress-adjusted' DE requirement 1 00% of 'stress-acljusted' DE requirement.
This procedure of increasing the plane of nutrition allows the gastrointestinal tract to become tolerant to the regime. In affected 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 cases. 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 modifying 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 activity 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-ester ification of NEFAs. The efficacy 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 patients 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 its 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 patients, 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 3-10 days. Early diagno sis and prompt initiation of therapy result in the best chances for survival.
19
HEPATIC AND BILIARY TRACT DISEASES
PREVENTION :.;:.:: = :.:..:. :.:.:.. .:.; _ - --"
..__
..
(1994) DMSO as a direct so!uhilizer of
_.
-
,.
Risk factors for hyperlipemia in susceptible classes of equids include
Cholelithiasis in horses: Ten cases (1982-1986) J. Am. V�l. AI�d. A.I.mr. 194:40;;-9.
obesity
•
stress
•
malnutrition
•
pregnancy and lac tation
•
parasitism
f:quinF Prado 2:105-1 14.
Am.
R"dV B,Johnston] K, Divers T.l, Acland H (1990)
Cltrasonographic filldings in horses with cholelithiasis:
Eight (as("s (1985-191l7) .f. Am. litl. Med. Assoc.
196: IH36-1 I.
Schneider [) A (l!N7) Choiestasis and biliary calculi in
Avoiding these factors will therefore help in prevent ing this disea�e. Particular emphasis should be placed providing
Johnston J K, Divers T.l, Reef V B, Acland H (191l9)
Ram...,,,,,, t\ W (1990) J)i'ea.'''.' of the li\""... F�I. �in. N.
•
on
bilirubinate stones. Hrj>fJlog",lrlJlml l'Tnl"f;J' 41 ( I ) :65-9.
adequate
nutrition
to
susceptible
animals without allowing them to become obese, and providing good routine parasite con trol measures. Food intake and general demeanor should be care fully monitored following periods of enforced s tress such as disease, transportation, inclement weather, change of environment, etc. Exercise regimes may be helpful in reducing insulin in sensitivi ty. Plasma triglyc eride levels may abo be measured at times of stress and during pregnancy and lactation. The early identi fication and treatment of hyperiipt'mia is far more like ly to result in recovery than identification laler in the course of the disease.
horse<. (;omj" Coni. Fdllf P,.,ul. V�t. 19(fi):744-il3.
Pyrrolizidine alkaloid intoxication, Chronic active hepatitis, Chronic liver disease Barton M H, :\1orris, D D (199il) Diseases ofth" l.iver. In
F.quinli Intl'17!{1[ A1�dirinf, S M R"ed and W M gayly (cds).
W B Saund"rs, l'hila(klphia, PI" 707-3H.
Carlson (; P ( 1 992) Icterus in the Horse. In lielmllal)
G(l.\lromlat>/o,;y (2nd "dn), :\ V Anderson, (cd.). Lea & Febigcr: Philadelphia, pp. fiHH-702.
Cornick] L, Carln G K, Bridges C H ( 1 9RR) Kkin gra," ,. a"ociated hepatotoxicosis in horst'S. j. /"m. \·'�I. M�d. A'.loc.
193:932-5.
]akov.-;ki R M (1994) Right l"'pati(" lobe mrophy ill hor�es: 17 cases ( 1 9R:'.-1993)
J Am.
1',1. l\1ni. A.\.Wf. 204,]()?i7-6 1 .
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
( 1 9Hfi) ClinicopaThologic study of horses slIn'iving
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19
CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
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402
Endocrine Problems of the Horse, T Watson (ed. ) . W B
Saunders, London pp 23-40. Watson T D G, Love S ( 1994) Equine hyperlipaemia. Compo Cont. Educ. Pract. Vet. 1 6:89-97. Watson T D G, Murphy D, Love S ( 1 992) Equine hyperlipaemia in the United Kingdom. Clinical features and blood biochemistry of 1 8 cases. Vet. Rec. 1 3 1 : 48-5 1 .
Wensing T H , Schotman Aj, Kronemanj ( 1974) Effect of treatment with glucose, galactose, and insulin in
hyperlipemia in ponies. Tijdschr. Dierfeneesk 99:919.
20
Acute diarrhea
General principles of treatment of acute diarrhea in adult horses _"l1'"& , ____________________
TJ Divers
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 influ ences (dehydration). Fluid replacement should include •
The most important treatment for horses with severe diarrhea is to give intravenous fluids to correct extracel lular fluid deficits (especially intravascular volume deficits) , 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. Although 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.
volume replacement (per cent dehydration x 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 of albu min and decreased oncotic pressure in most horses with acute colitis, it becomes increasingly difficult 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 405
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 benefits 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 5-1 0 g of the sodium chloride.
ORAL REHYDRATION WITHOUT INTRAVENOUS FLUIDS 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.
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 (0.04-l.6 mg/kg p.o.) may be used in non-infectious diarrheal conditions. Its primary benefit could be an antisecretory effect. Phenoxyben zamine 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 of the clinical findings 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 benefit. 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 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. 406
TJ Divers ETIOPATHOLOGY Salmonella spp. are gram-negative bacteria that belong to the Enterobacteriaceae family. Salmonella spp. are
ACUTE DIARRHEA
divided into serogroups (A through I) based upon their common 0 antigens. All Salmonella spp. are considered pathogenic, although a few serotypes are responsible for the majority of serious infections in horses; Salmonella typhimurium (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. newport (group C) and S. krefeld (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 fatty 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 significantly 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 fimbriae 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
mesenteric
lymph
nodes.
Virulence
20
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.
RISK FACTORS FOR SALMONELLOSIS AND EPIDEMIOLOGY 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 immunity, 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, i!nd 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-density 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.
CLINICAL SIGNS AND LABORATORY DIAGNOSIS The clinical signs are variable (Table 20. 1 ) and include fever, mild abdominal pain, anorexia, and depression 407
20
ACUTE AND CHRONIC DIARRHEA
Table 20.1 Clinical signsas_'eted WIth ilalmoneJlo. . . j . , .. :.. . . Adult horses
Fever Inappetence or anorexia Depression Abdominal pain Diarrhea - varying from nil to severe and watery Small colon impaction
Foals
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 significance. 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 (40°C) 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 confirm that a Salmonella sp. is the cause of the diarrhea and occasionally false negatives occur. Appropriate history (see above) , clinical find ings, eliminating other causes of diarrhea, and a heavy 408
growth of Salmonella spp. from feces is the most appro priate route to reach an ante-mortem definitive 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.
TREATMENT 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 cephalosporin) 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 justified 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 finding in Salmonellosis cases that die. Commercial plasma con tains an antibody against endotoxin but this property is probably not as important as albumin, anti-thrombin III, fibronectin, 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 sufficient volume to maintain urine output, return the blood urea and creatinine to
ACUTE DIARRHEA
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 EI (misoprostol, 2-4 Ilg/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 benefit. 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.
PROGNOSIS 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 findings in the adult horse. Meningitis, pneumonia, septic physitis, or septic arthritis worsen the prognosis in foals. Other complications 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
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 significant 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.
CONTROL AND PREVENTION 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 difficult 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 409
20
ACUTE AND CHRONIC DIARRHEA
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 typhimurium 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 Divers Clostridial diarrhea in adult horses may result from infections with toxigenic strains of Clostridium difficile or C. perJringens. C. perJringens type A with enterotoxin has been frequently incriminated as a cause of adult horse diarrhea, but has been difficult to document. An unclas sified type of C. perJringens that produces a beta2 toxin has been recently reported as a cause of diarrhea in adult horses. Toxigenic C. difficile 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. difficile is a more common cause of diarrhea in adult horses than are Salmonella spp.
ETIOPATHOLOGY Clostridium perJringens is thought to cause diarrhea by elaboration of either an enterotoxin or a newly described beta2 toxin. C. perfringens 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. perfringens 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. perfringens 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. perfringens enterotoxin may also induce a pro-inflammatory cytokine response with production of interferon 410
gamma, interleukin-l and 6. In humans, enterotoxi genic C. perfringens 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. perfringens producing a beta2 toxin is unknown. The type of C. perJringens producing this toxin is not described. Affected 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 findings for C. perfringens type A and enterotoxin. The etiopathology of C. difficile is well described in both horses and other species. Pathogenic strains of C. difficile 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. perfringens 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. difficilll-induced 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. diffi cile. Exposure to a toxigenic strain of the bacteria is a prerequisite. Clostridium difficile 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. difficile in normal feces. Foals with diarrhea, regardless of its etiology, may be another source of environmental contamination as toxigenic C. difficile can frequently be found in the feces of diarrheic foals, although cause and effect in the foals is more difficult to prove. In the majority of adult horses with C. difficile 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 C. difficile to proliferate in the colon. Antimicrobials that most com monly predispose to C. difficile 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-
ACUTE DIARRHEA
dispose to diarrhea, antimicrobials given by the par enteral route may also predispose to C. difficile colitis. Foals treated with erythromycin per os actually increase the risk of C. difficile 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. difficile 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. difficile colitis. Foals less than 4 months of age treated with ery thromycin rarely develop severe diarrhea. The risk of C. dilficile 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. difficile 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. difficile. Intestinal stasis associated with many cases of abdominal pain also pre disposes to overgrowth of the organism.
CLINICAL SIGNS AND CLINICAL PATHOLOGICAL FINDINGS The clinical signs and clinical pathological findings 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. difficile diar rhea can vary similarly to Salmonella spp. or Ehrlichia ris ticii. The most severe cases of C. difficile 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. difficile 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
20
neutrophils and toxic changes may be noted, but these findings are not different from other infectious causes of diarrhea in adult horses.
DIAGNOSIS The diagnosis of Clostridium perfringens as a cause of diar rhea in horses is difficult. There is usually no common predisposing event as in humans, i.e. outbreak of food poisoning or prior antibiotic administration as with C. difficile. 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. perfringens 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. per fringens 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. difficile 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. difficile-Iike 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. difficile toxin gene in the feces.
Feces with C. difficile are generally colored green to brown and are less commonly hemorrhagic. 411
20
ACUTE AND CHRONIC DIARRHEA
Hemorrhagic diarrhea was reported to be common in horses that had the novel beta2 toxin in the feces.
TREATMENT 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 • fluids (crystalloids and colloids) • anti-inflammatory drugs • intestinal protectants 2. antimicrobial therapy. The antimicrobials of choice are metronidazole or chloramphenicol. Metronidazole would be the first choice since most (but not all) C. difficile 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 facility in the US that had metronidazole-resistant strains of C. difficile. One advantage of chloramphenicol, although not as sensitive against most C. difficile 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. difficile 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. difficile and these should be evaluated further in the horse. If Clostridium perfringens is believed to be the cause of the diarrhea, oral metronidazole and/or intravenously administered penicillin may be used.
PREVENTION Prevention of Clostridium difficile infection may be diffi cult in intensive care hospitals with large numbers of foals and adult horses receiving broad-spectrum antibi otics. C. difficile forms heat-resistant spores but surface disinfection with hypochlorite may be successful in destroying most cells. Routine hand washing by all per412
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 fiber as soon as feasible after abdominal surgery might be helpful by increasing the normal bac terial metabolic products in the colon that are known to inhibit C. difficile 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. diffi cile 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. difficile. Foals should not be allowed to drink water from a shared water bucket immediately after being dosed with erythromycin.
Potomac horse fever JM Bartol 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 E. risticii's predilection for peripheral monocytes and macrophages. The dis ease was first reported along the Potomac River in Maryland in 1979, but presently has been confirmed throughout the United States, Canada, and in Europe. Several surveys have identified 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 adui t horses and yearlings, but not in foals. Currently there is evidence for the involvement of E. 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
ACUTE 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 E. 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 findings 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 E. risticii in circulating mononuclear cells and the resulting release of proinflammatory cytokines.
EPIDEMIOLOGY 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 E. risticii 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 E. risticii in a helminth or coprophagus arthropod, and inadvertent ingestion by a horse is likely. Neorickettsia
20
spp., also in the family Ehrlichieae, are transmitted through ingestion of infected helminths. Similarities in DNA structure between E. risticii and Neorickettsia 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 fish in japan, also transmitted by flukes, was isolated and found to share 99 per cent DNA homology with E. risticii. Thus, more evidence is pro vided for the potential of helminth transmission in the horse. Similarly, E. risticii 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 seasonality of the disease. More recently E. risticii, or a nearly identical organism, has been found in freshwater stream operculate snails (Pleuroceridae: Juga 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. risticiiwas 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. risticii positive metacerariae were identified 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 E. 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 E. 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 E. risticii, as compared to the 1984 isolate, were isolated from clinically sick horses in 413
20
ACUTE AND CHRONIC DIARRHEA
the early 1990s. It is known that PHF is caused by diver gent strains. Multiple strains may account for incom plete vaccine efficacy since commercial vaccines are made of the single 1984 isolate. Divergent strains may also account for difficulties 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 identify only a single type strain of E. risticii. E. risticii may also cause abortion. Abortions in the seventh month of gestation have been seen with both experimental E. 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. E. 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 confirmed 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 history of illness.
CLINICAL SIGNS 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 monocyto414
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 find ings are similar to those found in acute endotoxemia, diarrhea caused by Salmonella spp. is the primary differ ential diagnoses.
DIAGNOSIS 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 amplification to identify 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. risticii organisms are identified in the buffy coat component of the sample. The PCR is a sen sitive and specific 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 definitive 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 first titer is sufficient time to collect the second sample. A four-fold or greater change in IFA titer is diagnostically significant 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 first 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.
ACUTE DIARRHEA
of pentoxifylline in the treatment of endotoxemia in horses.
TREATMENT AND PREVENTION Treatment considerations for PHF are similar to those for any acute colitis in the horse 1. addressing hydration status, acid-base deficits, 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. a plasma transfusion of at least 3-6 liters is beneficial 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. Specific 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, efficacy of any one prophylactic treat ment for laminitis is difficult 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 observations 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 efficacious in laminitis prevention but it has not been proven. Currently studies are being performed to evaluate the efficacy
20
Presently vaccination efficacy is questionable. There are numerous cases of clinical PHF in vaccinated horses. A possible explanation is the identification of new disease-causing strains of Ehrlichia risticii. Studies on vaccine efficacy 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 severity of disease and is therefore strongly recommended. Possible explanations for the marginal nature of the vaccines include deficiencies 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 ND Cohen INTRODUCTION Non-steroidal anti-inflammatory drugs (NSAIDs) 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.
MECHANISMS OF TOXICITY The major toxicities related to NSAIDs include • •
gastrointestinal tract damage renal damage. 415
20
ACUTE AND CHRONIC DIARRHEA
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 NSAlDs is related to inhibi tion of the cyclooxygenase enzymes. Two isoforms of the cyclooxygenase enzyme have been identified • •
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, fibroblasts, 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 affinities 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 severity 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. 41 6
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 finding is important because NSAlDs are often administered to chronically lame horses. In some areas, concurrent use of two or more NSAlDs is com mon. Combination of two NSAlDs will prolong their pharmacologic effect and increase the risk of toxicity.
CLINICAL SIGNS 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 difficulty 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.
CLINICAL PATHOLOGY 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 findings 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
ACUTE DIARRHEA
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 hyperfib 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 fibrino 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.
DIAGNOSIS Diagnosis is usually made on the basis of history of NSAID use, clinicopathologic findings, 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 difficult to identifY without celiotomy and enterotomy. It has been sug gested that isotope-labeled white blood cell scinti graphic scans may identifY colonic ulceration; the sensitivity 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.
TREATMENT 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 benefit to reduce the absorption of the ingested NSAID. Treatment for gastric ulceration with a proton-pump inhibitor (e.g. omeprazole) , an Hz-blocker
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 ' may be of benefit I 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 2 1 , Right dorsal colitis. Horses with strictures of the pylorus, duodenum, jejunum, or colon may require surgical management.
PREVENTION 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. As described above, administration of misoprostol can prevent or limit the severity of NSAID-induced enteropathy.
Toxic colitides ND Cohen INTRODUCTION 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 2 1 ) .
Cause Cantharidin is a toxic principle found in many of the 'blister' beetles (Epicauta spp. ) (Figure 20.1) that cause 417
20
ACUTE AND CHRONIC DIARRHEA
Inappetance Depression Playing with water Salivation Pollakidipsia Pollakiuria Sweating Pyrexia Tachycardia Tachypnea Congested mucous membranes Figure 20.1 Beetle, Epicauta sp., associated with blister beetle toxicosis (photograph courtesy of Dr DG Schmitz)
Colic Diarrhea Hematuria or hemoglobinuria Synchronous diaphragmatic flutter Muscle fasciculations Stiff gait Sudden death
blistering of mucosal surfaces. Cantharidin toxicosis results from ingestion of dead blister beetles in alfalfa hay or, 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 4-6 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. Clinical Signs (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 418
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 6-8 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-specific, 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 identified macro- or microscopically in the gastrointestinal contents or feces of affected horses. Clinicopathologic findings often include hypocalcemia, hypomagnesemia, hypopro teinemia, and elevated creatine phosphokinase.
ACUTE DIARRHEA
The toxin can be identified 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 finding 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 two 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 benefit 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
.
20
flunixin meglumine, so xylazine, detomidine, or romifi 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 fields. Because they do not migrate far, avoiding simul taneous cutting and crimping of forage from the perimeter of fields 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.
OTHER TOXINS A variety 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 ( Quercus spp.) may be toxic to horses. Clinical signs in horses may be peracute or acute, including colic, hem orrhagic diarrhea, and sudden death. Renal toxicity can also occur. Rarely, ingestion of acorns can cause gastric impaction. Diagnosis is based on history of exposure, finding 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. 419
20
ACUTE AND CHRONIC DIARRHEA
Table
JGAPlal'lu ���_,��"�:i�b'�.
Acorn/oak Algae Avocado Castor bean Oleander Selenium-accumulating plants (e.g. Astra/agulus spp.) Heath (Erica spp.) Japanese yew Potato St John's wort (Klamath weed)
�r,:,:'��:::ko.�r��'''�' '
;'
,
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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 Astragulus 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. 420
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. Specific treatment for arsenic intoxication includes sodium thiosulfate ( 20-30 g diluted in 300 ml water p.o.) or dimercaprol (BAL) . The latter com pound is administered intramuscularly as an antidote for trivalent arsenical intoxication (3 mg/kg) , and its efficacy 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 increasingly 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 o f mercury-treated seed grains o r 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, identifying 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
ACUTE DIARRHEA
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 benefit. 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.
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 scientific study of that disease. The signs of symptomatic grain overload may include • • • • • •
MA
Ball
• • • • •
INTRODUCTION 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 corn 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 fiber in the cecum and large intestine generates a greater amount of heat than the digestion of concentrates.
colic abdominal distension lameness caused by laminitis trembling sweating diarrhea.
Clinical examination findings relate to endotoxic and hypovolemic shock, gastritis, and ileus, and may include •
Grain overload
20
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 findings are variable depending o n the indi vidual case.
MANAGEMENT Treatment options for grain overload are summarized in Table 20.6. The most immediate concern following the overingestion of soluble carbohydrates is gastritis and
Nasogastric intubation Activated charcoal Mineral oil Magnesium sulfate Flunixin meglumine Aspirin Antihistamines - doxylamine or diphenhydramine Intravenous polyionic fluids - lactated Ringer's solution hypertonic saline sodium bicarbonate Plasma
There are several sequelae to the sudden ingestion of soluble carbohydrates ranging from mild colic and the
Pentoxifylline Frog supports Glyceryl trinitrate
42 1
20
ACUTE AND CHRONIC DIARRHEA
subsequent overdistension of the stomach. In such cases, the horse typically 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 ( 1 0 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 first 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 presen t (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 nificant benefit as the initial fluid, but must be followed within several hours by a volume replacement quantity 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 benefit as well as the administration of pentoxirylline (8.4 tng/kg p.o. t.i.d. ) . A� a potential prophylaxis against laminitis treat ment should focus on maintaining laminar circulation. 422
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 Divers There are many causes of acute diarrhea in adult horses other than salmonellosis, clostridiosis, ehrlichiosis, can tharidin toxicosis, cyathostomosis (see Chapter 2 1 ) , 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.
TOXICITIES 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 leguminicola) , most commonly found as
*Consultant on-line database, White, M E, College of Veterinary Medicine, Cornell University, Ithaca, NY: www.vet.Comell.edulconsultant
ACUTE DIARRHEA
20
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. Hoary 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 amara (Simarubaceae) wood chips.
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 motility and may cause colic and/ or pas sage of loose stool. Massive exposure of the immuno logically naive horse to large strongyles may cause colic and diarrhea, although this is more common in foals (acute strongyle syndrome ) .
DRUGS
BACTERIAL INFECTIONS
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 sufficient quantities or for prolonged periods. Misoprostol and chenodeoxycholic acid are secretagogues causing active secretion of chlorine and bicarbonate ions and passive efflux 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.
Additional bacterial, fungal, and viral agents that may cause diarrhea include Aeromonas spp., Mycobacterium avium, Aspergillus 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. Mycobacterium 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.
DERANGED INTESTINAL MOTILITY 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 toxicity. 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
423
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ACUTE AND CHRONIC DIARRHEA
ASPERGILLOSIS Aspergillus colitis is well documented in horses. In vir tually all cases, the Aspergillus 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.
BIBLIOGRAPHY General principles of treatment of acute diarrhea in adult horses Brooks H W, Hall G A, Wagstafls 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] ( 1 998) Induced diarrhea in horses Part 2: Response to administration of oral rehydration solution. VetJ 1 55 : 1 6 1-70.
Salmonellosis Cohen N D, Martin L], Simpson R B ( 1 996) 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 ( 1 997) A clinical trial of probiotic administration for prevention of Salmonella shedding in the postoperative period in horses with colic. J Vet. Intern. Med. 1 1 ( 1 ) :36-4 1 . Spier S .I ( 1 993) Salmonellosis. Vet. Clin. N. Am. J<-'quine Pract. 9 ( 2 ) : 385-94.
Clostridial diarrhea in adult horses Baverud V, Franklin A, Gunnarsson A, et al. ( 1 998) Clostridial difficile 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 difflcile toxin A in feces of horses with diarrhea and colic. J Am. Vet. Med. Assoc. 2 1 5 (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. Microbiol. 37( 2 ) : 358-6 1 . .lang S S, Hansen L M , Breher.I E, e t al. ( 1 997) Antimicrobial susceptibilities of equine isolates of Clostridium difficile 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. ( 1 998) Detection of Ehrlichia risticii, the agent of Potomac horse
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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. ( 199 1 ) 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 K, Vemulapalli R , Biswas B ( 1 998) Association of deficiency 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) Identification of Ehrlichia risticii as the causative agent of two equine abortions following natural maternal infection. J Vet. Diagn. Invest. 7:201-5. Palmer .l E ( 1 993) 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 definitive host of the helminithic vector of Ehrlichia risticii. Proc 1 8th Annual ACVlM Forum
Pusterla N, Leutenegger C M, Sigrist B, et al (2000) Detection and quatification 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. Microbiol. 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. Bacteriol. 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. Rev. 1 6 (2) : 1 81-206. Johnston S A, Fox S M ( 1 997) Mechanisms of action of anu inflammatory medications used for treatment of osteoarthritis.J Am. Vet. Med. Assoc. 2 1 0 ( 1 0) : 1 486-- 1 492. MacKay R.I, French T W, Nguyen H T, Mayhew I G ( 1 983) Effects of large doses of phenylbutazone administration to horses. Am. .f. Vet. Res. 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 ( 1 98 1 ) Phenylbutazone toxicosis in equidae: a biochemical and pathophysiological study. Am . .f. Vet. Res. 42 ( 1 0) : 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 : 1 0 1 8-2 1 . Schmitz D G ( 1 989) Cantharidin toxicosis in horses . .f. Vet. Int. Med. 3:208-15.
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Smith B P (ed) ( 1990 and 1996) Large Animal Intemal Medicine ( 1 st and 2nd edns) . C V Mosby, St Louis.
Acute d iarrhea in adult horses - other causes Dave B , Rubin W ( 1 999) 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.
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Freeman D E , Ferrante P L, Palmer] E ( 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. A m. ]. Vet. Res. 53(8) : 1 347-53.
Hathcock T L, Schumacher], Wright], Stringfellow] ( 1999) The prevalence of Aeromonas species in feces of horses with diarrhea. ]. Vet. Int. Med. 1 3:357-60.
42 5
21 Chronic diarrhea
Differential diagnosis and evaluation of chronic diarrhea in the adult horse T Mair
INTRODUCTION
diarrhea
- variable consistency - persistent or recurrent
pyrexia inappetence depression
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 find 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 definitive 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 post-mortem examination.
The clinical signs associated with diseases causing chronic diarrhea are summarized in Table 21.1.
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
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ACUTE AND CHRONIC DIARRHEA
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.
Clinical history Management, nutrition, parasite control Signalment Physical examination
DIFFERENTIAL DIAGNOSIS
Hematology and plasma fibrinogen
The more common causes of chronic diarrhea are listed in Table 2l.2.
Serum biochemistry Serum protein electrophoresis Abdominocentesis Fecal examinations - worm egg count examination for larvae
Cyathostomosis
other parasitological
Mixed strongyle infections
examinations white blood cells bacteriology
Peritonitis Alimentary lymphosarcoma Inflammatory bowel diseases
Sugar absorption tests
- granulomatous enteritis/
Rectal biopsy
colitis - Iymphocytic-plasmacytic
Ultrasonography
enteritis/colitis - eosinophilic enteritis/colitis
Exploratory surgery and bowel wall/colonic lymph node biopsies
NSAID toxicity
Salmonellosis Chronic liver disease* Sand enteropathy Chronic 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
chronic diarrhea, but even after exhaustive tests the clinician and owner of an affected horse should be aware that a definitive diagnosis may not be attainable. Some of the important components of the examination of affected horses are summarized in Table 2l.3. As 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 full clinical history and evaluation of management and nutrition are important. These aspects are dis cussed more fully in Chapter 18, Differential 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
A
EVALUATION OF CHRONIC DIARRHEA Thorough and repeated clinical and laboratory evalua tions are often required to diagnose the cause of 428
CHRONIC DIARRHEA
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). Physical examination 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 hyperfibrino 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
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 severity 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 fiber 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 larval 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 identifY larvae. 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
21
ACUTE AND CHRONIC DIARRHEA
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 nificant 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 significant 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.
General principles of treatment of chronic diarrhea in adult horses T Mair
INTRODUCTION As in acute colitis and diarrhea, chronic diarrhea can
result in significant lumenal loss of fluid, electrolytes, and protein. Since the precise causes of chronic diarrhea are frequently difficult to establish, specific 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 •
Ultrasonography Ultrasonography is complementary to rectal examina tion and can be helpful in the evaluation of chronic diarrhea. Abnormalities that may be identified 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).
• •
• •
dryness of mucous membranes skin turgor speed of distention of the jugular vein when compressed PCV 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. =
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
• •
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-
CHRONIC DIARRHEA
nal lumen with resulting hypoproteinemia and hypo albuminemia. These horses may benefit 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 specific 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
• •
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.
ANTIBIOTICS 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,yor 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 amides or metronidazole (the reason for this is uncer tain). Antibiotics are indicated in horses with chronic diarrhea due to peritonitis (see Chapter 17).
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 benefit.
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-specific 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 benefit could be an antisecretory effect • 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-inflammatory properties but is relatively ineffective 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
21
ACUTE AND CHRONIC DIARRHEA
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 activity 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 benefit 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.
and is probably responsible for subclinical production losses that are difficult to quantify. When the parasite burden becomes high, overt clinical disease is more likely to be manifested, particularly in young horses. The most clearly defined disease syndrome associ ated with cyathostome infection is the acute diarrheal syndrome called larval cyathostomosis (previously known as larval cyathostomiasis or acute larval 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-specific 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 different clinical presentations in individual cases.
ETIOLOGY AND PATHOGENESIS
Larval cyathostomosis 0011111111
T Mair
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. Interval treatment using these drugs has been highly effective at reducing the prevalence of large strongyles such as Strongylus vulgaris, but it is rela tively ineffective at controlling the cyathostomes. Even in well-managed horses, cyathostome infection is likely 432
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 larvae 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 larvae cannot ingest nutrients so they survive on the pasture by consuming limited, intracellular energy reserves. The duration of their survival is inversely proportional to the environmental temperature because they utilize their energy reserves faster in hot weather. The environmen tal constraints on the cyathostome life cycle result in
CHRONIC DIARRHEA
Northern temperate areas
Southern temperate areas
Development
Persistence
Development
Persistence
Spring
+++
+++
++
++
Summer
++
+
Autumn
+++
+++
++
++
+++
+
+
Winter +++
21
excellent
++
good
+
fair
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 first stage larvae (Ll) develop in the presence of warmth and moisture via second stage larvae (L2) to infective third stage larvae (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 fibroblastic 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 fifth 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 as 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 typhlitis and
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-specific 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 first 4-6 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
21
ACUTE AND CHRONIC DIARRHEA
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 larvae 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 (dehydra434
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. History and epidemiology 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 fingers 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 confirm the presence of L4 and L5. Larvae may be difficult 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 Campylobacter spp. Hematological examination Routine hematological examination usually reveals leukocytosis and neutrophilia. Some cases may also show anemia and/or mild eosinophilia. Serum biochemistry 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 electrophoresis This may show elevated beta-globulin levels and some times elevated alpha-globulin levels.
CHRONIC DIARRHEA
Histological 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 five occasions is advocated. The following larvici dal doses of these drugs are suggested • • •
fenbendazole ivermectin moxidectin
7.5-10.0 mg/kg p.o. s.i.d. for 5 days 0.2 mg/kg p.o. 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
21
of cyathostomes may limit the effectiveness of fenben 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 activity 2. the steroid-induced immunosuppression may encourage resumption of larval 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 beneficial 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 acljusted on an empiri cal basis thereafter. Side effects can be seen with higher 435
21
ACUTE AND CHRONIC DIARRHEA
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 first 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 subcutaneous edema, and cyathostome larvae were identified in the feces.
PREVENTION Prevention of larval 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
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 identified 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 larval cyathostomosis. All four horses demonstrated a variable number of other signs of larval cyathostomosis, such as diarrhea, pyrexia, 436
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. Strongylus 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 artery 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
CHRONIC DIARRHEA
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 Strongylus vulgaris 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 difficult. Since clin ical disease is usually caused by the immature, migratory larval 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-specific 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 affect the small intestine and
21
are associated with malabsorption and chronic weight loss (see Chapter 18). However, if the large intestine is affected 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 findings 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 confirm bowel wall thickening. Moderate to severe hypoalbuminemia and mild to moderate hyperglobu linemia are often present. Elevated serum alkaline phosphatase may be present. Non-specific hematologi cal abnormalities (anemia, leukocytosis, neutrophilia, hyperfibrinogenemia) may also be identified. Diagnosis of inflammatory or neoplastic bowel infiltrates 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-specific 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 significant 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
21
ACUTE AND CHRONIC DIARRHEA
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 refill time, and a toxic rim at the gum/incisor margin.
DIAGNOSIS Sand may be identified 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 identify 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 (pev 45-55% and total protein 72-80 gil (7.2-8.0 g/dl». Plasma fibrinogen 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, identification of sand particles in the sample of peritoneal fluid is diagnostic when seen.
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 efficacy 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 fiber 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 intervals 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 fields with adequate growth to prevent ingestion of sand are vital to avoid this condition.
Equine right dorsal colitis NO Cohen
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
INTRODUCTION Right dorsal colitis has been clinically and experimen tally associated with administration of phenylbutazone
CHRONIC DIARRHEA
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.
21
Physical examination of horses with RDC may reveal few abnormalities and clinical signs are non-specific. Horses may have signs of acute abdominal pain (colic). Often 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 PCV 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 findings, 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 hyperfibrinogenemia, associated with inflammation, and leukopenia and neutropenia, possibly caused by endotoxemia, can be seen in some horses with RDC. Hypocalcemia is frequently observed 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
21
ACUTE AND CHRONIC DIARRHEA
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 fluid 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 findings observed is specific for RDC. Consequently diagnosis is difficult. 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 2 1.1 ). 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 findings of signal ment and history, clinical signs, and clinicopathologic findings, particularly hypoalbuminemia. The chief complaint is often non-specific and history of recurrent episodes of anorexia, lethargy, and colic is frequently described. History of administration of non steroidal anti-inflammatory 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 difficult, particularly in cases where blame may be an issue. The amount and duration of NSAID administered may be important. It is, however, important 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 findings, how ever, can be seen in horses with gastric and small intesti440
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. Definitive 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 identifYing 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 identifY colonic ulceration; the sensitivity and availabil ity of the procedure is likely to be quite limited.
TREATMENT Initially RDC was described as a condition requmng surgical management and carrying 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 benefit 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 difficult 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.
CH RONIC DIARRHEA
21
Minimizing stress for the horse
Psyllium mucilloid
Physiologic stress and dehydration appear to increase the risk of gastrointestinal ulceration induced by NSAIDs. 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
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.
• •
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 pelleted concentrate, and restricting or eliminating ingestion of roughage. These changes aim to decrease the mechanical and physio logic load of the colon. A complete pelleted diet (i.e. pellets containing both concentrate and adequate dietary roughage) will decrease intestinal fill in the colon, therehy decreasing the mechanical load of the colon. A diet lower in fiber should decrease the physio logic load of the colon because the cecum and large colon are the primary sites in horses of fiber 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 amounts 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.
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 benefit in horses with RDC. The drug can be administered orally (2.5-5 J.1g/kg q. 12 h or 2 J.1g/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 J.1g/kg q. 6 h.
Sucra/fa te 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
21
ACUTE AND CHRONIC DIARRHEA
Metronidazole and sulfasalazine In humans, NSAID-induced enteropathy has been treated with sulfasalazine and metronidazole with vary ing success. These agents 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- 1 5 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 benefits of feeding omega-3+/omega to fatty acid diets to prevent or help repair intestinal mucosal injury are unknown in the horse.
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
Intestinal protectants and adsorbants
INTRODUCTION
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.
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 • • •
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 recur442
• • • • • • • • •
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)
CHRONIC DIARRHEA
•
pancreatic diseases (see Chapter
•
peritonitis (see Chapter
17)
21
tion may persist for several months. Systemic antibiotics
17).
are of questionable value in these cases even when
Toxic causes of diarrhea are described in Chapter
20.
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
IDIOPATHIC CHRONIC DIARRHEA
no longer be detected.
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 significant 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 h orses with idiopathic chronic diarrhea will respond to dietary modification. 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 benefit 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 beneficial in the man agement of idiopathic diarrhea include the following (see also General principles of treatment of chronic
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 identified 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
(5-20 mg kg-l dayl) and/or (10 mg/kg b.i.d.) might be considered.
horses, although isoniazid rifampin
diarrhea in adult horses)
NEOSPORA CANINUM
•
iodochlorhydroxyquin
•
metronidazole or poten tiated sulfonamides
•
anthelmintics ( larvicidal doses)
Neospora caninum has been diagnosed as a possible cause
•
transfaunation
of colitis in a middle aged horse that demonstrated
•
probiotics
signs of chronic diarrhea and anemia. At necropsy,
•
codeine phosphate and other motility-modifYing
tachyzoites of N.
drugs
the colon and mesenteric lymph nodes.
•
caninum were identified in sections of
acetic acid (vinegar) .
HISTOPLASMOSIS CHRONIC SALMONELLOSIS Histoplasmosis has been identified in a small number of Chronic salmonellosis appears to be a rare cause of
horses affected by chronic diarrhea and weight loss.
chronic diarrhea in adult horses. Although
Although there are enzootic areas of histoplasmosis in
Salmonella
spp. can frequently be cultured from the feces of horses with chronic diarrhea, other underlying causes of the
the USA, cases are rarely reported.
Histoplasma capsula tum has been diagnosed as a cause of granulomatous
lymphosarcoma,
colitis, resulting in chronic diarrhea and protein-losing
inf1ammatory bowel disease, etc.) may be present. Some
enteropathy. The organism can also cause peritonitis,
horses recovering from acute salmonellosis will be
pulmonary
affected
achieved by bowel wall biopsy. Skin tests are unreliable.
diarrhea
(such
by
as
chronic
cyathostomosis,
or
intermittent
remain persistent shedders of
diarrhea
and
Salmonella spp.; this situa-
infection,
and
abortion.
Diagnosis
is
No attempts at treatment have been reported.
443
21
ACUTE AND CHRONIC DIARRHEA
GIARDIASIS
PERITONITIS
Giardia equi infection has been described as a rare cause of chronic diarrhea, decreased appetite, and abdominal pain in adult horses, but the significance 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 difficult 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.
Diarrhea is an unusual presenting clinical sign associ ated with peritonitis. The disease is described in detail in Chapter 1 7 .
TRICHOMONAS EQUI " �W-'''' ,,", i''-�,h".' ,,' "'"' ,," ',' ",*""m"1)...,""�+,tI"C �,,, oii!> "'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 fluidity 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 identified. Diagnosis is achieved by identifYing 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 significant cause of diarrhea in adult horses.
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 specific cause was identified, and no treatment was described.
INTESTINAL FIBROSIS Diarrhea has been recorded in horses and ponies affected by intestinal fibrosis. 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 fibrosis of the small intestine. The only reported treatment has been resec tion of affected segments of bowel.
BIBLIOGRAPHY Differential diagnosis and evaluation of chronic diarrhea in the adult horse Love S, Mair T S, Hillyer M H ( 1 992) Chronic diarrhoea in adult horses: a review of 5 1 referred cases. Vet. Rec. 1 30:2 1 7-19. Mair T S, Cripps P ], Ricketts, S W ( 1 993) Diagnostic and prognostic value of serum protein electrophoresis in horses with chronic diarrhoea. Equine Vet. ] 25:324-6. Merritt A M ( 1 983) Chronic diarrhoea. In Current Therapy in Equine Medicine 1st edn, N E Robinson (ed. ) . W B Saunders, Philadelphia, p. 2 1 6. Morris D D , Whitlock R H , Palmer] E ( 1 983) Fecal leukocytes and epithelial cells in horses with diarrhea. Cornell Vet. 73:
HEPATIC DISEASE Chronic hepatic disease is a rare cause of diarrhea. Alterations in intestinal microflora, portal hyperten sion, and deficiency of bile acids may be involved in the pathogenesis. The diagnosis and treatment of chronic hepatic diseases are discussed in Chapter I g . 444
265-74. Pearson E G , Smith B B and McKim] M ( 1 987) Fecal blood determinations and interpretation . Proe. Am. Assaf. Equine Praet. 33:77-8 1 Ragle C A and Meagher D M ( 1987) Abdominal auscultation as an aid to diagnosis of sand colic. Proc. Am. Assoc. Equine Praet. 33:521-523 Rantanen N W ( 1 986) Diseases of the abdomen. Vet. Clin. N. Am. Equine Praet. 2:67-88
CHRONIC DIARRHEA
General principles of treatment of chronic diarrhea in adult horses
21
Wallace K D, Selcer B A, Tyler D E and Brown] ( 1 989) Transrectal ultrasonography of the cranial meseneric artery of the horse. Am. J Vet. Res. 50: 1 699-1703.
Hansen T 0 ( 1 994) Treatment of chronic diarrhoea in horses. Camp. Cant. Educ. Pract. Vet. 1 6 : 1 490-2. Harris P A, Frape D L, ]effcott L B , Lucas D M, Meyer H and Savage C] ( 1 995) Nutritional aspects of me tabolic diseases. In The Equine Manual, A] Higgins and I M Wright (eds ) . W B Saunders, London, pp. 1 75-85.
Chronic inflammatory bowel disease and intestinal neoplasia Love S, Mair T S and Hillyer M H ( 1 992) Chronic diarrhoea in adult horses: a review of 5 1 referred cases. Vet. Rec. 1 30:2 1 7-219
Larval cyathostomosis Giles C], Urquhart K A and Longstaffe ] A ( 1 985) Larval cyathostomiasis (immature trichonema-induced enteropathy) : a report of 1 5 clinical cases. Equine Vet. J 27:29-40 Love S, Mair T S and Hillyer M H ( 1 992) Chronic diarrhoea in adult horses: a review of 51 referred cases. Vet. Rec.
Platt H ( 1 986) Chronic inflammatory and Iymphoproliferative diseases of the equine small intestine. J Camp. Patho!. 96:671-684 Roberts M C ( 1985) Malabsorption syndromes in the horse. Camp. Cant. Educ. Pract. Vet. 7:S637-S646 Scrutchfield L ( 1 987) Chronic diarrhea. In Current Therapy in Equine Medicine 2nd edn, N E Robinson (ed. ) . W B Saunders, Philadelphia, pp. 1 00-102
1 30 : 2 1 7-2 1 9 Mair T S ( 1 993) Recurrent diarrhoea i n aged ponies associated with larval cyathostomiasis. Equine Vet. J 25:1 61-1 63 Mair T S ( 1 994) Outbreak of larval cyathostomiasis among a group of yearling and two-year-old horses. Vet. Rec. 1 35:598-600 Mair T S, Cripps P] and Ricketts S W ( 1 993) Diagnostic and prognostic value of serum protein electrophoresis in horses with chronic diarrhoea. Equine Vet. J 25:32-326 Mair T S and Pearson G R ( 1 995) Multifocal non strangulating intestinal infarction associated with larval cyathostomiasis in a pony. Equine Vet.J 2 7 : 1 54-155 Mair T S, Sutton D G M and Love, S (2000) Caeco-caecal and caeco-colic intussusceptions associated with larval cyathostomosis in four young horses. Equine Vet. J 32:77-80
Sand enteropathy Bertone ]], Traub-Dargatz ] L, Wrigley R W ( 1 988) . Diarrhea associated with sand in the gastrointestinal tract of horses. J Am. Vet. Med. Assoc. 1 93 : 1 409- 1 4 1 2 Denberg T ( 1 979) Equine colic associated with sand impaction of the large colon. Can. Vet. J 20:269-272 Hammock P D, Freeman D E and Baker G ] ( 1998) Failure of psyllium mucilloid to hasten evacuation of sand from the equine large intestine. Vet. Surg. 27:547-554 Hansen T 0 ( 1 994) Treatment of chronic diarrhea in horses Camp. Cant. Educ. Pract. Vet. 1 6: 1 490-1492 Jones S L, Snyder] R and Spier S] ( 1 998) Obstructive conditions of the large intestine. In Equine Internal Medicine, S M Reed and W M Bayly (eds ) . W B Saunders, Philadelphia, pp. 682-694
Paul] W ( 1 998) Equine larval cyathostomosis. Camp. Cant. Educ. Pract. Vet. 20:509-5 1 4 Reid S W], Mail' T S , Hillyer M H and Love S ( 1 995) Epidemiological risk factors associated with a diagnosis of clinical cyathostomiasis in the horse. Equine Vet. J 27:1 27-130 Reilly G A C, CassidyJ P and Taylor S M ( 1 993) Two cases of diarrhoea in horses associated with larvae of the small
Equine right dorsal colitis Cohen N D , Carter G K, Mealey R H, Taylor T S ( 1 995) Medical management of right dorsal colitis in 5 horses ( 1 987-1993 ) . J Vet. Int. Med. 9:272-276 Karcher L F, Dill S G, Anderson W I, et al ( 1 990) Right dorsal colitis. J Vet. Int. Med. 4:247-253
strongyles. Vet. Rec. 1 32:267-268 Uhlinger C A ( 1 990) Effects of three anthelmintic schedules on the incidence of colic in horses. Equine Vet. J 22:25 1-254 Uhlinger C A ( 1 99 1 ) Equine small strongyles: epidemiology, pathology and control. Camp. Cant. Educ. Pract. Vet. 1 3:863 Xiao L H, Herd R P and Majewski G A ( 1 994) Comparative efficacy of moxidectin and ivermectin aginst hypobiotic and encysted cyathostomes and other equine parasites. Vet. Parasitol. 53:83-90
Chronic diarrhea in adult horses - other causes Barker I K. and Remmler 0 ( 1 970) Experimental Eimeria leuckarti infection in ponies. Vet. Rec. 86:448-449 Bennett S P and Franco D A ( 1 969) Equine protozoan diarrhea (equine intestinal trichomoniasis) at Trinidad racetracks. J Am. Vet. Med. Assoc. 154:58-60 Chineme C N, Tulpule S S and ]amdar M N ( 1979) Enteritis associated with Eimeria leuckarti infetion in donkeys. Vet.
Strongylosis Austin S M ( 1 994) Large strongyles in horses. Camp. Cant. Educ. Pract. Vet. 1 6:650-657 Greatorex ] C ( 1 977) Diagnosis and treatment of 'verminous aneurism' formation in the horse. Vet. Rec. 1 0 1 : 1 84-187 Love S ( 1 992) Parasite-associated equine diarrhea. Camp. Cant. Educ. Pract. Vet. 14:642-649 Wallace K D, Selcer B A and BechtJ L ( 1 989) Technique for transrectal ultrasonography of the cranial mesenteric artery of the horse. Am. J Vet. Res. 50: 1 695-1697
Rec. 1 05 : 1 26 Cline] M, Schlafer D W, Callihan D R, Vanderwall D and Drazek F J ( 1 99 1 ) Abortion and granulomatous colitis due to Mycobacterium avium complex infection in a horse. Vet. Patho!. 28:89-9 1 Damron G W ( 1976) Gastrointestinal trichomonads in horses: occurrence and identification. Am. J Vet. Res. 37:25-28 Goetz T E and Coffman] R ( 1984) Ulcerative colitis and protein losing enteropathy associated with intestinal salmonellosis and histoplasmosis in a horse. Equine Vet. J 1 6:439-441
445
21
ACUTE AND CHRONIC DIARRHEA
Gray M L, Harmon B G, Sales L and Dubey J P ( 1 996) Visceral neosporosis in a 1 0-year-old horse.]. Vet. Diagn. Invest. 8: 1 30-133 Johnson P J, Pace L W, Mrad D R, Turnquist S E, Moore L A and Ganjam V K ( 1 997) Small intestinal fibrosis in two horses . ]. Am. Vet. Med. Assoc. 2 1 1 : 1 0 1 3-- 1 0 1 7 Kirkptrick C E and Skand D L ( 1 989) Giardiasis i n a horse. ]. Am. Vet. Med. Assoc. 197: 1 63-164
infection with Eimeria leuckarti: prevalence of oocysts in feces of horse foals on several farms in Kentucky during 1986. Am. ]. Vet. Res. 49:96-98 Merritt, A.M. ( 1 994) Chronic diarrhoea in horses: a summary. Vet. Med. 130: 2 1 7-219 Milne E M, Woodman M P, Rowland A C, Patrick CJ and Arthur SJ ( 1 994) Intestinal lymphangectasia as cause of chronic diarrhoea in a horse. Vet. Rec. 134:603-604
Kirkptrick C E ( 1 989) Giardiasis in large animals. Compo Cont. Educ. Pract. Vet. 1 1 :80-84
Platt H ( 1986) Chronic inflammatory and
LofstedtJ andJakowski R M ( 1 989) Diagnosis of avian tuberculosis n a horse by use of liver biopsy. ]. Am. Vet.
]. Compo Palhol. 96:671-684 Scrutchfield L ( 1 987) Chronic diarrhea. In Current Therapy in
Med. Assoc. 194:260-262 Love S ( 1 992) Parasite-associated diarrhea. Compo Cont. Educ. Pract. Vet. 1 4:642-649 Love S, Mair T S and Hillyer M H ( 1 992) Chronic diarrhoea in adult horses: a review of 51 referred cases. Vet. Rec. 1 30:2 1 7-2 1 9 Lyons E T , DrudgeJ H and Tolliver S C ( 1 988) Natural
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lymphoproliferative diseases of the equine small intestine.
E-quine Medicine 2nd edn, N E Robinson ( ed . ) . W B Saunders, Philadelphia, pp. 100-102 Traub-DargatzJ L, Schultheiss P C, Kiper M L, et al. ( 1 992) Intestinal fibrosis with partial obstruction in five horses and two ponies. ]. Am. Vet. Med. Assoc. 201 603-607 Wheeldon E B and Greig W A ( 1977) Globidium leuckarti infection in a horse with diarrhoea. Vet. Rec. 100: 1 02-103
22 Clinical evaluation of the foal
Evaluation of the foal with colic
•
CS Cable
•
•
•
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 difficult 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 3 1 5-365) time to suckling reflex - normally suckles within 20 minutes time to standing - mean 57 minutes (range 1 5- 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 m aternal 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. Rhodococcus equi) .
Furthermore, previous or concurrent disease in the affected foal such as septicemia or musculoskeletal disorders m ay predispose to gastrointestinal ileus, ulceration, and/or peritonitis. Neonates undergoing intensive care, especially those with premature body 449
22
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 1 2-36 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 born, 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 without restraint. 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 or 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 m ay 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 lidocaine enemas. At the author' s hospital foals have been seen to develop sec ondary uroperitoneum, because of excessive straining to urinate or defecate. Physical examination 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 ).
CLINICAL EVALUATION OF THE FOAL
22
TeWl U.1 "rmal\fIl." ·tf hSrt rate�telplratotYiF.te. capilfary rE\flfl time,and rHtlI:tempe.'''''' 'fI�. . Age
Heart rate (bpm)
Respiratory rate (breaths per min)
Temperature (OC)
Capillary refill time (sec)
newborn
40-80 (at birth)
60-80 (first hour) 20-40 (first day)
37.2-38.9
<2
130-150 (during attempts to stand) 70- 100 (first day) 7 days
70-100
20-40
38.0-39.0
<2
3 months
30-60
12-20
37.5-38.5
<2
Cardiovascular system The cardiovascular system should be evaluated care fully. Mucous membranes should be moist and pink, with a capillary refill time of 1-2 seconds. Tachycardia can represent pain, hypovolemia, endotoxemia, and/ or septicemia. 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.
Respiratory system 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 possibility of fractured ribs - displaced rib fractures can lead to laceration of the lung tissue and pneumothorax.
Gastrointestinal system 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
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 defini 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.
Rectal examination A digital rectal examination can be performed, espe cially in the neonate to check for the presence of retained meconium. The m econium 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 taken first. If the foal is febrile and' colicky' , enteritis should be suspected.
Auscultation and palpation Auscultation of the abdomen can be performed to determine if there is gastrointestinal motility. 451
22
GASTROINTESTINAL DISEASE IN THE FOAL
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.
Examination of the eyes 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 fibrin in the anterior chamber may make the normally brown iris appear green.
OTHER DIAGNOSTIC PROCEDURES Nasogastric intubation Another diagnostic procedure that can be performed on foals of all ages is the passage of a nasogastric tube. Obtaining gastric reflux in the neonate can be difficult, 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 difficult 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 identified. Contrast radiography can be used to identify obstruction of the gastrointestinal tract and/or disrup tion of the u rinary 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 identify 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 fluid is iden tified to decrease the risk of enterocentesis. Ultrasonography can also be used to identify abscesses or enlarged lymph nodes within the gastrointestinal
CLINICAL EVALUATION OF THE FOAL
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 1 00 per cent sensitivity, specificity, 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 findings (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 confirm 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 (4-6 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
22
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 significant 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 heavily 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 nan ts. 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
22
GASTROINTESTINAL DISEASE IN THE FOAL
confirm 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 nificant fluid loss or sequestration. Portable electrolyte units such as the I-Stat, can make electrolyte and blood gas analysis in the field 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 field 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 difficulty 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/ill) 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 confirmed. 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 list 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.
Diagnostic imaging procedures in the foal JM Reimer Ultrasonography of the gastrointestinal tract of the foal is particularly rewarding because of the h igh incidence of small intestinal disorders and the reduced digestive development of the colon in the foal. In contrast to the value of ultrasonography in identifying 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 a,bdomen should be clipped as for exploratory celiotomy. In lieu 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-filled, 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 difficult 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-filled seg ments of intestine will often obscure visualization of
CLINICAL EVALUATION OF THE FOAL
underlying structures. Transducer frequencies in the range of 7.5-5.0 MHz are recommended for evaluation of the gastrointestinal tract of the foal. D epth 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 filled with fluid contents or meconium).
22
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 motility may be difficult 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
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 fluid 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 ingesta 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
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
22
GASTROINTESTINAL DISEASE IN THE FOAL
Figure 22.5 Normal small intestine dorsal to the spleen, as visualized from the ventral abdomen in a neonatal foal
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 22.7 Distended fluid-filled loop of small intestine (amotile in real time) in a foal with ileus due to enteritis
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 22.9 Gas-bubble-Iaden fluid in the colon (long axis view) of a young foal with colitis
456
Figure 22.10 Small intestinal intussusception, short axis view
CLINICAL EVALUATION OF THE FOAL
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 difficult. 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 as hyper motile fluid-filled 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 benefit. 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-filled or edematous intes tine, or intussuscepted intestine; will tend to gravitate to the most dependent area of the abdomen.
Figure
22. 1 1
Meconium
(arrows)
in
a
22
foal with a
meconium impaction. Because meconium may be seen in the intestine normally, the diagnosis of meconium impaction should not be based on the results of ultra sonography alone
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 identified in foals with peri tonitis, uroperitoneum, hemoperitoneum, and transu dates. Effusions due to accumulation of transudate may be identified 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 identified in cases
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 significant pneumoperitoneum. Abdominocentesis should be performed to confirm the type of fluid present as the ultrasound appearance of effusions is not specific. 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
22
GASTROINTESTINAL DISEASE IN THE FOAL
Figure 22. 1 3 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
portability 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 identified 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- 1 5 rnA and 80-120 kVp, with an 8:1 grid, film 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. 1 5 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 of the contrast material
CLIN ICAL EVALUATION OF THE FOAL
22
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 type 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 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
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 An initial step in the physical examination is to take
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 sufficient 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) .
Differential diagnosis and evaluation of the foal with abdominal distention CS Cable 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
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 difficulty 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 difficulty 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
22
GASTROINTESTINAL DISEASE IN THE FOAL
within the rectum and small colon. For identifYing 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.
EXPLORATORY SURGERY
ABDOMINOCENTESIS
NEONATES
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 infiltration. 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. As 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.
Neonatal foals are those within the first 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
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 (6-8) than that refluxed from the stomach which is more acidic. 460
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.
• •
• • • • •
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 firm and dry and often lead to difficulty in passage through the newborn foal's narrow pelvis and rectum. Colts are thought to be more commonly affected than fillies. 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
CLIN ICAL EVALUATION OF THE FOAL
22
retained m econium. Plain radiographs can reveal the retained m econium 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.
can now be tested prior to breeding to determine if they carry 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.
Intestinal atresia (see Chapter 1 6)
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 fillies 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 m any foals will have stranguria or oliguria, foals with defects within the urinary 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 m ay 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 confirmed 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 confirmed 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
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 first 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-specific 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
Uroperitoneum
461
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GASTROINTESTINAL DISEASE IN THE FOAL
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 occur 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 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 importantly 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 in 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 obstruc462
•
• •
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 different 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 typically 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.
CLI NICAL EVALUATION OF THE FOAL
Medical therapy in the foal with abdominal pain G Perkins
22
H ypovolemic shock is suspected when the following are observed • • • •
decreased distensibility of the j ugular vein prolonged capillary refill time cold extremities increased heart rate decreased pulse pressure decreased skin turgor.
INTRODUCTION
•
This section provides a general guide to the medical management of a foal with colic. The goals of medical therapy are to
Increases in the packed cell volume and total protein are indicators of dehydration but are not specific. Azotemia, 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 beneficial in the management of colic in foals and adult horses. Calculations for fluid volume are
• • • • • •
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 persists.
Treatment for gastric ulceration is covered elsewhere
(see Chapter 23) . Foals are more likely to show signs o f colic with en teritis 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) .
•
volume deficit
ongoing losses
=
=
x
(body weight (kg»
(60 - 1 20 ml x (body weight (kg»
(estimated volume)
per day plus
=
(liters) to be given over 1 day The electrolyte abnormalities most commonly encountered with gastrointestinal disease in the foal include
•
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
(% dehydration)
maintenance fluids
•
FLUID THERAPY
=
• • •
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 deficit (base deficit) deficit (mEq)
x
(0.4)
x
(body weight (kg»
=
HC03
or • • • • •
decreased skin turgor dry mucous membranes decreased urinary output sunken eyes muscle weakness.
(normal HC03 - measured HC03) x (0.4) (body weight (kg» HC03 deficit (mEq)
x
=
One half of the deficit should be replaced over 1-4 hours and the remainder over the following 463
22
GASTROI NTESTINAL DISEASE IN THE FOAL
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 deficit 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 (O. l IU /kg regular insulin i.v.) can also be used but is generally 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 En teral nutrition III 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 fun ction. 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
1 00 kcal/kg/d 100 kcal x 50 kg 5000 kcal
=
Non-nitrogen calorie distribution 40% dextrose = 2000 kcal dextrose 60% lipid = 3000 kcal lipid
fr21iln A. Ratio of 300 non-nitrogen cal/g of nitrogen 5000 total daily kcal / 300 (ratio) = 1 6. 5 9 nitrogen
B. C.
16.5 9 nitrogenl16% nitrogen in protein = 1 00 9 protein Example to determine volume of an amino 8.4% acid solution: 100g nitrogen/0.084 a m i no acid solution = 1 1 76.5 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
CLIN ICAL EVALUATION OF T H E FOAL
decreasing inflammation that is causing ileus. Non steroidal anti-inflammatory drugs (NSAIDs) can be of benefit but should be used judiciously because of the ulcerogenic effects 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 difficult 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.
22
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 H2blocker, has also been shown to have effects on gas trointestinal motility and positive effects on gastric emptying disorders. Ranitidine w.ould be a wise choice since it is also useful in treating gastric ulceration. An 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.
Surgical decision for the foal with colic CS Cable INTRODUCTION Foals with colic are challenging cases to manage. Often the most difficult 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
22
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 difficult. 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 As 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 surgery 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 difficult 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 severity of distension can be monitored by repeat edly measuring around the foal' s abdomen at specific points with a tape to detect changes. Foals with severe abdominal distension can have great difficulty 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 difficult 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 identify 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 identify bacterial enteritis, especially if an overwhelming population of one type of bacteria is found. Foals tend to be more sensitive to gastrointestinal pain than adults, and this makes it difficult 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 As 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
CLIN ICAL EVALUATION OF THE FOAL
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 identifying 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 1 500-3000/111 ( 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 specific 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 identify problems with the oral cavity, 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 identify lesions of the car dia, stomach (e.g. gastric ulcers) , or duodenal stric tures. Barium administered via an enema can help identify lesions of the rectum, small colon, and even
22
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 identified 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. I mproved 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 ( 1 995) Assessing the history, signalment, and examination findings in foals with colic. Vet. Med. 8:765-9. Chaffin M K, Cohen N D ( 1 995) Diagnostic tests and procedures in foals with colic. Vet. Med. 8:770-6. Cohen N D, Chaffin M K ( 1 995) Assessment and initial management of colic in foals. Compo Cont. Educ. Pract. Vet. 1 7 ( 1 ) :93-102. Cudd T A ( 1 990) Evaluation of acute abdominal pain. In Equine Clinical Neonatology, A M Koterba, W H Drummond, P C Kosch (eds. ) . Lea and Febiger, Philadelphia, pp. 367-78. Cudd T A, Wilson ] H ( 1 990) 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.
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GASTROINTESTINAL DISEASE I N THE FOAL
Klohnen A, Vachon A M, Fisher A T ( 1996) Use of diagnostic ultrasonography in horses with signs of acute abdominal pain.] Am. Vet. Med. Assoc. 209 ( 9 ) : 1597-160 1 . Koterba A M ( 1 990) Physical examination. I n A M Koterba, W H Drummond, P C Kosch (eds.) Equine Clinical Neonatology, Lea and Febiger, Philadelphia, pp 71-83. Murray M] ( 1 997) Foal stomach and duodenum. In Equine Endoscopy] L Traub-Dargatz, C M Brown (eds.) 2nd edn. Mosby, Baltimore, pp 159-7 1 . Orsini,] A ( 1 997) Abdominal surgery i n foals. Vet. Clin. North Am. Equine Pract. 1 3 ( 2) :393-413.
Diagnostic imaging procedures in the foal Fisher A T, Yarbrough T Y ( 1 995) 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 Ultrasound, WB Saunders, Philadelphia, pp. 364-403. Reimer] M and Bernard W V ( 1 998) 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 Ultrasonography. Mosby, St Louis, pp. 200-1 1 .
Differential diagnosis and evaluation of the foal with abdominal distension Benamou A E, Blikslager A T, Sellon D C ( 1 995) Intestinal atresia in foals. Compo Cont. Educ. Pract. Vet. 1 7 ( 1 2 ) : 1 5 10-16. Chaffin M K, Cohen N D ( 1995) Assessing the history, signalment and examination findings in foals with colic. Vet. Med. 8:765-776. Cohen N D, Chaffin M K ( 1 994) Intestinal obstruction and other causes of abdominal pain in foals. Compo Cont. Educ. Pract. Vet. 1 6 (6) :780-90. Cohen N D, Chaffin 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 ( 1 995) 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, Chaffin M K ( 1 995) Assessment and initial management of colic in foals. Compo Cont. Educ. Pract. Vet. 1 7 ( 1 ) :93-103. MacAllister C G, Morgan S], Borne A T, Pollet R A ( 1 993) Comparison of adverse effects of phenylbutazone, flunixin meglumine and ketoprofen in horses. ] Am. Vet. Med. Assoc. 202 ( 1 ) :71-7. Spurlock S L, Ward M V ( 1 99 1 ) Parenteral nutrition in equine patients: principles and theory. Compo Cont. Educ. Pract. Vet., 1 3 (3) :461-8. Vaala W E ( 1 998) Neonatology. In Manual o/Equine Emergencies: Treatment and Procedures,] A Orsini, T] Divers (eds ) . W B Saunders, Philadelphia, pp. 473-503.
Surgical decision for the foal with colic Bernard W V ( 1 992) Differentiating enteritis and conditions that require surgery in foals. Compo Cont. Educ. Pract. Vet. 14: 535-7. Cable C S, Fubini S L, Erb H N et aL ( 1 996) Abdominal surgery in foals: a review of 1 19 cases ( 1 977-1994) . Equine Vet. ] 29(4) :257-6 1 . Klohnen A , Vachon A M, Fisher A T ( 1 996) Use of diagnostic ultrasonography in horses with signs of acute abdominal pain. ] Am. Vet. Med. Assoc. 209(9) : 1 597-60 1 . Orsini,] A ( 1 997) Abdominal surgery i n foals. Vet. Clin. N. Am. Equine Pract. 1 3 (2) :393-4 13. Ragle C A ( 1 999) The acute abdomen: diagnosis, preoperative management and surgical approaches. In Equine Surgery, ] A Auer. and] A Stick (eds) : 2nd edn WB Saunders, Philadelphia, p 224-32. Vatistas N ], Snyder] R, Wilson W D ( 1996) Surgical treatment for colic in the foal (67 cases) : 1980-1992. Equine Vet. ] 28 ( 2 ) : 1 39-45.
23 Stomach diseases of the foal MJ Murray
Gastroduodenal ulceration
and prevention of gastroduodenal ulcers in foals have changed.
INTRODUCTION
ETIOPATHOGENESIS
There are many similarities between gastric ulceration in foals and adult horses, but there are also important differences
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 stratified 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 stratified. In the last month of gestation the basal layers of the squamous mucosa become more numer ous, epithelial cells become flattened and stratified, and a superficial 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 superficial 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
• •
•
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 affecting the esophagus, stomach, and duodenum have been recognized as important conditions in foals for many years. In a 1964 report of post-mortem findings of severely ulcerated stomachs from foals, the author suggested that lesions might have resulted from Gasterophilus 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 findings, and methods of treatment
469
23
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 acidification 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 i�ury, 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 observed 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 superficial 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 insufficiencies 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 identified 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 susceptibility 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.
ULCER SYNDROMES 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 duode-
STOMACH DISEASES OF THE FOAL
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.
23
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 benefit these foals. Duodenal ulceration and duodenitis
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 sufficient 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.
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 confined to the duodenum. Gastric ulceration, and often esophagitis, accompanies duodenal ulceration, because of impaired gastric emptying. In fact, presenting signs often appear to relate more to complications of duodenal ulceration rather than the duodenal disease itself. Duodenal ulceration can be difficult to confirm 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 specific 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.
Sudden onset severe gastric ulcers
Gastric outlet obstruction or pseudo obstruction
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, typically in the gastric antrum and at the pylorus (Plate 23.3), but also in the gastric squamous mucosa. It is
Gastric emptying results from coordinated myoelectric activity that originates in the gastric antrum and is propagated toward the pylorus and into the proximal duodenum. Inflammation, erosion, and ulceration affecting the pylorus or duodenum can impair gastric emptying and cause pseudo-obstruction. Fibrosis may 471
23
GASTROINTESTINAL DISEASE IN THE FOAL
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 fibrosis and stricture (Plate 23.5), the long-term prognosis is less favorable. Signs associated with impaired gastric emptying include • • • • • •
poor appetite abdominal discomfort belching poor body condition spontaneous nasal reflux of gastric contents ptyalism (secondary to esophagitis).
If impaired gastric emptying 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. 6-8 h initially, then 0.35 mg/kg p.o., q. 8 h. If impaired emptying 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 fibrinous 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 fibrin clots within the omentum. Careful inspection of a Wright's or gram stained slide for bacteria may confirm a perforated vis cus. Occasionally, a perforation in the stomach or in the duodenal ampulla will be sealed by the greater omen472
tum. In these cases there will be evidence of peritonitis (fever, shock, peripheral blood leukocytosis or leuko penia, hyperfibrinogenemia, 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 • • • • • • •
•
abdominal discomfort poor nursing bruxism dorsal recumbency depression ptyalism 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 specific 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-specific 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.
DIAGNOSIS Although the clinical signs described for gastroduode nal ulceration in foals may be non-specific 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
STOMACH DISEASES OF THE FOAL
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, urine 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 .or 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 fibrinous 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.
23
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 sufficient to alleviate pain, but insufficient to facilitate healing. In such cases, there can be a false belief in treatment success, only to have catastrophic complications develop later.
TREATMENT (Tables 23.1. 23.2) 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. As with adult horses, misoprostol can cause abdominal discomfort and diarrhea in foals, and 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
23
GASTROINTESTINAL DISEASE IN THE FOAL
T,b" U.1
Typical tre.tmlmw':us�ln ttl.mlldlcal
man.rUnt of g��� ulctl'atlon.lnfOJls
Tlble�34 �nttnued Scenario 3: Foal is not nursing well, it has frequent mild
Recommended
Drug (size)
dosage
abdominal discomfort, and is lethargic. Physical examination and results of minimum database are within normal limits. Endoscopy reveals extensive erosion and ulceration of the gastric squamous mucosa, ulceration in
Antacid MaaloxTC
240 ml (8 oz.), q. 4 h
Mylanta double strength
240 ml (8 oz.), q. 2 h
(150 mg/ml) Ranitidine (300 mg tablets)
mucosa at the pylorus. Treatment recommendation
H2antagonist Cimetidine (800 mg tablets)
the glandular mucosa of the antrum, and hyperemia of the
duration
25 mg/kg p.o., q. 8 h 7 mg/kg Lv., q. 6-8 h 7 mg/kg p.o., q. 8 h 1.5 mg/kg Lv., q. 8 h
(25 mg/ml)
Initial treatment • •
Proton pump inhibitor 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)
cimetidine, 7 mg/kg Lv., q. 6 h, or
ranitidine, 1.5 mg/kg Lv., q. 8 h, and bethanecol, 0.02 mg/kg s.c., q. 8 h
•
•
omeprazole paste, 4 mg/kg s.i.d. or
Mucosal protectant 10-20 mglkg p.o., q. 8 h 1.51J9/kg p.o., q. 8-12 h
ingests feed
•
3 weeks
•
3 weeks
ranitidine, 7 mglkg p.o., q. 8 h, and
sucralfate, 10-20 mg/kg p.o., q. 8 h, and
Misoprostol (200 IJg tablets)
2-4 days, until foal nurses or
Subsequent treatment
bethanecol, 0.35 mglkg p.o., q. 8 h Sucralfate (1 9 tablets)
Treatment
10-21 days Repeat endoscopy
•
after treatment
up to 2.5 IJg/kg p.o.,
Scenario 4: Foal is presented because of depression and mild
q. 8 h
abdominal discomfort. Physical examination reveals signs of
Bethanecol (5.15 mg/ml)
0.02 mg/kg s.c., q. 6-8 h
fluid with the appearance of increased neutrophils and a
Bethanecol (50 mg tablets)
0.35 mg/kg p.o., q. 8 h
cardiovascular shock and fever. CBC reveals leukopenia and mild anemia. Peritoneal centesis yields a small volume of
Motility modifier
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 contractility the endoscope cannot
TJIjIt al�a. GllideliMs fOI'ti1emedlcal """___t of IastrOduOi:!tn.' !.Iletl'S in fOJls, fQ!.Ir
be advanced into the duodenum.
.
dlfft_dl�c1Isca�· . .
.
Scenario 1: Foal has mild signs of diminished nursing, occasional mild abdominal discomfort, mild lethargy. Physical examination and results of minimum database are within normal limits. Endoscopy not done. Treatment recommendation
• • •
omeprazole paste, 4 mg/kg, s.Ld., or ranitidine, 7 mg/kg p.o., q. 8 h, or cimetidine, 25 mglkg p.o., q. 6 h
Treatment recommendation
Treatment duration •
2-3 weeks
•
2-3 weeks
•
2-3 weeks
Initial treatment •
cimetidine, 7 mg/kg Lv., q. 6 h. or
•
ranltidine, 1.5 mg/kg Lv., q. 8 h, and
4-7 days, until foal nurses or
bethanecol, 0.02 mg/kg s.c., q. 8 h
ingests feed
Subsequent treatment •
omeprazole paste, 4 mg/kg s.Ld. or
•
ranltldlne, 7 mg/kg p.o., q. 8 h, and
Repeat endoscopy after 4-7 days, then every 7-14 days Associated treatment 2-4 weeks
•
broad spectrum antimicrobial treatment anti-Inflammatory therapy
•
Treatment
•
as needed
duration
•
intravenous fluid support
•
•
intravenous nutritional support
•
•
Treatment recommendation
• •
474
omeprazole paste, 4 mg/kg s.i.d., or ranitidine, 7 mg/kg p.o., q. 8 h, and sucralfate, 10-20 mg/kg p.o., q. 8 h
3-12 weeks
sucralfate, 10-20 mg/kg p.o., q. 8 h, and 3-4 weeks bethaneco.l, 0.35 mg/kg p.o., q. 8 h 3-12 weeks
Scenario 2: Foal is not nursing well, it has frequent mild abdominal discomfort, and is lethargic. Physical examination and results of minimum database are within normal limits. Endoscopy not done.
Treatment duration
.
•
3-4 weeks
•
3-4 weeks
as needed while foal is nil per os
STOMACH DISEASES OF THE FOAL
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 4--6 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.
PREVENTION 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. 6-8 h, or ranitidine 7 mg/kg p.o., q. 8 h. Use of a mucosal protectant such as 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 affect the foal's milk or
23
feed intake, and thus contribute to ulcer formation in individual animals.
Gastric endoparasitism MJ Murray Endoparasitism of the stomach of foals is relatively uncommon because modern anthelmintics and para site control programs are highly effective against para sitic species that may infect the stomach. Gasterophilus spp. ( G. intestinalis, G. nasalis, and G. haemorrhoidalis) are the most common gastric endoparasites, but occasion ally infection with spirurid nematodes (Draschia mega stoma, Habronema muscae, H. majus) and the minute worm (Trichostrongylus axei) occur.
GASTEROPHILUS SPP. 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 larvae make a small defect in the mucosa, but even with a large number of larvae 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
23
GASTROINTESTINAL DISEASE IN THE FOAL
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 definitive 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 24-48 hours of treat ment. The benzimadazole and pyrimidine anthelmintics are ineffective in eliminating Gasterophilus larvae.
Gastric abscess MJ Murray Abscessation in the wall of the stomach is an infrequent finding. 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 hyperfibrinogenemia 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.
SPIRURID NEMATODES The spirurid nematodes that can infect the equine stomach are Draschia 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.
MINUTE STOMACH WORM Typically, infection with Trichostrongylus axei is light and causes no clinical problem. The larvae 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 effectively eliminated by the benzimadazole anthelmintics and ivermectin.
476
BIBLIOGRAPHY 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. Proc. Am. Assoc. Equine Pract. 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.Proc. Second Equine Colic Res. Symp. pp.126-8.
Gastric endoparasitism Drudge] H, Lyons E T (1986) Internal parasites 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 definitive, diagnos tic information in the adult horse but is not generally feasible in the foal because of its small size. It therefore can be difficult to distinguish medical from surgical cases of colic. Frequently a 'watch and wait' or 'medical treatment first' 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 configuration 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 figure-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 superficial 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 hernial sac, its reducibility, and the nature of the tissue surrounding the ring. A thickened fibrotic 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 fistula. 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, firm, 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 identified, 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 fistula is involved, special care should be taken to clean the fis tula and isolate it from the surgical field 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. As 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 volvulus 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 3month-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
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 acljacent mesentery to rupture. Chyloabdomen
Figure 24.3 A large Meckel's diverticulum with a diameter equal to that of the small intestine
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
24
GASTROINTESTINAL DISEASE IN THE FOAL
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-specific, 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 fibrinogen 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 difficult to docu ment. There can sometimes be an outbreak of duo denal ulcers in a herd. Ulcers with outflow obstruction can be difficult to confirm by contrast radiography. Diagnostic signs on plain radiographic films include aspiration pneumonia, dilated fluid-filled esophagus, and gastric distension; gas may be present in the hepatic duct. Endoscopy is more sensitive and specific 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
SMALLINTESTINAL DISEASES ASSOCIATED WITH COLIC IN THE FOAL
24
Small intestinal impaction Ascarid impaction (see Chapter 13)
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. As 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. After correcting the volvulus, resection and anastomosis can be p t;:rformed.
Intestinal stages of Parascaris 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 firm 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 5month-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
24
GASTROINTESTINAL DISEASE IN THE FOAL
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 difficult 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.
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 Ultrasonography, W B Saunders, Philadelphia, with permission
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 identify 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 Iow a 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 unthrifty and 482
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 Ultrasonography, W B Saunders, Philadelphia, with 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.
SMALLINTESTINAL DISEASES ASSOCIATED WITH COLIC IN THE FOAL
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
24
6 weeks of age. Foals with mesenteric abscesses (Streptococcus spp. and Rhodococcus 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 hyperfib 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 significant 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
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
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 significantly worse than survival rates of adults. 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 1month-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 survival is about 40 per cent, similar to the reported long-term survival of older horses undergoing colic surgery (45 per cent) . As 483
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GASTROINTESTINAL DISEASE IN THE FOAL
expected, colic surgery survival rates vary widely accord ing to the diagnosis, the compromised condition of many surgical colic patients is also a significant 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 difficult to distinguish medical from surgical cases of colic. Frequently a 'watch and wait' or 'medical treatment first' approach can carry as much risk as exploratory surgery.
Hooper R N (1989) Small intestinal strangulation caused by Meckel's diverticulum in a horse.]. 194(7):943-4.
Am. Vet. Med. Assoc.
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).]. Vet. Med. Assoc. 190:692-4. OrsiniJ A (1997) Abdominal surgery in foals.
Equine Pract.
BIBLIOGRAPHY
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 urn hilical hernias 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
484
Vet. Clin. N. Am.
13(2) :393-413.
Priester W A, Glass M D, Waggoner, N S (1970) Congenital
Crowe M W, Swerczek T W (1985) Equine congenital defects. Am.]. Vet. Res. 46(2): 353-8.
a hospital population.
Am.
Am.]. Vet. Res. 52:637-9.
defects in domesticated animals: general considerations. Am.] Vet. Res. 31:1871-9. RobertsonJ T (1982) Obstructive diseases - congenital diseases. In:
Equine Medicine and Surgery 3rd edn,
RA
Mansmann, E S McAllister, P W Pratt (eds). American
Veterinary Publications, Santa Barbara, CA, 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 20:178-81.
Vet.].
YovichJ V, Horney F D (1983) Congenital jejunal diverticulum in a foal.]. Am. Vet. Med. Assoc. 183:1092.
25 Large and small colon diseases associated with colic in the foal
WV Bernard
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.
INTRODUCTION
Clinical signs
Retained meconium
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 first 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 first 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 fied 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
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
25
GASTROINTESTINAL DISEASE IN THE FOAL
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 specific, and other differentials of abdominal pain should be considered.
DIAGNOSIS Diagnosis of the condition is based upon clinical signs, physical examination findings, and other diagnostic testing. Digital examination can identifY 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 identifY gastric reflux, and peritoneal fluid analysis may be use ful in ruling out other causes of abdominal pain. Abdominal ultrasound can be used to identifY 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 identifY meconium and/or gas distension of the small or large intestine. Contrast radiography (barium enema), can be very useful if other diagnostics are not definitive. 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 soft, 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. So�t 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 beneficial 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 beneficial 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.
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
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-filled intestinal segments.
CLINICAL PATHOLOGY There are no pathognomonic pre-mortem tests for atre sia coli. As 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, fluid, and gas, and the rectal segment is usually atretic (Figure 25.2). Other congenital abnormalities of the cardiac
present in this foal.
and central nervous system have been reported in foals affected with atresia coli, and may be discovered on post-mortem examination.
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 majority 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. Confirmation 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
25
GASTROINTESTINAL DISEASE IN THE FOAL
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 monofilament 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 first 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 theOvero 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 ofOvero 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 two alleles of a specific mutation in the gene that codes for endothelin receptor B. Allele-specific 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 first transmembrane domain of the seven transmembrane domain g-protein coupled receptor. This alteration in the protein composition is thought to be sufficient 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
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. As the foal becomes moribund, alterations in blood clinical chemistry and hematological parameters can be seen, presumably because of dehydration and endotoxemia.
PATHOLOGY
25
DIAGNOSIS Confirmation 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.
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).
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 HISTOPATHOLOGY Myenteric ganglia are absent in the ileum, cecum, and colon of affected foals.
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 Surgery, 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
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.
207:734-7. (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. foals.] Am. Vet. Med. Assoc.
Nappert G, Laverty S, Drolet R, Naylor]
489
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GASTROINTESTINAL DISEASE IN THE FOAL
Ileocolonic aganglionosis Gariepy C E, Cass D T, Yanagisawa M
progeny of overo spotted horses. J. Am. Vet. Med. Assoc.
(1996)
Null mutation of
endothelin receptor B gene in spotting lethal rats causes aganglionic megacolon and white coat color. Proc. Nat.
Acad. Sci.
93:867-72. (1982) Ileocolonic aganglionosis in white
Hultgren B D
490
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.
Gen.
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
27
GASTROINTESTINAL DISEASE IN THE FOAL
being immunologically naive. The causative or associ ated viruses include • • • • • • •
equine herpesvirus Type-l (EHV-l) adenovirus coronavirus equine viral arteritis (EVA) rotavirus parvovirus viral infections that have not been completely identified 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 sacrifice to confirm a diagnosis may be elected, foals represent a population of companion animals where viral infections may be sus pected but not confirmed, since the time involved in treatment can compromise ante-mortem diagnosis and post-mortem viral isolation. Koch's postulates are rarely documented in identifYing 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 difficult 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 prokinetics 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 findings, electrolyte and acid-base imbal ances, and clinical signs. Oral supplementation should include access to fresh and electrolyte water, and a salt block. Potassium deficits 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 benefit 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 efficacy. Analgesic use in viral diarrheas should emphasize the discriminating use of ulcerogenic non-steroidal anti-inflammatory drugs
DIARRHEA IN THE FOAL
(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 specific 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 deficient. 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 efficacy of this treatment remains unproven. A commercial modified 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-
27
tion of new clinical cases. Viral particles were noted on fecal electron microscopy without a definitive identifi 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 severity.
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, Escherichia coli, Streptococcus 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 significance 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 gastrointesti495
27
GASTROINTESTINAL DISEASE IN THE FOAL
nal tract via the fecal-oral route. The bacteria must combat a number of non-specific 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 fimbriae 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 variety 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 Congested mucous membranes Prolonged capillary refill time Diarrhea
DIARRHEA IN THE FOAL
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.
27
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.
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.
An inversion of the neutrophil:lymphocyte ratio can indicate sepsis. A rebound neutrophilic leukocytosis
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
27
GASTROINTESTINAL DISEASE IN THE FOAL
than in adult horses) . A minimum of three to five 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 Dextrose Partial or total parenteral nutrition Antibiotics Polymyxin B Flunixin meglumine Pentoxifylline Bismuth subsalicylate Activated charcoal Live yogurt Anti-ulcer 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 containing Hyperimmune plasma patient. 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. Pentoxifylline (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 toxifylline increases red blood cell deformability,
DIARRHEA IN THE FOAL
decreases blood viscosity, 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 beneficial 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 10 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 first 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 immunity 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
27
because of sequestering of IgG within the intravascular space or at sites of inflammation, and can benefit 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 difficult. Animals identified 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 five 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
Clostridium perfringens 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 sufficient 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 first week of life. C. perfringens type C produces a beta toxin which causes severe intestinal necrosis and hem orrhagic diarrhea. As 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 unconfirmed, exposure to the organism may be via the mare rather than environmen tal contamination. 499
27
GASTROINTESTINAL DISEASE IN THE FOAL
Clostridium peifringens type A has been incriminated as a cause of diarrhea in foals of all ages. Proof of the relationship between C. perfringens type A in the foal's stool, and diarrhea in foals has been difficult. As in adult horses, C. peifringens 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. perfringens type A from non-pathogenic strains. C. perfringens type A enterotoxin and/or its enterotoxin gene can be found in both normal and diseased foals. C. perfringens type A may cause diarrhea in foals, but more research is needed to prove cause and effect. A similar situation exists with C. dijjicile and its relationship to foal diar rhea. C. dijjicile 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. dijjicile diarrhea. Proving cause and effect has been dif ficult since normal foals may have both C. dijjicile and its toxin in their stool. This situation is also well-known in children. It may be that C. dijjicile 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 Cryptosporidium spp., Bacteroides fragilis, rotavirus type A, or a virus similar to rotavirus but smaller than type A.
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 Clostridium spp. culture (anaerobic media) and toxin assay (c. diffi cile toxin A and B, and C. peifringens 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. peifringens organisms in the feces may be helpful in determining significance, 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. perfringens (> 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
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. Clostridium perfringens type C generally causes a hemorrhagic enteritis with blood-stained diarrhea (Plate 27. 1 ) . Diarrhea associated with C. dijjicile or C. perfringens 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 rnA with rare earth 500
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
DIARRHEA IN THE FOAL
a large number of gram-positive rods. Spores are more commonly seen with C. difficile and the organism can often be more curved in appearance and have a darker gram-positive stain than C. perfringens. Genotyping would be needed to determine C. perfringens type (A-E) . Blood cultures should be performed on young foals « I week of age) with diarrhea as C. perfringens 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 fluids. If the foal appears weak add 10 g dextrose/I unless the blood glucose concentration is normal. If the
27
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). Clostridium perfringens 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-lg 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
Analgesics
-
dipyrone butorphanol
- flunixin meglumine Neostigmine Lactated Ringer's solution Potassium chloride Dextrose Sodium bicarbonate Plasma Dobutamine Antibiotics H2-blockers -
penicillin amikacin metronidazole ranitidine famotidine
Pepto bismol/yogurt
The prognosis with Clostridium perfringens 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 fluid. Less severely affected cases respond dramatically to treatment and may appear normal within 2-3 days. C. difficile and C. perfrin 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 significant problems in a few foals.
CONTROL
Clostridium perfringens type C diarrhea is often an iso lated event on a farm requiring few control measures. 501
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GASTROINTESTINAL DISEASE IN THE FOAL
Cleaning the mare's udder prior to the foal nursing may be the most appropriate control measure and should be routinely recommended. C. perfringens type 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. difficile 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 efficacy is not proven. Hospitalized foals, either with or without diarrhea may be shedding C. difficile 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 amplification 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 Corynebacterium, the organism was reclassified 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 IS 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. tuberculosis) 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 infiltration.
EPIDEMIOLOGY AND PATHOGENESIS Because the bacterium resides endemically in types 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 identifying 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.
DIARRHEA IN THE FOAL
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 RJwdococcus. 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 significant amplification 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 Rhodowccus 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
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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 atypical 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 Rhodococcus 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 Rhodococcus equi may include several manifestations. Enterocolitis in the form of diffuse infiltration 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 infiltrate can be seen to fill the lam ina propria, distort villi, and displace intestinal glands and crypts. These areas of granulomatous infiltrate 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 firm. 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 identifYing clinically affected foals. 503
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GASTROINTESTINAL DISEASE IN THE FOAL
In the intestinal form of infection, it is likely that
Rhodococcus 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 variety 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.
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 Rhodococcus 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 Rhodococcus 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.
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 two 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 dis504
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 Cryptosporidium parvum is being increasingly recog nized. The purpose of this chapter is to review the epidemiology, clinical signs, diagnosis, treatment, and prevention of C. parvum infection in horses.
DIARRHEA IN THE FOAL
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 a t breeding farms may b e 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 2day-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.
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Immune status Immunocompromised foals, such as those with severe combined immunodeficiency 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 vary 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 affected. 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
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GASTROINTESTINAL DISEASE IN THE FOAL
distinguishing oocysts from yeast is an important diag nostic issue. In veterinary diagnostic laboratories, three tech niques are commonly used • • •
flotation of oocysts 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 (4-6 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 specificity making it a poor choice for a screening test. However, it is useful clinically as a diagnostic test because of its good sensi tivity, availability, 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 specific 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 Cryptosporidium parvum. Paromomycin was effective in treating a cat with cryptosporidiosis. Doses used in calves have ranged from 50-100 mg/kg administered orally once or twice daily. No data exist for the use of this drug in foals. Adverse effects of paromomycin in humans include diarrhea, nausea, and abdominal cramps. As for all other agents used to treat cryptosporidial infection, experimental and clinical evidence also exists indicat ing a lack of effectiveness 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 efits 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 deficiency 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 difficult. 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
DIARRHEA IN THE FOAL
27
extremes of temperature or desiccation. Oocysts can be killed by steam, 1 0 % formalin, 5% ammonia, and undi luted commercial bleach, although prolonged expo sure is necessary which can be difficult to achieve. Good sanitation may help by decreasing the oocyst burden in the foals' environment. Specific 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.
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.
ZOONOTIC CONSIDERATIONS
SEPTICEMIA
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 immunodeficiency 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 is a common clinical sign in the septicemic foal. Septicemia usually develops in the first 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 Escherichia coli, Actinobacillus spp., Klebsiella pneumoniae, and Streptococcus 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.
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. Erythromycin is widely used in combina-
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
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GASTROINTESTINAL DISEASE IN THE FOAL
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 effective in removing the sand and dirt.
EQUINE HERPESVIRUS __�_�_Wil*�I#lI**WA"'�»lIi!lfW"_;{'"",'��ty"'*'_ 'lli
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.
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 infections 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 severity 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
CANDIDIASIS J-P Lavoie and R Drolet
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. As 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
Strongyloides 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 estab508
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 classified as Lawsonia intracellularis, 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 4-7 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.
DIARRHEA IN THE FOAL
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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 Rhodococcus 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 identifying 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 intracellu laris 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 sensitivity in horses. The use of serology for the diagnosis of Lawsonia intracellularis 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 o f 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.
BIBLIOGRAPHY Foal heat d iarrhea Becht] L, Semrad S D ( 1 986) Gastrointestinal diseases of foals. Compo Cont. Educ. Pract. Vet. 8 ( 7 ) : S367-S374. Masri M D, Merritt A M, Gronwall R, Burrows C F ( 1 986) Fecal composition in foal heat diarrhea. Equine Vet. J
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Viral d iarrhea Cohen N ( 1 997) Diarrheal diseases of foals. In: Current
Therapy in Equine Medicine 4th edn, N Robinson (ed. ) , W B Saunders, Philadelphia, p. 631. Fenger C ( 1 998) Neonatal and perinatal diseases. In: Equine Internal Medicine, S Reed and W Bayly (eds). W B Saunders, Philadelphia, pp. 962-3. Smith B ( 1996) Diarrhea. In: Large Animal Internal Medicine 2nd edn, B P Smith (ed. ) . C V Mosby, St Louis, pp . 1l9-123 .
Salmonellosis in the foal Clarke R C, Gyles C L ( 1993) Salmonella. In: Pathogenesis oj
Bacterial Injections in Animals, 2nd edn, C L Gyles and C 0 Thoen (eds). Iowa State University Press, Ames, lA,
pp. 133-53. Jones S L, Spier SJ ( 1 998) Inflammatory diseases of the large intestine causing diarrhea. In: Equine Internal Medicine. S M Reed and W M Bayly (eds) . Philadelphia, W B Saunders, Philadelphia, pp. 663-7. Kowalski J ]. Bacterial and mycotic infections. In: Equine
Internal Medicine. S M Reed and W M Bayly (eds ) . Philadelphia, W B Saunders, Philadelphia, p p . 68-70. Madigan J E ( 199 1 ) Neonatal salmonellosis. In: Manual oJ
Equine Neonatal Medicine, 2ndedn , J E Madigan (ed. ) . Live Oak Publishing, Woodland, CA; pp. 133-5. Madigan J E ( 1 995) Diarrhea in neonatal foals. In: Large Animal internal Medicine, 2nd edn, B P Smith (ed . ) . Mosby Year Book, St Louis, MO; pp. 391-4. Spier S J ( 1993) Salmonellosis. Vet. Clin. N. Am. Equine Pract.; 9:2 385-7. Vaala W E ( 1 996) Failure of passive-transfer: diagnosis, treatment and prevention. In: Proceedings oj Equine Stud Medicine. Post Graduate Foundation of Veterinary Science, University of Sydney, Sydney, Australia; pp. 3 1-8. Vaala W E ( 1 996) Neonatal foal diarrhea. In: Proceedings oj Equine Stud Medicine. Post Graduate Foundation of Veterinary Science, University of Sydney, Sydney, Australia; pp. 133-5. Vaala W E ( 1 996) Neonatal septicemia. In: Proceedings oJEquine Stud Medicine. Post Graduate Foundation of Veterinary Science. University of Sydney, Sydney, Australia; pp. 21 1-18.
Clostridial enterocolitis i n foals East L M, Savage CJ, Traub-DargatzJ L et at. ( 1 998) Enterocolitis associated with Clostridium perJringens infection in neonatal foals: 54 cases ( 1 988-1997) . J Am.
Vet. Med. Assoc. 2 1 2 ( 1 1 ) : 1 751-6. Meer R R, Songer J G ( 1997) Multiplex polymerase chain reaction assay for genotyping Clostridium perJringens. Am.J
Vet. Res. 58(7):702-5. Netherwood T, Binns M, Townsend H et at. ( 1998) The Clostridium perfringens enterotoxin from equine isolates; its characterization, sequence and role in foal diarrhea.
Epidemiol. Inject. 120:193-200.
Rhodococcus equi as an agent of intestinal disease Anzai T et at. ( 1 997) Comparison of tracheal aspiration with other tests for diagnosis of Rhodococcus equi pneumonia in foals. Vet. Microbiol. 56(3-4 ) : 335-45. Barton M D, Hughes K L ( 1 984) Ecology of Rhodococcus equi.
Vet. Microbioi.; 9:65-76. 510
Brumbaugh G W, Davis L E , Thurman J C , et al. ( 1990) Influence of Rhodococcus equi o n the respiratory burst of resident alveolar macrophages from adult horses. Am. J
Vet. Res.; 5 1 : 766-71 . Giguere S , PrescottJ F ( 1 997) Strategies for the control of
Rhodococcus equi infections on enzootic farms. Proc. Am. Assoc. Equine Pract.; (43) :65-70. Hondalus M K ( 1 997) Rhodococcus equi: Pathogenesis and virulence. Proc. Am. Assoc. Equine Pract. ; 43:71-8. PrescottJ F, Hoffman A M ( 1 993) Rhodococcus equi, Vet. Clin. N. Am. Equine Pract.; 9 (2) :375-84. PrescottJ F et al. ( 1 996) Use of a virulence-associated protein based ELISA for Rhodococcus equi serology in horses. Equine Vet.J 28(5) : 344-9. Takai S et al. ( 1 986) Quantitative fecal culture for early diagnosis of Corynebacterium (Rhodococcus) equi enteritis in foals. Can. J Vet. Res.; 50 (4) :479-84. Tizard I ( 1 996) Immunity at body surfaces. In: Veterinary Immunology 5th edn, I R Tizard ( ed . ) . W B Saunders, Philadelphia, pp. 254-55. Zink M C, YagerJ A, Smart N L ( 1 986) Corynebacterium equi infections in horses, 1958-1984: a review of 1 3 1 cases. Can. J Vet. Res. 27:213. Zink M C, Yager J A, Prescott J F et al. ( 1 987) Electron microscopic investigation of intracellular events after ingestion of Rhodococcus equi by foal alveolar macrophages.
Vet. Microbiol.; 14:295-305.
Equine cryptosporidial d iarrhea Cohen N D, Snowden K ( 1 996) Cryptosporidial diarrhea in foals. Comp. Cont. Educ. Pract. Vet. 18:298-306. Cole D J, Cohen N D, Snowden K, Smith R ( 1 998) Prevalence and risk factors for fecal shedding of Cryptosporidium parvum oocysts in horses. J Am. Vet. Med. Assoc. 2 1 3: 1 296-1 302. Cole D j, Snowden K, Cohen N D , Smith R ( 1 999) Detection of Cryptosporidium parvum in horses: thresholds of acid-fast stain, immunofluorescence assay, and flow cytometry. J
Clin. Microbiol. 37. Xiao L, Herd R P ( 1 994) Review of equine Cryptosporidium infection. Equine Vet. J 26:9-13.
Diarrhea - other causes BechtJ L, Semrad S D ( 1 986) Gastrointestinal diseases of foals. Compo Cont. Educ. Pract. Vet. 8:S367-S374. Klei T R ( 1986) Other parasites - recent advances. Vet. Clin.
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: 2 1 63-6. McClure JJ, AddisonJ D, Miller R 1 ( 1 985) Immunodeficiency 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.
Proliferative enteropathy in foals Duhamel G E, Wheeldon E B ( 1 982) Intestinal adenomatosis in a foal. Vet. Patho!.; 19:447-9.
DIARRHEA IN THE FOAL
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 ( 1 998) Proliferative enteropathy in foals: a cause of colic, diarrhea and
27
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. Bacteriol; 45:820-5. Williams N M, Harrison L R, Gebhart C] ( 1 996) Proliferative
protein-losing enteropathy. Proc. Am. Assoc. Equine Pract.
enteropathy in a foal caused by Lawsonia intmcellularis-like
44:1 34-5.
bacterium . ] Vet. Diag. Invest; 8:254-6.
51 1
26 Diseases of the rectum and anus in the foal EM Santschi
Atresia recti and ani
supply to a portion of the gut, leading to ischemic local necrosis. However the cause of the vascular insult is unknown.
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 Ag e
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 fistula or rectourethral fistu 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
Atresia recti and ani are congenital conditions, there fore clinical signs of colic and bloating in foals with this
no feces. Caudal abdominal radiographs may help delineate the extent of atresias. Elevating the foal's hindquarters will cause gas to fill the terminal patent
condition are only seen within 48 hours of birth.
gut and the caudal blind pouch can be determined.
Gender and genetics 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
PATHOLOGY Gross pathology 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
26
GASTROINTESTINAL DISEASE IN THE FOAL
TREATMENT
a two-layer closure. The mucosa of the fistula is removed and the submucosal tissues sutured together.
Treatment of atresia ani requires surgical anastomosis of the terminal rectum and the skin, and closure of any
The rectal mucosa is then closed separately. There is little information about correction of atresia recti. Surgical correction (via rectal pull through) is dif
urethral or vaginal fistulae. 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
ficult because of the inaccessibility of the blind-ended segments in the pelvic cavity. Permanent colostomy might be an option for salvage.
dally. The terminal rectum is opened and sutured to the skin. It is helpful to first suture the rectum using four equally spaced interrupted sutures and then filling in between them with interrupted sutures.
BIBLIOGRAPHY
Closure of urethral or vaginal fistulae with the rec tum requires dissection of the border of the fistulae and
Benamou A E, Blikslager A T, Sellon D C (1995) Intestinal atresia in foals. Compo Cont. Educ. Pract. Vet. 17:1510-16.
492
28 Hepatic diseases in foals
Portosystemic shunts
Only five cases of congenital portosystemic vascular anomalies have been reported in horses, of these five cases
LA Fortier
•
INTRODUCTION Portosystemic shunts (PSS) are anomalies of the porto systemic circulation that allow direct communication
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
between the portal circulation and a systemic vein such
ical signs, and blood tests, while a definitive diagnosis
as the vena cava. The shunting vessel(s) circumvents
requires hepatic scintigraphy or positive-contrast por
portal blood from entering the hepatic circulation and
tography. Medical management may provide temporary
being
cleared
of
toxic
metabolites
by
the
liver.
congenital or acquired
•
intrahepatic or extrahepatic
•
single or multiple. chapter
from
the
signs
of
hepatic
encephalopathy.
progressive deterioration occurs.
•
This
relief
However, without surgical ligation of the shunt vessel(s)
Portosystemic shunts are classified as
PATHOPHYSIOLOGY
primarily
addresses
congenital
PSS,
although the fundamental pathophysiology and med
Portosystemic shunts divert portal blood away from the
ical management described applies to acquired shunts
liver thereby allowing noxious substances such
as well.
ammonia, mercaptans, short-chain fatty acids, and false
Intrahepatic
shunts
represent
ductus venosus to close normally
a
failure
of
the
2-3 days following
as
neurotransmitters that are normally cleared by the liver to remain in the systemic circulation,
resulting in
Ammonia has been widely
birth. Embryologically the ductus venosus provides a
hepatic encephalopathy.
direct communication between the left umbilical vein
suggested as the major neurotoxin of hepatic disease.
and the caudal vena cava. In the neonate, when the
Hyperammonemia emerges from decreased hepatic
ductus venosus fails to close, portal blood drains into
conversion of ammonia to urea and is a characteristic
the left hepatic vein just prior to entering the caudal
sign of PSS in horses. Ammonia exert� its toxic effects
vena cava. Congenital extrahepatic shunts most com
on neuronal cell membranes and impairs neurotrans
monly originate from the portal vein but may also
mission through competing with potassium and subse
originate from
the
left
gastric vein,
splenic
vein,
quently inhibiting
the
sodium-potassium-dependent
cranial or caudal mesenteric vein, or gastroduodenal
adenosine
vein, and typically empty in the caudal vena cava or
75-80 per cent of total hepatic blood flow and 50 per
azygous vein.
cent of hepatic oxygen supply. Portal blood therefore
triphosphatase.
Portal
blood
comprises
51 3
28
GASTROINTESTINAL DISEASE IN THE FOAL
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 findings on blood laboratory results in foals with PSS. The cause of poikilocytosis in PSS remains unde fined and the microcytosis is believed to result from metabolic toxins interfering with iron uptake and metabolism or disrupting erythrocyte membrane integrity. Neither poikilocytosis nor microcytosis are specific 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 between 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 typically include PSS, bacterial or viral meningitis, and idiopathic cerebral edema. A definitive 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 definitive 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
Abnormalities noted with P55
hemogram
microcytosis, poikilocytosis
serum biochemistry panel
hyperbilirubinemia, hypoglycemia
:t
blood ammonia
usually increased more than 7 x normal
serum bile acids
increased
cerebrospinal fluid*
:t increased nucleated cell count, red blood cell count, and total protein
:t *
indicates all these conditions are present following seizures
HEPATIC DISEASES IN FOALS
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. An iodinated contrast agent such as Renografin-76 is injected as needed (typically 50-80 ml) to opacify 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 identify the PSS, however, a positive-contrast portogram 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 surgery are attempted. Gaining manage ment of the hepatic encephalopathy may require sev eral days of intense medical therapy. Extreme caution
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
28
GASTROINTESTINAL DISEASE IN THE FOAL
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 identification. A patent ductus venosus represents the most difficult 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 observed 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 five 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 heritability 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 sibility 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 flank approach instead of a ventral midline celiotomy, and most importantly, appropriate and aggressive preoperative and postopera tive management.
Tyzzer's disease WV 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 filamentous 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.
HEPATIC DISEASES IN FOALS
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. pilifarmis can be challeng ing as the signs are non-specific 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 identifies 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 significant 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 finding on necropsy associated with this disease.
DIAGNOSIS Ante-mortem diagnosis is difficult as there is no rapid definitive diagnostic test. Signalments with appropriate age classification, 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 specific, 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.
28
Gross necropsy identifies typical white spots in the hepatic parenchyma. Histopathology confirms a diag nosis of Tyzzer's disease. Warthin Starry stains identifY filamentous bacteria in affected tissue (Plate 28.1). Routine bacterial culture techniques are unrewarding.
TREATMENT Successful treatment of a definitively 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 underwent a post-mortem examination. The livers 517
28
GASTROINTESTINAL DISEASE IN THE FOAL
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 utero 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.
• •
fibroblastic-fibrocytic 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
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 first 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
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 finding 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
HEPATIC DISEASES IN FOALS
bacteria EScherichia coli, Actinobacillus equuli, Klebsiella 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 findings would include leukocytic infil trate (primarily neutrophils) in the periportal tissue and sinusoids, Kupffer 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 variety 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 definitive 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
28
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 differences lactic acidemia increased vascular permeability.
SIRS and its profound systemic effects lead to defective cellular mitochondrial function and specific visceral microcirculatory defects. The final 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 acetylcysteine, a glutathione donor, used for its anti oxidant properties non-steroidal anti-inflammatory drugs 51 9
28
GASTROINTESTINAL DISEASE IN THE FOAL
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 findings, 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) EHV-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 EHV-l infections are fatal, although there are two reported cases of neonatal foals with con firmed EHV-l viremia that survived. Common clinical presentations for foals born infected with EHV-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 findings. 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
HEPATIC DISEASES IN FOALS
and/or failure (persistent hypoxemia, hypercapnia). The foals usually die within 3-5 days. Typical post mortem examination findings 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. Definitive 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 significance 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
28
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 infiltrate (predominately lymphocytes and eosinophils) around the portal triads, and fibrosis. The diagnostic findings 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 hepatica) 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.
Large strongyles Both Strongylus 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, fibrinous inflammation, and then penetrate the bile duct, where fibrosis 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 infiltrate, possible fibrosis, possible larvae identification 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
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 often reveal an enlarged, pale liver and icterus. Histopathologic findings are quite characteristic, including hepatocellular dissociation, mixed leukocytic infiltration of portal triads and giant cell hepatopathy. Originally, the cause of giant cell hepatopathy was not known, but was subsequently identified 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 identifying the spirochete on micro scopic samples. 521
28
GASTROINTESTINAL DISEASE IN THE FOAL
Ehrlichia ristic;; Ehrlichia risticii, 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. risticii 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.
EX
JE Adolf and TJ Divers 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
• • • •
gross liver atrophy hepatocyte necrosis prominent bile duct proliferation occasional periportal fibrosis.
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
Toxic disorders
•
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 findings were similar among affected foals
Non-steroidal anti-inflammatory drugs (NSAIDs) 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 effects were noted. Carprofen in particular has been associated with hepa tocellular toxicosis in dogs. NSAID-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 NSAID-induced hepa totoxicity in foals, the monitoring of liver enzymes in foals receiving NSAIDs, especially carprofen, is warranted.
OTHER HEPATOTOXINS
�����----------------------
With the exception of iron toxicity, reports 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
HEPATIC DISEASES IN FOALS
• • • • • • •
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 type 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 JE Adolf and TJ Divers
28
In the most recent report, amino acid profiles 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 Rhodococcus equi polyarthritis and pneu monia. Based on the hematology and serum biochem istry, bacteriologic findings, 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 files. 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 echogenic foci in the liver parenchyma. As 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
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, were 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 findings in the liver were variable and included lymphocytic-plasmacytic periportal hepatitis, portal fibrosis, 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.
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
28
GASTROINTESTINAL DISEASE IN THE FOAL
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 ISOERYTHROLYSIS Rarely, a foal develops significant 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
Center S A, Magne M L (1990) Historical, physical examination, and clinicopathologic features of portosystemic vascular anolamies in the dog and cat. Semin. Vet. Med. Surg. (Sm. Anim.) 5:83-99. Fortier L A, Fubini S L, Flanders] A, Divers T] (1996) The diagnosis and surgical correction of congenital portosystemicvascular anomalies in two calves and two foals. Vet. Surg. 25:154-60. Lawrence D, Bellah] R, Diaz R (1992) Results of surgical management of portosystemic shunts in dogs: 20 cases (1985-1990 ) . ]. Am. Vet. Assoc. 201(11) :1750-3. Lindsay W A, Ryder] K, Beck K A, McGuirk S M (1998) Hepatic encephalopathy caused by a portacaval shunt in a foal. Vet. Med. 83:798-805. Mathews K, Gofton N (1987) Congenital extrahepatic portosystemic shunt occlusion in the dog: Gross observations during surgical correction.]' Am. Anim. Hosp. Assoc. 24:387-94. Olgilvie G K, Engelking L R, Anwer M S (1985) Effects of plasma sample storage on blood ammonia, bilirubin, and urea nitrogen concentrations: Cats and horses. Am.]. Vet. Res. 46:2619-22. Youmans K R, Hunt G B (1999) Experimental evaluation of four methods of progressive venous attenuation in dogs. Vet. Surg. 28:38-47.
Tyzzer's disease Williams N E (1998) Tyzzer's disease. Equine Disease Quarterly 6:4-5. Divers T D (1997) Tyzzer's disease. In Current Therapy in Equine Medicine 4th edn. N F Robinson (ed.) . W B Saunders, Philadelphia, pp. 218-9.
Congenital disorders Biliary atresia
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. As in humans, icterus and liver enzyme elevations would be present if there was suffi cient liver damage. Treatment would include support ive care (i.e. oxygen therapy) and addressing the needs of any other affected organ system.
Van der Leur R] T, Kroneman] (1982) Biliary atresia in a foal. Equine Vet.]. 14: 91-3.
Serous cysts Kelly W R (1993) The liver and biliary system. In Pathology of Domestic Animals, K V F ]ubb, P C Kennedy and N Palmer (eds ) . Harcourt-Brace]ovanovich Publishers, San Diego, pp. 319-406.
Neoplastic conditions
BIBLIOGRAPHY
Roperto F, Galati P (1984) Mixed hamartoma of the liver in an equine foetus. Equine Vet.]' 16:218-20. Neu S M (1993) Hepatoblastoma in an equine fetus.]. Vet. Diagn. Invest. 5:634-7.
Portosystemic shunts
Infectious processes
Beech], Dubielzig R, Bester R (1977) Portal vein anomaly and hepatic encephalopathy in a horse.]. Am. Vet. Med. Assoc. 170(2) :164-6. Birchard S], Sherding R G (1992) Feline portosystemic shunts. Compend. Cont. Educ. 14(10):1295-300. Buonanno A M, Carlson G P, Kantrowitz F (1998) Clinical and diagnostic features of a portosystemic shunt in a foal. ]. Am. Vet. Med. Assoc. 192:387-90.
Septicemia and/or endotoxemia
524
Hawthorne T B (1990) Neonatal hyperbilirubinemia. In Equine Clinical Neonatology, A M Koterba, W H Drummond and P C Kosch (eds ) . Lea and Febiger, Philadelphia, pp. 589-601. Miller D], Keeton G R, Webber B L, et al. (1976) Jaundice in severe bacterial infection. Gastroenterology 71:94-7.
HEPATIC DISEASES I N FOALS
Fahrlander H, Huber F, Gloor F ( 1 964) Intrahepatic retention of bile in severe bacterial infections.
Gastroenterology 47:590-9. Gossett K A, French D D ( 1 984) Effect of age on liver enzyme activities in serum of healthy quarter horses. Am.]. Vet.
Res. 45: 354-6. Paradis M R ( 1 994) Update of neonatal septicemia. Vet. Clin. N. Am. Equine Pract. 10: 1 09-35. Fly D E ( 1 988) Multiple system organ failure. Surg. Clin. N. Am. 68:1 07-22. Gullo A ( 1 999) Sepsis and organ dysfunction/failure. An overview. Mineroa Anestesiol. 65:529-40.
28
Leptospirosis Poonacha K B, Donahue J M, Giles R C, et al. Leptospirosis in equine fetuses, stillborn foals and placentas. Vet. Patho!.
30:362-9.
Ehrlichia risticii Long M T, Goetz T E, Kakoma I, et al. ( 1 995) Evaluation of fetal infection and abortion in pregnant ponies experimentally infected with Ehrlichia risticii. Am.] 11et.
Res. 56: 1 307-16.
Ascending infection Reef V B, Collatos C, Spencer P A, et a!. ( 1 989) Clinical, ultrasonograpbic, and surgical findings in foals with umbilical remnant infections . ]. Am. 11et. Med. Assoc.
195:69-72. Campbell-Thompson M L, Brown M P, Slone D E, et al. ( 1 986) Gastroenterotomy for treatment of gastroduodenal ulcer disease in 14 foals. ] Am. 11et. Med. Assoc. 1 88:840-4. Orsini J A, Donawick W J ( 1989) Hepaticojejunostomy for treatment of common bepatic duct obstructions associated with duodenal stenosis in two foals. Vet. Surg. 1 8:34-8.
Equine herpesvirus Type- 1 Murray M J , Piero F,Jeffrey S C, et al. ( 1 998) Neonatal equine herpesvirus Type I infection on a thoroughbred breeding farm. ] Vet. Intern. Med. 1 2:36-41 . Perkins G, Ainsworth D M , Erb H N , et al. ( 1 999) Clinical, haematological and biochemical findings in foals with equine herpesvirus-l infection compared with septic and premature foals. Equine Vet. ] 3 1 :422-6. Golenz M R, Madigan J E, Zinki J ( 1 995) A comparison of the clinical, clinicopathological and bone marrow characteristics of foals with equine herpes and neonatal septicemia. In Proceedings Annu Am Coli Vet Intern Med
Toxic disorders Iron toxicity Divers T J, Warner A, Vaala W E, et al. ( 1 983) Toxic hepatic failure in newborn foals. ] Am. 11et. Med. Assoc.
183:1407-1 3. Mullaney T P, Brown C M ( 1 988) Iron toxicity in neonatal foals. Equine Vet. ]. 20: 1 1 9-24.
NSAID toxicity Lewis J H ( 1 984) Hepatic toxicity of nonsteroidal anti inflammatory drugs. Clin. Pharmacol. Ther. 3 : 1 28-38. MacPhail C M, Lappin M R, Meyer D J, et al. ( 1 998) Hepatocellular toxicosis associated with administration of carprofen in 21 dogs . ]. Am. Vet. Med. Assoc.
2 1 2 : 1 895-9 0 1 .
Other hepatotoxins Pearson E G ( 1 996) Other hepatotoxins. In Large Animal Internal Medicine, B P Smith (ed . ) . Mosby-Year Book, Philadelphia, pp. 930-3.
Forum 585-7.
Cytomegalovirus
Other liver diseases
Rossdale P D ( 1 972) Modern concepts of neonatal diseases in foals. Equine 11et.] 4: 1 1 7-28.
Hyperammonemia in Morgans
Large strongyles and ascarids Uhlinger C A ( 1 996) Parasite control programs. In Large Animal internal Medicine, B P Smith (ed. ) . Mosby-Year Book, Philadelphia, pp. 1 685-710.
Divers T J, Tennant B C, Murray M J , et al. ( 1 994) Unusual cases of liver disease in Morgan foals. Gastroent. 11iewpoint
2:6.
McConnico RS, Duckett W M , Wood P A ( 1 997) Persistent hyperammonemia in two related Morgan weanlings. ]. 11et.
Intern. Med. 1 1 :264-6.
Flukes
Perinatal asphyxia
Owen J M ( 1 977) Liver fluke infection in horses and ponies.
Saili A, Saina M S, Gathwala G, et al. ( 1 990) Liver dysfunction in severe birth asphyxia. Ind. Pediatr. 27: 1 291 .
Equine Vet.] 9:29-3 1 .
525
Index
Abdomen
auscultation 4,110 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 fetal hydrops 321 foals 451 differential 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 surgery 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 Acorns 419,423 Acremonium coenophialum 422-423 Actinobacillus lignieresii 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 Alpha2 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 type II cells 382,385,522 Ameloblastomas 73,79 Aminocaproic acid 218,334,359 Amitraz 280,420
Ammonia toxicity
see Hyperammonemia Amsinckia intermedia 389 Amylase activity 349
Analgesia in colic 119-122,124 dosages and efficacy 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 recovery 154-155
pregnant mare and 351 Anesthesia, local laparoscopy 46,48-49 Anisognathism 69
Anoplocephala magna 54 Anoplocephala perjoliata 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 effects 58 treatments 57-58
see also specific agents 527
INDEX
Anti-arrhythmic therapy 236-237
Antibiotic-induced diarrhea 410,411, 412,423,507
Antibiotic tberapy
abdominal abscesses 331-332
Autotransfusion 334,359
hyperlipemia and 394,395
Avocado toxicity 419
recurrent volvulus 291-292
AV block,profound 236 Azotemia 138, 373 Bacteria
distributive shock 203
clostridial disease 410-411,412,501
see also specific diseases Bacteroides fragilis 75-76
periradicular disease 75-76
Bermuda grass 259
post-anestbesia myopathy/neuropathy
Bethanecol 124,213-214,244,246
peritoneal fluid analysis 18
endotoxemia 195
Barium enema 459-460
peritonitis 328
Berteroa incana 423
and 220
Bezoars 302-303
postoperative colitis 232
Bicarbonate estimation 12, 123,154,203,
salmonellosis 408,409,499
Bile acids 383, 391
preoperative 141
thrombophlebitis 137
463-464
Biliary calculi 386-389
Antifreezes 421
Biliary tract disease 386-389
Anti-inflammatory agents
Biochemistry
in distributive shock 203
ileus and 213
in peritonitis 328
Antimesenteric enterotomy 295 Antimesenteric teniotomy 295
Antioxidant status 221
Antithrombin III activity 223-224,227
Arabian borses 295,350
Arachidonic acid metabolism 104,147, 192
Bilirubin levels 382,383, 384,387 hyperlipemia 397-398 parameters 11-12
parasite-associated diseases 57 in peritonitis 326-327
Biopsy
control programs 59 egg survival 53
Cancer cachexia 374-375
Candidiasis 508
Cantharidin toxicosis 417-419 Capnograph 151
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
electrolyte status and 234-236
endoscopic 26
in malabsorption syndromes 379
see also specific
sites
Bismuth subsalicylate 195,406,431
Blister beetles 417-418,419
biology and lifecycle 54
Calcium gluconate 154
laparoscopic 44,48
Arterial rupture,at parturition 357-359
A.carids 521
see also Hypercalcemia,Hypocalcemia
Calcium borogluconate 140,405-406,419
aftercare and prognosis 237 anti-arrhythmic treatment 236-237
Bismuth,synthetic 412
Arteritis,mesenteric 55,262,436-437
post-anesthetic myopathy and 222
chronic diarrhea and 430
Arsenic intoxication 420
Arterial oxygen levels 145
postoperative pain 206,207,208
Calcium 235
Carbohydrates
Biliary atresia 517-518
adhesions and 210
Butorphanol 24,47,119,121, 148,154
Bile salt therapy 388
Anti-endotoxin therapy 123,193,203,
Antihistamines 422
Bull's eye sign 29,30,456,457,482
Capillary refill time (CRT) 3-4,110
Bile fluid leakage 19
213,230
Bruxism 471
Bile duct hyperplasia 387
Anticoagulant therapy 226-227
Antidiarrbeal agents 435-436
Brotizolam 348 Buccal mucosal flaps 85-86,87
biliary tract disease 388
chronic diarrbea 431
post-parturient,cecal perforation 274
Bite plate 72,73
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
electrocardiography 232
pathogenesis 234
prevalence and significance 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
fecal tests 57,521
Blood substitutes 202
Caslick procedure 353
impaction 56, 262,481-482
Blood transfusions 202,218,333-334,359
Castration 17,327,331,332,477
ill thrift 56
pathogenesis 55,521 treatment 58,521
Ascites 320, 503
Blood tests,anesthesia and 152 Blood volume 199
Blue-green algae 419
Body condition score 367-368
Aspartate aminotransferase 220, 221-222,
Body weight balance 367
Aspergillosis 424
Borborygmi 4
383,387,390,392
A.lpergillus spp.
378,384,423,424
Asphyxia,perinatal 524
Aspiration pneumonia 64,79,89,92,507 Aspirin 207,226,422 Astragulus spp. 420
Atipamazole 234,236
Atracurium 150
Atresia ani 461, 491-492
Atresia coli 461, 486-489
Atresia recti 461,491-492 Atrial fibrillation 234
Atropine 121-122,150,236,420 Aural fistulae 73
Auscultation 4, 110 colic 254
foals 451-452
Auto suturing device 42,43
528
Bone scintigraphy 34-36
Bots 60
Castor bean plant 420 Cathartics 281,486 Catheters 134-137
complications 135,137,226
considerations 134-135 guidelines for use 226
management 137,226
during transport 132-133
Botulism 64
materials 132
Bowel sounds 4,110, 206
treatment of thrombophlebitis 137,226
Bougienage 93
Bowel wall biopsy 342,372,380
replacement 136
types 135-136
Bradydysrhythmias 232,234,236
Cecal acidosis 275-276
Brood mare
Cecal content transfer 431
Breath hydrogen tests 38
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
Cecal bypass 271
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
INDEX
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 Central 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 investigation 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 difficile 230-231,410-412,500, 501
antibiotic-associated infection 124
Clostridium peifringens 258,261,410,411, 412,499-502
Clostridium piliformis 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 hawthorn fruit 280 Codeine phosphate 57,431,435-436 Colic acute, decision to refer 126-129 cecal diseases 267-278,see also specific disorders chronic and recurrent causes 339,340 defined 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 specific conditions medical therapies 119-125 aims 119 analgesia 119-122,124 anti-endotoxin therapy 123 anti-inflammatory 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
small intestinal 249-266 epidemiology 250-251 outcome and prognosis 483-484 postoperative management and complications 483 risk factors 250-251 see also specific 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 filling 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 postoperative 230-232 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
Dental abscess 35
Colostrum 449,499,507
Dental caries 74
Colostomy 310-312 bovine 506
Combined immunodeficiency syndrome (eID) 350
Compartment syndrome 221,222 Conduction block 221,222
strongylosis 436-437
Trichomonas equi 444
Dental anatomy 69
Diarrhea in foals 493-511 antibiotic-induced 507
Dental cysts 73
Dental disease 69-77
developmental disorders 72-77
infectious 74-76
candidiasis 508
clostridial enterocolitis 499-502
cryptosporidial 504-507 equine herpesvirus 508
signs 71-72
fetal 507
Copper levels 357
Dental eruption time 70
Corticosteroids 57,193,210,334,338,
Dental scintigraphy 34-36
Creatine kinase activity 220,221-222
Dentigerous cysts 73
Rhodococcus equi 502-504
Cryptosporidial diarrhea 504-507
Dermatitis 391,406
septicemia 507
Coronary bands, dermatitis 391
379,392,435
Crypt enterocytes, proliferating 509 zoonotic considerations 507
CryjJtosporidium spp. 60,350,504-507
Crystalloid therapy 138-140,192,
201-202,359,405 Cushing's disease 322 Cyathostomes
Dental nomenclature 69-70
Dental tumors 73
strongyle infection 508
Desflurane 149
Dessicated feed 245,246
Detomidine 24,47,119, 121,206,207,
208,234
Dexamethasone 193, 236,379,392
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
Dioctyl sodium succinate 122,246,281,
Diarrhea
Disinfection procedures 232 Disseminated intravascular coagulation
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
malabsorption and 372-373
toxic colitides 417-421
weight loss and 372-373
toxicities 422-423
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
oral rehydration 406
cantharidin toxicosis 417-419
see also Potomac horse Salmonellosis
cecal 268-269 foals 465
gastric 120,206, 246,247
ileus and 213
Decompression tract 159 Deglutition 63-64
compromised 65-67
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 fibrosis 444 intestinal lymphangiectasia 444 intestinal neoplasia 437 larval cyathostomosis
see
Cyathostomosis
Neospora caninum 443
other causes 442-444
in anesthesia 152-153 clinical parameters 12
peritonitis 444
fluid therapy
sand enteropathy 437-438
530
see
Fluid therapy
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
Duodenal perforation 472
Dehydration
estimation of 138
clinical findings 201
differential diagnosis 428
intestinal tuberculosis 443
acute diarrhea 405-406
Distributive shock 198
Draschia megastoma 476
437
Dehiscence 182,197,216,217,311 abdominal pain and 138-140
Abdominal distention,
clinical signs 427-428
Eimeria leukarti 444
Database, on-line 422
see
specific sites
Drainage, peritoneal 229
Cytotoxins 407,410,411,496
Decompression
(DIC) 195-196,382
Distention
chronic inflammatory bowel disease
defined 427
Dantrolene 222
fever,
Diarrhea, chronic 427-446
Cytomegalovirus 521
Cytosine arabinoside 338
423
Dipyrone 119, 120,207
hemorrhagic, clostridial 412
principles of treatment 405-406
treatment 58,435-436
Dioctahedral smectite 412
infectious, postoperative colitis
epidemiology 434
etiology and pathogenesis 432-433
Digestible energy (DE) input 399-400
Diaphragmatic hernia 261,480 Diaphragm, displaced 245, 246
intussusceptiollS 55,272,274
viral 493-495
Diazepam 24, 148,348 Dimercaprol 420
clinical features 55-56 diarrhea 56,57
Strongyloides westeri 508
Dextrans 192,211
Diabetes mellitus 349-350
control programs 58-60
proliferative enteropathy 508-509 salmonellosis 495-499
Depression 108, 382, 387
anthelmintic resistance 54,59,60 biology and lifecycle 54
foal heat 493
nutritional causes 507-508
salmonellosis (chronic) 443
Draining tract 182
Dry sickness (mal seco) 251,343 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
defined 63
diagnosis 64-65
normal deglutition 63-64 post-laryngoplasty 66 weight loss and 371
Ear teeth 73
ECN, equine-clinicians' network 93
INDEX
Edrophonium 150 Ehrlichia nsticii 412-414,415,522 FimPria 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 hyperlipemia and 398-399 peritonitis 326--327 Electrolyte therapy abdominal pain and 138-140 expected abnormalities 138 ill anesthesia 152-1.�3,154 chronic diarrhea 430 in colic 122-123 ")als 463-464 Elephant on a tub posture 345 ELISA 231,494, 495 Eltmac 120, 192,207 Emaciation 368 Iff 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 postoperative 192-196 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 ultrasonography 32,33 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 infiltrates, 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 clinical signs and diagnosis 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 general surgical considerations 90-92 complications/ prognosis 96--97 incisional closure 91-92 surgical approaches 91 see also specific disorders Esophageal diverticulum 93, 95 Esophageal fistula 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, 66-- 6 7
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) 12,56-- 57, 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 distributive shock 200 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
expected abnormalities 138 cecal impaction 270 colic 122-123 diarrhea acute 405-406 chronic 430 viral 494-495 distributive shock 202-203 during transport 132-133 endotoxemia 192 foals 463-464 hepatoencephalopathy 383-384 hyperlipemia and 398-399 hypovolemic shock 201-202,334, :�58-359
intestinal impaction 139,140,280-281 peritonitis 327 salmonellosis 408-409,499 Flunixin meglumine in distributive shock 203 in endotoxemia 123,192,195 pain relief 119,120 postoperative pain 206,207,208 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 intestinal atresia 304 iron overload 393,522 large and small colon disease and colic 485-490
medical therapy of pain 463-465 analgesics 464-465 decompression 465 fluid therapy 463-464 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 gastroduodenal ulceration 469-475 ulcer syndromes 470-472 Foals, clinical evaluation 449-468 abdominal distention, differential diagnosis 459-462 abdominocentesis 453,460 clinicopathological data 453-454, 466-467
endoscopy 453 history 449-450, 459, 466 nasogastric intubation 452, 460 physical examination 450-453, 459, 466
radiography 452,457-458,459-460, 467
rectal examination 451 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/pseudoobstruction 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 NSAID 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/pseudoobstruction 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 chronic diarrhea 429 parameters 11 parasite-associated diseases 57 peritonitis 326-327 weight loss 369-370
INDEX
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 I I Hemoperitoneum 18,19,201,332-334 Hemorrhage at parturition 357-359 fecal examination 429,430 hematology profile 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 hyperlipemia 394-401 primary hyperammonemia 384-386 pyrrolizidine alkaloid intoxication 389-391
right hepatic lobe atrophy 394 Sfe also specific 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 fibrosis 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 clinical signs and diagnosis 382-383 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 Histoplasma 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 (HYPP) 220-221,405
Hyperlipemia 350,394-401 associated diseases 395 clinical signs and diagnosis 396-398 epidemiology 394-395 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,
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 findings 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 definition 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 specific 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
439-440
clinical signs 216-217 predisposing factors 216 treatment 217-219 Incisional drainage 182,217,218 Incisional hemorrhage 216-217,218 Incisional hernias 182,217, 218-219,
440
Incisional infections 33-34, 182,217,218 Incisor caps 73-74 Incisor profile 71 Infiltrative bowel disease 30,32-33,372 malabsorption and 377-378
Hypoglossal nerve injuries 65 Hypoglycemia 350 Hypokalemia 154,235,464 Hypomagnesemia 235 Hypoproteinemia 370,430-431,433,439,
322
533
INDEX
Inflammatory bowel disease chronic (CIBD) 372,377-378,379,437 Inflammatory diseases parasite-associated 54-55,57 scintigraphy 36-37 ultrasonography 30,32-33 Inflammatory response adhesions and 209-210 hematology profile 11 peritoneal fluid analysis and 18 in peritonitis 323-324 in salmonellosis 496 weight loss and 369-370 Infundibular disease/necrosis 74 Ingesta prehension 63 reduction pre-laparoscopy 46 Inguinal hernias 261,477-478 rectal examination 114 reduction 452,477 ruptured 478 ultrasonography 29, 30 Inguinal rings, palpation 8 Inspiratory time:expiratory time (I:E) 152 Insufflation 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 pathophysiology 103-105 adhesion formation 105 endotoxemia 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 examination 114 rectal prolapse repair 313-314 repair of rectal tear 309 small intestinal 261-262 ultrasonography 29-30,456,457 see also specific sites
534
Intussusceptum 262 Intussuscipiens 261 Iodochlorohydroxyquin 432 Iron toxicity 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 filling 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 deficiency 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 postoperative 229-230 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 defined 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 rectal examination 115-117 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 clinical signs 285-288 rectal examination 115-116 treatment 286-287 ultrasonography 30,31 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 exteriorization 162-164 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 activity 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
INDEX
Lipoproteins, very low density (VLDL)
Megaesophagus 67, 96
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
Melanomas 19, 44, 45 Melena 13 Mercury toxicity 78, 420
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 weight loss and 372-373 Malabsorption syndromes 376-380 causes 377-378 alimentary lymphosarcoma 378 chronic inflammatory bowel disease
377-378 enteric infections 378 small intestinal resection 377 clinical signs and diagnosis 378 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 (MAP) 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
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
Multisystemic eosinophilic epitheliotrophic disease 378 Muscle atrophy 376 Muscle fiber necrosis 220 Muscle weakness, overall 220 Mustard plant toxicity 423 Mycobacterial infection, intestinal 377,
378, 423, 443 Mycobacterium spp. 423, 443
Mycosis 64 Mycotoxicosis 384 Mycotoxins 251, 384, 420 Myeloencephalitis 376 Myocarditis, immune-mediated 236 Myonecrosis 221
Mesodiverticular bands 260, 478-479 Mesothelioma 320 Mesperidine 148 Metabolic acidosis 12 in colic 153-154, 154
Myopathy, post-anesthetic 2 19-222 pathogenesis 220 prevention and prognosis 222
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)
Naloxone 334, 359 Narcotic analgesics 121 Nasal edema 137
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 Modified Triadan System 70 Monocytosis 11 Morgans 303, 381, 385-386, 523 Morphine 119, 121, 148, 208 Motility
therapy 222
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 isoerythrolysis 524 Neonates abdominal distention 460-462 normal parameters 449, 450-451 Neoplasia see Gastrointestinal neoplasia and specific tumors Neospora caninum 443 Neostigmine 123, 2 14, 281-282, 465, 495 Nephrosplenic entrapment see Large
abnormal, medical therapy 123-125 bowel sounds 4 disturbances acute diarrhea 423 cecal impaction and 269 intestinal obstruction 104-105 modification in chronic diarrhea 431 normal physiology 211-212 ultrasonography 32 Motility enhancers see Prokinetic agen t� Motor neuron disease 376
colon displacement, left dorsal Nephrosplenic ligament, palpation 7 Neurofibroma 338
Mouth disorders of 78-79 physical examination 4, 78 Moxidectin control programs 59 therapeutic regimens 58, 60, 435
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
Mucosal ulcers 378
therapy 222 Neurotoxins 382 Neutropenia 1 1 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
Mucosa-periosteal sliding flap 85 Mucous membranes 3-4, 201
Nociceptors 204-205, 208 Non-esterified fatty acid (NEFA) 395-396,
colic and 110 toxic line 1 10 Multiple organ dysfunction syndrome (MODS) 200, 201, 519 Multiple organ failure (MOF) 519
Non-strangulating infarction large colon 55, 58, 293 small colon 304 small intestine 55, 58, 262
toxicity 58, 435 Mucosal disease, esophageal 93 Mucosal protectant 473, 474
397,399, 400
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 196-198 long-term care 197-198 in chronic diarrhea 432 foals with abdominal pain 464 in grass sickness 347-348 hyperlipemia 399-400 right dorsal colitis 441 Nutrition-induced diarrhea 507-508 Oat stones 302-303 Obstruction see Intestinal obstruction, specific 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, chronic 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, viability and 166, 167, 168 Oxygen therapy 154, 155, 203, 359 Oxytetracycline 415 Oxytocin 361 Oxyuris equi 60 Pacemaker activity 249, 250, 268 Packed cell volume (PCV) 11 in colic 112
536
Pain acute abdominal, prognosis 141-142 classification of severity 107-108, 205-206 clinical signs 107-108 colic chronic and recurrent 339, 340-341 decision for surgery 130 decision to refer 127 small intestinal obstruction 253 management during transport 133 mechanisms of 107, 204-205 meconium retention 486 medical therapy in foals 463-465 analgesics 464-465 decompression 465 fluid therapy 463-464 nutrition 464 prokinetics 465 ovulation-related 340, 352 parietal 107, 205 parturition 357 persistent low-grade 371 postoperative 204-209 clinical signs 205-206 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 Paranoplocephala 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 specific parasites and diseases Parasympatholytic drugs 150, 307, 308 Parenteral nutrition 197 foals 464 Parietal hernia 261 Parrot mouth 72 Partial pressure of carbon diol'
INDEX
Peritonitis 321. 322-330 acute 325. 326 bile 3RR chemical 462
chronic 325. 326-327 classification and etiology 323. 324
clinical signs 324-325 copulation-induced 353 in foals 462 gastric rupture 472 investigation and diagnosis 325-327
medical treatment 327-330 pathophysiology 323-324 peracute 325. 326 peritoneal fluid analysis 18. 1 9
postoperative 227-229 causes 227-228 clinical signs and diagnosis 228-229 treatment 229 prognosis 330
signalment and history 324 surgical treatment 329-330 ultrasonography 32. 457 Pethidine 1 1 9 . 121 Pharyngeal cysts 66 Pharyngeal hemiplegia 64 Pharyngeal neoplasia 66 Pharyngeal paralysis 64. 66
Pharyngeal phase of deglutition 63. 66 Pharyngeal stripping wave 63 Pharyngeal swallow reflexes 63 Phenothiazines 59. 121 Phenoxybenzamine 406. 431 Phenylbutazone 1 1 9. 120. 192. 195. 207. 230 toxicity 120. 207. 274. 4 1 7 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; specific conditions Phytoconglobates 302-303
Pink-rosewater diarrhea 495 Pinworm 60 Piperazines 59 Placenta. retained 36 1 . 414 Placentitis 507
Plank in the flank technique 356 Plant toxins 389. 393. 419-420 Plasma fibrinogen concentration 1 1 Plasmalyte 2 0I
Plasma therapy 123. 140. 192. 1 93. 203. 327. 430 Platelet plug formation 223 Pneumatosis intestinalis 483 Pneumoperitoneum 4 1 . 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-control 5 1 5 Portosystemic shunts 513-516 Positive end-expiratory 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 impaction at anastomosis 215-216 incisional complications 2 1 6-219 myopathy/neuropathy 2 1 9-222 nutritional support 196-198 immediate 196-197 long-term care 1 97-198
peritonitis 227-229 postoperative monitoring 189-191 protocols 190- 1 9 1 postoperative pain 204-209 postoperative shock and organ failure 1 98-204 thrombophlebitis 222-227 treatment of endotoxemia 1 9 1 - 1 96 Potassium supplements 1 40. 154. 235.
405. 464 Potomac horse fever 412-415 clinical signs and diagnosis 412-413. 414
epidemiology 413-414 treatment and prevention 4 1 5
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 2 1 3-215. 281 -282. 348. 465. 473. 474 Proliferative enteropathy 508-509 Propanol 236. 237 Propantheline bromide 307 Propofol 149 Propulsion. normal physiology 2 1 1 - 2 1 2 Propylene glycol 421 Protamine zinc insulin 350 Protein-losing enteropathies cyathostomosis 433 weight loss and 372-373 Protein metabolism. abnormal hepatic 382 Prothrombin time (PT) 382. 383. 387 Proton pump 241 inhibitors 243. 244. 473, 474
Pseudocysts 75
Psyllium. dry 438 Psyllium mucilloid 122, 283, 284. 438. 441 Ptosis. bilateral 345 Ptyalism 78. 471 . 472 Pulmonary disease. chronic 376 Pulmonary edema 155. 201 Pulmonary function anesthesia and 146. 1 5 1 - 1 52. 154-155 in colic 145-146 Rhodococcus equi infection 503
Pulmonary hypertension 155 Pulmonary neoplasia 375 Pulpitis 74. 75 Pulse 3, 7. 8
Pulse oximetry 1 5 1 - 1 52, 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
Quercus 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 gastroduodenal ulceration 472-473 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 1 9. 130. 253 chronic and recurrent 341
foals 451 in peritonitis 327
recognition of abnormalities cecum 1 1 4-1 1 5 descending colon and rectum 1 1 7-1 18 large colon 1 15-1 1 7
small intestine 1 1 3-1 1 4 rectal tears and 305. 307 technique 6-8. 1 1 2-1 1 3 complications 7 lubrication 6 palpation of normal horse 7-8 videolaparoscopy and 45-46 Rectal liner 309-31 0 Rectal prolapse 312-313 Rectal prosthesis 309-3 1 0 Rectal tears 305-31 2 causes 305 classification 306-307
537
INDEX
Rectal tears - continued clinical signs and diagnosis 307 prevention 307
prognosis 312 treatment colostomy 310-312 definitive 308 immediate 307-308 primary repair 308-309 rectal liner, temporary 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 l O, 129-130, 152 foals 450-451 Restraint anesthesia and 147 endoscopy 24 foals 450,452 nasogastric intubation 4-5 rectal examination 6
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
clinical signs 503-504
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 Romifidine 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, 496-- 498 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 epidemiology 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 36--3 7
labeled white blood cells 36--37, 417, 440 techniques and agents 34, 35 Scours,36-- hour 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--2 97 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 (SAP) 12
Serum hepatitis see Theiler's disease Serum protein electrophoresis 57, 372, 429 Severe combined immunodeficiency (SCID) 505, 506 Sevoflurane 149, 152 Shear mouth 77 Shock,postoperative 198-204 classification 198-199 clinical findings 200-201 defined 198 pathophysiology 199-200 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 usitis 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 impaction at anastomosis 215-216 intestinal atresia 304 intramural hematoma 303 mesocolic rupture 303
non-strangulating infarction 304 obstruction,ultrasonography 30, 32 rectal examination 117-118
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
clinical signs and diagnosis 253-254 foals,radiography 458 medical treatment 257-258 pathophysiology 251-253 prognosis 263-264 rectal examination 113-114 simple 251-252
strangulating 252-253,261 surgical correction 254-257 ultrasonography 29-30,32 Small intestine anatomy and physiology 249-250 causes of disease 258-262 colic
clinical signs and diagnosis 253-254 epidemiology 250-251 foals 477-484 medical,prognosis 263-264
outcome and prognosis 262-263, 483-484
postoperative management and complications 483 risk factors 250-251 surgical,prognosis 262-263 see also specific diseases edematous 456, 457
exteriorization 161-162
impaction at anastomosis 215
malabsorption syndromes 372, 376--380 maldigestion 372 resection anastomosis 255-257 malabsorption and 377 nutritional support and 197-198
viability 164-167, 172-173 , 255 ultrasonography,foals 4!15-457
Sodium chloride,as laxative 122 Sodium thiosulfate 420 Soft palate
anatomy and physiology 79-80 dorsal displacement (DDSP) 65, 66 repair 85-86 see also Cleft palate
INDEX
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 Squamous cell carcinoma 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 specific 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 Streptococcus bovis 229 Streptococcus equi 331
Streptococcus zooepidemicus 314 Slress
gastric lesions in foals 471 right dorsal colitis and 440,441 Strongyles,large biology and lifecycle 54
clinical features of infection 55,56 control programs 58,59 hepatic disease 521 investigations 56-- 57 mixed infections see Strongylosis pathogenesis 54-55 treatment 57
Strongyles,small see Cyathostomes Strongyloides westeri 60,508 Strongylosis 436--437 clinical signs 56,436 diagnosis 437 diarrhea and 508 Strongylus edendatus 54,349,521 Strongylus equinus 54,349,521 Strongylus vulgaris 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
156--157 closure of abdomen 181-184 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--1 87 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 adhesions and 180-181 auto suturing device 42,43 bite size 183
materials 168 closure of abdomen 182-183
strength 182-183 patterns 168-172, 172,183
sinuses 182,183,218 Swallowing 63-64 difficulties see Dysphagia Sweating,effects of 138 Sympathomimetics 153 Systemic inflammatory response
syndrome (SIRS) 191-192,200,519
Table,laparoscopy 43,48-49
Tachydysrhythmias 153 Tapeworms
biology and lifecycle 54 colic 56,57,58 control programs 59 in ileal impaction 259 in intussusceptions 273 pathogenesis 54, 55
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 166--167 Theiler's disease 381-384 clinical signs and diagnosis 381-383 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
clinical signs 224-225 defined 222 pathogenesis 223-224,226 prevention 226-- 227 septic 222,224,225,227 treatment 227 Thrombosis,catheter-related 135,136, 137 Thrombus formation 223 Thromoboembolic arteritis 262,436-- 437 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
Trichomonas equi 444 Trichostrongylus axei 476
Trichothecenes 420
Triclabendazole 521
Triglycerides 395, 396, 397-398, 399, 400,
479
Uterine Uterine Uterine Uterine Uterine Uterine
artery rupture 357-359 contractions, normal 357 horn, inversion 360-361 prolapse 360-361 rupture 357, 360 torsion 354-356
Triodontophorus spp. 54
Utero-ovarian artery rupture 357, 358 Uterus, dorsoretroflexion 354
Tympanitic colic see Colic, distention Tympany, bowel sounds 4 Typhlectomy 158 Typhlotomy 270-271 Tyzzer's disease 5 1 6-51 7
Vaccines
Tromethamine 154 Tuberculosis, intestinal 377, 378, 423, 443
Ultrasonography 26-34 abdominocentesis and 15, 16 biliary tract disease 387, 388 cecal intussusceptions 274 clinical indications for 29 colic 29, 1 3 1
chronic and recurrent 342 postoperative 33-34 small intestinal obstruction 253 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 infiltrative 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
Ehrlichia risticii 414, 4 1 5
mutant core polysaccharide 123
R. equi 504
rotavirus 495
Salmonella spp. 499 Vaginal injuries 353 Vascular hyporeactivity 200 Vasculitis, immune-mediated 391 Vasodilators, and laminitis 230
Venous admixture 145, 152, 155 Ventral body wall hernias 321-322 Ventral edema 3 1 7, 320, 321 Ventricular arrhythmias 232-234, 236,
237
Ventricular premature depolarizations
233
Ventricular tachycardia 232, 233-234,
236, 237
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 difficulties 371 protein-losing enteropathies 373
Vesicular stomatitis 78 Viability of gut 164-168, 172-173, 185,
pulmonary disease, chronic 376 clinical pathology 369-370 cyathostome-associated 55-56, 436
Video-endoscopy 21-22, 23 Video-fluoroscopy 65 Videolaparoscopy 42, 45-46, 48-49
environmental factors 368-369
255, 377
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 1 6-1 1 7 strangulation 291 treatment 290, 291 small colon 303 small intestinal 29, 260, 261 foals 455, 456, 462, 480-481
definition 367 differential diagnosis and evaluation
367-376
gastrointestinal neoplasia 335 nutrition, assessment of 368-369
in right dorsal colitis 439 ultrasonography, indications for 29 White cell count (WBC) 1 1 , 1 1 2 Wooden tongue 78 Wound healing 1 8 1 , 196 Wry nose 80 Xanthine metabolism 104, 105 Xylazine
abdominal pain relief 1 1 9, 120-121 in anesthesia 147-148, 154
in endoscopy 24 postoperative pain 206, 207, 208
sedation 47, 452 side effects 1 2 1 Xylose absorption test 2 1 , 372 Yohimbine 1 24, 147, 2 1 4
Zolazepam 1 49 Zoonotic considerations 410, 507 Z-plasty, double opposing 85
