Manual of Equine Gastroenterology

WB SAUNDERS An imprint of Elsevier Science Limited 2002 2002. All rights reserved. © Harcourt Publishers Limited © El...

Author: Tim Mair BVSC PhD DEIM DESTS DipECEIM MRCVS | Thomas Divers DVM Dipl ACVIM ACVECC | Norm Ducharme DVM

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WB SAUNDERS An imprint of Elsevier Science Limited

2002 2002. All rights reserved.

© Harcourt Publishers Limited © Elsevier Science Limited

�

is a registered trademark of Elsevier Science Limited

The right of Tim Mair, Tom Divers and Norman Ducharme to be identified as editors of this work has been asserted by them in accordance with the Copyright, Designs and Patents Act

1988

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without either the prior per

1-3 Baxter's 3AF), or a licence permitting restricted copying in the United Kingdom issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London WIT 4LP. mission of the publishers (Permissions Manager, Elsevier Science Limited, Robert Stevenson House,

Place, Leith Walk, Edinburgh EHI

2002 2002

First published Reprinted ISBN

0 7020 2486 4

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.

Typeset by Phoenix Photosetting, Chatham, Kent Printed in the UK by Bath Press Limited The publisher's policy is to use paper manufactured from sustainable forests

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


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


Sefton Equine Referral Hospital


Royal Veterinary College

Cornell University

University of London


Hatfield, Herts, UK G Barrie Edwards T Douglas Byars

Professor of Equine Studies

Director of Internal Medicine

University of Liverpool


Leahurst


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


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


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


Departement de Science Cliniques

Cornell University

Universite de Montreal


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


Faculty of Veterinary Medicine

Cornell University

University College Dublin


Dublin, Republic of Ireland

xii

CONTRIBUTORS

Tim S Mair

Claude A Ragle


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


Michael J Murray


Rood and Riddle Equine Hospital Professor in Equine Medicine Marion Dupont Scott Equine Medical Centre

BA Rucker

Leesburg, Virginia, USA


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


South Wirral, UK


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


University of Cambridge

Cornell University

Cambridge, UK


-

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


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


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


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


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 •

• •


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


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


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

'''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

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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 . . " . ..' . . "
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

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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

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"

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


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


(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


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


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


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

3

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 • • •


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-


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


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


•

•

•

•

• •

•

•

•

•

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

•


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


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

=

=

=

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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

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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

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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.


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


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


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!

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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.


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


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


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


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.


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


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


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


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


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


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


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.

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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.

88

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


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 •

•

•

•


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

7


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

7


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


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

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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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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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COLIC

process, such as colitis, proximal enteritis, peritonitis, or pleuritis. Body temperature elevation can also occur early after stomach or intestinal rupture, leading to sep tic peritonitis. Decreased temperature (hypothermia) , in addition to tachycardia, is indicative of the develop ment of circulatory compromise and potential shock. Respiratory rate The respiratory rate of a horse with colic will usually be elevated because of pain or metabolic acidosis. Dyspnea or shallow breathing can result from pressure applied to the diaphragm by severe gastric or intestinal disten tion. The rate and character of respiration should be noted, but these do not usually provide any direct insight into the causes of colic. Heart rate A horse's heart rate can usually be obtained by auscul tation of the heart at the thorax, it can also be obtained by palpation of the facial artery or other peripheral arter ies. Palpation of a peripheral pulse can offer a reflection of cardiovascular function and tissue perfusion. The absence of a palpable pulse may indicate cardiovascular compromise . In relation to gastrointestinal origins, it may be wise to palpate the digital arteries in order to detect the potential early development of laminitis. The normal equine heart rate is 24-40 bpm. Elevations of heart rate in horses with colic are usually the result of anxiety, pain, and hypovolemia. Heart rate elevation is a good indicator of the severity of pain and indirectly, the original intestinal disorder. Pulse assess ment should always be used in addition to other physi cal examination data to determine the potential presence of a surgical condition. Horses with a functional or mild intestinal obstruction can have intermittent heart rate spikes, whereas horses with strangulating lesions usually have sustained heart rate elevations up to 80-90 bpm. A sustained elevation in heart rate is critical to a more com plete understanding of the diagnosis and prognosis. Mucous membranes and jugular vein filling The character and color of mucous membranes can reflect the circulatory status of the patient. Normal mucous membranes are moist and pink. Physiological capillary 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

9

COLIC

CLINICAL PATHOLOGY For many horses, laboratory assessment of blood is not essential for treatment success. However, with severe or changing cases WBC, packed cell volume ( PCV) and total plasma proteins (TPP) are often helpful. The PCV and TPP are useful for assessment of the degree of dehydration, and are necessary to monitor the 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


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

9

COLIC

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


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

9

COLIC

(Figure 9.9 ) . The majority of the colon is palpable on the left side of the abdomen with the tenia coursing from the left craniodorsal abdomen to the left caudo ventral abdomen and if 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

116


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

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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


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,


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.


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


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.


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.


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

9

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.


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.

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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

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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

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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

1 43

9

COLIC

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


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


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-

10

sistencies in determining the level for zero cause con siderable variability in this normal value. Nevertheless, CVP is a valuable tool for measuring changing cardio vascular status. If the venous return to the heart is low, as is the case in relative or absolute hypovolemia, then 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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COLIC

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


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-

10

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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COLIC

anaerobic metabolism in poorly perfused tissues. Moderate metabolic acidemia (pH 7.40-7.25, base excess O.O-S.O mEq/l) usually resolves after rehydration with balanced electrolyte solution. Severe acidemia has multiple adverse effects including desensitization of adrenoceptors that are important in treating hypoper fusion in anesthesia. Conventional therapy involves sodium bicarbonate (S.4% w/v, 1 mEq/ml) given intra venously over 1 5-30 minutes at a dose 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-


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

10

surgeon. The site of the lesion (s) and anesthetic con siderations (e.g. possible impairment of venous return for mares late in gestation) dictate the position of the animal and the abdominal approach required. If there is no financial constraint the decision on where to make the abdominal incision must be based on which approach gives the best access to the anticipated lesion, and gives the least morbidity to the patient. Other fac tors, for example the facilities and equipment that are available, must also be considered. Invasive surgical approaches are described in this chapter, but in some horses laparoscopy (although it allows only partial abdominal exploration ) can be useful, albeit mainly as a diagnostic procedure. This section describes the stan dard surgical approaches for horses with gastrointesti nal disease (see Chapter 3 for details on laparoscopic approaches) .

PREOPERATIVE PREPARATION There are two main approaches to the equine abdomen (Figure 10.la, b) 1. ventral incisions such as midline or paramedian 2. left or right flank incisions made either through the paralumbar fossa or by a 1 7th or 1 8th rib resection. Surgical entry into the abdomen is made with the horse under general anesthesia in dorsal or lateral recum bency, except for paralumbar fossa celiotomies that can be done with the animal standing. The surgical area is clipped, and a 5 cm linear band is shaved at the intended incision site to allow better adhesion of the adhesive impervious dressings applied as part of the incisional draping in the operating room. In addition, ventral abdominal approaches require, in males, sutur ing of the prepuce using a continuous pattern to pre vent intraoperative urine 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

10

COLIC

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-


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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COLIC

is desired. This approach allows significantly greater abdominal exposure of the left or right abdominal viscera compared to the paralumbar fossa/flank celiotomy. It is generally done on the right side for procedures such as typhlectomy, resection of the right dorsal colon, or improved access to the ileocecal valve (Figure 10.3) . It is done on the left side for procedures such as closure of the nephrosplenic space and correc tion of nephrosplenic entrapment. Either the 1 7th or 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.


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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COLIC

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


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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

10

COLIC

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.

10


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

10

COLIC

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


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


Anastomotic problems

No 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


Expensive treatment

Expensive treatment


No 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

10

COLIC

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

10

COLIC

that the equipment is expensive, only small areas of tis sue can be evaluated, and contact between probe and tissue should be constant. Pulse oximetry can be used to assess oxygen saturation, but it has not been evaluated in the horse and it may not be as sensitive to decreases in local tissue blood flow as surface oximetry. Fluorescein fluorescence might be more suitable for assessing large intestine than for small intestine because the large intestine has a lower risk of adhesions in seg ment� that produce a viable pattern. The 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

10

COLIC

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

10

COLIC

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"Wyslcrn

hich is activated

.....

(lurinK i�chcmic reperfur.ion i njury. ROS can attack \inlts 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 !futun' 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 oherved. 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

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 \\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 Ssted, 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�
(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;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. 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
October 24--27, Lexington,

Kenlucky.

Orsini J A ( 1 99(1) Shock. In I-AplilU' Surgtry, ht edn. J A AU
Postoperative pain

BIBLIOGRAPHY

C!.lrk.! 0, CI Hrk T P ( l 999) Analgesia. In V;'I. elin. N. "'m. r �"inePracl., S A Turner (ed.). W B Saunde�,

Treatment of endotoxemia Baflon M 1-1, Bruce E 1-1, �loore.J "", �I al. ( 1 99S) Effect of Ilimor Ilec)"()_si� ranof antibody giv(�n to horses during "arl�' experimentaHy induced 'i():7�)2-7_

endotoxem ia. Am.J.

V;'I. &.

Philadelphia, 15(3):705-23.

Drossman D A ( 1 998) Chronic funnional abdominal pain. In Gastroj"te.,linai and Liv"Disrase6th "dn, �I Feldman, B F Scharschmidt, M H SIeisenger Philadelphia, 1998, PI' 90-7.

(eds) W B Saunders,

237

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COLIC

Glasgow R E and Mulvihill SJ ( 1 99R) Ahrlominal pain, induding (he acute abdomcn. In Gll-llroinuslillal and LiTltT Dismlf 6!h edn, M Feldman, B F Scharschmidt, "'1 H Sleisengcr (cds). lA' B Saundns, Philadelphia, PI' 80-89. Muir W W ( 1 99S) Anaesthesia and pain management in h(>r�c�. l:'qw'ne Vft. j.,-duc. 10(6):3:1.1-340. , \\ hit� :-: A ( 1990) Examination and diagn"-'is of th" acute abdomen. In 17lt Equint Actlln\bdmnn!, N A While (cct.) . Lea and Fcbigcr. Philadelphia, PI" 102-42. While ;-.; A and Byars D T ( 1 990) Analgesia. In The Equine Awlr tlbdmllro, 1\ A White (cd.). Lea and Fcbig-cr. Philadelphia, pp 154-9.

Abdominal adhesions 13:1587-97.

!�axter G M, Broome T E, Moore J :\ ( 1 989) Abdominal adh('sions �fu�r small intestinal surg('I)' in the horse. V�I, SUTf{.

1 8 409-414.

Raxter G M,Jackman R R, Eanes S C, �I aL ( 1 993) F�i!ure of calcium channel hlock,,,]e to prevent intra-abdominal adhl�sions in ponies. 1i.1. S"rg. 22:496-�O. Baxter G M, Parks A H. Prasse K W (1991) Effecl� of explor�to[1' l�parolOm}' on plasma �nd peritoneal ",,�guJati()n/!ibrinoJysi� in horse.�. Am.]. V,I. lV.I. fi2:1121-7, (:oll�I'" C, Barton M H, I'rasse K W, �I al ( 1 99,,) Intravascular and peritoneal coagulation and librinolysis i n horses with anile !!;as!roimestinal tract disease. ./. .-i.m. l'ft. Med, Ass",..

2()7:46!>-70.

DiZ.".ega G S ( 1 994) C(lnt('mpor�ry arihe,ion prn'e!ltion,

Fnhl. SimI. 61;219--3fi.

Du{'harme N G, Hackett R P, Ducharme G R, ,I aI, ( 1 983) Surgic�1 lre�lment of colic: Results in J il l horses, V,/. Surg.

12:206-209. Ellis H ( 1 982) The c�uses and prewnlion of inf.estinal adh2:88-91.

.\-fudlel: P 0 �:, l lunt R 1, Alkn D, Parks A H. H�\' W P ( 1 995) · Illlfapt'riloneal use or sodium rarboxymethylcellulo'l' in horses undergoing exploratory celiotomy. Vel. Surg.

24:112-117.

Parker.! E, Fubini S i., Car B D, el "t. (1987) Th" liSt' 01

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:;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,"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. 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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COLIC

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 la360°

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

289

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COLIC

the cecal base is typical. Mild edema of the colonic wall may be evident on rectal palpation or ultrasonographic evaluation.

Treatment The treatment for non-strangulated colon volvulus is surgical. Progressive colon tympany and signs of severe abdominal pain clearly indicate the need for surgery in horses with 270-360° colonic volvulus. In horses with a 90-270° volvulus, clinical signs are relatively mild and resemble those of colonic impaction. Such horses are often treated conservatively for many days. However, unless the presence of a treatable impaction is 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

290

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

15

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

15

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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


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.

15

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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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-


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


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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 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


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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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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-

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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


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

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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


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

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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

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" 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

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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

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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

< 1.016 100 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.

326

In order to improve the culture rate, peritoneal fluid should be collected into blood culture medium - if the horse has already been given antibiotics, fluid should first be passed through an antimicrobial-removal device.

Hematology, serum/plasma electrolytes and biochemistry The hematological and biochemical changes that may be seen in peritonitis are listed below, these changes vary depending on the stage, severity, and type of 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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17

COLIC

Antibiotic therapy Antimicrobial therapy should be initiated immediately after peritoneal fluid samples have been obtained for culture. Antibiotic therapy, therefore, needs to be started before the results of culture and susceptibility are available. In most cases of septic peritonitis a 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

328

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 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
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

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.

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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

17

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

•

•

•

•


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

18


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 • • • •


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 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


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'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 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

20

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 "'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

446

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 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


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


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

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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

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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

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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


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

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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.


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

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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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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.].

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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

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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.

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defects in domesticated animals: general considerations. Am.] Vet. Res. 31:1871-9. RobertsonJ T (1982) Obstructive diseases - congenital diseases. In:

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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.

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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

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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


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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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


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


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


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


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: 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


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

27


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.


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

27

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

27


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.


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.

27

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

27


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


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

27


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.


27

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

1 8 (4) :301- 6. 509

27


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.


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


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


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


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.


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.

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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


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


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


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


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

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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


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


• • • • • • •

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

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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

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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-

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