Gastrointestinal System
Identifieur interne : 000227 ( Pmc/Corpus ); précédent : 000226; suivant : 000228Gastrointestinal System
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- Equine Emergencies ; 2013.
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DOI: 10.1016/B978-1-4557-0892-5.00018-0
PubMed: NONE
PubMed Central: 7152054
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Gastrointestinal System</title></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmc">7152054</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7152054</idno><idno type="RBID">PMC:7152054</idno><idno type="doi">10.1016/B978-1-4557-0892-5.00018-0</idno><idno type="pmid">NONE</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000227</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000227</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Gastrointestinal System</title></analytic><series><title level="j">Equine Emergencies</title><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader></TEI><pmc article-type="chapter-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Equine Emergencies</journal-id><journal-title-group><journal-title>Equine Emergencies</journal-title></journal-title-group></journal-meta><article-meta><article-id pub-id-type="pmc">7152054</article-id><article-id pub-id-type="publisher-id">B978-1-4557-0892-5.00018-0</article-id><article-id pub-id-type="doi">10.1016/B978-1-4557-0892-5.00018-0</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Gastrointestinal System</article-title></title-group><contrib-group><contrib contrib-type="editor"><name><surname>Orsini</surname><given-names>James A.</given-names></name><degrees>DVM, DACVS</degrees></contrib></contrib-group><aff>Associate Professor of Surgery, New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, Pennsylvania</aff><contrib-group><contrib contrib-type="editor"><name><surname>Divers</surname><given-names>Thomas J.</given-names></name><degrees>DVM, DACVIM, DACVECC</degrees></contrib></contrib-group><aff>Professor, Large Animal Medicine, Cornell University College of Veterinary Medicine, Cornell University Hospital for Animals, Cornell University, Ithaca, New York</aff><pub-date pub-type="pmc-release"><day>6</day><month>12</month><year>2013</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><year>2014</year></pub-date><pub-date pub-type="epub"><day>6</day><month>12</month><year>2013</year></pub-date><fpage>157</fpage><lpage>237</lpage><permissions><copyright-statement>Copyright © 2014 Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder>Elsevier Inc.</copyright-holder><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions></article-meta></front><body><sec id="s0010"><title>Diagnostic and Therapeutic Procedures</title><p id="p0010"><italic><bold>Barbara Dallap Schaer and James A. Orsini</bold></italic></p><sec id="s0015"><title>Nasogastric Tube Placement</title><p id="p0015">Placement of a nasogastric tube is used for the administration of large volumes of enteral medication(s), fluids, and electrolytes. This is also an important diagnostic and therapeutic procedure in the evaluation and treatment of a horse with signs of colic. Nasogastric intubation, followed by creation of a siphon, is performed to evacuate any accumulated fluid or gas in the stomach due to functional or mechanical proximal obstruction of the gastronintestinal tract. Fluid is removed to alleviate gastric pain caused by visceral distention, and most importantly to prevent gastric rupture. Nasogastric intubation is indicated in suspected cases of esophageal obstruction to confirm the diagnosis and relieve the esophageal obstruction. Nasogastric tubes are commercially available that are specifically designed for treatment of esophageal obstruction (directions included with tube).<xref rid="fn0010" ref-type="fn">1</xref> Every clinician develops his or her own technique for passing a nasogastric tube. The following description may be useful for the less experienced.</p><sec id="s0020"><title>Equipment</title><p id="p0020"><list list-type="simple" id="ulist0010"><list-item id="u0010"><label>•</label><p id="p0025">Nasogastric tube (sized appropriately)</p></list-item><list-item id="u0015"><label>•</label><p id="p0030">Bucket half-filled with warm water</p></list-item><list-item id="u0020"><label>•</label><p id="p0035">400-mL nylon dose syringe, <italic>or</italic></p></list-item><list-item id="u0025"><label>•</label><p id="p0040">Veterinary injection pump (fluid pump)<xref rid="fn0015" ref-type="fn">2</xref></p></list-item></list></p></sec><sec id="s0025"><title>Procedure</title><p id="p0045"><list list-type="simple" id="ulist0015"><list-item id="u0030"><label>•</label><p id="p0050">Immerse the nasogastric tube in warm water until it is clean and flexible.</p></list-item><list-item id="u0035"><label>•</label><p id="p0055">Adequately restrain the horse. This may require a chain shank over the nose or under the lip, a twitch, chemical restraint, or a combination thereof.</p></list-item><list-item id="u0040"><label>•</label><p id="p0060">Stand on the horse's left side, place the right hand over the nose, and use the thumb to reflect the alar fold of the left nostril dorsally. Do not obstruct airflow in the right nostril. Apply pressure to the bridge of the nose so that the head is flexed more ventrally to promote swallowing of the tube.</p></list-item><list-item id="u0045"><label>•</label><p id="p0065">Using the left hand, guide the tube ventrally and medially along the ventral nasal meatus. The middle nasal meatus is immediately dorsal and must be avoided.</p></list-item><list-item id="u0050"><label>•</label><p id="p0070">Advance the tube slowly, and refrain from forcing the tube if excessive resistance is encountered. If the patient is tossing its head, hold the tube in the nostril using the thumb of the right hand. Mild sedation with an α<sub>2</sub>-agonist (e.g., xylazine, detomidine) can be used as an adjunct to physical restraint.</p></list-item><list-item id="u0055"><label>•</label><p id="p0075">The tube encounters some resistance as it reaches the epiglottis. Many horses swallow the tube immediately, but it may be necessary to rotate the tube approximately 180 degrees to facilitate passage into the esophagus. Gently “bumping” the epiglottis with the end of the tube, or blowing into the tube may encourage some patients to swallow. Try to pass the tube on the patient's first swallow because subsequent attempts to stimulate swallowing become progressively more difficult. If no swallow reflex is elicited, attempt to pass the tube using the opposite nostril.</p></list-item><list-item id="u0060"><label>•</label><p id="p0080">Be absolutely certain the tube is in the esophagus and not in the trachea. There are several ways to ensure correct placement. <bold><italic>Important:</italic></bold><italic>All must be confirmed before the tube is advanced farther and before any medication is delivered:</italic><list list-type="simple" id="ulist0020"><list-item id="u0065"><label>•</label><p id="p0085">Resistance is encountered when the tube moves down the esophagus. The tube passes down the trachea relatively easily, and the tube passing over the tracheal rings is palpable.</p></list-item><list-item id="u0070"><label>•</label><p id="p0090">Negative pressure (aspiration is not possible) is obtained with suction if the tube is in the esophagus because the lumen collapses. Suction on the end of a tube in the trachea does not result in negative pressure.</p></list-item><list-item id="u0075"><label>•</label><p id="p0095">The end of the tube is seen advancing down the neck to the left of midline when in the esophagus. The tube is not seen if it is in the trachea. The tube should be palpated as it passes toward the thoracic inlet, or more easily, as it rests beside the proximal trachea (usually to the left). Exact tube placement is confirmed by gently pushing the trachea dorsally with one hand while using the fingertips to feel the tube in the esophagus. This is the most reliable assessment of correct tube placement. In a small percentage of horses, the tube in the esophagus is palpated on the right side.</p></list-item></list></p></list-item><list-item id="u0080"><label>•</label><p id="p0100">Blow into the tube to facilitate advancement through the cardia into the stomach. Once the tube is in the stomach, gas that smells like ingesta is emitted.</p></list-item><list-item id="u0085"><label>•</label><p id="p0105">Attempt to obtain reflux before administering large volumes of fluid. <bold><italic>Practice Tip:</italic></bold><italic>To obtain reflux, create a siphon by establishing a column of water between the stomach and the free end of the nasogastric tube.</italic> Administer one or two dose syringes full of warm water to fill the tube, aspirate a small amount of fluid, detach the syringe, and lower the tube end. Several attempts are often needed before gastric fluid is successfully siphoned off the stomach. If there is high index of suspicion of gastric distention, ultrasound evidence of the stomach imaged at the most caudal intercostal space, or clinical signs of proximal obstruction (high heart rate, small intestinal distention on abdominal palpation per rectum, etc.), be persistent in attempting to decompress the stomach.</p></list-item><list-item id="u0090"><label>•</label><p id="p0110">If no net reflux is obtained after an appropriate number of attempts, it should be safe to administer enteral medication or fluid. Lift the tube end above the patient's head to complete delivery of the medication. Before removing the tube, lower the tube end to ensure that there is not excessive pressure on the stomach. Evacuate the contents of the tube before removing the tube.</p></list-item><list-item id="u0095"><label>•</label><p id="p0115">Crimp the tube or leave the dose syringe attached during removal so that fluid does not drain into the pharynx or nasal passage.</p><p id="p0120">A normal horse usually has gastric reflux of less than 2 L of fluid. To determine the amount of reflux, measure the total volume obtained minus the volume started with in a single bucket. Alternatively, total volume obtained minus the amount used to create the siphon can be calculated if two buckets are used.</p></list-item><list-item id="u10975"><label>•</label><p id="p13330"><italic><bold>Important:</bold> Do not administer enteral fluids to patients with significant reflux.</italic> It is <italic>not</italic> absorbed and increases the likelihood of gastric rupture. Excessive reflux is often the result of proximal intestinal obstruction, either mechanical or functional. Patients with a large quantity of reflux should have a nasogastric tube left in place and secured to the halter in an attempt to prevent gastric rupture. The tube should have a Heimlich valve placed over the end to allow fluid and gas to escape. Retrieval of reflux should be repeated every few hours in these cases.</p></list-item></list></p></sec><sec id="s0030"><title>Complications</title><p id="p0125"><list list-type="simple" id="ulist0025"><list-item id="u0100"><label>•</label><p id="p0130">Accidentally administering a large volume of fluid into the lungs of a patient can be fatal. For this reason, one must literally “see, feel, smell, and hear” the tube in the correct position. If a large volume of fluid is accidentally administered into the trachea, immediate communication with the owner followed by prompt medical attention is warranted. Extreme caution should be used with enteral administration of mineral oil; mineral oil aspiration is often fatal.</p></list-item><list-item id="u0105"><label>•</label><p id="p0135">Bleeding from the nose is an occasional complication. The conchal mucosa is extremely vascular and easily injured. Most nosebleeds eventually stop without serious consequences.</p></list-item><list-item id="u0110"><label>•</label><p id="p0140">If a nosebleed occurs prior to reaching the stomach, rinse the tube and attempt to pass it gently through the other nostril.</p></list-item><list-item id="u0115"><label>•</label><p id="p0145">A smaller diameter tube is less likely to damage the mucosa. Make sure the tube has no nicks or sharp edges that could cause mucosal injury. If bleeding continues for more than 10 to 15 minutes or is believed to be excessive, an intranasal spray of 10 mg phenylephrine hydrochloride diluted in 10 mL of sterile saline solution infused through a nasal catheter may help to stop the nose bleed.</p></list-item></list></p></sec></sec><sec id="s0035"><title>Abdominocentesis</title><p id="p0150">Peritoneal fluid analysis can be a useful tool in evaluating the patient with acute gastrointestinal disease, intermittent abdominal pain, diarrhea, or chronic weight loss (see <xref rid="s0055" ref-type="sec">p. 159</xref>).</p><sec id="s0040"><title>Equipment</title><p id="p0155"><list list-type="simple" id="ulist0030"><list-item id="u0120"><label>•</label><p id="p0160">Twitch or possibly sedation, if necessary</p></list-item><list-item id="u0125"><label>•</label><p id="p0165">Clippers</p></list-item><list-item id="u0130"><label>•</label><p id="p0170">Material for sterile scrub</p></list-item><list-item id="u0135"><label>•</label><p id="p0175">Sterile gloves</p></list-item><list-item id="u0140"><label>•</label><p id="p0180">Sterile 18- to 22-gauge, <inline-graphic xlink:href="if018-001-9781455708925.gif"></inline-graphic>-inch (3.8-cm) needles, metal teat cannula (3.75 inches [9.4 cm] long), <inline-graphic xlink:href="if018-002-9781455708925.gif"></inline-graphic>-inch spinal needle, or metal bitch urinary catheter (10.5 inches [26.3 cm] long) (the latter two may be necessary for larger or obese horses)</p></list-item><list-item id="u0145"><label>•</label><p id="p0185">2% local anesthetic (with 25-gauge needle and 3-mL syringe)</p></list-item><list-item id="u0150"><label>•</label><p id="p0190">#15 blade if using a cannula or urinary catheter</p></list-item><list-item id="u0155"><label>•</label><p id="p0195">Sterile gauze sponge</p></list-item><list-item id="u0160"><label>•</label><p id="p0200">Tubes containing ethylenediaminetetraacetic acid (EDTA) and plain Vacutainer tubes for analysis</p></list-item><list-item id="u0165"><label>•</label><p id="p0205">Sterile vial, Port-a-Cul culture and transport system, or blood culture bottle for culture and sensitivity</p></list-item></list></p></sec><sec id="s0045"><title>Procedure</title><p id="p0210"><list list-type="simple" id="ulist0035"><list-item id="u0170"><label>•</label><p id="p0215">Choose an area in the most dependent portion of the abdomen (usually directly on the midline 5 cm caudal to the xyphoid). A right paramedian approach may be used to avoid the spleen. Alternatively, ultrasonography can be used to gauge the depth of the peritoneum and to attempt to position the abdominocentesis site in a location away from viscera.</p></list-item><list-item id="u0175"><label>•</label><p id="p0220">Clip the area chosen for abdominocentesis.</p></list-item><list-item id="u0180"><label>•</label><p id="p0225">Perform an aseptic scrub and perform a local block under appropriate restraint if using anything larger than a 25-gauge needle.</p></list-item><list-item id="u0185"><label>•</label><p id="p0230">Properly restrain the horse using twitch, lip chain, sedation, or a combination thereof.</p></list-item><list-item id="u0190"><label>•</label><p id="p0235">Don sterile gloves and maintain sterility throughout the procedure. If using a teat cannula or bitch catheter, incise through the skin and subcutaneous tissues at anesthetized site using #15 scalpel blade.</p></list-item><list-item id="u0195"><label>•</label><p id="p0240">While standing next to the patient, select insertion site for needle or teat cannula. Position your body to avoid injury from patient reaction to needle insertion. Insert the needle with a controlled, quick movement through the skin only, and then advance it gently through the muscular layers and peritoneum. If using a teat cannula or bitch urinary catheter, insertion through a gauze sponge minimizes contamination. If drops of abdominal fluid are not seen at the needle hub, reposition and rotate the needle or attach a syringe and aspirate. If necessary, place a second needle a few inches/cm from the first to release the negative pressure in the abdomen.</p></list-item><list-item id="u0200"><label>•</label><p id="p0245">Consider ultrasound examination to locate fluid pockets; however, peritoneal fluid can still be obtained even if <italic>not</italic> seen on ultrasonography.</p></list-item><list-item id="u10980"><label>•</label><p id="p13335">Once the end of the needle or cannula is in the abdomen, use caution when slowly redirecting and manipulating it to avoid penetrating viscera.<list list-type="simple" id="ulist0040"><list-item id="u0205"><label>•</label><p id="p0250">Allow the abdominal fluid to drop directly into the EDTA Vacutainer tube. If clinically indicated, fluid may be also submitted for microbiologic culture and sensitivity and peritoneal lactate and glucose concentrations.</p></list-item></list></p></list-item><list-item id="u10985"><label>•</label><p id="p13340"><italic><bold>Practice Tip:</bold> Most horses react to the needle or cannula penetrating the peritoneum (the response can vary from twinging to kicking) and a difference in resistance is felt between penetrating the muscle and peritoneum.</italic></p></list-item></list></p></sec><sec id="s0055"><title>Complications</title><p id="p0305"><list list-type="simple" id="ulist0055"><list-item id="u0250"><label>•</label><p id="p0310">Cellulitis or abscess formation can occur after a break in aseptic technique or during sampling of heavily contaminated peritoneal fluid. Accidental enterocentesis (aspiration of bowel contents) is <italic>not</italic> uncommon, but rarely causes a problem other than sample contamination. If an enterocentesis occurs, the area should be carefully monitored for 3 to 5 days; swelling with pain may indicate septic cellulitis requiring antibiotic therapy. A blunt-tipped cannula decreases the likelihood of bowel puncture, but caution is advised as puncture can still occur if the bowel wall is diseased or weighted ventrally along the abdominal wall (i.e., with sand impaction). Ultrasound-guided abdominocentesis is useful in foals to decrease the risk of intestinal laceration.</p></list-item><list-item id="u0255"><label>•</label><p id="p0315">Accidental splenic aspiration causes sample contamination, or in rare severe cases, significant hemorrhage.</p></list-item><list-item id="u0260"><label>•</label><p id="p0320">Omental herniation has been reported to occur in foals after abdominocentesis performed with a teat cannula in the rostral to middle abdomen. If this occurs, transect the omentum at or near the body wall, close aseptically prepared skin/subcutaneous tissues, apply an antiseptic cream or ointment, and cover with an abdominal bandage.</p></list-item></list></p></sec></sec><sec id="s0050"><title>Peritoneal Fluid Analysis</title><p id="p0255">Changes in peritoneal fluid are recognized fairly quickly after the onset of gastrointestinal disease (<xref rid="t0010" ref-type="table">Table 18-1</xref>). In cases of acute strangulating obstruction, changes in peritoneal fluid are often seen within hours of the onset of clinical signs. More insidious lesions, such as nonstrangulating obstruction, enteritis, and peritonitis, may produce less dramatic changes in peritoneal fluid concurrent with the progression of clinical signs. Inguinal herniation, intussusception, and entrapment of bowel in the omental bursa may initially result in local peritonitis with normal peritoneal fluid.<list list-type="simple" id="ulist0045"><list-item id="u0210"><label>•</label><p id="p0260">Normal peritoneal fluid is clear and light yellow, with a specific gravity of approximately 1.005 mg/dL.</p></list-item><list-item id="u0215"><label>•</label><p id="p0265">Turbidity results from increased protein or cellular content, which may be caused by septic peritonitis or inflammation of a segment of intestine. The color of the fluid can reflect the type of cells present. Cloudy white-to-yellow or even orange fluid represents large numbers of white blood cells, as in septic peritonitis.</p></list-item><list-item id="u0220"><label>•</label><p id="p0270">In strangulating obstruction, segments of bowel become compromised following arterial occlusion and diminished venous and lymphatic drainage from the affected segment. Initially, red blood cells and protein leak out of vessels resulting in a modified transudate. An increased total protein level and red blood cell count (serosanguineous fluid) may be seen early in the disease process. Peritoneal fluid becomes increasingly turbid as bowel ischemia progresses and white blood cells migrate.</p></list-item><list-item id="u0225"><label>•</label><p id="p0275">Necrotic bowel leaks bacteria and endotoxin, accelerating chemotaxis of white blood cells into the peritoneal cavity. Red-brown or green-colored fluid may indicate rupture of the stomach or intestine; peritoneal fluid obtained in these cases contains plant material and large numbers of several types of bacteria.</p></list-item><list-item id="u0230"><label>•</label><p id="p0280">Nucleated cell counts may be increased in the case of gastrointestinal rupture, but in the face of large volumes of free water and plant material, cell lysis may dramatically decrease nucleated cell count numbers. A low cell count in the face of grossly appearing abnormal peritoneal fluid does not rule out gastrointestinal rupture, particularly if the index of clinical suspicion is high.</p></list-item><list-item id="u0235"><label>•</label><p id="p0285">Dark red fluid may be obtained when a vessel or the spleen is entered. In rare instances, hemoperitoneum results from rupture of a vessel; the sample contains no platelets and may have evidence of erythrophagocytosis. The packed cell volume (PCV) may be compared with that of a systemic sample to differentiate samples from the spleen (PCV is higher) and from a vessel (PCV is the same). Stippling of red color in the yellow peritoneal fluid generally indicates iatrogenic bleeding from the centesis.</p></list-item></list><table-wrap position="float" id="t0010"><label>Table 18-1</label><caption><p>Correlation of Peritoneal Fluid Parameters and Intraperitoneal Disorders</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">Condition</th><th align="left">Appearance<xref rid="tn0010" ref-type="table-fn">*</xref></th><th align="left">Total Protein<xref rid="tn0010" ref-type="table-fn">*</xref> (g/dL)</th><th align="left">Total Nucleated Cells/L<xref rid="tn0010" ref-type="table-fn">*</xref></th><th align="left">Cytologic Findings<xref rid="tn0010" ref-type="table-fn">*</xref></th></tr></thead><tbody><tr><td align="left">Normal<xref rid="tn0015" ref-type="table-fn">†</xref></td><td align="left">Yellow, clear</td><td align="left"><2.0</td><td align="left"><7.5 × 10<sup>9</sup></td><td align="left">40%-80% neutrophils<break></break>20%-80% mononuclear</td></tr><tr><td colspan="5"><hr></hr></td></tr><tr><td align="left">Nonstrangulating obstruction</td><td align="left">Yellow, clear to slightly turbid</td><td align="left"><3.0</td><td align="left"><3.0-15.0 × 10<sup>9</sup></td><td align="left">Predominantly neutrophils (well preserved)</td></tr><tr><td colspan="5"><hr></hr></td></tr><tr><td align="left">Strangulating obstruction</td><td align="left">Red-brown, turbid</td><td align="left">2.5-6.0</td><td align="left">5.0-50.0 × 10<sup>9</sup></td><td align="left">Predominantly neutrophils (degenerate)</td></tr><tr><td colspan="5"><hr></hr></td></tr><tr><td align="left">Proximal duodenitis-jejunitis</td><td align="left">Yellow-red, turbid</td><td align="left">3.0-4.5</td><td align="left"><10.0 × 10<sup>9</sup></td><td align="left">Predominantly neutrophils (well preserved)</td></tr><tr><td colspan="5"><hr></hr></td></tr><tr><td align="left">Bowel rupture</td><td align="left">Red-brown, green, turbid with or without particulate matter</td><td align="left">5.0-6.5</td><td align="left">>20.0 × 10<sup>9</sup> (20-150 × 10<sup>9</sup>)</td><td align="left">>95% neutrophils (severely degenerate); intracellular and extracellular bacteria, with or without plant matter</td></tr><tr><td colspan="5"><hr></hr></td></tr><tr><td align="left">Septic peritonitis</td><td align="left">Yellow-white, turbid</td><td align="left">>3.0</td><td align="left">>20.0 × 10<sup>9</sup> (20-100 × 10<sup>9</sup>)</td><td align="left">Predominantly neutrophils (degenerate)</td></tr><tr><td colspan="5"><hr></hr></td></tr><tr><td align="left">Postceliotomy</td><td align="left">Yellow-red, turbid</td><td align="left">Variable</td><td align="left">Variable</td><td align="left">Predominantly neutrophils (slightly to moderately degenerate); no intracellular bacteria</td></tr><tr><td colspan="5"><hr></hr></td></tr><tr><td align="left">Enterocentesis</td><td align="left">Brown-green, with or without particulate matter</td><td align="left">Variable</td><td align="left"><1.0 × 10<sup>9</sup></td><td align="left">Free bacteria, few cells, plant matter</td></tr><tr><td colspan="5"><hr></hr></td></tr><tr><td align="left">Intraabdominal hemorrhage</td><td align="left">Dark red</td><td align="left">Initially similar to peripheral blood, WBC count increases with time</td><td align="left"></td><td align="left">PCV less than PCV of peripheral blood, erythrocytophagia, few to no platelets</td></tr></tbody></table><table-wrap-foot><fn id="sp0015"><p><italic>WBC,</italic> White blood cell; <italic>PCV,</italic> packed cell volume.</p></fn><fn id="sp0020"><p><bold><italic>Note:</italic></bold> Absence of gross or cytologic abnormalities in the peritoneal fluid does not rule out compromised intestine.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tn0010"><label>*</label><p id="np0020">Most common findings; exceptions can occur.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tn0015"><label>†</label><p id="np0025">Including peripartum mares.</p></fn></table-wrap-foot></table-wrap></p><p id="p0290">Cytologic examination should include a white blood cell count and differential, total protein, evaluation of cellular appearance, and examination for the presence of bacteria or plant material. A direct smear is made with Wright or Gram stain or both.<list list-type="simple" id="ulist0050"><list-item id="u10990"><label>•</label><p id="p13345"><italic><bold>Practice Tip:</bold> White blood cell counts are normally lower in foals.</italic> A moderate amount of blood contamination in the sample (≤17%) should <italic>not</italic> affect any parameters except the number of red blood cells.</p></list-item><list-item id="u10995"><label>•</label><p id="p13350"><italic><bold>Practice Tip:</bold> White blood cell count and total protein levels can be mildly increased in a patient that has undergone abdominal surgery even with manipulation of the intestines only.</italic> A sample with increased white blood cell numbers in which most neutrophils appear toxic and degenerate is evidence of septic peritonitis, even if the sample is obtained after celiotomy.</p></list-item><list-item id="u0240"><label>•</label><p id="p0295"><italic><bold>Practice Tip:</bold> Peritoneal fluid lactate that is greater than plasma lactate may suggest strangulation or infarction of bowel.</italic></p></list-item><list-item id="u0245"><label>•</label><p id="p0300">Peritoneal glucose concentrations that are less than blood glucose can occur with septic peritonitis.</p></list-item></list></p></sec><sec id="s0060"><title>Cecal or Colonic Trocarization</title><p id="p0325">Cecal trocarization can be performed to decompress the cecum in patients with cecal tympany; colonic trocarization may be necessary as a salvage procedure or in an emergent situation in which the degree of colonic distention seems to be significantly contributing to rapid physiologic deterioration. In most cases, trocarization is performed in situations in which surgical intervention is not a viable option or in cases in which the degree of large bowel distention appears life-threatening in the face of prolonged transport time to a surgical facility.</p><p id="p0330">Cecal gas distention is suspected in patients with colic when a “ping” is heard on simultaneous percussion and auscultation in the right paralumbar fossa and is confirmed with rectal palpation. Cecal tympany can be a primary or secondary disorder. Decompression might stimulate cecal motility and relieve the pain caused by distention. The procedure can be performed in patients with extreme abdominal distention before surgery if difficulties with ventilation or compromise of venous return are a concern once the patient is anesthetized. Cecal or colonic decompression in these patients may decrease intraabdominal pressure and improve venous return and ease of ventilation. If the patient is not a surgical candidate, trocarization might resolve colic in cases of tympany or simple colonic displacements. Cecal trocarization is not without risk, and the procedure should be performed only in situations in which there appears to be an obvious clinical benefit outweighing the risks.</p><sec id="s0065"><title>Equipment</title><p id="p0335"><list list-type="simple" id="ulist0060"><list-item id="u0265"><label>•</label><p id="p0340">Twitch</p></list-item><list-item id="u0270"><label>•</label><p id="p0345">Clippers</p></list-item><list-item id="u0275"><label>•</label><p id="p0350">Material for aseptic scrub</p></list-item><list-item id="u0280"><label>•</label><p id="p0355">2% local anesthetic, 5-mL syringe, and 22-gauge, <inline-graphic xlink:href="if018-003-9781455708925.gif"></inline-graphic>-inch (3.8-cm) needle</p></list-item><list-item id="u0285"><label>•</label><p id="p0360">Sterile gloves</p></list-item><list-item id="u0290"><label>•</label><p id="p0365">14- or 16-gauge, 5-inch (12.5-cm) pliable intravenous catheter</p></list-item><list-item id="u0295"><label>•</label><p id="p0370">30-inch extension set</p></list-item><list-item id="u0300"><label>•</label><p id="p0375">Small cup of tap water</p></list-item></list></p></sec><sec id="s0070"><title>Procedure</title><p id="p0380"><list list-type="simple" id="ulist0065"><list-item id="u0305"><label>•</label><p id="p0385">Consider using a twitch if the patient is not sedated. Sedation is <italic>not</italic> always necessary but may minimize risk to patient and personnel.</p></list-item><list-item id="u0310"><label>•</label><p id="p0390">Clip an area in the right paralumbar fossa where the “ping” is best heard, or alternatively in cases of severe colonic distention, on the left side where the ping is heard or gas distention is palpated per rectum.</p></list-item><list-item id="u0315"><label>•</label><p id="p0395">Infiltrate 3 to 5 mL of local anesthetic subcutaneously and in the underlying muscle at the trocarization site.</p></list-item><list-item id="u0320"><label>•</label><p id="p0400">Perform aseptic scrub.</p></list-item><list-item id="u0325"><label>•</label><p id="p0405">Wearing sterile gloves, insert the catheter and stylet through the skin, subcutaneous tissue, and abdominal muscle. The catheter should remain perpendicular to the skin. Remove the plastic cap on the catheter; if the catheter is in the cecum, gas escapes. When the catheter is in the cecum, remove the stylet entirely or withdraw the stylet approximately one-half inch to prevent collapse of the catheter by the abdominal wall.</p></list-item><list-item id="u0330"><label>•</label><p id="p0410">Attach the extension set and place the free end in the cup of water. Bubbles are produced as long as gas is escaping from the cecum; suction may be used if available.</p></list-item><list-item id="u0335"><label>•</label><p id="p0415">If gas is no longer retrievable, withdraw the catheter; <italic>do not</italic> attempt to redirect.</p></list-item><list-item id="u0340"><label>•</label><p id="p0420">Administer antibiotics (e.g., 300 mg [3 mL] gentocin or 750 mg [3 mL] amikacin) through the catheter as it is being removed.</p></list-item></list></p></sec><sec id="s0075"><title>Complications</title><p id="p0425"><list list-type="simple" id="ulist0070"><list-item id="u0345"><label>•</label><p id="p0430">Low-grade, localized peritonitis, which can affect peritoneal fluid parameters, is expected to occur after this procedure.</p></list-item><list-item id="u0350"><label>•</label><p id="p0435">Clinical evidence of disseminated peritonitis and subsequent complications related to cecal or colonic wall trauma are rare but can occur. Abdominal wall abscessation at the puncture site may occur; however, this is unusual.</p></list-item><list-item id="u0355"><label>•</label><p id="p0440">Signs of infection should raise suspicion of a more serious problem and be managed promptly with the appropriate therapy. Injecting antibiotics through the catheter during removal may minimize this complication and is recommended.</p></list-item><list-item id="u0360"><label>•</label><p id="p0445">Repeat trocarization is <italic>not</italic> recommended because clinical peritonitis can develop.</p></list-item><list-item id="u0365"><label>•</label><p id="p0450">Local cellulitis or abscess can occur at the trocarization site. The inflammation is usually self-limiting but should be monitored and managed appropriately.</p></list-item></list></p><sec id="s0080"><title>Transrectal Trocarization of the Large Colon</title><p id="p0455"><list list-type="simple" id="ulist0075"><list-item id="u0370"><label>•</label><p id="p0460">Dr. Massimo Magri in Italy recently reported a transrectal technique for decompressing the colon when there is severe colonic distention. <italic><bold>Note:</bold> The technique appears to have merit in horses with severe abdominal distention, providing relief from severe pain. This permits a more complete examination to be performed, and in some cases, resolution of the distention allows intestinal motility to resume and/or the colon to fall in a more normal position (if displaced). It can be curative in some horses if there is</italic> not <italic>a strangulating lesion.</italic> Buscopan can be given before the procedure if there are strong rectal contractions on the initial abdominal palpation per rectum. The procedure appears to be safe and quick but requires mechanical suction to remove the gas. Dr. Magri has developed a special cylinder that encloses the needle so that there is no danger of the needle puncturing the rectum until it is placed against the distended colon; the device is then activated as it enters the colon. The other end of the instrument is connected to suction. Information is available in Equine Veterinary Education Journal [Eq Vet Ed April 2013; 25(4):184-188].</p></list-item></list></p><sec id="s0085"><title>Complications</title><p id="p0465"><list list-type="simple" id="ulist0080"><list-item id="u0375"><label>•</label><p id="p0470">Problems associated with transrectal trocarization of the large colon are similar to those listed for the transcutaneous procedure. (See previous section, <xref rid="p0290" ref-type="p">p. 160</xref>.)</p></list-item></list></p></sec></sec></sec></sec><sec id="s0090"><title>Esophagostomy</title><p id="p0475">Esophagostomy is used for the placement of an indwelling feeding tube. Most commonly the procedure is performed with the horse standing under sedation and local anesthesia. Depending on the temperament of the patient, the type of obstruction, financial concerns, and the surgeon's preference, the procedure may also be performed under general anesthesia. Placement of a nasogastric tube before surgery is recommended to identify the esophagus and minimize the dissection of surrounding tissues. A ventrolateral approach is used most commonly when an esophagostomy is performed for placement of a feeding tube. This approach typically provides improved access to the middle and distal cervical esophagus as opposed to a ventral approach. A surgeon experienced in other esophageal approaches should be consulted if another procedure is contemplated for feeding tube placement.</p><sec id="s9005"><title>Equipment</title><p id="p13355"><list list-type="simple" id="ulist9015"><list-item id="u11000"><label>•</label><p id="p13360">Twitch</p></list-item><list-item id="u11005"><label>•</label><p id="p13365">Clippers</p></list-item><list-item id="u11010"><label>•</label><p id="p13370">Material for aseptic scrub</p></list-item><list-item id="u11015"><label>•</label><p id="p13375">2% local anesthetic, 5-mL syringe, and 22 guage, <inline-graphic xlink:href="if018-011-9781455708925.gif"></inline-graphic>-inch (3.8-cm) needle</p></list-item><list-item id="u11020"><label>•</label><p id="p13380">Sterile gloves</p></list-item><list-item id="u11025"><label>•</label><p id="p13385">Small surgical pack</p></list-item><list-item id="u11030"><label>•</label><p id="p13390">Appropriate suture material as needed</p></list-item><list-item id="u11035"><label>•</label><p id="p13395">Penrose drains, <inline-graphic xlink:href="if018-012-9781455708925.gif"></inline-graphic>-inch (1.27 cm)</p></list-item><list-item id="u11040"><label>•</label><p id="p13400">Stomach tube in the esophagus to identify the esophagus in the surgery field</p></list-item></list></p></sec><sec id="s0095"><title>Procedure</title><p id="p0480"><list list-type="simple" id="ulist0085"><list-item id="u0380"><label>•</label><p id="p0485">An approximately 5-cm incision is made ventral to the jugular vein at or near the junction of the middle and distal cervical esophagus (<xref rid="f0010" ref-type="fig">Fig. 18-1</xref>, <italic>A-C</italic>).<fig id="f0010"><label>Figure 18-1</label><caption><p>Technique of esophagostomy for placement of an indwelling feeding tube. <bold>A,</bold> Location of esophagus on left side of neck. <bold>B,</bold> Incision into esophageal lumen. <bold>C,</bold> Feeding tube passed normograde to stomach.</p></caption><graphic xlink:href="f018-001-9781455708925"></graphic></fig></p></list-item><list-item id="u0385"><label>•</label><p id="p0490">Separate the sternocephalicus and brachiocephalicus muscles.</p></list-item><list-item id="u0390"><label>•</label><p id="p0495">Identify and gently retract the carotid sheath, which contains the vagosympathetic trunk and recurrent laryngeal nerve and artery.</p></list-item><list-item id="u11220"><label>•</label><p id="p0500"><italic><bold>Practice Tip:</bold> The vagosympathetic trunk and recurrent laryngeal nerve must be identified and avoided during the surgical procedure.</italic></p></list-item><list-item id="u0395"><label>•</label><p id="p0505">Incise the deep cervical adventitia overlying the esophagus; elevation of the esophagus with two <inline-graphic xlink:href="if018-004-9781455708925.gif"></inline-graphic>″ Penrose drains or Allis tissue forceps may aid in the dissection.</p></list-item><list-item id="u0400"><label>•</label><p id="p0510">Once an appropriately sized lumen into the esophagus has been created, the original stomach tube can be retracted, and the selected feeding tube can be inserted into the newly created esophagostomy. Depending on surgeon preference and suspected duration of the esophagostomy, mucosa may be sutured to the skin to minimize subcutaneous contamination. The tube should be firmly secured in place, often with tape and skin sutures.</p></list-item></list></p></sec><sec id="s0100"><title>Complications</title><p id="p0515"><list list-type="simple" id="ulist0095"><list-item id="u0405"><label>•</label><p id="p0520">Even with delicate tissue handling, laryngeal hemiplegia from damage to the recurrent laryngeal nerve can be a sequela to the surgery.</p></list-item><list-item id="u0410"><label>•</label><p id="p0525">Further complications can include esophageal stricture and dissecting infections while the tube is in place or following tube removal.</p></list-item></list></p></sec></sec></sec><sec id="s0105"><title>Aging Guidelines</title><p id="p0530"><italic><bold>David L. Foster</bold></italic></p><p id="p0535"><list list-type="simple" id="ulist0100"><list-item id="u0415"><label>•</label><p id="p0540">Aging of horses by the teeth becomes less exact as the individual advances in years.</p></list-item><list-item id="u0420"><label>•</label><p id="p0545">Bracketing age into 0 to 2 years, 2 to 5 years, 5 to 10 years, 10 to 20 years, and >20 years is generally a useful starting point.</p></list-item><list-item id="u0425"><label>•</label><p id="p0550">Specific aging of the horse is accomplished by the following:<list list-type="simple" id="ulist0105"><list-item id="u0430"><label>•</label><p id="p0555">Noting the eruption of the deciduous incisors</p></list-item><list-item id="u0435"><label>•</label><p id="p0560">Shedding of the juvenile incisors</p></list-item><list-item id="u0440"><label>•</label><p id="p0565">Eruption and wear of the permanent incisors</p></list-item></list></p></list-item></list></p><p id="p0570">Once the deciduous incisors are shed and the permanent incisors are erupted, aging is less clear with advancing age. The degree of wear, general shape, length, and other features contribute to suggest an “approximate” age. As the horse ages, small variations of the teeth, oral configuration, and diet contribute to the appearance, angulation, and wear of the teeth.<list list-type="simple" id="ulist0110"><list-item id="u0445"><label>•</label><p id="p0575">General guidelines are described as follows:<list list-type="simple" id="ulist0115"><list-item id="u0450"><label>•</label><p id="p0580">Foals use the “rule-of-8”:<list list-type="simple" id="ulist0120"><list-item id="u0455"><label>○</label><p id="p0585">First incisors erupt at 8 days.</p></list-item><list-item id="u0460"><label>○</label><p id="p0590">Second incisors erupt at 8 weeks.</p></list-item><list-item id="u0465"><label>○</label><p id="p0595">Third incisors erupt at 8 months.</p></list-item></list></p></list-item><list-item id="u0470"><label>•</label><p id="p0600">Two-year-olds shed the central deciduous incisors.</p></list-item><list-item id="u0475"><label>•</label><p id="p0605">Three-year-olds shed the second deciduous incisors.</p></list-item><list-item id="u0480"><label>•</label><p id="p0610">Four-year-olds shed the third deciduous incisors.</p></list-item><list-item id="u0485"><label>•</label><p id="p0615">Five-year-olds have all permanent incisors.</p></list-item><list-item id="u0490"><label>•</label><p id="p0620">Seven-year-olds have all the incisors erupted, and the corner mandibular incisors (303/403) have their table surface in wear and a large central “cup.”</p></list-item><list-item id="u0495"><label>•</label><p id="p0625">Ten-year-olds: Galvayne's groove appears on 103/203 (maxillary I3); 301/401 and 302/402 have developed a “round” table surface. All cups are lost from the mandibular incisors.</p></list-item><list-item id="u0500"><label>•</label><p id="p0630">At greater than 10 years of age, it becomes increasingly more difficult to determine age accurately by dental examination.</p></list-item><list-item id="u0505"><label>•</label><p id="p0635">The length, angulation, degree of wear, and shape of incisors are “markers” of an individual's age but become increasingly unreliable with advancing age.</p></list-item></list></p></list-item></list></p><sec id="s0110"><sec id="s0115"><title>Using Tattoos and Brands to Age Horses</title><p id="p0640">Several horse breed registries mark the year of birth in the tattoo or freeze brand applied to their horses.</p><sec id="s0120"><title>Thoroughbreds</title><p id="p0645"><list list-type="simple" id="ulist0125"><list-item id="u0510"><label>•</label><p id="p0650">All racing Thoroughbreds in the United States receive a lip tattoo.</p></list-item><list-item id="u0515"><label>•</label><p id="p0655">A letter followed by four or five numbers (representing the registration number) completes the tattoo.</p></list-item><list-item id="u0520"><label>•</label><p id="p0660">The letter denotes the year of birth: A—1971 through Z—1996; all letters of the alphabet are used.</p></list-item><list-item id="u0525"><label>•</label><p id="p0665">The alphabet is repeated every 26 years; all Thoroughbreds born in 1997 are tattooed beginning with the letter A; 1998, B; 1999, C, to the end of the alphabet (<xref rid="b0010" ref-type="boxed-text">Box 18-1</xref>).<boxed-text id="b0010"><label>Box 18-1</label><caption><title>Thoroughbred Tattoos</title></caption><p id="p0670">A = 1971, 1997</p><p id="p0675">B = 1972, 1998</p><p id="p0680">C = 1973, 1999</p><p id="p0685">D = 1974, 2000</p><p id="p0690">E = 1975, 2001</p><p id="p0695">F = 1976, 2002</p><p id="p0700">G = 1977, 2003</p><p id="p0705">H = 1978, 2004</p><p id="p0710">I = 1979, 2005</p><p id="p0715">J = 1980, 2006</p><p id="p0720">K = 1981, 2007</p><p id="p0725">L = 1982, 2008</p><p id="p0730">M = 1983, 2009</p><p id="p0735">N = 1984, 2010</p><p id="p0740">O = 1985, 2011</p><p id="p0745">P = 1986, 2012</p><p id="p0750">Q = 1987, 2013</p><p id="p0755">R = 1988, 2014</p><p id="p0760">S = 1989, 2015</p><p id="p0765">T = 1990, 2016</p><p id="p0770">U = 1991, 2017</p><p id="p0775">V = 1992, 2018</p><p id="p0780">W = 1993, 2019</p><p id="p0785">X = 1994, 2020</p><p id="p0790">Y = 1995, 2021</p><p id="p0795">Z = 1996, 2022</p></boxed-text></p></list-item><list-item id="u0530"><label>•</label><p id="p0800">An exception is made for foreign-bred horses that, once properly identified, receive a lip tattoo beginning with an asterisk followed by a number and no letter; this serves as the full registration number.</p></list-item></list></p></sec><sec id="s0125"><title>Standardbreds</title><p id="p0805"><list list-type="simple" id="ulist0130"><list-item id="u0535"><label>•</label><p id="p0810">The Standardbred tattoo system can be used to determine the year of birth. However, it is an idiosyncratic system and is difficult to apply in the field without a tattoo list.</p></list-item><list-item id="u0540"><label>•</label><p id="p0815">In the United States, a system is used that records the full registration number, a letter to denote the year of birth, and four more characters, one of which may be another letter (<xref rid="t0015" ref-type="table">Table 18-2</xref>).<table-wrap position="float" id="t0015"><label>Table 18-2</label><caption><p>Standardbred Tattoos</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">Born in 1981 or Earlier</th><th align="left">Born in 1982 or Later</th><th align="left"></th></tr></thead><tbody><tr><td align="left">First three digits are numbers. The fourth can be a letter or a number. The fifth is a letter indicating year of foaling. <italic>The letters M, N, O, Q, and U are not used.</italic></td><td align="left">The first character is a letter, indicating year of foaling. The second can be a letter or a number. The last three digits are numbers. <italic>The letters I, O, Q, U, and Y are not used.</italic></td><td align="left"></td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">A = 1961</td><td align="char">A = 1982</td><td align="char">A = 2003</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">B = 1962</td><td align="char">B = 1983</td><td align="char">B = 2004</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">C = 1963</td><td align="char">C = 1984</td><td align="char">C = 2005</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">D = 1964</td><td align="char">D = 1985</td><td align="char">D = 2006</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">E = 1965</td><td align="char">E = 1986</td><td align="char">E = 2007</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">F = 1966</td><td align="char">F = 1987</td><td align="char">F = 2008</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">G = 1967</td><td align="char">G = 1988</td><td align="char">G = 2009</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">H = 1968</td><td align="char">H = 1989</td><td align="char">H = 2010</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">I = 1969</td><td align="char">J = 1990</td><td align="char">J = 2011</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">J = 1970</td><td align="char">K = 1991</td><td align="char">K = 2012</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">K = 1971</td><td align="char">L = 1992</td><td align="char">L = 2013</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">L = 1972</td><td align="char">M = 1993</td><td align="char">M = 2014</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">P = 1973</td><td align="char">N = 1994</td><td align="char">N = 2015</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">R = 1974</td><td align="char">P = 1995</td><td align="char">P = 2016</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">S = 1975</td><td align="char">R = 1996</td><td align="char">R = 2017</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">T = 1976</td><td align="char">S = 1997</td><td align="char">S = 2018</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">V = 1977</td><td align="char">T = 1998</td><td align="char">T = 2019</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">W = 1978</td><td align="char">V = 1999</td><td align="char">V = 2020</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">X = 1979</td><td align="char">W = 2000</td><td align="char">W = 2021</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">Y = 1980</td><td align="char">X = 2001</td><td align="char">X = 2022</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="char">Z = 1981</td><td align="char">Z = 2002</td><td align="char">Z = 2023</td></tr></tbody></table></table-wrap></p></list-item><list-item id="u0545"><label>•</label><p id="p0820">Standardbreds rotate the year of birth letter from the first position to the last in the tattoo character series once all letters are used. Not all letters of the alphabet are used in any given series.</p></list-item><list-item id="u0550"><label>•</label><p id="p0825">Any Standardbred born after 1995 may have its identification markings as a lip tattoo or a freeze brand applied to the upper right side of the neck.</p></list-item><list-item id="u0555"><label>•</label><p id="p0830">For example, 4321A could be a lip tattoo assigned to a horse born in 1961.</p></list-item><list-item id="u0560"><label>•</label><p id="p0835">A Standardbred born in 1995 could have a lip tattoo or a freeze brand of P4321.</p></list-item></list></p></sec><sec id="s0130"><title>Arabian Horse Registry of America/U.S. Bureau of Land Management Registry</title><p id="p0840"><list list-type="simple" id="ulist0135"><list-item id="u0565"><label>•</label><p id="p0845">Registry uses a freeze-brand encryption to identify full- and partial-bred Arabian horses and mustangs (<xref rid="f0015" ref-type="fig">Fig. 18-2</xref>).<fig id="f0015"><label>Figure 18-2</label><caption><p>Freeze branding system for breed registration can be useful in individual age identification. A number is assigned to each angle or double bar configuration <italic>(top).</italic> Sample registration is depicted below the freeze branding system.</p></caption><graphic xlink:href="f018-002-9781455708925"></graphic><attrib>(Courtesy Michael Q. Lowder, DVM, MS.)</attrib></fig></p></list-item><list-item id="u0570"><label>•</label><p id="p0850">The first figure represents the breed.</p></list-item><list-item id="u0575"><label>•</label><p id="p0855">If the figure is rotated to the right (clockwise), it represents a half-breed.</p></list-item><list-item id="u0580"><label>•</label><p id="p0860">The next stacked figures represent the year of birth and are followed by the horse's registration number.</p></list-item></list></p></sec><sec id="s0135"><title>Racing Quarter Horses</title><p id="p0865"><list list-type="simple" id="ulist0140"><list-item id="u0585"><label>•</label><p id="p0870">Racing Quarter Horses are identified by lip tattoos, but they do <italic>not</italic> indicate the year of birth as in Thoroughbreds and Standardbreds.</p></list-item></list></p></sec></sec></sec><sec id="s0140"><title>Equine Dental Nomenclature</title><p id="p0875">Two nomenclature systems are used for horses:<list list-type="simple" id="ulist0145"><list-item id="u0590"><label>•</label><p id="p0880">Anatomic descriptive system (<xref rid="f0020" ref-type="fig">Fig. 18-3</xref>)<fig id="f0020"><label>Figure 18-3</label><caption><p>Numbering and anatomic descriptive systems used to identify equine teeth.</p></caption><graphic xlink:href="f018-003-9781455708925"></graphic></fig></p></list-item><list-item id="u0595"><label>•</label><p id="p0885">Triadan (numeric) nomenclature system (<xref rid="f0025" ref-type="fig">Fig. 18-4</xref>)<fig id="f0025"><label>Figure 18-4</label><caption><p>In the Triadan system, juvenile or deciduous teeth are identified by replacing the first digit with 5, 6, 7, or 8. For example, 203 for the permanent tooth would be identified by the number 603 for the deciduous tooth.</p></caption><graphic xlink:href="f018-004-9781455708925"></graphic></fig></p></list-item></list></p><p id="p0890">The use of a concise nomenclature system promotes communication between professionals; accurate record keeping; and organized oral examinations. In the anatomic system (see <xref rid="f0020" ref-type="fig">Fig. 18-3</xref>), a letter defines the type of tooth being described. All lowercase letters used denote deciduous teeth, capital letters permanent teeth: I, incisors; C, canines; P, premolars; and M, molars. A number then is assigned to the letter that denotes the location of the tooth in the oral cavity (e.g., first molar and second incisor). The oral cavity is divided into four quadrants. The horse's right maxillary arcade is the first arcade. The other three quadrants are assigned sequentially in a clockwise manner from the examiner's position facing the horse. The anatomic letter then has the positional number placed around the letter to represent the location of the tooth. For example, a right mandibular second incisor would be defined as <sub>2</sub>I; a left maxillary second incisor would be defined as I<sup>2</sup>.</p><p id="p0895">The right mandibular arcade of an adult male would be noted in the anatomic system as follows: <sub>1</sub>I, <sub>2</sub>I, <sub>3</sub>I, <sub>1</sub>C, <sub>2</sub>P, <sub>3</sub>P, <sub>4</sub>P, <sub>1</sub>M, <sub>2</sub>M, <sub>3</sub>M (assuming that the first premolar is <italic>not</italic> present).</p><p id="p0900">The Triadan digital nomenclature system assigns a three-digit number to each tooth (see <xref rid="f0025" ref-type="fig">Fig. 18-4</xref>). The first number defines the quadrant in which the tooth resides. The quadrants are numbered one through four starting with the horse's right maxillary arcade and progressing clockwise relative to the examiner facing the horse, as is the case for the anatomic nomenclature system. The following two numbers in this system define the position of the tooth relative to the centerline of the oral cavity. The first or central incisor is assigned “01,” the next (middle) incisor “02,” and so on. The right mandibular arcade of an adult male would be described in the Triadan system as follows: 401, 402, 403, 404, 406, 407, 408, 409, 410, 411. This supposes that 405 (the lower first premolar or wolf tooth) is <italic>not</italic> present.</p></sec><sec id="s0145"><title>Dental Radiology Ambulatory Techniques</title><p id="p0905"><italic><bold>Edward T. Earley</bold></italic></p><sec id="s0150"><title>Extraoral Radiographs</title><p id="p0910">Refer to <xref rid="t0020" ref-type="table">Table 18-3</xref>.<table-wrap position="float" id="t0020"><label>Table 18-3</label><caption><p>Extraoral Technique Chart</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">View</th><th align="left">Distance (cm)</th><th align="left">kV</th><th align="left">mA</th><th align="left">Time (second)</th><th align="left">mA-s</th></tr></thead><tbody><tr><td align="left">Dorsal ventral</td><td align="char">40-50</td><td align="center">78</td><td align="center">25</td><td align="char">0.04</td><td align="char">1</td></tr><tr><td colspan="6"><hr></hr></td></tr><tr><td align="left">Lateral</td><td align="char">40-50</td><td align="center">74</td><td align="center">25</td><td align="char">0.04</td><td align="char">1</td></tr><tr><td colspan="6"><hr></hr></td></tr><tr><td align="left">D OBL rostral cheek teeth</td><td align="char">40-50</td><td align="center">70</td><td align="center">25</td><td align="char">0.03</td><td align="char">0.75</td></tr><tr><td colspan="6"><hr></hr></td></tr><tr><td align="left">D OBL caudal cheek teeth</td><td align="char">40-50</td><td align="center">74</td><td align="center">25</td><td align="char">0.04</td><td align="char">1</td></tr><tr><td colspan="6"><hr></hr></td></tr><tr><td align="left">V OBL rostral cheek teeth</td><td align="char">40-50</td><td align="center">74</td><td align="center">25</td><td align="char">0.04</td><td align="char">1</td></tr><tr><td colspan="6"><hr></hr></td></tr><tr><td align="left">V OBL caudal cheek teeth</td><td align="char">40-50</td><td align="center">80</td><td align="center">25</td><td align="char">0.05</td><td align="char">1.25-2.0</td></tr></tbody></table><table-wrap-foot><fn id="sp0055"><p>Cassettes: 10 × 12 inches and 14 × 17 inches with rare earth intensifying screens.</p></fn><fn id="sp0060"><p>Film: Green, 400 speed.</p></fn><fn id="sp0065"><p><italic>D,</italic> Dorsal; <italic>OBL,</italic> oblique <italic>V,</italic> ventral.</p></fn></table-wrap-foot></table-wrap></p><sec id="s0155"><title>Dorsal Ventral View (DV)</title><p id="p0915"><list list-type="simple" id="ulist0150"><list-item id="u0600"><label>•</label><p id="p0920">A 14- × 17-inch cassette is recommended (<xref rid="f0030" ref-type="fig">Fig. 18-5</xref>).<fig id="f0030"><label>Figure 18-5</label><caption><p>Dorsoventral positioning.</p></caption><graphic xlink:href="f018-005-9781455708925"></graphic></fig></p></list-item><list-item id="u0605"><label>•</label><p id="p0925">Center the beam on the rostral aspect of the facial crest (<xref rid="f0030" ref-type="fig">Fig. 18-5</xref>).</p></list-item><list-item id="u0610"><label>•</label><p id="p0930">Bungee cords can be used to support the cassette (<xref rid="f0035" ref-type="fig">Figs. 18-6</xref>and <xref rid="f0040" ref-type="fig">18-7</xref>).<fig id="f0035"><label>Figure 18-6</label><caption><p>Dorsoventral position with bungee cords.</p></caption><graphic xlink:href="f018-006-9781455708925"></graphic></fig><fig id="f0040"><label>Figure 18-7</label><caption><p>Dorsoventral radiograph.</p></caption><graphic xlink:href="f018-007-9781455708925"></graphic></fig></p></list-item></list></p></sec><sec id="s0160"><title>Lateral View (LAT)</title><p id="p0935"><list list-type="simple" id="ulist0155"><list-item id="u0615"><label>•</label><p id="p0940">A 14- × 17-inch cassette is recommended (<xref rid="f0045" ref-type="fig">Fig. 18-8</xref>).<fig id="f0045"><label>Figure 18-8</label><caption><p>Lateral positioning.</p></caption><graphic xlink:href="f018-008-9781455708925"></graphic></fig></p></list-item><list-item id="u0620"><label>•</label><p id="p0945">Opened-mouth technique is recommended (<xref rid="f0050" ref-type="fig">Fig. 18-9</xref>).<fig id="f0050"><label>Figure 18-9</label><caption><p>Lateral view.</p></caption><graphic xlink:href="f018-009-9781455708925"></graphic></fig></p></list-item><list-item id="u0625"><label>•</label><p id="p0950">Center the beam at the rostral aspect of the facial crest (<xref rid="f0050" ref-type="fig">Figs. 18-9</xref> and <xref rid="f0055" ref-type="fig">18-10</xref>).<fig id="f0055"><label>Figure 18-10</label><caption><p>Lateral radiograph.</p></caption><graphic xlink:href="f018-010-9781455708925"></graphic></fig></p></list-item></list></p><sec id="s0165"><title>Lateral 30-Degree Dorsal–Lateral Oblique (L 30-Degree D-LO) or (D OBL)</title><p id="p0955"><list list-type="simple" id="ulist0160"><list-item id="u0630"><label>•</label><p id="p0960">A 10- × 12-inch cassette is recommended.</p></list-item><list-item id="u0635"><label>•</label><p id="p0965">The film is oriented to the side of the lesion.</p></list-item><list-item id="u0640"><label>•</label><p id="p0970">The cassette is positioned slightly ventral to accommodate the oblique image (<xref rid="f0060" ref-type="fig">Fig. 18-11</xref>).<fig id="f0060"><label>Figure 18-11</label><caption><p>Dorsal oblique positioning.</p></caption><graphic xlink:href="f018-011-9781455708925"></graphic></fig></p></list-item><list-item id="u0645"><label>•</label><p id="p0975">The view is taken at 30° dorsal to the lateral view.</p></list-item><list-item id="u0650"><label>•</label><p id="p0980">The image is focusing on the maxillary arcade corresponding to the same side as the cassette (<xref rid="f0065" ref-type="fig">Fig. 18-12</xref>).<fig id="f0065"><label>Figure 18-12</label><caption><p>Positioning for an opened-mouth lateral dorsal oblique.</p></caption><graphic xlink:href="f018-012-9781455708925"></graphic></fig></p></list-item><list-item id="u0655"><label>•</label><p id="p0985">An opened-mouth technique helps separate the arcades (<xref rid="f0070" ref-type="fig">Fig. 18-13</xref>).<fig id="f0070"><label>Figure 18-13</label><caption><p>Lateral dorsal oblique radiograph.</p></caption><graphic xlink:href="f018-013-9781455708925"></graphic></fig></p></list-item></list></p></sec><sec id="s0170"><title>Lateral 45-Degree Ventral Lateral Oblique (L 45-Degree V-LO) or (V OBL)</title><p id="p0990"><list list-type="simple" id="ulist0165"><list-item id="u0660"><label>•</label><p id="p0995">A 10- × 12-inch cassette is recommended.</p></list-item><list-item id="u0665"><label>•</label><p id="p1000">The film is oriented to the side of the lesion (<xref rid="f0075" ref-type="fig">Fig. 18-14</xref>).<fig id="f0075"><label>Figure 18-14</label><caption><p>Ventral oblique positioning.</p></caption><graphic xlink:href="f018-014-9781455708925"></graphic></fig></p></list-item><list-item id="u0670"><label>•</label><p id="p1005">The cassette should be positioned slightly dorsal to accommodate the oblique image (<xref rid="f0080" ref-type="fig">Figs. 18-15</xref>and <xref rid="f0085" ref-type="fig">18-16</xref>).<fig id="f0080"><label>Figure 18-15</label><caption><p>Imaging the left mandibular arcade (lateral ventral oblique).</p></caption><graphic xlink:href="f018-015-9781455708925"></graphic></fig><fig id="f0085"><label>Figure 18-16</label><caption><p>Positioning for the right mandibular arcade (right ventral oblique).</p></caption><graphic xlink:href="f018-016-9781455708925"></graphic></fig></p></list-item><list-item id="u0675"><label>•</label><p id="p1010">The view is taken at 45° ventral to the lateral view.</p></list-item><list-item id="u0680"><label>•</label><p id="p1015">The image is focusing on the mandibular arcade corresponding to the same side as the cassette (<xref rid="f0090" ref-type="fig">Figs. 18-17</xref>and <xref rid="f0095" ref-type="fig">18-18</xref>).<fig id="f0090"><label>Figure 18-17</label><caption><p>Technique for the rostral cheek teeth.</p></caption><graphic xlink:href="f018-017-9781455708925"></graphic></fig><fig id="f0095"><label>Figure 18-18</label><caption><p>Technique for the caudal cheek teeth.</p></caption><graphic xlink:href="f018-018-9781455708925"></graphic></fig></p></list-item><list-item id="u0685"><label>•</label><p id="p1020">An opened-mouth technique helps separate the arcades.</p></list-item></list></p></sec><sec id="s0175"><title>Opened-Mouth Techniques</title><p id="p1025"><list list-type="simple" id="ulist0170"><list-item id="u0690"><label>•</label><p id="p1030">The mouth can be held open with a small section of polyvinyl chloride pipe placed between the incisors (3 to 4 inches in length and <inline-graphic xlink:href="if018-005-9781455708925.gif"></inline-graphic> to 2 inches in diameter; <xref rid="f0100" ref-type="fig">Figs. 18-19</xref>and <xref rid="f0105" ref-type="fig">18-20</xref>).<fig id="f0100"><label>Figure 18-19</label><caption><p>Adapted polyvinyl chloride pipe with an elastic strap.</p></caption><graphic xlink:href="f018-019-9781455708925"></graphic></fig><fig id="f0105"><label>Figure 18-20</label><caption><p>Adapted polyvinyl chloride pipe in use.</p></caption><graphic xlink:href="f018-020-9781455708925"></graphic></fig></p></list-item><list-item id="u0695"><label>•</label><p id="p1035">A Stubbs full-mouth speculum<xref rid="fn0020" ref-type="fn">3</xref> can be used to hold the mouth open and to support the cassette. Use of a longer elastic strap (draft poll strap) is best so that the buckle is placed up near the poll/ear and out of the radiographic view (<xref rid="f0065" ref-type="fig">Figure 18-12</xref>, <xref rid="f0110" ref-type="fig">Figure 18-21</xref>, <xref rid="f0115" ref-type="fig">Figure 18-22</xref>, <xref rid="f0120" ref-type="fig">Figure 18-23</xref>).<fig id="f0110"><label>Figure 18-21</label><caption><p>Stubbs full-mouth speculum.</p></caption><graphic xlink:href="f018-021-9781455708925"></graphic></fig><fig id="f0115"><label>Figure 18-22</label><caption><p>Elastic “draft poll strap” <italic>(left)</italic> and an elastic “regular poll strap” <italic>(right).</italic></p></caption><graphic xlink:href="f018-022-9781455708925"></graphic></fig><fig id="f0120"><label>Figure 18-23</label><caption><p>Placement of the cassette using the Stubbs full-mouth speculum.</p></caption><graphic xlink:href="f018-023-9781455708925"></graphic></fig></p></list-item></list></p></sec><sec id="s0180"><title>Radiograph Orientation</title><p id="p1040"><list list-type="simple" id="ulist0175"><list-item id="u0700"><label>•</label><p id="p1045">When identifying multiple views of dental radiographs, it is recommended to orient the radiographs in a fashion so that each view is instantly recognizable.</p></list-item><list-item id="u0705"><label>•</label><p id="p1050">Using a technique that is common for small animal and human dental radiology leaves <italic>no</italic> room for confusion between the left and right arcades.</p></list-item><list-item id="u0710"><label>•</label><p id="p1055">The viewing technique always orients the radiograph in the same plane as viewing the horse from that position (see <xref rid="f0120" ref-type="fig">Fig. 18-23</xref>).</p></list-item><list-item id="u0715"><label>•</label><p id="p1060">When viewing a radiograph of the left arcades (200 and 300 arcades), the nose would always be facing the left (see <xref rid="f0070" ref-type="fig">Figure 18-13</xref>, <xref rid="f0090" ref-type="fig">Figure 18-17</xref>, <xref rid="f0095" ref-type="fig">Figure 18-18</xref>).</p></list-item><list-item id="u0720"><label>•</label><p id="p1065">When viewing a radiograph of the right arcades (100 and 400 arcades), the nose would always be facing the right (see <xref rid="f0055" ref-type="fig">Fig. 18-10</xref>).</p></list-item><list-item id="u0725"><label>•</label><p id="p1070">A DV image is facing the horse from the front. As a result, the right side of the horse is always oriented to the left on a DV radiograph.</p></list-item></list></p></sec></sec><sec id="s0185"><title>Intraoral Radiographs</title><p id="p1075">Refer to <xref rid="t0025" ref-type="table">Table 18-4</xref>.<table-wrap position="float" id="t0025"><label>Table 18-4</label><caption><p>Intraoral Technique Chart</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">View</th><th align="left">Distance (cm)</th><th align="center">kV</th><th align="left">mA</th><th align="left">Time (second)</th><th align="center">mA-s</th></tr></thead><tbody><tr><td align="left">Maxillary cheek teeth</td><td align="char">30-40</td><td align="left">60-70</td><td align="center">30</td><td align="char">0.02</td><td align="left">0.60-0.70</td></tr><tr><td colspan="6"><hr></hr></td></tr><tr><td align="left">Maxillary incisors</td><td align="char">30-40</td><td align="center">60</td><td align="center">30</td><td align="char">0.02</td><td align="center">0.60</td></tr><tr><td colspan="6"><hr></hr></td></tr><tr><td align="left">Mandibular incisors</td><td align="char">30-40</td><td align="center">60</td><td align="center">30</td><td align="char">0.02</td><td align="center">0.60</td></tr></tbody></table><table-wrap-foot><fn id="sp0170"><p>Flexible cassettes with screens (100 or 200 speed); 200 speed is used most commonly.</p></fn><fn id="sp0175"><p>Film: Green, 400 speed. Cut 8- × 10-inch film into 4- × 8-inch strips.</p></fn></table-wrap-foot></table-wrap></p><sec id="s0190"><title>Bisecting Angle Technique: Maxillary Cheek Teeth</title><p id="p1080"><list list-type="simple" id="ulist0180"><list-item id="u0730"><label>•</label><p id="p1085">Place a flexible cassette<xref rid="fn0025" ref-type="fn">4</xref> in the mouth over the tongue against the palate.</p></list-item><list-item id="u0735"><label>•</label><p id="p1090">Estimate the angle between the maxillary cheek teeth and the film.</p></list-item><list-item id="u0740"><label>•</label><p id="p1095">Estimate an angle that “bisects” or “equally splits” the angle of the maxillary cheek teeth and the film.</p></list-item><list-item id="u0745"><label>•</label><p id="p1100">The line drawn at 90° to the bisecting angle is the projection needed for the radiograph (<xref rid="f0125" ref-type="fig">Fig. 18-24</xref>).<fig id="f0125"><label>Figure 18-24</label><caption><p>Bisecting angle.</p></caption><graphic xlink:href="f018-024-9781455708925"></graphic><attrib>(Courtesy Dr. Dave Klugh.)</attrib></fig></p></list-item><list-item id="u0750"><label>•</label><p id="p1105">If the angle is too steep (acute), the image of the tooth is shortened (<xref rid="f0130" ref-type="fig">Fig. 18-25</xref>).<fig id="f0130"><label>Figure 18-25</label><caption><p>Shortening of the tooth image.</p></caption><graphic xlink:href="f018-025-9781455708925"></graphic><attrib>(Courtesy Dr. Robert Baratt.)</attrib></fig></p></list-item><list-item id="u0755"><label>•</label><p id="p1110">If the angle is too flat (obtuse), the image of the tooth is lengthened (<xref rid="f0135" ref-type="fig">Fig. 18-26</xref>).<fig id="f0135"><label>Figure 18-26</label><caption><p>Lengthening of the tooth image.</p></caption><graphic xlink:href="f018-026-9781455708925"></graphic><attrib>(Courtesy Dr. Robert Baratt.)</attrib></fig></p></list-item><list-item id="u0760"><label>•</label><p id="p1115"><xref rid="f0140" ref-type="fig">Fig. 18-27</xref>demonstrates the resulting intraoral radiograph of the 100 arcade with proper placement of the flexible cassette.<fig id="f0140"><label>Figure 18-27</label><caption><p>Intraoral radiograph (100 arcade).</p></caption><graphic xlink:href="f018-027-9781455708925"></graphic></fig></p></list-item><list-item id="u0765"><label>•</label><p id="p1120"><xref rid="f0145" ref-type="fig">Fig. 18-28</xref>demonstrates the proper orientation of the x-ray beam for a bisecting angle technique.<fig id="f0145"><label>Figure 18-28</label><caption><p>Bisecting angle technique using a Stubbs full-mouth speculum.</p></caption><graphic xlink:href="f018-028-9781455708925"></graphic></fig></p></list-item><list-item id="u0770"><label>•</label><p id="p1125">The Stubbs full-mouth speculum works well for this radiograph because there is minimal obstruction of the view from the metal cheek piece (<xref rid="f0150" ref-type="fig">Fig. 18-29</xref>).<fig id="f0150"><label>Figure 18-29</label><caption><p>Lateral view of the bisecting angle technique.</p></caption><graphic xlink:href="f018-029-9781455708925"></graphic></fig></p></list-item></list></p></sec><sec id="s0195"><title>Bisecting Angle Technique: Maxillary Incisors</title><p id="p1130"><list list-type="simple" id="ulist0185"><list-item id="u0775"><label>•</label><p id="p1135">Place the flexible cassette (film side up) above the tongue, between the maxillary and mandibular incisors (<xref rid="f0155" ref-type="fig">Fig. 18-30</xref>).<fig id="f0155"><label>Figure 18-30</label><caption><p>Bisecting angle technique for the maxillary incisors.</p></caption><graphic xlink:href="f018-030-9781455708925"></graphic></fig></p></list-item><list-item id="u0780"><label>•</label><p id="p1140">Estimate the angle between the maxillary incisors and the flexible cassette (the angle of the incisors flattens with age).</p></list-item><list-item id="u11045"><label>•</label><p id="p13405">Approximate the bisecting angle and align the x-ray beam at 90 degrees to the bisecting angle.</p></list-item><list-item id="u0785"><label>•</label><p id="p1145">Align the x-ray beam at 90° to the bisecting angle.</p></list-item></list></p></sec><sec id="s0200"><title>Bisecting Angle Technique: Mandibular Incisors</title><p id="p1150"><list list-type="simple" id="ulist0190"><list-item id="u0790"><label>•</label><p id="p1155">Place the flexible cassette (film side down) under the tongue, between the maxillary and mandibular incisors (<xref rid="f0160" ref-type="fig">Fig. 18-31</xref>).<fig id="f0160"><label>Figure 18-31</label><caption><p>Bisecting angle technique for the mandibular incisors.</p></caption><graphic xlink:href="f018-031-9781455708925"></graphic></fig></p></list-item><list-item id="u0795"><label>•</label><p id="p1160">Estimate the angle between the mandibular incisors and the flexible cassette.</p></list-item><list-item id="u11050"><label>•</label><p id="p13410">Approximate the bisecting angle and align the x-ray beam at 90 degrees to the bisecting angle.</p></list-item><list-item id="u0800"><label>•</label><p id="p1165">Align the x-ray beam at 90° to the bisecting angle.</p></list-item></list></p></sec><sec id="s0205"><title>Radiograph Orientation</title><p id="p1170"><list list-type="simple" id="ulist0195"><list-item id="u0805"><label>•</label><p id="p1175">When viewing the incisors, the same dental techniques are applied as with the cheek teeth. The right arcade is always oriented on the left side of the radiograph.</p></list-item><list-item id="u0810"><label>•</label><p id="p1180">The maxillary incisors are directed in a downward orientation (<xref rid="f0165" ref-type="fig">Fig. 18-32</xref>).<fig id="f0165"><label>Figure 18-32</label><caption><p>Orientation of maxillary incisors.</p></caption><graphic xlink:href="f018-032-9781455708925"></graphic></fig></p></list-item><list-item id="u0815"><label>•</label><p id="p1185">The mandibular incisors are directed in an upward orientation (<xref rid="f0170" ref-type="fig">Fig. 18-33</xref>).<fig id="f0170"><label>Figure 18-33</label><caption><p>Orientation of the mandibular incisors.</p></caption><graphic xlink:href="f018-033-9781455708925"></graphic></fig></p></list-item></list></p></sec></sec></sec></sec></sec><sec id="s0210"><title>Upper Gastrointestinal Emergencies</title><sec id="s0215"><title>Teeth</title><p id="p1190"><italic><bold>Edward T. Earley, David L. Foster, and James A. Orsini</bold></italic></p><p id="p1195"><list list-type="simple" id="ulist0200"><list-item id="u0820"><label>•</label><p id="p1200">The nomenclature used for the mouth is a mixture of classic, archaic, and modern systems. A consistent, coherent nomenclature improves communication between veterinarians and assists in maintaining records. Most veterinarians use the Triadan nomenclature system (see “<xref rid="s0140" ref-type="sec">Equine Dental Nomenclature</xref>” earlier in text, <xref rid="s0140" ref-type="sec">p. 164</xref>, and <xref rid="f0020" ref-type="fig">Fig. 18-3</xref>) because it is specific and understandable.</p></list-item><list-item id="u0825"><label>•</label><p id="p1205">No oral examination is complete unless a full-mouth speculum is used to see and safely palpate the horse's mouth. A good light source, examination mirror, and a dental probe are also necessary.</p></list-item><list-item id="u0830"><label>•</label><p id="p1210">Only severe oral problems prevent a horse from eating.</p></list-item><list-item id="u0835"><label>•</label><p id="p1215">Drooling or quidding should alert the clinician to an oral emergency.</p></list-item></list></p><p id="p1220"><bold><italic>Practice Tip:</italic></bold><italic>Rabies and other neurologic diseases such as botulism and tetanus must be considered in differential diagnoses in a horse with clinical signs of drooling or quidding! Proper safety precautions should be taken to protect the examiner and assistants.</italic></p><p id="p9000"><list list-type="simple" id="ulist9000"><list-item id="u0840"><label>•</label><p id="p1225">Vaccination history, physical examination, gloves, and eye protection are essential for performing a safe oral examination.</p></list-item><list-item id="u0845"><label>•</label><p id="p1230">Examine the ventral aspects of the tongue and the caudal buccal tissues, which are frequently overlooked.</p></list-item><list-item id="u0850"><label>•</label><p id="p1235">Fractured teeth may have exposed pulp tissue that requires vital pulpotomy. This procedure needs specialized equipment not commonly available in the field. Removing the tooth is an alternative but is complicated by the loss of exposed crown resulting from the fracture.</p></list-item></list></p><sec id="s0220"><title>Emergency Care: Dental-Oral</title><sec id="s9010"><title>Tongue Lacerations</title><p id="p13415"><list list-type="simple" id="ulist0205"><list-item id="u0855"><label>•</label><p id="p1245">Most emergencies are traumatic.</p></list-item><list-item id="u0860"><label>•</label><p id="p1250">Lacerations are cleaned, anesthetized, debrided, and apposed with absorbable suture material such as polydioxanone.<xref rid="fn0030" ref-type="fn">5</xref></p></list-item><list-item id="u0865"><label>•</label><p id="p1255">Supportive treatment decreases healing time: anti-inflammatory drugs (phenylbutazone or flunixin meglumine), antibiotics, and oral flushes with 1% chlorhexidine diacetate (Nolvasan) diluted to 1 : 200 (5.0 mL/L) in water q12h.</p></list-item><list-item id="u0870"><label>•</label><p id="p1260">Lacerations of the tongue are occasionally seen. These can be transverse lacerations caused by inappropriate use of a bit, linear lesions produced by instruments during routine dental care, wounds caused by mandibular tooth fragments, incomplete shedding of the mandibular premolars, sharp edges of the lingual aspect of the mandibular cheek teeth, or wounds that occur when horses bite their tongues while racing and jumping.</p></list-item><list-item id="u0875"><label>•</label><p id="p1265"><bold><italic>Practice Tip:</italic></bold><italic>An infected deep laceration of the tongue causes severe pain and manifests with the chief complaint of difficulty eating, drooling, quidding, and depression.</italic></p></list-item><list-item id="u0880"><label>•</label><p id="p1275">Clinical signs vary from bleeding, sialorrhea/ptyalism, protruding tongue, fever, malodor from the mouth, poor or no appetite, and dysphagia.</p></list-item><list-item id="u0885"><label>•</label><p id="p1280">Sedation is needed to completely evaluate lacerations and injuries involving the mouth.</p></list-item><list-item id="u0890"><label>•</label><p id="p1285">Fresh lacerations are primarily repaired and older wounds are best left to heal by secondary intention.</p></list-item></list></p></sec><sec id="s0225"><title>Injury to the Incisor Teeth</title><p id="p1290">This section serves as a reference for colleagues presented with incisor fractures as an emergency. Our intent is not to give detailed instructions on how to perform these procedures. If a fracture is diagnosed that requires special treatment, it is recommended that one refer the case to an equine practitioner with advanced training in dentistry. In all incisor fracture cases, quality radiographs are a prerequisite to determine treatment options and prognosis.<list list-type="simple" id="ulist0210"><list-item id="u0895"><label>•</label><p id="p1295">Self-inflicted injury to the deciduous incisors is common in young horses.</p></list-item><list-item id="u0900"><label>•</label><p id="p1300">Avulsions of the juvenile teeth occur when the teeth are “caught” on a relatively immovable object such as a stall guard, webbing, feed tub, or bucket. The individual panics and pulls back with partial avulsion of the incisor teeth.</p></list-item><list-item id="u0905"><label>•</label><p id="p1305">The injuries may <italic>not</italic> be noticed for hours or even days.</p></list-item></list></p><sec id="s0230"><title>Presentation</title><p id="p1310"><list list-type="simple" id="ulist0215"><list-item id="u0910"><label>•</label><p id="p1315">Juvenile teeth displaced rostrally</p></list-item><list-item id="u0915"><label>•</label><p id="p1320">Torn mucosal border of the lingual/palatal aspect of the affected teeth</p></list-item><list-item id="u0920"><label>•</label><p id="p1325">Contaminated exposed root area of the affected teeth</p></list-item></list></p></sec><sec id="s0235"><title>First Priority</title><p id="p1330">Consider the viability of the permanent incisors originating below the deciduous teeth. Aggressive debridement and repositioning of the deciduous teeth can injure the developing permanent teeth. Removal of the juvenile teeth is best, rather than risking damage to the permanent tooth buds while attempting a repair of the injury. The delicate tooth buds frequently are injured by the sharp, apical edges of the unstable, partially avulsed deciduous teeth.<list list-type="simple" id="ulist0220"><list-item id="u0925"><label>•</label><p id="p1335">Radiographs of the affected incisors are recommended (see <xref rid="s0140" ref-type="sec">p. 164</xref>).</p></list-item><list-item id="u0930"><label>•</label><p id="p1340">Remove the unstable juvenile teeth.</p></list-item><list-item id="u0935"><label>•</label><p id="p1345">Debride the wound edges.</p></list-item><list-item id="u0940"><label>•</label><p id="p1350">Allow the wound to heal by secondary intention, using analgesic, antibiotic, and oral flushes as necessary.</p></list-item></list></p><p id="p1355">Often the permanent teeth develop and erupt without problems. Young horses missing several deciduous incisors rarely have difficulties, whereas the loss of permanent incisors over the many years these teeth are in service causes significant incisor malalignment requiring dental care to maintain incisor balance.<list list-type="simple" id="ulist9020"><list-item id="u11055"><label>•</label><p id="p1360"><italic><bold>Practice Tip:</bold> Trauma to the incisors produced by an external source (e.g., kicks and collisions) typically drives the teeth into the oral cavity. If this occurs in the juvenile incisors, injury to the permanent incisors is more likely than if the trauma is produced by an outward rotation of the incisors.</italic></p></list-item><list-item id="u11060"><label>•</label><p id="p1365"><italic><bold>Practice Tip:</bold> Use a pair of bungee cords placed under the lips and attached to the halter to retract the lips and better expose the injury.</italic><boxed-text id="b0015"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0240"><title>Injury to the Incisor Teeth</title><p id="p1370"><list list-type="simple" id="ulist0225"><list-item id="u0945"><label>•</label><p id="p1375">Restrain and sedate the patient.</p></list-item><list-item id="u0950"><label>•</label><p id="p1380">Support the head with a head stand or overhead device.</p></list-item><list-item id="u0955"><label>•</label><p id="p1385">Desensitize the area with either local infiltration or a regional block.</p></list-item><list-item id="u0960"><label>•</label><p id="p1390">Examine the injury.</p></list-item><list-item id="u0965"><label>•</label><p id="p1395">Radiographs are usually indicated in such injuries.</p></list-item><list-item id="u0970"><label>•</label><p id="p1400">Extract nonviable teeth and debride the wound.</p></list-item><list-item id="u0975"><label>•</label><p id="p1405">Suture soft tissue if possible (usually not possible).</p></list-item><list-item id="u0980"><label>•</label><p id="p1410">Administer analgesics, antibiotics, and oral flushes postoperatively.</p></list-item></list></p></sec><sec id="s0245"><title>Stabilization via Cerclage Wire</title><p id="p1415"><list list-type="simple" id="ulist0230"><list-item id="u0985"><label>•</label><p id="p1420">Severe destabilization limited to a portion of the incisors may be treated with the use of stabilizing wires. If the repair can be achieved without incorporating the cheek teeth into the repair, the treatment can be performed successfully in the standing horse. However, if the cheek teeth are required to be incorporated into the repair, general anesthesia is indicated.</p></list-item><list-item id="u0990"><label>•</label><p id="p1425">Sedate and restrain the patient.</p></list-item><list-item id="u0995"><label>•</label><p id="p1430">Radiograph the injury.</p></list-item><list-item id="u1000"><label>•</label><p id="p1435">Administer local anesthesia.</p></list-item><list-item id="u1005"><label>•</label><p id="p1440">Debride the occlusal fragments of any fractured crowns. Treat the exposed pulps of any fractured teeth that are intended to be saved. Otherwise, remove the tooth. <italic>Do not</italic> attempt to wire teeth with deeply fractured crowns; they <italic>do not</italic> survive.</p></list-item><list-item id="u1010"><label>•</label><p id="p1445">Reduce the fracture and return the teeth to their normal orientation.</p></list-item><list-item id="u1015"><label>•</label><p id="p1450">Stabilization of the injury via cerclage wire requires the passing of the wire through the interdental space of a stable tooth that is not involved in the fracture.</p></list-item><list-item id="u1020"><label>•</label><p id="p1455">Use a small ASIF (Association for the Study of Internal Fixation) drill bit and a hand chuck or drill. Take care <italic>not</italic> to enter the pulp chambers of any teeth while drilling the pathway for the wire.</p></list-item><list-item id="u1025"><label>•</label><p id="p1460">Direct the drill through the interdental space at or just below the gingival border.</p></list-item><list-item id="u1030"><label>•</label><p id="p1465">Insert a 14-gauge needle into the drill hole to serve as a wire guide.</p></list-item><list-item id="u1035"><label>•</label><p id="p1470">Healthy canine teeth may be incorporated into the repair, and slight notching of the crown provides the wire some purchase on the conical tooth.</p></list-item><list-item id="u1040"><label>•</label><p id="p1475">Once the cerclage wire is in place, tighten it by twisting the free ends of the wire. Then cut the wire and bend the free ends inward. It is recommended to apply a protective covering to the wire ends to prevent oral trauma (e.g., dental acrylic or polymethyl methacrylate).</p></list-item><list-item id="u1045"><label>•</label><p id="p1480">When appropriate, bonding agents may be incorporated into the repair to stabilize the repair further.</p></list-item><list-item id="u1050"><label>•</label><p id="p1485">Six-month follow-up radiographs are necessary posttreatment to evaluate the health of the teeth.</p></list-item></list></p><p id="p1490">External trauma to the deciduous incisors caused by kicks, collisions, and falls is treated as described for self-inflicted injury. Generally, these injuries almost always result in injury to the permanent tooth buds. Gentle debridement of the wound and anatomic replacement and stabilization of the teeth with stainless steel wires may correct incomplete or minor avulsion of the teeth.</p><p id="p1495">If the avulsion involves permanent incisors, a more aggressive attempt to “rescue” these teeth is needed. Debridement of the contaminated wound followed by repositioning and stabilization of the area with cerclage wire can reclaim some of the teeth.</p><p id="p1500"><italic><bold>Note:</bold></italic> It is important to determine whether the permanent incisors are fractured and, if so, to remove the fractured ends and evaluate the remaining apical portion of the tooth for viability.</p><p id="p1505"><italic><bold>Practice Tip:</bold> Geriatric horses with newly fractured incisors often have a history of a sleep disorder and have fallen on their muzzle after “passing out.”</italic></p></sec><sec id="s0250"><title>Regional and Local Anesthesia of the Incisors</title><p id="p1510"><list list-type="simple" id="ulist0235"><list-item id="u1055"><label>•</label><p id="p1515">Use 5 to 10 mL of lidocaine with a <inline-graphic xlink:href="if018-006-9781455708925.gif"></inline-graphic>-inch, 22-gauge needle.</p></list-item><list-item id="u1060"><label>•</label><p id="p1520">Local infusion of the lidocaine in the loose mucosa on the labial, palatal, or lingual aspect of the affected teeth successfully desensitizes the teeth.</p></list-item><list-item id="u1065"><label>•</label><p id="p1525">Regional anesthesia of the incisors is achieved by blocking the mental foramen (mandibular incisors) or the infraorbital foramen (maxillary incisors).</p></list-item></list></p></sec></boxed-text><boxed-text id="b0020"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0255"><title>Fractured Incisors—Other Management Principles</title><sec id="s0260"><title>Vital Pulpotomy</title><p id="p1530"><list list-type="simple" id="ulist0240"><list-item id="u1070"><label>•</label><p id="p1535">A <italic>vital pulpotomy</italic> refers to the surgical removal of a portion of the pulp in a vital tooth.</p></list-item><list-item id="u1075"><label>•</label><p id="p1540">The diseased portion of the pulp is removed down to the healthy pulp.</p></list-item><list-item id="u1080"><label>•</label><p id="p1545">A thin layer of Ca(OH)<sub>2</sub> is applied to help initiate the formation of a dentinal bridge.</p></list-item><list-item id="u1085"><label>•</label><p id="p1550">Next, a glass ionomer is applied as an attempt to create a permanent seal over the pulp canal.</p></list-item><list-item id="u1090"><label>•</label><p id="p1555">Following the glass ionomer, a flowable composite is used to help restore part of the crown.</p></list-item><list-item id="u1095"><label>•</label><p id="p1560">The vital tooth continues to erupt. <xref rid="f0175" ref-type="fig">Fig. 18-34</xref>demonstrates the eruption of 201 (see <xref rid="s0140" ref-type="sec">p. 164</xref> for Triadan terminology) over a 14-month period (compared with <xref rid="f0180" ref-type="fig">Fig. 18-35</xref>at the time of the injury).<fig id="f0175"><label>Figure 18-34</label><caption><p>Fractured 201 with an acute pulp exposure.</p></caption><graphic xlink:href="f018-034-9781455708925"></graphic></fig><fig id="f0180"><label>Figure 18-35</label><caption><p>Fourteen months after vital pulpotomy.</p></caption><graphic xlink:href="f018-035-9781455708925"></graphic></fig></p></list-item><list-item id="u1100"><label>•</label><p id="p1565">The radiograph of 101 at 14 months postprocedure shows that the pulp horn is still viable (<xref rid="f0185" ref-type="fig">Fig. 18-36</xref>).<fig id="f0185"><label>Figure 18-36</label><caption><p>Intraoral radiograph of the maxillary incisors at 14 months after vital pulpotomy.</p></caption><graphic xlink:href="f018-036-9781455708925"></graphic></fig></p></list-item><list-item id="u1110"><label>•</label><p id="p1575">A remnant of 202 was removed at the time of the vital pulpotomy.</p></list-item><list-item id="u1105"><label>•</label><p id="p1570">As the tooth continues to erupt, the exposed crown could have an additional restoration performed using a compactable composite.</p></list-item></list></p></sec><sec id="s0265"><title>Crown Restoration</title><p id="p1580"><list list-type="simple" id="ulist0245"><list-item id="u1115"><label>•</label><p id="p1585">A chronic crown fracture can develop a caries lesion that slowly erodes the enamel and dentin.</p></list-item><list-item id="u1120"><label>•</label><p id="p1590"><xref rid="f0190" ref-type="fig">Fig. 18-37</xref>involves 402 with a crown fracture at the mesial border and a caries lesion on the labial aspect of the tooth.<fig id="f0190"><label>Figure 18-37</label><caption><p>Initial presentation of 402.</p></caption><graphic xlink:href="f018-037-9781455708925"></graphic></fig></p></list-item><list-item id="u1125"><label>•</label><p id="p1595">The pulp was exposed to Ca(OH)<sub>2</sub> 6 months before, and as a result, a strong dentinal response was seen clinically and radiographically.</p></list-item><list-item id="u1130"><label>•</label><p id="p1600">The necrotic and fractured portion of the crown was removed, and part of the gingival margin was removed on the labial aspect of 402 (<xref rid="f0195" ref-type="fig">Fig. 18-38</xref>).<fig id="f0195"><label>Figure 18-38</label><caption><p>Fractured and necrotic crown removed.</p></caption><graphic xlink:href="f018-038-9781455708925"></graphic></fig></p></list-item><list-item id="u1135"><label>•</label><p id="p1605">The tooth was etched and bonded. An initial layer of a glass ionomer was applied.</p></list-item><list-item id="u1140"><label>•</label><p id="p1610">Following the glass ionomer, baseplate wax was used to form an abutment for the restoration (<xref rid="f0200" ref-type="fig">Fig. 18-39</xref>).<fig id="f0200"><label>Figure 18-39</label><caption><p>Baseplate wax used as an abutment.</p></caption><graphic xlink:href="f018-039-9781455708925"></graphic></fig></p></list-item><list-item id="u1145"><label>•</label><p id="p1615">Next, a flowable composite was used to help fill in the irregularities of the damaged crown.</p></list-item><list-item id="u1150"><label>•</label><p id="p1620">Following the flowable composite, a compactable composite was applied in two layers in order to build the restoration to the same level as the original crown.</p></list-item><list-item id="u1155"><label>•</label><p id="p1625">Next the baseplate wax was removed, and the composite was reduced to the mesial and distal edges of the original crown (<xref rid="f0205" ref-type="fig">Fig. 18-40</xref>).<fig id="f0205"><label>Figure 18-40</label><caption><p>Final restoration.</p></caption><graphic xlink:href="f018-040-9781455708925"></graphic></fig></p></list-item><list-item id="u1160"><label>•</label><p id="p1630">A postoperative radiograph shows the restoration of 402 (<xref rid="f0210" ref-type="fig">Fig. 18-41</xref>).<fig id="f0210"><label>Figure 18-41</label><caption><p>Postrestoration radiographs.</p></caption><graphic xlink:href="f018-041-9781455708925"></graphic></fig></p></list-item></list></p></sec><sec id="s0270"><title>Periodontal Splinting</title><p id="p1635"><list list-type="simple" id="ulist0250"><list-item id="u1165"><label>•</label><p id="p1640">Periodontal splinting with polyethylene fibers is used for support until the periodontal ligaments reattach to the damaged tooth.</p></list-item><list-item id="u1170"><label>•</label><p id="p1645">This example involves 101, in which a partial enamel and dentin fracture occurred at the level of the reserve crown (<xref rid="f0215" ref-type="fig">Fig. 18-42</xref>).<fig id="f0215"><label>Figure 18-42</label><caption><p>Small fracture of the reserve crown of 101 removed.</p></caption><graphic xlink:href="f018-042-9781455708925"></graphic></fig></p></list-item><list-item id="u1175"><label>•</label><p id="p1650">The pulp canal is <italic>not</italic> involved with the fracture.</p></list-item><list-item id="u1180"><label>•</label><p id="p1655">An initial gingival incision was made to remove the fragment.</p></list-item><list-item id="u1185"><label>•</label><p id="p1660">Following removal of the fragment, the damaged portion of 101 was restored with a flowable composite.</p></list-item><list-item id="u1190"><label>•</label><p id="p1665">The polyethylene fibers were bonded to 101 and the two neighboring incisors (102 and 201) (<xref rid="f0220" ref-type="fig">Fig 18-43</xref>).<fig id="f0220"><label>Figure 18-43</label><caption><p>Periodontal splinting using polyethylene fibers and composite.</p></caption><graphic xlink:href="f018-043-9781455708925"></graphic></fig></p></list-item><list-item id="u1195"><label>•</label><p id="p1670">A flowable composite was worked into the fiber in an effort to strengthen the splint.</p></list-item><list-item id="u1200"><label>•</label><p id="p1675">A radiograph demonstrates the restoration and splint 6 months following the procedure (<xref rid="f0225" ref-type="fig">Fig. 18-44</xref>).<fig id="f0225"><label>Figure 18-44</label><caption><p>Radiographs 6 months after periodontal splint and restoration.</p></caption><graphic xlink:href="f018-044-9781455708925"></graphic></fig></p></list-item></list></p></sec></sec></boxed-text></p></list-item></list></p></sec></sec></sec></sec><sec id="s0275"><title>Acute Salivation (Ptyalism)</title><p id="p1680"><italic><bold>Thomas J. Divers</bold></italic></p><p id="p1685"><list list-type="simple" id="ulist0255"><list-item id="u1205"><label>•</label><p id="p1690">Acute salivation (ptyalism/sialorrhea) can be caused by the inability to swallow normally produced saliva (i.e., choke, see <xref rid="s0290" ref-type="sec">p. 177</xref>; neurologic disorders, particularly botulism; equine protozoal myeloencephalitis [EPM]; and guttural pouch mycosis) or from injury to the mouth or pharynx.</p></list-item><list-item id="u1210"><label>•</label><p id="p1695">Ptyalism can be caused by excessive production of saliva, most commonly from red clover toxicity (slaframine), mouth injury/irritations, and gastric ulcers with esophagitis in foals.</p></list-item><list-item id="u1215"><label>•</label><p id="p1700">A thorough physical examination and history are important to differentiate local causes from a focal manifestation of a generalized disease (i.e., red clover toxicity) to arrive at an accurate diagnosis.</p></list-item><list-item id="u1220"><label>•</label><p id="p1705"><bold><italic>Practice Tip:</italic></bold><italic>The most common causes of ptyalism are choke and red clover poisoning in some geographic areas in adults. In foals, the most common cause is gastric and esophageal ulceration (see</italic><xref rid="s0370" ref-type="sec">p. 182</xref><italic>).</italic></p></list-item><list-item id="u1225"><label>•</label><p id="p1710">The cause of salivation can be determined by oral examination in some cases. Evaluate the entire oral cavity, looking for a laceration, ulcerations, vesicular disease, foreign body (especially in the tongue or caught between the upper dental arcade), tooth root or soft tissue abscess, a fractured tooth (see <xref rid="s0240" ref-type="sec">p. 173</xref>), injury to the palate, strangles, or evidence of chemical injury. Kicks to the incisors and head or catching the mouth on bucket handles, for example, are all common causes of mouth injury. Tongue injuries are often self-inflicted in horses with cerebral disorders. Stomach tube injury or irritation may cause ptyalism. Sedation (detomidine with butorphanol) and the careful use of an equine mouth speculum may be needed to allow a safe and complete examination of the mouth.</p></list-item><list-item id="u1230"><label>•</label><p id="p1715"><italic><bold>Practice Tip:</bold> Without proper sedation, the mouth speculum becomes a dangerous weapon to the examiner if the patient “tosses” his head.</italic></p></list-item><list-item id="u1235"><label>•</label><p id="p1720">Excessive biting on the speculum also can result in a tooth fracture. General anesthesia may be required to perform a complete oral examination in some horses, particularly those with foreign bodies and injury to the caudal pharynx.</p></list-item></list></p><sec id="s0280"><title>Localized Causes of Salivation</title><p id="p1725"><list list-type="simple" id="ulist0260"><list-item id="u1240"><label>•</label><p id="p1730">The most common equine foreign bodies are a wooden stick large enough to lodge between the upper arcade of teeth, a small stick penetrating the soft tissues of the pharyngeal cavity or soft palate, and a metallic foreign body in the tongue or pharynx. Reaction to oral medications is a common cause of mouth irritation.</p></list-item><list-item id="u1245"><label>•</label><p id="p1735">Evaluate the tongue for blisters, ulceration, foreign body, or cellulitis.</p></list-item><list-item id="u1250"><label>•</label><p id="p1740">Burrs or grass awns (e.g., Foxtail, sandbur, cheat grass, tickle grass [see www1.extension.umn.edu/agriculture/horse/pasture/mouth-blisters/docs/mouth-blisters.pdf for pictures]) can become stuck in the mouth while eating hay contaminated with these plants and cause salivation. This may be a problem of a particular farm or batch of hay.</p></list-item><list-item id="u1255"><label>•</label><p id="p1745">Patients that have licked mercury blister compounds are prone to severe oral erosions; this product is rarely used today. Enrofloxacin (Baytril 100) causes severe stomatitis in some horses. A pharmaceutical procedure for mixing the drug in a gel is reported to reduce the likelihood of oral irritation; however, stomatitis may still occur in a few horses. Oral metronidazole may cause excess salivation but it does <italic>not</italic> cause oral erosions. Nonsteroidal anti-inflammatory drug (NSAID) therapy, on occasion, may cause oral ulcers; however, excessive salivation from these drugs is uncommon.</p></list-item><list-item id="u1260"><label>•</label><p id="p1750">Most vesicular lesions in the mouth are idiopathic, but one must consider vesicular stomatitis, which appears more commonly in New Mexico and Colorado every few years. Suspicious oral ulcers should be reported to the state veterinarian. Immune-mediated pemphigus vesicular formation in the oral cavity occurs but is unusual.</p></list-item><list-item id="u1265"><label>•</label><p id="p1755"><italic>Actinobacillus lignieresii, Actinomyces</italic> spp., and <italic>Corynebacterium</italic> spp. infection can cause wooden tongue and/or mandibular region abscesses in horses.</p></list-item><list-item id="u1270"><label>•</label><p id="p1760">Consider also sialadenitis (inflammation of a salivary gland), sialolith in horses and donkeys, fractured teeth, or fractured bones of the mouth, hyoid apparatus or temporohyoid. Primary pharyngitis or acute epiglottitis, retropharyngeal lymphadenopathy, guttural pouch empyema, pharyngeal edema, and esophageal obstruction are other causes of ptyalism.</p></list-item><list-item id="u1275"><label>•</label><p id="p1765">Swelling of the tongue caused by tumors (rhabdomyosarcoma, squamous cell carcinoma), foreign body, injury, or eosinophilic myositis may cause salivation and some dysphagia.</p></list-item><list-item id="u1280"><label>•</label><p id="p1770">Facial paralysis and masseter myopathy (selenium deficiency) are other causes of salivation. With facial paralysis or brainstem disease affecting the cranial nerves V or VII, horses may pack food in their cheek on the affected side. With masseter myopathy the tongue may protrude.</p></list-item></list></p></sec><sec id="s0285"><title>Neurologic or Toxic Causes of Salivation</title><p id="p1775"><list list-type="simple" id="ulist0265"><list-item id="u1285"><label>•</label><p id="p1780">Neurologic causes of excessive salivation include:<list list-type="simple" id="ulist0270"><list-item id="u1290"><label>•</label><p id="p1785">Botulism</p></list-item><list-item id="u1295"><label>•</label><p id="p1790">EPM</p></list-item><list-item id="u1300"><label>•</label><p id="p1795">West Nile virus (WNV)</p></list-item><list-item id="u1305"><label>•</label><p id="p1800">Rabies</p></list-item><list-item id="u1310"><label>•</label><p id="p1805">Other encephalitides</p></list-item><list-item id="u1315"><label>•</label><p id="p1810">Moldy corn poisoning</p></list-item><list-item id="u1320"><label>•</label><p id="p1815">Yellow star thistle</p></list-item><list-item id="u1325"><label>•</label><p id="p1820">Ivermectin toxicity</p></list-item><list-item id="u1330"><label>•</label><p id="p1825">Propylene glycol toxicity</p></list-item><list-item id="u1335"><label>•</label><p id="p1830">Hepatic encephalopathy (see specific neurologic diseases, Chapter 20, p. 277)</p></list-item></list></p></list-item><list-item id="u1340"><label>•</label><p id="p1835">Cantharidin (blister beetle) toxicity may cause both local irritation and systemic effects—colic, hematuria, etc<italic>.</italic> (see Chapter 34, p. 584).</p></list-item><list-item id="u1345"><label>•</label><p id="p1840">Iatrogenic bethanechol administration (a parasympathomimetic)</p></list-item><list-item id="u1350"><label>•</label><p id="p1845">Pasture-associated salivation (slobbers) most commonly caused by ingestion of white or red clover infected with <italic>Rhizoctonia leguminicola:</italic><list list-type="simple" id="ulist0275"><list-item id="u1355"><label>•</label><p id="p1850">Most common in the southeastern United States and some areas of South America</p></list-item><list-item id="u1360"><label>•</label><p id="p1855">Has also been reported with feeding of alfalfa</p></list-item><list-item id="u1365"><label>•</label><p id="p1860">Black spores can be seen on the leaves of the infected plant (see Chapter 34, p. 587).</p></list-item><list-item id="u1370"><label>•</label><p id="p1865">Clinical disease occurs mostly in grazing horses but can occur from feeding stored hay.<list list-type="simple" id="ulist9090"><list-item id="u1375"><label>○</label><p id="p1870">Toxin is slowly degraded in hay stored for several months.</p></list-item></list></p></list-item><list-item id="u1380"><label>•</label><p id="p1875">Lacrimation, frequent urination, and diarrhea may also occur as a result of cholinergic activation.</p></list-item><list-item id="u1385"><label>•</label><p id="p1880">Signs may start within 30 minutes of ingesting the toxin.</p></list-item><list-item id="u1390"><label>•</label><p id="p1885">Signs generally resolve within 1 day of removing affected horses from pasture.</p></list-item></list></p></list-item></list></p><sec id="s0290"><title>Diagnosis</title><p id="p1890">Ancillary diagnostic tests include radiography, ultrasonography, and endoscopy of the mouth and pharyngeal area. Ultrasonography may define an area that can be sampled for cytologic examination and culture. Radiographs are helpful in identifying a foreign body or diseased tooth. Observe from a distance whether the ability to prehend, masticate, and swallow is retained. In some cases, a complete oral examination with the horse under general anesthesia may be necessary before an etiology is determined. When multiple horses have oral vesicular lesions, testing for vesicular stomatitis is performed (serology and aspiration of a vesicle for virus isolation). Outbreaks of vesicular lesions in horses may occur unrelated to vesicular stomatitis; the cause usually is not identified in those outbreaks. For toxin-related causes, an index of suspicion regarding possible exposure to toxins or chemical irritants that may have been ingested is important.<boxed-text id="b0025"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0295"><title>Diseases of the Mouth Causing Excessive Salivation</title><p id="p1895">Treatments may include the following:<list list-type="simple" id="ulist0285"><list-item id="u1395"><label>•</label><p id="p1900">Removal of foreign bodies—radiographs may be needed to localize the foreign body</p></list-item><list-item id="u1400"><label>•</label><p id="p1905">Extraction of diseased tooth causing clinical signs</p></list-item><list-item id="u1405"><label>•</label><p id="p1910">Remove from pasture if clover associated “slobbers” is the cause</p></list-item><list-item id="u1410"><label>•</label><p id="p1915">Antibiotics for infection-related cause (i.e., wooden tongue)</p></list-item><list-item id="u1415"><label>•</label><p id="p1920">Intravenously administer fluids if dehydrated and unable to swallow normally</p></list-item><list-item id="u1420"><label>•</label><p id="p1925">NSAIDs for mouth wounds or fractures</p></list-item><list-item id="u1425"><label>•</label><p id="p1930">Other symptomatic treatment:<list list-type="simple" id="ulist0290"><list-item id="u1430"><label>•</label><p id="p1935">Nolvasan mouth wash (mix 1 part of 2% chlorhexidine gluconate [Durvet<xref rid="fn0035" ref-type="fn">6</xref>] with 10 parts water), colloidal or chelated silver mouth rinse solution, or 2% potassium permanganate as a mouth disinfectant/antiseptic wash. Nolvasan wash is good for foals with mouth “thrush” <italic>(Candida)</italic> also.</p></list-item><list-item id="u1435"><label>•</label><p id="p1940">Furacin (nitrofurazone) in a prednisolone spray for pharyngeal edema, inflammation, and epiglottitis. Penicillin is often the first-choice antibiotic for mouth wounds/infections because many commensal oral organisms are sensitive to penicillin. Some patients may need a tracheostomy (see Chapter 25, p. 456) if laryngeal-pharyngeal swelling is compromising the airway. <bold><italic>Practice Tip:</italic></bold><italic>Fluid therapy—it is important to remember that in horses, the anion of highest concentration in saliva is chloride and there is a relatively low concentration of bicarbonate. On rare occasion, horses have an acid-base disturbance caused by saliva loss; hypochloremic metabolic alkalosis may occur (if acid-base changes are present they are generally mild). For those cases, fluid therapy consisting of 0.9% sodium chloride and 20 mEq/L KCl is usually recommended.</italic></p></list-item></list></p></list-item></list></p></sec></boxed-text></p><p id="p1945"><boxed-text id="b0030"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0300"><title>Systemic Causes of Excess Salivation</title><p id="p1950">Treatment for the specific disease (see neurologic disorders or toxicities <xref rid="s0275" ref-type="sec">p. 176</xref>).</p></sec></boxed-text></p></sec></sec></sec><sec id="s0305"><title>Esophagus</title><p id="p1955"><list list-type="simple" id="ulist0295"><list-item id="u1440"><label>•</label><p id="p1960">The most common clinical problem affecting the esophagus of a horse is obstruction of the esophageal lumen (choke). This disorder occurs as a single acute episode or as a chronic, intermittent problem. In either case, these conditions are emergencies. If the condition recurs, a diverticulum or stricture should be considered as a possible cause.</p></list-item><list-item id="u1445"><label>•</label><p id="p1965"><italic><bold>Practice Tip:</bold> Megaesophagus and chronic choke are common in Friesians and carry a poor prognosis for long-term survival; Friesian horses may also have gastric emptying problems.</italic></p></list-item></list></p><sec id="s0315"><title>Esophageal Obstruction</title><p id="p1970"><list list-type="simple" id="ulist0300"><list-item id="u1450"><label>•</label><p id="p1975">Esophageal obstruction, most often acute, results from obstruction of the esophageal lumen with food (e.g., dried beet pulp, hay, pellets, wood chips, or bedding). These problems occur among horses with ravenous eating habits, especially older horses being fed pelleted feed.</p></list-item><list-item id="u1455"><label>•</label><p id="p1980">Other risk factors are immediately feeding the nervous and excited horse upon arrival at a hospital or exhausted horses at rest stops. Occasionally, choke occurs when a heavily sedated horse is permitted to eat. Most cases of esophageal choke are in adult horses, but it may occur in younger horses.</p></list-item><list-item id="u1460"><label>•</label><p id="p1985"><bold><italic>Practice Tip:</italic></bold><italic>Geriatric horses are predisposed to choke because of decreased saliva production and sometimes poor mastication of feed.</italic></p></list-item><list-item id="u1465"><label>•</label><p id="p1990">The most common clinical signs of esophageal choke are excessive salivation, retching, coughing with saliva, and food dripping from the nostrils. In most instances, if the obstruction is in the cervical region (the most common sites for obstruction are proximal esophagus and just cranial to the thoracic inlet) and of recent origin, enlargement of the esophagus can be palpated.</p></list-item><list-item id="u1470"><label>•</label><p id="p1995">Over time, swelling and muscle spasm in this region make it difficult to delineate the mass. The likelihood that the obstruction is in the cervical portion of the esophagus increases if the patient “retches” immediately after attempting to swallow. There is a 10- to 12-second delay between the swallow and the onset of retching if the obstruction is in the distal esophagus.</p></list-item></list></p><sec id="s0320"><title>Diagnosis of Choke</title><p id="p2000"><list list-type="simple" id="ulist0305"><list-item id="u1475"><label>•</label><p id="p2005">History and clinical signs are nearly diagnostic but in most cases the obstruction is confirmed by passing a nasogastric tube and encountering an obstruction in the esophagus.</p></list-item><list-item id="u1480"><label>•</label><p id="p2010"><italic><bold>Practice Tip:</bold> The initial aim of treatment is to reduce the patient's level of anxiety, allow the esophageal muscles to relax, and to adequately hydrate the horse.</italic></p></list-item></list><boxed-text id="b0035"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0325"><title>Medical Management of Esophageal Obstruction</title><p id="p2015"><list list-type="simple" id="ulist0310"><list-item id="u1485"><label>•</label><p id="p2020">Tranquilize the patient with acepromazine and/or additional sedation with xylazine to relax the entire esophagus and lower the horse's head.</p></list-item><list-item id="u1490"><label>•</label><p id="p2025"><bold><italic>Important:</italic></bold> If choke is suspected, advise owners to remove hay and water immediately. These conservative treatments frequently are enough to relax the esophagus and allow the obstruction to pass on its own within 4 to 6 hours.</p></list-item><list-item id="u1495"><label>•</label><p id="p2030"><italic><bold>Practice Tip:</bold> If the horse has choked previously or there is a belief that the choke is of longer than 6 hours' duration, it is considered a medical emergency.</italic> Most veterinarians upon arrival prefer to pass a stomach tube following tranquilization, not only to confirm the diagnosis but also to provide a gentle water lavage at the level of the obstruction <italic>while the horse's head is kept down</italic> along with very gently “pushing” the obstruction. This is recommended on the first visit unless you believe the obstruction is <italic>very proximal,</italic> just caudal to the larynx. In this situation, if there is <italic>no</italic> evidence of laryngeal obstruction and it is a first-time choke, administer a tranquilizer, withhold feed and water, and allow 3 to 4 hours for this to resolve before attempting lavage.</p></list-item><list-item id="u1500"><label>•</label><p id="p2035">N-butylscopolammonium bromide (Buscopan), 0.3 mg/kg IV or IM (7 mL/450 kg), may also help resolve the obstruction by decreasing esophageal tone. Because of its anticholinergic effect, N-butylscopolammonium bromide given intravenously causes a transient (20 to 30 minutes) increase in heart rate. It is recommended for most cases, but because the most common site for choke, the proximal and mid-cervical area, involves skeletal muscle, the benefit is questionable.</p></list-item><list-item id="u1505"><label>•</label><p id="p2040">Oxytocin, 0.11 to 0.22 IU/kg IV q6h, is of questionable value, but it may help resolve the obstruction by decreasing esophageal smooth muscle tone. Smooth muscle constitutes only the distal third of the esophagus. Oxytocin administration may be associated with transient abdominal discomfort, sweating, and muscle tremors. <bold><italic>Note:</italic></bold> Oxytocin should <italic>not</italic> be administered to pregnant mares because of the potential abortifacient properties.</p></list-item><list-item id="u1510"><label>•</label><p id="p2045">If the above treatment is unsuccessful in relieving choke in 4 to 6 hours, consider lavage. With the patient sedated with xylazine or detomidine, causing the patient to lower their head, pass a stomach tube to the proximal limit of the obstruction; gently introduce a small volume of water through the tube and against the obstructing mass. This process should be repeated several times to break up the obstruction. As long as the head is kept low, large volumes of water can be pumped (stomach pump) into a medium-size stomach tube and against the obstruction.</p></list-item><list-item id="u1515"><label>•</label><p id="p2050"><bold><italic>Practice Tip:</italic></bold><italic>In the beginning and before a large volume of water is pumped, it is important to make sure the fluid is able to easily exit around the tube! Gently pressing the tube against the obstruction while flushing may cause the obstruction to move down the esophagus. Once a food obstruction begins to move, the choke is usually quickly resolved. If the obstruction is caused by a rope or another non-plant foreign body, pushing the object further down the esophagus may be contraindicated in case surgical removal is needed.</italic><list list-type="simple" id="ulist0315"><list-item id="u1520"><label>•</label><p id="p2055">The Rüsch esophageal flush probe<xref rid="fn0040" ref-type="fn">7</xref> for choked horses (<xref rid="f0230" ref-type="fig">Fig. 18-45</xref>) uses a pressurized water (room temperature-to-warm) source (hose/faucet). The operator needs to check that the primary tube through which choked material and water exit (egress) is <italic>not</italic> blocked, preventing overpressurization of the esophagus proximal to the obstruction! The valve between the water extension hosing and the proximal end of the ingress inner tube allows the water flow to be turned off at any time.<fig id="f0230"><label>Figure 18-45</label><caption><p>Close-up, cross section of the Rüsch esophageal flush probe and its placement within the esophagus to treat “choke.”</p></caption><graphic xlink:href="f018-045-9781455708925"></graphic></fig></p></list-item><list-item id="u1525"><label>•</label><p id="p2060">Another aggressive lavage method is a warmed, cuffed endotracheal tube passed intranasally into the esophagus, providing the security of an inflatable cuff and preventing aspiration of water during lavage of the esophagus. Warming the tube before passage facilitates passage by making it more flexible. Fluid can be pumped through the endotracheal tube or through a small-diameter stomach tube that has been passed inside the larger endotracheal tube. The lavage solution is most commonly warm water.</p></list-item></list></p></list-item></list></p><p id="p2065"><italic><bold>Important:</bold></italic> Careful manipulation is important to avoid esophageal injury and secondary stricture or esophageal perforation.<list list-type="simple" id="ulist0320"><list-item id="u1530"><label>•</label><p id="p2070">An alternative procedure is to pass the endotracheal tube into the trachea and inflate the cuff to protect the trachea from aspirated material before flushing the esophagus.</p></list-item><list-item id="u1535"><label>•</label><p id="p2075">If the obstruction <italic>cannot</italic> be cleared or if the patient becomes unmanageable under sedation, general anesthesia, with the head positioned “down,” is required for a more aggressive lavage. In the weanling or yearling that is difficult to restrain, this might be the easiest approach.</p></list-item><list-item id="u1540"><label>•</label><p id="p2080"><italic><bold>Practice Tip:</bold> If flushing is planned following short-acting anesthesia, always pass the nasogastric tube before general anesthesia; passing the tube into the esophagus of an anesthetized horse is difficult!</italic></p></list-item><list-item id="u1545"><label>•</label><p id="p2085">Intravenously administered fluids are an important supportive treatment in prolonged cases of choke to prevent dehydration and “drying” of the esophageal obstruction.</p></list-item><list-item id="u1550"><label>•</label><p id="p2090">Prophylactic antimicrobial agents are indicated for many choke cases because of the high risk of aspiration pneumonia. Antibiotics (e.g., penicillin G procaine, 22,000 IU/kg IM q12h and gentocin 6.6 mg/kg IV or IM q24h; ceftiofur, 2.2 to 4.4 mg/kg IM q12h; or trimethoprim-sulfamethoxazole, 20 to 30 mg/kg PO q12h) are usually administered for 5 to 7 days after relieving the obstruction. If the choke is of more than 6 hours' duration, the caretaker did <italic>not</italic> immediately remove hay and water, or if crackles are heard on thoracic auscultation, metronidazole (15 to 25 mg/kg PO or 25 to 30 mg/kg per rectum q8h) should be added to one of the above treatment protocols. If endoscopy is performed following relief of the choke and severe mucosal erosions are noted, metronidazole should be given per rectum; in these cases, sucralfate should also be administered PO.<list list-type="simple" id="ulist0325"><list-item id="u1555"><label>•</label><p id="p2095">If there is concern that the choke has caused damage to the mucosa (based on the duration of choke, an effort is made to relieve the choke or irritating material causing the choke), the esophagus should be evaluated endoscopically in 24 to 48 hours and before refeeding.</p></list-item><list-item id="u1560"><label>•</label><p id="p2100">If there is concern about more severe aspiration than normal (most choke cases have some aspiration), a thoracic ultrasound should be performed 24 hours after alleviation of the choke (see p. 95).</p></list-item></list></p></list-item><list-item id="u1565"><label>•</label><p id="p2105">After relieving the choke, if a large amount of food is seen in the trachea during endoscopic examination and the horse is <italic>not</italic> coughing, the patient can be further tranquilized so that the head is positioned ventrally. Using a bronchoalveolar lavage (BAL) tube and with brief periods of suction (10 to 15 seconds at a time) gently lavage the trachea with small (30 mL) amounts of warm balanced crystalloid infused through the endoscope at the thoracic bifurcation of the trachea. If the initial lavage and suctioning do <italic>not</italic> yield particulate matter, <italic>do not</italic> continue the lavage.</p></list-item><list-item id="u11065"><label>•</label><p id="p13420">If they are known, correct the predisposing causes for the choke (e.g., improper feed and poor dentition).</p></list-item><list-item id="u1570"><label>•</label><p id="p2110">Once the obstruction is resolved, initially offer <italic>only</italic> water, because esophageal dilation after obstruction increases the likelihood of re-impaction for 48 hours. Recommend withholding feed for 48 hours or, if this is impractical, feed small amounts of a soft “soupy mash” diet to prevent recurrence of the obstruction. <italic><bold>Note:</bold></italic> Feeding mash is recommended for ponies and miniature horses at risk of hyperlipemia! Endoscopic examination, after the obstruction is relieved, provides evaluation of the esophageal mucosa and information concerning the likelihood of secondary complications (e.g., reobstruction, stricture, and perforation).</p></list-item></list></p></sec></boxed-text></p><p id="p2115"><boxed-text id="b0040"><caption><title><inline-graphic xlink:href="icon02-9781455708925.gif"></inline-graphic> What Not to Do</title></caption><sec id="s0330"><title>Medical Management of Esophageal Choke</title><p id="p2120"><list list-type="simple" id="ulist0330"><list-item id="u1575"><label>•</label><p id="p2125"><italic>Do not</italic> leave feed or water in the stall after choke is recognized!</p></list-item><list-item id="u1580"><label>•</label><p id="p2130"><italic>Do not</italic> use butorphanol, which may suppress the cough reflex.</p></list-item><list-item id="u1585"><label>•</label><p id="p2135"><italic>Do not</italic> use mineral oil as a lubricant for the esophagus; some will be aspirated and can cause severe granulomatous pneumonia.</p></list-item><list-item id="u1590"><label>•</label><p id="p2140"><italic>Do not</italic> be too aggressive in forcing the choke down the esophagus in the first 3 to 4 hours.</p></list-item><list-item id="u1595"><label>•</label><p id="p2145"><italic>Do not</italic> feed dried beet pulp or immediately feed a horse that has become excited or has received heavy sedation!</p></list-item><list-item id="u1600"><label>•</label><p id="p2150"><italic>Do not</italic> try to flush the esophagus without the head lowered!</p></list-item><list-item id="u1605"><label>•</label><p id="p2155">If the choke is a first time event and <italic>cannot</italic> be relieved after 1 hour of flushing, give the horse and yourself a break and try again later in the day or the following day as long as the horse can be tranquilized, food and water is removed, and IV fluids are being administered.</p></list-item><list-item id="u1610"><label>•</label><p id="p2160"><italic>Do not</italic> use atropine to relax the esophagus; use Buscopan instead.</p></list-item><list-item id="u1615"><label>•</label><p id="p2165"><italic>Do not</italic> forget follow-up care. Horses with esophageal obstruction of prolonged (>4 hours) duration, repeat offenders, and those <italic>not</italic> having hay and water immediately removed should be reexamined 24 hours after relieving the choke and ideally have both ultrasound examination of the lungs and endoscopy of the esophagus performed.<list list-type="simple" id="ulist0335"><list-item id="u1620"><label>•</label><p id="p2170">If the horse has an increase in respiratory rate 12 to 24 hours following relief of the obstruction, the patient should be closely examined and may need antibiotic treatment for pneumonia!</p></list-item></list></p></list-item><list-item id="u1625"><label>•</label><p id="p2175"><italic>Do not</italic> refeed too soon.<list list-type="simple" id="ulist0340"><list-item id="u1630"><label>•</label><p id="p2180">Begin refeeding with a gruel (thoroughly soaked and watery mash or pellets).</p></list-item><list-item id="u1635"><label>•</label><p id="p2185">Ponies, miniature horses, and pregnant mares may need nutritional support (IV dextrose and/or amino acids) if feed is withheld or cannot be consumed for more than 24 hours; monitor triglyceride values in these cases.</p></list-item></list></p></list-item></list></p></sec></boxed-text><boxed-text id="b0045"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0335"><title>Surgical Management</title><p id="p2190">If all attempts to dislodge the obstruction are unsuccessful, surgical intervention is indicated. Although several procedures are used to manage strictures, diverticula, tumors, and other rare causes of obstruction, cervical esophagotomy is the only emergency procedure.<list list-type="simple" id="ulist0345"><list-item id="u1640"><label>•</label><p id="p2195">Cervical esophagotomy is performed with a nasogastric tube placed in the esophagus and the horse under local or general anesthesia. The anesthesia protocol depends on the temperament of the patient, the type of obstruction, cost, and the surgeon's preference. Make an incision on the midline or ventral to the left jugular vein over the obstruction. Once the obstructed portion of the esophagus is identified, attempt extraluminal massage and manual breakdown of the mass before entering the esophageal lumen. If this maneuver is unsuccessful, make a 2-cm longitudinal incision distal to the obstruction on the ventral or ventrolateral aspect of the esophagus (see <xref rid="s0075" ref-type="sec">p. 161</xref>). These sites are used to aid in ventral drainage if the incision is left open to heal by secondary intention or if dehiscence of the primary incision occurs. A <inline-graphic xlink:href="if018-007-9781455708925.gif"></inline-graphic>-inch Penrose drain is used to occlude the esophagus distal to the esophagotomy, and a stallion catheter is introduced retrograde into the esophageal lumen. Gentle intermittent pressure lavage is attempted to retropulse the obstruction into the pharynx. If retrograde pulsion fails, the esophagotomy incision is extended, and sponge forceps are used to remove the obstruction.</p></list-item><list-item id="u1645"><label>•</label><p id="p2200">A stomach tube is passed, normograde and retrograde, to ensure a patent lumen. Suture the esophagus in a simple continuous pattern using 3-0 monofilament polydioxanone (PDS, Ethicon) or polypropylene suture placed in the mucosa and submucosa with the knots in the lumen of the esophagus. Close the muscular layer of the esophagus using an interrupted pattern of absorbable material. Position a suction drain adjacent to the esophagus and close the subcutaneous tissues. The suction drain remains in place for 48 hours, all food is withheld, parenteral nutrition is provided, and fluids are administered intravenously. Feed the patient a slurry of pelleted feed for 8 to 10 days, beginning on postoperative day 5.</p></list-item><list-item id="u1650"><label>•</label><p id="p2205">An alternative is to use a second esophagotomy distal to the site of the obstruction to feed the patient a gruel and water mixture through an indwelling stomach tube sutured in place. This tube can be used for 10 days to allow the sutured proximal esophagotomy time to heal by primary intention. If dehiscence occurs, a traction diverticulum can develop but usually is associated with few complications.</p></list-item><list-item id="u1655"><label>•</label><p id="p2210">If necrotic tissue is debrided at the obstruction site, a stomach tube is recommended. Suture the tube in place and feed the individual a gruel and water mixture through the tube for 10 days. The stoma is left to heal by secondary intention after tube removal.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s0340"><title>Prognosis and Complications</title><p id="p2215">The prognosis for survival with simple esophageal obstruction is excellent. The prognosis is favorable for horses with pulsion diverticula but poor if strictures occur that require resection and anastomosis of the esophagus. Aspiration pneumonia is a serious sequela, to be recognized early and managed aggressively. Use clinical examination and ultrasonography to determine the severity of aspiration pneumonia. The incidence of these complications seems related to the time to resolution of the primary obstruction and whether feed and water were properly withheld. Treat the patient aggressively with particular care to avoid possible iatrogenic complications. Choke in miniature horse foals is relatively common and can be difficult to relieve.</p></sec></sec><sec id="s0345"><title>Esophageal Perforation</title><p id="p2220">Causes for esophageal perforation (rupture) include the following:<list list-type="simple" id="ulist0350"><list-item id="u1660"><label>•</label><p id="p2225">Chronic obstruction</p></list-item><list-item id="u1665"><label>•</label><p id="p2230">Swallowed perforating foreign body such as a needle or thorn</p></list-item><list-item id="u1670"><label>•</label><p id="p2235">Penetrating external wounds, even rarely a misguided needle puncture</p></list-item><list-item id="u1675"><label>•</label><p id="p2240">Repeated or traumatic nasogastric intubation</p></list-item><list-item id="u1680"><label>•</label><p id="p2245"><italic><bold>Note:</bold></italic> Horses that are extremely difficult to tube and then have a large tube left in for several days sometimes have pressure necrosis of the most proximal dorsal esophagus. Rarely following nasogastric tubing does esophageal perforation occur, but if it occurs and is <italic>not</italic> recognized for several days, a communication with the mediastinum may result in fatal pleuritis.</p></list-item><list-item id="u1685"><label>•</label><p id="p2250">Extension of infection or injury (e.g., kick) from surrounding tissues</p></list-item><list-item id="u1690"><label>•</label><p id="p2255">Clinical signs vary from a fistula draining saliva and feed material with open perforations to severe cervical swelling, cellulitis, abscessation, and subcutaneous emphysema with closed esophageal perforation. Dyspnea may develop and necessitate emergency tracheotomy.</p></list-item><list-item id="u1695"><label>•</label><p id="p2260">Confirm the diagnosis with endoscopy, radiography, or contrast radiography. <italic>Small perforations are difficult to detect with endoscopy.</italic> Survey radiographs may reveal subcutaneous emphysema, and positive-contrast studies may demonstrate leakage of fluid and gas medium into the surrounding tissues.</p></list-item></list><boxed-text id="b0050"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0350"><title>Esophageal Perforation</title><p id="p2265"><list list-type="simple" id="ulist0355"><list-item id="u1700"><label>•</label><p id="p2270">Acute (6 to 12 hours) perforations can be debrided and closed primarily if sufficient viable esophageal tissue is present.</p></list-item><list-item id="u1705"><label>•</label><p id="p2275">Maintain affected horses with nothing by mouth for 48 to 72 hours after surgery to allow time for mucosal healing and to minimize postoperative fistula formation.</p></list-item><list-item id="u1710"><label>•</label><p id="p2280">Administer broad-spectrum antimicrobial therapy. Antimicrobial combinations commonly used include the following:<list list-type="simple" id="ulist0360"><list-item id="u1715"><label>•</label><p id="p2285">Na<sup>+</sup>/K<sup>+</sup> penicillin, 22,000 to 44,000 IU/kg IV q6h, and aminoglycosides: gentamicin, 6.6 mg/kg IV q24h, or amikacin, 19.8 mg/kg IV q24h</p></list-item><list-item id="u1720"><label>•</label><p id="p2290">Metronidazole 25 to 35 mg/kg per rectum q6h, for anaerobes</p></list-item></list></p></list-item><list-item id="u1725"><label>•</label><p id="p2295">Administer intravenous, balanced, polyionic fluids to correct electrolyte and acid-base abnormalities, or if aminoglycosides are being administered, to preserve sufficient renal perfusion.</p></list-item><list-item id="u1730"><label>•</label><p id="p2300">Administer NSAIDs.</p></list-item><list-item id="u1735"><label>•</label><p id="p2305">Administer tetanus prophylaxis.</p></list-item><list-item id="u1740"><label>•</label><p id="p2310">If primary closure is <italic>not</italic> possible, which is usually the case, establish adequate ventral drainage to minimize extension of the cellulitis along fascial planes, which could result in septic mediastinitis and pleuritis. The wound is left to heal by second intention.</p></list-item><list-item id="u1745"><label>•</label><p id="p2315">Nutritional supplementation through an esophagostomy and indwelling nasogastric tube distal to the site of perforation, or total parenteral nutrition, may be needed during the convalescent period.</p></list-item><list-item id="u1750"><label>•</label><p id="p2320">If severe nonperforating tears are noted on endoscopy, these can be managed with intravenous nutrition until salivation is no longer present, after which a gruel can be fed. The value of sucralfate in these cases is unproven but it is often used.</p></list-item></list></p></sec></boxed-text></p><sec id="s0355"><title>Prognosis</title><p id="p2325"><list list-type="simple" id="ulist0365"><list-item id="u1755"><label>•</label><p id="p2330">The prognosis for acute esophageal perforation is fair if prompt, aggressive therapy is instituted and primary closure of the defect is possible.</p></list-item><list-item id="u1760"><label>•</label><p id="p2335">In chronic cases, the prognosis is guarded because of the high probability of secondary complications such as esophageal stricture, reobstruction, and septic mediastinitis or pleuritis.</p></list-item></list></p></sec></sec></sec><sec id="s0360"><title>Stomach and Duodenum</title><sec id="s0365"><title>Gastric Ulcers</title><p id="p2340"><italic><bold>James A. Orsini and Thomas J. Divers</bold></italic></p><p id="p2345">For information regarding clinical signs of gastric ulcers and guidelines for their diagnosis, see <xref rid="t0030" ref-type="table">Tables 18-5</xref>and <xref rid="t0035" ref-type="table">18-6</xref>.<boxed-text id="b0055"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0370"><title>Gastric Ulceration in Adult Horses*</title><p id="p2495"><table-wrap position="float" id="t0040"><label>Table 18-7</label><table frame="hsides" rules="groups"><thead><tr><th align="left">Therapeutic Goals</th><th align="left">Specific Treatment Options</th></tr></thead><tbody><tr><td align="left"><bold>Suppress Gastric Acid Secretion</bold></td><td align="left">Proton pump inhibitors:<break></break>Omeprazole (Gastrogard, Ulcergard): 2-4 mg/kg PO q24h<break></break>Omeprazole (Losec): 0.5 mg/kg IV q24h<break></break>Esomeprazole sodium: 0.5 mg/kg IVPantoprazole 1.5 mg/kg IV q24h<break></break>Histamine (H<sub>2</sub>) receptor antagonists:<break></break>Cimetidine (Tagamet): 16-25 mg/kg PO or 6.6 mg/kg IV q6-8h<break></break>Ranitidine (Zantac): 6.6 mg/kg PO or 1.5 mg/kg IV q8h<break></break>Famotidine (Pepcid): 2.8-4 mg/kg PO or 0.23-0.5 mg/kg IV q8-12h</td></tr><tr><td colspan="2"><hr></hr></td></tr><tr><td align="left"><bold>Protect the Ulcerated Mucosa</bold></td><td align="left">Mucosal protection/repair:<break></break>Sucralfate (Carafate): 20-40 mg/kg PO q6-8h<break></break>Misoprostol (Cytotec): 2.5-5 μg/kg PO q12-24h (<bold><italic>Note</italic></bold><italic>:</italic> May cause diarrhea)<break></break>Antacids (buffer already secreted acid):<break></break>Mg(OH)<sub>2</sub> and Al(OH)<sub>3</sub> must be given PO q2-4h<break></break>If severe colic is present, add 30-40 mL of 2% lidocaine to the above for a 500-kg horse.</td></tr><tr><td colspan="2"><hr></hr></td></tr><tr><td align="left"><bold>Stimulate Gastric Emptying</bold></td><td align="left">Gastric prokinetics include bethanechol, metoclopramide, erythromycin, and cisapride. <italic>Do not use if outflow obstruction is present or suspected.</italic></td></tr><tr><td colspan="2"><hr></hr></td></tr><tr><td align="left"><bold>Prophylaxis</bold></td><td align="left">Omeprazole: 1-2 mg/kg PO q24h</td></tr></tbody></table></table-wrap></p></sec></boxed-text><boxed-text id="b0060"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0375"><title>Gastroduodenal Ulceration in Foals<xref rid="tn0020" ref-type="table-fn">*</xref></title><p id="p2500"><table-wrap position="float" id="t0045"><label>Table 18-8</label><table frame="hsides" rules="groups"><thead><tr><th align="left">Situation</th><th align="left">Treatment Recommendations</th></tr></thead><tbody><tr><td align="left">Subacute or chronic ulceration (mild to moderate clinical signs)</td><td align="left"><list list-type="simple" id="olist0390"><list-item id="o1910"><label>1.</label><p id="p2505">Administer oral sucralfate <italic>plus</italic> an acid blocker (H<sub>2</sub> receptor antagonist or proton pump inhibitor):<list list-type="simple" id="ulist0395"><list-item id="u1915"><label>•</label><p id="p2510">Use adult dosages (see <xref rid="t0040" ref-type="table">Table 18-7</xref>)</p></list-item><list-item id="u1920"><label>•</label><p id="p2515">Wait 1-2 hours between sucralfate and other oral meds</p></list-item><list-item id="u1925"><label>•</label><p id="p2520">If <italic>no</italic> improvement after 3-5 days, consider outflow obstruction or other disorder</p></list-item><list-item id="u1930"><label>•</label><p id="p2525">For foals unable to receive oral medication, use pantoprazole or ranitidine IV</p></list-item></list></p></list-item><list-item id="o1935"><label>2.</label><p id="p2530">Manage pain with xylazine or butorphanol:<list list-type="simple" id="ulist0400"><list-item id="u1940"><label>•</label><p id="p2535"><italic>Do not</italic> use NSAIDs unless absolutely necessary; even COX-2 selective NSAIDs may inhibit ulcer healing</p></list-item><list-item id="u1945"><label>•</label><p id="p2540">If inadequate response, make an “antacid cocktail”(500 mL Pepto-Bismol or Mylanta + 100 mL Maalox liquid + 4 sucralfate crushed tablets + 1 cup activated charcoal powder + 500 mL warm water) and give via soft NG tube to sedated foal</p></list-item><list-item id="u1950"><label>•</label><p id="p2545">May also add 15 mL of 2% lidocaine to cocktail for rapid pain relief</p></list-item></list></p></list-item><list-item id="o1955"><label>3.</label><p id="p2550">Provide supportive care as needed:<list list-type="simple" id="ulist0405"><list-item id="u1960"><label>•</label><p id="p2555">Fluid therapy for diarrhea, for example</p></list-item><list-item id="u1965"><label>•</label><p id="p2560">Give misoprostol (see <xref rid="t0040" ref-type="table">Table 18-7</xref>) if ulcers were caused by NSAIDs</p></list-item></list></p></list-item></list><break></break>Be aware of possible complications/sequelae, including gastric or duodenal perforation, duodenal stricture, cholangitis, and aspiration pneumonia.</td></tr><tr><td colspan="2"><hr></hr></td></tr><tr><td align="left">Emergency care (acute, severe clinical signs)</td><td align="left"><list list-type="simple" id="olist0410"><list-item id="o1970"><label>1.</label><p id="p2565">Follow care as outlined for subacute/chronic cases, but give ulcer meds IV.</p></list-item><list-item id="o1975"><label>2.</label><p id="p2570">If severe gastroesophageal reflux, marked salivation, esophageal distention, and esophageal ulceration, give one of the following prokinetics until signs improve:<list list-type="simple" id="ulist0415"><list-item id="u1980"><label>•</label><p id="p2575">Bethanechol: 0.03-0.04 mg/kg IV or SQ q6-8h</p></list-item><list-item id="u1985"><label>•</label><p id="p2580">Metoclopramide (Reglan): 0.25 mg/kg <italic>slowly</italic> over 1 hour IV q4-8h; can be given SQ</p></list-item><list-item id="u1990"><label>•</label><p id="p2585">Lidocaine: 1.3 mg/kg bolus IV, followed by constant-rate infusion at 0.04 mg/kg/h IV; use of this dose in foals less than 3 weeks old could result in increased risk of toxicity because of delayed hepatic metabolism</p></list-item></list></p></list-item></list></td></tr><tr><td colspan="2"><hr></hr></td></tr><tr><td align="left">Prophylaxis</td><td align="left"><list list-type="simple" id="olist0420"><list-item id="o1995"><label>1.</label><p id="p2590">Minimize risk factors where possible (e.g., minimize NSAID use, use COX-2 selective NSAIDs when necessary, promptly treat diarrhea).</p></list-item><list-item id="o2000"><label>2.</label><p id="p2595">Give antiulcer meds to stressed foals:<list list-type="simple" id="ulist0425"><list-item id="u2005"><label>•</label><p id="p2600">Use oral sucralfate, an acid inhibitor, or both.</p></list-item><list-item id="u2010"><label>•</label><p id="p2605">Sucralfate may be used alone in recumbent, critically ill foals or in foals at increased risk of nosocomial enteric infections.</p></list-item><list-item id="u2015"><label>•</label><p id="p2610">An acid inhibitor should be added once the foal is able to stand.</p></list-item></list></p></list-item><list-item id="o2020"><label>3.</label><p id="p2615">Check for duodenal stricture if the problem is not acute.</p></list-item></list></td></tr></tbody></table><table-wrap-foot><fn><p><italic>COX,</italic> Cyclooxygenase; <italic>NG,</italic> nasogastric; <italic>NSAID,</italic> nonsteroidal anti-inflammatory drug.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tn0020"><label>*</label><p id="np0055">Clinical response to H<sub>2</sub> receptor antagonist or proton pump inhibitor should occur in 3 to 5 days after starting treatment. If <italic>not,</italic> consider other differential diagnoses, such as outflow problems and inadequate treatment.</p></fn></table-wrap-foot></table-wrap></p></sec></boxed-text><table-wrap position="float" id="t0030"><label>Table 18-5</label><caption><p>Clinical Signs of Gastroduodenal Ulceration in Horses</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">Adults</th><th align="left">Foals</th></tr></thead><tbody><tr><td align="left"><list list-type="simple" id="ulist0370"><list-item id="u1765"><p id="p2350">Poor appetite</p></list-item><list-item id="u1770"><p id="p2355">Depression or other behavioral changes</p></list-item><list-item id="u1775"><p id="p2360">Poor performance, which might be related to decreased feed consumption, anemia, decreased stride length, or chronic pain/stress</p></list-item><list-item id="u1780"><p id="p2365">Mild to moderate signs of abdominal pain</p></list-item><list-item id="u1785"><p id="p2370">Poor hair coat</p></list-item><list-item id="u1790"><p id="p2375">Loss of body weight, body condition score <5/9</p></list-item><list-item id="u1795"><p id="p2380">Positive response to ulcer treatment</p></list-item></list></td><td align="left"><list list-type="simple" id="ulist0375"><list-item id="u1800"><p id="p2385">High-risk group: 1 to 4 months of age</p></list-item><list-item id="u1805"><p id="p2390">Bruxism/odontoprisis (teeth grinding)</p></list-item><list-item id="u1810"><p id="p2395">Ptyalism (hypersalivation) generally indicates an outflow problem and esophagitis</p></list-item><list-item id="u1815"><p id="p2400">Rolling onto back, especially after nursing</p></list-item><list-item id="u1820"><p id="p2405">Other signs of abdominal pain</p></list-item><list-item id="u1825"><p id="p2410">Poor appetite</p></list-item><list-item id="u1830"><p id="p2415">Interruption of nursing (discomfort)</p></list-item><list-item id="u1835"><p id="p2420">Diarrhea or history of diarrhea</p></list-item></list></td></tr></tbody></table></table-wrap><table-wrap position="float" id="t0035"><label>Table 18-6</label><caption><p>Diagnosis of Gastric Ulcers</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">Adults</th><th align="left">Foals</th></tr></thead><tbody><tr><td align="left"><list list-type="simple" id="ulist0380"><list-item id="u1840"><p id="p2425">Clinical Signs: See <xref rid="t0030" ref-type="table">Table 18-5</xref>.</p></list-item><list-item id="u1845"><p id="p2430">Endoscopy is the only reliable diagnostic tool to confirm a presumptive diagnosis of gastric ulcers. For video or fiber-optic endoscopy, use a 200- (minimum) to 300-cm length scope.</p></list-item><list-item id="u1860"><p id="p2445">Grades of gastric ulceration (<xref rid="f0240" ref-type="fig">Fig. 18-46</xref>):<list list-type="simple" id="ulist9025"><list-item id="u1865"><p id="p2450">Grade 0/normal—epithelium intact</p></list-item><list-item id="u1870"><p id="p2455">Grade 1/mild ulceration—reddening, hyperkeratosis, and single or multifocal ulcer lesions</p></list-item><list-item id="u1875"><p id="p2460">Grade 2/moderate ulceration—large or multifocal lesions or extensive superficial lesions</p></list-item><list-item id="u1880"><p id="p2465">Grade 3/severe ulceration—extensive, coalescing lesions and deep lesions</p></list-item></list></p></list-item></list><break></break></td><td align="left"><list list-type="simple" id="ulist0385"><list-item id="u1885"><p id="p2470">Clinical Signs: See <xref rid="t0030" ref-type="table">Table 18-5</xref>.</p></list-item><list-item id="u1890"><p id="p2475">Ancillary Tests:<list list-type="simple" id="ulist9030"><list-item id="u1895"><p id="p2480">Gastroduodenal endoscopy (see Fig. 11-24)</p></list-item><list-item id="u1900"><p id="p2485">Barium contrast radiography</p></list-item><list-item id="u1905"><p id="p2490">Occult fecal blood tests are <italic>not</italic> sensitive; a negative result does not rule out gastroduodenal ulceration.</p></list-item></list></p></list-item></list></td></tr></tbody></table></table-wrap><fig id="f0240"><label>Figure 18-46</label><caption><p><bold>A,</bold> Grade 0 ulcer (normal). Intact mucosal epithelium (may have reddening and/or hyperkeratosis). <bold>B,</bold> Grade 1 ulcer (mild). Small single or multiple ulcers. <bold>C,</bold> Grade 2 ulcer (moderate). Large single or multiple ulcers. <bold>D,</bold> Grade 3 ulcer (severe). Extensive (often coalescing) ulcers with areas of deep ulceration.</p></caption><graphic xlink:href="f018-046-9781455708925"></graphic></fig></p></sec><sec id="s0380"><title>Duodenal or Gastric Perforation</title><p id="p2620">Duodenal or gastric perforation usually occurs in foals younger than 8 weeks.<list list-type="simple" id="ulist0430"><list-item id="u2025"><label>•</label><p id="p2625">Risk factors include the use of NSAIDs and stresses to the foal, including diarrhea.</p></list-item><list-item id="u2030"><label>•</label><p id="p2630">Many cases occur with minimal warning signs of gastric ulceration.</p></list-item></list></p><sec id="s0385"><title>Common Clinical Signs</title><p id="p2635"><list list-type="simple" id="ulist0435"><list-item id="u2035"><label>•</label><p id="p2640">Foals often are found acutely depressed or “colicky” with a tense/guarded abdomen.</p></list-item><list-item id="u2040"><label>•</label><p id="p2645">Foals have increased heart and respiratory rates.</p></list-item><list-item id="u2045"><label>•</label><p id="p2650">Foals may have a high fever, yet they may continue to nurse.</p></list-item><list-item id="u2050"><label>•</label><p id="p2655">Often, diarrhea accompanies duodenal perforation; the diarrhea is often present before the perforation or as a consequence of endotoxemia.</p></list-item></list></p></sec><sec id="s0395"><title>Diagnosis</title><p id="p2660"><list list-type="simple" id="ulist0440"><list-item id="u11070"><label>•</label><p id="p13425">Clinical signs</p></list-item><list-item id="u2055"><label>•</label><p id="p2665">Ultrasonography: large amounts of flocculent fluid are seen</p></list-item><list-item id="u2060"><label>•</label><p id="p2670">Abdominocentesis: may confirm septic peritonitis</p></list-item></list><boxed-text id="b0065"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0400"><title>Duodenal or Gastric Perforation</title><p id="p2675">Humane destruction is generally the outcome, except for those patients with a small duodenal perforation that may be found at exploratory surgery and sealed by the omentum. Acute gastric perforations in young foals with milk found in the abdomen have been successfully repaired.</p></sec></boxed-text></p></sec><sec id="s0405"><title>Prevention</title><p id="p2680"><list list-type="simple" id="ulist0445"><list-item id="u2065"><label>•</label><p id="p2685">NSAIDs should be administered to young foals <italic>only</italic> when absolutely necessary, as in the management of endotoxemia or colic, especially in foals with diarrhea.</p></list-item><list-item id="u2070"><label>•</label><p id="p2690">If an NSAID has been administered to a foal, initiate treatment with omeprazole, 2 to 4 mg/kg PO q24h.</p></list-item><list-item id="u2075"><label>•</label><p id="p2695"><italic><bold>Practice Tip:</bold> Do not rely on sucralfate alone to prevent ulcers if NSAIDs are being used.</italic></p></list-item><list-item id="u2080"><label>•</label><p id="p2700"><italic><bold>Practice Tip:</bold> Firocoxib, 0.09 mg/kg IV q24h; meloxicam 0.6 mg/kg PO or IV q12 to 24h; and carprofen, 1.4 mg/kg q12 to 24h PO or IV, may be the safest NSAIDs to use when more long-term therapy for skeletal disorders is required in foals.</italic></p></list-item></list></p></sec></sec><sec id="s0410"><title>Acute Grain Overload</title><p id="p2705">Clinicians often are called in an emergency to examine and treat a horse that has accidentally ingested a large quantity of grain (a commercially prepared concentrate or a cereal grain hay such as barley).<boxed-text id="b0070"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0415"><title>Acute Grain Overload</title><p id="p2710">If the patient has <italic>no</italic> abnormal clinical signs at examination, the following treatment is recommended:<list list-type="simple" id="ulist0450"><list-item id="u2085"><label>•</label><p id="p2715">Pass a stomach tube and check for gastric reflux; if there is <italic>no</italic> reflux, use gravity flow (funnel) to administer 1 lb (450 g) Epsom salts (MgSO<sub>4</sub>) or 1 lb (450 g) activated charcoal, or half of each, mixed in 1 gallon (3.8 L) warm water (per 500-kg adult).</p></list-item><list-item id="u2090"><label>•</label><p id="p2720">Administer 1 mg/kg followed by 0.3 mg/kg flunixin meglumine IV or PO q8h for 48 hours.</p></list-item><list-item id="u2095"><label>•</label><p id="p2725">Administer diphenhydramine 1.0 mg/kg IM q12h or 0.5 mg/kg doxylamine succinate SQ q6h for 24h; other antihistamines may be substituted.</p></list-item><list-item id="u2100"><label>•</label><p id="p2730">Remove all feed for 24 hours.</p></list-item><list-item id="u2105"><label>•</label><p id="p2735">Cryoprophylaxis for laminitis should be performed if there is an increased risk for the disease (see Chapter 43, p. 712).</p></list-item><list-item id="u11075"><label>•</label><p id="p13430">Di-trioctahedral (DTO) smectite (Biosponge), 0.5 to 3 lb/1.1 to 6.6 kg per 450 kg, PO or NG tube q12-24h; gastrointesintal adsorbent.</p></list-item></list></p></sec></boxed-text></p><sec id="s0420"><title>Prognosis</title><p id="p2740">Prognosis should be excellent if treatment is given before clinical signs develop.</p></sec></sec><sec id="s0425"><title>Symptomatic Grain Overload</title><p id="p2745"><list list-type="simple" id="ulist0455"><list-item id="u2110"><label>•</label><p id="p2750">The clinical signs most frequently seen with symptomatic grain overload are<list list-type="simple" id="ulist0460"><list-item id="u2115"><label>•</label><p id="p2755">Colic</p></list-item><list-item id="u2120"><label>•</label><p id="p2760">Significant abdominal distention</p></list-item><list-item id="u2125"><label>•</label><p id="p2765">Severe lameness (laminitis)</p></list-item><list-item id="u2130"><label>•</label><p id="p2770">Trembling</p></list-item><list-item id="u2135"><label>•</label><p id="p2775">Sweating</p></list-item><list-item id="u2140"><label>•</label><p id="p2780">Polypnea</p></list-item><list-item id="u2145"><label>•</label><p id="p2785">Less frequently, diarrhea</p></list-item></list></p></list-item><list-item id="u2150"><label>•</label><p id="p2790">Clinical findings include:<list list-type="simple" id="ulist0465"><list-item id="u2155"><label>•</label><p id="p2795">Bright red to purple membranes</p></list-item><list-item id="u2160"><label>•</label><p id="p2800">Tachycardia</p></list-item><list-item id="u2165"><label>•</label><p id="p2805">Absence of intestinal sounds (some pings may be heard on simultaneous auscultation and percussion of the abdomen)</p></list-item><list-item id="u2170"><label>•</label><p id="p2810">Gastric reflux</p></list-item><list-item id="u2175"><label>•</label><p id="p2815">Colonic distention with tight bands palpated on rectal examination</p></list-item></list></p></list-item><list-item id="u2180"><label>•</label><p id="p2820">CBC usually reveals severe polycythemia, neutropenia with a left shift, and vacuolization of neutrophils (toxic changes).</p></list-item></list><boxed-text id="b0075"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0430"><title>Symptomatic Grain Overload</title><p id="p2825"><list list-type="simple" id="ulist0470"><list-item id="u2185"><label>•</label><p id="p2830">Give intravenous fluid therapy. Administer hypertonic saline solution initially, but this must be followed within 1 to 2 hours by administration of a polyionic fluid at 2 to 4 L/h for the adult; 500 mL of 23% calcium borogluconate, can be administered but must be diluted with several liters of the polyionic fluids. Add KCl, 20 to 40 mEq, to each liter of fluid after urination is documented. <italic><bold>Practice Tip:</bold> A ratio of 10 : 1 of polyionic fluid : hypertonic fluid is the accepted rule-of-thumb when using hypertonic saline as part of fluid replacement therapy.</italic></p></list-item><list-item id="u2190"><label>•</label><p id="p2835">Administer plasma if possible (2 to 4 L for an adult). Hyperimmune plasma containing antibodies against endotoxin is preferred but is not essential.</p></list-item><list-item id="u2195"><label>•</label><p id="p2840">Administer flunixin meglumine 1 mg/kg IV q12h initially and 0.3 mg/kg q8h after signs of colic are no longer evident.</p></list-item><list-item id="u2200"><label>•</label><p id="p2845">Administer lidocaine (1.3 mg/kg as a slow bolus IV followed by 0.05 mg/kg/min) to improve intestinal motility, provide analgesia, and to impair neutrophil margination that may be a trigger factor for laminitis.</p></list-item><list-item id="u2205"><label>•</label><p id="p2850">Pass a nasogastric tube and leave it in place to relieve gastric distention. If there is <italic>no</italic> gastric reflux, administer <inline-graphic xlink:href="if018-008-9781455708925.gif"></inline-graphic> lb (225 g) of charcoal and <inline-graphic xlink:href="if018-009-9781455708925.gif"></inline-graphic> lb of magnesium sulfate in <inline-graphic xlink:href="if018-010-9781455708925.gif"></inline-graphic> gallon (1.9 L) warm water (per 500-kg adult) by means of gravity flow.</p></list-item><list-item id="u2210"><label>•</label><p id="p2855">Polymyxin B, 2000 to 6000 IU/kg IV q12h for 1 to 2 days, can be used to bind circulating endotoxin if renal function is normal.</p></list-item><list-item id="u2215"><label>•</label><p id="p2860">Pentoxifylline, 10 mg/kg PO or IV q12h, may be administered:<list list-type="simple" id="ulist0475"><list-item id="u2220"><label>•</label><p id="p2865">If there is no gastric reflux</p></list-item><list-item id="u2225"><label>•</label><p id="p2870">Administer slowly intravenously as a compounded solution</p></list-item><list-item id="u2230"><label>•</label><p id="p2875">It may inhibit inflammatory cytokine production</p></list-item></list></p></list-item><list-item id="u2245"><label>•</label><p id="p2890">Administer aggressive and early therapy for laminitis if signs of founder are present (see Chapter 43, p. 709).<list list-type="simple" id="ulist9035"><list-item id="u2235"><label>•</label><p id="p2880">Remove feed, bed heavily, apply dental packing or pads to the feet.</p></list-item><list-item id="u2240"><label>•</label><p id="p2885"><bold>Ice legs and feet for a minimum of 2 days or until clinical signs resolve, using ice boots or equivalent cyrotherapy.</bold></p></list-item></list></p></list-item><list-item id="u2250"><label>•</label><p id="p2895">If there is considerable cecal or colonic distention, perform trocarization (see <xref rid="p0290" ref-type="p">p. 160</xref>) and infuse 1 × 10<sup>6</sup> units of penicillin into the cecal/colon lumen. Penicillin preparation instilled is not important for the antimicrobial effect targeting <italic>Streptococcus bovis.</italic></p></list-item></list></p></sec></boxed-text></p><sec id="s0435"><title>Prognosis</title><p id="p2900"><list list-type="simple" id="ulist0480"><list-item id="u2255"><label>•</label><p id="p2905">The prognosis, if there are moderate to severe clinical signs, is poor. If severe abdominal pain and significant abdominal distention are present, affected patients usually die within 24 to 48 hours even with the most aggressive therapy.</p></list-item><list-item id="u2260"><label>•</label><p id="p2910">If signs of laminitis occur before signs of the presence of intestinal disease abate, the prognosis is grave.</p></list-item></list></p></sec></sec><sec id="s0440"><title>Acute Gastric Dilation</title><p id="p2915"><italic><bold>P.O. Eric Mueller, John F. Peroni, and James N. Moore</bold></italic></p><p id="p2920"><list list-type="simple" id="ulist0485"><list-item id="u2265"><label>•</label><p id="p2925">Primary gastric dilation is believed to be associated with:<list list-type="simple" id="ulist0490"><list-item id="u2270"><label>•</label><p id="p2930">The ingestion of highly fermentable feed, such as grass clippings</p></list-item><list-item id="u2275"><label>•</label><p id="p2935">The ingestion of excessive amounts of corn or other grain</p></list-item></list></p></list-item><list-item id="u2280"><label>•</label><p id="p2940">Secondary gastric dilation occurs when fluid from the small intestine accumulates in the stomach because of:<list list-type="simple" id="ulist0495"><list-item id="u2285"><label>•</label><p id="p2945">Ileus</p></list-item><list-item id="u2290"><label>•</label><p id="p2950">Obstruction of the small-intestinal lumen</p></list-item><list-item id="u2295"><label>•</label><p id="p2955">Strangulating obstruction involving the small intestine</p></list-item><list-item id="u2300"><label>•</label><p id="p2960">Severe inflammation of the small intestine</p></list-item></list></p></list-item><list-item id="u2305"><label>•</label><p id="p2965">In one study of 50 horses with gastric rupture, horses drinking water from a bucket, stream, or pond were at greater risk of gastric rupture than were those with access to an automatic waterer.</p></list-item><list-item id="u2310"><label>•</label><p id="p2970">Foals with duodenal/pyloric obstruction have significant gastric dilation; however, because of the gradual obstruction and dilation, abdominal pain (colic) is <italic>not</italic> pronounced.</p></list-item><list-item id="u2315"><label>•</label><p id="p2975">Horses exhibit signs of severe pain and increased heart and respiratory rates caused by pain and diaphragmatic pressure.</p></list-item><list-item id="u2320"><label>•</label><p id="p2980">If the dilation is primary, the mucous membranes are pale, and on rectal examination, the spleen can be palpated because it is displaced caudally by the enlarged stomach. <italic><bold>Practice Tip:</bold> Ultrasound examination of the left side of the abdomen is helpful in imaging the size of the stomach. It is abnormal if the stomach extends to the caudal limits of the last rib!</italic> If the dilation results from a problem involving the small intestine, the patient may exhibit signs of toxicity, the peritoneal fluid may reflect intraabdominal ischemia (discoloration with erythrocytes, increased WBC count and protein concentration), and several loops of distended small intestine may be palpable on rectal examination.</p></list-item><list-item id="u2325"><label>•</label><p id="p2985">In some cases, spontaneous regurgitation may occur immediately before the stomach ruptures along its greater curvature.</p></list-item></list><boxed-text id="b0080"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0445"><title>Acute Gastric Dilation</title><p id="p2990"><list list-type="simple" id="ulist0500"><list-item id="u2330"><label>•</label><p id="p2995">For acute abdominal pain, the primary goal is to relieve intragastric pressure by passing a medium or large-bore stomach tube. Lidocaine may be needed to relax the cardiac sphincter; it may be necessary to create a “siphon” effect to ensure that all excess fluid is removed from the stomach (see <xref rid="s0010" ref-type="sec">p. 157</xref>).</p></list-item><list-item id="u2335"><label>•</label><p id="p3000">Once emergency care is given, perform a complete physical examination to determine the cause. In primary dilation, the patient should remain pain-free once the intragastric pressure is relieved.</p></list-item><list-item id="u2340"><label>•</label><p id="p3005">If the dilation results from a small-intestinal problem, relief is transient. Intravenous lidocaine (1.3 mg/kg as a slow IV bolus followed by 0.04 mg/kg/min CRI [constant rate infusion]) and polymyxin, 2000 to 6000 IU/kg IV q8h, are used for gastric dilation caused by nonobstructing small-intestinal disease such as proximal enteritis.</p></list-item><list-item id="u2345"><label>•</label><p id="p3010">If the stomach ruptures, the patient immediately appears comfortable, but then rapid deterioration occurs as the result of endotoxic and cardiovascular shock. Ingesta are evident in the peritoneal fluid, and the serosa of the intestines is roughened on rectal examination. Humane destruction is recommended.</p></list-item></list></p></sec></boxed-text></p><sec id="s0450"><title>Prognosis</title><p id="p3015"><list list-type="simple" id="ulist0505"><list-item id="u2350"><label>•</label><p id="p3020">The prognosis for primary dilation is excellent, provided intragastric pressure is rapidly relieved.</p></list-item><list-item id="u2355"><label>•</label><p id="p3025">The prognosis for secondary gastric dilation depends on the underlying disease and the duration of the condition before treatment is started.</p></list-item></list></p></sec></sec><sec id="s0455"><title>Gastric Impaction</title><p id="p3030">Gastric impaction occurs infrequently. The most common causes are the following:<list list-type="simple" id="ulist0510"><list-item id="u2360"><label>•</label><p id="p3035">Grain overload</p></list-item><list-item id="u2365"><label>•</label><p id="p3040">Dry, impacted ingesta<list list-type="simple" id="ulist0515"><list-item id="u2370"><label>•</label><p id="p3045">Poor dentition</p></list-item></list></p></list-item><list-item id="u2375"><label>•</label><p id="p3050">Squamous cell carcinoma of the stomach</p></list-item><list-item id="u2380"><label>•</label><p id="p3055">Ingestion of persimmons</p></list-item><list-item id="u2385"><label>•</label><p id="p3060">Severe hepatic disease</p></list-item></list></p><p id="p3065">If the impaction is associated with causes other than squamous cell carcinoma, the patient may show signs of moderate to severe pain. Most often these patients do <italic>not</italic> show evidence of systemic toxicity unless the grain overload has progressed, resulting in signs of acute laminitis. Gastroscopic examination and ultrasound (finding an enlarged stomach) are helpful procedures in making the diagnosis; on extremely rare occasions, the stomach may be palpated rectally with gastric impaction. Horses with impacted ingesta in the stomach may be in uncontrollable pain, which necessitates immediate exploratory surgery. The diagnosis in these cases is made at surgery. Horses with more chronic impactions may have mild to moderate pain. The diagnosis can be made by ultrasound examination, demonstrating an enlarged stomach and gastroscopic examination, showing large amounts of feed present after <italic>not</italic> being fed for more than 16 hours.</p><p id="p3070"><italic><bold>Practice Tip:</bold> Friesians may be genetically predisposed to both esophageal and gastric motility disorders.</italic><boxed-text id="b0085"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0460"><title>Gastric Impaction</title><p id="p3075"><list list-type="simple" id="ulist0520"><list-item id="u2390"><label>•</label><p id="p3080">For severe impactions, surgery is recommended. At surgery, administer 2 to 3 L of water through a 3-inch (7.5-cm) intraabdominal needle placed through the gastric wall. Redirect the end of the needle, infiltrating different areas of the mass, and gently massage the impaction.</p></list-item><list-item id="u2395"><label>•</label><p id="p3085">Postoperative care includes:<list list-type="simple" id="ulist0525"><list-item id="u2400"><label>•</label><p id="p3090">Lavage of the stomach</p></list-item><list-item id="u2405"><label>•</label><p id="p3095">Drainage through a large-bore gastric tube</p></list-item></list></p></list-item></list></p><p id="p3100">If persimmon impaction is suspected, or visualized on gastroscopic examination, repeated administration of Coca-Cola (1 L) by nasogastric tube has been reported to be effective.<list list-type="simple" id="ulist0530"><list-item id="u2410"><label>•</label><p id="p3105">For horses with milder pain and less severe distention, based upon ultrasound examination, withhold food and administer 6 L of isotonic electrolyte via gravity flow every 6 to 12 hours.</p></list-item></list></p></sec></boxed-text></p><sec id="s0465"><title>Prognosis</title><p id="p3110"><list list-type="simple" id="ulist0535"><list-item id="u2415"><label>•</label><p id="p3115">Guarded for horses with acute severe pain.</p></list-item><list-item id="u2420"><label>•</label><p id="p3120">Much better for horses with more mild pain—a recent report from Finland (Vainio et al., 2011) even suggests it is good.</p></list-item><list-item id="u2425"><label>•</label><p id="p3125">Poor for horses with liver failure and gastric impaction.</p></list-item></list></p></sec></sec></sec><sec id="s0470"><title>Acute Abdomen—Colic</title><sec id="s0475"><title>Classification and Pathophysiology of Colic</title><p id="p3135">A variety of enteric diseases can result in the manifestation of abdominal pain (colic) in horses. Abnormalities of the equine gastrointestinal tract are broadly classified as physical or functional obstructions. With a nonstrangulating physical obstruction, the mesenteric blood supply is intact, but the bowel lumen is occluded. This can be caused by intraluminal masses or reduction of the lumen by intramural thickening or extramural compression. Strangulating obstruction implies luminal occlusion and reduction or occlusion of the mesenteric blood supply. Incarceration of the intestine through internal or external hernias, intussusception, or a greater than 180-degree twist of a segment of intestine on its mesentery can result in a strangulating obstruction.</p><p id="p13435">Functional obstruction, referred to as adynamic or paralytic ileus:<list list-type="simple" id="ulist0540"><list-item id="u2430"><label>•</label><p id="p3140">Can be idiopathic</p></list-item><list-item id="u2435"><label>•</label><p id="p3145">Can result from inflammatory disease (e.g., duodenitis/proximal jejunitis and colitis)</p></list-item><list-item id="u2440"><label>•</label><p id="p3150">Can be caused by serosal irritation from surgical manipulation</p></list-item></list></p><p id="p3155">Intestinal obstruction prevents the aboral movement of gastrointestinal contents and results in distention of the intestine. As the distention increases, venous drainage from the intestinal wall is impaired, and the mucosa becomes congested and edematous. If the obstruction persists for a prolonged time (>24 hours) significant compromise of intestinal vascular integrity can result in mucosal ischemia. With progressive distention, gastric, cecal, or colonic rupture can result. In strangulating obstruction, these events are combined with rapid tissue hypoxia and ischemia of the affected segment and lead to necrosis and transmural leakage of bacteria and endotoxin. Cardiovascular deterioration rapidly follows transperitoneal absorption of endotoxin, resulting in hypovolemia and endotoxic shock.</p><sec id="s0480"><title>Diagnosis</title><sec id="s0485"><title>Early History</title><p id="p3160"><list list-type="simple" id="ulist0545"><list-item id="u2445"><label>•</label><p id="p3165">Previous episode of colic, duration of colic, recent changes in management (feed, water, deworming, medication, exercise routine), breeding, pregnancy</p></list-item></list></p></sec><sec id="s0490"><title>Recent History</title><p id="p3170"><list list-type="simple" id="ulist0550"><list-item id="u2450"><label>•</label><p id="p3175">Degree of and change in pain (looking at flank, pawing, kicking at abdomen, rolling), last defecation, sweating, treatment, and response to treatment</p></list-item></list></p></sec><sec id="s0495"><title>Physical Examination</title><p id="p3180">Assess the following parameters immediately and completely during initial examination of the patient with a history of acute abdominal pain:<list list-type="simple" id="ulist0555"><list-item id="u2455"><label>•</label><p id="p3185">Attitude</p></list-item><list-item id="u2460"><label>•</label><p id="p3190">Abdominal shape (distention)</p></list-item><list-item id="u2465"><label>•</label><p id="p3195">Body temperature, pulse, and respiratory rate</p></list-item><list-item id="u2470"><label>•</label><p id="p3200">Skin turgor, mucous membrane moisture and color, and capillary refill time (CRT)</p></list-item><list-item id="u2475"><label>•</label><p id="p3205">Abdominal auscultation and percussion</p></list-item><list-item id="u2480"><label>•</label><p id="p3210">Nasogastric intubation—quantity and characteristics of fluid</p></list-item><list-item id="u2485"><label>•</label><p id="p3215">Abdominal palpation per rectum</p></list-item></list></p><p id="p3220">The physical examination starts with observation of external appearance and attitude. Abdominal distention is generally a sign of large-intestinal disease in adult horses, but it can occur with severe small-intestinal distention, especially in foals. Multiple abrasions, particularly around the periorbital area, indicate that the patient recently experienced severe abdominal pain. Recent enlargement of an umbilical or abdominal hernia, or of the scrotum may indicate intestinal incarceration with obstruction or strangulation. Rectal temperature of 39° C (102° F) or greater may be suggestive of colitis or peritonitis; if possible, the rectal temperature should be taken in all colic cases prior to abdominal palpation per rectum. Assess the degree of pain with the patient in a quiet environment.</p><sec id="s0500"><title>Signs of Abdominal Pain in Order of Severity—Severe to Most Severe</title><p id="p3225"><list list-type="simple" id="ulist0560"><list-item id="u2490"><label>•</label><p id="p3230">Lying down for long periods</p></list-item><list-item id="u2495"><label>•</label><p id="p3235">Inappetence</p></list-item><list-item id="u2500"><label>•</label><p id="p3240">Restlessness</p></list-item><list-item id="u2505"><label>•</label><p id="p3245">Quivering of the upper lip</p></list-item><list-item id="u2510"><label>•</label><p id="p3250">Turning the head toward the flank</p></list-item><list-item id="u2515"><label>•</label><p id="p3255">Repeated stretching as if to urinate</p></list-item><list-item id="u2520"><label>•</label><p id="p3260">Kicking the abdomen with the hind feet</p></list-item><list-item id="u2525"><label>•</label><p id="p3265">Crouching as if wanting to lie down</p></list-item><list-item id="u2530"><label>•</label><p id="p3270">Sweating</p></list-item><list-item id="u2535"><label>•</label><p id="p3275">Dropping to the ground and rolling</p></list-item><list-item id="u2540"><label>•</label><p id="p3280"><italic><bold>Practice Tip:</bold> Severe, unrelenting pain may require analgesics before examination</italic> (<xref rid="t0055" ref-type="table">Table 18-9</xref>).<table-wrap position="float" id="t0055"><label>Table 18-9</label><caption><p>Analgesics and Relative Efficacy for Control of Acute Abdominal Pain</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left">Analgesic</th><th align="left">Trade Name</th><th align="left">Dosage</th><th align="left">Efficacy</th></tr></thead><tbody><tr><td align="left">Flunixin meglumine</td><td align="left">Banamine</td><td align="left">0.25-1.1 mg/kg IV</td><td align="left">Excellent</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Detomidine hydrochloride</td><td align="left">Dormosedan</td><td align="left">10-40 µg/kg IV or IM<xref rid="tn0025" ref-type="table-fn">*</xref></td><td align="left">Excellent</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Xylazine hydrochloride</td><td align="left">Rompun</td><td align="left">0.2-1.1 mg/kg IV or IM<xref rid="tn0025" ref-type="table-fn">*</xref></td><td align="left">Good</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Butorphanol tartrate</td><td align="left">Torbugesic</td><td align="left">0.02-0.08 mg/kg IV or IM<xref rid="tn0030" ref-type="table-fn">†</xref><xref rid="tn0035" ref-type="table-fn">‡</xref></td><td align="left">Good</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Ketoprofen</td><td align="left">Ketofen</td><td align="left">1.1-2.2 mg/kg IV</td><td align="left">Good</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">N-butylscopolammonium bromide</td><td align="left">Buscopan</td><td align="left">0.3 mg/kg IV (7 mL/450 kg)<xref rid="tn0040" ref-type="table-fn">§</xref><xref rid="tn0045" ref-type="table-fn">||</xref></td><td align="left">Good</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Morphine sulfate</td><td align="left"></td><td align="left">0.3-0.66 mg/kg IV<xref rid="tn0035" ref-type="table-fn">‡</xref><xref rid="tn0050" ref-type="table-fn">¶</xref></td><td align="left">Good</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Pentazocine</td><td align="left">Talwin</td><td align="left">0.3-0.6 mg/kg IV<xref rid="tn0035" ref-type="table-fn">‡</xref></td><td align="left">Poor</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Chloral hydrate</td><td align="left"></td><td align="left">30-60 mg/kg IV titrated</td><td align="left">Poor</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Dipyrone</td><td align="left">Novin</td><td align="left">10 mg/kg IV or IM</td><td align="left">Poor</td></tr><tr><td colspan="4"><hr></hr></td></tr><tr><td align="left">Phenylbutazone</td><td align="left">Butazolidin</td><td align="left">2.2-4.4 mg/kg IV</td><td align="left">Poor</td></tr></tbody></table><table-wrap-foot><fn id="tn0025"><label>*</label><p id="np0065">Repeated administration may compromise cardiac output and colonic motility.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tn0030"><label>†</label><p id="np0070">Doses in upper range may cause ataxia.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tn0035"><label>‡</label><p id="np0075">Indicates a controlled substance.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tn0040"><label>§</label><p id="np0080">Causes transient increase in heart rate.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tn0045"><label>||</label><p id="np0085">Available in Europe as a compositum with dipyrone.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tn0050"><label>¶</label><p id="np0090"><italic>Use only with xylazine</italic> (0.66 to 1.1 mg/kg IV) to avoid central nervous system excitement.</p></fn></table-wrap-foot></table-wrap></p></list-item></list></p><p id="p3285">Consider previous treatment by the owner, trainer, or RDVM when assessing the severity of abdominal pain. Depression with mild to moderate abdominal pain and fever may indicate an inflammatory condition (enteritis or colitis). In the absence of extreme muscle exertion, suspect inflammatory disease (enteritis, colitis, peritonitis) as the cause of abdominal pain accompanied by fever. Loud “fluid and bubbling” sounds can be heard on abdominal auscultation in some patients with impending colitis. Ultrasound examination can be helpful in delineating enteritis (distended, thickened small intestine with increased motility) from strangulating obstruction (distended small intestine with no motility).</p><p id="p3290">Tachycardia and tachypnea can serve as indicators of abdominal pain, cardiovascular shock, and endotoxemia.</p><p id="p3295">Skin turgor, mucous membrane moisture and color, and CRT can aid in assessment of dehydration resulting from intestinal dysfunction. Mucous membrane moisture and color change from moist and pale pink to dry and red with a decrease in circulating blood volume. With the onset of shock and endotoxemia, mucous membrane color can progress to reddish blue or purple (cyanosis).</p><p id="p3300">Auscultate for intestinal borborygmi in all abdominal quadrants. Pain and inflammation related to the gastrointestinal tract result in decreased borborygmi. Increased borborygmi can be present early with enteritis or colitis, only to progress to ileus and cessation of the sounds as the bowel becomes progressively inflamed and distended. Increased borborygmi are present early in patients with intestinal obstruction, but intestinal sounds decrease as the obstruction becomes complete. Simultaneous auscultation and percussion may reveal high-pitched sounds (pinging) caused by cecal (right flank) or colonic (left flank) tympany. A sound similar to an ocean wave can be heard in some patients with sand impaction; if a sand impaction is suspected, perform auscultation of the rostral-ventral abdomen for 5 minutes listening for the characteristic sound.</p><p id="p3305">Perform nasogastric intubation immediately when a patient demonstrates abdominal pain. Gastric decompression is essential to determine whether gastric distention is present and to provide relief to patients with primary or secondary gastric distention. Nasogastric reflux can be caused by small-intestinal obstruction or secondary ileus from large-intestinal disease. Horses with proximal enteritis characteristically have large volumes of reflux (10 to 20 L). Blood-tinged, foul-smelling reflux fluid may indicate small-intestinal strangulating obstruction or severe proximal enteritis. If small-intestinal obstruction or enteritis is suspected, it is important to leave the tube in place to prevent spontaneous gastric rupture and subsequent death.</p><p id="p3310">A careful rectal examination is mandatory when examining a horse that has abdominal pain. The rectal temperature should be taken before the rectal examination. Before beginning the abdominal palpation per rectum, note the amount and consistency of fecal material in the rectum. Absence of fecal material or the presence of dry, fibrin- and mucus-covered feces is abnormal and suggests delayed intestinal transit. Fetid, watery fecal material often is seen in horses with colitis. Examination should be performed in a consistent, systematic manner to minimize missing a lesion. Intraabdominal structures palpable in a normal horse (<xref rid="f0245" ref-type="fig">Fig. 18-47</xref>), starting in the left cranial abdominal quadrant and progressing clockwise, are subsequently identified.<fig id="f0245"><label>Figure 18-47</label><caption><p>Caudal view of a standing horse shows the abdominal structures palpable in normal patients during rectal examination. Beginning in the left dorsal abdominal quadrant and progressing in a clockwise direction, palpable structures include the caudal border of the spleen, nephrosplenic ligament, caudal pole of the left kidney, small colon containing fecal balls, root of the mesentery, cecal base and ventral taenia, portions of the left ventral and dorsal colon, and the pelvic flexure.</p></caption><graphic xlink:href="f018-047-9781455708925"></graphic></fig></p></sec><sec id="s0505"><title>Palpable Intraabdominal Structures</title><p id="p3315"><list list-type="simple" id="ulist0565"><list-item id="u2545"><label>•</label><p id="p3320">Caudal border of the spleen</p></list-item><list-item id="u2550"><label>•</label><p id="p3325">Nephrosplenic (renosplenic) ligament</p></list-item><list-item id="u2555"><label>•</label><p id="p3330">Caudal pole of the left kidney</p></list-item><list-item id="u2560"><label>•</label><p id="p3335">Mesenteric root</p></list-item><list-item id="u2565"><label>•</label><p id="p3340">Ventral cecal band (no tension)</p></list-item><list-item id="u2570"><label>•</label><p id="p3345">Cecal base (empty)</p></list-item><list-item id="u2575"><label>•</label><p id="p3350">Small colon containing distinct fecal balls</p></list-item><list-item id="u2580"><label>•</label><p id="p3355">Pelvic flexure</p></list-item></list></p><p id="p3360">The small intestine is <italic>not</italic> palpable, except for the infrequent and chance palpation of the ileum in some horses or unless an underlying abnormality exists. Determination of the presence of bowel distention of any form is important in formulating a working diagnosis.</p></sec><sec id="s0510"><title>Abnormal Rectal Examination Findings</title><p id="p3365"><list list-type="simple" id="ulist0570"><list-item id="u2585"><label>•</label><p id="p3370">Cecal distention</p></list-item><list-item id="u2590"><label>•</label><p id="p3375">Gas- or ingesta-distended small intestine (<xref rid="f0250" ref-type="fig">Fig. 18-48</xref>), large colon (<xref rid="f0255" ref-type="fig">Fig. 18-49</xref>), or small colon<fig id="f0250"><label>Figure 18-48</label><caption><p>Caudal view of a standing horse shows severe small intestinal distention. Multiple loops of gas- and fluid-distended small intestine are palpable.</p></caption><graphic xlink:href="f018-048-9781455708925"></graphic></fig><fig id="f0255"><label>Figure 18-49</label><caption><p>Caudal view of a standing horse reveals right dorsal displacement of the large colon. The left ventral and dorsal colons are displaced lateral to the cecum. The colon and associated taenia are palpated immediately cranial to the pelvic canal, coursing from the right caudal abdomen, transversely across the abdomen, and then continuing beyond the examiner's reach toward the left cranial abdomen.</p></caption><graphic xlink:href="f018-049-9781455708925"></graphic></fig></p></list-item><list-item id="u2595"><label>•</label><p id="p3380">Significant intramural or mesenteric edema</p></list-item><list-item id="u2600"><label>•</label><p id="p3385">Bowel malposition (see <xref rid="f0255" ref-type="fig">Fig. 18-49</xref>)</p></list-item><list-item id="u2605"><label>•</label><p id="p3390">Herniation</p></list-item><list-item id="u2610"><label>•</label><p id="p3395">Impaction</p></list-item><list-item id="u2615"><label>•</label><p id="p3400">Intussusception</p></list-item><list-item id="u2620"><label>•</label><p id="p3405">Intraabdominal mass, abscess, or hematoma</p></list-item><list-item id="u2625"><label>•</label><p id="p3410">Enterolithiasis</p></list-item><list-item id="u2630"><label>•</label><p id="p3415">Volvulus of the mesenteric root</p></list-item></list></p><p id="p3420">Always examine the internal inguinal rings, urethra, and bladder (male) and reproductive tract and bladder (female). Sequential rectal examinations are often helpful in determining the rate and severity of disease and the need for surgical intervention.</p></sec></sec><sec id="s0515"><title>Ultrasonography</title><p id="p3425">Ultrasonography is an important component of the examination and is covered in detail in Chapter 14, p. 85).</p></sec><sec id="s0520"><title>Response to Analgesics</title><p id="p3430">The degree of pain demonstrated by a horse with gastrointestinal disease is variable and depends on the characteristic “pain threshold” of the individual horse and the severity of disease present. <italic><bold>Practice Tip:</bold> In general, the greater the pain, the more severe the disease. In the later stages of disease, abdominal pain may be replaced by considerable depression and cardiovascular deterioration as a result of bowel necrosis and systemic endotoxemia.</italic> Pain control is accomplished with gastric decompression through a nasogastric tube and administration of peripherally and centrally acting analgesics (see <xref rid="t0055" ref-type="table">Table 18-9</xref>). Assessment of a patient's response to analgesics is helpful in determining the severity of disease and likelihood of successfully treating the patient with medical management alone. Horses demonstrating unrelenting pain <italic>not</italic> responsive to analgesics require immediate surgical exploration or humane destruction.</p></sec><sec id="s0525"><title>Clinicopathologic Evaluation</title><p id="p3435"><list list-type="simple" id="ulist0575"><list-item id="u2635"><label>•</label><p id="p3440">PCV</p></list-item><list-item id="u2640"><label>•</label><p id="p3445">Total plasma protein (TPP)</p></list-item><list-item id="u2645"><label>•</label><p id="p3450">Complete blood count (CBC)</p></list-item><list-item id="u2650"><label>•</label><p id="p3455">Blood gases</p></list-item><list-item id="u2655"><label>•</label><p id="p3460">Electrolyte determination</p></list-item><list-item id="u2660"><label>•</label><p id="p3465">Lactate</p></list-item></list></p><sec id="s0530"><title>Packed Cell Volume and Total Plasma Protein</title><p id="p3470">Hypovolemia resulting from intestinal dysfunction results in dehydration. The PCV and TPP are the most accurate measurements to support a clinical assessment of dehydration in most patients with abdominal pain.<table-wrap position="float" id="t0050"><table frame="hsides" rules="groups"><thead><tr><th align="left"></th><th align="left">PCV (%)<xref rid="fn0045" ref-type="fn">8</xref></th><th align="left">TPP (g/dL)</th></tr></thead><tbody><tr><td align="left">Mild dehydration</td><td align="center">45-50</td><td align="center">7.5-8.0</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="left">Moderate dehydration</td><td align="center">50-60</td><td align="center">8.0-9.0</td></tr><tr><td colspan="3"><hr></hr></td></tr><tr><td align="left">Severe dehydration</td><td align="center">60</td><td align="center">9.0</td></tr></tbody></table></table-wrap></p><p id="p3475"><italic><bold>Practice Tip:</bold> Significant increases in PCV without corresponding increases or decreases in TPP may indicate protein loss into the intestinal lumen, peritoneal cavity, or sympathetic and endotoxin-induced splenic contraction.</italic></p></sec><sec id="s0535"><title>Complete Blood Count</title><p id="p3480">Most simple or strangulating obstructions do <italic>not</italic> cause a significant change in the white blood cell (WBC) count until the terminal stages of diseases. Acute inflammatory diseases (enteritis, colitis), however, often cause leukopenia (<4000 cells/µL) with a left shift and toxic changes noted in the neutrophils. Significant leukopenia (<1000 cells/µL) also occurs with fulminant septic peritonitis resulting from acute bowel rupture. Mature neutrophilia and high TPP and fibrinogen levels may indicate chronic peritonitis caused by abdominal abscessation.</p></sec><sec id="s0540"><title>Blood Gases</title><p id="p3485">Acidemia may be seen with advanced hypovolemic shock. Evaluation of blood gases is important for appropriate management of severe acid-base abnormalities, especially in patients who need general anesthesia and surgical treatment. Patients with simple colon displacements may have an insignificant base excess, whereas patients with strangulating obstruction usually have an obvious base deficit.</p></sec><sec id="s9015"><title>Lactate</title><p id="p23340">Blood and peritoneal lactate is an important laboratory test in the evaluation and monitoring of the acute abdomen.<list list-type="simple" id="ulist9040"><list-item id="u2675"><label>•</label><p id="p3505">Blood and peritoneal fluid lactate determinations can be performed stall-side.</p></list-item><list-item id="u2680"><label>•</label><p id="p3510">Elevated blood lactate concentration suggests a global decrease in perfusion (hypotension/dehydration) and/or local ischemia or strangulation.</p></list-item><list-item id="u2685"><label>•</label><p id="p3515"><bold><italic>Practice Tip:</italic></bold><italic>The initial value of the blood lactate is</italic> not <italic>as important prognostically as the change in lactate after early treatments; absence of a decline in blood lactate 2 to 4 hours after aggressive treatments, including resuscitation with hypertonic saline and/or polyionic crystalloids, is suggestive of a serious and possibly strangulating condition.</italic></p></list-item><list-item id="u2690"><label>•</label><p id="p3520"><bold><italic>Practice Tip:</italic></bold><italic>More significant elevations in peritoneal fluid in comparison to blood lactate is highly suggestive of a strangulation obstruction.</italic></p></list-item></list></p></sec><sec id="s0545"><title>Electrolytes</title><p id="p3490">Measurement of serum electrolytes rarely is helpful in making a diagnosis. A rare exception is acute abdominal pain caused by hypocalcemia and ileus (synchronous diaphragmatic flutter may be present).<list list-type="simple" id="ulist0580"><list-item id="u2665"><label>•</label><p id="p3495">Electrolyte determinations are vital for appropriate management before, during, and after surgical treatment.<list list-type="simple" id="ulist0585"><list-item id="u2670"><label>•</label><p id="p3500">Hyponatremia and hypochloremia may suggest impending colitis.</p></list-item></list></p></list-item></list></p></sec></sec><sec id="s0550"><title>Abdominocentesis</title><p id="p3525">Abdominocentesis (see <xref rid="u0085" ref-type="list-item">p. 158</xref>) is a useful diagnostic tool for assessment of intestinal compromise. Abdominocentesis is performed with an 18-gauge, sterile hypodermic needle or a blunt cannula (teat cannula or canine female urinary catheter). Collect fluid in a sterile tube containing EDTA for cytologic analysis of the fluid and into a second sterile tube without additives for culture and sensitivity, if indicated. Fluid analysis includes specific gravity and protein determinations and cell types, numbers, and morphology (see <xref rid="t0010" ref-type="table">Table 18-1</xref>). Ultrasonography may be useful in locating peritoneal fluid. Use caution in performing abdominocentesis on foals; needle perforation of the bowel can cause adhesions, and using the teat cannula method can result in herniation of omentum unless performed in the most caudal part of the abdomen.</p><p id="p3530">Normal peritoneal fluid is<list list-type="simple" id="ulist0590"><list-item id="u2695"><label>•</label><p id="p3535">Odorless</p></list-item><list-item id="u2700"><label>•</label><p id="p3540">Nonturbid</p></list-item><list-item id="u2705"><label>•</label><p id="p3545">Clear to pale yellow</p></list-item><list-item id="u2710"><label>•</label><p id="p3550">The nucleated cell count should be less than 3000 to 5000 cells/µL, with a total protein concentration less than 2.5 g/dL.</p></list-item><list-item id="u2715"><label>•</label><p id="p3555">In early, simple obstruction of the small or large intestine, peritoneal fluid typically remains normal.</p></list-item><list-item id="u2720"><label>•</label><p id="p3560">In a strangulating obstruction or severe intestinal inflammation, the peritoneal fluid can become serosanguineous with increases in nucleated cell count and total protein concentration.</p></list-item><list-item id="u2725"><label>•</label><p id="p3565">Dark, turbid fluid with the smell of ingesta, increased nucleated cell counts, and increased protein concentration signifies bowel necrosis and leakage.</p></list-item><list-item id="u2730"><label>•</label><p id="p3570">The presence of plant material and intracellular bacteria indicates bowel rupture (<xref rid="f0260" ref-type="fig">Fig. 18-50</xref>). (If this material has been collected by needle aspiration, it should be repeated with a teat cannula before the diagnosis of ruptured viscus is made.)<fig id="f0260"><label>Figure 18-50</label><caption><p>Peritoneal fluid (×400). Ruptured intestine.</p></caption><graphic xlink:href="f018-050-9781455708925"></graphic></fig></p></list-item><list-item id="u2735"><label>•</label><p id="p3575">The presence of blood-tinged fluid indicates:<list list-type="simple" id="ulist0595"><list-item id="u2740"><label>•</label><p id="p3580">Splenic puncture</p></list-item><list-item id="u2745"><label>•</label><p id="p3585">Intraabdominal hemorrhage</p></list-item><list-item id="u2750"><label>•</label><p id="p3590">Iatrogenic hemorrhage</p></list-item><list-item id="u2755"><label>•</label><p id="p3595">Intestinal necrosis</p></list-item></list></p></list-item></list></p><p id="p3600"><bold><italic>Practice Tip:</italic></bold><italic>With splenic puncture, the PCV of the fluid is greater than the peripheral PCV, and the fluid contains large numbers of small lymphocytes. Fluid from intraabdominal hemorrhage reveals a PCV less than that of peripheral blood, erythrocytophagia, and few to no platelets.</italic></p><p id="p3605"><italic><bold>Important:</bold></italic> The absence of gross or cytologic abnormalities in the peritoneal fluid does <italic>not</italic> exclude the presence of compromised intestine.<list list-type="simple" id="ulist0600"><list-item id="u2760"><label>•</label><p id="p3610">Some strangulating lesions, such as intussusception, external hernia, and epiploic foramen incarceration may <italic>not</italic> demonstrate abnormalities in the peritoneal fluid because of sequestration of the fluid in the omentum, intussuscipiens, or hernial sac.</p></list-item><list-item id="u2765"><label>•</label><p id="p3615">If sand impaction is suspected or if considerable cecal or colonic distention is present, abdominocentesis should be performed only to confirm suspected bowel rupture.</p></list-item></list></p><p id="p3620"><bold><italic>Practice Tip:</italic></bold><italic>If physical examination reveals other findings consistent with a surgical lesion and referral for surgery is considered, abdominocentesis should</italic> not <italic>be performed in the field because of the risk to the patient and the examiner.</italic></p></sec></sec><sec id="s0555"><title>Medical Versus Surgical Management</title><p id="p3625">Considerations in determining the need for exploratory surgery are as follows (<xref rid="b0090" ref-type="boxed-text">Box 18-2</xref>):<list list-type="simple" id="ulist0605"><list-item id="u2770"><label>•</label><p id="p3680">Pain</p></list-item><list-item id="u2775"><label>•</label><p id="p3685">Response to analgesic therapy</p></list-item><list-item id="u2780"><label>•</label><p id="p3690">Cardiovascular status</p></list-item><list-item id="u2785"><label>•</label><p id="p3695">Blood and peritoneal fluid lactate evaluation (see <xref rid="s0540" ref-type="sec">p. 189</xref>)</p></list-item><list-item id="u2790"><label>•</label><p id="p3700">Rectal examination findings</p></list-item><list-item id="u2795"><label>•</label><p id="p3705">Ultrasonographic findings</p></list-item><list-item id="u2800"><label>•</label><p id="p3710">Quantity of gastric reflux</p></list-item><list-item id="u2805"><label>•</label><p id="p3715">Abdominocentesis results</p></list-item></list><boxed-text id="b0090"><label>Box 18-2</label><caption><title>Indications for Exploratory Celiotomy in Horses Demonstrating Acute Abdominal Pain</title></caption><p id="p3630"><list list-type="simple" id="ulist9010"><list-item id="u10935"><p id="p13580">Severe, unrelenting abdominal pain*</p></list-item><list-item id="u10940"><p id="p3635">Pain refractory to analgesics*</p></list-item><list-item id="u10945"><p id="p3640">Abnormal rectal examination<sup>†</sup></p></list-item><list-item id="u10950"><p id="p3645">Abnormal ultrasonographic examination<sup>†</sup></p></list-item><list-item id="u10955"><p id="p3650">Increased heart rate<sup>†</sup></p></list-item><list-item id="u10960"><p id="p3655">Large quantities of gastric reflux<sup>†</sup></p></list-item><list-item id="u10965"><p id="p3660">Absence of borborygmi<sup>†</sup></p></list-item><list-item id="u10970"><p id="p3665">Serosanguineous abdominal fluid with increased protein and nucleated cell count<sup>†</sup></p></list-item></list></p><p id="p3670">*These parameters alone are indications for emergency exploratory celiotomy.</p><p id="p3675"><sup>†</sup>These parameters are NOT sole indications for emergency exploratory celiotomy but must be evaluated in view of other clinical findings.</p></boxed-text></p><p id="p3720">A history of abdominal pain often requires reassessment of these parameters over time. A change in one or more clinical criteria may determine the need for surgical or medical management. <italic><bold>Practice Tip:</bold> Manifestation of pain and the response to analgesic therapy are the most valuable measurements in assessing the need for surgical intervention. Patients demonstrating unrelenting pain or recurrent pain after administration of analgesics are considered surgical candidates.</italic></p><p id="p3725">Rectal examination is the <italic>second</italic> most valuable criterion for surgery. Demonstration of pain concurrent with abnormal rectal examination findings is a strong indicator. Failure of medical therapy, abnormalities identified during ultrasound examination of the abdomen, systemic cardiovascular deterioration, increases in blood lactate or peritoneal fluid lactate higher than blood lactate and/or changes in peritoneal fluid (color, protein, etc.) results supporting intestinal degeneration are additional justification for surgical intervention.<boxed-text id="b0095"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0560"><title>Medical Versus Surgical Management—Acute Abdomen</title><p id="p3730">Treatment of horses demonstrating acute abdominal pain is directed at the following:<list list-type="simple" id="ulist0610"><list-item id="u2810"><label>•</label><p id="p3735">Pain relief</p></list-item><list-item id="u2815"><label>•</label><p id="p3740">Stabilization of cardiovascular and metabolic status</p></list-item><list-item id="u2820"><label>•</label><p id="p3745">Minimizing the deleterious effects of endotoxemia</p></list-item><list-item id="u2825"><label>•</label><p id="p3750">Establishing a patent and functional intestine. This can be accomplished with one or more of the following therapeutic modalities:<list list-type="simple" id="ulist0615"><list-item id="u2830"><label>•</label><p id="p3755">Analgesic therapy (see <xref rid="t0055" ref-type="table">Table 18-9</xref>)</p></list-item><list-item id="u2835"><label>•</label><p id="p3760">Fluid therapy and cardiovascular support</p></list-item><list-item id="u2840"><label>•</label><p id="p3765">Laxatives and cathartics</p></list-item><list-item id="u2845"><label>•</label><p id="p3770">Antiendotoxin therapy</p></list-item><list-item id="u2850"><label>•</label><p id="p3775">Therapy for ischemia-reperfusion injury</p></list-item><list-item id="u2855"><label>•</label><p id="p3780">Antimicrobial therapy</p></list-item><list-item id="u2860"><label>•</label><p id="p3785">Nutritional support</p></list-item><list-item id="u2865"><label>•</label><p id="p3790">Surgical intervention</p></list-item></list></p></list-item></list></p></sec></boxed-text></p><sec id="s0565"><title>Analgesic Therapy</title><p id="p3795">Pain relief is accomplished by means of gastric decompression with a nasogastric tube and administration of peripherally and centrally acting analgesics (see <xref rid="t0055" ref-type="table">Table 18-9</xref>). Perform gastric decompression (see <xref rid="s0010" ref-type="sec">p. 157</xref>) q2h using an indwelling nasogastric tube; it may be necessary to repeat up to q2h to prevent distention, which can potentially lead to pain, gastric rupture, and death. Patients being referred for possible exploratory surgery should have an indwelling nasogastric tube in place during transport to the referral facility if there has been a need for repeated gastric decompression.</p></sec><sec id="s0570"><title>Fluid Therapy and Cardiovascular Support</title><p id="p3800">Intravenous administration of polyionic, balanced electrolyte solutions is necessary to maintain intravascular fluid volume. Administration of colloid solutions such as hydroxyethyl starch (6% Hetastarch,<xref rid="fn0050" ref-type="fn">9</xref> 5 to 10 mL/kg IV) improves systemic blood pressure and cardiac output. Hypertonic saline solution is the ideal resuscitation crystalloid but <italic>must</italic> be followed by adequate fluid replacement with balanced crystalloid solutions (ideally within 1 hour after administration of the hypertonic solution). <italic><bold>Practice Tip:</bold> The ratio of crystalloid to colloid solution (ratio of saline to 7% hypertonic) should be 10 : 1 (10 L saline or other crystalloid to 1 L of hypertonic saline).</italic> Monitor hydration status with clinical assessment and measurement of PCV and TPP. Monitor blood gas and serum electrolyte values, and adjust the intravenous solutions to correct the deficits.</p><p id="p3805">If the plasma protein concentration is <4.5 g/dL and the patient is dehydrated, administer plasma (2 to 10 L IV slowly), 25% human albumin, or a synthetic colloid (Hetastarch or VetStarch/Abbott Labs, up to 10 mL/kg) to maintain plasma oncotic pressure and avoid inducing pulmonary edema during rehydration with intravenous fluids.</p></sec><sec id="s0575"><title>Laxatives</title><p id="p3810">Laxatives are used to increase gastrointestinal water content, soften ingesta, facilitate intestinal transit, and manage impaction of the cecum and large and small colons. For maximal effect, oral and intravenous fluids should be administered concurrently. Do <italic>not</italic> administer laxatives orally to patients with nasogastric reflux.</p><sec id="s0580"><title>Commonly Used Laxatives</title><p id="p3815"><list list-type="simple" id="ulist0620"><list-item id="u2870"><label>•</label><p id="p3820">Mineral oil (6 to 8 L/500 kg body mass) can be administered to facilitate manure passage after the impaction begins to resolve; however, mineral oil is <italic>not</italic> useful for penetrating or hydrating the primary impaction.</p></list-item><list-item id="u2875"><label>•</label><p id="p3825">Magnesium sulfate (Epsom salts, 500 g diluted in warm water per 500 kg body mass, daily). <italic>Do not</italic> use for longer than 3 days or to treat patients with decreased renal function in order to avoid enteritis and possible magnesium intoxication. Its use is preferred for large-colon impactions.</p></list-item><list-item id="u2880"><label>•</label><p id="p3830">Psyllium hydrophilic mucilloid (Metamucil, 400 g/500 kg body mass q6-12h) until the impaction resolves. Especially useful for sand impaction.</p></list-item><list-item id="u11080"><label>•</label><p id="p13445"><italic><bold>Practice Tip:</bold> Mixing psyllium with water makes a thick paste that clogs the pump and tube. Alternatively, mix psyllium with mineral oil for easier administration.</italic></p></list-item><list-item id="u2885"><label>•</label><p id="p3835">Dioctyl sodium sulfosuccinate (DSS, 10 to 20 mg/kg up to 2 doses, 48 hours apart). Can cause mild abdominal pain and diarrhea.</p></list-item></list></p></sec></sec><sec id="s0585"><title>Antiendotoxin Therapy</title><p id="p3840">Antiserum (500 to 1000 mL) directed against the gram-negative core antigens of endotoxin<xref rid="fn0055" ref-type="fn">10</xref> can be administered intravenously diluted in balanced electrolyte solution. Endoserum should be slowly warmed to room temperature and administered slowly to avoid undesirable side effects, such as tachycardia and muscle fasciculations. Hyperimmune plasma,<xref rid="fn0060" ref-type="fn">11</xref> directed against the J-5 mutant strain of <italic>Escherichia coli,</italic> or normal equine plasma (2 to 10 L), administered intravenously slowly, can be equally as or more beneficial, supplying protein, fibronectin, complement, antithrombin III, and other inhibitors of hypercoagulability. Polymyxin B,<xref rid="fn0065" ref-type="fn">12</xref> 2000 to 6000 IU/kg IV q12h for 24 to 48 hours, binds and neutralizes circulating endotoxin and may be beneficial in the management of systemic endotoxemia.</p><p id="p13450">Pentoxifylline (Trental) is used to treat endotoxemia, 7.5 to 10 mg/kg PO, IV, q8-12h.</p></sec><sec id="s0590"><title>Therapy for Ischemia-Reperfusion Injury</title><p id="p3845">If ischemia is suspected, dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, can be administered intravenously (100 mg/kg q8-12h) diluted to a 10% solution in a balanced electrolyte solution. Efficacy has not been verified. Kinetic studies support use every 12 hours at the anti-inflammatory dose.</p><p id="p3850">Lidocaine infusion (1.3 mg/kg bolus followed by 0.05 mg/kg/min) has been shown to reduce bowel mucosal injury from repercussion injury when the lidocaine was given before the experimental injury occurred.</p></sec><sec id="s0595"><title>Antimicrobials</title><p id="p3855"><list list-type="simple" id="ulist0625"><list-item id="u2890"><label>•</label><p id="p3860">Antimicrobial agents are not administered routinely to patients that demonstrate acute abdominal pain unless an underlying infectious agent is suspected. Broad-spectrum antimicrobials may be indicated if the patient has sepsis and neutropenia (<2000 cells/µL) to minimize bacteremia and organ colonization by enteric organisms and if the patient is undergoing exploratory celiotomy.</p></list-item><list-item id="u2895"><label>•</label><p id="p3865">Penicillin (22,000 to 44,000 IU/kg IV q6h or IM q12h) and metronidazole (30 mg/kg per rectum q8h or 15 mg/kg IV q8-12h) often is administered to patients with duodenitis or proximal jejunitis. The suspected targeted agent is <italic>Clostridium perfringens</italic> type A.</p></list-item></list></p></sec><sec id="s0600"><title>Nutritional Support</title><p id="p3870">See Chapter 51, p. 768.</p><p id="p3875">Horses demonstrating abdominal pain should have hay and grain withheld for at least 12 to 18 hours. If they <italic>do not</italic> have gastric reflux, they should be allowed free-choice water and should have access to trace mineral salt. A patient that responds to initial medical treatment should be returned gradually to a normal diet over 24 to 48 hours (moist bran and alfalfa pellet mash, grazing grass, hay, then grain). Patients being referred for possible exploratory surgery should <italic>not</italic> be fed during transport to the referral facility.</p></sec><sec id="s0605"><title>Surgical Intervention</title><p id="p3880">Candidates for exploratory celiotomy (see <xref rid="b0090" ref-type="boxed-text">Box 18-2</xref>) have the following signs:<list list-type="simple" id="ulist0630"><list-item id="u2900"><label>•</label><p id="p3885">Unrelenting pain</p></list-item><list-item id="u2905"><label>•</label><p id="p3890">Recurrent pain after administration of analgesics</p></list-item><list-item id="u2910"><label>•</label><p id="p3895">Palpable abnormalities detected on rectal examination</p></list-item><list-item id="u2915"><label>•</label><p id="p3900">Ultrasonographic findings demonstrating an obstructive pattern or intussusception</p></list-item><list-item id="u2920"><label>•</label><p id="p3905">Systemic cardiovascular deterioration</p></list-item><list-item id="u2925"><label>•</label><p id="p3910">Changes in peritoneal fluid results indicating intestinal degeneration</p></list-item><list-item id="u2930"><label>•</label><p id="p3915">Failure of medical therapy</p></list-item></list>Ventral midline celiotomy is the surgical approach of choice. Specific treatments are discussed with each gastrointestinal disorder.</p></sec></sec></sec></sec></sec><sec id="s0610"><title>Lower Gastrointestinal Emergencies</title><p id="p3920">For gastric diseases causing colic, see <xref rid="s0355" ref-type="sec">p. 181</xref>.</p><sec id="s0615"><title>Disorders of the Small Intestine</title><sec id="s0620"><title>Intussusception</title><p id="p3925">Small-intestinal intussusception usually occurs in younger horses and involves an invagination of a segment of intestine <italic>(intussusceptum)</italic> and mesentery into the lumen of an adjacent distal segment of intestine <italic>(intussuscipiens).</italic> Continued peristalsis draws more intestine and its mesentery into the intussuscipiens, causing venous congestion, edema, infarction, and necrosis of the involved segment. Small-intestinal obstruction and strangulation result. Intussusception results from alterations in intestinal motility.</p><sec id="s0625"><title>Predisposing Factors</title><p id="p3930"><list list-type="simple" id="ulist0635"><list-item id="u2935"><label>•</label><p id="p3935">Enteritis, especially foals</p></list-item><list-item id="u2940"><label>•</label><p id="p3940">Maladjustment of septic foals in intensive care units</p></list-item><list-item id="u2945"><label>•</label><p id="p3945">Abrupt dietary changes</p></list-item><list-item id="u2950"><label>•</label><p id="p3950">Heavy ascarid <italic>(Parascaris equorum)</italic> or tapeworm <italic>(Anoplocephala perfoliata)</italic> infestation</p></list-item><list-item id="u2955"><label>•</label><p id="p3955">Anthelmintic treatment</p></list-item><list-item id="u2960"><label>•</label><p id="p3960">Intestinal anastomosis</p></list-item><list-item id="u2965"><label>•</label><p id="p3965">In most cases, <italic>no</italic> specific factor is identified.</p></list-item><list-item id="u2970"><label>•</label><p id="p3970"><italic><bold>Practice Tip:</bold> Jejunojejunal and jejunoileal intussusception are more common in foals, whereas ileocecal intussusception is more common in adults.</italic></p></list-item></list></p></sec><sec id="s0630"><title>Diagnosis</title><p id="p3975"><list list-type="simple" id="ulist0640"><list-item id="u2975"><label>•</label><p id="p3980">Clinical signs of jejunojejunal and ileocecal intussusception vary with the degree and duration of the condition.</p></list-item><list-item id="u2980"><label>•</label><p id="p3985">Most commonly, intussusception leads to complete intestinal obstruction and strangulation of the intussusceptum, causing an acute onset of unrelenting abdominal pain, although it may rarely be a cause of a more chronic colic.</p></list-item><list-item id="u2985"><label>•</label><p id="p3990">Nasogastric reflux develops, and progressive dehydration and hypovolemia rapidly follow.</p></list-item><list-item id="u2990"><label>•</label><p id="p3995">Rectal examination reveals loops of distended small intestine, and occasionally the intussusception can be palpated. With ileocecal intussusception, a turgid segment of bowel may be palpable within the cecum.</p></list-item><list-item id="u2995"><label>•</label><p id="p4000">Increased peritoneal protein concentration and nucleated cell count reflect devitalization of the affected bowel. Changes in the peritoneal fluid, however, may not accurately reflect the degree of intestinal compromise because of isolation of the devitalized intussusceptum within the intussuscipiens (see <xref rid="s0055" ref-type="sec">p. 159</xref>).</p></list-item><list-item id="u3000"><label>•</label><p id="p4005">In foals, jejunal intussusception is usually identified with ultrasound.</p></list-item><list-item id="u3005"><label>•</label><p id="p4010">Chronic ileocecal intussusception with partial obstruction causes the following:<list list-type="simple" id="ulist0645"><list-item id="u3010"><label>•</label><p id="p4015">Intermittent or continuous abdominal pain</p></list-item><list-item id="u3015"><label>•</label><p id="p4020">Weight loss</p></list-item><list-item id="u3020"><label>•</label><p id="p4025">Poor general physical condition</p></list-item><list-item id="u3025"><label>•</label><p id="p4030">Varying degrees of anorexia</p></list-item><list-item id="u3030"><label>•</label><p id="p4035">Depression</p></list-item></list></p></list-item><list-item id="u3035"><label>•</label><p id="p4040">Chronic ileocecal intussusception can continue for weeks to months and eventually leads to an acute episode of severe abdominal pain compatible with a complete obstruction of the intestine.</p></list-item></list><boxed-text id="b0100"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0635"><title>Intussusception</title><sec id="s0640"><title>Initial Therapy Is Supportive</title><p id="p4045"><list list-type="simple" id="ulist0650"><list-item id="u3040"><label>•</label><p id="p4050">Gastric decompression</p></list-item><list-item id="u3045"><label>•</label><p id="p4055">Balanced polyionic intravenous fluids, such as lactated Ringer's solution</p></list-item><list-item id="u3050"><label>•</label><p id="p4060">Analgesics such as xylazine, butorphanol tartrate, or flunixin meglumine</p></list-item><list-item id="u3055"><label>•</label><p id="p4065">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0655"><list-item id="u3060"><label>•</label><p id="p4070">Pain</p></list-item><list-item id="u3065"><label>•</label><p id="p4075">Nasogastric reflux</p></list-item><list-item id="u3070"><label>•</label><p id="p4080">Heart rate</p></list-item><list-item id="u3075"><label>•</label><p id="p4085">Mucous membranes</p></list-item><list-item id="u3080"><label>•</label><p id="p4090">Hematocrit, PCV/TPP</p></list-item><list-item id="u3085"><label>•</label><p id="p4095">Borborygmi</p></list-item></list></p></list-item><list-item id="u3090"><label>•</label><p id="p4100">Surgical exploration is indicated if intussusception is suspected.</p></list-item></list></p></sec><sec id="s0645"><title>Exploratory Surgery</title><p id="p4105"><list list-type="simple" id="ulist0660"><list-item id="u3095"><label>•</label><p id="p4110">Ventral midline exploratory celiotomy</p></list-item><list-item id="u3100"><label>•</label><p id="p4115">Manual reduction of the intussusception</p></list-item><list-item id="u3105"><label>•</label><p id="p4120">Resection and anastomosis of the affected intestine</p></list-item></list></p><p id="p4125">Some intussusceptions <italic>cannot</italic> be reduced because of the length of bowel involved, venous congestion, and edema. These cases require en bloc resection and anastomosis. Even if the intestinal segment appears viable, consider resection and anastomosis because of the possibility of mucosal necrosis, serosal inflammation, and postoperative adhesion formation.</p></sec></sec></boxed-text></p></sec><sec id="s0650"><title>Prognosis</title><p id="p4130">Prognosis is good with early diagnosis and surgical repair but poor if the intussusception is advanced and irreducible because of the likelihood of ileus, peritonitis, and postoperative adhesion formation.</p></sec></sec><sec id="s0655"><title>Volvulus</title><p id="p4135"><list list-type="simple" id="ulist0665"><list-item id="u3110"><label>•</label><p id="p4140">Volvulus is the rotation of a segment of intestine around the long axis of its mesentery.</p></list-item><list-item id="u3115"><label>•</label><p id="p4145">Although most cases are <italic>not</italic> accompanied by a predisposing lesion, the following can lead to volvulus:<list list-type="simple" id="ulist0670"><list-item id="u3120"><label>•</label><p id="p4150">Adhesions</p></list-item><list-item id="u3125"><label>•</label><p id="p4155">Infarction</p></list-item><list-item id="u3130"><label>•</label><p id="p4160">Intestinal incarceration</p></list-item><list-item id="u3135"><label>•</label><p id="p4165">Pedunculated lipoma</p></list-item><list-item id="u3140"><label>•</label><p id="p4170">Mesodiverticular bands</p></list-item></list></p></list-item><list-item id="u3145"><label>•</label><p id="p4175">Abrupt dietary changes and verminous arteritis also have been implicated.</p></list-item><list-item id="u3150"><label>•</label><p id="p4180">The length and segment of the intestine involved are variable.</p></list-item><list-item id="u3155"><label>•</label><p id="p4185">The ileum is frequently included because of its fixed attachment at the ileocecal junction.</p></list-item></list></p><sec id="s0660"><title>Diagnosis</title><p id="p4190"><list list-type="simple" id="ulist0675"><list-item id="u3160"><label>•</label><p id="p4195">Acute onset of progressive, moderate to severe, continuous pain that may initially respond to analgesics.</p></list-item><list-item id="u3165"><label>•</label><p id="p4200">Analgesic efficacy rapidly decreases as the disease progresses.</p></list-item><list-item id="u3170"><label>•</label><p id="p4205">Rapid, progressive cardiovascular deterioration occurs as evidenced by poor peripheral perfusion (rapid, weak pulse; hyperemic or cyanotic mucous membranes; and a prolonged CRT).</p></list-item><list-item id="u3175"><label>•</label><p id="p4210">Hypovolemia and hemoconcentration develop rapidly.</p></list-item><list-item id="u3180"><label>•</label><p id="p4215">Nasogastric reflux often is present, but decompression may <italic>not</italic> provide pain relief as it does in simple obstruction.</p></list-item><list-item id="u3185"><label>•</label><p id="p4220">Rectal examination usually reveals moderate to severe small-intestinal distention (see <xref rid="f0250" ref-type="fig">Fig. 18-48</xref>) and occasionally a tight mesenteric root. Placing mild tension on the mesentery may elicit a pain response.</p></list-item><list-item id="u3190"><label>•</label><p id="p4225">Lack of palpable small-intestinal distention does not rule out the possibility of a strangulating lesion because the distended intestine may be beyond the reach of the examining arm.</p></list-item><list-item id="u3195"><label>•</label><p id="p4230">Abdominal ultrasonography reveals dilated, nonmotile small intestine.</p></list-item><list-item id="u3200"><label>•</label><p id="p4235">Abdominocentesis may yield normal or serosanguineous fluid with increased peritoneal protein concentration (>3.0 g/dL) and nucleated cell count (>5000 cells/µL). The devitalized portion of intestine may be isolated from the peritoneal cavity (e.g., a volvulus within the omental bursa), and results of peritoneal fluid analysis therefore may not accurately reflect the degree of intestinal change.</p></list-item><list-item id="u3205"><label>•</label><p id="p4240">Peritoneal fluid lactate is elevated, often higher than blood lactate. Serial sampling of peritoneal lactate demonstrates increased lactate concentrations over time.</p></list-item></list><boxed-text id="b0105"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0665"><title>Volvulus</title><sec id="s0670"><title>Initial Therapy Is Supportive</title><p id="p4245"><list list-type="simple" id="ulist0680"><list-item id="u3210"><label>•</label><p id="p4250">Gastric decompression</p></list-item><list-item id="u3215"><label>•</label><p id="p4255">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution) with plasma</p></list-item><list-item id="u3220"><label>•</label><p id="p4260">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u3225"><label>•</label><p id="p4265">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0685"><list-item id="u3230"><label>•</label><p id="p4270">Pain</p></list-item><list-item id="u3235"><label>•</label><p id="p4275">Nasogastric reflux</p></list-item><list-item id="u3240"><label>•</label><p id="p4280">Heart rate</p></list-item><list-item id="u3245"><label>•</label><p id="p4285">Mucous membranes</p></list-item><list-item id="u3250"><label>•</label><p id="p4290">Hematocrit, PCV/TPP</p></list-item><list-item id="u3255"><label>•</label><p id="p4295">Borborygmi</p></list-item></list></p></list-item><list-item id="u3260"><label>•</label><p id="p4300">Surgical exploration if volvulus is suspected</p></list-item></list></p></sec><sec id="s0675"><title>Exploratory Surgery</title><p id="p4305"><list list-type="simple" id="ulist0690"><list-item id="u3265"><label>•</label><p id="p4310">Perform a ventral midline exploratory celiotomy.</p></list-item><list-item id="u3270"><label>•</label><p id="p4315">Identify the strangulated portion of intestine.</p></list-item><list-item id="u3275"><label>•</label><p id="p4320">Determine the direction of rotation of the affected segment by means of palpation of the mesentery.</p></list-item><list-item id="u3280"><label>•</label><p id="p4325">After correction, evaluate intestinal viability and perform resection and anastomosis if needed.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s0680"><title>Prognosis</title><p id="p4330"><list list-type="simple" id="ulist0695"><list-item id="u3285"><label>•</label><p id="p4335">Prognosis depends on the duration of illness and amount of intestine involved in the volvulus.</p></list-item><list-item id="u3290"><label>•</label><p id="p4340">Prognosis is good with early detection and rapid treatment.</p></list-item><list-item id="u3295"><label>•</label><p id="p4345">For patients with long-standing strangulation, postoperative peritonitis, ileus, and adhesion formation are common sequelae.</p></list-item><list-item id="u3300"><label>•</label><p id="p4350"><italic><bold>Practice Tip:</bold> When resection of more than 50% of the small intestine is needed, there is a high incidence of postoperative complications (malabsorption, weight loss, and liver damage).</italic></p></list-item></list></p></sec></sec><sec id="s0685"><title>Herniation</title><p id="p4355"><list list-type="simple" id="ulist0700"><list-item id="u3305"><label>•</label><p id="p4360">Herniation of the small intestine is classified as:<list list-type="simple" id="ulist0705"><list-item id="u3310"><label>•</label><p id="p4365">Internal</p></list-item><list-item id="u3315"><label>•</label><p id="p4370">External</p></list-item></list></p></list-item><list-item id="u3320"><label>•</label><p id="p4375">Internal hernias occur within the abdominal cavity and do <italic>not</italic> involve a hernial sac. Examples are:<list list-type="simple" id="ulist0710"><list-item id="u3325"><label>•</label><p id="p4380">Displacement of the small intestine through the epiploic foramen</p></list-item><list-item id="u3330"><label>•</label><p id="p4385">Mesenteric defects</p></list-item><list-item id="u3335"><label>•</label><p id="p4390">Rents in the gastrosplenic and broad ligaments</p></list-item></list></p></list-item><list-item id="u3340"><label>•</label><p id="p4395">External hernias extend outside the limits of the abdominal cavity and include:<list list-type="simple" id="ulist0715"><list-item id="u3345"><label>•</label><p id="p4400">Inguinal</p></list-item><list-item id="u3350"><label>•</label><p id="p4405">Umbilical</p></list-item><list-item id="u3355"><label>•</label><p id="p4410">Ventral abdominal</p></list-item><list-item id="u3360"><label>•</label><p id="p4415">Diaphragmatic</p></list-item></list></p></list-item></list></p></sec><sec id="s0690"><title>Epiploic Foramen Herniation</title><p id="p4420"><list list-type="simple" id="ulist0720"><list-item id="u3365"><label>•</label><p id="p4425">The epiploic foramen is a potential opening, approximately 4 to 6 cm in length, separating the omental bursa from the peritoneal cavity.</p></list-item><list-item id="u3370"><label>•</label><p id="p4430">The foramen is bounded dorsally by the caudate lobe of the liver and caudal vena cava and ventrally by the right lobe of the pancreas and the portal vein.</p></list-item><list-item id="u3375"><label>•</label><p id="p4435">The epiploic foramen is limited cranially by the hepatoduodenal ligament and caudally by the junction of the pancreas and mesoduodenum.</p></list-item><list-item id="u3380"><label>•</label><p id="p4440"><italic><bold>Practice Tip:</bold> Adults (older than 8 years) may be predisposed to epiploic foramen entrapment because of enlargement of this space caused by atrophy of the right caudate lobe of the liver.</italic></p></list-item><list-item id="u3385"><label>•</label><p id="p4445">Aerophagia (wind sucking) has also been associated with a predisposition to herniation through the epiploic foramen.</p></list-item><list-item id="u3390"><label>•</label><p id="p4450">Herniation through the foramen occurs more commonly from left-to-right (from the medial side) displacement but may also occur from right-to-left (from the lateral side) displacement.</p></list-item><list-item id="u3395"><label>•</label><p id="p4455">Gastrosplenic ligament herniation may appear clinically similar to epiploic herniation.</p></list-item></list></p><sec id="s0695"><title>Diagnosis</title><p id="p4460"><list list-type="simple" id="ulist0725"><list-item id="u3400"><label>•</label><p id="p4465">Acute onset of moderate to severe pain that may initially be responsive to analgesics.</p></list-item><list-item id="u3405"><label>•</label><p id="p4470">The effectiveness of analgesics decreases as the disease progresses.</p></list-item><list-item id="u3410"><label>•</label><p id="p4475">Rapid cardiovascular deterioration occurs, with hypovolemia and hemoconcentration.</p></list-item><list-item id="u3415"><label>•</label><p id="p4480">Nasogastric reflux is usually present, but decompression may not provide pain relief.</p></list-item><list-item id="u3420"><label>•</label><p id="p4485">Rectal examination reveals moderate to severe small-intestinal distention (see <xref rid="f0250" ref-type="fig">Fig. 18-48</xref>) in most cases.</p></list-item><list-item id="u3425"><label>•</label><p id="p4490">Some horses may have mild signs of pain with no nasogastric reflux or palpable intestinal distention. The lack of palpable small-intestinal distention does <italic>not</italic> rule out a strangulating lesion because the distended intestine may be beyond the reach of the examiner.</p></list-item><list-item id="u3430"><label>•</label><p id="p4495">Ultrasonography generally reveals distended nonmotile small intestine.</p></list-item><list-item id="u3435"><label>•</label><p id="p4500">Abdominocentesis is useful in determining the severity of the lesion and the need for surgical intervention.</p></list-item><list-item id="u3440"><label>•</label><p id="p4505">Peritoneal fluid analysis may reveal normal or serosanguineous fluid with increased protein concentration (>3.0 g/dL) and nucleated cell count (>5000 cells/µL). Lactate is increased in peritoneal fluid but may be within normal range in plasma on rare occasion. The devitalized portion of intestine within the omental bursa may be isolated from the rest of the peritoneal cavity. Therefore, fluid obtained at abdominocentesis may <italic>not</italic> accurately reflect the severity of intestinal compromise.</p></list-item></list><boxed-text id="b0110"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0700"><title>Epiploic Foramen Herniation</title><sec id="s0705"><title>Initial Therapy Is Supportive</title><p id="p4510"><list list-type="simple" id="ulist0730"><list-item id="u3445"><label>•</label><p id="p4515">Gastric decompression</p></list-item><list-item id="u3450"><label>•</label><p id="p4520">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution)</p></list-item><list-item id="u3455"><label>•</label><p id="p4525">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u3460"><label>•</label><p id="p4530">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0735"><list-item id="u3465"><label>•</label><p id="p4535">Pain</p></list-item><list-item id="u3470"><label>•</label><p id="p4540">Nasogastric reflux</p></list-item><list-item id="u3475"><label>•</label><p id="p4545">Heart rate</p></list-item><list-item id="u3480"><label>•</label><p id="p4550">Mucous membranes</p></list-item><list-item id="u3485"><label>•</label><p id="p4555">Hematocrit, PCV/TPP</p></list-item><list-item id="u3490"><label>•</label><p id="p4560">Borborygmi</p></list-item></list></p></list-item><list-item id="u3495"><label>•</label><p id="p4565">Surgical intervention if epiploic entrapment is suspected</p></list-item></list></p></sec><sec id="s0710"><title>Exploratory Surgery</title><p id="p4570"><list list-type="simple" id="ulist0740"><list-item id="u3500"><label>•</label><p id="p4575">Surgery frequently is needed to confirm the diagnosis.</p></list-item><list-item id="u3505"><label>•</label><p id="p4580">Perform a ventral midline exploratory celiotomy.</p></list-item><list-item id="u3510"><label>•</label><p id="p4585">Perform decompression of the bowel, careful manual dilation of the foramen, and reduction of the hernia.</p></list-item><list-item id="u3515"><label>•</label><p id="p4590"><italic><bold>Important Note:</bold></italic> Traumatic dilation of the foramen can result in life-threatening rupture of the caudal vena cava or portal vein.</p></list-item><list-item id="u3520"><label>•</label><p id="p4595">Evaluate intestinal viability, and perform resection and anastomosis if necessary.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s0715"><title>Prognosis</title><p id="p4600">Prognosis depends on the duration of illness, the length of intestine requiring resection, and difficulty encountered reducing the hernia.</p></sec></sec><sec id="s0720"><title>Gastrosplenic Ligament Incarceration</title><p id="p4605"><list list-type="simple" id="ulist0745"><list-item id="u3525"><label>•</label><p id="p4610">Incarceration of the small intestine through the gastrosplenic ligament is uncommon.</p></list-item><list-item id="u3530"><label>•</label><p id="p4615">Anatomically, the ligament attaches the greater curvature of the stomach to the hilum of the spleen and continues ventrally with the greater omentum.</p></list-item><list-item id="u3535"><label>•</label><p id="p4620">Defects in the ligament are generally acquired as the result of trauma.</p></list-item><list-item id="u3540"><label>•</label><p id="p4625">The distal jejunum is most commonly involved, with herniation occurring in a caudal to cranial direction.</p></list-item></list></p><sec id="s0725"><title>Diagnosis</title><p id="p4630">Clinical signs are similar to those of epiploic foramen herniation:<list list-type="simple" id="ulist0750"><list-item id="u3545"><label>•</label><p id="p4635">Acute onset of severe abdominal pain, nasogastric reflux, small-intestinal distention on rectal examination, and rapid systemic deterioration occur.</p></list-item><list-item id="u3550"><label>•</label><p id="p4640">Distended small intestine may <italic>not</italic> be palpable early in the disease because of the cranial location in the abdomen.</p></list-item><list-item id="u3555"><label>•</label><p id="p4645">Abdominal ultrasonography generally reveals distended nonmotile small intestine in the left cranial abdomen, between the spleen and left body wall.</p></list-item><list-item id="u3560"><label>•</label><p id="p4650">Abdominocentesis may yield normal to serosanguineous fluid with an increased total protein and nucleated cell count. The severity of the signs depends on the location, duration, and extent of the lesion.</p></list-item><list-item id="u3565"><label>•</label><p id="p4655">Exploratory celiotomy is frequently needed for a definitive diagnosis.</p></list-item></list><boxed-text id="b0115"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0730"><title>Gastrosplenic Ligament Incarceration</title><sec id="s0735"><title>Initial Therapy Is Supportive</title><p id="p4660"><list list-type="simple" id="ulist0755"><list-item id="u3570"><label>•</label><p id="p4665">Gastric decompression</p></list-item><list-item id="u3575"><label>•</label><p id="p4670">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution)</p></list-item><list-item id="u3580"><label>•</label><p id="p4675">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u3585"><label>•</label><p id="p4680">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0760"><list-item id="u3590"><label>•</label><p id="p4685">Pain</p></list-item><list-item id="u3595"><label>•</label><p id="p4690">Nasogastric reflux</p></list-item><list-item id="u3600"><label>•</label><p id="p4695">Heart rate</p></list-item><list-item id="u3605"><label>•</label><p id="p4700">Mucous membranes</p></list-item><list-item id="u3610"><label>•</label><p id="p4705">Hematocrit, PCV/TPP</p></list-item><list-item id="u3615"><label>•</label><p id="p4710">Borborygmi</p></list-item></list></p></list-item><list-item id="u3620"><label>•</label><p id="p4715">Surgical intervention if strangulating obstruction is suspected</p></list-item></list></p></sec><sec id="s0740"><title>Exploratory Surgery</title><p id="p4720"><list list-type="simple" id="ulist0765"><list-item id="u3625"><label>•</label><p id="p4725">Perform a ventral midline exploratory celiotomy.</p></list-item><list-item id="u3630"><label>•</label><p id="p4730">Reduce the hernia.</p></list-item><list-item id="u3635"><label>•</label><p id="p4735">The ligament is relatively avascular, and digital enlargement of the rent facilitates reduction of the incarceration with minimal risk of life-threatening bleeding.</p></list-item><list-item id="u3640"><label>•</label><p id="p4740">Resection and anastomosis of devitalized bowel is performed.</p></list-item><list-item id="u3645"><label>•</label><p id="p4745">The defect in the ligament is <italic>not</italic> closed.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s0745"><title>Prognosis</title><p id="p4750">Prognosis depends on the duration of illness and length of intestine resected.</p></sec></sec><sec id="s0750"><title>Mesenteric Defects</title><p id="p4755"><list list-type="simple" id="ulist0770"><list-item id="u3650"><label>•</label><p id="p4760">Defects or rents in the <italic>mesentery, broad ligaments, or greater omentum</italic> produce a potential space for intestinal incarceration or strangulation.</p></list-item><list-item id="u3655"><label>•</label><p id="p4765">Mesenteric defects most often occur in the small-intestinal mesentery (<xref rid="f0265" ref-type="fig">Fig. 18-51</xref>), and less commonly, in the large and small colon mesentery.<fig id="f0265"><label>Figure 18-51</label><caption><p><bold>A,</bold> Intraabdominal view of a loop of jejunum passing through a mesenteric rent. <bold>B,</bold> Strangulation of the loop of small intestine occurs as the thicker-walled ileum becomes lodged in the mesenteric rent, thereby impairing blood flow in the affected intestine.</p></caption><graphic xlink:href="f018-051ab-9781455708925"></graphic></fig></p></list-item><list-item id="u3660"><label>•</label><p id="p4770">Defects commonly are acquired as a result of blunt abdominal trauma or surgical manipulation of bowel and mesentery. A segment of intestine may pass through the defect and become incarcerated or strangulated.</p></list-item><list-item id="u3665"><label>•</label><p id="p4775">A mesodiverticular band, a congenital remnant of a vitelline artery and its associated mesentery, extends from one side of the mesentery to the antimesenteric border of the jejunum or ileum and is a common site of incarceration. This tissue normally atrophies during the first trimester. Failure to atrophy results in formation of a triangulated mesenteric sac. A loop of intestine can become incarcerated in the sac; the result is mesenteric rupture, herniation, and strangulation.</p></list-item></list></p><sec id="s0755"><title>Diagnosis</title><p id="p4780">Clinical signs are similar to those of volvulus:<list list-type="simple" id="ulist0775"><list-item id="u3670"><label>•</label><p id="p4785">Acute onset of abdominal pain.</p></list-item><list-item id="u3675"><label>•</label><p id="p4790">Nasogastric reflux with small-intestinal distention on rectal examination.</p></list-item><list-item id="u3680"><label>•</label><p id="p4795">Abdominal ultrasonography generally reveals distended nonmotile small intestine.</p></list-item><list-item id="u3685"><label>•</label><p id="p4800">Systemic cardiovascular deterioration.</p></list-item><list-item id="u3690"><label>•</label><p id="p4805">Abdominocentesis reveals normal to serosanguineous fluid with increased protein concentration, nucleated cell count, and lactate.</p></list-item><list-item id="u3695"><label>•</label><p id="p4810">The severity of the signs depends on the location, duration, and severity of the lesion.</p></list-item></list><boxed-text id="b0120"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0760"><title>Mesenteric Defects</title><sec id="s0765"><title>Initial Therapy Is Supportive</title><p id="p4815"><list list-type="simple" id="ulist0780"><list-item id="u3700"><label>•</label><p id="p4820">Gastric decompression</p></list-item><list-item id="u3705"><label>•</label><p id="p4825">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution)</p></list-item><list-item id="u3710"><label>•</label><p id="p4830">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u3715"><label>•</label><p id="p4835">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0785"><list-item id="u3720"><label>•</label><p id="p4840">Pain</p></list-item><list-item id="u3725"><label>•</label><p id="p4845">Nasogastric reflux</p></list-item><list-item id="u3730"><label>•</label><p id="p4850">Heart rate</p></list-item><list-item id="u3735"><label>•</label><p id="p4855">Mucous membranes</p></list-item><list-item id="u3740"><label>•</label><p id="p4860">Hematocrit, PCV/TPP</p></list-item><list-item id="u3745"><label>•</label><p id="p4865">Borborygmi</p></list-item></list></p></list-item><list-item id="u3750"><label>•</label><p id="p4870">Surgical intervention if a strangulating obstruction is suspected</p></list-item></list></p></sec><sec id="s0770"><title>Exploratory Surgery</title><p id="p4875"><list list-type="simple" id="ulist0790"><list-item id="u3755"><label>•</label><p id="p4880">Surgery is needed for definitive diagnosis.</p></list-item><list-item id="u3760"><label>•</label><p id="p4885">Ventral midline exploratory celiotomy is performed.</p></list-item><list-item id="u3765"><label>•</label><p id="p4890">The incarceration is reduced.</p></list-item><list-item id="u3770"><label>•</label><p id="p4895">The hernial ring may require manual dilation to reduce the hernia.</p></list-item><list-item id="u3775"><label>•</label><p id="p4900">The mesenteric defect is closed.</p></list-item><list-item id="u3780"><label>•</label><p id="p4905">Resection and anastomosis of devitalized bowel is performed.</p></list-item><list-item id="u3785"><label>•</label><p id="p4910"><italic><bold>Important Note:</bold></italic> Defects near the root of the mesentery are difficult to close because of limited exposure.</p></list-item><list-item id="u3790"><label>•</label><p id="p4915"><italic><bold>Practice Tip:</bold> Dorsally located mesenteric defects that</italic> cannot <italic>be closed may be repaired at a second surgery using a standing laparoscopic approach.</italic></p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s0775"><title>Prognosis</title><p id="p4920">Prognosis depends on the duration of illness and the length of intestine that requires resection. The prognosis is poor if difficulty is encountered reducing the hernia and closing the defect.</p></sec></sec><sec id="s0780"><title>Inguinal Hernia</title><p id="p4925"><list list-type="simple" id="ulist0795"><list-item id="u3795"><label>•</label><p id="p4930">Acquired inguinal hernias in stallions are associated with breeding or strenuous exercise and cause acute abdominal pain.</p></list-item><list-item id="u3800"><label>•</label><p id="p4935">A sudden increase in intraabdominal pressure or an enlarged internal inguinal ring may predispose to inguinal hernia.</p></list-item><list-item id="u3805"><label>•</label><p id="p4940">Inguinal hernias are commonly unilateral and occur frequently among Standardbred, Saddlebred, and Tennessee Walking horses.</p></list-item><list-item id="u3810"><label>•</label><p id="p4945">Inguinal herniation and evisceration can also occur as a sequela to castration!</p></list-item><list-item id="u3815"><label>•</label><p id="p4950">Congenital inguinal hernias in foals usually close spontaneously as the foal matures and only occasionally require surgical correction if the hernia <italic>cannot</italic> be reduced or if it is very large.</p></list-item><list-item id="u3820"><label>•</label><p id="p4955">Scrotal herniation may require surgical correction when the intestine ruptures the parietal tunic.</p></list-item></list></p><sec id="s0785"><title>Diagnosis</title><p id="p4960"><list list-type="simple" id="ulist0800"><list-item id="u3825"><label>•</label><p id="p4965">Acquired inguinal and scrotal herniation in a stallion can produce acute intestinal obstruction that necessitates emergency surgical intervention.</p></list-item><list-item id="u3830"><label>•</label><p id="p4970">Incarcerated bowel is strangulated; hypovolemic and endotoxic shock occur and cause systemic cardiovascular deterioration.</p></list-item><list-item id="u3835"><label>•</label><p id="p4975">The hernia is usually indirect and unilateral, with the incarcerated intestinal segment descending through the vaginal ring and contained within the tunica vaginalis.</p></list-item><list-item id="u3840"><label>•</label><p id="p4980">Affected horses have a rapid onset of moderate to severe abdominal pain.</p></list-item><list-item id="u3845"><label>•</label><p id="p4985">Palpation of the scrotum may reveal a firm, swollen, cold testicle on the affected side, but early in the disease process scrotal swelling may be absent.</p></list-item><list-item id="u3850"><label>•</label><p id="p4990">A swollen and slightly turgid tail of the epididymis may be palpated in early cases owing to passive congestion.</p></list-item><list-item id="u3855"><label>•</label><p id="p4995">The loop of herniated small bowel may be palpable per rectum passing through the internal inguinal ring. Palpate just below the brim of the pelvis and to each side.</p></list-item><list-item id="u3860"><label>•</label><p id="p5000">Ultrasonography generally reveals distended nonmotile bowel within the inguinal ring or scrotum.</p></list-item><list-item id="u3865"><label>•</label><p id="p5005">Signs of strangulating obstruction are the following:<list list-type="simple" id="ulist0805"><list-item id="u3870"><label>•</label><p id="p5010">Tachycardia</p></list-item><list-item id="u3875"><label>•</label><p id="p5015">Dehydration</p></list-item><list-item id="u3880"><label>•</label><p id="p5020">Endotoxemia</p></list-item><list-item id="u3885"><label>•</label><p id="p5025">Cardiovascular deterioration, which develops with time</p></list-item></list></p></list-item><list-item id="u3890"><label>•</label><p id="p5030">Abdominocentesis reveals fluid with an increased total protein level and nucleated cell count. Peritoneal fluid analysis may not accurately reflect the severity of intestinal compromise because of sequestration of fluid within the scrotum.</p></list-item><list-item id="u3895"><label>•</label><p id="p5035">Herniation and rupture of the vaginal tunic in newborn foals can cause mild to more severe pain and depression, local edema, and subsequent abscessation.</p></list-item></list><boxed-text id="b0125"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0790"><title>Inguinal Hernia</title><sec id="s0795"><title>Initial Therapy Is Supportive</title><p id="p5040"><list list-type="simple" id="ulist0810"><list-item id="u3900"><label>•</label><p id="p5045">Gastric decompression</p></list-item><list-item id="u3905"><label>•</label><p id="p5050">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution)</p></list-item><list-item id="u3910"><label>•</label><p id="p5055">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u3915"><label>•</label><p id="p5060">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0815"><list-item id="u3920"><label>•</label><p id="p5065">Pain</p></list-item><list-item id="u3925"><label>•</label><p id="p5070">Nasogastric reflux</p></list-item><list-item id="u3930"><label>•</label><p id="p5075">Heart rate</p></list-item><list-item id="u3935"><label>•</label><p id="p5080">Mucous membranes</p></list-item><list-item id="u3940"><label>•</label><p id="p5085">Hematocrit, PCV/TPP</p></list-item><list-item id="u3945"><label>•</label><p id="p5090">Borborygmi</p></list-item></list></p></list-item><list-item id="u3950"><label>•</label><p id="p5095">Surgical intervention if inguinal or scrotal herniation is suspected in adult horses</p></list-item></list></p></sec><sec id="s0800"><title>Exploratory Surgery</title><p id="p5100"><list list-type="simple" id="ulist0820"><list-item id="u3955"><label>•</label><p id="p5105">Ventral midline exploratory celiotomy.</p></list-item><list-item id="u3960"><label>•</label><p id="p5110">Inguinal incision is used to achieve adequate surgical exposure and reduction.</p></list-item><list-item id="u3965"><label>•</label><p id="p5115">Reduction, resection, and anastomosis of the affected bowel are performed.</p></list-item><list-item id="u3970"><label>•</label><p id="p5120">Unilateral castration and inguinal herniorrhaphy are usually required.</p></list-item><list-item id="u3975"><label>•</label><p id="p5125"><italic><bold>Practice Tip:</bold> Inguinal herniation in newborn colts may be contained in the vaginal tunic or may rupture the tunic and lie subcutaneously. Those within the vaginal tunic may be manually reduced and generally correct spontaneously. Those that rupture the tunic or those that are large and</italic> cannot <italic>be reduced, require immediate surgical repair through inguinal and scrotal incisions.</italic></p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s0805"><title>Prognosis</title><p id="p5130"><list list-type="simple" id="ulist0825"><list-item id="u3980"><label>•</label><p id="p5135">Prognosis is good if reduction and repair are performed within hours of herniation before strangulation occurs.</p></list-item><list-item id="u3985"><label>•</label><p id="p5140">The prognosis worsens with increasing duration before correction.</p></list-item><list-item id="u3990"><label>•</label><p id="p5145">The prognosis for breeding soundness is good if only one testicle is involved.</p></list-item></list></p></sec></sec><sec id="s0810"><title>Diaphragmatic Hernia</title><p id="p5150"><list list-type="simple" id="ulist0830"><list-item id="u3995"><label>•</label><p id="p5155">Diaphragmatic hernia can be congenital or acquired and is an unusual cause of abdominal pain in horses.</p></list-item><list-item id="u4000"><label>•</label><p id="p5160">Most often it results from strenuous exercise, a hard fall, hitting something while running, or being hit by a car.</p></list-item><list-item id="u4005"><label>•</label><p id="p5165">Pregnant or periparturient mares also are at risk.</p></list-item></list></p><sec id="s0815"><title>Diagnosis</title><p id="p5170"><list list-type="simple" id="ulist0835"><list-item id="u4010"><label>•</label><p id="p5175">Clinical signs of diaphragmatic hernia include abdominal pain, tachypnea, and dyspnea.</p></list-item><list-item id="u4015"><label>•</label><p id="p5180">The severity of signs depends on the size of the hernia opening and degree of visceral herniation.</p></list-item><list-item id="u4020"><label>•</label><p id="p5185">The presence of viscera within the thoracic cavity may reduce the intensity of lung sounds and cause dullness on percussion.</p></list-item><list-item id="u4025"><label>•</label><p id="p5190">Radiography or ultrasonography (<xref rid="f0270" ref-type="fig">Fig. 18-52</xref>) is helpful in finding thickened or ingesta-filled loops of intestine in the thoracic cavity (finding bowel on both sides of the diaphragm).<fig id="f0270"><label>Figure 18-52</label><caption><p>Ultrasound of the thorax of a 20-year-old gelding with mild pain, sternal edema, and thoracic effusion. The 5-mHz scan shows multiple loops of thickened small intestine and fluid in the thoracic cavity. To the middle left of the image, a caudal tip of consolidated lung is present <italic>(arrow),</italic> and to the bottom right of the image, diaphragm <italic>(arrowhead)</italic>.</p></caption><graphic xlink:href="f018-052-9781455708925"></graphic></fig></p></list-item><list-item id="u4030"><label>•</label><p id="p5195">Blood gas measurement may indicate respiratory compromise and hypoxemia.</p></list-item><list-item id="u4035"><label>•</label><p id="p5200">Thoracocentesis and abdominocentesis may yield blood-tinged fluid with an increased total protein level and nucleated cell count, which are evidence of the presence of devitalized bowel. Be <italic>cautious</italic> performing a thoracocentesis if a diaphragmatic hernia is suspected; the bowel could be entered.</p></list-item><list-item id="u4040"><label>•</label><p id="p5205">Exploratory celiotomy often is necessary for a definitive diagnosis.</p></list-item></list><boxed-text id="b0130"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0820"><title>Diaphragmatic Hernia</title><sec id="s0825"><title>Initial Therapy Is Supportive</title><p id="p5210"><list list-type="simple" id="ulist0840"><list-item id="u4045"><label>•</label><p id="p5215">Gastric decompression</p></list-item><list-item id="u4050"><label>•</label><p id="p5220">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution)</p></list-item><list-item id="u4055"><label>•</label><p id="p5225">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u4060"><label>•</label><p id="p5230">Supplemental oxygen therapy if necessary</p></list-item><list-item id="u4065"><label>•</label><p id="p5235">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0845"><list-item id="u4070"><label>•</label><p id="p5240">Pain</p></list-item><list-item id="u4075"><label>•</label><p id="p5245">Nasogastric reflux</p></list-item><list-item id="u4080"><label>•</label><p id="p5250">Heart rate</p></list-item><list-item id="u4085"><label>•</label><p id="p5255">Mucous membranes</p></list-item><list-item id="u4090"><label>•</label><p id="p5260">Hematocrit, PCV/TPP</p></list-item><list-item id="u4095"><label>•</label><p id="p5265">Borborygmi</p></list-item></list></p></list-item></list></p></sec><sec id="s0830"><title>Exploratory Surgery</title><p id="p5270"><list list-type="simple" id="ulist0850"><list-item id="u4100"><label>•</label><p id="p5275">Ventral midline exploratory celiotomy</p></list-item><list-item id="u4105"><label>•</label><p id="p5280">Reduction, resection, and anastomosis of the affected bowel</p></list-item><list-item id="u4110"><label>•</label><p id="p5285">Closure of the diaphragmatic defect by suturing or use of a synthetic mesh (Marlex,<xref rid="fn0070" ref-type="fn">13</xref> Proxplast,<xref rid="fn0075" ref-type="fn">14</xref> high-density polyethylene [HDPE]<xref rid="fn0080" ref-type="fn">15</xref>)</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s0835"><title>Prognosis</title><p id="p5290">The prognosis is guarded to poor because of difficult surgical exposure and a high incidence of postoperative complications, including septic pleuritis, implant failure, and hernia recurrence. The prognosis is better in young horses as a result of the improved surgical exposure.</p></sec></sec><sec id="s0840"><title>Pedunculated Lipoma</title><p id="p5295"><list list-type="simple" id="ulist0855"><list-item id="u4115"><label>•</label><p id="p5300">Pedunculated lipoma is a common cause of small-intestinal strangulation or obstruction in horses older than 10 years.</p></list-item><list-item id="u4120"><label>•</label><p id="p5305">Lipomas attach to the mesentery by a fibrovascular stalk of variable length.</p></list-item><list-item id="u4125"><label>•</label><p id="p5310">They are frequently incidental findings at exploratory surgery or necropsy.</p></list-item><list-item id="u4130"><label>•</label><p id="p5315">These masses have the potential to incarcerate a segment of small intestine (or rarely small colon) and produce strangulating obstruction (<xref rid="f0275" ref-type="fig">Fig. 18-53</xref>).<fig id="f0275"><label>Figure 18-53</label><caption><p><bold>A,</bold> Movement of a loop of jejunum into a half-hitch formed by a pedunculated lipoma on its stalk. <bold>B,</bold> Strangulation of the loop of jejunum by the pedunculated lipoma.</p></caption><graphic xlink:href="f018-053a-9781455708925"></graphic><graphic xlink:href="f018-053b-9781455708925"></graphic></fig></p></list-item></list></p><sec id="s0845"><title>Diagnosis</title><p id="p5320"><italic><bold>Practice Tip:</bold> Pedunculated lipoma should always be considered in the differential diagnosis when a horse older than 10 years has signs of small-intestinal obstruction.</italic><list list-type="simple" id="ulist0860"><list-item id="u4135"><label>•</label><p id="p5330">Acute abdominal pain</p></list-item><list-item id="u4140"><label>•</label><p id="p5335">Hemoconcentration</p></list-item><list-item id="u4145"><label>•</label><p id="p5340">Decreased borborygmi</p></list-item><list-item id="u4150"><label>•</label><p id="p5345">Nasogastric reflux usually is present but may be absent early in the disease. Multiple loops of small intestine are palpable on rectal examination (see <xref rid="f0250" ref-type="fig">Fig. 18-48</xref>) or are evident on abdominal ultrasonographic examination. Increases in peritoneal total protein concentration and nucleated cell count reflect the degree of intestinal compromise.</p></list-item></list><boxed-text id="b0135"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0855"><title>Pedunculated Lipoma</title><sec id="s0860"><title>Initial Therapy Is Supportive</title><p id="p5350"><list list-type="simple" id="ulist0865"><list-item id="u4155"><label>•</label><p id="p5355">Gastric decompression</p></list-item><list-item id="u4160"><label>•</label><p id="p5360">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution)</p></list-item><list-item id="u4165"><label>•</label><p id="p5365">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u4170"><label>•</label><p id="p5370">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0870"><list-item id="u4175"><label>•</label><p id="p5375">Pain</p></list-item><list-item id="u4180"><label>•</label><p id="p5380">Nasogastric reflux</p></list-item><list-item id="u4185"><label>•</label><p id="p5385">Heart rate</p></list-item><list-item id="u4190"><label>•</label><p id="p5390">Mucous membranes</p></list-item><list-item id="u4195"><label>•</label><p id="p5395">Hematocrit, PCV/TPP</p></list-item><list-item id="u4200"><label>•</label><p id="p5400">Borborygmi</p></list-item></list></p></list-item><list-item id="u4205"><label>•</label><p id="p5405">Surgical intervention if a strangulating obstruction is suspected</p></list-item></list></p></sec><sec id="s0865"><title>Exploratory Surgery</title><p id="p5410"><list list-type="simple" id="ulist0875"><list-item id="u4210"><label>•</label><p id="p5415">Ventral midline exploratory celiotomy</p></list-item><list-item id="u4215"><label>•</label><p id="p5420">Ligation and transection of lipoma</p></list-item><list-item id="u4220"><label>•</label><p id="p5425">Resection and anastomosis of the affected intestine</p></list-item><list-item id="u4225"><label>•</label><p id="p5430">Removal of any lipomas found at surgery to minimize recurrence</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s0870"><title>Prognosis</title><p id="p5435">Prognosis is often favorable with early diagnosis and prompt treatment. If devitalized intestine <italic>cannot</italic> be resected or if peritonitis is severe, the prognosis is guarded to poor.</p></sec></sec><sec id="s0875"><title>Ileal Impaction</title><p id="p5440"><list list-type="simple" id="ulist0880"><list-item id="u4230"><label>•</label><p id="p5445">The ileum is the most common site of small-intestinal intraluminal impaction (<xref rid="f0280" ref-type="fig">Fig. 18-54</xref>). The incidence varies with geographic location.<fig id="f0280"><label>Figure 18-54</label><caption><p>Obstruction of the lumen of the ileum by ingesta. The wall of the ileum has been rendered transparent to facilitate visualization of the impaction.</p></caption><graphic xlink:href="f018-054-9781455708925"></graphic></fig></p></list-item><list-item id="u4235"><label>•</label><p id="p5450">This condition is more common in Europe and the southeastern United States; the cause is unknown.</p></list-item><list-item id="u4240"><label>•</label><p id="p5455">An association with fine, high-roughage forage and coastal Bermuda hay has been implicated.</p></list-item><list-item id="u4245"><label>•</label><p id="p5460">Ingesta accumulate in the ileum causing obstruction. Spasmodic contraction and absorption of water from the ileal lumen exacerbate the impaction.</p></list-item><list-item id="u4250"><label>•</label><p id="p5465">Mesenteric vascular thrombotic disease, tapeworm infestation <italic>(A. perfoliata),</italic> and ascarid impaction <italic>(P. equorum)</italic> are less common causes.</p></list-item><list-item id="u11085"><label>•</label><p id="p5470"><italic><bold>Practice Tip:</bold> Ileal hypertrophy should be considered in older horses with a history of chronic colic.</italic></p></list-item><list-item id="u4255"><label>•</label><p id="p5475">On the rare occasion, idiopathic hypertrophy of large portions of the small bowel may cause chronic colic. The hypertrophy in these cases can be easily seen on abdominal ultrasound examination. Prognosis is guarded in these cases and are best managed by dietary (low roughage) control.</p></list-item><list-item id="u4260"><label>•</label><p id="p5480">Focal or diffuse eosinophilic inflammatory disease of the small intestine and left dorsal colon may also present with thickened bowel and either acute or chronic colic.</p></list-item><list-item id="u4265"><label>•</label><p id="p5485">Of the inflammatory bowel disorders (lymphocytic-plasmacytic, eosinophilic, granulomatous, lymphosarcoma, etc.) eosinophilic cases seem to have the highest incidence of colic as a clinical sign. Medical management (corticosteroids) for eosinophilic enteritis has a fair to guarded outcome although for focal disease surgical removal is usually successful.</p></list-item></list></p><sec id="s0880"><title>Diagnosis</title><p id="p5490">Clinical signs are variable and depend on the duration of the impaction:<list list-type="simple" id="ulist0890"><list-item id="u4270"><label>•</label><p id="p5495">Moderate to severe abdominal pain is caused by focal intestinal distention and spasmodic contraction around the impaction. Affected horses usually have a transient response to analgesics.</p></list-item><list-item id="u4275"><label>•</label><p id="p5500">Rectal palpation reveals multiple loops of moderately to severely distended small intestine (see <xref rid="f0250" ref-type="fig">Fig. 18-48</xref>). Early examination may reveal 5- to 8-cm diameter, firm, smooth-surfaced ileum originating at the cecal base and coursing from the right of the midline obliquely downward and to the left side.</p></list-item><list-item id="u4280"><label>•</label><p id="p5505">Abdominal ultrasonography generally reveals distended nonmotile small intestine.</p></list-item><list-item id="u4285"><label>•</label><p id="p5510">Nasogastric reflux may be absent in the early stages. During the 8 to 10 hours after the initial episode of colic, small intestinal and gastric distention develops and results in recurrence of signs of pain and progressive dehydration.</p></list-item><list-item id="u4290"><label>•</label><p id="p5515">Gastric decompression often provides temporary pain relief. Borborygmi diminish or disappear, and intestinal distention without motility is seen on ultrasound examination.</p></list-item><list-item id="u4295"><label>•</label><p id="p5520">CBC, electrolytes, blood gases, and findings at abdominocentesis frequently are within normal limits.</p></list-item><list-item id="u4300"><label>•</label><p id="p5525">Hemoconcentration and increased total peritoneal protein level and nucleated cell count may occur with long-standing impaction.</p></list-item></list><boxed-text id="b0140"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0885"><title>Ileal Impaction</title><sec id="s0890"><title>Initial Therapy Is Supportive</title><p id="p5530"><list list-type="simple" id="ulist0895"><list-item id="u4305"><label>•</label><p id="p5535">Gastric decompression</p></list-item><list-item id="u4310"><label>•</label><p id="p5540">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution)</p></list-item><list-item id="u4315"><label>•</label><p id="p5545">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u4320"><label>•</label><p id="p5550">Monitoring of physiologic and clinical parameters:<list list-type="simple" id="ulist0900"><list-item id="u4325"><label>•</label><p id="p5555">Pain</p></list-item><list-item id="u4330"><label>•</label><p id="p5560">Nasogastric reflux</p></list-item><list-item id="u4335"><label>•</label><p id="p5565">Heart rate</p></list-item><list-item id="u4340"><label>•</label><p id="p5570">Mucous membranes</p></list-item><list-item id="u4345"><label>•</label><p id="p5575">Hematocrit, PCV/TPP</p></list-item><list-item id="u4350"><label>•</label><p id="p5580">Borborygmi</p></list-item></list></p></list-item><list-item id="u4355"><label>•</label><p id="p5585">The impaction may respond to medical therapy (one to three doses of xylazine may resolve the impaction based on its use in several horses), and is believed to cause relaxation of the intestine; N-butylscopolammonium bromide (Buscopan) may have a similar effect.</p></list-item><list-item id="u4360"><label>•</label><p id="p5590">6 to 8 L of water via nasogastric tube if <italic>no</italic> net reflux</p></list-item><list-item id="u4365"><label>•</label><p id="p5595">If medical therapy is unsuccessful, surgical intervention is necessary.</p></list-item></list></p></sec><sec id="s0895"><title>Exploratory Surgery</title><p id="p5600"><list list-type="simple" id="ulist0905"><list-item id="u4370"><label>•</label><p id="p5605">Ventral midline exploratory celiotomy</p></list-item><list-item id="u4375"><label>•</label><p id="p5610">Reduce the obstruction by extraluminal massage</p></list-item><list-item id="u4380"><label>•</label><p id="p5615">Mix the impaction with jejunal fluid or infuse of the impaction with sterile saline solution or sodium carboxymethylcellulose with or without 2% lidocaine to facilitate reduction</p></list-item><list-item id="u4385"><label>•</label><p id="p5620">With significant mural edema and congestion, jejunal enterotomy may be necessary to facilitate emptying of the ileal contents without excessive manipulation of the bowel</p></list-item><list-item id="u4390"><label>•</label><p id="p5625">Resection and anastomosis (ileocecostomy or jejunocecostomy) is rarely necessary but may be required if additional problems exist, such as ileal hypertrophy or mesenteric vascular thrombotic disease.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s0900"><title>Prognosis</title><p id="p5630">Prognosis is good for both medical and surgical treatment if no concurrent abnormalities exist (e.g., ileal hypertrophy) and is guarded if ileocecostomy or jejunocecostomy is needed because of postoperative ileus and the high incidence of intraabdominal adhesions.</p></sec></sec><sec id="s0905"><title>Ascarid Impaction</title><p id="p5635"><list list-type="simple" id="ulist0910"><list-item id="u4395"><label>•</label><p id="p5640">Heavy ascarid <italic>(P. equorum)</italic> infestation can lead to intraluminal obstruction in foals, weanlings, and yearlings.</p></list-item><list-item id="u4400"><label>•</label><p id="p5645">Affected horses have a history of a poor parasite control program leading to heavy infestation with ascarids.</p></list-item><list-item id="u4405"><label>•</label><p id="p5650"><bold><italic>Practice Tip:</italic></bold><italic>Impaction commonly follows (24 to 48 hr) after treatment with an anthelmintic (e.g., pyrantel, ivermectin), tranquilizers, or general anesthetics.</italic></p></list-item><list-item id="u4410"><label>•</label><p id="p5655">Fenbendazole, although a highly effective anthelmintic, is <italic>not</italic> commonly implicated in the development of ascarid impaction.</p></list-item><list-item id="u4415"><label>•</label><p id="p5660">Intestinal rupture, peritonitis, and intussusception are possible sequelae.</p></list-item><list-item id="u4420"><label>•</label><p id="p5665">Foals develop immunity to the parasite by 6 months to 1 year of age. Consequently, this condition is uncommon in adults.</p></list-item></list></p><sec id="s0910"><title>Diagnosis</title><p id="p5670">Clinical signs depend on the duration and degree of small-intestinal obstruction and include the following:<list list-type="simple" id="ulist0915"><list-item id="u4425"><label>•</label><p id="p5675">Unthriftiness</p></list-item><list-item id="u4430"><label>•</label><p id="p5680">Poor hair coat</p></list-item><list-item id="u4435"><label>•</label><p id="p5685">Mild to severe abdominal pain</p></list-item><list-item id="u4440"><label>•</label><p id="p5690">Nasogastric reflux that usually is present and may contain ascarids</p></list-item><list-item id="u4445"><label>•</label><p id="p5695">Rectal examination and abdominal ultrasonography that reveal multiple loops of distended small intestine. Ascarids may be seen within the lumen on ultrasound examination (<xref rid="f0285" ref-type="fig">Fig 18-55, A and B</xref>).<fig id="f0285"><label>Figure 18-55</label><caption><p><bold>A,</bold> Ultrasound image of the ventral abdomen of a 3-month-old foal with colic and distended small intestine because of a <italic>Parascaris equorum</italic> impaction. The hyperechoic circle is a <italic>Parascaris equorum</italic> seen on cross section. <bold>B,</bold> The same foal as in <xref rid="f0280" ref-type="fig">Fig 18-54</xref>; Three <italic>Parascaris equorum</italic> parasites are seen longitudinally. The foal was dewormed the previous day.</p></caption><graphic xlink:href="f018-055a-9781455708925"></graphic><graphic xlink:href="f018-055b-9781455708925"></graphic></fig></p></list-item><list-item id="u11090"><label>•</label><p id="p5700"><italic><bold>Practice Tip:</bold> The final diagnosis is based on signalment, history, and the presence of signs of small-intestinal obstruction.</italic><boxed-text id="b0145"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0915"><title>Ascarid Impaction</title><sec id="s0920"><title>Partial Obstruction of the Intestine with Ascarids</title><p id="p5705"><list list-type="simple" id="ulist0920"><list-item id="u4450"><label>•</label><p id="p5710">Intestinal lubricants (e.g., mineral oil)</p></list-item><list-item id="u4455"><label>•</label><p id="p5715">Balanced polyionic intravenous fluids (e.g., lactated Ringer's solution)</p></list-item><list-item id="u4460"><label>•</label><p id="p5720">Analgesics (e.g., xylazine, butorphanol tartrate, and/or flunixin meglumine)</p></list-item><list-item id="u4465"><label>•</label><p id="p5725">Low-efficacy or slow-onset anthelmintics (fenbendazole, ivermectin), which are preferred to prevent future recurrence</p></list-item></list></p></sec><sec id="s0925"><title>Ventral Midline Exploratory Surgery to Relieve the Obstruction</title><p id="p5730"><list list-type="simple" id="ulist0925"><list-item id="u4470"><label>•</label><p id="p5735">Surgery is required with complete obstruction or if medical therapy is unsuccessful.</p></list-item><list-item id="u4475"><label>•</label><p id="p5740">Multiple enterotomies (<xref rid="f0290" ref-type="fig">Fig. 18-56</xref>) may be needed to remove the ascarids, although massaging the parasites into the cecum may improve the prognosis.<fig id="f0290"><label>Figure 18-56</label><caption><p>Intraoperative image demonstrating a small intestinal enterotomy in a weanling to facilitate removal of an ascarid impaction.</p></caption><graphic xlink:href="f018-056-9781455708925"></graphic></fig></p></list-item></list></p></sec></sec></boxed-text></p></list-item></list></p></sec><sec id="s0930"><title>Prognosis</title><p id="p5745">Prognosis is good if medical treatment is successful and guarded if surgery and multiple enterotomies are performed because of the high occurrence of intraabdominal adhesions.</p></sec></sec><sec id="s0935"><title>Duodenitis and Proximal Jejunitis</title><p id="p5750"><list list-type="simple" id="ulist0930"><list-item id="u4480"><label>•</label><p id="p5755">Duodenitis and proximal jejunitis are characterized by transmural inflammation, edema, and hemorrhage in the duodenum and proximal jejunum (<xref rid="f0295" ref-type="fig">Fig. 18-57</xref>).<fig id="f0295"><label>Figure 18-57</label><caption><p>Caudal right view of inflammation and distention of the duodenum and jejunum caused by proximal enteritis.</p></caption><graphic xlink:href="f018-057-9781455708925"></graphic></fig></p></list-item><list-item id="u4485"><label>•</label><p id="p5760">The stomach and proximal small intestine are moderately distended with fluid, whereas the distal jejunum and ileum usually are flaccid.</p></list-item><list-item id="u4490"><label>•</label><p id="p5765">Histologic lesions include hyperemia and edema of the mucosa and submucosa, villous epithelial degeneration and sloughing, neutrophil infiltration, hemorrhage in the muscular layer, and fibrinopurulent exudation on the serosa.</p></list-item><list-item id="u4495"><label>•</label><p id="p5770">The cause of this extensive intestinal damage is unknown; <italic>Clostridium perfringens</italic> and <italic>Clostridium difficile</italic> are presumed causative agents and frequently can be cultured from the gastric reflux.</p></list-item><list-item id="u4500"><label>•</label><p id="p5775"><italic>Salmonella</italic> is rarely cultured from gastric contents.</p></list-item><list-item id="u4505"><label>•</label><p id="p5780">Proximal small-intestinal distention, gastric reflux, dehydration, and hypovolemic and endotoxic shock result from the intestinal damage. The inflammation and damage can alter intestinal motility, causing adynamic ileus.</p></list-item></list></p><sec id="s0940"><title>Diagnosis</title><sec id="s0945"><title>Clinical Signs</title><p id="p5785"><list list-type="simple" id="ulist0935"><list-item id="u4510"><label>•</label><p id="p5790">Acute abdominal pain</p></list-item><list-item id="u4515"><label>•</label><p id="p5795">Large volumes of nasogastric reflux fluid (red to greenish brown; spontaneous reflux may even be seen in a few cases)</p></list-item><list-item id="u4520"><label>•</label><p id="p5800">Absent borborygmi</p></list-item><list-item id="u4525"><label>•</label><p id="p5805">Tachycardia</p></list-item><list-item id="u4530"><label>•</label><p id="p5810">Dehydration</p></list-item><list-item id="u4535"><label>•</label><p id="p5815">Slight increase in body temperature (38.6° C to 39.1° C [101.5° F to 102.4° F])</p></list-item><list-item id="u4540"><label>•</label><p id="p5820">Hyperemic mucous membranes</p></list-item><list-item id="u4545"><label>•</label><p id="p5825">Increased hematocrit</p></list-item><list-item id="u4550"><label>•</label><p id="p5830">Moderate to severe small-intestinal distention on rectal examination; early in the disease, small-intestinal distention may be absent</p></list-item><list-item id="u4555"><label>•</label><p id="p5835">Distended proximal small intestine with thickened wall and mild to moderate motility at ultrasound examination</p></list-item></list></p></sec><sec id="s0950"><title>Clinical Laboratory Findings</title><p id="p5840"><list list-type="simple" id="ulist0940"><list-item id="u4560"><label>•</label><p id="p5845">Increased PCV and TPP (hemoconcentration)</p></list-item><list-item id="u4565"><label>•</label><p id="p5850">Increased creatinine concentration indicating prerenal or renal azotemia</p></list-item><list-item id="u4570"><label>•</label><p id="p5855">Increased peritoneal total protein concentration</p></list-item><list-item id="u4575"><label>•</label><p id="p5860">Mild to moderate increase in nucleated cell count (5000 to 25,000 cells/mL) in peritoneal fluid</p></list-item><list-item id="u4580"><label>•</label><p id="p5865">Hypokalemia</p></list-item><list-item id="u4585"><label>•</label><p id="p5870">Occasionally, metabolic acidosis</p></list-item><list-item id="u4590"><label>•</label><p id="p5875">CBC that may reveal a normal, increased (neutrophilia caused by inflammation) or decreased (neutropenia and left shift caused by endotoxemia and consumption) WBC count</p></list-item><list-item id="u4595"><label>•</label><p id="p5880">Gram stain of the gastric reflux fluid that shows a large number of large gram-positive rods (<xref rid="f0300" ref-type="fig">Fig. 18-58</xref>)<fig id="f0300"><label>Figure 18-58</label><caption><p>Gram stain of gastric fluid from a horse with proximal duodenitis-jejunitis that demonstrates many large gram-positive rods (compatible with <italic>Clostridium perfringens</italic>).</p></caption><graphic xlink:href="f018-058-9781455708925"></graphic></fig></p></list-item><list-item id="u4600"><label>•</label><p id="p5885"><italic><bold>Practice Tip:</bold> The clinical findings can be confused with those of strangulating or nonstrangulating obstruction. After nasogastric decompression, abdominal pain usually subsides and is replaced by depression in patients with duodenitis and proximal jejunitis. The presence of persistent abdominal pain with serosanguineous abdominal fluid supports the diagnosis of strangulating obstruction, but serosanguineous abdominal fluid can also be present with proximal enteritis.</italic></p></list-item></list><boxed-text id="b0150"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0955"><title>Duodenitis and Proximal Jejunitis</title><p id="p5890"><list list-type="simple" id="ulist0945"><list-item id="u4605"><label>•</label><p id="p5895">Voluminous gastrointestinal reflux is produced for 1 to 7 days, requiring gastric decompression through an indwelling nasogastric tube every 2 hours to prevent distention, pain, and gastric rupture.</p></list-item><list-item id="u4610"><label>•</label><p id="p5900">Food and oral medication are withheld until small-intestinal borborygmi return.</p></list-item><list-item id="u4615"><label>•</label><p id="p5905">Intravenous administration of a balanced crystalloid solution is required to maintain intravascular fluid volume.</p></list-item><list-item id="u4620"><label>•</label><p id="p5910">Monitoring of blood gases and serum electrolytes (Na<sup>+</sup>, K<sup>+</sup>, Cl<sup>−</sup>, HCO<sub>3</sub><sup>−</sup>, Ca<sup>2+</sup>) daily and adjustment of the intravenous solution are necessary to correct any deficiencies.</p></list-item><list-item id="u4625"><label>•</label><p id="p5915">Administer low-dose flunixin meglumine, 0.25 mg/kg IV q8h, to minimize the adverse effects of arachidonic acid metabolites (thromboxane A<sub>2</sub> and prostaglandins).</p></list-item><list-item id="u4630"><label>•</label><p id="p5920">Antiserum (Endoserum) directed against gram-negative core antigens (endotoxin) is administered intravenously diluted in a balanced electrolyte solution. Hyperimmune plasma directed against the J-5 mutant strain of <italic>E. coli</italic> (Polymune-J or Foalimmune) or normal equine plasma (2 to 10 L) administered intravenously slowly may be equally beneficial, supplying protein, fibronectin, complement, antithrombin III, and other inhibitors of hypercoagulability.</p></list-item><list-item id="u4635"><label>•</label><p id="p5925">Polymyxin B, 2000 to 6000 IU/kg IV slowly q12h as needed, if the horse shows evidence of significant toxemia and after urination is seen.</p></list-item><list-item id="u4640"><label>•</label><p id="p5930">Nonfractionated heparin, 100 U/kg SQ q12h, or preferably low-molecular-weight heparin, 50 to 100 U/kg SQ q24h, may decrease the incidence of laminitis.</p></list-item><list-item id="u4645"><label>•</label><p id="p5935">DMSO 10% solution can be administered intravenously (100 mg/kg q8h or q12h) but efficacy is in question.</p></list-item><list-item id="u4650"><label>•</label><p id="p5940">Na<sup>+</sup> or K<sup>+</sup> penicillin (22,000 to 44,000 IU/kg IV q6h) or procaine penicillin (22,000 to 44,000 IU/kg IM q12h) can be administered, in addition to metronidazole (30 mg/kg per rectum q8h or 15 mg/kg IV q6h) for <italic>C. perfringens</italic> or <italic>C. difficile,</italic> as the suggested causative pathogen.</p></list-item><list-item id="u4655"><label>•</label><p id="p5945">Motility modifiers can be useful in reducing gastric reflux and may decrease the cost of treatment and complications associated with frequent passage of the nasogastric tube.</p></list-item><list-item id="u4660"><label>•</label><p id="p5950">Recommendations for motility modifiers are as follows:<list list-type="simple" id="ulist0950"><list-item id="u4665"><label>•</label><p id="p5955">2% lidocaine, slow intravenous bolus, 1.3 mg/kg (approximately 30 mL/450-kg adult) followed by 0.05 mg/kg per minute infusion; the motility modifying effect is believed secondary to the anti-inflammatory effect.</p></list-item><list-item id="u4670"><label>•</label><p id="p5960">Cisapride, 0.1 to 0.2 mg/kg IV q8h, 0.3 mg/kg PO q8h; adverse effects can occur with the IV administration</p></list-item></list></p></list-item><list-item id="u4675"><label>•</label><p id="p5965">Monitor serum creatinine concentration and urine output after fluid therapy because secondary renal failure is common.</p></list-item><list-item id="u4680"><label>•</label><p id="p5970">Laminitis is a common complication. The feet should be monitored, and treatment should be incorporated in the medical therapy, including the following (see Chapter 43, p. 709):<list list-type="simple" id="ulist0955"><list-item id="u4685"><label>•</label><p id="p5975">Ice distal limbs and feet with ice boots for 48 hours or until toxic neutrophils and band cells are <italic>no</italic> longer present in the CBC.</p></list-item><list-item id="u4690"><label>•</label><p id="p5980">Heavily bed the stall with shavings or sand.</p></list-item><list-item id="u4695"><label>•</label><p id="p5985">Removing shoes, trim and balance feet, and apply Styrofoam, dental putty, or other hoof and frog support to enlist mechanical support of the entire foot.</p></list-item><list-item id="u4700"><label>•</label><p id="p5990">Apply lower limb support bandages.</p></list-item><list-item id="u4705"><label>•</label><p id="p5995">Administer phenylbutazone, after discontinuing flunixen meglumine, (2.2 to 4.4 mg/kg PO or IV q12h) if laminitis develops.</p></list-item><list-item id="u4710"><label>•</label><p id="p6000">Administer acepromazine (0.02 mg/kg IM q8h) for its vasodilatory properties.</p></list-item><list-item id="u4715"><label>•</label><p id="p6005">Administer DMSO intravenously as listed before.</p></list-item><list-item id="u11095"><label>•</label><p id="p13455">Pentoxifylline (Trental), 7.5 to 10 mg/kg PO, IV, q8-12h; recommended for endotoxemia, laminitis, vasodilator and rheologic effects.</p></list-item></list></p></list-item><list-item id="u4720"><label>•</label><p id="p6010">With prolonged (>7 days) nasogastric reflux, bowel decompression or intestinal bypass through a standing right flank laparotomy or ventral midline celiotomy can be used to augment medical therapy.</p></list-item><list-item id="u4725"><label>•</label><p id="p6015">Some surgeons, particularly in the United Kingdom, believe that immediate exploratory laparotomy and decompression results in a more rapid recovery.</p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s0960"><title>Prognosis</title><p id="p6020"><list list-type="simple" id="ulist0960"><list-item id="u4730"><label>•</label><p id="p6025">With aggressive medical management, the disease resolves in most cases.</p></list-item><list-item id="u4735"><label>•</label><p id="p6030">Sequelae that adversely affect the prognosis include:<list list-type="simple" id="ulist0965"><list-item id="u4740"><label>•</label><p id="p6035">Laminitis</p></list-item><list-item id="u4745"><label>•</label><p id="p6040">Renal failure</p></list-item><list-item id="u4750"><label>•</label><p id="p6045">Intraabdominal adhesion formation</p></list-item><list-item id="u4755"><label>•</label><p id="p6050">Pharyngeal or esophageal injury</p></list-item><list-item id="u4760"><label>•</label><p id="p6055">Gastric rupture</p></list-item></list></p></list-item><list-item id="u4765"><label>•</label><p id="p6060"><italic><bold>Practice Tip:</bold> Patients with red gastric reflux fluid appear to be more prone to complications than are horses without such reflux.</italic></p></list-item></list></p></sec></sec><sec id="s0965"><title>Nonstrangulating Infarction</title><p id="p6065"><list list-type="simple" id="ulist0970"><list-item id="u4770"><label>•</label><p id="p6070">Nonstrangulating infarction is an inadequate blood supply (necrosis caused by loss of blood supply) of the intestine without a strangulating lesion.</p></list-item><list-item id="u4775"><label>•</label><p id="p6075">Postmortem examination commonly reveals the cause to be thrombus formation at the cranial mesenteric artery from damage by migration of the fourth and fifth stages of <italic>Strongylus vulgaris</italic> larvae.</p></list-item><list-item id="u4780"><label>•</label><p id="p6080">Infarction is hypothesized to be the result of hypoxia induced by vasospasm.</p></list-item></list></p><sec id="s0970"><title>Diagnosis</title><p id="p6085">A poor parasite control program may predispose horses to nonstrangulating ischemia and infarction. The disease also occurs in horses regularly treated with anthelmintics. Clinical signs of variable severity range from depression to moderately severe abdominal pain:<list list-type="simple" id="ulist0975"><list-item id="u4785"><label>•</label><p id="p6090">Heart rate, respiratory rate, and body temperature may be normal or increased.</p></list-item><list-item id="u4790"><label>•</label><p id="p6095">Hyperemic mucous membranes suggest endotoxemia or inflammation caused by migrating parasites.</p></list-item><list-item id="u4795"><label>•</label><p id="p6100">Rectal examination and abdominal ultrasound examination findings may be normal or include distended small intestine.</p></list-item><list-item id="u4800"><label>•</label><p id="p6105">Pain, fremitus, or thickening is commonly evident on palpation of the mesenteric root.</p></list-item><list-item id="u4805"><label>•</label><p id="p6110">Auscultation of the abdomen may reveal normal, increased, or decreased borborygmi.</p></list-item><list-item id="u4810"><label>•</label><p id="p6115">Gastric reflux may be present because of functional obstruction of the intestinal segment.</p></list-item><list-item id="u4815"><label>•</label><p id="p6120">PCV, TPP, and creatinine level may be increased because of dehydration.</p></list-item><list-item id="u4820"><label>•</label><p id="p6125">Peripheral blood examination may reveal a normal, decreased (neutropenia with a left shift resulting from endotoxemia), or increased (neutrophilia resulting from inflammation) WBC count.</p></list-item><list-item id="u4825"><label>•</label><p id="p6130">TPP may be increased because of chronic inflammation caused by parasites or decreased as a result of protein loss through damaged intestinal mucosa.</p></list-item><list-item id="u4830"><label>•</label><p id="p6135">Abdominal fluid may be normal or contain an increased amount of total protein (>3.0 mg/dL), and the WBC count can be as high as 200,000 cells/µL.</p></list-item></list><boxed-text id="b0155"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0975"><title>Nonstrangulating Infarction</title><p id="p6140"><list list-type="simple" id="ulist0980"><list-item id="u4835"><label>•</label><p id="p6145">Balanced crystalloid intravenous fluids to correct dehydration and enhance reperfusion of the affected intestinal segments</p></list-item><list-item id="u4840"><label>•</label><p id="p6150">Maintain gastric decompression</p></list-item><list-item id="u4845"><label>•</label><p id="p6155">Broad-spectrum antimicrobial drugs, K<sup>+</sup> penicillin, 22,000 IU/kg IV q6h; gentamicin, 6.6 mg/kg IV q24h, if peritonitis is present</p></list-item><list-item id="u4850"><label>•</label><p id="p6160">Flunixin meglumine, 0.25 mg/kg IV q8h, to reduce thromboxane production and increase mesenteric perfusion</p></list-item><list-item id="u4855"><label>•</label><p id="p6165">DMSO 10% solution, 100 mg/kg IV q8-12h, to decrease superoxide radical injury during reperfusion</p></list-item><list-item id="u4860"><label>•</label><p id="p6170">Aspirin (20 mg/kg PO every other day) and fractionated heparin (40 to 100 IU/kg IV or SQ q6-12h) or preferably low-molecular-weight heparin (40 to 50 U/kg IM) to diminish and/or prevent thrombosis. Monitor the hematocrit closely for red blood cell agglutination and declining hematocrit resulting from nonfractionated heparin administration.</p></list-item><list-item id="u11100"><label>•</label><p id="p13460">Pentoxifylline (Trental), 7.5 to 10 mg/kg, PO, IV, q8-12h to treat endotoxemia, vasodilator and rheologic properties.</p></list-item><list-item id="u4865"><label>•</label><p id="p6175">Exploratory surgery for patients unresponsive to medical therapy</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s0980"><title>Prognosis</title><p id="p6180"><list list-type="simple" id="ulist0985"><list-item id="u4870"><label>•</label><p id="p6185">Prognosis is poor for patients that need surgery for intestinal resection.</p></list-item><list-item id="u4875"><label>•</label><p id="p6190">Ischemia that is <italic>not</italic> obvious at the time of exploratory surgery may progress to infarction.</p></list-item><list-item id="u4880"><label>•</label><p id="p6195">Ileus and adhesions are common postoperative complications.</p></list-item><list-item id="u4885"><label>•</label><p id="p6200">Large segments of affected intestine may be too extensive for resection.</p></list-item><list-item id="u4890"><label>•</label><p id="p6205">Identification and resection of diseased small- or large-intestinal segments sometimes is successful with fluorescein dye, Doppler ultrasonography, or surface oximetry to determine intestinal viability.</p></list-item></list></p></sec></sec><sec id="s0985"><title>Acute Ileus of the Small Intestine</title><p id="p6210"><list list-type="simple" id="ulist0990"><list-item id="u4895"><label>•</label><p id="p6215">Acute colic caused by ileus of the small intestine and stomach is occasionally seen, mostly in postparturient mares.</p></list-item><list-item id="u4900"><label>•</label><p id="p6220">Affected horses are generally very painful and both ultrasound and rectal examinations confirm small-intestinal distention without motility (ultrasound exam).</p></list-item><list-item id="u4905"><label>•</label><p id="p6225">Peritoneal fluid and blood lactate measurements are suggestive of a nonstrangulating lesion.</p></list-item><list-item id="u4910"><label>•</label><p id="p6230">Hypocalcemia may be the cause in some cases with demonstrated serum hypocalcemia; otherwise the cause of the disorder is unknown.</p></list-item></list><boxed-text id="b0160"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s0990"><title>Small-Intestinal Ileus in the Postparturient Mare</title><p id="p6235"><list list-type="simple" id="ulist0995"><list-item id="u4915"><label>•</label><p id="p6240">Pass a nasogastric tube to prevent gastric rupture.</p></list-item><list-item id="u4920"><label>•</label><p id="p6245">Provide intravenous fluids with calcium as required.</p></list-item><list-item id="u4925"><label>•</label><p id="p6250">Administer analgesics, preferably NSAIDs (which have minimal effect on intestinal motility) to control abdominal pain that can be severe.</p></list-item><list-item id="u4930"><label>•</label><p id="p6255">Administer lidocaine CRI.</p></list-item><list-item id="u4935"><label>•</label><p id="p6260">If severe colic continues and small-intestinal distention does not improve after the previous actions, surgical decompression may be required.</p></list-item><list-item id="u4940"><label>•</label><p id="p6265">Prognosis is good if appropriate treatment is begun before gastric rupture.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s0995"><title>Eosinophilic Enteritis Causing Intestinal Obstruction</title><p id="p6270"><list list-type="simple" id="ulist1000"><list-item id="u4945"><label>•</label><p id="p6275">There are several infiltrative or inflammatory bowel diseases (either small intestine or large intestine) of the horse.</p></list-item><list-item id="u4950"><label>•</label><p id="p6280">Eosinophilic infiltration is the most common one to cause colic and sometimes may cause focal obstruction of the small intestine or left dorsal colon.</p></list-item><list-item id="u4955"><label>•</label><p id="p6285">Diagnosis can occur based on histopathology of resected tissue taken at surgery, or based on response to corticosteroid treatment.</p></list-item><list-item id="u11120"><label>•</label><p id="p13475">Horses with focal lesions have been shown to also have eosinophilic infiltrates in the normal appearing intestine.</p></list-item></list></p></sec></sec><sec id="s1000"><title>Disorders of the Large Intestine</title><sec id="s1005"><title>Cecal Impaction</title><p id="p6295"><list list-type="simple" id="ulist1005"><list-item id="u4960"><label>•</label><p id="p6300">Cecal impaction generally occurs as the result of other diseases, especially those associated with:<list list-type="simple" id="ulist1010"><list-item id="u4965"><label>•</label><p id="p6305">Endotoxemia</p></list-item><list-item id="u4970"><label>•</label><p id="p6310">Surgery</p></list-item><list-item id="u4975"><label>•</label><p id="p6315">Chronic pain, secondary to septic metritis, infectious arthritis, fractures, and corneal disease</p></list-item><list-item id="u11105"><label>•</label><p id="p13465">Cecal impaction can also be a sequelae of stall rest in a horse previously in a high level of work.</p></list-item></list></p></list-item><list-item id="u4980"><label>•</label><p id="p6320">Most cases have large amounts of dry ingesta in the cecum (true impaction), whereas other cases have a large volume of fluid contents (cecal dysfunction).</p></list-item></list></p><sec id="s1010"><title>Diagnosis</title><sec id="s1015"><title>Clinical Findings</title><p id="p6325"><list list-type="simple" id="ulist1015"><list-item id="u4985"><label>•</label><p id="p6330">Anorexia</p></list-item><list-item id="u4990"><label>•</label><p id="p6335">Reduced fecal output or smaller than normal fecal balls</p></list-item><list-item id="u4995"><label>•</label><p id="p6340">Mild to severe abdominal pain</p></list-item><list-item id="u5000"><label>•</label><p id="p6345"><italic><bold>Practice Tip:</bold> Occasionally, there are few prodromal signs, such as only slight depression.</italic></p></list-item><list-item id="u5005"><label>•</label><p id="p6350">Abdominal distention may be present but is often absent.</p></list-item><list-item id="u11110"><label>•</label><p id="p13470">With severe impaction, abdominal auscultation reveals a high right-sided “cecal ping.”</p></list-item><list-item id="u5010"><label>•</label><p id="p6355">Heart rate varies with the severity of pain, and mucous membranes usually are pink and tacky.</p></list-item><list-item id="u5015"><label>•</label><p id="p6360">Nasogastric reflux is unusual unless the impaction is of prolonged duration or cecal dysfunction results in ileus of the small intestine.</p></list-item><list-item id="u5020"><label>•</label><p id="p6365">PCV, TPP, and creatinine levels are increased as a consequence of dehydration.</p></list-item><list-item id="u5025"><label>•</label><p id="p6370">In cases of cecal perforation, peritoneal total protein concentration and nucleated cell count are increased.</p></list-item><list-item id="u5030"><label>•</label><p id="p6375">The diagnosis is confirmed on rectal examination; the ventral cecal taenia is tight and displaced ventrally and medially. Dry ingesta are palpable in the body and base of the cecum, and moderate amounts of gas fill the base (<xref rid="f0305" ref-type="fig">Fig. 18-59</xref>). Cecal distention can make the dorsal and medial cecal taeniae readily palpable and leave the left colon and small colon empty.<fig id="f0305"><label>Figure 18-59</label><caption><p>Caudal view of the abdomen demonstrating cecal distention caused by a cecal impaction.</p></caption><graphic xlink:href="f018-059-9781455708925"></graphic></fig></p></list-item></list><boxed-text id="b0165"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1020"><title>Cecal Impaction</title><sec id="s1025"><title>Medical Management of Mild to Moderate Cecal Impaction</title><p id="p6380"><list list-type="simple" id="ulist1020"><list-item id="u5035"><label>•</label><p id="p6385">Give nothing by mouth ; water is fine if there is <italic>no</italic> gastric reflux.</p></list-item><list-item id="u5040"><label>•</label><p id="p6390">Administer three times the daily maintenance requirement of fluid (60 to 90 L/450 kg/day), balanced crystalloid solutions with 20 mEq/L KCl IV, and water orally to rehydrate the impaction: 6 to 8 L of water/500 kg q2h through an indwelling nasogastric tube. Administer intravenous lidocaine (1.3 mg/kg slow bolus followed by 0.05 mg/kg/min CRI) to enhance motility, especially for cecal dysfunction.</p></list-item><list-item id="u5045"><label>•</label><p id="p6395">Administer laxatives to facilitate rehydration of impacted material (see Laxatives, <xref rid="s0565" ref-type="sec">p. 190</xref>)</p></list-item><list-item id="u5050"><label>•</label><p id="p6400">Reintroduce feed slowly to avoid recurrence.</p></list-item><list-item id="u5055"><label>•</label><p id="p6405">Feed grass, water-soaked pellets, and bran mashes for the first 24 to 48 hours after feed is reintroduced.</p></list-item></list></p></sec><sec id="s1030"><title>Conditions Requiring Surgical Management</title><p id="p6410"><list list-type="simple" id="ulist1025"><list-item id="u5060"><label>•</label><p id="p6415">Uncontrollable pain</p></list-item><list-item id="u5065"><label>•</label><p id="p6420">Severe impaction (extremely tight medial cecal band)</p></list-item><list-item id="u5070"><label>•</label><p id="p6425">Unsuccessful medical therapy</p></list-item><list-item id="u5075"><label>•</label><p id="p6430">Characteristics of peritoneal fluid suggesting cecal compromise</p></list-item><list-item id="u5080"><label>•</label><p id="p6435">The surgical options through ventral midline celiotomy include the following:<list list-type="simple" id="ulist1030"><list-item id="u5085"><label>•</label><p id="p6440">Extraluminal massage</p></list-item><list-item id="u5090"><label>•</label><p id="p6445">Typhlotomy and evacuation (most commonly performed)</p></list-item><list-item id="u5095"><label>•</label><p id="p6450">Partial or complete typhlectomy</p></list-item><list-item id="u5100"><label>•</label><p id="p6455">Cecocolic anastomosis</p></list-item><list-item id="u5105"><label>•</label><p id="p6460">Ileocolic anastomosis</p></list-item><list-item id="u5110"><label>•</label><p id="p6465">Jejunocolic anastomosis</p></list-item></list></p></list-item></list></p><p id="p6470"><italic><bold>Practice Tip:</bold> Jejunocolic or ileocolic anastomosis is considered superior to cecocolic anastomosis because it has fewer long-term sequelae. Complete typhlectomy through a right paralumbar laparotomy is difficult, and fecal contamination of the abdomen is a complication.</italic></p></sec></sec></boxed-text></p></sec></sec><sec id="s1035"><title>Prognosis</title><p id="p6475"><list list-type="simple" id="ulist1035"><list-item id="u5115"><label>•</label><p id="p6480">Prognosis is good for patients with mild to moderate cecal impaction without underlying cecal dysfunction.</p></list-item><list-item id="u5120"><label>•</label><p id="p6485">Severe cecal impaction necessitating surgical treatment is complicated by peritonitis, adhesions, perforation, and death.</p></list-item><list-item id="u5125"><label>•</label><p id="p6490">The prognosis for severe impaction is guarded.</p></list-item></list></p><p id="p6495"><italic><bold>Important Note:</bold></italic> Cecal distention with “fluidy” contents may also occur and cause a similar clinical condition. This appears to be a primary motility disturbance and is often more troublesome than “dry” cecal impaction.</p></sec></sec><sec id="s1040"><title>Cecal Perforation</title><p id="p6500">The site is generally the medial or caudal surface of the base owing to excessive tension on the cecal wall as a result of severe impaction. Perforation also is associated with late gestation and parturition. The pathogenesis remains unknown; tapeworm <italic>(A. perfoliata)</italic> infestation has been implicated.</p><sec id="s1045"><title>Diagnosis</title><p id="p6505"><list list-type="simple" id="ulist1040"><list-item id="u5130"><label>•</label><p id="p6510">The horse has signs of cardiovascular shock resulting from septic peritonitis.</p></list-item><list-item id="u5135"><label>•</label><p id="p6515">The rate of deterioration is related directly to the degree of peritoneal contamination.</p></list-item><list-item id="u5140"><label>•</label><p id="p6520">Rectal examination reveals enlargement of the cecum with emphysema and roughening of the serosa of the cecal base.</p></list-item><list-item id="u5145"><label>•</label><p id="p6525">The peritoneal fluid, obtained with a teat cannula, has an increased or a decreased nucleated cell count and increased total protein concentration; degenerative WBCs and intracellular and extracellular bacteria and plant material are present.</p></list-item></list><boxed-text id="b0170"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1050"><title>Cecal Perforation—Symptomatic Only</title><p id="p6530"><list list-type="simple" id="ulist1045"><list-item id="u5150"><label>•</label><p id="p6535">Balanced, polyionic, intravenous fluids</p></list-item><list-item id="u5155"><label>•</label><p id="p6540">Broad-spectrum antimicrobial agents</p></list-item><list-item id="u5160"><label>•</label><p id="p6545">Flunixin meglumine</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1055"><title>Prognosis</title><p id="p6550">Prognosis is poor and may be grave if fecal contamination occurs due to resulting septic peritonitis and endotoxic shock.</p></sec></sec><sec id="s1060"><title>Large Colon Impaction</title><p id="p6555"><list list-type="simple" id="ulist1050"><list-item id="u5165"><label>•</label><p id="p6560">Large colon impaction most commonly occurs at two sites of narrowing:<list list-type="simple" id="ulist1055"><list-item id="u5170"><label>•</label><p id="p6565">Pelvic flexure</p></list-item><list-item id="u5175"><label>•</label><p id="p6570">Transverse colon</p></list-item></list></p></list-item><list-item id="u5180"><label>•</label><p id="p6575">At these locations, retropulsive contractions (propagation in an oral direction) retain ingesta for microbial digestion. These contractile patterns can contribute to impaction.</p></list-item></list></p><sec id="s1065"><title>Predisposing Factors</title><p id="p6580"><list list-type="simple" id="ulist1060"><list-item id="u5185"><label>•</label><p id="p6585">Poor dentition</p></list-item><list-item id="u5190"><label>•</label><p id="p6590">Ingestion of coarse roughage</p></list-item><list-item id="u5195"><label>•</label><p id="p6595">Inadequate fluid intake</p></list-item><list-item id="u5200"><label>•</label><p id="p6600">Stress associated with transportation</p></list-item><list-item id="u5205"><label>•</label><p id="p6605">Intense exercise resulting in hypomotility</p></list-item><list-item id="u5210"><label>•</label><p id="p6610">Inadequate water intake</p></list-item><list-item id="u5215"><label>•</label><p id="p6615">Excessive fluid loss through sweating</p></list-item></list></p></sec><sec id="s1070"><title>Diagnosis</title><sec id="s1075"><title>Clinical Findings</title><p id="p6620"><list list-type="simple" id="ulist1065"><list-item id="u5220"><label>•</label><p id="p6625">Anorexia</p></list-item><list-item id="u5225"><label>•</label><p id="p6630">Abdominal distention</p></list-item><list-item id="u5230"><label>•</label><p id="p6635">Decreased fecal output</p></list-item><list-item id="u5235"><label>•</label><p id="p6640">Mild, initially intermittent, to severe abdominal pain</p></list-item><list-item id="u5240"><label>•</label><p id="p6645">Heart rate varying with the degree of pain; pink and tacky mucous membranes</p></list-item><list-item id="u5245"><label>•</label><p id="p6650">Nasogastric reflux is uncommon unless ileus of the small intestine or compression of loops of small intestine occurs.</p></list-item><list-item id="u5250"><label>•</label><p id="p6655">PCV, TPP, and creatinine concentration are increased when clinical dehydration is present.</p></list-item><list-item id="u5255"><label>•</label><p id="p6660">With complete luminal obstruction, abdominal distention is significant.</p></list-item><list-item id="u5260"><label>•</label><p id="p6665">Rectal examination reveals impacted ingesta with varying degrees of distention of the pelvic flexure and ventral colon; in severe cases, the colon is palpable in the pelvic canal.</p></list-item><list-item id="u5265"><label>•</label><p id="p6670">Impaction in the transverse colon is <italic>not</italic> palpable.</p></list-item><list-item id="u5270"><label>•</label><p id="p6675">In chronic, severe cases, distention of the colonic wall can cause pressure necrosis of the intestinal wall and peritonitis. The peritoneal fluid protein level and nucleated cell count reflect intestinal compromise. Abdominal pain usually is severe and unrelenting, and signs of toxemia (hyperemia, cyanotic mucous membranes, or both), tachycardia, and tachypnea are apparent.</p></list-item></list><boxed-text id="b0175"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1080"><title>Large Colon Impaction</title><p id="p6680"><list list-type="simple" id="ulist1070"><list-item id="u5275"><label>•</label><p id="p6685">Withhold food to prevent continued accumulation of ingesta.</p></list-item><list-item id="u5280"><label>•</label><p id="p6690">Allow access to water if there is <italic>no</italic> nasogastric reflux.</p></list-item><list-item id="u5285"><label>•</label><p id="p6695">Provide medical management:<list list-type="simple" id="ulist1075"><list-item id="u5290"><label>•</label><p id="p6700">Patients with mild impaction respond to administration of water and mineral oil, magnesium sulfate (preferred), or DSS and electrolytes through a nasogastric tube.</p></list-item><list-item id="u5295"><label>•</label><p id="p6705">Intravenous fluids (4 to 5 L/h per 450 kg) and laxative therapy are needed for moderate to severe colon impaction.</p></list-item><list-item id="u5300"><label>•</label><p id="p6710">Administer analgesics as needed. N-butylscopolammonium bromide (Buscopan) is used successfully along with laxatives by many clinicians, although there remains some controversy with this treatment.</p></list-item></list></p></list-item><list-item id="u5305"><label>•</label><p id="p6715">Surgical decision based on the following:<list list-type="simple" id="ulist1080"><list-item id="u5310"><label>•</label><p id="p6720">Unsuccessful medical management</p></list-item><list-item id="u5315"><label>•</label><p id="p6725">Unrelenting abdominal pain</p></list-item><list-item id="u5320"><label>•</label><p id="p6730">Rectal examination that reveals large colon displacement</p></list-item><list-item id="u5325"><label>•</label><p id="p6735">Endotoxemia, cardiovascular deterioration</p></list-item><list-item id="u5330"><label>•</label><p id="p6740">Changes in peritoneal fluid indicating intestinal compromise</p></list-item></list></p></list-item><list-item id="u5335"><label>•</label><p id="p6745">Ventral midline exploratory celiotomy:<list list-type="simple" id="ulist1085"><list-item id="u5340"><label>•</label><p id="p6750">Defines extent of impaction</p></list-item><list-item id="u5345"><label>•</label><p id="p6755">May reveal other abnormalities: e.g., colon displacement, enterolith</p></list-item><list-item id="u5350"><label>•</label><p id="p6760">Perform a pelvic flexure enterotomy</p></list-item><list-item id="u5355"><label>•</label><p id="p6765">Lavage the lumen of colon to evacuate ingesta</p></list-item></list></p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1085"><title>Prognosis</title><p id="p6770"><list list-type="simple" id="ulist1090"><list-item id="u5360"><label>•</label><p id="p6775">Prognosis is good for medical management of mild-to-moderate severe large colon impaction.</p></list-item><list-item id="u5365"><label>•</label><p id="p6780">Prognosis is fair to good for surgical correction of severe impaction, unless necrosis of the intestinal wall or colonic devitalization results in intestinal perforation.</p></list-item></list></p></sec></sec><sec id="s1090"><title>Sand Impaction</title><p id="p6785"><list list-type="simple" id="ulist1095"><list-item id="u5370"><label>•</label><p id="p6790">Ingestion of sand while grazing or eating hay, or especially grain spillage on closely grazed pastures in areas with sandy soil, may result in sand impaction.</p></list-item><list-item id="u5375"><label>•</label><p id="p6795">The ingested sand settles in the large colon, where it accumulates and eventually results in a nonstrangulating luminal obstruction.</p></list-item></list></p><sec id="s1095"><title>Diagnosis</title><sec id="s1100"><title>Clinical Signs</title><p id="p6800"><list list-type="simple" id="ulist1100"><list-item id="u5380"><label>•</label><p id="p6805">Clinical signs are similar to those of large colon impaction; the signs of pain are frequently acute. The horse may have a history of chronic colic or diarrhea.</p></list-item><list-item id="u5385"><label>•</label><p id="p6810">Auscultation of the cranial ventral abdomen, for 4 to 5 minutes, may reveal a sound similar to an “ocean wave.”</p></list-item><list-item id="u5390"><label>•</label><p id="p6815">Sand may be palpated on rectal examination and found in feces placed in water; the ingesta floats in water, and the sand settles to the bottom of the container.</p></list-item><list-item id="u5395"><label>•</label><p id="p6820">The impaction is commonly palpable on rectal examination in the pelvic flexure or cecum, whereas impaction in the right dorsal (most common) or transverse colon is <italic>not</italic> palpable.</p></list-item><list-item id="u11125"><label>•</label><p id="p13480"><italic><bold>Practice Tip:</bold> The lack of sand found on rectal examination or in manure does not rule out a diagnosis of sand impaction, as in severe impactions no sand is moving aborally.</italic></p></list-item><list-item id="u5400"><label>•</label><p id="p6825"><italic><bold>Practice Tip:</bold> Abdominocentesis, if performed, should be done with extreme caution to avoid enterocentesis caused by the location of the sand-filled colon on the ventral abdominal floor.</italic></p></list-item><list-item id="u5405"><label>•</label><p id="p6830">Abdominal radiographs may be helpful. The radiographic pattern has been described by Kendall et al. (See online Bibliography for complete citation.) The irritating effect of the sand on the colonic mucosa can cause diarrhea or low-grade fever.</p></list-item><list-item id="u5410"><label>•</label><p id="p6835">Under the weight of the sand, degeneration and necrosis of the bowel wall can result in endotoxemia and peritonitis.</p></list-item></list><boxed-text id="b0180"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1105"><title>Sand Impaction</title><sec id="s1110"><title>Medical Management</title><p id="p6840"><list list-type="simple" id="ulist1105"><list-item id="u5415"><label>•</label><p id="p6845">Horse frequently responds to early administration of fluids and laxatives (mineral oil). Psyllium hydrophilic mucilloid (Metamucil) is the most effective laxative: 400 g/500 kg q6h until the impaction resolves. <italic><bold>Practice Tip:</bold> Once in contact with cold water, the mucilloid forms a gel that can be difficult to pump through a nasogastric tube; therefore, the tube must be in place and the mixture administered immediately. The gel lubricates and binds with the sand, moving it distally and relieving the obstruction</italic>. <italic>Alternatively, mixing the psyllium with mineral oil instead of water maintains the psyllium in solution, thereby facilitating easier administration by nasogastric tube.</italic></p></list-item><list-item id="u5420"><label>•</label><p id="p6850">Continue psyllium treatment at 400 g/500 kg once a day for 7 days to remove residual sand. Alternating psyllium and mineral oil may prevent obstruction associated with retrograde movement of sand and psyllium.</p></list-item></list></p></sec><sec id="s1115"><title>Surgical Management</title><p id="p6855"><list list-type="simple" id="ulist1110"><list-item id="u5425"><label>•</label><p id="p6860">Perform a ventral midline exploratory celiotomy for patients that do <italic>not</italic> respond to medical treatment or have other abnormalities, such as colonic displacement.</p></list-item><list-item id="u5430"><label>•</label><p id="p6865">Remove sand through a pelvic flexure enterotomy.</p></list-item><list-item id="u5435"><label>•</label><p id="p6870">Sand can cause extensive damage to the colonic wall, leading to postoperative complications such as postoperative ileus, intestinal wall degeneration, and peritonitis.</p></list-item></list></p></sec><sec id="s1120"><title>Preventive Management</title><p id="p6875"><list list-type="simple" id="ulist1115"><list-item id="u5440"><label>•</label><p id="p6880"><italic>Do not</italic> overgraze pastures.</p></list-item><list-item id="u5445"><label>•</label><p id="p6885">Provide a hay supplement when needed, and <italic>do not</italic> place feed on the ground.</p></list-item><list-item id="u5450"><label>•</label><p id="p6890">Add prophylactic psyllium treatment to feed to remove sand from the colon: Administer psyllium, 400 g/500 kg once a day for 7 days, for preventive treatment every 4 to 12 months, depending on sand exposure risk.</p></list-item><list-item id="u5460"><label>•</label><p id="p6900">Consider using flavored or soluble psyllium, which may be more palatable than unflavored forms.</p></list-item></list></p></sec></sec></boxed-text></p></sec></sec><sec id="s1125"><title>Prognosis</title><p id="p6905"><list list-type="simple" id="ulist1120"><list-item id="u5465"><label>•</label><p id="p6910">Prognosis is good for mild to moderately severe sand impaction.</p></list-item><list-item id="u5470"><label>•</label><p id="p6915">The surgical prognosis for severe sand impaction is good unless necrosis or devitalization of the intestinal wall results in rupture of the colon.</p></list-item></list></p></sec></sec><sec id="s1130"><title>Cecocolic Intussusception</title><p id="p6920"><list list-type="simple" id="ulist1125"><list-item id="u5475"><label>•</label><p id="p6925">Cecocolic intussusception is an unusual cause of intestinal obstruction that results from invagination of the apex of the cecum through the cecocolic orifice into the right ventral colon.</p></list-item><list-item id="u5480"><label>•</label><p id="p6930">The entire cecum can invaginate into the colon and become strangulated.</p></list-item><list-item id="u5485"><label>•</label><p id="p6935">The cause is unknown; however, conditions causing aberrant intestinal motility, such as parasite infestation, diet changes, impaction, mural lesions, and the presence of motility-altering drugs, have been implicated.</p></list-item><list-item id="u5490"><label>•</label><p id="p6940"><italic><bold>Practice Tip:</bold> Cecocolic intussusception is more common among horses younger than 3 years.</italic></p></list-item></list></p><sec id="s1135"><title>Diagnosis</title><p id="p6945"><list list-type="simple" id="ulist1130"><list-item id="u5495"><label>•</label><p id="p6950">Patients with strangulating intussusception may show signs of acute, severe abdominal pain.</p></list-item><list-item id="u5500"><label>•</label><p id="p6955">In contrast, affected horses with chronic nonstrangulating intussusception may have mild to moderate abdominal pain; depression; weight loss; and scant, soft feces.</p></list-item><list-item id="u5505"><label>•</label><p id="p6960">The intussusception is frequently palpable per rectum as a large mass in the right caudal abdomen; if the ileum is involved, distended small intestine is palpable.</p></list-item><list-item id="u5510"><label>•</label><p id="p6965">In some cases, the intussusception may be observed on ultrasound examination</p></list-item><list-item id="u5515"><label>•</label><p id="p6970">The presence of a firm mass palpable in the cecal base or the right ventral colon is confirmatory.</p></list-item><list-item id="u5520"><label>•</label><p id="p6975">Abdominocentesis reveals increases in peritoneal total protein and nucleated cell count. These changes may <italic>not</italic> be evident until late in the disease because the cecum is sequestered within the ventral colon.</p></list-item><list-item id="u5525"><label>•</label><p id="p6980">Failure to respond to medical therapy leads to exploratory surgery and a definitive diagnosis.</p></list-item></list><boxed-text id="b0185"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1140"><title>Cecocolic Intussusception</title><p id="p6985"><list list-type="simple" id="ulist1135"><list-item id="u5530"><label>•</label><p id="p6990">Perform a ventral midline exploratory celiotomy.</p></list-item><list-item id="u5535"><label>•</label><p id="p6995">Reduce the intussusception—this can be difficult because of mural edema and adhesions between the serosal surfaces.</p></list-item><list-item id="u5540"><label>•</label><p id="p7000">If extraluminal reduction is successful, assess cecal viability and, if required, perform complete or partial typhlectomy.</p></list-item><list-item id="u5545"><label>•</label><p id="p7005">Reduction and resection of the devitalized portion of cecum can be performed through an enterotomy in the right ventral colon if extraluminal reduction is impossible.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1145"><title>Prognosis</title><p id="p7010"><list list-type="simple" id="ulist1140"><list-item id="u5550"><label>•</label><p id="p7015">Prognosis is fair if the apex of the cecum is involved and extraluminal reduction is possible.</p></list-item><list-item id="u5555"><label>•</label><p id="p7020">Prognosis is poor if reduction requires enterotomy or the entire cecum is involved due to the risk of septic peritonitis.</p></list-item></list></p></sec></sec><sec id="s1150"><title>Large Colon Displacement</title><p id="p7025"><list list-type="simple" id="ulist1145"><list-item id="u5560"><label>•</label><p id="p7030">The left ventral and dorsal colons are freely movable, allowing for intestinal displacement and volvulus.</p></list-item><list-item id="u5565"><label>•</label><p id="p7035">The cause is unknown, with the following implicated:<list list-type="simple" id="ulist1150"><list-item id="u5570"><label>•</label><p id="p7040">Alterations in colonic motility</p></list-item><list-item id="u5575"><label>•</label><p id="p7045">Excessive gas production</p></list-item><list-item id="u5580"><label>•</label><p id="p7050">Rolling resulting from abdominal pain or dietary changes</p></list-item><list-item id="u5585"><label>•</label><p id="p7055">Excessive concentrate intake</p></list-item><list-item id="u5590"><label>•</label><p id="p7060">Grazing lush pastures</p></list-item><list-item id="u5595"><label>•</label><p id="p7065">Parasite infestation</p></list-item></list></p></list-item><list-item id="u5600"><label>•</label><p id="p7070">Generally, <italic>no</italic> causative factor is identified.</p></list-item><list-item id="u5605"><label>•</label><p id="p7075"><italic><bold>Practice Tip:</bold> Large colon displacement is more common in geldings.</italic></p></list-item><list-item id="u5610"><label>•</label><p id="p7080">Right dorsal displacement of the colon is displacement of the left colon lateral to the cecum between the cecum and the right body wall (<xref rid="f0310" ref-type="fig">Fig. 18-60</xref>). The pelvic flexure commonly moves lateral to the cecum, in a cranial to caudal direction, and rests at the sternum. Displacement may be accompanied by a variable degree of volvulus.<fig id="f0310"><label>Figure 18-60</label><caption><p><bold>A,</bold> View of an early stage in the development of right displacement of the colon. The colon has begun to move caudally ventral to the cecum. <bold>B,</bold> Final stage of right displacement of the colon in which the colon is positioned caudal to the cecum and has rotated such that the ventral colon is dorsal and the dorsal colon is ventral.</p></caption><graphic xlink:href="f018-060a-9781455708925"></graphic><graphic xlink:href="f018-060b-9781455708925"></graphic></fig></p></list-item><list-item id="u5615"><label>•</label><p id="p7085">Left dorsal displacement of the colon is a displacement of the left colon to a position between the dorsal body wall and the nephrosplenic (renosplenic) ligament (<xref rid="f0315" ref-type="fig">Fig. 18-61</xref>). The large colon is hypothesized to pass through the nephrosplenic space from a cranial to caudal direction or migrates dorsally, lateral to the spleen.<fig id="f0315"><label>Figure 18-61</label><caption><p><bold>A,</bold> View from the left side of the horse with the ascending colon in its normal position. <bold>B,</bold> Displacement of the ascending colon over the dorsal edge of the spleen, with rotation of the colon on its long axis. <bold>C,</bold> A final stage in displacement of the colon over the nephrosplenic ligament. Weight of the displaced colon borne by the ligament impedes venous blood flow from the spleen, thereby causing the spleen to engorge. <bold>D,</bold> Caudal view of the final stage of the displacement, with the colon entrapped over the nephrosplenic ligament and engorgement of the spleen.</p></caption><graphic xlink:href="f018-061a-9781455708925"></graphic><graphic xlink:href="f018-061b-9781455708925"></graphic><graphic xlink:href="f018-061c-9781455708925"></graphic><graphic xlink:href="f018-061d-9781455708925"></graphic></fig></p></list-item></list></p><sec id="s1155"><title>Diagnosis</title><sec id="s1160"><title>Clinical Signs</title><p id="p7090"><list list-type="simple" id="ulist1155"><list-item id="u5620"><label>•</label><p id="p7095">Signs include abdominal pain and abdominal distention, the severity of which depends on the duration and amount of colonic tympany. The signs generally develop rapidly and are more severe than with impaction because of tension on the mesentery and greater colonic tympany.</p></list-item><list-item id="u5625"><label>•</label><p id="p7100">The displacement may occasionally place pressure on the duodenum and cause nasogastric reflux.</p></list-item><list-item id="u5630"><label>•</label><p id="p7105">Peritoneal fluid usually is normal in the early stages of displacement; with chronic displacement, the amount of peritoneal fluid, total protein, and nucleated cell count may be increased.</p></list-item><list-item id="u5635"><label>•</label><p id="p7110">Right dorsal displacement is characterized on rectal palpation by mild to severe gas distention of the cecum, colon, or both, with large colon taeniae palpable lateral to the cecum or horizontally crossing the pelvic inlet (see <xref rid="f0255" ref-type="fig">Fig. 18-49</xref>).</p></list-item><list-item id="u5640"><label>•</label><p id="p7115"><italic><bold>Practice Tip:</bold> Gamma-glutamyltransferase and direct bilirubin may be greatly increased with right dorsal displacement because of biliary obstruction. For other gastrointestinal (GI) displacements to cause these changes is unusual.</italic></p></list-item><list-item id="u5645"><label>•</label><p id="p7120">Ultrasound examination of the mid to lower right abdomen in horses with right dorsal displacement may reveal distended vessels within the displaced and rotated right colon (see Chapter 14, p. 86).</p></list-item><list-item id="u5650"><label>•</label><p id="p7125">Left dorsal displacement is characterized on rectal palpation by mild to severe gas distention of the cecum, colon, or both, with palpable large-colon taeniae coursing cranially and to the left, dorsal to the nephrosplenic ligament.</p></list-item><list-item id="u5655"><label>•</label><p id="p7130">Signs of pain are elicited when the nephrosplenic area is palpated per rectum and the spleen is displaced caudally, away from the left body wall because of tension on the ligament.</p></list-item><list-item id="u5660"><label>•</label><p id="p7135">Ultrasound examination of the upper left abdomen in horses with left dorsal displacement reveals colonic gas such that the left kidney and dorsal edge of the spleen <italic>cannot</italic> be visualized. If the colon is rotated slightly, mesenteric vessels may be seen (see Chapter 14, p. 87).</p></list-item><list-item id="u5665"><label>•</label><p id="p7140">Several loops of moderately distended small intestine may be palpable if the small intestine is involved secondarily.</p></list-item><list-item id="u5670"><label>•</label><p id="p7145">Decompression of the stomach and cecum provides temporary pain relief.</p></list-item></list></p></sec></sec><sec id="s1190"><title>Prevention of Reccurence</title><p id="p7290">Surgical prophylactic procedures are recommended in horses with recurrent left dorsal displacement (two or more occurrences):<list list-type="simple" id="ulist1190"><list-item id="u5795"><label>•</label><p id="p7295">Colopexy or partial resection of the large colon at the time of the initial celiotomy</p></list-item><list-item id="u5800"><label>•</label><p id="p7300">Standing laparoscopic ablation of the nephrosplenic space with suture or mesh at a subsequent surgery</p></list-item></list></p></sec><sec id="s1195"><title>Prognosis</title><p id="p7305">Prognosis is good to excellent for complete recovery. The incidence of adhesions and laminitis with large colon displacement is low.<boxed-text id="b0190"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1165"><title>Large Colon Displacement</title><sec id="s1170"><title>Right Dorsal Displacement</title><p id="p7150"><list list-type="simple" id="ulist1160"><list-item id="u5675"><label>•</label><p id="p7155">If abdominal pain is <italic>not</italic> severe, withhold feed and administer, to an adult horse, 6 L q4h of electrolyte solution by nasogastric tube; correction may occur in 24 to 36 hours.</p></list-item><list-item id="u5680"><label>•</label><p id="p7160">Ventral midline exploratory celiotomy if surgical exploration is indicated (see Box 18-2)</p></list-item><list-item id="u5685"><label>•</label><p id="p7165">Examine the colon for volvulus and correction of the displacement.</p></list-item><list-item id="u5690"><label>•</label><p id="p7170">Enterotomy is not always necessary and is at the surgeon’s discretion. If the colon is secondarily impacted, an enterotomy is recommended.</p></list-item></list></p></sec><sec id="s1175"><title>Left Dorsal Displacement: Nonsurgical Correction</title><p id="p7175"><list list-type="simple" id="ulist1165"><list-item id="u5695"><label>•</label><p id="p7180">The two most common nonsurgical methods are oral fluids and withholding feed as described earlier or to administer phenylephrine (8 to 16 mg/450 kg in 1 L of 0.9% sodium chloride slowly IV over 15 minutes):<list list-type="simple" id="ulist1170"><list-item id="u5700"><label>•</label><p id="p7185">To contract the spleen</p></list-item><list-item id="u5705"><label>•</label><p id="p7190">Follow the phenylephrine with light exercise for 5 to 10 minutes</p></list-item><list-item id="u5710"><label>•</label><p id="p7195">Repeat a rectal examination</p></list-item><list-item id="u5715"><label>•</label><p id="p7200">Repeat ultrasound examination to confirm the abnormality is corrected.</p></list-item></list></p></list-item><list-item id="u5720"><label>•</label><p id="p7205"><italic><bold>Practice Tip:</bold> Do not use the phenylephrine treatment protocol for severely volume-depleted patients, those with cardiovascular instability, or horses more than 16 years of age</italic>. Significant pressor effect and reflex bradycardia may cause severe hypoperfusion in severely dehydrated horses. In aged horses, phenylephrine administration may result in significant internal hemorrhaging.</p></list-item><list-item id="u5725"><label>•</label><p id="p7210">If unsuccessful, the phenylephrine treatment may be repeated several times and is reported to have a success rate of 70% to 90% in patients with a stable cardiovascular system and without severe colonic distention or devitalization.</p></list-item><list-item id="u5730"><label>•</label><p id="p7215">Proper rolling procedure (<xref rid="f0320" ref-type="fig">Fig. 18-62</xref>):<list list-type="simple" id="ulist1175"><list-item id="u5735"><label>•</label><p id="p7220">Administer general anesthesia with the patient positioned in right lateral recumbency.</p></list-item><list-item id="u5740"><label>•</label><p id="p7225">Place hobbles on the pelvic limbs, and position the patient in dorsal recumbency.</p></list-item><list-item id="u5745"><label>•</label><p id="p7230">Lift the pelvic limbs to raise the hind end of the patient off the ground; vigorously perform ballottement of the abdomen.</p></list-item><list-item id="u5750"><label>•</label><p id="p7235">The large colon falls cranially and to the right.</p></list-item><list-item id="u11130"><label>•</label><p id="p13485">The 360 rotation is completed by rolling the patient into sternal recumbency and then back to right lateral recumbency.</p></list-item><list-item id="u5755"><label>•</label><p id="p7240">When in right lateral recumbency, the colon should rest in a position medial and ventral to the spleen. Allow the horse to recover.</p></list-item><list-item id="u5760"><label>•</label><p id="p7245">Rectal palpation is performed to assess the position of the colon with the patient in lateral recumbency or after recovery.</p></list-item></list><fig id="f0320"><label>Figure 18-62</label><caption><p>Nonsurgical correction of a left dorsal displacement of the large colon. <bold>A,</bold> Caudal view of the standing horse with the left ventral and dorsal colons entrapped over the nephrosplenic ligament. <bold>B,</bold> The patient is anesthetized and placed in right lateral recumbency. <bold>C,</bold> Hobbles are placed on the pelvic limbs, and the patient is positioned in dorsal recumbency; the pelvic limbs are lifted to raise the hind end off the ground; the large colon falls cranially, lateral, and to the right <italic>(arrow).</italic><bold>D,</bold> The patient is then positioned in left lateral recumbency; this allows the colon to continue to fall ventral and lateral to the spleen <italic>(arrow).</italic><bold>E,</bold> The 360-degree rotation is then completed by rolling the patient into sternal recumbency (not shown) and then back to right lateral recumbency, with the colon coming to rest in a position medial to the spleen. <bold>F,</bold> The patient is allowed to recover; if the procedure is successful, the colon assumes a position ventral and medial to the spleen. Rectal palpation is performed to assess the position of the colon.</p></caption><graphic xlink:href="f018-062a-9781455708925"></graphic><graphic xlink:href="f018-062b-9781455708925"></graphic><graphic xlink:href="f018-062c-9781455708925"></graphic><graphic xlink:href="f018-062d-9781455708925"></graphic><graphic xlink:href="f018-062e-9781455708925"></graphic><graphic xlink:href="f018-062f-9781455708925"></graphic></fig></p></list-item></list></p></sec><sec id="s1180"><title>Potential Complications of Nonsurgical Correction (Rolling)</title><p id="p7250"><list list-type="simple" id="ulist1180"><list-item id="u5765"><label>•</label><p id="p7255">Worsening or recurrence of displacement</p></list-item><list-item id="u5770"><label>•</label><p id="p7260">Iatrogenic colonic or cecal volvulus, splenic vessel rupture, and internal hemorrhage</p></list-item><list-item id="u5775"><label>•</label><p id="p7265">Cecal or colonic rupture</p></list-item></list></p></sec><sec id="s1185"><title>Left Dorsal Displacement</title><p id="p7270">Surgical correction is performed in the following cases:<list list-type="simple" id="ulist1185"><list-item id="u5780"><label>•</label><p id="p7275">Marked colonic distention with persistent and severe pain</p></list-item><list-item id="u5785"><label>•</label><p id="p7280">Evidence of intestinal devitalization is found during peritoneal fluid analysis.</p></list-item><list-item id="u5790"><label>•</label><p id="p7285">Increased risk is present for colonic or cecal rupture and the resulting fatal peritonitis.</p></list-item></list></p></sec></sec></boxed-text></p></sec></sec><sec id="s1200"><title>Large Colon Volvulus</title><p id="p7310"><list list-type="simple" id="ulist1195"><list-item id="u5805"><label>•</label><p id="p7315">Large colon volvulus is rotation of the ventral and dorsal colons on their long axes and frequently includes the cecum.</p></list-item><list-item id="u5810"><label>•</label><p id="p7320">Viewing the left ventral and dorsal colon from behind, or with the horse in dorsal recumbency, the colons usually twist in a counterclockwise direction (<xref rid="f0325" ref-type="fig">Fig. 18-63</xref>).<fig id="f0325"><label>Figure 18-63</label><caption><p>Large colon volvulus. <bold>A,</bold> Ventral view of a horse in dorsal recumbency with a 360-degree <italic>counterclockwise (arrow)</italic> volvulus of the large colon. <bold>B,</bold> Right lateral view of a horse in dorsal recumbency with 180-degree counterclockwise <italic>(arrow)</italic> volvulus of the large colon.</p></caption><graphic xlink:href="f018-063ab-9781455708925"></graphic></fig></p></list-item><list-item id="u5815"><label>•</label><p id="p7325">The large colon and cecum can rotate on the vertical axis of the mesentery (volvulus).</p></list-item><list-item id="u5820"><label>•</label><p id="p7330">Rotation of 360 degrees causes the colon to lie in an apparently normal position with the mesenteric root occluded.</p></list-item><list-item id="u5825"><label>•</label><p id="p7335"><bold><italic>Practice Tip:</italic></bold><italic>Large colon volvulus is one of the most severe acute abdominal emergencies in horses.</italic></p></list-item><list-item id="u5830"><label>•</label><p id="p7340">The cause is unknown, but hypomotility caused by dietary changes, electrolyte imbalances, and stress can predispose the colon to excessive gas accumulation and volvulus.</p></list-item><list-item id="u5835"><label>•</label><p id="p7345">A higher incidence of colonic volvulus occurs among periparturient mares.</p></list-item><list-item id="u5840"><label>•</label><p id="p7350">Large colon volvulus recurs in 20% to 30% of corrected cases.</p></list-item></list></p><sec id="s1205"><title>Diagnosis</title><p id="p7355"><list list-type="simple" id="ulist1200"><list-item id="u5845"><label>•</label><p id="p7360">Colonic volvulus (>180 degrees) causes an acute onset of severe abdominal distention and continuous abdominal pain only mildly responsive to or refractory to analgesic therapy. Xylazine or detomidine alone or in combination with butorphanol provides transient pain relief.</p></list-item><list-item id="u5850"><label>•</label><p id="p7365">Tachycardia, tachypnea, and blanched or congested mucous membranes are usually clinically evident.</p></list-item><list-item id="u5855"><label>•</label><p id="p7370">Respiratory acidosis can develop if colonic distention impairs normal respiratory function.</p></list-item><list-item id="u5860"><label>•</label><p id="p7375">Serosanguineous peritoneal fluid with an increased total protein concentration and nucleated cell count reflect the presence of intestinal ischemia and necrosis.</p></list-item><list-item id="u5865"><label>•</label><p id="p7380">Rectal palpation reveals severe colonic distention, frequently accompanied by mural and mesenteric edema resulting from venous congestion. Taeniae traversing the abdomen may be palpable, but a comprehensive rectal examination is frequently impossible because of the considerable colonic distention and degree of pain.</p></list-item><list-item id="u5870"><label>•</label><p id="p7385">Rotations (twists) between 180 degrees and 270 degrees may manifest as moderate pain only and slow deterioration.</p></list-item></list><boxed-text id="b0195"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1210"><title>Large Colon Volvulus</title><p id="p7390"><list list-type="simple" id="ulist1205"><list-item id="u5875"><label>•</label><p id="p7395">Successful treatment requires early diagnosis and emergency surgical correction.</p></list-item><list-item id="u5880"><label>•</label><p id="p7400">Ventral midline exploratory celiotomy is performed.</p></list-item><list-item id="u5885"><label>•</label><p id="p7405">Decompression and enterotomy often are necessary to facilitate correction.</p></list-item><list-item id="u5890"><label>•</label><p id="p7410">Affected colon typically appears bluish gray initially and becomes red to black after reperfusion.</p></list-item><list-item id="u5895"><label>•</label><p id="p7415">Nonviable colon requires resection or humane destruction of the horse.</p></list-item><list-item id="u5900"><label>•</label><p id="p7420">Up to 95% of the ascending colon may be resected without adversely affecting colonic function.</p></list-item><list-item id="u5905"><label>•</label><p id="p7425">Plasma, DMSO, and heparin may be useful in attenuating “reperfusion injury.”</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1215"><title>Prevention of Recurrence</title><p id="p7430"><list list-type="simple" id="ulist1210"><list-item id="u5910"><label>•</label><p id="p7435">In brood mares or nonperformance horses, colopexy, or suturing the lateral taenia of the left ventral colon to the abdominal wall, is performed by some surgeons to reduce the risk of recurrence.</p></list-item><list-item id="u5915"><label>•</label><p id="p7440">Tearing of the adhesion, suture failure, and colonic rupture are reported complications of this procedure.</p></list-item><list-item id="u5920"><label>•</label><p id="p7445"><italic><bold>Practice Tip:</bold> Elective colonic resection is performed to minimize the likelihood of recurrence; this procedure is preferred for performance athletes.</italic></p></list-item></list></p></sec><sec id="s1220"><title>Prognosis</title><p id="p7450"><list list-type="simple" id="ulist1215"><list-item id="u5925"><label>•</label><p id="p7455">Prognosis depends on early diagnosis and surgical intervention.</p></list-item><list-item id="u5930"><label>•</label><p id="p7460">Intestinal ischemia and necrosis rapidly progress to hypovolemia, endotoxemia, peritonitis, and irreversible shock.</p></list-item><list-item id="u5935"><label>•</label><p id="p7465">The prognosis is poor unless surgery is performed within a few hours of the onset of clinical signs.</p></list-item><list-item id="u5940"><label>•</label><p id="p7470">In some patients, postoperative absorptive dysfunction, diarrhea, and protein-losing enteropathy occur and may be short-lived or permanent.</p></list-item></list></p></sec></sec><sec id="s1225"><title>Atresia Coli</title><p id="p7475"><list list-type="simple" id="ulist1220"><list-item id="u5945"><label>•</label><p id="p7480">Atresia coli is congenital absence or closure of a portion of the intestine. It manifests in three forms:<list list-type="simple" id="ulist1225"><list-item id="u5950"><label>•</label><p id="p7485">Membrane atresia: A tissue diaphragm occludes the lumen of the colon or rectum.</p></list-item><list-item id="u5955"><label>•</label><p id="p7490">Cord atresia: A fibrous cord connects the noncommunicating ends of the colon.</p></list-item><list-item id="u5960"><label>•</label><p id="p7495">Blind-end atresia: The most common type; there is <italic>no</italic> connection or mesentery between noncommunicating ends of colon.</p></list-item></list></p></list-item><list-item id="u5965"><label>•</label><p id="p7500">Atresia coli results from ischemia of the affected segment during development; the condition is believed to be hereditary.</p></list-item><list-item id="u5970"><label>•</label><p id="p7505">Lethal white foal disease is an autosomal recessive pigmentary disorder in which newborn paint foals have albinism coupled with congenital defects of the intestinal tract, most commonly atresia coli. These defects are <italic>not</italic> compatible with life.</p></list-item></list></p><sec id="s1230"><title>Diagnosis</title><p id="p7510"><list list-type="simple" id="ulist1230"><list-item id="u5975"><label>•</label><p id="p7515">Abdominal pain in the newborn during the first 12 to 24 hours of life and lack of meconium stool are the first signs.</p></list-item><list-item id="u5980"><label>•</label><p id="p7520">Digital palpation of the rectum reveals mucus and no meconium.</p></list-item><list-item id="u5985"><label>•</label><p id="p7525">Abdominal radiography may reveal an enlarged segment of colon with no obvious obstruction; contrast radiography is needed to confirm the diagnosis.</p></list-item><list-item id="u5990"><label>•</label><p id="p7530">Abdominal distention and pain are indications for surgical exploration.</p></list-item><list-item id="u5995"><label>•</label><p id="p7535">Meconium impaction is the primary condition to rule out (see Disorders of the Small Colon and Rectum, in the following section).</p></list-item></list><boxed-text id="b0200"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1235"><title>Atresia Coli</title><p id="p7540"><list list-type="simple" id="ulist1235"><list-item id="u6000"><label>•</label><p id="p7545">Surgical correction is the only treatment.</p></list-item><list-item id="u6005"><label>•</label><p id="p7550">Ventral midline exploratory celiotomy is performed.</p></list-item><list-item id="u6010"><label>•</label><p id="p7555">The distance and size disparity between the affected bowel segments make anastomosis difficult.</p></list-item><list-item id="u6015"><label>•</label><p id="p7560">The aboral segment often is too small for end-to-end anastomosis. Side-to-side anastomosis may be needed but often is <italic>not</italic> possible because of the excessive distance between the proximal and distal intestinal segments; therefore, euthanasia is recommended.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1240"><title>Prognosis</title><p id="p7565">Prognosis is guarded because of the difficult technical aspects of performing the anastomosis in this part of the intestine.</p></sec></sec><sec id="s1245"><title>Nonstrangulating Infarction</title><p id="p7570">See Disorders of the Small Intestine, <xref rid="s0585" ref-type="sec">p. 191</xref>.</p></sec><sec id="s1250"><title>Ulcerative Colitis (NSAID Toxicity)</title><p id="p7575">See <xref rid="s1920" ref-type="sec">p. 232</xref> and Appendix 6, p. 823.</p></sec></sec><sec id="s1255"><title>Disorders of the Small Colon and Rectum</title><sec id="s1260"><title>Small Colon Impaction and Foreign Body Obstruction</title><p id="p7580"><list list-type="simple" id="ulist1240"><list-item id="u11115"><label>•</label><p id="p6290">Inflammatory bowel disease frequently predisposes the colon, especially the small colon, to impaction and may be associated with positive fecal cultures for <italic>Salmonella</italic> organisms. In many cases, a predisposing factor is never identified.</p></list-item><list-item id="u6020"><label>•</label><p id="p7585">Dehydration of fecal matter can cause impaction of the small colon, and a foreign body or an enterolith (see <xref rid="s1285" ref-type="sec">Enterolithiasis</xref>, <xref rid="s9020" ref-type="sec">p. 212</xref>) can cause an obstruction.</p></list-item><list-item id="u6025"><label>•</label><p id="p7590">Complete obstruction causes severe abdominal pain; tympany and secondary ileus of the proximal small and large colons result from the obstruction.</p></list-item></list></p><sec id="s9020"><title>Diagnosis</title><p id="p13490"><list list-type="simple" id="ulist9045"><list-item id="u6030"><label>•</label><p id="p7595">The diagnosis is confirmed on rectal examination with palpation of the impaction or gas-distended loops of small colon. The small colon is identified on rectal examination by its characteristic single, wideband on the antimesenteric surface and ropelike mesenteric band.</p></list-item><list-item id="u6035"><label>•</label><p id="p7600">Foreignbody impaction occurs more commonly among horses younger than 4 years of age because they are curious. For example, they eat portions of hay nets, rubber fencing, bits of rope, and string.</p></list-item><list-item id="u6040"><label>•</label><p id="p7605">Impaction is sometimes accompanied by inflammatory bowel disease, such as salmonellosis.</p></list-item><list-item id="u6045"><label>•</label><p id="p7610">If impactions are recurring, myenteric ganglionitis should be considered.</p></list-item><list-item id="u6050"><label>•</label><p id="p7615"><bold><italic>Practice Tip:</italic></bold><italic>Small colon impaction is common among miniature horses and is generally</italic> not <italic>associated with an inflammatory/infectious disease.</italic></p></list-item></list><boxed-text id="b0205"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1265"><title>Small Colon Impaction and Foreign Body Obstruction</title><sec id="s1270"><title>Medical Management</title><p id="p7620"><list list-type="simple" id="ulist1245"><list-item id="u6055"><label>•</label><p id="p7625">Analgesics</p></list-item><list-item id="u6060"><label>•</label><p id="p7630">Large volumes of balanced, polyionic intravenous fluid</p></list-item><list-item id="u6065"><label>•</label><p id="p7635">6 to 8 L of water or magnesium sulfate in water q2h through an indwelling nasogastric tube if <italic>no</italic> gastric reflux is recovered</p></list-item><list-item id="u6070"><label>•</label><p id="p7640">Warm water enemas or gravity administered (by soft tube) electrolyte solution to soften the fecal material</p></list-item><list-item id="u6075"><label>•</label><p id="p7645">Misoprostil (2.5 to 5 µg/kg PO, q12-24h) has been used to increase perfusion to the bowel and fluid secretion into the colon in cases where surgery is <italic>not</italic> an option. Do <italic>not</italic> administer to pregnant mares; pregnant women should not handle the drug.</p></list-item><list-item id="u11135"><label>•</label><p id="p7650"><italic><bold>Caution:</bold></italic> Use extreme care to prevent rectal perforation during administration of enemas.</p></list-item></list></p></sec><sec id="s1275"><title>Surgical Management</title><p id="p7655"><list list-type="simple" id="ulist1250"><list-item id="u6080"><label>•</label><p id="p7660">Needed with unrelenting pain, severe gas distention, or failure of medical treatment</p></list-item><list-item id="u6085"><label>•</label><p id="p7665">Perform a ventral midline exploratory celiotomy.</p></list-item><list-item id="u6090"><label>•</label><p id="p7670">Use enemas and extraluminal massage of the small colon to break down the impaction.</p></list-item><list-item id="u6095"><label>•</label><p id="p7675">Perform an enterotomy to remove a foreign body or enterolith.</p></list-item><list-item id="u6100"><label>•</label><p id="p7680">Perform pelvic flexure enterotomy and evacuation of large colon ingesta</p></list-item><list-item id="u6105"><label>•</label><p id="p7685">Patients with small colon impaction frequently have culture results positive for <italic>Salmonella</italic> organisms. The condition of these horses can become endotoxic with secondary laminitis, peritonitis, and adhesions. The role of <italic>Salmonella</italic> infection in the development of the impaction is unknown.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s1280"><title>Prognosis</title><p id="p7690"><list list-type="simple" id="ulist1255"><list-item id="u6110"><label>•</label><p id="p7695">Prognosis is fair to good for patients with foreign body obstruction or simple impaction of the small colon.</p></list-item><list-item id="u6115"><label>•</label><p id="p7700">Prognosis is guarded if the culture result for <italic>Salmonella</italic> organisms is positive.</p></list-item><list-item id="u6120"><label>•</label><p id="p7705">Rectal examination of horses with small colon impaction presents greater risk of iatrogenic perforation.</p></list-item></list></p></sec></sec><sec id="s1285"><title>Enterolithiasis</title><p id="p7710"><list list-type="simple" id="ulist1260"><list-item id="u6125"><label>•</label><p id="p7715">Enteroliths are concretions of magnesium and ammonium phosphate crystals deposited around a nidus, frequently a piece of wire, stone, or nail.</p></list-item><list-item id="u6130"><label>•</label><p id="p7720">There may be one or multiple concretions, and they do <italic>not</italic> cause a surgical problem until they become lodged in the transverse or small colon (<xref rid="f0330" ref-type="fig">Fig. 18-64</xref>).<fig id="f0330"><label>Figure 18-64</label><caption><p>Obstruction of the descending colon by a polyhedral-shaped enterolith. Note the presence of an additional enterolith in the lumen of the right dorsal colon. The wall of the colon has been rendered transparent to facilitate visualization of the enteroliths.</p></caption><graphic xlink:href="f018-064-9781455708925"></graphic></fig></p></list-item><list-item id="u6135"><label>•</label><p id="p7725">The specific geographic distribution of the condition—California, Florida, Indiana—has led to speculation that undetermined constituents of the soil and water in these areas may be inciting causes.</p></list-item><list-item id="u6140"><label>•</label><p id="p7730"><italic><bold>Practice Tip:</bold> Enterolithiasis is seen most commonly in middle-aged horses (5 to 10 years of age), and the condition is overrepresented in Arabians and miniature horses.</italic></p></list-item></list></p><sec id="s1290"><title>Diagnosis</title><p id="p7735"><list list-type="simple" id="ulist1265"><list-item id="u6145"><label>•</label><p id="p7740">Affected horses may have a history of chronic weight loss and recurring acute bouts of mild to moderate abdominal pain or acute, severe abdominal distention and pain with <italic>no</italic> history of colic.</p></list-item><list-item id="u6150"><label>•</label><p id="p7745">The obstruction most commonly is at the proximal small colon or transverse colon. Smaller enteroliths can be located distally in the small colon. When the obstruction is complete, pain is severe, and distention of the colon is considerable.</p></list-item><list-item id="u6155"><label>•</label><p id="p7750">With complete obstruction, heart and respiratory rates are increased, and mucous membranes are pink.</p></list-item><list-item id="u6160"><label>•</label><p id="p7755">Rectal examination reveals colonic and cecal distention.</p></list-item><list-item id="u6165"><label>•</label><p id="p7760">Peritoneal fluid is generally normal unless the wall of the colon is compromised.</p></list-item><list-item id="u6170"><label>•</label><p id="p7765">Abdominal radiography may confirm the diagnosis of enterolithiasis, but in the field, imaging can be performed only on miniature horses.</p></list-item><list-item id="u6175"><label>•</label><p id="p7770">Patients with chronic enterolithiasis often have concurrent gastric ulcers, which can confound the diagnosis.</p></list-item></list><boxed-text id="b0210"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1295"><title>Enterolithiasis</title><p id="p7775"><list list-type="simple" id="ulist1270"><list-item id="u6180"><label>•</label><p id="p7780">Perform ventral midline exploratory celiotomy.</p></list-item><list-item id="u6185"><label>•</label><p id="p7785">Decompress the distended colon and cecum.</p></list-item><list-item id="u6190"><label>•</label><p id="p7790">Remove small, freely movable enteroliths through a pelvic flexure enterotomy.</p></list-item><list-item id="u6195"><label>•</label><p id="p7795">Remove large enteroliths in the transverse colon and proximal small colon through a large colon enterotomy at the diaphragmatic flexure.</p></list-item><list-item id="u6200"><label>•</label><p id="p7800"><italic><bold>Practice Tip:</bold> If an enterolith has a polyhedral shape, multiple enteroliths are present</italic>.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1300"><title>Prognosis</title><p id="p7805">Prognosis is good; the survival rate is 65% to 90%.</p></sec></sec><sec id="s1305"><title>Meconium Impaction</title><p id="p7810"><list list-type="simple" id="ulist1275"><list-item id="u6205"><label>•</label><p id="p7815">A common cause of acute pain in newborn foals is retention of meconium in the small colon and rectum.</p></list-item><list-item id="u6210"><label>•</label><p id="p7820">Impaction occurs more frequently in males, weak newborns after a dystocia, and foals born at more than 340 days of gestation.</p></list-item></list></p><sec id="s1310"><title>Clinical Signs</title><p id="p7825"><list list-type="simple" id="ulist1280"><list-item id="u6215"><label>•</label><p id="p7830">Acute abdominal pain during the first 24 hours after foaling</p></list-item><list-item id="u6220"><label>•</label><p id="p7835">Tachycardia</p></list-item><list-item id="u6225"><label>•</label><p id="p7840">Repeated attempts to defecate</p></list-item><list-item id="u6230"><label>•</label><p id="p7845">Rolling</p></list-item><list-item id="u6235"><label>•</label><p id="p7850">Abnormal stance (back arched dorsally)</p></list-item><list-item id="u6240"><label>•</label><p id="p7855">Swishing the tail</p></list-item><list-item id="u6245"><label>•</label><p id="p7860">Abdominal tympany if obstruction of the small colon is complete (<xref rid="f0335" ref-type="fig">Fig. 18-65</xref>)<fig id="f0335"><label>Figure 18-65</label><caption><p>Radiograph demonstrates the abdomen of a 2-day-old foal with meconium impaction of the colon causing severe gas distention <italic>(arrow)</italic>. Surgery was needed to correct the problem.</p></caption><graphic xlink:href="f018-065-9781455708925"></graphic></fig></p></list-item><list-item id="u6250"><label>•</label><p id="p7865">The foal appears transiently normal for short periods and nurses. The diagnosis often is confirmed with digital palpation of meconium impaction in the distal small colon and rectum.</p></list-item><list-item id="u6255"><label>•</label><p id="p7870">The impaction may be seen on either radiographs or abdominal ultrasound in many cases.</p></list-item></list></p></sec><sec id="s9030"><title>Diagnosis</title><p id="p13500"><list list-type="simple" id="ulist9050"><list-item id="u11140"><label>•</label><p id="p13505">Repeated attempts to defecate without producing stool</p></list-item><list-item id="u11145"><label>•</label><p id="p13510">Digital palpation of the meconium impaction</p></list-item><list-item id="u11150"><label>•</label><p id="p13515">Radiographic or ultrasound confirmation</p></list-item></list><boxed-text id="b0215"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1315"><title>Meconium Impaction</title><p id="p7875"><list list-type="simple" id="ulist1285"><list-item id="u6260"><label>•</label><p id="p7880">Enemas with warm, soapy water (500 to 1000 mL) delivered by means of gravity flow through a soft rubber tube. Fleet enemas may also be used (4 ounces) but are more irritating and, with repeated use, may cause hyperphosphatemia.</p></list-item><list-item id="u6265"><label>•</label><p id="p7885">Acetylcysteine enema—the foal must be adequately sedated with valium (5 to 10 mg IV/50-kg foal). A soft Foley catheter is inserted 2 to 3 inches inside the rectum and the balloon distended with 30 mL of air. One hundred to 200 mL of a 4% acetylcysteine solution is slowly infused without pressure into the rectum through the Foley catheter and left in place for 30 minutes before the balloon is deflated and the catheter is removed.</p></list-item><list-item id="u6270"><label>•</label><p id="p7890">N-butylscopolammonium bromide can be used in the enema (0.3 mg/kg) or intravenously (0.2 mg/kg) to relax the bowel.</p></list-item><list-item id="u6275"><label>•</label><p id="p7895">Administer intravenous, balanced polyionic fluids.</p></list-item><list-item id="u6280"><label>•</label><p id="p7900">Administer mineral oil by nasogastric tube.</p></list-item><list-item id="u6285"><label>•</label><p id="p7905">Administer sedatives as needed.</p></list-item><list-item id="u6290"><label>•</label><p id="p7910">Perform ventral midline exploratory celiotomy for refractory patients and for those with proximal impaction, accompanied by enemas and extraluminal massage of the affected colon.</p></list-item><list-item id="u6295"><label>•</label><p id="p7915">Small colon enterotomy rarely is necessary.</p></list-item><list-item id="u11155"><label>•</label><p id="p7920"><italic><bold>Important Note:</bold></italic> Repeated enemas or enemas with caustic solutions result in rectal edema and irritation and a syndrome that mimics meconium impaction. Foals receiving several enemas often become very toxic because of injury of the rectal mucosa.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1320"><title>Prognosis</title><p id="p7925">Prognosis is excellent.</p></sec></sec><sec id="s1325"><title>Mesocolic Rupture</title><p id="p7930"><list list-type="simple" id="ulist1290"><list-item id="u6300"><label>•</label><p id="p7935">Mesocolic rupture affects mares during parturition and results in tearing of the mesentery of the small colon (<xref rid="f0340" ref-type="fig">Fig. 18-66</xref>).<fig id="f0340"><label>Figure 18-66</label><caption><p>Intraoperative photograph demonstrating a rupture of the small colon mesentery in a mare after a severe rectal prolapse during foaling.</p></caption><graphic xlink:href="f018-066-9781455708925"></graphic></fig></p></list-item><list-item id="u6305"><label>•</label><p id="p7940">The condition is a complication of prolapse of the rectum and may be accompanied by prolapse of the bladder, uterus, vagina, small intestine, or a combination of these organs.</p></list-item><list-item id="u6310"><label>•</label><p id="p7945">Multiparous mares older than 11 years of age are at greatest risk.</p></list-item><list-item id="u6315"><label>•</label><p id="p7950">Clinical signs of abdominal pain develop during the first 24 hours postpartum and are complicated by intraabdominal bleeding and peritonitis.</p></list-item><list-item id="u6320"><label>•</label><p id="p7955">The mare's clinical condition deteriorates rapidly if the blood supply to the small colon is compromised or the intestine is entrapped in the mesocolic rent.</p></list-item><list-item id="u6325"><label>•</label><p id="p7960">Rectal examination reveals impaction or tympany of the small colon.</p></list-item></list><boxed-text id="b0220"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1330"><title>Mesocolic Rupture</title><p id="p7965"><list list-type="simple" id="ulist1295"><list-item id="u6330"><label>•</label><p id="p7970">Perform ventral midline exploratory celiotomy.</p></list-item><list-item id="u6335"><label>•</label><p id="p7975">Perform resection and anastomosis of the affected small colon.</p></list-item><list-item id="u6340"><label>•</label><p id="p7980">A colostomy will be necessary if the tear involves the mesorectum.</p></list-item></list></p></sec></boxed-text></p><sec id="s1335"><title>Prognosis</title><p id="p7985">Prognosis is poor because of ischemia of the small colon, difficult surgical exposure, and complications associated with the colostomy, such as prolapse of the proximal small colon through the colostomy stoma and adhesions.</p></sec></sec><sec id="s1340"><title>Rectal Tear</title><p id="p7990"><list list-type="simple" id="ulist1300"><list-item id="u6345"><label>•</label><p id="p7995"><italic><bold>Practice Tip:</bold> A complication of performing a rectal examination is the risk of a rectal tear.</italic></p></list-item><list-item id="u6350"><label>•</label><p id="p8000">The incidence is highest among young, nervous, anxious equine patients; older horses with a weakened or edematous rectal wall, such as those with small-colon impactions; and patients that strain during rectal examination.</p></list-item><list-item id="u6355"><label>•</label><p id="p8005">The incidence is higher among Arabians than it is among other breeds, presumably because of the smaller size of Arabians.</p></list-item><list-item id="u6360"><label>•</label><p id="p8010">Stallions and geldings are at greater risk than are mares. The tears most often occur at the 10 to 12 o'clock position 25 to 30 cm from the anus.</p></list-item><list-item id="u6365"><label>•</label><p id="p8015">The tear is most often longitudinal and is hypothesized to occur where blood vessels penetrate the intestinal wall.</p></list-item><list-item id="u6370"><label>•</label><p id="p8020">Spontaneous tears or impaction of a segment of the rectum can occur.</p></list-item><list-item id="u6375"><label>•</label><p id="p8025">Rectal tears are classified as follows:<list list-type="simple" id="ulist1305"><list-item id="u6380"><label>•</label><p id="p8030"><italic>Grade I:</italic> Mucosa or submucosa</p></list-item><list-item id="u6385"><label>•</label><p id="p8035"><italic>Grade II:</italic> Muscular layer only</p></list-item><list-item id="u6390"><label>•</label><p id="p8040"><italic>Grade III:</italic> Mucosa, submucosa, and muscular layers without serosal penetration (3a), including mesorectum (3b)</p></list-item><list-item id="u6395"><label>•</label><p id="p8045"><italic>Grade IV:</italic> Tears involving all layers and extending into the peritoneal cavity</p></list-item></list></p></list-item><list-item id="u6400"><label>•</label><p id="p8050"><italic><bold>Important Note:</bold></italic> Grades III and IV are life-threatening, with cellulitis, abscessation, and acute septic peritonitis as sequelae. The diagnosis is confirmed with careful examination of the tear after the patient is sedated and the rectum evacuated. Intraluminally administered lidocaine gel or epidural anesthesia facilitates rectal examination.</p></list-item></list></p><sec id="s1345"><title>Clinical Signs</title><p id="p8055"><list list-type="simple" id="ulist1310"><list-item id="u6405"><label>•</label><p id="p8060">Blood on rectal sleeve up on withdrawal of the examining arm</p></list-item><list-item id="u6410"><label>•</label><p id="p8065">Sudden relaxation of the rectum while the horse is straining</p></list-item><list-item id="u6415"><label>•</label><p id="p8070">Hemorrhagic feces or straining to defecate</p></list-item><list-item id="u6420"><label>•</label><p id="p8075">Idiopathic tears—immediate clinical signs may <italic>not</italic> be apparent. Signs of abdominal pain, endotoxemia, and depression may develop within 2 to 3 hours after rectal examination.</p></list-item></list></p></sec><sec id="s9035"><title>Diagnosis</title><p id="p13520"><list list-type="simple" id="ulist9055"><list-item id="u11160"><label>•</label><p id="p13525">Confirmation of a suspected rectal tear is based on the clinical signs.</p></list-item><list-item id="u11165"><label>•</label><p id="p13530">Careful examination of the rectum under sedation or epidural anesthesia</p></list-item><list-item id="u11170"><label>•</label><p id="p13535">Endoscopic (proctoscopy) of the rectum if physical examination does not confirm diagnosis (use sedation or epidural anesthesia)</p></list-item><list-item id="u11175"><label>•</label><p id="p13540">Immediate referral to a surgical facility for follow-up diagnostic procedures</p></list-item></list><boxed-text id="b0225"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1350"><title>Rectal Tear</title><p id="p8080"><list list-type="simple" id="ulist1315"><list-item id="u6425"><label>•</label><p id="p8085">Immediately begin administration of broad-spectrum antimicrobial agents.</p></list-item><list-item id="u6430"><label>•</label><p id="p8090">Include metronidazole, 15 to 20 mg/kg PO q8hr, or suppository q6h for anaerobes.</p></list-item><list-item id="u6435"><label>•</label><p id="p8095">Provide intravenous, balanced polyionic fluids.</p></list-item><list-item id="u6440"><label>•</label><p id="p8100">Administer NSAIDs.</p></list-item><list-item id="u6445"><label>•</label><p id="p8105">Adequately restrain and sedate the horse, administer N-butylscopolamine bromide (Buscopan, 0.3 mg/kg IV) and 50 mL of 2% lidocaine in 120 mL of lube per rectum. With a well lubricated bare arm, determine the location (distance cranial to the anus) and severity of the tear.</p></list-item><list-item id="u6450"><label>•</label><p id="p8110">Gently evacuate feces from the rectum and tear.</p></list-item><list-item id="u6455"><label>•</label><p id="p8115">Inform the owner about the possible occurrence of a rectal tear and the potential sequelae without implying admission of guilt or wrongdoing</p></list-item></list></p><sec id="s1355"><title>Grade I Tears</title><p id="p8120"><list list-type="simple" id="ulist1320"><list-item id="u6460"><label>•</label><p id="p8125">These tears are managed conservatively unless the tear can be sutured easily with 2-0 or 0 polydioxanone (PDS, Ethicon) in a simple continuous pattern.</p></list-item><list-item id="u6465"><label>•</label><p id="p8130">These tears heal with minimal or <italic>no</italic> complications.</p></list-item></list></p></sec><sec id="s1360"><title>Grade II Tears</title><p id="p8135"><list list-type="simple" id="ulist1325"><list-item id="u6470"><label>•</label><p id="p8140">Because of the lack of frank blood in the lumen of the rectum, grade II tears frequently are <italic>not</italic> diagnosed at the time of injury.</p></list-item><list-item id="u6475"><label>•</label><p id="p8145">These tears are identified weeks later when a perirectal fistula or abscess develops.</p></list-item></list></p></sec><sec id="s1365"><title>Grade III or IV Tears</title><p id="p8150"><list list-type="simple" id="ulist1330"><list-item id="u6480"><label>•</label><p id="p8155">Administer Buscopan to reduce peristalsis.</p></list-item><list-item id="u6485"><label>•</label><p id="p8160">Administer epidural anesthesia (xylazine, 0.17 mg/kg in 6 mL saline) to minimize straining.</p></list-item><list-item id="u6490"><label>•</label><p id="p8165">Pack the rectal lumen from the anus to cranial to the tear (moistened rolled cotton or gauze packing suitable).</p></list-item><list-item id="u6495"><label>•</label><p id="p8170">Transport to a surgical referral facility for primary suture repair and/or a diverting colostomy.</p></list-item><list-item id="u6500"><label>•</label><p id="p8175">A rectal liner<xref rid="fn0085" ref-type="fn">16</xref> or primary surgical repair of the tear is used in the management of grade III lacerations to bypass the site of injury and potentially avoid the need for a colostomy.</p></list-item><list-item id="u6505"><label>•</label><p id="p8180">A colostomy may be performed to divert feces from the site and prevent peritoneal contamination.</p></list-item><list-item id="u11180"><label>•</label><p id="p8185"><italic><bold>Important Note:</bold></italic> Grade IV tears often necessitate a colostomy. For most grade III tears, a colostomy is recommended (<xref rid="f0345" ref-type="fig">Fig. 18-67</xref>).<fig id="f0345"><label>Figure 18-67</label><caption><p>Colostomy technique. <bold>A,</bold> Loop colostomy. <bold>B,</bold> Diverting colostomy positioned in the left flank. <italic>Arrows</italic> indicate the location of the rectal tear. Loop colostomy is performed at the initial flank incision. The diverting colostomy is performed in a separate incision, cranial to the initial flank incision <italic>(dotted line).</italic></p></caption><graphic xlink:href="f018-067ab-9781455708925"></graphic></fig></p></list-item><list-item id="u6510"><label>•</label><p id="p8190">Loop colostomy is performed with the patient under general anesthesia or under sedation and local anesthesia. The colostomy exits through the left flank (<xref rid="f0345" ref-type="fig">Fig. 18-67, A</xref>).</p></list-item><list-item id="u6515"><label>•</label><p id="p8195">An alternative is to oversew the proximal end of the distal small colon; the distal end of the proximal small colon exits from the flank as a diverting colostomy (<xref rid="f0345" ref-type="fig">Fig. 18-67, B</xref>).</p></list-item><list-item id="u6520"><label>•</label><p id="p8200">If the patient is placed under general anesthesia, large colon enterotomy is performed to reduce fecal bulk exiting from the colostomy.</p></list-item><list-item id="u6525"><label>•</label><p id="p8205">A rectal liner<sup>16</sup> or primary surgical repair of the tear is used in the management of grade III tears to bypass the tear and potentially avoid the need for a colostomy.</p></list-item><list-item id="u6530"><label>•</label><p id="p8210">Grades III and IV tears heal by secondary intention; the loop colostomy is reversed after the tear heals.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s1370"><title>Prognosis</title><p id="p8215"><list list-type="simple" id="ulist1340"><list-item id="u6535"><label>•</label><p id="p8220">Prognosis is excellent for grades I and II rectal tears.</p></list-item><list-item id="u6540"><label>•</label><p id="p8225">Prognosis is guarded for grade III tears.</p></list-item><list-item id="u6545"><label>•</label><p id="p8230">Prognosis is guarded to poor for grade IV tears.</p></list-item></list></p></sec></sec><sec id="s1375"><title>Rectal Prolapse</title><p id="p8235"><list list-type="simple" id="ulist1345"><list-item id="u6550"><label>•</label><p id="p8240">Rectal prolapse is caused by straining because of constipation, obstipation, dystocia, colitis, urethral obstruction, or foreign body impaction of the distal small colon or rectum.</p></list-item><list-item id="u6555"><label>•</label><p id="p8245">In some cases <italic>no</italic> known predisposing cause can be identified.</p></list-item><list-item id="u6560"><label>•</label><p id="p8250">The condition occurs more commonly in mares and is classified according to severity as follows:<list list-type="simple" id="ulist1350"><list-item id="u6565"><label>•</label><p id="p8255">Type I prolapse involves only the rectal mucosa and submucosa and appears as a large circular anal swelling.</p></list-item><list-item id="u6570"><label>•</label><p id="p8260">Type II involves the entire rectal wall and is called “complete” prolapse; the ventral portion of prolapsed tissue is thicker than the dorsal portion.</p></list-item><list-item id="u6575"><label>•</label><p id="p8265">Type III includes invaginated peritoneal rectum or small colon and is difficult to differentiate from type II prolapse.</p></list-item><list-item id="u6580"><label>•</label><p id="p8270">Type IV involves intussuscepted peritoneal rectum or small colon beyond the anus. A palpable invagination adjacent to the intussuscepted intestine differentiates type IV from type III prolapse.</p></list-item></list></p></list-item></list></p><p id="p8275"><italic><bold>Important Note:</bold></italic> Internal rupture of the small colon mesentery should be suspected in type IV rectal prolapse involving greater than 30 cm of rectum (see Mesocolic Rupture, <xref rid="s1300" ref-type="sec">p. 213</xref>).<boxed-text id="b0230"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1380"><title>Rectal Prolapse</title><sec id="s1385"><title>Type I or Type II Prolapse</title><p id="p8280"><list list-type="simple" id="ulist1355"><list-item id="u6585"><label>•</label><p id="p8285">Identify and correct underlying cause of prolapse if possible.</p></list-item><list-item id="u6590"><label>•</label><p id="p8290">Reduce the edema in the tissues with topical application of glycerin or dextrose and apply petroleum jelly (Vaseline).</p></list-item><list-item id="u6595"><label>•</label><p id="p8295">Reduce the prolapse under epidural anesthesia. An indwelling epidural catheter may be needed.</p></list-item><list-item id="u6600"><label>•</label><p id="p8300">Tranquilize the patient unless contraindicated.</p></list-item><list-item id="u6605"><label>•</label><p id="p8305">Administer Buscopan</p></list-item><list-item id="u6610"><label>•</label><p id="p8310">Place a purse-string suture in the anus.</p></list-item><list-item id="u6615"><label>•</label><p id="p8315">Administer stool softeners, such as mineral oil.</p></list-item><list-item id="u6620"><label>•</label><p id="p8320">Perform submucosal resection if medical treatment is unsuccessful.</p></list-item></list></p></sec><sec id="s1390"><title>Type III or IV Prolapse</title><p id="p8325"><list list-type="simple" id="ulist1360"><list-item id="u6625"><label>•</label><p id="p8330">Perform celiotomy to reduce the intussusception.</p></list-item><list-item id="u6630"><label>•</label><p id="p8335">Perform colostomy for type IV prolapse if the blood supply to the affected bowel is compromised.</p></list-item></list></p></sec></sec></boxed-text></p><sec id="s1395"><title>Prognosis</title><p id="p8340"><list list-type="simple" id="ulist1365"><list-item id="u6635"><label>•</label><p id="p8345">Prognosis is good for types I and II prolapse.</p></list-item><list-item id="u6640"><label>•</label><p id="p8350">Prognosis is guarded to poor for types III and IV.</p></list-item></list></p></sec></sec></sec><sec id="s1400"><title>Colic in the Late-Term Pregnant Mare</title><p id="p8355"><list list-type="simple" id="ulist1370"><list-item id="u6645"><label>•</label><p id="p8360">Colic in a mare during the last trimester of pregnancy often is a diagnostic challenge.</p></list-item><list-item id="u6650"><label>•</label><p id="p8365">GI disorders must be ruled out with careful clinical examination, but the large, gravid uterus often prevents a complete rectal examination.</p></list-item><list-item id="u6655"><label>•</label><p id="p8370">The effect of the colic episode on the fetus is always of concern because abortion can result in substantial emotional and financial loss.</p></list-item><list-item id="u6660"><label>•</label><p id="p8375">The overall postcolic abortion rate among mares is between 16% and 18%.</p></list-item><list-item id="u6665"><label>•</label><p id="p8380">Endotoxemia and intraoperative <italic>hypoxia</italic> or <italic>hypotension</italic> during colic surgery in the last 60 days of gestation have been associated with a higher incidence of abortion.</p></list-item><list-item id="u6670"><label>•</label><p id="p8385">Causes of colic in late-term pregnant mares <italic>not</italic> associated with the GI tract include the following:<list list-type="simple" id="ulist1375"><list-item id="u6675"><label>•</label><p id="p8390">Abortion and premature parturition</p></list-item><list-item id="u6680"><label>•</label><p id="p8395">Uterine torsion</p></list-item><list-item id="u6685"><label>•</label><p id="p8400">Hydrallantois</p></list-item><list-item id="u6690"><label>•</label><p id="p8405">Ruptured prepubic tendon</p></list-item><list-item id="u6695"><label>•</label><p id="p8410">Uterine artery bleed</p></list-item></list></p></list-item></list><boxed-text id="b0235"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1405"><title>Colic in the Late-Term Pregnant Mare</title><p id="p8415"><list list-type="simple" id="ulist1380"><list-item id="u6700"><label>•</label><p id="p8420">Pregnant mares with colic and endotoxemia during the first 2 months of pregnancy may benefit from treatment with progestin supplementation, altrenogest (22 to 44 mg PO q24h for a 450-kg adult) or injectable progesterone (150 to 300 mg/450 kg IM q24h) for 100 to 200 days of pregnancy. Although the benefit of this treatment in late pregnancy is not evidence based, it is generally used.</p></list-item><list-item id="u6705"><label>•</label><p id="p8425">Administration of NSAIDs may alleviate the adverse effects of endotoxemia in pregnancy.</p></list-item><list-item id="u6710"><label>•</label><p id="p8430">Glucose should be administered to late pregnant mares recovering from colic or surgery.</p></list-item></list></p></sec></boxed-text></p><sec id="s1410"><title>Abortion and Premature Parturition</title><p id="p8435"><list list-type="simple" id="ulist1385"><list-item id="u6715"><label>•</label><p id="p8440">Mares may have signs of mild to moderate abdominal pain and minimal udder development. Vaginal examination reveals loss of the cervical plug and relaxation of the cervix.</p></list-item><list-item id="u6720"><label>•</label><p id="p8445">This finding alone does <italic>not</italic> indicate impending abortion because similar findings occur in many normal mares days or weeks before delivery.</p></list-item><list-item id="u6725"><label>•</label><p id="p8450">Rectal examination often reveals the fetus to be positioned within the birth canal.</p></list-item></list><boxed-text id="b0240"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1415"><title>Abortion and Premature Parturition</title><p id="p8455"><list list-type="simple" id="ulist1390"><list-item id="u6730"><label>•</label><p id="p8460">Treatment is supportive and is directed at an uncomplicated delivery and postpartum care of the mare.</p></list-item><list-item id="u6735"><label>•</label><p id="p8465">Postmortem examination of the aborted fetus and placenta may determine the cause of the abortion, such as equine herpesvirus 1 (see Abortion Evaluation, Chapter 24, p. 433). The mare should be isolated until the results of the examination are available.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1420"><title>Uterine Torsion</title><p id="p8470"><list list-type="simple" id="ulist1395"><list-item id="u6740"><label>•</label><p id="p8475">Uterine torsion can be a cause of colic in late-term pregnant mares.</p></list-item><list-item id="u6745"><label>•</label><p id="p8480">Uterine torsion usually occurs between 8 months of gestation and term, but rarely at term.</p></list-item><list-item id="u6750"><label>•</label><p id="p8485">Unlike the case in cows, in which the torsion most often is diagnosed at term, mares affected usually are <italic>not</italic> in labor when clinical signs are first evident.</p></list-item><list-item id="u6755"><label>•</label><p id="p8490">Also unlike the disorder in cows, torsion in mares is usually cranial to the cervix and vagina, thereby minimizing the benefit of a vaginal examination in making the diagnosis.</p></list-item><list-item id="u6760"><label>•</label><p id="p8495">The degree of torsion ranges from 180 to 540 degrees and occurs in either direction with equal frequency.</p></list-item><list-item id="u6765"><label>•</label><p id="p8500">Uterine rupture can occur as the result of torsion but is an uncommon complication.</p></list-item></list></p><sec id="s1425"><title>Diagnosis</title><p id="p8505"><list list-type="simple" id="ulist1400"><list-item id="u6770"><label>•</label><p id="p8510">Mild to moderate intermittent abdominal pain is the most consistent sign; however, some mares may demonstrate severe, unrelenting pain.</p></list-item><list-item id="u6775"><label>•</label><p id="p8515">A mild increase in heart and respiratory rates also may be present.</p></list-item><list-item id="u6780"><label>•</label><p id="p8520">Diagnosis is made with the signalment, history, and findings on rectal examination.</p></list-item><list-item id="u6785"><label>•</label><p id="p8525">Rectal palpation of the broad ligaments reveals the ligaments to be tight as they cross the caudal abdomen below and above the cervix.</p></list-item><list-item id="u6790"><label>•</label><p id="p8530">Palpation of the dorsal-most ligament, and occasionally the body of the uterus, indicates the direction of the torsion (<xref rid="f0350" ref-type="fig">Fig. 18-68, A</xref>).<fig id="f0350"><label>Figure 18-68</label><caption><p><bold>A,</bold> Normal orientation of uterus and broad ligament. <bold>B,</bold> Clockwise uterine torsion. <bold>C,</bold> Counterclockwise uterine torsion.</p></caption><graphic xlink:href="f018-068a-9781455708925"></graphic><graphic xlink:href="f018-068b-9781455708925"></graphic><graphic xlink:href="f018-068c-9781455708925"></graphic><attrib>(Art by Kip Carter [The University of Georgia], © University of Georgia Research Foundation, Inc. Used under license.)</attrib><permissions><copyright-statement>© 2014 </copyright-statement><copyright-year>2014</copyright-year><license><license-p>Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.</license-p></license></permissions></fig></p></list-item><list-item id="u6795"><label>•</label><p id="p8535">In clockwise torsion, as viewed from behind, the left broad ligament is pulled tight over the uterus and courses to the right in a horizontal to oblique direction (<xref rid="f0350" ref-type="fig">Fig. 18-68, B</xref>). The right broad ligament is pulled ventrally and diagonally to the left, and because of its more ventral and caudal position in the abdomen, may be the easier of the two ligaments to identify during rectal palpation.</p></list-item><list-item id="u6800"><label>•</label><p id="p8540">In counterclockwise torsion, the opposite is true (<xref rid="f0350" ref-type="fig">Fig.18-68, C</xref>).</p></list-item></list><boxed-text id="b0245"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1430"><title>Uterine Torsion</title><p id="p8545"><list list-type="simple" id="ulist1405"><list-item id="u6805"><label>•</label><p id="p8550">Early recognition and intervention are imperative for a successful outcome for the mare and the foal.</p></list-item><list-item id="u6810"><label>•</label><p id="p8555">The optimal method of correction depends on the condition of the mare and fetus and the stage of gestation.</p></list-item></list></p><sec id="s1435"><title>Nonsurgical Correction: Rolling</title><p id="p8560">See Chapter 24, Fig. 24-10.</p></sec><sec id="s1440"><title>Surgical Correction (Preferred)</title><sec id="s1445"><title>Flank Celiotomy</title><p id="p8565"><list list-type="simple" id="ulist1410"><list-item id="u6815"><label>•</label><p id="p8570">Flank celiotomy provides the least stress for the foal and mare, and it can be performed during any stage of gestation.</p></list-item><list-item id="u6820"><label>•</label><p id="p8575">The procedure is performed with the standing mare under sedation (xylazine or detomidine with or without butorphanol) and local anesthetic infiltration along the proposed incision site.</p></list-item><list-item id="u6825"><label>•</label><p id="p8580">Controversy exists as to the preferred side of entry relative to the direction of the torsion. Many surgeons prefer to enter the abdomen from the side to which the torsion is directed (e.g., right flank for clockwise torsion).</p></list-item><list-item id="u6830"><label>•</label><p id="p8585">If the abdomen is entered from the side to which the torsion is directed (e.g., right flank for clockwise torsion), the surgeon's hand is passed ventrally to the uterus, and the uterus is lifted and rotated upward to correct the torsion.</p></list-item><list-item id="u6835"><label>•</label><p id="p8590">If the abdomen is entered on the side opposite that to which the torsion is directed (e.g., left flank for clockwise torsion), the surgeon's hand passes dorsally to the uterus, and the uterus is pulled toward the surgeon to correct the torsion.</p></list-item><list-item id="u6840"><label>•</label><p id="p8595">Alternatively, in late-term pregnancies, a left and right flank incision may be made simultaneously with two surgeons to facilitate reduction.</p></list-item><list-item id="u6845"><label>•</label><p id="p8600">Correction can be facilitated by means of grasping the limbs of the fetus through the wall of the uterus and gently “rocking” the uterus to gain enough momentum for complete rotation and final correction.</p></list-item></list></p></sec><sec id="s1450"><title>Ventral Midline Celiotomy</title><p id="p8605"><list list-type="simple" id="ulist1415"><list-item id="u6850"><label>•</label><p id="p8610">Ventral midline celiotomy provides the best exposure for assessment and manipulation of the gravid uterus.</p></list-item><list-item id="u6855"><label>•</label><p id="p8615">Indications for ventral midline celiotomy include uterine rupture, uterine tearing, and uterine devitalization.</p></list-item><list-item id="u6860"><label>•</label><p id="p8620">This approach also allows identification and correction of concurrent intestinal disorders.</p></list-item><list-item id="u6865"><label>•</label><p id="p8625">The procedure can be performed during any stage of gestation.</p></list-item><list-item id="u6870"><label>•</label><p id="p8630">Standard ventral midline celiotomy is performed.</p></list-item><list-item id="u6875"><label>•</label><p id="p8635">If hysterotomy is indicated, the ventral midline approach provides the best surgical exposure.</p></list-item><list-item id="u6880"><label>•</label><p id="p8640">Ventral midline celiotomy should be reserved for cases <italic>not</italic> amenable to nonsurgical correction or flank celiotomy because of the associated risks of general anesthesia to the mare and foal.</p></list-item></list></p></sec></sec></sec></boxed-text></p></sec><sec id="s1455"><title>Prognosis</title><p id="p8645"><list list-type="simple" id="ulist1420"><list-item id="u6885"><label>•</label><p id="p8650">Prognosis is good to excellent for complete recovery and future breeding soundness of the mare with uterine torsion.</p></list-item><list-item id="u6890"><label>•</label><p id="p8655">Fetal viability depends on the duration and degree of torsion.</p></list-item><list-item id="u6895"><label>•</label><p id="p8660">The abortion rate after uterine torsion is reported to be between 30% and 40%.</p></list-item><list-item id="u6900"><label>•</label><p id="p8665">Prognosis for both the mare and foal is more favorable if uterine torsion occurs before the last 30 days of gestation.</p></list-item></list></p></sec></sec><sec id="s1460"><title>Uterine Rupture</title><p id="p8670"><list list-type="simple" id="ulist1425"><list-item id="u6905"><label>•</label><p id="p8675">Uterine rupture can be a complication of manipulation during dystocia or can occur during apparently normal foaling.</p></list-item><list-item id="u6910"><label>•</label><p id="p8680">Rupture also can be a sequela to uterine torsion or hydrallantois.</p></list-item><list-item id="u6915"><label>•</label><p id="p8685">The tear usually occurs at the dorsal aspect of the uterus (see Chapter 24, p. 444).</p></list-item></list></p><sec id="s1465"><title>Diagnosis</title><p id="p8690"><list list-type="simple" id="ulist1430"><list-item id="u6920"><label>•</label><p id="p8695">Suspect uterine rupture in any mare demonstrating postpartum abdominal pain.</p></list-item><list-item id="u6925"><label>•</label><p id="p8700">Large ruptures may result in significant blood loss and produce signs of hemorrhagic shock.</p></list-item><list-item id="u6930"><label>•</label><p id="p8705">Diagnosis is confirmed on vaginal and uterine examination.</p></list-item></list><boxed-text id="b0250"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1470"><title>Uterine Rupture</title><p id="p8710"><list list-type="simple" id="ulist1435"><list-item id="u6935"><label>•</label><p id="p8715">If a uterine tear is suspected, irrigating solutions should <italic>not</italic> be infused into the uterus.</p></list-item><list-item id="u6940"><label>•</label><p id="p8720">Administer the following:<list list-type="simple" id="ulist1440"><list-item id="u6945"><label>•</label><p id="p8725">Broad-spectrum antimicrobial agents</p></list-item><list-item id="u6950"><label>•</label><p id="p8730">Balanced, polyionic intravenous fluids</p></list-item><list-item id="u6955"><label>•</label><p id="p8735">Plasma or synthetic colloids</p></list-item><list-item id="u6960"><label>•</label><p id="p8740">NSAIDs</p></list-item><list-item id="u6965"><label>•</label><p id="p8745">Peritoneal drainage</p></list-item></list></p></list-item><list-item id="u6970"><label>•</label><p id="p8750">Allow small tears to heal by secondary intention.</p></list-item><list-item id="u6975"><label>•</label><p id="p8755">Close large tears primarily; general anesthesia and ventral midline celiotomy may be necessary.</p></list-item><list-item id="u6980"><label>•</label><p id="p8760">Cervical tears may be repaired under standing epidural anesthesia.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1475"><title>Prognosis</title><p id="p8765"><list list-type="simple" id="ulist1445"><list-item id="u6985"><label>•</label><p id="p8770">Prognosis depends on the size of the tear, duration before recognition and treatment, degree of peritoneal contamination, and nature of the intrauterine contents.</p></list-item><list-item id="u6990"><label>•</label><p id="p8775">Prognosis is good for small tears recognized early and poor for large tears with an emphysematous fetus and gross peritoneal contamination.</p></list-item></list></p></sec></sec><sec id="s1480"><title>Hydrallantois</title><p id="p8780">See Chapter 24, p. 436.</p></sec><sec id="s1485"><title>Ruptured Prepubic Tendon</title><p id="p8785"><list list-type="simple" id="ulist1450"><list-item id="u6995"><label>•</label><p id="p8790">The prepubic tendon is a strong, thick, fibrous structure that attaches to the cranial border of the pelvis and provides attachment for the rectus abdominis, oblique abdominis, gracilis, and pectineus muscles.</p></list-item><list-item id="u7000"><label>•</label><p id="p8795">The tendon forms the medial borders of the external inguinal rings.</p></list-item><list-item id="u7005"><label>•</label><p id="p8800">Hydrallantois, twins, or fetal giants may predispose to prepubic tendon rupture.</p></list-item></list></p><sec id="s1490"><title>Diagnosis</title><p id="p8805"><list list-type="simple" id="ulist1455"><list-item id="u7010"><label>•</label><p id="p8810">Prepubic tendon rupture must be differentiated from ventral hernia, which also occurs most frequently in late-term pregnant mares.</p></list-item><list-item id="u7015"><label>•</label><p id="p8815">Ventral hernia may respond favorably to surgical repair; however, the prognosis for prepubic tendon rupture is poor.</p></list-item></list></p><sec id="s1495"><title>Clinical Signs</title><p id="p8820"><list list-type="simple" id="ulist1460"><list-item id="u7020"><label>•</label><p id="p8825">Severe, progressive, ventral abdominal swelling and edema with the pelvis tilted cranially and ventrally (<xref rid="f0355" ref-type="fig">Fig. 18-69</xref>). The mammary gland also assumes a more cranioventral position.<fig id="f0355"><label>Figure 18-69</label><caption><p>Photograph demonstrating a prepubic tendon rupture in a horse.</p></caption><graphic xlink:href="f018-069-9781455708925"></graphic><attrib>(Courtesy Dr. Stefan Witte.)</attrib></fig></p></list-item><list-item id="u7025"><label>•</label><p id="p8830"><italic><bold>Practice Tip:</bold> Mild to moderate abdominal pain usually is apparent, and the mare is reluctant to walk. In contrast, mares with a ventral hernia are</italic> not <italic>reluctant to walk, and the pelvis and mammary gland are in a normal position.</italic></p></list-item><list-item id="u7030"><label>•</label><p id="p8835">Identification of the defect by means of external palpation may be difficult because of excessive edema formation.</p></list-item><list-item id="u7035"><label>•</label><p id="p8840">Rectal examination and ultrasonography are helpful in differentiating prepubic tendon rupture from ventral herniation.</p></list-item></list><boxed-text id="b0255"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1500"><title>Ruptured Prepubic Tendon</title><p id="p8845"><list list-type="simple" id="ulist1465"><list-item id="u7040"><label>•</label><p id="p8850">In mares near term, early induction of parturition and assisted foaling may be required. For pregnancy >315 days, give 100 mg of dexamethasone daily for 3 days to “speed” maturation of the foal.</p></list-item><list-item id="u7045"><label>•</label><p id="p8855">Exploratory celiotomy and cesarean section should be performed immediately on mares that demonstrate intractable pain or systemic deterioration or in which a concurrent incarcerating intestinal lesion is suspected.</p></list-item><list-item id="u7050"><label>•</label><p id="p8860">Stabilized mares should be confined to stall rest, placed in abdominal support bandages, and administered NSAIDs.</p></list-item><list-item id="u7055"><label>•</label><p id="p8865">Low-bulk, pelleted feed should be fed to decrease the volume of ingesta.</p></list-item><list-item id="u7060"><label>•</label><p id="p8870">These mares may foal normally; however, they should be observed closely and assisted with foaling if necessary.</p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1505"><title>Prognosis</title><p id="p8875"><list list-type="simple" id="ulist1470"><list-item id="u7065"><label>•</label><p id="p8880">Stabilized mares not in pain may raise a foal successfully but should <italic>not</italic> be used for breeding.</p></list-item><list-item id="u7070"><label>•</label><p id="p8885">The likelihood of long-term survival is poor.</p></list-item></list></p></sec></sec><sec id="s1510"><title>Abdominal Pain After Foaling</title><p id="p8890"><list list-type="simple" id="ulist1475"><list-item id="u7075"><label>•</label><p id="p8895">Abdominal pain is common in mares and is usually mild and associated with bruising of the pelvic canal and secondary ileus.</p></list-item><list-item id="u7080"><label>•</label><p id="p8900">More serious conditions include:<list list-type="simple" id="ulist1480"><list-item id="u7085"><label>•</label><p id="p8905">Uterine hemorrhage</p></list-item><list-item id="u7090"><label>•</label><p id="p8910">Small colon impaction</p></list-item><list-item id="u7095"><label>•</label><p id="p8915">Rupture of the small colon mesentery</p></list-item><list-item id="u7100"><label>•</label><p id="p8920">Large colon volvulus</p></list-item><list-item id="u7105"><label>•</label><p id="p8925">Ruptured uterus, cecum, and/or bladder</p></list-item></list></p></list-item><list-item id="u7110"><label>•</label><p id="p8930">These problems must be ruled out by clinical, laboratory, and ultrasound examination and must be surgically corrected if necessary.</p></list-item><list-item id="u7115"><label>•</label><p id="p8935">Peritoneal fluid analysis in normal post foaling mares can occur and is similar to normal horse laboratory values</p></list-item><list-item id="u7120"><label>•</label><p id="p8940">Medical therapy alone may be appropriate for small colon impaction and occasionally small dorsal tears of the uterus and/or bladder.</p></list-item></list></p></sec></sec><sec id="s1515"><title>Peritonitis</title><p id="p8945"><list list-type="simple" id="ulist1490"><list-item id="u7125"><label>•</label><p id="p8950">Peritonitis, inflammation of the peritoneal cavity, is classified according to the following:<list list-type="simple" id="ulist1495"><list-item id="u7130"><label>•</label><p id="p8955">Origin: primary or secondary</p></list-item><list-item id="u7135"><label>•</label><p id="p8960">Onset: peracute, acute, or chronic</p></list-item><list-item id="u7140"><label>•</label><p id="p8965">Extent of involvement: diffuse or localized</p></list-item><list-item id="u7145"><label>•</label><p id="p8970">Presence of bacteria: septic or nonseptic</p></list-item></list></p></list-item><list-item id="u7150"><label>•</label><p id="p8975">Peritonitis usually is acute, diffuse, and results from GI compromise or infectious disease.</p></list-item><list-item id="u7155"><label>•</label><p id="p8980">Severity depends on the causative agent, virulence of the organism, host defenses, extent and site of involvement, recognition of problems, and treatment.</p></list-item><list-item id="u7160"><label>•</label><p id="p8985">Generally the aboral sites, cecum to small colon, contain more bacteria and anaerobes and therefore are associated with more severe disease.</p></list-item><list-item id="u7165"><label>•</label><p id="p8990">The organisms frequently cultured are enteric aerobes (<italic>E. coli, Actinobacillus</italic> organisms, <italic>Streptococcus equi, S. zooepidemicus,</italic> and <italic>Rhodococcus</italic> organisms) and anaerobes (<italic>Bacteroides, Peptostreptococcus,</italic> and <italic>Clostridium</italic>), and in rare cases, <italic>Fusobacterium</italic> organisms.</p></list-item></list></p><sec id="s1520"><title>Causes</title><p id="p8995"><list list-type="simple" id="ulist1500"><list-item id="u7170"><label>•</label><p id="p9900">Idiopathic</p></list-item><list-item id="u7175"><label>•</label><p id="p9005">Perforation of the GI or genitourinary tract</p></list-item><list-item id="u7180"><label>•</label><p id="p9010"><bold><italic>Practice Tip:</italic></bold><italic>Infectious disease</italic> (Actinobacillus) <italic>is a common cause of peritonitis in adult horses without known predisposing causes. Some horses may even have repeat occurrences separated by months or years.</italic></p></list-item><list-item id="u7185"><label>•</label><p id="p9015">Trauma</p></list-item><list-item id="u7190"><label>•</label><p id="p9020">Iatrogenic after abdominal surgery</p></list-item></list></p></sec><sec id="s1525"><title>Diagnosis</title><p id="p9025"><list list-type="simple" id="ulist1505"><list-item id="u7195"><label>•</label><p id="p9030">Clinical signs depend on the causative agent and the extent and duration of disease.</p></list-item><list-item id="u7200"><label>•</label><p id="p9035">Local peritonitis has minimal systemic signs.</p></list-item><list-item id="u7205"><label>•</label><p id="p9040">Diffuse peritonitis has signs of endotoxemia and septicemia, abdominal pain, pyrexia, anorexia, weight loss, and diarrhea.</p></list-item><list-item id="u7210"><label>•</label><p id="p9045">Peracute peritonitis resulting from intestinal rupture causes severe signs of endotoxemia, depression, and rapid cardiovascular deterioration; severe abdominal pain, sweating, muscle fasciculations, tachycardia, red to purple mucous membranes with increased CRT; and dehydration.</p></list-item><list-item id="u7215"><label>•</label><p id="p9050">In acute diffuse peritonitis, death occurs 4 to 24 hours after the primary insult.<list list-type="simple" id="ulist1510"><list-item id="u7220"><label>•</label><p id="p9055">Fever and abdominal pain may <italic>not</italic> occur and depend on the stage of endotoxic shock.</p></list-item><list-item id="u7225"><label>•</label><p id="p9060">Ileus and gastric reflux may develop as the result of peritoneal and serosal inflammation.</p></list-item><list-item id="u7230"><label>•</label><p id="p9065">Rectal examination may yield normal findings or dry, emphysematous, “gritty” serosa and peritoneum and distention of the large and small intestine from ileus.</p></list-item></list></p></list-item><list-item id="u7235"><label>•</label><p id="p9070">Affected horses with localized, subacute to chronic peritonitis have signs of depression, anorexia, weight loss, intermittent fever, ventral edema, intermittent abdominal pain, and mild dehydration. Usually large amounts of echogenic fluid are found within the abdominal cavity on ultrasound and there is thickening of the intestinal walls.</p></list-item></list></p><sec id="s1530"><title>Clinical Laboratory Findings</title><p id="p9075"><list list-type="simple" id="ulist1515"><list-item id="u7240"><label>•</label><p id="p9080">Increased PCV</p></list-item><list-item id="u7245"><label>•</label><p id="p9085">Increased (hemoconcentration) or decreased (protein loss into the peritoneal cavity) TPP concentration</p></list-item><list-item id="u7250"><label>•</label><p id="p9090">Hyperfibrinogenemia</p></list-item><list-item id="u7255"><label>•</label><p id="p9095">Increased creatinine concentration: prerenal or renal azotemia</p></list-item><list-item id="u7260"><label>•</label><p id="p9100">Metabolic acidosis</p></list-item></list></p></sec><sec id="s1535"><title>Results of Complete Blood Count</title><p id="p9105"><list list-type="simple" id="ulist1520"><list-item id="u7265"><label>•</label><p id="p9110">Significant leukopenia: neutropenia and left shift caused by endotoxemia and consumption in peracute and acute peritonitis</p></list-item><list-item id="u7270"><label>•</label><p id="p9115">Leukocytosis: neutrophilia caused by inflammation with hyperfibrinogenemia in chronic peritonitis</p></list-item></list></p></sec><sec id="s1540"><title>Peritoneal Fluid Analysis</title><p id="p9120"><list list-type="simple" id="ulist1525"><list-item id="u7275"><label>•</label><p id="p9125">Collect peritoneal fluid in an EDTA tube for cytologic examination, measurement of total protein, and WBC count. Collect samples for bacterial culture in a sterile tube (see <xref rid="u0085" ref-type="list-item">p. 158</xref>).</p></list-item><list-item id="u7280"><label>•</label><p id="p9130">Total protein concentration and nucleated cell count is increased: 20,000 to 400,000 cells/µL</p></list-item><list-item id="u7285"><label>•</label><p id="p9135">Cytologic examination shows free or phagocytized bacteria in leukocytes.</p></list-item><list-item id="u7290"><label>•</label><p id="p9140">Perform Gram stain for initial evaluation and selection of antimicrobial agents while awaiting culture and susceptibility results.</p></list-item></list><boxed-text id="b0260"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1545"><title>Peritonitis</title><p id="p9145"><list list-type="simple" id="ulist1530"><list-item id="u7295"><label>•</label><p id="p9150">Prompt and aggressive treatment is needed.</p></list-item><list-item id="u7300"><label>•</label><p id="p9155">Perform the following:<list list-type="simple" id="ulist1535"><list-item id="u7305"><label>•</label><p id="p9160">Manage the primary disease; however, with <italic>Actinobacillus</italic> peritonitis there is usually <italic>no</italic> other disorder and antibiotics with even low-level supportive care results in a rapid recovery.</p></list-item><list-item id="u7310"><label>•</label><p id="p9165">Provide analgesics.</p></list-item><list-item id="u7315"><label>•</label><p id="p9170">Reverse the endotoxic and hypovolemic shock.</p></list-item><list-item id="u7320"><label>•</label><p id="p9175">Correct metabolic and electrolyte abnormalities.</p></list-item><list-item id="u7325"><label>•</label><p id="p9180">Correct dehydration.</p></list-item><list-item id="u7330"><label>•</label><p id="p9185">Correct hypoproteinemia.</p></list-item><list-item id="u7335"><label>•</label><p id="p9190">Administer broad-spectrum antimicrobial therapy.</p></list-item><list-item id="u7340"><label>•</label><p id="p9195">Administer intravenous balanced electrolyte solution to maintain intravascular fluid volume.</p></list-item></list></p></list-item><list-item id="u7345"><label>•</label><p id="p9200">Hypertonic saline solution (7% NaCl, 1 to 2 L IV) improves systemic blood pressure and cardiac output. Hypertonic saline solution administered initially must be followed by adequate fluid replacement with a balanced crystalloid solution (see Chapter 32, p. 567).</p></list-item><list-item id="u7350"><label>•</label><p id="p9205">A TPP concentration <4.5 g/dL necessitates administration of plasma, 2 to 10 L IV slowly, to maintain plasma oncotic pressure and minimize pulmonary edema during rehydration with intravenous fluids.</p></list-item><list-item id="u7355"><label>•</label><p id="p9210">Antiserum (Endoserum) against gram-negative core antigens (endotoxin) can be administered intravenously diluted in a balanced electrolyte solution. Hyperimmune plasma directed against the J-5 mutant strain of <italic>E. coli</italic> (Polymune-J, Foalimmune) or normal equine plasma (2 to 10 L) administered intravenously, slowly, may be equally beneficial for supplying protein, fibronectin, complement, antithrombin III, and other inhibitors of hypercoagulability.</p></list-item><list-item id="u7360"><label>•</label><p id="p9215">Administer polymyxin B, 2000 to 6000 IU/kg IV q12h as needed.</p></list-item><list-item id="u7365"><label>•</label><p id="p9220">Administer flunixin meglumine, 0.66 to 1.1 mg/kg IV q12h, or low dose, 0.25 mg/kg IV q8h, to reduce the adverse effects of arachidonic acid metabolites. NSAIDs should be used with caution in the care of hypovolemic, hypoproteinemic patients to avoid GI and renal toxicity.</p></list-item><list-item id="u7370"><label>•</label><p id="p9225">Monitor blood gas and serum electrolyte levels and correct deficiencies.</p></list-item><list-item id="u7375"><label>•</label><p id="p9230">Start antimicrobial therapy immediately after a peritoneal fluid sample has been obtained for culture and susceptibility.</p></list-item><list-item id="u7380"><label>•</label><p id="p9235">Antimicrobial combinations commonly used include the following:<list list-type="simple" id="ulist1540"><list-item id="u7385"><label>•</label><p id="p9240">Na<sup>+</sup>/K<sup>+</sup> penicillin, 22,000 to 44,000 IU/kg IV q6h, and</p></list-item><list-item id="u7390"><label>•</label><p id="p9245">Aminoglycosides: gentamicin, 6.6 mg/kg IV q24h; or amikacin, 15 to 25 mg/kg IV q24h; or enrofloxacin, 5.0 mg/kg q24h IV or 7.5 mg/kg q24h PO.</p></list-item><list-item id="u7395"><label>•</label><p id="p9250">Metronidazole, 15 to 25 mg/kg PO, or suppository q8h for anaerobes</p></list-item></list></p></list-item><list-item id="u7400"><label>•</label><p id="p9255">Duration of antimicrobial therapy depends on the following:<list list-type="simple" id="ulist1545"><list-item id="u7405"><label>•</label><p id="p9260">Severity of the peritonitis</p></list-item><list-item id="u7410"><label>•</label><p id="p9265">Causative agent</p></list-item><list-item id="u7415"><label>•</label><p id="p9270">Response to treatment</p></list-item><list-item id="u7420"><label>•</label><p id="p9275">Complications: thrombophlebitis, abdominal abscessation</p></list-item></list></p></list-item><list-item id="u7425"><label>•</label><p id="p9280">After stabilization, perform surgical intervention to correct the primary problem (if known) and reduce peritoneal contamination by abdominal drainage, peritoneal lavage, and peritoneal dialysis.</p></list-item><list-item id="u7430"><label>•</label><p id="p9285">Use clinical signs and sequential evaluation of clinicopathologic parameters and peritoneal fluid to assess response to treatment. Generalized septic peritonitis may necessitate 1 to 6 months of antimicrobial therapy.</p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1550"><title>Prognosis</title><p id="p9290"><list list-type="simple" id="ulist1550"><list-item id="u7435"><label>•</label><p id="p9295">Prognosis depends on:<list list-type="simple" id="ulist1555"><list-item id="u7440"><label>•</label><p id="p9300">Severity and duration of the disease</p></list-item><list-item id="u7445"><label>•</label><p id="p9305">Primary causative agent</p></list-item><list-item id="u7450"><label>•</label><p id="p9310">Complications, which include:<list list-type="simple" id="ulist1560"><list-item id="u7455"><label>○</label><p id="p9315">Intraabdominal adhesion formation</p></list-item><list-item id="u7460"><label>○</label><p id="p9320">Laminitis</p></list-item><list-item id="u7465"><label>○</label><p id="p9325">Endotoxic shock</p></list-item></list></p></list-item></list></p></list-item><list-item id="u7470"><label>•</label><p id="p9330">Prognosis is fair to good in mild, acute, diffuse peritonitis if prompt, aggressive management of the underlying problem is successful or if it is unknown.</p></list-item><list-item id="u7475"><label>•</label><p id="p9335">Prognosis is good in <italic>Actinobacillus</italic> peritonitis.</p></list-item><list-item id="u7480"><label>•</label><p id="p9340">Prognosis is poor if there is significant abdominal contamination or intestinal perforation.</p></list-item></list></p></sec></sec></sec><sec id="s1555"><title>Acute Diarrhea</title><sec id="s1560"><title>Diarrhea in Nursing Foals</title><p id="p9345"><italic><bold>Nathan Slovis</bold></italic></p><sec id="s1565"><title>Necrotizing Enterocolitis</title><p id="p9350"><list list-type="simple" id="ulist1565"><list-item id="u7485"><label>•</label><p id="p9355">Necrotizing enterocolitis is a common cause of diarrhea and colic in foals, usually during the first week of life. The diarrhea can be hemorrhagic.</p></list-item></list></p><sec id="s9045"><title>Causes</title><p id="p13545"><list list-type="simple" id="ulist9065"><list-item id="u11185"><label>•</label><p id="p13550">Cases of necrotizing enterocolitis generally are considered to be caused by perinatal asphyxia syndrome, the anaerobic bacteria <italic>C. difficile, C. perfringens</italic> type C, or <italic>Bacteroides fragilis.</italic></p></list-item><list-item id="u11190"><label>•</label><p id="p13555"><italic><bold>Practice Tip:</bold> Recumbency and feeding milk replacer are considered to increase the risk of acquiring the disease. Cases of clostridial diarrhea frequently become a farm problem.</italic></p></list-item><list-item id="u7490"><label>•</label><p id="p9360">Perinatal asphyxia syndrome (PAS) produces hypoxic ischemic encephalopathy (HIE) resulting in neurologic deficits ranging from hypotonia to grand mal seizures. Foals affected with perinatal asphyxia also experience gastrointestinal disturbances ranging from mild ileus and delayed gastric emptying to severe, bloody diarrhea and necrotizing enterocolitis (NEC).</p></list-item><list-item id="u7495"><label>•</label><p id="p9365">It has been postulated that when the preterm infant is stressed by periods of hypoxia or hypotension, blood flow is redistributed, via input from the adrenergic system, away from the splanchnic bed. During the period of reperfusion, oxygen free radicals are generated; these free radicals can cause the tissue damage that is typically seen with reperfusion injury.</p></list-item><list-item id="u7500"><label>•</label><p id="p9370">If the hypoxic event is severe enough, then NEC can occur resulting in:<list list-type="simple" id="ulist1570"><list-item id="u7505"><label>•</label><p id="p9375">Bloody diarrhea</p></list-item><list-item id="u7510"><label>•</label><p id="p9380">Pneumatosis intestinalis</p></list-item><list-item id="u7515"><label>•</label><p id="p9385">Ascites</p></list-item><list-item id="u7520"><label>•</label><p id="p9390">Intestinal perforation</p></list-item></list></p></list-item><list-item id="u7525"><label>•</label><p id="p9395"><italic><bold>Practice Tip:</bold> A diagnosis of hypoxic ischemic ileus is presumptive when the patient has a history of:</italic><list list-type="simple" id="ulist1575"><list-item id="u7530"><label>•</label><p id="p9400"><italic>Peripartum asphyxia (placentitis, premature placental separation)</italic></p></list-item><list-item id="u7535"><label>•</label><p id="p9405"><italic>Negative fecal diagnostics for infectious diseases</italic></p></list-item><list-item id="u7540"><label>•</label><p id="p9410"><italic>Abdominal ultrasonography reveals distended small intestine with decreased motility</italic></p></list-item></list></p></list-item><list-item id="u7545"><label>•</label><p id="p9415"><italic><bold>C. difficile</bold></italic> produces several toxins; only the effects of toxin A and B are well known.<list list-type="simple" id="ulist1580"><list-item id="u7550"><label>•</label><p id="p9420">When established in the colon, pathogenic strains of <italic>C. difficile</italic> produce toxins that cause diarrhea and colitis. <italic><bold>Note:</bold></italic> Strains that do not produce these toxins are not pathogenic.</p></list-item></list></p></list-item><list-item id="u7555"><label>•</label><p id="p9425"><italic><bold>C. perfringens</bold></italic> produces four major toxins, with one relatively newer toxin identified (β<sub>2</sub>).<list list-type="simple" id="ulist1585"><list-item id="u7560"><label>•</label><p id="p9430">Recently an unassigned type of <italic>C. perfringens</italic> that produces alpha toxin and the newly discovered β<sub>2</sub>-toxin was described. The toxin was isolated from piglets with necrotic enterocolitis and was also found in horses with enterocolitis. Because the alpha toxin, produced by all types of <italic>C. perfringens</italic> including nonpathogenic type A strains, is not considered a primary cause of digestive lesions, it was suggested that the β<sub>2</sub>-toxin, which is present in this new type of <italic>C. perfringens,</italic> is responsible for the lesions.</p></list-item><list-item id="u7565"><label>•</label><p id="p9435"><italic>C. perfringens</italic> diarrhea in foals is considered to result from infection with type C (beta toxin) (sporadic cases) or enterotoxin from <italic>C. perfringens</italic> type A, which may be associated with a high morbidity<italic>.</italic></p></list-item></list></p></list-item></list></p></sec><sec id="s1570"><title>Clinical Signs</title><p id="p9440"><list list-type="simple" id="ulist1590"><list-item id="u7570"><label>•</label><p id="p9445">Colic that frequently precedes the production of diarrhea by several hours</p></list-item><list-item id="u7575"><label>•</label><p id="p9450">Abdominal distention</p></list-item><list-item id="u7580"><label>•</label><p id="p9455">Fever</p></list-item><list-item id="u7585"><label>•</label><p id="p9460">Potentially hemorrhagic diarrhea (not noted in most type A cases but common in type C cases)</p></list-item></list></p><p id="p9465"><italic><bold>Practice Tip:</bold></italic> C. perfringens <italic>type C cases usually have normal IgG, bloody diarrhea, and are almost always in foals younger than 8 days of age and sporadic in occurrence as opposed to the sometimes outbreak of presumed</italic> C. perfringens <italic>type A</italic> and Clostridium difficile <italic>diarrhea in neonatal foals, which often do</italic> not <italic>have bloody feces.</italic><list list-type="simple" id="ulist1595"><list-item id="u7590"><label>•</label><p id="p9470">Anorexia</p></list-item></list></p></sec><sec id="s1575"><title>Diagnosis</title><p id="p9475"><list list-type="simple" id="ulist1600"><list-item id="u7595"><label>•</label><p id="p9480">Clinical signs</p></list-item><list-item id="u7600"><label>•</label><p id="p9485">Rule out other causes of abdominal pain (see <xref rid="s0450" ref-type="sec">p. 185</xref>).</p></list-item><list-item id="u7605"><label>•</label><p id="p9490">Meconium impaction and enteritis are the most common causes of colic in foals.</p></list-item><list-item id="u7610"><label>•</label><p id="p9495">Perform abdominal ultrasonography:<list list-type="simple" id="ulist1605"><list-item id="u7615"><label>•</label><p id="p9500">Enterocolitis leads to hypomotile, thickened loops of small intestine (<xref rid="f0365" ref-type="fig">Fig. 18-70</xref>), whereas a physical obstruction (<xref rid="f0360" ref-type="fig">Fig. 18-71</xref>) typically does <italic>not</italic> demonstrate diffuse amotility, and the walls are not as thick.<fig id="f0365"><label>Figure 18-70</label><caption><p>Foal diarrhea: Ultrasound finding in a 3-day-old foal with hemorrhagic diarrhea due to <italic>Clostridium perfringens</italic> type C. The same organism was cultured from the feces and blood. With antibiotic and supportive treatments the foal recovered in 3 days.</p></caption><graphic xlink:href="f018-070-9781455708925"></graphic></fig><fig id="f0360"><label>Figure 18-71</label><caption><p>Classic sonographic view of an obstructive intestinal lesion, which was a midjejunal intussusception.</p></caption><graphic xlink:href="f018-071-9781455708925"></graphic></fig></p></list-item><list-item id="u7620"><label>•</label><p id="p9505">One may see “pneumatosis intestinalis,” intramural gas echoes in the small or large bowel wall.</p></list-item></list></p></list-item><list-item id="u7625"><label>•</label><p id="p9510">Perform abdominal radiography (85 kVp, 20 mA-s, rare earth screens) if necessary.<list list-type="simple" id="ulist1610"><list-item id="u7630"><label>•</label><p id="p9515">Similar to ultrasonography, radiography shows more diffuse gas distention of the small bowel as opposed to a smaller area of distention seen with problems such as intussusception.</p></list-item></list></p></list-item><list-item id="u7635"><label>•</label><p id="p9520">Abdominocentesis should be performed only in cases with difficulty differentiating surgical from medical problems.<list list-type="simple" id="ulist1615"><list-item id="u7640"><label>•</label><p id="p9525">Use a teat cannula or bitch catheter rather than performing a needle aspirate.</p></list-item><list-item id="u7645"><label>•</label><p id="p9530">Indiscriminant “centesis” is fraught with complications including enterocentesis and peritonitis.</p></list-item><list-item id="u7650"><label>•</label><p id="p9535">Use ultrasound to identify an area to sample.</p></list-item></list></p></list-item><list-item id="u7655"><label>•</label><p id="p9540">Clinical pathology results are as follows:<list list-type="simple" id="ulist1620"><list-item id="u7660"><label>•</label><p id="p9545">Blood cultures frequently are positive for <italic>C. perfringens</italic> in foals with severe clostridial enteritis. They may also be blood culture positive for <italic>Enterococcus</italic> spp.</p></list-item><list-item id="u7665"><label>•</label><p id="p9550">CBC generally reveals a leukopenia with toxic neutrophils.</p></list-item><list-item id="u7670"><label>•</label><p id="p9555">Serum chemistry showing hyponatremia, hypochloremia, and frequently a low total CO<sub>2</sub> is indicative of acidosis.</p></list-item><list-item id="u7675"><label>•</label><p id="p9560">Hypoproteinemia is secondary to the effects of clostridial toxins leading to extravasation of plasma proteins.</p></list-item><list-item id="u7680"><label>•</label><p id="p9565">Metabolic acidosis is also consistent with clostridial enterocolitis and hypovolemia or gastrointestinal tract loss of bicarbonate.</p></list-item><list-item id="u7685"><label>•</label><p id="p9570">Hyponatremia may also be attributable to the gastrointestinal tract losses, as well as to an excess of free water associated with water or milk consumption by these foals.</p></list-item></list></p></list-item><list-item id="u7690"><label>•</label><p id="p9575">Fecal diagnostics for clostridial enteritis are as follows:<list list-type="simple" id="ulist1625"><list-item id="u7695"><label>•</label><p id="p9580">Direct fecal smear with Gram stain<list list-type="simple" id="ulist1630"><list-item id="u7700"><label>○</label><p id="p9585">A presumptive diagnosis may be made (until culture and toxin analysis) by demonstration of abundant gram-positive bacteria in a fecal smear.</p></list-item><list-item id="u7705"><label>○</label><p id="p9590">However, this test may not be sensitive because <italic>C. perfringens</italic> was isolated from 59% of samples in which no gram-positive rods were seen.</p></list-item></list></p></list-item><list-item id="u7710"><label>•</label><p id="p9595"><italic>C. difficile</italic> toxin assays: toxin types A and B. More recently two new enzyme immunoassays have been introduced that:</p></list-item><list-item id="u7715"><label>•</label><p id="p9600">Detect toxin A/toxin B (<italic>C. difficile</italic> TOX A/B test<xref rid="fn0090" ref-type="fn">17</xref>)</p></list-item><list-item id="u7720"><label>•</label><p id="p9605">Detect antigen of <italic>C. difficile</italic> and toxin A (TRIAGE Micro<xref rid="fn0095" ref-type="fn">18</xref>)<list list-type="simple" id="ulist1635"><list-item id="u7725"><label>○</label><p id="p9610">These tests have a good sensitivity (69% to 87%) and specificity (99% to 100%).</p></list-item><list-item id="u7730"><label>○</label><p id="p9615"><italic>C. difficile</italic> TOX A/B test, Techlab has been validated for use in feces of horses.</p></list-item><list-item id="u7735"><label>○</label><p id="p9620"><italic><bold>Practice Tip:</bold> Do</italic> not <italic>use</italic> Styrofoam cups <italic>to submit a fecal sample because they can bind the clostridial toxins. Fecal samples can be stored for up to 72 hours between 2° and 8° C.</italic></p></list-item><list-item id="u7740"><label>○</label><p id="p9625">Most cases appear to be positive for toxins on examination of a single fecal sample although repeat testing may further improve sensitivity.</p></list-item></list></p></list-item><list-item id="u7745"><label>•</label><p id="p9630">The toxin must be demonstrated in feces to confirm diagnosis.</p></list-item><list-item id="u7750"><label>•</label><p id="p9635">The presence of <italic>C. difficile</italic> in culture is not diagnostic because many strains do <italic>not</italic> produce toxin or disease</p></list-item><list-item id="u7755"><label>•</label><p id="p9640">Some healthy foals may have <italic>C. difficile</italic>–toxin positive stool.</p></list-item></list></p></list-item><list-item id="u7760"><label>•</label><p id="p9645"><italic>C. perfringens</italic> toxin assay: enterotoxin assay<list list-type="simple" id="ulist1640"><list-item id="u7765"><label>•</label><p id="p9650">Enzyme-linked immunosorbent assay (ELISA) is commercially available for <italic>C. perfringens</italic> enterotoxin (Tech Lab).<list list-type="simple" id="ulist1645"><list-item id="u7770"><label>○</label><p id="p9655">Labile-toxin assay must be run within one-half hour of sample collection or sample should be frozen for testing.</p></list-item></list></p></list-item><list-item id="u7775"><label>•</label><p id="p9660">Obtain a fecal anaerobic culture.</p></list-item><list-item id="u7780"><label>•</label><p id="p9665">Commercial anaerobic kits are available<xref rid="fn0100" ref-type="fn">19</xref>; it is best to use anaerobic blood plates.</p></list-item></list></p></list-item><list-item id="u7785"><label>•</label><p id="p9670">Pure growth of <italic>C. perfringens</italic> is <italic>indicative</italic> of disease, but toxin must be identified to confirm disease.</p></list-item><list-item id="u7790"><label>•</label><p id="p9675">Polymerase chain reaction (PCR):<list list-type="simple" id="ulist1650"><list-item id="u7795"><label>•</label><p id="p9680">Incorporated primers for <italic>C. difficile</italic> toxin A and B</p></list-item><list-item id="u7800"><label>•</label><p id="p9685">Incorporated primers that allowed for classification of <italic>C. perfringens</italic> types A, B, C, D, and E, as well as genes for β<sub>2</sub>-toxin and enterotoxin (CPE)</p></list-item><list-item id="u7805"><label>•</label><p id="p9690">PCR testing of feces would be needed to confirm <italic>C. perfringens</italic> type C. One option for testing is at Iowa State University Diagnostic Laboratory (515-294-1950).</p></list-item></list></p></list-item></list></p></sec><sec id="s1580"><title>Prognosis</title><p id="p9695"><list list-type="simple" id="ulist1655"><list-item id="u7810"><label>•</label><p id="p9700">Initially, the prognosis is considered guarded because the intestinal necrosis may progress rapidly. (This is especially true with the infrequent and sporadic cases of <italic>C. perfringens</italic> type C.)</p></list-item><list-item id="u7815"><label>•</label><p id="p9705">If the foal survives the initial 48 hours, the prognosis generally improves significantly.</p></list-item></list><boxed-text id="b0265"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1585"><title>Clostridial Diarrhea</title><sec id="s1590"><title>Pain Relief</title><p id="p9710"><list list-type="simple" id="ulist1660"><list-item id="u7820"><label>•</label><p id="p9715">Attempt to control pain <italic>without</italic> the use of high doses of flunixin meglumine; a single full dose is many times necessary to control the pain.<list list-type="simple" id="ulist1665"><list-item id="u7825"><label>•</label><p id="p9720">Dipyrone, 3 to 5 mL IV; xylazine, 0.6 to 1.0 mg/kg IV; butorphanol, 0.02 to 0.04 mg/kg IV or IM; or ketoprofen, 1 mg/kg IV. Meloxicam 0.6 mg/kg IV is another more COX-2 selective option but is expensive in the United States.</p></list-item><list-item id="u7830"><label>•</label><p id="p9725">If the foal remains painful and is gas-distended <italic>and</italic> obstructive disease is ruled out, administer neostigmine, 0.2 to 1 mg SQ (total dose) q1h for 3 treatments then q6h along with analgesics or sedation.</p></list-item></list></p></list-item></list></p></sec><sec id="s1595"><title>Antibiotics</title><p id="p9730"><list list-type="simple" id="ulist1670"><list-item id="u7835"><label>•</label><p id="p9735">Sodium or potassium penicillin, 22,000 to 44,000 IU/kg IV q6h</p></list-item><list-item id="u7840"><label>•</label><p id="p9740"><italic><bold>Note:</bold></italic> The most common organism cultured from the blood of neonatal foals with enterocolitis is <italic>Enterococcus</italic> spp. (fecal streps). These are gram-positive facultative anaerobic cocci found in the intestinal tract that are resistant to most cephalosporins (therefore, ceftiofur is <italic>not</italic> a good choice for treating septic foals with enterocolitis); ampicillin (15 mg/kg q8h IV) is preferred over penicillin for enterococci but <italic>not</italic> as good as penicillin for <italic>Clostridium</italic> spp.</p></list-item><list-item id="u7845"><label>•</label><p id="p9745">Amikacin, 21 to 25 mg/kg IV q24h (Use <italic>only</italic> when urine production is normal.)</p></list-item><list-item id="u7850"><label>•</label><p id="p9750">Metronidazole, 15 mg/kg PO q8 to 12h or 10 mg/kg IV q6 to 8h; use if abundant gram-positive rods are found on fecal smear or <italic>C. difficile</italic> toxins are identified.</p></list-item></list></p></sec></sec><sec id="s1600"><title>Intravenous Fluids</title><p id="p9755"><list list-type="simple" id="ulist1675"><list-item id="u7855"><label>•</label><p id="p9760">Continual administration is unlikely if the mare is in the same stall as the foal. One to 2 L of fluids can be administered, as a bolus, over 20 to 30 minutes q4h to q12h a day.</p></list-item><list-item id="u7860"><label>•</label><p id="p9765">Lactated Ringer's solution, Normosol-R, or Plasma-Lyte preferred</p></list-item><list-item id="u7865"><label>•</label><p id="p9770">If severe, acute hyponatremia is present, correction of sodium to 125 mEq/L can be rapid, but further correction should be gradual to prevent neurologic signs.<list list-type="simple" id="ulist1680"><list-item id="u7870"><label>•</label><p id="p9775">Potassium chloride, 20 mEq/L if foal is urinating: Most foals on large volumes of IV fluids require supplemental potassium, particularly if they are anorectic.</p></list-item><list-item id="u7875"><label>•</label><p id="p9780">Sodium bicarbonate: based on results of a clinical chemistry TCO<sub>2</sub> or blood gas and <italic>only</italic> after correcting dehydration.</p></list-item><list-item id="u7880"><label>•</label><p id="p9785">Dextrose solution: If the foal appears weak and serum glucose measurement cannot be obtained, add 55 mL of 50% dextrose to 1 L of fluid for a 2.5% solution; 110 mL for a 5% solution.</p></list-item></list></p></list-item><list-item id="u7885"><label>•</label><p id="p9790">Plasma, 2 L or more IV<list list-type="simple" id="ulist1685"><list-item id="u7890"><label>•</label><p id="p9795">Hyperimmune for endotoxin is preferable.</p></list-item><list-item id="u7895"><label>•</label><p id="p9800">A hyperimmunized <italic>Clostridium difficile Toxin A and B</italic> plasma is currently available.<xref rid="fn0105" ref-type="fn">20</xref></p></list-item><list-item id="u7900"><label>•</label><p id="p9805">Oral and IV administration of <italic>C. perfringens</italic> type A, C, and D hyperimmunized plasma may be given to the neonate.<xref rid="fn0110" ref-type="fn">21</xref></p></list-item><list-item id="u7905"><label>•</label><p id="p9810">The oral dosage ranges from 50 to 100 mL every 6 hours for 48 to 72 hours.</p></list-item><list-item id="u7910"><label>•</label><p id="p9815">If the foal is severely ill, use nasogastric intubation with 250 to 500 mL of the hyperimmunized plasma. Subjectively, foals given the hyperimmunized plasma have formed feces quicker than the foals not treated with the plasma.</p></list-item></list></p></list-item><list-item id="u7915"><label>•</label><p id="p9820"><italic><bold>Note</bold>:</italic> The efficacy of the plasma in treating diarrhea/toxic insult is currently anecdotal.</p></list-item></list></p></sec><sec id="s1605"><title>Intestinal Protectants</title><p id="p9825"><list list-type="simple" id="ulist1690"><list-item id="u7920"><label>•</label><p id="p9830">Lactaid<xref rid="fn0115" ref-type="fn">22</xref> (1 tablet every feeding or q2h), lactase,<xref rid="fn0120" ref-type="fn">23</xref> or yogurt (1 to 2 oz q6h): foals are likely to be lactose intolerant with clostridial infection.</p></list-item><list-item id="u7925"><label>•</label><p id="p9835">Di-tri-octahedral smectite, Bio-Sponge<xref rid="fn0125" ref-type="fn">24</xref> or Anti-Diarrhea Gel<xref rid="fn0130" ref-type="fn">25</xref><list list-type="simple" id="ulist9070"><list-item id="u7930"><label>•</label><p id="p9840">Studies have shown in vitro adsorption of clostridial toxins by these products.</p></list-item></list></p></list-item><list-item id="u7935"><label>•</label><p id="p9845">Bentonite clay can also be used for treatment because it adsorbs <italic>C. perfringens</italic> alpha, beta, and beta-2 exotoxins without interfering with absorption of equine colostral antibodies or metronidazole.</p></list-item><list-item id="u7940"><label>•</label><p id="p9850">Bismuth subsalicylate, 30 to 60 mL PO q2-6h</p></list-item><list-item id="u7945"><label>•</label><p id="p9855">Probiotics: clinical evidence is in question; <italic>Lactobacillus pentosus</italic> WE7 may actually be detrimental to recovery. Following omeprazole or ranitidine treatment, to raise gastric pH, fecal transfaunation from a healthy foal or the mare may be indicated.</p></list-item><list-item id="u11195"><label>•</label><p id="p13560">Gastric ulcer prophylaxis:<list list-type="simple" id="ulist9075"><list-item id="u7965"><label>•</label><p id="p9875">Sucralfate, 22 mg/kg PO q6h <italic>and</italic></p></list-item><list-item id="u7950"><label>•</label><p id="p9860">Omeprazole, 1-4 mg/kg PO q24h <italic>or</italic></p></list-item><list-item id="u7955"><label>•</label><p id="p9865">Ranitidine, 1.5 mg/kg IV(expensive) or 6.6 mg/kg PO q8h <italic>or</italic></p></list-item><list-item id="u7960"><label>•</label><p id="p9870">Famotidine, 0.23 to 0.5 mg/kg IV q8 to 12h or 2.8 to 4 mg/kg PO q8 to 12h</p></list-item></list></p></list-item></list></p></sec><sec id="s1610"><title>Supportive Care</title><p id="p9880"><list list-type="simple" id="ulist1695"><list-item id="u7970"><label>•</label><p id="p9885">Keep the foal dry and warm.</p></list-item><list-item id="u7975"><label>•</label><p id="p9890">Apply a desiccant to the hind quarters; frequently wash and dry the tail.</p></list-item></list></p></sec><sec id="s1615"><title>Prevention</title><p id="p9895"><list list-type="simple" id="ulist1700"><list-item id="u7980"><label>•</label><p id="p9990">Numerous prophylactic measures can be instituted on farms with a history of <italic>C. perfringens</italic>–associated enterocolitis in foals.</p></list-item><list-item id="u7985"><label>•</label><p id="p9905">Institute optimal hygienic efforts to ensure a clean foaling stall, and at parturition, clean the mare's udder before and after birth and the perineal and hind limb area to reduce exposure of the foal to fecal pathogens.</p></list-item><list-item id="u7990"><label>•</label><p id="p9910">Some farms have eliminated foal diarrhea outbreak by foaling the mares out on pasture.</p></list-item><list-item id="u7995"><label>•</label><p id="p9915">Oral administration of <italic>Lactobacillus acidophilus</italic> (found in yogurt and commercial probiotics) have been successfully used in chickens to minimize the overgrowth of <italic>C. perfringens.</italic></p></list-item><list-item id="u8000"><label>•</label><p id="p9920">Prophylactic use of metronidazole (10 mg/kg PO q12h) has also been instituted after birth with reports of mixed results.</p></list-item><list-item id="u8005"><label>•</label><p id="p9925">In mares with a history of good milk production, feed a ration containing low to moderate amounts of digestible energy 1 week before parturition and 1 week after parturition to reduce excessive milk production, and therefore, excessive milk intake by the foal. Use this only on farms with high morbidity of disease.</p></list-item><list-item id="u8010"><label>•</label><p id="p9930">Specific preventative methods addressing <italic>C. perfringens</italic> include: immunization of mares with a toxoid vaccine (aluminum hydroxide adsorbed culture supernatant PLUS recombinant beta-2 toxoid. Vaccine strain is <italic>C. perfringens</italic> type A and carries genes for alpha, beta-2, and CPE) recently developed (2007) by Hagyard Equine Medical Institute (<ext-link ext-link-type="uri" xlink:href="http://www.hagyardpharmacy.com" id="iw0010">www.hagyardpharmacy.com</ext-link>).<list list-type="simple" id="ulist1705"><list-item id="u8015"><label>•</label><p id="p9935">Other oral enteric protectants include the oral and/or IV administration of hyperimmunized plasma, previously mentioned.</p></list-item><list-item id="u8020"><label>•</label><p id="p9940">Specific immune treatments for <italic>C. perfringens</italic> types C and D provide some protection against alpha toxin; it is generally believed that this protection is inadequate against <italic>C. perfringens</italic> type A organisms.</p></list-item></list></p></list-item><list-item id="u8025"><label>•</label><p id="p9945">If clostridial disease is a historical problem on a farm, administration of the following has occasionally appeared to be of clinical benefit:<list list-type="simple" id="ulist1710"><list-item id="u8030"><label>•</label><p id="p9950">Prophylactic treatment of all newborns with penicillin G procaine, 22,000 units/kg IM q12h for 3 days, or combined with metronidazole, 15 mg/kg PO q12h for 3 to 5 days</p></list-item></list></p></list-item><list-item id="u8035"><label>•</label><p id="p9955">Strict isolation protocol of affected individuals</p></list-item><list-item id="u8040"><label>•</label><p id="p9960">Barrier protocol for handlers</p></list-item><list-item id="u8045"><label>•</label><p id="p9965">Disinfect stalls using:<list list-type="simple" id="ulist1715"><list-item id="u8050"><label>•</label><p id="p9970">Hypochlorite and phenolic compounds. <italic><bold>Important:</bold></italic> Hypochlorite is <italic>not</italic> effective in organic debris so must clean with detergent first.</p></list-item><list-item id="u8055"><label>•</label><p id="p9975"><italic>C. perfringens</italic> types C and D antitoxin is available for other large animal species, but safety and efficacy in foals are not well documented.</p></list-item></list></p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1620"><title>Foal Salmonellosis</title><sec id="s1625"><title>Clinical Signs</title><p id="p9980"><list list-type="simple" id="ulist1720"><list-item id="u8060"><label>•</label><p id="p9985">Variable diarrhea that may be scant or profuse, watery, or hemorrhagic</p></list-item><list-item id="u8065"><label>•</label><p id="p19980">Fever, usually >103° F, anorexia, tachycardia, tachypnea, and abdominal pain</p></list-item><list-item id="u8070"><label>•</label><p id="p9995">These signs are often related to bacteremia/endotoxemia rather than electrolyte derangements and dehydration</p></list-item><list-item id="u8075"><label>•</label><p id="p10000">Other signs of bacteremia include the following:<list list-type="simple" id="ulist1725"><list-item id="u8080"><label>•</label><p id="p10005">Green-tinted iris (presumed septicemia-induced uveitis), injected sclera and mucous membranes</p></list-item><list-item id="u8085"><label>•</label><p id="p10010">Lameness associated with septic arthritis or physitis</p></list-item><list-item id="u8090"><label>•</label><p id="p10015">Abnormal lung sounds associated with pneumonia of hematogenous origin</p></list-item><list-item id="u8095"><label>•</label><p id="p10020">Lethargy, stupor, or seizures associated with meningitis or from severe electrolyte derangements (e.g., hyponatremia)</p></list-item></list></p></list-item></list></p></sec><sec id="s1630"><title>Laboratory Findings</title><p id="p10025"><list list-type="simple" id="ulist1730"><list-item id="u8100"><label>•</label><p id="p10030">Leukopenia as a result of neutropenia is common.<list list-type="simple" id="ulist1735"><list-item id="u8105"><label>•</label><p id="p10035">Neutrophils frequently demonstrate toxic changes.</p></list-item></list></p></list-item><list-item id="u8110"><label>•</label><p id="p10040">Fibrinogen concentration may be elevated.</p></list-item><list-item id="u8115"><label>•</label><p id="p10045">Low platelet count may indicate the presence of disseminated intravascular coagulation.</p></list-item><list-item id="u8120"><label>•</label><p id="p10050"><italic><bold>Practice Tip:</bold> Hyponatremia, hypochloremia, acidosis, and azotemia are the most common laboratory findings with salmonellosis and most other causes of infectious diarrhea.</italic><list list-type="simple" id="ulist1740"><list-item id="u8125"><label>•</label><p id="p10055">Acidosis may mask life-threatening hypokalemia by raising the plasma potassium at the expense of total body potassium.</p></list-item><list-item id="u8130"><label>•</label><p id="p10060">Low serum potassium may result from a combination of decreased intake, increased loss in diarrheic feces, fluid therapy causing kaluresis and polyuric acute renal failure.</p></list-item></list></p></list-item></list></p></sec><sec id="s1635"><title>Diagnosis</title><p id="p10065"><list list-type="simple" id="ulist1745"><list-item id="u8135"><label>•</label><p id="p10070">For <italic>Salmonella</italic> spp., fecal cultures use selective media and selenite enrichment media.</p></list-item><list-item id="u8140"><label>•</label><p id="p10075">Other organisms of possible significance for foal diarrhea include <italic>E. coli, Aeromonas hydrophila, Yersinia psuedotuberculosis, Enterococcus</italic> spp., <italic>Campylobacter</italic> spp., <italic>Streptococcus</italic> spp., <italic>Clostridium</italic> spp., coronavirus, rotavirus, and <italic>Pseudomonas</italic> spp.</p></list-item><list-item id="u8145"><label>•</label><p id="p10080">Blood cultures frequently are positive (BBL, Becton, Dickinson and Company) in foals with salmonellosis.</p></list-item><list-item id="u8150"><label>•</label><p id="p10085">PCR</p></list-item><list-item id="u8160"><label>•</label><p id="p10095"><italic><bold>Practice Tip:</bold> The Enhanced rapid test system (Reveal</italic><xref rid="fn0135" ref-type="fn">26</xref><italic>2.0</italic> Salmonella <italic>test system) for the detection of</italic> Salmonella <italic>spp. should be performed on suspicious cultures (black or green colonies noted on Hektoen agar).</italic></p></list-item></list></p><p id="p10100"><boxed-text id="b0270"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1640"><title>Foal Salmonellosis</title><p id="p10105"><list list-type="simple" id="ulist1750"><list-item id="u8165"><label>•</label><p id="p10110">Treatment emphasis is on fluid therapy, antibiotics, and nursing care.</p></list-item></list></p><sec id="s1645"><title>Fluid Therapy</title><p id="p10115"><list list-type="simple" id="ulist1755"><list-item id="u8170"><label>•</label><p id="p10120">Polyionic fluids, Lactated Ringer's, Normosol-R and Plasma-Lyte are the best choices because sodium chloride is an acidifying solution.</p></list-item><list-item id="u8175"><label>•</label><p id="p10125">Use hypertonic saline only if polyionic fluids do <italic>not</italic> alleviate hypotension associated with severe disease <italic>or</italic> it can be administered in 1- to 2-mL/kg boluses at 30- to 60-minute intervals for severe hyponatremia.</p></list-item><list-item id="u8180"><label>•</label><p id="p10130">Goal for initial correction of severe hyponatremia should be sodium concentration of 125 to 130 mEq/L, <italic>no higher. <bold>Practice Tip:</bold> Chronic (days) hyponatremia should be corrected more slowly.</italic></p></list-item><list-item id="u8185"><label>•</label><p id="p10135">Add potassium chloride to fluids; 20 mEq/L, if foal is urinating and serum potassium <3.5 mEq/L.</p></list-item><list-item id="u8190"><label>•</label><p id="p10140"><italic><bold>Note:</bold></italic> Potassium administration should <italic>not</italic> exceed 0.5 mEq/kg/h.<list list-type="simple" id="ulist9095"><list-item id="u8300"><label>•</label><p id="p10260">Two tablespoons of Lite Salt (50% KCl) can be added to a pint of yogurt to safely assist in providing potassium to foals.</p></list-item></list></p></list-item><list-item id="u8195"><label>•</label><p id="p10145">If acidosis persists in the face of adequate fluid therapy and normal L-lactate (the metabolic acidosis is believed to be due to either D-lactate production or bicarbonate loss in the feces), add sodium bicarbonate to fluids.<list list-type="simple" id="ulist1760"><list-item id="u8200"><label>•</label><p id="p10150">Use an isotonic solution or 12.5 g baking soda added to a gallon of sterile water; be careful of too rapid correction of hyponatremia.</p></list-item><list-item id="u8205"><label>•</label><p id="p10155">General rule in bicarbonate administration is to give as a bolus half of the calculated deficit and then to correct remaining deficit over 12 to 24 hours.</p></list-item><list-item id="u8210"><label>•</label><p id="p10160">If sodium bicarbonate is used, more potassium supplementation is necessary!</p></list-item></list></p></list-item></list></p></sec><sec id="s1650"><title>Antibiotic Therapy</title><p id="p10165"><list list-type="simple" id="ulist1765"><list-item id="u8215"><label>•</label><p id="p10170">Ticarcillin/clavulanic acid, 44 mg/kg IV q6h; or ceftiofur, 5 mg/kg IV q8h; or ceftazidime, 20 to 40 mg/kg IV q6 to 8h, often combined with:<list list-type="simple" id="ulist1770"><list-item id="u8220"><label>•</label><p id="p10175">Amikacin, 21 to 25 mg/kg IV q24h; <italic>do not</italic> administer amikacin until the foal has been observed to urinate a normal volume.</p></list-item><list-item id="u8225"><label>•</label><p id="p10180">Enrofloxacin, 6 mg/kg IV q24h or 7.5 mg/kg PO q24h for resistant strains of salmonellosis; risk of drug-induced joint disease limits this treatment to foals with life-threatening and highly drug resistant salmonellosis! Marbofloxacin 2 mg/kg q24h PO can be used as a replacement for Enrofloxacin.<list list-type="simple" id="ulist1775"><list-item id="u8230"><label>○</label><p id="p10185">Monitor foals for joint effusion (nonseptic synovitis), lameness, flexoral laxity, or anemia because these can be commonly encountered when using this medication.</p></list-item><list-item id="u8235"><label>○</label><p id="p10190">Empirical treatment with Adequan, 1 vial IM every 3 days, has helped decrease the incidence of synovitis.</p></list-item></list></p></list-item></list></p></list-item></list></p></sec><sec id="s1655"><title>Additional Therapy</title><p id="p10195"><list list-type="simple" id="ulist1780"><list-item id="u8240"><label>•</label><p id="p10200">Endotoxemia treatment:<list list-type="simple" id="ulist1785"><list-item id="u8245"><label>•</label><p id="p10205">A minimum of 1 L of hyperimmune (to endotoxin) plasma</p></list-item><list-item id="u8250"><label>•</label><p id="p10210">Consider low-molecular-weight heparin, 50 units/kg SQ q24h, if evidence of disseminated intravascular coagulation exists (i.e., decreased platelets, prolonged clotting profile, decreased antithrombin III activity).</p></list-item><list-item id="u8255"><label>•</label><p id="p10215">Flunixin meglumine, 0.25 mg/kg IV q8h, <italic>only</italic> with serious endotoxemia and after initiation of intravenous fluid administration</p></list-item></list></p></list-item><list-item id="u8260"><label>•</label><p id="p10220">Ulcer prophylaxis <italic>and</italic><list list-type="simple" id="ulist1790"><list-item id="u8280"><label>•</label><p id="p10240">Sucralfate, 22 mg/kg PO q6h</p></list-item><list-item id="u8265"><label>•</label><p id="p10225">Omeprazole, 4.0 mg/kg q24h <italic>or</italic></p></list-item><list-item id="u8270"><label>•</label><p id="p10230">Ranitidine, 1.5 mg/kg IV or 6.6 mg/kg PO q8h <italic>or</italic></p></list-item><list-item id="u8275"><label>•</label><p id="p10235">Famotidine, 0.7 mg/kg IV q24h or 2.8 mg/kg PO q24h</p></list-item></list></p></list-item><list-item id="u8290"><label>•</label><p id="p10250">Intestinal protectants<list list-type="simple" id="ulist1795"><list-item id="u8295"><label>•</label><p id="p10255">Di-tri-octahedral smectite (Bio-Sponge) or (Hagyard Anti-Diarrhea Gel), yogurt, bismuth subsalicylate, or activated charcoal may be beneficial.</p></list-item></list></p></list-item><list-item id="u8305"><label>•</label><p id="p10265">Nursing care<list list-type="simple" id="ulist1800"><list-item id="u8310"><label>•</label><p id="p10270">Keep foal clean; apply petroleum jelly to perineal region.</p></list-item><list-item id="u8315"><label>•</label><p id="p10275">Wrap tail with plastic bag and Elasticon (around base of tail with separate piece extending dorsally up to midsacral region).</p></list-item><list-item id="u8320"><label>•</label><p id="p10280"><italic>Do not</italic> wrap tightly; monitor for frequent slipping.</p></list-item><list-item id="u8325"><label>•</label><p id="p10285"><italic>Do not</italic> use Vetwrap<italic>.</italic></p></list-item></list></p></list-item><list-item id="u8330"><label>•</label><p id="p10290">For abdominal pain, use the following:<list list-type="simple" id="ulist1805"><list-item id="u8285"><label>•</label><p id="p10245">Dipyrone, firocoxib and reportedly carprofen are considered less ulcerogenic than flunixin meglumine and can be used when several treatments with NSAIDs are needed.</p></list-item><list-item id="u8335"><label>•</label><p id="p10295">Dipyrone, 4 to 10 mL IV; xylazine, 0.3 to 1.0 mg/kg IV; butorphanol, 0.02 to 0.04 mg/kg IV or IM; ketoprofen, 1 mg/kg IV. The continuous administration of lidocaine, IV, can also be used, although in young foals, hepatic metabolism can be delayed.</p></list-item><list-item id="u8340"><label>•</label><p id="p10300">If ileus is clinically present <italic>and</italic> obstructive disease is ruled out, administer neostigmine, 0.2 to 1 mg SQ q1h for 3 treatments then q6h along with analgesics or sedation.</p></list-item></list></p></list-item><list-item id="u8345"><label>•</label><p id="p10305">For uveitis, use topical ophthalmic corticosteroid with or without antibiotic (if no corneal ulcer) and atropine.</p></list-item><list-item id="u8350"><label>•</label><p id="p10310">Keep the mare and foal together; the mare is likely fecal positive for <italic>Salmonella</italic> spp., and separation creates extra stress on the foal and the mare.</p></list-item><list-item id="u8355"><label>•</label><p id="p10315">Follow strict isolation protocol!</p></list-item></list></p></sec><sec id="s1660"><title>Prevention</title><p id="p10320"><list list-type="simple" id="ulist1810"><list-item id="u8360"><label>•</label><p id="p10325">Prevention of <italic>Salmonella</italic> consists of proper hygiene. Before the foal is able to nurse, the udder and perineal regions of the mare are to be thoroughly washed with dilute chlorhexidine or Ivory soap and water.</p></list-item><list-item id="u8365"><label>•</label><p id="p10330">During an outbreak, at risk foals should also be intubated with 6 to 8 oz of colostrum before contact with the mare.</p></list-item><list-item id="u8370"><label>•</label><p id="p10335">An experimental inactivated bacterin (<italic>Salmonella typhimurium</italic> and <italic>newport</italic>) vaccine has been developed by Hagyard Equine Medical Institute and Dr. John Timmoney at the Gluck Research Center in Lexington, Kentucky. This vaccine is currently being used on endemic farms since 2007.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s1665"><title>Prognosis</title><p id="p10340"><list list-type="simple" id="ulist1815"><list-item id="u8375"><label>•</label><p id="p10345">The prognosis is considered fair <italic>if</italic> the foal responds positively to initial therapy over the first 48 hours.</p></list-item><list-item id="u8380"><label>•</label><p id="p10350">If the foal continues to deteriorate during the first 48 hours in spite of aggressive therapy or septic foci develop in joints, lungs, or meninges, the prognosis is guarded.</p></list-item><list-item id="u8385"><label>•</label><p id="p10355"><italic><bold>Practice Tip:</bold> It is unusual for both the mare and foal to have diarrhea associated with</italic> Salmonella <italic>spp., but it is likely that the mare cultures fecal positive for the organism.</italic></p></list-item><list-item id="u8390"><label>•</label><p id="p10360">Keep the pair isolated from other horses on the farm.</p></list-item><list-item id="u8395"><label>•</label><p id="p10365">Generally, a minimum of three, and preferably five, negative cultures should be obtained from the mare and foal before reintroducing the pair to the general herd.</p></list-item></list></p></sec></sec><sec id="s1670"><title>Rotavirus Diarrhea</title><p id="p10370"><list list-type="simple" id="ulist1820"><list-item id="u8400"><label>•</label><p id="p10375"><italic><bold>Practice Tip:</bold> This is the most common infectious diarrhea in nursing foals (group A rotavirus).</italic></p></list-item><list-item id="u8405"><label>•</label><p id="p10380">Rotavirus causes diarrhea in foals up to 6 months of age but is more common in younger foals.</p></list-item><list-item id="u8410"><label>•</label><p id="p10385">The virus is associated with an increased incidence of gastric ulceration.</p></list-item><list-item id="u8415"><label>•</label><p id="p10390">The virus is highly contagious; often several foals on a farm are affected simultaneously.</p></list-item></list></p><sec id="s1675"><title>Clinical Signs</title><p id="p10395"><list list-type="simple" id="ulist1825"><list-item id="u8420"><label>•</label><p id="p10400">Watery yellow to yellow-green diarrhea</p></list-item><list-item id="u8425"><label>•</label><p id="p10405">Nonfetid diarrhea with a distinctive odor</p></list-item><list-item id="u8430"><label>•</label><p id="p10410">Lethargy, anorexia frequently observed before the onset of diarrhea</p></list-item><list-item id="u8435"><label>•</label><p id="p10415">Neonates may become tympanic and colicky</p></list-item></list></p></sec><sec id="s1680"><title>Diagnosis</title><p id="p10420"><list list-type="simple" id="ulist1830"><list-item id="u8440"><label>•</label><p id="p10425">ELISA (Virogen rotatest, Rotazyme<xref rid="fn0140" ref-type="fn">27</xref>)<list list-type="simple" id="ulist9100"><list-item id="u8445"><label>•</label><p id="p10430">Foals that have had diarrhea for several days may have negative results.</p></list-item></list></p></list-item><list-item id="u8450"><label>•</label><p id="p10435">PCR<list list-type="simple" id="ulist1835"><list-item id="u11200"><label>•</label><p id="p10440">There is documented analysis of several equine samples positive for rotavirus by PCR that tested negative in an immunoassay with human rotavirus specificity. <bold><italic>Practice Tip:</italic></bold><italic>This underscores the importance of equine–specific test reagents for veterinary medicine and the risk of false-negative results when using nonspecies-matched reagents.</italic></p></list-item><list-item id="u8455"><label>•</label><p id="p10445">Sequences showed 98% identities to equine rotavirus isolates deposited in GenBank.</p></list-item><list-item id="u8460"><label>•</label><p id="p10450">These results suggest that the immunoassay with human specificity <italic>does not</italic> detect all equine isolates.</p></list-item></list></p></list-item><list-item id="u8465"><label>•</label><p id="p10455">Laboratory findings usually are relatively mild compared with <italic>Salmonella</italic> spp.</p></list-item><list-item id="u8470"><label>•</label><p id="p10460">For CBC, toxic neutrophils and the presence of band neutrophils are not common.</p></list-item><list-item id="u8475"><label>•</label><p id="p10465">Serum chemistry reveals hypochloremia, hyponatremia, hypokalemia, and acidosis.</p></list-item></list></p><p id="p10470"><boxed-text id="b0275"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1685"><title>Rotavirus Diarrhea</title><p id="p10475"><list list-type="simple" id="ulist1840"><list-item id="u8480"><label>•</label><p id="p10480">Gastric ulcer prophylaxis is indicated.</p></list-item><list-item id="u8485"><label>•</label><p id="p10485">May be self-limiting</p></list-item><list-item id="u8490"><label>•</label><p id="p10490">Monitor hydration status and laboratory parameters for indications to initiate fluid therapy.</p></list-item><list-item id="u8495"><label>•</label><p id="p10495">See previous section on fluid therapy for foal diarrhea.</p></list-item><list-item id="u8500"><label>•</label><p id="p10500">Intestinal protectants are necessary (see previous section for dosages):<list list-type="simple" id="ulist1845"><list-item id="u8505"><label>•</label><p id="p10505">Bismuth subsalicylate</p></list-item><list-item id="u8510"><label>•</label><p id="p10510">Di-tri-octahedral smectite (Bio-Sponge)</p></list-item><list-item id="u8515"><label>•</label><p id="p10515">Hagyard Anti-Diarrhea Gel</p></list-item><list-item id="u8520"><label>•</label><p id="p10520">Yogurt</p></list-item></list></p></list-item><list-item id="u8525"><label>•</label><p id="p10525">Lactaid should be administered because rotavirus-infected foals are likely to have maldigestion.</p></list-item><list-item id="u8530"><label>•</label><p id="p10530">Lactase<xref rid="fn0145" ref-type="fn">28</xref> 6000 Food Chemical Codex (FCC) lactase U/50 kg PO q3 to 8h for 10 to 14 days has also been used to improve digestion of milk lactose.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1690"><title>Prevention</title><p id="p10535"><list list-type="simple" id="ulist1850"><list-item id="u8535"><label>•</label><p id="p10540">Take measures to prevent spread of the disease.<list list-type="simple" id="ulist1855"><list-item id="u8540"><label>•</label><p id="p10545">Isolate all affected foals.</p></list-item><list-item id="u8545"><label>•</label><p id="p10550">Control the entry of birds and pets into the barn.</p></list-item><list-item id="u8550"><label>•</label><p id="p10555">Personnel should enter stall last during daily cleaning and feeding.<list list-type="simple" id="ulist1860"><list-item id="u8555"><label>○</label><p id="p10560">Wear boots, coveralls, and gloves when entering the stall.</p></list-item><list-item id="u8560"><label>○</label><p id="p10565"><italic>Do not</italic> share buckets and utensils between stalls.</p></list-item><list-item id="u8565"><label>○</label><p id="p10570">If possible, assign one person to care only for affected foals.</p></list-item><list-item id="u8570"><label>○</label><p id="p10575">Provide foot-baths outside stall using phenolic compounds or hypochlorite.</p></list-item></list></p></list-item></list></p></list-item><list-item id="u8575"><label>•</label><p id="p10580">Vaccination of brood mares confers moderate protection and is considered at least to decrease the severity of the disease.</p></list-item><list-item id="u8580"><label>•</label><p id="p10585"><italic><bold>Practice Tip:</bold> On rare occasion with rotavirus and other causes of foal diarrhea, the foal becomes bloated and colicky following nursing; use lactaid, lidocaine CRI if possible, and restrict the amount of time the foal nurses for a couple of days (if required).</italic></p></list-item></list></p></sec><sec id="s1695"><title>Prognosis</title><p id="p10590">Prognosis is considered good to excellent.</p></sec></sec><sec id="s1700"><title>Enterotoxigenic <italic>Escherichia Coli</italic></title><p id="p10595"><list list-type="simple" id="ulist1865"><list-item id="u8585"><label>•</label><p id="p10600">Usually affects a single foal on the farm</p></list-item><list-item id="u8590"><label>•</label><p id="p10605">Infection with pili-positive and enterotoxin-positive <italic>E. coli</italic></p></list-item></list></p><sec id="s1705"><title>Clinical Signs</title><p id="p10610"><list list-type="simple" id="ulist1870"><list-item id="u8595"><label>•</label><p id="p10615">Watery diarrhea, usually not fetid</p></list-item><list-item id="u8600"><label>•</label><p id="p10620">Moderate to severe depression</p></list-item><list-item id="u8605"><label>•</label><p id="p10625">Fever not typically present</p></list-item><list-item id="u8610"><label>•</label><p id="p10630">Signs of gastric ulceration usually present</p></list-item></list></p></sec><sec id="s1710"><title>Diagnosis</title><p id="p10635"><list list-type="simple" id="ulist1875"><list-item id="u8615"><label>•</label><p id="p10640">Laboratory findings typically demonstrate acidosis.</p></list-item><list-item id="u8620"><label>•</label><p id="p10645">Rule out other causes of diarrhea.</p></list-item><list-item id="u8625"><label>•</label><p id="p10650">Aerobic fecal culture shows heavy growth of mucoid colonies.</p></list-item><list-item id="u8630"><label>•</label><p id="p10655">Submit culture to a laboratory that tests for <italic>adhesion</italic> and <italic>enterotoxin</italic>.</p></list-item></list><boxed-text id="b0280"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1715"><title><italic>E. Coli</italic> Diarrhea</title><p id="p10660"><list list-type="simple" id="ulist1880"><list-item id="u8635"><label>•</label><p id="p10665">Treatment is similar to other causes of foal diarrhea with consideration that <italic>E. coli</italic> or <italic>Enterococcus</italic> spp. may become bacteremic.</p></list-item><list-item id="u8640"><label>•</label><p id="p10670">Amikacin use should be limited to foals producing normal volumes of urine.</p></list-item><list-item id="u8645"><label>•</label><p id="p10675"><italic>E. coli</italic> antibody specifically against K99 pili is commercially available as an oral paste<xref rid="fn0150" ref-type="fn">29</xref> for foals, but field value is not well documented.</p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1720"><title>Cryptosporidiosis</title><p id="p10680"><list list-type="simple" id="ulist1885"><list-item id="u8650"><label>•</label><p id="p10685"><italic><bold>Practice Tip:</bold></italic> Cryptosporidium <italic>is a protozoal pathogen with significant zoonotic potential.</italic></p></list-item><list-item id="u8655"><label>•</label><p id="p10690">Oocysts are infective when shed.</p></list-item><list-item id="u8660"><label>•</label><p id="p10695">Zoonotic potential exists.</p></list-item><list-item id="u8665"><label>•</label><p id="p10700">Diarrhea is a result of infection with <italic>Cryptosporidium parvum</italic> and typically occurs in immunocompromised (often hospitalized) foals, although <italic>C. parvum</italic> has been associated with diarrhea in otherwise healthy foals.</p></list-item><list-item id="u8670"><label>•</label><p id="p10705">Infection often is noted in Arabian foals with combined immunodeficiency.</p></list-item><list-item id="u8675"><label>•</label><p id="p10710">Infection may occur in foals that have secondary immunosuppression associated with chronic, catabolic disease or another enteric pathogen.</p></list-item><list-item id="u8680"><label>•</label><p id="p10715">Diagnosis is based on detection of oocysts in fecal samples.<list list-type="simple" id="ulist1890"><list-item id="u8685"><label>•</label><p id="p10720">Kinyoun acid-fast stain, immunofluorescence, PCR and flow cytometry are useful.</p></list-item><list-item id="u8690"><label>•</label><p id="p10725"><italic><bold>Note:</bold> Cryptosporidium</italic> can also be found in the feces of normal foals.</p></list-item><list-item id="u8695"><label>•</label><p id="p10730"><italic>Eimeria</italic> and <italic>Giardia</italic> spp. may be noted in samples; the pathogenicity of these organisms in the horse has not been conclusively documented.</p></list-item></list></p></list-item></list><boxed-text id="b0285"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1725"><title>Cryptosporidiosis</title><p id="p10735"><list list-type="simple" id="ulist1895"><list-item id="u8700"><label>•</label><p id="p10740">Supportive care—fluids and nutrition!</p></list-item><list-item id="u8705"><label>•</label><p id="p10745">Total parenteral nutrition (TPN) may be required.</p></list-item><list-item id="u8710"><label>•</label><p id="p10750">Administer paromomycin, 100 mg/kg PO q24h for 5 days or nitazoxanide (NTZ) 2 g PO q12h for 3 days. (The equine product is no longer available; however, for valuable foals, NTZ, approved for human use, can be acquired.)</p></list-item><list-item id="u8715"><label>•</label><p id="p10755">Efficacy and safety have <italic>not</italic> been proven in foals but nitazoxanide is effective in calves.</p></list-item><list-item id="u8720"><label>•</label><p id="p10760">Transmission is from foal to foal.</p></list-item></list></p><sec id="s1730"><title>Prevention</title><p id="p10765"><list list-type="simple" id="ulist1900"><list-item id="u8725"><label>•</label><p id="p10770">Use barrier precautions with patients.</p></list-item><list-item id="u8730"><label>•</label><p id="p10775">Extreme heat and cold are considered the best methods to kill oocysts.</p></list-item><list-item id="u8735"><label>•</label><p id="p10780">Concentrated hypochlorite solutions may be used.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s1735"><title>Fetal Diarrhea</title><p id="p10785"><list list-type="simple" id="ulist1905"><list-item id="u8740"><label>•</label><p id="p10790">It is <italic>not</italic> unusual to deliver a newborn and see the foal covered in amniotic fluid stained with fetal diarrhea.</p></list-item><list-item id="u8745"><label>•</label><p id="p10795"><italic><bold>Practice Tip:</bold> This problem generally signifies an unthrifty newborn that is at high risk for the development of aspiration pneumonia.</italic></p></list-item></list></p><sec id="s1740"><title>Clinical Signs</title><p id="p10800"><list list-type="simple" id="ulist1910"><list-item id="u8750"><label>•</label><p id="p10805">Foals may be clinically normal, but typically they are depressed, demonstrate poor suckle reflex, and may exhibit signs of ischemic-hypoxic encephalopathy.</p></list-item><list-item id="u8755"><label>•</label><p id="p10810">Foals are reluctant or unable to stand and nurse.</p></list-item><list-item id="u8760"><label>•</label><p id="p10815">Signs of sepsis may be severe.</p></list-item><list-item id="u8765"><label>•</label><p id="p10820">Toxic mucous membranes and poor perfusion are evident.</p></list-item></list><boxed-text id="b0290"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1745"><title>Fetal Diarrhea</title><p id="p10825"><list list-type="simple" id="ulist1915"><list-item id="u8770"><label>•</label><p id="p10830">Suction the trachea for 10-second intervals at a time, while administering intranasal oxygen, to remove meconium-stained amniotic fluid.</p></list-item><list-item id="u8775"><label>•</label><p id="p10835">Administer broad-spectrum antibiotics (see <italic>Salmonella</italic> spp., <xref rid="s1605" ref-type="sec">p. 223</xref>).</p></list-item><list-item id="u8780"><label>•</label><p id="p10840">Administer IV fluids and plasma.</p></list-item><list-item id="u8785"><label>•</label><p id="p10845">Give colostrum orally.</p></list-item><list-item id="u8790"><label>•</label><p id="p10850">If respiratory signs begin to worsen, administer the following:<list list-type="simple" id="ulist1920"><list-item id="u8795"><label>•</label><p id="p10855">Dexamethasone, 0.1 to 0.25 mg/kg IV once, or prednisolone sodium succinate, 100 mg IV once.</p></list-item><list-item id="u8800"><label>•</label><p id="p10860">The dose may be repeated for 2 to 3 days if there is a positive response to the initial dose.</p></list-item></list></p></list-item></list></p></sec></boxed-text><boxed-text id="b0295"><caption><title><inline-graphic xlink:href="icon02-9781455708925.gif"></inline-graphic> What Not to Do</title></caption><sec id="s1750"><title>Meconium Aspiration from Fetal Diarrhea</title><p id="p10865"><list list-type="simple" id="ulist1925"><list-item id="u8805"><label>•</label><p id="p10870"><italic>Do not</italic> suction trachea for prolonged periods without supplemental oxygen.</p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1755"><title><italic>Enterococcus Durans</italic> (Previously Group D Streptococcus)</title><p id="p10875"><list list-type="simple" id="ulist1930"><list-item id="u8810"><label>•</label><p id="p10880"><italic>Enterococcus durans</italic> is a gram-positive coccus in the alimentary tract that has been implicated as a cause of enteritis in foals, piglets, calves, and puppies. <italic>E. durans</italic> has been reported as a cause of diarrhea in 5 of 7 foals that developed diarrhea during the first 10 days of life.</p></list-item><list-item id="u8815"><label>•</label><p id="p10885">In one Australian study, <italic>E. durans</italic> was isolated from a foal that had severe diarrhea, then used to experimentally infect 7 foals by stomach tube exposure. All 7 foals developed profuse watery diarrhea within 24 hours of inoculation with varying degrees of depression, anorexia, abdominal tenderness, and dehydration.</p></list-item><list-item id="u8820"><label>•</label><p id="p10890">The pathogenesis of diarrhea and enteric disease remains unknown. Diarrhea induced by <italic>E. durans</italic> is <italic>not</italic> associated with enterotoxin production or substantial mucosal injury.</p></list-item><list-item id="u8825"><label>•</label><p id="p10895">Decreased activity of brush border digestive enzymes, such as lactase and alkaline phosphatase, suggests there is a direct mechanical interference with digestion and absorption at the brush border.</p></list-item></list><boxed-text id="b0300"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1760"><title><italic>Enterococcus Durans</italic> Diarrhea</title><p id="p10900"><list list-type="simple" id="ulist1935"><list-item id="u8830"><label>•</label><p id="p10905">Subjectively, systemic treatment with some β-lactams appears to decrease the diarrhea duration (ampicillin or penicillin). The organism is highly resistant to cephalosporins.</p></list-item><list-item id="u8835"><label>•</label><p id="p10910">The ideal treatment is to improve husbandry on the farm.</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1765"><title>Coronavirus</title><p id="p10915"><list list-type="simple" id="ulist1940"><list-item id="u8840"><label>•</label><p id="p10920">Equine coronavirus (ECoV, a beta coronavirus) was isolated and characterized only recently but was described as an infectious agent in sick foals in 1976.</p></list-item><list-item id="u8845"><label>•</label><p id="p10925">Several studies and case reports have identified coronaviruses in foals with enteric disease but the pathogenicity and etiologic role in enteric disease have <italic>not</italic> been examined. A recent prevalence study in central Kentucky clearly shows that healthy foals without signs of GI disease are equally infected with equine coronavirus as sick animals. This finding suggests low pathogenicity of ECoV in foals. However, when analyzed as a coinfecting agent, ECoV is significantly associated with diseased foals; all ECoV infections in the GI diseased group were associated with coinfections (15 of 15) while foals in the healthy group were mostly monoinfected (8 of 10). <italic><bold>Practice Tip:</bold> This finding supports the theory that (certain) viruses primarily act as immune-suppressing agents allowing opportunistic infections to take place.</italic></p></list-item><list-item id="u8850"><label>•</label><p id="p10930">Opportunistic infections can be of different origin, including bacterial or protozoal, as shown in the study. Coinfection data in piglets clearly indicate that coronavirus and bacterial coinfections have a significant effect on the magnitude of the inflammatory immune response and the amount of tissue damage compared with single infected foals. Furthermore, in young turkeys, coronavirus and enteropathogenic <italic>E. coli</italic> (EPEC) were shown to synergistically interact and cause severe growth depression and high mortality when compared with monoinfected turkeys.</p></list-item><list-item id="u8855"><label>•</label><p id="p10935">These observations suggest a role for coronavirus in foals and the diagnostic value of detecting ECoV in apparently healthy foals to assess their potential susceptibility for coinfections.</p></list-item><list-item id="u8860"><label>•</label><p id="p10940">In coronavirus-infected healthy foals, the focus should be directed toward epidemiologic aspects to reduce the likelihood of coinfections. Additional information is needed to determine equine coronavirus virulence factors and the relative importance as a coinfecting agent contributing to GI disease in foals.</p></list-item></list></p><sec id="s1770"><title>Diagnosis</title><p id="p10945"><list list-type="simple" id="ulist1945"><list-item id="u8865"><label>•</label><p id="p10950">PCR, virus isolation, or electron microscopy of fecal sample.</p></list-item></list><boxed-text id="b0305"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1775"><title>Coronavirus Diarrhea</title><p id="p10955"><list list-type="simple" id="ulist1950"><list-item id="u8870"><label>•</label><p id="p10960">See treatment under Rotavirus Diarrhea, <xref rid="s1665" ref-type="sec">p. 225</xref>.</p></list-item><list-item id="u8875"><label>•</label><p id="p10965">Currently there is an ultrapurified Bentonite clay that is available for use in horses that has the same composition as a product being investigated in humans suffering from rotavirus or coronavirus gastrointestinal infections.<xref rid="fn0155" ref-type="fn">30</xref></p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1780"><title>Lactase Deficiency (Dietary)</title><p id="p10970"><list list-type="simple" id="ulist1955"><list-item id="u8880"><label>•</label><p id="p10975">Lactose intolerance has been diagnosed in foals as either:<list list-type="simple" id="ulist1960"><list-item id="u8885"><label>•</label><p id="p10980">Lactose malabsorption<list list-type="simple" id="ulist1965"><list-item id="u8890"><label>○</label><p id="p10985">Physiologic problem that arises from the consumption of too much lactose and the capacity for lactase to hydrolyze it to glucose and galactose.</p></list-item><list-item id="u8895"><label>○</label><p id="p10990">An example is overfeeding or incorrectly prepared milk replacer.</p></list-item></list></p></list-item><list-item id="u8900"><label>•</label><p id="p10995">Secondary lactase deficiency<list list-type="simple" id="ulist1970"><list-item id="u8905"><label>○</label><p id="p11000">For example, a lactase deficiency that is the result of injury of the brush border (location of lactase enzyme) during enterocolitis.</p></list-item></list></p></list-item><list-item id="u8910"><label>•</label><p id="p11005">Primary lactase deficiency<list list-type="simple" id="ulist1975"><list-item id="u8915"><label>○</label><p id="p11010">These foals have low or completely absent lactase concentrations.</p></list-item></list></p></list-item></list></p></list-item></list></p><sec id="s1785"><title>Diagnosis</title><p id="p11015"><list list-type="simple" id="ulist1980"><list-item id="u8920"><label>•</label><p id="p11020">Based on response to treatment and/or the lactose tolerance test.<list list-type="simple" id="ulist9080"><list-item id="u8925"><label>•</label><p id="p11025">Lactose monohydrate (1 g/kg body weight in a 20% water solution) is administered by nasogastric tube after fasting for 4 hours; plasma glucose concentrations are monitored.</p></list-item><list-item id="u8930"><label>•</label><p id="p11030"><italic><bold>Practice Tip:</bold> Fluoride oxalate may need to be used as an anticoagulant if the sample</italic> cannot <italic>be immediately cooled and there is more than 1 hour between collection and submission of the sample before dosing; monitor every 30 minutes for 2 hours.</italic></p></list-item><list-item id="u8935"><label>•</label><p id="p11035">Normal digestion of lactose results in a doubling of the normal glucose concentration in 60 to 90 minutes.</p></list-item></list></p></list-item></list><boxed-text id="b0310"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1790"><title>Lactase Deficiency</title><p id="p11040"><list list-type="simple" id="ulist1985"><list-item id="u8940"><label>•</label><p id="p11045">Supplement with lactase enzyme (6000 Food Chemical Codex units/50-kg foal) orally every 3 to 8 hours or a tablet of Lactaid.</p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1795"><title>Acute Pancreatitis in the Neonatal Foal</title><p id="p11050"><list list-type="simple" id="ulist1990"><list-item id="u8945"><label>•</label><p id="p11055">Acute onset of diarrhea almost immediately followed by signs of septic shock and gross hyperlipemia with marked elevations in amylase and lipase are characteristic of pancreatitis in foals.</p></list-item><list-item id="u8950"><label>•</label><p id="p11060">The cause of the pancreatitis is unknown but most foals are approximately 3 days of age and were healthy and vigorous nursers on days 1 and 2.</p></list-item><list-item id="u8955"><label>•</label><p id="p11065">The first sign is often diarrhea. Abdominal ultrasound may reveal increased peritoneal fluid and an abnormal appearing mass in the area of the pancreas.</p></list-item><list-item id="u8960"><label>•</label><p id="p11070">Peritoneal fluid is inflammatory, with both hemorrhage and lipids causing a milky pink color, and may have higher amylase and lipase than values in plasma.</p></list-item></list><boxed-text id="b0315"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1800"><title>Acute Pancreatitis in the Neonatal Foal</title><p id="p11075"><list list-type="simple" id="ulist1995"><list-item id="u8965"><label>•</label><p id="p11080">IV fluids</p></list-item><list-item id="u8970"><label>•</label><p id="p11085">Systemic antibiotics</p></list-item><list-item id="u8975"><label>•</label><p id="p11090">Plasma</p></list-item><list-item id="u8980"><label>•</label><p id="p11095">Low-molecular-weight heparin</p></list-item><list-item id="u8985"><label>•</label><p id="p11100">Selenium and vitamin E</p></list-item><list-item id="u8990"><label>•</label><p id="p11105">Flunixin meglumine</p></list-item><list-item id="u8995"><label>•</label><p id="p11110">Parenteral nutrition (excluding lipids)</p></list-item></list></p><p id="p11115"><italic><bold>Note:</bold></italic> One foal survived the acute disease and was treated with oral pancreatic enzymes and milk feeding and succumbed to fibrinous peritonitis due to the inflammatory pancreatitis.</p></sec></boxed-text></p></sec></sec><sec id="s1805"><title>Diarrhea in Weanlings and Yearlings</title><p id="p11120"><italic><bold>Thomas J. Divers</bold></italic></p><sec id="s1810"><title>Proliferative Enteropathy: <italic>Lawsonia Intracellularis</italic></title><p id="p11125"><list list-type="simple" id="ulist2000"><list-item id="u9000"><label>•</label><p id="p11130">Affects many mammals, including foals most commonly 4 to 7 months of age.<list list-type="simple" id="ulist2005"><list-item id="u9005"><label>•</label><p id="p11135">The organism can be found in the feces of normal foals and adult horses (especially on farms that have had clinical cases).</p></list-item></list></p></list-item><list-item id="u9010"><label>•</label><p id="p11140">Worldwide distribution</p></list-item><list-item id="u9015"><label>•</label><p id="p11145">Obligate intracellular bacterium</p></list-item><list-item id="u9020"><label>•</label><p id="p11150">Different strains of the organism; the “pig” strain appears to be relatively nonpathogenic in foals while strain(s) isolated from some wild animals may be pathogenic to foals.</p></list-item><list-item id="u9025"><label>•</label><p id="p11155"><italic><bold>Practice Tip:</bold> Hypoproteinemia is the hallmark laboratory finding.</italic></p></list-item></list></p><sec id="s1815"><title>Clinical Signs</title><p id="p11160"><list list-type="simple" id="ulist2010"><list-item id="u9030"><label>•</label><p id="p11165">Rapid weight loss, often in the face of a normal appetite</p></list-item><list-item id="u9035"><label>•</label><p id="p11170">Poor hair coat and a pot-bellied appearance</p></list-item><list-item id="u9040"><label>•</label><p id="p11175">Ventral edema and lethargy</p></list-item><list-item id="u9045"><label>•</label><p id="p11180">Diarrhea in approximately 50% of cases and abdominal pain in 10% to 15%</p></list-item><list-item id="u9050"><label>•</label><p id="p11185">Fever is rare</p></list-item><list-item id="u9055"><label>•</label><p id="p11190">Uncommonly, an acute necrotizing form of <italic>Lawsonia</italic> occurs with acute, severe systemic inflammation, necrosis of the bowel, and secondary bacterial invasion may be a clinical presentation.</p></list-item></list></p></sec><sec id="s1820"><title>Laboratory Findings</title><p id="p11195"><list list-type="simple" id="ulist2015"><list-item id="u9060"><label>•</label><p id="p11200">CBC results are variable; most common abnormalities are low total protein, leukocytosis, and anemia</p></list-item><list-item id="u9065"><label>•</label><p id="p11205">Serum chemistry: classically hypoproteinemia caused by <italic>hypoalbuminemia</italic></p></list-item><list-item id="u9070"><label>•</label><p id="p11210">May have electrolyte abnormalities from diarrhea or edema: hyponatremia, hypochloremia</p></list-item><list-item id="u9075"><label>•</label><p id="p11215">Increased creatinine kinase</p></list-item></list></p></sec><sec id="s1825"><title>Diagnosis</title><p id="p11220"><list list-type="simple" id="ulist2020"><list-item id="u9080"><label>•</label><p id="p11225">Fecal PCR for the organism is the <italic>best</italic> test.<list list-type="simple" id="ulist2025"><list-item id="u9085"><label>•</label><p id="p11230">Multiple fecal samples or fecal sample and rectal swab together may improve sensitivity</p></list-item></list></p></list-item><list-item id="u9090"><label>•</label><p id="p11235">Serum neutralization titer: potentially evaluate acute and convalescence titers</p></list-item><list-item id="u9095"><label>•</label><p id="p11240">Abdominal ultrasonography: “wagon-wheel” small-intestinal wall edema is the characteristic appearance (<xref rid="f0370" ref-type="fig">Fig. 18-72</xref>)<fig id="f0370"><label>Figure 18-72</label><caption><p>Severe edema in the wall of the small intestine in a weanling with diarrhea and hypoproteinemia that was fecal positive by polymerase chain reaction for <italic>Lawsonia intracellularis.</italic></p></caption><graphic xlink:href="f018-072-9781455708925"></graphic></fig></p></list-item><list-item id="u9100"><label>•</label><p id="p11245">Postmortem: Warthin-Starry silver stain of affected tissues</p></list-item></list><boxed-text id="b0320"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1830"><title>Lawsonia</title><p id="p11250"><list list-type="simple" id="ulist2030"><list-item id="u9105"><label>•</label><p id="p11255">Antibiotic therapy usually is indicated for at least 21 days:<list list-type="simple" id="ulist2035"><list-item id="u9110"><label>•</label><p id="p11260">Oxytetracycline, 6.6 mg/kg IV q12h or 10 mg/kg IV q24h—the primary and preferred treatment by clinicians, although an invitro sensitivity on swine isolates suggests that macrolides have better activity.</p></list-item><list-item id="u9115"><label>•</label><p id="p11265"><bold><italic>Note:</italic></bold> Serum creatinine should be monitored with tetracycline treatment. <italic><bold>Practice Tip:</bold> Many Lawsonia foals are dehydrated and because of the low albumin, there is more non-bound/free tetracycline in the plasma, both of which may increase risk of renal failure!</italic></p></list-item><list-item id="u9120"><label>•</label><p id="p11270">Doxycycline, 10 mg/kg PO q12h or minocycline, 4 mg/kg PO q12h, are the secondary preferred treatment. <italic><bold>Note:</bold></italic> The absorption of doxycycline varies in individual horses but is likely higher in foals than adult horses</p></list-item><list-item id="u9125"><label>•</label><p id="p11275">It is common practice to start treatment with oxytetracycline IV and then switch to doxycycline or minocycline PO.</p></list-item><list-item id="u9130"><label>•</label><p id="p11280">Chloramphenicol, 44 mg/kg PO q6 to 8h</p></list-item><list-item id="u9135"><label>•</label><p id="p11285">Azithromycin, 10mg/kg PO q24h for 5 days then EOD (every other day) with or without rifampin, 5 mg/kg PO q12h.</p></list-item></list></p></list-item><list-item id="u9140"><label>•</label><p id="p11290">Supportive care:<list list-type="simple" id="ulist2045"><list-item id="u9145"><label>•</label><p id="p11295">Administer IV fluid therapy in cases with severe diarrhea to correct electrolyte imbalances and dehydration (<xref rid="u7710" ref-type="list-item">p. 222</xref>).</p></list-item><list-item id="u9150"><label>•</label><p id="p11300">For severe hypoproteinemia, consider oncotic support.<list list-type="simple" id="ulist2050"><list-item id="u9155"><label>○</label><p id="p11305">Hetastarch, Vetstarch or Pentastarch, 7 to 10 mg/kg IV</p></list-item><list-item id="u9160"><label>○</label><p id="p11310">May consider IV plasma, a minimum of 2 L</p></list-item></list></p></list-item><list-item id="u9165"><label>•</label><p id="p11315">For ulcer prophylaxis, see <xref rid="s1605" ref-type="sec">p. 223</xref>.</p></list-item><list-item id="u9170"><label>•</label><p id="p11320">Foals with <italic>Lawsonia</italic> infection and acute severe systemic inflammation should be treated for septic shock as detailed under treatment of systemic inflammation (see Chapter 32, p. 567).</p></list-item></list></p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1835"><title>Prognosis</title><p id="p11325"><list list-type="simple" id="ulist2055"><list-item id="u9175"><label>•</label><p id="p11330">Prognosis is considered favorable with appropriate therapy in most cases; the physical appearance of the foals may take <italic>months</italic> to improve.</p></list-item><list-item id="u9180"><label>•</label><p id="p11335">There are a small number of foals that do not respond to treatment.</p></list-item><list-item id="u9185"><label>•</label><p id="p11340">A vaccine approved for swine has been used rectally on farms with endemic disease caused by <italic>Lawsonia.</italic></p></list-item></list></p></sec></sec><sec id="s1840"><title><italic>Rhodococcus Equi</italic> Enterocolitis</title><p id="p11345"><list list-type="simple" id="ulist2060"><list-item id="u9190"><label>•</label><p id="p11350"><italic>Rhodococcus equi</italic> may cause diarrhea in foals from approximately 3 weeks of age up to 9 months of age.<list list-type="simple" id="ulist2065"><list-item id="u9195"><label>•</label><p id="p11355">Infection is of the lymphoid tissue (Peyer's patches) in the intestinal mucosa.</p></list-item><list-item id="u9200"><label>•</label><p id="p11360">May present as insidious onset of diarrhea, often with fever that is persistent.</p></list-item><list-item id="u9205"><label>•</label><p id="p11365">Fever, marked leukocytosis, and high fibrinogen are <italic>not</italic> found as commonly as with <italic>R. equi</italic> pneumonia.</p></list-item><list-item id="u9210"><label>•</label><p id="p11370">Usually one foal is affected at a time, although outbreaks may occur.</p></list-item></list></p></list-item><list-item id="u9215"><label>•</label><p id="p11375">Other organ systems <italic>may</italic> be infected simultaneously.<list list-type="simple" id="ulist2070"><list-item id="u9220"><label>•</label><p id="p11380">Pulmonary tissue demonstrates pyogranulomatous pneumonia.</p></list-item><list-item id="u9225"><label>•</label><p id="p11385">Lymphoid tissue in the intestinal tract demonstrates ulcerative enterocolitis.</p></list-item><list-item id="u9230"><label>•</label><p id="p11390">Abdominal abscessation is associated with the mesenteric lymph nodes (<xref rid="f0375" ref-type="fig">Fig. 18-73</xref>).<fig id="f0375"><label>Figure 18-73</label><caption><p>Abdominal abscess in the region of the mesenteric root caused by infection with <italic>Rhodococcus equi.</italic></p></caption><graphic xlink:href="f018-073-9781455708925"></graphic></fig></p></list-item><list-item id="u9235"><label>•</label><p id="p11395">Septic physitis and osteomyelitis can occur.</p></list-item><list-item id="u9240"><label>•</label><p id="p11400">Uveitis or synovitis may be noted.</p></list-item></list></p></list-item></list></p><sec id="s1845"><title>Diagnosis</title><p id="p11405"><list list-type="simple" id="ulist2075"><list-item id="u9245"><label>•</label><p id="p11410">If diarrhea is the only syndrome caused by <italic>R. equi,</italic> the diagnosis is more difficult.</p></list-item><list-item id="u9250"><label>•</label><p id="p11415">Perform radiography/ultrasonography of the thorax and abdomen to evaluate for changes associated with <italic>R. equi.</italic> Negative results <italic>do not</italic> rule out <italic>R. equi</italic> enteritis.</p></list-item><list-item id="u9255"><label>•</label><p id="p11420">Tentative diagnosis is based on ruling out other causes of diarrhea plus the following:<list list-type="simple" id="ulist2085"><list-item id="u9260"><label>•</label><p id="p11425">Findings show 10<sup>5</sup> organisms per gram of feces or 100 colonies of <italic>R. equi</italic> per plate from a fecal swab.</p></list-item><list-item id="u9265"><label>•</label><p id="p11430">Additionally, the pathogenicity of the organism can be documented based on detecting the presence of virulence-associated antigen plasmids (VapA-P).</p></list-item><list-item id="u9270"><label>•</label><p id="p11435">Many strains of <italic>R. equi</italic> are <italic>not</italic> virulent.</p></list-item><list-item id="u9275"><label>•</label><p id="p11440">Healthy foals frequently have positive fecal cultures for <italic>R. equi:</italic> The combination of high numbers of <italic>R. equi</italic> colonies combined with the presence of VapA-P and other indications of <italic>R. equi</italic> infection (e.g., synovitis) helps guide therapy.</p></list-item></list></p></list-item></list><boxed-text id="b0325"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1850"><title>Rhodococcus <italic>Equi</italic> Enterocolitis</title><p id="p11445"><list list-type="simple" id="ulist2090"><list-item id="u9280"><label>•</label><p id="p11450">Clarithromycin, 7.5 mg/kg PO q12h, or azithromycin, 10 mg/kg PO q24h for 5 to 10 days, followed by 10 mg/kg q48h; either one is combined with rifampin, 5 mg/kg PO q12.</p></list-item><list-item id="u9285"><label>•</label><p id="p11455">Ideally, the rifampin should be given 2 hours after the macrolide treatment to decrease competition for intestinal absorption.</p></list-item><list-item id="u9290"><label>•</label><p id="p11460">Fluid therapy and intestinal protectants as for Salmmonellosis (see <xref rid="s1635" ref-type="sec">p. 224</xref>)</p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1855"><title>Prognosis</title><p id="p11465"><list list-type="simple" id="ulist2095"><list-item id="u9295"><label>•</label><p id="p11470">Prognosis varies.</p></list-item><list-item id="u9300"><label>•</label><p id="p11475">Prognosis is fair to good with appropriate treatment.</p></list-item><list-item id="u9305"><label>•</label><p id="p11480">The prognosis worsens if there is concurrent bone infection or abdominal abscessation!<list list-type="simple" id="ulist2100"><list-item id="u9310"><label>•</label><p id="p11485"><italic><bold>Practice Tip:</bold> Foals that have signs of weight loss before the development of diarrhea frequently have abdominal abscessation.</italic></p></list-item></list></p></list-item></list></p></sec></sec><sec id="s1860"><title>Antibiotic-Induced Diarrhea</title><p id="p11490"><list list-type="simple" id="ulist2105"><list-item id="u9315"><label>•</label><p id="p11495">Antibiotic-induced diarrhea most commonly is associated with the administration of macrolides, or less commonly, trimethoprim-sulfamethoxazole or rifampicin.<list list-type="simple" id="ulist2110"><list-item id="u9320"><label>•</label><p id="p11500">Foals tend to tolerate macrolides fairly well while nursing, but in transition to a more functional cecum and colon and adult diet, erythromycin, azithromycin, and clarithromycin may cause colic, severe diarrhea, and toxemia in older foals and weanlings.</p></list-item><list-item id="u9325"><label>•</label><p id="p11505">Most antibiotic-associated diarrhea cases occur in the first 2 to 6 days of therapy.</p></list-item><list-item id="u9330"><label>•</label><p id="p11510">A common scenario is that an older foal (>3 months)develops pneumonia and treatment for <italic>R. equi</italic> pneumonia is begun; two days later the foal is colicky, sometimes bloated, toxic (endotoxemic), and has diarrhea.</p></list-item><list-item id="u9335"><label>•</label><p id="p11515"><italic><bold>Practice Tip:</bold> Always be sure of the diagnosis of</italic> R. equi <italic>in foals over 3 months of age before beginning macrolide treatments</italic>; <italic>R. equi pneumonia is rare in foals over 4 months of age!</italic></p></list-item><list-item id="u9340"><label>•</label><p id="p11520"><italic>C. difficile</italic> infection is the cause of the diarrhea in some of the cases. In milder cases, it appears to be more of a dysbiosis.</p></list-item></list></p></list-item></list></p><sec id="s1865"><title>Clinical Signs</title><p id="p11525"><list list-type="simple" id="ulist2115"><list-item id="u9345"><label>•</label><p id="p11530">Abdominal distention and colic generally precede the onset of diarrhea.</p></list-item><list-item id="u9350"><label>•</label><p id="p11535">Signs of endotoxemia may be severe.<list list-type="simple" id="ulist2120"><list-item id="u9355"><label>•</label><p id="p11540">Injected mucous membranes and sclera are evident.</p></list-item><list-item id="u9360"><label>•</label><p id="p11545">Tachycardia and tachypnea are present.</p></list-item><list-item id="u9365"><label>•</label><p id="p11550">Extremities may be cold.</p></list-item></list></p></list-item></list></p></sec><sec id="s1870"><title>Laboratory Findings</title><p id="p11555"><list list-type="simple" id="ulist2125"><list-item id="u9370"><label>•</label><p id="p11560">Nonspecific findings associated with dehydration are as follows:<list list-type="simple" id="ulist2130"><list-item id="u9375"><label>•</label><p id="p11565">Elevated PCV and serum creatinine</p></list-item><list-item id="u9380"><label>•</label><p id="p11570">Hypochloremia and hyponatremia</p></list-item></list></p></list-item><list-item id="u9385"><label>•</label><p id="p11575">Possibly leukopenia or leukocytosis<list list-type="simple" id="ulist2135"><list-item id="u9390"><label>•</label><p id="p11580">Neutrophils frequently toxic</p></list-item></list></p></list-item></list></p></sec><sec id="s1875"><title>Diagnosis</title><p id="p11585"><list list-type="simple" id="ulist2140"><list-item id="u9395"><label>•</label><p id="p11590">Submit feces for culture.<list list-type="simple" id="ulist2145"><list-item id="u9400"><label>•</label><p id="p11595"><italic>Salmonella</italic> spp. and <italic>R. equi</italic></p></list-item><list-item id="u9405"><label>•</label><p id="p11600">Anaerobic culture</p></list-item></list></p></list-item><list-item id="u9410"><label>•</label><p id="p11605">Submit feces for toxin assays.<list list-type="simple" id="ulist2150"><list-item id="u9415"><label>•</label><p id="p11610"><italic>C. difficile</italic> and <italic>C. perfringens</italic></p></list-item></list></p></list-item></list><boxed-text id="b0330"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1880"><title>Antibiotic-Induced Diarrhea</title><p id="p11615"><list list-type="simple" id="ulist2155"><list-item id="u9420"><label>•</label><p id="p11620">Provide pain relief:<list list-type="simple" id="ulist2160"><list-item id="u9425"><label>•</label><p id="p11625">Avoid full-dose flunixin meglumine if possible; use dipyrone, 22 mg/kg IV; butorphanol, 0.05 mg/kg IV or IM; or xylazine, 0.5 to 1.0 mg/kg IV.<list list-type="simple" id="ulist2165"><list-item id="u9430"><label>○</label><p id="p11630"><italic>Do not</italic> use NSAIDs in excess as right dorsal colitis (RDC) can occur in weanlings although it is <italic>not</italic> nearly as common as in adult horses.</p></list-item></list></p></list-item></list></p></list-item><list-item id="u9435"><label>•</label><p id="p11635">Provide IV fluids: Plasma-Lyte, Normosol-R, Lactated Ringer's solution; <italic>volume replacement is the most important consideration.</italic><list list-type="simple" id="ulist2170"><list-item id="u9440"><label>•</label><p id="p11640">Supplement volume replacement with 20 mEq/L of KCl unless the following are true:<list list-type="simple" id="ulist2175"><list-item id="u9445"><label>○</label><p id="p11645">The patient is oliguric, the serum creatinine concentration >5 mg/dL, or the serum potassium >5.0 mEq/L.</p></list-item></list></p></list-item></list></p></list-item><list-item id="u9450"><label>•</label><p id="p11650">Supplement with bicarbonate if the horse is acidotic (pH <7.1) and does <italic>not</italic> respond to initial therapy.</p></list-item><list-item id="u9455"><label>•</label><p id="p11655">Treat endotoxemia (see <xref rid="s1635" ref-type="sec">p. 224</xref>).<list list-type="simple" id="ulist2180"><list-item id="u9460"><label>•</label><p id="p11660">Administer plasma, 1 to 2 L IV, to improve hemodynamics.<list list-type="simple" id="ulist2185"><list-item id="u9465"><label>○</label><p id="p11665">Endotoxin hyperimmune plasma is preferred.</p></list-item></list></p></list-item><list-item id="u9470"><label>•</label><p id="p11670">Administer flunixin meglumine, 0.25 mg/kg IV q8h if colic present.</p></list-item></list></p></list-item><list-item id="u9475"><label>•</label><p id="p11675">Administer antibiotics:<list list-type="simple" id="ulist2190"><list-item id="u9480"><label>•</label><p id="p11680">Metronidazole, 15 to 25 mg/kg PO q8h to q12h</p></list-item><list-item id="u9485"><label>•</label><p id="p11685">If no improvement occurs in 3 to 4 days, discontinue oral antibiotics.</p></list-item></list></p></list-item><list-item id="u9490"><label>•</label><p id="p11690">Bacteriotherapy:<list list-type="simple" id="ulist2195"><list-item id="u9495"><label>•</label><p id="p11695">Bacteriotherapy is transfaunation. The donor intestinal fluid is best if it is taken from the cecum of a horse that is being humanely destroyed for noninfectious causes, is <italic>Salmonella</italic> culture negative, and has a normal appetite (e.g., laminitis case).</p></list-item><list-item id="u9500"><label>•</label><p id="p11700">Fecal collection from the rectum of a healthy, properly dewormed horse would be second best choice.</p></list-item><list-item id="u9505"><label>•</label><p id="p11705">One to 2 L of fluid can be collected from the cecal contents or feces collected from the rectum and placed in a warm balanced electrolyte solution so that 1 to 2 L of fluid can be collected; these can be given via nasogastric tube; once is often sufficient if cecal contents are used.</p></list-item><list-item id="u9510"><label>•</label><p id="p11710">The transfaunation fluid can be kept in a refrigerator (ideally in a glass bottle with air evacuated but with a pressure release valve!) or frozen if there is a several day delay in treatment or if it needs to be repeated.</p></list-item></list></p></list-item><list-item id="u9515"><label>•</label><p id="p11715">Provide supportive care:<list list-type="simple" id="ulist2200"><list-item id="u9520"><label>•</label><p id="p11720">Ulcer prophylaxis including sucralfate (see <xref rid="s1605" ref-type="sec">p. 223</xref>).</p></list-item><list-item id="u9525"><label>•</label><p id="p11725">Intestinal protectants:<list list-type="simple" id="ulist2205"><list-item id="u9530"><label>○</label><p id="p11730">Treat with di-tri-octahedral smectite (Bio-Sponge)</p></list-item><list-item id="u9535"><label>○</label><p id="p11735">Bismuth subsalicylate</p></list-item></list></p></list-item></list></p></list-item></list></p></sec></boxed-text></p></sec></sec><sec id="s1885"><title>Salmonellosis</title><p id="p11740"><boxed-text id="b0335"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1890"><title>Salmonellosis</title><p id="p11745"><list list-type="simple" id="ulist2210"><list-item id="u9540"><label>•</label><p id="p11750">Treat weanlings as you would treat a foal (see <xref rid="s1605" ref-type="sec">p. 223</xref>) with Salmonellosis.</p></list-item><list-item id="u9545"><label>•</label><p id="p11755">Treat yearlings as you would an adult horse (see <xref rid="s1985" ref-type="sec">p. 235</xref>) with salmonellosis.</p></list-item><list-item id="u9550"><label>•</label><p id="p11760">Lesions in the colon of a weanling with salmonellosis can be severe, with marked thickening noted on ultrasound exam (<xref rid="f0380" ref-type="fig">Fig. 18-74</xref>).<fig id="f0380"><label>Figure 18-74</label><caption><p>Marked thickening of the colon in a 6-month-old Thoroughbred filly that did <italic>not</italic> survive <italic>Salmonella</italic> diarrhea in spite of intensive therapy, including parenteral nutrition.</p></caption><graphic xlink:href="f018-074-9781455708925"></graphic></fig></p></list-item></list></p></sec></boxed-text></p></sec><sec id="s1895"><title>Other Causes of Diarrhea in Weanlings</title><p id="p11765"><list list-type="simple" id="ulist2215"><list-item id="u9555"><label>•</label><p id="p11770"><italic>Neorickettsia risticii:</italic><list list-type="simple" id="ulist2220"><list-item id="u9560"><label>•</label><p id="p11775">There are no studies to confirm the frequency of Potomac horse fever in weanlings.</p></list-item><list-item id="u9565"><label>•</label><p id="p11780">The diagnosis and treatment are the same as in adult horses (see the following).</p></list-item></list></p></list-item><list-item id="u9570"><label>•</label><p id="p11785"><italic>Listeria</italic> species:<list list-type="simple" id="ulist2225"><list-item id="u9575"><label>•</label><p id="p11790">This bacterium is a sporadic cause of diarrhea in nursing up to weanling foals.</p></list-item><list-item id="u9580"><label>•</label><p id="p11795">In younger foals, bacteremia and shock may occur, whereas in older foals the disease does not appear to be as severe.</p></list-item><list-item id="u9585"><label>•</label><p id="p11800">Treat with penicillin 22,000 units/kg IV q6h.</p></list-item><list-item id="u9590"><label>•</label><p id="p11805">Supportive intestinal treatments are recommended.</p></list-item></list></p></list-item><list-item id="u9595"><label>•</label><p id="p11810"><italic>Brachyspira pilosicoli:</italic><list list-type="simple" id="ulist2230"><list-item id="u9600"><label>•</label><p id="p11815">This is an uncommon cause of diarrhea (mostly chronic) in weanlings.</p></list-item><list-item id="u9605"><label>•</label><p id="p11820">The anaerobic bacteria damage the brush border of the colon causing diarrhea. Infection may occur from contaminated water.</p></list-item><list-item id="u9610"><label>•</label><p id="p11825">Diagnosis includes ruling out other more common causes, histologic finding on postmortem samples, and fecal PCR testing.</p></list-item><list-item id="u9615"><label>•</label><p id="p11830">Treatment is metronidazole, 15 to 20 mg/kg PO q8h.</p></list-item></list></p></list-item><list-item id="u9620"><label>•</label><p id="p11835">Parasites:<list list-type="simple" id="ulist2235"><list-item id="u9625"><label>•</label><p id="p11840">Acute heavy infection with <italic>Parascaris equorum</italic> or <italic>Strongylus</italic> spp. may cause diarrhea but diarhea is uncommon with even heavy infection from these parasites!<list list-type="simple" id="ulist2240"><list-item id="u9630"><label>○</label><p id="p11845">Unthriftiness and colic are the more common clinical signs.</p></list-item><list-item id="u9635"><label>○</label><p id="p11850">In yearlings, weight loss and protein-losing enteropathy may occur.</p></list-item></list></p></list-item></list></p></list-item></list></p></sec></sec><sec id="s1900"><title>Acute Infectious and Toxic Diarrheal Diseases in the Adult Horse</title><p id="p11855"><italic><bold>J. Barry David and Thomas J. Divers</bold></italic></p><p id="p11860"><list list-type="simple" id="ulist2245"><list-item id="u9640"><label>•</label><p id="p11865">Acute diarrhea in the adult horse often presents as a medical emergency.</p></list-item><list-item id="u9645"><label>•</label><p id="p11870">The horse sometimes exhibits signs of abdominal pain, which may initially be difficult to differentiate from a surgical colic.</p></list-item><list-item id="u9650"><label>•</label><p id="p11875">A complete history and physical examination including abdominal ultrasound examination and analysis of the laboratory measurements of a CBC and serum chemistry are important in the workup of a horse with acute colitis.</p></list-item></list></p><sec id="s1905"><title>Presentation</title><p id="p11880"><list list-type="simple" id="ulist2250"><list-item id="u9655"><label>•</label><p id="p11885">Abdominal pain, lethargy, and fever are common signs that may precede the production of diarrhea in adult horses with colitis.</p></list-item><list-item id="u9660"><label>•</label><p id="p11890">Occasionally, the patient may present with a colonic impaction and fever.</p></list-item><list-item id="u9665"><label>•</label><p id="p11895"><italic><bold>Practice Tip:</bold> Acute infectious diarrhea in adult horses is considered a medical emergency.</italic></p></list-item><list-item id="u9670"><label>•</label><p id="p11900">Elevations of heart and respiratory rates are common, as is the appearance of dark or injected mucous membranes accompanied by the typical signs of dehydration.</p></list-item><list-item id="u9675"><label>•</label><p id="p11905">The findings of abdominal auscultation generally are those of hypomotility, decreased frequency and intensity of borborygmi or an increase in gas/fluid interface sounds.</p></list-item><list-item id="u9680"><label>•</label><p id="p11910"><italic><bold>Practice Tip:</bold> Any form of colitis may result in laminitis.</italic></p></list-item></list></p></sec><sec id="s1910"><title>Causes of Acute Colitis in Adult Horses</title><sec id="s1915"><title>Potomac Horse Fever (PHF)</title><p id="p11915"><list list-type="simple" id="ulist2255"><list-item id="u9685"><label>•</label><p id="p11920"><italic>Neorickettsia risticii</italic> infection</p></list-item><list-item id="u9690"><label>•</label><p id="p11925">A common cause of fever in endemic areas with approximately 20% of cases developing diarrhea and/or laminitis</p></list-item><list-item id="u9695"><label>•</label><p id="p11930">Seasonal occurrence in endemic areas—more common in June to November in the Northeast, North Central, and Mid-Atlantic regions of North America. It also causes disease in some South American countries.</p></list-item><list-item id="u9700"><label>•</label><p id="p11935">Infection may occur in pastured or stabled horses.<list list-type="simple" id="ulist2260"><list-item id="u9705"><label>•</label><p id="p11940">In pastured horses, infection may result from <italic>N. risticii</italic>–infected trematodes (cercariae) of fresh water snails released into water or in the pasture near a wet area (as snail slime trails).</p></list-item><list-item id="u9710"><label>•</label><p id="p11945">This may be especially common during hot weather and may occur during droughts as wet areas in the pasture concentrate both the available grass and either snails or especially aquatic insects, which may have ingested the <italic>N. risticii</italic>–infected metacercariae, that die in the pasture.</p></list-item><list-item id="u9715"><label>•</label><p id="p11950">These aquatic insects are responsible for transporting <italic>N. risticii</italic> to feed buckets when they are attracted to light in the stables at night.</p></list-item></list></p></list-item><list-item id="u9720"><label>•</label><p id="p11955">After infection, presumably by ingestion, infected horses may become febrile within 1 to 3 days. This fever often goes unnoticed and most horses never show clinical signs.</p></list-item><list-item id="u9725"><label>•</label><p id="p11960">Approximately 20% of horses a second fever, leukopenia, toxemia, and sometimes diarrhea develop 5 to 7 days later as the organism moves from the blood to the colon (trophism) and causes colitis.</p></list-item><list-item id="u9730"><label>•</label><p id="p11965">No stress factors are required for this cause of colitis.</p></list-item><list-item id="u9735"><label>•</label><p id="p11970">Vaccine efficacy is in question because there appear to be a number of strains of this intracellular bacteria.</p></list-item><list-item id="u9740"><label>•</label><p id="p11975">Clinical signs are often indistinguishable from <italic>Salmonella</italic> spp.</p></list-item><list-item id="u9745"><label>•</label><p id="p11980"><bold><italic>Practice Tip:</italic></bold><italic>Except for more pronounced colic with both right dorsal colitis and blister beetle toxicity, most causes of acute colitis in horses have a similar clinical and clinical pathology presentation.</italic></p></list-item><list-item id="u9750"><label>•</label><p id="p11985"><italic><bold>Important:</bold></italic> Laminitis appears to be more commonly associated with PHF than other causes of colitis.<list list-type="simple" id="ulist2265"><list-item id="u9755"><label>•</label><p id="p11990">Laminitis may occur with only fever and protein-losing enteropathy without diarrhea in some PHF cases!</p></list-item></list></p></list-item></list>Diagnosis and treatment for all causes of colitis are listed on <xref rid="s1950" ref-type="sec">pp. 233-237</xref>.</p></sec><sec id="s1920"><title>Salmonellosis</title><p id="p11995"><list list-type="simple" id="ulist2270"><list-item id="u9760"><label>•</label><p id="p12000">May be associated with stress</p></list-item><list-item id="u9765"><label>•</label><p id="p12005">1% to 5% carriers in most studies<list list-type="simple" id="ulist2275"><list-item id="u9770"><label>•</label><p id="p12010">Closer to 1% except for colic cases</p></list-item></list></p></list-item><list-item id="u9775"><label>•</label><p id="p12015">Other risk factors for disease include:<list list-type="simple" id="ulist2280"><list-item id="u9780"><label>•</label><p id="p12020">Off feed, abdominal surgery</p></list-item><list-item id="u9785"><label>•</label><p id="p12025">Housed on large brood mare farms</p></list-item><list-item id="u9790"><label>•</label><p id="p12030">Antibiotics (both oral and systemic)</p></list-item></list></p></list-item><list-item id="u9795"><label>•</label><p id="p12035">Dose and gastric pH are also important in determining disease risk</p></list-item><list-item id="u9800"><label>•</label><p id="p12040">Virulence of serovar seems to be of some importance in determining disease; <italic>S. typhimurium, S. agona,</italic> and <italic>S. newport</italic> seem to be especially prominent causes of clinical diarrhea in the horse although many other serovars have caused salmonellosis in horses. There is <italic>no</italic> recognized correlation between multi-drug resistant (MDR) strains (i.e., DT-104) and virulence.</p></list-item><list-item id="u9805"><label>•</label><p id="p12045">Rarely bloody diarrhea</p></list-item><list-item id="u9810"><label>•</label><p id="p12050">May be a farm problem<list list-type="simple" id="ulist2285"><list-item id="u9815"><label>•</label><p id="p12055">It is <italic>not</italic> unusual to have a farm problem involving mostly foals or mostly adults.</p></list-item><list-item id="u9820"><label>•</label><p id="p12060">One age group is clinically ill while the accompanying foal or mare is culture positive and often not ill.</p></list-item></list></p></list-item></list>Diagnosis and treatment for all causes of colitis are listed on <xref rid="s1950" ref-type="sec">pp. 233-237</xref> .</p></sec><sec id="s1925"><title>NSAID Toxicity</title><p id="p12065"><list list-type="simple" id="ulist2290"><list-item id="u9825"><label>•</label><p id="p12070">Phenylbutazone and flunixin meglumine have been implicated in causing the disease.<list list-type="simple" id="ulist2295"><list-item id="u9830"><label>•</label><p id="p12075">The drugs <italic>may</italic> have been administered in appropriate dosages to uniquely sensitive or dehydrated horses and ponies or may have been overdosed.</p></list-item></list></p></list-item><list-item id="u9835"><label>•</label><p id="p12080">Phenylbutazone is generally considered to have the highest tendency to create GI problems but flunixin may pose an equal risk.</p></list-item><list-item id="u9840"><label>•</label><p id="p12085">NSAIDs may cause the problem when administered orally or intravenously.</p></list-item><list-item id="u9845"><label>•</label><p id="p12090">Patients typically develop <italic>hypoproteinemia</italic> as a result of <italic>hypoalbuminemia</italic> early in the course of the disease. <italic><bold>Note:</bold></italic> It would be difficult to diagnosis RDC in a horse unless the plasma protein is low.</p></list-item><list-item id="u9850"><label>•</label><p id="p12095">The most severe form of the disease affects the right dorsal colon and the diarrheal/colic disease associated with NSAIDs is often referred to as right dorsal colitis (RDC). The mechanism for this is unknown.</p></list-item></list>Diagnosis and treatments are listed on <xref rid="s1950" ref-type="sec">pp. 233-237</xref>.</p></sec><sec id="s1930"><title>Cyathostomiasis</title><p id="p12100"><list list-type="simple" id="ulist2300"><list-item id="u9855"><label>•</label><p id="p12105">Occurs most commonly in yearlings or young adults</p></list-item><list-item id="u9860"><label>•</label><p id="p12110">Generally poor body condition patients with a questionable history of parasite control</p></list-item><list-item id="u9865"><label>•</label><p id="p12115">Most commonly occurs in October through April</p></list-item><list-item id="u9870"><label>•</label><p id="p12120">Often insidious in onset of diarrhea without fever or may occur after deworming</p></list-item></list>Diagnosis and treatment are listed on <xref rid="s1950" ref-type="sec">pp. 233, 234</xref>.</p></sec><sec id="s1935"><title>Antibiotic-Associated Colitis</title><p id="p12125"><list list-type="simple" id="ulist2305"><list-item id="u9875"><label>•</label><p id="p12130">Illness generally occurs 2 to 6 days after start of antibiotic administration.<list list-type="simple" id="ulist2310"><list-item id="u9880"><label>•</label><p id="p12135">Almost any antibiotic can cause the problem; there may be some differences based on geographic location: ceftiofur (both Naxcel and Exceed), trimethoprim-sulfamethoxazole, oral penicillin V, Quartermaster in the guttural pouch, macrolides (especially when given to horses >4 months of age), rifampicin, and less commonly oxytetracycline/doxycycline, and enrofloxacin.</p></list-item></list></p></list-item><list-item id="u9885"><label>•</label><p id="p12140">Decreased roughage consumption and switching from intravenous to orally administered antibiotics may predispose the patient to antibiotic-associated colitis.</p></list-item><list-item id="u9890"><label>•</label><p id="p12145">Illness is believed to result from the death of beneficial GI flora, allowing an overgrowth of toxigenic <italic>C. difficile</italic> and/or <italic>C. perfringens,</italic> or in many cases, a dysbiosis (change in normal intestinal flora). Horses with dysbiosis without clostridiosis are generally <italic>not</italic> as sick but may be totally inappetent.</p></list-item></list>Diagnosis and treatments are listed on <xref rid="s1950" ref-type="sec">pp. 233-237</xref>.</p></sec><sec id="s1940"><title>Colitis X</title><p id="p12150"><list list-type="simple" id="ulist2315"><list-item id="u9895"><label>•</label><p id="p12155">Acute colitis and associated endotoxemia and anaphylaxis may have multiple causes including anaphylaxis, acute clostridiosis, or rapid overgrowth of other pathogenic bacteria such as some strains of <italic>E. coli, Proteus</italic> spp., <italic>Enterococcus</italic> spp., and/or <italic>Pseudomonas</italic> spp.</p></list-item><list-item id="u9900"><label>•</label><p id="p12160">Colon wall edema is a characteristic finding and sometimes hemorrhagic regions are noted during postmortem examination.</p></list-item><list-item id="u9905"><label>•</label><p id="p12165">Aerobic and anaerobic cultures should be performed.</p></list-item></list></p></sec><sec id="s1945"><title>Coronavirus</title><p id="p12170"><list list-type="simple" id="ulist2320"><list-item id="u9910"><label>•</label><p id="p12175">There have been several outbreaks of beta coronavirus-associated fever; leukopenia; anorexia; and sometimes, diarrhea or colic in adult horses.</p></list-item><list-item id="u9915"><label>•</label><p id="p12180">The incidence of diarrhea in horses is approximately 20%. On one farm, nine horses were infected—all with fever, anorexia, and leukopenia but no clinical diarrhea.</p></list-item><list-item id="u9920"><label>•</label><p id="p12185">The degree of anorexia is marked in many cases.</p></list-item><list-item id="u9925"><label>•</label><p id="p12190">Diagnosis is based on PCR-positive coronavirus feces and ruling out other causes.</p></list-item><list-item id="u9930"><label>•</label><p id="p12195">Nasal swabs do <italic>not</italic> detect coronavirus-infected horses. The PCR testing can be performed by IDEXX (diarrhea panel) or other molecular laboratories such as U.C. Davis or Cornell University Diagnostic Laboratory that have experience in testing horses for the virus.</p></list-item><list-item id="u9935"><label>•</label><p id="p12200">Treatment is generally supportive and prognosis is good.</p></list-item><list-item id="u9940"><label>•</label><p id="p12205">Coronavirus is highly contagious in horses; quarantine for 2 weeks is recommended plus fecal PCR testing.</p></list-item></list></p></sec></sec><sec id="s1950"><title>General Diagnostic Tests for Adult Colitis</title><p id="p12210"><list list-type="simple" id="ulist2325"><list-item id="u9945"><label>•</label><p id="p12215">Perform a complete physical examination: a horse presenting with acute abdominal pain and fever is likely to have an early case of colitis or, less likely, peritonitis.</p></list-item><list-item id="u9950"><label>•</label><p id="p12220">Obtain a detailed history, including vaccinations, deworming, antibiotic administration, NSAID use, the presence of other clinical cases of diarrhea on the farm, previous cases of salmonellosis and PHF on the farm, types of feeds and changes in the feeding program, and the duration of the signs.</p></list-item><list-item id="u9955"><label>•</label><p id="p12225">Most cases of <italic>C. difficile</italic> colitis occur 2 to 5 days after starting antibiotic treatment. Antibiotic dybiosis can occur almost immediately after beginning antibiotics.</p></list-item><list-item id="u9960"><label>•</label><p id="p12230">Isolate the patient from herd mates until the results of fecal diagnostics are known and/or the clinical signs have resolved.</p></list-item><list-item id="u9965"><label>•</label><p id="p12235">Perform general diagnostic tests for acute colitis:<list list-type="simple" id="ulist2330"><list-item id="u9970"><label>•</label><p id="p12240">Whole blood and serum for a CBC, serum chemistry, and other diagnostic analyses.</p></list-item><list-item id="u9975"><label>•</label><p id="p12245">Ancillary stall-side tests may include serum lactate, electrolytes, creatinine, and blood gas with ionized calcium.</p></list-item><list-item id="u9980"><label>•</label><p id="p12250">If you are located in an endemic area of PHF, submit serum samples for serologic testing and whole blood for PCR. Whole blood PCR is most useful in the early stages of the disease.</p></list-item><list-item id="u9985"><label>•</label><p id="p12255">If coronavirus is suspected, fecal PCR testing is recommended.</p></list-item><list-item id="u9990"><label>•</label><p id="p12260">Submit fecal cultures for <italic>Salmonella</italic> spp.</p></list-item><list-item id="u9995"><label>•</label><p id="p12265">Submit fecal samples for detection of clostridial diseases (toxin assays): Tox A and B for <italic>C. difficile</italic> and enterotoxin and beta-2 toxin gene for <italic>C. perfringens</italic> type A.<xref rid="fn0160" ref-type="fn">31</xref></p></list-item></list></p></list-item><list-item id="u10000"><label>•</label><p id="p12270">Abdominal ultrasonography should be performed.<list list-type="simple" id="ulist2335"><list-item id="u10005"><label>•</label><p id="p12275">Edema or thickness of the bowel wall may be visualized in some cases, especially in horses with NSAID toxicity (RDC) (<xref rid="f0385" ref-type="fig">Fig. 18-75</xref>and <xref rid="f0390" ref-type="fig">18-76</xref>, <italic>B</italic>). The right dorsal colon can usually be identified between the 11th to 13th intercostal spaces against the liver, duodenum, dorsal to the right ventral colon, which has increased numbers of sacculations.<fig id="f0385"><label>Figure 18-75</label><caption><p>Ultrasound examination of the right abdomen at midlevel of an adult horse with right dorsal colitis demonstrates marked edema of the colon wall. The liver is to the right.</p></caption><graphic xlink:href="f018-075-9781455708925"></graphic></fig></p></list-item><list-item id="u10010"><label>•</label><p id="p12280">With RDC, the hypoechoic layer is bordered by a hyperechoic layer on both the serosal and mucosal sides and the thickened hypoechoic layer is less echogenic than liver. The thickness of the hypoechoic layer is usually 50% to 75% of total mural thickness of the right dorsal colon.</p></list-item><list-item id="u10015"><label>•</label><p id="p12285">Frequently, ingesta of a nearly homogeneous fluid nature are observed swirling in the large colon (<xref rid="f0390" ref-type="fig">Fig. 18-76</xref>) of horses with colitis. Normal colonic sacculations with an air interface are lost.<fig id="f0390"><label>Figure 18-76</label><caption><p><bold>A,</bold> Homogeneous appearing, fluid-filled large intestine seen on an ultrasound examination of a horse that developed diarrhea 4 hours later. <bold>B,</bold> Edema of the right dorsal colon associated with an overdose of phenylbutazone in a 2-year-old Thoroughbred filly.</p></caption><graphic xlink:href="f018-076-9781455708925"></graphic></fig></p></list-item></list></p></list-item><list-item id="u10020"><label>•</label><p id="p12290">Palpation per rectum is not generally needed, unless the horse is distended and/or is painful. In fact, palpation may initiate rectal prolapse in some colitis cases.<list list-type="simple" id="ulist2340"><list-item id="u10025"><label>•</label><p id="p12295">Edema or thickness of the colon wall may be appreciated.</p></list-item><list-item id="u10030"><label>•</label><p id="p12300">Early in the course of disease mild to moderate impaction may be part of the clinical presentation.</p></list-item></list></p></list-item><list-item id="u10035"><label>•</label><p id="p12305">Abdominocentesis is not routine for colitis cases because it may enhance the formation of ventral edema sometimes leading to scrotal cellulitis in stallions. Perform <italic>only</italic> if peritonitis is suspected.<list list-type="simple" id="ulist9085"><list-item id="u10040"><label>•</label><p id="p12310">Elevated protein is typical in peritoneal fluid samples from horses with colitis.</p></list-item></list></p></list-item><list-item id="u10045"><label>•</label><p id="p12315">Routine blood work includes the following:<list list-type="simple" id="ulist2345"><list-item id="u10050"><label>•</label><p id="p12320">CBC<list list-type="simple" id="ulist2350"><list-item id="u10055"><label>○</label><p id="p12325">Leukopenia with toxic appearing neutrophils is commonly seen.</p></list-item></list></p></list-item><list-item id="u10060"><label>•</label><p id="p12330">Serum chemistry panel<list list-type="simple" id="ulist2355"><list-item id="u10065"><label>○</label><p id="p12335">Hyponatremia, hypochloremia, and azotemia are common findings in acute cases.</p></list-item><list-item id="u10070"><label>○</label><p id="p12340">Hypoproteinemia and hypoalbuminemia are manifestations of significant disease.</p></list-item><list-item id="u10075"><label>○</label><p id="p12345">Hyperammonemia (overproduction of ammonia in the gut) may sporadically occur with any of the infectious causes of diarrhea.</p></list-item></list></p></list-item><list-item id="u10080"><label>•</label><p id="p12350">Use serial serum lactate concentration as a prognostic indicator.<list list-type="simple" id="ulist2360"><list-item id="u10085"><label>○</label><p id="p12355">Look for at least a 30% reduction in 4 to 8 hours or a 50% reduction in 24 hours after initiation of treatment for an improved prognosis.</p></list-item></list></p></list-item></list></p></list-item></list></p></sec><sec id="s1955"><title>Laboratory Testing for Specific Diseases</title><sec id="s1960"><title>Potomac Horse Fever</title><p id="p12360"><list list-type="simple" id="ulist2365"><list-item id="u10090"><label>•</label><p id="p12365">An (IFA) titer >1 : 640 is somewhat diagnostic in an unvaccinated individual; >1 : 2560 is often diagnostic in a vaccinated individual.<xref rid="fn0165" ref-type="fn">32</xref> Sensitivity and specificity of these numbers are unproven.</p></list-item><list-item id="u10095"><label>•</label><p id="p12370">Remember that values may be low in an acute case, as seroconversion may occur later in the course of the disease.</p></list-item><list-item id="u10100"><label>•</label><p id="p12375">Potomac horse fever PCR requires a whole blood sample (EDTA tube) shipped on ice overnight to one of several laboratories in the country. The PCR may be negative in many cases as the organism has moved from the blood to the colon.<list list-type="simple" id="ulist2370"><list-item id="u10110"><label>•</label><p id="p12385">The PCR is available at Cornell Diagnostic Laboratory, University of California—Davis, University of Connecticut, and other laboratories</p></list-item></list></p></list-item></list></p></sec><sec id="s1965"><title>Salmonella</title><p id="p12390"><list list-type="simple" id="ulist2375"><list-item id="u10115"><label>•</label><p id="p12395"><italic>Salmonella</italic> spp. fecal cultures generally are performed in multiple cultures (3 to 5 days in a row).<list list-type="simple" id="ulist2380"><list-item id="u10120"><label>•</label><p id="p12400">Do <italic>not</italic> refrigerate samples; transport them in selenite or Ames transport media.</p></list-item><list-item id="u10125"><label>•</label><p id="p12405">If samples are cultured in-house, use selective media.<list list-type="simple" id="ulist2385"><list-item id="u10130"><label>○</label><p id="p12410">Positive culture provides species for basic epidemiologic studies and the capability to perform antibiotic sensitivity studies.</p></list-item><list-item id="u10135"><label>○</label><p id="p12415"><italic>Citrobacter</italic> spp. in the feces may require extra steps of testing to differentiate from salmonella.</p></list-item></list></p></list-item><list-item id="u10140"><label>•</label><p id="p12420">Serotype data, antimicrobial resistance patterns, and Pulse-Field-Gel-Electrophoresis (PFGE) can be used to determine epidemiology of an outbreak.</p></list-item></list></p></list-item><list-item id="u10145"><label>•</label><p id="p12425"><italic>Salmonellae</italic> spp. PCR testing is available through an Enhanced Rapid Test System (Reveal 2.0 <italic>Salmonella</italic> test system<xref rid="fn0170" ref-type="fn">33</xref>) for the detection of <italic>Salmonella</italic> spp. A culture would need to be performed to determine antibiogram.<list list-type="simple" id="ulist2390"><list-item id="u10150"><label>•</label><p id="p12430">PCR is performed on suspicious cultures (black or green colonies noted on Hektoen agar).</p></list-item><list-item id="u10155"><label>•</label><p id="p12435">This testing is especially useful during outbreaks for both early detection of infected horses and environmental culturing and quickly separates <italic>Salmonella</italic> and <italic>Citrobacter</italic> spp.</p></list-item></list></p></list-item></list></p></sec><sec id="s1970"><title>Clostridiosis</title><p id="p12440"><list list-type="simple" id="ulist2395"><list-item id="u10160"><label>•</label><p id="p12445">Clostridial disease frequently is implicated as the causative agent of antibiotic-induced colitis.</p></list-item><list-item id="u10165"><label>•</label><p id="p12450">Gram stain on direct fecal smear may show an overwhelming number of gram-positive rods, which may be <italic>indicative</italic> of clostridial colitis although sensitivity of the Gram stain is likely low.</p></list-item><list-item id="u10170"><label>•</label><p id="p12455">The definitive diagnosis of <italic>C. difficile</italic> requires identification of the presence of clostridial toxins in the feces.</p></list-item><list-item id="u10175"><label>•</label><p id="p12460">A commercial ELISA assay for toxins A and B has been studied and is considered reliable and adequate for use in the horse.<xref rid="fn0175" ref-type="fn">34</xref></p></list-item><list-item id="u10180"><label>•</label><p id="p12465">For the diagnosis of <italic>C. perfringens,</italic> pure growth in anaerobic fecal culture is considered <italic>suggestive</italic> that the organism is the cause of disease.<list list-type="simple" id="ulist2400"><list-item id="u10185"><label>•</label><p id="p12470">Commercial enterotoxin assay is available (see <xref rid="u7710" ref-type="list-item">p. 222</xref>) and is required for a more definitive diagnosis.<list list-type="simple" id="ulist2405"><list-item id="u10190"><label>○</label><p id="p12475">Because the toxin is considered labile, the assay must be performed within a half-hour of collection of fresh manure or the manure sample must be frozen within a half-hour and kept frozen until testing. PCR testing is also available at some laboratories.</p></list-item></list></p></list-item></list></p></list-item></list></p></sec><sec id="s1975"><title>NSAID-Induced Colitis</title><p id="p12480"><list list-type="simple" id="ulist2410"><list-item id="u10195"><label>•</label><p id="p12485">Ultrasonography of the abdominal cavity <italic>may</italic> demonstrate bowel wall edema of the right dorsal colon (see <xref rid="f0385" ref-type="fig">Fig. 18-75</xref>). The thickness of the RDC may vary from dramatic to subtle. There is a commercial fecal test for albumin loss (SUCCEED Equine Fecal Blood Test<xref rid="fn0180" ref-type="fn">35</xref>), but sensitivity/specificity data from independent scientific publications are needed.</p></list-item></list></p></sec><sec id="s1980"><title>Cyathostomiasis</title><p id="p12490"><list list-type="simple" id="ulist2415"><list-item id="u10200"><label>•</label><p id="p12495">Fecal test for parasites is generally recommended but seldom reveals a cause for the diarrhea. Identifying cyathostome larvae on a rectal mucosal biopsy or appearance of the adults in the manure is supportive of cyathostomiasis.</p></list-item></list></p></sec><sec id="s1985"><title>Coronavirus</title><p id="p12500"><list list-type="simple" id="ulist2420"><list-item id="u10205"><label>•</label><p id="p12505">Feces should be submitted for PCR testing at a laboratory that is experienced in the testing (e.g., U.C.-Davis, Cornell diagnostic laboratory, or other locations).</p></list-item></list><boxed-text id="b0340"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1990"><title>General Therapy for Colitis, Regardless of the Cause</title><p id="p12510"><list list-type="simple" id="ulist2425"><list-item id="u10210"><label>•</label><p id="p12515">Crystalloid fluids: the hallmark of therapy<list list-type="simple" id="ulist2430"><list-item id="u10215"><label>•</label><p id="p12520">Plasma-Lyte, Normosol-R, and lactated Ringer's solution are preferred in most cases.<list list-type="simple" id="ulist2435"><list-item id="u10220"><label>○</label><p id="p12525">KCl, 20 to 40 mEq added to each liter: the <italic>safe</italic> rate of KCl administration is 0.5 mEq/kg/h.</p></list-item><list-item id="u10225"><label>○</label><p id="p12530">Most horses with diarrhea are expected to have a total body decrease in potassium regardless of the plasma K<sup>+</sup> concentration. If the plasma K<sup>+</sup> is above 6 meq/L, this could be an indication of acute renal failure.</p></list-item></list></p></list-item></list></p></list-item><list-item id="u10230"><label>•</label><p id="p12535">Hypertonic saline, 4 mL/kg IV bolus for hypovolemic shock<list list-type="simple" id="ulist2440"><list-item id="u10235"><label>•</label><p id="p12540">Follow the administration of hypertonic saline immediately with crystalloid therapy in a 10 : 1 ratio; 10 L crystalloid for each liter of hypertonic saline.</p></list-item><list-item id="u10240"><label>•</label><p id="p12545">Sodium bicarbonate: Use <italic>only</italic> if the patient is severely acidotic (pH <7.1) and hypertonic saline followed by large volume lactated Ringer's or Plasmalyte have <italic>not</italic> corrected the metabolic acidosis but the L-lactate is decreasing. This scenario could indicate an intestinal overproduction of D-lactate.</p></list-item></list></p></list-item><list-item id="u10245"><label>•</label><p id="p12550">Treat endotoxemia:<list list-type="simple" id="ulist2445"><list-item id="u10250"><label>•</label><p id="p12555">Plasma: Administer a minimum of 2 L.<list list-type="simple" id="ulist2450"><list-item id="u10255"><label>○</label><p id="p12560">Plasma contains several opsonins such as fibronectin and antithrombin III, in addition to antibodies.</p></list-item><list-item id="u10260"><label>○</label><p id="p12565">Hyperimmune plasma from horses exposed to endotoxin is preferred.</p></list-item></list></p></list-item><list-item id="u10265"><label>•</label><p id="p12570">Plasma also provides oncotic support if the patient is hypoproteinemic.</p></list-item><list-item id="u10270"><label>•</label><p id="p12575">Flunixin meglumine, 0.25 mg/kg IV q8h—<italic>except in cases of RDC</italic>.<list list-type="simple" id="ulist2455"><list-item id="u10275"><label>○</label><p id="p12580">Continue administration until signs of endotoxemia are alleviated.</p></list-item></list></p></list-item><list-item id="u10280"><label>•</label><p id="p12585">Pentoxifylline, 10 mg/kg PO or IV q12h<list list-type="simple" id="ulist2460"><list-item id="u10285"><label>○</label><p id="p12590">Shown in vivo to decrease cytokine production during endotoxin challenge (if given before endotoxin challenge) and protects against multiple organ injury</p></list-item><list-item id="u10290"><label>○</label><p id="p12595">May cause red blood cells to be more deformable</p></list-item></list></p></list-item><list-item id="u10295"><label>•</label><p id="p12600">Polymyxin B sulfate, 6000 units/kg IV q12h if renal function is normal<list list-type="simple" id="ulist2465"><list-item id="u10300"><label>○</label><p id="p12605">Considered to directly bind endotoxin and may provide an initial notable clinical response.</p></list-item></list></p></list-item><list-item id="u10305"><label>•</label><p id="p12610">Clopidogrel (Plavix), 4 mg/kg PO q24h on day 1 and 2 mg/kg PO q24h on subsequent treatments may inhibit platelet activation and may decrease the likelihood of laminitis and colon and jugular venous thrombosis; the absorption of the drug in horses with colitis is unknown.</p></list-item></list></p></list-item><list-item id="u10310"><label>•</label><p id="p12615">Treatment of hypoproteinemia:<list list-type="simple" id="ulist2470"><list-item id="u10315"><label>•</label><p id="p12620">Plasma: A significant amount of plasma is required to increase plasma oncotic pressure.</p></list-item><list-item id="u10320"><label>•</label><p id="p12625">Hydroxyethyl starch (Hetastarch, VetStarch or Pentastarch), 5 to 10 mL/kg IV<list list-type="simple" id="ulist2475"><list-item id="u10325"><label>○</label><p id="p12630">Increases colloid oncotic pressure</p></list-item><list-item id="u10330"><label>○</label><p id="p12635">Synthetic colloid may “plug” leaky endothelial cell gaps</p></list-item><list-item id="u10335"><label>○</label><p id="p12640">May assist in reducing bowel wall edema</p></list-item></list></p></list-item></list></p></list-item><list-item id="u10340"><label>•</label><p id="p12645">Intravenous multiple B-vitamins can be given daily but must be administered slowly.</p></list-item><list-item id="u10345"><label>•</label><p id="p12650">Intestinal protectants should be administered in most cases.<list list-type="simple" id="ulist2480"><list-item id="u10350"><label>•</label><p id="p12655">Di-tri-octahedral smectite (Bio-Sponge<xref rid="fn0185" ref-type="fn">36</xref>) is most commonly used for clostridial diarrhea. Bismuth subsalicylate and/or activated charcoal may be beneficial.</p></list-item></list></p></list-item><list-item id="u10355"><label>•</label><p id="p12660">Unless patient is clinically painful, provide free-choice water and offer an additional electrolyte bucket:<list list-type="simple" id="ulist2485"><list-item id="u10365"><label>•</label><p id="p12670">Add a commercial electrolyte mixture per label directions, <italic>or</italic></p></list-item><list-item id="u10370"><label>•</label><p id="p12675">Add to each 1 to 2 L of water the following:<list list-type="simple" id="ulist2490"><list-item id="u10375"><label>○</label><p id="p12680">30 mL of 50% dextrose</p></list-item><list-item id="u10380"><label>○</label><p id="p12685">12 g baking soda</p></list-item><list-item id="u10385"><label>○</label><p id="p12690">10 g KCl</p></list-item></list></p></list-item></list></p></list-item><list-item id="u10390"><label>•</label><p id="p12695"><italic>Prophylaxis for laminitis</italic>: cryotherapy is the <italic>only</italic> proven method of prevention. This can be performed using 5-L fluid bags attached to the feet and/or commercially available boots that fit over the coronary band; both filled with <italic>crushed</italic> ice slurry (see Chapter 43, p. 712). The top of the bag can be taped to the fetlock area using Elasticon or duct tape. For horses with larger feet or those that “walk out” of the 5-L fluid bags, commercial boots can be purchased and filled with <italic>crushed</italic> ice slurry.</p></list-item><list-item id="u10395"><label>•</label><p id="p12700">Provide a highly digestible fiber (low-residue) feed, if possible, particularly with NSAID toxicity.<list list-type="simple" id="ulist2495"><list-item id="u10400"><label>•</label><p id="p12705">A complete pelleted ration with the addition of 1 to 2 oz of dietary linseed or corn oil is an option.</p></list-item><list-item id="u10405"><label>•</label><p id="p12710">Most importantly, keep the horse eating unless bloated, gastric reflux, or “colicy.”</p></list-item><list-item id="u10410"><label>•</label><p id="p12715">Offer the horse pasture/grass, if available.</p></list-item></list></p></list-item><list-item id="u10415"><label>•</label><p id="p12720">Minimize risk of thrombophlebitis:<list list-type="simple" id="ulist2500"><list-item id="u10420"><label>•</label><p id="p12725">Use polyurethane catheters.</p></list-item><list-item id="u10425"><label>•</label><p id="p12730">Sample blood from vessels other than the jugular veins.</p></list-item><list-item id="u10430"><label>•</label><p id="p12735">Monitor catheter site frequently; alternate catheter sites.</p></list-item></list></p></list-item><list-item id="u10435"><label>•</label><p id="p12740">Prevent exposure to other horses; isolate the patient if possible.</p></list-item><list-item id="u10440"><label>•</label><p id="p12745">Wrap tail; use caution to not wrap the tail too tight. <italic>Do not</italic> use Vetwrap<italic>.</italic></p></list-item></list></p></sec></boxed-text></p><p id="p12750"><boxed-text id="b0345"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s1995"><title>Specific Treatments for Adult Colitis</title><sec id="s2000"><title>Salmonellosis</title><p id="p12755"><list list-type="simple" id="ulist2505"><list-item id="u10445"><label>•</label><p id="p12760">Administration of antibiotics is of questionable clinical benefit in adult horses. Although no evidence indicates that they help this condition, most clinicians prefer parenteral administration; there can be translocation of other organisms from the diseased intestine.</p></list-item><list-item id="u10450"><label>•</label><p id="p12765">If possible, choose antibiotic based on fecal culture and sensitivity report.</p></list-item><list-item id="u10455"><label>•</label><p id="p12770">Risks associated with antibiotic use include the following:<list list-type="simple" id="ulist2510"><list-item id="u10460"><label>•</label><p id="p12775">Fungal pneumonia and colitis, further dysbiosis</p></list-item><list-item id="u10465"><label>•</label><p id="p12780">Nephrotoxicity associated with aminoglycosides and decreased renal blood flow because of hypovolemia and endotoxemia</p></list-item><list-item id="u10470"><label>•</label><p id="p12785">Outcome in adult horse salmonellosis does not appear to be affected by antibiotic use. Enrofloxacin, 7.5 mg/kg IV q24h is frequently used.</p></list-item></list></p></list-item></list></p></sec><sec id="s2005"><title>Potomac Horse Fever</title><p id="p12790"><list list-type="simple" id="ulist2515"><list-item id="u10475"><label>•</label><p id="p12795">Oxytetracycline, 6.6 mg/kg IV q12h or 10 mg/kg IV q24h<list list-type="simple" id="ulist2520"><list-item id="u10480"><label>•</label><p id="p12800"><italic><bold>Caution:</bold></italic> May be nephrotoxic in dehydrated horses!</p></list-item></list></p></list-item><list-item id="u10485"><label>•</label><p id="p12805">Better prognosis when administered early in the course of the disease.</p></list-item></list></p></sec><sec id="s2010"><title>Antibiotic-Associated Colitis</title><p id="p12810"><list list-type="simple" id="ulist2525"><list-item id="u10490"><label>•</label><p id="p12815">Metronidazole, 15 to 25 mg/kg PO q6 to 8h; it is very rare for metronidazole to cause diarrhea<list list-type="simple" id="ulist2530"><list-item id="u10495"><label>•</label><p id="p12820">Improvement should occur within 3 days; consider discontinuing antibiotic therapy if clinical improvement is not seen.</p></list-item></list></p></list-item><list-item id="u10500"><label>•</label><p id="p12825">Di-tri-octahedral smectite (Bio-Sponge), generally 3 lb administered by nasogastric tube 2 to 3 times, 8 hours apart.</p></list-item><list-item id="u10505"><label>•</label><p id="p12830">Administer commercial plasma with antibodies targeting <italic>Clostridium difficile</italic> toxins.</p></list-item><list-item id="u11215"><label>•</label><p id="p13575">Bacteriotherapy using the cecal contents of healthy recently euthanized horses has caused a marked improvement in horses with antibiotic-induced diarrhea; the feces returning to normal “overnight”; one treatment is often sufficient. Fecal transfaunation can be performed if cecal contents are not available, but it does not seem as successful as a cecal transfaunation. This treatment is recommended for either clostridial diarrhea or dybiosis.</p></list-item></list></p></sec><sec id="s2015"><title>NSAID Toxicity</title><p id="p12835"><list list-type="simple" id="ulist2535"><list-item id="u10510"><label>•</label><p id="p12840">Plasma: 4 to 8 L IV</p></list-item><list-item id="u10515"><label>•</label><p id="p12845">Hetastarch, VetStarch, or Pentastarch: 7 to 10 mL/kg IV</p></list-item><list-item id="u10520"><label>•</label><p id="p12850">Sucralfate: 22 mg/kg PO q6 to12 to 24h</p></list-item><list-item id="u10525"><label>•</label><p id="p12855">Misoprostol: 2 to 4 µg/kg PO q12h to q24h<list list-type="simple" id="ulist2540"><list-item id="u10530"><label>•</label><p id="p12860">Mild diarrhea, increased rectal temperature, and mild colic have been reported after administration.</p></list-item><list-item id="u10535"><label>•</label><p id="p12865">The drug is associated with abortion. <bold><italic>Do not</italic> use misoprostol in the pregnant mare, and it must <italic>not</italic> be handled by pregnant women!</bold></p></list-item></list></p></list-item></list></p></sec><sec id="s2020"><title>Cyathostomiasis</title><p id="p12870"><list list-type="simple" id="ulist2545"><list-item id="u10540"><label>•</label><p id="p12875">Moxidectin<xref rid="fn0190" ref-type="fn">37</xref>: 400 to 500 µg/kg PO once, along with dexamethasone 0.04 mg/kg IV or IM q24h for 3 days</p></list-item><list-item id="u10545"><label>•</label><p id="p12880">Fenbendazole: 10 mg/kg PO q24h for 5 successive days is frequently used but efficacy is questionable.</p></list-item><list-item id="u10550"><label>•</label><p id="p12885">Corticosteroids used in combination with moxidectin may improve recovery.</p></list-item></list></p></sec><sec id="s2025"><title>Coronavirus</title><p id="p12890"><list list-type="simple" id="ulist2550"><list-item id="u10555"><label>•</label><p id="p12895">No specific treatment</p></list-item></list></p></sec></sec></boxed-text></p><p id="p12900"><boxed-text id="b0350"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s2030"><title>Abdominal Pain Associated with Acute Colitis</title><p id="p12905"><list list-type="simple" id="ulist2555"><list-item id="u10560"><label>•</label><p id="p12910">Rule out obstructive GI tract disease:<list list-type="simple" id="ulist2560"><list-item id="u10565"><label>•</label><p id="p12915">Nasogastric intubation: evaluate for gastric reflux.</p></list-item><list-item id="u10570"><label>•</label><p id="p12920">Abdominal ultrasonography</p></list-item><list-item id="u10575"><label>•</label><p id="p12925">Abdominocentesis and palpation per rectum if colitis is not the obvious diagnosis</p></list-item></list></p></list-item><list-item id="u10580"><label>•</label><p id="p12930">Treat ileus:<list list-type="simple" id="ulist2565"><list-item id="u10585"><label>•</label><p id="p12935">Calcium borogluconate 23%: 500 mL added to 10 L of crystalloid fluids</p></list-item><list-item id="u10590"><label>•</label><p id="p12940">Lidocaine: 1.3 mg/kg as a slow IV bolus followed by a constant rate infusion of 0.05 mg/kg/min</p></list-item></list></p></list-item></list></p><sec id="s2035"><title>Analgesics</title><p id="p12945"><list list-type="simple" id="ulist2570"><list-item id="u10595"><label>•</label><p id="p12950">NSAIDs: Flunixin meglumine and possibly ketoprofen <italic>initially</italic> at the recommended full dose, except in cases of NSAID-induced colitis.<list list-type="simple" id="ulist2575"><list-item id="u10600"><label>•</label><p id="p12955">Firocoxib (0.09 mg/kg IV) is the safest selection for NSAID use in horses with colitis; however, even COX-2 specific inhibitors may slow healing of the damaged bowel. If firocoxib is used to control pain in horses with colitis, a low dose (0.3 mg/kg) of flunixin may be added to the treatment to inhibit thromboxane.<list list-type="simple" id="ulist2580"><list-item id="u10605"><label>○</label><p id="p12960">It is generally recommended to decrease the dosage of NSAIDs early in the treatment of the infectious diarrheal disease to protect the GI mucosa. There is no evidence that NSAID use prevents laminitis in these cases.</p></list-item></list></p></list-item><list-item id="u11210"><label>•</label><p id="p13570">Concurrent treatment with lidocaine CRI and flunixin meglumine is reported to lessen the negative effects of NSAIDs on bowel healing.</p></list-item></list></p></list-item><list-item id="u10610"><label>•</label><p id="p12965">Sedatives: xylazine, detomidine, and butorphanol may be used on a short-term basis.</p></list-item><list-item id="u10615"><label>•</label><p id="p12970">If the patient is distended because of colonic gas and remains nonresponsive to standard analgesic regimens, consider the following:<list list-type="simple" id="ulist2585"><list-item id="u10620"><label>•</label><p id="p12975">Cecal or colonic decompression (see <xref rid="p0290" ref-type="p">p. 160</xref>) if “ping” is present in right dorsal abdomen (cecal) or marked gas distention of the colon is found on rectal examination</p></list-item><list-item id="u10625"><label>•</label><p id="p12980">Neostigmine, 0.005 to 0.01 mg/kg SQ q1h, for 3 to 5 treatments to stimulate colonic motility</p></list-item><list-item id="u10630"><label>•</label><p id="p12985">Chloral hydrate for narcosis and as a last resort to control the “colicky” horse, administered to effect, generally 30 to 60 mg/kg IV.</p></list-item><list-item id="u10635"><label>•</label><p id="p12990">Butylscopolammonium bromide (Buscopan, 0.3 mg/kg IV) decreases pain associated with intestinal distention but inhibition of motility and delayed passage of the soft feces may worsen ileus and toxemia.</p></list-item></list></p></list-item></list></p></sec></sec></boxed-text></p></sec></sec><sec id="s2040"><title>Prognosis for Acute Colitis in Adult Horses</title><p id="p12995"><list list-type="simple" id="ulist2590"><list-item id="u10640"><label>•</label><p id="p13000">The prognosis for acute colitis in adult horses is variable.</p></list-item><list-item id="u10645"><label>•</label><p id="p13005">Factors that worsen the prognosis include the development of laminitis, renal failure, and systemic inflammatory response syndrome.</p></list-item><list-item id="u10650"><label>•</label><p id="p13010">The prognosis for a performance horse is considered poor if laminitis occurs and is not markedly improved after 3 days of treatment.</p></list-item><list-item id="u10655"><label>•</label><p id="p13015">The presence of scant, watery diarrhea for more than 24 hours and purple mucous membranes indicate a less favorable prognosis.</p></list-item><list-item id="u10660"><label>•</label><p id="p13020">Patients with a PCV >65% or refractory erythrocytosis may recover but often fail to gain weight, founder, or cascade into renal failure.</p></list-item><list-item id="u10665"><label>•</label><p id="p13025">The majority of cases are azotemic, which is generally a prerenal cause.</p></list-item><list-item id="u10670"><label>•</label><p id="p13030">The patient's serum creatinine concentration and serum potassium concentration should move rapidly toward the normal range within the first 36 hours of fluid therapy or primary renal failure should be considered.</p></list-item><list-item id="u10675"><label>•</label><p id="p13035">If blood lactate and cTn-I concentrations do not decrease after resuscitation therapy, the prognosis is guarded.</p></list-item><list-item id="u10680"><label>•</label><p id="p13040">If urine production is <italic>not</italic> seen after the administration of several liters of intravenous fluids or after the administration of 2 L of hypertonic saline and the serum potassium concentration is >5.5 mg/L, the patient is likely in acute renal failure (see Chapter 26, p. 489).</p></list-item><list-item id="u10685"><label>•</label><p id="p13045">The prognosis for acute renal failure is fair if the patient becomes polyuric with continued intravenous fluid administration.</p></list-item></list></p></sec><sec id="s2045"><title>Toxic Causes of Acute Colitis/Diarrhea in Horses</title><p id="p13050"><list list-type="simple" id="ulist2595"><list-item id="u10690"><label>•</label><p id="p13055">There are many causes of acute diarrhea and most cause additional clinical signs other than diarrhea:<list list-type="simple" id="ulist2600"><list-item id="u10695"><label>•</label><p id="p13060">Ionophore toxicity (see Chapter 34, p. 602)</p></list-item><list-item id="u10700"><label>•</label><p id="p13065">Hoary alyssum (see Chapter 34, p. 600)</p></list-item><list-item id="u10705"><label>•</label><p id="p13070">Clover poisoning (see Chapter 34, p. 604)</p></list-item><list-item id="u10710"><label>•</label><p id="p13075">Sand or gravel ingestion (see <xref rid="s1055" ref-type="sec">p. 204</xref>)</p></list-item><list-item id="u10715"><label>•</label><p id="p13080">Anaphylaxis (see Appendix 4, p. 814)</p></list-item><list-item id="u10720"><label>•</label><p id="p13085">Endotoxemia (see <xref rid="s1985" ref-type="sec">p. 235</xref>)</p></list-item><list-item id="u10725"><label>•</label><p id="p13090">Acute grain overload (see <xref rid="s0410" ref-type="sec">p. 184</xref>)</p></list-item></list></p></list-item><list-item id="u10730"><label>•</label><p id="p13095">Dietary changes and excitement may also cause acute diarrhea; however, these horses are generally <italic>not</italic> ill.</p></list-item><list-item id="u10735"><label>•</label><p id="p13100">Perhaps the most severe toxin affecting the horse's intestinal tract causing both colic and diarrhea is blister beetle poisoning.</p></list-item></list></p><sec id="s2050"><title>Cantharidin Intoxication (Blister Beetle Poisoning)</title><sec id="s2055"><title>Presentation</title><p id="p13105"><list list-type="simple" id="ulist2605"><list-item id="u10740"><label>•</label><p id="p13110">Elevated heart rate and respiratory rate are associated with the most common clinical sign of abdominal pain.</p></list-item><list-item id="u10745"><label>•</label><p id="p13115">The severity of the signs is directly related to the degree and duration of intoxication.</p></list-item><list-item id="u10750"><label>•</label><p id="p13120">Oral ulcers/erosions are frequently noted; the horse may appear to play in the water.</p></list-item><list-item id="u10755"><label>•</label><p id="p13125">Horses experiencing cantharidin intoxication are typically anorexic, lethargic, and may exhibit signs of urinary tract dysfunction such as pollakiuria, hematuria, and stranguria.</p></list-item><list-item id="u10760"><label>•</label><p id="p13130">Signs associated with profound hypocalcemia include a stiff, stilted gait and thumps (synchronous diaphragmatic flutter).</p></list-item><list-item id="u10765"><label>•</label><p id="p13135">Severe cases may have neurologic signs or acutely die.</p></list-item></list></p></sec><sec id="s2060"><title>Cause</title><p id="p13140"><list list-type="simple" id="ulist2610"><list-item id="u10770"><label>•</label><p id="p13145">Cantharidin is a toxin found in the hemolymph and gonads of the male <italic>Epicauta</italic> spp. beetles (<xref rid="f0395" ref-type="fig">Fig. 18-77</xref>).<fig id="f0395"><label>Figure 18-77</label><caption><p>Three-striped blister beetle.</p></caption><graphic xlink:href="f018-077-9781455708925"></graphic><attrib>(Courtesy Dr. David Schmitz, Texas A&M College of Veterinary Medicine.)</attrib></fig></p></list-item><list-item id="u10775"><label>•</label><p id="p13150">The beetles are most common in the Southwest, and they swarm in alfalfa fields when mating in mid- to late summer.</p></list-item><list-item id="u10780"><label>•</label><p id="p13155">Modern hay harvesting methods of cutting and crimping hay in a single pass kills swarms of beetles.</p></list-item><list-item id="u10785"><label>•</label><p id="p13160">Cantharidin creates mucosal lesions throughout the GI tract, and it is rapidly excreted by the kidneys, which in turn leads to renal parenchymal damage and hemorrhagic cystitis.</p></list-item><list-item id="u10790"><label>•</label><p id="p13165">Myocardial damage occurs by an unknown mechanism.</p></list-item><list-item id="u10795"><label>•</label><p id="p13170"><italic><bold>Practice Tip:</bold> As few as 5 to 10 beetles may be fatal to a horse.</italic></p></list-item></list><boxed-text id="b0355"><caption><title><inline-graphic xlink:href="icon01-9781455708925.gif"></inline-graphic> What to Do</title></caption><sec id="s2065"><title>Blister Beetle Intoxication</title><p id="p13175"><list list-type="simple" id="ulist2615"><list-item id="u10800"><label>•</label><p id="p13180">Supportive treatment:<list list-type="simple" id="ulist2620"><list-item id="u10805"><label>•</label><p id="p13185">Provide pain relief<list list-type="simple" id="ulist2625"><list-item id="u10810"><label>○</label><p id="p13190">Flunixin meglumine, 1.1 mg/kg IV q12h</p></list-item><list-item id="u10815"><label>○</label><p id="p13195">Butorphanol, 0.04 to 0.1 mg/kg IV or IM or consider a constant rate infusion of butorphanol or lidocaine</p></list-item></list></p></list-item><list-item id="u10820"><label>•</label><p id="p13200">Evacuate GI tract:<list list-type="simple" id="ulist9985"><list-item id="u10825"><label>○</label><p id="p13205">Mineral oil by nasogastric intubation provides laxative effects and binds the lipid-soluble toxin; but recent work suggests it also increases absorption and toxicity. Therefore, administration of activated charcoal or smectite in addition to magnesium sulfate would seem more appropriate.</p></list-item></list></p></list-item><list-item id="u10830"><label>•</label><p id="p13210">Establish diuresis and base choice of fluids on serum chemistry results and urine production.<list list-type="simple" id="ulist2630"><list-item id="u10835"><label>○</label><p id="p13215">Cases are frequently hypocalcemic and hypomagnesemic.<list list-type="simple" id="ulist2635"><list-item id="u10840"><label>-</label><p id="p13220">Administer 500 mL of 23% calcium borogluconate diluted in 5 to 10 L of intravenous fluids.</p></list-item><list-item id="u10845"><label>-</label><p id="p13225">Administer 5 to 10 g of magnesium sulfate diluted in fluids.</p></list-item></list></p></list-item></list></p></list-item><list-item id="u10850"><label>•</label><p id="p13230">Administer anti-inflammatory agents:<list list-type="simple" id="ulist2640"><list-item id="u10855"><label>○</label><p id="p13235">Dexamethasone, 0.1 to 0.2 mg/kg IV once</p></list-item></list></p></list-item><list-item id="u10860"><label>•</label><p id="p13240">Provide ulcer prophylaxis:<list list-type="simple" id="ulist2645"><list-item id="u10865"><label>○</label><p id="p13245">Sucralfate 20 mg/kg PO q6 to 12h and</p></list-item><list-item id="u10870"><label>○</label><p id="p13250">Ranitidine, 6.6 mg/kg PO q8h</p><p id="p13255">or</p></list-item><list-item id="u10875"><label>○</label><p id="p13260">Omeprazole 4 mg/kg PO q24h</p></list-item></list></p></list-item><list-item id="u10880"><label>•</label><p id="p13265">Administer broad-spectrum antibiotics:<list list-type="simple" id="ulist2650"><list-item id="u10885"><label>○</label><p id="p13270">Avoid aminoglycosides and sulfonamides</p></list-item></list></p></list-item></list></p></list-item></list></p><sec id="s2070"><title>Diagnosis</title><p id="p13275"><list list-type="simple" id="ulist2655"><list-item id="u10890"><label>•</label><p id="p13280">Submit several hundred milliliters of stomach contents and urine to Texas Veterinary Medical Diagnostic Lab, College Station, Texas, or other labs that assay the toxin.</p></list-item><list-item id="u10895"><label>•</label><p id="p13285">Examine hay for the presence of <italic>Epicauta</italic> spp.</p></list-item><list-item id="u10900"><label>•</label><p id="p13290">Submit GI contents and kidneys from postmortem samples.</p></list-item></list></p></sec></sec></boxed-text></p></sec><sec id="s2075"><title>Prognosis</title><p id="p13295"><list list-type="simple" id="ulist2660"><list-item id="u10905"><label>•</label><p id="p13300">The prognosis for cantharidin intoxication is considered guarded in most cases.</p></list-item><list-item id="u10910"><label>•</label><p id="p13305">Clinicopathologic findings that worsen the prognosis include:<list list-type="simple" id="ulist2665"><list-item id="u10915"><label>•</label><p id="p13310">Azotemia</p></list-item><list-item id="u10920"><label>•</label><p id="p13315"><italic>Markedly</italic> elevated cardiac troponin I (cTn-I) concentrations or concentrations that do not decrease with therapy</p></list-item></list></p></list-item><list-item id="u10925"><label>•</label><p id="p13320">The risk of intoxication can be reduced by feeding only alfalfa hay harvested before June (first cutting). <italic><bold>Important:</bold></italic> Storing or pelleting hay <italic>does not</italic> denature cantharidin.</p></list-item><list-item id="u10930"><label>•</label><p id="p13325">Client education for those producing their own hay is essential to minimizing exposure to blister beetles.</p></list-item></list></p></sec></sec></sec></sec><sec id="s9050"><title>References</title><p id="p19790">References can be found on the companion website at <ext-link ext-link-type="uri" xlink:href="http://www.equine-emergencies.com" id="iw0025">www.equine-emergencies.com</ext-link>.</p></sec></sec></body><back><fn-group><fn id="fn0010"><label>1</label><p id="np0010">Rüsch esophagus flush probe, Oesophagus-sprelsonde (Willy Ruesch AG, Kernen, Germany).</p></fn><fn id="fn0015"><label>2</label><p id="np0015">Veterinary injection pump (Nasco, Inc., Fort Atkinson, Wisconsin).</p></fn><fn id="fn0020"><label>3</label><p id="np0030">Stubbs Equine Innovations, Inc., Johnson City, Texas.</p></fn><fn id="fn0025"><label>4</label><p id="np0035">Diagnostic Imaging Systems, Inc., Rapid City, South Dakota.</p></fn><fn id="fn0030"><label>5</label><p id="np0040">PDS (Ethicon, Somerville, New Jersey).</p></fn><fn id="fn0035"><label>6</label><p id="np0045">Information available at durvet.com.</p></fn><fn id="fn0040"><label>7</label><p id="np0050">MEDVET (Kernen, Germany).</p></fn><fn id="fn0045"><label>8</label><p id="np0060">These values are not relevant to nursing foals, which generally have lower PCV and protein values.</p></fn><fn id="fn0050"><label>9</label><p id="np0095">6% Hetastarch (Braun Medical, Irvine, California).</p></fn><fn id="fn0055"><label>10</label><p id="np0100">Endoserum (Immvac, Columbia, Missouri).</p></fn><fn id="fn0060"><label>11</label><p id="np0105">Polymune-J (San Luis Obispo, California) or Foalimmune (Lake Immunogenics, Inc., Ontario, New York).</p></fn><fn id="fn0065"><label>12</label><p id="np0110">Polymyxin B (Bedford Laboratories, Bedford, Ohio).</p></fn><fn id="fn0070"><label>13</label><p id="np0115">Polypropylene (Davol A Bard Company, Warwick, Rhode Island).</p></fn><fn id="fn0075"><label>14</label><p id="np0120">Plastics (Goshen Laboratories, Goshen, New York).</p></fn><fn id="fn0080"><label>15</label><p id="np0125">HDPE (MEDPOR, DermNet, New Zealand).</p></fn><fn id="fn0085"><label>16</label><p id="np0130">Rectal Ring (Regal Plastic Co., Detroit Lakes, Minnesota).</p></fn><fn id="fn0090"><label>17</label><p id="np0135">TOX A/B test (Techlab, Blacksburg, Virginia).</p></fn><fn id="fn0095"><label>18</label><p id="np0140">TRIAGE Micro (BIOSITE, San Diego California, 1-888-BIOSITE).</p></fn><fn id="fn0100"><label>19</label><p id="np0145">BD GasPak EZ (Becton, Dickinson and Company, Sparks, Maryland).</p></fn><fn id="fn0105"><label>20</label><p id="np0150">Lake Immunogenics <italic>Clostridium difficile</italic> Toxin A and B Antibody Select HI Plasma (Ontario, New York 14519).</p></fn><fn id="fn0110"><label>21</label><p id="np0155">Lake Immunogenics <italic>Clostridium perfringens</italic> Type A, C, and D Antibody Select HI Plasma (Ontario, New York 14519).</p></fn><fn id="fn0115"><label>22</label><p id="np0160">LACTAID (McNeil Consumer Healthcare, Fort Washington, Pennsylvania 19034).</p></fn><fn id="fn0120"><label>23</label><p id="np0165">Lactase enzyme (6000 Food Chemical Codex units/50-kg foal) orally every 3 to 8 hours (McNeil Consumer Healthcare, Fort Washington, Pennsylvania 19034).</p></fn><fn id="fn0125"><label>24</label><p id="np0170">Bio-Sponge (Platinum Performance, Buellton, California 93427).</p></fn><fn id="fn0130"><label>25</label><p id="np0175">Anti-Diarrhea Gel (Hagyard Medical Institute, 4250 Iron Works Pike, Lexington, Kentucky 40511-8412).</p></fn><fn id="fn0135"><label>26</label><p id="np0180">Reveal (Neogen, Lansing, Michigan 48912).</p></fn><fn id="fn0140"><label>27</label><p id="np0185">Rotazyme (Abbott Laboratories, Diagnostics Div., North Chicago, Illinois).</p></fn><fn id="fn0145"><label>28</label><p id="np0190">Lactase enzyme (6000 Food Chemical Codex units/50-kg foal) orally every 3 to 8 hours (McNeil Consumer Healthcare, Fort Washington, Pennsylvania 19034).</p></fn><fn id="fn0150"><label>29</label><p id="np0195">Equine Coli Endotox (Novartis Animal Health US, Inc., 800-843-3386).</p></fn><fn id="fn0155"><label>30</label><p id="np0200">Bentonite clay (Hagyard Pharmacy, 4250 Iron Works Pike Lexington, Kentucky).</p></fn><fn id="fn0160"><label>31</label><p id="np0205">Department of Veterinary Science and Microbiology, University of Arizona, Tucson, Arizona.</p></fn><fn id="fn0165"><label>32</label><p id="np0210">There may be an increase in control (background) IFA values in recent years, and it is possible that the titers have lost accuracy in confirming a diagnosis.</p></fn><fn id="fn0170"><label>33</label><p id="np0215">Neogen (Lansing, Michigan 48912).</p></fn><fn id="fn0175"><label>34</label><p id="np0220">Tox A/B test (Techlab, Blacksburg, Virginia).</p></fn><fn id="fn0180"><label>35</label><p id="np0225">SUCCEED Equine Fecal Blood Test (Freedom Health, LLC, Aurora, Ohio).</p></fn><fn id="fn0185"><label>36</label><p id="np0230">Bio-Sponge (Platinum Performance, 90 Thomas Road, PO Box 990, Buellton, California 93427).</p></fn><fn id="fn0190"><label>37</label><p id="np0235">Moxidectin (American Cyanamid, Wayne, New Jersey).</p></fn></fn-group></back></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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