The gastrointestinal and digestive system

Chapter 10


The gastrointestinal and digestive system





Chapter contents



INTRODUCTION


DISEASES OF THE ESOPHAGUS



DISEASES OF THE STOMACH



DISEASES OF THE SMALL INTESTINE CAUSING COLIC



DISEASES OF THE LARGE INTESTINE CAUSING COLIC



Introduction


Non-strangulating obstructions



Strangulating obstructions



Functional obstructions



LARGE COLON DISEASES CAUSING PERITONITIS



GASTROINTESTINAL DISEASES CAUSING CHRONIC WEIGHT LOSS



GASTROINTESTINAL DISEASES CAUSING ACUTE DIARRHEA



LIVER DISEASE IN HORSES



PERITONITIS





DISEASES OF THE ESOPHAGUS



ESOPHAGEAL IMPACTION




Etiology and pathogenesis

Obstruction or “choke” is the most common of the esophageal disorders in the horse. Common predisposing factors include feed changes, poor dentition, trauma, inadequate water intake, foreign bodies, and ingestion of dry, coarse feed items (dry grains, ears of corn and pelleted feeds). Gluttonous horses that rapidly eat feed without proper mastication or ingest bedding also are at risk of developing esophageal impaction. The lodging of dry material in the esophagus may initiate impaction formation.


Irritation of the esophageal mucosa and esophageal distension may cause esophageal spasm, thereby worsening esophageal impaction. Long-standing impaction can result in ulceration and necrosis of the esophageal wall. Ulceration of the esophageal wall can lead to esophageal spasm leading to recurrence of impaction. Severe necrosis can result in perforation.



Clinical findings and diagnosis

The horse with a physical obstruction of the esophagus may exhibit dysphagia, coughing and nasal regurgitation of food material, water and saliva from the mouth and nostrils. The horse may make repeated attempts at ingestion followed by extension of the head and neck to facilitate swallowing. This is often accompanied by odynophagia (painful swallowing), head-tossing and other signs of agitation and frustration.


The time from ingestion to the onset of clinical signs is dependent on the location of the obstruction within the esophagus and can vary from immediately after ingestion to 10–12s following ingestion. After an initial excitatory period, forced attempts at swallowing become less frequent, and distress and frustration are replaced by depression, anorexia, electrolyte imbalances and dehydration. Intermittent signs of obstruction may indicate a more complex underlying disease and justify further diagnostic evaluation. Aspiration pneumonia (q.v.) is a frequent complication of esophageal obstruction.


Diagnosis of esophageal obstruction often is based on clinical signs. Esophageal obstruction can be confirmed by attempting to pass a nasogastric tube, which cannot be passed beyond the site of obstruction. Palpation of the neck may reveal enlargement of the cervical esophagus. Crepitation and diffuse cervical enlargement may denote cellulitis (q.v.) resulting from perforation of the esophageal wall. Thoracic auscultation and ultrasound should be performed to ascertain and monitor the development of aspiration pneumonia.


Transtracheal aspiration (q.v.) provides a sample for cytology and bacterial culture as an aid in determining the identity and antimicrobial sensitivity of the bacterial organisms causing pneumonia. Gram-positive cocci (especially Streptococcus spp.), Gram-negative enteric bacteria (Escherichia coli, Proteus spp., Klebsiella spp. and Pseudomonas spp.) and anaerobic bacteria are all common. Aspiration pneumonia (q.v.) sometimes results in severe consolidation, abscessation or pleuritis, which can best be evaluated with thoracic radiography and ultrasonography.


Horses with esophageal obstruction that recurs or does not resolve after conservative therapy should be evaluated for esophageal foreign body, ulceration, stricture, diverticulum and megaesophagus (q.v.).


Endoscopy and radiography are helpful for definitive diagnosis. The endoscope length must be 200 cm to examine the entire esophagus. A flexible endoscope with insufflation and irrigation capabilities is necessary for a thorough and complete examination. Endoscopic examination is best performed by fully inserting the endoscope into the insufflated esophagus and then slowly withdrawing it. Ulceration, stricture, diverticulum or dilatation may be seen. With the esophagus relaxed, normal longitudinal mucosal folds should be seen. The mucosa should be white to pale pink in color. Insufflation causes flattening of these folds and permits evaluation of luminal diameter. Transverse folds can be iatrogenically produced by moving the endoscope aborally and should not be mistaken for mural lesions.


Survey radiographs may reveal the presence of a feed impaction or foreign body. Radiography performed within 24–48 h after relieving the obstruction may reveal dilatation of the esophagus in the area of the obstruction, visible as air contrast. Barium, given orally as a paste (85% with 120 mL water), or as a liquid (72% with 420 mL water) under pressure via a nasogastric tube, will delineate the longitudinal mucosal folds and localize the obstruction. Escape of barium into the surrounding tissues indicates rupture of the esophagus.


Liquid barium (480 mL) followed by air (480 mL) provides a double contrast study and is best for evaluation of the mucosal lesions, such as circumferential mucosal ulcers secondary to feed impactions. Swallowing during contrast studies may produce radiographic artifacts that mimic an esophageal stricture. Xylazine (0.25–1.1 mg/kg IV) and butorphanol (0.02–0.08 mg/kg IV) or detomidine (0.01–0.02 mg/kg IV) given 5 min before the study helps to eliminate this artifact by suppressing the swallow reflex.


Manometric techniques to evaluate esophageal dysfunction are routinely used in human medicine and have been developed for use in horses. The availability and technical difficulty of this procedure, however, has limited its use in equine practice.



Treatment and prognosis

Prompt therapy is vital to successful management of esophageal impactions. Feed impactions become more inspissated over time, thereby making removal more difficult and complications more likely. Impactions present for only a few hours can sometimes be relieved by sedating the animal with xylazine (0.25–1.1 mg/kg IV) and butorphanol (0.02–0.08 mg/kg IV) or detomidine (0.01–0.02 mg/kg IV) to reduce swallowing, thereby decreasing the frequency of contractions of the esophagus. Access to food and water should be prevented.


Nasal intubation with gentle warm water lavage under xylazine sedation is successful in relieving most simple impactions. If gentle lavage fails, a cuffed nasogastric tube may be placed in the sedated animal thereby allowing the lavage to be performed under moderate pressure without reflux of fluid back into the pharynx. External massage may increase the efficacy of lavage. If this is unsuccessful, the animal should be muzzled to prevent food or water intake and administered balanced, isotonic IV fluids. After softening the impaction by rehydration of the patient, sedation and lavage should be repeated. Excessively aggressive lavage can result in severe aspiration or esophageal damage and/or perforation. Attempting to remove the impaction by applying pressure with a nasogastric tube often lodges the impaction in the narrower, more distal esophagus or causes perforation of the esophagus.


Relaxation of the esophagus would facilitate removal of the obstruction by preventing esophageal spasm. Detomidine, xylazine, butorphanol and guaifenesin only slightly reduce the strength of contractions of the esophagus but these sedatives do reduce the frequency of contractions of the esophagus by reducing the attempts to swallow. Oxytocin (0.11–0.22IU/kg IM) and acepromazine (0.04–0.06 mg/kg IV) have a slight effect on the strength of contraction of the esophagus, thereby minimally reducing the impact of spasm.


Because these medications lack a pronounced effect on esophageal contraction, general anesthesia and intubation with a cuffed endotracheal tube may be necessary in cases that are refractory to standing warm water lavage. This technique reduces the likelihood of aspiration, provides more esophageal muscular relaxation, and reduces the chance of perforation.


Following relief, feed should be withheld for at least 24 h to allow esophageal function to return to normal. After 24–48 h, frequent interval, small volume, soft, moist mashes (alfalfa pellets or complete feed) and/or grass should be fed for 1–7 days. Feeding of hay and other dry feeds should not be resumed until it is felt that the esophagus has healed and returned to normal function. In some cases, endoscopic examination is needed to assess resolution of secondary esophageal damage. Horses should not be allowed to ingest bedding or other foreign material. Fresh water should be available at all times and electrolyte abnormalities corrected with oral or IV solutions. Broad-spectrum antimicrobial therapy should be instituted for at least 7 days for aspiration pneumonia (q.v.). Long-term antimicrobial therapy is necessary in cases in which significant lung damage due to aspiration has occurred. Any underlying problems (e.g. management and dentition) should be corrected.


Impactions that do not respond to conservative therapy should be definitively identified, localized and relieved by surgical intervention. Either extraluminal massage or longitudinal esophagotomy may be performed. The goals of surgery are to relieve the obstruction and to return the esophagus to near normal size and function with minimal contamination and stricture formation at the surgical site. This requires strict asepsis and meticulous surgical technique. Longitudinal esophagotomy with primary closure of the incision results in minimal complications when performed in a region of normal esophagus. This procedure has a favorable prognosis for first intention healing and is preferred over manipulations that may induce further esophageal trauma. Postoperative therapy includes withholding of feed and water for 48–72 h with IV fluid therapy to correct electrolyte and acid–base abnormalities. Broad-spectrum antimicrobial drugs should be administered perioperatively if esophagotomy is performed or if there is a risk of aspiration pneumonia (q.v.). Beginning 48 h after surgery, frequent interval, small volume, soft, moist mashes should be fed for 7–10 days.


Impactions of short duration that are properly managed have a good prognosis. Reimpaction with premature ingestion of coarse feed and aspiration pneumonia (q.v.) are the most common complications. Impactions of long duration (≥24 h) are accompanied by damage to the esophageal wall and more severe aspiration and have a more guarded prognosis. Esophageal impactions requiring surgery have a guarded prognosis. Stricture formation, fistula formation, incisional dehiscence and descending cellulitis with resulting pleuritis are all possible complications, which occur with a higher incidence when the esophageal wall is compromised. Esophageal impactions leading to perforation have a grave prognosis.



ESOPHAGEAL FOREIGN BODY






Treatment and prognosis

If a secondary impaction is present, it must be relieved before attempting to remove a foreign body. Non-surgical methods for removal include endoscopically guided retrieval or pushing the object into the stomach by use of a nasogastric tube. Because the risk of esophageal trauma and perforation with these techniques is great, surgery is preferred.


Longitudinal esophagotomy with primary closure results in minimal complications when performed in a region of normal esophagus. Postoperative therapy includes withholding of feed and water for 48–72 h with IV fluid therapy to correct electrolyte and acid-base abnormalities. Broad-spectrum antimicrobial drugs should be administered. Following the initial postoperative period, frequent interval, small volume, soft, moist mashes should be fed for 7–10 days.



ESOPHAGEAL STRICTURE




Etiology and pathogenesis

Narrowing of the esophageal lumen due to stricture formation is usually present as an annular lesion and may be classified into three types:



Strictures usually result from circumferential damage to the esophagus, which heals with fibrous tissue. Impactions of extended duration with resultant circumferential mucosal irritation and ulceration, esophageal trauma resulting from attempts at relieving an obstruction, and surgical correction of previous annular lesions (q.v.) are common forms of trauma leading to stricture. Gastrointestinal disease resulting in secondary reflux esophagitis (q.v.) may result in stricture formation. Severe external cervical trauma occasionally will cause esophageal damage that heals with a stricture.



Clinical findings and diagnosis

The clinical signs associated with esophageal stricture are caused by secondary feed impaction at the proximal aspect of the constricted segment. Thus the clinical presentation of stricture is similar to that of esophageal obstruction. Endoscopic examination after removal of the secondary feed impaction will generally reveal the stricture. Maximal reduction in esophageal lumen size occurs up to 30 days after esophageal trauma or surgery; therefore, follow-up examination may be necessary. If the impaction is corrected without detection of the stricture, recurrent obstruction is likely.


Stricture formation usually impedes the passage of a nasogastric tube into the stomach and may be identified endoscopically or by positive pressure contrast radiography. Swallowing during contrast studies may produce radiographic artifacts that mimic an esophageal stricture. IV xylazine, given 5 min prior to examination, suppresses the swallow reflex and reduces this swallowing artifact.



Treatment and prognosis

Conservative management of stricture formation is directed at dilating the stenotic segment of esophagus and is most successful in early cases. Post-surgical strictures and those following circumferential mucosal ulceration may be dilated by feeding small quantities of a low bulk diet over a period of several months. Grass and mashes made of complete feed or alfalfa pellets are satisfactory diets. Concurrent non-steroidal anti-inflammatory drug (NSAID) therapy, phenylbutazone (2.2–4.4 mg/kg b.i.d. PO or IV), may be helpful. Following circumferential esophageal ulceration, maximal reduction in luminal diameter occurs at approximately 30 days post obstruction but this returns to normal by 60 days from the original insult. Therefore, if possible, it is important to postpone surgical intervention for at least 60 days, to assess maximal luminal diameter and corresponding clinical response to conservative therapy. Bougienage (passing a cylinder into a passage) has also been used in the management of equine esophageal stricture.


Chronic strictures (≥60 days in duration) have a mature cicatrix that is usually unresponsive to conservative attempts at dilatation. These may be corrected by esophagomyotomy, partial or complete resection and anastomosis, or a patch graft (q.v.) using the sternocephalicus or brachiocephalicus muscle.


Mural strictures respond well to esophagomyotomy and have the best prognosis for recovery without re-stricture. In this procedure the esophagus is incised longitudinally through the stricture to the level of the mucosa. The myotomy is not closed but the surrounding tissues are apposed.


Longitudinal esophagomyotomy and mucosal resection are used to relieve strictures caused by mucosal rings or webs and annular cicatricial lesions involving all layers of the wall. In cases of extensive stricture formation where the mucosa cannot be closed, regeneration of the mucosa will occur within the muscularis and adventitia. This procedure is indicated when myotomy fails to correct the stricture, since it carries a greater risk of re-stricture than myotomy alone.


The diameter of the esophageal lumen may also be increased in cases of extensive stricture and annular stenosis through use of a patch graft utilizing the sternocephalicus or brachiocephalicus muscle. Under general anesthesia, the surgical procedure begins by approaching the esophagus via the ventral midline or laterally. After nasogastric intubation, a longitudinal incision is initially made through the muscularis from a point 3 cm distal to and extending 3 cm proximal to the stricture. The incision is then extended through the submucosa and mucosa. The caudal portion of the muscle belly of the brachiocephalicus or sternocephalicus is mobilized by blunt dissection. The muscle should maintain its proximal and distal attachments and should be freely movable as to not exert tension on the closure with movement of the neck. Routine closure with suction drains is performed, and extraoral alimentation is preferred for 10 days. Indwelling nasogastric tubes will only stimulate salivation and increase the incidence of fistula formation.


Complete resection and anastomosis of the esophagus should be reserved for cases of rupture in which the muscularis is severely compromised. Placement of an esophagostomy tube distal to the lesion for extraoral alimentation greatly facilitates healing and minimizes incisional complications. An indwelling nasogastric tube is not recommended due to stimulation of saliva formation, thus increasing the incidence of fistula formation.


The prognosis for correction of esophageal strictures is guarded. Conservative management of early strictures is sometimes successful. However, surgical management of chronic strictures often is complicated by re-stricture, fistula formation, incisional dehiscence and descending cellulitis with resulting pleuritis (q.v.). Surgical procedures and diseases of the esophagus in the cervical area may also result in laryngeal hemiplegia (q.v.) because of the close proximity of the recurrent laryngeal nerves.



ESOPHAGEAL DIVERTICULUM




Etiology and pathogenesis

Diverticula of the esophagus are a rare cause of dysfunction. They are usually acquired lesions and may be classified into two types. A traction or true diverticulum results from periesophageal fibrosis, causing an outward tenting of all the layers of the esophageal wall. These commonly develop at a site of an esophagotomy or traumatic wound of the esophagus that is allowed to heal by second intention. They may also occur at a surgical or traumatic site where leakage of saliva has induced inflammation or abscess formation.


A pulsion or false diverticulum results from protrusion of mucosa and submucosa through a defect in the muscular layers of the esophageal wall. Pulsion diverticula may result from fluctuations in intraluminal pressure and damage of esophageal musculature by impacted feed material. In the horse external trauma is the most common cause of diverticula.



Clinical findings and diagnosis

Diverticula of the esophagus should be suspected when enlargement of the cervical area and dysphagia are present, yet a nasogastric tube can be passed into the stomach without difficulty. Positive contrast radiography confirms the diagnosis. During barium swallow esophograms, traction diverticula are spherical and have a wide area of communication with the esophagus. Pulsion diverticula are flask shaped and have a narrow area of communication with the esophagus. Positive pressure contrast studies that distend the esophageal lumen and outline the opening of the diverticula may assist in differentiation between the two types. Endoscopy is also useful in localizing the lesion and determining the size of the opening of the evagination.


Traction diverticula, even when large, produce minimal clinical signs and rarely require treatment. Pulsion diverticula, however, tend to enlarge progressively, thereby increasing the possibility of esophageal obstruction and rupture.



Treatment and prognosis

Diverticulectomy should be performed when the mucosal sac is very large and the communication with the esophagus is narrow. Pulsion diverticula may be repaired surgically by either diverticulectomy with resection of the mucosal–submucosal sac followed by reconstruction of the mucosa, submucosa and muscularis, or inversion of the mucosal–submucosal sac with reconstruction of the muscularis.


Mucosal inversion is the preferred procedure for most cases because it minimizes the risk of postoperative complications such as dehiscence or leakage, infection, fistula formation and postoperative re-obstruction. Soft, moist feed mashes should be fed for 4–6 days following surgery and treatment with antimicrobial drugs is indicated when contamination is encountered during surgery. Prognosis is dependent on the type, size and duration of the diverticulum. If the esophageal lumen is not invaded and the integrity of the esophageal wall is intact, the overall prognosis for recovery is good.



INTRAMURAL CYST







ESOPHAGITIS




Etiology and pathogenesis

Esophagitis may be caused by ingested irritants (e.g. topical irritant medications or blisters, blister beetles or cantharidin toxicity), prolonged use of a nasogastric tube, or reflux of gastric or gastroduodenal contents (q.v.). NSAID therapy can lead to esophageal ulceration. The result can be inflammation, erosion and ulceration of the esophageal mucosa. Chronic inflammation produces pain and may decrease esophageal motility. In severe cases, megaesophagus can result.


Lower esophageal and gastric inflammation may reduce the tone of the lower esophageal sphincter, thereby causing or perpetuating inflammation of the lower esophagus. Reflux esophagitis most often occurs in foals with gastric paresis or gastric outlet obstruction caused by gastric ulceration. Duodenogastric reflux may occur in horses with duodenitis/proximal jejunitis or small intestinal obstruction.




Treatment and prognosis

Exposure to the caustic agent should be removed and the esophagus allowed to rest. Slurries made of pelleted feed and grass should be fed frequently in small amounts. The animal should not be allowed to eat coarse roughage. Reflux esophagitis should be treated with the proton pump antagonist, omeprazole (4.4 mg/kg PO), or H2-receptor antagonists such as cimetidine (20 mg/kg PO t.i.d. or 4.4 mg/kg IV q.i.d.) and ranitidine (6 mg/kg PO or IV b.i.d.) to decrease gastric acid production.


Metoclopramide (0.02–0.1 mg/kg SC q 4–12 h) and bethanechol (0.03 mg/kg SC or 0.4 mg/kg PO q 6–8 h) increase the tone of the lower esophageal sphincter and distal esophageal and gastric motility and, therefore, may be useful in foals with gastric paresis and reflux esophagitis. Metoclopramide and bethanechol should not be used in animals with gastric outflow obstruction. Metoclopramide sometimes causes neurologic side effects. The prognosis with esophagitis is usually good. In the case of some ingested toxins (e.g. cantharidin), the resulting systemic disease is of greater consequence than the esophagitis. The prognosis is poor if severe megaesophagus (q.v.) develops.



MEGAESOPHAGUS




Etiology and pathogenesis

Megaesophagus is esophageal dilatation resulting in accumulation of food material and fluid within the esophageal lumen. Megaesophagus can be idiopathic or secondary to numerous primary disease processes. Congenital idiopathic megaesophagus has been reported in a few weanling foals. Secondary megaesophagus most often results from reflux esophagitis and chronic esophageal obstruction, such as that caused by vascular ring anomalies, lymphosarcoma involving cervical or mediastinal lymph nodes, or abscessation (q.v.).


Neuromuscular diseases may disrupt esophageal motility and cause chronic dilatation and ineffectual esophageal contraction. Dysphagia associated with esophageal disease has been reported in horses with botulism, equine protozoal myeloencephalitis, equine herpesvirus, and damage to the vagus nerve from trauma, neoplasia and lymphadenopathy (q.v.).



Clinical findings and diagnosis

Clinical signs of megaesophagus include nasal reflux of food and water. Aspiration pneumonia (q.v.) is a common sequel and, therefore, fever, coughing and dyspnea are often present. In cases of secondary megaesophagus, signs of the primary disease process (e.g. weakness, ataxia, etc.) are common.


Esophageal dilatation can be demonstrated by contrast radiography and endoscopy. Dilatation and accumulation of contrast material on sequential radiographs confirm the presence of impaired esophageal clearance. On esophagoscopy, dilatation, absence of peristaltic waves, and pooling of feed or fluid are observed. In cases of esophageal obstruction or esophagitis, the primary lesion may be observed via contrast radiography and esophagoscopy. A thorough neurologic examination and CSF analysis are indicated if megaesophagus is suspected to be a complication of a primary neurologic disease (q.v.).



Treatment and prognosis

In secondary megaesophagus, therapy for the obstruction, esophagitis, neurologic disease or neuromuscular disease should be instituted. There is no specific therapy for idiopathic megaesophagus; however, metoclopramide (0.02–0.1 mg/kg SC q 4–12 h) and bethanechol (0.03 mg/kg SC or 0.4 mg/kg PO q 6–8 h) may be used to improve distal esophageal peristalsis. Because aspiration causes mixed bacterial contamination of the lung, broad-spectrum antimicrobial coverage is necessary. Dietary management is necessary to prevent further pulmonary soilage and to maintain nutrition and hydration. If the resulting dysphagia is severe and prolonged, parenteral or enteral feeding will be necessary. If the dysphagia is incomplete, a slurry of pelleted feed or grass may be fed.


The prognosis depends upon the severity and cause of the dilatation. The prognosis for return of esophageal function is poor if the dilatation is severe and long-standing. Cases in which nasal reflux of food material and pulmonary soilage can be avoided by proper dietary management have a better prognosis. The prognosis in secondary megaesophagus depends upon the prognosis associated with the primary disease process. In foals with congenital megaesophagus, function may return to normal as the foal matures.



ESOPHAGEAL NEOPLASIA







DISEASES OF THE STOMACH



GASTRIC ULCERATION




Etiology and pathogenesis

The specific etiology of gastric ulceration in horses is unknown. Gastric acid hypersecretion, disturbances of gastric mucosal blood flow, impaired production of prostaglandin (PG) E or the gastric mucus/bicarbonate layer, and gastric emptying disorders are potentially involved in the initiation of gastric ulceration. Furthermore, after ulceration occurs, gastric acid prevents healing of the gastric mucosa. Other disease processes (e.g. foal diarrhea and neonatal sepsis), stressful conditions (e.g. horses in show and race training) and medication (e.g. NSAIDs [q.v.]) are factors commonly associated with a higher incidence of ulceration.


Modern management practices in which horses are stall confined and eating high energy feeds intermittently (e.g. twice daily) rather than grazing continuously on roughage are major factors in development of gastroduodenal ulceration.



Clinical signs and diagnosis

Clinical signs in foals with gastric ulcers depend upon the region of the stomach involved. In most foals with gastric ulcers, lesions are distributed throughout the squamous mucosa. These foals may be asymptomatic or exhibit poor growth, rough haircoat, a “pot belly” appearance, bruxism, salivation, colic, dorsal recumbency and, sometimes, diarrhea. Lesions can occasionally result in hemorrhage that rarely is associated with anemia or hypoproteinemia. Healing of antral or pyloric lesions can lead to pyloric stricture and obstruction (q.v.).


Gastric ulcer syndrome (GUS) also occurs in yearlings and mature horses with an overall prevalence of approximately 10%. Studies have found squamous ulceration in 70–100% of racehorses and around 60% of other performance horses. Ulceration of the glandular mucosa of the stomach occurs in 60% of horses in a hospital setting. Clinical signs in mature horses classically include anorexia and chronic intermittent colic of varying severity. Vague clinical signs include poor performance or failure to perform to expectations, decreased body condition, poor-quality haircoat and decreased concentrate consumption. Colic signs in some horses with gastric ulceration are post prandial. Many horses with endoscopic evidence of disease may appear to be clinically normal.


Gastroduodenal ulceration is diagnosed by observation of typical clinical signs, endoscopic findings and response to therapy. A presumptive diagnosis of gastric ulceration can be made when typical clinical signs are observed, other causes of these signs are ruled out, and a response to administration of agents used to treat gastroduodenal ulceration is observed.


Confirmation of the presence of gastroduodenal ulceration is only made by endoscopic examination. Lesions occur predominantly in the squamous mucosa adjacent to the margo plicatus. Lesions at the cardia are common and require retroflexion of the endoscope to be observed. In foals >1 mo of age and horses, fasting and sedation will facilitate this procedure. In some neonatal foals, the stomach can be examined with a 100 cm endoscope; however, in older foals a 200 cm endoscope is needed. A 200 cm endoscope is required for examination of the duodenum in foals up to 6 mo of age. Examination of the duodenum in older animals requires a 300 cm endoscope.



Treatment and prognosis

The therapeutic strategy for gastric ulceration is reduction of gastric acid secretion, thereby allowing healing of the damaged mucosa, by use of proton pump antagonists (omeprazole 4 mg/kg daily) or H2-receptor antagonists (cimetidine 20 mg/kg PO t.i.d. or 4.4 mg/kg IV q.i.d.; ranitidine 6.6 mg/kg PO or IV b.i.d.). Appetite, signs of colic and diarrhea should begin to improve within 48 h of therapy, which should be continued for approximately 28 days.


Because many cases require therapy of longer duration, assessment of ulcer healing via endoscopic examination is useful for determining the duration of therapy. Recurrence has been documented after endoscopic confirmation of healing in some horses. Maintenance therapy (omeprazole 2–4 mg/kg daily) has been used in some cases to prevent recurrence of gastric ulceration. A recent study of performance horses revealed that the occurrence and recurrence of gastric ulceration was the same with a lower dose of omeprazole (1 mg/kg/day) as that in horses treated with omeprazole at 2 mg/kg/day. Studies to document the overall impact of preventative therapy on the incidence of gastric ulceration have not been performed.


Other drugs may be useful in combination with H2-receptor antagonists. Sucralfate (2–4g PO q.i.d.) has been used in combination with H2-receptor antagonists for treatment of gastric ulcers in horses. Sucralfate promotes synthesis of PGE, stimulates mucus secretion and protects ulcerated mucosa during healing. PGE inhibits gastric acid secretion and promotes mucosal blood flow, mucus production and mucosal cell division. PGE analogues have been effective therapy for gastric ulcers in humans but have not been used clinically in horses due to expense. Antacids have limited efficacy in treatment of gastric ulcers in horses due to the large doses (200 mL/500 kg BW) required.


The prognosis with gastric ulceration is good if appropriate therapy is continued for an adequate period of time and if complications do not develop. On the other hand, animals with duodenal ulceration are less responsive to therapy and more likely to develop complications. Complications that may result from gastroduodenal ulceration include gastroesophageal reflux, megaesophagus with aspiration pneumonia, gastric paresis, pyloric or duodenal stricture, gastric or duodenal perforation, and ascending cholangitis and hepatitis (q.v.).



GASTRITIS







GASTRIC IMPACTION







GASTRIC NEOPLASIA





Clinical findings and diagnosis

Gastric squamous cell carcinoma occurs most frequently in older horses. Presenting signs often include weight loss. Horses may develop intermittent colic due to obstruction of the cardia or metastasis to other abdominal organs. Colic occurring immediately after eating is especially common. Obstruction of the cardia can result in megaesophagus (q.v.) and/or nasal regurgitation of food. Horses with thoracic metastasis often develop thoracic effusion, which may cause tachypnea (q.v.). Melena, anemia and hypoproteinemia may occur in horses with gastrointestinal bleeding. Occasionally squamous cell carcinoma causes gastric rupture (q.v.) and peritonitis (q.v.). Diagnosis can be made by cytologic examination of peritoneal fluid in horses with abdominal metastasis.




PYLORIC HYPERTROPHY







DISEASES OF THE SMALL INTESTINE CAUSING COLIC



INTRODUCTION


Approximately 34% of all colic cases at referral institutions involve small intestine diseases.


Abnormalities of the equine small intestine may be broadly classified as either physical or functional obstructions. Non-strangulating physical obstructions may be caused by either intraluminal masses or reduction of the lumen by intramural thickening or extramural compression. Strangulating obstructions can follow incarceration of intestine through internal or external hernias, intussusception, or a greater than 180° twist of a segment of intestine on its own mesentery.


Functional obstruction, referred to as adynamic or paralytic ileus, may be either idiopathic in origin, result from inflammatory disease (e.g. duodenitis and proximal jejunitis [q.v.]), or result from serosal irritation due to surgical manipulation. The majority of cases of small intestinal colic (58–80%) are caused by strangulating lesions and the remainder by simple and functional obstructions. The ileum is involved in 41–46% of all small intestinal obstructions.


Intestinal obstruction prevents the aboral movement of gastrointestinal contents, thereby resulting in distension of the intestine. As the distension increases, venous drainage from the intestinal wall is impaired and the mucosa becomes congested and edematous. If the obstruction persists for a prolonged period of time, significant compromise of intestinal vascular integrity may result in mucosal ischemia. Shock (q.v.) will develop with prolonged ileus due to decreased oral intake and accumulation of fluid in the intestinal lumen. With progressive distension, gastric rupture (q.v.) may occur.


In strangulating obstructions, the above events are combined with rapid tissue hypoxia and ischemia of the affected segment leading to necrosis and transmural leakage of endotoxin. Cardiovascular deterioration rapidly follows transperitoneal absorption of endotoxin resulting in hypovolemia and endotoxic shock (q.v.). For these reasons it is important that small intestinal lesions are identified early in the disease process, based on a thorough history and physical examination.


Abdominal pain, small intestinal distension (identified by transrectal palpation and abdominal ultrasound examination), nasogastric reflux and decreased or absent borborygmi are common clinical signs in patients with small intestinal disease. The expression of abdominal pain can depend on the temperament of the horse, the degree of restraint, administration of sedatives or analgesics, and mental attitude. Reduced or absent borborygmi may be encountered with obstruction developing at any site in the gastrointestinal tract. Ultrasonographic examination can also be used to assess the presence or absence of intestinal motility in individual segments of bowel. Strangulating obstructions usually cause severely distended, turgid small intestine.


With both non-strangulating and functional obstructions, mild to moderate distension of small intestine commonly is present. The severity of small intestinal distension can be assessed via rectal examination and ultrasonographic examination of the abdomen. In cases of ileal impaction, ileocecal and jejunojejunal intussusception, and inguinal hernias, transrectal palpation may reveal the specific etiology of the obstruction. Small intestinal distension may also occur with large intestinal obstruction or displacement, causing secondary extraluminal compression of the small intestine.


Therapy for small intestinal lesions includes controlling pain, maintenance of cardiovascular and metabolic status, and establishing a patent and functional intestine. Pain control is accomplished by gastric decompression via a nasogastric tube and administration of visceral and centrally acting analgesics ( Table 10.1). Maintenance and support of cardiovascular and metabolic status is achieved by IV administration of balanced, isotonic fluids. In most cases of physical obstruction, ventral midline exploratory celiotomy is necessary for identification and correction of the inciting lesion.


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Jul 8, 2016 | Posted by in EQUINE MEDICINE | Comments Off on The gastrointestinal and digestive system

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