Gastrointestinal Disorders PDF

Gastrointestinal Michal Mazaki-Tovi ORAL DISORDERS I. Oronasal ﬁstulas and palatal defects A. Congenital defect in brachiocephalic breeds, miniature schnauzers, cocker spaniels, beagles, and cats B. Acquired defect from trauma or maxillary periodontal pocket C. Clinical signs include sneezing after eating and mucopurulent nasal discharge D. Diagnosis is by physical examination E. Surgery is treatment of choice II. Stomatitis and gingivitis A. Etiology includes periodontal disease, physical injury, chemical injury, systemic infections (herpesvirus, calicivirus in cats; Nocardia in dogs), oral candidiasis, necrotizing ulcerative stomatitis, immunosuppression secondary to feline leukemia virus (FeLV) or feline immunodeﬁciency virus (FIV), uremia, plasma cell stomatitis (cats), feline eosinophilic granuloma complex, canine oral eosinophilic granuloma, autoimmune disorders, niacin deﬁciency, or oral neoplasia B. Clinical signs include hypersalivation, halitosis, oral bleeding, dysphagia, anorexia, and weight loss C. Diagnosis by history and physical examination primarily. Radiographs and laboratory tests may help to identify the underlying cause D. Treatment 1. Treat the underlying cause 2. Symptomatic treatment includes dental prophylaxis, systemic antibiotics III. Tonsillitis A. Primary tonsillitis may occur in young, small- breed dogs, or tonsillitis may be secondary to chronic infections of the nasopharynx, vomiting, chronic regurgitation, or coughing B. Clinical signs include retching, cough, fever, and anorexia C. Diagnosis is based on physical examination and history D. Treat with antibiotics, and treat the underlying disorder IV. Tonsillar neoplasia A. Squamous cell carcinoma and lymphoma are the most common causes B. Clinical signs may include retching, coughing, and cervical mass (metastases to regional lymph nodes) 226 SECTION II SMALL ANIMAL 4. Sialoadenosis is a diagnosis of exclusion. Cyto- logic and histologic evaluations of the salivary glands are unremarkable. A dramatic rapid re- sponse to phenobarbital supports the diagnosis D. Treatment 1. Cervical mucoceles are treated by surgical excision of the mandibular and sublingual salivary glands (for cervical and pharyngeal mucoceles) or zygomatic salivary gland (for zygomatic mucocele). Ranulas may be treated by surgical marsupialization 2. Sialoadenitis: Treat with systemic antibiotics, drainage of the abscess, and application of warm compresses 3. Sialoadenosis: Treat with long-term therapy (phenobarbital or potassium bromide) is usually required 4. Neoplasia: Treat with surgical removal. Postop- erative chemotherapy, radiation therapy, or both may be beneﬁcial for adenocarcinoma ESOPHAGUS AND DISORDERS OF SWALLOWING I. Overview A. Cause is either a structural disorder or a motility disorder B. Clinical signs include regurgitation, dysphagia, odynophagia, ptyalism, exaggerated swallowing, weight loss, polyphagia, anorexia, cough, dys- pnea, and fever C. Diagnosis is based on history and a careful physi- cal examination to detect alterations of swallow- ing. Imaging is most important for the diagnosis. Endoscopy can also be used. Consider Spirocerca lupi infection in the southern United States D. Treatment includes speciﬁc therapy for the underlying condition, along with general symp- tomatic management II. Oropharyngeal dysphagia A. Causes 1. Oral dysphagia involves difﬁculty with prehen- sion or transport of food to the pharynx 2. Pharyngeal dysphagia involves problems with transport of a bolus from the oropharynx through the cranial esophageal sphincter and includes cricopharyngeal achalasia and crico- pharyngeal asynchrony 3. Caused by morphologic (e.g., foreign body, dental disease, oral neoplasia, stomatitis, retro- pharyngeal abscess, cleft palate, etc.) or func- tional (e.g., neuromuscular) disorders B. Clinical signs 1. Oral dysphagia is characterized by abnormal prehension and mastication 2. Pharyngeal dysphagia is characterized by re- peated unsuccessful attempt to swallow with gagging, retching, and spitting of food. Aspira- tion pneumonia is common 3. Regurgitation may occur with concurrent megaesophagus and generalized muscle weak- ness, or neurologic deﬁcits may occur when there is an underlying neuromuscular disorder 3. Imaging a. Survey and contrast thoracic radiography may suggest megaesophagus and aspiration pneumonia (as described above) b. Barium swallow ﬂuoroscopy can detect esophageal motility disorders 4. Routine laboratory tests a. A CBC may reveal neutrophilia and a left shift with aspiration pneumonia b. Biochemical proﬁle may reveal abnormali- ties associated with underlying disorders c. Acetylcholine receptor antibody titer to evaluate for acquired myasthenia gravis is indicated even in the absence of generalized signs, as myasthenia gravis may be focal 5. Ancillary tests to evaluate for underlying causes as indicated 6. Esophagoscopy is indicated when an obstruc- tive disease or reﬂux esophagitis is suspected D. Treatment is symptomatic and supportive in most cases 1. Feed frequent small meals with the animal in an upright position. Liquid food is better toler- ated in most cases, but different food types should be tried to identify the best option. Gastrostomy tube may be required in some cases 2. Administer antibiotic therapy for aspiration pneumonia E. Idiopathic Megaesophagus is usually irreversible and supportive care is required for life IV. Esophageal foreign body A. Foreign bodies commonly found in dogs are bones and in cats vomited hairballs. These usually lodge at the thoracic inlet, base of the heart, or hiatus of the diaphragm. Complications include esophagitis, esophageal perforation and mediastinitis, esophageal stricture, and broncho- esophageal ﬁstula B. Clinical signs include acute onset of gagging, sali- vation, dysphagia, and regurgitation. Depression, fever, cough, and dyspnea may suggest aspiration pneumonia C. Diagnosis is usually conﬁrmed with radiography, barium contrast esophageal radiography, or esophagoscopy. Bones or metal foreign bodies are usually apparent on survey thoracic and cervical radiographs. Evaluate thoracic radiographs for aspiration pneumonia. Findings of pneumomediastinum, pneumothorax, and mediastinal or pleural effusion suggest esopha- geal perforation D. Endoscopic removal is preferred in most cases 1. If the object cannot be extracted orally, advance it to the stomach to be removed by gastrostomy (bones may dissolve). Withhold food and water for 24 hours after the procedure. Administer antibiotics if indicated 2. An esophagotomy is indicated if the foreign body cannot be retrieved orally or advanced into the stomach E. Prognosis is excellent unless perforation or aspi- ration pneumonia is present 228 SECTION II SMALL ANIMAL VIII. Esophageal diverticula A. Diverticula are pouchlike sacculations of the esophageal wall and may be congenital or acquired. Diverticula may become impacted, leading to esophagitis B. Clinical signs include regurgitation, distress after eating, intermittent thoracic pain, and respiratory distress C. Thoracic radiography may reveal a gas- or food- ﬁlled mass in the area of the esophagus. Barium esophagram or esophagoscopy may conﬁrm the diagnosis D. Large diverticula require surgical resection, but small diverticula can be managed by feeding frequent small meals of soft food with the animal in an upright position IX. Esophageal ﬁstula A. Fistulas are communications between the esop- hagus and airways, most commonly the bronchi. Acquired ﬁstulas are more common than con- genital ﬁstulas and may be caused by eso- phageal foreign body, trauma, malignancy, or infection. Bronchoesophageal ﬁstulas are frequently associated with esophageal diverticula B. Clinical signs are related to contamination of the airways with ﬂuid and food. Coughing, fever, and dyspnea are common C. Diagnosis is based on physical examination ﬁndings, thoracic radiography, and conﬁrmation with a barium esophagram D. Treatment is surgical resection of the ﬁstula with appropriate antibiotic therapy E. Prognosis is poor if complications (e.g., pulmonary abscess, pleuritis) are present X. Vascular ring anomalies A. Causes (Figure 16-1) 1. Persistent right aortic arch (PRAA) accounts for 95% of vascular ring anomalies in dogs and cats. The right rather than the left fourth aor- tic arch is retained, resulting in compression of the esophagus between the ligamentum LA RAA A LS PA E Figure 16-1 Schematic of persistent right left, shows the ligamentum arteriosum (LA) connecting aortic arch (RAA) to the main or left pulmonary tion of the esophagus (E) between these structures CVC, Caudal vena cava; LAt, left atrium; LSA, Thrall DE. Textbook of Veterinary Diagnostic 2007, Saunders.) C. Endoscopy and biopsy are required for a deﬁni- tive diagnosis D. Surgical excision is required STOMACH DISORDERS I. Vomiting A. A common clinical sign associated with gastroin- testinal (GI) and non-GI disorders 1. Frequently is preceded by nausea (hypersali- vation, repeated licking and swallowing), retching, and abdominal contractions 2. Vomitus consists of stomach and duodenal con- tents (food, mucus, and foamy or bile-stained ﬂuid with a neutral or acidic pH) and may contain blood (hematemesis) 3. Projectile vomiting usually indicates gastric outlet or upper small bowel obstruction 4. Vomiting of undigested food more than 12 hours after eating suggests delayed gastric emptying B. Diagnosis 1. Careful review of history and physical exami- nation is required. Include oral and rectal examinations, abdominal palpation, review of vaccination and deworming history 2. Laboratory evaluation includes routine hema- tology, biochemistry, urinalysis, and additional tests as indicated. Fecal ﬂotation tests may be indicated 3. Imaging a. Routine abdominal radiographs may iden- tify radiopaque foreign bodies, GI obstruc- tion, or mural thickening. Barium contrast may additionally identify radiolucent for- eign bodies. Barium mixed with food and barium-impregnated plastic spheres (BIPS) may detect gastric retention disorders. Use aqueous iodide contrast if perforation is suspected b. Abdominal ultrasonography is useful to evaluate non-GI causes of vomiting (e.g., pancreatitis, hepatic, or renal disease) and GI disorders (e.g., intussusception, or masses) 4. Endoscopy or exploratory laparotomy may be necessary C. Symptomatic and supportive treatment 1. Fluid therapy. Intravenous therapy is preferred. 2. Withhold food for 12 to 24 hours, then offer a highly digestible diet (chicken and rice) for 2 to 3 days. Gradually reintroduce the routine diet over 2 to 3 days 3. Antiemetics. Phenothiazines are widely used but may decrease seizure threshold. Metoclo- pramide should not be used in animals with seizures. Butorphanol is also commonly used. Avoid anticholinergic drugs II. Acute gastritis A. Common, usually mild and self-limiting. Possible causes include dietary indiscretion, foreign body causing mechanical irritation, chemical irritants, and drugs 230 SECTION II SMALL ANIMAL ECL Cell Acetylcholine antagonists Histamine Figure 16-2 Representation of a gastric Histamine type 2 (H2) antagonists (blockers) (ECL) cells by gastrin stimulation. Acetylcholine secretion is limited by systemic side effects. adenosine monophosphate production. Proton pump they interrupt the ﬁnal common pathway of acid. (From Birchard SJ, Sherding RG. Saunders 2. Clinical signs include intermittent vomiting (weeks to months), and is not consistently associated with eating 3. Endoscopy is the diagnostic method of choice. Mucosal abnormalities include irregularity, ﬁrmness, or ulceration. Laparotomy may be indicated for biopsies B. Eosinophilic gastritis and granuloma 1. Eosinophilic inﬁltration is usually diffuse but may present as a granulomatous lesion in dogs. An allergic or immunologic hypersensi- tivity has been suggested. Eosinophilic gastri- tis is rarely associated with hypereosinophilic syndrome in cats 2. Clinical signs include chronic vomiting, he- matemesis, melena, anorexia, and weight loss 3. Endoscopy is the diagnostic method of choice. Laparotomy may be indicated to obtain gastric biopsies C. Therapy for chronic gastritis 1. Treat any underlying disorder 2. Dietary trial with an easily digestible, moder- ately fat-restricted, carbohydrate-based diet, with a novel protein source. Feed frequent small meals, and assess response after 3 to 4 weeks 3. H2 blockers may be useful. Promotility drugs may be indicated 4. Prednisolone or azathioprine may be used if there is no response to dietary trial or H2 blockers 5. Antibacterial therapy is used for Helicobacter infection B. Clinical signs are similar to those of gastric outﬂow obstruction C. Abdominal radiograph may suggest delayed gastric emptying as described for gastric outﬂow obstruction. However, the gastric outﬂow region appears normal D. Treat the underlying cause. Feed a diet low in fat and high in digestible carbohydrate. Feed small amounts frequently. A liquid diet may be better tolerated. Use promotility drugs as needed VIII. Hypertrophic gastropathy is a heterogeneous group of disorders A. Cause is unknown in most cases. Possible causes include stress in excitable small-breed dogs, chronic irritation from aspirin therapy, or hyper- gastrinemia B. Clinical signs include chronic intermittent vomit- ing, anorexia, weight loss, abdominal distension, hematemesis, and concurrent diarrhea in basenjis. Typically occurs in small-breed dogs with chronic intermittent vomiting C. Metabolic alkalosis may occur with profuse vom- iting and gastric outﬂow obstruction. centrations may be elevated. Radiography delayed gastric emptying. Surgery is obtain a full-thickness biopsy D. Surgical excision may be necessary to relieve outﬂow obstruction. Promotility drugs may be needed after surgery. Treatment may also include H2 blockers, sucralfate, or prednisolone if indicated IX. Gastric neoplasia A. Adenocarcinoma is most common in dogs, and lymphoma is most common in cats. Leiomyosar- coma and ﬁbrosarcoma are less common B. Leiomyomas are the second most common gas- tric tumors in dogs. Benign adenomatous polyps occur infrequently in dogs and cats C. Clinical signs include progressive vomiting, he- matemesis, anorexia, and weight loss. Clinical signs may be absent with benign tumors unless obstruction occurs D. Contrast radiography and endoscopy are most useful for diagnosis E. Removal by partial gastrectomy is the treatment of choice, with chemotherapy if indicated. Prognosis is good for benign tumors but poor for adenocarcinoma X. Gastric dilatation-volvulus (GDV) A. GDV causes complete obstruction of gastric out- ﬂow, which impairs venous return through the vena cava causing hypovolemic and endotoxic shock B. The cause is unknown. Older large-breed, deep-chested dogs are predisposed. Risk factors include having a ﬁrst-degree relative affected by GDV, lean body conformation, rapid eating, eating from a raised bowl, eating one meal daily, exercise or stress after a meal, and a fearful temperament C. Clinical signs include acute onset of abdominal distension, nonproductive retching, salivating, and respiratory distress D. Physical examination usually reveals tympani on abdominal percussion and ﬁndings indicative of hypovolemia or shock. Hypokalemia and 232 SECTION II SMALL ANIMAL Table 16-1 Physical Findings in Intestinal Disease Physical Finding Potential Clinical General Physical Examination Dehydration Diarrheal ﬂuid loss Depression or Electrolyte imbalance, weakness debilitation Emaciation or Chronic malabsorption, malnutrition protein-losing Dull unthrifty hair Malabsorption of coat protein, and vitamins Fever Infection, transmural inﬂammation, Edema, ascites, Protein-losing enteropathy pleural effusion Pallor (anemia) Gastrointestinal mia of chronic Intestinal Palpation Masses Foreign body, neoplasia, granuloma Thickened loops Inﬁltration (inﬂammation, lymphoma) “Sausage loop” Intussusception Aggregated loops Linear intestinal foreign body, peritoneal adhesions Pain Inﬂammation, obstruction, ischemia, peritonitis Gas of ﬂuid Obstruction, ileus, diarrhea distention Mesenteric Inﬂammation, infection, neoplasia lymphadenopathy Rectal Palpation Masses Polyp, granuloma, Circumferential Stricture, spasm, narrowing Coarse mucosal Colitis, neoplasia texture From Birchard SJ, Sherding RG. Saunders Manual of Small Animal clinical Practice, 3rd ed. St Louis, 2006, Saunders, p. 704. be decreased in EPI, enteropathies that impair absorption in the distal small intestine, or small intestinal bacterial overgrowth 6. Imaging, including plain radiography, barium radiography, or ultrasonography 7. Endoscopy or laparotomy D. Nonspeciﬁc treatment of diarrhea 1. Dietary management a. Acute diarrhea: Restrict food intake for at least 24 hours and then give bland, low-fat foods (e.g., boiled rice and chicken or low- fat cottage cheese) in small amounts at frequent intervals. Gradually reintroduce the animal’s regular diet when the diarrhea has been resolved for 48 hours b. Chronic diarrhea: Give three or four meals a day, and use appropriate diets (ﬁber- supplemented if large bowel diarrhea; novel protein diets with inﬂammatory bowel disease [IBD]). 2. Routes of infection include prenatal, milk- borne, ingestion of infective larvae or paratenic hosts, or skin penetration by infec- tive larvae. Eggs are passed in the feces after 2-3 weeks 3. Clinical signs are associated mostly with blood-sucking activity and include melena, bloody diarrhea, pallor, emaciation, and dehy- dration. Acute blood loss in neonates may lead to death. Chronic blood loss in older animals results in iron deﬁciency anemia 4. Diagnose on routine fecal ﬂotation 5. Treat with pyrantel pamoate (safest for pups), fenbendazole, or febantel C. Whipworms 1. Trichuris vulpis is common in dogs. The adult nematode attaches to the colonic and cecal mucosa, where it feeds on blood and tissue ﬂuids, thereby causing colitis and typhlitis 2. Infection occurs by ingestion of infective ova, and the life cycle is direct. Ova may remain infectious in the environment for 4 to 5 years 3. Acute, chronic, or intermittent signs of large bowel–type diarrhea occur commonly. Hematochezia may sometimes occur 4. Ova can be identiﬁed on fecal ﬂotation. Hyperkalemia and hyponatremia may occur with severe diarrhea 5. Treat with fenbendazole or febantel. Retreat every 2 to 3 months if dogs have access to contaminated ground D. Strongyloides 1. Found in the southern Gulf States. Strongyloides stercoralis resides in the proximal small intes- tines in dogs. Strongyloides tumefaciens resides in the large intestines in cats 2. Infectious larvae are ingested or penetrate the skin, and adult worms develop in the small intestine following migration in the circulation and lung. Larvae are passed in the feces 3. S. stercoralis may cause acute hemorrhagic en- teritis that may be fatal in pups. S. tumefaciens is usually asymptomatic. Colonic nodular pro- liferations develop in some cats and are associ- ated with chronic diarrhea 4. Ova containing ﬁrst-stage larvae can be iden- tiﬁed in feces by ﬂotation techniques. Free larvae may be identiﬁed by direct microscopic examination of fresh feces or by the Baermann technique 5. Treat with fenbendazole, diethylcarbamazine, or pyrantel pamoate E. Tapeworms 1. Dipylidium caninum is the most common tape- worm in dogs and cats. Others include Taenia pisiformis in the dog and Taenia taeniaeformis in the cat 2. Fleas and lice are intermediate hosts for D. caninum. Taenia spp. infection occurs by ingestion of cysticercus-infected tissues from intermediate hosts 3. Most infections are asymptomatic. Mild decline in body condition or anal pruritus may occur 234 SECTION II SMALL ANIMAL 2. Diagnosis is made by identiﬁcation of tropho- zoites in saline fecal suspensions 3. Treat with metronidazole VI. Viral infections A. Canine parvovirus, coronavirus, and rotavirus cause viral enteritis and diarrhea in dogs. Canine parvovirus is acute, severe, highly contagious enteritis B. Coronavirus and rotavirus are less prevalent and cause mild clinical signs except in neonates C. Canine distemper virus also causes diarrhea VII. Bacterial infections A. Salmonella 1. Transmitted by the fecal-oral route, mainly through ingestion of contaminated food or water. Migratory birds have been reported a source of infection in cats, raw-food diets in dogs 2. Clinical signs of enterocolitis include acute watery or mucoid diarrhea, containing blood in severe cases, vomiting, tenesmus, and fever. Some animals may have chronic or intermit- tent diarrhea, and many are asymptomatic carriers 3. Diagnosis is by isolation of the bacteria from fecal or blood samples 4. Treat with antibiotics (enroﬂoxacin or trimethoprim-sulfa), and correct ﬂuid deﬁcits. Mortality is high in neonates 5. Salmonellosis is a zoonotic disease B. Campylobacter 1. Most infected dogs are clinically normal carriers. Exposure is high with overcrowding and poor sanitation 2. Clinical signs include watery-mucoid diarrhea. Hematochezia, vomiting, and tenesmus may occur. Fever is usually mild or absent. Some animals may have chronic or intermittent diarrhea 3. Diagnosis is by isolation of Campylobacter from feces 4. Treat with erythromycin, enroﬂoxacin, or azithromycin. Carrier state may persist C. Clostridium perfringens 1. These bacteria normally reside in the bowel in the vegetative form but can release their toxin (CPE) during sporulation endogenously within the bowel or exogenously in contaminated food 2. Clinical signs include watery to soft diarrhea, with hematochezia or tenesmus. C. perfringens has been associated with acute hemorrhagic gastroenteritis with severe hemoconcentration in dogs 3. A deﬁnite diagnostic test is not available. Fecal cultures are not useful because C. perfringens is a part of the normal ﬂora. Fecal assays for CPE are available 4. Treat with ampicillin, amoxicillin-clavulonate, tylosin, or clindamycin. Metronidazole seems to work less consistently. Long-term treatment may be required in chronic or recurrent cases. Fiber-containing diet or supplementation with colonic submucosal vessels, thickened folds, or decreased distensibility. Normal endoscopic appearance does not rule out IBD b. Mucosal histopathology shows diffuse inﬁltration of the lamina propria with mature lymphocytes and plasma cells in association with mucosal damage c. Evaluate for dietary hypersensitivity 4. Treatment a. Dietary therapy with a novel protein source, or ﬁber supplementation may be helpful b. Medical therapy (1) Oral prednisolone is the most consis- tently effective medical therapy. Metro- nidazole is also often used for long-term therapy (2) Other agents that may be indicated in- clude cobalamin, azathioprine, chloram- bucil, cyclosporine, or motility-modifying antidiarrheal drugs 5. Persistence or recurrence of IBD is likely despite therapy B. Eosinophilic gastroenteritis 1. An uncommon form of IBD, characterized by inﬁltration of the GI tract with mature eosino- phils. Food allergy and parasitism are possible causes, but most cases are idiopathic. Feline hypereosinophilic syndrome is characterized by multiorgan severe eosinophilic inﬁltration 2. Clinical signs include chronic vomiting, and small or large bowel diarrhea. Protein-losing enteropathy may be present, and granulomas can cause intestinal obstruction 3. Diagnosis is based on demonstration of eosino- philic inﬂammation in intestinal biopsies 4. Treatment includes fenbendazole to exclude parasites and a feeding trial to exclude food allergy. Oral prednisolone is the most effec- tive treatment, and response to treatment is rapid C. Regional granulomatous enterocolitis 1. An uncommon form of IBD characterized by transmural granulomatous inﬂammation result- ing in a mass-like thickening of the bowel wall. The ileocolic junction is most often involved. The lesion may contain many eosinophils 2. Clinical signs include chronic large bowel diar- rhea containing mucus and fresh blood and sometimes tenesmus and abdominal pain 3. Diagnosis requires biopsy to detect fungi and acid-fast organisms. Eosinophilia, neutrophilia, monocytosis, and panhypoproteinemia may be present 4. Treat as for lymphocytic-plasmacytic IBD. Surgical excision may be required D. Histiocytic ulcerative colitis 1. Chronic idiopathic IBD of young boxer dogs characterized by inﬁltration of the colon by distinctive periodic acid-Schiff (PAS)-positive histiocytes 2. Clinical signs include severe, bloody-mucoid large bowel diarrhea in young boxers 236 SECTION II SMALL ANIMAL C. Diagnosis is by histologic documentation of villous atrophy in jejunal biopsies D. Treatment 1. For gluten-sensitive enteropathy, eliminate gluten-containing cereal grains (wheat, barley, and rye) from the diet for life. Breeding of affected animals is discouraged 2. For idiopathic villous atrophy, dietary manage- ment with gluten-restricted diet is sometimes beneﬁcial. Folate, cobalamin, antibiotics, or prednisolone may be beneﬁcial E. Prognosis is guarded. Clinical signs often persist despite treatment XIV. Small intestinal bacterial overgrowth A. Causes 1. An overproliferation of microﬂora within the proximal small intestine that results in malab- sorption and diarrhea 2. May develop secondary to other disorders (e.g., intestinal obstruction, dysfunction of the ileocolic junction, motility disorders, hypose- cretion of gastric acid, exocrine pancreatic insufﬁciency) 3. Immunoglobulin A deﬁciency may breed predilection in German shepherds, basenjis, and shar-peis B. Clinical signs consist of chronic watery diarrhea and steatorrhea. Blood or mucus is usually absent C. Diagnosis requires quantitative aerobic and anaer- obic cultures of duodenal juice taken by endos- copy, intestinal intubation, or laparotomy after an 18-hour fast. This may be impractical. Indirect evi- dence to support the diagnosis includes response to antibiotics, elevated serum folate and decreased serum cobalamin, presence of predisposing disor- der, and minimal changes in intestinal biopsies D. Treat with tetracycline, tylosin, and metronida- zole for 10 to 14 days. Some animals need contin- uous treatment XV. Intestinal neoplasia A. Benign tumors include adenomatous polyps, adenomas, and leiomyomas B. Malignant tumors include adenocarcinoma and lymphoma most commonly. Less common malig- nancies include carcinoid tumors, leiomyosar- coma, ﬁbrosarcoma, mastocytoma, hemangiosar- coma, and anaplastic sarcoma C. Clinical signs are initially vague and progress to vomiting and diarrhea. Signs may vary with loca- tion of neoplasia D. Deﬁnitive diagnosis requires biopsy. Abdominal radiography or ultrasonography may detect intes- tinal masses E. Surgical resection is the treatment of choice, with appropriate adjunct therapy XVI. Intestinal obstruction A. Cause can be intraluminal, intramural, or extramural B. Pathophysiology 1. Proximal vs. distal obstruction a. The more proximal and complete the ob- struction, the more acute and severe the signs 3. Laboratory evaluation (CBC, biochemical pro- ﬁle, and urinalysis) may identify underlying systemic disease, dehydration, or electrolyte disorders 4. Abdominal radiography can conﬁrm the diag- nosis; evaluate the extent of colonic impaction; and identify megacolon, radiopaque foreign bodies, pelvic or spinal lesions, and prostatic enlargement. Barium enema contrast radiogra- phy may identify intraluminal obstruction (Figure 16-3) 5. Abdominal ultrasonography may be useful to evaluate the prostate and pelvic canal area 6. Other tests may be indicated to evaluate thyroid function and neuromuscular disorders (e.g., my- elography, magnetic resonance imaging, electro- myography, and nerve conduction studies) D. Treatment overview 1. Control any identiﬁed predisposing factor 2. Simple constipation without systemic signs can be managed using rectal suppositories or oral laxatives combined with dietary modiﬁca- tion and promotion of water intake. Severe constipation may initially require evacuation of impacted feces from the colon with correction of dehydration and electrolyte imbalances 3. Prevent recurrence using dietary modiﬁcation, laxatives, and promotility agents as needed 4. Surgical management is required for obstruct- ing neoplasms, strictures, and pelvic malfor- mations. Subtotal colectomy is often required to manage advanced megacolon E. Initial relief of constipation 1. Rectal suppositories of docusate (emollient), glycerin (lubricant), or bisacodyl (stimulant) may be used to promote defecation in patients with mild constipation 2. Enema therapy is used to soften hard, impacted feces. Administer the warmed enema solution through a rubber catheter or feeding tube. Enema solutions include tap water, isotonic sa- line, lactulose (osmotic), docusate (emollient), or mineral oil (lubricant). Phosphate enemas Figure 16-3 Barium enema in a 12-year-old tion and megacolon. (From Ettinger SJ, Feldman Internal Medicine, 6th ed. St Louis, 2005, Saunders.) 238 SECTION II SMALL ANIMAL B. Pathogenesis is unknown. Predisposing factors may include persistent straining, neurogenic atro- phy of the muscles, and male hormones. May be a complication of megacolon in cats C. Clinical signs include perineal swelling that may be unilateral (usually right-sided) or bilateral D. Diagnosis is based on palpation E. Laxative therapy and stool softening may be sufﬁ- cient in mild cases. Castration of male dogs may prevent progression of the disorder. Corrective perineal herniorrhaphy and castration are re- quired in most cases VI. Anorectal foreign bodies and fecaliths A. Ingested foreign bodies (e.g., bones, sticks, needles) may become lodged within the rectum or at the anal sphincter B. Clinical signs include dyschezia and tenesmus C. Diagnosis is usually conﬁrmed by rectal examination D. Most foreign bodies and fecaliths may be removed by rectal palpation VII. Anorectal stricture (stenosis) A. Strictures may result from trauma caused by foreign body or during treatment of obstipation, anorectal surgery, chronic inﬂammation (anal sac, perineal ﬁstula, proctitis), or adenocarcinoma B. Clinical signs include dyschezia, tenesmus, hematochezia, and secondary constipation C. Diagnosis is made by digital rectal palpation, proctoscopy, or barium enema contrast radiography D. Treat conservatively in most cases. Balloon dilatation may be successful VIII. Anal spasm A. Idiopathic spasm of the anal sphincter when the animal attempts to defecate. Defensive con- traction of the sphincter in response to painful defecation may play a role B. Clinical signs include pain on attempts to defe- cate and anxiety C. Occurs most frequently in German shepherd dogs, and digital palpation of the rectum is pain- ful. Exclude other causes of painful defecation D. Treat conservatively. Resection of the pudendal nerve may be required IX. Anal and rectal atresia A. Atresia ani and rectal atresia are congenital malformations B. Clinical signs include inability Disorders 16 CH A P TE R C. Diagnosis is based on oral examination and biopsy ﬁndings D. Treat with chemotherapy E. Prognosis is poor V. Salivary gland diseases A. Causes 1. Mucoceles (sialoceles) result from damage to the duct or gland and leakage of saliva into the tissues. Common sites include cervical and sublingual (ranulas) mucoceles 2. Fistulas are common and usually the result of trauma to the parotid salivary gland or duct 3. Sialoadenitis is uncommon and usually affects the zygomatic salivary gland 4. Sialoadenosis is a syndrome of unknown cause in dogs, characterized by mandibular salivary gland enlargement, associated with hypersali- vation, retching, regurgitation, and vomiting. Response to phenobarbital is often excellent 5. Neoplasia of the salivary glands is rare B. Clinical signs 1. Clinical signs of mucoceles depend on the gland affected. Cervical mucoceles present as soft nonpainful masses; ranulas cause dysphagia and blood-tinged saliva; pharyngeal mucocele may cause breathing or swallowing difﬁculty; and zygomatic mucoceles may cause exophthalmos 2. Fistulas present as a small skin opening drain- ing serous ﬂuid 3. Zygomatic sialoadenitis causes exophthalmos, pain on opening the mouth, and mucopurulent discharge from the duct. Parotid sialoadenitis presents as a painful, warm parotid gland and discharge 4. Sialoadenosis is usually associated with chronic signs, including hypersalivation, retching, regurgitation, and vomiting 5. Neoplasia usually presents as a nonpainful mass in the region of the salivary gland C. Diagnosis 1. The diagnosis of mucoceles is usually based on palpation and aspiration of viscid, muci- nous ﬂuid that is consistent with saliva 2. Sialography may be used to diagnose ﬁstulas but is usually not necessary 3. Sialoadenitis is diagnosed based on complete blood cell count (CBC) and histopathology ﬁndings 225 C. Diagnosis 1. Signalment may suggest breed dispositions for congenital neuromuscular disorders (e.g., hereditary muscular dystrophy in Bouvier) 2. Morphologic diseases can be detected by visual examination of the oropharynx, and generalized neuromuscular abnormalities may be detected by complete physical and neuro- logic examination 3. Imaging a. Radiographs of the oropharyngeal area may identify morphologic disorders (e.g., foreign body) b. Thoracic radiographs may reveal aspiration pneumonia or concurrent megaesophagus c. Fluoroscopy with a barium swallow is required for the diagnosis of functional abnormalities d. Ancillary testing is usually required for the diagnosis of generalized neuromuscular disorders D. Treatment and prognosis depend on the underly- ing disorder. Administer supportive treatment as needed III. Esophageal hypomotility A. Causes 1. May be segmental or diffuse (megaesophagus); congenital or acquired 2. Megaesophagus is idiopathic in most dogs 3. Acquired megaesophagus may occur second- ary to diseases causing diffuse neuromuscular dysfunction (e.g., myasthenia gravis, dysauto- nomia, polyneuropathy, polymyositis, botulism, tick paralysis, anticholinesterase, lead, or thallium toxicity, hypothyroidism, hypoadre- nocorticism), esophagitis, or hiatal hernia (common in cats) B. Regurgitation is the primary clinical sign and may not be related to eating. Dyspnea, cough, and fever suggest aspiration pneumonia. Signs of an underlying disorder may be present C. Diagnosis: Idiopathic megaesophagus is a diagno- sis of exclusion 1. Signalment and history a. Breeds predisposed for idiopathic mega- esophagus include German shepherd dog, Great Dane, greyhound, golden retriever, Labrador retriever, Irish setter, miniature schnauzer, Newfoundland, shar-pei, wire- haired fox terrier, and Siamese cat b. Congenital disorders are suggested when signs are ﬁrst noted at the time of weaning c. History of chronic or recurrent respiratory infections may indicate secondary aspira- tion pneumonia 2. Physical examination a. May be unremarkable except for weight loss. Distension of the cervical esophagus may become evident by compressing the thorax while the nostrils are closed b. Nasal discharge and additional signs associ- ated with underlying disorders may be present CHAPTER 16 Gastrointestinal Disorders 227 V. Esophageal perforation A. Foreign bodies are the most common cause; penetrating wounds are also common. Iatrogenic perforation may occur during esophagoscopy B. Clinical signs include anorexia, depression, odynophagia, and a rigid stance. Cervical swell- ing, cellulitis, or a draining ﬁstula may be present with cervical esophageal perforation. Cough, dyspnea, and fever may occur with mediastinitis or pleuritis C. Thoracic radiography may show pneumomedias- tinum, pneumothorax, and mediastinal or pleural effusion. The CBC usually reveals neutrophilia with a left shift D. Surgical repair is needed if the perforation is large, or mediastinitis or pleuritis occur E. Medical management is sufﬁcient for small tears. Give parenteral antibiotics, ﬂuid therapy, and nothing per os for 5 to 7 days. Consider feeding by gastrostomy tube or parenteral nutritional support VI. Esophagitis A. Causes of esophagitis include foreign bodies, oral medications (doxycycline), thermal injury, caustic injury, Pythium insidiosum infection, and gastro- esophageal reﬂux associated with chronic vomit- ing, hiatal hernia, general anesthesia, or indwelling nasogastric (NG) tube B. Clinical signs are nonspeciﬁc for esophageal dis- ease and may be absent with mild esophagitis C. Esophagoscopy is the most sensitive method of diagnosis 1. Findings include mucosal erythema, hemor- rhage, erosions, ulcers, strictures (in severe cases) 2. With gastroesophageal reﬂux, lesions are most severe in the distal esophagus, the gastroesoph- ageal junction may appear dilated, and reﬂux of gastric contents into the esophagus may be noted D. Treatment 1. General therapy involves antibiotic therapy and frequent feeding of small portions of soft food 2. For reﬂux esophagitis, give promotility agents (metoclopramide), histamine type 2 (H2)- receptor blockers, sucralfate, and prednisolone E. Prognosis is good for mild to moderate esophagitis and guarded or poor for severe esophagitis VII. Esophageal stricture A. Strictures may be the result of severe esophagitis or esophageal surgery B. Regurgitation usually occurs immediately after eating, but it might not be related to eating in chronic cases C. If due to injury, signs of stricture usually occur within 14 days D. Radiography may show distention of the esopha- gus proximal to the stricture. Contrast studies or endoscopy may be helpful in the diagnosis E. Treatment is usually by balloon catheter dilata- tion. Prednisolone helps prevent further ﬁbrosis and stricture arteriosum, the aorta, the pulmonary trunk, and base of the heart 2. There is a familial tendency in some breeds (e.g., German shepherd dog, Irish setter) B. Clinical signs include regurgitation that begins at the time of weaning, failure to gain weight, and cough and dyspnea (with aspiration pneumonia) C. Survey thoracic radiography ﬁndings suggesting PRAA include esophageal dilatation cranial to the heart, absence of the normal bulge of the aortic arch, and leftward tracheal deviation cranial to the heart. Barium esophagram may conﬁrm the location of the esophageal obstruction D. Treatment involves surgical ligation and antibiotic therapy if indicated. Prognosis for recovery of esophageal function is better if the surgery is performed early XI. Hiatal disorders A. Causes 1. Hiatal hernias: A sliding hiatal hernia is a pro- trusion of the distal esophagus and stomach through an enlarged esophageal hiatus into the thorax. A congenital form has been described in shar-peis. It may also occur secondary to high positive intraabdominal pressure (e.g., ab- dominal trauma, vomiting), chronic upper air- way obstruction (e.g., brachycephalic syndrome), or tetanus 2. Gastroesophageal intussusception, an invagina- tion of the stomach into the distal esophagus, is seen with congenital idiopathic megaesophagus B. Clinical signs of small hiatal hernias are due pri- marily to reﬂux esophagitis (regurgitation, hyper- salivation). When large portions of the stomach are displaced, signs of gastric and esophageal obstruction occur and may include dyspnea, hematemesis, collapse, rapid deterioration, and death C. Radiography, barium esophagram, or endoscopy may conﬁrm the diagnosis D. Surgery is indicated for the treatment of large hernias. Small hernias may be managed medically with treatment for reﬂux esophagitis and frequent feeding of small portions of low-fat soft-food diet XII. Periesophageal obstruction A. Extraluminal compression can be caused by E cervical or mediastinal masses B. Clinical signs include chronic progressive regurgi- tation, dysphagia, and hypersalivation in addition CVC to other signs related to neoplasia C. Thoracic radiography usually reveals an intratho- LAt racic mass D. Treat the underlying cause XIII. Esophageal neoplasia A. Primary neoplasia is rare. Leiomyoma is the most common neoplasia in dogs, and squamous cell carcinoma is most common in cats. Osteosar- aortic arch. This view, from the coma and ﬁbrosarcoma in dogs may develop with the descending right artery (PA) causing constric- malignant transformation of a granuloma caused and the heart base. by Spirocerca lupi. Other tumors occasionally left subclavian artery. (From metastasize to the esophagus Radiology, 5th ed. St Louis, B. Clinical signs include regurgitation, dysphagia, and ptyalism CHAPTER 16 Gastrointestinal Disorders 229 B. Clinical signs include acute onset of nausea and vomiting C. Diagnosis is supported by response to therapy in 1 to 2 days D. Treat the underlying cause, withhold food for 12 to 24 hours, then offer a bland diet. Correct dehydration if present; consider antiemetic and acid control therapy III. Gastric foreign bodies A. Gastric foreign bodies are most common in dogs. Linear foreign bodies are more likely in cats B. The most common clinical sign is acute-onset vomiting, but some may present with chronic vomiting. Additional signs may relate to the foreign body ingested (zinc or lead toxicity) C. Gastric foreign body should be considered in all animals with acute vomiting. Radiography may identify the object and reveal a distended stomach D. Endoscopic removal is preferred. Asymptomatic animals may be managed conservatively. Per- form gastrostomy if object cannot be removed via endoscopy IV. Gastroduodenal ulceration and bleeding A. Causes include nonsteroidal antiinﬂammatory drugs (NSAIDs), glucocorticoids, chronic gastritis, hepatic disease, renal failure, neurologic disease, hypoadrenocorticism, gastric neoplasia, mast cell tumors, gastrinoma, or stress B. Clinical signs include anorexia, vomiting, hemate- mesis, melena, abdominal pain, and weight loss. Acute onset abdominal pain, depression, and collapse suggest ulcer perforation and septic shock C. Diagnosis 1. Carefully review drug history for administra- tion of ulcerogenic drugs 2. Laboratory evaluation may show regenerative anemia or microcytic hypochromic anemia with chronic blood loss. Evaluate for underly- ing disorders 3. Radiographs or GI contrast studies may be useful 4. Abdominocentesis is indicated if perforation is suspected 5. Endoscopy or laparotomy may be useful D. Treat with H2 blockers to control gastric acid secretion, and sucralfate for mucosal protection. Give antibiotics or other supportive therapy as needed (Figure 16-2) V. Chronic Gastritis A. Lymphocytic-plasmacytic gastritis is a common histologic diagnosis 1. Etiology a. Idiopathic chronic gastritis is usually attrib- uted to dietary allergy or intolerance, oc- cult parasitism, or a reaction to bacterial antigens, or unknown pathogens b. Speciﬁc causes include infection with Physaloptera rara, Ollulanus tricuspis (cats), Pythium insidiosum (dogs), or Helicobacter, enterogastric reﬂux, or chronic mucosal irritation Antacids Anticholinergic H+ agents ATPase X H2-receptor + X Proton pump inhibitors – Prostaglandin E2 Misoprostol Gastrin parietal cell showing the site of action of various therapeutic agents used to decrease gastric acid secretion. competitively inhibit acid secretion stimulated by histamine, which is released from nearby enterochromafﬁn-like also indirectly stimulates histamine release from the ECL cells. Use of anticholinergic drugs to inhibit acid Prostaglandin (PGE2) analogues, such as misoprostol, inhibit acid secretion by blocking histamine-induced cyclic inhibitors such as omeprazole and pantoprazole have broad-spectrum antisecretory activity because acid secretion by inhibiting hydrogen potassium adenosine triphosphatase. Antacids neutralize luminal gastric Manual of Small Animal Clinical Practice, 3rd ed. St Louis, 2006, Saunders.) 6. Surgery may be indicated to correct gastric outﬂow obstruction D. The prognosis is good when the underlying cause is identiﬁed. Long-term management is usually required VI. Gastric outﬂow obstruction A. Causes include foreign bodies, chronic hyper- trophic pyloric gastropathy, congenital pyloric stenosis, pyloric mass, gastric dilatation-volvulus, or extrinsic compression B. Clinical signs include projectile vomiting of undi- gested food, abdominal distention, belching, and weight loss C. Diagnosis 1. Laboratory ﬁndings are unremarkable unless profuse vomiting occurs and results in hypoka- lemia, hyponatremia, hypochloremia, and metabolic alkalosis 2. The ﬁnding of a distended stomach ﬁlled with food more than 12 hours after eating suggests delayed gastric emptying. Endos- copy may be useful to identify foreign bodies and masses D. Surgery is the deﬁnitive therapy. Administer ﬂuid therapy and gastric promotility drugs if necessary VII. Gastric motility disorders A. Possible factors include drugs (e.g., anticholiner- gic, adrenergic, or narcotic), gastric or abdominal inﬂammation, metabolic abnormalities (e.g., hy- pokalemia, endotoxemia, hypothyroidism), neurogenic causes (e.g., dysautonomia), nervous inhibition (stress, pain), or prolonged mechanical obstruction CHAPTER 16 Gastrointestinal Disorders 231 metabolic acidosis are often present. Radiogra- phy shows overdistension of the stomach with gas, pyloric displacement, and compartmentaliza- tion of the stomach on lateral view. Splenomegaly is also seen. Pneumoperitoneum suggests gastric perforation E. Initial medical management 1. Decompress the stomach, preferably by intubation 2. Administer ﬂuids and treat for shock 3. Control infection and endotoxemia with antibiotics and glucocorticoids 4. Treat cardiac arrhythmias; correct hypokalemia F. Surgical management is aimed at repositioning of the stomach and spleen, resecting devitalized gas- tric and splenic tissue, and permanently ﬁxing the stomach to prevent future recurrences of volvulus G. Prevention involves feeding frequent, small por- tions of food, and restricting exercise and access to water for 1 hour after eating XI. Surgery of the stomach. See Chapter 27 for a review of surgical procedures Gastrin con- shows INTESTINAL DISORDERS required to I. Diarrhea overview A. Acute vs. chronic diarrhea 1. Acute diarrhea has a sudden onset, with dura- tion of 3 weeks or less. Treatment is mainly supportive and nonspeciﬁc 2. Chronic diarrhea persists for 4 weeks or longer or has episodic recurrence B. Small bowel vs. large bowel 1. Small bowel diarrhea is characterized by a large volume of feces with a rancid smell. May be associated with excessive ﬂatulence and weight loss. Steatorrhea may occur in mal- digestive or malabsorptive disorders 2. Large bowel diarrhea is characterized by frequent urges to defecate, straining, and small quantities of feces. Hematochezia, mucus, or exudates may be present C. Diagnostic approach for diarrhea (Table 16-1) 1. History: Consider extraintestinal causes of diarrhea. Review the mode of onset; duration; clinical course; fecal characteristics; correla- tion with diet, medication, or stressful events; response to treatment; and association with other signs 2. Physical examination: Perform rectal examina- tion, and palpate abdomen. Look for signs of systemic disease 3. Routine laboratory tests (CBC, biochemistry proﬁle) and thyroid proﬁle in cats to exclude hyperthyroidism 4. Fecal examination for parasites, bacteria, blood, and fecal fat 5. Serum folate and cobalamin assays. Serum folate may be decreased in enteropathies that impair absorption in the proximal small intes- tine, and increased with overproliferation of the normal intestinal ﬂora, or exocrine pancre- atic insufﬁciency (EPI). Serum cobalamin may 2. Fluid therapy to correct dehydration and electrolyte abnormalities 3. Antidiarrheal drugs are used short-term to Associations control ﬂuid loss. Loperamide or diphenoxyl- ate are most effective 4. Corticosteroids are indicated for IBD, and NSAIDs may be used in chronic colitis severe 5. Antibiotic should be used only to treat speciﬁc bacterial enteropathogens 6. Fenbendazole therapy for common intestinal enteropathy nematodes and Giardia spp. fatty acids, 7. Cobalamin therapy in chronic small intestinal disease or exocrine pancreatic insufﬁciency II. Dietary diarrhea neoplasia A. Dietary indiscretions include overeating, inges- tion of spoiled garbage, and ingestion of abrasive or indigestible foreign material that can trauma- blood loss, ane- tize the GI mucosa. Common in dogs inﬂammation B. Diagnosis is by review of history C. Self-limiting with feeding of a restricted diet and prevention of indiscriminant eating III. Drug- and toxin-induced diarrhea A. Many medications may cause diarrhea (e.g. NSAIDs, digitalis, lactulose, antihelmintics, antibiotics, many antineoplastic drugs). Dexamethasone has been associated with hemorrhagic gastroenterocolitis, especially in dogs with intervertebral disc disease B. Many exogenous toxins cause diarrhea (e.g., bac- terial enterotoxins causing food poisoning, heavy metals, insecticides) C. Diagnosis is based on a review of the history D. Diarrhea usually resolves with discontinuation of the medication or dose reduction, and with elimi- nation of the toxin from the body. Give supportive neoplasia treatment as indicated neoplasia IV. Intestinal parasites: Helminths A. Ascarids 1. Toxocara canis is the most prevalent intesti- nal parasites of dogs. Toxocara cati occurs in cats 2. Routes of infection include transplacental (T. canis), milk-borne (T. canis, T. cati), inges- tion of infective eggs (all), ingestion of a paratenic host (T. canis), or an intermediate host (T. leonina) 3. Clinical signs occur most often in puppies and kittens and may include abdominal discomfort, potbelly, stunted growth, and diarrhea. Intesti- nal obstruction caused by large masses of worms or severe lung damage due to migration occurs rarely 4. Diagnose on routine fecal examination 5. Treat with pyrantel pamoate 6. Toxocaral visceral larval migrans can occur in humans when larva penetrate the skin B. Hookworms 1. Ancylostoma caninum, the most common hook- worm in the dog, is a bloodsucker. Ancylostoma tubaeforme, the common hookworm in the cat, feeds on tissue. Ancylostoma braziliense (southern United States) and Uncinaria steno- cephala (Canada) are less common in dogs and cats and are only mildly pathogenic CHAPTER 16 Gastrointestinal Disorders 233 4. Diagnosis is made by identiﬁcation of proglot- tids in the feces 5. Treat with praziquantel. Control ﬂeas and lice V. Intestinal parasites: Protozoa A. Coccidia 1. Primary enteric disease is caused by Isospora spp. and Cryptosporidium. Toxoplasma gondii and Neospora caninum cause multisystemic infections 2. Infection usually occurs by ingestion of sporu- lated oocysts from feces contamination 3. Diarrhea is the characteristic sign. It may vary from soft to ﬂuid and may contain mucus or blood. Vomiting, weight loss, and dehydration may also occur. Most infected animals are asymptomatic. Clinical signs commonly occur in newborns in unsanitary and stressful conditions 4. Isospora can be identiﬁed in fresh feces. Fecal immunoassay or polymerase chain reaction (PCR) is available for Cryptosporidium 5. Treat Isospora with sulfadimethoxine, trimethoprim-sulfa, or furazolidone. Treat Cryptosporidium with azithromycin. Cryptospo- ridium is zoonotic B. Giardia 1. Infective cysts pass through feces into the environment, and infection occurs by ingestion of contaminated food or water 2. Clinical signs result from intestinal malabsorp- tion and include large volume of feces, steator- rhea, and weight loss. Diarrhea may be acute or chronic, intermittent, or continuous. Most infected animals are asymptomatic 3. Diagnosis is by microscopic examination of feces or a fecal immunoassay for antigen 4. Treat with fenbendazole. Giardia may be resis- tant to metronidazole. Furazolidone is effective in cats. Clean the environment, and bathe animals C. Tritrichomonas foetus in cats 1. T. foetus causes mild to severe lymphoplasma- cytic colitis and chronic large intestinal diar- rhea in young cats 2. Clinical signs consist of diarrhea that may wax and wane in an otherwise healthy animal 3. Fecal PCR assay is the most accurate method of diagnosis. Trophozoites are observed in fresh fecal smears in a low percentage of cases 4. Treat with antibiotics, treat concurrent infec- tions, and improve environmental conditions D. Entamoeba 1. E. histolytica infection occurs by drinking contaminated water 2. Clinical signs include bloody-mucoid diarrhea 3. Diagnosis can be made by detecting tropho- zoites in fecal smears or cysts in zinc sulfate ﬂotation 4. Treat with metronidazole E. Balantidium 1. B. coli rarely causes chronic ulcerative colitis in dogs psyllium may help to reduce bacterial prolifer- ation and sporulation D. Clostridium difﬁcile 1. C. difﬁcile and its toxin may be found in normal dogs and cats and also in animals with mild diarrhea or acute hemorrhagic diarrhea. Pseu- domembranous colitis as seen in people is not seen in dogs and cats 2. Fecal cultures are not useful because C. difﬁcile is a part of the normal ﬂora. Fecal assays for toxins A and B are available 3. Treatment with metronidazole is recommended VIII. Fungal infections A. Intestinal pythiosis and zygomycosis 1. Pythium insidiosum and Zygomycetes can invade the digestive tract, causing granulomatous tissue reactions 2. Pythiosis is most common in young large- breed dogs in the southern Gulf States. It is rare in cats 3. Clinical signs include chronic intractable diarrhea (may be bloody) and vomiting, depression, and progressive weight loss 4. Conﬁrmation of diagnosis requires histologic identiﬁcation in biopsies 5. Treatment involves radical surgical excision of the affected segments. A combination of amphotericin B, itraconazole, and terbinaﬁne may be successful. Prognosis is guarded to poor B. Histoplasmosis is a multisystemic infection with intestinal involvement caused by Histoplasma capsulatum IX. Intestinal protothecosis A. Caused by algae that may rarely colonize the intestinal tract of dogs and cause severe necro- tizing or ulcerating enterocolitis B. Clinical signs include large bowel diarrhea with hematochezia. Additional signs are related to invasion of other organs (visceral organs, eye, central nervous system [CNS]) C. Identify organisms in feces, cytology prepara- tions, and biopsies D. Treat with a combination of amphotericin B and itraconazole X. Chronic IBD A. Lymphocytic-plasmacytic IBD 1. This is the most common form of IBD in dogs and cats. Factors that may play a role include mucosal hypersensitivity to antigens, and genetic factors (basenji, German shepherd dog, soft-coated wheaten terrier, and shar-pei) 2. Clinical signs include vomiting, diarrhea, and weight loss. Protein-losing enteropathy may be present. Signs may be intermittent and last for months to years 3. IBD is a diagnosis of exclusion of all known causes of lymphocytic-plasmacytic inﬂamma- tion of the intestinal tract a. Abnormalities on endoscopic examination include mucosal erythema, petechiae ero- sions, or ulcers, increased mucus, friability, or granularity, decreased visibility of the CHAPTER 16 Gastrointestinal Disorders 235 3. Diagnosis is based on breed and presence of PAS-positive histiocytes in a biopsy 4. Treat with enroﬂoxacin with metronidazole. Feed a highly digestible diet E. Neutrophilic (suppurative) enterocolitis 1. Cause is unknown 2. Clinical signs consist of large bowel diarrhea that can be either acute or chronic 3. Diagnosis is based on biopsy 4. Treat with antibiotics, antiinﬂammatory, and immunosuppressive agents XI. Fiber-responsive diarrhea A. Chronic, noninﬂammatory, mucoid large bowel diarrhea B. Clinical signs include intermittent mucoid diar- rhea (without hematochezia). Working dogs and excitable dogs are predisposed C. Diagnosis is based on exclusion of known causes of colonic disease (e.g., dietary, infectious, parasitic, IBD), including a normal colonoscopic biopsy D. Feed a digestible diet with ﬁber supplementation (psyllium). Consider motility-modifying antidiar- rheal drugs if dietary modiﬁcation is unsuccessful XII. Protein-losing enteropathy A. A variety of intestinal diseases associated with accelerated loss of plasma proteins into the gut either caused by impaired lymphatic drainage or mucosal injury B. Most frequently occurs with chronic enteropa- thies (e.g., lymphangiectasia, IBD, histoplasmosis, lymphoma) C. Clinical signs include severe hypoalbuminemia (subcutaneous edema, ascites, hydrothorax) and chronic intermittent or persistent diarrhea D. Diagnosis 1. Typical laboratory ﬁndings in intestinal lymphangiectasia include hypoalbuminemia, hypoglobulinemia, lymphopenia, hypocholes- terolemia, and hypocalcemia. Perform liver function tests and urine protein determination to exclude other causes of hypoalbuminemia 2. Radiography and ultrasonography may detect abdominal and thoracic effusions 3. Deﬁnitive diagnosis requires identiﬁcation of the characteristic lymphatic lesions in biop- sies. Full-thickness biopsies may be required for the diagnosis E. Treatment is similar to that of lymphocytic- plasmacytic IBD. Dietary fat restriction is war- ranted. Response to therapy is unpredictable XIII. Villous atrophy is associated with intestinal malab- sorption and chronic diarrhea A. Causes 1. Primary causes include gluten-sensitive enter- opathy of Irish setters and idiopathic canine villous atrophy in German shepherds 2. Secondary causes include diffuse inﬁltrative in- testinal diseases (e.g., chronic IBD, lymphoma), and enteric infections (e.g., coronavirus, Giardia, bacterial overgrowth) B. Clinical signs include small bowel diarrhea and weight loss b. Gastric outlet obstruction causes hypoch- loremic metabolic alkalosis. More distant obstructions cause varying degrees of metabolic acidosis 2. Simple vs. strangulated obstruction: Simple obstructions occlude the lumen; strangulated obstructions cause vascular compromise of the obstructed bowel segment C. Clinical signs depend on the location, complete- ness, duration of the obstruction, and presence of strangulation. Signs include acute onset of vomit- ing, anorexia, depression, abdominal distension or pain, diarrhea, melena, hematochezia, and shock D. Diagnosis 1. Abdominal palpation may identify foreign bodies, intussusceptions (“sausage loop”), or distended bowel loops 2. Radiographic ﬁndings include gas or ﬂuid distention of the bowel, retention of contrast material, and luminal ﬁlling defects E. Treatment involves surgical removal of the obstruction, management of complications, and supportive medical treatment explain the CONSTIPATION AND ANORECTAL DISEASES I. Constipation A. Cause 1. Ingestion of foreign material (e.g., hair in cats, bones in dogs) 2. Environmental conditions (e.g., unfamiliar sur- roundings) may cause inhibition of defecation 3. Painful defecation resulting from anorectal disease (e.g., anal sacculitis) or orthopedic disorders that limit positioning may lead to inhibition of defecation 4. Rectocolonic obstruction may be caused by intraluminal causes (e.g., foreign body, perineal hernia) or external compression (e.g., prostatic enlargement, pelvic fractures) 5. Neuromuscular disease may interfere with co- lonic innervations or smooth muscle function or with positioning for defecation. Examples include intervertebral disc disease at the lumbosacral region, dysautonomia, and hypo- thyroidism 6. Fluid and electrolyte disorders: Dehydration causes feces to become dry and hard; hypoka- lemia and hypercalcemia can impair colonic smooth muscle function 7. Drug-related (e.g., anticholinergics, opiates, loperamide, antihistamines, barium sulfate) B. Clinical signs include reduced or absent defeca- tion, dyschezia, abdominal discomfort, and para- doxical diarrhea (ﬂuids secreted by the irritated mucosa may pass around the retained feces). Prolonged constipation may lead to anorexia, vomiting, and dehydration C. Diagnosis 1. Review history to identify an underlying cause 2. Physical examination, including rectal examina- tion and abdominal palpation CHAPTER 16 Gastrointestinal Disorders 237 may cause life-threatening hyperphosphatemia in cats and small dogs 3. Manual extraction of impacted feces under general anesthesia may be necessary in severe cases. Use colonic irrigation with warm saline to soften the feces, extract the feces by trans- abdominal manipulation into the distal rectum for digital or forceps removal F. Oral laxative therapy 1. High-ﬁber bulk-forming laxatives are available as commercial high-ﬁber diets or ﬁber supple- ments (e.g., wheat bran, psyllium) 2. Lubricant laxatives: Flavored petrolatum is preferred. Mineral oil may lead to inhalation lipid pneumonia and should not be given orally 3. Emollient laxatives: Docusate is a mild laxative, and its efﬁcacy depends on patient hydration 4. Osmotic laxatives: Lactulose is the most clini- cally useful and effective. It is safe for long- term use 5. Stimulant laxatives: Bisacodyl is the most effective, but long-term use may damage the myenteric plexus. Contraindicated in the presence of an obstructive lesion 6. Promotility drugs are contraindicated in the presence of an obstructive lesion. Cisapride is the most effective II. Megacolon in cats A. Most cases are idiopathic. Obstructive rectoco- lonic disorder is found in up to 25% of the cases (perineal hernia, anorectal stricture, or neoplasia). Neurologic dysfunction may account for up to 5% of the cases (Manx cat deformity, dysautonomia) B. Clinical signs occur mostly in middle-aged and older cats. Males are predisposed. Signs consist of progressive constipation and obstipation C. Diagnosis is based on ﬁnding severe colonic dilatation and impaction with feces on abdominal palpation and abdominal radiography D. Treat medically, including evacuation of feces, lactulose, and cisapride. Most cats eventually require subtotal colectomy III. Proctitis A. Usually associated with colitis B. Clinical signs may include tenesmus, diarrhea, and hematochezia IV. Anorectal prolapse A. Occurs most frequently in puppies and kittens with persistent straining to defecate because of endoparasitism. Anal sphincter incompetence in Manx cats may be a predisposing factor B. A partial prolapse appears as a red, swollen, doughnut-shaped ring of prolapsed mucosa. Complete prolapse appears as an edematous, cylindrical-shaped mass C. Diagnosis based on physical examination. Differ- entiate from intussusception D. Treat underlying disorders, and manually reduce the prolapse. Surgical treatment may be required V. Perineal hernia cat with idiopathic constipa- A. Weakened perineal musculature fails to support EC. Textbook of Veterinary the rectal wall, resulting in persistent rectal dis- tention. Occurs mostly in aged, intact male dogs XI. Anal sac disease A. Impaction is usually bilateral. The anal sac is dis- tended, mildly painful, and not readily expressed. Anal sacculitis may be unilateral or bilateral and associated with moderate to severe pain and purulent contents. Anal sac abscesses are usually unilateral and are characterized by marked distension of the sac with pus, erythema of the overlying skin, and fever B. Clinical signs include scooting the hind end on the ﬂoor, tenesmus, and licking and biting the anal area C. Diagnosis is based on examination of the anal sacs D. Manually evacuate, irrigate with povidone-iodine solution, and treat with systemic antibiotics based on culture and sensitivity. A high-ﬁber diet may help to prevent recurrence. Anal sacculec- tomy may be required XII. Perianal ﬁstula A. Perianal ﬁstulas are deep ulcerating tracts in the perianal tissues. They occur most frequently in German shepherd dogs and Irish setters B. Clinical signs commonly include dyschezia, tenes- mus, and severe anal discomfort. Hematochezia, constipation, fecal incontinence, and purulent perianal discharge may be present C. Diagnosis is established by examination of the perineal area. The anal sacs may be involved D. Medical therapy with hair removal and cleansing, systemic antibiotic therapy, and immunosuppres- sive therapy is often effective. Surgical therapy is indicated in refractory cases E. Prognosis is better when treatment is early. Fecal incontinence and anal stenosis are complications of extensive disease or surgical procedure XIII. Pseudocoprostasis A. Occurs when the anal opening is obstructed by surrounding hair. Diarrhea and obesity may be predisposing factors B. Clinical signs include constipation, restlessness, and biting the anal region. Dermatitis may occur C. Diagnosis is established by visual examination D. Treatment includes clipping of the hair, cleansing, and antibiotic treatment when needed XIV. Rectal, anal, and perianal tumors A. Benign rectal polyps 1. Common in middle-aged and older dogs. They are usually solitary, focal, pedunculated, or sessile masses 2. Clinical signs include hematochezia, dyschezia,

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