Gastrointestinal Disease and Its Management

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GERIATRICS

GASTROINTESTINAL DISEASE AND ITS MANAGEMENT Albert E. Jergens, DVM, MS

Gastrointestinal (GI) diseases are common in the geriatric dog and cat and present the clinician with formidable diagnostic and therapeutic challenges. Although primary signs (dysphagia, vomiting, diarrhea, icterus) of digestive system dysfunction predominate in most animals, secondary signs having variable specificity for GI disease are also commonly seen as found in the list on this page. The veterinarian who is presented with an aged animal with GI signs must determine the likely site(s) of the problem, the severity of the animal's condition, and the appropriate diagnostic evaluation and treatment that address the problem most directly. This article will provide an overview of those GI diseases that are most commonly seen with advancing age in dogs and cats. Emphasis is placed on the diagnostic approach and specific management of each disease by organ system. Comments concerning prognosis and patient monitoring are included to assist the clinician when advising his or her clients. A comprehensive listing of all drugs, their dosages, and the clinical indications for their use may be found in Table 1.

Signs of Gastrointestinal Disease Vomiting* Diarrhea* Weight loss* Icterus* Anorexia*

Hematochezia* Behavioral changes Tenesmus* Hematemesis/Melena* Regurgitation*

Flatulence Dysphagia Abdominal pain* Bloat

*Common signs.

From the Department of Veterinary Clinical Sciences College of Veterinary Medicine, Iowa State University, Ames, Iowa

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 27 • NUMBER 6 • NOVEMBER 1997

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Table 1. SUMMARY OF DRUGS AVAILABLE FOR TREATMENT OF GASTROINTESTINAL DISEASES Drug

Dosage

Indications/Comments

Diseases of the Oral Cavity and Pharynx Amoxicillin 22 mg/kg BID PO (D,C) Metronidazole

20 mg/kg BID PO (D,C)

Prednisone

1 mg/kg BID PO (D,C)

Azathioprine

1.1 mg/kg EOD PO (C) 2.2 mglkg SID PO (D) Test dose of 1 mg IM, then 1 mglkg IM weekly until remission (C)

Aurothioglucose

Diseases of the Esophagus Amoxicillin

22 mglkg BID PO (D,C)

Sulfadiazine/Trimethoprim

30 mg/kg SID PO (D,C)

Sucralfate

Crush 1-g tablet and mix with 10 mL of water; give 5 mL of slurry TID (D,C) 1-4 mg/kg TID-QID PO (D,C)

Cimetidine

Ranitidine

2 mg/kg BID PO (D)

Famotidine

1 mglkg SID PO (D)

Omeprazole

2 mg/kg SID PO (D)

Metoclopramide

0.2-0.5 mg/kg SID-TID PO, IV(D,C) 0.5 mg/kg TID PO (D)

Cisapride Diseases of the Stomach Cimetidine

Misoprostil

See section on diseases the esophagus See section on diseases the esophagus See section on diseases the esophagus See section on diseases the esophagus See section on diseases the esohagus See section on diseases the oral cavity See section on diseases the oral cavity 3 ftg/kg TID PO (D)

Chlorpromazine Deferoxamine

0.2-{).4 mg/kg SID- TID (D) 50 mg/kg IV (D)

Ranitidine Omeprazole Cisapride Metoclopramide Metronidazole Prednisone

Useful for lymphocytic-plasmacytic stomatitis; good anaerobic spectrum Useful for lymphocytic-plasmacytic stomatitis; good anaerobic spectrum Reduces cellular infiltrates via immunosuppression Potent immunosuppressive agent; watch for myelosuppression in cats Closely screen cats for cytopenias and proteinuria

Treatment of aspiration pneumonia seen with megaesophagus Treatment of aspiration pneumonia seen with megaesophagus Topical mucosal protectant for reflux esophagitis

H, acid blocker used for reflux esophagitis; inhibits hepatic microsomal enzymes H, acid blocker; causes less microsomal inhibition H2 acid blocker; causes less microsomal inhibition Gastric acid proton pump inhibitor; use in severe cases of reflux esophagitis Reduces gastroesophageal reflux and enhances gastric motility Reduces gastroesophageal reflux and enhances gastric motility

of

Gastric antacid

of

Gastric antacid

of

Gastric antacid

of

Gastric prokinetic agent

of

Gastric prokinetic agent and centrally acting antiemetic Immunosuppressive drug; reduces cellular infiltrates Immunosuppressive drug; reduces cellular infiltrates For nonsteroidal anti-inflammatory druginduced gastritis with ulceration Phenothiazine centrally acting antiemetic Free radical scavenger; reduces repertusion injury of gastric dilatation volvlus Table continued on opposite page

of of

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Table 1. SUMMARY OF DRUGS AVAILABLE FOR TREATMENT OF GASTROINTESTINAL DISEASES (Continued). Drug

Dosage

Diseases of the Small Intestine Prednisone See section on diseases of the oral cavity

Metronidazole

See section on diseases of the oral cavity

Oxytetracycline

20 mg/kg TID PO (d)

Diseases of the Large Intestine Prednisone See section on diseases of the oral cavity See section on diseases of Metronidazole the oral cavity Sulfasalazine 12.5 mg/kg QID PO (D)

Dioctyl sodium sulfosuccinate Lactulose Cisapride Diseases of the Liver Prednisone Metronidazole Lactulose

Indications/Comments

Immunosuppressive drug; reduces mucosal infiltrates seen with inflammatory bowel disease and protein-losing enteropathy Immunosuppressive drug; reduces mucosal infiltrates seen with inflammatory bowel disease and protein-losing enteropathy Treatment of small intestinal bacterial overgrowth

50 mg SID PO (C)

Immunosuppressive drug; useful for inflammatory bowel disease colitis Immunosuppressive drug; useful for inflammatory bowel disease colitis First-choice drug for inflammatory bowel disease colitis in dogs; use cautiously in cats and at a reduced dosage Emollient laxative for constipation

0.5 mUkg BID-TID PO (C) 0.1-0.5 mg/kg BID PO (C)

Hyperosmotic laxative for constipation Colonic prokinetic agent for constipation

1 mg/kg BID PO (D,C)

Useful as an anti-inflammatory and antibiotic agent Treatment of hepatic encephalopathy Treatment of hepatic encephalopathy

Furosemide Spironolactone Trientene Zinc acetate

10 mg/kg TID PO (D,C) 1-5 mL BID PO (C) 2-10 mL BID PO (D) 2 mg/kg BID PO (D,C) 1- 2 mg/kg BID PO (D) 10- 14 mg/kg BID PO (D) 4-10 mg/kg BID PO (D)

Urodeoxycholic acid

10-15 mg/kg SID PO (D,C)

Treatment of ascites Treatment of ascites Hepatic decoppering agent Hepatic decoppering agent; give 1 hour prior to meal Mitigates hepatocyte injury and promotes choleresis

D = dog, C = cat, PO = oral administration, IM = intramuscular administration, IV = intravenous administration, SID = once daily, BID = twice daily, TID = three times daily, QID = four times daily, EOD = every other day

DISEASES OF THE ORAL CAVITY AND PHARYNX Gingivitis/Stomatitis/Glossitis Causes

Inflammation of the oral cavity may occur as stomatitis, gingivitis, or glossitis. Chronic oral lesions are most commonly seen in cats but may also affect dogs. The cause is often unknown, but dental disease, immune-mediated disease (hypersensitivity to oral bacterial antigens), autoimmune disorders (such as the Pemphigus diseases), and concurrent infection with feline immunodeficiency virus (FIV) or feline leukemia virus (FeLV) have been incriminated. 11 Uremic stomatitis may be seen with both acute and chronic renal disease.

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Diagnosis

Clinical signs include halitosis, ptyalism, inappetence, weight loss, and oropharyngeal dysphagia. Oral examination (often requiring anesthesia) may reveal erythema, hemorrhage, ulceration, and dental resorptive lesions. Laboratory findings are nonspecific but may confirm hypergammaglobulinemia. Serology for detection of FeLV and FIV infection is recommended. Biopsy is rarely indicated and usually reveals lymphocytic-plasmacytic inflammation. Treatment

Chronic feline oral inflammation must be treated aggressively. The teeth should be thoroughly scaled and polished to remove all plaque and calculus. Use of systemic antibiotics (metronidazole, amoxicillin) is palliative but not curativeY Use of immunosuppressive drugs such as corticosteroids, azathioprine, gold salts (aurothioglucose), and chlorambucil is reported to be beneficial.54 The author has successfully used a combination of corticosteroids and gold salts in refractory cases. Prognosis/Patient Monitoring

A guarded to poor prognosis should be given to chronically affected cats. Repeated dental scalings and tooth extractions are performed as needed. Longterm, intermittent or continuous immunosuppressive therapy is needed in most cases to maintain remission. Gold salts should be used cautiously (see Table 1).

Oropharyngeal Neoplasia Causes

Malignant tumors of the oropharynx are common in old dogs and cats. Melanoma and squamous cell carcinoma most commonly involve the tonsils and gingiva in dogs.14 Squamous cell carcinomas and fibrosarcomas predominantly occur along the base of the tongue or gingiva of cats. 44 Diagnosis

Clinical signs include anorexia, ptyalism, halitosis, and oropharyngeal dysphagia. Oral examination reveals the presence of a mass lesion with demonstrable bony lysis via oral radiography. Definitive diagnosis depends on biopsy with histopathology. The lesion should be evaluated for metastasis by palpation/ aspiration of regional lymph nodes and performance of thoracic radiography. Treatment

Aggressive surgery should be pursued for tumors located along the rostral mandible or maxilla. Surgery combined with radiation therapy alone and with

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radiation therapy in combination with chemotherapy is palliative in animals having nonresectable masses. Prognosis/Patient Monitoring

A guarded prognosis is warranted in animals w ith rostrally located masses that are completely excised surgically. Animals having non-resectable masses, tonsillar masses, and evidence of regional (lymph node) or distant (thorax) metastasis have a poor prognosis. DISEASES OF THE ESOPHAGUS Adult-Onset Megaesophagus Causes

Adult-onset megaesophagus (ME) is defined as generalized esophageal dilatation and aperistalsis which manifests in animals after maturity. The etiopathogenesis in many cases is unknown, leading to a classification of idiopathic ME. A variety of acquired disease conditions have been associated with or hypothesized to cause ME. A list of diseases associated with ME and esophageal hypomotility is found on this page. Diagnosis

Regurgitation must be clearly differentiated from vomiting. Signs seen w ith ME usually include regurgitation of food and liquids, pytalism, repeated swallowing attempts, and odynophagia due to excessive dilatation or inflammation. Severe cachexia may result from malnutrition. Respiratory distress (moist cough, crackles, dyspnea) is often observed in animals with aspiration pneumonia. It should be noted whether regurgitation is associated with other signs (e.g., muscle pain and a stiff gait caused by myositis or weakness seen with neuromus-

Some Diseases Associated with Megaesophagus and Esophageal Hypomotility Neuromuscular Idiopathic megaesophagus Myasthenia gravis Systemic lupus erythematosus Polymyositis/polymyopathy Botulism Tetanus Canine distemper Dysautonomia

Toxicity Lead Thallium Anticholinesterase Miscellaneous Hypoadrenocorticism Hypothyroidism Pyloric stenosis Gastric dilatation- volvulus Esophagitis

Adapted from Jones BD, Jergens AE, Guilford WG: Diseases of the esophagus. In Ettinger SJ (ed): Textbook of Veterinary Internal Medicine, ed 3. Philadelphia, WB Saunders, 1989, p 1262; with permission.

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cular disease) indicative of acquired ME. Survey neck and thoracic radiographs usually reveal the presence of a dilated air-, fluid-, or ingesta-filled esophagus. An esophagram confirms dilatation and provides evidence of other structural abnormalities. Pulmonary alveolar opacities are seen with aspiration pneumonia. Laboratory tests should include a minimum database as well as ancillary tests based on clinical suspicion as specified in the list on this page. Acetylcholine receptor antibody titer testing should be performed in all cases of unexplained ME when focal myasthenia gravis is suspected.43 Treatment

Animals with acquired forms of ME are treated specifically for the disorder causing esophageal dilatation. Idiopathic forms of ME are treated symptomatically by feeding multiple, small-sized meals from an elevated position. Diets that have a bulky consistency (in contrast to a gruel) work best in the author's experience. Animals with pneumonia are treated with broad-spectrum antibiotics. Promotility drugs (metoclopramide, cisapride) are currently of unproven benefit, although anecdotal reports indicate possible clinical improvement in some dogs with ME. 49 Prognosis/Patient Monitoring

The prognosis with adult-onset ME is generally poor. Many animals die or are euthanized because of their disease. Animals with acquired disease may

Suggested Diagnostic Tests in Animals with Megaesophagus First-choice tests Complete blood count Serum biochemistries (include cholesterol) Urinalysis Thoracic radiographs Esophagram Second-choice tests Antinuclear antibody Acetylcholine receptor antibody titer* T4 ; thyrotropin/corticotropin stimulation tests Creatine kinase Tertiary tests Electromyogram Muscle/nerve biopsy Toxicology Cerebrospinal fluid tap/analysis Central nervous system imaging *Data compiled at Comparative Neuromuscular Laboratory, Basic Science Building, Room B200, University of California, San Diego, La Jolla CA 92093-0614. Adapted from Twedt DC: Diseases of the esophagus. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, ed 4. Philadelphia, WB Saunders, 1995, p 1124; with permission.

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respond to specific drug therapy. The prognosis with ME caused by focal myasthenia gravis is more favorable with up to one half of affected dogs responding to supportive therapy.43

Gastroesophageal Reflux Causes

Gilstroesophageal (GE) reflux may be caused by general anesthesia, hiatal defects, persistent vomiting, and anticholinergic therapy.10• 46 Refluxed gastric fluids contain acid, pepsin, trypsin, and bile salts, which are directly injurious to the esophageal mucosa. Prolonged acidification times and reduced or absent esophageal clearance (as seen with general anesthesia) contribute to the pathogenesis of esophageal inflammation.45 Mild esophagitis is usually limited to the mucosa, although severe esophagitis extends into the muscular layer and may cause ulceration and stricture formation. Diagnosis

Animals may have a history of recent anesthesia or chronic vomiting. Animals with mild esophagitis may be asymptomatic. Moderate to severe esophagitis causes anorexia, dysphagia, odynophagia (painful swallowing), and ptyalism. Survey I contrast radiographs are often unremarkable. Esophagoscopy is the most reliable means to diagnose esophagitis.50 Lesions are most prominent in the distal esophagus, adjacent to the lower esophageal sphincter (LES), and include marked erythema, erosions, and mucosal granularity (Fig. 1).

Figure 1. Endoscopic appearance of severe distal esophagitis in a 9-year-old dog. Note the marked mucosal erythema surrounding the partially dilated lower esophageal sphincter.

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Treatment

Food and water should be withheld for 24 to 48 hours with acute lesions. Once feeding resumes, small and frequent meals of a low-fat, high-protein diet should be provided to maximize LES tone.23 A slurry of sucralfate should be given orally to promote esophageal healing and mucosal cytoprotection.24 Histamine H 2-receptor antagonists (cimetidine, ranitidine, famotidine) or proton pump inhibitors (omeprazole) are used to reduce gastric acidity and the effects of GE reflux. Promotility drugs (metoclopramide, cisapride) should be administered to enhance gastric emptying and to increase LES tone.52 Severe esophagitis requires gastrostomy tube placement for provision of nutrition and to bypass the inflamed mucosa. Prognosis/Patient Monitoring

The prognosis in most cases of esophagitis caused by GE reflux is good with appropriate medical management. Mild lesions are treated for 5 to 7 days, and moderate to severe esophagitis is treated for 3 to 4 weeks. Complications of severe disease include segmental or generalized esophageal hypomotility and stricture. Esophageal Neoplasia Causes

Primary tumors of the esophagus are rare in the dog and cat. Fibrosarcoma in the dog and squamous cell carcinoma in the cat are the most common malignant neoplasms.56 Leiomyomas are the most common benign tumors. Neoplasms may also occur as metastatic lesions or as periesophageal masses (Fig. 2).

Figure 2. Periesophageal mass observed endoscopically in a 5-year-old cat having chronic regurgitation. Percutaneous fine-needle aspiration of the mass revealed a cytologic diagnosis of lymphosarcoma.

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Figure 3. Esophagram (ventrodorsal view) of the same cat as in Figure 2. Note the marked luminal stenosis and lateral deviation of the trachea (arrows) caused by the periesophageal mass. The metallic densities visualized in both axillary regions are from a previous gunshot injury.

Esophageal dysphagia in animals with neoplasia results from mechanical obstruction and disruption of esophageal motility. 31 Diagnosis

Signs are consistent with a slowly progressive stenosis. Regurgitation, dysphagia, and intermittent vomiting are seen with lower sphincter involvement. Anorexia, weight loss, and depression are more characteristic of advanced disease. Physical examination might reveal a palpable neck mass or cervical dilatation associated with ME. Survey radiographs are useful in detecting intrathoracic masses and tracheal deviation caused by cervical tumors. An esophagram confirms gross mucosal irregularities and stenosis caused by intrinsic/ extrinsic compression (Fig. 3). Esophagoscopy allows direct visualization of intraluminal mass lesions such as leiomyomas which frequently arise near the LES (Fig. 4A).

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Figure 4. A, Endoscopic appearance of a leiomyoma located in the distal esophagus of a 12-year-old Rottweiler. Note the broad based attachment of the neoplasm to the surrounding esophageal mucosa. B, Gross appearance of the esophageal leiomyoma following complete surgical excision.

Treatment

Treatment options are limited with malignant tumors as they are often quite advanced by the time of diagnosis. Chemotherapy, radiation therapy, and surgery all tend to provide poor results. Benign esophageal tumors such as leiomyomas may be successfully removed surgically (Fig. 4B). 42 Prognosis/Patient Monitoring

The prognosis for benign tumors that are completely excised is good to excellent. The prognosis is grave for malignant neoplasia, where symptomatic

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therapy with upright feedings, gastrostomy tube placement, and antibiotics for aspiration pneumonia is palliative at best. DISEASES OF THE STOMACH Chronic Gastritis Causes

Chronic gastritis is defined as focal or generalized gastric mucosal inflammation of chronic duration. Classification of chronic gastropathies is generally based on the predominant cellular infiltrate present, with lymphocytic-plasmacytic gastritis being most common. The etiopathogenesis of chronic nonspecific gastritis in dogs and cats is unknown, but immune-mediated or autoimmune processes are thought to be involved. Clinical consequences of gastric inflammation include deranged gastric motility, interference with gastric secretory function, and gastric erosion and ulceration. The role(s) of gastric spirillar organisms (Helicobacter species) in the pathogenesis of chronic gastritis/ gastric ulceration in dogs and cats has not been fully elucidated. Diagnosis

Animals with chronic gastritis often have a history of intermittent vomiting. The vomitus may consist of food, mucus, or bile-stained liquid. Hematemesis is uncommon but implies a breach in the gastric mucosal barrier as seen with erosions or ulcers. Other signs may include anorexia, weight loss, and melena with severe or long-standing disease. Physical examination is often unremarkable. Routine laboratory tests and survey abdominal radiographs are usually normal. Contrast radiography and ultrasonography are useful in detecting gastric retention or mucosal hypertrophy. Gastroscopy and mucosal biopsy are required for definitive diagnosis. Mucosal granularity and friability are the most frequent characteristics of these lesions observed endoscopically (Fig. 5). Endoscopic examination and biopsy of the small intestine should also be performed, because inflammatory infiltrates may involve the intestinal mucosa. Treatment

An antigen-restricted, highly digestible, low-fat, controlled diet should be fed. Small and frequent meals lessen the likelihood of vomiting. Clinical or endoscopic signs of ulceration warrant short-term (7-10 days) use of histamine H 2-receptor blockers or omeprazole. Antiemetic agents are rarely needed, because vomiting episodes are infrequent. Prokinetic drugs (metoclopramide, cisapride) are useful in animals with delayed gastric emptying. Prokinetic agents should not be used when mucosal hypertrophy has predisposed to gastricoutflow obstruction. Corticosteroids (prednisone) or metronidazole is used for 2 to 4 weeks to reduce mucosal cellular infiltrates. Metronidazole is the immunomodulator drug of choice in patients with severe erosive or ulcerative disease. Prognosis/Patient Monitoring

The prognosis in most cases is good to excellent. Corticosteroid dosage should be decreased gradually by 25% at 2-week intervals. The bland diet

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Figure 5. Marked, focal granularity of the gastric body in an 8-year-old dog as observed endoscopically. Biopsy specimens procured from this lesion and contiguous normal-appearing gastric mucosa confirmed a diagnosis of severe lymphocytic-plasmacytic gastritis.

should be continued for 2 to 4 weeks beyond resolution of clinical signs. Intermittent, short-term corticosteroid therapy may be required for flare-ups. Gastric Ulceration Causes

Gastric ulceration denotes a breach in the gastric mucosa that extends deeply into the muscular layer of the stomach. Gastric erosions, which are superficial mucosal defects that do not penetrate the muscularis mucosa, are much more common in the author's experience. The causes of gastric erosion and ulceration are extensive/4 as indicated in the list on page 1385. Major differential diagnoses for ulceration in aged animals include drugs (especially nonsteroidal anti-inflammatory drugs (NSAIDs), renal disease, hepatic disease, and benign (e.g., chronic gastritis) and malignant (e.g., neoplastic) infiltrative diseases. Diagnosis

Clients should be carefully queried concerning ulcerative drug use. Clinical signs are variable and often relate to the underlying etiology. Vomiting (food, mucus, or fresh or digested blood) is the most common sign. Melena and small bowel diarrhea may also be reported. Animals with ulcers or diffuse erosions may exhibit abdominal pain. Anorexia, weight loss, and hematemesis predominate in animals with ulceration caused by gastric neoplasia, especially adenocarcinoma. Systemic causes for ulceration and erosion should be ruled out by performing routine blood work and urinalysis. Laboratory tests may indicate evidence of metabolic disease (e.g., azotemia, elevated liver enzymes) or anemia

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Causes of Gastrointestinal Ulceration and Erosion Drugs-nonsteroidal anti-inflammatory drugst Mucosal ischemia* Renal disease* Liver disease* Chronic gastritis* Alimentary neoplasiat Inflammatory bowel disease* Neurologic disease* *More commonly erosive. tMore commonly ulcerative.

as a consequence of chronic blood loss. Contrast abdominal radiography is useful for detecting ulceration and other gross mucosal abnormalities but is poorly sensitive for erosive disease. Once systemic diseases have been ruled out, gastroscopy with mucosal biopsy I cytology is the diagnostic modality of choice (Fig. 6). Ulcers are best biopsied along the ulcer rim as it interfaces with adjacent normal mucosa. Gastric erosions may be biopsied directly. Treatment

The precipitating cause(s) should be identified and removed. Oral intake of food and water (or nothing per os) should be restricted to reduce gastric secretions and to minimize vomiting. Fluids (lactated Ringer's solution) should

Figure 6. Endoscopic appearance of benign gastric ulceration involving the incisure angu· laris in a 9-year-old Cocker Spaniel. Note the focal, crateriform appearance of this lesion that also contains a central crater of necrotic, fibrinopurulent debris.

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be given parenterally to correct hydration and electrolyte disturbances if present. The use of a single antiulcer drug is generally recommended, considering the cost, convenience, and efficacy seen with single-agent therapy in humans. 32 The author utilizes the following drug therapies: (1) for erosions, an H 2-receptor blocker or sucralfate; (2) for ulcers, an H 2-receptor blocker or sucralfate or omeprazole; and (3) for NSAID-induced gastritis, synthetic prostaglandins (misoprostil). Centrally acting antiemetics (metoclopramide, phenothiazines) should be used for patients with intractable vomiting. Surgery should be performed in animals with perforating ulcers and resectable neoplastic masses causing ulceration. Prognosis/Patient Monitoring

A good prognosis is given to animals with benign erosive disease. Many animals will improve following specific treatment for the underlying cause combined with symptomatic antiulcer therapy. A guarded to poor prognosis is warranted with ulceration caused by renal/liver diseases and malignant neoplasia. Gastric Dilatation Volvulus Causes

Gastric dilatation volvulus (GDV) is defined as acute abdominal tympany due to gastric overdistension caused by accumulated gas and fluid accompanied by gastric volvulus. No single cause for GDV in dogs has been identified, although the following risk factors should be considered: increased breed size, body conformation (high thoracic depth: width ratios), laxity of gastric ligaments, defective eructation, advancing age, and delayed gastric emptying.13• 15 GDV traps gas and ingesta in the stomach causing a myriad of systemic consequences, including gastric ischemia, venous obstruction, cardiac dysfunction, poor tissue perfusion, shock, impaired respiration, and reperfusion injury. Diagnosis

The diagnosis is largely based on the history and clinical findings. Affected animals are typically large-breed, deep-chested dogs with an acute history of abdominal distension, depression, and retching. Abdominal palpation confirms marked gastric distension. Evidence of circulatory failure (tachycardia, weak pulses, poor capillary refill time) is usually evident. Laboratory tests reveal hemoconcentration and a variable acid-base status. Right lateral abdominal radiographs confirm GDV by showing compartmentalization of the stomach caused by displacement of the pylorus to the left of the midline and dorsal to the fundus (Fig. 7). Treatment

Cornerstones of therapy include gastric decompression, correction of metabolic disturbances (hypovolemia, electrolyte, and acid-base derangements), and anatomic repositioning (gastropexy). Aggressive intravenous fluid therapy (crystalloids such as lactated Ringer's solution administered at a rate of 90 mL/kg for 1-2 hours or plasma expanders such as hetastarch or dextran-70 administered at a rate of 20 mL/kg in dogs slowly to effect) is essentiaL Histamine H 2-

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Figure 7. Lateral abdominal radiographic view of gastric dilation volvulus in a dog. Note the dilated, air-filled stomach that appears compartmentalized due to dorsal displacement of the pylorus above the gastric fundus. Courtesy of Kristina G. Miles.

blockers (cimetidine, ranitidine) are administered to combat gastric ulceration. Antibiotics (ampicillin or cephalexin combined with amikacin) should be parenterally administered to septic dogs and those with GI necrosis. Free radical scavengers such as deferoxamine and allopurinol may protect abdominal organs against reperfusion injury. 28 Cardiac arrhythmias (premature ventricular contractions) are best treated with lidocaine hydrochloride (2-4 mg/kg administered intravenously slowly) or procainamide (12-20 mg/ kg administered intramuscularly every 6 hours). Surgery is performed as expeditiously as is possible and safe for the patient. Prognosis/Patient Monitoring

The prognosis in dogs with GDV is guarded. Mortality with acute GDV is high and ranges from 15% to 68%.5• 37 Factors associated with increased perioperative mortality in dogs with surgically managed GDV include gastric necrosis,

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gastric resection, splenectomy, and preoperative cardiac arrhythmias. 5 Complications are common during recovery from GDV and include cardiac arrhythmias, disseminated intravascular coagulation, and delayed gastric emptying. The diet should be modified to include daily multiple, small meals of a highly digestible, low-fat ration postoperatively.

Gastric Neoplasia Causes

The majority of neoplasms occurring in the gastric mucosa of dogs and cats are malignant.40 The most common malignant tumor in dogs is adenocarcinoma, with lymphosarcoma being the second most common. Lymphosarcoma is the most common malignant gastric tumor in cats. Aged dogs may also develop benign tumors such as adenomatous polyps and leiomyoma (smooth muscle tumor). Gastric neoplasia impairs gastric function by causing pyloric outflow obstruction (mass effect), disrupting mucosal integrity, or altering normal motility patterns responsible for gastric emptying. Diagnosis

Gastric neoplasia should be suspected in animals having chronic vomiting, anorexia, and weight loss. Other signs in dogs include hematemesis, abdominal pain, melena, and anemia caused by ulceration. Cats suspicious for gastric neoplasia should be screened for FeLV antigenemia and antibodies to FIV. Laboratory tests are nonspecific, although contrast radiography might reveal focal/ diffuse mucosal irregularities or evidence of ulceration. Ultrasonography may detect the presence of mesenteric lymphadenopathy and gastric mural thickening. Gastroscopy is the preferred diagnostic tool, where direct visual assessment and procurement of mucosal biopsies may be performed. Endoscopic characteristics of lesions of gastric neoplasia are variable but include ulceration/ erosion, friability, granularity, and the presence of mass lesions (Fig. 8). Multiple, deep mucosal biopsy specimens should be obtained to avoid histopathologic misdiagnosis of superficial inflammation.5 1 Thoracic radiographs should be performed to assess for evidence of thoracic metastasis when adenocarcinoma is suspected. Treatment

Adenocarcinomas are generally diffuse and have metastasized at the time of diagnosis, making surgical resection impossible. Reports of chemotherapy for canine adenocarcinoma have not been published. Gastric lymphosarcoma can be treated with combination chemotherapy using a cytoxan-oncovin-prednisone (COP) protocol. Treatment of gastric leiomyoma is by surgical excision and generally carries a good prognosis. 33 Prognosis/Patient Monitoring

The prognosis is poor for adenocarcinoma. Animals with lymphosarcoma warrant a guarded prognosis when treated with chemotherapy. The prognosis is excellent in animals with complete surgical excision of leiomyom a.

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Figure 8. Severe, focal ulceration involving the incisure angularis of a 12-year-old Chow Chow having intermittent hematemesis. Endoscopic mucosal biopsies obtained from the ulcer rim confirmed a diagnosis of gastric adenocarcinoma.

DISEASES OF THE SMALL INTESTINE Inflammatory Bowel Disease Causes

Inflammatory bowel disease (IBD) encompasses a group of idiopathic, chronic GI disorders in dogs and cats characterized by persistent signs of gastroenteritis and accompanied by histologic evidence of mucosal inflammation. Although the cause(s) for IBD remain unknown, there is general consensus that host hypersensitivity responses to antigens within the bowel lumen or mucosa are involved. 47 Potential initiating events of mucosal inflammation include increased intestinal permeability or aberrant mucosal immune responses to gut antigens. Classification of IBD is arbitrarily based on the predominant cellular infiltrate present (e.g., lymphocytic-plasmacytic, eosinophilic, suppurative, or granulomatous inflammation), with lymphocytic-plasmacytic enterocolitis diagnosed most frequently. Diagnosis

A diagnosis of IBD requires the following stringent diagnostic criteria: (1) persistent signs (> 2 weeks' duration) of gastroenteritis, (2) incomplete clinical response to dietary trials, (3) histologic diagnosis of inflammatory cellular infiltrates, and (4) failure to demonstrate other causes for gastrointestinal inflammation.22 Predominant clinical findings include chronic vomiting, diarrhea, anorexia, weight loss, and signs of large bowel d ysfunction (tenesmus, hematochezia, mucoid stools). Signs are often intermittent and cyclical. Physical examination is variable, as animals may be well fleshed with mild disease or may exhibit marked cachexia with severe lesions and those causing protein losing

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Causes of Gastrointestinal Mucosal Inflammation Dietary sensitivity Bacterial overgrowth Giardiasis

Toxoplasmosis Gastric nematodiasis Lymphangiectasia

Campylobacteriosis Alimentary neoplasia Gastric spirochetes?

enteropathy (PLE). Abdominal pain and thickened intestinal loops may be noted on abdominal palpation. Diagnosis of IBD is made by excluding other known causes for GI inflammation as found in the list on this page. Definitive diagnosis requires intestinal biopsy (preferably via endoscopic techniques) and histologic confirmation of mucosal cellular infiltrates (Fig. 9A, B). Treatment

Management of IBD varies widely and includes the use of controlled diets, immunosuppressive drugs, and bulking agents. A variety of diets that are highly digestible, antigen restricted, and contain a minimum of fat, lactose, and additives are available commercially. Most animals will require adjunctive therapy with immunosuppressive drugs to induce remission of s igns. Oral corticosteroids (e.g., prednisone) and metronidazole a re used most frequently for the therapy of canine and feline IBD. The use of more potent cytotoxic drugs such as azathioprine and cyclophosphamide is uncommonly required and should be reserved for use in refractory patients that fail to respond to traditional drug therapies. 20 Prognosis/ Patient Monitoring

The prognosis for IBD is good for control but poor for cure. Immunosuppressive drug dosages should be tapered gradually by 25% at 2-week intervals, and animals should be maintained on dietary therapy. Some animals will require intermittent high-dose or long-term, low-dose drug therapy for maintenance of remission. Protein Losing Enteropathy Causes

PLE refers to a variety of intestinal diseases that are associated with panhypoproteinemia caused by an excessive loss of plasma proteins into the GI lumen. The most important causes for PLE in older animals include mucosal inflammatory disorders (IBD, intestinal neoplasia, G I ulceration/ erosion, mycotic enteritis) and intestinal lymphangiectasia.48 Severe mucosal disease with protein leakage results from exudation, bleeding, or increased intestinal p ermeability. Lymphangiectasia occurs secondarily to obstruction of intestinal lymph drainage with reflux of protein-rich lymph into the gut. The occurrence of PLE is much greater in dogs than in cats. Diagnosis

The panhypoproteinemia (low albumin and globulins) characteristic of PLE must be clearly differentiated fr om the selective hypoalbuminemia seen with

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Figure 9. A, Endoscopic appearance of marked duodenal granularity in an 8-year-old dog with severe lymphocytic-plasmacytic enteritis. B, Duodenal histopathology from this dog showing a diffuse lamina propria! infiltrate of lymphocytes and plasma cells accompanied by multiple crypt abscesses (arrows).

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liver disease and protein losing nephropathy. Affected animals usually exhibit signs of weight loss, chronic watery diarrhea (with mucosal inflammation), vomiting, edema, and ascites. A routine database (complete blood count, biochemistries, urinalysis, serum bile acids) confirms panhypoproteinemia and eliminates liver disease and glomerular injury as causes for hypoalbuminemia. A diagnosis of PLE is suspected on the basis of history and physical examination but is confirmed only by intestinal biopsy (endoscopy or laparotomy) with histologic evaluation and interpretation. Treatment

Treatment is directed at correction of the underlying disease if identified. Many cases are idiopathic, prompting nonspecific dietary and drug therapy to reduce enteric protein loss. Animals should be fed high-quality protein, low-fat diets to facilitate digestion and to minimize intestinal lymph flow / loss into the gut. The caloric content of the diet may be increased by supplementation with medium chain triglyceride (MCT) oil. Oral corticosteroids (prednisone) are often useful in reducing mucosal inflammation seen with noninfectious enteropathies. Prognosis/Patient Monitoring

The prognosis for PLE is guarded to poor. Many animals are anorexic and severely protein-caloric depleted at the time of diagnosis. Those animals with correctable causes of mucosal inflammation should be treated for the specific cause. Animals with lymphangiectasia show a uniformly poor response to therapy in the author's experience.

Small Intestinal Neoplasia Causes

The majority of tumors in the small intestines of dogs and cats are malignant. In dogs, adenocarcinoma, lymphosarcoma, and leiomyosarcomas are most common, although lymphosarcoma and adenocarcinoma predominate in cats. The majority (70%) of affected cats with adenocarcinoma are Siamese.36 Benign adenomatous polyps of the duodenum have also been reported in cats.29 Diagnosis

Vomiting, anorexia, weight loss, and melena are the salient signs with malignant intestinal neoplasia. Physical examination may reveal a palpable abdominal mass or ascites in cats with adenocarcinoma and peritoneal metastasis.36 Routine laboratory tests rarely reveal significant findings. Survey I contrast radiographs may demonstrate a mass, mucosal irregularities suspicious for infiltrative disease, or radiographic evidence of intestinal obstruction. Ultrasonography is very useful for confirming mass lesions, mural thickenings, and mesenteric lymphadenopathy indicative of regional metastasis. 38 Thoracic radiographs are indicated to screen for pulmonary metastasis. Definitive diagnosis requires intestinal biopsy obtained via endoscopy, laparotomy, or ultrasound guidance.

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Treatment

Surgical resection of mass lesions (adenocarcinoma) is recommended. Cats with focal adenocarcinoma and evidence of metastatic disease (e.g., mesenteric lymphadenopathy) should still undergo surgery. 26 Alimentary forms of lymphosarcoma are treated with a combination chemotherapy protocol using doxorubicin, vincristine, cyclophosphamide, and prednisone. Prognosis/Patient Monitoring

The prognosis for focal lesions in which complete surgical excision can be performed is guarded to good. Animals having diffuse disease are generally poorly responsive to chemotherapy, although a subset of cats with alimentary lymphosarcoma may have long-term survivaJ.3° Further weight loss and debilitation in cachectic patients can be avoided by providing adjunctive enteral nutrition (gastrostomy or jejunostomy tube) at initiation of therapy.

Miscellaneous Causes tor Malabsorption

A variety of other less common but significant causes for malabsorption may affect the alimentary tract in geriatric dogs and cats. Exocrine Pancreatic Insufficiency

Exocrine pancreatic insufficiency (EPI) may occur secondarily to chronic pancreatitis and, rarely, to pancreatic neoplasia. The most reliable and sensitive test currently available for diagnosis of EPI is assay of serum trypsin-like immunoreactivity.55 Specific therapy entails dietary management and supplementation with pancreatic enzymes. Bile Salt Insufficiency

Because bile acids are responsible for normal digestion and absorption of dietary fat, a deficiency of bile salts will result in lipid malabsorption. Causes of bile salt insufficiency include inflammatory hepatobiliary diseases (e.g., cholecystitis, cholangiohepatitis) and extrahepatic biliary obstruction. Animals often manifest overt signs and laboratory evidence of hepatic dysfunction (icterus, elevated liver enzymes), and therapy is directed at the primary cause of the disorder. Small Intestinal Bacterial Overgrowth

Polymicrobial overgrowth in the gut lumen may occur secondarily to a variety of structural (obstruction) and functional (canine EPI) intestinal disorders. Both biochemical and morphologic injury to the small intestinal mucosa contribute to the pathogenesis of malabsorption seen with small intestinal bacterial overgrowth. 4 Diagnosis of small intestinal bacterial overgrowth is ideally based on bacteriologic confirmation of the offending flora from duodenal secretions.4 Therapy includes correction of the identifying cause and use of an antibiotic having a broad spectrum of activity such as oxytetracycline.

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DISEASES OF THE LARGE INTESTINE Chronic Idiopathic (Lymphocytic-Piasmacytic) Colitis Causes

Similarly to small intestinal IBD, the cause and pathogenesis for chronic idiopathic colitis are unknown. Immune mechanisms are theorized based on the similarities to ulcerative colitis in humans, the histologic appearance of mononuclear cellular infiltrates in involved tissues, and the beneficial therapeutic response generally observed with drugs that are known to alter immune responses such as corticosteroids, metronidazole, and sulfasalazine. Idiopathic colitis is the most common cause for chronic large bowel diarrhea in dogs and cats in the author's experience. Diagnosis

Affected animals show classic signs of large bowel dysfunction, including chronic intermittent tenesmus, mucoid feces, and hematochezia. Systemic signs of illness are not observed. Physical examination is usually unremarkable with the exception of rectal palpation which may reveal pain and fresh blood. The diagnostic workup is identical to that for small intestinal IBD with the exception that abdominal radiographs are less likely to provide useful information. Endoscopy with mucosal biopsy is the diagnostic tool of choice. Mucosal abnormalities observed during colonoscopy may include granularity, friability, loss of submucosal vascularity, and focal or diffuse erosive lesions (Fig. 10). Brush cytology is a useful adjunct to endoscopic biopsy in the diagnosis of colonic inflammatory disorders. 21 Histologic examination of endoscopic biopsy specimens confirms mucosal inflammation and accompanying colonic glandular changes.

Figure 10. Multiple, linear erosions involving the descending colonic mucosa in a 10-yearold dog having chronic vomiting and tenesmus. Endoscopic biopsy of these mucosal lesions confirmed a diagnosis of lymphocytic-plasmacytic and suppurative colitis.

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Treatment

Nutritional management and the use of immunomodulating drugs to reduce cellular infiltrates are cornerstones of therapy. An antigen-restricted, highly digestible diet divided into several meals daily should be fed. Dietary fiber (whether soluble or insoluble fiber is best remains to be determined) is also provided because it improves colonic motility, binds irritating substances, and promotes the production of beneficial volatile fatty acids such as butyrate. 41 Both oral corticosteroids and sulfasalazine are effective drugs in the management of canine IBD colitis. Disagreement exists concerning which drug(s) to use and the optimal duration of drug therapy for chronic colitis. The corticosteroid protocol outlined for small bowel IBD is generally appropriate for idiopathic colitis. Combination drug therapy using corticosteroids along with metronidazole or sulfasalazine will lessen steroid side effects. The use of more potent immunosuppressive drugs is rarely needed. Prognosis/Patient Monitoring

The prognosis for control is good. Drug therapy should be tapered gradually as outlined for small bowel IBD. Animals will likely require long-term dietary therapy (including fiber supplementation). Feline Constipation Causes

Constipation denotes infrequent or difficult passage of feces and is a common problem in middle-aged and older cats. Intractable constipation that fails to respond to therapy is referred to as obstipation, which may or may not progress to megacolon. Constipation is by far the most common of the clinical syndromes in the author's experience. A recently published excellent and thorough review53 indicates that in cats, the vast majority of cases of constipation/ obstipation are idiopathic, orthopedic (pelvic canal stenosis), or neurologic (nerve injury) in origin. Diagnosis

Affected cats usually present with a history of constipation. Systemic signs of depression, anorexia, weight loss, and vomiting are seen with long-standing cases. Abdominal palpation reveals marked colonic impaction of hard feces and, often, evidence of dehydration. Routine blood work and urinalysis should be performed to screen for metabolic causes of colonic hypomotility. Abdominal radiographs confirm the extent of fecal impaction and identify potential causes such as spinal abnormalities or pelvic fractures. A neurologic examination should be performed in cats suspected of having sacral spinal abnormalities. Treatment

Optimal therapeutic regimens for feline constipation have not been formulated. Principles of therapy utilized by this author include evacuation of impacted feces w ith tepid water enemas (5-10 mL/kg every 12 hours), use of dietary fiber (psyllium) as a bulking agent, administration of an emollient laxative (dioctyl sodium sulfosuccinate) to soften feces, and administration of

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lactulose to stimulate colonic fluid secretion and propulsive motility. Cisapride is also reported to be of benefit in cats with mild to moderate constipation by stimulating colonic motility and facilitating fecal elimination.53 Prognosis/Patient Monitoring

The prognosis in cats with mild to moderate constipation is good with aggressive medical therapy. Cats having severe constipation with systemic signs (depression, inappetence, vomiting, and dehydration) and cats with idiopathic megacolon warrant a poor prognosis. Colectomy should be considered the therapeutic modality of choice in these severely affected animals. 27 Colonic Neoplasia Causes

Adenocarcinoma and lymphosarcoma are the predominant malignant tumors affecting the large intestine in dogs and cats. Leiomyosarcomas may involve the canine cecum. Diagnosis

Tenesmus and hematochezia most often occur with colonic tumors. Signs may persist for weeks to months and may not be accompanied by systemic signs. Distal colonic and rectal adenocarcinomas may be readily palpable via rectal examination. The diagnostic evaluation is the same as for small intestinal neoplasia. Definitive diagnosis requires histologic evaluation of biopsy specimens obtained endoscopically. Treatment

Treatment is identical to that for small intestinal tumors. Surgical excision of localized mass lesions is recommended. Prognosis/Patient Monitoring

Alimentary lymphosarcoma has a guarded prognosis. Dogs with leiomyosarcomas and single, pedunculated colorectal adenocarcinoma may have long survival times following surgery. 6' 9 No adjunctive therapy for adenocarcinoma in cats has been reported. DISEASES OF THE LIVER

Due to the spectrum of potential diseases affecting the hepatobiliary system in aged dogs and cats, only the most salient will be succinctly reviewed. Canine Chronic Hepatitis Causes

Canine chronic hepatitis is characterized by chronic and progressive hepatocellular inflammation, regeneration, and fibrosis of unknown cause. Recent evi-

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dence suggests that liver-specific antibodies may contribute to the pathogenesis of tissue injury. 2 Continual hepatic inflammation often leads to cirrhosis and fulminant hepatic failure. Doberman Pinschers and Cocker Spaniels appear to be genetically predisposedY· 16 Diagnosis

Signs may be intermittent and chronic but indicate primary hepatic dysfunction. Specific signs include depression, anorexia, and vomiting. Ascites, icterus, and central nervous systems signs manifest in the later stages of the disease. Laboratory tests show increased alanine aminotransferase, serum alkaline phosphatase, total bilirubin, and serum bile acids. Hypoalbuminemia and a low blood urea nitrogen concentration are also frequently seen. Diagnostic imaging generally reveals a small liver size with a mixed echogenic parenchyma. Definitive diagnosis requires hepatic biopsy which shows inflammation, fibrosis, and, often, copper accumulation. Treatment

A multiregimen therapeutic plan should be initiated. The identifiable cause should be corrected if possible; a high-quality (normal protein, low residue) diet should be fed; corticosteroids (prednisone) should be used to reduce inflammation/fibrosis; hepatic encephalopathy should be managed with a special diet, metronidazole, and lactulose; and ascites should be controlled with sodium restriction and diuretics. Supplemental therapy may include the administration of antibiotics (for secondary infection), copper chelators (trientine, zinc), and ursodeoxycholic acid (for choleresis and immunomodulation). Prognosis/Patient Monitoring

The prognosis is guarded. The liver enzymes and bile acids should be reassessed periodically. Drugs used to treat ascites and hepatic encephalopathy should be modified accordingly. Feline Cholangitis-Cholangiohepatitis Syndrome Causes

Feline cholangitis-cholangiohepatitis (CCH) syndrome refers to a group of inflammatory hepatobiliary disorders that are characterized histologically into suppurative and nonsuppurative types. Disorders associated with CCS are varied but include biliary tract obstruction, bacterial infection, sepsis, IBD, pancreatitis, and cholecystitis? Diagnosis

Most cats with suppurative CCH present with acute (< 5 days) icterus, fever, vomiting/diarrhea, anorexia, and depression. 18 Cats with nonsuppurative CCH generally have a longer duration (e.g., several weeks) of illness. Palpable hepatomegaly is present in about 50% of all cats. Supportive laboratory abnormalities include elevated alanine aminotransferase, serum alkaline phosphatase, total bilirubin, serum bile acids, and serum globulins. Imaging reveals variable

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hepatomegaly and increased hepatic parenchymal echogenicity. Hepatic biopsy and histopathology are necessary to differentiate suppurative from nonsuppurative CCH. Aerobic/anaerobic cultures of hepatic biopsy specimens or biliary secretions should be performed in cats suspicious for suppurative CCH. Treatment

The biliary obstruction or other inciting cause should be corrected. Ursodeoxycholic acid is beneficial as a choleretic and immunomodulating agent. Antibiotics should be used based on culture/ susceptibility patterns in cats with suppurative CCH. Corticosteroids are used in cats with nonsuppurative CCH to reduce lymphocytic-plasmacytic infiltrates. Prognosis/Patient Monitoring

The prognosis in all cats is guarded. Mortality may be high in cats with suppurative CCH during the immediate postoperative period following surgical correction of biliary obstruction. Cats with nonsuppurative CCH often show incomplete remission on glucocorticoid therapy. Periodically (every 2-4 weeks), the veterinarian should reassess hepatic enzymes and bile acids as markers of hepatic inflammation/function.

Hepatic Lipidosis Causes

The cause of feline hepatic lipidosis is unknown. Excessive triglycerides may accumulate in the liver as a consequence of nutritional, metabolic, hormonal, toxic, or ischemic imbalances affecting lipid metabolism. 25 The disease syndrome is associated with acute hepatic failure. Diagnosis

Many cats are obese prior to the development of lipidosis. Prolonged partial/complete anorexia is a consistent clinical sign. Other signs include icterus, hepatomegaly, depression, vomiting, and weight loss. The history is often suggestive and is substantiated by elevation in alanine aminotransferase, serum alkaline phosphatase (marked), and total bilirubin. Diagnostic imaging confirms hepatomegaly with diffuse parenchymal hyperechogenicity. Hepatic biopsy or aspirate cytology confirms hepatocellular vacuolation. Treatment

Therapy is supportive, because the underlying cause(s) for lipidosis is rarely identified. Any hydration and electrolyte deficiencies that are present should be corrected. Aggressive nutritional support is the cornerstone of therapy. A gastrostomy tube placed endoscopically or surgically is typically used to deliver long-term (1- 3 months) nutritional therapy. A variety of balanced, caloric-dense, high-protein, commercial diets may be fed. Signs of HE should be treated as previously described. Vomiting caused by H E can be controlled with centrally acting antiemetics such as m etoclopramide.

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Prognosis/Patient Monitoring

The prognosis in most cases is good with aggressive medical (nutritional) therapy. 19 Periodically (weekly), the veterinarian should re-evaluate liver enzymes and body weight. Oral food should be offered daily. Cats should be carefully screened (via trypsin-like immunoreactivity [TLI] assay, ultrasonography, pancreatic biopsy) for concurrent pancreatic inflammation which can complicate recovery from hepatic lipidosis. 1 Glucocorticoid Hepatopathy Causes

Glucocorticoid hepatopathy is a disease in dogs characterized by diffuse glycogen deposition within hepatocytes. Hepatocyte vacuolation causes cellular swelling, sinusoidal compression, and diffuse hepatomegaly. It may be caused by chronic stress or illness, pharmacologic administration of glucocorticoids, or hyperadrenocorticism (most commonly).8 Diagnosis

The history may indicate chronic treatment with corticosteroids. Clinical signs of polyuria/ polydipsia, symmetrical alopecia, hepatomegaly, and muscle wasting support a diagnosis of Cushing's disease. Laboratory tests reveal relative polycythemia and marked elevation in SAP, cholesterol, and triglycerides. Hepatomegaly is confirmed via radiography or ultrasonography. The veterinarian should confirm the presence of and cause for hyperadrenocorticism by performing adrenal function tests. Treatment

Treatment is directed at the specific endocrine, metabolic, or inflammatory cause for the hepatopathy. Prognosis/Patient Management

Generally, a good prognosis is given for dogs with vacuolar hepatopathy caused by Cushing's disease that are treated appropriately. In these animals, the hepatopathy will resolve over several months' (6 months) duration. In another subset of Cushingnoid animals that receive no therapy or insufficient treatment, resolution of hepatic lesions will be incomplete. The veterinarian should monitor hepatic enzyme levels at 1- to 3-month intervals to assess response to therapy. Hepatobiliary Neoplasia Causes

The liver is affected by both primary and metastatic neoplasia. The most common primary tumor types in dogs are hepatocellular carcinomas and adenomas. Intrahepatic bile duct tumors (most are benign cystadenomas) are the most common primary histologic type diagnosed in cats. 35 Lymphosarcoma (usually due to multicentric disease) is also common in cats. The liver is much more

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likely to be affected by metastatic disease (due to its rich blood supply from the abdominal viscera) than by primary neoplasms. Diagnosis

Neoplasia should be considered in aged dogs and cats with nonspecific lethargy, anorexia, and weight loss. A palpable cranial abdominal mass is often evident on physical examination. Nonspecific hepatic enzyme elevations are evident on serum biochemistries. Thoracic radiographs are performed to screen for pulmonary metastasis. Abdominal radiographs reveal hepatomegaly or the presence of a focal hepatic mass causing asymmetry. Ultrasonography is useful in detecting the origin of the hepatic mass and in obtaining needle-guided biopsies of hepatic lesions for histologic evaluation. Treatment

Surgery (hepatic lobectomy) is the therapy of choice in dogs with solitary hepatic carcinomas. Dogs having diffuse hepatic neoplasia will respond variably to chemotherapy. More than one third of cats with solitary hepatic tumors have a benign tumor that can be cured with surgery. 39 Prognosis/Patient Monitoring

Dogs with solitary hepatocellular carcinomas and cats with benign hepatic tumors warrant a good prognosis with successful surgery. The prognosis is poor in animals having diffuse neoplastic disease. Hepatic lymphosarcoma is treated with a COP chemotherapy protocol as previously described. References 1. Akol KG, Washabau RJ, Saunders HM, et a!: Acute pancreatitis in cats with hepatic lipidosis. J Vet Intern Med 7:205, 1993 2. Armstrong PJ, Weiss DJ, Gagne JM: Inflammatory liver disease. In August JR (ed): Consultations in Feline Internal Medicine, ed 3. Philadelphia, WB Saunders, 1997, p 68 3. Batt RM, McLean L: Comparison of the biochemical changes in the ej junal mucosa of dogs with aerobic and anaerobic bacterial overgrowth. Gastroenterology 93:986, 1987 4. Batt RM, Needham JR, Carter MW: Bacterial overgrowth associated with a naturally occurring enteropathy in the German Shepherd dog. Res Vet Sci 35:42, 1983 5. Brourman JD, Schertel ER, Allen DA, et al: Factors associated with perioperative mortality in dogs with surgically managed gastric dilatation-volvulus: 137 cases (19881993). JAVMA 208:1855, 1996 6. Bruecker KA, Withrow SJ: Intestinal leiomyosarcomas in six dogs. J Am Anim Hasp Assoc 24:281, 1988 7. Center SA: Diseases of the gallbladder and biliary tree. In Guilford WG, Center SA, Strombeck DR, et al (eds): Strombeck's Small Animal Gastroenterology, ed 3. Philadelphia, WB Saunders, 1996, p 860 8. Center SA: Hepatic lipidosis, glucocorticoid hepatopathy, vacu olar hepatopathy, storage disorders, amyloidosis, and iron toxicity. In Guilford WG, Center SA, Strombeck DR, et a! (eds): Strombeck's Small Animal Gastroenterology, ed 3. Philadelphia, WB Saunders, 1996, p 766 9. Church EM, Mehlhaff CJ, Patnaik AK: Colorectal adenocarcinoma in dogs: 78 cases (1973-1984). JAVMA 191:727, 1987 10. Dent J, Dodds WJ, Hogan WJ, et a!: Factors that influence induction of gastroesophageal reflux in normal human subjects. Dig Dis Sci 33:270, 1988

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11. Diehl K, Rosychuk RAW: Feline gingivitis-stomatitis-pharyngitis. Vet Clin North Am Small Anim Pract 23:139, 1993 12. Franklin JE, Saunders GK: Chronic active hepatitis in Doberman Pinschers. Compend Cantin Educ Pract Vet 10:1247, 1988 13. Glickman LT, Glickman LW, Perez CM, et al: Analysis of risk factors for gastric dilatation and dilatation-volvulus in dogs. JAVMA 204:1465, 1994 14. Goldschmidt MH: Benign and malignant melanocytic neoplasms of domestic animals. Am J Dermatopathol 7:203, 1985 15. Hall JA, Willer RL, Seim HB, et al: Gross and histologic evaluation of hepatogastric ligaments in clinically normal dogs and dogs with gastric dilatation-volvulus. A m J Vet Res 56:1611, 1995 16. Hardy RM: Chronic hepatitis in Cocker Spaniels - another syndrome? In Proceedings of the American College of Veterinary Internal Medicine, Washington, DC, 1993, p 256 17. Harvey CE: Plasmacytic-lymphocytic stomatitis. In August JR (ed): Consultations in Feline Internal Medicine, vol 2. Philad elphia, WB Saunders, 1994, p 59 18. Hirsch VM, Doige CE: Suppurative cholangitis in cats. JAVMA 182:1223, 1983 19. Jacobs G, Cornelius L, Allen S, eta!: Treatment of idiopathic hepatic lipidosis in cats: 11 cases (1986-1987). JAVMA 195:635, 1989 20. Jergens AE: Current concepts in inflammatory bowel disease therapy. In Proceedings of the American College of Veterinary Internal Medicine, Lake Buena Vista, FL, 1995, p 769 21. Jergens AE, Andreasen CB, Hagemoser WA: The use of endoscopic cytology in the diagnosis o f gastrointestinal disease. J Vet Intern Med 11:115, 1997 22. Je rgens AE, Moore FM, Haynes JS, et a!: Idiopathic inflammatory bowel disease in dogs a nd cats: 84 cases (1987- 1990). JAVMA 201:1603, 1992 23. Jones BD, Jergens AE, Guilford WG: Diseases of the esophagus. In Ettinger SJ (ed): Textbook of Veterinary Internal Medicine, vol 2, ed 3. Philadelphia, WB Saunders, 1989, p 1255 24. Katz PO, Geisenger KR, Hassan M, et al: Acid-induced esophagitis in cats is prevented by sucralfate but not synthetic prostaglandin E. Dig Dis Sci 33:217, 1 988 25. Kelly WR: The liver and biliary system. In Jubb KVF, Kennedy PC, Palmer N (eds): Pathology of D omestic Animals, ed 4. New York, Academic Press, 1993, p 319 26. Kosovsky JE, Matthiesen DT, Patnaik AK: Small intestinal adenocarcinoma in cats: 32 cases (1978-1985). JAVMA 192:233, 1988 27. Kudisch M, Pavletic M: Subtotal colectomy with surgical stapling instruments via a trans-cecal approach for treatment of acquired megacolon in cats. Vet Surg 22:457, 1993 28. Lantz GC, Badylak SF, Hiles MC, et al: Treatment of reperfusion injury in dogs with experimentally induced gastric dilatation-volvulus. Am JVet Res 53:1594, 1992 29. MacDonald JM, Mullen HS, Moroff SD: Adenomatous polyps of the duodenum in cats: 18 cases (1985- 1990). JAVMA 178:479, 1993 30. Mahoney OM, Moore AS, Cotter SM, et a!: A limentary lymphoma in cats: 28 cases (1988- 1993). JAVMA 207:1593, 1995 31. Matros L, Jergens AE, Miles KG, et a!: Megaesophagus and hypomotility associated with esophageal leiomyoma in a dog. J Am Anim Hosp Assoc 30:15, 1994 32. Matz ME: Drug induced gastric hemorrhage, erosion, and ulceration. In Proceedings of the American College of Veterinary Internal Medicine, San Diego, 1992, p 75 33. McPherron MA, Wit hrow SJ, Seim HB, et al:Colorectal leiomyomas in seven dogs. J Am Anim Hosp Assoc 28:43, 1992 34. Moreland KJ: Ulcer disease of the upper gastrointestinal tract in small animals: Pathophysiology, diagnosis, and management. Compend Contin Educ Pract Vet 10:1265, 1988 35. Patnaik AK: A m orphologic and immunocytochemical study of hepatic neoplasms in cats. Vet Pathol 29:405, 1992 36. Patnaik AK, Liu S-K, Johnston GF: Feline intestinal adenocarcinoma: A clinicopathologic study o f 22 cases. Vet Pathol 13:1, 1976 37. Pass M, Johnston D : T eatment r of gastric dilatation and torsion in the dog. J S mall Anim Pract 14:131, 1973

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38. Penninck DG, Nyland TG, Kerr LY, et a!: Ultrasonographic evaluation of gastrointestinal diseases in small animals. Vet Radio! 31:134, 1990 39. Peterson SL: Intrahepatic biliary cystadenoma in a cat. Feline Pract 14:29, 1984 40. Priester WA, McKay FA: The occurrence of tumors in domestic animals. National Cancer Institute Monograph 54. US Department of Health and Human Services, Bethesda, MD, 1980 41. Reinhart D, Lebenthal E: Intestinal mucosal energy metabolism - a new approach to therapy of gastrointestinal disease. J Pediatr Gastroenterol Nutr 10:1, 1990 42. Rolfe DS, Twedt DC, Seim HB: Chronic regurgitation or vomiting caused by esophageal leiomyoma in three dogs. JAm Anim Hosp Assoc 30:425, 1994 43. Shelton GD, Willard MD, Cardinet GH, eta!: Acquired myasthenia gravis: Selective involvement of esophageal, pharyngeal, and facial muscles. J Vet Intern Med 4:281, 1990 44. Stebbins KE, Morse CE, Goldschmidt MH: Feline oral neoplasia: A ten year survey. Vet Pathol 26:121, 1989 45. Strombeck DR, Guilford WG: Diseases of swallowing. In Strombeck DR, Guilford WG (eds): Small Animal Gastroenterology, ed 2. Davis, Stonegate Publishing, 1990, p 140 46. Strombeck DR, Harrold D: Effects of atropine, acepromazine, meperedine, and xylazine on gastroesophageal sphincter pressure in the dog. Am J Vet Res 46:963, 1985 47. Strombeck DR, Guilford WG: Idiopathic inflammatory bowel diseases. In Strombeck DR, Guilford WG (eds): Small Animal Gastroenterology, ed 2. Davis, Stonegate Publishing, 1990, p 357 48. Tams TR, Tewdt DC: Canine protein-losing gastroenteropathy syndrome. Compend Contin Educ Pract Vet 3:105, 1981 49. Tams TR: Cisapride: Clinical experience with the newest GI prokinetic drug. In Proceedings of the American College of Veterinary Internal Medicine, San Francisco, 1994, p 100 . 50. Tams TR: Esophagoscopy. In Tams TR (ed): Small Animal Endoscopy. Mosby Yearbook, St. Louis, 1990, p 47 51. Tams TR: Gastroscopy. In Tams TR (ed): Small Animal Endoscopy. Mosby Yearbook, St. Louis, 1990, p 89 52. Washabau RJ, Hall JE: Cisapride. JAVMA 207:1285, 1995 53. Washabau RJ, Hasler AH: Constipation, obstipation, and megacolon. In August JR (ed): Consultations in Feline Internal Medicine, ed 3. Philadelphia, WB Saunders, 1997, p 104 54. White SD, Rosychuk RAW, Janik TA, et al: Plasma cell stomatitis-pharyngitis in cats: 40 cases (1973-1991). JAVMA 200:1377, 1992 55. Williams DA, Batt RM: Sensitivity and specificity of radioimmunoassay of serum trypsin-like immunoreactivity for the diagnosis of canine exocrine pancreatic insufficiency. JAVMA 192:195, 1988 56. Withrow SJ: Esophageal cancer. In Withrow SJ, MacEwen EG (eds): Clinical Veterinary Oncology. Philadelphia, JB Lippincott, 1989, p 190

Address reprint requests to Albert E. Jergens, DVM, MS Department of Veterinary Clinical Sciences College of Veterinary Medicine Iowa State University Ames, IA 500ll