key: cord-0040565-60hxcrr3
authors: Moore, Lisa E.
title: Diseases of the Stomach
date: 2009-05-15
journal: Handbook of Small Animal Practice
DOI: 10.1016/b978-1-4160-3949-5.50035-2
sha: 271f085395507c70cc5cdc5fa17a91b759ee4e00
doc_id: 40565
cord_uid: 60hxcrr3

nan

Diseases of the Stomach | Lisa E. Moore 339 V. Nuclear scintigraphy may also be used to identify delayed gastric emptying. VI. Abdominal ultrasonography can be used to detect thickening of the pylorus. VII. Endoscopy may be normal if the mucosa is not thickened. VIII. At surgery, the pylorus is palpably thickened, and gastrotomy reveals a thickening of the muscular layer.

I. Other causes of mechanical pyloric outfl ow obstruction: mucosal hypertrophy, intraluminal masses (e.g., polyps, neoplasia, foreign bodies) II. Causes of a functional delay in emptying: electrolyte disorders, pain, peritonitis, acute pancreatitis, dysautonomia, gastric ulceration

I. After the animal has been stabilized with appropriate fl uid and electrolyte therapy, the defi nitive treatment is surgery. II. Surgical procedures include pyloromyotomy or various pyloroplasty techniques. III. Prognosis following adequate surgical correction is good.

I. Parasites affecting the stomach of cats include Ollulanus tricuspis and Physaloptera spp. (less common). II. Gastric parasites of dogs include Physaloptera spp. III. Parasites attach to the gastric mucosa, causing infl ammation and gastritis.

I. Infections in both dogs and cats may be inapparent. II. Intermittent vomiting is the most common clinical sign. III. Variable anorexia may also occur.

I. Ollulanus spp. can be diffi cult to diagnose.

A. The parasites and eggs are usually missed on routine parasitologic (usually not passed in the feces) and endoscopic (very small in size) examinations.

I. It is a congenital disease of boxers and Boston terriers. II. Stenosis of the pyloric canal occurs from hypertrophy of the pyloric circular muscle.

I. The cause is unknown, but an oversecretion of gastrin has been postulated. II. A functional abnormality has also been proposed, as some animals with pyloric outfl ow obstruction do not have muscular thickening.

I. Stenosis of the pyloric canal causes gastric outfl ow obstruction. II. Elevated levels of gastrin can lead to thickening of the pyloric smooth muscle from its trophic effects. III. Gastrin can also lead to hypertrophy of the mucosa, which can worsen the outfl ow obstruction.

I. Clinical signs are related to delayed gastric emptying. II. Generally, animals vomit food >12 hours after eating.

A. The vomiting may be explosive. B. The food in the vomitus is usually digested, but may appear undigested. III. Abdominal distention may be noted. IV. Weight loss may occur from inability to retain food. V. Anorexia is uncommon.

I. Pyloric outfl ow obstruction is suspected based on the pattern of vomiting. II. Laboratory fi ndings may show hypokalemia, hypochloremia, and metabolic alkalosis. III. Plain radiography often shows a stomach distended with gas and fl uid. IV. Contrast radiography may show delayed gastric emptying and a narrowing of the pyloric canal that is referred to as the beak sign.

B. The best method of diagnosis is microscopic examination of the vomitus. C. Organisms may also be seen on histopathology. D. Chronic hypertrophic fi brosing gastritis may also be seen on histopathology. II. Diagnosis of Physaloptera spp. is a little easier.

A. Eggs may be found on fecal fl otation, but may not be routinely isolated. B. The parasites can be seen with endoscopy and appear as 1-to 4-cm-long, white worms attached to the stomach.

I. Other causes of acute gastritis (see below) II. Causes of chronic and secondary gastritis Treatment and Monitoring I. Ollulanus spp.: fenbendazole 10 mg/kg PO SID for 3 days II. Physaloptera spp.: pyrantel pamoate 5 mg/kg PO for two doses, 3 weeks apart III. Prognosis is excellent for recovery after treatment.

I. Helicobacter gastritis is infl ammation of the stomach caused by various species of the genus Helicobacter. II. Many cats and dogs that have colonization of the stomach with these spiral organisms do not have concurrent infl ammation.

I. The organisms are spiral-shaped, gram-negative, motile bacteria. II. Various species have been isolated from the stomachs of cats, dogs, ferrets, cheetahs, and others. III. Helicobacter heilmannii and Helicobacter felis are the most common species that naturally occur in dogs and cats. IV. Helicobacter pylori has been found in laboratory cats, but not in dogs. V. These bacteria may be normal inhabitants of the stomach.

I. The pathophysiology of this disease is unclear. II. The organisms produce urease (urea ˜ NH 3 + HCO 3 ) that buffers acid and allows colonization of the superfi cial mucus and gastric glands of the stomach. III. The bacteria have been observed intracellularly. IV. In infected animals, degeneration of gastric glands, as well as vacuolation and necrosis of parietal cells, has been seen. A. The infl ammation is generally mononuclear (lymphocytes, plasma cells) and can vary in the degree of severity. B. Lymphoid follicle hyperplasia can be seen. V. Infected animals may have up-regulation of various cytokines.

I. Chronic vomiting is the most common sign. II. Diarrhea, anorexia, pica, and polyphagia have also been reported. III. Uncommonly, fever and/or bloody diarrhea may be seen.

I. Laboratory tests are usually normal, but may show nonspecifi c changes (e.g., stress leukogram). II. Abdominal radiography and ultrasonography are usually normal. III. The best method of diagnosis currently is endoscopic biopsy.

A. Organisms can be visualized on the epithelium or in the mucus layer. B. Warthin-Starry silver stains enhance visualization of the organisms. C. Multiple biopsy samples are taken as the colonization can be patchy. D. Endoscopy also allows evaluation of the mucosa for the type and severity of infl ammation and for other changes. IV. The rapid urease test may be performed and is based on the production of urease by almost all Helicobacter spp. A. The test is also known as the Campylobacter-like organism (CLO) test. B. Gastric tissue is incubated in broth with a pH indicator (phenol red) so that a color change indicates production of ammonia via urease. C. The degree of color change is proportional to the density of organisms. D. Results are available in 1 to 24 hours. E. This test has a sensitivity of 70% to 90% (Happonen et al., 1996) . V. Brush cytology of gastric mucus is a relatively sensitive method of detecting organisms but does not allow determination of whether infl ammation is present. VI. Culture is not usually performed because the organisms are hard to grow in the laboratory. VII. The C13 urea breath test also has been used in dogs and cats; however, it is not widely available. VIII. Polymerase chain reaction (PCR) assays of gastric tissue allows diagnosis as well as identifi cation of the species present; however, it is not widely available. IX. Serological testing is widely used as a screening test in humans, but tests designed for humans should not be used in dogs and cats because the primary organism affecting humans (H. pylori) is not generally found in dogs or cats. X. Serological testing is also diffi cult in animals because multiple species of Helicobacter may occur.

I. Other causes of chronic vomiting: chronic gastritis, pyloric outfl ow obstruction II. Vomiting caused by nongastrointestinal diseases Treatment I. The best therapy has yet to be identifi ed in the dog and cat. II. "Triple therapy" is recommended in symptomatic humans and involves administration of an acid-inhibiting drug, bismuth compounds, and an antibiotic (e.g., clarithromycin, amoxicillin). III. Most of the therapies tried in dogs and cats have not been 100% successful; many animals, although initially cleared of the organism, become reinfected. IV. Combinations that have been tried include the following:

A. Metronidazole, amoxicillin, and famotidine B. Azithromycin, tinidazole, bismuth, and ranitidine C. Clarithromycin, metronidazole, bismuth, and ranitidine D. Amoxicillin, metronidazole, and omeprazole E. Amoxicillin, metronidazole, and clarithromycin V. Therapy is usually given for 2 to 3 weeks.

I. Monitoring is generally via physical examination and clinical signs. II. To defi nitively determine if the organisms have been cleared, invasive testing may need to be repeated, but this is usually not done if the clinical signs resolve.

I. Gastric pythiosis in dogs is caused by the aquatic oomycete Pythium insidiosum. II. It has been documented only as a cutaneous and subcutaneous infection in cats; however, unpublished information indicates it can occur rarely as a gastrointestinal (GI) infection in cats. III. The organism may dwell in water or soil. IV. In the United States, the infection occurs most commonly in the Gulf Coast states, but it has been recognized as far north as New Jersey and Illinois, and as far west as Oklahoma, Missouri, and Kansas.

I. Pythiosis occurs most commonly in young, male, largebreed dogs-especially outdoor, working dogs. A. Affected dogs are usually exposed to areas of warm, fresh water. B. The animals are usually immunocompetent. II. The infective form is likely the zoospore and may cause infection by encysting in damaged GI mucosa. III. Infection is characterized by severe transmural thickening of the stomach, and the gastric outfl ow tract is one of the most common sites of infection. IV. Infl ammation is usually in the submucosa, with variable mucosal ulceration. V. The disease may extend through to the serosal surface, and associated lymph nodes may be enlarged.

I. Severe weight loss and vomiting are common. II. Lethargy is not usually seen unless obstruction has occurred. III. Diarrhea and hematochezia may be seen when other parts of the GI tract are involved.

I. Laboratory abnormalities may include eosinophilia, anemia, hyperglobulinemia, and hypoalbuminemia. II. Abdominal radiography and ultrasonography reveal thickening of the gastric (usually pyloric) wall. III. Associated lymphadenopathy also is usually seen on ultrasonography. IV. Defi nitive diagnosis requires identifi cation of the organism. V. Cytology of aspirates of enlarged lymph nodes or thickened stomach wall shows pyogranulomatous, suppurative, or eosinophilic infl ammation, but the organism is seen only occasionally. VI. A presumptive diagnosis can be made based on histopathology.

A. Findings include granulomatous, eosinophilic to pyogranulomatous infl ammation with fi brosis. B. Organisms are usually found in the center of granulomas or in areas of necrosis. C. The organisms are easier to visualize with Gomori's methamine silver (GMS) staining. D. Immunohistochemistry techniques may also be used. VII. Culture of the organism is diffi cult unless special sample handling and culture techniques are used. VIII. A serological enzyme-linked immunosorbent assay (ELISA) has been developed for the detection of antibodies and is highly sensitive and specifi c in dogs and cats. IX. Western immunoblot analysis also can be used.

I. Gastric neoplasia II. Hypertrophic gastritis III. Other systemic fungal infections.

A. The organisms may not be present in enlarged lymph nodes, so they are not routinely resected. B. Medical therapy for 2 to 3 months (as follows) is recommended following resection because of the possibility of recurrence. II. If resection is not possible, antifungal therapy can be tried.

A. Response is often poor, but up to 15% of dogs may respond (Grooters, 2003) . B. Itraconazole 10 mg/kg PO SID and terbinafi ne 5 to 10 mg/kg PO are recommended for 6 to 9 months. C. Alternatively, amphotericin B lipid complex is given at 2 to 3 mg/kg IV QOD up to a cumulative dose of 24 to 27 mg/kg.

I. It is infl ammation of the stomach that has an acute onset. II. It implies that the cause and the infl ammation can be eliminated, so that the stomach returns to normal health, with no residual infl ammation or fi brosis.

I. Ingestion of pathogenic bacteria rarely cause gastritis because they are usually unable to colonize the stomach. II. The main exception is the spiral bacteria (Helicobacter spp., see Helicobacter gastritis). III. Viruses (e.g., parvovirus, distemper virus, coronavirus) may cause gastritis as part of a more widespread condition. IV. Bacterial toxins produced by Clostridium spp., Escherichia coli, and Klebsiella spp. have been suggested. V. Physical damage from foreign bodies and thermal injury can result in gastritis. VI. Chemicals, such as cleaning agents, fl oor fi nishes, and various plant toxins, are also potential causes. VII. Certain drugs (aspirin) may be directly cytotoxic to the stomach, whereas others exert their toxic effects by indirect mechanisms. VIII. Garbage ingestion is a common cause of acute gastritis in dogs. IX. Many metabolic diseases cause gastritis (e.g., renal and hepatic failure, hypoadrenocorticism).

I. Acute vomiting is the most common clinical sign, especially after eating or drinking. II. Blood is occasionally present in vomitus. III. Varying degrees of anorexia, depression, and abdominal pain may also be noted. 5. Serotonergic 5HT 4 agonists a. Sites of action are the myenteric neurons. b. They are used primarily for delayed gastric emptying, rather than as an antiemetic. c. An example is cisapride (Propulsid) 0.1 to 0.5 mg/ kg PO BID to TID (dog, cat). 6. Motilin agonists a. Site of action is the GI smooth muscle (motilin receptors). b. They are used for delayed gastric emptying, rather than as an antiemetic. c. Side effects include vomiting. d. An example in the dog is erythromycin 0.5 to 1 mg/kg PO, IV TID. V. Inhibition of gastric acid secretion is usually not needed;

however, H 2 blockers may be used if gastric bleeding is noted (see next section). VI. Antibiotics are not indicated unless a specifi c bacterial pathogen is suspected or documented, or disruption of the gastric mucosal barrier is signifi cant. VII. Locally acting protectants (sucralfate, bismuth subsalicylate) are usually not needed, but may be used safely if desired (see next section).

I. Ulceration may be acute and caused by chemicals, gastric dilatation-volvulus, drugs, disseminated intravascular coagulation (DIC), shock, or foreign bodies. II. Ulcers may arise with chronic disorders, such as infl ammatory bowel disease (IBD), neoplasia, renal failure (acute or chronic), and hepatic failure. III. The most common causes include nonsteroidal antiinfl ammatory drugs (NSAIDs), neoplasia, shock, renal and hepatic failure, and hypoadrenocorticism.

I. NSAIDs inhibit prostaglandin production, which results in loss of an important part of the gastric mucosal barrier. A. Certain drugs (aspirin) can be directly cytotoxic to the epithelial cells. B. Risk factors for ulcer formation include higher doses, long-term administration, and concurrent administration with another NSAID or a corticosteroid. II. Certain neoplasms commonly cause gastric ulceration.

A. Mast cell tumors release histamine, which causes an increase in H + production. B. Gastrinomas release gastrin, which also results in increased H + production. III. Shock results in disruption of blood fl ow to the stomach, leading to ischemia and ulceration. IV. Renal and hepatic failure causes abnormal metabolism of gastrin (among other substances), with increased production of H + . V. In the preceeding situations, reparative mechanisms of the mucosa are overwhelmed and superfi cial damage (erosions) occurs, or severe lesions that penetrate to the muscularis or deeper (ulcers) develop.

I. Clinical signs are variable, with vomiting being the most common. II. The vomitus may contain fresh or digested blood ("coffee grounds"). III. Anorexia may be noted. IV. Abdominal pain can occur that may be ameliorated by food (from buffering action of food). V. Animals may develop acute abdominal pain from gastric perforation and peritonitis, with few or no prior clinical signs.

I. Laboratory fi ndings may be normal. II. The cause of ulceration may be detected by laboratory fi ndings (e.g., azotemia, hepatic failure). III. Acute or chronic microcytic, hypochromic anemia may be seen. IV. Abdominal ultrasonography reveals changes in the gastric wall consistent with ulceration and focal or diffuse accumulation of peritoneal fl uid if a perforation is present. V. Any free abdominal fl uid may be sampled with ultrasound guidance. VI. Defi nitive diagnosis requires visualization of the ulceration/ erosion via endoscopy.

I. Other causes of vomiting II. Other causes of GI bleeding and melena, including thrombocytopenia and other clotting disorders Treatment I. Treat any underlying conditions and stabilize the animal with appropriate fl uid therapy, electrolyte replacement, and transfusion therapy as necessary. II. If the animal is receiving a drug that may cause an ulceration, discontinue the drug. III. Institute specifi c treatment with antacids.

A. Acid neutralizers 1. These agents neutralize acid that has already been produced by the stomach. 2. They can be very effective, but must be given at least six times per day.

Magnesia), aluminum hydroxide (Amphojel), and calcium carbonate (Tums). 4. Aluminum-containing antacids decrease absorption of phosphorus and may stimulate mucosal defense mechanisms. 5. Calcium-containing antacids may cause constipation. B. H 2 -receptor antagonists 1. These agents selectively and reversibly bind to H 2 receptors on the oxyntic cell, thus inhibiting the acid secretagogue effect of histamine.

2. Although these drugs only partially inhibit acid secretion, they often allow healing to occur. 3. Cimetidine (5 to 10 mg/kg PO, SC TID to QID in dogs and cats) reversibly inhibits the hepatic microenzyme system (cytochrome P-450), and can interfere with clearance of drugs metabolized by this route. 4. Ranitidine may be six to ten times more potent than cimetidine. a. Ranitidine inhibits microsomal enzymes less than cimetidine. b. Ranitidine may have gastric prokinetic properties. c. Dose is 1 to 4 mg/kg PO, SC, IV BID to TID (dogs and cats). 5. Famotidine has potency similar to ranitidine in dogs, with a longer elimination half-life. a. Dose in dogs is 0.5 mg/kg PO, SC, IV SID to BID b. Dose is not established for cats. C. Proton pump antagonist 1. These drugs irreversibly inhibit the hydrogenpotassium-ATPase pump at the apical border of the oxyntic cells. 2. A single daily dose results in virtual antacidity. 3. They also inhibit hepatic microsomal enzymes similar to cimetidine. 4. They are superior to H 2 blockers for treatment of severe refl ux esophagitis and indolent gastroduodenal ulceration in dogs. 5. Dose of omeprazole is 0.7 to 2 mg/kg PO SID in dogs; very little experience exists in cats. IV. Gastric protectants are also useful.

A. Misoprostol is a synthetic prostaglandin E1 analog that inhibits gastric acid secretion and stimulates gastric mucosal defense mechanisms in dogs. 1. Its primary therapeutic use is prophylaxis against gastric mucosal injury caused by NSAIDS. 2. Its main adverse effect is diarrhea. 3. Do not use it in pregnant animals, and do not allow pregnant women to handle it (can cause abortion). 4. Dose in dogs is 1 to 5 mg/kg PO BID to TID. B. Sucralfate is a complex salt of sucrose sulfate and aluminum hydroxide. 1. In an acidic environment, sucralfate binds to exposed submucosa and polymerizes. 2. Its primary action is to stimulate mucosal defense and reparative mechanisms, as well as inhibit pepsin activity. 3. Sucralfate stimulates bicarbonate and mucus secretion, increases the viscosity of gastric mucus, and stimulates the release of prostaglandins (facilitates mucosal blood fl ow and repair). 4. It is not absorbed from the GI tract, but may inhibit absorption of other drugs. 5. It may cause constipation. 6. Dose is 0.25 to 1 g PO BID to QID in dogs and 0.125 to 0.25 g PO BID to TID in cats.

C. Bismuth subsalicylate (Pepto-Bismol) has cytoprotective properties by complexing with glycoproteins to retard hydrogen ion diffusion through the mucosa and by decreasing pepsin output. 1. It also has antibacterial activity. 2. Dose in dogs is 0.5 to 1 mL/kg PO every 4 to 8 hours.

3. It must be used with caution in cats because of the salicylate component (0.25 mL/kg PO BID). V. Antiemetics are used as needed (see Acute Gastritis). VI. Prokinetic agents enhance GI motility, specifi cally gastric emptying.

A. Metoclopramide has antiemetic and prokinetic properties. 1. It increases gastroesophageal sphincter (GES) pressure and hastens gastric emptying. 2. Dose in both dogs and cats is 0.2 to 0.4 mg/kg PO, SC, IM TID to QID or 2 mg/kg/day IV as a constant rate infusion. B. Cisapride has prokinetic and antiemetic effects, but is used primarily as a prokinetic agent. 1. It increases GES pressure, accelerates gastric emptying, enhances colonic propulsive motility, and probably enhances motility of the small intestine. 2. Dose in both dogs and cats is 0.1 to 0.5 mg/kg PO BID to TID. 3. Cisapride is available through a few compounding pharmacies. C. Erythromycin has an action similar to endogenous motilin, as well as an antiemetic action. 1. It accelerates gastric emptying and has intestinal promotility affects. 2. Dose is 0.5 to 1 mg/kg PO, IV TID in dogs. D. Ranitidine and nizatidine may stimulate gastric, intestinal, and colonic motility, but their clinical effi cacy is unknown. VII. Uncommonly, gastric ulcers may bleed profusely or may be so deep that perforation is imminent, making partial gastrectomy and resection of the affected area necessary.

I. Laboratory tests are repeated to ensure that electrolytes have normalized and anemia (if present) is stable or improving. II. Endoscopy can be repeated to determine defi nitively if the ulceration has healed, but is not usually done unless clinical signs persist.

I. It is defi ned as chronic infl ammation of the stomach where no cause can be found. II. The condition may be immune-mediated, and is considered a form of IBD that is localized to the stomach. III. Postulated causes include food allergy, loss of tolerance to bacterial (normal fl ora) antigens, genetic susceptibility, or an abnormal immune response (host hypersensitivity).

I. The pathophysiology of IBD is complex and poorly understood. II. Chronic gastritis is a diagnosis of exclusion. III. Histopathologic fi ndings include occasional microerosions of the epithelium, infi ltration of the interstitium with lymphocytes, plasma cells or eosinophils. A. Fibrosis of gastric tissue is seen after prolonged, untreated infl ammation. B. Lesions can be patchy or diffuse. IV. In cats, eosinophilic gastritis may be seen as part of a more generalized disease (hypereosinophilic syndrome).

I. Vomiting is the most common clinical sign. II. Mild weight loss is seen less commonly. III. Variable anorexia and depression may occur.

I. Laboratory tests are usually normal or show nonspecifi c changes (e.g., stress leukogram, eosinophilia). II. Abdominal radiographs are usually normal. III. Abdominal ultrasonography may show a thickened stomach wall and/or enlargement of gastric lymph nodes. IV. Known causes of gastritis must be excluded.

A. Negative fecal examination and no response to deworming B. No history of NSAID use V. Gastric biopsy is necessary for defi nitive diagnosis.

A. Endoscopic biopsies are often adequate. B. Biopsies also may be obtained via exploratory laparotomy. VI. At endoscopy, the mucosa may appear grossly normal, granular, friable, hyperemic, edematous, or eroded.

I. Other causes of primary gastritis: food intolerance, parasites, foreign body II. Other causes of secondary gastritis: renal or hepatic failure, hypoadrenocorticism Treatment I. Treatment often involves a combination of dietary changes and/or drug therapy. II. Feed small, frequent meals of a low-fi ber, low-to-moderatefat diet to hasten gastric emptying. III. Diets can be of three types.

A. An easily and highly digestible commercial diet or a home-cooked diet can be prepared. B. A novel protein diet can be tried. C. A hypoallergenic diet consisting of hydrolyzed protein sources can be tried. D. The dietary change may be effective alone, or may be used in combination with drug therapy. IV. Antiinfl ammatory or immunosuppressive drugs are indicated if nutritional management alone does not control the clinical signs.

A. Give prednisone at 2 mg/kg PO SID for dogs and 2 to 4 mg/kg PO SID for cats for 2 to 4 weeks, then gradually tapered over 3 to 6 months. B. Some animals may be weaned completely off corticosteroids, whereas others must remain on chronic low doses (usually 0.5 to 1 mg/kg PO QOD). V. If the animal is refractory to steroid therapy, relapses, or has unacceptable side effects, alternative drugs may be needed. A. Metronidazole may be helpful. B. Other options include azathioprine or cyclosporine in dogs and chlorambucil or cyclosporine in cats. VI. Mucosal protectants are used as needed if erosions are present. VII. Inhibition of gastric acid secretion with H 2 blockers or a proton pump inhibitor may be benefi cial. VIII. Prokinetic agents may be of value if delayed gastric emptying is a concurrent problem.

I. Repeat laboratory tests to ensure that the animal is stable.

A. Some animals with severe idiopathic gastritis may have gastric bleeding, so the monitor the packed cell volume (PCV). B. Some animals may develop side effects (e.g., diabetes mellitus) secondary to corticosteroid use, so monitor blood glucose as well. II. Repeat endoscopy and biopsy to defi nitively determine if the infl ammation is under control; however, they are not usually done unless clinical signs persist.

I. It is a very uncommon condition. II. The etiology is unknown, but it may be immune-mediated or the terminal stage of idiopathic gastritis.

I. The pathophysiology is unknown. II. Histopathology shows a reduced gastric mucosal parenchyma (loss of glands and cells), some infl ammatory cells (lymphocytes and plasma cells), fl attened epithelium, shortened gastric pits, metaplastic cells, and fi brosis. III. Achlorhydria (loss of ability to produce H + ) often results and leads to small intestinal bacterial overgrowth, which in turn may lead to malabsorption.

I. Intermittent vomiting is the most common clinical sign. II. Mild weight loss may be seen, and anorexia and depression may occur.

I. Laboratory tests are usually normal, but may show nonspecifi c changes (e.g., stress leukogram). II. Abdominal radiographs and ultrasonography are usually normal.

III. Endoscopy with biopsy is the method of choice for diagnosis. IV. The mucosa may appear grossly normal or discolored and thin (more common), with submucosal blood vessels visible under the mucosa. A. Prednisone is given at 1 to 2 mg/kg PO SID for 2 to 3 weeks then gradually tapered over 3 to 6 months. B. Additional antiinfl ammatory agents are uncommonly needed.

I. Laboratory monitoring is done for side effects secondary to corticosteroid use (e.g., blood glucose, alkaline phosphatase). II. Endoscopy and biopsy can be repeated to determine defi nitively if the infl ammation is under control, but are not usually done unless clinical signs persist.

I. Hypertrophic gastritis is characterized by focal or diffuse mucosal proliferation along with infl ammation. II. In the focal form, polypoid lesions may occur. III. Widespread mucosal thickening is less common.

I. The etiology of this uncommon condition is unknown. II. Genetics may play a role because it is more common in smallbreed dogs (e.g., Lhasa apso, shih tzu, Maltese, basenji). III. An immune-mediated cause has also been postulated. IV. Male dogs are predisposed.

I. The pathophysiology is unknown, but hypergastrinemia may be involved, as gastrin is trophic to the gastric mucosa. II. Histopathology shows hypertrophy and hyperplasia of the mucosa, metaplasia of glandular epithelium, and variable amounts of fi brous tissue and infl ammatory cells (lymphocytes, plasma cells).

I. Intermittent vomiting is the most common clinical sign. II. Mild weight loss may be seen with variable anorexia and depression.

I. Laboratory tests and abdominal radiographs are usually normal or show nonspecifi c changes (e.g., stress leukogram). II. On endoscopy the mucosa is diffusely or focally thickened, usually in the area of the antrum, and biopsy confi rms the diagnosis. III. Measurement of serum gastrin concentration is done to rule out a gastrin-secreting tumor.

I. Other GI causes of vomiting: food intolerance, parasites, foreign body. II. Non-GI causes of vomiting: renal or hepatic failure, hypoadrenocorticism.

I. Change the diet to small, frequent meals of an easily digested diet, or try a novel protein diet. II. Mucosal protectants may be benefi cial if erosions are present. III. Inhibition of gastric acid secretion with H 2 blockers or a proton pump inhibitor may be helpful. IV. Prokinetic agents are of value if delayed gastric emptying from a motility problem is present, but they are indicated if hypertrophied mucosa causes a physical obstruction. V. Prednisone may be tried (1 to 2 mg/kg PO SID for 2 to 3 weeks, then gradually tapered over 3 to 6 months) if infl am mation is present and nutritional management does not control the signs. VI. Surgical resection of focal areas of hypertrophy is performed, especially when bleeding polypoid lesions or gastric outfl ow obstruction are present.

I. Laboratory monitoring is done for side effects secondary to corticosteroid use (e.g., blood glucose, alkaline phosphatase). II. Endoscopy and biopsy can be repeated to determine defi nitively if the infl ammation is under control, but they are not usually done unless clinical signs persist.

I. Food is retained in the stomach for an abnormally long time. II. The stomach is usually completely empty within 10 to 12 hours after a normal meal.

Chronic hypertrophic pyloric gastropathy in 14 dogs

Ultrasonographic appearance of chronic hypertrophic pyloric gastropathy in the dog

Demonstration of Ollulanis tricuspis in the stomach of domestic cats by biopsy

Use of [ 13 C] urea breath test for detection of gastric infection with Helicobacter spp. in dogs

Lymphoma updates

Endoscopy of the gastroduodenal mucosa after carprofen, meloxicam and ketoprofen administration in dogs

Grooters AM: Pythiosis, lagenidiosis, and zygomycosis in small animals

Ultrasonographic appearance of feline alimentary lymphoma

Food sensitivity in cats with chronic idiopathic gastrointestinal problems

Chronic gastric diseases

Effect of triple therapy on eradication of canine gastric Helicobacters and gastric disease

Comparison of diagnostic methods for detecting gastric Helicobacter-like organisms in dogs and cats

Identifying and controlling helminths of the feline esophagus, stomach, and liver

Biopsy of the gastrointestinal tract

Omeprazole: a potent antiulcer drug

The effect of misoprostol on aspirin induced gastroduodenal lesions in dogs

Leiomyosarcoma in dogs: 44 cases

Feline infl ammatory bowel disease: pathogenesis, diagnosis, and relationship to lymphosarcoma

Ultrasonographic appearance of primary gastric neoplasia in 21 dogs

Diagnosing Helicobacter infections in dogs and cats

Endoscopic diagnosis of chronic hypertrophic pyloric gastropathy in dogs

Alimentary lymphoma in cats: 28 cases (1988-1993)

Use of synthetic prostaglandin E1(misoprostol) administration for prevention of aspirin induced gastroduodenal ulceration in arthritic dogs

Use of a urea breath test to evaluate short-term treatments for cats naturally infected with Helicobacter heilmann II

Helicobacter infection in dogs and cats: facts and fi ction

Ultrasonography of alimentary lymphosarcoma in the cat

Ultrasonographic evaluation of gastrointestinal diseases in small animals

The gastroduodenal effects of buffered aspirin, carprofen, and etodolac in healthy dogs

Feline gastrointestinal lymphoma

Chronic hypertrophic pyloric gastropathy: a review of 16 cases

Subnormal concentrations of serum cobalamin (Vitamin B12) in cats with gastrointestinal disease

The relationship of Helicobacter spp. infection to gastric disease in dogs and cats

Helicobacter spp. infection in cats: evaluation of the humoral immune response and prevalence of gastric Helicobacter spp

Canine gastric adenocarcinoma and leiomyosarcoma: a retrospective study of 21 cases (1986-1999) and literature review

Small Animal Endoscopy

Gastrointestinal motility disorders and gastrointestinal prokinetic therapy

Antiemetic therapy

Canine gastritis

Quantitative analysis of infl ammatory and immune responses in dogs with gastritis and their relationship to Helicobacter spp. infection

A. Mechanical obstruction from gastric mucosal hypertrophy, pyloric muscular stenosis, foreign bodies, polyps, neoplasia, pythiosis B. Functional obstruction or motility disorders from acute or chronic gastritis, acute pancreatitis, gastric ulceration, gastric neoplasia II. Delayed gastric emptying may also be secondary to non-GI disease.A. Metabolic acidosis, electrolyte disorders (hyper-or hypocalcemia, hypokalemia) B. Diabetes mellitus, pain, peritonitis, trauma, abdominal surgery C. Drugs (narcotics), dysautonomia, hypoadrenocorticism, hepatic failure, uremia Pathophysiology I. Pathophysiology depends on the underlying cause. II. Mechanical obstruction is a physical impedance to outfl ow of contents from the stomach. III. Functional obstruction arises from an alteration in normal gastric motility causing defective gastric propulsion, and may be related to an abnormality of neuronal or smooth muscle function or coordination.

I. Acute or chronic vomiting is the most common clinical sign. A. Whether the vomiting is acute or chronic depends on the underlying condition. B. The vomiting often occurs long after ingestion of the meal at a time when the stomach would normally be empty (>10 to 12 hours after eating). C. The vomiting may be explosive or projectile. II. Abdominal discomfort is sometimes noted. III. Anorexia and depression are uncommon. IV. Weight loss may be seen with chronic disease. V. Various other clinical signs are seen depending on the underlying cause, such as polyuria and polydipsia with diabetes mellitus and renal failure.

I. Regardless of the cause, laboratory tests often shows hypochloremic metabolic alkalosis secondary to loss or pooling of HCl in the stomach. II. Other laboratory changes depend on the underlying cause (e.g., hyperglycemia with diabetes mellitus, azotemia with renal failure). III. Contrast radiography is one of the best methods to identify a mechanical outfl ow obstruction. IV. Fluoroscopy is also helpful when a functional disorder is suspected. V. Endoscopy can be used to help determine the cause of a mechanical obstruction, but it is not very helpful if a functional problem is present. 

I. Bilious vomiting syndrome is an idiopathic disorder associated with duodenogastric refl ux of bile. II. Duodenogastric refl ux stimulates the vomiting refl ex.

I. Dogs tend to vomit small amounts of bile fi rst thing in the morning on an empty stomach. II. The physical examination is usually normal.

I. Diagnosis is suggested based on the pattern of vomiting and lack of other clinical signs. II. Laboratory tests are normal. III. Defi nitive diagnosis is by exclusion of other causes of chronic vomiting.

I. A small meal given just before bed often helps. II. A prokinetic drug at bedtime may be added if needed. III. Prognosis is good to excellent for control of the condition.

I. Adenocarcinoma is the most common gastric neoplasm of the dog, and lymphoma is the most common tumor of the cat. II. Other tumors affecting the stomach include the fi brosarcoma, leiomyoma, leiomyosarcoma, and plasmacytoma.

I. Neoplastic cells infi ltrate the stomach in either a focal (adenocarcinoma) or diffuse (lymphoma) pattern, and may be mucosal or transmural. II. Mucosal ulceration is common. III. Lymphoma in cats has been described as large or small cell in type.

I. Chronic vomiting, weight loss, and inappetence are the most common clinical signs. II. Vomitus may include old blood (coffee grounds appearance), and melena may be seen in some cases.

I. Laboratory tests may be normal or show nonspecifi c changes (e.g., stress leukogram).A. Anemia may be seen with bleeding tumors. B. The anemia may be acute and nonregenerative, or chronic (microcytic, hypochromic). II. Survey abdominal radiographs may reveal a mass effect or gastric wall thickening. A. Positive contrast techniques or pneumogastrography may be helpful (see Chapter 4). B. Both techniques are performed after abdominal ultrasonography, because they interfere with visualization of the stomach and other organs. III. Abdominal ultrasonography may reveal a gastric mass, enlarged lymph nodes, or evidence of metastasis (liver). IV. Defi nitive diagnosis requires biopsy and histopathology. V. Endoscopy may be performed to obtain a biopsy diagnosis, but does not determine whether metastasis is present. VI. Surgery can be performed for diagnostic purposes, as well as for therapy.

I. Other causes of chronic vomiting: GI and non-GI in origin II. Other neoplasia of the GI track and abdomen

I. Treatment depends on the tumor type. II. The recommended therapy for lymphoma is multi-drug chemotherapy (see Chapter 69). A. Remission times are much shorter for dogs than cats. B. Small-cell lymphoma in cats is usually treated with prednisone (or prednisolone) and chlorambucil. 1. Prednisone is started at 5 mg PO BID and chlorambucil at 15 mg/m 2 PO SID for 4 days and repeated every 3 weeks. 2. An alternative regimen is to give chlorambucil at 6 mg/m 2 PO QOD. 3. Long-term remissions may be achieved in these cats. III. Recommended therapy for other types of gastric neoplasia is surgical resection. A. The primary mass is resected and >2-to 3-cm margins are included if possible.B. With adenocarcinomas, large margins are diffi cult and metastases are often present at the time of diagnosis. C. Prognosis may be better for leiomyosarcoma if the mass is resectable. D. Adjunctive chemotherapy has not been shown be benefi cial for most gastric tumors, although carboplatin and doxorubicin may be alternated every 3 weeks for three treatments each. E. Median survival times are often short (approximately 4 months).