Issues

Gastroduodenal Ulceration/Erosion (GUE)

 

Ulcers are defects that extend completely through the mucosa; erosions only extend part way through the mucosa.

 

PATHOPHYSIOLOGY

Gastroduodenal ulcers/erosions (GUE) result from various factors which damage or overwhelm normal gastric mucosal defense and repair mechanisms.

Factors protecting the stomach from GUE include the mucus-bicarbonate layer, gastric epithelial cell turnover, gastric mucosal blood flow, and locally produced prostaglandins.

 

SYSTEMS AFFECTED

Gastrointestinal—ulcers and/or erosion are most common in the stomach and then the proximal duodenum; however, neoplasia and some drugs (e.g., flunixin meglumine) can cause ulceration anywhere in GI tract.

Cardiovascular—hemorrhage may cause anemia, tachycardia, systolic heart murmur, and/or hypotension.

Peritoneal cavity—perforation may cause peritonitis/sepsis/SIRS.

 

INCIDENCE/PREVALENCE

40–60% in exercising Alaskan sled dogs.

Relatively common in dogs receiving NSAIDs or dexamethasone.

 

SIGNALMENT

Species

Primarily dog; cat uncommonly affected.

 

Breed Predilections

Chow chows, rough-coated collies, Staffordshire bull terriers, and Belgian shepherd dogs have increased incidence of gastric carcinoma.

 

Mean Age and Range

All ages

 

Predominant Sex

Male dogs are predisposed to gastric carcinoma.

 

SIGNS

General Comments

Patients can be asymptomatic, hyporexic, vomiting, and/or have GI bleeding. The severity of clinical signs is not necessarily proportional to the size/number of GUE.

 

Historical Findings

• Some animals with GUE are asymptomatic (e.g., patients taking NSAIDs or dexamethasone, dogs working in extreme environments).
• Hyporexia is the most common clinical sign.
• Vomiting, hematemesis, and/or melena may be seen (in decreasing order of frequency).
• Cranial abdominal pain (“praying position”) is rarely seen.
• Weakness, pallor, lethargy, and/or collapse if severe anemia or SIRS develops.
• Physical Examination Findings
• Physical examination is often normal.
• Melena is rare.
• Pale mucous membranes and weakness if severely anemic (infrequent).
• Tachycardia, hypotension, and prolonged capillary refill time if hypovolemic shock or perforation/SIRS occur.

CAUSES

Drugs

NSAIDs—COX-2 selective NSAIDs are usually safer than non-selective NSAIDs, however, GUE and perforation can occur with all COX-2 selective NSAIDs. Coadministration of glucocorticoids (either systemic or local) enhances the ulcerogenic potential of NSAIDs. Some NSAIDs are renowned for being extremely ulcerogenic (flunixin meglumine, naproxen, indomethacin).

Glucocorticoids: dexamethasone is probably the most ulcerogenic. Prednisolone is much less likely to cause GUE unless there are additional stress factors (e.g., hypoxemia, hypoperfusion) affecting the GI mucosa.

Gastrointestinal Diseases

Gastrointestinal neoplasia: carcinomas are the most common cause of neoplastic ulceration, but leiomyomas/leiomyosarcomas are renowned for causing severe hemorrhage.

Pythiosis can cause severe GUE. It is a regionally important disease and is becoming increasingly widespread in North America.

Foreign bodies can be associated with GUE, but they are usually not an important cause in the stomach. Intestinal foreign bodies (especially linear foreign bodies) commonly cause intestinal ulceration/perforation.

Gastric hyperacidity.

Infectious Diseases

Pythiosis

Metabolic Diseases

Hepatic disease

Hypoadrenocorticism

Pancreatitis

Toxicity

Heavy metal poisoning (arsenic, zinc, thallium, iron, or lead are rare causes)

 

Neoplasia

GI neoplasia (carcinoma, lymphoma, leiomyoma, GI stromal tumor [GIST])

Paraneoplastic hyperacidity (mastocytosis, gastrinoma)

Stress/Major Medical Illness

Shock/severe hypotension (e.g., secondary to trauma or surgery)

SIRS (heat stroke, sepsis)

Burns

Sustained strenuous exercise (especially in extreme environments, either cold or hot)

 

RISK FACTORS

Ulcerogenic drugs (NSAIDs, dexamethasone)

Hypovolemic shock/SIRS

Extreme exercise

 

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

Esophageal disease (neoplasia, esophagitis, foreign body) diagnose with radiography and/or esophagoscopy.

Coagulopathies (thrombocytopenia, anticoagulant poisoning): diagnose with platelet count, and coagulation testing.

Bronchopulmonary disease causing hemoptysis: diagnose with radiography and/or bronchoscopy.

Regurgitation or vomiting of blood (hematemesis) swallowed from the respiratory tract or swallowed with food.

Pepto-Bismol, sucralfate, or activated charcoal cause stool to resemble melena.

 

CBC/BIOCHEMISTRY/URINALYSIS

Acute blood loss (i.e., 3–5 days): non-regenerative anemia/hypoalbuminemia.

Blood loss > 7 days: regenerative anemia/hypoalbuminemia.

Chronic blood loss: iron deficiency anemia (i.e., microcytic, hypochromic, variable reticulocytosis) and hypoalbuminemia.

BUN:creatinine ratio may be elevated with acute, severe GI hemorrhage, but this is hard to evaluate without recent pre-bleed laboratory values.

OTHER LABORATORY TESTS

Fecal flotation (parasitism)

Bile acids (hepatic insufficiency)

Resting serum cortisol (screen for hypoadrenocorticism)

Serum gastrin concentrations (gastrinoma is rare)

 

IMAGING

Abdominal radiography (GI foreign body, abdominal mass, pancreatitis, pneumoperitoneum, effusion, hepatic disease).

Barium contrast radiography is very insensitive for GUE.

Ultrasonography has high specificity but questionable sensitivity for GI lesions (e.g., infiltrates, altered layering, ulcer); cannot detect erosions.

 

DIAGNOSTIC PROCEDURES

Endoscopy is the most sensitive test for GUE. It also allows the biopsy of lesions. Can try to biopsy margin including normal and abnormal tissue; however, it is optimal to biopsy normal-appearing tissue around GUE plus the periphery of the ulcer. Be careful about biopsying the center of ulcers as this occasionally causes perforation.

Fine-needle aspirates or biopsies of infiltrative lesions in the GI tract.

Abdominocentesis may reveal septic peritonitis if the ulcer perforates.

Exploratory surgery can be done to look for GUE, but it can be hard to see GUE or other mucosal lesions from the serosal surface. It is easy to look into the stomach through gastrostomy incision and miss lesions.

 

PATHOLOGIC FINDINGS

GUE is grossly visible.

The gastric body and antrum are the most common sites of GUE (especially from NSAIDs and dexamethasone), but GUE can occur anywhere in the stomach.

Proximal duodenal ulceration is classic but not diagnostic for excessive gastric acid secretion (mast cell tumor, gastrinoma).

Microscopically can see inflammation, neoplasia, or fungal organisms.

 

TREATMENT

APPROPRIATE HEALTH CARE

VERY IMPORTANT: Remove underlying cause if possible, especially drugs, toxins, and/or poor perfusion. Some GUE resolves spontaneously if the cause is removed.

 

SUPPORTIVE CARE

IV fluids if needed to maintain hydration, gastric mucosal perfusion, and/or treat shock.

Transfusions if the patient has severe GI hemorrhage.

 

ACTIVITY

Based upon the patient’s condition

 

DIET

Discontinue oral intake if vomiting.

When feeding is resumed, feed small amounts of low-fat/low-fiber diet.

 

CLIENT EDUCATION

Dogs are especially prone to NSAID-induced GUE because these drugs usually have a longer half-life in dogs than in humans.

Never administer an NSAID (especially if sold for human use) unless specifically told to use it by a veterinarian. For example, a low dose of aspirin at 0.5 mg/kg q24h is frequently used to prevent thromboembolic disease in dogs at increased risk.

Hyporexia is often the first sign of GUE and may be the only evidence in patients receiving NSAIDs.

Adverse effects of NSAIDs are reduced by giving drugs with food.

Proton pump inhibitors help prevent NSAID-induced GUE, but misoprostol is probably the most effective prophylactic drug.

No drug is effective in preventing dexamethasone-induced GUE.

 

SURGICAL CONSIDERATIONS

If GI blood loss is potentially life-threatening, perform gastroduodenoscopy to identify sites of hemorrhage and then either surgically resect lesions or cauterize sites endoscopically (either electrically or chemically).

Surgical excision of ulcers is indicated if medical treatment shows no evidence of helping after 5–7 days.

Rarely need to do intraoperative endoscopy to locate lesions that cannot be found at surgery.

Rarely may need to have surgeon telescope intestines over the tip of the endoscope to allow a thorough examination of the entire jejunal mucosa.

 

MEDICATIONS

DRUG(S) OF CHOICE

Proton pump inhibitors (PPIs) are currently the most potent inhibitors of gastric acid secretion. They irreversibly block the parietal cell proton pump. They require 3–5 days to achieve maximum efficacy, but immediate effects are still superior to that of H2 receptor antagonists. They can be used as first-line therapy for any GUE, but they are especially indicated for gastrinomas. Omeprazole (1–2 mg/kg PO q12–24h, dog), esomeprazole, or lansoprazole (1 mg/kg PO q24h, dog) can be administered orally whereas pantoprazole (1 mg/kg IV q24h, dog) can be administered parenterally.

Histamine (H2) receptor antagonists competitively inhibit gastric acid secretion. Ranitidine (1–2 mg/kg SC, PO, IV q8–12h, dog and cat); famotidine (0.5—1 mg/kg PO, IV q12–24h, dog and cat); nizatidine (5 mg/kg PO q24h, dog). Famotidine is the most potent. Cimetidine should be avoided in light of its short half-life and relative ineffectiveness. Lafutidine is a new H2 receptor antagonist that is supposed to be as effective as a PPI, but there is currently no experience with its use in veterinary medicine.

Sucralfate (0.5–1 g PO q6–8h) protects ulcerated tissue by binding to ulcer sites and stimulating prostaglandin synthesis.

Antiemetics if vomiting is frequent or nausea is severe. Maropitant (1 mg/kg SC q24h for 5 days, dog; 2 mg/kg PO q24h for 5 days, dog); ondansetron (0.5 mg/kg IV q12h, dog; 0.2 mg/kg IV q12h, cat).

Oral antacids (e.g., calcium carbonate) are poorly effective and not recommended.

 

POSSIBLE INTERACTIONS

Sucralfate may slow the absorption of other drugs.

Antacids may slow the absorption of other drugs.

 

ALTERNATIVE DRUG(S)

Misoprostol, synthetic prostaglandin E1 analogue, (2–5 μg/kg PO q8–12h) used prophylactically to prevent NSAID-induced ulcers. Can be used to treat any existing ulcer. Do not use it in pregnant patients (causes abortion).

 

FOLLOW-UP

PATIENT MONITORING

If medications are going to be effective, the patient should show evidence of clinical improvement within 5–7 days.

 

PREVENTION/AVOIDANCE

Administer NSAIDs with food.

Concurrent use of PPI when chronically administering NSAIDs helps prevent GUE. If PPIs are inadequate, misoprostol is usually more effective.

COX-2 selective or dual LOX/COX inhibitors are less likely to cause GUE than non-selective NSAIDs, but they can still cause GUE and perforation/peritonitis.

 

POSSIBLE COMPLICATIONS

Hemorrhage, ulcer perforation, and/or septic peritonitis

 

EXPECTED COURSE AND PROGNOSIS

Varies with underlying causes.

GUE not due to local malignancy can usually (not always) be treated successfully medically (especially if one can remove the cause). However, if perforation has occurred, surgery is necessary.

 

MISCELLANEOUS

ASSOCIATED CONDITIONS

Anemia

 

AGE-RELATED FACTORS

Neoplasia more common in older animals.

 

Visit your veterinarian as early recognition, diagnosis, and treatment are essential.

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