Issues

Gastritis, Chronic

• Intermittent vomiting of > 1–2 weeks in duration secondary to gastric inflammation.
• The presence of gastric erosions or ulcers is dependent on the inciting cause and duration.

 

PATHOPHYSIOLOGY

Chronic irritation of the gastric mucosa by chemical irritants, drugs, foreign bodies, infectious agents, or hyperacidity syndromes results in an inflammatory response in the mucosal surface that may extend to involve submucosal layers.

Chronic allergen exposure or immune-mediated disease may also produce chronic inflammation.

 

SYSTEMS AFFECTED

Gastrointestinal—esophagitis may result from chronic vomiting or gastroesophageal reflux.

Respiratory—aspiration pneumonia is infrequently seen secondary to chronic vomiting; it is more likely if concurrent esophageal disease exists or if the patient is debilitated.

 

INCIDENCE/PREVALENCE

Relatively common

 

SIGNALMENT

Species

Dog and cat

 

Breed Predilections

Old, small-breed dogs (i.e., Lhasa apso, Shih Tzu, miniature poodle) are more commonly affected with antral mucosal hyperplasia and hypertrophy.

 

Mean Age and Range

Varies with the underlying cause

 

Predominant Sex

Varies with the underlying cause

 

SIGNS

Historical Findings

• Vomitus is frequently bile-stained and may contain undigested food, flecks of blood, or digested blood (“coffee grounds”).
• The frequency varies from daily to every few weeks and increases as gastritis progresses.
• Vomiting may be stimulated by eating or drinking.
• Early morning vomiting before eating may indicate bilious vomiting syndrome.
• May see weight loss with chronic anorexia.
• May see melena with ulceration (not common).
• Increased water intake.
• Diarrhea, if the concurrent intestinal disease
• Physical Examination Findings
• Generally, within normal limits.
• May be thin with persistent anorexia.
• May have pale mucous membranes with anemia from chronic blood loss.
• May find cranial abdominal pain (rarely noted).

 

CAUSES

• Inflammatory—immune-mediated, dietary allergy or intolerance, idiopathic.
• Dietary indiscretion—plant material, foreign objects, chemical irritants.
• Toxins—fertilizers, herbicides, cleaning agents, heavy metals.
• Metabolic/endocrine disease—azotemia, chronic liver disease, hypoadrenocorticism, pancreatitis.
• Neoplastic—common: gastrointestinal lymphoma, gastric adenocarcinoma, small cell lymphoma (especially cats, recent increase in dogs); infrequent: gastric polyps, gastrinoma, leiomyosarcoma, plasma cell tumor, mast cell tumor.
• Parasitism—Physaloptera spp. (dogs, cats), Ollulanus tricuspid and Gnathostoma spp. (cats).
• Drugs—NSAIDs, glucocorticoids.
• Infectious—Helicobacter spp., Pythiosis, viral (distemper in dogs, feline leukemia virus in cats).
• Miscellaneous—duodenogastric reflux (bilious vomiting syndrome), stress, achlorhydria.

 

RISK FACTORS

Medications—NSAIDs, glucocorticoids.

Environmental—unsupervised/free-roaming pets are more likely to ingest inappropriate foods or materials.

Ingestion of a dietary antigen to which an allergy or intolerance has been acquired.

 

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

• Although the causes listed above are included in the differential diagnosis of chronic gastritis, an identifiable cause is often not found for gastric inflammation.
• Must differentiate chronic vomiting from chronic regurgitation (active vs. passive vomiting).
• Small intestinal inflammation and gastric or small intestinal neoplasia often present with signs and physical exam findings similar to those of gastric inflammation.
• Idiopathic gastritis—diagnosis of exclusion; often characterized by a predominantly lymphoplasmacytic infiltrate (superficial or diffuse).
• Eosinophilic gastritis, hypertrophic gastritis, granulomatous/histiocytic gastritis, and atrophic gastritis are less common; often overlap of histologic changes exists in the types of inflammatory infiltrates.
• Atrophic gastritis differs in the endoscopic examination—resulting in visualization of the submucosal vessels secondary to thinning of the gastric mucosa.
• Hypertrophic gastritis—prominent mucosal folds that do not flatten with gastric insufflation.

 

CBC/BIOCHEMISTRY/URINALYSIS

• Hemogram was usually unremarkable unless systemic disease is present.
• Hemoconcentration if severe dehydration.
• May see nonregenerative (anemia of chronic disease) or regenerative anemia (blood loss).
• With ulceration—microcytic, hypochromic anemia associated with an iron deficiency if prolonged, severe blood loss.
• May see eosinophilia with eosinophilic gastroenteritis.
• Azotemia with low urine specific gravity in uremic gastritis.
• Increased serum hepatic enzyme activities, total bilirubin, or hypoalbuminemia with chronic hepatic disease.
• Hyperkalemia and hyponatremia suggest Addison’s disease.
• Hyponatremia, hypokalemia, hypochloremia, and an elevated bicarbonate level with acidotic urine suggest a gastric outflow obstruction (hypochloremic metabolic alkalosis).

 

OTHER LABORATORY TESTS

Elevated serum gastrin level without azotemia suggests gastrinoma.

 

IMAGING

Survey abdominal radiographs—usually normal, but may reveal radiodense foreign objects, a thickened gastric wall, or gastric outflow obstruction with persistent gastric distension.

Contrast radiography—may detect foreign objects, gastric outflow obstruction, delayed gastric emptying, or gastric wall defects or thickening.

Ultrasonography—may detect gastric wall thickening, ulceration, and gastric foreign objects.

 

DIAGNOSTIC PROCEDURES

Gastroscopy—is usually adequate for visualization of the gastric mucosa and for biopsy but in most cases, one should also evaluate and biopsy the duodenum.

Gastric biopsy and histopathology are required for diagnosis, even if gastric mucosa appears normal.

Foreign objects can be identified and retrieved via endoscopy.

Exploratory celiotomy is indicated if a perforated ulcer or submucosal lesion of the gastric wall is suspected and partial gastrectomy or full-thickness biopsy is required.

Fecal flotation may reveal intestinal parasites.

 

PATHOLOGIC FINDINGS

Idiopathic gastritis—inflammatory infiltrates vary; can be lymphocytes, plasma cells, neutrophils, eosinophils, and/or histiocytes.

Mucosal changes can be degenerative, hyperplastic, or atrophic.

May see varying degrees of edema and fibrous tissue; may see Helicobacter spp. Must be noted within gastric glands to be significant and should be accompanied by lymphofollicular gastritis; special stains can be requested for fungal hyphae and Helicobacter.

May see lymphoplasmacytic inflammation along with Helicobacter spp. Treatment for Helicobacter may result in the resolution of clinical signs without immunosuppressive therapy.

If hyperplastic changes are noted, a gastrin level should be obtained before institution or after discontinuation of antacids, H2 blockers or proton pump blockers.

 

TREATMENT

APPROPRIATE HEALTH CARE

Most patients are stable at presentation unless vomiting is severe enough to cause dehydration.

Can typically manage as an outpatient, pending diagnostic testing or undergoing clinical trials of special diets or medications.

If the patient is dehydrated or if vomiting becomes severe, hospitalize and institute appropriate intravenous crystalloid fluid therapy (see Vomiting, Acute).

 

DIET

Soft, low-fat food ideally from a single carbohydrate and protein source.

Non-fat cottage cheese, boiled skinless white meat chicken, boiled hamburger or tofu as a protein source, and rice, pasta, or potato as a carbohydrate source, in a ratio of 1:3.

Frequent, small meals (q4–6h or more frequently).

Can use novel protein source or hydrolyzed protein diet if the dietary allergy is suspected.

Feed diets for a minimum of 2–3 weeks to assess the adequacy of the response.

Feed a late-night meal to help prevent bilious vomiting syndrome in the early morning hours.

 

CLIENT EDUCATION

Gastritis has numerous causes.

Diagnostic workup—may be extensive; usually requires a biopsy for a definitive diagnosis.

 

SURGICAL CONSIDERATIONS

Surgical management if a granulomatous mass or hypertrophy is causing a gastric outflow obstruction.

Gastrotomy for removal of foreign objects if endoscopic retrieval is unsuccessful or is not available.

 

MEDICATIONS

DRUG(S) OF CHOICE

Treat any gastric erosions and ulcers (see Gastroduodenal Ulcer Disease).

Give glucocorticoids (prednisone 2–4 mg/kg PO q24h [rarely requires the high end of dose to start]; taper by 25% every 2–3 weeks over 2–3 months) for chronic gastritis secondary to suspected immune-mediated mechanisms if no clinical response to dietary management. Never exceed a total dose of 60 mg of prednisone no matter how heavy the dog is.

Treatment for Helicobacter gastritis—amoxicillin (22 mg/kg PO q12h), Pepto-Bismol (15 mg/kg PO q6–8h), and metronidazole (10 mg/kg PO q12h) for 3 weeks (see Helicobacter Infection).

Antiemetics (maropitant 1 mg/kg PO/SC q24h) for fluid and electrolyte disorders caused by frequent or profuse vomiting (see Vomiting, Acute).

Metoclopramide (0.2–0.4 mg/kg PO q6–8h), cisapride (0.5–1 mg/kg PO q8h to q12h), or low-dose erythromycin (0.5–1 mg/kg PO q8h) to increase gastric emptying and normalize intestinal motility if gastric emptying is delayed or gastroduodenal reflux is present. Metoclopramide is most effective as a CRI administered at 1–2 mg/kg q24h.

 

CONTRAINDICATIONS

Do not use prokinetics, metoclopramide, or cisapride if gastric outflow obstruction is present.

Antacids are not indicated with atrophic gastritis and achlorhydria.

 

PRECAUTIONS

Steroids are immunosuppressive, making close monitoring for secondary infections important.

Steroids may also inhibit the normal gastric mucosal barrier, leading to ulceration.

ALTERNATIVE DRUG(S)

Synthetic prostaglandin E1 (misoprostol 1–3 μg/kg PO q6–8h) to prevent gastric mucosal ulcers with NSAID toxicity.

For additional immunosuppression when in need of an immediate response, add chlorambucil (0.1–0.2 mg/kg q24h for 7 days then q48h). Often used in place of azathioprine but can be used in addition. A recent study suggests that this addition may be superior to adding azathioprine.

Immunosuppressive drugs such as azathioprine (2.2 mg/kg PO q24h, tapering to q48h after 2–3 weeks in dogs) if an immune-mediated mechanism is suspected and response to dietary management and glucocorticoid administration is inadequate. Expect a response to occur in 2–3 weeks. Avoid the use of azathioprine in cats because the drug is markedly myelosuppressive.

 

FOLLOW-UP

PATIENT MONITORING

Resolution of clinical signs indicates a positive response.

Recheck electrolytes and acid-base status if initially abnormal.

Complete blood counts should be obtained weekly and then reduced to q4–6 weeks for patients on myelosuppressive drugs (i.e., azathioprine, chlorambucil). Additional chemistry monitoring q2–3 months as well.

Repeat diagnostic workup and consider possible rebiopsy if signs decrease but do not resolve.

Repeat diagnostic workup and consider rebiopsy if signs resolve and then recur several months to years later, especially in cats. IBD can progress to small cell lymphoma in the cat.

 

PREVENTION/AVOIDANCE

Avoid medications (e.g., corticosteroids, NSAIDs) and foods that cause gastric irritation or allergic response in the patient.

Prevent free-roaming and the potential for dietary indiscretion.

 

POSSIBLE COMPLICATIONS

Progression of gastritis from superficial to atrophic gastritis.

Gastric erosions and ulcers with progressive mucosal damage.

Aspiration pneumonia.

Electrolyte or acid-base imbalances.

EXPECTED COURSE AND PROGNOSIS

Varies with the underlying cause

 

MISCELLANEOUS

AGE-RELATED FACTORS

Young animals are more likely to ingest foreign objects.

 

PREGNANCY/FERTILITY/BREEDING

Prednisone has been used safely in pregnant women; corticosteroids have been associated with an increased incidence of congenital defects, abortion, and fetal death.

Azathioprine has been used safely in pregnant women and may be a good substitute for corticosteroids in pregnant animals.

Do not administer misoprostol to pregnant animals.

 

ABBREVIATIONS

IBD = inflammatory bowel disease

NSAID = nonsteroidal anti-inflammatory drug

 

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

You may also visit – https://www.facebook.com/angkopparasahayop