Gastritis in Small Animals
Gastritis is a general term used to describe a syndrome of acute or chronic vomiting secondary to inflammation of the gastric mucosa. Irritation, infection, antigenic stimulation, or injury (eg, chemical, erosion, ulceration) of the gastric mucosa stimulates the release of inflammatory and vasoactive mediators with subsequent disruption of gastric epithelial cells, increased gastric acid secretion, and impaired gastric barrier function. Visceral receptors sensitive to gastric distention, gastric inflammation, and tonicity of gastric contents send impulses via vagal and sympathetic nerves to the vomiting center of the medulla oblongata, thereby stimulating the vomiting reflex.
In acute gastritis, vomiting of sudden onset is presumed or confirmed to be secondary to inflammation of the gastric mucosa. Causes include dietary indiscretion or intolerance (eg, ingestion of novel, spoiled, or contaminated foods, or of foreign material), drug or toxin ingestion (eg, antibiotics, NSAIDs, corticosteroids, plants, chemicals), systemic illness (eg, pancreatitis, uremic gastropathy, hypoadrenocorticism), endoparasitism (eg, Physaloptera sp [dog], Ollulanus sp [cat]), or bacterial (eg, Helicobacter-associated disease) or viral (eg, canine parvovirus gastroenteritis, feline panleukopenia) infection. Vomiting of sudden onset is characteristic. The vomitus may contain bile, food, froth, blood (frank or digested), or evidence of an ingested substance (eg, grass, bones, foreign material, etc). Additional clinical signs depend on the severity and frequency of vomiting as well as on the underlying cause.
Diagnosis is usually based on a thorough history, clinical findings, and response to symptomatic treatment. A specific diagnosis should be sought if the animal has had access to foreign objects or toxins, if clinical signs do not resolve within 2 days of symptomatic therapy, if hematemesis or melena are present, if the animal is systemically unwell, or if abnormalities are noted on abdominal palpation. Dogs may signal the presence of cranial abdominal discomfort by adopting a “praying” posture (hindquarters raised and chest and forelegs held close to floor), which seems to provide some sense of relief. A CBC, serum biochemical profile, and urinalysis may be followed by more specific clinicopathologic testing (eg, basal serum cortisol concentration, adrenocorticotropic hormone [ACTH] stimulation test, evaluation of vomitus for specific toxins). Diagnostic imaging, including plain and/or barium contrast abdominal radiographs and abdominal ultrasound, may be indicated.
Treatment of acute gastritis is generally symptomatic and supportive. Small amounts of oral fluids can be given frequently, with the volume increasing as vomiting subsides. Ice (crushed or cubes) can be provided as the only source of water initially. Subcutaneous administration of an isotonic balanced electrolyte solution may be sufficient to correct mild fluid deficits (<5%). If dehydration is moderate to severe or the clinical condition of the animal warrants IV fluid therapy, a more extensive diagnostic evaluation is indicated. If vomiting is acute, oral intake should be discontinued for ≥24 hr. Small amounts of a bland, low-fat, easily digestible diet (eg, boiled lean beef, chicken, or cottage cheese and rice, or a commercially available prescription diet) fed frequently can be introduced, with gradual transition to the usual diet over 3–5 days.
Antiemetic drugs should be used to control vomiting only after an etiologic diagnosis has been made or if vomiting is protracted or severe enough to cause dehydration or electrolyte imbalances. Metoclopramide (0.3 mg/kg, PO or SC, tid, or 1–2 mg/kg/day as a constant-rate infusion) increases gastric contractions; relaxes the pyloric sphincter; and increases gastric, duodenal, and proximal jejunal peristalsis. It is contraindicated in confirmed or suspected GI obstructions. Alternative antiemetics include maropitant (1 mg/kg/day, SC, or 2 mg/kg/day, PO, for 5 days) and ondansetron (0.1–1 mg/kg, PO, once to twice daily). Gastroprotectants such as H2-receptor antagonists (eg, famotidine 0.5–1 mg/kg, PO, SC, or IV, bid) or proton pump inhibitors (eg, omeprazole 0.7–2 mg/kg/day, PO, or pantoprazole 1 mg/kg/day, IV) may also be indicated. In dogs, omeprazole may provide better gastric acid suppression and better prevention of exercise-induced gastritis than famotidine.
Chronic gastritis should be considered in animals with intermittent or persistent vomiting that lasts >7 days and that cannot be attributed to dietary indiscretion or intolerance; drug, toxin, or foreign body ingestion; systemic illness; endoparasitism; infection (bacterial or viral); or neoplasia. The most common clinical sign is intermittent vomiting of food or bile. Systemic illness, weight loss, and GI ulceration are infrequent and should raise suspicion of a more serious condition or diffuse GI inflammation (eg, inflammatory bowel disease, pythiosis, etc).
Histologic evaluation of endoscopic or surgical gastric biopsies is required for definitive diagnosis and classification of chronic gastritis. A CBC, serum biochemical profile, urinalysis, total thyroid hormone concentration (cats), basal serum cortisol concentration possibly with an ACTH-stimulation test (to exclude canine hypoadrenocorticism), and fecal evaluation for endoparasitism are indicated but are frequently unremarkable in animals with chronic gastritis. Diagnostic imaging (plain and/or barium contrast abdominal radiographs, abdominal ultrasound) can identify foreign objects, neoplasia, pyloric stenosis, gastric antral mucosal hypertrophy, discrete or multifocal mucosal or mural abnormalities, intra-abdominal lymphadenomegaly, or other intra-abdominal pathology, and is indicated before gastric biopsy.
Lymphocytic-plasmacytic gastritis and eosinophilic gastritis are characterized by diffuse infiltration of the gastric mucosa and lamina propria with lymphocytes and plasma cells, or eosinophils, respectively. Similar cellular infiltrates may be seen in the small intestine. Concomitant lymphoid hyperplasia, mucosal atrophy, or mucosal fibrosis is infrequently seen. Dietary allergy or intolerance, occult parasitism, or hyperimmune response to normal antigens have been proposed as possible causes. Eosinophilic gastritis with eosinophilia and/or skin lesions should raise suspicion for dietary sensitivity or hypereosinophilic syndrome (cats).
Animals with mild clinical signs and mild histologic lesions may respond to symptomatic care (see Acute Gastritis), empirical deworming, and exclusive feeding of a hypoallergenic or novel protein diet (eg, balanced homemade diet or many commercially available options). In addition to symptomatic care, empirical deworming, and dietary modification, animals with moderate to severe, histologically confirmed disease generally require immunosuppressive therapy. Prednisone (or prednisolone in cats) is started at 2 mg/kg/day, PO (dogs), or 2–4 mg/kg/day, PO (cats), and tapered to the lowest dosage that controls clinical signs. Assuming continued clinical remission, prednisone therapy is ultimately discontinued and strict adherence to dietary therapy maintained. If clinical signs persist despite gastroprotectant therapy, dietary modification, and prednisone therapy, treatment with an additional immunosuppressive agent (dogs: azathioprine 2 mg/kg, PO, every 24–48 hr; cats >4 kg: chlorambucil 2 mg [total dose], PO, every 48 hr for 2–4 wk then tapered to 2 mg every 72–96 hr; cats <4 kg: chlorambucil 2 mg [total dose] every 72 hr; dogs and cats: cyclosporine 3–5 mg/kg/day, PO) can be considered.
Chronic atrophic gastritis is often characterized by marked mononuclear cell infiltration, thinning of the gastric mucosa, and atrophy of the gastric glands. A unique, breed-associated form of atrophic gastritis in Norwegian Lundehunds has not been associated with Helicobacter spp infection but has been associated with gastric adenocarcinoma. The role, if any, of Helicobacter spp infection in the development of atrophic gastritis is unknown. However, if Helicobacter spp organisms are identified in gastric biopsy specimens, treatment is indicated (see Helicobacter Infection in Small Animals). Additional treatment options include dietary management and immunosuppression as for lymphocytic-plasmacytic and eosinophilic gastritis (see above); however, data with respect to treatment efficacy and prognosis are lacking.
Chronic hypertrophic gastropathy is characterized by diffuse or focal hypertrophy of the gastric mucosa, muscularis, or both, with variable inflammatory infiltrates. The lesion is often most pronounced in the pyloric region, with resultant gastric outflow obstruction. Projectile vomiting of food within hours of eating may be described. Older, male, small-breed dogs are overrepresented (eg, Lhasa Apso, Shih Tzu, Maltese, Miniature Poodle). Hypergastrinemia due to exaggerated secretion (eg, gastrin-secreting neoplasia, Basenji gastroenteropathy) or inadequate clearance (eg, hepatic or renal disease, achlorhydria) may initiate mucosal hypertrophy. Surgical correction via pyloroplasty and/or removal of hypertrophied tissue may be required to alleviate clinical signs.