Acute Gastritis

Acute gastritis is a sudden, self-limiting or rapidly progressive inflammatory condition of the gastric mucosa, characterized by mucosal edema, hyperemia, and neutrophilic infiltration. It is one of the most common gastrointestinal disorders in dogs and cats, often resulting from dietary indiscretion, ingestion of irritants, infectious agents, or systemic diseases. The condition disrupts the gastric mucosal barrier, leading to increased permeability, altered acid secretion, and clinical signs such as vomiting, anorexia, and abdominal discomfort. Acute gastritis is typically reversible with appropriate management, but severe cases can progress to hemorrhagic gastritis, gastric ulceration, or systemic complications.

The etiology of acute gastritis is diverse and includes dietary indiscretion (e.g., ingestion of spoiled food, garbage, foreign bodies, or toxic plants), infectious agents (viral: canine parvovirus, feline panleukopenia virus; bacterial: Helicobacter spp., Salmonella, Campylobacter; fungal: Histoplasma, Pythium; parasitic: Physaloptera, Ollulanus tricuspis), toxins (e.g., nonsteroidal anti-inflammatory drugs, corticosteroids, heavy metals, household chemicals), metabolic diseases (e.g., uremia, hepatic failure, hypoadrenocorticism), and stress. In many cases, the exact cause remains undetermined (idiopathic).

Acute gastritis is extremely common in both dogs and cats, with no strong breed or sex predilection. Young animals are more prone to dietary indiscretion and infectious causes, while older animals may develop gastritis secondary to chronic diseases or drug therapy. Certain breeds, such as the Yorkshire Terrier and Standard Poodle, may have a higher incidence of gastric mucosal barrier dysfunction. The condition is seen worldwide, with seasonal peaks associated with increased outdoor activity and exposure to toxins or infectious agents.

The gastric mucosa is protected by a complex barrier comprising mucus, bicarbonate, tight junctions, and rich blood flow. Acute gastritis occurs when this barrier is breached by noxious agents, leading to direct mucosal injury, increased permeability, and back-diffusion of hydrogen ions. This triggers an inflammatory cascade with neutrophil infiltration, release of pro-inflammatory cytokines (e.g., TNF-α, IL-1β), and activation of the cyclooxygenase pathway. The resulting mucosal edema, hyperemia, and hemorrhage contribute to clinical signs. In severe cases, disruption of the microvasculature can lead to ischemia, necrosis, and ulceration. Vomiting is mediated by stimulation of the chemoreceptor trigger zone and vagal afferents.

Predisposing factors include young age (exploratory behavior), inadequate dietary supervision, ingestion of non-food items (pica), concurrent systemic diseases (renal, hepatic, endocrine), administration of ulcerogenic drugs (NSAIDs, corticosteroids), stress (hospitalization, travel), and immunosuppression. In cats, ingestion of foreign bodies (linear foreign bodies) is a common cause. Genetic factors may influence mucosal resistance, but specific gene associations are not well-defined.

Clinical signs typically develop acutely and include vomiting (often with bile or foam, occasionally blood), anorexia, lethargy, and mild to moderate dehydration. Abdominal pain may be evident on palpation. In severe cases, hematemesis, melena, and signs of shock (tachycardia, pale mucous membranes, weak pulses) may occur. Physical examination may reveal a tense, painful abdomen, and in cases of gastric dilation, a tympanic sound on percussion. Systemic signs such as fever are uncommon unless secondary infection or sepsis occurs.

Differential diagnoses include: 1) Gastric foreign body (history of pica, radiopaque object on radiography, ultrasonographic evidence); 2) Gastric ulceration (NSAID use, chronic vomiting, hematemesis, contrast radiography or endoscopy); 3) Pancreatitis (elevated pancreatic lipase, ultrasonographic changes); 4) Inflammatory bowel disease (chronic history, lymphocytic-plasmacytic infiltrate on biopsy); 5) Gastrointestinal lymphoma (weight loss, mass on imaging, biopsy); 6) Renal failure (azotemia, isosthenuria); 7) Hypoadrenocorticism (hyperkalemia, hyponatremia, ACTH stimulation test); 8) Hepatic disease (elevated liver enzymes, bile acids); 9) Infectious gastroenteritis (parvovirus, salmonellosis; fecal PCR, serology); 10) Toxin ingestion (ethylene glycol, chocolate; history, specific toxicology).

Diagnostic workup begins with a thorough history and physical examination. Initial laboratory tests include a complete blood count, serum biochemistry profile, and urinalysis to rule out metabolic causes. Fecal examination (direct smear, floatation) and fecal PCR for infectious agents are recommended if infectious etiology is suspected. Abdominal radiography is indicated to rule out foreign bodies or obstruction. Abdominal ultrasonography can assess gastric wall thickness, peristalsis, and adjacent organs. If clinical signs persist or are severe, upper gastrointestinal endoscopy with mucosal biopsy is the gold standard for definitive diagnosis and to rule out chronic conditions. In cases of suspected toxin exposure, specific toxicology tests may be performed.

Hematology may show mild hemoconcentration (increased PCV) due to dehydration, and stress leukogram (neutrophilia, lymphopenia) or leukopenia in viral infections. Serum biochemistry may reveal mild elevations in liver enzymes (ALT, ALP) due to hepatic hypoxia or concurrent disease, electrolyte imbalances (hypokalemia, hyponatremia, hypochloremia) from vomiting, and metabolic alkalosis (initially) or acidosis (in severe cases). Urinalysis may show concentrated urine (USG >1.030) unless renal disease is present. Specific biomarkers such as canine pancreatic lipase immunoreactivity (cPLI) or feline pancreatic lipase immunoreactivity (fPLI) are useful to rule out pancreatitis. In cases of suspected hypoadrenocorticism, an ACTH stimulation test is indicated. Serology or PCR for infectious agents (e.g., parvovirus) may be performed.

Abdominal radiography is often unremarkable in acute gastritis, but may show a gas-filled stomach or evidence of foreign bodies. Ultrasonography may reveal thickened gastric wall (usually <5 mm in dogs), loss of normal layering, and increased echogenicity of the mucosa. Doppler ultrasound can assess gastric wall perfusion. Endoscopy is the most sensitive imaging modality, allowing direct visualization of mucosal erythema, erosions, or hemorrhage, and enables biopsy collection. CT and MRI are rarely needed but may be useful to evaluate for complications such as gastric outflow obstruction or perforation.

Cytology from gastric brushing or fine-needle aspiration may show neutrophils, macrophages, and cellular debris. Histopathology of gastric mucosal biopsies typically reveals neutrophilic infiltration of the lamina propria, mucosal edema, hyperemia, and occasionally epithelial erosion or ulceration. Special stains (e.g., Warthin-Starry silver stain) may be used to identify Helicobacter-like organisms. In chronic cases, lymphocytic-plasmacytic infiltration may be present, but in acute gastritis, neutrophils predominate.

Treatment of acute gastritis is primarily supportive and symptomatic. The mainstay is to withhold food for 12-24 hours (but not water) to allow gastric rest, followed by a bland diet (e.g., boiled chicken and rice) in small, frequent meals. Fluid therapy with balanced crystalloids (e.g., Lactated Ringer's solution) is essential to correct dehydration and electrolyte imbalances. Antiemetics such as maropitant (1 mg/kg IV, SC, or PO q24h) or ondansetron (0.5-1 mg/kg IV q12h) are indicated for persistent vomiting. Gastroprotectants like famotidine (0.5-1 mg/kg IV, SC, or PO q12h) or omeprazole (0.7-1 mg/kg PO q24h) may be used to reduce gastric acid secretion. Sucralfate (0.5-1 g per dog or 250-500 mg per cat PO q8h) can be administered as a mucosal protectant. In cases of severe hemorrhagic gastritis, blood transfusion may be necessary. Antibiotics are not routinely indicated unless a bacterial infection is confirmed or suspected. If a specific cause is identified (e.g., toxin, foreign body), it should be addressed accordingly.

The prognosis for acute gastritis is generally excellent with appropriate supportive care. Most animals recover within 24-72 hours. However, the prognosis worsens if the underlying cause is severe (e.g., ingestion of caustic toxins, gastric perforation) or if complications such as sepsis or disseminated intravascular coagulation develop. Mortality rates are low (<5%) in uncomplicated cases. Negative prognostic indicators include persistent hematemesis, severe dehydration, shock, and lack of response to antiemetic therapy within 48 hours.

Follow-up is typically not required for uncomplicated cases, but owners should be advised to monitor for recurrence of vomiting, lethargy, or anorexia. If clinical signs persist beyond 48 hours or recur, further diagnostic evaluation is warranted. For animals with a known cause (e.g., NSAID toxicity), periodic monitoring of renal and hepatic function may be necessary. In cases of chronic or recurrent gastritis, long-term dietary management and periodic re-evaluation are recommended.

Pearls: 1) Always consider dietary indiscretion as the most common cause; 2) Use maropitant as a first-line antiemetic due to its broad-spectrum action; 3) Provide aggressive fluid therapy to correct dehydration and electrolyte imbalances; 4) Reintroduce food gradually after a 12-24 hour fast. Pitfalls: 1) Avoid using corticosteroids in acute gastritis as they may exacerbate mucosal damage; 2) Do not use NSAIDs for pain control; 3) Do not delay diagnostic imaging if a foreign body is suspected; 4) Avoid overuse of antibiotics without evidence of bacterial infection.

Based on Plumb's Veterinary Drug Handbook, the following protocols are recommended: 1) Maropitant (Cerenia): 1 mg/kg IV, SC, or PO q24h for up to 5 days; 2) Ondansetron: 0.5-1 mg/kg IV q12h; 3) Famotidine: 0.5-1 mg/kg IV, SC, or PO q12h; 4) Omeprazole: 0.7-1 mg/kg PO q24h; 5) Sucralfate: 0.5-1 g (dogs) or 250-500 mg (cats) PO q8h, given 30-60 minutes before meals; 6) Metoclopramide: 1-2 mg/kg/day as a CRI or 0.2-0.4 mg/kg PO q8h (less preferred due to variable efficacy); 7) Fluid therapy: Lactated Ringer's solution or Normosol-R at a rate of 40-60 mL/kg/day for maintenance plus replacement of estimated deficits. For severe vomiting, add potassium chloride (20-30 mEq/L) to fluids. Adjust dosages in renal or hepatic impairment; contraindications include hypersensitivity to the drug. Drug interactions: Maropitant may interact with CYP450 inhibitors; famotidine may alter absorption of other drugs.

Evidence-based literature supports the use of maropitant as an effective antiemetic in dogs and cats with acute gastritis (Benchaoui et al., 2007). Studies have shown that maropitant is superior to metoclopramide in controlling vomiting (Sedlacek et al., 2008). The use of H2 receptor antagonists (e.g., famotidine) is common but evidence for their efficacy in acute gastritis is limited; however, they are recommended in cases of gastric ulceration or hemorrhage (Tolbert et al., 2011). Proton pump inhibitors (e.g., omeprazole) are more effective at raising gastric pH and are preferred in severe cases (Tolbert et al., 2015). Sucralfate has been shown to promote mucosal healing in experimental models (Okabe et al., 1983). Consensus guidelines from ACVIM and ECVIM recommend supportive care with fluid therapy and antiemetics as the mainstay of treatment for acute gastritis (Marks et al., 2013).