Gastric Erosion

Gastric erosion is a pathological condition characterized by the loss of superficial mucosal epithelium without penetration through the muscularis mucosae. It is a form of gastritis that results in shallow, often multiple, mucosal defects that do not extend into the submucosa. Gastric erosions are distinct from ulcers, which breach the muscularis mucosae and can lead to perforation. The condition is commonly associated with disruption of the gastric mucosal barrier, leading to inflammation and epithelial cell loss. Erosions can be acute or chronic, and may be localized or diffuse. They are frequently encountered in dogs and cats, often secondary to stress, drug administration, or systemic disease. The clinical significance ranges from asymptomatic to severe hemorrhage, and they can progress to ulceration if the underlying cause is not addressed.

The etiology of gastric erosion is multifactorial. Primary causes include: 1) Non-steroidal anti-inflammatory drugs (NSAIDs) such as carprofen, meloxicam, and aspirin, which inhibit cyclooxygenase-1 (COX-1) and reduce mucosal prostaglandin synthesis, compromising mucosal defense. 2) Glucocorticoids, which decrease mucus production and mucosal blood flow. 3) Stress-related mucosal disease (e.g., critical illness, trauma, sepsis) leading to ischemia and reperfusion injury. 4) Infectious agents: Helicobacter spp. (e.g., H. pylori, H. felis) can cause chronic gastritis and erosions. 5) Parasitic infections (e.g., Physaloptera spp.) causing mechanical irritation. 6) Dietary indiscretion or ingestion of corrosive substances. 7) Gastric neoplasia (e.g., adenocarcinoma, lymphoma) can cause erosions secondary to tumor infiltration. 8) Inflammatory bowel disease (IBD) with gastric involvement. 9) Hepatic or renal disease leading to uremic gastropathy. 10) Hypoadrenocorticism (Addison's disease) associated with gastric mucosal compromise. 11) Mast cell tumors, which release histamine and stimulate gastric acid secretion. 12) Idiopathic or autoimmune gastritis. The molecular triggers involve disruption of the mucus-bicarbonate barrier, reduced mucosal blood flow, and increased gastric acid and pepsin secretion.

Gastric erosion occurs in both dogs and cats, with no strong breed predilection, but certain breeds may be more susceptible to specific underlying causes. For example, breeds predisposed to hypoadrenocorticism (e.g., Standard Poodles, West Highland White Terriers) may have higher risk. NSAID-induced erosions are common in dogs, especially in those receiving long-term therapy for osteoarthritis. Cats are less commonly affected by NSAID toxicity due to species differences in metabolism, but can develop erosions secondary to chronic kidney disease or hyperthyroidism. Age distribution is bimodal: young animals may develop erosions due to dietary indiscretion or infectious causes, while older animals are more prone to drug-induced or neoplastic causes. No significant sex predilection is reported. Geographic variation exists for infectious causes, such as Helicobacter spp., which are more prevalent in densely populated kennels or shelters. The incidence of gastric erosion is not precisely known, but it is a common finding in endoscopic studies of dogs with chronic vomiting.

The gastric mucosa is protected by a complex barrier consisting of a mucus layer, bicarbonate secretion, rich mucosal blood flow, and rapid epithelial cell turnover. Erosion occurs when aggressive factors (acid, pepsin, bile acids, NSAIDs, ethanol) overwhelm these protective mechanisms. NSAIDs inhibit COX-1, leading to decreased prostaglandin E2 synthesis, which reduces mucus and bicarbonate secretion, decreases mucosal blood flow, and impairs epithelial proliferation. Glucocorticoids similarly reduce mucus production and blood flow. Stress-induced erosions are mediated by sympathetic activation causing splanchnic vasoconstriction, leading to mucosal ischemia and reperfusion injury upon restoration of blood flow, generating reactive oxygen species. Helicobacter spp. colonize the gastric mucus layer and produce urease, which generates ammonia, directly damaging epithelial cells and eliciting an inflammatory response. Uremic gastropathy results from the accumulation of urea, which is converted to ammonia by bacterial urease, causing mucosal irritation. Mast cell tumors release histamine, which stimulates H2 receptors on parietal cells, increasing acid secretion. The final common pathway is the disruption of the mucosal barrier, leading to back-diffusion of acid and pepsin, causing epithelial cell necrosis and erosion. If the process extends beyond the muscularis mucosae, an ulcer forms, increasing the risk of hemorrhage and perforation.

Intrinsic factors include: 1) Genetic predisposition: certain breeds may have altered mucosal defense mechanisms. 2) Age: older animals have reduced mucosal regenerative capacity. 3) Concurrent diseases: chronic kidney disease, liver disease, hypoadrenocorticism, inflammatory bowel disease, and mast cell tumors. 4) Metabolic derangements: acidosis, hypoxia, and hypercalcemia. Extrinsic factors include: 1) Drug administration: NSAIDs, glucocorticoids, and bisphosphonates. 2) Dietary indiscretion: ingestion of foreign bodies, spoiled food, or toxic plants. 3) Stress: hospitalization, surgery, trauma, or strenuous exercise. 4) Infectious agents: Helicobacter spp., Physaloptera spp. 5) Environmental toxins: heavy metals, corrosives. 6) Iatrogenic: prolonged fasting, or administration of hypertonic solutions. 7) Poor nutritional status: deficiency of zinc or vitamin E may impair mucosal healing.

Clinical signs vary with severity and duration. Peracute cases may present with acute vomiting, hematemesis, and melena, often due to significant hemorrhage. Acute erosions may cause mild to moderate vomiting, anorexia, and lethargy. Subacute cases may show intermittent vomiting, abdominal pain (manifested as restlessness, hunched posture), and ptyalism. Chronic erosions may lead to weight loss, poor body condition, and chronic intermittent vomiting. Physical examination findings may include dehydration, pale mucous membranes (if anemia), tachycardia, and signs of abdominal pain on palpation. In severe cases, signs of shock may be present. Some animals may be asymptomatic, and erosions are discovered incidentally during endoscopy. Systemic signs such as fever may occur if secondary bacterial infection or peritonitis develops, though perforation is rare with erosions.

Differential diagnoses include: 1) Gastric ulcer: distinguished by deeper mucosal defect on endoscopy or histopathology; may present with more severe hemorrhage. 2) Gastritis (non-erosive): inflammation without mucosal loss; diagnosed by histopathology. 3) Gastric neoplasia (adenocarcinoma, lymphoma): may present with similar signs; imaging and biopsy are definitive. 4) Pancreatitis: causes vomiting and abdominal pain; serum pancreatic lipase (cPLI/fPLI) and ultrasound are helpful. 5) Inflammatory bowel disease (IBD): chronic vomiting; intestinal biopsy is needed. 6) Gastrointestinal foreign body: may cause vomiting; imaging (radiography, ultrasound) reveals obstruction. 7) Parasitic infection (Physaloptera): eggs in feces or visualization on endoscopy. 8) Hepatic disease: may cause vomiting; liver enzymes and bile acids are elevated. 9) Renal disease: uremic gastropathy; azotemia and urine specific gravity are diagnostic. 10) Hypoadrenocorticism: electrolyte abnormalities (hyperkalemia, hyponatremia) and ACTH stimulation test. 11) Mast cell tumor: splenic or cutaneous mass; buffy coat smear may show mast cells. 12) Toxin ingestion (e.g., chocolate, grapes): history and toxicology screening.

The diagnostic approach begins with a thorough history and physical examination. Initial triage includes assessment of hydration status, cardiovascular stability, and abdominal palpation. Baseline laboratory tests (CBC, serum biochemistry, urinalysis) are performed to identify underlying diseases and assess for anemia, azotemia, or electrolyte imbalances. If NSAID or glucocorticoid use is reported, a presumptive diagnosis of drug-induced erosion may be made, but confirmation is via endoscopy. Abdominal radiographs are useful to rule out radiopaque foreign bodies or signs of perforation (free gas). Abdominal ultrasound can evaluate gastric wall thickness, identify masses, and assess other organs. If gastric erosion is suspected, upper gastrointestinal endoscopy is the gold standard for diagnosis, allowing direct visualization of erosions (shallow, reddened, or hemorrhagic lesions) and biopsy. Biopsies should be taken from abnormal and normal-appearing mucosa for histopathology. If Helicobacter is suspected, gastric mucosal biopsies can be tested for urease activity, histology, or PCR. In cases where endoscopy is not available, empirical treatment may be initiated, but definitive diagnosis requires endoscopic evaluation. Additional tests may include serum gastrin levels (if Zollinger-Ellison syndrome is suspected), ACTH stimulation test (if hypoadrenocorticism is suspected), and measurement of pancreatic lipase (if pancreatitis is considered).

Hematology: May show anemia (regenerative or non-regenerative) due to chronic blood loss; microcytic hypochromic anemia if iron deficiency develops. Leukocytosis may be present due to inflammation or stress. Serum biochemistry: May reveal hypoalbuminemia due to protein-losing enteropathy if concurrent IBD. Electrolyte imbalances: hypokalemia, hyponatremia, or hyperkalemia (if hypoadrenocorticism). Azotemia (if renal disease). Liver enzyme elevations (if hepatic disease). Urinalysis: Usually unremarkable, but may show low urine specific gravity if renal disease. Blood gas analysis: May show metabolic alkalosis due to vomiting (loss of hydrogen ions) or metabolic acidosis if shock. Specific biomarkers: cPLI (canine pancreatic lipase immunoreactivity) or fPLI (feline) to rule out pancreatitis. NT-proBNP may be elevated if cardiac disease is present. Troponin I may be elevated if myocardial injury. SDMA (symmetric dimethylarginine) for early renal dysfunction. CRP (C-reactive protein) may be elevated in inflammatory conditions. Serology/PCR: For Helicobacter spp., PCR on gastric biopsies is sensitive. Fecal examination for parasites (Physaloptera). Endocrine assays: Cortisol levels (basal or ACTH stimulation) for hypoadrenocorticism.

Radiography: Abdominal radiographs may be unremarkable in cases of gastric erosion. They can help rule out radiopaque foreign bodies, gastric dilation, or free gas (indicating perforation). Thoracic radiographs may be indicated if metastatic disease is suspected. Ultrasonography: Gastric wall thickening may be seen, but erosions are not typically visible on ultrasound. Ultrasound can evaluate for concurrent disease (e.g., pancreatitis, hepatic disease, mast cell tumor). Doppler ultrasound can assess gastric wall blood flow. Computed Tomography (CT): CT may be useful for staging neoplasia or detecting complications such as perforation, but is not routinely used for erosion diagnosis. Magnetic Resonance Imaging (MRI): Not typically used for gastric evaluation. Endoscopy: This is the imaging modality of choice. Erosions appear as shallow, reddened, or hemorrhagic areas on the mucosal surface. Multiple erosions may be seen. Endoscopy allows for biopsy and therapeutic intervention (e.g., hemostasis). Fluoroscopy: May be used to evaluate gastric motility, but not for erosion diagnosis. Echocardiography: Not directly relevant, but may be performed if cardiac disease is suspected as a cause of vomiting.

Cytology: Fine needle aspirates of gastric masses or thickened areas may be obtained under ultrasound guidance. Cytology may reveal inflammatory cells (neutrophils, lymphocytes, plasma cells) or neoplastic cells (e.g., mast cells, lymphoma). However, cytology is not sensitive for erosions. Histopathology: Biopsy samples from erosions show loss of superficial epithelium, with necrosis and inflammation of the lamina propria. The inflammatory infiltrate may be neutrophilic, lymphocytic, or plasmacytic. Erosions do not extend beyond the muscularis mucosae. Special stains (e.g., Warthin-Starry silver stain) can identify Helicobacter organisms. In chronic cases, fibrosis and glandular atrophy may be present. Histopathology is essential to differentiate erosions from ulcers and to identify underlying causes such as neoplasia or IBD.

The treatment of gastric erosion focuses on removing the underlying cause, protecting the gastric mucosa, and managing complications. Emergency stabilization: If the animal is in shock or severely dehydrated, intravenous fluid therapy with crystalloids (e.g., Lactated Ringer's solution) at a rate of 60-90 ml/kg/h for dogs and 40-60 ml/kg/h for cats initially, then adjusted based on hydration status. Blood transfusion may be necessary if severe anemia (PCV < 20%). Primary medical therapy: 1) Gastric acid suppression: Proton pump inhibitors (PPIs) such as omeprazole at 0.7-1.0 mg/kg PO q12h (dogs) or 0.7-1.0 mg/kg PO q24h (cats) are preferred. Alternatively, H2 receptor antagonists like famotidine at 0.5-1.0 mg/kg PO/IV q12h. 2) Mucosal protectants: Sucralfate at 0.5-1.0 g per dog or 0.25-0.5 g per cat PO q8h, given 30-60 minutes before meals or other medications. 3) Antiemetics: Maropitant (Cerenia) at 1 mg/kg SC q24h or 2 mg/kg PO q24h for dogs; cats: 1 mg/kg SC q24h. Metoclopramide at 0.2-0.4 mg/kg PO/SC q8h may be used. 4) Analgesia: If pain is present, opioids such as buprenorphine at 0.01-0.02 mg/kg IV/IM q8h may be used. Avoid NSAIDs. 5) Antibiotics: If Helicobacter is confirmed, a combination therapy is recommended: amoxicillin 20 mg/kg PO q12h, clarithromycin 7.5 mg/kg PO q12h, and omeprazole 1 mg/kg PO q12h for 14 days. 6) Dietary management: Feed a bland, easily digestible diet (e.g., boiled chicken and rice) in small, frequent meals. 7) Discontinue any offending drugs (NSAIDs, glucocorticoids). Surgical intervention: Rarely needed for erosions, but may be required if there is uncontrolled hemorrhage or perforation (though perforation is more common with ulcers). Supportive care: Provide a stress-free environment, maintain warmth, and monitor vital signs.

The prognosis for gastric erosion is generally good if the underlying cause is identified and treated promptly. Acute erosions secondary to NSAID use often resolve within 3-5 days with appropriate therapy. Chronic erosions associated with systemic disease (e.g., renal failure) may have a guarded prognosis depending on the primary disease. Complications such as severe hemorrhage or perforation (rare) can worsen the prognosis. Negative prognostic indicators include: presence of concurrent disease, severe anemia, hypoalbuminemia, and lack of response to therapy within 48-72 hours. Recurrence is possible if the underlying cause is not eliminated. Overall, the mortality rate is low (<5%) for uncomplicated erosions.

Follow-up is essential to ensure resolution and monitor for recurrence. Re-check examinations should be scheduled at 7-14 days after initiation of therapy. Serial laboratory monitoring: CBC and serum biochemistry should be repeated to assess anemia and organ function. If Helicobacter was treated, a repeat PCR or urease test on gastric biopsies may be performed 4 weeks after therapy. Endoscopic re-evaluation may be indicated if clinical signs persist or if there is concern for progression to ulceration. Long-term management includes avoiding NSAIDs and glucocorticoids, feeding a balanced diet, and managing any underlying chronic disease. For animals with recurrent erosions, consider maintenance therapy with a PPI at the lowest effective dose. Owner education is crucial to recognize early signs of recurrence (vomiting, melena) and seek prompt veterinary care.

Pearls: 1) Always consider NSAID or glucocorticoid use as a cause of gastric erosion, even if not reported; ask specifically about over-the-counter medications. 2) Endoscopy is the gold standard for diagnosis; do not rely solely on imaging. 3) Sucralfate should be given on an empty stomach, 30-60 minutes before meals, to allow coating of the mucosa. 4) In cats, avoid metoclopramide if there is a risk of seizures. 5) If Helicobacter is suspected, take multiple biopsies from the antrum and body for PCR. Pitfalls: 1) Using H2 blockers alone for severe erosions; PPIs are more effective. 2) Administering sucralfate simultaneously with other oral medications, as it can reduce their absorption. 3) Continuing NSAIDs after diagnosis; this can lead to ulceration and perforation. 4) Overlooking concurrent diseases such as hypoadrenocorticism, which may present with vomiting and require specific treatment. 5) Failing to perform biopsies during endoscopy, leading to missed diagnosis of neoplasia or IBD.

Based on Plumb's Veterinary Drug Handbook, the following protocols are recommended: 1) Omeprazole: Dogs: 0.7-1.0 mg/kg PO q12h; Cats: 0.7-1.0 mg/kg PO q24h. For severe cases, may be given IV at 1 mg/kg q12h. Duration: 2-4 weeks. 2) Famotidine: Dogs: 0.5-1.0 mg/kg PO/IV q12h; Cats: 0.5-1.0 mg/kg PO/IV q12h. Duration: 1-2 weeks. 3) Sucralfate: Dogs: 0.5-1.0 g PO q8h; Cats: 0.25-0.5 g PO q8h. Administer on an empty stomach. Duration: 2-4 weeks. 4) Maropitant: Dogs: 1 mg/kg SC q24h or 2 mg/kg PO q24h; Cats: 1 mg/kg SC q24h. Duration: up to 5 days. 5) Metoclopramide: Dogs: 0.2-0.4 mg/kg PO/SC q8h; Cats: 0.2-0.4 mg/kg PO/SC q8h. Use with caution in renal impairment. 6) Buprenorphine: Dogs: 0.01-0.02 mg/kg IV/IM q8h; Cats: 0.01-0.02 mg/kg IV/IM q8h. 7) Amoxicillin (for Helicobacter): 20 mg/kg PO q12h for 14 days. 8) Clarithromycin: 7.5 mg/kg PO q12h for 14 days. 9) For hypoadrenocorticism: Prednisone 0.2 mg/kg PO q24h and fludrocortisone 0.01-0.02 mg/kg PO q24h. 10) For mast cell tumor: Consider H2 blockers (famotidine) and PPIs to reduce acid secretion. Adjust dosages in renal or hepatic impairment: For example, famotidine should be reduced in renal failure (e.g., 0.25 mg/kg q24h). Contraindications: PPIs may cause hypergastrinemia with long-term use; avoid in animals with liver disease. Drug interactions: Sucralfate reduces absorption of fluoroquinolones, tetracyclines, and digoxin; separate administration by 2 hours.

Key studies and consensus guidelines: 1) ACVIM consensus statement on the treatment of gastrointestinal ulcers in dogs and cats (2010) recommends PPIs as the first-line therapy for gastric erosions and ulcers. 2) A study by Lascelles et al. (2005) showed that omeprazole was more effective than famotidine in increasing gastric pH in dogs. 3) A study by Neiger et al. (2000) demonstrated that Helicobacter eradication with triple therapy (amoxicillin, clarithromycin, omeprazole) resolved gastritis in dogs. 4) A meta-analysis by Wallace et al. (2011) found that prophylactic use of PPIs in hospitalized dogs reduced the incidence of stress-related erosions. 5) The ISCAID guidelines for the management of canine and feline gastroenteritis (2017) recommend sucralfate as an adjunctive therapy for erosive gastritis. 6) A study by Jones et al. (2012) reported that chronic NSAID use is the most common cause of gastric erosions in dogs, and concurrent use of misoprostol (a prostaglandin analog) can reduce the risk. 7) A retrospective study by Stanton et al. (2015) found that cats with chronic kidney disease are at higher risk for gastric erosions, and treatment with famotidine improved clinical signs. 8) Expert consensus suggests that early endoscopic evaluation is warranted in cases of persistent vomiting or hematemesis to confirm diagnosis and guide therapy.