Gastric Erosions

Gastric erosions are superficial breaks in the gastric mucosa that do not penetrate through the muscularis mucosae, usually 5 mm or less in diameter, often multiple, found in the antrum and body of the stomach. They are distinguished from ulcers, which are deeper (more than 5 mm in diameter with depth through the muscularis mucosae).

• Prevalence: found on 5 to 20% of endoscopies for dyspepsia, and in 40 to 70% of regular NSAID users. They are often asymptomatic.
• Causes:
  • NSAIDs and aspirin (the commonest), through inhibition of cyclooxygenase-1 with reduced protective prostaglandins, and direct mucosal injury. Even low dose aspirin (75 to 100 mg daily) causes erosions, and the risk is increased by age above 65 years, previous ulcer, corticosteroids, anticoagulants, and combinations of antiplatelet drugs.
  • Helicobacter pylori infection (a chronic gastritis with erosions, in up to 30 to 50% of cases of chronic erosive gastritis).
  • Alcohol (direct injury), smoking, bile reflux (after gastric surgery, cholecystectomy), and corrosive and caustic ingestion.
  • Stress related mucosal disease (critically ill patients, burns, trauma, mechanical ventilation for more than 48 hours, coagulopathy, shock, sepsis, and intracranial injury).
  • Drugs: potassium chloride, bisphosphonates, iron tablets, doxycycline, mycophenolate, chemotherapy (5-fluorouracil, methotrexate), and corticosteroids (with NSAIDs).
  • Others: radiation, Crohn disease, cytomegalovirus and other infections, uraemia, portal hypertensive gastropathy, ischaemia, eosinophilic gastritis, and autoimmune gastritis. Complete (varioliform) erosions are seen in lymphocytic gastritis (associated with coeliac disease and Helicobacter pylori).
• Complications: upper gastrointestinal bleeding (haematemesis, melaena, anaemia, which is usually mild to moderate but can be significant, particularly with anticoagulants and in critically ill patients), iron deficiency anaemia, progression to ulceration, and rarely perforation or gastric outlet obstruction (from scarring).
• Many patients have no symptoms, and erosions are discovered incidentally at endoscopy.

• Epigastric pain or burning, early satiety, nausea, bloating, belching, and loss of appetite. Pain may be worse or relieved by food. Symptoms correlate poorly with the severity of the erosions.
• Bleeding presentations: coffee ground vomiting, haematemesis, melaena, iron deficiency anaemia, and fatigue. Alarm features of massive bleeding include dizziness, syncope, tachycardia, and hypotension.
• Exposure history: NSAIDs and aspirin, alcohol, smoking, previous peptic ulcer, anticoagulants, corticosteroids, stress (surgery, intensive care), and diet.
• Examination: epigastric tenderness, pallor, and, with bleeding, tachycardia and hypotension. Often normal.
• Differential diagnosis: peptic ulcer disease, functional dyspepsia, gastro oesophageal reflux disease, gastric cancer, gastroparesis, biliary or pancreatic disease, Helicobacter pylori gastritis, eosinophilic gastritis, Zollinger-Ellison syndrome, Menetrier disease, and cardiac disease.
• Red flags: haematemesis or melaena, anaemia, weight loss, persistent vomiting, dysphagia, a palpable mass, age over 55 years with new dyspepsia, a family history of gastric cancer, and recurrent symptoms despite treatment.

• Upper endoscopy is the diagnostic test, showing flat or raised erosions (sometimes with a central umbilication, "varioliform" erosions, or haemorrhagic erosions), erythema and oedema, usually in the antrum. Perform it for alarm features, age over 55 years with new dyspepsia, persistent symptoms after treatment, bleeding, or anaemia.
• Biopsies: take samples from the antrum and body for histology (Helicobacter pylori, gastritis type, intestinal metaplasia, lymphocytic or eosinophilic infiltrates), and biopsy any ulcerated or suspicious lesion to exclude malignancy.
• Helicobacter pylori testing in all patients with erosions or dyspepsia: urea breath test (accurate, noninvasive) or stool antigen test, both requiring 2 weeks off proton pump inhibitors and 4 weeks off antibiotics and bismuth. Serology is used only when other tests are unsuitable (it cannot confirm cure), and rapid urease test or histology on biopsy.
• Blood tests: full blood count, ferritin, urea and electrolytes (urea is raised in upper bleeding), clotting, liver function, and group and save when bleeding. Check coeliac serology for lymphocytic gastritis, and gastrin when recurrent ulceration suggests Zollinger-Ellison syndrome.
• Assess bleeding risk with a validated bleeding score where bleeding is present (haemoglobin, urea, systolic blood pressure, pulse, melaena, syncope, hepatic disease, cardiac failure).

• Remove or reduce the cause:
  • Stop NSAIDs (and aspirin if there is no cardiovascular indication). If NSAIDs must continue, use the lowest dose for the shortest time, switch to paracetamol 1 g orally 6 hourly (maximum 4 g per day) or topical NSAIDs, or use a selective COX-2 inhibitor (celecoxib 100 to 200 mg once to twice daily) with a proton pump inhibitor in high risk patients. If aspirin is needed for secondary cardiovascular prevention, continue it with a proton pump inhibitor.
  • Alcohol cessation or reduction (below 14 units per week), smoking cessation, and avoidance of irritant foods and drugs.
  • Review and stop other offending medicines when possible (potassium chloride tablets, bisphosphonates, iron).
• Acid suppression: omeprazole 20 to 40 mg orally once daily (or esomeprazole 20 to 40 mg, lansoprazole 30 mg, pantoprazole 40 mg) taken 30 to 60 minutes before breakfast, for 4 to 8 weeks, with healing in more than 90%. Continue a proton pump inhibitor for as long as the NSAID or antiplatelet drug is continued in at risk patients (age above 65 years, previous ulcer or bleeding, anticoagulants, corticosteroids, dual antiplatelet therapy). Use pantoprazole with clopidogrel because omeprazole and esomeprazole reduce its activation.
• Helicobacter pylori eradication when positive (it reduces ulcer relapse and bleeding risk, and treats the gastritis):
  • Triple therapy for 14 days where clarithromycin resistance is below 15% and the patient has not taken a macrolide before: a proton pump inhibitor (omeprazole 20 to 40 mg or esomeprazole 20 to 40 mg) twice daily, amoxicillin 1 g twice daily, and clarithromycin 500 mg twice daily.
  • Bismuth quadruple therapy for 10 to 14 days (preferred first line where clarithromycin resistance is high, or after a prior macrolide, and as second line therapy): a proton pump inhibitor twice daily, bismuth subcitrate potassium 120 mg (or bismuth subsalicylate 262 mg) 4 times daily, tetracycline 500 mg 4 times daily, and metronidazole 400 to 500 mg 3 to 4 times daily.
  • Penicillin allergy: bismuth quadruple therapy. Where metronidazole resistance is high, extend to 14 days with higher metronidazole doses (500 mg 4 times daily), or use a rifabutin based or high dose dual regimen under specialist guidance.
  • Vonoprazan based dual therapy (vonoprazan 20 mg twice daily with amoxicillin 1 g 3 times daily for 14 days) or triple therapy where available.
  • Test for cure at least 4 weeks after the end of antibiotics and 2 weeks after stopping proton pump inhibitors (urea breath test or stool antigen test), and use a second line regimen without repeating the same antibiotics for failures. Check adherence, and avoid alcohol with metronidazole.
• Gastroprotection for patients who must continue NSAIDs: proton pump inhibitor (omeprazole 20 mg daily is preferred), or misoprostol 200 micrograms orally 4 times daily with food (diarrhoea and abdominal pain are common, and it is contraindicated in pregnancy and women who may become pregnant).
• Other agents: sucralfate 1 g orally 4 times daily (1 hour before meals and at bedtime) for 4 to 8 weeks (separates from other drugs by 2 hours, and caution in renal impairment because of aluminium), and antacids or alginate (calcium carbonate 500 to 1000 mg as needed) for symptom relief. H2 receptor antagonists (famotidine 20 mg twice daily) are less effective than proton pump inhibitors for NSAID erosions.
• Stress related mucosal disease: prophylaxis for critically ill patients with risk factors (mechanical ventilation for more than 48 hours, coagulopathy, shock, head injury, burns): pantoprazole 40 mg IV or orally once daily, or famotidine 20 mg IV 12 hourly, stopping when the risk resolves and enteral feeding is established. Avoid unnecessary continuation at discharge.
• Bleeding erosions: resuscitate, check haemoglobin, give pantoprazole or omeprazole 80 mg IV bolus then 8 mg per hour for 72 hours (or 40 mg IV 12 hourly) for high risk lesions, perform urgent endoscopy within 24 hours, with endoscopic treatment when active bleeding, and transfuse for haemoglobin below 70 g/L (or below 80 g/L with cardiovascular disease). Manage anticoagulants and antiplatelets with specialist advice.
• Specific causes: bile reflux (cholestyramine 4 g 1 to 3 times daily, and surgical review), Crohn disease and eosinophilic gastritis (specialist therapy), lymphocytic gastritis (gluten free diet if coeliac disease), and portal hypertensive gastropathy (non-selective beta blocker propranolol 20 to 40 mg twice daily, and iron for anaemia).
• Iron deficiency: ferrous sulphate 200 mg (65 mg elemental iron) orally once daily or on alternate days for 3 months after normalisation of haemoglobin, and investigate for other sources of blood loss (colonoscopy, coeliac serology) in men and postmenopausal women.
• Special groups:
  • Pregnancy: avoid NSAIDs, use antacids and alginate, and omeprazole 20 mg daily or famotidine for symptoms. Defer Helicobacter pylori eradication until after delivery and breastfeeding, unless there is bleeding ulceration. Misoprostol is contraindicated.
  • Elderly: higher risk of bleeding, so use gastroprotection with all NSAIDs and antiplatelet drugs, avoid NSAIDs where possible, and review polypharmacy.
  • Children: Helicobacter pylori infection is a cause of gastritis. Treat only when ulcer disease or erosions with symptoms are proven, with amoxicillin 50 mg/kg per day in 2 divided doses, clarithromycin 15 mg/kg per day in 2 divided doses, and omeprazole 1 mg/kg per day in 2 divided doses for 14 days, or metronidazole based regimens depending on resistance.
  • Anticoagulated and antiplatelet patients: continue gastroprotection and review the need for combined therapy.
  • Renal impairment: avoid NSAIDs and aluminium containing sucralfate, and adjust antibiotic doses.
  • Liver disease: avoid NSAIDs, and use propranolol for portal hypertensive gastropathy.
• Follow up: review at 4 to 8 weeks and repeat endoscopy only for gastric ulcers, alarm features, or persistent symptoms. Confirm Helicobacter pylori eradication. Refer to a gastroenterologist for bleeding, refractory disease, suspected malignancy, or rare causes.