Stress gastritis

Aetiology

Physical trauma
Shock
Sepsis
Haemorrhage
Respiratory failure
CNS disease causing elevated intra-cranial pressure with resultant vagal nerve stimulation (Cushing ulcer)
Burns involving >30% TBSA (Curling ulcer)

Likely multifactorial relating to reduction in blood flow - leads to impaired defence systems including reduction in mucus and bicarbonate secretion
Gastric mucosal changes usually develop 1-2 days after a traumatic event
Risk factors for developing clinically significant bleeding from stress gastritis
- Coagulopathy
- Respiratory failure requiring mechanical ventilation

Endoscopy
- Characterised by multiple superficial non-ulcerating erosions, typically beginning in the proximal stomach and progressing distally
- Early lesions are typically multiple and shallow, with discrete areas of erythema along with focal haemorrhage or adherent clot. Frank bleeding can result if it erodes into the submucosa. Almost always seen purely in the fundus and not in the distal stomach.
- Later lesions appear identical to regenerating mucosa around a healing gastric ulcer

Prophylaxis - controversial as to what defines high-risk, but high-risk patients should be given IV PPI
Early enteral feeding is protective
Endoscopic control is usually difficult due to diffuse inflammation, and re-bleeding rate is high
Octreotide can probably help
Reports of vasopressin administration into left gastric artery (contra-indicated in cardiac and liver disease) or embolisation (which is probably the best option)
Surgery
- Standard
  - Most lesions are in the proximal stomach or fundus, so a long anterior gastrotomy should expose them
  - Oversew all areas of bleeding
  - Consider performing a truncal vagotomy and pyloroplasty
- Last-ditch
  - Subtotal gastrectomy