Gastric Perforation

Gastric perforation is full thickness disruption of the stomach wall with escape of gas and gastric contents into the peritoneal cavity.

Causes include peptic ulcer disease, gastric malignancy, trauma, iatrogenic endoscopic injury, foreign body, severe gastric distension and ischaemia.

The key distinctions are:

• Free versus contained perforation
• Benign versus malignant pathology
• Stable versus septic patient
• Small repairable defect versus extensive tissue destruction

Free perforation causes sudden severe epigastric pain followed by rapidly progressive peritoneal irritation.

Typical findings include:

• Epigastric or generalised guarding
• Abdominal rigidity
• Tachycardia
• Reduced bowel sounds
• Progressive sepsis

A contained perforation may present with more localised pain and relatively preserved physiology.

Shock, altered consciousness, oliguria or metabolic acidosis indicates advanced contamination and physiological failure.

CT abdomen with IV contrast: identify free gas and the site of gastric wall disruption while determining whether contamination is free or contained.

Check full blood count, renal function, electrolytes, coagulation, lactate and crossmatch according to severity.

A gastric perforation must raise concern for underlying malignancy, particularly when the lesion is large, chronic appearing or indurated.

Keep fasting.

Establish IV access, correct hypovolaemia and insert a nasogastric tube when major gastric distension or persistent vomiting is present.

Start Gram negative and anaerobic coverage promptly.

Stable community acquired perforation:

Ceftriaxone 2 g IV every 24 hours plus metronidazole 500 mg IV every 12 hours.

Severe sepsis, extensive contamination or healthcare associated infection:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, adjusted for renal function.

Give intravenous acid suppression:

Pantoprazole 40 mg IV every 12 hours.

Iatrogenic perforation

A perforation recognised during endoscopy can often be closed immediately.

Defects below approximately 2 cm can frequently be closed with through the scope or over the scope clips. Larger accessible defects may require endoscopic suturing. Successful closure still requires fasting, observation, IV fluids and antibiotics.

Generalised peritonitis, failed endoscopic closure, delayed perforation or uncontrolled leakage requires surgery.

Spontaneous gastric perforation

Free perforation with peritonitis requires operative source control.

Small benign appearing defects can undergo primary closure with or without omental reinforcement.

Large, indurated or suspicious gastric perforations require tissue diagnosis and may require wedge resection or gastrectomy when oncologically and physiologically appropriate. Gastric malignancy accounts for a clinically important minority of gastric perforations.

If emergency physiology does not permit oncological gastrectomy, control the perforation first and establish definitive histology, then plan staged cancer treatment after recovery.

After adequate source control for established intra abdominal infection, approximately 4 days of antibiotics is generally sufficient unless infection remains uncontrolled.