The most common cause of gastric perforation is peptic ulcer. Perforation occurs as the ulcer deepens and penetrates the muscular layer, the plasma membrane layer and finally the stomach or duodenal wall. Several different consequences can occur after perforation. If the bottom of the ulcer has been adhered to the adjacent organs such as pancreas and liver before perforation, forming a penetrating ulcer, this is a chronic perforation, and in a few cases the bottom of the ulcer is adhered to the transverse colon, forming a gastrocolic fistula after perforation. Most of the above two cases occur in the perforation of ulcers in the posterior wall of the stomach and duodenum. If the ulcer is perforated and rapidly adheres to the greater omentum or nearby organs, an abscess may form around the perforation. Acute free perforation is the most serious complication of ulcer disease, the perforation site is mostly in the anterior wall of the first duodenal segment and the prepyloric area, because the perforation occurs quickly, local adhesions occur at the end, the gastric contents leak directly into the abdominal cavity, forming diffuse peritonitis, which requires first aid. Small perforations without peritonitis can be treated conservatively by fasting, placing a nasogastric tube to aspirate gastric contents, giving fluids to replenish water and electrolytes, and applying antibacterial drugs to prevent secondary infection in the abdominal cavity. Post-full meal perforations, often with diffuse peritonitis, require emergency surgery within 6-12 hours. Chronic perforation, which progresses more slowly, can cause adhesions and fistulas to adjacent organs and often requires surgical treatment. Gastric perforation can be classified as acute, subacute or chronic according to its clinical presentation.