GIANT GASTRIC ULCER
Giant gastric ulcers are rare in the overall group of gastric ulcers, especially since upper endoscopy evaluation has become available and ulcer treatments with proton pump inhibitors and for H. pylori have also become available. The site of origin is usually on the posterior wall of the gastric body and may progressively involve the lesser curvature by extension. The ulcers may penetrate the gastrohepatic ligament and even involve the liver and pancreas. They are particularly deceptive because the flattened floor of the ulcer is extensive, so that it resembles an atrophic area of gastric mucosa. A very similar pathologic picture can be produced acutely by the corrosive action of acids or alkalis. When caustic agents are involved, however, the contrast material puddles in the prepyloric region and on the posterior wall of the stomach if the patient assumes a supine position immediately after the accident of ingestion.
In the past, giant gastric ulcers were usually thought to be carcinomas. They now are considered benign lesions that can be properly treated with vigorous medical management. Upper endoscopy is needed for biopsies to evaluate for carcinoma and to assess for H. pylori. Benign ulcers are treated with proton pump inhibitors; healing can take months. Surgical exploration may lead to extensive surgery. Ulcers of this magnitude, and particularly those in the prepyloric region in the absence of a caustic ingestion history, must be considered malignant until proven otherwise by biopsy. Adenomatous changes of serious malignant importance can occur in giant ulcer craters just as they can in the smaller ulcers of the stomach.
Patients with giant benign gastric ulcers are older than patients with smaller ulcers and have more aggressive disease, reflected by a higher incidence of bleeding, anorexia, weight loss, and emergency admission. Patients usually have a long history of ulcer disease, and usually ulcer symptoms have been present for at least 4 to 6 months. The great majority of these patients are over the age of 50. The patient may have lost much weight and may show advanced stages of malnutrition. Many have fairly far advanced peripheral vascular disease, with involvement of the mesenteric arterioles in an arteriosclerotic process, and, perhaps because of this diminished blood supply, the ulcer has proceeded to its large size. Perforation or massive hemorrhage as a terminal event is not unusual.