ACUTE GASTRIC ULCER
The cause of gastric or duodenal ulcers was a matter of debate during several decades; there are now known to be two main causes. H. pylori infection is a factor in many peptic ulcers, both gastric and duodenal; its causative role appears to be decreasing, however. Aspirin and other NSAIDs are also a known cause of gastric ulcers. A significant minority of these ulcers have causes other than H. pylori infection or NSAID use.
Small superficial erosions of the gastric mucosa, even those with a tendency to bleed, may cause few or no symptoms, though they are noted quite often by the endoscopist. Acute ulcers are characterized by a some-what greater defect of the mucosa and sometimes of the uppermost stratum of the submucosa. Their size varies considerably between the extremes of a few millimeters to 3 to 4 cm. Acute ulcers are usually multiple; the greater their number, the smaller their size. Single acute ulcers are rare. The site of predilection for acute ulcers is the prepyloric region, but occasionally very small ones may arise in the mucosa of the body and along the greater curvature. In contrast, larger acute ulcers are sometimes found along the so-called Magenstrasse, a groove along the lesser curvature that is the route food and liquids tend to take in moving toward the pylorus.
In its earliest stages, an acute ulcer appears as a shallow necrotic region, with a slightly raised soft margin surrounded by tissue which may or may not show a mild inflammatory reaction. The floor of the ulcer can appear black, as a consequence of the chemical changes produced by the hydrochloric acid on the blood that oozes from the lesion. At times the bleeding may be more pronounced, or even severe, with a relatively small ulcer. Should the ulcerative process reach the muscularis mucosae, this layer retracts, drawing the edges of the ulcer downward in opposition to each other. The original shape of the acute ulcer is oval, but it assumes a slitlike shape when the stomach wall contracts.
Although it is generally agreed that acute ulcers may become subacute or chronic, as a rule they have a good and relatively rapid healing tendency. The healing process starts with growth of the epithelium from the margins across the area from which the necrotic parts have been sloughed. From the newly formed epithelium, the growth is downward. Even the muscularis mucosae, if involved in the process, may be completely restored.
The diagnosis of an acute ulcer is not often made on clinical grounds, except when endoscopy is employed. The symptoms, if any, are negligible and certainly less pronounced than with an acute diffuse gastritis.
A special type of acute peptic ulcer of the stomach or duodenum, the so-called stress ulcer, has been discussed widely; its pathophysiologic relationship has not yet been completely clarified. It may develop following extensive burns (Curling ulcer), in the course of tetanus, after brain surgery (Cushing ulcer), or in the course of therapy with corticosteroids (steroid ulcer) or NSAIDs. The specific features of this ulcer type are the rapidity with which it comes into existence, the lack of any inflammatory reaction around the ulcer, complete absence of pain, and a pronounced tendency to perforation and bleeding. The frequency of ulcer formation during steroid therapy, however, has been controversial, with recent studies showing only a marginal increase in ulcer formation in patients receiving steroid treatment.