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.
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| Plate 4-43 |
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.
