Partial Gastrectomy and Carcinoma

The polypoid appearance of the distal portions of the gastric stump in patients who have undergone gastrectomy has been referred to as gastritis cysticapolyposa. Several studies, mostly conducted in Europe and Asia, have reported a high prevalence of low-grade dysplasia in these polypoid areas, as well as an increased incidence of gastric adenocarcinoma 2 to 3 decades after gastrectomy. The implications of these findings, potentially important because of the suggestion that patients who undergo partial gastrectomy may need endoscopic surveillance, seem less urgent in the present era, when partial gastrectomy for peptic ulcer disease has become an exceedingly rare operation.

HEMORRHAGIC GASTROPATHY

Hemorrhagic gastropathy (hemorrhagic gastritis) refers to a group of conditions characterized by subepithelial hemorrhages and erosions. These mucosal lesions do not cause major bleeding unless ulcers develop. Three major factors are involved in the pathogenesis of hemorrhagic gastropathy: use of NSAIDs, ingestion of large quantities of alcohol, and severe physical stress.

Aspirin and other NSAIDs may induce mucosal edema, hyperemia, and multiple erosions and ulcerations. Such lesions may occur suddenly, without warning symptoms such as pain or discomfort, in first-time NSAID users and in patients who have taken NSAIDs regularly for years. Except for generic risk factors such as older age, female sex, and previous episodes, there is no known trait to identify NSAID users prospectively who may be susceptible to severe gastric injury.

Similar mucosal lesions, although usually less severe and only rarely evolving to ulcerations, can be caused by ingestion of large quantities of alcohol. Because alcohol and aspirin may act synergistically to break down mucosal defenses, one wonders how many hemorrhagic gastropathies have been caused by attempts to prevent hangovers by taking aspirin after an alcoholic binge.

The most severe degrees of hemorrhagic gastropathy are those induced by stress. Originally described in 1842 by Thomas Curling, stress-induced gastroduodenal mucosal breakdowns (known as Curling ulcers) can be found in most patients admitted to an intensive care unit; approximately 20% are a source of overt bleeding, and 2% to 5% of these ulcers cause life-threatening hemorrhage.

Pathogenesis

The pathogenesis of stress-induced hemorrhagic gastritis is not known, but lumenal acid seems to be essential. Acid exerts its deleterious effects when the mucosal defense mechanisms (e.g., the mucous-bicarbonate barrier and the epithelial layer) lose their integrity. Vascular disturbances—in association with stasis, vasoconstriction, and increased vascular permeability—may further contribute to mucosal vulnerability. Aspirin and NSAIDs act by interfering with prostaglandin synthesis, as noted earlier. Alcohol causes direct damage to the gastric mucosa; at a concentration of 12.5% (that of table wine), it induces hyperemia and petechiae, and concentrations greater than 40% (“hard liquors”) cause necrosis of the surface epithelium and capillaries and subsequent interstitial hemorrhage.

Дата добавления: 2015-11-14