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Endoscopic study of acute gastric lesions following cerebral apoplexy



Endoscopic study of acute gastric lesions following cerebral apoplexy



Journal of Nippon Medical School 49(3): 340-352



The features of acute gastric lesions and its pathogenesis, observed after attacks of the cerebral apoplexy, were investigated. Endoscopic examination was performed within 10 days after the cerebral apoplexy attacks and repeated observations were made at 10 day intervals. Acute lesions in the upper G.I. [gastrointestinal] tract were seen in 25 of 45 cases of cerebral apoplexy with 23 of those being acute gastric lesion (51.1%). Acute gastric lesions are classified as ulcer, erosion, mucosal hemorrhage and ecchymosis. Of 11 cases manifested as rheumatemesis or melena, however, the remainder of them remained asymptomatic. The features of the acute ulcers were multiple (3 .apprx. 10), and tended to be localized in the fundic gland area. The acute ulcers of the larger sizes (above 10 mm) were hemorrhagic. Most of these ulcers were located along the longitudinal direction of the stomach. The erosive lesions were frequently of the multiple type and tended to localize in the pyloric gland region. On the other hand, mucosal hemorrhage and ecchymosis were widely distributed in the gastric mucosa. Fourteen cases of the 23 cases of acute gastric lesions were fatal and the cause of death in 12 cases was cerebral apoplexy per se. Twelve ulcers in 4 cases healed within 8-53 days. The erosion, mucosal hemorrhage and ecchymosis, also healed within 20 days in 6 cases. However, complications of pneumonia, liver dysfunction and uremia occurred during the deterioration of the disease. In reviewing the interrelationship between cerebral apoplexy and acute gastric lesion, an association was frequently observed with cerebral hemorrhage and subarachnoid hemorrhage and was seen in cerebral infarction in a lesser frequency. Moreover, acute gastric lesion was frequently observed in the combined types of cerebral apoplexy (with the bleeding parts extending from the area around the capsula interna of the thalamus and hypothalamus) and was also frequent in cases of internal carotid arterial occlusion of cerebral infarction. The lesion was also frequently observed in cases of serious disturbance of consciousness and increased cerebrospinal pressure. In relation to gastric secretion and the serum gastrin, the gastric acid secretion was significantly increased immediately after attacks of cerebral apoplexy. This was more pronounced if the patient showed evidence for acute gastric lesion complications. However, no direct interrelationship was confirmed between acute gastric lesion and serum gastrin. As a therapeutic attempt for bleeding from acute gastric lesion, antiacid and anticholinergic drugs, as well as antipepsin drugs were given. Bleeding ceased in 3 of 5 cases which clearly demonstrated evidence for hematemesis or melena. Moreover, in all 3 cases which demonstrated evidence for intagastric hemorrhage, hemorrhage ceased after the medication. The above-mentioned therapeutic effect is apparently effective for hemorrhage of acute gastric lesion which is complicated with cerebral apoplexy.

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Accession: 005359634

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