Seven cases are described of gastrointestinal haemorrhage occurring in association with a cerebro- vascular accident. In five instances the intracranial lesion was a cerebral haemorrhage, and in two it was a subarachnoid haemor- rhage. Haematemesis occurred in five cases, and melaena in one ; in the seventh case no clinical evidence of bleeding was obtained, but blood was found in the stomach at autopsy.
In the five cases of cerebral haemorrhage death occurred within 24 hours of the onset. At autopsy the outstanding feature in the digestive tract in each of these cases was the presence of numerous punctate haemorrhages and ecchy- moses in the mucosa of the stomach. There were also erosions in two cases, and erosions and small acute ulcers in one.
A histological study was made of the early lesions in the gastric mucosa. With the benzidine stain (Lepehne -Pickworth method), described for the demonstration of the vascular pattern of the central nervous system, areas of vascular disturbance in the stomach were clearly outlined. The predominant lesion was found to be a wedge -shaped haemorrhage situated superficially in the gastric mucosa. The observation of Hagemann (1909) that this superficial mucosal haemorrhage is of venous origin, and owes its characteristic shape to the anatomical arrangement of the mucosal venules, has been confirmed. The superficial haemorrhage is followed by local necrosis of the mucosa, and diges- tion or sloughing of the necrotic area leads to the formation of an erosion or, if the muscularis mucosae is penetrated, an acute ulcer.
Haematemesis was the presenting feature in one of the two cases of sub - arachnoid haemorrhage. This patient died six days after the onset of the illness ; at necropsy the stomach appeared normal, but microscopic examination revealed evidence of widespread focal mucosal damage. The other patient with sub - arachnoid haemorrhage survived, and radiological examination of the upper gastrointestinal tract one month after the onset of the haematemesis gave a negative result.
The pathogenesis of acute gastrointestinal lesions associated with intracranial disease is discussed.