Clinical and pathological study of rebleeding of intracranial aneurysm--based on 7 cases expired by rebleeding during hospital stay (author's transl)

Abstract

Seven patients who had expired due to rebleeding of ruptured intracranial aneurysm during hospitalization were studied clinically and pathologically to evaluate the risk factors and the warning signs of rebleeding, and to evaluate therapeutic methods in acute stages of ruptured intracranial aneurysm. It was evident from clinical observations that rebleeding was preceded by increase or fluctuation in blood pressure lasting from several hours to several days. And also this instability of blood pressure, which was followed by rebleeding, was caused by several psychological and physical factors, such as transportation to the neurosurgical ward, defecation and voiding, angiography and brain scan, ventricular drainage and deterioration of the neurological state. There were 20 episodes of rebleeding in these 7 cases; 15 of which occurred within 14 days after the previous attack. Among the risk factors concerning the clinical feature, all factors mentioned above which resulted from the increase or instability of blood pressure, prolonged headache and nuchal rigidity suggesting minor leakage from aneurysm and acute stage after bleeding were considered to be of great importance. Age and sex had no significance. Both hypertension in the past and upon admission were of less significance as risk factors. The grade of the patient upon admission was also not meaningful because five patients were in good condition, Grade I or II. In the risk factors examined angiographically, aneurysm over 10 mm in size, aneurysm with loculi and vasospasm were all significant, but there was no special localization to suggest the tendency of rebleeding. As warning sign of rebleeding, increase or instability of blood pressure, deterioration of the neurological state and worsening of the headache and nuchal rigidity seemed to have great significance. Postmortum study was performed on 4 cases. Extensive brain edema was seen in all of them and cerebral herniation in three (Cases 2, 3 and 4) ; Case 2 had a small hematoma in the insule, Case 3 showed large cerebral infarction in the contralateral hemisphere to the ruptured aneurysm and Case 4 had intraventricular hemorrhage. The cause of death in Case 1 seemed that the vital center suddenly ceased to function because of severe ischemia. Ruptured intracranial aneurysm should be treated surgically beofre rebleeding. However, if an early operation was impossible due to the patient's poor condition or some other reasons, conservative treatment is inevitable under high risk of rebleeding. Rebleeding of aneurysm depends upon two major factors; the first is the intensity of the ruptured aneurysmal wall, i.e. thrombus and adhesion around the aneurysm vs. fibrinolytic process; the second is the intensity of the power acting on the wall, i.e. blood pressure. Therefore, antifibrinolytic therapy and control of the blood pressure are essential in nonsurgical treatment of ruptured aneurysm, and control of increased intracranial pressure due to brain edema and/or hemorrhage is important. Close observation of the patient's condition, especially of the blood pressure and of the neurological state, is of great importance in the prediction of rebleeding.