Rebleeding from ruptured intracranial aneurysms in North Eastern Province of Japan. A cooperative study

Object: Rebleeding from ruptured intracranial aneurysms is a major cause of death and disability. With regard to the factors that precipitate the rebleeding and influence the time course after initial bleeding, previous reports differ in their results, and the number of patients investigated was not sufficient for valid conclusions. This study was thus designed to clarify the factors related to rebleeding from ruptured intracranial aneurysms in a large group of patients of the North Eastern Province of Japan. Methods: We found 181 patients with rebleeding after hospitalization among 5612 cases of ruptured intracranial aneurysms from January 1997 to December 2001 in 33 major hospitals in the North Eastern Province of Japan. We analyzed the data with respect to the time course after bleeding and rebleeding, the arterial blood pressure, the situation when rebleeding occurred, the methods of neuroimaging, the level of consciousness, the treatment and the outcome. Results: Of 181 patients who were hospitalized, rebleeding occurred in 65 (35.9%) within 3 h and 88 (48.6%) within 6 h after the initial subarachnoid hemorrhage (SAH). The consciousness level before the rebleeding varied widely in distribution, but belonged to the drowsiness or less [Japan coma scale (JCS) single-digit] in 83 patients (45.8%), but after rebleeding, JCS triple-digits (semicoma to coma) included 152 patients (84.0%). Systolic arterial blood pressure prior to rebleeding was most commonly between 120 and 140 mmHg. Rebleeding did occur more frequently during angiography (totally 29 patients, 20%) and much less frequently during 3D-CTA and MRA procedures (a single case). Treatment consisted of aneurysm neck clipping in 72 patients (40.0%), endovascular therapy with coils in 4 patients (2.2%) and conservative ones in 103 patients (56.9%). As to outcome, 109 patients with rebleeding (60.2%) died in 3 months following initial SAH. Conclusion: Rebleeding occurs more frequently in the earlier period after the initial SAH than previously believed. Thus, more aggressive pharmacologically induced systemic arterial hypotension appears lobe important for preventing rebleeding but ultimate outcome of more aggressive hypotension is yet to be determined. If feasible, in order to avoid catheter-angiography related rebleeding, evaluations solely with 3D-CTA and MRA should be in consideration and earlier surgical intervention seems essential as rebleeding does occur often within the first 3 h of onset. (0 2007 Published by Elsevier B.V.