Outcome in patients subjected to early aneurysm operation and intravenous nimodipine.
B. Ljunggren, Jonathan Brandt, Hans Säveland
Abstract
B. Ljunggren, Jonathan Brandt, Hans Säveland
Abstract
A consecutive series of 120 individuals with subarachnoid hemorrhage (SAH) from a ruptured supratentorial aneurysm were subjected to early aneurysm operation followed by subsequent intravenous administration of the calcium antagonist nimodipine during the critical period for symptomatic vasospasm. One hundred and one patients were in Hunt and Hess neurological Grades I-III, and 19 were in Grade IV or V prior to surgery. In 50 individuals the aneurysm was located in the anterior cerebral artery complex (ACA), in 34 it originated from the internal carotid artery complex (ICA), and in 36 individuals the ruptured aneurysm arose from the middle cerebral artery (MCA). 74% of the patients made a good neurological recovery, the morbidity was 20%, and the mortality was 6%. Of the Grade I-III patients, 82% made a good neurological recovery, and the mortality was 5%. Delayed ischemic deterioration (DID) with permanent dysfunction occurred in five patients, all with ruptured ACA aneurysms. No single patient in the ICA or MCA populations developed DID with fixed neurological deficit (FND). The low incidence of symptomatic vasospasm following early aneurysm surgery suggests that intravenous nimodipine exerts an additional anti-ischemic effect. Analysis of blood concentration of nimodipine did not make it likely that therapeutical failures in the ACA aneurysm patients could be ascribed to individual deviations in the pharmacokinetics of nimodipine.
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A consecutive series of 120 individuals with subarachnoid hemorrhage (SAH) from a ruptured supratentorial aneurysm were subjected to early aneurysm operation followed by subsequent intravenous administration of the calcium antagonist nimodipine during the critical period for symptomatic vasospasm. One hundred and one patients were in Hunt and Hess neurological Grades I-III, and 19 were in Grade IV or V prior to surgery. In 50 individuals the aneurysm was located in the anterior cerebral artery complex (ACA), in 34 it originated from the internal carotid artery complex (ICA), and in 36 individuals the ruptured aneurysm arose from the middle cerebral artery (MCA). 74% of the patients made a good neurological recovery, the morbidity was 20%, and the mortality was 6%. Of the Grade I-III patients, 82% made a good neurological recovery, and the mortality was 5%. Delayed ischemic deterioration (DID) with permanent dysfunction occurred in five patients, all with ruptured ACA aneurysms. No single patient in the ICA or MCA populations developed DID with fixed neurological deficit (FND). The low incidence of symptomatic vasospasm following early aneurysm surgery suggests that intravenous nimodipine exerts an additional anti-ischemic effect. Analysis of blood concentration of nimodipine did not make it likely that therapeutical failures in the ACA aneurysm patients could be ascribed to individual deviations in the pharmacokinetics of nimodipine.
Key concepts: Nimodipine, Medicine, Aneurysm, Vasospasm, Subarachnoid hemorrhage, Anesthesia, Cerebral vasospasm, Middle cerebral artery