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Delayed Ischemic Deterioration in Patients with Early Aneurysm Operation and Intravenous Nimodipine

S S Hans, Ljunggren Bengt, Brandt Lennart, Messeter Kenneth

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Abstract

A consecutive series of 100 individuals with aneurysmal subarachnoid hemorrhage were subjected to early aneurysm operation followed by subsequent intravenous administration of the calcium antagonist nimodipine during the critical period for symptomatic vasospasm. A total of 85 patients were in Hunt and Hess neurological Grades I through III, and 15 were in Grade IV or V before operation. In 39 individuals the aneurysm was located in the anterior cerebral artery complex (ACA), in 29 it originated from the internal carotid artery complex (ICA), and in 32 individuals the ruptured aneurysm arose from the middle cerebral artery (MCA). Of the patients, 71% made a good neurological recovery; the morbidity was 22%, and the mortality was 7%. Of the Grade I-III patients, 79% made a good neurological recovery, and the mortality was 6%. Delayed ischemic cerebral deterioration with permanent dysfunction occurred in five patients, all with ruptured ACA aneurysms. No single patient in the ICA or MCA populations developed delayed ischemic deterioration with fixed neurological deficit despite the presence of several potential risk factors, especially among the MCA aneurysm patients.

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What this paper is about

A consecutive series of 100 individuals with aneurysmal subarachnoid hemorrhage were subjected to early aneurysm operation followed by subsequent intravenous administration of the calcium antagonist nimodipine during the critical period for symptomatic vasospasm. A total of 85 patients were in Hunt and Hess neurological Grades I through III, and 15 were in Grade IV or V before operation. In 39 individuals the aneurysm was located in the anterior cerebral artery complex (ACA), in 29 it originated from the internal carotid artery complex (ICA), and in 32 individuals the ruptured aneurysm arose from the middle cerebral artery (MCA). Of the patients, 71% made a good neurological recovery; the morbidity was 22%, and the mortality was 7%. Of the Grade I-III patients, 79% made a good neurological recovery, and the mortality was 6%. Delayed ischemic cerebral deterioration with permanent dysfunction occurred in five patients, all with ruptured ACA aneurysms. No single patient in the ICA or MCA populations developed delayed ischemic deterioration with fixed neurological deficit despite the presence of several potential risk factors, especially among the MCA aneurysm patients.

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Available abstract

A consecutive series of 100 individuals with aneurysmal subarachnoid hemorrhage were subjected to early aneurysm operation followed by subsequent intravenous administration of the calcium antagonist nimodipine during the critical period for symptomatic vasospasm. A total of 85 patients were in Hunt and Hess neurological Grades I through III, and 15 were in Grade IV or V before operation. In 39 individuals the aneurysm was located in the anterior cerebral artery complex (ACA), in 29 it originated from the internal carotid artery complex (ICA), and in 32 individuals the ruptured aneurysm arose from the middle cerebral artery (MCA). Of the patients, 71% made a good neurological recovery; the morbidity was 22%, and the mortality was 7%. Of the Grade I-III patients, 79% made a good neurological recovery, and the mortality was 6%. Delayed ischemic cerebral deterioration with permanent dysfunction occurred in five patients, all with ruptured ACA aneurysms. No single patient in the ICA or MCA populations developed delayed ischemic deterioration with fixed neurological deficit despite the presence of several potential risk factors, especially among the MCA aneurysm patients.

Key concepts: Medicine, Nimodipine, Aneurysm, Subarachnoid hemorrhage, Vasospasm, Middle cerebral artery, Internal carotid artery, Anesthesia

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