부산대학교 도서관

The prognosis for the severe stage of a ruptured cerebral aneurysm is generally poor. We have had 35 cases of good recovery out of 175 patients with severe ruptured cerebral aneurysms (Hunt-Kosnik Grade IV and V). We analyzed and compared the CT findings, rebleeding, change of consciousness level, surgical procedure, symptomatic vasospasm and Glasgow outcome scale for the 175 cases.In the most severe cases, where the patients died due to severe brain edema whether or not they were treated surgically, the CT findings demonstrated 1) small ventricle, 2) massive ventricle hemorrhage, 3) severe midline shift due to acute subdural hematoma or acute brain swelling in addition to a bilateral thick clot on the basal cistern.Cases with an uphill consciousness level within six hours after admission showed promise of very good recovery, due to early surgical operation for ruptured cerebral aneurysms.There are two big factors which contribute to a poor prognosis after severe subarachnoid hemorrhage. One of them is rebleeding and the other is the appearance of symptomatic vasospasm. So, from the viewpoint of preventing rebleeding, using venous infusion of diltiazem (Ca++ antagonist) for control of blood pressure (systolic pressure 120 130mmHg, diastolic pressure 70 90mmHg) and delaying angiography at least six hours after the last attack of ruptured aneurysms is important. We haven't experienced a case of rebleeding after using this treatment.For prevention of symptomatic vasospasm, we have administrated the intracisternal nicardipine treatment (4mg 2×1/10 days) after early surgery. There was no significant change of occurrence rate of symptomatic vasospasm between a nicardipine treated group and a non-nicardipine-treated group. However, the symptoms were almost transient(80%) in the nicardipine-treated group. Those of the non-nicardipine-treated group were only 10%.In conclusion, we have adopted the following therapy for severe subarachnoid hemorrhage: 1) in-jected a venous infusion of diltiazem for the control of blood pressure and delayed angiography more than six hours after the last attack, 2) intracisternal administration of nicardipine for preven-tion of symptomatic vasospasm, 3) dopamine and fluoro-carbon if symptomatic vasospasm occurred, 4) barbiturate coma therapy in cases whose consciousness level showed a downhill course due to brain edema, 5) hyperbaric therapy for permanent symptomatic spasm.