Background and Purpose-The rationale behind early aneurysm surgery in patients with subarachnoid hemorrhage (SAH) is the prevention of rebleeding as early as possible after SAH. In addition, by clipping the aneurysm as early as possible, one can apply treatment for cerebral ischemia more vigorously (induced hypertension) without the risk of rebleeding. Hypervolemic hemodilution is now a well-accepted treatment for delayed cerebral ischemia. We compared the prospectively collected clinical data and outcome of patients admitted to the intensive care unit in the period 1977 to 1982 with those of patients admitted in the period 1989 to 1992 to measure the effect of the change in medical management procedures on patients admitted in our hospital with SAH. Methods-We studied 348 patients admitted within 72 hours after aneurysmal SAH. Patients with negative angiography results and those in whom death appeared imminent on admission were excluded. The first group (group A) consisted of 176 consecutive patients admitted from 1977 through 1982. Maximum daily fluid intake was 1.5 to 2 L. Hyponatremia was treated with fluid restriction (Ͻ1 L/24 h). Antihypertensive treatment with diuretic agents was given if diastolic blood pressure was Ͼ110 mm Hg. Patients in the second group (172 consecutive patients; group B) were admitted from 1989 through 1992. Daily fluid intake was at least 3 L, unless cardiac failure occurred. Diuretic agents and antihypertensive medications were avoided. Cerebral ischemia was treated with vigorous plasma volume expansion under intermittent monitoring of pulmonary wedge pressure, cardiac output, and arterial blood pressure, aiming for a hematocrit of 0.29 to 0.33. Aneurysm surgery was planned for day 12. Results-Patients admitted in group B had less favorable characteristics for the development of cerebral ischemia and for good outcome when compared with patients in group A. Despite this, we found a significant decrease in the frequency of delayed cerebral ischemia in patients of group B treated with tranexamic acid (Pϭ0.00005 by log rank test) and significantly improved outcomes among patients with delayed cerebral ischemia (Pϭ0.006 by 2 test) and among patients with deterioration from hydrocephalus (Pϭ0.001 by 2 test). This resulted in a significant improvement of the overall outcome of patients in group B when compared with those in group A (Pϭ0.006 by 2 test). The major cause of death in group B was rebleeding (Pϭ0.011 by 2 test). Conclusions-We conclude that the outcome in our patients with aneurysmal SAH was improved but that rebleeding remains a major cause of death. Patient outcome can be further improved if we can increase the efficacy of preventive measures against rebleeding by performing early aneurysm surgery. (Stroke. 1998;29:924-930.)

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With the exception of the presence of a parenchymal hematoma, the site of the ruptured aneurysm can be predicted by CT only in ruptured anterior cerebral artery or anterior communicating artery aneurysms.

Interobserver variability in the prediction of delayed cerebral ischemia by means of blood on CT was investigated in 159 patients with aneurysmal subarachnoid hemorrhage, admitted within 72 hours after the bleed. The authors found considerable interobserver variability in the assessment of the amount of blood in the individual cisterns. A high sum score was an independent predictor for delayed cerebral ischemia only for rater 1 (rater 1: hazard ratio, 3.26; 95% confidence interval [CI], 1.14 to 7.75; rater 2: hazard ratio, 1.72; 95% CI, 0.72 to 4.09). The authors conclude that interobserver variability limits the predictive power of the amount of blood on CT for the occurrence of cerebral ischemia.

Visual failure is an uncommon presenting symptom of an intracranial aneurysm. It is even more uncommon in aneurysms arising from the anterior cerebral artery (ACA). We presented 2 patients with an aneurysm of the A1 segment of the anterior cerebral artery causing visual field defects. One patient presented with a complete homonymous hemianopia due to compression of the optic tract by a giant aneurysm of the proximal left A1 segment. The second patient had an almost complete unilateral anopia caused by compression of the optic nerve and chiasm by an aneurysm of the distal part of the A1 segment with a small chiasmatic hemorrhage and ventricular rupture.