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The major causes of mortality and morbidity in patients surviving the rupture of a saccular aneurysm are subsequent bleeding and vasospasm. The purpose of this study was to evaluate the influence of early treatment of ruptured aneurysms with Guglielmi detachable coils on the incidence of subsequent bleeding. Thirteen patients were treated within 72 hours of initial aneurysm rupture with Guglielmi detachable coils. Excluding three patients who died 2, 4, and 12 weeks after initial hemorrhage, all others have been followed up for intervals between 6 and 36 months (mean, 16 mo). None of these have had either clinical or radiographic evidence of subsequent bleeding. Assuming that there is a 30% incidence of subsequent bleeding in conservatively (nonsurgically) treated patients, the 0% subsequent bleed rate observed in this subgroup was significant at a P value of 0.01. Only one procedure-related complication occurred in this series, and 9 of 13 (69%) aneurysms were 100% occluded at the time of initial treatment. All aneurysms were at least 90% occluded at the end of initial treatment. In addition to reducing the risk of subsequent bleeding, early treatment facilitated the institution of an aggressive approach for management of both vasospasm and increased intracranial pressure. Patient outcome, as measured by the Glasgow Outcome Scale, was good in 9 of 13 (69%), poor in 1 of 13 (8%), and death in 3 of 13 (23%) patients. The results of this study suggest that early Guglielmi detachable coil treatment of ruptured aneurysms may be effective in reducing the incidence of subsequent bleeding and can be performed with a low incidence of complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Although hemin is known to exert toxic effects on a variety of cell types, its possible participation in the genesis of cerebral vasospasm has received little attention. The authors measured the concentration of hemin in experimental subarachnoid clot and studied its effects on the morphology and 45Ca++ uptake of vascular smooth-muscle cells dissociated from canine carotid artery. Craniectomies were performed in five dogs under general anesthesia, and 3 to 5 ml of autologous whole blood was deposited in the supraclinoid subarachnoid compartment. The concentration of hemin recovered by Folch extraction from clotted material removed 7 days after surgery was 390 +/- 247 microM (mean +/- standard error of the mean). Mean vascular smooth-muscle cell length after 40 minutes of exposure to 50 microM hemin was 37.3 +/- 1.2 microns (control 51.6 +/- 1.6 microns) (p < 0.01). The mean percent permeation of 45Ca++, measured by a dual label technique, of cells exposed to hemin was 200.9% +/- 23% (control 102.9% +/- 4.3%) (p < 0.01). These findings indicate that hemin accrues in subarachnoid hematoma, that it exerts a constrictive effect on vascular smooth-muscle cells, and that this effect is associated with an increased uptake of Ca++. This study demonstrates that hemin should be included in the list of potential agents that participate in the development of cerebral vasospasm.

In an effort to determine which blood elements play a critical role in the development of cerebral vasospasm, adult cats were subjected to prepontine injection of either autogenous whole blood or erythrocyte-free blood containing latex beads as a substitute morphologic marker. Seven or 10 days later the cats were anesthetized and perfused with fixative, and the basilar arteries were prepared for light and electron microscopy. Successful clot deposition was confirmed by the presence of numerous erythrocytes or latex beads within the adventitia of vessels. In agreement with previous studies, instillation of whole blood produced luminal narrowing associated with profound ultrastructural changes in all layers of the vascular wall. No significant alterations, however, occurred in arteries bathed in erythrocyte-free blood. These findings suggest first, that erythrocytes are essential for the development of the vasculopathy associated with chronic cerebral vasospasm, and second, that the role, if any, of other blood elements is not autonomous.

Loss of catecholamine histofluorescence, increased sensitivity to norepinephrine, and changes in alpha1 receptor binding have led to the proposal that denervation hypersensitivity may play a role in cerebrovascular spasm. Because the significance of these alterations has remained unclear, the present study was undertaken to determine whether there was direct ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage. Under general anesthesia, adult cats were subjected to pre-pontine injection of blood or serum (5 to 7 ml) via a transclival approach. The animals were sacrificed 4, 7, or 10 days later and basilar artery segments were prepared for electron microscopy. Control vessels appeared normal, whereas those bathed in blood revealed unequivocal changes in neural and supporting elements, including: 1) disintegration of both clear- and dense-core vesicles; 2) fragmentation of varicosities; 3) loss of Schwann cell cytoplasm; and 4) axonal degeneration. These changes were most pronounced 7 days after instillation of blood, and correlated in time with maximal injury of the media and endothelium. Although the development of smooth-muscle hypersensitivity remains unsettled, this study indicates that prolonged exposure to blood can cause extensive denervation of cerebral arteries.