Cerebral Vasospasm After Subarachnoid Hemorrhage
Section snippets
FREQUENCY OF OCCURRENCE AND RELATED AND UNRELATED CLINICAL FEATURES
Depending on the criteria used to define it, cerebral vasospasm has been reported to occur in 21 to 78% of all patients after a subarachnoid hemorrhage,1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 although most studies estimate its frequency of occurrence to be between 40 and 60%. Most often, angiographic vasospasm occurs in cerebral arteries near the source of the subarachnoid hemorrhage and tends to occur in the segments of cerebral arteries that are intimately related to the densest collections
TEMPORAL PROFILE
Experimental cerebral vasospasm after subarachnoid hemorrhage seems to be a biphasic event.21, 22 In dogs, arterial narrowing begins immediately after subarachnoid hemorrhage and reaches maximal intensity by 30 minutes. Within 2 days, this early phase of vasospasm reverses spontaneously. Early spasm, however, has been difficult to substantiate in humans.23, 24 Although this difficulty may reflect the transient nature of acute vasospasm, the fact that human cerebral arteries contract less
HEMODYNAMIC CONSEQUENCES
Differences in hemodynamic properties facilitate classification of cerebral arteries into at least two types: proximal large conducting vessels on the surface of the brain and distal small penetrating arterioles. In normal subjects, cerebral arterial resistance and, consequently, cerebral blood flow are primarily regulated at the level of the penetrating arterioles rather than by the conducting arteries. With modification of resistance in this arteriolar bed, cerebral blood flow is maintained
VASCULAR PATHOLOGIC FEATURES
Transmission electron microscopic examination of vasospastic cerebral arteries after experimentally induced subarachnoid hemorrhage in dogs and monkeys shows structural differences between arteries in the early phase of vasospasm and those in the chronic phase. Arteries examined within 48 hours after experimentally induced subarachnoid hemorrhage have few pathologic changes. The internal elastic lamina may appear corrugated as a result of arterial contraction. Subtle changes in the
FUNCTIONAL ABNORMALITIES OF VASOSPASTIC ARTERIES
Despite the fact that numerous investigators have successfully prevented or treated experimental vasospasm with a wide variety of vasodilating drugs, clinically the final result has been disappointing.61 Lack of a reliable animal model of chronic vasospasm prompted many investigators to study acute in vitro or in vivo vasospasm; consequently, these observations were irrelevant to the human situation. Recently, a canine model of subarachnoid hemorrhage has been described which reliably
PATHOGENESIS
Although the mechanism responsible for these vascular changes remains unknown, circumstantial evidence is consistent with several possibilities.
TREATMENT
Treatment of symptomatic vasospasm today relies on efforts directed at enhancing cardiac output, inducing arterial hypertension, and expanding the intravascular volume in an attempt to increase cerebral perfusion and promote cerebral blood flow.84, 85, 86 The techniques used vary from clinic to clinic and have recently been reviewed by Heros and associates.87 Major differences in treatment protocols focus on the ideal hematocrit needed to optimize oxygen delivery but not hinder cerebral blood
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Cerebral vasospasm after subarachnoid hemorrhage: Developing treatments
2021, Brain HemorrhagesCitation Excerpt :One of the most common complications for patients who suffer from SAH is cerebral vasospasm. The leading cause of morbidity and mortality, vasospasm develops in approximately 50% percentage of these patients.6–8 The biggest risk factor is the severity of SAH as shown on computed tomography (CT) scan, though other factors included age, clinical grade, presence of intraventricular or intracerebral hemorrhage, aneurysm size and location, and acute hydrocephalus.9
A comparison of the effects of tirilazad on subarachnoid hemorrhage-induced blood-brain barrier permeability in male and female rats
1997, Journal of Stroke and Cerebrovascular DiseasesThe neurosurgical patient
1994, Bailliere's Clinical AnaesthesiologySubarachnoid hemorrhage: An update of pathogenesis, diagnosis and management
1994, Journal of the Neurological SciencesNeurologic evaluation in a canine model of single and double subarachnoid hemorrhage
1993, Journal of Neuroscience Methods
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Mayo Graduate School of Medicine, Rochester, Minnesota. This investigation was supported in part by Research Grant NS-6663 from the National Institutes of Health, Public Health Service.