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JOURNAL ARTICLE
REVIEW
Risk Factors for Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage: A Review of the Literature.
World Neurosurgery 2016 January
OBJECTIVE: To examine the literature on risk factors for cerebral vasospasm (CV), one of the most serious complications following aneurysmal subarachnoid hemorrhage (SAH), with special reference to the definition of CV.
METHODS: Using standard search engines, including PubMed, the medical literature on risk factors for CV after SAH was reviewed, and the best definition representative of CV was searched.
RESULTS: Severe SAH evident on computed tomography scan was the only consistent risk factor for CV after SAH. Effects of risk factors on CV, including age, clinical grade, rebleeding, intraventricular or intracerebral hemorrhage on computed tomography scan, acute hydrocephalus, aneurysm site and size, leukocytosis, interleukin-6 level, and cardiac abnormalities, appeared to be associated with the severity of SAH rather than each having a direct effect. Cigarette smoking, hypertension, and left ventricular hypertrophy on electrocardiogram were associated with CV without any relationship to SAH severity. With regard to parameters representative of CV, the grade of angiographic vasospasm (i.e., the degree of arterial narrowing evident on angiography) was the most adequate. Nevertheless, few reports on the risk factors associated with angiographic vasospasm grade have been reported to date.
CONCLUSIONS: Severe SAH evident on computed tomography scan appears to be a definite risk factor for CV after SAH, followed by cigarette smoking, hypertension, and left ventricular hypertrophy on electrocardiogram. To understand the pathogenesis of CV, further studies on the relationships between risk factors, especially factors not related to the severity of SAH, and angiographic vasospasm grade are necessary.
METHODS: Using standard search engines, including PubMed, the medical literature on risk factors for CV after SAH was reviewed, and the best definition representative of CV was searched.
RESULTS: Severe SAH evident on computed tomography scan was the only consistent risk factor for CV after SAH. Effects of risk factors on CV, including age, clinical grade, rebleeding, intraventricular or intracerebral hemorrhage on computed tomography scan, acute hydrocephalus, aneurysm site and size, leukocytosis, interleukin-6 level, and cardiac abnormalities, appeared to be associated with the severity of SAH rather than each having a direct effect. Cigarette smoking, hypertension, and left ventricular hypertrophy on electrocardiogram were associated with CV without any relationship to SAH severity. With regard to parameters representative of CV, the grade of angiographic vasospasm (i.e., the degree of arterial narrowing evident on angiography) was the most adequate. Nevertheless, few reports on the risk factors associated with angiographic vasospasm grade have been reported to date.
CONCLUSIONS: Severe SAH evident on computed tomography scan appears to be a definite risk factor for CV after SAH, followed by cigarette smoking, hypertension, and left ventricular hypertrophy on electrocardiogram. To understand the pathogenesis of CV, further studies on the relationships between risk factors, especially factors not related to the severity of SAH, and angiographic vasospasm grade are necessary.
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