Post-hemorrhage delayed cerebral vasospasm: has there been progression in the last 25 years?

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IBRAHIM AMER ALJAEZI
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Delayed cerebral vasospasm is the most predominant cause of mortality and morbidity after subarachnoid hemorrhage (SAH). In this paper, recent and updated literature on delayed cerebral vasospasm after SAH was reviewed, covering risk factors, pathogenies, and treatments. A literature research was carried out using two appropriate databases over a 25-year period. For the risk factors and treatments, clinical studies were summarized in tables by extracting information from the study (author, published year, sample size, endpoint or outcome, and result). Studies that examine cerebral vasospasm and poor outcomes after an SAH were included, as well as clinical studies. Smoking mostly has a clear trend of being a risk factor for a poor outcome; patients less than 50 years old are more vulnerable to vasospasm incidence; females tend to be at higher risk for vasospasm incidence and a poor clinical outcome. There is no confirmed evidence that hyperglycemia and genetic factors (eNOS T-786C and APOE4) are considered risk factors for cerebral vasospasm incidence and a poor outcome. Concerning pathogenesis, experimental studies, clinical studies, and multiple reviews were included. For the treatment part (balloon angioplasty, Triple H therapy, statin, clazosentan, magnesium sulfate, nitric oxide donor, and cilostozal), only clinical studies and clinical trials were included; experimental trials were excluded. Among a wide range of discussed therapies, only a balloon angioplasty and cilostazol are substantially to have a promising results in managing cerebral vasospasm incidence and poor outcomes. However, a high level of evidence should be considered to confirm the benefits of both of these treatments by conducting a large randomized, double-blinded study.
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