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Case Reports
Journal Article
Review
Cerebral venous thrombosis presenting with subarachnoid hemorrhage. Case report and review.
American Journal of Emergency Medicine 2009 January
OBJECTIVE: The objective of the study is to demonstrate the pitfalls in the diagnosis of cerebral venous thrombosis (CVT) especially when subarachnoid hemorrhage (SAH) is associated and discuss the diagnostic value of computed tomography (CT) imaging as well as the use of other diagnostic modalities. In addition, we will briefly summarize the pathophysiology of SAH in the setting of CVT.
METHODS: We reviewed 16 articles, which included 26 different case reports of SAH associated with CVT. In addition, we presented our experience with a case of SAH secondary to CVT.
RESULTS: Nonenhanced CT was able to detect SAH in 86% of cases and CVT in only 36%. Further imaging testing was necessary to further characterize the extent of the thrombosis. The location of the SAH varied, but it never involved the skull base. Risk factors for CVT development included hypercoagulable states, oral contraceptives use, history of recent fracture or surgery, family or personal history of deep vein thrombosis, smoking, and hyperlipidemia and migraines. Sixty-two percent of patients had acute onset severe headaches, 35% presented with nuchal rigidity, and 35% presented with seizures.
CONCLUSIONS: Cerebral venous thrombosis must be considered in the differential diagnosis of patients presenting with a broad range of neurological presentations especially in the presence of new onset of seizures. Computed tomographic offers many clues to the diagnosis of CVT when concomitant SAH is present. These include the presence of SAH at cerebral convexities with associated basal cisterns and skull base sparing. Recognition of these subtleties will allow prompt and appropriate management and, when in doubt, encourage further investigations.
METHODS: We reviewed 16 articles, which included 26 different case reports of SAH associated with CVT. In addition, we presented our experience with a case of SAH secondary to CVT.
RESULTS: Nonenhanced CT was able to detect SAH in 86% of cases and CVT in only 36%. Further imaging testing was necessary to further characterize the extent of the thrombosis. The location of the SAH varied, but it never involved the skull base. Risk factors for CVT development included hypercoagulable states, oral contraceptives use, history of recent fracture or surgery, family or personal history of deep vein thrombosis, smoking, and hyperlipidemia and migraines. Sixty-two percent of patients had acute onset severe headaches, 35% presented with nuchal rigidity, and 35% presented with seizures.
CONCLUSIONS: Cerebral venous thrombosis must be considered in the differential diagnosis of patients presenting with a broad range of neurological presentations especially in the presence of new onset of seizures. Computed tomographic offers many clues to the diagnosis of CVT when concomitant SAH is present. These include the presence of SAH at cerebral convexities with associated basal cisterns and skull base sparing. Recognition of these subtleties will allow prompt and appropriate management and, when in doubt, encourage further investigations.
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