Why the study?
Does subarachnoid hemorrhage and subsequent surgery alter platelet aggregability and thromboxane release?
Does subarachnoid hemorrhage and subsequent surgery alter platelet aggregability and thromboxane release?
Subarachnoid hemorrhage and subsequent surgery cause dynamic changes in platelet aggregability and thromboxane release, which are most prominent in patients who develop delayed postoperative ischemic deterioration.
May flag SAH patients at risk for delayed ischemia post-surgery; leaves open whether antiplatelet modulation improves outcomes.
We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in platelet-rich plasma from 88 patients with subarachnoid hemorrhage and 26 healthy controls. During the first 3 days after subarachnoid hemorrhage, the patients showed significantly decreased (p less than 0.05) platelet aggregability and thromboxane release relative to the controls, but these effects disappeared in a few days. Platelet count increased for 3 weeks after subarachnoid hemorrhage. Surgery in 67 patients was followed by significant increases in platelet aggregability (p less than 0.05) and thromboxane release (p less than 0.001). Greatest thromboxane release was found in the eight patients showing delayed (postoperative) ischemic deterioration with a permanent neurologic deficit. Although platelet hyperaggregability and increased thromboxane release were particularly prominent in these eight patients, the role of these hematologic parameters in the pathogenesis of delayed ischemic deterioration remains unclear.
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Juvela et al. (1990) studied this question.
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