Clinical Bedside Studies of Cerebral Blood Flow in Severe Subarachnoid Hemorrhage Using Xenon CT
Abstract: Aneurysmal subarachnoid hemorrhage (SAH) is frequently complicated by delayed cerebral ischemia (DCI), contributing to poor outcome. Particularly for patients in poor neurological state, prediction of the acute clinical course is difficult, as is the early detection of DCI. Repeated measurement of global and regional cerebral blood flow (CBF) could potentially identify patients at risk of deterioration and guide in the clinical management.The studies in this thesis are based on bedside measurements of CBF by xenon-enhanced CT with the aim to assess and characterize global and regional CBF disturbances at different phases in the acute course after severe SAH. Furthermore, the effects of hemodynamic augmentation by hypervolemia, hemodilution and hypertension (HHH-therapy) on CBF and cerebral energy metabolism in patients with DCI are addressed.In Paper I, CBF disturbances at the early phase (day 0–3) after SAH were found common and often heterogeneous with substantial regions of near ischemic CBF. Older age and more severe hemorrhage (graded according to Fisher from CT) were factors associated with more compromised CBF. In Paper II, exploring the temporal dynamics of CBF, low initial CBF was associated with a persistent low level of CBF at day 4–7. The association was more pronounced when patients receiving HHH-therapy were separated, and indicates that patients with low CBF, even without clinical signs of DCI, could benefit from careful surveillance and optimization of circulation. In Paper III, the effects on CBF from HHH-therapy in patients with DCI was assessed. Hematocrit decreased during treatment, while the increase in systemic blood pressure was modest. Global CBF and CBF of the worst perfused regions increased, and the proportion of regions with critically low flow decreased accordingly. In Paper IV, the effects of HHH was further assessed in patients also monitored with cerebral microdialysis (CMD). CBF improved during HHH-therapy, while the cerebral energy metabolic CMD parameters stayed statistically unchanged. None of the patients developed metabolic signs of severe ischemia, but a disturbed energy metabolic pattern was common, possibly explained by mitochondrial dysfunction.
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