Neurocritical care
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Delayed cerebral ischemia (DCI) contributes to morbidity following aneurysmal subarachnoid hemorrhage; however, its etiology remains poorly understood. DCI is not only a consequence of angiographic vasospasm, but also involves microthrombosis and neuroinflammation, two events with unexplained phenomenology. The vascular endothelial glycocalyx mediates platelet aggregation and endothelial cell-leukocyte interactions and may play an important role in DCI pathogenesis. ⋯ These preliminary data support the hypothesis that glycocalyx injury occurs in SAH, and might contribute to DCI by regulating cerebral microthrombosis and delayed neuroinflammation.
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While systolic dysfunction has been observed following traumatic brain injury (TBI), the relationship between early hemodynamics and the development of systolic dysfunction has not been investigated. Our study aimed to determine the early hemodynamic profile that is associated with the development of systolic dysfunction after TBI. ⋯ Patients who develop systolic dysfunction following TBI have a distinctive hemodynamic profile, with early hypertension and tachycardia, followed by a decrease in blood pressure over the first day after TBI. This profile suggests an early maladaptive catecholamine-excess state as a potential underlying mechanism of TBI-induced systolic dysfunction.
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Hemodynamic instability responsive to fluid resuscitation is common after a traumatic brain injury (TBI), also in the absence of systemic hemorrhage. The present study tests if an isolated severe TBI induces a decrease in plasma volume (PV). ⋯ The results support that an isolated severe head trauma triggers a significant and rapid reduction in PV, most likely due to vascular leak.