Neurocritical care
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Traumatic brain injury (TBI) generates regional alterations in cerebral metabolism, leading to the potential evolution of persistent metabolic dysfunction. In the case of penetrating, firearm-related TBI, the pathophysiological mechanisms underlying these acute-phase metabolic derangements are not entirely understood-hindering the potential effectiveness of therapeutic intervention. The use of cerebral microdialysis to monitor biochemical alterations that occur, post-TBI, provides critical insight into the events that perpetuate neurological deterioration. ⋯ Microdialysis studies may significantly improve the understanding of the metabolic alterations that occur in patients who sustain a variety of forms of neurotrauma. Ultimately, monitoring these variations in brain tissue chemistry will improve the insight into the neuropathological mechanisms underlying penetrating traumatic brain injury, and enhance the therapeutic approach of these patients.
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Endothelin-1 (ET-1) is a potent vasoconstrictor and is thought to be responsible for secondary ischemia and vasogenic edema after traumatic brain injury (TBI). Both CSF and plasma concentrations have been shown to be increased after TBI, but there is little evidence to confirm an intracranial site of production. ⋯ These findings confirm the synthesis of Big ET and its cleavage to ET-1 within the brain after TBI. More work is needed to elucidate the pathophysiological role and the outcome impact of ET-1 generation after TBI.
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Medical management of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) includes hypertensive, hypervolemic, and hemodilution ("triple-H") therapy. However, there is little information regarding the indications and guidance used to initiate and adjust triple-H therapy. ⋯ There are substantial differences in the administration of prophylactic triple-H, but there was high agreement on indication for therapeutic use. There was wide variability in the extent of ICU monitoring, diagnostic approach, physiologic parameters and values used as target of therapy. NICU availability was associated with more intensive monitoring. Lack of evidence and guidelines for triple-H therapy might largely explain these findings.
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Studies devoted to intensive glucose control suggested that the intensive insulin therapy (IIT) approach could effectively reduce complications associated with critical illness. A program of IIT with the goal of achieving a blood glucose of 80-120 mg/dL was, therefore, adopted in this study. To explore the impact of this approach in patients admitted to a neurocritical care unit, we compared the short-term outcomes of patients treated before and after our policy change. ⋯ IIT was not only able to reduce overall mean glucose levels, but also resulted in significantly more episodes of hypoglycemia, increased mortality, and increased length of stay. The relationship between hypoglycemia and mortality indicates that efforts to control glucose levels should also aggressively avoid induction of hypoglycemia.
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Although neurogenic stunned myocardium (NSM) after aneurysmal subarachnoid hemorrhage (SAH) is well described, its clinical significance remains poorly defined. We investigated the influence of left ventricular (LV) dysfunction and cerebral vasospasm on cerebral infarction, serious cardiovascular events, and functional outcome after SAH. ⋯ LV dysfunction after SAH increases the risk of cerebral infarction from vasospasm, hypotension, and pulmonary edema, but with aggressive ICU support does not affect short-term survival or functional outcome. Antihypertensive medication may confer cardioprotection and reduce the risk of catecholamine-mediated injury after SAH.