Neurocritical care
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Randomized Controlled Trial Multicenter Study
TURN Score Predicts 24-Hour Cerebral Edema After IV Thrombolysis.
Cerebral edema is associated with poor outcome after IV thrombolysis. We recently described the TURN score (Thrombolysis risk Using mRS and NIHSS), a predictor of severe outcome after IV thrombolysis. Our purpose was to evaluate its ability to predict 24-h cerebral edema. ⋯ Cerebral edema at 24 h is associated with poor outcome and 90-day mortality. TURN predicts ischemic stroke patients who will develop 24-h cerebral edema after IV thrombolysis.
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The manner in which brain death protocols in the United States address family objection to death by neurologic criteria has not been explored. ⋯ The majority of protocols reviewed did not mention how to handle circumstances in which families object to determination of brain death or discontinuation of organ support after brain death. The creation of guidelines on management of these complex situations may be helpful to prevent distress to families and hospital staff.
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Delirium symptoms are associated with later worse functional outcomes and long-term cognitive impairments, but the neuroanatomical basis for delirium symptoms in patients with acute brain injury is currently uncertain. We tested the hypothesis that hematoma location is predictive of delirium symptoms in patients with intracerebral hemorrhage, a model disease where patients are typically not sedated or bacteremic. ⋯ Higher odds ratio for delirium was increased due to hematoma location. The location of neurological injury could be of high prognostic value for predicting delirium symptoms.
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Aneurysmal subarachnoid hemorrhage (SAH) is a common condition with relatively poor clinical outcome. Pulmonary complication after SAH is an important contributor to poor outcome. Previous studies have shown that labile zinc and inflammatory mediators participate in many pathophysiological processes. The present study investigated the effects of SAH on the levels of labile zinc and certain proinflammatory factors in rat lung and determined the effect of erythropoietin (EPO) on the pulmonary labile zinc and the inflammatory factor after SAH in rats. ⋯ EPO can protect lung from SAH-induced injury by attenuating pulmonary inflammation and labile zinc accumulation in vivo.
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Propofol exhibits neuroprotective effects mediated by the inhibition of excitatory amino acid (EAA) neurotransmitter release and potentiation of inhibitory amino acid (IAA) neurotransmitters. To our knowledge, this is the first study to investigate the effects of propofol on the EAA and IAA balance in neurogenic pulmonary edema (NPE). ⋯ The current findings suggest that propofol improves NPE likely via IAA accumulation and the regulation of EAA and IAA balance, which may represent an effective treatment for NPE.