Neurocritical care
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While tight glucose control has been widely adopted in the critical care setting, the optimal target glucose level following acute traumatic brain injury (TBI) remains debatable. This observational study was conducted to delineate the relationship between glucose levels and clinical outcomes during acute phase (first 5 days) of TBI. ⋯ Findings from our study suggest a glucose level > or =160 mg/dl within the first 24 h of admission following TBI is associated with poor outcomes irrespective of severity of injury, and this presents a timeframe for which active therapeutic interventions may improve clinical outcomes. Prospective efficacy trials are needed to corroborate these findings.
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Hypertonic saline (3% NaCl) infusions can be used to treat acute neurologic hyponatremia (ANH) in critically ill patients with neurological and neurosurgical disorders such as subarachnoid hemorrhage. Adjustments in the rate of hypertonic saline infusions to treat ANH are needed to achieve a goal sodium range and are usually made on an empiric basis. To date, no data are available to determine how reliably such adjustments achieve stable, normal serum sodium concentrations or how often iatrogenic hypernatremia occurs during the course of treatment with hypertonic saline. ⋯ Our hypertonic saline sliding-scale protocol for treatment of ANH can be used reliably and achieves normal sodium concentrations in a safe manner with minimal overshoot.
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Since the establishment of the concept of declaring death by brain criteria, a large extent of variability in the determination of brain death has been reported. There are no standardized practical guidelines, and major differences exist in the requirements for the declaration of brain death throughout the USA and internationally. The American Academy of Neurology published evidence-based practice parameters for the determination of brain death in adults in 1995, requiring the irreversible absence of clinical brain function with the cardinal features of coma, absent brainstem reflexes, and apnea, as well as the exclusion of reversible confounders. ⋯ Every step in the determination of brain death bears potential pitfalls which can lead to errors in the diagnosis of brain death. These pitfalls are presented here, and possible solutions identified. Suggestions are made for improvement in the standardization of the declaration of brain death.
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Excessive use of adrenergic agents may result in stunned myocardium. ⋯ IABP counterpulsation may be one therapeutic option for patients with vasospasm after SAH when high doses of vasopressors can induce severe myocardial dysfunction. However, this invasive device may not be sufficient to maintain adequate cerebral perfusion and fatal embolic events can complicate the clinical course.
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Delayed ischemic neurological deficit associated to cerebral vasospasm is the most common cause of sequelae and death that follows the rupture of an aneurysm. The objective of this study was to evaluate the safety and efficacy of intra-arterial Milrinone in patients with symptomatic refractory cerebral vasospasm. ⋯ Intra-arterial Milrinone infusion seems to be a safe and effective treatment for patients who develop refractory symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage.