Neurocritical care
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Patients with traumatic brain injury commonly receive phenytoin for seizure prophylaxis. Due to the non-linear pharmacokinetics of phenytoin and narrow therapeutic window, phenytoin concentrations are monitored to ensure efficacy and prevent toxicity. Because phenytoin is hepatically metabolized, polymorphisms within cytochrome P450 enzymes can affect phenytoin concentrations. ⋯ This case reveals the clinical significance of genetic polymorphisms and the effect on phenytoin dosage requirements. Because pharmacogenomic testing is expensive and not readily available, routine monitoring of phenytoin concentrations is warranted. Further, established polymorphisms should be documented to prevent toxicity of drugs metabolized by similar pathways.
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Case Reports
Cerebral air embolism resulting in fatal stroke in an airplane passenger with a pulmonary bronchogenic cyst.
Cerebral air embolism is a rare cause of stroke, but may occur in patients undergoing invasive cardiac and pulmonary procedures, as well as in divers suffering pulmonary barotrauma from rapid ascent. Cerebral air embolism during air travel, however, is particularly rare. ⋯ This case suggests the importance of considering cerebral air embolism in patients with stroke associated with air travel; restricting air travel in patients with intrapulmonary cysts may be prudent.
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Little is known about the effects of hemodialysis on the injured brain, however; concern exists over the use of intermittent hemodialysis in patients with acute brain injury (ABI) due to its hemodynamic effects and increased intracranial pressure (ICP) associated with therapy. Continuous renal replacement therapy (CRRT) has become the preferred method of renal support in these patients though there is limited data to support its safety. Furthermore, exacerbations of cerebral edema have been reported. CRRT is an option for the treatment of hypervolemia and in theory may improve intracranial compliance. We report the case of a poly-trauma patient with severe traumatic brain injury (TBI) in which CRRT was implemented solely for refractory intracranial hypertension. ⋯ Though unproven, CRRT may be beneficial in patients with IH due to gentle removal of fluid, solutes, and inflammatory cytokines. Given the limited data on safety of CRRT in patients with ABI, we encourage further reports.
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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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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.