Neurocritical care
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Brain tissue oxygen (PbtO(2)) monitors are utilized in a threshold-based fashion, triggering actions based on the presumption of tissue compromise when PbtO(2) is less than 20 mmHg. Some early published practice guidelines suggest that seizure is a potential culprit when PbtO(2) crosses this threshold; evidence for this is not well defined. ⋯ Seizures were neither associated with a PbtO(2) value of <20 mmHg nor associated with a drop in PbtO(2) value across a clinically significant threshold. However, we cannot rule out the existence of any relationship between PbtO(2) and seizure with this limited data set. Prospective research using electronically recorded data is required to more effectively examine the relationship between PbtO(2) and seizure.
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Comparative Study
Dose-dependent influence of sevoflurane anesthesia on neuronal survival and cognitive outcome after transient forebrain ischemia in Sprague-Dawley rats.
Volatile anesthetics reduce postischemic neurohistopathological injury and improve neurological outcome in various animal models. However, the isoflurane concentrations above 1 minimum alveolar concentration (MAC) have been associated with reduced neuronal survival and impaired functional outcome. The aim of this study was to evaluate if 1.8 MAC sevoflurane alters postischemic neuronal survival and neurologic outcome compared with 0.45 MAC sevoflurane. ⋯ Postischemic neuronal survival was increased with 1.8 MAC compared with 0.45 MAC sevoflurane. Therefore, experimental models of cerebral ischemia should account for neuroprotective effects of sevoflurane with increasing concentrations. To ensure minimal interference of sevoflurane on neuronal survival, a low inspired concentration should be used and fluctuations in the depth of anesthesia should be limited.
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Stroke is common after aneurysmal subarachnoid hemorrhage (aSAH). Transcranial Doppler ultrasound (TCD) monitoring is often employed to identify vasospasm and allow intervention to avoid infarction. The required duration of monitoring has not been established. We aim to determine if 10 days of TCD monitoring identifies all patients at risk for infarction. ⋯ TCD identification of vasospasm after day 10 is rare. Stroke is more likely to result from poor detection than from brevity of TCD monitoring. Improved or alternative monitoring is needed to effectively identify ischemia and prevent stroke.
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Posterior reversible encephalopathy syndrome (PRES) is a rare complication of hemodynamic augmentation for subarachnoid hemorrhage (SAH)-associated vasospasm. The roles of hyperperfusion and hypoperfusion in the genesis of PRES remain uncertain. ⋯ PRES is a rare complication of hemodynamic augmentation that should be considered in the differential diagnosis of delayed neurological decline in patients with aneurysmal SAH-associated cerebral vasospasm. The markedly asymmetric distribution of PRES lesions with sparing of the territory affected by vasospasm supports the hypothesis that hyperperfusion underlies the pathophysiology of this disorder.
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The pathogenesis of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) remains obscure. The authors assessed the relationship of tumor necrosis factor alpha (TNF-α) and TNF-α gene polymorphisms with occurrence of DCI and poor outcome at 3 months. ⋯ It is unlikely that serum TNF-α or TNF-α genotype play an important role in the occurrence of DCI after SAH.