Neurocritical care
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Observational Study
Fluid Responsiveness and Brain Tissue Oxygen Augmentation After Subarachnoid Hemorrhage.
The objective of this study was to investigate the relationship between cardiac index (CI) response to a fluid challenge and changes in brain tissue oxygen pressure (PbtO(2)) in patients with subarachnoid hemorrhage (SAH). ⋯ Bolus fluid resuscitation resulting in augmentation of CI can improve cerebral oxygenation after SAH.
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Patients suffering from severe traumatic brain injury (TBI) often develop secondary brain lesions that may worsen outcome. S100B, a biomarker of brain damage, has been shown to increase in response to secondary cerebral deterioration. The aim of this study was to analyze the occurrence of secondary increases in serum levels of S100B and their relation to potential subsequent radiological pathology present on CT/MRI-scans. ⋯ Secondary increases in serum levels of S100B, even as low as ≥0.05 μg/L, beyond 48 h after TBI are strongly correlated to the development of clinically significant secondary radiological findings.
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Case Reports
Apnea Testing for Brain Death in Severe Acute Respiratory Distress Syndrome: A Possible Solution.
A 42-year-old man with a subarachnoid hemorrhage complicated by anoxic brain injury, respiratory failure requiring mechanical ventilation, and severe acute respiratory distress syndrome (ARDS) presented a clinical conundrum for safe apnea testing in brain death determination due to profound hypoxemia. ⋯ A recruitment maneuver and CPAP valve may be used in severe ARDS for safe apnea testing in brain death determination.
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Optimal management of physiological parameters in neurological/neurosurgical intensive care units (NICUs) is largely unclear as high-quality evidence is lacking. The aim of this survey was to investigate if standards exist in the use of clinical scores, systemic and cerebral monitoring and the targeting of physiology values and in what way this affects clinical management in German NICUs. ⋯ Although apparently aiming for standardization in neurocritical care, German NICUs show substantial differences in NM and monitoring-associated interventions. In terms of scoring and monitoring methods, German NICUs seem to be quite conservative. These survey results suggest a need of prospective and randomized interventional trials in neurocritical care to help define standards and target values.
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Therapeutic hypothermia protects neurons after severe brain damage. This effect has been mainly achieved at the core temperatures of 32-34 °C; however, the optimum temperature of therapeutic hypothermia is not fully defined. Here we studied whether hypothermic culture at 35 °C had the same effects on the decrease of time-dependent expression of tumor necrosis factor (TNF)-α, interleukin (IL)-10, and nitric oxide (NO) by stimuli-activated microglia as that at 33 °C, as determined in our previous reports, and whether these factors directly induced neuronal cell death. ⋯ Hypothermic culture at 35 °C decreased the production of early-phase TNF-α and late-phase IL-10 and NO from ATP- and TLR-activated microglia as observed at 33 °C, albeit with diminished effects. Moreover, these factors caused the death of neuronal cells in a concentration-dependent manner. These results suggest that the attenuation of microglial production of TNF-α, IL-10, and NO by therapeutic hypothermia leads to the inhibition of neuronal cell death. Minimal hypothermia at 35 °C may be sufficient to elicit neuroprotective effect.