Articles: brain-injuries.
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In the last two decades our understanding of the pathophysiology of severe head injury has significantly increased. It has become evident that secondary neuronal damage may occur and should be prevented. It is ischemia, similar to that seen with stroke and aneurysmal subarachnoid hemorrhage, that causes secondary brain damage. ⋯ Moreover, there are some new pharmacological concepts for changing the threshold for ischemia in brain tissue. At the present time, however, valid data concerning clinical use are still not available. Therefore, mild hyperventilation and sedation during the initial post-traumatic phase and lowering of intracranial pressure by osmotherapeutics remain the most important treatment modalities, as they were 20 years ago.
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Journal of neurotrauma · Nov 1996
Review Practice Guideline GuidelineThe use of mannitol in severe head injury. Brain Trauma Foundation.
Mannitol is effective in reducing ICP, and we recommend its use in the management of traumatic intracranial hypertension. Serum osmolalities greater than 320 mOSsm/L and hypovolemia should be avoided. Some data suggest that bolus administration is preferable to continuous infusion.
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J Int Neuropsychol Soc · Nov 1996
Randomized Controlled Trial Clinical TrialThe impact of posttraumatic seizures on 1-year neuropsychological and psychosocial outcome of head injury.
This study examined the relationship of posttraumatic seizures and head injury severity to neuropsychological performance and psychosocial functioning in 210 adults who were prospectively followed and assessed 1 year after moderate to severe traumatic head injury. Eighteen percent (n = 38) of the patients experienced 1 or more late seizures (i.e., seizures occurring 8 or more days posttrauma) by the time of the 1-year followup. ⋯ However, after the effects of head injury severity were controlled, there were no significant differences in neuropsychological and psychosocial outcome at 1 year as a function of having seizures. These findings suggest that worse outcomes in patients who develop posttraumatic seizures up to 1 year posttrauma largely reflect the effects of the brain injuries that cause seizures, rather than the effect of seizures.
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Journal of neurosurgery · Nov 1996
Monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue PO2 versus jugular vein oxygen saturation.
Monitoring of cerebral oxygenation is considered to be of great importance in minimizing secondary hypoxic and ischemic brain damage following severe head injury. Although the threshold for cerebral hypoxia in jugular bulb oximetry (measurement of O2 saturation in the jugular vein (SjvO2)) is generally accepted to be 50% oxygen saturation, a comparable value in brain tissue PO2 (PtiO2) monitoring, a new method for direct assessment of PO2 in the cerebral white matter, has not yet been established. Hence, the purpose of this study was to compare brain PtiO2 with SjvO2 in severely head injured patients during phases of reduced cerebral perfusion pressure (CPP) to define a threshold in brain PtiO2 monitoring. ⋯ This study demonstrates that monitoring brain PtiO2 is a safe, reliable, and sensitive diagnostic method to follow cerebral oxygenation. In comparison to SjvO2, PtiO2 is more suitable for long-term monitoring. It can be used to minimize episodes of secondary cerebral maloxygenation after severe head injury and may, hopefully, improve the outcome in severely head injured patients.