Articles: brain-injuries.
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J Neurosurg Anesthesiol · Jan 1995
Comparative StudyBrain edema and neurologic status with rapid infusion of 0.9% saline or 5% dextrose after head trauma.
We previously reported that intravenous (i.v.) administration of large volumes (0.2 ml/g) of either an isotonic dextrose-free solution or 5% dextrose solution given over 18 h after closed head trauma (CHT) in rats did not significantly affect neurological severity score or brain tissue specific gravity. However, it is possible that with more rapid administration, isotonic or 5% dextrose i.v. solutions may alter neurological outcome after CHT. Our study examined whether neurological severity score, brain tissue specific gravity and water content, and blood composition were significantly altered when 0.25 ml/g of either 0.9% saline or 5% dextrose was given i.v. over 0.5 h (rather than over 18 h) after CHT. ⋯ There were no statistically significant differences in neurologic outcome and brain edema between the untreated and the saline-treated groups. However, 5% dextrose i.v. increased mortality (group 6 and 11, 50 and 0% survivors, respectively), decreased specific gravity in the noncontused hemisphere, and worsened neurologic outcome with and without CHT. Blood osmolality remained stable in comparison to the baseline value of 291.9 +/- 7.4 mOsm/kg (mean +/- SD).(ABSTRACT TRUNCATED AT 250 WORDS)
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Critical care medicine · Jan 1995
Colloid infusion after brain injury: effect on intracranial pressure, cerebral blood flow, and oxygen delivery.
We sought to determine the effects of colloid osmotic pressure on cerebral edema formation after brain injury. We hypothesized that an increase in plasma oncotic pressure accompanying a colloid infusion would be associated with a decrease in intracranial pressure and increases in cerebral blood flow and oxygen delivery when compared with isotonic crystalloid. ⋯ Colloid infusion after a focal cryogenic injury does not increase cerebral oxygen delivery or reduce either cerebral edema formation or intracranial pressure when compared with lactated Ringer's solution. Colloid is not superior to isotonic crystalloid in the management of isolated brain injury.
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Diagnostic and therapeutic measures after severe head-injury in the intensive care unit are discussed. The main goal of all efforts consists in minimizing secondary brain damage. Adequate shock therapy in the initial phase proves crucial for the later outcome. ⋯ Surgical and conservative modalities of therapy are further examined. Controversial methods (barbiturates, steroids, some osmotic active agents) as well as new concepts of therapy are also included. The clinician is provided with a critical discussion of the value of the different methods from our point of experience.
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The Journal of pediatrics · Jan 1995
Comparative StudySomatosensory evoked potentials for prediction of outcome in acute severe brain injury.
The purpose of this study was to evaluate prospectively short-latency somatosensory evoked potentials (SEPs) as a predictor of outcome in acute, severe brain injury, and to compare this with the predictive power of the motor component of the Glasgow Coma Scale score and computed tomographic scan. Outcome was measured with the Glasgow Outcome Scale at a minimum of 6 months after injury. We studied 109 patients (aged 0.1 to 16.8 years) with SEPs within 4 days of the onset of coma. ⋯ Of the 59 patients with unfavorable outcome, 76% could be identified with SEPs compared with 36% with examination of motor function. We suggest that SEPs be performed in children with acute severe brain injury because they add an important tool to the physician's prognostic armamentarium. We conclude that in the absence of the above mentioned identifiable clinical situations, absent SEPs predict 100% unfavorable outcome, and this finding may warrant consideration of withdrawal of treatment in children with brain injuries.
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Posttraumatic agitation is perhaps the most dramatic behavioral consequence of severe traumatic brain injury. The mechanism for this behavior remains to be determined. ⋯ Concurrent neurologic or medical decline during the recovery from an acute traumatic brain injury may precipitate delirium, which has many clinical features that overlap with posttraumatic agitation. Hence, the differential diagnosis of posttraumatic agitation includes all medical and neurologic etiologies for transient declines in consciousness and cognition.