Journal of neurotrauma
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Journal of neurotrauma · Aug 2000
Impaired autoregulation of cerebral blood flow in an experimental model of traumatic brain injury.
In order to study the pathophysiology and the intracranial hemodynamics of traumatic brain injury, we have developed a modified closed-head injury model of impact-acceleration that expresses several features of severe head injury in humans, including acute and long-lasting intracranial hypertension, diffuse axonal injury, neuronal necrosis, bleeding, and edema. In view of the clinical relevance of impaired autoregulation of cerebral blood flow after traumatic brain injury, and aiming at further characterization of the model, we investigated the autoregulation efficiency 24 h after experimental closed-head injury. Cortical blood flow was continuously monitored with a laser-Doppler flowmeter, and the mean arterial blood pressure was progressively decreased by controlled hemorrhage. ⋯ The break point tended towards higher values in the closed head injury group (62.2 +/- 20.8 mm Hg versus 46.9 +/- 12.7 mm Hg; mean +/- SD, p = 0.198). It is concluded that cerebral autoregulation in this modified closed head injury model is impaired 24 h after traumatic brain injury. This finding, in addition to other characteristic features of severe head injury established earlier in this model, significantly contributes to its clinical relevance.
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Journal of neurotrauma · Aug 2000
Cerebral metabolic response to traumatic brain injury sustained early in development: a 2-deoxy-D-glucose autoradiographic study.
Following fluid percussion (FP) traumatic brain injury (TBI), adult rats exhibit dynamic regional changes in cerebral glucose metabolism characterized by an acute (hours) increase and subsequent chronic (weeks) decrease in metabolic rates. The injury-induced hyperglycolysis is the result of ionic fluxes across cell membranes and the degree and extent of metabolic depression is predictive of neurobehavioral deficits. Given that younger animals appear to exhibit similar physiological responses to injury yet show an improved rate of recovery compared to adults, we wanted to determine if this injury-induced dynamic metabolic response to TBI is different if the injury is sustained early in life. ⋯ This hyperglycolytic state subsided within 30 min, and by 1 day all cerebral structures, except the ipsilateral cerebellar cortex, showed lower rates of glucose metabolism (ranging from 5.7% to 63.0% below controls). This period of posttraumatic metabolic depression resolved within 3 days for all structures measured. Compared to previous adult studies these results suggest that the young rat pup, although exhibiting acute hyperglycolysis, is not subjected to a prolonged period of metabolic depression, which supports the findings that at this level of injury severity, these young animals show remarkable neurological sparing following TBI.
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Journal of neurotrauma · Jun 2000
Review Practice Guideline GuidelineThe Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Recommendations for intracranial pressure monitoring technology.
In patients who require ICP monitoring, a ventricular catheter connected to an external strain gauge transducer or catheter tip pressure transducer device is the most accurate reliable method of monitoring ICP and enables therapeutic CSF drainage. Clinically significant infections or hemorrhage associated with ICP devices causing patient morbidity are rare and should not deter the decision to monitor ICP. ⋯ These devices are advantageous when ventricular ICP is not obtained or if there is obstruction in the fluid couple. Subarachnoid or subdural fluid coupled devices and epidural ICP devices are currently less accurate.
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Journal of neurotrauma · Jun 2000
Review Practice Guideline GuidelineThe Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Use of barbiturates in the control of intracranial hypertension.
High-dose barbiturate therapy is efficacious in lowering ICP and decreasing mortality in the setting of uncontrollable ICP refractory to all other conventional medical and surgical ICP-lowering treatments. Utilization of barbiturates for the prophylactic treatment of ICP is not indicated. The potential complications attendant on this form of therapy mandate that its use be limited to critical care providers and that appropriate systemic monitoring be undertaken to avoid or treat any hemodynamic instability. When barbiturate coma is utilized, consideration should also be given to monitoring arteriovenous oxygen saturation as some patients treated in this fashion may develop oligemic cerebral hypoxia.
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Journal of neurotrauma · Jun 2000
Review Practice Guideline GuidelineThe Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Indications for intracranial pressure monitoring.
ICP monitoring per se has never been subjected to a prospective randomized clinical trial (PRCT) to establish its efficacy (or lack thereof) in improving outcome from severe head injury. Hence, there are insufficient data to support its use as a standard. However, there is a large body of published clinical experience that indicates that ICP monitoring (1) helps in the earlier detection of intracranial mass lesions, (2) can limit the indiscriminate use of therapies to control ICP which themselves can be potentially harmful, (3) can reduce ICP by CSF drainage and thus improve cerebral perfusion, (4) helps in determining prognosis, and (5) may improve outcome. ⋯ ICP monitoring in patients with a normal CT scan with two or more of these risk factors is suggested as a guideline. Routine ICP monitoring is not indicated in patients with mild or moderate head injury. However, it may be undertaken in certain conscious patients with traumatic mass lesions at the discretion of the treating physician.