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Lack of effect of induction of hypothermia after acute brain injury.
Treatment with hypothermia, with the body temperature reaching 33 degrees C within eight hours after injury, is not effective in improving outcomes in patients with severe brain injury.
Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia.
The results support the hypothesis that early ischemia after traumatic brain injury may be an important factor determining neurological outcome, and suggest that early hyperventilation or lowering of blood pressure to prevent brain edema may be harmful.
Mitochondrial dysfunction and calcium perturbation induced by traumatic brain injury.
Data indicate that CCII-induced TBI perturbs cellular Ca2+ homeostasis and results in excessiveCa2+ adsorption to the mitochondrial membrane, which subsequently inhibits the respiratory chain-linked electron transfer and energy transduction.
Acute secondary adrenal insufficiency after traumatic brain injury: A prospective study*
Lower cortisol levels were associated with lower blood pressure and higher vasopressor use, and consideration should be given to monitoring cortisol levels in intubated TBI patients, particularly those receiving high-dose pentobarbital or propofol.
Phase II Clinical Trial of Moderate Hypothermia after Severe Traumatic Brain Injury in Children
Moderate hypothermia after severe TBI in children was found to be safe relative to standard management and NORM in children of all ages and in children with delay of initiation of treatment up to 24 hours, and functional outcome tended to improve from the 3- to 6-month cognitive assessment in HYPO compared with NORM.
Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial.
It is concluded that prophylactic hyperventilation is deleterious in head-injured patients with motor scores of 4-5 and that the course of ICP was most stable in the HV + THAM group, although mean ICP could be kept well below 25 mm Hg in all three groups.
Clinical trials in head injury.
This workshop proved to be very informative and yielded many insights into previous and future TBI trials, and it is hoped that these lessons will enhance the planning and design of future efforts in this important field of research.
Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography.
- G. Bouma, J. Muizelaar, W. Stringer, S. Choi, P. Fatouros, H. Young
- MedicineJournal of neurosurgery
- 1 September 1992
Data support the hypothesis that ischemia is an important secondary injury mechanism after traumatic brain injury, and that trauma may share pathophysiological mechanisms with stroke in a large number of cases; this may have important implications for the use of hyperventilation and antihypertensive drugs in the acute management of severely head-injured patients.
Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow.
The data indicate that a decline in blood pressure should be avoided in head-injured patients, even when baseline blood pressure is high, and induced hypertension did not consistently reduce ICP in patients with intact autoregulation and should be attempted after thorough assessment of the cerebrovascular status and under careful monitoring of its effects.
Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulation.
Data support the hypothesis that, within broad limits, CBF is not related to cardiac output, even when autoregulation is impaired, and the effect of intravascular volume expansion appears to be mediated by decreased blood viscosity rather than cardiac output augmentation.