Re-exposure to the hypobaric hypoxic brain injury of high altitude: plasma S100B levels and the possible effect of acclimatisation on blood-brain barrier dysfunction.

Hypobaric hypoxic brain injury results in elevated peripheral S100B levels which may relate to blood-brain barrier (BBB) dysfunction. A period of acclimatisation or dexamethasone prevents altitude-related illnesses and this may involve attenuation of BBB compromise. We hypothesised that both treatments would diminish the S100B response (a measure of BBB dysfunction) on re-ascent to the hypobaric hypoxia of high altitude, in comparison to an identical ascent completed 48 h earlier by the same group. Twelve healthy volunteers, six of which were prescribed dexamethasone, ascended Mt Fuji (summit 3700 m) and serial plasma S100B levels measured. The S100B values reduced from a baseline 0.183 µg/l (95 % CI 0.083-0.283) to 0.145 µg/l (95 % CI 0.088-0.202) at high altitude for the dexamethasone group (n = 6) and from 0.147 µg/l (95 % CI 0.022-0.272) to 0.133 µg/l (95 % CI 0.085-0.182) for the non-treated group (n = 6) [not statistically significant (p = 0.43 and p = 0.82) for the treated and non-treated groups respectively]. [These results contrasted with the statistically significant increase during the first ascent, S100B increasing from 0.108 µg/l (95 % CI 0.092-0.125) to 0.216 µg/l (95 % CI 0.165-0.267) at high altitude]. In conclusion, an increase in plasma S100B was not observed in the second ascent and this may relate to the effect of acclimatisation (or hypoxic pre-conditioning) on the BBB. An exercise stimulated elevation of plasma S100B levels was also not observed during the second ascent. The small sample size and wide confidence intervals, however, precludes any statistically significant conclusions and a larger study would be required to confirm these findings.

A review of the current management of severe traumatic brain injury.

Traumatic brain injury accounts for up to half of trauma related fatalities. This review describes current management practices including pre-hospital care, surgical interventions and various treatment modalities for intracranial hypertension. The lack of class I evidence for the majority of interventions is highlighted.

The role of decompressive craniectomy in the management of traumatic brain injury: a critical review.

Brain swelling and intracranial hypertension following severe head injury are known to contribute to secondary brain damage, and have been shown to adversely affect patient outcome. The use of unilateral craniectomy following the evacuation of a mass lesion, such as acute subdural haematoma or traumatic intracerebral haematoma, is accepted practice. The following review focuses on a bi-fronto-temporal decompressive craniectomy, used as an isolated operation for the control of intracranial hypertension, secondary to diffuse brain swelling refractory to medical management. Though the operation is being increasingly used, current opinion is still divided regarding its overall effects on outcome. This review examines the experimental and clinical evidence for and against the use of decompressive craniectomy, highlights the lack of class I evidence relevant to this topic and emphasises the necessity for well-designed prospective randomised controlled trials.