2009
DOI: 10.1097/ta.0b013e318157dbec
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Effect of 35°C Hypothermia on Intracranial Pressure and Clinical Outcome in Patients With Severe Traumatic Brain Injury

Abstract: Cooling patients to 35 degrees C is safe and the ICP reduction effects of 35 degrees C hypothermia are similar to those of 33 degrees C hypothermia.

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Cited by 64 publications
(58 citation statements)
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“…There is also a randomized trial evidence of benefit in human brain ischemia after cardiac arrest and neonatal hypoxia ischemia. [54][55][56][57] Hypothermia has been shown to decrease elevated ICP in several neurological disorders, [58][59][60][61] including several phase II stroke clinical trials. 62,63 These studies used long durations of cooling (24-72 hours) and often encountered problems of systemic infection and rebound ICP elevation during patient rewarming.…”
Section: Strokementioning
confidence: 99%
“…There is also a randomized trial evidence of benefit in human brain ischemia after cardiac arrest and neonatal hypoxia ischemia. [54][55][56][57] Hypothermia has been shown to decrease elevated ICP in several neurological disorders, [58][59][60][61] including several phase II stroke clinical trials. 62,63 These studies used long durations of cooling (24-72 hours) and often encountered problems of systemic infection and rebound ICP elevation during patient rewarming.…”
Section: Strokementioning
confidence: 99%
“…To this end, we revisit the utility of hypothermia, now moving from the moderate hypothermia used in our previous studies to mild hypothermia (35°C) to determine whether a relatively modest drop in temperature can exert any protective effects, which, obviously, could prove of clinical utility. [25][26][27] Additionally, to better understand the potential involvement of damaging oxygen radicals in the process of repetitive injury and the benefits of their therapeutic attenuation, we revisit our previous studies, 22,23 now using postrepetitive administration of either superoxide dismutase (SOD) or Tempol, based upon the recognition that SOD will dismutate the superoxide anion, whereas Tempol serves as a nitroxide antioxidant that decomposes both the superoxide radical and the peroxynitrite-derived radical species, all of which have been implicated in the pathogenesis of various forms of axonal and vascular change after TBI. [28][29][30][31][32][33] In the current communication, we report that the use of even mild hypothermia (35°C) exerts significant axonal and vascular protection when the hypothermia is initiated relatively late (1 h) after repetitive injury, with both SOD and Tempol providing comparable protection when administered in the same time frame.…”
mentioning
confidence: 99%
“…In AIS 3-4 patients who died from degeneration in intracerebral lesion, the period from admission to death was significantly shorter in the MTH group than in the fever control group (medians [IQR]: 10 [6-13] vs. 17 [13][14][15][16][17][18][19][20][21][22][23][24][25], p < 0.05).…”
Section: Period From Admission To Deathmentioning
confidence: 99%