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JOURNAL ARTICLE
RANDOMIZED CONTROLLED TRIAL
Mild hypothermia therapy reduces blood glucose and lactate and improves neurologic outcomes in patients with severe traumatic brain injury.
Journal of Critical Care 2011 June
PURPOSE: The study aimed to investigate the association between blood glucose or lactate and the outcomes of severe traumatic brain injury (TBI), and to evaluate the effect of mild hypothermia therapy on glucose and lactate levels.
METHODS: Eighty-one patients with TBI were randomly divided into normothermia (n = 41) and mild hypothermia (n = 40) group. Body temperature of hypothermia group was maintained at 32.7°C for 72 hours. Arterial blood glucose and lactic acid were determined before and after hypothermia therapy. Glasgow Outcome Scale (GOS) score was assessed 3 months after the treatment.
RESULTS: The mean glucose (7.04 ± 0.51 vs 9.71 ± 1.63 mmol/L, P < .05) in the hypothermia group was lower than in the normothermia group after hypothermia therapy. There were more patients with good neurologic function (GOS 4-5) in the hypothermia group than in the normothermia group (75.0% vs 51.2%, P = .038). Multivariate regression analysis showed that blood glucose greater than 10 mmol/L (adjusted risk ratio, 5.7; 95% confidence interval, 1.4-13.2; P < .05) was an independent predictor for poor neurologic outcomes in these patients, and hypothermia therapy was an independent predictor for favorable outcomes (risk ratio, 4.9; 95% confidence interval, 1.0-15.6; P < .05). No significant association between lactate and GOS scores was identified in the multivariate analysis.
CONCLUSION: Hyperglycemia after TBI was associated with poor clinical outcomes, but the predictive value of blood lactate level requires further investigation. Hypothermia therapy improves neurologic outcomes in patients with severe TBI, and reduction in blood glucose may be partially responsible for the improved outcomes.
METHODS: Eighty-one patients with TBI were randomly divided into normothermia (n = 41) and mild hypothermia (n = 40) group. Body temperature of hypothermia group was maintained at 32.7°C for 72 hours. Arterial blood glucose and lactic acid were determined before and after hypothermia therapy. Glasgow Outcome Scale (GOS) score was assessed 3 months after the treatment.
RESULTS: The mean glucose (7.04 ± 0.51 vs 9.71 ± 1.63 mmol/L, P < .05) in the hypothermia group was lower than in the normothermia group after hypothermia therapy. There were more patients with good neurologic function (GOS 4-5) in the hypothermia group than in the normothermia group (75.0% vs 51.2%, P = .038). Multivariate regression analysis showed that blood glucose greater than 10 mmol/L (adjusted risk ratio, 5.7; 95% confidence interval, 1.4-13.2; P < .05) was an independent predictor for poor neurologic outcomes in these patients, and hypothermia therapy was an independent predictor for favorable outcomes (risk ratio, 4.9; 95% confidence interval, 1.0-15.6; P < .05). No significant association between lactate and GOS scores was identified in the multivariate analysis.
CONCLUSION: Hyperglycemia after TBI was associated with poor clinical outcomes, but the predictive value of blood lactate level requires further investigation. Hypothermia therapy improves neurologic outcomes in patients with severe TBI, and reduction in blood glucose may be partially responsible for the improved outcomes.
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