4.6 Article

Tight glycemic control increases metabolic distress in traumatic brain injury: A randomized controlled within-subjects trial

期刊

CRITICAL CARE MEDICINE
卷 40, 期 6, 页码 1923-1929

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/CCM.0b013e31824e0fcc

关键词

cerebral metabolism; glucose; insulin; microdialysis; positron emission tomography; traumatic brain injury

资金

  1. NINDS [NS049471, P01 NS 058489-01A2]
  2. UCLA Brain Injury Research Center

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Objective: To determine the effects of tight glycemic control on brain metabolism after traumatic brain injury using brain positron emission tomography and microdialysis. Design: Single-center, randomized controlled within-subject crossover observational trial. Setting: Academic intensive care unit. Methods: We performed a prospective, unblinded randomized controlled within-subject crossover trial of tight (80-110 mg/dL) vs. loose (120-150 mg/dL) glycemic control in patients with severe traumatic brain injury to determine the effects of glycemic control on brain glucose metabolism, as measured by [F-18] deoxy-D-glucose brain positron emission tomography. Brain microdialysis was done simultaneously. Measurements and Main Results: Thirteen severely injured traumatic brain injury patients underwent the study between 3 and 8 days (mean 4.8 days) after traumatic brain injury. In ten of these subjects, global brain and gray matter tissues demonstrated higher glucose metabolic rates while glucose was under tight control as compared with loose control (3.2 +/- 0.6 vs. 2.4 + 0.4, p = .02 [whole brain] and 3.8 +/- 1.4 vs. 2.9 +/- 0.8, p = .05 [gray matter]). However, the responses were heterogeneous with pericontusional tissue demonstrating the least state-dependent change. Cerebral microdialysis demonstrated more frequent critical reductions in glucose (p = .02) and elevations of lactate/pyruvate ratio (p = .03) during tight glycemic control. Conclusion: Tight glycemic control results in increased global glucose uptake and an increased cerebral metabolic crisis after traumatic brain injury. The mechanisms leading to the enhancement of metabolic crisis are unclear, but delivery of more glucose through mild hyperglycemia may be necessary after traumatic brain injury. (Crit Care Med 2012; 40:1923-1929)

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