To determine the effects of tight glycemic control on brain metabolism after traumatic brain injury using brain positron emission tomography and microdialysis.
Single-center, randomized controlled within-subject crossover observational trial.
Academic intensive care unit.
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 [18F] deoxy-D-glucose brain positron emission tomography. Brain microdialysis was done simultaneously.
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.
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.
From the Departments of Neurology (PV), Neurosurgery (PV, DLM, NS, MF, ME, TG, DAH), and Nuclear Medicine (S-CH, WS), UCLA School of Medicine, Los Angeles, CA.
*See also p. 1995.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (http://journals.lww.com/ccmjournal). Supplemental data can be viewed at: Supplemental Digital Content 1, http://links.lww.com/CCM/A445.
Supported, in part, by NINDS NS049471, P01 NS 058489-01A2, and the UCLA Brain Injury Research Center.
The authors have not disclosed any potential conflicts of interest.
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