Objective: Previous animal studies showed contradictory clinical observations on whether acute hyperglycemia contributes to poor outcome in traumatic brain injury (TBI). Herein, we tried to clarify this issue.
Methods: Striking with depths of 3.0-4.25mm at right occipitoparietal brain region and with depth of 3.75mm at right/left occipitoparietal or right/left frontoparietal brain region were performed, respectively. Blood glucose and insulin levels were traced every four hours from 1 to 72h after striking. HOMA2-%S and HOMA2-%β were calculated. Modified neurological severity scores (mNSS) were used to evaluate neurological deficit within 72h.
Results: Striking with depths of 3.5-4.25mm induced increase in blood glucose lasting up to 24h after striking. The levels of blood glucose after striking with depths of 3.75-4.25mm were significantly different from that of striking with the depth of 3.0mm. Striking with depth of 3.75mm at right/left occipitoparietal region induced higher blood glucose in 24h than that at right/left frontoparietal region. Insulin concentration increased slowly during 72h after striking. Striking also induced decrease in insulin sensitivity and secretion lasting 72h. Evaluation of mNSS revealed that severe striking (beyond 3.75mm) worsened nerve function than slight striking (<3.0mm). Intervention of acute hyperglycemia could decrease the mNSS from 2 to 7 days after TBI.
Conclusion: Our results suggested that only severe TBI could induce acute hyperglycemia by itself, and early care of acute hyperglycemia could benefit the outcome of TBI patients.
Keywords: Acute hyperglycemia; Controlled cortical impact; Outcome; Traumatic brain injury.
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