Department of Anesthesia and Intensive Care, Fondazione IRCCS Cà Granda-Ospedale Maggiore Policlinico, Milan, Italy.
Crit Care Med. 2012 Jun;40(6):1785-91. doi: 10.1097/CCM.0b013e318246bd45.
To clarify the dynamics of glucose delivery to the brain and the effects of changes in blood glucose after severe traumatic brain injury.
Retrospective analysis of a prospective observational cohort study.
Neurosurgical intensive care unit of a university hospital.
Seventeen patients with acute traumatic brain injury monitored with cerebral and subcutaneous microdialysis.
None.
For continuous, accurate systemic monitoring, glucose was measured in the interstitial space of subcutaneous adipose tissue using microdialysis, and 39 specific episodes of spontaneous rises in glucose were identified. During these episodes, there was a significant positive linear relationship between systemic glucose levels and brain glucose concentrations measured by microdialysis (p < .0001). The basal lactate/pyruvate ratio, with a threshold of 25, was adopted to distinguish between disturbed and presumably preserved cerebral oxidative metabolism. Using normal vs. elevated lactate/pyruvate ratio as variable factor, the relationship between brain and systemic glucose during the episodes could be described by two significantly distinct parallel lines (p = .0001), which indicates a strong additive effect of subcutaneous glucose and lactate/pyruvate ratio in determining brain glucose. The line describing the relationship under disturbed metabolic conditions was lower than in presumably intact metabolic conditions, with a significant difference of 0.648 ± 0.192 mM (p = .002). This let us to accurately predict that in this situation systemic glucose concentrations in the lower range of normality would result in critical brain glucose levels.
The linear relationship between systemic and brain glucose in healthy subjects is preserved in traumatic brain-injured patients. As a consequence, in brain tissue where oxidative metabolism is disturbed, brain glucose concentrations might possibly drop below the critical threshold of 0.8 mM to 1.0 mM when there is a reduction in systemic glucose toward the lower limits of the "normal" range.
阐明严重创伤性脑损伤后葡萄糖向大脑输送的动力学和血糖变化的影响。
对一项前瞻性观察队列研究的回顾性分析。
大学医院神经外科重症监护病房。
17 例接受脑和皮下微透析监测的急性创伤性脑损伤患者。
无。
为了进行连续、准确的系统监测，使用微透析测量皮下脂肪组织间质中的葡萄糖，确定了 39 个自发血糖升高的特定发作。在这些发作期间，系统血糖水平与微透析测量的脑葡萄糖浓度之间存在显著的正线性关系（p<0.0001）。采用基础乳酸/丙酮酸比值（阈值为 25）来区分氧化代谢紊乱和可能正常的脑区。使用正常与升高的乳酸/丙酮酸比值作为变量因素，发作期间脑和系统葡萄糖之间的关系可以用两条明显不同的平行线来描述（p=0.0001），这表明皮下葡萄糖和乳酸/丙酮酸比值在确定脑葡萄糖方面具有很强的相加效应。描述代谢紊乱条件下关系的线低于假定完整代谢条件下的线，差异显著为 0.648±0.192 mM（p=0.002）。这使我们能够准确预测，在这种情况下，系统血糖浓度处于正常范围的较低水平时，会导致脑葡萄糖水平达到临界值。
在创伤性脑损伤患者中，健康受试者的系统血糖与脑血糖之间的线性关系得以保留。因此，在氧化代谢紊乱的脑组织中，当系统血糖向“正常”范围的较低限降低时，脑葡萄糖浓度可能会降至 0.8 mM 至 1.0 mM 的临界阈值以下。
