Purpose: High arterial lactate is associated with disturbed systemic physiology. Lactate can also be used as alternative cerebral fuel and it is involved in regulating cerebral blood flow. This study explored the relation of endogenous arterial lactate to systemic physiology, pressure autoregulation, cerebral energy metabolism, and clinical outcome in traumatic brain injury (TBI).
Method: A retrospective study including 115 patients (consent given) with severe TBI treated in the neurointensive care unit, Uppsala university hospital, Sweden, 2008-2018. Data from cerebral microdialysis, arterial blood gases, hemodynamics and intracranial pressure were analyzed the first ten days post-injury.
Results: Arterial lactate peaked on day 1 post-injury (mean 1.7 ± 0.7 mM) and gradually decreased. Higher arterial lactate correlated with lower age (p-value < 0.05), higher Marshall score (p-value < 0.05) and higher arterial glucose (p-value < 0.001) in a multiple regression analysis. Higher arterial lactate was associated with poor pressure autoregulation (p-value < 0.01), but not to worse cerebral energy metabolism. Higher arterial lactate was also associated with unfavorable clinical outcome (p-value < 0.05).
Conclusions: High endogenous arterial lactate is a biomarker of poor systemic physiology and may disturb cerebral blood flow autoregulation.
Keywords: Cerebral energy metabolism; Clinical outcome; Lactate; Neurointensive-care; Pressure reactivity; Traumatic brain injury.
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