LAUSR

Following traumatic brain injury (TBI), cerebral metabolism can become deranged, contributing to secondary injury. Cerebral microdialysis (CMD) allows cerebral metabolism assessment and is often used with other neuro-monitoring modalities. CMD-derived parameters such as the lactate/pyruvate ratio (LPR) show a failure of oxidative energy generation. CMD-based abnormal metabolic states can be described following TBI, informing the aetiology of physiological derangements. This systematic review summarises the published literature on microdialysis-based abnormal metabolic classifications following TBI. Original research studies where the populations were patients with traumatic brain injury were included. Studies that described CMD-based classifications of metabolic abnormalities were included in the narrative results synthesis. A total of 825 studies underwent two-step screening after duplicates were removed. Fifty-three articles that used CMD in TBI patients were included. Of these, 14 described abnormal metabolic states based on CMD parameters. Classifications were heterogeneous between studies. LPR was the most frequently used parameter in the classifications; high LPR values were described as metabolic crisis. Ischaemia was consistently defined as high LPR with low CMD substrate levels (glucose or pyruvate). Mitochondrial dysfunction, describing inability to use energy substrate despite availability, was identified based on raised LPR with near normal levels of pyruvate. This is the first systematic review summarising the published literature on microdialysis-based abnormal metabolic states following TBI. Although variability exists between individual classifications, there is broad agreement around broad definitions of metabolic crisis, ischaemia and mitochondrial dysfunction. Identifying the aetiology of deranged cerebral metabolism after TBI is important to offer targeted treatment interventions.