Abstract
Background:Ischemic and hypoxic secondary brain insults are common and detrimental in traumatic brain injury (TBI). Treatment aims to maintain an adequate cerebral blood flow with sufficient arterial oxygen content. It has been suggested that arterial hyperoxia may be beneficial to the injured brain to compensate for cerebral ischemia, overcome diffusion barriers, and improve mitochondrial function. In this study, we investigated the relation between arterial oxygen levels and cerebral energy metabolism, pressure autoregulation, and clinical outcome.Methods:This retrospective study was based on 115 patients with severe TBI treated in the neurointensive care unit, Uppsala university hospital, Sweden, 2008 to 2018. Data from cerebral microdialysis (MD), arterial blood gases, hemodynamics, and intracranial pressure were analyzed the first 10 days post-injury. The first day post-injury was studied in particular.Results:Arterial oxygen levels were higher and with greater variability on the first day post-injury, whereas it was more stable the following 9 days. Normal-to-high mean pO2 was significantly associated with better pressure autoregulation/lower pressure reactivity index (P = .02) and lower cerebral MD-lactate (P = .04) on day 1. Patients with limited cerebral energy metabolic substrate supply (MD-pyruvate below 120 µM) and metabolic disturbances with MD-lactate-/pyruvate ratio (LPR) above 25 had significantly lower arterial oxygen levels than those with limited MD-pyruvate supply and normal MD-LPR (P = .001) this day. Arterial oxygenation was not associated with clinical outcome.Conclusions:Maintaining a pO2 above 12 kPa and higher may improve oxidative cerebral energy metabolism and pressure autoregulation, particularly in cases of limited energy substrate supply in the early phase of TBI. Evaluating the cerebral energy metabolic profile could yield a better patient selection for hyperoxic treatment in future trials.
Highlights
Ischemic and hypoxic secondary injury events are common in traumatic brain injury (TBI).[1,2] Maintaining an adequate cerebral blood flow (CBF) and delivery of oxygen is essential in TBI management.[3]
High intracranial pressure (ICP) and low cerebral perfusion pressure (CPP) are associated with low pBtO2, but most hypoxic insults occur in the absence of these predictors[4] and are probably caused by microvascular thrombosis or diffusion barriers such as cerebral edema.[8,9]
The treatment may compensate for ischemic hypoxia, overcome cerebral diffusion barriers, and improve mitochondrial function, thereby improving oxidative cerebral energy metabolism and reducing secondary brain injuries.[2]
Summary
Ischemic and hypoxic secondary injury events are common in traumatic brain injury (TBI).[1,2] Maintaining an adequate cerebral blood flow (CBF) and delivery of oxygen is essential in TBI management.[3]. Increasing the fraction of the inspired O2 (FIO2), for example, by normobaric hyperoxia (NBO), in order to increase arterial and brain oxygenation, has been suggested as treatment for cerebral hypoxia in TBI.[10] The treatment may compensate for ischemic hypoxia, overcome cerebral diffusion barriers, and improve mitochondrial function, thereby improving oxidative cerebral energy metabolism and reducing secondary brain injuries.[2] Normobaric hyperoxia may increase pBtO2,11 but the effect on Received January 23, 2020. We investigated the relation between arterial oxygen levels and cerebral energy metabolism, pressure autoregulation, and clinical outcome. Evaluating the cerebral energy metabolic profile could yield a better patient selection for hyperoxic treatment in future trials
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