It is well known that hypoxemia is associated with worse outcome in TBI . The influence of hyperoxia on outcome remains controversial. Suggested mechanisms of potential negative effects include cerebral vasoconstriction in a similar manner as hypocarbia, oxidative stress and inflammation.
Most studies investigating hyperoxia and outcome in TBI and other patient groups used (arbitrary) cutoff values for hyperoxia such as 200, 250 or 300 mmHg, respectively. Whether the analysis of different cutoff values adequately approximates oxygen exposure is questionable due to the multifactorial and dynamic nature of oxygen physiology in combination with continuous supplemental oxygen exposure in the majority of cases. A study in pediatric post-cardiopulmonary resuscitation (CPR) patients by van Zellem et al. introduced a new innovative method in defining and measuring hyperoxia and oxygen exposure: the cumulative analysis using the area-under-the-curve (AUC) PaO2 calculation, which is a commonly used approach to estimate drug exposure in pharmacological studies. Although each method of oxygen exposure analysis has its limitations, our hypothesis is that the longitudinal, cumulative approach better addresses the (patho-)physiology of cerebral hyperoxia as it takes time- and dose-dependent factors into account.