LAUSR

We read with great interest the article recently published by Humaloja et al. “The Association Between Arterial Oxygen Level and Outcome in Neurocritically Ill Patients Is not Affected by Blood Pressure” [1]. The authors examined the association between different partial pressure of arterial oxygen (PaO2) and blood pressure patterns and 1-year mortality in various types of brain injury. The main results revealed that PaO2 was not an independent predictor of mortality, whereas an higher mean arterial pressure (MAP) predicted lower mortality. After a careful reading of this article, we would suggest to the authors some explanations to their study conclusions. The authors stated as a strength the large number of patients with brain injury. However, when the population is composed of traumatic brain injury, intracranial hemorrhage, subarachnoid hemorrhage, or acute ischemic stroke, the same treatment is difficult to achieve for all conditions. For the initial phase, aneurysmal subarachnoid hemorrhage, for example, needs a lower MAP target at the acute phase, whereas acute ischemic stroke could need a higher target [2]. The autoregulation loss in severe traumatic brain injury is a major parameter to guide treatment as precise PaO2 and MAP targets [3]. As mentioned above, theses different threshold values should be closely monitored and personalized starting in the first few hours. The study period covers the first 24 h of patient care in the intensive care unit, allowing individual monitoring. Depending on the initial pathology, cerebral oxygenation monitoring could integrate an intracranial pressure device, partial brain tissue oxygen, transcranial doppler, pressure reactivity index, etc. [4]. The oxygen demand (temperature, agitation, seizures, etc.), utilization, delivery (cerebral perfusion pressure, autoregulation, arterial CO2, etc.), or its diffusion (endothelial swelling) are all variables that have an impact on clinical outcomes. That’s why the authors should not only considerer PaO2 and MAP as variables but integrate these threshold values in a global optimization strategy. Furthermore, optimal PaO2 and MAP at the acute phase are obviously not the same if we manage thrombectomy for acute ischemic stroke or extraventricular drain for subarachnoid hemorrhage. Hence, it is difficult to find a relationship between a minimal PaO2 or MAP values and 1-year mortality in this heterogeneous population. The same treatment (or target) does not fit all neurocritically ill patients and could explain these work results.