Protocolized Brain Oxygen Optimization in Subarachnoid Hemorrhage.

Brain tissue hypoxia (PbtO2 < 20 mmHg) is common after subarachnoid hemorrhage (SAH) and associated with poor outcome. Recent data suggest that brain oxygen optimization is feasible and reduces the time spent with PbtO2 < 20 mmHg from 45 to 16% in patients with severe traumatic brain injury. Here, we intended to quantify the brain tissue hypoxia burden despite implementation of a protocolized treatment approach in poor-grade SAH patients and to identify the simultaneous occurrence of pathologic values potentially amenable to treatment. We present a bi-centric observational cohort study including 100 poor-grade SAH patients admitted to two tertiary care centers who underwent multimodal brain monitoring and were managed with a PbtO2-targeted protocolized approach. PbtO2 optimization (≥ 20 mmHg) included a stepwise neuro-intensive care approach, aiming to prevent low cerebral perfusion pressure (CPP), and blood hemoglobin, and to keep normocapnia, normoxemia, and normothermia. Based on routine blood gas analysis, hemoglobin, PaCO2, and PaO2 data were matched to 2-h averaged data of continuous CPP, PbtO2, core temperature, and to hourly cerebral microdialysis (CMD) samples over the first 11 days. Patients had a Glasgow Coma Scale of 3 (IQR 3–4) and were 58 years old (IQR 48–66). Overall incidence of brain tissue hypoxia was 25%, which was not different between both sites despite differences in the treatment approach. During brain tissue hypoxia, episodes of CPP < 70 mmHg (27%), PaCO2 < 35 mmHg (19%), PaO2 < 80 mmHg (14%), Hb < 9 g/dL (11%), metabolic crisis (CMD-lactate/pyruvate ratio > 40, and CMD-glucose < 0.7 mmol/L; 7%), and temperature > 38.3 °C (4%) were common. Our results demonstrate that brain tissue hypoxia remains common despite implementation of a PbtO2-targeted therapy in poor-grade SAH patients, suggesting room for further optimization.