Brain Oxygen-Directed Management of Aneurysmal Subarachnoid Hemorrhage. Temporal Patterns of Cerebral Ischemia During Acute Brain Attack, Early Brain Injury, and Territorial Sonographic Vasospasm.

Background: Neurocritical management of aneurysmal subarachnoid hemorrhage focuses on delayed cerebral ischemia (DCI) after aneurysm repair.

Methods: This study conceptualizes the pathophysiology of cerebral ischemia and its management using a brain oxygen-directed protocol (intracranial pressure [ICP] control, eubaric hyperoxia, hemodynamic therapy, arterial vasodilation, and neuroprotection) in patients with subarachnoid hemorrhage, undergoing aneurysm clipping (n = 40).

Results: The brain oxygen-directed protocol reduced Lbo (Pbto [partial pressure of brain tissue oxygen] <20 mm Hg) from 67% to 15% during acute brain attack (<24 hours of ictus), by increasing Pbto from 11.31 ± 9.34 to 27.85 ± 6.76 (P < 0.0001) and then to 29.09 ± 17.88 within 72 hours. Day-after-bleed, Fio change, ICP, hemoglobin, and oxygen saturation were predictors for Pbto during early brain injury. Transcranial Doppler ultrasonography velocities (>20 cm/second) increased at day 2. During DCI caused by territorial sonographic vasospasm (TSV), middle cerebral artery mean velocity (V) increased from 45.00 ± 15.12 to 80.37 ± 38.33/second by day 4 with concomitant Pbto reduction from 29.09 ± 17.88 to 22.66 ± 8.19. Peak TSV (days 7-12) coincided with decline in Pbto. Nicardipine mitigated Lbo during peak TSV, in contrast to nimodipine, with survival benefit (P < 0.01). Intravenous and cisternal nicardipine combination had survival benefit (Cramer Φ = 0.43 and 0.327; G = 28.32; P < 0.001). This study identifies 4 zones of Lbo during survival benefit (Cramer Φ = 0.43 and 0.3) TSV, uncompensated; global cerebral ischemia, compensated, and normal Pbto. Admission Glasgow Coma Scale score (not increased ICP) was predictive of low Pbto (β = 0.812, R = 0.661, F = 58.41; P < 0.0001) during early brain injury. Coma was the only credible predictor for mortality (odds ratio, 7.33/>4.8∗; χ = 7.556; confidence interval, 1.70-31.54; P < 0.01) followed by basilar aneurysm, poor grade, high ICP and Lbo during TSV. Global cerebral ischemia occurs immediately after the ictus, persisting in 30% of patients despite the high therapeutic intensity level, superimposed by DCI during TSV.

Conclusions: We propose implications for clinical practice and patient management to minimize cerebral ischemia.