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 Lbo2 (Pbto2 [partial pressure of brain tissue oxygen] <20 mm Hg) from 67% to 15% during acute brain attack (<24 hours of ictus), by increasing Pbto2 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, Fio2 change, ICP, hemoglobin, and oxygen saturation were predictors for Pbto2 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 (Vm) increased from 45.00 ± 15.12 to 80.37 ± 38.33/second by day 4 with concomitant Pbto2 reduction from 29.09 ± 17.88 to 22.66 ± 8.19. Peak TSV (days 7-12) coincided with decline in Pbto2. Nicardipine mitigated Lbo2 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; G2 = 28.32; P < 0.001). This study identifies 4 zones of Lbo2 during survival benefit (Cramer Φ = 0.43 and 0.3) TSV, uncompensated; global cerebral ischemia, compensated, and normal Pbto2. Admission Glasgow Coma Scale score (not increased ICP) was predictive of low Pbto2 (ß = 0.812, R2 = 0.661, F1,30 = 58.41; P < 0.0001) during early brain injury. Coma was the only credible predictor for mortality (odds ratio, 7.33/>4.8∗; χ2 = 7.556; confidence interval, 1.70-31.54; P < 0.01) followed by basilar aneurysm, poor grade, high ICP and Lbo2 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.

Oral anticoagulant use around the time of atrial fibrillation ablation: a review of the current evidence of individual oral anticoagulant use for periprocedural atrial fibrillation ablation thromboembolic prophylaxis.

Atrial fibrillation is the most common arrhythmia and ablation is becoming more prevalent as a treatment option. Appropriate treatment of atrial fibrillation mandates thromboembolic prophylaxis, and atrial fibrillation ablation periprocedural management of oral anticoagulation is paramount because of the unique susceptibility for thromboembolism that exists for a patient undergoing ablation. Uninterrupted warfarin therapy is the current standard approach for periprocedural atrial fibrillation anticoagulation. Novel oral anticoagulants, including direct thrombin and factor Xa inhibitors, are being used more frequently for thromboembolic prophylaxis in atrial fibrillation patients, but the best strategy for using novel oral anticoagulants in periprocedural anticoagulation is unknown. Optimal periprocedural anticoagulation management strategies with oral anticoagulants, limitations of using novel oral anticoagulants, and future directions in this field are discussed.