Department of Neurosurgery, University of Pennsylvania, 3 Silverstein Pavilion, 3400 Spruce Street, Philadelphia, PA 19104, USA.
Neurocrit Care. 2011 Jun;14(3):361-9. doi: 10.1007/s12028-011-9526-7.
Brain tissue oxygen (PbtO(2)) monitoring is used in severe traumatic brain injury (TBI) patients. How brain reduced PbtO(2) should be treated and its response to treatment is not clearly defined. We examined which medical therapies restore normal PbtO(2) in TBI patients.
Forty-nine (mean age 40 ± 19 years) patients with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) admitted to a University-affiliated, Level I trauma center who had at least one episode of compromised brain oxygen (PbtO(2) <25 mmHg for >10 min), were retrospectively identified from a prospective observational cohort study. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), and PbtO(2) were monitored continuously. Episodes of compromised PbtO(2) and brain hypoxia (PbtO(2) <15 mmHg for >10 min) and the medical interventions that improved PbtO(2) were identified.
Five hundred and sixty-four episodes of compromised PbtO2 were identified from 260 days of PbtO2 monitoring. Medical management used in a "cause-directed" manner successfully reversed 72% of the episodes of compromised PbtO(2), defined as restoration of a "normal" PbtO(2) (i.e. ≥ 25 mmHg). Ventilator manipulation, CPP augmentation, and sedation were the most frequent interventions. Increasing FiO(2) restored PbtO(2) 80% of the time. CPP augmentation and sedation were effective in 73 and 66% of episodes of compromised brain oxygen, respectively. ICP reduction using mannitol was effective in 73% of treated episodes, though was used only when PbtO(2) was compromised in the setting of elevated ICP. Successful medical treatment of brain hypoxia was associated with decreased mortality. Survivors (n = 38) had a 71% rate of response to treatment and non-survivors (n = 11) had a 44% rate of response (P = 0.01).
Reduced PbtO(2) may occur in TBI patients despite efforts to maintain CPP. Medical interventions other than those to treat ICP and CPP can improve PbtO(2). This may increase the number of therapies for severe TBI in the ICU.
脑组织氧（PbtO2）监测用于严重创伤性脑损伤（TBI）患者。如何治疗脑氧降低以及对治疗的反应尚不清楚。我们研究了哪些医学治疗方法可以恢复 TBI 患者的正常 PbtO2。
从一项前瞻性观察队列研究中，回顾性确定了 49 名（平均年龄 40±19 岁）严重 TBI（格拉斯哥昏迷量表[GCS]≤8）的患者，这些患者在入住大学附属一级创伤中心后至少出现过一次脑氧合受损（PbtO2<25mmHg 持续>10min）。连续监测颅内压（ICP）、脑灌注压（CPP）和 PbtO2。确定了 PbtO2 受损和脑缺氧（PbtO2<15mmHg 持续>10min）的发作以及改善 PbtO2 的医学干预措施。
从 260 天的 PbtO2 监测中发现了 564 次 PbtO2 受损发作。以“病因导向”的方式进行的医学治疗成功地逆转了 72%的 PbtO2 受损发作，定义为恢复“正常”PbtO2（即≥25mmHg）。呼吸机操作、CPP 增加和镇静是最常见的干预措施。增加 FiO2 恢复 PbtO2 的时间为 80%。CPP 增加和镇静分别有效于 73%和 66%的脑氧受损发作。甘露醇降低 ICP 有效于 73%的治疗发作，尽管仅在 ICP 升高时 PbtO2 受损时才使用。成功的脑缺氧医学治疗与死亡率降低相关。幸存者（n=38）的治疗反应率为 71%，非幸存者（n=11）的治疗反应率为 44%（P=0.01）。
尽管努力维持 CPP，但 TBI 患者的 PbtO2 仍可能降低。除了治疗 ICP 和 CPP 的干预措施外，其他医学干预措施也可以改善 PbtO2。这可能会增加 ICU 中严重 TBI 的治疗方法数量。
