背景:主要目的是探索包括颅内压(ICP)在内的整体大脑生理变量之间的关联。脑血管反应性(PRx),脑灌注压(CPP),以及与创伤性脑损伤(TBI)中与脑组织氧合(pbtO2)相关的基于PRx的最佳CPP值(ΔCPPopt;实际CPP-CPPopt)的偏差。
方法:总共425名TBI患者进行ICP-和pbtO2监测至少12小时,在神经重症监护病房接受治疗的人,Addenbrooke医院,剑桥,英国,包括2002年至2022年。采用广义加性模型(GAMs)和线性混合效应模型,PRx,CPP,和CPPopt与pbtO2有关。PbtO2<20mmHg,ICP>20mmHg,PRx>0.30,CPP<60mmHg,ΔCPPopt<-5mmHg被认为是脑损伤。
结果:PbtO2<20mmHg出现在17%的监测时间的中位数中,与ICP>20mmHg的组合少于5%,PRx>0.30,CPP<60mmHg,或ΔCPPott<-5mmHg。在GAM分析中,在较大范围的ICP([0;50]mmHg)和PRx[-1;1]上,pbtO2保持在25mmHg左右,但在低于20mmHg的极低CPP低于30mmHg和低于-30mmHg时,CPPopt会恶化。在线性混合效应模型中,ICP,CPP,PRx,与pbtO2显著相关,但固定效应只能解释pbtO2变化的很小程度。
结论:PbtO2低于20mmHg是相对常见的,并且通常在没有ICP干扰的情况下发生,PRx,CPP,和ΔCPPopt。有显著的,但是整体大脑生理变量与pbtO2之间的联系较弱,这表明pbtO2缺氧通常是复杂且独立的病理生理事件。因此,其他变量可能对解释pbtO2更重要,同样,pbtO2可能不是确定整体脑血流优化(如CPPopt治疗)是否成功的合适结果指标。
The primary aim was to explore the association of global cerebral physiological variables including intracranial pressure (ICP), cerebrovascular reactivity (PRx), cerebral perfusion pressure (CPP), and deviation from the PRx-based optimal CPP value (∆CPPopt; actual CPP-CPPopt) in relation to brain tissue oxygenation (pbtO2) in traumatic brain injury (TBI).
A total of 425 TBI patients with ICP- and pbtO2 monitoring for at least 12 h, who had been treated at the neurocritical care unit, Addenbrooke\'s Hospital, Cambridge, UK, between 2002 and 2022 were included. Generalized additive models (GAMs) and linear mixed effect models were used to explore the association of ICP, PRx, CPP, and CPPopt in relation to pbtO2. PbtO2 < 20 mmHg, ICP > 20 mmHg, PRx > 0.30, CPP < 60 mmHg, and ∆CPPopt < - 5 mmHg were considered as cerebral insults.
PbtO2 < 20 mmHg occurred in median during 17% of the monitoring time and in less than 5% in combination with ICP > 20 mmHg, PRx > 0.30, CPP < 60 mmHg, or ∆CPPopt < - 5 mmHg. In GAM analyses, pbtO2 remained around 25 mmHg over a large range of ICP ([0;50] mmHg) and PRx [- 1;1], but deteriorated below 20 mmHg for extremely low CPP below 30 mmHg and ∆CPPopt below - 30 mmHg. In linear mixed effect models, ICP, CPP, PRx, and ∆CPPopt were significantly associated with pbtO2, but the fixed effects could only explain a very small extent of the pbtO2 variation.
PbtO2 below 20 mmHg was relatively frequent and often occurred in the absence of disturbances in ICP, PRx, CPP, and ∆CPPopt. There were significant, but weak associations between the global cerebral physiological variables and pbtO2, suggesting that hypoxic pbtO2 is often a complex and independent pathophysiological event. Thus, other variables may be more crucial to explain pbtO2 and, likewise, pbtO2 may not be a suitable outcome measure to determine whether global cerebral blood flow optimization such as CPPopt therapy is successful.