背景:脑自动调节受损和脑灌注不足可能在脓毒症相关性脑病(SAE)患者的高发病率和高死亡率中起关键作用。大脑自动调节的床边评估可能有助于个性化优化脑灌注的血液动力学目标。我们假设近红外光谱(NIRS)衍生的脑血氧饱和度可以确定可增强SAE患者自动调节的血压范围,并且自动调节障碍与脑病的严重程度有关。
方法:使用基于NIRS的多模式监测连续12小时随访可直接归因于脓毒症的急性脑病的成年患者。我们使用区域脑氧饱和度与平均动脉压(MAP)之间的时间相关性来确定脑氧饱和度指数(COx)作为脑自动调节的量度。在3个连续的4小时内,每个患者的平均COx值按MAP排序,构建自动调节曲线;最佳压力(MAPOPT),定义为与最稳健的自动调节相关的MAP(最低COX),在每个时期都被确定。用格拉斯哥昏迷量表(GCS)测量脑病的严重程度。
结果:六例颅外脓毒症患者符合严格的标准,包括没有药物镇静或神经系统疾病。在所有患者中均确定了最佳MAP,范围为55至115mmHg。此外,MAPOPT在监测期间随时间在个体患者中变化。受干扰的自动调节,基于COx,在控制和不控制脓毒症的年龄和严重程度的情况下,与较差的神经系统状况(GCS<13)相关(调整后的比值比[OR]:2.11;95%置信区间[CI]:1.77-2.52;P<.001;OR:2.97;95%CI:1.63-5.43;P<.001)。
结论:在SAE患者的高保真组中,连续,基于NIRS的监测可以识别改善自动调节的血压范围。考虑到大脑自动调节功能与脑病严重程度之间的关联,这一点很重要。与目前的做法相比,使用床边自动调节监测个性化血压目标可能会更好地保持SAE中的脑灌注。
BACKGROUND: Impaired cerebral autoregulation and cerebral hypoperfusion may play a critical role in the high morbidity and mortality in patients with sepsis-associated encephalopathy (SAE). Bedside assessment of cerebral autoregulation may help individualize hemodynamic targets that optimize brain perfusion. We hypothesize that near-infrared spectroscopy (NIRS)-derived cerebral oximetry can identify blood pressure ranges that enhance autoregulation in patients with SAE and that disturbances in autoregulation are associated with severity of encephalopathy.
METHODS: Adult patients with acute encephalopathy directly attributable to sepsis were followed using NIRS-based multimodal monitoring for 12 consecutive hours. We used the correlation in time between regional cerebral oxygen saturation and mean arterial pressure (MAP) to determine the cerebral oximetry index (COx) as a measure of cerebral autoregulation. Autoregulation curves were constructed for each patient with averaged COx values sorted by MAP in 3 sequential 4-hour periods; the optimal pressure (MAPOPT), defined as the MAP associated with most robust autoregulation (lowest COx), was identified in each period. Severity of encephalopathy was measured with Glasgow coma scale (GCS).
RESULTS: Six patients with extracranial sepsis met the stringent criteria specified, including no pharmacological sedation or neurologic premorbidity. Optimal MAP was identified in all patients and ranged from 55 to 115 mmHg. Additionally, MAPOPT varied within individual patients over time during monitoring. Disturbed autoregulation, based on COx, was associated with worse neurologic status (GCS < 13) both with and without controlling for age and severity of sepsis (adjusted odds ratio [OR]: 2.11; 95% confidence interval [CI]: 1.77-2.52; P < .001; OR: 2.97; 95% CI: 1.63-5.43; P < .001).
CONCLUSIONS: In this high-fidelity group of patients with SAE, continuous, NIRS-based monitoring can identify blood pressure ranges that improve autoregulation. This is important given the association between cerebral autoregulatory function and severity of encephalopathy. Individualizing blood pressure goals using bedside autoregulation monitoring may better preserve cerebral perfusion in SAE than current practice.