Santos Gabriela A, Petersen Nils, Zamani Amir A, Du Rose, LaRose Sarah, Monk Andrew, Sorond Farzaneh A, Tan Can Ozan
From the Department of Neurology, Stroke Division (G.A.S., S.L., A.M., F.A.S.), Department of Radiology (A.A.Z.), and Department of Neurosurgery (R.D.), Harvard Medical School, Brigham and Women's Hospital; Cerebrovascular Research Laboratory and Department of Physical Medicine and Rehabilitation (C.O.T.), Harvard Medical School, Spaulding Rehabilitation Hospital, Boston, MA; and Division of Neurocritical Care and Emergency Neurology (N.P.), Yale School of Medicine and Yale-New Haven Hospital, New Haven, CT.
Neurology. 2016 May 24;86(21):1950-6. doi: 10.1212/WNL.0000000000002696. Epub 2016 Apr 22.
To understand the physiologic basis of impaired cerebral autoregulation in subarachnoid hemorrhage (SAH) and its relationship to neurologic outcomes.
The cohort included 121 patients with nontraumatic SAH admitted to a neurointensive critical care unit from March 2010 to May 2015. Vasospasm was ascertained from digital subtraction angiography and delayed cerebral ischemia (DCI) was defined as new cerebral infarction on high-resolution CT. Cerebral blood flow and beat-by-beat pressure were recorded daily on days 2-4 after admission. Autoregulatory capacity was quantified from pressure flow relation via projection pursuit regression. The main outcome was early alterations in autoregulatory mechanisms as they relate to vasospasm and DCI.
Forty-three patients developed only vasospasm, 9 only DCI, and 14 both. Autoregulatory capacity correctly predicted DCI in 86% of training cohort patients, generalizing to 80% of the patients who were not included in the original model. Patients who developed DCI had a distinct autoregulatory profile compared to patients who did not develop secondary complications or those who developed only vasospasm. The rate of decrease in flow was significantly steeper in response to transient reductions in pressure. The rate of increase in flow was markedly lower, suggesting a diminished ability to increase flow despite transient increases in pressure.
The extent and nature of impairment in autoregulation accurately predicts neurologic complications on an individual patient level, and suggests potentially differential impairments in underlying physiologic mechanisms. A better understanding of these can lead to targeted interventions to mitigate neurologic morbidity.
了解蛛网膜下腔出血(SAH)时脑自动调节功能受损的生理基础及其与神经学预后的关系。
该队列包括2010年3月至2015年5月入住神经重症监护病房的121例非创伤性SAH患者。通过数字减影血管造影确定血管痉挛,延迟性脑缺血(DCI)定义为高分辨率CT上的新发脑梗死。入院后第2 - 4天每天记录脑血流量和逐搏血压。通过投影追踪回归从压力 - 流量关系量化自动调节能力。主要结局是与血管痉挛和DCI相关的自动调节机制的早期改变。
43例患者仅发生血管痉挛,9例仅发生DCI,14例两者均发生。自动调节能力在86%的训练队列患者中正确预测了DCI,并推广到未纳入原始模型的80%的患者。与未发生继发性并发症或仅发生血管痉挛的患者相比,发生DCI的患者具有独特的自动调节特征。压力短暂降低时,血流下降速率明显更陡。血流增加速率明显更低,表明尽管压力短暂升高,但增加血流的能力减弱。
自动调节功能受损的程度和性质可在个体患者水平准确预测神经学并发症,并提示潜在的基础生理机制差异受损。更好地理解这些情况可导致有针对性的干预措施,以减轻神经学发病率。