Pressure autoregulation, intracranial pressure, and brain tissue oxygenation in children with severe traumatic brain injury
Pressure autoregulation, intracranial pressure, and brain tissue oxygenation in children with severe traumatic brain injury
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DOI：
10.3171/2009.6.peds096
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发表时间：
2009-11-01
影响因子：
1.9
通讯作者：
Peter, Jonathan C.
中科院分区：
文献类型：
--
作者：
Figaji, Anthony A.;Zwane, Eugene;Peter, Jonathan C.
物体。脑压自动调节是血压变化时稳定脑血流量的重要神经保护机制。在本研究中，作者探讨了自动调节与临床因素的关系。布尔奇科颅内压、脑组织氧分压(PbtO(2))和儿童重型颅脑损伤(TBI)后的预后。在这项前瞻性观察性研究中，我们特别研究了状态01：自动调节如何影响血压变化对ICP和PbtO(2)方法的影响。对24例重症患者进行了52次自动调节试验。TBI。患者平均年龄6.3±3.2岁。复苏后格拉斯哥昏迷评分为6分(3~8分)。所有患者均进行持续的颅内压和MID监测。应用经颅多普勒超声检测平均动脉压升高20%后大脑中动脉血流速度的自动调节指数(ARI)，将自动调节受损定义为ARI&0 4，完整自动调节定义为ART>；=0 4。采用多元Logistic回归分析自动调节(包括连续变量和二分变量)与预后、临床和生理变量的关系。29%的患者(7例)自我调节功能受损(ART<；04)。格拉斯哥昏迷评分与ARI显著相关(p=0.02，r=0.32)，而其他临床因素与自身调节状态无关。在自我调节功能受损或正常的患者中，检测时的基础值包括：颅内压、PbtO(2)、PbtO(2)/PaO2、平均动脉压和大脑中动脉血流速度。ART(连续型和二分型)与颅内压改变呈负相关(连续型ARI，p 0.005，二分型ARI，p=0.02)。当ARI较低(自身调节较弱)时，颅内压随血压升高而升高，ART(连续型和二分型)也与PbtO(2)的变化呈负相关。(连续艺术。0.002点。二分ARI，p=0.02)。在大多数患者中，PbtO(2)随着血压的升高而增加，即使在ARI相对较高的情况下也是如此(较强的自我调节)。但这种反应的规模仍然与艺术有关。结论ART与预后无明显关系。这些数据说明了自我调节的强度对颅内压和微循环反应的影响。对于血压的变化和个体间这种反应的变异性，研究结果表明，自动调节测试可能有助于儿童重型颅脑损伤的临床决策，并有助于更好地为个别患者确定最佳血压或脑灌注压目标。(DOI：10.3171/2009.6.PEDS096)
Object. Cerebral pressure autoregulation is an important neuroprotective mechanism that stabilizes cerebral blood flow when blood pressure (BP) changes In this study the authors examined the association between autoregulation and clinical factors. BR. intracranial pressure (ICP), brain tissue oxygen tension (PbtO(2)), and outcome after pediatric severe traumatic brain injury (TBI). In particular we examined how the Status 01: autoregulation influenced the effect of BP changes on ICP and PbtO(2)Methods In this prospective observational study. 52 autoregulation tests were performed in 24 patients with severe. TBI. The patients had a mean age of 6.3 +/- 3.2 years. and a postresuscitation Glasgow Coma Scale score of 6 (range 3-8). All patients underwent continuous ICP and MID, monitoring. and transcranial Doppler ultrasonography was, used to examine the autoregulatory index (ARI) based on blood flow velocity of the middle cerebral artery after increasing mean arterial pressure by 20% of the baseline value Impaired autoregulation was defined as an ARI < 0 4 and intact autoregulation as an ART >= 0 4 The relationships between autoregulation (measured as both a Continuous and dichotomous variable), outcome, and clinical and physiological variables were examined using Multiple logistic regression analysisResults. Autoregulation was impaired (ART < 0 4) in 29% of patients (7 patients). The initial Glasgow Coma Scale score was significantly associated with the ARI (p = 0.02, r = 0.32) but no other clinical factors were associated with autoregulation Status. Baseline values at the time of testing for ICP, PbtO(2), the ratio PbtO(2)/PaO2, mean arterial pressure, and middle cerebral artery blood flow velocity were similar in the patients with impaired or intact autoregulation. There was an inverse relationship between ART (continuous and dichotomous) with a chancle in ICP (continuous ARI, p 0.005, dichotomous ARI, p = 0 02): that is. ICP increased with the BP increase when ARI was low (weak autoregulation) The ART (continuous and dichotomous) was also inversely associated with a change in PbtO(2). (continuous ART. p 0.002. dichotomous ARI, p = 0 02). The PbtO(2) increased when BP was increased in most patients, even when the ARI was relatively high (stronger autoregulation). but the magnitude of this response was still associated with the ART. There was no relationship between the ART and OutcomeConclusion. These data demonstrate the influence of the strength of autoregulation on the response of ICP and MO. to BP changes and the variability of this response between individuals The findings suggest that autoregulation testing may assist clinical decision-making in pediatric severe TBI and help better define optimal BP or cerebral perfusion pressure targets for individual patients. (DOI: 10.3171/2009.6.PEDS096)