Extended neuromonitoring: new therapeutic opportunities?
Extended neuromonitoring: new therapeutic opportunities?
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扩展神经监测：新的治疗机会？
DOI：
10.1080/01616412.1998.11740617
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发表时间：
1998
影响因子：
1.9
通讯作者：
Bullock,R
中科院分区：
文献类型：
--
作者：
Zauner,A;Doppenberg,E;Soukup,J;Menzel,M;Young,HF;Bullock,R
为了优化脑损伤的治疗，需要对危重病人的底物递送进行持续监测。底物输送中断是导致脑缺血损伤易损性的主要因素，大多数患者在严重颅脑损伤、脑卒中或蛛网膜下腔出血后易发生缺血性损伤。在缺血期间保护大脑的一种方法是通过缺血组织的残余血流增加氧气的输送。在严重头部损伤后，低温也是保护脑细胞免受缺血有害影响的重要手段，因为它降低了代谢需求。在这项研究中，我们连续测量了脑氧、脑二氧化碳、脑pH和脑温度，以及每小时的脑葡萄糖和乳酸。在60名头部严重受伤的患者中，通过一个三腔螺栓将一个多参数传感器与一个脑室造瘘导管和一个微透析探头一起插入脑组织。在6小时内，通过逐步增加吸入氧（FiO2）从30%到60%到100%来增加脑氧输送，以测试增强氧张力对组织氧的影响。在大多数患者中，脑氧最初很低，并在监测期间逐渐增加，达到稳定的状态水平，约为30-40 mmHg。在那些死亡或植物人中，脑氧降至无氧水平。颅内压升高（n = 25）、低血压（n = 15）和呼吸困难（n = 9）的发作引起脑CO2立即升高。多元逻辑回归分析显示，脑氧是这些患者预后的最强预测因子。通过增加FiO2，氧气输送增加700%以上，乳酸产量同时下降（p < 0.01）。脑温与直肠温度、脑氧、脑血流量密切相关。自发性低体温患者预后较差（p < 0.01）。更全面地了解影响脑代谢和底物递送的动态因素可以通过扩展的神经监测获得。[神经科学学报，1998；[20]（增刊1）：585-590]
In order to optimize therapy for the injured brain it is desirable to continuously monitor substrate delivery in the critically ill patient. Interruption of substrate delivery is a major factor of the great vulnerability to ischemic damage, which affects a majority of patients after severe head injury, stroke or subarachnoid hemorrhage. An approach to protecting the brain during ischemia is to increase the delivery of oxygen via residual blood flow through ischemic tissue. Hypothermia is also an important means of protecting brain cells from the deleterious effects of ischemia, after severe head injury, because it reduces metabolic demands. In this study we continuously measured brain oxygen, brain CO2, brain pH and brain temperature, as well as hourly brain glucose and lactate. A multiparameter sensor was inserted into brain tissue, via a three lumen bolt, along with a ventriculostomy catheter and a microdialysis probe in 60 severely head injured patients. Brain oxygen delivery was increased by stepwise increase of inspired oxygen (FiO2) from 30% to 60% to 100% over a period of 6 h, in order to test the effect ofenhanced oxygen tension, on tissue oxygen. In most patients brain oxygen was initially low, and progressively increased, over the monitoring period, to a steady state level, around 30-40 mmHg. In those who died or remained vegetative, brain oxygen fell to anerobic levels. Episodes of increased ICP (n = 25), hypotension (n = 15), and respiratory difficulties (n = 9) caused an immediate increase in brain CO2 . Multiple logistic regression analysis showed brain oxygen to be the strongest predictor for outcome in these patients. By increasing FiO2, an increase in oxygen delivery ofmore than 700%, and a simultaneous decline in lactate production was seen (p < 0.01). Brain temperature was closely related to rectal temperature, brain oxygen, and cerebral blood flow. Patients who were spontaneously hypothermic had a poor outcome (p < 0.01). A fuller understanding of cfynamic factors affecting brain metabolism and substrate delivery may be obtained with extended neuromonitoring. [Neural Res 1998;20 (Suppl1): 585–590]