ваrbituric酸性衍生物急性中毒。巴比妥昏迷

Vladimir Alexandrovsky, Mariya Vladimirovna Kareva, P. Rozhkov
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摘要

介绍。研究的目的。总结作者多年来对巴比妥酸衍生物急性中毒的诊断和治疗经验,并详细介绍巴比妥中毒的临床研究结果,证明巴比妥中毒对身体有毒性损害作用,引起中枢神经系统功能的深度抑制,主要作用于脑干皮层和自主神经中枢。材料和方法。对在N.V. Sklifosovsky急诊医学研究所急诊毒理学部接受治疗的385例不同严重程度的巴比妥类药物急性中毒患者进行了分析。评估急性中毒的临床和脑电图。对两组患者的脑电图数据进行考虑和分析,有可能确定大脑的生物电活动类型。这些类型的脑电图对医生的信息价值是与临床和毒理学数据的特征进行比较。结果。总结巴比妥酸盐中毒的临床和脑电图变化的结果,指出已确定的脑生物电活动类型与某些临床症状相对应,并表明不同程度的中毒严重程度。这使得执业医生可以在记录昏迷患者的脑电图后,对急性巴比妥酸盐中毒做出初步诊断,有目的地进行毒理学研究,并在接受分析之前开始特定治疗。催眠药对中枢神经系统产生直接刺激作用。随着小剂量的bembromegrid的引入,人们注意到大脑生物电活动的适度激活。我们治疗这种中毒患者的经验表明,大剂量bemegrid对中枢神经系统有负面影响,可导致异种生物抑制的抑制阶段(根据N.E. Vvedensky)。结论。巴比妥酸衍生物中毒目前已严重危及患者的生命和健康。这使得在疾病早期阶段及时诊断和治疗措施的问题具有相关性。
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Acute poisoning with ваrbituric acid derivatves. Barbituric coma
Introduction. Aim of the study. To summarize the authors’ many years of experience in the diagnosis and treatment of acute poisoning with barbituric acid derivatives and to present the results of a detailed study of the clinic of barbituric intoxication, which prove a toxic damaging effect on the body, causing a deep inhibition of the functions of the central nervous system (CNS) with a predominant effect on the cortex and autonomic centers of the brain trunk. Material and methods. The analysis of 385 patients with acute poisoning with barbiturates of varying severity who were treated in the emergency toxicology department of the N.V. Sklifosovsky Research Institute for Emergency Medicine was carried out. The clinical and encephalographic picture of acute poisoning was assessed. The EEG data of two groups of patients were considered and analyzed, with the possibility of determining the type of bioelectric activity of the brain. The informative value of these types of EEG for a physician is in comparison with the characteristics of clinical and toxicological data. Results. Summarizing the obtained results of clinical and electroencephalographic changes in barbiturate poisoning, it was noted that the identified types of brain bioelectrical activity correspond to certain clinical symptoms and indicate different degrees of poisoning severity. This makes it possible for a practicing physician, after recording an EEG in a patient in a coma, to make a preliminary diagnosis of acute barbiturate poisoning, to purposefully conduct a toxicological study, and to begin specific treatment before receiving an analysis. Analeptic bemegrid causes a direct stimulating effect on the central nervous system. With the introduction of small doses of bеmegrid, a moderate activation of the bioelectrical activity of the brain was noted. Our experience in treating patients with this poisoning showed a negative effect of large doses of bemegrid on the central nervous system, which can lead to an inhibitory phase of parabiotic inhibition (according to N.E. Vvedensky). Conclusion. Poisoning with barbituric acid derivatives currently poses a serious danger to the life and health of patients. This makes the issue of timely diagnosis and treatment measures in the early stages of the disease relevant.
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