Aspects of the formation of encephalopathy and myocardiopathy in sepsis

Q3 Medicine
M. V. Petrova, A. V. Butrov, V. V. Kulabukhov, D. V. Cheboksarov, O. V. Ryzhova
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The search for domestic publications was carried out in the database on the RSCI website, foreign – in the PubMed, Google Scholar databases in the period 2000–2023. When analyzing the PubMed database, the query «sepsis neuroinflammation» found 5272 links. We also studied works on the following keywords: «neurotransmitters and sepsis». Publications describing the clinical picture, diagnosis, and sepsis were analyzed. A total of 40 articles were analyzed Such systems as immune, nervous and endocrine are interconnected due to regulatory peptides. Stable functioning of the central nervous system (CNS), or rather adequate secretion of neuropeptides are necessary for a normal immune response. Neuronal anti-inflammatory regulation of tissue macrophages is characterized by a local, rapid response to the pathogen through neuromediators. Confirmation of the neuropeptide theory of immunity regulation is the verification of neuropeptide receptors on peripheral blood lymphocytes and monocytes. These results indicate a possible mechanism of a «vicious» circle that occurs in infectious-septic complications and leads to damage to vital organs. To date, there are no widely available means for accurate monitoring of brain function at the patient’s bedside. There is no evidence or recommendations to support monitoring of cerebral perfusion or function in sepsis patients. At the same time, modern research on the phenotyping of patients taking into account brain dysfunction (sepsis associated encephalopathy) is based on the basic postulates of the pathophysiology and biochemistry of sepsis, but does not offer any methods of instrumental diagnosis of this condition, except for the use of validated delirium, coma scales (Glasgow coma scale, FOUR, CAM-ICU, etc.). Despite the described pathogenesis, there is currently no single definition of cardiac cardiomyopathy. However, most authors describe the fundamental features of this pathology: acute reversible one- or two-ventricular systolic or diastolic dysfunction with reduced contractility, not due to coronary heart disease. Primary cellular myocardial dysfunction in sepsis can manifest in several ways, including impaired function of the left and/or right ventricles during systole or diastole, as well as with insufficient cardiac output (CO) and oxygen delivery. To explain the changes in myocardial contractility associated with sepsis, several mechanisms have been proposed taking into account the host response. Since most of the parameters of the echo signal depend on the conditions of the volemic status, the evaluation of the echo signal should be repeated at several time points and supplemented with the definition of cardiac biomarkers. Conclusion. Analyzing the literature data on sepsis-associated encephalopathy and septic cardiomyopathy, it is possible to judge the interconnectedness of these events indirectly through damage to neurons during infectious-septic complications. Especially neuro-humoral mechanisms of regulation of the response to an infectious agent should be evaluated in patients with CCS, not only relying on laboratory diagnostics, but also using instrumental methods of visualization of brain, heart, and kidney damage. Such methods include magnetic resonance imaging (MRI), electroencephalogram (EEG), cerebral oximetry (CMRO2), echocardiography, ultrasound examination of the kidneys, etc","PeriodicalId":33000,"journal":{"name":"Vestnik anesteziologii i reanimatologii","volume":"40 6","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2023-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Vestnik anesteziologii i reanimatologii","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.24884/2078-5658-2023-20-5-84-91","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

Abstract

Relevance . The severe brain damage in most cases leads the patient to a long-term chronic critical condition (CCS). Regardless of the underlying disease that led to CCS, patients will have a certain imbalance of neurohumoral regulation and characteristic cognitive, muscle-reflex disorders. This cohort of patients is characterized not only by a cascade of typical pathological processes in the brain, but also by the consistent involvement of the cardiovascular system, respiratory organs, digestive organs, water metabolism, hormonal regulation, immunity, the addition of infectious-septic complications closes the circle of pathological processes, which often leads to death. Materials and methods . The search for domestic publications was carried out in the database on the RSCI website, foreign – in the PubMed, Google Scholar databases in the period 2000–2023. When analyzing the PubMed database, the query «sepsis neuroinflammation» found 5272 links. We also studied works on the following keywords: «neurotransmitters and sepsis». Publications describing the clinical picture, diagnosis, and sepsis were analyzed. A total of 40 articles were analyzed Such systems as immune, nervous and endocrine are interconnected due to regulatory peptides. Stable functioning of the central nervous system (CNS), or rather adequate secretion of neuropeptides are necessary for a normal immune response. Neuronal anti-inflammatory regulation of tissue macrophages is characterized by a local, rapid response to the pathogen through neuromediators. Confirmation of the neuropeptide theory of immunity regulation is the verification of neuropeptide receptors on peripheral blood lymphocytes and monocytes. These results indicate a possible mechanism of a «vicious» circle that occurs in infectious-septic complications and leads to damage to vital organs. To date, there are no widely available means for accurate monitoring of brain function at the patient’s bedside. There is no evidence or recommendations to support monitoring of cerebral perfusion or function in sepsis patients. At the same time, modern research on the phenotyping of patients taking into account brain dysfunction (sepsis associated encephalopathy) is based on the basic postulates of the pathophysiology and biochemistry of sepsis, but does not offer any methods of instrumental diagnosis of this condition, except for the use of validated delirium, coma scales (Glasgow coma scale, FOUR, CAM-ICU, etc.). Despite the described pathogenesis, there is currently no single definition of cardiac cardiomyopathy. However, most authors describe the fundamental features of this pathology: acute reversible one- or two-ventricular systolic or diastolic dysfunction with reduced contractility, not due to coronary heart disease. Primary cellular myocardial dysfunction in sepsis can manifest in several ways, including impaired function of the left and/or right ventricles during systole or diastole, as well as with insufficient cardiac output (CO) and oxygen delivery. To explain the changes in myocardial contractility associated with sepsis, several mechanisms have been proposed taking into account the host response. Since most of the parameters of the echo signal depend on the conditions of the volemic status, the evaluation of the echo signal should be repeated at several time points and supplemented with the definition of cardiac biomarkers. Conclusion. Analyzing the literature data on sepsis-associated encephalopathy and septic cardiomyopathy, it is possible to judge the interconnectedness of these events indirectly through damage to neurons during infectious-septic complications. Especially neuro-humoral mechanisms of regulation of the response to an infectious agent should be evaluated in patients with CCS, not only relying on laboratory diagnostics, but also using instrumental methods of visualization of brain, heart, and kidney damage. Such methods include magnetic resonance imaging (MRI), electroencephalogram (EEG), cerebral oximetry (CMRO2), echocardiography, ultrasound examination of the kidneys, etc
败血症中脑病和心肌病的形成
的相关性。在大多数情况下,严重的脑损伤导致患者长期慢性危重状态(CCS)。无论导致CCS的潜在疾病是什么,患者都会有一定的神经体液调节失衡和特征性的认知、肌肉反射障碍。这组患者的特点不仅是脑内典型病理过程的级联,而且心血管系统、呼吸器官、消化器官、水代谢、激素调节、免疫系统的一致参与,感染-脓毒症并发症的加入关闭了病理过程的循环,往往导致死亡。材料和方法。检索2000-2023年期间国内出版物在RSCI网站数据库中进行,国外出版物在PubMed、Google Scholar数据库中进行。在分析PubMed数据库时,查询“败血症神经炎症”发现了5272个链接。我们还研究了以下关键词的作品:“神经递质和败血症”。对描述临床表现、诊断和败血症的出版物进行分析。本文共分析了40篇文章,其中免疫系统、神经系统和内分泌系统由于调节肽而相互联系。中枢神经系统(CNS)的稳定功能,或者更确切地说,神经肽的充足分泌是正常免疫反应所必需的。神经元抗炎调节组织巨噬细胞的特点是通过神经介质对病原体的局部快速反应。神经肽免疫调节理论的证实是对外周血淋巴细胞和单核细胞上神经肽受体的验证。这些结果表明了一种可能的“恶性”循环机制,这种恶性循环发生在感染性-败血性并发症中,并导致重要器官的损害。到目前为止,还没有广泛可用的方法来精确监测病人床边的大脑功能。没有证据或建议支持监测脓毒症患者的脑灌注或功能。同时,考虑脑功能障碍(脓毒症相关脑病)的患者表型的现代研究是基于脓毒症的病理生理学和生物化学的基本假设,但除了使用经过验证的谵妄、昏迷量表(Glasgow昏迷量表、FOUR量表、CAM-ICU量表等)外,没有提供任何仪器诊断方法。尽管描述了发病机制,但目前对心肌病没有单一的定义。然而,大多数作者描述了这种病理的基本特征:急性可逆性单室或双室收缩或舒张功能障碍伴收缩力降低,而不是由于冠心病。脓毒症的原发性细胞性心肌功能障碍可表现为多种方式,包括收缩或舒张时左心室和/或右心室功能受损,以及心输出量(CO)和氧输送不足。为了解释与脓毒症相关的心肌收缩力的变化,考虑到宿主的反应,提出了几种机制。由于回波信号的大多数参数取决于容量状态的条件,因此回波信号的评估应在几个时间点重复,并辅以心脏生物标志物的定义。结论。分析脓毒症相关脑病和脓毒症心肌病的文献资料,可以通过感染-脓毒症并发症期间神经元的损伤间接判断这些事件的关联性。尤其是CCS患者对感染因子反应的神经-体液调节机制应进行评估,不仅依赖于实验室诊断,还应使用仪器方法可视化脑、心脏和肾脏损伤。这些方法包括磁共振成像(MRI)、脑电图(EEG)、脑氧饱和度(CMRO2)、超声心动图、肾脏超声检查等
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来源期刊
Vestnik anesteziologii i reanimatologii
Vestnik anesteziologii i reanimatologii Medicine-Emergency Medicine
CiteScore
1.10
自引率
0.00%
发文量
62
审稿时长
8 weeks
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