SEPSIS ASSOCIATED ENCEPHALOPATHY AND ABDOMINAL SEPSIS: CURRENT STATE OF PROBLEM

The aim of the work is to analyze literature data on the current status of sepsis and sepsis associated encephalopathy (including against background of abdominal sepsis). For this purpose, 59 scientific publications of PubMed, Google Scholar and Research Gate scientific platforms were retrospectively analyzed. Results of the study: Sepsis-Associated Encepha-lopathy (SAE) is a syndrome of general cerebral dysfunction, due to the systemic response of the body to the infection, with exception of direct CNS infection and other types of encephalopathies. In view of absence of unambiguous specific clinical criteria for SAE, its diagnosis is based on exclusion method that use a complex of instruments, including EEG, MRI, laboratory determination of NSE and S100b in blood. In surgical ICU, abdominal sepsis ranks second in levels of mortality. In accordance with the changes in sepsis nomenclature in 2016 and tactical approaches to the man-agement of septic patients, the SOFA scale, which includes a systemic assessment of organ failure, including cerebral insufficiency, based on the GCS, is an optimal tool in as-sessing the condition of patients with suspected abdominal sepsis. At the same time, the GCS itself is considered to be the most optimal in assessing the severity of SAE. The degree of peritonitis severity is usually assessed separately, using the Mannheim Peritonitis Index. Data on the pathobiology of abdominal sepsis and SAE are based primarily on experimental studies and do not reflect a complete picture of the processes. Taking into account modern ideas about the "compartmentalization of the immune response" for sepsis, we should take a more balanced view of the interpretation of pathophysiological stereotypic reactions developing in differ-ent organs, and for clinical and experimental comparisons it is optimal to use similar conditions for the development of the septic process – for example, the abdominal source of sepsis. Conclusion: Despite the significant contribution of abdominal sepsis and sepsis-associated pathology to the overall mortality rate of surgical ICU patients, as well as a large number of studies in this field, there is still no unam-biguous opinion on the mechanisms of the development of a septic condition, and in particular, complications such as SAE . From the literature it is known that the triggering factor in the development of a septic cascade of events is the hyperactivation of inflammatory cytokines system, which has disadaptive nature and leads to the development of "cytokine storm". SAE is a consequence of this process. Damage to the CNS appears to be a complex process based on a complex system of neuro-immune-endocrine signals. In SAE morpho-genesis a large number of white spots remain. In experimental studies, the role of damage of BBB, the reactivation of neuroglia as well as ischemic damage are emphasized. However, the deficiency of clinical-anatomical studies causes a certain discrepancy between the scientific concepts of sepsis, based on experimental models, and real clinical studies. "CLP" is recognized as the "gold standard" of the experimental animal model of sepsis and SAE, during which animals can recreate a close to the clinical picture of abdominal sepsis with cerebral dysfunction. Further clinical-anatomical and simultaneous experimental studies of abdominal sepsis and SAE will help to determine the thinner links of pathogenesis and morphogenesis of the sepsis-associated pathology of the CNS.