Annotation. Polytrauma is considered the main cause of death among people younger 45 years. Among trauma patiens 15-20% regularly take alcohol, close to 32% of patients who needed intensive therapy to alcohol withdrawal syndrome (AWS), and 5-20% of the progressed to alcohol delirium. The aim of the study is to analyze the dynamics of autoimmune response to markers of neurodestruction in the blood of patients with moderate polytrauma and alcohol withdrawal, complicated by alcohol delirium and assessment of cognitive functions depending on the method of sedation. The study involved 80 patients with moderate polytrauma with alcohol withdrawal, complicated by alcohol delirium. The median age was 45 years (39-54). Patients in Group 1 (n=40) were given dexmedetomidine as a sedation method, and in Group 2 (n=40) diazepam sedation was used according to the symptom-trigger protocol. The content of antibodies to neuron-specific enolase (NSE), myelin basic protein (MBP), total human brain antigen (THBA), S-100 calcium were determined by enzyme-linked immunosorbent assay on days 1, 3, 7 and 14 after alcohol delirium. Assessment of cognitive function was performed (after withdrawal from sedation if present) on days 4 and 14 using the Montreal Cognitive Assessment Scale (MoCa). Mathematical processing of the obtained results was performed in accordance with the generally accepted methods of statistical analysis. The critical value of the significance level (p) was taken as ≤5%. Signs, the distribution of which differed from normal, are presented in the form of Me (median), the confidence interval within the first and third quarters [QI - QIII]. To assess the causal role of various factors in the development of lesions used χ-square with the inclusion of the Yates correction and the odds ratio. In the first 24 hours after the manifestation of AD, the levels of autoantibodies in the two groups of patients did not differ significantly from the level of healthy volunteers. Estimation of the level of antibodies to the S-100B protein showed that in group 1 this indicator increased by a maximum of 24.4% and amounted to 15.8 [14.7 - 17.6], while in the second group increased by 32.6% and became 17.5 [15.3 - 19.7]. From the 7th day, the number of antibodies began to decrease in both groups and was 15.6 [13.6 - 16.8] in group 1 and 16.3 [14.1-19.2] in group 2 on the 7th day, and 14.0 [11.6 - 15.3] and 15.2 [ 13.1 - 18.3], respectively, on the 14th day after hospitalization in ICU. The level of antibodies to NSE was maximum on the 3rd day of the study and was 29.8 [28.4 - 31.8] in patients of group 1, which is higher than the initial level by 26.8%, and in patients of group 2 was 31.6 [29.5 -33.2], which exceeds baseline by 33.9% (p=0.0114 between groups 1 and 2). Subsequently, there was a decrease in the level of antibodies to NSE on the 7th and 14th day after the onset of AD, while maintaining a significant difference between the comparison groups. Antibodies to MBP did not differ between groups up to and including day 3, but were significantly higher than in healthy volunteers. On the 7th day, the level of antibodies to MBP in group 1 was 26.8 [24.4 - 28.8], which corresponded to the values of the control group, and in group 2 was 29.3 [27.7 - 31.5], which is significantly more than the first group (p = 0.0017). In the study on day 14, this trend was maintained: the level of antibodies to OBM among patients in group 2 was 28.6 [27.0 - 30.8], while in group 1 it was 26.2 [23.7 - 28.2]. Antibody levels to THBA on day 3 were significantly higher than baseline and were 30.8 [28.4 - 34.5] in group 1 and 32.7 [30.6 - 36.1] in group 2 (p=0.0056). On day 7 and day 14, the number of antibodies THBA in patients of group 1 did not differ significantly from the control group, while in patients of group 2 they were significantly higher on day 7 - 31.5 [29.4 - 34.9] and normalized on day 14. When analyzing the results of the MoCa test after eliminating the main manifestations of alcohol withdrawal syndrome (4 days after admission to ICU), the number of points in the study groups was significantly lower than the control values: in group 1 1.3 times (p <0.0001), in group 2 – 1.6 times (p<0.0001). The differences between the studied groups of patients are significant (p = 0.000087). Thus, the use of dexmedetomidine for the sedation of patients with hypertension and polytrauma reduces autumnal neurodestruction, which improves the prognosis for the restoration of cognitive function.
Injuries are one of the leading causes of death and disability in the world. It is known that from 25% to 85% of patients are in a state of alcohol intoxication during hospitalization in the polytrauma department, 5-20% of them develop alcoholic delirium as a complication of alcohol withdrawal.The aim of the study was to analyze the indicators of lipid peroxidation and antioxidant protection in patients with moderate polytrauma and with a state of alcohol withdrawal complicated by alcoholic delirium, depending on the method of sedation. Material and research methods. The study included 80 patients with polysystemic trauma of moderate severity and with a state of alcohol withdrawal complicated by alcoholic delirium. The median age was 45 years [39-54]. Patients in Group 1 (n = 40) were given dexmedetomidine as a sedation method, and in Group 2 (n = 40) they used sedation with diazepam according to the symptom-trigger protocol. The content of the main indicators of the oxidative system was determined in the serum of patients: active products of thiobarbituric acid, diene conjugates, 8-isoprostane to assess the intensity of lipid peroxidation. The state of the antioxidant system was assessed by the content of superoxide dismutase, catalase, glutathione peroxidase. Conclusions. The use of dexmedetomidine for sedation of patients with alcohol withdrawal and alcoholic delirium and polytrauma reduces the manifestations of lipid peroxidation due to faster recovery of enzyme systems of antioxidant protection.