Sepsis and septic shock remain a major problem in critical care medicine being the most common causes of death in the intensive care unit. Currently, such methods of extracorporeal blood purification as hemodiafiltration, high-volume hemofiltration, high cut-off (HCO) membrane hemofiltration are among preferable options for treatment of severe systemic disorders and pathological conditions including sepsis.

The purpose of the review is to show the potentialities and prospects of the use of various extracorporeal hemocorrection methods, including those that are commonly employed in medical practice, and novel ones, either recently developed, or still under the development in experimental settings according to sepsis patho-physiology. The selected 82 papers represent comprehensible clinical and experimental data from the literature of the last five years and several earlier publications remained of current interest in a medical practice.

The review presents current methods of extracorporeal hemocorrection (EHC) in patients with sepsis. The clinical pathophysiology of sepsis is described in relation to treatment options that target endotoxemia and «cytokine storm». We consider commonly used EHC methods (hemodiafiltration, high-volume hemofiltration, high cut-off membrane hemofiltration and others) and novel promising technologies that include extracorporeal kidney support device, immune support system, leukocyte inhibition module, and artificial spleen, which have been recently developed and are still under investigation in the intensive care.

Conclusion. Currently, EHC methods are increasingly used not only to support renal function, but also as pathogenetic therapy option for multiple organ support and immunomodulation by reducing the level of cir-culating inflammatory mediators. Exploration of novel extracorporeal blood purification techniques for the pathogenetic treatment of patients with sepsis seems encouraging and promising.

Massive anoxic brain injury caused by cardiac arrest leads to wakefulness suppression up to coma. The prediction of outcome is based on the analysis of the clinical features and the results of instrumental tests. One of the well-known signs of an unfavorable prognosis is involuntary motor activity, which is most commonly represented by myoclonus. In case of their cortical origin, they are accompanied by epileptiform activity in the electroencephalogram (EEG).

Material and methods. We present a case series and literature review concerning a very rare fatal sign, non-rhythmic spontaneous eye opening accompanied by a «burst-suppression» pattern (BS) in the EEG. All patients suffered from transient acute hypotension or arrhythmia that required cardiopulmonary resuscitation (CPR) in three cases. A literature search found only 11 publications describing post-anoxic tonic eye-opening (PATEO).

Results. The PATEO with BS was observed for less than a day followed by cessation of brain bioelectric activity in all patients. Only two patients exhibited isolated eye-opening and closing, while the rest had axial and limbs myoclonus just after CPR. In one case, eyelid opening was followed by a clonic movement of the head to the right, the EEG bursts were prolonged and had spike-like morphology. Three patients received antiepileptic and sedative therapy. All patients died in 3-43 days after the fatal cardiovascular event.

Visual superposition of bursts in EEG and myogram of m. orbicularis oculi demonstrating identical morphology for EEG and myographic bursts was described for the first time. Our cases and literature review confirm that, regardless of the intensive treatment, patients with PATEO have fatal outcomes.

Conclusion. The clinical and electrographic PATEO with BS phenomenon always indicates a lethal prognosis. The origin of PATEO is still under discussion. We suggest that it could be caused by disinhibition of subcortical and stem structures during extensive death of cerebral cortical neurons.

The aim of the study. To identify alterations of motor connectome in patients with varying degrees of hemi-paresis after severe traumatic brain injury (TBI) versus healthy volunteers.

Material and methods. The study included 29 patients with TBI aged 18 to 35 years and 23 healthy volunteers aged 20 to 32 years. Participants underwent a comprehensive clinical and neuroimaging study. Motor impairment was evaluated via muscle strength assessment using a five-score scale. The fMRI data were processed using a dedicated CONN software package. Anatomical 3-D connection masks of the whole brain motor functional system in the predetermined regions of interest (ROIs) were used for the assessment. Then the group indicators of functional connectivity (statistical significance of the connection) were computed.

Results. It was established that the structure of connections in healthy individuals performing active movement with the right (leading) hand is determined by formation of focus in the cortical and subcortical ROIs in the contralateral hemisphere. With passive movement of the right hand the pale ball becomes functionally active in addition to the activated areas. The striopallidar system structures became active on both sides, and connectivity with the additional motor cortex and the motor cortex of the ipsilateral hemisphere emerged as the paresis increased during active movement. The focus of motor activity during passive movement was determined in the motor cortex and putamen, which makes it possible to use a passive test in patients with gross motor disorders or unconsciousness for a full assessment of the entire structural and functional brain connectome.

Conclusion. As hemiparesis increased in patients after severe traumatic brain injury, a decrease in the total number of connection appeared; simultaneous engagement of ancient primordial structures, such as bilateral activation of pale globes, demonstrated neuroplasticity.

Up to 70% of patients hospitalized for COVID-19 need respiratory support, up to 10% need high-flow oxygen therapy, non-invasive and invasive ventilation. However, standard methods of respiratory support are ineffective in 0.4-0.5% of patients. In case of potentially reversible critical refractory respiratory failure that patients may require ECMO. Management of patients with extremely severe COVID-19 associates with numerous clinical challenges, including critical illness, multiple organ dysfunction, blood coagulation disorders, requiring prolonged ICU stay and care, use of multiple pharmacotherapies including immunosuppressive drugs. Pharmacological suppression of immunity is associated with a significant increase in the risk of secondary bacterial and fungal infections. Currently, data on epidemiology of secondary infections in patients with COVID-19 undergoing ECMO is limited.

Aim. To study the prevalence and etiology of secondary infections associated with positive blood cultures in patients with extremely severe COVID-19 requiring ECMO.

Materials and methods. A single-center retrospective non-interventional epidemiological study including 125 patients with extremely severe COVID-19 treated with ECMO in April 2020 to December 2021.

Results. Out of 700 blood culture tests performed in 125 patients during the study, 250 tests were positive confirming bacteremia/fungemia. Isolated pathogens varied depending on the duration of ECMO: gram-positive bacteria (primarily coagulase-negative staphylococci) dominated from the initiation of ECMO support; increased duration of ECMO associated with an increasing the proportion of pathogens common in ICU (Klebsiella pneumoniae and/or Acinetobacter baumannii with extensively drug resistant and pan-drug resistant phenotypes, and vancomycin-resistant Enterococcus faecium). When ECMO lasted more than 7-14 days, opportunistic pathogens (Candida species, Stenotrophomonas maltophilia, Providencia stuartii, non-diphtheria corynebacteria, Burkholderia species and others) prevailed as etiological agents.

Conclusion. Longer duration of ECMO resulted in increasing the rates of infectious complications. In patients undergoing ECMO for more than 14 days, the microbiological landscape becomes extremely diverse, which hampers choosing an empirical antimicrobial therapy. Since potential pathogens causing secondary infections in patients during ECMO are difficult to predict, rapid identification of rare opportunistic pathogens and their sensitivity profile, followed by targeted administration of antimicrobials, seems most beneficial.

Objective. To evaluate a potential of cystatin C blood concentration to predict acute kidney injury (AKI) in patients with severe and extremely severe pneumonia associated with a COVID-19.

Materials and methods. An observational prospective study of 117 patients with severe and extremely severe pneumonia associated with a COVID-19 in an ICU setting was conducted in 2020-2022 (site: multi-functional Medical Center, 1586 Military Clinical Hospital of the Ministry of Defense of Russia, Moscow Region, Russia). Routine laboratory tests and instrumental examinations were performed according to generally accepted protocols. Cystatin C concentrations in blood (s-CysC) and urine (u-CysC) were measured by immunoturbidimetric method.

Results. AKI was diagnosed in 21 (17.9%) patients, kidney dysfunction without AKI was found in 22 (18.8%) patients with severe and extremely severe pneumonia associated with COVID-19. s-CysC and u-CysC levels in the group of patients with AKI were statistically significantly higher compared to the levels in the group of patients without AKI. The levels of s-CysC obtained within Day 1 — T (-1), and Day 2 — T (-2) prior to AKI onset turned out to be the independent factors for AKI development in patients with severe and extremely severe pneumonia associated with COVID-19: OR 5.37, Wald chisquare 5.534 (CI: 1.324; 21.788); P=0.019 and OR 3.225, Wald chi-square 4.121 (CI: 1.041; 9.989); P=0.042, respectively. s-CysC T (-2) value is informative, and s- CysC T (-1) is a highly informative predictor of AKI development in severe and extremely severe pneumonia associated with COVID-19: ROC AUC 0.853 (95% CI, 0.74-0.966), P<0.001) with 90% sensitivity and 73% specificity at a cut-off of 1.67 mg/L, and ROC AUC 0.905 (95% CI, 0.837-0.973), P<0.001) with 90% sensitivity and 73% specificity at a cut-off of 1.69 mg/l, respectively. Serum CysC levels started increasing 3 days prior to AKI onset, outpacing the increase of SCr levels. The u-CysC levels were not predictive of AKI development. Impaired renal function probability was increasing with patients' age (P<0.0001).

Conclusions. Serum CysC seems to be a statistically significant predictor of AKI. s-CysC levels started increasing 3 days prior to AKI onset, surpassing the increase of SCr levels in patients with severe and extremely severe pneumonia associated with COVID-19. Urine CysC did not achieve statistical significance as a predictor for AKI, although u-CysC concentrations were significantly higher on days 3, 2, 1 prior to AKI onset and on the day of AKI onset in the group of patients with AKI.

Objective. To identify predictors of newborn infants mortality before medical evacuation.

Materials and methods. The observational, cohort, retrospective study included 564 newborns: 526 patients survived and 38 died after 604 visits of the resuscitation-consultation Center transport team (critical care transport — CCT team). Patient's anamnesis, objective data of a patient at the time of examination by CCT team, the volume of intensive care provided and treatment adjustments during preparation for the transfer, records of patient's monitored parameters and indicators of prognosis were analyzed.

Results. Compared to survivors, non-survivors neonates exhibited significant increases in premature new-borns (gestation period <29 weeks in 55.26% vs 10.27% in survivors, P<0.001) and significantly increased need in a high-frequency ventilation (7.89% [1.66-21.38] vs 0.57% [0.12-1.66] in survivors, P=0.005), and in cate-cholamines support (use of adrenaline was 13.51% [4.54-28.77] in non-survivors vs 0.76% [0.21-1.94] in survivors, P<0.001). Both early and late neonatal infections predominated in non-survivors: ([26.32% [13.40-43.10] vs 8,75% [6,47-11,49, early infection, non-survivors vs. survivors, respectively, P=0.002) and (23.6% 8 [11.44-40.24] vs 10.46% [7.97-13.39], late infection, non-survivors vs. survivors, respectively, P=0.028). Significant differences in the fraction of inspired oxygen (30% [30-30] vs 45% [30-60], P<0.001), oxygenation saturation index (2.71 [2.54-3.03] vs 4.48 [2.55-7.67], P<0.001), and SpO₂/FiO₂ ratio (316.67 [313.33-320] vs 207.25 [151.67-313.33] P<0.001) were found between the groups of survived vs. non-survived neonates, respectively. Logistic regression model revealed following markers of neonatal mortality: birth weight, development of early and late neonatal infection, and the oxygenation saturation index.

Conclusion. Low birth weight, development of early or late neonatal infection and an increase in the oxygenation saturation index are the risk factors of death in newborns requiring medical evacuation.

Necrotizing enterocolitis is a devastating emergency, multifactorial disease. Inter-alpha inhibitor proteins are serine protease inhibitors involved in many physiological and pathological activities.

Aim: this study was designed in order to assess the value of inter-alpha inhibitor proteins in predicting and improving accuracy of diagnosis of NEC in newborn infants with non-precise abdominal and intestinal manifestations.

Materials and Methods. This study was prospective longitudinal research that included 80 newborn infants presented with non-specific abdominal manifestations. Infants were divided into two groups. Group A; infants who developed necrotizing enterocolitis, they had stage II or III necrotizing enterocolitis according to modified Bell's criteria. Group B; included infants who did not develop necrotizing enterocolitis. Serum inter alpha inhibitor proteins level was measured by ELISA.

Results. In necrotizing enterocolitis group, the median inter-alpha inhibitor protein level was (9.38 mg/L), this was significantly lower than non-necrotizing enterocolitis group (44.40 mg/L), P<0.01. Inter-alpha inhibitor protein was reduced in stage IA than stage IIIB. Inter-alpha inhibitor protein values were decreased in preterm and full term infants with sensitivity of 98 % and specificity of 96% at cutoff <19.42 and <19.96 mg/L. The cut off in non-survival cases was >13.29 mg/L with sensitivity of 53.33 % and specificity of 92.31%.

Conclusion. Inter-alpha inhibitor protein levels were reduced in full term and preterm infants with necrotizing enterocolitis, consequently it may improve diagnosis of necrotizing enterocolitis in newborn infants. It has prognostic value and correlate with severity of necrotizing enterocolitis. It might predict non-survival cases.

Aim of the study. To determine the effects of xenon exposure at a dose of 0.5 MAC of different duration on the content and enzyme-inactivating phosphorylation of the glycogen synthase kinase-3β (GSK3β) in the perifocal zone of ischemic cerebral infarction in an experimental setting.

Materials and methods. The Long method was used for modelling brain ischemia/reperfusion in 39 rats weighing 300-350 g. Study group animals was exposed to xenon at a dose of 0.5 MAC during 30, 60 and 120 minutes whereas control group animals received an oxygen-air mixture. Sham-operated animals served as a comparison group. The levels of GSK3β and phospho-GSK3β in brain homogenates were determined by blotting using specific antibodies.

Results. In ischemic stroke model, the content of GSK3β did not significantly change in control animals compared to comparison group. However, control group animals exhibited significant (2.7-fold, P<0.001) decrease in the content of its phospho-GSK3β in the perifocal zone of ischemic cerebral infarction. Inhalation of 0.5 MAC xenon during 30 minutes did not lead to an increase in phosphorylation of the GSK3β enzyme (P=0.9), however, 60 and 120 minutes of 0.5 MAC xenon exposures resulted in the increase in phosphorylated form of the enzyme by a factor of 2.1 (P=0.005) and 2.3 (P=0.001), respectively, compared to the control group.

Conclusion. The results reveal a possible molecular mechanism (i. e., execution of neuroprotective and anti-inflammatory effects of xenon due to GSK-Зβ inactivation) and show the prospects for using 60 and 120 minutes of 0.5 MAC xenon exposures in ischemic brain damage after a stroke, traumatic brain injury and other brain lesions.