Traumatic brain injury (TBI) remains one of the leading causes of disability, and current approaches to neuroprotection have limited efficacy. The inert gas krypton is considered a promising neuroprotective agent; however, data on its effects in TBI and on components of the neurovascular unit (NVU) are limited. Objective. To evaluate the neuroprotective potential of krypton in rats with traumatic brain injury (TBI) in vivo and in NVU cell cultures subjected to oxygen-glucose deprivation (OGD) in vitro . Materials and Methods. The study included 48 Wistar rats divided into 3 groups: SO (sham operated), TBI (N₂/O₂ 70/30 %), and TBI + iKr (Kr/O₂ 70/30 %). A model of controlled open brain contusion injury was used. On day 14, we assessed neurological deficits (limb placing test, LPT), the extent of brain injury (T2-weighted MRI slices), morphological changes (hematoxylin-eosin staining), and the expression of GFAP and Caspase-3 (fluorescent immunohistochemistry, IHC). IL-1β, IL-6, and TNF-α mRNA levels in the injury zone were determined by PCR. In vitro studies investigated the effect of krypton preconditioning (Kr/O₂ 79/21 %, 24 h) on the survival of neuronal (SH-SY5Y), glial (C6), and vascular endothelial (Ea.Hy926) cells during OGD (4–6 h). Results. A significant neurological deficit of 2.5 (2; 5.25) scores was determined by the TBI modeling accompanied by a large volume of brain damage of 33 (28; 39) mm³. Krypton inhalation led to a reduction in the lesion volume to 18 (15; 26) mm³ and accelerated the recovery of sensorimotor functions: starting on day 7, the indicators in the TBI + iKr group were statistically significantly better than in the TBI group, and by day 14, they approached the values of the SO (control) group. In the TBI + iKr group, IL-1β and TNF-α levels in the affected hemisphere were nearly 50% lower than in the TBI group, while remaining higher than in the SO group; changes in IL-6 levels were insignificant. Histologically, less significant cerebral edema, spongiosis, and neuronal degeneration were observed in the TBI + iKr group. Immunohistochemical analysis revealed a trend toward more pronounced reactive gliosis (GFAP) with no differences in Caspase-3. In vitro , krypton preconditioning under OGD conditions did not improve the survival of neuronal, glial, and endothelial cells. Conclusion. Krypton exerted significant neuroprotective effect in experimental TBI in rats, reducing neurological deficits, the extent of structural damage, and the severity of the inflammatory response. The absence of a protective effect in NVU cellular models underscores the essential role of systemic and intercellular interactions in the neuroprotective action of krypton and warrants further research into its mechanisms of action and dosing optimization.

The aim of the study . To evaluate the effectiveness of multimodal selective lipopolysaccharide (LPS) hemoadsorption in combination with renal replacement therapy (RRT) in patients with gram-negative sepsis or septic shock. Materials and methods. The study included 39 patients. In the main prospective group, patients received extracorporeal therapy in addition to standard of care (ET group, n = 10). In the retrospective comparison group, patients received only standard therapy (ST group, n = 29). Results . In the ET group, the average SOFA score decreased by 3.4 [95% CI: 0.8; 5.2] scores after 72 hours of treatment, while in the ST group, the average SOFA value increased by 1.7 [95% CI: 0; 3.4] scores over the same period, p adj = 0.002. Hospital mortality was 1/10 (10%) in the ET group and 19/29 (66%) in the ST group, and OR = 0.06 [95% CI: 0.01; 0.4] p = 0.003. The analysis, including consideration of severity of the condition at a baseline as a potential confounding factor, confirmed the robustness of the results: statistically significant differences in SOFA dynamics and mortality remained. Conclusion . The use of selective hemoadsorption in combination with renal replacement therapy reduces the severity of organ dysfunction and mortality in patients with sepsis or septic shock.

There is a general agreement on the need to analyze critical incidents in the operating room (OR) in order to develop effective ways to predict associated fatal consequences, as well as to develop decision support cognitive tools that can be used in both routine and crisis situations. Research objective . Developing and testing of a confidential questionnaire on perioperative critical incidents by anaesthesiologists and other intensivists, assessment of the initial results of the tool application including its possible relevance to further implementation in the Russian Federation health care Materials and methods . The survey was conducted by anonymous questioning among doctors of large hospitals in St. Petersburg from 01.06.2024 to 31.12.2024 using an on-line form. Results . Of the 32 questionnaires received, 27 (84.4%) were completed and contained complete information, which was systematized and analyzed. Respondents reported most often on critical incidents in male patients (15 patients, 55.6%), and in the age group of 45–59 years (8 cases, 29.6%). Most of the incidents occurred during minimally invasive video assisted surgery (18 cases, 66.7%). In 14 cases (51.8%), critical incidents were related to human error, and in 9 (33.3%) cases, they were related to unexpected complications in the perioperative period. Most of the respondents (20 out of 27, 74.1%) noted that the incidents could have been prevented with more accurate anesthesia monitoring and relying on more sophisticated and performant anesthetic equipment in the Intensive Care Unit. Doctors positively evaluated the trial version of the anonymous questionnaire (22 out of 27, 81.5%), noting its simplicity and usefulness in identifying problems. Several respondents suggested adding open-ended questions to provide a more detailed description of the incidents. Conclusion . The study confirmed the usefulness of designing and implementing a national questionnaire on perioperative critical incidents in Russia. The data obtained demonstrate that such a tool, combined with improving the staff training, equipment upgrade, and standardization of protocols, can significantly contribute to enhancing patient safety in anesthesia. Ensuring the confidentiality of the provided data is crucial for obtaining statistically significant information. The development, implementation, and expansion of the proposed tool's database under the auspices of the Federation of Anesthesiologists and Resuscitation Specialists on a regular basis will undoubtedly contribute to improving the quality and safety of anesthesiology and resuscitation services in Russia.

The aim of the study was to identify potential predictors of functional outcome (FO) in patients with subtypes of ischemic stroke (IS) who did not receive reperfusion therapy.Materials and methods. A prospective study included 229 patients with ischemic stroke divided . into three groups based on the IS subtype: Group 1 — 84 patients with cardioembolic IS; Group 2 — 65 patients with atherothrombotic IS; Group 3 — 80 patients with lacunar IS. Changes in the modified Rankin Scale (mRS) scores were considered as FO criteria calculated as the difference between the scores on admission and on the 21st day after IS onset — ∆mRS. In order to optimize the performance of the machine learning (ML) model, a binary FO approach was chosen for assessment on the 21st day after IS onset: mRS ≥ 3 scores corresponded to an unfavorable non-lethal outcome, and mRS = 0–2 scores corresponded to a favorable FO. We analyzed the interrelation with FO (correlation coefficient, r) and the predictive ability (ML (decision tree), information gain, i. g.) of 29 parameters, including demographic features; comorbidities; instrumental examination findings; NIHSS, BI, CDR scores; serum concentrations of cytokines on the 2nd day of hospital stay.Results. The following significant (P<0.0001) predictors of unfavorable non-lethal FO were identified: female sex (i. g. = 0.346), recurrent IS (i. g = 0.248), diabetes mellitus (i. g. = 0.442), and CXCL2 concentration (i.g. = 0.306) in Group 1; WMHs severity (i. g. = 0.206), diabetes mellitus (i. g. = 0.340), content of CCL2 (i. g. = 0.116), CCL3 (i. g. = 0.202) and CCL23 (i. g. = 0.101) in Group 2; age (i. g. = 0.106), 2nd –3rd degree obesity (i. g. = 0.150), WMHs severity (i. g. = 0.300), CXCL5 content (i. g. = 0.143) and MIF (i. g. = 0.145) in Group 3. Concentrations of CCL25 (i. g. = 0.108) and IL-6 (i. g. = 0.401) were found as predictors of favorable FO (P<0.0001) in Group 1; 1st degree obesity (i. g. = 0.118) and TNF-α concentration (i. g. = 0.211) in Group 2; arterial hypertension (AH) (i. g. = 0.113) and 1st degree obesity in Group 3.Conclusion. Study results made evident the variances in combination of factors affecting FO, depending on IS pathogenetic subtype. Despite undoubtful value of the data obtained, further research is needed to expand the potentiality in predicting acute IS outcome and confirm the relevance of identified markers.

Objective: to clarify the pathogenesis of ischemic stroke in infectious diseases of the lower respiratory tract.Material and methods. We searched the PubMed database for original research articles, clinical reports, review articles, editorials, commentaries, and short communications published before June 25, 2025. Additional studies that were not captured through the primary database search were analyzed after manually examining the reference lists of the selected articles. Articles were selected based on the relevance of the title and abstract to the purpose of this review. Data from 160 sources were included in the analysis.Results. We have identified and analyzed in detail the mechanisms of ischemic stroke development in respiratory infections: activation of the coagulation system and disruption of natural anticoagulant and fibrinolytic mechanisms (1); interaction of the hemostasis system with innate immunity (2); the effect of infectious agents on the progression of atherosclerosis and the stability of the atherosclerotic plaque (3); the formation of thromboemboli in the pulmonary veins (4).Conclusion. Both bacterial and viral infections can initiate a procoagulant state mediated by tissue factor, von Willebrand factor, platelet activation, neutrophil extracellular traps and decreased activity of endogenous anticoagulants. The infectious process localized in the lungs, characterized by damage to the pulmonary vascular endothelium, alveolocytes, intraalveolar fibrin deposition, edema, cellular infiltration, in concert with hemostasis alterations create conditions for the formation of thrombi in the pulmonary vessels. Thus, the pulmonary veins and venules can be a source of cerebral thromboembolism. This mechanism of thromboembolic stroke development largely explains causes of acute cerebrovascular events in patients with lower respiratory tract infection without cardiovascular risk factors. Another mechanism of ischemic stroke is associated with direct or indirect effects of pathogens on the stability of atherosclerotic plaques in cerebral vessels, which, together with systemic procoagulant imbalance, leads to the formation of atherothrombosis. Given the significant pathogenetic relationship between acute infectious lung diseases and cardioembolic and atherothrombotic strokes, clinical alertness regarding acute cerebrovascular events should be included in monitoring and management of such patients.

Aim. To identify personalized morphological neuronal phenotypes based on the distribution pattern of the neuronal protein NeuN in the cerebral cortex layers.Materials and Methods. A histologic study of the cerebral cortex was performed in rats (N=10). Tissue sections were stained with hematoxylin and eosin, and the neuronal nuclear protein NeuN was visualized by immunohistochemical staining. Analysis was performed by microscopy and image analysis software.Results. NeuN immunohistochemical staining revealed distinct localization and intensity patterns within cortical neurons. Contrary to the definition of NeuN as a nuclear neuronal protein, its localization was observed in both the nucleus and cytoplasm in most neurons. The following neuronal phenotypes were identified based on NeuN staining patterns: 1) Neurons with stained nuclei but unstained cytoplasm; 2) Neurons with stained cytoplasm but unstained nuclei; 3) Neurons with stained nuclei and cytoplasm; 4) Fully stained neurons with no visible nuclei; 5) Neurons with stained processes (dendrites/axons). A significant difference was found between mean intensity of NeuN-positive neurons depending on the localization in the layers of the cerebral cortex.Conclusion. Given the critical biological role of NeuN, the identified neuronal phenotypes based on NeuN localization warrant further research as they may reflect the functional states of neurons. The interpretation of the absence of NeuN staining as a marker of neuronal damage is not scientifically justified. Future studies using NeuN immunohistochemical staining should consider not only the total number of NeuN-positive neurons, but also their distinct phenotypes.

Scoring systems based on assessment of disease severity and patient condition are widely used for routing and predicting length of stay in the ICU. However, their effectiveness varies in patients with sepsis.The aim of the study. To evaluate the effectiveness of scoring systems in routing and predicting ICU length of stay in patients with severe community-acquired pneumonia (CAP).Materials and methods. Medical records of 664 patients from the Intensive Care for Severe CAP database of I. I. Mechnikov Northwestern State Medical University (2013–2023) were analyzed using the following scoring scales: CURB-65, PSI/PORT, SMART-COP, SCAP, REA-ICU, NEWS2, IDSA/ATS criteria, APACHE IV, CFS, and CCI. Statistical analysis was performed using Statistica 10.0, SPSS, and Stat Research (Center for Statistical Research) software.Results. Among the study cohort, 96 patients (15%) had bacterial severe CAP (bCAP) and 568 patients (85%) had viral severe CAP (vCAP), all of whom were admitted to the ICU. A NEWS2 score ≥2 was observed in 74 (77.1%) bCAP patients and all vCAP patients (P<0.001). In contrast, 437 (76.9%) vCAP patients and 74 (77.1%) bCAP patients were classified as high risk according to SMART-COP (P=0.966). Delayed ICU admission (>7 days) was observed in older patients with severe bCAP, but did not significantly affect ICU length of stay or outcomes. A strong correlation was found between adverse outcome and predicted mortality using APACHE IV (η=0.966 for vCAP and η=0.807 for bCAP). However, no correlation was observed between predicted and actual ICU length of stay for both vCAP and bCAP patients (R²=0.0257, Kendall's W=0.018 for vCAP; R²=0.0294, Kendall's W=0.050 for bCAP). The predictive model accuracy for ICU stay >1 day or >14 days was not satisfactory. Model with vCAP patients adjusted for age (≥60 years) and APACHE IV exhibited moderate predictive accuracy for prolonged ICU stay (AUROC 0.610).Conclusion. Differences were found in the applicability of the NEWS2, REA-ICU, and IDSA/ATS major criteria scoring systems for ICU routing of bCAP and vCAP patients. APACHE IV showed a strong correlation between predicted and actual mortality, but no correlation between predicted and actual ICU length of stay in severe CAP patients was found.

The aim of this study was to assess the incidence of cardiovascular complications (CVC) within 12 months after vascular surgery and to analyze inpatient perioperative examination data to identify potential predictors. Materials and Methods. A prospective cohort study included 103 patients aged 66 years [61–70] who underwent vascular surgery. Clinical outcomes within 12 months after surgery, including CVC and/or other cardiac events (composite outcome) and cardiac death, were assessed by telephone interviews with patients or their relatives. Patient physiological parameters, comorbidities, cardiac risk indices (CRI), platelet-lymphocyte ratio (PLR), concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP), and other parameters were obtained and analyzed from medical records. Logistic regression and ROC analysis were used to assess the predictive power of the investigated indicators. Results. The composite outcome was recorded in 33 % of cases and cardiac death occurred in 6.8 %. The risk of the composite outcome was associated with ASA class (OR 2.7413; 95 % CI 1.1126–6.7541), whereas the risk of perioperative myocardial infarction or cardiac arrest was associated with CRI (OR 1. 6051; 95 % CI 0.6645–2.0215), American University of Beirut (AUB) CRI (OR 2.1106; 95 % CI 1.0260–4.3414), PLR (1.0120; 95 % CI 1.0018–1.0222), and NT-proBNP concentration during hospitalization. Concurrent congestive heart failure (OR 5.0658; 95 % CI 1.2400–20.6956), revised CRI (OR 2.1024; 95 % CI 1.0572–4.1813), Khoronenko CRI (OR 103.76; 95 % CI 1.8752–5796.55), AUB CRI (OR 3.1902; 95 % CI 1.1040–9.2181), and NT-proBNP concentration all increased the risk of cardiac death. Predischarge NT-proBNP levels < 179 pg/mL (OR 1.0071; 95 % CI 1.0038–1.0104; AUC 0.795) and maximum postoperative NT-proBNP levels were reliable predictors of the composite outcome. The most effective predictor of postoperative mortality was a maximum NT-proBNP concentration > 303 pg/mL after surgery (OR 1.0039; 95 % CI 1.0015–1.0063; AUC 0.836). Conclusion. CVC developed in 33 % of patients within 12 months after vascular surgery, with cardiac death occurring in 6.8 % of cases. An NT-proBNP concentration > 179 pg/mL before hospital discharge or a maximum NT-proBNP concentration > 248 pg/mL in the postoperative period predicted CVC within one year. Postoperative NT-proBNP concentration > 303 pg/mL was a strong predictor of one-year cardiac mortality. Other factors associated with the risk of postoperative CVC did not provide an accurate prognosis.

The aim of the study was to evaluate neonatal outcomes in preterm infants.Materials and methods. The study included 58 premature neonates divided into 2 groups: «A» (N=34) with an adverse neonatal period ending in death and «B» (N=24) who survived. Clinical assessment of the infant, measurement of blood gases, acid-base balance (ABB) and lactate, recording of lung ventilation parameters, calculation of mean airway pressure, oxygenation index (OI) and ventilation efficiency index (VEI), neurosonography and, in case of death, pathological and histological examination of the brain were performed.Results. Elevated lactate was found in 24 patients (70.5%) in group A and in 12 patients (50%) in group B. The mean lactate levels in groups A and B were 8.1±3.3 and 6.3±2.8 mmol/L, respectively. In group A, 19 (55.9%) infants had severe acidosis, corresponding to a pH of 7.19 to 6.80. In group B, only 8 (33.3%) infants had a pH between 7.0 and 7.19. At birth, neonates in both groups were found to have a base deficit (BD), which was significantly lower in group A than in group B (P=0.004). There were no trends toward reduction of acidosis or normalization of ABB in infants in group A. Plasma BE levels in group B had returned to normal by 96 hours postpartum. The frequency of grade II, III peri/intraventricular hemorrhage (PIVH) and hemorrhage of other localization in group A were 8 (23.5%), 9 (26.5%), and 3 (8.8%), respectively. In group B, grade I PIVH and hemorrhage of other localization occurred in 5 (20.8%) and 1 (4.2%) cases, respectively. In neonates with grade II PIVH, severe lactic acidosis was diagnosed at birth: venous blood pH was 6.97 [6.8; 7.22], BE was (–21.6) [–30; –7.2] mmol/L, lactate level was 8.5 [6.3; 12.9] mmol/L, and pO₂ was 50.5 [20.5; 64] mm Hg. In infants with grade III PIVH, pH was –7.26 [7.12; 7.28], BE was (–8.1) [–8.9; –7] mmol/L, lactate was 7.6 [4.8; 8.9] mmol/L, and pO₂ was 33 [30; 50] mm Hg. Cell damage of varying severity affected all brain structures, as evidenced by absence or deformation of nuclei and nucleoli, and peripheral chromatin condensation. Morphological immaturity of brain structures was another negative factor.Conclusion. Lactic acidosis diagnosed at birth in premature infants is one of the indicators of perinatal hypoxia severity. Critical pH, BE, and lactate levels, as well as lack of response to treatment, contribute to structural brain damage and worsen prognosis. Severe changes in oxygen and lactate levels that persist for two days after birth lead to severe PIVH and irreversible brain changes.

Most patients with critical illness, regardless of the cause, develop activation of innate and adaptive immunity. This is often a critical process leading to organ dysfunction.The aim of the review is to systematize information on monitoring the immune system in critical illness for physicians of different specialties (anesthesiology and intensive care, surgery, general practice, obstetrics and gynecology).The review includes information from 83 recent national and international publications (mostly from 2023), available in the public domain and found by keyword search.We have summarized the current understanding of the relationship between infections and the human immune system, as well as the clinical application of traditional markers of immune status. We provided data on novel promising markers for the assessment of immunity in patients with various diseases.Limitations of the studies reviewed include the need for additional large-scale clinical trials of even the most promising markers, as well as a synthesis of the evidence for their performance. In addition, immune monitoring is likely to increase the cost of patient care, necessitating the development of more affordable research methods.Conclusion. Almost all disorders in critically ill patients are associated with changes in the immune system. Management of patients based on their immune profile requires determination of a personalized strategy for immune modulation, treatment, and prevention of infection. Advanced monitoring of immune system functions will contribute to the personalization of medicine, and the continuous development of biological technologies will allow to improve its methods.