Magnitude of heart rate (HR) fluctuation during sepsis and septic shock can significantly impact tissue perfusion and organ dysfunction.

The aim of the study is to examine and compare the predictive characteristics of a composite index based on clinical parameters and demographic variables for early risk stratification of mortality in patients with sepsis.

Materials and Methods. In a multicenter retrospective cohort study, data from 257 patients with sepsis or septic shock were analyzed, including age, sex, height, weight, severity of illness, comorbidities, bedside hemodynamic and respiratory monitoring parameters upon admission to the ICU, and 3 hours after the initiation of intensive therapy, as well as treatment outcomes. Statistical characteristics of the generated Prognostic Index for Compensation of Reduced Cardiorespiratory Function (PICRCF) were assessed, calculated as the ratio of the product obtained by multiplying heart rate by respiratory rate and by age to the product obtained by multiplying of diastolic blood pressure by body surface area (BSA). To identify clinical and laboratory predictors of fatal outcomes, all patients were divided into two groups: survivors and those who died during treatment.

Results. The hospital mortality rate in the analyzed patient sample was 48%. Differences were found between those who died and those who survived in terms of age, scores on the Glasgow (RR), heart rate (HR), and blood pressure (BP), as well as PICRCF values both upon admission ((PICRCF 0) and after 3 hours of intensive care ((PICRCF 3). Notably, (PICRCF 3 demonstrated the highest discriminative performance among all studied predictors (AUC 0.800; 95% CI 0.744–0.855) with a cutoff value of 1.1 (sensitivity 69%, specificity 85%). In the Cox proportional hazards model, (PICRCF 3 was the only independent predictor of mortality (OR 1.313 (95% CI 1.062–1.623), p = 0.012). Additionally, PICRCF values were associated with the number of days without organ replacement support.

Conclusion. The indicators reflecting the state of the cardiovascular and respiratory systems, indexed according to anthropometric and age characteristics, have several advantages over standard prognostic scales in the early risk stratification of patients with sepsis. The simplicity, accessibility, and rapid measuring of the components for calculating PICRCF allow for dynamic assessment of the patient's condition from the first minutes of admission to the ICU.

The heated helium-oxygen mixture (t-He/O₂, heliox ) reduces resistance in the airways and improves ventilation in affected zones of the lungs. Inhaled nitric oxide (NO) is a selective pulmonary vasodilator that lowers pressure in the pulmonary artery and enhances the ventilation-perfusion matchig, which also contributes to the optimization of oxygenation.

The aim of the study is to assess the efficacy and safety of adding inhaled NO, t-He/O₂, and their combination to standard respiratory therapy in patients with polytrauma and pulmonary contusion.

Materials and Methods: We conducted an open prospective randomized study. 186 patients were divided into 4 groups: the NO group (n = 43), the t-He/O₂ group (n = 49), the t-He/O₂ + NO group (n = 48), and the control group (oxygen therapy, O₂, n = 46). The respiratory therapy course lasted 12 days. We assessed the dynamics of computed tomography (MSCT) signs of pulmonary contusion, as well as the arterial blood gas (ABG) parameters (PaO₂, PaCO₂, SaO₂, lactate, pH) on days 1, 4, 8, and 12.

Results. The most remarkable improvements were documented in the combination therapy group (t-He/O₂ + NO). By day 12, this group showed a statistically significant 69% reduction in the extent of lung injury on MSCT (p = 0.018), an increase in PaO₂ to 95.1 mm Hg (p < 0.001), a decrease in PaCO₂ to 35.8 mm Hg (p < 0.001), and a reduction in lactate to 1.38 mmol/L (p = 0.0025). The same parameters in the monotherapy groups NO or t-He/O₂ also markedly improved compared to the control group (O₂). No therapy-related adverse events were reported.

Conclusion. Employment of inhaled t-He/O₂ and NO, especially in combination, as a part of the total care plan of patients with polytrauma and pulmonary contusion, contributes to a significant improvement in gas exchange and regression of radiographic signs of lung tissue injury. Thereby, described method is recommended for early respiratory therapy in intensive care units.

The aim of the study was to investigate the neuroprotective properties of lithium chloride in a model of photochemically induced stroke in rats.

Materials and Methods. The experimental work was conducted in the organoprotection laboratory for critical conditions at the V. A. Negovsky Research Institute of General Reanimatology, Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology. The study included 32 outbred Wistar rats, randomized into 2 equal groups: the NaCl (control) group, treated with physiological saline solution, and the LiCl group, which received a 4.2% lithium chloride solution (63 mg/kg). The solutions were administered intravenously 120 minutes after inducing a stroke. The ischemic stroke model was generated using photochemically induced thrombosis in cerebral sensorimotor cortex vessels. Neurological deficit was assessed using the «limb placement test». Ischemic lesion volume was measured using MRI (7 Tesla). Immunohistochemical analysis included markers for NeuN (survived mature neurons), Cas-3 (neuronal apoptosis), and Iba-1 (microglial activation). Statistical analysis was performed using the Shapiro–Wilk test, Student's t-test, and the Mann–Whitney U test with significance at p < 0.05.

Results. Lithium chloride infusion resulted in a 30% reduction in the ischemic lesion volume compared to the control group (p = 0.0236). The LiCl group showed an increase in signal intensity (relative units, RU) in the NeuN-positive neurons in the penumbra (80 RU vs 41 RU in the control group, p = 0.0001), a 25% decrease in signal intensity in Cas-3-positive cells (p = 0.0008), and a 58% decrease in signal intensity in Iba-1-positive cells (p < 0.0001). Neurological deficit in the LiCl group was less detectable (NaCL vs LiCl: 9,8 ± 1,2 vs 12,5 ± 1,5 scores, respectively, p < 0.0001).

Conclusion. Lithium chloride demonstrated significant neuroprotective properties in a model of ischemic stroke, reducing the volume of damage and favoring the suppression of apoptosis and inflammation. The findings validate the potential of lithium chloride as a therapeutic agent for treatment of ischemic stroke, owing in particular to ability to modulate key pathogenic mechanisms of the disease. The results underscore the need for further clinical research to assess the efficacy and safety of lithium in medical practice.

The aim of the study was to identify the characteristics of dynamic reactive neuronal changes in sensorimotor cortex (SMC) layers III and V of the rat brain in the remote period (up to 270 days) following bilateral common carotid arteries ligation (CCAL).

Methods. The experiment was conducted on 66 male Wistar rats (a prospective cohort study with sequential terminal outcomes): intact control (n = 6) and groups with survival at 30, 90, 150, 210, and 270 days post-bilateral CCAL (n = 6 in each group after adjusting for mortality). Histological methods (Nissl and hematoxylin-eosin staining) were used to assess the total neuronal numerical density (NND), the density of four types of reactive altered cells (hyperchromatic shriveled cells — HCSC; hyperchromatic non-shriveled cells — HCNSC; hypochromatic cells — HCC; shadow cells — SC) and the neuroglial index (NGI). Paired and multiple comparison methods, linear mixed models (LMM) with random intercept for the animal (to account for the paired data structure), Jonckheere–Terpstra test, quadratic trend test, correlation analysis, and ∆-analysis were applied.

Results. A biphasic reduction in NND was observed in layer III of the SMC (maximum of -44.6% at 30 days, p < 0.001) with a wave-like dynamics (quadratic trend: F = 16.4, p < 0.001). HCNSC peak at 30 days (+683%) followed by a decrease, while HCC showed a delayed peak at 150 days (+500%); both parameters showed a mixed pattern (steadily increasing trend: Z = 1.88, p=0.030 for HCNSC; Z = 2.45, p = 0.007 for HCC; quadratic component: F = 8.2 and 7.4, p < 0.01). SCs demonstrated non-monotonous dynamics (quadratic trend: F = 19.2, p < 0.001) with a delayed peak at 210 days. NGI peaked at 30 days (transient gliosis, +95.5%, steadily decreasing trend, Z = –4.92, p < 0.001). The decrease in NND was less pronounced in layer V of the SMC, (–11.6% at 150 days, p = 0.048), but there was an extreme increase in HCSC at 30 days (+945% from control, with a continuously decreasing trend, Z = –2.94, p = 0.002), a monotonous depletion of HCC (linear increasing trend, Z = 4.82, p < 0.001), and a prolonged building up gliosis (NGI +42% by 270 days, mixed pattern: steadily increasing trend Z = 4.15, p < 0.001; quadratic component F = 5.1, p = 0.028). LMM confirmed a significant «Layer × Time» interaction for all parameters (F = 24.1–71.2; p < 0.001). A correlational analysis revealed moderate positive correlations between the layers (for SCs: r = 0.58; r_partial = 0.52; p = 0.004; for HCSC: r = 0.52; p = 0.008; for NGI: r = 0.44; p = 0.016). The ∆-analysis showed consistency in changes for SC, HCSC, and NGI. The extremum moments for SC (210 days) and HCSC (30 days) were synchronous in both layers. Temporal precedence of layer III was found for NGI (early peak of gliosis at 30 days compared to 270 days in layer V), as well as for HCSC and HCC (30–150 days compared to 90 days in layer V). Temporal precedence of layer V was identified for the first peak of SC (90 days compared to 210 days in layer III).

Conclusion. Chronic ischemia induces various damage scenarios: layer III is characterized by a biphasic reduction in NND, asynchronous peaks of HCSC (30 days) and HCC (150 days), a delayed SC peak (210 days), and transient gliosis (a model of damage with delayed degeneration); layer V exhibits an extreme early increase in HCSC (30 days), early peak of SC (90 days), and prolonged gliosis (a model of progressive degeneration). Correlation and ∆-analysis indicate moderate synchrony in the degeneration processes; no convincing evidence of cascading damage propagation from superficial layers to deeper ones was obtained.

Superior mesenteric artery (SMA) syndrome is a rare cause of high duodenal obstruction.

We report a case of an asthenic male (BMI 17.9 kg/m²) presenting with acute bowel obstruction.

Methods. Multiphase CT demonstrated marked pre-stenotic dilation of the D2 of the duodenum (max 8.8 cm) and compression of the D3 between the aorta and SMA, with an aortomesenteric angle of 11–12° and distance of 7 mm. A morphological, asymptomatic nutcracker phenomenon was present without hematuria. CT-suggested colitis was ruled out endoscopically and histologically. After consultation with vascular surgeon and shared decision-making, the patient opted for enteral bypass. The patient’s preoperative anaesthesiology assessment revealed no contraindications to general anaesthesia for the planned laparoscopic procedure. A laparoscopic laterolateral, anisoperistaltic duodenojejunostomy was performed using a linear stapler (minimal blood loss; operative time 76 minutes) with a perianastomotic drain.

Results. Postoperatively, the nasogastric tube was removed on POD2, oral intake resumed from POD3, and the drain removed on POD4. Transient rise in CRP/leukocytosis on POD2 (negative presepsin) was managed empirically with ampicillin/sulbactam (Clavien–Dindo II). Patient was discharged on POD6 (7-day stay). At three months follow-up he remained symptom-free with objective nutritional gain (BMI + 2.3 kg/m²).

Conclusion. This case supports laparoscopic duodenojejunostomy as a safe and effective definitive option in hemodynamically stable patients with CT-quantified SMA obstruction. A concomitant asymptomatic nutcracker phenomenon does not require vascular intervention nor alter operative strategy.

The aim is to demonstrate the successful use of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) in a patient developing acute myocardial infarction (AMI) and cardiogenic shock due to spontaneous coronary artery dissection in the third trimester of pregnancy.

Patient and investigative techniques. We analyzed laboratory and hemodynamic parameters, mechanical ventilation settings and ECMO circuit parameters in a 32-week pregnant woman with acute myocardial infarction and cardiogenic shock caused by spontaneous coronary artery dissection. We reviewed all stages of patient’s management from hospital admission, including initiation of ECMO, performing of cesarean section under extracorporeal support, and patient's transportation to tertiary center for heart transplantation.

Results. The use of VA-ECMO in a patient with AMI at 32 weeks of gestation provided biventricular circulatory support, which allowed to stabilize severe cardiogenic shock and safely place coronary stents, providing sufficient placental blood flow to preserve the life of the fetus. A cesarean section (CS) was performed under VA-ECMO support resulting in delivery of a live baby-girl weighing 1.8 kg with an Apgar score of 5/6. The mother was transported after CS to the V. I. Shumakov National Medical Research Center for Transplantation and Artificial Organs, Ministry of Health of the Russian Federation, where emergency orthotopic heart transplantation (OHT) was performed.

Conclusion. We present a case report of spontaneous coronary artery dissection leading to AMI and cardiogenic shock and requiring life-saving circulatory support with VA-ECMO. The case demonstrates the urgent need of both treatment arms including established protocol of coronary angiography with percutaneous coronary intervention, and timely employed individual approach, that include VA-ECMO, intra-aortic balloon pump, and left ventricular decompression. The use of high-tech methods and a professionally employed multidisciplinary approach saved the lives of both the mother and the child.

The combination of syndromes and organ failure manifestations that develop after an acute critical illness (ACI) and demand the continuation of intensive care does not currently have a single definition. Meanwhile, the steadily increasing number of patients with such manifestations poses a challenge to the entire healthcare system. The complex pathogenesis and the differences in subtypes of chronic critical illness (CCI) necessitate a personalized approach to management of these patients.

Objective. To clarify the available data on the terminology of CCI, its prevalence, development timelines, clinical manifestations, pathogenesis, subtypes, and outcomes.

Materials and Methods. A literature review wasconducted using the PubMed, Google Scholar, and eLibrary databases. The review included 60 papers covering approaches to CCI definition, associated terminology, the investigation on of pathogenesis, clinical aspects, and CCI subtypes.

Results. Several case definitions were identified for CCI, reflecting the attitude toward this condition — either as one of the phases of acute critical illness or as a new disease. Additionally, two main approaches to diagnosing CCI were established: the first based on the duration of patient's stay in post-anesthesia care and intensive therapy (PACU/ICU) due to the need for intensive care, and the second based on the emergence of newly identified specific clinical and laboratory manifestations. The development of CCI is an unfavorable outcome of acute critical illness, leading to increased patient disability and a rise in mortality.

Conclusion. Further research is needed for deeper insights into development of CCI, establishing unified approaches to its definition, assessing risk factors, identifying its subtypes and associated organ dysfunctions.