Systemic inflammation is an integral pathophysiological component of many critical illnesses. The systemic inflammatory response is based on a cascade of interactions leading to hypercytokinemia and, as a consequence, multiple organ failure, which is one of the main causes of mortality in intensive care units.

Aim of the study. To evaluate the activity of the negative regulation system of T-cell response by determining the plasma levels of PD-1, PD-L1 and PD-L2 molecules in pneumonia patients with influenza A (H1N1).

Materials and methods. 85 patients with pneumonia and underlying influenza A (H1N1) were examined. Among them there were 30 patients with severe pneumonia, and 55 patients with non-severe pneumonia. Plasma levels of PD-1, PD-L1, PD-L2 molecules was determined by flow cytofluorometry method.

Results. In patients with severe pneumonia and underlying influenza A (H1N1), the plasma level of PD-1 receptor increased 4.6-fold, while the concentration of its ligands PD-L1 and PD-L2 increased 10.6 and 2.2-fold, respectively.

Conclusion. Significant increase in levels of PD-1 and its ligands PD-L1 and PD-L2 in patients with pneumonia and underlying influenza A (H1N1) indicates the involvement of negative regulation system of T-cell response in the cascade of immunological reactions and is associated with the severe disease. Possible correction of immune reactions realized through PD-1/PD-L1/PD-L2 complex in critically ill patients is a promising research avenue.

The aim of the study: to evaluate the efficacy of extracorporeal liver support systems in patients with acute liver failure of various etiologies.

Material and methods. The study included 117 patients with acute liver failure of various etiologies. The main group consisted of 71 patients who received complex intensive therapy, including MARS-therapy and hemodiafiltration. The comparison group included 46 patients who received albumin dialysis (24 patients) and hemodiafiltration (22 patients) alone. The mean age of the patients was 34±5.6 years, the majority (56.4%) were men. Dynamic assessment of patients' severity was performed using Sequential Organ Failure Assessment (SOFA) and Model for End-Stage Liver Disease (MELD) scales.

Results. A more significant reduction of SOFA and MELD scores was noted as early as by day 10 of intensive therapy in the main group with sequential use of extracorporeal liver detoxification methods — to 2.7±0.2 vs. 8.3±0.5 points (P=0.021) on SOFA and to 16.7±0.4 vs. 23.4±1.4 points (P=0.023) MELD scales. The use of a comprehensive approach to extracorporeal detoxification in acute decompensated liver failure increased the regression rate of multiple organ failure from 51.2 to 74.6% and reduced mortality from 47.8 to 25.4% (χ²=6.266; d_f=1; P=0.013). At the same time, the cumulative proportion of survivors depending on the type of complication within 30 days was 88.4% in the main group and 69.0% in the comparison group (χ²=4.164; d_f=1; P=0.042).

Conclusion. A comprehensive approach to extracorporeal detoxification is highly effective, providing a more significant reduction of SOFA and MELD scores, increasing the proportion of regression of multiple organ dysfunction and reducing mortality.

The clinical manifestation of shock is characterized by systemic circulatory disturbances andblood flow, hypoxic and metabolic disorders. The leading role in the pathogenesis of traumatic shock (the subtype of a hypovolemic shock), is assigned to the severity of the damaging effect, the time interval sufficient for the development of a pathophysiological response, mismatch between body tissue perfusion and the metabolic requirements, and impaired aerobic oxidation in tissues. The use of a comprehensive multicomponent intensive care strategy matching the pathophysiological changes is a difficult challenge for a critical care physician.

The aim of the review is to demonstrate the specific features and sequence of events occurring in the body during the development of traumatic shock, the pattern of manifestations of clinical signs, and potential use of intensive therapy methods tailored to the pathophysiological responses in traumatic shock.

Material. The information search was carried out in the PubMed and RSCI databases, among which 80 sources were finally selected, representing current therapeutic approaches, the results of scientific research and clinical guidelines related to the scope of this review.

Results. The main stages of traumatic shock pathogenesis were reviewed. The basic patterns of cardiovascular and respiratory failure development were analyzed, the criteria of their severity were evaluated, and the complexity of the selection of intensive therapy was shown.

Conclusion. Respiratory support, stabilization of cardiac and circulatory parameters and optimization of oxygen status are the most important components of treatment of patients with traumatic shock. Current methods of respiratory failure control allow to estimate promptly the severity of respiratory dysfunction, reveal the cause and correct existing disorders in an individualized way taking into account the better availability of mechanical ventilation. Replacement of circulating blood volume is aimed both at achieving hemodynamic effect and restoring the concentration of sources of oxygen carriers and plasma pro- and anticoagulant factors. The earliest and most comprehensive intensive therapy can improve the prognosis and outcome in patients with traumatic shock.

We present a case of cardiogenic shock due to neurogenic stress cardiomyopathy (NSC) in a patient with nontraumatic subarachnoid hemorrhage caused by a ruptured aneurysm of the right pericallosal artery. Due to the catecholamine-resistant shock, levosimendan was administered under advanced hemodynamic control, including transpulmonary thermodilution and echocardiography. This resulted in an improved cardiac contractility and reduced demand for catecholamines. Full stabilization of hemodynamic parameters was achieved by day 5. In the discussion section we reviewed available published case reports of using levosimendan in stress cardiomyopathy treatment.

Isolated neuropathy of the superficial peroneal nerve (SPN) is a relatively rare type of peripheral neuropathy. It is linked to the mechanical entrapment of the SPN in predisposed locations of its anatomical pathway. Associated clinical findings are insufficient lifting of the latero-dorsal part of the foot, stepping on the lateral border of the foot, and commonly, a strong pain localized in the nerve dermatome.

Case report. We describe a case of a 14-year-old female patient with right leg pain lasting 24 months. Repeated neurological examinations with negative findings on electromyography (EMG) were performed. The patient underwent a Steindler surgery for a suspected diagnosis of a heel spur, without any improvement. Despite complex pharmacotherapy, chronic pain developed. The patient was unable to walk, being bound to a wheelchair. Amputation of her lower limb under the knee was also considered. SPN entrapment was diagnosed at a physical examination at EuroPainClinics. Decompression of the SPN under local anaesthesia was performed at the clinic.

Results. The symptoms improved immediately after the procedure, and following 2 months of rehabilitation, the patient was completely symptom-free. Her clinical state remains unchanged until this day.

Conclusions. SPN entrapment is not a common diagnosis in the group of pain syndromes. Regarding the lower limb, it is imperative to include it on the list of differential diagnoses in cases of pain and functional disorders of the lateral muscle groups of the calf and leg. In the case of SPN entrapment, EMG findings may be negative.

Aim of the study: to investigate chest compression parameters by city hospital staff under simulated conditions with and without the use of a sensor device for quality control of chest compressions.

Materials and Methods. The study was conducted in Moscow's multidisciplinary hospitals. The study included 359 medical staff members. The participants were divided into 4 groups: physicians (n=97) and nurses (n=82) from intensive care units (ICU) and physicians (n=92) and nurses (n=88) from specialized departments. Participants performed 2 minutes of chest compressions without a chest compressions quality control (CCQC) sensor, followed by 2 minutes of chest compressions using a defibrillator sensor with audiovisual prompts from the device turned on. The percentage of target compressions, rate and depth of compressions were analyzed.

Results. Compression parameters in the group of ICU doctors were outside the reference range (% target compression — 0.5 (0.0; 14.5)%, rate 124.1±17.8 per minute, depth 5.6±1.1 cm), in the group of ICU nurses, the percentage of target compressions was 0.0 (0.0; 3.5)%, rate — 123.6±23.7 per minute, depth — 5.3±1.2 cm, in the group of specialist doctors the percentage of target compressions was 0.0 (0.0; 1.2) %, rate — 123.8±23.2 per minute, depth — 5.8±1.2 cm, in specialized nurses group the percentage of target compressions was 0.0 (0.0; 6.1)%, rate — 119.7±29.5 per minute, depth — 5.6±1.2 cm. There was a significant improvement in compression performance in all groups when the sensor device was used: in ICU physicians the percentage of target compressions was 81.6 (64.80; 87.90)%, rate — 124.1±17.8 per minute, depth — 5.5±0.2 cm; in ICU nurses the percentage of target compressions was 69.1 (47.4; 80.6), rate — 123.6±23.7 per minute, depth — 5.3±0.3 cm, in specialist doctors the percentage of target compressions was 69.30 (50.50; 78.70), rate — 123.8±23.2 per minute, depth — 5.4±0.3 cm, in specialized nurses the percentage of target compressions reached 63.70 (42.90; 75.80), rate — 119.7±29.5 per minute, depth — 5.4±0.3 cm. There were no differences in analysed compression parameters between staff in different departments or positions.

Conclusion. Compression parameters (percentage of target compressions, rate, depth) were not influenced by the department where the staff member worked and the position held (doctor or nurse). The use of a compression quality sensor device has improved compression parameters by reducing rate and normalizing depth. The use of the sensor does not increase the percentage of target compressions to the maximum values, indicating the need for training by an instructor.

The aim of the study was to determine experimentally the effect of hemodilution by the 2:1 sterofundin/gelofusine (SG) solution on hemostatic parameters in vitro and in vivo.

Material and methods. Experiments were carried out on 75 male Wistar rats weighing 270–380 g and anesthetized with intramuscular tiletamine-zolazepam (40 mg/kg) + xylazine (10 mg/kg). Animals were divided randomly into 4 groups: Group 1 — in vitro 25-percent dilution of carotid blood samples by the SG solution (n=12), Group 2 — in vitro 37.5-percent dilution of similar samples (n=11), Group 3 — in vivo 25-percent dilution (n=10), Group 4 — the controls (n=42) with no dilution. The first stage of the study compared the in vitro dilution groups with the control group and with each other; the second stage compared the in vivo dilution group with the control group. The parameters of low-frequency piezoelectric tromboelastography (LFPTEG), clotting tests and complete blood count were studied to evaluate the effect of hemodilution.

Results. At a 25-percent hemodilution with 2:1 CG solution in vitro and in vivo, the hemostatic parameters retained within the reference limits, but a trend to increased intensity of the enzymatic reactions of the coagulation cascade and a significant increase in clot polymerization in vitro due to relative anticoagulant deficiency became evident. In vitro 37.5-percent blood dilution significantly reduced the blood level of fibrinogen and platelet count, inhibited the intensity of the proteolytic stage of coagulation, reduced the clot density at the T3 gelation point, at 5 minutes after reaching it and the maximum amplitude (MA) of the LFPTEG curve, as well as significantly reduced anticoagulant activity of the blood. The observed changes in hemostatic parameters were significantly outside the reference limits, which may affect the interpretation of the experimental results and be clinically important. We found negative correlation between clot density and platelet activity at 25-percent dilution in vivo, whereas at 37.5-percent dilution in vitro an additional positive correlations between platelet count and fibrinogen levels were determined.

Conclusion. A 25-percent hemodilution with 2:1 CG solution should be considered «safe» for the in vivo hemostatic system providing minimal effect on the in vitro parameters in the exper-iment.