Global statistics show that approximately 489,000 people died annually from heat-related causes over the past two decades. Higher temperatures are associated with increased risk of mortality due to general accidents and four main subtypes, including road traffic accidents, falls, drownings, and unintentional injuries. Elevated temperatures and periods of anomalously hot weather already increase the global health hazard and cause significant economic losses. Mortality from general overheating is high and ranges from 33 to 80 %, with terminal events including shock, arrhythmias, myocardial infarction, renal failure, and neurological dysfunction. Residual neurological disorders were observed in 17 % of survivors. General overheating affects military personnel, athletes, workers in hot industries, and civilian populations exposed to or having formed risk factors for general inadvertent body overheating. Therefore, identifying and, where possible, preventing these risk factors is currently relevant. Exogenous hyperthermia contributing and predisposing factors are identified, timely detection and prevention of which will allow medical and social workers to limit the detrimental effects of hot conditions on public health.

Stress-induced hyperthermia (SIH) is a physiological response of the body to psychological stress. Currently, 88 % of the population is in a state of chronic stress. Psychogenic hyperthermia is more common in young women. Psychogenic fever is not associated with an immunological inflammatory process, there is no increase in inflammatory mediators. The mechanism of the development of stress-induced hyperthermia is the activation of the sympathoadrenal system, vasoconstriction, an increase in the level of corticosterone and the thermogenesis of brown fat. Constant sympathetic stimulation leads to the formation of thermogenin-expressing loci in white adipose tissue. Dopaminergic and noradrenergic compounds do not affect the intensity of hyperthermia. Taking nonsteroidal analgesics does not affect this type of hyperthermia. Antipsychotics are ineffective for psychogenic hyperthermia. Effective drugs that have anxiolytic properties, which significantly reduce the basal body temperature when the dose is increased. Serotonergic receptors play a key role in modulating behavioural, autonomic, and endocrine responses to stress. Effective GABA agonists and antidepressants. For the treatment of the chronic variant of SIH, the use of fluoxetine is recommended. Psychoeducation is used as non-medicinal methods of treating functional fever; psychotherapy with an adjustment environment (verbal or non-verbal release of unreacted negative emotions and conflicts); cognitive-behavioral or other psychological therapy, meditation, relaxation training; yoga and practices aimed at reducing stress and mental disorders.

Background. A combat gunshot wound is significantly different from a civilian trauma. It is characterized by the prevalence of penetrating injuries, which increases the volume of blood loss at the pre-hospital stage, and the destruction of large masses of muscle tissue (rhabdomyolysis), which leads to acute kidney injury. Moreover, combat trauma occurs in conditions of chronic background stress as a result of severe emotional and physical strain, uncomfortable weather conditions, and deprivation of sleep, drinking and food. So, such a phenomenon as voluntary dehydration is common among soldiers in combat conditions. In wounded, oliguria is often considered a result of acute kidney injury, but it can also be a symptom of severe dehydration. The purpose of our work was to analyze three clinical cases of oliguria caused by dehydration in wounded with combat trauma to better understand the severity of the condition of such victims and to improve medical aid for them. Materials and methods. The article describes three cases of men aged 35, 50 and 44 years with combat gunshot wounds to the extremities, who were admitted to the tertiary care hospital on the second day after the injury with oliguria (0.18–0.19 ml/kg/hr) and high creatinine (333 to 457 μmol/L). Results. All three patients were conscious, breathing spontaneously, had stable hemodynamics, and moderate anemia after pre-hospital blood transfusions. Focused ultrasound study revealed hyperdynamic left ventricle and small inferior vena cava with complete inspiratory collapse, which suggested hypovolemia. Upon further investigation of the medical history, patients admitted not drinking any liquid for one to two days prior to injury. Tissue hydrophilicity test was conducted which showed severe dehydration in all three cases. Infusion volume was calculated using P.I. Shelestiuk nomogram (modified by O.V. Kravets et al.) and amounted to 60 ml/kg of balanced crystalloid solutions. Upon starting rehydration, diuresis was restored within two hours and amounted to 0.7–2.1 ml/kg/h in all three patients. Creatinine levels normalized in 2–4 days. Patients were transferred to another hospital in a moderate condition in 4–5 days. Conclusions. Oliguria is a frequent complication of combat gunshot injury. Although it is most often associated with acute kidney injury from rhabdomyolysis, it should also be considered that in a combat environment, soldiers’ access to water may be limited and the injury may be accompanied by dehydration. In the cases presented, the differential diagnosis of the causes of oliguria in the wounded made it possible to detect signs of severe dehydration, abstain from the inappropriate use of saluretics, quickly compensate for the fluid deficit, and to avoid the development of kidney damage and the need for renal replacement therapy.

ОСОБЛИВОСТІ АНЕСТЕЗІОЛОГІЧНОГО ЗАБЕЗПЕЧЕННЯ

Background. Acute kidney injury (AKI) is a common complication of polytrauma that requires renal replacement therapy (RRT) in 10 to 28 % of cases. RRT methods can be divided into discrete, or intermittent, and continuous. There are currently no clear recommendations regarding the choice of the RRT method. The purpose was to study the effect of intermittent venovenous hemodiafiltration (HDF) on indicators of renal function, hemodynamics, homeostasis and inflammation in multiple trauma victims with rhabdomyolysis and AKI. Materials and methods. Fifty victims with multiple trauma complicated by rhabdomyolysis and AKI were examined. We investigated the levels of total creatine kinase and myoglobin, indicators of kidney function, frequency of vasopressor support, indicators of general blood analysis, liver complex, coagulogram, acid-base and gas composition of blood. The study was conducted upon admission, before the start and after the end of each HDF session and on the last day of treatment. Results. Multiple trauma with massive rhabdomyolysis led to AKI, manifested by oliguria and hyperazotemia (and from the 3rd day, by hyperkalemia), as well as cardiovascular failure, anemia, liver dysfunction, and inflammatory response. AKI progression to renal failure despite conservative therapy led to the beginning of HDF on 3.6 ± 0.8 days of hospital stay. HDF allowed to effectively reduce indicators of the renal complex and normalize the potassium level, and at the same time did not have a negative effect on hemostasis or other indicators of homeostasis. 72.9 % of victims needed two HDF sessions, 47.9 % — three, 31.3 % — four or more. The most pronounced reduction of hyperazotemia was observed after the second session. Among the survivors, restoration of adequate diuresis by the day 14 was observed in 39.3 % of cases. The mortality rate was 34.0 %. Laboratory markers of renal function were not significantly different between survivors and deceased; the difference was in markers of liver function, coagulogram and acid-base balance, as well as the need for vasopressor support. That is, the mortality was due to the progression not so much of kidney failure, but of the failure of other organs and systems. It should also be noted that the injury severity score among survivors was 23.5 ± 4.0 points, and among non-survivors — 40.5 ± 6.8 points (p < 0.001). Conclusions. Multiple trauma with massive rhabdomyolysis leads to the development of multiple organ failure. Intermittent HDF allows to quickly and effectively reduce azotemia and normalize potassium levels without adversely affecting coagulation or other indicators of homeostasis. Most multiple trauma victims need 2 or more sessions of HDF. Mortality remains high and primarily depends on the severity of anatomical injuries and the addition of other organs and systems failure.

Recently discovered specific markers open up new possibilities for the diagnosis of acute kidney injury (AKI) in burn disease in order to optimize the treatment of such patients. Early diagnosis with the involvement of biomarkers prevents the sudden death of burn patients and allows predicting the course of the pathological condition. There are several characteristics that an “ideal” AKI biomarker should conform to: being non-invasive, locally specific, highly sensitive, being a stable molecule at different temperatures and pH values, having the ability to rapidly increase in response to kidney injury (quantify it), remaining at high levels during the episode and decreasing during the recovery period. There is a difference between the biomarkers that can be freely filtered in the glomerulus, so any increase in their plasma concentration (due to damage to other renal tissues) can lead to a high concentration of indicators in the urine (loss of specificity), and high-molecular-weight markers that are not freely filtered and therefore are more specific when measured in urine. Renal function in burn patients is usually determined by blood and urine tests, as biopsy can cause iatrogenic damage and is not commonly used in this cohort. After the onset of AKI, the level of biomarkers remains elevated for a certain period. None of the described indicators is monospecific for AKI; this makes estimating the time of AKI quite difficult. It has been proven that the combination of three biomarkers at two different time points in adults and the combination of two indicators at two time intervals in children allows to increase the reliability of determining AKI up to 0.78

Cannabis potentially interacts with drugs commonly used for anesthesia, which can be life-threatening. Dysfunctions of various organs and systems in cannabis users classify them as patients at increased perioperative risk. When planning anesthesia, acute cannabis intoxication and chronic use should be considered, as patients with acute intoxication may require lower doses of anesthetics (but emergence from anesthesia will be significantly prolonged compared to nonintoxicated states). Chronic exposure to cannabinoids outside of acute intoxication leads to downregulation of receptors, which may result in increased anesthesia tolerance when patients abstain from cannabis before anesthesia. Regional anesthesia methods are preferred in cannabis-dependent individuals. Tolerance to propofol is increased in cannabis users. Acute cannabis intoxication mostly causes additive effects with general anesthesia drugs. Chronic cannabis use mostly results in cross-tolerance to general anesthesia drugs. Anesthesiologists, surgeons, and intensive care physicians should understand the impact of cannabis on the action of general anesthesia drugs to implement safe perioperative management.

Over the past decade, the prevalence of cannabis use among patients requiring surgery has increased by more than 3.5 times, with currently one in seven surgical patients reporting cannabis consumption. Adjusted analysis demonstrated a 1.19 times increased risk of postoperative morbidity and mortality in cannabis users compared to non-users. Despite some discrepancies in the conclusions of many researchers regarding the impact of preoperative cannabis use on specific details of the postoperative period, all authors unanimously confirmed significant harm from cannabinoid dependence to patients' health. Pathological conditions caused by cannabis use are independent risk factors for postoperative complications, increased rates of rehospitalization and surgical interventions, prolonged hospital stays, and increased financial costs. Anesthesiologists' and surgeons' awareness of the pathophysiology of cannabis-dependent individuals will help prevent severe postoperative complications in this patient population and reduce the cost of surgical treatment. Medical cannabis-based preparations will undoubtedly be quite useful in the treatment of many diseases and pathological conditions, but they should be thoroughly studied prior to use in multicenter randomized controlled trials focusing on potential side effects in accordance with regional conditions.

Nowadays, smoking is one of the significant factors for the development of inflammatory periodontal diseases. The effect of nicotine on the microcirculation is manifested in the deterioration of the trophic level of the gums and a decrease in their resistance to infection. Atrophy of acinar parts of small salivary glands develops and other morphological changes characteristic of progressive sialadenitis occur. A change in the microflora of the oral cavity was found depending on the duration of smoking. Epithelial dysplasia, which covers the entire thickness of the epithelium, but does not affect the connective tissue, is called carcinoma. Worldwide, more than 300 million people use smokeless tobacco. Malignant changes at the site of precancerous diseases occur after a couple of years of using the product. In smokers, nicotine blocks H-cholinergic receptors and reduces sensitivity to local anesthetics. Nicotine promotes the production of the CYP2E1 enzyme, which is responsible for the metabolism of halogen anesthetics: halothane, enflurane, diethyl ether, trichlorethylene, chloroform, isoflurane and methoxyflurane. Chronic smokers show reduced pain tolerance. Before morphine loading, the assessment of pain threshold in nicotine-dependent individuals was significantly lower than in non-smokers. Smokers require higher doses of opiates and benzodiazepines than nonsmokers. Smoking reduces the potency of aminosteroid muscle relaxants, the required doses of vecuronium and rocuronium in smokers were 25 % higher than in patients leading a healthy lifestyle. Smokers also need more frequent doses to maintain neuromuscular block. Quitting smoking 4–6 weeks (ideally 8 weeks) before general anesthesia reduces the frequency of peri- and postoperative complications.

The central nervous system is very sensitive to hyperthermia, which causes neurological complications through alteration of the cerebellum, basal ganglia, anterior horn cells, and peripheral nerves. Cerebellar damage is associated with generalized atrophy and signs of Purkinje cell involvement. Heat shock (stroke) is a critical condition caused by hyperthermia, typified by symmetrical damage to the cerebellum. The critical core temperature for the brain is 40–41 °C, but damage to the cerebellum can occur at lower temperatures. In the central nervous system, cerebellar Purkinje cells are most susceptible to hyperpyrexia-induced dysfunction. The degree of their loss correlates with the severity and duration of hyperthermia. Heat hyperpyrexia-induced cerebellar atrophy usually involves both the vermis and the cerebellar hemispheres. Heat stroke can also cause neurological dysfunction, most commonly due to cerebellar damage. During the acute stage, typical neurological disorders are cerebellar ataxia, cognitive impairment, dysphagia, and aphasia. The convalescent period is characterized by transient cerebellar dysfunction; diffuse cerebellar atrophy has been described, and cerebellar degeneration is a well-known consequence of heat stroke. In permanent cerebellar dysfunction after heat stroke, permanent neurological deficit is relatively rare, and the most common manifestation is cerebellar syndrome. The most common X-ray finding in heat stroke is diffuse cerebellar atrophy with preserved brain volume, which is caused by diffuse loss of Purkinje cells and, according to computed tomography and magnetic resonance imaging, mostly affects the vermis or the cerebellar hemispheres, with the hemispheres of the brain mostly remain intact. Cerebellar disorders caused by heat stroke is a complex neurological problem. To rule out an alternative diagnosis, a thorough special examination with neuroimaging is necessary.

Paroxysmal sympathetic hyperactivity (PSH) is a separate form of fever of central origin and is a neurological syndrome characterized by simultaneous paroxysmal occurrence of hypertension, hyperpyrexia, tachycardia, tachypnea, increased sweating and dystonic posture due to sympathetic activation in brain damage. PSH is a syndrome that can manifest itself in a wide range of clinical symptoms. Paroxysmal sympathetic hyperacti-vity is an example of a clinical correlate of central and autonomic nervous system dysfunction. Almost all cases of PSH are associated with craniocerebral trauma, hypoxia, and acute cerebrovascular accident. There is a disengagement theory and a model of the excitation-inhibition relationship of the PSH pathogenesis. In 2014, an expert consensus group proposed a PSH-assessment measure (PSH-AM), which can not only serve as a reliable diagnostic criterion but also stratify the severity of PSH. Assuming clinical evaluation as the current gold standard, PSH-AM has a sensiti-vity of 94 % when used retrospectively. In the treatment of patients with traumatic brain injury, PSH-AM can help avoid misdiagnosis, increase diagnostic efficiency, save time, and reduce economic costs. Hypodiagnosis of PSH can lead to an increase in mortality, disability, length of hospital stay and material costs, but timely diagnosis will allow optimizing treatment for PSH.

Cold urticaria (CU) is an allergic reaction that manifests itself as hives-like rashes or red spots in response to general or local cooling of the body. Th e disease can be acquired or hereditary, and in the cold season it can affect all segments of the population. Th is pathological condition, at first glance, does not seem to be a very dangerous variant of a local cold injury, but in persons who are prone to exposure to low temperatures, especially with a burdened cold history, it may be accompanied by chronicity of the process and complicated by neurovasculitis, obliterating endarteritis and secondary Raynaud’s syndrome, may decrease the quality of life of the victims and become a cause of disability. The pathophysiology of CU is largely unknown, but it is likely to be related to immunoglobulin E (IgE) and mast cell activation. Cooling has been reported to induce the release of neutrophilic and eosinophilic chemotactic factors, prostaglandin D2, and tumor necrosis factor (TNF-α). Less common immunologic fi ndings in patients with CU include cryoglobulinemia consisting of monoclonal IgG and mixed IgG/IgM and IgG/IgA cryoglobulin types. The mechanisms of development of CU are mainly determined by the formation of cryoglobulins (cold hemolysins) and subsequent degranulation of mast cells. Th e diagnosis of CU depends on the patient’s history and the results of cold provocation tests. Patients with CU are recommended first of all not to overcool, to take warm showers, to wear warm clothes and a hat, and not to consume cold food and drinks. Treatment options include second-generation H1 antihistamines and glucocorticosteroids. New promising option is omalizumab, a humanized monoclonal antibody derived from a recombinant DNA molecule that targets and selectively binds to circulating IgE and affects mast cells function. In patients with CU undergoing general anesthesia, premedication including antihistamines and corticosteroids is recommended, along with strict maintenance of perioperative normotermia.

Background. Traumatic injuries often lead to rhabdomyolysis, the destruction of muscle tissue, which causes leakage of the intracellular contents of myocytes into the bloodstream. The most common systemic complication of rhabdomyolysis is acute kidney injury (AKI). It occurs with a frequency of 10 to 55 % and is associated with a poor prognosis, especially with multiple organ failure. The aim of our work was to investigate the impact of multiple trauma complicated by rhabdomyolysis and AKI on the state of the body’s main systems. Materials and methods. We examined 96 victims with multiple trauma complicated by rhabdomyolysis and AKI. Upon admission, we examined the frequency of vasopressor support, rate of diuresis, indicators of the blood count, biochemistry (hepatic, renal complex, electrolytes, creatine kinase, myoglobin), coagulogram, acid-base and gas composition of blood. Results. Severe multiple trauma caused a massive rhabdomyolysis with an increase in creatine kinase to 7058.3 ± 2726.2 units/l, myoglobin to 1433.1 ± 121.9 μg/l. The mean empirical blood loss volume was 2762.5 ± 363.4 mL, leading to posthemorrhagic anemia and thrombocytopenia. 56.3 % of victims needed vasopressor support. Stress hyperglycemia up to 9.2 ± 1.7 mmol/l was observed. Liver dysfunction manifested by a decrease in total protein to 45.3 ± 2.3 g/l, albumin to 26.9 ± 1.5 g/l, which created a risk of interstitial edema. A significant cytolytic syndrome was formed with an increase in alanine aminotransferase to 466.5 ± 141.4 U/l, aspartate aminotransferase to 822.9 ± 187.9 U/l. Moderate hypocoagulation was observed with a decrease in the prothrombin index to 74.6 ± 4.3 % and an increase in the international normalized ratio to 1.4 ± 0.1; activated partial thromboplastin time and fibrinogen level remained within normal limits. The inflammatory reaction manifested by leukocytosis up to (15.3 ± 1.3) × 109/l. AKI was accompanied by an increase in creatinine to 402.1 ± ± 58.6 μmol/l, urea to 19.9 ± 3.0 mmol/l. Diuresis on the first day after admission averaged 0.47 ± 0.08 ml/kg/h. Hyperkalemia was observed in 47.2 % of victims: in 26.5 % of cases, potassium level was from 5.5 to 6.5 mmol/l, in 13.2 %, from 6.5 to 7.5 mmol/l, in 7.5 %, more than 7.5 mmol/l. These disorders were accompanied by subcompensated mixed acidosis. Conclusions. Multiple trauma complicated by rhabdomyolysis and acute kidney injury forms multiple organ failure with a high frequency of vasopressors need, post-hemorrhagic anemia, stress hyperglycemia, impairment of protein synthetic, pigment, enzymatic functions of the liver, coagulopathy, inflammatory syndrome, mixed acidosis and kidney damage per se, which manifested by oliguria, hyperazotemia and hyperkalemia.

Abstract. Acute kidney injury (AKI) develops in 20 % of multiple trauma victims in intensive care units. In 10 % – 28 % of cases, these victims require renal replacement therapy. The aim of our study was to study the effect of continuous veno-venous hemodiafiltration (CVVHDF) on indicators of kidney function, hemodynamics, homeostasis and inflammation in victims of multiple trauma, complicated by rhabdomyolysis and AKI. Materials and methods. 71 victims with multiple trauma complicated by massive rhabdomyolysis and AKI were examined. The levels of total creatine kinase and myoglobin, indicators of kidney function, frequency of vasopressor support, indicators of general blood count, liver complex, coagulogram, and blood gas were studied. The study was conducted at admission, before and after each CVVHDF session and on the last day of treatment. The results. Multiple trauma with massive rhabdomyolysis resulted in AKI with oliguria, hyperazotemia, and hyperkalemia, as well as cardiovascular failure, anemia, hepatic dysfunction, and an inflammatory response. In the case of progressing renal failure despite conservative therapy, CVVHDF was started on day 2.7±0.5. After 1 session of CVVHDF, hyperazotemia was significantly reduced, and potassium levels were normalized. Indicators of the blood count and liver complex did not change. Due to the use of heparin in the circuit, there was a significant prolongation of activated partial thromboplastin time, which did not exceed the target values. 1 session of CVVHDF was sufficient for 71.8 % of victims. Among the survivors, restoration of diuresis was observed in 63.9 %. The mortality rate was 42.3 %. However, there was no significant difference in azotemia levels between survivors and non-survivors, but non-survivors had higher potassium levels, more severe thrombocytopenia, cardiovascular and hepatic failure, and hypocoagulation. In addition, the ISS score in non-survivors was 37.8 % (p=0.001) higher than in the survivors. Conclusions. Multiple trauma, complicated by massive rhabdomyolysis, causes the development of multiple organ failure, primarily renal. CVVHDF allows to effectively reduce the levels of azotemia and normalize the level of potassium after the first session, while avoiding abrupt fluctuations in the indicators of the function of other organs and systems. A single session of CVVHDF is sufficient to restore renal function in most patients. Mortality remains high and depends directly on the severity of anatomical injuries and the addition of insufficiency of other organs and systems.

The non-medical use of cannabis can negatively impact the morpho-functional state of almost all organs and systems of the human body. During acute intoxication and established drug dependence, it can unevenly distort the effects of drugs for local and general anesthesia, leading to life-threatening complications. Part 1 of this review presents the results of acute and chronic cannabis use on homeostasis. Cerebral vasospasm and atherosclerosis are identified as major etiological factors for cannabis-related cerebrovascular diseases. Young to middle-aged individuals (30–50 years), male gender (male-to-female ratio 3.7:1), and chronic use (86%) are significant independent predictors of neurovascular toxicity, cerebral hypoperfusion, and stroke. Cannabis smoking causes damage to the respiratory mucosa similar to tobacco. Regular cannabis smokers can expect irritation of the upper respiratory tract, swelling, obstruction, chronic cough, bronchitis, lung emphysema, and bronchospasm. Some reports advocate the use of dexamethasone during surgery to alleviate these symptoms. The detrimental effects of chronic cannabis use on liver and kidney functions are somewhat overstated. Disturbances in immune system, thermoregulation, blood clotting, and carbohydrate metabolism in the absence of anesthetic precautions can significantly complicate the patient's condition in the perioperative period. Cannabinoids can interact with drugs from various groups. Awareness of the pathophysiological and biochemical consequences of cannabis use allows anesthesiologists to anticipate and effectively manage perioperative complications in this patient category

Based on the understanding of the pathophysiology of heat stroke, it has been suggested that heat stroke can be considered as a form of hyperthermia that is associated with a systemic inflammatory response leading to a syndrome of multiple organ dysfunction in which encephalopathy predominates. Mechanisms of neuronal injury in heat stroke include: cellular effects (damage to membranes, mitochondria, and DNA, stimulation of excitotoxic mechanisms, protein denaturation), local effects (ischemia, inflammatory changes, edema, cytokine release, vascular damage), systemic effects (changes in cerebral blood flow, endotoxemia, translocation of bacteria through a dysfunctional gastrointestinal tract). Neurological manifestations of heat stroke develop in 3 stages according to the time of occurrence: acute, convalescent and late. In the acute stage, cerebral dysfunction prevails. Overheating of the body directly caused polyetiological cerebral dysfunction with deep suppression of consciousness in the acute stage; circulatory shock, hypoxia and cerebral ischemia, excessive accumulation of cytotoxic free radicals and oxidant brain damage developed. During the convalescence stage, cerebral dysfunction gradually decreases. This stage is characterized by transient cerebellar dysfunction. For the late stage, long-term neurological and cardiovascular complications with a constant risk of death are typical. When late stage with permanent neurologic deficits develop, cerebellar dysfunction is the most common symptom. The delayed onset of degeneration and deafferentation suggests that the syndrome is not caused by the primary lesion itself but may be a consequence of postsynaptic hypersensitivity or secondary reorganization of the involved pathways.

Preeclampsia remains one of the main causes of obstetric and perinatal complications. The frequency of preeclampsia in the structure of pregnancy complications varies from 6 % to 12 % in healthy pregnant women and from 20 % to 40 % in pregnant women with extragenital pathology. There is growing interest in investigating the exact pathophysiological mechanism of the preeclampsia process as this may identify new potential screening biomarkers. There is evidence that inflammatory mechanisms are a key link between placental ischemia and endothelial dysfunction. It has been hypothesized that impaired regulatory systems are unable to regulate the resolution of inflammatory pathways, contributing to an exaggerated immune response. It is appropriate to call pregnancy a unique immune state that is modulated, but not suppressed. Modulation of the immune system leads to differentiated reactions depending on the stage of pregnancy. Each stage of pregnancy is characterized by a unique inflammatory state. The first and third trimesters are pro-inflammatory, while the second trimester is an anti-inflammatory phase. Proinflammatory mediators, such as IL-6, directly and indirectly through TNF-α, bradykinin, thrombin cause degradation of the endothelial glycocalyx, which leads to an increase in the permeability of the vascular wall with the progression of capillary leakage into the interstitial space. Inflammatory damage to the glycocalyx that occurs during preeclampsia increases intercellular permeability associated with leakage of fluid and albumin into the interstitial space. As a result of damage to the endothelium, there is an increase in the volume of extracellular fluid, which is manifested in women with severe preeclampsia in the form of edema with pathological fluid retention. Further studies are needed to clarify the role of inflammatory mediators in predicting the risk of developing preeclampsia. Further study of the problem will reveal potential targets for treatment, primarily related to inhibition of inflammatory processes and prevention of damage to the endothelial glycocalyx.

BACKGROUND. According to the modern standards, in case of an acute blood loss, the pathogenetic provision of fluid therapy is based on the ROSE/D concept. According to this concept, after the initial emergency restoration of circulating blood volume, the fluid compartments should be optimized with further stabilization of the condition. OBJECTIVE. To study the fluid compartments in mine-explosive injuries victims. MATERIALS AND METHODS. 28 servicemen aged 20 to 51 years (average age 34.6±10.3 years) who were in the intensive care unit (ICU) with mine-explosive injuries of various localization (chest, abdomen, limbs) were examined. The victims were given fluid therapy in a restrictive mode. The condition of fluid compartments was determined by the method of bioimpedance measurement and calculation methods. RESULTS. On the first day of ICU stay, the total amount of water in the body exceeded the norm by 3 %. At the same time, the volume of intracellular water was significantly lower than normal by 22 %. On the second day, the total amount of water in the body normalized, but the indicator of intracellular water increased by 9.5 % of the reference. CONCLUSIONS. It is shown that despite the restoration of the circulating blood volume, there is an intracellular fluid deficit, which, even in the conditions of the restrictive fluid therapy, is replaced by a slight compensatory intracellular hyperhydration the next day when the intravascular volume of fluid is normalized.

Nowadays, rewarming of the affected tissues is the primary method of treatment for patients with cold injuries. But the warming manipulation has its own characteristics and limitations, depending on specific circumstances. Untimely and incorrectly performed rewarming can lead to a significant increase in the level of dangerous complications, mortality, and disability. The rewarming strategy is implemented according to one of the two scenarios. If there is a risk of freezing again, the injured area is not actively rewarmed; it is just immobilized, and thermo‑insulating bandages are applied. Slow warming with body heat is also acceptable. If the frozen area can be warmed and kept warm without refreezing until the evacuation is completed, a quick warming with warm water or special heating blankets is preferable. Recommendations on the ideal water temperature significantly differ among authors and include a wide range between 37 °C and 43 °C. The extent of damage to the tissues becomes obvious only after thawing. The traditional classification system of local cold injuries distinguishes four degrees of frostbite. First‑degree frostbite presents with superficial damage to the skin; second‑degree frostbite involves deep skin damage; third‑degree frostbite results in full‑thickness skin damage, including the subcutaneous and surrounding tissues; and fourth‑degree frostbite causes deep necrosis of the subcutaneous structures. Depending on the extent of damage, patients may experience constant and severe pain during rewarming, so analgesics should be prescribed to relieve it. It is recommended to use topical agents (creams, gels, and ointments) to improve circulation and prevent and treat infection. Tissue necrosis with severe frostbite requires surgical treatment of wounds. The authors hope that the provided information will be useful to doctors‑of‑first‑ contact and in hospital conditions in order to optimize the treatment of local cold injuries.

Background. Modern literary sources indicate that of the five main channels through which a person receives information (sight, hearing, taste, smell, and tactile sensations), subjects of learning mainly use only three — auditory, visual, and tactile that determine auditory, visual and kinesthetic. Purpose was to determine the types of perception of information by interns and participants of training in the specialty “Anesthesiology and intensive care” to optimize the postgraduate training process. Materials and methods. An anonymous survey of 48 interns and 51 practicing doctors in the specialty “Anesthesiology and intensive care” was conducted using a special questionnaire, followed by interpretation and analysis according to the dominant channels of obtaining information and their combinations. Results. When evaluating the leading (dominant) sensory modalities in the group of intern doctors, a significant advantage of auditory perception among other channels of receiving information was determined. The evaluation of the leading sensory types in the group of training participants who have their own specific work experience in the specialty showed a significant predominance of the kinesthetic informational channel, which is slightly inferior to the auditory sensory type, and only 11.2 % of the respondents account for the visual modality. The involvement of most sensory analyzers and the combination of modalities in the educational process contributes not only to the holistic perception, analysis and assimilation of educational information, but also to the formation of multimodal thinking. Therefore, during the educational process, multimodal technologies should be used, which allow providing educational material in several formats at the same time. Conclusions. 1. Interns mostly demonstrated the dominance of audio-kinesthetic and polymodal types of information acquisition. 2. Anesthesiologists with some practical experience are more inclined to monokinesthetic and audio-kinesthetic information modality. 3. The polymodal type of providing educational information is optimal in postgraduate education of medical workers. 4. The introduction of short-term trainings on mastering practical skills into the educational process creates an optimal combination of ways to obtain educational information and consolidate memory by subjects of training.