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Relevance. The pathogenesis of COVID-19 remains one of the most pressing. The literature discusses the role of iron as a factor supporting inflammatory processes, hypercoagulability and microcirculation crisis in severe COVID-19.The aim of study. was to identify changes in iron metabolism in patients with severe COVID-19 and hyperferritinemia.Material and methods. In this study, we used a content analysis of available scientific publications and our own observations of the peculiarities of the clinical picture and laboratory parameters in patients with a severe course of COVID-19 who had hyperferretinemia at the height of the disease. The main group consisted of 30 patients hospitalized in the Department of Anesthesiology, Resuscitation and Intensive Care of N.A. Semashko City clinical Hospital No. 38 with the diagnosis COVID-19, bilateral polysegmental pneumonia, severe course and hyperferritinemia. The diagnosis of a new coronavirus infection was confirmed by visualization of bilateral viral lung lesions with chest CT-scan, positive PCR test for SARS-CoV-2 and the presence of immunoglobulins to SARS-CoV-2. The control group consisted of 20 healthy volunteers. The study evaluated the biochemical parameters of iron metabolism, fibrinolysis and markers of inflammation. Changes associated with impaired iron metabolism were assessed by the level of serum iron, transferrin, daily and induced iron excretion in the urine. Statistical processing was carried out using nonparametric methods.Results. All patients with severe COVID-19 and hyperferritinemia showed signs of impaired iron metabolism, inflammation and fibrinolysis — a decrease in the level of transferrin (p˂0.001), serum iron (p˂0.005), albumin (p˂0.001), lymphocytes (p˂0.001) and an increase in leukocytes (p˂0.001), neutrophils (p˂0.001), CRP (p˂0.005), IL-6 (p˂0.001), D-dimer (p˂0.005), daily urinary iron excretion (p˂0.005) and induced urinary iron excretion (p˂0.001).Conclusions. The study showed that in the pathogenesis of the severe course of COVID-19, there is a violation of iron metabolism and the presence of a free iron fraction. The appearance of free iron can be caused by damage to cells with the “release” of iron from cytochromes, myoglobin, hemoglobin, or violation of the binding of iron to transferrin, which may be the result of a change in the protein structure or violation of the oxidation of iron to the trivalent state. When assessing the degree of viral effect on the body, one should take into account the effect of various regulators of iron metabolism, as well as an assessment of the level of free iron not associated with transferrin.

Abstract In 21 male patients aged 20 to 40 years, metabolic disorders in post-toxic delirious syndrome caused by gamma-hydroxybutyric acid poisoning and its precursors were studied. In the examined group of patients, hyperammonemia was detected in 71.4% of cases, metabolic lactic acidosis was revealed in 76.2%. The direct correlation between the severity of metabolic disorders and delirious syndrome according to DRS-R-98 scale was established. The statistically significant increase in capillary blood levels of lactate on day 3 of psychotic period was 4.9 mlmol/L and ammonia on day 5 was 187.0 mmol/L. The greatest severity of metabolic disorders was found in patients over the age of 27 years who systematically use the studied substances with narcotic effects for 7 months or more and combine their intake with other psychoactive substances.

This clinical case of acute poisoning due to bite of snake Dendroaspis viridis seems interesting to share because of its rare incidence inRussiaand management peculiarities: the critical care was conducted without specific antidote therapy due to absence of the antidote.The prevailing clinical presentation included signs of toxic myopathy combined with paresis of skeletal and breathing muscles that led to development of acute respiratory failure and metabolic disorders. The processes described were induced by the action of snake poison dendrotoxins featuring the activities of potassium channel blockers and acetyl cholinesterase inhibitors.The proper critical care included conduct of syndrome therapy aimed at maintaining life support systems adequately to condition (replacement of the breathing and circulation functions), antibiotic therapy and desensitizing treatment and metabolic care by administration of drugs characterized by antihypoxant/antioxidant mechanism of action.The comprehensive therapy applied has resulted in a favorable outcome of acute poisoning by snake green mamba without development of possible complications even when the specific antidote drug has not been included into the treatment protocol.

Purpose: to contribute to relief of metabolic disorders associated with hypoxia by including a succinate correcting tissue metabolism into the scheme of intensive care of acute severe methadone poisoning complicated by the crush syndrome.Materials and methods. We examined the dynamics of clinical manifestation of acute methadone poisoning complicated by crush syndrome: changes in clinical and biochemical parameters, coagulation test findings, blood gas composition and acid-base state, ECG and X-ray findings.Results. By the 7th day after patient's admission in the ICU, stabilization of hemodynamics, recovery of spontaneous breathing and consciousness, reduction of swelling and the beginning of the formation of pressure ulcers were observed; on the 8 the day, restoration of urination and characteristics of urine were registered. On the 12th day, the patient was transferred to the toxicology unit being in a state of moderate severity and demonstrating positive changes in all clinical parameters.Conclusion. The inclusion of a drug with antioxidant/antihypoxant properties in the infusion therapy scheme allows to relieve metabolic disorders associated with hypoxia, and thereby increase the effectiveness of treatment: i.e. to relief clinical and laboratory manifestations and reduce the ICU stay.

This review presents current data on the mechanism of action, selective toxicity, toxicokinetics and toxicodynamics of diacetylmorphine (heroin). Acute diacetylmorphine poisoning is considered under taking into account the developing a critical state, in which the poisoning severity is determined by severe metabolic disorders associated with the progression of hypoxia. The main lifethreatening complications of acute diacetyl morphine poisoning are described including those associated with the nervous system, respiratory, circulatory and urinary systems. Since hypoxia is the principal damaging factor, the the mechanisms of oxygen transport disorders and the pathogenesis of activation of free radical oxidation in acute diacetylmorphine poisoning are discussed. The improvement of intensive care strategy for severe forms of acute diacetylmorphine poisoning by the inclusion of a substrate antihypoxant Reamberin into the list of routine critical care prescriptions is emphesized.

Objective: to improve intensive therapy for acute ethanol intoxications complicated by the development of delirium tremens. Subjects and methods. The data of examination and treatment were analyzed in 173 patients with acute severe ethanol intoxications complicated by the development of delirium tremens, out of them 105 patients received Cytoflavin incorporated into a treatment regimen and 68 patients were treated according to convention al procedures. In addition to physical examination, the clinical course of the disease, blood gas composition and water electrolyte balance parameters, and circulating blood volume were estimated by a dye hematocrit method. Results. Correction of somatic dysfunctions and metabolic disorders with Cytoflavin along with medical sleep was found to lead to rapid arrest of the signs of the psychosis, to prevent brain edema, to have a positive impact on the further status of patients, to considerably reduce the period of asthenization and to ameliorate its manifestations. Conclusion. The findings may serve as a basis for the wide use of Cytoflavin in a treatment regimen in narco logical practice since it leads to normalization of metabolic processes and hence to a more rapid recovery.

Objective: to study the specific features of the clinical course of acute intoxications with venoms due to the bites of Naja (cobra) naja and Naja kaouthia and those of intensive therapy in patients with the severest forms of this condition. Subjects and methods. Two clinical cases of acute intoxications with venoms due to Naja naja and Naja kaouthia bites were examined. The specific features of their clinical picture over time, changes in clinical and biochemical indicators, blood gas composition, and acidbase balance, coagulogram readings, ECG and radiological findings were studied. Results. Acute intoxication with venoms due to serious cobrabites was found to be characterized by the development of toxicohypoxic encephalopathy, toxic myopathy with skeletal and respiratory muscle paresis to develop acute respiratory and cardiovascular failure, coagulopathy, and metabolic disorders. Specific therapy (with an anti-ophidic serum in one case) resulted in drastically worsening health conditions as fulminant acute respiratory distress syndrome. A package of intensive therapy measures should include actions based on general resuscitation approaches — maintenance of life support systems (breathing, blood circulation), anti-sensitizing therapy, correction of metabolic disturbances with substrate antihypoxants (cytofavin, reamberin), and antimicrobial therapy. Conclusion. In the severest acute intoxications due to cobra snakebites, specific therapy methods (with anti-ophidic serum) should be used with extreme caution and particular emphasis should be laid on the general resuscitation-based principles.

Objective: to examine the capacities of pharmacological correction of impairments in oxygen-transporting systems and metabolic processes with perfluorane and cytoflavin in critically ill patients with acute intoxication with neurotropic poisons.Subjects and methods. Metabolic sequels of severe hypoxia, free radical processes, and endogenous intoxications were studied in 62 patients with the severest acute intoxication with neurotropic poisons.Results. The studies have established that hypoxia and metabolic changes lead to the development of endotoxicosis. Intensifying endotoxicosis in turn enhances hypoxic lesion. Thus, the major task of intensive care is to restore oxygen delivery and to diminish metabolic disturbances and endotoxicosis. Ways of correcting hypoxia and metabolic disturbances are considered in the severe forms of acute poisoning.

Monitoring of the blood circulation and liquid sectors in patients with lung lesion due to severe acute intoxications makes it possible to perform infusion therapy that does not induce thoracic hyperhydration. The inclusion of gelofusin and cytoflavin into the infusion regimen by the proposed procedure substantially enhances the efficiency of treatment of patients with this pathology even when acute lung lesion syndrome develops.

Objective. To conduct an experimental study of the impact of the time of administration of succinic acid preparations on central nervous system (CNS) function and gas exchange while simulating metabolic therapy for severe poisoning by ethyl alcohol. The study was performed on 74 male albino rats weighing 140—180 g. Acute severe and very severe intoxication was simulated, by intraabdominally administering 30% ethanol to the rats. Cytoflavin was used to simulate experimental therapy. The rate of gas exchange was estimated by the oxygen uptake determined by the closed chamber method in a Regnault apparatus (Germany). Spontaneous bioelectrical activity was recorded in the frontooccipital lead by the routine procedure. External pain stimulation and rhythmical photostimulation were employed to evaluate cerebral responsiveness. Heterodirectional EEG changes in the «early» and «late» administration of succinate were not followed by the similar alterations of gas exchange: oxygen consumption in both the «early» and «late» administration of succinate remained significantly lower than in the control animals. With the late administration of succinate to the animals with mixed (toxic and hypoxic) coma, the so-called discrepancy between the noticeably increased energy production and brutally diminished metabolism occurred. It may be just the pathological mechanism that was the basis for higher mortality in the late succinate administration group. The findings and their analysis make it possible to advance a hypothesis that succinate may cause metabolic desynchronization if activation of metabolic processes takes place under severe tissue respiratory tissue depression. In these cases, there is a severe damage to tissue and chiefly the brain. This manifests itself as EEG epileptiform activity splashes preceding the animals’ death. Therefore, resuscitation aimed at restoring the transport of oxygen and its involvement in tissue energy processes should be followed by the administration of succinic acid preparations. The drug of this kind is now perfluorane, as demonstrated by experimental and clinical studies. It should be noted that the more potent a metabolic agent is, the more strictly the rules of its use should be observed.

The most severe sequels of acute lung lesions are manifested by the impairment of ventilation-perfusion relations, by the development of primary pulmonary hypertension, by circulatory disorders and the increased content of extravascular fluid in the lung, whose diagnosis is extremely difficult. The purpose of the study was to access the capacities of early diagnosis of systemic hemodynamic and pulmonary circulatory disorders in acute lung lesion in patients with critical states. Hydro- and hemodynamics was evaluated in 32 persons in the early phase of intoxications with neurotropic poisons, in 15 with severe concomitant injury, and in 22 patients with critical states intensively treated cardiac surgery. Hemodynamics was determined, by concomitantly using the integral body rheography technique after M. I. Tishchenko and transthoracic impedance cardiogra-phy. The rheographic techniques could evaluate the state of systemic hemodynamics, the nature and effectiveness of pulmonary pulsatile blood flow, that depended on pulmonary hypertension, and increased thoracic fluid. The determination of the level of lactate and its arterial and venous blood ration with consideration of lactate clearance enabled the authors to evaluate both the effectiveness of systemic perfusion and impaired metabolic processes in the lung. Drastically decreased pulsatile blood flow, ineffective volumetric load, low oxygenation index, increased thoracic fluid volume, and the ratios of the arterial to venous blood concentration of lactate with its normal clearance may be early signs of acute lung lesion.

Objective: to determine the impact of reamberin incorporation into intensive care on the antioxidant defense system and the activity of lipid peroxidation in patients with toxic-hypoxic encephalopathy. Subjects and methods. The investigation enrolled 84 patients with acute severe poisoning by a mixture of psychotropic substances (hypnotics, neuroleptics, antidepressants, 1,4-benzodiazepine derivatives, ethanol). Oxygen balance parameters (oxygen consumption, oxygen utilization quotient, and arteriovenous oxygen difference) were calculated. The antiradical defense system was evaluated determining the levels of reduced glutathione and free sulfhydryl groups of proteins activity of the antiradical enzymes glutathione peroxidase, glutathione-S-transferase, and catalase in red blood cells. Lipid peroxidation rate in red blood cells was determined by measuring the concentration of malondialdehyde. Results. The incorporation of reamberin into intensive care was found to be accompanied by a reduction in tissue hypoxia, more rapid recovery of the antioxidant defense system, and a decrease in the activity of lipid peroxidation processes. Сorrection of metabolic disturbances in its turn leads to the improved clinical course of acute poisoning, which manifests itself as a reduction in the duration of coma, the length of stay in the intensive care unit, and mortality. Conclusion. The reduction in the severity of metabolic disturbances associated with the development of hypoxia and free radical disorders leads to substantial improvement of the clinical course and outcomes of toxic-hypoxic encephalopathy. Key words: toxic-hypoxic encephalopathy, hypoxia, antioxidant system, lipid peroxida-tion, reamberin.

The paper considers the problems of diagnosis of severe thallium salt poisoning in early-stage intoxication, which are associated with the fact that alopecia, a clinical typical symptom of thallium toxicity, appears in the period exceeding two weeks. At the same time, in severe poisoning a fatal outcome occurs much more early and the first signs of intoxication are highly diversified and nonspecific. The clinical manifestations with no specificity at the early period of intoxication in conjunction with the absence of certain history data result in late (sometimes postmortem) diagnosis in the vast majority of cases, particularly, in criminal cases. This comprises a danger of acute severe thallium poisoning since unrecognized intoxication leads to incorrect treatment and patient death. While making a differential diagnosis, attention should be given to a set of a number of symptoms that arouse suspicion of thallium poisoning, which is an indication for chemical and analytical studies of biological environments in these patients. This paper summarizes the available data on ethyology, pathogenesis and cliniu-cal manifestations of severe thallium poisoning and demonstrate own cases of thallium intoxication occurred recently in Yaroslavl and Saint Petersburg. Basic strategy of thallium poisoning treatment is presented and discussed. Key words: acute poisoning, thallium compounds, antidote therapy, diffeferential diagnosis.

Objective: to study the clinical patterns due to course of severe methadone poisoning and to assess the results of reamberine use in the complex of intensive therapy for this condition. Subjects and methods. Sixty-eight patients with acute severe methadone poisoning were examined and treated. The clinical manifestations of intoxication and impairment in the tissue component of oxygen transport were evaluated. Results. The severity of its clinical picture, besides directly toxic effect of methadone was characterized by the depth and magnitude of hypoxia that clinically manifested both as cerebral edema/swelling and pulmonary edema and, in cases of hyperhypoxia, as severest disorders in the cardiovascular system. The incorporation of the antihypoxant reamberine into an intensive care program for severe acute methadone poisoning was found to result in a rapider reduction of tissue hypoxia, which substantially diminished the degree of occurring complications and improved the clinical course of acute intoxications. Conclusion. Thus, correction of metabolic aftereffects and alleviation of hypoxic lesions result in a reduction in the duration of coma, the length of stay on mechanical ventilation, the rate and severity of secondary pulmonary complications and mortality rates.

Цель настоящей работы — изучить возможность фармакологической коррекции нарушений иммунной системы путем использования цитофлавина у больных с острыми отравлениями нейротропными ядами, осложнившимися развитием пневмонии. У 24-х больных с тяжелыми формами острых отравлений нейротропными ядами исследованы нарушения метаболизма, связанные с развитием тяжелой гипоксии тканей, и иммунной системы. В результате проведенных исследований установлено, что одним из ведущих факторов развития пневмонии при тяжелых отравлениях являются нарушения метаболизма и иммунная недостаточность. Коррекция метаболических расстройств, в свою очередь, снижает степень нарушений иммунной системы и сокращает сроки разрешения пневмонии. Ключевые слова: острые отравления, нарушения метаболизма, перекисное окисление липидов, сукцинат, цитофлавин.

Objective: to evaluate the efficiency of therapy in patients with acute intoxication with neurotropic poisons and protracted hypoxia complicated by pneumonia under guidance of impedance study of pulmonary circulation and pulmonary hydration. Subjects and methods. Ninety-six patients with acute intoxication with neurotropic poisons were examined and treated. They were divided into 3 groups: 1) 60 patients without signs of acute lung injury (ALI); 2) 17 with ALI in whom impedance methods for diagnosis and therapy monitoring were used; 3) 19 with ALI who were treated without impedance study. Systemic and pulmonary circulation and pulmonary hydration were evaluated via the one-stage application of integral body rheography (IBR) by the procedure developed by M. I. Tishchenko, thoracic rheography (TRG) after B. B. Sramek, and integral two-frequency impedance study. Results. In patients with ALI, increased thoracic fluid was accompanied by the decreased differential rheogram amplitude, which suggested the diminished pulsating component of blood flow, but the higher amplitude ratio of the differential rheograms obtained at IBR and TRG indicated the presence of impaired regional pulmonary circulation. The patients with ALI, followed by evolving pneumonia had lower differential rheogram amplitudes measured by TRG; they tended to have higher thoracic fluid levels and lower ejection rates. Conclusion. In patients with acute severe intoxication with neurotropic poisons, the risk for ALI is determined by the severity of intoxication and the duration and depth of hypoxia. The development of a critical condition determines the degree of pulmonary hyperhydration that depends on the pattern of cardiovascular abnormalities (a fall of single cardiac performance and pulmonary microcirculato-ry disorders). Monitoring of blood circulatory and microcirculatory disorders determines the basic treatment options and outcome. Key words: acute intoxication with neurotropic poisons, acute lung injury, pneumonia, integral body rheography, thoracic rheography, integral two-frequency impedance study.

Objective: to evaluate the efficiency of methods for diagnosing and treating critically ill patients with acute respiratory failure (ARF) in acute poisoning by neurotropic substances. Subjects and methods. Two hundred and thirty-three patients with acute severe intoxication with neurotropic poisons were examined. All the patients were admitted for toxic-hypoxic coma and ARF; in this connection all the patients underwent artificial ventilation (AV). The patients were divided into 3 groups: 1) those in whom the traditional treatments (AV, detoxifying therapy, and infusional and cardiotropic support) could restore the basic parameters of vital functions, as judged from the recovered oxygenation index; these patients had no metabolic shifts; 2) those who had signs of pulmonary hyperhydration, low cardiac output and moderate metabolic disorders, as suggested by elevated lactate levels; 3) seriously ill patients in whom the interval between the time of poisoning to care delivery was more than 20 hours; the patients of this group had the most significant metabolic disorders. Results. Correction of ARF in critically ill patients with acute poisoning should include, in addition to the rational parameters of AV and detoxifying therapy, agents for targeted therapy for sequels of hypoxia and energy deficiency states. For maximally rapid and effective oxygen transport recovery, the addition of perfluorane to the complex therapy cardinally improves the results of treatment and reduces mortality rates. Conclusion. The complexity of the pathogenesis of ARF and its sequels is a ground for diagnosing and correcting not only ventilation disturbances, but also pulmonary microcirculatory disorders and metabolic disturbances. Key words: acute intoxication with neu-rotropic poisons, acute respiratory failure, pulmonary hyperhydration, hypoxia, metabolic disturbances.