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Delirium complicating regular use of psychoactive substances remains one of the major issues of critical care, toxicology, and psychiatry. However, the pathogenetic mechanisms of delirium development in patients with 1,4-butanediol poisoning have been poorly studied until now.The aim of the study was to reveal specific patterns of delirium in patients with 1,4-butanediol poisoning as well as to study the changes in systemic hemodynamic parameters, respiratory function, and body fluid compartments during the treatment.Material and methods. The study was prospective and treatment-randomized. Forty-eight male patients aged 20 to 45 years with delirium and acute 1,4-butanediol poisoning were enrolled. Of them, 24 patients were administered with succinate-containing drug 40 ml daily, 24 patients received standard treatment without antihypoxic agents. We studied the evolution of delirium, changes in anaerobic metabolism parameters, systemic hemodynamics, respiratory function, and the volume of fluid compartments. Impedance measurement method adjusted for interference was used in the study.Results. At the «peak» of delirium (days 1–3), the hyperdynamic circulation, increased systemic arterial tone, stroke output, respiratory function parameters, and metabolic lactate acidosis were recorded. A decrease in total fluid volume and extracellular fluid volume was clearly observed during day 1 of intoxication delirium along with increased permeability of cell membranes. On day 3 of delirium, a decrease in intracellular fluid volume and increase in extracellular fluid volume were noted. After the cytoflavin administration, shorter delirium duration (7.5 [6; 8] days), more rapid correction of lactate acidosis, stabilization of respiratory parameters and stabilization of cell membrane permeability by day 5 were found. In the control group, delirium persisted for up to 14 [11; 15] days (z=-5.9; P=0.00011) with more frequent development of complications such as nosocomial pneumonia (χ2=8.4, P<0.001).Conclusion. The severity of delirium in acute poisoning with 1,4-butanediol was associated with metabolic lactate acidosis, changes in systemic hemodynamics and pulmonary function. A positive effect of adjunctive antihypoxic therapy with succinate-containing agent on cardio-respiratory parameters, cell membrane permeability, water balance due to elimination of tissue hypoxia and prompt switching to tissue aerobic metabolism has been found.
Delirium complicating regular use of psychoactive substances remains one of the major issues of critical care, toxicology, and psychiatry. However, the pathogenetic mechanisms of delirium development in patients with 1,4-butanediol poisoning have been poorly studied until now.The aim of the study was to reveal specific patterns of delirium in patients with 1,4-butanediol poisoning as well as to study the changes in systemic hemodynamic parameters, respiratory function, and body fluid compartments during the treatment.Material and methods. The study was prospective and treatment-randomized. Forty-eight male patients aged 20 to 45 years with delirium and acute 1,4-butanediol poisoning were enrolled. Of them, 24 patients were administered with succinate-containing drug 40 ml daily, 24 patients received standard treatment without antihypoxic agents. We studied the evolution of delirium, changes in anaerobic metabolism parameters, systemic hemodynamics, respiratory function, and the volume of fluid compartments. Impedance measurement method adjusted for interference was used in the study.Results. At the «peak» of delirium (days 1–3), the hyperdynamic circulation, increased systemic arterial tone, stroke output, respiratory function parameters, and metabolic lactate acidosis were recorded. A decrease in total fluid volume and extracellular fluid volume was clearly observed during day 1 of intoxication delirium along with increased permeability of cell membranes. On day 3 of delirium, a decrease in intracellular fluid volume and increase in extracellular fluid volume were noted. After the cytoflavin administration, shorter delirium duration (7.5 [6; 8] days), more rapid correction of lactate acidosis, stabilization of respiratory parameters and stabilization of cell membrane permeability by day 5 were found. In the control group, delirium persisted for up to 14 [11; 15] days (z=-5.9; P=0.00011) with more frequent development of complications such as nosocomial pneumonia (χ2=8.4, P<0.001).Conclusion. The severity of delirium in acute poisoning with 1,4-butanediol was associated with metabolic lactate acidosis, changes in systemic hemodynamics and pulmonary function. A positive effect of adjunctive antihypoxic therapy with succinate-containing agent on cardio-respiratory parameters, cell membrane permeability, water balance due to elimination of tissue hypoxia and prompt switching to tissue aerobic metabolism has been found.
The aim of the study was to establish objective reliable morphological signs of fatal poisoning with 4-hydroxybutanoic acid (4-HBA).Material and methods. The 49 acts of forensic medical examination of corpses with «Acute poisoning with 4-hydroxybutanoic acid» as the main cause of death were analyzed. The work was done in the Saint Petersburg Bureau of Forensic Medical Expertise.The results of morphological (macro - and microscopic) as well as forensic chemical studies of biological tissues were evaluated.The results were statistically processed using Statistic for Windows software (version 10). The numerical characteristics of the variables (M ± SD, Me [Q25; Q75]), χ2 — Pearson's criterion, and Spearman's correlation coefficient were applied for statistical processing.Results. The average lethal dose of 4-HBA in arterial blood was found to be equal to 273,6 ± 125,1 mg/l. In a forensic chemical study the combined use of 4-HBA and other narcotic substances (NS) and psychoactive substances (PAS) was diagnosed in 48.9% of cases. Of the causes leading to death, non-violent and «non-criminal» death due to 4-HBA poisoning was established more often - in 67.3% (33) of cases, a fall of the victim from a height with a fatal outcome - in 22.4% (11), less often violent death as a result of blunt and acute trauma - in 4.09% (2) cases.Among the macroscopic signs of acute lethal poisoning with 4-HBA were an increased mass of internal organs (heart, lungs, spleen, liver) in direct connection with the concentration of the toxicant in the blood. Microscopic signs of acute lethal poisoning by a toxicant included blood circulation features characteristic of sudden death.Concomitant pathology was diagnosed in 32.6% of cases in the form of degenerative changes in internal organs. In turn, hepatitis C and human immunodeficiency virus (HIV) were detected in 26.5% (13) of the dead.Conclusions. Thus, the signs characteristic for acute fatal poisoning with 4-HBA include the features of hemocirculation characteristic of sudden death. The brain is most severely affected, which is manifested by destructive edema. Poisoning is also characterized by the presence of serous pulmonary edema. Macroscopic signs of poisoning were revealed, including an increase in the weight of the heart, lungs, spleen and liver in direct connection with the concentration of the toxicant in the blood.It should be noted that the concomitant pathology in the form of dystrophic changes in the internal organs indicates the long-term nature of the use of the toxicant leading to pronounced metabolic disorders.
Introduction. The article considers a case of a favorable outcome of acute oral poisoning with a mixture of narcotic and psychoactive substances of severe degree, complicated by the development of acute respiratory failure and exotoxic shock. Clinical observation. An episode of acute oral poisoning with a mixture of narcotic and psychoactive substances of severe degree (baclofen, (4-amino-3-(4-chlorophenyl) is presented-butyric acid – ethylglucuronide >2000 mg/ml), methadone 83 mg/ml, methylenedioxypyrovaleron 57 ng/ml, complicated by the development of exotoxic shock in a 32-year-old patient. The clinical picture of acute poisoning was manifested by depression of consciousness to the level of coma II, acute respiratory failure, mixed respiratory and metabolic acidosis (pH 7.18; partial pressure of carbon dioxide 64.0 mmHg, lactic acidosis up to 5 mmol/l), swelling of the brain, exotoxic shock (BP – 60/20 mmHg, heart rate – 110 beats per minute). Intensive therapy included: respiratory, infusion, detoxification, anticoagulation, antibacterial therapy, correction of acid-base state disorders, water-electrolyte balance, nutritional support, normalization of metabolic disorders through the use of a substrate antihypoxant. The calculation of the required amount of sodium bicarbonate was carried out according to the Mellengaard-Astrup formula: the amount of mmol of sodium bicarbonate is equal to the product of VE • body weight in kg • 0.3. According to the calculation, the amount of required bicarbonate was 195 mmol, that is, in terms of 5% bicarbonate solution – 195 ml. Conclusion. As a result of basic resuscitation care in the form of artificial lung ventilation, correction of mixed respiratory and metabolic acidosis by using sodium bicarbonate, infusion therapy to correct hypovolemia, ensuring optimal perfusion of organs and tissues, elimination of key links of hypoxia by using cytoflavin, improvement of rheological properties of blood and symptomatic therapy allowed for a favorable outcome of severe poisoning with a mixture of narcotic and psychoactive substances complicated by the development of exotoxic shock.
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