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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.

A case of acute oral poisoning by 1.4-butanediol, complicated by the development of severe hypoxia in a 34-year-old patient actively engaged in bodybuilding, is presented. The psychoactive substance was used by the patient to increase sexual activity and physical stamina. The duration of systematic daily intake was 4 months. The toxicogenic stage of acute poisoning was caused by a single dose of 50 ml of undiluted 13% 1.4-butanediol together with ethanol, manifested by convulsive syndrome, depression of consciousness to the level of coma II, acute respiratory failure with aspiration syndrome, respiratory acidosis (pH 7.22; partial pressure carbon dioxide 61.2 mm Hg), lactic acidosis up to 7 mmol / L, hyperammonemia up to 240 μmol / L, cerebral edema (decrease in white matter density to 21.6 ± 1.7 HU units), loss of vascular tone resistance (pareso arterioles) and a significant increase in cerebral blood flow rate to 115 ± 20.1 ml / 100 g per minute, increasing the volume of extracellular fluid (+ 130% of the proper volumes). Intensive therapy was complex, including infusion and detoxification therapy, correction of acid-base disorders, hypoxic disorders by using a substrate antihypoxant (Cytoflavin) in a daily dosage of 0.57 ml / kg body weight daily, for 9 days. The article discusses the toxicokinetics and toxicodynamics of 1.4-butanediol, radiation diagnostics and the clinical picture of acute poisoning, the features of its course, and pathogenetic approaches to therapy.Представлен случай острого перорального отравления 1,4-бутандиолом, осложнившегося развитием тяжелой гипоксии у пациента 34 лет, активно занимающегося бодибилдингом. Психоактивное вещество использовалось с целью повышения сексуальной активности и физической выносливости. Длительность систематического ежедневного приема составила 4 мес. Острое отравление возникло после однократного приема 50 мл неразведенного 13% 1,4-бутандиола вместе с этанолом, проявилось судорожным синдромом, угнетением сознания до уровня комы II, острой дыхательной недостаточностью с аспирационным синдромом, дыхательным ацидозом (pH 7,22; парциальное давление углекислоты 61,2 мм рт.ст.), лактатацидозом до 7 ммоль/л, гипераммониемией до 240 мкмоль/л, отеком головного мозга (снижение показателей плотности белого вещества до 21,6±1,7 ед. HU), утратой тонуса сосудистого сопротивления (парез артериол) и значительным повышением скорости церебрального кровотока до 115±20,1 мл/100 г в 1 мин, повышением объема внеклеточной жидкости (+130% от должных объемов). Интенсивная терапия носила комплексный характер и включала инфузионно-детоксикационную терапию, коррекцию нарушений кислотно-основного состояния, гипоксических расстройств путем применения субстратного антигипоксанта (Цитофлавин) в суточной дозировке 0,57 мл/кг массы тела ежедневно на протяжении 9 дней. Обсуждаются токсикокинетика и токсикодинамика 1,4–бутандиола, лучевая диагностика и клиническая картина острого отравления, особенности его течения, патогенетические подходы к терапии.

The article presents a case-report of delirium syndrome in a 29-year-old patient who systematically consumed 1.4-butanediol. Psychopathological symptoms developed in the toxicogenic phase and continued to increase during the first days of treatment, followed by transformation into a deliberate delirium and toxic nephropathy. Comprehensive treatment, including infusion-detoxification therapy, correction of acid-base and hypoxic disorders using cytoflavin, had a positive effect on the clinical course of poisoning and allowed for a favorable outcome of acute exogenous psychosis.Приведено наблюдение делириозного синдрома на фоне острого отравления у пациента 29 лет, систематически употреблявшего 1,4-бутандиол. Психопатологическая симптоматика развилась в токсикогенной фазе и продолжила нарастать в течение первых суток с последующей трансформацией в мусситирующий делирий и токсическую нефропатию. Проведенное лечение, включавшее инфузионно-детоксикационную терапию, коррекцию нарушений кислотно-основного состояния и гипоксических расстройств с применением цитофлавина, оказало положительное влияние на клиническое течение заболевания, что позволило обеспечить благоприятный исход острого экзогенного психоза.