Acute barium poisoning is a rare but extremely dangerous type of poisoning in the structure of chemical injuries. The article provides a brief overview of the pathogenesis, clinical course and principles of intensive therapy of acute intoxication with this metal, as well as clinical examples of severe poisoning with barium salts with a negative and positive outcome in victims who used counterfeit barium carbonate instead of barium sulfate.

Acetic acid has a local cauterizing effect like coagulation necrosis and significant resorptive hemato-, nephro- and hepatotoxic effect due to hemolysis of erythrocytes, development of toxic coagulopathy, syndrome of disseminated intravascular coagulation. Developing severe hypoxia, microcirculation disorder, and impaired liver and kidney function significantly worsen proliferative processes in the area of chemical burn, leading to the development of such serious complications as late esophageal and gastric bleeding and cicatrical stenosis of the esophagus and stomach. Therefore, the prevention of these complications should include not only local treatment of the burn surface, but also complex therapy aimed at restoring the function of affected organs at the early hospital stage and rehabilitation stage. The article describes the case of practical application of an intensive care algorithm, which includes the use of microcirculation improvers, Cytoflavin — an antihypoxant on the basis of succinic acid, Actovegin — a stimulant of proliferation, prolonged use of glucocorticoids, active nutritional support with a protein-carbohydrate mixture, all initiated upon arrival.