[Case of death occurred after an injection of aetoxisclerol. The responsibility of the product should be discussed]. / L'aetoxisclerol accusé à tort d'entraîner une mort subite.

A 35-year-old woman has suffered from faintness with cardiovascular failure at the end of a sclerotherapy session for varix management. The injected product was Aeloxisclerol (DCI lauromacrogal 400). The death came up very quickly. The autopsy didn't reveal any traumatic lesion. The anaphylactic choc could be ruled out. Macroscopically, the heart showed a right ventricular dilatation. The toxicological analysis didn't reveal any medicinal substances. Histology showed the presence of lipid degeneration of all the right-ventricle wall The discussion is carried out on the role played by this previous health-state on the onset of death, and also on the incidence of sclerotherapy using this product. and the onset of death. We are carrying out this discussion by taking in mind the nature of the product injected and the information available in the literature concerning the lipid degeneration of cardiac muscle. Quickly after this case, the AFSSAPS (The French Agency for Sanitary Security of Health Products) has emitted an written alert which correlates with the requirements of principles of precaution although it is not founded on the totality of investigation results done for this medicolegal case.

An experimental study on hepatotoxicity of sclerosant ethanolamine oleate flowed into portal vein.

Although endoscopic injection sclerotherapy has been a main treatment option for gastroesophageal varices, intraportal inflow of the sclerosant, ethanolamine oleate, induce liver damage. The aim of this study was to clarify the liver damage due to intraportal inflow of ethanolamine oleate. Ethanolamine oleate suspension was injected into livers of male Wistar rats via the portal (ileocolic) vein. Degrees of liver damage were evaluated by serum levels of transaminases and by histological examination. Intraportal injection of ethanolamine oleate led to extensive liver necrosis, which was marked 1 day after the injection and recovered by 7 days after injection. Liver necrosis became severe as the dose of the injected sclerosant increased. Histologically, neither portal thrombosis nor embolism was evident. Carbon powder particles of India ink, which were injected together with ethanolamine oleate, reached and deposited in sinusoids of the necrotic portions of the liver. These findings suggested that the liver damage had not developed simply as a result of impairment of portal blood flow. Ethanolamine oleate may itself have direct hepatotoxic effects.