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Cases of ingesting button batteries by children are not common clinical situations in forensic medicine. Although it can be a cause of death when associated with digestive perforations, no cases of sudden death have been reported in the literature. We report the case of a 17-month-old girl who presented at home with haematemesis, followed by failed cardiopulmonary resuscitation. The child had been treated on two occasions for nasopharyngitis, 14 and 18 days prior to her death. The post-mortem scan revealed a radio-opaque foreign body in the oesophagus. The autopsy revealed the presence of a round button battery, 20 mm in diameter, blocking the lumen of the oesophagus in its upper third, associated with two parietal oesophageal ruptures opposite each other. There was limited digestive haemorrhage, but above all significant bronchial inhalation of blood. Toxicology analyses showed slightly increased blood levels of the heavy metals of which the battery was composed (lithium, chromium, manganese and molybdenum). The anatomopathological analyses confirmed the recent nature of these ruptures. Ingestions of button batteries localised at the level of the oesophagus are the cases linking to the highest risk of complications, particularly for batteries with a diameter of more than 20 mm and in children under the age of 4. The main difficulty in such clinical situations is identifying when the ingestion occurred, as more often than not, no witnesses are present. We discuss the advantages of anatomopathology and toxicology examinations targeted towards heavy metals in these forensic situations. [ABSTRACT FROM AUTHOR]

Cardiotoxicity is a rare, but well-recognized complication of treatments with the anti-cancer drug 5-fluorouracil (5FU). The underlying mechanism, however, is not fully elucidated. A spasm of the coronary arteries is often considered to be the leading cause of myocardial ischemia and decreased contractility associated with 5FU. As spasm cannot account for all reported adverse cardiac effects, the present study was undertaken to search for alternative mechanisms. Groups of six rabbits were given either a single intravenous dose of 50 mg/kg 5FU or four intravenous doses of 15 mg/kg 5FU at 7-day intervals. A third group served as control. The heart was removed shortly after death or scheduled sacrifice of the animals, to perform macroscopic and microscopic examinations of the heart and to evidence apoptosis by the TUNEL method. Following a single dose of 50 mg/kg 5FU, all animals rapidly developed a massive hemorrhagic myocardial infarct with spasms of the proximal coronary arteries. Repeated infusions of 15 mg/kg 5FU induced left ventricular hypertrophy, foci of myocardial necrosis, thickening of intra-myocardial arterioles, and disseminated apoptosis in myocardial cells of the epicardium, as well as endothelial cells of the distal coronary arteries. These results indicate that a spasm of the coronary arteries is not the only mechanism of 5FU cardiotoxicity, and that apoptosis of myocardial and endothelial cells can result in inflammatory lesions mimicking toxic myocarditis. [ABSTRACT FROM AUTHOR]