Search

Brugada syndrome is a congenital arrhythmogenic disease, characterized by alterations in sodium channels in the absence of structural myocardial changes. It leads to ventricular electrical instability, causing arrhythmias with high risk of sudden cardiac death. Patients affected by Brugada syndrome show electrocardiographic alterations either at baseline or after stimulation. Symptomatology and electrocardiographic alterations are the most important prognostic elements. The only effective treatment is the implantation of an automatic implantable cardioverter-defibrillator, which dramatically reduces arrhythmic mortality. This device is used only in symptomatic patients for abortive sudden cardiac death or syncope with electrocardiographic alterations, whereas in most patients just a careful follow-up is required. In this article we evaluate the medical-legal aspects of patients with Brugada syndrome, in forensic pathology, social insurance, private insurance, medical professional liability and ability to work. First of all, we analyze the question of medical professional liability, mostly in case of a wrong identification of prognostic factors. Then we consider the medical-legal evaluation of Brugada syndrome in the field of social insurance, in relation to the clinical picture and particularly to the frequency of arrhythmic events. As far as private insurance is concerned, we dwell upon patients' insurability in the various types of policies, refundable medical expenses and evaluation of pathology in health insurance. Finally, we discuss the question of ability to work, with special regard to armed forces and police, whose committees do not provide a specific evaluation for Brugada syndrome by making identical use of automatic implantable cardioverter-defibrillators and pacemakers, thus ignoring the great clinical differences between these two devices.

We studied the persistence of rigor mortis by using physical manipulation. We tested the mobility of the knee on 146 corpses kept under refrigeration at Torino's city mortuary at a constant temperature of +4 degrees C. We found a persistence of complete rigor lasting for 10 days in all the cadavers we kept under observation; and in one case, rigor lasted for 16 days. Between the 11th and the 17th days, a progressively increasing number of corpses showed a change from complete into partial rigor (characterized by partial bending of the articulation). After the 17th day, all the remaining corpses showed partial rigor and in the two cadavers that were kept under observation "à outrance" we found the absolute resolution of rigor mortis occurred on the 28th day. Our results prove that it is possible to find a persistence of rigor mortis that is much longer than the expected when environmental conditions resemble average outdoor winter temperatures in temperate zones. Therefore, this datum must be considered when a corpse is found in those environmental conditions so that when estimating the time of death, we are not misled by the long persistence of rigor mortis.

In 1984, 313 samples of imported liquid milk and 159 samples of imported cheese were checked for aflatoxin M1; 225 of the milk samples came from FR Germany and 88 from France, while 82 of the cheese samples came from France, 34 from FR Germany and 43 from the Netherlands. The number of positive samples was small both for German (13.8%) and for French (12.5%) milks, and the contamination levels were very low (maximum 23 ng/l). As regards the cheeses, aflatoxin M1 was detected in 19.5, 26.5 and 53.5% of the French, German and Dutch samples respectively, but only 2 French samples exceeded 250 ng/kg, the limit set by Swiss law. In 1985, two surveys were carried out on 276 milk samples mostly obtained from individual farms and on 416 cheese samples taken from all parts of the country. As regards the milk samples, 70 (25.3%) contained aflatoxin M1, but generally at very low levels; in fact only 7 (2.5%) of the samples exceeded 50 ng/l. Aflatoxin M1 was found in 130 (31.3%) of the cheese samples, but here again only 9 (2.2%) exceeded 250 ng/kg. There was no significant difference in aflatoxin M1 levels between Italian, German and French cheese samples but these were significantly lower (P less than 0.01) than in Dutch samples.