Entrapment and rupture of the guide wire during PTCA: case report and medico-legal considerations.

Background: In recent years, due to the increase of complaints for medical malpractice, the Sicilian Regional Health System has adopted proceedings for the direct management of claims by each healthcare facility with the aim of reducing costs of insurance premiums and their relative taxes. Thus this management has led to increased awareness and management of clinical risk through the introduction of mandatory sentinel event monitoring. Case report: A 55-year-old man with acute ischemic heart disease, due to three-vasal coronary diasease, underwent angioplasty perfomed on the second diagonal branch of the anterior descending artery. Simultaneously following the discovery of a major middle tract stenosis, he underwent further angioplasty surgery during which guidewire entrapment occurred, precisely in the proximal section of the vessel, resulting in the rupture and persistence of some fragments despite attempts to extract them. Subsequent antiplatelet therapy was prescribed and no further procedures were indicated for the removal of the guide wire, meanwhile a persistent reactive anxious-depressive state was established. Conclusion: The medico-legal analysis of the case excluded liabilty since it was a fortuitous, unpredictable and inevitable event. However, the patient had not been adequately informed about the possibility of the complication presented, which resulted in prolonged hospitalization and compensation for the psychological disorder suffered as a result of the adverse event. The attempted economic agreement was unsuccessful. A civil lawsuit was subsequently filed by the patient and the Judge's report confirmed the corporate CMC assessment and ruled out that the side effects related to the guideline fragment.

[Genetic polymorphisms (GSTT1 e GSTM1) and urinary excretion of t,t-muconic acid among refinery workers]. / Polimorfismi genetici (GSTT1 e GSTM1) ed escrezione urinaria di acido t,t-muconico in lavoratori di una raffineria.

Many xenobiotics agents are metabolized by enzymes mechanisms through Phase I, activating substances procancerogene through oxidative reactions, and / or through mechanisms Phase II, acting on metabolic intermediate products of oxidative processes with conjugation reactions with endogenous mediators, in order to generate hydrophilic products that can be easily excreted by the body. Among the enzymes Phase II is a heterogeneous group represented by glutathione S-transferase. Genetic polymorphisms encoding for these enzymes (GSTs) are responsible phenotypic expression of enzymes specifically involved in the detoxification and elimination of different genotoxic agents (IPA, toluene, benzene). Accordingly, the authors have investigated a population of subjects professionally exposed to benzene (used in active refining and storage of crude oil) in order to assess the genetic profile in relation to possible null genotype (responsible for the failure phenotypic expression of protein) of polymorphism GSTT1 and GSTM1 and correlate the impact that the genotype effect of normal metabolic pathway t, t-muconico.

[Sudden death from hypoglycemia]. / La morte improvvisa da ipoglicemia.

The sudden death by hypoglycemia is an aspect of the forensic pathology frequently neglected. Authors initially described the pathogenesis of different hypoglycemia forms, distinguishing the primary ones due to hyperinsulinism and the secondary ones due to functional insufficiency of other organs (hypophysis, thyroid, adrenal gland, liver); after that Authors described three cases of sudden death induced hypoglycemia by hyperinsulinism: two were unweaned with nesidioblastosis and one adolescent. In any form of hypoglycemia the central nervous system damage is present with evident neuronal degenerative-necrotic phenomena, widespread edema with microhemorrhage, swollen and dissociation of myelin sheath, glial cells hyperplasia. Death caused by primary hypoglycemia is histopathologically different from the secondary one because of the maintenance of hepatic glycogen content in the former, that increase in striated muscles, including the heart, in spite of the constant secretion of catecholamine from the adrenal medulla. Glycogen is depleted in secondary hypoglycemia. In the primary form, behind the adrenal medulla hyperfunction, the increased functional activity of the adrenal cortex is moderate, contrasting with the seriousness of the syndrome, due prevalently to inhibit the gluconeogenesis response conditioned by the persistence of stored glycogen in the liver, heart and striated muscles. The rare anoxic processes coming with resynthesis of hepatic glycogen have to be considered in the differential diagnosis. The primary hypoglycemic death, especially in unweaned, is frequently promoted by other processes inducing hypoxia (fetal asphyxia outcome, pneumonia, etc.) or worsening the hypoglycemia (hypothyroidism, etc.). The secondary hypoglycemias are characterized by the normality of exocrine pancreas and by organic alterations that cause glycogen depletion from the liver.