title: [Sudden death from hypoglycemia].
abstract: 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.
authors.affiliation: Istituto di Clinica Oncologica e di Ricerca sui tumori, Università di Messina.
authors.forename: A
authors.initials: A
authors.lastname: Asmundo
authors.forename: M
authors.initials: M
authors.lastname: Aragona
authors.forename: P
authors.initials: P
authors.lastname: Gualniera
authors.forename: F
authors.initials: F
authors.lastname: Aragona
mesh_terms: D000293:Adolescent; D000313:Adrenal Medulla / Q000503:physiopathology; D000328:Adult; D001921:Brain / Q000473:pathology; D003645:Death, Sudden / Q000209:etiology* / Q000473:pathology; D005260:Female; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications / Q000473:pathology; D006984:Hypertrophy; D007003:Hypoglycemia / Q000401:mortality* / Q000473:pathology; D007223:Infant; D007231:Infant, Newborn; D007515:Islets of Langerhans / Q000473:pathology; D008099:Liver / Q000378:metabolism; D008297:Male; D009186:Myelin Sheath / Q000473:pathology; D009336:Necrosis; D009474:Neurons / Q000473:pathology; D010182:Pancreatic Diseases / Q000150:complications / Q000473:pathology