Leg massage by mother resulting in fatal pulmonary thromboembolism.

We report the sudden death of a 23-year-old male with hairline ankle fracture after massage of the leg by his mother. Autopsy confirmed the cause of death as pulmonary thromboembolism due to deep vein thrombosis of the leg veins which was dislodged and travelled to his lungs consequent to the leg massage. The treating doctors did not warn the patient of the risk of developing pulmonary thromboembolism.

Accidental selenium toxicosis in lambs.

Acute selenium toxicosis occurred in 3-week-old lambs after accidental over-supplementation by intramuscular injection and caused dyspnea, cyanosis, and sudden death. Pathological lesions included myocardial necrosis, skeletal muscle necrosis, pulmonary edema, hydrothorax, and hydropericardium.

Toxicose accidentelle au sélénium chez des agneaux. Une toxicose aiguë au sélénium s'est produite chez des agneaux âgés de 3 semaines après une supplémentation excédentaire accidentelle par injection intramusculaire et elle a causé des signes de dyspnée, de cyanose et de mort soudaine. Les lésions pathologiques incluaient une nécrose du myocarde, une nécrose du muscle squelettique, un œdème pulmonaire, de l'hydrothorax et de l'hydropéricarde.(Traduit par Isabelle Vallières).

Acute selenium toxicosis in polo ponies.

Just prior to an international polo event, 21 horses from one team exhibited clinical signs of central nervous system disturbance, hyperexcitability, sweating, ataxia, tachycardia, dyspnea, pyrexia, and rapid death. The suspected cause of this peracute onset of illness and death included intentional contamination of feed or iatrogenic administration of performance-enhancing drugs resulting in a severe adverse reaction. Six horses were submitted to the Bronson Animal Disease Diagnostic Laboratory for necropsy and toxicological examination. The clinical signs and sudden death, the similarity to earlier work by the lead author of selenium toxicosis in calves, as well as published reports, prompted investigators to focus on selenium testing. Sixty-four hours following receipt, the laboratory detected toxic selenium concentrations in the tissues of these animals. Following further investigation of the case by regulatory officials, it was determined that all affected horses had received an intravenous injection of a compounded "vitamin/mineral" supplement just prior to the onset of signs. The compounded supplement contained toxic levels of selenium. The present report illustrates the in-depth laboratory investigation of the cause of acute death in 6 polo ponies due to selenium toxicosis. In addition to solving this high profile case, the toxic levels of selenium found in livers (6.13 ± 0.31 mg/kg wet weight), kidneys (6.25 ± 0.3 mg/kg wet weight), and sera (1.50 ± 0.11 µg/ml) of these affected animals may provide important diagnostic criteria for future interpretations of selenium concentrations in tissues of horses.

Sudden death associated with myocardial contraction band necrosis in Boer goat kids.

Parenteral selenium (Se) and vitamin E (Vit E) were administered to all newborn kids at a Boer goat farm where there was previous high neonatal mortality assumed to be due to nutritional myopathy. All treated kids were affected by severe respiratory distress and died within 8 hours of Se/Vit E administration. Gross lesions included severe pulmonary edema, hydrothorax, and hydropericardium. The primary histopathologic finding was severe, acute, and monophasic myocardial contraction band necrosis. The diagnosis was accidental acute selenosis based on trace mineral analysis of the liver. This case highlights an important differential diagnosis in cases of acute myocardial contraction band necrosis and sudden death in goats and emphasizes the need for caution when administering parenteral Se/Vit E preparations.

Death and hypnosis: two remarkable cases.

The Journal of the American Medical Association reported The First Recorded Death in Hypnosis in its issue of October 27, 1894. Ninety-nine years later, on September 23, 1993 a healthy 24-year old mother of two was found dead at home, fully clothed and draped across the foot of one of her children's bed, 5 hours after volunteering as a subject for a stage hypnosis show. The suggestion given to terminate the trance had been that when the hypnotist said, "Goodnight", several subjects would feel 10,000 volts of electricity through the seat of their chairs. Unknown to the hypnotist, she had been phobic about electricity ever since a childhood shock, and would not even change a light bulb or plug in a cord. The coroner's verdict was death by natural causes.

[Death on a sauna stove]. / Verbrennung auf dem Saunaofen.

A 67-year-old woman noticed a strange smell from the cellar of her house. When she followed the smell, she found her 64-year-old husband with the face and upper part of his body lying on the stove of the private sauna. He was dead when the emergency doctor arrived. The autopsy revealed upper gastrointestinal bleeding from mucosal lesions in the esophagus with an agonal fall on the sauna stove as the cause of death. In addition, there were signs of chronic alcohol and drug abuse.

Hiponatremia sintomática secundaria a tratamiento conjunto anticomicial y antidepresivo: ¿riesgo de muerte súbita en epilepsia? / Symptomatic secondary hyponatremia due to combined treatment anticonvulsant and antidepressant: risk of sudden death in epilepsy?

La notable incidencia de epilepsia en nuestro medio, con la presencia, cada vez más frecuente, de refractariedad terapéutica, obliga a la politerapia anticomicial. Si partimos del hecho, de que muchas de las epilepsias tienen una base secundaria, con trastornos comportamentales asociados, podemos comprender la cada vez más habitual asociación entre fármacos anticomiciales y antidepresivos. Presentamos el caso clínico de una mujer de 37 años, afecta de epilepsia farmacorresistente asociada a síndrome depresivo exógeno, en tratamiento conjunto con Carbamacepina, Lamotrigina y Venlafaxina que sufre cuadro sincopal secundario a hiponatremia sintomática, cuya patogénesis radica en un mecanismo de secreción inadecuada de hormona antidiurética (SIADH). La relevancia de este caso radica en el hecho de que la hiponatremia generada por esta combinación farmacológica, hasta ahora, no ha sido descrita en la literatura. Esta anomalía electrolítica puede derivar en efectos secundarios neurológicos y cardiovasculares, en ocasiones tan relevantes, como para producir el fenómeno conocido como muerte súbita en el paciente epiléptico (SUDEP). Recomendamos, por ello, un estricto control iónico en aquellos pacientes en tratamiento conjunto anticomicial y antidepresivo, a fin de evitar episodios paroxísticos vasculares y minimizar el riesgo de SUDEP

The notable incidence of epilepsy in the general population, with the presence, more and more frequent of refractory therapeutic, it forces the anticonvulsant polytherapy. If we depart from the fact, that many of the epilepsies have a secondary cause, with affective disorders associate, we can understand the most habitual association of anticonvulsant and antidepressant. We present the clinical case of a 37-year-old-woman with refractory therapeutic epilepsy associated to exogenous depressive syndrome, in combined treatment with Carbamazepine, Lamotrigine and Venlafaxine, that suffers a episode of syncope secondary to symptomatic hyponatraemia, generated by syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The relevance of this case resides in the fact that the hyponatraemia generated by this pharmacological combination, up to now, it has not been described in the literature. This electrolytic anomaly can derive in secondary neurological and cardiovascular effects, in so outstanding occasions, as to produce the phenomenon denominated sudden death in the epileptic patient (SUDEP). We recommended a strict ionic control in those patients that require anti-epileptic and anti-depressant treatment combined, in order to avoiding paroxistic vascular episodes and to minimize the risk of SUDEP

Sudden death during worker transportation due to massive pulmonary thromboembolism: a case report.

This is a report on a 30-year-old black man who suddenly died in the worker transportation vehicle in which he had been quietly sitting for thirty minutes. No information about his medical or surgical history or any family history has been obtained. This case is intended to highlight the fact that forensic autopsy is a valuable tool to recognize the cause of death and that fatal pulmonary thromboembolism still remains a post-mortem diagnosis. In this case report, the autopsy found a fresh saddle pulmonary thromboembolus associated with partially organized thrombi of the inferior vena cava. Can a prolonged seated position encourage thrombus formation? We think that seat-related factors and especially patient-related factors intervene together in the development of thromboembolic events. In our medico-legal unit, having no means to search for these factors, we speculated on the various causes that could be involved in the occurrence of venous thromboembolism in our subject. We emphasize the importance of focusing research on genetic factors and the impact of traditional medicine in African people.

Sudden death from pituitary apoplexy in a patient presenting with an isolated sixth cranial nerve palsy.

A 68-year-old diabetic, hypertensive man presented with a left sixth cranial nerve palsy. MRI demonstrated an inhomogeneous sellar mass encroaching on the left cavernous sinus. Two days later, a left third cranial nerve palsy developed. Within 24 hours, the patient went into cardiac arrest and died. An autopsy showed hemorrhage within a pituitary macroadenoma ("pituitary apoplexy"). Pituitary apoplexy should be considered a cause of acute isolated sixth cranial nerve palsy and may represent a life-threatening emergency that can be averted with emergent hormonal replacement and hypophysectomy.

The structural basis of moderate disability after traumatic brain damage.

The objective was to discover the nature of brain damage in survivors of head injury who are left with moderate disability. Macroscopic and microscopic examination was carried out on the brains of 20 persons who had died long after a head injury that had been treated in a neurosurgical unit. All had become independent but had various disabilities (moderate disability on the Glasgow outcome scale) Most deaths had been sudden, which had led to their referral from forensic pathologists. Post-traumatic epilepsy was a feature in 75%. An intracranial haematoma had been evacuated in 75%, and in 11 of the 15 with epilepsy. Diffuse axonal injury was found in six patients, five of the mildest type (grade 1) and one of grade 2. No patient had diffuse thalamic damage but one had a small focal ischaemic lesion in the thalamus. No patient had severe ischaemic brain damage, but three had moderate lesions which were bilateral in only one. No patient had severe cortical contusions. In conclusion, the dominant lesion was focal damage from an evacuated intracranial haematoma. Severe diffuse damage was not found, with diffuse axonal injury only mild and thalamic damage in only one patient.

Delayed cerebral ischaemia: the pathological substrate.

Ischaemic complications both at the level of the cortex and the hypothalamus are well recognised after an aneurysmal subarachnoid haemorrhage. We have studied histological changes in the cortex (53 patients) and hypothalamus (48 patients) in patients who died after an aneurysmal subarachnoid haemorrhage. Cortical ischaemic lesions were demonstrated in 41 of the 53 patients studied. These changes were more common in patients who had impaired control of systemic blood pressure (p = 0.0004) and in patients who died gradually (p = 0.0003). Hypothalamic lesions were found in 24 of 48 patients studied; 23 of these patients had widespread associated changes in the cerebral cortex. Patients with moderate/severe cortical changes tended to have hypothalamic lesions and it was uncommon for patients with no cortical lesions to have changes in the hypothalamus (p = 0.0007). We believe that these histological changes are due to diffuse microangiopathy which develops slowly after a subarachnoid haemorrhage and affects the cortex and hypothalamus. Because the cortical lesions are widespread we postulate that they may be implicated in the aetiology of the well described psychosocial or cognitive problems in patients who survive a subarachnoid haemorrhage.

Clinical features of Kleine-Levin syndrome with localized encephalitis.

We report the clinico-pathological findings regarding a 9 year-old girl with some clinical features of Kleine-Levin syndrome who died suddently as a result of pulmonary embolism in the course of femoro-iliac thrombophlebitis. Neuropathological examination provided evidence of perivascular inflammatory infiltrates and microglial proliferation of nodular type located in the diencephalon and midbrain. These findings suggest that a localized encephalitis may be the underlying condition in Kleine-Levin syndrome.

[Analysis of 59 cases of non-traumatic sudden death in various neurological diseases].

Sudden death is a common complication of myocardial infarction, necrotic pancreatitis and other diseases. Physicians usually neglect the possibility of neurological disorders. 59 cases of sudden death among 314 autopsied cases with neurological diseases were analyzed. The most frequent cause of neurological sudden death was cerebrovascular disease (CVD). It was present in 53 (89.9%) cases. 48 of them had hemorrhagic CVD. 37 of these 48 cases were due to hypothalamic lesions. In 37 cases general autopsy was performed; pathological abnormalities of heart, lungs, stomach etc, were found in 28 of them. In conclusion, the size and location of the lesion correlated with the prognosis of the disease. Concomitant multiple organ damage may deteriorate the lesion. Awareness of sudden death resulting from CVD may elevate the rate of correct diagnosis.

[Morpho-biochemical study of catecholamine metabolism in the myocardium of dogs with fibrillation and autolysis]. / Morfobiokhimicheskoe issledovanie obmena katekholaminov v miokarde sobak pri fibrilliatsii i autolize.

The balance of catecholamines (CA) and their metabolites in the canine heart during myocardial fibrillation and 1, 2, 3, 4, 5, 6 hours after death was studied. The fibrillation was caused by low myocardial electrostimulation. The comparative neuro-morphometric analysis of the CA-containing structures in 1 and 5 min of the fibrillation and the determination of the norepinephrine, its precursors and metabolites by HPLC-ED method was done. There was an increase of the myocardial norepinephrine (20%), 3-4-dihydroxyphenylethyleneglycol (25%) and decrease of the dopamine (50%) contents without any qualitative changes of CA metabolism. Autolysis leads to the successive decrease of the norepinephrine and dopamine contents without any qualitative changes of the CA metabolism too. These data suggest that autopsies could be used for the determination of the myocardial CA content and the qualitative characteristics of the CA metabolism before death in those who died suddenly.

Membrane cerebral lipids in Rett syndrome.

The lipid membrane composition of cerebral tissue from 5 patients with classic Rett syndrome, ages 12-30 years, and from 14 age-matched controls was studied. The results demonstrated a selective loss of myelin-associated lipids and an enrichment of gangliosides in temporal white matter. The ganglioside pattern revealed an increase of astroglial cell-associated gangliosides and reduced proportions of gangliosides GD1a and GT1b. This latter finding may be crucial in synaptic function. The fatty acid compositions of ethanolamine phosphoglyceride, choline phosphoglyceride, and galactosylceramide were normal.

[Skin damage caused by fatal benzene fume inhalation]. / Hautschädigung bei tödlicher Benzindampfinhalation.

Two young men tried to stop a leaking patrol pipe of a private car in a workshop pit. One of them died from petrol-vapour-poisoning. Toxicological analyses by means of headspace gas chromatography permitted the identification of gasoline vapour. The other victim lost consciousness for a few hours and survived. By investigation of both victims alterations of skin were observed and interpreted as combustions with burns and blisters. Therefore the law-enforcement agency supposed an explosion or deflagration of gasoline vapour. In reality the experts on burnings could not gain any indication of an explosion and we proved the skin alterations to be a dermatotoxic effect of petrol.

[Heat thrombosis of burned skin]. / Zur Hitzethrombosierung verbrannter Haut.

The vital reaction to heat-induced thrombosis is discussed here using a case of sudden death in the Sauna. The dead body was lying for about one hour in the heat (90 degrees C). Beside the beginning formation of bubbles there was subcutaneous blood vessel exposition, especially in parts outside of the Livor mortis. The cause of death was viral infection with florid Myocarditis.