Acute selenium poisoning: suicide by ingestion

Selenium is a ubiquitous element in the environment essential to the human diet and widely utilized in industrial processes. Fatal human selenium intoxication is rare. The authors report a case in which investigators recovered a bottle of gun-bluing agent beside a 24-year-old man. He exhibited signs and symptoms typical of acute selenium intoxication presenting with nausea and vomiting, followed by pulmonary edema and rapid cardiovascular collapse approximately 3 to 4 h after ingestion. Classic electrocardiographic (EKG) changes, which have been reported to occur in acute selenium intoxication, included sinus tachycardia with ST wave alteration. Toxicological results confirmed elevated blood and tissue concentrations. The cause of death was ascribed to acute selenium intoxication, which ensued rapidly after oral consumption. The manner of death was suicide. This case report, which presents an overview of acute and chronic selenium poisoning, underscores the value of thorough toxicologic analyses of tissue and body fluids in humans.     

3-Methoxytyramine in the putamen as a gauge of the postmortem interval

The armamentarium of the forensic thanatologist includes the examiner's subjective assessment of bodily changes together with comprehensive evaluation of environmental and associated factors to estimate the postmortem interval (PMI). Of the various objective means, postmortem accumulation of potassium in vitreous humor is a widely used gauge. In view of the considerable variability inherent in these techniques, an additional marker with greater accuracy would be a welcome supplement to these indices. We have developed a method of estimating PMI from the level of 3-methoxytyramine (3-MT) in the dorsal putamen of the brain. The supernatant of a sample of putamen, sonicated in 6 volumes (weight/volume) of 0.1 M perchloric acid and centrifuged at 51 000 times gravity for 10 min, was analyzed for 3-MT using high-pressure liquid chromatography with electrochemical detection. The change of 3-MT in the putamen is linearly related to the PMI (range: 5.5 to 60 h), irrespective of patient age (1 to 84 years). This observation is attributable to several factors, including high substrate (dopamine) concentration, preservation of catechol-O-methyl transferase activity, and an inactivation of monoamine oxidase activity, as a result of a decrease in tissue pO2.     

Sudden Death Due To Acute Cocaine Toxicity—Excited Delirium in a Body Packer

Excited delirium denotes a life-threatening medical condition characterized by the acute onset of agitated and violent behavior that often results in a sudden and unexplained death. Cocaine-induced excited delirium refers to fatal cocaine intoxication with the following symptoms occurring sequentially: hyperthermia, delirium with agitation, respiratory arrest, and death. We present a case of cocaine-induced excited delirium in a cocaine “body packer” or a “mule”, specifically an individual who attempts to smuggle cocaine within the body. Investigators at the scene initially suspected homicide due to the victim's sharp and blunt force injuries. Three rubber packets containing cocaine were removed from the victim's rectum. Blood toxicological analysis revealed an alcohol concentration of 0.016 g/100 and cocaine >1 mg/L. The forensic pathologist should consider cocaine-induced excited delirium when an individual exhibits aggressive behavior, unexpected strength, and resistance to pain who dies suddenly. Further analysis should be performed during the scene investigation and autopsy for evidence of body packing.     

Comparison of chemical methods for determining postmortem interval

Accurate determination of postmortem interval (PMI) is a problem for the forensic thanatologist, especially in unwitnessed deaths. A number of objective chemical methods for determining PMI have been developed, the most widely used being accumulation of potassium in the vitreous humor. The authors previously have reported a chemical method for determining PMI from the predictable accumulation or clearance of the dopaminergic metabolite 3-methoxytyramine (3-MT) in the putamen of the brain. They have extended their previous study to compare directly the accuracy of determining PMI from the level of 3-MT in putamen with the level of potassium in vitreous humor. The data indicate that 3-MT is at least as accurate as, if not more accurate than, potassium accumulation in vitreous humor, although 3-MT levels can be affected by the cause of death and drugs present at the time of death. Nevertheless, determination of both the 3-MT and potassium levels can afford the most accurate method of determining PMI; preliminary nomograms for determining PMI from both variables are presented.     

Sudden and unexpected death from pituitary tumor apoplexy

Pituitary tumor apoplexy refers to a clinical syndrome precipitated by the expansion of a pituitary adenoma by hemorrhage or infarction. Individuals may present with myriad signs, including sudden onset of severe headache, visual changes, altered mental status, cranial nerve palsies, and hormonal dysfunction. This disorder constitutes a medical emergency and warrants an expedited evaluation, diagnosis, and treatment to prevent the potential sequelae of permanent visual loss, endocrine abnormalities, or death. We report a case of sudden death from undiagnosed pituitary tumor apoplexy. The decedent was evaluated by medical personnel on three occasions in the week prior to her death for severe headache, nausea, vomiting, and photophobia. Postmortem examination demonstrated a hemorrhagic infarction of a pituitary adenoma with necrosis and expansion out of the sella turcica. The recognition of and treatment for a patient with pituitary tumor apoplexy requires a rapid multidisciplinary effort. Failure of prompt diagnosis may be fatal and require a medico-legal death investigation for sudden and unexpected death.     

Iatrogenic catheter-related cardiac tamponade: a case report of fatal hydropericardium following subcutaneous implantation of a chemotherapeutic injection port

The need to obtain dependable access to the vascular system constitutes a significant component in the treatment and management of critically ill patients. Intravenous chemotherapy administered to cancer patients over an extended period of time often results in loss of peripheral vascular access due to vein sclerosis, "exhaustion" or tissue necrosis. Medical investigators have designed and steadily upgraded a variety of devices constructed to improve venous access for long-term utilization. As with the introduction of any foreign object into the body, each of these devices has complications which may be life threatening and occasionally fatal. We present an unusual case of iatrogenic acute hydropericardium and cardiac tamponade caused by the percutaneous infusion of chemotherapeutic fluid via a right subclavian central venous implant system (Port-a-Cath). Failure to implant and monitor the device with a radiograph following placement according to manufacturer's guidelines and accepted standards of medical practice were causally related to an unusual complication, namely, perforation of the right cardiac ventricle by the catheter tip, resulting in sudden and unexpected cardiac death.     

Sudden and unexpected death resulting from splenic artery aneurysm rupture: two case reports of pregnancy-related fatal rupture of splenic artery aneurysm

Rupture of a splenic artery aneurysm is a rare and usually catastrophic event, most commonly associated with pregnancy. In spite of increasingly common reliance on abdominal angiography, magnetic resonance imaging, and computerized tomography during the past quarter century, clinicians uncommonly recognize any of the various splanchnic arterial aneurysms absent premonitory signs or symptoms. Accordingly, rupture of a visceral aneurysm, including splenic artery aneurysm, typically presents as sudden, unexpected obtundation or death. As a consequence, the initial recognition and diagnosis of splenic artery aneurysm rupture take place only at autopsy. This report presents two such cases of sudden death resulting from splenic artery aneurysm in a pregnant woman and a postpartum woman, respectively.     

Sudden unexpected death in epilepsy: neuropathologic findings

Sudden unexpected death in epilepsy refers to sudden death of an individual with a clinical history of epilepsy, in whom a postmortem examination fails to uncover a gross anatomic, toxicologic, or environmental cause of death. Evidence of terminal seizure activity may not be present. One to two percent of natural deaths certified by the medicolegal death investigator are attributed to epilepsy. Detailed microscopic examination of the brain has increasingly afforded the identification of structural changes representative of epileptogenic foci. The authors present 70 cases of death attributed to sudden unexpected death in epilepsy. These cases were classified as follows: individuals who lacked a gross brain lesion, those who had a brain lesion demonstrable at autopsy, and those who lacked neuropathologic evaluation because of decomposition or because only an external examination was done. All of the subjects had a clinical history of seizures. The authors confirm that various microscopic findings, including neuronal clusters, increased perivascular oligodendroglia, gliosis, cystic gliotic lesions, decreased myelin, cerebellar Bergmann's gliosis, and folial atrophy, are present in a higher percentage of the brains of sudden unexpected death in epilepsy subjects than in the brains of age- and sex-matched control subjects.