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.     

Sudden death due to undiagnosed intracranial hemangiopericytoma

A previously healthy 9-year-old Japanese boy with a 4-day history of vomiting and headache died suddenly and unexpectedly. An external examination revealed no abnormalities other than foam around the mouth and nose. An internal examination revealed severe pulmonary edema and hemorrhagic hemangiopericytoma arising from the choroid plexus of the right lateral ventricle. The cause of death was thought to be neurogenic pulmonary edema caused by the rapid growth of a hemangiopericytoma, with intratumoral hemorrhage.     

Sevoflurane concentrations in blood, brain, and lung after sevoflurane-induced death

Sevoflurane concentrations in blood, brain, and lung were measured in an individual apparently dying from sevoflurane inhalation. Sevoflurane is a volatile nonflammable fluorinated methyl isopropyl ether inhaled anesthetic, chemically related to desflurane and isoflurane. The incidence of abuse of sevoflurane is lower than that of other drugs of abuse possibly due to its inaccessibility to the general public and less pleasurable and addicting effects. The dead subject was an anesthetist found prone in bed holding an empty bottle of sevoflurane (Ultane). Serum, urine, and liver were screened for numerous drugs and metabolites using enzyme immunoassays and gas chromatography-mass spectrometry. Analysis did not reveal presence of any drug, including ethanol, other than sevoflurane. Sevoflurane was determined by headspace gas chromatography and revealed concentrations of 15 microg/mL in blood and 130 mg/kg in brain and lung. Autopsy revealed pulmonary edema and frothing in the lung, pathological findings associated with death by sevoflurane or hypoxia. The cause of death was ruled as sevoflurane toxicity and the manner of death as accident.     

Methamphetamine body packer: acute poisoning death due to massive leaking of methamphetamine

We encountered three methamphetamine (MA) body packers presenting simultaneously, one of whom died. Three Nigerian men (39, 35, and 37 years old) who attempted to smuggle were found to contain 35 (498 g), 21 (292 g), and 5 packages (73 g) of methamphetamine hydrochloride (MA-HCl) in their stomachs, respectively. Packages were wrapped with plastic film and Scotch tape. The 39-year-old man died with acute poisoning from c. 20 g of MA-HCl that had leaked from the packages into the stomach. His plasma MA concentration was 8.6 microg/mL when he was hospitalized (17 h before his death). Autopsy findings showed extreme pulmonary congestion and edema as well as moderate hepatic edema and several petechiae. Quantitative analysis was performed by gas chromatography/mass spectrometry. Extremely high concentrations of MA and its metabolite amphetamine (AP) were found in cardiac blood (63.5 microg/mL and 1.2 microg/mL), urine (4,518 microg/mL and 72.4 microg/mL), gastric contents (8,490 microg/mL and 16.9 microg/mL), and in all other autopsy samples. These high concentrations confirmed that the cause of death was acute MA poisoning. Furthermore, impurity-profiling analysis of the seized MA revealed that the MA smuggled by the three suspects originated from the same batch.     

Report of a fatal, acute tripelennamine intoxication.

A death resulting from tripelennamine overdose in a 19-year-old male Caucasian is reported. The patient died 7 h after ingesting approximately twenty 50-mg tripelennamine tablets. A concentration of 1.0 mg/100 ml was found in the blood. All tissue concentrations were measured by ultraviolet spectroscopy and verified by gas-liquid chromatography. Significant findings included pulmonary edema and multiple small petechial hemorrhages in the soft tissue of the scalp.     

Forensic evaluation of sudden death due to tuberculosis

Abstract:  The emergence of drug-resistant tuberculosis (TB) poses a major threat to TB control efforts. We report a case of a 50-year-old man with pulmonary TB. The scene investigation had initially suspected for homicide; however, the result of medico-legal autopsy demonstrated natural cause of death. Statistical data suggest that the rates of national mortality by respiratory TB decreased in the last decades in Hungary; however, an increasing TB mortality was detected in the capital Budapest. Facing a new mortality trend in TB, the forensic scene investigation and determination of manner of death represent new challenges for practitioners.     

Postmortem investigation of lamotrigine concentrations

Lamotrigine is a relatively new anticonvulsant. Therapeutic plasma concentrations generally range from 1 to 4 mg/L, although several studies have shown that good control of epilepsy has been achieved with concentrations reaching 10 mg/L generally, with little toxicity. In overdose, however, the drug has been linked to ECG changes that may suggest a possible arrythmogenic effect and hence cardiac toxicity. Lamotrigine has also been shown to cause encephalopathy and thus neurotoxicity. There is no information concerning postmortem lamotrigine concentrations and their interpretation. We describe lamotrigine concentrations in postmortem specimens including blood, liver, bile, vitreous humour, and urine from eight cases. A high performance liquid chromatography (HPLC) method is described with extraction procedures for the various tissues. Two possible groups were identified. The first being the "broader therapeutic" group with blood concentrations ranging from 0.9 to 7.2 mg/L and corresponding liver concentrations ranging from 16 to 36 mg/kg. The second being a "supratherapeutic" group with blood concentrations ranging from 20 to 39 mg/L and corresponding liver concentrations ranging from 53 to 350 mg/kg. Although none of the eight cases described were attributed to overdose by lamotrigine alone, the cause of death for one of the three cases in the "supratherapeutic" group was given as mixed drug toxicity. Cause of death for the remaining two cases in this group was reported as epilepsy. However, both these cases showed elevated concentrations of lamotrigine and both were co-medicated with valproic acid. Such co-administration has been shown in the literature to lead to elevated lamotrigine concentrations and a reduction in lamotrigine dose has been recommended. With such data, we highlight the importance of monitoring lamotrigine concentrations in cases co-medicated, particularly with valproic acid.     

Acute epiglottitis (supraglottitis)

During an autopsy the clinician, as well as the pathologist, should insist on a culture and adequate examination of the neck. Failure to examine the neck structures in this catastrophic illness may result in an incorrect determination of the cause of death [12,13]. Many autopsy surgeons assume pneumonia is present but later find only microscopic evidence of pulmonary edema. By then the decedent has been buried. Untreated fatalities are seldom reported [3,5,14]. Future reports should include statistics from the medical examiner's or coroner's office in their jurisdiction. This will promote knowledge of the true incidence of acute epiglottitis.     

Ecstasy and suicide

Deaths due to the ring-derivative amphetamines are not common and are usually accidental involving dehydration and hyperthermia. Suicides from 3,4-methylenedioxymethamphetamine (MDMA) and related ring-derivative amphetamines overdose are rare. A 15-year-old female who had a history of depression and previous suicide attempts was found dead with a suicide note. Toxicology demonstrated lethal serum concentrations of MDMA (9.3 mg/L), with 34 mg/kg of MDMA in the liver, 2.4 mg/L in the urine, and 530 mg/kg in the stomach. The cause of death was MDMA toxicity, the manner suicide. While MDMA may be detected in victims in other drug-related or traumatic deaths, it is only rarely used in isolation in suicide, with a predominance in the 21- to 25-year-old range. Despite the rarity of such events, the possibility of a nonaccidental manner of death should be considered when high levels of MDMA and associated amphetamines are found at autopsy.     

Fatal acute alcohol intoxication in an ALDH2 heterozygote: a case report

On an evening in November, a 25-year-old man was found dead in his bedroom. There were many empty snap-out sheets for flunitrazepam tablets in the trash at his bedside. He had been beaten by a gang of young people earlier in the morning of the same day. At the medico-legal autopsy, although there were many bruises and/or abrasions on the whole body, only slight subdural hemorrhage was observed, and none of them was thought to be the cause of death. Flunitrazepam and its metabolites were not detected in his body fluid by gas chromatography-mass spectrometry (GC-MS). Marked lung edema and a severe congestion of organs were observed. His blood alcohol concentration from the femoral vein was 2.00 mg/ml. Fatal cases of acute alcohol intoxication usually have shown higher alcohol concentration (2.25-6.23 mg/ml). Although the genotype of aldehyde dehydrogenase 2 (ALDH2) has not previously been mentioned as a contributing factor in determining the cause of death, in this case the genotype of ALDH2 was ALDH2*1/2 and thus is important. Those who possess the ALDH2*2 gene show high concentrations of acetaldehyde (AcH) at even comparatively lower alcohol levels. Consequently, the cause of death was considered to be acute alcohol intoxication including AcH poisoning.     

Ascertainment of the cause and tempo of death in forensic medical practice

In order to develop a method of ascertaining a cause of death and of evaluating its tempo the authors undertook a histological study and a study of a dehydration degree in 76 cases of death due to the below reasons: mechanical trauma, mechanical asphyxia, burn shock, and carbon monoxide intoxication. Acute emphysema of lungs, lack of edemas in lungs and brain, desquamation of pulmonary macrophages, hyperemia of renal capillaries, primary urine in some glomerules, prevalence of ischemic changes with karyopyknosis in medulla and hypohydration of brain were typical of fast death. Prevalence of dystelectasis in lungs, emptying of pulmonary capillaries, evident edema of lungs and brain, desquamation of pulmonary macrophages, lack of primary urine in glomerular capsules, acute circulatory disorders of renal hemodynamics with sweating of fibrin and erythrocyte glomerules into cavities, necrotic nephrosis, pigment cylinders in renal tubules, thrombi in vessels, prevalence of chromatolysis, karyolysis and cytolysis in medulla, pronounced glial reaction as well as pronounced edema of brain and its hyperhydration were typical of slow death.     

Fatal acute selenium toxicity

Selenium is used widely in industry and as a dietary supplement. Reports of acute selenium toxicity are infrequent, however, and the relationship of toxicity to selenium concentrations in blood and tissues has not been established. We describe a patient who died eight days after ingesting selenious acid in the form of gun blueing. The patient's clinical course demonstrated many of the features of inorganic selenium toxicity described in animals; hypotension as a result of both vasodilation and decreased cardiac output, adult respiratory distress syndrome, severe myopathy which contributed to respiratory failure, and a garlicky odor to the breath. Four days after ingestion the serum selenium concentration was twenty times normal and urinary excretion seventy times normal. Postmortem tissue selenium concentrations were up to 40 times normal.     

Postmortem Diagnosis of Fatal Hypothermia by Fourier Transform Infrared Spectroscopic Analysis of Edema Fluid in Formalin-Fixed,Paraffin-Embedded Lung Tissues

The goal of this study was to investigate whether pulmonary edema could become a specific diagnostic marker for fatal hypothermia using Fourier transform infrared (FTIR) spectroscopy in combination with chemometrics. The spectral profile analysis indicated that hypothermia fatalities associated with pulmonary edema fluid contained more β-sheet protein conformational structures than the control causes of death, which included sudden cardiac death, brain injury, cerebrovascular disease, mechanical asphyxiation, intoxication, and drowning. Subsequently, the results of principal component analysis (PCA) further revealed that the content of β-sheet protein conformational structures in the pulmonary edema fluid was the main discriminatory marker between fatal hypothermia and the other causes of death. Ultimately, a robust postmortem diagnostic model for fatal hypothermia using a partial least-squares discriminant analysis (PLS-DA) algorithm was constructed. Pulmonary edema fluid spectra collected from eight new forensic autopsy cases that did not participate in the construction of the diagnostic model were predicted using the model. The results showed the causes of death of all these eight cases were correctly classified. In conclusion, this preliminary study demonstrates that FTIR spectroscopy in combination with chemometrics could be a promising approach for the postmortem diagnosis of fatal hypothermia.     

Investigations on the cause of death in a polytoxicomanic patient treated with wires and intermaxillary fixation for a chronic, infected mandibular fracture

The case of a 36-year-old male and former patient is presented who died for initially unknown reasons, with intermaxillary wire fixation for the treatment of an infected mandibular fracture still in place. The combined investigation of forensic experts and maxillofacial surgeons excluded aspiration and asphyxia as cause of death. Evidence was found for lethal methadone concentrations after intravenous drug abuse and a broncho pneumonia. Despite the clear evidence of a fatal intoxication in this case, caution must be exercised when dealing with individuals carrying intermaxillary fixation.     

Sudden death as a complication of bacterial endocarditis

Three cases are reported to demonstrate the range of possible lesions and wide variation in lethal mechanisms that may be found in cases of unexpected death subsequently shown to be due to bacterial endocarditis. Case 1: A 36-year-old man was found dead on his bedroom floor surrounded by drug paraphernalia. At autopsy, acute myocardial ischemia was present caused by coronary artery ostial occlusion complicating acute bacterial endocarditis of the aortic valve. Case 2: A 54-year-old man with chronic renal failure was found dead in bed at home. At autopsy, a left middle cerebral artery territory cerebral infarct was present due to septic embolization from bacterial endocarditis involving the aortic valve. Case 3: A 23-year-old man was found collapsed in a pool of blood. At autopsy, upper airway hemorrhage from an arteriobronchial fistula was present caused by septic pulmonary infarction from previous endocarditis of a congenital ventricular septal defect. This report demonstrates that bacterial endocarditis may still be a cause of sudden and unexpected death presenting to forensic mortuaries and that the underlying mechanisms may involve complex sequences of pathological changes that compromise vascular function.     

Pulmonary embolization by chorionic villi causing maternal death after a car crash

Throughout the last century, there has been a marked decline in obstetric maternal deaths, resulting in an increase in the proportion of nonobstetric deaths among pregnant women. Trauma, in particular, has become a leading cause of maternal death. We report the case of a 20-year-old primigravid woman who was involved in a motor vehicle crash at 36 weeks gestation. The woman developed abruptio placentae, followed by disseminated intravascular coagulation, adult respiratory distress syndrome, and shock, and died the day after the crash. Widespread pulmonary embolization by chorionic villi was identified at autopsy. This report discusses traumatic maternal deaths, with emphasis on the differences in injury pattern observed in pregnant trauma victims in comparison with other adults. It is important that the pathologist be aware of these problems so that an accurate cause of death can be identified in cases of maternal death after trauma. Also discussed is the relationship between trauma and placental abruption and the mechanism of death in the patient. To the authors' knowledge, this is the first reported case of extensive embolism of chorionic villi to the lungs after trauma.     

The trials of Steven Truscott.

Determination of time of death (postmortem interval) is one of the most difficult problems confronting forensic pathologists. One noteworthy such case is that of Steven Truscott, a 14-year-old Canadian youth who was convicted of the June 1959 rape-murder of 12-year-old Lynne Harper in rural southwestern Ontario. The two had been seen together on the evening when Lynne was last seen alive. At her autopsy approximately 48 h later, the prosecutor, relying almost entirely on examination of the gastric contents, placed the time of death during the period in which the two were apparently in each other's company. Truscott's defense was unable to refute this opinion, and Truscott was sentenced first to death, then to life imprisonment. Isabel LeBourdais, a Canadian journalist, published a book defending Truscott that eventually led to a judicial rehearing, but his conviction was upheld. The examination of gastric contents is only one measure employed in the often difficult determination of time of death. It has not been made inherently more reliable in this regard since 1959. It is crucial, therefore, to use all available evidence in determining time of death.     

An Autopsy Case of Sudden Unexplained Death Caused by Malaria*

Abstract: Sudden unexplained deaths, especially those unwitnessed can lead to forensic issues and would necessitate the need for a meticulous and complete postmortem examination including ancillary investigations to discover the cause of death. We herein report a case of sudden unexplained death caused by malaria in an apparently healthy individual. This fatal case is presented to remind the forensic pathologist of the possibility of malaria as a cause of sudden unexplained death in malaria‐endemic regions. In the present case, histopathological examination demonstrated the presence of parasitized red blood cells with malarial pigment in the blood capillaries in the brain, myocardium, pericardium, lungs, kidneys, liver, and the spleen. Cerebral malaria with acute renal insufficiency or pulmonary edema with an acute respiratory distress syndrome might have been the cause of death.     

The Importance of Microscopic Examination of the Lungs in Decedents with Sustained Central Intravascular Catheters: A Nine‐Case Series

Indwelling intravascular catheters provide convenient access to healthcare personnel and also recreational intravenous drug users who inject suspensions of oral medications. A nine‐case series of autopsies of clinically stable decedents with indwelling catheters and sudden death is herein presented. Pulmonary histologic findings were consistent with intravenous administration of oral medications in all cases. In eight, the mechanism of death was directly attributed to occlusive vascular embolization of foreign material, with or without contribution of acute drug toxicity. In one, the mechanism of death was solely attributed to acute drug toxicity. Acute, massive embolization of foreign material may explain sudden death by vascular obstruction, whereas chronic repeated injections lead to obliteration of the pulmonary vasculature, increased pulmonary vascular resistance, and cardiac failure. Therefore, a complete autopsy with histologic examination of the lungs and toxicology testing is recommended in patients with indwelling catheters to determine the cause and mechanism of death.