Lethal Bentazone Intoxication – A Report of Two Cases

This study presents two cases of lethal bentazone poisonings, their clinical presentation, the course of the disease and the autopsy findings. The first is a 50‐year‐old male who had sprayed corn with a solution of bentazone and was admitted to the hospital with sweating, fever, nausea, vomiting of aqueous and hemorrhagic content, and bloody, watery stools. He was treated according to the symptoms including extracorporeal hemodialysis, but eventually suffered from multiorgan failure (acute respiratory failure, acute liver failure, coagulopathy, acute renal failure, metabolic acidosis, and gastrointestinal bleeding) and died 11.35 h after admittance. The cause of death was probable bentazone intoxication. The second case, also a male, aged 49 who committed suicide by ingesting a bentazone solution. He was transferred to the hospital prostrated and cyanotic and died 14.15 h after admittance despite all efforts by the hospital staff. The cause of death was acute bentazone intoxication.     

Variable Presentations of Lethal Colloid Cysts

Four cases of colloid cysts that led to death are reported to demonstrate their nonspecific and protean presentations at autopsy: a 27‐year‐old man with severe occipital headache, blurred vision, drowsiness and vomiting; a 44‐year‐old man with recent memory disturbance; a 54‐year‐old man with head and neck pains, tiredness, urinary incontinence, confusion, and drowsiness; and a 66‐year‐old man with severe frontal headache, gait disturbance, vomiting, and syncope with a previous episode of confusion and disorientation. Each death was due to an occult colloid cyst obstructing the foramen of Monro causing acute hydrocephalus. Nonspecific manifestations may mean that the diagnosis of colloid cyst is only made at the time of autopsy. The possibility of rare cases being familial may necessitate medical review of family members. Forensic evaluation should identify how a colloid cyst was related to the mechanism of death and whether there are any features that were associated with precipitate decline.     

Subaortic Pseudoaneurysm of the Left Ventricle Complicating Staphyloccal Endocarditis*

Abstract: Subaortic pseudoaneurysms are rare but can be a cause of sudden death in young individuals. This case report involves a 20‐year‐old Vietnamese male who died suddenly from rupture of a subaortic pseudoaneurysm with resultant hemopericardium with tamponade. He had a history of bicuspid aortic valve with recent but healed Staphylococcal endocarditis. A review of the literature reveals few similar cases and enlightens the association between aortic bicuspid valve, endocarditis, and subvalvular aortic aneurysm. The pathogenesis as well as recent studies that identified aneurysm predisposing genes in patients with bicuspid aortic valve will be discussed.     

Medium‐Chain Acyl‐CoA Dehydrogenase Deficiency in Adulthood: A Potential Diagnosis in a Patient with Mental Status Changes Suspected of Drug Toxicity

Medium‐chain acyl‐CoA dehydrogenase (MCAD) deficiency is a rare but important component of the differential diagnosis for adults with a history of premortem mental status changes and the postmortem finding of hepatic steatosis. This case report describes a 30‐year‐old white man who, following a period of nausea and vomiting, was admitted to the hospital with sudden mental status deterioration followed rapidly by clinical deterioration and death. Treating physicians in this case suspected acute illicit drug toxicity with synthetic cathinones based on social history. Clinicians and medical examiners should be aware that the presentation, signs, and symptoms described may indicate an underlying inborn error of metabolism such as MCAD deficiency and take action accordingly.     

Ketoacidosis and Adrenocortical Insufficiency

We herein report an autopsy case involving a 27‐year‐old Caucasian woman suffering from chronic adrenocortical insufficiency with a background of a polyendocrine disorder. Postmortem biochemistry revealed pathologically decreased aldosterone, cortisol, and dehydroepiandrosterone levels in postmortem serum from femoral blood as well as decreased cortisol and 17‐hydroxycorticosteroid in urine. Decreased vitreous sodium and increased 3‐beta‐hydroxybutyrate and C‐reactive protein concentrations were observed. The cause of death was determined to be acute adrenocortical insufficiency. Fasting ketoacidosis was postulated to have precipitated the Addisonian crisis. Traumatic causes of death and third‐party involvement were excluded. The case highlights the importance of systematically performing exhaustive postmortem biochemical investigations to formulate appropriate hypothesis regarding the pathophysiological mechanisms involved in the death process.     

Forensic Analysis Reveals Acute Decompensation of Chronic Heart Failure in a 3500‐Year‐Old Egyptian Dignitary

Naturally preserved and embalmed bodies from archeological contexts represent a powerful source of information for forensic investigators. They allow one to ascertain pathology, cause of death, to enhance diagnostic methodology, and to improve the analysis of altered remains. We investigated the complete head and lung remnants of a 3,500‐year‐old Egyptian dignitary by radiological, microscopic, and genetic approaches. The individual, a middle‐aged male, suffered from severe periodontitis, mild atherosclerosis, and experienced cardiogenic pulmonary insufficiency with recurrent mini‐bleeds and pulmonary edema. Histology and ancient DNA analyses excluded the presence of Mycobacterium tuberculosis or of any other pathogenic species. Based on our collection of evidence, we propose that acute decompensation complicating chronic cardiac insufficiency was the likely cause of death. The underlying causes for this failure remain unknown although chronic hypertension appears to be the most likely candidate. Our finding represents the earliest reported case of chronic heart failure in ancient mummies.     

Fatal Injury Caused by a Ram (Ovis Aries) Attack

Animal‐inflicted injuries to humans are a major public health problem around the world resulting in great morbidity, money loss, and mortality. They are related to wild and domestic animals alike. Animals can cause injuries by various mechanisms—biting, stinging, crushing, goring, stomping, butting, kicking, pecking, etc. We present a case of a ram's attack with fatal consequences. A 4‐year‐old, 120 kg jezersko‐sol?ava breed ram with prior history of aggressive behavior inflicted multiple injuries to his 83‐year‐old owner, who died in the hospital a few hours later due to severe blunt force injuries sustained in the attack. The autopsy revealed the cause of death to be multiple injuries of the thorax and the head. Sheep, even though they are not considered aggressive or large farm animals such as cattle and horses, can inflict serious injuries with devastating results.     

Acute Bacterial Meningitis with Coincident Methamphetamine Use: A Case Report and Review of the Literature

Methamphetamine is a synthetic stimulant that can adversely affect the central nervous system and the immune system. Through various mechanisms, methamphetamine is toxic to neurons, endothelial cells, lymphocytes, granulocytes, and macrophages resulting in systemic damage. Reported is the sudden demise of an otherwise healthy 31‐year‐old woman with a history of stimulant abuse. At autopsy, acute bacterial meningitis was identified. Microbiology cultures grew a single isolate of Streptococcus pneumoniae. Toxicology was positive for amphetamine (0.13 mg/L) and methamphetamine (0.8 mg/L). The cause of death was classified as acute bacterial meningitis with methamphetamine use. Either the acute bacterial meningitis or the methamphetamine toxicity would have been sufficient to result in death; however, the concurrent pathophysiology of the two entities must be understood. A review of the current literature assesses the mechanisms of injury attributed to acute and chronic methamphetamine use, bacterial meningitis, and the synergy between the two.     

Driving Under the Influence of Synthetic Cannabinoid Receptor Agonist XLR‐11

The case of a 22‐year‐old male Caucasian driver is presented. He was involved in a traffic collision. At the roadside, he displayed blank stare and mellow speech with a barely audible voice. A DRE found low body temperature, rigid muscle tone, normal pulse, lack of horizontal and vertical gaze nystagmus, nonconvergence of the eyes, dilated pupil size, and normal Pupillary reaction to light. A standard toxicology DUID protocol was performed on the driver's whole blood including ELISA and GC‐MS drug screens with negative results. Additional drug screening was undertaken for bath salts and synthetic cannabinoid receptor agonists by LC‐MS/MS by a commercial laboratory and identified the synthetic cannabinoid receptor agonist XLR‐11 in the driver's blood. XLR‐11 was subsequently quantified at 1.34 ng/mL. This is the first documented case involving a driver operating a motor vehicle under the influence of the synthetic cannabinoid receptor agonist XLR‐11.     

Carbon Monoxide Poisoning and Death in a Large Enclosed Ventilated Area

A 55‐year‐old man with a medical history of tobacco use suddenly collapsed while power washing an empty indoor pool in a hotel. The decedent was transported to the local hospital where he was pronounced. A postmortem examination revealed atherosclerotic heart disease and bilateral pulmonary edema and congestion. A postmortem blood carbon monoxide (CO) level was 27% saturation, and a CO performed on hospital admission blood was 49% saturation. CO poisoning is a common cause of toxicological morbidity and mortality in the United States. The circumstances most often occur in an enclosed environment and may be intentional or unintentional. CO poisoning has been reported in open, well‐ventilated spaces, but rarely results in death. A warning label was present on the engine clearly stating the dangers of CO emission. However, there was a false sense of security due to the large size of the pool room and the presence of industrial blowers that were being used for ventilation.     

Metal Railing Fences and Accidental Death

Two cases of accidental deaths caused by the sharp ends of fence or gate posts are reported. Case 1: A 47‐year‐old man was found hanging by his ankle in an inverted position on fencing. He had attempted a shortcut to a railway platform by climbing over a metal rail fence. He had slipped and been impaled through his ankle by the sharp end of the fence post, resulting in death from positional asphyxia. Case 2: An 18‐year‐old male slipped while climbing over a gate and died after being impaled on a spear tip finial, which had lacerated his external iliac vein. Death was due to exsanguination. These cases demonstrate two rare examples of accidental deaths from impalement by the ends of sharp fence posts. Mechanisms of death in such circumstances involve suspension with positional asphyxia and vascular injury with exsanguination.     

The Biological Effects of Kambo: Is There a Relationship Between its Administration and Sudden Death?

Kambo is a substance obtained from the skin secretions of a frog, Phyllomedusa bicolor, popular in the Amazon region, which is administered via the transdermal route. We report a case of 42‐year‐old man found dead in his house. Near the corpse, a plastic box labeled as “Kambo sticks” was found. The man was a chronic consumer of Kambo and no previous pathology or genetic disease emerged in clinical history from the declaration of his general practitioner. Autopsy investigations and toxicological analysis were performed. The histopathological examination showed left ventricular hypertrophy. Toxicological screening was negative for ethanol and other drugs. Phyllocaerulein, phyllokinin, and deltorphin A were isolated from the Kambo sticks but, only deltorphin A was detected in blood sample. We describe the first forensic case of death associated with Kambo administration. We attempt to explain how its use could be related to the cause of sudden death in this case.     

A Fatal Leopard Attack

Abstract: A rare case of a big cat fatal attack is presented. A male leopard that had escaped from its unlocked cage attacked a 26‐year‐old male zoo worker. The man sustained penetrating injuries to the neck with consequent external bleeding. The man died while being transported to the hospital as a result of the injuries sustained. The wounds discovered on the victim’s body corresponded with the known methods of leopard attacks and with findings on the carcasses of animals killed by leopards in the wild. The conclusion of the medicolegal investigation was that the underlying cause of death was a bite wound to the neck which lacerated the left internal jugular vein, the two main branches of the left external carotid artery, and the cervical spine. The cause of death was massive external bleeding. Special attention is paid to the general pattern of injuries sustained from big cat attacks.     

Sudden Death from Cardiopulmonary Arrest on Arrival of a Patient with Pulmonary Tuberculosis: A Case Diagnosed by Postmortem CT and Autopsy

Sudden death due to massive hemoptysis during management of tuberculosis occurs in a considerable number of patients. However, when massive airway hemorrhage occurs in a patient in whom tuberculosis has not been confirmed and a blood is not apparent externally on the face/body, it is difficult to immediately identify the cause of death as airway obstruction by tuberculous bleeding in the airway. We encountered an 83‐year‐old Japanese woman with her medical history included treatment of tuberculosis in her 20s who was in cardiopulmonary arrest on arrival (CPAOA), and the cause of sudden death could not initially be identified. Postmortem CT (PMCT) and autopsy revealed that the cause of sudden death was airway obstruction/asphyxia by tuberculous massive airway hemorrhage. Identification of the cause of death facilitated a subsequent active contact investigation and led to prevention of secondary tuberculosis infection.     

Left Ventricular Aneurysm: Sudden Unexpected Deaths in a 29‐Year‐Old Man

Left ventricular aneurysm (LVA) is an abnormal dilated heart structure, either congenital or acquired. LVA is a rare cardiac condition with no symptoms in most cases, thus occasionally diagnosed during investigations of other diseases. Its association with certain cardiac complications and sudden cardiac deaths has been reported. However, its role as a cause of sudden unexpected death is rare. The author reported a sudden cardiac death in a 29‐year‐old man with LVA. Without a significant coronary artery disease and known etiologies of LVA, such an abnormal heart structure in the present case was considered congenital LVA. As no other possible mechanisms of death could be identified other than LVA with its associated pathologic lesions, mural thrombi, and dilated cardiomegaly, his death was attributable to fatal cardiac arrhythmia (most commonly ventricular tachycardia) secondary to LVA.     

Sudden Death Due to Undiagnosed Rheumatic Heart Disease in a Child

We report the case of a 5‐year‐old boy who died from complications of rheumatic heart disease with atypical presentation. He was hospitalized for recent inflammatory and neurological symptoms. He was diagnosed with viral encephalitis. He died the day after he was discharged. The macroscopic autopsy findings were unremarkable. Histology revealed typical rheumatic heart disease. Neuropathology showed cerebral infarction due to an embolic event linked with the rheumatic valvulitis. The cause of death was determined as heart failure due to rheumatic heart disease secondary to an undiagnosed acute rheumatic fever. It is related to an autoimmune response to infection with group A streptococcus. It mainly affects children in developing countries. In our case, viral encephalitis was consistent with the medical history and the proper diagnosis was made on histological analysis. Forensic pathologists should consider this diagnosis facing a sudden unexpected death in childhood, even in industrialized countries.     

Diagnosis of Hemorrhagic Stroke in an Exhumed Brain After Three Years of Burial in a Deep Grave

Abstract: We present the forensic neuropathologic analysis of an exhumed decomposed brain following long‐term interment in a 50‐year‐old white woman, who had been buried for 34 months. Next of kin authorized exhumation of the body for an autopsy to determine the cause of death. The embalmed body was anatomically intact and revealed decompositional changes with mold colonies. Internal viscera showed intact histomorphology. The brain revealed diffuse congestive swelling and extracellular edema with dissecting parenchymal hemorrhage and hematoma originating from the left putamen and thalamus and extending to the left lateral ventricle. Excitotoxic neuronal injury as well as penumbric parenchymal changes was noted. Cause of death was determined to be a hypertensive cerebral parenchymal hemorrhage. This case and our previously reported case are sentinel cases, which should encourage and guide the forensic neuropathologic work‐up and investigation of causes of death in spite of long‐term burial in deep graves.     

Ascending Aortic Rupture through a Penetrating Atherosclerotic Ulcer: A Rare Cause of Sudden Unexpected Death

Spontaneous rupture of the aorta through an atherosclerotic lesion without preexisting aortic aneurysm, dissection, or history of trauma is very rare. Without prompt aortic repair, all cases result in sudden death with a definitive diagnosis made only intraoperatively or during autopsy. The phenomenon has been uniformly found in individuals with hypertension. The author reports a sudden unexpected death caused by spontaneous rupture of the ascending aorta in a 57‐year‐old man with a history of hypertension. The ascending aortic wall showed a longitudinal intimal tear measuring approximately 1 cm in length and rupture of the ascending aorta through an atherosclerotic ulcer, leading to massive hemopericardium and eventual death. Chronic hypertension and a penetrating atherosclerotic ulcer of the ascending aorta were the apparent underlying etiologies of the aortic rupture in the present case. This case illustrates not only the association between a rupture and a penetrating atherosclerotic ulcer with a silent death, but also raises awareness of possible such deaths.     

Accidental death from hydromorphone ingestion

Abstract: A 15‐year‐old male orally consumed an unknown but fatal amount of sustained release hydromorphone. He was naïve to opioid use. No other drugs or alcohol were involved. The cause of death was acute aspiration‐related bronchopneumonia, secondary to hydromorphone ingestion; the manner of death was accidental. Hydromorphone and hydromorphone‐3‐glucuronide were quantified in postmortem fluids by tandem liquid chromatography–mass spectrometry. The hydromorphone concentrations in the peripheral blood, urine, and vitreous humor were 57, 4460, and 31 ng/mL, respectively. The hydromorphone‐3‐glucuronide concentrations in the corresponding three fluids were 459, 36,400, and 40 ng/mL. Hydromorphone‐3‐glucuronide accumulation probably did not contribute significantly to the opiate toxicity. The proposed minimum lethal hydromorphone blood concentration in the nontolerant user is in the vicinity of 60 ng/mL.