Postmortem diffusion of n-butane and i-butane used for anticontagious plugging spray

Blood and tissue samples from a forensic autopsy of a man in his late 60s, who developed dementia and died of multiple head traumas due to a fall from a moving vehicle, contained certain amounts of n-butane and i-butane. The concentration of n-butane was in the range of 0.48–70.5 μL/g, which would be considered as toxic or lethal levels. We had to distinguish whether the cause of his unexplained behavior was due to his pre-existing condition (dementia), or from a confused state induced by butane abuse. No traces of butane use were found at the scene. Police investigation revealed that a propellant used in an anticontagious plugging spray had been administered to him during a postmortem treatment in the emergency hospital. In order to prove the postmortem butane diffusion had resulted from the spray administration and to estimate the diffused concentration, experimental simulation was conducted by using rats. As a result of postmortem treatment with the spray, n-butane at concentrations of 0.54–15.5 μL/mL or g were found in the rat blood and tissues. In this case, we provided further evidence that the postmortem butane diffusion, caused by using the anticontagious plugging spray containing butane gas as a propellant administered to a cadaver during a postmortem procedure prior to forensic autopsy, should be distinguished from cases of actual butane poisoning.     

A fatal case considered to be due to cardiac arrhythmia associated with butane inhalation

An autopsy case of a 14-year-old boy whose death is considered to be a result of cardiac arrhythmia after butane inhalation and sample preservation for butane analysis are reported. The electrocardiogram taken in the ambulance revealed ventricular fibrillation. There were no autopsy findings as to the cause of death. n-Butane, isobutane and propane were identified in the blood, brain and lung of the cadaver by headspace gas chromatography. Based on these results, the cause of death was concluded to be cardiac arrhythmia due to butane inhalation. As a follow-up, n-butane, isobutane and propane concentrations in the blood kept at -30 degrees C showed the unchanged values with a coefficient of variation of within 10% for 2 weeks.     

Two cases of oral aspirin overdose

A 30-year-old woman and a 27-year-old man were found in a parked car after the man had telephoned his father to tell him of their suicide attempt. In spite of emergent hospitalization and intensive care, the woman died. Due to the possibility of his assisting her suicide, medicolegal autopsy and toxicological analysis were performed. On forensic autopsy, no external injuries or pathological findings were detected. The man recovered after 5 days of hospitalization. In spite of a negative toxicological screening test, the police investigation revealed that they may have taken 120 tablets (330 mg/tablet; 39,600 mg total dose) of aspirin (acetylsalicylic acid) orally; therefore, we analyzed the concentrations of acetylsalicylic acid and two kinds of metabolite in specimens obtained at autopsy and on emergent hospitalization using high performance liquid chromatography. Acetylsalicylic acid and/or the two metabolites were found in the woman’s specimens. These substances were also present in the man’s specimens. It is still unclear why the man survived in spite of what appeared to be a fatal aspirin overdose. It was very straightforward to diagnose aspirin poisoning in these cases; however, we have to be aware of poisoning by drugs which are not included in simple drug screening examinations.     

A case of medical liability involving an unexpected systemic amyloidosis

The authors present a case of fatal amyloid cardiomyopathy, which was diagnosed only upon autopsy. A 57-year-old man was admitted to the hospital for scheduled percutaneous cardiac procedure of transcatheter radiofrequency ablation due to persistent atrial fibrillation and atrial flutter. Ventricular fibrillation was recorded in the monitor 2 h after the surgical procedure. Therefore, he was defibrillated and intubated, but he died for nosocomial pneumonia 26 days after being admitted. A judicial autopsy was ordered by the prosecutor due to an alleged medical malpractice. The autopsy confirmed the cause of death being pneumonia, but also revealed an occult restrictive cardiomyopathy with a thick and firm myocardium. Viscera samples were then collected for microscopic examination. Histopathologic analysis showed diffuse amyloid deposits in the myocardium, especially in the perivascular and subendocardial spaces. Amyloid deposits were also detected in all the other organs, except for the brain. Furthermore, immunohistochemistry for light chains was performed on the heart tissue sample, resulting to be positive. In the case presented herein, autopsy and histopathologic examination were crucial to diagnose an occult systemic amyloidosis (AL-type). In fact, it has been observed that the rarity of systematic amyloidosis and its unusual clinical onset were at first mistakenly perceived as a medical malpractice due to a technical error within the catheter ablation for atrial fibrillation. As a consequence, upon discussing the clinical and medicolegal implications concerning the case, the focus was placed on the undiagnosed systemic amyloidosis and on the causality between surgical procedure and the patient’s death.     

A fatal suicidal sodium nitrite ingestion determined six days after death

Sodium nitrite (SN) is an inorganic salt that appears as a slightly yellowish crystalline solid, odorless, and highly soluble in water at room temperature. It is highly toxic to humans at specific doses because it can oxidize hemoglobin to methemoglobin, causing severe tissue hypoxia. A 20-year-old woman was unconscious in her bedroom and died shortly after that. Two days later, following the discovery of a jar of SN and a paper in which were written instructions on how to take it (and the website from which the procedure was learned) in the same room were death occurred, the Judicial Authority ordered the execution of the autopsy on the exhumed body of the young woman. The autopsy procedure was performed ∼ 2h after exhumation. It showed greyish-purple hypostasis, labial cyanosis, stomach distension and greenish color but empty, subpleural petechiae, brownish fluid in the pleural cavities (∼300 ml), congested and edematous lungs and diffuse visceral congestion. At autopsy, foamy liquid was observed at the lung section and subsequent squeezing. In addition, the autopsy showed edema and hemorrhagic petechiae of the laryngeal, glottal, and tracheal submucosa and green-brownish foamy liquid in the tracheal lumen. The cause of death was attributed tocardiac arrest induced by anoxia resulting from acute methemoglobinemia caused by sodium nitrite poisoning, intensified by severe malnutrition. Manner of death was suicidal.     

Histological microaggregates as a sign of systemic dissemination due to oral ingestion of povidone-iodine (Betadine®)

Povidone-iodine (PVP-I) in the formulation of Betadine® is widely used in several medical fields, whereas its suicidal ingestion is an unusual occurrence. Therefore, the biological signs of this fatal poisoning remain unclear and elusive, similarly to the histological lesions induced by PVP-I. In fact, there are no forensic articles concerning the histological signs of PVP-I acute poisoning. Specifically, this short communication reports the unique case of a man who ingested 125 ml of Betadine® 10% to commit suicide, for which he died three days later. The autopsy examination showed either local or systemic signs of caustic ingestion; moreover, the histological analysis showed both intra- and extra-cytoplasmic amorphous and brownish microaggregates in almost all the organs. Histological and histochemical techniques resulted to be negative for the detection of physiological and known pigments (e.g., formalin, lipofuscin, hemosiderin). Likewise, such pigments were not associated neither with the man’s diseases nor with his medications. Therefore, the authors supposed that they were povidone-iodine microaggregates, which have been deposited in the organs through the blood circulation. In conclusion, the complete postmortem histological examination could allow the identification and the characterization of PVP-I microaggregates as evidence of systemic toxicity from Betadine®, when dealing with a forensic case of ingestion of povidone-iodine.     

Undiagnosed late-onset chylothorax accompanied by fatal acute pulmonary thromboembolism after surgical treatment of lung cancer: An autopsy case and review of the literature

Late-onset chylothorax is a relatively rare and essentially benign postoperative complication. We describe an autopsy case of undiagnosed hemi-chylothorax accompanied by fatal acute pulmonary thromboembolism after pulmonary resection and lymph node dissection for lung cancer, reviewing the literature. The patient was a 60-year-old woman. She complained of dyspnea on the 20th postoperative day, which gradually increased. The patient suddenly died 2 days later. Autopsy demonstrated right chylothorax (1000 ml), and fatal acute pulmonary thromboembolism, mainly on the left side, originating from the lower extremities. Postoperative chylothorax, causing respiratory and pulmonary circulatory disturbance, may provide an important predisposition to ward fatality due to pulmonary thromboembolism even among those showing a milder type; thus careful management is necessary.     

Delayed asphyxia due to inhalation injury

We report the case of a 53-year-old man who was found dead in his apartment 2 days after a little fire during which he had suffered from second to third degree burns at 2% of the body surface, also involving the skin around the mouth and the nose. At autopsy, severe acute emphysema and mucopurulent obstructive laryngotracheobronchitis were observed. The histology showed desquamative loss of the respiratory epithelium up to the middle bronchi; the bronchial lumen was filled with clumps of mucopurulent secretions mixed with necrotic epithelial cells. The cause of death was a delayed asphyxia due to inhalation injury.     

Milk of calcium pericardial effusion confirmed with postmortem computed tomography and autopsy findings: A case report

We present the postmortem computed tomography and autopsy findings of a 60-year-old man who developed milk of calcium pericardial effusion and died of constrictive epicarditis. He experienced out-of-hospital cardiopulmonary arrest, and spontaneous circulation returned at the hospital. However, 7 h after recovery, the patient died. He had a swollen neck, had been experiencing coughing from 4 to 5 days earlier, and had no significant medical or surgical history. On computed tomography (CT), highly dense pericardial fluid (CT value: 130–150 Hounsfield units) and multiple calcifications along the epicardium and pericardium were visualized. The epicardium and pericardium were thick, hard, rough, and widely calcified with mild adhesions on autopsy. The pericardial cavity contained a pale, reddish brown, turbid, and highly viscous liquid. Bacteriological tests of pericardial fluid cultures revealed the presence of group G β-hemolytic streptococci. Hence, we diagnosed the patient’s cause of death as heart failure due to constrictive epicarditis. We believe that this case of milk of calcium pericardial effusion is the first case confirmed with postmortem CT and autopsy findings.     

Volatile lipophilic substances management in case of fatal sniffing

Death due to inhalation of aliphatic hydrocarbons such as butane and propane is a particularly serious problem worldwide, resulting in several fatal cases of sniffing these volatile substances in order to “get high”. Despite the number of cases published, there is not a unique approach to case management of fatal sniffing. In this paper we illustrate the volatile lipophilic substances management in a case of a prisoner died after sniffing a butane-propane gas mixture from prefilled camping stove gas canisters, discussing the comprehensive approach of the crime scene, the autopsy, histology and toxicology.A large set of accurate values of both butane and propane was obtained by gas chromatography–mass spectrometry analyzing the following post-mortem biological samples: peripheral blood, heart blood, vitreous humor, liver, lung, heart, brain/cerebral cortex, fat tissue, kidney, and allowed an in depth discussion about the cause of death. A key role is played by following the proper sampling approach during autopsy.     

Fulminant sepsis due to anaerobic bacterial infection in immuno-compromised state

We experienced two autopsy cases of fulminant sepsis due to anaerobes. Case 1: A 67-year-old female with uncontrolled diabetes mellitus (DM) was admitted to a hospital because of sudden onset of mid-abdominal pain. She was diagnosed with infectious colitis and given a laxative and an enema. However, 9 h later, her blood pressure suddenly dropped with metabolic acidosis, and she died 20 h after admission. Autopsy revealed massive pneumohemia and a dark-brown colored mucosal surface from the terminal ileum to the sigmoid colon. Histopathological findings were compatible with marginal ischemic colitis. Anaerobes were positive in blood culture. Case 2: A 53-year-old male with alcoholic liver cirrhosis (LC) was found dead in his room. He had been alive 24 h before the discovery, but postmortem changes appeared to accelerate more rapidly than usual cases. Autopsy revealed severe LC with muddy ascites and many Gram-negative rods in several organs. These cases suggest the possibility of sepsis as causes of death, especially in immuno-compromised hosts when unexplained putrefactive changes are seen on forensic autopsy.     

Sudden death due to a novel nonsense mutation in Marfan syndrome

BackgroundMarfan syndrome is a hereditary connective tissue disease accompanied by autosomal dominant inheritance; that mainly arises from a mutation in the fibrillin-1 gene (FBN1). Aortic dissection and rupture are the common and lethal complications of MFS and may cause sudden unexpected death.MethodA man aged 34 was admitted to the hospital due to persistent pain in his abdomen 12 h post-drinking and suddenly died 10 h later. A forensic autopsy was performed to identify the underlying mechanism of death. Due to the high suspected of MFS, Sanger sequencing was performed, and a novel mutation was detected in the deceased. To clarify the underlying mechanism of this mutation, real-time quantitative polymerase chain reaction was conducted and Western blot analysis was performed in vitro.ResultsA novel PTC mutation c.933C > A in FBN1 was found. Through family history inspection and Sanger sequencing, other MFS patients in the present family were confirmed. The pathologic changes in the aorta in the present case showed media cystic degeneration, disordered arrangement of elastic fibers and a significant reduction in fibrillin 1 compared with the control. The mutation led to significant reduction inFBN1 mRNA and fibrillin-1 in cells in vitro, and overexpression of phospho-Smad2 was observed.ConclusionWe confirmed a novel pathogenic PTC mutation in the FBN1gene through Sanger sequencing, and the pathological changes and underlying mechanisms were also identified. The present work not only extends the pathogenic mutation spectrum of MFS, but also stresses the role of forensic autopsy, genetic analysis and functional validation of novel mutations in cases of sudden death associated with congenital diseases.     

Acute fatal poisoning with Tolfenpyrad

The authors present a fatal case of poisoning with Tolfenpyrad (TFP), a pesticide first approved in Japan in 2002. A man in his fifties was found dead in the supine position at his son's home and the small towel with a smell of naphthalene was found nearby. Forensic autopsy was unremarkable, except for a very small amount of light pink fluid in the stomach, with naphthalene odour. The toxicological analyses revealed the presence of TFP and its major metabolite PTCA (4-[4-[(4-chloro-3-ethyl-1-methylpyrazol-5-yl)carbonylaminomethyl]phenoxy]benzoic acid), together with naphthalene and methyl naphthalenes in the post-mortem sample, with liquid chromatography–mass spectrometry (LC–MS) and gas chromatography–mass spectrometry (GC–MS) respectively. The plasma concentrations of each substance were quantified as 1.97 μg/ml (TFP), 2.88 μg/ml (PTCA), 1.70 μg/ml (naphthalene), 0.67 μg/ml (1-methyl naphthalene) and 1.44 μg/ml (2-methyl naphthalene). According to these results together with autopsy findings, the cause of his death was determined to be acute Tolfenpyrad poisoning. This is the first case report of fatal poisoning attributable to an intake of TFP product.     

Sudden unexpected death due to Fournier’s gangrene

A 43-year-old Japanese male vagrant collapsed suddenly in a police station. The man was resuscitated in hospital but died about 13 h later. An autopsy revealed necrotizing fasciitis in the genitalia and lower abdominal wall. The man was considered to have died from endotoxic shock following on Fournier’s gangrene. Received: 16 July 1996 / Received in revised form: 23 December 1996     

Confluent muscle pallor: a macroscopic marker of cocaine-induced rhabdomyolysis

A 39-year-old man presenting with acute delirium is reported who suffered an unexpected cardiac arrest shortly after being sedated. Death followed 2 days later from hypoxic-ischemic encephalopathy. At autopsy, marked pallor and edema of his left sternomastoid muscle was observed which was shown on microscopy to be due to confluent coagulative necrosis. Myoglobin casts in his renal tubules corresponded to an antemortem creatine phosphokinase level of 31,940 U/l. Death was due to rhabdomyolyisis and excited delirium complicating cocaine toxicity with hypoxic-ischemic encephalopathy, against a background of atherosclerotic coronary artery disease. Extensive confluent pallor in a single muscle may be a useful marker of chronic cocaine exposure associated with hyperthermia and muscle necrosis. Confirmatory toxicology is required.     

Acute myocardial infarction in a young woman: Unexpected findings of a coronary occlusion

In clinical and forensic practice, the cause of death is often attributed to acute myocardial infarction, among which the coronary atherosclerosis being the Captain of the Men of Death. However, other reasons such as coronary septic embolization with neutrophilic granulocyte myocarditis although rare, can also cause sudden unexpected death. This paper reports a case with this rare cause—a 21-year-old woman diagnosed with “acute gastroenteritis” who died 4 days later. A forensic autopsy revealed an inflammatory polypous embolic located at 1.0 cm from the left anterior descending branch (LAD) with serve neutrophilic granulocyte myocarditis, which resulted in embolic at the opening of the left main coronary artery, acute myocardial infarction and eventually leading to her death. Histopathological examination showed large amounts of neutrophilic granulocyte infiltration in the arterial layer forming the septic embolic and eventually resulting in coronary occlusion. To find the real cause of septic embolic, myocarditis, bacterial, fungal, protozoan and virus detection was performed through RT-PCR, with negative findings. Septic embolic leading coronary occlusion in left main coronary artery and LAD is rarely reported in forensic practice, we hope this report can pave the way on understanding this rare disease to make correct diagnosis in medical practice.     

Ethyl glucuronide and ethyl sulfate in autopsy samples 27 years after death

The unique case of a 50-year-old known alcoholic whose corpse was exhumed 27 years after death is reported. The man apparently committed suicide by hanging, but many years later the case was questioned and homicide—linked to a long-lasting serial killer case—was suspected. Thus, the corpse was exhumed, and at the autopsy it was found to be naturally mummified. This fact permitted the analysis of body tissues with the aim to investigate the persistence of ethanol conjugates in the biological material 27 years after death. Fragments of liver and kidney, a blood clot, and a hair strand were collected and submitted to liquid chromatography tandem mass spectrometry analysis. Ethyl glucuronide (EtG) and ethyl sulfate (EtS) were identified and quantified in the liver, the kidney, and the blood clot. Hair analysis was found to be severely affected by ion suppression even after solid phase extraction. Consequently, EtG was identified in all hair segments (0–3 cm, 3–6 cm, and 6–10 cm), but no reliable quantification could be carried out. In summary, our findings demonstrate that, notwithstanding the expected conjugate degradation, EtG and EtS can be indicative of ante-mortem use of alcohol even many years after death.     

Multidirectional analysis for a colchicine poisoning case revealed detail cause of death and its mechanism

The appearance of Meadow saffron (Colchicum autumnale), which contains colchicine, closely resembles Alpine leek (Allium victorialis), a popular edible wild vegetable in Northern Japan. This often results in the accidental ingestion of Meadow saffron and acute colchicine poisoning deaths. Here, we report on a case of acute colchicine poisoning death caused by the accidental ingestion of Meadow saffron. A man in his 70 s had been given wild vegetables from his neighborhood, which were then cooked and eaten by himself and his wife. Several hours later, they suffered from abdominal pain, vomiting, and diarrhea. They immediately went to the hospital and received routine treatment. While his wife made a full recovery, he died at home two days after consumption of the vegetables. A forensic autopsy was conducted five days after ingestion of the Meadow saffron and a lethal concentration (21.5 ng/mL) of colchicine in the peripheral blood sample was detected by liquid chromatography-tandem mass spectrometry. Distribution of colchicine in body fluids, tissues and gastrointestinal contents was also investigated. Some of the plants he had eaten were identified as Alpine leek or Meadow saffron by genetic analysis of his stomach contents. Histopathological examination showed apoptotic cells and cell cycle arrest at the metaphase in the intestinal crypts and testis. In addition, we detected high concentrations of endotoxins and tumor necrosis factor-α in his blood, indicating that intestinal mucosal injury induced by colchicine poisoning had allowed endotoxins to invade the body, causing death by endotoxin shock.     

Central nervous system lymphoma not detectable on single-photon emission CT with thallium 201.

A 33-year-old man with acquired immunodeficiency syndrome had an erosive supraglottic mass visible on CT scans of the neck; biopsy was postponed because of the patient''s debilitated condition. Two weeks later, he was admitted with altered mental status; an MR image of the brain obtained at that time showed multiple bilateral mass lesions, the largest of which was 5 cm. Findings on a thallium-201 single-photon emission CT (SPECT) scan of the brain were normal. Ten days later, the patient died and autopsy showed both the neck and the brain lesions to be large-cell lymphoma. This case is counterevidence to the reported 100% sensitivity of thallium-201 brain SPECT for demonstrating lymphoma of the central nervous system.