Dental anesthetic death. An unusual autoerotic episode

The details of an unusual autoerotic death are presented; the postulated method of induction of cerebral hypoxia was inhalation of nitrous oxide from a dental anesthetic machine; the theme of dental anesthesia, presumably an elaborate bondage fetish, recurred in documentary material found at the scene.     

Asphyxial deaths from the recreational use of nitrous oxide.

The recreational use of nitrous oxide is widespread. Nitrous oxide for recreational use is usually obtained from anesthesia tanks or whipped-cream machine chargers or cans. Twenty previously described deaths associated with recreational nitrous-oxide use describe anesthesia tanks and whipped-cream machine dispensors as a source. Five deaths associated with nitrous oxide use are presented; two involving whipped-cream cannisters as the source, two involving anesthesia tanks, and one involving a racing fuel tank as a source of nitrous oxide. Autopsy findings in our cases were subtle or negative, but usually suggestive of asphyxia. Through a laboratory simulation, we have confirmed that nitrous oxide displaces oxygen in a closed space, which probably leads to asphyxia. A review of the literature, neuropharmacology, and pathophysiology of nitrous oxide use is also presented.     

Accidental death by nitrous oxide inhalation

Nitrous oxide is a popular inhalation anesthetic-analgesic agent. Its euphoric action and its availability have led to its abuse. We report a case of fatal accidental asphyxia due to nitrous oxide abuse. The deceased was a hospital worker who had access to the hospital supply of nitrous oxide. His death was due to hypoxemia and asphyxiation, secondary to nitrous oxide inhalation.     

Atypical autoerotic death: part II

Autoerotic fatalities encompass a wide array of means and mechanisms used to attain sexual gratification. The most commonly encountered autoerotic practice, specifically, autoerotic asphyxia, denotes death resulting from failure of a release mechanism of the apparatus designed to attain cerebral hypoxia for heightened arousal. Historically, the majority of victims of autoerotic death are Caucasian males under the age of 30. While autoerotic death is most often associated with a constrictive cervical ligature tied to either other parts of the victim's body or to an inanimate object such as a door, several other methods have been reported. These modalities include ligature around the thorax or abdomen, plastic bags covering the face, electrical current, inhalation of a toxic gas or chemicals, or partial or total submersion, known as aquaerotic asphyxiation. This study highlights 11 cases of atypical autoerotic death, including asphyxia with a plastic bag, electrocution, and inhalation of butane and nitrous oxide (N2O). Whereas the manner of death in the majority of autoerotic death cases is deemed accidental, we present and analyze unique and equivocal cases representing 4 different manners of death: accident, natural, suicide, and homicide. The 11 victims were all Caucasian and between the ages of 17 and 55. Ten decedents were males, 1 female. A comprehensive investigation incorporating a thorough scene analysis, gathering of the victim's history, and complete postmortem examination is necessary to elucidate both the cause and manner of death in these atypical cases.     

Gases released from tissue and analyzed by infrared and gas chromatography/mass spectroscopy techniques

Two techniques for analyzing contaminants released as gases from postmortem tissues were described and compared. One technique used gas chromatography/mass spectrometry (GC/MS); the other, infrared spectroscopy (IR). Brain, lung, liver, blood and urine specimens were obtained from suspected drug-overdose victims whose deaths were contributed to or caused by inhalation of unknown gases or vapors during the period immediately preceding death. Gases from the postmortem tissues and liquid samples were separately admitted into an evacuated IR gas cell, the IR spectra recorded, and gas samples then removed for GC/MS analysis. Nitrous oxide, glue, and paint solvent constituents were identified and measured. Only the brain and lung tissues contained measurable amounts of inhalants. Both IR and GC/MS methods were adequate for normal confirmatory analyses; the GC/MS system was judged superior for fast routine efforts normally hampered by incomplete sample history.     

Inhalant deaths in South Australia: a 20-year retrospective autopsy study

A 20-year retrospective study of inhalant deaths in South Australia, autopsied at Forensic Science SA, was undertaken from January 1983 to December 2002. Thirty-nine cases were identified from an autopsy pool of 18,880 cases, with a male to female ratio of 12:1. Sixty-four percent of the victims (N = 25) died during voluntary inhalation of volatile substances and 28% (N = 11) committed suicide utilizing a volatile substance or gas. The remaining 3 cases involved a workplace accident (N = 1) and 2 cases of autoerotic death where inhalants were being used to augment solitary sexual activity. The mean age of the 28 victims of accidental inhalant death of 21 years (range, 13-45 years) was considerably less than that of the 11 suicide victims of 31.5 years (range, 17-48 years). No homicides were found. Approximately one quarter of the victims were Aboriginal (N = 11), 10 of whom had died as a result of gasoline inhalation ("petrol sniffing"). Other common substances of abuse were aliphatic hydrocarbons such as butane. The study has shown that those most at risk for accidental or suicidal inhalant deaths were young males, with 92% of victims overall being male, and with 77% of victims being under 31 years of age. Gasoline inhalation remains a significant problem in Aboriginal communities in South Australia.     

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.     

Three cases of sudden death due to butane or propane gas inhalation: analysis of tissues for gas components

We report three cases of sudden death due to inhalation of portable cooking stove fuel (case 1), cigarette lighter fuel (case 2), and liquefied petroleum gas (LPG) (case 3). Specimens of blood, urine, stomach contents, brain, heart, lung, liver, kidney, and fat were collected and analyzed for propylene, propane, isobutane, and n-butane by headspace gas chromatography. n-Butane was the major substance among the volatiles found in the tissues of cases 1 and 2, and propane was the major substance in case 3. A combination of the autopsy findings and the gas analysis results revealed that the cause of death was ventricular fibrillation induced by hard muscle exercise after gas inhalation in cases 1 and 2, and that the cause of death in case 3 might be hypoxia. It is possible that the victim in case 3 was under anesthetic toxicity of accumulated isobutane which is a minor component of liquefied petroleum gas.     

Trends and pattern of drug abuse deaths in Maryland teenagers

The Office of the Chief Medical Examiner of Maryland recorded a total of 149 drug abuse deaths of teenagers aged 13-19 years between 1991 and 2006. Of these deaths, 96 (64.4%) were caused by the use of narcotic drugs only, 29 (19.5%) by both narcotics and cocaine, four (2.7%) by both narcotics and methylenedioxymethamphetamine, six (4.0%) by cocaine only, and 14 (9.4%) by volatile substances (e.g., butane, Freon, nitrous oxide, and propane). The annual death rate from drug abuse for teenagers increased from 1.4 deaths per 100,000 population in 1991 to 2.7 deaths per 100,000 population in 2006 (chi-square test for time trend, p<0.01). The increase in teenager drug abuse deaths occurred in 1999 and since has remained at a higher rate. Further analysis revealed that the increase in drug abuse deaths was attributable to a large degree to narcotic drugs, particularly heroin/morphine and methadone, and was confined to teenagers residing in the suburban and rural areas.     

Suicide by nitrous oxide poisoning

Fatal nitrous oxide poisoning usually occurs accidentally during the administration of general anesthesia. It seldom occurs during autoerotic behavior or in acute drug abuse. We report an unusual case of a health professional who committed suicide by inhaling nitrous oxide.     

The happy land homicides: 87 deaths due to smoke inhalation

We reviewed all 87 deaths from the Happy Land Social Club fire. All deaths were due to smoke inhalation. The carboxyhemoglobin (COHb) concentrations ranged from 37 to 93% with a mean of 76.5%. The vast majority (97%) of the decedents had a COHb concentration over 50%. Cyanide blood concentrations ranged from 0 to 5.5 mg/L with a mean of 2.2 mg/L. Nine decedents had no cyanide detected, and seven had cyanide concentrations of less than 1 mg/L. Fewer than one third of the decedents had thermal injuries, and most were partial thickness burns involving less than 20% body surface area. Ethanol was detected in 72% of decedents with a range of 0.01 to 0.29 g% and a mean blood concentration of 0.11 g%. Cocaine or cannabinoid use was identified in 9% of the decedents. All decedents were visually identified, and all had soot in the airway extending to the major bronchi. Carboxyhemoglobin concentrations corresponded well with deaths from smoke inhalation. Cyanide concentrations did not correspond with the extent of smoke inhalation, and the role of cyanide in contributing to these deaths is doubtful. Hydrogen chloride inhalation, as evidenced by comparison of the pH of tracheal mucosa to controls, was not a factor.     

Deaths caused by carbon monoxide poisoning in an open environment (outdoors)

Three deaths as a result of inhalation of carbon monoxide from the exhaust fumes of automobiles are reported. All deaths occurred outside and not in a structure. The individuals were white males, ages 24 to 26 years. Blood carboxyhemoglobin concentrations ranged from 58 (in a decomposing body) to 81%. The three cases illustrate the fact that even in the outdoors death from carbon monoxide inhalation can occur if an individual is in close proximity to a rich source of carbon monoxide.     

Determination of butane in respiratory gases by means of GC/MS and GC/MS-MS

Butane is inhaled in order to achieve a pleasurable state of intoxication. An overdose can lead to death. In two deaths from our own investigation material the circumstances were suspicious for the inhalation of liquid gas, and the presence of butane should be demonstrated in the respiratory gases. For detection, a method of ion trap gas chromatography/mass spectrometry (GC/MS) and tandem-mass spectrometry (GC/MS-MS) was developed, whereby the gas samples from the lung tissue were directly injected into the GC. The GC/MS tests revealed the presence of butane. Moreover, it was found that during the MS-MS tests reaction products appeared which had formed in the ion trap. Systematic investigations of these reaction products showed that these appeared regularly and could be used as additional backup for the proof of butane. Thus phenomena in the ion trap were used which would not have been expected to occur in normal mass spectrometry or tandem-MS and had not been described in the forensic literature so far. The detected amount of butane could be quantified by means of serial dilutions with nitrogen and room air. The described method shows that small molecules or gases can be demonstrated with the ion trap mass spectrometer.     

Volatile substance abuse--post-mortem diagnosis

A substantial number of children and adolescents world-wide abuse volatile substances with the intention to experience an euphoric state of consciousness. Although the ratio of deaths to nonfatal inhalation escapades is low, it is an important and preventable cause of death in young people. In the analytical investigation of volatile substances proper sample collection, storage and handling are important in view of the volatile nature of the compounds. Volatile organic compounds in post-mortem matrices such as blood, urine and tissues are generally determined by gas chromatography after extracting the compounds with methods such as static and dynamic headspace or even with pulse-heating and solvent extraction. In post-mortem cases, metabolites in urine seem less relevant, however, trichloroethanol and trichloroacetic acid were determined in several cases. When interpreting qualitative and quantitative results, researchers should be aware of false conclusions. The main reason why scepticism is necessary is the occurrence of losses of analytes during sampling, sample handling and storage, which results in false quantitation.     

Reporting a sudden death due to accidental gasoline inhalation

The investigation of uncertain fatalities requires accurate determination of the cause of death, with assessment of all factors that may have contributed to it. Gasoline is a complex and highly variable mixture of aliphatic and aromatic hydrocarbons that can lead to cardiac arrhythmias due to sensitization of the myocardium to catecholamines or acts as a simple asphyxiant if the vapors displace sufficient oxygen from the breathing atmosphere. This work describes a sudden occupational fatality involving gasoline. The importance of this petroleum distillate detection and its quantitative toxicological significance is discussed using a validated analytical method. A 51 year-old Caucasian healthy man without significant medical history was supervising the repairs of the telephone lines in a manhole near to a gas station. He died suddenly after inhaling gasoline vapors from an accidental leak. Extensive blistering and peeling of skin were observed on the skin of the face, neck, anterior chest, upper and lower extremities, and back. The internal examination showed a strong odor of gasoline, specially detected in the respiratory tract. The toxicological screening and quantitation of gasoline was performed by means of gas chromatography with flame ionization detector and confirmation was performed using gas chromatography-mass spectrometry. Disposition of gasoline in different tissues was as follows: heart blood, 35.7 mg/L; urine, not detected; vitreous humor, 1.9 mg/L; liver, 194.7 mg/kg; lung, 147.6 mg/kg; and gastric content, 116,6 mg/L (2.7 mg total). Based upon the toxicological data along with the autopsy findings, the cause of death was determined to be gasoline poisoning and the manner of death was accidental. We would like to alert on the importance of testing for gasoline, and in general for volatile hydrocarbons, in work-related sudden deaths involving inhalation of hydrocarbon vapors and/or exhaust fumes.     

The course of respiration and circulation in death by carbon dioxide poisoning

To investigate the effects of very high concentrations of carbon dioxide (CO2) upon the course of respiration and circulation, dogs were allowed to breathe high concentrations of CO2 while intrathoracic pressure, blood pressure (BP) in the femoral artery, electrocardiogram and electroencephalogram readings were registered. The respiratory movements either increased just after inhalation of high concentrations of CO2 and then ceased in 1 min, or decreased and continued for a while according to the concentrations of CO2. The BP showed an initial depression, then returned to the original level, then fell again rapidly or maintained an appreciable level for a while until circulatory breakdown. In the dogs allowed to breathe the gas mixture of 80% CO2 with 20% O2, the respiratory movement ceased in 1 min, and the terminal respirations were seen with the circulatory breakdown after apnoea of several minutes. These findings showed that the cause of death in breathing high concentrations of CO2 is not hypoxia, but the CO2 poisoning.     

Pulmonary siderophages and unexpected infant death

It has been proposed that the presence of siderophages in the lungs of infants who die unexpectedly should be considered a marker of a previous hypoxic event, which may preclude a diagnosis of sudden infant death syndrome. The authors retrospectively reviewed all infant deaths (<1 year old) going to autopsy at the Denver Office of the Medical Examiner from January 1999 to January 2001. Lung sections were stained with Prussian blue, and siderophages were counted in 20 high-power fields per lobe sampled. Cell counts were performed by two independent pathologists who were blinded to history and cause of death, with good reproducibility. Iron stain results were then categorized by average number of siderophages per 20 high-power field (category 1 = <5, category 2 = 5-100, category 3A = 100-500, category 3B = >100 in a single lobe, category 4 = >500). The results were subsequently correlated to case history, autopsy findings, and cause/manner of death. Forty-three cases were reviewed. The causes of death included sudden infant death syndrome (16), asphyxia (5), undetermined (6), and other (16). Those deaths were categorized by the above criteria as follows: category 1. (32), category 2. (6), category 3. (4), and category 4. (1). All sudden infant death syndrome deaths were in category 1. Categories 1 and 2 also included deaths in which hypoxia might have been present before death because of such factors as pneumonia and congenital heart disease. Categories 3 and 4 included a known homicidal asphyxia in which repeated episodes of intentional smothering were documented, 2 probable asphyxias, 1 nonaccidental trauma, and 1 undetermined. All 5 cases had questionable circumstances surrounding the death of the infant. Pulmonary siderophages were described in only 1 of the 43 autopsy reports. It was concluded that pulmonary siderophages can be markedly increased in cases of repeated asphyxia. Siderophages may also be increased in cases where hypoxia may have been present for another reason, but not to the same degree. Siderophages are not increased in sudden infant death syndrome. Because iron-laden macrophages often are not recognized on routine examination with hematoxylin and eosin staining, iron stains may be helpful in the evaluation of infant deaths. If siderophages are present in increased amounts without an obvious explanation, further investigation is warranted.     

Animal experiments on the detection of an exposure to "chemical mace" (author's transl)]

To answer the question whether a negative result of gas chromatographic blood analysis for components of chemical mace proves that no or at most only slight tear gas exposure can have occurred, animal experiments were carried out. In the blood of 10 guinea pigs, which were exposed to the contents of chemical mace for 1--6 h, the solvants 1,1,2-trichloro-1,2,2-trifluorethane (freon 113) and 1,1,1-trichloroethane could easily be detected--even 23 h after the end of exposure or after a storage of the blood samples for 18 weeks--whereas the lacrimator chloracetophenone (CN) could not be found at all. In vitro experiments showed that CN relatively quickly reacts with components of blood. Therefore, blood samples should be analyzed for CN after withdrawal as soon as possible. In case of inhalation of the contents of chemical mace, i.e., after the comparatively mildest form of CN application, most probably no traces of the lacrimator at all can pass into the blood due to the quick reaction of CN with proteins of the respiratory surface of the lung.     

Ultrastructure of acute ammonia toxicity in the human lung

A tanker truck carrying anhydrous ammonia (NH3) fell off a freeway, releasing a dense cloud of NH3 gas, killing several people. The driver was dead upon impact. To our knowledge, pulmonary NH3 toxicity in humans has not been studied previously by electron microscopy (EM). Therefore, in two cases, the paraffin-embedded tissue blocks of lung were deparaffinized and reembedded in plastic for 1-mu sections and EM examination. The lung tissue of a third case, the truck driver, was similarly processed as a control. Light-microscopic pulmonary findings in the acute NH3 deaths included denudation of the tracheobronchial epithelium, edema of the lamina propria, and marked alveolar edema, congestion, and hemorrhage. In contrast, in the truck driver's lungs, the bronchial epithelium was intact, and there was no gross odor of NH3. Massive pulmonary hemorrhages in his lungs were attributed to trauma rather than NH3 inhalation. EM examination of the lungs of the truck driver showed no discernible toxic alterations in either the capillary endothelial cells or the Type I or II alveolar epithelial cells, and alveolar and capillary basement membranes were intact. In contrast, EM study of the lungs from two individuals dying acutely of NH3 inhalation showed marked swelling and imbitional edema of Type I alveolar epithelial cells; however, alveolar basement membranes and capillary endothelial cells appeared as usual. These electron-microscopic findings demonstrate the Type I epithelial cell to be the target cell of acute alveolar wall injury in NH3 inhalation.     

Accidental autoerotic death by volatile substance abuse or nonsexually motivated accidents?

In contrast to typical autoerotic fatalities, when death is due to asphyxia mostly by mechanical compression of the neck, atypical autoerotic accidental deaths (AADs) involve sexual self-stimulation by other means such as electrocution or inhalation of chemical agents. Especially in lethal cases of volatile substance abuse (VSA), a differentiation between suicide or sexually or nonsexually motivated accident is often complicated in practical casework. Considering the small number of AADs involving chemical substance abuse reported in the literature, the number of unreported cases seems to be very high. We report about 5 lethal cases of VSA; analysis was performed using headspace solid-phase microextraction (HS-SPME) and gas chromatography-mass spectrometry (GC/MS). When headspace sampling is not performed at autopsy, the analysis of volatile substances can be very complicated. In 2 cases, an AAD was diagnosed considering findings at the scene, reconstruction of the event, and discussion of the circumstances of the death. These findings demonstrate the importance of VSA in atypical autoerotic asphyxia. Therefore, in cases of suspected lethal inhalational intoxications, as a matter of principle, headspace asservation should be performed at autopsy and an autoerotic motivational background should be taken into consideration for differential diagnosis.