Autoerotic Deaths in Hamburg, Germany: Autoerotic accident or death from internal cause in an autoerotic setting? A retrospective study from 2004-2018.

INTRODUCTION: Autoerotic deaths are rare events. The death scene is often bizarre and the death unexpected, thus often requiring forensic autopsies. Our analysis will provide an overview of the expected range of causes and manners of death in cases of autoerotic deaths. METHODS: A retrospective analysis was carried out on all scientific and forensic autopsies and postmortem examinations performed at the Department of Legal Medicine in Hamburg, Germany, over the period of 2004-2018. RESULTS: 25 cases of autoerotic fatalities were identified over this 15-year-period or one to two cases per year, respectively. Autopsies were carried out on 23 of these cases. 16 (64%) of the cases involved autoerotic accidents and 7 (28%) from internal causes of death during an autoerotic act. Two cases had not undergone an autopsy. On average, those who were involved in autoerotic accidents had been younger in age (average age: 37 years) than the individuals who died from internal disease (average age: 61 years). Only one woman was involved. The most common cause of death in autoerotic accidents was strangulation (hanging: 8 cases, ligature strangulation: 1 case), followed by smothering of the respiratory tract (4 cases). Fatal intoxication was diagnosed in three of the cases. Fatalities with natural cause of death solely involved cardiovascular causes of death. CONCLUSIONS: Autoerotic deaths involved a wide range of natural and non-natural causes of death. The reconstruction of such unusual cases and detection of non-natural fatalities requires thorough investigation of the scene of death as well as a postmortem external and internal examination including a chemical toxicological and blood alcohol analysis.

Delayed onset of liver injury after intentional chloroform overdose: a case report and literature review.

Chloroform is a recognised cause of acute liver injury, although now rarely encountered in clinical practice. We present a case of inhalational chloroform self-poisoning in a 47-year-old man that presented to hospital initially with reduced conscious level and later developed acute liver injury that was treated with intravenous acetylcysteine. This paper reviews the existing literature and presents a summary of the mechanisms of chloroform hepatotoxicity. Published cases show that there is a characteristic delay of 24 to 48 hours between chloroform exposure and elevation of liver transaminase activity. Therefore, clinicians need to provide an appropriate duration of monitoring in order to detect the occurrence of this important toxic effect.

Hazards of Improper Dispensary: Literature Review and Report of an Accidental Chloroform Injection.

Several clear, transparent solutions are used in endodontics. Inappropriate dispensing methods can lead to accidental injection or accidental irrigation. These accidents can cause permanent tissue damage including damage to the bone, periodontium, nerves, and vasculature. This article reports on the consequences of an accidental chloroform injection. Nonsurgical retreatment of tooth #8 was planned as part of a restorative treatment plan in a 69-year-old woman. The dentist accidentally injected chloroform instead of local anesthesia because chloroform was loaded into the anesthetic syringe. The patient experienced severe pain and swelling and soft tissue necrosis and suffered permanent sensory and motor nerve damage. A review of the literature was performed on accidents caused by improper dispensary, namely accidental injections and accidental irrigations. The data were extracted and summarized. Sodium hypochlorite, chlorhexidine, formalin, formocresol, 1:1000 adrenaline, benzalkonium chloride, and lighter fuel were accidentally injected as an intraoral nerve block or as infiltration injections. Bone and soft tissue necrosis, tooth loss, and sensory nerve damage (anesthesia and paresthesia) were the most common consequences reported. Such disastrous events can be prevented by appropriate labeling and separate dispensing methods for each solution. There is a need for disseminating information on toxicity and biocompatibility of materials/solutions used in endodontics. The authors recommend training dental students and endodontic residents on immediate and long-term therapeutic management of patients when an accidental injection or accidental irrigation occurs.

Chloroform ingestion causing severe gastrointestinal injury, hepatotoxicity and dermatitis confirmed with plasma chloroform concentrations.

CONTEXT: Poisoning due to chloroform ingestion is rare. The classic features of acute chloroform toxicity include central nervous system (CNS) and respiratory depression, and delayed hepatotoxicity. CASE DETAILS: A 30-year-old female ingested 20-30 mL of 99% chloroform solution, which caused rapid loss of consciousness, transient hypotension and severe respiratory depression requiring endotracheal intubation and ventilation. She was alert by 12 h and extubated 16 h post-overdose. At 38-h post-ingestion, her liver function tests started to rise and she was commenced on intravenous acetylcysteine. Her alanine transaminase (1283 U/L), aspartate transaminase (734 U/L) and international normalized ratio (2.3) peaked 67- to 72-h post-ingestion. She also developed severe abdominal pain, vomiting and diarrhoea. An abdominal CT scan was consistent with severe enterocolitis, and an upper gastrointestinal endoscopy showed erosive oesophagitis, severe erosive gastritis and ulceration. She was treated with opioid analgesia, proton pump inhibitors, sucralfate and total parenteral nutrition. Secretions caused a contact dermatitis of her face and back. Nine days post-ingestion she was able to tolerate food. Her liver function tests normalized and the dermatitis resolved. Chloroform was measured using headspace gas chromatograph mass spectrometry, with a peak concentration of 2.00 µg/mL, 4 h 20 min post-ingestion. The concentration-time data fitted a 1-compartment model with elimination half-life 6.5 h. DISCUSSION: In addition to early CNS depression and delayed hepatotoxicity, we report severe gastrointestinal injury and dermatitis with chloroform ingestion. Recovery occurred with good supportive care, acetylcysteine and management of gastrointestinal complications.

Of Penguins, Pinnipeds, and Poisons: Anesthesia on Elephant Island.

Although Ernest Shackleton's Endurance Antarctic expedition of 1914 to 1916 is a famous epic of survival, the medical achievements of the two expedition doctors have received little formal examination. Marooned on Elephant Island after the expedition ship sank, Drs. Macklin and McIlroy administered a chloroform anesthetic to crew member Perce Blackborow to amputate his frostbitten toes. As the saturated vapor pressure of chloroform at 0°C is 71.5 mmHg and the minimum alveolar concentration is 0.5% of sea-level atmospheric pressure (3.8 mmHg), it would have been feasible to induce anesthesia at a low temperature. However, given the potentially lethal hazards of a light chloroform anesthetic, an adequate and constant depth of anesthesia was essential. The pharmacokinetics of the volatile anesthetic, administered via the open-drop technique in the frigid environment, would have been unfamiliar to the occasional anesthetist. To facilitate vaporization of the chloroform, the team burned penguin skins and seal blubber under overturned lifeboats to increase the ambient temperature from -0.5° to 26.6°C. Chloroform degrades with heat to chlorine and phosgene, but buildup of these poisonous gases did not occur due to venting of the confined space by the stove chimney. The anesthetic went well, and the patient-and all the ship's crew-survived to return home.

Systemic inflammatory response due to chloroform intoxication--an uncommon complication.

Well-known adverse effects of chloroform are drowsiness, nausea, and liver damage. Two cases with an uncommon complication due to chloroform intoxication are presented. In the first case, a general physician, because of nausea and dyspnea, admitted a 34-year-old woman to hospital. She developed a toxic pulmonary edema requiring mechanical ventilation for a few days, and a systemic inflammatory response syndrome (SIRS) with elevated white blood cell counts, a moderate increase of C-reactive protein, and slightly elevated procalcitonin levels. There were inflammatory altered skin areas progressing to necrosis later on. However, bacteria could be detected neither in blood culture nor in urine. Traces of chloroform were determined from a blood sample, which was taken 8 h after admission. Later, the husband confessed to the police having injected her chloroform and put a kerchief soaked with chloroform over her nose and mouth. In the second case, a 50-year-old man ingested chloroform in a suicidal attempt. He was found unconscious in his house and referred to a hospital. In the following days, he developed SIRS without growth of bacteria in multiple blood cultures. He died several days after admission due to multi-organ failure. SIRS in response to chloroform is a rare but severe complication clinically mimicking bacterial-induced sepsis. The mechanisms leading to systemic inflammation after chloroform intoxication are currently unclear. Possibly, chloroform and/or its derivates may interact with pattern recognition receptors and activate the same pro-inflammatory mediators (cytokines, interleukins, prostaglandins, leukotrienes) that cause SIRS in bacterial sepsis.

Poisoning: fact or fiction?

Analytical toxicology is a complex discipline. Simply detecting a poison in a biological sample does not necessarily mean that the individual from whom the sample was obtained had been poisoned. An analysis can prove exposure and perhaps give an indication of the magnitude of exposure, but the results have to be placed in proper context. Even if sampling was ante-mortem an analysis does not necessarily prove the effects that the drug or poison had on the victim immediately before or at the time of sampling. Tolerance is one big issue, the mechanism of exposure (how the drug got into the body) is another, and of course with post-mortem work there are always additional considerations such as site of sample collection and the possibility of post-mortem change in analyte concentration. There are also questions of quality and reliability, and whether a particular analysis and the interpretation placed upon the result are appropriate in a particular case.

Chloroform poisoning--a case report.

Chloroform, a halogenated hydrocarbon, causes central nervous system (CNS) depression, cardiac arrhythmias, hepatotoxicity, and renal failure. We describe a successful outcome in a case of chloroform ingestion with renal and hepatotoxicity with N-acetylcysteine (NAC) administration and hemodialysis support.

Two fatalities associated with chloroform inhalation. Variation of toxicological and pathological findings.

We report a forced double suicide involving a wife and husband in their late 80s resulting from chloroform inhalation. Macro- and microscopic examinations revealed marked pulmonary edema and extensive contraction band necrosis of the cardiac muscles. Toxicological analysis revealed high levels of chloroform in the blood (41.4 µg/ml in the wife and 29.1 µg/ml in the husband) and in the adipose tissue (128 µg/g in the wife and 131 µg/g in the husband). From these findings, we conclude that the cause of death of both was acute heart failure due to chloroform poisoning. In addition, the pathological examination of the husband revealed submucosal hemorrhage at the root of the tongue and trachea, erosion of the stomach, and upper jejunum, none of which were present in the wife. Furthermore, hyperemia of the mucous membrane of the husband was more marked than that of the wife. Toxicological analysis also revealed that the chloroform levels in the liver and brain of the husband were higher than those of the wife, although the chloroform level in the blood of the husband was lower than that of the wife. We presume that the wife may have inhaled a greater amount of chloroform, and that the wife's circulation may have arrested before irritation of the mucous membranes became apparent. The husband may have inhaled a smaller amount of chloroform in longer duration, leading to irritation of the mucous membranes prior to the fatal heart failure. These findings suggest that toxicological and pathological outcomes of chloroform poisoning may vary between patients, and that they may reflect the dose and duration of chloroform inhalation.

Acute chloroform ingestion successfully treated with intravenously administered N-acetylcysteine.

Chloroform, a halogenated hydrocarbon, causes central nervous system depression, cardiac arrhythmias, and hepatotoxicity. We describe a case of chloroform ingestion with a confirmatory serum level and resultant hepatotoxicity successfully treated with intravenously administered N-acetylcysteine (NAC). A 19-year-old man attempting suicide ingested approximately 75 mL of chloroform. He was unresponsive and intubated upon arrival. Intravenously administered NAC was started after initial stabilization was complete. His vital signs were normal. Admission laboratory values revealed normal serum electrolytes, AST, ALT, PT, BUN, creatinine, and bilirubin. Serum ethanol level was 15 mg/dL, and aspirin and acetaminophen were undetectable. The patient was extubated but developed liver function abnormalities with a peak AST of 224 IU/L, ALT of 583 IU/L, and bilirubin level reaching 16.3 mg/dL. NAC was continued through hospital day 6. Serum chloroform level obtained on admission was 91 µg/mL. The patient was discharged to psychiatry without known sequelae and normal liver function tests. The average serum chloroform level in fatal cases of inhalational chloroform poisoning was 64 µg/mL, significantly lower than our patient. The toxicity is believed to be similar in both inhalation and ingestion routes of exposure, with mortality predominantly resulting from anoxia secondary to central nervous system depression. Hepatocellular toxicity is thought to result from free radical-induced oxidative damage. Previous reports describe survival after treatment with orally administered NAC, we report the first use of intravenously administered NAC for chloroform ingestion. Acute oral ingestion of chloroform is extremely rare. Our case illustrates that with appropriate supportive care, patients can recover from chloroform ingestion, and intravenously administered NAC may be of benefit in such cases.

Lethal complications after poisoning with chloroform--case report and literature review.

Chloroform is a potent central nervous system and respiratory depressant. The toxicities associated with chloroform frequently occur after inhalation. Hepatotoxicity is secondary to production of a toxic metabolite, with a peak elevation of liver enzymes 72 hours after exposure. Acute liver failure after chloroform inhalation is rarely described, this syndrome being produced mainly by viral hepatitis, idiosyncratic drug-induced liver injury, and acetaminophen ingestion. This report describes the case of a 46-year-old woman who presented to emergency department with coma, signs of respiratory failure, and solvent odor of her breath after chloroform inhalation and binge drinking. In evolution appeared lethal acute liver failure and rhabdomyolysis, despite maximum supportive care. Necroptic examination revealed microvesicular steatosis and tubular renal necrosis, specific for chloroform toxicity. This case illustrates the dramatic impact on liver of two well-recognized hepatotoxins. Mechanisms of chloroform and alcohol-induced liver toxicity are reviewed.

A chloroform-related death: analytical and forensic aspects.

Chloroform is still encountered occasionally in clinical and forensic toxicology, hence knowledge of the special problems presented in the detection and measurement of this compound in biological specimens may be required. The aim of this paper is to review the available documentation on this topic in the context of a chloroform-related death. Early one morning in February 1999 a 34-year-old female was found dead fully clothed on a path near to a neighbour's garden. Amfetamine intoxication combined with hypothermia was accepted as the cause of the death in the absence of any other identifiable cause. Further investigation 17 months later revealed a blood chloroform concentration of 31 mg/L and the cause of death was revised to chloroform poisoning. A murder trial ensued, the indictment specifying forced inhalation as the route of exposure. The liver chloroform concentration measured 38 months after collection was reported as 1064 mg/kg and opinions were offered at trial that the autopsy findings, which included a gastritis, but no evidence of injury to the inside of the mouth and oesophagus, excluded the possibility of ingestion of a toxic dose of chloroform. It was asserted that the explanation for the high liver concentration was that the liver had concentrated chloroform from blood after death against a concentration gradient. At appeal against conviction 7 years later the conviction was quashed. It was found that the liver concentration should have been reported at trial as 1 mg/kg. Moreover, chloroform found in the stomach contents (162 mg/kg) 86 months after collection was irrefutable evidence that some, if not all, of the chloroform had been ingested. Screening for volatile poisons should always be considered if a cause of death is not immediately obvious, especially in young people and in known substance abusers. If the presence of an unstable or volatile analyte is suspected then sample collection, transport, and storage must be performed with the analysis in mind. Quantitative analysis of all available specimens should proceed forthwith once the presence of an unstable analyte is established if the cause of death is in doubt or if prosecution may follow. In the case of chloroform especial precautions are needed: (i) headspace analysis should be performed at 35 degrees C to preclude the possibility of artefactual formation from trichloroacetic acid, (ii) precautions to prevent cross-contamination of biological samples in the laboratory must be taken, and (iii) interpretation of analytical results must take account of the widespread presence of chloroform in the environment on the one hand, and that the toxicity of chloroform varies greatly depending on the circumstances and intensity of exposure on the other.

A case of acute toxic hepatitis after suicidal chloroform and dichloromethane ingestion.

Chloroform and dichloromethane are halogenated hydrocarbons that have been used as a potent anesthetic agent or a general industrial solvent. Short-term exposure to chloroform anesthesia and long-term exposure to chloroform and dichloromethane in workplaces can produce adverse health effects, such as hepatitis, cardiac arrhythmia, and carbon monoxide intoxication. Most of the related reports, however, involve the inhalation of such substances by humans. Limited reports are available regarding the adverse clinical effects of these substances in the case of a person's immediate ingestion of them. A 23-year-old man with an altered mental status after attempting suicide through the oral ingestion of unknown chemicals was brought to the emergency department (ED). We identified that the patient was poisoned with chloroform and dichloromethane by analysis of contents of the suspected chemicals in the bottle through gas chromatography. Abnormal liver enzymes were noted on postingestion day 2, and jaundice occurred on postingestion day 3. The radiologic findings from computed tomographic (CT) scanning showed severe fatty infiltration of the liver parenchyma. The patient received supportive cares and was restored to health from hepatic dysfunction and was discharged without complications after 2 weeks of admission.

An unusual autoerotic fatality associated with chloroform inhalation.

We report the death of a young male attributed to chloroform poisoning during autoerotic asphyxia. He was found lying on the floor of his apartment, prone on a piece of foam and a towel. His eyes were bound with a towel, his lower face and nose were almost entirely covered with duct tape surrounding a rubber hose in his mouth. The other end of the hose was loosely sitting inside an open bottle which was in a box beside him. He was bound-up by an intricate system of ropes, handles, and rods, ending with a noose around his neck. Toxicology testing indicated chloroform concentrations of 18.1 mg/L in femoral blood and 1.5 mg/L in urine. Chloroform was measured by headspace gas chromatography with flame-ionization detection using 1,1,1-trichloroethane as the internal standard. The cause of death was recorded as "chloroform toxicity" with "autoerotic asphyxia" as a contributing factor, and the manner of death was "accidental".

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.

Diagnostic radiopacity and hepatotoxicity following chloroform ingestion: a case report.

BACKGROUND: Diagnostic imaging can help in the management of toxicologic emergencies. The authors report on a patient who presented to the emergency department with coma and suppressed respirations after ingestion of an unknown substance. METHODS: Ingestion of chloroform with radiopaque material in the bowel on abdominal radiograph was documented. The patient was treated with haemoperfusion, activated charcoal, and laxatives to decrease the toxicities. RESULTS: Hepatotoxicity occurred on post-ingestion day 3 and elevation of liver enzymes reached peak levels on post-ingestion day 5. The patient received N-acetylsystein and supportive care during hospitalisation. The patient improved from hepatic dysfunction and was discharged without complication on post-ingestion day 11. CONCLUSION: Radiographic studies in toxicology may confirm a diagnosis and assist in therapeutic intervention.