Among the new psychoactive substances encountered in forensic investigations is the opioid, acetyl fentanyl. The death of a 28-year-old man from recreational use of this compound is reported. The decedent was found in the bathroom of his residence with a tourniquet secured around his arm and a syringe nearby. Postmortem examination findings included marked pulmonary and cerebral edema and needle track marks. Toxicological analysis revealed acetyl fentanyl in subclavian blood, liver, vitreous fluid, and urine at concentrations of 235 ng/mL, 2400 ng/g, 131 ng/mL, and 234 ng/mL, respectively. Acetyl fentanyl was also detected in the accompanying syringe. Death was attributed to recreational acetyl fentanyl abuse, likely through intravenous administration. The blood acetyl fentanyl concentration is considerably higher than typically found in fatal fentanyl intoxications. Analysis of this case underscores the need for consideration of a wide range of compounds with potential opioid-agonist activity when investigating apparent recreational drug-related deaths.

Effects of benzodiazepines on postmortem opioid parent and parent/metabolite blood concentration ratios were determined for fentanyl-, hydrocodone-, methadone-, or oxycodone-related accidental deaths. These opioids are partially metabolized by the CYP3A4 enzyme system, which is also affected by diazepam and alprazolam. Opioid/metabolite combinations examined were as follows: fentanyl/norfentanyl, hydrocodone/dihydrocodeine, methadone/EDDP, and oxycodone/oxymorphone. Parent opioid concentrations were analyzed for 877 deaths. Parent/metabolite concentration ratios were analyzed for 349 deaths, excluding cases with co-intoxicants present known to interfere with opioid elimination. Alprazolam in combination with diazepam significantly decreased median hydrocodone concentrations by 48% (p = 0.01) compared to hydrocodone alone. The methadone parent/metabolite concentration ratio was reduced by 35% in the presence of diazepam compared to methadone alone (p = 0.03). Benzodiazepines did not statistically significantly affect fentanyl or oxycodone concentrations. Possible factors affecting opioid concentrations and possible toxicity development, including any differential effects on specific opioids, should continue to be explored.

Cocaine is one of the most widely abused drugs and one that is frequently encountered in forensic toxicology laboratories. Most often, the detection of cocaine would lead toxicologists and forensic pathologists to believe that the drug was used illicitly; however, cocaine is an effective local anesthetic and vasoconstrictor and is used clinically in surgeries of the eye, ear, nose, and throat. Therefore, it is important to note that the presence of cocaine and its metabolites in forensic samples cannot always be attributed to abuse and that a thorough investigation and review of medical records is warranted before an informed conclusion can be made. In this case report, a 54-year-old male died three days after an altercation in which he suffered multiple injuries. In addition to natural disease and injuries documented at autopsy, cocaine and its metabolites were detected in the decedent's urine, and a review of surgical records showed that earlier on the day of death, he was administered cocaine clinically during a procedure to repair nasal bone fractures. If not for this comprehensive investigation and review of surgical records, the assumption of cocaine abuse might have otherwise been made and the cause and manner of death incorrectly established.

Carbon monoxide (CO) toxicity associated with exposure to an environmental, exogenous source, is routinely investigated in the field of forensics. Paramedics responded to the home of a 60-year-old woman who complained of persistent nausea, dizziness, and fatigue. Her initial carboxyhemoglobin (COHb) saturation was 25% as measured by paramedics in the field via pulse CO-oximetry (SpCO) and was, 2 hours later, confirmed by hospital laboratory spectrophotometric analysis to be 16% after initial treatment in the emergency department. The clinical presentation of environmental CO exposure and subsequent death notification to the North Carolina Office of the Chief Medical Examiner prompted an extensive investigation into the suspected residential source of CO, which ultimately ruled out all exogenous sources. The medicolegal death investigator later discovered an updated hematology consultation note, which determined the actual source of the CO to be endogenously produced from disease. Herein, we report an unusual fatality involving enhanced endogenous CO production caused by warm autoimmune hemolytic anemia. This unique case report and brief literature review of disease-related elevation of endogenous CO will shed light on this lesser-known phenomenon alerting the forensic community to its potential occurrence and need for consideration when sources of environmental exposure have been exhausted. K E Y W O R D Scarbon monoxide toxicity, carboxyhemoglobin, endogenous carbon monoxide, forensic pathology, medicolegal death investigation, warm autoimmune hemolytic anemia Highlights• Endogenous carbon monoxide (CO) production can reach clinically measurable levels in the setting of hemolytic anemia.• Endogenous CO may mimic symptoms of an environmental exposure in forensic investigations.• Among cases of warm autoimmune hemolytic anemia, those mediated by complement component 3 (C3) can sometimes be fatal.