Optic Nerve Atrophy in Heroin Intoxication

Drug dependence is one of important social problems in modern society. It became more actual because of the high morbidity in young working-age patients. The central nervous system is the main target for psychoactive substances. Long-term drug intoxication results in functional and structural brain alterations, it leads to cognitive impairment and disturbances of higher mental functions rendering patients’ disadapted in their work and daily life activities. Eye disorders due to drug abuse are multifaceted and can vary from conjunctival damage to severe endogenous endophthalmitis. Opioid dependence can result not only from intentional self-administration of narcotic drugs, but also from long-term prescribed use of these medicinal products owing to their potent analgesic effect exhibited in somatically ill patients with severe chronic pain. Opioid derivatives act as partial or full agonists of three types of opioid receptors (δ, κ, and µ) extensively expressed by the neurons of the central and, to a lesser extent, peripheral nervous system. The most dangerous complication of intoxication with this group narcotic drugs is opioid induced-respiratory depression resulting in hypoxaemia and hypercapnia. The paper presents a case report of bilateral optic nerve atrophy that developed in a young female patient after a long period of intravenous heroin use. There are practically no reports of optic nerve damage due to heroin intoxication in the current literature. Possible optic nerve atrophy mechanisms under discussion include generalized hypoxia developing against a background of chronic heroin intoxication and direct toxicity of admixtures used to dilute home-made narcotic drugs. In view of the growing use of these substances, physicians have to consider their effects in the differential diagnosis in patients with atypical eye disorders.

Opioid overdoses: Emerging clinical challenges

Objective: Analysis of a large consecutive case series of cases brought to an Emergency Department (ED).Design: Retrospective chart review.Setting: Emergency Department in Broward County, Florida.Patients: Medical records of patients with registered diagnoses of opioid overdose in 2016 and 2017.Outcomes: Demographics, toxicology results, mental-health comorbidities, use/response to naloxone, and hospital disposition.Results: Seven hundred and seventy nine opioid-overdose cases were identified (35 percent female, 65 percent male; age 36.2). Heroin intoxication was registered in 77 percent of discharge diagnoses, and 17.7 percent were prescription pain medications. Urine samples were collected in 39 percent and 81.5 percent of patients received naloxone (mean dose 4.0 mg ± 2.2). Sixty-five percent of cases were discharged home, 17.5 percent left the ED against medical advice, and 17.5 percent were admitted to the hospital/intensive care unit/behavioral unit.Conclusion: There is an alarming number of visits to the ED due to opioid overdoses with differences in age and gender. Clinicians are facing diagnostic, treatment and follow-up challenges for the management of these cases.

Wound botulism presenting as dysphagia to an ENT ward

A 44-year-old man with a background of heroin injection drug use was referred to the ear, nose and throat team with a sore throat and dysphagia. He was treated with intravenous antibiotics and steroids for suspected uvulitis. He developed progressive bulbar weakness and symmetrical descending weakness of the upper extremities over a 12-hour period and was intubated prior to transfer to the intensive care unit.Botulinum heptavalent antitoxin was administered, and subsequent PCR assay confirmed Clostridium botulinum neurotoxin B from his most recent injection site. He was found unconscious on the ward 3 days following extubation. Postmortem confirmed he died from heroin intoxication.This case highlights the importance of considering wound botulism in injection drug users presenting with unexplained weakness, particularly of the lower cranial nerves. Botulism is not characteristically associated with signs of localised or systemic infection in contrary to other bacterial complications of injection drug use.

Four cases of death involving the novel synthetic cannabinoid 5F-Cumyl-PEGACLONE

Purpose Cumyl-PEGACLONE was the first synthetic cannabinoid (SC) with a γ-carbolinone core structure detected in forensic casework and, since then, it has dominated the German SC-market. Here the first four cases of death involving its fluorinated analog, 5F-Cumyl-PEGACLONE, a recently emerged γ-carbolinone derived SC, are reported. Methods Complete postmortem examinations were performed. Postmortem samples were screened by immunoassay, gas chromatography mass spectrometry (GC–MS) or liquid chromatography tandem mass spectrometry. For quantification of SCs, the standard addition method was employed. Herbal blends were analyzed by GC–MS. In each case of death, the Toxicological Significance Score (TSS) was assigned to the compound. Results 5F-Cumyl-PEGACLONE was identified at concentrations ranging 0.09–0.45 ng/mL in postmortem femoral blood. In case 1, signs of hypothermia and kidney bleedings were noted. Despite a possible tolerance due to long term SC use, a TSS of 3 was assigned. In case 2, an acute heroin intoxication occurred and a contributory role (TSS = 1) of 5F-Cumyl-PEGACLONE was suggested. In case 3, a prisoner was found dead. GC–MS analysis of herbal blends, retrieved in his cell together with paraphernalia, confirmed the presence of 5F-Cumyl-PEGACLONE and a causative role was deemed probable (TSS = 2). In case 4, the aspiration of gastric content due to a SC-induced coma was observed (TSS = 3). Conclusions 5F-Cumyl-PEGACLONE is an emerging and extremely potent SC which raises serious public health concerns. A comprehensive analysis of circumstantial, clinical, and postmortem findings, as well as an in-depth toxicological analysis is necessary for a valid interpretation and for the assessment of the toxicological significance.

Heroin overdose masquerades as methomyl poisoning: a case report

Background Methomyl is the most common cause of suicidal death but heroin is the most common cause of accidental death. The problem is to determine the exact cause and manner of death between methomyl or heroin toxicity. The evidence from autopsy includes crime scene investigation, toxicological analysis by liquid chromatography with mass spectrometry, and knowledge of methomyl and heroin intoxication. Case presentation A 35-year-old Thai man and a 30-year-old Thai woman were found showing evidence of cyanosis, with a fine froth around the nose and mouth. Postmortem interval time was 24 hours. According to the police’s and hotel owner’s records, the couple stayed together for 1 day before being found dead in bed, naked, with a foul and a fine froth around the nose and mouth. A methomyl insecticide sachet and a plastic box containing white powder form of heroin were found at the scene. Laboratory tests of the male corpse identified the presence of methomyl in the blood of the stomach and morphine, codeine, methadone, and tramadol in the systemic blood. Blood cholinesterase enzyme activity and morphine concentration was 3416 U/L or 53% (normal 6400 U/L) and 0.058 μg/ml respectively. Laboratory test of the female corpse identified the presence of methomyl in the stomach and blood, and cholinesterase enzyme activity was 1965 U/L or 30.7%. Conclusions Cause of death of the male corpse was deemed to be due to heroin intoxication as the blood concentration of morphine was more than the lethal concentration with a morphine/codeine ratio of more than 1:1. Methomyl intoxication of the male corpse was unlikely to be the cause of death because methomyl systemic blood concentration was found to be very low, < 2.5 μg/ml, and cholinesterase enzyme levels did not indicate lethal activity (< 10–15% of normal). The main problem regarding an insurance claim is that the policy will not pay out in the case of heroin-associated deaths, as it is an addictive drug. The policy would pay out on death by suicide with methomyl insecticide, which was not prohibited by the insurance company after 1 year of insurance. So, it is not clear whether or not the family will receive money from the insurance company.

The Elephant in the Room

Over a three-month period in early 2017, the Hennepin County Medical Examiner’s Office investigated nine apparent opioid toxicity deaths that occurred in three separate urban, suburban, and rural counties in our jurisdiction. All decedents were known substance abusers and had reportedly recently used heroin; most were found with drug paraphernalia. Complete autopsies variably showed classic stigmata of opioid overdose with no significant injury or natural disease to explain death. Initial toxicology screens failed to identify heroin or other narcotic substances. Several cases were presumptively positive for fentanyl by immunoassay, yet failed to confirm positive for fentanyl. Following American Board of Forensic Toxicology reporting standards, these cases were reported as negative for fentanyl by the laboratory. Due to the discrepant scene and toxicology findings suggestive of an opioid toxicity death, further discussion between the medical examiners and toxicologists prompted additional testing at a referral laboratory. This resulted in quantifiable blood carfentanil in all cases (mean 0.26 ng/mL, range 0.12 – 0.64 ng/mL). Cointoxicants included ethanol (n=2), methamphetamine (n=3), benzodiazepines (n=3), and cocaine (n=1). No case had definitive evidence of acute heroin intoxication, but two cases had low concentrations of morphine present (0.03 and 0.06 ng/mL), and two others had 6-monoacetyl morphine in the urine without morphine in the blood, suggesting recent use. All deaths were certified as accidental acute or mixed carfentanil toxicity. These cases present additional information about carfentanil-related deaths and highlight the importance of collaboration between forensic pathologists and toxicologists.