Fentanyl-contaminated cocaine outbreak with laboratory confirmation in New York City in 2019
BACKGROUND:Illicitly manufactured fentanyl and fentanyl analogues (IMFs) are being increasingly suspected in overdose deaths. However, few prior outbreaks have been reported thus far of patients with laboratory-confirmed IMF toxicity after reporting intent to use only nonopioid substances. Herein we report a case series of nine patients without opioid use disorder who presented to two urban emergency departments (EDs) with opioid toxicity after insufflating a substance they believed to be cocaine. CASE REPORTS/METHODS:Over a period of under three hours, nine patients from five discrete locations were brought to two affiliated urban academic EDs. All patients denied prior illicit opioid use. All patients endorsed insufflating cocaine shortly prior to ED presentation. Soon after exposure, all developed lightheadedness and/or respiratory depression. Seven patients received naloxone en route to the hospital; all had improvement in respiratory function by arrival to the ED. None of the patients required any additional naloxone administration in the ED. All nine patients were discharged home after observation. Blood +/- urine samples were obtained from eight patients. All patients who provided specimens tested positive for cocaine metabolites and had quantifiable IMF concentrations, as well as several detectable fentanyl derivatives, analogues, and synthetic opioid manufacturing intermediates. DISCUSSION/CONCLUSIONS:IMF-contamination of illicit drugs remains a public health concern that does not appear to be restricted to heroin. This confirmed outbreak demonstrates that providers should elevate their level of suspicion for concomitant unintentional IMF exposure even in cases of non-opioid drug intoxication. Responsive public health apparatuses must prepare for future IMF-contamination outbreaks.
Fentanyl-contaminated cocaine poisonings: A case series with laboratory confirmation [Meeting Abstract]
Background: The opioid epidemic remains a significant public health problem in the United States. Illicitly manufactured fentanyl and fentanyl analogues (IMFs) are being increasingly identified in overdose deaths. Fentanyl is approximately 100 times more potent than morphine, and IMFs have become an economical way to adulterate or replace heroin among illicit drug distributors and patients with opioid use disorder (OUD). While adulteration by IMFs is increasingly recognized among patients with OUD, what has received less attention is the contamination of non-opioid illicit substances, such as cocaine, with IMFs. There are few prior outbreaks that have been reported thus far of patients with laboratory-confirmed IMF toxicity after reporting intent to use only nonopioid substances. Herein we report a case series of nine patients without OUD who presented to two urban emergency departments (EDs) with opioid toxicity after insufflating a substance they believed to be cocaine. Case Reports: Over a period of under three hours, nine patients from five discrete locations were brought to two affiliated urban academic EDs. All patients were in their third decade of life and denied prior illicit opioid use. Two patients reported prior opioid exposure in the form of prescribed analgesics only, both more than one year prior. One patient reported a remote history of deep venous thrombosis; all others denied any significant past medical history. All patients endorsed insufflating cocaine shortly prior to ED presentation. Over the seconds to minutes following insufflation, all patients developed lightheadedness, and seven patients lost consciousness. In all cases of loss of consciousness, Emergency Medical Services responded and found the patients to have varying degrees of respiratory depression. These seven patients received naloxone en route to the hospital (Table 1) and all had improvement in respiratory function by arrival to the ED. None of the patients required any additional naloxone administration in the ED. All nine patients reported nausea and/or emesis which resolved with symptomatic treatment. All nine patients were discharged to home after an observation period. Blood samples were obtained from eight patients, and urine samples from six of these. One patient declined laboratory testing. All patients who provided specimens tested positive for cocaine metabolites and had quantifiable IMF concentrations, as well as several detectable fentanyl derivatives, analogues, and synthetic opioid manufacturing intermediates. (Table 2) Discussion: The geographic and temporal proximity of our patients' presentations, combined with the overlap in fentanyl precursors and analogues found on laboratory testing strongly suggests a common source, though sample product was not available for confirmation. Interpretation of this data is subject to a number of limitations, including variations in time between exposure and lab collection limiting interpatient comparability.
Conclusion(s): IMF-contamination of illicit drugs remains a public health concern that does not appear to be restricted to heroin. Increasing prevalence implies that providers should elevate their level of suspicion for concomitant IMF exposure even in cases of non-opioid drug intoxication. Responsive public health apparatuses need to prepare for future IMF-contamination outbreaks. (Table Presented)
A Novel Approach to Patient Education: Emergency Physicians in the Classroom [Meeting Abstract]
A RANKL Wrinkle: Denosumab-Induced Hypocalcemia
The human monoclonal antibody denosumab inhibits osteoclast-mediated bone resorption by binding to receptor activator of nuclear factor kappaB ligand (RANKL), which is upregulated by tumor cells. Denosumab is indicated to prevent skeletal-related events (SREs) from osteoporosis and metastatic bone disease. We report a case of denosumab-induced hypocalcemia to highlight potential toxicity and treatment considerations. A 66-year-old man with prostate cancer, small cell lung cancer, and bone metastases presented with fatigue, weakness, and muscle spasm. Sixteen days prior, he received cycle 6 of cisplatin and etoposide, leuprolide, and denosumab (120 mg subcutaneously). His examination demonstrated a slight resting tremor, normal strength, and negative Chvostek sign. Laboratory analysis revealed hemoglobin, 8.0 g/dL; total calcium, 5.2 mg/dL (pre-denosumab, 8.9 mg/dL); and magnesium, 0.7 mg/dL. He initially received two units packed red blood cells, intravenous calcium and magnesium, and vitamin D. During his hospitalization, he required multiple doses of intravenous and oral calcium, magnesium, and vitamin D. Despite ongoing oral supplementation, his post-discharge serum calcium fluctuated significantly, requiring close monitoring and frequent dose adjustments. Denosumab's unique antiresorptive properties yield fewer SREs. The trade-off is increased hypocalcemia risk, which may be severe and require aggressive, prolonged supplementation and monitoring.
Authors' response to: "Beta-blocker treatment of caffeine-induced tachydysrhythmias"
Letter in response to: "Stimulant-induced hyperthermia and ice-water submersion: practical considerations", by John R. Richards et al., DOI -10.3109/15563650.2015.1104536 [Letter]
A RANKLing Case: Denosumab-Induced Hypocalcemia [Meeting Abstract]
Evolution of the NBOMes: 25C- and 25B- Sold as 25I-NBOMe
INTRODUCTION: The NBOMes (N-benzyl-oxy-methyl derivatives of known 2C phenylethylamines) are a new and growing class of potent synthetic stimulants. Case reports provide the bulk of available safety and clinical data for clinicians. We report two cases of NBOMe intoxication with 25C-NBOMe (the first lab-confirmed US case) and 25B-NBOMe, respectively, both confirmed via triple quadrapole mass spectrometry. CASE REPORTS: Case 1: A 16-year-old girl had a generalized seizure after reported use of 25I-NBOMe. She presented with altered mental status, lower extremity rigidity, and elevated CPK (6042 U/L). Despite treatment with benzodiazepines, her lower extremity rigidity persisted and CPK peaked at 47,906 U/L. She was discharged on hospital day 8. Serum and urine specimens confirmed presence of 25C-NBOMe. Case 2: A 15-year-old boy developed bizarre behavior after reported use of 25I-NBOMe. In the ED, he had two generalized seizures and persistent muscle rigidity. CPK peaked at 429 U/L. Seizures were managed with benzodiazepines, and he was discharged within 24 h. Serum specimens revealed 25B-NBOMe. DISCUSSION: NBOMes are amphetamine derivatives and highly potent 5-HT2A receptor agonists. Clinical manifestations are a product of enhanced central sympathetic and serotonergic tone. We report two cases of NBOMe intoxication in patients who believed they used 25I-NBOME, while lab confirmation proved otherwise. Whether unique clinical manifestations are specific to the NBOMe variant, dose, route of administration, or other factors is unknown. Laboratory confirmation may play a role in identifying unexpected NBOMe variants, while contributing to the epidemiologic data on these novel substances.
Ice water submersion for rapid cooling in severe drug-induced hyperthermia
Abstract Context. The optimal method of cooling hyperthermic patients is controversial. Although controlled data support ice water submersion, many authorities recommend a mist and fan technique. We report two patients with drug-induced hyperthermia, to demonstrate the rapid cooling rates of ice water submersion. Case details. Case 1. A 27-year-old man presented with a sympathomimetic toxic syndrome and a core temperature of 41.4 degrees C after ingesting 4-fluoroamphetamine. He was submerged in ice water and his core temperature fell to 38 degrees C within 18 minutes (a mean cooling rate of 0.18 degrees C/min). His vital signs stabilized, his mental status improved and he left on hospital day 2. Case 2. A 32-year-old man with a sympathomimetic toxic syndrome after cocaine use was transported in a body bag and arrived with a core temperature of 44.4 degrees C. He was intubated, sedated with IV benzodiazepines, and submerged in ice water. After 20 mins his temperature fell to 38.8 degrees C (a cooling rate of 0.28 degrees C/min). He was extubated the following day, and discharged on day 10. Discussion. In these two cases, cooling rates exceeded those reported for mist and fan technique. Since the priority in hyperthermia is rapid cooling, clinical data need to be collected to reaffirm the optimal approach.
Start me up! Recurrent ventricular tachydysrhythmias following intentional concentrated caffeine ingestion
CONTEXT: Nearly pure caffeine is sold as a "dietary supplement," with instructions to ingest 1/64th to 1/16th of one teaspoon (50-200 mg). We report a patient with refractory cardiac dysrhythmias treated with defibrillation, beta-adrenergic blockade, and hemodialysis to highlight concentrated caffeine's dangers. CASE DETAILS: A 20-year-old woman presented with severe agitation, tremor, and vomiting approximately 1-2 h after suicidal ingestion of concentrated caffeine (powder and tablets). Within minutes, ventricular fibrillation commenced. Defibrillation, intubation, and amiodarone administration achieved return of spontaneous circulation (ROSC). Shortly thereafter, she developed pulseless ventricular tachycardia (VTach), with ROSC after defibrillation and lidocaine. She subsequently experienced 23 episodes of pulseless VTach, each responsive to defibrillation. Activated charcoal was administered via orogastric tube. An esmolol infusion was started. Hemodialysis was initiated once she was hemodynamically stable. She was extubated the following day, continued on oral metoprolol, and transferred to psychiatry on hospital day seven, achieving full neurological recovery. Serum caffeine concentrations performed approximately six and 18 h post-ingestion (pre/post-dialysis) were 240.8 mcg/mL and 150.7 mcg/mL. DISCUSSION: Severe caffeine toxicity can produce difficult to treat, life-threatening dysrhythmias. Concentrated caffeine, marketed for dietary supplementation, presents a substantial public health risk that demands action to limit consumer availability.