I'm seeing fewer and fewer reports recently of cocaine cut with (significant amounts of) levamisole on ecstasydata.org, so we can only hope so.
As it turns out, that's not the worst thing cocaine could be cut with.
Tomassoni AJ, Hawk KF, Jubanyik K, et al.
Multiple Fentanyl Overdoses — New Haven, Connecticut, June 23, 2016. MMWR Morb Mortal Wkly Rep 2017;66:107–111. DOI:
http://dx.doi.org/10.15585/mm6604a4.
On the evening of June 23, 2016, a white powder advertised as cocaine was purchased off the streets from multiple sources and used by an unknown number of persons in New Haven, Connecticut. During a period of less than 8 hours, 12 patients were brought to the emergency department (ED) at Yale New Haven Hospital, experiencing signs and symptoms consistent with opioid overdose. The route of intoxication was not known, but presumed to be insufflation (“snorting”) in most cases. Some patients required doses of the opioid antidote naloxone exceeding 4 mg (usual initial dose = 0.1–0.2 mg intravenously), and several patients who were alert after receiving naloxone subsequently developed respiratory failure. Nine patients were admitted to the hospital, including four to the intensive care unit (ICU); three required endotracheal intubation, and one required continuous naloxone infusion. Three patients died. The white powder was determined to be fentanyl, a drug 50 times more potent than heroin, and it included trace amounts of cocaine. The episode triggered rapid notification of public health and law enforcement agencies, interviews of patients and their family members to trace and limit further use or distribution of the fentanyl, immediate naloxone resupply and augmentation for emergency medical services (EMS) crews, public health alerts, and plans to accelerate naloxone distribution to opioid users and their friends and families. Effective communication and timely, coordinated, collaborative actions of community partners reduced the harm caused by this event and prevented potential subsequent episodes.
Shortly after 4:00 p.m. on June 23, 2016, four patients with symptoms and signs of opioid overdose, characterized by central nervous system and respiratory depression, miosis (pinpoint pupil constriction), hypotension, and bradycardia, arrived in rapid succession at the York Street Campus (two patients) and St. Raphael Campus (two patients) EDs of Yale New Haven Hospital in downtown New Haven. Within 6 hours, seven additional patients arrived at the York Street Campus ED and one more at the St. Raphael ED; these patients included two who were pronounced dead on arrival and four critically ill patients requiring endotracheal intubation and ICU admission (Figure). The patients represented four geographic clusters (i.e., at least one other victim found in the same vehicle or parking lot, or in the same house or an adjacent house), and were transported by EMS crews responding to bystander 911 calls. All of the patients had clinical signs of opioid overdose and received at least one dose of naloxone from EMS (Table 1). Twelve patients met the case definition for suspected fentanyl exposure (i.e., clinical signs of opioid toxicity and response to naloxone, with laboratory confirmation of fentanyl or fentanyl metabolites in blood, or history of direct association with a laboratory-confirmed fentanyl exposure) (Table 1). Among the four patients admitted to the ICU, three required endotracheal intubation and mechanical ventilation for respiratory failure that was relatively refractory to large doses of naloxone, and one required a continuous naloxone infusion for 12 hours. Two of the three intubated patients suffered acute kidney injury and pulmonary or gastrointestinal hemorrhage, one of whom (patient K) died 3 days later from multisystem organ failure. The third patient survived with permanent cardiac injury. Other intoxicated patients who arrived at the ED with signs or symptoms of the opioid toxidrome were excluded from this analysis because of inconsistent history (e.g., patient reported using a nonfentanyl opioid) or toxicology test results that did not identify fentanyl.
Shortly after arrival in the ED, serum toxicology screens, designed to detect a panel of nonopioid toxins, were performed for all patients, and qualitative urine immunoassay toxicology screens for drugs of abuse were performed for nine patients (A, C, D, F, G, H, J, K, and L) (Table 2). The urine immunoassay screening tests cannot detect fentanyl and its analogs; however, all but one of the nine tested positive for cocaine. The one patient with a negative urine cocaine screen (patient A) acknowledged past cocaine use. Serum and urine specimens were later analyzed at the University of California, San Francisco (UCSF) using liquid chromatography high-resolution mass spectrometry (LC-HRMS) (1) to detect 215 common illicit and pharmaceutical drugs and metabolites, followed by additional analyses in attempts to identify 7,038 novel drugs and metabolites (2,3). Levels of fentanyl, cocaine, benzoylecgonine (a cocaine metabolite that persists in body fluids and is an indicator of cocaine use) and levamisole (a veterinary antihelminthic that has been used as a cocaine adulterant) were quantified. Nine patients (B, C, D, F, G, H, J, K, and L) had fentanyl detected in blood that was collected during their hospitalization and tested at UCSF (Table 2). One patient who reported cocaine use before symptom onset (patient A) and who was found in the vicinity of patients B, C, and D at the time of intoxication, was discharged before the full scope of the outbreak had been recognized and did not receive confirmatory toxicology testing. The Connecticut Medical Examiner’s Office performed postmortem toxicology screens on specimens obtained from two patients who died en route to the hospital (patients E and I).
Serum samples from the hospitalized patients analyzed at UCSF demonstrated fentanyl levels of 0.5–9.5 ng/mL (Table 2) (therapeutic range for analgesia = 0.6–3.0 ng/mL) (4); postmortem levels in the first two patients who died were 11 ng/mL (patient E) and 13 ng/mL (patient I). Norfentanyl, a major metabolite of fentanyl, was detected in the serum of nine patients; norfentanyl was not detected in postmortem testing of patients E and I, presumably because death occurred before metabolism of fentanyl to norfentanyl. All hospitalized patients had detectable serum levels of cocaine, cocaine metabolites (benzoylecgonine and ecgonine methyl ester), cocaethylene (a compound formed in vivo when ethanol is ingested in the presence of cocaine), or levamisole by LC-HRMS confirmatory testing (Table 2), all suggesting recent cocaine use. The absence of other opioids, such as heroin, methadone, or oxycodone, in serum (only one patient [D] was hydrocodone positive) was consistent with reports by the patients that most were not habitual opioid users.
Additional substances detected in serum and urine were reported qualitatively (Table 2) and reflected nicotine (cotinine), cannabinoid (tetrahydrocannabinol), and hydroxyzine (antihistamine) use, or receipt of naloxone. Postmortem toxicology screens identified fentanyl as a cause of death for patients E and I, both of whom arrived in the ED in cardiac arrest. In addition to the clinical specimens, one 32-mg forensic sample of the illicit drug material collected by law enforcement was tested at the Drug Enforcement Administration laboratory. Analysis of that product recovered from an involved crime scene found 6.6% (± 0.8% ) fentanyl by weight with trace amounts of cocaine and an inert adulterant.
Within a few hours of recognition of the outbreak, a multiagency response involving the New Haven Office of Emergency Management, New Haven and Connecticut Departments of Public Health, the Drug Enforcement Administration, local police, Connecticut Poison Control Center, and the New Haven Mayor’s Office was undertaken. Initial actions included 1) rapid notification of public health and law enforcement agencies by ED and EMS personnel; 2) real-time interviews of patients and family members in an attempt to trace and limit further use or distribution of the fentanyl; 3) advice to EMS crews to increase naloxone doses in treating suspected cases; 4) public health alerts regarding the event, including notices of the sale of a high potency opioid marketed as cocaine causing deaths in the region; and 5) plans to accelerate distribution of naloxone to opioid users and their friends and families. The high naloxone requirements necessitated both immediate naloxone resupply and augmentation for local EMS crews, including the transfer of 700 naloxone kits from the Connecticut Department of Public Health to hospitals and EMS crews the following morning. Actions of multiple partners led to the arrest 4 days later of three persons allegedly responsible for the illicit fentanyl sales.