Pediatric Cannabis Single-Substance Exposures Reported to the Michigan Poison Center From 2008-2019 After Medical Marijuana Legalization.

BACKGROUND: Legalization of medical and recreational cannabis is a major contributor to pediatric cannabis exposures. The trends and magnitude of pediatric cannabis exposures in Michigan after medical cannabis legalization in 2008 have not been assessed. OBJECTIVE: To describe the temporal trends of pediatric cannabis exposures reported to the Michigan Poison Center (MiPC) after medical cannabis was legalized in 2008 and 1 year after legalization of recreational cannabis in 2018. METHODS: Retrospective electronic chart review of pediatric (<18 years old) single-substance cannabis exposures reported to the MiPC from January 1, 2008 to December 31, 2019. Routes of cannabis exposure were reported as ingestion, inhalation, and unknown. Types of ingested cannabis products were also documented. RESULTS: Between 2008 and 2019, 426 pediatric cannabis single exposures were reported. The median patient age was 6.0 years (interquartile range 2-15 years). Age distribution was bimodal. A total of 327 (76.8%) exposures were from cannabis ingestion, 79 (18.5%) from inhalation, 2 (0.5%) from both ingestion and inhalation, and 18 (4.2%) from unknown route. The doubling time for number of cases was 2.1 years, and the total number of annual reported cases increased after 2016. Teenagers (13-17 years) had the highest number of inhalational exposures, whereas young children (0-5 years) had the highest number of ingestions. CONCLUSION: Single-substance pediatric cannabis exposures reported to the Michigan Poison Center increased after medical cannabis was legalized in 2008 through recreational legalization in 2018.

Pennies for Your Thoughts: A Case Series of Pancytopenia Due to Zinc-induced Copper Deficiency in the Same Patient.

A 47-year-old schizophrenic male presented on three separate occasions with pancytopenia and sideroblastic anemia due to copper deficiency from massive zinc penny ingestion. The poisoning was treated differently on each visit: intravenous (IV) copper plus surgical decontamination and chelation with calcium disodium versenate (CaNa2EDTA); IV copper plus whole bowel irrigation; and IV copper with surgical decontamination only. Serum zinc half-lives were 80.0 hours, 233.2 hours, and 83.9 hours, respectively. Importantly, chelation with CaNa2EDTA did not significantly alter the elimination half-life. This is the first reported case of the same patient being treated on three different occasions with three different regimens for this condition.

Consensus statements on the approach to patients in a methanol poisoning outbreak.

Background: Methanol poisoning is an important cause of mortality and morbidity worldwide. Although it often occurs as smaller sporadic events, epidemic outbreaks are not uncommon due to the illicit manufacture and sale of alcoholic beverages.Objective: We aimed to define methanol poisoning outbreak (MPO), outline an approach to triaging an MPO, and define criteria for prioritizing antidotes, extracorporeal elimination treatments (i.e., dialysis), and indications for transferring patients in the context of an MPO.Methods: We convened a group of experts from across the world to explore geographical, socio-cultural and clinical considerations in the management of an MPO. The experts answered specific open-ended questions based on themes aligned to the goals of this project. This project used a modified Delphi process. The discussion continued until there was condensation of themes.Results: We defined MPO as a sudden increase in the number of cases of methanol poisoning during a short period of time above what is normally expected in the population in that specific geographic area. Prompt initiation of an antidote is necessary in MPOs. Scarce hemodialysis resources require triage to identify patients most likely to benefit from this treatment. The sickest patients should not be transferred unless the time for transfer is very short. Transporting extracorporeal treatment equipment and antidotes may be more efficient.Conclusion: We have developed consensus statements on the response to a methanol poisoning outbreak. These can be used in any country and will be most effective when they are discussed by health authorities and clinicians prior to an outbreak.

Carfentanil-Associated Mortality in Wayne County, Michigan, 2015-2017.

OBJECTIVES: To identify opioids associated with a spike in opioid-related mortality in Wayne County, Michigan, from July 2016 through February 2017. METHODS: We reviewed records from the Wayne County Medical Examiner's Office of 645 people who died because of accidental nonmedically prescribed opioid overdoses from July 2015 through July 2017. We analyzed basic demographics, locations of death, and all opioid toxicology results. Decedents who died in hospitals were excluded. RESULTS: Of the 645 people who died because of nonmedically prescribed opioid overdoses, 65% were male and 63% were White, with an average age of 43 years. Carfentanil was detected in 129 (20%) cases. During the 8-month mortality spike, carfentanil was detected in 114 of 419 cases (average = 27.2%; range = 6.4%-45.2%). Substances most frequently detected with carfentanil included morphine (57%), 6-monoacetylmorphine (38%), fentanyl (43%), norfentanyl (33%), tetrahydrocannabinol (34%), and cocaine (29%). CONCLUSIONS: The Wayne County spike in mortality temporally corresponded with the detection of carfentanil and a proportional increase in opioid overdose deaths with detectable carfentanil. Public Health Implications. The abrupt decrease in carfentanil-detected mortality coincided with an announcement indicating an impending ban on fentanyl analogs from China, which suggests that source control is an effective countermeasure.

Characteristics of Tianeptine Exposures Reported to the National Poison Data System - United States, 2000-2017.

Tianeptine (marketed as Coaxil or Stablon) is an atypical tricyclic drug used as an antidepressant in Europe, Asia, and Latin America. In the United States, tianeptine is not approved by the Food and Drug Administration (FDA) for medical use and is an unscheduled pharmaceutical agent* (1). Animal and human studies show that tianeptine is an opioid receptor agonist (2). Several case studies have reported severe adverse effects and even death from recreational abuse of tianeptine (3-5). To characterize tianeptine exposures in the United States, CDC analyzed all exposure calls related to tianeptine reported by poison control centers to the National Poison Data System (NPDS)† during 2000-2017. Tianeptine exposure calls, including those for intentional abuse or misuse, increased across the United States during 2014-2017, suggesting a possible emerging public health risk. Most tianeptine exposures occurred among persons aged 21-40 years and resulted in moderate outcomes. Neurologic, cardiovascular, and gastrointestinal signs and symptoms were the most commonly reported health effects, with some effects mimicking opioid toxicity. A substantial number of tianeptine exposure calls also reported clinical effects of withdrawal. Among 83 tianeptine exposures with noted coexposures, the most commonly reported coexposures were to phenibut, ethanol, benzodiazepines, and opioids.

A 29-year analysis of acute peak salicylate concentrations in fatalities reported to United States poison centers.

BACKGROUND/OBJECTIVES: The threshold salicylate concentration commonly recommended to initiate extracorporeal elimination, in the absence of significant end-organ toxicity, is 100 mg/dL. Unfortunately, the grade of evidence to support this decision is low. Our primary aim is to describe highest reported salicylate concentrations in patients who died from acute salicylate ingestions. Our secondary aim is to determine if age or coingestants varied with highest reported salicylate concentration. METHODS: We analyzed acute salicylate fatalities reported to the National Poison Data System (NPDS) between 1 January 1986 and 31 December 2014. Included were patients who died during the index hospitalization and for which acute salicylate toxicity was the primary cause of death. We used descriptive statistics with standard deviations (SD) or 95% confidence intervals (CI) where appropriate. We created a general linear model that evaluated the association of age and coingestions with salicylate concentrations. We divided the patients into age quartiles to assess a possible interaction between age and salicylate concentration. RESULTS: We identified 602 acute salicylate fatalities that fit inclusion criteria. The mean peak reported fatal salicylate concentration across all age groups was 99.19 mg/dL (± 50.2 mg/dL). The median peak fatal salicylate concentration was 97.0 mg/dL. The oldest quartile had a lower mean concentration (age >57 years; 90.4 mg/dL) than the youngest quartile (age <30 years; 111.6 mg/dL, mean difference 21.2 mg/dL, 95%CI 6.1-36.3). Fatalities with a coingestant had a lower mean concentration of 91.5 mg/dL compared to 104.8 mg/dL among those ingesting salicylates alone (mean difference 13.4 mg/dL, 95%CI 21.4-5.3). Increasing age and the presence of any coingestions were negatively associated with fatal concentrations (estimates; 95%CI 0.41; 0.61-0.021 and -14.43; 22.45-6.42, respectively). When opioids were a coingestant, mean concentration was 72.8 (mean difference 32.1 95%CI 23.1-41.1). CONCLUSIONS: Using the current recommended hemodialysis threshold of 100 mg/dL, more than half of the patients would be deprived of this critical life-saving therapy. Additionally, increasing age and ingestion of other substances, especially opioids, are associated with lower peak fatal salicylate concentrations. A prospective, randomized controlled trial considering salicylate concentrations and other clinical factors may provide further guidance for hemodialysis.

Basal Ganglion Hemorrhage as Delayed Complication of Diethylene Glycol Ingestion.

Diethylene glycol (DEG), an organic compound (HOCH2CH2)2O is a commonly used solvent. Mass poisoning outbreaks have been reported because of frequent contaminations. A PubMed search for diethylene resulted in 795 publications with 151 specifically discussing the toxicity. Of the 151 reported toxicity reviews/case reports, only 6 publications discussed the long-term neurological effects of diethylene toxicity. We report a fatal case of oral ingestion of DEG with complications from delayed toxicity. She died 7 days after the second admission. Autopsy disclosed a right basal ganglia hemorrhage within the brain and microscopic deposits of polarizable crystals into small cerebral blood vessels. Both kidneys illustrate tubular necrosis with scattered tubular deposition of polarizable calcium oxalate crystals. PubMed search leads to only 2 reported cases of basal ganglia hemorrhage (based on radiological findings) after ethylene glycol intoxication. Our case is the first reportable case of basal ganglia hemorrhage after DEG ingestion.

Organophosphate and carbamate poisoning.

Organophosphates (OPs) and carbamates have a wide variety of applications, most commonly as pesticides used to eradicate agricultural pests or control populations of disease-carrying vectors. Some OP and carbamates have therapeutic indications such as physostigmine. Certain organophosphorus compounds, known as nerve agents, have been employed in chemical warfare and terrorism incidents. Both classes inhibit acetylcholinesterase (AChE) enzymes, leading to excess acetylcholine accumulation at nerve terminals. In the setting of toxicity from either agent class, clinical syndromes result from excessive nicotinic and muscarinic neurostimulation. The toxic effects from OPs and carbamates differ with respect to reversibility, subacute, and chronic effects. Decontamination, meticulous supportive care, aggressive antimuscarinic therapy, seizure control, and administration of oximes are cornerstones of management.

Usefulness of intravenous lipid emulsion for cardiac toxicity from cocaine overdose.

The investigators describe the clinical course of a 26-year-old-man who was brought to the emergency department in a comatose state with status epilepticus after smoking a large amount of crack cocaine. In the emergency department, he was intubated because of depressed mental status and respiratory acidosis. His troponin I remained negative, and electrocardiography showed wide-complex tachycardia with a prolonged corrected QT interval. Because of the corrected QT interval prolongation and wide-complex tachycardia, the patient was started on intravenous magnesium sulfate and sodium bicarbonate. Despite these interventions, no improvement in cardiac rhythm was observed, and electrocardiography continued to show wide-complex tachycardia. The patient became more unstable from a cardiovascular standpoint, with a decrease in blood pressure to 85/60 mm Hg. He was then given 100 ml of 20% lipid emulsion (Intralipid). Within 10 minutes of starting the infusion of 20% lipid emulsion, wide-complex tachycardia disappeared, with an improvement in systemic blood pressure to 120/70 mm Hg. Repeat electrocardiography after the infusion of intravenous lipid emulsion showed regular sinus rhythm with normal QRS and corrected QT intervals. The patient was successfully extubated on day 8 of hospitalization and discharged home on day 10. His cardiac rhythm and blood pressure remained stable throughout his further stay in the hospital.

Lethal serotonin syndrome after methylone and butylone ingestion.

INTRODUCTION: A new generation of designer phenethylamines have emerged and aggressively marketed as "legal highs." The drugs are labeled "not for human consumption" to avoid widespread recognition and prosecution under the existing analog drug laws. The newest generation includes methylone and butylone. Methylone and butylone have minor structural changes and similar pharmacodynamics properties to scheduled drugs. CASE REPORT: We report a case of a healthy 24-year-old who ingested a capsule containing methylone and butylone sold as "Ecstasy" at a concert. The patient presented to the emergency department, comatose febrile, tachycardic, tachypnic, and hypertensive. On exam, she was diaphoretic, tremulous, hyperreflexic, and had sustained clonus. The patient was aggressively cooled, and despite maximal supportive care, the patient progressed to multi-system organ failure and ultimately expired. We obtained and analyzed both her urine and a capsule found on her person similar to the capsules ingested. In both samples, laboratory analysis identified only methylone and butylone. CONCLUSION: This is the first reported death for methylone or butylone and the first human or animal ingestion of butylone. Clinicians and public health officials should work together as new designer drugs emerge.

Acute clenbuterol overdose resulting in supraventricular tachycardia and atrial fibrillation.

OBJECTIVE: We are presenting a case illustrating the complex metabolic and rhythm disturbances associated with acute clenbuterol intoxication. BACKGROUND: Clenbuterol is a long-acting beta2-adrenergic agonist primarily used in veterinary medicine in the United States. It has become a common drug of abuse by body builders because of its reported anabolic and lipolytic properties. In this case report, a body builder using veterinary clenbuterol developed significant electrolyte and cardiac manifestations. CASE REPORT: A 31-year-old man presented to the emergency department approximately 30 minutes after ingesting 1.5 ml (a tenfold dosing error) of Ventipulmin syrup (72.5 mcg/ml clenbuterol HCl). The product was brought to the emergency department (ED) by the patient. He reported no current use of anabolic steroids. He presented in an anxious state with complaints of palpitations and shortness of breath. Vital signs upon examination were as follows: BP, 122/77 mmHg (16.3/10.3 kPa); HR 254 bpm; RR, 22 bpm; Temperature, 97.1 degrees F (36 degrees C); and oxygen saturation, 100% on ambient air. His electrocardiogram (ECG) demonstrated supraventricular tachycardia with a ventricular rate of 254 bpm. Esmolol was recommended for rate control after the unsuccessful use of adenosine and diltiazem. Laboratory studies showed potassium, 2.1 mmol/L; magnesium, 1.3 mg/dL (0.54 mmol/L); phosphorus, 1.0 mg/dL (0.32 mmol/L); serum glucose, 209 mg/dL (11.6 mmol/L); creatinine, 0.8 mg/dL (70.7 micromol/L); AST, 20 U/L; ALT, 55 U/L; hemoglobin, 12.6 g/dL (126 g/L); CPK total, 87 U/L; and troponin I, 0.23 mug/L. The patient's urine was negative for any drugs of abuse. Clenbuterol levels were not obtained. A second ECG, 16 hours post ingestion, reflected atrial fibrillation with a ventricular rate of 125 to 147 bpm. On hospital day 3, he was electively cardioverted to sinus rhythm; heart rate and rhythm returned to normal, and he was discharged with oral metoprolol. DISCUSSION: Clenbuterol is approved for use in countries outside the U.S. as a bronchodilator for the treatment of acute asthma exacerbations in humans. Although clenbuterol is not a steroid hormone, it possesses anabolic properties that increase muscle mass. Its longer duration of action compared to other beta2-agonists (such as albuterol) make it a desired agent for body-building because of its high and prolonged serum level. The mechanism for the short and long-term cardiovascular complications of clenbuterol is complex. The anabolic effects of clenbuterol are associated with its beta2-adrenoreceptor agonist activity on striated skeletal muscles. In addition, clenbuterol promotes lipolysis through adipocyte beta3-adrenoreceptors. CONCLUSION: Considering the significant number of body-building enthusiasts, physicians will continue to encounter clenbuterol abuse in their clinical practices.