Unintentional Pediatric Marijuana Exposures Prior to and After Legalization and Commercial Availability of Recreational Marijuana in Washington State.

BACKGROUND: Washington State was one of the first states to legalize recreational marijuana. Increased availability of marijuana may result in more unintentional pediatric exposure, which often presents as altered mental status with unknown cause. OBJECTIVES: To quantify unintentional pediatric marijuana exposures reported to the Washington Poison Center (WAPC) prior to and after legalization and commercial availability of recreational marijuana. METHODS: Data were obtained from the WAPC database, toxiCALL®. Patients ≤ 9 years old with a reported marijuana exposure between July 2010 and July 2016 were included in the analysis. Patient and exposure characteristics were summarized and median exposure frequencies were calculated for the periods prior to and after legalization. RESULTS: There were 161 cases meeting the inclusion criteria that occurred between July 2010 and July 2016. Of these, 130 (81%) occurred in the 2.5-year period after legalization of recreational marijuana in January 2013. The median age of exposed children was 2 years (range 0-9 years). Eighty-one percent of the exposures occurred in the child's own home. The number of exposures per month increased after recreational marijuana was legalized in November 2012, and increased further once recreational marijuana shops were legally allowed to open in July 2014. CONCLUSION: Reported unintentional pediatric marijuana exposure has increased in the state of Washington since recreational marijuana was legalized. As marijuana becomes more available, clinicians should be aware of the risk of unintentional pediatric marijuana exposure, and this should inform lawmakers regarding regulations around childhood exposure to marijuana.

Survival After Severe Rhabdomyolysis Following Monensin Ingestion.

INTRODUCTION: Monensin is a veterinary antibiotic with a narrow therapeutic window that has led to lethal intoxication in many animal species. Only two prior cases of human toxicity have been reported, both fatal. We present the first case of survival from severe toxicity following monensin ingestion. CASE: A 58-year-old man presented with 8 days of vomiting and abdominal pain. Due to delusions of central nervous system toxoplasmosis, he ingested 300 mg of monensin. His laboratory studies revealed severe rhabdomyolysis without renal dysfunction. Total creatine kinase (CK) peaked above 100,000 U/L. His CK decreased to 5192 U/L after 15 days of aggressive hydration and sodium bicarbonate therapy. His ejection fraction on echocardiogram decreased from 69 to 56%. DISCUSSION: Reports on acute clinical effects after human exposure to monensin are limited. Ingestion is known to cause skeletal and cardiac muscle rhabdomyolysis and necrosis. Animal studies demonstrate that monensin's toxicity is due to increases in intracellular sodium concentrations and Ca2+ release. To date, no effective antidotal treatment has been described. CONCLUSIONS: Monensin is a veterinary medication not approved for human use by the US Food and Drug Administration. Though poorly studied in humans, this case demonstrates the severe harm that may occur following ingestion.

A review of acetaminophen poisoning.

Acetaminophen poisoning remains one of the more common drugs taken in overdose with potentially fatal consequences. Early recognition and prompt treatment with N-acetylcysteine can prevent hepatic injury. With acute overdose, the Rumack-Matthew nomogram is a useful tool to assess risk and guide management. Equally common to acute overdose is the repeated use of excessive amounts of acetaminophen. Simultaneous ingestion of several different acetaminophen-containing products may result in excessive dosage. These patients also benefit from N-acetylcysteine. Standard courses of N-acetylcysteine may need to be extended in patients with persistently elevated plasma concentrations of acetaminophen or with signs of hepatic injury.

Validation of a pre-existing formula to calculate the contribution of ethanol to the osmolar gap.

PURPOSE: The aim of this study was to validate the formula derived by Purssell et al. that relates blood ethanol concentration to the osmolar gap and determine the best coefficient for use in the formula. The osmolar gap is often used to help diagnose toxic alcohol poisoning when direct measurements are not available. METHODOLOGY: Part I of the study consisted of a retrospective review of 603 emergency department patients who had a concurrent ethanol, basic metabolic panel and a serum osmolality results available. Estimated osmolarity (excluding ethanol) was calculated using a standard formula. The osmolar gap was determined by subtracting estimated osmolarity from the actual osmolality measured by freezing point depression. The relationship between the osmolar gap and the measured ethanol concentration was assessed by linear regression analysis. In Part II of this study, predetermined amounts of ethanol were added to aliquots of plasma and the estimated and calculated osmolarities were subjected to linear regression analysis. RESULTS: In the cases of 603 patients included in Part I of the study, the median ethanol concentration in these patients was 166 mg/dL (Q1: 90, Q3: 254) and the range ethanol concentrations was 10-644 mg/dL. The mean serum osmolality was 338 mOsm/kg (SD: 30) and a range of 244-450 mOsm/kg. The mean osmolar gap was 47 (SD: 29) and a range of - 15 to 55. There was a significant proportional relationship between ethanol concentration and osmolar gap (r(2) = 0.9882). The slope of the linear regression line was 0.2498 (95% CI: 0.2472-0.2524). The slope of the linear regression line derived from the data in Part II of the study was 0.2445 (95% CI: 0.2410-0.2480). CONCLUSIONS: The results of our study are in fairly close agreement with previous studies that used smaller samples and suggest that an accurate conversion factor for estimating the contribution of ethanol to the osmolar gap is [Ethanol (mg/dL)]/4.0.

Refractory hypotension due to Rogaine® (minoxidil) ingestion managed with midodrine.

BACKGROUND: Minoxidil (Rogaine®) is a direct vasodilator that can cause significant toxicity when ingested. We report a case of ingestion of topical minoxidil [Rogaine® (Johnson & Johnson Healthcare Products, Division of McNeil-PPC, Inc)] resulting in refractory hypotension that was successfully managed with the oral α (1) agonist midodrine. CASE REPORT: A 48-year-old male who ingested an eight ounce bottle of Rogaine® presented to the emergency department. The patient presented with a blood pressure of 57/45 mmHg and a pulse of 84 beats per minute. The patient received IV fluids and multiple vasopressors to maintain an adequate mean arterial pressure. Midodrine, an oral α (1) vasopressor, was added 10 hours post ingestion and was able to maintain an adequate mean arterial pressure. Over the next two days, midodrine was titrated down as his blood pressure returned to baseline. CONCLUSION: Midodrine may serve as an additional option to treat toxicant induced hypotension.