Delayed hyperthermia from chlorfenapyr overdose.

We describe the hospital course of a 42-year-old patient who presented to the Emergency Department following an ingestion of an unknown quantity of chlorfenapyr, an organochlorine pesticide that acts as a mitochondrial uncoupler (MU). There is limited data on chlorfenapyr toxicity in humans, but reports indicate a 100% mortality rate after a 7-10 day quiescent period.3-6 Our patient was admitted for a 5-day asymptomatic observation period before becoming critically ill. Supportive care, antioxidant therapy, and late hemodialysis (HD) proved futile. The patient expired from complications due to uncontrollable hyperthermia on hospital day 6. This case represents the first reported fatality due to chlorfenapyr in North America, and illustrates: 1) its potency as a human toxin, 2) the futility of extracorporeal decontamination once late toxicity has set in; 3) the potential need for early and aggressive decontamination in the ED; and 4) the need for a better understanding of this unique poison.

Retrospective Chart Review of Synthetic Cannabinoid Intoxication with Toxicologic Analysis.

INTRODUCTION: Use of synthetic cannabinoids (SC) has recently emerged as a new drug epidemic. Our emergency departments (EDs) received a surge of SC users presenting with lethargy and bradycardia, contrasting prior reports of SC-induced tachycardia and agitation. Our goal was to describe these novel presentations and characterize the compounds. METHODS: We present a case series of patients with SC intoxication who presented to our toxicology service covering two tertiary care EDs between 2/11/2015 and 6/23/2015. A retrospective chart review recorded initial vital signs, chief complaint and clinical course. Urine, blood and xenobiotic samples were analyzed using either liquid chromatography/mass spectrometry or gas chromatography/mass spectrometry. We compared resulting spectra against databases containing numerous SCs or metabolites and scored based on a reference comparison. RESULTS: Between 2/11/2015 and 6/23/2015, we identified 141 visits. Males comprised 139 visits (age range 21-68 years; median 35, interquartile range 20). Sixty-eight percent presented with lethargy or loss of consciousness. Hypotension (SBP <90 mmHg) and bradycardia (HR<60 bpm) were seen in 10% and 24% of visits, respectively. While most patients were discharged after observation, three were admitted to the intensive care unit and seven to telemetry. Admissions were for vital sign instability, bradycardia requiring pacing, prolonged sedation and respiratory failure requiring mechanical ventilation.Laboratory analysis revealed SC in the XLR-11 family in 18/36 drug, 9/12 blood, and 23/31 urine samples. Carboxamide indazole derivative (CID) family compounds were detected in 13/36 drug samples, 21/31 urine samples, but no blood samples; 11/31 drug samples contained both XLR-11 and CID. Other compounds detected included PB-22 and nicotine. No JWH compounds, opiates, imidazoline receptor agonists, benzodiazepines or other sedative-hypnotics were detected. CONCLUSION: Unlike their predecessors, novel SC may be associated with significant central nervous system depression and bradycardia. While prior reports indicated that SC mostly contained JWH compounds, none were detected in these samples. The most commonly identified compounds in this series were CID and alkyl SC derivatives, such as INACA compounds and XLR-11. These tend to be full agonists at the cannabinoid receptor and are presumably more potent. The lack of other depressants suggests that the clinical findings are due to the combination of these compounds and not coingestants or adulterants. SC intoxication should be considered for patients with undifferentiated psychomotor depression and bradycardia.

Hand Compartment Syndrome Due to N-acetylcysteine Extravasation.

N-acetylcysteine (NAC) is the antidote for acetaminophen (APAP)-induced hepatotoxicity. Both intravenous (IV) and oral (PO) NAC formulations are available with equal efficacy. Adverse events from either preparation are rare. We describe a hand compartment syndrome after extravasation of NAC requiring emergent fasciotomy during phase three of treatment for suspected APAP toxicity. Extravasation injuries leading to compartment syndrome are rare. It is unclear whether IV NAC induced a direct tissue-toxic insult, or functioned as a space-occupying lesion to cause a compartment syndrome. Compartment syndrome from extravasation of NAC is possible. In cases where IV access is difficult, PO NAC is an alternative.

A Massive Overdose of Dalfampridine.

Multiple sclerosis (MS) is an immune mediated inflammatory disease that attacks myelinated axons in the central nervous system. Dalfampridine (4-aminopyridine) was approved by the Food and Drug Administration in January 2010 for treatment of MS. Our patient was a 34-year-old male with a history of MS, who was brought to the emergency department after being found unresponsive. His current medications were valacyclovir, temazepam, dalfampridine (4-AP) and a tysabri intravenous (IV) infusion. Fifteen minutes after arrival the patient seized. The seizures were refractory to benzodiazepines, barbiturates and phenytoin. The 4-AP level was 530 ng/mL (25 ng/mL and 49 ng/mL). The patient stopped seizing on hospital day 3 and was discharged 14 days later with normal mental status and neurologic exam. 4-AP is a potassium channel blocker that blocks the potassium ion current of repolarization following an action potential. The blockade of the potassium channel at the level of the membrane widens the action potential and enhances the release of acetylcholine, thus increasing post-synaptic action potentials. The treatment of patients with 4-AP overdose is supportive. Animal data suggest that patients with toxic levels of 4-AP may respond to phenytoin. Our case illustrates the highest recorded level of 4-AP in an overdose. Our patient appeared to be refractory to a combination of high doses of anticonvulsants and only improved with time.

The synthetic cannabinoid withdrawal syndrome.

BACKGROUND: Little is known about the effects of synthetic cannabinoids. There has been only one previous report of a withdrawal syndrome from synthetic cannabinoids. We report two cases of a withdrawal syndrome from prolonged habitual use of synthetic cannabinoids. DISCUSSION: Withdrawal from delta-9-THC has been described as a syndrome of anxiety, myalgias, chills, and anorexia. Synthetic cannabinoids are potent than delta-9-THC and thus the withdrawal syndrome is similar but more severe; however the symptoms do not seem to improve with delta-9-THC. The differences in presentation could be due to the fact that synthetic products may contain several heterogeneous compounds, including amphetamine-like substances. CONCLUSIONS: The acute withdrawal syndrome appears to be characterized mainly by anxiety and tachycardia in the absence of any neurological findings or electrolyte disturbances. We describe two patients with symptoms consistent with withdrawal presumably due to synthetic cannabinoid use. The most appropriate treatment for such patients remains unknown, however benzodiazepines are a reasonable first line approach and quetiapine may have some efficacy.

Case series: inhaled coral vapor--toxicity in a tank.

INTRODUCTION: Palytoxin (PTX) is considered a severe marine toxin. Although rare, reports of human exposure from consumption of PTX have described significant morbidity and mortality. PTX is the suspected agent in Haff disease, in which rhabdomyolysis occurs within 24 h of eating contaminated fish such as buffalo fish. PTX is primarily present in soft corals or in dinoflagellates, and it can contaminate crustaceans and other fish as it bioaccumulates up the food chain. Only 23 cases have been reported in the USA, including two recent cases in New York City. Reports of inhalational exposure to PTX are uncommon. CASE REPORTS: We describe a case series of six patients, including four adults and two children, with inhalational exposure to PTX aerosolized from Palythoa corals. Their symptoms included some degree of respiratory involvement, myalgias, paresthesias, low-grade fevers, and gastrointestinal symptoms. Fortunately, there were no serious outcomes and all patients survived without sequelae. DISCUSSION: Although rare, exposure to palytoxin is not restricted to people visiting marine environments because of Palythoa coral in some home aquariums. Routes of exposure go beyond consumption of fish that feed on the coral and include dermal as well as inhalational exposure. Palytoxin exposure should be considered in the differential diagnosis of patients who own or work with fish tanks and present with symptoms that include respiratory complaints, myalgias, neuromuscular dysfunction, hemolysis, and cardiac toxicity. There is no known antidotal therapy and treatment should focus on meticulous supportive care.