Toxic boost: Acute, reversible neurotoxicity after ingestion of methylcyclopentadienyl manganese tricarbonyl (MMT) mistaken for an energy drink.

Methylcyclopentadienyl manganese tricarbonyl (MMT) is an organometallic compound used as a gasoline additive for its antiknock properties. Human ingestion of MMT has not previously been reported. We present the case of a 54-year-old man who developed seizures and altered mental status after drinking 12 oz. of MMT-containing NOS Octane Booster Racing Formula. Due to label similarities, he mistook this for the NOS High Performance energy drink. The patient was intubated due to persistent seizures despite benzodiazepine treatment and admitted to the intensive care unit. He had two further seizures while intubated, but he was successfully extubated on the 4th day post-ingestion. He was confused and ataxic following extubation, but one day later his symptoms resolved and he was discharged without further incident. This case highlights the importance of responsible labeling of consumables. It is important for clinicians and poison centers to report any such instances to the United States Food and Drug Administration.

Iatrogenic pediatric hydroxocobalamin overdose.

INTRODUCTION: Hydroxocobalamin, a precursor molecule to vitamin B12, has emerged as the preferred empiric treatment for patients rescued from enclosed-space fires with concern for inhalational injury and potential concomitant cyanide toxicity. Limited data exist on the effects of hydroxocobalamin toxicity, particularly in pediatric patients. CASE REPORT: We report a case of a healthy three-year old girl who was rescued from an apartment fire and electively intubated by prehospital providers. Due to concern for potential cyanide toxicity, she received 5 g (373 mg/kg) of intravenous hydroxocobalamin, an amount equivalent to one standard adult dose but over five times the appropriate weight-adjusted dose for this 13.4-kilogram child. On hospital arrival, patient was noted to have chromaturia and diffuse erythroderma without cutaneous burns. She was extubated 4 h after prehospital intubation and discharged home the following morning in good condition with persistent erythroderma. Skin color returned to normal within two days. DISCUSSION: We believe this to be the first reported case of iatrogenic pediatric hydroxocobalamin overdose for the treatment of suspected cyanide toxicity. Erythroderma and chromaturia are expected side effects of hydroxocobalamin, even at therapeutic levels. Along with minor airway burns, the only other finding was a transient and hemodynamically neutral bradycardia, which began shortly after prehospital intubation. As this bradycardia occurred prior to hydroxocobalamin administration, more likely culprits include vagal nerve stimulation from direct laryngoscopy, and sinoatrial muscarinic receptor stimulation caused by repeated doses of succinylcholine. In all, we were unable to appreciate any complications due to excess hydroxocobalamin administration.

Reversal of Pediatric Opioid Toxicity with Take-Home Naloxone: a Case Report.

BACKGROUND: Take-home naloxone, an opioid antagonist, has become part of a multimodal approach to curbing opioid-related mortality. However, there is little information about the utility of take-home naloxone in pediatric patients. We report a case of opioid toxicity after exposure to methadone in a pediatric patient, which was successfully reversed with take-home naloxone. CASE: A previously healthy 22-month-old girl ingested an unknown amount of liquid methadone. The child became progressively somnolent. The mother administered intranasal naloxone at home with reversal of somnolence. The patient presented to the emergency department and had recurrence of symptoms. The patient was placed on a naloxone infusion and discharged from a tertiary care facility, uneventfully, 2 days after ingestion. RESULTS: To our knowledge, we report the first case of pediatric opioid toxicity reversed by take-home naloxone. In the setting of rising opioid-related mortality, providers and public health officials should consider expanding access of take-home naloxone for children at high risk for opioid overdose.

Flibanserin toxicity in a toddler following ingestion.

INTRODUCTION: Flibanserin is a medication recently approved by the FDA for treatment of generalized hypoactive sexual desire disorder (HSDD) in premenopausal women. Its mechanism of action is not fully understood but is thought to modulate serotonin receptors and increase levels of norepinephrine and dopamine. While much is known about toxicity of other drugs which affect these systems, there is little information about toxicity of flibanserin at this time. CASE: We present a case of a 2-year-old boy who ingested an estimated 600 mg of his mother's flibanserin. Following ingestion, the child developed facial twitching and unresponsiveness to pain, concerning for seizure-like activity. In the emergency department (ED) he was found to have hypertension, mydriasis, slurred speech, and normal labs. He responded well to supportive care including administration of benzodiazepines. Shortly after admission to the hospital, his temperature increased to 38.4 °C. Toxicology testing revealed the presence of 1-(3-trifluoromethylphenyl)-piperazine (TFMPP), a flibanserin metabolite. TFMPP is a recreational drug used as an alternative to 3,4-methylenedioxymethamphetamine (more commonly known as "MDMA" or "ecstasy"). DISCUSSION: This case highlights potential toxicity associated with ingestion of flibanserin.

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.

Hemorrhagic Encephalopathy From Acute Baking Soda Ingestion.

Baking soda is a readily available household product composed of sodium bicarbonate. It can be used as a home remedy to treat dyspepsia. If used in excessive amounts, baking soda has the potential to cause a variety of serious metabolic abnormalities. We believe this is the first reported case of hemorrhagic encephalopathy induced by baking soda ingestion. Healthcare providers should be aware of the dangers of baking soda misuse and the associated adverse effects.

Toxic Alcohol Ingestion: Prompt Recognition And Management In The Emergency Department.

Identifying patients with potential toxic alcohol exposure and initiating appropriate management is critical to avoid significant patient morbidity. Sources of toxic alcohol exposure include ethylene glycol, methanol, diethylene glycol, propylene glycol, and isopropanol. Treatment considerations include the antidotes fomepizole and ethanol, and hemodialysis for removal of the parent compound and its toxic metabolites. Additional interventions include adjunctive therapies that may improve acidosis and enhance clearance of the toxic alcohol or metabolites. This issue reviews common sources of alcohol exposure, basic mechanisms of toxicity, physical examination and laboratory findings that may guide rapid assessment and management, and indications for treatment.

A Retrospective Study of Clinical Effects of Powdered Caffeine Exposures Reported to Three US Poison Control Centers.

INTRODUCTION: Anhydrous caffeine, often sold on the Internet as a powdered caffeine product, is sold as "pure caffeine" to be used as an additive to beverages and has also been used as an ingredient in energy supplement products. METHODS: This is a retrospective multiple-poison center chart review of calls regarding powdered caffeine to poison centers covering Oregon, Alaska, Guam, Washington, and Utah between January 1, 2013 and June 30, 2015. RESULTS: There were 40 calls to three poison centers over 30 months for powdered caffeine exposure. The majority of patients were over age 19 (52.5 %; 21/40) and male (70 %; 28/40). Sixty percent (24/40) of the patients were symptomatic but only 10 % (4/40) required admission; 52.5 % (21/40) of the patient calls were for inadvertent overdose of powdered caffeine; one patient overdosed in a self-harm attempt. DISCUSSION: Powdered caffeine calls to three poison centers during a 30-month study period were rare, and severe caffeine toxicity due to exposure was found in few patients. The majority of symptoms were reported after an inadvertent powdered caffeine overdose. CONCLUSIONS: An analysis of calls to three poison centers for powdered caffeine found that exposures were uncommon, but did result in toxicity, and highlighted that the lack of clear dosing instructions on product packaging may place patients at risk of inadvertent overdose.

Toxic alcohol ingestion: prompt recognition and management in the emergency department [digest].

Identifying patients with potential toxic alcohol exposure and initiating appropriate management is critical to avoid significant patient morbidity. Sources of toxic alcohol exposure include ethylene glycol, methanol, diethylene glycol, propylene glycol, and isopropanol. Treatment considerations include the antidotes fomepizole and ethanol, and hemodialysis for removal of the parent compound and its toxic metabolites. Additional interventions include adjunctive therapies that may improve acidosis and enhance clearance of the toxic alcohol or metabolites. This issue reviews common sources of alcohol exposure, basic mechanisms of toxicity, physical examination and laboratory findings that may guide rapid assessment and management, and indications for treatment. [Points & Pearls is a digest of Emergency Medicine Practice].

Digoxin-Specific Antibody Fragment Dosing: A Case Series.

Digoxin-specific antibody fragments (DSFab) are used for the treatment of poisoning by cardiac glycosides, such as pharmaceutical digoxin. Dosing of this therapy for chronic and acute poisonings is based on the steady-state serum concentrations of digoxin, historical data in acute ingestions, or empiric regimens purportedly based on the average requirements. Empiric dosing for adult patients involves utilization of 3-6 vials for chronic poisoning and 10-20 vials for acute poisoning. The aim of this study was to describe the average dosing requirements based on the steady-state serum concentration of digoxin or historical data and compare this with the empiric dosing regimens. We performed a retrospective analysis of cases over an 11-year period presented to the Illinois Poison Center where administration of DSFab was recommended. We identified 140 cases of chronic digoxin poisoning and 26 cases or acute digoxin poisoning for analysis. The average dose of DSFab recommended in the cases of chronic digoxin poisoning was 3.05 vials (SD ± 1.31). The average dose of DSFab recommended in the cases of acute digoxin poisoning was 6.33 vials (SD ± 5.26). These values suggest that empiric dosing regimens may overestimate the need for DSFab in cases of both chronic and acute poisonings of pharmaceutical digoxin.

Death following intentional ingestion of e-liquid.

CONTEXT: Electronic cigarette (e-cigarette) use is growing within the United States, resulting in both intentional and unintentional exposures to concentrated liquid nicotine or "e-liquid." Nicotine has been culpable for severe poisoning and deaths in the past. However, sources of nicotine have traditionally been from cigarettes, cigars, or pesticides. Fatalities due to liquid nicotine are rare, and fatalities following ingestion of e-liquid are even scarcer. CASE: We present a case of a 24-year-old woman who intentionally ingested up to 3000 mg of liquid nicotine intended for e-cigarette use. She was found in pulseless electrical activity and had return of spontaneous circulation (ROSC) after undergoing approximately 10 min of cardiopulmonary resuscitation with a blood pressure of 74/53 mmHg and a pulse rate of 106 beats/min. Despite aggressive supportive care, she ultimately died after she was found to have multiple acute infarcts, consistent with severe anoxic brain injury, on magnetic resonance imaging. The patient's toxicologic testing, obtained shortly after ROSC, was notable for plasma nicotine and cotinine levels each >1000 ng/mL. DISCUSSION: This fatality highlights the potential toxicity associated with suicidal ingestion of liquid nicotine.

Variability in hyperbaric oxygen treatment for acute carbon monoxide poisoning.

CONTEXT: In patients with acute carbon monoxide (CO) poisoning, we have noted wide clinical variability in both criteria for hyperbaric oxygen (HBO2) treatment as well as HBO2 treatment regimens. Our aim was to survey Midwest hyperbaric centers for insight into specific criteria and protocols for treating acute CO toxicity with HBO2. METHODS: Hyperbaric centers were identified from the published list of the Undersea and Hyperbaric Medical Society. Ninety-three centers from nine Midwestern states were contacted via telephone. A standard script was used to minimize surveyor bias. RESULTS: Thirty centers that treat CO poisonings were identified. One did not participate in the study. Nineteen reported a specific level of carboxyhemoglobin (COHb) that served as an independent indication for initiation of HBO2 treatment. Four centers used the COHb level as the exclusive indication for HBO2 treatment. Ten centers relied solely on reported symptoms, while the remaining centers used a combination of symptoms plus COHb levels. There were 19 separate treatment protocols. CONCLUSION: No uniform practice for either the initiation or implementation of HBO2 therapy for CO poisoning exists among U.S. Midwest hyperbaric centers responding to a survey. We see opportunity for specific targeted educational programs as well as further study.

Care of the pacemaker/implantable cardioverter defibrillator patient in the ED.

As the population ages and the prevalence of cardiovascular disease increases, patients with pacemakers and implantable cardioverter defibrillators (ICDs) more commonly present to the emergency department. These patients can have complex medical issues related to and independent of their pacemaker/ICD that require careful management by the emergency physician. This article will review the major diagnostic and therapeutic considerations in the emergency care of patients with pacemakers and ICDs.