Alpha Lipoic Acid Toxicity: The First Reported Mortality in an Adult Patient After Multiorgan Failure.

BACKGROUND: Alpha lipoic acid (ALA) is an anti-oxidant found in many over-the-counter supplements and is used in treatments for diabetes, hypertension, and obesity. Although it is a safe oral molecule, there have been eight cases of ALA toxicity reported. Three reported cases were among adult patients and five were among pediatric patients. A 14-year-old girl died after ingestion of 6 g of ALA leading to multi-organ failure. CASE REPORT: A 42-year-old woman presented to the emergency department 4 h after an intentional overdose of 10 tablets of ALA 600 mg each (6 g, 92.3 mg/kg). She developed refractory seizures, metabolic acidosis, thrombocytopenia, rhabdomyolysis, depressed cardiac contractility, kidney injury, and supraventricular tachycardia. Her condition deteriorated and she developed multi-organ failure. The patient was started on dual pressors, anti-epileptic medications, high-dose insulin and euglycemia protocol, and methylene blue (1 mg/kg). Despite aggressive resuscitation, she required intubation and died. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This was the ninth case and the first reported adult mortality from ALA toxicity with multi-organ failure. Our case shared some similar findings with previously reported cases, including refractory seizures, metabolic acidosis, thrombocytopenia, and rhabdomyolysis. Refractory supraventricular tachycardia and severe agitation have not been reported with ALA toxicity previously. The range of toxicity of ALA is not well established. A reported dose of 6 g caused death in a pediatric patient as well as our patient, but others survived doses of 6 g and 18 g. Toxicologists and emergency physicians should be prepared for clinical deterioration and consider aggressive resuscitation in severe ALA toxicity.

Psychiatric Outcomes of Patients With Severe Agitation Following Administration of Prehospital Ketamine.

BACKGROUND: Ketamine is an emerging drug used in the management of undifferentiated, severe agitation in the prehospital setting. However, prior work has indicated that ketamine may exacerbate psychotic symptoms in patients with schizophrenia. The objective of this study was to describe psychiatric outcomes in patients who receive prehospital ketamine for severe agitation. METHODS: This is a retrospective cohort study, conducted at two tertiary academic medical centers, utilizing chart review of patients requiring prehospital sedation for severe agitation from January 1, 2014, to June 30, 2016. Patients received either intramuscular (IM) versus intravenous (IV) ketamine or IM versus IV benzodiazepine. The primary outcome was psychiatric inpatient admission with secondary outcomes including ED psychiatric evaluation and nonpsychiatric inpatient admission. Generalized estimating equations and Fisher's exact tests were used to compare cohorts. RESULTS: During the study period, 141 patient encounters met inclusion with 59 (42%) receiving prehospital ketamine. There were no statistically significant differences between the ketamine and benzodiazepine cohorts for psychiatric inpatient admission (6.8% vs. 2.4%, difference = 4.3%, 95% CI = -2% to 12%, p = 0.23) or ED psychiatric evaluation (8.6% vs. 15%, difference = -6.8%, 95% CI = -18% to 5%, p = 0.23). Patients with schizophrenia who received ketamine did not require psychiatric inpatient admission (17% vs. 10%, difference = 6.7%, 95% CI = -46% to 79%, p = 0.63) or ED psychiatric evaluation (17% vs. 50%, difference = -33%, 95% CI = -100% to 33%, p = 0.55) significantly more than those who received benzodiazepines, although the subgroup was small (n = 16). While there was no significant difference in the nonpsychiatric admission rate between the ketamine and benzodiazepine cohorts (35% vs. 51%, p = 0.082), nonpsychiatric admissions in the benzodiazepine cohort were largely driven by intubation (63% vs. 3.8%, difference = 59%, 95% CI = 38% to 79%, p < 0.001). CONCLUSIONS: Administration of prehospital ketamine for severe agitation was not associated with an increase in the rate of psychiatric evaluation in the emergency department or psychiatric inpatient admission when compared with benzodiazepine treatment, regardless of the patient's psychiatric history.

Designer benzodiazepines: a report of exposures recorded in the National Poison Data System, 2014-2017.

IMPORTANCE: Exposures to novel psychoactive substances are reported with increasing frequency in both the medical literature and the lay press. While the majority of reports describe synthetic cannabinoids and cathinones, a lesser understood family is the "designer benzodiazepines". The current literature describing human exposures to these compounds is comprised of case reports and small case series. OBJECTIVE: The primary objectives of this study are to describe epidemiologic trends and clinical effects of designer benzodiazepine use. METHODS: Data regarding single agent exposures to designer benzodiazepines between 1 January 2014 and 31 December 2017 was obtained from the National Poison Data System. Substances queried include: adinazolam, clonazolam, cloniprazepam, diclazepam, etizolam, flubromazepam, flubromazolam, meclonazepam, nifoxipam, norflurazepam, and pyrazolam. Data was summarized descriptively. RESULTS: 234 single agent exposures in 40 states were reported during the study period. The annual number of exposures increased each year, from 26 in 2014 to 112 in 2017, amounting to a 330% increase. The most common exposures were etizolam (n = 162) and clonazolam (n = 50). The most common clinical effects were drowsiness/lethargy (65%), and slurred speech (17%). 3% required intubation, 36% of cases required hospital admission, 22% to the intensive care unit. There was 1 death in the study population. CONCLUSIONS: The incidence of exposures to designer benzodiazepines is rising. Clinical effects are generally consistent with a sedative-hypnotic toxidrome. Severe effects, including death, seemed relatively uncommon in the study population.

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.