Matthew Valento

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.

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.

Mixed propranolol and tizanidine overdose treated with intravenous lipid emulsion

abstract We describe a case of mixed propranolol and tizanidine overdose and response to treatment with intravenous lipid emulsion (ILE) in conjunction with glucagon therapy. A 35-year-old male was unresponsive after intentional overdose of propanolol and tizanidine. He was bradycardic, hypertensive, and obtunded on the first medical contact. He received glucagon with moderate improvement in heart rate, followed by a bolus of ILE. Minutes after receiving ILE he became alert and responsive, and had further improvement in heart rate. This case suggests that ILE may reverse the effects of propanolol and tizanidine toxicity in overdose.

Severe iron poisoning treated with prolonged deferoxamine infusion: a case report

ABSTRACT The incidence of iron poisoning, once the most common cause of fatal pediatric unintentional ingestions, and the use of its antidote deferoxamine have declined. We describe a case of a 17-year-old girl who presented to a hospital following an intentional polysubstance ingestion, which included ferrous sulfate. She developed severe gastrointestinal symptoms including hematemesis, as well as anion gap metabolic acidosis, coagulopathy, and liver toxicity. She was treated with a prolonged course of greater than 24 h with deferoxamine due to a markedly elevated serum iron concentration of 2565 g/dL and worsening clinical status. Clinical features and management of complex iron poisoning are discussed. This case demonstrates the benefit of early poison control center and medial toxicology involvement in instances regarding the off-label usage of deferoxamine in the treatment of severe iron toxicity.

Letter in response to “fatal cardiac glycoside poisoning due to mistaking foxglove for comfrey”

We read with great interest the recent article by Wu et al. titled “Fatal cardiac glycoside poisoning due to mistaking foxglove for comfrey” [1]. In the article, authors present a case of cardiac glycoside poisoning in a woman after ingestion of alleged “comfrey” tea. The patient developed progressive bradycardia and hypotension followed by refractory ventricular dysrhythmias and death. We report a similar case of fatal cardiac glycoside poisoning in a patient who also sought comfrey leaves for an herbal tea but mistakenly brewed and ingested foxglove. A 69-year-old woman presented to the emergency department with complaints of nausea, vomiting and generalized weakness. These symptoms began shortly after drinking a homemade tea composed of leaves believed to be comfrey (Symphytum spp.). Her vital signs on arrival were: blood pressure, 153/76mmHg; pulse rate, 30 BPM; and respiratory rate, 20 breaths/min. She appeared pale, with diaphoresis. An initial EKG showed junctional bradycardia (34 BPM), and the cardiac monitor showed occasional sinus pauses of up to six seconds. Laboratory studies were notable for hyperkalemia (serum potassium 6.6mmol/L). Shortly after arrival to the ED, the patient’s blood pressure dropped to 75/40mmHg with a pulse of 30–40 BPM. Intravenous fluids and atropine were administered with minimal response. Hyperkalemia was treated with insulin, glucose and sodium bicarbonate, though repeat potassium concentration after these interventions was 8.2mmol/L. Clinical deterioration progressed to cardiac arrest. Unintentional foxglove (Digitalis purpurea) poisoning was suspected after consultation with poison control, and the hospital’s entire supply of digoxin-specific antibody (6 vials) was administered. Despite ongoing CPR and administration of atropine, epinephrine, magnesium, calcium, isoproterenol, dopamine and transvenous pacing, return of spontaneous circulation was not achieved, and the patient expired. A serum digoxin concentration ultimately returned at 55 ng/mL (therapeutic range 0.5–2.0 ng/mL). Our case exhibits many similarities to the case described by Wu et al. Both patients, seeking comfrey leaves for an herbal tea, brewed and ingested foxglove, with fatal results. Nausea, vomiting, bradycardia and hyperkalemia were common early features. Serum digoxin concentrations were markedly elevated in both patients, demonstrating the laboratory assay’s ability to qualitatively assist in making the diagnosis of nondigoxin cardiac glycoside exposure. Furthermore, in both cases, there was delay to treatment with digoxinspecific antibody (Fab) fragments and insufficient hospital supply of the antidote. Comfrey leaves are not easily distinguishable from those of the foxglove plant, especially when the plants are not in bloom. Both these cases and a small number of previously reported non-fatal cases highlight the risk of severe cardiac glycoside poisoning from such plant misidentification (Table 1) [2–7]. Clinical manifestations of acute cardiac glycoside poisoning are often nonspecific, which can mislead clinicians and delay diagnosis. Large doses of antidote may be required in patients poisoned by naturally occurring cardiac glycosides because binding of digoxin-specific Fab fragments is less efficient than in patients with pharmaceutical digoxin poisoning [8]. These cases together suggest a pattern of early GI symptoms with bradycardia, hyperkalemia and elevated digoxin concentrations, followed by refractory ventricular dysrhythmias in patients who mistake digitalis for foraged comfrey. We recommend empiric treatment with digoxin-specific antibodies be considered early in the course of patients presenting with these symptoms following ingestion of an unidentified plant, especially in patients foraging for comfrey.

Flibanserin toxicity in a toddler following ingestion

Abstract 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.

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.