Persistent Hyperinsulinemia Following High-Dose Insulin Therapy: A Case Report.

INTRODUCTION: Overdoses of beta-adrenergic antagonists and calcium channel antagonists represent an uncommonly encountered but highly morbid clinical presentation. Potential therapies include fluids, calcium salts, vasopressors, intravenous lipid emulsion, methylene blue, and high-dose insulin. Although high-dose insulin is commonly used, the kinetics of insulin under these conditions are unknown. CASE REPORT: We present a case of a 51-year-old male who sustained a life-threatening overdose after ingesting approximately 40 tablets of a mixture of amlodipine 5 mg and metoprolol tartrate 25 mg. Due to severe bradycardia and hypotension, he was started on high-dose insulin (HDI) therapy; this was augmented with epinephrine. Despite the degree of his initial shock state, he ultimately recovered, and HDI was discontinued. Insulin was infused for a total of approximately 37 hours, most of which was dosed at 10 U/kg/hour; following discontinuation, serial serum insulin levels were drawn and remained at supraphysiologic levels for at least 24 hours and well above reference range for multiple days thereafter. CONCLUSION: The kinetics of insulin following discontinuation of high-dose insulin therapy are largely unknown, but supraphysiologic insulin levels persist for some time following therapy; this may allow for simple discontinuation rather than titration of insulin at the end of therapy. Dextrose replacement is frequently needed; although the duration is often difficult to predict, prolonged infusions may not be necessary.

Survival After Cardiac Arrest: ECMO Rescue Therapy After Amlodipine and Metoprolol Overdose.

Extracorporeal membrane oxygenation (ECMO) use in poisoned patients is increasing, but is rare post cardiac arrest. We report a case of ECMO use with complete recovery in a patient who arrested twice after a cardiotoxicant overdose. A 17-year-old male presented after an unknown overdose. He rapidly became hypotensive and bradycardic and received aggressive supportive care without improvement. He was transferred to our institution and suffered a cardiac arrest shortly after arrival. Six minutes of advanced cardiac life support resulted in return of spontaneous circulation. High-dose insulin, lipid emulsion, and ECMO were initiated. While awaiting ECMO deployment, he again became pulseless. Compressions resumed, and after 30 min, ROSC was achieved, and he was cannulated for veno-arterial ECMO. Within 48 h, he was decannulated, and then weaned off epinephrine 2 days later. Upon extubation, he was neurologically intact. Amlodipine and metoprolol were later confirmed in serum. Adolescent poisoned patients represent an ideal population for ECMO due to lack of comorbidities. As experience with ECMO in overdose increases, additional research is needed to determine appropriate indications and timing for its use. ECMO is an option for patients poisoned with a cardiotoxicant drug, even following witnessed cardiac arrest.

Successful treatment of metoprolol-induced cardiac arrest with high-dose insulin, lipid emulsion, and ECMO.

ß-Adrenergic antagonist toxicity causes cardiovascular collapse often refractory to standard therapy. Alternative therapies include high-dose insulin, lipid emulsion, and venoarterial extracorporeal membrane oxygenation (VA-ECMO). A 47-year-old man ingested 10 g of metoprolol tartrate in a suicide attempt. Upon emergency department presentation, he was comatose, bradycardic, and hypotensive. Glucagon (14 mg IV) and vasopressor/inotropic support (epinephrine 0.1 µg/[kg min], dobutamine 10 µg/[kg min]) were administered. Despite these therapies, he developed cardiac arrest for 55 minutes, requiring epinephrine (5 mg IV) and vasopressin (40 U IV) with multiple episodes of return of spontaneous circulation. Additional vasopressor administration (vasopressin 0.04 U/min, norepinephrine 0.5 µg/[kg min]) did not improve his hemodynamics. High-dose insulin (250 U IV) and 20% lipid emulsion (100 mL bolus with 200 mL/30 min infusion) were administered, and VA-ECMO was initiated with hemodynamic improvement. His postarrest neurologic examination demonstrated lack of brainstem reflexes and cortical motor response. He awoke 11.5 hours after time of ingestion. Venoarterial extracorporeal membrane oxygenation was discontinued at hospital day 3, and the patient was discharged on hospital day 10 with excellent neurologic recovery. A serum metoprolol level measured 25,000 ng/mL (therapeutic 20-340 ng/mL). High-dose insulin has been shown to be beneficial in ß-adrenergic antagonist cardiotoxicity. Lipid emulsion is thought to act as a lipid extractor, lowering serum and tissue levels. Venoarterial extracorporeal membrane oxygenation was used with the above therapies, restoring organ perfusion and allowing intrinsic drug metabolism and elimination. High-dose insulin, lipid emulsion, and VA-ECMO should be considered for refractory cardiac arrest secondary to ß-adrenergic antagonist toxicity such as metoprolol.

Massive Atenolol, Lisinopril, and Chlorthalidone Overdose Treated with Endoscopic Decontamination, Hemodialysis, Impella Percutaneous Left Ventricular Assist Device, and ECMO.

BACKGROUND: Overdose of cardiovascular medications is increasingly associated with morbidity and mortality. We present a case of substantial atenolol, chlorthalidone, and lisinopril overdose treated by multiple modalities with an excellent outcome. CONCLUSION: Aggressive medical intervention did not provide sufficient hemodynamic stability in this patient with refractory cardiogenic and distributive shock. Impella® percutaneous left ventricular assist device and extracorporeal membrane oxygenation provided support while the effects of the overdose subsided. We present concentrations demonstrating removal of atenolol with continuous venovenous hemodiafiltration. This is the first report of esophagogastroduo denoscopy decontamination of this overdose with a large pill fragment burden.