LIFE-SAVER INSULIN: "THE MORE THE BETTER"

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Calcium channel blockers (CCB) are cardiovascular drugs that act on L-type calcium channels. Toxic exposures related to CCB is estimated to be 4.16% of all prescription overdoses. Toxicity leads to peripheral vasodilation, conduction blockade, and reduction in myocardial contractility. Additionally, high doses of CCBs inhibit the release of endogenous insulin and induce a state of hypoinsulinemia. In this state, myocardial cells are unable to uptake glucose for metabolic activity, which can be detrimental in the setting of shock. Treatment of CCB overdose revolves around administration of fluids, calcium, vasopressors, and ionotropic agents. Furthermore, cases involving cardiogenic shock should consider prompt addition of hyperinsulinemic-euglycemic therapy (HIET). The mechanisms by which HIET treats CCB overdose is theorized to be due to improved glucose uptake by myocardial cells, a concentration dependent ionotropic effect and systemic vasodilation. CASE PRESENTATION: A 41-year-old male with hypertension and major depressive disorder presented in shock after he intentionally ingested 600mg amlodipine in combination with alcohol. Despite aggressive initial measures with intravenous fluids, glucagon, calcium gluconate and high-dose vasopressor therapy ((nor-)epinephrine, vasopressin and angiotensin II), his condition worsened. He was intubated and started on HIET (bolus of intravenous insulin 1unit/kg followed by an infusion which was steadily increased to 8units/kg/hr). A continuous infusion of D25W was administered to maintain euglycemia and plasmapheresis was started to aid in the removal of amlodipine.The patient's course was further complicated by acute renal failure which led to overt volume overload. Continuous renal replacement therapy (CRRT) and eventually intermittent hemodialysis were started. Ultimately, he was gradually weaned off vasopressor support over 7 days while on HIET. DISCUSSION: The presented case highlights the importance of HIET in treating refractory cardiogenic shock caused by CCB overdose. Concomitant renal failure can be additive to the patient's clinical picture due to high quantities of intravenous volume needed with HIET. To our knowledge this is the first case to successfully utilize prolonged HIET with CRRT for CCB overdose. This case demonstrates that there may be promise in the utility of prolonged HIET for cases of complex CCB overdose with refractory shock. Due to lack of large sample sizes and randomized controlled studies, consideration for prolonged therapy or its role in renal failure should be given on a case-by-case scenario. CONCLUSIONS: Prolonged HIET is a promising treatment for cases of complex CCB overdose with refractory shock. REFERENCE #1: Gummin DD, Mowry JB, Spyker DA, Brooks DE, Fraser MO, Banner W. 2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 34th Annual Report. Clin Toxicol (Phila) 2017;55:1072–252 REFERENCE #2: Graudins A, Lee HM, Druda D. Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies. BrJ Clin Pharmacol 2016;81:453–61 DISCLOSURES: No relevant relationships by Shijo Benjamin, source=Web Response No relevant relationships by Md Islam, source=Web Response No relevant relationships by Maulin Patel, source=Web Response No relevant relationships by Mirja Wirtz, source=Web Response