HIGH DOSE INSULIN AND VA ECMO FOR POISON-INDUCED CARDIOGENIC SHOCK

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SESSION TITLE: Critical Care 2 SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/09/2018 05:00 PM - 06:00 PM INTRODUCTION: High dose insulin therapy (HDI) is an emerging and increasingly well described intervention for poison-induced cardiogenic shock (PICS). PICS due to beta-blocker or calcium channel blocker overdose is both frequent and life-threatening [1]. When traditional therapies such as fluid resuscitation, cardiac pacing, atropine, calcium, glucagon, vasopressors and inotropes fail to provide hemodynamic stability, HDI can be effective [2-7]. While the current literature is limited to case series and animal models [2-7], we present a case of successful HDI in a patient with beta-blocker toxicity. CASE PRESENTATION: We report a 36-year-old female who presented in cardiogenic shock secondary to polypharmacy overdose, including significant amounts of propranolol. She suffered cardiopulmonary arrest shortly after arrival to the hospital. Despite aggressive resuscitation, she required emergent venoarterial extracorporeal membrane oxygenation (VA ECMO) support to achieve hemodynamic stability. HDI was subsequently initiated by assessing hemodynamic responsiveness to progressively increased bolus doses, starting with 1 unit per kilogram. HDI was continued with an insulin infusion at 15 units/kilogram/hour. She demonstrated an excellent response, and was successfully transitioned off VA ECMO support and all vasoactive medications. The following day, the insulin drip was carefully weaned to avoid large potassium shifts. The patient was eventually discharged to home, neurologically intact with normal biventricular function by echocardiogram. DISCUSSION: This patient demonstrated a rapid and robust response to HDI in the setting of profound cardiogenic shock. Despite requiring escalation of care to VA ECMO, HDI allowed for rapid discontinuation of this salvage therapy. Several mechanisms of action have been postulated for HDI, including a direct positive inotropic effect and multiple favorable metabolic properties [3,5,8-12]. HDI also induces vasodilation, which improves both microcirculation and systemic perfusion [5,11]. While evidence for specific dosing regimens remains limited, the doses used in this case are consistent with previously described values including bolus doses of 1 unit per kilogram and infusions of 10 units/kilogram/hour or more [13-15]. CONCLUSIONS: In patients with PICS due to either calcium channel blockers or beta-blockers, HDI can be a definitive and life-saving treatment. While large clinical trials are lacking, sufficient evidence exists to consider this therapy in patients with PICS refractory to traditional treatment [16]. Note: All sixteen references available in uploaded document Reference #1: DeWitt CR, et al. Pharmacology, pathophysiology and management of calcium channel blocker and beta blocker toxicity. Toxicol Rev 2004, 23:223-38 Reference #2: Yuan TH, Kerns WP, Tomaszewski CA, Ford MD, Kline JA. Insulin-glucose as adjunctive therapy of severe calcium channel antagonist poisoning. J Toxicol Clin Toxicol 1999, 37:463-74 Reference #3: Megarbane B, et al. The role of insulin and glucose (hyperinsulinemia/euglycemia) therapy in acute calcium channel antagonist and beta-blocker poisoning. Toxicol Rev 2004, 23:215-22 DISCLOSURES: No relevant relationships by Benjamin Abrams, source=Web Response No relevant relationships by David Douin, source=Web Response No relevant relationships by Scott Wolf, source=Web Response