Background: To examine the effectiveness and adverse events of High Dose Insulin (HDI) therapy in consecutive overdose patients in cardiogenic shock after implementation of an HDI guideline (1–10 units/kg/h, while avoiding or tapering off vasopressors).
Methods: This is an observational consecutive case series of patients with toxin-induced cardiogenic shock treated by our toxicology service from February 2007 to March 2010.
Results: Twelve patients (pts) were treated with HDI. The age range was 19–65 years (mean 43). Seven pts failed pre-existing vasopressor therapy, and six of these were tapered off vasopressors while on HDI; one completed therapy with HDI and a vasopressor. Two pts had pulseless electrical activity (PEA) cardiac arrest prior to HDI therapy. Intravenous fat emulsion was administered to two pts; in one with initiation of HDI during cardiac arrest, and in one who appeared to be unresponsive to HDI at 10 units/kg/hr with known hypertrophic cardiomyopathy (a condition that may worsen with inotropic/vasodilator therapy). An initial HDI bolus was used in 11 of 12 pts. The mean maximum HDI infusion rate was 8.7 units/kg/h (range = 1–21). The mean duration of HDI was 28.8 h (range = 3–60). The mean duration of glucose infusion post-HDI was 21.0 h. The primary toxins were ¦Â-blocker (BB) in five, Ca++ channel blocker (CCB) in one, combined BB/CCB in four, TCA in one, and polydrug in one.
Clinical outcomes: Eleven of twelve pts survived. One pt expired 9 h into HDI therapy from cardiac arrest shortly after the HDI infusion was stopped and a vasopressor re-initiated (guideline deviation).
Adverse events: Overall, five pts experienced a total of 11 hypoglycemic events. Hypokalemia (<3.0 mEq/L) developed in seven pts (minimum 2.3 mEq/L). KCl was infused in these pts.
Adverse sequelae: Necrotic digits occurred in one pt with a prior clotting disorder after receiving high dose norepinephrine and INR reversal with FFP and subsequent HDI. One patient was discharged with mild anoxic injury thought due to prolonged PEA arrest prior
to HDI therapy.
Conclusion: HDI therapy, based on a 1–10 units/kg/h dosing guideline and recommending avoidance of vasopressors, was highly effective in the treatment of toxin-induced cardogenic shock. HDI related adverse events were mild and infrequent. Known adverse sequelae were not related to HDI therapy.