(764) Nitroprusside-Induced Cyanide Toxicity in an Infant With Complex Congenital Cardiac Disease

Introduction: Sodium nitroprusside (SNP) is a potent vasodilator commonly administered in the critical care setting to manage severe hypertension. It relaxes vascular smooth muscle by releasing nitric oxide and is favored due to its rapid onset and short duration of action. However, potentially fatal toxicity may occur as a result of the accumulation of cyanide ions which interfere with cellular respiration resulting in anaerobic metabolism and lactic acidosis. Patients receiving SNP who have hepatic and renal dysfunction are at higher risk of developing cyanide and thiocyanate toxicity.

Description: We describe the case of a 2-week-old female infant with pulmonary valve atresia/intact ventricular septum who underwent balloon atrial septostomy followed by central shunt placement. Her post-procedure course was complicated by a coronary ischemic event resulting in cardiac arrest and initiation of veno-arterial ECMO using a PediMag blood pump. While on ECMO, the patient developed hepatic and renal dysfunction. To maximize systemic perfusion with a target ECMO flow of 100ml/kg/min, blood pressure (BP) control was attempted using SNP and fenoldopam infusions while other agents were avoided due to ongoing poor myocardial function. Despite SNP doses of up to 10mcg/kg/min, the patient’s mean arterial BP remained significantly elevated. During this time, she developed worsening lactic acidosis thought to be due to worsening perfusion. With maneuvers to increase ECMO flow, she developed severe hemolysis (plasma free hemoglobin 509mg/dL, normal < 5mg/dL) and worsening lactic acidosis (peak 9.3mmol/L, normal < 1.25mmol/L). Methemoglobin levels were normal and cyanide and thiocyanite levels were sent. Due to concern for cyanide toxicity, SNP infusion was discontinued and the patient was treated empirically with hydroxocobalamin (70mg/kg). Subsequently, blood lactate levels rapidly normalized. Labs later resulted showing a cyanide level of 5.9mg/L (normal < 0.1mg/L) and a thiocyanate level of 23.0mcg/ml (normal < 4.0mcg/ml).

Discussion: This case illustrates the importance of vigilant monitoring of cyanide and thiocyanate levels for patients receiving SNP infusion for BP control, particularly while attempting to maximize ECMO flow in the post-resuscitation period when hepatic and renal dysfunction may be evolving.