Lactic acidosis caused by sodium nitroprusside in a newborn with congenital heart disease

Sodium nitroprusside (SNP) is an antihypertensive agent used frequently in the critical care setting. Co-adminstration of the antidote sodium thiosulphate with SNP usually prevents increases in cyanide concentrations during anaesthesia or long-term SNP infusion [2, 3,4]. We report on a newborn with congenital heart disease who developed severe lactic acidosis due to the administration of SNP despite co-medication with sodium thiosulphate. A 3800 g female newborn was born at term by normal spontaneous vaginal delivery. The pregnancy was reported to be normal. On day 3 of life, a loud systolic murmur was heard on physical examination. For further work-up the patient was transferred to our hospital. On echocardiography, complex congenital heart disease was diagnosed (double inlet left ventricle, dysplasia of the right ventricle, atrial and ventricular septal defects with right ventricular outlet, transposition of the great arteries, hypoplastic ascending aorta). Due to the presence of a hypoplastic ascending aorta distal to the orifices of the coronary arteries, treatment consisted of the administration of prostaglandin E1 (50 ng/kg per min) to allow for adequate systemic perfusion via the patent ductus arteriosus. Because of a mismatch between pulmonary and systemic blood flow, continuous treatment with SNP was started to shift perfusion from the pulmonary bed to the systemic circulation by reducing the afterload. The starting dose of SNP (0.2 lg/kg per min) was gradually increased to a maximum of 2.5 lg/kg per min over a 24 h period. To avoid iatrogenic intoxication with cyanide, the patient received concomitant medication with sodium thiosulphate (ratio SNP/sodium thiosulphate of 1:10 as recommended by the manufacturer). On day 6 of SNP medication, the patient became tachydyspnoeic with sternal retractions. Skin colour and capillary refill time were normal. No significant changes in oxygen saturation or in blood pressure were noticed (average oxygen saturation 80%–85%). Blood gas analysis revealed profound lactic acidosis (pH 7.26, pO2 48.5 mmHg, pCO2 21.3 mmHg, lactate 19 mmol/l, base excess -16.4 mmol/l). At this time point, capillary oxygen saturation was 81.5%. Severe hyperglycaemia was also noted (430 mg/dl). SNP was immediately stopped; the patient was intubated and ventilated with FiO2 100%. Due to the mechanism of action of SNP (inactivating cytochrome oxidase a-3 and blocking cellular aerobic metabolism) the metabolism of oxygen was disturbed as shown by small differences between arterio-venous oxygen saturation (87.5% versus 65.3%). During the following 6 h, the lactic acidosis completely resolved and a substantial increase in the difference between arterio-venous oxygen saturation was seen (87% versus 52%). Cardiac failure with low-cardiac output as the cause of lactic acidosis was ruled out by echocardiography. Also, renal failure as a possible cause for the accumulation of SNP was excluded (normal serum creatinine; urine output 2–3 ml/kg per h). Toxicological analysis done 24 h after the development of lactic acidosis still showed elevated levels of thiocyanate (41 mg/l; therapeutic level <30 mg/l). The further clinical course was uneventful. Our case report draws attention to the fact that despite concomitant administration of sodium thiosulphate, SNP may cause severe lactic acidosis by accumulation of cyanide. Due to the alterations in oxygen S. Meyer AE A. Baghai AE N.-L. Sailer AE S. Gottschling Department of Paediatric Intensive Care, University Children’s Hospital of the Saarland, Homburg/Saar, Germany