Prolonged lactic acidosis following congenital cardiac surgery: A case report highlighting the potential role of thiamine deficiency

Background

Lactic acidosis is a critical metabolic derangement frequently observed following pediatric cardiac surgery, often attributed to low cardiac output and resultant tissue hypoperfusion. However, thiamine deficiency can disrupt aerobic metabolism, leading to excessive lactate accumulation. Infants undergoing complex surgical interventions risk developing thiamine deficiency in the postoperative period, especially if prolonged parenteral nutrition is administered without adequate supplementation.

Case description

A full-term female neonate diagnosed with transposition of the great arteries underwent an arterial switch operation on day 11 of life. Her postoperative course was complicated by feeding intolerance, suspected necrotizing enterocolitis (NEC), and prolonged parenteral nutrition (TPN). Despite the resolution of sepsis and NEC being ruled out, persistent lactic acidosis and feeding intolerance continued. On postoperative day 57, thiamine deficiency was suspected and treated with intravenous supplementation. After thiamin therapy, there was a rapid decline in lactate levels (from 14 mmol/L to <2 mmol/L within 24 h) and resolution of clinical symptoms.

Conclusion

This case illustrates how thiamine deficiency may contribute to persistent lactic acidosis and feeding intolerance in neonates receiving prolonged TPN following complex cardiac surgery, underscoring the value of considering nutritional deficiencies in the differential diagnosis. Early recognition and timely supplementation can significantly improve outcomes, emphasizing the need for clinical awareness and routine thiamine supplementation in high-risk postoperative care.