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Severe Lactic Acidosis in a Critically Ill Child: Think About Thiamine! A Case Report
Clémence Didisheim1, Diana Ballhausen2, Marie-Louise Choucair3
1Department of Pediatrics, Pediatric Intensive Care Unit, University Hospital and Medicine and Biology Faculty of Lausanne, Lausanne, Switzerland.
Insights
A teenager with leukemia developed severe lactic acidosis during chemotherapy. Thiamine supplementation rapidly normalized lactate levels, highlighting its importance in critically ill pediatric patients.
Area of Science:
- Biochemistry
- Pediatric Critical Care
- Nutritional Science
Background:
- Leukemia patients undergoing chemotherapy are at risk for nutritional deficiencies.
- Parasitic infections can complicate management and increase nutritional demands.
- Severe illness can precipitate metabolic derangements, including lactic acidosis.
Observation:
- A teenage leukemia patient on maintenance chemotherapy presented with parasitic infection and required parenteral nutrition.
- The patient developed refractory shock, necessitating extracorporeal membrane oxygenation.
- Despite hemodynamic support, worsening lactic acidosis persisted until thiamine administration.
Findings:
- Thiamine supplementation led to rapid normalization of lactic acidosis within 12 hours.
- Thiamine is a crucial coenzyme for aerobic glycolysis; deficiency impairs this pathway.
- Lactate accumulation occurred due to a shift towards anaerobic glycolysis secondary to thiamine deficiency.
Implications:
- Thiamine deficiency should be considered in pediatric patients with unexplained lactic acidosis, especially those with risk factors.
- Early recognition and supplementation of thiamine can be life-saving in critically ill children.
- This case underscores the importance of comprehensive nutritional assessment and management in immunocompromised pediatric patients.
Abstract:
In this article, we presented a teenager, in maintenance chemotherapy for leukemia, who was admitted for digestive symptoms related to a parasitic infection and required nutritional support with parenteral nutrition. After 6 weeks, his condition worsened with refractory shock of presumed septic origin, necessitating extracorporeal membrane oxygenation. Despite hemodynamic stabilization, his lactic acidosis worsened until thiamine supplementation was started. Lactate normalized within 12 hours. Thiamine is an essential coenzyme in aerobic glycolysis, and deficiency leads to lactate accumulation through anaerobic glycolysis. Thiamine deficiency is uncommon in the pediatric population. However, it should be considered in patients at risk of nutritional deficiencies with lactic acidosis of unknown origin.
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