Prevention of metabolic decompensation in an infant with mutase deficient methylmalonic aciduria undergoing cardiopulmonary bypass

World J Pediatr. 2014 Feb;10(1):83-5. doi: 10.1007/s12519-014-0458-0. Epub 2014 Jan 25.

Abstract

Background: Effects of circulatory arrest upon an inborn error of metabolism patient are unknown.

Methods: A retrospective chart review was performed of outcome and biochemical parameters obtained during palliative cardiac surgery for a mutase-deficient methylmalonic aciduria patient with Ebstein's cardiac anomaly was performed.

Results: The levels of ammonia, methylmalonic acid, free carnitine, and propionylcarnitine of the patient were improved. The patient survived surgery following institution of four metabolic treatment principles: 1) restriction of toxic substrate; 2) promotion of anabolism via administration of carbohydrate and lipid calories; 3) administration of detoxifying levocarnitine and sodium benzoate; and 4) cobalamin enzymatic co-factor administration. The patient died from post-operative dysrhythmia and was posthumously determined to have compound heterozygosity for mutations predicting severe, cobalamin non-responsive disease: c.322C>T/c.1233del3 (p.R108C/p.ΔI412).

Conclusion: Metabolic decompensation is preventable during cardiopulmonary bypass and cardioplegia using four principles of metabolic treatment.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Metabolism, Inborn Errors / complications*
  • Amino Acid Metabolism, Inborn Errors / metabolism*
  • Amino Acid Metabolism, Inborn Errors / therapy
  • Cardiopulmonary Bypass*
  • Heart Defects, Congenital / surgery*
  • Humans
  • Infant, Newborn
  • Male
  • Palliative Care

Supplementary concepts

  • Methylmalonic acidemia