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Lactic acidosis in children with acute exacerbation of severe asthma

Pulin B Koul, Milan Minarik, Balagangadhar R Totapally

    European Journal of Emergency Medicine : Official Journal of the European Society for Emergency Medicine
    |January 2, 2007
    PubMed

    Insights

    Intensive use of nebulized beta2-agonists for severe pediatric asthma may cause lactic acidosis. Symptoms improved after reducing or stopping the medication, suggesting a direct link.

    Area of Science:

    • Pediatric Intensive Care Medicine
    • Respiratory Medicine
    • Clinical Biochemistry

    Background:

    • Acute severe asthma in children requires intensive treatment.
    • Nebulized beta2-agonists are a cornerstone therapy for acute severe asthma.
    • Potential adverse effects of high-dose beta2-agonist therapy require ongoing investigation.

    Observation:

    • Four pediatric patients with acute severe asthma developed lactic acidosis during intensive nebulized beta2-agonist treatment.
    • Peak lactic acidosis concentrations ranged from 5.2 to 13 mmol/l.
    • Lactic acidosis resolved within 24 hours after discontinuing or decreasing beta2-agonist dosage.

    Findings:

    • Intensive nebulized beta2-agonist therapy is a potential cause of lactic acidosis in pediatric patients with severe asthma.
    • The severity of lactic acidosis correlated with beta2-agonist dosage.
    • Discontinuation or dose reduction of beta2-agonists led to rapid improvement of lactic acidosis.

    Implications:

    • Clinicians should consider lactic acidosis as a potential complication of intensive beta2-agonist therapy in pediatric severe asthma.
    • Monitoring lactate levels may be warranted in pediatric patients receiving high-dose beta2-agonists.
    • Further research is needed to elucidate the mechanism and confirm the association between beta2-agonists and lactic acidosis in this population.

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