Abstract
Lactic acidosis is a common complication of status asthmaticus in adults. However, data is sparse in children. The aim of this study was to describe the prevalence and risk factors for lactic acidosis in children hospitalised for acute moderate or severe asthma. A total of 154 children 2–17 years of age were enrolled in a prospective observational study conducted in a tertiary hospital. All had capillary blood gas assessment 4 h after the first dose of salbutamol in hospital. The primary endpoint was the prevalence of lactic acidosis. Potential contributing factors such as age, sex, BMI, initial degree of asthma severity, type of salbutamol administration (nebuliser or inhaler), steroids, ipratropium bromide, and glucose-containing maintenance fluid represented secondary endpoints. All in all, 87% of patients had hyperlactatemia (lactate concentration > 2.2 mmol/l). Lactic acidosis (lactate concentration > 5 mmol/l and anion gap ≥ 16 mmol/l) was observed in 26%. In multivariate analysis, age more than 6 years (OR = 2.8, 95% CI 1.2–6.6), glycemia above 11 mmol/l (OR = 3.2 95% CI 1.4–7.4), and salbutamol administered by nebuliser (OR = 10, 95% CI 2.7–47) were identified as risk factors for lactic acidosis in children with moderate or severe asthma.Conclusion: Lactic acidosis is a frequent and early complication of acute moderate or severe asthma in children.What is Known:• Lactic acidosis during acute asthma is associated with b2-mimetics administration.• Salbutamol-related lactic acidosis is self-limited but important to recognise, as compensatory hyperventilation of lactic acidosis can be mistaken for respiratory worsening and lead to inappropriate supplemental bronchodilator administration.What is New:• Lactic acidosis is a frequent complication of acute asthma in the paediatric population.• Age older than 6 years, hyperglycaemia, and nebulised salbutamol are risk factors for lactic acidosis during asthma.
Highlights
Asthma is characterised by chronic airway inflammation and hyperresponsiveness
Lactic acidosis during acute asthma is associated with b2-mimetics administration
Salbutamol-related lactic acidosis is self-limited but important to recognise, as compensatory hyperventilation of lactic acidosis can be mistaken for respiratory worsening and lead to inappropriate supplemental bronchodilator administration
Summary
Asthma is characterised by chronic airway inflammation and hyperresponsiveness. During an acute exacerbation, inhomogeneous airway narrowing and obstruction lead to hypoxemia. Compensatory hyperventilation mediated by pulmonary mechanoreceptors conducts to respiratory alkalosis, the most frequent acid-base disturbance observed in acute asthma. Progressive respiratory insufficiency may occur with hypercapnia and respiratory acidosis [1]. Lactic acidosis is another blood gas alteration observed during moderate or severe asthma. Others have suggested that b2-adrenergic agents like bronchodilators used to treat asthma lead to increased gluconeogenesis, glycogenolysis, glycolysis, and lipolysis, cumulating in lactic acid production [3,4,5,6]. Depending on the mechanism of lactate formation, two types of lactic acidosis exist that can be distinguished calculating the lactate to pyruvate ratio (L/P). Type A (L/P ratio < 25/1) is related to impaired oxygenation, and type B (L/P > 25/1) is caused by excessive b2-receptor stimulation [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
