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Department of Pulmonary Medicine, PGIMER, Chandigarh, India
Correspondence to: Ritesh Agarwal, MD, DM, Assistant Professor, Department of Pulmonary Medicine, PGIMER, Sector-12, Chandigarh-160012, India; e-mail: riteshpgi{at}gmail.com
To the Editor:
We read with interest the article by Buysse et al (March 2005),1 who evaluated the clinical effect of sodium bicarbonate (NaHCO3) on carbon dioxide levels in 17 children with life-threatening asthma. They show a significant decrease of PCO2 after NaHCO3 infusion and improvement of respiratory distress in the majority. However, certain points need clarification.
First, the authors claim that NaHCO3 per se has beneficial effects in asthma. The authors assume that other therapies remained unchanged during the time period between the blood gas analysis before and after the administration of NaHCO3, and attribute this to clinical improvement secondary to NaHCO3. However, one should also remember that the patients had received glucocorticoids, and the improvement during that time could be due to the latent period of onset of action of glucocorticoids. Hence, this is only a crude estimate of the efficacy of NaHCO3, and it requires adjustment for other variables, such as salbutamol, ipratropium, and glucocorticoids, by a multivariable analysis.
Secondly, the fear of administration of NaHCO3 is mainly (or only) in patients with pure respiratory acidosis and not mixed metabolic and respiratory acidosis. In the present study, the majority of patients had mixed metabolic and respiratory acidosis, which otherwise is not an absolute contraindication. Although several risks are associated with NaHCO3, the most prominent concern is an acute worsening of intracellular acidosis.2 Approximately 10 to 15% of HCO3 immediately converts to carbon dioxide, so that a typical 1 mEq/kg dose administered rapidly results in approximately 200 mL of carbon dioxide (equivalent to 1 min of carbon dioxide production for an average-size adult).3 In general, treating primary respiratory acidosis with NaHCO3 should be discouraged,4 and should be administered to patients with acute severe asthma who have mixed metabolic and respiratory acidosis pending larger trials or in strict trial conditions.
References
Erasmus MC-Sophia Childrens Hospital, Rotterdam, the Netherlands
Correspondence to: Corinne Buysse, MD, Erasmus MC-Sophia Childrens Hospital, Dr. Molewaterplein 60, 3015 GJ Rotterdam, the Netherlands; email: c.buysse{at}erasmusmc.nl
To the Editor:
We thank Dr. Agarwal for his comments regarding our article in CHEST (March 2005).1 On the first point, we stated in our article that the administration of large doses of sodium bicarbonate to patients with life-threatening asthma (LTA) led to reduction of PCO2. A causal relation between the administration of sodium bicarbonate and clinical improvement was indeed not proven in our study. We certainly would not like to credit sodium bicarbonate as the sole factor that caused clinical improvement in this series of patients. By nature, treatment of children with LTA is directed at several key points in the pathophysiology. Our data do suggest a beneficial effect of sodium bicarbonate in this treatment. Dr. Agarwal argues that clinical improvement could be due to a delayed effect of glucocorticoids. However, since there was a prompt improvement of the clinical condition, we think this is unlikely.
On the second point, although we agree with some theoretical points made by Dr. Agarwal, we think a key point is overlooked. LTA is commonly associated with metabolic or mixed acidosis, which reduces the effectiveness of ß-agonist. Our hypothesis was that children with LTA could benefit from treating their acidosis, regardless of the origin, by giving these patients sodium bicarbonate irrespective of respiratory insufficiency.
References
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