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Egypt J Pediatr Allergy Immunol, (October 2004), Volume No. 2, Issue 02  
 
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Egypt J Pediatr Allergy Immunol 2004 ; 2 ( 02 ) : 83-89 -
, ESP - 106  
Lactatemia during treatment of status asthmaticus in children
Zeinab M. Radwan   Tarek F. Ali   Hisham W. Bader   Sally M. Gouda      
Background: Transient increase of lactate levels with or without metabolic acidosis has been seldom reported as a complication of ?2-adrenergic therapy administered during asthma attacks in children. Objective: The study is aimed to investigate the frequency of lactatemia in children with acute asthma treated with nebulized ?2-agonists, and to delineate its causes and effects on prognosis. Methods: We studied 32 asthmatic children; 68.8% had intermittent asthma, and 31.2% had mild persistent asthma. Their ages ranged from 6 to 8 years with a mean of 6.480.68 years. Patients were enrolled during acute asthma exacerbation (62.5% had severe and 37.5% had moderate attacks)from the Cairo University Children's Hospital. Patients underwent clinical evaluation, and routine investigations (CBC, PEFR, and total serum IgE) then received nebulized salbutamol at 0.1 mg/kg/dose (minimum 2.5 mg) every 20 min for three doses together with O2. Plasma lactate was determined before, 1 h after, and 24 h following the inhalation therapy. Blood gases were also evaluated before and after the ?2-agonist treatment. Results: At 1 h post-treatment, all patients had appreciable lactatemia (4.440.78 mmol/L, p<0.001) compared to the pre-treatment level with a rise of 257121.5%. Patients with severe attacks demonstrated a higher mean value compared to those with moderate attacks (4.690.8 mmol/L versus 4.020.6 mmol/L, p<0.05). At 24 h post-treatment, lactate levels returned to the normal values in most patients (1.910.59 mmol/L, p<0.001) as compared to the 1 h post-treatment level. None of our patients developed metabolic acidosis and all of them showed significant clinical improvement. Our results strongly accuse nebulized salbutamol as the possible pathogenetic factor for lactatemia during therapy of acute asthma attacks, while overworked respiratory muscles and hypoxemia have been excluded as contributing factors. Conclusion: Transient lactatemia is not uncommon during ?2-agonist therapy in asthmatic children with acute exacerbation, and is harmless in most cases. Prediction of lactic acidosis prevents inappropriate intensification of therapy especially in patients with more severe attacks or impending respiratory failure.