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Archives de pédiatrie
Volume 21, n° 10
pages 1120-1122 (octobre 2014)
Doi : 10.1016/j.arcped.2014.06.024
Received : 10 July 2013 ;  accepted : 27 June 2014
Acidose lactique chez un nourrisson au cours d’une crise d’asthme grave
Lactic acidosis in a child with acute severe asthma
 

C. Perrin a, , N. Savy a, M. Lang a, N. Caron b, A. Labbé a, b
a Service de réanimation pédiatrique, CHU Estaing, 1, place Raymond et Lucie Aubrac, 63003 Clermont-Ferrand, France 
b Service des urgences pédiatriques, CHU Estaing, 1, place Raymond et Lucie Aubrac, 63003 Clermont-Ferrand, France 

Auteur correspondant.
Résumé

La survenue d’une acidose lactique dans l’asthme aigu grave (AAG) est classique chez l’adulte mais peu décrite chez l’enfant. Sa reconnaissance peut avoir des conséquences sur la prise en charge thérapeutique de la crise d’asthme. Une petite fille de 2 ans a été hospitalisée en réanimation pédiatrique pour un AAG, traité par oxygénothérapie à haut débit, méthylprednisolone et salbutamol par voie intraveineuse. Elle a présenté une acidose métabolique (pH=7,29) avec hypocapnie (26 mmHg), chute des bicarbonates (12 mmol/L), trou anionique (20 mmol/L) et augmentation des lactates (8 mmol/L). La recherche d’une maladie métabolique sous-jacente a été négative. L’évolution a été favorable avec amélioration spontanée de l’acidose lactique permettant la sortie de l’unité de réanimation après 72 heures. L’origine d’une acidose lactique au cours de l’AAG est multifactorielle. Bien que sa résolution soit spontanée, il est essentiel de la reconnaître car elle peut modifier la symptomatologie respiratoire et conduire à une escalade thérapeutique inappropriée.

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Summary

Lactic acidosis is a recognized event in adult patients with acute severe asthma (ASA). Only a few cases have been reported in children. Hereinafter is reported the case of a 2-year-old girl hospitalized in the pediatric intensive care unit for ASA, which was treated with high-flow oxygen therapy and intravenous methylprednisolone and salbutamol. During hospitalization, she had metabolic acidosis with a 7.29 pH, a 26mmHg hypocapnia, and a decrease in bicarbonates to 12 mmol/L. The anion gap was increased to 20 mmol/L and lactates to 8 mmol/L. The work-up for a congenital metabolic disease was normal. Progression was propitious with spontaneous improvement of lactic acidosis, and the child was discharged from the intensive care unit after 72 h. The origin of lactic acidosis during ASA seems to be multifactorial. Although its recovery can be spontaneous, it is important to know how to identify it because it can worsen respiratory symptoms and can lead to incongruous therapeutic escalation.

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