Salbutamol-induced lactic acidosis in status asthmaticus survivor

Abstract Background Salbutamol-induced lactic acidosis is a rare presentation that could manifest in specific clinical context as acute asthmatic attack treatment. An increase of glycolysis pathway leading to pyruvate escalation is the mechanism of hyperlactatemia in β2-adrenergic agonist drug. Case...

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Main Authors: Vorakamol Phoophiboon, Parima Singhagowinta, Sangdao Boonkaya, Thitiwat Sriprasart
Format: Article
Language:English
Published: BMC 2021-01-01
Series:BMC Pulmonary Medicine
Subjects:
Online Access:https://doi.org/10.1186/s12890-021-01404-x
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author Vorakamol Phoophiboon
Parima Singhagowinta
Sangdao Boonkaya
Thitiwat Sriprasart
author_facet Vorakamol Phoophiboon
Parima Singhagowinta
Sangdao Boonkaya
Thitiwat Sriprasart
author_sort Vorakamol Phoophiboon
collection DOAJ
description Abstract Background Salbutamol-induced lactic acidosis is a rare presentation that could manifest in specific clinical context as acute asthmatic attack treatment. An increase of glycolysis pathway leading to pyruvate escalation is the mechanism of hyperlactatemia in β2-adrenergic agonist drug. Case presentation A 40-year-old man who had poor-controlled asthma, presented with progressive dyspnea with coryza symptom for 6 days. He was intubated and admitted into medical intensive care unit due to deteriorated respiratory symptom. Severe asthmatic attack was diagnosed and approximate 1.5 canisters of salbutamol inhaler was administrated within 24 h of admission. Initial severe acidosis consisted of acute respiratory acidosis from ventilation-perfusion mismatch and acute metabolic acidosis resulting from bronchospasm and hypoxia-related lactic acidosis, respectively. The lactate level was normalized in 6 h after hypoxemia and ventilation correction. Given the lactate level re-elevated into a peak of 4.6 mmol/L without signs of tissue hypoxia nor other possible etiologies, the salbutamol toxicity was suspected and the inhaler was discontinued that contributed to rapid lactate clearance. The patient was safely discharged on the 6th day of admission. Conclusion The re-elevation of serum lactate in status asthmaticus patient who had been administrated with the vast amount of β2-adrenergic agonist should be considered for salbutamol-induced lactic acidosis and promptly discontinued especially when there were no common potentials.
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spelling doaj.art-2c13d15da40d4dd1894ff91b7477f8f32022-12-21T22:00:00ZengBMCBMC Pulmonary Medicine1471-24662021-01-012111410.1186/s12890-021-01404-xSalbutamol-induced lactic acidosis in status asthmaticus survivorVorakamol Phoophiboon0Parima Singhagowinta1Sangdao Boonkaya2Thitiwat Sriprasart3Division of Pulmonary and Critical Care Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn UniversityDepartment of Medicine, Faculty of Medicine, Chulalongkorn UniversityDepartment of Medicine, Faculty of Medicine, Chulalongkorn UniversityDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn UniversityAbstract Background Salbutamol-induced lactic acidosis is a rare presentation that could manifest in specific clinical context as acute asthmatic attack treatment. An increase of glycolysis pathway leading to pyruvate escalation is the mechanism of hyperlactatemia in β2-adrenergic agonist drug. Case presentation A 40-year-old man who had poor-controlled asthma, presented with progressive dyspnea with coryza symptom for 6 days. He was intubated and admitted into medical intensive care unit due to deteriorated respiratory symptom. Severe asthmatic attack was diagnosed and approximate 1.5 canisters of salbutamol inhaler was administrated within 24 h of admission. Initial severe acidosis consisted of acute respiratory acidosis from ventilation-perfusion mismatch and acute metabolic acidosis resulting from bronchospasm and hypoxia-related lactic acidosis, respectively. The lactate level was normalized in 6 h after hypoxemia and ventilation correction. Given the lactate level re-elevated into a peak of 4.6 mmol/L without signs of tissue hypoxia nor other possible etiologies, the salbutamol toxicity was suspected and the inhaler was discontinued that contributed to rapid lactate clearance. The patient was safely discharged on the 6th day of admission. Conclusion The re-elevation of serum lactate in status asthmaticus patient who had been administrated with the vast amount of β2-adrenergic agonist should be considered for salbutamol-induced lactic acidosis and promptly discontinued especially when there were no common potentials.https://doi.org/10.1186/s12890-021-01404-xSalbutamol-induced lactic acidosisStatus asthmaticusLactic acidosisSalbutamol’s adverse effectCase report
spellingShingle Vorakamol Phoophiboon
Parima Singhagowinta
Sangdao Boonkaya
Thitiwat Sriprasart
Salbutamol-induced lactic acidosis in status asthmaticus survivor
BMC Pulmonary Medicine
Salbutamol-induced lactic acidosis
Status asthmaticus
Lactic acidosis
Salbutamol’s adverse effect
Case report
title Salbutamol-induced lactic acidosis in status asthmaticus survivor
title_full Salbutamol-induced lactic acidosis in status asthmaticus survivor
title_fullStr Salbutamol-induced lactic acidosis in status asthmaticus survivor
title_full_unstemmed Salbutamol-induced lactic acidosis in status asthmaticus survivor
title_short Salbutamol-induced lactic acidosis in status asthmaticus survivor
title_sort salbutamol induced lactic acidosis in status asthmaticus survivor
topic Salbutamol-induced lactic acidosis
Status asthmaticus
Lactic acidosis
Salbutamol’s adverse effect
Case report
url https://doi.org/10.1186/s12890-021-01404-x
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AT parimasinghagowinta salbutamolinducedlacticacidosisinstatusasthmaticussurvivor
AT sangdaoboonkaya salbutamolinducedlacticacidosisinstatusasthmaticussurvivor
AT thitiwatsriprasart salbutamolinducedlacticacidosisinstatusasthmaticussurvivor