Treating acute asthma – salbutamol may not always be the right answer

Sturney, Sharon; Suntharalingam, Jay

doi:10.7861/clinmedicine.12-2-181

Cited by 9 publications

(2 citation statements)

References 8 publications

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“…Forty-two articles [4, reported on 47 patients (Table 1), who were found to have a blood lactic acid level ≥5.0 mmol/L on treatment with a short-acting (N = 46) or a long-acting (N = 1) ß 2 -agonist, which subsequently decreased by ≥3.0 mmol/L or to ≤2.5 mmol/L ( Figure 2). This was noticed 3 to 56, median 13 h later: in 24 cases after discontinuing [4,[9][10][11][14][15][16]18,19,22,24,25,29,[32][33][34]36,38,40,41,47,48], in 17 cases after reducing [12,13,20,22,23,26,28,30,31,35,37,39,42,43,45], and in 6 cases (all of these patients were affected by asthma) without modifying [8,12,17,21,27,46], the dosage of the selective ß 2 -agonist. None of the patients was managed with further drugs potentially associated with hyperlactate...…”

Section: Individual Casesmentioning

confidence: 99%

Selective ß2-Adrenoceptor Agonists and Relevant Hyperlactatemia: Systematic Review and Meta-Analysis

Liedtke

Lava

Milani

et al. 2019

JCM

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Selective ß2-agonists have been imputed as potential cause of l-hyperlactatemia since the 1970s. To document the prevalence of hyperlactatemia associated with selective ß2-agonists and to investigate the predisposing factors, we searched for published articles until April 2019 pertaining to the interplay of administration of selective ß2-agonists and circulating l-lactic acid in the Excerpta Medica, Web of Science, and the U.S. National Library of Medicine databases. Out of the 1834 initially retrieved records, 56 articles were included: 42 papers reporting individual cases, 2 observational studies, and 12 clinical trials. Forty-seven individual patients receiving a selective ß2-agonist were found to have l-lactatemia ≥5.0 mmol/L, which decreased by ≥3.0 mmol/L or to ≤2.5 mmol/L after discontinuing (N = 24), reducing (N = 17) or without modifying the dosage of the selective ß2-agonist (N = 6). Clinical trials found that l-lactic acid significantly increased in healthy volunteers administered a ß2-agonist. l-lactatemia ≥5.0 mmol/L was observed in 103 (24%) out of 426 patients with asthma or preterm labor managed with a selective ß2-agonist and was more common in patients with asthma (30%) than in premature labor (5.9%). A significant relationship was also noted between l-lactate level and intravenous albuterol dose or its circulating level. In conclusion, relevant l-hyperlactatemia is common on high dose treatment with a selective ß2-agonist.

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Section: Individual Casesmentioning

confidence: 99%

Selective ß2-Adrenoceptor Agonists and Relevant Hyperlactatemia: Systematic Review and Meta-Analysis

Liedtke

Lava

Milani

et al. 2019

JCM

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“…Finally, theophylline and glucocorticoids may have a role in the increased lactate production during acute severe asthma. Theophylline is a non-selective 5’-phosphodiesterase inhibitor and potentiates the activity of β-adrenergic agents by increasing the intracellular concentration of cAMP [79,80,81]. Glucocorticoids are also known to increase the β-receptor’s sensitivity to β-adrenergic agonists [82].…”

Section: Metabolic Acidosismentioning

confidence: 99%

Acid-Base Disturbances in Patients with Asthma: A Literature Review and Comments on Their Pathophysiology

Vasileiadis

Alevrakis

Ampelioti

et al. 2019

JCM

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Asthma is a common illness throughout the world that affects the respiratory system function, i.e., a system whose operational adequacy determines the respiratory gases exchange. It is therefore expected that acute severe asthma will be associated with respiratory acid-base disorders. In addition, the resulting hypoxemia along with the circulatory compromise due to heart–lung interactions can reduce tissue oxygenation, with a particular impact on respiratory muscles that have increased energy needs due to the increased workload. Thus, anaerobic metabolism may ensue, leading to lactic acidosis. Additionally, chronic hypocapnia in asthma can cause a compensatory drop in plasma bicarbonate concentration, resulting in non-anion gap acidosis. Indeed, studies have shown that in acute severe asthma, metabolic acid-base disorders may occur, i.e., high anion gap or non-anion gap metabolic acidosis. This review briefly presents studies that have investigated acid-base disorders in asthma, with comments on their underlying pathophysiology.

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Medication‐Induced Hyperlactatemia and Lactic Acidosis: A Systematic Review of the Literature

2019

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Hyperlactatemia and lactic acidosis are two syndromes that are associated with morbidity and mortality. Medication-induced hyperlactatemia and lactic acidosis are diagnoses of exclusion and have the potential to be overlooked. The purposes of this systematic review are to identify published reports of medication-induced lactate level elevations to aid clinicians in diagnosing and comprehending the underlying mechanism of this rare adverse drug effect and to provide management strategies. The PubMed database was searched for case reports, case series, retrospective studies, and prospective studies describing cases of medication-induced lactate level elevation, including lactic acidosis and hyperlactatemia, published between January 1950 and June 2017. A standardized search strategy was used, and the articles identified underwent two rounds of independent evaluation by two reviewers to assess for inclusion. Articles were included if they described at least one patient older than 12 years with hyperlactatemia or lactic acidosis caused by a medication with United States Food and Drug Administration (FDA) approval and if alternative etiologies for an elevated lactate level were ruled out. Metformin and nucleoside/nucleotide reverse transcriptase inhibitors were excluded since the pathophysiology and incidence of lactic acidosis have been well established for these agents. Overall, 1918 articles were identified, and 101 met inclusion criteria. A total of 286 patients experienced medication-induced lactate level elevations, from which 59 unique medications were identified. The most commonly identified agents were epinephrine and albuterol. Medication-induced lactate level elevation was classified as lactic acidosis (64.0%), hyperlactatemia (31.1%), or not specified (4.9%). The doses ingested included FDA-labeled doses (86%), intentional overdoses (10.8%), or prescribed doses exceeding the FDA-labeled dose (3.1%). Medications were continued without a change (40.8%), were permanently discontinued (34.4%), were continued with a dosage reduction (11.6%), or were initially withheld then resumed after lactate level normalized (2.9%); medication management for the remaining 10.0% was not reported. Forty-six patients died (16%). Six deaths were attributed by treating clinicians to be secondary to medication-induced lactic acidosis. Management strategies were heterogeneous, and treatment included supportive care, exogenous bicarbonate therapy, medication specific antidotes, and decontamination strategies. Unexplained lactate level elevations should prompt clinicians to assess for medication-induced lactate level elevations. Pharmacists are members of the health care team that are well positioned to serve as experts in the diagnosis and management of medication-induced lactate level elevations. KEY WORDS adverse drug reactions, hyperlactatemia, systematic review, lactate, lactic acidosis. (Pharmacotherapy 2019;39(9):946-963)

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Treating acute asthma – salbutamol may not always be the right answer

Cited by 9 publications

References 8 publications

Selective ß2-Adrenoceptor Agonists and Relevant Hyperlactatemia: Systematic Review and Meta-Analysis

Selective ß2-Adrenoceptor Agonists and Relevant Hyperlactatemia: Systematic Review and Meta-Analysis

Acid-Base Disturbances in Patients with Asthma: A Literature Review and Comments on Their Pathophysiology

Medication‐Induced Hyperlactatemia and Lactic Acidosis: A Systematic Review of the Literature

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