Lactic acidosis is an important cause of metabolic acidosis in hospitalised patients. This usually occurs either due to over production or under utilisation of lactate1 . Most cases of lactic acidosis are due to marked tissue hypoperfusion or hypoxia in systemic shock.

Asymptomatic lactic acidosis has been reported previously during acute severe asthma and attributed to fatiguing respiratory muscles, hypoxaemia and liver ischaemia. It has also been linked to β2 agonist therapy in asthma, although lactic acidosis causing increasing dyspnoea in the asthmatic patient has only been recorded rarely.

We present a case of lactic acidosis in a patient with acute severe asthma who did not have any overt signs of sepsis or tissue hypoperfusion.

Mr IL was a 49 years old male who was known to have moderate asthma. He had multiple previous admissions to hospital with exacerbation of asthma but had never required an intensive care admission and had never been intubated. His other comorbidities included atrial fibrillation, ischaemic heart disease and depression.

His usual medications included salbutamol, budesonide and salmeterol inhalers, aspirin, atorvastatin and digoxin. He was a mechanic by trade with no obvious occupational sensitisation. He had no pets at home. He was a smoker with a 20 pack year history. Recent lung function tests showed an FEV1/FVC of 0.68 with a post bronchodilator FEV1 of 4.17 L (95% predicted).

He was admitted with a 1 week history of worsening shortness of breath, dry cough and wheeze. His baseline blood tests including full blood count, C reactive protein, liver and renal function were normal. Chest radiograph was unremarkable.

Arterial blood gas showed no evidence of hypoxia or acidosis. He was treated as acute severe asthma with back to back nebulisers, intravenous hydrocortisone and magnesium sulphate resulting in gradual improvement in bronchospasm and peak expiratory flow rate.

Despite optimal treatment, his breathing started to deteriorate. Arterial blood gas at this time showed lactic acidosis with normal oxygenation (Table 1). There was no clinical or biochemical evidence of haemodynamic compromise or sepsis. A presumptive diagnosis of lactic acidosis secondary to salbutamol was made. The nebulisers were withheld and he has transferred to high dependency unit for closer monitoring. The acidosis completely resolved in the following 12 hours on stopping salbutamol and the patient made an uneventful recovery.

Lactate is a product of anaerobic glucose metabolism and is generated from pyruvate. Normal plasma lactate concentration is 0.5-2 meq/L. Most cases of lactic acidosis are due to marked tissue hypoperfusion or hypoxia in systemic shock2 .

Lactic acidosis can occur in acute severe asthma due to inadequate oxygen delivery to the respiratory muscles to meet an elevated oxygen demand3 or due to fatiguing respiratory muscles4 . A less recognised cause of lactic acidosis is treatment with salbutamol. The mechanism of this complication is poorly understood.

Salbutamol is the most commonly used short acting βagonist. Stimulation of β adrenergic receptors leads to a variety of metabolic effects including increase in glycogenolysis, gluconeogenesis and lipolysis5 thus contributing to lactic acidosis.

Table 2 shows an assortment of previously published case reports and case series of lactic acidosis in the context of acute asthma.

Table 1: Serial Arterial Blood Gases (On admission, 4 hours later and on stopping salbutamol)

Table 2: Details of etiology and consequences of lactic acidosis in previously published case reports

In this case, the patient developed lactic acidosis secondary to treatment with salbutamol nebulisers. The acidosis resolved spontaneously without any specific treatment.

Lactic acidosis secondary to β agonist administration may be a common scenario which can be easily misinterpreted and confuse the clinical picture. Acidosis itself results in hyperventilation which could be mistaken for failure to treat the response. This may in turn lead to inappropriate intensification of treatment.

Competing Interests: None Declared

1. Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest 2000; 117:260–267
2. Prakash S, Mehta S: Lactic acidosis in asthma: Report of two cases and review of the literature. Canadian Respiratory Journal. 2002, 9(3):203- 208
3. Stratakos G, Kalomenidis J, Routsi C, Papiris S, Roussos C. Transient lactic acidosis as a side effect of inhaled salbutamol. Chest. 2002 Jul;122(1):385-6
4. Mountain RD, Heffner JE, Brackett NC Jr, Sahn SA. Acid-base disturbances in acute asthma. Chest. 1990 Sep;98(3):651-5
5. Haffner CA, Kendall MJ. Metabolic effects of β2 agonists. J Clin Pharm Ther 1992; 17:155–164
6. Roncoroni AJ, Adrougué HJ, De Obrutsky CW, Marchisio ML, Herrera MR. Metabolic acidosis in status asthmaticus. Respiration. 1976;33(2):85–94
7. Appel D, Rubenstein R, Schrager K, Williams MH., Jr. Lactic acidosis in severe asthma. Am J Med. 1983 Oct;75(4):580–584
8. Braden GL, Johnston SS, Germain MJ, Fitzgibbons JP, Dawson JA. Lactic acidosis associated with the therapy of acute bronchospasm. N Engl J Med. 1985 Oct 3;313(14):890-1
9. O'Connell MB, Iber C. Continuous intravenous terbutaline infusions for adult patients with status asthmaticus. Ann Allergy. 1990 Feb;64(2 Pt 2):213-8
10. Mountain RD, Heffner JE, Brackett NC, Jr, Sahn SA. Acid-base disturbances in acute asthma.Chest. 1990 Sep;98(3):651–655
11. Maury E, Ioos V, Lepecq B, Guidet B, Offenstadt G. A paradoxical effect of bronchodilators.Chest. 1997 Jun;111(6):1766–1767
12. Manthous CA. Lactic acidosis in status asthmaticus : three cases and review of the literature.Chest. 2001 May;119(5):1599–1602
13. Creagh-Brown BC, Ball J. An under-recognized complication of treatment of acute severe asthma. Am J Emerg Med. 2008 May;26(4):514.e1-3
14. Veenith TV, Pearce A. A case of lactic acidosis complicating assessment and management of asthma. Int Arch Med. 2008 Apr 15;1(1):3
15. R Saxena, G Marais. Salbutamol: beware of the paradox! BMJ Case Reports 2010; doi:10.1136/bcr.01.2010.2665