A case of lactic acidosis complicating assessment and management of asthma
© Veenith and Pearce. 2008
Received: 30 January 2008
Accepted: 15 April 2008
Published: 15 April 2008
Lactic acidosis often occurs in severely unwell patients presenting to Accident and Emergency. It is commonly associated with either hypoxia or decreased tissue perfusion secondary due to cardiovascular collapse or sepsis.
We present a case of severe lactic acidosis in the presence of normal tissue perfusion and oxygenation in a 31-year-old patient with poorly-controlled asthma. Acidosis promptly reversed on discontinuation of inhaled beta-agonists.
Lactic acidosis secondary to inhaled beta-agonist administration may be a common scenario which can be misinterpreted very easily and can confuse the clinical picture. Further studies will be needed to establish the exact aetiology of this lactic acid production.
Lactic acidosis is diagnosed by a metabolic acidosis, associated with an elevated serum lactate concentration. It often occurs in severely unwell patients presenting to Accident and Emergency, and is commonly associated with either hypoxia or decreased tissue perfusion secondary due to cardiovascular collapse or sepsis. Many drugs may also result in an increase in serum lactate, including Salbutamol.
Ms XF is a 31 year old Caucasian female who has a diagnosis of uncontrolled asthma which has required repeated admissions over approximately ten years . She is otherwise well with no significant co-morbidities.
Her usual medications are inhaled Salbutamol, Fluticasone accuhaler, nebulised Salbutamol, Salmeterol, Monteleucast 10 mg, Theophylline 300 mg bd, Vitamin D3 and Lansoprazole.
The patient was admitted with a history of cough with green sputum, wheezing and shortness of breath over three days. Initially she treated herself with Salbutamol inhalers and nebulised bronchodilators without improvement. She continued to deteriorate and in A&E she was treated with "back to back" salbutamol nebulisers and transferred to ITU. On admission she had no evidence of hypoxia, infection and hypovolemia as evidenced by clinical examination along with invasive monitoring and investigations such as blood gases, FBC, CRP, and CXR.
Arterial blood gas analysis before and after stopping salbutamol. The patient's clinical condition and blood gases improved dramatically after cessation of salbutamol. ABGs after 11 hours and 48 hours post-withdrawal of salbutamol are shown.
Minimal wheeze, SOB+ Reduced dose of Salbutamol
No wheeze, hyperventilation+
Minimal wheeze Nebulised salbutamol discontinued
No wheeze Continued improvement
Discharged to ward.
In this particular patient, salbutamol and its resultant metabolic acidosis caused us difficulty in assessment and management of her asthma.
Salbutamol is a beta agonist associated with a multitude of systemic side effects. One of the least recognised side effects of salbutamol with clinical consequence is lactic acidosis. Lactic acidosis is commonly associated with either hypoxia or decreased tissue perfusion either due to cardiovascular collapse or sepsis . There are many views regarding the pathogenesis of lactic acidosis in asthma; the most accepted one being due to fatiguing respiratory muscles . Another accepted explanation could be due to effects of ischemia and hypoxia on liver which was unlikely in the above case as this patient had normal liver function .
In healthy volunteers salbutamol will increase the oxygen consumption by increasing metabolic rate and serum lactate. This will affect patients with severe asthma, who already limited ventilatory reserve, by increasing their symptoms . In pregnant patients the lactate levels increase when given Ritodrine (beta agonist) for tocolysis . An increase in serum lactate has also been documented paediatric patients, followed by administration of nebulised salbutamol . This resolved after the discontinuation of the drug. Lactic acidosis is much more prominent in intravenous salbutamol than nebulised salbutamol, so intravenous salbutamol should not be routinely prescribed .
In this patient, resolution of wheezing was accomplished by intensive treatment with salbutamol but at the cost of lactic acidosis. This was important because acidosis by itself can result in hyperventilation and a sense of dyspnoea which could be easily mistaken for failure to respond to the treatment, as this particular case exemplifies. Lactic acidosis secondary to inhaled beta-agonist administration may be a common scenario which can be misinterpreted very easily and can confuse the clinical picture. Further studies will be needed to establish the exact aetiology of this lactic acid production.
List of abbreviations
Full Blood count
C Reactive Protein
Arterial Blood Gases
Accident and Emergency
Intensive Treatment Unit
Peak expiratory flow rate
This patient was consented for publication for this case report.
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