Specialist Registrar, Department of Anaesthetics, Addenbrookes Hospital, Cambridge, UK
Foundation House Officer Year 2, Neurosciences Critical Care Unit, Addenbrookes Hospital, Cambridge, UK
Abstract
Introduction
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.
Case presentation
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.
Conclusion
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.
Introduction
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.
Case presentation
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
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.
In ITU she complained of worsening breathlessness, despite an objective improvement in peak expiratory flow rate and wheeze. Her arterial blood gases at that time showed a compensated metabolic acidosis with high lactate. We excluded all common causes of a metabolic acidosis in this clinical setting including hypoxia, hypovolemia and sepsis. We suspected that the lactic acidosis may have been secondary to nebulised salbutamol, and consequently reduced the dosing interval. This resulted in a reduction in the serum lactic acid level. When the nebulised salbutamol was subsequently stopped the lactic acidosis promptly reversed (Table
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.
Time/Date
pH
PaCO2
PaO2
HCO3
BE
Lactate
PEFR
Symptoms/Treatment
11/1/06
21.20 hrs
7.39
3.03 KPa
20.5 KPa
13.6 mmol/l
-11 mmol/l
14.6 mmol/l
230 L/min
Minimal wheeze, SOB+
11/1/06
24.00 hrs
7.32
3.01 KPa
18.6 KPa
11.7 mmol/l
-14 mmol/l
11.06 mmol/l
240 L/min
No wheeze, hyperventilation+
12/1/06
3.00 hrs
7.28
2.29 KPa
11.4 KPa
8.3 mmol/l
-19 mmol/l
15.2 mmol/l
230 L/min
SOB+++, hyperventilation
12/1/06
7.00 hrs
7.3
2.13 KPa
13.8 KPa
8.0 mmol/l
-18 mmol/l
10.09 mmol/l
300 L/min
Minimal wheeze
12/1/06
23.00 hrs
7.43
3.46 KPa
12.3 KPa
17.6 mmol/l
-7 mmol/l
6.3 mmol/l
300 L/min
No wheeze Continued improvement
14/1/06
10.00 hrs
7.53
3.39 KPa
9.6 KPa
21.0 mmol/l
-2 mmol/l
1.1 mmol/l
320 L/min
Discharged to ward.
In this particular patient, salbutamol and its resultant metabolic acidosis caused us difficulty in assessment and management of her asthma.
Discussion
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
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
Conclusion
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
FBC – Full Blood count, CRP – C Reactive Protein, CXR – Chest X-ray, ABG – Arterial Blood Gases, A&E – Accident and Emergency, ITU – Intensive Treatment Unit, PEFR – Peak expiratory flow rate, ECG – Electrocardiogram.
Competing interests
The author(s) declare that they have no competing interests.
Authors' contributions
Both author(s) are involved in writing this case report.
Acknowledgements
This patient was consented for publication for this case report.