Endgames Case Report

Metabolic alkalosis in a patient with dyspnoea

BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.f2710 (Published 02 May 2013) Cite this as: BMJ 2013;346:f2710
  1. Richard Windsor, foundation year 2, obstetrics and gynaecology1,
  2. Will Petchey, registrar, renal medicine2
  1. 1Queen Elizabeth Hospital, King’s Lynn PE30 4ET, UK
  2. 2Norfolk and Norwich University Hospital, Norwich, UK
  1. Correspondence to: R Windsor Richard.windsor{at}doctors.org.uk

A 56 year old woman with poorly controlled asthma was admitted to hospital with a suspected lower respiratory tract infection, having become increasingly anxious and short of breath over the past 24 hours. She had been unwell for the past week, and her general practitioner had started her on amoxicillin and oral steroids. She was a never smoker, had a history of ischaemic heart disease and atrial fibrillation, and had a high body mass index. This was not the first time she had been admitted to hospital with an exacerbation of her asthma, having been admitted several times previously. Her regular drugs included fluticasone, salbutamol, furosemide, omeprazole, simvastatin, and diltiazem.

On examination she had a normal temperature, a respiratory rate of 26 breaths/min, sparse crackles at her left lung base, together with widespread expiratory wheeze. The table details her initial arterial blood gases on air and other blood test results.

Initial arterial blood gases on air and other blood test results

View this table:

Questions

  • 1 What is the likely cause of this patient’s metabolic alkalosis?

  • 2 Which of the drugs that she was taking on admission can also cause metabolic alkalosis?

  • 3 Does this alkalosis require therapeutic correction?

Answers

1 What is the likely cause of this patient’s metabolic alkalosis?

Short answer

This patient has post-hypercapnic metabolic alkalosis, which occurs when the carbon dioxide level in the blood drops rapidly owing to an increased respiratory rate in a patient with compensated chronic retention of carbon dioxide. In this case, hyperventilation was caused by a combination of anxiety, relative hypoxia, and concomitant pneumonia.

Long answer

Risk factors for chronic retention of carbon dioxide include chronic obstructive pulmonary disease, diseases that cause respiratory muscle weakness, abnormal curvature of the thoracic spine, and, as in this case, a high body mass index.1 The normal physiological response in patients who chronically retain carbon dioxide is for the resulting acidosis to be compensated for by an increase in serum bicarbonate. In this case, the patient’s increased respiratory rate caused her chronically raised arterial carbon dioxide level to drop back within the normal range. In this situation, the increased plasma concentration of bicarbonate causes metabolic alkalosis.2 This post-hypercapnic alkalosis is most often seen in patients with chronic obstructive pulmonary disease who require ventilation, but it is not unusual in younger patients with carbon dioxide retention who become tachypnoeic.

2 Which of the drugs that she was taking on admission can also cause metabolic alkalosis?

Short answer

Furosemide.

Long answer

Loop diuretics can cause a metabolic alkalosis through two mechanisms. Initially, contraction alkalosis is caused by a reduction in total extracellular fluid and urinary chloride wasting, which without proportionate bicarbonate wasting effectively raises serum bicarbonate concentrations.3 However, the loss of potassium (kaliuresis) also plays an important role.4 Blockade of the sodium/potassium/chloride transporter in the ascending limb of the loop of Henlé by furosemide not only inhibits potassium reabsorption but also results in increased sodium delivery to the distal tubules. Here, under the influence of aldosterone, the sodium is exchanged for potassium (sodium/potassium ATPase). The resulting loss of potassium increases renal ammoniagenesis, increasing the concentration of ammonium in the urine and the loss of hydrogen ions in the urine. Aldosterone also stimulates hydrogen ATPase in the collecting ducts, thereby further increasing fractional excretion of hydrogen ions.5

Other classes of drugs that may cause metabolic alkalosis include thiazide diuretics, high dose glucocorticoids, lactate containing intravenous solutions, and bicarbonate containing antacids.5 6 Non-drug causes include severe potassium depletion (for example, dietary limitation), chloride depletion (vomiting, nasogastric drainage), impairment of renal chloride transport (Bartter syndrome and Gitelman’s syndrome), and corticosteroid excess, either real or apparent (primary hyperaldosteronism, Cushing’s syndrome, liquorice ingestion).5 7

3 Does this alkalosis require therapeutic correction?

Short answer

No.

Long answer

In this setting, no—the high level of bicarbonate will be physiologically corrected within hours to days, or carbon dioxide concentrations will rise again. However, correction of a protracted primary metabolic alkalosis will depend on chloride and potassium repletion and correction of any underlying metabolic or endocrine problems.2 Indications for treatment are opinion based, with no formal guidelines. However, the presence of symptomatic or serious hypokalaemia (<3.0 mmol/L) or alkalotic symptoms (such as hypoventilation, apnoeic episodes, diarrhoea, flocillation, muscle excitability, twitching, irritability, confusion, seizures, coma) would seem appropriate. There is some evidence that attempts at weaning are more likely to fail in ventilated patients with chronic obstructive pulmonary disease and uncorrected metabolic alkalosis; however, clear treatment guidelines are yet to be established.8

Patient outcome

Further investigation supported a diagnosis of lobar pneumonia and acute exacerbation of asthma. She responded well to antibiotics, oral steroids, and bronchodilators and was discharged home after three days with theophylline and montelukast added to her regular drugs.

Notes

Cite this as: BMJ 2013;346:f2710

Footnotes

  • Competing interests: We have read and understood the BMJ Group policy on declaration of interests and declare the following interests: None.

  • Provenance and peer review: Not commissioned; externally peer reviewed.

  • Patient consent obtained.

References