Metabolic Alkalosis

Metabolic alkalosis is a primary rise in serum bicarbonate producing a rise in pH, compensated by hypoventilation with a rise in PaCO₂.

It is among the commonest acid-base disturbances in hospital inpatients, largely because vomiting, nasogastric drainage and diuretics are so common.

Two distinct processes are always involved, and separating them clarifies management.

• A generation step creates the alkalosis ; loss of gastric acid, diuretic use, mineralocorticoid excess, or bicarbonate administration.

• A maintenance step prevents the kidney from excreting the excess bicarbonate, and is usually chloride depletion, volume depletion, hypokalaemia, or mineralocorticoid excess. Since a healthy kidney can excrete bicarbonate readily, an alkalosis that persists always implies a maintenance factor, and treating that factor is what resolves it.

Causes are classified by urine chloride into saline-responsive and saline-resistant, which is the practical division that determines treatment.

• Blood gas showing raised pH and raised bicarbonate, with compensatory hypoventilation raising PaCO₂ by roughly 0.7 mmHg per 1 mmol/L rise in bicarbonate. Compensation is limited by hypoxaemia, so PaCO₂ rarely exceeds about 55 mmHg

• Urine chloride is the essential discriminating test:

  • Below 20 mmol/L ; saline-responsive: vomiting, nasogastric aspiration, prior diuretic use, post-hypercapnic alkalosis, villous adenoma, congenital chloride diarrhoea

  • Above 20 mmol/L ; saline-resistant: current diuretics, primary hyperaldosteronism, Cushing's syndrome, Liddle syndrome, Bartter and Gitelman syndromes, severe hypokalaemia, licorice ingestion

• Blood pressure further subdivides the saline-resistant group: hypertension points to mineralocorticoid excess, while normotension points to Bartter or Gitelman syndrome, diuretic use, or surreptitious vomiting

• Potassium and magnesium, which are almost always low and which perpetuate the alkalosis

• Consider surreptitious vomiting or diuretic misuse where no cause is apparent, particularly with a normal blood pressure and a puzzling picture

• Aldosterone and renin where mineralocorticoid excess is suspected

Saline-responsive:

• 0.9% saline to restore volume and chloride, which allows renal bicarbonate excretion
• Potassium chloride, which is essentially always required; the alkalosis will not resolve while hypokalaemia persists, since potassium depletion drives hydrogen ion into cells and promotes renal bicarbonate reabsorption
• Magnesium replacement, without which potassium cannot be corrected
• Treat the source: antiemetics, reduce or replace nasogastric losses, manage gastric outlet obstruction, and review diuretic dosing
• Proton pump inhibitors reduce gastric acid loss in patients on continuous nasogastric drainage, which is a simple and effective preventive measure

Saline-resistant:

• Saline is ineffective and may cause harm through volume overload
• Acetazolamide promotes bicarbonate excretion, and is particularly useful in diuretic-associated alkalosis in heart failure, where a saline load is undesirable
• Potassium-sparing diuretics (spironolactone, amiloride) where ongoing diuresis is needed
• Treat mineralocorticoid excess specifically: spironolactone or surgical management for primary hyperaldosteronism, and appropriate treatment for Cushing's syndrome
• Correct severe potassium depletion, which can itself sustain the alkalosis

Severe alkalosis (pH above approximately 7.55) risks arrhythmia, seizures, reduced cerebral perfusion and tetany from reduced ionised calcium; hydrochloric acid infusion via central access or haemodialysis are options in extremis and warrant critical care involvement.

Referral: nephrology for saline-resistant alkalosis and suspected tubular disorders; endocrinology for mineralocorticoid excess.