What is the treatment for metabolic alkalosis?

Treatment of Metabolic Alkalosis

The cornerstone of treatment for metabolic alkalosis is addressing the underlying cause while correcting volume status, electrolyte abnormalities (particularly chloride and potassium), and in severe cases, using carbonic anhydrase inhibitors like acetazolamide. 1

Pathophysiology and Classification

Metabolic alkalosis is characterized by elevated serum bicarbonate (>26 mmol/L) and arterial pH (>7.43), often accompanied by hypokalemia 2. Understanding the cause is essential for proper treatment:

Classification by Volume Status:

• Chloride-responsive (volume-depleted):

  • Urinary chloride <20 mEq/L
  • Common causes: vomiting, nasogastric suction, diuretic use
  • Responds to normal saline administration

• Chloride-resistant (volume-expanded):

  • Urinary chloride >20 mEq/L
  • Common causes: mineralocorticoid excess, Bartter syndrome
  • Requires specific treatment of underlying cause

Treatment Algorithm

1. Address the Underlying Cause

• Stop offending medications (diuretics)
• Treat vomiting/nasogastric losses
• Manage conditions like Bartter syndrome or mineralocorticoid excess

2. Volume Repletion and Electrolyte Correction

• For chloride-responsive alkalosis:

  • Administer isotonic saline (0.9% NaCl) to restore effective arterial blood volume 3
  • This corrects volume depletion and provides chloride, enabling the kidneys to excrete excess bicarbonate

• Potassium repletion:

  • Correct hypokalemia with potassium chloride (not potassium bicarbonate or citrate)
  • Hypokalemia maintains alkalosis by promoting bicarbonate reabsorption and hydrogen secretion

3. Pharmacologic Interventions

• Acetazolamide (carbonic anhydrase inhibitor):

  • Indicated for severe or persistent metabolic alkalosis, especially in heart failure or when volume overload limits saline administration 4
  • Dosage: 250-500 mg IV/PO every 6-8 hours
  • Mechanism: Inhibits proximal tubular bicarbonate reabsorption, promoting bicarbonate excretion
  • Monitor for hypokalemia and worsening of volume depletion 5

• Hydrochloric acid (HCl):

  • Reserved for severe, life-threatening alkalosis (pH >7.55) unresponsive to other measures 6
  • Must be administered through central venous catheter at 0.1-0.2N concentration
  • Requires close monitoring in ICU setting

4. Special Situations

• Heart Failure with Metabolic Alkalosis:

  • Add aldosterone antagonists (spironolactone) to diuretic regimen 4
  • Use acetazolamide cautiously to enhance bicarbonate excretion
  • Avoid volume overload with judicious saline administration

• Bartter Syndrome:

  • Potassium chloride supplementation
  • NSAIDs (indomethacin) to reduce prostaglandin-mediated salt wasting 3
  • Potassium-sparing diuretics may be considered in individual cases but are not routinely recommended due to risk of worsening salt wasting 3

Monitoring and Follow-up

• Serial arterial blood gases or venous bicarbonate levels
• Electrolyte monitoring (especially potassium, chloride, sodium)
• Fluid status assessment

Common Pitfalls to Avoid

1. Using potassium bicarbonate or citrate instead of potassium chloride - these can worsen alkalosis

2. Overly aggressive volume repletion in patients with heart failure - can precipitate pulmonary edema

3. Failure to recognize mixed acid-base disorders - metabolic alkalosis can mask concurrent respiratory acidosis

4. Discontinuing acetazolamide too quickly - can lead to rebound alkalosis

5. Administering thiazide diuretics in Bartter syndrome - can lead to life-threatening hypovolemia 3

In severe cases of metabolic alkalosis with pH >7.55, particularly in critically ill patients, prompt and aggressive treatment is warranted as this level of alkalosis is associated with significantly increased mortality 7.