What is the treatment for metabolic alkalosis?

Treatment of Metabolic Alkalosis

The primary treatment for metabolic alkalosis is chloride replacement therapy with sodium chloride and potassium chloride supplementation, combined with discontinuation or dose reduction of causative diuretics when possible. 1

Initial Assessment and Management

Identify and address the underlying cause:

• Discontinue or reduce diuretic therapy (loop or thiazide diuretics) if clinically feasible 2, 1
• Assess for volume depletion, which is the most common perpetuating factor 3
• Measure urinary chloride to distinguish chloride-responsive (<20 mEq/L) from chloride-resistant (>20 mEq/L) alkalosis 2

Electrolyte Replacement Strategy

Potassium chloride is essential and must be prioritized:

• Target serum potassium levels of 4.5-5.0 mEq/L 2, 1
• Doses of 20-60 mEq/day are frequently required 2
• Critical pitfall: Never use potassium citrate or other non-chloride potassium salts, as these will worsen the alkalosis 2, 1

Chloride replacement:

• Administer intravenous or oral sodium chloride for volume repletion 1
• In vomiting-induced alkalosis, potassium chloride infusion restores renal bicarbonate excretion 4
• Correct hypokalemia to >3.5 mmol/L before addressing other interventions 2

Pharmacologic Interventions

Potassium-sparing diuretics are first-line for diuretic-induced alkalosis:

• Amiloride is the most effective option: start at 2.5 mg daily, titrate up to 5 mg daily 2
• Amiloride improves edema/hypertension while countering hypokalemia and metabolic alkalosis 2
• Spironolactone 25-100 mg daily is an alternative, particularly beneficial in heart failure patients 2, 1
• Critical warning: Avoid combining potassium-sparing diuretics with ACE inhibitors without close monitoring due to hyperkalemia risk 2, 1

Acetazolamide for refractory cases:

• Useful in heart failure patients with diuretic-induced alkalosis and adequate kidney function 2
• Dose: 500 mg intravenously 5
• Onset of action within 2 hours, with mean bicarbonate reduction of 6.4 mmol/L at 24 hours 5
• Consider when potassium-sparing diuretics are insufficient 1

Special Clinical Situations

Bartter or Gitelman syndrome (chloride-resistant alkalosis with urinary Cl >20 mEq/L):

• Sodium chloride supplementation: 5-10 mmol/kg/day 2
• Potassium chloride for potassium replacement 2
• NSAIDs to reduce prostaglandin-mediated salt wasting 2
• Consider gastric acid inhibitors with NSAIDs for gastric protection 2
• Obtain genetic testing for definitive diagnosis 2

Severe or refractory metabolic alkalosis:

• Hemodialysis with low-bicarbonate/high-chloride dialysate is the treatment of choice, especially with concurrent renal failure 2, 3
• Dilute hydrochloric acid (0.1-0.2 N) via central venous catheter for patients with hepatic dysfunction who cannot tolerate ammonium chloride 6
• Never administer sodium bicarbonate or alkalinization strategies—these are contraindicated and will worsen the alkalosis 2

Monitoring Requirements

Essential parameters to track:

• Serum electrolytes (potassium, sodium, chloride) 2, 1
• Acid-base status (pH, bicarbonate, base excess) 2
• Volume status and kidney function 1
• Adjust therapy based on clinical response and laboratory parameters 2, 1

Common Pitfalls to Avoid

• Using non-chloride potassium salts (citrate, gluconate, acetate) which exacerbate alkalosis 2, 1
• Failing to achieve adequate potassium repletion before expecting bicarbonate correction 4
• Overlooking Bartter syndrome in patients with unexplained alkalosis, especially with history of polyhydramnios and premature birth 2
• Using potassium-sparing diuretics in patients with significant renal dysfunction or existing hyperkalemia 2
• Administering high-dose loop diuretics (furosemide >160 mg/day) without monitoring, which worsens electrolyte disturbances 7