How is metabolic alkalosis treated?

Treatment of Metabolic Alkalosis

The primary treatment of metabolic alkalosis is discontinuing diuretics when possible, correcting volume depletion with saline, and aggressively replacing potassium chloride to maintain serum potassium at 4.5-5.0 mEq/L, with potassium-sparing diuretics (particularly amiloride) as the first-line pharmacologic intervention for diuretic-induced alkalosis. 1

Initial Assessment and Diagnosis

The first step is determining whether the alkalosis is chloride-responsive or chloride-resistant by checking urinary chloride 1:

• Urinary chloride <20 mEq/L: Chloride-responsive (volume depletion, diuretic use, vomiting/NG suction) 1
• Urinary chloride >20 mEq/L: Chloride-resistant (consider Bartter syndrome, Gitelman syndrome, mineralocorticoid excess) 1

Monitor serum electrolytes, acid-base status, and volume status throughout treatment 1. In severe cases (pH >7.55-7.60), recognize this carries significant morbidity and mortality risk 2.

Chloride-Responsive Metabolic Alkalosis (Most Common)

Step 1: Discontinue Precipitating Factors

• Stop or reduce diuretics if clinically feasible 1
• Remove nasogastric suction when possible 3

Step 2: Volume Repletion with Saline

• Administer normal saline (0.9% NaCl) to correct volume depletion 4, 3
• Volume expansion allows the kidneys to excrete excess bicarbonate 4
• This is the cornerstone of treatment for chloride-depletion alkalosis 5

Step 3: Aggressive Potassium Chloride Replacement

• Potassium chloride 20-60 mEq/day is frequently required to maintain serum potassium at 4.5-5.0 mEq/L 1
• Use only potassium chloride, never potassium citrate or other potassium salts, as these worsen metabolic alkalosis 1
• Hypokalemia perpetuates alkalosis by increasing renal bicarbonate reabsorption 4, 5
• Correct potassium to >3.5 mmol/L at minimum 1

Step 4: Add Potassium-Sparing Diuretics for Diuretic-Induced Alkalosis

Amiloride is the most effective first-line agent for correcting metabolic alkalosis in patients requiring ongoing diuresis 1:

• Amiloride 2.5 mg daily, titrate up to 5 mg daily 1
• Provides improvement in edema/hypertension while countering hypokalemia and alkalosis 1
• Spironolactone 25 mg daily, titrate to 50-100 mg daily, is an alternative 1
• In heart failure patients, adding an aldosterone antagonist (spironolactone) to the diuretic regimen is particularly beneficial 1

Critical caveat: Avoid potassium-sparing diuretics in patients with significant renal dysfunction (eGFR <30 mL/min) or existing hyperkalemia 1. Do not combine with ACE inhibitors without close monitoring due to hyperkalemia risk 1.

Step 5: Consider Acetazolamide for Refractory Cases

Acetazolamide 250-500 mg once or twice daily can be useful in patients with heart failure and diuretic-induced alkalosis who have adequate kidney function 1:

• Works by inhibiting renal bicarbonate reabsorption 1
• Particularly effective when switching to longer-acting loop diuretics is not sufficient 1
• Requires adequate renal function to be effective 1

Chloride-Resistant Metabolic Alkalosis (Bartter/Gitelman Syndrome)

For patients with urinary chloride >20 mEq/L suggesting salt-losing tubulopathies 1:

• Sodium chloride supplementation 5-10 mmol/kg/day 1
• Potassium chloride for potassium supplementation (never potassium citrate) 1
• NSAIDs to reduce prostaglandin-mediated salt wasting in symptomatic patients 1
• Gastric acid inhibitors (PPIs) together with NSAIDs to prevent GI complications 1
• Consider genetic testing for definitive diagnosis if Bartter or Gitelman syndrome is suspected 1

Severe or Refractory Metabolic Alkalosis

When conventional therapy fails or cannot be tolerated 4, 3:

Hemodialysis (Preferred for Severe Cases)

• Hemodialysis with low-bicarbonate/high-chloride dialysate is the treatment of choice for refractory metabolic alkalosis, especially with concurrent renal failure 1
• This is safer and more controlled than acid infusion 3

Hydrochloric Acid Infusion (Rarely Needed)

Only when rapid correction is essential and dialysis is unavailable 4, 6:

• Dilute hydrochloric acid 0.1-0.2 N (0.12-0.24 mol/L) via central venous catheter only 4, 6
• Maximum infusion rate: 0.2 mmol H+/kg/hour 6
• Calculate dose: HCl (mEq) = 0.5 × body weight (kg) × (measured HCO3- - desired HCO3-) 4
• Requires continuous monitoring for hemolysis and tissue necrosis 6
• Reserved for patients with hepatic dysfunction who cannot use ammonium chloride 4

Ammonium Chloride (Alternative Acid Therapy)

• Contraindicated in hepatic or severe renal dysfunction as it requires hepatic conversion 4
• When liver function is intact, this is preferred over hydrochloric acid 4

Critical Monitoring Parameters

Throughout treatment, monitor 1:

• Serum electrolytes every 2-4 hours in severe cases (sodium, potassium, chloride, bicarbonate)
• Arterial blood gases to assess pH and bicarbonate response
• Volume status clinically
• Renal function before using potassium-sparing diuretics or acetazolamide

Common Pitfalls to Avoid

• Never use potassium citrate or other non-chloride potassium salts—these worsen alkalosis 1
• Do not give sodium bicarbonate—this is contraindicated and worsens alkalosis 1
• Avoid potassium-sparing diuretics with ACE inhibitors without close potassium monitoring 1
• Do not overlook Bartter syndrome in patients with unexplained alkalosis, especially with history of polyhydramnios and premature birth 1
• Do not use ammonium chloride in hepatic dysfunction—use hydrochloric acid or dialysis instead 4
• Never infuse hydrochloric acid peripherally—central venous access is mandatory 6

Treatment Algorithm Summary

1. Identify and stop precipitating cause (diuretics, NG suction) 1
2. Check urinary chloride to classify as responsive vs. resistant 1
3. For chloride-responsive: Give saline + aggressive KCl replacement 1, 4
4. If diuretics must continue: Add amiloride 2.5-5 mg daily 1
5. If inadequate response: Add acetazolamide 250-500 mg daily (if adequate renal function) 1
6. For refractory cases: Hemodialysis with high-chloride dialysate 1
7. For chloride-resistant: Sodium chloride supplementation + NSAIDs (consider Bartter/Gitelman) 1