How to manage metabolic alkalosis in a child?

Management of Metabolic Alkalosis in Children

The management of metabolic alkalosis in children requires first determining the underlying etiology through urinary chloride measurement, then addressing the specific cause with targeted interventions including discontinuation of offending agents (especially diuretics), aggressive potassium chloride and sodium chloride supplementation, and consideration of acetazolamide or potassium-sparing diuretics in refractory cases. 1

Initial Diagnostic Assessment

The first critical step is measuring urinary chloride to classify the alkalosis type and guide treatment strategy 1:

• Urinary chloride <20 mEq/L indicates chloride-responsive (saline-responsive) alkalosis, typically from gastric losses, diuretic use, or volume depletion 1, 2
• Urinary chloride >20 mEq/L indicates chloride-resistant alkalosis, suggesting mineralocorticoid excess, Bartter syndrome, or Gitelman syndrome 1, 3

Additional essential laboratory evaluation includes 4:

• Serum electrolytes with particular attention to potassium, chloride, and magnesium 3
• Acid-base status (pH, bicarbonate, base excess) 4
• Assessment of volume status and hydration 4
• Blood urea nitrogen and hematocrit 4

Common pitfall: In euvolemic children with metabolic alkalosis and no obvious cause (no vomiting, nasogastric losses, or diuretic use), always consider Bartter or Gitelman syndrome, especially with hypokalemia and elevated urinary chloride despite no external losses 1, 3.

Management Based on Etiology

Diuretic-Induced Alkalosis

Discontinue or reduce diuretic doses if clinically feasible 1. This is the most direct intervention when diuretics are the culprit 4.

For patients requiring continued diuresis 1:

• Switch to longer-acting loop diuretics to reduce electrolyte fluctuations
• Add a potassium-sparing diuretic (amiloride 2.5-5 mg daily or spironolactone 25-100 mg daily) 1
• Consider acetazolamide in patients with adequate kidney function 1, 5

Electrolyte Replacement Therapy

Potassium chloride supplementation is absolutely essential when hypokalemia is present 1, 3:

• Use only potassium chloride (20-60 mEq/day), targeting serum potassium 4.5-5.0 mEq/L 1, 3
• Never use potassium citrate or potassium bicarbonate, as these worsen the metabolic alkalosis 1, 3
• The chloride component is critical for allowing renal bicarbonate excretion 6, 7

Sodium chloride supplementation addresses volume depletion and provides chloride for bicarbonate excretion 1, 3:

• In Bartter/Gitelman syndrome: 5-10 mmol/kg/day 1, 3
• In volume-depleted states: normal saline resuscitation 3

Magnesium replacement is critical as hypomagnesemia impairs both calcium homeostasis and potassium repletion 3.

Pharmacologic Interventions

Acetazolamide is useful in specific situations 1, 5:

• Dose: 500 mg IV as a single dose in children with adequate kidney function 1
• Mechanism: Carbonic anhydrase inhibition causes renal bicarbonate loss 5
• Particularly effective in heart failure patients with diuretic-induced alkalosis 1
• Contraindication: Avoid in patients with significant renal dysfunction 5

Potassium-sparing diuretics are first-line alternatives to acetazolamide 1:

• Amiloride 2.5 mg daily (can titrate to 5 mg daily) is most effective for metabolic alkalosis 1
• Spironolactone 25 mg daily (can titrate to 50-100 mg daily) 1
• These counter hypokalemia while improving the alkalosis 1
• Critical warning: Avoid combining with ACE inhibitors without close monitoring due to hyperkalemia risk 1

Special Condition: Bartter/Gitelman Syndrome

When Bartter or Gitelman syndrome is suspected (hypokalemic metabolic alkalosis, hypochloremia, elevated urinary chloride, normal blood pressure) 1, 3:

Diagnostic workup 3:

• Fractional excretion of chloride (>0.5% in Bartter despite volume depletion)
• Plasma renin and aldosterone (both markedly elevated)
• Urinary calcium (high in Bartter, low in Gitelman)
• Renal ultrasound for nephrocalcinosis
• Genetic testing (SLC12A1 for Bartter Type 1, KCNJ1 for Type 2)

Chronic management 1, 3:

• Sodium chloride supplementation 5-10 mmol/kg/day (cornerstone of therapy)
• Potassium chloride supplementation (not citrate or bicarbonate)
• NSAIDs (indomethacin or ibuprofen) to reduce prostaglandin-mediated salt wasting in symptomatic patients 1, 3
• Always combine NSAIDs with gastric acid inhibitors to prevent GI complications 1, 3
• Potassium-sparing diuretics can help maintain potassium but use cautiously as they may worsen volume depletion 3

Monitoring During Treatment

Daily monitoring initially 4:

• Serum electrolytes (sodium, potassium, chloride, bicarbonate)
• Body weight
• Fluid balance (urine output, urine specific gravity)
• Acid-base status

Adjust monitoring frequency based on clinical stability and response to therapy 4.

Refractory Cases

For severe, refractory metabolic alkalosis 1:

• Hemodialysis with low-bicarbonate/high-chloride dialysate is the treatment of choice, especially with concurrent renal failure
• Never use sodium bicarbonate or alkalinization strategies - these are contraindicated and worsen the alkalosis 1

Critical Pitfalls to Avoid

• Never correct severe metabolic alkalosis too rapidly - gradual correction over 48-72 hours prevents complications 4
• Avoid excessive chloride intake in preterm infants (>3.3 mmol/kg/day in first 3 days) as this can paradoxically cause metabolic acidosis 4
• Do not use loop diuretics unless hypervolemia, hyperkalemia, or renal acidosis are present, as they perpetuate the alkalosis 1
• Recognize that chronic metabolic alkalosis can inhibit central respiratory drive, particularly important when weaning from mechanical ventilation 4, 8
• In neonates on parenteral nutrition, ensure adequate potassium and phosphate supply parallel amino acid administration to avoid refeeding-like syndrome 4