What is contraction alkalosis?

Contraction Alkalosis: Pathophysiology and Management

Contraction alkalosis is a metabolic alkalosis that occurs when a reduction in extracellular fluid volume leads to increased bicarbonate concentration, characterized by elevated serum bicarbonate, decreased chloride, and increased arterial pH. 1

Pathophysiology

Contraction alkalosis develops through the following mechanisms:

• Volume contraction: When extracellular fluid volume decreases (due to diuretics, vomiting, etc.), there is a proportionally greater loss of water and sodium chloride than bicarbonate
• Chloride depletion: Low serum chloride (<98 mmol/L) is a hallmark finding 1
• Renal compensation: Volume depletion activates the renin-angiotensin-aldosterone system, which promotes:
  • Sodium reabsorption in exchange for potassium and hydrogen ions
  • Enhanced bicarbonate reabsorption in the proximal tubule
  • Impaired ability of the kidneys to excrete excess bicarbonate

Laboratory Findings

Characteristic laboratory findings include:

• Elevated serum bicarbonate (>26 mEq/L)
• Decreased serum chloride (<98 mmol/L)
• Decreased serum potassium (<3.5 mEq/L)
• Elevated arterial pH (>7.45)
• Low urinary chloride (<20 mEq/L) in volume depletion cases 1

Common Causes

• Diuretic therapy: Particularly thiazides and loop diuretics
• Vomiting or nasogastric suction: Loss of hydrochloric acid from the stomach
• Hypovolemia: From any cause leading to extracellular fluid contraction
• Medication interactions: As seen in the case of HCTZ and dicyclomine interaction 2

Clinical Presentation

Patients may present with:

• Symptoms of volume depletion (postural dizziness, confusion, weakness)
• Neuromuscular symptoms due to associated hypokalemia
• Respiratory compensation (hypoventilation)
• In severe cases: altered mental status, tetany, seizures

Management

Treatment should focus on addressing the underlying cause and correcting volume and electrolyte abnormalities:

1. Volume repletion:

   • Isotonic saline (0.9% NaCl) is first-line therapy to correct both volume depletion and chloride deficit 1
   • This promotes renal bicarbonate excretion and suppresses the renin-angiotensin-aldosterone system

2. Electrolyte correction:

   • Potassium chloride supplementation to correct hypokalemia (target 4.0-5.0 mEq/L) 1
   • Chloride replacement is crucial as it allows bicarbonate excretion

3. Addressing the underlying cause:

   • Discontinue or reduce offending diuretics
   • For diuretic-dependent patients, consider adding potassium-sparing diuretics like spironolactone 1

4. For severe or refractory cases:

   • Acetazolamide may be effective after correcting fluid and electrolyte abnormalities 3
   • In critically ill patients with kidney failure and severe alkalosis, consider low-bicarbonate dialysis 4

Special Considerations

• Avoid rapid correction of electrolytes to prevent complications
• Monitor serum electrolytes within 24 hours of initiating therapy 1
• Check magnesium levels, as hypomagnesemia can perpetuate hypokalemia 1
• Be cautious with potassium-sparing diuretics in patients with kidney dysfunction

Common Pitfalls

• Treating the alkalosis without addressing the underlying cause
• Using non-chloride potassium salts when hypochloremia is present
• Failing to recognize medication interactions that can precipitate contraction alkalosis
• Overlooking the need for ongoing monitoring of electrolytes during treatment

Contraction alkalosis is distinct from other forms of metabolic alkalosis in that it specifically results from a contracted extracellular fluid volume with proportionally greater retention of bicarbonate relative to water and chloride.