Identifying Contraction Alkalosis: Distinguishing Features from Other Types of Alkalosis
Contraction alkalosis is characterized by decreased extracellular fluid volume, elevated serum bicarbonate concentration, hypochloremia, and hypokalemia, typically occurring due to volume contraction. 1
Key Laboratory Findings in Contraction Alkalosis
- 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) - critical distinguishing feature
- Normal anion gap
Clinical Features of Contraction Alkalosis
- Signs of volume depletion:
- Postural pulse change ≥30 beats per minute
- Severe postural dizziness
- Confusion
- Non-fluent speech
- Extremity weakness
- Dry mucous membranes
- Dry tongue
- Furrowed tongue
- Sunken eyes (especially in older adults) 1
Distinguishing Contraction Alkalosis from Other Types of Alkalosis
1. Pathophysiological Mechanism
Contraction alkalosis occurs when extracellular fluid volume decreases while the absolute amount of bicarbonate remains relatively unchanged, leading to increased bicarbonate concentration. This is fundamentally different from other forms of metabolic alkalosis where bicarbonate is actively generated or retained. 1, 2
2. Urinary Chloride Levels
- Contraction alkalosis: Urinary chloride is typically low (<20 mEq/L) due to avid chloride reabsorption in response to volume depletion 1
- Diuretic-induced alkalosis: Urinary chloride is elevated during active diuretic use
- Vomiting-induced alkalosis: Initially high urinary chloride that decreases as volume depletion progresses 2
3. Volume Status
- Contraction alkalosis: Always presents with clinical evidence of volume depletion
- Other forms of alkalosis: May or may not have volume depletion 1, 2
4. Response to Treatment
- Contraction alkalosis: Responds primarily to volume repletion with isotonic saline (0.9% NaCl)
- Other forms: May require specific treatments addressing the underlying cause (e.g., stopping diuretics, correcting hypokalemia, treating hyperaldosteronism) 1, 2
5. Maintenance Factors
Contraction alkalosis is maintained primarily by:
- Volume depletion
- Chloride depletion
- Secondary hyperaldosteronism due to volume contraction
While other forms may be maintained by:
- Primary hyperaldosteronism
- Ongoing hydrogen ion losses (vomiting, nasogastric suction)
- Exogenous alkali administration 2
Diagnostic Algorithm for Contraction Alkalosis
- Confirm metabolic alkalosis: pH >7.45, HCO3- >26 mmol/L
- Assess volume status: Look for clinical signs of volume depletion
- Measure urinary chloride:
- If <20 mEq/L with volume depletion → contraction alkalosis
- If >20 mEq/L → consider other causes (diuretics, vomiting, Bartter syndrome)
- Check plasma renin and aldosterone:
- Contraction alkalosis: Both elevated (secondary hyperaldosteronism)
- Primary hyperaldosteronism: High aldosterone, low renin 2
Treatment Approach
For contraction alkalosis:
- Administer isotonic saline (0.9% NaCl) to correct volume depletion and chloride deficit
- Provide potassium chloride supplementation to correct hypokalemia
- Target potassium level of 4.0-5.0 mEq/L
- Monitor serum electrolytes within 24 hours of initiating therapy 1
Common Pitfalls to Avoid
- Using non-chloride containing solutions for volume repletion (will not correct the chloride deficit)
- Using potassium-sparing diuretics, which can worsen volume depletion
- Using thiazide diuretics, which may lead to life-threatening hypovolemia
- Using non-chloride potassium salts when hypochloremia is present 1
By understanding these distinguishing features, clinicians can accurately identify contraction alkalosis and differentiate it from other forms of metabolic alkalosis, leading to appropriate treatment strategies.