What is the diagnostic approach for metabolic alkalosis?

Diagnosis of Metabolic Alkalosis

Metabolic alkalosis is diagnosed through arterial blood gas analysis showing pH >7.45 and elevated serum bicarbonate (HCO3-) >26 mmol/L, along with assessment of urinary chloride levels to determine the underlying cause and guide treatment. 1, 2

Laboratory Evaluation

Essential Tests

• Arterial blood gases: Confirms alkalemia (pH >7.45) with elevated HCO3- (>26 mmol/L)
• Serum electrolytes: Including sodium, potassium, chloride, and bicarbonate
• Calculated anion gap: To rule out mixed acid-base disorders
• Urinary chloride concentration: Critical for determining the cause
  • Low urinary chloride (<10 mEq/L): Suggests chloride-responsive alkalosis
  • High urinary chloride (>20 mEq/L): Suggests chloride-resistant alkalosis

Additional Tests Based on Clinical Suspicion

• Plasma renin and aldosterone levels
• Serum magnesium and calcium
• Urine electrolytes (potassium, sodium)
• Renal function tests (creatinine, BUN)

Classification of Metabolic Alkalosis

1. By Urinary Chloride Response

• Chloride-responsive (urinary Cl- <10 mEq/L)

  • Volume contraction (vomiting, nasogastric suction)
  • Diuretic use (after discontinuation)
  • Post-hypercapnic states

• Chloride-resistant (urinary Cl- >20 mEq/L)

  • Mineralocorticoid excess
  • Severe hypokalemia
  • Bartter's and Gitelman's syndromes
  • Current diuretic use

2. By Pathophysiologic Mechanism

Generation Phase

• Hydrogen ion loss

  • Gastrointestinal: Vomiting, nasogastric suction
  • Renal: Diuretic therapy, hypokalemia

• Bicarbonate gain

  • Exogenous alkali administration
  • Massive blood transfusions
  • Milk-alkali syndrome

Maintenance Phase

Factors that maintain the alkalosis:

• Volume contraction
• Chloride depletion
• Hypokalemia
• Decreased GFR
• Hyperaldosteronism

Clinical Assessment

History

• Recent vomiting or nasogastric suction
• Diuretic use
• Excessive alkali intake
• Hypertension (suggesting mineralocorticoid excess)

Physical Examination

• Assess volume status (skin turgor, mucous membranes, jugular venous pressure)
• Blood pressure (hypertension or hypotension)
• Signs of hypokalemia (muscle weakness, cardiac arrhythmias)
• Signs of hypocalcemia (tetany, Chvostek's sign, Trousseau's sign)

Clinical Manifestations

• Neuromuscular irritability
• Tetany
• Seizures
• Cardiac arrhythmias
• Respiratory depression (compensatory hypoventilation)

Diagnostic Algorithm

1. Confirm metabolic alkalosis: Arterial pH >7.45 and HCO3- >26 mmol/L
2. Calculate the expected compensatory response: PaCO2 = 0.7 × (HCO3- - 24) + 40 ± 5 mmHg
3. Measure urinary chloride:
   • If <10 mEq/L: Chloride-responsive alkalosis
   • If >20 mEq/L: Chloride-resistant alkalosis
4. Evaluate volume status:
   • Hypovolemic: Consider vomiting, nasogastric suction, diuretics
   • Euvolemic/hypervolemic: Consider mineralocorticoid excess, severe hypokalemia
5. Check serum potassium:
   • Hypokalemia often accompanies and perpetuates metabolic alkalosis
6. Measure plasma renin and aldosterone if mineralocorticoid excess is suspected

Common Pitfalls in Diagnosis

• Failure to recognize mixed acid-base disorders: Metabolic alkalosis can coexist with respiratory acidosis or metabolic acidosis
• Overlooking hypokalemia: Critical to assess as it both causes and maintains metabolic alkalosis
• Misinterpreting compensatory responses: Respiratory compensation (hypoventilation) is limited by hypoxemia
• Not measuring urinary chloride at the appropriate time: Should be measured before treatment is initiated
• Confusing contraction alkalosis with true metabolic alkalosis: Volume contraction can concentrate bicarbonate without true excess

By systematically evaluating arterial blood gases, serum electrolytes, and urinary chloride, clinicians can accurately diagnose metabolic alkalosis and identify its underlying cause, which is essential for appropriate treatment 3, 4.