Metabolic alkalosis

Pathophysiology

• Chloride-Responsive
  • Condition that produces chloride loss also tends to reduce extracellular volume
    • Reduction in extracellular volume increases mineralocorticoid activity
      • Enhances Na reabsorption and K+/H+ secretion in renal tubule
        • K/H+ secretion -> HCO3 generation
          • Resulting urine is alkaline with little chloride
• Chloride-Resistant
  • Excess mineralocorticoid activity leads to same cascade as above
    • However, excess mineralocorticoid is not a/w hypovolemia so urine chloride is generally normal

DDX

1. Chloride-Responsive (urine Cl < 20 mEq/L)
   1. Loss of gastric secretions
      1. vomiting
      2. NG suction
      3. bulemia
   2. Loss of colonic secretions
      1. congenital chloridorrhea
      2. villous adenoma
   3. Thiazides/loop after D/C
   4. Post hypercapnia
   5. Cystic fibrosis
2. Chloride-resistant (urine Cl > 20 mEq/L)
   1. With HTN
      1. Primary hyperaldo
         1. adrenal adenoma
         2. bilateral adrenal
         3. hyperplasia
         4. adrenal carcinoma
      2. 11B-HSD2
         1. genetic, licorice
         2. chewing tobacco
         3. carbenoxolone
      3. CAH (11-Hydroxylase or 17-hydroxylase deficiency)
      4. Current diuretics + HTN
      5. Cushing syndrome
      6. Exogenous steroids
      7. Liddle syndrome
      8. Renovascular HTN
   2. Without HTN
      1. Bartter syndrome^
      2. Gitelman syndrome^
      3. Severe K+ depletion
      4. Current thiazides/loop
      5. Hypomagnesemia
3. Other causes
   1. Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
   2. Milk alkali syndrome
   3. Hypercalcemia
   4. Intravenous penicillin
   5. Refeeding alkalosis
   6. Massive blood transfusion

^ln children

Source

Emedicine, Tintinalli