Metabolic alkalosis

Background

Metabolic alkalosis generally occurs as a primary increase in serum bicarbonate (HCO3-) concentration, which can occur due to loss of H+ from the body or a gain in HCO3-.

Main Causes

  • Hydrogen ion loss (via vomiting)
  • Shift of hydrogen ions intracellularly (from hypokalemia)
  • Bicarbonate administration
  • Contraction alkalosis (Diuretic administration, diarrhea, or any excessive loss of volume)

Clinical Features

Symptoms are nonspecific and usually result from the concomitant hypokalemia or hypocalcemia. Common signs and symptoms include

  • Weakness/Fatigue
  • Vomiting or diarrhea
  • Hypoventilation

Differential Diagnosis

Chloride-Responsive

Urine Cl < 20 mEq/L

  1. Loss of gastric secretions;
  2. Loss of colonic secretions
    • Diarrhea
    • Congenital chloridorrhea
    • Villous adenoma
  3. Thiazides/loop diuretics
  4. Cystic fibrosis

Chloride-resistant

Urine Cl > 20 mEq/L

  • Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
    • Potassium acetate
  • Milk alkali syndrome
  • Hypercalcemia (inability to concentrate urine leads to hypovolemia)
  • Intravenous penicillin
  • Refeeding alkalosis
  • Massive blood transfusion
  • Primary hyperaldosteronism
  • CAH (11-Hydroxylase or 17-hydroxylase deficiency)
  • Cushing syndrome
  • Exogenous steroids
  • Liddle syndrome
  • Renovascular hypertension
  • Bartter syndrome (pediatrics)
  • Gitelman syndrome (pediatrics)
  • Severe K+ depletion
  • Hypomagnesemia

Evaluation

  • pH > 7.42 = alkalemia
  • HCO3 > 28 = metabolic alkalosis
  • Always determine if there is also a concurrent primary respiratory process
    • expected pCO2 = 40 + 0.6(measured HCO3 - 24)
    • if pCO2>pCO2 expected, then there is also a primary respiratory acidosis
    • if pCO2<pCO2 expected, then there is also primary respiratory alkalosis
  • Always calculate AG to determine if concurrent primary metabolic acidosis

Management

  1. Correct volume depletion
    • Normal saline
      • Repletion of extracellular volume decreased need for Na reaborption
      • Delivery of Cl to distal tubule increases Cl/bicarb exchange
  2. Correct potassium depletion
    • Giving K+ leads to movement of H+ out of cells → acidosis
    • Giving K+ stops hypokalemia-induced distal H+/K+ pump
  3. Correct chloride depletion
    • Must give a reabsorbable anion to replace HCO3
  4. Correct mineralocorticoid excess
  • Note: if patient is edematous (CHF, cirrhosis), do NOT give normal saline
    • If patient is hypokalemic, KCl will correct both hypoK AND alkalosis

See Also

References

    This article is issued from Wikem. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.