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 non specific 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;
   • Vomiting
   • NG suction
   • Bulemia
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)
• 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
   • Aldostorone antagonists if indicated (i.e. spironolactone)

• 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

• Acid-base disorders

References

Authors

Jordan Swartz, Ross Donaldson, Daniel Ostermayer, Genevieve Hasek, Neil Young, Jonathan Osgood, Michael Holtz