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Metabolic alkalosis, the overlooked disorder!

We pay great attention to metabolic acidosis compared to metabolic alkalosis

Clinical relevance

  • The four clinical scenarios in which you will encounter metabolic alkalosis the most are:
    • Volume depletion, particularly, those due to vomiting or over-diuresis.
    • Volume overload, particularly, those who are being actively diuresed.
    • Chronic respiratory acidosis when CO2 is acutely reduced with BIPAP or mechanical ventilation (post hypercapnic alkalosis) if associated with with stimulant for HCO3 gain typically volume depletion.
    • Iatrogenic from bicarbonate therapy oral or IV.

 

Pathophysiology

  • For metabolic alkalosis to develop, two conditions must present:
    • HCO3 gain (direct & indirect).
    • Sustained HCO3 renal absorption (Direct & indirect).
  • Almost all of the filtered HCO3 is reabsorbed in the proximal tubule. This process is very effective to keep the HCO3 22-26, any HCO3 above this concentration will be expelled in the urine returning the HCO3 level to normal.
  • The following factors increase proximal tubule HCO3 reabsorption:
    • Decreased intravascular volume whether from Volume depletion or volume overload.
    • Severe hypokalemia
    • Hypercapnia

 

Diagnosis

  • Metabolic alkalosis is defined by a serum HCO3 > 26 in the abscess of a primary respiratory acidosis.

 

Treatment

  • Stop the HCO3 gain (Treat the underlying cause).
  • Excrete the excess HCO3.
  • Discontinue any HCO3 or HCO3 precursors (Acetate or lactate) treatment

 

Hypokalemia

  • Potassium must be repleted to correct metabolic alkalosis.
  • Use KCL not K-acetate or lactate (Acetate and lactate are metabolized to HCO3 in the liver).
  • Don’t forget to check Mg and replete if needed.

 

Volume depletion

  • Volume depletion: Resuscitation with 0.9 NS (Saline responsive).
  • Urine Cl < 10 (Unlike Na, Urine chloride isn’t affected by diuretics).

 

Volume overload

 

Diuretics

Acetazolamide: Strong HCO3 urinary loss, modest diuresis, exacerbate hypokalemia.

Spironolactone/Amiloride/Triamterene: Weak HCO3 urinary loss, weak diuresis, potassium-sparing.

 

Post hypercapnic

  • Acute reduction of CO2 in patients with chronic CO2 retention.
  • Most of these patients have volume depletion which sustains the elevated HCO3 and minimizes urinary excretion.
  • Resuscitation with 0.9 NS.
  • Replete K & Mg

 

Other causes of metabolic alkalosis

  • Renal failure: rarely leads to metabolic alkalosis rather than acidosis → dialysis.
  • Barter syndrome = loop diuretics → Potassium repletion and Amiloride.
  • Gittleman syndrome = Thiazides diuretics → Potassium repletion and Amiloride.
  • Cushing syndrome.
  • Liddle syndrome → Potassium repletion and Amiloride/triamterene.
  • Primary hyperaldosteronism.

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