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For further information, see CMDT Part 21-19: Metabolic Alkalosis

Key Features

Essentials of Diagnosis

  • High serum HCO3 with alkalemia (high pH)

  • Evaluate effective circulating volume by physical examination

  • Urinary chloride concentration differentiates saline-responsive alkalosis from saline-unresponsive alkalosis

General Considerations

  • Etiology can be classified into chloride responsive or chloride unresponsive (Table 21–15)

  • Chloride responsive (UCl < 20 mEq/L)

    • Involves the loss of chloride and extracellular volume

    • In vomiting and nasogastric suction, loss of acid (HCl) generates the alkalosis and volume contraction from Cl loss maintains the alkalosis

    • Distally acting diuretics that cause chloride loss, eg, loop and thiazide diuretics, are a common cause of metabolic alkalosis; UCl levels can be unreliable when diuretics have been used since they increase UCl excretion

  • Chloride unresponsive (UCl > 20 mEq/L)

    • Implies a volume-expanded state as from hyperaldosteronism with accompanying hypokalemia from the renal mineralocorticoid effect

Table 21–15.Metabolic alkalosis.
Etiology

  • Chloride responsive (UCl < 20 mEq/L)

    • Excessive body bicarbonate content

      • Renal alkalosis

        • Diuretic therapy

        • Poorly reabsorbable anion therapy (carbenicillin, penicillin, sulfate, phosphate)

        • Posthypercapnia

      • Gastrointestinal alkalosis

        • Loss of HCl from vomiting or nasogastric suction

        • Intestinal alkalosis: chloride diarrhea

        • NaHCO3 (baking soda)

        • Sodium citrate, lactate, gluconate, acetate

        • Transfusions

        • Antacids

    • Normal body bicarbonate content: Contraction alkalosis

  • Chloride unresponsive (UCl > 20 mEq/L)

    • Excessive body bicarbonate content

      • Renal alkalosis, normotensive

        • Bartter syndrome (renal salt wasting and secondary hyperaldosteronism)

        • Severe potassium depletion

        • Refeeding alkalosis

        • Hypercalcemia and hypoparathyroidism

      • Renal alkalosis, hypertensive

        • Endogenous mineralocorticoids (primary hyperaldosteronism, hyperreninism, adrenal enzyme deficiency: 11-β- and 17-α-hydroxylase, Liddle syndrome)

        • Exogenous alkali

        • Exogenous mineralocorticoids

        • Licorice

Clinical Findings

Symptoms and Signs

  • No characteristic symptoms or signs

  • However, hypopnea can be present in severe cases

  • Alkalemia decreases oxygen delivery by shifting the oxygen disassociation curve of hemoglobin

  • Concomitant hypokalemia may cause weakness and hyporeflexia

Diagnosis

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