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Key Features

Essentials of Diagnosis

  • High serum HCO3 (> 32 mEq/L or > 32 mmol/L) with alkalemia (arterial pH > 4.45)

  • 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 saline responsive or saline unresponsive (Table 21–15)

  • Saline responsive

    • By far the more common disorder

    • Characterized by normotensive extracellular volume contraction

    • Less frequently, hypotension or orthostatic hypotension are seen

    • Generally associated with hypokalemia, due partly to the direct effect of alkalosis on renal potassium excretion and partly to secondary hyperaldosteronism from volume contraction

  • Saline unresponsive

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

Table 21–15.Metabolic alkalosis.
Etiology

  • Saline responsive (UCl < 25 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

  • Saline unresponsive (UCl > 40 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- and 17-hydroxylase, Liddle syndrome)

      • Exogenous alkali

      • Exogenous mineralocorticoids

      • Licorice

Clinical Findings

Symptoms and Signs

  • No characteristic symptoms or signs

  • Hypotension and orthostasis may occur

  • Weakness and hyporeflexia occur if serum K+ is markedly low

  • Tetany and neuromuscular irritability occur rarely

Diagnosis

Laboratory Tests

  • High serum HCO3 (> 32 mEq/L or > 32 mmol/L) with alkalemia (arterial pH > 4.45)

  • Arterial PCO2 is increased (> 48 mm Hg)

  • Serum potassium and chloride are decreased

  • There may be an increased anion gap

  • The spot urinary chloride can differentiate between a saline-response (< 25="" meq/l)="" and="" unresponsive="" (=""> 40 mEq/L) cause

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