What are the causes of metabolic alkalosis?

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Causes of Metabolic Alkalosis

Metabolic alkalosis is primarily caused by excessive hydrogen ion loss or bicarbonate gain, and is characterized by elevated plasma bicarbonate (>26 mmol/L) and blood pH (>7.43). 1 The causes can be categorized into four main groups based on their pathophysiological mechanisms.

Chloride Depletion Alkalosis

  • Gastrointestinal losses:
    • Vomiting or nasogastric suction (loss of gastric acid) 1, 2
    • Congenital chloridorrhea 2
  • Renal losses:
    • Diuretic therapy (especially loop and thiazide diuretics) 1, 3
    • Post-hypercapnic state 2
    • Severe chloride deficiency 4

Mineralocorticoid Excess Syndromes

  • Primary hyperaldosteronism 2, 5
  • Secondary hyperaldosteronism (renovascular hypertension, renin-secreting tumors) 2
  • Cushing syndrome 2
  • Bartter syndrome 2, 5
  • Gitelman syndrome 2, 5

Apparent Mineralocorticoid Excess Syndromes

  • Licorice ingestion (glycyrrhizic acid inhibits 11β-hydroxysteroid dehydrogenase) 2, 5
  • Congenital adrenal hyperplasia 5
  • Liddle syndrome 2

Exogenous Alkali Administration

  • Excessive oral or parenteral bicarbonate administration 2, 5
  • Administration of bicarbonate precursors (lactate, acetate, citrate) 5
  • Massive blood transfusions 2
  • Milk-alkali syndrome (excessive calcium carbonate intake) 2

Pathophysiological Mechanisms

Generation of Metabolic Alkalosis

  • Loss of hydrogen ions through the gastrointestinal tract or kidneys 1
  • Gain of bicarbonate through exogenous administration 5
  • Contraction alkalosis due to loss of chloride-rich, bicarbonate-poor fluid 2

Maintenance Factors

For metabolic alkalosis to persist, certain factors must impair the kidney's ability to excrete excess bicarbonate:

  • Volume depletion (reduces glomerular filtration rate) 1, 5
  • Chloride depletion (impairs bicarbonate excretion) 4
  • Hypokalemia (enhances bicarbonate reabsorption) 1, 5
  • Reduced GFR (decreases filtered bicarbonate load) 5
  • Hyperaldosteronism (increases hydrogen ion secretion) 2

Diagnostic Approach

  • Assess arterial blood gases showing elevated pH and bicarbonate 4
  • Evaluate compensatory increase in PaCO₂ 2
  • Determine volume status (supine and standing blood pressure) 4
  • Measure urinary chloride concentration:
    • Low urinary chloride (<10 mEq/L): chloride-responsive alkalosis 4
    • High urinary chloride (>20 mEq/L): chloride-resistant alkalosis 4
  • Assess renin-angiotensin-aldosterone axis 4
  • Check serum potassium and chloride levels 1

Treatment Principles

  • Address the underlying cause 3
  • Correct volume depletion with sodium chloride in chloride-responsive alkalosis 4
  • Replace potassium chloride in cases with hypokalemia 1
  • In severe cases, consider hydrochloric acid infusion (0.1 N HCl), though this carries risk of hemolysis 4
  • For emergency situations with severe alkalosis, dialysis with higher K⁺, Cl⁻, and low HCO₃⁻ bath may be appropriate 4
  • Carbonic anhydrase inhibitors may be used in selected cases 5

Clinical Impact

Severe metabolic alkalosis (arterial pH ≥7.55) is associated with significantly increased mortality in critically ill patients and can affect multiple organ systems including the central nervous system, myocardium, and skeletal muscle 2, 5.

References

Research

The patient with metabolic alkalosis.

Acta clinica Belgica, 2019

Research

Metabolic Alkalosis Pathogenesis, Diagnosis, and Treatment: Core Curriculum 2022.

American journal of kidney diseases : the official journal of the National Kidney Foundation, 2022

Research

Approach to metabolic alkalosis.

Emergency medicine clinics of North America, 2014

Research

Diagnosis and management of metabolic alkalosis.

Journal of the Indian Medical Association, 2006

Research

Metabolic alkalosis.

Journal of nephrology, 2006

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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