Metabolic Acidosis

Metabolic Acidosis

 

Metabolic acidosis is heralded by a decreased concentration of plasma bicarbonate.

Etiology

  • Production of organic acid exceeds rates of elimination
    • Beta-hydroxybutyrate and acetoacetic acid production during diabetic acidosis
    • Lactic acid production during lactic acidosis
  • Reduced excretion of acids due to:
    • Renal failure
    • Renal tubular acidosis
  • Excessive loss of bicarbonate due to:
    • Renal losses or gastrointestinal losses (eg, diarrhea)

Classification

  • Type is based on anion gap calculation
  • Anion gap = [Na] – [Cl ]+ [HCO3-]
    • Na = sodium, Cl = chloride, HCO3 = bicarbonate
    • Normal = 7-16 mmol
  • High anion gap acidosis (organic acidosis)
    • Methanol poisoning
      • Osmolar gap –  high
      • Retained acid – formate
      • No crystals in urine
    • Ethylene glycol poisoning
      • Osmolar gap –  high
      • Retained acids – hippurate, glycolate, oxalate
      • Oxalate crystals in urine
    • Diabetes mellitus – ketoacidosis
      • Osmolar gap – normal
      • Retained acids – acetoacetate, beta-hydroxybutyrate
    • Ethanol poisoning
      • Osmolar gap – high
      • Renal failure
      • Retained acids – sulfuric, phosphoric, organic
    • Starvation
      • Retained acid – beta-hydroxybutyrate
    • Salicylate toxicity
      • Retained acids – salicylate, organic
    • Lactic acidosis
      • Retained acid – lactate
    • Paraldehyde toxicity
      • Pyruvate may be helpful in differentiating inborn errors and cardiac ischemia
  • Normal anion gap acidosis (inorganic acidosis)
    • Gastrointestinal fluid loss
      • Severe diarrhea – results from loss of Na, K (potassium), HCO3-
      • Pancreatitis – loss of HCO3- production
      • Intestinal fistula – loss of Na, K, HCO3-
    • Renal tubular acidosis (RTA)
      • Proximal (type II) RTA – loss of HCO3- due to decreased tubular secretion of H+
      • Distal (type I) RTA – decreased reabsorption of HCO3-
      • Type IV RTA – inhibited Na reabsorption with abnormal K+ and H+ retention; decreased renal ammonia formation with reduced elimination of H+
    • Drug-induced hyperkalemia
      • Potassium sparing diuretics
      • Angiotensin-converting enzymes (ACE) inhibitors
      • Cyclosporine
      • Trimethoprim

Diagnosis

  • Laboratory testing
    • Initial suspicion that acidosis exists from values found on a basic metabolic laboratory panel (sodium, potassium, chloride and bicarbonate)
      • Decreased bicarbonate level along with arterial blood gases which demonstrates acidosis
    • Based on clinical scenario and anion gap calculation, further testing may be appropriate
      • Glucose serum or plasma to rule out diabetes mellitus
      • BUN/creatinine to rule out renal failure
      • Lactate/pyruvate levels to rule out lactic acidosis
      • Ethanol levels to rule out alcohol poisoning
      • Microscopic examination of urine for crystals to differentiate methanol from ethylene glycol
        • Methanol and ethylene glycol serum levels may also be necessary
      • Salicylate levels to rule out salicylate poisoning
      • Serum osmolality to calculate osmolar gap
      • Anion gap may also be elevated by toxicants such as iron, toluene, phenformin, paraldehyde and arsenic

See Also