Metabolic Acidosis

Diagnosis

Indications for Testing

• Patient with altered mental status
• Patient with initial laboratory results that indicate the presence of acidosis

Laboratory Testing

• Metabolic panel (Na, K, Cl, HCO3-) and arterial blood gases
  • Expect decreased bicarbonate level on both tests, along with acidosis on arterial blood gases
  • Calculate anion and osmolar gaps to further aid in differential
    • Anion gap = [Na] - ([Cl] + [HCO3-])
      • Normal = 7-16 mmol/L
    • Osmolar gap = calculated plasma osmolality - measured plasma osmolality (2[Na+] + [glucose]/18 + [blood urea nitrogen (BUN)]/2.8)
      • Normal = -10 to +10 mOsm/kg
• Based on clinical scenario and anion gap calculation, further testing may be appropriate
  • Glucose – evaluate for diabetes mellitus (DM)
  • BUN/creatinine – evaluate for renal failure
  • Lactate/pyruvate levels – evaluate for lactic acidosis
  • Beta-hydroxybutyrate acid – evaluate for DM, starvation
  • Ethanol levels – evaluate 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 – evaluate for salicylate poisoning
  • Anion gap may also be elevated by toxicants such as acetaminophen, iron, toluene, phenformin, paraldehyde, arsenic
  • Other testing (serum drug levels) based on results of above testing

Differential Diagnosis

Refer to the different types of metabolic acidosis in Background

Background

Classification

• Type of metabolic acidosis is based on anion/osmolar gap calculation
  • Anion gap = [Na] - ([Cl ] + [HCO₃^-])
  • Osmolar gap = calculated plasma osmolality - measured plasma osmolality (2[Na⁺] + [glucose]/18 + [BUN]/2.8)
  • Osmolar gap may be used to differentiate between different types within high anion gap acidosis

Normal anion gap acidosis (inorganic acidosis)

• Gastrointestinal fluid loss
  • Severe diarrhea – results from loss of Na, K, HCO₃^-
  • Pancreatitis – loss of HCO₃^- production
  • Intestinal fistula – loss of Na, K, HCO₃^-
• Drug-induced hyperkalemia
  • Potassium-sparing diuretics
  • Angiotensin-converting enzyme (ACE) inhibitors
  • Cyclosporine
  • Trimethoprim
• 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⁺

Low or negative anion gap (hyperchloremia)

• Lithium toxicity
• Monoclonal IgG gammopathy
• Iodide or bromide intoxication – causes pseudohyperchloremia
• Disorders of high calcium or magnesium levels

Pathophysiology

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