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metabolic acidosis

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metabolic acidosis Merck Manual diagnosis anion gap treatment

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Metabolic acidosis

A primary acid-base disorder with a decreased serum bicarbonate (HCO₃⁻), causing acidemia (usually pH < 7.35). The lungs compensate by hyperventilating to lower PaCO₂, sometimes producing deep, rapid Kussmaul breathing.

Causes

Classify it by the anion gap (AG):
[ AG = Na^+ - (Cl^- + HCO_3^-) ]

1. High-anion-gap metabolic acidosis

Accumulation of unmeasured acids.
Common causes:
  • Lactic acidosis: shock, sepsis, hypoxemia, seizures, ischemia
  • Ketoacidosis: diabetic, alcoholic, starvation
  • Kidney failure / uremia
  • Toxins or drugs: methanol, ethylene glycol, salicylates, propylene glycol, sometimes metformin in susceptible patients

2. Normal-anion-gap metabolic acidosis

Also called hyperchloremic metabolic acidosis. Usually due to bicarbonate loss or impaired renal acid excretion.
Common causes:
  • Diarrhea or intestinal fistula
  • Renal tubular acidosis
  • Carbonic anhydrase inhibitors, such as acetazolamide
  • Large-volume chloride-rich IV fluid administration
  • Early chronic kidney disease
  • Urinary diversion
A bicarbonate fall with a reciprocal chloride rise characterizes this group. Frameworks for Internal Medicine, p. 435.

Interpretation on ABG/electrolytes

Typical pattern:
  • ↓ pH
  • ↓ HCO₃⁻
  • ↓ PaCO₂ from respiratory compensation
Assess compensation with Winter's formula:
[ Expected\ PaCO_2 = 1.5 \times HCO_3^- + 8 \pm 2 ]
  • Measured PaCO₂ higher than expected: concurrent respiratory acidosis
  • Measured PaCO₂ lower than expected: concurrent respiratory alkalosis
Frameworks for Internal Medicine, p. 434.
For high-gap acidosis, calculate a delta gap to identify an additional metabolic alkalosis or normal-gap acidosis.

Clinical features

Severity and cause determine symptoms:
  • Tachypnea or Kussmaul respirations
  • Nausea, vomiting, abdominal pain
  • Fatigue, confusion, drowsiness
  • Hypotension or shock in severe lactic acidosis
  • Arrhythmias and hyperkalemia risk, particularly with severe acidemia

Evaluation

  1. Confirm with venous/arterial blood gas and serum electrolytes.
  2. Calculate anion gap and correct it for low albumin when applicable.
  3. Check glucose and blood/urine ketones.
  4. Measure lactate.
  5. Assess renal function and potassium.
  6. Consider toxic alcohols or salicylate level if clinically plausible.
  7. In normal-gap acidosis, urine studies may help distinguish gastrointestinal bicarbonate loss from renal tubular acidosis.

Management principles

  • Treat the cause, not just the pH:
    • DKA: fluids, insulin, potassium management
    • Sepsis/shock: perfusion restoration, antimicrobials/source control as indicated
    • Diarrhea: volume/electrolyte replacement
    • Toxic alcohol: urgent antidotal therapy and often dialysis
    • Renal failure: consider dialysis when indicated
  • Bicarbonate is not routine in high-anion-gap acidosis because the underlying acid-generating process must be corrected. It is generally more appropriate when bicarbonate has been lost, such as diarrhea or some renal tubular acidoses. In very severe acidemia, clinicians may consider IV bicarbonate in selected circumstances while treating the cause.
Recent evidence should not be taken as support for automatic buffer use: a 2026 systematic review of bicarbonate/buffer therapy in acute metabolic acidosis found the evidence base remains context-dependent (PMID 41808275).
Urgent assessment is needed for severe breathlessness, altered consciousness, shock, suspected DKA, poisoning, or very low pH/bicarbonate.
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