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Metabolic Acidosis: Causes, Diagnosis, and Emergency Treatment

Definition & Pathophysiology

Metabolic acidosis is a primary reduction in serum bicarbonate ([HCO₃⁻] <22 mEq/L) with compensatory respiratory alkalosis (pCO₂ ↓), resulting in pH <7.35. The bicarbonate buffer system (HCO₃⁻/H₂CO₃) is the primary extracellular buffer; kidneys regenerate HCO₃⁻ and excrete H⁺.

Major Etiologies (MUDPILES Mnemonic)

CategoryKey CausesMechanism
MethanolToxic alcohol ingestionFormic acid accumulation
UremiaAdvanced CKD/ESRDReduced H⁺ excretion, NH₄⁺ synthesis, HCO₃⁻ regeneration
DKA / DiarrheaDiabetic ketoacidosis; GI HCO₃⁻ lossKetoacids (β-OHB, AcAc); loss of alkaline stool
Paraldehyde / Propylene glycolRare; IV lorazepam vehicleOrganic acid accumulation
Iron / IsoniazidOverdoseLactic acidosis (mitochondrial toxin)
Lactic acidosisType A: Hypoperfusion (sepsis, shock, cardiac arrest); Type B: Mitochondrial dysfunction (metformin, NRTIs, thiamine def, malignancy)Anaerobic glycolysis → lactate; impaired clearance
Ethylene glycolAntifreeze ingestionGlycolic/oxalic acid
SalicylatesAspirin overdoseUncouples oxidative phosphorylation; mixed respiratory alkalosis + metabolic acidosis

RTA (Renal Tubular Acidosis): Type 1 (distal), Type 2 (proximal), Type 4 (hypoaldosteronism) — non-anion gap metabolic acidosis.

Clinical Presentation

  • Respiratory: Kussmaul respirations (deep, rapid) — compensatory hyperventilation
  • Neurologic: Confusion, lethargy, coma (severe)
  • Cardiovascular: Vasodilation, myocardial depression, arrhythmia risk (↓K⁺ in DKA; ↑K⁺ in renal)
  • GI: Nausea, vomiting, abdominal pain
  • Specific clues: Fruity breath (DKA), osmolar gap (toxic alcohols), anuria (uremia), metformin use (lactic)

Diagnostic Approach

  1. ABG/VBG: pH, pCO₂, HCO₃⁻
  2. Electrolytes → calculate Anion Gap (AG) = Na⁺ – (Cl⁻ + HCO₃⁻) (normal 8–12 mEq/L)
  3. High AG (>12): Additions (ketoacids, lactate, toxins) — MUDPILES
  4. Normal AG (hyperchloremic): Losses (diarrhea, RTA, ureterosigmoidostomy) or dilution
  5. Delta-delta: ΔAG/ΔHCO₃⁻ → identifies mixed disorders
  6. Lactate, ketones (β-OHB), toxicology, renal function, osmolar gap

Treatment Principles

  1. Treat the underlying cause (insulin/fluids for DKA, antibiotics/source control for sepsis, dialysis for uremia/toxins, stop metformin)
  2. IV Fluids: Isotonic crystalloid (NS/RL) for volume resuscitation; D5W + insulin for DKA
  3. Bicarbonate therapy: Controversial; generally reserved for pH <7.1 (or <7.2 with hemodynamic instability). Risks: paradoxical CSF acidosis, hypokalemia, volume overload, hypernatremia, left-shift O₂ curve. If given: 1–2 mmol/kg over 1–2 hrs; target pH >7.2.
  4. Electrolyte replacement: K⁺, Mg²⁺, PO₄³⁻ per protocol (especially DKA)
  5. Renal replacement therapy (CRRT/IHD): Refractory acidosis, volume overload, toxic alcohol, uremia

Metabolic acidosis is a medical emergency when severe. Rapid identification of etiology drives life-saving intervention.

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