Overview
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Physiologic disturbance resulting from excess acid production, failure of organic acid excretion, or inappropriate bicarbonate loss causing increased serum acidity.
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A marker of an underlying disease process.
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Severe when, in the presence of resp compensation, serum [HCO 3 ] is ≤10 mmol/L or pH < 7.20.
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Acute metabolic acidosis is associated with increased morbidity and mortality.
Etiology
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Broadly differentiated by calculating the AG: AG = [Na + ] − ([Cl − ] + [HCO 3 − ]). The AG corresponds to the presence of unmeasured anions in serum. The presence or absence of an elevated AG helps to determine the underlying cause and direct appropriate therapy. Normal AG is 7 ± 4 mEq/L and decreases 2.5 mEq/L for every 1 g/dL decrease in serum albumin. Corrected AG can be calculated:
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Corrected AG = Calculated AG − {2.5 ∗ (4.0 − [albumin])}.
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High AG metabolic acidosis: Results from an accumulation of excess acid in the serum. Specific causes are due to production of lactate or ketones (diabetic, alcoholic, or starvation ketoacidosis), toxic ingestion (methanol, ethylene glycol, salicylates), uremia, or medication side effects (propofol infusion syndrome, lactic acidosis associated with metformin).
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Normal AG (hyperchloremic) metabolic acidosis: Associated with excess HCO 3 − loss from the kidney or GI tract, failure of the kidney to excrete H + , or rapid IV infusion of unbuffered solutions (e.g., normal saline).
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Delta gap (ΔΔ): Used to determine the presence of concomitant metabolic derangements and is calculated as ΔAG/Δ [HCO 3 − ], where ΔAG = (calculated AG − expected AG) and Δ [HCO 3 − ] = (24−[HCO 3 − ]). ΔΔ < 1 indicates AG metabolic acidosis and concurrent non-AG acidosis. ΔΔ > 2 indicates AG metabolic acidosis and concurrent metabolic alkalosis. ΔΔ = 1 to 2 indicates a pure AG metabolic acidosis.