Calculate serum anion gap and albumin-corrected anion gap. Differentiate metabolic acidosis causes with clinical interpretation.
The Anion Gap Calculator computes the standard serum anion gap from sodium, chloride, and bicarbonate, then optionally shows the albumin-corrected anion gap. That helps separate elevated-gap metabolic acidosis from hyperchloremic, non-gap patterns and keeps low albumin from masking a clinically important gap.
In practice, the raw gap is most useful when bicarbonate is low or acid-base status is otherwise unclear. The corrected gap matters because each 1 g/dL fall in albumin below 4.0 g/dL lowers the expected baseline gap by about 2.5 mEq/L. This page keeps the raw gap, corrected gap, and delta-delta view together so the calculation can be checked quickly against the broader clinical picture.
The anion gap is a fast bedside way to frame metabolic acidosis. A widened gap points toward causes such as lactic acidosis, ketoacidosis, renal failure, or toxin exposure, while a normal-gap acidosis pushes the differential toward gastrointestinal bicarbonate loss, renal tubular acidosis, or saline-heavy resuscitation. Adding the albumin correction makes the number more dependable in hospitalized patients, where hypoalbuminemia is common.
Anion Gap = Na⁺ − (Cl⁻ + HCO₃⁻) Albumin-Corrected Anion Gap: Corrected AG = AG + 2.5 × (4.0 − measured albumin) Normal Ranges: • Anion Gap: 8–12 mEq/L (some labs 3–11) • Corrected AG: same reference range Classification: • Normal: 8–12 mEq/L • Elevated: > 12 mEq/L (suggests gap acidosis) • Low: < 8 mEq/L (consider lab error, hypoalbuminemia, or paraprotein)
Result: AG = 18 mEq/L, Corrected AG = 20.5 mEq/L — Elevated (Gap Acidosis)
AG = 140 − (104 + 18) = 18 mEq/L. This is elevated (normal 8–12). With albumin 3.0, the corrected AG = 18 + 2.5 × (4.0 − 3.0) = 20.5 mEq/L, confirming an even greater true gap. Common causes include diabetic ketoacidosis, lactic acidosis, uremia, and toxic ingestions.
The anion gap is one of the first calculations performed when evaluating a patient with altered mental status, shortness of breath, or suspected poisoning. An elevated anion gap immediately narrows the differential: is it a toxic ingestion (methanol, ethylene glycol), diabetic ketoacidosis, lactic acidosis from sepsis or shock, or renal failure? This simple calculation can be life-saving when time is critical.
The delta ratio (ΔAG/ΔHCO₃) is a powerful extension of the anion gap. In a pure anion-gap acidosis, every acid molecule that enters the blood replaces one bicarbonate, so the ratio is approximately 1:1. If the ratio exceeds 2, the bicarbonate is higher than expected, suggesting a coexisting metabolic alkalosis (e.g., DKA patient who is also vomiting). If below 1, bicarbonate is lower than expected, suggesting a concurrent non-gap acidosis.
The anion gap has limitations: it varies with laboratory assays, reference ranges differ between institutions, and it can be affected by pH-dependent changes in albumin charge. Stewart's strong ion approach offers a more physicochemical framework for acid-base analysis but is more complex. For bedside clinical use, the albumin-corrected anion gap remains the practical standard.
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This page reports the standard serum anion gap as sodium minus the sum of chloride and bicarbonate. When albumin is entered, it also shows an albumin-corrected gap using the conventional bedside adjustment of adding 2.5 mEq/L for every 1 g/dL that albumin falls below 4.0. If the gap is elevated, the page also calculates a simple delta-delta ratio to help flag a possible mixed acid-base disorder.
The output is intended as an acid-base screening aid rather than a diagnosis by itself. Reference ranges vary somewhat by laboratory and by whether potassium is included in the institutional formula, so the result still has to be interpreted with the measured bicarbonate, pH, lactate or ketones, renal function, and the broader clinical picture.
The anion gap represents unmeasured anions in the blood (proteins, phosphate, sulfate, organic acids). In a normal state, unmeasured anions minus unmeasured cations equals about 8–12 mEq/L. When acid accumulates (e.g., lactic acid, ketoacids), bicarbonate drops and unmeasured anions rise, widening the gap.
The classic mnemonic is MUDPILES: Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, and Salicylates. D-lactic acidosis and pyroglutamic acid are increasingly recognized causes. The most common causes in practice are lactic acidosis and DKA.
When the anion gap is normal but bicarbonate is low, it's called a non-gap (or hyperchloremic) metabolic acidosis. Causes include diarrhea (GI bicarbonate loss), renal tubular acidosis, carbonic anhydrase inhibitors, and ureteral diversions. The chloride rises to replace the lost bicarbonate.
Albumin is a negatively charged protein that accounts for most of the "unmeasured anions" in the normal anion gap. When albumin is low (common in illness, liver disease, malnutrition), the baseline anion gap drops. Without correction, a patient with hypoalbuminemia could have a falsely normal AG despite an underlying gap acidosis.
The delta-delta compares the change in anion gap (ΔAG = AG − 12) to the change in bicarbonate (ΔHCO₃ = 24 − measured HCO₃). A ratio near 1.0 suggests a pure gap acidosis. Greater than 2 suggests a concurrent metabolic alkalosis. Less than 1 suggests a concurrent non-gap acidosis.
Some institutions use the formula AG = (Na + K) − (Cl + HCO₃), which gives a normal range of 10–20. However, most modern references and board exams use the simplified formula without potassium (normal 8–12). Check which formula your institution prefers.