Calculate serum anion gap and albumin-corrected anion gap. Differentiate metabolic acidosis causes with clinical interpretation.
The Anion Gap Calculator computes the difference between measured cations and anions in your blood, a critical tool for diagnosing the cause of metabolic acidosis. The anion gap helps differentiate between "gap" acidosis (diabetic ketoacidosis, lactic acidosis, toxic ingestions) and "non-gap" acidosis (diarrhea, renal tubular acidosis).
This calculator also provides the albumin-corrected anion gap, which accounts for the fact that hypoalbuminemia (common in hospitalized patients) can mask a true elevated anion gap. Each 1 g/dL decrease in albumin below 4.0 g/dL reduces the apparent anion gap by approximately 2.5 mEq/L.
Enter your basic metabolic panel values to compute both raw and corrected anion gaps with clinical interpretation. Whether you are a beginner or experienced professional, this free online tool provides instant, reliable results without manual computation. By automating the calculation, you save time and reduce the risk of costly errors in your planning and decision-making process. This tool handles all the complex arithmetic so you can focus on interpreting results and making informed decisions based on accurate data.
The anion gap is one of the most fundamental diagnostic tools in emergency medicine and critical care. It helps clinicians rapidly narrow the differential diagnosis of metabolic acidosis, guiding treatment decisions. The albumin correction prevents dangerous false negatives in hypoalbuminemic patients. Having a precise figure at your fingertips empowers better planning and more confident decisions.
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.
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.