Anion Gap Calculator

How to Use This Calculator

1. Enter serum sodium, chloride, and bicarbonate for standard AG.
2. AG with K+ tab: add potassium for the 4-ion formula.
3. Differential tab: add albumin to get albumin-corrected AG and cause-based differential.
4. Professional tier adds delta-delta ratio and Winter's formula expected PCO2.

Formula

Example

Frequently Asked Questions

• What is the anion gap? ▼
  The anion gap (AG) is a calculated value representing the difference between the measured serum cations (primarily sodium) and the measured serum anions (chloride and bicarbonate): AG = Na − (Cl + HCO3). The "gap" exists because electroneutrality must be maintained in plasma — all positive charges must equal all negative charges — but we only measure some of the relevant ions. The unmeasured anions that fill this gap include albumin (the most important), phosphate, sulfate, and organic acids. In a healthy person with normal albumin, the AG is approximately 6–12 mEq/L (without potassium) or 10–16 mEq/L (when potassium is included in the formula). Potassium is often omitted from the formula in US practice because it is small and relatively constant, simplifying the calculation. The anion gap is most clinically useful when evaluating metabolic acidosis. If a patient has a low bicarbonate (metabolic acidosis) but a normal AG, the acidosis is compensated by hyperchloremia — a non-anion gap metabolic acidosis (NAGMA). If the AG is elevated above 12 mEq/L, unmeasured anions have accumulated in the blood — a high anion gap metabolic acidosis (HAGMA) — pointing to a specific set of causes remembered by the mnemonic MUDPILES.
• What does an elevated anion gap indicate? ▼
  An elevated anion gap (AG >12 mEq/L in standard practice, or >20 mEq/L if corrected for albumin) indicates accumulation of unmeasured anions in the blood, which always represents a high anion gap metabolic acidosis (HAGMA) when accompanied by a low bicarbonate. The classic mnemonic MUDPILES organizes the causes: M — Methanol (formic acid accumulation); U — Uremia (phosphate, sulfate, organic acids retained in renal failure); D — Diabetic ketoacidosis (and other ketoacidoses: alcoholic ketoacidosis, starvation ketoacidosis, beta-hydroxybutyrate); P — Propylene glycol (lactic acidosis from vehicle in IV medications like lorazepam); I — Isoniazid or Iron (both can cause lactic acidosis); L — Lactic acidosis (the most common cause in hospital settings — sepsis, shock, hypoxemia, metformin, mesenteric ischemia); E — Ethylene glycol (glycolic and oxalic acid); S — Salicylates (aspirin overdose, complex mixed acid-base disorder). The most common causes in hospitalized patients are lactic acidosis, diabetic ketoacidosis, and uremia. A very high AG (>30 mEq/L) is almost always due to lactic acidosis, ketoacidosis, or a toxic ingestion. When the AG is elevated, always check for whether the degree of AG elevation matches the degree of bicarbonate fall using the delta-delta ratio.
• Why correct the anion gap for albumin? ▼
  Albumin is the principal unmeasured anion that maintains the normal anion gap. Each 1 g/dL decrease in serum albumin below 4.4 g/dL reduces the anion gap by approximately 2.5 mEq/L. This means that a critically ill patient with albumin of 2.0 g/dL (very common in the ICU) has a "pseudonormal" anion gap that is actually 6 mEq/L lower than it would be with normal albumin. If such a patient develops lactic acidosis or DKA that would normally raise the AG to 20 mEq/L, their measured AG might only be 14 mEq/L — appearing only mildly elevated and potentially underestimated. The albumin correction formula (Figge et al. 1998) is: Corrected AG = measured AG + 2.5 × (4.4 − albumin). Multiple studies have demonstrated that uncorrected AG fails to detect up to 50% of true HAGMA in ICU patients with hypoalbuminemia. In any patient with low albumin — which includes most critically ill, malnourished, cirrhotic, or nephrotic patients — the albumin-corrected AG should always be used. If only the corrected AG is consistently applied, the corrected AG calculator (a separate tool) provides this directly from raw labs. The take-home: in patients with low albumin, a "normal" measured AG may actually represent a significant unmeasured anion burden.
• What is MUDPILES and how does it guide the workup? ▼
  MUDPILES is a mnemonic listing the major causes of high anion gap metabolic acidosis (HAGMA): Methanol, Uremia, DKA (and other ketoacidoses), Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates. When an elevated AG is detected, the clinical approach should be systematic. First, calculate the albumin-corrected AG to confirm the elevation is genuine. Second, consider the most likely causes based on clinical context: is the patient a diabetic (DKA)? In shock or sepsis (lactic acidosis)? In renal failure (uremia)? Have a history of ingestion (toxic alcohols, salicylates)? Third, order targeted investigations: serum lactate (lactic acidosis — the most common cause), urine and serum ketones (DKA, AKA, starvation), serum BUN/creatinine (uremia), serum salicylate level, osmolal gap (elevated osmolal gap suggests toxic alcohol — methanol or ethylene glycol, since these small molecules contribute to osmolality but are unmeasured anions only after metabolism). Fourth, use the delta-delta ratio (delta AG / delta bicarbonate) to detect mixed acid-base disorders: a ratio <0.4 suggests a concurrent non-AG metabolic acidosis; >2 suggests a concurrent metabolic alkalosis. This prevents anchoring on a single diagnosis when multiple processes are present simultaneously.
• How does anion gap help differentiate types of metabolic acidosis? ▼
  Metabolic acidosis is defined by a low serum bicarbonate, but the anion gap divides it into two fundamentally different categories with distinct pathophysiology and treatment. High anion gap metabolic acidosis (HAGMA, AG >12) occurs when acid is added to the blood (or alkali is lost via the kidneys specifically with unmeasured anion accumulation). The body buffers the acid by consuming bicarbonate; the acid's conjugate base (lactate, ketone, formate, oxalate, etc.) remains in the blood as an unmeasured anion, raising the AG. The treatment is to address the underlying cause (fluids/insulin for DKA, antimicrobials for septic lactic acidosis, dialysis for toxic alcohols or uremia). Non-anion gap metabolic acidosis (NAGMA, AG normal with low bicarbonate) occurs when bicarbonate is lost directly without accumulation of an unmeasured anion. This is compensated by chloride retention (hyperchloremia), leaving the AG unchanged. Causes include diarrhea (bicarbonate lost in stool), renal tubular acidosis (RTA types 1, 2, 4 — inability to excrete acid or absorb bicarbonate), carbonic anhydrase inhibitors (acetazolamide), adrenal insufficiency, and urinary diversions. The mnemonic HARDUP covers NAGMA causes: Hyperchloremia/hyperalimentation, Addisons, RTA, Diarrhea, Ureteral diversion, Pancreatic fistula. The urine anion gap (UAG = urine Na + urine K − urine Cl) helps further differentiate: a negative UAG suggests diarrhea (appropriate renal response); a positive UAG suggests RTA (impaired renal acid excretion).

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