Anion Gap Calculator
Calculate serum anion gap with albumin correction for acid-base disorders
Electrolyte Values
Results
Clinical Significance
Normal anion gap, typical healthy range
Medical Disclaimer: This calculator is for educational purposes only and should not replace professional medical advice. Anion gap calculation requires clinical context for proper interpretation. Always consult a physician for diagnosis and treatment. Results may be affected by lab variability, hypoalbuminemia, and other factors. Emergency evaluation is required for severely elevated anion gaps.
Understanding the Inputs
Formula and Scientific Basis
AG = Na⁺ - (Cl⁻ + HCO₃⁻)AG = (Na⁺ + K⁺) - (Cl⁻ + HCO₃⁻)Corrected AG = AG + 2.5 × (4 - Albumin)Example Calculation
Interpretation and Clinical Benchmarks
- Low AG (<3 mEq/L): Uncommon finding. Causes include hypoalbuminemia (most common—AG decreases 2.5 mEq/L per 1 g/dL albumin drop), multiple myeloma (paraproteinemia), lithium toxicity, hypercalcemia, hypomagnesemia, bromide toxicity (interferes with chloride assay), or lab error. Low AG itself is not dangerous but may indicate underlying pathology.
- Normal AG (10-14 mEq/L): Healthy acid-base balance. If metabolic acidosis exists with normal AG, consider normal anion gap acidosis (NAGMA) causes: diarrhea (most common—bicarbonate loss), renal tubular acidosis (RTA types 1, 2, 4), ureterosigmoidostomy, pancreatic fistula, rapid normal saline infusion. Use mnemonic HARDUPS: Hyperalimentation, Acetazolamide, RTA, Diarrhea, Ureterosigmoidostomy, Pancreatic fistula, Saline.
- Mild Elevation (15-20 mEq/L): Investigate cause. Common causes: early ketoacidosis (DKA, alcoholic, starvation), mild lactic acidosis (tissue hypoxia), renal insufficiency (uremia—decreased acid excretion), dehydration (concentration effect), fasting/starvation (ketone accumulation). Monitor closely and address underlying condition.
- Moderate Elevation (21-30 mEq/L): Urgent evaluation required. Primary causes: diabetic ketoacidosis (DKA—AG typically 20-30), lactic acidosis (shock, sepsis, hypoxia—lactate >4 mmol/L), uremia (end-stage renal disease—BUN >100), toxic ingestion (methanol, ethylene glycol, salicylates), alcoholic ketoacidosis. Requires hospitalization and targeted therapy.
- Severe Elevation (>30 mEq/L): Medical emergency requiring ICU-level care. Life-threatening causes: severe DKA (AG >35 possible), methanol poisoning (AG >40—causes optic nerve damage), ethylene glycol poisoning (antifreeze—causes renal failure), severe septic shock with lactic acidosis (lactate >10 mmol/L), advanced renal failure with uremia, massive rhabdomyolysis. Immediate intervention includes IV fluids, insulin (if DKA), dialysis (if toxin/uremia), vasopressors (if shock), fomepizole (if toxic alcohol), sodium bicarbonate (if pH <7.1).
Important Precautions
- Hypoalbuminemia: Falsely lowers AG by 2.5 mEq/L per 1 g/dL decrease. Always apply albumin correction in critically ill, malnourished, cirrhotic, or nephrotic patients.
- Paraproteinemia: Multiple myeloma produces cationic immunoglobulins that falsely lower AG. Confirm with serum protein electrophoresis (SPEP).
- Bromide toxicity: Bromide interferes with chloride assay, falsely elevating chloride and lowering AG. Suspect in psychiatric patients or seawater drowning.
- Lab variability: Different analyzers have different reference ranges (8-16 mEq/L range exists). Use your lab's specific normal range.
- Hyperlipidemia/hyperproteinemia: Pseudohyponatremia falsely lowers sodium, reducing AG. Corrected sodium: measured Na + [1.6 × (glucose - 100)/100].
- AG alone cannot diagnose specific cause—requires clinical context, arterial blood gas (ABG), lactate, ketones, renal function, toxicology screen
- Mixed acid-base disorders (e.g., DKA + vomiting) require delta ratio calculation to detect concurrent alkalosis
- Normal AG doesn't exclude acidosis—check pH and HCO₃⁻ for normal AG metabolic acidosis (NAGMA)
- AG may be normal early in toxin ingestion (methanol/ethylene glycol) before metabolism to toxic acids
- AG >30 mEq/L (critical elevation)
- Symptoms: altered mental status, Kussmaul respirations (deep rapid breathing), severe nausea/vomiting, abdominal pain
- Known diabetic with hyperglycemia (>250 mg/dL) and elevated AG
- Suspected toxic ingestion (methanol, ethylene glycol, aspirin)
- Severe dehydration, shock, or sepsis
Related Tools
Frequently Asked Questions
What is anion gap and why is it important?
The anion gap is the difference between measured cations (Na⁺, K⁺) and anions (Cl⁻, HCO₃⁻) in serum, representing unmeasured anions like albumin, phosphate, sulfate, and organic acids. It's crucial for diagnosing metabolic acidosis causes: high AG indicates accumulation of unmeasured anions (lactate, ketones, toxins, uremia), while normal AG with low HCO₃⁻ suggests bicarbonate loss (diarrhea) or renal acid retention (RTA). This distinction guides treatment—insulin for DKA, dialysis for uremia, fomepizole for toxic alcohols, or fluid repletion for diarrhea.
What is a normal anion gap range?
Normal anion gap is 10-14 mEq/L using the standard formula (Na⁺ - Cl⁻ - HCO₃⁻), or 12-16 mEq/L if potassium is included. Modern analyzers measuring chloride more accurately have lowered the normal range to 6-12 mEq/L at some labs. Always use your lab's specific reference range. Values below 3 mEq/L are abnormally low (hypoalbuminemia, paraproteinemia), 15-20 mEq/L are mildly elevated (early acidosis), 21-30 mEq/L are moderately elevated (DKA, lactic acidosis), and >30 mEq/L are critically elevated (life-threatening emergency).
Why is albumin correction necessary?
Albumin is a negatively charged protein contributing ~50% of unmeasured anions. When albumin is low (hypoalbuminemia—common in critically ill, cirrhotic, nephrotic, or malnourished patients), the uncorrected AG appears falsely normal even when high AG acidosis exists. Albumin correction adds 2.5 mEq/L for each 1 g/dL drop below 4 g/dL, revealing masked acidosis. For example, patient with AG 10 mEq/L and albumin 2.0 g/dL has corrected AG = 10 + 2.5 × (4-2) = 15 mEq/L, indicating mild acidosis that would have been missed without correction.
What causes high anion gap metabolic acidosis?
Use the MUDPILES mnemonic: Methanol (AG >40, optic neuritis, osmolar gap), Uremia (renal failure, BUN >100), Diabetic ketoacidosis (glucose >250, positive ketones, AG 20-30), Propylene glycol/Paraldehyde, Isoniazid/Iron toxicity, Lactic acidosis (shock, sepsis, hypoxia, lactate >4 mmol/L—most common ICU cause), Ethylene glycol (antifreeze, calcium oxalate crystals, renal failure), Salicylates (aspirin overdose, tinnitus, respiratory alkalosis + metabolic acidosis). Other causes: alcoholic ketoacidosis (chronic EtOH, starvation), starvation ketosis, rhabdomyolysis, 5-oxoproline (chronic acetaminophen use).
What is delta ratio and why does it matter?
Delta ratio = ΔAG / ΔHCO₃⁻ = (measured AG - 12) / (24 - measured HCO₃⁻). It detects mixed acid-base disorders that AG alone misses. Interpretation: <0.4 = hyperchloremic (normal AG) acidosis; 0.4-0.8 = mixed high AG + normal AG acidosis; 1.0-2.0 = pure high AG acidosis (classic DKA, lactic acidosis); >2.0 = high AG acidosis + concurrent metabolic alkalosis (e.g., DKA patient vomiting, or chronic respiratory acidosis with compensatory metabolic alkalosis). Example: DKA patient with AG 30, HCO₃⁻ 10 has delta ratio = (30-12)/(24-10) = 18/14 = 1.29, confirming pure high AG acidosis without mixed disorder.
When should I go to the emergency room for high anion gap?
Seek immediate ER evaluation if: (1) AG >30 mEq/L—critical elevation requiring ICU care; (2) Kussmaul respirations—deep, rapid breathing compensating for acidosis; (3) Altered mental status—confusion, lethargy, coma indicating severe acidosis or toxic ingestion; (4) Diabetic with glucose >250 mg/dL + fruity breath odor (DKA); (5) Suspected toxic ingestion—methanol (vision changes), ethylene glycol (flank pain, crystals in urine), aspirin (tinnitus); (6) Severe dehydration/shock with lactic acidosis. Delayed treatment of AG >30 can cause cardiac arrest (hyperkalemia), respiratory failure, cerebral edema, or multi-organ failure. Call 911 or go to nearest ER immediately.
References
- Emmett M, Narins RG. Clinical use of the anion gap. Medicine (Baltimore). 1977;56(1):38-54. Classic paper establishing anion gap's clinical utility.
- Figge J, Jabor A, Kazda A, Fencl V. Anion gap and hypoalbuminemia. Crit Care Med. 1998;26(11):1807-10. Study validating albumin correction formula (2.5 mEq/L per g/dL).
- Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol. 2007;2(1):162-74. Comprehensive review of AG interpretation and pitfalls.
- Rastegar A. Use of the deltaAG/deltaHCO3- ratio in the diagnosis of mixed acid-base disorders. J Am Soc Nephrol. 2007;18(9):2429-31. Delta ratio application for mixed disorders.
- Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N Engl J Med. 2014;371(15):1434-45. Modern acid-base assessment including AG and Stewart approach.