Combined Electrolyte Panel Pathway

Na · K · Mg · Ca · PO₄: Triage, Sequencing & Interplay · v1.2

How to use this tool: Sodium, potassium, magnesium, calcium and phosphate commonly derange together, in diuretic use, DKA, refeeding, tumour lysis and CKD. Enter at least one value, and more for a fuller reading. The tool interprets the panel as a whole, recognises combined patterns, flags the interactions and returns a sequenced correction plan.

1. The Electrolytes

Sodium (mEq/L)

Potassium (mEq/L)

Magnesium (mg/dL)

Total Calcium (mg/dL)

Albumin (g/dL, for Ca correction)

Phosphate (mg/dL)

2. Sodium Kinetics (for glucose correction & Adrogué-Madias)

Blood Glucose (mg/dL)

Weight (kg)

Sex (for TBW)

3. Shared Clinical Context ECG Findings (select all that apply) Peaked T / widened QRS / sine wave Hyperkalaemic changes U waves / ST depression / flat T Hypokalaemic / hypomagnesaemic changes QTc prolongation Hypocalcaemic change Active arrhythmia (VT / VF / Torsades de Pointes)

Symptom Severity

Volume Status (sodium pathway)

Renal Function

4. Common Shared Causes & Modifiers

Loop / Thiazide Diuretics Classic cause of combined Na, K, and Mg depletion.

DKA / Insulin Infusion Running K, Mg, and phosphate depleted; insulin shifts all three intracellularly. Pseudohyponatraemia from hyperglycaemia.

Refeeding / Alcoholism / Malnutrition The K-Mg-PO₄ depletion triad. Also raises ODS risk for sodium. Give thiamine before glucose.

Tumour Lysis Syndrome / Rhabdomyolysis Massive cellular release: high K, high PO₄, low Ca, AKI. Oncologic emergency.

Digoxin Therapy Low K and low Mg potentiate toxicity; IV calcium and high Ca are also unsafe with digoxin.

Why Correct in Sequence? The Core Principle

When multiple electrolytes are deranged, the order of correction determines success:

Immediate cardiac/neurological threats first. Severe hyperkalaemia with ECG changes (calcium), Torsades (magnesium), severe symptomatic hyponatraemia (hypertonic saline), and symptomatic hypocalcaemia (IV calcium) override metabolic sequencing.
Magnesium comes first. Both hypokalaemia and hypocalcaemia are refractory until magnesium is replaced.
Then potassium (with magnesium alongside), then calcium (caution if phosphate high), then phosphate, then sodium (potassium replacement itself raises sodium).

Sodium Correction Factor for Hyperglycaemia

This tool uses the Katz/Hillier hybrid: corrected Na = measured Na + 1.6 × ((glucose − 100)/100) for glucose up to 400 mg/dL, then 2.4 per 100 mg/dL for the increment above 400. Applying the higher 2.4 factor to the entire glucose elevation (a common coding error) overestimates corrected sodium in severe HHS and can lead to inappropriate withholding of free water. The relationship is non-linear and steeper at very high glucose, which the hybrid captures.

Note: there is no single universally-mandated factor - the classic Katz value is 1.6, Hillier (1999) argued 2.4 fits better across the range, and the piecewise hybrid used here is a pragmatic middle ground.

The Ca × PO₄ Product Uses TOTAL (Measured) Calcium

The calcium-phosphate solubility product and its > 55 mg²/dL² threshold (KDOQI) are calibrated to total (measured) calcium × phosphate - not albumin-corrected calcium. Using corrected calcium would falsely inflate the product in hypoalbuminaemic patients and could wrongly block necessary calcium replacement. This tool therefore grades hypo/hypercalcaemia severity on corrected calcium (correct for grading) but computes the Ca×PO₄ product on measured calcium (correct for the product).

The DKA Potassium Rule (fires independent of K entry)

Total body potassium is depleted in every DKA patient, even when serum K looks normal or high. Insulin drives K intracellularly and can precipitate fatal hypokalaemia. Do not start insulin until K is known and confirmed above 3.3 mEq/L. This tool surfaces the DKA potassium rule whenever DKA is flagged, whether or not a potassium value has been entered.

The Magnesium Gate & The Potassium Effect

Magnesium gate: low Mg drives renal K wasting (ROMK) and impairs PTH, so both hypokalaemia and hypocalcaemia are refractory until Mg is replaced. Potassium effect: replacing K raises serum Na (~1 mEq Na per mEq KCl); in a hyponatraemic patient this can overshoot the safe sodium limit and cause osmotic demyelination - count K replacement against the 24h sodium budget.

Recognisable Combined Patterns

Pattern	Signature	Key Action
Refeeding Syndrome	K↓ Mg↓ PO₄↓	Replace all three. Thiamine before glucose. Slow Na correction (high ODS risk).
Tumour Lysis Syndrome	K↑ PO₄↑ Ca↓ (+ high urate, AKI)	Hydration, rasburicase. Treat hyperK. Don't give calcium for asymptomatic hypocalcaemia.
CKD Mineral-Bone Disease	Ca↓ PO₄↑	Phosphate binders, calcitriol. Correct phosphate before calcium.
Diuretic Depletion	Na↓ K↓ Mg↓	Hold diuretic. Mg first, then K. Volume restore for Na.
DKA	Total body K, Mg, PO₄ depleted; pseudo-hypoNa	No insulin if K < 3.3. Replace K/Mg/PO₄. Correct glucose - Na follows.
Renal Retention	K↑ Mg↑ PO₄↑ (oliguric)	Membrane stabilisation if hyperK with ECG changes. Dialysis is definitive.

Adrogué-Madias Equation (replaces deficit-replacement)

ΔNa per 1 L infusate = (Infusate Na − Serum Na) / (Total Body Water + 1). This estimates how much 1 litre of a given fluid will move the serum sodium, and is preferred over closed-system "deficit" formulas (which ignore renal free water clearance and routinely cause ODS). This panel shows the ΔNa figure as a quick reference when sodium is low and weight is entered; for the full tier-gated infusion schedule, monitoring timeline, and overcorrection-rescue protocol, open the dedicated Acute Hyponatraemia Protocol.

Reference Ranges & Severity Bands

Electrolyte	Normal	Low (severe)	High (severe)
Sodium	135 - 145 mEq/L	< 120 (severe), < 110 (critical)	> 160 mEq/L
Potassium	3.5 - 5.0 mEq/L	< 2.5 mEq/L	≥ 6.5 mEq/L
Magnesium	1.8 - 2.4 mg/dL	< 1.0 mg/dL	> 7.0 mg/dL
Calcium (corrected)	8.5 - 10.5 mg/dL	< 6.0 mg/dL	> 14 mg/dL
Phosphate	2.5 - 4.5 mg/dL	< 1.0 mg/dL	> 7.0 mg/dL

Corrected Ca = measured Ca + 0.8 × (4.0 − albumin), used for severity grading. Mg: 1.8 to 2.4 mg/dL ≈ 0.75 to 1.0 mmol/L (divide mg/dL by 2.43). Phosphate: divide mg/dL by 3.1 for mmol/L.

Abbreviations: ACLS (Advanced Cardiac Life Support) · AKI (Acute Kidney Injury) · BD (Twice Daily) · Ca (Calcium) · CKD (Chronic Kidney Disease) · CKD-MBD (CKD Mineral-Bone Disease) · CPS (Calcium Polystyrene Sulphonate) · D5W (5% Dextrose in Water) · DKA (Diabetic Ketoacidosis) · ECG (Electrocardiogram) · eGFR (Estimated Glomerular Filtration Rate) · ESRD (End-Stage Renal Disease) · HF (Heart Failure) · HHS (Hyperosmolar Hyperglycaemic State) · IV (Intravenous) · K⁺ (Potassium) · KCl (Potassium Chloride) · KDOQI (Kidney Disease Outcomes Quality Initiative) · Mg (Magnesium) · MgSO₄ (Magnesium Sulphate) · Na⁺ (Sodium) · NaCl (Sodium Chloride) · NG (Nasogastric) · NPO (Nil Per Os) · NS (Normal Saline) · ODS (Osmotic Demyelination Syndrome) · PO₄ (Phosphate) · PTH (Parathyroid Hormone) · QTc (Corrected QT Interval) · ROMK (Renal Outer Medullary Potassium channel) · SBAR (Situation, Background, Assessment, Recommendation) · SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion) · SZC (Sodium Zirconium Cyclosilicate) · TBW (Total Body Water) · TdP (Torsades de Pointes) · TDS (Three Times Daily) · TLS (Tumour Lysis Syndrome) · VF (Ventricular Fibrillation) · VT (Ventricular Tachycardia)

Algorithm References & Evidence Base

Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: evaluating the correction factor for hyperglycemia. Am J Med. 1999;106(4):399-403.
Katz MA. Hyperglycemia-induced hyponatremia. N Engl J Med. 1973;289(16):843-844.
Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342(21):1581-1589.
Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol. 2007;18(10):2649-2652.
Mehanna HM, Moledina J, Travis J. Refeeding syndrome. BMJ. 2008;336(7659):1495-1498.
Howard SC, Jones DP, Pui CH. The tumor lysis syndrome. N Engl J Med. 2011;364(19):1844-1854.
National Kidney Foundation. K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in CKD. Am J Kidney Dis. 2003;42(4 Suppl 3):S1-S201.

How to Cite This Tool

AMA Style:
Umakanth S. Combined Electrolyte Panel Pathway. MEDiscuss. Published 2026. Accessed .

Vancouver Style:
Umakanth S. Combined Electrolyte Panel Pathway [Internet]. MEDiscuss.org; 2026 [cited ]. Available from:

Category Therapeutic & Management PathwaysPathway

Specialties Internal Medicine, Nephrology, Critical Care, Emergency Medicine

Written and maintained by Dr Shashikiran Umakanth.
Last revised: 29 July 2026

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Combined Electrolyte Panel Pathway

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