Magnesium (Blood)

Diagnostic Use

Serum concentrations may be normal even when body stores are depleted by up to 20%. Magnesium deficiency or loss is usually associated with loss of potassium and phosphate, the other major intracellular elements. Hypocalcaemia may be secondary to magnesium deficiency, which impairs both the release and action of PTH.

Decreased concentrations are usually due to inadequate intake (e.g. parenteral nutrition), gastrointestinal disorders (e.g. malabsorption (including PPI use in susceptible patients), prolonged diarrhoea or nasogastric function, pancreatitis), endocrine disorders (parathyroid disorders, hyperthyroidism, primary hyperaldosteronism, ketoacidosis, SIADH), and impaired renal conservation (idiopathic, renal tubular disorders, ethanol ingestion, post-transplantation, and drug therapy, including diuretics).

Increased concentrations are found with end stage renal failure, dehydration, hypothyroidism, and adrenocortical insufficiency. Symptomatic hypermagnesaemia is uncommon and is usually associated with excessive intake. Lithium therapy can cause an increase in serum magnesium.

Toxicity thresholds for general risk subjects:

a. Hyporeflexia, bradycardia, prolong PR, QRS, QT intervals can be found when plasma Mg is ≥2.0mmol/L
b. Flaccid paralysis, hypoventilation from respiratory depression, significant cardiac arrythmias/cardiac arrest can be found when plasma Mg is ≥ 4-5mmol/L

Reference Intervals

0.70 – 1.00 mmol/L