Hypomagnesaemia

Aetiologies

• Gastrointestinal loss (e.g. malabsorption, GIT fistula, short-bowel syndrome, diarrhoea, pancreatitis)
• Endocrine disorders (e.g. Hyperparathyroidism, Hyperthyroidism, Conn syndrome)
• Renal diseases (e.g. Renal Tubular Acidosis, diuretic phase of Acute Tubular Necrosis)
• Drugs such as Diuretics, aminoglycosides, PPIs
• Burns patients

Pathophysiology

• Causes ↓ ICF potassium and ↑ ICF sodium ⇒ ↑ resting potential → ↑ inward calcium current and therefore enhanced neurological and cardiac irritability
• Hypocalcaemia occurs because magnesium leads to impaired release of PTH and impaired peripheral action of PTH
• Magnesium is required for potassium reabsorption by the kidneys

Clinical Features

• Symptoms typically only occur at levels < 0.5 mmol/L
• Similar to Hypocalcaemia: tetany, seizures, positive Trosseau and Chvostek signs
• ECG changes:
  • Widening of QRS
  • Peaking of T waves
  • Prolonged PR interval
• Other associated labs:
  • Hypokalaemia
  • Hypocalcaemia
  • Low parathyroid hormone levels (despite hypocalcaemia)
  • Low vitamin D levels
  • Hypernatraemia
  • Normal anion gap metabolic acidosis

Investigations

• 24 hour urine magnesium
• Fractional excretion of magnesium
• Only ionised magnesium is physiologically active (~60% of plasma magnesium)
  • Low serum albumin lowers total plasma magnesium but ionised magnesium may be normal

Management

• Resuscitation for any dysrhythmias, seizures etc.
• Magnesium replacement (IV replacement preferred in malabsorption states and acute symptomatic states)
• Correct co-existing electrolyte abnormalities (hypokalaemia and hypocalcaemia)

Sources

• Hypomagnesaemia • LITFL • CCC Electrolytes
• Hypomagnesemia - Deranged Physiology