Hypomagnesaemia

Hypomagnesaemia is a low serum magnesium, and is both common and disproportionately consequential, because magnesium deficiency causes refractory hypokalaemia and refractory hypocalcaemia.

Failure to check and replace magnesium is one of the commonest reasons potassium and calcium replacement appears to fail.

Causes include gastrointestinal loss (diarrhoea, malabsorption, short bowel, prolonged nasogastric aspiration), renal loss (loop and thiazide diuretics, alcohol use disorder, hypercalcaemia, Gitelman and Bartter syndromes), drugs, notably proton pump inhibitors, which are a common and under-recognised cause with long-term use, alongside aminoglycosides, amphotericin, ciclosporin, cisplatin and digoxin and redistribution during refeeding and after correction of diabetic ketoacidosis.

Serum magnesium correlates poorly with total body stores, since most magnesium is intracellular. A normal serum level does not exclude significant depletion, particularly in chronic alcohol use or malabsorption.

• Frequently asymptomatic, and detected only when sought

• Neuromuscular: tremor, muscle cramps, weakness, tetany, and positive Chvostek's and Trousseau's signs: often attributed to hypocalcaemia, which usually coexists

• Neurological: irritability, apathy, confusion, and in severe deficiency seizures

• Cardiac: this is the main hazard. Prolonged PR and QT intervals, widened QRS, atrial and ventricular ectopy, atrial fibrillation, and torsades de pointes, for which magnesium is both cause and treatment

• Increased digoxin sensitivity and digoxin toxicity at therapeutic levels

• Associated hypokalaemia and hypocalcaemia that resist correction until magnesium is replaced

The clinical signature worth recognising is a patient whose potassium will not come up despite repeated replacement; magnesium should be checked before further potassium is given.

• Check magnesium in every case of hypokalaemia, hypocalcaemia or unexplained arrhythmia, and replace it in parallel with, not after, the other electrolytes

Severe, symptomatic, or arrhythmia:

• Intravenous magnesium sulfate, typically 2 g (8 mmol) over 10–20 minutes for torsades de pointes or seizures, and more slowly over hours for less acute severe deficiency
• Magnesium is the treatment of choice for torsades de pointes irrespective of the measured magnesium level
• Rapid infusion causes flushing, hypotension and, in excess, the features of hypermagnesaemia, so rate matters outside of a peri-arrest situation
• Monitor deep tendon reflexes and renal function during replacement, and reduce the dose in renal impairment where accumulation is a real risk

Mild to moderate:

• Oral magnesium salts, though diarrhoea is dose-limiting and often prevents adequate repletion, which is why the intravenous route is used more readily for magnesium than for other electrolytes
• Repletion is slow: because magnesium is predominantly intracellular and much of an intravenous dose is excreted renally, correcting total body deficit takes several days of sustained replacement even after the serum level normalises

Alongside:

• Identify and address the cause: review proton pump inhibitors and diuretics specifically, address alcohol use, and consider malabsorption
• Correct coexisting potassium and calcium disturbance, which will often improve substantially once magnesium is restored
• Potassium-sparing diuretics such as amiloride reduce renal magnesium wasting and are useful in chronic renal losses

Referral: nephrology for persistent unexplained renal magnesium wasting; gastroenterology where malabsorption is suspected.