Hypomagnesaemia
Low magnesium — causes, cardiac risks and safe replacement
Hypomagnesaemia (serum magnesium below 0.7 mmol/L) is a frequently overlooked electrolyte disturbance that is closely intertwined with potassium and calcium balance. It is common in patients on long-term PPIs, loop or thiazide diuretics, or receiving cisplatin chemotherapy. Recognising and correcting hypomagnesaemia is critical — refractory hypokalaemia will not respond to potassium replacement until magnesium is restored.
What is Hypomagnesaemia?
Hypomagnesaemia is defined as a serum magnesium level below 0.7 mmol/L (normal range 0.7–1.0 mmol/L). Magnesium is the second most abundant intracellular cation after potassium and acts as a co-factor for over 300 enzymatic reactions, including DNA synthesis, protein synthesis, and energy production. It is essential for neuromuscular function and maintaining cardiac rhythm. Hypomagnesaemia is classified as mild (0.5–0.7 mmol/L), moderate (0.3–0.5 mmol/L), or severe (<0.3 mmol/L). Because magnesium is primarily intracellular, serum levels may not accurately reflect total body stores — symptoms can occur even when serum levels appear only mildly reduced.
Causes & Risk Factors
The most common causes of hypomagnesaemia fall into two groups: gastrointestinal losses and renal wasting. Gastrointestinal causes include chronic diarrhoea, malabsorption syndromes (coeliac disease, IBD, short bowel syndrome), prolonged vomiting, post-bariatric surgery, and alcoholism (which combines poor intake, GI loss, and renal wasting). Renal wasting is caused by loop diuretics (furosemide), thiazide diuretics, osmotic diuresis in DKA, and nephrotoxic drugs including cisplatin, amphotericin B, aminoglycosides, and calcineurin inhibitors (ciclosporin, tacrolimus). A particularly important and often missed drug cause is long-term proton pump inhibitor (PPI) use — PPIs reduce intestinal magnesium absorption and the FDA issued a safety warning in 2011. The risk is amplified when PPIs are combined with diuretics.
Signs, Symptoms & Investigations
Mild hypomagnesaemia is commonly asymptomatic. As levels fall, symptoms include muscle cramps and weakness, tremor, tetany (positive Trousseau and Chvostek signs), hyper-reflexia, nausea, apathy, and in severe cases, generalised seizures. Cardiac effects are the most dangerous: hypomagnesaemia prolongs the QT interval and can precipitate Torsades de Pointes (a polymorphic ventricular tachycardia). It also commonly coexists with hypokalaemia and hypocalcaemia — refractory hypokalaemia (potassium that does not respond to replacement) should always prompt a magnesium check. Key investigations include serum magnesium, serum potassium, serum calcium, renal function and eGFR, ECG, and urine magnesium (to distinguish renal wasting from GI loss — >1 mmol/day suggests renal cause).
Management Overview
Management depends on severity and symptoms. Mild to moderate asymptomatic hypomagnesaemia is treated with oral magnesium — magnesium glycerophosphate (Neomag) is preferred due to better tolerability and less diarrhoea compared to magnesium oxide or hydroxide. Severe hypomagnesaemia (<0.5 mmol/L), symptomatic patients, those with cardiac arrhythmias, seizures, or those unable to take oral treatment require intravenous magnesium sulphate. For Torsades de Pointes, magnesium sulphate 8 mmol IV over 15 minutes is given urgently. A critical rule in clinical practice: always correct magnesium before potassium — without restoring magnesium, renal potassium conservation is impaired and hypokalaemia will not resolve. Long-term PPI users should have annual magnesium monitoring, and cisplatin patients require prophylactic magnesium supplementation.