Hypomagnesaemia !

Low magnesium in the blood. It causes cramps, tremor and dangerous heart rhythms and makes low potassium and calcium hard to correct.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

A serum magnesium below the normal range, usually under about 1.7–1.8 mg/dL (0.7 mmol/L). It is common in hospitalised and critically ill people and often travels with low potassium and low calcium. The page also covers its opposite, hypermagnesaemia, mostly seen with kidney failure or magnesium therapy.

Who gets it

Frequent in intensive care, in alcohol use disorder and in people on diuretics or long-term proton-pump inhibitors. Hypermagnesaemia is rare outside kidney failure and the use of magnesium sulfate in preeclampsia, a common obstetric scenario in Colombia.

Causes

Gastrointestinal loss: chronic diarrhoea, malabsorption, short bowel, long-term proton-pump inhibitor use
Kidney loss: loop and thiazide diuretics, osmotic diuresis in uncontrolled diabetes, aminoglycosides, amphotericin B, cisplatin, calcineurin inhibitors
Alcohol use disorder and malnutrition
Refeeding syndrome and recovery from diabetic ketoacidosis (shift into cells)
Inherited tubular disorders (Gitelman and Bartter syndromes)

Risk factors

Chronic alcohol use
Diuretic or long-term proton-pump inhibitor therapy
Chronic diarrhoea or bowel resection
Poorly controlled diabetes
Critical illness and parenteral nutrition

Pathophysiology

Magnesium is mainly inside cells and is reabsorbed in the thick ascending limb of the loop of Henle and the distal tubule. Low magnesium increases neuromuscular excitability. It also releases the brake on kidney potassium channels (so potassium is lost) and impairs parathyroid hormone release and action (so calcium falls); both stay low until magnesium is replaced.

Classification

Hypomagnesaemia: mild or severe (severe usually under 1.2 mg/dL or with symptoms)
Hypermagnesaemia: progressive loss of deep tendon reflexes, then respiratory depression and cardiac arrest as levels rise

Symptoms and signs

Muscle cramps, weakness and fatigue
Tremor, twitching and tetany (Chvostek and Trousseau signs)
Numbness and tingling
Nystagmus, confusion or seizures in severe cases
Palpitations
Hypermagnesaemia: flushing, nausea, low blood pressure, drowsiness and loss of reflexes

Diagnosis

Clinical: Suspect it in people with risk factors, neuromuscular irritability, arrhythmias or hard-to-correct low potassium or calcium. In obstetrics, magnesium therapy is monitored clinically with reflexes, breathing rate and urine output.
Tests: Serum magnesium (it may be normal despite low body stores), potassium, calcium, phosphate and creatinine. A 24-hour urine magnesium or fractional excretion separates kidney from gut loss. ECG may show a long QT, wide QRS or arrhythmias.
Imaging: Not needed.

Differential diagnosis

Hypocalcaemia from other causes (hypoparathyroidism, vitamin D deficiency)
Hypokalaemia from other causes
Alcohol withdrawal
Primary seizure disorders
Congenital or drug-induced long QT syndrome

Goal of treatment

Restore magnesium safely, prevent arrhythmias and seizures, correct accompanying potassium and calcium, and treat the cause.

Treatment

Medical: Oral magnesium salts for mild, asymptomatic deficiency; treating the cause (stopping or changing a diuretic or proton-pump inhibitor, managing diarrhoea).
Acute: Intravenous magnesium sulfate for severe or symptomatic deficiency, seizures or torsades de pointes; more cautious replacement in kidney failure.
Medical: Potassium-sparing diuretics can reduce kidney magnesium loss in selected people; hypokalaemia and hypocalcaemia are corrected alongside magnesium.
Follow-up: Nursing priorities: cardiac monitoring, serial levels, seizure precautions; during magnesium sulfate infusion, check deep tendon reflexes, breathing and urine output, with calcium gluconate kept available as the antidote for toxicity.

Complications

Ventricular arrhythmias, including torsades de pointes
Seizures
Persistent hypokalaemia and hypocalcaemia
Increased sensitivity to digoxin toxicity
Hypermagnesaemia: respiratory depression and cardiac arrest

Prognosis

Good when recognised and the cause is treated. Severe untreated deficiency can be fatal through arrhythmias or seizures; chronic causes such as alcohol use or long-term drugs tend to recur.

Prevention

Monitoring magnesium in people on diuretics, long-term proton-pump inhibitors, nephrotoxic drugs or parenteral nutrition
Checking and replacing magnesium before and during refeeding of malnourished people

Test yourself

Think of the answer, then tap the question to see it.

Why does hypokalaemia not correct until magnesium is replaced?

Low magnesium increases potassium secretion through kidney (ROMK) channels, so potassium keeps being lost.

Which arrhythmia is classically treated with intravenous magnesium sulfate?

Torsades de pointes (polymorphic ventricular tachycardia with a long QT).

How does hypomagnesaemia cause hypocalcaemia?

It impairs parathyroid hormone release and the tissue response to it.

What is the earliest clinical sign of magnesium sulfate toxicity in preeclampsia?

Loss of deep tendon (patellar) reflexes, before respiratory depression.

What is the antidote for magnesium toxicity?

Intravenous calcium gluconate (calcium salts).

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Magnesium deficiency: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2024).

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Kidneys highlighted on the Durgical 3D model