Hypomagnesaemia and hypermagnesaemia — Rapid

Synopsis

Recognise bidirectional magnesium toxicity, correct linked calcium and potassium disturbance, and adapt replacement or removal to renal function.

Serum magnesium represents a small extracellular fraction, so a result can underestimate tissue depletion; interpret symptoms, losses and companion electrolytes as well as the number.
Hypomagnesaemia causes neuromuscular irritability, seizure, QT-related ventricular arrhythmia and renal potassium wasting, and it impairs PTH release and action to produce hypocalcaemia.
Common low-magnesium drivers include diarrhoea, malabsorption, alcohol dependence, refeeding, diuretics, proton pump inhibitors, aminoglycosides, cisplatin, calcineurin inhibitors and uncontrolled diabetes.
MHRA warns that long-term proton pump inhibitors can cause insidious serious hypomagnesaemia; review the indication and measure magnesium in symptomatic or high-risk patients.
Use oral replacement for stable mild depletion when absorption is adequate, but intravenous magnesium is needed for serious symptoms, arrhythmia or inability to absorb treatment.
Renal impairment reduces magnesium clearance, so repeated standard replacement can accumulate and produce toxicity even if the initial concentration was low.
Hypermagnesaemia is usually iatrogenic or renal: ask about obstetric infusions, intravenous replacement, magnesium laxatives and antacids, especially in acute kidney injury.
Intravenous calcium antagonises severe magnesium effects temporarily but does not remove magnesium; fluids, renal excretion and dialysis decisions determine durable recovery.

Key red flags

Low-magnesium irritability

Tremor, fasciculation, cramps, hyperreflexia, carpopedal spasm, nystagmus, confusion or seizure reflects increased neuromuscular excitability and companion calcium disturbance.

Ventricular electrical risk

QT prolongation, ventricular ectopy and polymorphic ventricular tachycardia are more likely when potassium is also low or QT-prolonging medicines remain active.

High-magnesium hyporeflexia

Diminishing deep tendon reflexes, somnolence and progressive weakness are early bedside warnings during therapeutic magnesium or impaired renal clearance.

Cardiorespiratory depression

Hypotension, bradycardia, conduction block, shallow breathing or apnoea marks severe toxicity and requires calcium antagonism, ventilatory support and removal planning.

Investigation priorities

Repeat serum magnesium with renal profileFirst step

Confirm direction and severity and determine whether excretion can support replacement or recovery.

Management branches

LowTreat magnesium depletion by risk

Magnesium is low with symptoms, arrhythmia, linked electrolyte disturbance or an ongoing high-risk cause.

Assess ABCDE, ECG, renal function, potassium and calcium, identify ongoing gastrointestinal or renal losses and stop or modify causal medicines where clinically safe.
Use a locally selected oral preparation for stable mild disease; use monitored intravenous magnesium sulfate when severe symptoms, torsades, seizure or malabsorption makes enteral treatment inappropriate.
Recheck magnesium and companion electrolytes after each treatment stage, reducing dose for kidney impairment and treating the cause so replacement is retained.

Key medicines

Magnesium sulfate for severe deficiencySelect concentration, dose and infusion duration from the current licensed product and local hypomagnesaemia chart according to symptoms, measured magnesium, weight, ongoing loss and renal function; serious arrhythmia uses its dedicated resuscitation protocol.Use a pump and monitor ECG, reflexes, breathing, pressure, magnesium and renal output. Reduce substantially in renal impairment, distinguish deficiency treatment from obstetric regimens and stop for developing hyporeflexia, bradycardia or respiratory depression.

Oral magnesium preparationChoose the locally formulary-approved licensed salt and divided dose from the BNF or SmPC, titrating to tolerance, serum response and continuing losses rather than converting different salts by tablet count.Diarrhoea can limit absorption and worsen loss; check elemental magnesium, kidney function, medicine interactions and formulation excipients. Stop or reduce promptly if renal function declines or hypermagnesaemic symptoms develop.

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