Hypomagnesaemia and hypermagnesaemia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Magnesium supports ATP-dependent reactions, neuromuscular stability, ion channels and PTH physiology. Low magnesium increases acetylcholine release and electrical instability, producing tremor, cramps, tetany, nystagmus, seizure and torsades. It also opens renal potassium secretory pathways, which explains refractory hypokalaemia, and can create functional hypoparathyroidism with a low calcium.

High magnesium suppresses neuromuscular transmission and slows cardiac conduction. Nausea and flushing can progress to reduced reflexes, weakness, hypotension, bradycardia, heart block, respiratory paralysis and cardiac arrest. Because healthy kidneys excrete magnesium efficiently, important toxicity should prompt a search for kidney failure, concentrated replacement, magnesium-containing bowel preparations or dosing error.

Replacement doses and concentrations are product- and setting-specific. Obstetric eclampsia regimens are not general deficiency schedules, and a dose tolerated with normal filtration may be unsafe after acute kidney injury. Use the live BNF, licensed product information, local infusion chart and pharmacy support; involve renal, endocrine, toxicology or critical-care specialists for severe symptoms or unexpected accumulation.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Gastrointestinal magnesium loss

Poor intake, diarrhoea, malabsorption and nutrition-related illness reduce magnesium entry or increase losses, often alongside other electrolyte deficiencies.

Renal magnesium wasting

Diuretics, tubular injury and several other medicines increase urinary magnesium loss, while proton-pump inhibitors can cause depletion by impairing intestinal absorption.

Reduced excretion with magnesium exposure

Acute kidney injury or advanced renal failure allows replacement, antacid or bowel-preparation magnesium to accumulate to toxic concentrations.

Iatrogenic administration

Concentrated intravenous treatment or a dosing error can raise magnesium rapidly, particularly when filtration deteriorates during therapy.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Magnesium balance is disturbed
Altered intake, intestinal absorption, renal transport or administration changes extracellular magnesium and disrupts intracellular enzyme, membrane and neuromuscular function.
2
Deficiency increases excitability
Low magnesium increases neuromuscular activity and electrical instability, producing tremor, tetany, seizure and ventricular arrhythmia, especially when potassium is also low.
3
Linked electrolytes become refractory
Deficiency promotes renal potassium wasting and impairs PTH release or action, sustaining hypokalaemia and hypocalcaemia until magnesium is corrected.
4
Excess suppresses conduction
High magnesium inhibits neuromuscular transmission and cardiac conduction, progressing from reduced reflexes to weakness, hypotension, heart block and respiratory paralysis.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Low-magnesium irritabilityRed flag

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

Ventricular electrical riskRed flag

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

Refractory companion deficits

Potassium or calcium that remains low despite replacement should prompt magnesium measurement and cause review rather than endless escalation of the other electrolyte.

High-magnesium hyporeflexiaRed flag

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

Cardiorespiratory depressionRed flag

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

Hidden oral exposure

Magnesium-containing antacid, laxative, bowel preparation or supplement can accumulate in frail adults with constipation, reduced intake or kidney disease.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Repeat serum magnesium with renal profileFirst step
Why
Confirm direction and severity and determine whether excretion can support replacement or recovery.
Interpretation and limitations
Trend with creatinine and urine output; a normal serum result does not fully exclude depletion, while a high result in oliguria predicts prolonged toxicity.
02
Potassium, adjusted or ionised calcium and phosphate
Why
Identify linked deficiencies, refeeding and mineral precipitation risk.
Interpretation and limitations
Low magnesium can drive both hypokalaemia and hypocalcaemia; their improvement may lag until magnesium is restored, and phosphate replacement requires compatible prescribing.
03
Twelve-lead ECG and continuous monitoring when severe
Why
Detect QT-related arrhythmia in deficiency and conduction slowing in excess.
Interpretation and limitations
Torsades or ventricular ectopy demands immediate treatment, while PR or QRS prolongation, bradycardia and block suggest escalating hypermagnesaemic toxicity.
04
Acid–base, glucose and nutrition assessment
Why
Find DKA treatment, refeeding, alcohol-related illness or gastrointestinal loss driving redistribution and depletion.
Interpretation and limitations
A falling magnesium after insulin or nutrition can be part of a broader intracellular shift, requiring phosphate, potassium and thiamine-aware management.
05
Medication and administration record
Why
Locate PPIs, diuretics, nephrotoxic drugs and prescribed or non-prescribed magnesium exposure.
Interpretation and limitations
Compare the actual formulation, concentration, cumulative dose and renal trajectory; toxicity often reflects an appropriate original prescription that became unsafe as filtration fell.
06
Urinary magnesium assessment in recurrent depletion
Why
Distinguish gastrointestinal loss from inappropriate renal wasting after acute stabilisation.
Interpretation and limitations
Use a locally validated fractional excretion or timed method with renal advice; diuretics, replacement and low GFR can invalidate a simplistic spot interpretation.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Primary potassium disorder

Persistent hypokalaemia despite replacement suggests magnesium deficiency, whereas isolated potassium loss can correct without resolving a magnesium abnormality.

Primary hypoparathyroidism

Low calcium with non-raised PTH can arise from severe magnesium deficiency; recovery of PTH after magnesium correction distinguishes functional suppression.

Sedative or neurological toxicity

Reduced reflexes, weakness and respiratory depression can mimic hypermagnesaemia; measured magnesium and a renal or exposure history discriminate it.

Sampling artefact

Haemolysis and collection problems can distort a result, so an unexpected concentration should be confirmed while clinically significant toxicity is assessed.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01LowTreat magnesium depletion by riskFirst stepMagnesium is low with symptoms, arrhythmia, linked electrolyte disturbance or an ongoing high-risk cause.

1Assess ABCDE, ECG, renal function, potassium and calcium, identify ongoing gastrointestinal or renal losses and stop or modify causal medicines where clinically safe.
2Use 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.
3Recheck magnesium and companion electrolytes after each treatment stage, reducing dose for kidney impairment and treating the cause so replacement is retained.

02LinkedCorrect refractory potassium and calciumHypokalaemia or hypocalcaemia persists despite apparently adequate direct replacement.

1Measure magnesium and review diarrhoea, PPI, alcohol, diuretics, chemotherapy, aminoglycosides, nutrition and renal tubular injury.
2Replace magnesium through the severity-appropriate route while continuing cautious potassium or calcium treatment based on symptoms and ECG.
3Expect biochemical recovery to take time because intracellular magnesium stores and PTH function do not normalise instantly; avoid overshooting the companion electrolytes.

03HighReverse magnesium toxicityRaised magnesium is accompanied by reduced reflexes, weakness, hypotension, bradycardia or respiratory depression.

1Stop every magnesium source, use ABCDE with ventilatory support, obtain continuous ECG, repeat magnesium, calcium, potassium and renal tests and call senior critical-care and renal clinicians.
2Give intravenous calcium gluconate through the current emergency and product guidance to antagonise neuromuscular and cardiac effects, reassessing because its benefit is temporary.
3Restore renal perfusion if depleted, promote excretion only when cardiorenal status permits and arrange urgent dialysis for severe toxicity with renal failure or refractory cardiorespiratory compromise.

04PreventRemove the recurrent exposureThe acute magnesium abnormality has improved or repeated episodes have occurred.

1AlternativeReview the ongoing need for PPI, diuretic, laxative, antacid, supplement or chemotherapy and agree a monitored alternative rather than leaving a causal medicine unexplained.
2For nutrition risk, apply NICE CG32 refeeding precautions with gradual energy, thiamine and planned magnesium, phosphate and potassium surveillance.
3Set repeat magnesium and renal tests after discharge, particularly after intravenous replacement, acute kidney injury or continued medicine exposure.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Restores magnesium when severe neurological or electrical manifestations, malabsorption or inability to take oral treatment makes enteral replacement inadequate.

Magnesium sulfate for severe deficiency

Select 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.

Repletes stable mild or chronic magnesium deficiency without the infusion and accumulation risks of parenteral therapy.

Oral magnesium preparation

Choose 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.

Temporarily antagonises severe neuromuscular blockade and cardiac membrane effects while magnesium is cleared or removed by dialysis.

Intravenous calcium gluconate for magnesium toxicity

Use the dose equivalent to 2.5–5 mmol calcium described in current magnesium sulfate product information, administered through the organisation’s monitored emergency calcium protocol with repeat decisions based on clinical response.

It does not remove magnesium and may require further specialist dosing. Confirm calcium salt and concentration, secure the vein, monitor ECG, consider digoxin risk and continue respiratory and renal support.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Ventricular arrhythmia

Magnesium deficiency destabilises repolarisation and can cause torsades de pointes, particularly with hypokalaemia or QT-prolonging medicines.

Seizure and tetany

Low magnesium increases neuromuscular excitability and, especially with accompanying hypocalcaemia, can progress from tremor and tetany to seizure.

Respiratory paralysis

Severe magnesium excess suppresses neuromuscular transmission, weakening ventilation and potentially requiring airway support while magnesium is removed.

Heart block and shock

Toxic magnesium concentrations slow conduction and reduce vascular tone, causing bradycardia, hypotension and potentially cardiac arrest.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During intravenous replacement, repeat magnesium at the interval in the local chart and continue surveillance after completion because extracellular normalisation can precede stable total-body repletion.
Trend potassium and calcium until they remain stable without escalating replacement; improvement after magnesium confirms the linked mechanism but does not exclude ongoing loss.
Use continuous ECG for torsades, ventricular ectopy, severe deficiency or symptomatic excess, and repeat a formal tracing after clinically meaningful correction.
Check respiratory rate, oxygenation, pressure, heart rate and deep tendon reflexes during high-dose or repeated parenteral magnesium, especially in renal impairment.
Measure creatinine and urine output before and during replacement and toxicity care; new oliguria should stop an automatic next dose and trigger accumulation review.
For recurrent PPI or diuretic-associated disease, assign a post-change magnesium result and document whether the original medicine remains necessary.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Serum stores are incomplete

Most magnesium is intracellular or in bone, so symptoms and ongoing losses can persist after a single serum result enters the reference interval.

Low magnesium mimics low calcium

Tetany and seizure may reflect both direct neuronal irritability and functional PTH failure; measure ionised calcium when symptoms are severe.

Torsades is a specific emergency

Magnesium is used for torsades even when serum magnesium is not frankly low, but dosing follows the arrhythmia protocol rather than routine deficiency replacement.

Reflexes are bedside toxicology

Progressive loss of tendon reflexes during infusion is an actionable early toxicity signal before respiratory paralysis and cardiac arrest.

Calcium buys clearance time

In hypermagnesaemia, calcium opposes physiological effects for a limited period; renal excretion or dialysis determines the actual body burden.

PPI deficiency can be delayed

Symptoms may arise after months of treatment and recur after rechallenge, supporting a careful indication review rather than supplementation alone.

11Common pitfallsFrequent interpretation and management errors.

01
Escalating potassium or calcium indefinitely while never measuring the magnesium that is driving renal loss and impaired PTH action.
02
Using an obstetric magnesium regimen for ordinary deficiency without checking indication, renal function or local product concentration.
03
Continuing repeated intravenous magnesium after urine output falls and assuming the original low value still predicts current body burden.
04
Treating severe hypermagnesaemic bradycardia with calcium alone but making no plan to remove magnesium or support ventilation.
05
Ignoring non-prescription laxatives, antacids and supplements during medicines reconciliation in a patient with kidney failure.
06
Prescribing long-term oral magnesium for PPI-associated depletion without reviewing whether the PPI remains indicated or arranging follow-up tests.