Removing excess magnesium from the body requires prompt medical intervention, particularly in patients with kidney impairment or those experiencing symptoms of hypermagnesaemia. Whilst healthy kidneys naturally excrete surplus magnesium through urine, elevated levels can develop when renal function is compromised or excessive supplementation occurs. Treatment approaches range from stopping magnesium intake and administering intravenous calcium gluconate to emergency haemodialysis in severe cases. Understanding the causes, recognising warning signs, and seeking timely medical help are essential for safe management. This article explores evidence-based strategies for addressing magnesium overload and preventing potentially life-threatening complications.

Understanding Excess Magnesium in the Body

Hypermagnesaemia, or elevated magnesium levels in the blood, is a relatively uncommon condition that occurs when serum magnesium concentrations exceed the laboratory reference range (commonly >1.0–1.1 mmol/L). Unlike magnesium deficiency, which is more frequently encountered in clinical practice, excess magnesium typically develops in specific circumstances rather than through dietary intake alone. The kidneys play a crucial role in maintaining magnesium homeostasis by efficiently excreting excess amounts through urine, making hypermagnesaemia rare in individuals with normal renal function.

The condition most commonly arises in patients with chronic kidney disease (CKD) or acute kidney injury, where impaired renal excretion prevents the body from eliminating excess magnesium effectively. Other contributing factors include excessive magnesium supplementation, particularly in those taking high-dose supplements without medical supervision, and the use of magnesium-containing medications such as certain antacids, laxatives or bowel preparations. Additional causes include adrenal insufficiency, hypothyroidism, and lithium therapy. Elderly patients are at increased risk due to age-related decline in kidney function and polypharmacy.

Magnesium is the fourth most abundant cation in the body and the second most abundant intracellular cation after potassium. It serves as a cofactor for over 300 enzymatic reactions, including those involved in energy metabolism, protein synthesis, and neuromuscular function. Approximately 99% of total body magnesium is stored intracellularly in bone, muscle, and soft tissues, with only 1% present in extracellular fluid. This distribution means that serum magnesium levels may not always reflect total body stores, though they remain the standard measure for clinical assessment. It's worth noting that haemolysis or other sample collection issues can cause falsely elevated results, and repeat testing may sometimes be needed.

Understanding the mechanisms behind magnesium accumulation is essential for appropriate management. The condition requires prompt recognition and treatment, particularly in vulnerable populations with compromised renal function or those receiving intravenous magnesium therapy in hospital settings.

Symptoms of High Magnesium Levels (Hypermagnesaemia)

The clinical manifestations of hypermagnesaemia vary considerably depending on the severity and rate of magnesium accumulation. Mild elevations may produce minimal or no symptoms, whilst moderate to severe hypermagnesaemia can result in significant and potentially life-threatening complications. Early recognition of symptoms is crucial for timely intervention.

Mild to moderate hypermagnesaemia typically presents with:

• Nausea and vomiting – often the earliest gastrointestinal symptoms

• Facial flushing and sensation of warmth

• Lethargy and generalised weakness

• Reduced or absent deep tendon reflexes (hyporeflexia or areflexia)

• Muscle weakness affecting voluntary movement

As magnesium levels rise further, more serious neuromuscular and cardiovascular effects emerge. These include profound muscle weakness that may progress to flaccid paralysis, difficulty speaking (dysarthria), and impaired swallowing. The neuromuscular blockade occurs because excess magnesium interferes with calcium channels at the neuromuscular junction, reducing acetylcholine release and muscle excitability.

Severe hypermagnesaemia constitutes a medical emergency and may cause:

• Cardiac conduction abnormalities – bradycardia, prolonged PR interval, widened QRS complex on ECG

• Hypotension due to peripheral vasodilation

• Respiratory depression or respiratory failure requiring ventilatory support

• Complete heart block or cardiac arrest in extreme cases

• Altered consciousness ranging from drowsiness to coma

It's important to note that the severity of symptoms depends not only on absolute magnesium levels but also on the rate of rise, presence of other electrolyte abnormalities (particularly hypocalcaemia), and concomitant medications. Patients with renal impairment or those taking sedative drugs may experience toxicity at lower magnesium concentrations.

Patients receiving magnesium therapy, particularly intravenously for conditions such as pre-eclampsia or eclampsia, require careful monitoring. The loss of patellar reflexes serves as an important clinical warning sign that magnesium levels may be approaching dangerous concentrations. Any patient experiencing progressive weakness, breathing difficulties, or cardiac symptoms whilst taking magnesium-containing products should seek immediate medical attention.

Medical Treatments to Remove Excess Magnesium

The management of hypermagnesaemia depends on the severity of elevation, presence of symptoms, and underlying renal function. Treatment strategies aim to enhance magnesium elimination, antagonise its effects, and address the underlying cause. All cases of symptomatic hypermagnesaemia require hospital assessment and management.

Immediate cessation of magnesium intake forms the cornerstone of initial management. This includes discontinuing all magnesium supplements, magnesium-containing laxatives (such as magnesium hydroxide), antacids containing magnesium compounds (like magnesium carbonate or magnesium trisilicate mixtures), and any intravenous magnesium infusions. In patients with normal kidney function, this measure alone may be sufficient for mild cases, as the kidneys will naturally excrete excess magnesium over 12–24 hours.

Intravenous calcium gluconate serves as a direct antagonist to magnesium's effects, particularly on cardiac and neuromuscular tissues. Typically administered as 10 mL of 10% calcium gluconate given slowly over about 10 minutes with ECG monitoring, this treatment provides rapid but temporary reversal of life-threatening symptoms such as respiratory depression or severe cardiac conduction abnormalities. The dose may be repeated if needed. Calcium competes with magnesium at cellular receptor sites, effectively counteracting its toxic effects whilst the body eliminates the excess magnesium.

Intravenous fluid therapy with normal saline promotes renal magnesium excretion in patients with adequate kidney function. Volume expansion increases glomerular filtration rate and reduces tubular reabsorption of magnesium. This approach may be combined with loop diuretics such as furosemide (20–40 mg intravenously), which further enhance urinary magnesium losses by inhibiting reabsorption in the loop of Henle. This strategy requires monitoring of fluid status, urine output, and other electrolytes, and is only appropriate in patients with sufficient renal function.

Haemodialysis represents the definitive treatment for severe hypermagnesaemia, particularly in patients with renal impairment who cannot adequately excrete magnesium. Dialysis should be considered urgently in severe or symptomatic hypermagnesaemia with significant renal impairment, regardless of absolute magnesium level. Magnesium-free or low-magnesium dialysate is used to create a concentration gradient favouring magnesium removal. This intervention can reduce serum magnesium levels by approximately 50% within 3–4 hours of treatment.

Throughout treatment, close monitoring of vital signs, airway and ventilation, ECG, blood pressure, and urine output is essential. Regular checks of calcium, potassium, and renal function help guide ongoing management.

When to Seek Medical Help for High Magnesium

Recognising when to seek medical attention for suspected hypermagnesaemia can be lifesaving, as severe cases may progress rapidly to respiratory or cardiac arrest. Certain patient groups require heightened vigilance, and specific symptoms warrant immediate medical evaluation.

Seek emergency medical help (call 999 or attend A&E) if you experience:

• Severe muscle weakness affecting your ability to move or stand

• Difficulty breathing or shortness of breath

• Chest pain or irregular heartbeat

• Severe drowsiness or confusion

• Difficulty speaking or swallowing

• Loss of consciousness or unresponsiveness

These symptoms may indicate dangerously elevated magnesium levels requiring urgent intervention, particularly if you have been taking magnesium supplements or have kidney disease.

Contact your GP or NHS 111 for same-day advice if you develop:

• Persistent nausea and vomiting whilst taking magnesium supplements

• Unusual tiredness or weakness that progressively worsens

• Facial flushing accompanied by dizziness or lightheadedness

• Reduced reflexes or coordination difficulties

• Diarrhoea that becomes severe after starting magnesium-containing laxatives

High-risk groups who should exercise particular caution include patients with chronic kidney disease (stages 3–5), elderly individuals with declining renal function, those taking multiple medications that may contain magnesium, and patients receiving intravenous magnesium therapy in hospital. If you fall into these categories and take magnesium supplements, discuss appropriate monitoring with your GP.

Pregnant women receiving magnesium sulphate for pre-eclampsia or eclampsia should be under close hospital supervision with regular monitoring of reflexes, respiratory rate, and magnesium levels. Healthcare professionals should be alerted immediately if reflexes become absent, respiratory rate falls below 12 breaths per minute, or urine output decreases below 25–30 mL/hour. These are critical warning signs requiring immediate senior medical review and possible pause of magnesium infusion.

Patients with known kidney disease should inform all healthcare providers about their condition before accepting any over-the-counter medications, as many preparations contain magnesium. Kidney function monitoring forms part of routine CKD management, with additional tests including magnesium levels performed when clinically indicated or if using magnesium-containing products.

If you experience side effects from any medicines, report them through the MHRA Yellow Card scheme, which helps monitor medicine safety.

Preventing Magnesium Overload

Prevention of hypermagnesaemia centres on appropriate supplementation practices, medication awareness, and regular monitoring in at-risk populations. Most cases are avoidable through informed decision-making and medical supervision.

Supplement safety and appropriate dosing are paramount. The NHS recommends that adults should not exceed 400 mg of magnesium from supplements daily unless advised otherwise by a healthcare professional, as higher doses increase the risk of adverse effects, particularly diarrhoea and, in susceptible individuals, hypermagnesaemia. Many people obtain sufficient magnesium through a balanced diet including green leafy vegetables, nuts, seeds, whole grains, and legumes, making supplementation unnecessary. Before starting magnesium supplements, consult your GP or pharmacist, particularly if you have kidney disease, heart conditions, or take regular medications.

Medication review should include careful assessment of all magnesium-containing products. Common sources include:

• Laxatives – magnesium hydroxide (milk of magnesia), magnesium citrate

• Antacids – products containing magnesium trisilicate or magnesium carbonate

• Multivitamin preparations – check labels for magnesium content

• Epsom salts (magnesium sulphate) – primarily risky when ingested; topical use in baths is unlikely to cause significant magnesium absorption through intact skin

Patients with renal impairment should avoid these products or use them only under medical supervision with dose adjustments.

Regular monitoring is essential for high-risk groups. Patients with advanced CKD or those on dialysis should have serum magnesium checked according to their renal unit protocol. Those receiving long-term magnesium supplementation for conditions such as chronic constipation or magnesium deficiency should undergo periodic blood tests to ensure levels remain within the laboratory reference range (typically 0.7–1.0 mmol/L, though this varies between laboratories).

Patient education plays a vital role in prevention. Understanding that 'natural' does not mean 'risk-free' helps individuals make informed choices about supplements. Reading product labels, adhering to recommended doses, and recognising early warning signs of excess enable prompt action. Healthcare professionals should provide clear guidance about magnesium-containing products during medication reconciliation, particularly at hospital discharge or when prescribing new treatments.

For patients with kidney disease, dietary counselling may be appropriate, though dietary magnesium alone rarely causes hypermagnesaemia. The focus should remain on avoiding unnecessary supplementation and magnesium-containing medications whilst maintaining adequate nutrition through food sources.

Frequently Asked Questions