Magnesium Overload: When Supplements Turn Toxic

Abstract

Magnesium is an essential electrolyte involved in neuromuscular function, cardiac conduction, and enzymatic reactions. Oral magnesium supplements and magnesium-containing antacids/laxatives are widely available as over the counter medications. When taken in excess or when excretion is impaired, magnesium can accumulate and produce a spectrum of toxicity. This case report reviews pathophysiology, clinical presentation, diagnostic approach, electrocardiographic (ECG) findings, differential diagnosis, and management of magnesium tablet (oral) overdose, centred on a prototypical case: a young male presenting with profuse loose stools and new-onset arrhythmia. Key decision points (when to give calcium, when to dialyze) and pitfalls (confusing ECG changes with hyperkalaemia, missing co-ingestions, or failing to recognise renal impairment) are emphasised.

Introduction

Magnesium (Mg²⁺) is the second most abundant intracellular cation and crucial for neuromuscular conduction, cardiac electrophysiology, and serves as a cofactor for several enzymatic function.¹ Oral magnesium preparations (oxides, hydroxides, sulfates, citrate, carbonate, gluconate) are commonly used as supplements, antacids, and laxatives. In most individuals with normal renal function, excess oral magnesium is limited by poor intestinal absorption and the diarrhoeal effect of unabsorbed magnesium salts. However, overdose can occur with extremely large ingestions, repeated supratherapeutic dosing, or in persons with decreased renal excretion; severe toxicity is more frequent with parenteral (intravenous) magnesium but oral overdoses can still produce clinically significant hypermagnesemia and cardiac disturbances.² Early recognition is essential because timely antagonism and renal elimination can be lifesaving.

Case vignette

A young male presented to the emergency department with complaints of several episodes of profuse loose stools and light-headedness. He reported having taken multiple over-the-counter magnesium tablets for insomnia over the last day (self-medicated, higher than recommended dose). Each tablet contained 200 mg of elemental magnesium and he reported to have taken a total of 18 tablets the previous night. On arrival he was diaphoretic, heart rate 40–50/min, blood pressure 90/60 mmHg, and ECG showed bradyarrhythmia with PR prolongation and wide QRS complexes. There was no history of prior kidney disease. Initial point-of-care glucose was normal. Serum electrolytes and a 12-lead ECG were sent; supportive measures and antidote therapy were initiated. This vignette illustrates a common and important presentation of hypermagnesiemia — oral magnesium supplement excess leading to GI losses but systemic magnesium overload sufficient to produce conduction abnormalities.

Pathophysiology — How oral magnesium causes toxicity

1. Absorption and excretion
   • Oral magnesium is variably absorbed in the small intestine; unabsorbed magnesium increases intraluminal osmotic load causing diarrhoea (a protective mechanism). Nevertheless, with massive ingestion or repeated supratherapeutic dosing, absorbed magnesium can overwhelm renal excretion, especially when renal function is impaired. Kidneys are the main route of magnesium elimination.
2. Cellular/physiologic effects
   • Magnesium acts as a physiological calcium antagonist at cell membranes and neuromuscular junctions. High extracellular magnesium reduces release of acetylcholine at neuromuscular junctions and depresses cardiac conduction by affecting ion channel function. These effects underlie hypotension, muscle weakness, respiratory depression, and conduction abnormalities/arrhythmias. Calcium administration reverses many acute effects by opposing magnesium at membrane and receptor sites.³
3. Interaction with other electrolytes/conditions
   • Magnesium toxicity can mimic or coexist with hyperkalaemia, hypocalcaemia, or drug effects (beta blockers, calcium channel blockers, digitalis), which complicates ECG interpretation and management.

Clinical features

Clinical manifestations correlate imperfectly with serum magnesium concentration, but general patterns are:

• Mild (serum Mg  >2-4 mg/dL): nausea, vomiting, diarrhea (often the first sign after oral ingestion), abdominal cramping, lethargy.
• Moderate (serum magnesium ≈4–8 mg/dL): flushing, hypotension, depressed deep tendon reflexes, somnolence, mild bradycardia, ECG conduction changes (PR prolongation).
• Severe (serum magnesium >8–12 mg/dL and above): profound hypotension, bradycardia progressing to heart block or asystole, wide QRS, respiratory muscle weakness/arrest, coma, and death.

Electrocardiographic manifestations

ECG changes of hypermagnesemia reflect slowed atrioventricular conduction and depressed myocardial excitability:

• Sinus bradycardia and PR prolongation (early signs).
• Widening of QRS complex with progression, QRS changes may resemble severe hyperkalemia.
• High-grade AV block, ventricular arrhythmias or asystole in extreme toxicity.
• T wave changes are not specific; differentiation from hyperkalemia is critical because management differs. Clinically, hypermagnesemia often causes bradyarrhythmias and conduction delay rather than the classic peaked T waves of hyperkalemia, but overlap exists.⁴

Diagnostic evaluation

1. History and physical
   • Enquire about timing/amount/formulation of magnesium tablets (oxide, sulfate, citrate, gluconate), other antacids/laxatives, medications (ACE inhibitors, NSAIDs, diuretics, lithium), kidney disease, or herbal supplements. Document stool frequency/character and associated symptoms (weakness, oliguria).
2. Laboratory tests
   • Serum electrolytes: magnesium, potassium, sodium, calcium, creatinine, BUN, glucose.
   • Arterial/venous blood gas if respiratory compromise suspected.
   • ECG immediately to detect conduction disturbances.
   • Serum magnesium is the key test, but clinical status drives treatment; levels may lag behind symptoms. Also request renal function tests because impaired clearance increases severity and informs dialysis decisions.
3. Imaging/monitoring
   • Continuous cardiac monitoring if arrhythmia, hypotension, or altered mental status. Frequent reassessment of reflexes and respiratory function. Consider chest X-ray if aspiration/respiratory failure suspected.

Differential diagnosis

When a patient presents with diarrhea and arrhythmia, the following differential diagnosis are considered:

• Hyperkalaemia — causes ECG changes similar to conduction disturbance; check K⁺ immediately.
• Hypocalcaemia or hypercalcemia — can cause arrhythmias and neuromuscular signs.
• Digitalis toxicity — may produce arrhythmias with gastrointestinal prodrome.
• Other electrolyte disturbances (sodium abnormalities, severe acidosis).
• Sepsis, dehydration, and autonomic dysfunction causing hypotension and secondary arrhythmia.
• Drug intoxication (beta-blockers, calcium channel blockers, tricyclics) — may present with bradycardia and hypotension.
• Primary cardiac conduction disease (e.g., sick sinus syndrome) — less likely in a young person with acute GI symptoms and recent magnesium ingestion.

Management

General principles

Management is guided by clinical severity, not just the serum magnesium value.⁵ The goals are to:

1. Stop further magnesium absorption.
2. Antagonise life-threatening effects (with IV calcium administration).
3. Enhance elimination (renal excretion, dialysis if indicated).
4. Support airway, breathing, and circulation.

Immediate management:

1. Airway & breathing
   • Assess and secure airway if altered consciousness or respiratory muscle weakness. Provide supplemental oxygen; prepare for assisted ventilation if hypoventilation or respiratory arrest develops.
2. Cardiac monitoring & IV access
   • Continuous telemetry, large bore IV access, frequent vitals, and frequent neurologic checks (including deep tendon reflexes — hyporeflexia is an early sign).
3. Antidote — IV calcium
   • Rationale: Calcium (usually calcium gluconate) rapidly antagonises the cardiac and neuromuscular effects of magnesium by restoring ion gradient and excitability. It does not lower magnesium levels but gives immediate symptomatic improvement.
   • Dosing (common recommendation):
     • Calcium gluconate 10%: 10 mL (which contains ~1 g elemental calcium gluconate) IV over 5–10 minutes; may repeat every 10–20 minutes until improvement in hemodynamics/ECG. Some texts recommend 1–2 g (10–20 mL of 10% solution) as initial bolus for severe toxicity. Continuous infusion can be considered if recurrent signs persist, but serial dosing guided by response is typical. Always monitor for hypercalcemia and arrhythmia during administration.⁶
   • Alternative: Calcium chloride provides more elemental calcium but is more irritant to veins; use only via central line if chosen (and multiply dose accordingly).
4. Fluid resuscitation and diuresis to promote renal excretion
   • If the patient is euvolemic or hypovolemic, give isotonic crystalloid boluses to restore perfusion (and help renal Mg excretion). After volume resuscitation, loop diuretics (e.g., furosemide) can increase urinary magnesium elimination — use with caution and only after establishing adequate intravascular volume. Monitor electrolytes and urine output.
5. For GI decontamination (oral ingestion within recent hours)
   • Activated charcoal is not effective for magnesium salts (they are ionic and poorly adsorbed).
   • Consider whole-bowel irrigation or magnesium-free cathartics/enemas to hasten removal if a large amount of tablets is still in the gut and the ingestion was recent — expert and source guidance varies. For magnesium sulfate from oral ingestion, some sources recommend cathartics/emptying; always consult local poison control. Do not give additional oral cathartics that contain magnesium.

When to consider dialysis (renal replacement therapy)

Renal replacement therapy is the definitive method to remove magnesium rapidly.⁷ It is indicated when:

• Severe symptomatic hypermagnesemia (e.g., refractory hypotension, progressive neuromuscular depression, respiratory failure, life-threatening arrhythmia) despite calcium and supportive measures.
• Markedly elevated serum magnesium with impaired renal function — exact numeric cutoffs vary by guideline, but many sources recommend urgent dialysis for levels associated with severe symptoms (e.g., >8–12 mg/dL or values producing cardiopulmonary compromise) or when Mg is rising and the patient has renal failure.
• Persistent hypermagnesemia despite adequate diuresis.

Effectiveness: Haemodialysis can rapidly reduce serum magnesium (reports of ~50% reduction after a 3–4 hour session), but caution: dialysis may lower serum calcium and thus transiently worsen neuromuscular/cardiac effects — monitor calcium.⁸

Monitoring and follow-up

• Frequent reassessment (vital signs, neurological status, DTRs, respiratory rate, urine output).
• Serial labs: serum magnesium every 2–6 hours depending on severity until stable and trending downward; monitor potassium, calcium, creatinine.
• ECG monitoring until conduction abnormalities resolve and magnesium normalises.

Prognosis

Prognosis depends on amount ingested, timeliness of recognition/treatment, and renal function. Most oral magnesium overdoses in otherwise healthy persons cause only GI symptoms (diarrhoea) and resolve after stopping supplements. However, with large ingestions or impaired clearance, toxicity can progress to life-threatening cardiopulmonary compromise. Timely calcium administration, supportive care, and dialysis when indicated generally result in recovery; delayed recognition of severe hypermagnesemia increases mortality risk.

Prevention and patient education

• Safe dosing: For adults, the tolerable upper intake level (UL) for magnesium from supplements is commonly cited as 350 mg/day (elemental magnesium) for most adults — higher amounts in specific therapeutic contexts should be under medical supervision.⁹ Food sources typically do not cause toxicity. Patients must be counselled to follow labeled dosing and to avoid doubling doses.
• High-risk groups: patients with chronic kidney disease, elderly patients, and those on medications that reduce renal perfusion/excretion (e.g., ACE inhibitors, NSAIDs) should be cautioned about magnesium-containing OTC products.¹⁰ Healthcare providers should explicitly warn patients using laxatives or antacids containing magnesium.

References

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Dr Ramapriya
DrNB Post Graduate Critical Care Medicine
Kauvery Hospital, Alwarpet, Chennai.

Dr Muralidharan
Consultant Critical Care Medicine
Kauvery Hospital, Alwarpet, Chennai.