Epsom Salt Ingestion in Children: Hypermagnesemia, Not Tachycardia
Epsom salt (magnesium sulfate) ingestion in children causes bradycardia and cardiac depression, not tachycardia—this is a critical distinction that can be life-threatening if misunderstood. 1, 2, 3
Cardiovascular Effects of Hypermagnesemia
The cardiovascular manifestations of magnesium toxicity progress in a dose-dependent manner and are characterized by cardiac depression, not stimulation:
- At serum levels of 2.5-5 mmol/L: Prolonged PR, QRS, and QT intervals develop 4
- At levels of 4-6 mmol/L: Bradycardia, hypotension, and AV nodal conduction blocks occur 1, 2
- At levels of 6-10 mmol/L: Life-threatening cardiac arrest becomes imminent 1, 4, 2
Magnesium produces vasodilation and cardiac depression through its calcium-antagonist effects at the cellular level, which directly opposes the tachycardic response 1, 4. In documented pediatric cases of Epsom salt toxicity, bradydysrhythmia—not tachycardia—was the presenting cardiac manifestation 2, 3.
Clinical Presentation in Children
When children ingest toxic amounts of Epsom salt, the clinical picture includes:
- Bradycardia and hypotension as the primary cardiovascular findings 2, 5, 3
- Extreme muscle weakness and loss of deep tendon reflexes at levels >4 mmol/L 1, 6
- Altered mental status, confusion, and progressive CNS depression 2, 5, 6
- Respiratory depression requiring intubation in severe cases 5
- Vomiting and gastrointestinal symptoms 2
A fatal case in a 7-year-old who received an Epsom salt enema documented a serum magnesium of 41.2 mg/dL (33.9 mEq/L) with cardiac arrest as the terminal event 3.
Critical Pitfall to Avoid
Do not confuse the cardiovascular effects of magnesium toxicity with those of epinephrine or other catecholamines. The American Heart Association explicitly warns that epinephrine causes tachycardia in patients with a perfusing rhythm 1, but magnesium has the opposite effect—it is a cardiac depressant that causes bradycardia and hypotension 1, 4.
Emergency Management Algorithm
Step 1: Immediate Recognition and Stabilization
- Assess for bradycardia, hypotension, and altered mental status 2, 5
- Obtain serum magnesium level immediately; levels >6 mmol/L indicate imminent cardiac arrest risk 2
- Secure airway if respiratory depression or altered mental status is present 5
Step 2: Antidote Administration
- Give intravenous calcium immediately as the direct antidote: calcium chloride 10% 5-10 mL IV over 2-5 minutes, or calcium gluconate 10% 15-30 mL IV 4
- Calcium competitively antagonizes magnesium's cardiac and neuromuscular effects 4
- Multiple doses may be required with continuous cardiac monitoring 5
Step 3: Enhanced Elimination
- Administer generous IV fluids with furosemide to promote renal excretion 5
- Urgent hemodialysis should be initiated for severe hypermagnesemia (>6 mmol/L) or life-threatening features, as dialysis results in rapid correction of magnesium levels 4, 2, 5
- Dialysis is particularly critical in children because calcium gluconate alone may show minimal response in severe toxicity 2, 5
Step 4: Supportive Care
- Continuous cardiac monitoring for bradydysrhythmias and conduction blocks 2, 3
- Prepare for mechanical ventilation if hypoventilation develops 4
- Monitor for loss of patellar reflexes as a clinical marker of toxicity 1
Why This Distinction Matters
Hypermagnesemia from Epsom salt is unusual in patients with normal renal function but can occur with large ingestions 2, 6. The easy availability of magnesium products and the subtle initial symptoms make this a dangerous scenario 3. Mistaking bradycardia for tachycardia could lead to inappropriate treatment decisions, such as withholding calcium or administering beta-blockers, which would worsen the patient's condition.
The American Heart Association guidelines state that routine magnesium administration in cardiac arrest is not recommended (Class III: No Benefit) except for torsades de pointes 4, and if a patient was receiving magnesium prior to arrest, it should be immediately discontinued 4.