Clinical Features of hypermagnesemia
How does hypermagnesemia present?
Hypermagnesemia decreases neuromuscular transmission. The first sign will typically be diminished deep-tendon reflexes (DTR), followed eventually by complete loss of DTR. As the magnesium level rises, patients develop progressive somnolence, paralysis, and ultimately apnea.
Cardiovascular effects occur due to magnesium acting as both a calcium and potassium channel antagonist. This leads to PR, QRS, and QT prolongation presenting as bradycardia and hypotension. Ultimately, hypermagnesemia can cause complete heart block and cardiac arrest.
Magnesium is tightly linked to calcium metabolism. Hypermagnesemia inhibits parathyroid hormone (PTH) release, leading to mild hypocalcemia; this may be of little consequence but can worsen QT prolongation and compound cardiac arrhythmia.
The below table is the summary of signs and symptoms according to severity of hypermagnesemia.
| MAGNESIUM LEVEL | NEUROMUSCULAR | CARDIOVASCULAR | ELECTROLYTE | OTHER |
|---|---|---|---|---|
| 4–6 mEq/L 4.8–7.2 mg/dL | Diminished DTR | Flushing from vasomotor dilation, PR interval prolongation and QRS interval prolongation | Nausea, vomiting | |
| 6–10 mEq/L 7.2–12 mg/dL | Loss of DTR | Hypotension, bradycardia, | Hypocalcemia, suppression of PTH | Somnolence |
| >10 mEq/L >12 mg/dL | Paralysis, respiratory depression, apnea | AV dissociation, complete heart block, cardiac arrest | Coma |
DTR , Deep-tendon reflexes.
