Hypermagnesemia: Difference between revisions
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==Clinical Features== | ==Clinical Features== | ||
*[[Nausea and vomiting]] | *[[Nausea and vomiting]] | ||
*Loss of reflexes and diaphragmatic paralysis (at very high levels) | *Loss of reflexes and [[respiratory failure|diaphragmatic paralysis]] (at very high levels) | ||
{| class="wikitable" | {| class="wikitable" | ||
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*[[Renal Failure]] | *[[Renal Failure]] | ||
*[[Lithium]] | *[[Lithium]] | ||
*Volume depletion | *[[hypovolemia|Volume depletion]] | ||
*[[Rhabdo]] | *[[Rhabdo]] | ||
*IV Mg (goal in PET/eclampsia 5-7 mEq/L) | *IV Mg (goal in PET/[[eclampsia]] 5-7 mEq/L) | ||
*Massive PO intake (laxative abusers, accidental Epsom salts) | *Massive PO intake ([[bulimia nervosa|laxative abusers]], accidental Epsom salts) | ||
*Magnesium enemas<ref>Schelling Fatal hypermagnesemia. JR1. Clin Nephrol. 2000 Jan;53(1):61-5.</ref> | *Magnesium enemas<ref>Schelling Fatal hypermagnesemia. JR1. Clin Nephrol. 2000 Jan;53(1):61-5.</ref> | ||
Revision as of 01:06, 29 September 2019
Background
- High >3.5
- Magnesium is an effective calcium channel blocker both extracellularly and intracellularly[1]
- Intracellular magnesium profoundly blocks several cardiac potassium channels
Clinical Features
- Nausea and vomiting
- Loss of reflexes and diaphragmatic paralysis (at very high levels)
| Mg Level | Signs/Symptoms |
|---|---|
| 2-3 | Nausea |
| 3-4 | Somnolence |
| 4-8 | Loss of DTRs, muscle weakness |
| 8-12 | Respiratory depression |
| 12-15 | Hypotension, heart block, Cardiac Arrest, death |
Differential Diagnosis
- Renal Failure
- Lithium
- Volume depletion
- Rhabdo
- IV Mg (goal in PET/eclampsia 5-7 mEq/L)
- Massive PO intake (laxative abusers, accidental Epsom salts)
- Magnesium enemas[2]
Evaluation
- Magnesium level >3.5
Management
- IVF
- Furosemide 20-40mg IV
- Calcium chloride 10% 5-10mL IV or calcium gluconate 10% 15-30mL IV over 5min
- Consider hemodialysis for Mg >8 or poor renal function