Hypermagnesemia in Emergency Medicine Clinical Presentation

  • Author: Nona P Novello, MD; Chief Editor: Erik D Schraga, MD   more...
 
Updated: Jan 22, 2010
 

History

Common causes of hypermagnesemia include renal failure and iatrogenic manipulations. However, other diseases may result in increased magnesium; the degree of elevation determines the symptoms. Acute elevations of magnesium usually are more symptomatic than slow rises.

  • Magnesium levels of 2-4 mEq/L are associated with the following:
    • Nausea
    • Vomiting
    • Skin flushing
    • Weakness
    • Lightheadedness
  • High magnesium levels are associated with depressed levels of consciousness, respiratory depression, and cardiac arrest.
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Physical

Physical findings are related to the serum magnesium levels.

  • Serum magnesium levels of 3.5-5.0 mEq/L are associated with the following:
    • Disappearance of deep tendon reflexes
    • Muscle weakness
  • Serum magnesium levels of 5.0-6.0 mEq/L are related to the following:
    • Hypotension
    • Vasodilatation
  • Serum magnesium levels of 8.0-10.0 mEq/L are associated with the following:
    • Arrhythmia, including atrial fibrillation
    • Intraventricular conduction delay
    • Flaccid skeletal muscle paralysis
  • Levels of serum magnesium greater than 10.0 mEq/L are related to the following:
    • Asystole
    • Heart block
    • Ventilatory failure
    • Stupor or coma
    • Death
  • Elevated levels of magnesium also are associated with the following:
    • Delayed thrombin formation
    • Platelet clumping
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Causes

Most cases of hypermagnesemia are due to iatrogenic interventions and administration,[1] especially errors in calculating appropriate infusions. Additional causes include the following:

  • Ingestion of magnesium-containing substances such as vitamins, antacids, or cathartics by patients with chronic renal failure
  • Acute renal failure (in the absence of dialysis)
  • Excessive intravenous infusions of magnesium in patients being treated for eclampsia, asthma, torsade de pointes, or other cardiac arrhythmias
  • In neonates, treatment of maternal eclampsia with magnesium, which passes through the placental circulation
  • Decreased GI elimination and increased GI absorption of magnesium due to intestinal hypomotility from any cause
    • GI medications that decrease motility, including narcotics and anticholinergics
    • Hypomotility disorders such as bowel obstruction and chronic constipation
  • Tumor lysis syndrome, by releasing massive amounts of intracellular magnesium
  • Adrenal insufficiency (secondary hypermagnesemia)
  • Rhabdomyolysis, like tumor lysis syndrome, by releasing significant amounts of intracellular magnesium
  • Neoplasm with skeletal muscle involvement
  • Extracellular volume contraction, as in diabetic ketoacidosis (DKA)
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Contributor Information and Disclosures
Author

Nona P Novello, MD  Associate Chair, Department of Emergency Medicine, Franklin Square Hospital

Nona P Novello, MD is a member of the following medical societies: American College of Emergency Physicians and Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Howard A Blumstein, MD, FAAEM  Assistant Professor of Surgery, Medical Director, Department of Emergency Medicine, Wake Forest University School of Medicine

Howard A Blumstein, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Joseph J Sachter, MD, FACEP  Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center

Joseph J Sachter, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Jeffrey L Arnold, MD, FACEP  Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD  Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

References
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  3. Musso CG. Magnesium metabolism in health and disease. Int Urol Nephrol. 2009;41(2):357-62. [Medline].

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  10. Moe SM. Disorders of calcium, phosphorus, and magnesium. Am J Kidney Dis. Jan 2005;45(1):213-8. [Medline].

  11. Nadler JL, Rude RK. Disorders of magnesium metabolism. In: Clinical Disorders of Fluid and Electrolyte Metabolism. Vol 24. 1995:623-37.

  12. Qureshi T, Melonakos TK. Acute hypermagnesemia after laxative use. Ann Emerg Med. Nov 1996;28(5):552-5. [Medline].

  13. Usowicz MM, Gigg M, Jones LM. Allosteric interactions at L-type calcium channels between FPL 64176 and the enantiomers of the dihydropyridine Bay K 8644. J Pharmacol Exp Ther. Nov 1995;275(2):638-45. [Medline].

  14. Wilson RF, Barton C. Fluid and electrolyte problems. In: Emergency Medicine Comprehensive Study Guide. 1996:135-7.

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