eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Hypermagnesemia

Author: Nona P Novello, MD, Associate Chair, Department of Emergency Medicine, Franklin Square Hospital
Coauthor(s): Howard A Blumstein, MD, FAAEM, Assistant Professor, Surgery; Medical Director, Department of Emergency Medicine, Wake Forest University School of Medicine
Contributor Information and Disclosures

Updated: Nov 6, 2009

Introduction

Background

Magnesium is one of the body's major electrolytes. As the second most common intracellular cation, it plays a vital role in many cellular metabolic pathways.1 Magnesium is required for deoxyribonucleic acid (DNA) and protein synthesis. It is a necessary cofactor for most enzymes in phosphorylation reactions. It is also important for parathyroid hormone synthesis.

The total body content of this central cation is 2000 mEq, or 24 g. The magnesium is distributed in bone (67%), intracellularly (31%), and extracellularly (a mere 1%).2 The intracellular concentration is 40 mEq/L, while the normal serum concentration is 1.5-2.0 mEq/L. Of this serum component, 25-30% is protein bound, 10-15% is complexed, and the remaining 50-60% is ionized.

Magnesium is absorbed in the ileum and excreted in stool and urine. The minimum daily requirement of magnesium is 300-350 mg, or 15 mmol; this amount is easily obtainable with a normal daily intake of fruits, seeds, and vegetables because magnesium is a component of chlorophyll and is present in high concentrations in all green plants.

The kidney is the main regulator of magnesium concentrations. Absorption occurs primarily in the proximal tubule and thick ascending limb of the loop of Henle.

Hypermagnesemia is a rare electrolyte abnormality because the kidney is very effective in excreting excess magnesium.3

Pathophysiology

Magnesium excess affects the CNS, neuromuscular, and cardiac organ systems. It most commonly is observed in renal insufficiency and in patients receiving intravenous (IV) magnesium for treatment of a medical condition.4

Frequency

United States

Hypermagnesemia occurs only rarely in the United States.

Clinical

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.

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

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
  • Milk-alkali syndrome
  • Hypothyroidism
  • Hypoparathyroidism
  • Neoplasm with skeletal muscle involvement
  • Lithium intoxication
  • Extracellular volume contraction, as in diabetic ketoacidosis (DKA)

More on Hypermagnesemia

Overview: Hypermagnesemia
Differential Diagnoses & Workup: Hypermagnesemia
Treatment & Medication: Hypermagnesemia
Follow-up: Hypermagnesemia
References
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References

  1. Soave PM, Conti G, Costa R, Arcangeli A. Magnesium and anaesthesia. Curr Drug Targets. Aug 2009;10(8):734-43. [Medline].

  2. Kaze Folefack F, Stoermann Chopard C. [Magnesium metabolism disturbances]. Rev Med Suisse. Mar 7 2007;3(101):605-6, 608, 610-1. [Medline].

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

  4. Guillaume T, Krzesinski JM. [Management of serum magnesium abnormalities]. Rev Med Liege. Jul-Aug 2003;58(7-8):465-7. [Medline].

  5. Agus ZS, Wasserstein A, Goldfarb S. Disorders of calcium and magnesium homeostasis. Am J Med. Mar 1982;72(3):473-88. [Medline].

  6. Birrer RB, Shallash AJ, Totten V. Hypermagnesemia-induced fatality following epsom salt gargles(1). J Emerg Med. Feb 2002;22(2):185-8. [Medline].

  7. Gigg MA, Wolfson AB, Tayal VS. Electrolyte disturbances. In: Emergency Medicine Concepts and Clinical Practice. Vol 3. 1998:2445-8.

  8. Knochel JP. Disorders of magnesium metabolism. In: Harrison's Principles of Internal Medicine. Vol 2. 1994:2187-9.

  9. Londner M, Hammer D, Kelen G. Fluid and electrolyte problems. In: Emergency Medicine Comprehensive Study Guide. 2004:177-178.

  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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Further Reading

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Keywords

magnesium, high magnesium level, electrolytes, magnesium absorption, electrolyte abnormality, excess magnesium, renal insufficiency, intravenous magnesium, iatrogenic manipulation, adrenal insufficiency, secondary hypermagnesemia, hyperkalemia, hypercalcemia, magnesium toxicity, acute renal failure, maternal eclampsia, tumor lysis syndrome, rhabdomyolysis, milk-alkali syndrome, hypothyroidism, hypoparathyroidism, lithium intoxication, 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, 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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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.

CME Editor

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, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

 
 
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