eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Hypermagnesemia

Nona P Novello, MD, Associate Chair, Department of Emergency Medicine, Franklin Square Hospital
Howard A Blumstein, MD, FAAEM, Assistant Professor, Surgery; Medical Director, Department of Emergency Medicine, Wake Forest University School of Medicine

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)

Differential Diagnoses

Other Problems to Be Considered

Milk-alkali syndrome

Workup

Laboratory Studies

• Electrolytes, including potassium, magnesium, and calcium levels
  • A test for ionized magnesium is clinically available. However, it is used most often for monitoring magnesium infusions. The serum magnesium level is often used as an initial study in the ED.
  • Elevation in magnesium level is usually not found as an isolated electrolyte abnormality.
  • Hyperkalemia and hypercalcemia are often present concurrently.
• BUN and creatinine levels
  • Obtain renal function tests and calculate creatinine clearance to assess the ability of the kidney to excrete magnesium.
  • Serum magnesium levels rise when creatinine clearance is less than 30 mL/min.
• Check serum creatine phosphokinase (CPK) level or urine myoglobin level in patients in whom rhabdomyolysis is suspected.
• Arterial blood gases (ABG) may reveal a respiratory acidosis.
• Thyroid function tests
  • Hypothyroidism is a rare cause of hypermagnesemia.
  • Check these tests in the absence of any other good explanation.

Other Tests

• An ECG and cardiac monitor may show prolongation of the PR interval or intraventricular conduction delay, which are nonspecific findings.
• The ECG findings may reflect other electrolyte abnormalities such as hyperkalemia.

Treatment

Emergency Department Care

Although the effectiveness of dialysis in removing divalent cations is debated, some studies have demonstrated removal of a large amount of magnesium using this modality. Dialysis is best used when levels exceed 8 mEq/L, when life-threatening symptoms are present, or in patients with poor renal function.

• Assess the patient's ABCs and stabilize.
• Intubate if necessary.
• Treat hypotension with fluids.
• Treat arrhythmia as per advanced cardiac life support (ACLS) protocol or with treatment outlined below, if hypermagnesemia is known.
• Obtain appropriate studies as discussed in Workup.

Consultations

• Obtain a renal consultation for dialysis if the patient is severely hypermagnesemic.
• Arrange ICU monitoring if the symptoms are severe.

Medication

Treatment depends upon the level of magnesium and the presence of symptoms. In patients with mildly increased levels, simply stop the source of magnesium. In patients with higher concentrations or severe symptoms, other treatments are necessary. Calcium should be reserved for patients with life-threatening symptoms, such as arrhythmia or severe respiratory depression.

Intravenous fluids

Intravenous fluids work by dilution of the extracellular magnesium. Fluids are used with diuretics to promote increased excretion of magnesium by the kidney.

Normal saline or lactated Ringer solution

Both fluids are essentially isotonic, and, while some of their metabolic effects differ, the differences are clinically irrelevant for the purpose of promoting diuresis.

Dosing

Adult

1 L IV

Pediatric

20 mL/kg IV initially

Interactions

None reported

Contraindications

Poor renal function; inadequate urine output; pulmonary edema

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Administration of IV fluids requires close monitoring of cardiovascular and pulmonary function; fluids should be stopped when desired hemodynamic response is seen or pulmonary edema develops

Diuretics

These agents increase excretion of magnesium by the kidney.

Furosemide (Lasix)

Acts at loop of Henle to promote loss of magnesium in urine.

Dosing

Adult

20-80 mg/dose IV; single dose not to exceed 6 mg/kg

Pediatric

1 mg/kg/dose IV q6-12h prn

Interactions

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; aminoglycosides increase auditory toxicity—hearing loss of varying degrees may occur; may enhance anticoagulant activity of warfarin; may increase plasma lithium levels and toxicity

Contraindications

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, CO₂, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Mineral supplements

Calcium directly antagonizes the effects of magnesium. Reserved for patients with severe or symptomatic hypermagnesemia.

Calcium gluconate (Kalcinate)

Directly antagonizes neuromuscular and cardiovascular effects of magnesium. The 10% IV solution provides 100 mg/mL of calcium gluconate that equals 9 mg/mL (0.46 mEq/mL) of elemental calcium. One 10 mL ampule contains 93 mg of elemental calcium.

Dosing

Adult

100-200 mg 10% solution IV continuous infusion (2-4 mg/kg/h)

Pediatric

2 mg/kg of elemental calcium IV (about 20 mg/kg of calcium gluconate 10%)

Interactions

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels

Contraindications

Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia

Follow-up

Transfer

• Consider transfer if a patient with renal failure has a severe elevation of magnesium and no dialysis is available.

Prognosis

• Patients do well upon restoration of normal magnesium levels.

Patient Education

• Provide information regarding avoidance of medications that cause hypermagnesemia.

Miscellaneous

Medicolegal Pitfalls

• Not uncommonly, the cause of hypermagnesemia is iatrogenic.
• Complications of magnesium administration seen in the ED often are a function of the rate and/or concentration of delivery rather than the total amount administered.

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.

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

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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