eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Hypermagnesemia

Author: Anastasios K Konstantakos, MD, Clinical Associate Surgeon, Department of Cardiovascular Surgery, Billings Clinic, Billings, Montana
Contributor Information and Disclosures

Updated: May 5, 2009

Introduction

Background

Magnesium is the second most abundant intracellular cation and the fourth most abundant cation overall. Almost all enzymatic processes using phosphorus as an energy source require magnesium for activation.¹ Magnesium is involved in most biochemical reactions such as glycolysis and oxidative phosphorylation. Because magnesium is bound to adenosine triphosphate (ATP) inside the cell, shifts in intracellular magnesium concentration may help to regulate cellular bioenergetics.^2,3,4

Extracellularly, magnesium ions block neurosynaptic transmission by interfering with the release of acetylcholine. Magnesium ions also may interfere with the release of catecholamines from the adrenal medulla. In fact, magnesium has been proposed as being an endogenous endocrine modulator of the catecholamine component of the physiologic stress response.

Approximately 60% of total body magnesium is located in the bone, and the remainder is in the soft tissues. In this soft tissue intracellular compartment, which comprises about 38% of total body magnesium, relatively higher concentrations are found in the skeletal muscle and the liver. Because less than 2% is present in the extracellular fluid (ECF) compartment, serum levels do not necessarily reflect the status of total body stores of magnesium.

The reference range of serum concentration of magnesium is 1.8-2.5 mEq/L. Approximately one third of this magnesium is protein-bound. Analogous to plasma calcium, the free (ie, unbound) fraction of magnesium is the active component. Unfortunately, ionized serum magnesium cannot accurately be assessed at this time.

Less than 40% of dietary magnesium is absorbed; absorption takes place throughout the small intestine (predominantly in the ileum) and in the colon. A minimum daily intake of magnesium of 0.3 mEq/kg of body weight has been suggested to prevent deficiency. However, infants and children tend to have higher daily requirements of magnesium.

Elimination is predominantly renal; the threshold for urinary excretion nears the reference range of serum concentration. Thus, when serum levels are greater than 2.5 mEq/L, magnesium excretion dramatically increases. Conversely, the kidney retains a strong capacity to resorb magnesium, and the main site for reabsorption is the thick ascending loop of Henle.

Pathophysiology

Hypermagnesemia is defined as a serum concentration greater than 2.5 mEq/L. (The reference range of serum magnesium levels is 1.8-2.5 mEq/L.) Most cases of hypermagnesemia have been noted in patients with severe renal failure in whom magnesium intake has been excessive. This may result from iatrogenic administration of medications that contain magnesium. Fatal hypermagnesemia has resulted from the administration of enemas containing magnesium to patients with renal failure. In fact, hypermagnesemia is rarely observed in individuals with a glomerular filtration rate (GFR) that is within reference range. In patients with acute renal failure and hypermagnesemia, levels usually remain less than 4 mEq/L.

Rapid mobilization of magnesium from soft tissues may result in hypermagnesemia following trauma, shock, cardiac arrest, or burns.

Hypermagnesemia usually occurs in individuals with significant diabetic ketoacidosis and often turns into hypomagnesemia during treatment. Thus, the initial hypermagnesemia is likely a pseudo-elevation secondary to dehydration, and the resulting hypomagnesemia may reflect intracellular shifting following insulin administration.

Neonates with hypermagnesemia whose mothers have received intravenous magnesium sulfate for pregnancy-induced hypertension may present with respiratory impairment, generalized hypotonia, and GI hypomotility mimicking intestinal obstruction. Pregnancy in women who have congenital cardiac disease is associated with increased risk, but favorable outcomes occur in most cases.⁶

Frequency

United States

Although the occurrence of hypermagnesemia has not been precisely defined, the disorder tends to occur in certain patient populations, particularly in patients with preexisting renal insufficiency.

Age

Although no age predisposition to developing hypermagnesemia is noted per se, neonates whose mothers have been treated with magnesium sulfate for eclampsia may be born with significant elevations in serum magnesium concentration, which can range from 3-11 mEq/L.

Clinical

History

• Symptoms of hypermagnesemia are nonspecific at lower levels (2-4 mEq/L) and may include the following:
  • Nausea
  • Vomiting
  • Flushing
  • Lethargy
  • Weakness
  • Dizziness
• Higher levels may lead to a depressed sensorium, and cardiopulmonary arrest may occur at extreme levels (>10-15 mEq/L).

Physical

• Hypermagnesemia results in loss of deep-tendon reflexes at levels of 4-6 mEq/L. At magnesium levels of more than 5 mEq/L, CNS depression, which may range from drowsiness to coma, begins. Although concentrations of magnesium greater than 10 mEq/L lead to respiratory depression in adults, this may occur at much lower levels in the newborn.
• Hypermagnesemia has a negative effect on heart rate.⁷ Beginning with magnesium serum levels of 4.5 mEq/L, depression of sinoatrial node activity and atrial fibrillation may occur. Higher magnesium levels increase the P-R interval, widen the QRS complex, and can cause intraventricular conduction delays. Serum magnesium concentrations greater than 15 mEq/L can lead to complete heart block and asystole.
• At varying levels (5-8 mEq/L), hypermagnesemia may produce vasodepression of vascular smooth muscle leading to systemic hypotension.
• Although the absolute serum levels are important, the rate of rise is even more significant. For instance, a fast rise in serum level can produce cardiovascular symptoms more readily than can a slower rise in serum levels.

Causes

• Major predisposing factors for the development of hypermagnesemia include the following:
  • Renal failure (acute or chronic)
  • Iatrogenic overadministration of magnesium
  • Neonates born to mothers treated with magnesium sulfate for eclampsia

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