Hypermagnesemia in Emergency Medicine

Updated: Jun 23, 2022
Author: Nona P Novello, MD; Chief Editor: Erik D Schraga, MD 


Practice Essentials

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 occurs only rarely in the United States. Hypermagnesemia is a rare electrolyte abnormality because the kidney is very effective in excreting excess magnesium.[3]  

Pathophysiology and Etiology


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]


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)


Patients do well upon restoration of normal magnesium levels.


A study by Haider et al that screened 5339 patients with plasma magnesium concentrations reported that 36.9% of the 151 patients with hypermagnesemia died and that hypermagnesemia was a strong independent risk factor for mortality.[5]  A study by Stevens et al found that hypermagnesemia was associated with increased mortality in patients with severe COVID-19. The probability of survival at 30 days was 34% for patients with hypermagnesemia and 65% for those without hypermagnesemia.[6]


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.

Patient Education

Provide information to patients regarding avoidance of medications that cause hypermagnesemia.

For patient education resources, see Poisoning.




Common causes of hypermagnesemia include renal failure and iatrogenic manipulations.[7] 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 Examination

Physical findings are related to the serum magnesium levels.

Serum magnesium levels of 3.5-5 mEq/L are associated with the following:

  • Disappearance of deep tendon reflexes

  • Muscle weakness

Serum magnesium levels of 5-6 mEq/L are related to the following:

  • Hypotension

  • Vasodilatation

Serum magnesium levels of 8-10 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 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





Laboratory Studies

Electrolytes, including potassium, magnesium, and calcium levels[8, 9]

  • 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.



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.

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


Obtain a renal consultation for dialysis if the patient is severely hypermagnesemic.

Arrange ICU monitoring if the symptoms are severe.



Medication Summary

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

Class Summary

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.


Class Summary

These agents increase excretion of magnesium by the kidney.

Furosemide (Lasix)

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

Mineral supplements

Class Summary

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.