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
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]
Etiology
Most cases of hypermagnesemia are due to iatrogenic interventions and administration, [1] especially errors in calculating appropriate infusions. Additional causes include the following:
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Ingestion of magnesium-containing substances such as vitamins, antacids, or cathartics by patients with chronic renal failure
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Acute renal failure (in the absence of dialysis)
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Excessive intravenous infusions of magnesium in patients being treated for eclampsia, asthma, torsade de pointes, or other cardiac arrhythmias
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In neonates, treatment of maternal eclampsia with magnesium, which passes through the placental circulation
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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
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Tumor lysis syndrome, by releasing massive amounts of intracellular magnesium
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Adrenal insufficiency (secondary hypermagnesemia)
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Rhabdomyolysis, like tumor lysis syndrome, by releasing significant amounts of intracellular magnesium
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Neoplasm with skeletal muscle involvement
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Extracellular volume contraction, as in diabetic ketoacidosis (DKA)
Prognosis
Patients do well upon restoration of normal magnesium levels.
Morbidity/mortality
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
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.
